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Sample records for cigarette smoke induced

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

    NARCIS (Netherlands)

    Eijl, Teunis Jan Ahasuerus van

    2006-01-01

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

  2. 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.

  3. 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.

  4. Epigenetic Effects and Molecular Mechanisms of Tumorigenesis Induced by Cigarette Smoke: An Overview

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    Rong-Jane Chen

    2011-01-01

    Full Text Available Cigarette smoking is one of the major causes of carcinogenesis. Direct genotoxicity induced by cigarette smoke leads to initiation of carcinogenesis. Nongenotoxic (epigenetic effects of cigarette smoke also act as modulators altering cellular functions. These two effects underlie the mechanisms of tumor promotion and progression. While there is no lack of general reviews on the genotoxic and carcinogenic potentials of cigarette smoke in lung carcinogenesis, updated review on the epigenetic effects and molecular mechanisms of cigarette smoke and carcinogenesis, not limited to lung, is lacking. We are presenting a comprehensive review of recent investigations on cigarette smoke, with special attentions to nicotine, NNK, and PAHs. The current understanding on their molecular mechanisms include (1 receptors, (2 cell cycle regulators, (3 signaling pathways, (4 apoptosis mediators, (5 angiogenic factors, and (6 invasive and metastasis mediators. This review highlighted the complexity biological responses to cigarette smoke components and their involvements in tumorigenesis.

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

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    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.

  6. 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.

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

    Institute of Scientific and Technical Information of China (English)

    ZOU Ni; HONG Jiang; DAI Qiu-yan

    2009-01-01

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

  8. 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.

  9. A new experimental model of cigarette smoke-induced emphysema in Wistar rats

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    Rodrigo de las Heras Kozma

    2014-01-01

    Full Text Available OBJECTIVE: To describe a new murine model of cigarette smoke-induced emphysema. METHODS: Twenty-four male Wistar rats were divided into two groups: the cigarette smoke group, comprising 12 rats exposed to smoke from 12 commercial filter cigarettes three times a day (a total of 36 cigarettes per day every day for 30 weeks; and the control group, comprising 12 rats exposed to room air three times a day every day for 30 weeks. Lung function was assessed by mechanical ventilation, and emphysema was morphometrically assessed by measurement of the mean linear intercept (Lm. RESULTS: The mean weight gain was significantly (approximately ten times lower in the cigarette smoke group than in the control group. The Lm was 25.0% higher in the cigarette smoke group. There was a trend toward worsening of lung function parameters in the cigarette smoke group. CONCLUSIONS: The new murine model of cigarette smoke-induced emphysema and the methodology employed in the present study are effective and reproducible, representing a promising and economically viable option for use in studies investigating the pathophysiology of and therapeutic approaches to COPD.

  10. β-carotene protects rats against bronchitis induced by cigarette smoking

    Institute of Scientific and Technical Information of China (English)

    庞宝森; 王辰; 翁心植; 唐小奈; 张红玉; 牛淑洁; 毛燕玲; 辛平; 黄秀霞; 张海燕; 祝锦

    2003-01-01

    Objective To investigate the protective effects of β-carotene in rats against the development of chronic bronchitis induced by cigarette smoking. Results Long-term cigarette smoking caused an obvious increase in the amount of IL-6, IL-8 and LPO and a sharp decrease in the levels of NO and SOD in smoking animals compared to controls. β-carotene intake reversed all the changes induced by smoking and alleviated the pathological changes caused by chronic bronchitis. Conclusions Quantitative oral intake of β-carotene had protective effects against chronic bronchitis induced by long-term cigarette smoking, which was associated with the increased production of NO, the clearance of some oxidative free radicals (OFR) and the alleviation of chronic inflammation.

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

    OpenAIRE

    Aoshiba K; Nagai A

    2003-01-01

    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 inapprop...

  12. Influence of cigarette smoke and green tea on radiation-induced micronucleated polychromatic erythrocytes

    International Nuclear Information System (INIS)

    Objective: To observe the effects of cigarette smoke and green tea on radiation-induced bone marrow cell mutation, and to provide scientific information for prevention and treatment of radiation damage. Methods: There were 8 groups in the factorial experiment design with 3 factors at 2 levels. Mice were randomly divided into each group. There were 8 mice in each group. Mice in seven experimental groups were exposed to cigarette smoke, green tea, radiation or their mixtures respectively. One group was treated as the blank control group. The frequencies of micrnucleated polychromatic erythrocytes (MPCE) were scored by single blinded method. The data were analyzed with factorial experiments analysis of variance using SAS 8.0. Results: Analysis of variance showed that radiation, cigarette smoke and green tea were independently significant factors (P<0.01). Interactions between cigarette smoke and radiation or between green tea and radiation were statistically significant (P<0.01). Conclusion: Radiation and cigarette smoke can cause bone marrow cell mutations independently. There is synergistic effect between cigarette smoke and radiation. Green tea can inhibit radiation-induced cell mutation. (authors)

  13. Cigarette smoking accelerated brain aging and induced pre-Alzheimer-like neuropathology in rats.

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    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.

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

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    Zhi-Hua Chen

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

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

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    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.

  16. Cigarette Smoke-Induced Damage-Associated Molecular Pattern Release from Necrotic Neutrophils Triggers Proinflammatory Mediator Release

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    Heijink, Hilde; 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

    2015-01-01

    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 th

  17. 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.

  18. 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.

  19. 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.

  20. Persistence of Th17/Tc17 Cell Expression upon Smoking Cessation in Mice with Cigarette Smoke-Induced Emphysema

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    Min-Chao Duan

    2013-01-01

    Full Text Available Th17 and Tc17 cells may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD, a disease caused predominantly by cigarette smoking. Smoking cessation is the only intervention in the management of COPD. However, even after cessation, the airway inflammation may be present. In the current study, mice were exposed to room air or cigarette smoke for 24 weeks or 24 weeks followed by 12 weeks of cessation. Morphological changes were evaluated by mean linear intercepts (Lm and destructive index (DI. The frequencies of CD8+IL-17+(Tc17 and CD4+IL-17+(Th17 cells, the mRNA levels of ROR gamma and IL-17, and the levels of IL-8, TNF-alpha, and IFN-gamma in lungs or bronchoalveolar lavage fluid of mice were assayed. Here we demonstrated that alveolar enlargement and destruction induced by cigarette smoke exposure were irreversible and that cigarette smokeenhanced these T-cell subsets, and related cytokines were not significantly reduced after smoking cessation. In addition, the frequencies of Th17 and Tc17 cells in lungs of smoke-exposed mice and cessation mice were positively correlated with emphysematous lesions. More important, the frequencies of Tc17 cells were much higher than Th17 cells, and there was a significantly positive correlation between Th17 and Tc17. These results suggested that Th17/Tc17 infiltration in lungs may play a critical role in sustaining lung inflammation in emphysema. Blocking the abnormally increased numbers of Tc17 and Th17 cells may be a reasonable therapeutic strategy for emphysema.

  1. Persistence of Th17/Tc17 cell expression upon smoking cessation in mice with cigarette smoke-induced emphysema.

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    Duan, Min-Chao; Tang, Hai-Juan; Zhong, Xiao-Ning; Huang, Ying

    2013-01-01

    Th17 and Tc17 cells may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), a disease caused predominantly by cigarette smoking. Smoking cessation is the only intervention in the management of COPD. However, even after cessation, the airway inflammation may be present. In the current study, mice were exposed to room air or cigarette smoke for 24 weeks or 24 weeks followed by 12 weeks of cessation. Morphological changes were evaluated by mean linear intercepts (Lm) and destructive index (DI). The frequencies of CD8(+)IL-17(+)(Tc17) and CD4(+)IL-17(+)(Th17) cells, the mRNA levels of ROR gamma and IL-17, and the levels of IL-8, TNF-alpha, and IFN-gamma in lungs or bronchoalveolar lavage fluid of mice were assayed. Here we demonstrated that alveolar enlargement and destruction induced by cigarette smoke exposure were irreversible and that cigarette smokeenhanced these T-cell subsets, and related cytokines were not significantly reduced after smoking cessation. In addition, the frequencies of Th17 and Tc17 cells in lungs of smoke-exposed mice and cessation mice were positively correlated with emphysematous lesions. More important, the frequencies of Tc17 cells were much higher than Th17 cells, and there was a significantly positive correlation between Th17 and Tc17. These results suggested that Th17/Tc17 infiltration in lungs may play a critical role in sustaining lung inflammation in emphysema. Blocking the abnormally increased numbers of Tc17 and Th17 cells may be a reasonable therapeutic strategy for emphysema. PMID:24489575

  2. 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.

  3. Mechanisms of lung endothelial barrier disruption induced by cigarette smoke: role of oxidative stress and ceramides

    OpenAIRE

    Schweitzer, Kelly S.; Hatoum, Hadi; Brown, Mary Beth; Gupta, Mehak; Justice, Matthew J.; Beteck, Besem; Van Demark, Mary; Gu, Yuan; Presson, Robert G.; Hubbard, Walter C.; Petrache, Irina

    2011-01-01

    The epithelial and endothelial cells lining the alveolus form a barrier essential for the preservation of the lung respiratory function, which is, however, vulnerable to excessive oxidative, inflammatory, and apoptotic insults. Whereas profound breaches in this barrier function cause pulmonary edema, more subtle changes may contribute to inflammation. The mechanisms by which cigarette smoke (CS) exposure induce lung inflammation are not fully understood, but an early alteration in the epithel...

  4. Impacts of peroxisome proliferator-activated receptor-γ activation on cigarette smoke-induced exacerbated response to bacteria.

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    Morissette, Mathieu C; Shen, Pamela; Thayaparan, Danya; Stämpfli, Martin R

    2015-01-01

    Chronic obstructive pulmonary disease (COPD) is characterised by a state of chronic pulmonary inflammation punctuated by microbial exacerbations. Despite advances in treatment options, COPD remains difficult to manage. In this study, we investigated the potential of peroxisome proliferator-activated receptor (PPAR)γ activation as a new therapy against cigarette smoke-induced inflammation and its associated bacterial exacerbation. C57BL/6 mice were exposed to room air or cigarette smoke for either 4 days or 4 weeks and treated either prophylactically or therapeutically with rosiglitazone. The impact of rosiglitazone on cigarette smoke-induced exacerbated response to the bacterial pathogen nontypeable Haemophilus influenzae (NTHi) was studied using the therapeutic treatment protocol. We found that rosiglitazone was able to reduce cigarette smoke-induced neutrophilia both when administered prophylactically or therapeutically. Therapeutic intervention with rosiglitazone was also effective in preventing cigarette smoke-induced neutrophilia exacerbation following NTHi infection. Moreover, the anti-inflammatory effects of rosiglitazone did not lead to an increase in the pulmonary bacterial burden, unlike dexamethasone. Altogether, our data suggest that pharmacological activation of PPARγ may be an effective therapeutic approach to improve COPD management, as it is able to reduce cigarette smoke-induced inflammation and decrease the magnitude of bacterial exacerbations, without compromising the ability of the immune system to control the infection. PMID:25034559

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

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    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.

  6. 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. PMID:3698928

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

    Institute of Scientific and Technical Information of China (English)

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

    2012-01-01

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

  8. Inflammatory Diseases of the Lung Induced by Conventional Cigarette Smoke: A Review.

    Science.gov (United States)

    Crotty Alexander, Laura E; Shin, Stephanie; Hwang, John H

    2015-11-01

    Smoking-induced lung diseases were extremely rare prior to the 20th century. With commercialization and introduction of machine-made cigarettes, worldwide use skyrocketed and several new pulmonary diseases have been recognized. The majority of pulmonary diseases caused by cigarette smoke (CS) are inflammatory in origin. Airway epithelial cells and alveolar macrophages have altered inflammatory signaling in response to CS, which leads to recruitment of lymphocytes, eosinophils, neutrophils, and mast cells to the lungs-depending on the signaling pathway (nuclear factor-κB, adenosine monophosphate-activated protein kinase, c-Jun N-terminal kinase, p38, and signal transducer and activator of transcription 3) activated. Multiple proteins are upregulated and secreted in response to CS exposure, and many of these have immunomodulatory activities that contribute to disease pathogenesis. In particular, metalloproteases 9 and 12, surfactant protein D, antimicrobial peptides (LL-37 and human β defensin 2), and IL-1, IL-6, IL-8, and IL-17 have been found in higher quantities in the lungs of smokers with ongoing inflammation. However, many underlying mechanisms of smoking-induced inflammatory diseases are not yet known. We review here the known cellular and molecular mechanisms of CS-induced diseases, including COPD, respiratory bronchiolitis-interstitial lung disease, desquamative interstitial pneumonia, acute eosinophilic pneumonia, chronic rhinosinusitis, pulmonary Langerhans cell histiocytosis, and chronic bacterial infections. We also discuss inflammation induced by secondhand and thirdhand smoke exposure and the pulmonary diseases that result. New targeted antiinflammatory therapeutic options are currently under investigation and hopefully will yield promising results for the treatment of these highly prevalent smoking-induced diseases. PMID:26135024

  9. Smoking Cessation and the Microbiome in Induced Sputum Samples from Cigarette Smoking Asthma Patients.

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    Christian Munck

    Full Text Available Asthma is a common disease causing cough, wheezing and shortness of breath. It has been shown that the lung microbiota in asthma patients is different from the lung microbiota in healthy controls suggesting that a connection between asthma and the lung microbiome exists. Individuals with asthma who are also tobacco smokers experience more severe asthma symptoms and smoking cessation is associated with improved asthma control. In the present study we investigated if smoking cessation in asthma patients is associated with a change in the bacterial community in the lungs, examined using induced sputum. We found that while tobacco smokers with asthma have a greater bacterial diversity in the induced sputum compared to non-smoking healthy controls, smoking cessation does not lead to a change in the microbial diversity.

  10. Smoking Cessation and the Microbiome in Induced Sputum Samples from Cigarette Smoking Asthma Patients

    Science.gov (United States)

    Munck, Christian; Helby, Jens; Westergaard, Christian G.; Porsbjerg, Celeste; Backer, Vibeke; Hansen, Lars H.

    2016-01-01

    Asthma is a common disease causing cough, wheezing and shortness of breath. It has been shown that the lung microbiota in asthma patients is different from the lung microbiota in healthy controls suggesting that a connection between asthma and the lung microbiome exists. Individuals with asthma who are also tobacco smokers experience more severe asthma symptoms and smoking cessation is associated with improved asthma control. In the present study we investigated if smoking cessation in asthma patients is associated with a change in the bacterial community in the lungs, examined using induced sputum. We found that while tobacco smokers with asthma have a greater bacterial diversity in the induced sputum compared to non-smoking healthy controls, smoking cessation does not lead to a change in the microbial diversity. PMID:27391160

  11. Persistence of Th17/Tc17 Cell Expression upon Smoking Cessation in Mice with Cigarette Smoke-Induced Emphysema

    OpenAIRE

    Min-Chao Duan; Hai-Juan Tang; Xiao-Ning Zhong; Ying Huang

    2013-01-01

    Th17 and Tc17 cells may be involved in the pathogenesis of chronic obstructive pulmonary disease (COPD), a disease caused predominantly by cigarette smoking. Smoking cessation is the only intervention in the management of COPD. However, even after cessation, the airway inflammation may be present. In the current study, mice were exposed to room air or cigarette smoke for 24 weeks or 24 weeks followed by 12 weeks of cessation. Morphological changes were evaluated by mean linear intercepts (Lm)...

  12. Attenuation of acute lung inflammation induced by cigarette smoke in CXCR3 knockout mice

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    Cheng Deyun

    2008-12-01

    Full Text Available Abstract Background CD8+ T cells may participate in cigarette smoke (CS induced-lung inflammation in mice. CXCL10/IP-10 (IFNγ-inducible protein 10 and CXCL9/Mig (monokine induced by IFN-γ are up-regulated in CS-induced lung injury and may attract T-cell recruitment to the lung. These chemokines together with CXCL11/ITAC (IFN-inducible T-cell alpha chemoattractant are ligands for the chemokine receptor CXCR3 which is preferentially expressed chiefly in activated CD8+ T cells. The purpose of this investigation was to study the contribution of CXCR3 to acute lung inflammation induced by CS using CXCR3 knockout (KO mice. Methods Mice (n = 8 per group were placed in a closed plastic box connected to a smoke generator and were exposed whole body to the tobacco smoke of five cigarettes four times a day for three days. Lung pathological changes, expression of inflammatory mediators in bronchoalveolar lavage (BAL fluid and lungs at mRNA and protein levels, and lung infiltration of CD8+ T cells were compared between CXCR3-/- mice and wild type (WT mice. Results Compared with the WT littermates, CXCR3 KO mice showed less CS-induced lung inflammation as evidenced by less infiltration of inflammatory cells in airways and lung tissue, particularly fewer CD8+ T cells, lower levels of IFNγ and CXCR3 ligands (particularly CXCL10. Conclusion Our findings show that CXCR3 is important in promoting CD8+ T cell recruitment and in initiating IFNγ and CXCL10 release following CS exposure. CXCR3 may represent a promising therapeutic target for acute lung inflammation induced by CS.

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2012-03-15

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

  14. 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

  15. Vitamin C Prevents Cigarette Smoke-Induced Leukocyte Aggregation and Adhesion to Endothelium in vivo

    Science.gov (United States)

    Lehr, Hans-Anton; Frei, Balz; Arfors, Karl-E.

    1994-08-01

    A common feature of cigarette-smoke (CS)-associated diseases such as atherosclerosis and pulmonary emphysema is the activation, aggregation, and adhesion of leukocytes to micro- and macrovascular endothelium. A previous study, using a skinfold chamber model for intravital fluorescence microscopy in awake hamsters, has shown that exposure of hamsters to the smoke generated by one research cigarette elicits the adhesion of fluorescently labeled leukocytes to the endothelium of arterioles and small venules. By the combined use of intravital microscopy and scanning electron microscopy, we now demonstrate in the same animal model that (i) CS-induced leukocyte adhesion is not confined to the microcirculation, but that leukocytes also adhere singly and in clusters to the aortic endothelium; (ii) CS induces the formation in the bloodstream of aggregates between leukocytes and platelets; and (iii) CS-induced leukocyte adhesion to micro- and macrovascular endothelium and leukocyte-platelet aggregate formation are almost entirely prevented by dietary or intravenous pretreatment with the water-soluble antioxidant vitamin C (venules, 21.4 ± 11.0 vs. 149.6 ± 38.7 leukocytes per mm^2, P dietary means or supplementation, suggesting that vitamin C effectively contributes to protection from CS-associated cardiovascular and pulmonary diseases in humans.

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

    Science.gov (United States)

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

    2015-12-01

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

  17. 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.

  18. Mechanism of cigarette smoke condensate-induced acute inflammatory response in human bronchial epithelial cells

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    Mohapatra Shyam S

    2002-07-01

    Full Text Available Abstract Background To demonstrate the involvement of tobacco smoking in the pathophysiology of lung disease, the responses of pulmonary epithelial cells to cigarette smoke condensate (CSC — the particulate fraction of tobacco smoke — were examined. Methods The human alveolar epithelial cell line A549 and normal human bronchial epithelial cells (NHBEs were exposed to 0.4 μg/ml CSC, a concentration that resulted in >90% cell survival and Results NHBEs exposed to CSC showed increased expression of the inflammatory mediators sICAM-1, IL-1β, IL-8 and GM-CSF, as determined by RT-PCR. CSC-induced IL-1β expression was reduced by PD98059, a blocker of mitogen-actived protein kinase (MAPK kinase (MEK, and by PDTC, a NFκB inhibitor. Analysis of intracellular signaling pathways, using antibodies specific for phosphorylated MAPKs (extracellular signal-regulated kinase [ERK]-1/2, demonstrated an increased level of phosphorylated ERK1/2 with increasing CSC concentration. Nuclear localization of phosphorylated ERK1/2 was seen within 30 min of CSC exposure and was inhibited by PD98059. Increased phosphorylation and nuclear translocation of IκB was also seen after CSC exposure. A549 cells transfected with a luciferase reporter plasmid containing a NFκB-inducible promoter sequence and exposed to CSC (0.4 μg/ml or TNF-α (50 ng/ml had an increased reporter activity of approximately 2-fold for CSC and 3.5-fold for TNF-α relative to untreated controls. Conclusion The acute phase response of NHBEs to cigarette smoke involves activation of both MAPK and NFκB.

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

    Science.gov (United States)

    Nesi, Renata Tiscoski; de Souza, Priscila Soares; Dos Santos, Giulia Pedroso; Thirupathi, Anand; Menegali, Bruno T; Silveira, Paulo Cesar Lock; da Silva, Luciano Acordi; Valença, Samuel Santos; Pinho, Ricardo Aurino

    2016-01-01

    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. PMID:27042047

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

    Science.gov (United States)

    Pouwels, Simon D; Zijlstra, G Jan; 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

    2016-02-15

    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 chronic obstructive pulmonary disease (COPD). DAMPs can activate pattern recognition receptors (PRRs), triggering innate immune responses. We hypothesized that cigarette smoke (CS)-induced epithelial necroptosis and DAMP release initiate airway inflammation in COPD. Human bronchial epithelial BEAS-2B cells were exposed to cigarette smoke extract (CSE), and necrotic cell death (membrane integrity by propidium iodide staining) and DAMP release (i.e., double-stranded DNA, high-mobility group box 1, heat shock protein 70, mitochondrial DNA, ATP) were analyzed. Subsequently, BEAS-2B cells were exposed to DAMP-containing supernatant of CS-induced necrotic cells, and the release of proinflammatory mediators [C-X-C motif ligand 8 (CXCL-8), IL-6] was evaluated. Furthermore, mice were exposed to CS in the presence and absence of the necroptosis inhibitor necrostatin-1, and levels of DAMPs and inflammatory cell numbers were determined in bronchoalveolar lavage fluid. CSE induced a significant increase in the percentage of necrotic cells and DAMP release in BEAS-2B cells. Stimulation of BEAS-2B cells with supernatant of CS-induced necrotic cells induced a significant increase in the release of CXCL8 and IL-6, in a myeloid differentiation primary response gene 88-dependent fashion. In mice, exposure of CS increased the levels of DAMPs and numbers of neutrophils in bronchoalveolar lavage fluid, which was statistically reduced upon treatment with necrostatin-1. Together, we showed that CS exposure induces necrosis of bronchial epithelial cells and subsequent DAMP release in vitro, inducing the production of proinflammatory cytokines. In vivo, CS exposure induces neutrophilic airway inflammation that is sensitive to necroptosis inhibition. PMID:26719146

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

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    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.

  2. Cigarette Smoke Induces Immune Responses to Vimentin in both, Arthritis-Susceptible and -Resistant Humanized Mice.

    Science.gov (United States)

    Bidkar, Mitali; Vassallo, Robert; Luckey, David; Smart, Michele; Mouapi, Kelly; Taneja, Veena

    2016-01-01

    Rheumatoid arthritis (RA) is an autoimmune disease marked by chronic synovial inflammation and both, genetic and environmental factors are involved in its pathogenesis. Human leukocyte antigen (HLA) DRB1*0401 is associated with susceptibility to develop RA, while cigarette smoke (CS) exposure promotes seropositive disease with increased severity in DRB1*0401+ individuals. Smokers have higher levels of antibodies against citrullinated peptides. In this study, we determined whether the response to a known autoantigen, Vimentin (Vim) is shared epitope specific and how CS influences this response using transgenic-mice carrying RA-susceptible,*0401, and -resistant, *0402, genes. Following relatively brief exposure to CS, peptidyl arginine deiminase (PAD) enzyme expression was increased in murine lungs. Cigarette smoking led to production of Interferon (IFN)-γ with reduced levels of Interleukin (IL)-10 by splenocytes of *0401 mice. In contrast, CS augmented Th2 cytokines along with T-regulatory cells in *0402 mice. An increase in levels of antibodies to native and citrullinated Vim was observed in naïve mice of both strains following CS exposure. Our data showed that both arthritis-susceptible and -resistant mice can generate cellular and humoral immunity to Vim; however CS-induced modulation of host immunity is dependent on the interaction with the host HLA genes. PMID:27602574

  3. Cigarette smoking induces overexpression of c-Met receptor in microvessels of oral lichen planus

    OpenAIRE

    Kłosek, Sebastian K.; Sporny, Stanisław; Stasikowska-Kanicka, Olga; Kurnatowska, Anna J.

    2011-01-01

    Introduction Cigarette smoking is related to many pathological conditions; however, chemical substances affect the oral cavity first, so it is important to consider its influence on oral mucosa and oral potentially pre-malignant lesions. The aim of this study was to investigate the effect of smoking on microvessel density in oral lichen planus. Special emphasis was placed on examining the relationship between the expression of c-Met receptor in blood vessels and smoking habits. Material and m...

  4. Cigarette smoke modulates expression of human rhinovirus-induced airway epithelial host defense genes.

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    David Proud

    Full Text Available Human rhinovirus (HRV infections trigger acute exacerbations of chronic obstructive pulmonary disease (COPD and asthma. The human airway epithelial cell is the primary site of HRV infection and responds to infection with altered expression of multiple genes, the products of which could regulate the outcome to infection. Cigarette smoking aggravates asthma symptoms, and is also the predominant risk factor for the development and progression of COPD. We, therefore, examined whether cigarette smoke extract (CSE modulates viral responses by altering HRV-induced epithelial gene expression. Primary cultures of human bronchial epithelial cells were exposed to medium alone, CSE alone, purified HRV-16 alone or to HRV-16+ CSE. After 24 h, supernatants were collected and total cellular RNA was isolated. Gene array analysis was performed to examine mRNA expression. Additional experiments, using real-time RT-PCR, ELISA and/or western blotting, validated altered expression of selected gene products. CSE and HRV-16 each induced groups of genes that were largely independent of each other. When compared to gene expression in response to CSE alone, cells treated with HRV+CSE showed no obvious differences in CSE-induced gene expression. By contrast, compared to gene induction in response to HRV-16 alone, cells exposed to HRV+CSE showed marked suppression of expression of a number of HRV-induced genes associated with various functions, including antiviral defenses, inflammation, viral signaling and airway remodeling. These changes were not associated with altered expression of type I or type III interferons. Thus, CSE alters epithelial responses to HRV infection in a manner that may negatively impact antiviral and host defense outcomes.

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

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    Yan Han

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

  6. TLR9 expression is required for the development of cigarette smoke-induced emphysema in mice.

    Science.gov (United States)

    Foronjy, Robert F; Salathe, Matthias A; Dabo, Abdoulaye J; Baumlin, Nathalie; Cummins, Neville; Eden, Edward; Geraghty, Patrick

    2016-07-01

    The expression of Toll-like receptor (TLR)-9, a pathogen recognition receptor that recognizes unmethylated CpG sequences in microbial DNA molecules, is linked to the pathogenesis of several lung diseases. TLR9 expression and signaling was investigated in animal and cell models of chronic obstructive pulmonary disease (COPD). We observed enhanced TLR9 expression in mouse lungs following exposure to cigarette smoke. Tlr9(-/-) mice were resistant to cigarette smoke-induced loss of lung function as determined by mean linear intercept, total lung capacity, lung compliance, and tissue elastance analysis. Tlr9 expression also regulated smoke-mediated immune cell recruitment to the lung; apoptosis; expression of granulocyte-colony stimulating factor (G-CSF), the CXCL5 protein, and matrix metalloproteinase-2 (MMP-2); and protein tyrosine phosphatase 1B (PTP1B) activity in the lung. PTP1B, a phosphatase with anti-inflammatory abilities, was identified as binding to TLR9. In vivo delivery of a TLR9 agonist enhanced TLR9 binding to PTP1B, which inactivated PTP1B. Ptp1b(-/-) mice had elevated lung concentrations of G-CSF, CXCL5, and MMP-2, and tissue expression of type-1 interferon following TLR9 agonist administration, compared with wild-type mice. TLR9 responses were further determined in fully differentiated normal human bronchial epithelial (NHBE) cells isolated from nonsmoker, smoker, and COPD donors, and then cultured at air liquid interface. NHBE cells from smokers and patients with COPD expressed more TLR9 and secreted greater levels of G-CSF, IL-6, CXCL5, IL-1β, and MMP-2 upon TLR9 ligand stimulation compared with cells from nonsmoker donors. Although TLR9 combats infection, our results indicate that TLR9 induction can affect lung function by inactivating PTP1B and upregulating expression of proinflammatory cytokines. PMID:27288485

  7. Effects of cigarette smoking on priapism induced by quetiapine: a case report

    Directory of Open Access Journals (Sweden)

    Hosseini Seyed

    2012-10-01

    Full Text Available Abstract Priapism is defined as an unwanted, prolonged, and painful erection which is unrelated to sexual stimulation. Some case studies suggest that priapism is an adverse effect of antipsychotic medications. In our case study a 30 year-old Iranian male with schizophrenia was experiencing recurrent priapism associated with quetiapine use. There are three interesting facts about this case: Firstly, the patient suffered priapism after even low dose consumption of quetiapine. Secondly, this case had experienced priapism with risperidone, olanzapine, and even clozapine in the past, suggesting a possible pharmacodynamic interaction of antipsychotics and inner biological traits in this particular case. Thirdly, priapism induced by low dose quetiapine was resolved after cigarette smoking.

  8. 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.

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

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    Andrea C. Baeder

    2016-01-01

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

  10. Exacerbation of cigarette smoke-induced pulmonary inflammation by Staphylococcus aureus Enterotoxin B in mice

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    Brusselle Guy G

    2011-05-01

    Full Text Available Abstract Background Cigarette smoke (CS is a major risk factor for the development of COPD. CS exposure is associated with an increased risk of bacterial colonization and respiratory tract infection, because of suppressed antibacterial activities of the immune system and delayed clearance of microbial agents from the lungs. Colonization with Staphylococcus aureus results in release of virulent enterotoxins, with superantigen activity which causes T cell activation. Objective To study the effect of Staphylococcus aureus enterotoxin B (SEB on CS-induced inflammation, in a mouse model of COPD. Methods C57/Bl6 mice were exposed to CS or air for 4 weeks (5 cigarettes/exposure, 4x/day, 5 days/week. Endonasal SEB (10 μg/ml or saline was concomitantly applied starting from week 3, on alternate days. 24 h after the last CS and SEB exposure, mice were sacrificed and bronchoalveolar lavage (BAL fluid and lung tissue were collected. Results Combined exposure to CS and SEB resulted in a raised number of lymphocytes and neutrophils in BAL, as well as increased numbers of CD8+ T lymphocytes and granulocytes in lung tissue, compared to sole CS or SEB exposure. Moreover, concomitant CS/SEB exposure induced both IL-13 mRNA expression in lungs and goblet cell hyperplasia in the airway wall. In addition, combined CS/SEB exposure stimulated the formation of dense, organized aggregates of B- and T- lymphocytes in lungs, as well as significant higher CXCL-13 (protein, mRNA and CCL19 (mRNA levels in lungs. Conclusions Combined CS and SEB exposure aggravates CS-induced inflammation in mice, suggesting that Staphylococcus aureus could influence the pathogenesis of COPD.

  11. 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.

  12. Mechanisms of lung endothelial barrier disruption induced by cigarette smoke: role of oxidative stress and ceramides.

    Science.gov (United States)

    Schweitzer, Kelly S; Hatoum, Hadi; Brown, Mary Beth; Gupta, Mehak; Justice, Matthew J; Beteck, Besem; Van Demark, Mary; Gu, Yuan; Presson, Robert G; Hubbard, Walter C; Petrache, Irina

    2011-12-01

    The epithelial and endothelial cells lining the alveolus form a barrier essential for the preservation of the lung respiratory function, which is, however, vulnerable to excessive oxidative, inflammatory, and apoptotic insults. Whereas profound breaches in this barrier function cause pulmonary edema, more subtle changes may contribute to inflammation. The mechanisms by which cigarette smoke (CS) exposure induce lung inflammation are not fully understood, but an early alteration in the epithelial barrier function has been documented. We sought to investigate the occurrence and mechanisms by which soluble components of mainstream CS disrupt the lung endothelial cell barrier function. Using cultured primary rat microvascular cell monolayers, we report that CS induces endothelial cell barrier disruption in a dose- and time-dependent manner of similar magnitude to that of the epithelial cell barrier. CS exposure triggered a mechanism of neutral sphingomyelinase-mediated ceramide upregulation and p38 MAPK and JNK activation that were oxidative stress dependent and that, along with Rho kinase activation, mediated the endothelial barrier dysfunction. The morphological changes in endothelial cell monolayers induced by CS included actin cytoskeletal rearrangement, junctional protein zonula occludens-1 loss, and intercellular gap formation, which were abolished by the glutathione modulator N-acetylcysteine and ameliorated by neutral sphingomyelinase inhibition. The direct application of ceramide recapitulated the effects of CS, by disrupting both endothelial and epithelial cells barrier, by a mechanism that was redox and apoptosis independent and required Rho kinase activation. Furthermore, ceramide induced dose-dependent alterations of alveolar microcirculatory barrier in vivo, measured by two-photon excitation microscopy in the intact rat. In conclusion, soluble components of CS have direct endothelial barrier-disruptive effects that could be ameliorated by glutathione

  13. 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.

  14. 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. PMID:24615921

  15. Lipid-soluble cigarette smoking particles induce expression of inflammatory and extracellular-matrix-related genes in rat cerebral arteries

    DEFF Research Database (Denmark)

    Vikman, Petter; Xu, Cang-Bao; Edvinsson, Lars

    2009-01-01

    AIMS: Cigarette smoking is one of the strongest risk factors for stroke. However, the underlying molecular mechanisms that smoke leads to the pathogenesis of stroke are incompletely understood. METHODS: Dimethyl sulfoxide (DMSO)-soluble (lipid-soluble) cigarette smoking particles (DSP) were extra...

  16. Curcumin attenuates elastase- and cigarette smoke-induced pulmonary emphysema in mice.

    Science.gov (United States)

    Suzuki, Masaru; Betsuyaku, Tomoko; Ito, Yoko; Nagai, Katsura; Odajima, Nao; Moriyama, Chinatsu; Nasuhara, Yasuyuki; Nishimura, Masaharu

    2009-04-01

    Curcumin, a yellow pigment obtained from turmeric (Curcumina longa), is a dietary polyphenol that has been reported to possess anti-inflammatory and antioxidant properties. The effect of curcumin against the development of pulmonary emphysema in animal models is unknown. The aim of this study was to determine whether curcumin is able to attenuate the development of pulmonary emphysema in mice. Nine-week-old male C57BL/6J mice were treated with intratracheal porcine pancreatic elastase (PPE) or exposed to mainstream cigarette smoke (CS) (60 min/day for 10 consecutive days or 5 days/wk for 12 wk) to induce pulmonary inflammation and emphysema. Curcumin (100 mg/kg) or vehicle was administrated daily by oral gavage 1 h and 24 h before intratracheal PPE treatment and daily thereafter throughout a 21-day period in PPE-exposed mice and 1 h before each CS exposure in CS-exposed mice. As a result, curcumin treatment significantly inhibited PPE-induced increase of neutrophils in bronchoalveolar lavage fluid at 6 h and on day 1 after PPE administration, with an increase in antioxidant gene expression at 6 h and significantly attenuated PPE-induced air space enlargement on day 21. It was also found that curcumin treatment significantly inhibited CS-induced increase of neutrophils and macrophages in bronchoalveolar lavage fluid after 10 consecutive days of CS exposure and significantly attenuated CS-induced air space enlargement after 12 wk of CS exposure. In conclusion, oral curcumin administration attenuated PPE- and CS-induced pulmonary inflammation and emphysema in mice. PMID:19168576

  17. 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. PMID:25192219

  18. 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. PMID:27048661

  19. Andrographolide protects against cigarette smoke-induced oxidative lung injury via augmentation of Nrf2 activity

    OpenAIRE

    Guan, SP; Tee, W; Ng, DSW; Chan, TK; Peh, HY; Ho, WE; Cheng, C; Mak, JC; Wong, WSF

    2013-01-01

    BACKGROUND AND PURPOSE: Cigarette smoke is a major cause for chronic obstructive pulmonary disease (COPD). Andrographolide is an active biomolecule isolated from the plant Andrographis paniculata. Andrographolide has been shown to activate nuclear factor erythroid-2-related factor 2 (Nrf2), a redox-sensitive antioxidant transcription factor. As Nrf2 activity is reduced in COPD, we hypothesize that andrographolide may have therapeutic value for COPD. EXPERIMENTAL APPROACH: Andrographolide was ...

  20. 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.

  1. Airway epithelial cell PPARγ modulates cigarette smoke-induced chemokine expression and emphysema susceptibility in mice.

    Science.gov (United States)

    Solleti, Siva Kumar; Simon, Dawn M; Srisuma, Sorachai; Arikan, Meltem C; Bhattacharya, Soumyaroop; Rangasamy, Tirumalai; Bijli, Kaiser M; Rahman, Arshad; Crossno, Joseph T; Shapiro, Steven D; Mariani, Thomas J

    2015-08-01

    Chronic obstructive pulmonary disease (COPD) is a highly prevalent, chronic inflammatory lung disease with limited existing therapeutic options. While modulation of peroxisome proliferator-activating receptor (PPAR)-γ activity can modify inflammatory responses in several models of lung injury, the relevance of the PPARG pathway in COPD pathogenesis has not been previously explored. Mice lacking Pparg specifically in airway epithelial cells displayed increased susceptibility to chronic cigarette smoke (CS)-induced emphysema, with excessive macrophage accumulation associated with increased expression of chemokines, Ccl5, Cxcl10, and Cxcl15. Conversely, treatment of mice with a pharmacological PPARγ activator attenuated Cxcl10 and Cxcl15 expression and macrophage accumulation in response to CS. In vitro, CS increased lung epithelial cell chemokine expression in a PPARγ activation-dependent fashion. The ability of PPARγ to regulate CS-induced chemokine expression in vitro was not specifically associated with peroxisome proliferator response element (PPRE)-mediated transactivation activity but was correlated with PPARγ-mediated transrepression of NF-κB activity. Pharmacological or genetic activation of PPARγ activity abrogated CS-dependent induction of NF-κB activity. Regulation of NF-κB activity involved direct PPARγ-NF-κB interaction and PPARγ-mediated effects on IKK activation, IκBα degradation, and nuclear translocation of p65. Our data indicate that PPARG represents a disease-relevant pathophysiological and pharmacological target in COPD. Its activation state likely contributes to NF-κB-dependent, CS-induced chemokine-mediated regulation of inflammatory cell accumulation. PMID:26024894

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

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    Bracke Ken R

    2010-07-01

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

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

    NARCIS (Netherlands)

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

    2007-01-01

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

  4. Lipid-soluble cigarette smoking particles induce expression of inflammatory and extracellular-matrix-related genes in rat cerebral arteries

    Directory of Open Access Journals (Sweden)

    Petter Vikman

    2009-04-01

    Full Text Available Petter Vikman, Cang-Bao Xu, Lars EdvinssonDepartment of Clinical Sciences, Experimental Vascular Research, Lund, SwedenAims: Cigarette smoking is one of the strongest risk factors for stroke. However, the underlying molecular mechanisms that smoke leads to the pathogenesis of stroke are incompletely understood.Methods: Dimethyl sulfoxide (DMSO-soluble (lipid-soluble cigarette smoking particles (DSP were extracted from cigarette smoke (0.8 mg nicotine per cigarette; Marlboro®. Rat cerebral arteries were isolated and organ cultured in the presence of DSP (0.2 μl/ml, equivalent to the plasma level in smokers for 24 h. The expression of matrix metalloproteinase 9 and 13 (MMP9 and MMP13, angiotensin receptor 1 and 2 (AT1 and AT2, interleukin 6 and inducible nitric oxide synthase (iNOS were investigated at mRNA level by real-time PCR and/or at protein level by immunohistochemistry. In addition, the activity of three mitogen-activated protein kinases (p38, ERK 1/2 and SAPK/JNK and their downstream transcription factors (ATF-2, Elk-1 and c-Jun were examined.Results: We observed that compared with control (DMSO-treated cerebral arteries, the cerebral arteries treated by DSP exhibited enhanced expression of MMP13 and AT1 receptors, but not of AT2 receptors, at both mRNA and protein levels, suggesting that a transcriptional mechanism is most likely involved in the DSP effects. This is further supported by the findings that DSP induced phosphorylation of p38 mitogen-activated protein kinases inflammatory signal protein in parallel with activation of its downstream transcription factor ATF-2 and Elk-1. However, ERK 1/2 and SAPK/JNK activities were markedly expressed in the control (organ culture per se with DMSO, and DSP failed to further enhance the activation of ERK 1/2 and SAPK/JNK in the cerebral arteries.Conclusions: DSP induces cerebral vessel inflammation with activation of p38 MAPK inflammatory signal and the downstream transcriptional factors (ATF

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

    DEFF Research Database (Denmark)

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

    2010-01-01

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

  6. Tiotropium Attenuates Virus-Induced Pulmonary Inflammation in Cigarette Smoke-Exposed Mice.

    Science.gov (United States)

    Bucher, Hannes; Duechs, Matthias J; Tilp, Cornelia; Jung, Birgit; Erb, Klaus J

    2016-06-01

    Viral infections trigger exacerbations in chronic obstructive pulmonary disease (COPD), and tiotropium, a M3 receptor antagonist, reduces exacerbations in patients by unknown mechanisms. In this report, we investigated whether tiotropium has anti-inflammatory effects in mice exposed to cigarette smoke (CS) and infected with influenza virus A/PR/8/34 (H1N1) or respiratory syncytial virus (RSV) and compared these effects with those of steroid fluticasone and PDE4-inhibitor roflumilast. Mice were exposed to CS; infected with H1N1 or RSV; and treated with tiotropium, fluticasone, or roflumilast. The amount of cells and cytokine levels in the airways, lung function, and viral load was determined. NCI-H292 cells were infected with H1N1 or RSV and treated with the drugs. In CS/H1N1-exposed mice, tiotropium reduced neutrophil and macrophage numbers and levels of interleukin-6 (IL-6) and interferon-γ (IFN-γ) in the airways and improved lung function. In contrast, fluticasone increased the loss of body weight; failed to reduce neutrophil or macrophage numbers; increased IL-6, KC, and tumor necrosis factor-α (TNF-α) in the lungs; and worsened lung function. Treatment with roflumilast reduced macrophage numbers, IL-6, and KC in the lungs but had no effect on neutrophil numbers or lung function. In CS/RSV-exposed mice, treatment with tiotropium, but not fluticasone or roflumilast, reduced neutrophil numbers and IL-6 and TNF-α levels in the lungs. Viral load of H1N1 and RSV was significantly elevated in CS/virus-exposed mice and NCI-H292 cells after fluticasone treatment, whereas tiotropium and roflumilast had no effect. In conclusion, tiotropium has anti-inflammatory effects on CS/virus-induced inflammation in mice that are superior to the effects of roflumilast and fluticasone. This finding might help to explain the observed reduction of exacerbation rates in COPD patients. PMID:27016458

  7. A single serving of blueberry (V. corymbosum) modulates peripheral arterial dysfunction induced by acute cigarette smoking in young volunteers: a randomized-controlled trial.

    Science.gov (United States)

    Del Bo', Cristian; Porrini, Marisa; Fracassetti, Daniela; Campolo, Jonica; Klimis-Zacas, Dorothy; Riso, Patrizia

    2014-12-01

    Cigarette smoking causes oxidative stress, hypertension and endothelial dysfunction. Polyphenol-rich foods may prevent these conditions. We investigated the effect of a single serving of fresh-frozen blueberry intake on peripheral arterial function and arterial stiffness in young smokers. Sixteen male smokers were recruited for a 3-armed randomized-controlled study with the following experimental conditions: smoking treatment (one cigarette); blueberry treatment (300 g of blueberry) + smoking; control treatment (300 mL of water with sugar) + smoking. Each treatment was separated by one week of wash-out period. The blood pressure, heart rate, peripheral arterial function (reactive hyperemia and Framingham reactive hyperemia), and arterial stiffness (digital augmentation index, digital augmentation index normalized for a heart rate of 75 bpm) were measured before and 20 min after smoking with Endo-PAT2000. Smoking impaired the blood pressure, heart rate and peripheral arterial function, but did not affect the arterial stiffness. Blueberry consumption counteracted the impairment of the reactive hyperemia index induced by smoking (-4.4 ± 0.8% blueberry treatment vs. -22.0 ± 1.1% smoking treatment, p smoking treatment, p smoking treatment, mmHg, p smoking. No effect was observed for arterial stiffness and other vital signs. In conclusion, data obtained suggest a protective role of blueberry on reactive hyperemia, Framingham reactive hyperemia, and systolic blood pressure in subjects exposed to smoke of one cigarette. Future studies are necessary to elucidate the mechanisms involved.

  8. 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.

  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. 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.

  11. Injury of Mouse Brain Mitochondria Induced by Cigarette Smoke Extract and Effect of Vitamin C on It in vitro

    Institute of Scientific and Technical Information of China (English)

    YU-MEI YANG; GENG-TAO LIU

    2003-01-01

    To investigate the toxicity of cigarette smoke extract (CSE) and nicotine on mouse brain mitochondria as well as the protective effect of vitamin C in vitro. Method Mouse brain mitochondria in vitro was incubated with CSE or nicotine in the absence or presence of vitamin C for 60 minutes, and the changes of mitochondrial function and structure were measured. Results CSE inhibited mitochondrial ATPase and cytochrome C oxidase activities in a dose-dependent manner.However, no significant changes in the peroxidation indices were observed when mitochondrial respiratory enzymes activity was inhibited, and protection of mitochondria from CSE-induced injury by vitamin C was not displayed in vitro. The effect of CSE on mouse brain mitochondria swelling response to calcium stimulation was dependent on calcium concentrations. CSE inhibited swelling of mitochondria at 6.5 μmol/L Ca2+, but promoted swelling response at 250 μmol/L Ca2+. Nicotine, the major component of cigarette smoke, showed no significant damage in mouse brain mitochondria in vitro. The CSE treatment induced mitochondrial inner membrane damage and vacuolization of the matrix, whereas the outer mitochondrial membrane appeared to be preserved. Conclusion The toxic effect of CSE on brain mitochondria may be due to its direct action on enzymatic activity rather than through oxygen free radical injury. Nicotine is not the responsible component for the toxicity of CSE to brain mitochondria.

  12. Severe Reduction in Number and Function of Peripheral T Cells Does Not Afford Protection toward Emphysema and Bronchial Remodeling Induced in Mice by Cigarette Smoke.

    Science.gov (United States)

    De Cunto, Giovanna; Lunghi, Benedetta; Bartalesi, Barbara; Cavarra, Eleonora; Fineschi, Silvia; Ulivieri, Cristina; Lungarella, Giuseppe; Lucattelli, Monica

    2016-07-01

    The protein Lck (p56(Lck)) is a Src family tyrosine kinase expressed at all stages of thymocyte development and is required for maturation of T cells. The targeted disruption of Lck gene in mice results in severe block in thymocyte maturation with substantial reduction in the development of CD4(+)CD8(+) thymocytes, severe reduction of peripheral T cells, and disruption of T-cell receptor signaling with defective function of T-cell responses. To investigate the role of T lymphocyte in the development of cigarette smoke-induced pulmonary changes, Lck(-/-) mice and corresponding congenic wild-type mice were chronically exposed to cigarette smoke, and their lungs were analyzed by biochemical, immunologic, and morphometric methods. Smoking mice from both genotypes showed disseminated foci of emphysema and large areas of goblet cell metaplasia in bronchial and bronchiolar epithelium. Morphometric evaluation of lung changes and lung elastin determination confirmed that mice from both genotypes showed the same degree of emphysematous lesions. Thus, cigarette smoke exposure in the presence of severe reduction in number and function of peripheral T cells does not influence the development of pulmonary changes induced by cigarette smoke. The data obtained suggest that innate immunity is a leading actor in the early development of pulmonary changes in smoking mice and that the adaptive immune response may play a role at later stages. PMID:27157991

  13. 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...

  14. 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....

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

    Directory of Open Access Journals (Sweden)

    Yashodhar P Bhandary

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

  16. Characteristics of Smoking Used Cigarettes among an Incarcerated Population

    OpenAIRE

    Lantini, Ryan; van den Berg, Jacob J.; Roberts, Mary B.; Bock, Beth C.; Stein, L.A.R.; Parker, Donna R.; Friedmann, Peter D; Clarke, Jennifer G.

    2014-01-01

    Little is known about smoking behaviors involving shared and previously used cigarettes, which we refer to as “smoking used cigarettes.” Examples include: cigarette sharing with strangers, smoking discarded cigarettes (‘butts’), or remaking cigarettes from portions of discarded cigarettes. The current study focuses on the prevalence of and factors associated with smoking used cigarettes prior to incarceration among a US prison population. Questionnaires were administered to 244 male and femal...

  17. 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.

  18. 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.

  19. Icariin Ameliorates Cigarette Smoke Induced Inflammatory Responses via Suppression of NF-κB and Modulation of GR In Vivo and In Vitro

    OpenAIRE

    Li, Lulu; Sun, Jing; Xu, Changqing; Zhang, Hongying; Wu, Jinfeng; Liu, Baojun; Dong, Jingcheng

    2014-01-01

    Purpose To investigate the effects of icariin, a major constituent of flavonoids isolated from the herb Epimedium, on cigarette smoke (CS) induced inflammatory responses in vivo and in vitro. Methods In vivo, BALB/c mice were exposed to smoke of 15 cigarettes for 1 h/day, 6 days/week for 3 months and dosed with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). In vitro, A549 cells were incubated with icariin (10, 50 and 100 µM) followed by treatments with CSE (2.5%). Results We found...

  20. Cigarette smoking impairs sperm bioenergetics

    Directory of Open Access Journals (Sweden)

    Kazim R. Chohan

    2010-02-01

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

  1. 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

  2. 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.

  3. Genetic effects of fresh cigarette smoke in Saccharomyces cerevisiae

    Energy Technology Data Exchange (ETDEWEB)

    Gairola, C.

    1982-09-01

    Ability of fresh cigarette smoke from University of Kentucky reference cigarette 2R1 to induce gene conversion, reverse mutation and mitotic crossing-over in strain D7 of Saccharomyces cerevisiae was examined. A closed cell suspension-recycle system using 2 peristaltic pumps interconnected to a single-port reverse-phase smoking machine was developed to provide complete exposure of cells to smoke within 0.2--10 sec of its generation. The exposed cells showed a dose-dependent increase in the frequency of all the 3 genetic endpoints examined. Cell age was an important factor with younger cells being more sensitive than older. Filtration studies showed that the gas phase possessed as much as 25% of the total whole-smoke activity. Activated charcoal reduced the activity of smoke in direct proportion to its amount in the filter. Acetate filter did not appreciably alter the activity. A comparison of whole smoke from various cigarettes showed that: (1) the nicotine content of a cigarette does not affect the genetic activity of smoke; (2) burley and flue-cured tobaccos have differential activity in gene conversion and reverse mutation systems; and (3) the genetic effects of whole smoke are not peculiar to tobacco pyrolysis because similar effects are produced by smokes from lettuce and other non-tobacco cigarettes. It is concluded that the yeast D7 system can be used effectively for the quantitative evaluation of genetic effects of smoke from different cigarettes, and both whole cigarette smoke and its gas phase possess mutagenic as well as recombinogenic activity that can be modified by the use of filters.

  4. Genetic effects of fresh cigarette smoke in Saccharomyces cerevisiae.

    Science.gov (United States)

    Gairola, C

    1982-09-01

    Ability of fresh cigarette smoke from University of Kentucky reference cigarette 2R1 to induce gene conversion, reverse mutation and mitotic crossing-over in strain D7 of Saccharomyces cerevisiae was examined. A closed cell suspension-recycle system using 2 peristaltic pumps interconnected to a single-port reverse-phase smoking machine was developed to provide complete exposure of cells to smoke within 0.2--10 sec of its generation. The exposed cells showed a dose-dependent increase in the frequency of all the 3 genetic endpoints examined. Cell age was an important factor with younger cells being more sensitive than older. Filtration studies showed that the gas phase possessed as much as 25% of the total whole-smoke activity. Activated charcoal reduced the activity of smoke in direct proportion to its amount in the filter. Acetate filter did not appreciably alter the activity. A comparison of whole smoke from various cigarettes showed that: (1) the nicotine content of a cigarette does not affect the genetic activity of smoke; (2) burley and flue-cured tobaccos have differential activity in gene conversion and reverse mutation systems; and (3) the genetic effects of whole smoke are not peculiar to tobacco pyrolysis because similar effects are produced by smokes from lettuce and other non-tobacco cigarettes. It is concluded that the yeast D7 system can be used effectively for the quantitative evaluation of genetic effects of smoke from different cigarettes, and both whole cigarette smoke and its gas phase possess mutagenic as well as recombinogenic activity that can be modified by the use of filters. PMID:6755230

  5. 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.

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

    Science.gov (United States)

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

    2016-05-27

    Cigarette smoke (CS) is associated with many maladies, one of which is chronic obstructive pulmonary disease (COPD). As the disease progresses, patients are more prone to develop COPD exacerbation episodes by bacterial infection, particularly to nontypeable Haemophilus influenza (NTHi) infection. The present study aimed to develop a CS-exposed mouse model that increases inflammation induced by NTHi challenge and investigate the protective effects of andrographolide, a bioactive molecule with anti-inflammatory and antioxidant properties isolated from the plant Andrographis paniculata. Female BALB/c mice exposed to 2 weeks of CS followed by a single intratracheal instillation of NTHi developed increased macrophage and neutrophil pulmonary infiltration, augmented cytokine levels, and heightened oxidative damage. Andrographolide effectively reduced lung cellular infiltrates and decreased lung levels of TNF-α, IL-1β, CXCL1/KC, 8-OHdG, matrix metalloproteinase-8 (MMP-8), and MMP-9. The protective actions of andrographolide on CS-predisposed NTHi inflammation might be attributable to increased nuclear factor erythroid-2-related factor 2 (Nrf2) activation and decreased Kelch-like ECH-associated protein 1 (Keap1) repressor function, resulting in enhanced gene expression of antioxidant enzymes including heme oxygenase-1 (HO-1), glutathione reductase (GR), glutathione peroxidase-2 (GPx-2), glutamate-cysteine ligase modifier (GCLM), and NAD(P)H quinone oxidoreductase 1 (NQO1). Taken together, these findings strongly support a therapeutic potential for andrographolide in preventing lung inflammation caused by NTHi in cigarette smokers. PMID:27104764

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

    Science.gov (United States)

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

    2016-05-27

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

  8. Decitabine enhances stem cell antigen-1 expression in cigarette smoke extract-induced emphysema in animal model.

    Science.gov (United States)

    He, Zhi-Hui; Chen, Yan; Chen, Ping; He, Sheng-Dong; Ye, Ji-Ru; Liu, Da

    2016-01-01

    Stem cell antigen-1 (Sca-1) is a mouse glycosyl phosphatidylinositol-anchored protein and a cell surface marker found on hematopoietic stem cells (HSCs). Despite decades of study, its biological functions remain little known. Sca-1 is a typical marker of bone marrow-derived HSCs, it is also expressed by a mixture of tissue-resident stem, progenitor cells in nonhematopoietic organs. Endothelial progenitor cell (EPC) is a subtype of HSC and contributes to endothelial repair by homing in on locations of injury. Abnormal genetic methylation has been detected in smoking-related diseases. The present study aimed to investigate the lung function and histomorphology, the expression of Sca-1 gene in lung tissues, and bone marrow-derived EPCs in cigarette smoke extract (CSE)-induced emphysema mice, and to further determine whether Decitabine (Dec), the most widely used inhibitor of DNA methylation, could protect against the damages caused by CSE. The results of the present study demonstrated that Dec could partly protect against CSE-induced emphysema in mice, enhance Sca-1 expression in lung tissue, and bone marrow-derived EPCs. The results suggested that the depletion of the progenitor cell pool and DNA methylation of Sca-1 gene may be involved in the progression of emphysema in mice.

  9. Losartan attenuates chronic cigarette smoke exposure-induced pulmonary arterial hypertension in rats: Possible involvement of angiotensin-converting enzyme-2

    International Nuclear Information System (INIS)

    Chronic cigarette smoking induces pulmonary arterial hypertension (PAH) by largely unknown mechanisms. Renin-angiotensin system (RAS) is known to function in the development of PAH. Losartan, a specific angiotensin II receptor antagonist, is a well-known antihypertensive drug with a potential role in regulating angiotensin-converting enzyme-2 (ACE2), a recently found regulator of RAS. To determine the effect of losartan on smoke-induced PAH and its possible mechanism, rats were daily exposed to cigarette smoke for 6 months in the absence and in the presence of losartan. Elevated right ventricular systolic pressure (RVSP), thickened wall of pulmonary arteries with apparent medial hypertrophy along with increased angiotensin II (Ang II) and decreased ACE2 levels were observed in smoke-exposed-only rats. Losartan administration ameliorated pulmonary vascular remodeling, inhibited the smoke-induced RVSP and Ang II elevation and partially reversed the ACE2 decrease in rat lungs. In cultured primary pulmonary artery smooth muscle cells (PASMCs) from 3- and 6-month smoke-exposed rats, ACE2 levels were significantly lower than in those from the control rats. Moreover, PASMCs from 6-month exposed rats proliferated more rapidly than those from 3-month exposed or control rats, and cells grew even more rapidly in the presence of DX600, an ACE2 inhibitor. Consistent with the in vivo study, in vitro losartan pretreatment also inhibited cigarette smoke extract (CSE)-induced cell proliferation and ACE2 reduction in rat PASMCs. The results suggest that losartan may be therapeutically useful in the chronic smoking-induced pulmonary vascular remodeling and PAH and ACE2 may be involved as part of its mechanism. Our study might provide insight into the development of new therapeutic interventions for PAH smokers.

  10. Cigarette smoke extract-induced p120-mediated NF-κB activation in human epithelial cells is dependent on the RhoA/ROCK pathway

    Science.gov (United States)

    Zhang, Chao; Qin, Shenghui; Qin, Lingzhi; Liu, Liwei; Sun, Wenjia; Li, Xiyu; Li, Naping; Wu, Renliang; Wang, Xi

    2016-09-01

    Cigarette smoke exposure is a major cause of chronic obstructive pulmonary disease (COPD), but the underlying molecular inflammatory mechanisms remain poorly understood. Previous studies have found that smoke disrupts cell-cell adhesion by inducing epithelial barrier damage to the adherens junction proteins, primarily E-cadherin (E-cad) and p120-catenin (p120). Recently, the anti-inflammatory role of p120 has drawn increasing attention. In this study, we demonstrate that p120 has a role in the cigarette smoke extract-induced inflammatory response, presumably by regulating NF-κB signaling activation. Mechanistically, we show that p120-mediated NF-κB signaling activation in airway epithelial inflammation is partially RhoA dependent and is independent of E-cad. These results provide novel evidence for the role of p120 in the anti-inflammatory response.

  11. Cigarette smoke extract-induced p120-mediated NF-κB activation in human epithelial cells is dependent on the RhoA/ROCK pathway

    Science.gov (United States)

    Zhang, Chao; Qin, Shenghui; Qin, Lingzhi; Liu, Liwei; Sun, Wenjia; Li, Xiyu; Li, Naping; Wu, Renliang; Wang, Xi

    2016-01-01

    Cigarette smoke exposure is a major cause of chronic obstructive pulmonary disease (COPD), but the underlying molecular inflammatory mechanisms remain poorly understood. Previous studies have found that smoke disrupts cell-cell adhesion by inducing epithelial barrier damage to the adherens junction proteins, primarily E-cadherin (E-cad) and p120-catenin (p120). Recently, the anti-inflammatory role of p120 has drawn increasing attention. In this study, we demonstrate that p120 has a role in the cigarette smoke extract-induced inflammatory response, presumably by regulating NF-κB signaling activation. Mechanistically, we show that p120-mediated NF-κB signaling activation in airway epithelial inflammation is partially RhoA dependent and is independent of E-cad. These results provide novel evidence for the role of p120 in the anti-inflammatory response. PMID:27586697

  12. Cigarette smoke extract-induced p120-mediated NF-κB activation in human epithelial cells is dependent on the RhoA/ROCK pathway.

    Science.gov (United States)

    Zhang, Chao; Qin, Shenghui; Qin, Lingzhi; Liu, Liwei; Sun, Wenjia; Li, Xiyu; Li, Naping; Wu, Renliang; Wang, Xi

    2016-01-01

    Cigarette smoke exposure is a major cause of chronic obstructive pulmonary disease (COPD), but the underlying molecular inflammatory mechanisms remain poorly understood. Previous studies have found that smoke disrupts cell-cell adhesion by inducing epithelial barrier damage to the adherens junction proteins, primarily E-cadherin (E-cad) and p120-catenin (p120). Recently, the anti-inflammatory role of p120 has drawn increasing attention. In this study, we demonstrate that p120 has a role in the cigarette smoke extract-induced inflammatory response, presumably by regulating NF-κB signaling activation. Mechanistically, we show that p120-mediated NF-κB signaling activation in airway epithelial inflammation is partially RhoA dependent and is independent of E-cad. These results provide novel evidence for the role of p120 in the anti-inflammatory response. PMID:27586697

  13. The inhibitory mechanism of Cordyceps sinensis on cigarette smoke extract-induced senescence in human bronchial epithelial cells

    Directory of Open Access Journals (Sweden)

    Liu AL

    2016-07-01

    Full Text Available Ailing Liu,1,2,* Jinxiang Wu,1,* Aijun Li,2 Wenxiang Bi,3 Tian Liu,1 Liuzhao Cao,1 Yahui Liu,1 Liang Dong1 1Department of Pulmonary Diseases, Qilu Hospital, Shandong University, Jinan, Shandong, People’s Republic of China; 2Department of Pulmonary Diseases, Weihai Municipal Hospital, Weihai, Shandong, People’s Republic of China; 3Institute of Biochemistry and Molecular Biology, School of Medicine, Shandong University, Jinan, Shandong, People’s Republic of China *These authors contributed equally to this work Objectives: Cellular senescence is a state of irreversible growth arrest induced either by telomere shortening (replicative senescence or stress. The bronchial epithelial cell is often injured by inhaled toxic substances, such as cigarette smoke. In the present study, we investigated whether exposure to cigarette smoke extract (CSE induces senescence of bronchial epithelial cells; and Cordyceps sinensis mechanism of inhibition of CSE-induced cellular senescence.Methods: Human bronchial epithelial cells (16HBE cells cultured in vitro were treated with CSE and/or C. sinensis. p16, p21, and senescence-associated-galactosidase activity were used to detect cellular senescence with immunofluorescence, quantitative polymerase chain reaction, and Western blotting. Reactive oxygen species (ROS, PI3K/AKT/mTOR and their phosphorylated proteins were examined to testify the activation of signaling pathway by ROS fluorescent staining and Western blotting. Then, inhibitors of ROS and PI3K were used to further confirm the function of this pathway.Results: Cellular senescence was upregulated by CSE treatment, and C. sinensis can decrease CSE-induced cellular senescence. Activation of ROS/PI3K/AKT/mTOR signaling pathway was enhanced by CSE treatment, and decreased when C. sinensis was added. Blocking ROS/PI3K/AKT/mTOR signaling pathway can attenuate CSE-induced cellular senescence.Conclusion: CSE can induce cellular senescence in human bronchial

  14. E-Cigarettes a Gateway to Smoking for Teens

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_159340.html E-Cigarettes a Gateway to Smoking for Teens: Study ... who had never smoked, but who had used e-cigarettes, were substantially more likely to begin smoking ...

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

    Directory of Open Access Journals (Sweden)

    Botelho Fernando M

    2012-09-01

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

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

    Directory of Open Access Journals (Sweden)

    Hsi-Min Hsiao

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

  17. Characteristics of smoking used cigarettes among an incarcerated population.

    Science.gov (United States)

    Lantini, Ryan; van den Berg, Jacob J; Roberts, Mary B; Bock, Beth C; Stein, L A R; Parker, Donna R; Friedmann, Peter D; Clarke, Jennifer G

    2015-03-01

    Little is known about smoking behaviors involving shared and previously used cigarettes, which we refer to as "smoking used cigarettes." Examples include: cigarette sharing with strangers, smoking discarded cigarettes ("butts"), or remaking cigarettes from portions of discarded cigarettes. The current study focuses on the prevalence of and factors associated with smoking used cigarettes prior to incarceration among a U.S. prison population. Questionnaires were administered to 244 male and female inmates at baseline. Prevalence of smoking used cigarettes was assessed using 3 questions; 1 about sharing cigarettes with strangers, 1 about smoking a "found" cigarette, and 1 about smoking previously used cigarettes. Factors associated with those who engaged in smoking used cigarettes were then compared with those who did not engage in smoking used cigarettes. A majority of participants (61.5%) endorsed engaging in at least 1 smoking used cigarette behavior in the past prior to incarceration. Those who engaged in these behaviors were more likely to have a higher degree of nicotine dependence, to have started smoking regularly at a younger age, and to have lived in an unstable living environment prior to incarceration. Our results indicate that a history of smoking used cigarettes is common among incarcerated persons in the United States. Consistent with our hypothesis, engaging in smoking used cigarettes was found to be associated with a higher degree of nicotine dependence. (PsycINFO Database Record PMID:25180554

  18. Longitudinal Trajectories of Cigarette Smoking Following Rape

    OpenAIRE

    Ananda B. Amstadter; Resnick, Heidi S.; Nugent, Nicole R.; Acierno, Ron; Rheingold, Alyssa A.; Minhinnett, Robin; Kilpatrick, Dean G.

    2009-01-01

    Although prior research has identified increases in cigarette smoking following trauma exposure, no studies have examined longitudinal trajectories of smoking following rape. The present investigation identifies and characterizes longitudinal ( 6 months post-assault) trajectories of smoking (N = 152) following a rape in a sample of 268 sexual assault victims participating in a forensic medical exam. Further, we examine acute predictors of subsequent smoking trajec...

  19. 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

  20. 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.

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

    Directory of Open Access Journals (Sweden)

    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.

  2. Cigarette smoke upregulates rat coronary artery endothelin receptors in vivo

    DEFF Research Database (Denmark)

    Cao, Lei; Zhang, Yaping; Cao, Yong-Xiao;

    2012-01-01

    BACKGROUND: Cigarette smoking is a strong cardiovascular risk factor and endothelin (ET) receptors are related to coronary artery diseases. The present study established an in vivo secondhand smoke (SHS) exposure model and investigated the hypothesis that cigarette smoke induces ET receptor......(B) receptors of smoke exposed rats were higher than that of animals exposed to fresh air, suggesting that SHS upregulates ET(A) and ET(B) receptors in coronary arteries in vivo. Immunofluorescence staining showed that the enhanced receptor expression was localized to the smooth muscle cells of coronary...... arteries. The protein levels of phosphorylated (p)-Raf-1 and p-ERK1/2 in smoke exposed rats were significantly higher than in control rats, demonstrating that SHS induces the activation of the Raf/ERK/MAPK pathway. Treatment with Raf-1 inhibitor GW5074 suppressed SHS-induced enhanced contraction mediated...

  3. Naloxone does not affect cigarette smoking.

    Science.gov (United States)

    Nemeth-Coslett, R; Griffiths, R R

    1986-01-01

    In order to provide information about the hypothesis that endogenous opioids mediate the reinforcing properties of cigarette smoking, the present study examined the effects of naloxone, an opioid antagonist, on cigarette smoking in seven normal volunteers. The study used experimental procedures that had previously been shown sensitive for detecting the effects of other drugs, (including a nicotine antagonist) on smoking. Isolated subjects smoked their regular brand of cigarettes freely in a naturalistic laboratory environment while watching television or reading. Sixty minutes before each 2 h smoking session subjects received an IM injection of naloxone HCl (0.0625, 0.25, 1.0, or 4.0 mg/kg) or placebo. Each subject received each treatment three times in a mixed order across days. Naloxone did not significantly affect any measure of cigarette smoking including number of cigarettes, number of puffs, or expired air carbon monoxide level. Naloxone did, however, produce significant dose-related increases in subject ratings of yawning, stretching, and relaxation. The results of the present study provide no support for the endogenous opioid theory of smoking reinforcement. PMID:3088648

  4. Activation of C3a receptor is required in cigarette smoke-mediated emphysema

    OpenAIRE

    Yuan, Xiaoyi; Shan, Ming; You, Ran; Frazier, Michael V.; Hong, Monica Jeongsoo; Wetsel, Rick A.; Drouin, Scott; SERYSHEV, ALEXANDER; MD, Li-zhen Song; Cornwell, Lorraine; Rossen, Roger D.; Corry, David B.; Kheradmand, Farrah

    2014-01-01

    Exposure to cigarette smoke can initiate sterile inflammatory responses in the lung and activate myeloid dendritic cells (mDCs) that induce differentiation of T helper type 1 (Th1) and Th17 cells in the emphysematous lungs. Consumption of complement proteins increases in acute inflammation, but the contribution of complement protein 3 (C3) to chronic cigarette smoke-induced immune responses in the lung is not clear. Here we show that following chronic exposure to cigarette smoke, C3 deficient...

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

    Science.gov (United States)

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

    2016-01-12

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

  6. "Smoking wet": respiratory failure related to smoking tainted marijuana cigarettes.

    Science.gov (United States)

    Gilbert, Christopher R; Baram, Michael; Cavarocchi, Nicholas C

    2013-01-01

    Reports have suggested that the use of a dangerously tainted form of marijuana, referred to in the vernacular as "wet" or "fry," has increased. Marijuana cigarettes are dipped into or laced with other substances, typically formaldehyde, phencyclidine, or both. Inhaling smoke from these cigarettes can cause lung injuries. We report the cases of 2 young adults who presented at our hospital with respiratory failure soon after they had smoked "wet" marijuana cigarettes. In both patients, progressive hypoxemic respiratory failure necessitated rescue therapy with extracorporeal membrane oxygenation. After lengthy hospitalizations, both patients recovered with only mild pulmonary function abnormalities. To our knowledge, this is the first 2-patient report of severe respiratory failure and rescue therapy with extracorporeal oxygenation after the smoking of marijuana cigarettes thus tainted. We believe that, in young adults with an unexplained presentation of severe respiratory failure, the possibility of exposure to tainted marijuana cigarettes should be considered. PMID:23466531

  7. Cigarette smoking and progression in multiple sclerosis

    NARCIS (Netherlands)

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

    2007-01-01

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

  8. Icariin Ameliorates Cigarette Smoke Induced Inflammatory Responses via Suppression of NF-κB and Modulation of GR In Vivo and In Vitro

    Science.gov (United States)

    Li, Lulu; Sun, Jing; Xu, Changqing; Zhang, Hongying; Wu, Jinfeng; Liu, Baojun; Dong, Jingcheng

    2014-01-01

    Purpose To investigate the effects of icariin, a major constituent of flavonoids isolated from the herb Epimedium, on cigarette smoke (CS) induced inflammatory responses in vivo and in vitro. Methods In vivo, BALB/c mice were exposed to smoke of 15 cigarettes for 1 h/day, 6 days/week for 3 months and dosed with icariin (25, 50 and 100 mg/kg) or dexamethasone (1 mg/kg). In vitro, A549 cells were incubated with icariin (10, 50 and 100 µM) followed by treatments with CSE (2.5%). Results We found that icariin significantly protected pulmonary function and attenuated CS-induced inflammatory response by decreasing inflammatory cells and production of TNF-α, IL-8 and MMP-9 in both the serum and BALF of CS-exposed mice and decreasing production of TNF-α and IL-8 in the supernatant of CSE-exposed A549 cells. Icariin also showed properties in inhibiting the phosphorylation of NF-κB p65 protein and blocking the degradation of IΚB-α protein. Further studies revealed that icariin administration markedly restore CS-reduced GR protein and mRNA expression, which might subsequently contribute to the attenuation of CS-induced respiratory inflammatory response. Conclusion Together these results suggest that icariin has anti-inflammatory effects in cigarette smoke induced inflammatory models in vivo and in vitro, possibly achieved by suppressing NF-κB activation and modulating GR protein expression. PMID:25089961

  9. Icariin ameliorates cigarette smoke induced inflammatory responses via suppression of NF-κB and modulation of GR in vivo and in vitro.

    Directory of Open Access Journals (Sweden)

    Lulu Li

    Full Text Available To investigate the effects of icariin, a major constituent of flavonoids isolated from the herb Epimedium, on cigarette smoke (CS induced inflammatory responses in vivo and in vitro.In vivo, BALB/c mice were exposed to smoke of 15 cigarettes for 1 h/day, 6 days/week for 3 months and dosed with icariin (25, 50 and 100 mg/kg or dexamethasone (1 mg/kg. In vitro, A549 cells were incubated with icariin (10, 50 and 100 µM followed by treatments with CSE (2.5%.We found that icariin significantly protected pulmonary function and attenuated CS-induced inflammatory response by decreasing inflammatory cells and production of TNF-α, IL-8 and MMP-9 in both the serum and BALF of CS-exposed mice and decreasing production of TNF-α and IL-8 in the supernatant of CSE-exposed A549 cells. Icariin also showed properties in inhibiting the phosphorylation of NF-κB p65 protein and blocking the degradation of IΚB-α protein. Further studies revealed that icariin administration markedly restore CS-reduced GR protein and mRNA expression, which might subsequently contribute to the attenuation of CS-induced respiratory inflammatory response.Together these results suggest that icariin has anti-inflammatory effects in cigarette smoke induced inflammatory models in vivo and in vitro, possibly achieved by suppressing NF-κB activation and modulating GR protein expression.

  10. 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.

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

    Science.gov (United States)

    Nagler, R; Savulescu, D; Gavish, M

    2016-02-01

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

  12. The pathobiological impact of cigarette smoke on pancreatic cancer development (Review)

    OpenAIRE

    Wittel, Uwe A; Momi, Navneet; SEIFERT, GABRIEL; Wiech, Thorsten; Hopt, Ulrich T.; Batra, Surinder K.

    2012-01-01

    Despite extensive efforts, pancreatic cancer remains incurable. Most risk factors, such as genetic disposition, metabolic diseases or chronic pancreatitis cannot be influenced. By contrast, cigarette smoking, an important risk factor for pancreatic cancer, can be controlled. Despite the epidemiological evidence of the detrimental effects of cigarette smoking with regard to pancreatic cancer development and its unique property of being influenceable, our understanding of cigarette smoke-induce...

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

    Directory of Open Access Journals (Sweden)

    Yang Jin

    2008-08-01

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

  14. Smoked marijuana effects on tobacco cigarette smoking behavior.

    Science.gov (United States)

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

    1990-03-01

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

  15. 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...... are small and appear to be explicable. The Prevent model can be used for more general scenarios of effective health promotion, but it requires more data than the Peto et al method, which can be used only to estimate mortality related to smoking........ 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...

  16. 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...

  17. 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

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

    International Nuclear Information System (INIS)

    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

  19. Adjuvant and anti-inflammatory properties of cigarette smoke in murine allergic airway inflammation.

    Science.gov (United States)

    Trimble, Nancy J; Botelho, Fernando M; Bauer, Carla M T; Fattouh, Ramzi; Stämpfli, Martin R

    2009-01-01

    The impact of cigarette smoke on allergic asthma remains controversial both clinically and experimentally. The objective of this study was to investigate, in a murine model, how cigarette smoke affects immune inflammatory processes elicited by a surrogate allergen. In our experimental design, mice were concurrently exposed to cigarette smoke and ovalbumin (OVA), an innocuous antigen that, unless introduced in the context of an adjuvant, induces inhalation tolerance. We show that cigarette smoke exposure has adjuvant properties, allowing for allergic mucosal sensitization to OVA. Specifically, concurrent exposure to cigarette smoke and OVA for 2 weeks led to airway eosinophilia and goblet cell hyperplasia. In vivo OVA recall challenge 1 month after the last smoke exposure showed that concurrent exposure to OVA and cigarette smoke induced antigen-specific memory. Robust eosinophilia and OVA-specific IgG1 and IgE characterized the ensuing inflammatory response. Mechanistically, allergic sensitization was, in part, granulocyte macrophage colony-stimulating factor (GM-CSF) dependent, as a significant reduction in BAL eosinophilia was observed in mice treated with an anti-GM-CSF antibody. Of note, continuous smoke exposure attenuated the OVA recall response; decreased airway eosinophilia was observed in mice continuously exposed to cigarette smoke compared with mice that ceased the smoke exposure protocol. In conclusion, we demonstrate experimentally that while cigarette smoke acts as an adjuvant allowing for allergic sensitization, it also attenuates the ensuing eosinophilic inflammatory response. PMID:18635815

  20. Cigarette smoking and self-control

    OpenAIRE

    Kamhon Kan

    2006-01-01

    This paper empirically studies time inconsistent preferences in the context of cigarette smoking behavior. With hyperbolic discounting, an individual has time inconsistent preferences, which give rise to a lack of self-control, i.e., she may perpetually postpone the execution of a plan. This implies that a smoker who wants to quit has a demand for control devices, e.g., a smoking ban in public areas or a hike in cigarette excise taxes. This paper empirically tests this implication, using a sa...

  1. Prostacyclin reverses the cigarette smoke-induced decrease in pulmonary Frizzled 9 expression through miR-31.

    Science.gov (United States)

    Tennis, M A; New, M L; McArthur, D G; Merrick, D T; Dwyer-Nield, L D; Keith, R L

    2016-01-01

    Half of lung cancers are diagnosed in former smokers, leading to a significant treatment burden in this population. Chemoprevention in former smokers using the prostacyclin analogue iloprost reduces endobronchial dysplasia, a premalignant lung lesion. Iloprost requires the presence of the WNT receptor Frizzled 9 (Fzd9) for inhibition of transformed growth in vitro. To investigate the relationship between iloprost, cigarette smoke, and Fzd9 expression, we used human samples, mouse models, and in vitro studies. Fzd9 expression was low in human lung tumors and in progressive dysplasias. In mouse models and in vitro studies, tobacco smoke carcinogens reduced expression of Fzd9 while prostacyclin maintained or increased expression. Expression of miR-31 repressed Fzd9 expression, which was abrogated by prostacyclin. We propose a model where cigarette smoke exposure increases miR-31 expression, which leads to decreased Fzd9 expression and prevents response to iloprost. When smoke is removed miR-31 is reduced, prostacyclin can increase Fzd9 expression, and progression of dysplasia is inhibited. Fzd9 and miR-31 are candidate biomarkers for precision application of iloprost and monitoring of treatment progress. As we continue to investigate the mechanisms of prostacyclin chemoprevention and identify biomarkers for its use, we will facilitate clinical trials and speed implementation of this valuable prevention approach. PMID:27339092

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

    Mathieu C Morissette

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

  4. Epithelial-mesenchymal transition and cancer stem cells, mediated by a long non-coding RNA, HOTAIR, are involved in cell malignant transformation induced by cigarette smoke extract

    International Nuclear Information System (INIS)

    The incidence of lung diseases, including cancer, caused by cigarette smoke is increasing, but the molecular mechanisms of gene regulation induced by cigarette smoke remain unclear. This report describes a long noncoding RNA (lncRNA) that is induced by cigarette smoke extract (CSE) and experiments utilizing lncRNAs to integrate inflammation with the epithelial-mesenchymal transition (EMT) in human bronchial epithelial (HBE) cells. The present study shows that, induced by CSE, IL-6, a pro-inflammatory cytokine, leads to activation of STAT3, a transcription activator. A ChIP assay determined that the interaction of STAT3 with the promoter regions of HOX transcript antisense RNA (HOTAIR) increased levels of HOTAIR. Blocking of IL-6 with anti-IL-6 antibody, decreasing STAT3, and inhibiting STAT3 activation reduced HOTAIR expression. Moreover, for HBE cells cultured in the presence of HOTAIR siRNA for 24 h, the CSE-induced EMT, formation of cancer stem cells (CSCs), and malignant transformation were reversed. Thus, IL-6, acting on STAT3 signaling, which up-regulates HOTAIR in an autocrine manner, contributes to the EMT and to CSCs induced by CSE. These data define a link between inflammation and EMT, processes involved in the malignant transformation of cells caused by CSE. This link, mediated through lncRNAs, establishes a mechanism for CSE-induced lung carcinogenesis. - Highlights: • STAT3 directly regulates the levels of LncRNA HOTAIR. • LncRNA HOTAIR mediates the link between inflammation and EMT. • LncRNA HOTAIR is involved in the malignant transformation of cells caused by CSE

  5. Epithelial-mesenchymal transition and cancer stem cells, mediated by a long non-coding RNA, HOTAIR, are involved in cell malignant transformation induced by cigarette smoke extract

    Energy Technology Data Exchange (ETDEWEB)

    Liu, Yi; Luo, Fei; Xu, Yuan; Wang, Bairu; Zhao, Yue; Xu, Wenchao; Shi, Le; Lu, Xiaolin; Liu, Qizhan, E-mail: drqzliu@hotmail.com

    2015-01-01

    The incidence of lung diseases, including cancer, caused by cigarette smoke is increasing, but the molecular mechanisms of gene regulation induced by cigarette smoke remain unclear. This report describes a long noncoding RNA (lncRNA) that is induced by cigarette smoke extract (CSE) and experiments utilizing lncRNAs to integrate inflammation with the epithelial-mesenchymal transition (EMT) in human bronchial epithelial (HBE) cells. The present study shows that, induced by CSE, IL-6, a pro-inflammatory cytokine, leads to activation of STAT3, a transcription activator. A ChIP assay determined that the interaction of STAT3 with the promoter regions of HOX transcript antisense RNA (HOTAIR) increased levels of HOTAIR. Blocking of IL-6 with anti-IL-6 antibody, decreasing STAT3, and inhibiting STAT3 activation reduced HOTAIR expression. Moreover, for HBE cells cultured in the presence of HOTAIR siRNA for 24 h, the CSE-induced EMT, formation of cancer stem cells (CSCs), and malignant transformation were reversed. Thus, IL-6, acting on STAT3 signaling, which up-regulates HOTAIR in an autocrine manner, contributes to the EMT and to CSCs induced by CSE. These data define a link between inflammation and EMT, processes involved in the malignant transformation of cells caused by CSE. This link, mediated through lncRNAs, establishes a mechanism for CSE-induced lung carcinogenesis. - Highlights: • STAT3 directly regulates the levels of LncRNA HOTAIR. • LncRNA HOTAIR mediates the link between inflammation and EMT. • LncRNA HOTAIR is involved in the malignant transformation of cells caused by CSE.

  6. Innate cellular sources of interleukin-17A regulate macrophage accumulation in cigarette- smoke-induced lung inflammation in mice.

    Science.gov (United States)

    Bozinovski, Steven; Seow, Huei Jiunn; Chan, Sheau Pyng Jamie; Anthony, Desiree; McQualter, Jonathan; Hansen, Michelle; Jenkins, Brendan J; Anderson, Gary P; Vlahos, Ross

    2015-11-01

    Cigarette smoke (CS) is the major cause of chronic obstructive pulmonary disease (COPD). Interleukin-17A (IL-17A) is a pivotal cytokine that regulates lung immunity and inflammation. The aim of the present study was to investigate how IL-17A regulates CS-induced lung inflammation in vivo. IL-17A knockout (KO) mice and neutralization of IL-17A in wild-type (WT) mice reduced macrophage and neutrophil recruitment and chemokine (C-C motif) ligand 2 (CCL2), CCL3 and matrix metalloproteinase (MMP)-12 mRNA expression in response to acute CS exposure. IL-17A expression was increased in non-obese diabetic (NOD) severe combined immunodeficiency SCID) mice with non-functional B- and T-cells over a 4-week CS exposure period, where macrophages accumulated to the same extent as in WT mice. Gene expression analysis by QPCR (quantitative real-time PCR) of isolated immune cell subsets detected increased levels of IL-17A transcript in macrophages, neutrophils and NK/NKT cells in the lungs of CS-exposed mice. In order to further explore the relative contribution of innate immune cellular sources, intracellular IL-17A staining was performed. In the present study, we demonstrate that CS exposure primes natural killer (NK), natural killer T (NKT) and γδ T-cells to produce more IL-17A protein and CS alone increased the frequency of IL17+ γδ T-cells in the lung, whereas IL-17A protein was not detected in macrophages and neutrophils. Our data suggest that activation of innate cellular sources of IL-17A is an essential mediator of macrophage accumulation in CS-exposed lungs. Targeting non-conventional T-cell sources of IL-17A may offer an alternative strategy to reduce pathogenic macrophages in COPD. PMID:26201093

  7. p53 mediates cigarette smoke-induced apoptosis of pulmonary endothelial cells: inhibitory effects of macrophage migration inhibitor factor.

    Science.gov (United States)

    Damico, Rachel; Simms, Tiffany; Kim, Bo S; Tekeste, Zenar; Amankwan, Henry; Damarla, Mahendra; Hassoun, Paul M

    2011-03-01

    Exposure to cigarette smoke (CS) is the most common cause of emphysema, a debilitating pulmonary disease histopathologically characterized by the irreversible destruction of lung architecture. Mounting evidence links enhanced endothelial apoptosis causally to the development of emphysema. However, the molecular determinants of human endothelial cell apoptosis and survival in response to CS are not fully defined. Such determinants could represent clinically relevant targets for intervention. We show here that CS extract (CSE) triggers the death of human pulmonary macrovascular endothelial cells (HPAECs) through a caspase 9-dependent apoptotic pathway. Exposure to CSE results in the increased expression of p53 in HPAECs. Using the p53 inhibitor, pifithrin-α (PFT-α), and RNA interference (RNAi) directed at p53, we demonstrate that p53 function and expression are required for CSE-mediated apoptosis. The expression of macrophage migration inhibitory factor (MIF), an antiapoptotic cytokine produced by HPAECs, also increases in response to CSE exposure. The addition of recombinant human MIF prevents cell death from exposure to CSE. Further, the suppression of MIF or its receptor/binding partner, Jun activation domain-binding protein 1 (Jab-1), with RNAi enhances the sensitivity of human pulmonary endothelial cells to CSE via a p53-dependent (PFT-α-inhibitable) pathway. Finally, we demonstrate that MIF is a negative regulator of p53 expression in response to CSE, placing MIF upstream of p53 as an antagonist of CSE-induced apoptosis. We conclude that MIF can protect human vascular endothelium from the toxic effects of CSE via the antagonism of p53-mediated apoptosis. PMID:20448056

  8. 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…

  9. [Chemistry and toxicology of cigarette smoke in the lungs].

    Science.gov (United States)

    Munteanu, Ioana; Didilescu, Cristian

    2007-01-01

    Cigarettes appearance in the middle of 19th century turns tobacco into a general consumption product with ill-fated consequences. Technological process and the means by which tobacco dependence appears were hidden from medical world for a long time by the tobacco companies. Cigarette smoke represents a mixture of 4000 toxic substances including carcinogens, organic compounds, solvents, gas substances (CO). We can add another 600 additives which are used in the technological process. Tobacco dependence is defined by the daily cigarette consumption, difficult quitting and probability for withdraw symptoms. Among the smoke effects on respiratory system, we can identify two main mechanisms: inducing inflammation and mutagen if - carcinogenic effect. Inflammation consists of ciliary toxicity, increased mucus secretion and accumulation of activated inflammatory cells in the respiratory tract. The risk for lung cancer is directly related to the presence of CYPlA1 alleles and reduced glutathione S-reductase activity. PMID:17491209

  10. 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.

  11. Inhibition of immunological function mediated DNA damage of alveolar macrophages caused by cigarette smoke in mice.

    Science.gov (United States)

    Ishida, Takahiro; Hirono, Yuriko; Yoshikawa, Kenichi; Hutei, Yoshimi; Miyagawa, Mayuko; Sakaguchi, Ikuyo; Pinkerton, Kent E; Takeuchi, Minoru

    2009-12-01

    Exposure to cigarette smoke impairs the pulmonary immune system, including alveolar macrophage function, although the mechanisms by which this occurs are not fully elucidated. This study investigates the effect of cigarette smoke exposure on the antigen-presenting activity of alveolar macrophages, which is required for antigen-specific response to T cells. C57BL/6 mice were exposed to cigarette smoke for 10 days using a Hamburg II smoking machine, and alveolar macrophages were obtained by bronchoalveolar lavage. The antigen-presenting activity of alveolar macrophages was significantly inhibited in mice exposed to cigarette smoke compared with mice not exposed to cigarette smoke. Major histocompatibility complex class II cell surface molecule-positive cells, B7-1 molecule-positive cells, and interleukin-1beta messenger RNA gene expression in alveolar macrophages were significantly decreased in mice exposed to cigarette smoke compared with mice not exposed to cigarette smoke. In contrast, DNA damage and generation of superoxide and hydrogen peroxide in alveolar macrophages were significantly increased by cigarette smoke exposure. These results suggest that inhibition of the antigen-presenting activity of alveolar macrophages may result from decreased expression of major histocompatibility complex class II and B7-1 molecules and interleukin-1beta messenger RNA gene expression following cigarette smoke exposure. Furthermore, inhibition of antigen presentation in alveolar macrophage may result from DNA damage induced by excessive amounts of reactive oxygen species being generated by alveolar macrophages following cigarette smoke exposure. These findings suggest that cigarette smoke impairs the immunological function of alveolar macrophages and, as a result, increases the risk for pulmonary infection. PMID:19922407

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

    Science.gov (United States)

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

    2014-09-01

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

  13. Somatic-cell mutation induced by short exposures to cigarette smoke in urate-null, oxidative stress-sensitive Drosophila.

    Science.gov (United States)

    Uchiyama, Tomoyo; Koike, Ryota; Yuma, Yoko; Okamoto, Keinosuke; Arimoto-Kobayashi, Sakae; Suzuki, Toshinori; Negishi, Tomoe

    2016-01-01

    We previously reported that a urate-null strain of Drosophila is hypersensitive to cigarette smoke (CS), and we suggested that CS induces oxidative stress in Drosophila because uric acid is a potent antioxidant. Although the carcinogenic risk of CS exposure is widely recognized; documentation of in vivo genotoxic activity of environmental CS, especially gaseous-phase CS, remains inconclusive. To date, somatic-cell mutations in Drosophila resulting from exposure to CS have not been detected via the somatic mutation and recombination test (wing spot test) with wild-type flies, a widely used Drosophila assay for the detection of somatic-cell mutation; moreover, genotoxicity has not been documented via a DNA repair test that involves DNA repair-deficient Drosophila. In this study, we used a new Drosophila strain (y v ma-l; mwh) to examine the mutagenicity induced by gaseous-phase CS; these flies are urate-null due to a mutation in ma-l, and they are heterozygous for multiple wing hair (mwh), a mutation that functions as a marker for somatic-cell mutation. In an assay with this newly developed strain, a superoxide anion-producing weed-killer, paraquat, exhibited significant mutagenicity; in contrast, paraquat was hardly mutagenic with a wild-type strain. Drosophila larvae were exposed to CS for 2, 4 or 6h, and then kept at 25°C on instant medium until adulthood. After eclosion, mutant spots, which consisted of mutant hairs on wings, were scored. The number of mutant spots increased significantly in an exposure time-dependent manner in the urate-null females (ma-l (-/-)), but not in the urate-positive females (ma-l (+/-)). In this study, we showed that short-term exposure to CS was mutagenic in this in vivo system. In addition, we obtained suggestive data regarding reactive oxygen species production in larva after CS exposure using the fluorescence probe H2DCFDA. These results suggest that oxidative damage, which might be countered by uric acid, was partly responsible

  14. 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

    2012-01-01

    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

  15. Roflumilast N-oxide prevents cytokine secretion induced by cigarette smoke combined with LPS through JAK/STAT and ERK1/2 inhibition in airway epithelial cells.

    Directory of Open Access Journals (Sweden)

    Tatiana Victoni

    Full Text Available Cigarette smoke is a major cause of chronic obstructive pulmonary disease (COPD. Airway epithelial cells and macrophages are the first defense cells against cigarette smoke and these cells are an important source of pro-inflammatory cytokines. These cytokines play a role in progressive airflow limitation and chronic airways inflammation. Furthermore, the chronic colonization of airways by Gram-negative bacteria, contributes to the persistent airways inflammation and progression of COPD. The current study addressed the effects of cigarette smoke along with lipolysaccharide (LPS in airway epithelial cells as a representative in vitro model of COPD exacerbations. Furthermore, we evaluated the effects of PDE4 inhibitor, the roflumilast N-oxide (RNO, in this experimental model. A549 cells were stimulated with cigarette smoke extract (CSE alone (0.4% to 10% or in combination with a low concentration of LPS (0.1 µg/ml for 2 h or 24 h for measurement of chemokine protein and mRNAs and 5-120 min for protein phosphorylation. Cells were also pre-incubated with MAP kinases inhibitors and Prostaglandin E2 alone or combined with RNO, before the addition of CSE+LPS. Production of cytokines was determined by ELISA and protein phosphorylation by western blotting and phospho-kinase array. CSE did not induce production of IL-8/CXCL8 and Gro-α/CXCL1 from A549 cells, but increase production of CCL2/MCP-1. However the combination of LPS 0.1 µg/ml with CSE 2% or 4% induced an important production of these chemokines, that appears to be dependent of ERK1/2 and JAK/STAT pathways but did not require JNK and p38 pathways. Moreover, RNO associated with PGE2 reduced CSE+LPS-induced cytokine release, which can happen by occur through of ERK1/2 and JAK/STAT pathways. We report here an in vitro model that can reflect what happen in airway epithelial cells in COPD exacerbation. We also showed a new pathway where CSE+LPS can induce cytokine release from A549 cells, which is

  16. 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

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

    Science.gov (United States)

    Peron, Jean Pierre Schatzmann; de Brito, Auriléia Aparecida; Pelatti, Mayra; Brandão, Wesley Nogueira; Vitoretti, Luana Beatriz; Greiffo, Flávia Regina; da Silveira, Elaine Cristina; Oliveira-Junior, Manuel Carneiro; Maluf, Mariangela; Evangelista, Lucila; Halpern, Silvio; Nisenbaum, Marcelo Gil; Perin, Paulo; Czeresnia, Carlos Eduardo; Câmara, Niels Olsen Saraiva; Aimbire, Flávio; Vieira, Rodolfo de Paula; Zatz, Mayana; de Oliveira, Ana Paula Ligeiro

    2015-01-01

    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. PMID:26322981

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

    Directory of Open Access Journals (Sweden)

    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.

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

    International Nuclear Information System (INIS)

    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

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

    Institute of Scientific and Technical Information of China (English)

    徐凌; 蔡柏蔷; 朱元珏

    2004-01-01

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

  2. Teen Smoking Down, E-Cigarette Use Up

    Science.gov (United States)

    ... 159286.html Teen Smoking Down, E-Cigarette Use Up CDC survey finds adolescents hear some health messages, ... reported Thursday. However, use of e-cigarettes is up. Also on the good-news front: premarital sex ...

  3. Dose-responsiveness and persistence of microRNA expression alterations induced by cigarette smoke in mouse lung

    Energy Technology Data Exchange (ETDEWEB)

    Izzotti, Alberto; Larghero, Patrizia; Longobardi, Mariagrazia; Cartiglia, Cristina; Camoirano, Anna [Department of Health Sciences, University of Genoa, Genoa (Italy); Steele, Vernon E. [National Cancer Institute (NCI), Rockville, MD (United States); De Flora, Silvio, E-mail: sdf@unige.it [Department of Health Sciences, University of Genoa, Genoa (Italy)

    2011-12-01

    Our previous studies demonstrated that exposure to cigarette smoke (CS), either mainstream or environmental, results in a remarkable downregulation of microRNA expression in the lung of both mice and rats. The goals of the present study were to evaluate the dose responsiveness to CS and the persistence of microRNA alterations after smoking cessation. ICR (CD-1) neonatal mice were exposed whole-body to mainstream CS, at the doses of 119, 292, 438, and 631 mg/m{sup 3} of total particulate matter. Exposure started within 12 h after birth and continued daily for 4 weeks. The levels of bulky DNA adducts and 8-oxo-7,8-dihydro-2 Prime -deoxyguanosine (8-oxodGuo) were measured by {sup 32}P postlabeling procedures, and the expression of 697 mouse microRNAs was analyzed by microarray. The highest CS dose was lethal. Exposure to CS caused a dose-dependent increase of DNA alterations. DNA adducts and, even more sharply, 8-oxodGuo were reverted 1 and 4 weeks after smoking cessation. Exposure to CS resulted in an evident dysregulation of microRNA expression profiles, mainly in the sense of downregulation. The two lowest doses were not particularly effective, while the highest nonlethal dose produced extensive microRNA alterations. The expression of most downregulated microRNAs, including among others 7 members of the let-7 family, was restored one week after smoking cessation. However, the recovery was incomplete for a limited array of microRNAs, including mir-34b, mir-345, mir-421, mir-450b, mir-466, and mir-469. Thus, it appears that microRNAs mainly behave as biomarkers of effect and that exposure to high-dose, lasting for an adequate period of time, is needed to trigger the CS-related carcinogenesis process in the experimental animal model used.

  4. 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.

  5. Cigarette Smoke Delays Regeneration of the Olfactory Epithelium in Mice.

    Science.gov (United States)

    Ueha, Rumi; Ueha, Satoshi; Sakamoto, Takashi; Kanaya, Kaori; Suzukawa, Keigo; Nishijima, Hironobu; Kikuta, Shu; Kondo, Kenji; Matsushima, Kouji; Yamasoba, Tatsuya

    2016-08-01

    The olfactory system is a unique part of the mammalian nervous system due to its capacity for neurogenesis and the replacement of degenerating receptor neurons. Cigarette smoking is a major cause of olfactory dysfunction. However, the mechanisms by which cigarette smoke impairs the regenerative olfactory receptor neurons (ORNs) remain unclear. Here, we investigated the influence of cigarette smoke on ORN regeneration following methimazole-induced ORN injury. Administration of methimazole caused detachment of the olfactory epithelium from the basement membrane and induced olfactory dysfunction, thus enabling us to analyze the process of ORN regeneration. We found that intranasal administration of cigarette smoke solution (CSS) suppressed the recovery of ORNs and olfaction following ORN injury. Defective ORN recovery in CSS-treated mice was not associated with any change in the number of SOX2(+) ORN progenitor cells in the basal layer of the OE, but was associated with impaired recovery of GAP43(+) immature ORNs. In the nasal mucosa, mRNA expression levels of neurotrophic factors such as brain-derived neurotrophic factor, neurotrophin-3, neurotrophin-5, glial cell-derived neurotrophic factor, and insulin-like growth factor-1 (IGF-1) were increased following OE injury, whereas CSS administration decreased the ORN injury-induced IGF-1 expression. Administration of recombinant human IGF-1 prevented the CSS-induced suppression of ORN recovery following injury. These results suggest that CSS impairs regeneration of ORNs by suppressing the development of immature ORNs from ORN progenitors, at least partly by reducing IGF-1 in the nasal mucosa. PMID:27003941

  6. Cigarette Smoke Alters the Hematopoietic Stem Cell Niche

    Directory of Open Access Journals (Sweden)

    Robert W. Siggins

    2014-02-01

    Full Text Available Effects of tobacco smoke on hematologic derangements have received little attention. This study employed a mouse model of cigarette smoke exposure to explore the effects on bone marrow niche function. While lung cancer is the most widely studied consequence of tobacco smoke exposure, other malignancies, including leukemia, are associated with tobacco smoke exposure. Animals received cigarette smoke exposure for 6 h/day, 5 days/week for 9 months. Results reveal that the hematopoietic stem and progenitor cell (HSPC pool size is reduced by cigarette smoke exposure. We next examined the effect of cigarette smoke exposure on one supporting cell type of the niche, the mesenchymal stromal cells (MSCs. Smoke exposure decreased the number of MSCs. Transplantation of naïve HSPCs into irradiated mice with cigarette smoke exposure yielded fewer numbers of engrafted HSPCs. This result suggests that smoke-exposed mice possess dysfunctional niches, resulting in abnormal hematopoiesis. Co-culture experiments using MSCs isolated from control or cigarette smoke-exposed mice with naïve HSPCs in vitro showed that MSCs from cigarette smoke-exposed mice generated marked expansion of naïve HSPCs. These data show that cigarette smoke exposure decreases in vivo MSC and HSC number and also increases pro-proliferative gene expression by cigarette smoke-exposed MSCs, which may stimulate HSPC expansion. These results of this investigation are clinically relevant to both bone marrow donors with a history of smoking and bone marrow transplant (BMT recipients with a history of smoking.

  7. Adult Cigarette Smoking in the United States: Current Estimates

    Science.gov (United States)

    ... Health More CDC Sites Current Cigarette Smoking Among Adults in the United States Recommend on Facebook Tweet ... every day or some days. Current Smoking Among Adults in 2014 (Nation) By Gender 1 Men are ...

  8. 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.

  9. Resolvin-D1 inhibits interleukin-8 and hydrogen peroxide production induced by cigarette smoke extract in 16HBE cells via attenuating NF-κB activation

    Institute of Scientific and Technical Information of China (English)

    Dong Jiajia; Zhang Mingke; Liao Zenglin; Wu Wei; Wang Tao; Chen Lei; Yang Ting

    2014-01-01

    Background Cigarette smoke induced airway inflammation plays a role in pathogenesis of airway inflammation.Resolvin-D1 derived from omega-3 polyunsaturated fatty acids is an endogenous anti-inflammatory and proresolving lipid mediator.Resolvin-D1 ameliorated inflammatory responses in lung injury,asthma,peritonitis and atherosclerosis.We investigated whether resolvin-D1 suppressed the productions of chemokines and oxidative stress induced by cigarette smoke extract (CSE) in vitro and its possible mechanism.Methods We examined the proinfiammatory chemokine interleukin-8 and hydrogen peroxide (H2O2)productions induced by CSE in 16 human bronchial epithelial (16HBE)cells after resolvin-D1 treatment and their mechanisms.16HBE cells were treated with resolvin-D1 at up to 10 nmol/L,for 30 minutes before CSE up to 16% (v/v) exposure.Release of interlukin-8 proteins was assessed by enzyme linked immunosort assay (ELISA) and its mRNA level by RT-PCR.We evaluated extracellular H2O2 expression in the supematant.Phosphorylation of NF-KB/p65 and degradation of Ⅰ-KB in 16HBE cells were determined by Westem blotting analysis and NF-KB DNA binding activity by electrophoretic mobility shift assay (EMSA).Results 16HBE cells treated with 8% CSE showed significantly higher interlukin-8 production.Resolvin-D1 pretreatment inhibited CSE induced intedukin-8 production (mRNA and protein) in a dose and time dependent manner.Extracellular H2O2 level decreased after resolvin-D1 treatment.Resolvin-D1 attenuated CSE triggered Ⅰ-KB degradation and NF-KB/p65 activation dose dependently and inhibited NF-KB DNA binding activity.Conclusion Resolvin-D1 inhibits CSE induced interlukin-8 and H2O2 production in 16HBE cells by modulating NF-KB activation and has therapeutic potential for pulmonary inflammation.

  10. 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.

  11. 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. PMID:15520040

  12. 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.

  13. [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.

  14. Biological effects of inhaled cigarette smoke in beagle dogs

    International Nuclear Information System (INIS)

    A group of twenty dogs has received up to 7 yr of daily cigarette smoking (10 cigarettes per day, 5 days per week), using realistic methods of oral inhalation and nose-plus-mouth exhalation. Three dogs that received 20 cigarettes per day over 9 mo developed respiratory tract lesions, including pleural thickening, alveolar septal fibrosis, vesicular emphysema, and chronic bronchitis, more rapidly than dogs receiving 10 cigarettes per day

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

    OpenAIRE

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

    2016-01-01

    Abstract 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...

  16. 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.

  17. Cigarette smoke extracts promote vascular smooth muscle cell proliferation and enhances contractile responses in the vasculature and airway

    DEFF Research Database (Denmark)

    Xu, Cang-Bao; Lei, Ying; Chen, Qingwen;

    2010-01-01

    Cigarette smoke exposure is a strong risk factor for cardiovascular and respiratory diseases. However, the knowledge about how cigarette smoke induces damage to vasculature and airway is limited. The present study was designed to examine the effects of cigarette smoke particles extracted by heptane...... (heptane-soluble smoke particles, HSP), by water (water-soluble smoke particles, WSP) and by DMSO (DMSO-soluble smoke particles, DSP), which represent lipophilic, hydrophilic and ambiphoteric constituents from the cigarette smoke, respectively. Human aortic smooth muscle cell (HASMC) proliferation...... responses to sarafotoxin 6c, U46619 or bradykinin in rat mesenteric artery and/or in bronchi. ERK1/2 is activated by HSP and DSP in HASMCs and inhibition of ERK1/2 abrogated the smoke extracts-induced HASMC proliferation, while blockage of nicotinic receptors had no effects, suggesting that the toxic...

  18. Novel long chain fatty acid derivatives of quercetin-3-O-glucoside reduce cytotoxicity induced by cigarette smoke toxicants in human fetal lung fibroblasts.

    Science.gov (United States)

    Warnakulasuriya, Sumudu N; Ziaullah; Rupasinghe, H P Vasantha

    2016-06-15

    Smoking has become a global health concern due to its association with many disease conditions, such as chronic obstructive pulmonary disease (COPD), cardiovascular diseases (CVD) and cancer. Flavonoids are plant polyphenolic compounds, studied extensively for their antioxidant, anti-inflammatory, and anti-carcinogenic properties. Quercetin-3-O-glucoside (Q3G) is a flavonoid which is widely found in plants. Six novel long chain fatty acid [stearic acid, oleic acid, linoleic acid, α-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)] derivatives of Q3G were evaluated for their potential in protecting human lung fibroblasts against cytotoxicity induced by selected cigarette smoke toxicants: 4-(methylnitrosoamino)-1-(3-pyridinyl)-1-butanone (NNK), benzo-α-pyrene (BaP), nicotine and chromium (Cr[VI]). Nicotine and Cr[VI] induced toxicity in fibroblasts and reduced the percentage of viable cells, while BaP and NNK did not affect cell viability. The fatty acid derivatives of Q3G provided protection against nicotine- and Cr[VI]-induced cell death and membrane lipid peroxidation. Based on the evaluation of inflammatory markers of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2), the fatty acid derivatives of Q3G were found to be effective in lowering the inflammatory response. Overall, these novel fatty acid esters of Q3G warrant further investigation as potential cytoprotective agents. PMID:27071958

  19. 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.

  20. 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.

  1. Comparison of environmental tobacco smoke (ETS) concentrations generated by an electrically heated cigarette smoking system and a conventional cigarette.

    Science.gov (United States)

    Tricker, Anthony R; Schorp, Matthias K; Urban, Hans-Jörg; Leyden, Donald; Hagedorn, Heinz-Werner; Engl, Johannes; Urban, Michael; Riedel, Kirsten; Gilch, Gerhard; Janket, Dinamis; Scherer, Gerhard

    2009-01-01

    Smoking conventional lit-end cigarettes results in exposure of nonsmokers to potentially harmful cigarette smoke constituents present in environmental tobacco smoke (ETS) generated by sidestream smoke emissions and exhaled mainstream smoke. ETS constituent concentrations generated by a conventional lit-end cigarette and a newly developed electrically heated cigarette smoking system (EHCSS) that produces only mainstream smoke and no sidestream smoke emissions were investigated in simulated "office" and "hospitality" environments with different levels of baseline indoor air quality. Smoking the EHCSS (International Organisation for Standardization yields: 5 mg tar, 0.3 mg nicotine, and 0.6 mg carbon monoxide) in simulated indoor environments resulted in significant reductions in ETS constituent concentrations compared to when smoking a representative lit-end cigarette (Marlboro: 6 mg tar, 0.5 mg nicotine, and 7 mg carbon monoxide). In direct comparisons, 24 of 29 measured smoke constituents (83%) showed mean reductions of greater than 90%, and 5 smoke constituents (17%) showed mean reductions between 80% and 90%. Gas-vapor phase ETS markers (nicotine and 3-ethenylpyridine) were reduced by an average of 97% (range 94-99%). Total respirable suspended particles, determined by online particle measurements and as gravimetric respirable suspended particles, were reduced by 90% (range 82-100%). The mean and standard deviation of the reduction of all constituents was 94 +/- 4%, indicating that smoking the new EHCSS in simulated "office" and "hospitality" indoor environments resulted in substantial reductions of ETS constituents in indoor air. PMID:18951229

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

    Directory of Open Access Journals (Sweden)

    Jieming Zhong

    2016-05-01

    Full Text Available 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.

  3. 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.

  4. 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.

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

    Science.gov (United States)

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

    2013-01-01

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

  6. Information Management Strategies Within Conversations About Cigarette Smoking: Parenting Correlates and Longitudinal Associations With Teen Smoking

    OpenAIRE

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

    2012-01-01

    The present study examined smoking-specific and general parenting predictors of in vivo observed patterns of parent–adolescent discussion concerning adolescents’ cigarette smoking experiences and associations between these observed patterns and 24-month longitudinal trajectories of teen cigarette smoking behavior (nonsmokers, current experimenters, escalators). Parental solicitation, adolescent disclosure, and adolescent information management were coded from direct observations of 528 video-...

  7. Smoking and interstitial lung disease. The effect of cigarette smoking on the incidence of pulmonary histiocytosis X and sarcoidosis.

    Science.gov (United States)

    Hance, A J; Basset, F; Saumon, G; Danel, C; Valeyre, D; Battesti, J P; Chrétien, J; Georges, R

    1986-01-01

    Cigarette smoking produces marked alterations in the lung parenchyma and in the population of immune and inflammatory cells present in the lower respiratory tract. These cigarette-induced changes appear to influence the incidence of two different interstitial lung diseases, histiocytosis X and sarcoidosis. Smoking is a strong risk factor for the development of pulmonary histiocytosis X, since the incidence of smoking is very high among patients with histiocytosis X: 90% of the patients with histiocytosis X were smokers; 46% of the controls were smokers (p less than .001). In contrast, smoking appears to reduce the incidence of sarcoidosis: 31% of the patients with sarcoidosis were smokers (p less than .05 compared to controls). In an effort to understand how cigarette smoking influences the incidence of these two disorders, we compared the numbers and types of immune and inflammatory cells recovered by bronchoalveolar lavage from nonsmoking and smoking controls and patients with histiocytosis X and sarcoidosis. Although nonsmoking patients with histiocytosis X did not have a significant increase in the number of alveolar macrophages recovered by lavage (p greater than .2 compared to normals), smoking patients had an increase in the number of alveolar macrophages similar to that observed in the control population. In contrast, the number of macrophages recovered from patients with sarcoidosis who smoked was considerably less than that observed in normal smokers (p less than .05 comparing patients with sarcoidosis and controls who smoked 1-20 cigarettes/day). This difference in the intensity of the cigarette-induced macrophage alveolitis observed in the two patient groups may be important in explaining the opposite effects of cigarette smoking on the incidence of histiocytosis X and sarcoidosis. PMID:3488004

  8. 32P-postlabeling DNA adduct assay: cigarette smoke-induced dna adducts in the respiratory and nonrespiratory rat tissues. Book chapter

    International Nuclear Information System (INIS)

    An analysis of the tissue DNA adducts in rats by the sensitive (32)p-postlabeling assay showed one to eight detectable DNA adducts in lung, trachea, larynx, heart and bladder of the sham controls. Chronic exposure of animals to mainstream cigarette smoke showed a remarkable enhancement of most adducts in the lung and heart DNA. Since cigarette smoke contains several thousand chemicals and a few dozen of them are known or potential carcinogens, the difference between the DNA adducts of nasal and the other tissues may reflect the diversity of reactive constituents and their differential absorption in different tissues. In comparison to the lung DNA adducts, the adducts in nasal DNA were less hydrophobic. Identity of the predominant adducts was further investigated by comparison with several reference DNA adducts from 10 PAH and aromatic amines. Since some of these chemicals are present in cigarette smoke, the results suggest that these constituents of cigarette smoke may not be directly responsible for formation of DNA adducts in the lung and heart of the smoke-exposed animals

  9. Measuring cigarette smoking-induced cortical dopamine release: A [¹¹C]FLB-457 PET study.

    Science.gov (United States)

    Wing, Victoria C; Payer, Doris E; Houle, Sylvain; George, Tony P; Boileau, Isabelle

    2015-05-01

    Striatal dopamine (DA) is thought to have a fundamental role in the reinforcing effects of tobacco smoking and nicotine. Microdialysis studies indicate that nicotine also increases DA in extrastriatal brain areas, but much less is known about its role in addiction. High-affinity D2/3 receptor radiotracers permit the measurement of cortical DA in humans using positron emission tomography (PET). [(11)C]FLB-457 PET scans were conducted in 10 nicotine-dependent daily smokers after overnight abstinence and reinstatement of smoking. Voxel-wise [(11)C]-FLB-457-binding potential (BPND) in the frontal lobe, insula, and limbic regions was estimated in the two conditions. Paired t-tests showed BPND values were reduced following smoking (an indirect index of DA release). The overall peak t was located in the cingulate gyrus, which was part of a larger medial cluster (BPND change -12.1±9.4%) and this survived false discovery rate correction for multiple comparisons. Clusters were also identified in the left anterior cingulate cortex/medial frontal gyrus, bilateral prefrontal cortex (PFC), bilateral amygdala, and the left insula. This is the first demonstration of tobacco smoking-induced cortical DA release in humans; it may be the result of both pharmacological (nicotine) and non-pharmacological factors (tobacco cues). Abstinence increased craving but had minimal cognitive effects, thus limiting correlation analyses. However, given that the cingulate cortex, PFC, insula, and amygdala are thought to have important roles in tobacco craving, cognition, and relapse, these associations warrant investigation in a larger sample. [(11)C]FLB-457 PET imaging may represent a useful tool to investigate individual differences in tobacco addiction severity and treatment response. PMID:25502631

  10. Polonium in cigarette smoke and radiation exposure of lungs

    Science.gov (United States)

    Carvalho, Fernando P.; Oliveira, João M.

    2006-01-01

    Polonium (210Po), the most volatile of naturally-occurring radionuclides in plants, was analysed in three common brands of cigarettes produced in Portugal. The analyses were carried out on the unburned tobacco contained in cigarettes, on the ashes and butts of smoked cigarettes and on the mainstream smoke. 210Po in tobacco displays concentrations ranging from 3 to 37 mBq g-1, depending upon the cigarette brand. The 210Po activity remaining in the solid residue of a smoked cigarette varied from 0.3 to 4.9 mBq per cigarette, and the 210Po in the inhaled smoke varied from 2.6 to 28.9 mBq. In all brands of cigarettes tested, a large fraction of the 210Po content is not inhaled by the smoker and it is released into the atmosphere. Part of it may be inhaled by passive smokers. Depending upon the commercial brand and upon the presence or absence of a filter in the cigarette, 5 to 37 % of the 210Po in the cigarette can be inhaled by the smoker. Taking into account the average 210Po in surface air, the smoker of one pack of twenty cigarettes per day may inhale 50 times 210Po than a non smoker. Cigarette smoke contributes with 1.5 % to the daily rate of 210Po absorption into the blood, 0.39 Bq d-1, and, after systemic circulation it gives rise to a whole body radiation dose in the same proportion. However, in the smoker the deposition of 210Po in the lungs is much more elevated than normal and may originate an enhanced radiation exposure. Estimated dose to the lungs is presented and radiobiological effects of cigarette smoke are discussed.

  11. Cigarette smoking and genetic alterations in sporadic colon carcinomas

    NARCIS (Netherlands)

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

    2003-01-01

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

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

    Science.gov (United States)

    Gritz, Ellen R.

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

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

    Science.gov (United States)

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

    2016-01-01

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

  14. 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.

  15. 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.

  16. Effect of Cigarette Smoking on Epithelial to Mesenchymal Transition (EMT) in Lung Cancer.

    Science.gov (United States)

    Vu, Trung; Jin, Lin; Datta, Pran K

    2016-01-01

    Epithelial to mesenchymal transition (EMT) is a process that allows an epithelial cell to acquire a mesenchymal phenotype through multiple biochemical changes resulting in an increased migratory capacity. During cancer progression, EMT is found to be associated with an invasive or metastatic phenotype. In this review, we focus on the discussion of recent studies about the regulation of EMT by cigarette smoking. Various groups of active compounds found in cigarette smoke such as polycyclic aromatic hydrocarbons (PAH), nicotine-derived nitrosamine ketone (NNK), and reactive oxygen specicies (ROS) can induce EMT through different signaling pathways. The links between EMT and biological responses to cigarette smoke, such as hypoxia, inflammation, and oxidative damages, are also discussed. The effect of cigarette smoke on EMT is not only limited to cancer types directly related to smoking, such as lung cancer, but has also been found in other types of cancer. Altogether, this review emphasizes the importance of understanding molecular mechanisms of the induction of EMT by cigarette smoking and will help in identifying novel small molecules for targeting EMT induced by smoking. PMID:27077888

  17. Effect of Cigarette Smoking on Epithelial to Mesenchymal Transition (EMT in Lung Cancer

    Directory of Open Access Journals (Sweden)

    Trung Vu

    2016-04-01

    Full Text Available Epithelial to mesenchymal transition (EMT is a process that allows an epithelial cell to acquire a mesenchymal phenotype through multiple biochemical changes resulting in an increased migratory capacity. During cancer progression, EMT is found to be associated with an invasive or metastatic phenotype. In this review, we focus on the discussion of recent studies about the regulation of EMT by cigarette smoking. Various groups of active compounds found in cigarette smoke such as polycyclic aromatic hydrocarbons (PAH, nicotine-derived nitrosamine ketone (NNK, and reactive oxygen specicies (ROS can induce EMT through different signaling pathways. The links between EMT and biological responses to cigarette smoke, such as hypoxia, inflammation, and oxidative damages, are also discussed. The effect of cigarette smoke on EMT is not only limited to cancer types directly related to smoking, such as lung cancer, but has also been found in other types of cancer. Altogether, this review emphasizes the importance of understanding molecular mechanisms of the induction of EMT by cigarette smoking and will help in identifying novel small molecules for targeting EMT induced by smoking.

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

    Science.gov (United States)

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

    2014-06-01

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

  19. Acute effects of cigarette smoking on inflammation in healthy intermittent smokers

    Directory of Open Access Journals (Sweden)

    Vonk Judith M

    2005-03-01

    Full Text Available Abstract Background Chronic smoking is the main risk factor for chronic obstructive pulmonary disease. Knowledge on the response to the initial smoke exposures might enhance the understanding of changes due to chronic smoking, since repetitive acute smoke effects may cumulate and lead to irreversible lung damage. Methods We investigated acute effects of smoking on inflammation in 16 healthy intermittent smokers in an open randomised cross-over study. We compared effects of smoking of two cigarettes on inflammatory markers in exhaled air, induced sputum, blood and urine at 0, 1, 3, 6, 12, 24, 48, 96 and 192 hours and outcomes without smoking. All sputum and blood parameters were log transformed and analysed using a linear mixed effect model. Results Significant findings were: Smoking increased exhaled carbon monoxide between 0 and 1 hour, and induced a greater decrease in blood eosinophils and sputum lymphocytes between 0 and 3 hours compared to non-smoking. Compared to non-smoking, smoking induced a greater interleukin-8 release from stimulated blood cells between 0 and 3 hours, and a greater increase in sputum lymphocytes and neutrophils between 3 and 12 hours. Conclusion We conclude that besides an increase in inflammation, as known from chronic smoking, there is also a suppressive effect of smoking two cigarettes on particular inflammatory parameters.

  20. Effects of cigarette smoking on periodontium

    Directory of Open Access Journals (Sweden)

    Bokor-Bratić Marija

    2002-01-01

    Full Text Available Introduction The exact mechanisms by which smoking effects the periodontal tissues are not known. Studies in which plaque or calculus are taken into consideration come to conflicting conclusions regarding effects of smoking. Aim The aim of this study was to examine the oral hygiene and periodontal status in smokers and compare them with nonsmokers. Material and methods The study group comprised 83 smokers and 83 nonsmokers. The mean age (SD of smokers and nonsmokers was 42,4±7,0 years and 43,7±6,4 years, respectively. The age difference was not statistically significant. The average tobacco consumption of the smokers at the time of investigation was 14 cigarettes a day and they had been regular smokers for 21 years on average. Results The amount of dental plaque was evaluated in accordance with the criteria of Green-Vermillion by using disclosing solution. The periodontal condition was evaluated by Ramfjord Periodontal Disease Index. For gingival recession the distance from the cemento-enamel junction to the gingival margin was determined on mid-buccal and mid-lingual surfaces of all teeth. Each subject was radiographically examined with a full mouth intraoral survey. Alveolar bone loss was determined as the distance from the cemento-enamel junction to the point where lamina dura became continuous with the compact bone of the interdental septum. Mean alveolar bone loss based on all mesial and distal measurements was calculated for each subject. The amount of dental plaque was high in both smokers (2,60,60 and nonsmokers (1,50,70, whereas the differences were statistically significant (p<0.001. Conclusion Periodontal destruction, alveolar bone loss and gingival recession were significantly increased in smokers compared to nonsmokers (p<0.001. It is concluded that differences observed between smokers and nonsmokers with regard to periodontal condition are attributable to differences in oral hygiene. Smoking is a risk factor for periodontal

  1. 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

  2. Accelerated repair and reduced mutagenicity of DNA damage induced by cigarette smoke in human bronchial cells transfected with E.coli formamidopyrimidine DNA glycosylase.

    Directory of Open Access Journals (Sweden)

    Mara Foresta

    Full Text Available Cigarette smoke (CS is associated to a number of pathologies including lung cancer. Its mutagenic and carcinogenic effects are partially linked to the presence of reactive oxygen species and polycyclic aromatic hydrocarbons (PAH inducing DNA damage. The bacterial DNA repair enzyme formamidopyrimidine DNA glycosylase (FPG repairs both oxidized bases and different types of bulky DNA adducts. We investigated in vitro whether FPG expression may enhance DNA repair of CS-damaged DNA and counteract the mutagenic effects of CS in human lung cells. NCI-H727 non small cell lung carcinoma cells were transfected with a plasmid vector expressing FPG fused to the Enhanced Green Fluorescent Protein (EGFP. Cells expressing the fusion protein EGFP-FPG displayed accelerated repair of adducts and DNA breaks induced by CS condensate. The mutant frequencies induced by low concentrations of CS condensate to the Na(+K(+-ATPase locus (oua(r were significantly reduced in cells expressing EGFP-FPG. Hence, expression of the bacterial DNA repair protein FPG stably protects human lung cells from the mutagenic effects of CS by improving cells' capacity to repair damaged DNA.

  3. Nicotine- and tar-free cigarette smoke induces cell damage through reactive oxygen species newly generated by PKC-dependent activation of NADPH oxidase.

    Science.gov (United States)

    Asano, Hiroshi; Horinouchi, Takahiro; Mai, Yosuke; Sawada, Osamu; Fujii, Shunsuke; Nishiya, Tadashi; Minami, Masabumi; Katayama, Takahiro; Iwanaga, Toshihiko; Terada, Koji; Miwa, Soichi

    2012-01-01

    We examined cytotoxic effects of nicotine/tar-free cigarette smoke extract (CSE) on C6 glioma cells. The CSE induced plasma membrane damage (determined by lactate dehydrogenase leakage and propidium iodide uptake) and cell apoptosis {determined by MTS [3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium] reduction activity and DNA fragmentation}. The cytotoxic activity decayed with a half-life of approximately 2 h at 37°C, and it was abolished by N-acetyl-L-cysteine and reduced glutathione. The membrane damage was prevented by catalase and edaravone (a scavenger of (•)OH) but not by superoxide dismutase, indicating involvement of (•)OH. In contrast, the CSE-induced cell apoptosis was resistant to edaravone and induced by authentic H(2)O(2) or O(2)(-) generated by the xanthine/xanthine oxidase system, indicating involvement of H(2)O(2) or O(2)(-) in cell apoptosis. Diphenyleneiodonium [NADPH oxidase (NOX) inhibitor] and bisindolylmaleimide I [BIS I, protein kinase C (PKC) inhibitor] abolished membrane damage, whereas they partially inhibited apoptosis. These results demonstrate that 1) a stable component(s) in the CSE activates PKC, which stimulates NOX to generate reactive oxygen species (ROS), causing membrane damage and apoptosis; 2) different ROS are responsible for membrane damage and apoptosis; and 3) part of the apoptosis is caused by oxidants independently of PKC and NOX. PMID:22302021

  4. Coffee drinking enhances the analgesic effect of cigarette smoking

    DEFF Research Database (Denmark)

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

    2007-01-01

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

  5. Effects of cigarette smoke on the Meckel's cartilage of rat fetus: morphologic, morphometric and stereologic study.

    Science.gov (United States)

    Brandini, Daniela Atili; Sala, Miguel Angel; Lopes, Ruberval Armando; Semprini, Marisa; Contrera, Mary Garcia Duarte

    2005-01-01

    The purpose of this study was to investigate the effects of cigarette smoke on the development of the embryo mandible (Meckel's) cartilage in rat fetuses. When inhaled by female Wistar rats between the 9th and the 12th day of pregnancy, cigarette smoke (5 cigarettes a day) caused intrauterine growth retardation, providing smaller fetuses and placentas. In fetuses from the experimental group, the histopathologic examination revealed a poorly developed Meckel's cartilage with smaller chondroblasts showing a scanty cytoplasm with spherical and paler central nuclei, as well as more abundant cartilage matrix. Morphometric analysis revealed that Meckel's cartilage lacunae were smaller in the fetuses from the experimental group, although not showing any remarkable alteration in shape. The results suggested that inhalation of cigarette smoke by pregnant rats during the organogenic period induced growth retardation and delayed cellular differentiation in rat fetal Meckel's cartilage. PMID:16113936

  6. The Association between Cigarette Smoking and Acne Intensity

    OpenAIRE

    Taheri Ramin; Nasaji Zavareh Mohammad; Ghorbani Raheb; Mohmmadi Zahra

    2009-01-01

    Background: Acne vulgaris is a common chronic inflammatory disease of pilosebaceous unit. Different factors have been suggested to influence acne including diet, menstruation and occupation. The role of some of these factors on acne intensity is confirmed. The affect of Cigarette smoking on acne intensity has been suggested. In this research, we evaluated the association between cigarette smoking and the acne intensity.Materials and Methods: This cross-sectional study was performed on 278 sm...

  7. 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.

  8. 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...

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

    Science.gov (United States)

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

    2014-03-01

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

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

    Directory of Open Access Journals (Sweden)

    Venkatachalem Sathish

    2015-06-01

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

  11. EXPRESSIONS PROFILING PROJECT OF HUMAN EMBRYONIC LUNG CELLSEXPOSED TO PYROLYZED CIGARETTE SMOKE

    OpenAIRE

    Klaus Braun*, Gabriele Müller , Matthias Schick, Melanie Bewerunge-Hudler, Oliver Heil, Manfred Wiessler , Rüdiger Pipkorn , Wolfhard Semmler and Waldemar Waldeck

    2013-01-01

    In contrast to the problematic health and economic effects of acute and chronic smoke exposure on lung function and airway inflammation, there are still few data dealing with the effects of smoking. Smoke exposure can result in aberrant cell growth. In our experiments, pyrolyzed components of cigarettes have been shown to induce a strong stress response in cultured cells. We used human embryonic lung (HEL) cells, which respond with an altered expression of a broad spectrum of genes. Therefore...

  12. Cigarette smoking: knowledge and attitudes among Mexican physicians

    Directory of Open Access Journals (Sweden)

    TAPIA-CONYER ROBERTO

    1997-01-01

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

  13. Current cigarette smoking among adults - United States, 2005-2014.

    Science.gov (United States)

    Jamal, Ahmed; Homa, David M; O'Connor, Erin; Babb, Stephen D; Caraballo, Ralph S; Singh, Tushar; Hu, S Sean; King, Brian A

    2015-11-13

    Tobacco smoking is the leading cause of preventable disease and death in the United States, resulting in approximately 480,000 premature deaths and more than $300 billion in direct health care expenditures and productivity losses each year (1). To assess progress toward achieving the Healthy People 2020 objective of reducing the percentage of U.S. adults who smoke cigarettes to ≤12.0%,* CDC assessed the most recent national estimates of smoking prevalence among adults aged ≥18 years using data from the 2014 National Health Interview Survey (NHIS). The percentage of U.S. adults who smoke cigarettes declined from 20.9% in 2005 to 16.8% in 2014. Among daily cigarette smokers, declines were observed in the percentage who smoked 20–29 cigarettes per day (from 34.9% to 27.4%) or ≥30 cigarettes per day (from 12.7% to 6.9%). In 2014, prevalence of cigarette smoking was higher among males, adults aged 25–44 years, multiracial persons and American Indian/Alaska Natives, persons who have a General Education Development certificate, live below the federal poverty level, live in the Midwest, are insured through Medicaid or are uninsured, have a disability or limitation, or are lesbian, gay, or bisexual. Proven population-based interventions, including tobacco price increases, comprehensive smoke-free laws, high impact mass media campaigns, and barrier-free access to quitting assistance, are critical to reduce cigarette smoking and smoking-related disease and death among U.S. adults. PMID:26562061

  14. 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. PMID:15791675

  15. 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.

  16. Cigarette smoke induces C/EBP-β-mediated activation of miR-31 in normal human respiratory epithelia and lung cancer cells.

    Directory of Open Access Journals (Sweden)

    Sichuan Xi

    Full Text Available BACKGROUND: Limited information is available regarding mechanisms by which miRNAs contribute to pulmonary carcinogenesis. The present study was undertaken to examine expression and function of miRNAs induced by cigarette smoke condensate (CSC in normal human respiratory epithelia and lung cancer cells. METHODOLOGY: Micro-array and quantitative RT-PCR (qRT-PCR techniques were used to assess miRNA and host gene expression in cultured cells, and surgical specimens. Software-guided analysis, RNA cross-link immunoprecipitation (CLIP, 3' UTR luciferase reporter assays, qRT-PCR, focused super-arrays and western blot techniques were used to identify and confirm targets of miR-31. Chromatin immunoprecipitation (ChIP techniques were used to evaluate histone marks and transcription factors within the LOC554202 promoter. Cell count and xenograft experiments were used to assess effects of miR-31 on proliferation and tumorigenicity of lung cancer cells. RESULTS: CSC significantly increased miR-31 expression and activated LOC554202 in normal respiratory epithelia and lung cancer cells; miR-31 and LOC554202 expression persisted following discontinuation of CSC exposure. miR-31 and LOC554202 expression levels were significantly elevated in lung cancer specimens relative to adjacent normal lung tissues. CLIP and reporter assays demonstrated direct interaction of miR-31 with Dickkopf-1 (Dkk-1 and DACT-3. Over-expression of miR-31 markedly diminished Dkk-1 and DACT3 expression levels in normal respiratory epithelia and lung cancer cells. Knock-down of miR-31 increased Dkk-1 and DACT3 levels, and abrogated CSC-mediated decreases in Dkk-1 and DACT-3 expression. Furthermore, over-expression of miR-31 diminished SFRP1, SFRP4, and WIF-1, and increased Wnt-5a expression. CSC increased H3K4Me3, H3K9/14Ac and C/EBP-β levels within the LOC554202 promoter. Knock-down of C/EBP-β abrogated CSC-mediated activation of LOC554202. Over-expression of miR-31 significantly enhanced

  17. Epigallocatechin-3-gallate reduces DNA damage induced by benzo[a]pyrene diol epoxide and cigarette smoke condensate in human mucosa tissue cultures.

    Science.gov (United States)

    Baumeister, Philipp; Reiter, Maximilian; Kleinsasser, Norbert; Matthias, Christoph; Harréus, Ulrich

    2009-06-01

    Although epidemiological studies indicate cancer preventive effects of diets rich in fruit and vegetables, large clinical intervention studies conducted to evaluate dietary supplementation with micronutrients, mostly vitamins, showed disappointing results in large parts. In contrast, there is encouraging epidemiologic data indicating great chemopreventive potential of a large group of phytochemicals, namely polyphenols. This study shows the DNA protective effect epigallocatechin-3-gallate, a tea catechin, and one of the best-studied substances within this group, on carcinogen-induced DNA fragmentation in upper aerodigestive tract cells. Cell cultures from fresh oropharyngeal mucosa biopsies were preincubated with epigallocatechin-3-gallate in different concentrations before DNA damage was introduced with the metabolically activated carcinogen benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide or cigarette smoke condensate. Effects on resulting DNA fragmentation were measured using the alkaline single-cell microgel electrophoresis (comet assay). Epigallocatechin-3-gallate significantly reduced benzo[a]pyrene-7,8-dihydrodiol-9,10-epoxide-induced DNA damage by up to 51% (Pculture model. PMID:19491610

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

    Science.gov (United States)

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

    2012-01-01

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

  19. The effects of cigarette smoking on male fertility.

    Science.gov (United States)

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

    2015-04-01

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

  20. Prevalence of Cigarette smoking among Intermediate Qatari School Male Students

    International Nuclear Information System (INIS)

    Attempt was made to find out knowledge, attitudes and practices of Qatari male students and attending four intermediate schools in Doha, about cigarette smoking. 475 boys aged between 12-18 years were the subject of our study. A survey using self-administered questionnaire was carried out into habits, attitudes and knowledge about cigarette smoking. The importance of peer group pressure, parental smoking and early experimentation was confirmed, as was the general awareness of the health hazards of smoking. In contrast, the importance of religion and financial cost of smoking differed markedly. The prevalence of smoking amongst Qatari intermediate schools appears to be considerably less than their counterparts. The results of this research might be used by health planners and policy makers to establish a strategy to prevent smoking as early as possible to reduce morbidity and early mortality and health related economic burden. (author)

  1. Cigarette Smoke and Inflammation: Role in Cerebral Aneurysm Formation and Rupture

    Directory of Open Access Journals (Sweden)

    Nohra Chalouhi

    2012-01-01

    Full Text Available Smoking is an established risk factor for subarachnoid hemorrhage yet the underlying mechanisms are largely unknown. Recent data has implicated a role of inflammation in the development of cerebral aneurysms. Inflammation accompanying cigarette smoke exposure may thus be a critical pathway underlying the development, progression, and rupture of cerebral aneurysms. Various constituents of the inflammatory response appear to be involved including adhesion molecules, cytokines, reactive oxygen species, leukocytes, matrix metalloproteinases, and vascular smooth muscle cells. Characterization of the molecular basis of the inflammatory response accompanying cigarette smoke exposure will provide a rational approach for future targeted therapy. In this paper, we review the current body of knowledge implicating cigarette smoke-induced inflammation in cerebral aneurysm formation/rupture and attempt to highlight important avenues for future investigation.

  2. Psychosocial Correlates of Cigarette Smoking among College Students in China

    Science.gov (United States)

    Mao, Rong; Li, Xiaoming; Stanton, Bonita; Wang, Jing; Hong, Yan; Zhang, Hongshia; Chen, Xinguang

    2009-01-01

    The objectives are to examine the smoking practice and intention among Chinese college students and to explore the association between cigarette smoking and individual and psychosocial factors. Cross-sectional data were collected from 1874 students from 19 college campuses in Jiangsu province, China. Both bivariate and multivariate analyses were…

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

    Science.gov (United States)

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

    2012-01-01

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

  4. 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.

  5. 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. PMID:2532606

  6. The Association between Cigarette Smoking and Acne Intensity

    Directory of Open Access Journals (Sweden)

    Taheri Ramin

    2009-06-01

    Full Text Available Background: Acne vulgaris is a common chronic inflammatory disease of pilosebaceous unit. Different factors have been suggested to influence acne including diet, menstruation and occupation. The role of some of these factors on acne intensity is confirmed. The affect of Cigarette smoking on acne intensity has been suggested. In this research, we evaluated the association between cigarette smoking and the acne intensity.Materials and Methods: This cross-sectional study was performed on 278 smoker and 277non smoker males referred to dermatology clinics of Semnan during 2006-2007. The dermatologists interviewing the patients completed questionnaires based on clinical diagnosis and intensity of acne. Data analysis was performed using t-test, Mann-Whitney, Chi-square and Spearman coefficient tests. P-value less than 0.05 were considered significant. Results: Severe acne was observed in 16.6% of non-smokers and 22.7% of smokers. Distribution of acne intensity in both groups was significant (P=0.023. Association between duration of cigarette smoking and acne intensity was significant too (P<0.001. The association between dosage of cigarette smoking and acne intensity was also significant (P<0.001.Conclusion: Significant association between cigarette smoking and acne intensity showed that smoking withdrawal is helpful for reducing the acne intensity

  7. Effects of cigarette smoke on endothelial function of pulmonary arteries in the guinea pig

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    Martínez Anna

    2009-08-01

    Full Text Available Abstract Background Cigarette smoking may contribute to pulmonary hypertension in chronic obstructive pulmonary disease by altering the structure and function of pulmonary vessels at early disease stages. The objectives of this study were to evaluate the effects of long-term exposure to cigarette smoke on endothelial function and smooth muscle-cell proliferation in pulmonary arteries of guinea pigs. Methods 19 male Hartley guinea pigs were exposed to the smoke of 7 cigarettes/day, 5 days/week, for 3 and 6 months. 17 control guinea pigs were sham-exposed for the same periods. Endothelial function was evaluated in rings of pulmonary artery and aorta as the relaxation induced by ADP. The proliferation of smooth muscle cells and their phenotype in small pulmonary vessels were evaluated by immunohistochemical expression of α-actin and desmin. Vessel wall thickness, arteriolar muscularization and emphysema were assessed morphometrically. The expression of endothelial nitric oxide synthase (eNOS was evaluated by Real Time-PCR. Results Exposure to cigarette smoke reduced endothelium-dependent vasodilatation in pulmonary arteries (ANOVA p Conclusion In the guinea pig, exposure to cigarette smoke induces selective endothelial dysfunction in pulmonary arteries, smooth muscle cell proliferation in small pulmonary vessels and reduced lung expression of eNOS. These changes appear after 3 months of exposure and precede the development of pulmonary emphysema.

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

    Science.gov (United States)

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

    1991-12-01

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

  9. Children's hedonic judgments of cigarette smoke odor: effects of parental smoking and maternal mood.

    Science.gov (United States)

    Forestell, Catherine A; Mennella, Julie A

    2005-12-01

    Age-appropriate tasks were used to assess 3- to 8-year-old children's liking, identification, and preference for a variety of odors, including that of exhaled cigarette smoke. Children whose parents smoke took longer to decide whether they liked the cigarette odor and were significantly more likely to prefer the odor of cigarette to the neutral and unfamiliar odor of green tea compared with children of nonsmokers. Among children of smokers, relative preferences for the cigarette odor were related to maternal mood disturbance and depression scores. These findings suggest that some early learning about cigarette smoke odor is based on sensory experiences at home and anchors it to the emotional context in which their mothers smoke. PMID:16366814

  10. Children’s Hedonic Judgments of Cigarette Smoke Odor: Effects of Parental Smoking and Maternal Mood

    Science.gov (United States)

    Forestell, Catherine A.; Monell, Julie A. Mennella

    2006-01-01

    Age-appropriate tasks were used to assess 3-to 8-year-old children’s liking, identification, and preference for a variety of odors, including that of exhaled cigarette smoke. Children whose parents smoke took longer to decide whether they liked the cigarette odor and were significantly more likely to prefer the odor of cigarette to the neutral and unfamiliar odor of green tea compared with children of nonsmokers. Among children of smokers, relative preferences for the cigarette odor were related to maternal mood disturbance and depression scores. These findings suggest that some early learning about cigarette smoke odor is based on sensory experiences at home and anchors it to the emotional context in which their mothers smoke. PMID:16366814

  11. Acetyl radical generation in cigarette smoke: Quantification and simulations

    Science.gov (United States)

    Hu, Na; Green, Sarah A.

    2014-10-01

    Free radicals are present in cigarette smoke and can have a negative effect on human health. However, little is known about their formation mechanisms. Acetyl radicals were quantified in tobacco smoke and mechanisms for their generation were investigated by computer simulations. Acetyl radicals were trapped from the gas phase using 3-amino-2, 2, 5, 5-tetramethyl-proxyl (3AP) on solid support to form stable 3AP adducts for later analysis by high-performance liquid chromatography (HPLC), mass spectrometry/tandem mass spectrometry (MS-MS/MS) and liquid chromatography-mass spectrometry (LC-MS). Simulations were performed using the Master Chemical Mechanism (MCM). A range of 10-150 nmol/cigarette of acetyl radical was measured from gas phase tobacco smoke of both commercial and research cigarettes under several different smoking conditions. More radicals were detected from the puff smoking method compared to continuous flow sampling. Approximately twice as many acetyl radicals were trapped when a glass fiber particle filter (GF/F specifications) was placed before the trapping zone. Simulations showed that NO/NO2 reacts with isoprene, initiating chain reactions to produce hydroxyl radical, which abstracts hydrogen from acetaldehyde to generate acetyl radical. These mechanisms can account for the full amount of acetyl radical detected experimentally from cigarette smoke. Similar mechanisms may generate radicals in second hand smoke.

  12. Cigarette smoke worsens lung inflammation and impairs resolution of influenza infection in mice

    Directory of Open Access Journals (Sweden)

    Jones Jessica E

    2008-07-01

    Full Text Available Abstract Background Cigarette smoke has both pro-inflammatory and immunosuppressive effects. Both active and passive cigarette smoke exposure are linked to an increased incidence and severity of respiratory virus infections, but underlying mechanisms are not well defined. We hypothesized, based on prior gene expression profiling studies, that upregulation of pro-inflammatory mediators by short term smoke exposure would be protective against a subsequent influenza infection. Methods BALB/c mice were subjected to whole body smoke exposure with 9 cigarettes/day for 4 days. Mice were then infected with influenza A (H3N1, Mem71 strain, and analyzed 3 and 10 days later (d3, d10. These time points are the peak and resolution (respectively of influenza infection. Results Inflammatory cell influx into the bronchoalveolar lavage (BALF, inflammatory mediators, proteases, histopathology, viral titres and T lymphocyte profiles were analyzed. Compared to smoke or influenza alone, mice exposed to smoke and then influenza had more macrophages, neutrophils and total lymphocytes in BALF at d3, more macrophages in BALF at d10, lower net gelatinase activity and increased activity of tissue inhibitor of metalloprotease-1 in BALF at d3, altered profiles of key cytokines and CD4+ and CD8+ T lymphocytes, worse lung pathology and more virus-specific, activated CD8+ T lymphocytes in BALF. Mice smoke exposed before influenza infection had close to 10-fold higher lung virus titres at d3 than influenza alone mice, although all mice had cleared virus by d10, regardless of smoke exposure. Smoke exposure caused temporary weight loss and when smoking ceased after viral infection, smoke and influenza mice regained significantly less weight than smoke alone mice. Conclusion Smoke induced inflammation does not protect against influenza infection. In most respects, smoke exposure worsened the host response to influenza. This animal model may be useful in studying how smoke worsens

  13. 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.

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

    Directory of Open Access Journals (Sweden)

    Francesca Pirini

    2015-01-01

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

  15. ISE Analysis of Hydrogen Sulfide in Cigarette Smoke

    Science.gov (United States)

    Li, Guofeng; Polk, Brian J.; Meazell, Liz A.; Hatchett, David W.

    2000-08-01

    Many advanced undergraduate analytical laboratory courses focus on exposing students to various modern instruments. However, students rarely have the opportunity to construct their own analytical tools for solving practical problems. We designed an experiment in which students are required to build their own analytical module, a potentiometric device composed of a Ag/AgCl reference electrode, a Ag/Ag2S ion selective electrode (ISE), and a pH meter used as voltmeter, to determine the amount of hydrogen sulfide in cigarette smoke. Very simple techniques were developed for constructing these electrodes. Cigarette smoke is collected by a gas washing bottle into a 0.1 M NaOH solution. The amount of sulfide in the cigarette smoke solution is analyzed by standard addition of sulfide solution while monitoring the response of the Ag/Ag2S ISE. The collected data are further evaluated using the Gran plot technique to determine the concentration of sulfide in the cigarette smoke solution. The experiment has been successfully incorporated into the lab course Instrumental Analysis at Georgia Institute of Technology. Students enjoy the idea of constructing an analytical tool themselves and applying their classroom knowledge to solve real-life problems. And while learning electrochemistry they also get a chance to visualize the health hazard imposed by cigarette smoking.

  16. 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....

  17. The effects of shock as a punisher for cigarette smoking.

    Science.gov (United States)

    Powell, J; Azrin, N

    1968-01-01

    An attempt was made to reduce the cigarette smoking of three subjects by means of a special cigarette case that delivered aversive shock when opened. The number of cigarettes smoked was recorded by a counter in the cigarette case. The validity of the counter readings as a measure of smoking was obtained by a specially designed participant-observer technique. It was found that the rate of smoking decreased as a function of the intensity of the shock. Also, the smoking returned to its previously unpunished level after the shock punisher was discontinued. Both of these findings confirm the results of laboratory studies of punishment of simpler responses and extends them to more complex responses in a naturalistic situation. Surprisingly, the duration for which the apparatus was worn also decreased as a function of the intensity of the shock. This finding reveals that this aversive shock technique produced avoidance behavior that prevents the technique from having extensive applicability for eliminating smoking. The same limitation may apply to the use of aversive shock for eliminating other undesirable behaviors. PMID:16795161

  18. 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.

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

    Science.gov (United States)

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

    2014-12-01

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

  20. 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.

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

    Science.gov (United States)

    Keloglu-Isler, Esra; Erdogan, Irfan

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

  2. Alleviation of Severe Restless Legs Syndrome (RLS) Symptoms by Cigarette Smoking

    OpenAIRE

    Oksenberg, Arie

    2010-01-01

    Cigarette smoking is in general considered an aggravating factor for restless legs syndrome (RLS). The author presents a case in which cigarette smoking has produced for many years a consistent and effective alleviation of RLS symptoms.

  3. Psycho-social study of cigarette smoking.

    Science.gov (United States)

    Tandon, A K; Chaturvedi, P K; Dubey, A L; Narang, R K; Singh, S K; Chandra, S

    1990-04-01

    The present study has been carried out to assess the smoking habit among medical students and its relationship to demographic, social and psychological characteristics. Prevalence of smoking was found to be 30.79% in 854 students who responded to the questionnaire adequately. Smoking habit was more common among student who were married hailed from rural areas and the intensity of smoking increased with advancement in the career in medical profession. A strong association was observed between the habit and family history of smoking. The psychological factors associated with smoking were worry about examination unhappiness without justified cause and failure in friendship. PMID:21927445

  4. Menthol attenuates respiratory irritation responses to multiple cigarette smoke irritants.

    Science.gov (United States)

    Willis, Daniel N; Liu, Boyi; Ha, Michael A; Jordt, Sven-Eric; Morris, John B

    2011-12-01

    Menthol, the cooling agent in peppermint, is added to almost all commercially available cigarettes. Menthol stimulates olfactory sensations, and interacts with transient receptor potential melastatin 8 (TRPM8) ion channels in cold-sensitive sensory neurons, and transient receptor potential ankyrin 1 (TRPA1), an irritant-sensing channel. It is highly controversial whether menthol in cigarette smoke exerts pharmacological actions affecting smoking behavior. Using plethysmography, we investigated the effects of menthol on the respiratory sensory irritation response in mice elicited by smoke irritants (acrolein, acetic acid, and cyclohexanone). Menthol, at a concentration (16 ppm) lower than in smoke of mentholated cigarettes, immediately abolished the irritation response to acrolein, an agonist of TRPA1, as did eucalyptol (460 ppm), another TRPM8 agonist. Menthol's effects were reversed by a TRPM8 antagonist, AMTB. Menthol's effects were not specific to acrolein, as menthol also attenuated irritation responses to acetic acid, and cyclohexanone, an agonist of the capsaicin receptor, TRPV1. Menthol was efficiently absorbed in the respiratory tract, reaching local concentrations sufficient for activation of sensory TRP channels. These experiments demonstrate that menthol and eucalyptol, through activation of TRPM8, act as potent counterirritants against a broad spectrum of smoke constituents. Through suppression of respiratory irritation, menthol may facilitate smoke inhalation and promote nicotine addiction and smoking-related morbidities. PMID:21903934

  5. Prevalence and social environment of cigarette smoking in Cyprus youth

    Directory of Open Access Journals (Sweden)

    Jones Nathan R

    2008-06-01

    Full Text Available Abstract Background Tobacco use is the single most preventable cause of morbidity and mortality in humans. Limited data exist regarding the extent of the problem among Cyprus youth. We use the Global Youth Tobacco Survey to assess the prevalence of cigarette smoking among middle and high school students as well as the social environment in which this is taking place. Methods The survey was conducted by the Cyprus International Institute for the Environment and Public Health in association with Harvard School of Public Health. A two-stage cluster sample design was used to select a representative sample of students from middle and high schools registered with the Republic of Cyprus in 2005–2006. The study questionnaire consisted of 99 questions and participation in the survey was voluntary. Statistical analyses were performed taking into consideration the specific design of the study and the sample weights associated with each completed questionnaire. Results The prevalence of current smoking, defined as having smoked cigarettes on one or more days of the past 30 days, is 13% among boys and 7% among girls in middle schools, and 36% among boys and 23% among girls in high schools. Furthermore, 16% of middle school students and more than 24% of high school students that had never smoked indicated that they are likely to initiate smoking within the next year. Exposure to environmental tobacco smoke is also very high with 91% of students reporting being exposed to smoke in places outside home. In addition, more than 95% of current smokers reported that they had bought cigarettes in a store during the past month and were not refused cigarettes because of their age. Conclusion Smoking prevalence among Cyprus middle and high school students is high and there are indications of an increase in the prevalence of smoking among girls over the last few years. Susceptibility rates, exposure to second-hand smoke, and access to and availability of cigarettes to

  6. Cigarette smoke activates the proto-oncogene c-src to promote airway inflammation and lung tissue destruction.

    Science.gov (United States)

    Geraghty, Patrick; Hardigan, Andrew; Foronjy, Robert F

    2014-03-01

    The diagnosis of chronic obstructive pulmonary disease (COPD) confers a 2-fold increased lung cancer risk even after adjusting for cigarette smoking, suggesting that common pathways are operative in both diseases. Although the role of the tyrosine kinase c-Src is established in lung cancer, less is known about its impact in other lung diseases, such as COPD. This study examined whether c-Src activation by cigarette smoke contributes to the pathogenesis of COPD. Cigarette smoke increased c-Src activity in human small airway epithelial (SAE) cells from healthy donors and in the lungs of exposed mice. Similarly, higher c-Src activation was measured in SAE cells from patients with COPD compared with healthy control subjects. In SAE cells, c-Src silencing or chemical inhibition prevented epidermal growth factor (EGF) receptor signaling in response to cigarette smoke but not EGF stimulation. Further studies showed that cigarette smoke acted through protein kinase C α to trigger c-Src to phosphorylate EGF receptor and thereby to induce mitogen-activated protein kinase responses in these cells. To further investigate the role of c-Src, A/J mice were orally administered the specific Src inhibitor AZD-0530 while they were exposed to cigarette smoke for 2 months. AZD-0530 treatment blocked c-Src activation, decreased macrophage influx, and prevented airspace enlargement in the lungs of cigarette smoke-exposed mice. Moreover, inhibiting Src deterred the cigarette smoke-mediated induction of matrix metalloproteinase-9 and -12 in alveolar macrophages and lung expression of cathepsin K, IL-17, TNF-α, MCP-1, and KC, all key factors in the pathogenesis of COPD. These results indicate that activation of the proto-oncogene c-Src by cigarette smoke promotes processes linked to the development of COPD. PMID:24111605

  7. Smoking Wet”: Respiratory Failure Related to Smoking Tainted Marijuana Cigarettes

    OpenAIRE

    Gilbert, Christopher R.; Baram, Michael; Cavarocchi, Nicholas C.

    2013-01-01

    Reports have suggested that the use of a dangerously tainted form of marijuana, referred to in the vernacular as “wet” or “fry,” has increased. Marijuana cigarettes are dipped into or laced with other substances, typically formaldehyde, phencyclidine, or both. Inhaling smoke from these cigarettes can cause lung injuries.

  8. PSYCHO-SOCIAL STUDY OF CIGARETTE SMOKING

    OpenAIRE

    Tandon, A.K.; Chaturvedi, P. K.; Dubey, A.L.; R.K. Narang; Singh, S.K; Chandra, S.

    1990-01-01

    SUMMARY The present study has been carried out to assess the smoking habit among medical students and its relationship to demographic, social and psychological characteristics. Prevalence of smoking was found to be 30.79% in 854 students who responded to the questionnaire adequately. Smoking habit was more common among student who were married hailed from rural areas and the intensity of smoking increased with advancement in the career in medical profession. A strong association was observed ...

  9. Psychosocial correlates of cigarette smoking among college students in China.

    Science.gov (United States)

    Mao, Rong; Li, Xiaoming; Stanton, Bonita; Wang, Jing; Hong, Yan; Zhang, Hongshia; Chen, Xinguang

    2009-02-01

    The objectives are to examine the smoking practice and intention among Chinese college students and to explore the association between cigarette smoking and individual and psychosocial factors. Cross-sectional data were collected from 1874 students from 19 college campuses in Jiangsu province, China. Both bivariate and multivariate analyses were performed to assess the associations of smoking practice and smoking intention with various individual and psychosocial factors. There was a significant gender difference in both smoking practice and smoking intention. Overall, 53% of the participants (70% male and 31% female) reported ever having smoked in their lifetime and 29% of the sample (49% male and 5% female) reported having smoked in the past 30 days. About one-fourth of the sample (44% male and 6% female) thought they were likely to smoke in the next 6 months. Male gender, low family socioeconomic status, perception of more peer smoking, more perceived benefits of smoking, higher level of pro-smoking attitude, higher level of perceived cost of non-smoking and more involvement in other health risk were positively associated with being a past or current smoker. Likewise, male gender, older age, more friends smoking, greater perceived benefits of smoking, higher pro-smoking attitudes and more health risk involvement were associated with the likelihood to smoke in the next 6 months. The data suggest a substantial smoking experimentation among college students in China, which presents both a challenge and an opportunity to prevent a large proportion of experimenters from progressing to regular smokers. The findings in the current study can be used to inform the development of effective smoking intervention prevention programs among college students in China. PMID:18281711

  10. Hierarchical Composites to Reduce N-Nitrosamines in Cigarette Smoke

    Directory of Open Access Journals (Sweden)

    Yan Yan Li

    2015-03-01

    Full Text Available In order to reduce the harmful constituents in cigarette smoke, two hierarchical composites were synthesized. Based on, zeolites HZSM-5 or NaY fragments were introduced into the synthetic system of mesoporous silica SBA-15 or MCM-41 and assembled with the mesoporous materials. These porous composites combine the advantages of micro- and mesoporous materials, and exhibit higher effects than activated carbon on reducing tobacco specific nitrosamines (TSNA and some vapor phase compounds in smoke.

  11. Determination of Toxic Elements in Cigarettes Smoke, Using Neutron Activation Method

    International Nuclear Information System (INIS)

    The purpose of the experiments was to get information of the toxic elements content in cigarettes smoke which could be used to estimate the cigarettes smoke contribution in air pollution. The sample were cigarette smoke from the mixture of 7 popular brand cigarettes collected by The Centre Cigarettes Research, University of kentucky, USA. Neutron activation was done in the Hoger Onderwijs Reactor, IRI Delft Netherlands, using thermal neutron flux 4.8 x 10 16n cm-2 second-1 for 4 hours. Result of the analysis showed that the cigarettes smoke contained Cd, As, Sb, and Br which are toxic elements

  12. Rosiglitazone attenuates the metalloprotease/anti-metalloprotease imbalance in emphysema induced by cigarette smoke: involvement of extracellular signal-regulated kinase and NFκB signaling

    Directory of Open Access Journals (Sweden)

    Hou G

    2015-04-01

    Full Text Available Gang Hou, Yan Yin, Dan Han, Qiu-yue Wang, Jian Kang Department of Respiratory Medicine, the First Hospital of China Medical University, Shenyang, People’s Republic of China Objective: We investigated how rosiglitazone attenuated cigarette smoke (CS-induced emphysema in a rat model. In particular, we focused on its possible effects on the imbalance between metalloprotease (MMP and anti-MMP activity, mitogen-activated protein kinase (MAPK phosphorylation, and nuclear factor kappa-light-chain-enhancer of activated B cell (NFκB signaling pathway over-activation.Methods: A total of 36 Wistar rats were divided into three groups (n=12 each: animals were exposed to CS for 12 weeks in the absence (the CS group or presence of 30 mg/kg rosiglitazone (the rosiglitazone-CS [RCS] group; a control group was treated with the rosiglitazone vehicle only, without any CS exposure. Histopathology of lung tissue in all groups was evaluated to grade severity of the disease. Expression levels of peroxisome proliferator-activated receptor γ (PPARγ, MMP2, and MMP9 in lung tissue were determined and compared using Western blotting and immunohistochemistry. Activation of MAPKs, NFκB, and the nuclear factor of kappa light polypeptide gene enhancer in B-cell inhibitor, alpha (IκBα phosphorylation in lung tissue was examined by Western blotting.Results: Emphysema-related pathology, based on inter-alveolar wall distance and alveolar density, was less severe in the RCS group than in the CS group. Compared with the CS group, levels of PPARγ were higher in the RCS group, and levels of MMP2 and MMP9 proteins were lower in the RCS rats. Levels of activated MAPKs and NFκB were also lower, while the IκBαphosphorylation was increased in the lung tissue of RCS rats.Conclusion: Our findings suggest that oral administration of rosiglitazone attenuates the metalloprotease activity induced by CS, and the underlying mechanism might involve the activation of signaling pathways

  13. Attitudes toward E-Cigarettes, Reasons for Initiating E-Cigarette Use, and Changes in Smoking Behavior after Initiation: A Pilot Longitudinal Study of Regular Cigarette Smokers

    OpenAIRE

    Berg, Carla J.; Barr, Dana Boyd; Stratton, Erin; Escoffery, Cam; Kegler, Michelle

    2014-01-01

    Objectives We examined 1) changes in smoking and vaping behavior and associated cotinine levels and health status among regular smokers who were first-time e-cigarette purchasers and 2) attitudes, intentions, and restrictions regarding e-cigarettes. Methods We conducted a pilot longitudinal study with assessments of the aforementioned factors and salivary cotinine at weeks 0, 4, and 8. Eligibility criteria included being ≥18 years old, smoking ≥25 of the last 30 days, smoking ≥5 cigarettes pe...

  14. Perlite filtration of phenolic compounds from cigarette smoke.

    Science.gov (United States)

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

    2013-01-01

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

  15. Retail Food Availability, Obesity, and Cigarette Smoking in Rural Communities

    Science.gov (United States)

    Hosler, Akiko S.

    2009-01-01

    Context: Disparities in the availability of nutritionally important foods and their influence on health have been studied in US urban communities. Purpose: To assess the availability of selected retail foods and cigarettes, and explore ecologic relationships of the availability with obesity and smoking in rural communities. Methods: Inventories of…

  16. Lipid-soluble cigarette smoking particles induce expression of inflammatory and extracellular-matrix-related genes in rat cerebral arteries

    DEFF Research Database (Denmark)

    Vikman, Petter; Xu, Cang-Bao; Edvinsson, Lars

    2009-01-01

    receptor 1 and 2 (AT(1) and AT(2)), interleukin 6 and inducible nitric oxide synthase (iNOS) were investigated at mRNA level by real-time PCR and/or at protein level by immunohistochemistry. In addition, the activity of three mitogen-activated protein kinases (p38, ERK 1/2 and SAPK...... factor ATF-2 and Elk-1. However, ERK 1/2 and SAPK/JNK activities were markedly expressed in the control (organ culture per se with DMSO), and DSP failed to further enhance the activation of ERK 1/2 and SAPK/JNK in the cerebral arteries. CONCLUSIONS: DSP induces cerebral vessel inflammation...

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

    Directory of Open Access Journals (Sweden)

    F Sahin Mutlu

    2008-12-01

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

  18. Histone deacetylase 2 is phosphorylated, ubiquitinated, and degraded by cigarette smoke.

    Science.gov (United States)

    Adenuga, David; Yao, Hongwei; March, Thomas H; Seagrave, Jeanclare; Rahman, Irfan

    2009-04-01

    Cigarette smoke (CS)-induced lung inflammation involves the reduction of histone deacetylase 2 (HDAC2) abundance, which is associated with steroid resistance in patients with chronic obstructive pulmonary disease and in individuals with severe asthma who smoke cigarettes. However, the molecular mechanism of CS-mediated reduction of HDAC2 is not clearly known. We hypothesized that HDAC2 is phosphorylated and subsequently degraded by the proteasome in vitro in macrophages (MonoMac6), human bronchial and primary small airway epithelial cells, and in vivo in mouse lungs in response to chronic CS exposure. Cigarette smoke extract (CSE) exposure in MonoMac6 and in bronchial and airway epithelial cells led to phosphorylation of HDAC2 on serine/threonine residues by a protein kinase CK2-mediated mechanism, decreased HDAC2 activity, and increased ubiquitin-proteasome-dependent HDAC2 degradation. CK2 and proteasome inhibitors reversed CSE-mediated HDAC2 degradation, whereas serine/threonine phosphatase inhibitor, okadaic acid, caused phosphorylation and subsequent ubiquitination of HDAC2. CS-induced HDAC2 phosphorylation was detected in mouse lungs from 2 weeks to 4 months of CS exposure, and mice showed significantly lower lung HDAC2 levels. Thus, CS-mediated down-regulation of HDAC2 in human macrophages and lung epithelial cells in vitro and in mouse lung in vivo involves the induction of serine/threonine phosphorylation and proteasomal degradation, which may have implications for steroid resistance and abnormal inflammation caused by cigarette smoke. PMID:18927347

  19. Cigarette Smoking is Associated with Decreased Sperm Density

    Institute of Scientific and Technical Information of China (English)

    2002-01-01

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

  20. Attitudes toward Cigarette Smoking among College Students

    Science.gov (United States)

    Van Volkom, Michele

    2008-01-01

    The purpose of the current study was to gather data on the attitudes and smoking habits of university students. Data were collected from 250 undergraduates dealing with various aspects of smoking behavior. There were 80 smokers and 170 nonsmokers, including 21 former smokers. In addition to demographic information, participants were assessed with…

  1. Attachment of radon progeny to cigarette-smoke aerosols

    Energy Technology Data Exchange (ETDEWEB)

    Biermann, A.H.; Sawyer, S.R.

    1995-05-01

    The daughter products of radon gas are now recognized as a significant contributor to radiation exposure to the general public. It is also suspected that a synergistic effect exists with the combination cigarette smoking and radon exposure. We have conducted an experimental investigation to determine the physical nature of radon progeny interactions with cigarette smoke aerosols. The size distributions of the aerosols are characterized and attachment rates of radon progeny to cigarette-smoke aerosols are determined. Both the mainstream and sidestream portions of the smoke aerosol are investigated. Unattached radon progeny are very mobile and, in the presence of aerosols, readily attach to the particle surfaces. In this study, an aerosol chamber is used to contain the radon gas, progeny and aerosol mixture while allowing the attachment process to occur. The rate of attachment is dependent on the size distribution, or diffusion coefficient, of the radon progeny as well as the aerosol size distribution. The size distribution of the radon daughter products is monitored using a graded-screen diffusion battery. The diffusion battery also enables separation of the unattached radon progeny from those attached to the aerosol particles. Analysis of the radon decay products is accomplished using alpha spectrometry. The aerosols of interest are size fractionated with the aid of a differential mobility analyzer and cascade impactor. The measured attachment rates of progeny to the cigarette smoke are compared to those found in similar experiments using an ambient aerosol. The lowest attachment coefficients observed, {approximately}10{sup {minus}6} cm{sup 3}/s, occurred for the ambient aerosol. The sidestream and mainstream smoke aerosols exhibited higher attachment rates in that order. The results compared favorably with theories describing the coagulation process of aerosols.

  2. Cytogenetic effects of cigarette smoke on pulmonary alveolar macrophages of the rat

    International Nuclear Information System (INIS)

    This study was part of a larger investigation of the health effects resulting from different methods of exposing rats to cigarette smoke. Cytogenetic effects of cigarette smoke on rat pulmonary alveolar macrophages (PAMs) were evaluated. Fischer 344/N, male rats (4/group) were randomly assigned to 5 different exposure groups: (1) nose-only sham-exposed control, (2) whole-body sham-exposed control, (3) nose-only intermittent, (4) nose-only continuous, and (5) whole-body continuous. Sham controls were exposed to clean air. PAMs were obtained by lung lavage and chromosomal damage was measured. Multiple comparison demonstrated no significant differences between smoke-exposed groups and their respective sham-exposed controls, between the sham-exposed groups, or among the three smoke exposed groups. Highly significant smoke-induced differences in both structural and numerical aberrations were observed when data for the respective control groups and exposed groups were pooled and compared. Results from this study demonstrate the clastogenicity of cigarette smoke on rat PAM. (author)

  3. 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.

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

    Science.gov (United States)

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

    2016-01-01

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

  5. 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.

  6. Cigarette smoking and drug use in schoolchildren: IV--factors associated with changes in smoking behaviour.

    Science.gov (United States)

    Alexander, H M; Callcott, R; Dobson, A J; Hardes, G R; Lloyd, D M; O'Connell, D L; Leeder, S R

    1983-03-01

    Factors associated with changes in the smoking behaviour of approximately 6000 schoolchildren (two cohorts aged between 10 and 12 years in 1979) over 12 months are described. They were measured twice as part of a randomized controlled trial of a smoking prevention programme. Four groups were defined: (a) those who became smokers (adopters); (b) those who remained non-smokers; (c) those who became non-smokers (quitters), and, (d) those who remained smokers. Personal and social variables were ordered using a logistic regression model according to the strength of their association with adopting and quitting smoking. Factors distinguishing adopters from children who remained nonsmokers were, being a member of the older cohort, having friends who smoke, having siblings who smoke, approving of cigarette advertising and having a relatively large amount of money to spend each week. Factors distinguishing quitters from children who continued to smoke were, having siblings who do not smoke, being a member of the younger cohort, disapproving of cigarette advertising and having a relatively small amount of money to spend each week. Initial attitude scores were indicative of future smoking behaviour and where smoking behaviour changed, attitudes also changed so that the two remained congruent. The younger cohort improved their knowledge of smoking hazards over the year irrespective of their smoking behaviour. The older cohort showed significant differences in knowledge which were dependent upon smoking category, with 1980 smokers having lower knowledge scores than non-smokers and showing an apparent decrement in their previous knowledge. PMID:6341272

  7. 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.

  8. GENOTOXICITY OF TEN CIGARETTE SMOKE CONDENSATES IN FOUR TEST SYSTEMS: COMPARISONS BETWEEN ASSAYS AND CONDENSATES

    Science.gov (United States)

    What is the study? This the first assessment of a set of cigarette smoke condensates from a range of cigarette types in a variety (4) of short-term genotoxicity assays. Why was it done? No such comparative study of cigarette smoke condensates has been reported. H...

  9. GENOTOXICITY OF TEN CIGARETTE SMOKE CONDENSATES IN FOUR TEST SYSTEMS: COMPARISONS AMONG ASSAYS AND CONDENSATES

    Science.gov (United States)

    The particulate fraction of cigarette smoke, cigarette smoke condensate (CSC), is genotoxic in many short-term in vitro tests and carcinogenic in rodents. However, no study has evaluatedd a set of CSCs prepared from a diverse set of cigarettes in a variety of short-term genotoxic...

  10. Influence of cigarette smoking on human autonomic function

    Science.gov (United States)

    Niedermaier, O. N.; Smith, M. L.; Beightol, L. A.; Zukowska-Grojec, Z.; Goldstein, D. S.; Eckberg, D. L.

    1993-01-01

    BACKGROUND. Although cigarette smoking is known to lead to widespread augmentation of sympathetic nervous system activity, little is known about the effects of smoking on directly measured human sympathetic activity and its reflex control. METHODS AND RESULTS. We studied the acute effects of smoking two research-grade cigarettes on muscle sympathetic nerve activity and on arterial baroreflex-mediated changes of sympathetic and vagal neural cardiovascular outflows in eight healthy habitual smokers. Measurements were made during frequency-controlled breathing, graded Valsalva maneuvers, and carotid baroreceptor stimulation with ramped sequences of neck pressure and suction. Smoking provoked the following changes: Arterial pressure increased significantly, and RR intervals, RR interval spectral power at the respiratory frequency, and muscle sympathetic nerve activity decreased. Plasma nicotine levels increased significantly, but plasma epinephrine, norepinephrine, and neuropeptide Y levels did not change. Peak sympathetic nerve activity during and systolic pressure overshoots after Valsalva straining increased significantly in proportion to increases of plasma nicotine levels. The average carotid baroreceptor-cardiac reflex relation shifted rightward and downward on arterial pressure and RR interval axes; average gain, operational point, and response range did not change. CONCLUSIONS. In habitual smokers, smoking acutely reduces baseline levels of vagal-cardiac nerve activity and completely resets vagally mediated arterial baroreceptor-cardiac reflex responses. Smoking also reduces muscle sympathetic nerve activity but augments increases of sympathetic activity triggered by brief arterial pressure reductions. This pattern of autonomic changes is likely to influence smokers' responses to acute arterial pressure reductions importantly.

  11. Adenomatous Polyposis Coli-Mediated Accumulation of Abasic DNA Lesions Lead to Cigarette Smoke Condensate-Induced Neoplastic Transformation of Normal Breast Epithelial Cells

    Directory of Open Access Journals (Sweden)

    Aruna S. Jaiswal

    2013-04-01

    Full Text Available Adenomatous polyposis coli (APC is a multifunctional protein having diverse cellular functions including cell migration, cell-cell adhesion, cell cycle control, chromosomal segregation, and apoptosis. Recently, we found a new role of APC in base excision repair (BER and showed that it interacts with DNA polymerase β and 5′-flap endonuclease 1 and interferes in BER. Previously, we have also reported that cigarette smoke condensate (CSC increases expression of APC and enhances the growth of normal human breast epithelial (MCF10A cells in vitro. In the present study, using APC overexpression and knockdown systems, we have examined the molecular mechanisms by which CSC and its major component, Benzo[α]pyrene, enhances APC-mediated accumulation of abasic DNA lesions, which is cytotoxic and mutagenic in nature, leading to enhanced neoplastic transformation of MCF10A cells in an orthotopic xenograft model.

  12. Cytogenetic effects of the gaseous phase of cigarette smoke on root-tip cells of Allium sativum L

    Energy Technology Data Exchange (ETDEWEB)

    Pandey, K.N.; Benner, J.F.; Sabharwal, P.S.

    1978-02-01

    Chromosomal and mitotic abnormalities induced by the gaseous phase of cigarette smoke on the root-tips of garlic, Allium sativum L., were investigated. Chromosomal abnormalities in the form of breakages, bridges, lags, stickiness, and differential condensation were observed. In addition, multinucleate cells, polyploid cells, and multipolar mitotic divisions were observed. In general the results indicate that the percentage of abnormalities increased when root-tips were exposed to higher numbers of smoke puffs. The effect of the gaseous phase of cigarette smoke on the mitotic index is striking. It shows a slight increase at a low number of puffs and a decrease at high numbers, particularly at the 10, 15 and 20 puff levels. The results indicate that the gaseous phase of cigarette smoke induces significant effects on chromosome structure and number.

  13. The use of bupropion SR in cigarette smoking cessation

    Directory of Open Access Journals (Sweden)

    Scott Wilkes

    2008-03-01

    Full Text Available Scott WilkesDepartment of Primary and Community Care, School of Health, Natural and Social Sciences, University of Sunderland, Sunderland, United KingdomAbstract: Cigarette smoking remains the largest preventable cause of premature death in developed countries. Until recently nicotine replacement therapy (NRT has been the only recognised form of treatment for smoking cessation. Bupropion, the first non-nicotine based drug for smoking cessation was licensed in the United States of America (US in 1997 and in the United Kingdom (UK in 2000 for smoking cessation in people aged 18 years and over. Bupropion exerts its effect primarily through the inhibition of dopamine reuptake into neuronal synaptic vesicles. It is also a weak noradrenalin reuptake inhibitor and has no effect on the serotonin system. Bupropion has proven efficacy for smoking cessation in a number of clinical trials, helping approximately one in five smokers to stop smoking. Up to a half of patients taking bupropion experience side effects, mainly insomnia and a dry mouth, which are closely linked to the nicotine withdrawal syndrome. Bupropion is rarely associated with seizures however care must be taken when co-prescribing with drugs that can lower seizure threshold. Also, bupropion is a potent enzyme inhibitor and can raise plasma levels of some drugs including antidepressants, antiarrhythmics and antipsychotics. Bupropion has been shown to be a safe and cost effective smoking cessation agent. Despite this, NRT remains the dominant pharmacotherapy to aid smoking cessation.Keywords: bupropion, smoking cessation, nicotine addiction

  14. The Effects of Cigarette Smoke Condensate and Nicotine on Periodontal Tissue in a Periodontitis Model Mouse.

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    Mikiko Kubota

    Full Text Available Cigarette smoking is a major lifestyle-related risk factor for periodontal diseases. However, the pathophysiological role of cigarette smoking in periodontal disease has yet to be fully elucidated. Here we report that the systemic administration of cigarette smoke condensate or nicotine, which is the major ingredient of cigarette smoke, augmented alveolar bone loss. Concomitantly, the number of osteoclasts in periodontal tissues increased and the expression of receptor activator of nuclear factor κB ligand was upregulated at the ligated side in mice with periodontitis. Nicotine also attenuated alveolar bone repair after ligature removal. These observations highlight the destruction of periodontal tissue by smoking and the unfavorable clinical course of periodontal disease in patients with a cigarette smoking habit. The present study demonstrates that periodontal disease models are useful for elucidating the pathogenesis of cigarette smoking-related periodontal diseases.

  15. Microscopical examination of particles on smoked cigarette filters.

    Science.gov (United States)

    Linch, Charles A; Prahlow, Joseph A

    2008-01-01

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

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

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    Konopa Krzysztof

    2006-07-01

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

  17. Waterpipe Tobacco Smoking and Susceptibility to Cigarette Smoking Among Young Adults in the United States, 2012–2013

    Science.gov (United States)

    Haider, M. Rifat; Barnett, Tracey E.; Guo, Yi; Getz, Kayla R.; Thrasher, James F.; Maziak, Wasim

    2016-01-01

    Introduction Waterpipe tobacco smoking, also known as hookah and shisha, has surged in popularity among young people in the United States. Waterpipe is also increasingly becoming the first tobacco product that young people try. Given the limited access to and limited portability of waterpipes, waterpipe smokers who become more nicotine dependent over time may be more likely to turn to cigarettes. This study examined the relationship between waterpipe tobacco smoking and susceptibility to cigarette smoking among young adults in the United States. Methods Using data from the 2012–2013 National Adult Tobacco Survey, a nationally representative sample of US adults, we reported rates of current waterpipe smoking and susceptibility to cigarette smoking by demographic characteristics and by use of other tobacco products among survey participants aged 18 to 24 years. Multivariable logistic regression was used to examine the relationship between current waterpipe smoking and susceptibility to cigarette smoking, defined as the lack of a firm intention not to smoke soon or within the next year. Results Of 2,528 young adults who had never established cigarette smoking, 15.7% (n = 398) reported being waterpipe smokers (every day or some days [n = 97; 3.8%] or rarely [n = 301; 11.9%]); 44.2% (176/398) of waterpipe smokers reported being susceptible to cigarette smoking. Those who smoked waterpipe rarely were 2.3 times as susceptible to cigarette smoking as those who were not current waterpipe smokers (OR = 2.3; 95% CI, 1.6–3.4). Conclusion Current waterpipe smoking is associated with susceptibility to cigarette smoking among young adults in the United States. Longitudinal studies are needed to demonstrate causality between waterpipe smoking and initiation of cigarette smoking. PMID:26890407

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

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    Zakarya Bani Meri

    2013-01-01

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

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

    Science.gov (United States)

    Doherty, W J; Whitehead, D A

    1986-09-01

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

  20. Effects of elastase and cigarette smoke on alveolar epithelial permeability

    International Nuclear Information System (INIS)

    To determine whether instilled porcine pancreatic elastase (PPE) increases alveolar epithelial permeability, the authors measured alveolar epithelium permeability X surface area (PS) for [14C]sucrose and 125I-bovine serum albumin in isolated perfused lungs from hamsters previously exposed to PPE and/or cigarette smoke. Saline (0.5 ml) with 0, 5, or 20 units PPE was instilled intratracheally in anesthetized hamsters. Those exposed to smoke for 4-6 wk received 0 or 5 units; PS was measured 3 h later. Nonsmokers received 0, 5, or 20 units; PS was measured 3 h, 24 h, or 5 days later. Control PS values were (cm3/s X 10(-4), +/- SE) 0.84 +/- 0.11 for sucrose and 0.030 +/- 0.006 for BSA. Three and 24 h following 20 units PPE, (PS)sucrose was twice the control valve. (PS)BSA was four times control at 3 h but not significantly increased at 24 h. Five days after PPE both were back to control levels. Five units PPE or smoke exposure alone caused no PS changes. Smoke exposure and 5 units PPE caused (PS)sucrose to increase markedly (1.85 +/- 0.32); (PS)BSA was not significantly increased (0.076 +/- 0.026). Thus, instilled PPE causes reversible increases in alveolar epithelial PS; cigarette smoking potentiates this effect

  1. Cigarette advertising and media coverage of smoking and health.

    Science.gov (United States)

    Warner, K E

    1985-02-01

    In the US, media coverage of the health hazards of cigarette smoking is consored by the tobacco industry. Tobacco companies, which in 1983 alone spent US$2.5 billion on smoking promtion, are a major source of advertising revenue for many media organizations. As a result media organizations frequently refuse to publish antismoking information, tent to tone down coverage of antismoking news events, and often refuse to accept antismoking advertisements. In a 1983 "Newsweek" supplement on personal health, prepared by the American Medical Association, only 4 sentences were devoted to the negative effects of smoking. A spokesman for the association reported that "Newsweek" editors refused to allow the association to use the forum to present a strong antismoking message. In 1984 a similar type of health supplement, published by "Time," failed to mention smoking at all. An examination of 10 major women's magazines revealed that between 1967-79, 4 of the magazines published no articles about the hazards of smoking and only 8 such articles appeared in the other 6 magazines. All of these magazines carried smoking advertisements. During the same time period, 2 magazines, which refused to publish cigarette ads, published a total of 16 articles on the hazards of smoking. Small magazines which publish antismoking articles are especially vulnerable to pressure from the tobacco industry. For example, the tobacco industry canceled all its ads in "Mother Jones" after the magazine printed 2 antismoking articles. 22 out of 36 magazines refused to run antismoking advertisements when they were requested to do so. Due to poor media coverage, th public's knowledge of the hazards of smoking is deficient. Recent surveys found that 2/3 of the public did not know that smoking could cause heart attacks, and 1/2 of the respondents did not know that smoking is the major cause of lung cancer. An analysis of time trends in cigarette smoking indicates that the public does respond to antismoking

  2. Teens Using E-cigarettes May Be More Likely to Start Smoking Tobacco

    Science.gov (United States)

    ... are more likely than others to start smoking traditional cigarettes and other combustible tobacco products within the ... regular cigarettes, they do carry a risk of addiction.” Data were collected as part of a longitudinal ...

  3. 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

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

    Science.gov (United States)

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

    2007-08-01

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

  5. Smoking, epidemiology and e-cigarettes

    Directory of Open Access Journals (Sweden)

    Raschke RA

    2013-07-01

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

  6. Cigarette Smoking, Passive Smoking, Alcohol Consumption, and Hearing Loss

    OpenAIRE

    DAWES, P

    2014-01-01

    The objective of this large population-based crosssectional study was to evaluate the association between smoking, passive smoking, alcohol consumption, and hearing loss. The study sample was a subset of the UK Biobank Resource, 164,770 adults aged between 40 and 69 years who completed a speech-in-noise hearing test (the Digit Triplet Test). Hearing loss was defined as speech recognition in noise in the better ear poorer than 2 standard deviations below the mean wit...

  7. Detection of reactive oxygen species in mainstream cigarette smoke by a fluorescent probe

    Science.gov (United States)

    Liu, Li; Xu, Shi-jie; Li, Song-zhan

    2009-07-01

    A mass of reactive oxygen species(ROS) are produced in the process of smoking. Superfluous ROS can induce the oxidative stress in organism, which will cause irreversible damage to cells. Fluorescent probe is taken as a marker of oxidative stress in biology and has been applied to ROS detection in the field of biology and chemistry for high sensitivity, high simplicity of data collection and high resolution. As one type of fluorescent probe, dihydrorhodamine 6G (dR6G) will be oxidized to the fluorescent rhodamine 6G, which could be used to detect ROS in mainstream cigarette smoke. We investigated the action mechanism of ROS on dR6G, built up the standard curve of R6G fluorescence intensity with its content, achieved the variation pattern of R6G fluorescence intensity with ROS content in mainstream cigarette smoke and detected the contents of ROS from the 4 types of cigarettes purchased in market. The result shows that the amount of ROS has close relationship with the types of tobacco and cigarette production technology. Compared with other detecting methods such as electronic spin resonance(ESR), chromatography and mass spectrometry, this detection method by the fluorescent probe has higher efficiency and sensitivity and will have wide applications in the ROS detection field.

  8. Cigarette smoking, passive smoking, alcohol consumption, and hearing loss.

    Science.gov (United States)

    Dawes, Piers; Cruickshanks, Karen J; Moore, David R; Edmondson-Jones, Mark; McCormack, Abby; Fortnum, Heather; Munro, Kevin J

    2014-08-01

    The objective of this large population-based cross-sectional study was to evaluate the association between smoking, passive smoking, alcohol consumption, and hearing loss. The study sample was a subset of the UK Biobank Resource, 164,770 adults aged between 40 and 69 years who completed a speech-in-noise hearing test (the Digit Triplet Test). Hearing loss was defined as speech recognition in noise in the better ear poorer than 2 standard deviations below the mean with reference to young normally hearing listeners. In multiple logistic regression controlling for potential confounders, current smokers were more likely to have a hearing loss than non-smokers (odds ratio (OR) 1.15, 95 % confidence interval (CI) 1.09-1.21). Among non-smokers, those who reported passive exposure to tobacco smoke were more likely to have a hearing loss (OR 1.28, 95 %CI 1.21-1.35). For both smoking and passive smoking, there was evidence of a dose-response effect. Those who consume alcohol were less likely to have a hearing loss than lifetime teetotalers. The association was similar across three levels of consumption by volume of alcohol (lightest 25 %, OR 0.61, 95 %CI 0.57-0.65; middle 50 % OR 0.62, 95 %CI 0.58-0.66; heaviest 25 % OR 0.65, 95 %CI 0.61-0.70). The results suggest that lifestyle factors may moderate the risk of hearing loss. Alcohol consumption was associated with a protective effect. Quitting or reducing smoking and avoiding passive exposure to tobacco smoke may also help prevent or moderate age-related hearing loss. PMID:24899378

  9. 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).

  10. Comparison of three methods of exposing rats to cigarette smoke

    International Nuclear Information System (INIS)

    We compared smoke composition and biological effects resulting from exposures of rats for 5 wk to cigarette smoke by nose-only intermittent (NOI), nose-only continuous (NOC) and whole-body continuous (WBC) exposure methods. Exposure concentrations and times were adjusted to achieve the same daily concentration x time product for particulate matter. There were few differences in smoke composition or biological effects among exposure modes. WBC smoke was lower in particle-borne nicotine and higher in some organic vapors and carbon monoxide than smoke in nose-only modes. Body weight was depressed less by WBC than by NOI or NOC exposures. Plasma and urine nicotine levels were higher for WBC than for NOI or NOC, suggesting greater absorption from body surfaces or by grooming. Smoke exposures increased nasal epithelial proliferation, tracheal epithelial cell transformation, chromosomal aberrations in alveolar macrophages, and lung DNA adduct levels, and caused inflammatory changes in airway fluid and slight alterations of respiratory function, but there were no significant differences among exposure modes. The results indicate that WBC exposures should produce long-term effects similar to those of nose-only exposures, but might allow increased delivery of smoke to lungs while reducing stress, acute toxicity and the manpower requirements associated with performing these experiments. (author)

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

    Science.gov (United States)

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

    2007-10-01

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

  12. Cigarette smoke extracts inhibit prostacyclin synthesis by the rat urinary bladder.

    OpenAIRE

    Jeremy, J Y; Mikhailidis, D P; Dandona, P

    1985-01-01

    Since prostacyclin (PGI2) is known to have a cytoprotective effect on epithelia, and since cigarette smoking is associated with an increased risk of bladder cancer, we investigated the possibility that nicotine, cotinine (the principal metabolite of nicotine) and other components of cigarette smoke inhibit PGI2 secretion by the urinary bladder. Using the rat urinary bladder as a model, we found that cigarette smoke extracts, but not nicotine or cotinine, inhibit in vitro PGI2 synthesis. 2-Nap...

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

    OpenAIRE

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

    2014-01-01

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

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

    LENUS (Irish Health Repository)

    O'Cathail, S M

    2011-05-01

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

  15. Absorption of cholesterol and beta-sitosterol from cigarette smoke in Macaca mulatta

    Energy Technology Data Exchange (ETDEWEB)

    Malinow, M.R.; McLaughlin, P.; Aigner-Held, R.; Upson, B.; Isabelle, L.M.; Connor, W.E.; Lin, D.

    1986-04-01

    When smoke from single cigarettes containing (4-/sup 14/C)cholesterol or beta-(4-/sup 14/C)sitosterol was delivered to the lungs of Rhesus macaques, plasma contained radiolabeled sterols up to 50 days later. Since cholesterol, as well as plant sterols (campesterol, stigmasterol and beta-sitosterol), are normally present in cigarette smoke, our observations suggest that protracted absorption of sterols occurs after cigarette smoking.

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1979-05-01

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

  17. 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.

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

    Institute of Scientific and Technical Information of China (English)

    ZHOU Wen; XU Ying; WANG Dongfeng; ZHOU Shilu

    2013-01-01

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

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

    OpenAIRE

    Konopa Krzysztof; Jassem Ewa; Sieminska Alicja

    2006-01-01

    Abstract Background In the last decade Poland has successfully carried out effective anti-tobacco campaigns and introduced tobacco control legislation. This comprehensive strategy has focused on the general population and has led to a considerable decrease in tobacco consumption. Prisoners constitute a relatively small part of the entire Polish population and smoking habits in this group have been given little attention. The aim of the study was to assess the prevalence of cigarette smoking i...

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

    Science.gov (United States)

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

    2014-06-01

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

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

    Directory of Open Access Journals (Sweden)

    Gaur Dushyant

    2010-01-01

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

  2. Smoking, but not smokers: identity among college students who smoke cigarettes.

    Science.gov (United States)

    Levinson, Arnold H; Campo, Shelly; Gascoigne, Jan; Jolly, Olivia; Zakharyan, Armen; Tran, Zung Vu

    2007-08-01

    Cigarette smoking in college is often described as social smoking, but the term lacks definition and implicitly discounts dependence. We report on college students' use of the terms social smoker and smoker. Students who currently smoked cigarettes were asked whether they considered themselves smokers, and whether they smoked because they were social smokers. The survey was conducted during 1999-2004 at eight colleges; analysis was limited to 1,401 students aged 18-24 years. More than half of students (56.3%) denied being smokers ("deniers") despite current smoking behavior. Half of deniers, and fewer than half of admitters, called themselves social smokers. Deniers were highly likely to smoke infrequently, to say they were not addicted to cigarettes, to have mostly nonsmokers as close friends, to prefer dating nonsmokers, and to smoke for reasons other than stress relief. In contrast, social-smoker identity was associated only weakly with any attitude, behavior, or belief. Smoker and social-smoker identities were not significantly correlated with each other. Regardless of identity, more than half of the respondents wanted to quit smoking by graduation. Results suggest that denying being a smoker may be a widespread dissonance among college students who smoke. The possibility should be evaluated using population-level research, because it has potentially undermining implications for smoking cessation campaigns. Campus health centers should avoid using "smoker" self-assessment items on pre-exam questionnaires. Further research is needed to explore the psychosocial mechanisms involved with denier identity, to clarify the implications for public health communications, and to develop appropriate intervention strategies. PMID:17654297

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

    Science.gov (United States)

    Cui, Yanping; Ying, Mao; Fan, Hongqi

    2012-01-01

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

  4. Telephone surveys underestimate cigarette smoking among African-Americans

    Directory of Open Access Journals (Sweden)

    Hope eLandrine

    2013-09-01

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

  5. 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. PMID:27407178

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

    Science.gov (United States)

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

    1983-10-01

    Cadmium has been determined in 26 brands of cigarettes purchased in eight different countries throughout the world and in 16 different samples of cigarettes produced in Sweden between 1918 and 1968. In addition the amount of cadmium released from smoking one cigarette to the particulate phase collected from a smoking simulation machine, corresponding to the amount actually inhaled by a smoker, has been determined. The cadmium concentration in different brands of cigarettes ranged from 0.19 to 3.0 micrograms Cd/g dry wt, with a general tendency toward lower values in cigarettes from developing countries. No systematic change in the cadmium concentration of cigarettes with time could be revealed. The amount of cadmium inhaled from smoking one cigarette containing about 1.7 microgram Cd was estimated to be 0.14 to 0.19 microgram, corresponding to about 10% of the total cadmium content in the cigarette. PMID:6617614

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

    DEFF Research Database (Denmark)

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

    2009-01-01

    BACKGROUND: Cigarette smoking increases the risk of cardiovascular events related with several mechanisms. The most suggested mechanism is increased activity of sympathetic nervous system. Heart rate variability (HRV) and heart rate turbulence (HRT) has been shown to be independent and powerful...... predictors of mortality in a specific group of cardiac patients. The goal of this study was to assess the effect of heavy cigarette smoking on cardiac autonomic function using HRV and HRT analyses. METHODS: Heavy cigarette smoking was defined as more than 20 cigarettes smoked per day. Heavy cigarette smokers...... than control group (23 vs 10, P = 0.006). TO was correlated with the number of cigarettes smoked per day (r = 0.235, P = 0.004). While LF and LF/HF ratio were significantly higher, standard deviation of all NN intervals (SDNN), standard deviation of the 5-minute mean RR intervals (SDANN), root mean...

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

    Directory of Open Access Journals (Sweden)

    Michael A Ha

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

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

    Science.gov (United States)

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

    2015-01-01

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

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

    OpenAIRE

    Erika B Fulmer; Torsten B Neilands; Dube, Shanta R.; Kuiper, Nicole M.; Arrazola, Rene A.; Glantz, Stanton A.

    2015-01-01

    Purpose Youth are exposed to many types of protobacco influences, including smoking in movies, which has been shown to cause initiation. This study investigates associations between different channels of protobacco media and susceptibility to smoking cigarettes, cigarette experimentation, and current tobacco use among US middle and high school students. Methods By using data from the 2012 National Youth Tobacco Survey, structural equation modeling was performed in 2013. The analyses examined ...

  11. Cigarette Smoking Among Socioeconomically Disadvantaged Young Adults in Association With Food Insecurity and Other Factors

    OpenAIRE

    Kim, Jin E.; Tsoh, Janice Y.

    2016-01-01

    Introduction Low socioeconomic status is associated with high rates of cigarette smoking, and socioeconomic differences in cigarette smoking tend to emerge during young adulthood. To further our understanding of socioeconomic differences in smoking among young adults, we examined correlates of smoking, with attention to multiple socioeconomic indicators that have not been examined in this population. Methods We analyzed data from the 2011–2012 California Health Interview Survey. The analytic ...

  12. Cigarette Smoking Among Socioeconomically Disadvantaged Young Adults in Association With Food Insecurity and Other Factors

    OpenAIRE

    Jin E. Kim, PhD; Janice Y. Tsoh, PhD

    2016-01-01

    Introduction Low socioeconomic status is associated with high rates of cigarette smoking, and socioeconomic differences in cigarette smoking tend to emerge during young adulthood. To further our understanding of socioeconomic differences in smoking among young adults, we examined correlates of smoking, with attention to multiple socioeconomic indicators that have not been examined in this population. Methods We analyzed data from the 2011–2012 California Health Interview Survey. T...

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

    Directory of Open Access Journals (Sweden)

    Daniel A. Gundersen

    2012-01-01

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

  14. CT findings of respiratory bronchiolitis caused by cigarette smoking

    Energy Technology Data Exchange (ETDEWEB)

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

    1998-07-01

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

  15. The Length of Cigarette Smoking is the Principal Risk Factor for Developing COPD

    Directory of Open Access Journals (Sweden)

    Senaida Bišanović

    2012-01-01

    Full Text Available Background: The deterioration in lung function associated with Chronic Obstructive Pulmonary Disease (COPD is directly related to duration of smoking and the number of cigarettes smoked. Over 85% of lung cancers are attributed to smoking. The problem is, whether the length of smoking consumption period has more impact to COPD and lung cancer than the bigger number of cigarettes smoked per day?Examinees and methods: The sample has constituted of two groups of examinees, smokers, both gender, age 25-64 years old. The first group consisted of 240 examinees divided in 8 subgroups according to a number of years they have been smoking. The second group consisted of 180 examinees, which was divided in 6 subgroups, according to average number of cigarettes smoked daily during the smoking consumption period.Results: The prevalence of smoking was higher in men (65.7% vs. 62% than in women (34.3% vs. 38%. Smoking duration in the group of smokers according to the length of smoking consumption period was 20.34±10.63 y and in the group of smokers according to a number of cigarettes smoked daily 13.55±8.20y. COPD were registered as the most frequent lung disease, in the group of smokers according to a number of cigarettes smoked per day 52.2% and in the group according to the length of smoking consumption period 39.1%, and the middle values of FEV1 (82.77% vs. 97.64%, and FEV1/FVC (86.02% vs. 97.73% were lower in the group of smokers according to a number of cigarettes smoked.Conclusion: Chronic respiratory symptoms, impairment of lung function and diagnosis of COPD depended more on the length of smoking duration than a number of cigarettes smoked.

  16. Differential effect of cigarette smoking on antipyrine oxidation versus acetaminophen conjugation.

    Science.gov (United States)

    Scavone, J M; Greenblatt, D J; LeDuc, B W; Blyden, G T; Luna, B G; Harmatz, J S

    1990-01-01

    The effect of cigarette smoking on drug oxidation and conjugation was studied using antipyrine and acetaminophen as marker compounds. For the antipyrine study, healthy cigarette smokers (n = 30) and nonsmoking controls (n = 53) received a single 1.0-gram intravenous dose of antipyrine. For the acetaminophen study, 14 smokers and 15 nonsmokers received a 650-mg intravenous dose of acetaminophen. The clearance of antipyrine was significantly increased (0.93 vs. 0.60 ml/min/kg, p less than 0.0001) and elimination half-life was correspondingly reduced (8.9 vs. 13.0 h, p less than 0.0001) in smokers compared to nonsmoking controls. Total recovery of antipyrine and metabolites excreted in urine did not differ between groups, but there was a significantly increased fractional clearance of antipyrine via formation of 4-hydroxyantipyrine and 3-hydroxymethyl metabolites in smokers. Fractional clearance via formation of norantipyrine did not differ significantly between groups. Comparison of acetaminophen kinetics between smokers and nonsmokers indicated no significant differences in elimination half-life, clearance or volume of distribution. Thus, cigarette smoking is more likely to induce drug oxidation rather than drug conjugation. However, not all oxidative pathways are equally influenced; induction effects of smoking are highly substrate selective and pathway specific. PMID:2345775

  17. Nontypeable Haemophilus influenzae Clearance by Alveolar Macrophages Is Impaired by Exposure to Cigarette Smoke ▿ †

    Science.gov (United States)

    Martí-Lliteras, Pau; Regueiro, Verónica; Morey, Pau; Hood, Derek W.; Saus, Carles; Sauleda, Jaume; Agustí, Alvar G. N.; Bengoechea, José Antonio; Garmendia, Junkal

    2009-01-01

    Nontypeable Haemophilus influenzae (NTHI) is an opportunistic gram-negative pathogen that causes respiratory infections and is associated with progression of respiratory diseases. Cigarette smoke is a main risk factor for development of respiratory infections and chronic respiratory diseases. Glucocorticoids, which are anti-inflammatory drugs, are still the most common therapy for these diseases. Alveolar macrophages are professional phagocytes that reside in the lung and are responsible for clearing infections by the action of their phagolysosomal machinery and promotion of local inflammation. In this study, we dissected the interaction between NTHI and alveolar macrophages and the effect of cigarette smoke on this interaction. We showed that alveolar macrophages clear NTHI infections by adhesion, phagocytosis, and phagolysosomal processing of the pathogen. Bacterial uptake requires host actin polymerization, the integrity of plasma membrane lipid rafts, and activation of the phosphatidylinositol 3-kinase (PI3K) signaling cascade. Parallel to bacterial clearance, macrophages secrete tumor necrosis factor alpha (TNF-α) upon NTHI infection. In contrast, exposure to cigarette smoke extract (CSE) impaired alveolar macrophage phagocytosis, although NTHI-induced TNF-α secretion was not abrogated. Mechanistically, our data showed that CSE reduced PI3K signaling activation triggered by NTHI. Treatment of CSE-exposed cells with the glucocorticoid dexamethasone reduced the amount of TNF-α secreted upon NTHI infection but did not compensate for CSE-dependent phagocytic impairment. The deleterious effect of cigarette smoke was observed in macrophage cell lines and in human alveolar macrophages obtained from smokers and from patients with chronic obstructive pulmonary disease. PMID:19620348

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

    Science.gov (United States)

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

    2012-01-01

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

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

    Science.gov (United States)

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

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

    NARCIS (Netherlands)

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

    2014-01-01

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

  1. Application of Cigarette Smoke Characterisation Based on Optical Aerosol Spectrometry. Dynamics and Comparisons with Tar Values

    NARCIS (Netherlands)

    Dijk, W.D. van; Cremers, R.; Klerx, W.; Schermer, T.R.J.; Scheepers, P.T.J.

    2012-01-01

    Introduction: Cigarette smoking causes devastating disease worldwide. Current cigarette classification is based on standardised tar mass values obtained from smoking-machines. However, their ability to predict disease is poor, and these mass values are primarily determined by larger particles. The a

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

    Science.gov (United States)

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

    2013-01-01

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

  3. 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.

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

    Energy Technology Data Exchange (ETDEWEB)

    Rotenberg, K.S.; Adir, J.

    1983-06-15

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

  5. The remarkable decrease in cigarette smoking by American youth: Further evidence

    Directory of Open Access Journals (Sweden)

    Kenneth E. Warner

    2015-01-01

    Conclusion: Cigarette smoking, the most dangerous form of tobacco use, has decreased dramatically among American students. The fact that decreases are larger for more intensive measures of smoking indicates that simply tracking 30-day prevalence, often labeled “current smoking,” significantly understates the decrease in youth smoking over time.

  6. 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…

  7. Cigarette smoking causes hearing impairment among Bangladeshi population.

    Directory of Open Access Journals (Sweden)

    Ahmed Faisal Sumit

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

  8. SPONTANEOUS TUMORS IN MICE EXPOSED TO CIGARETTE SECOND-HAND SMOKE

    OpenAIRE

    Tume, L.F.

    2014-01-01

    Cigarette smoke inhaled second-hand is common with different types of cigarettes and can lead to an increased risk of developing tumors if the frequency is constant. In this experiment a group of four individuals (Mus musculus) were exposed to second-handcigarettesmoke three times a week for four months; later the occurrence of spontaneous tumors was observed in contrast to the control group. This study provides further evidence that second-hand cigarette smoke has components t...

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

    Science.gov (United States)

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

    2015-04-01

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

  10. Current cigarette smoking among adults--United States, 2005-2013.

    Science.gov (United States)

    Jamal, Ahmed; Agaku, Israel T; O'Connor, Erin; King, Brian A; Kenemer, John B; Neff, Linda

    2014-11-28

    Tobacco use is the leading cause of preventable disease and death in the United States, resulting in more than 480,000 premature deaths and $289 billion in direct health care expenditures and productivity losses each year. Despite progress over the past several decades, millions of adults still smoke cigarettes, the most commonly used tobacco product in the United States. To assess progress made toward the Healthy People 2020 target of reducing the proportion of U.S. adults who smoke cigarettes to ≤12.0% (objective TU-1.1), CDC used data from the 2013 National Health Interview Survey (NHIS) to provide updated national estimates of cigarette smoking prevalence among adults aged ≥18 years. Additionally, for the first time, estimates of cigarette smoking prevalence were assessed among lesbian, gay, or bisexual persons (LGB) using NHIS data. The proportion of U.S. adults who smoke cigarettes declined from 20.9% in 2005 to 17.8% in 2013, and the proportion of daily smokers declined from 16.9% to 13.7%. Among daily cigarette smokers, the proportion who smoked 20-29 cigarettes per day (CPD) declined from 34.9% to 29.3%, and the proportion who smoked ≥30 CPD declined from 12.7% to 7.1%. However, cigarette smoking remains particularly high among certain groups, including adults who are male, younger, multiracial or American Indian/Alaska Native, have less education, live below the federal poverty level, live in the South or Midwest, have a disability/limitation, or who are LGB. Proven population-based interventions, including tobacco price increases, comprehensive smoke-free policies in worksites and public places, high-impact anti-tobacco mass media campaigns, and easy access to smoking cessation assistance, are critical to reducing cigarette smoking and smoking-related disease and death among U.S. adults, particularly among subpopulations with the greatest burden. PMID:25426653

  11. Inhalation of {sup 210}Po and {sup 210}Pb from cigarette smoking in Poland

    Energy Technology Data Exchange (ETDEWEB)

    Skwarzec, B. E-mail: bosk@chemik.chem.univ.gda.pl; Ulatowski, J.; Struminska, D.I.; Borylo, A

    2001-07-01

    The carcinogenic effect of {sup 210}Po and {sup 210}Pb with respect to lung cancer is an important problem in many countries with very high cigarette consumption. Poland has one of the highest consumptions of cigarettes in the world. The results of {sup 210}Po determination on the 14 most frequently smoked brands of cigarettes which constitute over 70% of the total cigarette consumption in Poland are presented and discussed. Moreover, the polonium content in cigarette smoke was estimated on the basis of its activity in fresh tobaccos, ash, fresh filters and post-smoking filters. The annual effective doses were calculated on the basis of {sup 210}Po and {sup 210}Pb inhalation with the cigarette smoke. The results of this work indicate that Polish smokers who smoke one pack (20 cigarettes) per day inhale from 20 to 215 mBq of {sup 210}Po and {sup 210}Pb each. The mean values of the annual effective dose for smokers were estimated to be 35 and 70 {mu}Sv from {sup 210}Po and {sup 210}Pb, respectively. For persons who smoke two packs of cigarettes with higher radionuclide concentrations, the effective dose is much higher (471 {mu}Sv yr{sup -1}) in comparison with the intake in diet. Therefore, cigarettes and the absorption through the respiratory system are the main sources and the principal pathway of {sup 210}Po and {sup 210}Pb intake of smokers in Poland.

  12. 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.

  13. Cigarette smoke promotes drug resistance and expansion of cancer stem cell-like side population.

    Directory of Open Access Journals (Sweden)

    Yi An

    Full Text Available It is well known that many patients continue to smoke cigarettes after being diagnosed with cancer. Although smoking cessation has typically been presumed to possess little therapeutic value for cancer, a growing body of evidence suggests that continued smoking is associated with reduced efficacy of treatment and a higher incidence of recurrence. We therefore investigated the effect of cigarette smoke condensate (CSC on drug resistance in the lung cancer and head and neck cancer cell lines A549 and UMSCC-10B, respectively. Our results showed that CSC significantly increased the cellular efflux of doxorubicin and mitoxantrone. This was accompanied by membrane localization and increased expression of the multi-drug transporter ABCG2. The induced efflux of doxorubicin was reversed upon addition of the specific ABCG2 inhibitor Fumitremorgin C, confirming the role of ABCG2. Treatment with CSC increased the concentration of phosphorylated Akt, while addition of the PI3K inhibitor LY294002 blocked doxorubicin extrusion, suggesting that Akt activation is required for CSC-induced drug efflux. In addition, CSC was found to promote resistance to doxorubicin as determined by MTS assays. This CSC-induced doxurbicin-resistance was mitigated by mecamylamine, a nicotinic acetylcholine receptor inhibitor, suggesting that nicotine is at least partially responsible for the effect of CSC. Lastly, CSC increased the size of the side population (SP, which has been linked to a cancer stem cell-like phenotype. In summary, CSC promotes chemoresistance via Akt-mediated regulation of ABCG2 activity, and may also increase the proportion of cancer stem-like cells, contributing to tumor resilience. These findings underscore the importance of smoking cessation following a diagnosis of cancer, and elucidate the mechanisms of continued smoking that may be detrimental to treatment.

  14. Are the predictors of hookah smoking differ from those of cigarette smoking? report of a population-based study in Shiraz, Iran, 2010

    Directory of Open Access Journals (Sweden)

    Gholamreza Abdollahifard

    2013-01-01

    Results: Response rate was 98%. Prevalence of cigarette smoking was 9.7%. Among cigarette users, 12.6% reported smoking 2 years. Almost half of those surveyed (48.9% smoked 20 cpd. Almost a quarter (20.4% of the cigarette smokers tried to quit in the past year. Being male, married, aged 37-54, having higher perceived levels of stress, a non-manual occupation, and sedentary lifestyle were positively associated with cigarette smoking. Manual labor occupations, housewife/jobless status, and going frequently to restaurants were positive predictors of hookah smoking. Conclusions: Compared to cigarettes, hookah smoking was more prevalent among Iranian adults. Approximately, the prevalence of hookah smoking in women is the same as men, whereas cigarette use was 31 times more common in men. Cigarette and hookah smoking were associated with less healthy lifestyle habits in both men and women.

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2010-01-04

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

  16. Behavioral filter vent blocking on the first cigarette of the day predicts which smokers of light cigarettes will increase smoke exposure from blocked vents.

    Science.gov (United States)

    Strasser, Andrew A; Tang, Kathy Z; Sanborn, Paul M; Zhou, Jon Y; Kozlowski, Lynn T

    2009-12-01

    Filter vent blocking on best-selling light cigarettes increases smoke yield during standard machine testing but not in clinical investigations of smokers. The purpose of the study was to investigate the effect of (a) manipulating cigarette filter vent blocking and (b) blocking status of first cigarette of the day on carbon monoxide (CO) boost. Participants (n = 25; Marlboro Lights nonmenthol cigarette smokers, age range 21-60 years, minimum 15 daily cigarettes, and daily smoking for a minimum 5 years) completed the laboratory-based, within-subject, double-blind, cross-over design of 2 smoking sessions, one utilizing a smoking topography device, one without. Each session consisted of smoking 4 cigarettes; 2 with filter vents blocked and 2 with filter vents unblocked. Spent first daily cigarette filters collected between sessions were scored for evidence of filter vent blocking. Smoking cigarettes with blocked filter vents significantly increased CO boost in both laboratory sessions (p < .001). Those who blocked their first cigarette of the day (n = 10) had significantly greater CO boost when smoking a blocked cigarette, in relation to smoking an unblocked cigarette and in comparison with nonblockers (p = .04). Total puff volume was a significant predictor of CO boost when smoking unblocked and blocked cigarettes (ps < .04). Blocking filter vents significantly increased smoke exposure in relation to when filter vents are not blocked, particularly for those who block filter vents on their first cigarette of the day. Total puff volume predicted CO boost, and results suggest that smokers adjust their smoking behavior by cigarette blocking status. Those smokers who block filter vents may be increasing their exposure by 30%. PMID:19968405

  17. 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.

  18. 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. PMID:26934369

  19. The Impact of Lending, Borrowing, and Anti-Smoking Policies on Cigarette Consumption by Teens

    OpenAIRE

    Brett Katzman; Sara Markowitz; Kerry Anne McGeary

    2002-01-01

    A major factor contributing to smoking initiation and experimentation by teenagers is the ability to 'bum' cigarettes. Yet research until now has ignored the impact of a lending/borrowing market on the smoking decisions of teenagers. In this paper, we develop a theoretical model where smoking decisions are determined by an individual's utility maximization process that includes an incentive to lend cigarettes. Predictions from this model are tested using data from the Youth Risk Behavior Surv...

  20. E-cigarettes as smoking cessation aids: a survey among practitioners in Italy

    OpenAIRE

    Lazuras, Lambros; Muzi, Milena; Grano, Caterina; Lucidi, Fabio

    2015-01-01

    Objectives To describe experiences with and beliefs about e-cigarettes as safe and useful aids for smoking cessation among healthcare professionals providing smoking cessation services. Methods Using a cross-sectional design, anonymous structured questionnaires were completed by 179 healthcare professionals in public smoking cessation clinics across 20 regions in Italy. Results Service providers reported that considerably more smokers made inquiries about e-cigarettes in 2014 than in 2013. Th...

  1. Mediators and moderators of magazine advertisement effects on adolescent cigarette smoking.

    Science.gov (United States)

    Aloise-Young, Patricia A; Slater, Michael D; Cruickshank, Courtney C

    2006-01-01

    The purpose of the present study is to examine the relation between magazine advertising for cigarettes and adolescent cigarette smoking. Participants (242 adolescents) reported their frequency of reading 46 magazines and their attention to cigarette ads. Recognition of cigarette ads, passive peer pressure (i.e., normative beliefs), and the smoker image also were assessed. Results indicate that exposure to cigarette advertising and recognition of ads augment the effect of passive peer pressure on smoking. In addition, a positive smoker image was associated with attention to advertising and mediated the relation between attention and smoking. It is suggested that the effect of magazine ads on adolescents should be considered in policymaking on cigarette advertising. PMID:16624795

  2. 76 FR 57008 - Smoking of Electronic Cigarettes on Aircraft

    Science.gov (United States)

    2011-09-15

    ... (including electronic cigarettes) to charter flights of air carriers (i.e. U.S. carriers) and foreign air... vapor. Typically electronic cigarettes, also called ``e-cigarettes,'' are designed to look like traditional cigarettes. E-cigarettes are sometimes also made to look like cigars and pipes, and even...

  3. 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.

  4. Pharmacological Treatment for Pregnant Women who Smoke Cigarettes

    Directory of Open Access Journals (Sweden)

    Chan BC

    2003-09-01

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

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

    Science.gov (United States)

    Míguez Varela, M Del Carmen; Becoña, Elisardo

    2015-01-01

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

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

    Science.gov (United States)

    Míguez Varela, M Del Carmen; Becoña, Elisardo

    2015-01-01

    This article examined the relationship between cigarette smoking or alcohol consumption and cannabis use and problem gambling among a random and representative sample of 1447 Spanish adolescents (797 males and 650 females with an average of 12.8 years). An ad-hoc questionnaire was used to assess cigarette smoking, alcohol consumption (beer, wine and spirits) and cannabis use. Gambling was assessed with the South Oaks Gambling Screen Revised for Adolescents (SOGS-RA). Results indicated a positive and significant association between cigarette smoking and alcohol consumption and the two aforementioned variables. A larger percentage of cigarette smokers and drinkers was found among those participants who had consumed cannabis before or scored significantly in problem gambling. Additionally, multiple regression analysis confirmed that both cigarette smoking and alcohol consumption (beer and wine) were the most determinant variables for cannabis use and problem gambling. PMID:25879473

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

    Science.gov (United States)

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

    2016-01-01

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

  8. Adolescent elite athletes' cigarette smoking, use of snus, and alcohol.

    Science.gov (United States)

    Martinsen, M; Sundgot-Borgen, J

    2014-04-01

    The purpose was to examine cigarette smoking, use of snus, alcohol, and performance-enhancing illicit drugs among adolescent elite athletes and controls, and possible gender and sport group differences. First-year students at 16 Norwegian Elite Sport High Schools (n = 677) and two randomly selected high schools (controls, n = 421) were invited to participate. Totally, 602 athletes (89%) and 354 (84%) controls completed the questionnaire. More controls than athletes were smoking, using snus, and drinking alcohol. Competing in team sports was associated with use of snus [odds ratio = 2.8, 95% confidence interval (CI) 1.6 to 4.7] and a similar percentage of male and female handball (22.2% vs 18.8%) and soccer players (15.7% vs 15.0%) reported using snus. For controls, not participating in organized sport was a predictor for smoking (odds ratio = 4.9, 95% CI 2.2 to 10.9). Female athletes were more prone to drink alcohol than males (46.3% vs 31.0%, P performance-enhancing illicit drugs. In conclusion, use of legal drugs is less common among athletes, but this relationship depends on type of sport and competition level. The association between team sports and use of snus suggests that sport subcultures play a role. PMID:22830488

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

    Science.gov (United States)

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

    2016-06-01

    The Ames assay is useful for evaluating the mutagenic potentials of chemicals, and it has been used to evaluate the mutagenic potential of cigarette smoke (CS). In vitro direct exposure systems have been developed to mimic CS exposure in the human respiratory tract, and the Ames assay has been used with such systems. Ames tests were performed using the Vitrocell(®) direct exposure system in this study. The mutagenic potentials of whole mainstream CS and gas/vapor phase fractions produced by conventional combustible cigarettes under two smoking regimens were compared. Salmonella Typhimurium TA98 and TA100 were used with and without metabolic activation, and the number of revertants induced by exposure to each CS was determined. The amount of smoke particles to which cells were exposed were also determined, and dose-response curves describing the relationships between exposure to smoke particles and the number of revertants induced were plotted. The slopes of linear regressions of the dose-response curves were determined, and the slope for each CS was used as a mutagenic activity index for that CS. A new heated cigarette was also tested and smoke from the heated cigarette had a lower mutagenic activity in TA98 and TA100 with metabolic activation than did the conventional CS. The results indicate that the direct exposure system and the Ames test can be used to determine the mutagenic potentials of CS produced by different cigarettes under different conditions (i.e., using different Salmonella Typhimurium strains with and without metabolic activation, and using different smoking conditions). PMID:27265375

  10. The political obstacles to the control of cigarette smoking in the United States.

    Science.gov (United States)

    Sapolsky, H M

    1980-01-01

    The opportunity to affect significantly the consumption of cigarettes in the United States through government action appears quite limited. Fifty million Americans smoke cigarettes. The United States is a leading producer of tobacco leaf and utilizes a price support system which is designed to protect tobacco growers. The industry is profitable and politicaly well connected. Several states are important producers of tobacco while others benefit from the excise tax imposed on cigarettes. The opposition to smoking is relatively weak and divided. Nevertheless, the tobacco industry worries about the future market for cigarettes. PMID:7419892

  11. Does cigarette smoking affect body weight? causal estimates from the clean indoor air law discontinuity

    OpenAIRE

    Pieroni, Luca; Salmasi, Luca

    2012-01-01

    This paper examines the causal effects of smoking behavior on body weight in Italy. In 2005, the Italian government introduced a smoking ban in all indoor public places. We use a regression discontinuity design, which exploits this exogenous variation due to smoking restrictions across cohorts, to achieve identification in our model. Our estimates indicate that the smoking ban reduced cigarette consumption and the smoking participation rate. Most interestingly, we estimate a significant, alth...

  12. 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.

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

    Science.gov (United States)

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

    2016-01-01

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

  14. Metal status in human endometrium: Relation to cigarette smoking and histological lesions

    International Nuclear Information System (INIS)

    Human endometrium is a thick, blood vessel-rich, glandular tissue which undergoes cyclic changes and is potentially sensitive to the various endogenous and exogenous compounds supplied via the hematogenous route. As recently indicated, several metals including Cd, Pb, Cr and Ni represent an emerging class of potential metalloestrogens and can be implicated in alterations of the female reproductive system including endometriosis and cancer. In the present study, we investigated the content of five metals: Cd, Cr, Ni, Pb and Zn in 25 samples of human endometrium collected from Polish females undergoing diagnostic or therapeutic curettage of the uterine cavity. The overall mean metal concentration (analyzed using microwave induced plasma atomic emission spectrometry MIP-OES) decreased in the following order: Cr>Pb>Zn>Ni>Cd. For the first time it was demonstrated that cigarette smoking significantly increases the endometrial content of Cd and Pb. Concentration of these metals was also positively correlated with years of smoking and the number of smoked cigarettes. Tissue samples with recognized histologic lesions (simple hyperplasia, polyposis and atrophy) were characterized by a 2-fold higher Cd level. No relation between the age of the women and metal content was found. Our study shows that human endometrium can be a potential target of metal accumulation within the human body. Quantitative analyses of endometrial metal content could serve as an additional indicator of potential impairments of the menstrual cycle and fertility. - Highlights: • Cd, Cr, Ni, Pb and Zn are detectable in human endometrium. • Mean metal content in human endometrium decreases in Cr>Pb>Zn>Ni>Cd order. • Cigarettes smoking increases endometrial content of Cd and Pb. • Lesioned endometrial tissue was characterized by higher metal contents

  15. Metal status in human endometrium: Relation to cigarette smoking and histological lesions

    Energy Technology Data Exchange (ETDEWEB)

    Rzymski, Piotr, E-mail: rzymskipiotr@ump.edu.pl [Department of Biology and Environmental Protection, Poznan University of Medical Sciences, Rokietnicka 8, 60-806 Poznań (Poland); Rzymski, Paweł; Tomczyk, Katarzyna [Department of Mother' s and Child' s Health, Gynecologic and Obstetrical University Hospital, Poznan University of Medical Sciences, Poznań (Poland); Niedzielski, Przemysław; Jakubowski, Karol [Department of Analytical Chemistry, Faculty of Chemistry, Adam Mickiewicz University, Umultowska 89, 61-614 Poznań (Poland); Poniedziałek, Barbara [Department of Biology and Environmental Protection, Poznan University of Medical Sciences, Rokietnicka 8, 60-806 Poznań (Poland); Opala, Tomasz [Department of Mother' s and Child' s Health, Gynecologic and Obstetrical University Hospital, Poznan University of Medical Sciences, Poznań (Poland)

    2014-07-15

    Human endometrium is a thick, blood vessel-rich, glandular tissue which undergoes cyclic changes and is potentially sensitive to the various endogenous and exogenous compounds supplied via the hematogenous route. As recently indicated, several metals including Cd, Pb, Cr and Ni represent an emerging class of potential metalloestrogens and can be implicated in alterations of the female reproductive system including endometriosis and cancer. In the present study, we investigated the content of five metals: Cd, Cr, Ni, Pb and Zn in 25 samples of human endometrium collected from Polish females undergoing diagnostic or therapeutic curettage of the uterine cavity. The overall mean metal concentration (analyzed using microwave induced plasma atomic emission spectrometry MIP-OES) decreased in the following order: Cr>Pb>Zn>Ni>Cd. For the first time it was demonstrated that cigarette smoking significantly increases the endometrial content of Cd and Pb. Concentration of these metals was also positively correlated with years of smoking and the number of smoked cigarettes. Tissue samples with recognized histologic lesions (simple hyperplasia, polyposis and atrophy) were characterized by a 2-fold higher Cd level. No relation between the age of the women and metal content was found. Our study shows that human endometrium can be a potential target of metal accumulation within the human body. Quantitative analyses of endometrial metal content could serve as an additional indicator of potential impairments of the menstrual cycle and fertility. - Highlights: • Cd, Cr, Ni, Pb and Zn are detectable in human endometrium. • Mean metal content in human endometrium decreases in Cr>Pb>Zn>Ni>Cd order. • Cigarettes smoking increases endometrial content of Cd and Pb. • Lesioned endometrial tissue was characterized by higher metal contents.

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

    Science.gov (United States)

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

    2012-01-01

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

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

    Science.gov (United States)

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

    2012-10-01

    Little research has been conducted on the influence of macroeconomic environments on smoking among blue-collar workers, a group with high smoking prevalence and that is especially vulnerable to the effects of changing economic circumstances. Using data from 52,418 construction workers in the Tobacco Use Supplement to the United States Current Population Survey, we examined the association of labor market shock, cigarette prices, and state antismoking sentiments with smoking status and average number of cigarettes smoked daily. Data analysis included the use of multiple linear and logistic regressions, which employed the sampling and replicate weights to account for sampling design. Unemployed, American-Indian, lower-educated and lower-income workers had higher smoking rates. Labor market shock had a quadratic association, which was non-significant for smoking status and significant for number of cigarettes. The association of cigarette prices with smoking status became non-significant after adjusting for state-level antismoking sentiment. State-level antismoking sentiment had significant quadratic association with smoking status among employed workers and significant quadratic association with number of cigarettes for all smokers. The study highlights how both workplace-based smoking cessation interventions and antismoking sentiments could further contribute to disparities in smoking by employment status.

  18. Factors Related to Cigarette Smoking Initiation and Use among College Students

    Directory of Open Access Journals (Sweden)

    Ebert Sheryl

    2005-01-01

    Full Text Available Abstract The purpose of this cross-sectional study was to examine the impact of personality factors (neuroticism, extraversion, openness, agreeableness, and conscientiousness, cognitive factors (sense of coherence and self-efficacy, coping resources (family and friend social support and demographic factors (gender and ethnicity on cigarette smoking behaviors (initiation, frequency, and amount of cigarette smoking among college students. A total of 161 U.S. college students, aged 18–26, who enrolled in an introductory psychology course completed self-report questionnaires. The majority of the students had tried smoking (55%; among those who had tried, 42% were current smokers. The majority (77% who had smoked a whole cigarette did so at age 16 years or younger. Students who reported lower levels of conscientiousness and self-efficacy had a greater likelihood to had tried cigarette smoking. Also, students who had lower levels of self-efficacy reported smoking more frequently and greater quantities of cigarettes than students with higher levels of self-efficacy. Self-efficacy was the most significant predictor of smoking behaviors. Health promotion programs focused on self-efficacy may be an effective tool for reducing the initiation, frequency, and amount of cigarette smoking among college students.

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

    Science.gov (United States)

    Fromme, Hermann; Schober, Wolfgang

    2015-04-01

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

  20. Cigarette smoke exposure-associated alterations to noncoding RNA

    Directory of Open Access Journals (Sweden)

    Matthew Alan Maccani

    2012-04-01

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

  1. Method for the Determination of Ammonia in Mainstream Cigarette Smoke Using Ion Chromatography

    Science.gov (United States)

    Watson, Christina Vaughan; Feng, June; Valentin-Blasini, Liza; Stanelle, Rayman; Watson, Clifford H.

    2016-01-01

    Ammonia in mainstream smoke is present in both the particulate and vapor phases. The presence of ammonia in the cigarette filler material and smoke is of significance because of the potential role ammonia could have in raising the “smoke pH.” An increased smoke pH could shift a fraction of total nicotine to free-base nicotine, which is reportedly more rapidly absorbed by the smoker. Methods measuring ammonia in smoke typically employ acid filled impingers to trap the smoke. We developed a fast, reliable method to measure ammonia in mainstream smoke without the use of costly and time consuming impingers to examine differences in ammonia delivery. The method uses both a Cambridge filter pad and a Tedlar bag to capture particulate and vapor phases of the smoke. We quantified ammonia levels in the mainstream smoke of 50 cigarette brands from 5 manufacturers. Ammonia levels ranged from approximately 1μg to 23μg per cigarette for ISO smoking conditions and 38μg to 67μg per cigarette for Canadian intense smoking conditions and statistically significance differences were observed between brands and manufacturers. Our findings suggest that ammonia levels vary by brand and are higher under Canadian intense smoking conditions. PMID:27415766

  2. Method for the Determination of Ammonia in Mainstream Cigarette Smoke Using Ion Chromatography.

    Directory of Open Access Journals (Sweden)

    Christina Vaughan Watson

    Full Text Available Ammonia in mainstream smoke is present in both the particulate and vapor phases. The presence of ammonia in the cigarette filler material and smoke is of significance because of the potential role ammonia could have in raising the "smoke pH." An increased smoke pH could shift a fraction of total nicotine to free-base nicotine, which is reportedly more rapidly absorbed by the smoker. Methods measuring ammonia in smoke typically employ acid filled impingers to trap the smoke. We developed a fast, reliable method to measure ammonia in mainstream smoke without the use of costly and time consuming impingers to examine differences in ammonia delivery. The method uses both a Cambridge filter pad and a Tedlar bag to capture particulate and vapor phases of the smoke. We quantified ammonia levels in the mainstream smoke of 50 cigarette brands from 5 manufacturers. Ammonia levels ranged from approximately 1μg to 23μg per cigarette for ISO smoking conditions and 38μg to 67μg per cigarette for Canadian intense smoking conditions and statistically significance differences were observed between brands and manufacturers. Our findings suggest that ammonia levels vary by brand and are higher under Canadian intense smoking conditions.

  3. Cigarette and waterpipe smoking among Lebanese adolescents, a cross-sectional study, 2003-2004.

    Science.gov (United States)

    El-Roueiheb, Zana; Tamim, Hala; Kanj, Mayada; Jabbour, Samer; Alayan, Iman; Musharrafieh, Umayya

    2008-02-01

    Waterpipe or "argileh" is a form of smoking other than cigarettes that is currently spreading among people of all ages. The objective of the present study was to assess tobacco smoking practices (waterpipe and/or cigarette) among public and private adolescent school students in Beirut, Lebanon. A sample of 2,443 students selected from 10 private and 3 public schools with intermediate/secondary classes filled out a self-administered anonymous questionnaire that inquired about sociodemographic characteristics, and behavior about tobacco smoking. Binary analysis was performed as well as three regression models for the relationship between exclusive cigarettes smoking, exclusive waterpipe smoking and both cigarettes and waterpipe as the dependent variables and gender, type of school, and class as the independent variables. The current prevalence of cigarettes smoking was 11.4%, and that of waterpipe smoking was 29.6%. Gender was significantly associated with cigarettes (OR=3.2, 95% CI 1.8-5.6) but not waterpipe smoking. Public school students were, respectively, 3.2 (95% CI 1.8-5.6) and 1.7 (95% CI 1.4-2.1) times more likely to be exclusive cigarettes smokers, and exclusive waterpipe smokers. Class was not significantly associated with exclusive cigarette smoking; however, students attending secondary classes were 1.3 (95% CI 1.1-1.6) times more likely to be exclusive waterpipe smokers. The reasons behind the high prevalence of both types of smoking are presented and discussed. The present study calls for school-based prevention programs and other types of interventions such as tax increases, and age-restrictions on tobacco sales. More aggressive interventions to disseminate education and awareness among parents and students altogether are warranted.

  4. Sex differences in prevalence rates and predictors of cigarette smoking among in-school adolescents in Kilimanjaro, Tanzania.

    Science.gov (United States)

    Siziya, S; Ntata, P R T; Rudatsikira, E; Makupe, C M; Umar, E; Muula, A S

    2007-09-01

    An analysis of the Global Youth Tobacco Survey for Kilimanjaro, Tanzania was carried out to assess sex differences in the prevalence rates and predictors of current cigarette smoking among in-school adolescents. A total of 2323 adolescents participated in the study of whom 53% were females and 47% males. The prevalence of current cigarette smoking was 3.0% and 1.4% among males and females, respectively. The common factors that were significantly positively associated with cigarette smoking between sexes were: having more pocket money, closest friend smoked cigarettes, seeing actors smoke on TV, videos or movies, and seeing advertisements for cigarettes at social gatherings. Seeing anti-smoking messages at social gatherings were negatively associated with smoking among both sexes. While having had something such as a t-shirt or pen with a cigarette brand logo on it was positively associated with cigarette smoking among males, it was negatively associated with cigarette smoking among females. Male adolescents older than 15 years, those in their 9th year of schooling, and those who had seen cigarette brand names on TV were more likely to smoke. Meanwhile, male respondents who were in their 8th year of schooling, had seen anti-smoking media messages, and advertisements for cigarettes in newspapers or magazines were less likely to smoke. Among female adolescents, those who had parents who smoked, and surprisingly those who perceived that cigarette smoking as harmful were more likely to smoke. Interestingly, seeing advertisement for cigarettes on billboards was negatively associated with smoking among female adolescents. Interventions aimed to reduce adolescent smoking need to be designed and implemented with due consideration of sex differences in these associated factors. PMID:18087898

  5. Levels of Heavy Metals in Popular Cigarette Brands and Exposure to These Metals via Smoking

    Directory of Open Access Journals (Sweden)

    Muhammad Waqar Ashraf

    2012-01-01

    Full Text Available The levels of selected heavy metals in popular cigarette brands sold and/or produced in Saudi Arabia were determined by graphite furnace-atomic absorption spectrometry (GFAAS. Average concentrations of Cadmium and Lead in different cigarette brands were 1.81 and 2.46 μg g−1 (dry weight, respectively. The results obtained in this study estimate the average quantity of Cd inhaled from smoking one packet of 20 cigarettes to be in the range of 0.22–0.78 μg. Results suggest that the quantity of Pb inhaled of smoking one packet of 20 cigarettes is estimated to be 0.97–2.64 μg. The concentrations of Cd and Pb in cigarettes were significantly different between cigarette brands tested. The results of the present study were compared with those of other regional and international studies.

  6. Biological effects of cigarette smoke in cultured human retinal pigment epithelial cells.

    Directory of Open Access Journals (Sweden)

    Alice L Yu

    Full Text Available The goal of the present study was to determine whether treatment with cigarette smoke extract (CSE induces cell loss, cellular senescence, and extracellular matrix (ECM synthesis in primary human retinal pigment epithelial (RPE cells. Primary cultured human RPE cells were exposed to 2, 4, 8, and 12% of CSE concentration for 24 hours. Cell loss was detected by cell viability assay. Lipid peroxidation was assessed by loss of cis-parinaric acid (PNA fluorescence. Senescence-associated ß-galactosidase (SA-ß-Gal activity was detected by histochemical staining. Expression of apolipoprotein J (Apo J, connective tissue growth factor (CTGF, fibronectin, and laminin were examined by real-time PCR, western blot, or ELISA experiments. The results showed that exposure of cells to 12% of CSE concentration induced cell death, while treatment of cells with 2, 4, and 8% CSE increased lipid peroxidation. Exposure to 8% of CSE markedly increased the number of SA-ß-Gal positive cells to up to 82%, and the mRNA expression of Apo J, CTGF, and fibronectin by approximately 3-4 fold. Treatment with 8% of CSE also increased the protein expression of Apo J and CTGF and the secretion of fibronectin and laminin. Thus, treatment with CSE can induce cell loss, senescent changes, and ECM synthesis in primary human RPE cells. It may be speculated that cigarette smoke could be involved in cellular events in RPE cells as seen in age-related macular degeneration.

  7. Alteration of human hepatic drug transporter activity and expression by cigarette smoke condensate.

    Science.gov (United States)

    Sayyed, Katia; Vee, Marc Le; Abdel-Razzak, Ziad; Jouan, Elodie; Stieger, Bruno; Denizot, Claire; Parmentier, Yannick; Fardel, Olivier

    2016-07-01

    Smoking is well-known to impair pharmacokinetics, through inducing expression of drug metabolizing enzymes. In the present study, we demonstrated that cigarette smoke condensate (CSC) also alters activity and expression of hepatic drug transporters, which are now recognized as major actors of hepatobiliary elimination of drugs. CSC thus directly inhibited activities of sinusoidal transporters such as OATP1B1, OATP1B3, OCT1 and NTCP as well as those of canalicular transporters like P-glycoprotein, MRP2, BCRP and MATE1, in hepatic transporters-overexpressing cells. CSC similarly counteracted constitutive OATP, NTCP and OCT1 activities in human highly-differentiated hepatic HepaRG cells. In parallel, CSC induced expression of BCRP at both mRNA and protein level in HepaRG cells, whereas it concomitantly repressed mRNA expression of various transporters, including OATP1B1, OATP2B1, OAT2, NTCP, OCT1 and BSEP, and enhanced that of MRP4. Such changes in transporter gene expression were found to be highly correlated to those caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin, a reference activator of the aryl hydrocarbon receptor (AhR) pathway, and were counteracted, for some of them, by siRNA-mediated AhR silencing. This suggests that CSC alters hepatic drug transporter levels via activation of the AhR cascade. Importantly, drug transporter expression regulations as well as some transporter activity inhibitions occurred for a range of CSC concentrations similar to those required for inducing drug metabolizing enzymes and may therefore be hypothesized to be relevant for smokers. Taken together, these data established human hepatic transporters as targets of cigarette smoke, which could contribute to known alteration of pharmacokinetics and some liver adverse effects caused by smoking. PMID:27450509

  8. Anti-inflammatory effects of naringin in chronic pulmonary neutrophilic inflammation in cigarette smoke-exposed rats

    OpenAIRE

    Nie, YC; Wu, H.; Li, PB; Luo, YL; Long, K.; Xie, LM; Shen, JG; Su, WW

    2012-01-01

    Naringin, a well-known flavanone glycoside of grapefruit and citrus fruits, was found to be as an effective anti-inflammatory compound in our previous lipopolysaccharide-induced acute lung injury mouse model via blockading activity of nuclear factor κB. The current study sought to explore the anti-inflammatory effects of naringin on chronic pulmonary neutrophilic inflammation in cigarette smoke (CS)-induced rats. Seventy Sprague-Dawley rats were randomly divided into seven groups to study the...

  9. Acculturation, Gender, Depression, and Cigarette Smoking among U.S. Hispanic Youth: The Mediating Role of Perceived Discrimination

    Science.gov (United States)

    Lorenzo-Blanco, Elma I.; Unger, Jennifer B.; Ritt-Olson, Anamara; Soto, Daniel; Baezconde-Garbanati, Lourdes

    2011-01-01

    Hispanic youth are at risk for experiencing depressive symptoms and smoking cigarettes, and risk for depressive symptoms and cigarette use increase as Hispanic youth acculturate to U.S. culture. The mechanism by which acculturation leads to symptoms of depression and cigarette smoking is not well understood. The present study examined whether…

  10. E-cigarettes and smoking cessation: evidence from a systematic review and meta-analysis.

    Directory of Open Access Journals (Sweden)

    Muhammad Aziz Rahman

    Full Text Available E-cigarettes are currently being debated regarding their possible role in smoking cessation and as they are becoming increasingly popular, the research to date requires investigation.To investigate whether the use of e-cigarettes is associated with smoking cessation or reduction, and whether there is any difference in efficacy of e-cigarettes with and without nicotine on smoking cessation.A systematic review of articles with no limit on publication date was conducted by searching PubMed, Web of Knowledge and Scopus databases.Published studies, those reported smoking abstinence or reduction in cigarette consumption after the use of e-cigarettes, were included. Studies were systematically reviewed, and meta-analyses were conducted using Mantel-Haenszel fixed-effect and random-effects models. Degree of heterogeneity among studies and quality of the selected studies were evaluated.Six studies were included involving 7,551 participants. Meta-analyses included 1,242 participants who had complete data on smoking cessation. Nicotine filled e-cigarettes were more effective for cessation than those without nicotine (pooled Risk Ratio 2.29, 95%CI 1.05-4.97. Amongst 1,242 smokers, 224 (18% reported smoking cessation after using nicotine-enriched e-cigarettes for a minimum period of six months. Use of such e-cigarettes was positively associated with smoking cessation with a pooled Effect Size of 0.20 (95%CI 0.11-0.28. Use of e-cigarettes was also associated with a reduction in the number of cigarettes used.Included studies were heterogeneous, due to different study designs and gender variation. Whilst we were able to comment on the efficacy of nicotine vs. non-nicotine e-cigarettes for smoking cessation, we were unable to comment on the efficacy of e-cigarettes vs. other interventions for cessation, given the lack of comparator groups in the studies included in this meta-analysis.Use of e-cigarettes is associated with smoking cessation and reduction. More

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

    Science.gov (United States)

    Esakky, Prabagaran; Moley, Kelle H

    2016-11-01

    Paternal exposure to constituents of cigarette smoke (CS) is reportedly associated with infertility, birth defects and childhood cancers even though the mechanism behind this relationship is still unclear. Chronic cigarette smoking by men leads to poor sperm quality and quantity mainly through oxidative stress and also direct assault by CS metabolites. Among several carcinogenic and teratogenic components of cigarette smoke condensate (CSC), polycyclic aromatic hydrocarbons (PAHs) display a preeminent role in accelerating germ cell death via the cytoplasmic transcription factor, aryl hydrocarbon receptor (AHR) that is present across all stages of spermatogenesis. Activation of AHR by growth factors though benefits normal cellular functions, its mediation by CSC in a spermatocyte cell line [Gc2(spd)ts] adversely affects the expression of a battery of genes associated with antioxidant mechanisms, cell proliferation and apoptosis, and cell cycle progress. Besides, the CSC-mediated cross talk either between AHR and NRF2 or AHR-NRF2 and MAPKs pathways inhibits normal proliferation of the spermatogenic GC-2spd(ts) cells in vitro and cell death of spermatocytes in vivo. Pharmacological inactivation of CSC-induced AHR but not its genetic manipulation seems preventing DNA and cell membrane damage in Gc2(spd)ts. Data from recent reports suggest that the cigarette smoke affects both the genomic and epigenomic components of the sperm and attributes any associated changes to developmental defects in the offspring. Thus, the studies discussed here in this review shed light on possible mechanistic factors that could probably be responsible for the paternally mediated birth defects in the offspring following exposure to the toxic constituents of cigarette smoke. PMID:27424142

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

    DEFF Research Database (Denmark)

    Markussen Linnet, Karen; Obel, Carsten; Bonde, Else;

    2006-01-01

    born to women who smoked 10 or more cigarettes per day had a 60% increased risk of hyperactivity and distractibility perceived by the parents (OR 1.6; 95% CI 1.0-2.3; P characteristics. Additional adjustment...

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1975-06-01

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

  14. State Estimates of Adolescent Cigarette Use and Perceptions of Risk of Smoking: 2012 and 2013

    Science.gov (United States)

    ... most effective way to reduce the health and economic burden of tobacco-related disease in the future. ... smoking and its consequences, and improve prevention efforts. Keywords: cigarettes, National Survey on Drug Use and Health, ...

  15. Assessing the Feasibility of Using Contingency Management to Modify Cigarette Smoking by Adolescents

    OpenAIRE

    Roll, John M.

    2005-01-01

    Cigarette smoking is a leading cause of preventable death in the United States. Many smokers initiate this dangerous behavior during adolescence. This report describes a contingency management intervention designed to initate and maintain a period of abstinence from cigarettes by adolescent smokers. Results suggest that the intervention was generally successful and that further investigation of this topic is warranted.

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

    Science.gov (United States)

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

    2014-01-01

    Exposure to cigarette smoke (CS) is linked to the development of respiratory diseases, and there is a need to understand the mechanisms whereby CS causes damage. Although animal models have provided valuable insights into smoking-related respiratory tract damage, modern toxicity testing calls for reliable in vitro models as alternatives for animal experimentation. We report on a repeated whole mainstream CS exposure of nasal and bronchial organotypic tissue cultures that mimic the morphological, physiological, and molecular attributes of the human respiratory tract. Despite the similar cellular staining and cytokine secretion in both tissue types, the transcriptomic analyses in the context of biological network models identified similar and diverse biological processes that were impacted by CS-exposed nasal and bronchial cultures. Our results demonstrate that nasal and bronchial tissue cultures are appropriate in vitro models for the assessment of CS-induced adverse effects in the respiratory system and promising alternative to animal experimentation. PMID:25297719

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

    Directory of Open Access Journals (Sweden)

    Erika B Fulmer

    Full Text Available Youth are exposed to many types of protobacco influences, including smoking in movies, which has been shown to cause initiation. This study investigates associations between different channels of protobacco media and susceptibility to smoking cigarettes, cigarette experimentation, and current tobacco use among US middle and high school students.By using data from the 2012 National Youth Tobacco Survey, structural equation modeling was performed in 2013. The analyses examined exposure to tobacco use in different channels of protobacco media on smoking susceptibility, experimentation, and current tobacco use, accounting for perceived peer tobacco use.In 2012, 27.9% of respondents were never-smokers who reported being susceptible to trying cigarette smoking. Cigarette experimentation increased from 6.3% in 6th grade to 37.1% in 12th grade. Likewise, current tobacco use increased from 5.2% in 6th grade to 33.2% in 12th grade. Structural equation modeling supported a model in which current tobacco use is associated with exposure to static advertising through perception of peer use, and by exposure to tobacco use depicted on TV and in movies, both directly and through perception of peer use. Exposure to static advertising appears to directly increase smoking susceptibility but indirectly (through increased perceptions of peer use to increase cigarette experimentation. Models that explicitly incorporate peer use as a mediator can better discern the direct and indirect effects of exposure to static advertising on youth tobacco use initiation.These findings underscore the importance of reducing youth exposure to smoking in TV, movies, and static advertising.

  18. E-Cigarettes for Immediate Smoking Substitution in Women Diagnosed with Cervical Dysplasia and Associated Disorders.

    Science.gov (United States)

    James, Shirley A; Meier, Ellen M; Wagener, Theodore L; Smith, Katherine M; Neas, Barbara R; Beebe, Laura A

    2016-03-04

    The aim of this study was to determine if 31 women with cervical dysplasia and associated conditions exacerbated by smoking would be successful substituting cigarettes with their choice of either nicotine replacement therapy (NRT) or electronic cigarettes (EC). Women received motivational interviewing and tried both NRT and ECs, choosing one method to use during a six-week intervention period. Daily cigarette consumption was measured at baseline, six, and 12 weeks, with differences analyzed by the Wilcoxon signed-rank test. Study analysis consisted only of women choosing to use ECs (29/31), as only two chose NRT. At the 12-week follow-up, the seven day point prevalence abstinence from smoking was 28.6%, and the median number of cigarettes smoked daily decreased from 18.5 to 5.5 (p < 0.0001). The median number of e-cigarette cartridges used dropped from 21 at the six-week follow-up to 12.5 at the 12-week follow-up. After initiating EC use, women at risk for cervical cancer were able to either quit smoking or reduce the number of cigarettes smoked per day. Although a controlled trial with a larger sample size is needed to confirm these initial results, this study suggests that using ECs during quit attempts may reduce cigarette consumption.

  19. E-Cigarettes for Immediate Smoking Substitution in Women Diagnosed with Cervical Dysplasia and Associated Disorders

    Directory of Open Access Journals (Sweden)

    Shirley A. James

    2016-03-01

    Full Text Available The aim of this study was to determine if 31 women with cervical dysplasia and associated conditions exacerbated by smoking would be successful substituting cigarettes with their choice of either nicotine replacement therapy (NRT or electronic cigarettes (EC. Women received motivational interviewing and tried both NRT and ECs, choosing one method to use during a six-week intervention period. Daily cigarette consumption was measured at baseline, six, and 12 weeks, with differences analyzed by the Wilcoxon signed-rank test. Study analysis consisted only of women choosing to use ECs (29/31, as only two chose NRT. At the 12-week follow-up, the seven day point prevalence abstinence from smoking was 28.6%, and the median number of cigarettes smoked daily decreased from 18.5 to 5.5 (p < 0.0001. The median number of e-cigarette cartridges used dropped from 21 at the six-week follow-up to 12.5 at the 12-week follow-up. After initiating EC use, women at risk for cervical cancer were able to either quit smoking or reduce the number of cigarettes smoked per day. Although a controlled trial with a larger sample size is needed to confirm these initial results, this study suggests that using ECs during quit attempts may reduce cigarette consumption.

  20. Adolescents' responses to cigarette advertisements: links between exposure, liking, and the appeal of smoking

    OpenAIRE

    Arnett, J J; Terhanian, G.

    1998-01-01

    OBJECTIVE—To evaluate adolescents' responses to cigarette advertisements for different brands.
DESIGN—Adolescents were shown one print advertisement for each of five cigarette brands (Camel, Marlboro, Kool, Benson & Hedges, and Lucky Strike). They indicated on a structured questionnaire how many times they had seen the advertisement (or one almost like it), how much they liked it, whether or not they thought it made smoking more appealing, and whether or not it made them want to smoke cigaret...

  1. Factors Related to Cigarette Smoking Initiation and Use among College Students

    OpenAIRE

    Ebert Sheryl; Park Najin; Kang Duck-Hee; Ngamvitroj Anchalee; Von Ah Diane

    2005-01-01

    Abstract The purpose of this cross-sectional study was to examine the impact of personality factors (neuroticism, extraversion, openness, agreeableness, and conscientiousness), cognitive factors (sense of coherence and self-efficacy), coping resources (family and friend social support) and demographic factors (gender and ethnicity) on cigarette smoking behaviors (initiation, frequency, and amount of cigarette smoking) among college students. A total of 161 U.S. college students, aged 18–...

  2. Effects of cigarette smoke and chronic hypoxia on airways remodeling and resistance. Clinical significance

    OpenAIRE

    Olea, Elena; Prieto-Lloret, Jesús; Gonzalez-Martin, Carmen; Vega Agapito, Victoria; Gonzalez-Obeso, Elvira; Agapito, Teresa; Obeso, Ana; González, Constancio

    2011-01-01

    Previously we have reported that association of cigarette smoke (CS) and chronic hypoxia (CH) interact positively to physiopathologically remodel pulmonary circulation. In present study we have exposed guinea pigs to CS smoke (four cigarettes/day; 3 months; CS) and to chronic hypoxia (12% O2, 15 days; CH) alone or in combination (CSCH animals) and evaluated airways remodeling and resistance assessed as Penh (enhance pause). We measured Penh while animals breathe air, 10% O2 and 5% CO2 and fou...

  3. Cigarette smoking and risk of ovarian cancer: a pooled analysis of 21 case-control studies

    OpenAIRE

    Faber, Mette T.; Kjær, Susanne K.; Dehlendorff, Christian; Chang-Claude, Jenny; Klaus K. Andersen; Høgdall, Estrid; Webb, Penelope M.; Jordan, Susan J; Rossing, Mary Anne; Doherty, Jennifer A; Lurie, Galina; Pamela J Thompson; Carney, Michael E; Goodman, Marc T.; Ness, Roberta B.

    2013-01-01

    Purpose 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. Methods We used data from 21 case–control studies of ovarian cancer (19,066...

  4. The Impact of Menthol Cigarettes on Smoking Initiation among Non-Smoking Young Females in Japan

    Directory of Open Access Journals (Sweden)

    Yoneatsu Osaki

    2010-12-01

    Full Text Available Japan presents an excellent case-study of a nation with low female smoking rates and a negligible menthol market which changed after the cigarette market was opened to foreign competition. Internal tobacco industry documents demonstrate the intent of tobacco manufacturers to increase initiation among young females through development and marketing of menthol brands. Japanese menthol market share rose rapidly from less than 1% in 1980 to 20% in 2008. Menthol brand use was dominated by younger and female smokers, in contrast with non-menthol brands which were used primarily by male smokers. Nationally representative surveys confirm industry surveys of brand use and provide further evidence of the end results of the tobacco industry’s actions—increased female smoking in Japan. These findings suggest that female populations may be encouraged to initiate into smoking, particularly in developing nations or where female smoking rates remain low, if the tobacco industry can successfully tailor brands to them. The Japanese experience provides a warning to public health officials who wish to prevent smoking initiation among young females.

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

    Science.gov (United States)

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

    2015-01-01

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

  6. Views from the Coalface: What Do English Stop Smoking Service Personnel Think about E-Cigarettes?

    Directory of Open Access Journals (Sweden)

    Rosemary Hiscock

    2015-12-01

    Full Text Available The UK Stop Smoking Services (SSS are a source of information and advice on e-cigarettes for smokers and thus it is important to understand the knowledge of, and attitudes towards, e-cigarettes held by stop smoking practitioners. The datasets were English SSS quarterly monitoring returns (n = 207,883 and an online survey of English SSS practitioners, managers, and commissioners between 26th November and 15th December 2014 (n = 1801. SSS monitoring data suggested 2% of clients were using e-cigarettes to quit with SSS and that clients using e-cigarettes had similar quit rates to clients using Varenicline. Most SSS personnel are waiting for licenced e-cigarettes to become available before they will recommend them to clients. However, less than a quarter view e-cigarettes as “a good thing”. Managers and commissioners were more positive than practitioners. SSS personnel working for the NHS (hospitals and GP surgeries were less positive about e-cigarettes than those employed elsewhere. E-cigarettes were cited as the most important reason for the recent decline in service footfall. Thus dissemination of information about e-cigarettes needs to be examined and services should address their stance on e-cigarettes with some urgency.

  7. Views from the Coalface: What Do English Stop Smoking Service Personnel Think about E-Cigarettes?

    Science.gov (United States)

    Hiscock, Rosemary; Bauld, Linda; Arnott, Deborah; Dockrell, Martin; Ross, Louise; McEwen, Andy

    2015-12-21

    The UK Stop Smoking Services (SSS) are a source of information and advice on e-cigarettes for smokers and thus it is important to understand the knowledge of, and attitudes towards, e-cigarettes held by stop smoking practitioners. The datasets were English SSS quarterly monitoring returns (n = 207,883) and an online survey of English SSS practitioners, managers, and commissioners between 26th November and 15th December 2014 (n = 1801). SSS monitoring data suggested 2% of clients were using e-cigarettes to quit with SSS and that clients using e-cigarettes had similar quit rates to clients using Varenicline. Most SSS personnel are waiting for licenced e-cigarettes to become available before they will recommend them to clients. However, less than a quarter view e-cigarettes as "a good thing". Managers and commissioners were more positive than practitioners. SSS personnel working for the NHS (hospitals and GP surgeries) were less positive about e-cigarettes than those employed elsewhere. E-cigarettes were cited as the most important reason for the recent decline in service footfall. Thus dissemination of information about e-cigarettes needs to be examined and services should address their stance on e-cigarettes with some urgency.

  8. Views from the Coalface: What Do English Stop Smoking Service Personnel Think about E-Cigarettes?

    Science.gov (United States)

    Hiscock, Rosemary; Bauld, Linda; Arnott, Deborah; Dockrell, Martin; Ross, Louise; McEwen, Andy

    2015-12-01

    The UK Stop Smoking Services (SSS) are a source of information and advice on e-cigarettes for smokers and thus it is important to understand the knowledge of, and attitudes towards, e-cigarettes held by stop smoking practitioners. The datasets were English SSS quarterly monitoring returns (n = 207,883) and an online survey of English SSS practitioners, managers, and commissioners between 26th November and 15th December 2014 (n = 1801). SSS monitoring data suggested 2% of clients were using e-cigarettes to quit with SSS and that clients using e-cigarettes had similar quit rates to clients using Varenicline. Most SSS personnel are waiting for licenced e-cigarettes to become available before they will recommend them to clients. However, less than a quarter view e-cigarettes as "a good thing". Managers and commissioners were more positive than practitioners. SSS personnel working for the NHS (hospitals and GP surgeries) were less positive about e-cigarettes than those employed elsewhere. E-cigarettes were cited as the most important reason for the recent decline in service footfall. Thus dissemination of information about e-cigarettes needs to be examined and services should address their stance on e-cigarettes with some urgency. PMID:26703638

  9. Predisposing effects of cigarette advertising on children's intentions to smoke when older.

    Science.gov (United States)

    Aitken, P P; Eadie, D R; Hastings, G B; Haywood, A J

    1991-04-01

    Six hundred and forty Glasgow children, initially aged between 11 and 14 years, were interviewed twice, with approximately one year between interviews. Children whose intentions to smoke when older became more positive between the two interviews tended to be more aware of cigarette advertising at the time of the first interview (compared with children whose intentions to smoke were negative at both interviews). Children whose intentions to smoke became more negative between the interviews tended to be less appreciative of cigarette advertisements at the time of the first interview (compared with children whose intentions to smoke were positive at both interviews). Since both groups differed from their respective contrast groups before their declared intentions changed, these findings support the view that cigarette advertising has predisposing as well as reinforcing effects on children's attitudes and behaviour with respect to smoking.

  10. Summary of the Findings from a Study About Cigarette Smoking Among Teen-Age Girls and Young Women.

    Science.gov (United States)

    Yankelovich, Skelly and White, Inc., New York, NY.

    This paper presents the major results of a study for the American Cancer Society on cigarette smoking among teen-age girls and young women, and findings relevant to the prevention and quitting of smoking. The four major trends found in this study are: (1) a dramatic increase in cigarette smoking among females; (2) an intellectual awareness of the…

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

    Directory of Open Access Journals (Sweden)

    Dowling Nicole

    2010-05-01

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

  12. Effect of cigarette smoke extract on nitric oxide synthase in pulmonary artery endothelial cells.

    Science.gov (United States)

    Su, Y; Han, W; Giraldo, C; De Li, Y; Block, E R

    1998-11-01

    Cigarette smoking is associated with impaired endothelium-dependent vasodilation and reduced nitric oxide (NO) in the exhaled air of smokers. To explore the mechanism for the impairment of NO-mediated vasodilation, we studied the effect of cigarette smoke extract (CSE) on NO synthase (eNOS) activity and content in pulmonary artery endothelial cells (PAEC). Incubation of PAEC with CSE resulted in a time- and dose-dependent decrease in eNOS activity. The inhibitory effect of CSE on eNOS activity was not reversible. Both gas-phase and particulate-phase extracts of CSE contributed to the inhibition of eNOS activity. The protein kinase c (PKC) inhibitors staurosporine and chelerythrine did not affect the CSE-induced inhibition of eNOS activity. Catalase, superoxide dismutase (SOD), vitamin C, vitamin E, glutathione, and dithiothreitol (DTT) also did not prevent the CSE-induced inhibition of eNOS activity, and incubation of PAEC with 3 mM nicotine did not change the activity of eNOS. Treatment of PAEC with CSE also caused a nonreversible, time-dependent decrease in eNOS protein content detected by Western blot analysis, and in eNOS messenger RNA (mRNA) detected by Northern blot analysis. Treatment of PAEC with CSE had no effect on cell protein or glutathione contents or on lactate dehydrogenase (LDH) release. These results indicate that exposure to CSE causes an irreversible inhibition of eNOS activity in PAEC, and suggest that the decreased activity is secondary to reduced eNOS protein mass and mRNA. The decrease in eNOS activity may contribute to the high risk of pulmonary and cardiovascular disease in cigarette smokers. PMID:9806747

  13. Cigarette Smoke Decreases the Maturation of Lung Myeloid Dendritic Cells

    Science.gov (United States)

    Calero-Acuña, Carmen; Moreno-Mata, Nicolás; Gómez-Izquierdo, Lourdes; Sánchez-López, Verónica; López-Ramírez, Cecilia; Tobar, Daniela; López-Villalobos, José Luis; Gutiérrez, Cesar; Blanco-Orozco, Ana; López-Campos, José Luis

    2016-01-01

    Background Conflicting data exist on the role of pulmonary dendritic cells (DCs) and their maturation in patients with chronic obstructive pulmonary disease (COPD). Herein, we investigated whether disease severity and smoking status could affect the distribution and maturation of DCs in lung tissues of patients undergoing elective pneumectomy or lobectomy for suspected primary lung cancer. Materials and Methods A total of 75 consecutive patients were included. Spirometry testing was used to identify COPD. Lung parenchyma sections anatomically distant from the primary lesion were examined. We used flow cytometry to identify different DCs subtypes—including BDCA1-positive myeloid DCs (mDCs), BDCA3-positive mDCs, and plasmacytoid DCs (pDCs)—and determine their maturation markers (CD40, CD80, CD83, and CD86) in all participants. We also identified follicular DCs (fDCs), Langerhans DCs (LDCs), and pDCs in 42 patients by immunohistochemistry. Results COPD was diagnosed in 43 patients (16 current smokers and 27 former smokers), whereas the remaining 32 subjects were classified as non-COPD (11 current smokers, 13 former smokers, and 8 never smokers). The number and maturation of DCs did not differ significantly between COPD and non-COPD patients. However, the results of flow cytometry indicated that maturation markers CD40 and CD83 of BDCA1-positive mDCs were significantly decreased in smokers than in non-smokers (P = 0.023 and 0.013, respectively). Immunohistochemistry also revealed a lower number of LDCs in COPD patients than in non-COPD subjects. Conclusions Cigarette smoke, rather than airflow limitation, is the main determinant of impaired DCs maturation in the lung. PMID:27058955

  14. Potential Impact of Graphic Health Warnings on Cigarette Packages in Reducing Cigarette Demand and Smoking-Related Deaths in Vietnam.

    Science.gov (United States)

    Minh, Hoang Van; Chung, Le Hong; Giang, Kim Bao; Duc, Duong Minh; Hinh, Nguyen Duc; Mai, Vu Quynh; Cuong, Nguyen Manh; Manh, Pham Duc; Duc, Ha Anh; Yang, Jui-Chen

    2016-01-01

    Two years after implementation of the graphic health warning intervention in Vietnam, it is very important to evaluate the intervention's potential impact. The objective of this paper was to predict effects of graphic health warnings on cigarette packages, particularly in reducing cigarette demand and smoking-associated deaths in Vietnam. In this study, a discrete choice experiment (DCE) method was used to evaluate the potential impact of graphic tobacco health warnings on smoking demand. To predict the impact of GHWs on reducing premature deaths associated with smoking, we constructed different static models. We adapted the method developed by University of Toronto, Canada and found that GHWs had statistically significant impact on reducing cigarette demand (up to 10.1% through images of lung damage), resulting in an overall decrease of smoking prevalence in Vietnam. We also found that between 428,417- 646,098 premature deaths would be prevented as a result of the GHW intervention. The potential impact of the GHW labels on reducing premature smoking-associated deaths in Vietnam were shown to be stronger among lower socio-economic groups. PMID:27087188

  15. Potential Impact of Graphic Health Warnings on Cigarette Packages in Reducing Cigarette Demand and Smoking-Related Deaths in Vietnam.

    Science.gov (United States)

    Minh, Hoang Van; Chung, Le Hong; Giang, Kim Bao; Duc, Duong Minh; Hinh, Nguyen Duc; Mai, Vu Quynh; Cuong, Nguyen Manh; Manh, Pham Duc; Duc, Ha Anh; Yang, Jui-Chen

    2016-01-01

    Two years after implementation of the graphic health warning intervention in Vietnam, it is very important to evaluate the intervention's potential impact. The objective of this paper was to predict effects of graphic health warnings on cigarette packages, particularly in reducing cigarette demand and smoking-associated deaths in Vietnam. In this study, a discrete choice experiment (DCE) method was used to evaluate the potential impact of graphic tobacco health warnings on smoking demand. To predict the impact of GHWs on reducing premature deaths associated with smoking, we constructed different static models. We adapted the method developed by University of Toronto, Canada and found that GHWs had statistically significant impact on reducing cigarette demand (up to 10.1% through images of lung damage), resulting in an overall decrease of smoking prevalence in Vietnam. We also found that between 428,417- 646,098 premature deaths would be prevented as a result of the GHW intervention. The potential impact of the GHW labels on reducing premature smoking-associated deaths in Vietnam were shown to be stronger among lower socio-economic groups.

  16. Effect of Permeability of Tipping Paper on Cigarette Burning Temperature and the Property of Mainstream Smoke

    Science.gov (United States)

    Yao, Zhen-Yu; Shen, Yan; Huang, Hai-Qun; Xu, Ji-Cang

    2016-05-01

    Cigarette smoke analysis of tipping paper with different permeability was carried out. The infrared thermal imager was used to measure burning temperature of cigarette with different permeability tipping paper. The results indicated that with the increase of tipping paper permeability, Tar, CO and nicotine in cigarette mainstream were significantly linear decreased, puff count was increased. Tipping paper permeability had a great influence on cigarette burning temperature. With the increase of tipping paper permeability, the third puff burning temperature and the average peak temperature values were dropped obviously, but the changes of smoldering temperature were not obvious. In addition, smoldering average temperature was significantly lower than the third puff burning temperature and peak temperature.

  17. Factors associated with adolescent cigarette smoking in Greece: Results from a cross sectional study (GYTS Study

    Directory of Open Access Journals (Sweden)

    Gourgoulianis Konstantinos

    2008-09-01

    Full Text Available Abstract Background Data about the predictors of smoking among adolescents in Greece are sparse. We tried to identify factors associated with current cigarette smoking among in-school adolescents in Greece in the context of GYTS study. Methods A secondary analysis of data from a questionnaire study using the Global Youth Tobacco Survey methodology was conducted to identify factors associated with smoking among adolescents in Greece. Data were collected in 2004–2005. The outcome variable was cigarette smoking within the past 30 days preceding the survey while independent variables included age, gender, parental educational status, parental smoking, perception of harmfulness of smoking, and the amount of pocket money at the adolescent's disposal. Results 6141 adolescents (51.5% males and 48.5% females participated in the study. In multivariate analysis, cigarette smoking was associated with male gender (OR: 1.62; 95% CI: 1, 08–3.08, parental smoking (OR: 2.59; 95% CI: 1.45–5.89, and having pocket money ≥ 16 Euros (OR: 2.64; 95% CI: 1.19–5.98. Conclusion Male gender, parental smoking, and having pocket-money ≥ 16 Euros were independently associated with current smoking among Greek students. These findings could be taken into account in order to formulate a comprehensive anti-smoking strategy in Greece.

  18. 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

  19. Effects of cigarette smoke and chronic hypoxia on airways remodeling and resistance. Clinical significance.

    Science.gov (United States)

    Olea, Elena; Ferrer, Elisabet; Prieto-Lloret, Jesus; Gonzalez-Martin, Carmen; Vega-Agapito, Victoria; Gonzalez-Obeso, Elvira; Agapito, Teresa; Peinado, Victor; Obeso, Ana; Barbera, Joan Albert; Gonzalez, Constancio

    2011-12-15

    Previously we have reported that association of cigarette smoke (CS) and chronic hypoxia (CH) interact positively to physiopathologically remodel pulmonary circulation. In present study we have exposed guinea pigs to CS smoke (four cigarettes/day; 3 months; CS) and to chronic hypoxia (12% O(2), 15 days; CH) alone or in combination (CSCH animals) and evaluated airways remodeling and resistance assessed as Penh (enhance pause). We measured Penh while animals breathe air, 10% O(2) and 5% CO(2) and found that CS and CH animals have higher Penh than controls; Penh was even larger in CSCH animals. A rough parallelism between Penh and thickness of bronchiolar wall and muscular layer and Goblet cell number was noticed. We conclude that CS and CH association accelerates CS-induced respiratory system damage, evidenced by augmented airway resistance, bronchial wall thickness and muscularization and Goblet cell number. Our findings would suggest that appearance of hypoxia would aggravate any preexisting pulmonary pathology by increasing airways resistance and reactivity. PMID:22000990

  20. Blunt Chest Trauma in Mice after Cigarette Smoke-Exposure: Effects of Mechanical Ventilation with 100 % O2

    OpenAIRE

    Wagner, Katja; Gröger, Michael; McCook, Oscar; Scheuerle, Angelika; Asfar, Pierre; Stahl, Bettina; Huber-Lang, Markus; Ignatius, Anita; Jung, Birgit; Duechs, Matthias; Möller, Peter; Georgieff, Michael; Calzia, Enrico; Radermacher, Peter; Wagner, Florian

    2015-01-01

    Cigarette smoking (CS) aggravates post-traumatic acute lung injury and increases ventilator-induced lung injury due to more severe tissue inflammation and apoptosis. Hyper-inflammation after chest trauma is due to the physical damage, the drop in alveolar PO2, and the consecutive hypoxemia and tissue hypoxia. Therefore, we tested the hypotheses that 1) CS exposure prior to blunt chest trauma causes more severe post-traumatic inflammation and thereby aggravates lung injury, and that 2) hyperox...

  1. Cigarette Smoke Activates the Proto-Oncogene c-Src to Promote Airway Inflammation and Lung Tissue Destruction

    OpenAIRE

    Geraghty, Patrick; Hardigan, Andrew; Foronjy, Robert F.

    2014-01-01

    The diagnosis of chronic obstructive pulmonary disease (COPD) confers a 2-fold increased lung cancer risk even after adjusting for cigarette smoking, suggesting that common pathways are operative in both diseases. Although the role of the tyrosine kinase c-Src is established in lung cancer, less is known about its impact in other lung diseases, such as COPD. This study examined whether c-Src activation by cigarette smoke contributes to the pathogenesis of COPD. Cigarette smoke increased c-Src...

  2. E-cigarette use in young Swiss men : is vaping an effective way of reducing or quitting smoking ?

    OpenAIRE

    Gmel G.; Baggio S.; Mohler-Kuo M.; Daeppen J.B.; Studer J.

    2016-01-01

    QUESTION UNDER STUDY: To test longitudinally differences in conventional cigarette use (cigarettes smoked, cessation, quit attempts) between vapers and nonvapers. METHODS: Fifteen months follow-up of a sample of 5 128 20-year-old Swiss men. The onset of conventional cigarette (CC) use among nonsmokers, and smoking cessation, quit attempts, changes in the number of CCs smoked among smokers at baseline were compared between vapers and nonvapers at follow-up, adjusted for nicotine dependen...

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

    Science.gov (United States)

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

    2016-07-01

    Exposure to cigarette smoke is known to result in impaired host defense responses and immune suppressive effects. However, the effects of new and emerging tobacco products, such as e-cigarettes, on the immune status of the respiratory epithelium are largely unknown. We conducted a clinical study collecting superficial nasal scrape biopsies, nasal lavage, urine, and serum from nonsmokers, cigarette smokers, and e-cigarette users and assessed them for changes in immune gene expression profiles. Smoking status was determined based on a smoking history and a 3- to 4-wk smoking diary and confirmed using serum cotinine and urine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL) levels. Total RNA from nasal scrape biopsies was analyzed using the nCounter Human Immunology v2 Expression panel. Smoking cigarettes or vaping e-cigarettes resulted in decreased expression of immune-related genes. All genes with decreased expression in cigarette smokers (n = 53) were also decreased in e-cigarette smokers. Additionally, vaping e-cigarettes was associated with suppression of a large number of unique genes (n = 305). Furthermore, the e-cigarette users showed a greater suppression of genes common with those changed in cigarette smokers. This was particularly apparent for suppressed expression of transcription factors, such as EGR1, which was functionally associated with decreased expression of 5 target genes in cigarette smokers and 18 target genes in e-cigarette users. Taken together, these data indicate that vaping e-cigarettes is associated with decreased expression of a large number of immune-related genes, which are consistent with immune suppression at the level of the nasal mucosa. PMID:27288488

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

    Science.gov (United States)

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

    2016-07-01

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

  5. Prevalence of cigarette smoking and its predictors among school going adolescents of North India

    Directory of Open Access Journals (Sweden)

    Durgesh Thakur

    2014-01-01

    Full Text Available Background: Cigarettes smoking is a common mode of consuming tobacco in India. This habit usually starts in adolescence and tracks across the life course. Interventions like building decision making skills and resisting negative influences are effective in reducing the initiation and level of tobacco use. Aims and Objectives: The purpose of this study was to assess the prevalence of adolescent current cigarette smoking behavior and to investigate the individual and social factors, which influence them both to and not to smoke. Methodology: A cross-sectional study was carried out among school going adolescents in Shimla town of North India. After obtaining their written informed consent, a questionnaire was administered. Results: The overall prevalence of current cigarette smoking was 11.8%. The binary logistic regression model revealed that parents′ and peers′ smoking behavior influence adolescent smoking behavior. Individual self-harm tendency also significantly predicted cigarette smoking behavior. Parental active participation in keeping a track of their children′s free time activities predicted to protect adolescents from taking this habit. Conclusion: Our research lends support to the need for intervention on restricting adolescents from taking up this habit and becoming another tobacco industries′ addicted customer. Parents who smoke should quit this habit, which will not only restore their own health, but also protect their children. All parents should be counseled to carefully observe their children′s free time activities.

  6. Self-Reported Depressive Feelings and Cigarette Smoking among Mexican-American Adolescents.

    Science.gov (United States)

    Pesa, Jacqueline A.; Cowdery, Joan E.; Wang, Min Qi; Fu, Qiang

    1997-01-01

    Examined the relationship between depressive feelings and cigarette smoking in Mexican-American adolescents who participated in the 1993 Teenage Attitudes and Practices Survey II. Results suggest a relationship between certain feelings of depression and smoking, beyond that experienced by nonsmokers, which may be more evident in females.…

  7. Bone marrow mononuclear cells up-regulate toll-like receptor expression and produce inflammatory mediators in response to cigarette smoke extract.

    Directory of Open Access Journals (Sweden)

    Junmin Zhou

    Full Text Available Several reports link cigarette smoking with leukemia. However, the effects of cigarette smoke extract (CSE on bone marrow hematopoiesis remain unknown. The objective of this study was to elucidate the direct effects of cigarette smoke on human bone marrow hematopoiesis and characterize the inflammatory process known to result from cigarette smoking. Bone marrow mononuclear cells (BMCs from healthy individuals when exposed to CSE had significantly diminished CFU-E, BFU-E and CFU-GM. We found increased nuclear translocation of the NF-κB p65 subunit and, independently, enhanced activation of AKT and ERK1/2. Exposure of BMCs to CSE induced IL-8 and TGF-β1 production, which was dependent on NF-κB and ERK1/2, but not on AKT. CSE treatment had no effect on the release of TNF-α, IL-10, or VEGF. Finally, CSE also had a significant induction of TLR2, TLR3 and TLR4, out of which, the up-regulation of TLR2 and TLR3 was found to be dependent on ERK1/2 and NF-κB activation, but not AKT. These results indicate that CSE profoundly inhibits the growth of erythroid and granulocyte-macrophage progenitors in the bone marrow. Further, CSE modulates NF-κB- and ERK1/2-dependent responses, suggesting that cigarette smoking may impair bone marrow hematopoiesis in vivo as well as induce inflammation, two processes that proceed malignant transformation.

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

    Directory of Open Access Journals (Sweden)

    Lijuan He

    2016-07-01

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

  9. Cigarette Smoking Among Socioeconomically Disadvantaged Young Adults in Association With Food Insecurity and Other Factors

    Directory of Open Access Journals (Sweden)

    Jin E. Kim, PhD

    2016-01-01

    Full Text Available Introduction Low socioeconomic status is associated with high rates of cigarette smoking, and socioeconomic differences in cigarette smoking tend to emerge during young adulthood. To further our understanding of socioeconomic differences in smoking among young adults, we examined correlates of smoking, with attention to multiple socioeconomic indicators that have not been examined in this population. Methods We analyzed data from the 2011–2012 California Health Interview Survey. The analytic sample consisted of young adults aged 18–30 years who were considered socioeconomically disadvantaged as measured by education and poverty. Logistic regression analyses were conducted to examine factors associated with smoking status in this group, and multinomial logistic regression analyses were conducted to examine correlates of smoking frequency. Results In this sample (N = 1,511; 48% female, 66% Hispanic/Latino, 18% non-Hispanic white, 39.7% reported experiencing food insecurity in the past year. Smoking prevalence was significantly higher among young adults who reported being food insecure (26.9% than among those who reported being food secure (16.4%. Past-year food insecurity was significantly associated with current smoking, independent of sociodemographic characteristics and alcohol use. Specifically, food insecurity was significantly associated with daily but not nondaily smoking. Conclusion Socioeconomically disadvantaged young adults with food insecurity may be considered a high-risk group with respect to cigarette smoking. Efforts to reduce tobacco-related health disparities should address diverse sources of socioeconomic influences, including experiences of food insecurity.

  10. The cessation and detoxification effect of tea filters on cigarette smoke

    Institute of Scientific and Technical Information of China (English)

    2010-01-01

    To treat tobacco addiction,a tea filter was developed and studied for smoking cessation.This work reports the smoking cessation effect of tea when it was used as a component of cigarette filters.In one trial it was found that after using the tea filters for 2 months,the volunteer smokers decreased their cigarette consumption by 56.5%,and 31.7% of them stopped smoking.This work identified a new method and material,tea filter and theanine,which inhibit tobacco and nicotine addiction and provide an effective strategy for treating tobacco addiction.

  11. Measuring environmental emissions from tobacco combustion: Sidestream cigarette smoke literature review

    Science.gov (United States)

    Guerin, M. R.; Higgins, C. E.; Jenkins, R. A.

    The tobacco-derived environmental emission of most common concern is the smoke issuing from cigarettes between puffs. A literature review of smoke formation mechanisms, sampling methods and selected emission factors suggests that sidestream deliveries are actually much less variable than is commonly thought. Examples of devices used to generate and collect sidestream smoke for analysis are described and their advantages and disadvantages discussed. Emissions computed as is common practice from sidestream/mainstream ratios are compared to those determined directly. The ratio method can yield misleading results because of the sensitivity of mainstream deliveries to cigarette and burn characteristics.

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

    Directory of Open Access Journals (Sweden)

    Quirk Jeffrey T

    2004-09-01

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

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

    Science.gov (United States)

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

    2015-07-01

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

  14. Cigarette Smoking Among Urban American Indian Adults - Hennepin and Ramsey Counties, Minnesota, 2011.

    Science.gov (United States)

    Forster, Jean; Poupart, John; Rhodes, Kristine; Peterson-Hickey, Melanie; Lamont, Genelle; D'Silva, Joanne; Erickson, Darin

    2016-01-01

    In 2013, it was estimated that the prevalence of cigarette smoking among American Indians was 36.5%, the highest of all racial/ethnic groups in the continental United States (1). Among American Indians, considerable cultural and geographic variation in cigarette smoking exists. Smoking prevalence among American Indians is lowest in the Southwest and highest in the Upper Midwest/Northern Plains (2). Little information is available about tobacco use among urban American Indians, who might not have ever lived on a reservation or be enrolled in or affiliated with a tribe. In Minnesota, a significant proportion of American Indians reside in urban areas. Among Minnesota's residents who identify as American Indian alone or in combination with another race, 30% live in Hennepin County and Ramsey County, which encompass Minneapolis and St. Paul, respectively (collectively known as the Twin Cities). The predominant tribes (Ojibwe [Chippewa] and Dakota/Lakota/Nakota [Sioux]) traditionally have used locally grown tobacco (Nicotiana rustica), red willow, and other plants for religious ceremonies, although nonceremonial tobacco is often substituted for traditional plants. To assess prevalence of cigarette smoking among this population, it is important to distinguish ceremonial tobacco use (smoked or used in other ways) from nonceremonial tobacco use. To obtain estimates of cigarette smoking prevalence among American Indians in Hennepin and Ramsey counties, the American Indian Adult Tobacco Survey was administered to 964 American Indian residents in 2011, using respondent-driven sampling. Among all participants, 59% were current smokers, 19% were former smokers, and 22% had never smoked. Approximately 40% of employed participants reported that someone smoked in their workplace area during the preceding week. High prevalences of cigarette smoking and secondhand smoke exposure among urban American Indians in Minnesota underscores the need for a comprehensive and culturally

  15. Cigarette smoking impairs nitric oxide-mediated cerebral blood flow increase: Implications for Alzheimer's disease.

    Science.gov (United States)

    Toda, Noboru; Okamura, Tomio

    2016-08-01

    Cerebral blood flow is mainly regulated by nitrergic (parasympathetic, postganglionic) nerves and nitric oxide (NO) liberated from endothelial cells in response to shear stress and stretch of vasculature, whereas sympathetic vasoconstrictor control is quite weak. On the other hand, peripheral vascular resistance and blood flow are mainly controlled by adrenergic vasoconstrictor nerves; endothelium-derived NO and nitrergic nerves play some roles as vasodilator factors. Cigarette smoking impairs NO synthesis in cerebral vascular endothelial cells and nitrergic nerves leading to interference with cerebral blood flow and glucose metabolism in the brain. Smoking-induced cerebral hypoperfusion is induced by impairment of synthesis and actions of NO via endothelial nitric oxide synthase (eNOS)/neuronal NOS (nNOS) inhibition and by increased production of oxygen radicals, resulting in decreased actions of NO on vascular smooth muscle. Nicotine acutely and chronically impairs the action of endothelial NO and also inhibits nitrergic nerve function in chronic use. Impaired cerebral blood supply promotes the synthesis of amyloid β that accelerates blood flow decrease. This vicious cycle is thought to be one of the important factors involving in Alzheimer's disease (AD). Quitting smoking is undoubtedly one of the important ways to prevent and delay the genesis or slow the progress of impaired cognitive function and AD. PMID:27530818

  16. Rat lung macrophage tumor cytotoxin production: impairment by chronic in vivo cigarette smoke exposure.

    Science.gov (United States)

    Flick, D A; Gonzalez-Rothi, R J; Harris, J O; Gifford, G E

    1985-11-01

    Macrophages in the presence of bacteria-derived lipopolysaccharide (LPS) stimuli produce a soluble cytotoxin which is toxic to tumor cells. In this study, we examined various parameters of cytotoxin production from pulmonary lavage cells obtained from Fisher 344 cesarean-derived rats. Cultures of macrophages were derived from pulmonary lavage cells and stimulated in vitro with LPS. Cytotoxin production was assayed in vitro using an L-929 cell target assay. Pulmonary lavage preparations contained a relatively pure population of macrophages, and adherence studies revealed that nonadherent lavage cells contributed negligible amounts of cytotoxin, indicating that macrophages were responsible for cytotoxin production. After LPS stimulation, cytotoxin production became maximal within 10 h and thereafter plateaued. Doses of LPS above 0.1 microgram/ml were optimal for production, and in the absence of LPS, no cytotoxin was detected. Because cigarette smoke is the major etiological factor in the development of lung cancers and because smoking is known to profoundly alter the function of alveolar macrophages in humans and experimental animals, subsequent experiments examined the role of chronic cigarette smoke exposure on tumoricidal activity of lung macrophages. Rats were exposed in vivo for 8 wk to either cigarette smoke or air (sham-treated controls). When lavage cells were cultured and stimulated with LPS (1 microgram/ml), 5- to 10-fold less cytotoxin was produced by lavage cells from rats exposed to cigarette smoke. Similarly, using a direct cytotoxicity assay, lung macrophages of smoke-exposed animals also revealed marked impairment in cytotoxicity against L-929 cell targets, and this was noted over a wide range of macrophage:tumor target cell ratios. Another product of macrophages, interferon, was also decreased in rats exposed in vivo to cigarette smoke when compared to sham-treated controls. These results suggest that cigarette smoke exposure may impair pulmonary

  17. Relationship between nicotine dependence and temperament and character traits in adults with cigarette smoking

    OpenAIRE

    Zincir, Selma Bozkurt; Zincir, Nihat; Sünbül, Esra Aydın; Kaymak, Esra

    2012-01-01

    Objective: Cigarette smoking is one of the most important health problems today. Nicotine dependence and difficulty to cessate smoking are assumed to be originating both from psychopharmacological effects of nicotine and genetic and environmental factors. The other possible factor which mediates to keep on smoking behavior may be personality traits. Aims: To find out the associations between temperament and character traits and nicotine dependence levels among the adult outpatients presen...

  18. Cigarette Smoking, Reduction and Quit Attempts: Prevalence Among Veterans With Coronary Heart Disease

    OpenAIRE

    Shahoumian, Troy A.; Phillips, Barbara R.; Backus, Lisa I.

    2016-01-01

    Introduction Cigarette smoking increases the risk of illness and early death for people with coronary heart disease. In 2010, Brown estimated prevalence rates for smoking among veterans and nonveterans with or without coronary heart disease in the United States, based on the 2003 through 2007 data from the Behavioral Risk Factor Surveillance System (BRFSS). Recent changes in BRFSS methods promise more accurate estimates for veterans. To inform assessment of efforts to reduce smoking, we sough...

  19. Associations of psychological capital, demographic and occupational factors with cigarette smoking among Chinese underground coal miners

    OpenAIRE

    Liu, Li; Xu, Xin; Wu, Hui; Yang, Yilong; Wang, Lie

    2015-01-01

    Background As a specific male occupational group, underground coal miners have been commonly found to have a high prevalence of cigarette smoking. It is of urgent need to explore some factors that could be intervened to reduce smoking from personal or internal perspective. The purpose of the present study was to examine the associations of psychological capital (PsyCap), demographic and occupational factors with smoking among Chinese underground coal miners. Methods A cross-sectional survey w...

  20. Influence of American acculturation on cigarette smoking behaviors among Asian American subpopulations in California

    OpenAIRE

    AN, NING; Cochran, Susan D.; Mays, Vickie M; McCarthy, William J.

    2008-01-01

    Using combined data from the population-based 2001 and 2003 California Health Interview Surveys, we examined ethnic and gender-specific smoking behaviors and the effect of three acculturation indicators on cigarette smoking behavior and quitting status among 8,192 Chinese, Filipino, South Asian, Japanese, Korean, and Vietnamese American men and women. After adjustment for potential confounders, current smoking prevalence was higher and the quit rate was lower for Korean, Filipino, and Vietnam...

  1. A Comparative Study on Cigarette Smoking Control Strategies Used In Tanzania and the United Kingdom

    OpenAIRE

    Hussein, Hassan

    2006-01-01

    To identify and compare different smoking control strategies used in the United Kingdom and United Republic of Tanzania Descriptive cross-sectional study Data was collected by an interview and observation at various institutions and clinics in Dar Es Salaam, Tanzania and London, UK and analysed using Epi-Info 2002. It was found that both the two countries have very good strategies against cigarette smoking but UK has a better organized system which is more effective in lowering down smoking p...

  2. Cigarette smoking leads to reduced relaxant responses of the cutaneous microcirculation

    DEFF Research Database (Denmark)

    Edvinsson, Marie-Louise; Andersson, Sven; Xu, Cang-Bao;

    2008-01-01

    BACKGROUND: Smoking is a major risk factor for cardiovascular disease. The present study was undertaken to examine if cigarette smoking translates into reduced relaxant responses of the peripheral microcirculation. METHODS: The cutaneous forearm blood flow was measured by laser Doppler flowmetry......+/-111% in nonsmokers to 355+/-83% in smokers, pcigarette...... smoking results in reduced peripheral microvascular responses to both endothelial and smooth muscle cell stimulation in healthy subjects, suggesting a generalized microvascular vasomotor function....

  3. Cigarette smoking leads to reduced relaxant responses of the cutaneous microcirculation

    DEFF Research Database (Denmark)

    Edvinsson, M.L.; Andersson, S.E.; Xu, C.B.;

    2008-01-01

    BACKGROUND: Smoking is a major risk factor for cardiovascular disease. The present study was undertaken to examine if cigarette smoking translates into reduced relaxant responses of the peripheral microcirculation. METHODS: The cutaneous forearm blood flow was measured by laser Doppler flowmetry......+/-111% in nonsmokers to 355+/-83% in smokers, pcigarette...... smoking results in reduced peripheral microvascular responses to both endothelial and smooth muscle cell stimulation in healthy subjects, suggesting a generalized microvascular vasomotor function Udgivelsesdato: 2008...

  4. Effects of bupropion on simulated demand for cigarettes and the subjective effects of smoking

    Science.gov (United States)

    2010-01-01

    Introduction: The biobehavioral mechanism(s) mediating bupropion’s efficacy are not well understood. Behavioral economic measures such as demand curves have proven useful in investigations of the reinforcing effects of drugs of abuse. Behavioral economic measures may also be used to measure the effect of pharmacotherapies on the reinforcing effects of drugs of abuse. Methods: The effects of bupropion on simulated demand for cigarettes were investigated in a placebo-controlled double-blind clinical trial. Participants reported the number of cigarettes they would purchase and consume in a single day at a range of prices. The effects of medication on the subjective effects of smoking were also explored. Results: Demand for cigarettes was well described by an exponential demand equation. Bupropion did not significantly decrease the maximum number of cigarettes that participants said they would smoke in a single day nor did it significantly alter the relation between price per cigarette and demand. Baseline demand elasticity did not predict smoking cessation, but changes in elasticity following 1 week of treatment did. Medication group had no effect on any subjective effects of smoking. Discussion: Bupropion had no significant effects on demand for cigarettes. The exponential demand equation, recently introduced in behavioral economics, proved amenable to human simulated demand and might be usefully employed in other pharmacotherapy studies as it provides a potentially useful measure of changes in the essential value of the drug as a reinforcer. Such changes may be useful in predicting the efficacy of medications designed to reduce drug consumption. PMID:20194522

  5. Colonic inflammation in mice is improved by cigarette smoke through iNKT cells recruitment.

    Directory of Open Access Journals (Sweden)

    Muriel Montbarbon

    Full Text Available Cigarette smoke (CS protects against intestinal inflammation during ulcerative colitis. Immunoregulatory mechanisms sustaining this effect remain unknown. The aim of this study was to assess the effects of CS on experimental colitis and to characterize the intestinal inflammatory response at the cellular and molecular levels. Using the InExpose® System, a smoking device accurately reproducing human smoking habit, we pre-exposed C57BL/6 mice for 2 weeks to CS, and then we induced colitis by administration of dextran sodium sulfate (DSS. This system allowed us to demonstrate that CS exposure improved colonic inflammation (significant decrease in clinical score, body weight loss and weight/length colonic ratio. This improvement was associated with a significant decrease in colonic proinflammatory Th1/Th17 cytokine expression, as compared to unexposed mice (TNF (p=0.0169, IFNγ (p<0.0001, and IL-17 (p=0.0008. Smoke exposure also induced an increased expression of IL-10 mRNA (p=0.0035 and a marked recruitment of iNKT (invariant Natural Killer T; CD45+ TCRβ+ CD1d tetramer+ cells in the colon of DSS-untreated mice. Demonstration of the role of iNKT cells in CS-dependent colitis improvement was performed using two different strains of NKT cells deficient mice. Indeed, in Jα18KO and CD1dKO animals, CS exposure failed to induce significant regulation of DSS-induced colitis both at the clinical and molecular levels. Thus, our study demonstrates that iNKT cells are pivotal actors in the CS-dependent protection of the colon. These results highlight the role of intestinal iNKT lymphocytes and their responsiveness to environmental stimuli. Targeting iNKT cells would represent a new therapeutic way for inflammatory bowel diseases.

  6. Social Network Characteristics, Social Support, and Cigarette Smoking among Asian/Pacific Islander Young Adults.

    Science.gov (United States)

    Pokhrel, Pallav; Fagan, Pebbles; Cassel, Kevin; Trinidad, Dennis R; Kaholokula, Joseph Keawe'aimoku; Herzog, Thaddeus A

    2016-06-01

    Cigarette smoking may be one of the factors contributing to the high levels of cancer-related mortality experienced by certain Asian/Pacific Islander (A/PI) subgroups (e.g., Native Hawaiian). Given the collectivist cultural orientation attributed to A/PI groups, social strategies are recommended for substance abuse or smoking cessation treatment among A/PI. However, research examining how social network characteristics and social support relate to smoking across A/PI subgroups has been lacking. This study investigated the associations between social network characteristics (e.g., size, composition), perceived social support, and recent cigarette use across Native Hawaiian, Filipino, and East Asian (e.g., Japanese, Chinese) young adults (18-35 year old). Cross-sectional, self-report data were collected from N = 435 participants (M age = 25.6, SD = 8.3; 61% women). Ethnic differences were found in a number of pathways linking social network characteristics, perceived social support, and cigarette smoking. Larger network size was strongly associated with higher perceived social support and lower recent cigarette smoking among Native Hawaiians but not Filipinos or East Asians. Higher perceived social support was associated with lower recent smoking among East Asians and Filipinos but not Native Hawaiians. Implications are discussed with regard to smoking prevention and cessation among A/PI. PMID:27297612

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

    Institute of Scientific and Technical Information of China (English)

    Marcel Leppe; Josip Culig; Mirela Eric

    2012-01-01

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

  8. Social Network Characteristics, Social Support, and Cigarette Smoking among Asian/Pacific Islander Young Adults.

    Science.gov (United States)

    Pokhrel, Pallav; Fagan, Pebbles; Cassel, Kevin; Trinidad, Dennis R; Kaholokula, Joseph Keawe'aimoku; Herzog, Thaddeus A

    2016-06-01

    Cigarette smoking may be one of the factors contributing to the high levels of cancer-related mortality experienced by certain Asian/Pacific Islander (A/PI) subgroups (e.g., Native Hawaiian). Given the collectivist cultural orientation attributed to A/PI groups, social strategies are recommended for substance abuse or smoking cessation treatment among A/PI. However, research examining how social network characteristics and social support relate to smoking across A/PI subgroups has been lacking. This study investigated the associations between social network characteristics (e.g., size, composition), perceived social support, and recent cigarette use across Native Hawaiian, Filipino, and East Asian (e.g., Japanese, Chinese) young adults (18-35 year old). Cross-sectional, self-report data were collected from N = 435 participants (M age = 25.6, SD = 8.3; 61% women). Ethnic differences were found in a number of pathways linking social network characteristics, perceived social support, and cigarette smoking. Larger network size was strongly associated with higher perceived social support and lower recent cigarette smoking among Native Hawaiians but not Filipinos or East Asians. Higher perceived social support was associated with lower recent smoking among East Asians and Filipinos but not Native Hawaiians. Implications are discussed with regard to smoking prevention and cessation among A/PI.

  9. Composition and emissions of VOCs in main- and side-stream smoke of research cigarettes

    Science.gov (United States)

    Charles, Simone M.; Batterman, S. A.; Jia, Chunrong

    It is well known that mainstream (MS) and sidestream (SS) cigarette smoke contains a vast number of chemical substances. Previous studies have emphasized SS smoke rather than MS smoke to which smokers are exposed, and most have used chamber tests that have several disadvantages such as wall losses. Emissions from standard research cigarettes have been measured, but relatively few constituents have been reported, and only the 1R4F (low nicotine) cigarette type has been tested. This study provides a comprehensive characterization of total, MS and SS smoke emissions for the 1R5F (ultra low nicotine), 2R4F (low nicotine), and 1R3F (standard nicotine) research cigarettes research cigarettes, including emission factors for a number of toxic compounds (e.g., benzene) and tobacco smoke tracers (e.g., 2,5-dimethyl furan). Emissions of volatile organic compounds (VOCs) and particulate matter (PM) are quantified using a dynamic dilution emission measurement system that is shown to produce accurate, rapid and reproducible results for over 30 VOCs and PM. SS and MS emissions were accurately apportioned based on a mass balance of total emissions. As expected, SS emissions greatly exceeded MS emissions. The ultra low nicotine cigarette had lower emissions of most VOCs compared to low and standard nicotine cigarettes, which had similar emissions. Across the three types of cigarettes, emissions of benzene (296-535 μg cig -1), toluene (541-1003 μg cig -1), styrene (90-162 μg cig -1), 2-dimethyl furan (71-244 μg cig -1), naphthalene (15-18 μg cig -1) and other VOCs were generally comparable to or somewhat higher than literature estimates using chamber tests.

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

    Directory of Open Access Journals (Sweden)

    Rotsika Vasiliki

    2010-02-01

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

  11. Mainstream cigarette smoke accelerates the progression of nonalcoholic steatohepatitis by modulating Kupffer cell-mediated hepatocellular apoptosis in adolescent mice.

    Science.gov (United States)

    Park, Surim; Kim, Jong Won; Yun, Hyejin; Choi, Seong-Jin; Lee, Sang-Hyub; Choi, Kyung-Chul; Lim, Chae Woong; Lee, Kyuhong; Kim, Bumseok

    2016-08-10

    Cigarette smoking in adolescents is considered to be a major cause of preventable morbidity and mortality. The purpose of this study is to investigate the role of mainstream cigarette smoke (MSCS) on the progression of nonalcoholic steatohepatitis in adolescents. Three-week-old C57BL/6 mice were fed either a methionine and choline-deficient plus high fat (MCDHF) diet for 6 weeks. Each group was exposed to MSCS (300, 600 ug/L) or fresh air for 2h per day during the first 3 weeks of MCDHF diet feeding. MSCS increased MCDHF diet-induced NASH by increasing serum ALT/AST levels, steatosis, inflammation, and fibrosis. Furthermore, MSCS was associated with the degree of oxidative stress and hepatocellular apoptosis in NASH mice, but not prominent in controls. In vitro, cigarette smoke extract (CSE) activated Kupffer cells (KCs) to release inflammatory cytokines and oxidative stress, which induced hepatocellular apoptosis. In conclusion, MSCS exposure accelerates the progression and severity of NASH by modulating KC-mediated hepatocellular apoptosis. Our results support the regulation of CS in adolescents with steatohepatitis. PMID:27180087

  12. Electronic Cigarette Use Among High School Students and Its Association With Cigarette Use And Smoking Cessation, North Carolina Youth Tobacco Surveys, 2011 and 2013

    Science.gov (United States)

    Kowitt, Sarah D.; Sutfin, Erin L.; Patel, Tanha; Ranney, Leah M.; Goldstein, Adam O.

    2016-01-01

    Introduction Although adolescent cigarette use continues to decline in the United States, electronic cigarette (e‑cigarette) use among adolescents has escalated rapidly. This study assessed trends and patterns of e‑cigarette use and concurrent cigarette smoking and the relationships between e-cigarette use and smoking cessation intentions and behaviors among high school students in North Carolina. Methods Data came from high school students who completed the school-based, cross-sectional North Carolina Youth Tobacco Survey in 2011 (n = 4,791) and 2013 (n = 4,092). This study assessed changes in prevalence of e-cigarette and cigarette use from 2011 through 2013, and cessation-related factors associated with those students’ current and past use of e‑cigarettes in 2013. Results The prevalence of current e-cigarette use (use in the past 30 days) significantly increased from 1.7% (95% CI, 1.3%–2.2%) in 2011 to 7.7% (95% CI, 5.9%–10.0%) in 2013. Among dual users, current e-cigarette use was negatively associated with intention to quit cigarette smoking for good (relative risk ratio [RRR] = 0.51; 95% CI, 0.29–0.87) and with attempts to quit cigarette smoking in the past 12 months (RRR = 0.69; 95% CI, 0.49–0.97). Current e-cigarette smokers were less likely than those who only smoked cigarettes to have ever abstained from cigarette smoking for 6 months (RRR = 0.42; 95% CI, 0.21–0.82) or 1 year (RRR = 0.21; 95% CI, 0.09–0.51) and to have used any kind of aids for smoking cessation (RRR = 0.46; 95% CI, 0.29–0.74). Conclusion Public health practitioners and cessation clinic service providers should educate adolescents about the risks of using any nicotine-containing products, including e-cigarettes, and provide adequate tobacco cessation resources and counseling to adolescent tobacco users. PMID:27490368

  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. Molecular mechanism of reduction in pregnenolone synthesis by cigarette smoke

    International Nuclear Information System (INIS)

    Steroidogenic acute regulatory protein (StAR) facilitates the movement of cholesterol from the outer to inner mitochondrial membrane for the synthesis of pregnenolone. Here, we investigated the molecular mechanism of the reduction of pregnenolone synthesis by cigarette smoke condensate (CSC). Pre-exposure or post-exposure of cells with CSC led to reduced pregnenolone synthesis, in a fashion similar to its effect on isolated mitochondria. However, there was no difference in the expression of 30 kDa StAR in cells treated with moderately concentrated CSC by either regimen. The active form of 37 kDa StAR is degraded easily suggesting that the continuous presence of CSC reduces StAR expression. Mitochondrial import of 35S-methionine-labeled StAR followed by extraction of the StAR-mitochondrial complex with 1% digitonin showed similarly sized complexes in the CSC-treated and untreated mitochondria. Further analysis by sucrose density gradient centrifugation showed a specific complex, 'complex 2', in the untreated mitochondria but absent in the CSC-treated mitochondria. Mass spectrometric analysis revealed that complex 2 is the outer mitochondrial protein, VDAC1. Knockdown of VDAC1 expression by siRNA followed by co-transfection with StAR resulted in a lack of pregnenolone synthesis and 37 kDa StAR expression with reduced expression of the intermediate, 32 kDa StAR. Taken together, these results suggest that in the absence of VDAC1, active StAR expression is reduced indicating that VDAC1 expression is essential for StAR activity. In the absence of VDAC1-StAR interaction, cholesterol cannot be transported into mitochondria; thus the interaction with VDAC1 is a mandatory step for initiating steroidogenesis

  15. Deposition of lead and cadmium released by cigarette smoke in dental structures and resin composite.

    Science.gov (United States)

    Takeuchi, Cristina Yoshie Garcia; Corrêa-Afonso, Alessandra Marques; Pedrazzi, Hamilton; Dinelli, Welingtom; Palma-Dibb, Regina Guenka

    2011-03-01

    Cigarette smoke is a significant source of cadmium, lead, and toxic elements, which are absorbed into the human organism. In this context, the aim of this study was to investigate in vitro the presence of toxic elements, cadmium, and lead deriving from cigarette smoke in the resin composite, dentine, and dental enamel. Eight cylindrical specimens were fabricated from resin composite, bovine enamel, and root dentin fragments that were wet ground and polished with abrasive paper to obtain sections with 6-mm diameter and 2-mm thickness. All specimens were exposed to the smoke of 10 cigarettes/day during 8 days. After the simulation of the cigarette smoke, the specimens were examined with scanning electron microscopy (SEM) and the energy-dispersive X-ray analysis. In the photomicrographic analysis in SEM, no morphological alterations were found; however, the microanalysis identified the presence of cadmium, arsenic, and lead in the different specimens. These findings suggest that the deposition of these elements derived from cigarette smoke could be favored by dental structures and resin composite. PMID:20687130

  16. PROTECTIVE EFFECTS OF GINSENOSIDE RB1 AGAINST RAT NEURONAL INJURY INDUCED BY CIGARETTE SMOKE%人参皂甙Rb1对香烟烟雾诱导大鼠神经细胞损伤的保护作用

    Institute of Scientific and Technical Information of China (English)

    庄严; 柳忠兰; 王丹丹; 李欣; 陈丽丽; 曹亦宾

    2011-01-01

    [Objective] To investigate the effects of Ginsenoside Rb1 (GRb1) on rat neuroxicity induced by cigarette smoke. [ Methods] Male Wister rats were prepared under cigarette smoking for 12 weeks. The amount of cigarettes was 8, 20 and 40 per day, respectively. GRb1 (10. 20 and 40mg/kg) was administered intra-peritoneal to rats after rat smoking for 12 weeks. Cerebral cortex neuronal cells were prepared from these rats in vitro. After 24h of GRb1 treatment, flow cytometric analysis of Annexin V (marks apoptosis) and PI (propidium iodide, marks necrosis) labeling cells. Western-Blot experiment was used to detect the expression of Survivin. The contents of free Ca2+ were determined in each group. [ Results] Cigarette smoke induced cerebral cortex neuronal apoptosis and necrosis, apoptosis and necrosis rates were significantly increased compared with control group. Compared with control group, 8 rami/d cigarettes increased 34% in the level of Survivin, 20 or 40rami/d cigarettes decreased 48% and 67% in the level of Survivin. However, GRb1 markedly reduced apoptosis and necrosis due to toxicity of 20rami/d cigarettes compared with the vehicle-treated cigarette smoke group, the apoptosis was redueed by 30.6% and 40.3% , and necrosis was reduced by 32.5% and 39.4%, after treatment by GRb1 of 20 and 40mg/kg. Meanwhile. GRb1 obviously reversed the down-regulation of Survivin expression induced by cigarette smoking (up-regulation by 45.1% and 54.8% when compared with that of the vehicle-treated cigarette smoking group). A Ca2+ probe showed an obvious increase in the intracellular Ca2+ during cigarette smoking treatment. and GRb1 of 20 or 40mg/kg significantly showed down cigarette-induced Ca2+ onglux (P < 0.01). [Conclusion] The neuroprotective effect of GRb1 against cigarette smoke toxicity was associated with inhibition of the accumulation of intracellular Ca2+ and up-regulation of Survivin expression in cerebral cortex neurons

  17. Natural killer cells in obesity: impaired function and increased susceptibility to the effects of cigarette smoke.

    LENUS (Irish Health Repository)

    O'Shea, Donal

    2012-02-01

    BACKGROUND: Obese individuals who smoke have a 14 year reduction in life expectancy. Both obesity and smoking are independently associated with increased risk of malignancy. Natural killer cells (NK) are critical mediators of anti-tumour immunity and are compromised in obese patients and smokers. We examined whether NK cell function was differentially affected by cigarette smoke in obese and lean subjects. METHODOLOGY AND PRINCIPAL FINDINGS: Clinical data and blood were collected from 40 severely obese subjects (BMI>40 kg\\/m(2)) and 20 lean healthy subjects. NK cell levels and function were assessed using flow cytometry and cytotoxicity assays. The effect of cigarette smoke on NK cell ability to kill K562 tumour cells was assessed in the presence or absence of the adipokines leptin and adiponectin. NK cell levels were significantly decreased in obese subjects compared to lean controls (7.6 vs 16.6%, p = 0.0008). NK function was also significantly compromised in obese patients (30% +\\/- 13% vs 42% +\\/-12%, p = 0.04). Cigarette smoke inhibited NK cell ability to kill tumour cell lines (p<0.0001). NK cells from obese subjects were even more susceptible to the inhibitory effects of smoke compared to lean subjects (33% vs 28%, p = 0.01). Cigarette smoke prevented NK cell activation, as well as perforin and interferon-gamma secretion upon tumour challenge. Adiponectin but not leptin partially reversed the effects of smoke on NK cell function in both obese (p = 0.002) and lean controls (p = 0.01). CONCLUSIONS\\/SIGNIFICANCE: Obese subjects have impaired NK cell activity that is more susceptible to the detrimental effects of cigarette smoke compared to lean subjects. This may play a role in the increase of cancer and infection seen in this population. Adiponectin is capable of restoring NK cell activity and may have therapeutic potential for immunity in obese subjects and smokers.

  18. Natural killer cells in obesity: impaired function and increased susceptibility to the effects of cigarette smoke.

    LENUS (Irish Health Repository)

    O'Shea, Donal

    2010-01-01

    BACKGROUND: Obese individuals who smoke have a 14 year reduction in life expectancy. Both obesity and smoking are independently associated with increased risk of malignancy. Natural killer cells (NK) are critical mediators of anti-tumour immunity and are compromised in obese patients and smokers. We examined whether NK cell function was differentially affected by cigarette smoke in obese and lean subjects. METHODOLOGY AND PRINCIPAL FINDINGS: Clinical data and blood were collected from 40 severely obese subjects (BMI>40 kg\\/m(2)) and 20 lean healthy subjects. NK cell levels and function were assessed using flow cytometry and cytotoxicity assays. The effect of cigarette smoke on NK cell ability to kill K562 tumour cells was assessed in the presence or absence of the adipokines leptin and adiponectin. NK cell levels were significantly decreased in obese subjects compared to lean controls (7.6 vs 16.6%, p = 0.0008). NK function was also significantly compromised in obese patients (30% +\\/- 13% vs 42% +\\/-12%, p = 0.04). Cigarette smoke inhibited NK cell ability to kill tumour cell lines (p<0.0001). NK cells from obese subjects were even more susceptible to the inhibitory effects of smoke compared to lean subjects (33% vs 28%, p = 0.01). Cigarette smoke prevented NK cell activation, as well as perforin and interferon-gamma secretion upon tumour challenge. Adiponectin but not leptin partially reversed the effects of smoke on NK cell function in both obese (p = 0.002) and lean controls (p = 0.01). CONCLUSIONS\\/SIGNIFICANCE: Obese subjects have impaired NK cell activity that is more susceptible to the detrimental effects of cigarette smoke compared to lean subjects. This may play a role in the increase of cancer and infection seen in this population. Adiponectin is capable of restoring NK cell activity and may have therapeutic potential for immunity in obese subjects and smokers.

  19. Disparities in Adult Cigarette Smoking - United States, 2002-2005 and 2010-2013.

    Science.gov (United States)

    Martell, Brandi N; Garrett, Bridgette E; Caraballo, Ralph S

    2016-01-01

    Although cigarette smoking has substantially declined since the release of the 1964 Surgeon General's report on smoking and health,* disparities in tobacco use exist among racial/ethnic populations (1). Moreover, because estimates of U.S. adult cigarette smoking and tobacco use are usually limited to aggregate racial or ethnic population categories (i.e., non-Hispanic whites [whites]; non-Hispanic blacks or African Americans [blacks]; American Indians and Alaska Natives [American Indians/Alaska Natives]; Asians; Native Hawaiians or Pacific Islanders [Native Hawaiians/Pacific Islanders]; and Hispanics/Latinos [Hispanics]), these estimates can mask differences in cigarette smoking prevalence among subgroups of these populations. To assess the prevalence of and changes in cigarette smoking among persons aged ≥18 years in six racial/ethnic populations and 10 select subgroups in the United States,(†) CDC analyzed self-reported data collected during 2002-2005 and 2010-2013 from the National Survey on Drug Use and Health (NSDUH) (2) and compared differences between the two periods. During 2010-2013, the overall prevalence of cigarette smoking among the racial/ethnic populations and subgroups ranged from 38.9% for American Indians/Alaska Natives to 7.6% for both Chinese and Asian Indians. During 2010-2013, although cigarette smoking prevalence was relatively low among Asians overall (10.9%) compared with whites (24.9%), wide within-group differences in smoking prevalence existed among Asian subgroups, from 7.6% among both Chinese and Asian Indians to 20.0% among Koreans. Similarly, among Hispanics, the overall prevalence of current cigarette smoking was 19.9%; however, within Hispanic subgroups, prevalences ranged from 15.6% among Central/South Americans to 28.5% among Puerto Ricans. The overall prevalence of cigarette smoking was higher among men than among women during both 2002-2005 (30.0% men versus 23.9% women) and 2010-2013 (26.4% versus 21.1%) (p<0.05). These

  20. Waterpipe Tobacco Smoking and Susceptibility to Cigarette Smoking Among Young Adults in the United States, 2012–2013

    OpenAIRE

    Salloum, Ramzi G.; Haider, M. Rifat; Barnett, Tracey E; Guo, Yi; Getz, Kayla R.; Thrasher, James F.; Maziak, Wasim

    2016-01-01

    Introduction Waterpipe tobacco smoking, also known as hookah and shisha, has surged in popularity among young people in the United States. Waterpipe is also increasingly becoming the first tobacco product that young people try. Given the limited access to and limited portability of waterpipes, waterpipe smokers who become more nicotine dependent over time may be more likely to turn to cigarettes. This study examined the relationship between waterpipe tobacco smoking and susceptibility to ciga...

  1. 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, 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.

  2. Smoke chemistry, in vitro and in vivo toxicology evaluations of the electrically heated cigarette smoking system series K.

    Science.gov (United States)

    Werley, Michael S; Freelin, Susan A; Wrenn, Susan E; Gerstenberg, Birgit; Roemer, Ewald; Schramke, Heike; Van Miert, Erik; Vanscheeuwijck, Patrick; Weber, Susanne; Coggins, Christopher R E

    2008-11-01

    The Electrically Heated Cigarette Smoking System Series K (EHCSS) produces smoke through the controlled electrical heating of tobacco. Evaluation of the EHCSS was accomplished by comparison with commercial and reference cigarettes, using International Organization for Standardization (ISO) and alternative puffing regimens based on nicotine exposures measured in a short-term clinical study. Using the alternative puffing regimen and compared with conventional cigarettes on a per cigarette basis, the EHCSS had 50-60% reductions in tar and nicotine; at least 90% reductions in carbon monoxide, nitrogen oxides, 1,3-butadiene, isoprene, acrylonitrile, polyaromatic hydrocarbons, hydrogen cyanide, aromatic amines, tobacco specific nitrosamines, and phenol; and least a 40% reduction in 2-nitropropane. Other important smoke constituents in EHCSS smoke were reduced as well. The in vitro studies showed similar large reductions in biological activity. Ames mutagenicity of total particulate matter (TPM) from the EHCSS was reduced by 70-90%; cytotoxicity of the TPM was reduced by approximately 82% and 65% for the gas-vapor phase. In vivo testing under ISO smoking conditions in the mouse skin painting assay demonstrated later dermal tumor onset, lower dermal tumor incidence, reduced dermal tumor multiplicity, and a lower proportion of malignant dermal tumors in EHCSS smoke condensate-exposed mice. Thirty-five day and 90-day nose-only inhalation studies in rats showed reductions in pulmonary inflammation and other biological activity, including histopathological endpoints. We conclude that under the conditions of these in vitro and in vivo studies, the EHCSS demonstrated significantly lower biological activity compared to conventional cigarettes, and may suggest the potential for reductions in human smokers. PMID:18590791

  3. Cigarette smoking during early pregnancy reduces the number of embryonic germ and somatic cells

    DEFF Research Database (Denmark)

    Mamsen, Linn; Lutterodt, M C; Andersen, Elisabeth Anne Wreford;

    2010-01-01

    BACKGROUND: Cigarette smoking during pregnancy is associated with negative reproductive consequences for male fetuses in adult life such as reduced testicular volume and sperm concentration. The present study evaluates the number of germ and somatic cells present in human embryonic first......-trimester gonads in relation to maternal smoking. METHODS: The study includes 24 human first-trimester testes, aged 37-68 days post-conception, obtained from women undergoing legal termination of pregnancy. A questionnaire was used to obtain information about smoking and drinking habits during pregnancy. Validated...... = 0.004] and somatic cells by 37% (95% CI 59-3%, P = 0.023) was observed in testes prenatally exposed to maternal cigarette smoking, compared with unexposed. The effect of maternal smoking was dose-dependent being higher in the heavy smokers and remained consistent after adjusting for possible...

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

    Science.gov (United States)

    Jaspers, Ilona

    2014-01-01

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

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

    Science.gov (United States)

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

    2012-11-01

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

  6. Cigarette smoking and alcohol consumption among Chinese older adults: do living arrangements matter?

    Science.gov (United States)

    Zhang, Jiaan; Wu, Liyun

    2015-02-23

    This study used five waves of the Chinese Longitudinal Healthy Longevity Survey to examine the relationship between living arrangements, smoking, and drinking among older adults in China from 1998-2008. We found that living arrangements had strong implications for cigarette smoking and alcohol consumption among the elderly. First, the likelihood of smoking was lower among older men living with children, and older women living either with a spouse, or with both a spouse and children; and the likelihood of drinking was lower among both older men, and women living with both a spouse and children, compared with those living alone. Second, among dual consumers (i.e., being a drinker and a smoker), the amount of alcohol consumption was lower among male dual consumers living with children, while the number of cigarettes smoked was higher among female dual consumers living with others, compared with those living alone. Third, among non-smoking drinkers, the alcohol consumption was lower among non-smoking male drinkers in all types of co-residential arrangements (i.e., living with a spouse, living with children, living with both a spouse and children, or living with others), and non-smoking female drinkers living with others, compared with those living alone. Results highlighted the importance of living arrangements to cigarette smoking and alcohol consumption among Chinese elderly. Co-residential arrangements provided constraints on Chinese older adults' health-risk behaviors, and had differential effects for men and women.

  7. Cigarette Smoking and Alcohol Consumption among Chinese Older Adults: Do Living Arrangements Matter?

    Directory of Open Access Journals (Sweden)

    Jiaan Zhang

    2015-02-01

    Full Text Available This study used five waves of the Chinese Longitudinal Healthy Longevity Survey to examine the relationship between living arrangements, smoking, and drinking among older adults in China from 1998–2008. We found that living arrangements had strong implications for cigarette smoking and alcohol consumption among the elderly. First, the likelihood of smoking was lower among older men living with children, and older women living either with a spouse, or with both a spouse and children; and the likelihood of drinking was lower among both older men, and women living with both a spouse and children, compared with those living alone. Second, among dual consumers (i.e., being a drinker and a smoker, the amount of alcohol consumption was lower among male dual consumers living with children, while the number of cigarettes smoked was higher among female dual consumers living with others, compared with those living alone. Third, among non-smoking drinkers, the alcohol consumption was lower among non-smoking male drinkers in all types of co-residential arrangements (i.e., living with a spouse, living with children, living with both a spouse and children, or living with others, and non-smoking female drinkers living with others, compared with those living alone. Results highlighted the importance of living arrangements to cigarette smoking and alcohol consumption among Chinese elderly. Co-residential arrangements provided constraints on Chinese older adults’ health-risk behaviors, and had differential effects for men and women.

  8. Smoking Revolution” A Content Analysis of Electronic Cigarette Retail Websites

    Science.gov (United States)

    Grana, Rachel A.; Ling, Pamela M.

    2014-01-01

    Background Electronic cigarettes (e-cigarettes) have been increasingly available and marketed in the U.S. since 2007. As patterns of product adoption are frequently driven and reinforced by marketing, it is important to understand the marketing claims encountered by consumers. Purpose To describe the main advertising claims made on branded e-cigarette retail websites. Methods Websites were retrieved from two major search engines in 2011 using iterative searches with the following terms: electronic cigarette, e-cigarette, e-cig, and personal vaporizer. Fifty-nine websites met inclusion criteria, and 13 marketing claims were coded for main marketing messages in 2012. Results Ninety-five percent of the websites made explicit or implicit health-related claims, 64% had a smoking cessation-related claim, 22% featured doctors, and 76% claimed that the product does not produce secondhand smoke. Comparisons to cigarettes included claims that e-cigarettes were cleaner (95%) and cheaper (93%). Eighty-eight percent stated that the product could be smoked anywhere and 71% mentioned using the product to circumvent clean air policies. Candy, fruit, and coffee flavors were offered on most sites. Youthful appeals included images or claims of modernity (73%), increased social status (44%), enhanced social activity (32%), romance (31%), and use by celebrities (22%). Conclusions Health claims and smoking cessation messages that are unsupported by current scientific evidence are frequently used to sell e-cigarettes. Implied and overt health claims, the presence of doctors on websites, celebrity endorsements, and the use of characterizing flavors should be prohibited. PMID:24650842

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

    Science.gov (United States)

    Ozkol, Halil; Tülüce, Yasin; Koyuncu, Ismail

    2012-02-01

    This study was carried out to determine the preventive effect of Calendula officinalis L. (pot marigold) on rats exposed to cigarette smoke (CS). Rats were divided into three groups as control, CS and CS + pot marigold (PM). The rats in the CS and CS + PM groups were subjected to CS for 1 h twice a day for 23 days. PM (100 mg/kg body weight) was given to rats in the CS + PM group by gavage, 1 h before each administration period. While malondialdehyde, protein carbonyl contents and reduced glutathione level of the CS group increased, their levels diminished by PM administration. In addition, glutathione peroxidase (GPx), superoxide dismutase activities and β-carotene, vitamins A and C levels decreased in the CS group compared to control, however activities of these enzymes and concentration of vitamins were elevated by PM supplementation. This investigation showed that administration of PM supplied relative protection against subacute CS-induced cell injury. PMID:21505008

  10. Will any future increase in cigarette price reduce smoking in Saudi Arabia?

    Directory of Open Access Journals (Sweden)

    Omar A. Al-Mohrej

    2014-01-01

    Full Text Available Context: In Saudi Arabia, no studies have been conducted on the correlation between any possible cigarette′s price increase and its effects on cigarette consumption. Aims: The aim of this study was to determine the prevalence of cigarette smoking in Saudi Arabia and to predict the effect of price increase on cigarette consumption. Settings and Design: A cross-sectional study was conducted in April and May 2013. Methods: We developed an Arabic questionnaire with information on demographic and socioeconomic factors, smoking history, and personal opinion on the effect of price increase on cigarette consumption. The questionnaire was distributed in public places such as malls and posted on famous Saudi athlete media′s twitter accounts. Results: Among the 2057 included responses, 802 (39% were current smokers. The smokers′ population constituted of 746 (92% males, of which 546 (68% had a monthly income equal or greater to 800 US dollars, and 446 (55% were aged between 21 and 30 years. Multivariate analyses of the risk factors for smoking showed that male gender and older age were associated with greater risk. Despite the current low prices of 2.67 US dollars, 454 smokers (56% thought that cigarette prices are expensive. When asked about the price of cigarettes that will lead to smoking cessation, 443 smokers (55% expected that a price of 8.27 US dollars and more per pack will make them quit. Conclusions: Increasing the price of popular cigarettes pack from 2.67 US dollars to 8.27 US dollars is expected to lead to smoking cessation in a large number of smokers in the Saudi population.

  11. Induction of murine macrophage M2 polarization by cigarette smoke extract via the JAK2/STAT3 pathway.

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    Fengjiao Yuan

    Full Text Available Cigarette smoking is a major pathogenic factor in lung cancer. Macrophages play an important role in host defense and adaptive immunity. These cells display diverse phenotypes for performing different functions. M2 type macrophages usually exhibit immunosuppressive and tumor-promoting characteristics. Although macrophage polarization toward the M2 phenotype has been observed in the lungs of cigarette smokers, the molecular basis of the process remains unclear. In this study, we evaluated the possible mechanisms for the polarization of mouse macrophages that are induced by cigarette smoking (CS or cigarette smoke extract (CSE. The results showed that exposure to CSE suppressed the production of reactive oxygen species (ROS and nitric oxide (NO and down-regulated the phagocytic ability of Ana-1 cells. The CD163 expressions on the surface of macrophages from different sources were significantly increased in in vivo and in vitro studies. The M1 macrophage cytokines TNF-α, IL-12p40 and enzyme iNOS decreased in the culture supernatant, and their mRNA levels decreased depending on the time and concentration of CSE. In contrast, the M2 phenotype macrophage cytokines IL-10, IL-6, TGF-β1 and TGF-β2 were up-regulated. Moreover, phosphorylation of JAK2 and STAT3 was observed after the Ana-1 cells were treated with CSE. In addition, pretreating the Ana-1 cells with the STAT3 phosphorylation inhibitor WP1066 inhibited the CSE-induced CD163 expression, increased the mRNA level of IL-10 and significantly decreased the mRNA level of IL-12. In conclusion, we demonstrated that the M2 polarization of macrophages induced by CS could be mediated through JAK2/STAT3 pathway activation.

  12. 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.

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

    Directory of Open Access Journals (Sweden)

    Gerald A. Long

    2014-10-01

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

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

    Directory of Open Access Journals (Sweden)

    Dauphinee Amanda L

    2013-02-01

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

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

    Science.gov (United States)

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

    2013-11-01

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

  16. Fighting against cigarette smoking among medical students: a success story.

    Science.gov (United States)

    İçli, Fikri; Calışkan, Deniz; Gönüllü, Uğur; Sunguroğlu, Kadirhan; Akdur, Recep; Akbulut, Hakan; Özkan, Asiye; Ölmez, Senay; Gönüllü, İpek; İbiş, Erkan

    2014-09-01

    A survey in the year 2007 among medical students of Ankara University Medical School to assess the smoking rates showed that 25.1 % of them were smoking. Moreover, the smoking rate was 35 % at sixth grade students and 60 % of the smokers specified that they started smoking at medical school. This report provides a successful approach to decrease smoking among medical students by measures against starting smoking. An "Antismoking Group" composed of voluntary academic staff, nurses, students, psychologists, and a social worker of the medical school was established to engage in lowering the smoking rate and eliminating it eventually among our students. Several methods including regular monthly meetings, annual "Smoking or Health" symposiums, and lectures to first, second, and third grade students to increase their awareness related to harms of smoking and their role in the fight against smoking were carried out. Our surveys in the years 2009 (641 students) and 2012 (975 students) showed that total smoking rates dropped to 15.0 and 11.0 %, respectively (p students dropped from 35.0 % in 2007 to 21.8 and 8.8 % in the years 2009 and 2012, respectively (p students were 7.8 and 9.0 %, respectively. These close rates of smoking at the first and last years of medical school training and the significant drop in smoking rates in 5 years confirm that our group pursued a realistic and successful strategy against smoking. PMID:24189831

  17. Views from the Coalface: What Do English Stop Smoking Service Personnel Think about E-Cigarettes?

    OpenAIRE

    Rosemary Hiscock; Linda Bauld; Deborah Arnott; Martin Dockrell; Louise Ross; Andy McEwen

    2015-01-01

    The UK Stop Smoking Services (SSS) are a source of information and advice on e-cigarettes for smokers and thus it is important to understand the knowledge of, and attitudes towards, e-cigarettes held by stop smoking practitioners. The datasets were English SSS quarterly monitoring returns (n = 207,883) and an online survey of English SSS practitioners, managers, and commissioners between 26th November and 15th December 2014 (n = 1801). SSS monitoring data suggested 2% of clients were using e-...

  18. Allowing cigarette or marijuana smoking in the home and car: prevalence and correlates in a young adult sample

    OpenAIRE

    Padilla, Mabel; Berg, Carla J.; Schauer, Gillian L.; Lang, Delia L.; Kegler, Michelle C.

    2014-01-01

    Given the increased marijuana use, negative health consequences of marijuana secondhand smoke exposure (SHSe) and dearth of research regarding marijuana SHSe in personal settings, we examined the prevalence and correlates of allowing marijuana versus cigarette smoking in personal settings among 2002 online survey respondents at two southeastern US universities in 2013. Findings indicated that 14.5% allowed cigarettes in the home, 17.0% marijuana in the home, 35.9% cigarettes in cars and 27.3%...

  19. Hookah, Cigarette, and Marijuana Use: A Prospective Study of Smoking Behaviors among First-Year College Women

    OpenAIRE

    Fielder, Robyn L.; Carey, Kate B.; Carey, Michael P.

    2013-01-01

    Better understanding of the temporal sequence of hookah, cigarette, and marijuana use will help to inform smoking prevention efforts. To address this gap in the literature, we assessed all three of these smoking behaviors in a sample of 424 first-year college women. Using a longitudinal design, we investigated whether hookah use predicts initiating/resuming cigarette and/or initiating marijuana use, and whether cigarette and/or marijuana use predict initiating hookah use. Participants (67% Wh...

  20. Prevalence of and Susceptibility to Cigarette Smoking Among Female Students Aged 13 to 15 Years in Vietnam, 2007

    Directory of Open Access Journals (Sweden)

    Hoang Van Minh, MD, PhD

    2010-01-01

    Full Text Available IntroductionRecent reports show a sharp increase in smoking rates among girls. We describe prevalence of cigarette smoking and susceptibility to cigarette smoking among female students aged 13 to 15 years in Vietnam and examine the associated factors.MethodsWe used data from female secondary school students aged 13 to 15 years (grades 8-10 from the 2007 Global Youth Tobacco Survey that was conducted in 9 provinces in Vietnam. We used multivariate logistic regression analysis to determine associations between independent variables with smoking status and susceptibility to smoking.ResultsPrevalence of cigarette smoking among girls was 1.2% (95% confidence interval [CI], 0.9-1.5, and 1.5% (95% CI, 1.2-1.9 of girls were susceptible to smoking. Having friends who smoke was the strongest predictor of both smoking status and susceptibility to smoking. Attendance at school classes that described the harmful effects of smoking had significant effects in reducing cigarette smoking. Girls who were exposed to billboard cigarette advertising were more likely to be susceptible to smoking than were those who had not seen advertisements.ConclusionOur findings highlight the need for pursuing school-based intervention programs in Vietnam and for countering tobacco advertising and marketing practices that target young women.

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

    Directory of Open Access Journals (Sweden)

    Kenneth R Eyring

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

  2. Smoking motivators are different among cigarette and waterpipe smokers: The results of ITUPP.

    Science.gov (United States)

    Roohafza, Hamidreza; Heidari, Kamal; Alinia, Tahereh; Omidi, Razieh; Sadeghi, Masoumeh; Andalib, Elham; Ajami, Ali; Sarrafzadegan, Nizal

    2015-09-01

    The present study explores different drivers of cigarette and water pipe smoking among middle and high school students in Isfahan province. A questionnaire-based cross-sectional study was conducted. Trained staff collected questionnaires and saliva samples for response accuracy evaluation. Prevalence by demographic, parental and educational factors was calculated. Logistic regression was applied to compare behavior drivers of those who purely smoked cigarettes or a waterpipe. Waterpipe smokers were considered as the reference category. This study reported ORs along 95% confidence intervals; 5408 questionnaires were returned. The sample age was 15.37±01.70 on average. The self-reported prevalence of cigarette and waterpipe experimentation was 11.60% (n=624) and 20.70% (n=1,109), respectively; and 5.08% (n=311), 11.06% (n=619) for smokers, and 13.30% (n=711) for the whole sample. Psychological factors were the most important driver for cigarette smoking; bad event happening with odds of 2.38 (95% CI: 1.29-4.39); angriness 2.58 times (95% CI: 1.51-4.43); and distress by 2.49 times (95% CI: 1.42-4.40). Habitual situations were strong predictors of cigarette smoking, but not a predictor of waterpipe smoking, such as smoking after a meal (OR=3.11, 95% CI: 1.67-5.77); and smoking after waking up (OR=2.56, 95% CI: 1.42-4.40). Comprehensive and multifaceted preventive programs must tailor identified factors and increase family's awareness. PMID:26231400

  3. SMOKE ’EM IF YOU GOT ’EM: CIGARETTE BLACK MARKETS IN U.S. PRISONS AND JAILS

    OpenAIRE

    Lankenau, Stephen E.

    2001-01-01

    Since the mid-1980s, cigarette-smoking policies have become increasingly restrictive in jails and prisons across the United States. Cigarette black markets of various form and scale often emerge in jails and prisons where tobacco is prohibited or banned. Case studies of 16 jails and prisons were undertaken to understand the effects of cigarette bans versus restrictions on inmate culture and prison economies. This study describes how bans can transform largely benign cigarette “gray markets,” ...

  4. Smoke Gets in Your Eyes: Cigarette Tax Salience and Regressivity

    OpenAIRE

    Jacob Goldin; Tatiana Homonoff

    2013-01-01

    Recent evidence suggests consumers pay less attention to commodity taxes levied at the register than to taxes included in a good's posted price. If this attention gap is larger for high-income consumers than for low-income consumers, policymakers can manipulate a tax's regressivity by altering the fraction of the tax imposed at the register. We investigate income differences in attentiveness to cigarette taxes, exploiting state and time variation in cigarette excise and sales tax rates. Where...

  5. Hookah use predicts cigarette smoking progression among college smokers

    OpenAIRE

    Doran, N; Godfrey, KM; Myers, MG

    2015-01-01

    © The Author 2015. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved. Introduction: Hookah use is increasingly common among U.S. college students, but little is known regarding the relationship between hookah and cigarette use. The purpose of this study was to test the hypothesis that the added nicotine exposure from hookah use may accelerate the uptake of cigarettes. Methods: An ethnically diverse sample of college student...

  6. Cigarette smoking and its association with serum lipid/lipoprotein among Chinese nonagenarians/centenarians

    Directory of Open Access Journals (Sweden)

    Yan-Ling Zhang

    2012-07-01

    Full Text Available Abstract Objective Cigarette smoking had been confirmed as an increased risk for dyslipidemia, but none of the evidence was from long-lived population. In present study, we detected relationship between cigarette smoking habits and serum lipid/lipoprotein (serum Triglyceride (TG, Total cholesterol (TC, Low-density lipoprotein (LDL and high-density lipoprotein (HDL among Chinese Nonagenarians/Centenarian. Methods The present study analyzed data from the survey that was conducted on all residents aged 90 years or more in a district, there were 2,311,709 inhabitants in 2005. Unpaired Student’s t test, χ2 test, and multiple logistic regression were used to analyze datas. Results The individuals included in the statistical analysis were 216 men and 445 women. Current smokers had lower level of TC (4.05 ± 0.81 vs. 4.21 ± 0.87, t = 2.403, P = 0.017 and lower prevalence of hypercholesteremia (9.62% vs. 15.13%, χ2 = 3.018,P = 0.049 than nonsmokers. Unadjusted and adjusted multiple logistic regressions showed that cigarette smoking was not associated with risk for abnormal serum lipid/lipoprotein. Conclusions In summary, we found that among Chinese nonagenarians/centenarians, cigarette smoking habits were not associated with increased risk for dyslipidemia, which was different from the association of smoking habits with dyslipidemia in general population.

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

    Directory of Open Access Journals (Sweden)

    Maggie Folkesson

    2016-07-01

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

  8. Use of the zebrafish larvae as a model to study cigarette smoke condensate toxicity.

    Directory of Open Access Journals (Sweden)

    Lee D Ellis

    Full Text Available The smoking of tobacco continues to be the leading cause of premature death worldwide and is linked to the development of a number of serious illnesses including heart disease, respiratory diseases, stroke and cancer. Currently, cell line based toxicity assays are typically used to gain information on the general toxicity of cigarettes and other tobacco products. However, they provide little information regarding the complex disease-related changes that have been linked to smoking. The ethical concerns and high cost associated with mammalian studies have limited their widespread use for in vivo toxicological studies of tobacco. The zebrafish has emerged as a low-cost, high-throughput, in vivo model in the study of toxicology. In this study, smoke condensates from 2 reference cigarettes and 6 Canadian brands of cigarettes with different design features were assessed for acute, developmental, cardiac, and behavioural toxicity (neurotoxicity in zebrafish larvae. By making use of this multifaceted approach we have developed an in vivo model with which to compare the toxicity profiles of smoke condensates from cigarettes with different design features. This model system may provide insights into the development of smoking related disease and could provide a cost-effective, high-throughput platform for the future evaluation of tobacco products.

  9. Use of the zebrafish larvae as a model to study cigarette smoke condensate toxicity.

    Science.gov (United States)

    Ellis, Lee D; Soo, Evelyn C; Achenbach, John C; Morash, Michael G; Soanes, Kelly H

    2014-01-01

    The smoking of tobacco continues to be the leading cause of premature death worldwide and is linked to the development of a number of serious illnesses including heart disease, respiratory diseases, stroke and cancer. Currently, cell line based toxicity assays are typically used to gain information on the general toxicity of cigarettes and other tobacco products. However, they provide little information regarding the complex disease-related changes that have been linked to smoking. The ethical concerns and high cost associated with mammalian studies have limited their widespread use for in vivo toxicological studies of tobacco. The zebrafish has emerged as a low-cost, high-throughput, in vivo model in the study of toxicology. In this study, smoke condensates from 2 reference cigarettes and 6 Canadian brands of cigarettes with different design features were assessed for acute, developmental, cardiac, and behavioural toxicity (neurotoxicity) in zebrafish larvae. By making use of this multifaceted approach we have developed an in vivo model with which to compare the toxicity profiles of smoke condensates from cigarettes with different design features. This model system may provide insights into the development of smoking related disease and could provide a cost-effective, high-throughput platform for the future evaluation of tobacco products. PMID:25526262

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

    Science.gov (United States)

    Popa, Cristina

    2015-05-01

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

  11. Media Literacy and Cigarette Smoking in Hungarian Adolescents

    Science.gov (United States)

    Page, Randy M.; Piko, Bettina F.; Balazs, Mate A.; Struk, Tamara

    2011-01-01

    Objective: To assess smoking media literacy in a sample of Hungarian youth and to determine its association with current smoking and susceptibility to future smoking. Design: Quantitative cross-sectional survey. Setting: Four elementary and four high schools in Mako, Hungary. Method: A survey form was administered in regularly-scheduled classes to…

  12. Cigarette Smoking: Health Risks and How to Quit (PDQ)

    Science.gov (United States)

    ... smoke and want to quit. More people quit smoking with peer-counseling than with self-help programs. If you are a childhood cancer survivor and you smoke, talk to your doctor about peer-counseling programs. Drug treatment Treatment with drugs is also used to help ...

  13. Reduced exposure evaluation of an Electrically Heated Cigarette Smoking System. Part 6: 6-Day randomized clinical trial of a menthol cigarette in Japan.

    Science.gov (United States)

    Tricker, Anthony R; Kanada, Shigeto; Takada, Kohji; Martin Leroy, Claire; Lindner, Dirk; Schorp, Matthias K; Dempsey, Ruth

    2012-11-01

    A randomized, controlled, open-label, parallel-group, single-center study to determine biomarkers of exposure to 12 selected harmful and potentially harmful constituents (HPHC) in cigarette smoke, excretion of mutagenic material in urine, and serum Clara cell 16-kDa protein (CC16) in 102 male and female Japanese subjects who smoked Marlboro Ultra Lights Menthol cigarettes (M4J(M); 4 mg tar and 0.3mg nicotine) at baseline. Subjects were randomized to continue smoking M4J(M), or switch to smoking either the Electrically Heated Cigarette Smoking System menthol cigarette (EHCSS-K6(M); 5mg tar and 0.3mg nicotine) or the Lark One menthol cigarette (Lark1(M); 1mg tar and 0.1mg nicotine), or to no-smoking. The mean decreases from baseline to Day 5/6 were statistically significant (p ≤ 0.05) for exposure to 10 of 12 cigarette smoke HPHC including the primary endpoint (carbon monoxide) and urinary excretion of mutagenic material in the EHCSS-K6(M) group (-12.3% to -83.4%). Smaller, but statistically significant reductions (p ≤ 0.05) occurred in the Lark1(M) group (-3.3% to -35.2%), with the exception of urinary mutagens. The largest mean reductions (all p ≤ 0.05) in exposure to cigarette smoke HPHC and excretion of mutagenic material occurred in the no-smoking group (-1.4% to -93.6%). Serum CC16, an indicator of lung epithelial injury, was not significantly different between groups. PMID:22951347

  14. New interpretation of arterial stiffening due to cigarette smoking using a structurally motivated constitutive model

    DEFF Research Database (Denmark)

    Enevoldsen, Majken; Henneberg, K-A; Jensen, J A;

    2011-01-01

    Cigarette smoking is the leading self-inflicted risk factor for cardiovascular diseases; it causes arterial stiffening with serious sequelea including atherosclerosis and abdominal aortic aneurysms. This work presents a new interpretation of arterial stiffening caused by smoking based on data...... published for rat pulmonary arteries. A structurally motivated "four fiber family" constitutive relation was used to fit the available biaxial data and associated best-fit values of material parameters were estimated using multivariate nonlinear regression. Results suggested that arterial stiffening caused...

  15. Cigarette Smoking Practices and Its Determinants Among University Students in Southwest, Nigeria

    OpenAIRE

    OA Babatunde; OE Elegbede; LM Ayodele; OA Atoyebi; DO Ibirongbe; AO Adeagbo

    2012-01-01

    Background: Tobacco smoking is one of the largest causes of preventable morbidity and mortality globally, and is responsible for many causes of premature deaths. This study seeks to find out cigarette-smoking practices among University Students in Ekiti State, Nigeria and identify its determinants. Methodology: This study was a descriptive cross-sectional study of young adults in tertiary institutions. The sample size was 300 while multi stage sampling technique was adopted to select the stud...

  16. Relationship between salivary stress biomarker levels and cigarette smoking in healthy young adults: an exploratory analysis

    OpenAIRE

    SUZUKI, Nao; Nakanishi, Kosuke; Yoneda, Masahiro; Hirofuji, Takao; Hanioka, Takashi

    2016-01-01

    Background This study investigated the relationships among salivary stress biomarkers, cigarette smoking, and mood states. Methods The study population comprised 49 healthy sixth-year dental students at Fukuoka Dental College (39 men, 10 women; age, 23–31 years). Lifetime exposure to smoking was calculated using the Brinkman index (BI). Resting saliva samples were collected, and concentrations of cortisol, secretory immunoglobulin A (SIgA), interleukin (IL)-1β, interleukin-6, and tumor necros...

  17. Cigarette smoking in military pilots and intima-media thickness of the carotid arteries

    OpenAIRE

    Jovelić Stojan; Hajduković Zoran; Jovelić Aleksandra; Rađen Slavica

    2005-01-01

    Background. It is well known that smoking is associated with an increase in arterial wall thickness. However, most studies of this problem have been undertaken in age and sex heterogeneous groups, as well as in patients with already present other conventional risk factors. The aim of this study was to assess the effect of cigarette smoking on arterial wall thickness of the common carotid artery in asymptomatic pilots. Methods. The imaging of intima−media thickness of the posterior wall of the...

  18. Use of the Zebrafish Larvae as a Model to Study Cigarette Smoke Condensate Toxicity

    OpenAIRE

    Ellis, Lee D.; Soo, Evelyn C.; John C Achenbach; Michael G. Morash; Soanes, Kelly H.

    2014-01-01

    The smoking of tobacco continues to be the leading cause of premature death worldwide and is linked to the development of a number of serious illnesses including heart disease, respiratory diseases, stroke and cancer. Currently, cell line based toxicity assays are typically used to gain information on the general toxicity of cigarettes and other tobacco products. However, they provide little information regarding the complex disease-related changes that have been linked to smoking. The ethica...

  19. Cytotoxicity of eight cigarette smoke condensates in three test systems: comparisons between assays and condensates.

    Science.gov (United States)

    Richter, Patricia A; Li, Albert P; Polzin, Gregory; Roy, Shambhu K

    2010-12-01

    Cytotoxic properties of tobacco smoke are associated with chronic tobacco-related diseases. The cytotoxicity of tobacco smoke can be tested with short-term predictive assays. In this study, we compare eight mainstream cigarette smoke condensates (CSCs) from commercial and experimental cigarettes in three different cytotoxicity assays with unique and overlapping endpoints. The CSCs demonstrated cytotoxicity in all assays. In the multiple cytotoxicity endpoint (MCE) assay with TK-6 cells, the cigarette varieties that had the highest EC50s for reduced cell growth also showed a positive dose-response relationship for necrotic cells. In the IdMOC multiple cell-type co-culture (MCTCC) system, all CSCs reduced the viability of the cells. Low concentrations of some CSCs had a stimulatory effect in lung microvascular endothelial cells and small airway epithelial cells. In the neutral dye assay (NDA), except for a 100% flue-cured tobacco CSC, there was little consistency between CSCs producing morphological evidence of moderate or greater toxicity and the CSCs with the lowest EC50s in the MCE or MCTCC assays. Overall, cigarettes made with flue-cured tobacco were the most cytotoxic across the assays. When results were expressed on a per-mg of nicotine basis, lower tar cigarettes were the most cytotoxic in primary human respiratory cells. PMID:20719243

  20. 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, 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.

  1. Antismoking messages and current cigarette smoking status in Somaliland: results from the Global Youth Tobacco Survey 2004

    OpenAIRE

    Muula Adamson S; Rudatsikira Emmanuel; Siziya Seter

    2008-01-01

    Abstract Background Tobacco is a leading cause of death globally. There are limited reports on current cigarette smoking prevalence and its associated-antismoking messages among adolescents in conflict zones of the world. We, therefore, conducted secondary analysis of data to estimate the prevalence of current cigarette smoking, and to determine associations of antismoking messages with smoking status. Methods We used data from the Somaliland Global Youth Tobacco Survey (GYTS) of 2004 to esti...

  2. An Updated Global Picture of Cigarette Smoking Persistence among Adults

    Science.gov (United States)

    Troost, Jonathan P.; Barondess, David A.; Storr, Carla L.; Wells, J. Elisabeth; Al-Hamzawi, Ali Obaid; Andrade, Laura Helena; Bromet, Evelyn; Bruffaerts, Ronny; Florescu, Silvia; de Girolamo, Giovanni; de Graaf, Ron; Gureje, Oye; Haro, Josep Maria; Hu, Chiyi; Huang, Yueqin; Karam, Aimee N.; Kessler, Ronald C.; Lepine, Jean-Pierre; Matschinger, Herbert; Medina-Mora, Maria Elena; O'Neill, Siobhan; Posada-Villa, Jose; Sagar, Rajesh; Takeshima, Tadashi; Tomov, Toma; Williams, David R.; Anthony, James C.

    2012-01-01

    Background Cross-national variance in smoking prevalence is relatively well documented. The aim of this study is to estimate levels of smoking persistence across 21 countries with a hypothesized inverse relationship between country income level and smoking persistence. Methods Data from the World Health Organization World Mental Health Survey Initiative were used to estimate cross-national differences in smoking persistence–the proportion of adults who started to smoke and persisted in smoking by the date of the survey. Result There is large variation in smoking persistence from 25% (Nigeria) to 85% (China), with a random-effects meta-analytic summary estimate of 55% with considerable cross-national variation. (Cochran's heterogeneity Q statistic=6,845; p<0.001). Meta-regressions indicated observed differences are not attributable to differences in country income level, age distribution of smokers, or how recent the onset of smoking began within each country. Conclusion While smoking should remain an important public health issue in any country where smokers are present, this report identifies several countries with higher levels of smoking persistence (namely, China and India). PMID:23626929

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

    Science.gov (United States)

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

    1997-01-01

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

  4. The perceived influence of cigarette advertisements and smoking susceptibility among seventh graders.

    Science.gov (United States)

    Borzekowski, D L; Flora, J A; Feighery, E; Schooler, C

    1999-01-01

    A perceptual bias, the third person effect, has been observed where individuals believe themselves to differ from others regarding the perceived influence of media messages. Given the frequency with which youth encounter prosmoking messages and the reported negative effects of these messages, it is of value to study whether youth perceive cigarette advertisements to influence themselves and their friends and peers. This study examined the associations between exposure to social and information prosmoking environments, the perceived influence of cigarette advertisements on self, best friends, and other youth, and smoking susceptibility. A sample of 571 seventh graders completed surveys on tobacco advertisements and promotions. Using Student's-t, chi-square, ANOVA tests and proportional odds models, we found significant associations between perceived influence of cigarette advertisements and exposure to social and information prosmoking environments as well as smoking susceptibility. These data suggest that youth be taught that everyone is vulnerable to the tobacco industry's strategies and be given skills to resist prosmoking advertising.

  5. Differential Relationships between Religiosity, Cigarette Smoking, and Waterpipe Use: Implications for College Student Health

    Science.gov (United States)

    Klassen, Brian J.; Smith, Kathryn Z.; Grekin, Emily R.

    2013-01-01

    Objective: Using a framework informed by problem behavior theory, the authors examined differential relationships between religiosity and the frequency of cigarette and waterpipe tobacco smoking. Participants: Six hundred fourteen individuals beginning their freshman year at a large, public, midwestern university. Methods: Paper-and-pencil surveys…

  6. Physical Activity, Body Mass Index, Alcohol Consumption and Cigarette Smoking among East Asian College Students

    Science.gov (United States)

    Seo, Dong-Chul; Torabi, Mohammad R.; Chin, Ming-Kai; Lee, Chung Gun; Kim, Nayoung; Huang, Sen-Fang; Chen, Chee Keong; Mok, Magdalena Mo Ching; Wong, Patricia; Chia, Michael; Park, Bock-Hee

    2014-01-01

    Objective: To identify levels of moderate-intensity physical activity (MPA) and vigorous-intensity physical activity (VPA) in a representative sample of college students in six East Asian economies and examine their relationship with weight, alcohol consumption and cigarette smoking. Design: Cross-sectional survey. Setting: College students…

  7. Alcohol consumption, cigarette smoking, and endometrial cancer risk: Results from the Netherlands Cohort Study

    NARCIS (Netherlands)

    Loerbroks, A.; Schouten, L.J.; Goldbohm, R.A.; Brandt, P.A. van den

    2007-01-01

    Objective: To examine the association between alcohol consumption, cigarette smoking, and endometrial cancer. Methods: In 1986, the Netherlands Cohort Study was initiated. A self-administered questionnaire on dietary habits and other cancer risk factors was completed by 62,573 women. Follow-up for c

  8. Cigarette and Nargileh Smoking Practices among School Students in Beirut, Lebanon

    Science.gov (United States)

    Tamim, Hala; Al-Sahab, Ban; Akkary, Ghassan; Ghanem, Mary; Tamim, Nada; El Roueiheb, Zana; Kanj, Mayada; Afifi, Rima

    2007-01-01

    Objectives: To determine the prevalence and predictors of smoking nargileh and/or cigarettes among school students in Greater Beirut, Lebanon. Methods: A proportionate random sample of 2443 students from 13 public and private schools was selected and asked to complete self-administered anonymous questionnaires. Results: The prevalence of smoking…

  9. Effects of Initial Abstinence and Programmed Lapses on the Relative Reinforcing Effects of Cigarette Smoking

    Science.gov (United States)

    Chivers, Laura L.; Higgins, Stephen T.; Heil, Sarah H.; Proskin, Rebecca W.; Thomas, Colleen S.

    2008-01-01

    Fifty-eight smokers received abstinence-contingent monetary payments for 1 (n = 15) or 14 (n = 43) days. Those who received contingent payments for 14 days also received 0, 1, or 8 experimenter-delivered cigarette puffs on 5 evenings. The relative reinforcing effects of smoking were assessed in a 3-hr session on the final study day, when…

  10. Quantifying Littered Cigarette Butts to Measure Effectiveness of Smoking Bans to Building Perimeters

    Science.gov (United States)

    Seitz, Christopher M.; Strack, Robert W.; Orsini, Muhsin Michael; Rosario, Carrie; Haugh, Christie; Rice, Rebecca; Wyrick, David L.; Wagner, Lorelei

    2012-01-01

    Objective: The authors estimated the number of violations of a university policy that prohibited smoking within 25 ft of all campus buildings. Participants: The project was conducted by 13 student researchers from the university and a member of the local public health department. Methods: Students quantified cigarette butts that were littered in a…

  11. Defining Cigarette Smoking Status in Young Adults: A Comparison of Adolescent vs Adult Measures

    Science.gov (United States)

    Delnevo, Cristine D.; Lewis, M. Jane; Kaufman, Ira; Abatemarco, Diane J.

    2004-01-01

    Objective: To determine the agreement between 2 measures (adult vs adolescent) of current cigarette smoking among young adults. Methods: We examined data from 1007 young adults from the New Jersey Adult Tobacco Survey. The adult measure incorporates lifetime and present use, whereas the adolescent measure assesses past 30-day use. The kappa…

  12. Dietary behaviors, physical activity, and cigarette smoking among pregnant Puerto Rican women

    Science.gov (United States)

    Few studies have examined predictors of meeting health guidelines in pregnancy among Latina women. We assessed dietary behaviors, physical activity, and cigarette smoking in the Latina Gestational Diabetes Mellitus Study, a prospective cohort of 1231 prenatal care patients. Self-reported information...

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

    NARCIS (Netherlands)

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

    2011-01-01

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

  14. Externalizing Behavior Problems and Cigarette Smoking as Predictors of Cannabis Use: The TRAILS Study

    Science.gov (United States)

    Korhonen, Tellervo; van Leeuwen, Andrea Prince; Reijneveld, Sijmen A.; Ormel, Johan; Verhulst, Frank C.; Huizink, Anja C.

    2010-01-01

    Objective: To examine externalizing behavior problems and cigarette smoking as predictors of subsequent cannabis use. Method: Dutch adolescents (N = 1,606; 854 girls and 752 boys) from the TRacking Adolescents' Individual Lives Survey (TRAILS) ongoing longitudinal study were examined at baseline (ages 10-12 [T1]) and at two follow-up assessments…

  15. Why Does ADHD Confer Risk for Cigarette Smoking? A Review of Psychosocial Mechanisms

    Science.gov (United States)

    Glass, Kerrie; Flory, Kate

    2010-01-01

    Research has documented that adolescents and young adults with attention-deficit/hyperactivity disorder (ADHD) are at increased risk for cigarette smoking, but less attention has examined why this risk exists. The current paper reviews the literature on different psychosocial mechanisms [self-medication hypothesis, social factors (social modeling,…

  16. Externalizing behavior problems and cigarette smoking as predictors of cannabis use : the TRAILS Study

    NARCIS (Netherlands)

    Korhonen, T.; van Leeuwen, A.P.; Reijneveld, S.A.; Ormel, J.; Verhulst, F.C.; Huizink, A.C.

    2010-01-01

    Objective: To examine externalizing behavior problems and cigarette smoking as predictors Of Subsequent cannabis use. Method: Dutch adolescents (N = 1,606; 854 girls and 752 boys) from the TRacking Adolescents' Individual Lives Survey (TRAILS) ongoing longitudinal study were examined at baseline (ag

  17. Cytokinetics and histogenesis of cultured hamster tracheal epithelium. Effects of vitamin A and cigarette smoke condensate.

    NARCIS (Netherlands)

    Rutten, A.A.J.J.L.

    1988-01-01

    The studies reported in this thesis primarily deal with the influence of vitamin A (all-trans retinol) and cigarette smoke condensate on cellular proliferation, and differentiation and intercellular communication in tracheal epithelium. The experiments were carried out with Syrian Golden hamster tra

  18. The Effects of Maternal Alcohol Consumption and Cigarette Smoking during Pregnancy on Acoustic Cry Analysis.

    Science.gov (United States)

    Nugent, J. Kevin; And Others

    1996-01-01

    Measured the neurobehavioral integrity of Irish infants and maternal alcohol consumption and cigarette smoking. Subjects were 127 primiparous mothers. Results demonstrated significant cry effects on infants of heavily drinking mothers, supporting the conclusion that newborn infants show functional disturbances in the nervous system resulting from…

  19. Simple Fluorimetric Determination of Benzo[a]pyrene in Cigarette Smoke without Preseparation Procedure

    Institute of Scientific and Technical Information of China (English)

    2005-01-01

    Constant-energy synchronous fluorimetry was used for the identification of benzo[a]pyrene in mixtures with a detection limit of 1.34 nmol/L. The recovery experiments in cigarette smoke samples have also obtained satisfactory results of 99.1-103.5% for benzo[a]pyrene.

  20. Transcriptome sequencing reveals e-cigarette vapor and mainstream-smoke from tobacco cigarettes activate different gene expression profiles in human bronchial epithelial cells

    OpenAIRE

    Yifei Shen; Michael J. Wolkowicz; Tatyana Kotova; Lonjiang Fan; Timko, Michael P.

    2016-01-01

    Electronic cigarettes (e-cigarettes) generate an aerosol vapor (e-vapor) thought to represent a less risky alternative to main stream smoke (MSS) of conventional tobacco cigarettes. RNA-seq analysis was used to examine the transcriptomes of differentiated human bronchial epithelial (HBE) cells exposed to air, MSS from 1R5F tobacco reference cigarettes, and e-vapor with and without added nicotine in an in vitro air-liquid interface model for cellular exposure. Our results indicate that while e...

  1. Antismoking messages and current cigarette smoking status in Somaliland: results from the Global Youth Tobacco Survey 2004

    Directory of Open Access Journals (Sweden)

    Muula Adamson S

    2008-05-01

    Full Text Available Abstract Background Tobacco is a leading cause of death globally. There are limited reports on current cigarette smoking prevalence and its associated-antismoking