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Sample records for acute cigarette smoke-induced

  1. Inhalation of glycopyrronium inhibits cigarette smoke-induced acute lung inflammation in a murine model of COPD.

    PubMed

    Shen, Liang-liang; Liu, Ya-nan; Shen, Hui-juan; Wen, Chong; Jia, Yong-liang; Dong, Xin-wei; Jin, Fang; Chen, Xiao-ping; Sun, Yun; Xie, Qiang-min

    2014-02-01

    Glycopyrronium bromide (GB) is a muscarinic receptor antagonist that has been used as a long-acting bronchodilator in chronic obstructive pulmonary disease (COPD) patients. The aim of this study was to investigate the anti-inflammatory activity of inhaled GB in a cigarette smoke-induced acute lung inflammation mouse model. We found that aerosol pre-treatment with GB suppresses the accumulation of neutrophils and macrophages in the bronchoalveolar lavage fluid (BALF) in cigarette smoke (CS)-exposed mice. GB at doses of 300 and 600 μg/ml significantly inhibited the CS-induced increases in the mRNA and protein expression levels of interleukin (IL)-1β, tumor necrosis factor (TNF)-α, monocyte chemotactic protein (MCP)-1 and transforming growth factor (TGF)-β1 in lung tissues and the BALF. Moreover, GB at a dose of 600 μg/ml significantly inhibited the CS-induced changes in glutathione (GSH) and myeloperoxidase (MPO) activities in the BALF, decreased the CS-induced expression of matrix metalloproteinases (MMP)-9, and increased the CS-induced expression of tissue inhibitor of metalloproteinases (TIMP)-1, as determined through the immunohistochemical staining of lung tissue. Our results demonstrate the beneficial effects of inhaled GB on the inflammatory reaction in COPD. PMID:24389380

  2. Neu-164 and Neu-107, two novel antioxidant and anti-myeloperoxidase compounds, inhibit acute cigarette smoke-induced lung inflammation.

    PubMed

    Thatcher, Thomas H; Hsiao, Hsi-Min; Pinner, Elhanan; Laudon, Moshe; Pollock, Stephen J; Sime, Patricia J; Phipps, Richard P

    2013-07-15

    Cigarette smoke is a profound proinflammatory stimulus that causes acute lung inflammation and chronic lung disease, including chronic obstructive pulmonary disease (COPD, emphysema, and chronic bronchitis), via a variety of mechanisms, including oxidative stress. Cigarette smoke contains high levels of free radicals, whereas inflammatory cells, including macrophages and neutrophils, express enzymes, including NADPH oxidase, nitric oxide synthase, and myeloperoxidase, that generate reactive oxygen species in situ and contribute to inflammation and tissue damage. Neu-164 and Neu-107 are small-molecule inhibitors of myeloperoxidase, as well as potent antioxidants. We hypothesized that Neu-164 and Neu-107 would inhibit acute cigarette smoke-induced inflammation. Adult C57BL/6J mice were exposed to mainstream cigarette smoke for 3 days to induce acute inflammation and were treated daily by inhalation with Neu-164, Neu-107, or dexamethasone as a control. Inflammatory cells and cytokines were assessed by bronchoalveolar lavage and histology. mRNA levels of endogenous antioxidant genes heme oxygenase-1 and glutamate-cysteine ligase modifier subunit were determined by qPCR. Cigarette smoke exposure induced acute lung inflammation with accumulation of neutrophils and upregulation of proinflammatory cytokines, including IL-6, macrophage inflammatory protein-2, and keratinocyte-derived cytokine. Both Neu-164 and Neu-107 significantly reduced the accumulation of inflammatory cells and the expression of inflammatory cytokines as effectively as dexamethasone. Upregulation of endogenous antioxidant genes was dampened. Neu-164 and Neu-107 inhibit acute cigarette smoke-induced inflammation by scavenging reactive oxygen species in cigarette smoke and by inhibiting further oxidative stress caused by inflammatory cells. These compounds may have promise in preventing or treating lung disease associated with chronic smoke exposure, including COPD.

  3. Critical role of aldehydes in cigarette smoke-induced acute airway inflammation

    PubMed Central

    2013-01-01

    Background Cigarette smoking (CS) is the most important risk factor for COPD, which is associated with neutrophilic airway inflammation. We hypothesize, that highly reactive aldehydes are critical for CS-induced neutrophilic airway inflammation. Methods BALB/c mice were exposed to CS, water filtered CS (WF-CS) or air for 5 days. Levels of total particulate matter (TPM) and aldehydes in CS and WF-CS were measured. Six hours after the last exposure, inflammatory cells and cytokine levels were measured in lung tissue and bronchoalveolar lavage fluid (BALF). Furthermore, Beas-2b bronchial epithelial cells were exposed to CS extract (CSE) or WF-CS extract (WF-CSE) in the absence or presence of the aldehyde acrolein and IL-8 production was measured after 24 hrs. Results Compared to CS, in WF-CS strongly decreased (CS; 271.1 ± 41.5 μM, WF-CS; 58.5 ± 8.2 μM) levels of aldehydes were present whereas levels of TPM were only slightly reduced (CS; 20.78 ± 0.59 mg, WF-CS; 16.38 ± 0.36 mg). The numbers of mononuclear cells in BALF (p<0.01) and lung tissue (p<0.01) were significantly increased in the CS- and WF-CS-exposed mice compared to air control mice. Interestingly, the numbers of neutrophils (p<0.001) in BALF and neutrophils and eosinophils (p<0.05) in lung tissue were significantly increased in the CS-exposed but not in WF-CS-exposed mice as compared to air control mice. Levels of the neutrophil and eosinophil chemoattractants KC, MCP-1, MIP-1α and IL-5 were all significantly increased in lung tissue from CS-exposed mice compared to both WF-CS-exposed and air control mice. Interestingly, depletion of aldehydes in WF-CS extract significantly reduced IL-8 production in Beas-2b as compared to CSE, which could be restored by the aldehyde acrolein. Conclusion Aldehydes present in CS play a critical role in inflammatory cytokine production and neutrophilic- but not mononuclear airway inflammation. PMID:23594194

  4. Nedocromil sodium reduces cigarette smoke-induced bronchoconstrictor hyperresponsiveness to substance P in the guinea-pig.

    PubMed

    Dusser, D J; Lacroix, H; Desmazes-Dufeu, N; Mordelet-Dambrine, M; Roisman, G L

    1995-01-01

    Acute exposure to cigarette smoke provokes airway hyperresponsiveness to substance P and inactivates neutral endopeptidase (NEP). To determine whether nedocromil sodium can prevent cigarette smoke-induced hyperresponsiveness to substance P, we studied two groups of anaesthetized guinea-pigs. One group of guinea-pigs was pretreated with aerosolized 0.9% NaCl solution (90 breaths), the other group was pretreated with aerosolized nedocromil sodium (10(-4) M, 90 breaths). In each animal, pretreatment was followed by either exposure to the smoke of one cigarette or exposure to air. After acute exposure to cigarette smoke or to air, we measured the change in total pulmonary resistance (RL) induced by increasing concentrations of aerosolized substance P. In the absence of nedocromil sodium, the bronchoconstrictor responses to substance P were greater in cigarette smoke-exposed guinea-pigs than in air-exposed animals. Aerosolized nedocromil sodium had no effect on the response to substance P in air-exposed animals, but it reduced cigarette smoke-induced hyperresponsiveness to substance P. The preventive effect on cigarette smoke-induced hyperresponsiveness to substance P was observed at concentrations of aerosolized nedocromil sodium of 3 x 10(-5), 10(-4), and 3 x 10(-4) M. In vitro, cigarette smoke solution inhibited NEP activity from lung membrane preparations, but this inhibitory effect was not modified by nedocromil sodium (10(-4) M). We conclude that aerosolized nedocromil sodium reduces cigarette smoke-induced airway hyperresponsiveness to substance P in vivo. This action of nedocromil sodium is not due to a protective effect on cigarette smoke-induced inactivation of NEP in vitro.

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

    PubMed

    Vani, G; Anbarasi, K; Shyamaladevi, C S

    2015-01-01

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

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

    PubMed Central

    Vani, G.; Anbarasi, K.; Shyamaladevi, C. S.

    2015-01-01

    Cigarette smoking (CS) is a major health hazard that exerts diverse physiologic and biochemical effects mediated by the components present and generated during smoking. Recent experimental studies have shown predisposition to several biological consequences from both active and passive cigarette smoke exposure. In particular, passive smoking is linked to a number of adverse health effects which are equally harmful as active smoking. A pragmatic approach should be considered for designing a pharmacological intervention to combat the adverse effects of passive smoking. This review describes the results from a controlled experimental condition, testing the effect of bacoside A (BA) on the causal role of passive/secondhand smoke exposure that caused pathological and neurological changes in rat brain. Chronic exposure to cigarette smoke induced significant changes in rat brain histologically and at the neurotransmitter level, lipid peroxidation states, mitochondrial functions, membrane alterations, and apoptotic damage in rat brain. Bacoside A is a neuroactive agent isolated from Bacopa monnieri. As a neuroactive agent, BA was effective in combating these changes. Future research should examine the effects of BA at molecular level and assess its functional effects on neurobiological and behavioral processes associated with passive smoke. PMID:26413118

  7. Cigarette smoke induces methylation of the tumor suppressor gene NISCH

    PubMed Central

    Ostrow, Kimberly Laskie; Michalidi, Christina; Guerrero-Preston, Rafael; Hoque, Mohammad O.; Greenberg, Alissa; Rom, William; Sidransky, David

    2013-01-01

    We have previously identified a putative tumor suppressor gene, NISCH, whose promoter is methylated in lung tumor tissue as well as in plasma obtained from lung cancer patients. NISCH was observed to be more frequently methylated in smoker lung cancer patients than in non-smoker lung cancer patients. Here, we investigated the effect of tobacco smoke exposure on methylation of the NISCH gene. We tested methylation of NISCH after oral keratinocytes were exposed to mainstream and side stream cigarette smoke extract in culture. Methylation of the promoter region of the NISCH gene was also evaluated in plasma obtained from lifetime non-smokers and light smokers (< 20 pack/year), with and without lung tumors, and heavy smokers (20+ pack/year) without disease. Promoter methylation of NISCH was tested by quantitative fluorogenic real-time PCR in all samples. Promoter methylation of NISCH occurred after exposure to mainstream tobacco smoke as well as to side stream tobacco smoke in normal oral keratinocyte cell lines. NISCH methylation was also detected in 68% of high-risk, heavy smokers without detectable tumors. Interestingly, in light smokers, NISCH methylation was present in 69% of patients with lung cancer and absent in those without disease. Our pilot study indicates that tobacco smoke induces methylation changes in the NISCH gene promoter before any detectable cancer. Methylation of the NISCH gene was also found in lung cancer patients’ plasma samples. After confirming these findings in longitudinally collected plasma samples from high-risk populations (such as heavy smokers), examining patients for hypermethylation of the NISCH gene may aid in identifying those who should undergo additional screening for lung cancer. PMID:23503203

  8. A new experimental model of cigarette smoke-induced emphysema in Wistar rats*, **

    PubMed Central

    Kozma, Rodrigo de las Heras; Alves, Edson Marcelino; Barbosa-de-Oliveira, Valter Abraão; Lopes, Fernanda Degobbi Tenorio Quirino dos Santos; Guardia, Renan Cenize; Buzo, Henrique Vivi; de Faria, Carolina Arruda; Yamashita, Camila; Cavazzana, Manzelio; Frei, Fernando; Ribeiro-Paes, Maria José de Oliveira; Ribeiro-Paes, João Tadeu

    2014-01-01

    OBJECTIVE: To describe a new murine model of cigarette smoke-induced emphysema. METHODS: Twenty-four male Wistar rats were divided into two groups: the cigarette smoke group, comprising 12 rats exposed to smoke from 12 commercial filter cigarettes three times a day (a total of 36 cigarettes per day) every day for 30 weeks; and the control group, comprising 12 rats exposed to room air three times a day every day for 30 weeks. Lung function was assessed by mechanical ventilation, and emphysema was morphometrically assessed by measurement of the mean linear intercept (Lm). RESULTS: The mean weight gain was significantly (approximately ten times) lower in the cigarette smoke group than in the control group. The Lm was 25.0% higher in the cigarette smoke group. There was a trend toward worsening of lung function parameters in the cigarette smoke group. CONCLUSIONS: The new murine model of cigarette smoke-induced emphysema and the methodology employed in the present study are effective and reproducible, representing a promising and economically viable option for use in studies investigating the pathophysiology of and therapeutic approaches to COPD. PMID:24626269

  9. Ceramides mediate cigarette smoke-induced metabolic disruption in mice.

    PubMed

    Thatcher, Mikayla O; Tippetts, Trevor S; Nelson, Michael B; Swensen, Adam C; Winden, Duane R; Hansen, Melissa E; Anderson, Madeline C; Johnson, Ian E; Porter, James P; Reynolds, Paul R; Bikman, Benjamin T

    2014-11-15

    Cigarette smoke exposure increases lung ceramide biosynthesis and alters metabolic function. We hypothesized that ceramides are released from the lung during cigarette smoke exposure and result in elevated skeletal muscle ceramide levels, resulting in insulin resistance and altered mitochondrial respiration. Employing cell and animal models, we explored the effect of cigarette smoke on muscle cell insulin signaling and mitochondrial respiration. Muscle cells were treated with conditioned medium from cigarette smoke extract (CSE)-exposed lung cells, followed by analysis of ceramides and assessment of insulin signaling and mitochondrial function. Mice were exposed to daily cigarette smoke and a high-fat, high-sugar (HFHS) diet with myriocin injections to inhibit ceramide synthesis. Comparisons were conducted between these mice and control animals on standard diets in the absence of smoke exposure and myriocin injections. Muscle cells treated with CSE-exposed conditioned medium were completely unresponsive to insulin stimulation, and mitochondrial respiration was severely blunted. These effects were mitigated when lung cells were treated with the ceramide inhibitor myriocin prior to and during CSE exposure. In mice, daily cigarette smoke exposure and HFHS diet resulted in insulin resistance, which correlated with elevated ceramides. Although myriocin injection was protective against insulin resistance with either smoke or HFHS, it was insufficient to prevent insulin resistance with combined CS and HFHS. However, myriocin injection restored muscle mitochondrial respiration in all treatments. Ceramide inhibition prevents metabolic disruption in muscle cells with smoke exposure and may explain whole body insulin resistance and mitochondrial dysfunction in vivo.

  10. Human Adipose-derived Stem Cells Ameliorate Cigarette Smoke-induced Murine Myelosuppression via TSG-6

    PubMed Central

    Xie, Jie; Broxmeyer, Hal E.; Feng, Dongni; Schweitzer, Kelly S.; Yi, Ru; Cook, Todd G.; Chitteti, Brahmananda R.; Barwinska, Daria; Traktuev, Dmitry O.; Van Demark, Mary J.; Justice, Matthew J.; Ou, Xuan; Srour, Edward F.; Prockop, Darwin J.; Petrache, Irina; March, Keith L.

    2015-01-01

    Objective Bone marrow-derived hematopoietic stem and progenitor cells (HSC/HPC) are critical to homeostasis and tissue repair. The aims of this study were to delineate the myelotoxicity of cigarette smoking (CS) in a murine model, to explore human adipose-derived stem cells (hASC) as a novel approach to mitigate this toxicity, and to identify key mediating factors for ASC activities. Methods C57BL/6 mice were exposed to CS with or without i.v. injection of regular or siRNA-transfected hASC. For in vitro experiments, cigarette smoke extract (CSE) was used to mimic the toxicity of CS exposure. Analysis of bone marrow hematopoietic progenitor cells (HPC) were performed both by flow cytometry and colony forming unit assays. Results In this study, we demonstrate that as few as three days of CS exposure result in marked cycling arrest and diminished clonogenic capacity of HPC, followed by depletion of phenotypically-defined HSC/HPC. Intravenous injection of hASC substantially ameliorated both acute and chronic CS-induced myelosuppression. This effect was specifically dependent on the anti-inflammatory factor TSG-6, which is induced from xenografted hASC, primarily located in the lung and capable of responding to host inflammatory signals. Gene expression analysis within bone marrow HSC/HPC revealed several specific signaling molecules altered by CS and normalized by hASC. Conclusion Our results suggest that systemic administration of hASC or TSG-6 may be novel approaches to reverse cigarette smoking-induced myelosuppression. PMID:25329668

  11. Cigarette sidestream smoke induces phosphorylated histone H2AX.

    PubMed

    Toyooka, Tatsushi; Ibuki, Yuko

    2009-05-31

    Cigarette sidestream smoke (CSS) is a widespread environmental pollutant having highly genotoxic potency. In spite of the overwhelming evidence that CSS induces a wide range of DNA damage such as oxidative base damage and DNA adducts, evidence that CSS can result in DNA double strand breaks (DSBs) is little. In this study, we showed that CSS generated phosphorylated histone H2AX (gamma-H2AX), recently considered as a sensitive marker of the generation of DSBs, in a human pulmonary epithelial cell model, A549. Treatment with CSS drastically induced discrete foci of gamma-H2AX within the nucleus in a dose-dependent manner. CSS increased intracellular oxidation, and N-acetylcysteine (NAC), an antioxidant, significantly attenuated the formation of gamma-H2AX, suggesting that reactive oxygen species produced from CSS partially contributed to the phosphorylation. The generation of gamma-H2AX is considered to be accompanied the induction of DSBs. CSS in fact induced DSBs, which was also inhibited by NAC. DSBs are the worst type of DNA damage, related to genomic instability and carcinogenesis. Our results would increase the evidence of the strong genotoxicity of passive smoking. PMID:19486862

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

    PubMed

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

    2015-01-01

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

  13. Toll-like receptor-4 mediates cigarette smoke-induced cytokine production by human macrophages

    PubMed Central

    Karimi, Khalil; Sarir, Hadi; Mortaz, Esmaeil; Smit, Joost J; Hosseini, Hossein; De Kimpe, Sjef J; Nijkamp, Frans P; Folkerts, Gert

    2006-01-01

    Background The major risk factor for the development of COPD is cigarette smoking. Smoking causes activation of resident cells and the recruitment of inflammatory cells into the lungs, which leads to release of pro-inflammatory cytokines, chemotactic factors, oxygen radicals and proteases. In the present study evidence is found for a new cellular mechanism that refers to a link between smoking and inflammation in lungs. Methods Employing human monocyte-derived macrophages, different techniques including FACS analysis, Cytometric Bead Array Assay and ELISA were achieved to evaluate the effects of CS on pro-inflammatory cytokine secretion including IL-8. Then, Toll-like receptor neutralization was performed to study the involvement of Toll-like receptor-4 in IL-8 production. Finally, signaling pathways in macrophages after exposure to CS medium were investigated performing ELISA and Western analysis. Results We demonstrate that especially human monocytes are sensitive to produce IL-8 upon cigarette smoke stimulation compared to lymphocytes or neutrophils. Moreover, monocyte-derived macrophages produce high amounts of the cytokine. The IL-8 production is dependent on Toll-like receptor 4 stimulation and LPS is not involved. Further research resolved the cellular mechanism by which cigarette smoke induces cytokine production in monocyte-derived macrophages. Cigarette smoke causes subsequently a concentration-dependent phosphorylation of IRAK and degradation of TRAF6. Moreover, IκBα was phosphorylated which suggests involvement of NF-κB. In addition, NFκB -inhibitor blocked cigarette smoke-induced IL-8 production. Conclusion These findings link cigarette smoke to inflammation and lead to new insights/therapeutic strategies in the pathogenesis of lung emphysema. PMID:16620395

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

    PubMed Central

    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 given i.p. to BALB/c mice daily 2 h before 4% cigarette smoke exposure for 1 h over five consecutive days. Bronchoalveolar lavage fluid and lungs were collected for analyses of cytokines, oxidative damage markers and antioxidant activities. BEAS-2B bronchial epithelial cells were exposed to cigarette smoke extract (CSE) and used to study the antioxidant mechanism of action of andrographolide. Key Results Andrographolide suppressed cigarette smoke-induced increases in lavage fluid cell counts; levels of IL-1β, MCP-1, IP-10 and KC; and levels of oxidative biomarkers 8-isoprostane, 8-OHdG and 3-nitrotyrosine in a dose-dependent manner. Andrographolide promoted inductions of glutathione peroxidase (GPx) and glutathione reductase (GR) activities in lungs from cigarette smoke-exposed mice. In BEAS-2B cells, andrographolide markedly increased nuclear Nrf2 accumulation, promoted binding to antioxidant response element (ARE) and total cellular glutathione level in response to CSE. Andrographolide up-regulated ARE-regulated gene targets including glutamate-cysteine ligase catalytic (GCLC) subunit, GCL modifier (GCLM) subunit, GPx, GR and heme oxygenase-1 in BEAS-2B cells in response to CSE. Conclusions Andrographolide possesses antioxidative properties against cigarette smoke-induced lung injury probably via augmentation of Nrf2 activity and may have therapeutic potential for treating COPD. PMID:23146110

  15. Vitamin C prevents cigarette smoke-induced pulmonary emphysema in mice and provides pulmonary restoration.

    PubMed

    Koike, Kengo; Ishigami, Akihito; Sato, Yasunori; Hirai, Toyohiro; Yuan, Yiming; Kobayashi, Etsuko; Tobino, Kazunori; Sato, Tadashi; Sekiya, Mitsuaki; Takahashi, Kazuhisa; Fukuchi, Yoshinosuke; Maruyama, Naoki; Seyama, Kuniaki

    2014-02-01

    Vitamin C (VC) is a potent antioxidant and is essential for collagen synthesis. We investigated whether VC treatment prevents and cures smoke-induced emphysema in senescence marker protein-30 knockout (SMP30-KO) mice, which cannot synthesize VC. Two smoke-exposure experiments using SMP30-KO mice were conducted. In the first one (a preventive study), 4-month-old mice received minimal VC (0.0375 g/l) [VC(L)] or physiologically sufficient VC (1.5 g/l) [VC(S)] and exposed to cigarette smoke or smoke-free air for 2 months. Pulmonary evaluations followed when the mice were 6 months of age. The second study began after the establishment of smoke-induced emphysema (a treatment study). These mice no longer underwent smoke exposure but received VC(S) or VC(L) treatment for 2 months. Morphometric analysis was performed, and measurements of oxidative stress, collagen synthesis, and vascular endothelial growth factor in the lungs were evaluated. Chronic smoke exposure caused emphysema (29.6% increases of mean linear intercepts [MLI] and 106.5% increases of destructive index compared with the air-only group) in 6-month-old SMP30-KO mice, and this emphysema closely resembled human chronic obstructive pulmonary disease. Smoke-induced emphysema persisted in the VC(L) group after smoking cessation, whereas VC treatment provided pulmonary restoration (18.5% decrease of MLI and 41.3% decrease of destructive index compared with VC(L) group). VC treatment diminished oxidative stress, increased collagen synthesis, and improved vascular endothelial growth factor levels in the lungs. Our results suggest that VC not only prevents smoke-induced emphysema in SMP30-KO mice but also restores emphysematous lungs. Therefore, VC may provide a new therapeutic strategy for treating chronic obstructive pulmonary disease in humans.

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

    PubMed

    Anbarasi, K; Kathirvel, G; Vani, G; Jayaraman, G; Shyamala Devi, C S

    2006-01-01

    Cigarette smoking is associated with the development of several diseases and antioxidants play a major role in the prevention of smoking-related diseases. Apoptosis is suggested as a possible contributing factor in the pathogenesis of smoking-induced toxicity. Therefore the present study was designed to investigate the influence of chronic cigarette smoke exposure on apoptosis and the modulatory effect of bacoside A (triterpenoid saponin isolated from the plant Bacopa monniera) on smoking-induced apoptosis in rat brain. Adult male albino rats of Wistar strain were exposed to cigarette smoke and simultaneously administered with bacoside A (10 mg/kg b.w./day, orally) for a period of 12 weeks. Expression of brain hsp70 was analyzed by Western blotting. Apoptosis was identified by DNA fragmentation, terminal deoxynucleotidyl transferase-mediated deoxy uridine triphosphate nick end labeling (TUNEL) staining and transmission electron microscopy. The results showed that exposure to cigarette smoke induced hsp70 expression and apoptosis as characterized by DNA laddering, increased TUNEL-positive cells and ultrastructural apoptotic features in the brain. Administration of bacoside A prevented expression of hsp70 and neuronal apoptosis during cigarette smoking. We speculate that apoptosis may be responsible for the smoking-induced brain damage and bacoside A can protect the brain from the toxic effects of cigarette smoking.

  17. Respiratory Syncytial Virus Infections Enhance Cigarette Smoke Induced COPD in Mice

    PubMed Central

    Foronjy, Robert F.; Dabo, Abdoulaye J.; Taggart, Clifford C.; Weldon, Sinead; Geraghty, Patrick

    2014-01-01

    Respiratory syncytial viral (RSV) infections are a frequent cause of chronic obstructive pulmonary disease (COPD) exacerbations, which are a major factor in disease progression and mortality. RSV is able to evade antiviral defenses to persist in the lungs of COPD patients. Though RSV infection has been identified in COPD, its contribution to cigarette smoke-induced airway inflammation and lung tissue destruction has not been established. Here we examine the long-term effects of cigarette smoke exposure, in combination with monthly RSV infections, on pulmonary inflammation, protease production and remodeling in mice. RSV exposures enhanced the influx of macrophages, neutrophils and lymphocytes to the airways of cigarette smoke exposed C57BL/6J mice. This infiltration of cells was most pronounced around the vasculature and bronchial airways. By itself, RSV caused significant airspace enlargement and fibrosis in mice and these effects were accentuated with concomitant smoke exposure. Combined stimulation with both smoke and RSV synergistically induced cytokine (IL-1α, IL-17, IFN-γ, KC, IL-13, CXCL9, RANTES, MIF and GM-CSF) and protease (MMP-2, -8, -12, -13, -16 and cathepsins E, S, W and Z) expression. In addition, RSV exposure caused marked apoptosis within the airways of infected mice, which was augmented by cigarette smoke exposure. RSV and smoke exposure also reduced protein phosphatase 2A (PP2A) and protein tyrosine phosphates (PTP1B) expression and activity. This is significant as these phosphatases counter smoke-induced inflammation and protease expression. Together, these findings show for the first time that recurrent RSV infection markedly enhances inflammation, apoptosis and tissue destruction in smoke-exposed mice. Indeed, these results indicate that preventing RSV transmission and infection has the potential to significantly impact on COPD severity and progression. PMID:24587397

  18. Could charcoal filtration of cigarette smoke reduce smoking-induced disease? A review of the literature.

    PubMed

    Coggins, Christopher R E; Gaworski, Charles L

    2008-04-01

    A review of the published work with charcoal-filtered cigarettes indicates that there are reductions in the concentrations for many gas-vapor phase constituents found in mainstream smoke. However, charcoal filters provided no apparent capacity for reduction of smoke particulate phase components. The reductions in gas-vapor phase smoke chemistry analytes generally correspond with findings of reduced toxicological activity, principally related to a reduction in the cytotoxic action of the volatile smoke constituents. Results of a short-term clinical study show small reductions in the biomarkers of the gas-vapor phase smoke constituents in subjects smoking charcoal-filtered cigarettes, compared to subjects smoking non-charcoal filtered cigarettes. The very limited epidemiology data (a single study) fail to demonstrate a conclusive beneficial effect of charcoal-filtered cigarette products compared to non-charcoal filtered cigarette products. Review of the scientific literature is hindered due to the lack of documentation regarding the activity of the charcoal used in the filter, and the inconsistency in product designs used between the various different disciplines (chemistry, pre-clinical, clinical and epidemiology) that have conducted studies with charcoal filtered cigarettes. There do not appear to be any published studies using a combination of data from the different disciplines based on a consistently designed charcoal cigarette filter. Although the literature presently available would suggest that smoke filtration provided by current charcoal filter techniques alone may not be substantial enough to reduce smoking-related disease, the data are limited. Therefore, for the reduction of smoking-induced disease, it is difficult to come to a definitive conclusion regarding the potential health benefits of using charcoal as a smoke filtration technology. PMID:18289753

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

    Technology Transfer Automated Retrieval System (TEKTRAN)

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

  20. Soluble extracellular Klotho decreases sensitivity to cigarette smoke induced cell death in human lung epithelial cells.

    PubMed

    Blake, David J; Reese, Caitlyn M; Garcia, Mario; Dahlmann, Elizabeth A; Dean, Alexander

    2015-10-01

    Chronic obstructive pulmonary disease (COPD) is currently the third leading cause of death in the US and is associated with an abnormal inflammatory response to cigarette smoke (CS). Exposure to CS induces oxidative stress and can result in cellular senescence in the lung. Cellular senescence can then lead to decreased proliferation of epithelial cells, the destruction of alveolar structure and pulmonary emphysema. The anti-aging gene, klotho, encodes a membrane bound protein that has been shown to be a key regulator of oxidative stress and cellular senescence. In this study the role of Klotho (KL) with regard to oxidative stress and cellular senescence was investigated in human pulmonary epithelial cells exposed to cigarette smoke. Individual clones that stably overexpress Klotho were generated through retroviral transfection and geneticin selection. Klotho overexpression was confirmed through RT-qPCR, Western blotting and ELISA. Compared to control cells, constitutive Klotho overexpression resulted in decreased sensitivity to cigarette smoke induced cell death in vitro via a reduction of reactive oxygen species and a decrease in the expression of p21. Our results suggest that increasing Klotho level in pulmonary epithelial cells may be a promising strategy to reduce cellular senescence and mitigate the risk for the development of COPD.

  1. Nitrogen dioxide exposure attenuates cigarette smoke-induced cytokine production in mice.

    PubMed

    Brandsma, Corry-Anke; Hylkema, Machteld N; Luinge, Marjan A; Geerlings, Marie; Klok, Pieter A; Cassee, Flemming R; Timens, Wim; Postma, Dirkje S; Kerstjens, Huib A M

    2008-01-01

    Cigarette smoke is the most important cause for the development of chronic obstructive pulmonary disease (COPD). Since only a minority of smokers and some nonsmokers develop COPD, other factors must be involved as well. NO2 is an important air pollutant associated with respiratory symptoms in humans and emphysema development in animal models. We hypothesized that combined exposure to NO2 and cigarette smoke will enhance pulmonary inflammation and emphysema development. Mice were exposed to 20 ppm NO2 for 17 h/day, to 24 puffs of cigarette smoke 2 times per day, to their combination, or to control air for 5 days/wk during 4 wk. Following the last NO2 exposure and within 24 h after the last smoke exposure the mice were sacrificed. Lungs were removed and analyzed for several inflammatory parameters and emphysema. Cigarette smoke exposure increased eosinophil numbers and levels of tumor necrosis factor (TNF)-alpha, KC, monocyte chemoattractant protein (MCP)-1, and interleukin (IL)-6. NO2 exposure increased goblet cells, eosinophils, and the levels of IL-6, while it decreased the levels of IL-10. Four weeks of NO2, cigarette smoke, or their combination was not sufficient to induce significant emphysema, nor did it lead to increased numbers of lymphocytes, neutrophils, or macrophages in lung tissue. Instead, NO2 exposure attenuated the smoke-induced increases in levels of TNF-alpha, KC, and MCP-1. These dampening effects of NO2 may be due to modulating effects of NO2 on cytokine production by macrophages and epithelial cells, which have been reported earlier. The next step is to translate these findings of combined, controlled exposure in animals to the human situation.

  2. Forsythiaside inhibits cigarette smoke-induced lung inflammation by activation of Nrf2 and inhibition of NF-κB.

    PubMed

    Cheng, Li; Li, Fan; Ma, Rui; Hu, Xianping

    2015-09-01

    Cigarette smoke has been reported to be the major cause of chronic obstructive pulmonary disease (COPD). It causes persistent inflammation by regulating the redox-sensitive pathways. Forsythiaside, an active constituent isolated from the Chinese medicinal herb Forsythia suspensa, has been reported to have anti-inflammatory and anti-oxidant effects. Thus, in this study, we investigated the protective effects of forsythiaside against cigarette smoke-induced lung inflammation in mice. COPD mice model was established by cigarette smoke. Forsythiaside was given 2h before cigarette smoke exposure for five consecutive days. Bronchoalveolar lavage fluid and lung tissues were collected to assess pathological changes, lipid peroxidation, inflammatory cytokine production, Nrf-2, and NF-κB expression. Our results showed that forsythiaside attenuated the infiltration of inflammatory cells, NO and inflammatory cytokines TNF-α, IL-6 and IL-1β production, and reversed the CS-induced decrease of glutathione/glutathione disulfide (GSH/GSSG) ratio. Western blot analysis showed that forsythiaside inhibited cigarette smoke-induced NF-κB activation. In addition, forsythiaside dose-dependently up-regulated the expression of Nrf2 and HO-1. In conclusion, forsythiaside protected against cigarette smoke-induced lung injury through activating Nrf2 and inhibiting NF-κB signaling pathway.

  3. Cigarette smoking induces small airway epithelial epigenetic changes with corresponding modulation of gene expression.

    PubMed

    Buro-Auriemma, Lauren J; Salit, Jacqueline; Hackett, Neil R; Walters, Matthew S; Strulovici-Barel, Yael; Staudt, Michelle R; Fuller, Jennifer; Mahmoud, Mai; Stevenson, Christopher S; Hilton, Holly; Ho, Melisa W Y; Crystal, Ronald G

    2013-12-01

    The small airway epithelium (SAE), the first site of smoking-induced lung pathology, exhibits genome-wide changes in gene expression in response to cigarette smoking. Based on the increasing evidence that the epigenome can respond to external stimuli in a rapid manner, we assessed the SAE of smokers for genome-wide DNA methylation changes compared with nonsmokers, and whether changes in SAE DNA methylation were linked to the transcriptional output of these cells. Using genome-wide methylation analysis of SAE DNA of nonsmokers and smokers, the data identified 204 unique genes differentially methylated in SAE DNA of smokers compared with nonsmokers, with 67% of the regions with differential methylation occurring within 2 kb of the transcriptional start site. Among the genes with differential methylation were those related to metabolism, transcription, signal transduction and transport. For the differentially methylated genes, 35 exhibited a correlation with gene expression, 54% with an inverse correlation of DNA methylation with gene expression and 46% a direct correlation. These observations provide evidence that cigarette smoking alters the DNA methylation patterning of the SAE and that, for some genes, these changes are associated with the smoking-related changes in gene expression.

  4. An animal model of cigarette smoke-induced in utero growth retardation

    PubMed Central

    Esposito, Emily R.; Horn, Kristin H.; Greene, Robert M.; Pisano, M. Michele

    2009-01-01

    Maternal/fetal genetic constitution and environmental factors are vital to delivery of a healthy baby. In the United States (US), a low birth weight (LBW) baby is born every minute and a half. LBW, defined as weighing less than 5.5 lbs at birth, affects nearly 1 in 12 infants born in the US with resultant costs for the nation of more than 15 billion dollars annually. Infant birth weight is the single most important factor affecting neonatal mortality. Various environmental and genetic risk factors for LBW have been identified. Several risks are preventable, such as cigarette smoking during pregnancy. Over one million babies are exposed prenatally to cigarette smoke accounting for over 20% of the LBW incidence in the US. Cigarette smoke exposure in utero results in a variety of adverse developmental outcomes with intrauterine growth restriction and infant LBW being the most well documented. However, the mechanisms underlying the causes of LBW remain poorly understood. The purpose of this study was: (1) to establish an animal model of cigarette smoke-induced in utero growth retardation and LBW using physiologically relevant inhalation exposure conditions which simulate “active” and “passive” tobacco smoke exposures, and (2) to determine whether particular stages of development are more susceptible than others to the adverse effects of in utero smoke exposure on embryo/fetal growth. Pregnant C57BL/6J mice were exposed to cigarette smoke during three periods of gestation: pre-/peri-implantation (gestational days [gds] 1−5), post-implantation (gds 6−18), and throughout gestation (gds 1−17). Reproductive and fetal outcomes were assessed on gd 18.5. Exposure of dams to mainstream/sidestream cigarette smoke, simulating “active” maternal smoking, resulted in decreases in fetal weight and crown–rump length when exposed throughout gestation (gds 1−17). Similar results were seen when dams were exposed only during the first 5 days of gestation (pre

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

    PubMed

    Ni, Leng; Wang, Zhanqi; Yang, Genhuan; Li, Tianjia; Liu, Xinnong; Liu, Changwei

    2016-03-14

    Cigarette smoke is not only a profound independent risk factor of atherosclerosis, but also aggravates restenosis after vascular angioplasty. Heme oxygenase-1 (HO-1) is an endogenous antioxidant and cytoprotective enzyme. In this study, we investigated whether HO-1 upregulating by hemin, a potent HO-1 inducer, can protect against cigarette smoke-induced restenosis in rat's carotid arteries after balloon injury. Results showed that cigarette smoke exposure aggravated stenosis of the lumen, promoted infiltration of inflammatory cells, and induced expression of inflammatory cytokines and adhesion molecules after balloon-induced carotid artery injury. HO-1 upregulating by hemin treatment reduced these effects of cigarette smoke, whereas the beneficial effects were abolished in the presence of Zincprotoporphyrin IX, an HO-1 inhibitor. To conclude, hemin has potential therapeutic applications in the restenosis prevention after the smokers' vascular angioplasty.

  6. Protective effect of melatonin on cigarette smoke-induced restenosis in rat carotid arteries after balloon injury.

    PubMed

    Yang, Gen-Huan; Li, Yan-Chuan; Wang, Zhan-Qi; Liu, Bao; Ye, Wei; Ni, Leng; Zeng, Rong; Miao, Shi-Ying; Wang, Lin-Fang; Liu, Chang-Wei

    2014-11-01

    Vascular restenosis after the interventional angioplasty remains the main obstacle to a favorable long-term patency. Many researches suggest cigarette smoking is one of the most important causes of restenosis. This study was designed to investigate whether melatonin could protect against the cigarette smoke-induced restenosis in rat carotid arteries after balloon injury. Three groups of male rats (normal condition, cigarette smoke exposed, cigarette smoke exposed, and melatonin injected) were used in this study. An established balloon-induced carotid artery injury was performed, and the carotid arteries were harvested from these three groups 14 days later. The ratio of intima to media, the infiltration of inflammatory cells, the expression of inflammatory cytokines (NF-κB, IL-1β, IL-6, TNF-α, MCP-1), adhesion molecules (ICAM-1, VCAM-1), and eNOS were measured. The results showed that cigarette smoke exposure aggravated the stenosis of the lumen, promoted the infiltration of inflammatory cells and induced the expression of the inflammatory cytokines and adhesion molecules after the balloon-induced carotid artery injury. Moreover, cigarette smoke exposure can inhibit the expression of eNOS. Particularly, we surprised that melatonin could minimize this effect caused by cigarette smoke. These results suggested that melatonin could prevent the cigarette smoke-induced restenosis in rat carotid arteries after balloon injury and the mechanism of its protective effect may be the inhibition of the inflammatory reaction. This also implies melatonin has the potential therapeutic applicability in prevention of restenosis after the vascular angioplasty in smokers.

  7. Mitochondrial E3 Ubiquitin Protein Ligase 1 Mediates Cigarette Smoke-Induced Endothelial Cell Death and Dysfunction.

    PubMed

    Kim, Sun-Yong; Kim, Hyo Jeong; Park, Mi Kyeong; Huh, Jin Won; Park, Hye Yun; Ha, Sang Yun; Shin, Joo-Ho; Lee, Yun-Song

    2016-02-01

    By virtue of the critical roles of Akt in vascular endothelial cell (EC) survival and function, cigarette smoke-induced Akt reduction may contribute to EC death and dysfunction in smokers' lungs. One of the negative Akt regulatory mechanisms is K48-linked Akt ubiquitination and subsequent proteasomal degradation. Here, we assessed the involvement of mitochondrial E3 ubiquitin protein ligase 1 (MUL1), recently revealed as a novel Akt ubiquitin E3 ligase, in cigarette smoke-induced Akt ubiquitination and its contribution to pulmonary EC death and dysfunction. In human lung microvascular ECs (HLMVECs), cigarette smoke extract (CSE) noticeably elevated MUL1 expression and K48-linked Akt ubiquitination, whereas Akt, p-Akt, eNOS, and p-eNOS levels were decreased. MUL1 knockdown suppressed CSE-induced Akt ubiquitination/degradation and cytoplasmic reductions of Akt and p-Akt. Furthermore, MUL1 knockdown attenuated reductions of eNOS and p-eNOS and alleviated EC survival, migration, and tube formation in the presence of CSE exposure. In addition, overexpression of K284R Akt, a mutant for a MUL1-ubiquitination site, produced similar effects. In HLMVECs exposed to CSE, Akt-MUL1 interaction was increased in coimmunoprecipitation and in situ proximity ligation assays. Similarly, the proximity ligation assay signals were elevated in rat lungs exposed to cigarette smoke for 3 months, during which Mul1 levels were noticeably increased. Finally, we found that CSE-mediated MUL1 induction in HLMVECs is mediated by retinoic acid receptor-related orphan receptor α. Taken together, these data suggest that cigarette smoke-induced MUL1 elevation mediates Akt ubiquitination/degradation, potentially leading to pulmonary EC death and functional impairment.

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

    PubMed

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

    2015-12-01

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

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

    PubMed

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

    2015-10-01

    Matrix metalloproteinases (MMPs) are the main proteolytic enzymes involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). A radiolabeled MMP inhibitor, [(18)F]FB-ML5, was prepared, and its in vivo kinetics were tested in a mouse model of pulmonary inflammation. BALB/c mice were exposed for 4 days to cigarette smoke (CS) or air. On the fifth day, a dynamic microPET scan was made with [(18)F]FB-ML5. Standardized uptake values (PET-SUVmean) were 0.19 ± 0.06 in the lungs of CS-exposed mice (n = 6) compared to 0.11 ± 0.03 (n = 5) in air-exposed controls (p < 0.05), 90 min post-injection MMP-9 levels in bronchoalveolar lavage fluid (BALF) were increased from undetectable level to 4615 ± 1963 pg/ml by CS exposure. Increased MMP expression in a COPD mouse model was shown to lead to increased retention of [(18)F]FB-ML5.

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

    PubMed

    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.

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

    PubMed

    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

  12. Role of Cigarette Smoke-Induced Aggresome Formation in Chronic Obstructive Pulmonary Disease-Emphysema Pathogenesis.

    PubMed

    Tran, Ian; Ji, Changhoon; Ni, Inzer; Min, Taehong; Tang, Danni; Vij, Neeraj

    2015-08-01

    Cigarette smoke (CS) exposure is known to induce proteostasis imbalance that can initiate accumulation of ubiquitinated proteins. Therefore, the primary goal of this study was to determine if first- and secondhand CS induces localization of ubiquitinated proteins in perinuclear spaces as aggresome bodies. Furthermore, we sought to determine the mechanism by which smoke-induced aggresome formation contributes to chronic obstructive pulmonary disease (COPD)-emphysema pathogenesis. Hence, Beas2b cells were treated with CS extract (CSE) for in vitro experimental analysis of CS-induced aggresome formation by immunoblotting, microscopy, and reporter assays, whereas chronic CS-exposed murine model and human COPD-emphysema lung tissues were used for validation. In preliminary analysis, we observed a significant (P < 0.01) increase in ubiquitinated protein aggregation in the insoluble protein fraction of CSE-treated Beas2b cells. We verified that CS-induced ubiquitin aggregrates are localized in the perinuclear spaces as aggresome bodies. These CS-induced aggresomes (P < 0.001) colocalize with autophagy protein microtubule-associated protein 1 light chain-3B(+) autophagy bodies, whereas U.S. Food and Drug Administration-approved autophagy-inducing drug (carbamazepine) significantly (P < 0.01) decreases their colocalization and expression, suggesting CS-impaired autophagy. Moreover, CSE treatment significantly increases valosin-containing protein-p62 protein-protein interaction (P < 0.0005) and p62 expression (aberrant autophagy marker; P < 0.0001), verifying CS-impaired autophagy as an aggresome formation mechanism. We also found that inhibiting protein synthesis by cycloheximide does not deplete CS-induced ubiquitinated protein aggregates, suggesting the role of CS-induced protein synthesis in aggresome formation. Next, we used an emphysema murine model to verify that chronic CS significantly (P < 0.0005) induces aggresome formation. Moreover, we

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

    PubMed

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

    2015-12-01

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

  14. Cigarette smoke-induced cell death of a spermatocyte cell line can be prevented by inactivating the Aryl hydrocarbon receptor.

    PubMed

    Esakky, P; Hansen, D A; Drury, A M; Cusumano, A; Moley, K H

    2015-01-01

    Cigarette smoke exposure causes germ cell death during spermatogenesis. Our earlier studies demonstrated that cigarette smoke condensate (CSC) causes spermatocyte cell death in vivo and growth arrest of the mouse spermatocyte cell line (GC-2spd(ts)) in vitro via the aryl hydrocarbon receptor (AHR). We hypothesize here that inactivation of AHR could prevent the CSC-induced cell death in spermatocytes. We demonstrate that CSC exposure generates oxidative stress, which differentially regulates mitochondrial apoptosis in GC-2spd(ts) and wild type (WT) and AHR knockout (AHR-KO) mouse embryonic fibroblasts (MEFs). SiRNA-mediated silencing of Ahr augments the extent of CSC-mediated cellular damage while complementing the AHR-knockout condition. Pharmacological inhibition using the AHR-antagonist (CH223191) modulates the CSC-altered expression of apoptotic proteins and significantly abrogates DNA fragmentation though the cleavage of PARP appears AHR independent. Pretreatment with CH223191 at concentrations above 50 μM significantly prevents the CSC-induced activation of caspase-3/7 and externalization of phosphatidylserine in the plasma membrane. However, MAPK inhibitors alone or together with CH223191 could not prevent the membrane damage upon CSC addition and the caspase-3/7 activation and membrane damage in AHR-deficient MEF indicates the interplay of multiple cell signaling and cytoprotective ability of AHR. Thus the data obtained on one hand signifies the protective role of AHR in maintaining normal cellular homeostasis and the other, could be a potential prophylactic therapeutic target to promote cell survival and growth under cigarette smoke exposed environment by receptor antagonism via CH223191-like mechanism. Antagonist-mediated inactivation of the aryl hydrocarbon receptor blocks downstream events leading to cigarette smoke-induced cell death of a spermatocyte cell line. PMID:27551479

  15. Cigarette smoke-induced cell death of a spermatocyte cell line can be prevented by inactivating the Aryl hydrocarbon receptor

    PubMed Central

    Esakky, P; Hansen, D A; Drury, A M; Cusumano, A; Moley, K H

    2015-01-01

    Cigarette smoke exposure causes germ cell death during spermatogenesis. Our earlier studies demonstrated that cigarette smoke condensate (CSC) causes spermatocyte cell death in vivo and growth arrest of the mouse spermatocyte cell line (GC-2spd(ts)) in vitro via the aryl hydrocarbon receptor (AHR). We hypothesize here that inactivation of AHR could prevent the CSC-induced cell death in spermatocytes. We demonstrate that CSC exposure generates oxidative stress, which differentially regulates mitochondrial apoptosis in GC-2spd(ts) and wild type (WT) and AHR knockout (AHR-KO) mouse embryonic fibroblasts (MEFs). SiRNA-mediated silencing of Ahr augments the extent of CSC-mediated cellular damage while complementing the AHR-knockout condition. Pharmacological inhibition using the AHR-antagonist (CH223191) modulates the CSC-altered expression of apoptotic proteins and significantly abrogates DNA fragmentation though the cleavage of PARP appears AHR independent. Pretreatment with CH223191 at concentrations above 50 μM significantly prevents the CSC-induced activation of caspase-3/7 and externalization of phosphatidylserine in the plasma membrane. However, MAPK inhibitors alone or together with CH223191 could not prevent the membrane damage upon CSC addition and the caspase-3/7 activation and membrane damage in AHR-deficient MEF indicates the interplay of multiple cell signaling and cytoprotective ability of AHR. Thus the data obtained on one hand signifies the protective role of AHR in maintaining normal cellular homeostasis and the other, could be a potential prophylactic therapeutic target to promote cell survival and growth under cigarette smoke exposed environment by receptor antagonism via CH223191-like mechanism. Antagonist-mediated inactivation of the aryl hydrocarbon receptor blocks downstream events leading to cigarette smoke-induced cell death of a spermatocyte cell line. PMID:27551479

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

    PubMed

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

    2016-01-01

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

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

    PubMed

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

    2016-01-01

    Age-related macular degeneration (AMD) is a medical condition usually affecting older adults and resulting in a loss of vision in the macula, the center of the visual field. The dry form of this disease presents with atrophy of the retinal pigment epithelium, resulting in the detachment of the retina and loss of photoreceptors. Cigarette smoke is one main risk factor for dry AMD and increases the risk of developing the disease by three times. In order to understand the influence of cigarette smoke on retinal pigment epithelial cells, cultured human ARPE-19 cells were treated with cigarette smoke extract for 24 h. Using quantitative mass spectrometry more than 3000 proteins were identified and their respective abundances were compared between cigarette smoke-treated and untreated cells. Altogether 1932 proteins were quantified with at least two unique peptides, with 686 proteins found to be significantly differentially abundant with p > 0.05. Of these proteins the abundance of 64 proteins was at least 2-fold down-regulated after cigarette smoke treatment while 120 proteins were 2-fold up-regulated. The analysis of associated biological processes revealed an alteration of proteins involved in RNA processing and transport as well as extracellular matrix remodelling in response to cigarette smoke treatment. PMID:26427490

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

    PubMed

    Anbarasi, Kothandapani; Vani, Ganapathy; Devi, Chennam Srinivasulu Shyamala

    2005-01-01

    Chronic exposure to cigarette smoke affects the structure and function of mitochondria, which may account for the pathogenesis of smoking-related diseases. Bacopa monniera Linn., used in traditional Indian medicine for various neurological disorders, was shown to possess mitrochondrial membrane-stabilizing properties in the rat brain during exposure to morphine. We investigated the protective effect of bacoside A, the active principle of Bacopa monniera, against mitochondrial dysfunction in rat brain induced by cigarette smoke. Male Wistar albino rats were exposed to cigarette smoke and administered bacoside A for a period of 12 weeks. The mitochondrial damage in the brain was assessed by examining the levels of lipid peroxides, cholesterol, phospholipid, cholesterol/phospholipid (C/P) ratio, and the activities of isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, NADH dehydrogenase, and cytochrome C oxidase. The oxidative phosphorylation (rate of succinate oxidation, respiratory control ratio and ADP/O ratio, and the levels of ATP) was evaluated for the assessment of mitochondrial functional capacity. We found significantly elevated levels of lipid peroxides, cholesterol, and C/P ratio, and decreased levels of phospholipids and mitochondrial enzymes in the rats exposed to cigarette smoke. Measurement of oxidative phosphorylation revealed a marked depletion in all the variables studied. Administration of bacoside A prevented the structural and functional impairment of mitochondria upon exposure to cigarette smoke. From the results, we suggest that chronic cigarette smoke exposure induces damage to the mitochondria and that bacoside A protects the brain from this damage by maintaining the structural and functional integrity of the mitochondrial membrane.

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

    PubMed

    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

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

    PubMed

    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.

  1. Cigarette smoke-induced DNA adducts in the respiratory and nonrespiratory tissues of rats

    SciTech Connect

    Gairola, C.G.; Gupta, R.C. )

    1991-01-01

    Formation of DNA adducts is regarded as an essential initial step in the process of chemical carcinogenesis. To determine how chronic exposure to cigarette smoke affects the distribution of DNA adducts in selected respiratory and nonrespiratory tissues. The authors exposed male Sprague-Dawley rats daily to fresh mainstream smoke from the Univ. of Kentucky reference cigarettes (2R1) in a nose-only exposure system for 32 weeks. Blood carboxyhemoglobin, total particulate matter (TPM) intake, and pulmonary aryl hydrocarbon hydroxylase values indicated effective exposure of animals to cigarette smoke. DNA was extracted from three respiratory (larynx, trachea, and lung) and three nonrespiratory (liver, heart, and bladder) tissues and analyzed for DNA adducts by the {sup 32}P-postlabeling assay under conditions capable of detecting low levels of diverse aromatic/hydrophobic adducts. Data showed that the total DNA adducts in the lung, heart, and trachea, and larynx were increased by 10- to 20-fold in the smoke-exposed group. These data suggest selective formation of DNA adducts in the tissues.

  2. Glutathione Depletion Accelerates Cigarette Smoke-Induced Inflammation and Airspace Enlargement

    PubMed Central

    Gould, Neal S.; Min, Elysia; Huang, Jie; Chu, Hong Wei; Good, Jim; Martin, Richard J.; Day, Brian J.

    2015-01-01

    The study objective was to assess age-related changes in glutathione (GSH) adaptive response to cigarette smoke (CS) exposure. Older cigarette smokers show a decline (67%) in lung epithelial lining fluid (ELF) GSH and a 1.8-fold decreased GSH adaptive response to cigarette smoking with a concomitant elevation (47%) of exhaled nitric oxide compared with younger smokers. In order to isolate the changes in tissue GSH from other age-related effects, pharmacological inhibition of the rate limiting step in GSH synthesis was employed to examine the lung’s response to CS exposure in young mice. The γ-glutamylcysteine ligase inhibitor l-buthionine–sulfoximine (BSO) was administered in the drinking water (20 mM) to decrease by half the in vivo GSH levels to those found in aged mice and humans. Mice were then exposed to CS (3 h/day) for 5 or 15 days. Biochemical analysis of the ELF and lung tissue revealed an inhibition of the CS-induced GSH adaptive response by BSO with a concurrent increase in mixed protein–GSH disulfides indicating increased cysteine oxidation. The prevention of the GSH adaptive response led to an increase in pro-inflammatory cytokines present in the lung. Airspace enlargement is a hallmark of lung emphysema and was observed in mice treated with BSO and exposed to CS for as little as 15 days, whereas these types of changes normally take up to 6 months in this model. BSO treatment potentiated both lung elastase and matrix metalloproteinase activity in the CS group. These data suggest that age-related decline in the GSH adaptive response can markedly accelerate many of the factors thought to drive CS-induced emphysema. PMID:26149495

  3. Cadmium-enriched cigarette smoke-induced cytological and biochemical alterations in rat lungs

    SciTech Connect

    Gairola, C.G. )

    1989-01-01

    Male Sprague-Dawley rats were exposed daily for 52 wk in a nose-only exposure system to smoke from the University of Kentucky 2R1 reference cigarettes (SM) or from cigarettes made of cadmium-enriched tobacco (Cd-SM). At sacrifice, the animals were evaluated by bronchoalveolar lavage (BAL) for inflammatory cell response in the lungs, and the cells so obtained were analyzed for phagocytosis of particles (latex and IgG-coated SRBCs) and for their ability to release oxidants upon phagocytic challenge. Additionally, lung tissues were analyzed for Cd levels and lung homogenate fractions were assayed for aryl hydrocarbon hydroxylase (AHH) as well as total and selenium-dependent glutathione peroxidase (GSH-Px) activities. BAL cell counts showed a significant influx of inflammatory cells into the lungs of the Cd-SM group but not the SM group. The proportion of neutrophils in the BAL cells of the Cd-Sm group was elevated to 40 {plus minus} 9%, compared with less than 2% in the SM group. Phagocytosis of both types of particles by macrophages from SM and Cd-SM groups was similar to that of the control groups, except that a greater uptake of latex particles was seen is Cd-SM macrophages. The release of oxidants (superoxides and hydrogen peroxide) by the BAL cells was severely impaired in the Cd-SM group, whereas a slight stimulation was seen in the SM gropu. Pulmonary GSH-Px activity was the same in all groups. A significant induction of the pulmonary AHH activity was observed in the SM group only. The Cd levels in the lungs were approximately 8- and 200-fold greater than controls in SM and Cd-SM groups, respectively. These observation suggest a significant influence of tabacco Cd on the toxicity of cigarette smoke.

  4. Cigarette smoke-induced morphological transformation of Bhas 42 cells in vitro.

    PubMed

    Weisensee, Dirk; Poth, Albrecht; Roemer, Ewald; Conroy, Lynda L; Schlage, Walter K

    2013-05-01

    In vitro cell transformation assays detect transformed cells that have acquired the distinct characteristics of malignant cells and thus model one stage of in vivo carcinogenesis. These assays have been proposed as surrogate models for predicting the non-genotoxic carcinogenic potential of chemicals. The Bhas 42 cell transformation assay, a short-term assay that uses v-Ha-ras-transfected Balb/c 3T3 cells, can detect the tumour promoter-like activities of chemicals, but has not previously been used with cigarette smoke. The particulate phase of cigarette smoke (total particulate matter [TPM]) is known to induce tumours in vivo in the mouse skin painting assay. Therefore, we investigated the ability of this Bhas cell assay to form morphologically transformed foci in vitro when repeatedly challenged with TPM from a standard research cigarette. TPM induced a dose-dependent increase in Type III foci, and a significant increase (up to 20-fold) in focus formation at moderately toxic concentrations between 5 and 60µg TPM/ml, with a peak at 20µg/ml. Three batches of TPM were tested in three independent experiments. Precision (repeatability and reproducibility) was calculated by using 0, 5, 10, and 20µg TPM/ml. Repeatability and reproducibility, expressed as the relative standard deviation obtained from the normalised slopes of the dose-response curves, were 17.2% and 19.6%, respectively; the slopes were 0.7402 ± 0.1247, 0.9347 ± 0.1316, and 0.8772 ± 0.1767 (increase factor∗ml/mg TPM; mean ± SD) ; and the goodness of fit (r2) of the mean slopes, each derived from n = 6 repeats, was 0.9449, 0.8198, and 0.8344, respectively. This in vitro assay with Bhas 42 cells, which are regarded as already initiated in the two-stage paradigm of carcinogenesis (initiation and promotion), is able to detect cell transformation induced by cigarette smoke in a dose-dependent manner with a high sensitivity and good precision. Because this assay is fast and yields reliable results, it

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

    PubMed Central

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

    2016-01-01

    Reactive oxygen species (ROS) are important in the pathogenesis of pulmonary injury induced by cigarette smoke (CS) exposure, and physical exercise (Ex) is useful in combating impaired oxidative process. We verified the preventive effects of Ex on lung oxidative markers induced by smoking. In this study, 36 mice (C57BL-6, 30–35 g) were split into four groups: control, CS, Ex, and CS plus Ex. Ex groups were given prior physical training in water (2×30 min/d, 5 days/wk, 8 weeks). After training, the CS groups were subjected to passive exposure to four cigarettes, 3 × per day, for 60 consecutive days. After 24 hours from the last exposure, CS animals were sacrificed, and lung samples were collected for further analysis. Left lung sample was prepared for histological analysis, and right lung was used for biochemical analysis (superoxide, hydroxyproline, lipid peroxidation [thiobarbituric acid reactive species], protein carbonylation [carbonyl groups formation], superoxide dismutase [SOD], catalase [CAT], and glutathione peroxidase [GPx] activities). Group comparisons were evaluated by analysis of variance (ANOVA). Results were expressed as mean ± standard deviation, with P<0.05 considered significantly different. Preventive Ex impeded histological changes and increased the enzymatic defense system (SOD and GPx) by reducing oxidative damage in lipids and proteins. This preventive effect of prior physical Ex alleviates damage caused by CS exposure. PMID:27042047

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

    PubMed

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

    2016-01-01

    Reactive oxygen species (ROS) are important in the pathogenesis of pulmonary injury induced by cigarette smoke (CS) exposure, and physical exercise (Ex) is useful in combating impaired oxidative process. We verified the preventive effects of Ex on lung oxidative markers induced by smoking. In this study, 36 mice (C57BL-6, 30-35 g) were split into four groups: control, CS, Ex, and CS plus Ex. Ex groups were given prior physical training in water (2×30 min/d, 5 days/wk, 8 weeks). After training, the CS groups were subjected to passive exposure to four cigarettes, 3 × per day, for 60 consecutive days. After 24 hours from the last exposure, CS animals were sacrificed, and lung samples were collected for further analysis. Left lung sample was prepared for histological analysis, and right lung was used for biochemical analysis (superoxide, hydroxyproline, lipid peroxidation [thiobarbituric acid reactive species], protein carbonylation [carbonyl groups formation], superoxide dismutase [SOD], catalase [CAT], and glutathione peroxidase [GPx] activities). Group comparisons were evaluated by analysis of variance (ANOVA). Results were expressed as mean ± standard deviation, with P<0.05 considered significantly different. Preventive Ex impeded histological changes and increased the enzymatic defense system (SOD and GPx) by reducing oxidative damage in lipids and proteins. This preventive effect of prior physical Ex alleviates damage caused by CS exposure. PMID:27042047

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

    PubMed

    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

  8. Restoring cigarette smoke-induced impairment of efferocytosis in alveolar macrophages.

    PubMed

    Subramaniam, R; Mukherjee, S; Chen, H; Keshava, S; Neuenschwander, P; Shams, H

    2016-07-01

    Cigarette smoke has been associated with susceptibility to different pulmonary and airway diseases. Impaired alveolar macrophages (AMs) that are major phagocytes in the lung have been associated with patients with airway diseases and active smokers. In the current report, we show that exposure to second-hand cigarette smoke (SHS) significantly reduced efferocytosis in vivo. More importantly, delivery of recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF) to the alveolar space restored and refurbished the efferocytosis capability of AMs. Exposure to SHS significantly reduced expression of CD16/32 on AMs, and treatment with GM-CSF not only restored but also significantly increased the expression of CD16/32 on AMs. GM-CSF treatment increased uptake and digestion/removal of apoptotic cells by AMs. The latter was attributed to increased expression of Rab5 and Rab7. Increased efferocytosis of AMs was also tested in a disease condition. AMs from GM-CSF-treated, influenza-infected, SHS-exposed mice showed significantly better efferocytosis activity, and mice had significantly less morbidity compared with phosphate-buffered saline-treated group. GM-CSF-treated mice had increased amphiregulin levels in the lungs, which in addition to efferocytosis of AMs may have attributed to their protection against influenza. These results will have great implications for developing therapeutic approaches by harnessing mucosal innate immunity to treat lung and airway diseases and protect against pneumonia. PMID:26577570

  9. Mitochondrial iron chelation ameliorates cigarette-smoke induced bronchitis and emphysema in mice

    PubMed Central

    Cloonan, Suzanne M.; Glass, Kimberly; Laucho-Contreras, Maria E.; Bhashyam, Abhiram R.; Cervo, Morgan; Pabón, Maria A.; Konrad, Csaba; Polverino, Francesca; Siempos, Ilias I.; Perez, Elizabeth; Mizumura, Kenji; Ghosh, Manik C.; Parameswaran, Harikrishnan; Williams, Niamh C.; Rooney, Kristen T.; Chen, Zhi-Hua; Goldklang, Monica P.; Yuan, Guo-Cheng; Moore, Stephen C.; Demeo, Dawn L.; Rouault, Tracey A.; D’Armiento, Jeanine M.; Schon, Eric A.; Manfredi, Giovanni; Quackenbush, John; Mahmood, Ashfaq; Silverman, Edwin K.; Owen, Caroline A.; Choi, Augustine M.K.

    2015-01-01

    Chronic obstructive pulmonary disease (COPD) is linked to both cigarette smoking and genetic determinants. We have previously identified iron-responsive element binding protein 2 (IRP2) as an important COPD susceptibility gene, with IRP2 protein increased in the lungs of individuals with COPD. Here we demonstrate that mice deficient in Irp2 were protected from cigarette smoke (CS)-induced experimental COPD. By integrating RIP-Seq, RNA-Seq, gene expression and functional enrichment clustering analysis, we identified IRP2 as a regulator of mitochondrial function in the lung. IRP2 increased mitochondrial iron loading and cytochrome c oxidase (COX), which led to mitochondrial dysfunction and subsequent experimental COPD. Frataxin-deficient mice with higher mitochondrial iron loading had impaired airway mucociliary clearance (MCC) and higher pulmonary inflammation at baseline, whereas synthesis of cytochrome c oxidase (Sco2)-deficient mice with reduced COX were protected from CS-induced pulmonary inflammation and impairment of MCC. Mice treated with a mitochondrial iron chelator or mice fed a low-iron diet were protected from CS-induced COPD. Mitochondrial iron chelation also alleviated CS-impairment of MCC, CS-induced pulmonary inflammation and CS-associated lung injury in mice with established COPD, suggesting a critical functional role and potential therapeutic intervention for the mitochondrial-iron axis in COPD. PMID:26752519

  10. Mitochondrial iron chelation ameliorates cigarette smoke-induced bronchitis and emphysema in mice.

    PubMed

    Cloonan, Suzanne M; Glass, Kimberly; Laucho-Contreras, Maria E; Bhashyam, Abhiram R; Cervo, Morgan; Pabón, Maria A; Konrad, Csaba; Polverino, Francesca; Siempos, Ilias I; Perez, Elizabeth; Mizumura, Kenji; Ghosh, Manik C; Parameswaran, Harikrishnan; Williams, Niamh C; Rooney, Kristen T; Chen, Zhi-Hua; Goldklang, Monica P; Yuan, Guo-Cheng; Moore, Stephen C; Demeo, Dawn L; Rouault, Tracey A; D'Armiento, Jeanine M; Schon, Eric A; Manfredi, Giovanni; Quackenbush, John; Mahmood, Ashfaq; Silverman, Edwin K; Owen, Caroline A; Choi, Augustine M K

    2016-02-01

    Chronic obstructive pulmonary disease (COPD) is linked to both cigarette smoking and genetic determinants. We have previously identified iron-responsive element-binding protein 2 (IRP2) as an important COPD susceptibility gene and have shown that IRP2 protein is increased in the lungs of individuals with COPD. Here we demonstrate that mice deficient in Irp2 were protected from cigarette smoke (CS)-induced experimental COPD. By integrating RNA immunoprecipitation followed by sequencing (RIP-seq), RNA sequencing (RNA-seq), and gene expression and functional enrichment clustering analysis, we identified Irp2 as a regulator of mitochondrial function in the lungs of mice. Irp2 increased mitochondrial iron loading and levels of cytochrome c oxidase (COX), which led to mitochondrial dysfunction and subsequent experimental COPD. Frataxin-deficient mice, which had higher mitochondrial iron loading, showed impaired airway mucociliary clearance (MCC) and higher pulmonary inflammation at baseline, whereas mice deficient in the synthesis of cytochrome c oxidase, which have reduced COX, were protected from CS-induced pulmonary inflammation and impairment of MCC. Mice treated with a mitochondrial iron chelator or mice fed a low-iron diet were protected from CS-induced COPD. Mitochondrial iron chelation also alleviated CS-induced impairment of MCC, CS-induced pulmonary inflammation and CS-associated lung injury in mice with established COPD, suggesting a critical functional role and potential therapeutic intervention for the mitochondrial-iron axis in COPD.

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

    PubMed Central

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

    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

  12. Mitochondrial iron chelation ameliorates cigarette smoke-induced bronchitis and emphysema in mice.

    PubMed

    Cloonan, Suzanne M; Glass, Kimberly; Laucho-Contreras, Maria E; Bhashyam, Abhiram R; Cervo, Morgan; Pabón, Maria A; Konrad, Csaba; Polverino, Francesca; Siempos, Ilias I; Perez, Elizabeth; Mizumura, Kenji; Ghosh, Manik C; Parameswaran, Harikrishnan; Williams, Niamh C; Rooney, Kristen T; Chen, Zhi-Hua; Goldklang, Monica P; Yuan, Guo-Cheng; Moore, Stephen C; Demeo, Dawn L; Rouault, Tracey A; D'Armiento, Jeanine M; Schon, Eric A; Manfredi, Giovanni; Quackenbush, John; Mahmood, Ashfaq; Silverman, Edwin K; Owen, Caroline A; Choi, Augustine M K

    2016-02-01

    Chronic obstructive pulmonary disease (COPD) is linked to both cigarette smoking and genetic determinants. We have previously identified iron-responsive element-binding protein 2 (IRP2) as an important COPD susceptibility gene and have shown that IRP2 protein is increased in the lungs of individuals with COPD. Here we demonstrate that mice deficient in Irp2 were protected from cigarette smoke (CS)-induced experimental COPD. By integrating RNA immunoprecipitation followed by sequencing (RIP-seq), RNA sequencing (RNA-seq), and gene expression and functional enrichment clustering analysis, we identified Irp2 as a regulator of mitochondrial function in the lungs of mice. Irp2 increased mitochondrial iron loading and levels of cytochrome c oxidase (COX), which led to mitochondrial dysfunction and subsequent experimental COPD. Frataxin-deficient mice, which had higher mitochondrial iron loading, showed impaired airway mucociliary clearance (MCC) and higher pulmonary inflammation at baseline, whereas mice deficient in the synthesis of cytochrome c oxidase, which have reduced COX, were protected from CS-induced pulmonary inflammation and impairment of MCC. Mice treated with a mitochondrial iron chelator or mice fed a low-iron diet were protected from CS-induced COPD. Mitochondrial iron chelation also alleviated CS-induced impairment of MCC, CS-induced pulmonary inflammation and CS-associated lung injury in mice with established COPD, suggesting a critical functional role and potential therapeutic intervention for the mitochondrial-iron axis in COPD. PMID:26752519

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

    PubMed Central

    Mohamed, Mahaneem; Sulaiman, Siti Amrah; Jaafar, Hasnan; Sirajudeen, Kuttulebbai Nainamohamed Salam

    2011-01-01

    Cigarette smoke (CS) can cause testicular damage and we investigated the possible protective effect of honey against CS-induced testicular damage and oxidative stress in rats. CS exposure (8 min, 3 times daily) and honey supplementation (1.2 g/kg daily) were given for 13 weeks. Rats exposed to CS significantly had smaller seminiferous tubules diameter and epithelial height, lower Leydig cell count and increased percentage of tubules with germ cell loss. CS also produced increased lipid peroxidation (TBARS) and glutathione peroxidase (GPx) activity, as well as reduced total antioxidant status (TAS) and activities of superoxide dismutase (SOD) and catalase (CAT). However, supplementation of honey significantly reduced histological changes and TBARS level, increased TAS level, as well as significantly restored activities of GPx, SOD and CAT in rat testis. These findings may suggest that honey has a protective effect against damage and oxidative stress induced by CS in rat testis. PMID:22016605

  14. Decreased proteasomal function accelerates cigarette smoke-induced pulmonary emphysema in mice.

    PubMed

    Yamada, Yosuke; Tomaru, Utano; Ishizu, Akihiro; Ito, Tomoki; Kiuchi, Takayuki; Ono, Ayako; Miyajima, Syota; Nagai, Katsura; Higashi, Tsunehito; Matsuno, Yoshihiro; Dosaka-Akita, Hirotoshi; Nishimura, Masaharu; Miwa, Soichi; Kasahara, Masanori

    2015-06-01

    Chronic obstructive pulmonary disease (COPD) is a disease common in elderly people, characterized by progressive destruction of lung parenchyma and chronic inflammation of the airways. The pathogenesis of COPD remains unclear, but recent studies suggest that oxidative stress-induced apoptosis in alveolar cells contributes to emphysematous lung destruction. The proteasome is a multicatalytic enzyme complex that plays a critical role in proteostasis by rapidly destroying misfolded and modified proteins generated by oxidative and other stresses. Proteasome activity decreases with aging in many organs including lungs, and an age-related decline in proteasomal function has been implicated in various age-related pathologies. However, the role of the proteasome system in the pathogenesis of COPD has not been investigated. Recently, we have established a transgenic (Tg) mouse model with decreased proteasomal chymotrypsin-like activity, showing age-related phenotypes. Using this model, we demonstrate here that decreased proteasomal function accelerates cigarette smoke (CS)-induced pulmonary emphysema. CS-exposed Tg mice showed remarkable airspace enlargement and increased foci of inflammation compared with wild-type controls. Importantly, apoptotic cells were found in the alveolar walls of the affected lungs. Impaired proteasomal activity also enhanced apoptosis in cigarette smoke extract (CSE)-exposed fibroblastic cells derived from mice and humans in vitro. Notably, aggresome formation and prominent nuclear translocation of apoptosis-inducing factor were observed in CSE-exposed fibroblastic cells isolated from Tg mice. Collective evidence suggests that CS exposure and impaired proteasomal activity coordinately enhance apoptotic cell death in the alveolar walls that may be involved in the development and progression of emphysema in susceptible individuals such as the elderly.

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

    PubMed

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

    2016-02-15

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

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

    PubMed

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

    2016-02-15

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

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

    NASA Astrophysics Data System (ADS)

    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 < 0.01; arterioles, 8.5 ± 4.2 vs. 54.3 ± 21.6 leukocytes per mm^2, P < 0.01; aortas, 0.8 ± 0.4 vs. 12.4 ± 5.6 leukocytes per mm^2, P < 0.01; means ± SD of n = 7 animals, 15 min after CS exposure). No inhibitory effect was observed by pretreatment of the animals with the lipid-soluble antioxidants vitamin E or probucol. The protective effects of vitamin C on CS-induced leukocyte adhesion and aggregation were seen at vitamin C plasma levels (55.6 ± 22.2 μM, n = 7) that can easily be reached in humans by dietary means or supplementation, suggesting that vitamin C effectively contributes to protection from CS-associated cardiovascular and pulmonary diseases in humans.

  18. Nanoparticulate carbon black in cigarette smoke induces DNA cleavage and Th17-mediated emphysema.

    PubMed

    You, Ran; Lu, Wen; Shan, Ming; Berlin, Jacob M; Samuel, Errol Lg; Marcano, Daniela C; Sun, Zhengzong; Sikkema, William Ka; Yuan, Xiaoyi; Song, Lizhen; Hendrix, Amanda Y; Tour, James M; Corry, David B; Kheradmand, Farrah

    2015-10-05

    Chronic inhalation of cigarette smoke is the major cause of sterile inflammation and pulmonary emphysema. The effect of carbon black (CB), a universal constituent of smoke derived from the incomplete combustion of organic material, in smokers and non-smokers is less known. In this study, we show that insoluble nanoparticulate carbon black (nCB) accumulates in human myeloid dendritic cells (mDCs) from emphysematous lung and in CD11c(+) lung antigen presenting cells (APC) of mice exposed to smoke. Likewise, nCB intranasal administration induced emphysema in mouse lungs. Delivered by smoking or intranasally, nCB persisted indefinitely in mouse lung, activated lung APCs, and promoted T helper 17 cell differentiation through double-stranded DNA break (DSB) and ASC-mediated inflammasome assembly in phagocytes. Increasing the polarity or size of CB mitigated many adverse effects. Thus, nCB causes sterile inflammation, DSB, and emphysema and explains adverse health outcomes seen in smokers while implicating the dangers of nCB exposure in non-smokers.

  19. Cigarette smoke-induced mitochondrial fragmentation and dysfunction in human airway smooth muscle.

    PubMed

    Aravamudan, Bharathi; Kiel, Alexander; Freeman, Michelle; Delmotte, Philippe; Thompson, Michael; Vassallo, Robert; Sieck, Gary C; Pabelick, Christina M; Prakash, Y S

    2014-05-01

    The balance between mitochondrial fission and fusion is crucial for mitochondria to perform its normal cellular functions. We hypothesized that cigarette smoke (CS) disrupts this balance and enhances mitochondrial dysfunction in the airway. In nonasthmatic human airway smooth muscle (ASM) cells, CS extract (CSE) induced mitochondrial fragmentation and damages their networked morphology in a concentration-dependent fashion, via increased expression of mitochondrial fission protein dynamin-related protein 1 (Drp1) and decreased fusion protein mitofusin (Mfn) 2. CSE effects on Drp1 vs. Mfn2 and mitochondrial network morphology involved reactive oxygen species (ROS), activation of extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), protein kinase C (PKC) and proteasome pathways, as well as transcriptional regulation via factors such as NF-κB and nuclear erythroid 2-related factor 2. Inhibiting Drp1 prevented CSE effects on mitochondrial networks and ROS generation, whereas blocking Mfn2 had the opposite, detrimental effect. In ASM from asmatic patients, mitochondria exhibited substantial morphological defects at baseline and showed increased Drp1 but decreased Mfn2 expression, with exacerbating effects of CSE. Overall, these results highlight the importance of mitochondrial networks and their regulation in the context of cellular changes induced by insults such as inflammation (as in asthma) or CS. Altered mitochondrial fission/fusion proteins have a further potential to influence parameters such as ROS and cell proliferation and apoptosis relevant to airway diseases. PMID:24610934

  20. Angiotensin receptor blockade attenuates cigarette smoke-induced lung injury and rescues lung architecture in mice.

    PubMed

    Podowski, Megan; Calvi, Carla; Metzger, Shana; Misono, Kaori; Poonyagariyagorn, Hataya; Lopez-Mercado, Armando; Ku, Therese; Lauer, Thomas; McGrath-Morrow, Sharon; Berger, Alan; Cheadle, Christopher; Tuder, Rubin; Dietz, Harry C; Mitzner, Wayne; Wise, Robert; Neptune, Enid

    2012-01-01

    Chronic obstructive pulmonary disease (COPD) is a prevalent smoking-related disease for which no disease-altering therapies currently exist. As dysregulated TGF-β signaling associates with lung pathology in patients with COPD and in animal models of lung injury induced by chronic exposure to cigarette smoke (CS), we postulated that inhibiting TGF-β signaling would protect against CS-induced lung injury. We first confirmed that TGF-β signaling was induced in the lungs of mice chronically exposed to CS as well as in COPD patient samples. Importantly, key pathological features of smoking-associated lung disease in patients, e.g., alveolar injury with overt emphysema and airway epithelial hyperplasia with fibrosis, accompanied CS-induced alveolar cell apoptosis caused by enhanced TGF-β signaling in CS-exposed mice. Systemic administration of a TGF-β-specific neutralizing antibody normalized TGF-β signaling and alveolar cell death, conferring improved lung architecture and lung mechanics in CS-exposed mice. Use of losartan, an angiotensin receptor type 1 blocker used widely in the clinic and known to antagonize TGF-β signaling, also improved oxidative stress, inflammation, metalloprotease activation and elastin remodeling. These data support our hypothesis that inhibition of TGF-β signaling through angiotensin receptor blockade can attenuate CS-induced lung injury in an established murine model. More importantly, our findings provide a preclinical platform for the development of other TGF-β-targeted therapies for patients with COPD.

  1. Nanoparticulate carbon black in cigarette smoke induces DNA cleavage and Th17-mediated emphysema

    PubMed Central

    You, Ran; Lu, Wen; Shan, Ming; Berlin, Jacob M; Samuel, Errol LG; Marcano, Daniela C; Sun, Zhengzong; Sikkema, William KA; Yuan, Xiaoyi; Song, Lizhen; Hendrix, Amanda Y; Tour, James M; Corry, David B; Kheradmand, Farrah

    2015-01-01

    Chronic inhalation of cigarette smoke is the major cause of sterile inflammation and pulmonary emphysema. The effect of carbon black (CB), a universal constituent of smoke derived from the incomplete combustion of organic material, in smokers and non-smokers is less known. In this study, we show that insoluble nanoparticulate carbon black (nCB) accumulates in human myeloid dendritic cells (mDCs) from emphysematous lung and in CD11c+ lung antigen presenting cells (APC) of mice exposed to smoke. Likewise, nCB intranasal administration induced emphysema in mouse lungs. Delivered by smoking or intranasally, nCB persisted indefinitely in mouse lung, activated lung APCs, and promoted T helper 17 cell differentiation through double-stranded DNA break (DSB) and ASC-mediated inflammasome assembly in phagocytes. Increasing the polarity or size of CB mitigated many adverse effects. Thus, nCB causes sterile inflammation, DSB, and emphysema and explains adverse health outcomes seen in smokers while implicating the dangers of nCB exposure in non-smokers. DOI: http://dx.doi.org/10.7554/eLife.09623.001 PMID:26437452

  2. Cigarette smoke-induced oxidative stress in skeletal muscles of mice.

    PubMed

    Barreiro, Esther; del Puerto-Nevado, Laura; Puig-Vilanova, Ester; Pérez-Rial, Sandra; Sánchez, Francisco; Martínez-Galán, Lourdes; Rivera, Stephanie; Gea, Joaquim; González-Mangado, Nicolás; Peces-Barba, Germán

    2012-06-15

    Cigarette smoke (CS)-induced oxidative stress may cause muscle alterations in chronic conditions such as chronic obstructive pulmonary disease (COPD). We sought to explore in AKR/J mice exposed to CS for 6 months and in control animals, levels of protein oxidation, oxidized proteins (immunoblotting, proteomics) and antioxidant mechanisms in both respiratory and limb muscles, body weight modifications, systemic inflammation, and lung structure. Compared to control mice, CS-exposed animals exhibited a reduction in body weight gain at 3 months and thereafter, showed lung emphysema, and exhibited increased oxidative stress levels in their diaphragms and gastrocnemius at 6 months. Proteins involved in glycolysis, ATP production and distribution, carbon dioxide hydration, and muscle contraction were carbonylated in respiratory and limb muscles. Blood tumor necrosis factor (TNF)-alpha levels were significantly greater in CS-exposed mice than in control animals. In AKR/J mice, chronic exposure to CS induces lung emphysema concomitantly with greater oxidative modifications on muscle proteins in both respiratory and limb muscles, and systemic inflammation.

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

    PubMed

    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.

  4. TLR4 deficiency promotes autophagy during cigarette smoke-induced pulmonary emphysema.

    PubMed

    An, Chang Hyeok; Wang, Xiao Mei; Lam, Hilaire C; Ifedigbo, Emeka; Washko, George R; Ryter, Stefan W; Choi, Augustine M K

    2012-11-01

    Toll-like receptors (TLRs) exert important nonimmune functions in lung homeostasis. TLR4 deficiency promotes pulmonary emphysema. We examined the role of TLR4 in regulating cigarette smoke (CS)-induced autophagy, apoptosis, and emphysema. Lung tissue was obtained from chronic obstructive lung disease (COPD) patients. C3H/HeJ (Tlr4-mutated) mice and C57BL/10ScNJ (Tlr4-deficient) mice and their respective control strains were exposed to chronic CS or air. Human or mouse epithelial cells (wild-type, Tlr4-knockdown, and Tlr4-deficient) were exposed to CS-extract (CSE). Samples were analyzed for TLR4 expression, and for autophagic or apoptotic proteins by Western blot analysis or confocal imaging. Chronic obstructive lung disease lung tissues and human pulmonary epithelial cells exposed to CSE displayed increased TLR4 expression, and increased autophagic [microtubule-associated protein-1 light-chain-3B (LC3B)] and apoptotic (cleaved caspase-3) markers. Beas-2B cells transfected with TLR4 siRNA displayed increased expression of LC3B relative to control cells, basally and after exposure to CSE. The basal and CSE-inducible expression of LC3B and cleaved caspase-3 were elevated in pulmonary alveolar type II cells from Tlr4-deficient mice. Wild-type mice subjected to chronic CS-exposure displayed airspace enlargement;, however, the Tlr4-mutated or Tlr4-deficient mice exhibited a marked increase in airspace relative to wild-type mice after CS-exposure. The Tlr4-mutated or Tlr4-deficient mice showed higher levels of LC3B under basal conditions and after CS exposure. The expression of cleaved caspase-3 was markedly increased in Tlr4-deficient mice exposed to CS. We describe a protective regulatory function of TLR4 against emphysematous changes of the lung in response to CS.

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

    PubMed

    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

  6. Cigarette Smoke-Induced Placental Adrenomedullin Expression and Trophoblast Cell Invasion

    PubMed Central

    Kraus, Daniel M.; Feng, Liping; Heine, R. Phillips; Brown, Haywood L.; Caron, Kathleen M.; Murtha, Amy P.

    2014-01-01

    Smoking in pregnancy reduces preeclampsia risk, but the mechanism of this effect is unknown. Prior studies have demonstrated that women with preeclampsia have lower placental adrenomedullin (AM) expression, and cigarette smoke extract (CSE) treatment of placental trophoblast cells in culture increases AM cellular production. We hypothesized that CSE alters trophoblast invasion through an AM-mediated mechanism, and that placental AM expression is greater among smokers. HTR-8/SVneo trophoblast cells were incubated for 24 hours in Matrigel-invasion chambers with 6 treatment groups: nonstimulated (NS), AM, AM inhibitor (AM22-52), 1% CSE, AM + AM22-52, and 1% CSE + AM22-52. Cells that penetrated the lower surface of the chambers were quantified, invasion indices were calculated, and compared using a 1-way analysis of variance with Bonferroni corrections for multiple comparisons. Trophoblast cells treated with both AM and 1% CSE demonstrated increased cellular invasion compared to NS controls (1.5-fold [P < .01] and 1.45-fold [P < .01], respectively). Cotreatment with the AM inhibitor significantly attenuated the increased invasion seen with both AM and CSE alone. Next, the placental tissue was obtained from 11 smokers and 11 nonsmokers at term and processed for immunohistochemistry (IHC) and real-time quantitative polymerase chain reaction (PCR) for AM. Placentas from smokers demonstrated more intense AM staining and increased AM gene (ADM) expression compared to placentas from nonsmokers (P = .004 for IHC, P = .022 for PCR). The CSE increases trophoblast cell invasion through an AM-mediated process, and placental AM expression is increased among term smokers compared to nonsmokers. These findings provide evidence that the AM pathway may play a role in the protection from preeclampsia seen in smokers. PMID:23653390

  7. Attenuation of Cigarette Smoke-Induced Emphysema in Mice by Apolipoprotein A-1 Overexpression.

    PubMed

    Kim, Chorong; Lee, Ji-Min; Park, Sung-Woo; Kim, Ki-Sun; Lee, Myoung Won; Paik, Sanghyun; Jang, An Soo; Kim, Do Jin; Uh, Sootaek; Kim, Yonghoon; Park, Choon-Sik

    2016-01-01

    Chronic inflammation, oxidative stress, and proteolysis participate primarily in the pathogenesis of chronic obstructive pulmonary disease (COPD)/emphysema. COPD is a highly prevalent smoking-related disease for which no effective therapy exists to improve the disease course. Although apolipoprotein A-1 (ApoA1) has antiinflammatory and antioxidant properties as well as cholesterol efflux potential, its role in cigarette smoke (CS)-induced emphysema has not been determined. Therefore, we investigated whether human ApoA1 transgenic (TG) mice, with conditionally induced alveolar epithelium to overexpress ApoA1, are protected against the CS-induced lung inflammatory response and development of emphysema. In this study, ApoA1 levels were significantly decreased in the lungs of patients with COPD and in the lungs of mice exposed to CS. ApoA1 TG mice did not develop emphysema when chronically exposed to CS. Compared with the control TG mice, ApoA1 overexpression attenuated lung inflammation, oxidative stress, metalloprotease activation, and apoptosis in CS-exposed mouse lungs. To explore a plausible mechanism of antiapoptotic activity of ApoA1, alveolar epithelial cells (A549) were treated with CS extract (CSE). ApoA1 prevented CSE-induced translocation of Fas and downstream death-inducing signaling complex into lipid rafts, thereby inhibiting Fas-mediated apoptosis. Taken together, the data showed that ApoA1 overexpression attenuated CS-induced lung inflammation and emphysema in mice. Augmentation of ApoA1 in the lung may have therapeutic potential in preventing smoking-related COPD/emphysema.

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

    PubMed

    de Vries, M; Heijink, I H; Gras, R; den Boef, L E; Reinders-Luinge, M; Pouwels, S D; Hylkema, M N; van der Toorn, M; Brouwer, U; van Oosterhout, A J M; Nawijn, M C

    2014-08-01

    Exposure to cigarette smoke (CS) is the main risk factor for developing chronic obstructive pulmonary disease and can induce airway epithelial cell damage, innate immune responses, and airway inflammation. We hypothesized that cell survival factors might decrease the sensitivity of airway epithelial cells to CS-induced damage, thereby protecting the airways against inflammation upon CS exposure. Here, we tested whether Pim survival kinases could protect from CS-induced inflammation. We determined expression of Pim kinases in lung tissue, airway inflammation, and levels of keratinocyte-derived cytokine (KC) and several damage-associated molecular patterns in bronchoalveolar lavage in mice exposed to CS or air. Human bronchial epithelial BEAS-2B cells were treated with CS extract (CSE) in the presence or absence of Pim1 inhibitor and assessed for loss of mitochondrial membrane potential, induction of cell death, and release of heat shock protein 70 (HSP70). We observed increased expression of Pim1, but not of Pim2 and Pim3, in lung tissue after exposure to CS. Pim1-deficient mice displayed a strongly enhanced neutrophilic airway inflammation upon CS exposure compared with wild-type controls. Inhibition of Pim1 activity in BEAS-2B cells increased the loss of mitochondrial membrane potential and reduced cell viability upon CSE treatment, whereas release of HSP70 was enhanced. Interestingly, we observed release of S100A8 but not of double-strand DNA or HSP70 in Pim1-deficient mice compared with wild-type controls upon CS exposure. In conclusion, we show that expression of Pim1 protects against CS-induced cell death in vitro and neutrophilic airway inflammation in vivo. Our data suggest that the underlying mechanism involves CS-induced release of S100A8 and KC. PMID:24816488

  9. Genetic variation associates with susceptibility for cigarette smoke-induced neutrophilia in mice.

    PubMed

    Pouwels, Simon D; Heijink, Irene H; Brouwer, Uilke; Gras, Renee; den Boef, Lisette E; Boezen, H Marike; Korstanje, Ron; van Oosterhout, Antoon J M; Nawijn, Martijn C

    2015-04-01

    Neutrophilic airway inflammation is one of the major hallmarks of chronic obstructive pulmonary disease and is also seen in steroid resistant asthma. Neutrophilic airway inflammation can be induced by different stimuli including cigarette smoke (CS). Short-term exposure to CS induces neutrophilic airway inflammation in both mice and humans. Since not all individuals develop extensive neutrophilic airway inflammation upon smoking, we hypothesized that this CS-induced innate inflammation has a genetic component. This hypothesis was addressed by exposing 30 different inbred mouse strains to CS or control air for 5 consecutive days, followed by analysis of neutrophilic lung inflammation. By genomewide haplotype association mapping, we identified four susceptibility genes with a significant association to lung tissue levels of the neutrophil marker myeloperoxidase under basal conditions and an additional five genes specifically associated with CS-induced tissue MPO levels. Analysis of the expression levels of the susceptibility genes by quantitative RT-PCR revealed that three of the four genes associated with CS-induced tissue MPO levels had CS-induced changes in gene expression levels that correlate with CS-induced airway inflammation. Most notably, CS exposure induces an increased expression of the coiled-coil domain containing gene, Ccdc93, in mouse strains susceptible for CS-induced airway inflammation whereas Ccdc93 expression was decreased upon CS exposure in nonsusceptible mouse strains. In conclusion, this study shows that CS-induced neutrophilic airway inflammation has a genetic component and that several genes contribute to the susceptibility for this response. PMID:25637605

  10. C-reactive protein is associated with cigarette smoking-induced hyperfiltration and proteinuria in an apparently healthy population.

    PubMed

    Sauriasari, Rani; Sakano, Noriko; Wang, Da-Hong; Takaki, Jiro; Takemoto, Kei; Wang, BingLing; Sugiyama, Hitoshi; Sato, Yoshie; Takigawa, Tomoko; Takahashi, Noriko; Kanbara, Sakiko; Hitomi, Yoshiaki; Nakamura, Hiroyuki; Ogino, Keiki

    2010-11-01

    Although cigarette smoking is known to be an important risk factor for renal disease, the mechanism by which smoking induces progressive renal disease in a healthy population has not been established. We hypothesized that oxidative stress (measured as 8-iso-prostaglandin F(2α), 8-iso-PGF2a), inflammation (highly sensitive C-reactive protein (CRP), hs-CRP) and nitric oxide may be associated with an alteration in the estimated glomerular filtration rate (eGFR) and proteinuria in otherwise healthy smokers. A total of 649 eligible subjects were classified according to their smoking status. Plasma NOx was measured using ozone-based chemiluminescence, urinary 8-iso-PGF2a was measured using enzyme immunoassay and serum hs-CRP was measured using a latex aggregation nephelometry method. The levels of 8-iso-PGF2a and hs-CRP increased in current smokers (P=0.001 and P=0.029, respectively), although there was not an increase in the NOx level. The prevalence of a high eGFR increased in light smokers (odds ratio (OR) 1.15 (95% confidence interval (CI), 0.61-2.17)) and heavy smokers (OR 2.33 (95% CI, 1.06-5.10)) when compared with non- and past smokers (P for trend=0.024). The multivariable-adjusted mean values of the eGFR in current smokers, reported from the lowest to the highest quintiles of hs-CRP levels, were 82.1, 85.1, 86.4 and 88.5 ml per min per 1.73 m² (P for trend=0.027). The mean values of proteinuria were 28.6, 34.6, 37.2 and 39.5 mg g⁻¹ creatinine (P for trend=0.003). The correlation coefficient between hs-CRP and eGFR was increased significantly (P=0.03) across non- (r=0.03), past (r=-0.17), light (r=0.13) and heavy smokers (r=0.31). In conclusion, cigarette smoking is a risk factor for renal function alteration in healthy smokers and is characterized by a high eGFR and a high urinary protein associated with an increase in the hs-CRP. This finding suggests that hs-CRP may help mediate the alteration of renal function in smokers. PMID:20703235

  11. The standardized herbal formula, PM014, ameliorated cigarette smoke-induced lung inflammation in a murine model of chronic obstructive pulmonary disease

    PubMed Central

    2013-01-01

    Background In this study, we evaluated the anti-inflammatory effect of PM014 on cigarette smoke induced lung disease in the murine animal model of chronic obstructive pulmonary disease (COPD). Methods Mice were exposed to cigarette smoke (CS) for 2 weeks to induce COPD-like lung inflammation. Two hours prior to cigarette smoke exposure, the treatment group was administered PM014 via an oral injection. To investigate the effects of PM014, we assessed PM014 functions in vivo, including immune cell infiltration, cytokine profiles in bronchoalveolar lavage (BAL) fluid and histopathological changes in the lung. The efficacy of PM014 was compared with that of the recently developed anti-COPD drug, roflumilast. Results PM014 substantially inhibited immune cell infiltration (neutrophils, macrophages, and lymphocytes) into the airway. In addition, IL-6, TNF-α and MCP-1 were decreased in the BAL fluid of PM014-treated mice compared to cigarette smoke stimulated mice. These changes were more prominent than roflumilast treated mice. The expression of PAS-positive cells in the bronchial layer was also significantly reduced in both PM014 and roflumilast treated mice. Conclusions These data suggest that PM014 exerts strong therapeutic effects against CS induced, COPD-like lung inflammation. Therefore, this herbal medicine may represent a novel therapeutic agent for lung inflammation in general, as well as a specific agent for COPD treatment. PMID:24010767

  12. Trachea Epithelium as a “Canary” for Cigarette Smoking-induced Biologic Phenotype of the Small Airway Epithelium*

    PubMed Central

    Turetz, Meredith L.; O’Connor, Timothy P.; Tilley, Ann E.; Strulovici-Barel, Yael; Salit, Jacqueline; Dang, David; Teater, Matthew; Mezey, Jason; Clark, Andrew G.; Crystal, Ronald G.

    2013-01-01

    The initial site of smoking-induced lung disease is the small airway epithelium, which is difficult and time consuming to sample by fiberoptic bronchoscopy. We developed a rapid, office-based procedure to obtain trachea epithelium without conscious sedation from healthy nonsmokers (n=26) and healthy smokers (n=19, 27 ± 15 pack-yr). Gene expression differences (fold-change >1.5, p<0.01, Benjamini-Hochberg correction) were assessed with Affymetrix microarrays. 1,057 probe sets were differentially expressed in healthy smokers vs nonsmokers, representing >500 genes. Trachea gene expression was compared to an independent group of small airway epithelial samples (n=23 healthy nonsmokers, n=19 healthy smokers, 25 ± 12 pack-yr). The trachea epithelium is more sensitive to smoking, responding with 3-fold more differentially-expressed genes than small airway epithelium. The trachea transcriptome paralleled the small airway epithelium, with 156 of 167 (93%) genes that are significantly upand down-regulated by smoking in the small airway epithelium showing similar direction and magnitude of response to smoking in the trachea. Trachea epithelium can be obtained without conscious sedation, representing a less invasive surrogate “canary” for smoking-induced changes in the small airway epithelium. This should prove useful in epidemiologic studies correlating gene expression with clinical outcome in assessing smoking-induced lung disease. PMID:20443905

  13. Emodin Attenuates Cigarette Smoke Induced Lung Injury in a Mouse Model via Suppression of Reactive Oxygen Species Production.

    PubMed

    Xue, Wen-Hua; Shi, Xiu-Qin; Liang, Shu-Hong; Zhou, Lin; Liu, Ke-Feng; Zhao, Jie

    2015-11-01

    Emodin has antioxidative activities. Here, we investigated the effects of emodin on cigarette smoke (CS)-induced acute lung inflammation. Mice (C57BL/6) were exposed to CS. Emodin was administrated with intraperitoneal bolus injection of emodin (20 or 40 mg/kg) daily 1 h before CS exposure. Emodin inhibited CS-induced inflammatory cells infiltration in mouse lungs, especially at 40 mg/kg. Moreover, emodin resulted in significant reductions in total bronchoalveolar lavage fluid (BALF) cells, as compared with air exposure control, coupled with decreases in BALF cytokines. The activities of superoxide dismutase, catalase, and glutathione peroxidase were remarkably enhanced by emodin in CS-exposed mice. Emodin enhanced CS-induced expression of heme oxygenase-1 and nuclear factor-erythroid 2-related factor-2 (both are antioxidative genes) at both mRNA and protein levels, and profoundly promoted their activities in CS-treated mice. Collectively, our results suggested that emodin protects mouse lung from CS-induced lung inflammation and oxidative damage, most likely through its antioxidant activity.

  14. Cigarette smoke-induced oxidative stress suppresses generation of dendritic cell IL-12 and IL-23 through ERK-dependent pathways.

    PubMed

    Kroening, Paula R; Barnes, Terrance W; Pease, Larry; Limper, Andrew; Kita, Hirohito; Vassallo, Robert

    2008-07-15

    IL-12p70, a heterodimer composed of p35 and p40 subunits, is a key polarizing cytokine produced by maturing dendritic cells (DCs). We report that cigarette smoke extract (CSE), an extract of soluble cigarette smoke components, suppresses both p35 and p40 production by LPS or CD40L-matured DCs. Suppression of IL-12p70 production from maturing DCs was not observed in the presence of nicotine concentrations achievable in CSE or in the circulation of smokers. The suppressed IL-12p70 protein production by CSE-conditioned DCs was restored by pretreatment of DCs or CSE with the antioxidants N-acetylcysteine and catalase. Inhibition of DC IL-12p70 by CSE required activation of ERK-dependent pathways, since inhibition of ERK abrogated the suppressive effect of CSE on IL-12 secretion. Oxidative stress and sustained ERK phosphorylation by CSE enhanced nuclear levels of the p40 transcriptional repressor c-fos in both immature and maturing DCs. Suppression of the p40 subunit by CSE also resulted in diminished production of IL-23 protein by maturing DCs. Using a murine model of chronic cigarette smoke exposure, we observed that systemic and lung DCs from mice "smokers" produced significantly less IL-12p70 and p40 protein upon maturation. This inhibitory effect was selective, since production of TNF-alpha during DC maturation was enhanced in the smokers. These data imply that oxidative stress generated by cigarette smoke exposure suppresses the generation of key cytokines by maturing DCs through the activation of ERK-dependent pathways. Some of the cigarette smoke-induced inhibitory effects on DC function may be mitigated by antioxidants. PMID:18606709

  15. The contribution of benzene to smoking-induced leukemia.

    PubMed

    Korte, J E; Hertz-Picciotto, I; Schulz, M R; Ball, L M; Duell, E J

    2000-04-01

    Cigarette smoking is associated with an increased risk of leukemia; benzene, an established leukemogen, is present in cigarette smoke. By combining epidemiologic data on the health effects of smoking with risk assessment techniques for low-dose extrapolation, we assessed the proportion of smoking-induced total leukemia and acute myeloid leukemia (AML) attributable to the benzene in cigarette smoke. We fit both linear and quadratic models to data from two benzene-exposed occupational cohorts to estimate the leukemogenic potency of benzene. Using multiple-decrement life tables, we calculated lifetime risks of total leukemia and AML deaths for never, light, and heavy smokers. We repeated these calculations, removing the effect of benzene in cigarettes based on the estimated potencies. From these life tables we determined smoking-attributable risks and benzene-attributable risks. The ratio of the latter to the former constitutes the proportion of smoking-induced cases attributable to benzene. Based on linear potency models, the benzene in cigarette smoke contributed from 8 to 48% of smoking-induced total leukemia deaths [95% upper confidence limit (UCL), 20-66%], and from 12 to 58% of smoking-induced AML deaths (95% UCL, 19-121%). The inclusion of a quadratic term yielded results that were comparable; however, potency models with only quadratic terms resulted in much lower attributable fractions--all < 1%. Thus, benzene is estimated to be responsible for approximately one-tenth to one-half of smoking-induced total leukemia mortality and up to three-fifths of smoking-related AML mortality. In contrast to theoretical arguments that linear models substantially overestimate low-dose risk, linear extrapolations from empirical data over a dose range of 10- to 100-fold resulted in plausible predictions. PMID:10753092

  16. The contribution of benzene to smoking-induced leukemia.

    PubMed Central

    Korte, J E; Hertz-Picciotto, I; Schulz, M R; Ball, L M; Duell, E J

    2000-01-01

    Cigarette smoking is associated with an increased risk of leukemia; benzene, an established leukemogen, is present in cigarette smoke. By combining epidemiologic data on the health effects of smoking with risk assessment techniques for low-dose extrapolation, we assessed the proportion of smoking-induced total leukemia and acute myeloid leukemia (AML) attributable to the benzene in cigarette smoke. We fit both linear and quadratic models to data from two benzene-exposed occupational cohorts to estimate the leukemogenic potency of benzene. Using multiple-decrement life tables, we calculated lifetime risks of total leukemia and AML deaths for never, light, and heavy smokers. We repeated these calculations, removing the effect of benzene in cigarettes based on the estimated potencies. From these life tables we determined smoking-attributable risks and benzene-attributable risks. The ratio of the latter to the former constitutes the proportion of smoking-induced cases attributable to benzene. Based on linear potency models, the benzene in cigarette smoke contributed from 8 to 48% of smoking-induced total leukemia deaths [95% upper confidence limit (UCL), 20-66%], and from 12 to 58% of smoking-induced AML deaths (95% UCL, 19-121%). The inclusion of a quadratic term yielded results that were comparable; however, potency models with only quadratic terms resulted in much lower attributable fractions--all < 1%. Thus, benzene is estimated to be responsible for approximately one-tenth to one-half of smoking-induced total leukemia mortality and up to three-fifths of smoking-related AML mortality. In contrast to theoretical arguments that linear models substantially overestimate low-dose risk, linear extrapolations from empirical data over a dose range of 10- to 100-fold resulted in plausible predictions. PMID:10753092

  17. Protection of coronary endothelial cells from cigarette smoke-induced oxidative stress by a new Mn(II)-containing polyamine-polycarboxilate scavenger of superoxide anion.

    PubMed

    Becatti, Matteo; Boccalini, Giulia; Pini, Alessandro; Fiorillo, Claudia; Bencini, Andrea; Bani, Daniele; Nistri, Silvia

    2015-12-01

    Oxidative stress plays a major role in cardiovascular injury and dysfunction induced by cigarette smoke. Smoke-borne pro-oxidants impair endothelial function and predispose to thrombosis, inflammation and atherosclerosis. This in vitro study evaluates whether Mn(II)(4,10-dimethyl-1,4,7,10-tetraazacyclododecane-1,7-diacetate).2H2O (Mn(II)(Me2DO2A)), a polyamine-polycarboxilate, Mn(II)-containing O2(-) scavenger, has a direct protective action on guinea pig coronary endothelial (GPCE) cells exposed to cigarette smoke extracts (CSE). Mn(II)(Me2DO2A) (1-10μmol/l) was added to the culture medium together with CSE and maintained for 4h. In parallel experiments, the inactive congener Zn(II)(Me2DO2A), in which Zn(II) replaced the functional Mn(II) center in the same organic scaffold, was used as negative control. Mn(II)(Me2DO2A), mostly at the higher doses (5 and 10μmol/l), significantly increased GPCE cell viability (trypan blue assay), improved mitochondrial activity (MTT test, mitochondrial membrane potential Δψ), reduced cellular apoptosis (mPTP, caspase-3 activity, TUNEL assay), decreased intracellular ROS levels (H2DCFDA), lipoperoxidation (BODIPY 581/591) and decreased protein nitrosylation. Of note, Zn(II)(Me2DO2A) did not preserve cell viability. These findings suggest that Mn(II)(Me2DO2A) is a promising O2(-) scavenging compound able to protect from cigarette smoke-induced oxidative cell injury. In perspective, should its efficacy be confirmed in future in vivo studies, this molecule might represent a therapeutic or preventive drug to counteract cigarette smoke toxicity.

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

    PubMed

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

    2015-05-01

    Cigarette smoking, the major causative factor for the development of chronic obstructive pulmonary disease, is associated with neutrophilic airway inflammation. Cigarette smoke (CS) exposure can induce a switch from apoptotic to necrotic cell death in airway epithelium. Therefore, we hypothesized that CS promotes neutrophil necrosis with subsequent release of damage-associated molecular patterns (DAMPs), including high mobility group box 1 (HMGB1), alarming the innate immune system. We studied the effect of smoking two cigarettes on sputum neutrophils in healthy individuals and of 5-day CS or air exposure on neutrophil counts, myeloperoxidase, and HMGB1 levels in bronchoalveolar lavage fluid of BALB/c mice. In human peripheral blood neutrophils, mitochondrial membrane potential, apoptosis/necrosis markers, caspase activity, and DAMP release were studied after CS exposure. Finally, we assessed the effect of neutrophil-derived supernatants on the release of chemoattractant CXCL8 in normal human bronchial epithelial cells. Cigarette smoking caused a significant decrease in sputum neutrophil numbers after 3 hours. In mice, neutrophil counts were significantly increased 16 hours after repeated CS exposure but reduced 2 hours after an additional exposure. In vitro, CS induced necrotic neutrophil cell death, as indicated by mitochondrial dysfunction, inhibition of apoptosis, and DAMP release. Supernatants from CS-treated neutrophils significantly increased the release of CXCL8 in normal human bronchial epithelial cells. Together, these observations show, for the first time, that CS exposure induces neutrophil necrosis, leading to DAMP release, which may amplify CS-induced airway inflammation by promoting airway epithelial proinflammatory responses. PMID:25192219

  19. Water-Soluble alpha,beta-unsaturated aldehydes of cigarette smoke induce carbonylation of human serum albumin.

    PubMed

    Colombo, Graziano; Aldini, Giancarlo; Orioli, Marica; Giustarini, Daniela; Gornati, Rosalba; Rossi, Ranieri; Colombo, Roberto; Carini, Marina; Milzani, Aldo; Dalle-Donne, Isabella

    2010-03-01

    Cigarette smoking is a major risk factor for developing pulmonary and cardiovascular diseases as well as some forms of cancer. Understanding the mechanisms by which smoking contributes to disease remains a major research focus. Increased levels of carbonylated serum proteins are present in smokers; albumin is the major carbonylated protein in the bronchoalveolar lavage fluid of older smokers. We have investigated the susceptibility of human serum albumin (HSA) to alpha,beta-unsaturated aldehyde-induced carbonylation when exposed to whole-phase cigarette smoke extract (CSE). Fluorescence studies with fluorescent probes showed depletion of HSA Cys34 free thiol and marked decrease of free Lys residues. Spectrophotometric and immunochemical carbonyl assays after carbonyl derivatization with 2,4-dinitrophenylhydrazine revealed the formation of covalent carbonyl adducts. Nanoscale capillary liquid chromatography and electrospray tandem mass spectrometry analysis detected acrolein and crotonaldehyde Michael adducts at Cys34, Lys525, Lys351, and His39 at all the CSE concentrations tested. Lys541 and Lys545 were also found to form a Schiff base with acrolein. The carbonyl scavenger drugs, hydralazine and pyridoxamine, partially prevented CSE-induced HSA carbonylation. Carbonylation of HSA associated with cigarette smoking might result in modifications of its antioxidant properties and transport functions of both endogenous and exogenous compounds.

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

    PubMed

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

    2015-05-01

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

  1. A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer

    PubMed Central

    Cohen, Amit; Smith, Yoav

    2016-01-01

    Alteration in the expression of microRNAs (miRNAs) is associated with oncogenesis and cancer progression. In this review we aim to suggest that elevated levels of estrogens and their metabolites inside the lungs as a result of cigarette smoke exposure can cause widespread repression of miRNA and contribute to lung tumor development. Anti-estrogenic compounds, such as the components of cruciferous vegetables, can attenuate this effect and potentially reduce the risk of lung cancer (LC) among smokers. PMID:27413713

  2. A potential role for estrogen in cigarette smoke-induced microRNA alterations and lung cancer.

    PubMed

    Cohen, Amit; Burgos-Aceves, Mario Alberto; Smith, Yoav

    2016-06-01

    Alteration in the expression of microRNAs (miRNAs) is associated with oncogenesis and cancer progression. In this review we aim to suggest that elevated levels of estrogens and their metabolites inside the lungs as a result of cigarette smoke exposure can cause widespread repression of miRNA and contribute to lung tumor development. Anti-estrogenic compounds, such as the components of cruciferous vegetables, can attenuate this effect and potentially reduce the risk of lung cancer (LC) among smokers. PMID:27413713

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

    PubMed Central

    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

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

    PubMed

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

    2016-05-27

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

  5. Cigarette smoke induces molecular responses in respiratory tissues of ApoE(-/-) mice that are progressively deactivated upon cessation.

    PubMed

    Boué, Stéphanie; De León, Héctor; Schlage, Walter K; Peck, Michael J; Weiler, Horst; Berges, An; Vuillaume, Grégory; Martin, Florian; Friedrichs, Baerbel; Lebrun, Stefan; Meurrens, Kris; Schracke, Nadine; Moehring, Michaela; Steffen, Yvonne; Schueller, Jutta; Vanscheeuwijck, Patrick; Peitsch, Manuel C; Hoeng, Julia

    2013-12-01

    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. PMID:24096154

  6. Cigarette smoke-induced lung inflammation in COPD mediated via LTB4/BLT1/SOCS1 pathway

    PubMed Central

    Dong, Ran; Xie, Liang; Zhao, Kaishun; Zhang, Qiurui; Zhou, Min; He, Ping

    2016-01-01

    Background Evidence suggests that suppressor of cytokine signaling 1 (SOCS1) is crucial for the negative regulation of inflammation. We investigated the relationship between smoking, SOCS1, and leukotriene B4 (LTB4) in vitro and in clinical samples of COPD; besides which we detected the impact of LTB4 receptor 1 (BLT1) antagonist on inflammation. Methods SOCS1 expression in bronchial mucosa was determined by immunohistochemistry and real-time polymerase chain reaction. We also detect SOCS1 and BLT1 expression in alveolar macrophages from bronchoalveolar lavage fluid (BALF) by real time-PCR, in addition to measuring the level of cytokines in BALF using enzyme-linked immunosorbent assay. In vitro, we investigated the expression of SOCS1 in cigarette smoke extract-induced mouse macrophage cell line RAW264.7 by real-time polymerase chain reaction and Western blot, and detected the level of cytokines in the supernatant by enzyme-linked immunosorbent assay. Then, we investigated the effects of BLT1 antagonist U-75302 on SOCS1 expression in these cells. Results We obtained endobronchial biopsies (15 COPD patients and 12 non-COPD control subjects) and BALF (20 COPD patients and 20 non-COPD control subjects), and our results showed that SOCS1 expression significantly decreased in lung tissues from COPD patients. Inflammatory cytokines in BALF were higher in COPD and these inflammatory cytokines negatively correlate with SOCS1 levels. Further, the BLT1 antagonist restored SOCS1 expression and in turn inhibited inflammatory cytokine secretion in vitro. Conclusion Long-term cigarette smoke exposure induced SOCS1 degradation and LTB4 accumulation, which was associated with emphysema and inflammation. A BLT1 antagonist might be a potential therapeutic candidate for the treatment of COPD. PMID:26730186

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

    PubMed

    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

  8. The aryl hydrocarbon receptor suppresses cigarette-smoke-induced oxidative stress in association with dioxin response element (DRE)-independent regulation of sulfiredoxin 1.

    PubMed

    Sarill, Miles; Zago, Michela; Sheridan, Jared A; Nair, Parameswaran; Matthews, Jason; Gomez, Alvin; Roussel, Lucie; Rousseau, Simon; Hamid, Qutayba; Eidelman, David H; Baglole, Carolyn J

    2015-12-01

    The aryl hydrocarbon receptor (AhR) is a ubiquitously expressed receptor/transcription factor that mediates toxicological responses of environmental contaminants such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Emerging evidence indicates that the AhR suppresses apoptosis and proliferation independent of exogenous ligands, including suppression of apoptosis by cigarette smoke, a key risk factor for chronic obstructive pulmonary disease (COPD). As cigarette smoke is a potent inducer of oxidative stress, a feature that may contribute to the development of COPD, we hypothesized that the AhR prevents smoke-induced apoptosis by regulating oxidative stress. Utilizing primary lung fibroblasts derived from AhR(+/+) and AhR(-/-) mice as well as A549 human lung adenocarcinoma cells deficient in AhR expression (A549-AhR(ko)), we first show that AhR(-/-) fibroblasts and A549-AhR(ko) epithelial cells have a significant increase in cigarette smoke extract (CSE)-induced oxidative stress compared to wild type. CSE induced a significant increase in the mRNA expression of key antioxidant genes, including Nqo1 and Srxn1, predominantly in AhR(+/+) fibroblasts, with significantly less induction in AhR(-/-) cells. The induction of Srxn1, but not Nqo1, was independent of dioxin-response element (DRE) binding as AhR(DBD/DBD) lung fibroblasts, which express an AhR incapable of binding the DRE, increased Srxn1 to a degree similar to wild-type cells in response to CSE. There was no difference in Nrf2 expression or activation based on AhR expression. Lung fibroblasts derived from COPD subjects have significantly less AhR protein expression compared with both never-smokers (Normal) and smokers (At Risk). Consequently, COPD-derived fibroblasts were less robust in their induction of both Nqo1 and Srxn1 mRNA after exposure to CSE, which also failed to activate the AhR in the COPD fibroblasts. Taken together, these results support a new role for the AhR in regulating antioxidant defense in lung

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

    PubMed Central

    Jorgensen, Ellen; Stinson, Andy; Shan, Lin; Yang, Jin; Gietl, Diana; Albino, Anthony P

    2008-01-01

    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 diagnostic and

  10. Cigarette smoke-induced chronic obstructive pulmonary disease is attenuated by CCL20-blocker: a rat model

    PubMed Central

    Sun, Desheng; Ouyang, Yao; Gu, Yanhui; Liu, Xiansheng

    2016-01-01

    Aim To evaluate whether the effect of dendritic cells (DCs) on chronic obstructive pulmonary disease (COPD) can be relieved by blocking CCL20. Methods 30 Wistar rats were randomly divided into three groups: control, COPD, and COPD treated with CCL20 monoclonal antibody. In the latter two groups, COPD was induced by four-week cigarette smoke exposure and trachea injection of lipopolysaccharide solution on two occasions. CCL20 monoclonal antibody was injected intraperitoneally on the first day. All animals were sacrificed on the 29th day. Pathomorphology of the lung and bronchiole was analyzed using hematoxylin and eosin staining. The CCR6 content in the bronchoalveolar lavage fluid was detected using ELISA. DC distribution in the lung was examined by immunohistochemistry for OX62. Results COPD rat models showed pathological alterations similar to those in COPD patients. DCs, CCR6, and the severity of emphysema were significantly increased in the COPD group than in controls (all P values <0.001), and they were significantly reduced after anti-CCL20 treatment compared with the COPD group (all P values <0.05). Conclusion The interaction between CCR6 and its ligand CCL20 promotes the effect of DCs in the COPD pathogenesis, which can be reduced by blocking CCL20. PMID:27586551

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

    PubMed

    Nagler, R; Savulescu, D; Gavish, M

    2016-02-01

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

  12. Protecting the BBB endothelium against cigarette smoke-induced oxidative stress using popular antioxidants: Are they really beneficial?

    PubMed

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

    2015-11-19

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

  13. Selective inhibition by aspirin and naproxen of mainstream cigarette smoke-induced genotoxicity and lung tumors in female mice.

    PubMed

    Balansky, Roumen; Ganchev, Gancho; Iltcheva, Marietta; Micale, Rosanna T; La Maestra, Sebastiano; D'Oria, Chiara; Steele, Vernon E; De Flora, Silvio

    2016-05-01

    The role of nonsteroidal anti-inflammatory drugs (NSAIDs) in smoke-related lung carcinogenesis is still controversial. We have developed and validated a murine model for evaluating the tumorigenicity of mainstream cigarette smoke (MCS) and its modulation by chemopreventive agents. In the present study, the protective effects of the nonselective cyclooxygenase inhibitors aspirin and naproxen were investigated by using a total of 277 Swiss H neonatal mice of both genders. Groups of mice were exposed whole-body to MCS during the first 4 months of life, followed by an additional 3.5 months in filtered air in order to allow a better growth of tumors. Aspirin (1600 mg/kg diet) and naproxen (320 mg/kg diet) were given after weanling until the end of the experiment. After 4 months of exposure, MCS significantly enhanced the frequency of micronucleated normochromatic erythrocytes in the peripheral blood of mice, and naproxen prevented such systemic genotoxic damage in female mice. After 7.5 months, exposure of mice to MCS resulted in the formation of lung tumors, both benign and malignant, and in several other histopathological lesions detectable both in the respiratory tract and in the urinary tract. Aspirin and, even more sharply, naproxen significantly inhibited the formation of lung tumors in MCS-exposed mice, but this protective effect selectively occurred in female mice only. These results lend support to the views that estrogens are involved in smoke-related pulmonary carcinogenesis and that NSAIDs have antiestrogenic properties. The two NSAIDs proved to be safe and efficacious in the experimental model used. PMID:26104855

  14. Exposure to neonatal cigarette smoke causes durable lung changes but does not potentiate cigarette smoke-induced chronic obstructive pulmonary disease in adult mice.

    PubMed

    McGrath-Morrow, Sharon; Malhotra, Deepti; Lauer, Thomas; Collaco, J Michael; Mitzner, Wayne; Neptune, Enid; Wise, Robert; Biswal, Shyam

    2011-08-01

    The impact of early childhood cigarette smoke (CS) exposure on CS-induced chronic obstructive pulmonary disease (COPD) is unknown. This study was performed to evaluate the individual and combined effects of neonatal and adult CS exposure on lung structure, function, and gene expression in adult mice. To model a childhood CS exposure, neonatal C57/B6 mice were exposed to 14 days of CS (Neo CS). At 10 weeks of age, Neo CS and control mice were exposed to 4 months of CS. Pulmonary function tests, bronchoalveolar lavage, and lung morphometry were measured and gene expression profiling was performed on lung tissue. Mean chord lengths and lung volumes were increased in neonatal and/or adult CS-exposed mice. Differences in immune, cornified envelope protein, muscle, and erythrocyte genes were found in CS-exposed lung. Neonatal CS exposure caused durable structural and functional changes in the adult lung but did not potentiate CS-induced COPD changes. Cornified envelope protein gene expression was decreased in all CS-exposed mice, whereas myosin and erythrocyte gene expression was increased in mice exposed to both neonatal and adult CS, suggesting an adaptive response. Additional studies may be warranted to determine the utility of these genes as biomarkers of respiratory outcomes.

  15. The NF-κB family member RelB regulates microRNA miR-146a to suppress cigarette smoke-induced COX-2 protein expression in lung fibroblasts.

    PubMed

    Zago, Michela; Rico de Souza, Angela; Hecht, Emelia; Rousseau, Simon; Hamid, Qutayba; Eidelman, David H; Baglole, Carolyn J

    2014-04-21

    Diseases due to cigarette smoke exposure, including chronic obstructive pulmonary disease (COPD) and lung cancer, are associated with chronic inflammation typified by the increased expression of cyclooxygenase-2 (COX-2) protein. RelB is an NF-κB family member that suppresses cigarette smoke induction of COX-2 through an unknown mechanism. The ability of RelB to regulate COX-2 expression may be via miR-146a, a miRNA that attenuates COX-2 in lung fibroblasts. In this study we tested whether RelB attenuation of cigarette smoke-induced COX-2 protein is due to miR-146a. Utilizing pulmonary fibroblasts deficient in RelB expression, together with siRNA knock-down of RelB, we show the essential role of RelB in diminishing smoke-induced COX-2 protein expression despite robust activation of the canonical NF-κB pathway and subsequent induction of Cox-2 mRNA. RelB did not regulate COX-2 protein expression at the level of mRNA stability. Basal levels of miR-146a were significantly lower in Relb-deficient cells and cigarette smoke increased miR-146a expression only in Relb-expressing cells. Inhibition of miR-146a had no effects on Relb expression or induction of Cox-2 mRNA by cigarette smoke but significantly increased COX-2 protein. These data highlight the potential of a RelB-miR-146a axis as a novel regulatory pathway that attenuates inflammation in response to respiratory toxicants.

  16. REINFORCEMENT ENHANCING EFFECTS OF ACUTE NICOTINE VIA ELECTRONIC CIGARETTES

    PubMed Central

    Perkins, Kenneth A.; Karelitz, Joshua L.; Michael, Valerie C.

    2015-01-01

    Background Recent human studies confirm animal research showing that nicotine enhances reinforcement from rewards unrelated to nicotine. These effects of acute nicotine via tobacco smoking may also occur when consumed from non-tobacco products. Methods We assessed acute effects of nicotine via electronic cigarettes (“e-cigarettes”) on responding reinforced by music, video, or monetary rewards, or for no reward (control). In a fully within-subjects design, adult dependent smokers (N=28) participated in three similar experimental sessions, each following overnight abstinence (verified by CO≤10 ppm). Varying only in e-cigarette condition, sessions involved controlled exposure to a nicotine (labeled “36 mg/ml”) or placebo (“0”) e-cigarette, or no e-cigarette use. A fourth session involved smoking one’s own tobacco cigarette brand after no abstinence, specifically to compare responses under typical nicotine satiation with these acute e-cigarette conditions after abstinence. Results Reinforced responding for video reward, but not the other rewards, was greater due to use of the nicotine versus placebo e-cigarette (i.e., nicotine per se), while no differences were found between the placebo e-cigarette and no e-cigarette conditions (i.e., e-cigarette use per se). For nicotine via tobacco smoking, responding compared to the nicotine e-cigarette was similar for video but greater for music, while both video and music reward were enhanced relative to the non-nicotine conditions (placebo and no e-cigarette). Conclusions Acute nicotine from a non-tobacco product has some reinforcement enhancing effects in humans, in a manner partly consistent with nicotine via tobacco smoking and perhaps contributing to the rising popularity of nicotine e-cigarette use. PMID:26070455

  17. Pharmacological blockade of the DP2 receptor inhibits cigarette smoke-induced inflammation, mucus cell metaplasia, and epithelial hyperplasia in the mouse lung.

    PubMed

    Stebbins, Karin J; Broadhead, Alex R; Baccei, Christopher S; Scott, Jill M; Truong, Yen P; Coate, Heather; Stock, Nicholas S; Santini, Angelina M; Fagan, Patrick; Prodanovich, Patricia; Bain, Gretchen; Stearns, Brian A; King, Christopher D; Hutchinson, John H; Prasit, Peppi; Evans, Jilly F; Lorrain, Daniel S

    2010-03-01

    Prostaglandin D(2) (PGD(2)) is one of a family of biologically active lipids derived from arachidonic acid via the action of COX-1 and COX-2. PGD(2) is released from mast cells and binds primarily to two G protein-coupled receptors, namely DP1 and DP2, the latter also known as chemoattractant receptor-homologous molecule expressed on Th2 cells. DP2 is predominantly expressed on eosinophils, Th2 cells, and basophils, but it is also expressed to a lesser extent on monocytes, mast cells, and epithelial cells. Interaction of PGD(2) and its active metabolites with DP2 results in cellular chemotaxis, degranulation, up-regulation of adhesion molecules, and cytokine production. Chronic obstructive pulmonary disease (COPD) is a chronic progressive inflammatory disease characterized by elevated lung neutrophils, macrophages, and CD8+ T lymphocytes and mucus hypersecretion. Cigarette smoke contributes to the etiology of COPD and was used here as a provoking agent in a murine model of COPD. In an acute model, {2'-[(cyclopropanecarbonyl-ethyl-amino)-methyl]-6-methoxy-4'-trifluoro-methyl-biphenyl-3-yl}-acetic acid, sodium salt (AM156) and (5-{2-[(benzoyloxycarbonyl-ethyl-amino)-methyl]-4-trifluoromethyl-phenyl}-pyridin-3-yl)-acetic acid, sodium salt) (AM206), potent DP2 receptor antagonists, dose-dependently inhibited influx of neutrophils and lymphocytes to smoke-exposed airways. In a subchronic model, AM156 and AM206 inhibited neutrophil and lymphocyte trafficking to the airways. Furthermore, AM156 and AM206 treatment inhibited mucus cell metaplasia and prevented the thickening of the airway epithelial layer induced by cigarette smoke. These data suggest that DP2 receptor antagonism may represent a novel therapy for COPD or other conditions characterized by neutrophil influx, mucus hypersecretion, and airway remodeling.

  18. Cigarette smoke induced changes in rat pulmonary clearance of 99mTcDTPA. A comparison of particulate and gas phases.

    PubMed

    Minty, B D; Royston, D

    1985-12-01

    The rat model was developed to study the effects of cigarette smoke on pulmonary clearance of 99mTcDTPA. The method developed was sufficiently noninvasive to allow frequent repeat measurements to be made with a high degree of reproducibility. Animals exposed twice daily to 90 puffs of dilute whole cigarette smoke for 7 days showed an increase in 99mTcDTPA clearance from the lung which returned to normal within 3 wk of stopping exposure. Filtration of the smoke to remove all the particulate matter abolished the changes.

  19. 32P-postlabeling DNA adduct assay: cigarette smoke-induced dna adducts in the respiratory and nonrespiratory rat tissues. Book chapter

    SciTech Connect

    Gupta, R.C.; Gairola, C.G.

    1990-01-01

    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.

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

    PubMed

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

    2015-12-01

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

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

    PubMed

    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).

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

    PubMed Central

    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. 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

  3. Cigarette smoke-induced emphysema in A/J mice is associated with pulmonary oxidative stress, apoptosis of lung cells, and global alterations in gene expression

    PubMed Central

    Rangasamy, Tirumalai; Misra, Vikas; Zhen, Lijie; Tankersley, Clarke G.; Tuder, Rubin M.; Biswal, Shyam

    2009-01-01

    Cigarette smoking is the major risk factor for developing chronic obstructive pulmonary disease, the fourth leading cause of deaths in the United States. Despite recent advances, the molecular mechanisms involved in the initiation and progression of this disease remain elusive. We used Affymetrix Gene Chip arrays to determine the temporal alterations in global gene expression during the progression of pulmonary emphysema in A/J mice. Chronic cigarette smoke (CS) exposure caused pulmonary emphysema in A/J mice, which was associated with pronounced bronchoalveolar inflammation, enhanced oxidative stress, and increased apoptosis of alveolar septal cells. Microarray analysis revealed the upregulation of 1,190, 715, 260, and 246 genes and the downregulation of 1,840, 730, 442, and 236 genes in the lungs of mice exposed to CS for 5 h, 8 days, and 1.5 and 6 mo, respectively. Most of the genes belong to the functional categories of phase I genes, Nrf2-regulated antioxidant and phase II genes, phase III detoxification genes, and others including immune/inflammatory response genes. Induction of the genes encoding multiple phase I enzymes was markedly higher in the emphysematous lungs, whereas reduced expression of various cytoprotective genes constituting ubiquitin-proteasome complex, cell survival pathways, solute carriers and transporters, transcription factors, and Nrf2-regulated antioxidant and phase II-responsive genes was noted. Our data indicate that the progression of CS-induced emphysema is associated with a steady decline in the expression of various genes involved in multiple pathways in the lungs of A/J mice. Many of the genes discovered in this study could rationally play an important role in the susceptibility to CS-induced emphysema. PMID:19286929

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

    PubMed

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

    2015-10-01

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

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

    PubMed

    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

  6. Determinants of smoking-induced deprivation in China

    PubMed Central

    Yao, Tingting; Huang, Jidong; Sung, Hai-Yen; Ong, Michael K; Mao, Zhengzhong; Jiang, Yuan; Fong, Geoffrey T; Max, Wendy

    2015-01-01

    Objective Spending on cigarettes may deprive households of other items like food. The goal of this study was to examine the prevalence of and factors associated with this smoking-induced deprivation among adult smokers in China. Methods The data came from waves 1–3 of the International Tobacco Control (ITC) China Survey, conducted from 2006 to 2009 among urban adults aged 18 years or older in China. We focus on the samples of current smokers from six cities (N=7981). Smoking-induced deprivation was measured with the survey question, “In the last six months, have you spent money on cigarettes that you knew would be better spent on household essentials like food?” We examined whether sociodemographic factors, smoking intensity and price paid per pack of cigarettes were associated with smoking-induced deprivation using generalised estimating equations modelling. Findings 7.3% of smokers reported smoking-induced deprivation due to purchasing cigarettes. Low-income and middle-income smokers were more likely to have smoking-induced deprivation compared with high-income smokers (adjusted OR (AOR)=2.06, 95% CI 1.32 to 2.31; AOR=1.44, 95% CI 1.10 to 1.69); smokers living in Shenyang (AOR=1.68, 95% CI 1.25 to 2.24) and Yinchuan (AOR=2.50, 95% CI 1.89 to 3.32) were more likely to have smoking-induced deprivation compared with smokers living in Beijing. Retired smokers were less likely to have smoking-induced deprivation compared with employed smokers (AOR=0.67, 95% CI 0.52 to 0.87). There was no statistically significant relationship between smoking intensity, price paid per pack of cigarettes and smoking-induced deprivation. Conclusions Our findings indicate that certain groups of smokers in China acknowledge spending money on cigarettes that could be better spent on household essentials. Tobacco control policies that reduce smoking in China may improve household living standards by reducing smoking-induced deprivation. PMID:24827978

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

    PubMed

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

    2007-08-01

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

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

    PubMed

    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

  9. Cigarette smoke-induced neurogenic inflammation is mediated by alpha,beta-unsaturated aldehydes and the TRPA1 receptor in rodents.

    PubMed

    Andrè, Eunice; Campi, Barbara; Materazzi, Serena; Trevisani, Marcello; Amadesi, Silvia; Massi, Daniela; Creminon, Christophe; Vaksman, Natalya; Nassini, Romina; Civelli, Maurizio; Baraldi, Pier Giovanni; Poole, Daniel P; Bunnett, Nigel W; Geppetti, Pierangelo; Patacchini, Riccardo

    2008-07-01

    Cigarette smoke (CS) inhalation causes an early inflammatory response in rodent airways by stimulating capsaicin-sensitive sensory neurons that express transient receptor potential cation channel, subfamily V, member 1 (TRPV1) through an unknown mechanism that does not involve TRPV1. We hypothesized that 2 alpha,beta-unsaturated aldehydes present in CS, crotonaldehyde and acrolein, induce neurogenic inflammation by stimulating TRPA1, an excitatory ion channel coexpressed with TRPV1 on capsaicin-sensitive nociceptors. We found that CS aqueous extract (CSE), crotonaldehyde, and acrolein mobilized Ca2+ in cultured guinea pig jugular ganglia neurons and promoted contraction of isolated guinea pig bronchi. These responses were abolished by a TRPA1-selective antagonist and by the aldehyde scavenger glutathione but not by the TRPV1 antagonist capsazepine or by ROS scavengers. Treatment with CSE or aldehydes increased Ca2+ influx in TRPA1-transfected cells, but not in control HEK293 cells, and promoted neuropeptide release from isolated guinea pig airway tissue. Furthermore, the effect of CSE and aldehydes on Ca2+ influx in dorsal root ganglion neurons was abolished in TRPA1-deficient mice. These data identify alpha,beta-unsaturated aldehydes as the main causative agents in CS that via TRPA1 stimulation mediate airway neurogenic inflammation and suggest a role for TRPA1 in the pathogenesis of CS-induced diseases.

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

    PubMed

    Xueshibojie, Liu; Duo, Yu; Tiejun, Wang

    2016-10-15

    Taraxasterol, a pentacyclic-triterpene isolated from Taraxacum officinale, has been demonstrated to have anti-inflammatory effects. However, the protective effects of taraxasterol against cigarette smoke (CS)-induced lung inflammation have not been reported. This study aimed to investigate the protective effects and mechanism of taraxasterol on CS-induced lung inflammation in mice. CS-induced mouse lung inflammation model was used to investigate the protective effects of taraxasterol in vivo. Human bronchial epithelial cells (HBECs) were used to investigate the protective mechanism of taraxasterol in vitro. The results showed that taraxasterol attenuated CS-induced lung pathological changes, inflammatory cells infiltration, inflammatory cytokines TNF-α, IL-6 and IL-1β production. Taraxasterol also up-regulated CS-induced glutathione (GSH) production. In vitro, taraxasterol was found to inhibit CS-induced reactive oxygen species production, recruitment of TLR4 into lipid rafts, NF-κB activation, and IL-8 production. Furthermore, our results showed that antioxidant N-acetyl-L-cysteine (NAC) significantly inhibited CS-induced recruitment of TLR4 into lipid rafts as well as IL-8 production. In conclusion, our results suggested that taraxasterol had protective effects of CS-induced lung inflammation. PMID:27477353

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

    PubMed

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

    2012-01-01

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

  12. Cigarette-smoke-induced priming of neutrophils from smokers and non-smokers for increased oxidative burst response is mediated by TNF-α.

    PubMed

    Friedrichs, Bärbel; Neumann, Ute; Schüller, Jutta; Peck, Michael J

    2014-10-01

    In vitro treatment of human peripheral blood neutrophils from smokers and non-smokers with an aqueous cigarette smoke (CS) extract resulted in a concentration-dependent increase in surface expression of CD11b and CD66b and a corresponding decrease of CD62L, together with a concentration-dependent release of MMP-8, MMP-9, and lactoferrin, indicating considerable activation and degranulation. However, the burst response to N-formyl-methionyl-leucyl-phenylalanine (fMLP) was unchanged in CS-stimulated neutrophils from both smokers and non-smokers. When supernatants from CS-treated monocytic MonoMac-6 (MM6) cells were used for activation of neutrophils, concentration-dependent changes in surface marker expression, granule protein release, and the oxidative burst response to fMLP were observed, again with no major differences between smokers and non-smokers. CS-treated MM6 cells released significant amounts of IL-8 and TNF-α into the culture supernatant. However, antibody blocking experiments showed that only TNF-α mediated the increased burst response in neutrophils. These data show that, in the presence of secondary cells, CS is able to prime neutrophils for an increased burst response to fMLP which is mediated by TNF-α, released from the secondary cells in response to CS. Following stimulation with priming agents, peripheral blood neutrophils from healthy smokers show an equal burst response compared to those from non-smokers.

  13. Probing Cellular and Molecular Mechanisms of Cigarette Smoke-Induced Immune Response in the Progression of Chronic Obstructive Pulmonary Disease Using Multiscale Network Modeling

    PubMed Central

    Pan, Zhichao; Yu, Haishan; Liao, Jie-Lou

    2016-01-01

    Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disorder characterized by progressive destruction of lung tissues and airway obstruction. COPD is currently the third leading cause of death worldwide and there is no curative treatment available so far. Cigarette smoke (CS) is the major risk factor for COPD. Yet, only a relatively small percentage of smokers develop the disease, showing that disease susceptibility varies significantly among smokers. As smoking cessation can prevent the disease in some smokers, quitting smoking cannot halt the progression of COPD in others. Despite extensive research efforts, cellular and molecular mechanisms of COPD remain elusive. In particular, the disease susceptibility and smoking cessation effects are poorly understood. To address these issues in this work, we develop a multiscale network model that consists of nodes, which represent molecular mediators, immune cells and lung tissues, and edges describing the interactions between the nodes. Our model study identifies several positive feedback loops and network elements playing a determinant role in the CS-induced immune response and COPD progression. The results are in agreement with clinic and laboratory measurements, offering novel insight into the cellular and molecular mechanisms of COPD. The study in this work also provides a rationale for targeted therapy and personalized medicine for the disease in future. PMID:27669518

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

    PubMed

    Xueshibojie, Liu; Duo, Yu; Tiejun, Wang

    2016-10-15

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

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

    PubMed

    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.

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

    PubMed

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

    2014-06-01

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

  17. Lung Injury and Lung Cancer Caused by Cigarette Smoke-Induced Oxidative Stress: Molecular Mechanisms and Therapeutic Opportunities Involving the Ceramide-Generating Machinery and Epidermal Growth Factor Receptor

    PubMed Central

    Filosto, Simone; Chung, Samuel

    2014-01-01

    Abstract Chronic obstructive pulmonary disease (COPD) and lung cancer are frequently caused by tobacco smoking. However, these diseases present opposite phenotypes involving redox signaling at the cellular level. While COPD is characterized by excessive airway epithelial cell death and lung injury, lung cancer is caused by uncontrolled epithelial cell proliferation. Notably, epidemiological studies have demonstrated that lung cancer incidence is significantly higher in patients who have preexisting emphysema/lung injury. However, the molecular link and common cell signaling events underlying lung injury diseases and lung cancer are poorly understood. This review focuses on studies of molecular mechanism(s) underlying smoking-related lung injury (COPD) and lung cancer. Specifically, the role of the ceramide-generating machinery during cigarette smoke-induced oxidative stress leading to both apoptosis and proliferation of lung epithelial cells is emphasized. Over recent years, it has been established that ceramide is a sphingolipid playing a major role in lung epithelia structure/function leading to lung injury in chronic pulmonary diseases. However, new and unexpected findings draw attention to its potential role in lung development, cell proliferation, and tumorigenesis. To address this dichotomy in detail, evidence is presented regarding several protein targets, including Src, p38 mitogen-activated protein kinase, and neutral sphingomyelinase 2, the major sphingomyelinase that controls ceramide generation during oxidative stress. Furthermore, their roles are presented not only in apoptosis and lung injury but also in enhancing cell proliferation, lung cancer development, and resistance to epidermal growth factor receptor-targeted therapy for treating lung cancer. Antioxid. Redox Signal. 21, 2149–2174. PMID:24684526

  18. Acute eosinophilic pneumonia following recent cigarette smoking.

    PubMed

    Thakur, Lokendra K; Jha, Kunal Kishor

    2016-01-01

    In this report we describe the case of an 18 year old female who presented with fever, shortness of breath, and chest pain. Chest X-ray revealed diffuse bilateral infiltrates and eosinophilia was reported from her broncholaveolar lavage (BAL) fluid. She started smoking 3 weeks prior to the onset of symptoms and based on her clinical presentation, BAL findings and dramatic improvement, acute eosinophilic pneumonia (AEP) was diagnosed. PMID:27642564

  19. Acute effects of cigarette smoke exposure on experimental skin flaps

    SciTech Connect

    Nolan, J.; Jenkins, R.A.; Kurihara, K.; Schultz, R.C.

    1985-04-01

    Random vascular patterned caudally based McFarlane-type skin flaps were elevated in groups of Fischer 344 rats. Groups of rats were then acutely exposed on an intermittent basis to smoke generated from well-characterized research filter cigarettes. Previously developed smoke inhalation exposure protocols were employed using a Maddox-ORNL inhalation exposure system. Rats that continued smoke exposure following surgery showed a significantly greater mean percent area of flap necrosis compared with sham-exposed groups or control groups not exposed. The possible pathogenesis of this observation as well as considerations and correlations with chronic human smokers are discussed. Increased risks of flap necrosis by smoking in the perioperative period are suggested by this study.

  20. Inflammatory Transcriptome Profiling of Human Monocytes Exposed Acutely to Cigarette Smoke

    PubMed Central

    Wright, William R.; Parzych, Katarzyna; Crawford, Damian; Mein, Charles; Mitchell, Jane A.; Paul-Clark, Mark J.

    2012-01-01

    Background Cigarette smoking is responsible for 5 million deaths worldwide each year, and is a major risk factor for cardiovascular and lung diseases. Cigarette smoke contains a complex mixture of over 4000 chemicals containing 1015 free radicals. Studies show smoke is perceived by cells as an inflammatory and xenobiotic stimulus, which activates an immune response. The specific cellular mechanisms driving cigarette smoke-induced inflammation and disease are not fully understood, although the innate immune system is involved in the pathology of smoking related diseases. Methodology/Principle findings To address the impact of smoke as an inflammagen on the innate immune system, THP-1 cells and Human PBMCs were stimulated with 3 and 10% (v/v) cigarette smoke extract (CSE) for 8 and 24 hours. Total RNA was extracted and the transcriptome analysed using Illumina BeadChip arrays. In THP-1 cells, 10% CSE resulted in 80 genes being upregulated and 37 downregulated by ≥1.5 fold after 8 hours. In PBMCs stimulated with 10% CSE for 8 hours, 199 genes were upregulated and 206 genes downregulated by ≥1.5 fold. After 24 hours, the number of genes activated and repressed by ≥1.5 fold had risen to 311 and 306 respectively. The major pathways that were altered are associated with cell survival, such as inducible antioxidants, protein chaperone and folding proteins, and the ubiquitin/proteosome pathway. Conclusions Our results suggest that cigarette smoke causes inflammation and has detrimental effects on the metabolism and function of innate immune cells. In addition, THP-1 cells provide a genetically stable alternative to primary cells for the study of the effects of cigarette smoke on human monocytes. PMID:22363418

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

    PubMed Central

    Kitamura, S

    1987-01-01

    Nicotine and cigarette smoke extract show acute physiological effects: increasing tracheal pressure (PTR), pulmonary artery pressure (PPA), systemic blood pressure (PSYST), and left atrium pressure (PLA); and decreasing cardiac output (QAORTA) and blood flow to the left lower lobe (QLLL). In addition, cigarette smoking induces bronchoconstriction, thus decreasing peak flow, FVC, and FEV1.0 in healthy subjects. It has also been demonstrated that cigarette smoking caused temporary slowing of mucociliary clearance in the lung and that cigarette smoke increases the activity of aryl hydrocarbon hydroxylase which metabolizes benzo[alpha]pyrene. We demonstrated that serum angiotensin I converting enzyme (ACE) activity showed a significant increase immediately after smoking and returned to the control level 20 min after smoking. We also demonstrated that plasma histamine levels showed a marked decrease after smoking. Furthermore, the effects of cigarette smoke and related substances on prostaglandin, thromboxane, testosterone, cyclic nucleotides metabolism, and protein synthesis were also investigated. PMID:3305000

  2. Prevalence and Impact of Active and Passive Cigarette Smoking in Acute Respiratory Distress Syndrome

    PubMed Central

    Hsieh, S. Jean; Zhuo, Hanjing; Benowitz, Neal L.; Thompson, B. Taylor; Liu, Kathleen D.; Matthay, Michael A.; Calfee, Carolyn S.

    2014-01-01

    Objective Cigarette smoke exposure has recently been found to be associated with increased susceptibility to trauma- and transfusion-associated acute respiratory distress syndrome (ARDS). We sought to determine 1) the prevalence of cigarette smoke exposure in a diverse multi-center sample of ARDS patients, and 2) whether cigarette smoke exposure is associated with severity of lung injury and mortality in ARDS. Design Analysis of the Albuterol for the Treatment of ALI (ALTA) and Omega ARDS Network studies. Setting Acute Respiratory Distress Syndrome Network hospitals. Patients Three hundred eighty one patients with ARDS. Interventions None. Measurements NNAL (4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol), a validated tobacco-specific marker, was measured in urine samples from subjects enrolled in two NHLBI ARDS Network randomized controlled trials. Main Results Urine NNAL levels were consistent with active smoking in 36% of ARDS patients and with passive smoking in 41% of nonsmokers (vs 20% and 40% in general population, respectively). Patients with NNAL levels in the active smoking range were younger and had a higher prevalence of alcohol misuse, fewer comorbidities, lower severity of illness, and less septic shock at enrollment compared to patients with undetectable NNAL levels. Despite this lower severity of illness, the severity of lung injury did not significantly differ based on biomarker-determined smoking status. Cigarette smoke exposure was not significantly associated with death after adjusting for differences in age, alcohol use, comorbidities, and severity of illness. Conclusions In this first multicenter study of biomarker-determined cigarette smoke exposure in ARDS patients, we found that active cigarette smoke exposure was significantly more prevalent among ARDS patients compared to population averages. Despite their younger age, better overall health, and lower severity of illness, smokers by NNAL had similar severity of lung injury as patients with

  3. Acute one-cigarette smoking decreases ghrelin hormone in saliva: a pilot study.

    PubMed

    Kaabi, Yahia A; Khalifa, Mohiealdeen A

    2014-01-01

    Cigarette smoking is commonly associated with weight loss and mechanisms for these weight changes are still elusive. Ghrelin is a peptide hormone that works in a neuroendocrine fashion to stimulate hunger and the desire for food intake. Ghrelin is also secreted in saliva, probably to enhance food taste. In the current study, we tested the direct impact of acute cigarette smoking on total ghrelin found in saliva. Methods. Blood and saliva samples were collected from 30 healthy nonsmoker male volunteers before and after one-cigarette smoke. Total ghrelin in serum and saliva was measured by ELISA based method. Results. Data showed a statistically significant reduction in salivary ghrelin after smoking (P < 0.0001). In serum, total ghrelin levels were not affected before and after smoking (P = 0.1362). Additionally, positive correlation was observed between serum and salivary ghrelin before smoking (r = 0.4143 and P = 0.0158); however, this correlation was lost after smoking (r = 0.1147 and P = 0.5461). Conclusion. Acute one-cigarette smoking can negatively affect ghrelin levels in saliva that might contribute to the dull food taste in smokers. PMID:24808912

  4. Acute Effect of Cigarette Smoking on Pupil Size and Ocular Aberrations: A Pre- and Postsmoking Study

    PubMed Central

    Erdem, Uzeyir; Gundogan, Fatih C.; Dinc, Umut Aslı; Yolcu, Umit; Ilhan, Abdullah; Altun, Salih

    2015-01-01

    Aim. To evaluate the acute effects of cigarette smoking on photopic and mesopic pupil sizes and wavefront aberrations. Methods. Cigarette smoker volunteers were recruited in the study. Photopic and mesopic pupil sizes and total ocular aberrations were measured before smoking and immediately after smoking. All volunteers were asked to smoke a single cigarette containing 1.0 mg nicotine. Pupil sizes and total ocular aberrations were assessed by optical path difference scanning system (OPD-Scan II ARK-10000, NIDEK). Only the right eyes were considered for statistical analysis. The changes of pupil size and total ocular aberrations after smoking were tested for significance by Wilcoxon signed ranks test. Results. Mean photopic pupil size decreased from 3.52 ± 0.73 mm to 3.29 ± 0.58 mm (P = 0.001) after smoking. Mean mesopic pupil size was also decreased from 6.42 ± 0.75 mm to 6.14 ± 0.75 mm after smoking (P = 0.001). There was a decrease in all the measured components of aberrations (total wavefront aberration, higher-order aberration, total coma, total trefoil, total tetrafoil, total spherical aberration and total higher-order aberration) after smoking; however the differences were insignificant for all (P > 0.05). Conclusion. Our results indicate that pupil constricts after smoking. On the other hand, smoking does not alter ocular aberrations. PMID:25699189

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

    SciTech Connect

    Kitamura, S.

    1987-06-01

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

  6. Effects of acute cigarette smoking on total blood count and markers of oxidative stress in active and passive smokers

    PubMed Central

    Lymperaki, E; Makedou, K; Iliadis, S; Vagdatli, E

    2015-01-01

    Background: Free radicals, as a product of cigarette smoke, are considered to have deleterious effects causing oxidative stress. Acute active smoking seems to be followed by transient leukocytosis and delayed increase in neutrophil activation. The aim of the present study was to investigate the oxidative status of smokers and passive non-smokers, as well as the impact that acute cigarette smoking has on hematological parameters. Methods: Thirty-two healthy volunteers, 16 active smokers (Group A) aged 20-23 years and 16 age-matched, non-smokers (Group B), 18 women and 14 men in total, participated voluntarily in the study. All subjects did not have any food, drink, or cigarette smoking for eight hours before the study. Each time, two active smokers and two non-smokers were exposed simultaneously for half an hour to the smoke of two cigarettes smoked consecutively by the smokers. Blood was drawn before and after the exposure to cigarette smoke. Whole blood was analyzed immediately for total blood count parameters and serum was stored in -70◦C until serum levels of malondialdehyde (MDA) and vitamin E (VitE), and total antioxidant capacity (TAC) were determined. Results: No statistical significant difference was observed in the values of white blood cells and their subpopulations between the two groups and within the same group before and after exposure to cigarette smoke. In the group of smokers, granulocyte/lymphocyte ratio increased significantly, MDA levels showed significant elevation and protective VitE serum levels decreased significantly, whereas TAC was reduced, but not significantly, after the exposure. In the group of passive, non-smokers the results of the blood count parameters, MDA and VitE were similar to Group A, and there was a significant decrease in TAC, as well. Between the two groups, only hematocrit values and MDA levels differed significantly before the exposure to smoke, and no other significant difference was detected before or after the

  7. Smoking induces differential miRNA expression in human spermatozoa: a potential transgenerational epigenetic concern?

    PubMed

    Marczylo, Emma L; Amoako, Akwasi A; Konje, Justin C; Gant, Timothy W; Marczylo, Timothy H

    2012-05-01

    Recent work has suggested that environmental chemicals, including those contained in cigarette smoke, can have adverse effects on the exposed individuals as well as their future progeny. The mechanisms underlying transmission of environmentally induced phenotypes through the germ line are not well understood. However, a predominant process appears to be the establishment of permanent heritable epigenetic alterations, and a number of studies have implicated microRNAs in such processes. Here, we show that cigarette smoke induces specific differences in the spermatozoal microRNA content of human smokers compared with non-smokers, and that these altered microRNAs appear to predominantly mediate pathways vital for healthy sperm and normal embryo development, particularly cell death and apoptosis. microRNA-mediated perturbation of such pathways may explain how harmful phenotypes can be induced in the progeny of smokers.

  8. Cigarette smoke causes acute airway disease and exacerbates chronic obstructive lung disease in neonatal mice.

    PubMed

    Jia, Jie; Conlon, Thomas M; Ballester Lopez, Carolina; Seimetz, Michael; Bednorz, Mariola; Zhou-Suckow, Zhe; Weissmann, Norbert; Eickelberg, Oliver; Mall, Marcus A; Yildirim, Ali Önder

    2016-09-01

    Epidemiological evidence demonstrates a strong link between postnatal cigarette smoke (CS) exposure and increased respiratory morbidity in young children. However, how CS induces early onset airway disease in young children, and how it interacts with endogenous risk factors, remains poorly understood. We, therefore, exposed 10-day-old neonatal wild-type and β-epithelial sodium ion channel (β-ENaC)-transgenic mice with cystic fibrosis-like lung disease to CS for 4 days. Neonatal wild-type mice exposed to CS demonstrated increased numbers of macrophages and neutrophils in the bronchoalveolar lavage fluid (BALF), which was accompanied by increased levels of Mmp12 and Cxcl1 BALF from β-ENaC-transgenic mice contained greater numbers of macrophages, which did not increase following acute CS exposure; however, there was significant increase in airway neutrophilia compared with filtered air transgenic and CS-exposed wild-type controls. Interestingly, wild-type and β-ENaC-transgenic mice demonstrated epithelial airway and vascular remodeling following CS exposure. Morphometric analysis of lung sections revealed that CS exposure caused increased mucus accumulation in the airway lumen of neonatal β-ENaC-transgenic mice compared with wild-type controls, which was accompanied by an increase in the number of goblet cells and Muc5ac upregulation. We conclude that short-term CS exposure 1) induces acute airway disease with airway epithelial and vascular remodeling in neonatal wild-type mice; and 2) exacerbates airway inflammation, mucus hypersecretion, and mucus plugging in neonatal β-ENaC-transgenic mice with chronic lung disease. Our results in neonatal mice suggest that young children may be highly susceptible to develop airway disease in response to tobacco smoke exposure, and that adverse effects may be aggravated in children with underlying chronic lung diseases. PMID:27448665

  9. Acute fatal pericardial effusion induced by accidental ingestion of cigarette butts in a dog

    PubMed Central

    Kim, Jung-Hyun; Lim, Jae-Hyun

    2016-01-01

    A dog was referred for collapse and tachypnea after ingesting cigarette butts. Thoracic radiography and echocardiography indicated pericardial effusion, and an electrocardiogram showed tachycardia, variable QRS complexes, and ventricular premature complexes. This is the first description of fatal pericardial effusion associated with cigarette butt ingestion in a veterinary patient. PMID:26834265

  10. Acute fatal pericardial effusion induced by accidental ingestion of cigarette butts in a dog.

    PubMed

    Kim, Jung-Hyun; Lim, Jae-Hyun

    2016-02-01

    A dog was referred for collapse and tachypnea after ingesting cigarette butts. Thoracic radiography and echocardiography indicated pericardial effusion, and an electrocardiogram showed tachycardia, variable QRS complexes, and ventricular premature complexes. This is the first description of fatal pericardial effusion associated with cigarette butt ingestion in a veterinary patient.

  11. HDAC3 mediates smoking-induced pancreatic cancer

    PubMed Central

    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

  12. Smoking Induced Hemolysis: Spectral and microscopic investigations

    PubMed Central

    Masilamani, Vadivel; AlZahrani, Khalid; Devanesan, Sandhanasamy; AlQahtani, Hadi; AlSalhi, Mohamad Saleh

    2016-01-01

    Smoking is one of the major causes of lifestyle associated mortality and morbidity such as cancer of the oral cavity and lungs, and also cardiovascular diseases. In this study, we have provided evidences for the smoking-induced hemolysis using two methods: spectra of blood components and atomic force microscopic analysis of surface morphology. A total of 62 subjects (control = 31; smoker = 31: 21 male; 10 female in each set) were considered for the study. The findings indicate that smoking leads to potholes on the surface, swelling of shape, rupturing of erythrocytes, removal of hematoporphyrin and flushing into the plasma as metabolites of the erythrocyte. The overall morphology of the erythrocytes of the smoker group appears more like a Mexican hat. The mean surface roughness was 5.5 ± 3 nm for the smoker group, but 1.2 ± 0.2 nm for the control group. Such damages might help the toxins, (CO, peroxidants, aldehydes etc.,) to gain easy access and get strongly absorbed by the hemoglobin, leading to enhanced rates of hemolysis as shown by the spectral features of metabolites. This indicates that the average life span of the smoker’s erythrocytes is significantly less than that of the control group. PMID:26891995

  13. Acute stimulation of mesenchymal stem cells with cigarette smoke extract affects their migration, differentiation, and paracrine potential

    PubMed Central

    Wahl, Elizabeth A.; Schenck, Thilo L.; Machens, Hans-Günther; Egaña, J. Tomás

    2016-01-01

    Mesenchymal stem cells (MSCs) are known to play a key role in tissue regeneration, while smoking cigarettes is described to impair it. This work focuses on the effect cigarette smoke extract (CSE) has on the migration, differentiation, and paracrine potential of human adipose derived MSCs (AdMSCs). To mimic native conditions in vitro, AdMSCs were cultured in either monolayer or three-dimensional pellet cultures. While constant exposure to high concentrations of CSE had lethal effects on AdMSCs, lower concentrations of CSE impaired cell migration when compared to control conditions. The secretion of key interleukins was downregulated when CSE was exposed to the cells at low concentrations. Moreover, in this work AdMSCs were exposed to CSE while simultaneously being induced to differentiate into adipocytes, osteoblasts, and chondrocytes to determine the effect of CSE on the cells potential to differentiate. While adipogenic differentiation showed no significant variation, AdMSCs exposed to osteogenic and chondrogenic supplements showed both early and late genetic level variation when acutely exposed to low concentrations of CSE. Our results indicate that even a small amount of cigarette smoke can have detrimental effects on the regenerative potential of MSCs. PMID:26976359

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

    SciTech Connect

    Sobinoff, A.P.; Beckett, E.L.; Jarnicki, A.G.; Sutherland, J.M.; McCluskey, A.; Hansbro, P.M.; McLaughlin, E.A.

    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

  15. A single blueberry (Vaccinium corymbosum) portion does not affect markers of antioxidant defence and oxidative stress in healthy volunteers following cigarette smoking.

    PubMed

    Del Bo', Cristian; Porrini, Marisa; Campolo, Jonica; Parolini, Marina; Lanti, Claudia; Klimis-Zacas, Dorothy; Riso, Patrizia

    2016-03-01

    We previously reported that a portion of blueberries reversed endothelial dysfunction induced by acute cigarette smoking. Since smoking-induced endothelial dysfunction is associated with a condition of oxidative stress, we evaluated whether the observed effect was mediated by modulation of markers of oxidative stress and antioxidant defence. Fourteen out of 16 male healthy smokers previously enrolled, participated in a three-armed randomized controlled study with the following experimental conditions: smoking treatment (one cigarette); blueberry treatment (300g of blueberries) + smoking (one cigarette); control treatment (300ml of water with sugar) + smoking (one cigarette). The cigarette was smoked 100min after blueberry/control/water consumption. Each treatment was separated by 1 week of washout period. Plasma vitamin (C, B12 and folate) and aminothiol concentrations, endogenous [formamidopyrimidine-DNA glycosylase (FPG)-sensitive sites] and oxidatively induced DNA damage (resistance to H2O2-induced DNA damage) in peripheral blood mononuclear cells (PBMCs) were measured at baseline and 20, 60, 90, 120min and 24h after smoking. On the whole, analysis of variance did not show a significant effect of treatment on the modulation of markers of oxidative stress and antioxidant defence but revealed an effect of time for plasma concentrations of vitamin C (P = 0.003), B12 (P < 0.001), folate (P < 0.001), total cysteine (P = 0.007) and cysteine-glycine (P = 0.010) that increased following the three treatments after smoking. No significant effect of treatment was observed for the levels of FPG-sensitive sites (P > 0.05) and H2O2-induced DNA damage (P > 0.05) in PBMCs. In conclusion, the consumption of a single blueberry portion failed to modulate markers of oxidative stress and antioxidant defence investigated in our experimental conditions. Further studies are necessary to elucidate this finding and help clarifying the mechanisms of protection of blueberries against

  16. Acute systemic accumulation of acrolein in mice by inhalation at a concentration similar to that in cigarette smoke

    PubMed Central

    Tully, Melissa; Zheng, Lingxing; Acosta, Glen; Tian, Ran; Shi, Riyi

    2015-01-01

    Cigarette smoke is an important environmental factor associated with a wide array of public health concerns. Acrolein, a component of tobacco smoke and a known toxin to various cell types, may be a key pathological factor mediating the adverse effects linked with tobacco smoke. Although acrolein is known to accumulate in the respiratory system after acute nasal exposure, it is not clear if it accumulates systemically, and less is known in the nervous system. The aim of this study was to assess the degree of acrolein accumulation in the circulation and in the spinal cord following acute acrolein inhalation in mice. Using a laboratory-fabricated inhalation chamber, we found elevated urinary 3-HPMA, an acrolein metabolite, and increased acrolein adducts in the spinal cord after weeks of nasal exposure to acrolein at a concentration similar to that in tobacco smoke. The data indicated that acrolein is absorbed into the circulatory system and some enters the nervous system. It is expected that these findings may facilitate further studies to probe the pathological role of acrolein in the nervous system resulting from smoke and other external sources. PMID:25446876

  17. Acute systemic accumulation of acrolein in mice by inhalation at a concentration similar to that in cigarette smoke.

    PubMed

    Tully, Melissa; Zheng, Lingxing; Acosta, Glen; Tian, Ran; Shi, Riyi

    2014-12-01

    Cigarette smoke is an important environmental factor associated with a wide array of public health concerns. Acrolein, a component of tobacco smoke and a known toxin to various cell types, may be a key pathological factor mediating the adverse effects linked with tobacco smoke. Although acrolein is known to accumulate in the respiratory system after acute nasal exposure, it is not clear if it accumulates systemically, and less is known in the nervous system. The aim of this study was to assess the degree of acrolein accumulation in the circulation and in the spinal cord following acute acrolein inhalation in mice. Using a laboratory-fabricated inhalation chamber, we found elevated urinary 3-HPMA, an acrolein metabolite, and increased acrolein adducts in the spinal cord after weeks of nasal exposure to acrolein at a concentration similar to that in tobacco smoke. The data indicated that acrolein is absorbed into the circulatory system and some enters the nervous system. It is expected that these findings may facilitate further studies to probe the pathological role of acrolein in the nervous system resulting from smoke and other external sources.

  18. Acute prolapsed lumbar intervertebral disc. An epidemiologic study with special reference to driving automobiles and cigarette smoking.

    PubMed

    Kelsey, J L; Githens, P B; O'Conner, T; Weil, U; Calogero, J A; Holford, T R; White, A A; Walter, S D; Ostfeld, A M; Southwick, W O

    1984-09-01

    An epidemiologic case-control study to identify risk factors for acute prolapsed lumbar intervertebral disc was undertaken in Connecticut during 1979-1981. This paper focuses on nonoccupational factors of possible etiologic significance. Persons in their 30s were affected most frequently. Among surgical cases, the ratio of men to women was 1.5 to 1, while among probable and possible cases not undergoing surgery, the male to female ratio was about 1 to 1. Cigarette smoking in the past year was associated with an increased risk for prolapsed disc. The greater the number of hours spent in a motor vehicle, the higher the risk. Use of Swedish and Japanese cars was associated with a lower-than-average risk, while use of other cars was associated with a higher-than-average risk. For each type of car, older cars were associated with higher risks than newer cars. Variables that did not affect the risk for prolapsed lumbar disc in this study included height, weight, number of pregnancies, number of children, frequency of wearing shoes with high heels, smoking cigars or pipes, and participation in baseball or softball, golf, bowling, swimming, diving from a board, tennis, bicycling or jogging.

  19. The pathobiological impact of cigarette smoke on pancreatic cancer development (review).

    PubMed

    Wittel, Uwe A; Momi, Navneet; Seifert, Gabriel; Wiech, Thorsten; Hopt, Ulrich T; Batra, Surinder K

    2012-07-01

    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-induced pancreatic carcinogenesis is limited. Current data on cigarette smoke-induced pancreatic carcinogenesis indicate multifactorial events that are triggered by nicotine, which is the major pharmacologically active constituent of tobacco smoke. In addition to nicotine, a vast number of carcinogens have the potential to reach the pancreatic gland, where they are metabolized, in some instances to even more toxic compounds. These metabolic events are not restricted to pancreatic ductal cells. Several studies show that acinar cells are also greatly affected. Furthermore, pancreatic cancer progenitor cells do not only derive from the ductal epithelial lineage, but also from acinar cells. This sheds new light on cigarette smoke-induced acinar cell damage. On this background, our objective is to outline a multifactorial model of tobacco smoke-induced pancreatic carcinogenesis.

  20. Heme oxygenase-1 attenuates inflammation and oxidative damage in a rat model of smoke-induced emphysema.

    PubMed

    Wei, Jingjing; Fan, Guoquan; Zhao, Hui; Li, Jianqiang

    2015-11-01

    Emphysema is a serious disease of the respiratory system and is associated with inflammation and oxidative stress. Heme oxygenase-1 (HO-1), a rate-limiting enzyme involved in heme biosynthesis, exerts potent anti-inflammatory, antioxidant, anti-apoptotic and anti‑proliferative effects in various diseases. In the present study, we examined the effects of HO-1 on smoke‑induced emphysema, as well as the underlying mechanisms in a rat model of smoke-induced emphysema. Rats were either exposed to cigarette smoke or sham‑exposed for 20 weeks to establish the model of smoke-induced emphysema. The rats were subcutaneously injected with protoporphyrin IX [tin-protoporphyrin IX (SnPP) or ferriprotoporphyrin IX chloride (hemin)] during this period to examine the protective effects of HO-1. Subsequently, the development of emphysema, inflammatory cells, the levels of inflammatory mediators, particularly interleukin (IL)-17, tumor necrosis factor (TNF)‑α, monocyte chemotactic protein‑1 [MCP‑1, also known as chemokine (C-C motif) ligand 2 (CCL2)], IL-8 [also known as chemokine (C-X-C motif) ligand 8 (CXCL8)], macrophage inflammatory protein‑2α [MIP-2α, also known as chemokine (C-X-C motif) ligand 2 (CXCL2)] and IL-10, as well as the malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) content were determined. Exposure to smoke increased the total cell, neutrophil and macrophage counts in the bronchoalveolar lavage fluid (BALF). It also increased the levels of the inflammatory mediators, IL-17, TNF-α, MCP-1, IL-8 and MIP-2α, as well as the MDA content and induced emphysema. Treatment with hemin upregulated HO-1 expression and attenuated the development of smoke-induced emphysema by reducing inflammatory cell infiltration, decreasing the levels of inflammatory mediators and attenuating oxidative damage, to a certain extent. In conclusion, our findings demonstrate that HO-1 exerts anti-inflammatory and antioxidant effects, thus attenuating the

  1. Cigarette smoking and the thyroid.

    PubMed

    Bertelsen, J B; Hegedüs, L

    1994-01-01

    Relevant English language articles published from 1970 through 1993 regarding the possible influence of cigarette smoking on the thyroid were identified through a MEDLINE search and manual searches of identified articles. Thiocyanate in tobacco smoke influences the thyroid by a competitive inhibition of iodine uptake and organification in the gland. Also the stimulation of the sympathetic nervous system by cigarette smoke and benzpyrene, another constituent of tobacco, is thought to influence thyroid gland function. The thyroid hormones and TSH receptor autoantibodies are not affected by smoking, but serum TSH levels have been found to be slightly reduced. Smokers have a higher frequency of goiter and increased serum thyroglobulin levels, especially in iodine-deficient areas. Graves' ophthalmopathy is strongly associated with cigarette smoking; the more severe the eye disease the stronger the association. Graves' disease without ophthalmopathy is also associated with smoking, though this association is weaker. Thiocyanate level in cord blood equilibrates completely with the level in the mother, and a reverse correlation has been demonstrated between birth weight and thiocyanate level in cord blood. Cigarette smoking induces similar changes in thyroid function in the adult and the fetus. No separate study has elucidated the effects of cessation of smoking, but there seems to be longstanding effects induced by smoking, some probably irreversible.

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

    SciTech Connect

    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.

  3. Cigarette Smoke-Induced Interleukin-1 Alpha May Be Involved in the Pathogenesis of Adult Acne

    PubMed Central

    Yang, Yun Seok; Lim, Hee Kyeong; Hong, Kyung Kook; Shin, Min Kyung; Lee, Jin Woo; Lee, Sung Won

    2014-01-01

    Background Lipid peroxide (LPO) in comedones, which are produced as a result of sebum oxidation, might potentially induce interleukin-1α (IL-1α) and exacerbate comedogenesis and inflammatory changes in comedones. Objective To investigate the relationship of proinflammatory cytokines and LPO levels in the extracts of comedones with the acne of clinical difference between smokers and non-smokers, and with the severity and distribution of the acne lesions. Methods Twenty-two non-smoking and 21 smoking adult acne patients were evaluated by comedone extraction and measurement of proinflammatory cytokines and LPO levels. Acne severity and distribution of the lesions were also analyzed. Results Relative to the non-smoking group, smokers had significantly higher levels of IL-1α and LPO in comedones. Their levels showed a positive correlation. However, there were no statistically significant difference between the severity or distribution of the disease and the levels of LPO and IL-1α in comedones. Conclusion Smoking may be involved in the pathogenesis of adult acne by increasing the oxidative stress that results in subsequent accumulation of LPO in comedones. PMID:24648681

  4. Early response of gene clusters is associated with mouse lung resistance or sensitivity to cigarette smoke.

    PubMed

    Cavarra, Eleonora; Fardin, Paolo; Fineschi, Silvia; Ricciardi, Annamaria; De Cunto, Giovanna; Sallustio, Fabio; Zorzetto, Michele; Luisetti, Maurizio; Pfeffer, Ulrich; Lungarella, Giuseppe; Varesio, Luigi

    2009-03-01

    We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57BL/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, whereas ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype. The three strains of mice were exposed to smoke from three cigarettes per day, 5 days/wk, for 4 wk. Microarray analysis was carried out on total RNA extracted from the lung using the Affymetrix platform. Cigarette smoke modulates several clusters of genes (i.e., proemphysematous, acute phase response, and cell adhesion) in smoke-sensitive DBA/2 or C57BL/6J strains, but the same genes are not altered by smoke in ICR resistant mice. Only a few genes were commonly modulated by smoke in the three strains of mice. This pattern of gene expression suggests that the response to smoke is strain-dependent and may involve different molecular signaling pathways. Real-time quantitative PCR was used to verify the pattern of modulation of selected genes and their potential biological relevance. We conclude that gene expression response to smoke is highly dependent on the mouse genetic background. We speculate that the definition of gene clusters associated, to various degrees, with mouse susceptibility or resistance to smoke may be instrumental in defining the molecular basis of the individual response to smoke-induced lung injury in humans.

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

    PubMed Central

    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; Ligeiro de Oliveira, Ana Paula

    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

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

    PubMed

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

    2013-09-01

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

  7. Smoke-induced seed germination in California chaparral

    USGS Publications Warehouse

    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

  8. A multi-target antisense approach against PDE4 and PDE7 reduces smoke-induced lung inflammation in mice

    PubMed Central

    Fortin, Marylène; D'Anjou, Hélène; Higgins, Marie-Ève; Gougeon, Jasmine; Aubé, Paméla; Moktefi, Kamel; Mouissi, Sonia; Séguin, Serge; Séguin, Rosanne; Renzi, Paolo M; Paquet, Luc; Ferrari, Nicolay

    2009-01-01

    Background Recent development in the field of COPD has focused on strategies aimed at reducing the underlying inflammation through selective inhibition of the phosphodiesterase type IV (PDE4) isoform. Although the anti-inflammatory and bronchodilator activity of selective PDE4 inhibitors has been well documented, their low therapeutic ratio and dose-dependent systemic side effects have limited their clinical utility. This study examined the effect of 2'-deoxy-2'-Fluoro-β-D-Arabinonucleic Acid (FANA)-containing antisense oligonucleotides (AON) targeting the mRNA for the PDE4B/4D and 7A subtypes on lung inflammatory markers, both in vitro and in vivo. Methods Normal human bronchial epithelial (NHBE) cells were transfected with FANA AON against PDE4B/4D and 7A alone or in combination. mRNA levels for target PDE subtypes, as well as secretion of pro-inflammatory chemokines were then measured following cell stimulation. Mice were treated with combined PDE4B/4D and 7A AON via endo-tracheal delivery, or with roflumilast via oral delivery, and exposed to cigarette smoke for one week. Target mRNA inhibition, as well as influx of inflammatory cells and mediators were measured in lung lavages. A two-week smoke exposure protocol was also used to test the longer term potency of PDE4B/4D and 7A AONs. Results In NHBE cells, PDE4B/4D and 7A AONs dose-dependently and specifically inhibited expression of their respective target mRNA. When used in combination, PDE4B/4D and 7A AONs significantly abrogated the cytokine-induced secretion of IL-8 and MCP-1 to near baseline levels. In mice treated with combined PDE4B/4D and 7A AONs and exposed to cigarette smoke, significant protection against the smoke-induced recruitment of neutrophils and production of KC and pro-MMP-9 was obtained, which was correlated with inhibition of target mRNA in cells from lung lavages. In this model, PDE AONs exerted more potent and broader anti-inflammatory effects against smoke-induced lung inflammation

  9. Protocol for a human in vivo model of acute cigarette smoke inhalation challenge in smokers with COPD: monitoring the nasal and systemic immune response using a network biology approach

    PubMed Central

    Ross, Clare L; Galloway-Phillipps, Neil; Armstrong, Paul C; Mitchell, Jane A; Warner, Timothy D; Brearley, Christopher; Ito, Mari; Tunstall, Tanushree; Elkin, Sarah; Kon, Onn Min; Hansel, Trevor T; Paul-Clark, Mark J

    2015-01-01

    Introduction Cigarette smoke contributes to a diverse range of diseases including chronic obstructive pulmonary disease (COPD), cardiovascular disorders and many cancers. There currently is a need for human challenge models, to assess the acute effects of a controlled cigarette smoke stimulus, followed by serial sampling of blood and respiratory tissue for advanced molecular profiling. We employ precision sampling of nasal mucosal lining fluid by absorption to permit soluble mediators measurement in eluates. Serial nasal curettage was used for transcriptomic analysis of mucosal tissue. Methods and analysis Three groups of strictly defined patients will be studied: 12 smokers with COPD (GOLD Stage 2) with emphysema, 12 matched smokers with normal lung function and no evidence of emphysema, and 12 matched never smokers with normal spirometry. Patients in the smoking groups are current smokers, and will be given full support to stop smoking immediately after this study. In giving a controlled cigarette smoke stimulus, all patients will have abstained from smoking for 12 h, and will smoke two cigarettes with expiration through the nose in a ventilated chamber. Before and after inhalation of cigarette smoke, a series of samples will be taken from the blood, nasal mucosal lining fluid and nasal tissue by curettage. Analysis of plasma nicotine and metabolites in relation to levels of soluble inflammatory mediators in nasal lining fluid and blood, as well as assessing nasal transcriptomics, ex vivo blood platelet aggregation and leucocyte responses to toll-like receptor agonists will be undertaken. Implications Development of acute cigarette smoke challenge models has promise for the study of molecular effects of smoking in a range of pathological processes. Ethics and dissemination This study was approved by the West London National Research Ethics Committee (12/LO/1101). The study findings will be presented at conferences and will be reported in peer-reviewed journals

  10. Menthol Cigarettes

    MedlinePlus

    ... Use Supplement to the Current Population Survey (TUS-CPS) 2006/07. 2008, National Cancer Institute and Centers ... 07): http://cancercontrol.cancer.gov/brp/tcrb/tus-cps/ . U.S. Department of Commerce Census Bureau, Menthol Cigarette ...

  11. Electronic Cigarettes

    MedlinePlus

    ... and Figures Tobacco and Nicotine Smoked Tobacco Products Smokeless Tobacco Products Electronic Cigarettes New FDA Regulations HEALTH EFFECTS ... Secondhand Smoke Effects of Smoking on Your Health Smokeless Tobacco and Your Health Tobacco Use and Fertility Tobacco ...

  12. Cigarette smoking and acute myocardial infarction. A case-control study from the GISSI-2 trial. GISSI-EFRIM Investigators. Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto--Epidemiologia dei Fattori di Rischio dell'infarto Miocardioco.

    PubMed

    Negri, E; La Vecchia, C; Nobili, A; D'Avanzo, B; Bechi, S

    1994-08-01

    To make a further quantitative assessment of the relationship between cigarette smoking and the risk of myocardial infarction, a multicentric case-control study was conducted in Italy between September 1988 and June 1989 within the framework of the GISSI-2 trial. Ninety hospitals in various Italian Regions participated. 916 cases of acute myocardial infarction with no history of ischaemic heart disease and 1106 controls admitted to hospital for acute conditions not related to known or suspected risk factors for ischaemic heart disease were studied. Relative risks (RR) and 95% confidence intervals (CI) of myocardial infarction according to various measures of tobacco smoking, were adjusted for identified potential confounding factors using multiple logistic regression. Compared to lifelong non-smokers, the RR was 1.3 (95% CI 1.0 to 1.9) for ex-smokers, 2.0 (95% CI 1.4 to 2.9) for current smokers of less than 15 cigarettes per day, 3.1 (95% CI 2.2 to 4.2) for 15-24 cigarettes per day and 4.9 (95% CI 3.4 to 7.1) for 25 or more cigarettes per day. No trend in risk was evident for the duration, the RR being around 3 for subsequent categories. There was a significant interaction between smoking and age. Below the age 45, smokers of 25 or more cigarettes per day had a 33 times higher risk than non-smokers, compared to 7.5 at in the age group 45-54, 4.4 between the ages 55-64 and 2.5 at the age of 65 or over. The risk estimates were higher in women (RR for > or = 25 cigarettes per day = 10.1), in subjects in the lowest cholesterol tertile (RR = 11.9), with no history of diabetes (RR = 6.8), hypertension (RR = 9.5), no family history ischaemic heart disease (RR = 9.1) and low body mass index (RR = 9.3). The importance of smoking is confirmed as a cause of acute myocardial infarction: about 50% of all nonfatal infarctions in this Italian population could be attributable to cigarette smoking.(ABSTRACT TRUNCATED AT 250 WORDS)

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

    PubMed

    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

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

    PubMed

    Toda, Noboru; Okamura, Tomio

    2016-08-01

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

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

    PubMed Central

    Birru, Rahel L.; Di, Y. Peter

    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 SHS, 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. PMID:22973236

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

    PubMed Central

    Aoshiba, K; Nagai, A

    2003-01-01

    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. PMID:19570263

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

    PubMed Central

    Aoshiba, K; Nagai, A

    2003-01-01

    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.

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

    PubMed Central

    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

  19. Transient and Persistent Metabolomic Changes in Plasma following Chronic Cigarette Smoke Exposure in a Mouse Model

    PubMed Central

    Cruickshank-Quinn, Charmion I.; Mahaffey, Spencer; Justice, Matthew J.; Hughes, Grant; Armstrong, Michael; Bowler, Russell P.; Reisdorph, Richard; Petrache, Irina; Reisdorph, Nichole

    2014-01-01

    Cigarette smoke exposure is linked to the development of a variety of chronic lung and systemic diseases in susceptible individuals. Metabolomics approaches may aid in defining disease phenotypes, may help predict responses to treatment, and could identify biomarkers of risk for developing disease. Using a mouse model of chronic cigarette smoke exposure sufficient to cause mild emphysema, we investigated whether cigarette smoke induces distinct metabolic profiles and determined their persistence following smoking cessation. Metabolites were extracted from plasma and fractionated based on chemical class using liquid-liquid and solid-phase extraction prior to performing liquid chromatography mass spectrometry-based metabolomics. Metabolites were evaluated for statistically significant differences among group means (p-value≤0.05) and fold change ≥1.5). Cigarette smoke exposure was associated with significant differences in amino acid, purine, lipid, fatty acid, and steroid metabolite levels compared to air exposed animals. Whereas 60% of the metabolite changes were reversible, 40% of metabolites remained persistently altered even following 2 months of smoking cessation, including nicotine metabolites. Validation of metabolite species and translation of these findings to human plasma metabolite signatures induced by cigarette smoking may lead to the discovery of biomarkers or pathogenic pathways of smoking-induced disease. PMID:25007263

  20. Cardiovascular toxicity of nicotine: Implications for electronic cigarette use.

    PubMed

    Benowitz, Neal L; Burbank, Andrea D

    2016-08-01

    The cardiovascular safety of nicotine is an important question in the current debate on the benefits vs. risks of electronic cigarettes and related public health policy. Nicotine exerts pharmacologic effects that could contribute to acute cardiovascular events and accelerated atherogenesis experienced by cigarette smokers. Studies of nicotine medications and smokeless tobacco indicate that the risks of nicotine without tobacco combustion products (cigarette smoke) are low compared to cigarette smoking, but are still of concern in people with cardiovascular disease. Electronic cigarettes deliver nicotine without combustion of tobacco and appear to pose low-cardiovascular risk, at least with short-term use, in healthy users. PMID:27079891

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

    NASA Astrophysics Data System (ADS)

    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.

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

    PubMed Central

    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

  3. A Protocol for Detecting and Scavenging Gas-phase Free Radicals in Mainstream Cigarette Smoke

    PubMed Central

    Yu, Long-Xi; Dzikovski, Boris G.; Freed, Jack H.

    2012-01-01

    Cigarette smoking is associated with human cancers. It has been reported that most of the lung cancer deaths are caused by cigarette smoking 5,6,7,12. Although tobacco tars and related products in the particle phase of cigarette smoke are major causes of carcinogenic and mutagenic related diseases, cigarette smoke contains significant amounts of free radicals that are also considered as an important group of carcinogens9,10. Free radicals attack cell constituents by damaging protein structure, lipids and DNA sequences and increase the risks of developing various types of cancers. Inhaled radicals produce adducts that contribute to many of the negative health effects of tobacco smoke in the lung3. Studies have been conducted to reduce free radicals in cigarette smoke to decrease risks of the smoking-induced damage. It has been reported that haemoglobin and heme-containing compounds could partially scavenge nitric oxide, reactive oxidants and carcinogenic volatile nitrosocompounds of cigarette smoke4. A 'bio-filter' consisted of haemoglobin and activated carbon was used to scavenge the free radicals and to remove up to 90% of the free radicals from cigarette smoke14. However, due to the cost-ineffectiveness, it has not been successfully commercialized. Another study showed good scavenging efficiency of shikonin, a component of Chinese herbal medicine8. In the present study, we report a protocol for introducing common natural antioxidant extracts into the cigarette filter for scavenging gas phase free radicals in cigarette smoke and measurement of the scavenge effect on gas phase free radicals in mainstream cigarette smoke (MCS) using spin-trapping Electron Spin Resonance (ESR) Spectroscopy1,2,14. We showed high scavenging capacity of lycopene and grape seed extract which could point to their future application in cigarette filters. An important advantage of these prospective scavengers is that they can be obtained in large quantities from byproducts of tomato or wine

  4. A protocol for detecting and scavenging gas-phase free radicals in mainstream cigarette smoke.

    PubMed

    Yu, Long-Xi; Dzikovski, Boris G; Freed, Jack H

    2012-01-02

    Cigarette smoking is associated with human cancers. It has been reported that most of the lung cancer deaths are caused by cigarette smoking (5,6,7,12). Although tobacco tars and related products in the particle phase of cigarette smoke are major causes of carcinogenic and mutagenic related diseases, cigarette smoke contains significant amounts of free radicals that are also considered as an important group of carcinogens(9,10). Free radicals attack cell constituents by damaging protein structure, lipids and DNA sequences and increase the risks of developing various types of cancers. Inhaled radicals produce adducts that contribute to many of the negative health effects of tobacco smoke in the lung(3). Studies have been conducted to reduce free radicals in cigarette smoke to decrease risks of the smoking-induced damage. It has been reported that haemoglobin and heme-containing compounds could partially scavenge nitric oxide, reactive oxidants and carcinogenic volatile nitrosocompounds of cigarette smoke(4). A 'bio-filter' consisted of haemoglobin and activated carbon was used to scavenge the free radicals and to remove up to 90% of the free radicals from cigarette smoke(14). However, due to the cost-ineffectiveness, it has not been successfully commercialized. Another study showed good scavenging efficiency of shikonin, a component of Chinese herbal medicine(8). In the present study, we report a protocol for introducing common natural antioxidant extracts into the cigarette filter for scavenging gas phase free radicals in cigarette smoke and measurement of the scavenge effect on gas phase free radicals in mainstream cigarette smoke (MCS) using spin-trapping Electron Spin Resonance (ESR) Spectroscopy(1,2,14). We showed high scavenging capacity of lycopene and grape seed extract which could point to their future application in cigarette filters. An important advantage of these prospective scavengers is that they can be obtained in large quantities from byproducts of

  5. Acute secondhand smoke-induced pulmonary inflammation is diminished in RAGE knockout mice.

    PubMed

    Wood, Tyler T; Winden, Duane R; Marlor, Derek R; Wright, Alex J; Jones, Cameron M; Chavarria, Michael; Rogers, Geraldine D; Reynolds, Paul R

    2014-11-15

    The receptor for advanced glycation end-products (RAGE) has increasingly been demonstrated to be an important modulator of inflammation in cases of pulmonary disease. Published reports involving tobacco smoke exposure have demonstrated increased expression of RAGE, its participation in proinflammatory signaling, and its role in irreversible pulmonary remodeling. The current research evaluated the in vivo effects of short-term secondhand smoke (SHS) exposure in RAGE knockout and control mice compared with identical animals exposed to room air only. Quantitative PCR, immunoblotting, and immunohistochemistry revealed elevated RAGE expression in controls after 4 wk of SHS exposure and an anticipated absence of RAGE expression in RAGE knockout mice regardless of smoke exposure. Ras activation, NF-κB activity, and cytokine elaboration were assessed to characterize the molecular basis of SHS-induced inflammation in the mouse lung. Furthermore, bronchoalveolar lavage fluid was procured from RAGE knockout and control animals for the assessment of inflammatory cells and molecules. As a general theme, inflammation coincident with leukocyte recruitment was induced by SHS exposure and significantly influenced by the availability of RAGE. These data reveal captivating information suggesting a role for RAGE signaling in lungs exposed to SHS. However, ongoing research is still warranted to fully explain roles for RAGE and other receptors in cells coping with involuntary smoke exposure for prolonged periods of time.

  6. Modification of LCAT activity and HDL structure. New links between cigarette smoke and coronary heart disease risk.

    PubMed

    McCall, M R; van den Berg, J J; Kuypers, F A; Tribble, D L; Krauss, R M; Knoff, L J; Forte, T M

    1994-02-01

    The mechanism(s) through which smoking influences the progression of atherosclerosis is poorly understood. Recent evidence suggests that oxidants present in the gas phase of cigarette smoke are involved. We exposed human plasma to the filtered gas phase of cigarette smoke to assess its effects on plasma components involved in the antiatherogenic reverse cholesterol transport pathway. In our model, freshly isolated plasma (24 mL) was exposed to filtered air or gas-phase cigarette smoke for up to 6 hours at 37 degrees C. Lecithin-cholesterol acyltransferase (LCAT) activity was dramatically inhibited by cigarette smoke. A single 15-minute exposure to the smoke from an eighth of a cigarette was sufficient to reduce LCAT activity by 7%; additional exposures resulted in further decreases in activity. At 6 hours, only 22% of control LCAT activity remained in plasma exposed to smoke. Compared with control, gas-phase cigarette smoke-exposed plasma possessed high-density lipoprotein (HDL) with increased (16%) negative charge and with cross-linked apolipoproteins AI and AII. These data demonstrate that gas-phase cigarette smoke can inhibit a key enzyme (LCAT) and modify an integral lipid transport particle (HDL) that are essential components for the normal function of the reverse cholesterol transport pathway. Gas-phase cigarette smoke-induced modification of the reverse cholesterol transport pathway may provide a new mechanistic link between cigarette smoke and coronary heart disease risk.

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

    PubMed

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

    2005-01-01

    Cigarette smoking is implicated as a major risk factor in the development of cardiovascular and cerebrovascular diseases. Creatine kinase (CK) and its isoforms (CK-MM, MB, BB) have been advocated as sensitive markers in the assessment of cardiac and cerebral damage. Therefore, in the present study, we report the isoenzyme patterns of CK in rats upon exposure to cigarette smoke and the protective effect of Bacoside A against chronic smoking induced toxicity. Adult male albino rats were exposed to cigarette smoke and simultaneously administered with Bacoside A, the active constituent from the plant Bacopa monniera, for a period of 12 weeks. The activity of CK was assayed in serum, heart and brain, and its isoenzymes in serum were separated electrophoretically. Rats exposed to cigarette smoke showed significant increase in serum CK activity with concomitant decrease in heart and brain. Also cigarette smoke exposure resulted in a marked increase in all the three isoforms in serum. Administration of Bacoside A prevented these alterations induced by cigarette smoking. Cigarette smoking is known to cause free radical mediated lipid peroxidation leading to increased membrane permeability and cellular damage in the heart and brain resulting in the release of CK into the circulation. The protective effect of Bacoside A on the structural and functional integrity of the membrane prevented the leakage of CK from the respective tissues, which could be attributed to its free radical scavenging and anti-lipid peroxidative effect.

  8. Brain oxidative damage restored by Sesbania grandiflora in cigarette smoke-exposed rats.

    PubMed

    Ramesh, Thiyagarajan; Sureka, Chandrabose; Bhuvana, Shanmugham; Begum, Vavamohaideen Hazeena

    2015-08-01

    Cigarette smoking has been associated with high risk of neurological diseases such as stroke, Alzheimer's disease, multiple sclerosis, etc., The present study was designed to evaluate the restorative effects of Sesbania grandiflora (S. grandiflora) on oxidative damage induced by cigarette smoke exposure in the brain of rats. Adult male Wistar-Kyoto rats were exposed to cigarette smoke for a period of 90 days and consecutively treated with S. grandiflora aqueous suspension (SGAS, 1000 mg/kg body weight per day by oral gavage) for a period of 3 weeks. The levels of protein carbonyl, nitric oxide, and activities of cytochrome P450, NADPH oxidase and xanthine oxidase were significantly increased, whereas the levels of total thiol, protein thiol, non-protein thiol, nucleic acids, tissue protein and the activities of Na(+)/K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase were significantly diminished in the brain of rats exposed to cigarette smoke as compared with control rats. Also cigarette smoke exposure resulted in a significant alteration in brain total lipid, total cholesterol, triglycerides and phospholipids content. Treatment of SGAS is regressed these alterations induced by cigarette smoke. The results of our study suggest that S. grandiflora restores the brain from cigarette smoke induced oxidative damage. S. grandiflora could have rendered protection to the brain by stabilizing their cell membranes and prevented the protein oxidation, probably through its free radical scavenging and anti-peroxidative effect.

  9. Could zinc prevent reproductive alterations caused by cigarette smoke in male rats?

    PubMed

    Garcia, Patrícia Carvalho; Piffer, Renata Carolina; Gerardin, Daniela Cristina Cecatto; Sankako, Michele Kimie; Alves de Lima, Rodrigo Otávio; Pereira, Oduvaldo Câmara Marques

    2012-01-01

    The aim of the present study was to evaluate the effects of zinc on fertility through semen parameters, testosterone level and oxidative DNA damage to spermatozoa of rats exposed to cigarette smoke. Male Wistar rats (60 days old) were divided into four groups (n = 10 per group): control, cigarette-smoking (20 cigarettes per day), zinc (zinc chloride 20 mg kg⁻¹ day⁻¹) and zinc plus cigarette-smoking (zinc chloride 20 mg kg⁻¹ day⁻¹; 20 cigarettes per day). The treatment was applied for nine weeks and the following parameters were analysed: bodyweight, wet weights of the reproductive organs and the adrenal gland, plasma testosterone concentration, testicular function (seminal analysis and daily sperm production) and sperm DNA oxidative damage. The exposure to cigarette smoke decreased testosterone concentration, the percentage of normal morphology and the motility of spermatozoa. In addition, this exposure increased sperm DNA oxidative damage. Zinc treatment protected against the toxic damage that smoking caused to spermatozoa. This study showed a correlation between smoking and possible male infertility and subfertility, and also that the majority of smoking-induced changes in spermatozoa were prevented by zinc treatment. In conclusion, zinc, an antioxidant and stimulant of cell division, can be indicated as a promising treatment in men with infertility caused by the toxic components of cigarette smoke.

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

    PubMed Central

    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

  11. Phagocytosis of latex beads by alveolar macrophages from mice exposed to cigarette smoke.

    PubMed

    Ortega, E; Hueso, F; Collazos, M E; Pedrera, M I; Barriga, C; Rodríguez, A B

    1992-04-01

    Cigarette smoking is known to alter the numerical presence and function of alveolar macrophages. It has been speculated that these cigarette-smoke-induced alterations contribute to the depressed pulmonary defence mechanism commonly demonstrated in smokers. Studies of the phagocytic and bactericidal activities of alveolar macrophages from smokers and non-smokers have yielded conflicting results. The purpose of this study was to investigate the phagocytic capacity of alveolar macrophages from mice exposed to cigarette smoke in relation to the ability to ingest inert particles (latex beads). Measurements were made before (basal values), immediately after, and 1, 12 or 24 h after exposure. Significant decreases were observed in the number of latex beads ingested by 100 macrophages (phagocytic index) and in the phagocytic efficiency for ingesting latex (mean number of latex beads ingested per activated macrophages) immediately after and 1 h after exposure, and in the number of activated macrophages (those with phagocytic activity) immediately after exposure. PMID:1563261

  12. The Effect of Cigarette Smoke Exposure on Developing Folate Binding Protein-2 Null Mice

    PubMed Central

    Horn, Kristin H.; Esposito, Emily R.; Greene, Robert M.; Pisano, M. Michele

    2008-01-01

    Environmental tobacco smoke exposures have been linked to adverse health effects. Folate is essential for normal development, with deficiencies often causing fetal growth restriction. Mice lacking the folate binding protein-2 receptor (Folr2) exhibit increased susceptibility to teratogens. The purpose of the current study was to determine if the loss of Folr2 would increase sensitivity to cigarette smoke-induced effects on development. Pregnant Folr2−/−, Folr2+/+, and C57BL/6J mice were exposed to sidestream cigarette smoke during gestation. Exposure to sidestream smoke on gd 6–9 had no adverse effects on fetal outcomes. However, cigarette smoke exposure on gd 6–18 increased the number of fetal resorptions (Folr2−/− cohort) and decreased crown-rump length (Folr2+/+ fetuses). These data confirm an association between sidestream smoke exposure and fetal growth restriction, but do not suggest that loss of Folr2 increased susceptibility to these effects. PMID:18992323

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

    PubMed Central

    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

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

    PubMed

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

    2014-12-01

    Cigarette smoking causes oxidative stress, hypertension and endothelial dysfunction. Polyphenol-rich foods may prevent these conditions. We investigated the effect of a single serving of fresh-frozen blueberry intake on peripheral arterial function and arterial stiffness in young smokers. Sixteen male smokers were recruited for a 3-armed randomized-controlled study with the following experimental conditions: smoking treatment (one cigarette); blueberry treatment (300 g of blueberry) + smoking; control treatment (300 mL of water with sugar) + smoking. Each treatment was separated by one week of wash-out period. The blood pressure, heart rate, peripheral arterial function (reactive hyperemia and Framingham reactive hyperemia), and arterial stiffness (digital augmentation index, digital augmentation index normalized for a heart rate of 75 bpm) were measured before and 20 min after smoking with Endo-PAT2000. Smoking impaired the blood pressure, heart rate and peripheral arterial function, but did not affect the arterial stiffness. Blueberry consumption counteracted the impairment of the reactive hyperemia index induced by smoking (-4.4 ± 0.8% blueberry treatment vs. -22.0 ± 1.1% smoking treatment, p < 0.01) and Framingham reactive hyperemia (+28.3 ± 19.2% blueberry treatment vs. -42.8 ± 20.0% smoking treatment, p < 0.0001), and the increase of systolic blood pressure (+8.4 ± 0.02% blueberry treatment vs. +13.1 ± 0.02% smoking treatment, mmHg, p < 0.05) after cigarette smoking. No effect was observed for arterial stiffness and other vital signs. In conclusion, data obtained suggest a protective role of blueberry on reactive hyperemia, Framingham reactive hyperemia, and systolic blood pressure in subjects exposed to smoke of one cigarette. Future studies are necessary to elucidate the mechanisms involved.

  15. Cigars, Cigarettes, and Adolescents

    ERIC Educational Resources Information Center

    Brooks, Ashley; Larkin, Elizabeth M. Gaier; Kishore, Sonal; Frank, Scott

    2008-01-01

    Objective: To examine public health implications of adolescent use of cigars only, cigarettes only, and both cigarettes and cigars. Methods: A cross-sectional health risk survey was administered to a random sample of 4486 high school students in a Midwestern county. Results: More adolescents reported using both cigarettes and cigars (10.6%) than…

  16. 1α,25-dihydroxyvitamin D₃ counteracts the effects of cigarette smoke in airway epithelial cells.

    PubMed

    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.

  17. Toxicity of cigarette butts, and their chemical components, to marine and freshwater fish

    PubMed Central

    Gersberg, Richard M; Watanabe, Kayo; Rudolph, John; Stransky, Chris; Novotny, Thomas E

    2011-01-01

    Background Cigarette butts are the most common form of litter, as an estimated 4.5 trillion cigarette butts are thrown away every year worldwide. Many chemical products are used during the course of growing tobacco and manufacturing cigarettes, the residues of which may be found in cigarettes prepared for consumption. Additionally, over 4000 chemicals may also be introduced to the environment via cigarette particulate matter (tar) and mainstream smoke. Methods Using US Environmental Protection Agency standard acute fish bioassays, cigarette butt-derived leachate was analysed for aquatic toxicity. Survival was the single endpoint and data were analysed using Comprehensive Environmental Toxicity Information System to identify the LC50 of cigarette butt leachate to fish. Results The LC50 for leachate from smoked cigarette butts (smoked filter + tobacco) was approximately one cigarette butt/l for both the marine topsmelt (Atherinops affinis) and the freshwater fathead minnow (Pimephales promelas). Leachate from smoked cigarette filters (no tobacco), was less toxic, with LC50 values of 1.8 and 4.3 cigarette butts/l, respectively for both fish species. Unsmoked cigarette filters (no tobacco) were also found to be toxic, with LC50 values of 5.1 and 13.5 cigarette butts/l, respectively, for both fish species. Conclusion Toxicity of cigarette butt leachate was found to increase from unsmoked cigarette filters (no tobacco) to smoked cigarette filters (no tobacco) to smoked cigarette butts (smoked filter + tobacco). This study represents the first in the literature to investigate and affirm the toxicity of cigarette butts to fish, and will assist in assessing the potential ecological risks of cigarette butts to the aquatic environment. PMID:21504921

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

    PubMed

    1997-02-14

    During 1995, the American Association of Poison Control Centers (AAPCC) received 7917 reports of potentially toxic exposures to tobacco products among children aged < or = 6 years in the United States. Most cases of nicotine poisoning among children result from their ingestion of cigarettes or cigars. Acute nicotine poisoning is characterized by rapid onset of symptoms that may be severe when large amounts have been ingested. During January 1994-July 1996, the Rhode Island Poison Control Center (RIPCC) received 146 reports of ingestion of products containing nicotine by children aged < or = 6 years. To characterize risk factors for and outcomes associated with ingestion of cigarettes and cigarette butts among children aged < or = 6 years, the Rhode Island Department of Health (RIDH) analyzed data from the RIPCC and the 1996 Rhode Island Health Interview Survey (RIHIS). This report summarizes the findings of the study, which indicate that ingestion of cigarettes and cigarette butts by children aged < or = 6 years resulted in minor toxic effects and occurred more frequently in households where smoking was permitted in the presence of children and where cigarettes and cigarette wastes were accessible to children.

  19. NF-κB-mediated inflammation leading to EMT via miR-200c is involved in cell transformation induced by cigarette smoke extract.

    PubMed

    Zhao, Yue; Xu, Yuan; Li, Yuan; Xu, Wenchao; Luo, Fei; Wang, Bairu; Pang, Ying; Xiang, Quanyong; Zhou, Jianwei; Wang, Xinru; Liu, Qizhan

    2013-10-01

    Cigarette smoking constitutes a major human health hazard because it is the most important risk factor for lung cancer. Although evidence for smoking-induced lung cancer in humans is strong, the molecular mechanisms by which smoking causes cancer remain to be established. In this investigation, we evaluated the roles of inflammation and the epithelial-mesenchymal transition (EMT) in cigarette smoke extract (CSE)-induced transformation of human bronchial epithelial (HBE) cells. The results showed that chronic exposure to CSE induced EMT and transformation of these cells. Activation of nuclear factor-κB (NF-κB) by CSE increased levels of the proinflammatory interleukin-6 (IL-6), and acute and chronic exposures to CSE caused decreases in miR-200c levels. By blocking NF-κB with Bay11-7082 and IL-6 with anti-IL-6 antibody and enhancement of IL-6 with human recombinant IL-6, we found that the NF-κB signal pathway was involved in CSE-induced increases of IL-6, which suppressed miR-200c expression and promoted EMT. Moreover, IL-6 was necessary for maintenance of CSE-induced transformation and for malignant progression of HBE cells. Finally, blocking of NF-κB with Bay11-7082 prevented CSE-induced EMT and malignant transformation due to decreases of E-cadherin and miR-200c and elevations of IL-6, N-cadherin, and vimentin. Thus, we have defined a link between inflammation and EMT, processes involved in the malignant transformation of cells caused by CSE. This link, mediated through miRNAs, establishes a mechanism for CSE-induced lung carcinogenesis.

  20. NF-κB-mediated inflammation leading to EMT via miR-200c is involved in cell transformation induced by cigarette smoke extract.

    PubMed

    Zhao, Yue; Xu, Yuan; Li, Yuan; Xu, Wenchao; Luo, Fei; Wang, Bairu; Pang, Ying; Xiang, Quanyong; Zhou, Jianwei; Wang, Xinru; Liu, Qizhan

    2013-10-01

    Cigarette smoking constitutes a major human health hazard because it is the most important risk factor for lung cancer. Although evidence for smoking-induced lung cancer in humans is strong, the molecular mechanisms by which smoking causes cancer remain to be established. In this investigation, we evaluated the roles of inflammation and the epithelial-mesenchymal transition (EMT) in cigarette smoke extract (CSE)-induced transformation of human bronchial epithelial (HBE) cells. The results showed that chronic exposure to CSE induced EMT and transformation of these cells. Activation of nuclear factor-κB (NF-κB) by CSE increased levels of the proinflammatory interleukin-6 (IL-6), and acute and chronic exposures to CSE caused decreases in miR-200c levels. By blocking NF-κB with Bay11-7082 and IL-6 with anti-IL-6 antibody and enhancement of IL-6 with human recombinant IL-6, we found that the NF-κB signal pathway was involved in CSE-induced increases of IL-6, which suppressed miR-200c expression and promoted EMT. Moreover, IL-6 was necessary for maintenance of CSE-induced transformation and for malignant progression of HBE cells. Finally, blocking of NF-κB with Bay11-7082 prevented CSE-induced EMT and malignant transformation due to decreases of E-cadherin and miR-200c and elevations of IL-6, N-cadherin, and vimentin. Thus, we have defined a link between inflammation and EMT, processes involved in the malignant transformation of cells caused by CSE. This link, mediated through miRNAs, establishes a mechanism for CSE-induced lung carcinogenesis. PMID:23824089

  1. Resolvins attenuate inflammation and promote resolution in cigarette smoke-exposed human macrophages.

    PubMed

    Croasdell, Amanda; Thatcher, Thomas H; Kottmann, R Matthew; Colas, Romain A; Dalli, Jesmond; Serhan, Charles N; Sime, Patricia J; Phipps, Richard P

    2015-10-15

    Inflammation is a protective response to injury, but it can become chronic, leading to tissue damage and disease. Cigarette smoke causes multiple inflammatory diseases, which account for thousands of deaths and cost billions of dollars annually. Cigarette smoke disrupts the function of immune cells, such as macrophages, by prolonging inflammatory signaling, promoting oxidative stress, and impairing phagocytosis, contributing to increased incidence of infections. Recently, new families of lipid-derived mediators, "specialized proresolving mediators" (SPMs), were identified. SPMs play a critical role in the active resolution of inflammation by counterregulating proinflammatory signaling and promoting resolution pathways. We have identified dysregulated concentrations of lipid mediators in exhaled breath condensate, bronchoalveolar lavage fluid, and serum from patients with chronic obstructive pulmonary disease (COPD). In human alveolar macrophages from COPD and non-COPD patients, D-series resolvins decreased inflammatory cytokines and enhanced phagocytosis. To further investigate the actions of resolvins on human cells, macrophages were differentiated from human blood monocytes and treated with D-series resolvins and then exposed to cigarette smoke extract. Resolvins significantly suppressed macrophage production of proinflammatory cytokines, enzymes, and lipid mediators. Resolvins also increased anti-inflammatory cytokines, promoted an M2 macrophage phenotype, and restored cigarette smoke-induced defects in phagocytosis, highlighting the proresolving functions of these molecules. These actions were receptor-dependent and involved modulation of canonical and noncanonical NF-κB expression, with the first evidence for SPM action on alternative NF-κB signaling. These data show that resolvins act on human macrophages to attenuate cigarette smoke-induced inflammatory effects through proresolving mechanisms and provide new evidence of the therapeutic potential of SPMs.

  2. [The comparative analysis: the occurrence of acute respiratory system infections and chronic diseases among active smokers and non-smokers].

    PubMed

    Kałucka, Sylwia

    2006-01-01

    Cigarette smoking is one of the factors causing a lot of health problems. Breathing the smoke makes the development of arteriosclerosis and ischemic heart disease faster and the risk of myocardial infarction much higher. Toxic substances contained in the smoke induce inflammatory processes in bronchial tree, which finally leads to the destruction of lungs. One of the way of preventing complications in the circulatory system and stopping the inflammatory process in lungs is to give up the habit of smoking. Within the period of three years the group of more than 1000 people (smokers and non-smokers) was examined and the analysis of occurrence of acute respiratory system infections and chronic diseases was conducted. In the studies the questionnaire prepared by the author of the paper, some specialistic studies and medical reports were used. The achieved results show that more and more women smoke as many cigarettes as men and for as many years as they do. Both men and women who graduated either a grammar school or a university smoke more often than with elementary level of education. People who smoke suffer more often from numerous acute respiratory tract infections and must more often pay a visit to general practitioner. Considering the sex there are no statistically significant differences in the occurrence of chronic pulmonary diseases and the cardiovascular system. The achieved results show the changes of the attitude to smoking in Polish society. The increase of the consumption of cigarettes among women with high education is very worrying. It is a serious challenge for the whole medical staff. PMID:17288171

  3. Vapours of US and EU Market Leader Electronic Cigarette Brands and Liquids Are Cytotoxic for Human Vascular Endothelial Cells

    PubMed Central

    Putzhammer, Raphaela; Doppler, Christian; Jakschitz, Thomas; Heinz, Katharina; Förste, Juliane; Danzl, Katarina; Messner, Barbara; Bernhard, David

    2016-01-01

    The present study was conducted to provide toxicological data on e-cigarette vapours of different e-cigarette brands and liquids from systems viewed as leaders in the e-cigarette market and to compare e-cigarette vapour toxicity to the toxicity of conventional strong high-nicotine cigarette smoke. Using an adapted version of a previously constructed cigarette smoke constituent sampling device, we collected the hydrophilic fraction of e-cigarette vapour and exposed human umbilical vein endothelial cells (HUVECs) to the mixture of compounds present in the vapour of 4 different single-use e-cigarettes, 6 different liquid vapours produced by the same refillable e-cigarette, and one e-cigarette with an exchangeable liquid cartridge. After incubation of cells with various concentrations and for various periods of time we analysed cell death induction, proliferation rates, the occurrence of intra-cellular reactive oxygen species, cell morphology, and we also measured e-cigarette heating coil temperatures. Overall, conventional cigarette smoke extract showed the most severe impact on endothelial cells. However, some e-cigarette vapour extracts showed high cytotoxicity, inhibition of cell proliferation, and alterations in cell morphology, which were comparable to conventional high-nicotine cigarettes. The vapours generated from different liquids using the same e-cigarette show substantial differences, pointing to the liquids as an important source for toxicity. E-cigarette vapour-mediated induction of oxidative stress was significant in one out of the 11 analysed vapours. There is a high variability in the acute cytotoxicity of e-cigarette vapours depending on the liquid and on the e-cigarettes used. Some products showed toxic effects close to a conventional high-nicotine cigarette. Liquid nicotine, menthol content, and the formation of acute intracellular reactive oxygen species do not seem to be the central elements in e-cigarette vapour toxicity. PMID:27351725

  4. Alterations of gene expression in skin and lung of mice exposed to light and cigarette smoke.

    PubMed

    Izzotti, Alberto; Cartiglia, Cristina; Longobardi, Mariagrazia; Balansky, Roumen M; D'Agostini, Francesco; Lubet, Ronald A; De Flora, Silvio

    2004-10-01

    We previously showed that sunlight-mimicking light induces genotoxic damage not only in skin but also even in lung, bone marrow, and peripheral blood of hairless mice. Moreover, light and smoke acted synergically in the respiratory tract. To clarify the mechanisms involved, we investigated by cDNA-arrays the expression of 746 toxicologically relevant genes in skin and lungs of mice exposed for 28 days to light and/or environmental cigarette smoke. Glutathione-S-transferase-Pi and catalase were overexpressed in the lungs of mice exposed to light only. Moreover, the light induced in skin the expression of genes involved in carcinogenesis, photoaging, and production of genotoxic and oxidizing derivatives traveling at a distance. Smoke induced the expression of multiple genes in both skin and lung, which reflect adaptive responses and mechanisms related to cancer and, possibly, to emphysema and stroke. As shown in mice exposed to both light and smoke, the light tended to increase smoke-induced gene expression in lungs, while smoke tended to attenuate light-induced gene expression in skin. The oral administration of the nonsteroidal anti-inflammatory drug sulindac inhibited the light-induced overexpression of cyclooxygenase-2 and oxidative stress-related genes in skin, and down-regulated smoke-induced genes involved in oxidative stress, removal of damaged proteins, inflammation, and immune response in lung. These results provide a mechanistic insight explaining the systemic alterations induced by both light and smoke in mouse skin and lungs.

  5. Cigarette Smoke Extract-Induced Oxidative Stress and Fibrosis-Related Genes Expression in Orbital Fibroblasts from Patients with Graves' Ophthalmopathy

    PubMed Central

    Kau, Hui-Chuan; Wu, Shi-Bei; Tsai, Chieh-Chih; Liu, Catherine Jui-Ling; Wei, Yau-Huei

    2016-01-01

    Cigarette smoking is the most important risk factor for the development or deterioration of Graves' ophthalmopathy. Smoke-induced increased generation of reactive oxygen species may be involved. However, it remains to be clarified how orbital fibroblasts are affected by cigarette smoking. Our study demonstrated that Graves' orbital fibroblasts have exaggerated response to cigarette smoke extract challenge along with increased oxidative stress, fibrosis-related genes expression, especially connective tissue growth factor, and intracellular levels of transforming growth factor-β1 and interleukin-1β. The findings obtained in this study provide some clues for the impact of cigarette smoking on Graves' ophthalmopathy and offer a theoretical basis for the potential and rational use of antioxidants in treating Graves' ophthalmopathy. PMID:27340508

  6. Characterization of the third component of complement (C3) after activation by cigarette smoke

    SciTech Connect

    Kew, R.R.; Ghebrehiwet, B.; Janoff, A.

    1987-08-01

    Activation of lung complement by tobacco smoke may be an important pathogenetic factor in the development of pulmonary emphysema in smokers. We previously showed that cigarette smoke can modify C3 and activate the alternative pathway of complement in vitro. However, the mechanism of C3 activation was not fully delineated in these earlier studies. In the present report, we show that smoke-treated C3 induces cleavage of the alternative pathway protein, Factor B, when added to serum containing Mg-EGTA. This effect of cigarette smoke is specific for C3 since smoke-treated C4, when added to Mg-EGTA-treated serum, fails to activate the alternative pathway and fails to induce Factor B cleavage. Smoke-modified C3 no longer binds significant amounts of (/sup 14/C)methylamine (as does native C3), and relatively little (/sup 14/C)methylamine is incorporated into its alpha-chain. Thus, prior internal thiolester bond cleavage appears to have occurred in C3 activated by cigarette smoke. Cigarette smoke components also induce formation of noncovalently associated, soluble C3 multimers, with a Mr ranging from 1 to 10 million. However, prior cleavage of the thiolester bond in C3 with methylamine prevents the subsequent formation of these smoke-induced aggregates. These data indicate that cigarette smoke activates the alternative pathway of complement by specifically modifying C3 and that these modifications include cleavage of the thiolester bond in C3 and formation of noncovalently linked C3 multimers.

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

    SciTech Connect

    Rithidech, K.; Chen, B.T.; Mauderly, J.L.; Whorton, E.B. Jr.; Brooks, A.L. )

    1989-01-01

    To determine accurately the potential genetic damage induced by toxic inhaled agents, the cells that receive a high concentration of such agents should be analyzed. Pulmonary alveolar macrophages (PAMs) represent such cells. The authors compared the cytogenetic effects of cigarette smoke on PAMs of rats exposed repeatedly by different methods. This study was part of a larger investigation of the health effects resulting from different methods of exposing rats to cigarette smoke. Fischer 344/N male rats were randomly selected from five different exposure groups. The rats were exposed 6 hr/day, 5 days/week for 22-24 days. All smoke-exposed rats received the same daily concentrations {times} time product of cigarette smoke. Rats were injected intraperitoneally with colchicine at the end of exposure. PAMs were obtained by lung lavage and chromosomal damage was measured. Highly significant smoke-induced differences in both structural and numerical aberrations were observed in continuously exposed rats vs. sham controls, regardless route of exposure. The structural aberrations observed were chromatid-type deletions. Both hypoploid and hyperploid cells were detected. The data suggest that cigarette smoke is clastogenic and may disrupt spindle-fiber formation. These activities may play a role in the induction of human carcinogenesis caused by cigarette smoke exposure.

  8. Characterization of the third component of complement (C3) after activation by cigarette smoke.

    PubMed

    Kew, R R; Ghebrehiwet, B; Janoff, A

    1987-08-01

    Activation of lung complement by tobacco smoke may be an important pathogenetic factor in the development of pulmonary emphysema in smokers. We previously showed that cigarette smoke can modify C3 and activate the alternative pathway of complement in vitro. However, the mechanism of C3 activation was not fully delineated in these earlier studies. In the present report, we show that smoke-treated C3 induces cleavage of the alternative pathway protein, Factor B, when added to serum containing Mg-EGTA. This effect of cigarette smoke is specific for C3 since smoke-treated C4, when added to Mg-EGTA-treated serum, fails to activate the alternative pathway and fails to induce Factor B cleavage. Smoke-modified C3 no longer binds significant amounts of [14C]methylamine (as does native C3), and relatively little [14C]methylamine is incorporated into its alpha-chain. Thus, prior internal thiolester bond cleavage appears to have occurred in C3 activated by cigarette smoke. Cigarette smoke components also induce formation of noncovalently associated, soluble C3 multimers, with a Mr ranging from 1 to 10 million. However, prior cleavage of the thiolester bond in C3 with methylamine prevents the subsequent formation of these smoke-induced aggregates. These data indicate that cigarette smoke activates the alternative pathway of complement by specifically modifying C3 and that these modifications include cleavage of the thiolester bond in C3 and formation of noncovalently linked C3 multimers.

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

    PubMed

    Anbarasi, Kothandapani; Sabitha, Kuruvimalai Ekambaram; Devi, Chennam Srinivasulu Shyamala

    2005-09-01

    Despite a strong association between cigarette smoking and alarming increase in mortality rate from smoking-related diseases, around 35-40% of the world's population continues to smoke and many more are being exposed to environmental tobacco smoke. Since the role of free radicals and oxidative damage in the pathogenesis of smoking-related diseases has been suggested, bacoside A, a potent antioxidant was tested for its ability to protect against cigarette smoking-induced toxicity in terms of lactate dehydrogenase (LDH) and its isoenzymes. Rats were exposed to cigarette smoke and simultaneously administered with bacoside A, for a period of 12 weeks. Total LDH activity was assayed in serum, lung, heart, brain, liver and kidney, and serum LDH isoforms were separated electrophoretically. Cigarette smoke exposure resulted in significant increase in serum LDH and its isoenzymes with a concomitant decrease in these organs. These alterations were prevented by administration of bacoside A. Excessive oxidants from cigarette smoke is known to cause peroxidation of membrane lipids leading to cellular damage, thereby resulting in the leakage of LDH into the circulation. Bacoside A could have rendered protection to the organs by stabilizing their cell membranes and prevented the release of LDH, probably through its free radical scavenging and anti-lipid peroxidative effect.

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

    SciTech Connect

    Han Suxia; He Guangming; Wang Tao; Chen Lei; Ning Yunye; Luo Feng; An Jin; Yang Ting; Dong Jiajia; Liao Zenglin; Xu Dan; Wen Fuqiang

    2010-05-15

    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.

  11. Ending the cigarette pandemic.

    PubMed

    Richmond, J B

    1983-12-01

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

  12. Cigarette smoke inhibition of ion transport in canine tracheal epithelium

    SciTech Connect

    Welsh, M.J.

    1983-06-01

    To determine the effect of cigarette smoke on airway epithelial ion transport, the electrical properties and transepithelial Na and Cl fluxes were measured in canine tracheal epithelium. In vivo, the inhalation of the smoke from one cigarette acutely and reversibly decreased the electrical potential difference across the tracheal epithelium. In vitro, exposure of the mucosal surface of the epithelium to cigarette smoke decreased the short circuit current and transepithelial resistance. The decrease in short circuit current was due to an inhibition of the rate of Cl secretion with minimal effect on the rate of Na absorption. The effect of cigarette smoke was reversible, was not observed upon exposure of the submucosal surface to smoke, and was most pronounced when secretion was stimulated. The particulate phase of smoke was largely responsible for the inhibitory effect, since filtering the smoke minimized the effect. The effect of cigarette smoke was not prevented by addition of antioxidants to the bathing solutions, suggesting that the inhibition of Cl secretion cannot be entirely attributed to an oxidant mechanism. These results indicate that cigarette smoke acutely inhibits active ion transport by tracheal epithelium, both in vivo and in vitro. This effect may explain, in part, both the abnormal mucociliary clearance and the airway disease observed in cigarette smokers.

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

    PubMed

    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.

  14. E-Cigarettes (For Teens)

    MedlinePlus

    ... 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 ...

  15. Urinary cotinine levels of electronic cigarette (e-cigarette) users.

    PubMed

    Göney, Gülşen; Çok, İsmet; Tamer, Uğur; Burgaz, Sema; Şengezer, Tijen

    2016-07-01

    The popularity of electronic cigarettes (e-cigarettes) is rapidly increasing in many countries. These devices are designed to imitate regular cigarettes, delivering nicotine via inhalation without combusting tobacco but currently, there is a lack of scientific evidence on the presence or absence of nicotine exposure. Such research relies on evidence from e-cigarette users urine samples. In this study, we aimed to determine the levels and compare the amount of nicotine to which e-cigarette users, cigarette smokers and passive smokers are exposed. Therefore, urine samples were collected from e-cigarette users, cigarette smokers, passive smokers, and healthy nonsmokers. The urinary cotinine levels of the subjects were determined using gas chromatography-mass spectrometry. The mean (±SD) urinary cotinine levels were determined as 1755 ± 1848 ng/g creatinine for 32 e-cigarette users, 1720 ± 1335 ng/g creatinine for 33 cigarette smokers and 81.42 ± 97.90 ng/g creatinine for 33 passive smokers. A significant difference has been found between cotinine levels of e-cigarette users and passive smokers (p < 0.05). There were no statistically significant differences between e-cigarette users and cigarette smokers (p > 0.05). This is a seminal study to demonstrate the e-cigarette users are exposed to nicotine as much as cigarette smokers. PMID:27278718

  16. Urinary cotinine levels of electronic cigarette (e-cigarette) users.

    PubMed

    Göney, Gülşen; Çok, İsmet; Tamer, Uğur; Burgaz, Sema; Şengezer, Tijen

    2016-07-01

    The popularity of electronic cigarettes (e-cigarettes) is rapidly increasing in many countries. These devices are designed to imitate regular cigarettes, delivering nicotine via inhalation without combusting tobacco but currently, there is a lack of scientific evidence on the presence or absence of nicotine exposure. Such research relies on evidence from e-cigarette users urine samples. In this study, we aimed to determine the levels and compare the amount of nicotine to which e-cigarette users, cigarette smokers and passive smokers are exposed. Therefore, urine samples were collected from e-cigarette users, cigarette smokers, passive smokers, and healthy nonsmokers. The urinary cotinine levels of the subjects were determined using gas chromatography-mass spectrometry. The mean (±SD) urinary cotinine levels were determined as 1755 ± 1848 ng/g creatinine for 32 e-cigarette users, 1720 ± 1335 ng/g creatinine for 33 cigarette smokers and 81.42 ± 97.90 ng/g creatinine for 33 passive smokers. A significant difference has been found between cotinine levels of e-cigarette users and passive smokers (p < 0.05). There were no statistically significant differences between e-cigarette users and cigarette smokers (p > 0.05). This is a seminal study to demonstrate the e-cigarette users are exposed to nicotine as much as cigarette smokers.

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

    SciTech Connect

    Camlin, Nicole J.; McLaughlin, Eileen A.; Holt, Janet E.

    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.

  18. An improved in vitro model for testing the pulmonary toxicity of complex mixtures such as cigarette smoke.

    PubMed

    Aufderheide, Michaela; Knebel, Jan W; Ritter, Detlef

    2003-07-01

    Numerous approaches have been employed for testing the biological activity of cigarette smoke in vitro. None of them has managed to expose cultured lung cells in a realistic manner to the complex gaseous and particulate mixture that constitutes cigarette smoke. We have devised a system that makes this possible. The system presented here enables the direct exposure of human lung cells to native, unmodified cigarette mainstream smoke. It consists of a smoking machine, a dilution device for the smoke, analytical devices for online monitoring and a specially adapted exposure module based on the Cultex** cell cultivation system that is equipped with a gas-exposure top. Due to the special design of the exposure device and the optimised exposure conditions, this equipment allows cultured human lung cells to be exposed to freshly generated cigarette mainstream smoke. Exploratory experiments revealed that the smoke could be diluted over a wide concentration range in a reproducible way with respect to gas and particulate phases, and also demonstrated reproducible particle deposition depending on smoke concentration. Furthermore, it was shown that the exposed cells maintained their viability. Native cigarette mainstream smoke induced dose-dependent cellular effects in exposed cells with respect to cellular viability (viable cell number monitored by tetrazolium salt cleavage) and intracellular parameters (ATP and glutathione content). Therefore, fresh, physically and chemically unmodified cigarette mainstream smoke can be tested using this novel system.

  19. Analysis of the effects of cigarette smoke on staphylococcal virulence phenotypes.

    PubMed

    McEachern, Elisa K; Hwang, John H; Sladewski, Katherine M; Nicatia, Shari; Dewitz, Carola; Mathew, Denzil P; Nizet, Victor; Crotty Alexander, Laura E

    2015-06-01

    Cigarette smoking is the leading preventable cause of death, disease, and disability worldwide. It is well established that cigarette smoke provokes inflammatory activation and impairs antimicrobial functions of human immune cells. Here we explore whether cigarette smoke likewise affects the virulence properties of an important human pathogen, Staphylococcus aureus, and in particular methicillin-resistant S. aureus (MRSA), one of the leading causes of invasive bacterial infections. MRSA colonizes the nasopharynx and is thus exposed to inhalants, including cigarette smoke. MRSA exposed to cigarette smoke extract (CSE-MRSA) was more resistant to macrophage killing (4-fold higher survival; P < 0.0001). CSE-MRSA demonstrated reduced susceptibility to cell lysis (1.78-fold; P = 0.032) and antimicrobial peptide (AMP) (LL-37) killing (MIC, 8 μM versus 4 μM). CSE modified the surface charge of MRSA in a dose-dependent fashion, impairing the binding of particles with charge similar to that of AMPs by 90% (P < 0.0001). These changes persisted for 24 h postexposure, suggesting heritable modifications. CSE exposure increased hydrophobicity by 55% (P < 0.0001), which complemented findings of increased MRSA adherence and invasion of epithelial cells. CSE induced upregulation of mprF, consistent with increased MRSA AMP resistance. S. aureus without mprF had no change in surface charge upon exposure to CSE. In vivo, CSE-MRSA pneumonia induced higher mouse mortality (40% versus 10%) and increased bacterial burden at 8 and 20 h postinfection compared to control MRSA-infected mice (P < 0.01). We conclude that cigarette smoke-induced immune resistance phenotypes in MRSA may be an additional factor contributing to susceptibility to infectious disease in cigarette smokers.

  20. Effect of Cigarette Smoking on Concentrations of Cadmium and Lead and on the Oxidative Damage in Human Spermatozoa

    NASA Astrophysics Data System (ADS)

    Kiziler, Ali Riza; Aydemir, Birsen; Onaran, Ilhan; Alici, Bülent; Özkara, Hamdi; Akyolcu, Mehmet Can

    2007-04-01

    Cigarette smoking induced a significant oxidant effect to free radical-related male infertility. Semen and blood obtained from 50 subfertile men (n=26 smokers, n=24 nonsmokers) and from 45 fertile men (n=23 smokers, n=22 nonsmokers) volunteers were examined. The levels of ROS, MDA and protein carbonyls were significantly increased in smokers subfertile men. The results indicate that Cd and Pb levels of smoking subfertile men in seminal plasma and spermatozoa could affect semen quality and oxidative damage in human sperm cells.

  1. Low-Yield Cigarettes

    MedlinePlus

    ... Secondhand Smoke Smokeless Products Youth Tobacco Prevention Tobacco Industry and Products Federal Tax Increase Tobacco Ingredient Reporting ... be used. 3 In the past, the tobacco industry categorized low-yield cigarettes using measurements of tar ...

  2. E-Cigarettes

    MedlinePlus

    ... the liquid inside the cartridge. The liquid contains nicotine, flavorings, and other chemicals. The heated liquid turns ... about some dangers of e-cigarettes: They contain nicotine, which is addictive They contain other potentially harmful ...

  3. Analyzing Cigarette Smoke.

    ERIC Educational Resources Information Center

    Jaffe, Dan; Griffin, Dale; Ricker, Janet

    1997-01-01

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

  4. Cigarette Ads and Youth.

    ERIC Educational Resources Information Center

    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)

  5. Cigarette smoke extract immobilizes human spermatozoa and induces sperm apoptosis.

    PubMed

    Calogero, Aldo; Polosa, Riccardo; Perdichizzi, Anna; Guarino, Francesca; La Vignera, Sandro; Scarfia, Alessia; Fratantonio, Enza; Condorelli, Rosita; Bonanno, Oriana; Barone, Nunziata; Burrello, Nunziatina; D'Agata, Rosario; Vicari, Enzo

    2009-10-01

    Cigarette smoking by the male partner adversely affects assisted reproductive techniques, suggesting that it may damage sperm chromatin/DNA and consequently embryo development. The effects of graded concentrations of research cigarettes smoke extract (CSE) on motility, mitochondrial membrane potential (MMP), chromatin integrity and apoptosis were evaluated in spermatozoa obtained from 13 healthy, non-smoking men with normal sperm parameters, by flow cytometry. CSE suppressed sperm motility in a concentration- and time-dependent manner and increased the number of spermatozoa with low MMP, the main source of energy for sperm motility. In addition, CSE had a detrimental effect on sperm chromatin condensation and apoptosis. Indeed, it increased the number of spermatozoa with phosphatidylserine externalization, an early apoptotic sign, and fragmented DNA, a late apoptotic sign, in a concentration- and time-dependent manner. These effects of CSE were of similar or even greater magnitude to those obtained following incubation with tumour necrosis factor-alpha, a cytokine known for its negative impact on sperm function, used as positive control. Since transmission of smoking-induced sperm DNA alterations has been found in pre-implantation embryos, and this may predispose offspring to a greater risk of malformations, cancer and genetic diseases, men seeking to father a child are recommended to give up smoking.

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

    PubMed Central

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

    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

  7. An improved method of early diagnosis of smoking-induced respiratory changes using machine learning algorithms.

    PubMed

    Amaral, Jorge L M; Lopes, Agnaldo J; Jansen, José M; Faria, Alvaro C D; Melo, Pedro L

    2013-12-01

    The purpose of this study was to develop an automatic classifier to increase the accuracy of the forced oscillation technique (FOT) for diagnosing early respiratory abnormalities in smoking patients. The data consisted of FOT parameters obtained from 56 volunteers, 28 healthy and 28 smokers with low tobacco consumption. Many supervised learning techniques were investigated, including logistic linear classifiers, k nearest neighbor (KNN), neural networks and support vector machines (SVM). To evaluate performance, the ROC curve of the most accurate parameter was established as baseline. To determine the best input features and classifier parameters, we used genetic algorithms and a 10-fold cross-validation using the average area under the ROC curve (AUC). In the first experiment, the original FOT parameters were used as input. We observed a significant improvement in accuracy (KNN=0.89 and SVM=0.87) compared with the baseline (0.77). The second experiment performed a feature selection on the original FOT parameters. This selection did not cause any significant improvement in accuracy, but it was useful in identifying more adequate FOT parameters. In the third experiment, we performed a feature selection on the cross products of the FOT parameters. This selection resulted in a further increase in AUC (KNN=SVM=0.91), which allows for high diagnostic accuracy. In conclusion, machine learning classifiers can help identify early smoking-induced respiratory alterations. The use of FOT cross products and the search for the best features and classifier parameters can markedly improve the performance of machine learning classifiers. PMID:24001924

  8. Effects of using electronic cigarettes on nicotine delivery and cardiovascular function in comparison with regular cigarettes.

    PubMed

    Yan, X Sherwin; D'Ruiz, Carl

    2015-02-01

    The development of electronic cigarettes (e-cigs) has the potential to offer a less harmful alternative for tobacco users. This clinical study was designed to characterize e-cig users' exposure to nicotine, and to investigate the acute effects of e-cigs on the hemodynamic measurements (blood pressure and heart rate) in comparison with the effects of regular smoking. Five e-cigs and one Marlboro® cigarette were randomized for twenty-three participants under two exposure scenarios from Day 1 to Day 11: half-hour controlled administration and one hour ad lib use. The nicotine plasma concentrations after 1.5h of product use (C90) were significantly lower in the users of e-cigs than of Marlboro® cigarettes. The combination of glycerin and propylene glycol as the vehicle facilitated delivery of more nicotine than glycerin alone. The heart rate, systolic and diastolic blood pressure were significantly elevated after use of Marlboro® cigarettes, but the elevation was less after use of most of the e-cigs. Use of e-cigs had no impact on the exhaled CO levels, whereas the Marlboro® cigarette significantly increased the exhaled CO more than 8 times above the baseline. In conclusion, e-cigs could be a less harmful alternative for tobacco users. PMID:25460033

  9. The Effect of Different Doses of Cigarette Smoke in a Mouse Lung Tumor Model

    PubMed Central

    Santiago, Ludmilla Nadir; de Camargo Fenley, Juliana; Braga, Lúcia Campanario; Cordeiro, José Antônio; Cury, Patrícia M.

    2009-01-01

    Few studies have used Balb/c mice as an animal model for lung carcinogenesis. In this study, we investigated the effect of different doses of cigarette smoking in the urethane-induced Balb/c mouse lung cancer model. After injection of 3mg/kg urethane intraperitoneally, the mice were then exposed to tobacco smoke once or twice a day, five times a week, in a closed chamber. The animals were randomly divided into four groups. The control group (G0) received urethane only. The experimental groups (G1, G2 and G3) received urethane and exposure to the smoke of 3 cigarettes for 10 minutes once a day, 3 cigarettes for 10 minutes twice a day, and 6 cigarettes for 10 minutes twice a day, respectively. The mice were sacrificed after 16 weeks of exposure, and the number of nodules and hyperplasia in the lungs was counted. The results showed no statistically significant difference in the mean number of nodules and hyperplasia among the different groups, suggesting that the Balb/c mice are not suitable to study the pathogenesis of tobacco smoking-induced tumor progression in the lungs. PMID:19079653

  10. Metabolic Effects of Nicotine Gum and Cigarette Smoking: Potential Implications for Postcessation Weight Gain?

    ERIC Educational Resources Information Center

    Klesges, Robert C.; And Others

    1991-01-01

    Twenty smoking women participated in nicotine gum and smoking administration, after which resting energy expenditures (REEs) were measured. Results indicated acute increase in REE for both nicotine gum and cigarettes. Metabolic rates for nicotine gum slowly returned to baseline; rates for cigarettes quickly fell significantly below baseline.…

  11. Methylphenidate increases cigarette smoking in participants with ADHD

    PubMed Central

    Vansickel, Andrea R.; Stoops, William W.; Glaser, Paul E. A.; Poole, Megan M.

    2011-01-01

    Rationale Methylphenidate (Ritalin®) is commonly prescribed for behavioral problems associated with attention deficit/hyperactivity disorder (ADHD). The results of previous studies suggest that methylphenidate increases cigarette smoking in participants without psychiatric diagnoses. Whether methylphenidate increases cigarette smoking in participants diagnosed with ADHD is unknown. Objective In this within-subjects, repeated measures experiment, the acute effects of a range of doses of methylphenidate (10, 20, and 40 mg) and placebo were assessed in nine cigarette smokers who were not attempting to quit and met diagnostic criteria for ADHD but no other Axis I psychiatric disorders other than nicotine dependence. Methods Each dose of methylphenidate was tested once while placebo was tested twice. One hour after ingesting drug, participants were allowed to smoke ad libitum for 4 h. Measures of smoking included total cigarettes smoked, total puffs, and carbon monoxide levels. Snacks and decaffeinated drinks were available ad libitum; caloric intake during the 4-h smoking session was calculated. Results Methylphenidate increased the total number of cigarettes smoked, total number of puffs, and carbon monoxide levels. Methylphenidate decreased the number of food items consumed and caloric intake. Conclusions The results of this experiment suggest that acutely administered methylphenidate increases cigarette smoking in participants with ADHD, which is concordant with findings from previous studies that tested healthy young adults. These data indicate that clinicians may need to consider non-stimulant options or counsel their patients before starting methylphenidate when managing ADHD-diagnosed individuals who smoke. PMID:21590284

  12. Dioxins in cigarette smoke

    SciTech Connect

    Muto, H.; Takizawa, Y.

    1989-05-01

    Dioxins in cigarettes, smoke, and ash were determined using gas chromatography/mass spectrometry. The total concentration of polychlorinated dibenzo-p-dioxins (PCDDs) in cigarette smoke was approximately 5.0 micrograms/m3 at the maximum level, whereas various congeners from tetra-octa-chlorodibenzo-p-dioxin (-CDD) were detected. Particullary, the total concentration of hepta-CDD congeners was the highest among these congeners. Mass fragmentograms of various PCDD congeners were similar to those in flue gas samples collected from a municipal waste incinerator. The PCDD congeners that were not present in the cigarettes were found in the smoke samples. The 2,3,7,8-TCDD toxic equivalent value--an index for effects on humans--for total PCDDs in smoke was 1.81 ng/m3 using the toxic factor of the United States Environment Protection Agency. Daily intake of PCDDs by smoking 20 cigarettes was estimated to be approximately 4.3 pg.kg body weight/day. This value was close to that of the ADIs: 1-5 pg.kg body weight/day reported in several countries. A heretofore unrecognized health risk was represented by the presence of PCDDs in cigarette smoke.

  13. Economics and cigarettes.

    PubMed

    Schelling, T C

    1986-09-01

    Economic facts on cigarette consumption and production are summarized, and the health consequences of cigarette smoking are reviewed. The magnitude and distribution of these health consequences among the population are discussed in economic terms, that is, in an "accounting framework" comprising such disparate elements as lost lives, lost livelihoods, pain, fear, discomfort, medical costs, excise taxes, and the costs of regulating smoking behaviors. The importance of these factors and their potential influence on public policy and individual behavior are considered. Difficulties include assigning a monetary value to an expected extension of life, the "voluntary" nature of smoking (even though most smokers wish they could quit), deciding what to include as economic consequences of smoking, and the attribution to smoking of some share of the costs for diseases known to be affected by smoking. "Transfers," or purely financial transactions, in contrast to expenditures for goods and services, are explained as one assessment component of the economic impact of smoking-related diseases. The issue of the economic benefit to the United States as a whole and to the population engaged in the cigarette industry, because of the earnings and employment generated by cigarette purchases, is examined, as is the issue of cigarette purchases as a significant source of federal and state revenue. PMID:3774784

  14. Lumbrokinase from earthworm extract ameliorates second-hand smoke-induced cardiac fibrosis.

    PubMed

    Lai, Chao-Hung; Han, Chien-Kuo; Shibu, Marthandam Asokan; Pai, Pei Ying; Ho, Tsung-Jung; Day, Cecilia Hsuan; Tsai, Fuu-Jen; Tsai, Chang-Hai; Yao, Chun-Hsu; Huang, Chih-Yang

    2015-09-01

    Exposure to tobacco smoke has epidemiologically been linked to the occurrence of cardiovascular disease among nonsmokers but the associated molecular events are not well elucidated yet. When Sprague Dawley rats were exposed to second-hand tobacco cigarette smoke twice a day for a 30 days period at an exposure rate of 10 cigarettes/30 min, they showed adverse effects including reduced left ventricle weight, increased cardiac damages, deteriorated cardiac features, and cardiac fibrosis. Exposure to second-hand smoking (SHS) increased the molecular markers of cardiac fibrosis such as urokinase plasminogen activator and matrix metallopeptidases. The modulations in the protein levels were led by the activation of extracellular signal-regulated kinases (ERK1/2), the transcription factor-specificity protein 1 (SP1), and the fibrogenic master switch-connective for epithelial-mesenchymal transition tissue growth factor there by indicating their effective role in SHS-induced myocardial infraction. Dilong, an edible earthworm extract used in Chinese medicine and its bioactive fibrinolytic enzyme product-lumbrokinase, when administered in rats, restricted the SHS exposure induced cardiac fibrosis and provided cardio-protection. The results show that lumbrokinase and dilong administration can efficiently prevent epidemiological incidence of cardiac disease among SHS-exposed nonsmokers. PMID:24706507

  15. Interplay between Smoking-induced Genotoxicity and Altered Signaling in Pancreatic Carcinogenesis

    PubMed Central

    Batra, Surinder K.

    2012-01-01

    Despite continuous research efforts directed at early diagnosis and treatment of pancreatic cancer (PC), the status of patients affected by this deadly malignancy remains dismal. Its notoriety with regard to lack of early diagnosis and resistance to the current chemotherapeutics is due to accumulating signaling abnormalities. Hoarding experimental and epidemiological evidences have established a direct correlation between cigarette smoking and PC risk. The cancer initiating/promoting nature of cigarette smoke can be attributed to its various constituents including nicotine, which is the major psychoactive component, and several other toxic constituents, such as nitrosamines, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone, and polycyclic aromatic hydrocarbons. These predominant smoke-constituents initiate a series of oncogenic events facilitating epigenetic alterations, self-sufficiency in growth signals, evasion of apoptosis, sustained angiogenesis, and metastasis. A better understanding of the molecular mechanisms underpinning these events is crucial for the prevention and therapeutic intervention against PC. This review presents various interconnected signal transduction cascades, the smoking-mediated genotoxicity, and genetic polymorphisms influencing the susceptibility for smoking-mediated PC development by modulating pivotal biological aspects such as cell defense/tumor suppression, inflammation, DNA repair, as well as tobacco-carcinogen metabolization. Additionally, it provides a large perspective toward tumor biology and the therapeutic approaches against PC by targeting one or several steps of smoking-mediated signaling cascades. PMID:22623649

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

    PubMed

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

    2015-01-01

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

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

    PubMed Central

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

    2015-01-01

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

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

    PubMed

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

    2015-01-01

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

  19. Nicotine-containing versus de-nicotinized cigarettes: effects on craving and withdrawal.

    PubMed

    Gross, J; Lee, J; Stitzer, M L

    1997-01-01

    Nicotine exposure levels and subjective effects from smoking a de-nicotinized cigarette (Next) were examined under controlled conditions. Ten tobacco smokers smoked 20 puffs from their own brand (1.1 mg nicotine delivery, commercial cigarettes), a 0.7 mg nicotine "light" cigarette, or the Next de-nicotinized cigarette (< 0.1 mg nicotine) during independent experimental test sessions. The Next cigarette did not deliver and appreciable nicotine, did not elevate heart rate during smoking, and was rated as less satisfying than the smokers' own brand. Subjective ratings of cigarette carving and tobacco withdrawal symptoms increased during a 90 min post-smoking abstinence period. However, there were no measurable differences on these subjective ratings across the three cigarette test brands. It is concluded that nicotine can be removed from cigarettes without affecting the onset time course or intensity of cigarette cravings and other tobacco withdrawal symptoms in an acute abstinence model. Further studies to determine the subjective and physiological effects of nicotine-free cigarettes would contribute to a greater understanding of tobacco withdrawal and the processes involved in smoking maintenance.

  20. Heavy Cigarette Smokers in a Chinese Population Display a Compromised Permeability Barrier

    PubMed Central

    Xin, Shujun; Ye, Li; Lv, Chengzhi; Elias, Peter M.

    2016-01-01

    Cigarette smoking is associated with various cutaneous disorders with defective permeability. Yet, whether cigarette smoking influences epidermal permeability barrier function is largely unknown. Here, we measured skin biophysical properties, including permeability barrier homeostasis, stratum corneum (SC) integrity, SC hydration, skin surface pH, and skin melanin/erythema index, in cigarette smokers. A total of 99 male volunteers were enrolled in this study. Smokers were categorized as light-to-moderate (<20 cigarettes/day) or heavy smokers (≥20 cigarettes/day). An MPA5 was used to measure SC hydration and skin melanin/erythema index on the dorsal hand, forehead, and cheek. Basal transepidermal water loss (TEWL) and barrier recovery rates were assessed on the forearm. A Skin-pH-Meter pH900 was used to measure skin surface pH. Our results showed that heavy cigarette smokers exhibited delayed barrier recovery after acute abrogation (1.02% ± 13.06 versus 16.48% ± 6.07), and barrier recovery rates correlated negatively with the number of daily cigarettes consumption (p = 0.0087). Changes in biophysical parameters in cigarette smokers varied with body sites. In conclusion, heavy cigarette smokers display compromised permeability barrier homeostasis, which could contribute, in part, to the increased prevalence of certain cutaneous disorders characterized by defective permeability. Thus, improving epidermal permeability barrier should be considered for heavy cigarette smokers. PMID:27437403

  1. Cigarette smoke extract induces aberrant cytochrome-c oxidase subunit II methylation and apoptosis in human umbilical vascular endothelial cells.

    PubMed

    Yang, Min; Chen, Ping; Peng, Hong; Zhang, Hongliang; Chen, Yan; Cai, Shan; Lu, Qianjin; Guan, Chaxiang

    2015-03-01

    Cigarette smoke-induced apoptosis of vascular endothelial cells contributes to the pathogenesis of chronic obstructive pulmonary disease. However, the mechanisms responsible for endothelial apoptosis remain poorly understood. We conducted an in vitro study to investigate whether DNA methylation is involved in smoking-induced endothelial apoptosis. Human umbilical vascular endothelial cells (HUVECs) were exposed to cigarette smoke extract (CSE) at a range of concentrations (0-10%). HUVECs were also incubated with a demethylating reagent, 5-aza-2'-deoxycytidinem (AZA), with and without CSE. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay and flow cytometry using annexin V-FITC/propidium iodide staining. We found that CSE treatment significantly increased HUVEC apoptosis in a dose- and time-dependent manner. Quantitative real-time RT-PCR and immunoblot revealed that CSE treatment decreased cytochrome-c oxidase subunit II (COX II) mRNA and protein levels and decreased COX activity. Methylation-specific PCR and direct bisulfite sequencing revealed positive COX II gene methylation. AZA administration partly increased mRNA and protein expressions of COX II, and COX activity decreased by CSE and attenuated the toxic effects of CSE. Our results showed that CSE induced aberrant COX II methylation and apoptosis in HUVECs. PMID:25500741

  2. Alternative Complement Pathway Deficiency Ameliorates Chronic Smoke-Induced Functional and Morphological Ocular Injury

    PubMed Central

    Woodell, Alex; Coughlin, Beth; Kunchithapautham, Kannan; Casey, Sarah; Williamson, Tucker; Ferrell, W. Drew; Atkinson, Carl; Jones, Bryan W.; Rohrer, Bärbel

    2013-01-01

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

  3. MicroRNAs as modulators of smoking-induced gene expression changes in human airway epithelium

    PubMed Central

    Schembri, Frank; Sridhar, Sriram; Perdomo, Catalina; Gustafson, Adam M.; Zhang, Xiaoling; Ergun, Ayla; Lu, Jining; Liu, Gang; Zhang, Xiaohui; Bowers, Jessica; Vaziri, Cyrus; Ott, Kristen; Sensinger, Kelly; Collins, James J.; Brody, Jerome S.; Getts, Robert; Lenburg, Marc E.; Spira, Avrum

    2009-01-01

    We have shown that smoking impacts bronchial airway gene expression and that heterogeneity in this response associates with smoking-related disease risk. In this study, we sought to determine whether microRNAs (miRNAs) play a role in regulating the airway gene expression response to smoking. We examined whole-genome miRNA and mRNA expression in bronchial airway epithelium from current and never smokers (n = 20) and found 28 miRNAs to be differentially expressed (P < 0.05) with the majority being down-regulated in smokers. We further identified a number of mRNAs whose expression level is highly inversely correlated with miRNA expression in vivo. Many of these mRNAs contain potential binding sites for the differentially expressed miRNAs in their 3′-untranslated region (UTR) and are themselves affected by smoking. We found that either increasing or decreasing the levels of mir-218 (a miRNA that is strongly affected by smoking) in both primary bronchial epithelial cells and H1299 cells was sufficient to cause a corresponding decrease or increase in the expression of predicted mir-218 mRNA targets, respectively. Further, mir-218 expression is reduced in primary bronchial epithelium exposed to cigarette smoke condensate (CSC), and alteration of mir-218 levels in these cells diminishes the induction of the predicted mir-218 target MAFG in response to CSC. These data indicate that mir-218 levels modulate the airway epithelial gene expression response to cigarette smoke and support a role for miRNAs in regulating host response to environmental toxins. PMID:19168627

  4. Electronic Cigarettes on Hospital Campuses

    PubMed Central

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

    2015-01-01

    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. PMID:26729142

  5. Electronic Cigarettes on Hospital Campuses.

    PubMed

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

    2015-12-29

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

  6. Advertising media and cigarette demand.

    PubMed

    Goel, Rajeev K

    2011-01-01

    Using state-level panel data for the USA spanning three decades, this research estimates the demand for cigarettes. The main contribution lies in studying the effects of cigarette advertising disaggregated across five qualitatively different groups. Results show cigarette demand to be near unit elastic, the income effects to be generally insignificant and border price effects and habit effects to be significant. Regarding advertising effects, aggregate cigarette advertising has a negative effect on smoking. Important differences across advertising media emerge when cigarette advertising is disaggregated. The effects of public entertainment and Internet cigarette advertising are stronger than those of other media. Anti-smoking messages accompanying print cigarette advertising seem relatively more effective. Implications for smoking control policy are discussed.

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

    NASA Astrophysics Data System (ADS)

    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.

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

    EPA Science Inventory

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

  9. Electronic cigarettes: human health effects

    PubMed Central

    Callahan-Lyon, Priscilla

    2014-01-01

    Objective With the rapid increase in use of electronic nicotine delivery systems (ENDS), such as electronic cigarettes (e-cigarettes), users and non-users are exposed to the aerosol and product constituents. This is a review of published data on the human health effects of exposure to e-cigarettes and their components. Methods Literature searches were conducted through September 2013 using multiple electronic databases. Results Forty-four articles are included in this analysis. E-cigarette aerosols may contain propylene glycol, glycerol, flavourings, other chemicals and, usually, nicotine. Aerosolised propylene glycol and glycerol produce mouth and throat irritation and dry cough. No data on the effects of flavouring inhalation were identified. Data on short-term health effects are limited and there are no adequate data on long-term effects. Aerosol exposure may be associated with respiratory function impairment, and serum cotinine levels are similar to those in traditional cigarette smokers. The high nicotine concentrations of some products increase exposure risks for non-users, particularly children. The dangers of secondhand and thirdhand aerosol exposure have not been thoroughly evaluated. Conclusions Scientific evidence regarding the human health effects of e-cigarettes is limited. While e-cigarette aerosol may contain fewer toxicants than cigarette smoke, studies evaluating whether e-cigarettes are less harmful than cigarettes are inconclusive. Some evidence suggests that e-cigarette use may facilitate smoking cessation, but definitive data are lacking. No e-cigarette has been approved by FDA as a cessation aid. Environmental concerns and issues regarding non-user exposure exist. The health impact of e-cigarettes, for users and the public, cannot be determined with currently available data. PMID:24732161

  10. 27 CFR 40.352 - Cigarette tubes.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2011-04-01 2011-04-01 false Cigarette tubes. 40.352... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Manufacture of Cigarette Papers and Tubes Taxes § 40.352 Cigarette tubes. Cigarette...

  11. 27 CFR 40.352 - Cigarette tubes.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2012-04-01 2011-04-01 true Cigarette tubes. 40.352... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Manufacture of Cigarette Papers and Tubes Taxes § 40.352 Cigarette tubes. Cigarette...

  12. 27 CFR 40.352 - Cigarette tubes.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2014-04-01 2014-04-01 false Cigarette tubes. 40.352... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Manufacture of Cigarette Papers and Tubes Taxes § 40.352 Cigarette tubes. Cigarette...

  13. 27 CFR 40.352 - Cigarette tubes.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2013-04-01 2013-04-01 false Cigarette tubes. 40.352... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Manufacture of Cigarette Papers and Tubes Taxes § 40.352 Cigarette tubes. Cigarette...

  14. 27 CFR 40.352 - Cigarette tubes.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2010-04-01 2010-04-01 false Cigarette tubes. 40.352... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Manufacture of Cigarette Papers and Tubes Taxes § 40.352 Cigarette tubes. Cigarette...

  15. Exposure to cigarette smoke downregulates β2-adrenergic receptor expression and upregulates inflammation in alveolar macrophages.

    PubMed

    Wang, Wei; Li, Xiaoguang; Xu, Jie

    2015-01-01

    Cigarette smoke-triggered inflammation is important in the pathophysiology of chronic obstructive pulmonary disease (COPD). β2-Adrenergic receptor (β2-AR) is abundantly expressed on inflammatory cells, which is associated with inflammation regulation. To observe alterations in inflammation, pathological changes in lung tissues, and detect changes in β2-AR expression, rats were exposed for 4 months to cigarette smoke. Pathological changes were observed in lung tissue sections. The levels of inflammatory mediators tumor necrosis factor (TNF)-α, interleukin (IL)-1β in bronchoalveolar lavage fluid (BALF), and lung tissues were measured using enzyme-linked immunosorbent assay (ELISA). Nuclear factor (NF)-κB activity was detected by electrophoretic mobility shift assay (EMSA). Exposure to this regimen of cigarette smoke induced peribronchial and perivascular lymphocytic aggregates and parenchymal accumulation of macrophages in rats. EMSA demonstrated that smoke exposure enhanced NF-κB activation in rats' alveolar macrophages (AMs). Compared with the control group, smoke exposure induced a notable increase in TNF-α and IL-1β in BALF, lung tissues, and a decrease of β2-AR expression of AMs. The expression of β2-AR from AMs was inversely correlated with TNF-α and IL-1β levels of BALF. These data demonstrated that chronic smoke-triggered lung inflammation was accompanied by down-regulation of β2-AR in rat lungs' AMs.

  16. Effect of bacoside A on brain antioxidant status in cigarette smoke exposed rats.

    PubMed

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

    2006-02-16

    Free radicals mediated oxidative stress has been implicated in the pathogenesis of smoking-related diseases and antioxidant nutrients are reported to prevent the oxidative damage induced by smoking. Therefore, the present study was conducted to evaluate the antioxidant role of bacoside A (triterpenoid saponin isolated from Bacopa monniera) against chronic cigarette smoking induced oxidative damage in rat brain. Adult male albino rats were exposed to cigarette smoke for a period of 12 weeks and simultaneously administered with bacoside A (10 mg/kg b.w./day, p.o.). Antioxidant status of the brain was assessed from the levels of reduced glutathione, vitamin C, vitamin E, and vitamin A and the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. The levels of copper, iron, zinc and selenium in brain and serum ceruloplasmin activity were also measured. Oxidative stress was evident from the diminished levels of both enzymatic and non-enzymatic antioxidants. Alterations in the levels of trace elements with accumulation of copper and iron, and depletion of zinc and selenium were also observed. Bacoside A administration improved the antioxidant status and maintained the levels of trace elements. These results suggest that chronic cigarette smoke exposure enhances oxidative stress, thereby disturbing the tissue defense system and bacoside A protects the brain from the oxidative damage through its antioxidant potential.

  17. Tobacco smoke induces production of chemokine CCL20 to promote lung cancer.

    PubMed

    Wang, Gui-Zhen; Cheng, Xin; Li, Xin-Chun; Liu, Yong-Qiang; Wang, Xian-Quan; Shi, Xu; Wang, Zai-Yong; Guo, Yong-Qing; Wen, Zhe-Sheng; Huang, Yun-Chao; Zhou, Guang-Biao

    2015-07-10

    Tobacco kills nearly 6 million people each year, and 90% of the annual 1.59 million lung cancer deaths worldwide are caused by cigarette smoke. Clinically, a long latency is required for individuals to develop lung cancer since they were first exposed to smoking. In this study, we aimed to identify clinical relevant inflammatory factors that are critical for carcinogenesis by treating normal human lung epithelial cells with tobacco carcinogen nicotine-derived nitrosaminoketone (NNK) for a long period (60 days) and systematic screening in 84 cytokines/chemokines. We found that a chemokine CCL20 was significantly up-regulated by NNK, and in 78/173 (45.1%) patients the expression of CCL20 was higher in tumor samples than their adjacent normal lung tissues. Interestingly, CCL20 was up-regulated in 48/92 (52.2%) smoker and 29/78 (37.2%) nonsmoker patients (p = 0.05), and high CCL20 was associated with poor prognosis. NNK induced the production of CCL20, which promoted lung cancer cell proliferation and migration. In addition, an anti-inflammation drug, dexamethasone, inhibited NNK-induced CCL20 production and suppressed lung cancer in vitro and in vivo. These results indicate that CCL20 is crucial for tobacco smoke-caused lung cancer, and anti-CCL20 could be a rational approach to fight against this deadly disease.

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

    PubMed Central

    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 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. PMID:22934051

  19. Cigarette smoking contagion.

    PubMed

    Einstein, S; Epstein, A

    1980-01-01

    A ministudy was carried out with 50 male and female adults who are "regular" cigarette smokers to investigate the potential role(s) which contagion plays in smoking. Notwithstanding their reports that they were introduced to smoking by others 40% of the time, only 12% reported-remembered initiating someone else to smoking. The report of self-activated cigarette use is congruent with with most views about smoking, but not regarding drug use. As long as drug use intervention utilizes contagion as a concept, deviance as a classification and varieties of isolation as control techniques will be associated with drugs, users, and drug use. By definition, social substances have no source of contagion by others. The decision to use or abstain is viewed as being personal notwithstanding the reality that is related among other factors to a variety of market economies. PMID:7450935

  20. Electronic Cigarettes and Vaping: A New Challenge in Clinical Medicine and Public Health. A Literature Review

    PubMed Central

    Palazzolo, Dominic L.

    2013-01-01

    Electronic cigarette (e-cigarette) use, or vaping, in the United States and worldwide is increasing. Their use is highly controversial from scientific, political, financial, psychological, and sociological ideologies. Given the controversial nature of e-cigarettes and vaping, how should medical care providers advise their patients? To effectively face this new challenge, health care professionals need to become more familiar with the existing literature concerning e-cigarettes and vaping, especially the scientific literature. Thus, the aim of this article is to present a review of the scientific evidence-based primary literature concerning electronic cigarettes and vaping. A search of the most current literature using the pubmed database dating back to 2008, and using electronic cigarette(s) or e-cigarette(s) as key words, yielded a total of 66 highly relevant articles. These articles primarily deal with (1) consumer-based surveys regarding personal views on vaping, (2) chemical analysis of e-cigarette cartridges, solutions, and mist, (3) nicotine content, delivery, and pharmacokinetics, and (4) clinical and physiological studies investigating the effects of acute vaping. When compared to the effects of smoking, the scant available literature suggests that vaping could be a “harm reduction” alternative to smoking and a possible means for smoking cessation, at least to the same degree as other Food and Drug Administration-approved nicotine replacement therapies. However, it is unclear if vaping e-cigarettes will reduce or increase nicotine addiction. It is obvious that more rigorous investigations of the acute and long-term health effects of vaping are required to establish the safety and efficacy of these devices; especially parallel experiments comparing the cardiopulmonary effects of vaping to smoking. Only then will the medical community be able to adequately meet the new challenge e-cigarettes and vaping present to clinical medicine and public health. PMID

  1. Irritants in cigarette smoke plumes

    SciTech Connect

    Ayer, H.E.; Yeager, D.W.

    1982-11-01

    Concentrations of the irritants formaldehyde and acrolein in side stream cigarette smoke plumes are up to three orders of magnitude above occupational limits, readily accounting for eye and nasal irritation. ''Low-tar'' cigarettes appear at least as irritating as other cigarettes. More than half the irritant is associated with the particulate phase of the smoke, permitting deposition throughout the entire respiratory tract and raising the issue of whether formaldehyde in smoke is associated with bronchial cancer.

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

    PubMed

    Camlin, Nicole J; McLaughlin, Eileen A; Holt, Janet E

    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.

  3. 27 CFR 40.351 - Cigarette papers.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Manufacture of Cigarette Papers and Tubes Taxes § 40.351 Cigarette papers....

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

    PubMed Central

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

    2016-01-01

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

  5. Early events in the pathogenesis of chronic obstructive pulmonary disease. Smoking-induced reprogramming of airway epithelial basal progenitor cells.

    PubMed

    Shaykhiev, Renat; Crystal, Ronald G

    2014-12-01

    The airway epithelium is the primary site of the earliest pathologic changes induced by smoking, contributing to the development of chronic obstructive pulmonary disease (COPD). The normal human airway epithelium is composed of several major cell types, including differentiated ciliated and secretory cells, intermediate undifferentiated cells, and basal cells (BC). BC contain the stem/progenitor cell population responsible for maintenance of the normally differentiated airway epithelium. Although inflammatory and immune processes play a significant role in the pathogenesis of COPD, the earliest lesions include hyperplasia of the BC population, suggesting that the disease may start with this cell type. Apart from BC hyperplasia, smoking induces a number of COPD-relevant airway epithelial remodeling phenotypes that are likely initiated in the BC population, including mucous cell hyperplasia, squamous cell metaplasia, epithelial-mesenchymal transition, altered ciliated and nonmucous secretory cell differentiation, and suppression of junctional barrier integrity. Significant progress has been recently made in understanding the biology of human airway BC, including gene expression features, stem/progenitor, and other functions, including interaction with other airway cell types. Accumulating evidence suggests that human airway BC function as both sensors and cellular sources of various cytokines and growth factors relevant to smoking-associated airway injury, as well as the origin of various molecular and histological phenotypes relevant to the pathogenesis of COPD. In the context of these considerations, we suggest that early BC-specific smoking-induced molecular changes are critical to the pathogenesis of COPD, and these represent a candidate target for novel therapeutic approaches to prevent COPD progression in susceptible individuals.

  6. The Electronic Cigarette: The Good, the Bad, and the Ugly.

    PubMed

    Cooke, Andrew; Fergeson, Jennifer; Bulkhi, Adeeb; Casale, Thomas B

    2015-01-01

    Electronic cigarettes (EC) are battery-powered nicotine delivery systems that have increased in popularity since they entered the US market. EC has been reported to contain less carcinogens than traditional cigarettes, cause less acute lung effects in healthy individuals, and may help with smoking cessation. It has also been viewed as a potential safer alternative for asthmatic smokers, but its effects on lung functions are unclear. However, EC do carry some harmful aspects as they contain formaldehyde and formaldehyde-forming hemiacetals as well as potentially toxic particulate matter that deposits on surfaces. EC are an increasingly popular device that could serve as a gateway into traditional cigarette smoking or illicit drugs. The popularity of EC has brought with it money from large tobacco corporations and mass marketing. Lack of regulation has generated product inconsistency and potential health hazards. This review highlights what is known and what still needs to be answered about EC.

  7. The Electronic Cigarette: The Good, the Bad, and the Ugly.

    PubMed

    Cooke, Andrew; Fergeson, Jennifer; Bulkhi, Adeeb; Casale, Thomas B

    2015-01-01

    Electronic cigarettes (EC) are battery-powered nicotine delivery systems that have increased in popularity since they entered the US market. EC has been reported to contain less carcinogens than traditional cigarettes, cause less acute lung effects in healthy individuals, and may help with smoking cessation. It has also been viewed as a potential safer alternative for asthmatic smokers, but its effects on lung functions are unclear. However, EC do carry some harmful aspects as they contain formaldehyde and formaldehyde-forming hemiacetals as well as potentially toxic particulate matter that deposits on surfaces. EC are an increasingly popular device that could serve as a gateway into traditional cigarette smoking or illicit drugs. The popularity of EC has brought with it money from large tobacco corporations and mass marketing. Lack of regulation has generated product inconsistency and potential health hazards. This review highlights what is known and what still needs to be answered about EC. PMID:26164573

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

    PubMed Central

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

    2016-01-01

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

  9. Cigarette Smoking in Iran

    PubMed Central

    Meysamie, A; Ghaletaki, R; Zhand, N; Abbasi, M

    2012-01-01

    Background: Cigarette smoking is the largest preventable cause of death worldwide. No systematic review is available on the situation of the smoking in Iran, so we decided to provide an overview of the studies in the field of smoking in Iranian populations. Methods: Published Persian-language papers of all types until 2009 indexed in the IranMedex (http://www.iranmedex.com) and Magiran (http://www.magiran.com). Reports of World Health Organization were also searched and optionally employed. The studies concerning passive smoking or presenting the statistically insignificant side effects were excluded. Databases were searched using various combinations of the following terms: cigarette, smoking, smoking cessation, prevalence, history, side effects, and lung cancer by independent reviewers. All the 83 articles concerning the prevalence or side effects of the smoking habit in any Iranian population were selected. The prevalence rate of daily cigarette smoking and the 95% confidence interval as well as smoking health risk associated odds ratio (OR) were retrieved from the articles or calculated. Results: The reported prevalence rates of the included studies, the summary of smoking-related side effects and the ORs (95%CI) of smoking associated risks and the available data on smoking cessation in Iran have been shown in the article. Conclusion: Because of lack of certain data, special studies on local pattern of tobacco use in different districts, about the relationship between tobacco use and other diseases, especially non communicable diseases, and besides extension of smoking cessation strategies, studies on efficacy of these methods seems to be essential in this field. PMID:23113130

  10. Electronic cigarettes in the media.

    PubMed

    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.

  11. Electronic cigarettes in the media

    PubMed Central

    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

  12. Electronic cigarettes in the media.

    PubMed

    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

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

    PubMed

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

    2015-01-01

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

  14. Effects of omega-3 fatty acids on tobacco craving in cigarette smokers: A double-blind, randomized, placebo-controlled pilot study.

    PubMed

    Rabinovitz, Sharon

    2014-08-01

    Cigarette smoke induces oxidative stress with subsequent polyunsaturated fatty acids (PUFAs) peroxidation. Low concentrations of omega-3 PUFAs can affect neurotransmission, resulting in hypofunctioning of the mesocortical systems associated with reward and dependence mechanisms and thus may increase cigarette craving, hampering smoking cessation efforts. PUFA deficiency, in particular eicosapentaenoic acid (EPA; 20:5 n-3) and docosahexaenoic acid (DHA; 22:6 n-3), has also been linked to reduced psychological health and ability to cope with stress. Although stress is well linked to smoking urges and behavior, no research to date has examined the effects of PUFA supplementation on tobacco craving. In this double-blind, randomized, placebo-controlled pilot study, performed in regular cigarette smokers (n=48), administration of 2710 mg EPA/day and 2040 mg DHA/day for one month was accompanied by a significant decrease in reported daily smoking and in tobacco craving following cigarette cue exposure. Craving did not return to baseline values in the month that followed treatment discontinuation. This is the first study demonstrating that omega-3 PUFA supplementation reduces tobacco craving in regular smokers, compared to placebo treatment. Thus, omega-3 PUFAs may be of benefit in managing tobacco consumption. Further studies are needed on larger samples to explore the possible therapeutic implications for heavy cigarette smokers. PMID:24899596

  15. Electronic Cigarettes: Vulnerability of Youth

    PubMed Central

    2015-01-01

    Electronic cigarettes have become popular and are heavily promoted as a safer cigarette and an aid to quit smoking. Although they may have value in reducing cigarette use among smokers, they are of limited value in smoking cessation and pose many problems, particularly in children. Nicotine is highly addictive and affects virtually all cells in the body. It is particularly harmful to developing brains and other organs. The electronic nicotine delivery systems are largely uncontrolled and safety risks are manifold. Initiating nicotine use and increasing dependence in the population may be linked with increased tobacco and other addictive substance abuse even if the individual electronic cigarette delivers less harm than a combustible cigarette does. PMID:25830075

  16. Electronic cigarettes for smoking cessation.

    PubMed

    Bullen, Christopher

    2014-11-01

    Electronic cigarettes (e-cigarettes) are novel vaporising devices that, similar to nicotine replacement treatments, deliver nicotine but in lower amounts and less swiftly than tobacco smoking. However, they enjoy far greater popularity than these medications due in part to their behaviour replacement characteristics. Evidence for their efficacy as cessation aids, based on several randomised trials of now obsolete e-cigarettes, suggests a modest effect equivalent to nicotine patch. E-cigarettes are almost certainly far less harmful than tobacco smoking, but the health effects of long-term use are as yet unknown. Dual use is common and almost as harmful as usual smoking unless it leads to quitting. Population effects, such as re-normalising smoking behaviour, are a concern. Clinicians should be knowledgeable about these products. If patients who smoke are unwilling to quit or cannot succeed using evidence-based approaches, e-cigarettes may be an option to be considered after discussing the limitations of current knowledge.

  17. DNA typing from cigarette butts.

    PubMed

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

    2003-03-01

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

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

    PubMed Central

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

    2016-01-01

    Increasing evidence indicates that cigarette smoking is a strong predictor of electronic cigarettes (e-cigarettes) use, particularly in adolescents, yet the effects has not be systematically reviewed and quantified. Relevant studies were retrieved by searching three databases up to June 2015. The meta-analysis results were presented as pooled odds ratios (ORs) with 95% confidence intervals (CIs) calculated by a random-effects model. Current smokers were more likely to use e-cigarette currently (OR: 14.89, 95% CI: 7.70–28.78) and the probability was greater in adolescents than in adults (39.13 vs. 7.51). The probability of ever e-cigarettes use was significantly increased in smokers (OR: 14.67, 95% CI: 11.04–19.49). Compared with ever smokers and adults, the probabilities were much greater in current smokers (16.10 vs. 9.47) and adolescents (15.19 vs. 14.30), respectively. Cigarette smoking increases the probability of e-cigarettes use, especially in current smokers and adolescents. PMID:26771624

  19. Effect of cigarette tax increase on cigarette consumption in Taiwan

    PubMed Central

    Lee, J; Liao, D; Ye, C; Liao, W

    2005-01-01

    Objectives: This study evaluates the effect of a 5 New Taiwan Dollar (NT$5) Health and Welfare Tax increase on the consumption of domestic and imported cigarettes and cigars. Methods: Using statistics published annually from 1971 through 2000, we set up a model based on the Central Bureau of Statistics (CBS) demand model to estimate price and expenditure elasticity coefficients of cigarettes and cigars. Results: Our results showed that the price elasticity coefficients for domestic and imported cigarettes were –0.644 and –0.822. The consumption of imported cigarettes was reduced by 7.51 packs per capita, and the consumption of domestic cigarettes was reduced by 15.21 packs per capita. Total per capita consumption of cigarettes was reduced by 22.72 packs (18%). Conclusions: From the public health and financial perspectives, the increase in this excise tax on tobacco to the Taiwan government will have significant effect in reducing cigarette consumption; it will also generate additional tax revenues. PMID:15923453

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

    PubMed

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

    2016-01-12

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

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

    PubMed Central

    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

  2. Cigarette Smoking Accelerated Brain Aging and Induced Pre-Alzheimer-Like Neuropathology in Rats

    PubMed Central

    Ho, Yuen-Shan; Yang, Xifei; Yeung, Sze-Chun; Chiu, Kin; Lau, Chi-Fai; Tsang, Andrea Wing-Ting; Mak, Judith Choi-Wo; Chang, Raymond Chuen-Chung

    2012-01-01

    Cigarette smoking has been proposed as a major risk factor for aging-related pathological changes and Alzheimer's disease (AD). To date, little is known for how smoking can predispose our brains to dementia or cognitive impairment. This study aimed to investigate the cigarette smoke-induced pathological changes in brains. Male Sprague-Dawley (SD) rats were exposed to either sham air or 4% cigarette smoke 1 hour per day for 8 weeks in a ventilated smoking chamber to mimic the situation of chronic passive smoking. We found that the levels of oxidative stress were significantly increased in the hippocampus of the smoking group. Smoking also affected the synapse through reducing the expression of pre-synaptic proteins including synaptophysin and synapsin-1, while there were no changes in the expression of postsynaptic protein PSD95. Decreased levels of acetylated-tubulin and increased levels of phosphorylated-tau at 231, 205 and 404 epitopes were also observed in the hippocampus of the smoking rats. These results suggested that axonal transport machinery might be impaired, and the stability of cytoskeleton might be affected by smoking. Moreover, smoking affected amyloid precursor protein (APP) processing by increasing the production of sAPPβ and accumulation of β–amyloid peptide in the CA3 and dentate gyrus region. In summary, our data suggested that chronic cigarette smoking could induce synaptic changes and other neuropathological alterations. These changes might serve as evidence of early phases of neurodegeneration and may explain why smoking can predispose brains to AD and dementia. PMID:22606286

  3. Variation in, and causes of, toxicity of cigarette butts to a cladoceran and microtox.

    PubMed

    Micevska, T; Warne, M St J; Pablo, F; Patra, R

    2006-02-01

    Cigarette butts are the most numerically frequent form of litter in the world. In Australia alone, 24-32 billion cigarette butts are littered annually. Despite this littering, few studies have been undertaken to explore the toxicity of cigarette butts in aquatic ecosystems. The acute toxicity of 19 filtered cigarette types to Ceriodaphnia cf. dubia (48-hr EC50 (immobilization)) and Vibrio fischeri (30-min EC50 (bioluminescence)) was determined using leachates from artificially smoked cigarette butts. There was a 2.9- and 8-fold difference in toxicity between the least and most toxic cigarette butts to C. cf. dubia and V. fischeri, respectively. Overall, C. cf. dubia was more inherently sensitive than V. fischeri by a factor of approximately 15.4, and the interspecies relationship between C. cf. dubia and V. fischeri was poor (R(2) = 0.07). This poor relationship indicates that toxicity data for cigarette butts for one species could not predict or model the toxicity of cigarette butts to the other species. However, the order of the toxicity of leachates can be predicted. It was determined that organic compounds caused the majority of toxicity in the cigarette butt leachates. Of the 14 organic compounds identified, nicotine and ethylphenol were suspected to be the main causative toxicants. There was a strong relationship between toxicity and tar content and between toxicity and nicotine content for two of the three brands of cigarettes (R(2 )> 0.70) for C. cf. dubia and one brand for V. fischeri. However, when the cigarettes were pooled, the relationship was weak (R(2) < 0.40) for both test species. Brand affected the toxicity to both species but more so for V. fischeri.

  4. 19 CFR 159.5 - Cigars, cigarettes, and cigarette papers and tubes.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 19 Customs Duties 2 2012-04-01 2012-04-01 false Cigars, cigarettes, and cigarette papers and tubes..., and cigarette papers and tubes. The internal revenue taxes imposed on cigars, cigarettes, and cigarette papers and tubes under section 5701 or 7652, Internal Revenue Code of 1954 (26 U.S.C. 5701 or...

  5. 19 CFR 159.5 - Cigars, cigarettes, and cigarette papers and tubes.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

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

  6. 19 CFR 159.5 - Cigars, cigarettes, and cigarette papers and tubes.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 19 Customs Duties 2 2013-04-01 2013-04-01 false Cigars, cigarettes, and cigarette papers and tubes..., and cigarette papers and tubes. The internal revenue taxes imposed on cigars, cigarettes, and cigarette papers and tubes under section 5701 or 7652, Internal Revenue Code of 1954 (26 U.S.C. 5701 or...

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

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 19 Customs Duties 2 2011-04-01 2011-04-01 false Cigars, cigarettes, and cigarette papers and tubes..., and cigarette papers and tubes. The internal revenue taxes imposed on cigars, cigarettes, and cigarette papers and tubes under section 5701 or 7652, Internal Revenue Code of 1954 (26 U.S.C. 5701 or...

  8. 19 CFR 159.5 - Cigars, cigarettes, and cigarette papers and tubes.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 19 Customs Duties 2 2014-04-01 2014-04-01 false Cigars, cigarettes, and cigarette papers and tubes..., and cigarette papers and tubes. The internal revenue taxes imposed on cigars, cigarettes, and cigarette papers and tubes under section 5701 or 7652, Internal Revenue Code of 1954 (26 U.S.C. 5701 or...

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

    Technology Transfer Automated Retrieval System (TEKTRAN)

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

  10. 27 CFR 41.34 - Cigarette papers.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2012-04-01 2011-04-01 true Cigarette papers. 41.34... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.34 Cigarette papers. Cigarette papers are taxed at the...

  11. 27 CFR 41.38 - Cigarettes.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2010-04-01 2010-04-01 false Cigarettes. 41.38 Section... THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Classification of Large Cigars and Cigarettes § 41.38 Cigarettes. For...

  12. 27 CFR 41.38 - Cigarettes.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2011-04-01 2011-04-01 false Cigarettes. 41.38 Section... THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Classification of Large Cigars and Cigarettes § 41.38 Cigarettes. For...

  13. 27 CFR 41.34 - Cigarette papers.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2013-04-01 2013-04-01 false Cigarette papers. 41.34... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.34 Cigarette papers. Cigarette papers are taxed at the...

  14. 27 CFR 41.38 - Cigarettes.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2014-04-01 2014-04-01 false Cigarettes. 41.38 Section... THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Classification of Large Cigars and Cigarettes § 41.38 Cigarettes. For...

  15. 27 CFR 41.34 - Cigarette papers.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2014-04-01 2014-04-01 false Cigarette papers. 41.34... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.34 Cigarette papers. Cigarette papers are taxed at the...

  16. 27 CFR 40.351 - Cigarette papers.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2011-04-01 2011-04-01 false Cigarette papers. 40.351... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Manufacture of Cigarette Papers and Tubes Taxes § 40.351 Cigarette papers....

  17. 27 CFR 40.351 - Cigarette papers.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2013-04-01 2013-04-01 false Cigarette papers. 40.351... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Manufacture of Cigarette Papers and Tubes Taxes § 40.351 Cigarette papers....

  18. 27 CFR 41.34 - Cigarette papers.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

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

  19. 27 CFR 41.34 - Cigarette papers.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2011-04-01 2011-04-01 false Cigarette papers. 41.34... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.34 Cigarette papers. Cigarette papers are taxed at the...

  20. 27 CFR 40.351 - Cigarette papers.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

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

  1. 27 CFR 41.38 - Cigarettes.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2013-04-01 2013-04-01 false Cigarettes. 41.38 Section... THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Classification of Large Cigars and Cigarettes § 41.38 Cigarettes. For...

  2. 27 CFR 41.38 - Cigarettes.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2012-04-01 2011-04-01 true Cigarettes. 41.38 Section... THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Classification of Large Cigars and Cigarettes § 41.38 Cigarettes. For...

  3. 27 CFR 40.351 - Cigarette papers.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2012-04-01 2011-04-01 true Cigarette papers. 40.351... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Manufacture of Cigarette Papers and Tubes Taxes § 40.351 Cigarette papers....

  4. Functional Analysis and Treatment of Cigarette Pica.

    ERIC Educational Resources Information Center

    Piazza, Cathleen C.; And Others

    1996-01-01

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

  5. 27 CFR 41.35 - Cigarette tubes.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2013-04-01 2013-04-01 false Cigarette tubes. 41.35... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.35 Cigarette tubes. Cigarette tubes are taxed at the following...

  6. 27 CFR 41.35 - Cigarette tubes.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2011-04-01 2011-04-01 false Cigarette tubes. 41.35... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.35 Cigarette tubes. Cigarette tubes are taxed at the following...

  7. 27 CFR 41.35 - Cigarette tubes.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2014-04-01 2014-04-01 false Cigarette tubes. 41.35... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.35 Cigarette tubes. Cigarette tubes are taxed at the following...

  8. 27 CFR 41.35 - Cigarette tubes.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2012-04-01 2011-04-01 true Cigarette tubes. 41.35... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.35 Cigarette tubes. Cigarette tubes are taxed at the following...

  9. 27 CFR 41.35 - Cigarette tubes.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2010-04-01 2010-04-01 false Cigarette tubes. 41.35... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.35 Cigarette tubes. Cigarette tubes are taxed at the following...

  10. [Contact allergy from cigarette smoking].

    PubMed

    Rat, J P; Larregue, M

    1987-04-01

    Usually, recorded cases of allergic contact dermatitis to tobacco are confined to occupational diseases and involve agricultural workers and those engaged in manufacturing or selling the products, all of whom are in contact with tobacco leaves. We have found three cases of contact dermatitis caused by cigarette smoke, which are not occupational disease. We do not know what offending agent is, but in one case the patient is allergic to perfume and this may be the factor responsible, since she smokes only flavoured cigarettes. In addition, we need to know whether the allergen only appears during combustion and is therefore present only in cigarette smoke.

  11. Analysis of metals leached from smoked cigarette litter

    PubMed Central

    Moerman, J W

    2011-01-01

    Background Littered cigarette butts represent potential point sources for environmental contamination. In areas with substantial amounts of cigarette litter, environmental hazards may arise as chemical components are leached from the filters and smoked tobacco. Objective The three main aims of this study were: (1) to quantify the amount of Al, Ba, Cd, Cr, Cu, Fe, Pb, Mn, Ni, Sr, Ti and Zn leached from cigarette butts, (2) to determine the relationship between the pH of the aqueous soaking solution and metal concentration leached and (3) to determine the relationship between the period of soaking in aqueous solution and metal concentration leached. Methods Smoked cigarette butts and unsmoked cigarettes were added to phials containing aqueous solutions of pH 4.00, 5.00 and 6.00 (±0.05). The metal concentration of the resultant leachates was measured via inductively coupled plasma optical emission spectroscopy (ICP-OES) 1 day, 7 days and 34 days after sample addition. Results All metals were detected in leachates 1 day after sample addition (with the exception of Cd) and were released at varying rates. No clear relationship between pH within the range typical of precipitation and metal concentration leached was observed. Conclusions Based on the gradual release of multiple metals over the full 34-day study period, cigarette litter was found to be a point source for metal contamination. The apparent rapid leaching of other metals may increase the risk of acute harm to local organisms. PMID:21504922

  12. NF-{kappa}B inhibition is involved in tobacco smoke-induced apoptosis in the lungs of rats

    SciTech Connect

    Zhong Caiyun; Zhou Yamei; Pinkerton, Kent E.

    2008-07-15

    Apoptosis is a vital mechanism for the regulation of cell turnover and plays a critical role in tissue homeostasis and development of many disease processes. Previous studies have demonstrated the apoptotic effect of tobacco smoke; however, the molecular mechanisms by which tobacco smoke triggers apoptosis remain unclear. In the present study we investigated the effects of tobacco smoke on the induction of apoptosis in the lungs of rats and modulation of nuclear factor-kappa B (NF-{kappa}B) in this process. Exposure of rats to 80 mg/m{sup 3} tobacco smoke significantly induced apoptosis in the lungs. Tobacco smoke resulted in inhibition of NF-{kappa}B activity, noted by suppression of inhibitor of {kappa}B (I{kappa}B) kinase (IKK), accumulation of I{kappa}B{alpha}, decrease of NF-{kappa}B DNA binding activity, and downregulation of NF-{kappa}B-dependent anti-apoptotic proteins, including Bcl-2, Bcl-xl, and inhibitors of apoptosis. Initiator caspases for the death receptor pathway (caspase 8) and the mitochondrial pathway (caspase 9) as well as effector caspase 3 were activated following tobacco smoke exposure. Tobacco smoke exposure did not alter the levels of p53 and Bax proteins. These findings suggest the role of NF-{kappa}B pathway in tobacco smoke-induced apoptosis.

  13. Cardiology Patient Page: Electronic Cigarettes

    MedlinePlus

    ... Hookah Pens and Vapes: Adolescent and Young Adult Perceptions of Electronic Nicotine Delivery Systems Do stronger school ... the health behaviour in school-aged children survey Perception of electronic cigarettes in the general population: does ...

  14. E-Cigarettes (For Parents)

    MedlinePlus

    ... For Parents MORE ON THIS TOPIC Kids and Smoking Secondhand Smoke Nicotine: What Parents Need to Know Word! Nicotine Smoking Stinks! Smokeless Tobacco E-Cigarettes Smoking Secondhand Smoke How Can I Quit Smoking? Contact Us ...

  15. The fire-safe cigarette.

    PubMed

    Botkin, J R

    1988-07-01

    Fires caused by cigarettes through the ignition of upholstered furniture and mattresses are a serious public health problem, accounting for more than 1500 deaths and 7000 serious injuries per year in the United States. Fire-resistant fabrics and stuffings, public education, and smoke detectors have had a limited impact on this problem. The federal government recently has completed a three-year study of possible modifications in cigarette design. The study has demonstrated the technical feasibility of product design changes that would substantially reduce the propensity of cigarettes to ignite fires. Legislation currently is pending in Congress and in three state legislatures to mandate a cigarette fire safety standard. This legislation deserves strong support by the medical profession.

  16. Effect of hydrogen injected subcutaneously on testicular tissues of rats exposed to cigarette smoke

    PubMed Central

    Chen, Song; Jiang, Wei

    2015-01-01

    Smoking is one of the most common reasons inducing reactive oxygen species in semen. High concentration of active oxygen will cause decrease of sperm density and viability and induce oxidative injury of sperm DNA which has become the hot spot in male infertility. Although hydrogen was found to be an effective remover of active oxygen in liver, heart, kidney and brain, the same effect has not been discussed in reproductive system. The aim of this study was to investigate the protective effect of hydrogen against cigarette smoke-induced damage in rat reproductive system. Adult male Wistar rats were randomly divided into four groups to conduct this experiment, results showed that rats in SK+HSI group (passive smoking and hydrogen subcutaneous injection group) exhibited larger amount of sperm count, smaller sperm deformation rate, higher levels of testosterone and SOD in serum and testis, lower levels of MDA in testis and less morphologic abnormalities compared to SK+NSI group (passive smoking and nitrogen subcutaneous injection group). As a consequence, we concluded that injected subcutaneously exerted protective effects on reproductive system injury of male rats exposed to cigarette smoke through inhibiting oxidative damage. PMID:26131139

  17. Cigarette smoking and nickel exposure.

    PubMed

    Torjussen, William; Zachariasen, Hans; Andersen, Ivar

    2003-04-01

    The tobacco plant contains nickel and several other toxic metals, most probably absorbed from the soil, fertilizing products or from pesticides. It has been stated that nickel in a burning cigarette might form the volatile, gaseous compound, nickel tetracarbonyl, and thereby be introduced into the respiratory tract. Accordingly, the main objective of the present study was to find out if nickel content in inhaled smoke from ordinary cigarettes and nickel-contaminated cigarettes handmade by nickel process workers might be a supplementary source of nickel exposure to cigarette smoking process workers leading to additional risk of occupational respiratory cancer in these workers. Blood and urine samples from 318 randomly selected employees from Falconbridge Nickel Refinery in Kristiansand, Norway, allocated to 197 smokers and 121 non-smokers, were analysed for nickel content. Nickel quantities in tobacco from various cigarette brands, from nickel-contaminated cigarettes made by process workers or from cigarettes added known amounts of various nickel salts were analysed before being smoked. The cigarettes were smoked in a smoking machine device applying an electrostatic filter. Blood and urine, tobacco, ash and precipitates in the filter from the main stream smoke of the cigarettes were analysed for nickel quantities by atomic absorption spectrometry methods as previously described by the authors. The nickel concentrations in blood plasma and urine were quite similar among smokers and non-smokers, 6.2 and 48.1 microg L(-1) in smokers, and 6.4 and 50.5 microg L(-1) in non-smokers respectively. We recovered 1.1% or even less of nickel in the mainstream smoke after smoking the entire cigarettes without leaving any butt. Most of the tobacco nickel was recovered in the ash. We conclude that the inhaled nickel in the working atmosphere is probably the main source of the nickel exposure to the respiratory tract in these workers. It remains to be determined why cigarette

  18. Cigarette smoking and nickel exposure.

    PubMed

    Torjussen, William; Zachariasen, Hans; Andersen, Ivar

    2003-04-01

    The tobacco plant contains nickel and several other toxic metals, most probably absorbed from the soil, fertilizing products or from pesticides. It has been stated that nickel in a burning cigarette might form the volatile, gaseous compound, nickel tetracarbonyl, and thereby be introduced into the respiratory tract. Accordingly, the main objective of the present study was to find out if nickel content in inhaled smoke from ordinary cigarettes and nickel-contaminated cigarettes handmade by nickel process workers might be a supplementary source of nickel exposure to cigarette smoking process workers leading to additional risk of occupational respiratory cancer in these workers. Blood and urine samples from 318 randomly selected employees from Falconbridge Nickel Refinery in Kristiansand, Norway, allocated to 197 smokers and 121 non-smokers, were analysed for nickel content. Nickel quantities in tobacco from various cigarette brands, from nickel-contaminated cigarettes made by process workers or from cigarettes added known amounts of various nickel salts were analysed before being smoked. The cigarettes were smoked in a smoking machine device applying an electrostatic filter. Blood and urine, tobacco, ash and precipitates in the filter from the main stream smoke of the cigarettes were analysed for nickel quantities by atomic absorption spectrometry methods as previously described by the authors. The nickel concentrations in blood plasma and urine were quite similar among smokers and non-smokers, 6.2 and 48.1 microg L(-1) in smokers, and 6.4 and 50.5 microg L(-1) in non-smokers respectively. We recovered 1.1% or even less of nickel in the mainstream smoke after smoking the entire cigarettes without leaving any butt. Most of the tobacco nickel was recovered in the ash. We conclude that the inhaled nickel in the working atmosphere is probably the main source of the nickel exposure to the respiratory tract in these workers. It remains to be determined why cigarette

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

    PubMed

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

    2005-01-01

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

  20. Cigarette tax avoidance and evasion.

    PubMed

    Stehr, Mark

    2005-03-01

    Variation in state cigarette taxes provides incentives for tax avoidance through smuggling, legal border crossing to low tax jurisdictions, or Internet purchasing. When taxes rise, tax paid sales of cigarettes will decline both because consumption will decrease and because tax avoidance will increase. The key innovation of this paper is to compare cigarette sales data to cigarette consumption data from the Behavioral Risk Factor Surveillance System (BRFSS). I show that after subtracting percent changes in consumption, residual percent changes in sales are associated with state cigarette tax changes implying the existence of tax avoidance. I estimate that the tax avoidance response to tax changes is at least twice the consumption response and that tax avoidance accounted for up to 9.6% of sales between 1985 and 2001. Because of the increase in tax avoidance, tax paid sales data understate the level of smoking and overstate the drop in smoking. I also find that the level of legal border crossing was very low relative to other forms of tax avoidance. If states have strong preferences for smoking control, they must pair high cigarette taxes with effective policies to curb smuggling and other forms of tax avoidance or employ alternative policies such as counter-advertising and smoking restrictions. PMID:15721046

  1. Longitudinal Trajectories of Cigarette Smoking Following Rape

    PubMed Central

    Amstadter, Ananda B.; 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 (< 3 months, 3-6 months, and > 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 trajectories. Of participants endorsing smoking post-rape, a two-class solution was identified, with the majority of participants (74.6%) evidencing moderate smoking with a slight decrease over time and remaining participants showing heavy smoking with a slight increase over time. Having sustained an injury, minority status, and post-exam distress all predicted subsequent smoking trajectory. PMID:19370699

  2. Electronic Cigarette Use by College Students

    PubMed Central

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

    2013-01-01

    Background Electronic cigarettes, or ecigarettes, are battery operated devices that deliver nicotine via inhaled vapor. There is considerable controversy about the disease risk and toxicity of ecigarettes and empirical evidence on short- and long-term health effects is minimal. Limited data on e-cigarette use and correlates exist, and to our knowledge, no prevalence rates among U.S. college students have been reported. This study aimed to estimate the prevalence of ecigarette use and identify correlates of use among a large, multi-institution, random sample of college students. Methods 4,444 students from 8 colleges in North Carolina completed a Webbased survey in fall 2009. Results Ever use of ecigarettes was reported by 4.9% of students, with 1.5% reporting past month use. Correlates of ever use included male gender, Hispanic or “Other race” (compared to non-Hispanic Whites), Greek affiliation, conventional cigarette smoking and e-cigarette harm perceptions. Although e-cigarette use was more common among conventional cigarette smokers, 12% of ever e-cigarette users had never smoked a conventional cigarette. Among current cigarette smokers, e-cigarette use was negatively associated with lack of knowledge about e-cigarette harm, but was not associated with intentions to quit. Conclusions Although e-cigarette use was more common among conventional cigarette smokers, it was not exclusive to them. E-cigarette use was not associated with intentions to quit smoking among a sub-sample of conventional cigarette smokers. Unlike older, more established cigarette smokers, e-cigarette use by college students does not appear to be motivated by the desire to quit cigarette smoking. PMID:23746429

  3. Expectancies for Cigarettes, E-Cigarettes, and Nicotine Replacement Therapies Among E-Cigarette Users (aka Vapers)

    PubMed Central

    Marquinez, Nicole S.; Correa, John B.; Meltzer, Lauren R.; Unrod, Marina; Sutton, Steven K.; Simmons, Vani N.; Brandon, Thomas H.

    2015-01-01

    Introduction: Use of e-cigarettes has been increasing exponentially, with the primary motivation reported as smoking cessation. To understand why smokers choose e-cigarettes as an alternative to cigarettes, as well as to US Food and Drug Administration (FDA)–approved nicotine replacement therapies (NRT), we compared outcome expectancies (beliefs about the results of drug use) for the three nicotine delivery systems among vapers, i.e., e-cigarette users, who were former smokers. Methods: Vapers (N = 1,434) completed an online survey assessing 14 expectancy domains as well as perceived cost and convenience. We focused on comparisons between e-cigarettes and cigarettes to determine the attraction of e-cigarettes as a smoking alternative and between e-cigarettes and NRT to determine perceived advantages of e-cigarettes over FDA-approved pharmacotherapy. Results: Participants believed that e-cigarettes, in comparison to conventional cigarettes, had fewer health risks; caused less craving, withdrawal, addiction, and negative physical feelings; tasted better; and were more satisfying. In contrast, conventional cigarettes were perceived as better than e-cigarettes for reducing negative affect, controlling weight, providing stimulation, and reducing stress. E-cigarettes, compared to NRT, were perceived to be less risky, cost less, cause fewer negative physical feelings, taste better, provide more satisfaction, and be better at reducing craving, negative affect, and stress. Moderator analyses indicated history with ad libitum forms of NRT was associated with less positive NRT expectancies. Conclusions: The degree to which expectancies for e-cigarettes differed from expectancies for either tobacco cigarettes or NRT offers insight into the motivation of e-cigarette users and provides guidance for public health and clinical interventions to encourage smoking-related behavior change. PMID:25168035

  4. Doctors Divided on Safety, Use of Electronic Cigarettes

    MedlinePlus

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

  5. Identification of differentially expressed proteins in blood plasma of control and cigarette smoke-exposed mice by 2D differential in-gel electrophoresis/MS

    PubMed Central

    Tewari, Arun K.; Popova-Butler, Alexandra; El-Mahdy, Mohamed A.; Zweier, Jay L.

    2014-01-01

    Cigarette smoke exposure is known to induce obstructive lung disease and several cardiovascular disease states in humans and also in animal models. Smoking leads to oxidative stress and inflammation that are important in triggering pulmonary and cardiovascular disease. The objective of the current study was to quantify differences in expression levels of plasma proteins of cigarette smoke exposed and control mice, at the time of disease onset, and identify these proteins for use as potential biomarkers of the onset of smoking-induced disease. We utilized two dimensional difference in-gel electrophoresis/ mass spectroscopy (2D-DIGE/MS) to characterize these proteomic changes. 2D-DIGE of plasma samples identified 11 differentially expressed proteins in cigarette smoke exposed mice. From these 11 proteins, 9 were down-regulated and two were up-regulated. The proteins identified are involved in vascular function, coagulation, metabolism, and immune function. Among these, the alterations in fibrinogen (2.2 fold decrease), alpha-1-antitrypsin (1.8 fold increase) and arginase (4.5 fold decrease) are of particular interest since these have been directly linked to cardiovascular and lung pathology. Differences in expression levels of these proteins were also confirmed by immunoblotting. Thus, we observe that chronic cigarette smoke exposure in mice leads to prominent changes in the protein expression profile of blood plasma and these changes in turn can potentially serve as markers predictive of the onset and progression of cardiovascular and pulmonary disease. PMID:21500341

  6. Cigarette smoking in China: public health, science, and policy.

    PubMed

    Au, William W; Su, Daisy; Yuan, Jiang

    2012-01-01

    Throughout the world, cigarette smoking is a habit that causes serious health, economic, and social problems. Therefore, many countries have taken an active role to control and to ban smoking. The chronic smoking problem in China is particularly acute because China has the largest population of smokers in the world, over 300 million currently. If 30% of these smokers were to die of smoke-related diseases in the next 20 years, the impact from the more than 90 million premature deaths could be damaging to China. In addition, numerous non-smokers also experience health problems from exposure to environmental tobacco smoke. China's efforts to reduce or to ban smoking in certain public places have not been well-coordinated or enforced compared with those in other countries. Therefore, success has been minimal. Consequently, leaders in China should not be complacent about combating the serious national health problem. A multiprong approach in combination with the MPOWER policy from the World Health Organization that targets different levels of acquisition of the smoking habit must be used. Examples may include the government's reduced reliance on profits from the sale of cigarettes, the elimination of advertisements that encourage smoking among young individuals, the presentation of more graphic illustration of harmful effects from smoking on every pack of cigarettes, higher taxes/prices on cigarettes, and the implementation of enforceable bans on smoking in public places. As shown in other countries, such coordinated effort can be highly effective in the reduction of smoking and can have healthy consequences.

  7. E-Cigarette Awareness and Perceived Harmfulness

    PubMed Central

    Tan, Andy S.L.; Bigman, Cabral A.

    2014-01-01

    Background Electronic cigarettes, or e-cigarettes, are increasingly advertised as replacements for regular cigarettes or cessation aids for smokers. Purpose To describe the prevalence and correlates of e-cigarette awareness and perceived harmfulness among U.S. adults and analyze whether these variables are associated with smokers’ past year quit attempts and intention to quit. Methods Data were obtained from the Health Information National Trends Survey (HINTS 4 Cycle 2), conducted from October 2012 to January 2013. Data analyses were performed from June to August 2013. Results Overall, 77% of respondents were aware of e-cigarettes. Of these, 51% believed e-cigarettes were less harmful than cigarettes. Younger, white (compared with Hispanic), more educated respondents, and current or former smokers (compared with non-smokers) were more likely to be aware of e-cigarettes. Among those who were aware of e-cigarettes, younger, more educated respondents and current smokers (compared with former and non-smokers) were more likely to believe that e-cigarettes were less harmful. Awareness and perceived harm were not associated with smokers’ past year quit attempts or intention to quit. Conclusions Overall e-cigarette awareness increased while smokers’ perceived harm of e-cigarettes declined compared with earlier surveys. However, awareness and perceived harm of e-cigarettes did not show evidence of promoting smoking cessation at the population level. PMID:24794422

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

    PubMed

    Wang, Guoqing; Wang, Rui; Strulovici-Barel, Yael; Salit, Jacqueline; Staudt, Michelle R; Ahmed, Joumana; Tilley, Ann E; Yee-Levin, Jenny; Hollmann, Charleen; Harvey, Ben-Gary; Kaner, Robert J; Mezey, Jason G; Sridhar, Sriram; Pillai, Sreekumar G; Hilton, Holly; Wolff, Gerhard; Bitter, Hans; Visvanathan, Sudha; Fine, Jay S; Stevenson, Christopher S; Crystal, Ronald G

    2015-01-01

    Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD) and lung cancer remains significantly higher compared to healthy nonsmokers. Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE), we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 9 healthy nonsmokers and 10 healthy smokers, before and after they quit smoking for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy nonsmokers (p<0.01, fold-change >1.5), with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/β-catenin signaling pathway being the top identified enriched pathway of the target genes of the persistent dysregulated miRNAs. In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammatory diseases or lung cancer, it is likely that persistent smoking-related changes in SAE miRNAs play a role in the subsequent development of these disorders.

  9. [The angiopathic risk of inhaling smoke and the "less harmful cigarette". Utopia or chance? (author's transl)].

    PubMed

    Marshall, M

    1981-03-13

    The carbon monoxide concentrations already found in the work place causes functional damage to the cardiovascular system; CO loads such as occur in cigarette smoking may lead to additional morphologically detectable damage. Nicotine appears to act more through its acute circulatory functional and hemorheologic effects. Consequently the carbon monoxide in cigarette smoke must be considered a potentially dangerous factor for the vascular system, so that a "less harmful cigarette" in this connection must have a low concentration of carbon monoxide in the smoke. In order to be in the assuredly harmless range -- e.g. even for patients with coronary heart disease -- the COHb should lie below 3%. As long as this cannot be achieved, a "less harmful cigarette" remains utopian with regard to the angiopathic risk.

  10. Wnt5a Is Associated with Cigarette Smoke-Related Lung Carcinogenesis via Protein Kinase C

    PubMed Central

    Sung, Jae Sook; Ju, Hyun Jung; Kim, Hyun Kyung; Park, Kyong Hwa; Lee, Jong Won; Koh, In Song; Kim, Yeul Hong

    2013-01-01

    Wnt5a is overexpressed during the progression of human non-small cell lung cancer. However, the roles of Wnt5a during smoking-related lung carcinogenesis have not been clearly elucidated. We investigated the associations between Wnt5a and the early development of cigarette smoke related lung cancer using human bronchial epithelial (HBE) cells (NHBE, BEAS-2B, 1799, 1198 and 1170I) at different malignant stages established by exposure to cigarette smoke condensate (CSC). Abnormal up-regulation of Wnt5a mRNA and proteins was detected in CSC-exposed transformed 1198 and tumorigenic 1170I cells as compared with other non-CSC exposed HBE cells. Tumor tissues obtained from smokers showed higher Wnt5a expressions than matched normal tissues. In non-CSC exposed 1799 cells, treatment of recombinant Wnt5a caused the activations of PKC and Akt, and the blockage of Wnt5a and PKC significantly decreased the viabilities of CSC-transformed 1198 cells expressing high levels of Wnt5a. This reduced cell survival rate was associated with increased apoptosis via the down-regulation of Bcl2 and the induction of cleaved poly ADP-ribose polymerase. Moreover, CSC-treated 1799 cells showed induction of Wnt5a expression and enhanced colony-forming capacity. The CSC-induced colony forming efficiency was suppressed by the co-incubation with a PKC inhibitor. In conclusion, these results suggest that cigarette smoke induces Wnt5a-coupled PKC activity during lung carcinogenesis, which causes Akt activity and anti-apoptosis in lung cancer. Therefore, current study provides novel clues for the crucial role of Wnt5a in the smoking-related lung carcinogenesis. PMID:23349696

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

    PubMed

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

    2016-04-01

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

  12. E-cigarettes and E-hookahs

    MedlinePlus

    Electronic cigarettes; Electronic hookahs; Vaping; Electronic nicotine delivery systems; Smoking - electronic cigarettes ... cartridge into a vapor. The cartridge may contain nicotine or other flavors or chemicals. It also contains ...

  13. E-Cigarettes Emit Toxic Vapors

    MedlinePlus

    ... 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 ...

  14. 19 CFR 11.2a - Release from Customs custody without payment of tax on cigars, cigarettes and cigarette papers...

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 19 Customs Duties 1 2014-04-01 2014-04-01 false Release from Customs custody without payment of tax on cigars, cigarettes and cigarette papers and tubes. 11.2a Section 11.2a Customs Duties U.S... cigars, cigarettes and cigarette papers and tubes. Cigars, cigarettes, and cigarette papers and tubes...

  15. 19 CFR 11.2a - Release from Customs custody without payment of tax on cigars, cigarettes and cigarette papers...

    Code of Federal Regulations, 2010 CFR

    2010-04-01

    ... 19 Customs Duties 1 2010-04-01 2010-04-01 false Release from Customs custody without payment of tax on cigars, cigarettes and cigarette papers and tubes. 11.2a Section 11.2a Customs Duties U.S... cigars, cigarettes and cigarette papers and tubes. Cigars, cigarettes, and cigarette papers and tubes...

  16. 19 CFR 11.2a - Release from Customs custody without payment of tax on cigars, cigarettes and cigarette papers...

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 19 Customs Duties 1 2011-04-01 2011-04-01 false Release from Customs custody without payment of tax on cigars, cigarettes and cigarette papers and tubes. 11.2a Section 11.2a Customs Duties U.S... cigars, cigarettes and cigarette papers and tubes. Cigars, cigarettes, and cigarette papers and tubes...

  17. 19 CFR 11.2a - Release from Customs custody without payment of tax on cigars, cigarettes and cigarette papers...

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 19 Customs Duties 1 2012-04-01 2012-04-01 false Release from Customs custody without payment of tax on cigars, cigarettes and cigarette papers and tubes. 11.2a Section 11.2a Customs Duties U.S... cigars, cigarettes and cigarette papers and tubes. Cigars, cigarettes, and cigarette papers and tubes...

  18. 19 CFR 11.2a - Release from Customs custody without payment of tax on cigars, cigarettes and cigarette papers...

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 19 Customs Duties 1 2013-04-01 2013-04-01 false Release from Customs custody without payment of tax on cigars, cigarettes and cigarette papers and tubes. 11.2a Section 11.2a Customs Duties U.S... cigars, cigarettes and cigarette papers and tubes. Cigars, cigarettes, and cigarette papers and tubes...

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

    PubMed Central

    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

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

    PubMed

    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.

  1. Electronic cigarettes: a short review.

    PubMed

    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.

  2. Characterization of topographic EEG changes when smoking a cigarette.

    PubMed

    Shikata, H; Fukai, H; Ohya, I; Sakaki, T

    1995-06-01

    The acute effects of cigarette smoking on the human electroencephalogram (EEG) were investigated by the topographic mapping technique. Twenty-six subjects participated in this study, which involved sham smoking and real smoking of preferred cigarettes. Effects of smoking were analyzed by statistical and multivariate analysis. Analysis of variance and t-test results showed a significant decrease in the theta and alpha 1 bands but a significant increase in the alpha 2, beta 1, and beta 2 bands. Factor analysis and cluster analysis showed that there were two or three independent regions on the scalp that indicate the effects of smoking on topographic EEG. A hypothesis was formed that smoking has different effects on human EEG profiles for different brain regions and that there are individual variations in the EEG responses to smoking.

  3. Polonium-210 budget in cigarettes.

    PubMed

    Khater, Ashraf E M

    2004-01-01

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

  4. Reducing the addictiveness of cigarettes

    PubMed Central

    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 relevant journal articles, other government publications, and presentations made at scientific conferences.
DATA SYNTHESIS—The role of nicotine in causing and sustaining tobacco use was evaluated to project the impact of a nicotine reduction strategy on initiation and maintenance of, and relapse to, tobacco use. A range of potential concerns and barriers was addressed, including the technical feasibility of reducing cigarette nicotine content to non-addictive levels, the possibility that compensatory smoking would reduce potential health benefits, and whether such an approach would foster illicit ("black market") tobacco sales. Education, treatment, and research needs to enable a nicotine reduction strategy were also addressed. The Council on Scientific Affairs came to the following conclusions: (a) gradually eliminating nicotine from cigarettes is technically feasible; (b) a nicotine reduction strategy holds great promise in preventing adolescent tobacco addiction and assisting the millions of current cigarette smokers in their efforts to quit using tobacco products; (c) potential problems such as compensatory over-smoking of denicotinised cigarettes and black market sales could be minimised by providing alternate forms of nicotine delivery with less or little risk to health, as part of expanded access to treatment; and (d) such a strategy would need to be accompanied by relevant research and increased efforts to educate consumers and health professionals about

  5. Corrective Taxes and Cigarette Characteristics.

    PubMed

    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.

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

    PubMed

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

    2015-02-01

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

  7. Material coefficients of the strain energy function of pulmonary arteries in normal and cigarette smoke-exposed rats.

    PubMed

    Liu, S Q; Fung, Y C

    1993-11-01

    The effect of cigarette smoke on the stress-strain relationship of pulmonary arteries was studied in 2- and 3-month smoke-exposed rats. The animals were exposed to cigarette smoke in a smoke-generating system 10 times daily with one cigarette each time. The smoke density and the puffing duration and frequency of the system were regulated in accordance with reference values measured from human smokers. The mechanical properties of the pulmonary arteries about 450 microns in external diameter (at zero pressure) were determined in vitro by inflation and deflation tests. The average stress and middle-wall strain of the selected pulmonary arteries were determined on the basis of experimental data including inflation and deflation pressures during loading and unloading processes, respectively, and vessel diameter and length at various pressure levels, and vessel circumferential and longitudinal lengths at zero-stress state. A constitutive equation for the pulmonary arteries was derived from an energy function depending on circumferential and longitudinal Green's strains. The coefficients of the strain energy function of the pulmonary arteries were determined in both the smoke-exposed and control rats by fitting the experimental stress-strain data with the constitutive equation. It was found that the wall stress of the pulmonary arteries at a given strain and most of the coefficients of the strain energy function were increased in both the 2- and 3-month smoke-exposed rats in comparison with those in the corresponding controls. These results indicated that cigarette smoke induced an increase in the wall stiffness of the pulmonary arteries in the rats. PMID:8262988

  8. Cardiac-Specific Overexpression of Metallothionein Rescues against Cigarette Smoking Exposure-Induced Myocardial Contractile and Mitochondrial Damage

    PubMed Central

    Hu, Nan; Han, Xuefeng; Lane, Erin K.; Gao, Feng; Zhang, Yingmei; Ren, Jun

    2013-01-01

    Objectives Second hand cigarette smoke is an independent risk factor for cardiovascular disease. Although a tie between smoking and cardiovascular disease is well established, the underlying mechanisms still remains elusive due to the lack of adequate animal models. This study was designed to use a mouse model of exposure to cigarette smoke, a surrogate of environmental tobacco smoke, to evaluate the impact of cardiac overexpression of heavy metal scavenger metallothionein on myocardial geometry, contractile and intracellular Ca2+ properties and apoptosis following side-stream smoke exposure. Methods Adult male wild-type FVB and metallothionein transgenic mice were placed in a chamber exposed to cigarette smoke for 1 hour daily for 40 days. Echocardiographic, cardiomyocyte contractile and intracellular Ca2+ properties, fibrosis, apoptosis and mitochondrial damage were examined. Results Our data revealed that smoke exposure enlarged ventricular end systolic and diastolic diameters, reduced myocardial and cardiomyocyte contractile function, disrupted intracellular Ca2+ homeostasis, facilitated fibrosis, apoptosis and mitochondrial damage (cytochrome C release and aconitase activity), the effects of which were attenuated or mitigated by metallothionein. In addition, side-stream smoke expose enhanced phosphorylation of Akt and GSK3β without affecting pan protein expression in the heart, the effect of which was abolished or ameliorated by metallothionein. Cigarette smoke extract interrupted cardiomyocyte contractile function and intracellular Ca2+ properties, the effect of which was mitigated by wortmannin and NAC. Conclusions These data suggest that side-stream smoke exposure led to myocardial dysfunction, intracellular Ca2+ mishandling, apoptosis, fibrosis and mitochondrial damage, indicating the therapeutic potential of antioxidant against in second smoking-induced cardiac defects possibly via mitochondrial damage and apoptosis. PMID:23431404

  9. [The challenge of electronic cigarettes].

    PubMed

    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.

  10. Carbonyl compounds generated from electronic cigarettes.

    PubMed

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

    2014-10-28

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

  11. Non-cigarette tobacco and the lung.

    PubMed

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

    2014-02-01

    Cigarette smoking is known to cause a wide range of damaging health outcomes; however, the effects of non-cigarette tobacco products are either unknown or perceived as less harmful than cigarettes. Smokeless tobacco, cigar smoking, and waterpipe smoking have increased in usage over the past few decades. Some experts believe that their use is reaching epidemic proportions. Factors such as a perception of harm reduction, targeted advertising, and unrecognized addiction may drive the increased consumption of non-cigarette tobacco products. In particular, the need for social acceptance, enjoyment of communal smoking activities, and exotic nature of waterpipe smoking fuels, in part, its popularity. The public is looking for "safer" alternatives to smoking cigarettes, and some groups advertise products such as smokeless tobacco and electronic cigarettes as the alternatives they seek. Though it is clear that cigar and waterpipe tobacco smoking are probably as dangerous to health as cigarette smoking, there is an opinion among users that the health risks are less compared to cigarette smoking. This is particularly true in younger age groups. In the cases of smokeless tobacco and electronic cigarettes, the risks to health are less clear and there may be evidence of a harm reduction compared to cigarettes. In this article, we discuss commonly used forms of non-cigarette tobacco products, their impacts on lung health, and relevant controversies surrounding their use. PMID:23673789

  12. Self-reported smoking effects and comparative value between cigarettes and high dose e-cigarettes in nicotine-dependent cigarette smokers.

    PubMed

    McPherson, Sterling; Howell, Donelle; Lewis, Jennifer; Barbosa-Leiker, Celestina; Bertotti Metoyer, Patrick; Roll, John

    2016-04-01

    The objective of this experiment was to evaluate the comparative value of cigarettes versus high dose e-cigarettes among nicotine-dependent cigarette smokers when compared with money or use of their usual cigarette brand. The experiment used a within-subject design with four sessions. After baseline assessment, participants attended two 15-min unrestricted smoking sessions: one cigarette smoking session and one e-cigarette smoking session. Participants then attended two multiple-choice procedure (MCP) sessions: a session comparing cigarettes and money and a session comparing e-cigarettes and money. Participants (n=27) had used cigarettes regularly, had never used e-cigarettes, and were not currently attempting to quit smoking. The sample consisted primarily of males (72%), with a mean age of 34 years. When given the opportunity to choose between smoking a cigarette or an e-cigarette, participants chose the cigarette 73.9% of the time. Findings from the MCP demonstrated that after the first e-cigarette exposure sessions, the crossover value for cigarettes ($3.45) was significantly higher compared with the crossover value for e-cigarettes ($2.73). The higher participant preference, self-reported smoking effects, and higher MCP crossover points indicate that cigarettes have a higher comparative value than high dose e-cigarettes among e-cigarette naive smokers.

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

    PubMed Central

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

    2014-01-01

    The electronic nicotine delivery system, also known as the electronic cigarette, is generating considerable controversy, not only in the general population but also among health professionals. Smokers the world over have been increasingly using electronic cigarettes as an aid to smoking cessation and as a substitute for conventional cigarettes. There are few available data regarding the safety of electronic cigarettes. There is as yet no evidence that electronic cigarettes are effective in 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. PMID:25410845

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

    PubMed

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

    2014-10-01

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

  15. Investigating cigarette affordability in 60 cities using the cigarette price‐daily income ratio

    PubMed Central

    Kan, Ming‐yue

    2007-01-01

    Objective To investigate cigarette affordability in 60 cities. Methods Affordability of cigarettes is defined as the ratio of the price of one pack of cigarettes to daily income (cigarette price‐daily income ratio: CPDIR). Daily income data were calculated using the mean of the seven occupations with the lowest daily wage, as listed in the 2006 Union Bank of Switzerland survey; cigarette prices in 2006 were sourced from the Economist Intelligence Unit. Results Cigarette affordability in most of the surveyed cities remains high. There is a tendency for cities with high income economies to have a high level of cigarette affordability. Most of the cities in Western Europe and South and North America have high cigarette affordability, whereas 66.7% of their counterparts in Eastern Europe have medium cigarette affordability. In Asia, all cities with high cigarette affordability belong to the group of upper middle to high income economies, except for the Philippines. In Africa, Johannesburg and Nairobi have high and medium levels of cigarette affordability, respectively. Conclusion Cigarette affordability for most of the sampled cities, especially those in high income economies, is high. There is room for increasing cigarette prices via tax increases. There is a risk that the increase in cigarette prices in newly emerging economies lags behind the high speed of economic growth being experiencing. Tax increases should be given high priority. PMID:18048622

  16. ILLICIT CIGARETTE TRADE IN THAILAND

    PubMed Central

    Pavananunt, Pirudee

    2012-01-01

    The sale and consumption of illicit tobacco increases consumption, impacts public health, reduces tax revenue and provides an argument against tax increases. Thailand has some of the best tobacco control policies in Southeast Asia with one of the highest tobacco tax rates, but illicit trade has the potential to undermine these policies and needs investigating. Two approaches were used to assess illicit trade between 1991 and 2006: method 1, comparison of tobacco used based on tobacco taxes paid and survey data, and method 2, discrepancies between export data from countries exporting tobacco to Thailand and Thai official data regarding imports. A three year average was used to smooth differences due to lags between exports and imports. For 1991–2006, the estimated manufactured cigarette consumption from survey data was considerably lower than sales tax paid, so method 1 did not provide evidence of cigarette tax avoidance. Using method 2 the trade difference between reported imports and exports, indicates 10% of cigarettes consumed in Thailand (242 million packs per year) between 2004 and 2006 were illicit. The loss of revenue amounted to 4,508 million Baht (2002 prices) in the same year, that was 14% of the total cigarette tax revenue. Cigarette excise tax rates had a negative relationship with consumption trends but no relation with the level of illicit trade. There is a need for improved policies against smuggling to combat the rise in illicit tobacco consumption. Regional coordination and implementation of protocols on illicit trade would help reduce incentives for illegal tax avoidance. PMID:22299425

  17. Progression to Traditional Cigarette Smoking After Electronic Cigarette Use Among US Adolescents and Young Adults

    PubMed Central

    Primack, Brian A.; Soneji, Samir; Stoolmiller, Michael; Fine, Michael J.; Sargent, James D.

    2016-01-01

    IMPORTANCE Electronic cigarettes (e-cigarettes) may help smokers reduce the use of traditional combustible cigarettes. However, adolescents and young adults who have never smoked traditional cigarettes are now using e-cigarettes, and these individuals may be at risk for subsequent progression to traditional cigarette smoking. OBJECTIVE To determine whether baseline use of e-cigarettes among nonsmoking and nonsusceptible adolescents and young adults is associated with subsequent progression along an established trajectory to traditional cigarette smoking. DESIGN, SETTING, AND PARTICIPANTS In this longitudinal cohort study, a national US sample of 694 participants aged 16 to 26 years who were never cigarette smokers and were attitudinally nonsusceptible to smoking cigarettes completed baseline surveys from October 1, 2012, to May 1, 2014, regarding smoking in 2012–2013. They were reassessed 1 year later. Analysis was conducted from July 1, 2014, to March 1, 2015. Multinomial logistic regression was used to assess the independent association between baseline e-cigarette use and cigarette smoking, controlling for sex, age, race/ethnicity, maternal educational level, sensation-seeking tendency, parental cigarette smoking, and cigarette smoking among friends. Sensitivity analyses were performed, with varying approaches to missing data and recanting. EXPOSURES Use of e-cigarettes at baseline. MAIN OUTCOMES AND MEASURES Progression to cigarette smoking, defined using 3 specific states along a trajectory: nonsusceptible nonsmokers, susceptible nonsmokers, and smokers. Individuals who could not rule out smoking in the future were defined as susceptible. RESULTS Among the 694 respondents, 374 (53.9%) were female and 531 (76.5%) were non-Hispanic white. At baseline, 16 participants (2.3%) used e-cigarettes. Over the 1-year follow-up, 11 of 16 e-cigarette users and 128 of 678 of those who had not used e-cigarettes (18.9%) progressed toward cigarette smoking. In the primary

  18. Hand rolling cigarette papers as the reference point for regulating cigarette fire safety

    PubMed Central

    Laugesen, M; Duncanson, M; Fraser, T; McClellan, V; Linehan, B; Shirley, R

    2003-01-01

    Aim: To compare the burning characteristics of the tobacco and paper of manufactured and hand rolled cigarettes, and set a fire safety standard of manufacture to largely reduce the fire risk from discarded cigarettes. Methods: (1) Cigarette extinction test of ignition strength: 40 cigarettes per brand, lit and placed on 15 layers of filter paper, in accordance with ASTM test standard E2187-02. (2) Citrate extracted by 0.1N hydrochloric acid from cigarette papers and from tobacco in manufactured cigarettes, the supernatant analysed by high performance liquid chromatography using ultraviolet visual light spectrophotometer. (3) Survey of 750 nationally representative adults age 18 years and over, by telephone, including 184 smokers. Materials: (a) New Zealand made Holiday, and Horizon, and US made Marlboro manufactured cigarettes; (b) US manufactured Merit with banded paper; (c) Holiday, Horizon and Marlboro hand rolling tobaccos, hand rolled in Rizla cigarette papers; (d) manufactured cigarettes as in (a), reconstructed using Rizla hand rolling cigarette papers. Results: 1. (a) For each brand of manufactured cigarettes, 40/40 burnt full length; (b) for Merit banded paper cigarettes 29/40 (73%) burnt full length; (c) for each brand of hand rolled cigarettes 0/40 burnt full length; (d) 0/40 manufactured cigarettes reconstructed with Rizla hand rolling paper burnt full length. 2. Citrate content: (a) In manufactured cigarette papers: 0.3–0.8 mg; in tobacco of manufactured cigarettes: Holiday 0, Horizon 0, Marlboro 8.8 mg; (b) Merit: in banded paper 0.418 mg; in tobacco 10.23 mg; (c) In hand rolled cigarettes: in the papers < 0.08 mg; in hand rolled tobacco 13.3–15.0 mg; (d) In hand rolling papers of reconstructed cigarettes: < 0.018 mg. 3. Requiring manufactured cigarettes to compulsorily self-extinguish when left unattended was supported by 67% of smokers, 61% of manufactured cigarette smokers, 82% of hand rolled smokers, and by 68% of non-smokers. Conclusion: The

  19. Influence of cigarette smoking on human autonomic function

    NASA Technical Reports Server (NTRS)

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

    1993-01-01

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

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

    PubMed

    Carr, Ellen R

    2014-02-01

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

  1. State cigarette excise taxes - United States, 2009.

    PubMed

    2010-04-01

    Increasing the price of cigarettes can reduce smoking substantially by discouraging initiation among youths and young adults, prompting quit attempts, and reducing average cigarette consumption among those who continue to smoke. Increasing cigarette excise taxes is one of the most effective tobacco control policies because it directly increases cigarette prices, thereby reducing cigarette use and smoking-related death and disease. All states and the District of Columbia (DC) impose an excise tax on cigarettes. Because many states increased their cigarette excise taxes in 2009, CDC conducted a survey of these tax increases. For this report, CDC reviewed data contained in a legislative database to identify cigarette excise tax legislation that was enacted during 2009 by the 50 states and DC. During that period, 15 states (including DC), increased their state excise tax on cigarettes, increasing the national mean from $1.18 per pack in 2008 to $1.34 per pack in 2009. However, none of the 15 states dedicated any of the new excise tax revenue by statute to tobacco control. Additionally, for the first time, two states (Connecticut and Rhode Island) had excise tax rates of at least $3.00 per pack. Additional increases in cigarette excise taxes, and dedication of all resulting revenues to tobacco control and prevention programs at levels recommended by CDC, could result in further reductions in smoking and associated morbidity and mortality.

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

    PubMed

    Pandareesh, M D; Anand, T

    2014-01-01

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

  3. Secondhand Exposure to Vapors From Electronic Cigarettes

    PubMed Central

    Czogala, Jan; Fidelus, Bartlomiej; Zielinska-Danch, Wioleta; Travers, Mark J.; Sobczak, Andrzej

    2014-01-01

    Introduction: Electronic cigarettes (e-cigarettes) are designed to generate inhalable nicotine aerosol (vapor). When an e-cigarette user takes a puff, the nicotine solution is heated and the vapor is taken into lungs. Although no sidestream vapor is generated between puffs, some of the mainstream vapor is exhaled by e-cigarette user. The aim of this study was to evaluate the secondhand exposure to nicotine and other tobacco-related toxicants from e-cigarettes. Materials and Methods: We measured selected airborne markers of secondhand exposure: nicotine, aerosol particles (PM2.5), carbon monoxide, and volatile organic compounds (VOCs) in an exposure chamber. We generated e-cigarette vapor from 3 various brands of e-cigarette using a smoking machine and controlled exposure conditions. We also compared secondhand exposure with e-cigarette vapor and tobacco smoke generated by 5 dual users. Results: The study showed that e-cigarettes are a source of secondhand exposure to nicotine but not to combustion toxicants. The air concentrations of nicotine emitted by various brands of e-cigarettes ranged from 0.82 to 6.23 µg/m3. The average concentration of nicotine resulting from smoking tobacco cigarettes was 10 times higher than from e-cigarettes (31.60±6.91 vs. 3.32±2.49 µg/m3, respectively; p = .0081). Conclusions: Using an e-cigarette in indoor environments may involuntarily expose nonusers to nicotine but not to toxic tobacco-specific combustion products. More research is needed to evaluate health consequences of secondhand exposure to nicotine, especially among vulnerable populations, including children, pregnant women, and people with cardiovascular conditions. PMID:24336346

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

    PubMed Central

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

    2015-01-01

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

  5. 21 CFR 1141.14 - Misbranding of cigarettes.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 21 Food and Drugs 8 2014-04-01 2014-04-01 false Misbranding of cigarettes. 1141.14 Section 1141.14...) TOBACCO PRODUCTS CIGARETTE PACKAGE AND ADVERTISING WARNINGS Cigarette Package and Advertising Warnings § 1141.14 Misbranding of cigarettes. (a) A cigarette shall be deemed to be misbranded under section...

  6. 21 CFR 1141.14 - Misbranding of cigarettes.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 21 Food and Drugs 8 2013-04-01 2013-04-01 false Misbranding of cigarettes. 1141.14 Section 1141.14...) TOBACCO PRODUCTS CIGARETTE PACKAGE AND ADVERTISING WARNINGS Cigarette Package and Advertising Warnings § 1141.14 Misbranding of cigarettes. (a) A cigarette shall be deemed to be misbranded under section...

  7. 21 CFR 1141.14 - Misbranding of cigarettes.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 21 Food and Drugs 8 2012-04-01 2012-04-01 false Misbranding of cigarettes. 1141.14 Section 1141.14...) TOBACCO PRODUCTS CIGARETTE PACKAGE AND ADVERTISING WARNINGS; (Eff. 9-22-12) Cigarette Package and Advertising Warnings § 1141.14 Misbranding of cigarettes. (a) A cigarette shall be deemed to be...

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

    SciTech Connect

    Cheng, Ya-Hsin; Huang, Su-Chin; Lin, Chun-Ju; Cheng, Li-Chuan; Li, Lih-Ann

    2012-03-15

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

  9. Are E-cigarettes a safe and good alternative to cigarette smoking?

    PubMed

    Rom, Oren; Pecorelli, Alessandra; Valacchi, Giuseppe; Reznick, Abraham Z

    2015-03-01

    Electronic cigarettes (E-cigarettes) are devices that can vaporize a nicotine solution combined with liquid flavors instead of burning tobacco leaves. Since their emergence in 2004, E-cigarettes have become widely available, and their use has increased exponentially worldwide. E-cigarettes are aggressively advertised as a smoking cessation aid; as healthier, cheaper, and more socially acceptable than conventional cigarettes. In recent years, these claims have been evaluated in numerous studies. This review explores the development of the current E-cigarette and its market, prevalence of awareness, and use. The review also explores the beneficial and adverse effects of E-cigarettes in various aspects in accordance with recent research. The discussed aspects include smoking cessation or reduction and the health risks, social impact, and environmental consequences of E-cigarettes.

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

    PubMed

    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

  11. Menthol Cigarettes | Smokefree.gov

    Cancer.gov

    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.  

  12. The intractable cigarette ‘filter problem’

    PubMed Central

    2011-01-01

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

  13. Electronic cigarettes: product characterisation and design considerations

    PubMed Central

    Brown, Christopher J; Cheng, James M

    2014-01-01

    Objective To review the available evidence regarding electronic cigarette (e-cigarette) product characterisation and design features in order to understand their potential impact on individual users and on public health. Methods Systematic literature searches in 10 reference databases were conducted through October 2013. A total of 14 articles and documents and 16 patents were included in this analysis. Results Numerous disposable and reusable e-cigarette product options exist, representing wide variation in product configuration and component functionality. Common e-cigarette components include an aerosol generator, a flow sensor, a battery and a nicotine-containing solution storage area. e-cigarettes currently include many interchangeable parts, enabling users to modify the character of the delivered aerosol and, therefore, the product's ‘effectiveness’ as a nicotine delivery product. Materials in e-cigarettes may include metals, rubber and ceramics. Some materials may be aerosolised and have adverse health effects. Several studies have described significant performance variability across and within e-cigarette brands. Patent applications include novel product features designed to influence aerosol properties and e-cigarette efficiency at delivering nicotine. Conclusions Although e-cigarettes share a basic design, engineering variations and user modifications result in differences in nicotine delivery and potential product risks. e-cigarette aerosols may include harmful and potentially harmful constituents. Battery explosions and the risks of exposure to the e-liquid (especially for children) are also concerns. Additional research will enhance the current understanding of basic e-cigarette design and operation, aerosol production and processing, and functionality. A standardised e-cigarette testing regime should be developed to allow product comparisons. PMID:24732162

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

    ERIC Educational Resources Information Center

    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…

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

    PubMed Central

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

    2016-01-01

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

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

    PubMed Central

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

    2016-01-01

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

  17. 75 FR 69523 - Required Warnings for Cigarette Packages and Advertisements

    Federal Register 2010, 2011, 2012, 2013, 2014

    2010-11-12

    ... Experience 1. Getting Consumers' Attention 2. Influencing Consumers' Awareness of Cigarette-Related Health...; Iran; Jordan; Latvia; Malaysia; Mauritius; Mexico; Mongolia; New Zealand; Pakistan; Panama; Paraguay... cigarette smokers. Although the cigarette industry regularly loses customers through user cessation...

  18. Hazardous waste status of discarded electronic cigarettes.

    PubMed

    Krause, Max J; Townsend, Timothy G

    2015-05-01

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

  19. Effects of cigarette smoking on reproduction.

    PubMed

    Dechanet, C; Anahory, T; Mathieu Daude, J C; Quantin, X; Reyftmann, L; Hamamah, S; Hedon, B; Dechaud, H

    2011-01-01

    BACKGROUND Cigarette smoking is associated with lower fecundity rates, adverse reproductive outcomes and a higher risk of IVF failures. Over the last few decades, prevalence of smoking among women of reproductive age has increased. This review focuses on current knowledge of the potential effects of smoke toxicants on all reproductive stages and the consequences of smoke exposure on reproductive functions. METHODS We conducted a systematic review of the scientific literature on the impact of cigarette smoking and smoke constituents on the different stages of reproductive function, including epidemiological, clinical and experimental studies. We attempted to create hypotheses and find explanations for the deleterious effects of cigarette smoke observed in experimental studies. RESULTS Cigarette smoke contains several thousand components (e.g. nicotine, polycyclic aromatic hydrocarbons and cadmium) with diverse effects. Each stage of reproductive function, folliculogenesis, steroidogenesis, embryo transport, endometrial receptivity, endometrial angiogenesis, uterine blood flow and uterine myometrium is a target for cigarette smoke components. The effects of cigarette smoke are dose-dependent and are influenced by the presence of other toxic substances and hormonal status. Individual sensitivity, dose, time and type of exposure also play a role in the impact of smoke constituents on human fertility. CONCLUSIONS All stages of reproductive functions are targets of cigarette smoke toxicants. Further studies are necessary to better understand the deleterious effects of cigarette smoke compounds on the reproductive system in order to improve health care, help to reduce cigarette smoking and provide a better knowledge of the molecular mechanisms involved in reproductive toxicology.

  20. Price and cigarette consumption in Europe

    PubMed Central

    Gallus, S; Schiaffino, A; Vecchia, C La; Townsend, J; Fernandez, E

    2006-01-01

    Objective To analyse the variation in demand for tobacco according to price of cigarettes across the European region. Design Cross‐sectional study. Setting All the 52 countries of the European region. Participants For each European country, data were collected on annual per adult cigarette consumption (2000), smoking prevalence (most recent), retail price of a pack of local and foreign brand cigarettes (around 2000), the gross domestic product adjusted by purchasing power parities, and the adult population (2000). Main outcome measure Price elasticity of demand for cigarettes (that is, the change in cigarette consumption according to a change in tobacco price) across all the European countries, estimated by double‐log multiple linear regression. Results Controlling for male to female prevalence ratio, price elasticities for consumption were −0.46 (95% confidence interval (CI) −0.74 to −0.17) and −0.74 (95% CI −1.13 to −0.35) for local and foreign brand, respectively. The inverse relation between cigarette price and consumption was stronger in countries not in the European Union (price elasticity for foreign brand cigarettes of −0.8) as compared to European Union countries (price elasticity of −0.4). Conclusions The result that, on average, in Europe smoking consumption decreases 5–7% for a 10% increase in the real price of cigarettes strongly supports an inverse association between price and cigarette smoking. PMID:16565459

  1. Hazardous waste status of discarded electronic cigarettes.

    PubMed

    Krause, Max J; Townsend, Timothy G

    2015-05-01

    The potential for disposable electronic cigarettes (e-cigarettes) to be classified as hazardous waste was investigated. The Toxicity Characteristic Leaching Procedure (TCLP) was performed on 23 disposable e-cigarettes in a preliminary survey of metal leaching. Based on these results, four e-cigarette products were selected for replicate analysis by TCLP and the California Waste Extraction Test (WET). Lead was measured in leachate as high as 50mg/L by WET and 40mg/L by TCLP. Regulatory thresholds were exceeded by two of 15 products tested in total. Therefore, some e-cigarettes would be toxicity characteristic (TC) hazardous waste but a majority would not. When disposed in the unused form, e-cigarettes containing nicotine juice would be commercial chemical products (CCP) and would, in the United States (US), be considered a listed hazardous waste (P075). While household waste is exempt from hazardous waste regulation, there are many instances in which such waste would be subject to regulation. Manufactures and retailers with unused or expired e-cigarettes or nicotine juice solution would be required to manage these as hazardous waste upon disposal. Current regulations and policies regarding the availability of nicotine-containing e-cigarettes worldwide were reviewed. Despite their small size, disposable e-cigarettes are consumed and discarded much more quickly than typical electronics, which may become a growing concern for waste managers. PMID:25746178

  2. Deficiency in adiponectin exaggerates cigarette smoking exposure-induced cardiac contractile dysfunction: Role of autophagy.

    PubMed

    Hu, Nan; Yang, Lifang; Dong, Maolong; Ren, Jun; Zhang, Yingmei

    2015-10-01

    Second hand smoke is an independent risk factor for cardiovascular disease. Adiponectin (APN), an adipose-derived adipokine, has been shown to offer cardioprotective effect through an AMPK-dependent manner. This study was designed to evaluate the impact of adiponectin deficiency on second hand smoke-induced cardiac pathology and underlying mechanisms using a mouse model of side-stream smoke exposure. Adult wild-type (WT) and adiponectin knockout (APNKO) mice were placed in a chamber exposed to cigarette smoke for 1 hour daily for 40 days. Echocardiographic, cardiomyocyte function, and intracellular Ca2+ handling were evaluated. Autophagy and apoptosis were examined using western blot. 2',7'-dichlorodihydrofluorescein diacetate (H2DCFDA) staining was used to evaluate reactive oxygen species (ROS) generation. Masson trichrome staining was employed to measure interstitial fibrosis. Our data revealed that adiponectin deficiency provoked smoke exposure-induced cardiomyopathy (compromised fractional shortening, disrupted cardiomyocyte function and intracellular Ca2+ homeostasis, apoptosis and ROS generation). In addition, these detrimental effects of side-stream smoke were accompanied by defective autophagolysosome formation, the effect of which was exacerbated by adiponectin deficiency. Blocking autophagolysosome formation using bafilomycin A1 (BafA1) negated the cardioprotective effect of rapamycin against smoke extract. Induction of autophagy using rapamycin and AMPKα activation using AICAR rescued against smoke extract-induced myopathic anomalies in APNKO mice. Our data suggest that adiponectin serves as an indispensable cardioprotective factor against side-stream smoke exposure-induced myopathic changes possibly through facilitating autophagolysosome formation. PMID:26276084

  3. E-cigarettes and conventional cigarette use among US adolescents: A cross-sectional study

    PubMed Central

    Dutra, Lauren M.; Glantz, Stanton A.

    2014-01-01

    Importance E-cigarette use is increasing rapidly among adolescents and e-cigarettes are currently unregulated. Objective Examine e-cigarette use and conventional cigarette smoking. Design Cross-sectional analyses of survey data. Setting 2011 and 2012 National Youth Tobacco Surveys (NYTS) Participants Representative sample of US middle and high school students in 2011 (n=17,353) and 2012 (n=22,529) Exposures Ever and current e-cigarette use Main outcome measures Experimentation with, ever, and current smoking; smoking abstinence Results In pooled analyses, among cigarette experimenters (≥1 puff), ever e-cigarette use was associated with higher odds of ever smoking cigarettes (≥100 cigarettes; OR= 6.31, 95% CI [5.39-7.39) and current cigarette smoking (OR=5.96 [5.67-6.27]). Current e-cigarette use was positively associated with ever smoking cigarettes (OR=7.42 [5.63-9.79]) and current cigarette smoking (OR= 7.88 [6.01-10.32]. In 2011, current cigarette smokers who had ever used e-cigarettes were more likely to intend to quit smoking within the next year (OR=1.53 [1.03-2.28]). Among experimenters with conventional cigarettes, ever use of e-cigarettes was also associated with lower 30-day (OR=0.24 [0.21-0.28]), 6-month (OR=0.24 [0.21-0.28]), and 1-year (OR=0.25 [0.21-0.30]) abstinence from cigarettes. Current e-cigarette use was also associated with lower 30-day (OR=0.11 [0.08-0.15]), 6-month (OR=0.11 [0.08-0.15]), and 1-year (OR=0.12 [0.07-0.18]) abstinence. Among ever smokers of cigarettes (≥100 cigarettes), ever e-cigarette use was negatively associated with 30-day (OR=0.61, [0.42-0.89]), 6-month (OR=0.53, [0.33-0.83]) and one-year (OR=0.32 [0.18-0.56) abstinence from conventional cigarettes. Current e-cigarette use was also negatively associated with 30-day (OR=0.35 [0.18-0.69]), 6-month (OR=0.30 [0.13-0.68]), and one-year (OR=0.34 [0.13-0.87]) abstinence. Conclusions E-cigarette use was associated with higher odds of ever or current cigarette smoking, higher

  4. Cigarette litter: smokers' attitudes and behaviors.

    PubMed

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

    2012-06-01

    Cigarette butts are consistently the most collected items in litter clean-up efforts, which are a costly burden to local economies. In addition, tobacco waste may be detrimental to our natural environment. The tobacco industry has conducted or funded numerous studies on smokers' littering knowledge and behavior, however, non-industry sponsored research is rare. We sought to examine whether demographics and smokers' knowledge and beliefs toward cigarette waste as litter predicts littering behavior. Smokers aged 18 and older (n = 1,000) were interviewed about their knowledge and beliefs towards cigarette waste as litter. Respondents were members of the Research Now panel, an online panel of over three million respondents in the United States. Multivariate logistic regressions were conducted to determine factors significantly predictive of ever having littered cigarette butts or having littered cigarette butts within the past month (p-value < 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 waste and are harmful when disposed of

  5. Cigarette Litter: Smokers’ Attitudes and Behaviors

    PubMed Central

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

    2012-01-01

    Cigarette butts are consistently the most collected items in litter clean-up efforts, which are a costly burden to local economies. In addition, tobacco waste may be detrimental to our natural environment. The tobacco industry has conducted or funded numerous studies on smokers’ littering knowledge and behavior, however, non-industry sponsored research is rare. We sought to examine whether demographics and smokers’ knowledge and beliefs toward cigarette waste as litter predicts littering behavior. Smokers aged 18 and older (n = 1,000) were interviewed about their knowledge and beliefs towards cigarette waste as litter. Respondents were members of the Research Now panel, an online panel of over three million respondents in the United States. Multivariate logistic regressions were conducted to determine factors significantly predictive of ever having littered cigarette butts or having littered cigarette butts within the past month (p-value < 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 waste and are harmful when disposed of

  6. Cigarette litter: smokers' attitudes and behaviors.

    PubMed

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

    2012-06-01

    Cigarette butts are consistently the most collected items in litter clean-up efforts, which are a costly burden to local economies. In addition, tobacco waste may be detrimental to our natural environment. The tobacco industry has conducted or funded numerous studies on smokers' littering knowledge and behavior, however, non-industry sponsored research is rare. We sought to examine whether demographics and smokers' knowledge and beliefs toward cigarette waste as litter predicts littering behavior. Smokers aged 18 and older (n = 1,000) were interviewed about their knowledge and beliefs towards cigarette waste as litter. Respondents were members of the Research Now panel, an online panel of over three million respondents in the United States. Multivariate logistic regressions were conducted to determine factors significantly predictive of ever having littered cigarette butts or having littered cigarette butts within the past month (p-value < 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 waste and are harmful when disposed of

  7. Hazardous waste status of discarded electronic cigarettes

    SciTech Connect

    Krause, Max J.; Townsend, Timothy G.

    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. HIF-1α Plays a Critical Role in the Gestational Sidestream Smoke-Induced Bronchopulmonary Dysplasia in Mice

    PubMed Central

    Singh, Shashi P.; Chand, Hitendra S.; Gundavarapu, Sravanthi; Saeed, Ali Imran; Langley, Raymond J.; Tesfaigzi, Yohannes; Mishra, Neerad C.; Sopori, Mohan L.

    2015-01-01

    Rationale Smoking during pregnancy increases the risk of bronchopulmonary dysplasia (BPD) and, in mice, gestational exposure to sidestream cigarette smoke (SS) induces BPD-like condition characterized by alveolar simplification, impaired angiogenesis, and suppressed surfactant protein production. Normal fetal development occurs in a hypoxic environment and nicotinic acetylcholine receptors (nAChRs) regulate the hypoxia-inducible factor (HIF)-1α that controls apoptosis and angiogenesis. To understand SS-induced BPD, we hypothesized that gestational SS affected alveolar development through HIF-1α. Methods Pregnant BALB/c mice were exposed to air (control) or SS throughout the gestational period and the 7-day-old lungs of the progeny were examined. Results Gestational SS increased apoptosis of alveolar and airway epithelial cells. This response was associated with increased alveolar volumes, higher levels of proapoptotic factors (FOXO3a, HIPK2, p53, BIM, BIK, and BAX) and the antiangiogenic factor (GAX), and lower levels of antiapoptotic factors (Akt-PI3K, NF-κB, HIF-1α, and Bcl-2) in the lung. Although gestational SS increased the cells containing the proangiogenic bombesin-like-peptide, it markedly decreased the expression of its receptor GRPR in the lung. The effects of SS on apoptosis were attenuated by the nAChR antagonist mecamylamine. Conclusions Gestational SS-induced BPD is potentially regulated by nAChRs and associated with downregulation of HIF-1α, increased apoptosis of epithelial cells, and increased alveolar volumes. Thus, in mice, exposure to sidestream tobacco smoke during pregnancy promotes BPD-like condition that is potentially mediated through the nAChR/HIF-1α pathway. PMID:26361040

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

    PubMed Central

    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

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

    PubMed

    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

  11. A review on engineering of cellulosic cigarette paper to reduce carbon monoxide delivery of cigarettes.

    PubMed

    Shen, Jing; Li, Jinsong; Qian, Xueren; Ren, Wanshan; Fatehi, Pedram

    2014-01-30

    In cigarette production, the cellulosic paper essentially derived from flax fibers or other fiber materials is used as the wrapping material. During smoking of cigarettes, the highly toxic carbon monoxide is produced. To decrease the amount of carbon monoxide emission in the mainstream smoke, the engineering of all cigarette components including cellulosic cigarette paper and tobacco column is critical. This review summarizes the concepts related to engineering of cigarette paper. These mainly include permeability control, increased use of burn additives, optimization of fiber basis weight, engineering of calcium carbonate fillers, and incorporation of catalysts/oxidants. In particular, catalytic and/or oxidative conversion of carbon monoxide to carbon dioxide has been very widely reported. The control of permeability/diffusivity of cigarette paper is also of critical importance for enhanced diffusion of carbon monoxide out of the cigarette. The development of new concepts and combination of various concepts may lead to breakthroughs in this area.

  12. Characterization of SPECTRUM Variable Nicotine Research Cigarettes

    PubMed Central

    Richter, Patricia; Steven, Pappas R.; Bravo, Roberto; Lisko, Joseph G.; Damian, Maria; Gonzalez-Jimenez, Nathalie; Gray, Naudia; Keong, Lisa M.; Kimbrell, Jacob B.; Kuklenyik, Peter; Lawler, Tameka S.; Lee, Grace E.; Mendez, Magaly; Perez, Jose; Smith, Shakia; Tran, Hang; Tyx, Robert; Watson, Clifford H.

    2016-01-01

    Objective To provide researchers an extensive characterization of the SPECTRUM variable nicotine research cigarettes. Methods Data on cigarette physical properties, nicotine content, harmful and potentially harmful constituents in the tobacco filler was compiled. Results Data on physical properties, concentrations of menthol, nicotine and minor alkaloids, tobacco-specific nitrosamines, polycyclic aromatic hydrocarbons, ammonia, and toxic metals in the filler tobacco for all available varieties of Spectrum research cigarettes are provided. The similarity in the chemistry and physical properties of SPECTRUM cigarettes to commercial cigarettes renders them acceptable for use in behavioral studies. Baseline information on harmful and potentially harmful constituents in research tobacco products, particularly constituent levels such as minor alkaloids that fall outside typical ranges reported for commercial, provide researchers with the opportunity to monitor smoking behavior and to identify biomarkers that will inform efforts to understand the role of nicotine in creating and sustaining addiction. Conclusions Well characterized research cigarettes suitable for human consumption are an important tool in clinical studies for investigating the physiological impacts of cigarettes delivering various levels of nicotine, the impact of reduced nicotine cigarettes on nicotine addiction, and the relationship between nicotine dose and smoking behavior. PMID:26779559

  13. 47 CFR 73.4055 - Cigarette advertising.

    Code of Federal Regulations, 2010 CFR

    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....

  14. 47 CFR 73.4055 - Cigarette advertising.

    Code of Federal Regulations, 2014 CFR

    2014-10-01

    ... 47 Telecommunication 4 2014-10-01 2014-10-01 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....

  15. 47 CFR 73.4055 - Cigarette advertising.

    Code of Federal Regulations, 2013 CFR

    2013-10-01

    ... 47 Telecommunication 4 2013-10-01 2013-10-01 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....

  16. 47 CFR 73.4055 - Cigarette advertising.

    Code of Federal Regulations, 2011 CFR

    2011-10-01

    ... 47 Telecommunication 4 2011-10-01 2011-10-01 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....

  17. 47 CFR 73.4055 - Cigarette advertising.

    Code of Federal Regulations, 2012 CFR

    2012-10-01

    ... 47 Telecommunication 4 2012-10-01 2012-10-01 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....

  18. E-Cigarettes | Smokefree.gov

    Cancer.gov

    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.

  19. Debate, Research on E-Cigarettes Continues

    Cancer.gov

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

  20. Cigarette Warning Labels as Educational Devices.

    ERIC Educational Resources Information Center

    Newman, Ian M.; And Others

    This paper reports an investigation on the educational impact of warning labels on cigarette packages on adolescents. Subjects were asked to identify the locations of warning labels on cigarette packages and advertising and to restate the warning label. Results indicated that official warnings may be well known in general terms but poorly known in…

  1. Candy cigarettes: do they encourage children's smoking?

    PubMed

    Klein, J D; Forehand, B; Oliveri, J; Patterson, C J; Kupersmidt, J B; Strecher, V

    1992-01-01

    Candy and bubble gum cigarettes are packaged to resemble cigarette brands, and so they may encourage young children to smoke. Two studies of the role of these products in the development of children's attitudes and behaviors toward smoking were conducted. In the first study, six focus group interviews were conducted with 25 children in three age groups (4 through 5, 6 through 8, and 9 through 11 years old). Children in each group were shown five candy and snack foods and asked about their opinions and experiences with each item. In the second study, 195 seventh-grade students in a southeastern city school system were surveyed about their cigarette smoking and candy cigarette use. In the focus groups, candy cigarettes were recognized by most children. Young children played with the candy cigarettes more than with other candy or snack items and made general references to smoking behaviors. Older children made favorable references to smoking behavior; most knew which stores sold candy cigarettes, and many had chosen to buy and use these items, despite parental disapproval. Candy cigarettes may play a role in the development of children's attitudes toward smoking as an acceptable, favorable, or normative behavior. Elimination of these products should be part of efforts to prevent initiation of smoking by children. PMID:1728016

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

    PubMed

    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.

  3. Conditional risk assessment of adolescents’ electronic cigarette perceptions

    PubMed Central

    Chaffee, Benjamin W.; Gansky, Stuart A.; Halpern-Felsher, Bonnie; Couch, Elizabeth T.; Essex, Gwen; Walsh, Margaret M.

    2015-01-01

    Objectives Adapt an established instrument for measuring adolescents’ cigarette-related perceptions for new application with electronic cigarettes (e-cigarettes). Methods In this exploratory study, 104 male high school students (40% tobacco ever-users) estimated the probability of potential e-cigarette risks (eg, lung cancer) or benefits (eg, look cool). We calculated associations between risk/benefit composite scores, ever-use, and use intention for e-cigarettes and analogously for combustible cigarettes. Results E-cigarette ever-use was associated with lower perceived risks, with adjusted differences versus never-users greater for e-cigarettes than cigarettes. Risk composite score was inversely associated, and benefit score positively associated, with e-cigarette ever-use and use intention. Conclusion Conditional risk assessment characterized adolescents’ perceived e-cigarette risk/benefit profile, with potential utility for risk-perception measurement in larger future studies. PMID:25741686

  4. Cigarette ignition of soft furnishings: A literature review with commentary

    NASA Astrophysics Data System (ADS)

    Krasny, John F.

    1987-04-01

    Literature pertinent to the ignition by smoldering cigarettes of upholstered furniture and mattresses (soft furnishings) was searched through early 1986. This included literature on the smoldering behavior of cigarettes in air; their behavior on a variety of substrates simulating soft furnishings; mechanism of smoldering in substrates; relative cigarette ignition resistance of substrates; and relative propensity of commercial cigarette packings to ignite substrates. According to the reviewed literature, the smoldering behavior of cigarettes on substrates differs from that of cigarettes burning in air: on substrates, cigarette temperatures tend to be lower, and burning rates slower. These differences seem to be larger for substrates which ignite than for those which self-extinguish after the cigarette burns out. The characteristics of soft furnishings which insure resistance to cigarette ignition have been established, but those of cigarettes with low propensity to ignite furnishings have not. No mathematical model has been reported for the interaction of cigarette and substrate, but some empirical data do exist.

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

    PubMed

    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

  6. Do electronic cigarettes help with smoking cessation?

    PubMed

    2014-11-01

    Smoking causes around 100,000 deaths each year in the UK, and is the leading cause of preventable disease and early mortality. Smoking cessation remains difficult and existing licensed treatments have limited success. Nicotine addiction is thought to be one of the primary reasons that smokers find it so hard to give up, and earlier this year DTB reviewed the effects of nicotine on health. Electronic cigarettes (e-cigarettes) are nicotine delivery devices that aim to mimic the process of smoking but avoid exposing the user to some of the harmful components of traditional cigarettes. However, the increase in the use of e-cigarettes and their potential use as an aid to smoking cessation has been subject to much debate. In this article we consider the regulatory and safety issues associated with the use of e-cigarettes, and their efficacy in smoking cessation and reduction.

  7. Cigarette advertising and adolescent experimentation with smoking.

    PubMed

    Klitzner, M; Gruenewald, P J; Bamberger, E

    1991-03-01

    The extent to which cigarette advertising contributes to increases in smoking has been debated by public health professionals and the tobacco industry. One aspect of this debate has been the degree to which advertising influences smoking among adolescents. Previous research suggests that there are significant relationships between measures of advertising and smoking. However, potential simultaneous relationships between these measures have not been addressed. Observed correlations may arise from the effects of advertising on smoking or from smokers' selective exposure to advertisements. This study examined relationships between cigarette advertising and smoking experimentation. Using environmental and psychological measures of advertising exposure, it was demonstrated that adolescents who experimented with cigarettes were better able to recognize advertised products than those who had not, a selective exposure effect. Conversely, subjects who were better at recognizing advertised brands were more likely to have experimented with cigarettes, an effect due to their exposure to cigarette advertising.

  8. Electronic cigarettes: ambiguity and controversies of usage.

    PubMed

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

    2014-04-01

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

  9. Carbon monoxide kinetics following simulated cigarette smoking

    SciTech Connect

    Karnik, A.S.; Coin, E.J.

    1980-05-01

    Carbon monoxide kinetics were measured in the blood (% carboxyhemoglobin) and alveolar phase (ppM carbon monoxide) after simulated cigarette smoking. Cigarette smoking was siumlated using the same amount of carbon monoxide that 2R1F cigarettes manufactured by the Tobacco Research Institute would contain. Ten boluses of air containing carbon monoxide equivalent to smoking one cigarette were inhaled by six healthy nonsmoker volunteers. Carbon monoxide in the air phase was measured by an Ecolyzer and carboxyhemoglobin was measured by a CO-Oximeter. The mean rise in alveolar carbon monoxide immediately and 20 min after inhaling the last bolus was 3.3 and 3.1 ppM, respectively (p<.005). The mean rise in carboxyhemoglobin immediately and 20 min after inhalation of the last bolus was 0.8 and 0.5% respectively (P<.005). The changes in carboxyhemoglobin were found to be similar to changes that occur when one cigarette is actually smoked.

  10. Health Education and Cigarette Smoking

    PubMed Central

    Morison, James B.; Medovy, Herry; MacDonell, Gordon T.

    1964-01-01

    The smoking habits of Winnipeg school students were surveyed before and after a three-year program of health education on the hazards of smoking, directed to 8300 out of 48,000 students. The program consisted of informal approaches to students in elementary schools and a formal program of talks, lectures, films, and student participation for older students. There were fewer students at all ages who had never smoked a cigarette at the time of the second survey. There was a slight decrease in the number of regular smokers in high school, most marked in the school where the program was enthusiastically received and student participation was most active. A direct relationship between parental smoking and that of the student, and an inverse relationship between academic achievement and student smoking, were shown on both surveys. The majority of students believed that smoking caused lung cancer and other hazards to health, although this was less marked among smokers. The results indicated that an intensive program of health education directed to the teenagers in school was a potentially useful approach to the problem of cigarette smoking. PMID:14154295

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

    PubMed

    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.

  12. 27 CFR 41.32 - Cigarette tax rates.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2013-04-01 2013-04-01 false Cigarette tax rates. 41.32... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.32 Cigarette tax rates. Cigarettes are taxed at the following...

  13. 27 CFR 41.74 - Notice for cigarettes.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2014-04-01 2014-04-01 false Notice for cigarettes. 41..., DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Packages § 41.74 Notice for cigarettes. Every package of cigarettes, except...

  14. 27 CFR 41.74 - Notice for cigarettes.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2012-04-01 2011-04-01 true Notice for cigarettes. 41..., DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Packages § 41.74 Notice for cigarettes. Every package of cigarettes, except...

  15. 27 CFR 41.32 - Cigarette tax rates.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2011-04-01 2011-04-01 false Cigarette tax rates. 41.32... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.32 Cigarette tax rates. Cigarettes are taxed at the following...

  16. 27 CFR 41.74 - Notice for cigarettes.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2011-04-01 2011-04-01 false Notice for cigarettes. 41..., DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Packages § 41.74 Notice for cigarettes. Every package of cigarettes, except...

  17. 19 CFR 10.65 - Cigars and cigarettes.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 19 Customs Duties 1 2014-04-01 2014-04-01 false Cigars and cigarettes. 10.65 Section 10.65 Customs... Equipment for Vessels § 10.65 Cigars and cigarettes. (a) Imported cigars and cigarettes in bonded warehouse... cigarettes is made up of a number of units, each in a separate package, such units may be...

  18. 27 CFR 40.215 - Notice for cigarettes.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2011-04-01 2011-04-01 false Notice for cigarettes. 40..., DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES... cigarettes. Every package of cigarettes shall, before removal subject to tax, have adequately...

  19. 27 CFR 40.23 - Cigarette tax rates.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2010-04-01 2010-04-01 false Cigarette tax rates. 40.23... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes § 40.23 Cigarette tax rates. Cigarettes are taxed at the following rates under 26...

  20. 19 CFR 10.65 - Cigars and cigarettes.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 19 Customs Duties 1 2013-04-01 2013-04-01 false Cigars and cigarettes. 10.65 Section 10.65 Customs... Equipment for Vessels § 10.65 Cigars and cigarettes. (a) Imported cigars and cigarettes in bonded warehouse... cigarettes is made up of a number of units, each in a separate package, such units may be...

  1. 27 CFR 40.23 - Cigarette tax rates.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2013-04-01 2013-04-01 false Cigarette tax rates. 40.23... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes § 40.23 Cigarette tax rates. Cigarettes are taxed at the following rates under 26...

  2. 19 CFR 10.65 - Cigars and cigarettes.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 19 Customs Duties 1 2012-04-01 2012-04-01 false Cigars and cigarettes. 10.65 Section 10.65 Customs... Equipment for Vessels § 10.65 Cigars and cigarettes. (a) Imported cigars and cigarettes in bonded warehouse... cigarettes is made up of a number of units, each in a separate package, such units may be...

  3. 27 CFR 41.32 - Cigarette tax rates.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2010-04-01 2010-04-01 false Cigarette tax rates. 41.32... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.32 Cigarette tax rates. Cigarettes are taxed at the following...

  4. 27 CFR 40.23 - Cigarette tax rates.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2014-04-01 2014-04-01 false Cigarette tax rates. 40.23... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes § 40.23 Cigarette tax rates. Cigarettes are taxed at the following rates under 26...

  5. 27 CFR 40.215 - Notice for cigarettes.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2013-04-01 2013-04-01 false Notice for cigarettes. 40..., DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES... cigarettes. Every package of cigarettes shall, before removal subject to tax, have adequately...

  6. 27 CFR 41.32 - Cigarette tax rates.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2012-04-01 2011-04-01 true Cigarette tax rates. 41.32... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.32 Cigarette tax rates. Cigarettes are taxed at the following...

  7. 27 CFR 40.215 - Notice for cigarettes.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2014-04-01 2014-04-01 false Notice for cigarettes. 40..., DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES... cigarettes. Every package of cigarettes shall, before removal subject to tax, have adequately...

  8. 27 CFR 40.23 - Cigarette tax rates.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2011-04-01 2011-04-01 false Cigarette tax rates. 40.23... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes § 40.23 Cigarette tax rates. Cigarettes are taxed at the following rates under 26...

  9. 27 CFR 40.23 - Cigarette tax rates.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2012-04-01 2011-04-01 true Cigarette tax rates. 40.23... OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes § 40.23 Cigarette tax rates. Cigarettes are taxed at the following rates under 26...

  10. 27 CFR 41.74 - Notice for cigarettes.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2013-04-01 2013-04-01 false Notice for cigarettes. 41..., DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Packages § 41.74 Notice for cigarettes. Every package of cigarettes, except...

  11. 27 CFR 41.32 - Cigarette tax rates.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2014-04-01 2014-04-01 false Cigarette tax rates. 41.32... OF THE TREASURY (CONTINUED) TOBACCO IMPORTATION OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes Tax Rates § 41.32 Cigarette tax rates. Cigarettes are taxed at the following...

  12. Sources of Cigarettes among Adolescent Smokers: Free or Purchased?

    ERIC Educational Resources Information Center

    Jansen, Paul; Toomey, Traci L.; Nelson, Toben F.; Fabian, Lindsey E. A.; Lenk, Kathleen M.; Forster, Jean L.

    2011-01-01

    Few studies have described youth cigarette sources in terms of whether the cigarettes were free or purchased. Understanding the different ways youth obtain tobacco can guide development of interventions to more effectively reduce youth smoking. Purpose: To determine the propensity for youth to purchase cigarettes versus obtain cigarettes for free,…

  13. 27 CFR 40.215 - Notice for cigarettes.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... 27 Alcohol, Tobacco Products and Firearms 2 2012-04-01 2011-04-01 true Notice for cigarettes. 40..., DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES... cigarettes. Every package of cigarettes shall, before removal subject to tax, have adequately...

  14. Characteristics of Smoking Used Cigarettes among an Incarcerated Population

    PubMed Central

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

    2014-01-01

    Little is known about smoking behaviors involving shared and previously used cigarettes, which we refer to as “smoking used cigarettes.” Examples include: cigarette sharing with strangers, smoking discarded cigarettes (‘butts’), or remaking cigarettes from portions of discarded cigarettes. The current study focuses on the prevalence of and factors associated with smoking used cigarettes prior to incarceration among a US prison population. Questionnaires were administered to 244 male and female inmates at baseline. Prevalence of smoking used cigarettes was assessed using three questions; one about sharing cigarettes with strangers, one about smoking a “found” cigarette, and one about smoking previously used cigarettes. Factors associated with those who engaged in smoking used cigarettes were then compared to those who did not engage in smoking used cigarettes. A majority of participants (61.5%) endorsed engaging in at least one 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 US. Consistent with our hypothesis, engaging in smoking used cigarettes was found to be associated with a higher degree of nicotine dependence. PMID:25180554

  15. Development of an in vitro cytotoxicity model for aerosol exposure using 3D reconstructed human airway tissue; application for assessment of e-cigarette aerosol.

    PubMed

    Neilson, Louise; Mankus, Courtney; Thorne, David; Jackson, George; DeBay, Jason; Meredith, Clive

    2015-10-01

    Development of physiologically relevant test methods to analyse potential irritant effects to the respiratory tract caused by e-cigarette aerosols is required. This paper reports the method development and optimisation of an acute in vitro MTT cytotoxicity assay using human 3D reconstructed airway tissues and an aerosol exposure system. The EpiAirway™ tissue is a highly differentiated in vitro human airway culture derived from primary human tracheal/bronchial epithelial cells grown at the air-liquid interface, which can be exposed to aerosols generated by the VITROCELL® smoking robot. Method development was supported by understanding the compatibility of these tissues within the VITROCELL® system, in terms of airflow (L/min), vacuum rate (mL/min) and exposure time. Dosimetry tools (QCM) were used to measure deposited mass, to confirm the provision of e-cigarette aerosol to the tissues. EpiAirway™ tissues were exposed to cigarette smoke and aerosol generated from two commercial e-cigarettes for up to 6 h. Cigarette smoke reduced cell viability in a time dependent manner to 12% at 6 h. E-cigarette aerosol showed no such decrease in cell viability and displayed similar results to that of the untreated air controls. Applicability of the EpiAirway™ model and exposure system was demonstrated, showing little cytotoxicity from e-cigarette aerosol and different aerosol formulations when compared directly with reference cigarette smoke, over the same exposure time. PMID:26176715

  16. Patient–physician communication regarding electronic cigarettes

    PubMed Central

    Steinberg, Michael B.; Giovenco, Daniel P.; Delnevo, Cristine D.

    2015-01-01

    Introduction Smokers are likely asking their physicians about the safety of e-cigarettes and their potential role as a cessation tool; however, the research literature on this communication is scant. A pilot study of physicians in the United States was conducted to investigate physician–patient communication regarding e-cigarettes. Methods A total of 158 physicians were recruited from a direct marketing e-mail list and completed a short, web-based survey between January and April 2014. The survey addressed demographics, physician specialty, patient–provider e-cigarette communication, and attitudes towards tobacco harm reduction. Results Nearly two-thirds (65%) of physicians reported being asked about e-cigarettes by their patients, and almost a third (30%) reported that they have recommended e-cigarettes as a smoking cessation tool. Male physicians were significantly more likely to endorse a harm reduction approach. 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. PMID:26844056

  17. A public health strategy for e-cigarettes.

    PubMed

    Schneider, Sven; Diehl, Katharina

    2015-07-01

    The e-cigarette may present a new and significant Public Health problem: Studies published so far do not seem to indicate that e-cigarette use is just a passing trend. If e-cigarette use is less harmless than it is portrayed in many advertisements, Public Health would do well to start a serious discussion about a suitable prevention policy as soon as possible.The aim of this short paper is to discuss a range of measures designed to prevent e-cigarette consumption.Concretely, we suggest to monitor e-cigarette use, the e-cigarette industry and prevention policies, to implement a vapor-free policy, to develop help to quit e-cigarette use, to inform about the health risks of e-cigarette use, to establish regulations on e-cigarette advertising, promotion and sponsorship, and to introduce taxes on e-cigarettes.

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

    PubMed Central

    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 evidence indicates that electronic cigarettes are by far a less harmful alternative to smoking and significant health benefits are expected in smokers who switch from tobacco to electronic cigarettes. Research will help make electronic cigarettes more effective as smoking substitutes and will better define and further reduce residual risks from use to as low as possible, by establishing appropriate quality control and standards. PMID:25083263

  19. High School Students’ Use of Electronic Cigarettes to Vaporize Cannabis

    PubMed Central

    Kong, Grace; Camenga, Deepa R.; Cavallo, Dana A.; Krishnan-Sarin, Suchitra

    2015-01-01

    BACKGROUND AND OBJECTIVES: Electronic cigarette (e-cigarette) use is increasing rapidly among high school (HS) students. Of concern, e-cigarettes can be used to vaporize cannabis, although use rates among adolescents are unknown. We evaluated lifetime rates of using e-cigarettes to vaporize cannabis among all lifetime e-cigarette users (27.9%), all lifetime cannabis users (29.2%), and lifetime users of both e-cigarettes and cannabis (18.8%); common means of vaporizing cannabis including hash oil, wax infused with Δ-9-tetrahydrocannabinol (THC), and dried cannabis; and demographic predictors of using e-cigarettes to vaporize cannabis. METHODS: In the spring of 2014, 3847 Connecticut HS students completed an anonymous survey assessing e-cigarette and cannabis use. RESULTS: Vaporizing cannabis using e-cigarettes was common among lifetime e-cigarette users, lifetime cannabis users, and lifetime dual users (e-cigarette 18.0%, cannabis 18.4%, dual users 26.5%). Students reported using e-cigarettes to vaporize hash oil (e-cigarette 15.4%, cannabis 15.5%, dual users 22.9%) and wax infused with THC (e-cigarette 10.0%, cannabis 10.2%, dual users 14.8%) and using portable electronic vaporizers to vaporize dried cannabis leaves (e-cigarette 19.6%, lifetime cannabis 23.1%, lifetime dual users 29.1%). Binary logistic regression indicated that male students (odds ratio [OR] = 2.05), younger students (OR = 0.64), lifetime e-cigarette users (OR = 5.27), and lifetime cannabis users (OR = 40.89) were most likely to vaporize cannabis using e-cigarettes. Rates also differed by HS attended. CONCLUSIONS: Rates of vaporizing cannabis using e-cigarettes were high. These findings raise concerns about the lack of e-cigarette regulations and the potential use of e-cigarettes for purposes other than vaping nicotine. PMID:26347431

  20. Chinese “Herbal” Cigarettes are as Carcinogenic and Addictive as Regular Cigarettes

    PubMed Central

    Gan, Quan; Yang, Jie; Yang, Gonghuan; Goniewicz, Maciej; Benowitz, Neal L.; Glantz, Stanton A.

    2009-01-01

    Objective To examine the Chinese tobacco industry's claim that herbal cigarettes are less harmful than regular cigarettes. Design Cross-sectional study. Participants 135 herbal cigarette smokers and 143 regular smokers from one city in China completed a questionnaire on smoking behavior and provided a urine sample. Main Outcome Measures Cotinine and trans-3′-hydroxycotinine in all samples and polycyclic aromatic hydrocarbon metabolites (PAHs) (1-hydroxypyrene, naphthols, hydroxyfluorenes and hydroxyphnanthrenes) and the tobacco specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-butanol (NNAL) and NNAL-glucuronide in randomly selected 98 samples (47 from the herbal smokers' group and 51 from the regular smokers' group). Values were normalized by creatinine to correct for possible variability introduced by dilution or concentration of the urine. Results Health concern was among the main reasons that smokers switched to herbal cigarettes from regular cigarettes. Smokers reported increased consumption after switching to herbal cigarettes from regular cigarettes. For all the four markers analyzed (cotinine, trans-3′-hydroxycotinine, total NNAL, total PAHs), we observed no significant difference in the levels (p=0.169, p=0.146, p=0.171, p=0.554) between smokers of herbal cigarettes and smokers of regular cigarettes. Both total NNAL and total PAHs were significantly correlated with cotinine and trans-3′-hydroxycotinine (p<0.001 for all four correlations). Conclusions Our findings showed that herbal cigarettes did not deliver less carcinogens than regular cigarettes. The public needs to be aware of this fact and the Chinese tobacco industry should avoid misleading the public when promoting herbal cigarettes as safer products. PMID:19959701

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

    PubMed

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

    1992-06-01

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

  2. Radiation dose from cigarette tobacco

    SciTech Connect

    Papastefanou, C.

    2008-08-07

    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 {sup 226}Ra and {sup 210}Pb of the uranium series and {sup 228}Ra of the thorium series and/or man-made produced radionuclides, such as {sup 137}Cs 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 {sup 226}Ra varied from 42.5 to 178.6 {mu}Sv y{sup -1} (average 79.7 {mu}Sv y{sup -1}), while for {sup 228}Ra from 19.3 to 116.0 {mu}Sv y{sup -1} (average 67.1 {mu}Sv y{sup -1}) and for {sup 210}Pb from 47.0 to 134.9 {mu}Sv y{sup -1} (average 104.7 {mu}Sv y{sup -1}), that is the same order of magnitude for each radionuclide. The sum of the effective dose of the three natural radionuclides varied from 151.9 to 401.3 {mu}Sv y{sup -1} (average 251.5 {mu}Sv y{sup -1}). The annual effective dose from {sup 137}Cs of Chernobyl origin was three orders of magnitude lower as it varied from 70.4 to 410.4 nSv y{sup -1} (average 199.3 nSv y{sup -1})

  3. Effects of Experimental Income on Demand for Potentially Real Cigarettes

    PubMed Central

    Wilson, Arlington George; Bickel, Warren K.

    2015-01-01

    Introduction: Cigarette demand, or the change in cigarette consumption as a function of price, is a measure of reinforcement that is associated with level of tobacco dependence and other clinically relevant measures, but the effects of experimentally controlled income on real-world cigarette consumption have not been examined. Methods: In this study, income available for cigarette purchases was manipulated to assess the effect on cigarette demand. Tobacco-dependent cigarette smokers (n = 15) who smoked 10–40 cigarettes per day completed a series of cigarette purchasing tasks under a variety of income conditions meant to mimic different weekly cigarette budgets: $280, approximately $127, $70, or approximately $32 per week. Prices of $0.12, $0.25, $0.50, and $1.00 per cigarette were assessed in each income condition. Participants were instructed to purchase as many cigarettes as they would like for the next week and to only consume cigarettes purchased in the context of the study. One price in 1 income condition was randomly chosen to be “real,” and the cigarettes and the excess money in the budget for that condition were given to the participant. Results: Results indicate that demand elasticity was negatively correlated with income. Demand intensity (consumption at low prices) was unrelated to income condition and remained high across incomes. Conclusions: These results indicate that the amount of income that is available for cigarette purchases has a large effect on cigarette consumption, but only at high prices. PMID:25168032

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

    PubMed

    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

  5. [Cigarette prices, tobacco taxes and the proportion of contraband cigarettes in Germany].

    PubMed

    Effertz, T; Schlittgen, R

    2013-06-01

    Taxes on tobacco products are among the most efficient instruments against tobacco consumption and the arising cost of illness associated with them. The main argument of the tobacco industry against increases of excise taxes on cigarettes is a presumed substitution effect of smokers turning from consumption of legal cigarettes to smuggled ones. Besides deriving this proposition from the tobacco industry's own funded research, it has never been tested empirically. This article analyses the interdependence between contraband cigarettes and cigarette prices in Germany. Using VAR-modelling on the time-series of the variables of interest, we find no empirically valid correlation or causation between prices and untaxed contraband cigarettes. Furthermore, we find a positive relationship between contraband and legal taxed cigarettes, i. e., when the demand for legal cigarettes decreased in amount, so did the quantity of untaxed cigarettes. We conclude that the proposed relationship between prices and smuggled cigarettes as well as an overall substitution effect among smokers is non-existent. This has important implications for public health policy. The proposition that higher taxes on tobacco products incur social costs from increased smuggling activity cannot be corroborated empirically. Furthermore, this finding should encourage public health policy to keep using tobacco taxes as an instrument for prevention.

  6. [Cigarette prices, tobacco taxes and the proportion of contraband cigarettes in Germany].

    PubMed

    Effertz, T; Schlittgen, R

    2013-06-01

    Taxes on tobacco products are among the most efficient instruments against tobacco consumption and the arising cost of illness associated with them. The main argument of the tobacco industry against increases of excise taxes on cigarettes is a presumed substitution effect of smokers turning from consumption of legal cigarettes to smuggled ones. Besides deriving this proposition from the tobacco industry's own funded research, it has never been tested empirically. This article analyses the interdependence between contraband cigarettes and cigarette prices in Germany. Using VAR-modelling on the time-series of the variables of interest, we find no empirically valid correlation or causation between prices and untaxed contraband cigarettes. Furthermore, we find a positive relationship between contraband and legal taxed cigarettes, i. e., when the demand for legal cigarettes decreased in amount, so did the quantity of untaxed cigarettes. We conclude that the proposed relationship between prices and smuggled cigarettes as well as an overall substitution effect among smokers is non-existent. This has important implications for public health policy. The proposition that higher taxes on tobacco products incur social costs from increased smuggling activity cannot be corroborated empirically. Furthermore, this finding should encourage public health policy to keep using tobacco taxes as an instrument for prevention. PMID:22932830

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

    PubMed Central

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

    2015-01-01

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

  8. Histopathologic changes induced by cellophane wrapping of the pancreas are unaffected by cigarette smoke exposure in hamsters.

    PubMed

    Kim, Anthony W; Patel, Dhaval; Liu, Qiang; Gattuso, Paolo; Djuricin, Goldie; Kelly, Holly M; Girard, Scott; Cambria, Robert A; Freischlag, Julie A; Prinz, Richard A

    2002-01-01

    This study tests whether exposure to cigarette smoke alone or combined with cellophane wrapping of the pancreas increases the development of microscopic abnormalities in the pancreas of Syrian golden hamsters. Ninety hamsters were randomly divided into 4 groups. Thirty-five hamsters were exposed to 3 continuous hours of cigarette smoke daily for 3 months following celiotomy to cellophane wrap the gastric lobe of the pancreas (group 1). Thirty-two hamsters were not exposed to continuous cigarette smoke and had the wrap surgery alone (group 2). Twelve hamsters were exposed to cigarette smoke and had no surgery (group 3). Eleven hamsters had no exposure to cigarette smoke and no surgery (group 4). All of the hamsters were sacrificed after 3 months. The gastric (wrapped) and splenic (unwrapped) lobes of the pancreas were reviewed grossly and histologically. In all 4 groups, there were no gross abnormalities in either lobe of the pancreas. Histopathologic evaluation of the gastric lobes from group 1 showed that 13 of 35 lobes (37%) had pancreatitis (11 chronic, 1 acute, and 1 both). In group 2, 12 of 32 (38%) gastric lobes had pancreatitis (10 chronic, 2 acute). The incidence of pancreatitis in groups 1 and 2 was significantly higher than in groups 3 (0/12; p < 0.04) and 4 (0/11; p < 0.03), respectively. A significantly lower incidence of pancreatitis was found in the splenic lobes of all 4 groups when compared to gastric lobes in groups 1 and 2. Three of the 67 cellophane-wrapped glands had ductal hyperplasia. The effects of cellophane wrapping of the pancreas, both in the wrapped and unwrapped areas, induced changes of pancreatitis and hyperplasia that may be preneoplastic. Cigarette smoking, alone or combined with cellophane wrapping, did not cause these changes. Longer exposure to cigarette smoke may be needed to cause premalignant changes in the hamster pancreas.

  9. Cigarette Smoke Exposure Exacerbates Lung Inflammation and Compromises Immunity to Bacterial Infection

    PubMed Central

    Lugade, Amit A.; Bogner, Paul N.; Thatcher, Thomas H.; Sime, Patricia J.; Phipps, Richard P.; Thanavala, Yasmin

    2014-01-01

    The detrimental impact of tobacco on human health is clearly recognized and despite aggressive efforts to prevent smoking, close to one billion individuals worldwide continue to smoke. People with chronic obstructive pulmonary disease (COPD) are susceptible to recurrent respiratory infections with pathogens, including non-typeable Haemophilus influenzae (NTHI), yet the reasons for this increased susceptibility are poorly understood. As mortality rapidly increases with multiple exacerbations, development of protective immunity is critical to improving patient survival. Acute NTHI infection has been studied in the context of cigarette smoke exposure, but this is the first study to investigate chronic infection and the generation of adaptive immune responses to NTHI following chronic smoke exposure. After chronic NTHI infection, mice that had previously been exposed to cigarette smoke developed increased lung inflammation and compromised adaptive immunity relative to air-exposed controls. Importantly, NTHI-specific T cells from mice exposed to cigarette smoke produced lower levels of IFN-γ and IL-4, and B cells produced reduced levels of antibodies against outer membrane lipoprotein P6, with impaired IgG1, IgG2a and IgA class-switching. However, production of IL-17, which is associated with neutrophilic inflammation, was enhanced. Interestingly, cigarette smoke exposed mice exhibited a similar defect in the generation of adaptive immunity following immunization with P6. Our study has conclusively demonstrated that cigarette smoke exposure has a profound suppressive effect on the generation of adaptive immune responses to NTHI and suggests the mechanism by which prior cigarette smoke exposure predisposes COPD patients to recurrent infections, leading to exacerbations and contributing to mortality. PMID:24752444

  10. Disrupting nicotine reinforcement: from cigarette to brain.

    PubMed

    Rose, Jed E

    2008-10-01

    Cigarette smoking is a tenacious addiction that is maintained to a significant extent by the reinforcing effects of nicotine. An emerging theme in smoking cessation treatment is the development of methods for interfering with these reinforcing effects. By attenuating nicotine reinforcement, treatments may enhance a smoker's chances of successfully remaining abstinent. Several treatment approaches will be described, including the use of denicotinized cigarettes, nicotine vaccines, nicotinic receptor agonists and antagonists, and modulators of brain reinforcement processes. These techniques highlight the numerous sites along the path between the cigarette and the brain that can be targeted for intervention. In addition to unimodal therapies, treatment combinations will be discussed that might more effectively block cigarette reward and thereby further enhance smoking abstinence. PMID:18991961

  11. Sale of cigarettes to children in Exeter.

    PubMed

    Bradley, N C

    1983-09-01

    The sale of cigarettes to children in Exeter was investigated. Thirty-seven local shops were visited and the salespeople interviewed: 28 incorrectly understood the relevant law and seven had no knowledge of it. Only seven people said they tried to keep within the law. Only two of the 37 shops were displaying the Tobacco Advisory Council's explanatory notice sent to every cigarette retailer in the United Kingdom in 1981. Every shop sold cigarettes. It is proposed that: a notice explaining the law be displayed in all cigarette retailing shops; the tobacconist's licence (abolished in 1963) be reintroduced; and local civic and health authorities combine to educate retailers, their staff and the public. PMID:6631800

  12. Why Teens Choose E-Cigarettes

    MedlinePlus

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

  13. Multicomponent assessment and treatment of cigarette pica.

    PubMed Central

    Goh, H L; Iwata, B A; Kahng, S W

    1999-01-01

    We conducted a multicomponent assessment and treatment for 4 individuals who engaged in cigarette pica. During Phase 1, three stimulus preference assessments were conducted to identify (a) the reinforcing component of the cigarette, (b) potential alternative reinforcers that may be used during treatment, and (c) whether the alternative reinforcer would compete effectively with cigarettes. Results were successful in identifying the reinforcing component of the cigarette and suggested the feasibility of using alternative reinforcers during treatment to eliminate cigarette pica. During Phase 2, the effects of two treatment procedures were evaluated. Noncontingent reinforcement (NCR) with the alternative edible reinforcer reduced the pica of 2 of the participants, but effects were not maintained when the initial dense schedule of NCR was thinned. Subsequently, differential reinforcement of alternative behavior with the alternative edible reinforcer was effective in reducing pica for 3 participants. An evaluation of nine treatment procedures failed to identify an effective intervention for the remaining participant; consequently, preventive measures were designed to minimize occurrences of cigarette pica. PMID:10513026

  14. Children's perceptions of advertisements for cigarettes.

    PubMed

    Aitken, P P; Leathar, D S; O'Hagan, F J

    1985-01-01

    Groups of children aged between 6 and 16 years discussed a series of advertisements, including those for cigarettes. Clear patterns emerged in their recognition of cigarette brand imagery. For example, in response to an advertisement for holidays which also presents the brand imagery of John Player Special cigarettes, 22% of primary school children and 91% of secondary school children said it advertises cigarettes. There were consistent trends in responses to the symbolism portrayed. Younger children were very much tied to what was specifically shown in the advertisements; older ones tended to perceive more complex imagery. For example, whereas 10-year-olds said people who like the advertisement for Kim cigarettes (which has symbols for drinking) would smoke and drink, some 12-year-olds and most 14- and 16-year-olds saw Kim as feminine, sociable, trendy and sporty. It seems that some 12-year-olds and most 14- and 16-year-olds perceive cigarette advertisements much in the way that young adults do; therefore advertising campaigns targeted at older teenagers and young adults are likely to present qualities which younger teenagers find attractive. PMID:4071115

  15. Corneoscleral Laceration and Ocular Burns Caused by Electronic Cigarette Explosions

    PubMed Central

    Paley, Grace L.; Echalier, Elizabeth; Eck, Thomas W.; Hong, Augustine R.; Gregory, Darren G.; Lubniewski, Anthony J.

    2016-01-01

    Purpose: To report cases of acute globe rupture and bilateral corneal burns from electronic cigarette (EC) explosions. Methods: Case series. Results: We describe a series of patients with corneal injury caused by EC explosions. Both patients suffered bilateral corneal burns and decreased visual acuity, and one patient sustained a unilateral corneoscleral laceration with prolapsed iris tissue and hyphema. A review of the scientific literature revealed no prior reported cases of ocular injury secondary to EC explosions; however, multiple media and government agency articles describe fires and explosions involving ECs, including at least 4 with ocular injuries. Conclusions: Given these cases and the number of recent media reports, ECs pose a significant public health risk. Users should be warned regarding the possibility of severe injury, including sight-threatening ocular injuries ranging from corneal burns to full-thickness corneoscleral laceration. PMID:27191672

  16. Passive exposure to electronic cigarette (e-cigarette) use increases desire for combustible and e-cigarettes in young adult smokers

    PubMed Central

    King, Andrea C; Smith, Lia J; McNamara, Patrick J; Matthews, Alicia K; Fridberg, Daniel J

    2016-01-01

    Background Passive exposure to combustible cigarette use has been shown to act as a cue to increase smoking urge. Given the resemblance of e-cigarettes and other electronic nicotine delivery systems (ENDS) to combustible cigarettes, we examined whether these devices could also act as a cue to increase smoking desire and urges in those passively exposed. Methods Young adult daily smokers (age 18–35 years; N=60) completed subjective ratings before and after exposure to a study confederate drinking bottled water (control cue) and then smoking either a combustible or e-cigarette (active cue). Smoking desire and urge ratings were measured with visual analogue scale items for desire for a regular and an e-cigarette and the Brief Questionnaire of Smoking Urges. Results Passive exposure to both the e-cigarette and combustible cigarette cue significantly increased observers’ ratings of desire and urge to smoke a regular cigarette (all ps<0.05). Exposure to the e-cigarette cue but not the regular cigarette cue also increased desire to smoke an e-cigarette (p<0.01). Conclusions The results provide the first evidence in a controlled setting that electronic cigarette exposure may evoke smoking urges in young adult daily smokers. With replication, these findings may have relevance for ENDS regulation and policy. PMID:24848637

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

    ERIC Educational Resources Information Center

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

    2015-01-01

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

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

    ERIC Educational Resources Information Center

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

    PubMed

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

    2014-09-01

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

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

    SciTech Connect

    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. Use of the zebrafish larvae as a model to study cigarette smoke condensate toxicity.

    PubMed

    Ellis, Lee D; Soo, Evelyn C; Achenbach, John C; Morash, Michael G; Soanes, Kelly H

    2014-01-01

    The smoking of tobacco continues to be the leading cause of premature death worldwide and is linked to the development of a number of serious illnesses including heart disease, respiratory diseases, stroke and cancer. Currently, cell line based toxicity assays are typically used to gain information on the general toxicity of cigarettes and other tobacco products. However, they provide little information regarding the complex disease-related changes that have been linked to smoking. The ethical concerns and high cost associated with mammalian studies have limited their widespread use for in vivo toxicological studies of tobacco. The zebrafish has emerged as a low-cost, high-throughput, in vivo model in the study of toxicology. In this study, smoke condensates from 2 reference cigarettes and 6 Canadian brands of cigarettes with different design features were assessed for acute, developmental, cardiac, and behavioural toxicity (neurotoxicity) in zebrafish larvae. By making use of this multifaceted approach we have developed an in vivo model with which to compare the toxicity profiles of smoke condensates from cigarettes with different design features. This model system may provide insights into the development of smoking related disease and could provide a cost-effective, high-throughput platform for the future evaluation of tobacco products. PMID:25526262

  2. Use of the Zebrafish Larvae as a Model to Study Cigarette Smoke Condensate Toxicity

    PubMed Central

    Ellis, Lee D.; Soo, Evelyn C.; Achenbach, John C.; Morash, Michael G.; Soanes, Kelly H.

    2014-01-01

    The smoking of tobacco continues to be the leading cause of premature death worldwide and is linked to the development of a number of serious illnesses including heart disease, respiratory diseases, stroke and cancer. Currently, cell line based toxicity assays are typically used to gain information on the general toxicity of cigarettes and other tobacco products. However, they provide little information regarding the complex disease-related changes that have been linked to smoking. The ethical concerns and high cost associated with mammalian studies have limited their widespread use for in vivo toxicological studies of tobacco. The zebrafish has emerged as a low-cost, high-throughput, in vivo model in the study of toxicology. In this study, smoke condensates from 2 reference cigarettes and 6 Canadian brands of cigarettes with different design features were assessed for acute, developmental, cardiac, and behavioural toxicity (neurotoxicity) in zebrafish larvae. By making use of this multifaceted approach we have developed an in vivo model with which to compare the toxicity profiles of smoke condensates from cigarettes with different design features. This model system may provide insights into the development of smoking related disease and could provide a cost-effective, high-throughput platform for the future evaluation of tobacco products. PMID:25526262

  3. Comparison of Biological Responses in Rats Under Various Cigarette Smoke Exposure Conditions

    PubMed Central

    Tsuji, Hiroyuki; Fujimoto, Hitoshi; Matsuura, Daiki; Nishino, Tomoki; Lee, K Monica; Yoshimura, Hiroyuki

    2013-01-01

    A variety of exposure regimens of cigarette smoke have been used in animal models of lung diseases. In this study, we compared biological responses of smoke exposure in rats, using different smoke concentrations (wet total particulate matter [WTPM]), daily exposure durations, and total days of exposure. As a range-finding acute study, we first compared pulmonary responses between SD and F344 strains after a single nose-only exposure to mainstream cigarette smoke or LPS. Secondly, F344 rats were exposed to cigarette smoke for 2 or 13 weeks under the comparable daily exposure dose (WTPM concentration x daily exposure duration; according to Haber’s rule) but at a different WTPM concentration or daily exposure duration. Blood carboxylhemoglobin was increased linearly to the WTPM concentration, while urinary nicotine plus cotinine value was higher for the longer daily exposure than the corresponding shorter exposure groups. Gamma glutamyl transferase activity in bronchoalveolar lavage fluid (BALF) was increased dose dependently after 2 and 13 weeks of cigarette smoke exposure, while the neutrophil content in BALF was not increased notably. Smoke-exposed groups showed reduced body weight gain and increased relative lung and heart weights. While BALF parameters and the relative lung weights suggest pulmonary responses, histopathological examination showed epithelial lesions mainly in the upper respiratory organs (nose and larynx). Collectively, the results indicate that, under the employed study design, the equivalent daily exposure dose (exposure concentration x duration) induces equivalent pulmonary responses in rats. PMID:23914058

  4. Carcinogens in tobacco smoke: benzo[a]pyrene from Canadian cigarettes and cigarette tobacco.

    PubMed Central

    Kaiserman, M J; Rickert, W S

    1992-01-01

    We evaluated the benzo[a]pyrene (BaP) content in the smoke from 35 brands of Canadian cigarettes and 5 brands of Canadian tobaccos for roll-your-own cigarettes. For the cigarettes, mean values of BaP ranged from 3.36 ng to 28.39 ng per cigarette, roughly in proportion with declared tar values. The relationship between declared tar and yields of BaP, however, does not allow accurate prediction of one from the other. For the tobaccos, mean BaP values ranged from 22.92 ng to 26.27 ng (average, 24.7 ng) per cigarette. The implications of these findings are discussed with respect to overall exposure. PMID:1609904

  5. Smoking induces epithelial-to-mesenchymal transition in non-small cell lung cancer through HDAC-mediated downregulation of E-cadherin.

    PubMed

    Nagathihalli, Nagaraj S; Massion, Pierre P; Gonzalez, Adriana L; Lu, Pengcheng; Datta, Pran K

    2012-11-01

    Epidemiological studies have shown that most cases of lung cancers (85%-90%) are directly attributable to tobacco smoking. Although association between cigarette smoking and lung cancer is well documented, surprisingly little is known about the molecular mechanisms of how smoking is involved in epithelial-to-mesenchymal transition (EMT) through epigenetic changes. Here, we show that lung cancer patients with a smoking history have low E-cadherin levels and loss of E-cadherin is a poor prognostic factor in smokers. Moreover, the downregulation of E-cadherin correlates with the number of pack years. In an attempt to determine the role of long-term cigarette smoking on EMT, we observed that treatment of lung cell lines with cigarette smoke condensate (CSC) induces EMT through downregulation of epithelial markers, including E-cadherin and upregulation of mesenchymal markers. CSC decreases E-cadherin expression at the transcriptional level through upregulation of LEF1 and Slug, and knockdown of these two proteins increases E-cadherin expression. Importantly, chromatin immunoprecipitation assays suggest that LEF-1 and Slug binding to E-cadherin promoter is important for CSC-mediated downregulation of E-cadherin. The histone deacetylase (HDAC) inhibitor MS-275 reverses CSC-induced EMT, migration, and invasion through the restoration of E-cadherin expression. These results suggest that recruitment of HDACs by transcriptional repressors LEF-1 and Slug is responsible for E-cadherin suppression and EMT in cigarette smokers and provide a potential drug target toward the treatment of lung cancer.

  6. Cigarette smoke reversibly activates hypoxia-inducible factor 1 in a reactive oxygen species-dependent manner

    PubMed Central

    Daijo, Hiroki; Hoshino, Yuma; Kai, Shinichi; Suzuki, Kengo; Nishi, Kenichiro; Matsuo, Yoshiyuki; Harada, Hiroshi; Hirota, Kiichi

    2016-01-01

    Cigarette smoke (CS) is a major contributor to the development of a large number of fatal and debilitating disorders. However, the precise molecular mechanisms underlying the effects of CS in lung disease are largely unknown. To elucidate these pathophysiological processes, we examined the in vitro and in vivo effects of CS extract (CSE) and CS on the transcription factor, hypoxia-inducible factor 1 (HIF-1). CSE induced concentration- and time-dependent accumulation of HIF-1α protein in human lung epithelial-like cells under non-hypoxic conditions. Genes upregulated by HIF-1, including vascular endothelial growth factor and regulated in development and DNA damage response 1, both of which are involved in smoking-induced emphysematous changes, were increased by CSE treatment under non-hypoxic conditions in vitro and in vivo. Further investigation revealed that reactive oxygen species were generated in cells exposed to CSE and were required for CSE-mediated induction of HIF-1α protein, as was activation of phosphoinositide 3-kinase and mitogen-activated protein kinase pathways. In conclusion, we demonstrated that CSE and CS induced HIF-1 activation in vitro and in vivo, respectively. The evidence warrants further investigation to indicate that HIF-1 plays an important role in CS-induced gene expression, which is deeply involved in pulmonary cellular stress and small airway remodelling. PMID:27680676

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

    PubMed Central

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

    2009-01-01

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

  8. 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

    PubMed Central

    Barr, Dana Boyd; Stratton, Erin; Escoffery, Cam; Kegler, Michelle

    2015-01-01

    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 per day (cpd), smoking regularly ≥1 year, and not having started using e-cigarettes. Of 72 individuals screened, 40 consented, 36 completed the baseline survey, and 83.3% and 72.2% were retained at weeks 4 and 8, respectively. Results Participants reduced cigarette consumption from baseline to week 4 and 8 (p’s < 0.001); 23.1% reported no cigarette use in the past month at week 8. There was no significant decrease in cotinine from baseline to week 4 or 8 (p’s = ns). At week 8, the majority reported improved health (65.4%), reduced smoker’s cough (57.7%), and improved sense of smell (53.8%) and taste (50.0%). The majority believed that e-cigarettes versus regular cigarettes have fewer health risks (97.2%) and that e-cigarettes have been shown to help smokers quit (80.6%) and reduce cigarette consumption (97.2%). In addition, the majority intended to use e-cigarettes as a complete replacement for regular cigarettes (69.4%) and reported no restriction on e-cigarette use in the home (63.9%) or car (80.6%). Conclusions Future research is needed to document the long-term impact on smoking behavior and health among cigarette smokers who initiate use of e-cigarettes. PMID:25621193

  9. Rationale and approaches to the prevention of smoking-related diseases: overview of recent studies on chemoprevention of smoking-induced tumors in rodent models.

    PubMed

    De Flora, Silvio; Izzotti, Alberto; D'Agostini, Francesco; La Maestra, Sebastiano; Micale, Rosanna T; Ceccaroli, Chiara; Steele, Vernon E; Balansky, Roumen

    2014-01-01

    Tobacco smoke plays a dominant role in the epidemiology of lung cancer, cancer at other sites, and a variety of other chronic diseases. It is the leading cause of death in developed countries, and the global burden of cancer is escalating in less developed regions. For a rational implementation of strategies exploitable for the prevention smoking-related diseases, it is crucial to elucidate both the mechanisms of action of cigarette smoke and the protective mechanisms of the host organism. The imperative primary prevention goal is to avoid any type of exposure to smoke. Epidemiological studies have shown that a decrease in the consumption of cigarettes can be successful in attenuating the epidemic of lung cancer in several countries. Chemoprevention by means of dietary and/or pharmacological agents provides a complementary strategy aimed at decreasing the risk of developing smoking-associated diseases in addicted current smokers, who are unable to quit smoking, and especially in involuntary smokers and ex-smokers. The availability of new animal models that are suitable to detect the carcinogenicity of cigarette smoke and to assess the underlying molecular mechanisms provides new tools for evaluating both safety and efficacy of putative chemopreventive agents.

  10. Smoker reactions to a "radio message" that Light cigarettes are as dangerous as Regular cigarettes.

    PubMed

    Kozlowski, L T; Goldberg, M E; Sweeney, C T; Palmer, R F; Pillitteri, J L; Yost, B A; White, E L; Stine, M M

    1999-03-01

    The purpose of this study was to examine in a systematic, controlled fashion the reactions of smokers to scientifically correct information about the risks of smoking Light cigarettes (about 6-15 mg tar by the FTC method). Random-digit dialing, computer-assisted telephone interviews were used to locate daily smokers of Light cigarettes. In an experimental design, smokers were randomly assigned to listen (n = 293) or not (n = 275) to a persuasive simulated radio message on the risks of Light cigarettes; 108 of those who did not listen to the message in the first part of the interview were played the message in the second part, to evaluate some repeated-measures effects. Those who heard the message were more likely to report that one Light cigarette could give a smoker the same amount of tar as one Regular cigarette and that Light cigarettes were more dangerous: 55% said the message made them think more about quitting and 46% said the message increased the amount they wanted to quit; 42% said that after hearing the message they thought Light cigarettes were more dangerous. Using the Theory of Planned Behavior, structural equation modeling analysis indicated that the message acted to increase intention to quit smoking by increasing the desire to quit smoking. Seventy-three per cent of the smokers agreed that it was important to play such messages widely on the radio; 77% agreed that there should be a warning on packs that vent blocking increases tar; 61% agreed that the location of filter vents should be marked. The majority of smokers of Light cigarettes seem to value being informed that Light cigarettes are as dangerous for them as Regular cigarettes, and this information increases their intentions to quit smoking. PMID:11072390

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

    PubMed

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

    2015-10-01

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

  12. Effect of cigarette smoke condensate on gene promoter methylation in human lung cells

    PubMed Central

    2014-01-01

    Background In lung cancer, an association between tobacco smoking and promoter DNA hypermethylation has been demonstrated for several genes. However, underlying mechanisms for promoter hypermethylation in tobacco-induced cancer are yet to be fully established. Methods Promoter methylation was evaluated in control and cigarette smoke condensate (CSC) exposed human lung cells using the Methyl-Profiler DNA Methylation PCR System. PSAE cells were exposed to 0.3 or 1.0 μg/ml CSC for 72 hours and longer term for 14 and 30 days. NL-20 cells were exposed for 30 days to 10 or 100 μg/ml CSC. Results Promoters of several genes, including hsa-let-7a-3, CHD1, CXCL12, PAX5, RASSF2, and TCF21, were highly methylated (>90%); hsa-let-7a-3 was affected in both cell lines and under all exposure conditions. Level of methylation tended to increase with CSC concentration and exposure duration (statistical differences were not determined). Percentage methylation of TCF21, which was >98% at exposures of 10 or 100 μg/ml CSC, was found to be reduced to 28% and 42%, respectively, in the presence of the dietary agent genistein. Conclusions Using array techniques, several tumor suppressor genes in human lung cells were identified that undergo promoter hypermethylation, providing further evidence of their potential involvement in tobacco smoke-induced lung carcinogenesis and their use as potential biomarkers of harm in tobacco smoke exposure. Results from the study also demonstrated the potential of a dietary agent to exert chemopreventive activity in human tissue against tobacco smoke related diseases through modulation of DNA methylation. Additional studies are needed to confirm these findings. PMID:25214829

  13. Cigarette Smoke Exposure Triggers the Autophagic Cascade via Activation of the AMPK Pathway in Mice1

    PubMed Central

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

    2015-01-01

    We previously demonstrated that cigarette smoke (CS) exposure decreases primordial follicle counts and induces autophagy in ovarian granulosa cells in preference to apoptosis. Therefore, the objective of this study was to investigate molecular targets underlying smoke-induced activation of the reparative autophagy pathway in the ovary. Briefly, ovarian homogenates were prepared from adult female mice exposed to mainstream CS twice daily for 8 wk, using a whole-body exposure system. A gene array revealed that CS exposure induced a greater than 2-fold significant increase in the expression of proautophagic genes Cdkn1b, Map1lc3a, Bad, and Sqstm1/p62. A significant increase in Prkaa2, Pik3c3, and Maplc31b expression, as well as a significant decrease in Akt1 and Mtor expression, was detected by quantitative PCR. The 5′-AMP-activated protein kinase catalytic subunit (AMPK) alpha1 + alpha2 and ATG7 protein expression was significantly increased, whereas AKT1, mTOR, CDKN1B/p27, and CXCR4 proteins were significantly decreased in CS exposed versus control ovaries. Up-regulation of AMPK alpha1 + alpha2, a known initiator of autophagic signaling, and ATG7 further suggests activation of the autophagy cascade. Two prosurvival factors, AKT and mTOR, were decreased in expression, an outcome that favors induction of the autophagy pathway, whereas decreased levels of CDKN1B is suggestive of cell cycle dysregulation. In summary, our data suggest that CS exposure induces ovarian follicle loss through induction of the autophagic cascade via the AMPK pathway together with inhibition of antiautophagic markers AKT and mTOR. We further postulate that toxicant-induced dysregulation of reparative autophagy is a novel pathway central to impaired follicle development and subfertility. PMID:26377221

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

    PubMed

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

    2016-02-01

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

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

    PubMed

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

    2016-02-01

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

  16. Electronic cigarette use outcome expectancies among college students

    PubMed Central

    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

  17. Adverse effects of cigarette and noncigarette smoke exposure on the autonomic nervous system: mechanisms and implications for cardiovascular risk.

    PubMed

    Middlekauff, Holly R; Park, Jeanie; Moheimani, Roya S

    2014-10-21

    This review summarizes the detrimental effects of cigarette and noncigarette emission exposure on autonomic function, with particular emphasis on the mechanisms of acute and chronic modulation of the sympathetic nervous system. We propose that the nicotine and fine particulate matter in tobacco smoke lead to increased sympathetic nerve activity, which becomes persistent via a positive feedback loop between sympathetic nerve activity and reactive oxidative species. Furthermore, we propose that baroreflex suppression of sympathetic activation is attenuated in habitual smokers; that is, the baroreflex plays a permissive role, allowing sympathoexcitation to occur without restraint in the setting of increased pressor response. This model is also applicable to other nontobacco cigarette emission exposures (e.g., marijuana, waterpipes [hookahs], electronic cigarettes, and even air pollution). Fortunately, emerging data suggest that baroreflex sensitivity and autonomic function may be restored after smoking cessation, providing further evidence in support of the health benefits of smoking cessation.

  18. Adverse effects of cigarette and noncigarette smoke exposure on the autonomic nervous system: mechanisms and implications for cardiovascular risk.

    PubMed

    Middlekauff, Holly R; Park, Jeanie; Moheimani, Roya S

    2014-10-21

    This review summarizes the detrimental effects of cigarette and noncigarette emission exposure on autonomic function, with particular emphasis on the mechanisms of acute and chronic modulation of the sympathetic nervous system. We propose that the nicotine and fine particulate matter in tobacco smoke lead to increased sympathetic nerve activity, which becomes persistent via a positive feedback loop between sympathetic nerve activity and reactive oxidative species. Furthermore, we propose that baroreflex suppression of sympathetic activation is attenuated in habitual smokers; that is, the baroreflex plays a permissive role, allowing sympathoexcitation to occur without restraint in the setting of increased pressor response. This model is also applicable to other nontobacco cigarette emission exposures (e.g., marijuana, waterpipes [hookahs], electronic cigarettes, and even air pollution). Fortunately, emerging data suggest that baroreflex sensitivity and autonomic function may be restored after smoking cessation, providing further evidence in support of the health benefits of smoking cessation. PMID:25323263

  19. Aberrant promoter hypermethylation of the death-associated protein kinase gene is early and frequent in murine lung tumors induced by cigarette smoke and tobacco carcinogens.

    PubMed

    Pulling, Leah C; Vuillemenot, Brian R; Hutt, Julie A; Devereux, Theodora R; Belinsky, Steven A

    2004-06-01

    Loss of expression of the death-associated protein (DAP)-kinase gene by aberrant promoter methylation may play an important role in cancer development and progression. The purpose of this investigation was to determine the commonality for inactivation of the DAP-kinase gene in adenocarcinomas induced in mice by chronic exposure to mainstream cigarette smoke, the tobacco carcinogens 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and vinyl carbamate, and the occupational carcinogen methylene chloride. The timing for inactivation was also determined in alveolar hyperplasias that arise in lung cancer induced in the A/J mouse by NNK. The DAP-kinase gene was not expressed in three of five NNK-induced lung tumor-derived cell lines or in a spontaneously arising lung tumor-derived cell line. Treatment with 5-aza-2'-deoxycytidine restored expression; dense methylation throughout the DAP-kinase CpG island detected by bisulfite sequencing supported methylation as the inactivating event in these cell lines. Methylation-specific PCR detected inactivation of the DAP-kinase gene in 43% of tumors associated with cigarette smoke, a frequency similar to those reported in human non-small cell lung cancer. In addition, DAP-kinase methylation was detected in 52%, 60%, and 50% of tumors associated with NNK, vinyl carbamate, and methylene chloride, respectively. Methylation was observed at similar prevalence in both NNK-induced hyperplasias and adenocarcinomas (46% versus 52%), suggesting that inactivation of this gene is one pathway for tumor development in the mouse lung. Bisulfite sequencing of both premalignant and malignant lesions revealed dense methylation, substantiating that this gene is functionally inactivated at the earliest histological stages of adenocarcinoma development. This study is the first to use a murine model of cigarette smoke-induced lung cancer and demonstrate commonality for inactivation by promoter hypermethylation of a gene implicated in the development

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

    PubMed

    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

  1. C/EBPβ-mediated transcriptional regulation of bcl-xl gene expression in human breast epithelial cells in response to cigarette smoke condensate

    PubMed Central

    Connors, Shahnjayla K.; Balusu, Ramesh; Kundu, Chanakya N.; Jaiswal, Aruna S.; Gairola, C. Gary; Narayan, Satya

    2008-01-01

    In previous studies, we have shown that cigarette smoke condensate (CSC), a surrogate for cigarette smoke, is capable of transforming the spontaneously immortalized human breast epithelial cell line, MCF10A. These transformed cells displayed upregulation of the anti-apoptotic gene, bcl-xl. Upregulation of this gene may impede the apoptotic pathway and allow the accumulation of DNA damage that can lead to cell transformation and carcinogenesis. In the present study, we have determined the mechanism of CSC-mediated transcriptional upregulation of bcl-xl gene expression in MCF10A cells. We cloned the human bcl-xl promoter (pBcl-xLP) and identified putative transcription factor binding sites. Sequential deletion constructs that removed the putative cis-elements were constructed and transfected into MCF10A cells to determine the CSC-responsive cis-element(s) on the pBcl-xLP. Gel-shift, supershift, and chromatin immunoprecipitation (ChIP) analysis confirmed that C/EBPβ specifically bound to a C/EBP-binding site on the pBcl-xLP in vitro and in vivo. Additionally, overexpression of C/EBPβ-LAP2 stimulated pBcl-xLP activity and Bcl-xL protein levels, which mimicked the conditions of CSC treatment. Our results indicate that C/EBPβ regulates bcl-xl gene expression in MCF10A cells in response to CSC treatment, therefore making it a potential target for chemotherapeutic intervention of cigarette smoke-induced breast carcinogenesis. PMID:19043455

  2. Achieving appropriate regulations for electronic cigarettes

    PubMed Central

    Saitta, Daniela; Ferro, Giancarlo Antonio

    2014-01-01

    A growing body of scientific studies show that e-cigarettes may serve as an acceptable substitute for smoking tobacco cigarettes, thereby reducing or eliminating exposure to harmful elements in smoke. The success of e-cigarettes is such that sales of these products are rapidly gaining on traditional cigarettes. The rapidly evolving phenomenon is raising concerns for the health community, pharmaceutical industry, health regulators and state governments. Obviously, these products need to be adequately regulated, primarily to protect users. Depending on the form and intended scope, certain regulatory decisions may have diverse unintended consequences on public health and may face many different challenges. Ideally, before any regulations are enacted, the regulatory body will require sufficient scientific research to verify that a problem does exist, quantify the problem, explore all potential solutions including making no change at all, determine the possible consequences of each, and then select the solution that is best for public health. Here we present an overview on the existing and deeming regulatory decisions for electronic cigarettes. We challenge them, based on the mounting scientific evidence with the ultimate goal of proposing appropriate recommendations while minimizing potential unintended consequences of ill-informed regulation. PMID:24587890

  3. Naloxone does not affect cigarette smoking.

    PubMed

    Nemeth-Coslett, R; Griffiths, R R

    1986-01-01

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

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

    PubMed

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

    2014-01-01

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

  5. Naloxone does not affect cigarette smoking.

    PubMed

    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.

  6. Risk Factors for Exclusive E-Cigarette Use and Dual E-Cigarette Use and Tobacco Use in Adolescents

    PubMed Central

    Knight, Rebecca; Williams, Rebecca J.; Pagano, Ian; Sargent, James D.

    2015-01-01

    OBJECTIVE: To describe electronic cigarette (e-cigarette) use and cigarette use among adolescents and determine whether established risk factors for smoking discriminate user categories. METHODS: School-based survey of 1941 high school students (mean age 14.6 years) in Hawaii; data collected in 2013. The survey assessed e-cigarette use and cigarette use, alcohol and marijuana use, and psychosocial risk and protective variables (eg, parental support, academic involvement, smoking expectancies, peer smoking, sensation seeking). Analysis of variance and multinomial regression examined variation in risk and protective variables across the following categories of ever-use: e-cigarette only, cigarette only, dual use (use of both products), and nonuser (never used either product). RESULTS: Prevalence for the categories was 17% (e-cigarettes only), 12% (dual use), 3% (cigarettes only), and 68% (nonusers). Dual users and cigarette-only users were highest on risk status (elevated on risk factors and lower on protective factors) compared with other groups. E-cigarette only users were higher on risk status than nonusers but lower than dual users. E-cigarette only users and dual users more often perceived e-cigarettes as healthier than cigarettes compared with nonusers. CONCLUSIONS: This study reports a US adolescent sample with one of the largest prevalence rates of e-cigarette only use in the existing literature. Dual use also had a substantial prevalence. The fact that e-cigarette only users were intermediate in risk status between nonusers and dual users raises the possibility that e-cigarettes are recruiting medium-risk adolescents, who otherwise would be less susceptible to tobacco product use. PMID:25511118

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

    PubMed

    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 (P<0.001). By 2014, 20.5% of high school and 8.5% of middle school students reported ever use of e-cigarettes. Among ever e-cigarette users in 2014, 30.3% of high school and 42.2% of middle school students had never smoked traditional cigarettes. Given the concern that significant rates of e-cigarette use by U.S. adolescents may have a negative effect on public health, further review of e-cigarette advertising, marketing, sales, and use among U.S. youth is warranted.

  8. Heart Docs: Never Expose Kids to Cigarette Smoke

    MedlinePlus

    ... 160911.html Heart Docs: Never Expose Kids to Cigarette Smoke Secondhand smoke can raise children's risk of ... consider making their children's environment smoke-free because cigarette smoke exposure is harmful to children's long-term ...

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

    MedlinePlus

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

  10. Lung injury after cigarette smoking is particle-related

    EPA Science Inventory

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

  11. A Safer Cigarette? A Comparative Study. A Consensus Report.

    PubMed

    2000-01-01

    This special issue describes the scientific progress and scientific review process to develop a safer cigarette. A peer-review panel, the ECLIPSE Expert Panel, was convened to critically review the potential health hazards of this new cigarette to a reference, conventional cigarette that bums tobacco. This new cigarette is lit and smoked much like other cigarettes, but it burns very little tobacco and paper. Also, unlike other cigarettes, it does not burn down to a butt, nor does it produce loose ash. Such a product would be expected to have less "tar" and other combustion products than cigarettes that burn tobacco and should greatly reduce any sidestream smoke. This panel assessed the chemistry and physical characteristics, as well as the biological activity, of this new cigarette.

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

    PubMed

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

    1998-08-01

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

  13. E-Cigarettes a Gateway to Smoking for Teens

    MedlinePlus

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

  14. Percentage of U.S. Adolescents Who Smoke Cigarettes

    MedlinePlus

    ... U.S. Adolescents Who Smoke Cigarettes Percentage of U.S. Adolescents Who Smoke Cigarettes Tobacco use is the leading ... This measure is calculated by the Division of Adolescent and School Health, National Center for Chronic Disease ...

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

    MedlinePlus

    ... news/fullstory_160310.html Starting Monday, FDA Banning E-Cigarette Sales to Minors Agency also details other ... Aug. 8, 2016 (HealthDay News) -- The sale of e-cigarettes to minors will be banned starting Monday, ...

  16. Percentage of U.S. Adults Who Smoke Cigarettes

    MedlinePlus

    ... Coverage Percentage of Adults Who Smoke Cigarettes by Medicaid Coverage 6mph-3zwu Download these data » Click on ... Coverage Percentage of Adults Who Smoke Cigarettes by Medicare Coverage 5pgf-ueam Download these data » Click on ...

  17. Toxicological assessment of kretek cigarettes Part 3: kretek and American-blended cigarettes, inhalation toxicity.

    PubMed

    Piadé, J-J; Roemer, E; Dempsey, R; Weiler, H; Meurrens, K; Vanscheeuwijck, P; Schorp, M K

    2014-12-01

    A typical Indonesian kretek cigarette brand and an experimental kretek reference cigarette were compared to the reference cigarette 2R4F in two 90-day inhalation studies. Male and female rats were exposed nose-only to mainstream smoke for 6 hours daily, for 90 consecutive days. Biological endpoints were assessed according to OECD guideline 413, with special emphasis on respiratory tract histopathology and on lung inflammation (broncho-alveolar lavage fluid levels of neutrophils, macrophages and lymphocytes). Histopathological alterations included: in the nose, hyperplasia and squamous metaplasia of the respiratory epithelium and squamous metaplasia and atrophy of the olfactory epithelium; in the larynx, epithelial squamous metaplasia and hyperplasia; in the lungs, accumulation of macrophages in alveoli and goblet cell hyperplasia in bronchial epithelium. The findings were qualitatively consistent with observations from previous similar studies on conventional cigarettes. Compared to 2R4F cigarette, however, kretek smoke exposure was associated with a pronounced attenuation of pulmonary inflammation and less severe histopathological changes in the respiratory tract. Neutrophilic inflammation was also significantly lower (>70%). These results are consistent with the observations made on smoke chemistry and in vitro toxicology. They do not support any increased toxicity of the smoke of kretek cigarettes compared to conventional American-blended cigarettes. PMID:25455226

  18. Toxicological assessment of kretek cigarettes Part 3: kretek and American-blended cigarettes, inhalation toxicity.

    PubMed

    Piadé, J-J; Roemer, E; Dempsey, R; Weiler, H; Meurrens, K; Vanscheeuwijck, P; Schorp, M K

    2014-12-01

    A typical Indonesian kretek cigarette brand and an experimental kretek reference cigarette were compared to the reference cigarette 2R4F in two 90-day inhalation studies. Male and female rats were exposed nose-only to mainstream smoke for 6 hours daily, for 90 consecutive days. Biological endpoints were assessed according to OECD guideline 413, with special emphasis on respiratory tract histopathology and on lung inflammation (broncho-alveolar lavage fluid levels of neutrophils, macrophages and lymphocytes). Histopathological alterations included: in the nose, hyperplasia and squamous metaplasia of the respiratory epithelium and squamous metaplasia and atrophy of the olfactory epithelium; in the larynx, epithelial squamous metaplasia and hyperplasia; in the lungs, accumulation of macrophages in alveoli and goblet cell hyperplasia in bronchial epithelium. The findings were qualitatively consistent with observations from previous similar studies on conventional cigarettes. Compared to 2R4F cigarette, however, kretek smoke exposure was associated with a pronounced attenuation of pulmonary inflammation and less severe histopathological changes in the respiratory tract. Neutrophilic inflammation was also significantly lower (>70%). These results are consistent with the observations made on smoke chemistry and in vitro toxicology. They do not support any increased toxicity of the smoke of kretek cigarettes compared to conventional American-blended cigarettes.

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

    PubMed Central

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

    2015-01-01

    Objective: We reported association of haplotypes formed by IL-1b (IL1B)-511C/T (rs16944) and a variable number of tandem repeats (rs2234663) in intron 3 of IL-1 receptor antagonist (IL1RN) with rate of lung function decline in smoking-induced COPD. The aim of current study was to further investigate this association. Methods: We genotyped an additional 19 polymorphisms in IL1 cluster (including IL1A, IL1B and IL1RN) in non-Hispanic whites who had the fastest (n = 268) and the slowest (n = 292) decline of FEV1% predicted in the same study. We also analyzed the association of all 21 polymorphisms with serum CRP levels. Results: None of 21 polymorphisms showed significant association with rate of decline of lung function or CRP levels after adjusting for multiple comparisons. Before adjusting for multiple comparisons, only IL1RN_19327 (rs315949) showed significant association with lung function decline (P = 0.03, additive model). The frequencies of genotypes containing the IL1RN_19327A allele were 71.9% and 62.2%, respectively in the fast and slow decline groups (P = 0.02, odds ratio = 1.6, 95% confidence interval = 1.1-2.3); the IL1B_5200 (rs1143633) and rs2234663 in IL1RN were associated with serum CRP levels (P=0.04 and 0.03, respectively). Conclusions: No single marker was significantly associated with either rate of lung function decline or serum CRP levels. PMID:26722511

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

    PubMed

    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

  1. Association between Peer Cigarette Smoking and Electronic Cigarette Smoking among Adolescent Nonsmokers: A National Representative Survey

    PubMed Central

    Hwang, Jun Hyun; Park, Soon-Woo

    2016-01-01

    We assessed the association between electronic cigarette (e-cigarette) use and peer cigarette smoking, a major risk factor for the initiation of cigarette smoking in adolescents. Data from the 2013 Korea Youth Risk Behavior Web-based Survey of 65,753 nonsmokers aged 13–18 years were analyzed using multiple logistic regression. A total of 3.8% of the Korean adolescents were ‘ever e-cigarette’ users and 1.2% were current users. Adjusted odds ratios (ORs) for current and ever e-cigarette use compared to those whose closest friends were non-smokers ranged from 2.05 (95% confidence interval [CI], 1.82–2.30) to 5.50 (95% CI, 4.77–6.34), and from 2.23 (95% CI, 1.77–2.81) to 7.82 (95% CI, 5.97–10.25) for those who had ‘some’ close friends to ‘most/all’ friends who smoked, respectively. The slopes of the adjusted ORs for e-cigarette use in ‘never smokers’ were more than twice as steep as those in ‘former smokers’, showing a significant interaction effect between the proportion of smoking closest friends and cigarette smoking status (never or former smokers) (p<0.001 for interaction). Peer cigarette smoking had a significant association with e-cigarette use in adolescent nonsmokers, and this association was greater on never smokers than former smokers. PMID:27695093

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

    PubMed

    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.

  3. Cigarette smoking and invasive cervical cancer

    SciTech Connect

    Brinton, L.A.; Schairer, C.; Haenszel, W.; Stolley, P.; Lehman, H.F.; Levine, R.; Savitz, D.A.

    1986-06-20

    A case-control study of 480 patients with invasive cervical cancer and 797 population controls, conducted in five geographic areas in the United States, included an evaluation of the relationship of several cigarette smoking variables to cervical cancer risk. Although smoking was correlated with both age at first intercourse and number of sexual partners, a significant smoking-related risk persisted for squamous cell carcinoma after adjustment for these factors (relative risk, 1.5). Twofold excess risks were seen for those smoking 40 or more cigarettes per day and those smoking for 40 or more years. Increased risks, however, were observed only among recent and continuous smokers. In contrast to squamous cell cancer, no relationship was observed between smoking and risk of adenocarcinoma or adenosquamous carcinoma. These results suggest a causal relationship between cigarette smoking and invasive squamous cell cervical cancer, perhaps through a late-stage or promotional event, although the mechanisms of action require further elucidation.

  4. In search of the less hazardous cigarette.

    PubMed

    Givel, Michael

    2011-01-01

    Since the 1950s, despite considerable and long-term tobacco industry and government efforts, attempts to develop a less risky cigarette that reduces harmful ingredients, generally or specifically, have failed. Moreover, even under ideal conditions with adequate scientific testing, the efficacy of purportedly reducing the severe health effects cannot be scientifically verified for up to 20 years after introduction of a product on the market. A key and central provision in the 2009 U.S. Food and Drug Administration (FDA) legislation is to reduce the risk or harm of cigarettes. Because creating a less risky cigarette is not currently possible, this renders the efficacy of the 2009 FDA legislation highly uncertain, with a large risk that the proposed program may not reduce harm.

  5. Effects of cigarette smoking on erectile dysfunction.

    PubMed

    Kovac, J R; Labbate, C; Ramasamy, R; Tang, D; Lipshultz, L I

    2015-12-01

    Cigarette smoking is a leading cause of preventable morbidity and mortality in the United States. Although public policies have resulted in a decreased number of new smokers, smoking rates remain stubbornly high in certain demographics with 20% of all American middle-aged men smoking. In addition to the well-established harmful effects of smoking (i.e. coronary artery disease and lung cancer), the past three decades have led to a compendium of evidence being compiled into the development of a relationship between cigarette smoking and erectile dysfunction. The main physiologic mechanism that appears to be affected includes the nitric oxide signal transduction pathway. This review details the recent literature linking cigarette smoking to erectile dysfunction, epidemiological associations, dose dependency and the effects of smoking cessation on improving erectile quality.

  6. Adolescent cigarette smoking and health risk behavior.

    PubMed

    Busen, N H; Modeland, V; Kouzekanani, K

    2001-06-01

    During the past 30 years, tobacco use among adolescents has substantially increased, resulting in major health problems associated with tobacco consumption. The purpose of this study was to identify adolescent smoking behaviors and to determine the relationship among smoking, specific demographic variables, and health risk behaviors. The sample consisted of 93 self-selecting adolescents. An ex post facto design was used for this study and data were analyzed by using nonparametric statistics. Findings included a statistically significant relationship between lifetime cigarette use and ethnicity. Statistically significant relationships were also found among current cigarette use and ethnicity, alcohol use, marijuana use, suicidal thoughts, and age at first sexual intercourse. Nurses and other providers must recognize that cigarette smoking may indicate other risk behaviors common among adolescents.

  7. Are increases in cigarette taxation regressive?

    PubMed

    Borren, P; Sutton, M

    1992-12-01

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

  8. Triple Quad-ICP-MS Measurement of Toxic Metals in Mainstream Cigarette Smoke from Spectrum Research Cigarettes.

    PubMed

    Pappas, R Steven; Gray, Naudia; Gonzalez-Jimenez, Nathalie; Fresquez, Mark; Watson, Clifford H

    2016-01-01

    We previously reported toxic metal concentrations in the mainstream smoke from 50 varieties of commercial cigarettes available in the USA using quadrupole inductively coupled plasma-mass spectrometry (ICP-MS). However, efforts to continue producing high quality data on select mainstream cigarette smoke constituents demand continued improvements in instrumentation and methodology and application of the methodology to cigarettes that differ in design or construction. Here we report a new application of 'triple quad'-ICP-MS instrumentation to analyze seven toxic metals in mainstream cigarette smoke from the Spectrum variable nicotine research cigarettes. The Spectrum cigarettes are available for research purposes in different configurations of low or conventional levels of nicotine, mentholated or nonmentholated, and tar delivery ranges described as 'low tar' or 'high tar'. Detailed characterizations of specific harmful or potentially harmful constituents delivered by these research cigarettes will help inform researchers using these cigarettes in exposure studies, cessation studies and studies related to nicotine addiction or compensation.

  9. Prenatal and Early Postnatal Exposure to Cigarette Smoke Decreases BDNF/TrkB Signaling and Increases Abnormal Behaviors Later in Life

    PubMed Central

    Xiao, Lan; Kish, Vincent L.; Benders, Katherine M.

    2016-01-01

    Background: Cigarette smoke exposure during prenatal and early postnatal periods increases the incidence of a variety of abnormal behaviors later in life. The purpose of this study was to identify the possible critical period of susceptibility to cigarette smoke exposure and evaluate the possibe effects of cigarette smoke during early life on brain-derived neurotrophic factor/neurotrophic tyrosine kinase receptor B signaling in the brain. Methods: Three different age of imprinting control region mice were exposed to cigarette smoke or filtered air for 10 consecutive days beginning on either gestational day 7 by maternal exposure, or postnatal days 2 or 21 by direct inhalation. A series of behavioral profiles and neurotrophins in brain were measured 24 hours after mice received acute restraint stress for 1 hour on postnatal day 59. Results: Cigarette smoke exposure in gestational day 7 and postnatal day 2 produced depression-like behaviors as evidenced by significantly increased immobility in both tail suspension and forced-swim test. Increased entry latencies, but not ambulation in the open field test, were also observed in the gestational day 7 and postnatal day 2 cigarette smoke exposure groups. Genetic analysis showed that gestational day 7 cigarette smoke exposure significantly altered mRNA level of brain-derived neurotrophic factor/tyrosine kinase receptor B in the hippocampus. However, behavioral profiles and brain-derived neurotrophic factor/tyrosine kinase receptor B signaling were not significantly changed in PND21 cigarette smoke exposure group compared with FA group. Conclusions: These results suggest that a critical period of susceptibility to cigarette smoke exposure exists in the prenatal and early postnatal period, which results a downregulation in brain-derived neurotrophic factor/tyrosine kinase receptor B signaling in the hippocampus and enhances depression-like behaviors later in life. PMID:26503133

  10. Flavour chemicals in electronic cigarette fluids

    PubMed Central

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

    2016-01-01

    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 flavours (eg, bubble gum and cotton candy), also analysed were convenience samples of e-cigarette fluids in refill bottles from local ‘vape’ shops and online retailers. Results In many liquids, total flavour chemicals were found to be in the ∼1–4% range (10–40 mg/mL); labelled levels of nicotine were in the range of 0.6–2.4% (6 to 24 mg/mL). A significant number of the flavour chemicals were aldehydes, a compound class recognised as ‘primary irritants’ of mucosal tissue of the respiratory tract. Many of the products contained the same flavour chemicals: vanillin and/or ethyl vanillin was found in 17 of the liquids as one of the top three flavour chemicals, and/or at ≥0.5 mg/mL. Conclusions The concentrations of some flavour chemicals in e-cigarette fluids are sufficiently high for inhalation exposure by vaping to be of toxicological concern. Regulatory limits should be contemplated for levels of some of the more worrisome chemicals as well as for total flavour chemical levels. Ingredient labeling should also be required. PMID:25877377

  11. 16 CFR 1210.3 - Requirements for cigarette lighters.

    Code of Federal Regulations, 2012 CFR

    2012-01-01

    ... 16 Commercial Practices 2 2012-01-01 2012-01-01 false Requirements for cigarette lighters. 1210.3... REGULATIONS SAFETY STANDARD FOR CIGARETTE LIGHTERS Requirements for Child Resistance § 1210.3 Requirements for cigarette lighters. (a) A lighter subject to this part 1210 shall be resistant to successful operation by...

  12. 27 CFR 40.24 - Classification of cigarettes.

    Code of Federal Regulations, 2010 CFR

    2010-04-01

    ... cigarettes. 40.24 Section 40.24 Alcohol, Tobacco Products and Firearms ALCOHOL AND TOBACCO TAX AND TRADE BUREAU, DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes § 40.24 Classification of cigarettes. For tax purposes,...

  13. 16 CFR 1210.3 - Requirements for cigarette lighters.

    Code of Federal Regulations, 2011 CFR

    2011-01-01

    ... 16 Commercial Practices 2 2011-01-01 2011-01-01 false Requirements for cigarette lighters. 1210.3... REGULATIONS SAFETY STANDARD FOR CIGARETTE LIGHTERS Requirements for Child Resistance § 1210.3 Requirements for cigarette lighters. (a) A lighter subject to this part 1210 shall be resistant to successful operation by...

  14. 16 CFR 1210.3 - Requirements for cigarette lighters.

    Code of Federal Regulations, 2013 CFR

    2013-01-01

    ... 16 Commercial Practices 2 2013-01-01 2013-01-01 false Requirements for cigarette lighters. 1210.3... REGULATIONS SAFETY STANDARD FOR CIGARETTE LIGHTERS Requirements for Child Resistance § 1210.3 Requirements for cigarette lighters. (a) A lighter subject to this part 1210 shall be resistant to successful operation by...

  15. 27 CFR 40.24 - Classification of cigarettes.

    Code of Federal Regulations, 2012 CFR

    2012-04-01

    ... cigarettes. 40.24 Section 40.24 Alcohol, Tobacco Products and Firearms ALCOHOL AND TOBACCO TAX AND TRADE BUREAU, DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes § 40.24 Classification of cigarettes. For tax purposes,...

  16. 27 CFR 40.24 - Classification of cigarettes.

    Code of Federal Regulations, 2011 CFR

    2011-04-01

    ... cigarettes. 40.24 Section 40.24 Alcohol, Tobacco Products and Firearms ALCOHOL AND TOBACCO TAX AND TRADE BUREAU, DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes § 40.24 Classification of cigarettes. For tax purposes,...

  17. 27 CFR 40.24 - Classification of cigarettes.

    Code of Federal Regulations, 2014 CFR

    2014-04-01

    ... cigarettes. 40.24 Section 40.24 Alcohol, Tobacco Products and Firearms ALCOHOL AND TOBACCO TAX AND TRADE BUREAU, DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes § 40.24 Classification of cigarettes. For tax purposes,...

  18. 27 CFR 40.24 - Classification of cigarettes.

    Code of Federal Regulations, 2013 CFR

    2013-04-01

    ... cigarettes. 40.24 Section 40.24 Alcohol, Tobacco Products and Firearms ALCOHOL AND TOBACCO TAX AND TRADE BUREAU, DEPARTMENT OF THE TREASURY (CONTINUED) TOBACCO MANUFACTURE OF TOBACCO PRODUCTS, CIGARETTE PAPERS AND TUBES, AND PROCESSED TOBACCO Taxes § 40.24 Classification of cigarettes. For tax purposes,...

  19. 16 CFR 1210.3 - Requirements for cigarette lighters.

    Code of Federal Regulations, 2014 CFR

    2014-01-01

    ... 16 Commercial Practices 2 2014-01-01 2014-01-01 false Requirements for cigarette lighters. 1210.3... REGULATIONS SAFETY STANDARD FOR CIGARETTE LIGHTERS Requirements for Child Resistance § 1210.3 Requirements for cigarette lighters. (a) A lighter subject to this part 1210 shall be resistant to successful operation by...

  20. Cigarette staining and cleaning of a maxillofacial silicone

    SciTech Connect

    Yu, R.; Koran, A.; Raptis, C.N.; Craig, R.G.

    1983-07-01

    In this study, a maxillofacial silicone elastomer was stained with cigarette smoke. The stain was then removed by solvent extraction using 1,1,1-trichloroethane. The cigarette smoke produced large color changes in the elastomer as measured from spectrophotometric reflectance curves. The solvent was totally effective in removing the cigarette stain without changing the color of the silicone base.