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Sample records for cigarette smoke induces

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

    Directory of Open Access Journals (Sweden)

    G. Vani

    2015-01-01

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

  2. Effects of Exercise on Cardiovascular Dysfunctions Induced by Cigarette Smoking

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    Abdel-Sater Khaled A.

    2008-06-01

    Full Text Available Smoking is known to adversely affect many organs and systems in human, where the cardiovascular system is one of the important targets. However, the exact mechanisms by which cigarette smoke alters myocardial and endothelial cells function and induces cardiovascular pathology are not clear. There are no reports especially with nitric oxide (NO•, uric acid and hemodynamics after acute exercise in smokers up to date. This study is designed to investigate the role of oxidative stress, NO• and uric acid in the pathophysiologic mechanisms of smoking- induced cardiovascular diseases.40 apparently healthy subjects were studied. Depending on their previous physical conditioning status subjects were divided into equal four groups (n=10, physically active nonsmokers, physically active smokers, sedentary nonsmokers and sedentary smokers. Exercise tolerance was evaluated for each subject by using a running race (3 kilometers after a worming up period of 5 minutes.The obtained data revealed that regular exercise significantly decreased the plasma malonaldehyde, total cholesterol, LDL and uric acid levels below sedentary levels. Pre and post race plasma level of malonaldehyde and uric acid levels were significantly increased, while, plasma glutathione and NO• were decreased in sedentary smokers than the sedentary non smokers, physically active smokers and physically active non smokers.These findings point to the role of NO•, uric acid and lipid peroxide in the pathophysiologic mechanisms of smoking induced cardiovascular diseases. Sedentary smokers may be at an even greater risk of oxidative stress-related cardiovascular diseases. Finally, every body should include in a regular exercise.

  3. EGR-1 regulates Ho-1 expression induced by cigarette smoke

    International Nuclear Information System (INIS)

    As an anti-oxidant molecule, heme oxygenase-1 (HO-1) has been implicated in the protection of lung injury by cigarette smoke (CS). The mechanisms regulating its expression have not been defined. In this report, the role of early growth response 1 (EGR-1) in the regulation of Ho-1 expression was investigated. In C57BL/6 mice with CS exposure, HO-1 was greatly increased in bronchial epithelial cells and alveolar inflammatory cells. In primary cultured mouse lung fibroblasts and RAW264.7 cells exposed to cigarette smoke water extract (CSE), an increase in HO-1 protein level was detected. In addition, CSE induced HO-1 expression was decreased in Egr-1 deficient mouse embryo fibroblasts (Egr-1-/- MEFs). Nuclear localization of EGR-1 was examined in mouse lung fibroblasts after exposure to CSE. Luciferase reporter activity assays showed that the enhancer region of the Ho-1 gene containing a proposed EGR-1 binding site was responsible for the induction of HO-1. A higher increase of alveolar mean linear intercept (Lm) was observed in lung tissues, and a larger increase in the number of total cells and monocytes/macrophages from bronchial alveolar lavage fluid was found in CS-exposed mice by loss of function of EGR-1 treatment. In summary, the present data demonstrate that EGR-1 plays a critical role in HO-1 production induced by CS.

  4. 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.

  5. 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

  6. Point-of-sale cigarette marketing and smoking-induced deprivation in smokers: results from a population-based survey

    OpenAIRE

    Siahpush, Mohammad; Raees A. Shaikh; Robbins, Regina; Tibbits, Melissa; Kessler, Asia Sikora; Soliman, Ghada; McCarthy, Molly; Singh, Gopal K.

    2016-01-01

    Background Strict restrictions on outdoor cigarette marketing have resulted in increasing concentration of cigarette marketing at the point-of-sale (POS). The association between POS cigarette marketing and smoking-induced deprivation (SID) has never been studied. The aim of this study was to examine this association and how it is mediated by cravings to smoke, urges to buy cigarettes, and unplanned purchases of cigarettes. Methods Data from a telephone survey of 939 smokers were collected in...

  7. 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.

  8. 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...

  9. 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)

  10. Autophagy Has a Beneficial Role in Relieving Cigarette Smoke-Induced Apoptotic Death in Human Gingival Fibroblasts

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    Kim, Moon-Soo; Yun, Jeong-Won; Park, Jin-Ho; Park, Bong-Wook; Kang, Young-Hoon; Hah, Young-Sool; Hwang, Sun-Chul; Woo, Dong Kyun; Byun, June-Ho

    2016-01-01

    The deleterious role of cigarette smoke has long been documented in various human diseases including periodontal complications. In this report, we examined this adverse effect of cigarette smoke on human gingival fibroblasts (HGFs) which are critical not only in maintaining gingival tissue architecture but also in mediating immune responses. As well documented in other cell types, we also observed that cigarette smoke promoted cellular reactive oxygen species in HGFs. And we found that this cigarette smoke-induced oxidative stress reduced HGF viability through inducing apoptosis. Our results indicated that an increased Bax/Bcl-xL ratio and resulting caspase activation underlie the apoptotic death in HGFs exposed to cigarette smoke. Furthermore, we detected that cigarette smoke also triggered autophagy, an integrated cellular stress response. Interesting, a pharmacological suppression of the cigarette smoke-induced autophagy led to a further reduction in HGF viability while a pharmacological promotion of autophagy increased the viability of HGFs with cigarette smoke exposures. These findings suggest a protective role for autophagy in HGFs stressed with cigarette smoke, highlighting that modulation of autophagy can be a novel therapeutic target in periodontal complications with cigarette smoke.

  11. A kinetic analysis of strand breaks on large DNA induced by cigarette smoke extract

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    Kurita, Hirofumi; Takata, Tatsuya; Yasuda, Hachiro; Takashima, Kazunori; Mizuno, Akira

    2010-06-01

    We report a kinetic analysis of strand breakages on large DNA molecules induced by cigarette smoke extract (CSE), an extract of soluble cigarette smoke components. Previously, this DNA damage was analyzed by agarose gel electrophoresis, whereas we used fluorescence to kinetically analyze damage to individual DNA molecules. CSE caused a marked change in length of DNA molecules. The rate of CSE-induced double-strand breakage on large random-coiled DNA molecules was determined using a simple theoretical model, allowing the facile estimation of the rate of double-strand breaks on large DNA molecules.

  12. 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.

  13. STAT3 Modulates Cigarette Smoke-Induced Inflammation and Protease Expression

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    RobertForonjy

    2013-10-01

    Full Text Available Signal transducer and activator of transcription-3 (STAT3 regulates inflammation, apoptosis and protease expression, which are critical processes associated with airway injury and lung tissue destruction. However, the precise role of STAT3 in the development of airway diseases such as chronic obstructive pulmonary disease (COPD has not been established. This study shows that cigarette smoke activates STAT3 in the lungs of mice. Since cigarette smoke activated STAT3 in the lung, we then evaluated how the loss of STAT3 would impact on smoke-mediated lung inflammation, protease expression and apoptosis. STAT3+/+ and STAT3-/- mice were exposed to eight days of cigarette smoke. Compared to the STAT3+/+ mice bronchoalveolar lavage fluid (BALF cellularity was significantly elevated in the STAT3-/- mice both before and after cigarette smoke exposure, with the increase in cells primarily macrophages. In addition, smoke exposure induced significantly higher BALF protein levels of Interleukin-1α (IL-1α, and monocyte chemotactic protein-1 (MCP-1 and higher tissue expression of keratinocyte chemoattractant (KC in the STAT3-/- mice. Lung mRNA expression of MMP-12 was increased in STAT3-/- at baseline. However, the smoke-induced increase in MMP-10 expression seen in the STAT3+/+ mice was not observed in the STAT3-/- mice. Moreover, lung protein levels of the anti-inflammatory proteins SOCS3 and IL-10 were markedly lower in the STAT3-/- mice compared to the STAT3+/+ mice. Lastly, apoptosis, as determined by caspase 3/7 activity assay, was increased in the STAT3-/- at baseline to levels comparable to those observed in the smoke-exposed STAT3+/+ mice. Together, these results indicate that the smoke-mediated induction of lung STAT3 activity may play a critical role in maintaining normal lung homeostasis and function.

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

    Institute of Scientific and Technical Information of China (English)

    张劲农; 陶晓南; 谢建敏; 向敏; 付薇

    2003-01-01

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

  15. Inhaled cigarette smoke induces the formation of DNA adducts in lungs of rats

    International Nuclear Information System (INIS)

    Cigarette smoking causes a variety of adverse human health effects, including lung cancer. The molecular events associated with smoke-induced carcinogenesis are thought to be related in part to the genotoxic activities of the chemicals associated with smoke. The purpose of this investigation was to determine the molecular dosimetry of compounds in cigarette smoke in lungs of rats exposed by inhalation. These studies investigated the effects of exposure mode, sex, and time (adduct persistence) on the level of DNA adducts. Male and female F344/N rats were exposed 6 hr/day, 5 days/week for 22 days to cigarette smoke by nose-only intermittent (NOI), nose-only continuous (NOC), or whole-body continuous (WBC) exposures. Separate groups of rats were sham-exposed nose-only (NOS) or whole-body (WBS) to filtered air. All smoke exposure modes yielded daily smoke exposure concentration X time products of 600 mg particulate.hr/m3 for the first week and 1200 mg particulate.hour/m3 thereafter. Groups of rats were killed at 18 hr and 3 weeks after the 22-day exposure period and DNA adducts in lung tissues were quantified by the 32P-postlabeling method. There were significant (p less than 0.05) increases in levels of clearly resolved lung DNA adducts in male and female rats exposed to smoke compared to sham-exposed rats. There were no significant effects of exposure mode or sex on lung DNA adducts. Mean levels (+/- SE) of clearly resolved lung DNA adducts for both sexes combined in NOI, NOC, WBC, NOS, and WBS groups were 50 +/- 4, 52 +/- 6, 52 +/- 7, 21 +/- 6, and 22 +/- 4 adducts per 10(9) bases, respectively. Levels of clearly resolved DNA adducts were significantly less in lungs of rats killed 3 weeks after exposure and had declined to near control levels, suggesting that smoke-induced adducts are repaired by lung DNA repair enzymes

  16. 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.

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

    Science.gov (United States)

    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

  18. Cigarette smoke and plutonium

    International Nuclear Information System (INIS)

    Autoradiographic techniques with liquid photographic emulsion and cellulose nitrate track-etch film are being used to investigate the spatial distribution of inhaled plutonium in the lungs of beagle dogs exposed to cigarette smoke or to the plutonium aerosol only. More plutonium than expected was detected on the inner surfaces of bronchi, and particles were observed beneath the bronchial mucosa. 2 figures, 2 tables

  19. 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...

  20. Interleukin-22 exacerbates airway inflammation induced by short-term exposure to cigarette smoke in mice

    OpenAIRE

    Li, Jiu-rong; Zhou, Wei-xun; Huang, Ke-wu; Jin, Yang; Gao, Jin-Ming

    2014-01-01

    Aim: Interleukin-22 (IL-22) exhibits both proinflammatory and anti-inflammatory properties in various biological processes. In this study we explored the effects of exogenous recombinant IL-22 (rIL-22) on cigarette smoke (CS)-induced airway inflammation in mice. Methods: Male C57BL/6 mice were divided into groups: (1) CS group exposed to tobacco smoke for 3 consecutive days, (2) rIL-22 group received rIL-22 (100 mg/kg, ip), and (3) CS plus rIL-22 group, received rIL-22 (100 mg/kg, ip) before ...

  1. 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

  2. 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

  3. 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.

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

    DEFF Research Database (Denmark)

    Munck, Christian; Helby, Jens; Westergaard, Christian G;

    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 w....... 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....

  5. 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)...

  6. 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

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

    International Nuclear Information System (INIS)

    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

  8. Caffeic acid phenethyl ester protects lung alveolar epithelial cellsfrom cigarette smoke-induced damage

    OpenAIRE

    BARLAS, FIRAT BARIŞ; ERDOGAN, SUAT

    2015-01-01

    Background/aim: To evaluate the influence of caffeic acid phenethyl ester (CAPE) on cigarette smoke (CS)-induced cell damage, oxidative stress, and inflammation in human alveolar epithelial cells. Materials and methods: A549 alveolar epithelial cells were divided into control, CS exposure, CAPE, and CS+CAPE treatment groups. Undiluted CS-exposed medium (100%) and three dilutions (50%, 25%, and 10%) of CS-exposed media were applied to cultured A549 cells, which were analyzed after 3 h of inc...

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

    Directory of Open Access Journals (Sweden)

    Nesi RT

    2016-03-01

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

  10. Formation of cigarette smoke-induced DNA adducts in the rat lung and nasal mucosa

    International Nuclear Information System (INIS)

    The formation of DNA adducts in the nasal, lung, and liver tissues of rats exposed daily to fresh smoke from a University of Kentucky reference cigarette (2R1) for up to 40 weeks was examined. The amount of smoke total particulate matter (TPM) inhaled and the blood carboxyhemoglobin (COHb) values averaged 5-5.5 mg smoke TPM/day/rat and 5.5%, respectively. The pulmonary AHH activity measured at the termination of each experiment showed an average increase of about two- to threefold in smoke-exposed groups. These observations suggested that animals effectively inhaled both gaseous and particulate phase constituents of cigarette smoke. DNAs from nasal, lung, and liver tissue were extracted and analyzed by an improved 32P-postlabeling procedure. The data demonstrate the DNA-damaging potential of long term fresh cigarette smoke exposure and suggest the ability of the tissue to partially recover from such damage following cessation of the exposure

  11. 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.

  12. Cigarette Smoking and Dyspnea Perception

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    Scano Giorgio

    2004-03-01

    Full Text Available Abstract Cigarette smoking has been implicated as an important risk factor for the development of respiratory symptoms in adults. The relationship of dyspnea with cigarette smoking has been examined in smokers and ex-smokers and the beneficial effects of smoking cessation have been demonstrated. Recent studies reported that in subjects who smoke cigarettes the risk of developing respiratory symptoms is higher in a dose-dependent way. Environmental tobacco smoke heavily influences the incidence of respiratory symptoms in both adults and in children. Up to the present time, the mechanisms whereby cigarette smoking causes dyspnea perception remain to be defined. Abnormalities in sensory nerves might diminish the perception of bronchoconstriction in smokers. In this regard, it has been postulated that prolonged exposure to cigarette smoke may lead to chronic depletion of sensory nerve neurotransmitters. Eosinophil airway inflammation has been proposed as a determinant of breathlessness via mechanisms affecting either the mechanical pathways that control breathlessness or the afferent nerves involved in perception of dyspnea. An increased number of eosinophils in some smokers implies the possibility that smoking may trigger immunological or other reactions associated with eosinophilia. In conclusion, cigarette smoking is by far one of the greatest risk factors for most respiratory symptoms, including dyspnea. Smoking is associated with the development of symptoms in a dose-dependent way and eosinophilia and airway hyperresponsiveness (AHR increase the risk of developing dyspnea.

  13. 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.

  14. In vitro transformation of immortalized human bronchial epithelial cells BEAS-2B induced by radon and cigarette smoke

    International Nuclear Information System (INIS)

    Objective: To establish a model of malignant transformation of human cells in vitro to study the lung cancer induced by radon and cigarette smoke. Methods: The immortalized human bronchial epithelial cells BEAS-2B were divided into control group (C), radon group (Rn), cigarette smoke group (Sm) and combined group (Rn-Sm). Cells were planted onto transwell membrane one day before exposure and were directly exposed to radon and cigarette smoke pumped in a gas inhalation box. After the exposure cells were trypsinized into dishes for further growth and malignancy transformation phenotype was detected in order to compare the effects due to radon and cigarette smoke exposure. Results: BEAS-2B cells showed malignantly transformed phenotype by exposure to radon and cigarette smoke. A series of sequential steps emerged among transformed cells, including altered growth kinetics, resistance to serum has changed from 0. 31 ± 0. 18 to 1.92 ± 0. 27,2. 03 ± 0. 14,2.95 ± 0. 60, and anchorage-independence growth increased from (0.01 ±0.02)% to (4.89 ±0.30)%,(8.36 ±0.50)%,(11.74 ±0.69)%.After being subculture for 20 generations, cell apoptosis of the fifth generation cells exposed to radon,cigarette smoke and both was significant decreased from ( 11.76 ± 0. 17 ) % to (4. 62 ± 0. 42 ) %, ( 8.63 ±0. 15 )%, (3.68 ± 0. 33 )%. Conclusions: BEAS-2B cells could be malignancy transformed by radon and cigarette smoke in vitro, which could be used as a cell model in lung bronchial carcinogenesis. (authors)

  15. 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

  16. 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.

  17. Autophagy plays an essential role in cigarette smoke-induced expression of MUC5AC in airway epithelium.

    Science.gov (United States)

    Zhou, Jie-Sen; Zhao, Yun; Zhou, Hong-Bin; Wang, Yong; Wu, Yin-Fang; Li, Zhou-Yang; Xuan, Nan-Xia; Zhang, Chao; Hua, Wen; Ying, Song-Min; Li, Wen; Shen, Hua-Hao; Chen, Zhi-Hua

    2016-06-01

    Mucus hypersecretion is a common pathological feature of chronic airway inflammatory diseases including chronic obstructive pulmonary disease (COPD). However, the molecular basis for this condition remains incompletely understood. We have previously demonstrated a critical role of autophagy in COPD pathogenesis through mediating apoptosis of lung epithelial cells. In this study, we aimed to investigate the function of autophagy as well as its upstream and downstream signals in cigarette smoke-induced mucus production in human bronchial epithelial (HBE) cells and in mouse airways. Cigarette smoke extract (CSE), as well as the classical autophagy inducers starvation or Torin-1, significantly triggered MUC5AC expression, and inhibition of autophagy markedly attenuated CSE-induced mucus production. The CSE-induced autophagy was mediated by mitochondrial reactive oxygen species (mitoROS), which regulated mucin expression through the JNK and activator protein-1 pathway. Epidermal growth factor receptor (EGFR) was also required for CSE-induced MUC5AC in HBE cells, but it exerted inconsiderable effects on the autophagy-JNK signaling cascade. Airways of mice with dysfunctional autophagy-related genes displayed a markedly reduced number of goblet cells and attenuated levels of Muc5ac in response to cigarette smoke exposure. These results altogether suggest that mitoROS-dependent autophagy is essential for cigarette smoke-induced mucus hyperproduction in airway epithelial cells, and reemphasize autophagy inhibition as a novel therapeutic strategy for chronic airway diseases. PMID:27036871

  18. 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...

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

    Directory of Open Access Journals (Sweden)

    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.

  20. 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

  1. 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.

  2. 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.

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

    Science.gov (United States)

    Baeder, Andrea C.; Napa, Kiran; Richardson, Sarah T.; Taylor, Oliver J.; Andersen, Samantha G.; Wilcox, Shalene H.; Winden, Duane R.; Reynolds, Paul R.

    2016-01-01

    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. PMID:27034671

  4. 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.

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

    DEFF Research Database (Denmark)

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

    2009-01-01

    AIMS: Cigarette smoking is one of the strongest risk factors for stroke. However, the underlying molecular mechanisms that smoke leads to the pathogenesis of stroke are incompletely understood. METHODS: Dimethyl sulfoxide (DMSO)-soluble (lipid-soluble) cigarette smoking particles (DSP) were...... 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 AT(1) receptors, but not of AT(2) receptors, at both mRNA and protein...... 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...

  6. 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

  7. 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

  8. 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...

  9. 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

  10. 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

  11. 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 ...

  12. Cigarette smoke condensate induces aryl hydrocarbon receptor-dependent changes in gene expression in spermatocytes.

    Science.gov (United States)

    Esakky, Prabagaran; Hansen, Deborah A; Drury, Andrea M; Moley, Kelle H

    2012-12-01

    Cigarette smoke contains numerous compounds that cause oxidative stress and alter gene expression in many tissues, and cigarette smoking is correlated with male infertility. To identify mechanisms by which this occurs, we evaluated expression of antioxidant genes in mouse spermatocytes in response to cigarette smoke condensate (CSC). CSC exposure led to oxidative stress and dose-dependent up-regulation of Hsp90aa1, Ahr, Arnt, Sod1, Sod2, and Cyp1a1 expression in a mouse spermatocyte cell line. An antagonist of the aryl hydrocarbon receptor (AHR) abrogated several CSC-mediated changes in mRNA and protein levels. Consistent with these results, spermatocytes isolated by laser-capture microdissection from CSC-treated mice showed increased expression of several antioxidant genes. In vivo exposure to CSC was genotoxic to spermatocytes, resulting in apoptosis and disruptions to the seminiferous tubules. Our in vivo and in vitro data indicate that CSC-mediated damage to murine spermatocytes is AHR-dependent and is mediated by oxidative stress. PMID:23069111

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

    Directory of Open Access Journals (Sweden)

    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.

  14. Cigarette Smoke Induces Human Epidermal Receptor 2-Dependent Changes in Epithelial Permeability.

    Science.gov (United States)

    Mishra, Rangnath; Foster, Daniel; Vasu, Vihas T; Thaikoottathil, Jyoti V; Kosmider, Beata; Chu, Hong Wei; Bowler, Russell P; Finigan, James H

    2016-06-01

    The airway epithelium constitutes a protective barrier against inhaled insults, such as viruses, bacteria, and toxic fumes, including cigarette smoke (CS). Maintenance of bronchial epithelial integrity is central for airway health, and defective epithelial barrier function contributes to the pathogenesis of CS-mediated diseases, such as chronic obstructive pulmonary disease. Although CS has been shown to increase epithelial permeability, current understanding of the mechanisms involved in CS-induced epithelial barrier disruption remains incomplete. We have previously identified that the receptor tyrosine kinase human epidermal receptor (HER) 2 growth factor is activated by the ligand neuregulin-1 and increases epithelial permeability in models of inflammatory acute lung injury. We hypothesized that CS activates HER2 and that CS-mediated changes in barrier function would be HER2 dependent in airway epithelial cells. We determined that HER2 was activated in whole lung, as well as isolated epithelial cells, from smokers, and that acute CS exposure resulted in HER2 activation in cultured bronchial epithelial cells. Mechanistic studies determined that CS-mediated HER2 activation is independent of neuregulin-1 but required upstream activation of the epidermal growth factor receptor. HER2 was required for CS-induced epithelial permeability as knockdown of HER2 blocked increases in permeability after CS. CS caused an increase in IL-6 production by epithelial cells that was dependent on HER2-mediated extracellular signal-regulated kinases (Erk) activation. Finally, blockade of IL-6 attenuated CS-induced epithelial permeability. Our data indicate that CS activates pulmonary epithelial HER2 and that HER2 is a central mediator of CS-induced epithelial barrier dysfunction. PMID:26600084

  15. Cigarette smoking: health effects and control strategies.

    Science.gov (United States)

    Alberg, Anthony J

    2008-12-01

    Active cigarette smoking causes a broad spectrum of diseases that extend to many different organ systems. Its numerous deleterious health effects, combined with the substantial prevalence of cigarette smoking, make it a major worldwide cause of death. Smoking contributes so heavily to the mortality burden because it is a major cause of vascular disease, cancer and chronic obstructive pulmonary disease. In addition to these diseases, cigarette smoking also causes other respiratory symptoms, adversely affects reproductive outcomes and is a cause of diminished health status. Furthermore, exposure to secondhand smoke is an established cause of coronary heart disease and lung cancer, as well as a host of other adverse health effects. Given that cigarette smoking is such a major threat to global public health, controlling the worldwide epidemic of cigarette smoking would lead to enormous public health benefits. Strategies to control cigarette smoking at the societal level include smoke-free workplace legislation, increasing cigarette taxes and regulating cigarette advertising. On the individual level, preventing the initiation of cigarette smoking among youths is the optimal strategy; in practice, discovering efficacious primary prevention interventions has proven challenging. During the past two decades, major advances have been made in extending the menu of options available to assist dependent smokers in successfully quitting smoking. Successfully combating cigarette smoking requires a broad-based commitment to smoking control from multiple stakeholders, along with a multifaceted strategy that addresses both societal and individual factors. PMID:19198699

  16. Protective effect of EC-18, a synthetic monoacetyldiglyceride on lung inflammation in a murine model induced by cigarette smoke and lipopolysaccharide.

    Science.gov (United States)

    Shin, In-Sik; Ahn, Kyung-Seop; Shin, Na-Rae; Lee, Hyun-Jun; Ryu, Hyung Won; Kim, Jae Wha; Sohn, Ki-Young; Kim, Heung Jae; Han, Yong-Hae; Oh, Sei-Ryang

    2016-01-01

    The antler of Sika deer (Cervus nippon Temminck) has been used a natural medicine in Korea, China and Japan, and a monoacetyldiaglyceride (1-palmitoyl-2-linoleoyl-3-acetylglycerol, PLAG) was found in the antler of Sika deer as a constituent for immunomodulation. In this study, we investigated protective effects of EC-18 (a synthetic copy of PLAG) on inflammatory responses using a cigarette smoke with lipopolysaccharide (LPS)-induced airway inflammation model. Mice were exposed to cigarette smoke for 1h per day for 3days. Ten micrograms of LPS dissolved in 50μL of PBS was administered intra nasally 1h after the final cigarette smoke exposure. EC-18 was administered by oral gavage at doses of 30 and 60mg/kg for 3days. EC-18 significantly reduced the number of neutrophils, reactive oxygen species production, cytokines and elastase activity in bronchoalveolar lavage fluid (BALF) compared with the cigarette smoke and LPS induced mice. Histologically, EC-18 attenuated airway inflammation with a reduction in myeloperoxidase expression in lung tissue. Additionally, EC-18 inhibited the phosphorylation of NF-κB and IκB induced by cigarette smoke and LPS exposure. Our results show that EC-18 effectively suppresses neutrophilic inflammation induced by cigarette smoke and LPS exposure. In conclusion, this study suggests that EC-18 has therapeutic potential for the treatment of chronic obstructive pulmonary disease. PMID:26655742

  17. 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

  18. 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

  19. 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

  20. 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

  1. Immediate response to cigarette smoke

    Energy Technology Data Exchange (ETDEWEB)

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

    1982-06-01

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

  2. 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

  3. 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.

  4. 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.

  5. 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....

  6. Analysis of complex mixtures--cigarette smoke.

    Science.gov (United States)

    Borgerding, Michael; Klus, Hubert

    2005-07-01

    Mainstream cigarette smoke is a complex mixture that is inhaled into the respiratory system. The physical characteristics and chemical composition of mainstream smoke are reviewed and briefly compared with that of sidestream smoke. Special attention is paid to ageing effects and artifact formation during the sampling and testing of cigarette smoke, with specific examples of artifact formation during sampling discussed (nitrogen dioxide, methyl nitrite, etc.). Historically, the generation of cigarette smoke for chemical and biological testing has been based on standard smoke generation procedures that are intended for product comparisons. More recently, emerging global regulations have called for alternative smoke generation methods, with emphasis on results relevant to conditions of product use, e.g., estimates of maximum smoke emissions. Strategies for establishing such alternative smoke generation methods are discussed and the potential effects of alternative smoking conditions on analytical accuracy and precision are addressed. Current regulatory requirements that include Hoffmann analyte analysis (i.e., constituents reported to be associated with the risks of cigarette smoking) are also summarized and the potential effect of alternative smoke generation methods on individual constituent yields considered. Finally, a limited critique of emerging regulation that relates to mainstream cigarette smoke measurements, including a discussion of recent WHO recommendations, is offered. PMID:16092717

  7. 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

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

  9. 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...

  10. 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

  11. 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

  12. 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.

  13. 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 ...

  14. E-Cigarettes a Gateway to Smoking for Teens

    Science.gov (United States)

    ... nlm.nih.gov/medlineplus/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. Estimating mortality due to cigarette smoking

    DEFF Research Database (Denmark)

    Brønnum-Hansen, H; Juel, K

    2000-01-01

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

  16. 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

  17. 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...

  18. 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

  19. 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

  20. 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.

  1. Myeloid-specific Fos-related antigen-1 regulates cigarette smoke-induced lung inflammation, not emphysema, in mice.

    Science.gov (United States)

    Vaz, Michelle; Rajasekaran, Subbiah; Potteti, Haranatha R; Reddy, Sekhar P

    2015-07-01

    Heightened lung inflammation is a cardinal feature of chronic obstructive pulmonary disease (COPD). Cigarette smoke (CS)-induced macrophage recruitment and activation, accompanied by abnormal secretion of a number of inflammatory cytokines and matrix metalloproteinases, play a major role in the pathophysiology of COPD. The Fos-related antigen-1 (Fra-1) transcription factor differentially regulates several cellular processes that are implicated in COPD, such as inflammation and immune responses, cell proliferation and death, and extracellular remodeling. Although CS stimulates Fra-1 expression in the lung, the precise role of this transcription factor in the regulation of CS-induced lung inflammation in vivo is poorly understood. Here, we report that myeloid-specific Fra-1 signaling is important for CS-induced lung macrophagic inflammatory response. In response to chronic CS exposure, mice with Fra-1 specifically deleted in myeloid cells showed reduced levels of CS-induced lung macrophagic inflammation, accompanied by decreased expression levels of proinflammatory cytokines compared with their wild-type counterparts. Consistent with this result, bone marrow-derived Fra-1-null macrophages treated with CS showed decreased levels of proinflammatory mediators and matrix metalloproteinases. Interestingly, deletion of Fra-1 in myeloid cells did not affect the severity of emphysema. We propose that Fra-1 plays a key role in promoting chronic CS-induced lung macrophagic inflammation in vivo, and that targeting this transcription factor may be useful in dampening persistent lung inflammation in patients with COPD. PMID:25489966

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

    DEFF Research Database (Denmark)

    Cao, Lei; Zhang, Yaping; Cao, Yong-Xiao; Edvinsson, Lars; Xu, Cang-Bao

    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...... ET(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...

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

    OpenAIRE

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

    2015-01-01

    The present study has identified IL-17A as an alternative target to combat macrophage accumulation in cigarette smoke (CS)-related lung conditions and suggests that alternative innate cellular sources should be considered when developing strategies to combat excessive IL-17A signalling in chronic lung conditions.

  4. 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

  5. Protective effects of anisodamine on cigarette smoke extract-induced airway smooth muscle cell proliferation and tracheal contractility

    International Nuclear Information System (INIS)

    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.

  6. 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.

  7. 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...

  8. The Loss of Cellular Junctions in Epithelial Lung Cells Induced by Cigarette Smoke Is Attenuated by Corilagin

    Directory of Open Access Journals (Sweden)

    Ximena M. Muresan

    2015-01-01

    Full Text Available Cigarette smoke (CS contains over 4700 compounds, many of which can affect cellular redox balance through free radicals production or through the modulation of antioxidant enzymes. The respiratory tract is one of the organs directly exposed to CS and it is known that CS can damage the integrity of lung epithelium by affecting cell junctions and increasing epithelium permeability. In this study, we have used a human lung epithelial cell line, Calu-3, to evaluate the effect of CS on lung epithelial cell junctions levels, with special focus on the expression of two proteins involved in intercellular communication: connexins (Cx 40 and 43. CS exposure increased Cx40 gene expression but not of Cx43. CS also induced NFκB activation and the formation of 4HNE-Cxs adducts. Since corilagin, a natural polyphenol, is able to inhibit NFκB activation, we have determined whether corilagin could counteract the effect of CS on Cxs expression. Corilagin was able to diminish CS induced Cx40 gene expression, 4HNE-Cx40 adducts formation, and NFκB activation. The results of this study demonstrated that CS induced the loss of cellular junctions in lung epithelium, possibly as a consequence of Cx-4HNE adducts formation, and corilagin seems to be able to abolish these CS induced alterations.

  9. Cigarette smoking and progression in multiple sclerosis

    NARCIS (Netherlands)

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

    2007-01-01

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

  10. H2180 - cigarette smoke gas phase interaction

    International Nuclear Information System (INIS)

    the results of a stable isotope study of the interaction of H2180 with mainstream and sidestream gas phase smoke during and after smoke formation are reported. The objectives of the investigation were: (i) to study the interactions of the oxygen atom in water with oxygenated gas phase constituents which may have occurred during smoke trapping and subsequent analysis; (ii) to clarify previous results concerning the 180-enrichment of gas phase from a cigarette smoked in air containing 1802; (iii) to study, in the hope of gaining information concerning the role of water in gas phase smoke product formation, the incorporation of 180 in mainstream and sidestream gas phase smoke from cigarettes that had been dried and re-equilibrated with H2180. (UK)

  11. 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

  12. 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.

  13. Association between cigarette smoking and pulmonary tuberculosis

    International Nuclear Information System (INIS)

    Objectives: To determine the association between cigarette smoking and pulmonary tuberculosis. Methodology: In this retrospective study which was carried out in Razi hospital, in Ahvaz a city southwest Iran, medical charts of patients with tuberculosis between 2005 and 2007 were reviewed. Sixty one patients aged 15-96 years with documented pulmonary tuberculosis (smear positive) were selected as cases and 122 age and sex matched persons without tuberculosis(patients hospitalized in surgery and orthopedic wards) were selected randomly as controls. Data on smoking status, quantity of cigarette smoked, and duration of smoking was collected from medical charts. The data in the two groups were statistically compared with SPSS version 16. The chi square test was used to compare the frequency of cigarette smoking in two groups. Ninety-five percent confidence intervals were calculated when appropriate. Differences with a P value of <0.05 were considered significant. Results: Of total 61 case, 42 (68.9%) were smoker, while, of total 122 controls 22(18%) were smoker. The estimated odds ratio (OR) of the relation between smoking and tuberculosis was 10.1 [(95% confidence interval (CI) 4.3 to 23.5), P<0.001]. The mean of pocket - year of smoked cigarette (20/pocket) in cases and controls were 15.9 +- 13.7 and 13.5 +- 9.1, respectively (P=0.5). Conclusion: This study showed that pulmonary tuberculosis is associated to cigarette smoking. The association is not dose-dependent. Smoking may be a risk factor for TB acquisition. (author)

  14. Lethal impacts of cigarette smoke in cultured tobacco cells

    Directory of Open Access Journals (Sweden)

    Kawano Tomonori

    2011-07-01

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

  15. 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...

  16. Differential inhibitory effects of opioids on cigarette smoke, capsaicin and electrically-induced goblet cell secretion in guinea-pig trachea.

    OpenAIRE

    Kuo, H. P.; Rohde, J. A.; Barnes, P. J.; Rogers, D. F.

    1992-01-01

    1. Goblet cell secretion in guinea-pig airways is under neural control. Opioids have previously been shown to inhibit neurogenic plasma exudation and bronchoconstriction in guinea-pig airways. We have now examined the effects of morphine and opioid peptides on tracheal goblet cell secretion induced by either electrical stimulation of the cervical vagus nerves, exogenous capsaicin, or acute inhalation of cigarette smoke. The degree of goblet cell secretion was determined by a morphometric meth...

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

    International Nuclear Information System (INIS)

    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. 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. 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. 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 diagnostic and/or therapeutic potential. Furthermore

  18. 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

  19. Cigarette smoke induces molecular responses in respiratory tissues of ApoE−/− mice that are progressively deactivated upon cessation

    International Nuclear Information System (INIS)

    Cigarette smoking is the primary etiology of chronic obstructive pulmonary disease (COPD) and a risk factor for both lung and cardiovascular (CV) diseases, which are rarely investigated concomitantly. Although smoking cessation shows clear CV risk benefit, lung-related disease risk remains higher in former smokers than in never smokers. We sought to determine the differential molecular responses of murine respiratory tissues to better understand the toxicity pathways involved in smoking-related disease risk and those related to the benefits of smoking cessation. ApoE−/− mice were exposed to mainstream cigarette smoke (CS) or a smoking cessation-mimicking protocol for up to 6 months and transcriptomics analysis of nasal epithelium and lung parenchyma performed. We supported our gene expression profiling approach with standard lung histopathology and bronchoalveolar lavage fluid (BALF) analysis. Many BALF analytes involved in functions ranging from inflammation to cell proliferation and tissue remodeling were found elevated in BALF. Gene expression levels of these molecules were also increased in lung tissue, suggesting that the inflammatory response was the result of local tissue activation and the contribution of recruited inflammatory cells. Gene set enrichment analysis (GSEA) of expression data from murine lungs and nasal epithelium showed distinct activation patterns of inflammation, complement, and xenobiotic metabolism pathways during CS exposure that were deactivated upon smoking cessation. Pathways involved in cell proliferation and tissue remodeling were activated by CS and progressively deactivated upon smoke exposure cessation. Differential CS-mediated responses of pulmonary and nasal tissues reflect common mechanisms but also the varying degrees of epithelial functional specialization and exposure along the respiratory tract

  20. 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

  1. 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

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

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    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

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

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    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. 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

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

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    Victoria L Palmer

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

  6. Rat pleural mesothelial cells show damage after exposure to external but not internal cigarette smoke.

    OpenAIRE

    Sekhon, H S; Keeling, B; Churg, A.

    1993-01-01

    The combination of cigarette smoke and high-level occupational asbestos exposure produces a synergistic increase in the incidence of lung cancer; however, smoking does not affect the incidence of mesothelioma. Here we present the results of tests of two theories that have been proposed to explain this phenomenon; namely, that pleural mesothelial cells are resistant to cigarette smoke-induced damage and that the pleural connective tissue acts as a barrier that prevents smoke from reaching the ...

  7. 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.

  8. 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

  9. 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

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

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    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

  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. Cigarette smoking and innate immunity

    OpenAIRE

    Scott David A

    2005-01-01

    Abstract Background We examined female sedentary smokers' additional cardiovascular disease (CVD) risk behaviors and their associations to smoking cessation. Methods This study was part of a randomized controlled trial testing the effectiveness of exercise and nicotine gum in smoking cessation. Included in the analyses were 148 participants. Dietary habits and alcohol consumption were measured as additional CVD risk behaviors. High-fat diet and heavy alcohol use were considered those risk beh...

  13. Epigenetic silencing of p21 by long non-coding RNA HOTAIR is involved in the cell cycle disorder induced by cigarette smoke extract.

    Science.gov (United States)

    Liu, Yi; Wang, Bairu; Liu, Xinlu; Lu, Lu; Luo, Fei; Lu, Xiaolin; Shi, Le; Xu, Wenchao; Liu, Qizhan

    2016-01-01

    Long noncoding RNAs (lncRNAs), which are epigenetic regulators, are involved in human malignancies. Little is known, however, about the molecular mechanisms for lncRNA regulation of genes induced by cigarette smoke. We recently found that, in human bronchial epithelial (HBE) cells, the lncRNA, Hox transcript antisense intergenic RNA (HOTAIR), is associated with changes in the cell cycle caused by cigarette smoke extract (CSE). In the present study, we report that increased expression of HOTAIR and enhancer of zeste homolog 2 (EZH2), and tri-methylation of Lys 27 of histone H3 (H3K27me3), affect cell cycle progression during CSE-induced transformation of HBE cells. Inhibition of HOTAIR and EZH2 by siRNAs attenuated CSE-induced decreases of p21 levels. Further, ChIP assays verified that HOTAIR and EZH2 were needed to maintain the interaction of H3K27me3 with the promoter regions of p21; combined use of a HOTAIR plasmid and EZH2 siRNA supported this observation. Thus, HOTAIR epigenetic silencing of p21 via EZH2-mediated H3K27 trimethylation contributes to changes in the cell cycle induced by CSE. These observations provide further understanding of the regulation of CSE-induced lung carcinogenesis and identify new therapeutic targets. PMID:26506537

  14. Another Risk From Cigarette Smoking: Corneal Burn

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    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

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

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    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

  16. Multiplexed quantitative high content screening reveals that cigarette smoke condensate induces changes in cell structure and function through alterations in cell signaling pathways in human bronchial cells

    International Nuclear Information System (INIS)

    Human bronchial cells are one of the first cell types exposed to environmental toxins. Toxins often activate nuclear factor-κB (NF-κB) and protein kinase C (PKC). We evaluated the hypothesis that cigarette smoke condensate (CSC), the particulate fraction of cigarette smoke, activates PKC-α and NF-κB, and concomitantly disrupts the F-actin cytoskeleton, induces apoptosis and alters cell function in BEAS-2B human bronchial epithelial cells. Compared to controls, exposure of BEAS-2B cells to doses of 30 μg/ml CSC significantly activated PKC-α, while CSC doses above 20 μg/ml CSC significantly activated NF-κB. As NF-κB was activated, cell number decreased. CSC treatment of BEAS-2B cells induced a decrease in cell size and an increase in cell surface extensions including filopodia and lamellipodia. CSC treatment of BEAS-2B cells induced F-actin rearrangement such that stress fibers were no longer prominent at the cell periphery and throughout the cells, but relocalized to perinuclear regions. Concurrently, CSC induced an increase in the focal adhesion protein vinculin at the cell periphery. CSC doses above 30 μg/ml induced a significant increase in apoptosis in BEAS-2B cells evidenced by an increase in activated caspase 3, an increase in mitochondrial mass and a decrease in mitochondrial membrane potential. As caspase 3 increased, cell number decreased. CSC doses above 30 μg/ml also induced significant concurrent changes in cell function including decreased cell spreading and motility. CSC initiates a signaling cascade in human bronchial epithelial cells involving PKC-α, NF-κB and caspase 3, and consequently decreases cell spreading and motility. These CSC-induced alterations in cell structure likely prevent cells from performing their normal function thereby contributing to smoke-induced diseases.

  17. 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

  18. 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.

  19. 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

  20. 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 ...

  1. 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

  2. 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.

  3. Selenium and vitamin E deficiencies do not enhance lung inflammation from cigarette smoke in the hamster

    Energy Technology Data Exchange (ETDEWEB)

    Niewoehner, D.E.; Peterson, F.J.; Hoidal, J.R.

    1983-02-01

    The early lung inflammatory response to cigarette smoke may be oxidant-mediated. We fed Syrian hamsters a diet deficient in selenium and vitamin E to determine whether impairment of the lung's antioxidant defenses might worsen inflammation induced by cigarette smoke. After 8 wk, cigarette-smoke-exposed animals had characteristic inflammatory lesions in the distal airways. Increased numbers of phagocytes, predominantly macrophages, were recovered by lavage and these cells exhibited enhanced oxidative metabolism. Animals fed the deficient diet had profound depletions of selenium and vitamin E, but no alterations in the histologic appearance of smoke-induced inflammatory lesions, in the numbers of phagocytes recruited, or in the oxidative metabolism of these phagocytes. These results suggest that selenium and vitamin E are unimportant in protecting against cigarette-smoke-induced lung injury.

  4. 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

  5. Cigarette Smoking and Brain Regulation of Energy Homeostasis

    OpenAIRE

    HuiChen; SoniaSaad; ShaunSandow

    2012-01-01

    Cigarette smoking is an addictive behavior, 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...

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

    Directory of Open Access Journals (Sweden)

    Mok Joanie

    2010-09-01

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

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

    International Nuclear Information System (INIS)

    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/m3 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′-deoxyguanosine (8-oxodGuo) were measured by 32P 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.

  8. 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.

  9. Cigarette side-stream smoke lung and bladder carcinogenesis: inducing mutagenic acrolein-DNA adducts, inhibiting DNA repair and enhancing anchorage-independent-growth cell transformation.

    Science.gov (United States)

    Lee, Hyun-Wook; Wang, Hsiang-Tsui; Weng, Mao-wen; Chin, Chiu; Huang, William; Lepor, Herbert; Wu, Xue-Ru; Rom, William N; Chen, Lung-Chi; Tang, Moon-shong

    2015-10-20

    Second-hand smoke (SHS) is associated with 20-30% of cigarette-smoke related diseases, including cancer. Majority of SHS (>80%) originates from side-stream smoke (SSS). Compared to mainstream smoke, SSS contains more tumorigenic polycyclic aromatic hydrocarbons and acrolein (Acr). We assessed SSS-induced benzo(a)pyrene diol epoxide (BPDE)- and cyclic propano-deoxyguanosine (PdG) adducts in bronchoalveolar lavage (BAL), lung, heart, liver, and bladder-mucosa from mice exposed to SSS for 16 weeks. In SSS exposed mice, Acr-dG adducts were the major type of PdG adducts formed in BAL (p < 0.001), lung (p < 0.05), and bladder mucosa (p < 0.001), with no significant accumulation of Acr-dG adducts in heart or liver. SSS exposure did not enhance BPDE-DNA adduct formation in any of these tissues. SSS exposure reduced nucleotide excision repair (p < 0.01) and base excision repair (p < 0.001) in lung tissue. The levels of DNA repair proteins, XPC and hOGG1, in lung tissues of exposed mice were significantly (p < 0.001 and p < 0.05) lower than the levels in lung tissues of control mice. We found that Acr can transform human bronchial epithelial and urothelial cells in vitro. We propose that induction of mutagenic Acr-DNA adducts, inhibition of DNA repair, and induction of cell transformation are three mechanisms by which SHS induces lung and bladder cancers. PMID:26431382

  10. 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.

  11. 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 ...

  12. Causation of cigarette smoke-induced emphysema by p-benzoquinone and its prevention by vitamin C.

    Science.gov (United States)

    Ghosh, Arunava; Ganguly, Shinjini; Dey, Neekkan; Banerjee, Santanu; Das, Archita; Chattopadhyay, Dhruba J; Chatterjee, Indu B

    2015-03-01

    Cigarette smoke (CS) is the strongest risk factor for emphysema. However, the mechanism of the disease is not clear. One reason is that each puff of CS is a complex mixture of approximately 4,000 chemicals, and it is yet to be known which of these chemical(s) are directly involved in the pathogenesis of lung injury in emphysema. The purpose of this study was to demonstrate that p-benzoquinone (p-BQ) produced in the lungs of CS-exposed guinea pigs is a causative factor for destruction of alveolar cells resulting in emphysema that is prevented by vitamin C. Vitamin C-restricted guinea pigs were subjected to whole-body CS exposure from five Kentucky research cigarettes (3R4F) per day or intramuscular injection of p-BQ in amounts approximately produced in the lung from CS exposure with and without oral supplementation of vitamin C. Progressive exposure of CS or p-BQ treatment caused progressive accumulation of p-BQ in the lung that was accompanied by destruction of alveolar cells and emphysema. The pathogenesis involved was arylation, oxidative stress, inflammation, and apoptosis. Vitamin C (30 mg/kg body weight/d), a potential antagonist of p-BQ, prevented accumulation of p-BQ in the lung and the pathogenesis of emphysema. Our study provides the first proof that inactivation of p-BQ, a causative factor of emphysema in CS-exposed lung, could constitute a novel and effective approach in the prevention of emphysema. We consider that a moderately high dose of vitamin C may be a simple preventive therapy for emphysema in chronic smokers. PMID:25057895

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

    Science.gov (United States)

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

    2011-01-01

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

  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. DEVELOPMENTAL CIGARETTE SMOKE EXPOSURE: LIVER PROTEOME PROFILE ALTERATIONS IN LOW BIRTH WEIGHT PUPS

    OpenAIRE

    Canales, Lorena; Chen, Jing; Kelty, Elizabeth; Musah, Sadiatu; Webb, Cindy; Pisano, M. Michele; Neal, Rachel E.

    2012-01-01

    Cigarette smoke is composed of over 4000 chemicals many of which are strong oxidizing agents and chemical carcinogens. Chronic cigarette smoke exposure (CSE) induces mild alterations in liver histology indicative of toxicity though the molecular pathways underlying these alterations remain to be explored. Utilizing a mouse model of ‘active’ developmental CSE (gestational day (GD) 1 through postnatal day (PD) 21; cotinine > 50 ng/mL) characterized by low birth weight offspring, the impact of d...

  16. Activated charcoal filter effectively reduces p-benzosemiquinone from the mainstream cigarette smoke and prevents emphysema

    Indian Academy of Sciences (India)

    Neekkan Dey; Archita Das; Arunava Ghosh; Indu B Chatterjee

    2010-06-01

    In this paper, we have made a comparative evaluation of the cytotoxicity and pathophysiological effects of mainstream smoke from cellulose acetate (CA)-filtered cigarettes with that of charcoal-filtered cigarettes developed in our laboratory. Previously, we had demonstrated that the mainstream smoke from an Indian CA-filtered commercial cigarette contains p-benzosemiquinone (p-BSQ), a major, highly toxic, long-lived water-soluble radical. Here, we have examined 16 brands of different CA-filtered cigarettes including Kentucky research cigarettes, and observed that mainstream smoke from all the cigarettes contains substantial amounts of p-BSQ (100–200 g/cigarette). We also show that when the CA filter is replaced by a charcoal filter, the amount of p-BSQ in the mainstream smoke is reduced by 73–80%, which is accompanied by a reduction of carbonyl formation in bovine serum albumin to the extent of 70–90%. The charcoal filter also prevented cytotoxicity in A549 cells as evidenced by MTT assay, apoptosis as evidenced by FACS analysis, TUNEL assay, overexpression of Bax, activation of p53 and caspase 3, as well as emphysematous lung damage in a guinea pig model as seen by histology and morphometric analysis. The results indicate that the charcoal filter developed in our laboratory may protect smokers from cigarette smoke-induced cytotoxity, protein modification, apoptosis and emphysema.

  17. Reasons for quitting cigarette smoking and electronic cigarette use for cessation help.

    Science.gov (United States)

    Pokhrel, Pallav; Herzog, Thaddeus A

    2015-03-01

    Despite the lack of clarity regarding their safety and efficacy as smoking cessation aids, electronic cigarettes (e-cigarettes) are commonly used to quit smoking. Currently, little is understood about why smokers may use e-cigarettes for help with smoking cessation compared with other, proven cessation aids. This study aimed to determine the reasons for wanting to quit cigarettes that are associated with the use of e-cigarettes for cessation help versus the use of conventional nicotine replacement therapy (NRT) products (e.g., gums). Cross-sectional, self-report data were obtained from 1,988 multiethnic current daily smokers (M age = 45.1, SD = 13.0; 51.3% women) who had made an average of 8.5 (SD = 18.7) lifetime quit attempts but were not currently engaged in a cessation attempt. Reasons for wanting to quit smoking were assessed by using the Reasons for Quitting scale. Path analyses suggested that among reasons for quitting cigarettes, "immediate reinforcement"-a measure of wanting to quit cigarettes for extrinsic reasons such as bad smell, costliness and untidiness-was significantly associated with having tried e-cigarettes for cessation help, and "concerns about health" was associated with having tried NRT-only use. E-cigarettes appear to provide an alternative "smoking" experience to individuals who wish to quit cigarette smoking because of the immediate, undesirable consequences of tobacco smoking (e.g., smell, ash, litter) rather than concerns about health. Provided that the safety of e-cigarette use is ensured, e-cigarettes may be effectively used to reduce tobacco exposure among smokers who may not want to quit cigarettes for intrinsic motivation. PMID:25180551

  18. 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...

  19. 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

  20. 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-...

  1. 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…

  2. 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

  3. Polonium in cigarette smoke and radiation exposure of lungs

    International Nuclear Information System (INIS)

    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 more 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. (author)

  4. 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

  5. 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

  6. 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.

  7. 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...

  8. Microbiological components in mainstream and sidestream cigarette smoke

    Directory of Open Access Journals (Sweden)

    Larsson Lennart

    2012-08-01

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

  9. 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...

  10. 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...

  11. Cigarette smoking disparities among sexual minority cancer survivors

    OpenAIRE

    Charles Kamen; Blosnich, John R.; Megan Lytle; Janelsins, Michelle C.; Peppone, Luke J; Mustian, Karen M.

    2015-01-01

    Objective: Sexual minority (i.e., lesbian, gay, and bisexual) adults smoke cigarettes at higher rates than heterosexual adults. Smoking after receiving a cancer diagnosis is a major health concern, yet risk of continued smoking among sexual minority cancer survivors is as yet unknown. The current study examines current smoking among sexual minority vs. heterosexual adult cancer survivors. Method: Data drawn from the 2010 Behavioral Risk Factor Surveillance System survey in five states (Ala...

  12. Prevalence of Cigarette Smoking among Adult Cancer Survivors in Korea

    OpenAIRE

    Park, Jin Joo; Park, Hyun Ah

    2015-01-01

    Purpose Cigarette smoking is associated not only with increased risk of cancer incidence, but also influences prognosis, and the quality of life of the cancer survivors. Thus, smoking cessation after cancer diagnosis is necessary. However, smoking behavior among Korean cancer-survivors is yet unknown. Materials and Methods We investigated the smoking status of 23770 adults, aged 18 years or older, who participated in the Health Interview Survey of the Korea National Health and Nutrition Exami...

  13. 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

  14. 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.

  15. 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.

  16. 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.

  17. 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...

  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. 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.

  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 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

  2. 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

  3. 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.

  4. 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

  5. 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

  6. 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

    hyper-reactivity plays an important role in the pathogenesis of cardiovascular and airway diseases. Recent studies have demonstrated that endothelin receptor up-regulation mediates vascular and airway hyper-reactivity in response to endothelin-1 (ET-1, endothelin receptor agonist) in cardiovascular and......-activated protein kinase (MAPK) and subsequently results in the up-regulation of endothelin receptors in the vasculature and airways, which mediates vascular and airway hyper-reactivity, one of the important pathogenic characteristics of cardiovascular and airway diseases. Understanding the molecular mechanisms of...... how cigarette smoke causes up-regulation of endothelin receptors in the vasculature and airways may provide new strategies for the treatment of cigarette smoke-associated cardiovascular and lung diseases....

  7. Occluded Cigarette Smoke Exposure Causing Localized Chloracne-Like Comedones.

    Science.gov (United States)

    Patterson, Andrew T; Tian, Frances T; Elston, Dirk M; Kaffenberger, Benjamin H

    2015-01-01

    Many environmental acne disorders, including chloracne and oil acne, were previously thought to occur predominantly in occupational settings following polycyclic aromatic hydrocarbon exposure. Cigarette smoke has also been shown to contain a large number of these toxic polycyclic aromatic hydrocarbon components and strictly correlates with noninflammatory acneiform lesion development in postadolescent patients. We report a case of localized open comedones associated with occluded cigarette smoke exposure near the nasal cavity due to infrequently changed gauze following rhinectomy. The dermal uptake of polycyclic aromatic hydrocarbon components in cigarette smoke has the potential to function as a contributing factor in chloracne development. Several of these environmental and noninflammatory acne subtypes may share a common molecular propensity for enhanced comedogenesis originating from aryl hydrocarbon receptor pathway effects in the skin. Additional studies are needed to further elucidate the exact mechanistic pathways through which tobacco smoke impacts the integumentary system. PMID:26360246

  8. 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

  9. 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

  10. 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

  11. The use of bupropion SR in cigarette smoking cessation

    OpenAIRE

    Scott Wilkes

    2008-01-01

    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...

  12. Cigarette Smoking Causes Hearing Impairment among Bangladeshi Population

    OpenAIRE

    Sumit, Ahmed Faisal; Das, Anindya; Sharmin, Zinat; Ahsan, Nazmul; Ohgami, Nobutaka; Kato, Masashi; Akhand, Anwarul Azim

    2015-01-01

    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 sub...

  13. 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.

  14. 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.

  15. Nuclear and mitochondrial DNA alterations in newborns with prenatal exposure to cigarette smoke.

    Science.gov (United States)

    Pirini, Francesca; Guida, Elisa; Lawson, Fahcina; Mancinelli, Andrea; Guerrero-Preston, Rafael

    2015-02-01

    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. PMID:25648174

  16. 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.

  17. Enhancement of lung cancer by cigarette smoking in uranium and other miners

    International Nuclear Information System (INIS)

    There are substantial animal and epidemiological data related to cigarette smoking and lung cancer among miners exposed to elevated levels of radon daughters that appears to be in disagreement. An hypothesis is advanced that explains most of this disagreement as being derived from temporal differences of cancer expression. The hypothesis is that a given radiation exposure induced a finite number of lung cancers, which have shorter latent periods due to the cancer promotion activity of smoke among cigarette smokers. According to this hypothesis, the life-shortening effect is greater among smoking miners than nonsmoking miners, and the ultimate number of lung cancers among smoking miners will be only a little larger than among nonsmokers. The greater number will derive from the additive effect of radiation and smoking, plus the greater force of competing causes of death among elderly nonsmokers

  18. Smoking patterns in waterpipe smokers compared with cigarette smokers: an exploratory study of puffing dynamics and smoke exposure

    OpenAIRE

    Pulcu, Erdem; McNeill, Ann

    2014-01-01

    Aim: It is estimated that globally there are about 100 million people who smoke waterpipes daily yet exposure resulting from smoking waterpipes is under-researched relative to cigarette smoking. This exploratory study assesses smoke exposure and puffing profiles among waterpipe smokers in comparison with cigarette smokers in Turkey, where there is a concern that waterpipe smoking prevalence is increasing. Method: A convenience sample of waterpipe (n=20) and cigarette smokers (n=110) was recru...

  19. 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.

  20. Cigarette smoke and ozone effect on murine inflammatory responses.

    Science.gov (United States)

    Gardi, Concetta; Valacchi, Giuseppe

    2012-07-01

    Air pollution has been associated with many different diseases, such as cancer, and respiratory, cardiovascular, and cutaneous chronic diseases. These effects are enhanced in people exposed to combined air pollutants, such as ozone and cigarette smoke. Chronic exposure to these pollutants causes an increase in oxidative stress and inflammation and has been associated with an increase in pulmonary diseases and mortality. Clinical and epidemiological studies reported interindividual variability in the adverse health effects of air pollutants, suggesting a genetic predisposition. The identification of subgroups of the population who are particularly vulnerable to air pollution is, therefore, of importance. Mouse models are a useful tool for studying the mechanisms underlying different susceptibility, as they show differences in strain responses to both ozone and cigarette smoke. This review analyses the role of inflammation and the influence of genetic factors on the mechanisms of lung injury caused by ozone and cigarette smoke. PMID:22758642

  1. 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.

  2. Alternative Roles of STAT3 and MAPK Signaling Pathways in the MMPs Activation and Progression of Lung Injury Induced by Cigarette Smoke Exposure in ACE2 Knockout Mice.

    Science.gov (United States)

    Hung, Yi-Han; Hsieh, Wen-Yeh; Hsieh, Jih-Sheng; Liu, Fon-Chang; Tsai, Chin-Hung; Lu, Li-Che; Huang, Chen-Yi; Wu, Chien-Liang; Lin, Chih-Sheng

    2016-01-01

    Inflammation-mediated abnormalities in the renin-angiotensin system (RAS) and expression of matrix metalloproteinases (MMPs) are implicated in the pathogenesis of lung injury. Angiotensin converting enzyme II (ACE2), an angiotensin converting enzyme (ACE) homologue that displays antagonist effects on ACE/angiotensin II (Ang II) axis, could also play a protective role against lung diseases. However, the relationship between ACE2 and MMPs activation in lung injury is still largely unclear. The purpose of this study is to investigate whether MMPs activity could be affected by ACE2 and which ACE2 derived signaling pathways could be also involved via using a mouse model with lung injury induced by cigarette smoke (CS) exposure for 1 to 3 weeks. Wild-type (WT; C57BL/6) and ACE2 KO mice (ACE2(-/-)) were utilized to study CS-induced lung injury. Increases in the resting respiratory rate (RRR), pulmonary immunokines, leukocyte infiltration and bronchial hyperplasia were observed in the CS-exposed mice. Compared to WT mice, more serious physiopathological changes were found in ACE2(-/-) mice in the first week of CS exposure. CS exposure increased pulmonary ACE and ACE2 activities in WT mice, and significantly increased ACE in ACE2(-/-) mice. Furthermore, the activity of pulmonary MMPs was decreased in CS-exposed WT mice, whereas this activity was increased in ACE2(-/-) mice. CS exposure increased the pulmonary p-p38, p-JNK and p-ERK1/2 level in all mice. In ACE2(-/-) mice, a significant increase p-STAT3 signaling was detected; however, no effect was observed on the p-STAT3 level in WT mice. Our results support the hypothesis that ACE2 deficiency influences MMPs activation and STAT3 phosphorylation signaling to promote more pulmonary inflammation in the development of lung injury. PMID:27019629

  3. Exposure to Cigarette Smoke Reduces Vitamin D3 in the Blood Stream and Respiratory Tract

    Science.gov (United States)

    ... Search navigation Find an Allergist / Immunologist Search Your Symptoms Ask the ... April 2, 2014 Cigarette smoking and exposure to secondhand smoke have long been known to exacerbate respiratory ...

  4. 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

  5. Neurobehavioral phenotype of C57BL/6J mice prenatally and neonatally exposed to cigarette smoke.

    Science.gov (United States)

    Amos-Kroohs, Robyn M; Williams, Michael T; Braun, Amanda A; Graham, Devon L; Webb, Cynthia L; Birtles, Todd S; Greene, Robert M; Vorhees, Charles V; Pisano, M Michele

    2013-01-01

    Although maternal cigarette smoking during pregnancy is a well-documented risk factor for a variety of adverse pregnancy outcomes, how prenatal cigarette smoke exposure affects postnatal neurobehavioral/cognitive development remains poorly defined. In order to investigate the cause of an altered behavioral phenotype, mice developmentally exposed to a paradigm of 'active' maternal cigarette smoke is needed. Accordingly, cigarette smoke exposed (CSE) and air-exposed C57BL/6J mice were treated for 6h per day in paired inhalation chambers throughout gestation and lactation and were tested for neurobehavioral effects while controlling for litter effects. CSE mice exhibited less than normal anxiety in the elevated zero maze, transient hypoactivity during a 1h locomotor activity test, had longer latencies on the last day of cued Morris water maze testing, impaired hidden platform learning in the Morris water maze during acquisition, reversal, and shift trials, and impaired retention for platform location on probe trials after reversal but not after acquisition or shift. CSE mice also showed a sexually dimorphic response in central zone locomotion to a methamphetamine challenge (males under-responded and females over-responded), and showed reduced anxiety in the light-dark test by spending more time on the light side. No differences on tests of marble burying, acoustic startle response with prepulse inhibition, Cincinnati water maze, matching-to-sample Morris water maze, conditioned fear, forced swim, or MK-801-induced locomotor activation were found. Collectively, the data indicate that developmental cigarette smoke exposure induces subnormal anxiety in a novel environment, impairs spatial learning and reference memory while sparing other behaviors (route-based learning, fear conditioning, and forced swim immobility). The findings add support to mounting evidence that developmental cigarette smoke exposure has long-term adverse effects on brain function. PMID:23314114

  6. Neurobehavioral phenotype of C57BL/6J mice prenatally and neonatally exposed to cigarette smoke

    OpenAIRE

    Amos-Kroohs, Robyn M.; Williams, Michael T.; Braun, Amanda A.; Graham, Devon L.; WEBB, CYNTHIA L.; Birtles, Todd S.; Greene, Robert M.; Vorhees, Charles V.; Pisano, M. Michele

    2013-01-01

    Although maternal cigarette smoking during pregnancy is a well-documented risk factor for a variety of adverse pregnancy outcomes, how prenatal cigarette smoke exposure affects postnatal neurobehavioral/cognitive development remains poorly defined. In order to investigate the cause of an altered behavioral phenotype, mice developmentally exposed to a paradigm of ‘active’ maternal cigarette smoke is needed. Accordingly, cigarette smoke exposed (CSE) and air-exposed C57BL/6J mice were treated f...

  7. 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

  8. 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

  9. 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 ...

  10. 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

  11. 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.

  12. 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

  13. The combined effects of plutonium and cigarette smoke on the production of lung tumours

    International Nuclear Information System (INIS)

    An experiment was conducted to determine the effect of exposure to cigarette smoke on the incidence of plutonium induced lung tumours in mice. Approximately 130 female CBA/H mice were used. These were exposed to plutonium-239 dioxide to give an initial alveolar deposit of 100 Bq, then treated in one of three ways. One third received no further treatment and were held for a period of 18 months. The remainder were either sham-exposed or exposed to mainstream cigarette smoke for one year then held for a further 6 months. After this all the animals were killed. The control mice - that had received only plutonium -contained more tumours than mice that were also either sham-exposed or exposed to cigarette smoke. The lowest number of tumours was found in the group exposed to smoke. These results indicate that, under some circumstances, the effects of cigarette smoke and of alpha-irradiation of the lung can be antagonistic, contrasting with a common expectation of synergy. (author)

  14. Cigarette smoking increases white blood cell aggregation in whole blood.

    OpenAIRE

    Bridges, A B; Hill, A; Belch, J J

    1993-01-01

    We studied the effect of chronic cigarette smoking on white blood cell aggregation, increased aggregation predisposes to microvascular occlusion and damage. Current smokers had significantly increased white blood cell aggregation when compared with non smokers. The presence of chronically activated white blood cells in current smokers may be relevant in the pathogenesis of ischaemic vascular disease.

  15. Extended Treatment with Bupropion SR for Cigarette Smoking Cessation

    Science.gov (United States)

    Killen, Joel D.; Fortmann, Stephen P.; Murphy, Greer M.; Hayward, Chris; Arredondo, Christina; Cromp, DeAnn; Celio, Maria; Abe, Laurie; Wang, Yun; Schatzberg, Alan F.

    2006-01-01

    The authors present results of a randomized clinical trial of the efficacy of extended treatment with bupropion SR in producing longer term cigarette smoking cessation. Adult smokers (N = 362) received open-label treatment (11 weeks) that combined relapse prevention training, bupropion SR, and nicotine patch followed by extended treatment (14…

  16. Preventing Relapse to Cigarette Smoking by Behavioral Skill Training.

    Science.gov (United States)

    Hall, Sharon M.; And Others

    1984-01-01

    Crossed two relapse prevention conditions (skills training-vs-discussion control) with two levels of aversive smoking in volunteer subjects (N=123). Results indicated that relapse-prevention skill training did prevent relapse among cigarette smokers. Lighter smokers were more favorably influenced. (LLL)

  17. 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…

  18. 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...

  19. Cigarette smoking prevalence among psychiatric outpatients in Bucaramanga

    Directory of Open Access Journals (Sweden)

    Farelo Daniel

    2004-05-01

    Full Text Available Background: International investigations report a higher smoking prevalence among psychiatric patients than general population. However a Colombian research found similar smoking prevalence in both populations. Objective: Establishing cigarette smoking prevalence among psychiatric outpatients. Method: This is a transversal report, part of a bigger investagation. It included patients from 18 to 64 year-old, dwelling metropolitan area of Bucaramanga. Diagnosis was confirmed using SCID-I. Patients who smoked everyday during last month were considered smoker. Results: 185 patients were included. Mean age was 42.3 year, 62.7% was female, mean education was 7.0 years. Diagnosis was bipolar disorder in 42.7%, schizophrenia in 33.5%, major depressive disorder in 17.3%, and schizoaffective disorder in 6.5%. Cigarette smoking prevalence was 14.6% (CI 95% 9.4-19.8. Multivariate analysis showed association between smoking and older than 45 year old (PR 2.87, male sex (PR 2.31, higher year education (PR 2.35, and psychotic disorders (RP 3.63. Conclusion: Global smoking prevalence among psychiatric outpatients from Bucaramanga is lower than prevalence internationally reported. There is an association between smoking and psychotic disorders.

  20. 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.

  1. 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.

  2. 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

  3. Nitrated Fatty Acids Reverse Cigarette Smoke-Induced Alveolar Macrophage Activation and Inhibit Protease Activity via Electrophilic S-Alkylation

    Science.gov (United States)

    Reddy, Aravind T.; Lakshmi, Sowmya P.; Muchumarri, Ramamohan R.; Reddy, Raju C.

    2016-01-01

    Nitrated fatty acids (NFAs), endogenous products of nonenzymatic reactions of NO-derived reactive nitrogen species with unsaturated fatty acids, exhibit substantial anti-inflammatory activities. They are both reversible electrophiles and peroxisome proliferator-activated receptor γ (PPARγ) agonists, but the physiological implications of their electrophilic activity are poorly understood. We tested their effects on inflammatory and emphysema-related biomarkers in alveolar macrophages (AMs) of smoke-exposed mice. NFA (10-nitro-oleic acid or 12-nitrolinoleic acid) treatment downregulated expression and activity of the inflammatory transcription factor NF-κB while upregulating those of PPARγ. It also downregulated production of inflammatory cytokines and chemokines and of the protease cathepsin S (Cat S), a key mediator of emphysematous septal destruction. Cat S downregulation was accompanied by decreased AM elastolytic activity, a major mechanism of septal destruction. NFAs downregulated both Cat S expression and activity in AMs of wild-type mice, but only inhibited its activity in AMs of PPARγ knockout mice, pointing to a PPARγ-independent mechanism of enzyme inhibition. We hypothesized that this mechanism was electrophilic S-alkylation of target Cat S cysteines, and found that NFAs bind directly to Cat S following treatment of intact AMs and, as suggested by in silico modeling and calculation of relevant parameters, elicit S-alkylation of Cys25 when incubated with purified Cat S. These results demonstrate that NFAs’ electrophilic activity, in addition to their role as PPARγ agonists, underlies their protective effects in chronic obstructive pulmonary disease (COPD) and support their therapeutic potential in this disease. PMID:27119365

  4. 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

  5. Cigarette smoking among economically active population

    Directory of Open Access Journals (Sweden)

    Dorota Kaleta

    2013-06-01

    Full Text Available Background: Tobacco smoking is one of the major risk factors for chronic diseases and results in huge economic and social costs. The aim of the study was to evaluate the prevalence of smoking. Moreover, we evaluated the association between selected socio-economic factors and tobacco smoking among economically active individuals. Material and Methods: The study population covered 2254 economically active men and 1666 women. Data were derived from the Global Adult Tobacco Survey (GATS. Results: About 37.3% of men and 28.2% of women smoke regularly. Daily smoking was significantly associated with low level of education in men (primary vs. high education OR = 3.2, 95% CI: 1.9-5.3; p < 0.001; vocational vs. high education: OR = 2.1, 95% CI: 1.5-3.0; p < 0.001 and women (primary vs. high education OR = 2.8, CI: 1.4-5.5; p < 0.01; vocational vs. high education: OR = 1.9, 95% CI: 1.2-2.9; p < 0.01. Daily smoking was significantly associated with age of women (40-49 years vs. 20-29 years OR = 1.64, 95% CI: 1.1-2.44; p < 0.01, lack of awareness of health effects of smoking in both genders (men unaware vs. aware: OR = 2.9, 95% CI: 1.8-4.6; p < 0.01 and women unaware vs. aware: OR = 2,9, 95% CI: 1.5-5.7; p < 0.01. Smoking was associated with lack of complete smoking bans at workplaces of respondents. Conclusions: Comprehensive interventions are needed to reduce the prevalence of smoking among economically active individuals. Med Pr 2013;64(3:359–371

  6. Effects of smoking regimens and test material format on the cytotoxicity of mainstream cigarette smoke.

    Science.gov (United States)

    Li, Xiang; Shang, Pingping; Peng, Bin; Nie, Cong; Zhao, Le; Liu, Huimin; Xie, Jianping

    2012-03-01

    The purpose of this study was to evaluate the effects of test material format and smoking regimens on comparative toxicity testing of cigarette smoke. Total particulate matter (TPM) or whole smoke (WS) generated from three test cigarettes under International Organization for Standardization (ISO) or Health Canada Intensive (HCI) regimens were assessed for cytotoxicity using the neutral red uptake (NRU) cytotoxicity assay. Under both ISO and HCI regimens, the relative differences of cytotoxicity among the test cigarettes indicated by the EC50 values in WS were significantly higher than those in TPM. For TPM testing, cytotoxicity was decreased going from ISO regimen to HCI regimen, consistent with the reported reductions of toxicant output on a per unit of TPM basis under the HCI regimen. For WS, cytotoxicity increased for the two lower TPM cigarettes, and decreased for the higher TPM cigarette going from HCI regimen to ISO regimen. Results from this study demonstrated WS should be the preferable test material format for smoke toxicity testing whenever possible. Intensive smoking regimens, such as HCI, are less likely to underestimate smoke toxicant intakes by smokers, and should be included in the comparative toxicological testing strategy. PMID:22198610

  7. Associations of cigarette smoking with rheumatoid arthritis in African Americans

    Science.gov (United States)

    Mikuls, Ted R.; Sayles, Harlan; Yu, Fang; LeVan, Tricia; Gould, Karen A.; Thiele, Geoffrey M.; Conn, Doyt; Jonas, Beth L.; Callahan, Leigh F.; Smith, Edwin; Brasington, Richard; Moreland, Larry W.; Reynolds, Richard; Bridges, S. Louis

    2010-01-01

    Objective To examine the associations of cigarette smoking with rheumatoid arthritis (RA) in African Americans and to determine to whether this association is impacted by HLA-DRB1 shared epitope (SE). Methods Smoking status, cumulative smoking exposure, and SE status were measured in African American patients with RA and in healthy controls. Associations of smoking with RA were examined using age- and gender-adjusted logistic regression. Additive and multiplicative SE-smoking interactions were examined. Results After adjusting for age and gender, ever (OR = 1.45; 95% CI 1.07 to 1.97) and current smoking (OR = 1.56; 95% CI 1.07 to 2.26) were more common in African American RA cases (n = 605) than in controls (n = 255). The association of smoking with RA was limited to those with a cumulative exposure exceeding 10 pack-years, associations that were evident in both autoantibody positive and negative disease. There was evidence of a significant additive interaction between SE status and heavy smoking (≥ 10 pack-years) in RA risk (attributable proportion due to interaction [AP] of 0.58, p = 0.007) with an AP of 0.47 (p = 0.006) between SE status and ever smoking. There was no evidence of multiplicative interactions. Conclusion Among African Americans, cigarette smoking is associated not only with the risk of autoantibody positive RA but also with the risk of autoantibody negative disease. RA risk attributable to smoking is limited to African Americans with more than 10 pack-years of exposure and is more pronounced among individuals positive for HLA-DRB1 SE. PMID:20722010

  8. 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.

  9. Cigarette smoking and brain regulation of energy homeostasis.

    Science.gov (United States)

    Chen, Hui; Saad, Sonia; Sandow, Shaun L; Bertrand, Paul P

    2012-01-01

    Cigarette smoking is an addictive behavior, 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. PMID:22848202

  10. 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.

  11. 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

    2016-03-01

    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. PMID:26457812

  12. 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)

  13. 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

  14. 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

  15. 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.

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

    Directory of Open Access Journals (Sweden)

    Konopa Krzysztof

    2006-07-01

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

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

    Science.gov (United States)

    Mori, Kenta; Hasegawa, Shiori; Yamashita, Motozo; Yamada, Satoru; Kitamura, Masahiro; Murakami, Shinya

    2016-01-01

    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. PMID:27203240

  18. 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

  19. Emphysematous lung destruction by cigarette smoke. The effects of latent adenoviral infection on the lung inflammatory response.

    Science.gov (United States)

    Meshi, Bernard; Vitalis, Timothy Z; Ionescu, Diana; Elliott, W Mark; Liu, Chun; Wang, Xiang-Dong; Hayashi, Shizu; Hogg, James C

    2002-01-01

    This study was designed to test the hypothesis that cigarette smoke-induced inflammation and emphysema are amplified by the presence of latent adenoviral (Ad) infection, and to determine whether this emphysematous process can be reversed by all-trans-retinoic acid (RA) treatment. The results confirm that in guinea pigs, chronic cigarette-smoke exposure caused lesions similar to human centrilobular emphysema. They also show that latent Ad infection combined with cigarette-smoke exposure caused an excess increase in lung volume (P < 0.001), air-space volume (P < 0.001), and lung weight (P < 0.01), and further decrease in surface-to-volume ratio (P < 0.001) compared with smoke exposure alone. RA treatment failed to reverse these emphysematous changes. Analysis of inflammatory response in parenchymal and airway tissue showed that smoking caused an increase of polymorphonuclear leukocytes (PMNs) (P < 0.0002), macrophages (P < 0.001), and CD4 cells (P < 0.0009), and that latent Ad infection independently increased PMNs (P < 0.001), macrophages (P = 0.003), and CD8 cells (P < 0.001). We conclude that latent Ad infection amplifies the emphysematous lung destruction and increases the inflammatory response produced by cigarette-smoke exposure. In this study, the increase in CD4 was associated with cigarette smoke and the increase in CD8 cells with latent Ad infection. PMID:11751203

  20. 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.

  1. 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

  2. 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

  3. 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 ...

  4. 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

  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. 210Po radiation dose due to cigarette smoking

    International Nuclear Information System (INIS)

    The level of 210Po in eight brands of cigarettes and four brands of bidis popular in and around Nagercoil town was determined to evaluate the annual effective dose. The 210Po activity in a full cigarette ranged from 32.8±3.6 to 68.4±5.9 mBq and from 34.3±3.5 to 62.9±5.8 mBq in a bidi. In tobacco, the highest 210Po content was recorded in the brand C4 (23.0±1.2 mBq) whereas for bidis it was the highest in the brand B2 (21.1±1.1 mBq). The activity in mainstream varied from 15.2±0.75 to 36.8±2.1 mBq in a cigarette and from 20.7±3.1 to 39.8±4.0 mBq in a bidi. With regard to 210Po activity concentration, not much specificity was noted with respect to the tobacco brand. The data showed a relatively wide range of activity concentration of 210Po in the different cigarette/bidi brands and even within the same brand. The bidis showed a higher activity when compared to cigarettes. The popular brands concentrated more activity than the fine brands. Smokers who smoke one pack (10 cigarettes/bidis) per day may inhale about 100-300 mBq d-1 (0.1-0.3 Bq d-1) of 210Po. In this study, radiation dose values in the range of 153.5-372.9 μSv Y-'1 from cigarettes and from 209.2 to 402.7 μSvY-1 from bidis was estimated for the whole body. (author)

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

    OpenAIRE

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

    2013-01-01

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

  8. 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)

  9. 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.

  10. 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...

  11. 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. ...

  12. 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...

  13. 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.

  14. 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). PMID:27160659

  15. Cigarette smoke extract increases albumin flux across pulmonary endothelium in vitro

    International Nuclear Information System (INIS)

    Cigarette smoking causes lung inflammation, and a characteristic of inflammation is an increase in vascular permeability. To determine if cigarette smoke could alter endothelial permeability, we studied flux of radiolabeled albumin across monolayers of porcine pulmonary artery endothelium grown in culture on microporous membranes. Extracts (in either dimethylsulfoxide or phosphate-buffered saline) of cigarette smoke in a range estimate of concentrations simulating cigarette smoke exposure to the lungs in vivo caused a dose-dependent increase in albumin flux that was dependent on extracellular divalent cations and associated with polymerization of cellular actin. The effect was reversible, independent of the surface of endothelial cells exposed (either luminal or abluminal), and due primarily to components of the vapor phase of smoke. The effects occurred without evidence of cell damage, but subtle morphological changes were produced by exposure to the smoke extracts. These findings suggest that cigarette smoke can alter permeability of the lung endothelium through effects on cytoskeletal elements

  16. 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…

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

    Science.gov (United States)

    Cobb, Nathan K; Sonti, Rajiv

    2016-08-01

    E-cigarettes are a diverse set of devices that are designed for pulmonary delivery of nicotine through an aerosol, usually consisting of propylene glycol, nicotine, and flavorings. The devices heat the nicotine solution using a battery-powered circuit and deliver the resulting vapor into the proximal airways and lung. Although the current devices on the market appear to be safer than smoking combusted tobacco, they have their own inherent risks, which remain poorly characterized due to widespread product variability. Despite rising use throughout the United States, predominantly by smokers, limited evidence exists for their efficacy in smoking cessation. Pending regulation by the FDA will enforce limited disclosures on the industry but will not directly impact safety or efficacy. Meanwhile, respiratory health practitioners will need to tailor their discussions with patients, taking into account the broad range of existing effective smoking cessation techniques, including pharmaceutical nicotine replacement therapy. PMID:27407178

  18. 1α,25-dihydroxyvitamin D₃ counteracts the effects of cigarette smoke in airway epithelial cells.

    Science.gov (United States)

    Zhang, Ruhui; Zhao, Haijin; Dong, Hangming; Zou, Fei; Cai, Shaoxi

    2015-06-01

    Cigarette smoke extracts (CSE) alter calpain-1 expression via ERK signaling pathway in bronchial epithelial cells. 1α,25-dihydroxyvitamin D3 (1,25D3) inhibits cigarette smoke-induced epithelial barrier disruption. This study was aimed to explore whether the 1,25D3 counteracted the CSE effects in a human bronchial epithelial cell line (16HBE). In particular, transepithelial electrical resistance (TER) and permeability, expression and distribution of E-cadherin and β-catenin, calpain-1 expression, and ERK phosphorylation were assessed in the CSE-stimulated 16HBE cells. The CSE induced the ERK phosphorylation, improved the calpain-1 expression, increased the distribution anomalies and the cleaving of E-cadherin and β-catenin, and resulted in the TER reduction and the permeability increase. The 1,25D3 reduced these pathological changes. The 1,25D3 mediated effects were associated with a reduced ERK phosphorylation. In conclusion, the present study provides compelling evidences that the 1,25D3 may be considered a possible valid therapeutic option in controlling the cigarette smoke-induced epithelial barrier disruption. PMID:25880105

  19. Development of nitroxide radicals–containing polymer for scavenging reactive oxygen species from cigarette smoke

    International Nuclear Information System (INIS)

    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. (papers)

  20. 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.

  1. N-acetyl Cysteine Reduced Oxidative Damages in Guinea Pigs Exposed to Cigarette Smoke and / or Gamma Radiation

    International Nuclear Information System (INIS)

    The objective of this study was to evaluate the role of n-acetyl cysteine (NAC) supplementation on oxidative cigarette smoke induced-oxidative damage in irradiated guinea pigs. N-acetyl cysteine was injected (i.p) to guinea pigs at a dose of 150 mg/kg b. w/day pre-exposure to cigarette smoke for one hour daily for 30 successive days. Animals were submitted to fractionate whole body gamma radiation (2 Gy installment every two weeks up to 4 Gy total dose started on the 2nd week of the experiment). Animals were sacrificed during the first hours from the last treatment of cigarette smoke. The results obtained showed significant increase in malondialdehyde (MDA) content associated with decreased superoxide dismutase (SOD) activity and glutathione (GSH) concentration in cardiac and pulmonary tissues as compared with their equivalent in control animals. The activities of lactate dehydrogenase (LDH), creatine phosphokinase (CPK), aspartate transaminase (AST), concentration of nitric oxide (NO), total cholesterol, Triacylglycerol, LDL-cholesterol were significant increased in plasma associated with significant decreased HDL-cholesterol. The administration of NAC has significantly attenuated the cigarette smoke and/or irradiation-induced changes in all the studied parameters. It could be concluded that NAC reduced cigarette smoke and radiation hazards via neutralized their capability to generate excessive reactive oxygen species (ROS) and free radicals in the biological systems

  2. 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 imag....... 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....... imaging discovered multiple pulmonary nodules and liver lesions suspicious of widespread metastases; however, an extensive evaluation found no evidence of malignancy. Results of a lung biopsy revealed an area with multinucleated giant cells suggestive of a foreign body reaction to a lipophilic material...

  3. 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

  4. Cigarette smoking and smoking cessation in relation to risk of rheumatoid arthritis in women

    Science.gov (United States)

    2013-01-01

    Introduction Whereas the overall association between smoking and rheumatoid arthritis (RA) must be regarded as established, considerably less is known about how much smoking is needed to increase the risk of RA, that is, the effect of smoking intensity, duration and cessation. Methods The Swedish Mammography Cohort, including 34,101 women aged 54 to 89 years, was followed up from January 1, 2003 through December 31, 2010 (219 RA cases identified). Relative risks (RR) and their 95% confidence intervals (CI) were estimated as rate ratios using Cox proportional hazards model. Results There was a statistically significant association between smoking intensity (RR comparing 1 to 7 cigarettes/day vs never smoking 2.31 (95% CI: 1.59, 3.36)) as well as duration of smoking (comparing 1 to 25 years vs never smoking RR = 1.60 (95% CI: 1.07, 2.38)) and risk of RA. Compared to never smokers, the risk was still significantly elevated 15 years after smoking cessation (RR = 1.99 (95% CI: 1.23, 3.20)). However, among former smokers, the risk of RA seemed to be decreasing over time since stopping smoking: women who stopped smoking 15 years before the start of the follow-up had 30% lower risk of RA compared to those who stopped only a year before start of the follow-up (RR = 0.70 (95% CI: 0.24,2.02)). Conclusions This prospective study highlights that even light cigarette smoking is associated with increased risk of RA in women and that smoking cessation may reduce, though not remove, this risk. PMID:23607815

  5. 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

  6. 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

  7. Bronchial Responsiveness and Lung Function Related to Cigarette Smoking and Smoking Cessation

    Directory of Open Access Journals (Sweden)

    Shieh Ching Yang

    2002-10-01

    Full Text Available Background: The relationships between bronchial responsiveness and both cigarette smokingand smoking cessation are still controversial.Methods: To investigate the effects of cigarette smoking and smoking cessation onbronchial reactivity and the level of pulmonary function, bronchial responsivenessto methacholine using the forced oscillation method, the transferfactor, and spirometry were measured in 180 nonsmokers, 109 current smokers,and 82 ex-smokers. The following indices of bronchial responsivenesswere used: (1 baseline respiratory resistance (Rrs; (2 the cumulative doseof methacholine (DA causing an increase in Rrs by twice the baseline values(bronchial sensitivity; and (3 the slope of linearly decreased respiratoryconductance (SGrs representing bronchial reactivity.Results: Current smokers had significantly higher baseline Rrs ( p < 0.001 andbronchial responsiveness than did nonsmokers and ex-smokers. In 24.7% ofsmokers, Rrs increased by twice or more upon challenge with methacholine(responders, compared with 0% of nonsmokers ( p < 0.0001 and 19.5% ofex-smokers ( p = 0.28. SGrs for responders among ex-smokers was foundnot to differ from that for responders among smokers. However, smokershad a significantly lower DA of inhaled methacholine than did ex-smokers.Cigarette smoking was also associated with an appreciable reduction inFEV1/FVC (forced expiratory volume in 1s/forced vital capacity, DLCO(carbon monoxide diffusing capacity, and DLCO/VA (alveolar volume.Conclusion: There seems to be a partially reversible phenomenon that leads to improvementin airway responsiveness and DLCO upon smoking cessation.

  8. Comparison of cigarette smoke exposure atmospheres in different puffing modes

    International Nuclear Information System (INIS)

    Mainstream cigarette smoke generated using different puffing profiles was characterized for particle size distribution, vapor/gas concentration, and chemical composition. Three puffing profiles were compared: (1) a standard, 2-sec, 35 ml puff (SP), once per minute; (2) a puff of double the standard volume (70 mL), once per minute (DP); and (3) a double puff, twice per minute (2-DP). Results from samples collected with a multijet Mercer impactor indicated that the mass median aerodynamic diameter of smoke particles decreased with puff volume. The concentrations of specific chemicals from gas samples (CO, CO2, nitrogen oxides, and small molecular weight hydrocarbons), organic vapor samples (acetone, 2-methylfuran, benzene, meta- and para-xylene, ortho-xylene, and limonene), and particulate samples (nicotine, glycerol, hydroquinone, and palmitic acid) showed good agreement among the three puffing profiles. They support a prediction that the health effects of cigarette smoke generated from 2-DP or DP profiles would not be different from those resulting from SP profiles. (author)

  9. Deposition of cigarette smoke particles in the rat respiratory tract

    International Nuclear Information System (INIS)

    Male and female rats were exposed to mainstream cigarette smoke to determine the fractional deposition. Deposition studies were conducted by placing the rats in plethysmography tubes for respiratory minute volume measurements and exposing them to 14C-dotriacontane-labeled cigarette smoke at mass concentrations of 202 or 624 mg/m3 for 25 min. Immediately after the exposure, the rats were sacrificed and the 14C contents in various tissues and organs were analyzed. Results showed that the GI tract contained 16-31% of the total activity, indicating significant clearance from the large airways and nose to the GI tract during the exposure and during the 10-15 min between cessation of the exposure and the removal of the organs. Total deposition of the inhaled activity was 20.1 ± 1.6% for both exposure concentrations. The intrapulmonary deposition fractions (lung lobes plus airways below the lobar bronchi) were 12.4 ± 0.9% and 15.9 ± 1.4% for high and low concentrations, respectively, suggesting a slight enhancement in upper airway deposition for animals exposed to the higher smoke concentration. (author)

  10. The separate effects of tar and nicotine on the cigarette smoking manoeuvre

    International Nuclear Information System (INIS)

    The separate effects of tar and nicotine on the cigarette smoking manoeuvre were investigated. Each of ten asymptomatic habitual smokers smoked three different commercially available cigarettes in a randomised order. The brands were chosen such that two had the same tar yield (10 mg) and two had the same nicotine yield (1.4 mg). The volume of smoke inhaled into the lungs was measured by tracing the smoke with the inert gas 81Krm. Puffing indices were recorded using an electronic smoking analyser and flowhead/cigarette holder. There was no difference in the total volume of smoke puffed from each of the cigarette brands. With cigarettes of the samme tar level, the total inhaled smoke volume was lower with the higher nicotine cigarette (P<0.05): by contrast, with cigarettes of the same nicotine level, the toal inhaled smoke volume was lower with the lower tar cigarette (P<0.02). Tar and nicotine appear to exercise independent control over the volume of smoke inhaled. (author)

  11. 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.

  12. 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.

  13. Effect of cigarette smoke, nicotine, and carbon monoxide on the permeability of the arterial wall

    International Nuclear Information System (INIS)

    The association between cigarette smoking and the development of atherosclerosis is well established, but the mechanism that makes cigarettes such a potent risk factor is not understood. There is normally a constant insudation of plasma macromolecules into the arterial wall. Fibrinogen and lipids are two of the large molecules involved in atherosclerosis. Therefore, we studied the effect of cigarette smoke, nicotine, and carbon monoxide on the permeability of the canine arterial wall to 125I-labeled fibrinogen. The results show that inhaled cigarette smoke significantly and rapidly increases the permeability of the arterial wall to fibrinogen and that this effect can be produced with carbon monoxide alone but not with intravenous nicotine

  14. 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

  15. 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

  16. Cigarette smoking causes hearing impairment among Bangladeshi population.

    Science.gov (United States)

    Sumit, Ahmed Faisal; Das, Anindya; Sharmin, Zinat; Ahsan, Nazmul; Ohgami, Nobutaka; Kato, Masashi; Akhand, Anwarul Azim

    2015-01-01

    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. PMID:25781179

  17. Chronic cigarette smoking alters erythrocyte membrane lipid composition and properties in male human volunteers.

    Science.gov (United States)

    Padmavathi, Pannuru; Reddy, Vaddi Damodara; Kavitha, Godugu; Paramahamsa, Maturu; Varadacharyulu, Nallanchakravarthula

    2010-11-01

    Cigarette smoking is a major lifestyle factor influencing the health of human beings. The present study investigates smoking induced alterations on the erythrocyte membrane lipid composition, fluidity and the role of nitric oxide. Thirty experimental and control subjects (age 35+/-8) were selected for the study. Experimental subjects smoke 12+/-2 cigarettes per day for 7-10 years. In smokers elevated nitrite/nitrate levels in plasma and red cell lysates were observed. Smokers showed increased hemolysis, erythrocyte membrane lipid peroxidation, protein carbonyls, C/P ratio (cholesterol and phospholipid ratio), anisotropic (gamma) value with decreased Na(+)/K(+)-ATPase activity and sulfhydryl groups. Alterations in smokers erythrocyte membrane individual phospholipids were also evident from the study. Red cell lysate nitric oxide positively correlated with C/P ratio (r=0.565) and fluorescent anisotropic (gamma) value (r=0.386) in smokers. Smoking induced generation of reactive oxygen/nitrogen species might have altered erythrocyte membrane physico-chemical properties. PMID:20561918

  18. 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...

  19. Effects of cigarette smoke and dietary vitamin E levels on selected lung and hepatic biotransformation enzymes in mice

    Energy Technology Data Exchange (ETDEWEB)

    Graziano, M.J.; Gairola, C.; Dorough, H.W.

    1985-01-01

    Young male C57BL mice were exposed nose-only to cigarette smoke 20 min/day for 8 weeks while maintained on diets containing 0, 5, and 100 ppm of vitamin E. Smoking had no effect on hepatic aryl hydrocarbon hydroxylase (AHH), UDP-glucuronyltransferase, glutathione S-transferase, parathion desulfurase, or parathion esterase activity. Lung AHH activity was increased in all smoke-exposed mice, although the increase was significantly less in animals maintained on the vitamin E-free diet. All mice on the vitamin E-free diet showed reduced lung AHH activity and increased hepatic lipid peroxidation. No other biotransformations tested were significantly altered by varying vitamin E concentrations alone or in combination with cigarette smoke. For all vitamin E diets, both the smoke-exposed and sham-treated mice gained significantly less weight than the control animals. This effect was attributed to stress induced by restraint of the animals within the smoking apparatus. The results of these experiments show that both cigarette smoke and vitamin E-deficient diets may affect xenobiotic metabolism but that the combination does not appear to alter markedly their individual effects or to induce ones not previously observed.

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

    Science.gov (United States)

    Choi, Damee; Ota, Shotaro; Watanuki, Shigeki

    2015-12-01

    Previous studies have reported a paradox that cigarette smoking reduces stress psychologically; however, it increases the arousal level physiologically. To examine this issue, our study aimed to investigate whether cigarette smoking relieves stress by measuring the late positive potential (LPP), a component of the event-related potential (ERP). In Experiment 1, participants first watched emotionally neutral images; second, they received a break; and finally, they watched emotionally neutral images again. In the break, they smoked a cigarette (smoking condition) or simply rested without smoking (non-smoking condition). The procedure of Experiment 2 was the same as that of Experiment 1, except that the participants watched unpleasant images as stress stimuli before the break. In Experiment 1, the LPP decreased from before to after the break in the smoking condition, but not in the non-smoking condition, suggesting that smoking cigarettes in the neutral state reduces the arousal level. In Experiment 2, the LPP for 400-600 ms decreased from before to after the break, both in the smoking and non-smoking conditions; however, the LPP for 200-400 ms decreased from before to after the break only in the smoking condition. This suggests the possibility that cigarette smoking in the unpleasant state may facilitate a decrease in the arousal level faster than with non-smoking. In both Experiments 1 and 2, the subjective rating results also suggested that cigarette smoking decreased anxiety. Taken together, both the physiological (LPP) and the psychological responses from our study suggest that cigarette smoking perhaps relieves stress. PMID:26497442

  1. 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…

  2. Inhalation of 210Po and 210Pb from cigarette smoking in Poland

    International Nuclear Information System (INIS)

    The carcinogenic effect of 210Po and 210Pb 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 210Po 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 210Po and 210Pb 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 210Po and 210Pb each. The mean values of the annual effective dose for smokers were estimated to be 35 and 70 μSv from 210Po and 210Pb, respectively. For persons who smoke two packs of cigarettes with higher radionuclide concentrations, the effective dose is much higher (471 μSv yr-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 210Po and 210Pb intake of smokers in Poland

  3. 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.

  4. 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.

  5. 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.

  6. Effects of cigarette smoke exposure on pulmonary clearance of 239PuO2 in rats

    International Nuclear Information System (INIS)

    Groups of rats were exposed or sham exposed to cigarette smoke for 7 mo, at which time they were exposed to an aerosol of 239PuO2. Rats were then subjected to whole-body counting (17-keV X-rays) periodically, beginning at day 4 after plutonium exposure, and smoke exposures or sham exposures were resumed on day 7. Clearance of plutonium from the lungs of cigarette-smoke-exposed rats was significantly slower than that from the sham-exposed rats' lungs. The difference between the two groups became significant 7 days after the resumption of cigarette-smoke exposures

  7. Effect of the number of cigarettes smoked and of radon exposure on the lung cancer risk

    International Nuclear Information System (INIS)

    The relation between the extent of cigarette smoking and the lung cancer risk in people exposed to radon was examined. The changes in the airway geometry due to an increased production of mucus caused by smoking were taken into account. The mucous layer protects the target cells from the effects of ionizing radiation. The radiation risk per unit exposure decreases with the number of cigarettes smoked, in contrast to the total risk, which increases to stagnate in the range of extensive daily cigarette smoking. Lung damage in chronic smokers should be taken into account, though. (orig.)

  8. Trimetazidine Protects against Smoking-Induced Left Ventricular Remodeling via Attenuating Oxidative Stress, Apoptosis, and Inflammation

    OpenAIRE

    Zhou, Xiang; Li, Chao; Xu, Weiting; CHEN, JIANCHANG

    2012-01-01

    Trimetazidine, a piperazine derivative used as an anti-anginal agent, improves myocardial glucose utilization through inhibition of fatty acid metabolism. The present study was designed to investigate whether trimetazidine has the protective effects against smoking-induced left ventricular remodeling in rats. In this study, Wistar rats were randomly divided into 3 groups: smoking group (exposed to cigarette smoke), trimetazidine group (exposed to cigarette smoke and treated with trimetazidine...

  9. 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.

  10. 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...

  11. Carbon monoxide concentration in donated blood : relation to cigarette smoking and other sources

    OpenAIRE

    Åberg, Anna-Maja; Nilsson Sojka, Birgitta; Winsö, Ola; Abrahamsson, Pernilla; Johansson, Göran; Larsson, Jan Erik

    2009-01-01

    BACKGROUND: Carbon monoxide (CO) is normally present in the human body due to endogenous production of CO. CO can also be inhaled by exposure to external sources such as cigarette smoke, car exhaust, and fire. The purpose of this study was to investigate CO concentrations in blood from 410 blood donors at the blood center in Umea, Sweden. To further evaluate the effects of cigarette smoking on CO concentrations, the elimination time for CO was examined in six volunteer smokers after a smoked ...

  12. 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.

  13. Nicotine-specific and non-specific effects of cigarette smoking on endogenous opioid mechanisms.

    Science.gov (United States)

    Nuechterlein, Emily B; Ni, Lisong; Domino, Edward F; Zubieta, Jon-Kar

    2016-08-01

    This study investigates differences in μ-opioid receptor mediated neurotransmission in healthy controls and overnight-abstinent smokers, and potential effects of the OPRM1 A118G genotype. It also examines the effects of smoking denicotinized (DN) and average nicotine (N) cigarettes on the μ-opioid system. Positron emission tomography with (11)C-carfentanil was used to determine regional brain μ-opioid receptor (MOR) availability (non-displaceable binding potential, BPND) in a sample of 19 male smokers and 22 nonsmoking control subjects. Nonsmokers showed greater MOR BPND than overnight abstinent smokers in the basal ganglia and thalamus. BPND in the basal ganglia was negatively correlated with baseline craving levels and Fagerström scores. Interactions between group and genotype were seen in the nucleus accumbens bilaterally and the amygdala, with G-allele carriers demonstrating lower BPND in these regions, but only among smokers. After smoking the DN cigarette, smokers showed evidence of MOR activation in the thalamus and nucleus accumbens. No additional activation was observed after the N cigarette, with a mean effect of increases in MOR BPND (i.e., deactivation) with respect to the DN cigarette effects in the thalamus and left amygdala. Changes in MOR BPND were related to both Fagerström scores and changes in craving. This study showed that overnight-abstinent smokers have lower concentrations of available MORs than controls, an effect that was related to both craving and the severity of addiction. It also suggests that nicotine non-specific elements of the smoking experience have an important role in regulating MOR-mediated neurotransmission, and in turn modulating withdrawal-induced craving ratings. PMID:27095017

  14. 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.

  15. A-kinase-anchoring proteins coordinate inflammatory responses to cigarette smoke in airway smooth muscle.

    Science.gov (United States)

    Poppinga, Wilfred J; Heijink, Irene H; Holtzer, Laura J; Skroblin, Philipp; Klussmann, Enno; Halayko, Andrew J; Timens, Wim; Maarsingh, Harm; Schmidt, Martina

    2015-04-15

    β2-Agonist inhibitors can relieve chronic obstructive pulmonary disease (COPD) symptoms by stimulating cyclic AMP (cAMP) signaling. A-kinase-anchoring proteins (AKAPs) compartmentalize cAMP signaling by establishing protein complexes. We previously reported that the β2-agonist fenoterol, direct activation of protein kinase A (PKA), and exchange factor directly activated by cAMP decrease cigarette smoke extract (CSE)-induced release of neutrophil attractant interleukin-8 (IL-8) from human airway smooth muscle (ASM) cells. In the present study, we tested the role of AKAPs in CSE-induced IL-8 release from ASM cells and assessed the effect of CSE on the expression levels of different AKAPs. We also studied mRNA and protein expression of AKAPs in lung tissue from patients with COPD. Our data show that CSE exposure of ASM cells decreases AKAP5 and AKAP12, both capable of interacting with β2-adrenoceptors. In lung tissue of patients with COPD, mRNA levels of AKAP5 and AKAP12 were decreased compared with lung tissue from controls. Using immunohistochemistry, we detected less AKAP5 protein in ASM of patients with COPD Global Initiative for Chronic Obstructive Lung Disease (GOLD) stage II compared with control subjects. St-Ht31, which disrupts AKAP-PKA interactions, augmented CSE-induced IL-8 release from ASM cells and diminished its suppression by fenoterol, an effect mediated by disturbed ERK signaling. The modulatory role of AKAP-PKA interactions in the anti-inflammatory effects of fenoterol in ASM cells and the decrease in expression of AKAP5 and AKAP12 in response to cigarette smoke and in lungs of patients with COPD suggest that cigarette smoke-induced changes in AKAP5 and AKAP12 in patients with COPD may affect efficacy of pharmacotherapy. PMID:25637608

  16. 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

  17. 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

  18. 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

  19. 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...

  20. 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…

  1. 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

  2. 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.

  3. 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.

  4. 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.

  5. Selenium contents in tobacco and main stream cigarette smoke determined using neutron activation analysis

    International Nuclear Information System (INIS)

    In the domain of the essential trace elements, the role of selenium is extermely important. As one of the volatile elements is can be partly absorbed through the pulmonary system during smoking and transported to different organs of the body. Thus a knowledge of its concentration levels in various sorts of tobacco and in the smoke of commercial cigarettes, as well as in the same type of cigarettes from plants treated with selenium, is of interest for various research fields. The purpose of this contribution is to present reliable quantitative data on selenium contents in tobacco, soil, and main stream cigarette smoke, obtained by destructive neutron activation analysis

  6. Selenium contents in tobacco and main stream cigarette smoke determined using neutron activation analysis

    International Nuclear Information System (INIS)

    In the domain of the essential trace elements, the role of selenium is extremely important. As one of the volatile elements it can be partly absorbed through the pulmonary system during smoking and transported to different organs of the body. Thus a knowledge of its concentration levels in various sorts of tobacco and in the smoke of commercial cigarettes, as well as in the same type of cigarettes from plants treated with selenium, is of interest for various research fields. The purpose of this contribution is to present reliable quantitative data on selenium contents in tobacco, soil, and main stream cigarette smoke, obtained by destructive neutron activation analysis

  7. 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

  8. 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.

  9. 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

  10. 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.

  11. 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…

  12. 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...

  13. Cigarette smoking and health care professionals at Mayo Hospital, Lahore, Pakistan

    International Nuclear Information System (INIS)

    Objectives: To observe the frequency of cigarette smoking in doctors and paramedics and study various variables associated with it. Methods: An anonymous questionnaire was given to randomly selected 250 Doctors and 250 Paramedics at Mayo Hospital in 2009. Information about demographic characteristics, smoking status in family, number of cigarettes smoked per day, influence for starting smoking, reason for continuation of smoking and use of nicotine replacement therapy was obtained. Results: A total of 234 questionnaires from doctors and 207 from paramedics were received back (88.2% response rate). There were 280 males (163 Doctors; 117 Paramedics) and 161 females (71 Doctors; 90 Paramedics). Eighty seven (37.18%) Doctors and 74 (35.74%) Paramedics were smokers with 82 (50.31%) male doctors and 5 (7.04%) females. Similar results were obtained in Paramedics 72 (61.53%) males and 2 (2.22%) females. Of the smokers, majority started smoking between 11-20 years age with 39 (44.83%) Doctors and 48 (64.86%) Paramedics. Twenty three (26.44%) Doctors and 31 (41.89%) Paramedics smoked 11-20 cigarettes per day. Smoking was initiated due to the influence of friends by 48 (55.17%) Doctors and 56 (75.68%) Paramedics. Most smokers, 29 (33.33%) Doctors and 33 (44.59%) Paramedics found use of cigarette smoking as 'Relaxing'. Addiction was the main reason for difficulty in quitting cigarette smoking as reported by 33 (37.93%) Doctors and 31 (41.89%) Paramedics. Of the smokers, 61(70.11%) doctors and 50 (32.43%) paramedics had no intention to quit smoking in the next 6 months. Conclusion: A significant number of doctors and paramedics, especially males, in Pakistan smoke cigarettes, which requires proper attention. (author)

  14. Maternal cigarette smoking during pregnancy and life-course-persistent offending.

    Science.gov (United States)

    Piquero, Alex R; Gibson, Chris L; Tibbetts, Stephen G; Turner, Michael G; Katz, Solomon H

    2002-04-01

    Evidence exists documenting the relationship between maternal cigarette smoking and offspring criminal behavior. Although efforts to understand this relationship in a theoretical framework have only recently emerged, attempts made have been grounded in Moffitt's developmental taxonomy of antisocial behavior. Specifically, maternal cigarette smoking is generally viewed as a potential disruption in the offspring's neuropsychological development, which is subsequently associated with life-course-persistent offending. Using a birth cohort of 987 African Americans, the authors extend previous research by empirically assessing, prospectively, the link between maternal cigarette smoking and life-course-persistent offending while using different operationalizations of Moffitt's offending categorization. The authors' findings offer some support for the relationship between maternal cigarette smoking and life-course-persistent offending, which is dependent on how this concept is operationalized. PMID:12113165

  15. 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, ...

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

    International Nuclear Information System (INIS)

    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

  17. 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.

  18. Cigarette and waterpipe smoking among adolescents in Estonia: HBSC survey results, 1994–2006

    Directory of Open Access Journals (Sweden)

    Pärna Kersti

    2008-11-01

    Full Text Available Abstract Background Smoking is a major single cause of preventable morbidity and premature mortality. Tobacco use among adolescents is a significant public health problem as smoking behaviour is undeniably established in adolescence. While cigarette smoking among adolescents has been a significant public health problem for years, waterpipe smoking is considered to be a new global public health threat. The objectives of this study were to describe trends of cigarette smoking and the prevalence of waterpipe smoking and to study the association between cigarette and waterpipe smoking among adolescents in Estonia. Methods This study was based on a four-yearly HBSC survey of health behaviour among school-aged children conducted in 1994–2006 in Estonia. It was a school-based survey of a nationally representative sample using standardized methodology. The target group of the survey were 11-, 13-, and 15-year-old schoolchildren (N = 13826, 6656 boys and 7170 girls. Cigarette and waterpipe smoking was determined on a 4-stage scale: every day, at least once a week, less than once a week, not smoking. Logistic regression analysis was applied to examine gender- and age-specific smoking trends and to study the association between cigarette and waterpipe smoking. Results Prevalence of smoking was higher among boys than girls in all age groups during the whole study period. The prevalence of cigarette smoking increased in 1994–2002 and then slightly decreased in both genders. The increase in smoking was larger among girls. Among girls, daily smoking increased during the whole study period. Among 15-year-old schoolchildren one-third of the boys and one quarter of the girls were cigarette smokers, 21% of the boys and 12% of the girls were daily smokers in 2006. One fourth of the boys and one sixth of the girls were waterpipe smokers. A logistic regression analysis revealed a strong association between cigarette and waterpipe smoking among schoolchildren

  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. Glass fibers and vapor phase components of cigarette smoke as cofactors in experimental respiratory tract carcinogenesis

    Energy Technology Data Exchange (ETDEWEB)

    Feron, V.J.; Kuper, C.F.; Spit, B.J.; Reuzel, P.G.; Woutersen, R.A.

    1985-01-01

    Syrian golden hamsters were given intratracheal instillations of glass fibers with or without BP suspended in saline, once a fortnight for 52 weeks; the experiment was terminated at week 85. No tumors of the respiratory tract were observed in hamsters treated with glass fibers alone. There was no indication that glass fibers enhanced the development of respiratory tract tumors induced by BP. In another study Syrian golden hamsters were exposed to fresh air or to a mixture of 4 major vapor phase components of cigarette smoke, viz. isoprene (800----700 ppm), methyl chloride (1000----900 ppm), methyl nitrite (200----190 ppm) and acetaldehyde (1400----1200 ppm) for a period of at most 23 months. Some of the animals were also given repeated intratracheal instillations of BP or norharman in saline. Laryngeal tumors were found in 7/31 male and 6/32 female hamsters exposed only to the vapor mixture, whereas no laryngeal tumors occurred in controls. The tumor response of the larynx most probably has to be ascribed entirely to the action of acetaldehyde. Simultaneous treatment with norharman or BP did not affect the tumor response of the larynx. Acetaldehyde may occur in the vapor phase of cigarette smoke at levels up to 2000 ppm. Chronic inhalation exposure of rats to acetaldehyde at levels of 0 (controls), 750, 1500 or 3000----1000 ppm resulted in a high incidence of nasal carcinomas, both squamous cell carcinomas of the respiratory epithelium and adenocarcinomas of the olfactory epithelium. It was discussed that acetaldehyde may significantly contribute to the induction of bronchogenic cancer by cigarette smoke in man.

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

    OpenAIRE

    Trung Vu; Lin Jin; 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 aro...

  2. Impact of maternal cigarette smoke exposure on brain inflammation and oxidative stress in male mice offspring

    OpenAIRE

    Chan, Yik Lung; Saad, Sonia; Pollock, Carol; Oliver, Brian; Al-Odat, Ibrahim; Zaky, Amgad A.; Jones, Nicole; Chen, Hui

    2016-01-01

    Maternal cigarette smoke exposure (SE) during gestation can cause lifelong adverse effects in the offspring’s brain. Several factors may contribute including inflammation, oxidative stress and hypoxia, whose changes in the developing brain are unknown. Female Balb/c mice were exposed to cigarette smoke prior to mating, during gestation and lactation. Male offspring were studied at postnatal day (P) 1, P20 and 13 weeks (W13). SE dams had reduced inflammatory mediators (IL-1β, IL-6 and toll lik...

  3. REINFORCING EFFECTS OF NICOTINE AND NON-NICOTINE COMPONENTS OF CIGARETTE SMOKE

    OpenAIRE

    Rose, Jed E.; Salley, Al; Behm, Frederique M.; Bates, James E.; Westman, Eric C

    2010-01-01

    We assessed the reinforcing effects of nicotine and non-nicotine components of cigarette smoke, by presenting a concurrent choice paradigm in which participants had access to intravenous (IV) nicotine infusions vs. saline (placebo) infusions and puffs from denicotinized (“denic”) cigarettes vs. air (sham puffs). We also measured the effects on self-administration of prior satiation with each component. Sixteen smokers participated in 7 sessions, consisting of: 1) a baseline smoking assessment...

  4. 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...

  5. 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...

  6. Effect of Graphic Cigarette Warnings on Smoking Intentions in Young Adults

    OpenAIRE

    Blanton, Hart; Snyder, Leslie B.; Strauts, Erin; Larson, Joy G.

    2014-01-01

    Introduction Graphic warnings (GWs) on cigarette packs are widely used internationally and perhaps will be in the US but their impact is not well understood. This study tested support for competing hypotheses in different subgroups of young adults defined by their history of cigarette smoking and individual difference variables (e.g., psychological reactance). One hypothesis predicted adaptive responding (GWs would lower smoking-related intentions) and another predicted defensive responding (...

  7. Cigarette smoke extract induces COX-2 expression via a PKCalpha/c-Src/EGFR, PDGFR/PI3K/Akt/NF-kappaB pathway and p300 in tracheal smooth muscle cells.

    Science.gov (United States)

    Yang, Chuen-Mao; Lee, I-Ta; Lin, Chih-Chung; Yang, Ya-Lin; Luo, Shue-Fen; Kou, Yu Ru; Hsiao, Li-Der

    2009-11-01

    Exposure to cigarette smoke extract (CSE) leads to airway or lung inflammation, which may be mediated through cyclooxygenase-2 (COX-2) expression and its product prostaglandin E2 (PGE2) synthesis. The aim of this study was to investigate the molecular mechanisms underlying CSE-induced COX-2 expression in human tracheal smooth muscle cells (HTSMCs). Here, we describe that COX-2 induction is dependent on PKCalpha/c-Src/EGFR, PDGFR/PI3K/Akt/NF-kappaB signaling in HTSMCs. CSE stimulated the phosphorylation of c-Src, EGFR, PDGFR, and Akt, which were inhibited by pretreatment with the inhibitor of PKCalpha (Gö6976 or Gö6983), c-Src (PP1), EGFR (AG1478), PDGFR (AG1296), or PI3K (LY294002). Moreover, CSE induced a significant increase in COX-2 expression, which was reduced by pretreatment with these inhibitors or transfection with siRNA of PKCalpha, Src, or Akt. Furthermore, CSE-stimulated NF-kappaB p65 phosphorylation and translocation were also attenuated by pretreatment with Gö6976, PP1, AG1478, AG1296, or LY294002. CSE-induced COX-2 expression was also mediated through the recruitment of p300 associated with NF-kappaB in HTSMCs, revealed by coimmunoprecipitation and Western blot analysis. In addition, pretreatment with the inhibitors of NF-kappaB (helenalin) and p300 (garcinol) or transfection with p65 siRNA and p300 siRNA markedly inhibited CSE-regulated COX-2 expression. However, CSE-induced PGE2 generation was reduced by pretreatment with the inhibitor of COX-2 (NS-398). These results demonstrated that in HTSMCs, CSE-induced COX-2-dependent PGE2 generation was mediated through PKCalpha/c-Src/EGFR, PDGFR/PI3K/Akt leading to the recruitment of p300 with NF-kappaB complex. PMID:19717552

  8. 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.

  9. 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

  10. Properties of radioactive aerosols produced by interactions of indoor radon decay products with cigarette smoke and burning cigarettes

    International Nuclear Information System (INIS)

    Risks of lung cancer to smokers, attributable in part to exposure to indoor radon decay products, are dependent on properties of radon progeny-tagged smoke particles. The authors have investigated the properties and interactions of radon progeny-tagged smoke particles as they pass through burning cigarettes into mainstream smoke, using /sup 212/Pb-tagged smoke particles as tracers, cascade impactors for particle size determinations, and low-level β/sup -/ counting techniques. /sup 212/Pb-tagged particles of submicron size are destroyed in the burning zone of cigarettes. However, /sup 212/Pb-tagged smoke particles exceeding 1.0 μm diameter pass readily through the burning zone and tobacco rod into mainstream smoke. /sup 212/ Pb- tagged particles in mainstream smoke have an activity median aerodynamic diameter between 1.0 and 2.0 μm diameter. Particles > 2.0 μm diameter carry about 10 percent of the total activity, are selectively deposited at the carina of bifurcations, and are resistant to dissolution in lung fluid. These results indicate that indoor radon progeny on large particles in mainstream smoke can contribute substantially to the cumulative alpha radiation dose at ''hot spots'' in the bronchi of smokers

  11. Chronic respiratory effect of narguileh smoking compared with cigarette smoking in women from the East Mediterranean region

    Directory of Open Access Journals (Sweden)

    Yousser Mohammad

    2008-10-01

    Full Text Available Yousser Mohammad, Mouna Kakah, Yasser MohammadDepartment of Internal Medicine, Tishreen University School of Medicine, Lattakia, SyriaAbstract: Narguileh is a water pipe. Narguileh smoking is a traditional pattern of smoking among Eastern Mediterranean women, publicly considered as a harmless entertainment. We performed a survey aimed at tracking chronic respiratory symptoms and alteration in respiratory functions in 77 female narguileh smokers, 77 cigarette smokers, and controls. A questionnaire about respiratory symptoms, quantity, and duration of smoking was completed by each woman, and a flow-volume loop was performed with all women. Women were then categorized in subgroups according to a cumulative smoking duration of over 5 years, and cumulative quantity of 50 kilograms smoked. We obtained 8 subgroups for quantity and 10 for duration. Results showed a higher proportion of chronic bronchitis in narguileh smokers compared with cigarette smokers for both quantity and duration (p value < 0.001, as well as quasi-permanent alteration in maximum mid-expiratory flow (MMEF 25%–75% in narguileh smokers compared with cigarette smokers (p value < 0.001. Forced expired volume in one second was more altered in cigarette smokers than in narguileh smokers (p value > 0.001. These results will help to raise health authority awareness that narguileh smoking is also dangerous for women.Keywords: sheesha, narguileh, narguile, COPD, MMEF, smoking in women

  12. Polonium-210 concentration of cigarettes traded in Cuba and their estimated dose contribution due to smoking

    International Nuclear Information System (INIS)

    Cigarette smoking is one of the pathways that might contribute significantly to the increase in the radiation dose reaching man, due to the relatively large concentrations of polonium-210 found in tobacco leaves. The results of 200Po determination on the 11 most frequently smoked brands of cigarettes and cigars which constitute over 75% of the total cigarette consumption in Cuba are presented and discussed. Moreover, the polonium content in cigarette smoke was estimated on the basis of its activity in cigarettes, ash, fresh filters and post-smoking filters. 210Po was determined by gas flow proportional detector after spontaneous deposition of 210Po on a high copper-content disk. The annual committed equivalent dose for lungs and the annual effective dose for smokers between 12-17 years old and for adults were calculated on the basis of the 210Po inhalation through cigarette smoke. The results showed concentration ranging from 9.3 to 14.4 mBq per cigarette with a mean value of 11.8 ± 0.6 mBq.Cig-1. the results of this work indicate that Cuban smokers who smoke one pack (20 cigarettes) per day inhale from 62 to 98 mBq.d-1 of 210Po and smokers between 12-17 years old who consume 10 cigarettes daily inhale from 30-50 mBq.d-1. The average committed equivalent dose for lungs is estimated to be 466 ± 36 and 780 ± 60 μSv.year-1 for young and adult smokers, respectively and annual committed effective dose is calculated to be 60 ± 5 and 100 ± 8 μSv for these two groups of smokers, respectively. (Author)

  13. Prevalence and determinants of cigarette smoking among adolescents in Blantyre City, Malawi.

    Science.gov (United States)

    Muula, A S

    2007-01-01

    Tobacco smoking is a major risk factor for non-communicable diseases such as ischaemic heart disease, stroke, chronic obstructive airways disease and several cancers. There is little data about the prevalence and determinants of smoking among adolescents in southern Africa. This study aimed to determine the prevalence and determinants of cigarette smoking among adolescents in Blantyre City, Malawi. Cross-sectional data were obtained from school-going adolescents in Blantyre in 2001 using the Global Youth Tobacco Survey data collection instrument. Data were analysed to determine prevalence of current and ever cigarette smoking, and predictors of smoking. The prevalence of current smoking and ever smoking were 3.0% and 15.6%, respectively. Predictors of current tobacco smoking included male gender, having friends or parents who smoked, having been exposed to advertisements about tobacco brands on television and having seen a lot of advertisements in newspapers and magazines. School programmes that included being taught about smoking in class and a class discussion on the dangers of tobacco were not associated with reduced current smoking. Intervention programmes aiming to curb tobacco smoking among adolescents should focus on dealing also with parental smoking, peer influence and pay special attention toward male gender. School-based programmes to prevent smoking should be evaluated as some may have little impact in influencing current smoking status. PMID:17547101

  14. 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.

  15. 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…

  16. 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

  17. 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

  18. Effect of Cigarette Smoke on Wound Healing of the Septal Mucosa of the Rat.

    Science.gov (United States)

    Trombitas, Veronica; Nagy, Alina; Berce, Cristian; Tabaran, Flaviu; Albu, Silviu

    2016-01-01

    Objectives/Hypothesis. Proper wound healing following endoscopic sinus surgery (ESS) is influenced by several factors, like cigarette smoke (CS) exposure. This study aims to assess the influence of cigarette smoke on the healing of induced septal mucosal lesion in rats. Methods. Unilateral nasal wounds were created by means of the interdental brush in seventy-four-week-old male rats. Animals were randomly divided into two groups: control group and CS exposure group, each comprising 35 animals, divided into five groups (n = 7). Animals were sacrificed in groups of seven on day 2 and then on days 5, 14, and 28 and finally on day 42 following wound induction. Results. Histological analysis of mucosal specimens shows important changes at the CS exposure group. Starting with the infiltrates of neutrophils, eosinophils, macrophages, and lymphocytes, the histological changes were continued with the Goblet cell proliferation, ciliated cells loss, fibrosis, and epithelial and subepithelial hypertrophy. Conclusion. In this experimental model of nasal wound healing we demonstrated the deleterious effects of chronic CS exposure. The adverse effects of CS exposure are firstly a postponement of the healing process and secondly the persistence of inflammation which becomes chronic. PMID:27042668

  19. 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...

  20. 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...

  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. 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.

  3. Secondhand cigarette smoke as a cause of chronic carbon monoxide poisoning

    Energy Technology Data Exchange (ETDEWEB)

    Kachulis, C.J.

    1981-07-01

    Symptoms of carbon monoxide poisoning in a nonsmoking patient continued for several years until her husband stopped smoking cigarettes near her. Carbon monoxide poisoning should be considered in non-smokers when characteristic toxic symptoms occur (ie, lethargy, irritability, headache, blurred vision, slowed reaction time, and decreased concentration). Toxicity may develop simply from breathing second-hand smoke.

  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. PMID:27288488

  5. Sodium pertechnetate (Na99mTcO4) biodistribution in mice exposed to cigarette smoke

    International Nuclear Information System (INIS)

    The biological effects of cigarette smoke are not fully known. To improve our understanding of the action of various chemical agents, we investigated the biodistribution of sodium pertechnetate (Na99mTcO4) in mice exposed to cigarette smoke. Fifteen BALB/c male mice were exposed to the smoke of nine whole commercial cigarettes per day, 3 times/day, for up to 10 days to whole body exposure in a chamber. A control group of 5 BALB/c male mice was sham-smoked. One day later, the exposed and control groups of mice received (7.4 MBq/0.3 ml) of Na99mTcO4 before being killed at 30 min. Bones, brain, heart, intestine, kidney, liver, lungs, muscle, pancreas, spleen, stomach, testis and thyroid were weighed and these organs and blood radioactivity recorded with a gamma counter. The percentage per gram of tissue of injected dose (%ID/g) was determined for each organ. Cigarette smoke significantly decreased (p < 0.05) the %ID/g in red blood cells, bone, kidney, lung, spleen, stomach, testis and thyroid of the exposed mice. The toxic effects of cigarette smoke reduced the Na99mTcO4 biodistribution

  6. Effect of cigarette smoking on the detection of small radiographic opacities in inorganic dust diseases

    International Nuclear Information System (INIS)

    Whether cigarette smoking can cause radiographic opacities indistinguishable from those due to pneumoconiosis remains controversial. The situation becomes clearer when one limits the abnormalities to those that can be standardized under the International Labour Office (ILO) classification system. The bulk of the evidence indicates that, using the ILO system, cigarette smoking alone is not associated with radiographic opacities that would be mistaken for pneumoconiosis with sufficient frequency to be of any practical importance. The effects of cigarette smoking, as a cofactor, in conjunction with occupational dust exposure depend on the type of dust. No relationship has been convincingly demonstrated for coal dust or silica. Only with asbestos exposure does there appear to be a significant cigarette smoking-associated increase in the frequency of irregular radiographic opacities. This increase does not appear to translate into a restrictive impairment in pulmonary function. The limited information available indicates that the features of asbestosis on high-resolution computed tomography are not similarly related to cigarette smoking. Additional research is needed to substantiate the relationship between smoking and occupational exposure to dust of many types, and also the possible imaging and pathophysiologic significance of their interactions. 47 references

  7. 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.

  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. 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.

  10. 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.

  11. Laboratory Validation of Inertial Body Sensors to Detect Cigarette Smoking Arm Movements

    Directory of Open Access Journals (Sweden)

    Bethany R. Raiff

    2014-02-01

    Full Text Available Cigarette smoking remains the leading cause of preventable death in the United States. Traditional in-clinic cessation interventions may fail to intervene and interrupt the rapid progression to relapse that typically occurs following a quit attempt. The ability to detect actual smoking behavior in real-time is a measurement challenge for health behavior research and intervention. The successful detection of real-time smoking through mobile health (mHealth methodology has substantial implications for developing highly efficacious treatment interventions. The current study was aimed at further developing and testing the ability of inertial sensors to detect cigarette smoking arm movements among smokers. The current study involved four smokers who smoked six cigarettes each in a laboratory-based assessment. Participants were outfitted with four inertial body movement sensors on the arms, which were used to detect smoking events at two levels: the puff level and the cigarette level. Two different algorithms (Support Vector Machines (SVM and Edge-Detection based learning were trained to detect the features of arm movement sequences transmitted by the sensors that corresponded with each level. The results showed that performance of the SVM algorithm at the cigarette level exceeded detection at the individual puff level, with low rates of false positive puff detection. The current study is the second in a line of programmatic research demonstrating the proof-of-concept for sensor-based tracking of smoking, based on movements of the arm and wrist. This study demonstrates efficacy in a real-world clinical inpatient setting and is the first to provide a detection rate against direct observation, enabling calculation of true and false positive rates. The study results indicate that the approach performs very well with some participants, whereas some challenges remain with participants who generate more frequent non-smoking movements near the face. Future

  12. 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

  13. 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

  14. 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...

  15. 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...

  16. 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...

  17. 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...

  18. 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...

  19. Compliance of anti-smoking regulations by cigarette industry in Pakistan

    International Nuclear Information System (INIS)

    Background: The hazards of cigarette smoking and its increasing consumption are well known despite the ongoing tussle between the tobacco industry and global governments. To curb the menace of smoking, anti-smoking laws have been enforced from time to time by various governments. In 2003, Ministry of Health (MoH) Government of Pakistan has imposed certain regulations on cigarette manufacturing industry. The aim of this study was to highlight the compliance of the industry with these regulations. Methods: A cross-sectional study of major cigarette selling shops was conducted in Abbottabad. It was aimed at determining the availability of total cigarette brands and their compliance with the regulations and also to find out attributes of cigarette customers. Results: A total of 39 varieties of 18 cigarette brands are available in Abbottabad city, out of which 71.8% are imported varieties. A total of 38.4% varieties have displayed health warnings (28.2% pictorial health warning, 10.2% have written health warning. Majority of cigarette customers are between 20-40 years of age, while 5.6% customers include youngsters between 10-20 years of age. Female customers, accounting for 8% of total cigarette customers, buy only those brands which have not displayed the health warning. Conclusions: Observed compliance with governmental regulation for displaying health warning is 39% which is far less than desired. Sale of cigarette to children is also practiced. Ministry of Health (MoH) should assure the display of these warnings on all the brands so that smokers must be fully aware about the risk involved in smoking. (author)

  20. 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.

  1. 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

    2016-01-01

    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 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. PMID:26959042

  2. 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.

  3. 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.

  4. 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

  5. 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

  6. 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

  7. 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

  8. 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.

  9. 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.

  10. 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

  11. 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

  12. Cadmium, lead, and thallium in smoke particulate from counterfeit cigarettes compared to authentic US brands.

    Science.gov (United States)

    Pappas, R S; Polzin, G M; Watson, C H; Ashley, D L

    2007-02-01

    Smoking remains the leading cause of preventable disease in the United States. Exposure to tobacco smoke leads to cancer, heart and lung disease, and addiction. The origin of the tobacco and cigarette manufacturing practices of counterfeit cigarettes are unknown. Because toxic metals are incorporated into the tobacco lamina during cultivation, the ambient metal content of the soil could produce significant differences in metal levels in both the tobacco and smoke of counterfeit cigarettes. We compared mainstream smoke cadmium, thallium, and lead deliveries from counterfeit and authentic brands. Mainstream smoke levels of all three metals were far greater for counterfeit than the authentic brands, in some cases by an order of magnitude. Significant differences still existed even after normalizing mainstream smoke metal levels with nicotine delivery; the counterfeits typically delivered much higher levels of all three analytes. Our findings, based on 21 different counterfeit samples, suggest that counterfeit cigarettes potentially result in a markedly greater exposure to toxic heavy metals than authentic brands, even after correcting for differences in nicotine intake. In view of the unknown health risks associated with inhaling higher levels of toxic metals, it is prudent to minimize exposure to toxic substances whenever possible. PMID:17011104

  13. 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

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

    OpenAIRE

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

    2005-01-01

    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 fr...

  15. 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.

  16. 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

  17. The effect of cigarette smoke on the metabolism of arachidonic acid in isolated hamster lungs

    International Nuclear Information System (INIS)

    The effects of cigarette smoke on the metabolism of exogenous arachidonic acid (AA) were investigated in isolated hamster lungs. Arachidonate was injected into the pulmonary circulation and the metabolites were analysed from the nonrecirculating perfusion effluent by thin layer chromatography. After the pulmonary injection of 66 nmol of 14C-AA about 20% of the injected radioactivity appeared in the perfusion effluent mostly as metabolites in six minutes. When isolated lungs were ventilated with cigarette smoke during the perfusion, the amounts of PGF2 alpha, PGE2 and two unidentified metabolite groups increased in the lung effluent. In two other experimental series hamsters were exposed to cigarette smoke before the lung perfusion either once for 30 min or during one hour daily for ten consecutive days. Neither pre-exposures caused any changes in the amounts of arachidonate metabolites in the lung effluent

  18. Characterization of Indian cigarette tobacco and its smoke aerosol by nuclear and allied techniques

    International Nuclear Information System (INIS)

    Forty brands of tobacco used in Indian cigarettes, 20 brands of bidis (tobacco rolled in wrapper leaves), 15 brands of chewing tobacco and 15 brands of snuff tobacco were analyzed by nuclear and allied techniques. The elements measured into tobacco can be grouped into seven categories from less than 1 ppm to 5% by weight. Concentration level varied from 0.5-5% for (Ca, K, Cl), 400-1500 ppm (Fe), 200-600 ppm (Na), 100-300 ppm (Ti, Mn, Br and Sr), 10-100 ppm (Cu, Zn and Rb), 1-10 ppm (Cr, Ni, Pb and La) and less than 1 ppm (As, Co, Cd, Sb, Hg and Eu). Among the above elements Cr, Ni, As, Cd, Pb, Hg and Sb are considered toxic. The percentage transfer of the elements from cigarette tobacco to smoke particles during smoking was also estimated using a smoking machine and collecting the smoke particles on a filter paper. The results show that Br, Cr, Sb and Zn have high percentage transfer from tobacco to its smoke of the order of 2-15%. Out of these Sb has the highest 15%. Cobalt, Fe and Sc have lowest percentage of transfer of the order of less than 1%. The percent transfer of these elements from tobacco to tobacco smoke is higher in case of bidis (1.5-3.0 times) as compared to cigarettes. In cigarettes also non-filter cigarettes have higher transfer (2-3 times) as compared to filter tip cigarettes. (author)

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

    Directory of Open Access Journals (Sweden)

    Dauphinee Amanda L

    2013-02-01

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

  20. 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

  1. 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

    (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 was...

  2. 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.

  3. 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-...

  4. The Cigarette Smoke Carcinogen Benzo[a]pyrene Enhances Human Papillomavirus Synthesis▿

    OpenAIRE

    Alam, Samina; Conway, Michael J; Chen, Horng-Shen; Meyers, Craig

    2007-01-01

    Epidemiological studies suggest that cigarette smoke carcinogens are cofactors which synergize with human papillomavirus (HPV) to increase the risk of cervical cancer progression. Benzo[a]pyrene (BaP), a major carcinogen in cigarette smoke, is detected in the cervical mucus and may interact with HPV. Exposure of cervical cells to high concentrations of BaP resulted in a 10-fold increase in HPV type 31 (HPV31) viral titers, whereas treatment with low concentrations of BaP resulted in an increa...

  5. 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...

  6. 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%...

  7. DRD2/ANKK1 TaqI polymorphism and smoking behavior of Egyptian male cigarette smokers.

    Science.gov (United States)

    Radwan, Ghada N; El-Setouhy, Maged; Mohamed, Mostafa K; Hamid, Mohamed Abdel; Azem, Salwa Abdel; Kamel, Omima; Israel, Ebenezer; Loffredo, Christopher A

    2007-12-01

    Little is known about the genetic contribution to cigarette smoking and nicotine addiction in Egypt. The dopamine D2 receptor gene contains a TaqI repeat fragment length polymorphism creating two alleles with functional significance, DRD2*A1 and DRD2*A2. We investigated the relationship between these alleles and tobacco use in a study of 389 Egyptian male current smokers (mean age = 40 years; SD = 12). Participants were interviewed in 2004 on their smoking behaviors and quit attempts, and were given the Fagerström Test for Nicotine Dependence (FTND). Blood samples were obtained and genotyped for DRD2 A1and A2 alleles. The frequencies of A1/A2, A1/A2, and A2/A2 genotypes were 6%, 29%, and 65%, respectively. We found no statistically significant association between genotype and age at onset of smoking, years of smoking, FTND score, or average number of cigarettes smoked per day. DRD2 genotype was associated with the number of cigarettes smoked in the past 48 hr (42.2 in A1 carriers vs. 37.6 in A2, p = .03), the previous quit duration (28% in A1 vs. 40% in A2 quit for more than 1 month, p = .05), and the depth of inhalation (82% in A1 vs. 72% in A2 inhaled the smoke deeply, p = .03). Logistic regression analysis including DRD2 genotype, FTND score, age at smoking initiation, marital status, and education as predictors showed that maximum duration of quit time was associated with FTND score (p = .003), DRD2 genotype (p = .01), marital status (p = .03), and age at smoking initiation (p = .04). These findings suggest a modest association between DRD2 genotype and quitting behavior in male cigarette smokers in Egypt. PMID:18058350

  8. 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.

  9. 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...

  10. 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...

  11. 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, 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.

  12. 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,” ...

  13. 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 ...

  14. Sociocultural factors associated with cigarette smoking among women in Brazilian worksites: a qualitative study.

    Science.gov (United States)

    Scarinci, Isabel C; Silveira, Andréa F; dos Santos, Daniele Figueiredo; Beech, Bettina M

    2007-06-01

    This study examined the contextual factors associated with smoking initiation and cessation among women in Brazilian worksites (Curitiba, Paraná, Brazil). A total of 22 focus groups were conducted among 108 women in private and public worksites. The most frequently endorsed negative factors that contributed to smoking initiation included exposure to smoking-prompting behaviors through family members, peer pressure, media and easy access/low cost of cigarettes. Positive factors that served as protective mechanisms against initiation included smoking-related health effects and strong influence from parents and family members. The most salient negative factors associated with smoking cessation included stress/anxiety-relieving benefits, weight control, access/low cost of cigarettes, being around smokers and risk-exempting beliefs. Positive factors included smoking restrictions at home and workplace and concerns about appearance. Current and former smokers reported that they had never received any assistance from their physicians to quit smoking, nor did they rely on smoking cessation programs or aids or believe in their effectiveness. There are specific contextual factors that contribute to smoking initiation/cessation among women in Brazilian worksites which have important clinical, research and policy implications. PMID:17491118

  15. Cigarette smoking and risk of osteoarthritis in women in the general population: the Chingford study.

    OpenAIRE

    Hart, D.J.; Spector, T D

    1993-01-01

    Previous studies have suggested that smoking might be protective against the development of osteoarthritis (OA) of the knee. A group of 1003 women aged 45-64 years (mean 54.2 years) from the Chingford general population survey were studied to examine the effect of cigarette smoking on the prevalence of radiologically confirmed OA at different sites. Standard anteroposterior radiographs of the hand and knee were available in 985 women. Disease classification was made on the basis of radiologic...

  16. 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...

  17. 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...

  18. 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...

  19. Public Smoking Bans, Youth Access Laws, and Cigarette Sales at Vending Machines

    OpenAIRE

    Kvasnicka, Michael

    2010-01-01

    Tobacco control policies have proliferated in many countries in recent years, in particular youth access laws and public smoking bans. The effectiveness of youth access laws is still disputed, however, as are the costs of public smoking bans to the hospitality industry. Using a unique data set on cigarette sales at more than 100k vending machines that provides first objective evidence on the outgoing and customer behavior of smokers, we study both outcome dimensions by investigating several r...

  20. Cigarette smoking and risk of gestational diabetes: a systematic review of observational studies

    OpenAIRE

    Belizán José M; Duncan Bruce B; Pinto Maria; Wendland Eliana M; Schmidt Maria

    2008-01-01

    Abstract Background Gestational diabetes is a prevalent disease associated with adverse outcomes of pregnancy. Smoking as been associated with glucose intolerance during pregnancy in some but not all studies. Therefore, we aimed to systematically review all epidemiological evidence to examine the association between cigarette smoking during pregnancy and risk of developing gestational diabetes mellitus. Methods We conducted a systematic review of articles published up to 2007, using PubMed, E...

  1. 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...

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

    Science.gov (United States)

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

    2010-01-01

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

  3. The effects of cigarette smoke on some hematological parameters in human

    International Nuclear Information System (INIS)

    The effects of cigarette smoke on Red Blood Cells (RBCs) membrane were studied. Spontaneous hemolysis test indicated that RBCs which were separated from heavier smokers' blood (more than 20 cigarettes/day) have higher percentage of hemolysis when compared to those separated from nonsmokers blood (15±0.7%, 1.8±0.2%, respectively ). The results of osmotic fragility test for the above RBCs from both volunteers indicate, a slight shift to the left (MCF(50%)=4.4±0.05, 4.55±0.06g/l, respectively), this illustrate that the resistance to lysis was increased (the volume to the surface area ratio was decreased). In the analysis of phospho lipid's composition of RBCs, we observed that the percentage of diphosphoglyceride(DPG) and lysophosphatidylcholine (LPC) to the total phospholipids were increased for cigarette smokers. Also results obtained from measuring the superoxide radicals in smoker's blood have high optical density than that for nonsmokers, also for conjugated dienes. our results indicate that the cigarette smoke has many effects on RBCs specially on their membranes and phospho lipid's compost ion, and theses effects may be due to cigarette smoke contents and free radicals. (author). 35 refs., 4 figs

  4. Cigarette prices and smoking prevalence after a tobacco tax increase--Turkey, 2008 and 2012.

    Science.gov (United States)

    Kostova, Deliana; Andes, Linda; Erguder, Toker; Yurekli, Ayda; Keskinkılıç, Bekir; Polat, Sertaç; Culha, Gönül; Kilinç, Evin Aras; Taştı, Enver; Erşahin, Yılmaz; Ozmen, Mehmet; San, Ramazan; Ozcebe, Hilal; Bilir, Nazmi; Asma, Samira

    2014-05-30

    Raising the price of tobacco products has been shown to reduce tobacco consumption in the United States and other high-income countries, and evidence of this impact has been growing for low- and middle-income countries as well. Turkey is a middle-income country surveyed by the Global Adult Tobacco Survey (GATS) twice in a 4-year period, in 2008 and 2012. During this time, the country introduced a policy raising its Special Consumption Tax on Tobacco and implemented a comprehensive tobacco control program banning smoking in public places, banning advertising, and introducing graphic health warnings. The higher tobacco tax took effect in early 2010, allowing sufficient time for subsequent changes in prices and smoking to be observed by the time of the 2012 GATS. This report uses data from GATS Turkey to examine how cigarette prices changed after the 2010 tax increase, describe the temporally associated changes in smoking prevalence, and learn whether this smoking prevalence changed more in some demographic groups than others. From 2008 to 2012, the average price paid for cigarettes increased by 42.1%, cigarettes became less affordable, and smoking prevalence decreased by 14.6%. The largest reduction in smoking was observed among persons with lower socioeconomic status (SES), highlighting the potential role of tax policy in reducing health disparities across socioeconomic groups. PMID:24871250

  5. 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

  6. 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...

  7. Carbonyl compounds in gas and particle phases of mainstream cigarette smoke

    International Nuclear Information System (INIS)

    Carbonyl compounds (carbonyls) are important constituents of cigarette smoke and some are toxic and may be carcinogenic or mutagenic to humans. In this study carbonyl emissions in the gas and particle phases of mainstream cigarette smoke were assessed by GC-MS with pentafluorophenyl hydrazine (PFPH) derivatization. Seven brands of cigarettes and one brand of cigar common in the UK market and having differing nicotine, tar and carbon monoxide yields were investigated. Sixteen carbonyl components were identified in gaseous emissions and twenty in the particle phase. In the gaseous emissions, acetaldehyde presented as the predominant species, followed by formaldehyde, 2-propenal, and pentanal. In the particulate emissions, 1-hydroxy-2-propanone was the most abundant followed by formaldehyde, benzaldehyde, and 2,5-dimethylbenzaldehyde. Significant differences were found in carbonyl emissions among the brands of cigarettes. The gaseous carbonyl emissions varied in the range of 216-405 μg cigarette-1 (μg cig-1) and the particulate carbonyl emissions varied in the range of 23-127 μg cig-1. Positive correlations were found between the total emission of carbonyls, tar yield and carbon monoxide yield. Similar gas/particle (G/P) partitioning ratios of carbonyls were found among all cigarettes, which implies that G/P partitions of carbonyls in smoke mainly depend on the physical properties of the carbonyls. The gaseous carbonyl emissions were enhanced by 40% to 130% when some of the water, accounting for 8-12% of cigarettes in mass, was removed from the tobacco. Non-filtered cigarettes showed significantly higher carbonyl emissions compared to their filtered equivalents. Carbonyl particulate accounted for 11-19% by mass of total particulate matter from tobacco smoke. The cigar generated 806 μg cig-1 gaseous and 141 μg cig-1 particulate carbonyls, which is 2-4 times greater than the cigarettes. - Highlights: → Carbonyl emission factors in both gas (16 species) and

  8. Carbonyl compounds in gas and particle phases of mainstream cigarette smoke

    Energy Technology Data Exchange (ETDEWEB)

    Pang, Xiaobing, E-mail: pangxbyuanj@gmail.com [Department of Chemistry, University of York, Heslington, York, YO10 5DD (United Kingdom); Lewis, Alastair C., E-mail: ally.lewis@york.ac.uk [National Centre for Atmospheric Science, University of York, Heslington, York, YO10 5DD (United Kingdom)

    2011-11-01

    Carbonyl compounds (carbonyls) are important constituents of cigarette smoke and some are toxic and may be carcinogenic or mutagenic to humans. In this study carbonyl emissions in the gas and particle phases of mainstream cigarette smoke were assessed by GC-MS with pentafluorophenyl hydrazine (PFPH) derivatization. Seven brands of cigarettes and one brand of cigar common in the UK market and having differing nicotine, tar and carbon monoxide yields were investigated. Sixteen carbonyl components were identified in gaseous emissions and twenty in the particle phase. In the gaseous emissions, acetaldehyde presented as the predominant species, followed by formaldehyde, 2-propenal, and pentanal. In the particulate emissions, 1-hydroxy-2-propanone was the most abundant followed by formaldehyde, benzaldehyde, and 2,5-dimethylbenzaldehyde. Significant differences were found in carbonyl emissions among the brands of cigarettes. The gaseous carbonyl emissions varied in the range of 216-405 {mu}g cigarette{sup -1} ({mu}g cig{sup -1}) and the particulate carbonyl emissions varied in the range of 23-127 {mu}g cig{sup -1}. Positive correlations were found between the total emission of carbonyls, tar yield and carbon monoxide yield. Similar gas/particle (G/P) partitioning ratios of carbonyls were found among all cigarettes, which implies that G/P partitions of carbonyls in smoke mainly depend on the physical properties of the carbonyls. The gaseous carbonyl emissions were enhanced by 40% to 130% when some of the water, accounting for 8-12% of cigarettes in mass, was removed from the tobacco. Non-filtered cigarettes showed significantly higher carbonyl emissions compared to their filtered equivalents. Carbonyl particulate accounted for 11-19% by mass of total particulate matter from tobacco smoke. The cigar generated 806 {mu}g cig{sup -1} gaseous and 141 {mu}g cig{sup -1} particulate carbonyls, which is 2-4 times greater than the cigarettes. - Highlights: {yields} Carbonyl

  9. 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

  10. 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

  11. 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...

  12. 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…

  13. 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...

  14. 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…

  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. The endocrine effects of nicotine and cigarette smoke

    OpenAIRE

    Tweed, Jesse Oliver; Hsia, Stanley H.; Lutfy, Kabirullah; Friedman, Theodore C.

    2012-01-01

    With a current prevalence of approximately 20%, smoking continues to impact negatively upon health. Tobacco or nicotine use influences the endocrine system, with important clinical implications. In this review we critically evaluate the literature concerning the impact of nicotine as well as tobacco use on several parameters of the endocrine system and on glucose and lipid homeostasis. Emphasis is on the effect of smoking on diabetes mellitus and obesity and the consequences of smoking cessat...

  17. 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 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 estimate the prevalence of smoking. We also assessed whether being exposed to anti-smoking media, education and having discussed with family members on the harmful effects of smoking were associated with smoking. Logistic regression analysis was used to assess these associations. Current smoking was defined as having reported smoking cigarettes, even a single puff, in the last 30 days preceding the survey (main outcome. Results Altogether 1563 adolescents participated in the survey. However, 1122 had data on the main outcome. Altogether, 15.8% of the respondents reported having smoked cigarettes (10.3% among males, and 11.1% among females. Factors that were associated with reported non-smoking were: discussing harmful effects of smoking cigarettes with their family members (OR = 0.61, 95% CI 0.52, 0.71; being taught that smoking makes teeth yellow, causes wrinkles and smokers smell badly (OR = 0.62, 95% CI 0.52, 0.74; being taught that people of the respondent's age do not smoke (OR = 0.81, 95% CI 0.69, 0.95; and having reported that religious organizations discouraged young people smoking (OR = 0.70, 95% CI 0.60, 0.82. However, exposure to a lot many antismoking messages at social gatherings was associated with smoking. Exposure to antismoking print media was not associated with smoking status. Conclusion A combination of school and home based antismoking interventions may be effective in controlling adolescent smoking in Somaliland.

  18. Liquid chromatographic determination of benzo(a)pyrene in total particulate matter of cigarette smoke

    Energy Technology Data Exchange (ETDEWEB)

    Tomkins, B.A.; Jenkins, R.A.; Griest, W.H.; Reagan, R.R.; Holladay, S.K.

    1985-09-01

    The benzo(a)pyrene (BaP) delivery of reference and commercially available tobacco cigarettes, as well as reference and placebo marijuana cigarettes, is determined using a sequential liquid chromatographic/liquid chromatographic procedure. The total particulate matter of sample cigarette smoke is collected using a Cambridge filter pad, which is ultrasonically extracted with acetone. The resulting extract is filtered, then fractionated using semipreparative-scale normal phase liquid chromatography (LC). Quantitative determination is achieved using analytical-scale reverse phase LC equipped with a fluorescence detector. The method is precise (+/- 10-15% relative standard deviation) and yields 85% or better BaP recovery at the ng/cig. level. A single pad may be analyzed in 8 person-hours, while a more typical lot of 12 pads (6 pads each for 2 cigarette brands) may be analyzed in 10 person-days.

  19. 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...

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

    Institute of Scientific and Technical Information of China (English)

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

    2014-01-01

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

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

    International Nuclear Information System (INIS)

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2013-10-01

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

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

    OpenAIRE

    Gholamreza Abdollahifard; Veda Vakili; Mina Danaei; Mehrdad Askarian; Laura Romito; Palenik, Charles J

    2013-01-01

    Background: The aim of this study was to determine the prevalence of tobacco use and effect of lifestyle factors on cigarette and hookah use among adult residents of Shiraz, Iran. Methods: In 2010, 1,000 participants were recruited in a multistage, random sampling cross-sectional population-based survey. 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. Al...

  4. Scavenging of free radicals in gas-phase mainstream cigarette smoke by immobilized catalase at filter level.

    Science.gov (United States)

    Lu, Xin; Hua, Zhaozhe; Du, Guocheng; Ma, Xiaolong; Cao, Jianhua; Yang, Zhanping; Chen, Jian

    2008-03-01

    Catalase is well known as capable of inducing the decomposition of H(2)O(2). In this study, a kind of immobilized catalase (entrapped in cross-linked chitosan beads) was dispersed in conventional acetate filter as an antioxidant additive. Quantitative estimation of the free radicals in mainstream cigarette smoke (MCS) was performed to address the effect of this modified filter. It was found that the levels of PBN adduct and NO(*)/NO(2)(*) associated with the gas-phase mainstream cigarette smoke (GPCS) were efficiently decreased by approximately 40% through catalase filtering. Besides, the modified filter was found to lower the MCS-induced adverse biological effects including lipid peroxidation and mutagenicity. This was proved to be substantially attributed to the catalase-dependent breakdown of NO(*), which was stimulated by some of peroxides (most probably being H(2)O(2)), the dismutation products of tar particulate matters (TPM). These results highlighted a promising approach to reduce the smoking-associated health risks to passive smokers. Moreover, the mechanisms of catalase filtering may be helpful for the development of appropriate immobilized enzyme systems to be applied for reducing health risks associated with gaseous pollutants. PMID:18344119

  5. 76 FR 57008 - Smoking of Electronic Cigarettes on Aircraft

    Science.gov (United States)

    2011-09-15

    ... complete Privacy Act statement in the Federal Register published on April 11, 2000 (65 FR 19477-78), or you... CFR part 252, titled Smoking Aboard Aircraft, to implement section 41706. See 65 FR 36772. As a result... artificial smoke generators may cause acute ocular and upper airway irritation, and in a few cases...

  6. Cigarette smoking and risk of Hodgkin lymphoma and its subtypes

    DEFF Research Database (Denmark)

    Kamper-Jørgensen, Mads; Rostgaard, K; Glaser, S L;

    2013-01-01

    The etiology of Hodgkin lymphoma (HL) remains incompletely characterized. Studies of the association between smoking and HL have yielded ambiguous results, possibly due to differences between HL subtypes.......The etiology of Hodgkin lymphoma (HL) remains incompletely characterized. Studies of the association between smoking and HL have yielded ambiguous results, possibly due to differences between HL subtypes....

  7. Cigarette smoking disparities among sexual minority cancer survivors

    Directory of Open Access Journals (Sweden)

    Charles Kamen

    2015-01-01

    Conclusion: The current study offers preliminary evidence that sexual minority status is one variable among many that must be taken into account when assessing health behaviors post-cancer diagnosis. Future research should identify mechanisms leading from sexual minority status to increased rates of smoking and develop tailored smoking cessation interventions.

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

    DEFF Research Database (Denmark)

    Jacobsen, Katja Kemp; Lynge, Elsebeth; Vejborg, Ilse; Tjønneland, Anne; von Euler-Chelpin, My; Andersen, Zorana J

    2015-01-01

    PURPOSE: Smoking before first childbirth increases breast cancer risk, but the biological mechanism remains unknown and may involve mammographic density (MD), one of the strongest biomarkers of breast cancer risk. We aimed to examine whether active smoking and passive smoking were associated with...... intensity) and passive smoking were assessed at cohort baseline (1993-1997) via questionnaire, together with other breast cancer risk factors. Logistic regression was used to estimate associations (odds ratios, 95 % confidence intervals) between smoking and MD, adjusting for confounders. RESULTS: Two...... between smoking and MD was strongest in women who initiated smoking before age of 16 years (0.79, 0.64-0.96), smoked ≥15 cigarettes/day (0.83, 0.71-0.98), smoked ≥5 pack-years (0.62, 0.43-0.89), smoked >30 years (0.86, 0.75-0.99), and smoked ≥11 years before first childbirth (0.70, 0.51-0.96). Association...

  9. A feasibility study on oxidation state of arsenic in cut tobacco, mainstream cigarette smoke and cigarette ash by X-ray absorption spectroscopy

    International Nuclear Information System (INIS)

    This work describes the application of synchrotron-based X-ray Absorption Near-Edge Structure spectroscopy to study the oxidation state of arsenic in cigarette mainstream smoke, cut tobacco and cigarette ash. The level of arsenic in the total particulate matter of the smoke is approximately 1 ppm for the standard research reference cigarette 2R4F and its replacement 3R4F. Smoke particulate samples collected by a conventional glass-fiber membrane (commercially known as Cambridge filter pad) and a jet-impaction method were analyzed and compared. In addition smoke particulate samples were aged either at ambient temperature or at 195 K. X-ray Absorption Near-Edge Structure spectroscopy results revealed that the cut tobacco powder and cigarette ash contained almost exclusively AsV. The smoke particulate samples however contained a mixture of AsIII and AsV. The AsV in the smoke particulate was reduced to AsIII upon aging. Stabilizing the smoke particulate matter at 195 K by solid CO2 slowed down this aging reaction and revealed a higher percentage of AsV. This behavior is consistent with the redox properties of the arsenic species and the smoke particulate matrix.

  10. Modulation by metformin of molecular and histopathological alterations in the lung of cigarette smoke-exposed mice

    OpenAIRE

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

    2014-01-01

    The anti-diabetic drug metformin is endowed with anti-cancer properties. Epidemiological and experimental studies, however, did not provide univocal results regarding its role in pulmonary carcinogenesis. We used Swiss H mice of both genders in order to detect early molecular alterations and tumors induced by mainstream cigarette smoke. Based on a subchronic toxicity study, oral metformin was used at a dose of 800 mg/kg diet, which is 3.2 times higher than the therapeutic dose in humans. Expo...

  11. Cigarette smoke (CS) and nicotine delay neutrophil spontaneous death via suppressing production of diphosphoinositol pentakisphosphate

    Science.gov (United States)

    Xu, Yuanfu; Li, Hongmei; Bajrami, Besnik; Kwak, Hyunjeong; Cao, Shannan; Liu, Peng; Zhou, Jiaxi; Zhou, Yuan; Zhu, Haiyan; Ye, Keqiang; Luo, Hongbo R.

    2013-01-01

    Diphosphoinositol pentakisphosphate (InsP7), a higher inositol phosphate containing energetic pyrophosphate bonds, is beginning to emerge as a key cellular signaling molecule. However, the various physiological and pathological processes that involve InsP7 are not completely understood. Here we report that cigarette smoke (CS) extract and nicotine reduce InsP7 levels in aging neutrophils. This subsequently leads to suppression of Akt deactivation, a causal mediator of neutrophil spontaneous death, and delayed neutrophil death. The effect of CS extract and nicotine on neutrophil death can be suppressed by either directly inhibiting the PtdIns(3,4,5)P3/Akt pathway, or increasing InsP7 levels via overexpression of InsP6K1, an inositol hexakisphosphate (InsP6) kinase responsible for InsP7 production in neutrophils. Delayed neutrophil death contributes to the pathogenesis of CS-induced chronic obstructive pulmonary disease. Therefore, disruption of InsP6K1 augments CS-induced neutrophil accumulation and lung damage. Taken together, these results suggest that CS and nicotine delay neutrophil spontaneous death by suppressing InsP7 production and consequently blocking Akt deactivation in aging neutrophils. Modifying neutrophil death via this pathway provides a strategy and therapeutic target for the treatment of tobacco-induced chronic obstructive pulmonary disease. PMID:23610437

  12. Cigarette Smoking and its Relationship with Perceived Familial Support and Religiosity of University Students in Tabriz

    Directory of Open Access Journals (Sweden)

    Hamid Allahverdipour

    2015-11-01

    Full Text Available  Objective: The goal of the present study was to assess the prevalence of cigarette smoking and its relationship to other risk taking behaviors, perceived familial support and religiosity among college students in Tabriz, Iran .  Method:In this study, 1837 randomly selected students participated and completed a self-administered questionnaire inquiring demographic characteristics, risk taking behaviors, Aneshensel and Sucoff’s 13-items one-dimensional perceived Parental support scale and 28 - items Kendler’s general religiosity scale. Results: In general, 15.8 % of the students were cigarette smokers. The results indicated that being male (OR = 3.21, living alone or with friends (OR = 2.00, having a part-time job (OR = 1.98, alcohol consumption during the past 30 days (OR = 3.67, hookah use (OR = 5.23, substance abuse (OR = 1.69, familial support (OR = 0.97 and religiosity (OR = 0.98 have statistically significant relationships with cigarette smoking . Conclusion:Our study represents the co-occurrence of risky behaviors. Cultural context in the traditional communities seems to show the crucial role of familial support and religiosity traits with the female gender as predictive factors to not smoke cigarette and perform other risky behaviors.

  13. [Cigarette smoking among women attending cervical cancer screening program].

    Science.gov (United States)

    Walentowicz-Sadłecka, Małgorzata; Sadłecki, Paweł; Marszałek, Andrzej; Grabiec, Marek

    2012-01-01

    Cervical cancer is recognized as tobacco-related malignancy. HPV vaccination and introducing screening protocols were found as the best way to decrease cervical cancer related mortality. Besides the cytological screening programs of the uterine cervix smear, nowadays co-factors of carcinogenesis are taken into consideration, also. The aim of our study was to analyse data included in questionnaire of 310 women who underwent cytological examination wi thin cervical cancer screening program in our Department in 2011. There were no differences found between studied groups on rate of oral contraceptive or hormonal therapy use, as well as age and tobacco smoking. However, taking into account education and smoking, there was a significant correlation observed. Patients with higher education level smoked less often. The special attention should be paid to promote smoking cessation in the group of women who finished education on elementary level. PMID:23421059

  14. Parent involvement in cigarette smoking prevention: two pilot evaluations of the "Unpuffables Program".

    Science.gov (United States)

    Perry, C L; Pirie, P; Holder, W; Halper, A; Dudovitz, B

    1990-11-01

    Efforts to prevent the onset of cigarette smoking with young adolescents have been primarily successful in delaying onset, particularly with classroom curricula that emphasize social competencies. Maintenance of these reductions has been difficult to sustain into later adolescence, suggesting the need for programs to complement and supplement curricula. Since one group of adolescents more difficult to influence are those whose parents smoke, parental involvement in smoking prevention may be a powerful enhancer. This paper describes the "Unpuffables Program," an activity package program around smoking, for preadolescents and their parents. Two pilot evaluation studies in Minnesota and Massachusetts focus on the feasibility of and receptivity to the "Unpuffables Program." High awareness and participation rates were found in both settings. The program appears to provide an opportunity for smoking to be discussed at home, motivating smokers to consider cessation, and reinforcing nonsmoking parents' attitudes and behaviors. PMID:2283873

  15. Differential effects of cigarette smoke on oxidative stress and proinflammatory cytokine release in primary human airway epithelial cells and in a variety of transformed alveolar epithelial cells

    Directory of Open Access Journals (Sweden)

    Rahman Irfan

    2006-10-01

    Full Text Available Abstract Background Cigarette smoke mediated oxidative stress and inflammatory events in the airway and alveolar epithelium are important processes in the pathogenesis of smoking related pulmonary diseases. Previously, individual cell lines were used to assess the oxidative and proinflammatory effects of cigarette smoke with confounding results. In this study, a panel of human and rodent transformed epithelial cell lines were used to determine the effects of cigarette smoke extract (CSE on oxidative stress markers, cell toxicity and proinflammatory cytokine release and compared the effects with that of primary human small airway epithelial cells (SAEC. Methods Primary human SAEC, transformed human (A549, H1299, H441, and rodent (murine MLE-15, rat L2 alveolar epithelial cells were treated with different concentrations of CSE (0.2–10% ranging from 20 min to 24 hr. Cytotoxicity was assessed by lactate dehydrogenase release assay, trypan blue exclusion method and double staining with acridine orange and ethidium bromide. Glutathione concentration was measured by enzymatic recycling assay and 4-hydroxy-2-nonenal levels by using lipid peroxidation assay kit. The levels of proinflammatory cytokines (e.g. IL-8 and IL-6 were measured by ELISA. Nuclear translocation of the transcription factor, NF-κB was assessed by immunocytochemistry and immunoblotting. Results Cigarette smoke extract dose-dependently depleted glutathione concentration, increased 4-hydroxy-2-nonenal (4-HNE levels, and caused necrosis in the transformed cell lines as well as in SAEC. None of the transformed cell lines showed any significant release of cytokines in response to CSE. CSE, however, induced IL-8 and IL-6 release in primary cell lines in a dose-dependent manner, which was associated with the nuclear translocation of NF-κB in SAEC. Conclusion This study suggests that primary, but not transformed, lung epithelial cells are an appropriate model to study the inflammatory

  16. When “More doctors smoked Camels” Cigarette advertising in the journal

    OpenAIRE

    Alan Blum

    2010-01-01

    Even well into the twentieth century, cigarette smoking hadn't caught on among most men―and definitely not among women. But through mass media advertising and overseas tobacco funds for the boys at war, cigarettes became firmly entrenched by the 1920s. The tobacco companies were the first to offer women equal rights, of a sort, with slogans such as “I'm a Lucky girl,” “Blow some my way,” and “Do you inhale? Everybody’s doing it!” Readers of the Sunday funnies were told by ballplayers like Lou...

  17. Modulation by metformin of molecular and histopathological alterations in the lung of cigarette smoke-exposed mice.

    Science.gov (United States)

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

    2014-06-01

    The anti-diabetic drug metformin is endowed with anti-cancer properties. Epidemiological and experimental studies, however, did not provide univocal results regarding its role in pulmonary carcinogenesis. We used Swiss H mice of both genders in order to detect early molecular alterations and tumors induced by mainstream cigarette smoke. Based on a subchronic toxicity study, oral metformin was used at a dose of 800 mg/kg diet, which is 3.2 times higher than the therapeutic dose in humans. Exposure of mice to smoke for 4 months, starting at birth, induced a systemic clastogenic damage, formation of DNA adducts, oxidative DNA damage, and extensive downregulation of microRNAs in lung after 10 weeks. Preneoplastic lesions were detectable after 7.5 months in both lung and urinary tract along with lung tumors, both benign and malignant. Modulation by metformin of 42 of 1281 pulmonary microRNAs in smoke-free mice highlighted a variety of mechanisms, including modulation of AMPK, stress response, inflammation, NFκB, Tlr9, Tgf, p53, cell cycle, apoptosis, antioxidant pathways, Ras, Myc, Dicer, angiogenesis, stem cell recruitment, and angiogenesis. In smoke-exposed mice, metformin considerably decreased DNA adduct levels and oxidative DNA damage, and normalized the expression of several microRNAs. It did not prevent smoke-induced lung tumors but inhibited preneoplastic lesions in both lung and kidney. In conclusion, metformin was able to protect the mouse lung from smoke-induced DNA and microRNA alterations and to inhibit preneoplastic lesions in lung and kidney but failed to prevent lung adenomas and malignant tumors induced by this complex mixture. PMID:24683044

  18. Modulation by metformin of molecular and histopathological alterations in the lung of cigarette smoke-exposed mice

    International Nuclear Information System (INIS)

    The anti-diabetic drug metformin is endowed with anti-cancer properties. Epidemiological and experimental studies, however, did not provide univocal results regarding its role in pulmonary carcinogenesis. We used Swiss H mice of both genders in order to detect early molecular alterations and tumors induced by mainstream cigarette smoke. Based on a subchronic toxicity study, oral metformin was used at a dose of 800 mg/kg diet, which is 3.2 times higher than the therapeutic dose in humans. Exposure of mice to smoke for 4 months, starting at birth, induced a systemic clastogenic damage, formation of DNA adducts, oxidative DNA damage, and extensive downregulation of microRNAs in lung after 10 weeks. Preneoplastic lesions were detectable after 7.5 months in both lung and urinary tract along with lung tumors, both benign and malignant. Modulation by metformin of 42 of 1281 pulmonary microRNAs in smoke-free mice highlighted a variety of mechanisms, including modulation of AMPK, stress response, inflammation, NFκB, Tlr9, Tgf, p53, cell cycle, apoptosis, antioxidant pathways, Ras, Myc, Dicer, angiogenesis, stem cell recruitment, and angiogenesis. In smoke-exposed mice, metformin considerably decreased DNA adduct levels and oxidative DNA damage, and normalized the expression of several microRNAs. It did not prevent smoke-induced lung tumors but inhibited preneoplastic lesions in both lung and kidney. In conclusion, metformin was able to protect the mouse lung from smoke-induced DNA and microRNA alterations and to inhibit preneoplastic lesions in lung and kidney but failed to prevent lung adenomas and malignant tumors induced by this complex mixture

  19. Ontogenetic variation in rat liver, lung and kidney monooxygenase induction by low doses of benzo(A)pyrene and cigarette-smoke condensate

    Energy Technology Data Exchange (ETDEWEB)

    van Cantfort, J.; Gielen, J.E.

    1981-12-01

    The specific lung-AHH induction, which we previously observed after the inhalation of cigarette smoke, is not due to the route followed by the inhaled smoke, for the same phenomenon occurs after i.p. injection of either cigarette smoke condensate (CSC) or benzo(a)pyrene in low doses. In this respect lung AHH behaves completely differently from the liver and kidney enzyme, in which organs, basal AHH activity (which is low in the foetus) increases rapidly after birth to reach the adult level 2 months later, and is only inducible by CSC and low doses of BP in unweaned rats. In the lung, the basal AHH activity (low in the foetus) increases abruptly at birth, peaks in 5-day-old rats and then decreases slightly. Contrary to enzyme activity in other tissues, lung AHH cannot be induced in unweaned young animals. The enzyme subsequently becomes sensitive to inducing agents and is highly inducible in 90-day-old rats. Similar behaviour occurs in 2 other enzymes linked to cytochrome P1450: ethoxycoumarin deethylase and ethoxyresorufin deethylase. The results could be related to the particular susceptibility of the lung to develop cancer after the inhalation of cigarette smoke.

  20. Differential effects of cigarette smoke on oxidative stress and proinflammatory cytokine release in primary human airway epithelial cells and in a variety of transformed alveolar epithelial cells

    OpenAIRE

    Kode, Aruna; Yang, Se-Ran; Rahman, Irfan

    2006-01-01

    BACKGROUND:Cigarette smoke mediated oxidative stress and inflammatory events in the airway and alveolar epithelium are important processes in the pathogenesis of smoking related pulmonary diseases. Previously, individual cell lines were used to assess the oxidative and proinflammatory effects of cigarette smoke with confounding results. In this study, a panel of human and rodent transformed epithelial cell lines were used to determine the effects of cigarette smoke extract (CSE) on oxidative ...

  1. Differential effects of cigarette smoke on oxidative stress and proinflammatory cytokine release in primary human airway epithelial cells and in a variety of transformed alveolar epithelial cells

    OpenAIRE

    Rahman Irfan; Yang Se-Ran; Kode Aruna

    2006-01-01

    Abstract Background Cigarette smoke mediated oxidative stress and inflammatory events in the airway and alveolar epithelium are important processes in the pathogenesis of smoking related pulmonary diseases. Previously, individual cell lines were used to assess the oxidative and proinflammatory effects of cigarette smoke with confounding results. In this study, a panel of human and rodent transformed epithelial cell lines were used to determine the effects of cigarette smoke extract (CSE) on o...

  2. Primary Care Physicians' Beliefs and Practices Regarding E-Cigarette Use by Patients Who Smoke: A Qualitative Assessment.

    Science.gov (United States)

    El-Shahawy, Omar; Brown, Richard; Elston Lafata, Jennifer

    2016-01-01

    We explored primary care physicians' (PCPs') beliefs and practices about e-cigarettes. Cross-sectional, semi-structured interviews with PCPs in 2014 were conducted and audio-recorded. Participants were 15 general internal and family medicine physicians practicing in two settings in Virginia, USA. Interview recordings were transcribed, and the content analyzed using the Constant Comparative Method to identify key themes regarding PCPs' reported current practices and beliefs. Five themes were identified: (1) existing clinic processes do not include mechanisms to screen for noncombustible tobacco products (such as e-cigarettes); (2) e-cigarette discussions are becoming commonplace with patients initiating the discussions and seeking physician guidance regarding e-cigarette use; (3) a lack of knowledge regarding the potential harms and benefits of e-cigarettes, yet a willingness to support their patients' desire to use e-cigarettes (4) believing e-cigarettes are a safer alternative to smoking combustible tobacco products; and (5) abandoning concerns regarding the potential harms of e-cigarettes in the context of highly addicted patients and those with extensive comorbidities. Despite acknowledging limited knowledge regarding e-cigarettes, findings suggest that some PCPs are currently recommending e-cigarettes to their patients for smoking cessation and relative harm reduction, often personalizing recommendations based on the patient's perceived addiction level and current health status. Physicians need to be informed about the evolving evidence regarding the risks and benefits of e-cigarettes. PMID:27128928

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

    Institute of Scientific and Technical Information of China (English)

    Marcel Leppe; Josip Culig; Mirela Eric

    2012-01-01

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

  4. Characterization of biological activity of cigarette smoke using in vitro tests

    International Nuclear Information System (INIS)

    Studies were conducted to characterize the influence of exposure mode (whole-body continuous, nose only intermittent, nose-only continuous) on biological activity of cigarette smoke condensates. The mutagenic potency of the extracts was determined using Salmonella typhimurium tester strain TA-98 with and without the addition of S-9. The cytotoxicity of the cigarette smoke with and without the addition of S-9 was also determined using Chinese hamster ovary cells (CHO). Mutagenic activity was observed in the Ames test only after the addition of S-9. The optimum mutagenic activity was observed following addition of between 3 and 6% S-9. The average mutagenic potency, when cells were tested at the optimum level of S-9, was 1.5 revertants/mg extract. Cell killing by cigarette smoke extracts was the same for extracts derived from all three exposure modes. There was about 20% cell killing at concentrations of 300 mg extract/mL culture media. No differences were observed in either mutagenic or cytotoxic potency among the smoke extracts produced under different exposure conditions. (author)

  5. DNA methylation alterations in response to prenatal exposure of maternal cigarette smoking: A persistent epigenetic impact on health from maternal lifestyle?

    Science.gov (United States)

    Nielsen, Christina H; Larsen, Agnete; Nielsen, Anders L

    2016-02-01

    Despite increased awareness, maternal cigarette smoking during pregnancy continues to be a common habit causing risk for numerous documented negative health consequences in the exposed children. It has been proposed that epigenetic mechanisms constitute the link between prenatal exposure to maternal cigarette smoking (PEMCS) and the diverse pathologies arising in later life. We here review the current literature, focusing on DNA methylation. Alterations in the global DNA methylation patterns were observed after exposure to maternal smoking during pregnancy in placenta, cord blood and buccal epithelium tissue. Further, a number of specific genes exemplified by CYP1A1, AhRR, FOXP3, TSLP, IGF2, AXL, PTPRO, C11orf52, FRMD4A and BDNF are shown to have altered DNA methylation patterns in at least one of these tissue types due to PEMCS. Investigations showing persistence and indications of trans-generational inheritance of DNA methylation alterations induced by smoking exposure are also described. Further, smoking-induced epigenetic manifestations can be both tissue-dependent and gender-specific which show the importance of addressing the relevant sex, tissue and cell types in the future studies linking specific epigenetic alterations to disease development. Moreover, the effect of paternal cigarette smoking and second-hand smoke exposure is documented and accordingly not to be neglected in future investigations and data evaluations. We also outline possible directions for the future research to address how DNA methylation alterations induced by maternal lifestyle, exemplified by smoking, have direct consequences for fetal development and later in life health and behavior of the child. PMID:25480659

  6. The Effect of Cigarette Smoke on the Translocator Protein (TSPO) in Cultured Lung Cancer Cells.

    Science.gov (United States)

    Nagler, Rafael; Cohen, Shiri; Gavish, Moshe

    2015-12-01

    Lung cancer is prevalent in cigarette smokers. The mitochondrial membrane translocator protein (TSPO), is thought to protect cells from free radical damage. We examined the effect of cigarette smoke (CS) (containing free radicals) alone and in the presence of saliva (containing redox active free iron), on survival of H1299 lung cancer cells and on their mitochondrial characteristics, and whether TSPO binding was influenced by CS and by saliva. We exposed H1299 cells to CS in the presence/absence of saliva and also characterized TSPO binding in the cells using [3H]PK 11195 as a radioligand. CS induced a significant drop in mitochondrial potential (ΔΨm), while addition of saliva did not lead to further loss of ΔΨm (42.5% vs. 39.85%). Scatchard analysis of the saturation curve of [3H]PK 11195 binding (0.2-6 nM final concentration) yielded a straight-line plot (R =  0.9). Average Bmax value was 3274 ± 787 fmol/mg of protein, and average Kd value was 9.2 ± 1.3 nM. Benzodiazepine diazepam partially prevented decrease in cell survival following exposure to CS and redox active iron containing media (saliva) while benzodiazepine clonazepam did not, indicating that this effect is TSPO-specific. Exposure of cells to CS resulted in alternation of biomolecules expressed by CLs peroxidation, reduction of TSPO binding, and depletion of the mitochondrial potential. This irreversible damage was enhanced in the presence of saliva. All these modulations may result in cellular death increase following CS exposure, enhanced in the presence of saliva. PMID:25968977

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

    Directory of Open Access Journals (Sweden)

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

    2013-11-01

    Full Text Available 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 we performed a systematic analysis of the genetic expression behaviour, using the established whole genome microarray-technology which should be able to reveal the cellular effects. With these data we aim to generate a qualitative spectrum of cellular stress response activity. It is noticeable that after cells’ exposure to pyrolyzed tobacco smoke components the products of the most affected genes, e.g. ID1, inhibitor of DNA binding, are up-regulated as a rapid response after 2 h with a factor 3.8 and RPS2, ribosomal protein S2, is down-regulated to nearly 50 % after 24 hours. In databases they are documented as still uncharacterized and hypothetical proteins. The DDIT4 gene, encoding the DNA-damage-inducible transcript 4, associated with regulation and development of DNA processes after damage by ionizing radiation and in p53 mediated apoptotic processes, is up-regulated. The exposure leads to a rapid cellular stress response of genes like induction of the ID1, ID2, and ID3 genes, located on different chromosomes, already after two hours. They interact normally with DNA binding proteins under heterodimer formation and are considered as negative regulators of transcription. After 24 hours, a return back to normal was not observed and the genes remained stably down-regulated. The suppression of the GADD45B gene which is involved in the cell cycle regulation and after DNA damage a cell cycle arrest is mediated by the gene product. The C14orf4 gene (IRF2BPL

  8. Knowledge and perception about health risks of cigarette smoking among Iraqi smokers

    Directory of Open Access Journals (Sweden)

    Omar Thanoon Dawood

    2016-01-01

    Full Text Available Background: Smoking is a major public health problem, especially in Iraq. There is very little information had been documented regarding smoking risk factors and quit intention among Iraqi smokers. Objectives: The main objectives of this study are to determine smokers' knowledge and perception about smoking health risks; and to determine smoking behavior and quitting intentions among Iraqi smokers; as well as to predict the factors that may associate with quit intentions. Methods: A cross-sectional study was conducted at the outpatient clinic in Tikrit Teaching Hospital, Tikrit City, Iraq. Adult smokers who are smoking cigarette everyday and able to communicate with the researcher were invited to participate in the study. A self-administered questionnaire was used to collect data from 386 participants. Results: This study showed that smokers had low awareness about some risk effects of smoking such as lung cancer in nonsmokers (30.1%, impotence in male smokers (52.6%, premature ageing (64%, and stroke (66.3%. In addition, the high score of knowledge and perception was significantly associated with quitting intention. Conclusion: Smokers' knowledge and perception regarding smoking health effects were low, especially in terms of secondhand smokers. Many efforts needed from health policy-makers and health care professionals to disseminate information about the risks of smoking and health benefits of give up smoking.

  9. Cigarette Smoke Disrupted Lung Endothelial Barrier Integrity and Increased Susceptibility to Acute Lung Injury via Histone Deacetylase 6.

    Science.gov (United States)

    Borgas, Diana; Chambers, Eboni; Newton, Julie; Ko, Junsuk; Rivera, Stephanie; Rounds, Sharon; Lu, Qing

    2016-05-01

    Epidemiologic evidence indicates that cigarette smoke (CS) is associated with the development of acute lung injury (ALI). We have previously shown that brief CS exposure exacerbates lipopolysaccharide (LPS)-induced ALI in vivo and endothelial barrier dysfunction in vitro. In this study, we found that CS also exacerbated Pseudomonas-induced ALI in mice. We demonstrated that lung microvascular endothelial cells (ECs) isolated from mice exposed to CS had a greater permeability or incomplete recovery after challenges by LPS and thrombin. Histone deacetylase (HDAC) 6 deacetylates proteins essential for maintenance of endothelial barrier function. We found that HDAC6 phosphorylation at serine-22 was increased in lung tissues of mice exposed to CS and in lung ECs exposed to cigarette smoke extract (CSE). Inhibition of HDAC6 attenuated CSE-induced increases in EC permeability and CS priming of ALI. Similar barrier protection was provided by the microtubule stabilizer taxol, which preserved α-tubulin acetylation. CSE decreased α-tubulin acetylation and caused microtubule depolymerization. In coordination with increased HDAC6 phosphorylation, CSE inhibited Akt and activated glycogen synthase kinase (GSK)-3β; these effects were ameliorated by the antioxidant N-acetyl cysteine. Our results suggest that CS increases lung EC permeability, thereby enhancing susceptibility to ALI, likely through oxidative stress-induced Akt inactivation and subsequent GSK-3β activation. Activated GSK-3β may activate HDAC6 via phosphorylation of serine-22, leading to α-tubulin deacetylation and microtubule disassembly. Inhibition of HDAC6 may be a novel therapeutic option for ALI in cigarette smokers. PMID:26452072

  10. Sidestream cigarette smoke effects on cardiovascular responses in conscious rats: involvement of oxidative stress in the fourth cerebral ventricle

    OpenAIRE

    Valenti Vitor E; de Abreu Luiz; Sato Monica A; Ferreira Celso; Adami Fernando; Fonseca Fernando LA; Xavier Valdelias; Godoy Moacir; Monteiro Carlos B; Vanderlei Luiz Carlos M; Saldiva Paulo HN

    2012-01-01

    Abstract Background Cigarette exposure increases brain oxidative stress. The literature showed that increased brain oxidative stress affects cardiovascular regulation. However, no previous study investigated the involvement of brain oxidative stress in animals exposed to cigarette and its relationship with cardiovascular regulation. We aimed to evaluate the effects of central catalase inhibition on baroreflex and cardiovascular responses in rats exposed to sidestream cigarette smoke (SSCS). M...

  11. Does Vaping in E-Cigarette Advertisements Affect Tobacco Smoking Urge, Intentions, and Perceptions in Daily, Intermittent, and Former Smokers?

    Science.gov (United States)

    Maloney, Erin K; Cappella, Joseph N

    2016-01-01

    Visual depictions of vaping in electronic cigarette advertisements may serve as smoking cues to smokers and former smokers, increasing urge to smoke and smoking behavior, and decreasing self-efficacy, attitudes, and intentions to quit or abstain. After assessing baseline urge to smoke, 301 daily smokers, 272 intermittent smokers, and 311 former smokers were randomly assigned to view three e-cigarette commercials with vaping visuals (the cue condition) or without vaping visuals (the no-cue condition), or to answer unrelated media use questions (the no-ad condition). Participants then answered a posttest questionnaire assessing the outcome variables of interest. Relative to other conditions, in the cue condition, daily smokers reported greater urge to smoke a tobacco cigarette and a marginally significantly greater incidence of actually smoking a tobacco cigarette during the experiment. Former smokers in the cue condition reported lower intentions to abstain from smoking than former smokers in other conditions. No significant differences emerged among intermittent smokers across conditions. These data suggest that visual depictions of vaping in e-cigarette commercials increase daily smokers' urge to smoke cigarettes and may lead to more actual smoking behavior. For former smokers, these cues in advertising may undermine abstinence efforts. Intermittent smokers did not appear to be reactive to these cues. A lack of significant differences between participants in the no-cue and no-ad conditions compared to the cue condition suggests that visual depictions of e-cigarettes and vaping function as smoking cues, and cue reactivity is the mechanism through which these effects were obtained. PMID:25758192

  12. Cigarette Smoking and the Development of Premenstrual Syndrome

    OpenAIRE

    Bertone-Johnson, Elizabeth R.; Hankinson, Susan E; Johnson, Susan R.; Manson, JoAnn E.

    2008-01-01

    Moderate to severe premenstrual syndrome (PMS) affects as many as 20% of premenopausal women. Although smoking may be more common in women with PMS, it is unknown whether smoking is involved in PMS etiology. In 1991–2001, the authors conducted a case-control study nested within the prospective Nurses’ Health Study II. Participants were US women aged 27–44 years and free of PMS at baseline, including 1,057 who developed PMS over 10 years and 1,968 reporting no diagnosis of PMS and only minimal...

  13. Mortality and life expectancy in relation to long‐term cigarette, cigar and pipe smoking: The Zutphen Study

    OpenAIRE

    Streppel, M.T.; Boshuizen, H.C.; Ocké, M C; Kok, F.J.; Kromhout, D.

    2007-01-01

    Study objective: To study the effect of long-term smoking on all-cause and cause-specific mortality, and to estimate the effects of cigarette and cigar or pipe smoking on life expectancy. Design: A long-term prospective cohort study. Setting: Zutphen, The Netherlands. Participants: 1373 men from the Zutphen Study, born between 1900 and 1920 and studied between 1960 and 2000. Measurements: Hazard ratios for the type of smoking, amount and duration of cigarette smoking, obtained from a time-dep...

  14. The role of psychosocial and belief factors in self-reported cigarette smoking among university students in Malaysia

    Directory of Open Access Journals (Sweden)

    Sami Al-Dubai

    2014-01-01

    Full Text Available This study aimed to explore factors associated, specifically belief factors, with self-reported tobacco smoking status. A sample of 300 students was recruited from a private university in Malaysia. Data was collected using a pre-tested self-administrated questionnaire that investigated various factors including socio-demographics, socio-economic status, smoking behavior and beliefs on tobacco smoking. The main tobacco use in this study sample was cigarettes and the estimated prevalence of self-reported cigarette smoking was 10.3%. In bivariate analysis, self-reported cigarette smoking was significantly associated with socio-demographic, behavioral factors and faculty of study (P<0.05. In multivariate modeling, being male and a non-medical student, did not exercise, having a smoker father and brother or sister, suffering from financial difficulties and having the belief that smokers had more friends, all had statistically significant associations (P<0.05 with self-reported cigarette smoking. Social and interpersonal factors were associated with self-reported cigarette smoking status. A comprehensive health model focusing on changing the social norms of parent and sibling tobacco smoking and students’ beliefs, alongside nurturing skills of dealing with stressful situations, warrant implementation.

  15. Sidestream cigarette smoke effects on cardiovascular responses in conscious rats: involvement of oxidative stress in the fourth cerebral ventricle

    Directory of Open Access Journals (Sweden)

    Valenti Vitor E

    2012-03-01

    Full Text Available Abstract Background Cigarette exposure increases brain oxidative stress. The literature showed that increased brain oxidative stress affects cardiovascular regulation. However, no previous study investigated the involvement of brain oxidative stress in animals exposed to cigarette and its relationship with cardiovascular regulation. We aimed to evaluate the effects of central catalase inhibition on baroreflex and cardiovascular responses in rats exposed to sidestream cigarette smoke (SSCS. Methods We evaluated males Wistar rats (320-370 g, which were implanted with a stainless steel guide cannula into the fourth cerebral ventricle (4th V. Femoral artery and vein were cannulated for mean arterial pressure (MAP and heart rate (HR measurement and drug infusion, respectively. Rats were exposed to SSCS during three weeks, 180 minutes, 5 days/week (CO: 100-300 ppm. Baroreflex was tested with a pressor dose of phenylephrine (PHE, 8 μg/kg, bolus to induce bradycardic reflex and a depressor dose of sodium nitroprusside (SNP, 50 μg/kg, bolus to induce tachycardic reflex. Cardiovascular responses were evaluated before, 5, 15, 30 and 60 minutes after 3-amino-1,2,4-triazole (ATZ, catalase inhibitor, 0.001 g/100 μL injection into the 4th V. Results Central catalase inhibition increased basal HR in the control group during the first 5 minutes. SSCS exposure increased basal HR and attenuated bradycardic peak during the first 15 minutes. Conclusion We suggest that SSCS exposure affects cardiovascular regulation through its influence on catalase activity.

  16. Effect of cigarette smoking on evolution of ventilatory lung function in young adults: an eight year longitudinal study.

    OpenAIRE

    Jaakkola, M S; Ernst, P.; Jaakkola, J J; N'gan'ga, L W; Becklake, M R

    1991-01-01

    BACKGROUND: There are few data on the quantitative effects of cigarette smoking on lung function in young adults. These effects are important in the understanding of the early stages of chronic airflow obstruction. METHODS: A longitudinal study over eight years was carried out to estimate quantitatively the effect of cigarette smoking on ventilatory lung function in young adults and to examine the possibility that the effect is modified by other factors. The study population were 15 to 40 yea...

  17. Associations between cigarette smoking and cannabis dependence: A longitudinal study of young cannabis users in the United Kingdom

    OpenAIRE

    Hindocha, C; Shaban, N. D.; Freeman, T. P.; Das, R K; Gale, G.; Schafer, G.; Falconer, C. J.; Morgan, C. J.; Curran, H V

    2015-01-01

    Aims To determine the degree to which cigarette smoking predicts levels of cannabis dependence above and beyond cannabis use itself, concurrently and in an exploratory four-year follow-up, and to investigate whether cigarette smoking mediates the relationship between cannabis use and cannabis dependence. Methods The study was cross sectional with an exploratory follow-up in the participants’ own homes or via telephone interviews in the United Kingdom. Participants were 298 cannabis and tobacc...

  18. An Investigation on the Interaction of Plant Growth Substances and the Inhibitory Effects of Cigarette Smoke on Germination

    OpenAIRE

    MUNZUROGLU, Ömer

    1999-01-01

    In this work, the effects of cigarette smoke on the germination of a monocot ( Triticum aestivum cv. Cumhuriyet) and a dicot ( Cucumis sativus cv. Beit alpha) seeds and on the subsequent morphogenetic formations have been investigated. In addition, the interaction between externally applied plant growth substances and these phenomena have been dealt with. The results we have obtained may be summarized as follows: The application of cigarette smoke have inhibited the seed germination in b...

  19. Individualized Attempts To Reduce Cigarette Smoking among College Students.

    Science.gov (United States)

    Kane, Jeanette; Hodges, Jilda; Srebro, Karen; Authier, Charlene; Chambliss, Catherine

    An earlier study found it very difficult to attract large numbers of college-age smokers to a traditional counseling center based smoking cessation program, despite repeated efforts at advertising the availability of a free program. This study utilizes the program from the earlier study but tailors it more specifically to the needs of the target…

  20. Evaluation of Cigarette Smoking Attitudes and Behaviors among Students of a State High School in İstanbul

    OpenAIRE

    Ülkü Aka Aktürk; Özlem Saniye İçmeli; Selahattin Öztaş; Nagihan Durmuş Koçak; Aysun Şengül; Banu Musaffa Salepçi; Dilek Ernam

    2015-01-01

    Objective: We aimed to evaluate smoking habits of students, reasons of smoking and students’ level of knowledge on the adverse effects of smoking in a state high school in İstanbul. Methods: A 15-item questionnaire was administered to the students attending a state high school in İstanbul to evaluate their attitudes and behaviors towards cigarette smoking. The questionnaire was completed by each class of students at the same class period under the supervision of their teachers. Result...

  1. Evaluation of Cigarette Smoking Attitudes and Behaviors among Students of a State High School in İstanbul

    Directory of Open Access Journals (Sweden)

    Ülkü Aka Aktürk

    2015-08-01

    Full Text Available Objective: We aimed to evaluate smoking habits of students, reasons of smoking and students’ level of knowledge on the adverse effects of smoking in a state high school in İstanbul. Methods: A 15-item questionnaire was administered to the students attending a state high school in İstanbul to evaluate their attitudes and behaviors towards cigarette smoking. The questionnaire was completed by each class of students at the same class period under the supervision of their teachers. Results: The questionnaire was completed by 415 students at the respective school. While 349 students (84% never smoke, 66 (15.9% students were either current smokers or quitters. Fifty five of the students (13.2% were active smokers. When we looked at the reasons of smoking, they reported that 63.6% smoked cigarettes because their friends did; 47.2% smoked cigarettes due to exam-related stress; and 40% smoked cigarettes due to family problems. The rate of smoking friends in the smoker group was significantly higher than in the non-smoker group (p=0.0001. A logistic regression analysis showed that having smoking friends was associated with an 8-fold increase in the risk of smoking compared to having no smoking friends. Conclusion: The most common reasons of smoking at the school were friends who were smokers, exam-related stress and family problems. Having friends who smoke was associated with an 8-fold increase in the risk of smoking. We believe that counselling services’ close engagement with family problems of students and exam-related stress issues and helping them to cope with these problems may prevent their vulnerability to toxic substances.

  2. Cigarette Smoking in Same-Sex and Different-Sex Unions: The Role of Socioeconomic and Psychological Factors

    OpenAIRE

    Reczek, Corinne; Liu, Hui; Brown, Dustin

    2013-01-01

    Cigarette smoking has long been a target of public health intervention because it substantially contributes to morbidity and mortality. Individuals in different-sex marriages have lower smoking risk (i.e., prevalence and frequency) than different-sex cohabiters. However, little is known about the smoking risk of individuals in same-sex cohabiting unions. We compare the smoking risk of individuals in different-sex marriages, same-sex cohabiting unions, and different-sex cohabiting unions using...

  3. Thirty minute-exposure to aged cigarette smoke increases nasal congestion in nonsmokers.

    Science.gov (United States)

    Schick, Suzaynn F; van den Vossenberg, Glenn; Luo, Andy; Whitlatch, Aaron; Jacob, Peyton; Balmes, John; Shusterman, Dennis

    2013-01-01

    The aim of this study was to assess the effects of short exposures to experimentally aged cigarette smoke on the nose and upper airways. This crossover study compared the effects of 30-min exposures to (1) experimentally aged cigarette smoke at 1 mg/m³ particulate matter (PM)/14 ppm carbon monoxide (CO) and (2) conditioned filtered air on urinary metabolites of nicotine and tobacco-specific nitrosamines. Subjective nasal symptoms were assessed by questionnaire, objective nasal congestion was assessed by anterior rhinomanometry and nasal nitric oxide (NO) concentrations were determined. Experimentally aged cigarette smoke is a validated model for secondhand smoke (SHS). Twenty-six healthy nonsmokers (10 normal, 7 atopic/nonrhinitic, 7 atopic rhinitic, 2 nonatopic/rhinitic) were studied. A 30-min exposure to SHS increased nasal resistance in healthy nonsmokers. The rise in nasal resistance was most pronounced in rhinitic subjects. Significant increases were not noted when atopic subjects were considered independent of rhinitis status. Secondhand smoke exposure also elevated subjective nasal symptoms and urinary concentrations of metabolites of nicotine (cotinine and trans-3´-hydroxycotinine) and tobacco-specific nitrosamines [(4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol (NNAL)] in all subgroups of subjects. Exposure-related, subjective nasal symptoms were significantly higher in rhinitic than in normal subjects. Significant changes in nasal NO concentrations were not detected. Data indicate a 30-min exposure to secondhand smoke at 1 mg/m³ PM increases subjective upper respiratory symptoms, increases urinary cotinine and NNAL, and produces objective nasal airflow obstruction in human subjects. PMID:23859154

  4. Tobacco smoke-induced lung fibrosis and emphysema.

    Science.gov (United States)

    Morse, Danielle; Rosas, Ivan O

    2014-01-01

    Despite public health campaigns discouraging smoking, 1,000 American children every day become smokers, ensuring that tobacco-related health complications will be with us for decades to come. Smoking is the greatest risk factor for both chronic obstructive lung disease and interstitial lung disease. The facts that not every smoker develops chronic lung disease and that lung pathology differs markedly among smokers indicate that individual susceptibility must be a central determinant of lung injury responses to cigarette smoke. Comparative examination of pathogenic mechanisms of smoke-induced lung disease can shed light on the homeostatic pathways critical to maintaining lung health. In this review, we explore common and divergent biological forces tilting the lung homeostatic balance away from health and toward emphysema or pulmonary fibrosis. We emphasize recent insights that highlight the greatest contrasts or similarities in the pathogenesis of these two chronic lung disease phenotypes. PMID:24274738

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

    International Nuclear Information System (INIS)

    Nuclear workers may be exposed to radiation in various forms, such as low-LET γ-irradiation or α-irradiation from inhaled 239PuO2 particles. These workers may then have increased risk for lung cancer compared to the general population. Of additional concern is the possibility that interactions between radiation and other carcinogens may increase the risk of cancer induction, compared to the risks from either type of agent alone. An important and common lung carcinogen is cigarette smoke. The purpose of this project is to better determine the combined effects of chronically inhaled cigarette smoke and either inhaled 239PuO2 or external, thoracic X-irradiation on the induction of lung cancer in rats. Histologic and dosimetric evaluations of rats in the CS + 239PuO2 study continue, and the study of CS + X rays is beginning

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1995-12-01

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

  7. Cigarette Taxes and Older Adult Smoking: Evidence from the Health and Retirement Study.

    Science.gov (United States)

    MacLean, Johanna Catherine; Kessler, Asia Sikora; Kenkel, Donald S

    2016-04-01

    In this study, we use the Health and Retirement Study to test whether older adult smokers, defined as those 50 years and older, respond to cigarette tax increases. Our preferred specifications show that older adult smokers respond modestly to tax increases: a $1.00 (131.6%) tax increase leads to a 3.8-5.2% reduction in cigarettes smoked per day (implied tax elasticity = -0.03 to -0.04). We identify heterogeneity in tax elasticity across demographic groups as defined by sex, race/ethnicity, education, and marital status and by smoking intensity and level of addictive stock. These findings have implications for public health policy implementation in an aging population. Copyright © 2015 John Wiley & Sons, Ltd. PMID:25721732

  8. Effect of cigarette smoking on human health and promising remedy by mangroves

    Institute of Scientific and Technical Information of China (English)

    Chinnappan; Ravinder; Singh; Kandasamy; Kathiresan

    2015-01-01

    This article reviews the evils of cigarette smoking and the promise of mangroves to cure them.Chemicals in cigarette smoke are leading cause of death to both smokers and nonsmokers.Plant is the potential source to produce medicine for almost all the diseases.Mangroves are promising as a novel source of anti-cancer drugs in regulating the cancer pathways and stimulating immunity in the body system.Research on medicine from mangroves for the treatment of cancer has not only been shown to have an effect on cancer,but also provided important methods for the study of cancer therapy and mechanism.This report may help to explore the medicinal properties of the mangroves.

  9. Natural radionuclides in cigarette tobacco from Serbian market and effective dose estimate from smoke inhalation

    International Nuclear Information System (INIS)

    The activity concentrations of natural radionuclides (40K, 210Pb, 210Po, 226Ra and 228Ra) in 17 most frequently used cigarette brands in Serbia and corresponding effective doses due to smoke inhalation are presented. The mean annual effective doses for 210Pb and 210Po were estimated to be 47.3 and 724 μSv y-1 for 210Pb and 210Po, respectively. Serbia currently has the highest smoking rate in the world. The results of this study indicate the high contribution of the annual effective dose due to smoke inhalation to the total inhalation dose from natural radionuclides. The more effective implementation of actions for reducing smoking prevalence in Serbia is highly needed. (authors)

  10. Cigarette Smoke and the Induction of Urokinase Plasminogen Activator Receptor In Vivo: Selective Contribution of Isoforms to Bronchial Epithelial Phenotype.

    Science.gov (United States)

    Portelli, Michael A; Stewart, Ceri E; Hall, Ian P; Brightling, Christopher E; Sayers, Ian

    2015-08-01

    The urokinase plasminogen activator receptor (uPAR) gene (PLAUR) has been identified as an asthma susceptibility gene, with polymorphisms within that gene being associated with baseline lung function, lung function decline, and lung function in a smoking population. Soluble cleaved uPAR (scuPAR), a molecule identified as a marker of increased morbidity and mortality in a number of diseases, has been shown to be elevated in the airways of patients with asthma and in patients with chronic obstructive pulmonary disease. However, the functionality of soluble receptor isoforms and their relationship with an important initiator for obstructive lung disease, cigarette smoke, remains undefined. In this study, we set out to determine the effect of cigarette smoke on soluble uPAR isoforms, its regulatory pathway and the resultant effect on bronchial epithelial cell function. We identified a positive association between cigarette pack-years and uPAR expression in the airway bronchial epithelium of biopsies from patients with asthma (n = 27; P = 0.0485). In vitro, cigarette smoke promoted cleavage of uPAR from the surface of bronchial epithelial cells (1.5× induction; P bronchial epithelial cells. This suggests that cigarette smoke elevates soluble receptor isoforms in bronchial epithelial cells through direct (cleavage) and indirect (messenger RNA expression) means. These findings provide further insight into how cigarette smoke may influence changes in the airways of importance to airway remodeling and obstructive lung disease progression. PMID:25490122

  11. Cigarette smoking increases radon working level exposures to all occupants of the smoker's home

    International Nuclear Information System (INIS)

    This paper reports that the 1988 National Academy of Sciences report on radon health risks evaluated the combined effects of radon exposures and cigarettes on the lung cancer risk to smokers. This report showed that the risk of lung cancer is about 10 times greater for smokers than for nonsmokers at the same Working Level exposures. In 1986, the Surgeon General reported that 106,000 lung cancer deaths occurred among smokers. Therefore, the health risks of cigarettes alone or in combination with radon exposures are well recognized. What has not been studied is the effect of cigarette smoke on the Working Levels in homes that increases the exposure to radon decay products to all occupants, both smokers and nonsmokers. Preliminary studies in a radon chamber at Radon QC showed that the smoke from a single cigarette increased the Working Levels by a factor of five within four hours. Furthermore, the Working Levels remained at an elevated level for more than 24 hours. The equilibrium ratio of radon decay products to radon gas also went from about 14% up to 71%, with a slow decrease over 24 hours. Similar studies in the homes of a smoker and nonsmoker confirmed the laboratory observations. The studies in homes also showed the effects of thoron decay products

  12. Trends and Predictors of Cigarette Smoking Among HIV Seropositive and Seronegative Men: The Multicenter Aids Cohort Study.

    Science.gov (United States)

    Akhtar-Khaleel, Wajiha Z; Cook, Robert L; Shoptaw, Steven; Surkan, Pamela; Stall, Ronald; Beyth, Rebecca J; Teplin, Linda A; Plankey, Michael

    2016-03-01

    We measured the trend of cigarette smoking among HIV-seropositive and seronegative men over time from 1984 to 2012. Additionally, we examined the demographic correlates of smoking and smoking consumption. Six thousand and five hundred and seventy seven men who have sex with men (MSM) from the Multicenter AIDS Cohort Study (MACS) were asked detailed information about their smoking history since their visit. Prevalence of smoking and quantity smoked was calculated yearly from 1984 to 2012. Poisson regression with robust error variance was used to estimate prevalence ratios of smoking in univariate and multivariate models. In 2012, 11.8 and 36.9 % of men who were enrolled in the MACS before 2001 or during or after 2001 smoked cigarettes, respectively. In the multivariate analysis, black, non-Hispanic, lower education, enrollment wave, alcohol use, and marijuana use were positively associated with current smoking in MSM. HIV serostatus was not significant in the multivariate analysis. However, HIV variables, such as detectable viral load, were positively associated. Though cigarette smoking has declined over time, the prevalence still remains high among subgroups. There is still a need for tailored smoking cessation programs to decrease the risk of smoking in HIV-seropositive MSM. PMID:26093780

  13. The Demand For Cigarettes and Restrictions on Smoking in the Workplace

    OpenAIRE

    Chaloupka, Frank J.; Henry Saffer

    1988-01-01

    The purpose of this paper is to empirically test the effect that restrictive clean air laws have on the level of smoking. Restrictive clean air laws refers to the laws which prohibit smoking in private workplaces as well as in public places. The data employed in this study consist of a time series of cross sections of the fifty states of the U.S., and Washington D.C., over the time period from 1975 through 1985, Since states where sentiment is strongly against cigarettes are more likely to pa...

  14. Cigarette Smoking, N-Acetyltransferase 2 Acetylation Status, and Bladder Cancer Risk

    DEFF Research Database (Denmark)

    Marcus, P.M.; Hayes, R.B.; Vineis, P.;

    2000-01-01

    Tobacco use is an established cause of bladder cancer. The ability to detoxify aromatic amines, which are present in tobacco and are potent bladder carcinogens, is compromised in persons with the N-acetyltransferase 2 slow acetylation polymorphism. The relationship of cigarette smoking with bladder...... interaction between smoking and N-acetyltransferase 2 slow acetylation (OR, 1.3; 95% confidence interval, 1.0-1.6) that was somewhat stronger when analyses were restricted to studies conducted in Europe (OR, 1.5; confidence interval, 1.1-1.9), a pooling that included nearly 80% of the collected data. Using...

  15. Cigarette Smoking and Risk of Lung Cancer in Korean Men: The Seoul Male Cancer Cohort Study

    OpenAIRE

    Bae, Jong-Myon; Lee, Moo-Song; Shin, Myung-Hee; Kim, Dong-Hyun; Li, Zhong-Min; Ahn, Yoon-Ok

    2007-01-01

    Lung cancer is the leading cause of cancer deaths in Korea. The aim of this study was to estimate lung cancer risk of cigarette smoking in Korean men by a 10-yr follow-up prospective cohort study using the primary databases. The number of subjects was 14,272 men, who had full information of smoking habits among participants in the Seoul Male Cancer Cohort Study (SMCC). Total 125,053 person-years were calculated by determining the number of days from the start of follow-up, January 1, 1993, un...

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

    DEFF Research Database (Denmark)

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

    2006-01-01

    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 < 0.05). The results were adjusted for maternal lifestyle factors and socioeconomic characteristics. Additional adjustment for...... perinatal factors and parental psychiatric hospitalization did not change the results substantially (OR 1.7; 95% CI 1.1-2.6). We found no statistically significant association between maternal smoking in pregnancy and hostile-aggressive and anxious-fearful behaviour in the offspring. CONCLUSION: Exposure to...

  17. Genome-Wide Analysis of DNA Methylation and Cigarette Smoking in a Chinese Population

    Science.gov (United States)

    Zhu, Xiaoyan; Li, Jun; Deng, Siyun; Yu, Kuai; Liu, Xuezhen; Deng, Qifei; Sun, Huizhen; Zhang, Xiaomin; He, Meian; Guo, Huan; Chen, Weihong; Yuan, Jing; Zhang, Bing; Kuang, Dan; He, Xiaosheng; Bai, Yansen; Han, Xu; Liu, Bing; Li, Xiaoliang; Yang, Liangle; Jiang, Haijing; Zhang, Yizhi; Hu, Jie; Cheng, Longxian; Luo, Xiaoting; Mei, Wenhua; Zhou, Zhiming; Sun, Shunchang; Zhang, Liyun; Liu, Chuanyao; Guo, Yanjun; Zhang, Zhihong; Hu, Frank B.; Liang, Liming; Wu, Tangchun

    2016-01-01

    Background: Smoking is a risk factor for many human diseases. DNA methylation has been related to smoking, but genome-wide methylation data for smoking in Chinese populations is limited. Objectives: We aimed to investigate epigenome-wide methylation in relation to smoking in a Chinese population. Methods: We measured the methylation levels at > 485,000 CpG sites (CpGs) in DNA from leukocytes using a methylation array and conducted a genome-wide meta-analysis of DNA methylation and smoking in a total of 596 Chinese participants. We further evaluated the associations of smoking-related CpGs with internal polycyclic aromatic hydrocarbon (PAH) biomarkers and their correlations with the expression of corresponding genes. Results: We identified 318 CpGs whose methylation levels were associated with smoking at a genome-wide significance level (false discovery rate Zhang X, He M, Guo H, Chen W, Yuan J, Zhang B, Kuang D, He X, Bai Y, Han X, Liu B, Li X, Yang L, Jiang H, Zhang Y, Hu J, Cheng L, Luo X, Mei W, Zhou Z, Sun S, Zhang L, Liu C, Guo Y, Zhang Z, Hu FB, Liang L, Wu T. 2016. Genome-wide analysis of DNA methylation and cigarette smoking in Chinese. Environ Health Perspect 124:966–973; http://dx.doi.org/10.1289/ehp.1509834 PMID:26756918

  18. Interactions of Several Lipid-Related Gene Polymorphisms and Cigarette Smoking on Blood Pressure Levels

    Directory of Open Access Journals (Sweden)

    Rui-Xing Yin, Dong-Feng Wu, Jin-Zhen Wu, Xiao-Li Cao, Lynn Htet Htet Aung, Lin Miao, Xing-Jiang Long, Wan-Ying Liu, Lin Zhang, Meng Li

    2012-01-01

    Full Text Available The interactions of single nucleotide polymorphisms (SNPs and cigarette smoking on blood pressure levels are limited. The present study was undertaken to detect nine lipid-related SNPs and their interactions with cigarette smoking on blood pressure levels. Genotyping of ATP-binding cassette transporter A1 (ABCA-1 V825I, acyl-CoA:cholesterol acyltransferase-1 (ACAT-1 rs1044925, low density lipoprotein receptor (LDL-R AvaⅡ, hepatic lipase gene (LIPC -250G>A, endothelial lipase gene (LIPG 584C>T, methylenetetrahydrofolate reductase (MTHFR 677C>T, proprotein convertase subtilisin-like kexin type 9 (PCSK9 E670G, peroxisome proliferator-activated receptor delta (PPARD +294T>C, and Scavenger receptor class B type 1 (SCARB1 rs5888 was performed in 935 nonsmokers and 845 smokers. The interactions were detected by factorial regression analysis. The frequencies of genotypes (ACAT-1 and LIPG, alleles (ABCA-1, and both genotypes and alleles (LDL-R, LIPC, PPARD and SCARB1 were different between nonsmokers and smokers (P < 0.05-0.001. The levels of pulse pressure (PP, ABCA-1, and systolic, diastolic blood pressure (SBP, DBP and PP (LIPC in nonsmokers were different among the genotypes (P < 0.01-0.001. The levels of SBP (ABCA-1, ACAT-1, LIPG and PCSK9, DBP (ACAT-1, LDL-R, LIPC, PCSK9 and PPARD, and PP (LIPC, LIPG, MTHFR and PCSK9 in smokers were different among the genotypes (P < 0.01-0.001. The SNPs of ABCA-1, ACAT-1 and PCSK9; ACAT-1, LDL-R, MTHFR and PCSK9; and ABCA-1, LIPC, PCSK9 and PPARD were shown interactions with cigarette smoking to influence SBP, DBP and PP levels (P < 0.05-0.001; respectively. The differences in blood pressure levels between the nonsmokers and smokers might partly result from different interactions of several SNPs and cigarette smoking.

  19. Cigarette smoking in young-adult workers: a cross-sectional analysis from Abruzzo, Italy

    OpenAIRE

    Carlos Chiatti; Simone Chiadò Piat; Bruno Federico; Giovanni Capelli; Francesco Di Stanislao; Pamela Di Giovanni; Francesco Schioppa; Lamberto Manzoli

    2010-01-01

    Background: The “Valentino” cross-sectional study is aimed at evaluating the prevalence and pattern of cigarette smoking according to occupational group in a representative sample of workers aged 18-35 years from Abruzzo, Italy.

    Methods: Randomly selected workers anonymously self-compiled a structured questionnaire containing validated items. Job type was coded according to the I...

  20. Child Maltreatment and Adult Cigarette Smoking: A Long-term Developmental Model

    OpenAIRE

    Topitzes, James; Mersky, Joshua P.; Reynolds, Arthur J.

    2009-01-01

    Objective To examine: (a) child maltreatment’s association with young adult daily cigarette smoking, (b) variations in this association by gender, and (c) mediators of this association. Methods For all study participants (N = 1,125, 94% African American), data from multiple sources (e.g., child welfare records) were collected prospectively at child, adolescent, and young adult time points. Authors enlisted multivariate probit regression for objectives a and b versus exploratory and confirmato...

  1. Cigarette Smoking and its Relationship with Perceived Familial Support and Religiosity of University Students in Tabriz

    OpenAIRE

    Hamid Allahverdipour; Abbas Abbasi-Ghahramanloo; Asghar Mohammadpoorasl; Pouran Nowzari

    2015-01-01

     Objective: The goal of the present study was to assess the prevalence of cigarette smoking and its relationship to other risk taking behaviors, perceived familial support and religiosity among college students in Tabriz, Iran .  Method:In this study, 1837 randomly selected students participated and completed a self-administered questionnaire inquiring demographic characteristics, risk taking behaviors, Aneshensel and Sucoff’s 13-items one-dimensional perceived Parental support scale and 28 -...

  2. Cigarette Smoke (CS) and Nicotine Delay Neutrophil Spontaneous Death via Suppressing Production of Diphosphoinositol Pentakisphosphate

    OpenAIRE

    Xu, Yuanfu; Li, Hongmei; Bajrami, Besnik; Kwak, Hyunjeong; Cao, Shannan; Liu, Peng; Zhou, Jiaxi; Zhou, Yuan; Zhu, Haiyan; Ye, Keqiang; Luo, Hongbo

    2013-01-01

    Diphosphoinositol pentakisphosphate (InsP7), a higher inositol phosphate containing energetic pyrophosphate bonds, is beginning to emerge as a key cellular signaling molecule. However, the various physiological and pathological processes that involve InsP7 are not completely understood. Here we report that cigarette smoke (CS) extract and nicotine reduce InsP7 levels in aging neutrophils. This subsequently leads to suppression of Akt deactivation, a causal mediator of neutrophil spontaneous d...

  3. Chronic inhalation of cigarette smoke reduces phagocytosis in peripheral blood leukocytes

    OpenAIRE

    Tschernig, Thomas; Rabung, Andrea; Voss, Meike; Meier, Carola; Bals, Robert; Beisswenger, Christoph

    2015-01-01

    Background Phagocytosis activity of peripheral blood leukocytes in smokers or chronic obstructive pulmonary disease patients was found to be controversial and dependent on the phagocytic stimulus. Results We demonstrated that long-term exposure to cigarette smoke in mice clearly suppressed the phagocytosis of granulocytes and monocytes from peripheral blood. Conclusions Impaired phagocytosis activity of peripheral blood leukocytes may have a systemic effect and potentially contribute to smoki...

  4. CIGARETTE SMOKING IN SCHIZOPHRENIC PATIENTS THAT ARE CURRENTLY TREATED IN A MEXICAN HOSPITAL

    Directory of Open Access Journals (Sweden)

    Oscar Rodríguez-Mayoral

    2015-06-01

    Full Text Available Objective: tobacco smoking is the most commonly substance abused in psychiatric patients; among them, patients with schizophrenia are the highest abusers. Smoking is related to a decrease in the quality life and life expectancy, as well as interacting with psychotropic drugs. In Mexico, there is not basic descriptive knowledge about the main variables related to cigarette smoking in psychiatric population. The aim of this study was to know the relation among variables (beginning and course of the disease, use of other drugs and times of hospitalization among others and cigarette smoking in a Mexican population of hospitalized schizophrenic patients. Method: The relation between the main variables and smoking were evaluated in a Mexican population of schizophrenic patients while hospitalized. A casuistic sampling was performed in 96 patients diagnosed with schizophrenia and they were divided into three groups: 1 non-smokers, 2 ex-smokers and 3 smokers; according to their score on the Fagerström Test for Nicotine Dependence. Results: The results showed that hospitalized schizophrenic patients smoke 2.7 times more than the general population. Most of these patients showed moderate to high dependence of nicotine, as well as a higher risk for other drugs abuse (marihuana mainly. Most patients started smoking before the first positive symptoms of schizophrenia appeared, and their symptoms started at an earlier age than in patients without a smoking background. Conclusions: Similar studies will allow deepening into specific aspects that modify and or improve the prescribed treatments for each psychiatric patient in hospital settings.

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

    Directory of Open Access Journals (Sweden)

    Yun-Ching Huang

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

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

    Science.gov (United States)

    Huang, Yun-Ching; Chin, Chih-Chien; Chen, Chih-Shou; Shindel, Alan W; Ho, Dong-Ru; Lin, Ching-Shwun; Shi, Chung-Sheng

    2015-01-01

    Cigarette use is an independent risk factor for the development of erectile dysfunction (ED). While the association between chronic smoking and ED is well established, the fundamental mechanism(s) of cigarette-related ED are incompletely understood, partly due to no reliable animal model of smoking-induced ED. The present study was designed to validate an in vivo rat model of chronic cigarette-induced ED. Forty 12-week old male Sprague-Dawley rats were divided into 4 groups. Ten rats served as control group and were exposed only to room air. The remaining 30 rats were passively exposed to cigarette smoke (CS) for 4 weeks (n = 10), 12 weeks (n = 10), and 24 weeks (n = 10). At the 24-week time point all rats were assessed with intracavernous pressure (ICP) during cavernous nerve electrostimulation. Blood and urine were collected to measure serum testosterone and oxidative stress, respectively. Corporal tissue was assessed by Western blot for neuronal nitric oxide synthase (nNOS). Penile tissues were subjected to immunohistochemistry for endothelial, smooth muscle, and apoptotic content. Mean arterial pressure (MAP) was significantly higher in 24-week cigarette exposed animals compared to the control animals. Mean ICP/MAP ratio and cavernosal smooth muscle/endothelial contents were significantly lower in the 12- and 24-week rats compared to control animals. Oxidative stress was significantly higher in the 24-week cigarette exposed group compared to control animals. Mean nNOS expression was significantly lower, and apoptotic index significantly higher, in CS-exposed animals compared to control animals. These findings indicate that the rat model exposure to CS increases apoptosis and oxidative stress and decreases nNOS, endothelial and smooth muscle contents, and ICP in a dose dependent fashion. The rat model is a useful tool for further study of the molecular and cellular mechanisms of CS-related ED. PMID:26491965

  7. Toxicological assessment of kretek cigarettes Part 4: mechanistic investigations, smoke chemistry and in vitro toxicity.

    Science.gov (United States)

    Roemer, E; Dempsey, R; Lawless-Pyne, J; Lukman, S; Evans, A Deger; Trelles-Sticken, E; Wittke, S; Schorp, M K

    2014-12-01

    The smoke chemistry and in vitro toxicity of mainstream smoke (MS) was investigated in American-blended cigarettes with or without the addition of 2.5%, 5% or 10% eugenol to the tobacco and in Indonesian-blended cigarettes with and without the addition of cloves, cloves extracted with hot ethanol, and extracted cloves replenished with eugenol or clove oil. The addition of eugenol reduced the concentration of nearly all toxicants measured in MS as well as the in vitro cytotoxicity of the gas/vapor phase. Reductions were also seen in bacterial mutagenicity of the total particulate matter (TPM) assessed by the Ames Assay. The addition of extracted cloves led to increases and decreases of toxicant concentrations in MS. Replenishment with eugenol or clove oil decreased the toxicant concentrations; with most smoke constituent concentrations reduced below the concentration found in tobacco-only cigarettes. Cytotoxicity of the TPM was not affected by the clove preparations. However, GVP cytotoxicity was reduced (untreated cloves showing the highest reductions). Mutagenicity of TPM was decreased by the clove preparations. Mechanisms for the reductions, (up to 40%), are most likely due to dilution effects by eugenol, changed burning characteristics of the tobacco, and free radical scavenging by eugenol. PMID:25455230

  8. A double isotope dilution method for assaying of polycyclic aromatic hydrocarbons in cigarette smoke condensate

    International Nuclear Information System (INIS)

    This report describes a double isotope dilution method for analysis of the polycyclic aromatic hydrocarbons (PAH) phenanthrene, fluor-anthene, pyrene, and benzo[a]pyrene in cigarette smoke particulates. The first isotope dilution used deuterated analogues of the first three PAH as internal standards. The second isotope dilution, for benzo[a]pyrene, used the tritiated analogue as an internal standard. The PAH were isolated from extracts of cigarette smoke particulates using a two-step procedure based on selective extraction from aqueous dimethyl sulfoxide (DMSO) followed by chromatography on silica gel extraction columns. After isolation, aliquots of the samples were analyzed for phenanthrene, pyrene, and fluoranthene by gas chromatography with mass spectrometric detection (GC/MS). Separate aliquots of the samples were analyzed for benzo[a]pyrene by high pressure liquid chromatography with fluorescence detection followed by liquid scintillation spectrometry. PAH levels from cigarette smoke condensates collected from different exposure modes were compared; no exposure-related differences were found. (author)

  9. Effects of cigarette smoking on I-123 IMP clearance from the lung

    International Nuclear Information System (INIS)

    N-isopropyl-p-I-123-iodoamphetamine (I-123 IMP), originally developed as a brain scanning agent, is also taken up by the lung. To evaluate the cigarette smoking on the uptake of IMP by the lung, we studied I-123 IMP clearance from the lung on 14 volunteers; 5 non-smokers and 9 smokers. After the injection of 111 MBq (3mCi) of I-123 IMP into the medial cubital vein, the time-activity curve for 60 minutes and the regional activity using 1 frame per minute and a 64 x 64 matrix was obtained. I-123 IMP clearance curve was described as follows: C(t)=A1e-k1t+A2e-k2t (A1, A2: intercepts, and k1, k2: slopes of the exponential components). I-123 IMP clearance was delayed in smokers, and k2 was smaller in smokers. Also a significant correlations between k1, k2, and the number of cigarettes smoked per day were found. In conclusion, this study suggests that the delayed clearance and retention of I-123 IMP in the lung indicate the lung metabolic disorders due to cigarette smoking. (author)

  10. Effects of cigarette smoking on iodine 123 N-isopropyl-f-iodoamphetamine clearance from the lung

    International Nuclear Information System (INIS)

    Iodine 123 N-isopropyl-p-iodoamphetamine (123I-IMP), originally developed as a brain scanning agent, is also taken up by the lung. To evaluate the effects of cigarette smoking on the kinetics of IMP in the lung, we studied 123I-IMP clearance from the lung in 18 volunteers (8 non-smokers and 10 smokers). After the injection of 111 MBq of 123I-IMP into the medial cubital vein, the time-activity curve for 60 min and the regional activity using 1 frame per minute and a 64x64 matrix were obtained. The 123I-IMP clearance curve was described as follows: C(t)=A1e(-k1t)+A2e(-k2t)(A1, A2: intercepts, and k1, k2: slopes of the exponential components). 123I-IMP clearance was delayed in smokers, and k2 was smaller in smokers. Also, a correlation between k1, k2, and the number of cigarettes smoked per day was found (r=-0.65, r=-0.74, respectively, P123I-IMP in the lung indicate lung metabolic disorders due to cigarette smoking. (orig.)

  11. The Effect of Cigarette Smoking on Rheumatoid Arthritis.

    Directory of Open Access Journals (Sweden)

    Raouf Rahim Mirza

    2014-08-01

    Materials and Methods: This case control study which is carried out in the rheumatology division of Suliamaniya teaching hospital and clinic from 15th August 2009 to 15th June 2010, Ninety_ two patients 73(79% females and 19(21% males who fulfilled the American College of Rheumatology diagnostic criteria for diagnosis of adult rheumatoid arthritis were included compared to 92 controls. Detail history of smoking taken and disease activity assessed according to DAS28j(Disease activity score of 28 joints. Results: All forty six smoker patients had active disease , 38(82.6% had highly active disease according to DAS28j,these results are statistically significant (P-value =0.04, and 42(91.3% of them had rheumatoid factor which means the positive relation between smoking and seropositivity also (P-value =0.000. Conclusion: Majority of smokers demonstrated highly active disease according to DAS28j measurement for disease activity , and the relation of smoking with seropositivity found to be positive. [Cukurova Med J 2014; 39(4.000: 736-742

  12. Analysis of smoking by South Korean middle school students: shifting preferences in brand choice and rising popularity of Marlboro cigarettes.

    Science.gov (United States)

    Page, Randy M; Romero, Yarazeth Hernandez

    South Korean Global Youth Tobacco Surveys (GYTS) conducted in 2005 and 2008 were analyzed to determine changes in smoking behavior, cigarette brand choices, perceptions of smoking, and exposure to cigarette promotion/marketing and anti-smoking media messages. Results showed an increase in smoking prevalence, media exposure to cigarette advertising, and the offering of free cigarettes from cigarette company representatives, and a decrease in seeing anti-smoking messages and the perception that quitting smoking is difficult. There was a dramatic rise in the popularity of Marlboro as a brand choice among youth smokers in 2005 (9.1%) to 2008 (49.9%). These unfavorable trends suggest a pervasive tobacco industry influence among South Korean youth. Despite the regulations on advertising in South Korea that have been enacted and other anti-smoking policies which have been implemented, it appears that Philip Morris is particularly adept at circumventing advertising and market restrictions while effectively promoting Marlboro brand identity in youth. PMID:23896037

  13. Community-level Adult Daily Smoking Prevalence Moderates the Association between Adolescents’ Cigarette Smoking and Perceived Smoking by Friends

    OpenAIRE

    Thrul, Johannes; Lipperman-Kreda, Sharon; Grube, Joel W.; FRIEND, KAREN B.

    2013-01-01

    Few studies have investigated the complex interactions among the individual- and community-level social risk factors that underlie adolescents’ smoking behaviors. This study investigated whether community-level adult daily smoking prevalence is associated with adolescents’ smoking and whether it moderates the associations between perceived friends’ smoking approval and smoking behavior and adolescents’ own smoking. Self-reported data from 1,190 youths (50.3% female; 13–18 years old) in 50 mid...

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

    Directory of Open Access Journals (Sweden)

    Haider Raza

    2013-05-01

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

  15. Self-administration of nicotine and cigarette smoke extract in adolescent and adult rats.

    Science.gov (United States)

    Gellner, Candice A; Belluzzi, James D; Leslie, Frances M

    2016-10-01

    Although smoking initiation typically occurs during adolescence, most preclinical studies of tobacco use involve adult animals. Furthermore, their focus is largely on nicotine alone, even though cigarette smoke contains thousands of constituents. The present study therefore aimed to determine whether aqueous constituents in cigarette smoke affect acquisition of nicotine self-administration during adolescence in rats. Adolescent and adult male rats, aged postnatal day (P) 25 and 85, respectively, were food trained on a fixed ratio 1 (FR1) schedule, then allowed to self-administer one of 5 doses of nicotine (0, 3.75, 7.5, 15, or 30 μg/kg) or aqueous cigarette smoke extract (CSE) with equivalent nicotine content. Three progressively more difficult schedules of reinforcement, FR1, FR2, and FR5, were used. Both adolescent and adult rats acquired self-administration of nicotine and CSE. Nicotine and CSE similarly increased non-reinforced responding in adolescents, leading to enhanced overall drug intake as compared to adults. When data were corrected for age-dependent alterations in non-reinforced responding, adolescents responded more for low doses of nicotine and CSE than adults at the FR1 reinforcement schedule. No differences in adolescent responding for the two drugs were seen at this schedule, whereas adults had fewer responses for CSE than for nicotine. However, when the reinforcement schedule was increased to FR5, animals dose-dependently self-administered both nicotine and CSE, but no drug or age differences were observed. These data suggest that non-nicotine tobacco smoke constituents do not influence the reinforcing effect of nicotine in adolescents. PMID:27346207

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

    Directory of Open Access Journals (Sweden)

    Postma Dirkje S

    2007-07-01

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

  17. Comparison of the Cytotoxic Potential of Cigarette Smoke and Electronic Cigarette Vapour Extract on Cultured Myocardial Cells

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    Dimitris Tsiapras

    2013-10-01

    Full Text Available Background: Electronic cigarettes (ECs have been marketed as an alternative-to-smoking habit. Besides chemical studies of the content of EC liquids or vapour, little research has been conducted on their in vitro effects. Smoking is an important risk factor for cardiovascular disease and cigarette smoke (CS has well-established cytotoxic effects on myocardial cells. The purpose of this study was to evaluate the cytotoxic potential of the vapour of 20 EC liquid samples and a “base” liquid sample (50% glycerol and 50% propylene glycol, with no nicotine or flavourings on cultured myocardial cells. Included were 4 samples produced by using cured tobacco leaves in order to extract the tobacco flavour. Methods: Cytotoxicity was tested according to the ISO 10993-5 standard. By activating an EC device at 3.7 volts (6.2 watts—all samples, including the “base” liquid and at 4.5 volts (9.2 watts—four randomly selected samples, 200 mg of liquid evaporated and was extracted in 20 mL of culture medium. Cigarette smoke (CS extract from three tobacco cigarettes was produced according to ISO 3308 method (2 s puffs of 35 mL volume, one puff every 60 s. The extracts, undiluted (100% and in four dilutions (50%, 25%, 12.5%, and 6.25%, were applied to myocardial cells (H9c2; percent-viability was measured after 24 h incubation. According to ISO 10993-5, viability of 6.25% (viability: 76.9 ± 2.0% at 6.25%, 38.2 ± 0.5% at 12.5%, 3.1 ± 0.2% at 25%, 5.2 ± 0.8% at 50%, and 3.9 ± 0.2% at 100% extract concentration. Three EC extracts (produced by tobacco leaves were cytotoxic at 100% and 50% extract concentrations (viability range: 2.2%–39.1% and 7.4%–66.9% respectively and one (“Cinnamon-Cookies” flavour was cytotoxic at 100% concentration only (viability: 64.8 ± 2.5%. Inhibitory concentration 50 was >3 times lower in CS extract compared to the worst-performing EC vapour extract. For EC extracts produced by high-voltage and energy, viability was

  18. Effects of Cigarette Smoke Condensate on Oxidative Stress, Apoptotic Cell Death, and HIV Replication in Human Monocytic Cells.

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    Pss Rao

    Full Text Available While cigarette smoking is prevalent amongst HIV-infected patients, the effects of cigarette smoke constituents in cells of myeloid lineage are poorly known. Recently, we have shown that nicotine induces oxidative stress through cytochrome P450 (CYP 2A6-mediated pathway in U937 monocytic cells. The present study was designed to examine the effect of cigarette smoke condensate (CSC, which contains majority of tobacco constituents, on oxidative stress, cytotoxicity, expression of CYP1A1, and/or HIV-1 replication in HIV-infected (U1 and uninfected U937 cells. The effects of CSC on induction of CYP1 enzymes in HIV-infected primary macrophages were also analyzed. The results showed that the CSC-mediated increase in production of reactive oxygen species (ROS in U937 cells is dose- and time-dependent. Moreover, CSC treatment was found to induce cytotoxicity in U937 cells through the apoptotic pathway via activation of caspase-3. Importantly, pretreatment with vitamin C blocked the CSC-mediated production of ROS and induction of caspase-3 activity. In U1 cells, acute treatment of CSC increased ROS production at 6H (>2-fold and both ROS (>2 fold and HIV-1 replication (>3-fold after chronic treatment. The CSC mediated effects were associated with robust induction in the expression of CYP1A1 mRNA upon acute CSC treatment of U937 and U1 cells (>20-fold, and upon chronic CSC treatment to U1 cells (>30-fold. In addition, the CYP1A1 induction in U937 cells was mediated through the aromatic hydrocarbon receptor pathway. Lastly, CSC, which is known to increase viral replication in primary macrophages, was also found to induce CYP1 enzymes in HIV-infected primary macrophages. While mRNA levels of both CYP1A1 and CYP1B1 were elevated following CSC treatment, only CYP1B1 protein levels were increased in HIV-infected primary macrophages. In conclusion, these results suggest a possible association between oxidative stress, CYP1 expression, and viral replication in

  19. Cigarette smoking, nicotine dependence and anxiety disorders: a systematic review of population-based, epidemiological studies

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    Moylan Steven

    2012-10-01

    Full Text Available Abstract Background Multiple studies have demonstrated that rates of smoking and nicotine dependence are increased in individuals with anxiety disorders. However, significant variability exists in the epidemiological literature exploring this relationship, including study design (cross-sectional versus prospective, the population assessed (random sample versus clinical population and diagnostic instrument utilized. Methods We undertook a systematic review of population-based observational studies that utilized recognized structured clinical diagnostic criteria (Diagnostic and Statistical Manual of Mental Disorders (DSM or International Classification of Diseases (ICD for anxiety disorder diagnosis to investigate the relationship between cigarette smoking, nicotine dependence and anxiety disorders. Results In total, 47 studies met the predefined inclusion criteria, with 12 studies providing prospective information and 5 studies providing quasiprospective information. The available evidence suggests that some baseline anxiety disorders are a risk factor for initiation of smoking and nicotine dependence, although the evidence is heterogeneous and many studies did not control for the effect of comorbid substance use disorders. The identified evidence however appeared to more consistently support cigarette smoking and nicotine dependence as being a risk factor for development of some anxiety disorders (for example, panic disorder, generalized anxiety disorder, although these findings were not replicated in all studies. A number of inconsistencies in the literature were identified. Conclusions Although many studies have demonstrated increased rates of smoking and nicotine dependence in individuals with anxiety disorders, there is a limited and heterogeneous literature that has prospectively examined this relationship in population studies using validated diagnostic criteria. The most consistent evidence supports smoking and nicotine dependence as

  20. Radioactivity of cigarettes and the importance of (210)Po and thorium isotopes for radiation dose assessment due to smoking.

    Science.gov (United States)

    Kubalek, Davor; Serša, Gregor; Štrok, Marko; Benedik, Ljudmila; Jeran, Zvonka

    2016-05-01

    Tobacco and tobacco smoke are very complex mixtures. In addition to various chemical and organic compounds they also contain natural radioactive elements (radionuclides). In this work, the natural radionuclide activity concentrations ((234)U, (238)U, (228)Th, (230)Th, (232)Th, (226)Ra, (210)Pb and (210)Po) of nine different cigarette samples available on the Slovenian market are reported. In addition to (210)Po, the transfer of thorium isotopes from a cigarette to a smoker's body and lungs have been determined for the first time. Cigarette smoke and exhaled air from smokers' lungs were collected from volunteer smokers (C-4 brand) to determinate what quantity of (210)Po and thorium isotopes is transferred from the tobacco to the smoker's lungs. Cigarette ash and smoked filters were also collected and analysed. Among the determined isotopes, (210)Pb and (210)Po showed the highest activity concentrations. During the smoking of one cigarette approximately 22% of (210)Po (and presumably its predecessor (210)Pb), 0.6% of (228)Th, 24% of (230)Th, and 31% of (232)Th are transferred from the cigarette and retained in the smoker's body. The estimated annual effective dose for smokers is 61 μSv/year from (210)Po; 9 μSv/year from (210)Pb; 6 μSv/year from (228)Th; 47 μSv/year from (230)Th, and 37 μSv/year from (232)Th. These results show the importance of thorium isotopes in contributing to the annual effective dose for smoking. PMID:26942842

  1. Association between cigarette smoking, APC mutations and the risk of developing sporadic colorectal adenomas and carcinomas

    International Nuclear Information System (INIS)

    The association between colorectal cancer (CRC) and smoking has not been consistent. Incomplete smoking history and association to a specific subset of CRC tumors have been proposed as explanations. The adenomatous polyposis coli (APC) gene has been reported to have a 'gatekeeper' function in the colonic mucosa. To evaluate the hypothesis that cigarette smoking is associated with adenoma and carcinoma development and further to investigate whether this association is due to mutations in the APC gene, we used a study population consisting of 133 cases (45 adenomas and 88 carcinomas) and 334 controls. All tumors were sequenced in the mutation cluster region (MCR) of the APC gene. Cases and controls were drawn from a homogeneous cohort of Norwegian origin. The mutational spectra of the APC gene revealed no difference in frequencies of mutations in cases based on ever and never smoking status. An overall case-control association was detected for adenomas and 'ever smoking' OR = 1.73 (95% CI 0.83–3.58). For CRC cases several smoking parameters for dose and duration were used. We detected an association for all smoking parameters and 'duration of smoking > 30 years', yielded a statistically significant OR = 2.86 (1.06–7.7). When cases were divided based on APC truncation mutation status, an association was detected in adenomas without APC mutation in relation to 'ever smoking', with an OR = 3.97 (1.26–12.51). For CRC cases without APC mutation 'duration of smoking > 30 years', yielded a statistically significant OR = 4.06 (1.20–13.7). The smoking parameter 'starting smoking ≥ 40 years ago' was only associated with CRC cases with APC mutations, OR = 2.0 (0.34–11.95). A case-case comparison revealed similar findings for this parameter, OR = 2.24 (0.73–6.86). Our data suggest an association between smoking and adenoma and CRC development. This association was strongest for cases without APC truncation

  2. Association between cigarette smoking, APC mutations and the risk of developing sporadic colorectal adenomas and carcinomas

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    Hagen Per

    2006-03-01

    Full Text Available Abstract Background The association between colorectal cancer (CRC and smoking has not been consistent. Incomplete smoking history and association to a specific subset of CRC tumors have been proposed as explanations. The adenomatous polyposis coli (APC gene has been reported to have a "gatekeeper" function in the colonic mucosa. Methods To evaluate the hypothesis that cigarette smoking is associated with adenoma and carcinoma development and further to investigate whether this association is due to mutations in the APC gene, we used a study population consisting of 133 cases (45 adenomas and 88 carcinomas and 334 controls. All tumors were sequenced in the mutation cluster region (MCR of the APC gene. Cases and controls were drawn from a homogeneous cohort of Norwegian origin. Results The mutational spectra of the APC gene revealed no difference in frequencies of mutations in cases based on ever and never smoking status. An overall case-control association was detected for adenomas and "ever smoking" OR = 1.73 (95% CI 0.83–3.58. For CRC cases several smoking parameters for dose and duration were used. We detected an association for all smoking parameters and "duration of smoking > 30 years", yielded a statistically significant OR = 2.86 (1.06–7.7. When cases were divided based on APC truncation mutation status, an association was detected in adenomas without APC mutation in relation to "ever smoking", with an OR = 3.97 (1.26–12.51. For CRC cases without APC mutation "duration of smoking > 30 years", yielded a statistically significant OR = 4.06 (1.20–13.7. The smoking parameter "starting smoking ≥ 40 years ago" was only associated with CRC cases with APC mutations, OR = 2.0 (0.34–11.95. A case-case comparison revealed similar findings for this parameter, OR = 2.24 (0.73–6.86. Conclusion Our data suggest an association between smoking and adenoma and CRC development. This association was strongest for cases without APC truncation

  3. Anti-Inflammatory Effects of Lactobacillus Rahmnosus and Bifidobacterium Breve on Cigarette Smoke Activated Human Macrophages.

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    Esmaeil Mortaz

    Full Text Available Chronic obstructive pulmonary disease (COPD is a major global health problem with cigarette smoke (CS as the main risk factor for its development. Airway inflammation in COPD involves the increased expression of inflammatory mediators such as CXCL-8 and IL-1β which are important mediators for neutrophil recruitment. Macrophages are an important source of these mediators in COPD. Lactobacillus rhamnosus (L. rhamnosus and Befidobacterium breve (B. breve attenuate the development of 'allergic asthma' in animals but their effects in COPD are unknown.To determine the anti-inflammatory effects of L. rhamnosus and B. breve on CS and Toll-like receptor (TLR activation.We stimulated the human macrophage cell line THP-1 with CS extract in the presence and absence of L. rhamnosus and B. breve and measured the expression and release of inflammatory mediators by RT-qPCR and ELISA respectively. An activity assay and Western blotting were used to examine NF-κB activation.Both L. rhamnosus and B. breve were efficiently phagocytized by human macrophages. L. rhamnosus and B. breve significantly suppressed the ability of CS to induce the expression of IL-1β, IL-6, IL-10, IL-23, TNFα, CXCL-8 and HMGB1 release (all p<0.05 in human THP-1 macrophages. Similar suppression of TLR4- and TLR9-induced CXCL8 expression was also observed (p<0.05. The effect of L. rhamnosus and B. breve on inflammatory mediator release was associated with the suppression of CS-induced NF-κB activation (p<0.05.This data indicate that these probiotics may be useful anti-inflammatory agents in CS-associated disease such as COPD.

  4. Cigarette smoking in military pilots and intima-media thickness of the carotid arteries

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    Jovelić Stojan

    2005-01-01

    Full Text Available 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 distal 1 cm of both common carotid arteries was performed using a B mode ultrasound device, in 39 pilots (37.05 ± 6.66 years, for whom smoking was the single cardiovascular risk factor. Comparisons were made with 49 non-smokers (35.12 ± 7.39 years. Results. The posterior walls of both common carotid arteries were thicker in smokers (left, p < 0.05; right, p > 0,05. Intima-media thickness was significantly lower on the right side than on the left side in both smokers and nonsmokers (p < 0.01. Conclusion. Cigarette smoking as the single cardiovascular risk factor was associated with the wall thickness of the carotid arteries in our study. This finding indicated that early atherosclerosis was already present in pilots - smokers entering middle age.

  5. Cigarette smoking and radiation exposure in relation to cancer mortality, Hiroshima and Nagasaki

    International Nuclear Information System (INIS)

    Cancer mortality among 40,498 Hiroshima and Nagasaki residents was examined in relation to cigarette smoking habits and estimated atomic bomb radiation exposure. Relative risk models that are either multiplicative or additive in the two exposures (smoking radiation) were emphasized. Most analyses were directed toward all nonhematologic cancer, stomach cancer, lung cancer, or digestive cancer other than stomach, for which there were, respectively, 1,725, 658, 281, and 338 deaths in the follow-up period of this study. Persons heavily exposed to both cigarette smoke and radiation were found to have significantly lower cancer mortality than multiplcative relative risk models would suggest for all nonhematologic cancer, stomach cancer, and digestive cancer other than stomach. Surprisingly, the relative risk function appeared not only to be submultiplicative for these cancer sites, but to be subadditive as well. The lung cancer relative risk function could not be distinguished from either a multiplicative or an additive form. The number of deaths was sufficient to permit some more detailed study of all nonhematologic cancer mortality: Relative risk functions appeared to be consistent between males and females though a paucity of heavy smoking females limits the precision of this comparison. (author)

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1996-03-01

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

  7. Correlates of experimentation with smoking and current cigarette consumption among adolescents

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    Amanda Gimenes Bonilha

    2014-12-01

    Full Text Available OBJECTIVE: The aim of this study was to analyze social characteristics and stress as correlates of cigarette smoking in adolescence. The main intent was to identify elements that distinguish adolescents who had experimented with smoking and did not progress to regular smoking from those who became current smokers. METHODS: Students at 10 high schools in the city of Ribeirão Preto, Brazil, complet