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Sample records for cigarette smoke-induced pulmonary

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

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    Zhi-Hua Chen

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

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

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    Nesi RT

    2016-03-01

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

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

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    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

  4. 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

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

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    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

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

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    G. Vani

    2015-01-01

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

  7. 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.

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

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    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

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

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    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

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

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    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...

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

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    ZOU Ni; HONG Jiang; DAI Qiu-yan

    2009-01-01

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

  12. 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

  13. 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.

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

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    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

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

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    Jean Pierre Schatzmann Peron

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

  16. 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

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

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    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 ...

  18. 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.

  19. 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.

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

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    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.

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

    Institute of Scientific and Technical Information of China (English)

    林纯意

    2012-01-01

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

  2. 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

  3. 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.

  4. 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

  5. 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

  6. 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)...

  7. 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.

  8. 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

  9. 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

  10. Assessment of smoking-induced impairment of pulmonary perfusion using three-dimensional SPECT images

    International Nuclear Information System (INIS)

    The effects of smoking on ventilation-perfusion lung scintigrams were investigated. The subjects comprised 40 healthy males (28 smokers and 12 nonsmokers) without a history of cardiopulmonary disease and with normal chest radiographs. After acquisition of planar images of ventilation lung scintigrams with 370 MBq of 133Xe gas, planar images and SPECT images of pulmonary perfusion flow were obtained using 185 MBq of 99mTc-MAA. Planar imaging showed perfusion defects in only 5 smokers. In contrast, 16 subjects were found to have perfusion defects on SPECT images (p133Xe in 4 smokers, suggesting that smoking-induced abnormal perfusion on SPECT appears earlier than impaired ventilation on scintigrams. (author)

  11. 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...

  12. 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

  13. 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...

  14. Assessment of smoking-induced impairment of pulmonary perfusion using three-dimensional SPECT images

    Energy Technology Data Exchange (ETDEWEB)

    Miyasaka, Takashi [Toho Univ., Tokyo (Japan). School of Medicine

    1997-09-01

    The effects of smoking on ventilation-perfusion lung scintigrams were investigated. The subjects comprised 40 healthy males (28 smokers and 12 nonsmokers) without a history of cardiopulmonary disease and with normal chest radiographs. After acquisition of planar images of ventilation lung scintigrams with 370 MBq of {sup 133}Xe gas, planar images and SPECT images of pulmonary perfusion flow were obtained using 185 MBq of {sup 99m}Tc-MAA. Planar imaging showed perfusion defects in only 5 smokers. In contrast, 16 subjects were found to have perfusion defects on SPECT images (p<0.05), indicating the usefulness of SPECT images in detecting minor vascular damage of the lung. Although perfusion defects were common in the smokers (p<0.05), their relationship to the BRINKMAN index was uncertain. The perfusion defects found in the smokers were nonsegmental and commonly involved the right upper lobe. Ventilation scans revealed only delayed washout of {sup 133}Xe in 4 smokers, suggesting that smoking-induced abnormal perfusion on SPECT appears earlier than impaired ventilation on scintigrams. (author)

  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. 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

    proliferation and tumorigenicity of lung cancer cells; knock-down of miR-31 inhibited growth of these cells. CONCLUSIONS: Cigarette smoke induces expression of miR-31 targeting several antagonists of cancer stem cell signaling in normal respiratory epithelia and lung cancer cells. miR-31 functions as an oncomir during human pulmonary carcinogenesis.

  17. 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

  18. Long-term effects of acupuncture treatment on airway smooth muscle in a rat model of smoke-induced chronic obstructive pulmonary disease

    Science.gov (United States)

    Li, Jia; Wu, Song; Tang, Hongtu; Huang, Wei; Wang, Lushan; Zhou, Huanjiao; Zhou, Miao; Wang, Hua; Li, Jing

    2016-01-01

    Background Chronic obstructive pulmonary disease (COPD) is one of the most common lung diseases. It is a chronic inflammatory process characterised by airway obstruction and progressive lung inflammation, associated with difficulty breathing and insensitivity to corticosteroid therapy. Although there is some preliminary evidence to suggest a beneficial effect of acupuncture on COPD, its mechanism of action has not been investigated. Our aim was to examine the anti-inflammatory effects of acupuncture in a rat model of COPD induced by exposure to cigarette smoke (CS). Methods Sixty Sprague–Dawley rats were exposed to the smoke of 15 cigarettes for 1 h/day, 6 days/week for 3 months to induce COPD and treated with acupuncture at BL13 (Feishu), BL23 (Shenshu) and Dingchuan (COPD+Acupuncture, n=15), sham acupuncture (COPD+Sham, n=15) or left untreated (n=15). Exposed rats were compared with controls not exposed to CS (control, n=15). Pulmonary function was measured, and tumour necrosis factor-α (TNF-α) and interleukin-8 (IL-8) levels were determined in bronchoalveolar lavage fluid by ELISA. Histone deacetylase 2 (HDAC2) protein and mRNA expression were examined in lung tissue and in bronchus. Results Acupuncture treatment appeared to protect pulmonary function and reduce the COPD-induced inflammatory response by decreasing cell inflammation and the production of TNF-α and IL-8. Acupuncture also enhanced HDAC2 mRNA and protein expression, suggesting a possible direct effect on protein structure through post-translational modifications. Conclusions Our results suggest that acupuncture regulates inflammatory cytokines and contributes to lung protection in a rat model of smoke-induced COPD by modulating HDAC2. PMID:26345700

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

    Institute of Scientific and Technical Information of China (English)

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

    2016-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Min-Chao Duan

    2013-01-01

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

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

    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

  2. Early smoking-induced lung lesions in asymptomatic subjects. Correlations between high resolution dynamic CT and pulmonary function testing

    International Nuclear Information System (INIS)

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

  3. 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

  4. 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

  5. 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)

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

    Directory of Open Access Journals (Sweden)

    Victoria L Palmer

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

  7. 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.

  8. 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

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

    International Nuclear Information System (INIS)

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

  10. 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.

  11. 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.

  12. Protective effects of dandelion honey on initiative sigarette smoking induced pulmonary injury in mice%蒲公英蜂蜜对主动吸烟小鼠肺组织SOD的影响

    Institute of Scientific and Technical Information of China (English)

    赵华; 吴铁

    2009-01-01

    Objective To observe the protective effects of dandelion honey-extraction on cigarette smoking-induced pulmonary injury in mice. Methods Kunming mice were randomly divided into 3 groups:healthy control group,model group and dandelion honey group.Except healthy control group, the others were exposed to cigarette smoking, bid, 30 minutes/ day for 7 weeks.At the same time.the mice of dandelion honey group were given dandelion honey, bid for 7 weeks ,the mice of healthy control group were given distilled water.bid for 7 weeks.The pathologic changes of airways and lung tissues were determined.The active of SOD were measured. Results Cigarette smoking reduced the activity of SOD ain the model group,yet the activity of SOD increased in dandelion honey group. Conclusion Dandelion honey has the protective effect on cigarette smoking-induced injury.The mechanism may due to its antioxidation.%目的 观察蜂蜜对吸烟小鼠肺组织超氧化物歧化酶(SOD)的影响.方法 昆明种小鼠,随机分为3组,即正常对照组,吸烟模型组,蒲公英蜂蜜组.正常对照组小鼠不吸烟,其余两组连续吸烟7周,1d2次,30min/次.蒲公英蜂蜜组给予蒲公英蜂蜜每d2次,同时正常组每天用蒸馏水作对照.7周后处死动物,右肺组织做成匀浆,检测肺组织匀浆中SOD含量. 结果吸烟组小鼠肺部SOD活性明显降低,蒲公英蜂蜜组小鼠肺部的SOD活性增加. 结论蒲公英蜂蜜对小鼠吸烟造成肺组织病理损害有保护作用,其作用机制可能和蒲公英蜂蜜在肺部发挥的抗氧化作用等有关.

  13. 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

  14. 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)

  15. 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

  16. 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

  17. 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

  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. 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

  20. 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...

  1. 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

  2. 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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2013-09-01

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

  4. 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

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

    Science.gov (United States)

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

    1989-11-01

    Two weeks exposure of rats to cigarette smoke (CS) significantly (p less than 0.05) increased the secretion of fucose-containing glycoconjugates above normal in an in situ preparation of larynx and trachea. After equilibration mean basal secretion in CS-exposed rats was 24 micrograms (per 30 min collection) which was 8 times higher than that of unexposed animals (p less than 0.01). N-acetylcysteine (NAC) or S-carboxymethylcysteine (SCMC) given as 1% of the drinking water, before and after daily exposure to CS, significantly inhibited the development of the CS-induced increase in fucose secretion reducing the mean for basal secretion in each group to 7 and 5 micrograms, respectively (p less than 0.05). Neither NAC nor SCMC had significant effects on baseline glycoconjugate secretion in control animals. Albumin was inconsistently present in the secretions of both control and CS-exposed animals, whereas in those exposed to CS and also given one of the two cysteine derivatives there was a consistent increase in albumin transudation. PMID:2532606

  6. Pulmonary langerhans cell histiocytosis

    OpenAIRE

    Suri Harpreet S; Yi Eunhee S; Nowakowski Gregorz S; Vassallo Robert

    2012-01-01

    Abstract Pulmonary Langerhans Cell Histiocytosis (PLCH) is a relatively uncommon lung disease that generally, but not invariably, occurs in cigarette smokers. The pathologic hallmark of PLCH is the accumulation of Langerhans and other inflammatory cells in small airways, resulting in the formation of nodular inflammatory lesions. While the overwhelming majority of patients are smokers, mechanisms by which smoking induces this disease are not known, but likely involve a combination of events r...

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

    Directory of Open Access Journals (Sweden)

    Gang Chen

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

  8. 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

  9. Rapid improvement in abnormal pulmonary epithelial permeability after stopping cigarettes

    OpenAIRE

    Minty, Barbara D; Jordan, C.; Jones, J G

    1981-01-01

    A new, non-invasive method of measuring pulmonary epithelial damage in man was compared with traditional tests of small-airway function. Pulmonary epithelial permeability was expressed as the half-time clearance from the lung into blood of 99mTc-diethylene triaminepenta-acetic acid (99mTc-DTPA) deposited predominantly in the alveoli from an inhaled aerosol.

  10. 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...

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

    Directory of Open Access Journals (Sweden)

    Nagai A

    2003-09-01

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

  12. Autoimmunity in chronic obstructive pulmonary disease: clinical and experimental evidence

    OpenAIRE

    Kheradmand, Farrah; Shan, Ming; Xu, Chuang; Corry, David B.

    2012-01-01

    Over the past few decades, neutrophils and macrophages had co-occupied center stage as the critical innate immune cells underlying the pathobiology of cigarette smoke-induced chronic obstructive pulmonary disease and lung parenchymal destruction (i.e., emphysema). While chronic exposure to smoke facilitates the recruitment of innate immune cells into the lung, a clear role for adaptive immunity in emphysema has emerged. Evidence from human studies specifically point to a role for recruitment ...

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

    Science.gov (United States)

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

    2015-09-01

    This study was undertaken to determine the influence of Aloe vera (AV) on changes induced in pulmonary tissue of cigarette smoke (CS) inhaling mice. CS inhalation for 4 weeks caused pulmonary damage as evident by histoarchitectural alterations and enhanced serum and tissue lactate dehydrogenase (LDH) activities. CS inhalation also led to increased mucin production as revealed by mucicarmine and Alcian Blue-Periodic Acid Schiff (AB-PAS) staining. Studies on bronchoalveolar lavage fluid (balf) of CS exposed animals revealed structural changes in phospholipids and increase in surface tension when compared with control counterparts. These changes were accompanied by enhanced nitric oxide (NO) levels, citrulline levels, peroxidative damage, and differential modulation of antioxidant defense system. AV administration (seven weeks, 500 mg/kg b.w. daily) to CS inhaling mice led to modulation of CS induced pulmonary changes as revealed by lesser degree of histoarchitectural alterations, lesser mucin production, decreased NO levels, citrulline levels, peroxidative damage, and serum LDH activity. AV treatment to CS inhaling mice was associated with varying response to antioxidant defense system, however balf of CS + AV treated animals did not exhibit appreciable changes when compared with that of CS exposed animals. These observations suggest that AV has the potential to modulate CS induced changes in the pulmonary tissue which could have implications in management of CS associated pulmonary diseases, however, further investigations are required to explore its complete mechanism of action. PMID:24615921

  14. 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...

  15. Effects of Melatonin and Vitamin C on Smoke Induced Structural Changes in Liver

    OpenAIRE

    ÇOLAKOĞLU, Neriman; OZAN, Enver; SÖNMEZ, Mehmet Fatih; Yilmaz, Seval; Ozan, Gonca

    2005-01-01

    Objectives: This study was undertaken to investigate smoke-induced structural and biochemical changes and protective effects of co-administred of melatonin and vitamin C in the liver. Materials and Methods: Twenty-four Wistar adult female rats were used in this study. Animals were divided into four groups. The first group rats used as control. The second group of rats were inhaleted cigarette. Cigarette inhaleted third and fourth group rats recieved melatonin and vitamin C respectively. En...

  16. Emphysema and pulmonary impairment in coal miners: Quantitative relationship with dust exposure and cigarette smoking

    Science.gov (United States)

    Kuempel, E. D.; Vallyathan, V.; Green, F. H. Y.

    2009-02-01

    Coal miners have been shown to be at increased risk of developing chronic obstructive pulmonary diseases including emphysema. The objective of this study was to determine whether lifetime cumulative exposure to respirable coal mine dust is a significant predictor of developing emphysema at a clinically-relevant level of severity by the end of life, after controlling for cigarette smoking and other covariates. Clinically-relevant emphysema severity was determined from the association between individuals' lung function during life (forced expiratory volume in one second, FEV1, as a percentage of predicted normal values) and emphysema severity at autopsy (as the proportion of lung tissue affected). In a logistic regression model, cumulative exposure to respirable coal mine dust was a statistically significant predictor of developing clinically-relevant emphysema severity, among both ever-smokers and never-smokers. The odds ratio for developing emphysema associated with FEV1 <80% at the cohort mean cumulative coal dust exposure (87 mg/m3 x yr) was 2.30 (1.46-3.64, 95% confidence limits), and at the cohort mean cigarette smoking (among smokers: 42 pack-years) was 1.95 (1.39-2.79).

  17. Emphysema and pulmonary impairment in coal miners: Quantitative relationship with dust exposure and cigarette smoking

    International Nuclear Information System (INIS)

    Coal miners have been shown to be at increased risk of developing chronic obstructive pulmonary diseases including emphysema. The objective of this study was to determine whether lifetime cumulative exposure to respirable coal mine dust is a significant predictor of developing emphysema at a clinically-relevant level of severity by the end of life, after controlling for cigarette smoking and other covariates. Clinically-relevant emphysema severity was determined from the association between individuals' lung function during life (forced expiratory volume in one second, FEV1, as a percentage of predicted normal values) and emphysema severity at autopsy (as the proportion of lung tissue affected). In a logistic regression model, cumulative exposure to respirable coal mine dust was a statistically significant predictor of developing clinically-relevant emphysema severity, among both ever-smokers and never-smokers. The odds ratio for developing emphysema associated with FEV1 3 x yr) was 2.30 (1.46-3.64, 95% confidence limits), and at the cohort mean cigarette smoking (among smokers: 42 pack-years) was 1.95 (1.39-2.79).

  18. Emphysema and pulmonary impairment in coal miners: quantitative relationship with dust exposure and cigarette smoking

    Energy Technology Data Exchange (ETDEWEB)

    E.D. Kuempel; V. Vallyathan; F.H.Y. Green [National Institute for Occupational Safety and Health, Cincinnati, OH (United States)

    2009-07-01

    Coal miners have been shown to be at increased risk of developing chronic obstructive pulmonary diseases including emphysema. The objective of this study was to determine whether lifetime cumulative exposure to respirable coal mine dust is a significant predictor of developing emphysema at a clinically-relevant level of severity by the end of life, after controlling for cigarette smoking and other covariates. Clinically-relevant emphysema severity was determined from the association between individuals' lung function during life (forced expiratory volume in one second, FEV{sub 1}, as a percentage of predicted normal values) and emphysema severity at autopsy (as the proportion of lung tissue affected). In a logistic regression model, cumulative exposure to respirable coal mine dust was a statistically significant predictor of developing clinically-relevant emphysema severity, among both ever-smokers and never-smokers. The odds ratio for developing emphysema associated with FEV1 <80% at the cohort mean cumulative coal dust exposure (87 mg/m{sup 3} x yr) was 2.30 (1.46-3.64, 95% confidence limits), and at the cohort mean cigarette smoking (among smokers: 42 pack-years) was 1.95 (1.39-2.79). 20 refs., 2 figs., 2 tabs.

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

    Science.gov (United States)

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

    2012-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Mathieu C Morissette

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

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

    Directory of Open Access Journals (Sweden)

    Xiang Zhou

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

  2. 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...

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

    Directory of Open Access Journals (Sweden)

    Thomas E Sussan

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

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

    Science.gov (United States)

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

    2015-01-01

    Electronic cigarettes (E-cigs) have experienced sharp increases in popularity over the past five years due to many factors, including aggressive marketing, increased restrictions on conventional cigarettes, and a perception that E-cigs are healthy alternatives to cigarettes. Despite this perception, studies on health effects in humans are extremely limited and in vivo animal models have not been generated. Presently, we determined that E-cig vapor contains 7 x 10(11) free radicals per puff. To determine whether E-cig exposure impacts pulmonary responses in mice, we developed an inhalation chamber for E-cig exposure. Mice that were exposed to E-cig vapor contained serum cotinine concentrations that are comparable to human E-cig users. E-cig exposure for 2 weeks produced a significant increase in oxidative stress and moderate macrophage-mediated inflammation. Since, COPD patients are susceptible to bacterial and viral infections, we tested effects of E-cigs on immune response. Mice that were exposed to E-cig vapor showed significantly impaired pulmonary bacterial clearance, compared to air-exposed mice, following an intranasal infection with Streptococcus pneumonia. This defective bacterial clearance was partially due to reduced phagocytosis by alveolar macrophages from E-cig exposed mice. In response to Influenza A virus infection, E-cig exposed mice displayed increased lung viral titers and enhanced virus-induced illness and mortality. In summary, this study reports a murine model of E-cig exposure and demonstrates that E-cig exposure elicits impaired pulmonary anti-microbial defenses. Hence, E-cig exposure as an alternative to cigarette smoking must be rigorously tested in users for their effects on immune response and susceptibility to bacterial and viral infections. PMID:25651083

  5. 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

  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. 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

  8. 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

  9. Pulmonary functions of narghile smokers compared to cigarette smokers: a case-control study

    OpenAIRE

    Ben Saad, Helmi; Khemiss, Mehdi; Nhari, Saida; Ben Essghaier, Mejda; Rouatbi, Sonia

    2013-01-01

    Background: Studies of the lung function profiles of exclusive narghile smokers (ENS) are few, have some methodological limits, and present contradictory conclusions. The present study aimed to compare the plethysmographic profiles of ENS with age- and height-matched exclusive cigarette smokers (ECS).Methods: Males aged 35–60 living in Sousse, Tunisia, who have been smoking narghile exclusively for more than 10 narghile-years (n = 36) or cigarettes exclusively for more than 10 pack-years (n =...

  10. The expression and mechanisms of interleukin-17 in CD8+ T cells of mice with cigarette smoke-induced emphysema%肺气肿小鼠肺组织CD8+ IL-17+T细胞变化及作用机制

    Institute of Scientific and Technical Information of China (English)

    段敏超; 钟小宁; 黄颖; 何志义; 唐海娟

    2011-01-01

    Objective To evaluate the expression of Tc17 in a cigarette smoke-induced mice model of emphysema.To explore the probable mechanisms about how Tc17 cells to elevate in lungs of mice.Methods Forty male Balb/c mice were randomly divided into four groups,including control group ( 12 weeks,C12),control group (24 weeks,C24),smoke-exposure group (12 weeks,S12) and smoke-exposure group (24 weeks,S24 ),10 mice each group,Emphysema of mice was observed by HE pigmentation.Morphological changes were evaluated by mean linear intercepts (Lm) and destructive index (DI).The proportion of CD8+ IL-17 + Tc17,CD8+ IL-17 + CC chemokine receptor type 6 ( CCR6 ) + and 6CCR6 + Tc17 cells in lungs of mice was determined by flow cytometry.The mRNA expressions of retinoidrelated orphan nuclear receptor(RORγt) and IL-17 were evaluated by real-time PCR.The levels of IL-1 β,IL-6,IL-23,transforming growth factor β (TGFβ) and CC chemokine ligand 20 (CCL20) were tested by ELISA.Correlations among these indexes were analyzed.Results Lm and DI were significantly higher in S12 and S24 than in C12 and C24,S24 in particular (t value 4.378-15.188,all P < 0.05).The percentages of Tc17 in S12 and S24[(9.28 ± 1.12)%,( 13.13 ±3.56)%]was significantly increased as compared with that in C12 and C24[(2.40 ±0.60 )%,(2.64 ±0.96 )%],S24 in particular.The mRNA levels of RORγt and IL-17 in S12 and S24 were higher than in C12 and C24,S12 and S24 in particular.There was significant difference (all P <0.05 ).The frequency of Tc17 cells had a positive correlation with Lm and DI ( r value were 0.734 and 0.884 respectively,P < 0.01 ).The percentages of CD8+ IL-17 + CCR6 +T cells and CCR6 + Tc17 were significantly elevated in S12 and S24 compared to C12 and C24,S24 in particular (all P < 0.05 ).There was positive correlation between Tc17 cell ratio and CCL20 levels( r =0.899,P <0.01 ).The levels of IL-1 β,IL-6,IL-23 and TGFβ in S12 and S24 were significantly increased as compared with that in C12 and

  11. Particle doses in the pulmonary lobes of electronic and conventional cigarette users

    International Nuclear Information System (INIS)

    The main aim of the present study was to estimate size segregated doses from e-cigarette aerosols as a function of the airway generation number in lung lobes. After a 2-second puff, 7.7 × 1010 particles (DTot) with a surface area of 3.6 × 103 mm2 (STot), and 3.3 × 1010 particles with a surface area of 4.2 × 103 mm2 were deposited in the respiratory system for the electronic and conventional cigarettes, respectively. Alveolar and tracheobronchial deposited doses were compared to the ones received by non-smoking individuals in Western countries, showing a similar order of magnitude. Total regional doses (DR), in head and lobar tracheobronchial and alveolar regions, ranged from 2.7 × 109 to 1.3 × 1010 particles and 1.1 × 109 to 5.3 × 1010 particles, for the electronic and conventional cigarettes, respectively. DR in the right-upper lung lobe was about twice that found in left-upper lobe and 20% greater in right-lower lobe than the left-lower lobe. - Highlights: • Lobar doses were compared for mainstreams of electronic and conventional cigarettes. • Aerosol doses from e-cigarettes were more than double that from conventional ones. • Doses from a 2-s puff exceed the daily doses of a no smoking Australian subject. • Highest deposition densities occurred at the lobar bronchi. • Aerosol deposition was greater in the right than in the left lung lobes. - Lobar bronchi and right lung lobes represent sites where effects of the aerosol from e-cigarette smoke may be more likely to occur

  12. Pulmonary langerhans cell histiocytosis

    Directory of Open Access Journals (Sweden)

    Suri Harpreet S

    2012-03-01

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

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

    Science.gov (United States)

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

    2014-01-01

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2005-02-01

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

  15. HDAC3 mediates smoking-induced pancreatic cancer

    Science.gov (United States)

    Edderkaoui, Mouad; Xu, Shiping; Chheda, Chintan; Morvaridi, Susan; Hu, Robert W.; Grippo, Paul J.; Mascariñas, Emman; Principe, Daniel R.; Knudsen, Beatrice; Xue, Jing; Habtezion, Aida; Uyeminami, Dale; Pinkerton, Kent E.; Pandol, Stephen J.

    2016-01-01

    Smoking is a major risk factor for developing pancreatic adenocarcinoma (PDAC); however, little is known about the mechanisms involved. Here we employed a genetic animal model of early stages of PDAC that overexpresses oncogenic Kras in the pancreas to investigate the mechanisms of smoking-induced promotion of the disease in vivo. We confirmed the regulation of the interactions between the tumor microenvironment cells using in vitro cellular systems. Aerial exposure to cigarette smoke stimulated development of pancreatic intraepithelial neaoplasia (PanIN) lesions associated with a tumor microenvironment-containing features of human PDAC including fibrosis, activated stellate cells, M2-macrophages and markers of epithelial-mesenchymal transition (EMT). The pro-cancer effects of smoking were prevented by Histone Deacetylase HDAC I/II inhibitor Saha. Smoking decreased histone acetylation associated with recruitment of and phenotypic changes in macrophages; which in turn, stimulated survival and induction of EMT of the pre-cancer and cancer cells. The interaction between the cancer cells and macrophages is mediated by IL-6 produced under the regulation of HDAC3 translocation to the nucleus in the cancer cells. Pharmacological and molecular inhibitions of HDAC3 decreased IL-6 levels in cancer cells. IL-6 stimulated the macrophage phenotype change through regulation of the IL-4 receptor level of the macrophage. This study demonstrates a novel pathway of interaction between cancer cells and tumor promoting macrophages involving HDAC3 and IL-6. It further demonstrates that targeting HDAC3 prevents progression of the disease and could provide a strategy for treating the disease considering that the HDAC inhibitor we used is FDA approved for a different disease. PMID:26745602

  16. Pneumocystis murina Infection and Cigarette Smoke Exposure Interact To Cause Increased Organism Burden, Development of Airspace Enlargement, and Pulmonary Inflammation in Mice▿

    OpenAIRE

    Christensen, Paul J; Preston, Angela M.; Ling, Tony; Du, Ming; Fields, W. Bradley; Curtis, Jeffrey L.; Beck, James M.

    2008-01-01

    Chronic obstructive pulmonary disease (COPD) is characterized by the presence of airflow obstruction and lung destruction with airspace enlargement. In addition to cigarette smoking, respiratory pathogens play a role in pathogenesis, but specific organisms are not always identified. Recent reports demonstrate associations between the detection of Pneumocystis jirovecii DNA in lung specimens or respiratory secretions and the presence of emphysema in COPD patients. Additionally, human immunodef...

  17. Time to First Morning Cigarette and Risk of Chronic Obstructive Pulmonary Disease: Smokers in the PLCO Cancer Screening Trial.

    Directory of Open Access Journals (Sweden)

    Kristin A Guertin

    Full Text Available Time to first cigarette (TTFC after waking is an indicator of nicotine dependence. The association between TTFC and chronic obstructive pulmonary disease (COPD, the third leading cause of death in the United States, has not yet been reported.We investigated the cross-sectional association between TTFC and prevalent COPD among 6,108 current smokers in the Prostate, Lung, Colorectal, and Ovarian (PLCO Cancer Screening Trial. COPD was defined as a self-reported diagnosis of emphysema, chronic bronchitis, or both. Current smokers in PLCO reported TTFC, the amount of time they typically waited before smoking their first cigarette of the day after waking, in four categories: ≤ 5, 6-30, 31-60, or > 60 minutes. We used logistic regression models to investigate the association between TTFC and prevalent COPD with adjustments for age, gender, race, education, and smoking (cigarettes/day, years smoked during lifetime, pack-years, age at smoking initiation, and prior lung cancer diagnosis.COPD was reported by 19% of these 6,108 smokers. Individuals with the shortest TTFC had the greatest risk of COPD; compared to those with the longest TTFC (> 60 minutes the adjusted odds ratios (OR and 95% confidence intervals (CI for COPD were 1.48 (95% CI, 1.15-1.91, 1.64 (95% CI, 1.29-2.08, 2.18 (95% CI, 1.65-2.87 for those with TTFC 31-60 minutes, 6-30 minutes, and ≤ 5 minutes, respectively (P-trend 60 minutes, the adjusted OR (95% CI was 2.29 (1.69-3.12 for emphysema and 2.99 (1.95-4.59 for chronic bronchitis.Current smokers with shorter TTFC have increased risk of COPD compared to those with longer TTFC, even after comprehensive adjustment for established smoking covariates. Future epidemiologic studies, including prospective designs, should incorporate TTFC to better assess disease risk and evaluate the potential utility of TTFC as a COPD screening tool for smokers in the clinical setting.

  18. 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

  19. Electronic Cigarettes

    Science.gov (United States)

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

  20. Expiratory CT in cigarette smokers: correlation between areas of decreased lung attenuation, pulmonary function tests and smoking history

    International Nuclear Information System (INIS)

    The aim of this study was to determine the correlation between cigarette-smoke-related bronchial disease and air trapping as assessed by expiratory high-resolution CT (HRCT) scans. Thirty healthy subjects (11 non-smokers, 7 ex-smokers for > 2 years, 12 current smokers; age range 35-55 years) with a smoking history between 0 and 28.5 pack-years underwent pulmonary function tests (PFT) and HRCT in inspiration and expiration in supine and prone position. The extent of air trapping was scored in ventral and dorsal aspects of the upper, middle and lower lung portions. In 24 subjects (7 non-smokers, 7 ex-smokers, 10 current smokers) areas of focal air trapping were found, and were present significantly more often in dependent lung portions (p < 0.05) compared with non-dependent portions. No significant differences were found between apical and basal lung zones. Scores of focal air trapping were not significantly different between smokers and ex-smokers, but were significantly lower (p < 0.05) in non-smokers and showed a significant (p < 0.0005) correlation with pack-years. The degree of air trapping was also associated with several lung function tests, especially RV, DLCO, FRC, FEV1 and FEV1/VC. Air trapping is seen in smokers with normal PFT and correlates with the severity of the smoking history, independently of current smoking status. (orig.) (orig.)

  1. Expiratory CT in cigarette smokers: correlation between areas of decreased lung attenuation, pulmonary function tests and smoking history

    Energy Technology Data Exchange (ETDEWEB)

    Verschakelen, J.A.; Scheinbaum, K.; Bogaert, J.; Baert, A.L. [Department of Radiology, University Hospitals, Leuven (Belgium); Demedts, M.; Lacquet, L.L. [Department of Pneumology, University Hospitals, Leuven (Belgium)

    1998-10-01

    The aim of this study was to determine the correlation between cigarette-smoke-related bronchial disease and air trapping as assessed by expiratory high-resolution CT (HRCT) scans. Thirty healthy subjects (11 non-smokers, 7 ex-smokers for > 2 years, 12 current smokers; age range 35-55 years) with a smoking history between 0 and 28.5 pack-years underwent pulmonary function tests (PFT) and HRCT in inspiration and expiration in supine and prone position. The extent of air trapping was scored in ventral and dorsal aspects of the upper, middle and lower lung portions. In 24 subjects (7 non-smokers, 7 ex-smokers, 10 current smokers) areas of focal air trapping were found, and were present significantly more often in dependent lung portions (p < 0.05) compared with non-dependent portions. No significant differences were found between apical and basal lung zones. Scores of focal air trapping were not significantly different between smokers and ex-smokers, but were significantly lower (p < 0.05) in non-smokers and showed a significant (p < 0.0005) correlation with pack-years. The degree of air trapping was also associated with several lung function tests, especially RV, DLCO, FRC, FEV1 and FEV1/VC. Air trapping is seen in smokers with normal PFT and correlates with the severity of the smoking history, independently of current smoking status. (orig.) (orig.) With 4 figs., 4 tabs., 59 refs.

  2. 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

  3. Anti-inflammatory effects of montelukast on smoke-induced lung injury in rats

    Directory of Open Access Journals (Sweden)

    Basyigit Ilknur

    2010-04-01

    Full Text Available Abstract Aim To evaluate the effects of montelukast in smoke-induced lung injury. Methods 28 Wistar-Albino rats were enrolled into 4 groups with 7 rats per group. The healthy control group was exposed to fresh air while all rats in the 3 experimental groups were exposed to cigarette smoke for 20 weeks for 2 hours per day. After histopathological verification of smoke induced lung injury, montelukast (0.1 mg/kg dissolved in Na2CO3 was given in one group (MON, Na2CO3 only was given in another group (MON control and placebo was injected in the third group (COPD control intraperitoneally for 21 days. At the end of this period blood samples were obtained for serum TNF-α assessment and light and electron microscopy analyses were performed on the lung tissues of sacrificed rats. Results Serum TNF-α levels in the MON group were significantly lower than in the MON control and COPD control groups (38.84 ± 4.9 pg/ml, 77.5 ± 5.8 pg/ml and 79.2 ± 6.9 pg/ml respectively, p 0.05. Light and electron microscopic evaluation of the lungs demonstrated that the total histopathological damage score of the lung samples was significantly lower in the MON group than in MON controls and COPD controls (5.14 ± 0.5, 8.4 ± 0.6 and 8.7 ± 0.4 respectively, p 0.05. Conclusion These findings suggest that montelukast might have a protective effect on smoke-induced lung injury in rats both from a histopathological and inflammatory point of view.

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

    Institute of Scientific and Technical Information of China (English)

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

    2014-01-01

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

  5. Pathogenic mechanism of second hand smoke induced inflammation and COPD

    Directory of Open Access Journals (Sweden)

    Rahel eBirru

    2012-08-01

    Full Text Available Second hand smoke (SHS introduces thousands of toxic chemicals into the lung, including carcinogens and oxidants, which cause direct airway epithelium tissue destruction. It can also illicit indirect damage through its effect on signaling pathways related to tissue cell repair and by the abnormal induction of inflammation into the lung. After repeated exposure to second hand smoke, these symptoms can lead to the development of pulmonary inflammatory disorders, including chronic obstructive pulmonary disease (COPD. COPD is a severe pulmonary disease characterized by chronic inflammation and irreversible tissue destruction. There is no causal cure, as the mechanism behind the development and progression of the disease is still unknown. Recent discoveries implicate genetic predisposition associated with inflammatory response contributed to the development of COPD, linked to irregular innate and adaptive immunity, as well as a risk factor for cancer. The use of animal models for both cigarette smoke (CS and SHS associated in vivo experiments has been crucial in elucidating the pathogenic mechanisms and genetic components involved in inflammation related development of COPD.

  6. Exposure to Electronic Cigarettes Impairs Pulmonary Anti-Bacterial and Anti-Viral Defenses in a Mouse Model

    OpenAIRE

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

    2015-01-01

    Electronic cigarettes (E-cigs) have experienced sharp increases in popularity over the past five years due to many factors, including aggressive marketing, increased restrictions on conventional cigarettes, and a perception that E-cigs are healthy alternatives to cigarettes. Despite this perception, studies on health effects in humans are extremely limited and in vivo animal models have not been generated. Presently, we determined that E-cig vapor contains 7x1011 free radicals per puff. To de...

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

    Directory of Open Access Journals (Sweden)

    Gui Hua Xu

    2015-10-01

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

  8. Effect of alpha-tocopherol on pulmonary antioxidant defence system and lipid peroxidation in cigarette smoke inhaling mice

    Directory of Open Access Journals (Sweden)

    Bhatia Vipin

    2001-11-01

    Full Text Available Abstract Background Free radicals generated in biological systems by cigarette smoke (CS inhalation can cause oxidative stress in tissues, resulting in lipid peroxidation (LPO. In view of the antioxidant properties of α-tocopherol (AT, in the present study, effects of AT on antioxidant defence system and LPO were investigated in mice inhaling CS for different time intervals. Results Male Balb/c mice were fed orally with AT (5 I.U./Kg.b.wt. and /or exposed to CS for 2, 4, 6 or 8 weeks. No effect was observed on body growth, diet consumption, water intake and lung weight due to AT and /or CS treatment in any of the groups as compared to their control counterparts. After two weeks of treatment, no change in LPO, reduced glutathione (GSH levels and antioxidant enzymes were observed except for glutathione reductase (GR which increased in all the treated groups. A significant increase in pulmonary LPO levels was observed in mice exposed to CS inhalation for 4, 6 or 8 weeks. There was a gradual increase in the LPO levels as the extent of CS inhalation increased from 4 to 8 weeks. However, the extent of increase in LPO levels due to CS exposure for 4, 6 or 8 weeks in the mice treated with AT was comparatively less. A significant decrease in the GSH levels was also observed in all the animals exposed to CS for 4, 6 or 8 weeks. There was a significant increase in the activities of catalase, glutathione peroxidase (GSH-Px and GR observed in all the groups exposed to CS for 4,6 or 8 weeks. The increase in above antioxidant enzymes seems to be insufficient to combat the oxidative stress posed by CS inhalation. There was a marked decrease observed in the LPO levels in the animals treated with AT alone for 4, 6, or 8 weeks, when compared to their control counterparts. However, the supplementation of AT for 4, 6 or 8 weeks demonstrated a significant increase in GSH levels. Conclusion It appears from our studies that AT exhibits its antioxidant role either

  9. 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...

  10. 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...

  11. Menthol Cigarettes

    Science.gov (United States)

    ... cigarettes sold in the United States has the descriptor “menthol” on the cigarette pack. Menthol cigarettes are ... over 40 years [21]. Is menthol in other products? Yes. Menthol is added to many other products, ...

  12. 髓系细胞RelA/p65基因介导吸烟促进小鼠肺癌的生长机制%Mechanisms of myeloid cell RelA/p65 in cigarette smoking-induced lung cancer growth in mice

    Institute of Scientific and Technical Information of China (English)

    姚懿雯; 吴军录; 权文强; 周宏; 张宇; 万海英; 李冬

    2014-01-01

    鼠中均明显增加(P<0.05).WT小鼠在香烟刺激后,肿瘤组织中TNF-α、IL-6和KC的表达均明显升高(P<0.05).结论 吸烟促进了小鼠肺癌的生长,髓系细胞的RelA/p65基因介导了吸烟的促肿瘤生长效应,由RelA/p65基因调控的TNF-α表达可能参与了肺癌的发展.%Objective The aim of this study was to investigate the mechanism of cigarette smoking (CS)-induced lung cancer growth in mice.Methods RelA/p65-/-mice and WT mice were used to establish mouse models of lung cancer.Both mice were divided into two groups:air group and CS group,respectively.Tumor number on the lung surface was counted and maximal tumor size was evaluated using HE staining.Kaplan Meier (K-M) survival curve was used to analyze the survival rate of the mice.Expression of Ki-67,TNF-α and CD68 in the tumor tissue was determined by immunohistochemical analysis,and cyclin D1 and c-myc proteins were examined by Western blot.Apoptosis of tumor cells was analyzed using TUNEL staining.The concentrations of inflammatory cytokines TNF-α,[L-6 and KC in the mouse lung tissues were evaluated by ELISA.Results Compared with the WT air group,the lung weight,lung tumor multiplicity,as well as maximum tumor size in the WT mice exposed to CS were (1.5 ±0.1)g,(64.8 ±4.1) and (7.6 ± 0.2) mm,respectively,significantly increased than those in the WT mice not exposed to CS (P < 0.05 for all).However,there were no statistically significant differences between RelA/p65-/-mice before and after CS exposure (P > 0.05 for all).Kaplan-Meier survival analysis showed that CS exposure significantly shortened the life time of WT mice (P < 0.05),and deletion of RelA/p65 in myeloid cells resulted in an increased survival compared with that of the WT mice (P <0.05 for all).The ratios of Ki-67 positive tumor cells were (43.4 ±2.9)%,(60.6 ±5.4)%,(12.8 ±3.6)% and (15.0 ±4.2)% in the WT air group,WT CS groups,RelA/p65-/-air groups and RelA/p65-/-CS groups,respectively.After smoking,the number

  13. Forced oscillation technique in the detection of smoking-induced respiratory alterations: diagnostic accuracy and comparison with spirometry

    Directory of Open Access Journals (Sweden)

    Alvaro Camilo Dias Faria

    2010-01-01

    Full Text Available INTRODUCTION: Detection of smoking effects is of utmost importance in the prevention of cigarette-induced chronic airway obstruction. The forced oscillation technique offers a simple and detailed approach to investigate the mechanical properties of the respiratory system. However, there have been no data concerning the use of the forced oscillation technique to evaluate respiratory mechanics in groups with different degrees of tobacco consumption. OBJECTIVES: (1 to evaluate the ability of the forced oscillation technique to detect smoking-induced respiratory alterations, with special emphasis on early alterations; and (2 to compare the diagnostic accuracy of the forced oscillation technique and spirometric parameters. METHODS: One hundred and seventy subjects were divided into five groups according to the number of pack-years smoked: four groups of smokers classified as 60 pack-years and a control group. The four groups of smokers were compared with the control group using receiver operating characteristic (ROC curves. RESULTS: The early adverse effects of smoking in the group with 60 pack-years, the diagnostic performance of the forced oscillation technique was similar to that observed with spirometry. CONCLUSIONS: This study revealed that forced oscillation technique parameters were able to detect early smoking-induced respiratory involvement when pathologic changes are still potentially reversible. These findings support the use of the forced oscillation technique as a versatile clinical diagnostic tool in helping with chronic obstructive lung disease prevention, diagnosis, and treatment.

  14. Longitudinal follow-up study of smoking-induced emphysema progression in low-dose CT screening of lung cancer

    Science.gov (United States)

    Suzuki, H.; Matsuhiro, M.; Kawata, Y.; Niki, N.; Nakano, Y.; Ohmatsu, H.; Kusumoto, M.; Tsuchida, T.; Eguchi, K.; Kaneko, Masahiro; Moriyama, N.

    2014-03-01

    Chronic obstructive pulmonary disease is a major public health problem that is predicted to be third leading cause of death in 2030. Although spirometry is traditionally used to quantify emphysema progression, it is difficult to detect the loss of pulmonary function by emphysema in early stage, and to assess the susceptibility to smoking. This study presents quantification method of smoking-induced emphysema progression based on annual changes of low attenuation volume (LAV) by each lung lobe acquired from low-dose CT images in lung cancer screening. The method consists of three steps. First, lung lobes are segmented using extracted interlobar fissures by enhancement filter based on fourdimensional curvature. Second, LAV of each lung lobe is segmented. Finally, smoking-induced emphysema progression is assessed by statistical analysis of the annual changes represented by linear regression of LAV percentage in each lung lobe. This method was applied to 140 participants in lung cancer CT screening for six years. The results showed that LAV progressions of nonsmokers, past smokers, and current smokers are different in terms of pack-year and smoking cessation duration. This study demonstrates effectiveness in diagnosis and prognosis of early emphysema in lung cancer CT screening.

  15. 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.

  16. 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 ...

  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. 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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2013-07-01

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

  1. Smoke-induced seed germination in California chaparral

    Science.gov (United States)

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

    1998-01-01

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

  2. Sub-chronic exposure to second hand smoke induces airspace leukocyte infiltration and decreases lung elastance

    Directory of Open Access Journals (Sweden)

    John M. Hartney

    2012-07-01

    Full Text Available Exposure to second hand tobacco smoke is associated with the development and/or exacerbation of several different pulmonary diseases in humans. To better understand the possible effects of second hand smoke exposure in humans, we sub-chronically (4 weeks exposed mice to a mixture of mainstream and sidestream tobacco smoke at concentrations similar to second hand smoke exposure in humans. The inflammatory response to smoke exposures was assessed at the end of this time by enumeration of pulmonary leukocyte infiltration together with measurements of lung elastance and pathology. This response was measured in both healthy wild type (C57BL/6 mice as well as mouse mutants deficient in the expression of Arhgef1 (Arhgef1–/– that display constitutive pulmonary inflammation and decreased lung elastance reminiscent of emphysema. The results from this study show that sub-chronic second hand smoke exposure leads to significantly increased numbers of airspace leukocytes in both healthy and mutant animals. While sub-chronic cigarette smoke exposure is not sufficient to induce changes in lung architecture as measured by mean linear intercept, both groups exhibit a significant decrease in lung elastance. Together these data demonstrate that even sub-chronic exposure to second hand smoke is sufficient to induce pulmonary inflammation and decrease lung elastance in both healthy and diseased animals and in the absence of tissue destruction.

  3. 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.

  4. 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

  5. Does phosphodiesterase inhibition lessen facial flap necrosis in tobacco cigarette users?

    Science.gov (United States)

    Pfaff, Miles; Shah, Ajul; Steinbacher, Derek

    2014-02-01

    Tobacco cigarette smoking remains a serious risk factor for necrosis of local facial skin flaps. To date, no pharmacological therapies exist for cigarette smoke-induced impairment of skin flap tissue survival. Accumulating evidence suggest that phosphodiesterase-5 (PDE-5) inhibitor therapy may counteract the negative effects of cigarette smoke on flap survival. Here, we evaluate skin flap survival in a series of consecutive tobacco cigarette users treated with the PDE-5 inhibitor, sildenafil, who underwent local flap facial reconstruction. We included 11 patients (5 females; median age: 64) with a significant smoking history. Seventeen facial flaps were performed for 14 defects. All patients received sildenafil in the postoperative setting. One complication of necrosis of the flap distal margin was encountered. Follow-up was available for all patients. Our results demonstrate that facial reconstruction in tobacco cigarette smokers can be performed with improved success and that sildenafil therapy may mitigate the deleterious effects of smoking on flap survival. PMID:24488644

  6. Pathogenic mechanism of second hand smoke induced inflammation and COPD

    OpenAIRE

    Rahel eBirru; Y. Peter eDi

    2012-01-01

    Second hand smoke (SHS) introduces thousands of toxic chemicals into the lung, including carcinogens and oxidants, which cause direct airway epithelium tissue destruction. It can also illicit indirect damage through its effect on signaling pathways related to tissue cell repair and by the abnormal induction of inflammation into the lung. After repeated exposure to second hand smoke, these symptoms can lead to the development of pulmonary inflammatory disorders, including chronic obstructive...

  7. 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...

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

    Science.gov (United States)

    Kim, Kang-Hyun; Park, Tai Sun; Kim, You-Sun; Lee, Jae Seung; Oh, Yeon-Mok; Lee, Sang-Do; Lee, Sei Won

    2016-01-01

    Purpose Emphysema is an irreversible disease that is characterized by destruction of lung tissue as a result of inflammation caused by smoking. Resolvin D1 (RvD1), derived from docosahexaenoic acid, is a novel lipid that resolves inflammation. The present study tested whether RvD1 prevents smoking-induced emphysema and promotes lung tissue regeneration. Materials and methods C57BL/6 mice, 8 weeks of age, were randomly divided into four groups: control, RvD1 only, smoking only, and smoking with RvD1 administration. Four different protocols were used to induce emphysema and administer RvD1: mice were exposed to smoking for 4 weeks with poly(I:C) or to smoking only for 24 weeks, and RvD1 was injected within the smoking exposure period to prevent regeneration or after completion of smoking exposure to assess regeneration. The mean linear intercept and inflammation scores were measured in the lung tissue, and inflammatory cells and cytokines were measured in the bronchoalveolar lavage fluid. Results Measurements of mean linear intercept showed that RvD1 significantly attenuated smoking-induced lung destruction in all emphysema models. RvD1 also reduced smoking-induced inflammatory cell infiltration, which causes the structural derangements observed in emphysema. In the 4-week prevention model, RvD1 reduced the smoking-induced increase in eosinophils and interleukin-6 in the bronchoalveolar lavage fluid. In the 24-week prevention model, RvD1 also reduced the increased neutrophils and total cell counts induced by smoking. Conclusion RvD1 attenuated smoking-induced emphysema in vivo by reducing inflammation and promoting tissue regeneration. This result suggests that RvD1 may be useful in the prevention and treatment of emphysema. PMID:27313451

  9. Better understanding the influence of cigarette smoking and indoor air pollution on chronic obstructive pulmonary disease: A case-control study in Mainland China

    Energy Technology Data Exchange (ETDEWEB)

    Xu, F.; Yin, X.M.; Shen, H.B.; Xu, Y.C.; Ware, R.S.; Owen, N. [Nanjing Municipal Center for District Control & Prevention, Nanjing (China)

    2007-11-15

    This study investigated the relationship between the total amount of cigarettes smoked (TACS) and indoor air pollution, with the risk of COPD among urban and rural Chinese adults. A nested case-control study was performed using data collected in a large community survey (N = 29 319) conducted between October 2000 and March 2001 in Nanjing, China. The exposure to indoor respiratory pollutants of cooking and heating materials and to passive cigarette smoke was compared in patients diagnosed with COPD (n = 1743) and controls matched for age, gender and residence (n = 1743). The smoking rate among COPD patients was significantly higher than that among the controls. After controlling for possible confounders, the adjusted odds ratios for COPD increased across TACS tertiles: from lower (OR = 1.40, 95% confidence interval (CI): 1.09-1.79), to middle (OR = 1.55, 95% CI: 1.21-1.99), and upper (OR = 1.77, 95% CI: 1.37-2.29). Among smokers, women were significantly more likely to develop COPD than men (OR = 1.20, 95% CI: 1.02-1.41). There were no significant associations between COPD and domestic fuels used, kitchen ventilation or passive smoking. Heating in winter with coal was weakly but positively linked with COPD among non-smokers overall, among women non-smokers, and specifically for women living in urban as well as rural areas. This clear dose-response relationship exists between cigarette smoking and COPD; compared with men, women smokers were more susceptible to COPD. Exposure to other respiratory pollutants in the home was not significantly associated with the diagnosis of COPD.

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

    OpenAIRE

    Koubaa, Abdessalem; Triki, Moez; Trabelsi, Hajer; Masmoudi, Liwa; Zeghal, Khaled N; Sahnoun, Zouhair; Hakim, Ahmed

    2015-01-01

    Introduction: Pulmonary function is compromised in most smokers. Yet it is unknown whether exercise training improves pulmonary function and aerobic capacity in cigarette and hookah smokers and whether these smokers respond in a similar way as do non-smokers.Aim: To evaluate the effects of an interval exercise training program on pulmonary function and aerobic capacity in cigarette and hookah smokers.Methods: Twelve cigarette smokers, 10 hookah smokers, and 11 non-smokers participated in our ...

  11. Imaging-based assessment of dyspnea in cigarette smokers

    Science.gov (United States)

    Galvin, Jeffrey R.; Chang, Paul J.; Schwartz, David A.; Hunninghake, Gary W.; Helmers, Richard; Mori, Masaki

    1994-05-01

    Patients with pulmonary fibrosis frequently smoke cigarettes. The cause of dyspnea in these patients is often complex because of the coexistence of multiple disease processes. We investigated 10 cigarette smokers with pulmonary fibrosis who were referred for evaluation of new onset or worsening dyspnea. Chest radiographs and pulmonary function tests were obtained in addition to high-resolution computed tomography (HRCT). In those patients with HRCT evidence of both diseases, spirometry and lung volumes were most often normal. Although plain films provided a reasonable assessment of fibrosis, they underestimated the severity of emphysema. Quantitation of both emphysema and fibrosis by HRCT was reproducible and correlated with key pulmonary function tests. Our findings indicate that the HRCT scan is a useful diagnostic test in patients with pulmonary fibrosis who are also cigarette smokers.

  12. 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...

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

    Science.gov (United States)

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

    2009-01-01

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

  14. 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.

  15. Cold Smoke: smoke-induced density currents cause unexpected smoke transport near large wildfires

    OpenAIRE

    N. P. Lareau; Clements, C. B.

    2015-01-01

    The first observations of smoke-induced density currents originating from large wildfires are presented. Using a novel mobile Doppler lidar and additional in situ measurements, we document a deep (~ 2 km) smoke-filled density current that propagates more than 25 km at speeds up to 4.5 m s−1 near a large forest fire in northern California. Based on these observations we show that the dynamics governing the spread of the smoke layer result from differential solar heating between ...

  16. Cathepsin E Promotes Pulmonary Emphysema via Mitochondrial Fission

    OpenAIRE

    Zhang, Xuchen; Shan, Peiying; Homer, Robert; Zhang, Yi; Petrache, Irina; Mannam, Praveen; Lee, Patty J.

    2014-01-01

    Emphysema is characterized by loss of lung elasticity and irreversible air space enlargement, usually in the later decades of life. The molecular mechanisms of emphysema remain poorly defined. We identified a role for a novel cathepsin, cathepsin E, in promoting emphysema by inducing mitochondrial fission. Unlike previously reported cysteine cathepsins, which have been implicated in cigarette smoke-induced lung disease, cathepsin E is a nonlysosomal intracellular aspartic protease whose funct...

  17. DrugFacts: Electronic Cigarettes (e-Cigarettes)

    Science.gov (United States)

    ... Home » Publications » DrugFacts » Electronic Cigarettes (e-Cigarettes) DrugFacts: Electronic Cigarettes (e-Cigarettes) Email Facebook Twitter Revised May ... by ©iStock.com/kitiara65/ http://istockpho.to/1SWVugO Electronic cigarettes (also called e-cigarettes or electronic nicotine ...

  18. 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.

  19. Psychosocial Factors Associated With Adolescent Electronic Cigarette and Cigarette Use

    Science.gov (United States)

    Berhane, Kiros; Unger, Jennifer B.; Cruz, Tess Boley; Huh, Jimi; Leventhal, Adam M.; Urman, Robert; Wang, Kejia; Howland, Steve; Gilreath, Tamika D.; Chou, Chih-Ping; Pentz, Mary Ann; McConnell, Rob

    2015-01-01

    BACKGROUND: Use of electronic cigarettes (e-cigarettes) among adolescents has increased since their introduction into the US market in 2007. Little is known about the role of e-cigarette psychosocial factors on risk of e-cigarette or cigarette use in adolescence. METHODS: Information on e-cigarette and cigarette psychosocial factors (use and attitudes about use in the home and among friends) was collected from 11th- and 12th-grade participants in the Southern California Children’s Health Study during the spring of 2014. RESULTS: Of 2084 participants, 499 (24.0%) had used an e-cigarette, including 200 (9.6%) current users (past 30 days); 390 participants (18.7%) had smoked a combustible cigarette, and 119 (5.7%) were current cigarette smokers. Cigarette and e-cigarette use were correlated. Nevertheless, 40.5% (n = 81) of current e-cigarette users had never smoked a cigarette. Psychosocial factors (home use of each product, friends’ use of and positive attitudes toward e-cigarettes and cigarettes) and participant perception of the harm of e-cigarettes were strongly positively associated both with e-cigarette and cigarette use. Most youth who reported e-cigarette use had friends who used e-cigarettes, and almost half of current users reported that they did not believe there were health risks associated with e-cigarette use. CONCLUSIONS: Longitudinal studies of adolescents are needed to determine whether the strong association of e-cigarette psychosocial factors with both e-cigarette and cigarette use will lead to increased cigarette use or dual use of cigarettes and e-cigarettes, or whether e-cigarettes will serve as a gateway to cigarette use. PMID:26216326

  20. Infiltration of IL-17-Producing T Cells and Treg Cells in a Mouse Model of Smoke-Induced Emphysema.

    Science.gov (United States)

    Duan, Min-Chao; Zhang, Jian-Quan; Liang, Yue; Liu, Guang-Nan; Xiao, Jin; Tang, Hai-Juan; Liang, Yi

    2016-08-01

    Chronic obstructive pulmonary disease (COPD) is a progressive and irreversible chronic inflammatory disease associated with the accumulation of activated T cells. To date, there is little information concerning the intrinsic association among Th17, Tc17, and regulatory T (Treg) cells in COPD. The objective of this study was to investigate the variation of lungs CD4(+)Foxp3(+) Treg cells and IL-17-producing CD4 and CD8 (Th17 and Tc17) lymphocytes in mice with cigarette-induced emphysema. Groups of mice were exposed to cigarette smoke or room air. At weeks 12 and 24, mice were sacrificed to observe histological changes by HE stain. The frequencies of Th17 (CD4(+)IL-17(+)T), Tc17 (CD8(+)IL-17(+)T), and Treg (CD4(+)Foxp3(+)T) cells in lungs from these mice were analyzed by flow cytometry. The mRNA levels of orphan nuclear receptor ROR γt and Foxp3 were performed by real-time quantitative polymerase chain reaction. The protein levels of interleukin-17 (IL-17), IL-6, IL-10, and transforming growth factor-beta (TGF-β1) were measured by enzyme-linked immunosorbent assay. Cigarette smoke caused substantial enlargement of the air spaces accompanied by the destruction of the normal alveolar architecture and led to emphysema. The frequencies of Th17 and Tc17 cells, as well as the expressions of IL-6, IL-17, TGF-β1, and ROR γt were greater in the lungs of cigarette smoke (CS)-exposed mice, particularly in the 24-week CS-exposed mice. The frequencies of Treg cells and the expressions of IL-10 and Foxp3 were lower in CS-exposed mice compared to control group. More important, the frequencies of Tregs were negatively correlated with Th17 cells and with Tc17 cells. Interestingly, a significant portion of the cells that infiltrate the lungs was skewed towards a Tc17 phenotype. Our findings suggest the contribution of Th17, Tc17, and Treg cells in the pathogenesis of COPD. Rebalance of these cells will be helpful for developing and refining the new immunological therapies for COPD

  1. Antioxidant intervention of smoking-induced lung tumor in mice by vitamin E and quercetin

    International Nuclear Information System (INIS)

    Epidemiological and in vitro studies suggest that antioxidants such as quercetin and vitamin E (VE) can prevent lung tumor caused by smoking; however, there is limited evidence from animal studies. In the present study, Swiss mouse was used to examine the potential of quercetin and VE for prevention lung tumor induced by smoking. Our results suggest that the incidence of lung tumor and tumor multiplicity were 43.5% and 1.00 ± 0.29 in smoking group; Quercetin has limited effects on lung tumor prevention in this in vivo model, as measured by assays for free radical scavenging, reduction of smoke-induced DNA damage and inhibition of apoptosis. On the other hand, vitamin E drastically decreased the incidence of lung tumor and tumor multiplicity which were 17.0% and 0.32 ± 0.16, respectively (p < 0.05); and demonstrated prominent antioxidant effects, reduction of DNA damage and decreased cell apoptosis (p < 0.05). Combined treatment with quercetin and VE in this animal model did not demonstrate any effect greater than that due to vitamin E alone. In addition, gender differences in the occurrence of smoke induced-lung tumor and antioxidant intervention were also observed. We conclude that VE might prevent lung tumor induced by smoking in Swiss mice

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

    Directory of Open Access Journals (Sweden)

    Alexander Salskov

    2011-01-01

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

  3. 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

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

    Directory of Open Access Journals (Sweden)

    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.

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

    OpenAIRE

    Prajwal Gyawali; Victor Maduabuchi Oguoma

    2016-01-01

    Cigarette smoking has been implicated as a potential risk factor for development and progression of chronic obstructive pulmonary disease (COPD) and cardiovascular disease (CVD), including ischemic heart disease. Although, several methods are in existence to measuring cigarette toxicity, evidence regarding adoption of a gold standard technique is still imprecise. In this study, we reviewed articles describing methods of measuring cigarette toxicity in relation to clinical laboratory practice....

  6. Cigarette use, Cigarette Consumption and Price of Cigarette

    Institute of Scientific and Technical Information of China (English)

    JingMing Li

    2016-01-01

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

  7. Cold smoke: smoke-induced density currents cause unexpected smoke transport near large wildfires

    Directory of Open Access Journals (Sweden)

    N. P. Lareau

    2015-07-01

    Full Text Available First observations of smoke-induced density currents originating from large wildfires are presented. Using a novel mobile Doppler LiDAR and additional in situ measurements we document a deep (~ 2 km smoke-filled density current that propagates more than 25 km at speeds up to 4.5 m s−1 near a large forest fire in northern California. Based on these observations we show that the dynamics governing the spread of the smoke layer result from differential solar heating between the smoke-filled and smoke-free portions of the atmospheric boundary layer. A calculation of the theoretical density current speed agrees well with the observed propagation speed. Additional LiDAR and photographic documentation of other smoke-filled density currents demonstrate that these previously unknown phenomena are relatively common near large wildfires and can cause severe and unexpected smoke inundation of populated areas.

  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. Dynamics of the risk of smoking-induced lung cancer : A compartmental hidden markov model for longitudinal analysis

    NARCIS (Netherlands)

    Chadeau-Hyam, Marc; Tubert-Bitter, Pascale; Guihenneuc-Jouyaux, Chantal; Campanella, Gianluca; Richardson, Sylvia; Vermeulen, Roel; De Iorio, Maria; Galea, Sandro; Vineis, Paolo

    2014-01-01

    BACKGROUND:: To account for the dynamic aspects of carcinogenesis, we propose a compartmental hidden Markov model in which each person is healthy, asymptomatically affected, diagnosed, or deceased. Our model is illustrated using the example of smoking-induced lung cancer. METHODS:: The model was fit

  10. 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.

  11. [Autoimmunity in pathogenesis of chronic obstructive pulmonary disease].

    Science.gov (United States)

    Urboniene, Daiva; Sakalauskas, Raimundas; Sitkauskiene, Brigita

    2005-01-01

    For years, smoking induced inflammatory reaction, comprised mainly of neutrophils and macrophages, has been accepted to be the major component in pathogenesis of chronic obstructive pulmonary disease. New developments in molecular and cell biology have provided scientists with new knowledge and understanding of inflammatory processes in lung. Recent reports have underlined the role of autoimmunity and T lymphocytes as a potential important factor, which takes place in the pathogenesis of chronic obstructive pulmonary disease. This article reviews potential mechanism of T cell mediated immune response in chronic obstructive pulmonary disease. PMID:15827384

  12. E-Cigarettes (For Parents)

    Science.gov (United States)

    ... Tropical Delight: Melon Smoothie Pregnant? Your Baby's Growth E-Cigarettes KidsHealth > For Parents > E-Cigarettes Print A ... Using Them en español Los cigarrillos electrónicos About E-Cigarettes E-cigarettes are being marketed as a ...

  13. E-Cigarettes (For Teens)

    Science.gov (United States)

    ... How Can I Help a Friend Who Cuts? E-Cigarettes KidsHealth > For Teens > E-Cigarettes Print A ... Habit en español Los cigarrillos electrónicos What Are E-Cigarettes? E-cigarettes look high tech, so it's ...

  14. 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

  15. 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

  16. 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.

  17. Cigarette Ads and Youth.

    Science.gov (United States)

    Carol, Julia

    1988-01-01

    Points out ways the tobacco industry markets products to youth, including paid advertisements, sponsorship of sporting events, music concerts, and magazines. Relates several focal points for smoking prevention, which include deglamorization of cigarette advertisements and making smoking socially undesirable. (LS)

  18. 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...

  19. Comparative study of pulmonary function variables in relation to type of smoking.

    Science.gov (United States)

    Padmavathy, K M

    2008-01-01

    This study was intended to compare pulmonary function parameters in beedi smokers, cigarette smokers and subjects who smoked both beedi and cigarette on the basis of the dynamic ventilatory pulmonary function tests. The pulmonary function tests were done on 188 subjects which included, 48 beedi smokers, 48 cigarette smokers, 43 others who smoked both beedi as well as cigarette and 49 non-smokers (control). In beedi smokers the values of Forced Expiratory Volume in 1st second (FEV1), Peak Expiratory Flow Rate (PEFR), Forced Expiratory Flow (FEF) 25%-75%, FEV1/FVC%, BMI and weight were significantly lower (P < 0.01) than those of cigarette smokers and non-smokers. Moreover, the Forced Vital Capacity (FVC) and Maximal Voluntary Ventilation (MVV) of beedi smokers were significantly (P < 0.0001) lower than those of non-smokers. It may be concluded that pulmonary functions are more affected in beedi smokers than in cigarette smokers. PMID:19130865

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

    Institute of Scientific and Technical Information of China (English)

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

    2010-01-01

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

  1. The impact of emphysema in pulmonary fibrosis

    OpenAIRE

    Vincent Cottin

    2013-01-01

    Several groups have described a syndrome in which idiopathic pulmonary fibrosis (IPF) coexists with pulmonary emphysema. This comes as no surprise since both diseases are associated with a history of exposure to cigarette smoke. The syndrome of combined pulmonary fibrosis and emphysema (CPFE) is characterised by upper lobe emphysema and lower lobe fibrosis. Physiological testing of these patients reveals preserved lung volume indices contrasted by markedly impaired diffusion capacity. The inc...

  2. Cardiology Patient Page: Electronic Cigarettes

    Science.gov (United States)

    ... cigarettes and without exposing others to secondhand smoke. Marketing for e-cigarettes often describes them as emitting ... Us: Follow Circulation on Twitter Visit Circulation on Facebook Follow Circulation on Google Plus Follow Circulation on ...

  3. 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

  4. 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

  5. Role of IL-18 in second-hand smoke-induced emphysema

    NARCIS (Netherlands)

    Kratzer, A.; Salys, J.; Nold-Petry, C.; Cool, C.; Zamora, M.; Bowler, R.; Koczulla, A.R.; Janciauskiene, S.; Edwards, M.G.; Dinarello, C.A.; Taraseviciene-Stewart, L.

    2013-01-01

    Chronic second-hand smoke (SHS) exposure comprises the main risk factor for nonsmokers to develop chronic obstructive pulmonary disease (COPD). However, the mechanisms behind the chronic inflammation and lung destruction remain incompletely understood. In this study, we show that chronic exposure of

  6. 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

  7. 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

  8. 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...

  9. Electronic Cigarettes on Hospital Campuses

    Directory of Open Access Journals (Sweden)

    Clare Meernik

    2015-12-01

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

  10. Sub-chronic exposure to second hand smoke induces airspace leukocyte infiltration and decreased lung elastance

    OpenAIRE

    Hartney, John M.; Chu, HongWei; Pelanda, Roberta; Torres, Raul M.

    2012-01-01

    Exposure to second hand tobacco smoke is associated with the development and/or exacerbation of several different pulmonary diseases in humans. To better understand the possible effects of second hand smoke exposure in humans, we sub-chronically (4 weeks) exposed mice to a mixture of mainstream and sidestream tobacco smoke at concentrations similar to second hand smoke exposure in humans. The inflammatory response to smoke exposures was assessed at the end of this time by enumeration of pulmo...

  11. 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

  12. 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

  13. Analysis of cigarette-smoke-induced DNA adducts by butanol extraction and nuclease P1-enhanced 32P-postlabeling in human lymphocytes and granulocytes.

    OpenAIRE

    Savela, K; Hemminki, K

    1993-01-01

    In an earlier study, we analyzed the aromatic DNA adducts separated from lymphocytes and granulocytes of smokers and nonsmokers using the nuclease P1-enhanced 32P-postlabeling assay. Here we compare the butanol extraction and nuclease P1-enhanced procedure on the same kind of samples. The DNA adducts of 42 per 10(8) nucleotides from smokers' lymphocytes were statistically higher (p < 0.05) than those of 11 from nonsmokers', when analyzed by the nuclease P1 treatment, but not by the 1-butanol ...

  14. Multielement determination in a Chinese cigarette brand

    International Nuclear Information System (INIS)

    A cigarette brand manufactured in the Republic of China was analyzed by instrumental neutron activation analysis to determine the concentration of 27 elements in cigarette tobacco, cigarette wrapping paper, cigarette filter before and after smoking and in the dropped ash. The results were compared to the literature values for American and other international cigarette brands. (author) 28 refs.; 3 tabs

  15. 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.

  16. 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 ...

  17. 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...

  18. Pulmonary edema

    Science.gov (United States)

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

  19. Pharmacological and dietary antioxidant therapies for chronic obstructive pulmonary disease.

    Science.gov (United States)

    Biswas, S; Hwang, J W; Kirkham, P A; Rahman, I

    2013-01-01

    The progression and exacerbations of chronic obstructive pulmonary disease (COPD) are intimately associated with tobacco smoke/biomass fuel-induced oxidative and aldehyde/carbonyl stress. Alterations in redox signaling proinflammatory kinases and transcription factors, steroid resistance, unfolded protein response, mucus hypersecretion, extracellular matrix remodeling, autophagy/apoptosis, epigenetic changes, cellular senescence/aging, endothelial dysfunction, autoimmunity, and skeletal muscle dysfunction are some of the pathological hallmarks of COPD. In light of the above it would be prudent to target systemic and local oxidative stress with agents that can modulate the antioxidants/ redox system or by boosting the endogenous levels of antioxidants for the treatment and management of COPD. Identification of various antioxidant agents, such as thiol molecules (glutathione and mucolytic drugs, such as N-acetyl-L-cysteine, N-acystelyn, erdosteine, fudosteine, ergothioneine, and carbocysteine lysine salt), dietary natural product-derived polyphenols and other compounds (curcumin, resveratrol, green tea catechins, quercetin sulforaphane, lycopene, acai, alpha-lipoic acid, tocotrienols, and apocynin) have made it possible to modulate various biochemical aspects of COPD. Various researches and clinical trials have revealed that these antioxidants can detoxify free radicals and oxidants, control expression of redox and glutathione biosynthesis genes, chromatin remodeling, and ultimately inflammatory gene expression. In addition, modulation of cigarette smoke-induced oxidative stress and related cellular changes have also been reported to be effected by synthetic molecules. This includes specific spin traps like α-phenyl-N-tert-butyl nitrone, a catalytic antioxidant (ECSOD mimetic), porphyrins (AEOL 10150 and AEOL 10113), and a superoxide dismutase mimetic M40419, lipid peroxidation and protein carbonylation blockers/inhibitors, such as edaravone and lazaroids

  20. Complete pathological resolution of pulmonary Langerhans cell histiocytosis

    OpenAIRE

    Ninaber, Maarten; Dik, Hans; Peters, Elke

    2014-01-01

    Cigarette smoking is a major risk factor for pulmonary Langerhans cell histiocytosis (pLCH) and lung cancer. Resolution of pLCH may occur spontaneously, after smoking cessation or other interventions. However, despite clinicoradiological resolution, residual pulmonary Langerhans cells may be present and may lead to recurrent disease. We report the first case of pLCH with a complete histological resolution.

  1. Impact of heterozygote CFTR Mutations in COPD patients with Chronic Bronchitis

    OpenAIRE

    Raju, S. Vamsee; Tate, Jody H; Peacock, Sandra KG; Fang, Ping; Oster, Robert A.; Dransfield, Mark T.; Steven M Rowe

    2014-01-01

    Background Cigarette smoking causes Chronic Obstructive Pulmonary Disease (COPD), the 3rd leading cause of death in the U.S. CFTR ion transport dysfunction has been implicated in COPD pathogenesis, and is associated with chronic bronchitis. However, susceptibility to smoke induced lung injury is variable and the underlying genetic contributors remain unclear. We hypothesized that presence of CFTR mutation heterozygosity may alter susceptibility to cigarette smoke induced CFTR dysfunction. Con...

  2. Electronic cigarettes in the media.

    Science.gov (United States)

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

    2016-07-01

    Electronic cigarettes (e-cigarettes) are an increasingly popular source of nicotine and an increasingly popular topic in the media. Concerns about potential hazards associated with e-cigarette use and advertising, especially to adolescents, have led to studies on e-cigarettes in both traditional media (TV, mail, print, and outdoor advertising) and social media (websites, social networking sites, blogs, and e-mails). This review presents a narrative description of available studies related to e-cigarettes in the media. These articles have focused on promotion in both traditional and social media across a broad range of topics and have concentrated on target audiences, smoking cessation, harm reduction, and advertising. E-cigarette advertising is the most frequent topic in the published articles. Identifying the target audience also is a common objective in articles. The representation of e-cigarettes as a "healthier alternative" to traditional cigarettes and their use as a "smoking cessation aid" are main themes presented through all types of media. PMID:27365871

  3. Electronic cigarettes in the media

    Science.gov (United States)

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

    2016-01-01

    Electronic cigarettes (e-cigarettes) are an increasingly popular source of nicotine and an increasingly popular topic in the media. Concerns about potential hazards associated with e-cigarette use and advertising, especially to adolescents, have led to studies on e-cigarettes in both traditional media (TV, mail, print, and outdoor advertising) and social media (websites, social networking sites, blogs, and e-mails). This review presents a narrative description of available studies related to e-cigarettes in the media. These articles have focused on promotion in both traditional and social media across a broad range of topics and have concentrated on target audiences, smoking cessation, harm reduction, and advertising. E-cigarette advertising is the most frequent topic in the published articles. Identifying the target audience also is a common objective in articles. The representation of e-cigarettes as a “healthier alternative” to traditional cigarettes and their use as a “smoking cessation aid” are main themes presented through all types of media. PMID:27365871

  4. [Idiopathic Pulmonary Fibrosis].

    Science.gov (United States)

    Prasse, A

    2015-10-01

    Idiopathic pulmonary fibrosis (IPF) is the most common idiopathic interstitial pneumonia and a disease of the elderly. Cigarette smoking and longterm exposure to substances harming alveolar epithelial cells are risk factors for the development of IPF. There is also evidence for a genetic susceptibility. IPF is defined as the idiopathic variant of Usual Interstitial Pneumonitis (UIP). Diagnosis of IPF is complex and based on the exclusion of other diseases associated with an UIP pattern. The only cure is lung transplantation. In the last years there was a breakthrough in the treatment of IPF. With pirfenidone and nintedanib there are now two compounds approved for the treatment of IPF. PMID:26444136

  5. 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

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

    Science.gov (United States)

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

    2016-01-01

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

  7. 19 CFR 159.5 - Cigars, cigarettes, and cigarette papers and tubes.

    Science.gov (United States)

    2010-04-01

    ...; DEPARTMENT OF THE TREASURY (CONTINUED) LIQUIDATION OF DUTIES General Provisions § 159.5 Cigars, cigarettes, and cigarette papers and tubes. The internal revenue taxes imposed on cigars, cigarettes, and... 19 Customs Duties 2 2010-04-01 2010-04-01 false Cigars, cigarettes, and cigarette papers and...

  8. 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

  9. Inhalation of tobacco smoke induces increased proliferation of urinary bladder epithelium and endothelium in female C57BL/6 mice

    International Nuclear Information System (INIS)

    Cigarette smoking is the major environmental risk factor for bladder cancer in humans. Aromatic amines, potent DNA-reactive bladder carcinogens present in cigarette smoke, contribute significantly. However, increased cell proliferation, caused by direct mitogenesis or in response to cytotoxicity, may also play a role since urothelial hyperplasia has been observed in human cigarette smokers. We examined the urothelial effects of cigarette smoke (whole body inhalation exposure (Teague) system) in female C57BL/6 mice at various times in two studies, including reversibility evaluations. In both studies, no urothelial hyperplasia was observed by light microscopy in any group. However, in study 1, the Ki-67 labeling index (LI) of the urothelium was significantly increased in the smoke exposed group compared to controls through 3 months, but was not present at 6, 9 or 12 months even with continued exposures. In the groups that discontinued smoke exposure, it returned to the same levels as controls or lower. In study 2, the bromodeoxyuridine LI was similar to controls on day 1 but significantly increased at 5 days in the smoke exposed group. In the group that discontinued smoke exposure for 2 days, the LI was increased compared to controls but not significantly. Superficial urothelial cell cytotoxicity and necrosis were detectable by scanning electron microscopy at 5 days. Changes in LI of submucosal endothelial cells generally followed those of the urothelium and effects were reversible upon cessation of exposure. The increased urothelial proliferation appeared to be due to superficial cell cytotoxicity with consequent regeneration

  10. Youths' understandings of cigarette advertisements.

    Science.gov (United States)

    Freeman, Dan; Brucks, Merrie; Wallendorf, Melanie; Boland, Wendy

    2009-01-01

    This study addresses two questions: (1) when youths are exposed to advertisements for cigarettes, do they primarily see advertisements for brands or products, and (2) is there a relationship between youths' understandings of cigarette advertisements and their susceptibility to smoking? A sample of 271 participants ranging in age from 7 to 12 viewed a series of print advertisements that included cigarette and non-tobacco-related ads. While viewing each ad, participants were asked to indicate what they thought the advertisement was trying to sell. Responses were coded into one of three categories reflecting important differences in participants' comprehension of each advertisement - no understanding, product category understanding, or brand understanding. Results show that youths typically understand the type of product an advertisement is promoting; however, the levels of brand understanding observed for cigarette advertisements were low in an absolute sense, and significantly lower than brand understanding of non-tobacco-related advertisements. Results also show that understanding cigarette ads as promoting specific brands of cigarettes is positively related to susceptibility to smoking. Taken together, these findings provide a glimpse of the psychological mechanisms that may underlie the well established link between exposure to cigarette advertising and youth smoking. PMID:18812253

  11. Smoking-induced expression of the GPR15 gene indicates its potential role in chronic inflammatory pathologies.

    Science.gov (United States)

    Kõks, Gea; Uudelepp, Mari-Liis; Limbach, Maia; Peterson, Pärt; Reimann, Ene; Kõks, Sulev

    2015-11-01

    Despite the described clear epigenetic effects of smoking, the effect of smoking on genome-wide gene expression in the blood is obscure. We therefore studied the smoking-induced changes in the gene-expression profile of the peripheral blood. RNA was extracted from the whole blood of 48 individuals with a detailed smoking history (24 never-smokers, 16 smokers, and 8 ex-smokers). Gene-expression profiles were evaluated with RNA sequencing, and results were analyzed separately in 24 men and 24 women. In the male smokers, 13 genes were statistically significantly (false-discovery rate <0.1) differentially expressed; in female smokers, 5 genes. Although most of the differentially expressed genes were different between the male and female smokers, the G-protein-coupled receptor 15 gene (GPR15) was differentially expressed in both male and female smokers compared with never-smokers. Analysis of GPR15 methylation identified significantly greater hypomethylation in smokers compared with that in never-smokers. GPR15 is the chemoattractant receptor that regulates T-cell migration and immunity. Up-regulation of GPR15 could explain to some extent the health hazards of smoking with regard to chronic inflammatory diseases. PMID:26348578

  12. Cigarette Smoking and Dyspnea Perception

    Directory of Open Access Journals (Sweden)

    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. Marketing of menthol cigarettes and consumer perceptions

    Directory of Open Access Journals (Sweden)

    Rising Joshua

    2011-05-01

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

  14. A varying T cell subtype explains apparent tobacco smoking induced single CpG hypomethylation in whole blood

    OpenAIRE

    Bauer, Mario; Linsel, Gunter; Fink, Beate; Offenberg, Kirsten; Hahn, Anne Maria; Sack, Ulrich; Knaack, Heike; Eszlinger, Markus; Herberth, Gunda

    2015-01-01

    Background Many recent epigenetic studies report that cigarette smoking reduces DNA methylation in whole blood at the single CpG site cg19859270 within the GPR15 gene. Results Within two independent cohorts, we confirmed the differentially expression of the GPR15 gene when smokers and non-smokers subjects are compared. By validating the GPR15 protein expression at the cellular level, we found that the observed decreased methylation at this site in white blood cells (WBC) of smokers is mainly ...

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

    Institute of Scientific and Technical Information of China (English)

    Zongxian JIAO; Qilin AO; Xiaona GE; Mi XIONG

    2008-01-01

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

  16. A New Area to Fight: Electronic Cigarette

    Directory of Open Access Journals (Sweden)

    Şermin Börekçi

    2015-08-01

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

  17. 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

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

    Institute of Scientific and Technical Information of China (English)

    郭轶; 卢小刚; 代远斌

    2015-01-01

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

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

    Science.gov (United States)

    Fromme, Hermann; Schober, Wolfgang

    2015-04-01

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

  20. Patient–physician communication regarding electronic cigarettes

    Directory of Open Access Journals (Sweden)

    Michael B. Steinberg

    2015-01-01

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

  1. E-Cigarettes Emit Toxic Vapors

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_160107.html E-Cigarettes Emit Toxic Vapors: Study Levels depend on ... findings could be important to both makers of e-cigarettes and regulators who want to reduce the ...

  2. E-Cigarettes 'In' At Some Schools

    Science.gov (United States)

    ... nlm.nih.gov/medlineplus/news/fullstory_158580.html E-Cigarettes 'In' at Some Schools In certain places, ... study suggests. The researchers found that differences in e-cigarette use between schools increased over time. This ...

  3. Why Teens Choose E-Cigarettes

    Science.gov (United States)

    ... their prices, she suggested. Federal officials also could ban the use of flavors in e-cigarettes, as ... Drug Administration in May announced regulations that would ban sales of e-cigarettes to anyone younger than ...

  4. E-Cigarettes 'In' At Some Schools

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_158580.html E-Cigarettes 'In' at Some Schools In certain places, ... study suggests. The researchers found that differences in e-cigarette use between schools increased over time. This ...

  5. E-cigarettes also contain detrimental chemicals

    DEFF Research Database (Denmark)

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

    2014-01-01

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

  6. Flavour chemicals in electronic cigarette fluids

    OpenAIRE

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

    2015-01-01

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

  7. Electronic Cigarettes: Market Entry in Iceland?

    OpenAIRE

    Hinrik Hinriksson 1990

    2015-01-01

    Given that e-cigarettes will reach the required research and manufacturing standard, Artasan, an over-the-counter pharmaceutical company, are evaluating their potential distribution on the Icelandic market. Smoking consumption among Icelanders is of decreasing concern as daily cigarette use has reduced from 33% to only 11.6% in the last 26 years. However, sales of nicotine replacement therapies have evidently been increasing alongside the decreasing use of cigarettes. Globally, e-cigarette in...

  8. Electronic cigarettes: a short review.

    Science.gov (United States)

    Bertholon, J F; Becquemin, M H; Annesi-Maesano, I; Dautzenberg, B

    2013-01-01

    Marketed since 2004 as an alternative to nicotine delivery and advertised as a valid means to smoking cessation, the electronic (e)-cigarette has been the subject of much controversy but very little experimental study. This review provides a brief summary of the current knowledge of this product. Propylene glycol and glycerol, the main ingredients of the fluid that is vaporized, have proved to be harmless in the fog machines of the entertainment industry. However, in the case of the e-cigarette fluid, the composition is not properly labeled: additives like nicotine and flavors vary between and within brands and contamination with various chemicals has been detected. The short-term toxicity seems low, but the long-term toxicity is unknown. The usefulness of the e-cigarette in smoking cessation has still to be clinically established. PMID:24080743

  9. 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.

  10. 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

  11. E-cigarettes also contain detrimental chemicals

    DEFF Research Database (Denmark)

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

    2014-01-01

    This article reviews studies dealing with the content of electronic (e-) cigarettes. Based on measurements of the e-juice, the inhaled and the exhaled vapour, it is sound to assume that smoking e-cigarettes might have much less detrimental health effects than smoking conventional cigarettes. Howe...

  12. Corrective Taxes and Cigarette Characteristics.

    Science.gov (United States)

    Calcott, Paul; Petkov, Vladimir

    2016-07-01

    If cigarette design was exogenous, inefficiencies arising from smoking could be addressed either with a tax per packet or with an ad valorem tax. However, it is well known that the consequences of these two instruments differ when product characteristics are endogenous. We consider three such characteristics: nicotine, tar, and flavor. Implementation of the first-best social optimum typically requires the capacity to tax or regulate harmful ingredients. Without such a capacity, the next-best policy often combines a per-unit tax on cigarettes with an ad valorem subsidy. Copyright © 2015 John Wiley & Sons, Ltd. PMID:25919448

  13. 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.

  14. E-cigarettes: promise or peril?

    Science.gov (United States)

    Riker, Carol A; Lee, Kiyoung; Darville, Audrey; Hahn, Ellen J

    2012-03-01

    Electronic cigarettes (e-cigarettes) use a heating element to vaporize nicotine and other ingredients, simulating the visual, sensory, and behavioral aspects of smoking without the combustion of tobacco. An ever-growing number of companies around the world manufacture a wide variety of e-cigarette brands, despite scant information on the safety of the ingredients for human inhalation. This article provides an overview of the history, production, and marketing of e-cigarettes, the contents of e-cigarettes and vapor, how they are used, public health concerns, and implications for nursing practice, research, and policy development. PMID:22289406

  15. Carbonyl Compounds Generated from Electronic Cigarettes

    Directory of Open Access Journals (Sweden)

    Kanae Bekki

    2014-10-01

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

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

    Directory of Open Access Journals (Sweden)

    Marli Maria Knorst

    2014-10-01

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

  17. Pulmonary Rehabilitation

    Science.gov (United States)

    ... programs are certified by the American Association of Cardiovascular and Pulmonary Rehabilitation. These programs can be found on the AACVPR ... at 1-800-586-4872. American Association of Cardiovascular and Pulmonary Rehabilitation ... ...

  18. Pulmonary Fibrosis

    Science.gov (United States)

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

  19. Pulmonary edema

    Science.gov (United States)

    Pulmonary edema is an abnormal buildup of fluid in the lungs. This buildup of fluid leads to shortness of ... Pulmonary edema is often caused by congestive heart failure . When the heart is not able to pump efficiently, blood ...

  20. Pulmonary rehabilitation

    OpenAIRE

    Spruit, Martijn A.

    2001-01-01

    Pulmonary rehabilitation is a therapy that offers benefits to patients with chronic obstructive pulmonary disease that are complementary to those obtained by pharmacotherapy. The main objective of pulmonary rehabilitation is to restore muscle function and exercise tolerance, reverse other nonrespiratory consequences of the disease, and help patients to self-manage chronic obstructive pulmonary disease and its exacerbations and symptoms. To do so, a multidisciplinary program tailored to the pa...

  1. Pulmonary Embolism.

    Science.gov (United States)

    Rali, Parth; Gandhi, Viral; Malik, Khalid

    2016-01-01

    Pulmonary embolism covers a wide spectrum of presentation from an asymptomatic individual to a life-threatening medical emergency. It is of paramount importance to appropriately risk stratify patients with pulmonary embolism, particularly with those who present without hypotension. Right ventricular dysfunction can evolve after a patient has received a diagnosis of pulmonary embolism, necessitating aggressive measures rather than simple anticoagulation. In this review, we discuss definition, risk stratification, pathogenesis, diagnostic approach, and management, with particular focus on massive pulmonary embolism. PMID:26919674

  2. Learn About Pulmonary Fibrosis

    Science.gov (United States)

    ... www.lung.org > Lung Health and Diseases > Lung Disease Lookup > Pulmonary Fibrosis Learn About Pulmonary Fibrosis Pulmonary fibrosis is ... while processing XML file."); } }); } } --> Blank Section Header Lung Disease Lookup Pulmonary Fibrosis Learn About Pulmonary Fibrosis Pulmonary Fibrosis Symptoms, ...

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

    OpenAIRE

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

    2011-01-01

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

  4. 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...

  5. 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...

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

    OpenAIRE

    MaikeLeberl; AdelheidKratzer

    2013-01-01

    Chronic Obstructive Pulmonary Disease (COPD) is one of the foremost causes of death worldwide. It is primarily caused by tobacco smoke, making it an easily preventable disease, but facilitated by genetic α-1 antitrypsin deficiency. In addition to active smokers, health problems also occur in people involuntarily exposed to second hand smoke (SHS). Currently, the relationship between SHS and COPD is not well established. Knowledge of pathogenic mechanisms is limited, thereby halting the advanc...

  8. Pulmonary vasculature in COPD: The silent component.

    Science.gov (United States)

    Blanco, Isabel; Piccari, Lucilla; Barberà, Joan Albert

    2016-08-01

    Chronic obstructive pulmonary disease (COPD) is characterized by airflow obstruction that results from an inflammatory process affecting the airways and lung parenchyma. Despite major abnormalities taking place in bronchial and alveolar structures, changes in pulmonary vessels also represent an important component of the disease. Alterations in vessel structure are highly prevalent and abnormalities in their function impair gas exchange and may result in pulmonary hypertension (PH), an important complication of the disease associated with reduced survival and worse clinical course. The prevalence of PH is high in COPD, particularly in advanced stages, although it remains of mild to moderate severity in the majority of cases. Endothelial dysfunction, with imbalance between vasodilator/vasoconstrictive mediators, is a key determinant of changes taking place in pulmonary vasculature in COPD. Cigarette smoke products may perturb endothelial cells and play a critical role in initiating vascular changes. The concurrence of inflammation, hypoxia and emphysema further contributes to vascular damage and to the development of PH. The use of drugs that target endothelium-dependent signalling pathways, currently employed in pulmonary arterial hypertension, is discouraged in COPD due to the lack of efficacy observed in randomized clinical trials and because there is compelling evidence indicating that these drugs may worsen pulmonary gas exchange. The subgroup of patients with severe PH should be ideally managed in centres with expertise in both PH and chronic lung diseases because alterations of pulmonary vasculature might resemble those observed in pulmonary arterial hypertension. Because this condition entails poor prognosis, it warrants specialist treatment. PMID:27028849

  9. 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.

  10. Side-stream tobacco smoke-induced airway hyperresponsiveness in early postnatal period is involved nerve growth factor.

    Science.gov (United States)

    Wu, Z-X; Hunter, D D; Batchelor, T P; Dey, R D

    2016-03-01

    Epidemiological studies have shown that children are more susceptible to adverse respiratory effects of passive smoking than adults. The goal of this study is to elucidate the possible neural mechanism induced by exposure to passive smoking during early life. Postnatal day (PD) 2 and PD 21 mice were exposed to side-stream tobacco smoke (SS), a surrogate to secondhand smoke, or filtered air (FA) for 10 consecutive days. Pulmonary function, substance P (SP) airway innervation, neurotrophin gene expression in lung and nerve growth factor (NGF) release in bronchoalveolar lavage (BAL) fluid were measured at different times after the last SS or FA exposure. Exposure to SS significantly altered pulmonary function in PD2, accompanied with an enhanced SP innervation in airway. However, exposure to SS during the later developmental period (PD21) did not appear to affect pulmonary function and SP innervation of the airways. Interestingly, SS exposure in PD2 group significantly induced an increased gene expression on NGF, and decreased NGF receptor P75 in lung; parallel with high levels of NGF protein in BAL. Furthermore, pretreatment with NGF antibody significantly diminished SS-induced airway hyperresponsivenss and the increased SP airway innervation in the PD2 group. These findings suggest that enhanced NGF released in the lung contributes to SS-enhanced SP tracheal innervation and airway responsiveness in early life. PMID:26638730

  11. 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

  12. 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.

  13. HOW DO SMOKERS RESPOND TO CIGARETTE TAXES? EVIDENCE FROM CHINA'S CIGARETTE INDUSTRY.

    Science.gov (United States)

    Liu, Hong; Rizzo, John A; Sun, Qi; Wu, Fang

    2014-07-18

    This paper examines how Chinese smokers respond to tax-driven cigarette price increases by estimating a discrete choice model of demand for differentiated products, using annual nationwide brand-level cigarette sales data in China from 2005 to 2010. We allow for substitution between different cigarette brands and also incorporate key features of rational addiction theory into the model. Results show that the average own-price elasticity of demand for cigarettes at the brand level is -0.807, and the overall price elasticity of cigarettes at the market level is -0.488 in China. We find tax-induced substitution toward low-price cigarettes as well as high-tar cigarettes and that tax hikes encourage within-class substitution more than across-class substitution. These results have important policy implications for the potential effects of cigarette taxation. Copyright © 2014 John Wiley & Sons, Ltd. PMID:25044632

  14. [The challenge of electronic cigarettes].

    Science.gov (United States)

    Córdoba García, Rodrigo

    2014-01-01

    The electronic cigarette (e-cig) is a device with a conventional cigarette shape that releases a determined dose of nicotine vapour through an electronic heating process. The nicotine cartridges vary significantly in the amount of nicotine released, even within the same brand. Not all brands admit that they contain nicotine, but this is detected in the majority of units analysed. The e-cig usually contains a propellant, such as propylene glycol, which is a lung irritant. The short-term respiratory effect of the vapour of an e-cig is similar to that caused by the smoke of a cigarette, and is a cause of broncho-restriction. The majority of brands contain glycerine and at least one case of lipoid pneumonia has been detected due to this substance. Many brands contain traces of N-nitrosamines, heavy metals, and other products that are found in conventional cigarette smoke, but in a much higher proportion. There is currently no scientific evidence available that shows it is an effective device for quitting smoking, thus it should not be pro-actively recommended for this purpose, and may interfere with the use of demonstrated scientific evidence-based treatments for quitting smoking. It may have an undesirable effect on promoting the starting of smoking in adolescents or keeping adult smokers consuming nicotine and on gestural dependency. The toxicity of the vapour is not well known, but it is known that they are not innocuous, thus they should not be used in closed public spaces. PMID:24704194

  15. Reducing the addictiveness of cigarettes

    OpenAIRE

    HENNINGFIELD, J.; Benowitz, N.; Slade, J.; Houston, T; DAVIS, R.; Deitchman, S.

    1998-01-01

    OBJECTIVE—To assess the feasibility of reducing tobacco-caused disease by gradually removing nicotine from cigarettes until they would not be effective causes of nicotine addiction.
DATA SOURCES—Issues posed by such an approach, and potential solutions, were identified from analysis of literature published by the US Food and Drug Administration (FDA) in its 1996 Tobacco Rule, comments of the tobacco industry and other institutions and individuals on the rule, review of the reference lists of ...

  16. Menthol Cigarettes | Smokefree.gov

    Science.gov (United States)

    Menthol is a substance naturally found in mint plants such as peppermint and spearmint. It gives a cooling sensation. It is often used to relieve minor pain and irritation and prevent infection.    Menthol is added to many products. These include lozenges, syrups, creams and ointments, nasal sprays, powders, and candy. But none of these products are lighted or smoked when used. That makes them different from menthol cigarettes.  

  17. 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

  18. Cigarette Taxes and the Social Market

    OpenAIRE

    Hansen, Benjamin; Sabia, Joseph J.; Daniel I. Rees

    2011-01-01

    Previous researchers have argued that the social market for cigarettes insulates its participants from policies designed to curb youth smoking. Using state Youth Risk Behavior Survey data, we examine whether recent changes in state cigarette taxes affected how young smokers obtained their cigarettes. Our estimates suggest that tax increases reduce youth smoking participation primarily through their effect on third-party purchase, although there is evidence that they are negatively related to ...

  19. Cigarettes and Alcohol: Substitutes or Complements?

    OpenAIRE

    Decker, Sandra L.; Amy Ellen Schwartz

    2000-01-01

    Taxation of cigarettes and alcohol can raise revenue and reduce consumption of goods with negative external effects. Despite medical and psychological evidence linking their consumption, little previous work has investigated the significance of cross-price effects in cigarette and alcohol consumption. We use individual-level data from the Behavioral Risk Factor Surveillance System to investigate cigarette and alcohol consumption in the US, estimating both own and cross-price elasticities. Res...

  20. Cigarette package design: opportunities for disease prevention

    OpenAIRE

    Pollay RW; DiFranza JR; Clark DM

    2002-01-01

    Abstract Objective To learn how cigarette packages are designed and to determine to what extent cigarette packages are designed to target children. Methods A computer search was made of all Internet websites that post tobacco industry documents using the search terms: packaging, package design, package study, box design, logo, trademark and design study. All documents were retrieved electronically and analyzed by the first author for recurrent themes. Data Synthesis Cigarette manufacturers de...

  1. Pulmonary emphysema and smoking

    International Nuclear Information System (INIS)

    We assessed the relation between PE and smoking in 1,563 cases (1,068 men and 495 women) who underwent CT scaring for suspicion of respiratory disease on chest radiograph or some respiratory complaints. PE was diagnosed by the existence of low attenuation areas in CT scan and not by pulmonary function tests. CT was performed with 10 mm collimation in a standard algorithm. There were 2 subtypes of pulmonary emphysema: centrilobular and paraseptal emphysema. PE, regardless of the grade, was seen: in 189 out of 348 (54.3%) cases in males smokers and in only 2 out of 63 (3.2%) cases in male non-smokers; and in 5 out of 25 (20.0%) in female smokers and in 4 out of 203 (2.0%) in female non-smokers. PE was observed in more than half of male smokers. High incidence of PE was also observed in even younger generation, and severity would progress with advancing age and smoking. Both types of emphysema progress with age and amount of cigarette smoking. (author)

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

    Science.gov (United States)

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

    2008-01-01

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

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

    Directory of Open Access Journals (Sweden)

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

    2011-01-01

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

  4. Eicosanoid production and lymphatic responsiveness in human cigarette smokers compared with non-smokers.

    Science.gov (United States)

    Sinzinger, H; Kaliman, J; Oguogho, A

    2000-03-01

    Leg lymphatic segments were isolated from 10 patients (4 cigarette smokers and 6 non-smokers) undergoing conventional lymphography. Prostaglandin (PG) levels and PG synthesis in the lymphatics and in a variety of body fluids and the effects of eicosanoids on lymphatic contractility were determined. Leg lymphatics from 4 smokers generated less PGI2 and contained more 8-epi-PGF2 alpha when compared with leg lymphatics in 6 non-smokers. Similarly, levels of 8-epi-PGF2 alpha in smokers compared with non-smokers were higher in plasma (28.6 cf 19.7 pg/ml), leg lymph (146.7 cf 65.3 pg/ml), serum (299.0 cf 204.1 pg/ml), and urine (473.4 cf 241.0 pg/mg creatinine). Lymphatics from smokers also showed a higher contractile response, less 14C-arachidonic acid conversion to PGI2 and less PGI2-formation with various stimuli compared with non-smokers. Together these findings suggest that smoking induces oxidation injury, promotes altered (iso-)eicosanoid production and impacts on the function and dysfunction of peripheral lymphatics under normal circumstances and in a variety of clinical disorders. PMID:10769813

  5. 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

  6. Cigarette Litter: Smokers’ Attitudes and Behaviors

    Directory of Open Access Journals (Sweden)

    Julia C. Cartwright

    2012-06-01

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

  7. Hazardous waste status of discarded electronic cigarettes

    Energy Technology Data Exchange (ETDEWEB)

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

    2015-05-15

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

  8. Do cigarette and alcohol affect semen analysis?

    Directory of Open Access Journals (Sweden)

    Mehmet Zeynel Keskin

    2016-03-01

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

  9. Hazardous waste status of discarded electronic cigarettes

    International Nuclear Information System (INIS)

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

  10. 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

  11. Cigarette smoking and brain regulation of energy homeostasis

    Directory of Open Access Journals (Sweden)

    Hui eChen

    2012-07-01

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

  12. Living with Pulmonary Fibrosis

    Science.gov (United States)

    ... www.lung.org > Lung Health and Diseases > Lung Disease Lookup > Pulmonary Fibrosis Living With Pulmonary Fibrosis What to Expect ... while processing XML file."); } }); } } --> Blank Section Header Lung Disease Lookup Pulmonary Fibrosis Learn About Pulmonary Fibrosis Pulmonary Fibrosis Symptoms, ...

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

    Directory of Open Access Journals (Sweden)

    Olivia A. Wackowski

    2016-06-01

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

  14. Smokers' and E-Cigarette Users' Perceptions about E-Cigarette Warning Statements.

    Science.gov (United States)

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

    2016-01-01

    Cigarette warning labels are important sources of risk information, but warning research for other tobacco products is limited. This study aimed to gauge perceptions about warnings that may be used for e-cigarettes. We conducted six small focus groups in late 2014/early 2015 with adult current e-cigarette users and cigarette-only smokers. Participants rated and discussed their perceptions of six e-cigarette warning statements, and warnings in two existing Vuse and MarkTen e-cigarette ads. Participants were open to e-cigarette warnings and provided the strongest reactions to statements warning that e-liquid/e-vapor or e-cigarettes can be poisonous, contain toxins, or are "not a safe alternative to smoking". However, many also noted that these statements were exaggerated, potentially misleading, and could scare smokers away from reducing their harm by switching to e-cigarettes. Opinions on the Food and Drug Administration's proposed nicotine addiction warning and warnings that e-cigarettes had not been approved for smoking cessation or had unknown health effects were mixed. Participants perceived MarkTen's advertisement warning to be stronger and more noticeable than Vuse's. Care should be taken in developing e-cigarette warnings given their relative recentness and potential for harm reduction compared to other tobacco products. Additional research, including with varied audiences, would be instructive. PMID:27376310

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

    Science.gov (United States)

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

    2016-01-01

    Cigarette warning labels are important sources of risk information, but warning research for other tobacco products is limited. This study aimed to gauge perceptions about warnings that may be used for e-cigarettes. We conducted six small focus groups in late 2014/early 2015 with adult current e-cigarette users and cigarette-only smokers. Participants rated and discussed their perceptions of six e-cigarette warning statements, and warnings in two existing Vuse and MarkTen e-cigarette ads. Participants were open to e-cigarette warnings and provided the strongest reactions to statements warning that e-liquid/e-vapor or e-cigarettes can be poisonous, contain toxins, or are “not a safe alternative to smoking”. However, many also noted that these statements were exaggerated, potentially misleading, and could scare smokers away from reducing their harm by switching to e-cigarettes. Opinions on the Food and Drug Administration’s proposed nicotine addiction warning and warnings that e-cigarettes had not been approved for smoking cessation or had unknown health effects were mixed. Participants perceived MarkTen’s advertisement warning to be stronger and more noticeable than Vuse’s. Care should be taken in developing e-cigarette warnings given their relative recentness and potential for harm reduction compared to other tobacco products. Additional research, including with varied audiences, would be instructive. PMID:27376310

  16. 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

  17. 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

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

    Directory of Open Access Journals (Sweden)

    Abdessalem Koubaa

    2015-02-01

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

  19. E-Cigarettes | Smokefree.gov

    Science.gov (United States)

    You may have heard people talking about using electronic cigarettes (also called e-cigarettes or e-cigs) as a way to try to quit smoking. If you’re thinking about using an e-cig, here are three things you should know.

  20. 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.

  1. 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....

  2. 47 CFR 73.4055 - Cigarette advertising.

    Science.gov (United States)

    2010-10-01

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

  3. State cigarette excise taxes - United States, 2010-2011.

    Science.gov (United States)

    2012-03-30

    Increasing the price of cigarettes reduces the demand for cigarettes, thereby reducing youth smoking initiation and cigarette consumption and decreasing the prevalence of cigarette use in the United States overall, particularly among youths and young adults. The most common way governments have increased the price of cigarettes is by increasing cigarette excise taxes, which currently are imposed by all states and the District of Columbia. To update data on state cigarette excise taxes in 2009, CDC conducted a survey of changes in state cigarette excise taxes during 2010-2011. During that period, eight states increased their cigarette excise taxes, and one state decreased its tax; as a result, the mean state tax increased from $1.34 in 2009 to $1.46 in 2011. Previous evidence indicates that further increases in cigarette excise taxes would be expected to result in further reductions in demand for cigarettes, decreasing smoking and associated morbidity and mortality. PMID:22456118

  4. Electronic Cigarettes: Ambiguity and Controversies of Usage

    International Nuclear Information System (INIS)

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

  5. Pulmonary studies

    International Nuclear Information System (INIS)

    Radionuclide studies of the lung are described, as regards perfusion studies, ventilation studies and physiological considerations. The four principal applications for radionuclide studies of the lungs are outlined and the uses of these discussed in relation to particular entities including pulmonary embolic disease, congestive heart failure, asthma, acute, nonasthmatic, bronchial obstruction, chronic pulmonary disease and cancer. (Auth./C.F.)

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

    Science.gov (United States)

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

    2015-01-01

    Recent youth trends in the prevalence of e-cigarette and traditional cigarette use in Florida were examined in a cross-sectional, representative state sample from 2011 to 2014. Traditional cigarette use among youth declined during the study period. Experimentation with and past 30-day use of e-cigarettes among Florida youth tripled over 4 years. Past 30-day e-cigarette use exceeded traditional cigarette use in 2014; 10.8% of high school and 4.0% of middle school students reported recent e-cigarette use, compared with 8.7% of high school and 2.9% of middle school students for traditional cigarettes (Ptraditional cigarettes. Given the concern that significant rates of e-cigarette use by U.S. adolescents may have a negative effect on public health, further review of e-cigarette advertising, marketing, sales, and use among U.S. youth is warranted. PMID:25969979

  7. Radiation dose from cigarette tobacco

    International Nuclear Information System (INIS)

    The radioactivity in tobacco leaves collected from 15 different regions of Greece before cigarette production was studied in order to estimate the effective dose from cigarette tobacco due to the naturally occurring primordial radionuclides, such as 226Ra and 210Pb of the uranium series and 228Ra of the thorium series and or man-made radionuclides, such as 137Cs of Chernobyl origin. Gamma-ray spectrometry was applied using Ge planar and coaxial type detectors of high resolution and high efficiency. It was concluded that the annual effective dose due to inhalation for adults (smokers) for 226Ra varied from 42.5 to 178.6 μ Sv y-1 (average 79.7 μ Sv y-1), while for 228Ra from 19.3 to 116.0 μ Sv y-1 (average 67.1 μ Sv y-1) and for 210Pb from 47.0 to 134.9 μ Sv y-1 (average 104.7 μ Sv y-1), that is the same order of magnitude for each radionuclide. The sum of the effective doses of the three natural radionuclides varied from 151.9 to 401.3 μ Sv y-1 (average 251.5 μ Sv y-1). The annual effective dose from 137Cs of Chernobyl origin was three orders of magnitude lower as it varied from 70.4 to 410.4 nSv y-1 (average 199.3 nSv y-1). (authors)

  8. 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

  9. 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

  10. 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

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

    Directory of Open Access Journals (Sweden)

    Rubeena Bano

    2009-03-01

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

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

    International Nuclear Information System (INIS)

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

  13. 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

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

    OpenAIRE

    Anderson, Stacey J

    2010-01-01

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

  15. Price elasticity of demand for cigarettes : The Case of Sweden

    OpenAIRE

    Ahmed, Sadeq Mohamed; Vaziri, Kamran

    2014-01-01

    Due to health problems and the negative externalities associated with cigarette consumption, many governments try to discourage cigarette consumption by increasing its price through taxation. However, cigarette, like the other addictive goods, is viewed as that it is not sensitive to demand rules and the market forces. This study analyses the effect of price increase on cigarette consumption. We used Swedish time series data from 1970 to 2010. Our results reveal that though cigarette is addic...

  16. Public opinion regarding earmarked cigarette tax in Taiwan

    OpenAIRE

    Yang Chung-Lin; Yen Lee-Lan; Tsai Yi-Wen; Chen Pei-Fen

    2003-01-01

    Abstract Background Cigarette taxation has been perceived by academics and policy-makers as one of the most effective ways of reducing the use of cigarettes. On January 1 2002, the Taiwan government imposed a New Taiwan (NT) $5 per pack tax earmarked for the purpose of tobacco control. This study uses a survey collected prior to taxation to assess public attitudes toward cigarette taxation, public beliefs about the effectiveness of cigarette taxation at reducing cigarette use and public opini...

  17. Safety evaluation and risk assessment of electronic cigarettes as tobacco cigarette substitutes: a systematic review

    OpenAIRE

    Farsalinos, Konstantinos E; Polosa, Riccardo

    2014-01-01

    Electronic cigarettes are a recent development in tobacco harm reduction. They are marketed as less harmful alternatives to smoking. Awareness and use of these devices has grown exponentially in recent years, with millions of people currently using them. This systematic review appraises existing laboratory and clinical research on the potential risks from electronic cigarette use, compared with the well-established devastating effects of smoking tobacco cigarettes. Currently available evidenc...

  18. Pulmonary Atresia

    Science.gov (United States)

    ... to repair the defect. Return to main topic: Congenital Heart Disease See on other sites: MedlinePlus https://medlineplus.gov/ency/article/001091.htm Pulmonary atresia American Heart Association www. ...

  19. [Pulmonary rehabilitation].

    Science.gov (United States)

    Senjyu, Hideaki

    2016-05-01

    Pulmonary rehabilitation commenced in Japan in 1957. However, the development of pulmonary rehabilitation took a long time due to the lack of the necessary health and medical services. Pulmonary rehabilitation is a comprehensive intervention based on a thorough patient assessment followed by patient-tailored therapies that include, but are not limited to, exercise training, education, and behavior change, designed to improve the physical and psychological condition of people with chronic respiratory disease and to promote the long-term adherence to health-enhancing behaviors. The benefits of pulmonary rehabilitation include a decrease in breathlessness and an improvement in exercise tolerance. It is important that the gains in exercise tolerance lead to an increase in daily physical activity. PMID:27254948

  20. Pulmonary sequestration

    International Nuclear Information System (INIS)

    Pulmonary sequestration is a congenital affection consisting in the presence of a cystic mass of no-functional pulmonary tissue without an obvious communication with tracheobronchial tree and that receives all or most of its bloodstream of the anomalous vessels from systemic circulation. Taking into account that presentation of this affection is rare compared to other pulmonary affections (between the 1% and the 2% of all pulmonary resections) and that also the more usual is its definitive treatment before adulthood. The case of man aged 44 is presented coming to consultation due to frequent episodes of pneumonias from more 10 years ago diagnosed as a bronchiectasis. The more significant facts of embryology origin of this affection including: anatomical and pathological features, imaging diagnosis, surgical treatment details, and postoperative course. (author)

  1. PULMONARY SCEDOSPORIOSIS

    Directory of Open Access Journals (Sweden)

    SEVERO Luiz Carlos

    1998-01-01

    Full Text Available A case of a solitary pulmonary nodule due to Scedosporium apiospermum (Pseudallescheria boydii is related. A review of the pertinent literature was done and, in addition, similar lesions caused by other opportunistic fungi are commented.

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

    Directory of Open Access Journals (Sweden)

    Maike eLeberl

    2013-05-01

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

  3. Pulmonary Edema

    OpenAIRE

    Tanser, Paul H.

    1981-01-01

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

  4. Pulmonary hypertension

    OpenAIRE

    Anton Vonk Noordegraaf; Joanne A. Groeneveldt; Harm Jan Bogaard

    2016-01-01

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

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

    Science.gov (United States)

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

    2015-02-01

    Previous research has clearly demonstrated that smokers associate cigarette descriptors such as 'light', 'ultra-light' and 'low tar' with reduced health risks, despite evidence showing that cigarettes with these descriptor terms do not present lower health risk. In June 2010, regulations implemented by the US Food and Drug Administration went into effect to ban the use of 'light', 'mild' and 'low' on cigarette packaging. We surveyed smokers participating in human laboratory studies at our Center in Philadelphia, PA, USA shortly after the ban went into effect to determine the extent of awareness of recent cigarette packaging changes among smokers of light cigarettes. In our sample of 266 smokers, 76 reported smoking light cigarettes, but fewer than half of these smokers reported noticing changes to their cigarette packaging. Simple removal of a few misleading terms may be too subtle of a change to register with consumers of so-called 'low tar' cigarettes; more comprehensive regulation of cigarette packaging design may be necessary to gain smokers' attention and minimize misperceptions associated with tobacco pack design characteristics and color. PMID:25492058

  6. E-cigarettes and E-hookahs

    Science.gov (United States)

    Electronic cigarettes; Electronic hookahs; Vaping ... Until more is known about their long-term effects, the FDA and the American Cancer Association recommend steering clear of these devices. If you are trying to quit smoking, your ...

  7. 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...

  8. Types of Pulmonary Hypertension

    Science.gov (United States)

    ... from the NHLBI on Twitter. Types of Pulmonary Hypertension The World Health Organization divides pulmonary hypertension (PH) ... are called pulmonary hypertension.) Group 1 Pulmonary Arterial Hypertension Group 1 PAH includes: PAH that has no ...

  9. Cigarette smuggling in Europe: who really benefits?

    OpenAIRE

    Joossens, L.; Raw, M.

    1998-01-01

    Cigarette smuggling, now on the increase, is so widespread and well organised that it poses a serious threat to public health. This threat comes from two principal directions. First, smuggling makes cigarettes available cheaply, thereby increasing consumption. A third of annual global exports go to the contraband market, representing an enormous impact on consumption, and thus causing an increase in the burden of disease, especially in poorer countries. It is also costing government treasurie...

  10. Chronic obstructive pulmonary disease.

    Science.gov (United States)

    Barnes, Peter J; Burney, Peter G J; Silverman, Edwin K; Celli, Bartolome R; Vestbo, Jørgen; Wedzicha, Jadwiga A; Wouters, Emiel F M

    2015-01-01

    Chronic obstructive pulmonary disease (COPD) is a common disease with high global morbidity and mortality. COPD is characterized by poorly reversible airway obstruction, which is confirmed by spirometry, and includes obstruction of the small airways (chronic obstructive bronchiolitis) and emphysema, which lead to air trapping and shortness of breath in response to physical exertion. The most common risk factor for the development of COPD is cigarette smoking, but other environmental factors, such as exposure to indoor air pollutants - especially in developing countries - might influence COPD risk. Not all smokers develop COPD and the reasons for disease susceptibility in these individuals have not been fully elucidated. Although the mechanisms underlying COPD remain poorly understood, the disease is associated with chronic inflammation that is usually corticosteroid resistant. In addition, COPD involves accelerated ageing of the lungs and an abnormal repair mechanism that might be driven by oxidative stress. Acute exacerbations, which are mainly triggered by viral or bacterial infections, are important as they are linked to a poor prognosis. The mainstay of the management of stable disease is the use of inhaled long-acting bronchodilators, whereas corticosteroids are beneficial primarily in patients who have coexisting features of asthma, such as eosinophilic inflammation and more reversibility of airway obstruction. Apart from smoking cessation, no treatments reduce disease progression. More research is needed to better understand disease mechanisms and to develop new treatments that reduce disease activity and progression. PMID:27189863

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

    OpenAIRE

    Escudero Diaz, Paula

    2016-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Lee Jie-Min

    2007-06-01

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

  13. Pulmonary embolism

    International Nuclear Information System (INIS)

    Pulmonary embolism is a common medical problem whose incidence is likely to increase in our aging population. Although it is life-threatening, effective therapy exists. The treatment is not, however, without significant complications. Thus, accurate diagnosis is important. Unfortunately, the clinical manifestations of pulmonary embolism are nonspecific. Furthermore, in many patients the symptoms of an acute embolism are superimposed on underlying chronic heart or lung disease. Thus, a high index of suspicion is needed to identify pulmonary emboli. Laboratory parameters, including arterial oxygen tensions and electrocardiography, are as nonspecific as the clinical signs. They may be more useful in excluding another process than in diagnosing pulmonary embolism. The first radiologic examination is the chest radiograph, but the clinical symptoms are frequently out of proportion to the findings on the chest films. Classic manifestations of pulmonary embolism on the chest radiograph include a wedge-shaped peripheral opacity and a segmental or lobar diminution in vascularity with prominent central arteries. However, these findings are not commonly seen and, even when present, are not specific. Even less specific findings include cardiomegaly, pulmonary infiltrate, elevation of a hemidiaphragm, and pleural effusion. Many patients with pulmonary embolism may have a normal chest radiograph. The chest radiograph is essential, however, for two purposes. First, it may identify another cause of the patient's symptoms, such as a rib fracture, dissecting aortic aneurysm, or pneumothorax. Second, a chest radiograph is essential to interpretation of the radionuclide V/Q scan. The perfusion scan accurately reflects the perfusion of the lung. However, a perfusion defect may result from a variety of etiologies. Any process such as vascular stenosis or compression by tumor may restrict blood flow. 84 references

  14. Cigarette purchasing behaviors when prices are high.

    Science.gov (United States)

    Hyland, Andrew; Higbee, Cheryl; Bauer, Joseph E; Giovino, Gary A; Cummings, K Michael

    2004-01-01

    The objective of this study was to assess the cigarette purchase patterns of smokers in Erie and Niagara Counties following recent increases in the state excise tax for cigarettes. Data were collected with telephone interviews of a sample of 1,548 randomly selected people in Erie and Niagara Counties between October 2002 and March 2003. Purchase patterns were assessed for the 908 smokers in the sample who responded to questions about cigarette purchasing patterns. Thirty-three percent reported that their usual source of cigarettes is from a small store, large store, pharmacy, or vending machine, while 67% reported that their usual source is from an Indian reservation. Only one smoker reported the Internet was a usual source of cigarettes. The average price paid per pack was $4.80 in a small store and $1.91 on an Indian reservation. Price influences smoking behavior; however, the majority of smokers are taking advantage of readily available venues where less expensive, untaxed cigarettes are sold. This may undermine the public health benefit of higher prices and cause lost revenue to state and local governments. PMID:15643371

  15. Non-neoplastic pulmonary disease from inhaled radon daughters with uranium ore dust in beagle dogs

    International Nuclear Information System (INIS)

    Daily exposures of adult beagle dogs to inhaled radon daughters plus uranium ore dust, with and without concurrent cigarette smoking, for 2 to 5-1/2 yr have produced massive pulmonary fibrosis and severe emphysema. The cumulative exposure doses are similar to those associated with a 5-fold or greater increase in death rate of uranium miners due to chronic respiratory insufficiency, including pneumoconiosis, pulmonary fibrosis, and emphysema

  16. Defect of alveolar regeneration in pulmonary emphysema: Role of lung fibroblasts

    OpenAIRE

    Plantier, Laurent; Boczkowski, Jorge; Crestani, Bruno

    2007-01-01

    Pulmonary emphysema is characterized by the irreversible loss of pulmonary alveoli. Despite recent advances in the understanding this disease, its treatment remains palliative. In this review, we will successively review the data suggesting (1) that alveolar regeneration systems are functional in the mammalian lung and have the potential to regrow lost alveoli, (2) that cigarette smoke, the main etiologic factor of emphysema, inhibits those systems under experimental conditions, and (3) that ...

  17. Pulmonary imaging

    International Nuclear Information System (INIS)

    Studies in pulmonary imaging predominantly depict the distribution of pulmonary perfusion or the ventilation-perfusion balance for the detection of pulmonary embolism, obstructive airway disease, and lung carcinoma. Much work has been done using 133Xe to study both regional ventilation and blood flow. This work has led to a greater understanding of regional blood flow and ventilation, of lung anatomy and morphometry, of the mechanical factors that influence lung function, and of the biochemical and other nonrespiratory functions of the lung. The recent development of emission tomography and the potential for receptor- and function-oriented radiopharmaceuticals have allowed several important regional physiologic processes to be measured. The physical parameters measured in radionuclide emission studies are the temporal and spatial relations of the distribution of tracer in the lungs. Tracers that are diffusible will wash into and out of the lungs at a rate proportional not only to flow but also to membrane permeability. If the radionuclide label is attached to microspheres or macro-aggregates, the amount lodging in any portion of the lung can be related to relative flow in the lung. Metabolism of the lung is reflected by the rate of extraction and disappearance of various labeled radiopharmaceuticals. The problems encountered in assessing the value of ventilation-perfusion scans for the diagnosis of pulmonary embolism are concerned not only with improving specificity, but also with better estimation of the prior probability of pulmonary embolism in the patient being evaluated

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

    Science.gov (United States)

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

    2016-01-01

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

  19. Idiopathic pulmonary fibrosis

    Directory of Open Access Journals (Sweden)

    Noble Paul W

    2008-03-01

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

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

    Directory of Open Access Journals (Sweden)

    Ye Chun-Yuan

    2004-12-01

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

  1. Prothymosin α overexpression contributes to the development of pulmonary emphysema

    OpenAIRE

    SU, BH; Tseng, YL; Shieh, GS; Chen, YC; Shiang, YC; P. Wu; Li, KJ; Shiau, AL; Wu, CL

    2013-01-01

    Emphysema is one of the disease conditions that comprise chronic obstructive pulmonary disease. Prothymosin α transgenic mice exhibit an emphysema phenotype, but the pathophysiological role of prothymosin α in emphysema remains unclear. Here we show that prothymosin α contributes to the pathogenesis of emphysema by increasing acetylation of histones and nuclear factor-kappaB, particularly upon cigarette smoke exposure. We find a positive correlation between prothymosin α levels and the severi...

  2. Electronic cigarette use outcome expectancies among college students

    Science.gov (United States)

    Pokhrel, Pallav; Little, Melissa A.; Fagan, Pebbles; Muranaka, Nicholas; Herzog, Thaddeus A.

    2016-01-01

    Background E-cigarette use outcome expectancies and their relationships with demographic and e-cigarette use variables are not well understood. Based on past cigarette as well as e-cigarette use research, we generated self-report items to assess e-cigarette outcome expectancies among college students. The objective was to determine different dimensions of e-cigarette use expectancies and their associations with e-cigarette use and use susceptibility. Methods Self-report data were collected from 307 multiethnic 4- and 2-year college students [M age=23.5 (SD= 5.5); 65% Female; 35% current cigarette smokers] in Hawaii. Data analyses were conducted by using factor and regression analyses. Results Exploratory factor analysis among e-cigarette ever-users indicated 7 factors: 3 positive expectancy factors (social enhancement, affect regulation, positive sensory experience) and 4 negative expectancy factors (negative health consequences, addiction concern, negative appearance, negative sensory experience). Confirmatory factor analysis among e-cigarette never-users indicated that the 7-factor model fitted reasonably well to the data. Being a current cigarette smoker was positively associated with positive expectancies and inversely with negative expectancies. Higher positive expectancies were significantly associated with greater likelihood of past-30-day e-cigarette use. Except addiction concern, higher negative expectancies were significantly associated with lower likelihood of past-30-day e-cigarette use. Among e-cigarette never-users, positive expectancy variables were significantly associated with higher intentions to use e-cigarettes in the future, adjusting for current smoker status and demographic variables. Conclusions E-cigarette use expectancies determined in this study appear to predict e-cigarette use and use susceptibility among young adults and thus have important implications for future research. PMID:24630824

  3. 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.

  4. 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

  5. Pulmonary histiocytosis

    Directory of Open Access Journals (Sweden)

    Milenković Branislava

    2013-01-01

    Full Text Available Introduction. Langerhans cell histiocytosis encompasses a group of disorders of unknown origin with different clinical presentations and outcomes. It is characterized by infiltration of the involved tissues by large numbers of Langerhans cells, often organized into granulomas. The accumulation of these cells causes the classic lytic bone lesions, skin rashes, lymphadenopathy, splenomegaly, and dysfunction of organ such as the pituitary gland, lungs, liver, and bone marrow. Pulmonary histiocytosis. Adult pulmonary Langerhans cell histiocytosis is a rare disorder of unknown etiology. It occurs predominantly in male smokers, with an incidence peak between 20 and 40 years of age. High-resolution computed tomography of the chest can show nodules, cavitated nodules, and thickand thin-walled cysts. The definite diagnosis of pulmonary Langerhans cell histiocytosis requires identification of Langerhans’ cell granulomas infiltrating and destroying distal bronchioles, which is usually achieved by lung biopsy at a site selected by chest high-resolution computed tomography. Treatment. Treatment options for adults have never been clarified by a clinical trial. The published literature provides minimal data on the comparative efficacy of various treatment options which include surgery/curettage, steroids, radiation, and various chemotherapy regimens. The improved understanding of the mechanisms involved in the pathogenesis of pulmonary Langerhans cell histiocytosis should help in the development of specific therapeutic strategies and effective treatment.

  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. 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

  8. 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

  9. Matrix Remodeling in Pulmonary Fibrosis and Emphysema.

    Science.gov (United States)

    Kulkarni, Tejaswini; O'Reilly, Philip; Antony, Veena B; Gaggar, Amit; Thannickal, Victor J

    2016-06-01

    Pulmonary fibrosis and emphysema are chronic lung diseases characterized by a progressive decline in lung function, resulting in significant morbidity and mortality. A hallmark of these diseases is recurrent or persistent alveolar epithelial injury, typically caused by common environmental exposures such as cigarette smoke. We propose that critical determinants of the outcome of the injury-repair processes that result in fibrosis versus emphysema are mesenchymal cell fate and associated extracellular matrix dynamics. In this review, we explore the concept that regulation of mesenchymal cells under the influence of soluble factors, in particular transforming growth factor-β1, and the extracellular matrix determine the divergent tissue remodeling responses seen in pulmonary fibrosis and emphysema. PMID:26741177

  10. 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 ...

  11. E-Cigarette Poisonings Skyrocket Among Young Kids

    Science.gov (United States)

    ... nlm.nih.gov/medlineplus/news/fullstory_158738.html E-Cigarette Poisonings Skyrocket Among Young Kids: Study Swallowing ... poison control centers about young children's exposure to e-cigarettes have skyrocketed in recent years, new research ...

  12. 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 ...

  13. Doctors Divided on Safety, Use of Electronic Cigarettes

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_160650.html Doctors Divided on Safety, Use of Electronic Cigarettes When ... safety and using e-cigarettes to stop smoking, doctors' advice differs To use the sharing features on ...

  14. E-Cigarette Poisonings Skyrocket Among Young Kids

    Science.gov (United States)

    ... page: https://medlineplus.gov/news/fullstory_158738.html E-Cigarette Poisonings Skyrocket Among Young Kids: Study Swallowing ... poison control centers about young children's exposure to e-cigarettes have skyrocketed in recent years, new research ...

  15. 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 ...

  16. 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

  17. Tobacco and cigarette butt consumption in humans and animals

    OpenAIRE

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

    2011-01-01

    Discarded cigarette butts may present health risks to human infants and animals because of indiscriminate eating behaviours. Nicotine found in cigarette butts may cause vomiting and neurological toxicity; leachates of cigarette butts in aquatic environments may cause exposure to additional toxic chemicals including heavy metals, ethyl phenol and pesticide residues. This report reviews published and grey literature regarding cigarette butt waste consumption by children, pets and wildlife. Alth...

  18. Smokers' and e-cigarette users' perceptions of modified risk warnings for e-cigarettes.

    Science.gov (United States)

    Wackowski, Olivia A; O'Connor, Richard J; Strasser, Andrew A; Hammond, David; Villanti, Andrea C; Delnevo, Cristine D

    2016-12-01

    The 2009 Family Smoking Prevention and Tobacco Control Act opened the possibility for tobacco companies to apply to market their products as having "modified" or reduced risks. However, research on how to communicate comparative tobacco risks and how such messages are interpreted is limited. This study aimed to qualitatively examine perceptions of potential modified risk statements presented as warning labels for e-cigarettes. We conducted six focus groups between 2014 and 2015 with 27 adult e-cigarette users and cigarette-only smokers who provided comments on two versions of a modified risk warning for e-cigarettes: 1) "WARNING: No tobacco product is safe, but this product presents substantially lower risks to health than cigarettes" (as proposed by two companies for their smokeless tobacco products) and 2) "WARNING: This product may be harmful to health, but is substantially less harmful than cigarettes" (an alternative developed by our team). Although most personally believed that e-cigarettes are safer than cigarettes and some thought the messages were true and accurate, many were skeptical and uncomfortable with the warnings because they did not "seem like a warning" and because use of the phrase "substantially lower risks" could be misleading and difficult to understand. Several thought the second warning was stronger (e.g., more active, more specific). Modified risk messages about e-cigarettes may impact perceptions and use of the product. More research is needed to identify the framing, wording and placement (e.g. within or in addition to a warning) that could potentially increase population-level benefits and minimize harms. PMID:27486560

  19. Another Risk From Cigarette Smoking: Corneal Burn

    Directory of Open Access Journals (Sweden)

    Volkan Hürmeriç

    2012-12-01

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

  20. Cigarette advertising to counter New Year's resolutions.

    Science.gov (United States)

    Basil, M D; Basil, D Z; Schooler, C

    2000-01-01

    One process through which tobacco advertising may work is by reducing rates of quitting. Theories of addiction support the notion that relapse can be prompted by environmental cues. Further, because withdrawal symptoms occur over a predictable time frame, and because the most popular time to quit smoking is the beginning of the year, as a New Year's resolution, tobacco companies can make use of advertising to remind quitters of their need to smoke. Study 1 examined advertising in 10 popular magazines. It found a higher number of ads in January and February than the rest of the year after 1984. Study 2 examined cigarette advertising on the back cover of 10 other popular magazines. This study also found a higher rate of cigarette advertisements in January and February than for the rest of the year. The results suggest that cigarette marketers may be attempting to preempt quitting by cuing smoking behavior. PMID:11010347

  1. 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.

  2. Awareness of FDA-mandated cigarette packaging changes among smokers of ‘light’ cigarettes

    OpenAIRE

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

    2014-01-01

    Previous research has clearly demonstrated that smokers associate cigarette descriptors such as ‘light’, ‘ultra-light’ and ‘low tar’ with reduced health risks, despite evidence showing that cigarettes with these descriptor terms do not present lower health risk. In June 2010, regulations implemented by the US Food and Drug Administration went into effect to ban the use of ‘light’, ‘mild’ and ‘low’ on cigarette packaging. We surveyed smokers participating in human laboratory studies at our Cen...

  3. Emotions for sale: cigarette advertising and women's psychosocial needs

    OpenAIRE

    Anderson, Stacey J; Glantz, Stanton A. Ph.D.; Ling, P M

    2005-01-01

    Objective: To explore messages of psychosocial needs satisfaction in cigarette advertising targeting women and implications for tobacco control policy. Methods: Analysis of internal tobacco industry documents and public advertising collections. Results: Tobacco industry market research attempted to identify the psychosocial needs of different groups of women, and cigarette advertising campaigns for brands that women smoke explicitly aimed to position cigarettes as capable of...

  4. Cigarette Consumption, Taxation, and Household Income : Indonesia Case Study

    OpenAIRE

    Adioetomo, Sri Moertiningsih; Djutaharta, Triasih; Hendratno

    2005-01-01

    Cigarette consumption has been increasing in Indonesia, as in many other developing countries, causing a rising burden of disease and premature death. Higher excise taxes have proved effective in many countries in reducing cigarette consumption and raising government revenues. This study examines the effect of higher prices/taxes on the decision to smoke, the quantity of cigarettes consume...

  5. 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…

  6. 75 FR 69523 - Required Warnings for Cigarette Packages and Advertisements

    Science.gov (United States)

    2010-11-12

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

  7. Infliximab protects against pulmonary emphysema in smoking rats

    Institute of Scientific and Technical Information of China (English)

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

    2011-01-01

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

  8. 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...

  9. Can Higher Cigarette Taxes Improve Birth Outcomes?

    OpenAIRE

    Evans, William N.; Ringel, Jeanne S

    1997-01-01

    This study uses within-state variation in taxes over the 1989-1992 time period to test whether maternal smoking and birth outcomes are responsive to higher state cigarette taxes. Data on the outcomes of interest are taken from the Natality Detail files, generating a sample of roughly 10.5 million births. The results indicate that smoking participation declines when excise taxes are increased. The elasticity of demand for cigarettes is estimated to be appro- ximately -0.25. In addition, estima...

  10. 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

  11. Pulmonary aspergillosis.

    Science.gov (United States)

    Chabi, M L; Goracci, A; Roche, N; Paugam, A; Lupo, A; Revel, M P

    2015-05-01

    Aspergillosis is a mycotic disease usually caused by Aspergillus fumigatus, a saprophytic and ubiquitous airborne fungus. Aspergillus-related lung diseases are traditionally classified into four different forms, whose occurrence depends on the immunologic status of the host and the existence of an underlying lung disease. Allergic broncho-pulmonary aspergillosis (ABPA) affects patients with asthma or cystic fibrosis. Saprophytic infection (aspergilloma) occurs in patients with abnormal airways (chronic obstructive pulmonary disease, bronchiectasis, cystic fibrosis) or chronic lung cavities. Chronic necrotizing aspergillosis (semi-invasive form) is described in patients with chronic lung pathology or mild immunodeficiency. Invasive aspergillosis (angio-invasive or broncho-invasive forms) occurs in severely immuno-compromised patients. Knowledge of the various radiological patterns for each form, as well as the corresponding associated immune disorders and/or underlying lung diseases, helps early recognition and accurate diagnosis. PMID:25753544

  12. Pulmonary Hypertension

    OpenAIRE

    Newman, John H.

    2005-01-01

    The modern era in cardiopulmonary medicine began in the 1940s, when Cournand and Richards pioneered right-heart catheterization. Until that time, no direct measurement of central vascular pressure had been performed in humans. Right-heart catheterization ignited an explosion of insights into function and dysfunction of the pulmonary circulation, cardiac performance, ventilation–perfusion relationships, lung–heart interactions, valvular function, and congenital heart disease. It marked the beg...

  13. What Causes Pulmonary Hypertension?

    Science.gov (United States)

    ... from the NHLBI on Twitter. What Causes Pulmonary Hypertension? Pulmonary hypertension (PH) begins with inflammation and changes in the ... different types of PH. Group 1 pulmonary arterial hypertension (PAH) may have no known cause, or the ...

  14. Pulmonary Arterial Hypertension

    Science.gov (United States)

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

  15. Pulmonary manifestations of malaria

    International Nuclear Information System (INIS)

    We report on the two different types of pulmonary manifestations in acute plasmodium falciparum malaria. The more severe variant shows long standing interstitial pulmonary infiltrates, whereas in the more benign courses only short-term pulmonary edemas are visible. (orig.)

  16. Pulmonary Fibrosis Foundation

    Science.gov (United States)

    ... most current news and updates from the Pulmonary Fibrosis Foundation. Life with PF Education & Support About PF ... LEARN MORE We Imagine a World Without Pulmonary Fibrosis The Pulmonary Fibrosis Foundation mobilizes people and resources ...

  17. Pulmonary manifestations of malaria

    Energy Technology Data Exchange (ETDEWEB)

    Rauber, K.; Enkerlin, H.L.; Riemann, H.; Schoeppe, W.

    1987-05-01

    We report on the two different types of pulmonary manifestations in acute plasmodium falciparum malaria. The more severe variant shows long standing interstitial pulmonary infiltrates, whereas in the more benign courses only short-term pulmonary edemas are visible.

  18. Idiopathic Pulmonary Fibrosis

    Science.gov (United States)

    ... Explore Idiopathic Pulmonary Fibrosis What Is... How the Lungs Work Other Names Causes Signs & Symptoms Diagnosis Treatments Living With Clinical Trials Links Related Topics How the Lungs Work Lung Transplant Pulmonary Hypertension Pulmonary Rehabilitation Respiratory Failure ...

  19. Smoking Cessation in Chronic Obstructive Pulmonary Disease.

    Science.gov (United States)

    Tashkin, Donald P

    2015-08-01

    Smoking cessation is the most effective strategy for slowing down the progression of chronic obstructive pulmonary disease (COPD) and reducing mortality in the approximately 50% of patients with diagnosed COPD who continue to smoke. While behavioral interventions (including simple advice) have modest efficacy in improving smoking quit rates, the combination of counseling and pharmacotherapy is more effective than either alone. When combined with even brief counseling, nicotine replacement therapy (NRT), bupropion SR, and varenicline have all been shown to be effective in promoting smoking cessation and sustained abstinence in smokers with COPD to a degree comparable to that observed in the general smoking population. However, the recidivism rate is high after initial quitting so that at the end of 1 year, approximately 80% or more of patients are still smoking. Thus, new approaches to smoking cessation are needed. One approach is to combine different pharmacotherapies, for example, nicotine patch plus rapidly acting NRT (e.g., gum or nasal spray) and/or bupropion or even varenicline plus either NRT or bupropion, in a stepwise approach over a varying duration depending on the severity of nicotine dependence and nicotine withdrawal symptoms during the quit attempt, as proposed in the American College of Chest Physicians Tobacco Dependence Took Kit. Electronic (e)-cigarettes, which deliver vaporized nicotine without most of the noxious components in the smoke from burning tobacco cigarettes, also has potential efficacy as a smoking cessation aid, but their efficacy and safety as either substitutes for regular cigarettes or smoking cessation aids require additional study. This task is complicated because e-cigarettes are currently unregulated and hundreds of different brands are currently available. PMID:26238637

  20. Analysis of trace metals in various brands of cigarettes

    International Nuclear Information System (INIS)

    The present work deals with the analysis of trace metals in various brands of cigarettes belonging to four different countries. In the present research seven trace elements have been determined spectrophotometrically by the use of suitable analytical reagent of the respective metal ions. The metals which has been analysed quantitatively in forty one brand of cigarettes are aluminium, copper, chromium, nickel, iron titanium and zinc. The concentration per cigarette of these metals are in tolerable range. The concentration of above mentioned metal ions is highest in Pakistani cigarettes tobacco while the concentration of nickel is highest in American cigarettes. (author) 221 refs

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

    Science.gov (United States)

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

    2013-01-01

    Electronic cigarettes (e-cigarettes) have attracted considerable attention as a possible alternative to tobacco cigarettes, but uncertainties about their impact on health and indoor air quality as well as their commercial success without a clear regulatory framework are arousing concern. We have therefore tried to summarize the health-related implications of the use of e-cigarettes in order to help physicians and health professionals provide accurate information on this device. Given the lack of unequivocal scientific data on their toxicity and safety, we conclude that at the moment there is no reason to approve e-cigarettes as a safe alternative to tobacco smoke. PMID:24503808

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

    Directory of Open Access Journals (Sweden)

    Richard Barnes

    2009-05-01

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

  3. First Siena International Conference on Animal Models of Chronic Obstructive Pulmonary Disease, Certosa di Pontignano, University of Siena, Italy, September 30-October 2, 2001

    OpenAIRE

    Hele David

    2002-01-01

    Abstract The meeting proved of great interest to those developing an animal model of chronic obstructive pulmonary disease (COPD). COPD is caused by cigarette smoking, evidenced by deterioration in lung function. Lung function is only rarely assessed in animal models. A cigarette smoke driven pathology should provide the best in vivo model for COPD. However, as lesions produced this way take 8–12 months to develop other strategies have to be employed. Emphysematous lesions were also ...

  4. 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

  5. How Is Pulmonary Hypertension Treated?

    Science.gov (United States)

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

  6. Testing warning messages on smokers’ cigarette packages: A standardized protocol

    Science.gov (United States)

    Brewer, Noel T.; Hall, Marissa G.; Lee, Joseph G. L.; Peebles, Kathryn; Noar, Seth M.; Ribisl, Kurt M.

    2015-01-01

    Purpose Lab experiments on cigarette warnings typically use a brief one-time exposure that is not paired with the cigarette packs smokers use every day, leaving open the question of how repeated warning exposure over several weeks may affect smokers. This proof of principle study sought to develop a new protocol for testing cigarette warnings that better reflects real-world exposure by presenting them on cigarette smokers’ own packs. Methods We tested a cigarette pack labeling protocol with 76 US smokers ages 18 and older. We applied graphic warnings to the front and back of smokers’ cigarette packs. Results Most smokers reported that at least 75% of the packs of cigarettes they smoked during the study had our warnings. Nearly all said they would participate in the study again. Using cigarette packs with the study warnings increased quit intentions (ppack labeling protocol with six steps: (1) schedule appointments at brief intervals; (2) determine typical cigarette consumption; (3) ask smokers to bring a supply of cigarette packs to study appointments; (4) apply labels to smokers’ cigarette packs; (5) provide participation incentives at the end of appointments; and (6) refer smokers to cessation services at end of the study. When used in randomized controlled trials in settings with real-world message exposure over time, this protocol may help identify the true impact of warnings and thus better inform tobacco product labeling policy. PMID:25564282

  7. Reasons for Starting and Stopping Electronic Cigarette Use

    Directory of Open Access Journals (Sweden)

    Jessica K. Pepper

    2014-10-01

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

  8. Are Filter-Tipped Cigarettes Still Less Harmful than Non-Filter Cigarettes?—A Laser Spectrometric Particulate Matter Analysis from the Non-Smokers Point of View

    Directory of Open Access Journals (Sweden)

    Maria Schulz

    2016-04-01

    Full Text Available Background: Environmental tobacco smoke (ETS is associated with human morbidity and mortality, particularly chronic obstructive pulmonary disease (COPD and lung cancer. Although direct DNA-damage is a leading pathomechanism in active smokers, passive smoking is enough to induce bronchial asthma, especially in children. Particulate matter (PM demonstrably plays an important role in this ETS-associated human morbidity, constituting a surrogate parameter for ETS exposure. Methods: Using an Automatic Environmental Tobacco Smoke Emitter (AETSE and an in-house developed, non-standard smoking regime, we tried to imitate the smoking process of human smokers to demonstrate the significance of passive smoking. Mean concentration (Cmean and area under the curve (AUC of particulate matter (PM2.5 emitted by 3R4F reference cigarettes and the popular filter-tipped and non-filter brand cigarettes “Roth-Händle” were measured and compared. The cigarettes were not conditioned prior to smoking. The measurements were tested for Gaussian distribution and significant differences. Results: Cmean PM2.5 of the 3R4F reference cigarette: 3911 µg/m3; of the filter-tipped Roth-Händle: 3831 µg/m3; and of the non-filter Roth-Händle: 2053 µg/m3. AUC PM2.5 of the 3R4F reference cigarette: 1,647,006 µg/m3·s; of the filter-tipped Roth-Händle: 1,608,000 µg/m3·s; and of the non-filter Roth-Händle: 858,891 µg/m3·s. Conclusion: The filter-tipped cigarettes (the 3R4F reference cigarette and filter-tipped Roth-Händle emitted significantly more PM2.5 than the non-filter Roth-Händle. Considering the harmful potential of PM, our findings note that the filter-tipped cigarettes are not a less harmful alternative for passive smokers. Tobacco taxation should be reconsidered and non-smoking legislation enforced.

  9. Are Filter-Tipped Cigarettes Still Less Harmful than Non-Filter Cigarettes?—A Laser Spectrometric Particulate Matter Analysis from the Non-Smokers Point of View

    Science.gov (United States)

    Schulz, Maria; Gerber, Alexander; Groneberg, David A.

    2016-01-01

    Background: Environmental tobacco smoke (ETS) is associated with human morbidity and mortality, particularly chronic obstructive pulmonary disease (COPD and lung cancer. Although direct DNA-damage is a leading pathomechanism in active smokers, passive smoking is enough to induce bronchial asthma, especially in children. Particulate matter (PM) demonstrably plays an important role in this ETS-associated human morbidity, constituting a surrogate parameter for ETS exposure. Methods: Using an Automatic Environmental Tobacco Smoke Emitter (AETSE) and an in-house developed, non-standard smoking regime, we tried to imitate the smoking process of human smokers to demonstrate the significance of passive smoking. Mean concentration (Cmean) and area under the curve (AUC) of particulate matter (PM2.5) emitted by 3R4F reference cigarettes and the popular filter-tipped and non-filter brand cigarettes “Roth-Händle” were measured and compared. The cigarettes were not conditioned prior to smoking. The measurements were tested for Gaussian distribution and significant differences. Results: Cmean PM2.5 of the 3R4F reference cigarette: 3911 µg/m3; of the filter-tipped Roth-Händle: 3831 µg/m3; and of the non-filter Roth-Händle: 2053 µg/m3. AUC PM2.5 of the 3R4F reference cigarette: 1,647,006 µg/m3·s; of the filter-tipped Roth-Händle: 1,608,000 µg/m3·s; and of the non-filter Roth-Händle: 858,891 µg/m3·s. Conclusion: The filter-tipped cigarettes (the 3R4F reference cigarette and filter-tipped Roth-Händle) emitted significantly more PM2.5 than the non-filter Roth-Händle. Considering the harmful potential of PM, our findings note that the filter-tipped cigarettes are not a less harmful alternative for passive smokers. Tobacco taxation should be reconsidered and non-smoking legislation enforced. PMID:27092519

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

    Science.gov (United States)

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

    2015-01-01

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

  11. E-cigarettes: a rising trend among youth.

    Science.gov (United States)

    Ahern, Nancy R; Mechling, Brandy

    2014-06-01

    Electronic cigarettes, known as "e-cigarettes," were designed as a smoking cessation tool for adults. An unintended audience for the product has been found with adolescents, many of whom have never used conventional cigarettes. Broad consequences of e-cigarettes on adolescent health include nicotine addiction-and later nicotine withdrawal-and potential for nicotine overdose. U.S. Food and Drug Administration regulations are non-existent; empirical evidence regarding e-cigarettes is limited; and studies conducted with adolescent e-cigarette use are even less common. Prevention measures must target the manufacturers and retailers of these devices as well as adolescents, parents, schools, and health care professionals. Psychiatricmental health nurses are well positioned to raise awareness of the dangerous consequences of e-cigarette use in teens. PMID:24815950

  12. 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...

  13. 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...

  14. The Apoe(-/-) mouse model: a suitable model to study cardiovascular and respiratory diseases in the context of cigarette smoke exposure and harm reduction.

    Science.gov (United States)

    Lo Sasso, Giuseppe; Schlage, Walter K; Boué, Stéphanie; Veljkovic, Emilija; Peitsch, Manuel C; Hoeng, Julia

    2016-01-01

    Atherosclerosis-prone apolipoprotein E-deficient (Apoe(-/-)) mice display poor lipoprotein clearance with subsequent accumulation of cholesterol ester-enriched particles in the blood, which promote the development of atherosclerotic plaques. Therefore, the Apoe(-/-) mouse model is well established for the study of human atherosclerosis. The systemic proinflammatory status of Apoe(-/-) mice also makes them good candidates for studying chronic obstructive pulmonary disease, characterized by pulmonary inflammation, airway obstruction, and emphysema, and which shares several risk factors with cardiovascular diseases, including smoking. Herein, we review the results from published studies using Apoe(-/-) mice, with a particular focus on work conducted in the context of cigarette smoke inhalation studies. The findings from these studies highlight the suitability of this animal model for researching the effects of cigarette smoking on atherosclerosis and emphysema. PMID:27207171

  15. Pulmonary Hypertension in Pulmonary Langerhans Cell Granulomatosis

    OpenAIRE

    Matthias Held; Philipp Schnabel; Arne Warth; Berthold Jany

    2012-01-01

    Introduction. Pulmonary Langerhans cell granulomatosis is a rare disease with a variable course. In pulmonary Langerhans cell granulomatosis pulmonary hypertension is frequent and has an independent prognostic impact. A vasculopathy which ist not related to ventilatory disturbance and fibrosis has been identified. An arteriopathy and even a venulopathy have been described. Due to this possible venulopathy vasodilators carry a significant risk for pulmonary congestion and edema. No drugs have ...

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1990-04-01

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

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

    International Nuclear Information System (INIS)

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

  18. [Pulmonary embolism].

    Science.gov (United States)

    Söffker, Gerold; Kluge, Stefan

    2015-01-01

    Acute pulmonary embolism is an important differential diagnosis of acute chest pain. The clinical signs are often non-specific. However, diagnosis and therapy must be done quickly in order to reduce morbidity and mortality. The new (2014) European guidelines for acute pulmonary embolism (PE) focus on risk-adapted diagnostic algorithms and prognosis adapted therapy concepts. According to the hemodynamic presentation the division in a high-risk group (unstable patient with persistent hypotension or shock) or in non-high-risk groups (hemodynamically stable) was proposed. In the high-risk group the immediate diagnosis is usually done by multidetector spiral computed tomography (MDCT) and primarily the medical therapy of right ventricular dysfunction and thrombolysis is recommended.In the non-high-risk group, this is subdivided into an intermediate-risk group and low-risk group, the diagnosis algorithm based on the PE-pretest probability--determined by validated scores. Moreover, the diagnosis is usually secured by MDCT--the new gold standard in the PE-diagnosis, scores, or it can be primarily ruled out due to the high negative predictive value of D-dimer determination. To improve the prognostic risk stratification in non-high-risk group patients the additional detection of right ventricular dysfunction (MDCT, echocardiography), cardiac biomarkers (troponin, NT proBNP) and validated scores (e.g. Pulmonary Embolism Severity Index) is recommended. Therefore, the intermediate-risk group can be further subdivided. For treatment of non-high-risk group patients, the initial anticoagulation (except those with severe renal insufficiency) using low molecular weight heparin/fondaparinux and conversion to vitamin-K antagonists or alternatively with direct oral anticoagulants (DOAK) is recommended. Hemodynamically stable patients with right ventricular dysfunction and myocardial ischemia (Intermediate-high-risk group patients) but with clinically progressive hemodynamic

  19. Short-term exposure of mice to cigarette smoke and/or residual oil fly ash produces proximal airspace enlargements and airway epithelium remodeling

    OpenAIRE

    P.J.C. Biselli; F.D.T.Q.S. Lopes; H.T. Moriya; D.H.R.F. Rivero; A.C. Toledo; Saldiva, P H N; Mauad, T; M. A. Martins

    2011-01-01

    Chronic obstructive pulmonary disease (COPD) is associated with inflammatory cell reactions, tissue destruction and lung remodeling. Many signaling pathways for these phenomena are still to be identified. We developed a mouse model of COPD to evaluate some pathophysiological mechanisms acting during the initial stage of the disease. Forty-seven 6- to 8-week-old female C57/BL6 mice (approximately 22 g) were exposed for 2 months to cigarette smoke and/or residual oil fly ash (ROFA), a concentra...

  20. Serotonin and corticosterone rhythms in mice exposed to cigarette smoke and in patients with COPD:implication for COPD-associated neuropathogenesis

    OpenAIRE

    Isaac K Sundar; Yao, Hongwei; Huang, Yadi; Lyda, Elizabeth; Sime, Patricia J.; Sellix, Michael T.; Rahman, Irfan

    2014-01-01

    The circadian timing system controls daily rhythms of physiology and behavior, and disruption of clock function can trigger stressful life events. Daily exposure to cigarette smoke (CS) can lead to alteration in diverse biological and physiological processes. Smoking is associated with mood disorders, including depression and anxiety. Patients with chronic obstructive pulmonary disease (COPD) have abnormal circadian rhythms, reflected by daily changes in respiratory symptoms and lung function...

  1. Serotonin and Corticosterone Rhythms in Mice Exposed to Cigarette Smoke and in Patients with COPD: Implication for COPD-Associated Neuropathogenesis

    OpenAIRE

    Isaac K Sundar; Yao, Hongwei; Huang, Yadi; Lyda, Elizabeth; Sime, Patricia J.; Sellix, Michael T.; Rahman, Irfan

    2014-01-01

    The circadian timing system controls daily rhythms of physiology and behavior, and disruption of clock function can trigger stressful life events. Daily exposure to cigarette smoke (CS) can lead to alteration in diverse biological and physiological processes. Smoking is associated with mood disorders, including depression and anxiety. Patients with chronic obstructive pulmonary disease (COPD) have abnormal circadian rhythms, reflected by daily changes in respiratory symptoms and lung function...

  2. Electronic Cigarette Use Among Working Adults - United States, 2014.

    Science.gov (United States)

    Syamlal, Girija; Jamal, Ahmed; King, Brian A; Mazurek, Jacek M

    2016-01-01

    Electronic cigarettes (e-cigarettes) are battery-powered devices that deliver a heated aerosol, which typically contains nicotine, flavorings, and other additives, to the user. The e-cigarette marketplace is rapidly evolving, but the long-term health effects of these products are not known. Carcinogens and toxins such as diacetyl, acetaldehyde, and other harmful chemicals have been documented in the aerosol from some e-cigarettes (1-3). On May 5, 2016, the Food and Drug Administration (FDA) finalized a rule extending its authority to all tobacco products, including e-cigarettes.* The prevalence of e-cigarette use among U.S. adults has increased in recent years, particularly among current and former conventional cigarette smokers (4); in 2014, 3.7% of all U.S. adults, including 15.9% of current cigarette smokers, and 22.0% of former cigarette smokers, used e-cigarettes every day or some days (5). The extent of current e-cigarette use among U.S. working adults has not been assessed. Therefore, CDC analyzed 2014 National Health Interview Survey (NHIS) data for adults aged ≥18 years who were working during the week before the interview, to provide national estimates of current e-cigarette use among U.S. working adults by industry and occupation. Among the estimated 146 million working adults, 3.8% (5.5 million) were current (every day or some days) e-cigarette users; the highest prevalences were among males, non-Hispanic whites, persons aged 18-24 years, persons with annual household income <$35,000, persons with no health insurance, cigarette smokers, other combustible tobacco users, and smokeless tobacco users. By industry and occupation, workers in the accommodation and food services industry and in the food preparation and serving-related occupations had the highest prevalence of current e-cigarette use. Higher prevalences of e-cigarette use among specific groups and the effect of e-cigarette use on patterns of conventional tobacco use underscore the importance

  3. [Pulmonary circulation in embolic pulmonary edema].

    Science.gov (United States)

    Sanotskaia, N V; Polikarpov, V V; Matsievskiĭ, D D

    1989-02-01

    The ultrasonic method was used in acute experiments on cats with open chest under artificial lung ventilation to obtain blood flow in low-lobar pulmonary artery and vein, the blood pressure in pulmonary artery, as well as the left atrial pressure in fat (olive oil) and mechanical (Lycopodium spores) pulmonary embolism. It is shown that pulmonary embolism produces the decrease in the blood flow in pulmonary artery and vein, the increase of the pressure in pulmonary artery and left atria, the increase of lung vessels resistance. The decrease is observed of systemic arterial pressure, bradycardia, and extrasystole. After 5-10 min the restoration of arterial pressure and heart rhythm occur and partial restoration of blood flow in pulmonary artery and vein. In many experiments the blood flow in vein outdoes that in the artery--it allows to suppose the increase of the blood flow in bronchial artery. After 60-90 min there occur sudden decrease of systemic arterial pressure, the decrease of the blood flow in pulmonary artery and vein. The pressure in pulmonary artery and resistance of pulmonary vessels remain high. Pulmonary edema developed in all animals. The death occurs in 60-100 min after the beginning of embolism. PMID:2923969

  4. Social Inequality in Cigarette Consumption, Cigarette Dependence, and Intention to Quit among Norwegian Smokers

    Directory of Open Access Journals (Sweden)

    Marianne Lund

    2015-01-01

    Full Text Available Background. The study aim was to examine the influence of education and income on multiple measures of risk of smoking continuation. Methods. Three logistic regression models were run on cigarette consumption, dependence, and intention to quit based on nationally representative samples (2007–2012 of approximately 1 200 current smokers aged 30–66 years in Norway. Results. The relative risk ratio for current versus never smokers was RRR 5.37, 95% CI [4.26–6.77] among individuals with low educational level versus high and RRR 1.53, 95% CI [1.14–2.06] in the low-income group versus high (adjusted model. Low educational level was associated with high cigarette consumption, high cigarette dependence, and no intention to quit. The difference in predicted probability for having high cigarette consumption, high cigarette dependence, and no intention to quit were in the range of 10–20 percentage points between smokers with low versus those with high educational level. A significant difference between low- and high-income levels was observed for intention to quit. The effect of education on high consumption and dependence was mainly found in smokers with high income. Conclusion. Increased effort to combat social differences in smoking behaviour is needed. Implementation of smoking cessation programmes with high reach among low socioeconomic groups is recommended.

  5. 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

  6. 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.

  7. 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

  8. 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)

  9. Apelin and pulmonary hypertension

    DEFF Research Database (Denmark)

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

    2011-01-01

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

  10. Cigarette Cravings, Impulsivity, and the Brain.

    Science.gov (United States)

    Potvin, Stéphane; Tikàsz, Andràs; Dinh-Williams, Laurence Lê-Anh; Bourque, Josiane; Mendrek, Adrianna

    2015-01-01

    Craving is a core feature of tobacco use disorder as well as a significant predictor of smoking relapse. Studies have shown that appetitive smoking-related stimuli (e.g., someone smoking) trigger significant cravings in smokers impede their self-control capacities and promote drug seeking behavior. In this review, we begin by an overview of functional magnetic resonance imaging (fMRI) studies investigating the neural correlates of smokers to appetitive smoking cues. The literature reveals a complex and vastly distributed neuronal network underlying smokers' craving response that recruits regions involved in self-referential processing, planning/regulatory processes, emotional responding, attentional biases, and automatic conducts. We then selectively review important factors contributing to the heterogeneity of results that significantly limit the implications of these findings, namely between- (abstinence, smoking expectancies, and self-regulation) and within-studies factors (severity of smoking dependence, sex-differences, motivation to quit, and genetic factors). Remarkably, we found that little to no attention has been devoted to examine the influence of personality traits on the neural correlates of cigarette cravings in fMRI studies. Impulsivity has been linked with craving and relapse in substance and tobacco use, which prompted our research team to examine the influence of impulsivity on cigarette cravings in an fMRI study. We found that the influence of impulsivity on cigarette cravings was mediated by fronto-cingulate mechanisms. Given the high prevalence of cigarette smoking in several psychiatric disorders that are characterized by significant levels of impulsivity, we conclude by identifying psychiatric patients as a target population whose tobacco-smoking habits deserve further behavioral and neuro-imaging investigation. PMID:26441686

  11. [Are graphic warnings on cigarette packs useful?].

    Science.gov (United States)

    Etter, J F; Cornuz, J

    2009-07-01

    Based on the WHO Framework Convention on Tobacco Control recommendations, health warnings and messages should be printed on cigarettes packages. Scientific data show that such messages are effective by delivering important information directly to smokers, who believe these messages more and remember better than they do public education campaigns. These warnings also increase the chance of quitting. This narrative review summarizes the data at the time Switzerland requires such pictures on tobacco products. PMID:19634535

  12. Cigarette cravings, impulsivity and the brain

    Directory of Open Access Journals (Sweden)

    Stéphane Potvin

    2015-09-01

    Full Text Available Craving is a core feature of tobacco use disorder as well as a significant predictor of smoking relapse. Studies have shown that appetitive smoking-related stimuli (e.g. someone smoking trigger significant cravings in smokers which impedes their self-control capacities and promotes drug seeking behavior. In this review, we begin by an overview of functional magnetic resonance imaging (fMRI studies investigating the neural correlates of smokers to appetitive smoking cues. The literature reveals a complex and vastly distributed neuronal network underlying smokers’ craving response that recruits regions involved in self-referential processing, panning/regulatory processes, emotional responding, attentional biases, and automatic conducts. We then selectively review important factors contributing to the heterogeneity of results that significantly limit the implications of these findings, namely between- (abstinence, smoking expectancies and self-regulation and within-studies factors (severity of smoking dependence, sex-differences, motivation to quit and genetic factors. Remarkably, we found that little to no attention has been devoted to examine the influence of personality traits on the neural correlates of cigarette cravings in fMRI studies. Impulsivity has been linked with craving and relapse in substance and tobacco use, which prompted our research team to examine the influence of impulsivity on cigarette cravings in an fMRI study. We found that the influence of impulsivity on cigarette cravings was mediated by fronto-cingular mechanisms. Given the high prevalence of cigarette smoking in several psychiatric disorders that are characterized by significant levels of impulsivity, we conclude by identifying psychiatric patients as a target population whose tobacco smoking habits deserve further behavioral and neuro-imaging investigation.

  13. 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...

  14. Efficient Excise Taxation: The Evidence from Cigarettes.

    OpenAIRE

    Benjamin, Daniel K; William R. Dougan

    1997-01-01

    The authors develop a model in which optimizing policy makers in adjacent government jurisdictions levy excise taxes on a commodity that has a unique point of production from which all shipments emanate. From this model the authors derive an unusually specific predicted geographical pattern of those excise taxes in which these taxes rise at specific decreasing rate as one moves outward from the point of production. The authors compare these predictions to the observed pattern of cigarette tax...

  15. Exploring Cigarette Use among Male Migrant Workers in Nigeria

    Directory of Open Access Journals (Sweden)

    Olanrewaju Olusola Onigbogi

    2015-04-01

    Full Text Available Background There is limited knowledge about the use of cigarettes by blacks outside the United States (U.S. Nigeria creates an opportunity to explore smoking behaviours, smoking cessation (nicotine dependence and use of cigarettes in a country that has a large black population outside the U.S. Methods We conducted three Focus Group Discussions (FGDs involving twenty-four male migrant workers who reported that they were current cigarette smokers. Interviews were audio-taped and transcribed. Results Four major themes namely: reasons for initiating and continuing to smoke cigarettes, factors affecting brand choice, barriers to quitting, effect of smoking mentholated cigarette brands were identified. Conclusion This study provides insight into the use of mentholated and non-mentholated cigarettes and suggests the need for further studies to explore smoking behavior among Nigerians.

  16. Recent Advances in Cigarette Ignition Propensity Research and Development.

    Science.gov (United States)

    Alpert, Hillel R; O'Connor, Richard J; Spalletta, Ron; Connolly, Gregory N

    2010-04-01

    Major U.S. cigarette companies for decades conducted research and development regarding cigarette ignition propensity which has continued beyond fire safety standards for cigarettes that have recently been legislated. This paper describes recent scientific advances and technological development based on a comprehensive review of the physical, chemical, and engineering sciences, public health, and trade literature, U.S. and international patents, and research in the tobacco industry document libraries.Advancements since the first implementation of standards have made been in: a) understanding the key parameters involved in cigarette smoldering combustion and ignition of substrates; b) developing new cigarette and paper wrapper designs to reduce ignition propensity, including banded and non-banded cigarette paper approaches, c) assessing toxicology, and d) measuring performance. While the implications of manufacturers' non-safety related aims are of concern, this research indicates possible alternative designs should experience with fire loss and existing technologies on the market suggest need for improvement. PMID:20495669

  17. Electronic cigarettes: a survey of users

    Directory of Open Access Journals (Sweden)

    Etter Jean-François

    2010-05-01

    Full Text Available Abstract Background Little is known about users of electronic cigarettes, or their opinions, satisfaction or how and why they use such products. Methods An internet survey of 81 ever-users of ecigarettes in 2009. Participants answered open-ended questions on use of, and opinions about, ecigarettes. Results Respondents (73 current and 8 former users lived in France, Canada, Belgium or Switzerland. Most respondents (77% were men; 63% were former smokers and 37% were current smokers. They had used e-cigarettes for 100 days (median and drew 175 puffs per day (median. Participants used the ecigarette either to quit smoking (53 comments, to reduce their cigarette consumption (14 comments, in order not to disturb other people with smoke (20 comments, or in smoke-free places (21 comments. Positive effects reported with ecigarettes included their usefulness to quit smoking, and the benefits of abstinence from smoking (less coughing, improved breathing, better physical fitness. Respondents also enjoyed the flavour of ecigarettes and the sensation of inhalation. Side effects included dryness of the mouth and throat. Respondents complained about the frequent technical failures of ecigarettes and had some concerns about the possible toxicity of the devices and about their future legal status. Conclusions Ecigarettes were used mainly to quit smoking, and may be helpful for this purpose, but several respondents were concerned about potential toxicity. There are very few published studies on ecigarettes and research is urgently required, particularly on the efficacy and toxicity of these devices.

  18. Cigarette package design: opportunities for disease prevention

    Directory of Open Access Journals (Sweden)

    Pollay RW

    2003-01-01

    Full Text Available Abstract Objective To learn how cigarette packages are designed and to determine to what extent cigarette packages are designed to target children. Methods A computer search was made of all Internet websites that post tobacco industry documents using the search terms: packaging, package design, package study, box design, logo, trademark and design study. All documents were retrieved electronically and analyzed by the first author for recurrent themes. Data Synthesis Cigarette manufacturers devote a great deal of attention and expense to package design because it is central to their efforts to create brand images. Colors, graphic elements, proportioning, texture, materials and typography are tested and used in various combinations to create the desired product and user images. Designs help to create the perceived product attributes and project a personality image of the user with the intent of fulfilling the psychological needs of the targeted type of smoker. The communication of these images and attributes is conducted through conscious and subliminal processes. Extensive testing is conducted using a variety of qualitative and quantitative research techniques. Conclusion The promotion of tobacco products through appealing imagery cannot be stopped without regulating the package design. The same marketing research techniques used by the tobacco companies can be used to design generic packaging and more effective warning labels targeted at specific consumers.

  19. Pulmonary veno-occlusive disease

    Science.gov (United States)

    Pulmonary vaso-occlusive disease ... common among children and young adults. As the disease gets worse, it causes narrowed pulmonary veins, pulmonary artery hypertension , and congestion and swelling ...

  20. 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

  1. 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.

  2. Emotions for sale: cigarette advertising and women's psychosocial needs

    OpenAIRE

    Anderson, Stacey J; Glantz, Stanton A. Ph.D.; Ling, P M

    2005-01-01

    Objective: To explore messages of psychosocial needs satisfaction in cigarette advertising targeting women and implications for tobacco control policy. Methods: Analysis of internal tobacco industry documents and public advertising collections. Results: Tobacco industry market research attempted to identify the psychosocial needs of different groups of women, and cigarette advertising campaigns for brands that women smoke explicitly aimed to position cigarettes as capable of satisfying these ...

  3. Temperature distribution in a cigarette oven during baking

    OpenAIRE

    Zhang Qing; Shao Jia-Cun; Zhao Hang; Zhang Kai; Su Zhong-Di

    2015-01-01

    Baking treatment is one of the most important processes of cigarette production, which can significantly enhance quality of tobacco. Theoretical and numerical investigation on temperature distribution in a cigarette oven during baking was carried out. The finite volume method was used to simulate the flow field. The relationship between the uniformity of temperature field and impeller’s speed was given finally, which is helpful to optimize cigarette oven wi...

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

    OpenAIRE

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

    2015-01-01

    Marine debris is a global environmental issue. Smoked cigarette filters are the predominant coastal litter item; 4.5 trillion are littered annually, presenting a source of bioplastic microfibres (cellulose acetate) and harmful toxicants to marine environments. Despite the human health risks associated with smoking, little is known of the hazards cigarette filters present to marine life. Here we studied the impacts of smoked cigarette filter toxicants and microfibres on the polychaete worm Hed...

  5. 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)

  6. E-cigarettes: methodological and ideological issues and research priorities

    OpenAIRE

    Etter, Jean-François

    2015-01-01

    Cigarette combustion, rather than either tobacco or nicotine, is the cause of a public health disaster. Fortunately, several new technologies that vaporize nicotine or tobacco, and may make cigarettes obsolete, have recently appeared. Research priorities include the effects of vaporizers on smoking cessation and initiation, their safety and toxicity, use by non-smokers, dual use of vaporizers and cigarettes, passive vaping, renormalization of smoking, and the development of messages that effe...

  7. Recent Advances in Cigarette Ignition Propensity Research and Development

    OpenAIRE

    Alpert, Hillel R; O’Connor, Richard J; Spalletta, Ron; Connolly, Gregory N

    2010-01-01

    Major U.S. cigarette companies for decades conducted research and development regarding cigarette ignition propensity which has continued beyond fire safety standards for cigarettes that have recently been legislated. This paper describes recent scientific advances and technological development based on a comprehensive review of the physical, chemical, and engineering sciences, public health, and trade literature, U.S. and international patents, and research in the tobacco industry document l...

  8. Electronic cigarettes: incorporating human factors engineering into risk assessments

    OpenAIRE

    Yang, Ling; Rudy, Susan F.; Cheng, James M; Durmowicz, Elizabeth L

    2014-01-01

    Objective A systematic review was conducted to evaluate the impact of human factors (HF) on the risks associated with electronic cigarettes (e-cigarettes) and to identify research gaps. HF is the evaluation of human interactions with products and includes the analysis of user, environment and product complexity. Consideration of HF may mitigate known and potential hazards from the use and misuse of a consumer product, including e-cigarettes. Methods Five databases were searched through Januar...

  9. Electronic cigarettes and nicotine dependence: evolving products, evolving problems

    OpenAIRE

    Cobb, Caroline O.; Hendricks, Peter S.; Eissenberg, Thomas

    2015-01-01

    Electronic cigarettes (ECIGs) use an electric heater to aerosolize a liquid that usually contains propylene glycol, vegetable glycerin, flavorants, and the dependence-producing drug nicotine. ECIG-induced nicotine dependence has become an important concern, as some ECIGs deliver very little nicotine while some may exceed the nicotine delivery profile of a tobacco cigarette. This variability is relevant to tobacco cigarette smokers who try to switch to ECIGs. Products with very low nicotine de...

  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. Molecular mechanisms in progressive idiopathic pulmonary fibrosis.

    Science.gov (United States)

    Steele, Mark P; Schwartz, David A

    2013-01-01

    There is clear evidence that environmental exposures and genetic predisposition contribute to the pathogenesis of idiopathic pulmonary fibrosis (IPF). Cigarette smoking increases the risk of developing IPF several-fold, as do other exposures such as metal-fume and wood-dust exposure. Occupations that increase the risk of IPF are agricultural work, hairdressing, and stone polishing, supporting the role of environmental exposure in disease pathogenesis. Genetic predisposition to IPF is evident from its familial aggregation and the fact that pulmonary fibrosis develops in several rare genetic disorders. Mutations in surfactant proteins lead to pulmonary fibrosis and are associated with endoplasmic reticulum stress in alveolar type II epithelial cells. Mutations in telomerase have been found in several families with IPF, and shortened telomeres are found in sporadic cases of IPF. A common variant in mucin 5B predisposes to both familial and sporadic IPF and is present in the majority of cases, indicating sporadic IPF occurs in those with genetic predisposition. PMID:23020878

  12. The relationship between atherosclerosis and pulmonary emphysema

    Directory of Open Access Journals (Sweden)

    Vučević Danijela

    2014-01-01

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

  13. 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.

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

    International Nuclear Information System (INIS)

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2014-10-24

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

  16. Impact Assessment of Cigarette Smoke Exposure on Organotypic Bronchial Epithelial Tissue Cultures: A Comparison of Mono-Culture and Coculture Model Containing Fibroblasts.

    Science.gov (United States)

    Iskandar, Anita R; Xiang, Yang; Frentzel, Stefan; Talikka, Marja; Leroy, Patrice; Kuehn, Diana; Guedj, Emmanuel; Martin, Florian; Mathis, Carole; Ivanov, Nikolai V; Peitsch, Manuel C; Hoeng, Julia

    2015-09-01

    Organotypic 3D cultures of epithelial cells are grown at the air-liquid interface (ALI) and resemble the in vivo counterparts. Although the complexity of in vivo cellular responses could be better manifested in coculture models in which additional cell types such as fibroblasts were incorporated, the presence of another cell type could mask the response of the other. This study reports the impact of whole cigarette smoke (CS) exposure on organotypic mono- and coculture models to evaluate the relevancy of organotypic models for toxicological assessment of aerosols. Two organotypic bronchial models were directly exposed to low and high concentrations of CS of the reference research cigarette 3R4F: monoculture of bronchial epithelial cells without fibroblasts (BR) and coculture with fibroblasts (BRF) models. Adenylate kinase (AK)-based cytotoxicity, cytochrome P450 (CYP) 1A1/1B1 activity, tissue histology, and concentrations of secreted mediators into the basolateral media, as well as transcriptomes were evaluated following the CS exposure. The results demonstrated similar impact of CS on the AK-based cytotoxicity, CYP1A1/1B1 activity, and tissue histology in both models. However, a greater number of secreted mediators was identified in the basolateral media of the monoculture than in the coculture models. Furthermore, annotation analysis and network-based systems biology analysis of the transcriptomic profiles indicated a more prominent cellular stress and tissue damage following CS in the monoculture epithelium model without fibroblasts. Finally, our results indicated that an in vivo smoking-induced xenobiotic metabolism response of bronchial epithelial cells was better reflected from the in vitro CS-exposed coculture model. PMID:26085348

  17. A direct method for e-cigarette aerosol sample collection.

    Science.gov (United States)

    Olmedo, Pablo; Navas-Acien, Ana; Hess, Catherine; Jarmul, Stephanie; Rule, Ana

    2016-08-01

    E-cigarette use is increasing in populations around the world. Recent evidence has shown that the aerosol produced by e-cigarettes can contain a variety of toxicants. Published studies characterizing toxicants in e-cigarette aerosol have relied on filters, impingers or sorbent tubes, which are methods that require diluting or extracting the sample in a solution during collection. We have developed a collection system that directly condenses e-cigarette aerosol samples for chemical and toxicological analyses. The collection system consists of several cut pipette tips connected with short pieces of tubing. The pipette tip-based collection system can be connected to a peristaltic pump, a vacuum pump, or directly to an e-cigarette user for the e-cigarette aerosol to flow through the system. The pipette tip-based system condenses the aerosol produced by the e-cigarette and collects a liquid sample that is ready for analysis without the need of intermediate extraction solutions. We tested a total of 20 e-cigarettes from 5 different brands commercially available in Maryland. The pipette tip-based collection system condensed between 0.23 and 0.53mL of post-vaped e-liquid after 150 puffs. The proposed method is highly adaptable, can be used during field work and in experimental settings, and allows collecting aerosol samples from a wide variety of e-cigarette devices, yielding a condensate of the likely exact substance that is being delivered to the lungs. PMID:27200479

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

    DEFF Research Database (Denmark)

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

    2013-01-01

    girls and 361 boys aging 20-25 years old who entered Isfahan and Kashan Universities (Iran) in 2007. Demographic factors (age, gender, and age at smoking onset) cigarette and hookah smoking status, having a smoking father or smoking friends and four related social norms were recorded. Binary logistic...... regression analysis was used to separately determine associations between hookah and cigarette smoking and the four social norm variables. RESULTS: CIGARETTE AND HOOKAH SMOKERS HAD SIGNIFICANT DIFFERENCES WITH NONSMOKERS IN TWO SOCIAL NORMS: "Perceived smoking by important characters" [odds ratio (OR) = 1...... social norms leading to cigarette and hookah smoking may help policy makers develop comprehensive interventions to prevent smoking among adolescents....

  19. E-cigarette Ads and Youth PSA (:60)

    Centers for Disease Control (CDC) Podcasts

    2016-01-05

    This 60 second public service announcement is based on the January 2016 CDC Vital Signs report. Most electronic cigarettes, or e-cigarettes, contain nicotine, which is highly addictive and may harm brain development. More than 18 million middle and high school students were exposed to e-cigarette ads. Exposure to these ads may be contributing to an increase in e-cigarette use among youth. Learn what can be done to keep our youth safe and healthy.  Created: 1/5/2016 by National Center for Chronic Disease Prevention and Health Promotion (NCCDPHP).   Date Released: 1/5/2016.

  20. CDC Vital Signs-E-cigarette Ads and Youth

    Centers for Disease Control (CDC) Podcasts

    2016-01-05

    This podcast is based on the January 2016 CDC Vital Signs report. Most electronic cigarettes, or e-cigarettes, contain nicotine, which is highly addictive and may harm brain development. More than 18 million middle and high school students were exposed to e-cigarette ads. Exposure to these ads may be contributing to an increase in e-cigarette use among youth. Learn what can be done to keep our youth safe and healthy.  Created: 1/5/2016 by National Center for Chronic Disease Prevention and Health Promotion (NCCDPHP).   Date Released: 1/5/2016.

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

    OpenAIRE

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

    2015-01-01

    In recent years, the emerging electronic cigarette (e-cigarette) marketplace has shown great development prospects all over the world. Reddit, one of the most popular forums in the world, has a very large user group and thus great influence. This study aims to gain a systematic understanding of e-cigarette flavors based on data collected from Reddit. Flavor popularity, mixing, characteristics, trends, and brands are analyzed. Fruit flavors were mentioned the most (n = 15,720) among all the p...

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

    Science.gov (United States)

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

    2015-12-01

    E-cigarette use has increased rapidly over the past decade. There is growing concern about e-cigarette use and advertising given limited regulation of these products. This cross-sectional study reports on data collected at baseline from hospitalized cigarette smokers (N=944) recruited in monthly cohorts between December 2012 and September 2013. Participants were queried regarding e-cigarette awareness and use, and number and sources of e-cigarette advertisement exposures in the previous 6 months. Most Whites (99%) reported ever hearing of an e-cigarette compared to 96% of Blacks (p<0.001). Over two thirds (64%) of Whites reported ever using an e-cigarette compared to 30% of Blacks (p<0.001). There were significant trends in increasing e-cigarette use for both racial groups with an average increase of 13% each month (p<0.005) and in increasing e-cigarette advertisement exposure reported for the previous 6 months, with a 14% increase each month (p<0.0001). Whites reported 56% greater advertisement exposure than Blacks (mean=25 vs. 8 in month 1 to 79 vs. 45 in month 9, respectively; p<0.0001). For Blacks, advertisement exposure was significantly associated with e-cigarette use (p<0.001). Whites reported more advertisement exposure from stores and the Internet, and Blacks reported more advertisement exposure from radio or television. Results suggest that e-cigarette marketing is beginning to breach the Black population who are, as a consequence, "catching up" with Whites with regard to e-cigarette use. Given the significant disparities for smoking-related morbidity and mortality between Blacks and Whites, these findings identify new areas for future research and policy. PMID:25503053

  3. Cigarette Purchasing Patterns among New York Smokers: Implications for Health, Price, and Revenue

    OpenAIRE

    New York State Department of Health; ,

    2006-01-01

    Executive Summary Raising the price of cigarettes is one of the most effective interventions to prevent and reduce cigarette use. Local, state, and federal governments can change the price of cigarettes by raising or lowering cigarette excise taxes and by implementing and enforcing minimum price laws. Smokers can also adjust their behavior by choosing discount or “bargain” brands, buying fewer cigarettes, and avoiding paying cigarette taxes by purchasing from retailers that do not le...

  4. E-Cigarette Prevalence and Correlates of Use among Adolescents versus Adults: A Review and Comparison

    OpenAIRE

    Chapman, Shawna L. Carroll; Wu, Li-Tzy

    2014-01-01

    Perceived safer than tobacco cigarettes, prevalence of electronic cigarette (e-cigarette) use is increasing. Analyses of cartridges suggest that e-cigarettes may pose health risks. In light of increased use and the potential for consequences, we searched Google Scholar and Pubmed in July of 2013 using keywords, such as e-cigarette and vaping, to compare differences and similarities in prevalence and correlates of e-cigarette use among adolescents (grades 6-12) versus adults (aged ≥18 years). ...

  5. Decline and infiltrated pulmonary

    International Nuclear Information System (INIS)

    The case of a 45 year-old patient is analyzed, with diagnosis of rheumatoid arthritis from the 43 years, asymptomatic, without treatment and smoker antecedents from the 15 to the 35 years of 3 to 10 daily cigarettes

  6. 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.

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

    Energy Technology Data Exchange (ETDEWEB)

    Xu, Guang-Ni; Yang, Kai; Xu, Zu-Peng; Zhu, Liang; Hou, Li-Na; Qi, Hong; Chen, Hong-Zhuan, E-mail: hongzhuan_chen@hotmail.com; Cui, Yong-Yao, E-mail: yongyaocui@yahoo.com.cn

    2012-07-01

    Anisodamine, an antagonist of muscarinic acetylcholine receptors (mAChRs), has been used therapeutically to improve smooth muscle function, including microvascular, intestinal and airway spasms. Our previous studies have revealed that airway hyper-reactivity could be prevented by anisodamine. However, whether anisodamine prevents smoking-induced airway smooth muscle (ASM) cell proliferation remained unclear. In this study, a primary culture of rat ASM cells was used to evaluate an ASM phenotype through the ability of the cells to proliferate and express contractile proteins in response to cigarette smoke extract (CSE) and intervention of anisodamine. Our results showed that CSE resulted in an increase in cyclin D1 expression concomitant with the G0/G1-to-S phase transition, and high expression of M2 and M3. Functional studies showed that tracheal hyper-contractility accompanied contractile marker α-SMA high-expression. These changes, which occur only after CSE stimulation, were prevented and reversed by anisodamine, and CSE-induced cyclin D1 expression was significantly inhibited by anisodamine and the specific inhibitor U0126, BAY11-7082 and LY294002. Thus, we concluded that the protective and reversal effects and mechanism of anisodamine on CSE-induced events might involve, at least partially, the ERK, Akt and NF-κB signaling pathways associated with cyclin D1 via mAChRs. Our study validated that anisodamine intervention on ASM cells may contribute to anti-remodeling properties other than bronchodilation. -- Highlights: ► CSE induces tracheal cell proliferation, hyper-contractility and α-SMA expression. ► Anisodamine reverses CSE-induced tracheal hyper-contractility and cell proliferation. ► ERK, PI3K, and NF-κB pathways and cyclin D1 contribute to the reversal effect.

  8. Giant infantile pulmonary hemangioma

    International Nuclear Information System (INIS)

    We present a very unusual case of giant infantile pulmonary hemangioma presenting as a large solitary pulmonary mass. This was successfully managed with surgical resection. Histological examination revealed that the mass was positive for GLUT-1 receptor, a marker for infantile hemangioma. To our knowledge only a few cases of pulmonary hemangioma have been described previously in the literature. Pulmonary hemangiomas are very rare lesions, most of them presenting as a pulmonary mass. This case emphasizes the fact that this rare lesion should be considered in the differential of an enhancing pulmonary mass in an infant. (orig.)

  9. Support for Indoor Bans on Electronic Cigarettes among Current and Former Smokers

    Directory of Open Access Journals (Sweden)

    Stephanie K. Kolar

    2014-11-01

    Full Text Available Objectives: Electronic cigarette (e-cigarette use is increasing in the U.S. Although marketed as a safer alternative for cigarettes, initial evidence suggests that e-cigarettes may pose a secondhand exposure risk. The current study explored the prevalence and correlates of support for e-cigarette bans. Methods: A sample of 265 current/former smokers completed a cross-sectional telephone survey from June–September 2014; 45% Black, 31% White, 21% Hispanic. Items assessed support for home and workplace bans for cigarettes and e-cigarettes and associated risk perceptions. Results: Most participants were aware of e-cigarettes (99%. Results demonstrated less support for complete e-cigarette bans in homes and workplaces compared to cigarettes. Support for complete e-cigarette bans was strongest among older, higher income, married respondents, and former smokers. Complete e-cigarette bans were most strongly endorsed when perceptions of addictiveness and health risks were high. While both e-cigarette lifetime and never-users strongly supported cigarette smoking bans, endorsement for e-cigarette bans varied by lifetime use and intentions to use e-cigarettes. Conclusions: Support for indoor e-cigarette bans is relatively low among individuals with a smoking history. Support for e-cigarette bans may change as evidence regarding their use emerges. These findings have implications for public health policy.

  10. Pulmonary function in advanced pulmonary hypertension.

    OpenAIRE

    Burke, C. M.; Glanville, A R; Morris, A J; Rubin, D.; Harvey, J. A.; Theodore, J; Robin, E. D.

    1987-01-01

    Pulmonary mechanical function and gas exchange were studied in 33 patients with advanced pulmonary vascular disease, resulting from primary pulmonary hypertension in 18 cases and from Eisenmenger physiology in 15 cases. Evidence of airway obstruction was found in most patients. In addition, mean total lung capacity (TLC) was only 81.5% of predicted and 27% of our subjects had values of TLC less than one standard deviation below the mean predicted value. The mean value for transfer factor (TLC...

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

    Science.gov (United States)

    Paradise, Jordan

    2013-01-01

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

  12. Pulmonary Hyalinising Granuloma: A rare pulmonary disorder

    International Nuclear Information System (INIS)

    Pulmonary hyalinising granulomas are rare, non-infectious fibros lesions of the lung which can mimic metastatic disease. It was first described in literature by Engleman et al in the year 1977. Its etiology is unknown but they may be caused by an exaggerated immune response. The patient typically presents with cough, chest pain, dyspnoea or haemoptysis in association with multiple bilateral parenchymal nodules. We report the case of a 20 years old male who presented with a 12-month history of worsening dry cough. His plain chest radiograph and subsequent CT scan revealed bilateral pulmonary nodules. A CT guided biopsy of the pulmonary lesions was consistent with Pulmonary Hyalinising Granuloma [PHG].

  13. 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.

  14. 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.

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

    Directory of Open Access Journals (Sweden)

    Monique Williams

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

  16. CT assessment of progression in pulmonary emphysema

    International Nuclear Information System (INIS)

    The purpose of this study was to assess the progression of pulmonary emphysema (PE) using CT. We reviewed the records of 25 cases (all male smokers and age range of 36-85 years) in whom progression of PE was recognized using CT scanning. PE was diagnosed by the presence of low attenuation areas on CT scan. PE was divided into 2 subtypes: centrilobular emphysema (CLE) and paraseptal emphysema (PSE). There were 8 younger cases less than 50s. With respect to smoking habit, 6 cases had 1 pack per day at maximum whereas the remaining 19 cases had more over than 1.5 packs per day. Interval periods of observation were from 8 months minimum to 10 years maximum. PE, of both CLE and PSE subtype, was recognized even in younger cases less than 40 years of age, and progressed with cigarette consumption even a minimum during 8 months periods of observation. (author)

  17. Cigarette smoke regulates the expression of TLR4 and IL-8 production by human macrophages

    Directory of Open Access Journals (Sweden)

    Rahman Irfan

    2009-05-01

    Full Text Available Abstract Background Toll-like receptors (TLRs are present on monocytes and alveolar macrophages that form the first line of defense against inhaled particles. The importance of those cells in the pathophysiology of chronic obstructive pulmonary disease (COPD has well been documented. Cigarette smoke contains high concentration of oxidants which can stimulate immune cells to produce reactive oxygen species, cytokines and chemokines. Methods In this study, we evaluated the effects of cigarette smoke medium (CSM on TLR4 expression and interleukin (IL-8 production by human macrophages investigating the involvement of ROS. Results and Discussion TLR4 surface expression was downregulated on short term exposure (1 h of CSM. The downregulation could be explained by internalization of the TLR4 and the upregulation by an increase in TLR4 mRNA. IL-8 mRNA and protein were also increased by CSM. CSM stimulation increased intracellular ROS-production and decreased glutathione (GSH levels. The modulation of TLR4 mRNA and surface receptors expression, IRAK activation, IκB-α degradation, IL-8 mRNA and protein, GSH depletion and ROS production were all prevented by antioxidants such as N-acetyl-L-cysteine (NAC. Conclusion TLR4 may be involved in the pathogenesis of lung emphysema and oxidative stress and seems to be a crucial contributor in lung inflammation.

  18. E-cigarettes forbidden in offices and closed areas

    CERN Multimedia

    2013-01-01

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

  19. Pulmonary arteriovenous fistula

    Science.gov (United States)

    Pulmonary arteriovenous fistula is an abnormal connection between an artery and vein in the lungs. As a result, blood passes ... Pulmonary arteriovenous fistulas are usually the result of abnormal development of the blood vessels of the lung. Most occur in ...

  20. Pulmonary alveolar proteinosis

    Science.gov (United States)

    Alveolar proteinosis; Pulmonary alveolar phospholipoproteinosis ... In some cases, the cause of pulmonary alveolar proteinosis is unknown. In others, it occurs with lung infection or an immune problem. It also can occur with cancers of the blood system, ...

  1. Hantavirus Pulmonary Syndrome (HPS)

    Science.gov (United States)

    ... this page: About CDC.gov . Hantavirus Share Compartir Hantavirus Pulmonary Syndrome (HPS) Severe HPS. Image courtesy D. ... the workers showed evidence of infection or illness. Hantavirus Pulmonary Syndrome (HPS) Topics Transmission Where HPS is ...

  2. Extensive pulmonary alveolar microlithiasis

    OpenAIRE

    Rittayamai, Nuttapol; Muangman, Nisa; Ruangchira-Urai, Ruchira

    2013-01-01

    Pulmonary alveolar microlithiasis is a rare pulmonary disorder that is caused by abnormal sodium-dependent phosphate co-transporter from the mutation of SLC34A2 gene, leading to accumulation of microliths in the alveoli. We report the extensive pulmonary alveolar microlithiasis in an elderly woman who presented with progressive dyspnea for 2 months. Chest radiograph revealed diffuse pulmonary calcification. Tissue histopathology from open lung biopsy demonstrated widespread intra-alveolar lam...

  3. The pulmonary extracellular lining.

    OpenAIRE

    George, G; Hook, G E

    1984-01-01

    The extracellular lining of the lungs is reviewed. The pulmonary extracellular lining is a complex mixture of phospholipids, proteins and carbohydrates which is absolutely essential for the maintenance of normal pulmonary functions such as gas exchange. Without the lining the lungs would collapse. Alterations in the pulmonary extracellular lining may underlie some disease conditions induced by toxic agents, especially those which interfere with the formation of pulmonary surfactant. The extra...

  4. Symptoms, Diagnosis and Treatment for Pulmonary Fibrosis

    Science.gov (United States)

    ... www.lung.org > Lung Health and Diseases > Lung Disease Lookup > Pulmonary Fibrosis Pulmonary Fibrosis Symptoms, Causes & Risk Factors Pulmonary ... while processing XML file."); } }); } } --> Blank Section Header Lung Disease Lookup Pulmonary Fibrosis Learn About Pulmonary Fibrosis Pulmonary Fibrosis Symptoms, ...

  5. Current treatment in chronic obstructive pulmonary disease

    Institute of Scientific and Technical Information of China (English)

    李嘉惠

    2008-01-01

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

  6. Idiopathic pulmonary hemosiderosis

    OpenAIRE

    Sunilkumar, B M; Sathishkumar, K M; Somashekhar, A R; P.P. Maiya

    2010-01-01

    Recurrent or chronic pulmonary hemorrhage is rare in children. Idiopathic pulmonary hemosiderosis (IPH) manifests as hemoptysis, diffuse parenchymal infiltrates on chest radiographs and microcytic hypochromic anemia. The hemoptysis present may be mistaken for more common diseases, delaying the diagnosis and further management. Idiopathic pulmonary hemosiderosis is a disorder of unknown etiology. Treatment of IPH includes immunosuppressive drugs along with supportive measures.

  7. Elastase-induced pulmonary emphysema: insights from experimental models

    Directory of Open Access Journals (Sweden)

    Mariana A. Antunes

    2011-12-01

    Full Text Available Several distinct stimuli can be used to reproduce histological and functional features of human emphysema, a leading cause of disability and death. Since cigarette smoke is the main cause of emphysema in humans, experimental researches have attempted to reproduce this situation. However, this is an expensive and cumbersome method of emphysema induction, and simpler, more efficacious alternatives have been sought. Among these approaches, elastolytic enzymes have been widely used to reproduce some characteristics of human cigarette smoke-induced disease, such as: augmentation of airspaces, inflammatory cell influx into the lungs, and systemic inflammation. Nevertheless, the use of elastase-induced emphysema models is still controversial, since the disease pathways involved in elastase induction may differ from those occurring in smoke-induced emphysema. This indicates that the choice of an emphysema model may impact the results of new therapies or drugs being tested. The aim of this review is to compare the mechanisms of disease induction in smoke and elastase emphysema models, to describe the differences among various elastase models, and to establish the advantages and disadvantages of elastase-induced emphysema models. More studies are required to shed light on the mechanisms of elastase-induced emphysema.Diversos estímulos podem ser utilizados para reproduzir características histológicas e funcionais do enfisema humano, uma das principais causas de incapacidade e morte. Uma vez que a fumaça de cigarro é a principal causa de enfisema em humanos, estudos experimentais têm tentado reproduzir esta situação. No entanto, esse é um método dispendioso e complicado para a indução do enfisema e, alternativas mais simples e eficazes, têm sido pesquisadas. Entre essas abordagens, enzimas elastolíticas vêm sendo amplamente utilizadas para reproduzir algumas das características do enfisema humano, tais como: aumento dos espaços a

  8. A baseline understanding of state laws governing e-cigarettes

    Science.gov (United States)

    Gourdet, C K; Chriqui, J F; Chaloupka, F J

    2014-01-01

    Background Electronic cigarettes (e-cigarettes) have been available for purchase in the USA since 2007, and have grown rapidly in popularity. Currently, there are no federal restrictions on e-cigarettes; therefore, any regulations are under the purview of state and/or local governments. This study examines state laws governing e-cigarettes through youth access restrictions, smoke-free air requirements and/or excise taxation. Methods Codified statutory and administrative laws, attorney general opinions, executive orders, and revenue notices and rulings effective as of 15 November 2013 for all 50 states and the District of Columbia, were compiled using Boolean searches in Lexis-Nexis and Westlaw. All laws were analysed by two study authors to determine the presence and components of relevant provisions. Two categories of laws were identified; (1) explicit e-cigarette laws and (2) laws focused on tobacco-derived and/or nicotine-containing products. Results Thirty-four states’ laws address e-cigarettes either explicitly or as part of language applying to tobacco-derived or nicotine-containing products. Laws explicitly addressing e-cigarettes primarily focus on youth access (22 states) or smoke-free air (12 states); only Minnesota imposes an excise tax on e-cigarettes. Similarly, tobacco-derived or nicotine-containing products are primarily regulated through youth access restrictions (6 states), smoke-free air laws (5 states), or excise taxation (2 states). Conclusions In the current absence of federal law governing e-cigarettes, more than one-half of the states have taken the initiative to regulate these products. The opportunity exists for the remaining states to incorporate e-cigarette-related restrictions into their pre-existing tobacco control laws. PMID:24935897

  9. Clinical, High Resolution Computed Tomography and Pulmonary Function in Sulphur Mustard Victims

    OpenAIRE

    Javad Moghimi; Armita Valizadeh; Habib Heybar; Mahdi Yadollahzadeh; Ahmad Ahmadzadeh; Esmaeil Idani

    2012-01-01

    We aimed to evaluate clinical, high resolution computed tomography (HRCT) and pulmonary function test (PFT) findings after 18-23 years of exposure in veterans of sulphur mustard (SM) exposure. We performed a cross-sectional study of 106 patients. Inclusion criteria were 1: documented exposure to SM as confirmed by toxicological analysis of their urine and vesicular fluid after exposure 2: single exposure to SM that cause skin blisters and subsequent transient or permanent sequel. Cigarette sm...

  10. PULMONARY LANGERHANS CELL HISTIOCYTOSIS PRESENTING AS SIMULTANEOUS BILATERAL SPONTANEOUS PNEUMOTHORAX IN A NON-SMOKER PATIENT

    OpenAIRE

    M. Vaziri; A. Pazooki L. Zahedi

    2008-01-01

    Pulmonary Langerhans Cell Histiocytosis (PLCH) is a rare idiopathic disorder that primarily affects young adult cigarette smokers. Affected patients often present with cough and dyspnea and about 20% of patients present with or later develop pneumothorax. It is striking that more than 90% of patients are smokers. We report a very unusual case of PLCH in a 20-year- old male patient with no smoking history in whom a life- threatening complication such as simultaneous bilateral pneumothorax was ...

  11. Pulmonary Langerhans Cell Histiocytosis and Diabetes Insipidus in a Young Smoker

    OpenAIRE

    Earlam, K.; Souza, C.A.; Glikstein, R.; Gomes, M. M.; Pakhalé, S.

    2016-01-01

    Langerhans cell histiocytosis is characterized by the abnormal nodular proliferation of histiocytes in various organ systems. Pulmonary involvement seen in young adults is nearly always seen in the context of past or current cigarette smoking. Although it tends to be a single-system disease, extrapulmonary manifestations involving the skin, bone, and hypothalamic-pituitary-axis are possible. High resolution CT (HRCT) of the thorax findings includes centrilobular nodules and cysts that are biz...

  12. Pulmonary Langerhans Cell Histiocytosis with Lytic Bone Involvement in an Adult Smoker: Regression following Smoking Cessation

    OpenAIRE

    Routy, B.; J. Hoang; Gruber, J

    2015-01-01

    Langerhans cell histiocytosis (LCH) is a rare myeloid neoplasm characterized by the proliferation and dissemination of histiocytes. These in turn may cause symptoms ranging from isolated, infiltrative lesions to severe multisystem disease. Pulmonary Langerhans cell histiocytosis (PLCH) presents as a localized polyclonal proliferation of Langerhans cells in the lungs causing bilateral cysts and fibrosis. In adults, this rare condition is considered a reactive process associated with cigarette ...

  13. The Pulmonary Surfactant: Impact of Tobacco Smoke and Related Compounds on Surfactant and Lung Development

    OpenAIRE

    Scott, J Elliott

    2004-01-01

    Cigarette smoking, one of the most pervasive habits in society, presents many well established health risks. While lung cancer is probably the most common and well documented disease associated with tobacco exposure, it is becoming clear from recent research that many other diseases are causally related to smoking. Whether from direct smoking or inhaling environmental tobacco smoke (ETS), termed secondhand smoke, the cells of the respiratory tissues and the lining pulmonary surfactant are the...

  14. The Pulmonary Surfactant: Impact of Tobacco Smoke and Related Compounds on Surfactant and Lung Development

    OpenAIRE

    Scott J Elliott

    2004-01-01

    Abstract Cigarette smoking, one of the most pervasive habits in society, presents many well established health risks. While lung cancer is probably the most common and well documented disease associated with tobacco exposure, it is becoming clear from recent research that many other diseases are causally related to smoking. Whether from direct smoking or inhaling environmental tobacco smoke (ETS), termed secondhand smoke, the cells of the respiratory tissues and the lining pulmonary surfactan...

  15. A Modular Cell-Type Focused Inflammatory Process Network Model for Non-Diseased Pulmonary Tissue

    OpenAIRE

    Jurjen W. Westra; Schlage, Walter K.; Arnd Hengstermann; Stephan Gebel; Carole Mathis; Ty Thomson; Ben Wong; Vy Hoang; Emilija Veljkovic; Michael Peck; Lichtner, Rosemarie B; Dirk Weisensee; Marja Talikka; Renee Deehan; Julia Hoeng

    2013-01-01

    Exposure to environmental stressors such as cigarette smoke (CS) elicits a variety of biological responses in humans, including the induction of inflammatory responses. These responses are especially pronounced in the lung, where pulmonary cells sit at the interface between the body’s internal and external environments. We combined a literature survey with a computational analysis of multiple transcriptomic data sets to construct a computable causal network model (the Inflammatory Process Net...

  16. Diet, cigarettes and alcohol in laryngeal cancer

    Energy Technology Data Exchange (ETDEWEB)

    Freudenheim, J.L.; Graham, S.; Byers, T.E.; Marshall, J.R.; Haughey, B.P.; Swanson, M.K.; Wilkinson, G. (State Univ. of New York, Buffalo (United States))

    1991-03-11

    Diet and other risk factors for cancer of the larynx were examined in a case-control study among white males in Western New York, conducted in 1975-1985. Incident, pathologically-confirmed cases and age- and neighborhood-matched controls were interviewed to determine usual diet, and lifetime use of tobacco and alcohol. Because response rates were low for both cases and controls, this cannot be considered a population-based study. A strong association of risk with cigarette but not pipe and cigar smoking was found. Beer and hard liquor but not wine were associated with increased risk. After control for cigarettes, alcohol and education, the upper quartile odds ratio for fat was 2.40, while the odds ratio for high intake of carotenoids was 0.51. There was effect modification by smoking. Carotenoids were most negatively associated with risk among lighter smokers; dietary fat was most positively associated with risk among heavier smokers. Total calories, protein, and retinol were associated with increased risk; there was no relationship between laryngeal cancer and vitamins C and E or carbohydrate. This study again demonstrates the strong association between tobacco and alcohol and laryngeal cancer and also suggests that diets low in carotenoids and high fat may increase risk.

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

    OpenAIRE

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

    2009-01-01

    Background: Single cigarette use and its implications have rarely been studied among adults. Objective: To assess perceptions, prevalence and correlates of single cigarette purchase behaviour and its relation to harm reduction. Design: Focus group transcripts and cross-sectional data were analysed. Setting and participants: Focus groups among convenience samples of adult smokers in two Mexican cities and a population-based sample of 1079 adult smokers from the International Tobacco Control Po...

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

    Science.gov (United States)

    Fiore, Maria; La Vecchia, Carlo; Marzuillo, Carolina; Gualano, Maria Rosaria; Liguori, Giorgio; Cicolini, Giancarlo; Capasso, Lorenzo; D'Amario, Claudio; Boccia, Stefania; Siliquini, Roberta; Ricciardi, Walter; Villari, Paolo

    2015-01-01

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

  19. Effects of cigarette smoke and 3-methylcholanthrene on the disposition of phencyclidine and its N-ethylamine analogue in the isolated perfuse lung of rats

    International Nuclear Information System (INIS)

    The isolated perfused lung (IPL) of rats were used to examine the pulmonary disposition and metabolism of tritium-labeled phencyclidine (PCP) and N-ethyl-1-phenylcyclohexylamine (PCE). The IPL removed PCP and PCE from the perfusate and converted them to free and conjugated metabolities. At the conclusion of a 1-h perfusion, the lung accumulated at least 20% of the administered radioactivity and metabolized more than 30% of the added drug. Pretreatment of rats with 3-MC or cigarette smoke enhanced significantly PCP and PCE metabolism by the IPL. The concentration of conjugated PCE metabolite in the perfusate of the IPL was increased significantly by both 3-MC and cigarette smoke pretreatments whereas the concentration of conjugated PCP metabolite was not affected by cigarette smoke exposure and increased only slightly after 3-MC pretreatment. Pretreatment of rats with 3-MC or cigarette smoke also altered the amount of radioactivity accumulated by the lung tissue at the conclusion of a 1-h perfusion. Inasmuch as PCP and PCE are often abused by humans via smoke inhalation, a significant amount of these drugs may be stored or metabolized by the lung. (author)

  20. Pulmonary vascular diseases.

    Science.gov (United States)

    Mélot, C; Naeije, R

    2011-04-01

    Diseases of the pulmonary vasculature are a cause of increased pulmonary vascular resistance (PVR) in pulmonary embolism, chronic thromboembolic pulmonary hypertension (CTEPH), and pulmonary arterial hypertension or decreased PVR in pulmonary arteriovenous malformations on hereditary hemorrhagic telangiectasia, portal hypertension, or cavopulmonary anastomosis. All these conditions are associated with a decrease in both arterial PO2 and PCO2. Gas exchange in pulmonary vascular diseases with increased PVR is characterized by a shift of ventilation and perfusion to high ventilation-perfusion ratios, a mild to moderate increase in perfusion to low ventilation-perfusion ratios, and an increased physiologic dead space. Hypoxemia in these patients is essentially explained by altered ventilation-perfusion matching amplified by a decreased mixed venous PO2 caused by a low cardiac output. Hypocapnia is accounted for by hyperventilation, which is essentially related to an increased chemosensitivity. A cardiac shunt on a patent foramen ovale may be a cause of severe hypoxemia in a proportion of patients with pulmonary hypertension and an increase in right atrial pressure. Gas exchange in pulmonary arteriovenous malformations is characterized by variable degree of pulmonary shunting and/or diffusion-perfusion imbalance. Hypocapnia is caused by an increased ventilation in relation to an increased pulmonary blood flow with direct peripheral chemoreceptor stimulation by shunted mixed venous blood flow. PMID:23737196

  1. Lycopene inhibits NF-kB-mediated IL-8 expression and changes redox and PPARγ signalling in cigarette smoke-stimulated macrophages.

    Directory of Open Access Journals (Sweden)

    Rossella E Simone

    Full Text Available Increasing evidence suggests that lycopene, the major carotenoid present in tomato, may be preventive against smoke-induced cell damage. However, the mechanisms of such a prevention are still unclear. The aim of this study was to investigate the role of lycopene on the production of the pro-inflammatory cytokine IL-8 induced by cigarette smoke and the possible mechanisms implicated. Therefore, human THP-1 macrophages were exposed to cigarette smoke extract (CSE, alone and following a 6-h pre-treatment with lycopene (0.5-2 µM. CSE enhanced IL-8 production in a time- and a dose-dependent manner. Lycopene pre-treatment resulted in a significant inhibition of CSE-induced IL-8 expression at both mRNA and protein levels. NF-kB controlled the transcription of IL-8 induced by CSE, since PDTC prevented such a production. Lycopene suppressed CSE-induced NF-kB DNA binding, NF-kB/p65 nuclear translocation and phosphorylation of IKKα and IkBα. Such an inhibition was accompanied by a decrease in CSE-induced ROS production and NOX-4 expression. Lycopene further inhibited CSE-induced phosphorylation of the redox-sensitive ERK1/2, JNK and p38 MAPKs. Moreover, the carotenoid increased PPARγ levels which, in turn, enhanced PTEN expression and decreased pAKT levels in CSE-exposed cells. Such effects were abolished by the PPARγ inhibitor GW9662. Taken together, our data indicate that lycopene prevented CSE-induced IL-8 production through a mechanism involving an inactivation of NF-kB. NF-kB inactivation was accompanied by an inhibition of redox signalling and an activation of PPARγ signalling. The ability of lycopene in inhibiting IL-8 production, NF-kB/p65 nuclear translocation, and redox signalling and in increasing PPARγ expression was also found in isolated rat alveolar macrophages exposed to CSE. These findings provide novel data on new molecular mechanisms by which lycopene regulates cigarette smoke-driven inflammation in human macrophages.

  2. Lycopene Inhibits NF-kB-Mediated IL-8 Expression and Changes Redox and PPARγ Signalling in Cigarette Smoke–Stimulated Macrophages

    Science.gov (United States)

    Simone, Rossella E.; Russo, Marco; Catalano, Assunta; Monego, Giovanni; Froehlich, Kati; Boehm, Volker; Palozza, Paola

    2011-01-01

    Increasing evidence suggests that lycopene, the major carotenoid present in tomato, may be preventive against smoke-induced cell damage. However, the mechanisms of such a prevention are still unclear. The aim of this study was to investigate the role of lycopene on the production of the pro-inflammatory cytokine IL-8 induced by cigarette smoke and the possible mechanisms implicated. Therefore, human THP-1 macrophages were exposed to cigarette smoke extract (CSE), alone and following a 6-h pre-treatment with lycopene (0.5–2 µM). CSE enhanced IL-8 production in a time- and a dose-dependent manner. Lycopene pre-treatment resulted in a significant inhibition of CSE-induced IL-8 expression at both mRNA and protein levels. NF-kB controlled the transcription of IL-8 induced by CSE, since PDTC prevented such a production. Lycopene suppressed CSE-induced NF-kB DNA binding, NF-kB/p65 nuclear translocation and phosphorylation of IKKα and IkBα. Such an inhibition was accompanied by a decrease in CSE-induced ROS production and NOX-4 expression. Lycopene further inhibited CSE-induced phosphorylation of the redox-sensitive ERK1/2, JNK and p38 MAPKs. Moreover, the carotenoid increased PPARγ levels which, in turn, enhanced PTEN expression and decreased pAKT levels in CSE-exposed cells. Such effects were abolished by the PPARγ inhibitor GW9662. Taken together, our data indicate that lycopene prevented CSE-induced IL-8 production through a mechanism involving an inactivation of NF-kB. NF-kB inactivation was accompanied by an inhibition of redox signalling and an activation of PPARγ signalling. The ability of lycopene in inhibiting IL-8 production, NF-kB/p65 nuclear translocation, and redox signalling and in increasing PPARγ expression was also found in isolated rat alveolar macrophages exposed to CSE. These findings provide novel data on new molecular mechanisms by which lycopene regulates cigarette smoke-driven inflammation in human macrophages. PMID:21625550

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

    International Nuclear Information System (INIS)

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2015-09-15

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

  5. 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.

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

    OpenAIRE

    Lee Jie-Min

    2007-01-01

    Abstract Background Consumption of cigarettes and alcoholic beverages creates serious health consequences for individuals and overwhelming financial burdens for governments around the world. In Asia, a third stimulant – betel nuts – increases this burden exponentially. For example, individuals who simultaneously smoke, chew betel nuts and drink alcohol are approximately 123 times more likely to develop oral, pharyngeal and laryngeal cancer than are those who do not. To discourage consumption ...

  7. Who is using e-cigarettes in Canada? Nationally representative data on the prevalence of e-cigarette use among Canadians.

    Science.gov (United States)

    Reid, Jessica L; Rynard, Vicki L; Czoli, Christine D; Hammond, David

    2015-12-01

    The current study examined prevalence and correlates of electronic cigarette (e-cigarette) use in the Canadian population, using data from the nationally representative 2013 Canadian Tobacco, Alcohol and Drugs Survey (n=14,565). Sociodemographic correlates of e-cigarette use (ever, and in the past 30 days) were examined using logistic regression models. Overall, 8.5% of Canadians aged 15 and older reported having ever tried an e-cigarette; 1.8% had used one in the past 30 days. E-cigarette use was particularly high among smokers and young people. Overall, prevalence did not differ between males and females, for ever (P=0.24) or past 30-day use (P=0.30). Smoking status was the strongest correlate of e-cigarette use (ever and in the past 30 days, Pyoung adults aged 20-24 (20.1% ever; 3.9% past 30-day), and decreased with age. Among youth, the majority of e-cigarette users were never-smokers, while the majority of adult users were smokers. In Canada, e-cigarette use is particularly high among smokers and young people. Dual use with cigarettes was common, with most e-cigarette users also smoking conventional cigarettes. Continued monitoring of e-cigarette use and its relationship with smoking should be a priority, given the rapidly-evolving e-cigarette market and implementation of new policy measures. PMID:26348453

  8. Public opinion regarding earmarked cigarette tax in Taiwan

    Directory of Open Access Journals (Sweden)

    Yang Chung-Lin

    2003-12-01

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

  9. Cigarette taxes. The straw to break the camel's back.

    OpenAIRE

    Grossman, M.; F. J. Chaloupka

    1997-01-01

    Teenage cigarette smoking is sensitive to the price of cigarettes. The most recent research suggests that a 10% increase in price would reduce the number of teenagers who smoke by 7%. If the proposed 43-cent hike in the Federal excise tax rate on cigarettes contained in the Hatch-Kennedy Bill were enacted, the number of teenage smokers would fall by approximately 16%. This translates into more than 2.6 million fewer smokers and more than 850,000 fewer smoking-related premature deaths in the c...

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

    Directory of Open Access Journals (Sweden)

    Lei Wang

    2015-11-01

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

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

    Science.gov (United States)

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

    2015-11-01

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

  12. [Graphic images on cigarette packages not effective].

    Science.gov (United States)

    Kok, Gerjo; Peters, Gjalt-Jorn Y; Ruiter, Robert A C

    2013-01-01

    The Dutch Government intends to make graphic images on cigarette packages mandatory. However, contrary to other policy measures to reduce smoking, health warnings do not work. There is no acceptable evidence in favour of graphic images and behaviour change theories suggest methods of change that improve skills, self-efficacy and social support. Thus, theory- and evidence-based policy should focus on prohibiting the tobacco industry from glamourizing packaging and make health communications on packages mandatory. As to the type of communications to be used, theory and evidence suggest that warning of the negative consequences of smoking is not an effective approach. Rather, targeting the most important determinants of the initiation of smoking and its successful cessation - such as skills, self-efficacy and subjective norm - along with the most effective behaviour change methods appears to be the most expedient strategy. PMID:23548194

  13. 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

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

    Science.gov (United States)

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

    2014-07-01

    Despite the recent popularity of e-cigarettes, to date only limited data is available on their safety for both users and secondhand smokers. The present study reports a comprehensive inner and outer exposure assessment of e-cigarette emissions in terms of particulate matter (PM), particle number concentrations (PNC), volatile organic compounds (VOC), polycyclic aromatic hydrocarbons (PAH), carbonyls, and metals. In six vaping sessions nine volunteers consumed e-cigarettes with and without nicotine in a thoroughly ventilated room for two hours. We analyzed the levels of e-cigarette pollutants in indoor air and monitored effects on FeNO release and urinary metabolite profile of the subjects. For comparison, the components of the e-cigarette solutions (liquids) were additionally analyzed. During the vaping sessions substantial amounts of 1,2-propanediol, glycerine and nicotine were found in the gas-phase, as well as high concentrations of PM2.5 (mean 197 μg/m(3)). The concentration of putative carcinogenic PAH in indoor air increased by 20% to 147 ng/m(3), and aluminum showed a 2.4-fold increase. PNC ranged from 48,620 to 88,386 particles/cm(3) (median), with peaks at diameters 24-36 nm. FeNO increased in 7 of 9 individuals. The nicotine content of the liquids varied and was 1.2-fold higher than claimed by the manufacturer. Our data confirm that e-cigarettes are not emission-free and their pollutants could be of health concern for users and secondhand smokers. In particular, ultrafine particles formed from supersaturated 1,2-propanediol vapor can be deposited in the lung, and aerosolized nicotine seems capable of increasing the release of the inflammatory signaling molecule NO upon inhalation. In view of consumer safety, e-cigarettes and nicotine liquids should be officially regulated and labeled with appropriate warnings of potential health effects, particularly of toxicity risk in children. PMID:24373737

  15. Mechanisms responsible for pulmonary hypertension

    Institute of Scientific and Technical Information of China (English)

    2008-01-01

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

  16. Pulmonary arterial hypertension : an update

    NARCIS (Netherlands)

    Hoendermis, E. S.

    2011-01-01

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

  17. 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

  18. Pulmonary Extramedullary Hematopoiesis Involving the Pulmonary Artery

    OpenAIRE

    Varun Monga; Margarida Silverman

    2015-01-01

    Extramedullary hematopoiesis (EMH) occurs as a complication of hematologic disorders such as myelofibrosis, sickle cell anemia and thalassemia. The extramedullary tissue usually involves liver, spleen and lymph nodes, less frequently the chest. We present a recent case of a man with myeloproliferative neoplasm who developed pulmonary hemorrhage secondary to EMH in the lung and pulmonary artery. Radiation therapy was considered the best approach, but it didn’t work and the patient died a week ...

  19. Beyond corticosteroids: future prospects in the management of inflammation in COPD

    OpenAIRE

    Roche, N; Marthan, R.; P. Berger; A. Chambellan; Chanez, P; Aguilaniu, B; P-Y Brillet; P-R. Burgel; Chaouat, A.; Devillier, P; Escamilla, R.; Louis, R; H. Mal; J-F Muir; Pérez, T

    2011-01-01

    Inflammation plays a central role in the pathophysiology of chronic obstructive pulmonary disease (COPD). Exposure to cigarette smoke induces the recruitment of inflammatory cells in the airways and stimulates innate and adaptive immune mechanisms. Airway inflammation is involved in increased bronchial wall thickness, increased bronchial smooth muscle tone, mucus hypersecretion and loss of parenchymal elastic structures. Oxidative stress impairs tissue integrity, accelerates lung ageing and r...

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2014-11-15

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

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

    International Nuclear Information System (INIS)

    Background: There is scarce evidence about passive exposure to the vapour released or exhaled from electronic cigarettes (e-cigarettes) under real conditions. The aim of this study is to characterise passive exposure to nicotine from e-cigarettes' vapour and conventional cigarettes' smoke at home among non-smokers under real-use conditions. Methods: We conducted an observational study with 54 non-smoker volunteers from different homes: 25 living at home with conventional smokers, 5 living with nicotine e-cigarette users, and 24 from control homes (not using conventional cigarettes neither e-cigarettes). We measured airborne nicotine at home and biomarkers (cotinine in saliva and urine). We calculated geometric mean (GM) and geometric standard deviations (GSD). We also performed ANOVA and Student's t tests for the log-transformed data. We used Bonferroni-corrected t-tests to control the family error rate for multiple comparisons at 5%. Results: The GMs of airborne nicotine were 0.74 μg/m3 (GSD=4.05) in the smokers’ homes, 0.13 μg/m3 (GSD=2.4) in the e-cigarettes users’ homes, and 0.02 μg/m3 (GSD=3.51) in the control homes. The GMs of salivary cotinine were 0.38 ng/ml (GSD=2.34) in the smokers’ homes, 0.19 ng/ml (GSD=2.17) in the e-cigarettes users’ homes, and 0.07 ng/ml (GSD=1.79) in the control homes. Salivary cotinine concentrations of the non-smokers exposed to e-cigarette's vapour at home (all exposed ≥2 h/day) were statistically significant different that those found in non-smokers exposed to second-hand smoke ≥2 h/day and in non-smokers from control homes. Conclusions: The airborne markers were statistically higher in conventional cigarette homes than in e-cigarettes homes (5.7 times higher). However, concentrations of both biomarkers among non-smokers exposed to conventional cigarettes and e-cigarettes’ vapour were statistically similar (only 2 and 1.4 times higher, respectively). The levels of airborne nicotine and

  2. Effect of pulmonary hypertension on outcome of pulmonary tuberculosis

    OpenAIRE

    Majid Marjani; Parvaneh Baghaei; Majid Malekmohammad; Payam Tabarsi; Babak Sharif-Kashani; , Neda Behzadnia; Davood Mansouri; Mohammad Reza Masjedi; Ali Akbar Velayati

    2014-01-01

    Background: This study performed at the National Research Institute of Tuberculosis and Lung Disease, Tehran, Iran, aimed to evaluate the effect of concomitant pulmonary hypertension on the outcome of pulmonary tuberculosis. Methods: New cases of pulmonary tuberculosis were recruited for the study. Pulmonary hypertension was defined as systolic pulmonary arterial pressure ≥35 mm Hg estimated by transthoracic Doppler echocardiography. We assessed the relationship between pulmonary hypertensi...

  3. Surgically treated pulmonary stenosis

    DEFF Research Database (Denmark)

    Nielsen, Eva A; Hjortdal, Vibeke E

    additional four patients died after hospital discharge; therefore, the long-term mortality was 5%. The maximum follow-up period was 57 years, with a median of 33 years. In all, 16 patients (20%) required at least one re-intervention. Pulmonary valve replacement due to pulmonary regurgitation was the most...... re-intervention at the present stage. CONCLUSION: Surgical relief for pulmonary stenosis is efficient in relieving outflow obstruction; however, this efficiency is achieved at the cost of pulmonary regurgitation, leading to right ventricular dilatation and tricuspid regurgitation. When required......, pulmonary valve replacement is performed most frequently >20 years after the initial surgery. Lifelong follow-up of patients treated surgically for pulmonary stenosis is emphasised in this group of patients, who might otherwise consider themselves cured....

  4. Estimating the health consequences of replacing cigarettes with nicotine inhalers

    OpenAIRE

    Sumner, W.

    2003-01-01

    Background: A fast acting, clean nicotine delivery system might substantially displace cigarettes. Public health consequences would depend on the subsequent prevalence of nicotine use, hazards of delivery systems, and intrinsic hazards of nicotine.

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

    Data.gov (United States)

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

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

    OpenAIRE

    Carter, S.

    2003-01-01

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

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

    DEFF Research Database (Denmark)

    Rasch, Vibeke

    2003-01-01

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

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

    Data.gov (United States)

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

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

    Science.gov (United States)

    ... banned in the United States because of the ban on flavored cigarettes. hookahs or water pipes : Hookah ... Land Middle, Texas: why doesn't the U.S ban tobacco production? Eric Wargo Hi jgarcia, Because that ...

  10. 'Cool' Factor Often Spurs Teens to Try E-Cigarettes

    Science.gov (United States)

    ... learned about them from a store display or advertisement. Just over 10 percent (238 of the teens) ... on e-cigarette flavorings. In May, the U.S. Food and Drug Administration announced a new rule prohibiting ...

  11. Required warnings for cigarette packages and advertisements. Final rule.

    Science.gov (United States)

    2011-06-22

    The Food and Drug Administration (FDA) is amending its regulations to add a new requirement for the display of health warnings on cigarette packages and in cigarette advertisements. This rule implements a provision of the Family Smoking Prevention and Tobacco Control Act (Tobacco Control Act) that requires FDA to issue regulations requiring color graphics, depicting the negative health consequences of smoking, to accompany the nine new textual warning statements required under the Tobacco Control Act. The Tobacco Control Act amends the Federal Cigarette Labeling and Advertising Act (FCLAA) to require each cigarette package and advertisement to bear one of nine new textual warning statements. This final rule specifies the color graphic images that must accompany each of the nine new textual warning statements. PMID:21696017

  12. 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 ...

  13. Starting Monday, FDA Banning E-Cigarette Sales to Minors

    Science.gov (United States)

    ... to draw teenagers into a lifetime of smoking addiction. "Youth use e-cigarettes more than any other tobacco product on the market today, serving as an entry point to more traditional tobacco products and placing kids at risk to ...

  14. Current Cigarette Use Among Youth (YRBSS) PDF Slides

    Data.gov (United States)

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

  15. CDC STATE System E-Cigarette Legislation - Preemption

    Data.gov (United States)

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

  16. CDC STATE System E-Cigarette Legislation - Tax

    Data.gov (United States)

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

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

    Data.gov (United States)

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

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

    Data.gov (United States)

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

  19. CDC STATE System E-Cigarette Legislation - Licensure

    Data.gov (United States)

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

  20. Cigarette taxes. The straw to break the camel's back.

    Science.gov (United States)

    Grossman, M; Chaloupka, F J

    1997-01-01

    Teenage cigarette smoking is sensitive to the price of cigarettes. The most recent research suggests that a 10% increase in price would reduce the number of teenagers who smoke by 7%. If the proposed 43-cent hike in the Federal excise tax rate on cigarettes contained in the Hatch-Kennedy Bill were enacted, the number of teenage smokers would fall by approximately 16%. This translates into more than 2.6 million fewer smokers and more than 850,000 fewer smoking-related premature deaths in the current cohort of 0 to 17-year-olds. Adjusted for inflation, the current 24-cent-a-pack tax costs the buyer about half of the original cigarette tax of 8 cents imposed in 1951. A substantial tax hike would curb youth smoking; this strategy should move to the forefront of the antismoking campaign. PMID:9258294

  1. Excise Tax Rates On Packs Of Cigarettes PDF Slides

    Data.gov (United States)

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

  2. Cystic pulmonary hydatidosis

    Science.gov (United States)

    Sarkar, Malay; Pathania, Rajnish; Jhobta, Anupam; Thakur, Babu Ram; Chopra, Rajesh

    2016-01-01

    Cystic echinococcosis (CE) is a zoonotic parasitic disease caused by the larval stages of the cestode Echinococcus granulosus. Worldwide, pulmonary hydatid cyst is a significant problem medically, socially, and economically. Surgery is the definitive therapy of pulmonary hydatidosis. Benzimidazoles may be considered in patients with a surgical contraindication. This review will focus on pathogenesis, lifecycle, clinical features, and management of pulmonary hydatid disease. PMID:27051107

  3. Experimental pulmonary carcinogenesis by radon and its daughters

    International Nuclear Information System (INIS)

    Information on experimental pulmonary carcinogenesis by radon and its daughters has come mostly from experiments carried out in France and United States of America. In rats a dose response relation was estimated to be linear with dose at low dose region. Studies of rats exposed daily to radon and radon daughters indicated that the frequency of pulmonary cancer at total exposure greater than 3000 WLM was greater when the exposure rates were low. At low total exposures the dose-rate effect was less apparent. Cigarette smoke increased the pulmonary cancer in rats but decreased in dogs. The decrease may be due to a decrease of absorbed doses with increased secretion of mucus and to an enhancement of mucociliary clearance. After inhalation of 222Ru at equilibrium with radon daughters, rats were inoculated intrapleurally with asbestos fibres or glass fibres. The additive co-carcinogenic effects of this type of insult were demonstrated by the increased incidence of malignant thoracic tumours. As for species differences, dogs and hamsters are relatively resistant to cancer induction and rats are sensitive. While bronchogenic carcinomas are the most frequently observed radiation-induced pulmonary cancer in humans, bronchioloalveolar carcinomas are the most frequent type in most animal species. (author)

  4. How Is Pulmonary Hypertension Diagnosed?

    Science.gov (United States)

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

  5. Liver Disease and Pulmonary Hypertension

    Science.gov (United States)

    Liver Disease Pulmonary & PH Hypertension Did you know that if you have liver disease, you are at risk for pulmonary ... to the liver without cirrhosis. How does liver disease relate to pulmonary hypertension? Liver disease can cause what is known ...

  6. The Association between Cigarette Smoking and Acne Intensity

    OpenAIRE

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

    2009-01-01

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

  7. Impact of cigarette smoking in type 2 diabetes development

    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...

  8. Assessing Ultrafine Particles Exposure in Electronic Cigarette Vape Shops

    OpenAIRE

    Sen, Chanbopha

    2016-01-01

    Introduction: Vape shops have grown in popularity among adults and youth. The increased popularity of electronic cigarettes has triggered many new businesses to open within the last three years to sell electronic cigarettes devices, flavor liquids and provide a place for lounging. High levels of ultrafine particles (UFP) are generated when active vaping is occurring. Objectives: 1. Quantify and understand the spatial distribution of ultrafine particles in vape shops. 2. Identify factors that ...

  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. Social norms of cigarette and hookah smokers in Iranian universities

    OpenAIRE

    Roohafza, Hamidreza; Sadeghi, Masoumeh; Shahnam, Maryam; Shokouh, Pedram; Teimori, Soheila; Amirpour, Afshin; Sarrafzadegan, Nizal

    2013-01-01

    BACKGROUND First experiences of tobacco use usually occur in adolescence. The recognition of social norms leading to youth smoking is hence necessary. We tried to assess the social norms among Iranian young cigarette and hookah smokers. METHODS This cross-sectional study was conducted on 451 girls and 361 boys aging 20-25 years old who entered Isfahan and Kashan Universities (Iran) in 2007. Demographic factors (age, gender, and age at smoking onset) cigarette and hookah smoking status, having...

  11. Price Elasticity Estimates for Cigarette Demand in Vietnam

    OpenAIRE

    Patrick Eozenou; Burke Fishburn

    2009-01-01

    In this paper, we analyze a complete demand system to estimate the price elasticity for cigarette demand in Vietnam. Following Deaton (1990), we build a spatial panel using cross sectional household survey data. We consider a model of simultaneous choice of quantity and quality. This allows us to exploit unit values from cigarette consumption in order to disentangle quality choice from exogenous price variations. We then rely on spatial variations in prices and quantities demanded to estimate...

  12. Neural Circuitry of Impulsivity in a Cigarette Craving Paradigm

    OpenAIRE

    Bourque, Josiane; Mendrek, Adrianna; Dinh-Williams, Laurence; Potvin, Stéphane

    2013-01-01

    Impulsivity has been shown to play a pivotal role in the onset, pattern of consumption, relapse and, most notably, craving of illicit and licit drugs such as cigarette smoking. The goal of this study was to examine the neurobiological influence of trait impulsivity during cue-induced cigarette craving. Thirty-one chronic smokers passively viewed appetitive smoking-related and neutral images while being scanned and reported their feelings of craving. They completed the Barratt Impulsiveness Sc...

  13. Neural circuitry of impulsivity in a cigarette craving paradigm

    OpenAIRE

    StephanePotvin; JosianeBourque; AdriannaMendrek

    2013-01-01

    Impulsivity has been shown to play a pivotal role in the onset, pattern of consumption, relapse and, most notably, craving of illicit and licit drugs such as cigarette smoking. The goal of this study was to examine the neurobiological influence of trait impulsivity during cue-induced cigarette craving. Thirty-one chronic smokers passively viewed appetitive smoking-related and neutral images while being scanned and reported their feelings of craving. They completed the Barratt Impulsiveness Sc...

  14. Why ban the sale of cigarettes? The case for abolition

    OpenAIRE

    Proctor, Robert N.

    2013-01-01

    The cigarette is the deadliest artefact in the history of human civilisation. Most of the richer countries of the globe, however, are making progress in reducing both smoking rates and overall consumption. Many different methods have been proposed to steepen this downward slope, including increased taxation, bans on advertising, promotion of cessation, and expansion of smoke-free spaces. One option that deserves more attention is the enactment of local or national bans on the sale of cigarett...

  15. Neural correlates of cigarette health warning avoidance among smokers

    OpenAIRE

    Stothart, George; Maynard, Olivia M; Lavis, Rosie J; Munafo, Marcus R.

    2016-01-01

    BACKGROUND: Eye-tracking technology has indicated that daily smokers actively avoid pictorial cigarette package health warnings. Avoidance may be due to a pre-cognitive perceptual bias or a higher order cognitive bias, such as reduced emotional processing. Using electroencephalography (EEG), this study aimed to identify the temporal point at which smokers' responses to health warnings begin to differ.METHOD: Non-smokers (n=20) and daily smokers (n=20) viewed pictorial cigarette package health...

  16. Vaporous Marketing: Uncovering Pervasive Electronic Cigarette Advertisements on Twitter

    OpenAIRE

    Clark, Eric M.; Jones, Chris A.; Williams, Jake Ryland; Kurti, Allison N; Nortotsky, Michell Craig; Danforth, Christopher M.; Dodds, Peter Sheridan

    2015-01-01

    Background: Twitter has become the "wild-west" of marketing and promotional strategies for advertisement agencies. Electronic cigarettes have been heavily marketed across Twitter feeds, offering discounts, "kid-friendly" flavors, algorithmically generated false testimonials, and free samples. Methods:All electronic cigarette keyword related tweets from a 10% sample of Twitter spanning January 2012 through December 2014 (approximately 850,000 total tweets) were identified and categorized as Au...

  17. Price Elasticity Estimates of Cigarette Demand in Vietnam

    OpenAIRE

    Eozenou, Patrick; Fishburn, Burke

    2001-01-01

    In this paper, we analyze a complete demand system to estimate the price elasticity for cigarette demand in Vietnam. Following Deaton (1990), we build a spatial panel using cross sectional household survey data. We consider a model of simultaneous choice of quantity and quality. This allows us to exploit unit values from cigarette consumption in order to disentangle quality choice from exogenous price variations. We then rely on spatial variations in prices and quantities demanded to estimate...

  18. 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...

  19. Solitary pulmonary nodule

    Science.gov (United States)

    ... as aspergillosis , coccidioidomycosis , cryptococcosis , or histoplasmosis Primary lung cancer is the most common cause of cancerous (malignant) pulmonary nodules. This is cancer that starts in the ...

  20. 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…