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

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    Zhi-Hua Chen

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

  2. 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

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

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    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.

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

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    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

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

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    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.

  6. Cigarette smoke induces an unfolded protein response in the human lung: a proteomic approach.

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    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.

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

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    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.

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

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    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.

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

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    Toorn, Marco van der

    2009-01-01

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

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

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    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.

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

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    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

  12. 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.

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

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    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

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

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    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

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

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    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.

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

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

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    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

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

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    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

  19. 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.

  20. 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.

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

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    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.

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

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    张劲农; 陶晓南; 谢建敏; 向敏; 付薇

    2003-01-01

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

  3. 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

  4. 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

  5. Ibuprofen prevents synthetic smoke-induced pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Shinozawa, Y.; Hales, C.; Jung, W.; Burke, J.

    1986-12-01

    Multiple potentially injurious agents are present in smoke but the importance of each of these agents in producing lung injury as well as the mechanisms by which the lung injury is produced are unknown. In order to study smoke inhalation injury, we developed a synthetic smoke composed of a carrier of hot carbon particles of known size to which a single known common toxic agent in smoke, in this case HCI, could be added. We then exposed rats to the smoke, assayed their blood for the metabolites of thromboxane and prostacyclin, and intervened shortly after smoke with the cyclooxygenase inhibitors indomethacin or ibuprofen to see if the resulting lung injury could be prevented. Smoke exposure produced mild pulmonary edema after 6 h with a wet-to-dry weight ratio of 5.6 +/- 0.2 SEM (n = 11) compared with the non-smoke-exposed control animals with a wet-to-dry weight ratio of 4.3 +/- 0.2 (n = 12), p less than 0.001. Thromboxane B, and 6-keto-prostaglandin F1 alpha rose to 1660 +/- 250 pg/ml (p less than 0.01) and to 600 +/- 100 pg/ml (p greater than 0.1), respectively, in the smoke-injured animals compared with 770 +/- 150 pg/ml and 400 +/- 100 pg/ml in the non-smoke-exposed control animals. Indomethacin (n = 11) blocked the increase in both thromboxane and prostacyclin metabolites but failed to prevent lung edema.

  6. 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.

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

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    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.

  8. 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.

  9. 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.

  10. 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.

  11. 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

  12. 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

  13. 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.

  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. 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...

  17. 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.

  18. 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.

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

    Science.gov (United States)

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

    2015-05-01

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

  20. Linalool inhibits cigarette smoke-induced lung inflammation by inhibiting NF-κB activation.

    Science.gov (United States)

    Ma, Jianqun; Xu, Hai; Wu, Jun; Qu, Changfa; Sun, Fenglin; Xu, Shidong

    2015-12-01

    Linalool, a natural compound that exists in the essential oils of several aromatic plants species, has been reported to have anti-inflammatory effects. However, the effects of linalool on cigarette smoke (CS)-induced acute lung inflammation have not been reported. In the present study, we investigated the protective effects of linalool on CS-induced acute lung inflammation in mice. Linalool was given i.p. to mice 2h before CS exposure daily for five consecutive days. The numbers of macrophages and neutrophils in bronchoalveolar lavage fluid (BALF) were measured. The production of TNF-α, IL-6, IL-1β, IL-8 and MCP-1 were detected by ELISA. The expression of NF-κB was detected by Western blotting. Our results showed that treatment of linalool significantly attenuated CS-induced lung inflammation, coupled with inhibited the infiltration of inflammatory cells and TNF-α, IL-6, IL-1β, IL-8 and MCP-1 production. Meanwhile, treatment of linalool inhibited CS-induced lung MPO activity and pathological changes. Furthermore, linalool suppressed CS-induced NF-κB activation in a dose-dependent manner. In conclusion, our results demonstrated that linalool protected against CS-induced lung inflammation through inhibiting CS-induced NF-κB activation.

  1. 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.

  2. 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

  3. 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.

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

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    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.

  5. 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.

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

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    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

  7. 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.

  8. 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.

  9. 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.

  10. 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

  11. 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.

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

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    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.

  13. 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.

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

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    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.

  15. 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

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

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    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

  17. 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.

  18. 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

  19. 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.

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

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    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

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

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    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.

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

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    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.

  3. 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

  4. 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.

  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.

  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. 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.

  9. 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.

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

    Science.gov (United States)

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

    2013-06-15

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

  11. 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.

  12. 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.

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

    Institute of Scientific and Technical Information of China (English)

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

    2008-01-01

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

  14. Establishment of a Rabbit Model of Smoke-Induced Chronic Obstructive Pulmonary Disease%构建单纯烟熏至慢性阻塞性肺疾病兔模型

    Institute of Scientific and Technical Information of China (English)

    王培培; 邢珍; 刘全乐; 王锦川; 焦宝良; 王新生; 刘军超; 李福龙

    2013-01-01

    To establishment of a rabbit model of smoke-induced chronic obstructive pulmonary disease.Methods:Cut tobacco was used as irritant to prepare chronic obstructive pulmonary disease models,Those rabbits in smoke-induced model group were in self-made smoke cage,Pure cut tobacco 15g was burned at a time.Those rabbits in normal control group were not exposed to smoke.Exposed to smoker for 0.5 hour once,2 times per day,lasted for 70 days.All rabbits were anesthetized at no smoking for 1 week after the last smoke exposure,the arterial blood gases were analyzed before being sacrificed.Protein content in right lung bronchoalveolar lavage fluid (BALF) was measured and leukocyte count and classification were also done.The removed left lung tissues were stained with hematoxylin-eosin for histomorphology observation.Results:Totally 11 rabbits were involved in the analysis.When compared with normal control group,in smoke-induced model group,there were plenty of inflammatoty cells infiltrated in bronchial walls.Protein content and total mumber of leukocytes in BALF were increased significantly(p<0.05); PO2 and SaO2 were significantly lower (p<0.05),PCO2 were significantly higher (p<0.05).Conclusion:A smoke-induced chronic obstructive pulmonary disease rabbit model was established successfully,and it should endure a long time one-lung ventilation after being anesthetized.%目的:构建烟熏至慢性阻塞性肺疾病兔模型.方法:利用自制的方法采用单纯旱烟烟熏兔70d停1周,麻醉后行血气分析,处死后右肺进行支气管灌洗液分析,左肺作病理切片.结果:与正常饲养兔相比,烟熏兔肺泡灌洗液中蛋白含量显著增加,白细胞总数显著增加,分类中中性粒细胞比例增加:动脉氧分压(PO2)明显降低(P<0.05),二氧化碳分压(PCO2)增高(P<0.05),动脉血氧饱和度明显下降(p<0.05).结论:自制方法成功构建慢性阻塞性肺疾病兔模型,并能耐受麻醉过程中长时间单肺通气.

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

    Directory of Open Access Journals (Sweden)

    Nagai A

    2003-09-01

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

  16. 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.

  17. 构建单纯烟熏至慢性阻塞性肺疾病兔模型%Establishment of a Rabbit Model of Smoke-induced Chronic Obstructive Pulmonary Disease

    Institute of Scientific and Technical Information of China (English)

    王培培; 邢珍; 刘全乐; 王锦川; 焦宝良; 王新生; 刘军超; 李福龙

    2012-01-01

    objective: To establishment of a rabbit model of smoke-induced chronic obstructive pulmonary disease. Methods: Cut tobacco was used as irritant to prepare chronic obstructive pulmonary disease models, Those rabbits in smoke—induced model group were in self-made smoke cage, Pure cut tobacco 15g was burned at a time. Those rabbits in normal control group were not exposed to smoke. Exposed to smoker for 0.5 hour once, 2 times per day, lasted for 70 days. All rabbits were anesthetized at no smoking for 1 week after the last smoke exposure , the arterial blood gases were analyzed before being sacrificed. Protein content in right lung bronchoalveolar lavage fluid (BALF) was measured and leukocyte count and classification were also done. The removed left lung tissues were stained with hematoxylin—eosin for histomorphology observation. Results: Totally 11 rabbits were involved in the analysis. When compared with normal control group, in smoke—induced model group, there were plenty of inflammatoty cells infiltrated in bronchial walls. Protein content and total mumber of leukocytes in BALF were increased significantly (p<0.05); P02 and SaO2 were significantly lower (p<0.05), PCO2 were significantly higher (p<0.05). Conclusion: A smoke—induced chronic obstructive pulmonary disease rabbit model was established successfully,and it should endure a long time one—lung ventilation after beihg anesthetized.%目的:构建烟熏至慢性阻塞性肺疾病兔模型.方法:利用自制的方法采用单纯旱烟烟熏兔70 d停1周,麻醉后行血气分析,处死后右肺进行支气管灌洗液分析,左肺作病理切片.结果:与正常饲养兔相比,烟熏兔肺泡灌洗液中蛋白含量显著增加,白细胞总数显著增加,分类中中性粒细胞比例增加:动脉氧分压(PO2)明显降低(P<0.05),二氧化碳分压(PCO2)增高(P<0.05),动脉血氧饱和度明显下降(P<0.05).结论:自制方法成功构建慢性阻塞性肺疾病兔模型,并能耐受麻

  18. Aloe vera affects changes induced in pulmonary tissue of mice caused by cigarette smoke inhalation.

    Science.gov (United States)

    Koul, Ashwani; Bala, Shashi; Yasmeen; Arora, Neha

    2015-09-01

    This study was undertaken to determine the influence of Aloe vera (AV) on changes induced in pulmonary tissue of cigarette smoke (CS) inhaling mice. CS inhalation for 4 weeks caused pulmonary damage as evident by histoarchitectural alterations and enhanced serum and tissue lactate dehydrogenase (LDH) activities. CS inhalation also led to increased mucin production as revealed by mucicarmine and Alcian Blue-Periodic Acid Schiff (AB-PAS) staining. Studies on bronchoalveolar lavage fluid (balf) of CS exposed animals revealed structural changes in phospholipids and increase in surface tension when compared with control counterparts. These changes were accompanied by enhanced nitric oxide (NO) levels, citrulline levels, peroxidative damage, and differential modulation of antioxidant defense system. AV administration (seven weeks, 500 mg/kg b.w. daily) to CS inhaling mice led to modulation of CS induced pulmonary changes as revealed by lesser degree of histoarchitectural alterations, lesser mucin production, decreased NO levels, citrulline levels, peroxidative damage, and serum LDH activity. AV treatment to CS inhaling mice was associated with varying response to antioxidant defense system, however balf of CS + AV treated animals did not exhibit appreciable changes when compared with that of CS exposed animals. These observations suggest that AV has the potential to modulate CS induced changes in the pulmonary tissue which could have implications in management of CS associated pulmonary diseases, however, further investigations are required to explore its complete mechanism of action.

  19. 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.

  20. IMPACT OF CIGARETTE SMOKING ON RATES AND CLINICAL PROGNOSIS OF PULMONARY TUBERCULOSIS IN SOUTHERN MEXICO

    Science.gov (United States)

    Bonacci, Robert A.; Cruz-Hervert, Luis Pablo; García-García, Lourdes; Reynales-Shigematsu, Luz Myriam; Ferreyra-Reyes, Leticia; Bobadilla-del-Valle, Miriam; Canizales-Quintero, Sergio; Ferreira-Guerrero, Elizabeth; Báez-Saldaña, Renata; Téllez-Vázquez, Norma; Mongua-Rodríguez, Norma; Montero-Campos, Rogelio; Delgado-Sánchez, Guadalupe; Martínez-Gamboa, Rosa Areli; Cano-Arellano, Bulmaro; Sifuentes-Osornio, José; de León, Alfredo Ponce

    2012-01-01

    Objectives To examine the relationship between cigarette smoking and incidence and mortality rates of pulmonary tuberculosis (TB) and treatment outcomes. Materials From 1995-2010, we analyzed data from 1062 patients with TB and from 2001-2004, 2951 contacts in Southern Mexico. Patients with acid-fast bacilli or Mycobacterium tuberculosis in sputum samples underwent epidemiological, clinical and mycobacteriological evaluation and received treatment by the local DOTS program. Results Consumers of 1-10 (LS) or 11 or more (HS) cigarettes per day incidence (1.75 and 11.79) and mortality (HS,17.74) smoker-nonsmoker rate ratios were significantly higher for smokers. Smoker population was more likely to experience unfavorable treatment outcomes (HS, adjusted OR 2.36) and retreatment (LS and HS, adjusted hazard ratio (HR) 2.14 and 2.37). Contacts that smoked had a higher probability of developing active TB (HR 2.38) during follow up. Conclusions Results indicate the need of incorporating smoking prevention and cessation, especially among men, into international TB control strategies. PMID:22982014

  1. 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.

  2. 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:

  3. 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:

  4. 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.

  5. 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 ...

  6. Exposure to electronic cigarettes impairs pulmonary anti-bacterial and anti-viral defenses in a mouse model.

    Directory of Open Access Journals (Sweden)

    Thomas E Sussan

    Full Text Available Electronic cigarettes (E-cigs have experienced sharp increases in popularity over the past five years due to many factors, including aggressive marketing, increased restrictions on conventional cigarettes, and a perception that E-cigs are healthy alternatives to cigarettes. Despite this perception, studies on health effects in humans are extremely limited and in vivo animal models have not been generated. Presently, we determined that E-cig vapor contains 7 x 10(11 free radicals per puff. To determine whether E-cig exposure impacts pulmonary responses in mice, we developed an inhalation chamber for E-cig exposure. Mice that were exposed to E-cig vapor contained serum cotinine concentrations that are comparable to human E-cig users. E-cig exposure for 2 weeks produced a significant increase in oxidative stress and moderate macrophage-mediated inflammation. Since, COPD patients are susceptible to bacterial and viral infections, we tested effects of E-cigs on immune response. Mice that were exposed to E-cig vapor showed significantly impaired pulmonary bacterial clearance, compared to air-exposed mice, following an intranasal infection with Streptococcus pneumonia. This defective bacterial clearance was partially due to reduced phagocytosis by alveolar macrophages from E-cig exposed mice. In response to Influenza A virus infection, E-cig exposed mice displayed increased lung viral titers and enhanced virus-induced illness and mortality. In summary, this study reports a murine model of E-cig exposure and demonstrates that E-cig exposure elicits impaired pulmonary anti-microbial defenses. Hence, E-cig exposure as an alternative to cigarette smoking must be rigorously tested in users for their effects on immune response and susceptibility to bacterial and viral infections.

  7. Exposure to electronic cigarettes impairs pulmonary anti-bacterial and anti-viral defenses in a mouse model.

    Science.gov (United States)

    Sussan, Thomas E; Gajghate, Sachin; Thimmulappa, Rajesh K; Ma, Jinfang; Kim, Jung-Hyun; Sudini, Kuladeep; Consolini, Nicola; Cormier, Stephania A; Lomnicki, Slawo; Hasan, Farhana; Pekosz, Andrew; Biswal, Shyam

    2015-01-01

    Electronic cigarettes (E-cigs) have experienced sharp increases in popularity over the past five years due to many factors, including aggressive marketing, increased restrictions on conventional cigarettes, and a perception that E-cigs are healthy alternatives to cigarettes. Despite this perception, studies on health effects in humans are extremely limited and in vivo animal models have not been generated. Presently, we determined that E-cig vapor contains 7 x 10(11) free radicals per puff. To determine whether E-cig exposure impacts pulmonary responses in mice, we developed an inhalation chamber for E-cig exposure. Mice that were exposed to E-cig vapor contained serum cotinine concentrations that are comparable to human E-cig users. E-cig exposure for 2 weeks produced a significant increase in oxidative stress and moderate macrophage-mediated inflammation. Since, COPD patients are susceptible to bacterial and viral infections, we tested effects of E-cigs on immune response. Mice that were exposed to E-cig vapor showed significantly impaired pulmonary bacterial clearance, compared to air-exposed mice, following an intranasal infection with Streptococcus pneumonia. This defective bacterial clearance was partially due to reduced phagocytosis by alveolar macrophages from E-cig exposed mice. In response to Influenza A virus infection, E-cig exposed mice displayed increased lung viral titers and enhanced virus-induced illness and mortality. In summary, this study reports a murine model of E-cig exposure and demonstrates that E-cig exposure elicits impaired pulmonary anti-microbial defenses. Hence, E-cig exposure as an alternative to cigarette smoking must be rigorously tested in users for their effects on immune response and susceptibility to bacterial and viral infections.

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

    Science.gov (United States)

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

    2011-01-01

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

  9. A Cancer That Went Up in Smoke: Pulmonary Reaction to e-Cigarettes Imitating Metastatic Cancer

    DEFF Research Database (Denmark)

    Madsen, Lene Margrethe Ring; Vinther Krarup, Niels Henrik; Bergmann, Troels Korshøj;

    2016-01-01

    e-Cigarettes have gained worldwide popularity as a substitute for smoking, but concern has been raised regarding the long-term effects associated with their use. We report a case of a 45-year-old female consumer of e-cigarettes who presented with 4 months of abdominal pain and fever. Initial....... Upon cessation of e-cigarette use (known as vaping), the lung nodules disappeared, and the liver lesions regressed. Our case report suggests that vaping can induce an inflammatory reaction mimicking metastatic cancer....

  10. Effect of Simvastatin on 5-HT and 5-HTT in a Rat Model of Pulmonary Artery Hypertension

    Directory of Open Access Journals (Sweden)

    Xue Jiang

    2015-11-01

    Full Text Available Background/Aims: To investigaterole of serotonin (5-HT and serotonin transporter (5-HTT in a rat model of cigarette smoke-induced pulmonary artery hypertension (PAH and the effect of statins on regulating 5HT and 5-HTT. Methods: A rat model of COPD comorbid with PAH was established by cigarette smoke exposure with or without simvastatin administration. The smoking and the simvastatin plus smoking groups were exposed to cigarette smoke daily, and the latter received simvastatin at 5mg/kg, once a day. After 16 weeks of cigarette smoke exposure, body weight and mean pulmonary arterial pressure (mPAP were measured, bronchoalveolar lavage (BAL was performed, and lung tissues and blood samples were collected to determine cardiopulmonary pathology, physiological indices, blood levelof 5-HT and expression of 5-HTT in the lung. Results: In addition to alveolar structural damage (COPD-like injury, chronic cigarette smoke exposure lead to pulmonary artery remodeling and PAH as evidenced by significant elevation of mPAP, RVHI, WT%and WA%. Cigarette smoke exposure resulted in significant reduction in animal body weight, and simvastatin significantly prevented smoke-induced weight loss. The number of inflammatory cells in BALF was dramatically increased in smoke exposed rats, and simvastatin dampened the number of leukocytes, neutrophils, lymphocytes, and macrophages. In addition, circulating 5-HTand expression of 5-HTT in the lung were significantly increased in the smoked rats compared to control rats, and it was significantly reduced by simvastatin. Alteration of BALF inflammatory cells, 5-HT and 5-HTT was significantly correlated with changes of mPAP, RVHI, WT% and WA%. Conclusions: Cigarette smoke exposure could result in not only COPD, but also PAH, which may attribute to the alteration of blood 5-HT and lung tissue 5-HTT. Simvastatin could significantly inhibited 5-HT and 5-HTT expression, and by which mechanism, it may protect animals from development

  11. Cigarette smoking and pulmonary function in adult survivors of childhood cancer exposed to pulmonary-toxic therapy: results from the St. Jude lifetime cohort study.

    Science.gov (United States)

    Oancea, S Cristina; Gurney, James G; Ness, Kirsten K; Ojha, Rohit P; Tyc, Vida L; Klosky, James L; Srivastava, DeoKumar; Stokes, Dennis C; Robison, Leslie L; Hudson, Melissa M; Green, Daniel M

    2014-09-01

    Treatments for childhood cancer can impair pulmonary function. We assessed the potential impact of cigarette smoking on pulmonary function in 433 adult childhood cancer survivors (CCS) who received pulmonary-toxic therapy, using single breath diffusion capacity for carbon monoxide corrected for hemoglobin (DLCOcorr), forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and total lung capacity (TLC). FEV1/FVC median values among current [1.00; interquartile range (IQR): 0.94-1.04] and former smokers (0.98; IQR: 0.93-1.04) were lower than those who had never smoked (1.02; IQR: 0.96-1.06; P = 0.003). Median FEV1/FVC values were lower among those who smoked ≥ 6 pack-years (0.99; IQR: 0.92-1.03) and those who smoked <6 pack-years (1.00; IQR: 0.94-1.04), than among those who had never smoked (P = 0.005). Our findings suggest that CCSs have an increased risk for future obstructive and restrictive lung disease. Follow-up is needed to determine whether smoking imparts more than additive risk. Smoking prevention and cessation need to be a priority in this population.

  12. Pulmonary langerhans cell histiocytosis

    Directory of Open Access Journals (Sweden)

    Suri Harpreet S

    2012-03-01

    Full Text Available Abstract Pulmonary Langerhans Cell Histiocytosis (PLCH is a relatively uncommon lung disease that generally, but not invariably, occurs in cigarette smokers. The pathologic hallmark of PLCH is the accumulation of Langerhans and other inflammatory cells in small airways, resulting in the formation of nodular inflammatory lesions. While the overwhelming majority of patients are smokers, mechanisms by which smoking induces this disease are not known, but likely involve a combination of events resulting in enhanced recruitment and activation of Langerhans cells in small airways. Bronchiolar inflammation may be accompanied by variable lung interstitial and vascular involvement. While cellular inflammation is prominent in early disease, more advanced stages are characterized by cystic lung destruction, cicatricial scarring of airways, and pulmonary vascular remodeling. Pulmonary function is frequently abnormal at presentation. Imaging of the chest with high resolution chest CT scanning may show characteristic nodular and cystic abnormalities. Lung biopsy is necessary for a definitive diagnosis, although may not be required in instances were imaging findings are highly characteristic. There is no general consensus regarding the role of immunosuppressive therapy in smokers with PLCH. All smokers must be counseled on the importance of smoking cessation, which may result in regression of disease and obviate the need for systemic immunosuppressive therapy. The prognosis for most patients is relatively good, particularly if longitudinal lung function testing shows stability. Complications like pneumothoraces and secondary pulmonary hypertension may shorten life expectancy. Patients with progressive disease may require lung transplantation.

  13. CCR1 and CCR5 expression on inflammatory cells is related to cigarette smoking and chronic obstructive pulmonary disease severity

    Institute of Scientific and Technical Information of China (English)

    WANG Fei; HE Bei

    2012-01-01

    Background Chronic obstructive pulmonary disease (COPD) is a progressive disease associated with a cellular inflammatory response mostly concerned with cigarette smoking.Chemokine receptors CCR1/5 play an important role in the inflammatory cells recruitment in the lung of COPD patients.The aim of this study was to determine the impact of cigarette smoking on the expression of CCR1/5 on inflammatory cells in induced sputum,and the relationship between the receptors expression and COPD severity.Methods Differential cells in induced sputum were counted and the optical densities of CCR1 and CCR5 on inflammatory cells in induced sputum from COPD patients (n=29),healthy smokers (n=11),and nonsmokers (n=6) were measured using immunocytochemistry.Concentrations of CCL3,the ligand of CCR1/5,in supernatant of induced sputum were detected by enzyme-linked immunosorbent assay.Results The expressions of CCR1 and CCR5 on inflammatory cells in healthy smokers were significantly higher than those in nonsmokers,and the expression of CCR1 in patients with COPD was significantly increased when compared with nonsmokers but not healthy smokers.The expressions of CCR1 and CCR5 on inflammatory cells in severe and very severe COPD patients were higher compared with mild and moderate COPD patients.CCL3 level was positively correlated with the total cell counts in induced sputum and smoking history,and negatively correlated with percentage of predicted FEV1.Conclusions Cigarette smoking could increase the expression of CCR1 on the inflammatory cells.Both CCR1 and CCR5 expressions on the inflammatory cells in induced sputum could be associated with COPD severity.

  14. Development and characterization of a rat model of chronic obstructive pulmonary disease (COPD) induced by sidestream cigarette smoke.

    Science.gov (United States)

    Zheng, Hongao; Liu, Yuening; Huang, Tian; Fang, Zheman; Li, Guishuang; He, Shaoheng

    2009-09-28

    Cigarette smoke (CS) induced chronic obstructive pulmonary disease (COPD) has been emerging as a great health problem in China. However, lack of appropriate animal model slows down the progress in understanding pathogenesis of the disease. The aim of current study is to establish and evaluate a more adequate rat model of COPD. Study was performed with rats exposed to sidestream cigarette smoke 2h/d and 7d/wk for 2, 4, 6, 8, 10, 12, 24 and 36 wk in a CS chamber (carbon monoxide concentration was 231+/-11ppm). The lung function was determined by using the forced oscillation technique. Pathologic changes were determined by using histological analyses and mucin measurement. Following 36-wk exposure, airway resistance (Raw) and respiratory system elastance (Ers) in CS group rats was elevated by 28.5% and 37.5%, respectively. Up to 4.1-, 2.3- and 1.4-fold increase in the number of neutrophils, macrophages and lymphocytes was observed in the BALF of CS rats. Using quantitative histomorphology techniques, it was found that mean linear intercept (MLI) and mean alveolar airspace (MAA) of CS rats increased by 44.8% and 43.7%, respectively, indicating the occurrence of emphysema. The characteristics of chronic bronchitis including hyperplasia of bronchial epithelial cells, hypersecretion of mucus and development of peribronchial fibrosis were also found in rat lungs. CS group rats showed 43% body weight gain reduction. To conclude, a more adequate sidestream cigarette smoke rat COPD model was established, which will be beneficial for understanding the pathogenesis of the disease and for evaluation of drug effectiveness.

  15. 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.

  16. Early smoking-induced lung lesions in asymptomatic subjects. Correlations between high resolution dynamic CT and pulmonary function testing; Danno polmonare precoce da fumo in soggetti asintomatici. Studio correlativo con TC dinamica ad elevata risoluzione e test di funzionalita' respiratoria

    Energy Technology Data Exchange (ETDEWEB)

    Spaggiari, Enrica; Zompadori, Maurizio; Bna' , Claudio; Ormitti, Francesca; Svaerzellati, Nicola; Rabaiotti, Enrico [Parma Univ., Parma (Italy). Sezione di Diagnostica per Immagini e UO di Scienze Radiologiche Dipartimento di Scienze Cliniche; Verduri, Alessia; Chetta, Alfredo [Parma Univ., Parma (Italy). Sezione Clinica Pneumologica

    2005-02-01

    Purpose: To evaluate the prevalence and significance of the pathological effects of cigarette smoking on the lung and the sensitivity of high-resolution CT (HRCT) in the recognition of early smoking-induced lesions in asymptomatic former of current smokers. Materials and methods: We performed a prospective and consecutive analysis of 36 volunteers (16 males, 20 females), 10 non-smokers (3 males, 7 females) and 26 smokers (13 males, 13 females / 17 current smokers; 9 former smokers), all asymptomatic and with normal respiratory flows. These subjects underwent lung function testing and HRCT, after providing written informed consent for the study. The HRCT scans were obtained at three pre-selected levels (aortic arch, tracheal carina and venous hilum). The same scans were obtained in post-expiration phase. At the level of the apical segmental bronchus of the right upper lobe, we measured on the monitor wall thickening, and the total and internal diameters using the techniques reported in literature. Each study was independently evaluated by two radiologists that were blinded to all clinical and functional data: they also evaluated the presence, prevalence and type of emphysema, areas of patchy hyperlucency and oligoemia in the inspiration phase and areas of expiratory air trapping. The extension was evaluated with the visual score method. The data obtained were analysed with the Windows SPSS package for statistical analysis. Results: The two groups (non smokers and smokers) showed significant differences in some functional tests such as FEV1 (p<0.005) and Tiffeneau index (p<0.005) which were lower in current-smokers or former-smokers, although still within the normal range. The HRCT study did not show areas of emphysema or air trapping in non smokers. In the smokers' group, air trapping was observed in 30.7% of cases: 33% former-smokers and 29.4% current smokers (mean extension was 21.36% in former smokers and 9.48% in current smokers). Mean extension in the

  17. Prevalence of chronic obstructive pulmonary disease among adult male cigarettes smokers: a community-based study in Jordan

    Directory of Open Access Journals (Sweden)

    Al Omari M

    2014-07-01

    Full Text Available Mousa Al Omari,1 Basheer Y Khassawneh,2 Yousef Khader,1 Ali Shakir Dauod,1 George Bergus3 1Department of Community Medicine, Public Health and Family Medicine, Faculty of Medicine, Jordan University of Science and Technology, 2Department of Internal Medicine, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan; 3Department of Family Medicine, Carver College of Medicine, University of Iowa, Iowa City, IA, USA Abstract: Chronic obstructive pulmonary disease (COPD is a leading cause of morbidity and mortality worldwide. The prevalence of COPD among cigarette smokers in the Middle East is not well studied. A prospective descriptive study was performed in the north of Jordan. Male cigarette smokers (≥10 pack-year aged 35 years and older were recruited from the community. They completed a questionnaire and a postbronchodilator spirometry. Global Initiative for Chronic Obstructive Lung Disease (GOLD criteria (postbronchodilator forced expiratory volume in 1 second <70% was used to define COPD. A total of 512 subjects completed the study protocol. According to the GOLD criteria, 42 subjects (8.2% had COPD. Of those, 27 subjects (64.3% had symptomatic COPD. Using the GOLD criteria, eight subjects (19% with COPD had mild disease, 24 (57.1% had moderate disease, eight (19% had severe disease, and two (4.8% had very severe disease. Only 10.6% were aware of COPD as a smoking-related respiratory illness, and 6.4% had received counseling about risk for COPD by a physician. Chronic bronchitis (cough for 3 months in 2 consecutive years was reported by 15% of the subjects, wheezes by 44.1%, and dyspnea by 65.2%. Subjects with COPD reported having more chronic bronchitis 18/42 (42.9% and wheezing 28/42 (66.7% than subjects without COPD. The prevalence of COPD increased with increased number of pack-years smoked. In conclusion, COPD prevalence among cigarette-smoking men in Jordan is lower than in the developed world. COPD was largely

  18. Role of BAFF in pulmonary autoantibody responses induced by chronic cigarette smoke exposure in mice

    NARCIS (Netherlands)

    Morissette, Mathieu C; Gao, Yang; Shen, Pamela; Thayaparan, Danya; Bérubé, Jean-Christophe; Paré, Peter D; Brandsma, Corry-Anke; Hao, Ke; Bossé, Yohan; Ettinger, Rachel; Herbst, Ronald; Humbles, Alison A; Kolbeck, Roland; Zhong, Nanshan; Chen, Rongchang; Stämpfli, Martin R

    2016-01-01

    Emerging evidence suggests that autoimmune processes are implicated in the pathogenesis of chronic obstructive pulmonary disease (COPD). In this study, we assessed the expression of B-cell activating factor (BAFF) in smokers, and investigated the functional importance of BAFF in the induction and ma

  19. Klotho Reduction in Alveolar Macrophages Contributes to Cigarette Smoke Extract-induced Inflammation in Chronic Obstructive Pulmonary Disease.

    Science.gov (United States)

    Li, Lingling; Wang, Yujie; Gao, Wei; Yuan, Cheng; Zhang, Sini; Zhou, Hong; Huang, Mao; Yao, Xin

    2015-11-13

    Abnormal inflammation and accelerated decline in lung function occur in patients with chronic obstructive pulmonary disease (COPD). Klotho, an anti-aging protein, has an anti-inflammatory function. However, the role of Klotho has never been investigated in COPD. The aim of this study is to investigate the possible role of Klotho by alveolar macrophages in airway inflammation in COPD. Klotho levels were assessed in the lung samples and peripheral blood mononuclear cells of non-smokers, smokers, and patients with COPD. The regulation of Klotho expression by cigarette smoke extract (CSE) was studied in vitro, and small interfering RNA (siRNA) and recombinant Klotho were employed to investigate the role of Klotho on CSE-induced inflammation. Klotho expression was reduced in alveolar macrophages in the lungs and peripheral blood mononuclear cells of COPD patients. CSE decreased Klotho expression and release from MH-S cells. Knockdown of endogenous Klotho augmented the expression of the inflammatory mediators, such as MMP-9, IL-6, and TNF-α, by MH-S cells. Exogenous Klotho inhibited the expression of CSE-induced inflammatory mediators. Furthermore, we showed that Klotho interacts with IκBα of the NF-κB pathway. Dexamethasone treatment increased the expression and release level of Klotho in MH-S cells. Our findings suggest that Klotho plays a role in sustained inflammation of the lungs, which in turn may have therapeutic implications in COPD.

  20. 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.

  1. A Mitochondrial Perspective of Chronic Obstructive Pulmonary Disease Pathogenesis

    Science.gov (United States)

    Shadel, Gerald S.

    2016-01-01

    Chronic obstructive pulmonary disease (COPD) encompasses several clinical syndromes, most notably emphysema and chronic bronchitis. Most of the current treatments fail to attenuate severity and progression of the disease, thereby requiring better mechanistic understandings of pathogenesis to develop disease-modifying therapeutics. A number of theories on COPD pathogenesis have been promulgated wherein an increase in protease burden from chronic inflammation, exaggerated production of reactive oxygen species and the resulting oxidant injury, or superfluous cell death responses caused by enhanced cellular injury/damage were proposed as the culprit. These hypotheses are not mutually exclusive and together likely represent the multifaceted biological processes involved in COPD pathogenesis. Recent studies demonstrate that mitochondria are involved in innate immune signaling that plays important roles in cigarette smoke-induced inflammasome activation, pulmonary inflammation and tissue remodeling responses. These responses are reviewed herein and synthesized into a view of COPD pathogenesis whereby mitochondria play a central role.

  2. 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 ...

  3. 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.

  4. Anti-inflammatory effects of potato extract on a rat model of cigarette smoke–induced chronic obstructive pulmonary disease

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    Gui Hua Xu

    2015-10-01

    Full Text Available Objective: This study aimed to evaluate the therapeutic effects of potato extract (PE on cigarette smoke (CS–induced chronic obstructive pulmonary disease (COPD. Methods: PE was first prepared by frozen centrifugation, and its amino acid composition was detected. Toxicity of PE was analyzed by changes in morphology, behavior, routine blood indexes, and biochemical criteria of mice. Then, the COPD rat model was established by CS exposure, and PE, doxofylline, and prednisolone acetate were used to treat these rats. After 45 days of treatment, the morphology and behavior of rats were recorded. In addition, the histopathology of lung tissue was evaluated by chest x-ray and hematoxylin and eosin staining. The expression of interleukine-10 (IL-10, tumor necrosis factor-α (TNF-α, and granulocyte colony-stimulating factor (G-CSF was detected in serum and lung tissue by enzyme-linked immunosorbent assay (ELISA and immunohistochemistry, respectively. Results: Various amino acids were identified in PE, and no toxicity was exhibited in mice. The CS-induced COPD rat model was successfully established, which exhibited significant thickened and disordered lung markings on 90% of the rats. After administering doxofylline and prednisolone acetate, inflammation symptoms were improved. However, side effects such as emaciation, weakness, and loosening of teeth appeared. In the PE group, obviously improved histopathology was observed in lung tissues. Meanwhile, it was revealed that PE could increase the expression of IL-10 and reduce the expression of TNF-α and G-CSF in COPD rats, and doxofylline and prednisolone acetate also elicited similar results. Conclusion: Our study suggests PE might be effective in the treatment of CS-induced COPD by inhibiting inflammation.

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

    Science.gov (United States)

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

    2015-05-13

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

  6. The administration of a high refined carbohydrate diet promoted an increase in pulmonary inflammation and oxidative stress in mice exposed to cigarette smoke

    Directory of Open Access Journals (Sweden)

    Pena KB

    2016-12-01

    Full Text Available Karina Braga Pena,1 Camila de Oliveira Ramos,1 Nícia Pedreira Soares,1 Pamela Félix da Silva,1 Ana Carla Balthar Bandeira,2 Guilherme de Paula Costa,3 Sílvia Dantas Cangussú,1 André Talvani,3 Frank Silva Bezerra1 1Laboratory of Experimental Pathophysiology (LAFEx, 2Laboratory of Metabolic Biochemistry (LBM, 3Laboratory of Immunobiology of Inflammation (LABIIN, Department of Biological Sciences (DECBI, Center of Research in Biological Sciences (NUPEB, Federal University of Ouro Preto (UFOP, Ouro Preto, MG, Brazil Abstract: This study aimed to evaluate the effects of a high refined carbohydrate diet and pulmonary inflammatory response in C57BL/6 mice exposed to cigarette smoke (CS. Twenty-four male mice were divided into four groups: control group (CG, which received a standard diet; cigarette smoke group (CSG, which was exposed to CS; a high refined carbohydrate diet group (RG, which received a high refined carbohydrate diet; and a high refined carbohydrates diet and cigarette smoke group (RCSG, which received a high refined carbohydrate diet and was exposed to CS. The animals were monitored for food intake and body weight gain for 12 weeks. After this period, the CSG and RCSG were exposed to CS for five consecutive days. At the end of the experimental protocol, all animals were euthanized for subsequent analyses. There was an increase of inflammatory cells in the bronchoalveolar lavage fluid (BALF of CSG compared to CG and RCSG compared to CG, CSG, and RG. In addition, in the BALF, there was an increase of tumor necrosis factor alpha in RCSG compared to CG, CSG, and RG; interferon gamma increase in RCSG compared to the CSG; and increase in interleukin-10 in RCSG compared to CG and RG. Lipid peroxidation increased in RCSG compared to CG, CSG, and RG. Furthermore, the oxidation of proteins increased in CSG compared to CG. The analysis of oxidative stress showed an increase in superoxide dismutase in RCSG compared to CG, CSG, and RG and an

  7. The role of circulating serotonin in the development of chronic obstructive pulmonary disease.

    Directory of Open Access Journals (Sweden)

    Way K W Lau

    Full Text Available BACKGROUND: Cigarette smoking is a major risk factor in the development of age-related chronic obstructive pulmonary disease (COPD. The serotonin transporter (SERT gene polymorphism has been reported to be associated with COPD, and the degree of cigarette smoking has been shown to be a significant mediator in this relationship. The interrelation between circulating serotonin (5-hydroxytyptamine, 5-HT, cigarette smoking and COPD is however largely unknown. The current study aimed at investigating the mediation effects of plasma 5-HT on cigarette smoking-induced COPD and the relation between plasma 5-HT levels and age. METHODS: The association between plasma 5-HT, age and COPD was analyzed in a total of 62 COPD patients (ever-smokers and 117 control subjects (healthy non-smokers and ever-smokers. Plasma 5-HT levels were measured by enzyme-linked immuno assay (EIA. RESULTS: The elevated plasma 5-HT levels were significantly associated with increased odds for COPD (OR = 1.221, 95% CI = 1.123 to 1.319, p<0.0001. The effect remained significant after being adjusted for age and pack-years smoked (OR = 1.271, 95% CI = 1.134 to 1.408, p = 0.0003. Furthermore, plasma 5-HT was found to mediate the relation between pack-years smoked and COPD. A positive correlation (r = 0.303, p = 0.017 was found between plasma 5-HT levels and age in COPD, but not in the control subjects (r = -0.149, p = 0.108. CONCLUSION: Our results suggest that cigarette smoke-induced COPD is partially mediated by the plasma levels of 5-HT, and that these become elevated with increased age in COPD. The elevated plasma 5-HT levels in COPD might contribute to the pathogenesis of this disease.

  8. The Role of Circulating Serotonin in the Development of Chronic Obstructive Pulmonary Disease

    Science.gov (United States)

    Lau, Way K. W.; Chan-Yeung, Moira M. W.; Yip, Benjamin H. K.; Cheung, Amy H. K.; Ip, Mary S. M.; Mak, Judith C. W.

    2012-01-01

    Background Cigarette smoking is a major risk factor in the development of age-related chronic obstructive pulmonary disease (COPD). The serotonin transporter (SERT) gene polymorphism has been reported to be associated with COPD, and the degree of cigarette smoking has been shown to be a significant mediator in this relationship. The interrelation between circulating serotonin (5-hydroxytyptamine, 5-HT), cigarette smoking and COPD is however largely unknown. The current study aimed at investigating the mediation effects of plasma 5-HT on cigarette smoking-induced COPD and the relation between plasma 5-HT levels and age. Methods The association between plasma 5-HT, age and COPD was analyzed in a total of 62 COPD patients (ever-smokers) and 117 control subjects (healthy non-smokers and ever-smokers). Plasma 5-HT levels were measured by enzyme-linked immuno assay (EIA). Results The elevated plasma 5-HT levels were significantly associated with increased odds for COPD (OR = 1.221, 95% CI = 1.123 to 1.319, p<0.0001). The effect remained significant after being adjusted for age and pack-years smoked (OR = 1.271, 95% CI = 1.134 to 1.408, p = 0.0003). Furthermore, plasma 5-HT was found to mediate the relation between pack-years smoked and COPD. A positive correlation (r = 0.303, p = 0.017) was found between plasma 5-HT levels and age in COPD, but not in the control subjects (r = −0.149, p = 0.108). Conclusion Our results suggest that cigarette smoke-induced COPD is partially mediated by the plasma levels of 5-HT, and that these become elevated with increased age in COPD. The elevated plasma 5-HT levels in COPD might contribute to the pathogenesis of this disease. PMID:22319639

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

    NARCIS (Netherlands)

    Eijl, Teunis Jan Ahasuerus van

    2006-01-01

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

  10. 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

  11. Dynamic changes in spirometry and pathology of smoke-induced chronic obstructive pulmonary disease rat%烟熏法建立的慢性阻塞性肺疾病鼠肺功能和病理的动态变化

    Institute of Scientific and Technical Information of China (English)

    陈茜; 郭雪君; 管小俊

    2013-01-01

    Objective To observe the dynamic changes in spirometry and pathology of smokeinduced chronic obstructive pulmonary disease (COPD) rat,and provide a theoretical basis for the successful establishment of COPD rat model.Methods Thirty SD rats at 8 weeks of age were randomized divided into 6 weeks smoke-exposed group (E1 group) and 6 week sham-exposed group (C1 group),12weeks smoke-exposed group (E2 group) and 12 weeks sham-exposed group (C2 group),interval smokeexpose group (normal feeding 6 weeks after smoke for 12 weeks,E3 group).Using Buxco research system to obtain the spirometry data and HE staining to observe the pathological changes of lung tissue.Results ①Compared with C1 group,FRC,IC,VC and TLC of E1 group were increased (P <0.05),FEV100/FVC,FEV200/FVC were reduced by 22%,11% respectively (P <0.01).②Compared with C2 group,the FRC of E2 group was increased while IC,VC,TLC were decreased (P <0.05),FEV100/FVC and FEV200/FVC were reduced by 28% and 21% (P <0.01).③Compared with E2 group,IC,VC,TLC of E3 group were increased (P < 0.05),while no difference in FEV100/FVC,FEV200/FVC.④ The pathological examination of lungs from E1 group displayed narrowed alveolar septa which was the performance of mild emphysema,and with partial infiltration of characteristic inflammatory cells.The alveolar of E2 group displayed typical performance of emphysema with infiltration of a large number of inflammatory cell surrouding bronchioles and vesseles.E3 group displayed obvious emphysema while no significant inflammation was detected.C1 and C2 group showed the structural intergity of airway epithelium and alveolar septa.Conclusions Smoking time affects the spirometry and pathology of smoke induced rat typically.With 6 weeks smoking time,the rats performed early-stage COPD while with 12 weeks smoking time performed typical COPD.%目的 动态观察不同烟熏时间建立的慢性阻塞性肺疾病(COPD)大鼠肺功能和病理的改变,为成功建立COPD大

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

    OpenAIRE

    2010-01-01

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

  13. Meditative Movement as a treatment for pulmonary dysfunction in flight attendants exposed to second-hand cigarette smoke: Study protocol for a randomized trial.

    Directory of Open Access Journals (Sweden)

    Peter ePayne

    2016-03-01

    Full Text Available A study protocol is presented for the investigation of Meditative Movement (MM as a treatment for pulmonary dysfunction in Flight Attendants (FA who were exposed to second-hand cigarette smoke (SHCS while flying before the smoking ban. The study will have three parts, some of which will run concurrently. The first is a data gathering and screening phase, which will gather data on pulmonary and other aspects of the health of FA, and will also serve to screen participants for the other phases. Second is an exercise selection phase, in which a variety of MM exercises will be taught, over a 16-week period, to a cohort of 20 FA. A subset of these exercises will be selected on the basis of participant feedback on effectiveness and compliance. Third is a 52-week randomized controlled trial (RCT to evaluate the effectiveness of a digitally delivered form of the previously selected exercises on a group of 20 FA, as compared with an attention control group. Outcome measures to be used in all three parts of the study include the six-minute walk test as a primary measure, as well as a range of biomarkers, tests and questionnaires documenting hormonal, cardio-respiratory, autonomic and affective state. This study is registered at ClinicalTrials.gov. Identifier: NCT02612389.

  14. Effect of cigarette smoke extract on proliferation of rat pulmonary artery smooth muscle cells and the relevant roles of protein kinase C

    Institute of Scientific and Technical Information of China (English)

    HU Jing; XU Yong-jian; ZHANG Zhen-xiang; TIAN Feng

    2007-01-01

    Background Increased proliferation of pulmonary vascular cells and muscularisation of pulmonary vessels are frequently observed in human smokers and in animals exposed to cigarette smoke. To elucidate the molecular mechanisms leading to these changes, we studied the in vitro effect of cigarette smoke extract (CSE) on proliferation of pulmonary artery smooth muscle cells (PASMCs) and activation of protein kinase C (PKC), an important kinase implicated in cell proliferation.Methods PASMCs cultured from 12 normal Wistar rats were studied in the following conditions: (1) PASMCs were exposed to different concentrations of CSE for 24 hours, then MTT colorimetric assay was used for detection of cell proliferation. Cell viability was assessed by trypan blue exclusion. (2) PASMCs were pre-incubated with phorbol 12-myristate 13-acetate (PMA) for 24 hours or Ro31-8220 for 30 minutes before exposure to 5% CSE for 24 hours. Cell proliferation was examined by MTT colorimetric assay, cell cycle analysis and proliferating cell nuclear antigen (PCNA) immunocytochemical staining. (3) PASMCs were exposed to 5% CSE for 24 hours. Then PKC-α mRNA expression was detected by reverse transcription-polymerase chain reaction (RT- PCR) and protein expression by Western blotting, while PKC-α translocation was observed by immunofluorescence staining and confocal microscopy. (4) PASMCs were transfected with specific antisense oligodeoxynucleotides against PKC-α 6 hours before exposure to 5% CSE for 24 hours. PKC-α protein expression and cell proliferation were detected by methods described previously.Results (1) Low concentration of CSE (5%) increased proliferation of PASMCs, whereas high concentrations (20%,30%) were inhibitory as a result of cytotoxicity. (2) The value of absorbance (Value A), proliferation index (PI), S-phase cell fraction (SPF) and average optical density of PCNA staining in PASMCs from 5% CSE exposure group (0.306 ±0.033, 0.339 ± 0.033, 0.175 ± 0.021, 0.315 ± 0

  15. 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

  16. 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

  17. 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

  18. 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.

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

    Science.gov (United States)

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

    2016-03-15

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

  20. Relationships between pulmonary micro-RNA and proteome profiles, systemic cytogenetic damage and lung tumors in cigarette smoke-exposed mice treated with chemopreventive agents.

    Science.gov (United States)

    Izzotti, Alberto; Balansky, Roumen; D'Agostini, Francesco; Longobardi, Mariagrazia; Cartiglia, Cristina; La Maestra, Sebastiano; Micale, Rosanna T; Camoirano, Anna; Ganchev, Gancho; Iltcheva, Marietta; Steele, Vernon E; De Flora, Silvio

    2013-10-01

    Assessing the correlation between molecular endpoints and cancer induction or prevention aims at validating the use of intermediate biomarkers. We previously developed murine models that are suitable to detect both the carcinogenicity of mainstream cigarette smoke (MCS) and the induction of molecular alterations. In this study, we used 931 Swiss mice in two parallel experiments and in a preliminary toxicity study. The chemopreventive agents included vorinostat, myo-inositol, bexarotene, pioglitazone and a combination of bexarotene and pioglitazone. Pulmonary micro-RNAs and proteins were evaluated by microarray analyses at 10 weeks of age in male and female mice, either unexposed or exposed to MCS since birth, and either untreated or receiving each one of the five chemopreventive regimens with the diet after weaning. At 4 months of age, the frequency of micronucleated normochromatic erythrocytes was evaluated. At 7 months, the lungs were subjected to standard histopathological analysis. The results showed that exposure to MCS significantly downregulated the expression of 79 of 694 lung micro-RNAs (11.4%) and upregulated 66 of 1164 proteins (5.7%). Administration of chemopreventive agents modulated the baseline micro-RNA and proteome profiles and reversed several MCS-induced alterations, with some intergender differences. The stronger protective effects were produced by the combination of bexarotene and pioglitazone, which also inhibited the MCS-induced clastogenic damage and the yield of malignant tumors. Pioglitazone alone increased the yield of lung adenomas. Thus, micro-RNAs, proteins, cytogenetic damage and lung tumors were closely related. The molecular biomarkers contributed to evaluate both protective and adverse effects of chemopreventive agents and highlighted the mechanisms involved.

  1. 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.

  2. 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

  3. Neutralization of both IL-1α/IL-1β plays a major role in suppressing combined cigarette smoke/virus-induced pulmonary inflammation in mice.

    Science.gov (United States)

    Bucher, Hannes; Mang, Samuel; Keck, Martina; Przibilla, Michèl; Lamb, David; Schiele, Felix; Wittenbrink, Mareike; Fuchs, Klaus; Jung, Birgit; Erb, Klaus J; Peter, Daniel

    2017-03-15

    Smoking is an important risk factor for the development of chronic obstructive pulmonary disease (COPD) and viral infections are believed to be major triggers of exacerbations, which periodically lead to a worsening of symptoms. The pro-inflammatory IL-1 family members IL-1α and IL-1β are increased in COPD patients and might contribute to disease pathology. We investigated whether individual or combined inhibition of these cytokines reduced lung inflammation in cigarette smoke (CS)-exposed and H1N1-infected BALB/c mice. Animals were treated with individual or combined antibodies (Abs) directed against IL-1α, IL-1β or IL-1R1. Cells in BAL fluid and cytokines/chemokines in lung homogenate were determined. The viral load was investigated. Blocking IL-1α had significant suppressive effects on total cells, neutrophils, and macrophages. Furthermore, it reduced KC levels significantly. Blocking of IL-1β did not provide significant activity. In line with the in vivo findings, IL-1α Abs but not IL-1β Abs reduced levels of TNF-α and IL-6 in H1N1 infected primary human bronchial epithelial air-liquid-interface cell culture. Concomitant usage of Abs against IL-1α/IL-1β revealed strong effects in vivo and reduced total cells, neutrophils and macrophages. Additionally, levels of KC, IL-6, TNF-α, MCP-1, MIP-1α and MIP-1β were significantly reduced and ICAM-1 and MUC5 A/C mRNA expression was attenuated. The viral load decreased significantly upon combined IL-1α/IL-1β Ab treatment. Blocking the IL-1R1 provided significant effects on total cells, neutrophils and macrophages but was inferior compared to inhibiting both its soluble ligands IL-1α/IL-1β. Our results suggest that combined inhibition of IL-1α/IL-1β might be beneficial to reduce CS/H1N1-induced airway inflammation. Moreover, combined targeting of both IL-1α/IL-1β might be more efficient compared to individual neutralization IL-1α or IL-1β or inhibition of the IL-1R1.

  4. 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.

  5. 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.

  6. 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...

  7. 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.

  8. 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.

  9. 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.

  10. 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.

  11. 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.

  12. COMPARATIVE STUDY OF PULMONARY FUNCTION IN DIFFERENT TYPES OF SMOKERS

    Directory of Open Access Journals (Sweden)

    Abdul Majeed

    2015-12-01

    Full Text Available OBJECTIVES The aim and objective of this study is to compare the pulmonary function variables with the help of spirometer among beedi smokers, cigarette smokers and subjects who smoked both beedi and cigarette. BACKGROUND Smoking is a major public health problem and a major cause of many preventable diseases and premature deaths all over the world. Pulmonary function variables will differ based on the type of smoking i.e. Beedi smokers, cigarette smokers, subjects who smoked both beedi and cigarette. METHODS Cross sectional study done on 90 male smokers attending the Pulmonary Outpatient Department of Sri Ramachandra Medical College and Hospital. Spirometry was done to assess the pulmonary function. CONCLUSION Pulmonary function values showed significant reduction in beedi smokers than people who smoke both beedi and cigarette, followed by subjects who smoked cigarette alone.

  13. 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

  14. 烟熏联合脂多糖制备大鼠慢性阻塞性肺疾病动物模型%Establishment of rat chronic obstructive pulmonary disease model with cigarette inhalation and intratracheal instillation of LPS

    Institute of Scientific and Technical Information of China (English)

    顾延会; 欧阳瑶

    2012-01-01

    目的 通过动态观察大鼠慢性阻塞性肺疾病(COPD)动物模型制备过程中肺组织及小支气管的病理改变,以期进一步了解COPD疾病的发展过程.方法 采用2次气道内注入细菌内毒素脂多糖和连续被动吸烟4周的方法建立COPD大鼠模型.造模过程中取第7、14、21、28、42天大鼠肺组织进行病理HE染色.结果 造模28 d COPD大鼠模型均符合人类COPD的病理形态学特点,模型组大鼠在造模过程中逐渐出现肺气肿表现.结论 气道内注入脂多糖与烟熏的复合方法能成功制备较稳定大鼠COPD动物模型.%Objective To dynamically observe the pathogenic changes of lung tissue and small bronchia during constructing process of the rat model of chronic obstructive pulmonary disease(COPD) to further understand the developing process of COPD. Methods The COPD rat model was established by cigarette smoking inhalation for 4 weeks and twice intratracheal instillation of li-popolysaccharide(LPS). Then the model s lung tissues were taken on 7,14,21,28,42 d for pathological HE staining respectively. Results The COPD rat model on 28 d accorded with the pathomorphological characteristics of human COPD. The rats of COPD models gradually developed the manifestations of emphysema during the model-constructing process. Conclusion The stable COPD rat model may be successfully established by this combined methods of cigarette smoking inhalation and intratracheal instillation of LPS.

  15. 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.

  16. 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

  17. 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.

  18. 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.

  19. 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.

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

    DEFF Research Database (Denmark)

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

    2016-01-01

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

  1. Effect of different doses and courses of cigarette smoking on structure of pulmonary vessel in rats%烟雾暴露时间及吸入量对大鼠肺血管形态的影响

    Institute of Scientific and Technical Information of China (English)

    张红丽; 胡晓芸; 许建英; 杜永成

    2009-01-01

    Objective To investigate the influence of different doses and courses of cigarette smoking on the structure of pulmonary vessel and the expression of matrix metalloproteinase-9 (MMP-9) on pulmonary vessel in rats.Methods Forty male Wistar rats were randomly divided into normal control group,short-term massive smoking group,long-term trifle smoking group,long-term massive smoking group and long-term massive smoking then stop smoking group( anti-smoking group).Passive rat smoking models were established.The following morphologic parameters were measured by image analysis system:the ratio of pulmonary vascular wall's thickness and outer diameter (MT%),the ratio of pulmonary vessel wall's area and pulmonary vessel's area(MA%).The MMP-9 mRNA expression in the pulmonary vessel of rats were determined by in situ hybridization technique.Results ①In contrast to those of normal control group,MT% and MA% of short-term massive smoking group,long-term trifle smoking group and long-term massive smoking group increased (all P<0.05),and those increases were most significant in long-term massive smoking group,but MT% decreased in anti-smoking group (all P<0.05).②In contrast to normal control group,the MMP-9 mRNA expression of rat pulmonary vessel increased in short-term massive smoking group,long-term trifle smoking group and long-term massive smoking group increased (all P<0.05 ),but decreased in anti-smoking group(all P<0.05).③There was positive correlation between the level of MMP 9 mRNA and MT%(r=0.667,P<0.05),and there was positive correlation between the level of MMP-9 mRNA and MA% (r=0.619,P<0.05).Conclusions Smoking may induce rat pulmonary vessel destruction and reconstitution may be involved by up-regulating MMP-9 expression.%目的 探讨不同吸烟时间及吸烟量大鼠肺血管管壁结构的变化,以及基质金属蛋白酶9(matrix metalloproteinase-9,MMP-9)对肺血管结构改变的影响.方法 雄性Wistar大鼠40只随机分为5组:正常

  2. 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 ...

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

    Directory of Open Access Journals (Sweden)

    Coyle Anthony J

    2011-04-01

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

  4. 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.

  5. 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

  6. 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

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

    NARCIS (Netherlands)

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

    2012-01-01

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

  8. 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

  9. 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

  10. 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.

  11. 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.

  12. 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.

  13. 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 ...

  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. 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 ...

  16. 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 ...

  17. 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 ...

  18. E-Cigarettes (For Teens)

    Science.gov (United States)

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

  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. Quantitative differentiation of dendritic cells in lung tissues of smokers with and without chronic obstructive pulmonary disease

    Institute of Scientific and Technical Information of China (English)

    SU Yan-wei; XU Yong-jian; LIU Xian-sheng

    2010-01-01

    Background Chronic obstructive pulmonary disease (COPD) is thought to be an inflammatory immune response disease. In most cases, the disease is caused by cigarette smoke, but it has been demonstrated that only 10% to 20% of smokers will definitely suffer from COPD. Dendritic cells (DCs) are considered to be the promoter of immune responses.However, the underlying mechanisms involved are still unrevealed. In this study, we aimed to investigate the quantitative differentiation of pulmonary DC in smokers with or without COPD to explore the possible role of DCs in smokers suffering COPD.Methods Peripheral lung specimens from non-smokers without airflow obstruction (control group, n=7), smokers without airflow obstruction (smoker group, n=7) and patients with COPD (COPD group, n=7) were investigated to detect the quantity of S-100 and CD1a positive cells by immunohistochemical or immunofluorescent assay.Results In smokers with COPD, the number of S-100+ DCs was higher than in the controls and smokers without COPD (P 0.05). An inverse correlation was found between the number of DCs and forced expiratory volume in the first second (FEV1)% pred (r=-0.75, P <0.05), which was also found between the number of DCs and FEV1/forced vital capacity (FVC) (r=-0.72, P <0.05). The mean number of CD1a+ DCs, increased from non-smokers to non-COPD smokers to COPD patients, with significant differences between each group (P <0.01).Conclusions The quantity of DCs significantly increased in smokers with COPD compared with non-smokers or smokers without COPD. The results suggest that DCs may play an important role in the pathogenesis of smoking-induced COPD, and the upregulation of DCs may be a potential maker to identify the smokers who have more liability to suffer from COPD.

  1. A-kinase anchoring proteins contribute to loss of E-cadherin and bronchial epithelial barrier by cigarette smoke

    NARCIS (Netherlands)

    Oldenburger, Anouk; Poppinga, Wilfred J; Kos, Fleur; de Bruin, Harold G; Rijks, Wolter F; Heijink, Hilde; Timens, Wim; Meurs, Hermanus; Maarsingh, Harm; Schmidt, Martina

    2014-01-01

    Airway epithelium, which forms the first barrier towards environmental insults, is disturbed by cigarette smoking, a major risk factor for developing chronic obstructive pulmonary disease (COPD). A-kinase anchoring proteins (AKAP) maintain endothelial barrier function and coordinate subcellular loca

  2. Molecular phenotypes distinguish patients with relatively stable from progressive idiopathic pulmonary fibrosis (IPF.

    Directory of Open Access Journals (Sweden)

    Kathy Boon

    Full Text Available BACKGROUND: Idiopathic pulmonary fibrosis (IPF is a progressive, chronic interstitial lung disease that is unresponsive to current therapy and often leads to death. However, the rate of disease progression differs among patients. We hypothesized that comparing the gene expression profiles between patients with stable disease and those in which the disease progressed rapidly will lead to biomarker discovery and contribute to the understanding of disease pathogenesis. METHODOLOGY AND PRINCIPAL FINDINGS: To begin to address this hypothesis, we applied Serial Analysis of Gene Expression (SAGE to generate lung expression profiles from diagnostic surgical lung biopsies in 6 individuals with relatively stable (or slowly progressive IPF and 6 individuals with progressive IPF (based on changes in DLCO and FVC over 12 months. Our results indicate that this comprehensive lung IPF SAGE transcriptome is distinct from normal lung tissue and other chronic lung diseases. To identify candidate markers of disease progression, we compared the IPF SAGE profiles in stable and progressive disease, and identified a set of 102 transcripts that were at least 5-fold up regulated and a set of 89 transcripts that were at least 5-fold down regulated in the progressive group (P-valuecigarette-smoke induced inflammation, and Plunc (palate, lung and nasal epithelium associated, a gene not previously implicated in IPF. Interestingly, 26 of the up regulated genes are also increased in lung adenocarcinomas and have low or no expression in normal lung tissue. More importantly, we defined a SAGE molecular expression signature of 134 transcripts that sufficiently distinguished relatively stable from progressive IPF. CONCLUSIONS: These findings indicate that molecular signatures from lung parenchyma at the time of diagnosis could prove helpful in predicting the

  3. 香烟烟雾对支气管哮喘患者气道炎性反应及肺功能的影响%Influence of the cigarette smoke in the airway inflammation and pulmonary function of the asthmatic patients

    Institute of Scientific and Technical Information of China (English)

    张彩苹; 杜永成; 许建英

    2011-01-01

    Objective To explore the influence of the cigarette smoke in the airway inflammation and pulmonary function of the asthmatic patients. Methods Twenty-five cases of asthmatic patients with cigarette smoke exposure, 22 cases of asthmatic patients without cigarette smoke exposure and 20 cases of normal control persons were involved in this study. The proportion of various inflammatory cells in the induced sputum, the levels of serum interleukin (IL)-8 and IL-4 and lung function (FEV1% expected value,FEV1/FVC% ) were detected. Results The infiltrating of neutrophils was primarily found in sputum of the asthmatic patients with cigarette smoke exposure, but the infiltrating of eosinophils was mainly in sputum of the asthmatic patients without cigarette smoke exposure. The levels of serum IL-8 and IL-4 of peripheral blood of asthmatic patients with cigarette smoke exposure [(277.02 ±71.37), (171.69 ±31.01) ng/L] were significantly higher than those in asthmatic patients without cigarette smoke exposure [(158.88 ± 21.95 ),( 111.42 ± 21.69 ) ng/L] and normal control persons [( 116.78 ± 71.37 ), (73.94 ± 15.72 ) ng/L] (P < 0.01 ).The FEV1% expected value and FEV1/FVC% of the asthmatic patients with cigarette smoke exposure [(51.12 ± 13.30) %, ( 49.16 ± 11.09 )%] was lower than those of asthmatic patients without cigarette smokeexposure [(81.81 ± 5.82)%, (79.00 ± 3.86)%] and normal control persona [(95.50 ± 10.11 )%, (83.18 ±6.04)%] (P < 0.01 ). The level of serum IL-8 was positively correlated to the neutrophils percentage in the induced sputum (r =0.742,P< 0.01 ) ,while negatively correlated to the FEV1% expected value(r =-0.739,P < 0.01 ). Conclusion Cigarette smoke may influence the airway inflammation of the asthmatic patients and accelerate the deterioration of their lung function by promoting the producing of IL-8.%目的 探讨香烟烟雾对支气管哮喘(简称哮喘)患者气道炎性反应

  4. 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…

  5. 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 ...

  6. Pulmonary edema

    Science.gov (United States)

    Lung congestion; Lung water; Pulmonary congestion; Heart failure - pulmonary edema ... Pulmonary edema is often caused by congestive heart failure . When the heart is not able to pump efficiently, ...

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

    OpenAIRE

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

    2013-01-01

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

  8. 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

  9. Current research on cigarette toxicity: critical appraisal in view of clinical laboratory

    Directory of Open Access Journals (Sweden)

    Prajwal Gyawali

    2016-06-01

    Full Text Available Cigarette smoking has been implicated as a potential risk factor for development and progression of chronic obstructive pulmonary disease (COPD and cardiovascular disease (CVD, including ischemic heart disease. Although, several methods are in existence to measuring cigarette toxicity, evidence regarding adoption of a gold standard technique is still imprecise. In this study, we reviewed articles describing methods of measuring cigarette toxicity in relation to clinical laboratory practice. A critical analysis of the benefits and limitations of each method in relation to low-middle income countries is discussed. [Int J Res Med Sci 2016; 4(6.000: 1785-1793

  10. 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.

  11. 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.

  12. 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.

  13. 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.

  14. 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

    . The goal of this work was to use a structurally motivated nonlinear constitutive relation to quantify increased arterial stiffness based on available data. Specifically, we used a “four-fiber family model” that includes dominant effects of axial, circumferential, and symmetric-diagonal families of collagen...... 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...... describing the behaviour of the elastic fibers. These findings suggest that arterial stiffening in response to smoking is isotropic due to the changes in the material parameters seen in all fiber directions. Although changes are manifested in both elastic and collagen fibers, the predominant stiffening...

  15. 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

  16. Antioxidant properties of N-acetylcysteine: their relevance in relation to chronic obstructive pulmonary disease.

    NARCIS (Netherlands)

    Dekhuijzen, P.N.R.

    2004-01-01

    Oxidative stress has been implicated in the pathogenesis and progression of chronic obstructive pulmonary disease. Both reactive oxidant species from inhaled cigarette smoke and those endogenously formed by inflammatory cells constitute an increased intrapulmonary oxidant burden. Structural changes

  17. 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.

  18. 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

  19. Pulmonary embolus

    Science.gov (United States)

    ... Blood clot - lung; Embolus; Tumor embolus; Embolism - pulmonary; DVT-pulmonary embolism; Thrombosis - pulmonary embolism ... area). This type of clot is called a deep vein thrombosis (DVT) . The blood clot breaks off and travels ...

  20. 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.

  1. 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

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

    Science.gov (United States)

    Popa, Cristina

    2015-05-01

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

  3. 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.

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

    Science.gov (United States)

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

    2001-01-01

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

  5. 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.

  6. 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

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

    Science.gov (United States)

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

    2013-01-01

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

  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. 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.

  11. 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.

  12. 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.

  13. 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...

  14. 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,...

  15. 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.…

  16. 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....

  17. 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...

  18. 血管紧张素转化酶2在香烟提取物诱导的大鼠肺动脉平滑肌细胞增殖中的作用%Effects of angiotensin-converting enzyme 2 on cigarette smoke extract induced proliferation of rat pulmonary arterial smooth muscle cells

    Institute of Scientific and Technical Information of China (English)

    贺光明; 汪涛; 郭灵丽; 韩素霞; 徐丹; 文富强

    2010-01-01

    目的 探讨血管紧张素转化酶2(angiotensin-converting enzyme2,ACE2)在香烟提取物(cigarette smoke extract,CSE)诱导的大鼠肺动脉平滑肌细胞(pulmonary artery smooth muscle cells,PASMCs)增殖中的作用.方法 分离大鼠PASMCs并培养,加入1μmol/L或10μmol/L氯沙坦(一种特异性的血管紧张素II受体拮抗剂)预处理30min,加入2%CSE处理24h,用CCK-8检测试剂盒检测细胞增殖,Western blotting法检测细胞ACE2蛋白含量.结果 2%CSE能显著诱导大鼠PASMCs增殖,2%CSE处理后细胞表达ACE2水平较对照组明显降低;经过10μmol/L氯沙坦预处理的大鼠PASMCs增殖较单纯用2%CSE处理的细胞增殖减慢,但细胞ACE2表达水平相对升高.结论 CSE能诱导大鼠PASMCs增殖,这可能与CSE降低细胞ACE2表达水平有关,因此ACE2在吸烟引起的肺血管重构中可能具有保护作用.

  19. 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...

  20. 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.

  1. 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.

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

    Institute of Scientific and Technical Information of China (English)

    Zongxian JIAO; Qilin AO; Xiaona GE; Mi XIONG

    2008-01-01

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

  3. Uncommon features of pulmonary Langerhans' cell histiocytosis:analysis of 11 cases and a review of the literature

    Institute of Scientific and Technical Information of China (English)

    LING Chun-hua; JI Cheng; Daniel P Raymond; Patricia A Bourne; XU Hao-dong

    2010-01-01

    @@ Pulmonary Langerhans' cell histiocytosis (PLCH) is an isolated form of Langerhans' cell histiocytosis that usually develops in cigarette smokers.~(1,2) PLCH usually has typical light microscopic morphology with a spectrum of progressive changes.~(2-4)

  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. 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 ...

  6. 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 ...

  7. 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.

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

    Science.gov (United States)

    Fromme, Hermann; Schober, Wolfgang

    2015-04-01

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

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

    Directory of Open Access Journals (Sweden)

    Manuel Antonio Ballén

    2006-07-01

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

  10. 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

  11. Pulmonary Fibrosis

    Science.gov (United States)

    Pulmonary fibrosis is a condition in which the tissue deep in your lungs becomes scarred over time. This ... blood may not get enough oxygen. Causes of pulmonary fibrosis include environmental pollutants, some medicines, some connective tissue ...

  12. Pulmonary Rehabilitation

    Science.gov (United States)

    ... shortness of breath and increase your ability to exercise. You may have heard that pulmonary rehabilitation is only for people with COPD (chronic obstructive pulmonary disease). We now know that ...

  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.

  14. 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.

  15. 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.

  16. Pulmonary vasculitis.

    Science.gov (United States)

    Lally, Lindsay; Spiera, Robert F

    2015-05-01

    Pulmonary vasculitis encompasses inflammation in the pulmonary vasculature with involved vessels varying in caliber from large elastic arteries to capillaries. Small pulmonary capillaries are the vessels most commonly involved in vasculitis affecting the lung. The antineutrophil cytoplasmic antibody-associated vasculitides, which include granulomatosis with polyangiitis (formerly Wegener granulomatosis), microscopic polyangiitis, and eosinophilic granulomatosis with polyangiitis (formerly Churg-Strauss syndrome), are the small vessel vasculitides in which pulmonary vasculitis is most frequently observed and are the major focus of this review. Vasculitic involvement of the large pulmonary vessels as may occur in Behçet syndrome and Takayasu arteritis is also discussed.

  17. 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....

  18. 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....

  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. Preferential recruitment of neutrophils by endothelin-1 in acute lung inflammation induced by lipopolysaccharide or cigarette smoke

    Science.gov (United States)

    Bhavsar, Tapan; Liu, Xing Jian; Patel, Hardik; Stephani, Ralph; Cantor, Jerome O

    2008-01-01

    This study examined the role of endothelin-1 (ET-1) in recruiting inflammatory cells to the lung after induction of injury with either lipopolysaccharide (LPS) or cigarette smoke. Hamsters injected with either ET-1 or its precursor peptide (Big ET-1) prior to treatment with LPS or cigarette smoke had markedly increased concentrations of neutrophils in bronchoalveolar lavage fluid (BALF) despite a reduction in total numbers of BALF leukocytes. Furthermore, the effect of ET-1 on smoke-exposed animals was reversed by addition of an endothelin-A receptor antagonist. These results are consistent with preferential recruitment of neutrophils by ET-1, and suggest that inhibition of this proinflammatory mediator may decrease acute pulmonary inflammation associated with cigarette smoke and other pulmonary toxins. PMID:18990977

  1. 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...

  2. E-cigarettes and E-hookahs

    Science.gov (United States)

    ... this page: //medlineplus.gov/ency/patientinstructions/000761.htm E-cigarettes and E-hookahs To use the sharing features on this ... cigarettes because they believe these devices are safe. E-cigarettes and Children Many experts also have concerns ...

  3. 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.

  4. 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.

  5. 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.

  6. 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.

  7. 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.

  8. 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.

  9. Wood Bark Smoke Induces Lung and Pleural Plasminogen Activator Inhibitor 1 and Stabilizes Its mRNA in Porcine Lung Cells

    Science.gov (United States)

    2011-08-01

    Positive end-expiratory pressure; PaCO2 Partial pressure of carbon dioxide in arterial blood; PaO2 Partial pressure of oxygen in arterial blood; PIP Peak...inspiratory pressure; PFs Pleural fluids; PFR PaO2 -to-FIO2 ratio; scuPA Single-chain urokinase; SIALI Smoke-induced acute lung injury; TV tidal volume...hemoglobin level after smoke injury, peak inspiratory pressure, partial pressure of O2 in arterial blood ( PaO2 ), partial pressure of CO2 in arterial blood

  10. Teens and E-cigarettes

    Science.gov (United States)

    ... Age Adults in 2015 Teens and E-cigarettes Abuse of Prescription (Rx) Drugs Affects Young Adults Most Substance Use in Women and Men View All NIDA's Publication Series Brain Power DrugFacts Mind Over Matter Research Reports NIDA Home ...

  11. 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.

  12. Pulmonary hypertension

    Directory of Open Access Journals (Sweden)

    Lauro Martins Júnior

    2014-12-01

    Full Text Available Pulmonary hypertension is a pathological condition associated with various diseases, which must be remembered by the physicians, since early diagnosis may anticipate and avoid dangerous complications and even death if appropriate measures were not taken. The relationship with chronic obstructive pulmonary disease (COPD, important pathological process that is in increasing prevalence in developing countries, and leading position as cause of death, emphasizes its importance. Here are presented the classifications, pathophysiology, and general rules of treatment of pulmonary hypertension.

  13. 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...

  14. 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.

  15. 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.

  16. 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.

  17. 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.

  18. 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.

  19. 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

  20. 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…

  1. 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

  2. Estimating mortality due to cigarette smoking

    DEFF Research Database (Denmark)

    Brønnum-Hansen, Henrik; Juel, K

    2000-01-01

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

  3. 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.

  4. 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.

  5. 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.

  6. 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...

  7. 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...

  8. Pulmonary hypertension

    Science.gov (United States)

    ... that damage the lungs, such as scleroderma and rheumatoid arthritis Birth defects of the heart Blood clots in the lung ( pulmonary embolism ) Heart failure Heart valve disease HIV infection Low oxygen levels in the blood ...

  9. Pulmonary aspergilloma

    Science.gov (United States)

    ... grows on dead leaves, stored grain, bird droppings, compost piles, and other decaying vegetation. Cavities in the ... Histoplasmosis Lung cancer - small cell Pulmonary tuberculosis Sarcoidosis Review Date 8/31/2014 Updated by: Jatin M. ...

  10. Lung function profiles and aerobic capacity of adult cigarette and hookah smokers after 12 weeks intermittent training

    Directory of Open Access Journals (Sweden)

    Abdessalem Koubaa

    2015-02-01

    Full Text Available Introduction: Pulmonary function is compromised in most smokers. Yet it is unknown whether exercise training improves pulmonary function and aerobic capacity in cigarette and hookah smokers and whether these smokers respond in a similar way as do non-smokers. Aim: To evaluate the effects of an interval exercise training program on pulmonary function and aerobic capacity in cigarette and hookah smokers. Methods: Twelve cigarette smokers, 10 hookah smokers, and 11 non-smokers participated in our exercise program. All subjects performed 30 min of interval exercise (2 min of work followed by 1 min of rest three times a week for 12 weeks at an intensity estimated at 70% of the subject's maximum aerobic capacity (VO2max. Pulmonary function was measured using spirometry, and maximum aerobic capacity was assessed by maximal exercise testing on a treadmill before the beginning and at the end of the exercise training program. Results: As expected, prior to the exercise intervention, the cigarette and hookah smokers had significantly lower pulmonary function than the non-smokers. The 12-week exercise training program did not significantly affect lung function as assessed by spirometry in the non-smoker group. However, it significantly increased both forced expiratory volume in 1 second and peak expiratory flow (PEF in the cigarette smoker group, and PEF in the hookah smoker group. Our training program had its most notable impact on the cardiopulmonary system of smokers. In the non-smoker and cigarette smoker groups, the training program significantly improved VO2max (4.4 and 4.7%, respectively, v VO2max (6.7 and 5.6%, respectively, and the recovery index (7.9 and 10.5%, respectively. Conclusions: After 12 weeks of interval training program, the increase of VO2max and the decrease of recovery index and resting heart rate in the smoking subjects indicated better exercise tolerance. Although the intermittent training program altered pulmonary function only

  11. Cigarette smoking and brain regulation of energy homeostasis

    Directory of Open Access Journals (Sweden)

    Hui eChen

    2012-07-01

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

  12. Pulmonary hypertension

    OpenAIRE

    2016-01-01

    In 2015, more than 800 papers were published in the field of pulmonary hypertension. A Clinical Year in Review article cannot possibly incorporate all this work and needs to be selective. The recently published European guidelines for the diagnosis and treatment of pulmonary hypertension contain an inclusive summary of all published clinical studies conducted until very recently. Here, we provide an overview of papers published after the finalisation of the guideline. In addition, we summaris...

  13. Pulmonary Agenesis.

    Science.gov (United States)

    Chawla, Rakesh K; Madan, Arun; Chawla, Aditya; Arora, Harsh Nandini; Chawla, Kiran

    2015-01-01

    Unilateral opaque lung with ipsilateral mediastinal shift is an uncommon cause of respiratory distress in newborn which can be found on simple radiograph of the chest. Pulmonary agenesis is a rare cause of unilateral opaque lung in the newborn. Nearly 50% cases of pulmonary agenesis are associated with other congenital defects including cardiovascular, skeletal, gastrointestinal or genitourinary systems. We report an infant with agenesis of the right lung associated with other congenital anomalies.

  14. Pulmonary Edema

    OpenAIRE

    Tanser, Paul H.

    1981-01-01

    The physician who deals with pulmonary edema from a pathophysiologic basis will seldom make a diagnostic or therapeutic error. Recent additions to preload and afterload therapy have greatly helped in the emergency and ambulatory treatment of pulmonary edema due to left heart failure. Careful follow-up and patient self-monitoring are the most effective means of reducing hospitalization of chronic heart failure patients.

  15. 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.

  16. 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

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

    Science.gov (United States)

    Cobb, Nathan K; Sonti, Rajiv

    2016-08-01

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

  18. Dysfunction of pulmonary vascular endothelium in chronic obstructive pulmonary disease: basic considerations for future drug development.

    Science.gov (United States)

    Yang, Qin; Underwood, Malcolm J; Hsin, Michael K Y; Liu, Xiao-Cheng; He, Guo-Wei

    2008-09-01

    Chronic obstructive pulmonary disease (COPD) is one of the leading health problems worldwide and continues to be a major cause of morbidity and mortality in developed countries. The clinical features of COPD are chronic obstructive bronchiolitis and emphysema. Pulmonary vascular endothelial dysfunction is a characteristic pathological finding of COPD at different stages of the disease. Functional changes of pulmonary endothelial cells in COPD include antiplatelet abnormalities, anticoagulant disturbances, endothelial activation, atherogenesis, and compromised regulation of vascular tone which may adversely affect the ventilation-perfusion match in COPD. As the most important risk factor of COPD, cigarette smoking may initiate pulmonary vascular impairment through direct injury of endothelial cells or release of inflammatory mediators. Morphological changes such as denudation of endothelium and endothelial cell apoptosis have been observed in the pulmonary vasculature in COPD patients as well as functional alterations. Changes in the expression of tissue factor pathway inhibitor (TFPI), thrombomodulin, selectins, and adhesion molecules in pulmonary endothelial cells as well as complex regulation and interaction of vasoactive substances and growth factors released from endothelium may underlie the mechanisms of pulmonary endothelial dysfunction in COPD. The mechanism of endothelial repair/regeneration in COPD, although not fully understood, may involve upregulation of vascular endothelial growth factors in the early stages along with an increased number of bone marrow-derived progenitor cells. These factors should be taken into account when developing new strategies for the pharmacological therapy of patients with COPD.

  19. 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.

  20. 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)

  1. STUDY OF PULMONARY FUNCTION TESTS AMONG SMOKERS AND NON-SMOKERS IN A RURAL AREA

    Directory of Open Access Journals (Sweden)

    Rubeena Bano

    2009-03-01

    Full Text Available In India smoking is a common habit prevalent in both urban and rural areas. Cigarette smoking has extensive effects on respiratory function and is clearly implicated in the etiology of a number of respiratory diseases, particularly chronic bronchitis, emphysema, and bronchial carcinoma. An attempt has been made to study the pulmonary function tests among smoker and non-smoker population in a rural area.The pulmonary functions were done on a computerized spirometer in 100 male subjects comprising of 50 smokers and 50 non smokers. Almost all the pulmonary function parameters were significantly reducedin smokers and obstructive pulmonary impairment was commonest.

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

    Science.gov (United States)

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

    2011-10-01

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

  3. 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....

  4. 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.

  5. 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.

  6. 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.

  7. 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....

  8. 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.

  9. 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

  10. 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.

  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. 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.

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

    Directory of Open Access Journals (Sweden)

    Kong Chen

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

  14. Monitoring of cigarette smoking using wearable sensors and support vector machines.

    Science.gov (United States)

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

    2013-07-01

    Cigarette smoking is a serious risk factor for cancer, cardiovascular, and pulmonary diseases. Current methods of monitoring of cigarette smoking habits rely on various forms of self-report that are prone to errors and under reporting. This paper presents a first step in the development of a methodology for accurate and objective assessment of smoking using noninvasive wearable sensors (Personal Automatic Cigarette Tracker-PACT) by demonstrating feasibility of automatic recognition of smoke inhalations from signals arising from continuous monitoring of breathing and hand-to-mouth gestures by support vector machine classifiers. The performance of subject-dependent (individually calibrated) models was compared to performance of subject-independent (group) classification models. The models were trained and validated on a dataset collected from 20 subjects performing 12 different activities representative of everyday living (total duration 19.5 h or 21,411 breath cycles). Precision and recall were used as the accuracy metrics. Group models obtained 87% and 80% of average precision and recall, respectively. Individual models resulted in 90% of average precision and recall, indicating a significant presence of individual traits in signal patterns. These results suggest the feasibility of monitoring cigarette smoking by means of a wearable and noninvasive sensor system in free living conditions.

  15. Genome-wide joint meta-analysis of SNP and SNP-by-smoking interaction identifies novel loci for pulmonary function

    NARCIS (Netherlands)

    Hancock, Dana B; Artigas, María Soler; Gharib, Sina A; Henry, Amanda; Manichaikul, Ani; Ramasamy, Adaikalavan; Loth, Daan W; Imboden, Medea; Koch, Beate; McArdle, Wendy L; Smith, Albert V; Smolonska, Joanna; Sood, Akshay; Tang, Wenbo; Wilk, Jemma B; Zhai, Guangju; Zhao, Jing Hua; Aschard, Hugues; Burkart, Kristin M; Curjuric, Ivan; Eijgelsheim, Mark; Elliott, Paul; Gu, Xiangjun; Harris, Tamara B; Janson, Christer; Homuth, Georg; Hysi, Pirro G; Liu, Jason Z; Loehr, Laura R; Lohman, Kurt; Loos, Ruth J F; Manning, Alisa K; Marciante, Kristin D; Obeidat, Ma'en; Postma, Dirkje S; Aldrich, Melinda C; Brusselle, Guy G; Chen, Ting-hsu; Eiriksdottir, Gudny; Franceschini, Nora; Heinrich, Joachim; Rotter, Jerome I; Wijmenga, Cisca; Williams, O Dale; Bentley, Amy R; Hofman, Albert; Laurie, Cathy C; Lumley, Thomas; Morrison, Alanna C; Joubert, Bonnie R; Rivadeneira, Fernando; Couper, David J; Kritchevsky, Stephen B; Liu, Yongmei; Wjst, Matthias; Wain, Louise V; Vonk, Judith M; Uitterlinden, André G; Rochat, Thierry; Rich, Stephen S; Psaty, Bruce M; O'Connor, George T; North, Kari E; Mirel, Daniel B; Meibohm, Bernd; Launer, Lenore J; Khaw, Kay-Tee; Hartikainen, Anna-Liisa; Hammond, Christopher J; Gläser, Sven; Marchini, Jonathan; Kraft, Peter; Wareham, Nicholas J; Völzke, Henry; Stricker, Bruno H C; Spector, Timothy D; Probst-Hensch, Nicole M; Jarvis, Deborah; Jarvelin, Marjo-Riitta; Heckbert, Susan R; Gudnason, Vilmundur; Boezen, Hendrika; Barr, R Graham; Cassano, Patricia A; Strachan, David P; Fornage, Myriam; Hall, Ian P; Dupuis, Josée; Tobin, Martin D; London, Stephanie J

    2012-01-01

    Genome-wide association studies have identified numerous genetic loci for spirometic measures of pulmonary function, forced expiratory volume in one second (FEV(1)), and its ratio to forced vital capacity (FEV(1)/FVC). Given that cigarette smoking adversely affects pulmonary function, we conducted g

  16. [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.

  17. Validation of the smoking habits of a sample of the patient population seen in a pulmonary function laboratory.

    Science.gov (United States)

    Herbert, F A; Enarson, D A; Hackett, R L

    1989-12-01

    From a structured history of 32 current smokers seen in the pulmonary function laboratory of a community hospital, we determined the number of cigarettes they smoked in 24 h. We also asked them to estimate their cigarette butt lengths from a visual model and to collect all cigarette butts over the next 24 h and mail them to us. We counted the butts, individually measured their lengths, and compared these with their previous estimates in order to validate their claims. While in the laboratory, we determined the level of carboxyhemoglobin in the peripheral blood of each patient. Patients tended to estimate the numbers of cigarettes that they smoked in units of five. Light smokers returned more butts and heavy smokers returned fewer butts than the numbers they reported as usually smoking. All patients were able to precisely estimate the average length of their cigarette butts, and they left butts of consistent lengths. There was no association between the numbers of cigarettes smoked and the butt lengths. Carboxyhemoglobin levels were positively associated with the numbers of cigarettes smoked in 24 h and negatively associated with the butt length and the time elapsed since the last cigarette was smoked, but these were not associated with the amount of tar in the cigarettes or with the number of years the person had smoked.

  18. Pulmonary function in perlite workers.

    Science.gov (United States)

    Cooper, W C

    1976-11-01

    Pulmonary function was studied in 117 men employed in three plants engaged in the mining and processing of perlite. Of these, 38 had been employed for ten years or more; 18 for 15 years or more and four men for 20 years or more. Review of chest films confirmed previous studies which showed no changes indicative of pneumoconiosis. Measurement of forced vital capacity (FVC) by Jones Pulmonor and by Collins 9-liter spirometer did not show reductions correlated with length of exposure, after effects of cigarette smoking had been taken into account. There was instead a slight increase in FVC associated with years in the perlite industry. The distribution of individuals with FVC below 80% of predicted also showed no association with duration of perlite exposure. Although there were slight reductions in forced expiratory volume in one second (FEV1) and in FEV1/FVC% which were associated with years in the perlite industry and which could not be explained by cigarette smoking, these reductions were not statistically significant. In summary, the population of men available for study in the major perlite-producing area of the United States, who have worked for periods up to 23 years, showed no evidence of pneumoconiosis by chest radiography or by measurement of forced vital capacity. Nevertheless, continued control of dust to ensure exposures below nuisance dust levels is essential. Medical surveillance should also continue with records being retained for periodic reevaluation.

  19. 76 FR 36627 - Required Warnings for Cigarette Packages and Advertisements

    Science.gov (United States)

    2011-06-22

    ... 1141 Required Warnings for Cigarette Packages and Advertisements; Final Rule #0;#0;Federal Register... Cigarette Packages and Advertisements AGENCY: Food and Drug Administration, HHS. ACTION: Final rule. SUMMARY... display of health warnings on cigarette packages and in cigarette advertisements. This rule implements...

  20. Idiopathic pulmonary fibrosis.

    Science.gov (United States)

    Meltzer, Eric B; Noble, Paul W

    2008-01-01

    Idiopathic pulmonary fibrosis (IPF) is a non-neoplastic pulmonary disease that is characterized by the formation of scar tissue within the lungs in the absence of any known provocation. IPF is a rare disease which affects approximately 5 million persons worldwide. The prevalence is estimated to be slightly greater in men (20.2/100,000) than in women (13.2/100,000). The mean age at presentation is 66 years. IPF initially manifests with symptoms of exercise-induced breathless and dry coughing. Auscultation of the lungs reveals early inspiratory crackles, predominantly located in the lower posterior lung zones upon physical exam. Clubbing is found in approximately 50% of IPF patients. Cor pulmonale develops in association with end-stage disease. In that case, classic signs of right heart failure may be present. Etiology remains incompletely understood. Some environmental factors may be associated with IPF (cigarette smoking, exposure to silica and livestock). IPF is recognized on high-resolution computed tomography by peripheral, subpleural lower lobe reticular opacities in association with subpleural honeycomb changes. IPF is associated with a pathological lesion known as usual interstitial pneumonia (UIP). The UIP pattern consists of normal lung alternating with patches of dense fibrosis, taking the form of collagen sheets. The diagnosis of IPF requires correlation of the clinical setting with radiographic images and a lung biopsy. In the absence of lung biopsy, the diagnosis of IPF can be made by defined clinical criteria that were published in guidelines endorsed by several professional societies. Differential diagnosis includes other idiopathic interstitial pneumonia, connective tissue diseases (systemic sclerosis, polymyositis, rheumatoid arthritis), forme fruste of autoimmune disorders, chronic hypersensitivity pneumonitis and other environmental (sometimes occupational) exposures. IPF is typically progressive and leads to significant disability. The median

  1. Idiopathic pulmonary fibrosis

    Directory of Open Access Journals (Sweden)

    Noble Paul W

    2008-03-01

    Full Text Available Abstract Idiopathic pulmonary fibrosis (IPF is a non-neoplastic pulmonary disease that is characterized by the formation of scar tissue within the lungs in the absence of any known provocation. IPF is a rare disease which affects approximately 5 million persons worldwide. The prevalence is estimated to be slightly greater in men (20.2/100,000 than in women (13.2/100,000. The mean age at presentation is 66 years. IPF initially manifests with symptoms of exercise-induced breathless and dry coughing. Auscultation of the lungs reveals early inspiratory crackles, predominantly located in the lower posterior lung zones upon physical exam. Clubbing is found in approximately 50% of IPF patients. Cor pulmonale develops in association with end-stage disease. In that case, classic signs of right heart failure may be present. Etiology remains incompletely understood. Some environmental factors may be associated with IPF (cigarette smoking, exposure to silica and livestock. IPF is recognized on high-resolution computed tomography by peripheral, subpleural lower lobe reticular opacities in association with subpleural honeycomb changes. IPF is associated with a pathological lesion known as usual interstitial pneumonia (UIP. The UIP pattern consists of normal lung alternating with patches of dense fibrosis, taking the form of collagen sheets. The diagnosis of IPF requires correlation of the clinical setting with radiographic images and a lung biopsy. In the absence of lung biopsy, the diagnosis of IPF can be made by defined clinical criteria that were published in guidelines endorsed by several professional societies. Differential diagnosis includes other idiopathic interstitial pneumonia, connective tissue diseases (systemic sclerosis, polymyositis, rheumatoid arthritis, forme fruste of autoimmune disorders, chronic hypersensitivity pneumonitis and other environmental (sometimes occupational exposures. IPF is typically progressive and leads to significant

  2. Preferential recruitment of neutrophils by endothelin-1 in acute lung inflammation induced by lipopolysaccharide or cigarette smoke

    Directory of Open Access Journals (Sweden)

    Tapan Bhavsar

    2008-10-01

    Full Text Available Tapan Bhavsar, Xing Jian Liu, Hardik Patel, Ralph Stephani, Jerome O CantorSt John’s University, School of Pharmacy and Allied Health Sciences, New York, USAAbstract: This study examined the role of endothelin-1 (ET-1 in recruiting inflammatory cells to the lung after induction of injury with either lipopolysaccharide (LPS or cigarette smoke. Hamsters injected with either ET-1 or its precursor peptide (Big ET-1 prior to treatment with LPS or cigarette smoke had markedly increased concentrations of neutrophils in bronchoalveolar lavage fluid (BALF despite a reduction in total numbers of BALF leukocytes. Furthermore, the effect of ET-1 on smoke-exposed animals was reversed by addition of an endothelin-A receptor antagonist. These results are consistent with preferential recruitment of neutrophils by ET-1, and suggest that inhibition of this proinfl ammatory mediator may decrease acute pulmonary inflammation associated with cigarette smoke and other pulmonary toxins.Keywords: endothelin, lipopolysaccahride, cigarette smoke, neutrophils, lung

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

    Directory of Open Access Journals (Sweden)

    Nidhi Mehrotra

    2011-02-01

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

  4. 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

  5. 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.

  6. Phenotypes in COPD visualized by changes in neutrophil activation

    NARCIS (Netherlands)

    Lo Tam Loi, A.T.

    2014-01-01

    Chronic Obstructive Pulmonary Disease (COPD) is ranked number 3 by the WHO list of important diseases worldwide and is the only major disease with increasing mortality. 15-20% of the smokers will develop COPD. The pathogenesis of this (cigarette) smoke induced COPD is still unclear. It is becoming c

  7. 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...

  8. 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.

  9. 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.

  10. 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.

  11. 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.

  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. Estimating mortality due to cigarette smoking

    DEFF Research Database (Denmark)

    Brønnum-Hansen, H; Juel, K

    2000-01-01

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

  15. 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 ...

  16. 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.

  17. Pulmonary hypertension complicating pulmonary sarcoidosis

    NARCIS (Netherlands)

    Huitema, M P; Grutters, J C; Rensing, B J W M; Reesink, H J; Post, M C

    2016-01-01

    Pulmonary hypertension (PH) is a severe complication of sarcoidosis, with an unknown prevalence. The aetiology is multifactorial, and the exact mechanism of PH in the individual patient is often difficult to establish. The diagnostic work-up and treatment of PH in sarcoidosis is complex, and should

  18. 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 ...

  19. 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

  20. 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 ...

  1. 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…

  2. 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.

  3. [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.

  4. Pulmonary Arterial Hypertension

    Science.gov (United States)

    Pulmonary Arterial Hypertension What Is Pulmonary Hypertension? To understand pulmonary hypertension (PH) it helps to understand how blood ows throughout your body. While the heart is one organ, it ...

  5. 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.

  6. 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.

  7. How Is Pulmonary Hypertension Treated?

    Science.gov (United States)

    ... from the NHLBI on Twitter. How Is Pulmonary Hypertension Treated? Pulmonary hypertension (PH) has no cure. However, ... Types of Pulmonary Hypertension." ) Group 1 Pulmonary Arterial Hypertension Group 1 pulmonary arterial hypertension (PAH) includes PH ...

  8. Infliximab protects against pulmonary emphysema in smoking rats

    Institute of Scientific and Technical Information of China (English)

    ZHANG Xiang-yan; HAN Jing; ZHANG Cheng; SUN Qian-yun; LI Dan; LUO Rong-rong; WAN Zi-fen; YE Xian-wei; LIU Wei-jia; RAO Shan-shan

    2011-01-01

    Background It is widely accepted that tumor necrosis factor-α (TNF-a) plays an important role in the pathogenesis of emphysema. This study aimed at investigating the protective effects of anti-TNF-α antibody, infliximab, in the development of emphysema induced by passive smoking in rats.Methods Thirty-nine rats were randomly divided into a normal control group (group 1), an emphysema group (group 2),and an infliximab-intervention group (group 3). Rat models of emphysema were established by exposure to cigarette smoking daily for 74 days. After 1 month, the infliximab intervention group was treated with infliximab via subcutaneous injection. The levels of TNF-α, iL-8 and vascular endothelial growth factor (VEGF) in bronchoalveolar lavage fluid (BALF)were measured with enzyme linked immunosorbent assay (ELISA). The number and classification of cells in the BALF were measured. Lung tissue sections stained by hematoxylin and eosin (HE) were observed, and mean linear intercept (MLI) and mean alveolar numbers (MAN) were measured. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods were used to examine the percentage of positive cells and distribution of apoptotic cells.Results The levels of TNF-α and IL-8 in BALF were higher in group 2 than in group 1 and group 3. The MLI was greater in group 2 than that in group 1 and group 3 while MAN was decreased. The concentration of VEGF in BALF of group 2 was significantly decreased as compared with group 1. The total cells and neutrophils number was significantly increased in group 2 as compared with group 1 and group 3, so was the percentage of neutrophils. The number of TUNEL positive cells in the alveolar septa was significantly increased in group 2 as compared with group 1 and group 3.Conclusion Infliximab protects against cigarette smoking-induced emphysema by reducing airway inflammation,attenuating alveolar septa cell apoptosis and improving pathological changes.

  9. 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.

  10. 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

  11. 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

  12. 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.

  13. [Pulmonary strongyloidiasis].

    Science.gov (United States)

    Lozada, Heiler; Daza, Jorge E

    2016-10-01

    Strongyloidiasis is an infection caused by the parasite Strongyloides stercoralis, which can be asymptomatic and means a high morbidity and mortality in immunocompromised hosts, severe malnutrition and coinfection with HTLV-1 virus. The parasite has the potential to produce and multiply internal autoinfection in humans, thus an hyperinfection can be developed. A case of pulmonary infection by this parasite is presented in this study, infection which advanced into a respiratory failure and required mechanical ventilation and hemodynamic support in an intensive care unit. The standard treatment combined with ivermectin and albendazole was provided, achieving an appropriate response.

  14. 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.

  15. [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.

  16. 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.

  17. 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.

  18. 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, ...

  19. 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 ...

  20. 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 ...

  1. 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.

  2. 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 ...

  3. Lung injury after cigarette smoking is particle-related

    Science.gov (United States)

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

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

    Science.gov (United States)

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

    2012-02-01

    Cigarette smoking, the major cause of chronic obstructive pulmonary disease (COPD), induces aberrant airway epithelial structure and function. The underlying mechanisms are unresolved so far. We studied effects of cigarette smoke extract (CSE) on epithelial barrier function and wound regeneration in human bronchial epithelial 16HBE cells and primary bronchial epithelial cells (PBECs) from COPD patients, nonsmokers and healthy smokers. We demonstrate that CSE rapidly and transiently impairs 16HBE barrier function, largely due to disruption of cell-cell contacts. CSE induced a similar, but stronger and more sustained, defect in PBECs. Application of the specific epidermal growth factor receptor (EGFR) inhibitor AG1478 showed that EGFR activation contributes to the CSE-induced defects in both 16HBE cells and PBECs. Furthermore, our data indicate that the endogenous protease calpain mediates these defects through tight junction protein degradation. CSE also delayed the reconstitution of 16HBE intercellular contacts during wound healing and attenuated PBEC barrier function upon wound regeneration. These findings were comparable between PBECs from smokers, healthy smokers and COPD patients. In conclusion, we demonstrate for the first time that CSE reduces epithelial integrity, probably by EGFR and calpain-dependent disruption of intercellular contacts. This may increase susceptibility to environmental insults, e.g. inhaled pathogens. Thus, EGFR may be a promising target for therapeutic strategies to improve mucosal barrier function in cigarette smoking-related disease.

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

    Science.gov (United States)

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

    2013-11-01

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

  6. Pulmonary biomarkers in chronic obstructive pulmonary disease

    NARCIS (Netherlands)

    Barnes, Peter J.; Chowdhury, Badrul; Kharitonov, Sergei A.; Magnussen, Helgo; Page, Clive P.; Postma, Dirkje; Saetta, Marina

    2006-01-01

    There has been increasing interest in using pulmonary biomarkers to understand and monitor the inflammation in the respiratory tract of patients with chronic obstructive pulmonary disease (COPD). In this Pulmonary Perspective we discuss the merits of the various approaches by reviewing the current l

  7. [Idiopathic pulmonary hemosiderosis with dendriform pulmonary ossification].

    Science.gov (United States)

    Barrera, Ana Madeleine; Vargas, Leslie

    2016-12-01

    Pulmonary ossification is a rare and usually asymptomatic finding reported as incidental in lung biopsies. Similarly, idiopathic pulmonary hemosiderosis is a rare cause of pulmonary infiltrates. We report the case of a 64-year old man with chronic respiratory symptoms in whom these two histopathological findings converged.

  8. 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.

  9. 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.

  10. Another Risk From Cigarette Smoking: Corneal Burn

    Directory of Open Access Journals (Sweden)

    Volkan Hürmeriç

    2012-12-01

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

  11. 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.

  12. 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.

  13. 75 FR 69523 - Required Warnings for Cigarette Packages and Advertisements

    Science.gov (United States)

    2010-11-12

    ... Packages and Advertisements; Proposed Rule #0;#0;Federal Register / Vol. 75 , No. 218 / Friday, November 12... CFR Part 1141 RIN 0910-AG41 Required Warnings for Cigarette Packages and Advertisements AGENCY: Food... cigarette packages and in cigarette advertisements. The proposed rule would implement a provision of...

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1987-01-01

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

  15. Apelin and pulmonary hypertension

    DEFF Research Database (Denmark)

    Andersen, Charlotte Uggerhøj; Hilberg, Ole; Mellemkjær, Søren;

    2011-01-01

    Pulmonary arterial hypertension (PAH) is a devastating disease characterized by pulmonary vasoconstriction, pulmonary arterial remodeling, abnormal angiogenesis and impaired right ventricular function. Despite progress in pharmacological therapy, there is still no cure for PAH. The peptide apelin...... vasoconstriction, and has positive inotropic and cardioprotective effects. Apelin attenuates vasoconstriction in isolated rat pulmonary arteries, and chronic treatment with apelin attenuates the development of pulmonary hypertension in animal models. The existing literature thus renders APLNR an interesting...

  16. 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.

  17. 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.

  18. 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.

  19. 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.

  20. 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.

  1. 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.

  2. Reduction of aldehydes and hydrogen cyanide yields in mainstream cigarette smoke using an amine functionalised ion exchange resin

    Directory of Open Access Journals (Sweden)

    Duke Martin G

    2011-04-01

    Full Text Available Abstract Background Cigarette smoking is a well recognized cause of diseases such as lung cancer, chronic obstructive pulmonary disease and cardiovascular disease. Of the more than 5000 identified species in cigarette smoke, at least 150 have toxicological activity. For example, formaldehyde and acetaldehyde have been assigned as Group 1 and Group 2B carcinogens by IARC, and hydrogen cyanide has been identified as a respiratory and cardiovascular toxicant. Active carbon has been shown to be an effective material for the physical adsorption of many of the smoke volatile species. However, physical adsorption of acetaldehyde, formaldehyde and also hydrogen cyanide from smoke is less effective using carbon. Alternative methods for the removal of these species from cigarette smoke are therefore of interest. A macroporous, polystyrene based ion-exchange resin (Diaion®CR20 with surface amine group functionality has been investigated for its ability to react with aldehydes and HCN in an aerosol stream, and thus selectively reduce the yields of these compounds (in particular formaldehyde in mainstream cigarette smoke. Results Resin surface chemistry was characterized using vapour sorption, XPS, TOF-SIMS and 15N NMR. Diaion®CR20 was found to have structural characteristics indicating weak physisorption properties, but sufficient surface functionalities to selectively remove aldehydes and HCN from cigarette smoke. Using 60 mg of Diaion®CR20 in a cigarette cavity filter gave reductions in smoke formaldehyde greater than 50% (estimated to be equivalent to >80% of the formaldehyde present in the smoke vapour phase independent of a range of flow rates. Substantial removal of HCN (>80% and acetaldehyde (>60% was also observed. The performance of Diaion®CR20 was found to be consistent over a test period of 6 months. The overall adsorption for the majority of smoke compounds measured appeared to follow a pseudo-first order approximation to second order

  3. 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

  4. 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.

  5. [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.

  6. 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.

  7. 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...

  8. The effects of drugs, other foreign compounds, and cigarette smoke on the synthesis of protein by lung slices

    Energy Technology Data Exchange (ETDEWEB)

    Hellstern, K.; Curtis, C.G.; Powell, G.M. (University College, Cardiff (England)); Upshall, D.G. (Chemical Defence Establishment, Wiltshire (England))

    1990-04-01

    The incorporation of {sup 14}C-leucine into rabbit lung slices was monitored in the absence and presence of selected drugs and chemicals relevant to the perturbation of lung function and the development of lung disease. Known inhibitors of protein synthesis (cycloheximide and ricin) inhibited the incorporation of {sup 14}C-leucine. Marked inhibition was also recorded with the lung toxins paraquat and 4-ipomeanol. By contrast, orciprenaline, salbutamol, and terbutaline were without effect although some response was recorded with isoprenaline. The filtered gas phase of cigarette smoke and acrolein, one of its components, were inhibitory but protection was afforded by N-acetylcysteine. It is suggested that the inhibitory effects of cigarette smoke may be due to its acrolein content. It is further suggested that the use of lung slices and measurements of {sup 14}C-leucine incorporation provide valuable means for monitoring potential pulmonary toxins.

  9. Systems toxicology approaches enable mechanistic comparison of spontaneous and cigarette smoke-related lung tumor development in the A/J mouse model

    OpenAIRE

    2014-01-01

    The A/J mouse is highly susceptible to lung tumor induction and has been widely used as a screening model in carcinogenicity testing and chemoprevention studies. However, the A/J mouse model has several disadvantages. Most notably, it develops lung tumors spontaneously. Moreover, there is a considerable gap in our understanding of the underlying mechanisms of pulmonary chemical carcinogenesis in the A/J mouse. Therefore, we examined the differences between spontaneous and cigarette smoke-rela...

  10. Smoking and Pulmonary Fibrosis: Novel Insights

    Directory of Open Access Journals (Sweden)

    Katerina D. Samara

    2011-01-01

    Full Text Available The relationship between smoking and pulmonary fibrosis is under debate and intense investigation. The aim of this paper is to review the existing literature and identify further areas of research interest. Recently the negative influence of cigarette smoking on IPF outcome was highlighted, as non-smokers exhibit a better survival than ex-smokers and combined current- and ex-smokers. In patients with non-specific interstitial pneumonia (NSIP, a high prevalence of emphysema was recently demonstrated, providing an indirect support for a smoking pathogenetic hypothesis in NSIP. The coexistence of pulmonary fibrosis and emphysema has been extensively described in a syndrome termed combined pulmonary fibrosis and emphysema (CPFE. Connective tissue disorders (CTDs are a group of autoimmune diseases which affect the lung, as one of the most common and severe manifestations. However, the relationship between smoking and autoimmune disorders is still conflicting. Rheumatoid arthritis results from the interaction between genetic and environmental factors, while the best established environmental factor is tobacco smoking. Smoking has also a negative impact on the response of the RA patients to treatment. The aforementioned smoking-related implications give rise to further research questions and certainly provide one more important reason for physicians to advocate smoking cessation and smoke-free environment.

  11. The relationship between atherosclerosis and pulmonary emphysema

    Directory of Open Access Journals (Sweden)

    Vučević Danijela

    2014-01-01

    Full Text Available Introduction. The etiopathogenesis of atherosclerosis and subsequent pulmonary emphysema has not been fully elucidated. Experimental Studies Foam cells are of great importance in the development of these diseases. It is known that local cytokine secretion and modification of native lipoprotein particles, which are internalized by the vascular and alveolar macrophages via the scavenger receptors on the surfaces of these cells, lead to the formation of foam cells. Thus, the exacerbation of local inflammatory process in the vascular and lung tissue ensues due to a generation of reactive oxygen species, resulting in further lipoprotein modification and cytokine production. Accumulating evidence suggests that oxidants may facilitate the inflammatory response by impairing antiprotease function, directly attacking vascular and lung matrix proteins and by inactivating enzymes involved in elastin synthesis and vascular and lung repair. Clinical Studies Cigarette smoke is recognized as a rich source of oxidants. Nearly 90% of all patients with chronic obstructive pulmonary disease are smokers. The process of atherogenesis is also influenced by tobacco smoke. Conclusion The role of vascular and alveolar macrophages has become increasingly important in understanding the development of atherosclerosis and resulting pulmonary emphysema.[Projekat Ministarstva nauke Republike Srbije, br. 175015

  12. Sequential Treatments with Tongsai and Bufei Yishen Granules Reduce Inflammation and Improve Pulmonary Function in Acute Exacerbation-Risk Window of Chronic Obstructive Pulmonary Disease in Rats

    Directory of Open Access Journals (Sweden)

    Xiaofan Lu

    2016-01-01

    Full Text Available Background. Sequential treatments of Chinese medicines for acute exacerbation of chronic obstructive pulmonary disease (AECOPD risk window (RW have benefits for preventing reoccurrences of AEs; however, the effects on pulmonary function, pulmonary, and systemic inflammatory biomarkers remain unclear. Methods. Cigarette-smoke/bacterial infections induced rats were randomized into Control, COPD, AECOPD, Tongsai Granule/normal saline (TSG/NS, moxifloxacin + salbutamol/NS (MXF+STL/NS, TSG/Bufei Yishen Granule (BYG, MXF+STL/STL, and TSG+MXF+STL/BYG+STL groups and given corresponding medicine(s in AE- and/or RW phase. Body temperature, pulmonary function, blood cytology, serum amyloid A (SAA and C-reactive protein (CRP, pulmonary histomorphology and myeloperoxidase (MPO, polymorphonuclear (PMN elastase, interleukins IL-1β, IL-6, and IL-10, and tumor necrosis factor- (TNF- α expressions were determined. Results. Body temperature, inflammatory cells and cytokines, SAA, CRP, and pulmonary impairment were higher in AECOPD rats than stable COPD, while pulmonary function declined and recovered to COPD level in 14–18 days. All biomarkers were improved in treated groups with shorter recovery times of 4–10 days, especially in TSG+MXF+STL/BYG+STL group. Conclusion. Sequential treatments with Tongsai and Bufei Yishen Granules, during AECOPD-RW periods, can reduce inflammatory response and improve pulmonary function and shorten the recovery courses of AEs, especially the integrated Chinese and Western medicines.

  13. Sequential Treatments with Tongsai and Bufei Yishen Granules Reduce Inflammation and Improve Pulmonary Function in Acute Exacerbation-Risk Window of Chronic Obstructive Pulmonary Disease in Rats

    Science.gov (United States)

    Lu, Xiaofan; Li, Ya; Wang, Haifeng; Wu, Zhaohuan; Li, Hangjie; Wang, Yang

    2016-01-01

    Background. Sequential treatments of Chinese medicines for acute exacerbation of chronic obstructive pulmonary disease (AECOPD) risk window (RW) have benefits for preventing reoccurrences of AEs; however, the effects on pulmonary function, pulmonary, and systemic inflammatory biomarkers remain unclear. Methods. Cigarette-smoke/bacterial infections induced rats were randomized into Control, COPD, AECOPD, Tongsai Granule/normal saline (TSG/NS), moxifloxacin + salbutamol/NS (MXF+STL/NS), TSG/Bufei Yishen Granule (BYG), MXF+STL/STL, and TSG+MXF+STL/BYG+STL groups and given corresponding medicine(s) in AE- and/or RW phase. Body temperature, pulmonary function, blood cytology, serum amyloid A (SAA) and C-reactive protein (CRP), pulmonary histomorphology and myeloperoxidase (MPO), polymorphonuclear (PMN) elastase, interleukins IL-1β, IL-6, and IL-10, and tumor necrosis factor- (TNF-) α expressions were determined. Results. Body temperature, inflammatory cells and cytokines, SAA, CRP, and pulmonary impairment were higher in AECOPD rats than stable COPD, while pulmonary function declined and recovered to COPD level in 14–18 days. All biomarkers were improved in treated groups with shorter recovery times of 4–10 days, especially in TSG+MXF+STL/BYG+STL group. Conclusion. Sequential treatments with Tongsai and Bufei Yishen Granules, during AECOPD-RW periods, can reduce inflammatory response and improve pulmonary function and shorten the recovery courses of AEs, especially the integrated Chinese and Western medicines. PMID:27563333

  14. 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.

  15. 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.

  16. 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.

  17. Histoplasmosis - acute (primary) pulmonary

    Science.gov (United States)

    ... this page: //medlineplus.gov/ency/article/000098.htm Histoplasmosis - acute (primary) pulmonary To use the sharing features on this page, please enable JavaScript. Acute pulmonary histoplasmosis is a respiratory infection that is caused by ...

  18. Miliary pulmonary cryptococcosis

    Directory of Open Access Journals (Sweden)

    Shane Kelly

    2014-10-01

    Imaging features of pulmonary cryptococcosis are generally of well-defined pleural-based nodules and less commonly alveolar infiltrates, lymphadenopathy, pleural effusions or cavitating lesions. Miliary pulmonary infiltrates are an exceptionally rare presentation.

  19. Pulmonary Hemorrhage in Cryoglobulinemia

    Directory of Open Access Journals (Sweden)

    G Kirkpatrick

    2015-01-01

    Full Text Available Pulmonary manifestations of cryoglobulinemia are uncommon and their clinical behaviour is unpredictable, ranging from mild dyspnea to life-threatening presentations. A patient with cryoglobulinemia who presented with hypoxic respiratory failure attributed to pulmonary hemorrhage is reported.

  20. 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.

  1. 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.

  2. 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.

  3. Pulmonary Hypertension Association

    Science.gov (United States)

    ... at www.AHeartCures.org . Help Kickoff November’s Pulmonary Hypertension Awareness Month Want to help raise awareness for ... Heart2CurePH | Help promote Awareness Month Chronic Thromboembolic Pulmonary Hypertension (CTEPH) Awareness Chronic thromboembolic pulmonary hypertension (CTEPH) is ...

  4. Pulmonary Hypertension Overview

    Science.gov (United States)

    ... chest X-ray, a breathing test called a pulmonary function test and an echocardiogram (sometimes called an “echo”). Your doctor may also need to do other tests to find out whether another medical condition is causing your pulmonary hypertension. TreatmentHow is pulmonary hypertension treated?If the ...

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2013-10-01

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

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

    Directory of Open Access Journals (Sweden)

    Yi Eunhee S

    2010-04-01

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

  7. 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.

  8. 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.

  9. 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.

  10. [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.

  11. 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.

  12. 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.

  13. 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...

  14. 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...

  15. 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.

  16. Acute Exacerbation of Chronic Obstructive Pulmonary Disease: Cardiovascular Links

    Directory of Open Access Journals (Sweden)

    Cheryl R. Laratta

    2014-01-01

    Full Text Available Chronic obstructive pulmonary disease (COPD is a chronic, progressive lung disease resulting from exposure to cigarette smoke, noxious gases, particulate matter, and air pollutants. COPD is exacerbated by acute inflammatory insults such as lung infections (viral and bacterial and air pollutants which further accelerate the steady decline in lung function. The chronic inflammatory process in the lung contributes to the extrapulmonary manifestations of COPD which are predominantly cardiovascular in nature. Here we review the significant burden of cardiovascular disease in COPD and discuss the clinical and pathological links between acute exacerbations of COPD and cardiovascular disease.

  17. Current treatment in chronic obstructive pulmonary disease

    Institute of Scientific and Technical Information of China (English)

    李嘉惠

    2008-01-01

    Chronic obstructive pulmonary disease (COPD) is defined by fixed airflow limitation associated with an abnormal pulmonary and systemic inflammatory response of the lungs to cigarette smoke. COPD represents an increasing burden worldwide, reported to be the sixth leading cause of death in 1990 and the fourth in 2000. Discouragingly, it is projected to jump to third place by the year 2020.There is increasing evidence that COPD is a more complex systemic disease than an airway and lung disease. In particular, cachexia, skeletal muscle abnormalities, diabetes, coronary artery disease, heart failure, cancer and pulmonary vascular disease are the most common comorbidities. It is associated with a wide variety of systemic consequences, most notably systemic inflammation. Because COPD patients have in general ahigher cardiovascular risk than the average population, cardiovascular safety in a COPD medication is of critical importance.SINGH et al performed a systematic review and recta-analysis of 17 clinical trials enrolling 14 783 patients treated with inhaled anticholinergic drugs used for the treatment of COPD. Inhaled anticholinergics significantly increased the risk of cardiovascular death, MI, or stroke ( 1.8 % vs 1.2 % for control; RR, 1.58 (95 % CI,1.21 - 2.06); P < 0.001 ). However, UPLIIFT (Understanding the Potential Long-Term Impacts on Function with Tiotropium) , a large, 4-year, placebo controlled clinical trial with tiotropium in approximately 6 000 patients with COPD. The preliminary results of UPLIFT showed that there was no increased risk of stroke with tiotropium bromide compared to placebo.A meta-analysis is always considered less convincing than a large prospective trial designed to assess the outcome of interest. However, COPD is a systemic disease. COPD management needs to focus on four major areas: smoking cessation, pharmacologic therapy, exercise training, and pulmonary rehabilitation. Clinicians and patients should always carefully consider any

  18. 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.

  19. 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

  20. 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.

  1. 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.

  2. 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.

  3. 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...

  4. 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 ...

  5. 76 FR 66074 - Small Entity Compliance Guide: Required Warnings for Cigarette Packages and Advertisements...

    Science.gov (United States)

    2011-10-25

    ... Cigarette Packages and Advertisements; Availability AGENCY: Food and Drug Administration, HHS. ACTION... industry entitled ``Required Warnings for Cigarette Packages and Advertisements--Small Entity Compliance... entitled ``Required Warnings for Cigarette Packages and Advertisements--Small Entity Compliance Guide''...

  6. 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, ...

  7. 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.

  8. 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.

  9. 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.

  10. Pulmonary dysfunction and surgical risk. How to assess and minimize the hazards.

    Science.gov (United States)

    Okeson, G C

    1983-11-01

    Postoperative deterioration of pulmonary function can be considerable, resulting in hypoxemia and atelectasis, if such effects are not anticipated and efforts made to prevent or minimize them. The risk of postoperative pulmonary complications depends on the patient's age, degree of obesity, and cigarette consumption; the type of surgery to be performed; and the anesthetic agent used. Assessment of risk is based primarily on clinical and laboratory evaluations. The tests performed may vary from patient to patient, and specialized studies of regional pulmonary function are frequently required. Even though a patient may be identified as having a high risk of postoperative pulmonary complications, risk can often be decreased through a number of preoperative and intraoperative measures as well as a postoperative therapeutic program.

  11. 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.

  12. 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.

  13. 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.

  14. 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.

  15. 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.

  16. Multidetector computed tomography pulmonary angiography in childhood acute pulmonary embolism

    Energy Technology Data Exchange (ETDEWEB)

    Tang, Chun Xiang; Zhang, Long Jiang; Lu, Guang Ming [Medical School of Nanjing University, Department of Medical Imaging, Jinling Hospital, Nanjing, Jiangsu (China); Schoepf, U.J. [Medical School of Nanjing University, Department of Medical Imaging, Jinling Hospital, Nanjing, Jiangsu (China); Medical University of South Carolina, Department of Radiology and Radiological Science, Charleston, SC (United States); Medical University of South Carolina, Department of Pediatrics, Charleston, SC (United States); Chowdhury, Shahryar M. [Medical University of South Carolina, Department of Pediatrics, Charleston, SC (United States); Fox, Mary A. [Medical University of South Carolina, Department of Radiology and Radiological Science, Charleston, SC (United States)

    2015-09-15

    Pulmonary embolism is a life-threatening condition affecting people of all ages. Multidetector row CT pulmonary angiography has improved the imaging of pulmonary embolism in both adults and children and is now regarded as the routine modality for detection of pulmonary embolism. Advanced CT pulmonary angiography techniques developed in recent years, such as dual-energy CT, have been applied as a one-stop modality for pulmonary embolism diagnosis in children, as they can simultaneously provide anatomical and functional information. We discuss CT pulmonary angiography techniques, common and uncommon findings of pulmonary embolism in both conventional and dual-energy CT pulmonary angiography, and radiation dose considerations. (orig.)

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

    Directory of Open Access Journals (Sweden)

    Manuela Martins-Green

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

  18. 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.

  19. EFFECTS OF CIGARETTE SMOKE EXTRACT ON PROLIFERATION AND CTGF EXPRESSION OF HUMAN PULMONARY ARTERY SMOOTH MUSCLE CELLS%结缔组织生长因子在香烟提取物致人肺动脉平滑肌细胞增殖中的作用研究

    Institute of Scientific and Technical Information of China (English)

    卞维仕; 康振兴; 武善霞; 田锋; 杜庆伟

    2016-01-01

    Objective In order to explor the effects of cigarette smoke extract (CSE) on cell proliferation and the role of connective tissue growth factor (CTGF) .Methods In this study ,Cultured hPASMCs were divided into six groups :A :the normal control group ,B :hypoxia control group ,C :CSE group ,D :CSE and rhTGF‐β1 group ,E :CSE and CTGF sense oligonucleotide group ,F :CSE and CTGF antisense oligo‐nucleotide group .Then ,the expression of CTGF mRNA and protein of the supernatant of cells ,collagen content of cell culture supernatant .Results In Cell proliferation assay ,C group was more increased than in group A respectively ,Compared with D and C group , D group was more outstanding ,F groupwas decreased significantly ,compared with C group ( P 0 .05) .The results of CTGF mRNA ex‐pression and the content of type Ⅷ collagen in the su‐pernatant of cell culture were showed similar tendency to the protein expression .Conclusion CSE can in‐duce hPASMC proliferation ,CTGF may play an important role in it .%目的:探讨香烟提取物(CSE)对人肺动脉平滑肌细胞(hPASMC)增殖的影响及结缔组织生长因子(CTGF)在其中的作用。方法培养的hPASMC随机分为正常对照组(A)、缺氧对照组(B)、CSE组(C)、CSE+rhTGF‐β1组(D)、CSE+CTGF正义寡核苷酸组(E)、CSE+CTGF反义寡核苷酸组(F),分别检测细胞增殖、CTGF mRNA及蛋白表达、细胞培养上清液中I型胶原含量。结果细胞增殖检测,C组与A组比较明显升高,D组与C组比较,D组升高更卓著,F较C组下降显著( P均<0.01);E和C组之间无显著性差异( P >0.05)。hPASMC内CTGF蛋白表达量C组较A组明显升高,D较C组升高更明显,F较C组下降显著( P均<0.01);E组与C组之间无显著性差异( P >0.05);CTGF mRNA表达结果及细胞培养上清液中I型胶原含量均与蛋白表达有相似趋势。结论 CSE能诱导hPASMC增殖

  20. 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.

  1. 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.

  2. 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.

  3. Metal and silicate particles including nanoparticles are present in electronic cigarette cartomizer fluid and aerosol.

    Directory of Open Access Journals (Sweden)

    Monique Williams

    Full Text Available Electronic cigarettes (EC deliver aerosol by heating fluid containing nicotine. Cartomizer EC combine the fluid chamber and heating element in a single unit. Because EC do not burn tobacco, they may be safer than conventional cigarettes. Their use is rapidly increasing worldwide with little prior testing of their aerosol.We tested the hypothesis that EC aerosol contains metals derived from various components in EC.Cartomizer contents and aerosols were analyzed using light and electron microscopy, cytotoxicity testing, x-ray microanalysis, particle counting, and inductively coupled plasma optical emission spectrometry.The filament, a nickel-chromium wire, was coupled to a thicker copper wire coated with silver. The silver coating was sometimes missing. Four tin solder joints attached the wires to each other and coupled the copper/silver wire to the air tube and mouthpiece. All cartomizers had evidence of use before packaging (burn spots on the fibers and electrophoretic movement of fluid in the fibers. Fibers in two cartomizers had green deposits that contained copper. Centrifugation of the fibers produced large pellets containing tin. Tin particles and tin whiskers were identified in cartridge fluid and outer fibers. Cartomizer fluid with tin particles was cytotoxic in assays using human pulmonary fibroblasts. The aerosol contained particles >1 µm comprised of tin, silver, iron, nickel, aluminum, and silicate and nanoparticles (<100 nm of tin, chromium and nickel. The concentrations of nine of eleven elements in EC aerosol were higher than or equal to the corresponding concentrations in conventional cigarette smoke. Many of the elements identified in EC aerosol are known to cause respiratory distress and disease.The presence of metal and silicate particles in cartomizer aerosol demonstrates the need for improved quality control in EC design and manufacture and studies on how EC aerosol impacts the health of users and bystanders.

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

    Directory of Open Access Journals (Sweden)

    Postma Dirkje S

    2007-07-01

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

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

    Science.gov (United States)

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

    2016-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Marco Checa

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

  7. No sisyphean task: how the FDA can regulate electronic cigarettes.

    Science.gov (United States)

    Paradise, Jordan

    2013-01-01

    The adverse effects of smoking have fostered a natural market for smoking cessation and smoking reduction products. Smokers attempting to quit or reduce consumption have tried everything: "low" or "light" cigarettes; nicotine-infused chewing gum, lozenges, and lollipops; dermal patches; and even hypnosis. The latest craze in the quest to find a safer source of nicotine is the electronic cigarette. Electronic cigarettes (e-cigarettes) have swept the market, reaching a rapidly expanding international consumer base. Boasting nicotine delivery and the tactile feel of a traditional cigarette without the dozens of other chemical constituents that contribute to carcinogenicity, e-cigarettes are often portrayed as less risky, as a smoking reduction or even a complete smoking cessation product, and perhaps most troubling for its appeal to youth, as a flavorful, trendy, and convenient accessory. The sensationalism associated with e-cigarettes has spurred outcry from health and medical professional groups, as well as the Food and Drug Administration (FDA), because of the unknown effects on public health. Inhabiting a realm of products deemed "tobacco products" under recent 2009 legislation, e-cigarettes pose new challenges to FDA regulation because of their novel method of nicotine delivery, various mechanical and electrical parts, and nearly nonexistent safety data. Consumer use, marketing and promotional claims, and technological characteristics of e-cigarettes have also raised decades old questions of when the FDA can assert authority over products as drugs or medical devices. Recent case law restricting FDA enforcement efforts against e-cigarettes further confounds the distinction among drugs and medical devices, emerging e-cigarette products, and traditional tobacco products such as cigarettes, cigars, and smokeless tobacco. This Article investigates the e-cigarette phenomenon in the wake of the recently enacted Family Smoking Prevention and Tobacco Control Act of 2009

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

    Science.gov (United States)

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

    2016-01-01

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

  9. Mechanisms responsible for pulmonary hypertension

    Institute of Scientific and Technical Information of China (English)

    2008-01-01

    @@ Pulmonary hypertension is a pathophysiologic process characterized by progressive elevation of pulmonary vascular resistance and right heart failure, which is a common complication of many diseases. Pulmonary hypertension with no apparent causes (unknown etiology) is termed primary pulmonary hypertension or, more recently, idiopathic pulmonary arterial hypertension (IPAH).

  10. Pulmonary arterial hypertension : an update

    NARCIS (Netherlands)

    Hoendermis, E. S.

    2011-01-01

    Pulmonary arterial hypertension (PAH), defined as group 1 of the World Heart Organisation (WHO) classification of pulmonary hypertension, is an uncommon disorder of the pulmonary vascular system. It is characterised by an increased pulmonary artery pressure, increased pulmonary vascular resistance a

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

    Science.gov (United States)

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

    2014-11-01

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

  12. Cigarette smoke-mediated perturbations of the immune response: A new therapeutic approach with natural compounds.

    Science.gov (United States)

    Magrone, Thea; Jirillo, Emilio

    2016-09-27

    Cigarette smoke (CS) accounts for the outcome of several pathologies, even including lung cancer, cardiovascular disease and chronic obstructive pulmonary disease (COPD). Under healthy conditions, lung immune system becomes tolerant in response to various external stimuli. CS exposure alters the pulmonary immune equilibrium, thus leading to a condition of hyper activation of the local innate and adaptive immunity. COPD is one of the major complications of chronic CS exposure where a pro-inflammatory profile of the pulmonary and systemic immunity is predominant. In this review, alternative treatments with natural products to mitigate CS-mediated pulmonary inflammation are proposed. In particular, polyphenols, a class of natural compounds largely present in fruits and vegetables, have been shown to act as anti-inflammatory agents. Accordingly, recent experimental and clinical evidences support polyphenol-mediated potential health benefits in smokers. For instance, pomegranate juice is able to attenuate the damage provoked by CS on cultured human alveolar macrophages. In addition, maqui beery extract has been proven to normalize H2O2 and interleukin-6 levels in exhaled breath condensate in healthy smokers. However, some limitations of alternative treatments are represented by a better knowledge of the mechanism(s) of action exerted by polyphenols and by the lack of animal models of COPD. In any case, the potential targets of polyphenols in the course of COPD will be outlined with special reference to the activation of T regulatory cells as well as to the inhibition of the polymorphonuclear cell and monocyte respiratory burst and of the NF-kB pathway, respectively.

  13. Use and Perception of Electronic Cigarettes among College Students

    Science.gov (United States)

    Trumbo, Craig W.; Harper, Raquel

    2013-01-01

    Objective: This study provides insight into how electronic cigarettes (e-cigarettes) may affect the social normative environment for tobacco use among college students. Participants: Participants were 244 freshman and sophomore students. Methods: Students completed an online self-report survey in April 2011. Results: There is a higher acceptance…

  14. DEVELOPMENT OF SEPIOLITE TYPE FILTER TIPS OF CIGARETTE

    Institute of Scientific and Technical Information of China (English)

    2000-01-01

    Activating conditions of sepiolite are studied by determining specific surface method. Sepiolite is used in processing filter tip of cigarette of acetate silk and paper type first.Tar of cigarette with sepiolite filter tip is lowered to a lower tar level. Mechanism of the lowered tar content by sepiolite is analysed.

  15. E-cigarettes forbidden in offices and closed areas

    CERN Multimedia

    2013-01-01

    Be reminded that all people on the CERN site must comply with the following notice from the Medical Service: “In the same manner as for ordinary cigarettes, the use of e-cigarettes is forbidden in all offices and closed areas.” If you have any question, please write to medical.service@cern.ch HSE Unit/ GS-ME Department

  16. What Are Tobacco, Nicotine, and E-Cigarette Products?

    Science.gov (United States)

    ... e-cigarettes by the time they start 9th grade are more likely than others to start smoking traditional cigarettes ... now, smokers who want to quit have other good options with proven effectiveness. Find out more at teen.smokefree.gov and cdc.gov/tobacco/ ...

  17. 76 FR 57008 - Smoking of Electronic Cigarettes on Aircraft

    Science.gov (United States)

    2011-09-15

    ... for submitting comments. Mail: Docket Management Facility, U.S. Department of Transportation, 1200 New... Journal of Medicine article, ``E-Cigarette or Drug-Delivery Device? Regulating Novel Nicotine Products... which they evaluated five electronic cigarette brands. See Anna Trtchounian & Prue Talbot,...

  18. Solvent Chemistry in the Electronic Cigarette Reaction Vessel

    Science.gov (United States)

    Jensen, R. Paul; Strongin, Robert M.; Peyton, David H.

    2017-02-01

    Knowledge of the mechanism of formation, levels and toxicological profiles of the chemical products in the aerosols (i.e., vapor plus particulate phases) of e-cigarettes is needed in order to better inform basic research as well as the general public, regulators, and industry. To date, studies of e-cigarette emissions have mainly focused on chromatographic techniques for quantifying and comparing the levels of selected e-cigarette aerosol components to those found in traditional cigarettes. E-cigarettes heat and aerosolize the solvents propylene glycol (PG) and glycerol (GLY), thereby affording unique product profiles as compared to traditional cigarettes. The chemical literature strongly suggests that there should be more compounds produced by PG and GLY than have been reported in e-cigarette aerosols to date. Herein we report an extensive investigation of the products derived from vaporizing PG and GLY under mild, single puff conditions. This has led to the discovery of several new compounds produced under vaping conditions. Prior reports on e-cigarette toxin production have emphasized temperature as the primary variable in solvent degradation. In the current study, the molecular pathways leading to enhanced PG/GLY reactivity are described, along with the most impactful chemical conditions promoting byproduct production.

  19. Solvent Chemistry in the Electronic Cigarette Reaction Vessel

    Science.gov (United States)

    Jensen, R. Paul; Strongin, Robert M.; Peyton, David H.

    2017-01-01

    Knowledge of the mechanism of formation, levels and toxicological profiles of the chemical products in the aerosols (i.e., vapor plus particulate phases) of e-cigarettes is needed in order to better inform basic research as well as the general public, regulators, and industry. To date, studies of e-cigarette emissions have mainly focused on chromatographic techniques for quantifying and comparing the levels of selected e-cigarette aerosol components to those found in traditional cigarettes. E-cigarettes heat and aerosolize the solvents propylene glycol (PG) and glycerol (GLY), thereby affording unique product profiles as compared to traditional cigarettes. The chemical literature strongly suggests that there should be more compounds produced by PG and GLY than have been reported in e-cigarette aerosols to date. Herein we report an extensive investigation of the products derived from vaporizing PG and GLY under mild, single puff conditions. This has led to the discovery of several new compounds produced under vaping conditions. Prior reports on e-cigarette toxin production have emphasized temperature as the primary variable in solvent degradation. In the current study, the molecular pathways leading to enhanced PG/GLY reactivity are described, along with the most impactful chemical conditions promoting byproduct production. PMID:28195231

  20. Exploding E-Cigarettes Sending 'Vapers' to Burn Centers

    Science.gov (United States)

    ... https://medlineplus.gov/news/fullstory_161323.html Exploding E-Cigarettes Sending 'Vapers' to Burn Centers Users say they' ... 5, 2016 WEDNESDAY, Oct. 5, 2016 (HealthDay News) -- E-cigarette devices are randomly and unexpectedly exploding, burning and ...

  1. Flavorings Boost Toxicity of E-Cigarettes in Lab Study

    Science.gov (United States)

    ... news/fullstory_161111.html Flavorings Boost Toxicity of E-Cigarettes in Lab Study Increasing device's voltage, to get ... Sept. 22, 2016 (HealthDay News) -- Flavorings used in e-cigarettes can increase the toxicity of the vapor that ...

  2. Depressive Symptoms and Cigarette Smoking in a College Sample

    Science.gov (United States)

    Kenney, Brent A.; Holahan, Charles J.

    2008-01-01

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

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

    Science.gov (United States)

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

    2015-12-01

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

  4. Vector Unveils Reduced--Carcinogen Cigarette

    Institute of Scientific and Technical Information of China (English)

    裴小江

    2001-01-01

    11月5日,美国拥有排名第五的烟草公司的Vector集团(有限公司)声称他们制造出了一种牌子为Omni的香烟,这种经过碳过滤器加工的香烟,其致癌物质被削减了15%—60%。他们非常策略地称:While there is no suchthing as a safe cigarette,we believe that if you do smoke,Omni is the bestalternative。】

  5. The Importance of Conditioned Stimuli in Cigarette and E-Cigarette Craving Reduction by E-Cigarettes

    Directory of Open Access Journals (Sweden)

    Martijn Van Heel

    2017-02-01

    Full Text Available This study examined the impact of four variables pertaining to the use of e-cigarettes (e-cigs on cravings for tobacco cigarettes and for e-cigs after an overnight abstinence period. The four variables were the nicotine level, the sensorimotor component, the visual aspect, and the aroma of the e-cig. In an experimental study, 81 participants without prior vaping experience first got acquainted with using e-cigs in a one-week tryout period, after which they participated in a lab session assessing the effect of five minutes of vaping following an abstinence period of 12 h. A mixed-effects model clearly showed the importance of nicotine in craving reduction. However, also non-nicotine factors, in particular the sensorimotor component, were shown to contribute to craving reduction. Handling cues interacted with the level (presence/absence of nicotine: it was only when the standard hand-to-mouth action cues were omitted that the craving reducing effects of nicotine were observed. Effects of aroma or visual cues were not observed, or weak and difficult to interpret, respectively.

  6. The Importance of Conditioned Stimuli in Cigarette and E-Cigarette Craving Reduction by E-Cigarettes

    Science.gov (United States)

    Van Heel, Martijn; Van Gucht, Dinska; Vanbrabant, Koen; Baeyens, Frank

    2017-01-01

    This study examined the impact of four variables pertaining to the use of e-cigarettes (e-cigs) on cravings for tobacco cigarettes and for e-cigs after an overnight abstinence period. The four variables were the nicotine level, the sensorimotor component, the visual aspect, and the aroma of the e-cig. In an experimental study, 81 participants without prior vaping experience first got acquainted with using e-cigs in a one-week tryout period, after which they participated in a lab session assessing the effect of five minutes of vaping following an abstinence period of 12 h. A mixed-effects model clearly showed the importance of nicotine in craving reduction. However, also non-nicotine factors, in particular the sensorimotor component, were shown to contribute to craving reduction. Handling cues interacted with the level (presence/absence) of nicotine: it was only when the standard hand-to-mouth action cues were omitted that the craving reducing effects of nicotine were observed. Effects of aroma or visual cues were not observed, or weak and difficult to interpret, respectively. PMID:28212302

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

    Science.gov (United States)

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

    2004-12-01

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

  8. Tobacco and cigarette butt consumption in humans and animals.

    Science.gov (United States)

    Novotny, Thomas E; Hardin, Sarah N; Hovda, Lynn R; Novotny, Dale J; McLean, Mary Kay; Khan, Safdar

    2011-05-01

    Discarded cigarette butts may present health risks to human infants and animals because of indiscriminate eating behaviours. Nicotine found in cigarette butts may cause vomiting and neurological toxicity; leachates of cigarette butts in aquatic environments may cause exposure to additional toxic chemicals including heavy metals, ethyl phenol and pesticide residues. This report reviews published and grey literature regarding cigarette butt waste consumption by children, pets and wildlife. Although reports of human and animal exposures number in the tens of thousands, severe toxic outcomes due to butt consumption are rare. Nonetheless, the ubiquity of cigarette butt waste and its potential for adverse effects on human and animal health warrants additional research and policy interventions to reduce the stream of these pollutants in the environment.

  9. Handbook of pulmonary emergencies

    Energy Technology Data Exchange (ETDEWEB)

    Spaquolo, S.V.; Medinger, A

    1986-01-01

    This book presents information on the following topics: clinical assessment of the patient with pulmonary disease; interpretation of arterial blood gases in the emergency patient; life-threatening pneumonia; extrapulmonic ventilatory failure; acute inhalation lung disease; pulmonary edema; near drowning; chest trauma; upper airway emergencies; chronic lung disease with acute respiratory decompensation; acute respiratory failure in the patient with chronic airflow obstruction; asthma; hemoptysis; embolic pulmonary disease; superior vena cava syndrome; catastrophic pleural disease; ventilatory assistance and its complications; and ventilator emergencies.

  10. Waterpipes and electronic cigarettes: increasing prevalence and expanding science.

    Science.gov (United States)

    Pepper, Jessica K; Eissenberg, Thomas

    2014-08-18

    The prevalence of non-cigarette tobacco product use is on the rise across the globe, especially for waterpipes (also known as hookah, narghile, and shisha) and electronic cigarettes (e-cigarettes). The scientific literature reveals that waterpipe tobacco smoking is associated with exposure to a variety of toxicants that can cause short- and long-term adverse health events. In contrast, there is far less evidence of health harms related to e-cigarette use, although the variety of products in this category makes it difficult to generalize. We searched the PubMed database for all publications on waterpipes and e-cigarettes from January 2000 to March 2014. The number of publications on waterpipes rose in a slow, linear pattern during this time, while the number of publications on e-cigarettes showed exponential growth. The different trends suggest there may be more interest in studying a novel nicotine product (the e-cigarette) over a traditional tobacco product (the waterpipe). We posit that, although the specific research needs for these products are different, public health would be served best by a more equitable research approach. Scientists should continue to devote attention to understanding the unknown long-term health effects of e-cigarettes and their potential to serve as harm reduction or smoking cessation tools while simultaneously investigating how to reduce waterpipe smoking given that it exposes users to toxicants known to cause harm to health. Recent regulatory action in the United States, which proposes to include waterpipes and e-cigarettes under some of the same regulations as tobacco cigarettes, makes such research particularly timely.

  11. Epidemiology of menthol cigarette use in the United States

    Directory of Open Access Journals (Sweden)

    Asman Katherine

    2011-05-01

    Full Text Available Abstract Background Approximately one-fourth of all cigarettes sold in the United States have the descriptor “menthol” on the cigarette pack. It is important to determine what socio-demographic factors are associated with smoking menthol cigarettes if indeed these types of cigarettes are related to smoking initiation, higher exposure to smoke constituents, nicotine dependence, or reduced smoking cessation. Methods The National Cancer Institute (NCI conducted a review of the scientific literature on this topic which we completed by adding more recently published articles via PubMed. We also conducted further data analyses using the National Survey on Drug Use and Health, the National Youth Tobacco Survey, the Monitoring the Future Survey, and the National Health and Nutrition Examination Survey to provide up-to-date information on this topic. Results Menthol cigarettes are disproportionately smoked by adolescents, blacks/African Americans, adult females, those living in the Northeast of the United States and those with family incomes lower than $50,000. Based on self-reports of menthol cigarette use, menthol cigarette use among smokers have increased from 2004 to 2008. However, no increase was observed during these years for predominantly menthol brands like Newport™, Kool,™ and Salem™, however, this lack of significant trend may be due, at least in part, due to smaller numbers of smokers of specific brands or sub-brands, which provide estimates which are less precise. Conclusion Menthol cigarettes are disproportionately smoked by groups of U.S. cigarette smokers. It is likely that other disparities in menthol cigarette use exist that we have not covered or have not been studied yet.

  12. How Is Pulmonary Hypertension Diagnosed?

    Science.gov (United States)

    ... from the NHLBI on Twitter. How Is Pulmonary Hypertension Diagnosed? Your doctor will diagnose pulmonary hypertension (PH) ... To Look for the Underlying Cause of Pulmonary Hypertension PH has many causes, so many tests may ...

  13. Idiopathic pulmonary artery aneurysm.

    Science.gov (United States)

    Kotwica, Tomasz; Szumarska, Joanna; Staniszewska-Marszalek, Edyta; Mazurek, Walentyna; Kosmala, Wojciech

    2009-05-01

    Pulmonary artery aneurysm (PAA) is an uncommon lesion, which may be associated with different etiologies including congenital cardiovascular diseases, systemic vasculitis, connective tissue diseases, infections, and trauma. Idiopathic PAA is sporadically diagnosed by exclusion of concomitant major pathology. We report a case of a 56-year-old female with an idiopathic pulmonary artery dilatation identified fortuitously by echocardiography and confirmed by contrast-enhanced computed tomography. Neither significant pulmonary valve dysfunction nor pulmonary hypertension and other cardiac abnormalities which might contribute to the PAA development were found. Here, we describe echocardiographic and computed tomography findings and review the literature on PAA management.

  14. Miliary pulmonary cryptococcosis

    Science.gov (United States)

    Kelly, Shane; Marriott, Deborah

    2014-01-01

    A 32-year-old HIV positive male presents with fevers and a non-productive cough. Initial X-ray and subsequent computerised tomography of the chest shows a bilateral miliary pattern of pulmonary infiltration highly suggestive of disseminated tuberculosis. However subsequent results were consistent with disseminated cryptococcosis, including pulmonary involvement, with cryptococcus identified on transbronchial tissue biopsy, and on blood and cerebrospinal fluid cultures. Imaging features of pulmonary cryptococcosis are generally of well-defined pleural-based nodules and less commonly alveolar infiltrates, lymphadenopathy, pleural effusions or cavitating lesions. Miliary pulmonary infiltrates are an exceptionally rare presentation. PMID:25379393

  15. Regulation of pulmonary inflammation by mesenchymal cells

    NARCIS (Netherlands)

    Alkhouri, Hatem; Poppinga, Wilfred Jelco; Tania, Navessa Padma; Ammit, Alaina; Schuliga, Michael

    2014-01-01

    Pulmonary inflammation and tissue remodelling are common elements of chronic respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), and pulmonary hypertension (PH). In disease, pulmonary mesenchymal cells not only contribute to tissue

  16. Electronic Cigarette Topography in the Natural Environment.

    Directory of Open Access Journals (Sweden)

    R J Robinson

    Full Text Available This paper presents the results of a clinical, observational, descriptive study to quantify the use patterns of electronic cigarette users in their natural environment. Previously published work regarding puff topography has been widely indirect in nature, and qualitative rather than quantitative, with the exception of three studies conducted in a laboratory environment for limited amounts of time. The current study quantifies the variation in puffing behaviors among users as well as the variation for a given user throughout the course of a day. Puff topography characteristics computed for each puffing session by each subject include the number of subject puffs per puffing session, the mean puff duration per session, the mean puff flow rate per session, the mean puff volume per session, and the cumulative puff volume per session. The same puff topography characteristics are computed across all puffing sessions by each single subject and across all subjects in the study cohort. Results indicate significant inter-subject variability with regard to puffing topography, suggesting that a range of representative puffing topography patterns should be used to drive machine-puffed electronic cigarette aerosol evaluation systems.

  17. Cigarette smoke affects bonding to dentin.

    Science.gov (United States)

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

    2010-01-01

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

  18. Pulmonary arterial hypertension in pregnancy.

    Science.gov (United States)

    Običan, Sarah G; Cleary, Kirsten L

    2014-08-01

    Pulmonary hypertension is a medical condition characterized by elevated pulmonary arterial pressure and secondary right heart failure. Pulmonary arterial hypertension is a subset of pulmonary hypertension, which is characterized by an underlying disorder of the pulmonary arterial vasculature. Pulmonary hypertension can also occur secondarily to structural cardiac disease, autoimmune disorders, and toxic exposures. Although pregnancies affected by pulmonary hypertension and pulmonary arterial hypertension are rare, the pathophysiology exacerbated by pregnancy confers both high maternal and fetal mortality and morbidity. In light of new treatment modalities and the use of a multidisciplinary approach to care, maternal outcomes may be improving.

  19. Electronic Cigarettes Efficacy and Safety at 12 Months: Cohort Study.

    Directory of Open Access Journals (Sweden)

    Lamberto Manzoli

    Full Text Available To evaluate the safety and efficacy as a tool of smoking cessation of electronic cigarettes (e-cigarettes, directly comparing users of e-cigarettes only, smokers of tobacco cigarettes only, and smokers of both.Prospective cohort study. Final results are expected in 2019, but given the urgency of data to support policies on electronic smoking, we report the results of the 12-month follow-up.Direct contact and structured questionnaires by phone or via internet.Adults (30-75 years were included if they were smokers of ≥1 tobacco cigarette/day (tobacco smokers, users of any type of e-cigarettes, inhaling ≥50 puffs weekly (e-smokers, or smokers of both tobacco and e-cigarettes (dual smokers. Carbon monoxide levels were tested in a sample of those declaring tobacco smoking abstinence.Sustained smoking abstinence from tobacco smoking at 12 months, reduction in the number of tobacco cigarettes smoked daily.We used linear and logistic regression, with region as cluster unit.Follow-up data were available for 236 e-smokers, 491 tobacco smokers, and 232 dual smokers (overall response rate 70.8%. All e-smokers were tobacco ex-smokers. At 12 months, 61.9% of the e-smokers were still abstinent from tobacco smoking; 20.6% of the tobacco smokers and 22.0% of the dual smokers achieved tobacco abstinence. Adjusting for potential confounders, tobacco smoking abstinence or cessation remained significantly more likely among e-smokers (adjusted OR 5.19; 95% CI: 3.35-8.02, whereas adding e-cigarettes to tobacco smoking did not enhance the likelihood of quitting tobacco and did not reduce tobacco cigarette consumption. E-smokers showed a minimal but significantly higher increase in self-rated health than other smokers. Non significant differences were found in self-reported serious adverse events (eleven overall.Adding e-cigarettes to tobacco smoking did not facilitate smoking cessation or reduction. If e-cigarette safety will be confirmed, however, the use of e-cigarettes

  20. Toxicological evaluation of glycerin as a cigarette ingredient.

    Science.gov (United States)

    Carmines, E L; Gaworski, C L

    2005-10-01

    Glycerin is applied to cigarette tobacco at levels in the range of about 1-5% to improve moisture holding characteristics of tobacco and act as a surface active agent for flavor application. Neat material pyrolysis studies, smoke chemistry and biological activity studies (bacterial mutagenicity, cytotoxicity, in vivo micronucleus, and sub-chronic rodent inhalation) with mainstream smoke, or mainstream smoke preparations from cigarettes containing various target levels (5%, 10%, and 15%) of the glycerin were performed to provide data for an assessment of the use of glycerin as a cigarette tobacco ingredient. The actual levels of glycerin in the respective test cigarettes were determined to be 3.2%, 6.2% and 8.4% after cigarette production. At simulated tobacco burning temperatures up to 900 degrees C, neat glycerin did not pyrolyze extensively suggesting that glycerin would transfer intact to mainstream smoke (smoke was not analyzed for glycerin in this study). On a tar basis, nicotine in smoke was significantly decreased at 10% and 15% glycerin while water was increased at all addition levels. Addition of 10% or 15% glycerin also resulted in a statistically significant increase in acrolein (9%) and a decrease in acetaldehyde, propionaldehyde, aromatic amines, nitrogen oxides, tobacco specific nitrosamines, and phenols. Addition of 5% glycerin produced the same decrease in smoke constituents as the 10% and 15% groups but there was no concomitant increase in acrolein. Biological tests indicated no relevant differences in the genotoxic or cytotoxic potential of either mainstream smoke (or smoke preparations) from cigarettes with added glycerin compared to control cigarettes. Cigarette smoke atmosphere dilution, coupled with the lower nicotine delivery in the test cigarettes containing glycerin resulted in a lower nicotine delivery to the glycerin cigarette smoke exposed rats of the 90-day inhalation study. Smoke atmosphere acrolein was also reduced in a concentration

  1. Electronic Cigarette Use among College Students: Links to Gender, Race/Ethnicity, Smoking, and Heavy Drinking

    Science.gov (United States)

    Littlefield, Andrew K.; Gottlieb, Joshua C.; Cohen, Lee M.; Trotter, David R. M.

    2015-01-01

    Objective: Electronic cigarette (e-cigarette) use continues to rise, and current data regarding use of e-cigarettes among college students are needed. The purpose of this study was to examine e-cigarette use and the relation of such use with gender, race/ethnicity, traditional tobacco use, and heavy drinking. Participants and Methods: A sample of…

  2. [Electronic cigarettes: use, health risks, and effectiveness as a cessation method].

    Science.gov (United States)

    Willemsen, Marc C; Croes, Esther A; Kotz, Daniel; van Schayck, Onno C P

    2015-01-01

    The use of electronic cigarettes (e-cigarettes) among adults in the Netherlands is increasing but is still relatively low. Increasing numbers of young people abroad are experimenting with e-cigarettes but no trend data for the Netherlands are available to date. Young people who experiment with e-cigarettes are principally those young people who already smoke conventional cigarettes or have done so in the past; the same applies to adults. There are no indications that experimenting with e-cigarettes can lead to tobacco addiction. Although the vapour from e-cigarettes contains substances that are harmful to health, the health risks from the use of e-cigarettes are far smaller than those from smoking conventional cigarettes. Too few research data are available to be able to conclude that e-cigarettes are an effective aid to smoking cessation.

  3. Perceptions of E-Cigarettes among Black Youth in California

    Science.gov (United States)

    Hess, Catherine A.; Antin, Tamar M. J.; Annechino, Rachelle; Hunt, Geoffrey

    2017-01-01

    Research suggests that Black youth are less likely to use e-cigarettes than their white counterparts, yet little is known as to why. We examined perceptions of e-cigarettes among Black young adults (ages 18–25) to explore the meanings these youth ascribe to e-cigarettes and the role that identity plays in how these devices are viewed. Analysis of in-depth interviews with 36 Black smokers and non-smokers in the San Francisco Bay Area suggests that Black youth perceive e-cigarettes as serving distinct, yet overlapping roles: a utilitarian function, in that they are recognized as legitimate smoking cessation tools, and a social function, insofar as they serve to mark social identity, specifically a social identity from which our participants disassociated. Participants described e-cigarette users in highly racialized and classed terms and generally expressed disinterest in using e-cigarettes, due in part perhaps to the fact that use of these devices would signal alignment with a middle class, hipster identity. This analysis is discussed within a highly charged political and public health debate about the benefits and harms associated with e-cigarette use. PMID:28085031

  4. It's complicated: Examining smokers' relationships with their cigarette brands.

    Science.gov (United States)

    Johnson, Sarah E; Coleman, Blair N; Schmitt, Carol L

    2016-12-01

    Despite increased restrictions and taxes, decreased social acceptability, and widespread awareness of the harms of tobacco use, many in the U.S. continue to smoke cigarettes. Thus, understanding smokers' attitudes and motivations remains an important goal. This study adopts the consumer psychology concept of brand relationship to provide a new lens through which to examine smokers' attitudes about their cigarette use. Twelve focus groups (N = 143) were conducted with adult cigarette smokers from September to November, 2013. Using a semistructured moderator guide and "top of mind" worksheets, the discussion examined participants' attitudes toward (a) their own cigarette brand and (b) tobacco companies in general. Data were coded and analyzed following principles of thematic analysis. Adult smokers reported positive attitudes toward their cigarette brand, as their brand was strongly associated with the positive experience of smoking (e.g., satisfying craving and relief from withdrawal). In contrast, thinking about tobacco companies in general evoked negative reactions, revealing overwhelmingly negative attitudes toward the industry. Findings reveal a complicated relationship between smokers and their cigarette brand: simultaneously embracing their cigarettes and rejecting the industry that makes them. Taken together, these data suggest smokers maintain largely positive brand relationships, diverting negative feelings about smoking toward the tobacco industry. Finally, they highlight the synergy between branding and the subjective smoking experience, whereby positive brand attitudes are reinforced through withdrawal relief. Ultimately, this information could inform a more complete understanding of how smokers interpret and respond to tobacco communications, including marketing from their brand. (PsycINFO Database Record

  5. Pregnancy and pulmonary hypertension

    NARCIS (Netherlands)

    Pieper, Petronella G.; Lameijer, Heleen; Hoendermis, Elke S.

    2014-01-01

    Pulmonary hypertension during pregnancy is associated with considerable risks of maternal mortality and morbidity. Our systematic review of the literature on the use of targeted treatments for pulmonary arterial hypertension during pregnancy indicates a considerable decrease of mortality since a pre

  6. [Mediastino-pulmonary sarcoidosis].

    Science.gov (United States)

    Delaval, P; Desrues, B; Quinquenel, M L; Lineau, C; Lena, H

    1993-01-01

    Sarcoidosis is diffuse granulomatosis disease. The aetiology and pathogenesis are unknown. Many different localizations have been described together with immunological disturbances. Generally, the prognosis is favourable. Here we describe the pulmonary manifestations and their staging. Extra-pulmonary manifestations are then presented. Finally, the principle elements of the diagnosis and the treatment of sarcoidosis are discussed.

  7. Pulmonary Hypertension in Scleroderma

    Science.gov (United States)

    ... is a reduced diffusing capacity (DL CO ) on pulmonary function tests (PFTs). The DL CO measures the ability of ... catheterization to measure the actual pressure in the pulmonary ... the PH; to assess the function of the left side of the heart; and ...

  8. Pulmonary Function Tests

    OpenAIRE

    Ranu, H; Wilde, M.; Madden, B

    2011-01-01

    Pulmonary function tests are valuable investigations in the management of patients with suspected or previously diagnosed respiratory disease. They aid diagnosis, help monitor response to treatment and can guide decisions regarding further treatment and intervention. The interpretation of pulmonary functions tests requires knowledge of respiratory physiology. In this review we describe investigations routinely used and discuss their clinical implications.

  9. Types of Pulmonary Hypertension

    Science.gov (United States)

    ... on the cause of the condition. In all groups, the average pressure in the pulmonary arteries is higher than 25 ... mitral valve disease or long-term high blood pressure , can cause left ... of PH. Group 3 Pulmonary Hypertension Group 3 includes PH associated ...

  10. Pulmonary neuroendocrine (carcinoid) tumors

    DEFF Research Database (Denmark)

    Caplin, M E; Baudin, E; Ferolla, P

    2015-01-01

    BACKGROUND: Pulmonary carcinoids (PCs) are rare tumors. As there is a paucity of randomized studies, this expert consensus document represents an initiative by the European Neuroendocrine Tumor Society to provide guidance on their management. PATIENTS AND METHODS: Bibliographical searches were...... carried out in PubMed for the terms 'pulmonary neuroendocrine tumors', 'bronchial neuroendocrine tumors', 'bronchial carcinoid tumors', 'pulmonary carcinoid', 'pulmonary typical/atypical carcinoid', and 'pulmonary carcinoid and diagnosis/treatment/epidemiology/prognosis'. A systematic review...... of the relevant literature was carried out, followed by expert review. RESULTS: PCs are well-differentiated neuroendocrine tumors and include low- and intermediate-grade malignant tumors, i.e. typical (TC) and atypical carcinoid (AC), respectively. Contrast CT scan is the diagnostic gold standard for PCs...

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

    OpenAIRE

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

    2012-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Shepperd CJ

    2014-12-01

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

  13. Public opinion regarding earmarked cigarette tax in Taiwan

    Directory of Open Access Journals (Sweden)

    Yang Chung-Lin

    2003-12-01

    Full Text Available Abstract Background Cigarette taxation has been perceived by academics and policy-makers as one of the most effective ways of reducing the use of cigarettes. On January 1 2002, the Taiwan government imposed a New Taiwan (NT $5 per pack tax earmarked for the purpose of tobacco control. This study uses a survey collected prior to taxation to assess public attitudes toward cigarette taxation, public beliefs about the effectiveness of cigarette taxation at reducing cigarette use and public opinions about the allocation of this tax revenue. Methods Data were drawn from a national face-to-face interview on cigarette consumption in 2000. A total of 3,279 adults were aged 18 to 64 years; 49.9% of whom were male and 50.1% female, and with a smoking prevalence of 49.1% and 4.1%, respectively. The attitudes toward cigarette tax were analysed using multi-logit regressions. We analysed by logistic regression the potential changes in smoking behaviour that smokers might make in response to the five NT (New Taiwan dollar earmarked tax on cigarettes per pack. We summarized public opinions about the allocation of earmarked tax revenue using descriptive statistics. Results Current smokers (OR = 0.34 and former smokers (OR = 0.68 were less likely to support the cigarette tax than non-smokers. A favourable attitude toward the tax was positively associated with personal monthly income, especially among females. Among male smokers, the possibility of reducing/quitting smoking in response to the five-NT-dollar tax was negatively associated with the monthly expense for smoking. The two most frequently-suggested areas to receive money from the revenue collected from the earmarked tax were health education and cancer subsidy. Conclusions Smoking status and economic factors determine the attitude and potential responses of people toward the cigarette tax. Taiwan's five NT-dollar earmarked tax for cigarettes may have only a limited effect upon the reduction in cigarette

  14. An Examination of Electronic Cigarette Content on Social Media: Analysis of E-Cigarette Flavor Content on Reddit.

    Science.gov (United States)

    Wang, Lei; Zhan, Yongcheng; Li, Qiudan; Zeng, Daniel D; Leischow, Scott J; Okamoto, Janet

    2015-11-20

    In recent years, the emerging electronic cigarette (e-cigarette) marketplace has shown great development prospects all over the world. Reddit, one of the most popular forums in the world, has a very large user group and thus great influence. This study aims to gain a systematic understanding of e-cigarette flavors based on data collected from Reddit. Flavor popularity, mixing, characteristics, trends, and brands are analyzed. Fruit flavors were mentioned the most (n = 15,720) among all the posts and were among the most popular flavors (n = 2902) used in mixed blends. Strawberry and vanilla flavors were the most popular for e-juice mixing. The number of posts discussing e-cigarette flavors has increased sharply since 2014. Mt. Baker Vapor and Hangen were the most popular brands discussed among users. Information posted on Reddit about e-cigarette flavors reflected consumers' interest in a variety of flavors. Our findings suggest that Reddit could be used for data mining and analysis of e-cigarette-related content. Understanding how e-cigarette consumers' view and utilize flavors within their vaping experience and how producers and marketers use social media to promote flavors and sell products could provide valuable information for regulatory decision-makers.

  15. An Examination of Electronic Cigarette Content on Social Media: Analysis of E-Cigarette Flavor Content on Reddit

    Directory of Open Access Journals (Sweden)

    Lei Wang

    2015-11-01

    Full Text Available In recent years, the emerging electronic cigarette (e-cigarette marketplace has shown great development prospects all over the world. Reddit, one of the most popular forums in the world, has a very large user group and thus great influence. This study aims to gain a systematic understanding of e-cigarette flavors based on data collected from Reddit. Flavor popularity, mixing, characteristics, trends, and brands are analyzed. Fruit flavors were mentioned the most (n = 15,720 among all the posts and were among the most popular flavors (n = 2902 used in mixed blends. Strawberry and vanilla flavors were the most popular for e-juice mixing. The number of posts discussing e-cigarette flavors has increased sharply since 2014. Mt. Baker Vapor and Hangen were the most popular brands discussed among users. Information posted on Reddit about e-cigarette flavors reflected consumers’ interest in a variety of flavors. Our findings suggest that Reddit could be used for data mining and analysis of e-cigarette-related content. Understanding how e-cigarette consumers’ view and utilize flavors within their vaping experience and how producers and marketers use social media to promote flavors and sell products could provide valuable information for regulatory decision-makers.

  16. An Examination of Electronic Cigarette Content on Social Media: Analysis of E-Cigarette Flavor Content on Reddit

    Science.gov (United States)

    Wang, Lei; Zhan, Yongcheng; Li, Qiudan; Zeng, Daniel D.; Leischow, Scott J.; Okamoto, Janet

    2015-01-01

    In recent years, the emerging electronic cigarette (e-cigarette) marketplace has shown great development prospects all over the world. Reddit, one of the most popular forums in the world, has a very large user group and thus great influence. This study aims to gain a systematic understanding of e-cigarette flavors based on data collected from Reddit. Flavor popularity, mixing, characteristics, trends, and brands are analyzed. Fruit flavors were mentioned the most (n = 15,720) among all the posts and were among the most popular flavors (n = 2902) used in mixed blends. Strawberry and vanilla flavors were the most popular for e-juice mixing. The number of posts discussing e-cigarette flavors has increased sharply since 2014. Mt. Baker Vapor and Hangen were the most popular brands discussed among users. Information posted on Reddit about e-cigarette flavors reflected consumers’ interest in a variety of flavors. Our findings suggest that Reddit could be used for data mining and analysis of e-cigarette-related content. Understanding how e-cigarette consumers’ view and utilize flavors within their vaping experience and how producers and marketers use social media to promote flavors and sell products could provide valuable information for regulatory decision-makers. PMID:26610541

  17. Use of electronic cigarettes (e-cigarettes) impairs indoor air quality and increases FeNO levels of e-cigarette consumers.

    Science.gov (United States)

    Schober, Wolfgang; Szendrei, Katalin; Matzen, Wolfgang; Osiander-Fuchs, Helga; Heitmann, Dieter; Schettgen, Thomas; Jörres, Rudolf A; Fromme, Hermann

    2014-07-01

    Despite the recent popularity of e-cigarettes, to date only limited data is available on their safety for both users and secondhand smokers. The present study reports a comprehensive inner and outer exposure assessment of e-cigarette emissions in terms of particulate matter (PM), particle number concentrations (PNC), volatile organic compounds (VOC), polycyclic aromatic hydrocarbons (PAH), carbonyls, and metals. In six vaping sessions nine volunteers consumed e-cigarettes with and without nicotine in a thoroughly ventilated room for two hours. We analyzed the levels of e-cigarette pollutants in indoor air and monitored effects on FeNO release and urinary metabolite profile of the subjects. For comparison, the components of the e-cigarette solutions (liquids) were additionally analyzed. During the vaping sessions substantial amounts of 1,2-propanediol, glycerine and nicotine were found in the gas-phase, as well as high concentrations of PM2.5 (mean 197 μg/m(3)). The concentration of putative carcinogenic PAH in indoor air increased by 20% to 147 ng/m(3), and aluminum showed a 2.4-fold increase. PNC ranged from 48,620 to 88,386 particles/cm(3) (median), with peaks at diameters 24-36 nm. FeNO increased in 7 of 9 individuals. The nicotine content of the liquids varied and was 1.2-fold higher than claimed by the manufacturer. Our data confirm that e-cigarettes are not emission-free and their pollutants could be of health concern for users and secondhand smokers. In particular, ultrafine particles formed from supersaturated 1,2-propanediol vapor can be deposited in the lung, and aerosolized nicotine seems capable of increasing the release of the inflammatory signaling molecule NO upon inhalation. In view of consumer safety, e-cigarettes and nicotine liquids should be officially regulated and labeled with appropriate warnings of potential health effects, particularly of toxicity risk in children.

  18. Prevalence and management of pulmonary comorbidity in patients with lung and head and neck cancer

    DEFF Research Database (Denmark)

    Gottlieb, Magnus; Marsaa, Kristoffer; Godtfredsen, Nina S

    2015-01-01

    BACKGROUND: The simultaneous presence of cancer and other medical conditions (comorbidity) is frequent. Cigarette smoking is the major risk factor for as well head and neck cancer (HNC) and lung cancer (LC) as chronic obstructive pulmonary disease (COPD). COPD is the most common comorbidity in LC...... trial comparing usual care with optimized medical treatment of COPD in cancer patients. MATERIAL AND METHODS: All patients with HNC or LC referred for oncologic treatment in a university hospital during a 10-month period were invited to attend a pulmonary clinic for evaluation of lung function. Patients...... guidelines. Secondary outcome was feasibility, i.e. the proportion of eligible patients that accepted follow-up in the pulmonary clinic for 24 weeks in addition to oncological treatment. The design of the randomized trail is described in detail. RESULTS: In total 130 patients of whom 65% had LC and 35% HNC...

  19. Pulmonary mycoses among the clinically suspected cases of pulmonary tuberculosis

    OpenAIRE

    Tshering Ongmu Bhutia; Luna Adhikari

    2015-01-01

    Background: This study was carried with the main objectives: (1) to find out the occurrence of pulmonary mycoses in clinically suspected pulmonary tuberculosis cases at central referral hospital, Tadong, Sikkim. (2) To find out the various fungi causing pulmonary mycoses in clinically suspected pulmonary tuberculosis cases. Methods: 200 clinically suspected pulmonary tuberculosis cases who visited the department of microbiology for the diagnostic microscopic examination of sputum sample f...

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2014-11-15

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

  1. EffiCiency and Safety of an eLectronic cigAreTte (ECLAT) as Tobacco Cigarettes Substitute: A Prospective 12-Month Randomized Control Design Study

    OpenAIRE

    Pasquale Caponnetto; Davide Campagna; Fabio Cibella; Morjaria, Jaymin B; Massimo Caruso; Cristina Russo; Riccardo Polosa

    2013-01-01

    BACKGROUND: Electronic cigarettes (e-cigarettes) are becoming increasingly popular with smokers worldwide. Users report buying them to help quit smoking, to reduce cigarette consumption, to relieve tobacco withdrawal symptoms, and to continue having a 'smoking' experience, but with reduced health risks. Research on e-cigarettes is urgently needed in order to ensure that the decisions of regulators, healthcare providers and consumers are based on science. Methods ECLAT is a prospective 12-mont...

  2. Social norms of cigarette and hookah smokers in Iranian universities

    DEFF Research Database (Denmark)

    Roohafza, Hamidreza; Sadeghi, Masoumeh; Shahnam, Maryam;

    2013-01-01

    BACKGROUND: First experiences of tobacco use usually occur in adolescence. The recognition of social norms leading to youth smoking is hence necessary. We tried to assess the social norms among Iranian young cigarette and hookah smokers. METHODS: This cross-sectional study was conducted on 451...... girls and 361 boys aging 20-25 years old who entered Isfahan and Kashan Universities (Iran) in 2007. Demographic factors (age, gender, and age at smoking onset) cigarette and hookah smoking status, having a smoking father or smoking friends and four related social norms were recorded. Binary logistic...... regression analysis was used to separately determine associations between hookah and cigarette smoking and the four social norm variables. RESULTS: CIGARETTE AND HOOKAH SMOKERS HAD SIGNIFICANT DIFFERENCES WITH NONSMOKERS IN TWO SOCIAL NORMS: "Perceived smoking by important characters" [odds ratio (OR) = 1...

  3. CDC STATE System E-Cigarette Legislation - Tax

    Data.gov (United States)

    U.S. Department of Health & Human Services — 1995-2016. Centers for Disease Control and Prevention (CDC). State Tobacco Activities Tracking and Evaluation (STATE) System. E-Cigarette Legislation—Tax. The...

  4. CDC STATE System E-Cigarette Legislation - Smokefree Campus

    Data.gov (United States)

    U.S. Department of Health & Human Services — 1995-2016. Centers for Disease Control and Prevention (CDC). State Tobacco Activities Tracking and Evaluation (STATE) System. E-Cigarette Legislation—Smokefree...

  5. The Contribution of cocoa additive to cigarette smoking addiction

    NARCIS (Netherlands)

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

    2003-01-01

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

  6. CDC STATE System E-Cigarette Legislation - Preemption

    Data.gov (United States)

    U.S. Department of Health & Human Services — 1995-2016. Centers for Disease Control and Prevention (CDC). State Tobacco Activities Tracking and Evaluation (STATE) System. E-Cigarette Legislation—Preemption....

  7. Current Cigarette Use Among Adults (BRFSS) PDF Slides

    Data.gov (United States)

    U.S. Department of Health & Human Services — Download the current cigarette use among adults slides. These slides are available in PDF and PowerPoint formats. The PowerPoint version can be found at:...

  8. Excise Tax Rates On Packs Of Cigarettes PDF Slides

    Data.gov (United States)

    U.S. Department of Health & Human Services — Download the current excise tax rates on packs of cigarettes slides. These slides are available in PDF and PowerPoint formats. The PowerPoint version can be found...

  9. Most Americans Favor Larger Health Warnings on Cigarette Packs

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_164398.html Most Americans Favor Larger Health Warnings on Cigarette Packs ... According to the study's first author, Sarah Kowitt, "Most adults, including smokers, have favorable attitudes towards larger ...

  10. CDC STATE System E-Cigarette Legislation - Smokefree Indoor Air

    Data.gov (United States)

    U.S. Department of Health & Human Services — 1995-2016. Centers for Disease Control and Prevention (CDC). State Tobacco Activities Tracking and Evaluation (STATE) System. E-Cigarette Legislation—Smokefree...

  11. The Australian cigarette brand as product, person, and symbol

    OpenAIRE

    Carter, S

    2003-01-01

    Objective: To examine, for dominant Australian cigarette brands, brand identity (overriding brand vision), brand positioning (brand identity elements communicated to the consumer), brand image (consumers' brand perceptions) and brand equity (financial value).

  12. CDC STATE System E-Cigarette Legislation - Licensure

    Data.gov (United States)

    U.S. Department of Health & Human Services — 1995-2016. Centers for Disease Control and Prevention (CDC). State Tobacco Activities Tracking and Evaluation (STATE) System. E-Cigarette Legislation—Licensure....

  13. CDC STATE System E-Cigarette Legislation - Youth Access

    Data.gov (United States)

    U.S. Department of Health & Human Services — 1995-2016. Centers for Disease Control and Prevention (CDC). State Tobacco Activities Tracking and Evaluation (STATE) System. E-Cigarette Legislation—Youth Access....

  14. Cigarette, alcohol, and caffeine consumption: risk factors for spontaneous abortion

    DEFF Research Database (Denmark)

    Rasch, Vibeke

    2003-01-01

    OBJECTIVE: To study the association between cigarette, alcohol, and caffeine consumption and the occurrence of spontaneous abortion. METHODS: The study population consisted of 330 women with spontaneous abortion and 1168 pregnant women receiving antenatal care. A case-control design was utilized......; cases were defined as women with a spontaneous abortion in gestational week 6-16 and controls as women with a live fetus in gestational week 6-16. The variables studied comprise age, parity, occupational situation, cigarette, alcohol, and caffeine consumption. The association between cigarette, alcohol......, and caffeine consumption was studied using logistic regression analyzes while controlling for confounding variables. In addition stratified analyzes of the association between caffeine consumption and spontaneous abortion on the basis of cigarette and alcohol consumption were performed. RESULTS: Women who had...

  15. Comparison of carcinogen, carbon monoxide, and ultrafine particle emissions from narghile waterpipe and cigarette smoking: Sidestream smoke measurements and assessment of second-hand smoke emission factors

    Science.gov (United States)

    Daher, Nancy; Saleh, Rawad; Jaroudi, Ezzat; Sheheitli, Hiba; Badr, Thérèse; Sepetdjian, Elizabeth; Al Rashidi, Mariam; Saliba, Najat; Shihadeh, Alan

    2010-01-01

    The lack of scientific evidence on the constituents, properties, and health effects of second-hand waterpipe smoke has fueled controversy over whether public smoking bans should include the waterpipe. The purpose of this study was to investigate and compare emissions of ultrafine particles (UFP, carcinogenic polyaromatic hydrocarbons (PAH), volatile aldehydes, and carbon monoxide (CO) for cigarettes and narghile (shisha, hookah) waterpipes. These smoke constituents are associated with a variety of cancers, and heart and pulmonary diseases, and span the volatility range found in tobacco smoke. Sidestream cigarette and waterpipe smoke was captured and aged in a 1 m 3 Teflon-coated chamber operating at 1.5 air changes per hour (ACH). The chamber was characterized for particle mass and number surface deposition rates. UFP and CO concentrations were measured online using a fast particle spectrometer (TSI 3090 Engine Exhaust Particle Sizer), and an indoor air quality monitor. Particulate PAH and gaseous volatile aldehydes were captured on glass fiber filters and DNPH-coated SPE cartridges, respectively, and analyzed off-line using GC-MS and HPLC-MS. PAH compounds quantified were the 5- and 6-ring compounds of the EPA priority list. Measured aldehydes consisted of formaldehyde, acetaldehyde, acrolein, methacrolein, and propionaldehyde. We found that a single waterpipe use session emits in the sidestream smoke approximately four times the carcinogenic PAH, four times the volatile aldehydes, and 30 times the CO of a single cigarette. Accounting for exhaled mainstream smoke, and given a habitual smoker smoking rate of 2 cigarettes per hour, during a typical one-hour waterpipe use session a waterpipe smoker likely generates ambient carcinogens and toxicants equivalent to 2-10 cigarette smokers, depending on the compound in question. There is therefore good reason to include waterpipe tobacco smoking in public smoking bans.

  16. Nontypeable Haemophilus influenzae in chronic obstructive pulmonary disease and lung cancer

    Directory of Open Access Journals (Sweden)

    Seyed Javad Moghaddam

    2011-01-01

    Full Text Available Seyed Javad Moghaddam1, Cesar E Ochoa1,2, Sanjay Sethi3, Burton F Dickey1,41Department of Pulmonary Medicine, the University of Texas MD Anderson Cancer Center, Houston, TX, USA; 2Tecnológico de Monterrey School of Medicine, Monterrey, Nuevo León, Mexico; 3Department of Medicine, University at Buffalo, State University of New York, Buffalo, NY, USA; 4Center for Inflammation and Infection, Institute of Biosciences and Technology, Texas A&M Health Science Center, Houston, TX, USAAbstract: Chronic obstructive pulmonary disease (COPD is predicted to become the third leading cause of death in the world by 2020. It is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases, most commonly cigarette smoke. Among smokers with COPD, even following withdrawal of cigarette smoke, inflammation persists and lung function continues to deteriorate. One possible explanation is that bacterial colonization of smoke-damaged airways, most commonly with nontypeable Haemophilus influenzae (NTHi, perpetuates airway injury and inflammation. Furthermore, COPD has also been identified as an independent risk factor for lung cancer irrespective of concomitant cigarette smoke exposure. In this article, we review the role of NTHi in airway inflammation that may lead to COPD progression and lung cancer promotion.Keywords: COPD, NTHi, inflammation

  17. Pulmonary manifestations of leptospirosis

    Directory of Open Access Journals (Sweden)

    Sameer Gulati

    2012-01-01

    Full Text Available Leptospirosis has a spectrum of presentation which ranges from mild disease to a severe form comprising of jaundice and renal failure. Involvement of the lung can vary from subtle clinical features to deadly pulmonary hemorrhage and acute respiratory distress syndrome. Of late, it has been identified that leptospirosis can present atypically with predominant pulmonary manifestations. This can delay diagnosis making and hence optimum treatment. The purpose of this review is to bring together all the reported pulmonary manifestations of leptospirosis and the recent trends in the management.

  18. Anesthesia and pulmonary hypertension.

    Science.gov (United States)

    McGlothlin, Dana; Ivascu, Natalia; Heerdt, Paul M

    2012-01-01

    Anesthesia and surgery are associated with significantly increased morbidity and mortality in patients with pulmonary hypertension due mainly to right ventricular failure, arrhythmias, postoperative hypoxemia, and myocardial ischemia. Preoperative risk assessment and successful management of patients with pulmonary hypertension undergoing cardiac surgery involve an understanding of the pathophysiology of the disease, screening of patients at-risk for pulmonary arterial hypertension, analysis of preoperative and operative risk factors, thorough multidisciplinary planning, careful intraoperative management, and early recognition and treatment of postoperative complications. This article will cover each of these aspects with particular focus on the anesthetic approach for non-cardiothoracic surgeries.

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

    Science.gov (United States)

    Colman, Gregory J.; Remler, Dahlia K.

    2008-01-01

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

  20. Impact of cigarette smoking in type 2 diabetes development

    Institute of Scientific and Technical Information of China (English)

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

    2009-01-01

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

  1. Impact of cigarette smoking in type 2 diabetes development

    OpenAIRE

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

    2009-01-01

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

  2. Regulating the disposal of cigarette butts as toxic hazardous waste

    OpenAIRE

    Barnes, Richard L

    2011-01-01

    The trillions of cigarette butts generated each year throughout the world pose a significant challenge for disposal regulations, primarily because there are millions of points of disposal, along with the necessity to segregate, collect and dispose of the butts in a safe manner, and cigarette butts are toxic, hazardous waste. There are some hazardous waste laws, such as those covering used tyres and automobile batteries, in which the retailer is responsible for the proper disposal of the waste...

  3. Electronic cigarettes: A comparison of national regulatory approaches.

    Science.gov (United States)

    Rose, Adam; Filion, Kristian B; Eisenberg, Mark J; Franck, Caroline

    2015-10-03

    E-cigarettes have been readily available to global markets since 2004. However, regulations have lagged behind popular use and availability. As policies emerging from national health agencies have an important role to play in shaping consumer health, we examined the existing and upcoming national regulations surrounding e-cigarette availability and use in a convenience sample of English- and French-speaking countries, including Canada, the United States, the United Kingdom, France, Australia and New Zealand. There is substantial international variation in regulatory policies and the extent to which these are enforced. Of the countries considered in this review, the US has regulations that remain the most permissive, whereas those in Canada and New Zealand are the most conservative. However, regulations in Canada, Australia and New Zealand are easily bypassed through Internet imports and lenient enforcement. European health agencies are paving the way for Member States to take appropriate steps to regulate e-cigarettes according to their own jurisdictions. Currently, national regulations of e-cigarettes appear to be ill-defined in terms of shaping the future of e-cigarette availability and use. National regulations should be strengthened to reflect the public health implications of e-cigarettes and to emphasize their difference from consumer products.

  4. Do Cigarette Filters Contain Pig’s Blood ?

    Directory of Open Access Journals (Sweden)

    Birsen Can DEMİRDÖĞEN

    2010-09-01

    Full Text Available The news over the allegations raised by Prof. Simon Chapman from Australia Sydney University that hemoglobin protein obtained from pig blood is being used in cigarette filters has kept the agenda busy in recent days. It was stated that vegetarians and Muslims and Jews who are sensitive about pork products because of religious beliefs will not be pleased with this news. The analyses of the cigarette samples sent to our Agency in order to be examined for pig blood has been carried out at the Consumer Safety and Health Effects Research Laboratories. Presence of pig blood in cigarette filter was investigated by real time PCR technique. As a result, pig DNA was not determined in the cigarette filters that were analyzed. In order to analyze the presence of hemoglobin protein in cigarette filters, mass screening was conducted with UPLC-TOF-MS (Ultra performance liquid chromotography-time of flight mass spectrometry; as a result hemoglobin was not found in the analyzed cigarette filters. This research was a pilot study in nature and more detailed studies about the subject will be helpful.

  5. Change of Taste Sensitivity of Clove Cigarette Smokers in Medan

    Directory of Open Access Journals (Sweden)

    Marlina Simamora

    2013-07-01

    Full Text Available Tongue has taste buds that contain taste receptor which affected by many factors, including smoking habit. Objective: To analyze the differences of sweet and bitter taste sensitivity in the pedicab driver clove cigarette smokers compared to non-smokers in Medan Padang Bulan. Methods: This study was conducted by placing the sweet taste strips and bitter taste strips on four taste receptors of the tongue, with increasing solution concentration in 74 subjects. This was a cross sectional study on pedicab driver population in Medan Padang Bulan. Results: There were differences between clove cigarette smokers and non-smokers on sweet taste examination (p<0.005. There was a difference between clove cigarette smokers and non-smokers on examination bitter taste receptors (p<0.005. On the clove cigarette smokers, there was no significant difference between sweet taste and bitter taste on the receptors itself. Conclusion: Non-smokers are more sensitive to sweet taste than the clove cigarette smokers. Bitter taste sensitivity is greater in cigarettes smokers than in non-smokers. Taste receptors on all location of the tongue could taste sweet and bitter substances, but a certain location of taste receptors were more sensitive compared to others.

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

    Science.gov (United States)

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

    2011-06-01

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

  7. Bioaccumulation and biological effects of cigarette litter in marine worms

    Science.gov (United States)

    Wright, Stephanie L.; Rowe, Darren; Reid, Malcolm J.; Thomas, Kevin V.; Galloway, Tamara S.

    2015-01-01

    Marine debris is a global environmental issue. Smoked cigarette filters are the predominant coastal litter item; 4.5 trillion are littered annually, presenting a source of bioplastic microfibres (cellulose acetate) and harmful toxicants to marine environments. Despite the human health risks associated with smoking, little is known of the hazards cigarette filters present to marine life. Here we studied the impacts of smoked cigarette filter toxicants and microfibres on the polychaete worm Hediste diversicolor (ragworm), a widespread inhabitant of coastal sediments. Ragworms exposed to smoked cigarette filter toxicants in seawater at concentrations 60 fold lower than those reported for urban run-off exhibited significantly longer burrowing times, >30% weight loss, and >2-fold increase in DNA damage compared to ragworms maintained in control conditions. In contrast, ragworms exposed to smoked cigarette filter microfibres in marine sediment showed no significant effects. Bioconcentration factors for nicotine were 500 fold higher from seawater than from sediment. Our results illustrate the vulnerability of organisms in the water column to smoking debris and associated toxicants, and highlight the risks posed by smoked cigarette filter debris to aquatic life. PMID:26369692

  8. PCR-based typing of DNA extracted from cigarette butts.

    Science.gov (United States)

    Hochmeister, M N; Budowle, B; Jung, J; Borer, U V; Comey, C T; Dirnhofer, R

    1991-01-01

    Limited genetic marker information can be obtained from saliva by typing by conventional serological means. Thus, the application of PCR-based DNA typing methods was investigated as a potential approach for typing genetic markers in saliva. DNA was isolated from 200 cigarettes smoked by 10 different individuals (20 cigarettes per individual) and from 3 cigarette butts recovered from 2 crime scenes (adjudicated cases) using a Chelex 100 extraction procedure. The amount of recovered human DNA was quantified by slot-blot analysis and ranged from approximately less than 2-160 ng DNA per cigarette butt for the 200 samples, and 8 ng, 50 ng, and 100 ng for the cigarette butts from the adjudicated cases. The DNA was successfully amplified by the polymerase chain reaction (PCR) for the HLA-DQ alpha locus (99 out of 100 samples) as well as for the variable number of tandem repeat (VNTR) locus D1S80 (99 out of 100 samples). Amplification and typing of DNA was successful on all samples recovered from the crime scenes. The results suggest that PCR-based typing of DNA offers a potential method for genetically characterizing traces of saliva on cigarette butts.

  9. Electronic Vapor Cigarette Battery Explosion Causing Shotgun-like Superficial Wounds and Contusion

    Directory of Open Access Journals (Sweden)

    Siri Shastry, MD

    2016-03-01

    Full Text Available INTRODUCTION Electronic vapor cigarettes (E-cigarettes were created in 2003 as an alternative to traditional tobacco cigarettes. E-cigarettes have been available in the United States since 2006.1 The typical E-cigarette consists of a cartridge that contains liquid, an atomizer that heats the liquid (i.e. acts as a vaporizer, as well as a battery. The liquid contained within the cartridge contains nicotine, propylene glycol and/ or glycerol as well as flavorings. The consumer uses an E-cigarette through either pushing a button or inhalation, which triggers heating and therefore aerosolizes the liquid within the cartridge, emulating cigarette “smoke.” The newest E-cigarettes are larger than nicotine cigarettes and employ stronger, rechargeable batteries as a power source.2,3

  10. Insights in public health: Electronic cigarettes: marketing to Hawai'i's adolescents.

    Science.gov (United States)

    Williams, Rebecca J; Knight, Rebecca

    2015-02-01

    Electronic cigarettes (e-cigarettes) are an emerging phenomenon that is becoming increasingly popular among adolescents. Current e-cigarette use among adolescents has more than doubled in the past few years nationally and more than tripled in Hawai'i, despite the fact that safety in terms of health and injury from use is widely unknown. The use of e-cigarettes among adolescents is of particular concern because they may act as a gateway to smoking conventional tobacco cigarettes, substitute for cigarettes where smoking would normally not be allowed, and weaken the effect of clean air policies, and displace effective smoking cessation treatments. Additionally, the use of e-cigarettes may lead to the use of conventional cigarettes. There is special concern that e-cigarette companies are recruiting adolescents who would not have otherwise tried smoking by using tactics such as offering e-cigarettes in attractive flavorings and using the same successful strategies to market their product as tobacco companies have used for conventional cigarettes in past decades. It has been shown that exposure to cigarette marketing is related to initiation and progression in adolescent smoking. Yet, there remains no regulation on the marketing of e-cigarettes to adolescents. It can be extrapolated that expanded regulation that includes limits on the marketing of e-cigarettes may help decrease use among adolescents and prevent the possible increase of smoking rates.

  11. Cigarettes, social reinforcement, and culture: a commentary on "Tobacco as a social currency: cigarette gifting and sharing in China".

    Science.gov (United States)

    Ding, Ding; Hovell, Melbourne F

    2012-03-01

    As Rich and Xiao suggested, cigarette sharing and gifting play an important role in China's smoking epidemic. Understanding the cultural roots, history, and impacts of such practices should be emphasized in tobacco control efforts. "Tobacco as a social currency" is a consequence of the tobacco industry usurping traditional values and cultural customs to make cigarette gifting acceptable, desirable, and socially reinforcing. The cigarettes-social reinforcement link created by the tobacco industry can be broken by deglamorizing smoking and cigarette gifting and by reinforcing alternative healthful behaviors. A behavioral ecological perspective, with an emphasis of understanding and engineering cultures, should guide future health promotion efforts to reduce smoking and other risk practices in China.

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

    Science.gov (United States)

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

    2015-01-01

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

  13. Basic pulmonary function tests in pig farmers

    Directory of Open Access Journals (Sweden)

    Đuričić Slaviša M.

    2004-01-01

    Full Text Available INTRODUCTION Many epidemiological and clinical studies have demonstrated an increased risk for the symptoms of respiratory disorders consistent with chronic bronchitis and asthma and alterations of pulmonary function tests in pig farmers. AIM The aim of this study was to determine basic pulmonary function values in workers in swine confinement buildings and to compare them with the same values in the control group of unexposed persons. The next aim was to examine the association between these values with duration of professional exposure, cigarette smoking, age, and sex of the examined persons. METHODS We randomly selected for examination 145 workers of both sex who had worked for at least 2 previous years in pig farms and spent at least 3 hours per day, 6 days per week in a swine confinement building. The farmers worked at 6 different farms with 12,383 pigs on average on each farms. The subject was eligible for the study if he had had no history of atopic disease nor any serious chronic disease, and no acute respiratory infection within 3 previous months. As control group we examined 156 subjects who had lived and/or worked in the same areas and had had no history of exposure to farming environment or any other known occupational air pollutants. In both groups the study comprised cigarette smokers and persons who had never smoked. Pulmonary function data were collected according to the standard protocol with a Micro Spirometer, (Micro Medical Ltd, England, UK. The registered parameters were FEV1 and FVC At least three satisfactory forced maximal expirations were performed by each subject and the best value was accepted for analyses. The results were also expressed as a percentage of predicted values and FEV1/FVCxlOO was calculated. RESULTS There were no differences in the main demographic characteristics between two examined groups (Table1. Mean duration of work in pig farming was 11.6 years (SD=8.5; range 2-40. The average values of examined

  14. Pulmonary Langerhans Cell Histiocytosis: Case Series and Literature Review

    Science.gov (United States)

    Wei, Ping; Lu, Hai-Wen; Jiang, Sen; Fan, Li-Chao; Li, Hui-Ping; Xu, Jin-Fu

    2014-01-01

    Abstract Pulmonary Langerhans cell histiocytosis (PLCH) is a rare disease with insidious onset and nonspecific manifestations. The objective of this article was to characterize the clinical manifestations and features of PLCH by retrospectively analyzing clinical data of patients with PLCH in addition to simultaneous review of literature. A retrospective analysis was conducted on clinical data of patients with PLCH (n = 7), whose conditions were diagnosed by biopsy from pulmonary tissue (n = 6) or enlarged lymph nodes in the neck (n = 1) and confirmed by PLCH typical radiological features on computed tomography (CT) scan, between January 2001 and September 2012 at the Shanghai Pulmonary Hospital, Tongji University School of Medicine, Shanghai, China. The review of published reports was made to further emphasize the clinical manifestation and radiological features of PLCH. Long history of cigarette smoking was found in 6 patients. Two patients had recurrent pneumothorax and the other 2 had pulmonary arterial hypertension (World Health Organization group 5 pulmonary hypertension), diagnosed through ultrasonic cardiogram. The nodular shadows were revealed by chest CT scan in 5 patients, cystic shadows in 5 patients, and reticular shadows in 2 patients, as major manifestations, respectively; most of the lesions were located in the middle or upper segments of the lung. The obvious shrank of lesion was found in 1 patient after completely quitting smoking. The pathogenesis of PLCH might be closely associated with smoking. The cystic or nodular lesion was the typical radiological features. Further prospective studies with large sample size are required to further validate the study results and understand the clinical characteristics of PLCH to avoid misdiagnosis. PMID:25415669

  15. Pulmonary valve stenosis

    Science.gov (United States)

    ... valvuloplasty - pulmonary Images Heart valves References Carabello BA. Valvular heart disease. In: Goldman L, Schafer AI, eds. Goldman's Cecil ... Saunders; 2016:chap 69. Otto CM, Bownow RO. Valvular heart disease. In: Mann DL, Zipes DP, Libby P, Bonow ...

  16. Reperfusion pulmonary edema

    Energy Technology Data Exchange (ETDEWEB)

    Klausner, J.M.; Paterson, I.S.; Mannick, J.A.; Valeri, C.R.; Shepro, D.; Hechtman, H.B. (Harvard Medical School, Boston, MA (USA))

    1989-02-17

    Reperfusion following lower-torso ischemia in humans leads to respiratory failure manifest by pulmonary hypertension, hypoxemia, and noncardiogenic pulmonary edema. The mechanism of injury has been studied in the sheep lung lymph preparation, where it has been demonstrated that the reperfusion resulting in pulmonary edema is due to an increase in microvascular permeability of the lung to protein. This respiratory failure caused by reperfusion appears to be an inflammatory reaction associated with intravascular release of the chemoattractants leukotriene B{sub 4} and thromboxane. Histological studies of the lung in experimental animals revealed significant accumulation of neutrophils but not platelets in alveolar capillaries. The authors conclude that thromboxane generated and released from the ischemic tissue is responsible for the transient pulmonary hypertension. Second, it is likely that the chemoattractants are responsible for leukosequestration, and third, neutrophils, oxygen-derived free radicals, and thromboxane moderate the altered lung permeability.

  17. Pulmonary Valve Stenosis

    Science.gov (United States)

    ... growths called carcinoid tumors in the digestive system. Rheumatic fever. This complication of an infection caused by streptococcus ... valve stenosis later in life, including: Carcinoid syndrome Rheumatic fever Noonan's syndrome Mild to moderate pulmonary valve stenosis ...

  18. Management of pulmonary aspiration

    NARCIS (Netherlands)

    Janda, Matthias; Scheeren, Thomas W L; Nöldge-Schomburg, Gabriele F E

    2006-01-01

    Pulmonary aspiration of gastric contents in the perioperative phase is associated with increased postoperative morbidity and mortality. For the management of aspiration, differentiation between acid-associated aspiration pneumonitis and aspiration pneumonia as a consequence of a secondary bacterial

  19. E-Cigarette Policies on College Campuses: Student Use Behaviors, Awareness, and Policy Support.

    Science.gov (United States)

    Brown, Elizabeth M; Henes, Amy L; Olson, Lindsay T

    2016-12-01

    This study examined e-cigarette use and attitudes toward e-cigarette policies among students at colleges and universities with and without policies prohibiting e-cigarette use on campus. In April 2015, we fielded an online survey with a convenience sample of 930 students at 14 North Dakota colleges and universities. The survey included questions about e-cigarette use, observed e-cigarette use on campus, awareness of school e-cigarette policy, and support for policies prohibiting e-cigarette use on campus. Over 40 % of respondents had used e-cigarettes at least once, and most current users reported using them rarely (36 %). Nearly 29 % of respondents reported observing e-cigarette use on campus, and more than half of these reported seeing e-cigarette use indoors. More than 42 % did not know whether their school's policy prohibited e-cigarette use on campus, and students at schools with a policy were more likely to identify their campus policy correctly. Sixty-six percent of respondents were in favor of policies prohibiting e-cigarette use on campus, and those at schools with policies prohibiting e-cigarette use were more likely to support a campus e-cigarette policy. Policies prohibiting e-cigarette use on campus intend to restrict use, reduce prevalence, and shape social norms. This study indicates that support for campus e-cigarette policies is high, although awareness of whether e-cigarettes are included in college and university policies is low. These findings demonstrate the need for coordinated policy education efforts and may guide college administrators and student health services personnel as they consider how to implement and evaluate campus e-cigarette policies.

  20. Pulmonary mycosis in AIDS

    Energy Technology Data Exchange (ETDEWEB)

    Busi Rizzi, Elisa; Schinina, Vincenzo; Bellussi, Angelo; De Santis, Andrea; Mazzuoli, Giovanna; Giosue, Sandro; Bibbolino, Corrado

    2001-01-01

    We retrospectively reviewed our series of 35 pulmonary mycosis in patients with AIDS, observed from 1987 to 1999, to correlate the imaging and pathologic findings. We further evaluated the frequency of fungal pneumonia before and after the use of a highly active antiretroviral therapy (HAART). Early recognition of pulmonary mycosis is imperative in these patients and improved survival can be achieved with early CT detection and prompt institution of high-dose antifungal therapy.