WorldWideScience

Sample records for cigarette smoke-induced lung

  1. Cellular and molecular mechanisms of cigarette smoke-induced lung damage and prevention by vitamin C

    Roy Siddhartha

    2008-11-01

    Full Text Available Abstract Background Cigarette smoke-induced cellular and molecular mechanisms of lung injury are not clear. Cigarette smoke is a complex mixture containing long-lived radicals, including p-benzosemiquinone that causes oxidative damage. Earlier we had reported that oxidative protein damage is an initial event in smoke-induced lung injury. Considering that p-benzosemiquinone may be a causative factor of lung injury, we have isolated p-benzosemiquinone and compared its pathophysiological effects with cigarette smoke. Since vitamin C is a strong antioxidant, we have also determined the modulatory effect of vitamin C for preventing the pathophysiological events. Methods Vitamin C-restricted guinea pigs were exposed to cigarette smoke (5 cigarettes/day; 2 puffs/cigarette for 21 days with and without supplementation of 15 mg vitamin C/guinea pig/day. Oxidative damage, apoptosis and lung injury were assessed in vitro, ex vivo in A549 cells as well as in vivo in guinea pigs. Inflammation was measured by neutrophilia in BALF. p-Benzosemiquinone was isolated from freshly prepared aqueous extract of cigarette smoke and characterized by various physico-chemical methods, including mass, NMR and ESR spectroscopy. p-Benzosemiquinone-induced lung damage was examined by intratracheal instillation in guinea pigs. Lung damage was measured by increased air spaces, as evidenced by histology and morphometric analysis. Oxidative protein damage, MMPs, VEGF and VEGFR2 were measured by western blot analysis, and formation of Michael adducts using MALDI-TOF-MS. Apoptosis was evidenced by TUNEL assay, activation of caspase 3, degradation of PARP and increased Bax/Bcl-2 ratio using immunoblot analysis and confocal microscopy. Results Exposure of guinea pigs to cigarette smoke resulted in progressive protein damage, inflammation, apoptosis and lung injury up to 21 days of the experimental period. Administration of 15 mg of vitamin C/guinea pig/day prevented all these

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

    Kelsen, Steven G; Duan, Xunbao; Ji, Rong; Perez, Oscar; Liu, Chunli; Merali, Salim

    2008-05-01

    Cigarette smoking, which exposes the lung to high concentrations of reactive oxidant species (ROS) is the major risk factor for chronic obstructive pulmonary disease (COPD). Recent studies indicate that ROS interfere with protein folding in the endoplasmic reticulum and elicit a compensatory response termed the "unfolded protein response" (UPR). The importance of the UPR lies in its ability to alter expression of a variety of genes involved in antioxidant defense, inflammation, energy metabolism, protein synthesis, apoptosis, and cell cycle regulation. The present study used comparative proteomic technology to test the hypothesis that chronic cigarette smoking induces a UPR in the human lung. Studies were performed on lung tissue samples obtained from three groups of human subjects: nonsmokers, chronic cigarette smokers, and ex-smokers. Proteomes of lung samples from chronic cigarette smokers demonstrated 26 differentially expressed proteins (20 were up-regulated, 5 were down-regulated, and 1 was detected only in the smoking group) compared with nonsmokers. Several UPR proteins were up-regulated in smokers compared with nonsmokers and ex-smokers, including the chaperones, glucose-regulated protein 78 (GRP78) and calreticulin; a foldase, protein disulfide isomerase (PDI); and enzymes involved in antioxidant defense. In cultured human airway epithelial cells, GRP78 and the UPR-regulated basic leucine zipper, transcription factors, ATF4 and Nrf2, which enhance expression of important anti-oxidant genes, increased rapidly (< 24 h) with cigarette smoke extract. These data indicate that cigarette smoke induces a UPR response in the human lung that is rapid in onset, concentration dependent, and at least partially reversible with smoking cessation. We speculate that activation of a UPR by cigarette smoke may protect the lung from oxidant injury and the development of COPD.

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

    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

  4. Prevention of cigarette smoke induced lung cancer by low let ionizing radiation

    Sanders, Charles L. [Korea Advanced Institute of Science and Technology, Daejeon (Korea, Republic of)

    2008-12-15

    Lung cancer is the most prevalent global cancer, {approx}90% of which is caused by cigarette smoking. The LNT hypothesis has been inappropriately applied to estimate lung cancer risk due to ionizing radiation. A threshold of {approx}1 Gy for lung cancer has been observed in never smokers. Lung cancer risk among nuclear workers, radiologists and diagnostically exposed patients was typically reduced by {approx}40% following exposure to <100 mSv low LET radiation. The consistency and magnitude of reduced lung cancer in nuclear workers and occurrence of reduced lung cancer in exposed non-worker populations could not be explained by the HWE. Ecologic studies of indoor radon showed highly significant reductions in lung cancer risk. A similar reduction in lung cancer was seen in a recent well designed case-control study of indoor radon, indicating that exposure to radon at the EPA action level is associated with a decrease of {approx}60% in lung cancer. A cumulative whole-body dose of {approx}1 Gy gamma rays is associated with a marked decrease in smoking-induced lung cancer in plutonium workers. Low dose, low LET radiation appears to increase apoptosis mediated removal of {alpha}-particle and cigarette smoke transformed pulmonary cells before they can develop into lung cancer.

  5. Prevention of cigarette smoke induced lung cancer by low let ionizing radiation

    Sanders, Charles L.

    2008-01-01

    Lung cancer is the most prevalent global cancer, ∼90% of which is caused by cigarette smoking. The LNT hypothesis has been inappropriately applied to estimate lung cancer risk due to ionizing radiation. A threshold of ∼1 Gy for lung cancer has been observed in never smokers. Lung cancer risk among nuclear workers, radiologists and diagnostically exposed patients was typically reduced by ∼40% following exposure to <100 mSv low LET radiation. The consistency and magnitude of reduced lung cancer in nuclear workers and occurrence of reduced lung cancer in exposed non-worker populations could not be explained by the HWE. Ecologic studies of indoor radon showed highly significant reductions in lung cancer risk. A similar reduction in lung cancer was seen in a recent well designed case-control study of indoor radon, indicating that exposure to radon at the EPA action level is associated with a decrease of ∼60% in lung cancer. A cumulative whole-body dose of ∼1 Gy gamma rays is associated with a marked decrease in smoking-induced lung cancer in plutonium workers. Low dose, low LET radiation appears to increase apoptosis mediated removal of α-particle and cigarette smoke transformed pulmonary cells before they can develop into lung cancer

  6. Exercise training attenuated chronic cigarette smoking-induced up-regulation of FIZZ1/RELMα in lung of rats.

    Ma, Wan-li; Cai, Peng-cheng; Xiong, Xian-zhi; Ye, Hong

    2013-02-01

    FIZZ/RELM is a new gene family named "found in inflammatory zone" (FIZZ) or "resistin-like molecule" (RELM). FIZZ1/RELMα is specifically expressed in lung tissue and associated with pulmonary inflammation. Chronic cigarette smoking up-regulates FIZZ1/RELMα expression in rat lung tissues, the mechanism of which is related to cigarette smoking-induced airway hyperresponsiveness. To investigate the effect of exercise training on chronic cigarette smoking-induced airway hyperresponsiveness and up-regulation of FIZZ1/RELMα, rat chronic cigarette smoking model was established. The rats were treated with regular exercise training and their airway responsiveness was measured. Hematoxylin and eosin (HE) staining, immunohistochemistry and in situ hybridization of lung tissues were performed to detect the expression of FIZZ1/RELMα. Results revealed that proper exercise training decreased airway hyperresponsiveness and pulmonary inflammation in rat chronic cigarette smoking model. Cigarette smoking increased the mRNA and protein levels of FIZZ1/RELMα, which were reversed by the proper exercise. It is concluded that proper exercise training prevents up-regulation of FIZZ1/RELMα induced by cigarette smoking, which may be involved in the mechanism of proper exercise training modulating airway hyperresponsiveness.

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

    Gupta, R.C.; Sopori, M.L.; Gairola, C.G.

    1989-01-01

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

  8. Protocols to Evaluate Cigarette Smoke-Induced Lung Inflammation and Pathology in Mice.

    Vlahos, Ross; Bozinovski, Steven

    2018-01-01

    Cigarette smoking is a major cause of chronic obstructive pulmonary disease (COPD). Inhalation of cigarette smoke causes inflammation of the airways, airway wall remodelling, mucus hypersecretion and progressive airflow limitation. Much of the disease burden and health care utilisation in COPD is associated with the management of its comorbidities and infectious (viral and bacterial) exacerbations (AECOPD). Comorbidities, in particular skeletal muscle wasting, cardiovascular disease and lung cancer markedly impact on disease morbidity, progression and mortality. The mechanisms and mediators underlying COPD and its comorbidities are poorly understood and current COPD therapy is relatively ineffective. Many researchers have used animal modelling systems to explore the mechanisms underlying COPD, AECOPD and comorbidities of COPD with the goal of identifying novel therapeutic targets. Here we describe a mouse model that we have developed to define the cellular, molecular and pathological consequences of cigarette smoke exposure and the development of comorbidities of COPD.

  9. Molecular Mechanisms of Cigarette Smoke-Induced Proliferation of Lung Cells and Prevention by Vitamin C

    Neekkan Dey

    2011-01-01

    Full Text Available Lung cancer is the leading cause of cancer dearth. Cigarette smoking is the strongest risk factor for developing lung cancer, which is conceivably initiated by proliferation. Here, we show that low concentration of aqueous extract of cigarette smoke (AECS causes excessive proliferation of human lung epithelial cells (A549 without any apoptotic cell death. The causative factor responsible for AECS-induced proliferation has been identified as p-benzoquinone (p-BQ. Coimmunoprecipitation and immunoblot experiments indicate that p-BQ binds with epidermal growth factor receptor (EGFR. However, in contrast to EGF, it causes aberrant phosphorylation of EGFR that lacks c-Cbl-mediated ubiquitination and degradation resulting in persistent activation of EGFR. This is followed by activation of Hras + Kras and the downstream survival and proliferative signaling molecules Akt and ERK1/2, as well as the nuclear transcription factors c-Myc and c-Fos. Vitamin C and/or antibody to p-BQ prevents AECS/p-BQ-induced proliferation of lung cells apparently by inactivating p-BQ and thereby preventing activation of EGFR and the downstream signaling molecules. The results suggest that vitamin C and/or antibody to p-BQ may provide a novel intervention for preventing initiation of lung cancer in smokers.

  10. Simvastatin mitigates functional and structural impairment of lung and right ventricle in a rat model of cigarette smoke-induced COPD.

    Wang, Yajie; Jiang, Xue; Zhang, Lihai; Wang, Lihong; Li, Zhu; Sun, Wuzhuang

    2014-01-01

    This study is conducted to investigate an effect of simvastatin on cigarette smoke-induced COPD. Rats were exposed to air (control) and cigarette smoke (smoking) in presence and absence of simvastatin. Heart and lung tissues were harvested for histopathologic and morphometric analysis. Body weight of rat, mean liner intercept (MLI), mean alveolar number (MAN), lung function test, mean pulmonary artery pressure (mPAP), right ventricular hypertrophy index (RVHI) and 5-HTT level in serum and BALF were examined in experimental rats, respectively. Application of simvastatin mitigated peribronchiolar inflammation and pulmonary bullae formed in the smoke-exposed lungs with weight gain as compared to the smoking rats (P reversal of lung function decline (all P reverses lung function decline and attenuates structural impairments of lung and right ventricle possibly through reducing 5-HTT content in the model of COPD.

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

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

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

  12. Caspase 3 activity in isolated fetal rat lung fibroblasts and rat periodontal ligament fibroblasts: cigarette smoke-induced alterations

    James Elliot Scott

    2016-03-01

    Full Text Available Background Cigarette smoking is the leading cause of preventable death in the world. It has been implicated in the pathogenesis of pulmonary, oral and systemic diseases. Smoking during pregnancy is clearly a risk factor for the developing fetus and may be a major cause of infant mortality. Moreover, the oral cavity is the first site of exposure to cigarette smoke and may be a possible source for the spread of toxins to other organs of the body. Fibroblasts in general are morphologically heterogeneous connective tissue cells with diverse functions. Apoptosis or programmed cell death is a crucial process during embryogenesis and for the maintenance of homeostasis throughout life. Deregulation of apoptosis has been implicated in abnormal lung development in the fetus and disease progression in adults. Caspases, are proteases which belong to the family of cysteine aspartic acid proteases and are the key components for the downstream amplification of intra-cellular apoptotic signals. Of the 14 caspases known, caspase-3 is the key executioner of apoptosis. Fetal rat lung fibroblasts but not PDL viability is reduced by exposure to CSE. In addition Caspase 3 activity is elevated after CSE exposure in fetal lung fibroblasts but not in PDLs. Expression of caspase 3 is induced in CSE exposed lung fibroblasts but not in PDLs. Caspase 3 was localized to the cytoplasm in both cell types.

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

    Yang Jin

    2008-08-01

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

  14. Beta-cryptoxanthin protection against cigarette smoke-induced inflammatory responses in the lung is due to the action of its own molecule

    Higher intake of the dietary xanthophyll, beta-cryptoxanthin (BCX), has been associated with a lower risk of lung cancer death in smokers. We have previously shown that BCX feeding was effective in reducing both cigarette smoke (CS)-induced lung inflammation in ferrets and carcinogen-induced lung tu...

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

    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. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  16. Casticin, an active compound isolated from Vitex Fructus, ameliorates the cigarette smoke-induced acute lung inflammatory response in a murine model.

    Lee, Hyeonhoon; Jung, Kyung-Hwa; Lee, Hangyul; Park, Soojin; Choi, Woosung; Bae, Hyunsu

    2015-10-01

    The aim of this study was to determine of the effect of casticin, as an anti-inflammatory agent, on an acute lung inflammation in vivo model established through exposure to cigarette smoke (CS). Casticin is a phytochemical from Vitex species such as Vitex rotundifolia and Vitex agnus-castus that was recently shown to exert an anti-inflammatory effect in vivo. To demonstrate the effects of casticin, C57BL/6 mice were whole-body exposed to mainstream CS or fresh air for two weeks and treated with 1, 2, and 10mg/kg casticin via an i.p. injection. Immune cell infiltrations and cytokine productions were assessed from bronchoalveolar lavage Fluid (BALF), and lung histological analysis was performed. Treatment with casticin was observed to significantly inhibit the numbers of total cells, neutrophils, macrophages, and lymphocytes and reduce the levels of proinflammatory cytokines and chemokines in the BALF. In addition, casticin significantly decreased the infiltration of peribronchial and perivascular inflammatory cells and the epithelium thickness. The results of this study indicate that casticin has significant effects on the lung inflammation induced by CS in a mouse model. According to these outcomes, casticin may have therapeutic potential in inflammatory lung diseases, such as chronic obstructive pulmonary disease (COPD). Copyright © 2015 Elsevier B.V. All rights reserved.

  17. Rac1 signaling regulates cigarette smoke-induced inflammation in the lung via the Erk1/2 MAPK and STAT3 pathways.

    Jiang, Jun-Xia; Zhang, Shui-Juan; Shen, Hui-Juan; Guan, Yan; Liu, Qi; Zhao, Wei; Jia, Yong-Liang; Shen, Jian; Yan, Xiao-Feng; Xie, Qiang-Min

    2017-07-01

    Cigarette smoke (CS) is a major risk factor for the development of chronic obstructive pulmonary disease (COPD). Our previous studies have indicated that Rac1 is involved in lipopolysaccharide-induced pulmonary injury and CS-mediated epithelial-mesenchymal transition. However, the contribution of Rac1 activity to CS-induced lung inflammation remains not fully clear. In this study, we investigated the regulation of Rac1 in CS-induced pulmonary inflammation. Mice or 16HBE cells were exposed to CS or cigarette smoke extract (CSE) to induce acute inflammation. The lungs of mice exposed to CS showed an increase in the release of interleukin-6 (IL-6) and keratinocyte-derived chemokine (KC), as well as an accumulation of inflammatory cells, indicating high Rac1 activity. The exposure of 16HBE cells to CSE resulted in elevated Rac1 levels, as well as increased release of IL-6 and interleukin-8 (IL-8). Selective inhibition of Rac1 ameliorated the release of IL-6 and KC as well as inflammation in the lungs of CS-exposed mice. Histological assessment showed that treatment with a Rac1 inhibitor, NSC23766, led to a decrease in CD68 and CD11b positive cells and the infiltration of neutrophils and macrophages into the alveolar spaces. Selective inhibition or knockdown of Rac1 decreased IL-6 and IL-8 release in 16HBE cells induced by CSE, which correlated with CSE-induced Rac1-regulated Erk1/2 mitogen-activated protein kinase (MAPK) and signal transducer and activator of transcription-3 (STAT3) signaling. Our data suggest an important role for Rac1 in the pathological alterations associated with CS-mediated inflammation. Rac1 may be a promising therapeutic target for the treatment of CS-induced pulmonary inflammation. Copyright © 2017 Elsevier B.V. All rights reserved.

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

    Zhi-Hua Chen

    2008-10-01

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

  19. Transcriptomic Analysis of Lung Tissue from Cigarette Smoke-Induced Emphysema Murine Models and Human Chronic Obstructive Pulmonary Disease Show Shared and Distinct Pathways.

    Yun, Jeong H; Morrow, Jarrett; Owen, Caroline A; Qiu, Weiliang; Glass, Kimberly; Lao, Taotao; Jiang, Zhiqiang; Perrella, Mark A; Silverman, Edwin K; Zhou, Xiaobo; Hersh, Craig P

    2017-07-01

    Although cigarette smoke (CS) is the primary risk factor for chronic obstructive pulmonary disease (COPD), the underlying molecular mechanisms for the significant variability in developing COPD in response to CS are incompletely understood. We performed lung gene expression profiling of two different wild-type murine strains (C57BL/6 and NZW/LacJ) and two genetic models with mutations in COPD genome-wide association study genes (HHIP and FAM13A) after 6 months of chronic CS exposure and compared the results to human COPD lung tissues. We identified gene expression patterns that correlate with severity of emphysema in murine and human lungs. Xenobiotic metabolism and nuclear erythroid 2-related factor 2-mediated oxidative stress response were commonly regulated molecular response patterns in C57BL/6, Hhip +/- , and Fam13a -/- murine strains exposed chronically to CS. The CS-resistant Fam13a -/- mouse and NZW/LacJ strain revealed gene expression response pattern differences. The Fam13a -/- strain diverged in gene expression compared with C57BL/6 control only after CS exposure. However, the NZW/LacJ strain had a unique baseline expression pattern, enriched for nuclear erythroid 2-related factor 2-mediated oxidative stress response and xenobiotic metabolism, and converged to a gene expression pattern similar to the more susceptible wild-type C57BL/6 after CS exposure. These results suggest that distinct molecular pathways may account for resistance to emphysema. Surprisingly, there were few genes commonly modulated in mice and humans. Our study suggests that gene expression responses to CS may be largely species and model dependent, yet shared pathways could provide biologically significant insights underlying individual susceptibility to CS.

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

    G. Vani

    2015-01-01

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

  1. Respiratory syncytial virus infections enhance cigarette smoke induced COPD in mice.

    Robert F Foronjy

    Full Text Available 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.

  2. Src mediates cigarette smoke-induced resistance to tyrosine kinase inhibitors in NSCLC cells.

    Filosto, Simone; Baston, David S; Chung, Samuel; Becker, Cathleen R; Goldkorn, Tzipora

    2013-08-01

    The EGF receptor (EGFR) is a proto-oncogene commonly dysregulated in several cancers including non-small cell lung carcinoma (NSCLC) and, thus, is targeted for treatment using tyrosine kinase inhibitors (TKI) such as erlotinib. However, despite the efficacy observed in patients with NSCLC harboring oncogenic variants of the EGFR, general ineffectiveness of TKIs in patients with NSCLC who are current and former smokers necessitates identification of novel mechanisms to overcome this phenomenon. Previously, we showed that NSCLC cells harboring either wild-type (WT) EGFR or oncogenic mutant (MT) L858R EGFR become resistant to the effects of TKIs when exposed to cigarette smoke, evidenced by their autophosphorylation and prolonged downstream signaling. Here, we present Src as a target mediating cigarette smoke-induced resistance to TKIs in both WT EGFR- and L858R MT EGFR-expressing NSCLC cells. First, we show that cigarette smoke exposure of A549 cells leads to time-dependent activation of Src, which then abnormally binds to the WT EGFR causing TKI resistance, contrasting previous observations of constitutive binding between inactive Src and TKI-sensitive L858R MT EGFR. Next, we show that Src inhibition restores TKI sensitivity in cigarette smoke-exposed NSCLC cells, preventing EGFR autophosphorylation in the presence of erlotinib. Furthermore, we show that overexpression of a dominant-negative Src (Y527F/K295R) restores TKI sensitivity to A549 exposed to cigarette smoke. Importantly, the TKI resistance that emerges even in cigarette smoke-exposed L858R EGFR-expressing NSCLC cells could be eliminated with Src inhibition. Together, these findings offer new rationale for using Src inhibitors for treating TKI-resistant NSCLC commonly observed in smokers.

  3. Cigarette Smoke-Induced Emphysema and Pulmonary Hypertension Can Be Prevented by Phosphodiesterase 4 and 5 Inhibition in Mice

    Pichl, Alexandra; Bednorz, Mariola; Ghofrani, Hossein Ardeschir; Schermuly, Ralph Theo; Seeger, Werner; Grimminger, Friedrich; Weissmann, Norbert

    2015-01-01

    Rationale Chronic obstructive pulmonary disease (COPD) is a widespread disease, with no curative therapies available. Recent findings suggest a key role of NO and sGC-cGMP signaling for the pathogenesis of the disease. Previous data suggest a downregulation/inactivation of the cGMP producing soluble guanylate cyclase, and sGC stimulation prevented cigarette smoke-induced emphysema and pulmonary hypertension (PH) in mice. We thus aimed to investigate if the inhibition of the cGMP degrading phosphodiesterase (PDE)5 has similar effects. Results were compared to the effects of a PDE 4 inhibitor (cAMP elevating) and a combination of both. Methods C57BL6/J mice were chronically exposed to cigarette smoke and in parallel either treated with Tadalafil (PDE5 inhibitor), Piclamilast (PDE4 inhibitor) or both. Functional measurements (lung compliance, hemodynamics) and structural investigations (alveolar and vascular morphometry) as well as the heart ratio were determined after 6 months of tobacco smoke exposure. In addition, the number of alveolar macrophages in the respective lungs was counted. Results Preventive treatment with Tadalafil, Piclamilast or a combination of both almost completely prevented the development of emphysema, the increase in lung compliance, tidal volume, structural remodeling of the lung vasculature, right ventricular systolic pressure, and right ventricular hypertrophy induced by cigarette smoke exposure. Single, but not combination treatment prevented or reduced smoke-induced increase in alveolar macrophages. Conclusion Cigarette smoke-induced emphysema and PH could be prevented by inhibition of the phosphodiesterases 4 and 5 in mice. PMID:26058042

  4. Immune-regulating effects of exercise on cigarette smoke-induced inflammation

    Madani A

    2018-04-01

    Full Text Available Ashkan Madani,1 Katharina Alack,2 Manuel Jonas Richter,3,4 Karsten Krüger1 1Department of Exercise and Health, Institute of Sports Science, Leibniz University Hannover, Germany; 2Department of Sports Medicine, University of Giessen, Germany; 3Department of Internal Medicine, Justus Liebig University Giessen, Universities of Giessen and Marburg Lung Center (UGMLC, Germany; 4German Center for Lung Research (DZL, Giessen, Germany Abstract: Long-term cigarette smoking (LTCS represents an important risk factor for cardiac infarction and stroke and the central risk factor for the development of a bronchial carcinoma, smoking-associated interstitial lung fibrosis, and chronic obstructive pulmonary disease. The pathophysiologic development of these diseases is suggested to be promoted by chronic and progressive inflammation. Cigarette smoking induces repetitive inflammatory insults followed by a chronic and progressive activation of the immune system. In the pulmonary system of cigarette smokers, oxidative stress, cellular damage, and a chronic activation of pattern recognition receptors are described which are followed by the translocation of the NF-kB, the release of pro-inflammatory cytokines, chemokines, matrix metalloproteases, and damage-associated molecular patterns. In parallel, smoke pollutants cross directly through the alveolus–capillary interface and spread through the systemic bloodstream targeting different organs. Consequently, LTCS induces a systemic low-grade inflammation and increased oxidative stress in the vascular system. In blood, these processes promote an increased coagulation and endothelial dysfunction. In muscle tissue, inflammatory processes activate catabolic signaling pathways followed by muscle wasting and sarcopenia. In brain, several characteristics of neuroinflammation were described. Regular exercise training has been shown to be an effective nonpharmacological treatment strategy in smoke-induced pulmonary diseases

  5. Immune-regulating effects of exercise on cigarette smoke-induced inflammation

    Madani, Ashkan; Alack, Katharina; Richter, Manuel Jonas; Krüger, Karsten

    2018-01-01

    Long-term cigarette smoking (LTCS) represents an important risk factor for cardiac infarction and stroke and the central risk factor for the development of a bronchial carcinoma, smoking-associated interstitial lung fibrosis, and chronic obstructive pulmonary disease. The pathophysiologic development of these diseases is suggested to be promoted by chronic and progressive inflammation. Cigarette smoking induces repetitive inflammatory insults followed by a chronic and progressive activation of the immune system. In the pulmonary system of cigarette smokers, oxidative stress, cellular damage, and a chronic activation of pattern recognition receptors are described which are followed by the translocation of the NF-kB, the release of pro-inflammatory cytokines, chemokines, matrix metalloproteases, and damage-associated molecular patterns. In parallel, smoke pollutants cross directly through the alveolus–capillary interface and spread through the systemic bloodstream targeting different organs. Consequently, LTCS induces a systemic low-grade inflammation and increased oxidative stress in the vascular system. In blood, these processes promote an increased coagulation and endothelial dysfunction. In muscle tissue, inflammatory processes activate catabolic signaling pathways followed by muscle wasting and sarcopenia. In brain, several characteristics of neuroinflammation were described. Regular exercise training has been shown to be an effective nonpharmacological treatment strategy in smoke-induced pulmonary diseases. It is well established that exercise training exerts immune-regulating effects by activating anti-inflammatory signaling pathways. In this regard, the release of myokines from contracting skeletal muscle, the elevations of cortisol and adrenalin, the reduced expression of Toll-like receptors, and the increased mobilization of immune-regulating leukocyte subtypes might be of vital importance. Exercise training also increases the local and systemic

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

    Eijl, Teunis Jan Ahasuerus van

    2006-01-01

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

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

    Toorn, Marco van der

    2009-01-01

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

  8. Cigarette prices, cigarette expenditure and smoking-induced deprivation: findings from the International Tobacco Control Mexico survey.

    Siahpush, Mohammad; Thrasher, James F; Yong, Hua H; Cummings, K Michael; Fong, Geoffrey T; de Miera, Belén Saenz; Borland, Ron

    2013-07-01

    Mexico implemented annual tax increases between 2009 and 2011. We examined among current smokers the association of price paid per cigarette and daily cigarette expenditure with smoking-induced deprivation (SID) and whether the association of price or expenditure with SID varies by income. We used data (n=2410) from three waves of the International Tobacco Control Mexico survey (ie, 2008, 2010, 2011) and employed logistic regression to estimate the association of price paid per cigarette and daily cigarette expenditure with the probability of SID ('In the last 6 months, have you spent money on cigarettes that you knew would be better spent on household essentials like food?'). Price paid per cigarette increased from Mex$1.24 in 2008, to Mex$1.36 in 2010, to Mex$1.64 in 2011. Daily cigarette expenditure increased from Mex$6.9, to Mex$7.6 and to Mex$8.4 in the 3 years. There was no evidence of an association between price and SID. However, higher expenditure was associated with a higher probability of SID. There was no evidence that the association of price or expenditure with SID varied by income. Tax increases in Mexico have resulted in smokers paying more and spending more for their cigarettes. Those with higher cigarette expenditure experience more SID, with no evidence that poorer smokers are more affected.

  9. Surfactant Protein D is a candidate biomarker for subclinical tobacco smoke-induced lung damage

    Lock Johansson, Sofie; Tan, Qihua; Holst, Rene

    2014-01-01

    Variation in Surfactant Protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage. The associat......Variation in Surfactant Protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage...... or haplotypes, and expiratory lung function were assessed using twin study methodology and mixed-effects models. Significant inverse associations were evident between sSP-D and the forced expiratory volume in 1 second and forced vital capacity in the presence of current tobacco smoking but not in non...... with lung function measures in interaction with tobacco smoking. The obtained data suggest sSP-D as a candidate biomarker in risk assessments for subclinical tobacco smoke-induced lung damage. The data and derived conclusion warrant confirmation in a longitudinal population following chronic obstructive...

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

    Sun J

    2017-02-01

    /D: 0.160±0.034, P<0.01. In contrast, mean alveolar number was significantly decreased in the CSE group than that in the control group (13.5±2.0 of CSE vs 21.5±2.0 N/µm2 of control, P>0.01. Simvastatin slightly but not significantly prevented alteration of MLI, BWT/D, and mean alveolar number (MLI: 33.4±1.4 µm; BWT/D: 0.220±0.052; mean alveolar number: 15.5±2.5 N/µm2, P>0.05. Total white blood cell was significantly increased in the bronchoalveolar lavage fluid of smoking group (3.3±2.5×109 cells/L vs 1.1±1.3×109 cells/L of control, P<0.01, and it was significantly reduced by simvastatin (2.3±2.1×109 cells/L, P<0.01. CSE resulted in significantly increased accumulation of neutrophils and macrophages (neutrophils: 14.5%±1.3% of CSE group vs 9.1%±1.5% of control; macrophage: 91%±3% of CSE group vs 87%±2% of control, P<0.05, and simvastatin significantly reduced neutrophils (12.9%±2.0%, P<0.05 in the bronchoalveolar lavage fluid, but had no effect on macrophage (89%±1.6%, P>0.05. In response to CSE, MMP-8, MMP-9, and MMP-12 mRNA were upregulated more than sevenfold, while TIMP-1 and TIMP-4 increased two- to fivefold. Simvastatin significantly blocked upregulation of MMP-8 and -9 (P<0.01, but had no effect on MMP-12, TIMP-1 and TIMP-4 mRNA (P>0.05. In addition, simvastatin significantly blocked cigarette smoke-induced MMP-8 and -9 protein synthesis, while it had no significant effect on TIMP-1 and -4 protein synthesis even in the presence of cigarette smoke.Conclusion: CSE resulted in imbalance of MMPs and TIMPs, and by which mechanism, cigarette smoke may lead to insufficient lung tissue repair. Simvastatin partially blocked airway inflammation and MMP production and, thus, statins may modulate composition of the lung extracellular matrix. Keywords: tissue injury, tissue repair, smoking

  11. Cigarette Smoke-Induced Cell Death Causes Persistent Olfactory Dysfunction in Aged Mice

    Rumi Ueha

    2018-06-01

    Full Text Available Introduction: Exposure to cigarette smoke is a cause of olfactory dysfunction. We previously reported that in young mice, cigarette smoke damaged olfactory progenitors and decreased mature olfactory receptor neurons (ORNs, then, mature ORNs gradually recovered after smoking cessation. However, in aged populations, the target cells in ORNs by cigarette smoke, the underlying molecular mechanisms by which cigarette smoke impairs the regenerative ORNs, and the degree of ORN regeneration after smoking cessation remain unclear.Objectives: To explore the effects of cigarette smoke on the ORN cell system using an aged mouse model of smoking, and to investigate the extent to which smoke-induced damage to ORNs recovers following cessation of exposure to cigarette smoke in aged mice.Methods: We intranasally administered a cigarette smoke solution (CSS to 16-month-old male mice over 24 days, then examined ORN existence, cell survival, changes of inflammatory cytokines in the olfactory epithelium (OE, and olfaction using histological analyses, gene analyses and olfactory habituation/dishabituation tests.Results: CSS administration reduced the number of mature ORNs in the OE and induced olfactory dysfunction. These changes coincided with an increase in the number of apoptotic cells and Tumor necrosis factor (TNF expression and a decrease in Il6 expression. Notably, the reduction in mature ORNs did not recover even on day 28 after cessation of treatment with CSS, resulting in persistent olfactory dysfunction.Conclusion: In aged mice, by increasing ORN death, CSS exposure could eventually overwhelm the regenerative capacity of the OE, resulting in continued reduction in the number of mature ORNs and olfactory dysfunction.

  12. Propolis reversed cigarette smoke-induced emphysema through macrophage alternative activation independent of Nrf2

    Barroso, Marina Valente; Cattani-Cavalieri, Isabella; de Brito-Gitirana, Lycia; Fautrel, Alain; Lagente, Vincent; Schmidt, Martina; Porto, Luís Cristóvão; Romana-Souza, Bruna; Valença, Samuel Santos; Lanzetti, Manuella

    2017-01-01

    Chronic obstructive pulmonary disease (COPD) is an incurable and progressive disease. Emphysema is the principal manifestation of COPD, and the main cause of this condition is cigarette smoke (CS). Natural products have shown antioxidant and anti-inflammatory properties that can prevent acute lung

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

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

    2016-01-01

    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. 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. 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. 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.

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

    Jean Pierre Schatzmann Peron

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

  15. Modeling the influence of vitamin D deficiency on cigarette smoke-induced emphysema.

    Mardi A. Crane-Godreau

    2013-06-01

    Full Text Available Chronic obstructive pulmonary disease (COPD is a major cause of morbidity and mortality worldwide. While the primary risk factor for COPD is cigarette smoke exposure, vitamin D deficiency has been epidemiologically implicated as a factor in the progressive development of COPD-associated emphysema. Because of difficulties inherent to studies involving multiple risk factors in the progression of COPD in humans, we developed a murine model in which to study the separate and combined effects of vitamin D deficiency and cigarette smoke exposure. During a 16 week period, mice were exposed to one of four conditions, control diet breathing room air (CD-NS, control diet with cigarette smoke exposure (CD-CSE, vitamin D deficient diet breathing room air (VDD-NS or vitamin D deficient diet with cigarette smoke exposure (VDD-CSE. At the end of the exposure period, the lungs were examined by a pathologist and separately by morphometric analysis. In parallel experiments, mice were anesthetized for pulmonary function testing followed by sacrifice and analysis. Emphysema (determined by an increase in alveolar mean linear intercept length was more severe in the VDD-CSE mice compared to control animals and animals exposed to VDD or CSE alone. The VDD-CSE and the CD-CSE mice had increased total lung capacity and increased static lung compliance. There was also a significant increase in the matrix metalloproteinase-9: tissue inhibitor of metalloproteinases-1 ratio in VDD-CSE mice compared with all controls. Alpha-1 antitrypsin expression was reduced in VDD-CSE mice as well. In summary, vitamin D deficiency, when combined with cigarette smoke exposure, seemed to accelerate the appearance of emphysemas, perhaps by virtue of an increased protease-antiprotease ratio in the combined VDD-CSE animals. These results support the value of our mouse model in the study of COPD.

  16. Influence of green tea consumption on cigarette smoking-induced biochemical changes in plasma and blood

    Marthadu Shakeela Begum

    2017-12-01

    Full Text Available Cigarette smoking causes numerous adverse biochemical changes in plasma and blood leading to ill health effects for which therapeutic approaches are sought. The present study investigates the effect of green tea consumption on confirmed cigarette smokers. Blood samples were collected from 120 selected human male volunteers categorized in to four groups viz., controls, smokers, control volunteers consuming green tea with no habit of smoking and smokers consuming green tea were analysed. Results showed that altered plasma glucose, HbA1c, hemoglobin, hematocrit, total cholesterol, lipoprotein patterns (HDL, LDL, VLDL and lipid peroxidation along with vitamins (vitamin-D, vitamin-B12, vitamin-C and minerals (iron, total iron binding capacity, calcium, sodium, potassium, phosphorous, chloride followed by the activities of alanine aminotransferase (ALT, aspartate aminotransferase (AST, gamma glutamyl transferase (γGT and alkaline phosphatase (ALP. Furthermore, phytochemical analysis of green tea confirmed the presence of phenols, flavonoids and tannins. Antioxidants and free radical scavenging effects of green tea were assessed using 2, 2′-azino-bis (3-ethylbenzothiazoline-6-sulphonic acid (ABTS+ and 2, 2-diphenyl-1-picrylhydrazyl (DPPH+. Results of this study clearly demonstrated that the adverse changes observed in the above biochemical parameters in smokers were reversed upon green tea supplementation which can be attributed to the phytoconstituents present in green tea. In conclusion, both in vivo and in vitro studies revealed that phytocompounds present in green tea are able to scavenge free radicals and by there offers protection against smoking induced biochemical alterations.

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

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

    2016-04-28

    Strict restrictions on outdoor cigarette marketing have resulted in increasing concentration of cigarette marketing at the point-of-sale (POS). The association between POS cigarette marketing and smoking-induced deprivation (SID) has never been studied. The aim of this study was to examine this association and how it is mediated by cravings to smoke, urges to buy cigarettes, and unplanned purchases of cigarettes. Data from a telephone survey of 939 smokers were collected in Omaha, Nebraska. POS cigarette marketing was measured by asking respondents three questions about noticing pack displays, advertisements, and promotions such as cigarette price discounts within their respective neighborhoods. SID was measured with the following question: "In the last six months, has there been a time when the money you spent on cigarettes resulted in not having enough money for household essentials such as food? [yes/no]" We used structural equation modeling to examine the study aim. There was overwhelming evidence for an association between higher levels of POS cigarette marketing and a higher probability of SID (p marketing is associated with a higher probability of experiencing SID, policies that ban POS cigarette marketing might help some smokers afford essentials household items such as food more easily and thus have better standards of living.

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

    Yang, Jie; Li, Jun-Wen; Wang, Lu; Chen, Zhaoli; Shen, Zhi-Qiang; Jin, Min; Wang, Xin-Wei; Zheng, Yufei; Qiu, Zhi-Gang; Wang, Jing-feng

    2008-01-01

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

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

    Nesi RT

    2016-03-01

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

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

    Victoria L Palmer

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

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

    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.

  2. Sestrin-2, a repressor of PDGFRβ signalling, promotes cigarette-smoke-induced pulmonary emphysema in mice and is upregulated in individuals with COPD

    Heidler, Juliana; Fysikopoulos, Athanasios; Wempe, Frank; Seimetz, Michael; Bangsow, Thorsten; Tomasovic, Ana; Veit, Florian; Scheibe, Susan; Pichl, Alexandra; Weisel, Friederike; Lloyd, K. C. Kent; Jaksch, Peter; Klepetko, Walter; Weissmann, Norbert; von Melchner, Harald

    2013-01-01

    SUMMARY Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. COPD is caused by chronic exposure to cigarette smoke and/or other environmental pollutants that are believed to induce reactive oxygen species (ROS) that gradually disrupt signalling pathways responsible for maintaining lung integrity. Here we identify the antioxidant protein sestrin-2 (SESN2) as a repressor of PDGFRβ signalling, and PDGFRβ signalling as an upstream regulator of alveolar maintenance programmes. In mice, the mutational inactivation of Sesn2 prevents the development of cigarette-smoke-induced pulmonary emphysema by upregulating PDGFRβ expression via a selective accumulation of intracellular superoxide anions (O2−). We also show that SESN2 is overexpressed and PDGFRβ downregulated in the emphysematous lungs of individuals with COPD and to a lesser extent in human lungs of habitual smokers without COPD, implicating a negative SESN2-PDGFRβ interrelationship in the pathogenesis of COPD. Taken together, our results imply that SESN2 could serve as both a biomarker and as a drug target in the clinical management of COPD. PMID:24046361

  3. Airway Surface Dehydration Aggravates Cigarette Smoke-Induced Hallmarks of COPD in Mice.

    Seys, Leen J M; Verhamme, Fien M; Dupont, Lisa L; Desauter, Elke; Duerr, Julia; Seyhan Agircan, Ayca; Conickx, Griet; Joos, Guy F; Brusselle, Guy G; Mall, Marcus A; Bracke, Ken R

    2015-01-01

    Airway surface dehydration, caused by an imbalance between secretion and absorption of ions and fluid across the epithelium and/or increased epithelial mucin secretion, impairs mucociliary clearance. Recent evidence suggests that this mechanism may be implicated in chronic obstructive pulmonary disease (COPD). However, the role of airway surface dehydration in the pathogenesis of cigarette smoke (CS)-induced COPD remains unknown. We aimed to investigate in vivo the effect of airway surface dehydration on several CS-induced hallmarks of COPD in mice with airway-specific overexpression of the β-subunit of the epithelial Na⁺ channel (βENaC). βENaC-Tg mice and wild-type (WT) littermates were exposed to air or CS for 4 or 8 weeks. Pathological hallmarks of COPD, including goblet cell metaplasia, mucin expression, pulmonary inflammation, lymphoid follicles, emphysema and airway wall remodelling were determined and lung function was measured. Airway surface dehydration in βENaC-Tg mice aggravated CS-induced airway inflammation, mucin expression and destruction of alveolar walls and accelerated the formation of pulmonary lymphoid follicles. Moreover, lung function measurements demonstrated an increased compliance and total lung capacity and a lower resistance and hysteresis in βENaC-Tg mice, compared to WT mice. CS exposure further altered lung function measurements. We conclude that airway surface dehydration is a risk factor that aggravates CS-induced hallmarks of COPD.

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

    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. Cigarette smoke-induced alveolar epithelial-mesenchymal transition is mediated by Rac1 activation.

    Shen, Hui-juan; Sun, Yan-hong; Zhang, Shui-juan; Jiang, Jun-xia; Dong, Xin-wei; Jia, Yong-liang; Shen, Jian; Guan, Yan; Zhang, Lin-hui; Li, Fen-fen; Lin, Xi-xi; Wu, Xi-mei; Xie, Qiang-min; Yan, Xiao-feng

    2014-06-01

    Epithelial-mesenchymal transition (EMT) is the major pathophysiological process in lung fibrosis observed in chronic obstructive pulmonary disease (COPD) and lung cancer. Smoking is a risk factor for developing EMT, yet the mechanism remains largely unknown. In this study, we investigated the role of Rac1 in cigarette smoke (CS) induced EMT. EMT was induced in mice and pulmonary epithelial cells by exposure of CS and cigarette smoke extract (CSE) respectively. Treatment of pulmonary epithelial cells with CSE elevated Rac1 expression associated with increased TGF-β1 release. Blocking TGF-β pathway restrained CSE-induced changes in EMT-related markers. Pharmacological inhibition or knockdown of Rac1 decreased the CSE exposure induced TGF-β1 release and ameliorated CSE-induced EMT. In CS-exposed mice, pharmacological inhibition of Rac1 reduced TGF-β1 release and prevented aberrations in expression of EMT markers, suggesting that Rac1 is a critical signaling molecule for induction of CS-stimulated EMT. Furthermore, Rac1 inhibition or knockdown abrogated CSE-induced Smad2 and Akt (PKB, protein kinase B) activation in pulmonary epithelial cells. Inhibition of Smad2, PI3K (phosphatidylinositol 3-kinase) or Akt suppressed CSE-induced changes in epithelial and mesenchymal marker expression. Altogether, these data suggest that CS initiates EMT through Rac1/Smad2 and Rac1/PI3K/Akt signaling pathway. Our data provide new insights into the fundamental basis of EMT and suggest a possible new course of therapy for COPD and lung cancer. Copyright © 2014 Elsevier B.V. All rights reserved.

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

    Spaggiari, Enrica; Zompadori, Maurizio; Bna', Claudio; Ormitti, Francesca; Svaerzellati, Nicola; Rabaiotti, Enrico; Verduri, Alessia; Chetta, Alfredo

    2005-01-01

    Purpose: To evaluate the prevalence and significance of the pathological effects of cigarette smoking on the lung and the sensitivity of high-resolution CT (HRCT) in the recognition of early smoking-induced lesions in asymptomatic former of current smokers. Materials and methods: We performed a prospective and consecutive analysis of 36 volunteers (16 males, 20 females), 10 non-smokers (3 males, 7 females) and 26 smokers (13 males, 13 females / 17 current smokers; 9 former smokers), all asymptomatic and with normal respiratory flows. These subjects underwent lung function testing and HRCT, after providing written informed consent for the study. The HRCT scans were obtained at three pre-selected levels (aortic arch, tracheal carina and venous hilum). The same scans were obtained in post-expiration phase. At the level of the apical segmental bronchus of the right upper lobe, we measured on the monitor wall thickening, and the total and internal diameters using the techniques reported in literature. Each study was independently evaluated by two radiologists that were blinded to all clinical and functional data: they also evaluated the presence, prevalence and type of emphysema, areas of patchy hyperlucency and oligoemia in the inspiration phase and areas of expiratory air trapping. The extension was evaluated with the visual score method. The data obtained were analysed with the Windows SPSS package for statistical analysis. Results: The two groups (non smokers and smokers) showed significant differences in some functional tests such as FEV1 (p [it

  7. A murine model of elastase- and cigarette smoke-induced emphysema

    Rubia Rodrigues

    Full Text Available ABSTRACT Objective: To describe a murine model of emphysema induced by a combination of exposure to cigarette smoke (CS and instillation of porcine pancreatic elastase (PPE. Methods: A total of 38 C57BL/6 mice were randomly divided into four groups: control (one intranasal instillation of 0.9% saline solution; PPE (two intranasal instillations of PPE; CS (CS exposure for 60 days; and CS + PPE (two intranasal instillations of PPE + CS exposure for 60 days. At the end of the experimental protocol, all animals were anesthetized and tracheostomized for calculation of respiratory mechanics parameters. Subsequently, all animals were euthanized and their lungs were removed for measurement of the mean linear intercept (Lm and determination of the numbers of cells that were immunoreactive to macrophage (MAC-2 antigen, matrix metalloproteinase (MMP-12, and glycosylated 91-kDa glycoprotein (gp91phox in the distal lung parenchyma and peribronchial region. Results: Although there were no differences among the four groups regarding the respiratory mechanics parameters assessed, there was an increase in the Lm in the CS + PPE group. The numbers of MAC-2-positive cells in the peribronchial region and distal lung parenchyma were higher in the CS + PPE group than in the other groups, as were the numbers of cells that were positive for MMP-12 and gp91phox, although only in the distal lung parenchyma. Conclusions: Our model of emphysema induced by a combination of PPE instillation and CS exposure results in a significant degree of parenchymal destruction in a shorter time frame than that employed in other models of CS-induced emphysema, reinforcing the importance of protease-antiprotease imbalance and oxidant-antioxidant imbalance in the pathogenesis of emphysema.

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

    Yunye Ning

    Full Text Available BACKGROUND: Over-production of mucus is an important pathophysiological feature in chronic airway disease such as chronic obstructive pulmonary disease (COPD and asthma. Cigarette smoking (CS is the leading cause of COPD. Oxidative stress plays a key role in CS-induced airway abnormal mucus production. Hydrogen protected cells and tissues against oxidative damage by scavenging hydroxyl radicals. In the present study we investigated the effect of hydrogen on CS-induced mucus production in rats. METHODS: Male Sprague-Dawley rats were divided into four groups: sham control, CS group, hydrogen-rich saline pretreatment group and hydrogen-rich saline control group. Lung morphology and tissue biochemical changes were determined by immunohistochemistry, Alcian Blue/periodic acid-Schiff staining, TUNEL, western blot and realtime RT-PCR. RESULTS: Hydrogen-rich saline pretreatment attenuated CS-induced mucus accumulation in the bronchiolar lumen, goblet cell hyperplasia, muc5ac over-expression and abnormal cell apoptosis in the airway epithelium as well as malondialdehyde increase in the BALF. The phosphorylation of EGFR at Tyr1068 and Nrf2 up-regulation expression in the rat lungs challenged by CS exposure were also abrogated by hydrogen-rich saline. CONCLUSION: Hydrogen-rich saline pretreatment ameliorated CS-induced airway mucus production and airway epithelium damage in rats. The protective role of hydrogen on CS-exposed rat lungs was achieved at least partly by its free radical scavenging ability. This is the first report to demonstrate that intraperitoneal administration of hydrogen-rich saline protected rat airways against CS damage and it could be promising in treating abnormal airway mucus production in COPD.

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

    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

  10. Aryl hydrocarbon receptor-dependent retention of nuclear HuR suppresses cigarette smoke-induced cyclooxygenase-2 expression independent of DNA-binding.

    Zago, Michela; Sheridan, Jared A; Nair, Parameswaran; Rico de Souza, Angela; Gallouzi, Imed-Eddine; Rousseau, Simon; Di Marco, Sergio; Hamid, Qutayba; Eidelman, David H; Baglole, Carolyn J

    2013-01-01

    The aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that responds to man-made environmental toxicants, has emerged as an endogenous regulator of cyclooxygenase-2 (Cox-2) by a mechanism that is poorly understood. In this study, we first used AhR-deficient (AhR(-/-) ) primary pulmonary cells, together with pharmacological tools to inhibit new RNA synthesis, to show that the AhR is a prominent factor in the destabilization of Cox-2 mRNA. The destabilization of Cox-2 mRNA and subsequent suppression of cigarette smoke-induced COX-2 protein expression by the AhR was independent of its ability to bind the dioxin response element (DRE), thereby differentiating the DRE-driven toxicological AhR pathway from its anti-inflammatory abilities. We further describe that the AhR destabilizes Cox-2 mRNA by sequestering HuR within the nucleus. The role of HuR in AhR stabilization of Cox-2 mRNA was confirmed by knockdown of HuR, which resulted in rapid Cox-2 mRNA degradation. Finally, in the lungs of AhR(-/-) mice exposed to cigarette smoke, there was little Cox-2 mRNA despite robust COX-2 protein expression, a finding that correlates with almost exclusive cytoplasmic HuR within the lungs of AhR(-/-) mice. Therefore, we propose that the AhR plays an important role in suppressing the expression of inflammatory proteins, a function that extends beyond the ability of the AhR to respond to man-made toxicants. These findings open the possibility that a DRE-independent AhR pathway may be exploited therapeutically as an anti-inflammatory target.

  11. A murine model of elastase- and cigarette smoke-induced emphysema.

    Rodrigues, Rubia; Olivo, Clarice Rosa; Lourenço, Juliana Dias; Riane, Alyne; Cervilha, Daniela Aparecida de Brito; Ito, Juliana Tiyaki; Martins, Milton de Arruda; Lopes, Fernanda Degobbi Tenório Quirino Dos Santos

    2017-01-01

    To describe a murine model of emphysema induced by a combination of exposure to cigarette smoke (CS) and instillation of porcine pancreatic elastase (PPE). A total of 38 C57BL/6 mice were randomly divided into four groups: control (one intranasal instillation of 0.9% saline solution); PPE (two intranasal instillations of PPE); CS (CS exposure for 60 days); and CS + PPE (two intranasal instillations of PPE + CS exposure for 60 days). At the end of the experimental protocol, all animals were anesthetized and tracheostomized for calculation of respiratory mechanics parameters. Subsequently, all animals were euthanized and their lungs were removed for measurement of the mean linear intercept (Lm) and determination of the numbers of cells that were immunoreactive to macrophage (MAC)-2 antigen, matrix metalloproteinase (MMP)-12, and glycosylated 91-kDa glycoprotein (gp91phox) in the distal lung parenchyma and peribronchial region. Although there were no differences among the four groups regarding the respiratory mechanics parameters assessed, there was an increase in the Lm in the CS + PPE group. The numbers of MAC-2-positive cells in the peribronchial region and distal lung parenchyma were higher in the CS + PPE group than in the other groups, as were the numbers of cells that were positive for MMP-12 and gp91phox, although only in the distal lung parenchyma. Our model of emphysema induced by a combination of PPE instillation and CS exposure results in a significant degree of parenchymal destruction in a shorter time frame than that employed in other models of CS-induced emphysema, reinforcing the importance of protease-antiprotease imbalance and oxidant-antioxidant imbalance in the pathogenesis of emphysema. Descrever um modelo murino de enfisema induzido por exposição a fumaça de cigarro (FC) e instilação de elastase pancreática porcina (EPP). Trinta e oito camundongos C57BL/6 foram aleatoriamente divididos em quatro grupos: controle (uma instilação intranasal

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

    van der Toorn, Marco; Slebos, Dirk-Jan; de Bruin, Harold G.; Gras, Renee; Rezayat, Delaram; Jorge, Lucie; Sandra, Koen; van Oosterhout, Antoon J. M.

    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

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

    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.

  14. Cigarette smoke-induced emphysema : A role for the B cell?

    van der Strate, BWA; Postma, DS; Brandsma, CA; Melgert, BN; Luinge, MA; Geerlings, M; Hylkema, MN; van den Berg, Anke; Timens, W; Kerstjens, HAM

    2006-01-01

    Rationale: Little is known about what drives the inflammatory reaction in the development of chronic obstructive lung disease. B cells have been found. Objective: To study the involvement of B cells in the development of emphysema. Methods: The presence of B-cell follicles and their interaction with

  15. Cigarette smoke induced autophagy-impairment regulates AMD pathogenesis mechanisms in ARPE-19 cells.

    Viren Kumar Govindaraju

    Full Text Available Age related macular degeneration (AMD is one of the leading causes of blindness. Genetics, environmental insult, and age-related factors all play a key role in altering proteostasis, the homeostatic process regulating protein synthesis, degradation and processing. These factors also play a role in the pathogenesis of AMD and it has been well established that cigarette smoking (CS initiates AMD pathogenic mechanisms. The primary goal of this study is to elucidate whether CS can induce proteostasis/autophagy-impairment in retinal pigment epithelial (RPE cells. In our preliminary analysis, it was found that cigarette smoke extract (CSE induces accumulation of ubiquitinated proteins in the insoluble protein fraction (p < 0.01, which was subsequently mitigated through cysteamine (p < 0.01 or fisetin (p < 0.05 treatment. Further, it was verified that these CSE induced ubiquitinated proteins accumulated in the peri-nuclear spaces (p<0.05 that were cleared- off with cysteamine (p < 0.05 or fisetin (p < 0.05. Moreover, CSE-induced aggresome-formation (LC3B-GFP and Ub-RFP co-localization and autophagy-flux impairment was significantly (p<0.01 mitigated by cysteamine (p<0.05 or fisetin (p<0.05 treatment, indicating the restoration of CSE-mediated autophagy-impairment. CSE treatment was also found to induce intracellular reactive oxygen species (ROS, p < 0.001 while impacting cell viability (p < 0.001, which was quantified using CMH2DCFDA-dye (ROS and MTS (proliferation or propodium iodide staining (cell viability assays, respectively. Moreover, cysteamine and fisetin treatment ameliorated CS-mediated ROS production (p < 0.05 and diminished cell viability (p < 0.05. Lastly, CSE was found to induce cellular senescence (p < 0.001, which was significantly ameliorated by cysteamine (p < 0.001 or fisetin (p < 0.001. In conclusion, our study indicates that CS induced proteostasis/autophagy-impairment regulates mechanisms associated with AMD pathogenesis. Moreover

  16. MicroRNAs as Potential Mediators for Cigarette Smoking Induced Atherosclerosis

    Yuka Yokoyama

    2018-04-01

    Full Text Available Smoking increases the risk of atherosclerosis-related events, such as myocardial infarction and ischemic stroke. Recent studies have examined the expression levels of altered microRNAs (miRNAs in various diseases. The profiles of tissue miRNAs can be potentially used in diagnosis or prognosis. However, there are limited studies on miRNAs following exposure to cigarette smoke (CS. The present study was designed to dissect the effects and cellular/molecular mechanisms of CS-induced atherosclerogenesis. Apolipoprotein E knockout (ApoE KO mice were exposed to CS for five days a week for two months at low (two puffs/min for 40 min/day or high dose (two puffs/min for 120 min/day. We measured the area of atherosclerotic plaques in the aorta, representing the expression of miRNAs after the exposure period. Two-month exposure to the high dose of CS significantly increased the plaque area in aortic arch, and significantly upregulated the expression of atherosclerotic markers (VCAM-1, ICAM-1, MCP1, p22phox, and gp91phox. Exposure to the high dose of CS also significantly upregulated the miRNA-155 level in the aortic tissues of ApoE KO mice. Moreover, the expression level of miR-126 tended to be downregulated and that of miR-21 tended to be upregulated in ApoE KO mice exposed to the high dose of CS, albeit statistically insignificant. The results suggest that CS induces atherosclerosis through increased vascular inflammation and NADPH oxidase expression and also emphasize the importance of miRNAs in the pathogenesis of CS-induced atherosclerosis. Our findings provide evidence for miRNAs as potential mediators of inflammation and atherosclerosis induced by CS.

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

    Boué, Stéphanie; De León, Héctor; Schlage, Walter K.; Peck, Michael J.; Weiler, Horst; Berges, An; Vuillaume, Grégory; Martin, Florian; Friedrichs, Baerbel; Lebrun, Stefan

    2013-01-01

    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

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

    Joshua B. Lewis

    2016-10-01

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

  19. Establishment and Evaluation of a Rat Model of Sidestream Cigarette Smoke-Induced Chronic Obstructive Pulmonary Disease

    Genfa Wang

    2018-02-01

    Full Text Available Chronic obstructive pulmonary disease (COPD is a common cause of mortality worldwide. The current lack of an animal model that can be established within a certain time frame and imitate the unique features of the disease is a major limiting factor in its study. The present study established and evaluated an animal model of COPD that represents the early and advanced stage features using short-, middle-, and long-term sidestream cigarette smoke (CS exposure. One hundred and nine Sprague–Dawley rats were randomly divided into 10 groups for different periods of sidestream CS exposure or no exposure (i.e., normal groups. The rats were exposed to CS from 3R4F cigarettes in an exposure chamber. Histological analysis was performed to determine pathological changes. We also conducted open-field tests, lung function evaluations, and cytokine analysis of the blood serum, bronchoalveolar lavage fluid, and lung tissue. The lung tissue protein levels, blood gases, and were also analyzed. As the CS exposure time increased, the indicators associated with oxidative stress, inflammatory responses, and airway remodeling were greater in the CS exposure groups than in the normal group. At 24 and 36 weeks, the COPD model rats displayed the middle- and advanced-stage features of COPD, respectively. In the 8-week CS exposure group, after the CS exposure was stopped for 4 weeks, inflammatory responses and oxidative responses were ameliorated and lung function exacerbation was reduced compared with the 12-week CS exposure group. Therefore, we established a more adequate rat model of sidestream CS induced COPD, which will have great significance for a better understanding of the pathogenesis of COPD and drug effectiveness evaluation.

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

    Bannhi Das

    2014-01-01

    Full Text Available Cigarette smoke (CS is a major risk factor for emphysematous changes in the lungs and the underlying mechanism involves CS-induced cell death. In the present study we investigated the ability of nutrients to rescue CS-induced cell death. We observed that pre-treatment with excess leucine can partially rescue CS extract-induced cell death in Saccharomyces cerevisiae and alveolar epithelial A549 cells. Excess dietary leucine was also effective in alleviating effects of CS in guinea pig lungs. Further investigation to understand the underlying mechanism showed that CS exposure causes downregulation of leucine transporter that results in inactivation of mTOR, which is a positive regulator of protein synthesis and cell proliferation. Notably, leucine supplemented diet ameliorated even existing CS-induced emphysematous changes in guinea pig lung, a condition hitherto thought to be irreversible. Thus the current study documents a new mechanism by which CS affects cellular physiology wherein leucine transporter is a key target.

  1. Different profiles of notch signaling in cigarette smoke-induced pulmonary emphysema and bleomycin-induced pulmonary fibrosis.

    Li, Shi; Hu, Xiaofei; Wang, Zheng; Wu, Meng; Zhang, Jinnong

    2015-05-01

    Different profiles of Notch signaling mediate naive T cell differentiation which might be involved in pulmonary emphysema and fibrosis. C57BL/6 mice were randomized into cigarette smoke (CS) exposure, bleomycin (BLM) exposure, and two separate groups of control for sham exposure to CS or BLM. The paratracheal lymph nodes of the animals were analyzed by real-time PCR and immunohistochemistry. Morphometry of the lung parenchyma, measurement of the cytokines, and cytometry of the bronchoalveolar lavage fluid (BALF) were also done accordingly. In comparison with controls, all Notch receptors and ligands were upregulated by chronic CS exposure, especially Notch3 and DLL1 (P emphysema-like morphology and Th1-biased inflammation. While Notch3 and DLL1 were downregulated by BLM exposure (P pulmonary emphysema. Unable to initiate the Th1 response or inhibit it may lead to Th2 polarization and aberrant repair.

  2. Hydrogen-rich pure water prevents cigarette smoke-induced pulmonary emphysema in SMP30 knockout mice.

    Suzuki, Yohei; Sato, Tadashi; Sugimoto, Masataka; Baskoro, Hario; Karasutani, Keiko; Mitsui, Aki; Nurwidya, Fariz; Arano, Naoko; Kodama, Yuzo; Hirano, Shin-Ichi; Ishigami, Akihito; Seyama, Kuniaki; Takahashi, Kazuhisa

    2017-10-07

    Chronic obstructive pulmonary disease (COPD) is predominantly a cigarette smoke (CS)-triggered disease with features of chronic systemic inflammation. Oxidants derived from CS can induce DNA damage and stress-induced premature cellular senescence in the respiratory system, which play significant roles in COPD. Therefore, antioxidants should provide benefits for the treatment of COPD; however, their therapeutic potential remains limited owing to the complexity of this disease. Recently, molecular hydrogen (H 2 ) has been reported as a preventive and therapeutic antioxidant. Molecular H 2 can selectively reduce hydroxyl radical accumulation with no known side effects, showing potential applications in managing oxidative stress, inflammation, apoptosis, and lipid metabolism. However, there have been no reports on the efficacy of molecular H 2 in COPD patients. In the present study, we used a mouse model of COPD to investigate whether CS-induced histological damage in the lungs could be attenuated by administration of molecular H 2 . We administered H 2 -rich pure water to senescence marker protein 30 knockout (SMP30-KO) mice exposed to CS for 8 weeks. Administration of H 2 -rich water attenuated the CS-induced lung damage in the SMP30-KO mice and reduced the mean linear intercept and destructive index of the lungs. Moreover, H 2 -rich water significantly restored the static lung compliance in the CS-exposed mice compared with that in the CS-exposed H 2 -untreated mice. Moreover, treatment with H 2 -rich water decreased the levels of oxidative DNA damage markers such as phosphorylated histone H2AX and 8-hydroxy-2'-deoxyguanosine, and senescence markers such as cyclin-dependent kinase inhibitor 2A, cyclin-dependent kinase inhibitor 1, and β-galactosidase in the CS-exposed mice. These results demonstrated that H 2 -rich pure water attenuated CS-induced emphysema in SMP30-KO mice by reducing CS-induced oxidative DNA damage and premature cell senescence in the lungs. Our

  3. NF-κB inhibition is involved in tobacco smoke-induced apoptosis in the lungs of rats

    Zhong Caiyun; Zhou Yamei; Pinkerton, Kent E.

    2008-01-01

    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-κB) in this process. Exposure of rats to 80 mg/m 3 tobacco smoke significantly induced apoptosis in the lungs. Tobacco smoke resulted in inhibition of NF-κB activity, noted by suppression of inhibitor of κB (IκB) kinase (IKK), accumulation of IκBα, decrease of NF-κB DNA binding activity, and downregulation of NF-κB-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-κB pathway in tobacco smoke-induced apoptosis

  4. Quantitative assessment of smoking-induced emphysema progression in longitudinal CT screening for lung cancer

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

    2015-03-01

    Computed tomography has been used for assessing structural abnormalities associated with emphysema. It is important to develop a robust CT based imaging biomarker that would allow quantification of emphysema progression in early stage. This paper presents effect of smoking on emphysema progression using annual changes of low attenuation volume (LAV) by each lung lobe acquired from low-dose CT images in longitudinal screening for lung cancer. The percentage of LAV (LAV%) was measured after applying CT value threshold method and small noise reduction. Progression of emphysema was assessed by statistical analysis of the annual changes represented by linear regression of LAV%. This method was applied to 215 participants in lung cancer CT screening for five years (18 nonsmokers, 85 past smokers, and 112 current smokers). The results showed that LAV% is useful to classify current smokers with rapid progression of emphysema (0.2%/year, pemphysema in CT screening for lung cancer.

  5. 32P-postlabeling DNA adduct assay: cigarette smoke-induced dna adducts in the respiratory and nonrespiratory rat tissues. Book chapter

    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

  6. Cigarette smoke-induced differential expression of the genes involved in exocrine function of the rat pancreas.

    Wittel, Uwe A; Singh, Ajay P; Henley, Brandon J; Andrianifahanana, Mahefatiana; Akhter, Mohammed P; Cullen, Diane M; Batra, Surinder K

    2006-11-01

    Little is known about the molecular and biological aspects of the epidemiological association between smoking and pancreatic pathology, such as chronic pancreatitis and pancreatic cancer. Recently, we reported that tobacco smoke exposure induced morphological alterations in the rat pancreas. Here, we have investigated the alterations in the expression of genes associated with exocrine pancreatic function and cellular differentiation upon exposure to cigarette smoke. Female rats were exposed to environmental smoke inhalation for 2 d/wk (70 min/d) for 12 weeks. The expression profiles of trypsinogen, pancreas-specific trypsin inhibitor, cholecystokinin A receptor, cystic fibrosis transmembrane conductance regulator (CFTR), carbonic anhydrase, and Muc1 and Muc4 mucins transcripts were analyzed by RNA slot blot analysis. Muc4 expression was also examined by immunohistochemistry. Our data revealed that the ratio of trypsinogen to that of the protective pancreas-specific trypsin inhibitor was elevated upon cigarette smoke exposure. The expression of carbonic anhydrase and CFTR remained unaltered when inflammatory signs were not detected in histological examinations. On the other hand, when pancreatic inflammation was present, the levels of CFTR and carbonic anhydrase were increased, indicating ductal and/or centroacinar cell involvement. No changes in the expression of Muc1 and Muc4 mucins were observed. Our data show that cigarette smoke exposure leads to an increased vulnerability to pancreatic self-digestion. Moreover, the concomitant involvement of pancreatic ducts occurs only when focal pancreatic inflammation is present.

  7. Induced Pluripotent Stem Cells-Derived Mesenchymal Stem Cells Attenuate Cigarette Smoke-Induced Cardiac Remodeling and Dysfunction

    Yingmin Liang

    2017-07-01

    Full Text Available The strong relationship between cigarette smoking and cardiovascular disease (CVD has been well-documented, but the mechanisms by which smoking increases CVD risk appear to be multifactorial and incompletely understood. Mesenchymal stem cells (MSCs are regarded as an important candidate for cell-based therapy in CVD. We hypothesized that MSCs derived from induced pluripotent stem cell (iPSC-MSCs or bone marrow (BM-MSCs might alleviate cigarette smoke (CS-induced cardiac injury. This study aimed to investigate the effects of BM-MSCs or iPSC-MSCs on CS-induced changes in serum and cardiac lipid profiles, oxidative stress and inflammation as well as cardiac function in a rat model of passive smoking. Male Sprague-Dawley rats were randomly selected for exposure to either sham air (SA as control or 4% CS for 1 h per day for 56 days. On day 29 and 43, human adult BM-MSCs, iPSC-MSCs or PBS were administered intravenously to CS-exposed rats. Results from echocardiography, serum and cardiac lipid profiles, cardiac antioxidant capacity, cardiac pro- and anti-inflammatory cytokines and cardiac morphological changes were evaluated at the end of treatment. iPSC-MSC-treated group showed a greater effect in the improvement of CS-induced cardiac dysfunction over BM-MSCs-treated group as shown by increased percentage left ventricular ejection fraction and percentage fractional shortening, in line with the greater reversal of cardiac lipid abnormality. In addition, iPSC-MSCs administration attenuated CS-induced elevation of cardiac pro-inflammatory cytokines as well as restoration of anti-inflammatory cytokines and anti-oxidative markers, leading to ameliorate cardiac morphological abnormalities. These data suggest that iPSC-MSCs on one hand may restore CS-induced cardiac lipid abnormality and on the other hand may attenuate cardiac oxidative stress and inflammation via inhibition of CS-induced NF-κB activation, leading to improvement of cardiac remodeling and

  8. Interactions between ethanol and cigarette smoke in a mouse lung carcinogenesis model

    Balansky, Roumen; Ganchev, Gancho; Iltcheva, Marietta; Nikolov, Manasi; La Maestra, S.; Micale, Rosanna T.; Steele, Vernon E.; De Flora, Silvio

    2016-01-01

    Highlights: • Cigarette smoke and ethanol are known to synergize in the upper aerodigestive tract. • Their interactions in the lower respiratory tract have poorly been explored. • Prenatal and postnatal treatments of mice with ethanol caused pulmonary alterations. • However, ethanol attenuated smoke-induced preneoplastic and neoplastic lesions in lung. • The interaction between smoke and alcohol depends on life stage and target tissue. - Abstract: Both ethanol and cigarette smoke are classified as human carcinogens. They can synergize, especially in tissues of the upper aerodigestive tract that are targeted by both agents. The main objective of the present study was to evaluate the individual and combined effects of ethanol and smoke in the respiratory tract, either following transplacental exposure and/or postnatal exposure. We designed two consecutive studies in mouse models by exposing Swiss H mice to oral ethanol and/or inhaled mainstream cigarette smoke for up to 4 months, at various prenatal and postnatal life stages. Clastogenic effects and histopathological alterations were evaluated after 4 and 8 months, respectively. Ethanol was per se devoid of clastogenic effects in mouse peripheral blood erythrocytes. However, especially in mice exposed both transplacentally throughout pregnancy and in the postnatal life, ethanol administration was associated not only with liver damage but also with pro-angiogenetic effects in the lung by stimulating the proliferation of blood vessels. In addition, these mice developed pulmonary emphysema, alveolar epithelial hyperplasias, microadenomas, and benign tumors. On the other hand, ethanol interfered in the lung carcinogenesis process resulting from the concomitant exposure of mice to smoke. In fact, ethanol significantly attenuated some smoke-related preneoplastic and neoplastic lesions in the respiratory tract, such as alveolar epithelial hyperplasia, microadenomas, and even malignant tumors. In addition, ethanol

  9. Wnt5a is associated with cigarette smoke-related lung carcinogenesis via protein kinase C.

    Whang, Young Mi; Jo, Ukhyun; 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.

  10. Wnt5a is associated with cigarette smoke-related lung carcinogenesis via protein kinase C.

    Young Mi Whang

    Full Text Available 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.

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

    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).

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

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

    2012-01-01

    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

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

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

    2012-03-15

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

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

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

    2014-01-01

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

  15. Polonium in cigarette smoke and radiation exposure of lungs

    Carvalho, F.P.; Oliveira, J.M.

    2006-01-01

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

  16. Patients with lung cancer: Are electronic cigarettes harmful or useful?

    Dautzenberg, Bertrand; Garelik, Daniel

    2017-03-01

    E-cigarettes remain controversial because the scientific evidence of short term and long term effects on tolerance and the health value of a switch from tobacco to e-cigarettes is contested and controversial. Nevertheless the quality of e-cigarettes and e-liquids has improved. The main ingredients, propylene glycol, vegetable glycerine and nicotine are pharmaceutical-grade quality in most e-liquids. Flavors are almost all food grade. The high quality of ingredients has decreased the presence of impurities in e-liquids. The emissions of e-cigarettes do not contain solid particles or carbon monoxide. Nitrosamine content is at least one hundred times lower than in tobacco smoke. E-cigarette emissions in normal use do not contain any harmful constituents at significant levels except nicotine. UK public health authorities have stated that e-cigarette use is likely to be at least 95% less toxic than cigarette use. There are benefits from having a well-regulated legal market. In countries where e-liquid containing nicotine is not allowed, "do-it-yourself" liquids are common and have handling risks and may sometimes contain toxic impurities. Though e-cigarettes should never be assumed safe products for non-smokers, for smokers, the e-cigarette is at least 20 times less dangerous than the cigarette. Tobacco cessation specialists in countries where nicotine containing e-cigarettes are available increasingly provide counselling for e-cigarette use to stop smoking or to reduce smoking at the request of patients. Based on current knowledge, for patients with lung or other forms of cancer who would otherwise continue to smoke, e-cigarettes offer an alternative way to quit smoking while they undergo medical treatment. Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.

  17. Whole body exposure of mice to secondhand smoke induces dose-dependent and persistent promutagenic DNA adducts in the lung

    Kim, Sang-In; Arlt, Volker M.; Yoon, Jae-In; Cole, Kathleen J.; Pfeifer, Gerd P.; Phillips, David H.; Besaratinia, Ahmad

    2011-01-01

    Secondhand smoke (SHS) exposure is a known risk factor for lung cancer in lifelong nonsmokers. However, the underlying mechanism of action of SHS in lung carcinogenesis remains elusive. We have investigated, using the 32 P-postlabeling assay, the genotoxic potential of SHS in vivo by determining the formation and kinetics of repair of DNA adducts in the lungs of mice exposed whole body to SHS for 2 or 4 months (5 h/day, 5 days/week), and an ensuing one-month recovery period. We demonstrate that exposure of mice to SHS elicits a significant genotoxic response as reflected by the elevation of DNA adduct levels in the lungs of SHS-exposed animals. The increases in DNA adduct levels in the lungs of SHS-exposed mice are dose-dependent as they are related to the intensity and duration of SHS exposure. After one month of recovery in clean air, the levels of lung DNA adducts in the mice exposed for 4 months remain significantly higher than those in the mice exposed for 2 months (P < 0.0005), levels in both groups being significantly elevated relative to controls (P < 0.00001). Our experimental findings accord with the epidemiological data showing that exposure to smoke-derived carcinogens is a risk factor for lung cancer; not only does the magnitude of risk depend upon carcinogen dose, but it also becomes more irreversible with prolonged exposure. The confirmation of epidemiologic data by our experimental findings is of significance because it strengthens the case for the etiologic involvement of SHS in nonsmokers' lung cancer. Identifying the etiologic factors involved in the pathogenesis of lung cancer can help define future strategies for prevention, early detection, and treatment of this highly lethal malignancy.

  18. Associations of interleukin-1 gene cluster polymorphisms with C-reactive protein concentration and lung function decline in smoking-induced chronic obstructive pulmonary disease

    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

  19. Polonium in cigarette smoke and radiation exposure of lungs

    Carvalho, F.P.; Oliveira, J.M.

    2006-01-01

    210 Po was analysed in three common brands of cigarettes produced in Portugal. The analyses of polonium were performed using 209 Po as an internal isotopic tracer. Samples were dissolved with acids, polonium plated on a silver disc and measured by alpha spectrometry using silicon surface barrier detectors. The analyses were carried out on the unburned tobacco contained in the cigarettes, on the ashes of smoked cigarettes and on the mainstream smoke inhaled by the smoker. 210 Po in the tobacco display concentrations ranging from 3 to 37 mBq/g, depending upon the cigarette brand. The 210 Po remaining in the solid residue of a smoked cigarette varied between 0.3 to 4.9 mBq per cigarette, and the 210 Po in the inhaled smoke from one cigarette varied from 2.6 to 28.9 mBq. In all brands of cigarettes tested, about 50 % of the 210 Po content is not inhaled by the smoker and it is released into the atmosphere. Part of it may be inhaled by passive smokers. Depending upon the commercial brand and upon the presence or absence of a filter in the cigarette, 5 to 37 % of the 210 Po in the cigarette can be inhaled by the smoker. Taking into account the average 210 Po and 210 Pb in surface air, the smoker of one pack of twenty cigarettes per day may inhale 50 times more 210 Po than a non smoker. The average absorption of 210 Po into the blood taking all pathways into account is 0.39 Bq d -1 . This includes, namely, the ingestion of water and beverages, the ingestion of food, the inhalation of air and cigarette smoke. Cigarette smoke contributes with 1.5 % to this rate of 210 Po absorption into the blood and, after circulating in all organs, gives rise to a whole body radiation dose in the same proportion. However, in the smoker the deposition of 210 Po in the lungs is much more elevated than normal and may originate an enhanced radiation exposure of this organ. Estimated dose to the lungs is presented and radiobiological effects of cigarette smoking are discussed. (author)

  20. Cigarette smoke alters the secretome of lung epithelial cells.

    Mossina, Alessandra; Lukas, Christina; Merl-Pham, Juliane; Uhl, Franziska E; Mutze, Kathrin; Schamberger, Andrea; Staab-Weijnitz, Claudia; Jia, Jie; Yildirim, Ali Ö; Königshoff, Melanie; Hauck, Stefanie M; Eickelberg, Oliver; Meiners, Silke

    2017-01-01

    Cigarette smoke is the most relevant risk factor for the development of lung cancer and chronic obstructive pulmonary disease. Many of its more than 4500 chemicals are highly reactive, thereby altering protein structure and function. Here, we used subcellular fractionation coupled to label-free quantitative MS to globally assess alterations in the proteome of different compartments of lung epithelial cells upon exposure to cigarette smoke extract. Proteomic profiling of the human alveolar derived cell line A549 revealed the most pronounced changes within the cellular secretome with preferential downregulation of proteins involved in wound healing and extracellular matrix organization. In particular, secretion of secreted protein acidic and rich in cysteine, a matricellular protein that functions in tissue response to injury, was consistently diminished by cigarette smoke extract in various pulmonary epithelial cell lines and primary cells of human and mouse origin as well as in mouse ex vivo lung tissue cultures. Our study reveals a previously unrecognized acute response of lung epithelial cells to cigarette smoke that includes altered secretion of proteins involved in extracellular matrix organization and wound healing. This may contribute to sustained alterations in tissue remodeling as observed in lung cancer and chronic obstructive pulmonary disease. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  1. Will chronic e-cigarette use cause lung disease?

    Rowell, Temperance R.; Tarran, Robert

    2015-01-01

    Chronic tobacco smoking is a major cause of preventable morbidity and mortality worldwide. In the lung, tobacco smoking increases the risk of lung cancer, and also causes chronic obstructive pulmonary disease (COPD), which encompasses both emphysema and chronic bronchitis. E-cigarettes (E-Cigs), or electronic nicotine delivery systems, were developed over a decade ago and are designed to deliver nicotine without combusting tobacco. Although tobacco smoking has declined since the 1950s, E-Cig ...

  2. Lung function profiles and aerobic capacity of adult cigarette and ...

    Lung function profiles and aerobic capacity of adult cigarette and hookah smokers after 12 weeks intermittent training. ... All subjects performed 30 min of interval exercise (2 min of work followed by 1 min of rest) three times a week for 12 weeks at an intensity estimated at 70% of the subject's maximum aerobic capacity ...

  3. Inhibition of the Hedgehog Signaling Pathway Depresses the Cigarette Smoke-Induced Malignant Transformation of 16HBE Cells on a Microfluidic Chip.

    Qin, Yong-Xin; Yang, Zhi-Hui; Du, Xiao-Hui; Zhao, Hui; Liu, Yuan-Bin; Guo, Zhe; Wang, Qi

    2018-05-20

    The hedgehog signaling system (HHS) plays an important role in the regulation of cell proliferation and differentiation during the embryonic phases. However, little is known about the involvement of HHS in the malignant transformation of cells. This study aimed to detect the role of HHS in the malignant transformation of human bronchial epithelial (16HBE) cells. In this study, two microfluidic chips were designed to investigate cigarette smoke extract (CSE)-induced malignant transformation of cells. Chip A contained a concentration gradient generator, while chip B had four cell chambers with a central channel. The 16HBE cells cultured in chip A were used to determine the optimal concentration of CSE for inducing malignant transformation. The 16HBE cells in chip B were cultured with 12.25% CSE (Group A), 12.25% CSE + 5 μmol/L cyclopamine (Group B), or normal complete medium as control for 8 months (Group C), to establish the in vitro lung inflammatory-cancer transformation model. The transformed cells were inoculated into 20 nude mice as cells alone (Group 1) or cells with cyclopamine (Group 2) for tumorigenesis testing. Expression of HHS proteins was detected by Western blot. Data were expressed as mean ± standard deviation. The t-test was used for paired samples, and the difference among groups was analyzed using a one-way analysis of variance. The optimal concentration of CSE was 12.25%. Expression of HHS proteins increased during the process of malignant transformation (Group B vs. Group A, F = 7.65, P < 0.05). After CSE exposure for 8 months, there were significant changes in cellular morphology, which allowed the transformed cells to grow into tumors in 40 days after being inoculated into nude mice. Cyclopamine could effectively depress the expression of HHS proteins (Group C vs. Group B, F = 6.47, P < 0.05) and prevent tumor growth in nude mice (Group 2 vs. Group 1, t = 31.59, P < 0.01). The activity of HHS is upregulated during the CSE-induced malignant

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

    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 t...

  5. Bilirubin treatment suppresses pulmonary inflammation in a rat model of smoke-induced emphysema.

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

    2015-09-18

    Cigarette smoking is a significant risk factor for emphysema, which is characterized by airway inflammation and oxidative damage. To assess the capacity of bilirubin to protect against smoke-induced emphysema. Smoking status and bilirubin levels were recorded in 58 patients with chronic obstructive pulmonary diseases (COPD) and 71 non-COPD participants. The impact of smoking on serum bilirubin levels and exogenous bilirubin (20 mg/kg/day) on pulmonary injury was assessed in a rat model of smoking-induced emphysema. At sacrifice lung histology, airway leukocyte accumulation and cytokine and chemokine levels in serum, bronchoalveolar lavage fluid (BALF) and lung were analyzed. Oxidative lipid damage and anti-oxidative components was assessed by measuring malondialdehyde, superoxide dismutase (SOD) activity and glutathione. Total serum bilirubin levels were lower in smokers with or without COPD than non-smoking patients without COPD (P pulmonary injury by suppressing inflammatory cell recruitment and pro-inflammatory cytokine secretion, increasing anti-inflammatory cytokine levels, and anti-oxidant SOD activity in a rat model of smoke-induced emphysema. Copyright © 2015. Published by Elsevier Inc.

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

    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 models substantially overestimate low-dose risk, linear extrapolations from empirical data over a dose range of 10- to 100-fold resulted in plausible predictions.

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

    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. © The Author 2015. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.

  8. Cigarette smoking and risk of lung metastasis from esophageal cancer.

    Abrams, Julian A; Lee, Paul C; Port, Jeffrey L; Altorki, Nasser K; Neugut, Alfred I

    2008-10-01

    Whereas extensive research has explored the effect of environmental factors on the etiology of specific cancers, the influence of exposures such as smoking on risk of site-specific metastasis is unknown. We investigated the association of cigarette smoking with lung metastasis in esophageal cancer. We conducted a case-control study of esophageal cancer patients from two centers, comparing cases with lung metastases to controls without lung metastases. Information was gathered from medical records on smoking history, imaging results, site(s) of metastasis, and other patient and tumor characteristics. We used logistic regression to assess association. We identified 354 esophageal cancer cases; smoking status was known in 289 (82%). Among patients with lung metastases, 73.6% (39 of 53) were ever smokers, versus 47.8% (144 of 301) of patients without lung metastases [P=0.001; summary odds ratio (OR), 2.52; 95% confidence interval (95% CI), 1.17-5.45; stratified by histology]. Smoking was associated with a nonsignificant increased adjusted odds of lung metastasis (OR, 1.89; 95% CI, 0.80-4.46). Upper esophageal subsite (OR, 4.71; 95% CI, 1.20-18.5), but not histology (squamous OR 0.65,95% CI 0.27-1.60), was associated with lung metastasis. Compared with the combined never/unknown smoking status group, smoking was associated with a significantly increased odds of lung metastasis (OR, 2.35; 95% CI, 1.11-4.97). There was no association between liver metastasis and smoking (OR, 0.88; 95% CI, 0.42-1.83). Smoking is associated with increased odds of lung metastasis from esophageal cancer, and this relationship seems to be site specific. Future studies are needed to determine whether smoking affects the tumor cell or the site of metastasis, and whether this changes the survival outcome.

  9. Lung injury after cigarette smoking is particle related

    Rahul G Sangani

    2011-03-01

    Full Text Available Rahul G Sangani, Andrew J GhioEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, US Environmental Protection Agency, Chapel Hill, NC, USAAbstract: The specific component responsible and the mechanistic pathway for increased human morbidity and mortality after cigarette smoking are yet to be delineated. We propose that 1 injury and disease following cigarette smoking are associated with exposure to and retention of particles produced during smoking and 2 the biological effects of particles associated with cigarette smoking share a single mechanism of injury with all particles. Smoking one cigarette exposes the human respiratory tract to between 15,000 and 40,000 µg particulate matter; this is a carbonaceous product of an incomplete combustion. There are numerous human exposures to other particles, and these vary widely in composition, absolute magnitude, and size of the particle. Individuals exposed to all these particles share a common clinical presentation with a loss of pulmonary function, increased bronchial hyperresponsiveness, pathologic changes of emphysema and fibrosis, and comorbidities, including cardiovascular disease, cerebrovascular disease, peripheral vascular disease, and cancers. Mechanistically, all particle exposures produce an oxidative stress, which is associated with a series of reactions, including an activation of kinase cascades and transcription factors, release of inflammatory mediators, and apoptosis. If disease associated with cigarette smoking is recognized to be particle related, then certain aspects of the clinical presentation can be predicted; this would include worsening of pulmonary function and progression of pathological changes and comorbidity (eg, emphysema and carcinogenesis after smoking cessation since the particle is retained in the lung and the exposure continues.Keywords: particulate matter, smoking, oxidants, oxidative stress, air pollution

  10. Quantitative assessment of elemental carbon in the lungs of never smokers, cigarette smokers and coal miners

    Inhalation exposure to particulates such as cigarette smoke and coal dust is known to contribute to the development of chronic lung disease. The purpose of this study was to estimate the amount of elemental carbon (EC) deposits from autopsied lung samples from cigarette smokers, ...

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

    Whang, Young Mi; Jo, Ukhyun; 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 ...

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

    Elena Arellano-Orden

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

  13. Will chronic e-cigarette use cause lung disease?

    Rowell, Temperance R; Tarran, Robert

    2015-12-15

    Chronic tobacco smoking is a major cause of preventable morbidity and mortality worldwide. In the lung, tobacco smoking increases the risk of lung cancer, and also causes chronic obstructive pulmonary disease (COPD), which encompasses both emphysema and chronic bronchitis. E-cigarettes (E-Cigs), or electronic nicotine delivery systems, were developed over a decade ago and are designed to deliver nicotine without combusting tobacco. Although tobacco smoking has declined since the 1950s, E-Cig usage has increased, attracting both former tobacco smokers and never smokers. E-Cig liquids (e-liquids) contain nicotine in a glycerol/propylene glycol vehicle with flavorings, which are vaporized and inhaled. To date, neither E-Cig devices, nor e-liquids, are regulated by the Food and Drug Administration (FDA). The FDA has proposed a deeming rule, which aims to initiate legislation to regulate E-Cigs, but the timeline to take effect is uncertain. Proponents of E-Cigs say that they are safe and should not be regulated. Opposition is varied, with some opponents proposing that E-Cig usage will introduce a new generation to nicotine addiction, reversing the decline seen with tobacco smoking, or that E-Cigs generally may not be safe and will trigger diseases like tobacco. In this review, we shall discuss what is known about the effects of E-Cigs on the mammalian lung and isolated lung cells in vitro. We hope that collating this data will help illustrate gaps in the knowledge of this burgeoning field, directing researchers toward answering whether or not E-Cigs are capable of causing disease. Copyright © 2015 the American Physiological Society.

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

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

    2015-10-01

    Matrix metalloproteinases (MMPs) are the main proteolytic enzymes involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). A radiolabeled MMP inhibitor, [(18)F]FB-ML5, was prepared, and its in vivo kinetics were tested in a mouse model of pulmonary inflammation. BALB/c mice were exposed for 4 days to cigarette smoke (CS) or air. On the fifth day, a dynamic microPET scan was made with [(18)F]FB-ML5. Standardized uptake values (PET-SUVmean) were 0.19 ± 0.06 in the lungs of CS-exposed mice (n = 6) compared to 0.11 ± 0.03 (n = 5) in air-exposed controls (p FB-ML5.

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

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

    2014-01-01

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

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

    Boehm, R.; Holy, K.; Sedlak, A.

    2012-01-01

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

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

    Maennistoe, J.; Toivonen, H.; Hartiala, J.; Bakhle, Y.S.; Uotila, P.

    1981-01-01

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

  18. Radionuclides in cigarettes may lead to carcinogenesis via p16INK4a inactivation

    Prueitt, Robyn L.; Goodman, Julie E.; Valberg, Peter A.

    2009-01-01

    It is widely accepted that tobacco smoke is responsible for the vast majority of lung cancers worldwide. There are many known and suspected carcinogens present in cigarette smoke, including α-emitting radioisotopes. Epidemiologic studies have shown that increased lung cancer risk is associated with exposure to ionizing radiation, and it is estimated that the majority of smoking-induced lung cancers may be at least partly attributable to the inhaled and deposited radiation dose from radioisotopes in the cigarette smoke itself. Recent research shows that silencing of the tumor suppressor gene p16 INK4a (p16) by promoter methylation plays a role in smoking-related lung cancer. Inactivation of p16 has also been associated with lung cancer incidence in radiation-exposed workers, suggesting that radionuclides in cigarette smoke may be acting with other compounds to cause smoking-induced lung cancer. We evaluated the mechanism of ionizing radiation as an accepted cause of lung cancer in terms of its dose from tobacco smoke and silencing of p16. Because both radiation and cigarette smoking are associated with inactivation of p16, and p16 inactivation has been shown to play a major role in carcinogenesis, ionizing radiation from cigarette smoke likely plays a role in lung cancer risk. How large a role it plays, relative to chemical carcinogens and other modes of action, remains to be elucidated

  19. Smoking-induced gene expression changes in the bronchial airway are reflected in nasal and buccal epithelium

    Zhang Xiaohui

    2008-05-01

    Full Text Available Abstract Background Cigarette smoking is a leading cause of preventable death and a significant cause of lung cancer and chronic obstructive pulmonary disease. Prior studies have demonstrated that smoking creates a field of molecular injury throughout the airway epithelium exposed to cigarette smoke. We have previously characterized gene expression in the bronchial epithelium of never smokers and identified the gene expression changes that occur in the mainstem bronchus in response to smoking. In this study, we explored relationships in whole-genome gene expression between extrathorcic (buccal and nasal and intrathoracic (bronchial epithelium in healthy current and never smokers. Results Using genes that have been previously defined as being expressed in the bronchial airway of never smokers (the "normal airway transcriptome", we found that bronchial and nasal epithelium from non-smokers were most similar in gene expression when compared to other epithelial and nonepithelial tissues, with several antioxidant, detoxification, and structural genes being highly expressed in both the bronchus and nose. Principle component analysis of previously defined smoking-induced genes from the bronchus suggested that smoking had a similar effect on gene expression in nasal epithelium. Gene set enrichment analysis demonstrated that this set of genes was also highly enriched among the genes most altered by smoking in both nasal and buccal epithelial samples. The expression of several detoxification genes was commonly altered by smoking in all three respiratory epithelial tissues, suggesting a common airway-wide response to tobacco exposure. Conclusion Our findings support a relationship between gene expression in extra- and intrathoracic airway epithelial cells and extend the concept of a smoking-induced field of injury to epithelial cells that line the mouth and nose. This relationship could potentially be utilized to develop a non-invasive biomarker for

  20. Induction of the unfolded protein response by cigarette smoke is primarily an activating transcription factor 4-C/EBP homologous protein mediated process

    Geraghty P

    2011-06-01

    Full Text Available Patrick Geraghty, Alison Wallace, Jeanine M D'ArmientoDepartment of Medicine, Divisions of Molecular and Pulmonary Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USAPurpose: Cigarette smoke is the major risk factor associated with the development of chronic obstructive pulmonary disease (COPD. Recent studies propose a link between endoplasmic reticulum (ER stress and emphysema, demonstrated by increased ER stress markers under smoking conditions. Here, we investigate whether cigarette smoke-induced ER stress is cell specific and correlates with acute and chronic cigarette smoke exposure.Methods: Gene and protein expression changes in human primary lung cell cultures following cigarette smoke extract (CSE exposure were monitored by qPCR and Western blot analysis. Mice and guinea pigs were exposed to cigarette smoke and ER stress markers examined in whole lung homogenates. Inflammatory cells from the bronchoalveolar lavage fluid of 10 days smoke exposed mice were also examined.Results: Cigarette smoke induced a trend increase in the ER stress response through an activating transcription factor 4 (ATF4 mediated induction of C/EBP homologous protein (CHOP in primary small airway epithelial cells. Bronchial epithelial cells and macrophages responded similarly to CSE. Wild-type mice and guinea pigs exposed to acute levels of cigarette smoke exhibited increased levels of CHOP but not at significant levels. However, after long-term chronic cigarette smoke exposure, CHOP expression was reduced. Interestingly, inflammatory cells from smoke exposed mice had a significant increase in CHOP/ATF4 expression.Conclusion: A trend increase in CHOP levels appear in multiple human lung cell types following acute cigarette smoke exposure in vitro. In vivo, inflammatory cells, predominately macrophages, demonstrate significant cigarette smoke-induced ER stress. Early induction of CHOP in cigarette smoke may play a pivotal role in early

  1. Mast cell density in isolated monkey lungs on exposure to cigarette smoke.

    Walter, A; Walter, S

    1982-01-01

    The density and percentage of degranulated cells of the mast cell population were studied in the isolated lungs of 25 monkeys (Macaca radiata radiata) before and after acute exposure to cigarette smoke. In each animal one lung was used as the test lung while the other lung was used as its control. In the control lungs the total mean mast cell count was 9.5/mm2 and the proportion of degranulated cells was 9.7%. In the lungs exposed to smoke the total counts were lower (7.3/mm2) and the percent...

  2. Lung cancer specialist physicians' attitudes towards e-cigarettes: A nationwide survey.

    Shin, Dong Wook; Kim, Young Il; Kim, Seung Joon; Kim, Jung Soo; Chong, SeMin; Park, Young Sik; Song, Sang-Yun; Lee, Jin Han; Ahn, Hee Kyung; Kim, Eun Young; Yang, Sei Hoon; Lee, Myoung Kyu; Cho, Deog Gon; Jang, Tae Won; Son, Ji Woong; Ryu, Jeong-Seon; Cho, Moon-June

    2017-01-01

    Despite a sharp increase in e-cigarette use, there is debate about whether e-cigarettes are a viable alternative for harm reduction, and the forms that regulation should take. Healthcare providers can be effective in offering guidance to patients and their families and shaping regulatory policy. We described lung cancer specialists' attitudes toward e-cigarettes and its regulation. We undertook a nationwide survey of pulmonologists, thoracic surgeons, medical and radiological oncologists who are members of Korean Association for Lung Cancer. Survey items included beliefs and attitudes toward e-cigarettes, attitudes toward e-cigarette regulation and preparedness on discussing e-cigarettes with their patients. Most respondents believed that e-cigarettes are not safer than conventional tobacco cigarettes (75.7%) or smokeless tobacco (83.2%), and feared that discussing e-cigarettes with the patients would encourage use (65.4%). They did not consider it a smoking cessation treatment (78.3%), and thus would not recommend it to smokers who do not want to quit (82.2%) or who failed to quit with conventional smoking cessation treatment (74.1%). Most respondents supported all examples of e-cigarette regulations, including the safety and quality check (97.8%), warning label (97.8%), advertisement ban (95.1%), restriction of flavoring (78.4%), minimum purchasing age (99.5%), and restriction of indoor use (94.6%). Most learned about e-cigarettes from media and advertisements, or conversation with patients rather than through professional scientific resources, and reported discomfort when discussing e-cigarette with patients. Lung cancer specialist physicians in Korea doubt the safety of e-cigarette and use of e-cigarette as smoking cessation treatment, and supported strict regulation. However, only 20% reported that they obtained information on e-cigarettes from the scientific literature and many lacked adequate knowledge based on scientific evidence, suggesting the need for

  3. Cigarette Smoke Exposure during Pregnancy Alters Fetomaternal Cell Trafficking Leading to Retention of Microchimeric Cells in the Maternal Lung

    Vogelgesang, Anja; Scapin, Cristina; Barone, Caroline; Tam, Elaine

    2014-01-01

    Cigarette smoke exposure causes chronic oxidative lung damage. During pregnancy, fetal microchimeric cells traffic to the mother. Their numbers are increased at the site of acute injury. We hypothesized that milder chronic diffuse smoke injury would attract fetal cells to maternal lungs. We used a green-fluorescent-protein (GFP) mouse model to study the effects of cigarette smoke exposure on fetomaternal cell trafficking. Wild-type female mice were exposed to cigarette smoke for about 4 weeks and bred with homozygote GFP males. Cigarette smoke exposure continued until lungs were harvested and analyzed. Exposure to cigarette smoke led to macrophage accumulation in the maternal lung and significantly lower fetal weights. Cigarette smoke exposure influenced fetomaternal cell trafficking. It was associated with retention of GFP-positive fetal cells in the maternal lung and a significant reduction of fetal cells in maternal livers at gestational day 18, when fetomaternal cell trafficking peaks in the mouse model. Cells quickly clear postpartum, leaving only a few, difficult to detect, persisting microchimeric cells behind. In our study, we confirmed the postpartum clearance of cells in the maternal lungs, with no significant difference in both groups. We conclude that in the mouse model, cigarette smoke exposure during pregnancy leads to a retention of fetal microchimeric cells in the maternal lung, the site of injury. Further studies will be needed to elucidate the effect of cigarette smoke exposure on the phenotypic characteristics and function of these fetal microchimeric cells, and confirm its course in cigarette smoke exposure in humans. PMID:24832066

  4. Cigarettes, lung cancer, and coronary heart disease: the effects of inhalation and tar yield.

    Higenbottam, T; Shipley, M J; Rose, G

    1982-06-01

    Ten-year mortality rates for lung cancer and coronary heart disease have been related to cigarette smoking habits in 17 475 male civil servants aged 40-64 and in sample of 8089 male British residents aged 35-69. Both diseases were more frequent in smokers. Lung cancer rates were higher overall for "non-inhalers", particularly in heavy smokers. Tar yield correlated with the risk of lung cancer in non-inhalers but less so in inhalers. Conversely, coronary deaths were more common among inhalers, and the effect of tar/nicotine yield (such as it was) was confined to inhalers. It appears that there are subtle interactions between the amount smoked, the tar/nicotine yield of the cigarette, and the style of smoking. Thus the effects of a change in cigarette characteristics are hard to predict, and they may be different for respiratory and cardiovascular disease.

  5. Feasibility and acceptability of e-cigarettes as an aid to quitting smoking among lung cancer patients: a pilot study

    Allison Ford; Lesley Sinclair; Jennifer Mckell; Stephen Harrow; Jennifer Macphee; Andy Morrison; Linda Bauld

    2018-01-01

    Background Many patients diagnosed with lung cancer continue to smoke even though this can make their treatment less effective and increase side effects. E-cigarettes form part of the UK's tobacco harm reduction policy landscape and are, by far, smokers' most popular quit attempt method. This pilot study explores feasibility and acceptability of e-cigarettes to aid smoking cessation among lung cancer patients undergoing chemotherapy. Methods 27 smokers with stage IV lung cancer we...

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

    Katoh, Kunihiko; Takahashi, Tsuneo

    1990-01-01

    N-isopropyl-p-I-123-iodoamphetamine (I-123 IMP), originally developed as a brain scanning agent, is also taken up by the lung. To evaluate the cigarette smoking on the uptake of IMP by the lung, we studied I-123 IMP clearance from the lung on 14 volunteers; 5 non-smokers and 9 smokers. After the injection of 111 MBq (3mCi) of I-123 IMP into the medial cubital vein, the time-activity curve for 60 minutes and the regional activity using 1 frame per minute and a 64 x 64 matrix was obtained. I-123 IMP clearance curve was described as follows: C(t)=A 1 e -k1t +A 2 e -k2t (A 1 , A 2 : intercepts, and k 1 , k 2 : slopes of the exponential components). I-123 IMP clearance was delayed in smokers, and k 2 was smaller in smokers. Also a significant correlations between k 1 , k 2 , and the number of cigarettes smoked per day were found. In conclusion, this study suggests that the delayed clearance and retention of I-123 IMP in the lung indicate the lung metabolic disorders due to cigarette smoking. (author)

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

    Kato, Kunihiko; Harada, Satoshi; Takahashi, Tsuneo; Katsuragawa, Shigehiko; Yanagisawa, Toru

    1991-01-01

    Iodine 123 N-isopropyl-p-iodoamphetamine ( 123 I-IMP), originally developed as a brain scanning agent, is also taken up by the lung. To evaluate the effects of cigarette smoking on the kinetics of IMP in the lung, we studied 123 I-IMP clearance from the lung in 18 volunteers (8 non-smokers and 10 smokers). After the injection of 111 MBq of 123 I-IMP into the medial cubital vein, the time-activity curve for 60 min and the regional activity using 1 frame per minute and a 64x64 matrix were obtained. The 123 I-IMP clearance curve was described as follows: C(t)=A 1 e ( -k 1 t)+A 2 e ( -k 2 t)(A 1 , A 2 : intercepts, and k 1 , k 2 : slopes of the exponential components). 123 I-IMP clearance was delayed in smokers, and k 2 was smaller in smokers. Also, a correlation between k 1 , k 2 , and the number of cigarettes smoked per day was found (r=-0.65, r=-0.74, respectively, P 123 I-IMP in the lung indicate lung metabolic disorders due to cigarette smoking. (orig.)

  8. Buccal Epithelium, Cigarette Smoking, and Lung Cancer: Review of the Literature.

    Saba, Raya; Halytskyy, Oleksandr; Saleem, Nasir; Oliff, Ira A

    2017-01-01

    Lung cancer is currently the leading cause of cancer-related mortality among men and women in the United States, and optimal screening methods are still lacking. The field effect is a well-supported phenomenon wherein a noxious stimulus triggers genetic, epigenetic and molecular changes that are widespread throughout the entire exposed organ system. The buccal epithelium is an easily accessible part of the respiratory tree that has good potential of yielding a surrogate marker for the field effect in cigarette smokers, and thus, a noninvasive, reliable lung cancer screening method. Herein, we review the literature on the relationship between the buccal epithelium, cigarette smoking, and lung cancer. © 2017 S. Karger AG, Basel.

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

    Archer, V.E.

    1985-01-01

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

  10. Influenza Virus-Induced Lung Inflammation Was Modulated by Cigarette Smoke Exposure in Mice

    Han, Yan; Ling, Man To; Mao, Huawei; Zheng, Jian; Liu, Ming; Lam, Kwok Tai; Liu, Yuan; Tu, Wenwei; Lau, Yu-Lung

    2014-01-01

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

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

    Yan Han

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

  12. The effects of electronic cigarette emissions on systemic cotinine levels, weight and postnatal lung growth in neonatal mice.

    Sharon A McGrath-Morrow

    Full Text Available Electronic cigarette (E-cigarettes emissions present a potentially new hazard to neonates through inhalation, dermal and oral contact. Exposure to nicotine containing E-cigarettes may cause significant systemic absorption in neonates due to the potential for multi-route exposure. Systemic absorption of nicotine and constituents of E-cigarette emissions may adversely impact weight and lung development in the neonate. To address these questions we exposed neonatal mice to E-cigarette emissions and measured systemic cotinine levels and alveolar lung growth.Neonatal mice were exposed to E-cigarettes for the first 10 days of life. E-cigarette cartridges contained either 1.8% nicotine in propylene glycol (PG or PG vehicle alone. Daily weights, plasma and urine cotinine levels and lung growth using the alveolar mean linear intercept (MLI method were measured at 10 days of life and compared to room air controls. Mice exposed to 1.8% nicotine/PG had a 13.3% decrease in total body weight compared to room air controls. Plasma cotinine levels were found to be elevated in neonatal mice exposed to 1.8% nicotine/PG E-cigarettes (mean 62.34± 3.3 ng/ml. After adjusting for sex and weight, the nicotine exposed mice were found to have modestly impaired lung growth by MLI compared to room air control mice (p<.054 trial 1; p<.006 trial 2. These studies indicate that exposure to E-cigarette emissions during the neonatal period can adversely impact weight gain. In addition exposure to nicotine containing E-cigarettes can cause detectable levels of systemic cotinine, diminished alveolar cell proliferation and a modest impairment in postnatal lung growth.

  13. The effects of electronic cigarette emissions on systemic cotinine levels, weight and postnatal lung growth in neonatal mice.

    McGrath-Morrow, Sharon A; Hayashi, Madoka; Aherrera, Angela; Lopez, Armando; Malinina, Alla; Collaco, Joseph M; Neptune, Enid; Klein, Jonathan D; Winickoff, Jonathan P; Breysse, Patrick; Lazarus, Philip; Chen, Gang

    2015-01-01

    Electronic cigarette (E-cigarettes) emissions present a potentially new hazard to neonates through inhalation, dermal and oral contact. Exposure to nicotine containing E-cigarettes may cause significant systemic absorption in neonates due to the potential for multi-route exposure. Systemic absorption of nicotine and constituents of E-cigarette emissions may adversely impact weight and lung development in the neonate. To address these questions we exposed neonatal mice to E-cigarette emissions and measured systemic cotinine levels and alveolar lung growth. Neonatal mice were exposed to E-cigarettes for the first 10 days of life. E-cigarette cartridges contained either 1.8% nicotine in propylene glycol (PG) or PG vehicle alone. Daily weights, plasma and urine cotinine levels and lung growth using the alveolar mean linear intercept (MLI) method were measured at 10 days of life and compared to room air controls. Mice exposed to 1.8% nicotine/PG had a 13.3% decrease in total body weight compared to room air controls. Plasma cotinine levels were found to be elevated in neonatal mice exposed to 1.8% nicotine/PG E-cigarettes (mean 62.34± 3.3 ng/ml). After adjusting for sex and weight, the nicotine exposed mice were found to have modestly impaired lung growth by MLI compared to room air control mice (pE-cigarette emissions during the neonatal period can adversely impact weight gain. In addition exposure to nicotine containing E-cigarettes can cause detectable levels of systemic cotinine, diminished alveolar cell proliferation and a modest impairment in postnatal lung growth.

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

    Priest, N.D.; Moores, S.R.; Black, A.; Talbot, R.; Morgan, A.

    1989-01-01

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

  15. The effect of cigarette smoking on neutrophil kinetics in human lungs [see comments

    MacNee, W.; Wiggs, B.; Belzberg, A.S.; Hogg, J.C.

    1989-01-01

    Neutrophils may play a part in the pathogenesis of the centrilobular emphysema associated with cigarette smoking. The capillary bed of the lungs concentrates neutrophils approximately 100-fold with respect to erythrocytes, producing a large pool of marginated cells. We examined the effect of cigarette smoking on the kinetics of this pool of cells, using 99mTc-labeled erythrocytes to measure regional blood velocity and 111In-labeled neutrophils to measure the removal of neutrophils during the first passage through the pulmonary circulation, their subsequent washout from the lungs, and the effect of local blood velocity on the number of neutrophils retained in each lung region. We observed no difference in these measurements between subjects who had never smoked (n = 6) and smokers who did not smoke during the study (n = 12). However, subjects who did smoke during the study (n = 12) had a significantly slower rate of washout of radiolabeled neutrophils from the lung (0.08 +/- 0.04 of the total per minute, as compared with 0.13 +/- 0.06 in smokers who did not smoke during the experiment and 0.14 +/- 0.08 in non-smokers) (P = 0.02). We also observed an increase in the regional retention of labeled neutrophils with respect to blood velocity in 5 of the 12 subjects who smoked during the study, but in none of the other subjects. We conclude that the presence of cigarette smoke in the lungs of some subjects increases the local concentration of neutrophils, and suggest that the lesions that characterize emphysema may be a result of the destruction of lung tissue by neutrophils that remain within pulmonary microvessels

  16. Inhaled tobacco sterols: uptake by the lungs and disposition to selected organs of rats

    Holden, W.E.; Maier, J.M.; Liebler, J.M.; Malinow, M.R.

    1988-01-01

    Tobacco sterols (cholesterol, beta-sitosterol, campesterol, and stigmasterol) are present in tobacco smoke and appear in plasma of mammals exposed to cigarette smoke. Because tobacco sterols may be important in the pathogenesis of smoking-induced lung and vascular diseases, we studied the pattern of deposition of cigarette sterols in the lungs and appearance of cigarette sterols in plasma and body organs of rats. After exposure to twenty 5 ml puffs of smoke from tobacco labeled with [4- 14 C]cholesterol or beta-[4- 14 C]sitosterol, rats were killed just after exposure (day 0) and on days 2, 5, 8, 11, 15, and 30, and the lungs and selected body organs analyzed for activity. We found that cigarette sterols are associated with particulates in cigarette smoke, deposited mostly in distal airspaces and parenchyma of the lungs, and appear in plasma and several body organs for more than 30 days after this single exposure to cigarette smoke. Bronchoalveolar lavage fluid contained relatively small amounts of radiolabel for only the first few days, suggesting that most of the sterols were rapidly incorporated in lung parenchyma. Because disorders of sterol metabolism have been implicated in a variety of diseases including atherosclerosis and cancer, the significance of tobacco sterols to human smoking-induced diseases deserves further study

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

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

    1987-01-01

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

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

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

    1987-01-01

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

  19. Lung cancer death rates among nonsmokers and pipe and cigarette smokers

    Stocks, P; Campbell, J M

    1955-01-01

    This report discusses a two-year comparison of deaths from lung cancer with environmental histories, including smoking and pollution character of residence, of British men aged 45 to 74. In rural areas, lung cancer increases almost linearly with smoking, the increment being 1 death per 1000 for each 13 cigarettes. Pipe smoking is about 1/3 as hazardous as cigarette-smoking. In mixed rural-urban areas, rates in light and moderate smokers were higher than rural but not so with pipe or heavy smokers. There was a higher death rate in every group in urban area, but rate of mortality increase with increasing cigarette exposure was greater for those living in rural areas. Urban/rural ratio was about 9 for nonsmokers decreasing to almost 1 for heavy smokers. Smoking contributes 1/2 of lung cancer in urban area; urban factor contributes 3/8 (absolute excess in every group). Benzopyrene concentration of urban area was 8 to 11 times that of rural areas and gradient corresponds to urban/rural ratio for nonsmokers. Benzopyrene/death correlation was good if assumed combined intake is considered.

  20. Dual role of beta-carotene in combination with cigarette smoke aqueous extract on the formation of mutagenic lipid peroxidation products in lung membranes: dependence on pO2.

    Palozza, P; Serini, S; Trombino, S; Lauriola, L; Ranelletti, F O; Calviello, G

    2006-12-01

    Results from some intervention trials indicated that supplemental beta-carotene enhanced lung cancer incidence and mortality in chronic smokers. The aim of this study was to verify the hypothesis that high concentrations of the carotenoid, under the pO2 present in lung (100-150 mmHg), may exert deleterious effects through a prooxidant mechanism. To test this hypothesis, we examined the interactions of beta-carotene and cigarette smoke condensate (tar) on the formation of lipid peroxidation products in rat lung microsomal membranes enriched in vitro with varying beta-carotene concentrations (from 1 to 10 nmol/mg prot) and then incubated with tar (6-25 microg/ml) under different pO2. As markers of lipid peroxidation, we evaluated the levels of conjugated dienes and malondialdehyde, possessing mutagenic and pro-carcinogenic activity. The exposure of microsomal membranes to tar induced a dose-dependent enhancement of lipid peroxidation, which progressively increased as a function of pO2. Under a low pO2 (15 mmHg), beta-carotene acted clearly as an antioxidant, inhibiting tar-induced lipid peroxidation. However, the carotenoid progressively lost its antioxidant efficiency by increasing pO2 (50-100 mmHg) and acted as a prooxidant at pO2 ranging from 100 to 760 mmHg in a dose-dependent manner. Consistent with this finding, the addition of alpha-tocopherol (25 microM) prevented the prooxidant effects of the carotenoid. beta-Carotene auto-oxidation, measured as formation of 5,6-epoxy-beta,beta-carotene, was faster at high than at low pO2 and the carotenoid was more rapidly consumed in the presence of tar. These data point out that the carotenoid may enhance cigarette smoke-induced oxidative stress and exert potential deleterious effects at the pO2 normally present in lung tissue.

  1. Cigarette smoke regulates VEGFR2-mediated survival signaling in rat lungs

    Stevenson Christopher S

    2010-02-01

    Full Text Available Abstract Background Vascular endothelial growth factor (VEGF and VEGF receptor 2 (VEGFR2-mediated survival signaling is critical to endothelial cell survival, maintenance of the vasculature and alveolar structure and regeneration of lung tissue. Reduced VEGF and VEGFR2 expression in emphysematous lungs has been linked to increased endothelial cell death and vascular regression. Previously, we have shown that CS down-regulated the VEGFR2 and its downstream signaling in mouse lungs. However, the VEGFR2-mediated survival signaling in response to oxidants/cigarette smoke (CS is not known. We hypothesized that CS exposure leads to disruption of VEGFR2-mediated endothelial survival signaling in rat lungs. Methods Adult male Sprague-Dawley rats were exposed CS for 3 days, 8 weeks and 6 months to investigate the effect of CS on VEGFR2-mediated survival signaling by measuring the Akt/PI3-kinase/eNOS downstream signaling in rat lungs. Results and Discussion We show that CS disrupts VEGFR2/PI3-kinase association leading to decreased Akt and eNOS phosphorylation. This may further alter the phosphorylation of the pro-apoptotic protein Bad and increase the Bad/Bcl-xl association. However, this was not associated with a significant lung cell death as evidenced by active caspase-3 levels. These data suggest that although CS altered the VEGFR2-mediated survival signaling in the rat lungs, but it was not sufficient to cause lung cell death. Conclusion The rat lungs exposed to CS in acute, sub-chronic and chronic levels may be representative of smokers where survival signaling is altered but was not associated with lung cell death whereas emphysema is known to be associated with lung cell apoptosis.

  2. Cigarette smoking and lung cancer: a continuing controversy.

    Burch, P R

    1982-09-01

    During the late 1950s Sir Ronald Fisher questioned the already popular, but in his view precipitate, causal interpretation of the association between smoking and lung cancer. His pungently expressed views began a controversy that has smouldered and sometimes flared ever since. The most recent attack on Fisher's constitutional hypothesis was launched by Reif and in this paper I consider the validity of his criticisms. A range of evidence shows that it is not yet possible to distinguish between constitutional and causal-plus-constitutional interpretations although recent studies indicate that a pure causal hypothesis is incapable of explaining the full association as observed in Western populations. Unfortunately, errors of diagnosis and death certification still impede the rigorous testing of adequately formulated hypotheses.

  3. E-cigarette smoke damages DNA and reduces repair activity in mouse lung, heart, and bladder as well as in human lung and bladder cells

    Lee, Hyun-Wook; Park, Sung-Hyun; Weng, Mao-wen; Wang, Hsiang-Tsui; Huang, William C.; Lepor, Herbert; Wu, Xue-Ru; Chen, Lung-Chi; Tang, Moon-shong

    2018-01-01

    Significance E-cigarette smoke (ECS) delivers nicotine through aerosols without burning tobacco. ECS is promoted as noncarcinogenic. We found that ECS induces DNA damage in mouse lung, bladder, and heart and reduces DNA-repair functions and proteins in lung. Nicotine and its nitrosation product 4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone can cause the same effects as ECS and enhance mutations and tumorigenic cell transformation in cultured human lung and bladder cells. These results indica...

  4. Lung Deposition Analyses of Inhaled Toxic Aerosols in Conventional and Less Harmful Cigarette Smoke: A Review

    Yu Feng

    2013-09-01

    Full Text Available Inhaled toxic aerosols of conventional cigarette smoke may impact not only the health of smokers, but also those exposed to second-stream smoke, especially children. Thus, less harmful cigarettes (LHCs, also called potential reduced exposure products (PREPs, or modified risk tobacco products (MRTP have been designed by tobacco manufacturers to focus on the reduction of the concentration of carcinogenic components and toxicants in tobacco. However, some studies have pointed out that the new cigarette products may be actually more harmful than the conventional ones due to variations in puffing or post-puffing behavior, different physical and chemical characteristics of inhaled toxic aerosols, and longer exposure conditions. In order to understand the toxicological impact of tobacco smoke, it is essential for scientists, engineers and manufacturers to develop experiments, clinical investigations, and predictive numerical models for tracking the intake and deposition of toxicants of both LHCs and conventional cigarettes. Furthermore, to link inhaled toxicants to lung and other diseases, it is necessary to determine the physical mechanisms and parameters that have significant impacts on droplet/vapor transport and deposition. Complex mechanisms include droplet coagulation, hygroscopic growth, condensation and evaporation, vapor formation and changes in composition. Of interest are also different puffing behavior, smoke inlet conditions, subject geometries, and mass transfer of deposited material into systemic regions. This review article is intended to serve as an overview of contributions mainly published between 2009 and 2013, focusing on the potential health risks of toxicants in cigarette smoke, progress made in different approaches of impact analyses for inhaled toxic aerosols, as well as challenges and future directions.

  5. Intratracheal transplantation of endothelial progenitor cells attenuates smoking-induced COPD in mice

    Shi Z

    2017-03-01

    Full Text Available Zhihui Shi,1 Yan Chen,1 Jun Cao,2 Huihui Zeng,1 Yue Yang,1 Ping Chen,1 Hong Luo,1 Hong Peng,1 Shan Cai,1 Chaxiang Guan3 1Department of Internal Medicine, Division of Respiratory Disease, The Second Xiangya Hospital, Central-South University, 2Department of Internal Medicine, Division of Respiratory Disease, The People’s Hospital of Hunan Province, 3Department of Physiology, Xiangya Medical School, Central-South University, Changsha, Hunan, People’s Republic of China Background: Endothelial progenitor cells (EPCs might play a protective role in COPD. The aim of this study was to investigate whether intratracheal allogeneic transplantation of bone-marrow-derived EPCs would attenuate the development of smoking-induced COPD in mice.Methods: Isolated mononuclear cells from the bone marrow of C57BL/6J mice were cultured in endothelial cell growth medium-2 for 10 days, yielding EPCs. A murine model of COPD was established by passive 90-day exposure of cigarette smoke. On day 30, EPCs or phosphate-buffered saline alone was administered into the trachea. On day 90, EPCs or 30 µL phosphate-buffered saline alone was administered into the trachea, and on day 120, inflammatory cells, antioxidant activity, apoptosis, matrix metalloproteinase (MMP-2, and MMP-9 were measured.Results: After EPC treatment, the lung function of the mice had improved compared with the untreated mice. Mean linear intercept and destructive index were reduced in the EPCs-treated group compared with the untreated group. In addition, the EPCs-treated mice exhibited less antioxidant activity in bronchoalveolar lavage fluid compared with the untreated mice. Moreover, decreased activities of MMP-2, MMP-9, and TUNEL-positive cells in lung tissues were detected in EPCs-treated mice.Conclusion: Intratracheal transplantation of EPCs attenuated the development of pulmonary emphysema and lung function disorder probably by alleviating inflammatory infiltration, decelerating apoptosis

  6. Ascorbate attenuates pulmonary emphysema by inhibiting tobacco smoke and Rtp801-triggered lung protein modification and proteolysis.

    Gupta, Indranil; Ganguly, Souradipta; Rozanas, Christine R; Stuehr, Dennis J; Panda, Koustubh

    2016-07-19

    Cigarette smoking causes emphysema, a fatal disease involving extensive structural and functional damage of the lung. Using a guinea pig model and human lung cells, we show that oxidant(s) present in tobacco smoke not only cause direct oxidative damage of lung proteins, contributing to the major share of lung injury, but also activate Rtp801, a key proinflammatory cellular factor involved in tobacco smoke-induced lung damage. Rtp801 triggers nuclear factor κB and consequent inducible NOS (iNOS)-mediated overproduction of NO, which in combination with excess superoxide produced during Rtp801 activation, contribute to increased oxido-nitrosative stress and lung protein nitration. However, lung-specific inhibition of iNOS with a iNOS-specific inhibitor, N6-(1-iminoethyl)-L-lysine, dihydrochloride (L-NIL) solely restricts lung protein nitration but fails to prevent or reverse the major tobacco smoke-induced oxidative lung injury. In comparison, the dietary antioxidant, ascorbate or vitamin C, can substantially prevent such damage by inhibiting both tobacco smoke-induced lung protein oxidation as well as activation of pulmonary Rtp801 and consequent iNOS/NO-induced nitration of lung proteins, that otherwise lead to increased proteolysis of such oxidized or nitrated proteins by endogenous lung proteases, resulting in emphysematous lung damage. Vitamin C also restricts the up-regulation of matrix-metalloproteinase-9, the major lung protease involved in the proteolysis of such modified lung proteins during tobacco smoke-induced emphysema. Overall, our findings implicate tobacco-smoke oxidant(s) as the primary etiopathogenic factor behind both the noncellular and cellular damage mechanisms governing emphysematous lung injury and demonstrate the potential of vitamin C to accomplish holistic prevention of such damage.

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

    Hellstern, K.; Curtis, C.G.; Powell, G.M.; Upshall, D.G.

    1990-01-01

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

  8. Feasibility and acceptability of e-cigarettes as an aid to quitting smoking among lung cancer patients: a pilot study

    Allison Ford

    2018-03-01

    Full Text Available Background Many patients diagnosed with lung cancer continue to smoke even though this can make their treatment less effective and increase side effects. E-cigarettes form part of the UK's tobacco harm reduction policy landscape and are, by far, smokers' most popular quit attempt method. This pilot study explores feasibility and acceptability of e-cigarettes to aid smoking cessation among lung cancer patients undergoing chemotherapy. Methods 27 smokers with stage IV lung cancer were recruited from one NHS site in Scotland between May-16 and June-17. They were provided with a 2 nd generation e-cigarette kit at a baseline home visit conducted by a researcher and a volunteer who was an experienced e-cigarette user. Participants were followed-up weekly for four weeks and at 16 weeks. Participants´ response to, and use of, e-cigarettes was explored along with cessation outcomes (self-reported and CO verified. In-depth qualitative interviews were conducted with health professionals (n=8 engaged with lung cancer patients to obtain their views on the study. Results Overall, participants were motivated to stop smoking and took easily to using e-cigarettes. Minor issues arose around choice of flavour, and some side effects were noted, although participants reported difficulty in distinguishing these from treatment side effects. Seven participants were lost to follow-up. Preliminary findings show that at 4-week follow-up: average CO reading had reduced from 14 (range 3-37 to 8 (range 1-29, and 70% of participants reported daily e-cigarette use, however, use was dependent on individuals' day-to-day health. Health professionals interviewed were generally supportive of e-cigarettes as a tool for quitting, and suggested future efforts should concentrate on patients with curable cancer. Conclusions E-cigarettes have a potential role to play for lung cancer patients. Future smoking cessation research should take account of the impact of cancer treatment on

  9. Systematic review of the epidemiological evidence comparing lung cancer risk in smokers of mentholated and unmentholated cigarettes

    Lee Peter N

    2011-04-01

    Full Text Available Abstract Background US mentholated cigarette sales have increased considerably over 50 years. Preference for mentholated cigarettes is markedly higher in Black people. While menthol itself is not genotoxic or carcinogenic, its acute respiratory effects might affect inhalation of cigarette smoke. This possibility seems consistent with the higher lung cancer risk in Black men, despite Black people smoking less and starting smoking later than White people. Despite experimental data suggesting similar carcinogenicity of mentholated and non-mentholated cigarettes, the lack of convincing evidence that mentholation increases puffing, inhalation or smoke uptake, and the similarity of lung cancer rates in Black and White females, a review of cigarette mentholation and lung cancer is timely given current regulatory interest in the topic. Methods Epidemiological studies comparing lung cancer risk in mentholated and non-mentholated cigarette smokers were identified from MedLine and other sources. Study details were extracted and strengths and weaknesses assessed. Relative risk estimates were extracted, or derived, for ever mentholated use and for long-term use, overall and by gender, race, and current/ever smoking, and meta-analyses conducted. Results Eight generally good quality studies were identified, with valid cases and controls, and appropriate adjustment for age, gender, race and smoking. The studies afforded good power to detect possible effects. However, only one study presented results by histological type, none adjusted for occupation or diet, and some provided no results by length of mentholated cigarette use. The data do not suggest any effect of mentholation on lung cancer risk. Adjusted relative risk estimates for ever use vary from 0.81 to 1.12, giving a combined estimate of 0.93 (95% confidence interval 0.84-1.02, n = 8, with no increase in males (1.01, 0.84-1.22, n = 5, females (0.80, 0.67-0.95, n = 5, White people (0.87, 0.75-1.03, n = 4

  10. Systematic review of the epidemiological evidence comparing lung cancer risk in smokers of mentholated and unmentholated cigarettes

    2011-01-01

    Background US mentholated cigarette sales have increased considerably over 50 years. Preference for mentholated cigarettes is markedly higher in Black people. While menthol itself is not genotoxic or carcinogenic, its acute respiratory effects might affect inhalation of cigarette smoke. This possibility seems consistent with the higher lung cancer risk in Black men, despite Black people smoking less and starting smoking later than White people. Despite experimental data suggesting similar carcinogenicity of mentholated and non-mentholated cigarettes, the lack of convincing evidence that mentholation increases puffing, inhalation or smoke uptake, and the similarity of lung cancer rates in Black and White females, a review of cigarette mentholation and lung cancer is timely given current regulatory interest in the topic. Methods Epidemiological studies comparing lung cancer risk in mentholated and non-mentholated cigarette smokers were identified from MedLine and other sources. Study details were extracted and strengths and weaknesses assessed. Relative risk estimates were extracted, or derived, for ever mentholated use and for long-term use, overall and by gender, race, and current/ever smoking, and meta-analyses conducted. Results Eight generally good quality studies were identified, with valid cases and controls, and appropriate adjustment for age, gender, race and smoking. The studies afforded good power to detect possible effects. However, only one study presented results by histological type, none adjusted for occupation or diet, and some provided no results by length of mentholated cigarette use. The data do not suggest any effect of mentholation on lung cancer risk. Adjusted relative risk estimates for ever use vary from 0.81 to 1.12, giving a combined estimate of 0.93 (95% confidence interval 0.84-1.02, n = 8), with no increase in males (1.01, 0.84-1.22, n = 5), females (0.80, 0.67-0.95, n = 5), White people (0.87, 0.75-1.03, n = 4) or Black people (0.90, 0

  11. Simvastatin inhibits smoke-induced airway epithelial injury: implications for COPD therapy.

    Davis, Benjamin B; Zeki, Amir A; Bratt, Jennifer M; Wang, Lei; Filosto, Simone; Walby, William F; Kenyon, Nicholas J; Goldkorn, Tzipora; Schelegle, Edward S; Pinkerton, Kent E

    2013-08-01

    Chronic obstructive pulmonary disease (COPD) is the third leading cause of death. The statin drugs may have therapeutic potential in respiratory diseases such as COPD, but whether they prevent bronchial epithelial injury is unknown. We hypothesised that simvastatin attenuates acute tobacco smoke-induced neutrophilic lung inflammation and airway epithelial injury. Spontaneously hypertensive rats were given simvastatin (20 mg·kg(-1) i.p.) daily for either 7 days prior to tobacco smoke exposure and during 3 days of smoke exposure, or only during tobacco smoke exposure. Pretreatment with simvastatin prior to and continued throughout smoke exposure reduced the total influx of leukocytes, neutrophils and macrophages into the lung and airways. Simvastatin attenuated tobacco smoke-induced cellular infiltration into lung parenchymal and airway subepithelial and interstitial spaces. 1 week of simvastatin pretreatment almost completely prevented smoke-induced denudation of the airway epithelial layer, while simvastatin given only concurrently with the smoke exposure had no effect. Simvastatin may be a novel adjunctive therapy for smoke-induced lung diseases, such as COPD. Given the need for statin pretreatment there may be a critical process of conditioning that is necessary for statins' anti-inflammatory effects. Future work is needed to elucidate the mechanisms of this statin protective effect.

  12. The Role of Nicotine in the Effects of Maternal Smoking during Pregnancy on Lung Development and Childhood Respiratory Disease. Implications for Dangers of E-Cigarettes.

    Spindel, Eliot R; McEvoy, Cindy T

    2016-03-01

    Use of e-cigarettes, especially among the young, is increasing at near-exponential rates. This is coupled with a perception that e-cigarettes are safe and with unlimited advertising geared toward vulnerable populations, the groups most likely to smoke or vape during pregnancy. There is now wide appreciation of the dangers of maternal smoking during pregnancy and the lifelong consequences this has on offspring lung function, including the increased risk of childhood wheezing and subsequent asthma. Recent evidence strongly supports that much of the effect of smoking during pregnancy on offspring lung function is mediated by nicotine, making it highly likely that e-cigarette use during pregnancy will have the same harmful effects on offspring lung function and health as do conventional cigarettes. In fact, the evidence for nicotine being the mediator of harm of conventional cigarettes may be most compelling for its effects on lung development. This raises concerns about both the combined use of e-cigarettes plus conventional cigarettes by smokers during pregnancy as well as the use of e-cigarettes by e-cigarette-only users who think them safe or by those sufficiently addicted to nicotine to not be able to quit e-cigarette usage during pregnancy. Thus, it is important for health professionals to be aware of the risks of e-cigarette usage during pregnancy, particularly as it pertains to offspring respiratory health.

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

    Yi Eunhee S

    2010-04-01

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

  14. Cigarette smoke exposure inhibits extracellular MMP-2 (gelatinase A activity in human lung fibroblasts

    Cappello Francesco

    2007-03-01

    Full Text Available Abstract Background Exposure to cigarette smoke is considered a major risk factor for the development of lung diseases, since its causative role has been assessed in the induction and maintenance of an inflamed state in the airways. Lung fibroblasts can contribute to these processes, due to their ability to produce proinflammatory chemotactic molecules and extracellular matrix remodelling proteinases. Among proteolytic enzymes, gelatinases A and B have been studied for their role in tissue breakdown and mobilisation of matrix-derived signalling molecules. Multiple reports linked gelatinase deregulation and overexpression to the development of inflammatory chronic lung diseases such as COPD. Methods In this study we aimed to determine variations in the gelatinolytic pattern of human lung fibroblasts (HFL-1 cell line exposed to cigarette smoke extract (CSE. Gelatinolytic activity levels were determined by using gelatin zymography for the in-gel detection of the enzymes (proenzyme and activated forms, and the subsequent semi-quantitative densitometric evaluation of lytic bands. Expression of gelatinases was evaluated also by RT-PCR, zymography of the cell lysates and by western blotting. Results CSE exposure at the doses used (1–10% did not exert any significant cytotoxic effects on fibroblasts. Zymographic analysis showed that CSE exposure resulted in a linear decrease of the activity of gelatinase A. Control experiments allowed excluding a direct inhibitory effect of CSE on gelatinases. Zymography of cell lysates confirmed the expression of MMP-2 in all conditions. Semi-quantitative evaluation of mRNA expression allowed assessing a reduced transcription of the enzyme, as well as an increase in the expression of TIMP-2. Statistical analyses showed that the decrease of MMP-2 activity in conditioned media reached the statistical significance (p = 0.0031 for 24 h and p = 0.0012 for 48 h, while correlation analysis showed that this result was

  15. [Elevated expression of endothelin 2 in lung tissues of asthmatic rats after exposed to cigarette smoke and its mechanism].

    Han, Fangfang; Zhu, Shuyang; Chen, Bi; Li, Jingjing

    2017-08-01

    Objective To study the effect of cigarette smoke exposure on the expression of endothelin 2 (ET-2) in bronchial epithelium of asthmatic rats. Methods Asthma models were established through intraperitoneal injection of 1 mL chicken ovalbumin (OVA)/Al(OH) 3 mixture (asthma model group, n=6); based on the asthma models, exposure to smoking gas lasted four weeks with 10 cigarettes per day (smoke-exposed asthma group, n=6); based on the smoke-exposed asthma models, the rats were treated with intraperitoneal injection of dexamethasone 2 mg/(kg.d), intragastric administration of ET receptor inhibitor bosentan 100 mg/(kg.d) and combined use, respectively named dexamethasone treated group, bosentan treated group, and dexamethasone-bosentan treated group, 6 rats in every group. What's more, other 6 rats were only subjected to intraperitoneal injection of 1 mL normal saline as normal controls; in addition to the injection of saline, cigarette smoke control group (n=6) was set up by the exposure to smoking gas for four weeks with 10 cigarettes per day. Bronchoalveolar lavage fluid (BALF) was collected from the upper lobe of the left lung for cell counting and classification. Pathological changes of the right upper lung lobe tissues were observed by HE staining. In other lung tissues, the expression of JNK1/2 was detected by Western blotting; ET-2 was tested by Western blotting and immunohistochemistry; thiobarbituric acid reactive substances (TBARS) assay and trace enzyme standard method were used to measure malondialdehyde (MDA) and glutathione (GSH), respectively. Results Compared with normal control group, the number of airway inflammation cells increased in the BALF, and the expressions of ET-2, JNK1/2, MDA and GSH increased in the lung tissues of cigarette smoke control group, asthma model group and cigarette smoke-exposed asthma group. Compared with cigarette smoke-exposed asthma group, the number of airway inflammation cells decreased in the BALF, and the expressions of

  16. Oxidative damage induced by cigarette smoke exposure in mice: impact on lung tissue and diaphragm muscle,

    Samanta Portão de Carlos

    2014-08-01

    Full Text Available OBJECTIVE: To evaluate oxidative damage (lipid oxidation, protein oxidation, thiobarbituric acid-reactive substances [TBARS], and carbonylation and inflammation (expression of phosphorylated AMP-activated protein kinase and mammalian target of rapamycin [p-AMPK and p-mTOR, respectively] in the lung parenchyma and diaphragm muscles of male C57BL-6 mice exposed to cigarette smoke (CS for 7, 15, 30, 45, or 60 days. METHODS: Thirty-six male C57BL-6 mice were divided into six groups (n = 6/group: a control group; and five groups exposed to CS for 7, 15, 30, 45, and 60 days, respectively. RESULTS: Compared with control mice, CS-exposed mice presented lower body weights at 30 days. In CS-exposed mice (compared with control mice, the greatest differences (increases in TBARS levels were observed on day 7 in diaphragm-muscle, compared with day 45 in lung tissue; the greatest differences (increases in carbonyl levels were observed on day 7 in both tissue types; and sulfhydryl levels were lower, in both tissue types, at all time points. In lung tissue and diaphragm muscle, p-AMPK expression exhibited behavior similar to that of TBARS. Expression of p-mTOR was higher than the control value on days 7 and 15 in lung tissue, as it was on day 45 in diaphragm muscle. CONCLUSION: Our data demonstrate that CS exposure produces oxidative damage, not only in lung tissue but also (primarily in muscle tissue, having an additional effect on respiratory muscle, as is frequently observed in smokers with COPD.

  17. Double-hit mouse model of cigarette smoke priming for acute lung injury.

    Sakhatskyy, Pavlo; Wang, Zhengke; Borgas, Diana; Lomas-Neira, Joanne; Chen, Yaping; Ayala, Alfred; Rounds, Sharon; Lu, Qing

    2017-01-01

    Epidemiological studies indicate that cigarette smoking (CS) increases the risk and severity of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). The mechanism is not understood, at least in part because of lack of animal models that reproduce the key features of the CS priming process. In this study, using two strains of mice, we characterized a double-hit mouse model of ALI induced by CS priming of injury caused by lipopolysaccharide (LPS). C57BL/6 and AKR mice were preexposed to CS briefly (3 h) or subacutely (3 wk) before intratracheal instillation of LPS and ALI was assessed 18 h after LPS administration by measuring lung static compliance, lung edema, vascular permeability, inflammation, and alveolar apoptosis. We found that as little as 3 h of exposure to CS enhanced LPS-induced ALI in both strains of mice. Similar exacerbating effects were observed after 3 wk of preexposure to CS. However, there was a strain difference in susceptibility to CS priming for ALI, with a greater effect in AKR mice. The key features we observed suggest that 3 wk of CS preexposure of AKR mice is a reproducible, clinically relevant animal model that is useful for studying mechanisms and treatment of CS priming for a second-hit-induced ALI. Our data also support the concept that increased susceptibility to ALI/ARDS is an important adverse health consequence of CS exposure that needs to be taken into consideration when treating critically ill individuals.

  18. Cigarette smoking and federal black lung benefits in bituminous coal miners.

    Roy, T M; Collins, L C; Snider, H L; Anderson, W H

    1989-02-01

    The records of 1000 consecutive coal miners applying for benefits under the Federal Coal Mine Health and Safety Act were examined to determine the contribution of age, dust accumulation, and cigarette smoking to the profile of the miner who satisfies the current pulmonary criteria for disability. Using the presence of pneumoconiosis on chest radiograph as the indication of significant coal dust accumulation, the miners were separated into Group A--those without pneumoconiosis (n = 316) and Group B--those with pneumoconiosis (n = 684). The federal spirometric criteria for disability identified 55/316 miners in Group A (14.5%) and 99/684 miners in Group B (17.4%) potentially eligible for an award (P = .27). The mean ages of miners in both groups did not differ significantly, nor was there difference in the mean ages of groups that did or did not meet the federal criteria. In both groups, those miners potentially eligible for a financial award smoked more cigarettes than did their counterparts (Group A, 31.0 v 18.5 pack-years, P less than .001; Group B, 31.3 v 23.6 pack-years, P less than .001). There was no difference in the smoking histories of the miners from either group who met the federal criteria. Our data indicate that, in the case of bituminous coal miners, the present federal legislation intended to identify and remunerate those who suffer lung impairment from chronic occupational exposure to coal dust is biased in favor of those who sustain additional damage to their ventilatory capacity by smoking cigarettes.

  19. Carbon monoxide is not responsible for the cigarette smokeinduced changes in the pulmonary metabolism of arachidonic acid and prostaglandin E2

    Maennistoe, J.; Puustinen, T.; Uotila, P.

    1985-01-01

    Cigarette smoke is known to interfere with the pulmonary metabolism of arachidomic acid and prostaglandin E 2 (PGE 2 ). We investigated the possible role of carbon monoxide in these cigarette smoke-infuced alterations. 4 C-Arachidonic acid (50 nmol) was indused into the pulmonary circulation of isolated perfused hamster lungs and the radioactive metabolites in the perfusion effluent, as well as the distribution of incorporated radioactive arachidonic acid within the lung lipids, were analysed. Carbon monoxide, added into the ventilatory air, had no effect on the oxidative metabolism of arachidonic acid or on the distribution of radioactive arachidonic acid within the lung. In addition, carbon monoxide had no effect on the metabolism of PGE 2 following infusion of 100 nmol of 14 C-PGE 2 into the rat pulmonary circulation. The present study suggests that carbon monoxide is not responsible for the cigarette smoke-induced changes in the pulmonary metabolism of arachidonic acid and PGE 2 . (author)

  20. Benfotiamine Counteracts Smoking-Induced Vascular Dysfunction in Healthy Smokers

    Alin Stirban

    2012-01-01

    Full Text Available Background. Smoking induces endothelial dysfunction (ED mainly by exacerbating oxidative stress (OS and inflammation. Benfotiamine, a thiamine prodrug with high bioavailability, prevents nicotine-induced vascular dysfunction in rats. It remained unknown whether this effect also occurs in humans. Methods. Therefore, 20 healthy volunteers (mean age: 38 years were investigated twice, 7–10 days apart in a randomized, cross-over, and investigator-blinded design. Vascular function was assessed by flow-mediated vasodilatation (FMD of the brachial artery and by measurements of the soluble vascular cell adhesion molecule (sVCAM-1. Investigations were performed after an overnight fast as well as 20 minutes after one cigarette smoking. On another day, the same procedure was applied following a 3-day oral therapy with benfotiamine (1050 mg/day. Ten patients were randomized to start with smoking alone, and ten started with benfotiamine. Results. Results are expressed as (mean ± SEM. Smoking acutely induced a decrease in FMD by 50% (∗∗P<0.001 versus baseline an effect significantly reduced by benfotiamine treatment to 25%∗§ (∗P<0.05 versus baseline, §P<0.05 versus smoking alone. Smoking-induced elevation in sVCAM-1 was also prevented by benfotiamine. The endothelium-independent vasodilatation remained unaltered between days. Conclusion. In healthy volunteers, smoking blunts vascular function mirrored by a decrease in FMD and an increase in sVCAM-1. Short-term treatment with benfotiamine significantly reduces these effects, showing protective vascular properties.

  1. Cigarette use and the estimation of lung cancer attributable to radon in the United States

    Lubin, J.H.; Steindorf, K.

    1995-01-01

    Residential exposure to radioactive radon and its decay products has been estimated to account for 10-12% of all lung cancer deaths in the US. It has been difficult to evaluate fully the impact of cigarette smoking, the most important cause of lung cancer, on this estimate, because factors for patterns of tobacco use have not been included in the risk models, since risk models are derived from studies of underground miners exposed to radon and detailed data on smoking are limited. Lung cancer risk estimates for exposure to radon progeny in smoker and non-smoker populations are obtained by applying the same risk model to each population group, thereby assuming the joint effects of smoking and exposure to radon progeny are multiplicative. However, in miners, joint relative risks (RR) for the two exposures are most consistent with an intermediate relationship between multiplicative and additive, so that the present approach likely results in an overestimate of risk in smokers and an underestimate of risk in nonsmokers. One approach for adjusting risk models to incorporate smoking status is based on the relative magnitude of the effects of radon progeny in smokers and nonsmokers and therefore may not be applicable to non-miner populations if the proportion of smokers and the RR for smoking differ. We show that the modification can be derived explicitly by assuming an arithmetic mixture model for the joint RR for smoking and exposure to radon progeny. In this way, smoking parameters in the population of interest (the proportion of smokers and the RR of smoking) can be used directly to adjust radon progeny risk models and obtain risk estimates that are specific for smokers and nonsmokers. With an intermediate RR relationship for smoking and radon progeny, the attributable percentage of lung cancer deaths from residential radon may be twofold greater in nonsmokers than in smokers. 20 refs., 1 fig., 3 tabs

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

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

    2016-01-01

    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. PMID:21649527

  3. Exercise Inhibits the Effects of Smoke-Induced COPD Involving Modulation of STAT3

    Maysa Alves Rodrigues Brandao-Rangel

    2017-01-01

    Full Text Available Purpose. Evaluate the participation of STAT3 in the effects of aerobic exercise (AE in a model of smoke-induced COPD. Methods. C57Bl/6 male mice were divided into control, Exe, COPD, and COPD+Exe groups. Smoke were administered during 90 days. Treadmill aerobic training begun on day 61 until day 90. Pulmonary inflammation, systemic inflammation, the level of lung emphysema, and the airway remodeling were evaluated. Analysis of integral and phosphorylated expression of STAT3 by airway epithelial cells, peribronchial leukocytes, and parenchymal leukocytes was performed. Results. AE inhibited smoke-induced accumulation of total cells (p<0.001, lymphocytes (p<0.001, and neutrophils (p<0.001 in BAL, as well as BAL levels of IL-1β (p<0.001, CXCL1 (p<0.001, IL-17 (p<0.001, and TNF-α (p<0.05, while increased the levels of IL-10 (p<0.001. AE also inhibited smoke-induced increases in total leukocytes (p<0.001, neutrophils (p<0.05, lymphocytes (p<0.001, and monocytes (p<0.01 in blood, as well as serum levels of IL-1β (p<0.01, CXCL1 (p<0.01, IL-17 (p<0.05, and TNF-α (p<0.01, while increased the levels of IL-10 (p<0.001. AE reduced smoke-induced emphysema (p<0.001 and collagen fiber accumulation in the airways (p<0.001. AE reduced smoke-induced STAT3 and phospho-STAT3 expression in airway epithelial cells (p<0.001, peribronchial leukocytes (p<0.001, and parenchymal leukocytes (p<0.001. Conclusions. AE reduces smoke-induced COPD phenotype involving STAT3.

  4. Waterpipe smoking induces epigenetic changes in the small airway epithelium.

    Matthew S Walters

    Full Text Available Waterpipe (also called hookah, shisha, or narghile smoking is a common form of tobacco use in the Middle East. Its use is becoming more prevalent in Western societies, especially among young adults as an alternative form of tobacco use to traditional cigarettes. While the risk to cigarette smoking is well documented, the risk to waterpipe smoking is not well defined with limited information on its health impact at the epidemiologic, clinical and biologic levels with respect to lung disease. Based on the knowledge that airway epithelial cell DNA methylation is modified in response to cigarette smoke and in cigarette smoking-related lung diseases, we assessed the impact of light-use waterpipe smoking on DNA methylation of the small airway epithelium (SAE and whether changes in methylation were linked to the transcriptional output of the cells. Small airway epithelium was obtained from 7 nonsmokers and 7 light-use (2.6 ± 1.7 sessions/wk waterpipe-only smokers. Genome-wide comparison of SAE DNA methylation of waterpipe smokers to nonsmokers identified 727 probesets differentially methylated (fold-change >1.5, p<0.05 representing 673 unique genes. Dominant pathways associated with these epigenetic changes include those linked to G-protein coupled receptor signaling, aryl hydrocarbon receptor signaling and xenobiotic metabolism signaling, all of which have been associated with cigarette smoking and lung disease. Of the genes differentially methylated, 11.3% exhibited a corresponding significant (p<0.05 change in gene expression with enrichment in pathways related to regulation of mRNA translation and protein synthesis (eIF2 signaling and regulation of eIF4 and p70S6K signaling. Overall, these data demonstrate that light-use waterpipe smoking is associated with epigenetic changes and related transcriptional modifications in the SAE, the cell population demonstrating the earliest pathologic abnormalities associated with chronic cigarette smoking.

  5. Relationship of radioactive radon daughters and cigarette smoking in the genesis of lung cancer in uranium miners

    Saccomanno, G.; Huth, G.C.; Auerbach, O.; Kuschner, M.

    1988-01-01

    This article documents the study of 383 cases of lung cancer in uranium miners and presents for the first time the relationship of radioactive radon gas and cigarette smoking. There is evidence that alpha radiation from radon gas at exposure levels above 465 working level months (WLM) is a strong contributor to the development of lung cancer. Cigarette smoking plays the most significant role in causing lung tumor; this is also noticed in nonminers who smoke cigarettes. A synergistic or additive effect of these two carcinogens is strongly suggested. The data indicate that small cell tumors develop in younger nonsmoking miners exposed to radon levels above 465 WLM. Lung cancers develop in smoking miners at lower levels of radon exposure than in nonsmoking miners. Based on an average mining experience of 15 years, there is substantial evidence that the present maximum allowable limit of 0.3 working levels (WL), or 4 working level months (WLM) per year, is safe, representing a margin of safety of approximately 10:1. Furthermore, a comparison of these data with the radon levels in some homes, averaging in the neighborhood of 0.025 WL, would indicate that health risks at these levels are negligible. It is suggested that 20 picocuries/liter, which equals 0.10 WL, be the maximum allowable level in homes

  6. Knockdown of versican 1 blocks cigarette-induced loss of insoluble elastin in human lung fibroblasts.

    Xu, Lu-lu; Lu, Yun-tao; Zhang, Jing; Wu, Lian; Merrilees, Mervyn J; Qu, Jie-ming

    2015-08-15

    COPD lung is characterized by loss of alveolar elastic fibers and an increase in the chondroitin sulfate (CS) matrix proteoglycan versican V1 (V1). V1 is a known inhibitor of elastic fiber deposition and this study investigates the effects of knockdown of V1, and add-back of CS, on CCL-210 lung fibroblasts treated with cigarette smoke extract (CSE) as a model for COPD. CSE inhibited fibroblast proliferation, viability, tropoelastin synthesis, and elastin deposition, and increased V1 synthesis and secretion. V1 siRNA decreased V1 and constituent CS, did not affect tropoelastin production, but blocked the CSE-induced loss in insoluble elastin. Exogenous CS reduced insoluble elastin, even in the presence of V1 siRNA. These findings confirm that V1 and CS impair the assembly of tropoelastin monomers into insoluble fibers, and further demonstrate that specific knockdown of V1 alleviates the impaired assembly of elastin seen in cultures of pulmonary fibroblasts exposed to CSE, indicating a regulatory role for this protein in the pathophysiology of COPD. Copyright © 2015 Elsevier B.V. All rights reserved.

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

    Coyle Anthony J

    2011-04-01

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

  8. Gene and metabolite time-course response to cigarette smoking in mouse lung and plasma.

    Mikaela A Miller

    Full Text Available Prolonged cigarette smoking (CS causes chronic obstructive pulmonary disease (COPD, a prevalent serious condition that may persist or progress after smoking cessation. To provide insight into how CS triggers COPD, we investigated temporal patterns of lung transcriptome expression and systemic metabolome changes induced by chronic CS exposure and smoking cessation. Whole lung RNA-seq data was analyzed at transcript and exon levels from C57Bl/6 mice exposed to CS for 1- or 7 days, for 3-, 6-, or 9 months, or for 6 months followed by 3 months of cessation using age-matched littermate controls. We identified previously unreported dysregulation of pyrimidine metabolism and phosphatidylinositol signaling pathways and confirmed alterations in glutathione metabolism and circadian gene pathways. Almost all dysregulated pathways demonstrated reversibility upon smoking cessation, except the lysosome pathway. Chronic CS exposure was significantly linked with alterations in pathways encoding for energy, phagocytosis, and DNA repair and triggered differential expression of genes or exons previously unreported to associate with CS or COPD, including Lox, involved in matrix remodeling, Gp2, linked to goblet cells, and Slc22a12 and Agpat3, involved in purine and glycerolipid metabolism, respectively. CS-induced lung metabolic pathways changes were validated using metabolomic profiles of matched plasma samples, indicating that dynamic metabolic gene regulation caused by CS is reflected in the plasma metabolome. Using advanced technologies, our study uncovered novel pathways and genes altered by chronic CS exposure, including those involved in pyrimidine metabolism, phosphatidylinositol signaling and lysosome function, highlighting their potential importance in the pathogenesis or diagnosis of CS-associated conditions.

  9. Benefits of E-Cigarettes Among Heavy Smokers Undergoing a Lung Cancer Screening Program: Randomized Controlled Trial Protocol.

    Lucchiari, Claudio; Masiero, Marianna; Veronesi, Giulia; Maisonneuve, Patrick; Spina, Stefania; Jemos, Costantino; Omodeo Salè, Emanuela; Pravettoni, Gabriella

    2016-02-03

    Smoking is a global public health problem. For this reason, experts have called smoking dependence a global epidemic. Over the past 5 years, sales of electronic cigarettes, or e-cigarettes, have been growing strongly in many countries. Yet there is only partial evidence that e-cigarettes are beneficial for smoking cessation. In particular, although it has been proven that nicotine replacement devices may help individuals stop smoking and tolerate withdrawal symptoms, e-cigarettes' power to increase the quitting success rate is still limited, ranging from 5% to 20% dependent on smokers' baseline conditions as shown by a recent Cochrane review. Consequently, it is urgent to know if e-cigarettes may have a higher success rate than other nicotine replacement methods and under what conditions. Furthermore, the effects of the therapeutic setting and the relationship between individual characteristics and the success rate have not been tested. This protocol is particularly innovative, because it aims to test the effectiveness of electronic devices in a screening program (the COSMOS II lung cancer prevention program at the European Institute of Oncology), where tobacco reduction is needed to lower individuals' lung cancer risks. This protocol was designed with the primary aim of investigating the role of tobacco-free cigarettes in helping smokers improve lung health and either quit smoking or reduce their tobacco consumption. In particular, we aim to investigate the impact of a 3-month e-cigarettes program to reduce smoking-related respiratory symptoms (eg, dry cough, shortness of breath, mouth irritation, and phlegm) through reduced consumption of tobacco cigarettes. Furthermore, we evaluate the behavioral and psychological (eg, well-being, mood, and quality of life) effects of the treatment. This is a prospective, randomized, placebo-controlled, double-blind, three-parallel group study. The study is organized as a nested randomized controlled study with 3 branches: a

  10. Benfotiamine counteracts smoking-induced vascular dysfunction in healthy smokers.

    Stirban, Alin; Nandrean, Simona; Kirana, Stanley; Götting, Christian; Veresiu, Ioan Andrei; Tschoepe, Diethelm

    2012-01-01

    Background. Smoking induces endothelial dysfunction (ED) mainly by exacerbating oxidative stress (OS) and inflammation. Benfotiamine, a thiamine prodrug with high bioavailability, prevents nicotine-induced vascular dysfunction in rats. It remained unknown whether this effect also occurs in humans. Methods. Therefore, 20 healthy volunteers (mean age: 38 years) were investigated twice, 7-10 days apart in a randomized, cross-over, and investigator-blinded design. Vascular function was assessed by flow-mediated vasodilatation (FMD) of the brachial artery and by measurements of the soluble vascular cell adhesion molecule (sVCAM)-1. Investigations were performed after an overnight fast as well as 20 minutes after one cigarette smoking. On another day, the same procedure was applied following a 3-day oral therapy with benfotiamine (1050 mg/day). Ten patients were randomized to start with smoking alone, and ten started with benfotiamine. Results. Results are expressed as (mean ± SEM). Smoking acutely induced a decrease in FMD by 50% ((∗∗)P benfotiamine treatment to 25%(∗§) ((∗)P benfotiamine. The endothelium-independent vasodilatation remained unaltered between days. Conclusion. In healthy volunteers, smoking blunts vascular function mirrored by a decrease in FMD and an increase in sVCAM-1. Short-term treatment with benfotiamine significantly reduces these effects, showing protective vascular properties.

  11. Electronic cigarette aerosols and copper nanoparticles induce mitochondrial stress and promote DNA fragmentation in lung fibroblasts

    Lerner, Chad A.; Rutagarama, Pierrot; Ahmad, Tanveer; Sundar, Isaac K.; Elder, Alison; Rahman, Irfan, E-mail: irfan_rahman@urmc.rochester.edu

    2016-09-02

    Oxidants or nanoparticles have recently been identified as constituents of aerosols released from various styles of electronic cigarettes (E-cigs). Cells in the lung may be directly exposed to these constituents and harbor reactive properties capable of incurring acute cell injury. Our results show mitochondria are sensitive to both E-cig aerosols and aerosol containing copper nanoparticles when exposed to human lung fibroblasts (HFL-1) using an Air-Liquid Interface culture system, evident by elevated levels of mitochondrial ROS (mtROS). Increased mtROS after aerosol exposure is associated with reduced stability of OxPhos electron transport chain (ETC) complex IV subunit and nuclear DNA fragmentation. Increased levels of IL-8 and IL-6 in HFL-1 conditioned media were also observed. These findings reveal both mitochondrial, genotoxic, and inflammatory stresses are features of direct cell exposure to E-cig aerosols which are ensued by inflammatory duress, raising a concern on deleterious effect of vaping. - Graphical abstract: Oxidants and possibly reactive properties of metal particles in E-cig aerosols impart mitochondrial oxidative stress and DNA damage. These biological effects accompany inflammatory response which may raise concern regarding long term E-cig use. Mitochondria may be particularly sensitive to reactive properties of E-cig aerosols in addition to the potential for them to induce genotoxic stress by generating increased ROS. - Highlights: • Mitochondria are sensitive to both E-cig aerosols and metal nanoparticles. • Increased mtROS by E-cig aerosol is associated with disrupted mitochondrial energy. • E-cig causes nuclear DNA fragmentation. • E-cig aerosols induce pro-inflammatory response in human fibroblasts.

  12. Electronic cigarette aerosols and copper nanoparticles induce mitochondrial stress and promote DNA fragmentation in lung fibroblasts

    Lerner, Chad A.; Rutagarama, Pierrot; Ahmad, Tanveer; Sundar, Isaac K.; Elder, Alison; Rahman, Irfan

    2016-01-01

    Oxidants or nanoparticles have recently been identified as constituents of aerosols released from various styles of electronic cigarettes (E-cigs). Cells in the lung may be directly exposed to these constituents and harbor reactive properties capable of incurring acute cell injury. Our results show mitochondria are sensitive to both E-cig aerosols and aerosol containing copper nanoparticles when exposed to human lung fibroblasts (HFL-1) using an Air-Liquid Interface culture system, evident by elevated levels of mitochondrial ROS (mtROS). Increased mtROS after aerosol exposure is associated with reduced stability of OxPhos electron transport chain (ETC) complex IV subunit and nuclear DNA fragmentation. Increased levels of IL-8 and IL-6 in HFL-1 conditioned media were also observed. These findings reveal both mitochondrial, genotoxic, and inflammatory stresses are features of direct cell exposure to E-cig aerosols which are ensued by inflammatory duress, raising a concern on deleterious effect of vaping. - Graphical abstract: Oxidants and possibly reactive properties of metal particles in E-cig aerosols impart mitochondrial oxidative stress and DNA damage. These biological effects accompany inflammatory response which may raise concern regarding long term E-cig use. Mitochondria may be particularly sensitive to reactive properties of E-cig aerosols in addition to the potential for them to induce genotoxic stress by generating increased ROS. - Highlights: • Mitochondria are sensitive to both E-cig aerosols and metal nanoparticles. • Increased mtROS by E-cig aerosol is associated with disrupted mitochondrial energy. • E-cig causes nuclear DNA fragmentation. • E-cig aerosols induce pro-inflammatory response in human fibroblasts.

  13. A Correlative Study of Smokeless Tobacco induced Lesion and Smoke-induced Leukoplakia in Various Aspects

    Parita K Chitroda

    2011-01-01

    Full Text Available Various oral mucosal lesions are attributed to tobacco use. The presence of these conditions vanes with particular type of tobacco used (smoking or smokeless and the form in which it is used, such as cigarettes, pipes, cigars and chewing moist snuff. The frequency and duration of use as well as the ways in which the tobacco product is used also contributes to the clinical presentation and seventy of the lesion. The present study is mainly focused on the correlation between the smokeless tobacco-induced lesion and smoke-induced leukoplakia on various aspects with an objective to determine smokeless tobacco as a possible cause for leukoplakia.

  14. Secretion of the endoplasmic reticulum stress protein, GRP78, into the BALF is increased in cigarette smokers.

    Aksoy, Mark O; Kim, Victor; Cornwell, William D; Rogers, Thomas J; Kosmider, Beata; Bahmed, Karim; Barrero, Carlos; Merali, Salim; Shetty, Neena; Kelsen, Steven G

    2017-05-02

    Identification of biomarkers of cigarette smoke -induced lung damage and early COPD is an area of intense interest. Glucose regulated protein of 78 kD (i.e., GRP78), a multi-functional protein which mediates cell responses to oxidant stress, is increased in the lungs of cigarette smokers and in the serum of subjects with COPD. We have suggested that secretion of GRP78 by lung cells may explain the increase in serum GRP78 in COPD. To assess GRP78 secretion by the lung, we assayed GRP78 in bronchoalveolar lavage fluid (BALF) in chronic smokers and non-smokers. We also directly assessed the acute effect of cigarette smoke material on GRP78 secretion in isolated human airway epithelial cells (HAEC). GRP78 was measured in BALF of smokers (S; n = 13) and non-smokers (NS; n = 11) by Western blotting. GRP78 secretion by HAEC was assessed by comparing its concentration in cell culture medium and cell lysates. Cells were treated for 24 h with either the volatile phase of cigarette smoke (cigarette smoke extract (CSE) or the particulate phase (cigarette smoke condensate (CSC)). GRP78 was present in the BALF of both NS and S but levels were significantly greater in S (p = 0.04). GRP78 was secreted constitutively in HAEC. CSE 15% X 24 h increased GRP78 in cell-conditioned medium without affecting its intracellular concentration. In contrast, CSC X 24 h increased intracellular GRP78 expression but did not affect GRP78 secretion. Brefeldin A, an inhibitor of classical Golgi secretion pathways, did not inhibit GRP78 secretion indicating that non-classical pathways were involved. The present study indicates that GRP78 is increased in BALF in cigarette smokers; that HAEC secrete GRP78; and that GRP78 secretion by HAEC is augmented by cigarette smoke particulates. Enhanced secretion of GRP78 by lung cells makes it a potential biomarker of cigarette smoke-induced lung injury.

  15. Receptor for advanced glycation endproducts (RAGE maintains pulmonary structure and regulates the response to cigarette smoke.

    Lisa Wolf

    Full Text Available The receptor for advanced glycation endproducts (RAGE is highly expressed in the lung but its physiological functions in this organ is still not completely understood. To determine the contribution of RAGE to physiological functions of the lung, we analyzed pulmonary mechanics and structure of wildtype and RAGE deficient (RAGE-/- mice. RAGE deficiency spontaneously resulted in a loss of lung structure shown by an increased mean chord length, increased respiratory system compliance, decreased respiratory system elastance and increased concentrations of serum protein albumin in bronchoalveolar lavage fluids. Pulmonary expression of RAGE was mainly localized on alveolar epithelial cells and alveolar macrophages. Primary murine alveolar epithelial cells isolated from RAGE-/- mice revealed an altered differentiation and defective barrier formation under in vitro conditions. Stimulation of interferone-y (IFNy-activated alveolar macrophages deficient for RAGE with Toll-like receptor (TLR ligands resulted in significantly decreased release of proinflammatory cytokines and chemokines. Exposure to chronic cigarette smoke did not affect emphysema-like changes in lung parenchyma in RAGE-/- mice. Acute cigarette smoke exposure revealed a modified inflammatory response in RAGE-/- mice that was characterized by an influx of macrophages and a decreased keratinocyte-derived chemokine (KC release. Our data suggest that RAGE regulates the differentiation of alveolar epithelial cells and impacts on the development and maintenance of pulmonary structure. In cigarette smoke-induced lung pathology, RAGE mediates inflammation that contributes to lung damage.

  16. Apocynin and ebselen reduce influenza A virus-induced lung inflammation in cigarette smoke-exposed mice.

    Oostwoud, L C; Gunasinghe, P; Seow, H J; Ye, J M; Selemidis, S; Bozinovski, S; Vlahos, R

    2016-02-15

    Influenza A virus (IAV) infections are a common cause of acute exacerbations of chronic obstructive pulmonary disease (AECOPD). Oxidative stress is increased in COPD, IAV-induced lung inflammation and AECOPD. Therefore, we investigated whether targeting oxidative stress with the Nox2 oxidase inhibitors and ROS scavengers, apocynin and ebselen could ameliorate lung inflammation in a mouse model of AECOPD. Male BALB/c mice were exposed to cigarette smoke (CS) generated from 9 cigarettes per day for 4 days. On day 5, mice were infected with 1 × 10(4.5) PFUs of the IAV Mem71 (H3N1). BALF inflammation, viral titers, superoxide production and whole lung cytokine, chemokine and protease mRNA expression were assessed 3 and 7 days post infection. IAV infection resulted in a greater increase in BALF inflammation in mice that had been exposed to CS compared to non-smoking mice. This increase in BALF inflammation in CS-exposed mice caused by IAV infection was associated with elevated gene expression of pro-inflammatory cytokines, chemokines and proteases, compared to CS alone mice. Apocynin and ebselen significantly reduced the exacerbated BALF inflammation and pro-inflammatory cytokine, chemokine and protease expression caused by IAV infection in CS mice. Targeting oxidative stress using apocynin and ebselen reduces IAV-induced lung inflammation in CS-exposed mice and may be therapeutically exploited to alleviate AECOPD.

  17. Chronic cigarette smoke exposure adversely alters 14C-arachidonic acid metabolism in rat lungs, aortas and platelets

    Lubawy, W.C.; Valentovic, M.A.; Atkinson, J.E.; Gairola, G.C.

    1983-01-01

    Male rats were exposed to freshly generated cigarette smoke once daily, 5 times a week for 10 weeks. Inhalation of smoke was verified by elevated carboxyhemoglobin in blood sampled immediately after smoke exposure and by increased lung aryl hydrocarbon hydroxylase activity 24 hours after the last smoke exposure. Aortic rings isolated from smoke-exposed rats synthesized less prostacyclin (PGI2) from 14 C-arachidonic acid than rings from sham rats. Platelets from smoke-exposed rats synthesized more thromboxane (TXA2) from 14 C-arachidonic acid than platelets from room controls but not those from sham rats. Lung microsomes from smoke-exposed rats synthesized more TXA2 and had a lower PGI2/TXA2 ratio than lung microsomes from room controls and shams. It is concluded that chronic cigarette smoke exposure alters arachidonic acid metabolism in aortas, platelets and lungs in a manner resulting in decreased PGI2 and increased TXA2, thereby creating a condition favoring platelet aggregation and a variety of cardiovascular diseases

  18. Radon, cigarette smoke, and lung cancer: A re-analysis of the Colorado Plateau uranium miners' data [see comments

    Moolgavkar, S.H.; Luebeck, E.G.; Krewski, D.; Zielinski, J.M.

    1993-01-01

    Much of our knowledge regarding the interaction of radon and tobacco smoke in the etiology of human lung cancer derives from studies of uranium miners. In this article, we present a re-analysis of lung cancer mortality in the Colorado Plateau miners' cohort within the framework of the two-mutation clonal expansion model of carcinogenesis. This analysis takes into account the patterns of exposure to radon and cigarette smoke experienced by individuals in the cohort. A simultaneous re-analysis of the British doctors' cohort indicated that those model parameters relating to the effects of tobacco were comparable in the two data sets. We found no evidence of interaction between radon and tobacco smoke with respect to their joint effect on the first or second stage mutation rates or on the rate of proliferation of initiated cells. The age-specific relative risks associated with joint exposure to radon and cigarette smoke, however, were supra-additive but submultiplicative. The analysis also confirmed that fractionation of radon exposures leads to higher lung cancer risks. Finally, we present some estimates of lung cancer risk from environmental radon exposure for non-smokers and smokers

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

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

    2005-02-01

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

  20. What's in a Cigarette?

    ... Toluene - used to manufacture paint What's in an e-cigarette? Get the facts about nicotine, flavorings, colorings and other chemicals found in e-cigarettes. Find out more » Learn about the American Lung ...

  1. Role and mechanism of hydrogen sulfide in cigarette smoke induced chronic obstructive pulmonary disease related pulmonary vascular remodeling in rats%硫化氢对吸烟所致慢性阻塞性肺疾病大鼠模型肺血管重塑的作用及机制

    李敏霞; 陈亚红; 廖程程; 林帆; 白宇; 米文君; 孙云; 齐永芬

    2017-01-01

    ) group, CS+Sodium hydrosulfide (NaHS) group and CS+DL-propargylglycine (PPG) group.Rats in control group were fed normally and breathed clear air , and for the rest groups , passive cigarette smoke inhalation method were adopted to establish COPD model.After 8 weeks, the rats in corresponding groups were treated by NaHS or PPG.After 16 weeks, the markers of pulmonary vascular remodeling in all groups were measured.Proliferation marker proliferative cell nuclear antigen ( PCNA) and oxidative stress marker 3-neurotrophin ( 3-NT ) in all groups were measured by immunohistochemistry ( IHC ).Results Compared with control group ,the airway resistance was increased (0.859 ±0.283 vs 0.578 ±0.088, P<0.05) and the pathological scores was much higher in CS group , which suggested that the COPD model was successful.The degree of small resistance pulmonary artery medial wall thickness and full vascular muscularization of CS group were much higher (0.54 ±0.20 vs 0.37 ±0.12, 0.39 ±0.08;0.61 ±0.16 vs 0.20 ±0.12, 0.34 ±0.13, all P<0.01)than control group and CS +NaHS group, there was no significant difference between CS+PPG group and CS group.In accordance with the results of morphometric analysis , the proliferation marker PCNA was more in CS group when compared with control group and CS +NaHS group (0.27 ±0.08 vs 0.12 ±0.06, 0.14 ±0.06, both P<0.05), there was no significant difference between CS+PPG group and CS group.Furthermore , the IHC also showed that 3-NT significantly increased in CS group compared with control group and CS +NaHS group (0.26 ±0.08 vs 0.18 ±0.04, 0.19 ±0.06, both P<0.01 ) , there was no significant difference between CS +PPG group and CS group as well.In addition, the small resistance pulmonary artery medial wall thickness had strong correlation with the expression level of oxidative stress marker 3-NT ( r=0.906, P<0.001).Conclusion H2 S significantly attenuates cigarette smoke induced COPD related pulmonary vascular remodeling , which could be

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

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

    2010-01-01

    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.

  3. Quantifying potential health impacts of cadmium in cigarettes on smoker risk of lung cancer: a portfolio-of-mechanisms approach.

    Cox, Louis Anthony Tony

    2006-12-01

    This article introduces an approach to estimating the uncertain potential effects on lung cancer risk of removing a particular constituent, cadmium (Cd), from cigarette smoke, given the useful but incomplete scientific information available about its modes of action. The approach considers normal cell proliferation; DNA repair inhibition in normal cells affected by initiating events; proliferation, promotion, and progression of initiated cells; and death or sparing of initiated and malignant cells as they are further transformed to become fully tumorigenic. Rather than estimating unmeasured model parameters by curve fitting to epidemiological or animal experimental tumor data, we attempt rough estimates of parameters based on their biological interpretations and comparison to corresponding genetic polymorphism data. The resulting parameter estimates are admittedly uncertain and approximate, but they suggest a portfolio approach to estimating impacts of removing Cd that gives usefully robust conclusions. This approach views Cd as creating a portfolio of uncertain health impacts that can be expressed as biologically independent relative risk factors having clear mechanistic interpretations. Because Cd can act through many distinct biological mechanisms, it appears likely (subjective probability greater than 40%) that removing Cd from cigarette smoke would reduce smoker risks of lung cancer by at least 10%, although it is possible (consistent with what is known) that the true effect could be much larger or smaller. Conservative estimates and assumptions made in this calculation suggest that the true impact could be greater for some smokers. This conclusion appears to be robust to many scientific uncertainties about Cd and smoking effects.

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

    Abdessalem Koubaa

    2015-02-01

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

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

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

    1998-10-01

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

  6. E-cigarettes: voltage- and concentration-dependent loss in human lung adenocarcinoma viability.

    Otręba, Michał; Kośmider, Leon; Knysak, Jakub; Warncke, Jared D; Sobczak, Andrzej

    2018-04-17

    E-cigarettes are used by millions of people despite the fact that the harmful effect of aerosol emitted from these products to the human organism is still not clear. In this paper, toxicity of vapor generated using different solutions and battery output voltage on A549 cells viability is presented. The obtained EC 50 values for commercially available propylene glycol/glycerol solution 1:1 e-liquids based on 3.2 V (0.127%), 4.0 V (0.112%) and 4.8 V (0.038%) were about 1.5-4.5 times higher than in tobacco smoke (0.0086%). Furthermore, it was shown that the increase of battery output voltage decreased A549 cell viability. In addition, commercially available extracts were more cytotoxic than laboratory made extracts. Owing to the expansiveness of e-cigarettes, it is very important to estimate their impact on public health. Our results not only confirm less cytotoxicity of e-liquid aerosol than cigarette smoke, but also demonstrate that solutions used in e-liquids and, for the first time, battery output voltage have a significant impact on cytotoxicity of e-cigarette vapor. Thus, the results of this study are very important for the current and future legal regulations on e-cigarettes. Copyright © 2018 John Wiley & Sons, Ltd.

  7. Glutathione Peroxidase-1 Suppresses the Unfolded Protein Response upon Cigarette Smoke Exposure

    Patrick Geraghty

    2016-01-01

    Full Text Available Oxidative stress provokes endoplasmic reticulum (ER stress-induced unfolded protein response (UPR in the lungs of chronic obstructive pulmonary (COPD subjects. The antioxidant, glutathione peroxidase-1 (GPx-1, counters oxidative stress induced by cigarette smoke exposure. Here, we investigate whether GPx-1 expression deters the UPR following exposure to cigarette smoke. Expression of ER stress markers was investigated in fully differentiated normal human bronchial epithelial (NHBE cells isolated from nonsmoking, smoking, and COPD donors and redifferentiated at the air liquid interface. NHBE cells from COPD donors expressed heightened ATF4, XBP1, GRP78, GRP94, EDEM1, and CHOP compared to cells from nonsmoking donors. These changes coincided with reduced GPx-1 expression. Reintroduction of GPx-1 into NHBE cells isolated from COPD donors reduced the UPR. To determine whether the loss of GPx-1 expression has a direct impact on these ER stress markers during smoke exposure, Gpx-1−/− mice were exposed to cigarette smoke for 1 year. Loss of Gpx-1 expression enhanced cigarette smoke-induced ER stress and apoptosis. Equally, induction of ER stress with tunicamycin enhanced antioxidant expression in mouse precision-cut lung slices. Smoke inhalation also exacerbated the UPR response during respiratory syncytial virus infection. Therefore, ER stress may be an antioxidant-related pathophysiological event in COPD.

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

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

    1987-01-01

    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 [ 14 C]methylamine (as does native C3), and relatively little [ 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

  9. Gene expression signature of cigarette smoking and its role in lung adenocarcinoma development and survival.

    Maria Teresa Landi

    2008-02-01

    Full Text Available Tobacco smoking is responsible for over 90% of lung cancer cases, and yet the precise molecular alterations induced by smoking in lung that develop into cancer and impact survival have remained obscure.We performed gene expression analysis using HG-U133A Affymetrix chips on 135 fresh frozen tissue samples of adenocarcinoma and paired noninvolved lung tissue from current, former and never smokers, with biochemically validated smoking information. ANOVA analysis adjusted for potential confounders, multiple testing procedure, Gene Set Enrichment Analysis, and GO-functional classification were conducted for gene selection. Results were confirmed in independent adenocarcinoma and non-tumor tissues from two studies. We identified a gene expression signature characteristic of smoking that includes cell cycle genes, particularly those involved in the mitotic spindle formation (e.g., NEK2, TTK, PRC1. Expression of these genes strongly differentiated both smokers from non-smokers in lung tumors and early stage tumor tissue from non-tumor tissue (p1.5, for each comparison, consistent with an important role for this pathway in lung carcinogenesis induced by smoking. These changes persisted many years after smoking cessation. NEK2 (p<0.001 and TTK (p = 0.002 expression in the noninvolved lung tissue was also associated with a 3-fold increased risk of mortality from lung adenocarcinoma in smokers.Our work provides insight into the smoking-related mechanisms of lung neoplasia, and shows that the very mitotic genes known to be involved in cancer development are induced by smoking and affect survival. These genes are candidate targets for chemoprevention and treatment of lung cancer in smokers.

  10. Vapors produced by electronic cigarettes and e-juices with flavorings induce toxicity, oxidative stress, and inflammatory response in lung epithelial cells and in mouse lung.

    Chad A Lerner

    Full Text Available Oxidative stress and inflammatory response are the key events in the pathogenesis of chronic airway diseases. The consumption of electronic cigarettes (e-cigs with a variety of e-liquids/e-juices is alarmingly increasing without the unrealized potential harmful health effects. We hypothesized that electronic nicotine delivery systems (ENDS/e-cigs pose health concerns due to oxidative toxicity and inflammatory response in lung cells exposed to their aerosols. The aerosols produced by vaporizing ENDS e-liquids exhibit oxidant reactivity suggesting oxidants or reactive oxygen species (OX/ROS may be inhaled directly into the lung during a "vaping" session. These OX/ROS are generated through activation of the heating element which is affected by heating element status (new versus used, and occurs during the process of e-liquid vaporization. Unvaporized e-liquids were oxidative in a manner dependent on flavor additives, while flavors containing sweet or fruit flavors were stronger oxidizers than tobacco flavors. In light of OX/ROS generated in ENDS e-liquids and aerosols, the effects of ENDS aerosols on tissues and cells of the lung were measured. Exposure of human airway epithelial cells (H292 in an air-liquid interface to ENDS aerosols from a popular device resulted in increased secretion of inflammatory cytokines, such as IL-6 and IL-8. Furthermore, human lung fibroblasts exhibited stress and morphological change in response to treatment with ENDS/e-liquids. These cells also secrete increased IL-8 in response to a cinnamon flavored e-liquid and are susceptible to loss of cell viability by ENDS e-liquids. Finally, exposure of wild type C57BL/6J mice to aerosols produced from a popular e-cig increase pro-inflammatory cytokines and diminished lung glutathione levels which are critical in maintaining cellular redox balance. Thus, exposure to e-cig aerosols/juices incurs measurable oxidative and inflammatory responses in lung cells and tissues that

  11. Murine lung tumor response after exposure to cigarette mainstream smoke or its particulate and gas/vapor phase fractions

    Stinn, W.; Arts, J.H.E.; Buettner, A.; Duistermaat, E.; Janssens, K.; Kuper, C.F.; Haussmann, H.-J.

    2010-01-01

    Knowledge on mechanisms of smoking-induced tumorigenesis and on active smoke constituents may improve the development and evaluation of chemopreventive and therapeutic interventions, early diagnostic markers, and new and potentially reduced-risk tobacco products. A suitable laboratory animal disease

  12. Influenza A virus infection and cigarette smoke impair bronchodilator responsiveness to β-adrenoceptor agonists in mouse lung.

    Donovan, Chantal; Seow, Huei Jiunn; Bourke, Jane E; Vlahos, Ross

    2016-05-01

    β2-adrenoceptor agonists are the mainstay therapy for patients with asthma but their effectiveness in cigarette smoke (CS)-induced lung disease such as chronic obstructive pulmonary disease (COPD) is limited. In addition, bronchodilator efficacy of β2-adrenoceptor agonists is decreased during acute exacerbations of COPD (AECOPD), caused by respiratory viruses including influenza A. Therefore, the aim of the present study was to assess the effects of the β2-adrenoceptor agonist salbutamol (SALB) on small airway reactivity using mouse precision cut lung slices (PCLS) prepared from CS-exposed mice and from CS-exposed mice treated with influenza A virus (Mem71, H3N1). CS exposure alone reduced SALB potency and efficacy associated with decreased β2-adrenoceptor mRNA expression, and increased tumour necrosis factor α (TNFα) and interleukin-1β (IL-1β) expression. This impaired relaxation was restored by day 12 in the absence of further CS exposure. In PCLS prepared after Mem71 infection alone, responses to SALB were transient and were not well maintained. CS exposure prior to Mem71 infection almost completely abolished relaxation, although β2-adrenoceptor and TNFα and IL-1β expression were unaltered. The present study has shown decreased sensitivity to SALB after CS or a combination of CS and Mem71 occurs by different mechanisms. In addition, the PCLS technique and our models of CS and influenza infection provide a novel setting for assessment of alternative bronchodilators. © 2016 The Author(s).

  13. Benefits of Tobacco Free Cigarette among heavy smokers undergoing a lung cancer screening program: Randomized Controlled Study

    Lucchiari, C.; Masiero, M..A.; Veronesi, G.; Maisonneuve, P.; Spina, S.; Jemos, C.; Saia, E.; Pravettoni, G.

    2016-01-01

    Background Smoking is a global public health problem. For this reason, experts have called smoking dependence a global epidemic. Over the past 5 years, sales of electronic cigarettes, or e-cigarettes, have been growing strongly in many countries. Yet there is only partial evidence that e-cigarettes are beneficial for smoking cessation. In particular, although it has been proven that nicotine replacement devices may help individuals stop smoking and tolerate withdrawal symptoms, e-cigarettes? ...

  14. High-Mobility Group Box 1 Disrupts Metabolic Function with Cigarette Smoke Exposure in a Ceramide-Dependent Manner

    Oliver J. Taylor

    2017-05-01

    Full Text Available We have previously found that cigarette smoke disrupts metabolic function, in part, by increasing muscle ceramide accrual. To further our understanding of this, we sought to determine the role of the cytokine high-mobility group box 1 (HMGB1, which is increased with smoke exposure, in smoke-induced muscle metabolic perturbations. To test this theory, we determined HMGB1 from lungs of human smokers, as well as from lung cells from mice exposed to cigarette smoke. We also treated cells and mice directly with HMGB1, in the presence or absence of myriocin, an inhibitor of serine palmitoyltransferase, the rate-limiting enzyme in ceramide biosynthesis. Outcomes included assessments of insulin resistance and muscle mitochondrial function. HMGB1 was significantly increased in both human lungs and rodent alveolar macrophages. Further testing revealed that HMGB1 treatment elicited a widespread increase in ceramide species and reduction in myotube mitochondrial respiration, an increase in reactive oxygen species, and reduced insulin-stimulated Akt phosphorylation. Inhibition of ceramide biosynthesis with myriocin was protective. In mice, by comparing treatments of HMGB1 injections with or without myriocin, we found that HMGB1 injections resulted in increased muscle ceramides, especially C16 and C24, which were necessary for reduced muscle mitochondrial respiration and compromised insulin and glucose tolerance. In conclusion, HMGB1 may be a necessary intermediate in the ceramide-dependent metabolic consequences of cigarette smoke exposure.

  15. The antioxidant and anti-inflammatory properties of lycopene in mice lungs exposed to cigarette smoke.

    Campos, Keila Karine Duarte; Araújo, Glaucy Rodrigues; Martins, Thais Lourenço; Bandeira, Ana Carla Balthar; Costa, Guilherme de Paula; Talvani, André; Garcia, Camila Carrião Machado; Oliveira, Laser Antônio Machado; Costa, Daniela Caldeira; Bezerra, Frank Silva

    2017-10-01

    Lycopene is a carotenoid with known antioxidant and anti-inflammatory properties. We aimed to evaluate the in vitro and in vivo effects of lycopene on reducing the redox imbalance and inflammation induced by cigarette smoke (CS). For the in vitro study, J774A.1 (macrophages) cells were incubated in the presence of 0.5, 1.0, 2.0, 4.0, 8.0, 10.0 and 25 μM of lycopene for 3, 6 and 24 h or in the presence of 0.1%, 0.25%, 0.5%, 0.625%, 1.25%, 2.25%, 5% and 10% cigarette smoke extract (CSE) for 3, 6 and 24 h to assess cell viability and measurement of intracellular reactive oxygen species (ROS). For the in vivo study, 40 mice were divided into 5 groups: a control exposed to ambient air (CG), a vehicle-control group that received 200 μl of sunflower oil by orogastric gavage, a group exposed to CS and two groups administered lycopene (diluted in sunflower oil) at doses of either 25 or 50 mg/kg/day prior to exposure to CS (LY25+CS and LY50+CS). The total treatment time lasted 5 days. A cell viability decrease was observed at 10- and 25-μM concentrations of lycopene in 3, 6 and 24 h compared with CG. There was an increase of ROS production in 24 h in CS compared with CG. Lycopene concentrations of 1 μM and 2 μM were able to reduce the production of ROS in 24 h compared with CS. In the bronchoalveolar lavage fluid, the total number of leukocytes increased in the CS group compared with the control groups (CG). Administration with lycopene at the highest dose suppressed this CS-induced increase in leukocytes. Lipid peroxidation and DNA damage increased in the CS group compared with that in the controls, and this increase was suppressed by lycopene at the highest dose. In contrast, superoxide dismutase activity decreased in the CS group compared with that in the controls. Catalase activity also increased in the CS group compared with that in both control groups, and this increase was suppressed in LY25+CS and LY50+CS. There was an increase in the levels of tumor necrosis

  16. Smoking induces long-lasting effects through a monoamine-oxidase epigenetic regulation.

    Jean-Marie Launay

    Full Text Available BACKGROUND: Postulating that serotonin (5-HT, released from smoking-activated platelets could be involved in smoking-induced vascular modifications, we studied its catabolism in a series of 115 men distributed as current smokers (S, never smokers (NS and former smokers (FS who had stopped smoking for a mean of 13 years. METHODOLOGY/PRINCIPAL FINDINGS: 5-HT, monoamine oxidase (MAO-B activities and amounts were measured in platelets, and 5-hydroxyindolacetic acid (5-HIAA--the 5-HT/MAO catabolite--in plasma samples. Both platelet 5-HT and plasma 5-HIAA levels were correlated with the 10-year cardiovascular Framingham relative risk (P<0.01, but these correlations became non-significant after adjustment for smoking status, underlining that the determining risk factor among those taken into account in the Framingham risk calculation was smoking. Surprisingly, the platelet 5-HT content was similar in S and NS but lower in FS with a parallel higher plasma level of 5-HIAA in FS. This was unforeseen since MAO-B activity was inhibited during smoking (P<0.00001. It was, however, consistent with a higher enzyme protein concentration found in S and FS than in NS (P<0.001. It thus appears that MAO inhibition during smoking was compensated by a higher synthesis. To investigate the persistent increase in MAO-B protein concentration, a study of the methylation of its gene promoter was undertaken in a small supplementary cohort of similar subjects. We found that the methylation frequency of the MAOB gene promoter was markedly lower (P<0.0001 for S and FS vs. NS due to cigarette smoke-induced increase of nucleic acid demethylase activity. CONCLUSIONS/SIGNIFICANCE: This is one of the first reports that smoking induces an epigenetic modification. A better understanding of the epigenome may help to further elucidate the physiopathology and the development of new therapeutic approaches to tobacco addiction. The results could have a larger impact than cardiovascular

  17. Tobacco expenditure, smoking-induced deprivation and financial stress: results from the International Tobacco Control (ITC) Four-Country Survey.

    Siahpush, Mohammad; Borland, Ron; Yong, Hua-Hie; Cummings, K Michael; Fong, Geoffrey T

    2012-07-01

    While higher tobacco prices lead to a reduction in smoking prevalence, there is a concern that paying more for cigarettes can lead to excess financial burden. Our primary aim was to examine the association of daily cigarette expenditure with smoking-induced deprivation (SID) and financial stress (FS). We used data from wave 7 (2008-2009) of the International Tobacco Control (ITC) Four-Country Survey which is a survey of smokers in Canada, the USA, the UK and Australia (n = 5887). Logistic regressions were used to assess the association of daily cigarette expenditure with SID and FS. In multivariate analyses, a one standard deviation increase in daily cigarette expenditure was associated with an increase of 24% (P = 0.004) in the probability of experiencing SID. While we found no association between daily cigarette expenditure and FS, we found that SID is a strong predictor of FS (odds ratio 6.25; P < 0.001). This suggests that cigarette expenditure indirectly affects FS through SID. Results showed no evidence of an interaction between cigarette expenditure and income or education in their effect on SID or FS. Our results imply that spending more on tobacco may result in SID but surprisingly has no direct effect on FS. While most smokers may be adjusting their incomes and consumption to minimise FS, some fail to do so occasionally as indexed by the SID measure. Future studies need to prospectively examine the effect of increased tobacco expenditure on financial burden of smokers. © 2012 Australasian Professional Society on Alcohol and other Drugs.

  18. Cigarette smoke and plutonium

    Anon.

    1981-01-01

    The overall objective of this study is to determine whether cigarette smoking increases the probability of plutonium-induced lung cancer. Initial experiments, designed to characterize the effect of chronic cigarette smoke exposure on pulmonary clearance of plutonium aerosols, are described

  19. The intractable cigarette ‘filter problem’

    Harris, Bradford

    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 resea...

  20. Rapid fall in lung density following smoking cessation in COPD

    Shaker, Saher B; Stavngaard, Trine; Laursen, Lars Christian

    2011-01-01

    Whether smoking-induced lung inflammation subsides after smoking cessation is currently a matter of debate. We used computed tomography (CT) to evaluate the effect of smoking cessation on lung density in patients with COPD....

  1. Cigarette smoke–induced induction of antioxidant enzyme activities in airway leukocytes is absent in active smokers with COPD

    Dove, Rosamund E.; Leong-Smith, Pheneatia; Roos-Engstrand, Ester; Pourazar, Jamshid; Shah, Mittal; Behndig, Annelie F.; Mudway, Ian S.; Blomberg, Anders

    2015-01-01

    Background Oxidative injury to the airway has been proposed as an important underlying mechanism in the pathogenesis of chronic obstructive pulmonary disease (COPD). As the extent of oxidant-mediated damage is dependent on the endogenous antioxidant defences within the airways, we examined whether COPD was associated with deficiencies in the antioxidant network within the respiratory tract lining fluids (RTLFs) and resident airway leukocytes. We hypothesised that COPD would be associated with both basal depression of antioxidant defences and impaired adaptive antioxidant responses to cigarette smoke. Methods Low molecular weight and enzymatic antioxidants together with metal-handling proteins were quantified in bronchoalveolar lavage fluid and airway leukocytes, derived from current (n=9) and ex-smoking COPD patients (n=15), as well as from smokers with normal lung function (n=16) and healthy never smokers (n=13). Results Current cigarette smoking was associated with an increase in ascorbate and glutathione within peripheral RTLFs in both smokers with normal lung function compared with healthy never smokers and in COPD smokers compared with COPD ex-smokers. In contrast, intra-cellular antioxidant enzyme activities (glutathione peroxidase, glutathione reductase, and catalase) were only up-regulated in smokers with normal lung function compared with healthy never smokers and not in actively smoking COPD patients relative to COPD ex-smokers. Conclusions We found no evidence of impaired basal antioxidant defences, within either the RTLFs or airway leukocytes in stable ex-smoking COPD patients compared with healthy never smoking controls. Current cigarette smoking induced an up-regulation of low molecular weight antioxidants in the RTLFs of both control subjects with normal lung function and patients with COPD. Importantly, the present data demonstrated a cigarette smoke–induced increase in intra-cellular antioxidant enzyme activities only within the smokers with

  2. A whole-blood transcriptome meta-analysis identifies gene expression signatures of cigarette smoking

    Huan, T. (Tianxiao); R. Joehanes (Roby); C. Schurmann (Claudia); K. Schramm (Katharina); L.C. Pilling (Luke); M.J. Peters (Marjolein); R. Mägi (Reedik); D.L. Demeo (Dawn L.); G.T. O'Connor (George); L. Ferrucci (Luigi); A. Teumer (Alexander); G. Homuth (Georg); R. Biffar (Reiner); U. Völker (Uwe); C. Herder (Christian); M. Waldenberger (Melanie); A. Peters (Annette); S. Zeilinger (Sonja); A. Metspalu (Andres); A. Hofman (Albert); A.G. Uitterlinden (André); D.G. Hernandez (Dena); A. Singleton (Andrew); S. Bandinelli (Stefania); P.J. Munson (Peter); H. Lin (Honghuang); E.J. Benjamin (Emelia); T. Esko (Tõnu); H.J. Grabe (Hans Jörgen); H. Prokisch (Holger); J.B.J. van Meurs (Joyce); D. Melzer (David); D. Levy (Daniel)

    2016-01-01

    textabstractCigarette smoking is a leading modifiable cause of death worldwide. We hypothesized that cigarette smoking induces extensive transcriptomic changes that lead to target-organ damage and smoking-related diseases. We performed a metaanalysis of transcriptome-wide gene expression using whole

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

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

    2013-01-01

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

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

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

    2013-09-01

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

  5. SEGEL: A Web Server for Visualization of Smoking Effects on Human Lung Gene Expression.

    Xu, Yan; Hu, Brian; Alnajm, Sammy S; Lu, Yin; Huang, Yangxin; Allen-Gipson, Diane; Cheng, Feng

    2015-01-01

    Cigarette smoking is a major cause of death worldwide resulting in over six million deaths per year. Cigarette smoke contains complex mixtures of chemicals that are harmful to nearly all organs of the human body, especially the lungs. Cigarette smoking is considered the major risk factor for many lung diseases, particularly chronic obstructive pulmonary diseases (COPD) and lung cancer. However, the underlying molecular mechanisms of smoking-induced lung injury associated with these lung diseases still remain largely unknown. Expression microarray techniques have been widely applied to detect the effects of smoking on gene expression in different human cells in the lungs. These projects have provided a lot of useful information for researchers to understand the potential molecular mechanism(s) of smoke-induced pathogenesis. However, a user-friendly web server that would allow scientists to fast query these data sets and compare the smoking effects on gene expression across different cells had not yet been established. For that reason, we have integrated eight public expression microarray data sets from trachea epithelial cells, large airway epithelial cells, small airway epithelial cells, and alveolar macrophage into an online web server called SEGEL (Smoking Effects on Gene Expression of Lung). Users can query gene expression patterns across these cells from smokers and nonsmokers by gene symbols, and find the effects of smoking on the gene expression of lungs from this web server. Sex difference in response to smoking is also shown. The relationship between the gene expression and cigarette smoking consumption were calculated and are shown in the server. The current version of SEGEL web server contains 42,400 annotated gene probe sets represented on the Affymetrix Human Genome U133 Plus 2.0 platform. SEGEL will be an invaluable resource for researchers interested in the effects of smoking on gene expression in the lungs. The server also provides useful information

  6. Rapid fall in lung density following smoking cessation in COPD

    Shaker, Saher B; Stavngaard, Trine; Laursen, Lars Christian

    2011-01-01

    Whether smoking-induced lung inflammation subsides after smoking cessation is currently a matter of debate. We used computed tomography (CT) to evaluate the effect of smoking cessation on lung density in patients with COPD.......Whether smoking-induced lung inflammation subsides after smoking cessation is currently a matter of debate. We used computed tomography (CT) to evaluate the effect of smoking cessation on lung density in patients with COPD....

  7. Mechanisms of protein misfolding in conformational lung diseases.

    McElvaney, N G

    2012-08-01

    Genetic or environmentally-induced alterations in protein structure interfere with the correct folding, assembly and trafficking of proteins. In the lung the expression of misfolded proteins can induce a variety of pathogenetic effects. Cystic fibrosis (CF) and alpha-1 antitrypsin (AAT) deficiency are two major clinically relevant pulmonary disorders associated with protein misfolding. Both are genetic diseases the primary causes of which are expression of mutant alleles of the cystic fibrosis transmembrane conductance regulator (CFTR) and SERPINA1, respectively. The most common and best studied mutant forms of CFTR and AAT are ΔF508 CFTR and the Glu342Lys mutant of AAT called ZAAT, respectively. Non-genetic mechanisms can also damage protein structure and induce protein misfolding in the lung. Cigarette-smoke contains oxidants and other factors that can modify a protein\\'s structure, and is one of the most significant environmental causes of protein damage within the lung. Herein we describe the mechanisms controlling the folding of wild type and mutant versions of CFTR and AAT proteins, and explore the consequences of cigarette-smoke-induced effects on the protein folding machinery in the lung.

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

    Izzotti, Alberto; Larghero, Patrizia; Longobardi, Mariagrazia; Cartiglia, Cristina; Camoirano, Anna; Steele, Vernon E.; De Flora, Silvio

    2011-01-01

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

  9. [Initiation, promotion, initiation experiments with radon and cigarette smoke: Lung tumors in rats]. Progress report

    Moolgavkar, S.H.

    1994-01-01

    During the past several years, the authors have made considerable progress in modeling carcinogenesis in general, and in modeling radiation carcinogenesis, in particular. They present an overview of their progress in developing stochastic carcinogenesis models and applying them to experimental and epidemiologic data sets. Traditionally, cancer models have been used for the analysis of incidence (or prevalence) data in epidemiology and time to tumor data in experimental studies. The relevant quantities for the analysis of these data are the hazard function and the probability of tumor. The derivation of these quantities is briefly described here. More recently, the authors began to use these models for the analysis of data on intermediate lesions on the pathway to cancer. Such data are available in experimental carcinogenesis studies, in particular in initiation and promotion studies on the mouse skin and the rat liver. If however, quantitative information on intermediate lesions on the pathway to lung cancer were to be come available at some future date, the methods that they have developed for the analysis of initiation-promotion experiments could easily be applied to the analysis of these lesions. The mathematical derivations here are couched in terms of a particular two-mutation model of carcinogenesis. Extension to models postulating more than two mutations is not always straightforward

  10. Mercapturic Acids Derived from the Toxicants Acrolein and Crotonaldehyde in the Urine of Cigarette Smokers from Five Ethnic Groups with Differing Risks for Lung Cancer.

    Park, Sungshim L; Carmella, Steven G; Chen, Menglan; Patel, Yesha; Stram, Daniel O; Haiman, Christopher A; Le Marchand, Loic; Hecht, Stephen S

    2015-01-01

    The Multiethnic Cohort epidemiology study has clearly demonstrated that, compared to Whites and for the same number of cigarettes smoked, African Americans and Native Hawaiians have a higher risk for lung cancer whereas Latinos and Japanese Americans have a lower risk. Acrolein and crotonaldehyde are two important constituents of cigarette smoke which have well documented toxic effects and could play a role in lung cancer etiology. Their urinary metabolites 3-hydroxypropylmercapturic acid (3-HPMA) and 3-hydroxy-1-methylpropylmercapturic acid (HMPMA), respectively, are validated biomarkers of acrolein and crotonaldehyde exposure. We quantified levels of 3-HPMA and HMPMA in the urine of more than 2200 smokers from these five ethnic groups, and also carried out a genome wide association study using blood samples from these subjects. After adjusting for age, sex, creatinine, and total nicotine equivalents, geometric mean levels of 3-HPMA and HMPMA were significantly different in the five groups (P acrolein and crotonaldehyde may be involved in lung cancer etiology, and that their divergent levels may partially explain the differing risks of Native Hawaiian and Latino smokers. No strong signals were associated with 3-HPMA in the genome wide association study, suggesting that formation of the glutathione conjugate of acrolein is mainly non-enzymatic, while the top significant association with HMPMA was located on chromosome 12 near the TBX3 gene, but its relationship to HMPMA excretion is not clear.

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

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

    1997-09-01

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

  12. Lung Cancer

    Lung cancer is one of the most common cancers in the world. It is a leading cause of cancer death in men and women in the United States. Cigarette smoking causes most lung cancers. The more cigarettes you smoke per day and ...

  13. Electronic cigarette: A review

    Vinay Mahishale

    2014-01-01

    Full Text Available The principal addictive component of tobacco smoke is nicotine. The mechanisms of nicotine addiction are highly complex and are responsible for maintenance of smoking behaviour. Use of electronic cigarettes (E-cigarettes, devices that deliver a nicotine containing vapor has increased rapidly across the world. They are marketed as a "healthier alternatives" to conventional cigarettes. There is extensive debate over long-term safety and efficacy of these devices on public health. Studies show that the vapor generated from the E-cigarettes has a variable amount of nicotine and potential harmful toxins. Until robust research demonstrates the safety of E-cigarettes and efficacy in the treatment of tobacco dependence, their role as safe smoking cessation tool is unclear. This review highlights the recent data regarding E-cigarettes toxicity, impact on lung function, and efficacy in smoking reduction and cessation.

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

    Ritchideh, K.; Chen, B.T.; Mauderly, J.L.; Brooks, A.L.

    1988-01-01

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

  15. The radioactive cigarettes

    Ulatowski, J.; Skwarzec, B.

    2002-01-01

    The carcinogenic effect of 210 Po and 210 Pb on lung cancer is an important problem in many countries with very high cigarette consumption. Poland has one of the highest consumption of cigarettes in the world. The results of 210 Po determination in fourteen most frequently smoked brands of cigarettes which constitute over 70% total cigarette consumption in Poland, are presented and discussed. Moreover, polonium content in cigarette smoke was estimated on the basis of its activity in fresh tobacco, ash, fresh filter and post smoking filter. The annual effective doses were calculated on the basis of 210 Po and 210 Pb inhalation with cigarette smoke. The results of this work indicate that Polish smokers who smoke one pack (20 cigarettes) per day inhale from 20 to 215 mBq of 210 Po and 210 Pb (each of them). The highest 210 Po content per sample was found in the cheep 'Popularne' brand (24.12 mBq), the lowest in 'Caro' (4.23 mBq). The mean values and annual effective dose for smokers were estimated to be 35 and 70 μSv from 210 Po and 210 Pb, respectively. For persons who smoke 2 packs of cigarettes with higher radionuclide concentrations, the effective dose is much higher (471 μSv/y) in comparison with intake in diet. Therefore, cigarettes and the absorption through the respiratory system are the main sources and principal pathway of 210 Po and 210 Pb intake of smokers in Poland. (author)

  16. Mercapturic Acids Derived from the Toxicants Acrolein and Crotonaldehyde in the Urine of Cigarette Smokers from Five Ethnic Groups with Differing Risks for Lung Cancer.

    Sungshim L Park

    Full Text Available The Multiethnic Cohort epidemiology study has clearly demonstrated that, compared to Whites and for the same number of cigarettes smoked, African Americans and Native Hawaiians have a higher risk for lung cancer whereas Latinos and Japanese Americans have a lower risk. Acrolein and crotonaldehyde are two important constituents of cigarette smoke which have well documented toxic effects and could play a role in lung cancer etiology. Their urinary metabolites 3-hydroxypropylmercapturic acid (3-HPMA and 3-hydroxy-1-methylpropylmercapturic acid (HMPMA, respectively, are validated biomarkers of acrolein and crotonaldehyde exposure. We quantified levels of 3-HPMA and HMPMA in the urine of more than 2200 smokers from these five ethnic groups, and also carried out a genome wide association study using blood samples from these subjects. After adjusting for age, sex, creatinine, and total nicotine equivalents, geometric mean levels of 3-HPMA and HMPMA were significantly different in the five groups (P < 0.0001. Native Hawaiians had the highest and Latinos the lowest geometric mean levels of both 3-HPMA and HMPMA. Levels of 3-HPMA and HMPMA were 3787 and 2759 pmol/ml urine, respectively, in Native Hawaiians and 1720 and 2210 pmol/ml urine in Latinos. These results suggest that acrolein and crotonaldehyde may be involved in lung cancer etiology, and that their divergent levels may partially explain the differing risks of Native Hawaiian and Latino smokers. No strong signals were associated with 3-HPMA in the genome wide association study, suggesting that formation of the glutathione conjugate of acrolein is mainly non-enzymatic, while the top significant association with HMPMA was located on chromosome 12 near the TBX3 gene, but its relationship to HMPMA excretion is not clear.

  17. Electronic Cigarettes

    ... topics, including trends in e-cigarette use; health effects of e-cigarettes, nicotine, and secondhand e-cigarette aerosol; e-cigarette marketing and advertising; and evidence-based strategies to reduce e-cigarette use among young people. ...

  18. Estudo imunohistoquímico do remodelamento pulmonar em camundongos expostos à fumaça de cigarro Immunohistochemical study of lung remodeling in mice exposed to cigarette smoke

    Samuel Santos Valença

    2008-10-01

    metalloproteinases is associated with cytokines, and evidence suggests that the matrix metalloproteinase-12 (MMP-12 plays an important role. Our objective was to investigate tissue inhibitor of metalloproteinase-2 (TIMP-2, tumor necrosis factor-alpha (TNF-α and interleukin-6 (IL-6 detection by immunohistochemical methods in mouse lung. METHODS: Male C57BL/6 mice were exposed 3 times a day to smoke of 3 cigarettes over a period of 10, 20, 30 or 60 days in an inhalation chamber (groups CS10, CS20, CS30 and CS60, respectively. Controls were exposed to the same conditions in room air. RESULTS: A progressive increase in the number of alveolar macrophages was observed in the bronchoalveolar lavage fluid of the exposed mice. The mean linear intercept, an indicator of alveolar destruction, was greater in all exposed groups when compared to control group. In the CS10, CS20 and CS30 mice, the immunohistochemical index (II for MMP-12 increased in parallel with a decrease in II for TIMP-2 in the CS10, CS20 and CS30 mice. The II for the cytokines TNF-α and IL-6 was greater in all exposed groups than in the control group. Emphysema, with changes in volume density of collagen and elastic fibers, was observed in the CS60 group. CONCLUSIONS: These findings suggest that cigarette smoke induces emphysema with major participation of TNF-α and IL-6 without participation of neutrophils.

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

    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. Smoke-induced seed germination in California chaparral

    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

  1. Cigarette smoking prior to first cancer and risk of second smoking-associated cancers among survivors of bladder, kidney, head and neck, and stage I lung cancers.

    Shiels, Meredith S; Gibson, Todd; Sampson, Joshua; Albanes, Demetrius; Andreotti, Gabriella; Beane Freeman, Laura; Berrington de Gonzalez, Amy; Caporaso, Neil; Curtis, Rochelle E; Elena, Joanne; Freedman, Neal D; Robien, Kim; Black, Amanda; Morton, Lindsay M

    2014-12-10

    Data on smoking and second cancer risk among cancer survivors are limited. We assessed associations between smoking before first cancer diagnosis and risk of second primary smoking-associated cancers among survivors of lung (stage I), bladder, kidney, and head/neck cancers. Data were pooled from 2,552 patients with stage I lung cancer, 6,386 with bladder cancer, 3,179 with kidney cancer, and 2,967 with head/neck cancer from five cohort studies. We assessed the association between prediagnostic smoking and second smoking-associated cancer risk with proportional hazards regression, and compared these estimates to those for first smoking-associated cancers in all cohort participants. Compared with never smoking, current smoking of ≥ 20 cigarettes per day was associated with increased second smoking-associated cancer risk among survivors of stage I lung (hazard ratio [HR] = 3.26; 95% CI, 0.92 to 11.6), bladder (HR = 3.67; 95% CI, 2.25 to 5.99), head/neck (HR = 4.45; 95% CI, 2.56 to 7.73), and kidney cancers (HR = 5.33; 95% CI, 2.55 to 11.1). These estimates were similar to those for first smoking-associated cancer among all cohort participants (HR = 5.41; 95% CI, 5.23 to 5.61). The 5-year cumulative incidence of second smoking-associated cancers ranged from 3% to 8% in this group of cancer survivors. Understanding risk factors for second cancers among cancer survivors is crucial. Our data indicate that cigarette smoking before first cancer diagnosis increases second cancer risk among cancer survivors, and elevated cancer risk in these survivors is likely due to increased smoking prevalence. The high 5-year cumulative risks of smoking-associated cancers among current smoking survivors of stage I lung, bladder, kidney, and head/neck cancers highlight the importance of smoking cessation in patients with cancer. © 2014 by American Society of Clinical Oncology.

  2. Overexpression of matrix metalloproteinase-12 (MMP-12) correlates with radiation-induced lung fibrosis

    Jung, Myung Gu; Jeong, Ye Ji; Lee, Haejune; Lee, Sujae

    2014-01-01

    MMPs are classified into five subgroups: collagenases (MMP-1, MMP-8, MMP-13), gelatinases (MMP-2, MMP-9), stromelysins (MMP-3, MMP-10, MMP-11), as well as metalloelastase (MMP-12), the membrane-type MMPs (MMP14, MMP15), and other MMPS (e. g., MMP-19, and MMP20). MMP-12 (matrix metalloproteinase12), also known as macrophage metalloelastase, was first identified as an elastolytic metalloproteinase secreted by inflammatory macrophages 30 years ago. MMP-12 degrades extracellular matrix (ECM) components to facilitate tissue remodeling. It can degrade elastin and other substrates, such as type IV collagen, fibronectin, laminin, gelatin, vitronectin, entactin, heparin, and chondroitin sulfates. In the lung, MMP-12 is identified in alveolar macrophages of cigarette smokers as an elastolytic MMP. Inactivation of the MMP-12 gene in knockout mice demonstrates a critical role of MMP-12 in smoking-induced chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the effects of MMP-12 by radiation in lung, so we evaluate that MMP-12 expression pattern in normal lung tissue and cancer cell following radiation. Radiation induced lung injury most commonly occurs as a result of radiation therapy administered to treat cancer. The present study demonstrates that MMP-12 was highly increased in the lung damaged by radiation Thus, MMP-12 might be of potential relevance as a clinically diagnostic tool and sensitive biomarker for radiation induced lung injury and fibrosis

  3. Overexpression of matrix metalloproteinase-12 (MMP-12) correlates with radiation-induced lung fibrosis

    Jung, Myung Gu; Jeong, Ye Ji; Lee, Haejune [Korea Institute of Radiological and Medical Sciences, Seoul (Korea, Republic of); Lee, Sujae [Hanyang Univ., Seoul (Korea, Republic of)

    2014-05-15

    MMPs are classified into five subgroups: collagenases (MMP-1, MMP-8, MMP-13), gelatinases (MMP-2, MMP-9), stromelysins (MMP-3, MMP-10, MMP-11), as well as metalloelastase (MMP-12), the membrane-type MMPs (MMP14, MMP15), and other MMPS (e. g., MMP-19, and MMP20). MMP-12 (matrix metalloproteinase12), also known as macrophage metalloelastase, was first identified as an elastolytic metalloproteinase secreted by inflammatory macrophages 30 years ago. MMP-12 degrades extracellular matrix (ECM) components to facilitate tissue remodeling. It can degrade elastin and other substrates, such as type IV collagen, fibronectin, laminin, gelatin, vitronectin, entactin, heparin, and chondroitin sulfates. In the lung, MMP-12 is identified in alveolar macrophages of cigarette smokers as an elastolytic MMP. Inactivation of the MMP-12 gene in knockout mice demonstrates a critical role of MMP-12 in smoking-induced chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the effects of MMP-12 by radiation in lung, so we evaluate that MMP-12 expression pattern in normal lung tissue and cancer cell following radiation. Radiation induced lung injury most commonly occurs as a result of radiation therapy administered to treat cancer. The present study demonstrates that MMP-12 was highly increased in the lung damaged by radiation Thus, MMP-12 might be of potential relevance as a clinically diagnostic tool and sensitive biomarker for radiation induced lung injury and fibrosis.

  4. Disrupting the Btk Pathway Suppresses COPD-Like Lung Alterations in Atherosclerosis Prone ApoE−/− Mice Following Regular Exposure to Cigarette Smoke

    Jon M. Florence

    2018-01-01

    Full Text Available Chronic obstructive pulmonary disease (COPD is associated with severe chronic inflammation that promotes irreversible tissue destruction. Moreover, the most broadly accepted cause of COPD is exposure to cigarette smoke. There is no effective cure and significantly, the mechanism behind the development and progression of this disease remains unknown. Our laboratory has demonstrated that Bruton’s tyrosine kinase (Btk is a critical regulator of pro-inflammatory processes in the lungs and that Btk controls expression of matrix metalloproteinase-9 (MMP-9 in the alveolar compartment. For this study apolipoprotein E null (ApoE−/− mice were exposed to SHS to facilitate study in a COPD/atherosclerosis comorbidity model. We applied two types of treatments, animals received either a pharmacological inhibitor of Btk or MMP-9 specific siRNA to minimize MMP-9 expression in endothelial cells or neutrophils. We have shown that these treatments had a protective effect in the lung. We have noted a decrease in alveolar changes related to SHS induced inflammation in treated animals. In summary, we are presenting a novel concept in the field of COPD, i.e., that Btk may be a new drug target for this disease. Moreover, cell specific targeting of MMP-9 may also benefit patients affected by this disease.

  5. Cigarette smoke and plutonium

    Filipy, R.E.

    1985-01-01

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

  6. Contribution of alpha- and beta-defensins to lung function decline and infection in smokers: an association study

    Anthonisen Nicholas R

    2006-05-01

    Full Text Available Abstract Background Alpha-defensins, which are major constituents of neutrophil azurophilic granules, and beta-defensins, which are expressed in airway epithelial cells, could contribute to the pathogenesis of chronic obstructive pulmonary disease by amplifying cigarette smoke-induced and infection-induced inflammatory reactions leading to lung injury. In Japanese and Chinese populations, two different beta-defensin-1 polymorphisms have been associated with chronic obstructive pulmonary disease phenotypes. We conducted population-based association studies to test whether alpha-defensin and beta-defensin polymorphisms influenced smokers' susceptibility to lung function decline and susceptibility to lower respiratory infection in two groups of white participants in the Lung Health Study (275 = fast decline in lung function and 304 = no decline in lung function. Methods Subjects were genotyped for the alpha-defensin-1/alpha-defensin-3 copy number polymorphism and four beta-defensin-1 polymorphisms (G-20A, C-44G, G-52A and Val38Ile. Results There were no associations between individual polymorphisms or imputed haplotypes and rate of decline in lung function or susceptibility to infection. Conclusion These findings suggest that, in a white population, the defensin polymorphisms tested may not be of importance in determining who develops abnormally rapid lung function decline or is susceptible to developing lower respiratory infections.

  7. N-acetyl cysteine reverts the proinflammatory state induced by cigarette smoke extract in lung Calu-3 cells

    Ángel G. Valdivieso

    2018-06-01

    Full Text Available Chronic obstructive pulmonary disease (COPD and cystic fibrosis (CF are lethal pulmonary diseases. Cigarette consumption is the main cause for development of COPD, while CF is produced by mutations in the CFTR gene. Although these diseases have a different etiology, both share a CFTR activity impairment and proinflammatory state even under sterile conditions. The aim of this work was to study the extent of the protective effect of the antioxidant N-acetylcysteine (NAC over the proinflammatory state (IL-6 and IL-8, oxidative stress (reactive oxygen species, ROS, and CFTR levels, caused by Cigarette Smoke Extract (CSE in Calu-3 airway epithelial cells. CSE treatment (100 µg/ml during 24 h decreased CFTR mRNA expression and activity, and increased the release of IL-6 and IL-8. The effect on these cytokines was inhibited by N-acetyl cysteine (NAC, 5 mM or the NF-kB inhibitor, IKK-2 (10 µM. CSE treatment also increased cellular and mitochondrial ROS levels. The cellular ROS levels were normalized to control values by NAC treatment, although significant effects on mitochondrial ROS levels were observed only at short times (5´ and effects on CFTR levels were not observed. In addition, CSE reduced the mitochondrial NADH-cytochrome c oxidoreductase (mCx I-III activity, an effect that was not reverted by NAC. The reduced CFTR expression and the mitochondrial damage induced by CSE could not be normalized by NAC treatment, evidencing the need for a more specific reagent. In conclusion, CSE causes a sterile proinflammatory state and mitochondrial damage in Calu-3 cells that was partially recovered by NAC treatment. Keywords: Cigarette smoke extract, Mitochondria, CFTR, ROS, COPD, Cystic fibrosis

  8. Overexpression of the p53 tumor suppressor gene product in primary lung adenocarcinomas is associated with cigarette smoking

    Westra, W. H.; Offerhaus, G. J.; Goodman, S. N.; Slebos, R. J.; Polak, M.; Baas, I. O.; Rodenhuis, S.; Hruban, R. H.

    1993-01-01

    Mutations in the p53 tumor suppressor gene are frequently observed in primary lung adenocarcinomas, suggesting that these mutations are critical events in the malignant transformation of airway cells. These mutations are often associated with stabilization of the p53 gene product, resulting in the

  9. Lung dosimetry for inhaled radon progeny in smokers

    Baias, P. F.; Hofmann, W.; Winkler-Heil, R.; Cosma, C.; Duliu, O. G.

    2010-01-01

    Cigarette smoking may change the morphological and physiological parameters of the lung. Thus the primary objective of the present study was to investigate to what extent these smoke-induced changes can modify deposition, clearance and resulting doses of inhaled radon progeny relative to healthy non-smokers (NSs). Doses to sensitive bronchial target cells were computed for four categories of smokers: (1) Light, short-term (LST) smokers, (2) light, long-term (LLT) smokers, (3) heavy, short-term (HST) smokers and (4) heavy, long-term (HLT) smokers. Because of only small changes of morphological and physiological parameters, doses for the LST smokers hardly differed from those for NSs. For LLT and HST smokers, even a protective effect could be observed, caused by a thicker mucus layer and increased mucus velocities. Only in the case of HLT smokers were doses higher by about a factor of 2 than those for NSs, caused primarily by impaired mucociliary clearance, higher breathing frequency, reduced lung volume and airway obstructions. These higher doses suggest that the contribution of inhaled radon progeny to the risk of lung cancer in smokers may be higher than currently assumed on the basis of NS doses. (authors)

  10. Electronic cigarette (e-cigarette

    Erdinc Nayir

    2016-04-01

    Full Text Available Electronic cigarette (e-cigarette is a device developed with an intent to enable smokers to quit smoking and avoid the unhealthful effects of cigarettes. The popularity of e-cigarette has increased rapidly in recent years. The increase in its use during the adolescence period is attention-grabbing. Despite the fact that e-cigarette has become popular in a dramatic way, there are certain differences of opinion regarding its long-term effects on health, in particular. While some people assert that it is less harmful than conventional cigarettes, some others assert the contrary. Although e-cigarette contains less toxic substances compared to conventional cigarette, it contains certain carcinogens existing in conventional cigarette such as formaldehyde and acetaldehyde. It also contains heavy metals (nickel, chrome that conventional cigarette does not contain; and therefore, raises concerns about health. E-cigarette leads to upper and lower respiratory tract irritation as well as an increased airway resistance and an increased bacterial colonization in the respiratory tract. It may also cause tahcycardia and increase diastolic blood pressure. Although e-cigarette has been found to have certain benefits in terms of smoking cessation, most of the studies have shown unfavorable results. In this collected work, the effects of e-cigarette on health and its role in smoking cessation are discussed in detail.

  11. Quantitative proteomics analysis using 2D-PAGE to investigate the effects of cigarette smoke and aerosol of a prototypic modified risk tobacco product on the lung proteome in C57BL/6 mice.

    Elamin, Ashraf; Titz, Bjoern; Dijon, Sophie; Merg, Celine; Geertz, Marcel; Schneider, Thomas; Martin, Florian; Schlage, Walter K; Frentzel, Stefan; Talamo, Fabio; Phillips, Blaine; Veljkovic, Emilija; Ivanov, Nikolai V; Vanscheeuwijck, Patrick; Peitsch, Manuel C; Hoeng, Julia

    2016-08-11

    Smoking is associated with several serious diseases, such as lung cancer and chronic obstructive pulmonary disease (COPD). Within our systems toxicology framework, we are assessing whether potential modified risk tobacco products (MRTP) can reduce smoking-related health risks compared to conventional cigarettes. In this article, we evaluated to what extent 2D-PAGE/MALDI MS/MS (2D-PAGE) can complement the iTRAQ LC-MS/MS results from a previously reported mouse inhalation study, in which we assessed a prototypic MRTP (pMRTP). Selected differentially expressed proteins identified by both LC-MS/MS and 2D-PAGE approaches were further verified using reverse-phase protein microarrays. LC-MS/MS captured the effects of cigarette smoke (CS) on the lung proteome more comprehensively than 2D-PAGE. However, an integrated analysis of both proteomics data sets showed that 2D-PAGE data complement the LC-MS/MS results by supporting the overall trend of lower effects of pMRTP aerosol than CS on the lung proteome. Biological effects of CS exposure supported by both methods included increases in immune-related, surfactant metabolism, proteasome, and actin cytoskeleton protein clusters. Overall, while 2D-PAGE has its value, especially as a complementary method for the analysis of effects on intact proteins, LC-MS/MS approaches will likely be the method of choice for proteome analysis in systems toxicology investigations. Quantitative proteomics is anticipated to play a growing role within systems toxicology assessment frameworks in the future. To further understand how different proteomics technologies can contribute to toxicity assessment, we conducted a quantitative proteomics analysis using 2D-PAGE and isobaric tag-based LC-MS/MS approaches and compared the results produced from the 2 approaches. Using a prototypic modified risk tobacco product (pMRTP) as our test item, we show compared with cigarette smoke, how 2D-PAGE results can complement and support LC-MS/MS data, demonstrating

  12. Ibuprofen prevents synthetic smoke-induced pulmonary edema

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

    1986-12-01

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

  13. Electronic cigarette (e-cigarette)

    Erdinc Nayir; Burak Karacabey; Onder Kirca; Mustafa Ozdogan

    2016-01-01

    Electronic cigarette (e-cigarette) is a device developed with an intent to enable smokers to quit smoking and avoid the unhealthful effects of cigarettes. The popularity of e-cigarette has increased rapidly in recent years. The increase in its use during the adolescence period is attention-grabbing. Despite the fact that e-cigarette has become popular in a dramatic way, there are certain differences of opinion regarding its long-term effects on health, in particular. While some people assert ...

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

    Guoqing Wang

    Full Text Available Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD and lung cancer remains significantly higher compared to healthy nonsmokers. Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE, we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 9 healthy nonsmokers and 10 healthy smokers, before and after they quit smoking for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy nonsmokers (p1.5, with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/β-catenin signaling pathway being the top identified enriched pathway of the target genes of the persistent dysregulated miRNAs. In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammatory diseases or lung cancer, it is likely that persistent smoking-related changes in SAE miRNAs play a role in the subsequent development of these disorders.

  15. Hydrogen-rich saline inhibits tobacco smoke-induced chronic obstructive pulmonary disease by alleviating airway inflammation and mucus hypersecretion in rats.

    Liu, Zibing; Geng, Wenye; Jiang, Chuanwei; Zhao, Shujun; Liu, Yong; Zhang, Ying; Qin, Shucun; Li, Chenxu; Zhang, Xinfang; Si, Yanhong

    2017-09-01

    Chronic obstructive pulmonary disease induced by tobacco smoke has been regarded as a great health problem worldwide. The purpose of this study is to evaluate the protective effect of hydrogen-rich saline, a novel antioxidant, on chronic obstructive pulmonary disease and explore the underlying mechanism. Sprague-Dawley rats were made chronic obstructive pulmonary disease models via tobacco smoke exposure for 12 weeks and the rats were treated with 10 ml/kg hydrogen-rich saline intraperitoneally during the last 4 weeks. Lung function testing indicated hydrogen-rich saline decreased lung airway resistance and increased lung compliance and the ratio of forced expiratory volume in 0.1 s/forced vital capacity in chronic obstructive pulmonary disease rats. Histological analysis revealed that hydrogen-rich saline alleviated morphological impairments of lung in tobacco smoke-induced chronic obstructive pulmonary disease rats. ELISA assay showed hydrogen-rich saline lowered the levels of pro-inflammatory cytokines (IL-8 and IL-6) and anti-inflammatory cytokine IL-10 in bronchoalveolar lavage fluid and serum of chronic obstructive pulmonary disease rats. The content of malondialdehyde in lung tissue and serum was also determined and the data indicated hydrogen-rich saline suppressed oxidative stress reaction. The protein expressions of mucin MUC5C and aquaporin 5 involved in mucus hypersecretion were analyzed by Western blot and ELISA and the data revealed that hydrogen-rich saline down-regulated MUC5AC level in bronchoalveolar lavage fluid and lung tissue and up-regulated aquaporin 5 level in lung tissue of chronic obstructive pulmonary disease rats. In conclusion, these results suggest that administration of hydrogen-rich saline exhibits significant protective effect on chronic obstructive pulmonary disease through alleviating inflammation, reducing oxidative stress and lessening mucus hypersecretion in tobacco smoke-induced chronic obstructive pulmonary disease rats

  16. Electronic cigarette

    Wang, Tao

    2016-01-01

    As we know E-cigarette is becoming increasingly popular all over the world. It is a new product that the most of smoking people would like to buy and use. However, we are not realizing advantages and disadvantages of e-cigarette clearly. My objective was to research the development of electronic cigarette whether it is under control or a good way of marketing. The thesis has two main parts. They include answers to questions what is electronic cigarette and how to manage the whole industry...

  17. The intractable cigarette 'filter problem'.

    Harris, Bradford

    2011-05-01

    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. 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. 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. 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 production. The synthetic plastic cellulose acetate

  18. Lethal impacts of cigarette smoke in cultured tobacco cells

    Kawano Tomonori

    2011-07-01

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

  19. Ventilatory Function and Cigarette Smoking in Cement Handlers in ...

    Introduction: Occupational exposure to dust and cigarette smoking play important roles in the pathogenesis of lung diseases, particularly in developing countries. To determine the effects of outdoor cement dust exposure and cigarette smoking on lung health, we compared ventilatory function in cement handlers (smokers ...

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

    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.

  1. OZONE MODULATES LUNG TOXICITY IN A MOUSE MODEL OF SMOKE-INDUCED EMPHYSEMA. (R826442)

    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...

  2. INHIBITION OF TOBACCO SMOKE-INDUCED LUNG INFLAMMATION BY A CATALYTIC ANTIOXIDANT

    AMathematical Model for the Kinetics of the Male Reproductive Endocrine SystemLaura K. Potter1,2, H.A. Barton2 and R.W. Setzer21Curriculum in Toxicology, UNC-Chapel Hill, NC; 2US EPA, ORD, NHEERL, ETD, RTP, NCIn this presentation a model for the hormonal regul...

  3. Branched-chain amino acid-rich diet improves skeletal muscle wasting caused by cigarette smoke in rats.

    Tomoda, Koichi; Kubo, Kaoru; Hino, Kazuo; Kondoh, Yasunori; Nishii, Yasue; Koyama, Noriko; Yamamoto, Yoshifumi; Yoshikawa, Masanori; Kimura, Hiroshi

    2014-04-01

    Cigarette smoke induces skeletal muscle wasting by a mechanism not yet fully elucidated. Branched-chain amino acids (BCAA) in the skeletal muscles are useful energy sources during exercise or systemic stresses. We investigated the relationship between skeletal muscle wasting caused by cigarette smoke and changes in BCAA levels in the plasma and skeletal muscles of rats. Furthermore, the effects of BCAA-rich diet on muscle wasting caused by cigarette smoke were also investigated. Wistar Kyoto (WKY) rats that were fed with a control or a BCAA-rich diet were exposed to cigarette smoke for four weeks. After the exposure, the skeletal muscle weight and BCAA levels in plasma and the skeletal muscles were measured. Cigarette smoke significantly decreased the skeletal muscle weight and BCAA levels in both plasma and skeletal muscles, while a BCAA-rich diet increased the skeletal muscle weight and BCAA levels in both plasma and skeletal muscles that had decreased by cigarette smoke exposure. In conclusion, skeletal muscle wasting caused by cigarette smoke was related to the decrease of BCAA levels in the skeletal muscles, while a BCAA-rich diet may improve cases of cigarette smoke-induced skeletal muscle wasting.

  4. Reduced-Nicotine Cigarettes in Young Smokers: Impact of Nicotine Metabolism on Nicotine Dose Effects.

    Faulkner, Paul; Ghahremani, Dara G; Tyndale, Rachel F; Cox, Chelsea M; Kazanjian, Ari S; Paterson, Neil; Lotfipour, Shahrdad; Hellemann, Gerhard S; Petersen, Nicole; Vigil, Celia; London, Edythe D

    2017-07-01

    The use of cigarettes delivering different nicotine doses allows evaluation of the contribution of nicotine to the smoking experience. We compared responses of 46 young adult smokers to research cigarettes, delivering 0.027, 0.110, 0.231, or 0.763 mg nicotine, and conventional cigarettes. On five separate days, craving, withdrawal, affect, and sustained attention were measured after overnight abstinence and again after smoking. Participants also rated each cigarette, and the nicotine metabolite ratio (NMR) was used to identify participants as normal or slow metabolizers. All cigarettes equally alleviated craving, withdrawal, and negative affect in the whole sample, but normal metabolizers reported greater reductions of craving and withdrawal than slow metabolizers, with dose-dependent effects. Only conventional cigarettes and, to a lesser degree, 0.763-mg nicotine research cigarettes increased sustained attention. Finally, there were no differences between ratings of lower-dose cigarettes, but the 0.763-mg cigarettes and (even more so) conventional cigarettes were rated more favorably than lower-dose cigarettes. The findings indicate that smoking-induced relief of craving and withdrawal reflects primarily non-nicotine effects in slow metabolizers, but depends on nicotine dose in normal metabolizers. By contrast, relief of withdrawal-related attentional deficits and cigarette ratings depend on nicotine dose regardless of metabolizer status. These findings have bearing on the use of reduced-nicotine cigarettes to facilitate smoking cessation and on policy regarding regulation of nicotine content in cigarettes. They suggest that normal and slow nicotine metabolizers would respond differently to nicotine reduction in cigarettes, but that irrespective of metabolizer status, reductions to <0.763 mg/cigarette may contribute to temporary attentional deficits.

  5. Novel and Reversible Mechanisms of Smoking-Induced Insulin Resistance in Humans

    Bergman, Bryan C.; Perreault, Leigh; Hunerdosse, Devon; Kerege, Anna; Playdon, Mary; Samek, Ali M.; Eckel, Robert H.

    2012-01-01

    Smoking is the most common cause of preventable morbidity and mortality in the United States, in part because it is an independent risk factor for the development of insulin resistance and type 2 diabetes. However, mechanisms responsible for smoking-induced insulin resistance are unclear. In this study, we found smokers were less insulin sensitive compared with controls, which increased after either 1 or 2 weeks of smoking cessation. Improvements in insulin sensitivity after smoking cessation...

  6. Epidemiology of Lung Cancer

    Brock, Malcolm V.; Ford, Jean G.; Samet, Jonathan M.; Spivack, Simon D.

    2013-01-01

    Background: Ever since a lung cancer epidemic emerged in the mid-1900s, the epidemiology of lung cancer has been intensively investigated to characterize its causes and patterns of occurrence. This report summarizes the key findings of this research. Methods: A detailed literature search provided the basis for a narrative review, identifying and summarizing key reports on population patterns and factors that affect lung cancer risk. Results: Established environmental risk factors for lung cancer include smoking cigarettes and other tobacco products and exposure to secondhand tobacco smoke, occupational lung carcinogens, radiation, and indoor and outdoor air pollution. Cigarette smoking is the predominant cause of lung cancer and the leading worldwide cause of cancer death. Smoking prevalence in developing nations has increased, starting new lung cancer epidemics in these nations. A positive family history and acquired lung disease are examples of host factors that are clinically useful risk indicators. Risk prediction models based on lung cancer risk factors have been developed, but further refinement is needed to provide clinically useful risk stratification. Promising biomarkers of lung cancer risk and early detection have been identified, but none are ready for broad clinical application. Conclusions: Almost all lung cancer deaths are caused by cigarette smoking, underscoring the need for ongoing efforts at tobacco control throughout the world. Further research is needed into the reasons underlying lung cancer disparities, the causes of lung cancer in never smokers, the potential role of HIV in lung carcinogenesis, and the development of biomarkers. PMID:23649439

  7. Inflammatory Effects of Menthol vs. Non-menthol Cigarette Smoke Extract on Human Lung Epithelial Cells: A Double-Hit on TRPM8 by Reactive Oxygen Species and Menthol

    Tzong-Shyuan Lee

    2017-04-01

    Full Text Available Clinical studies suggest that smokers with chronic obstructive pulmonary disease who use menthol cigarettes may display more severe lung inflammation than those who smoke non-menthol cigarette. However, the mechanisms for this difference remain unclear. Menthol is a ligand of transient receptor potential melastatin-8 (TRPM8, a Ca2+-permeant channel sensitive to reactive oxygen species (ROS. We previously reported that exposure of human bronchial epithelial cells (HBECs to non-menthol cigarette smoke extract (Non-M-CSE triggers a cascade of inflammatory signaling leading to IL-8 induction. In this study, we used this in vitro model to compare the inflammatory effects of menthol cigarette smoke extract (M-CSE and Non-M-CSE and delineate the mechanisms underlying the differences in their impacts. Compared with Non-M-CSE, M-CSE initially increased a similar level of extracellular ROS, suggesting the equivalent oxidant potency. However, M-CSE subsequently produced more remarkable elevations in intracellular Ca2+, activation of the mitogen-activated protein kinases (MAPKs/nuclear factor-κB (NF-κB signaling, and IL-8 induction. The extracellular ROS responses to both CSE types were totally inhibited by N-acetyl-cysteine (NAC; a ROS scavenger. The intracellular Ca2+ responses to both CSE types were also totally prevented by NAC, AMTB (a TRPM8 antagonist, or EGTA (an extracellular Ca2+ chelator. The activation of the MAPK/NF-κB signaling and induction of IL-8 to both CSE types were suppressed to similar levels by NAC, AMTB, or EGTA. These results suggest that, in addition to ROS generated by both CSE types, the menthol in M-CSE may act as another stimulus to further activate TRPM8 and induce the observed responses. We also found that menthol combined with Non-M-CSE induced greater responses of intracellular Ca2+ and IL-8 compared with Non-M-CSE alone. Moreover, we confirmed the essential role of TRPM8 in these responses to Non-M-CSE or M-CSE and the

  8. Identification of Novel Targets for Lung Cancer Therapy Using an Induced Pluripotent Stem Cell Model.

    Shukla, Vivek; Rao, Mahadev; Zhang, Hongen; Beers, Jeanette; Wangsa, Darawalee; Wangsa, Danny; Buishand, Floryne O; Wang, Yonghong; Yu, Zhiya; Stevenson, Holly; Reardon, Emily; McLoughlin, Kaitlin C; Kaufman, Andrew; Payabyab, Eden; Hong, Julie A; Zhang, Mary; Davis, Sean R; Edelman, Daniel C; Chen, Guokai; Miettinen, Markku; Restifo, Nicholas; Ried, Thomas; Meltzer, Paul S; Schrump, David S

    2018-04-01

    Despite extensive studies, the genetic and epigenetic mechanisms that mediate initiation and progression of lung cancers have not been fully elucidated. Previously, we have demonstrated that via complementary mechanisms, including DNA methylation, polycomb repressive complexes, and noncoding RNAs, cigarette smoke induces stem-like phenotypes that coincide with progression to malignancy in normal respiratory epithelia as well as enhanced growth and metastatic potential of lung cancer cells. To further investigate epigenetic mechanisms contributing to stemness/pluripotency in lung cancers and potentially identify novel therapeutic targets in these malignancies, induced pluripotent stem cells were generated from normal human small airway epithelial cells. Lung induced pluripotent stem cells were generated by lentiviral transduction of small airway epithelial cells of OSKM (Yamanaka) factors (octamer-binding transcription factor 4 [Oct4], sex-determining region Y box 2 [SOX2], Kruppel-like factor 4 [KLF4], and MYC proto-oncogene, bHLH transcription factor [MYC]). Western blot, real-time polymerase chain reaction, and chromatin immunoprecipitation sequencing analysis were performed. The lung induced pluripotent stem cells exhibited hallmarks of pluripotency, including morphology, surface antigen and stem cell gene expression, in vitro proliferation, and teratoma formation. In addition, lung induced pluripotent stem cells exhibited no chromosomal aberrations, complete silencing of reprogramming transgenes, genomic hypermethylation, upregulation of genes encoding components of polycomb repressive complex 2, hypermethylation of stem cell polycomb targets, and modulation of more than 15,000 other genes relative to parental small airway epithelial cells. Additional sex combs like-3 (ASXL3), encoding a polycomb repressive complex 2-associated protein not previously described in reprogrammed cells, was markedly upregulated in lung induced pluripotent stem cell as well as human

  9. Secondhand Exposure to Vapors From Electronic Cigarettes

    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

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

    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.

  11. Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner

    Garcia-Arcos, Itsaso; Geraghty, Patrick; Baumlin, Nathalie; Campos, Michael; Dabo, Abdoulaye Jules; Jundi, Bakr; Cummins, Neville; Eden, Edward; Grosche, Astrid; Salathe, Matthias; Foronjy, Robert

    2016-01-01

    Background The use of electronic (e)-cigarettes is increasing rapidly, but their lung health effects are not established. Clinical studies examining the potential long-term impact of e-cigarette use on lung health will take decades. To address this gap in knowledge, this study investigated the effects of exposure to aerosolised nicotine-free and nicotine-containing e-cigarette fluid on mouse lungs and normal human airway epithelial cells. Methods Mice were exposed to aerosolised phosphate-buf...

  12. Combined effects of cigarette smoking, gene polymorphisms and methylations of tumor suppressor genes on non small cell lung cancer: a hospital-based case-control study in China

    Jin, Yongtang; Xu, Heyun; Zhang, Chunye; Kong, Yunming; Hou, Yong; Xu, Yingchun; Xue, Shaoli

    2010-01-01

    Cigarette smoking is the most established risk factor, and genetic variants and/or gene promoter methylations are also considered to play an essential role in development of lung cancer, but the pathogenesis of lung cancer is still unclear. We collected the data of 150 cases and 150 age-matched and sex-matched controls on a Hospital-Based Case-Control Study in China. Face to face interviews were conducted using a standardized questionnaire. Gene polymorphism and methylation status were measured by RFLP-PCR and MSP, respectively. Logistic regressive model was used to estimate the odds ratios (OR) for different levels of exposure. After adjusted age and other potential confounding factors, smoking was still main risk factor and significantly increased 3.70-fold greater risk of NSCLC as compared with nonsmokers, and the ORs across increasing levels of pack years were 1, 3.54, 3.65 and 7.76, which the general dose-response trend was confirmed. Our striking findings were that the risk increased 5.16, 8.28 and 4.10-fold, respectively, for NSCLC with promoter hypermethylation of the p16, DAPK or RARβ gene in smokers with CYP1A1 variants, and the higher risk significantly increased in smokers with null GSTM1 and the OR was 17.84 for NSCLC with p16 promoter hypermethylation, 17.41 for DAPK, and 8.18 for RARβ in smokers with null GSTM1 compared with controls (all p < 0.01). Our study suggests the strong combined effects of cigarette smoke, CYP1A1 and GSTM1 Polymorphisms, hypermethylations of p16, DAPK and RARβ promoters in NSCLC, implying complex pathogenesis of NSCLC should be given top priority in future research

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

    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.

  14. Lung

    DeNardo, G.L.; Blankenship, W.J.; Burdine, J.A. Jr.; DeNardo, S.J.

    1975-01-01

    At present no simple statement can be made relative to the role of radionuclidic lung studies in the pediatric population. It is safe to assume that they will be used with increasing frequency for research and clinical applications because of their sensitivity and ready applicability to the pediatric patient. Methods comparable to those used in adults can be used in children older than 4 years. In younger children, however, a single injection of 133 Xe in solution provides an index of both regional perfusion and ventilation which is easier to accomplish. This method is particularly valuable in infants and neonates because it is rapid, requires no patient cooperation, results in a very low radiation dose, and can be repeated in serial studies. Radionuclidic studies of ventilation and perfusion can be performed in almost all children if the pediatrician and the nuclear medicine specialist have motivation and ingenuity. S []ontaneous pulmonary vascular occlusive disease which occurs in infants and pulmonary emboli in children are easily detected using radionuclides. The pathophysiologic defects of pulmonary agenesis, bronchopulmonary sequestration, and foreign body aspiration may be demonstrated by these techniques. These techniques also appear to be useful in following patients with bronchial asthma, cystic fibrosis, congenital emphysema, and postinfection pulmonary abnormalities. (auth)

  15. Comparison of Nasal Epithelial Smoking-Induced Gene Expression on Affymetrix Exon 1.0 and Gene 1.0 ST Arrays

    Xiaoling Zhang

    2013-01-01

    Full Text Available We have previously defined the impact of tobacco smoking on nasal epithelium gene expression using Affymetrix Exon 1.0 ST arrays. In this paper, we compared the performance of the Affymetrix GeneChip Human Gene 1.0 ST array with the Human Exon 1.0 ST array for detecting nasal smoking-related gene expression changes. RNA collected from the nasal epithelium of five current smokers and five never smokers was hybridized to both arrays. While the intersample correlation within each array platform was relatively higher in the Gene array than that in the Exon array, the majority of the genes most changed by smoking were tightly correlated between platforms. Although neither array dataset was powered to detect differentially expressed genes (DEGs at a false discovery rate (FDR <0.05, we identified more DEGs than expected by chance using the Gene ST array. These findings suggest that while both platforms show a high degree of correlation for detecting smoking-induced differential gene expression changes, the Gene ST array may be a more cost-effective platform in a clinical setting for gene-level genomewide expression profiling and an effective tool for exploring the host response to cigarette smoking and other inhaled toxins.

  16. Higher cigarette prices influence cigarette purchase patterns.

    Hyland, A; Bauer, J E; Li, Q; Abrams, S M; Higbee, C; Peppone, L; Cummings, K M

    2005-04-01

    To examine cigarette purchasing patterns of current smokers and to determine the effects of cigarette price on use of cheaper sources, discount/generic cigarettes, and coupons. Higher cigarette prices result in decreased cigarette consumption, but price sensitive smokers may seek lower priced or tax-free cigarette sources, especially if they are readily available. This price avoidance behaviour costs states excise tax money and dampens the health impact of higher cigarette prices. Telephone survey data from 3602 US smokers who were originally in the COMMIT (community intervention trial for smoking cessation) study were analysed to assess cigarette purchase patterns, use of discount/generic cigarettes, and use of coupons. 59% reported engaging in a high price avoidance strategy, including 34% who regularly purchase from a low or untaxed venue, 28% who smoke a discount/generic cigarette brand, and 18% who report using cigarette coupons more frequently that they did five years ago. The report of engaging in a price avoidance strategy was associated with living within 40 miles of a state or Indian reservation with lower cigarette excise taxes, higher average cigarette consumption, white, non-Hispanic race/ethnicity, and female sex. Data from this study indicate that most smokers are price sensitive and seek out measures to purchase less expensive cigarettes, which may decrease future cessation efforts.

  17. Glycerol particle cigarettes: a less harmful option for chronic smokers.

    Sutherland, G; Russell, M A; Stapleton, J A; Feyerabend, C

    1993-01-01

    In 20 smokers who switched to a new type of virtually tar free cigarette for three days, average nicotine intake was reduced by 44%, carbon monoxide intake increased by 19%, while estimated tar intake was reduced by about 90%. Such cigarettes pose substantially less risk of cancer and chronic obstructive lung disease than conventional cigarettes, and their acceptability and safety could be improved by increasing nicotine yield, reducing carbon monoxide yield, and improving the flavour. PMID:8511737

  18. The intractable cigarette ‘filter problem’

    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

  19. Polonium-210 budget in cigarettes

    Khater, A.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 μSv from 210 Po and 210

  20. Inflammatory Response and Barrier Dysfunction by Different e-Cigarette Flavoring Chemicals Identified by Gas Chromatography-Mass Spectrometry in e-Liquids and e-Vapors on Human Lung Epithelial Cells and Fibroblasts.

    Gerloff, Janice; Sundar, Isaac K; Freter, Robert; Sekera, Emily R; Friedman, Alan E; Robinson, Risa; Pagano, Todd; Rahman, Irfan

    2017-03-01

    Recent studies suggest that electronic cigarette (e-cig) flavors can be harmful to lung tissue by imposing oxidative stress and inflammatory responses. The potential inflammatory response by lung epithelial cells and fibroblasts exposed to e-cig flavoring chemicals in addition to other risk-anticipated flavor enhancers inhaled by e-cig users is not known. The goal of this study was to evaluate the release of the proinflammatory cytokine (interleukin-8 [IL-8]) and epithelial barrier function in response to different e-cig flavoring chemicals identified in various e-cig e-liquid flavorings and vapors by chemical characterization using gas chromatography-mass spectrometry analysis. Flavorings, such as acetoin (butter), diacetyl, pentanedione, maltol (malt), ortho-vanillin (vanilla), coumarin, and cinnamaldehyde in comparison with tumor necrosis factor alpha (TNFα), were used in this study. Human bronchial epithelial cells (Beas2B), human mucoepidermoid carcinoma epithelial cells (H292), and human lung fibroblasts (HFL-1) were treated with each flavoring chemical for 24 hours. The cells and conditioned media were then collected and analyzed for toxicity (viability %), lung epithelial barrier function, and proinflammatory cytokine IL-8 release. Cell viability was not significantly affected by any of the flavoring chemicals tested at a concentration of 10 μM to 1 mM. Acetoin and diacetyl treatment induced IL-8 release in Beas2B cells. Acetoin- and pentanedione-treated HFL-1 cells produced a differential, but significant response for IL-8 release compared to controls and TNFα. Flavorings, such as ortho-vanillin and maltol, induced IL-8 release in Beas2B cells, but not in H292 cells. Of all the flavoring chemicals tested, acetoin and maltol were more potent inducers of IL-8 release than TNFα in Beas2B and HFL-1 cells. Flavoring chemicals rapidly impaired epithelial barrier function in human bronchial epithelial cells (16-HBE) as measured by electric cell surface

  1. Lung disease with chronic obstruction in opium smokers in Singapore

    Da Costa, J. L.; Tock, E. P. C.; Boey, H. K.

    1971-01-01

    Fifty-four opium smokers with chronic obstructive lung disease were studied for two-and-a-half years. Forty-eight patients had a cough for at least two years before the onset of inappropriate exertional dyspnoea. Fine, bubbling adventitious sounds suggesting small airway disease were heard on auscultation over the middle and lower lobes in 38 patients. The prevalence of inflammatory lung disease and chronic respiratory failure in this series is suggested as the main cause for the frequent finding of right ventricular hypertrophy and congestive heart failure. Physiological studies revealed moderate to severe airways obstruction with gross over-inflation and, in 32 patients, an additional restrictive defect probably due to peribronchiolar fibrosis. Radiological evidence of chronic bronchitis and bronchiolitis was observed in 45 patients, `pure' chronic bronchiolitis in six patients, and `widespread' emphysema in 25 patients respectively. Necropsy examinations in nine patients, however, showed destructive emphysema of variable severity in all. Chronic bronchiolitis often associated with striking bronchiolectasis was present in six cases. More severe bronchiolar rather than bronchial inflammation was noted. The heavy opium smokers had characteristic nodular shadows on chest radiography, sometimes associated with a striking reticular pattern not seen in `pure' cigarette smokers. This was due to gross pigmented dust (presumably carbon) deposition in relation to blood vessels, lymphatics, and bronchioles, and also within the alveoli. It is speculated that the initial lesion is an acquired bronchiolitis. Opium smoking induces an irritative bronchopathy favouring repeated attacks of acute bronchiolitis and eventually resulting in obliterative bronchiolitis, peribronchiolar fibrosis, chronic bronchitis, and destructive emphysema. Images PMID:5134057

  2. Patients are asking about e-cigarettes. What do we tell them?

    Worsley, D.J.; Jones, K.; Marshman, Z.

    2014-01-01

    Provides an overview of what e-cigarettes are and who is using them.\\ud Considers the safety, quality and efficacy of e-cigarettes.\\ud Outlines the current and proposed legislation on e-cigarettes.\\ud Suggests advice for health professionals to give patients about e-cigarettes.\\ud Lists the questions to consider when deciding whether to permit or prohibit use of e-cigarettes on premises.\\ud Abstract\\ud E-cigarettes are electronic devices that deliver vaporised nicotine liquid into the lungs. ...

  3. Epidemiology of Lung Cancer.

    Schwartz, Ann G; Cote, Michele L

    2016-01-01

    Lung cancer continues to be one of the most common causes of cancer death despite understanding the major cause of the disease: cigarette smoking. Smoking increases lung cancer risk 5- to 10-fold with a clear dose-response relationship. Exposure to environmental tobacco smoke among nonsmokers increases lung cancer risk about 20%. Risks for marijuana and hookah use, and the new e-cigarettes, are yet to be consistently defined and will be important areas for continued research as use of these products increases. Other known environmental risk factors include exposures to radon, asbestos, diesel, and ionizing radiation. Host factors have also been associated with lung cancer risk, including family history of lung cancer, history of chronic obstructive pulmonary disease and infections. Studies to identify genes associated with lung cancer susceptibility have consistently identified chromosomal regions on 15q25, 6p21 and 5p15 associated with lung cancer risk. Risk prediction models for lung cancer typically include age, sex, cigarette smoking intensity and/or duration, medical history, and occupational exposures, however there is not yet a risk prediction model currently recommended for general use. As lung cancer screening becomes more widespread, a validated model will be needed to better define risk groups to inform screening guidelines.

  4. How risky is it to use e-cigarettes? Smokers’ beliefs about their health risks from using novel and traditional tobacco products

    Emery, Sherry L.; Ribisl, Kurt M.; Rini, Christine M.; Brewer, Noel T.

    2015-01-01

    We sought to understand smokers’ perceived likelihood of health problems from using cigarettes and four non-cigarette tobacco products (NCTPs: e-cigarettes, snus, dissolvable tobacco, and smokeless tobacco). A US national sample of 6,607 adult smokers completed an online survey in March 2013. Participants viewed e-cigarette use as less likely to cause lung cancer, oral cancer, or heart disease compared to smoking regular cigarettes (all p e-cigarettes as more likely to cause oral cancer than smoking cigarettes but less likely to cause lung cancer. The dramatic increase in e-cigarette use may be due in part to the belief that they are less risky to use than cigarettes, unlike the other NCTPs. Future research should examine trajectories in perceived likelihood of harm from e-cigarette use and whether they affect regular and electronic cigarette use. PMID:25348584

  5. Effects of electronic cigarette smoking on human health.

    Meo, S A; Al Asiri, S A

    2014-01-01

    Electronic cigarette smoking is gaining dramatic popularity and is steadily spreading among the adolescents, high income, urban population around the world. The aim of this study is to highlight the hazards of e-cigarette smoking on human health. In this study, we identified 38 published studies through a systematic database searches including ISI-web of science and pub-med. We searched the related literature by using the key words including Electronic cigarette, E-cigarette, E-vapers, incidence, hazards. Studies in which electronic cigarette smoking hazards was investigated were included in the study. No limitations on publication status, study design of publication were implemented. Finally we included 28 publications and remaining 10 were excluded. E-smoking can cause, nausea, vomiting, headache, dizziness, choking, burn injuries, upper respiratory tract irritation, dry cough, dryness of the eyes and mucous membrane, release of cytokines and pro-inflammatory mediators, allergic airway inflammation, decreased exhaled nitric oxide (FeNO) synthesis in the lungs, change in bronchial gene expression and risk of lung cancer. Electronic cigarettes are swiftly promoted as an alternative to conventional cigarette smoking, although its use is highly controversial. Electronic cigarettes are not a smoking cessation product. Non-scientific claims about e-cigarettes are creating confusion in public perception about e-cigarette and people believe that e-cigarettes are safe and less addictive, but its use is unsafe and hazardous to human health. E-cigarette smoking should be regulated in the same way as traditional cigarettes and must be prohibited to children and adolescents.

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

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

    2016-01-01

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

  7. Posttranscriptional silencing of the lncRNA MALAT1 by miR-217 inhibits the epithelial–mesenchymal transition via enhancer of zeste homolog 2 in the malignant transformation of HBE cells induced by cigarette smoke extract

    Lu, Lu; Luo, Fei; Liu, Yi; Liu, Xinlu; Shi, Le; Lu, Xiaolin; Liu, Qizhan

    2015-01-01

    Lung cancer is regarded as the leading cause of cancer-related deaths, and cigarette smoking is one of the strongest risk factors for the development of lung cancer. However, the mechanisms for cigarette smoke-induced lung carcinogenesis remain unclear. The present study investigated the effects of an miRNA (miR-217) on levels of an lncRNA (MALAT1) and examined the role of these factors in the epithelial–mesenchymal transition (EMT) induced by cigarette smoke extract (CSE) in human bronchial epithelial (HBE) cells. In these cells, CSE caused decreases of miR-217 levels and increases in lncRNA MALAT1 levels. Over-expression of miR-217 with a mimic attenuated the CSE-induced increase of MALAT1 levels, and reduction of miR-217 levels by an inhibitor enhanced expression of MALAT1. Moreover, the CSE-induced increase of MALAT1 expression was blocked by an miR-217 mimic, indicating that miR-217 negatively regulates MALAT1 expression. Knockdown of MALAT1 reversed CSE-induced increases of EZH2 (enhancer of zeste homolog 2) and H3K27me3 levels. In addition to the alteration from epithelial to spindle-like mesenchymal morphology, chronic exposure of HBE cells to CSE increased the levels of EZH2, H3K27me3, vimentin, and N-cadherin and decreased E-cadherin levels, effects that were reversed by MALAT1 siRNA or EZH2 siRNA. The results indicate that miR-217 regulation of EZH2/H3K27me3 via MALAT1 is involved in CSE-induced EMT and malignant transformation of HBE cells. The posttranscriptional silencing of MALAT1 by miR-217 provides a link, through EZH2, between ncRNAs and the EMT and establishes a mechanism for CSE-induced lung carcinogenesis. - Highlights: • CSE exposure decreases miR-217 levels and increases MALAT1 levels. • miR-217 negatively regulates MALAT1 expression. • MALAT1, via EZH2, is involved in the EMT of CSE-transformed HBE cells.

  8. Alpha radioactivity in cigarette smoke

    Cohen, B.S.; Eisenbud, M.; Harley, N.H.

    1980-01-01

    The α activity of cigarette smoke tar deposited onto membrane filters was found to be associated with the relatively insoluble fraction. Perfusion of the tar with physiological saline resulted in no change in the mean measured activity, but there was more variability in the measured values for the perfused tar than for the initial tar samples. Analysis of cigarette smoke condensate shows that radium and thorium are present, but over 99% of the α activity results from 210 Po. Repeat measurements after a time lapse of 2 1/2 years indicate that the initial 210 Pb content of the tar is roughly 30 to 40% of the original 210 Po content for both unprocessed and perfused samples. An increase in the α activity concentration of smoke deposited in lung tissue may result from the lack of solubility of the radioactive material compared with other smoke constituents

  9. How close are we to definitively identifying the respiratory health effects of e-cigarettes?

    Ratajczak, Alexsandra; Feleszko, Wojciech; Smith, Danielle M; Goniewicz, Maciej

    2018-07-01

    Use of electronic cigarettes (e-cigarettes) is frequently promoted as a less harmful alternative to cigarette smoking. The impact of repeated inhalation of e-cigarette aerosols on respiratory health is not well understood. Areas covered: Using results from laboratory, observational, and clinical studies, we synthesize evidence relevant to potential respiratory health effects that may result from inhalation of e-cigarette aerosols. Expert commentary: Chemical analyses reveal that e-cigarette aerosols contain numerous respiratory irritants and toxicants. There are documented cytotoxic effects of e-cigarette constituents on lung tissue. Studies among ex-smokers who switched to e-cigarettes note reduced exposure to numerous respiratory toxicants, reduced asthma exacerbations, and chronic obstructive pulmonary disease symptoms. Regular exposure to e-cigarette aerosols is associated with impaired respiratory functioning. Potential respiratory health risks resulting from secondhand e-cigarette aerosol exposure have not been sufficiently evaluated. Current evidence indicates that although e-cigarettes are not without risk, these products seemingly pose fewer respiratory health harms issues compared to tobacco cigarettes. Data from prospective studies and randomized controlled trials examining the impact of e-cigarette use on lung health are needed to better understand respiratory health risks tied to use of these products.

  10. The mode of lymphoblastoid cell death in response to gas phase cigarette smoke is dose-dependent

    Baltatzis George E

    2009-09-01

    Full Text Available Abstract Background Cigarette smoke (CS is the main cause in the development of chronic obstructive pulmonary disease (COPD, the pathogenesis of which is related to an extended inflammatory response. In this study, we investigated the effect of low and high doses of gas phase cigarette smoke (GPS on cultured lymphocyte progenitor cells, using techniques to assess cell viability and to elucidate whether cells die of apoptosis or necrosis upon exposure to different doses of GPS. Methods In our approach we utilised a newly-established system of exposure of cells to GPS that is highly controlled, accurately reproducible and simulates CS dosage and kinetics that take place in the smokers' lung. This system was used to study the mode of cell death upon exposure to GPS in conjunction with a range of techniques widely used for cell death studies such as Annexin V staining, activation of caspase -3, cytoplasmic release of cytochrome C, loss of mitochondrial membrane potential and DNA fragmentation. Results Low doses of GPS induced specific apoptotic indexes in CCRF-CEM cells. Specifically, cytochrome C release and cleaved caspase-3 were detected by immunofluorescence, upon treatment with 1-3 puffs GPS. At 4 h post-exposure, caspase-3 activation was observed in western blot analysis, showing a decreasing pattern as GPS doses increased. Concomitant with this behaviour, a dose-dependent change in Δψm depolarization was monitored by flow cytometry 2 h post-exposure, while at 4 h Δψm collapse was observed at the higher doses, indicative of a shift to a necrotic demise. A reduction in DNA fragmentation events produced by 5 puffs GPS as compared to those provoked by 3 puffs GPS, also pointed towards a necrotic response at the higher dose of GPS. Conclusion Collectively, our results support that at low doses gas phase cigarette smoke induces apoptosis in cultured T-lymphocytes, whereas at high doses GPS leads to necrotic death, by-passing the characteristic

  11. Electronic Cigarette Toxicity.

    Payne, J Drew; Michaels, David; Orellana-Barrios, Menfil; Nugent, Kenneth

    2017-04-01

    Electronic cigarettes (e-cigarettes) are often advertised as a healthier product when compared with traditional cigarettes. Currently, there are limited data to support this and only a threat of federal regulation from the US Food and Drug Administration. Calls to poison control centers about e-cigarette toxicity, especially in children, and case reports of toxic exposures have increased over the past 3 years. This research letter reports the frequency of hazardous exposures to e-cigarettes and characterizes the reported adverse health effects associated with e-cigarette toxicity.

  12. How risky is it to use e-cigarettes? Smokers' beliefs about their health risks from using novel and traditional tobacco products.

    Pepper, Jessica K; Emery, Sherry L; Ribisl, Kurt M; Rini, Christine M; Brewer, Noel T

    2015-04-01

    We sought to understand smokers' perceived likelihood of health problems from using cigarettes and four non-cigarette tobacco products (NCTPs: e-cigarettes, snus, dissolvable tobacco, and smokeless tobacco). A US national sample of 6,607 adult smokers completed an online survey in March 2013. Participants viewed e-cigarette use as less likely to cause lung cancer, oral cancer, or heart disease compared to smoking regular cigarettes (all p cause oral cancer than smoking cigarettes but less likely to cause lung cancer. The dramatic increase in e-cigarette use may be due in part to the belief that they are less risky to use than cigarettes, unlike the other NCTPs. Future research should examine trajectories in perceived likelihood of harm from e-cigarette use and whether they affect regular and electronic cigarette use.

  13. Comparison of measured NH4 level and NO emission to declared tar and nicotine values of hundred cigarette brands

    Brunt TM; Verlaan APJ; Cleven RFMJ; Rambali B; Vleeming W; LEO; LAC; LPI

    2003-01-01

    The general hypothesis exists that NH4 level in cigarettes and NO level in cigarette smoke do affect the nicotine availability in the lungs and subsequently play a role in the tobacco addiction. The objective of this report was to investigate whether correlations exist between the cigarette

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

    Abdel-Sater Khaled A.

    2008-06-01

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

  15. How risky is it to use e-cigarettes? Smokers’ beliefs about their health risks from using novel and traditional tobacco products

    Pepper, Jessica K.; Emery, Sherry L.; Ribisl, Kurt M.; Rini, Christine M.; Brewer, Noel T.

    2014-01-01

    We sought to understand smokers’ perceived likelihood of health problems from using cigarettes and four non-cigarette tobacco products (NCTPs: e-cigarettes, snus, dissolvable tobacco, and smokeless tobacco). A US national sample of 6,607 adult smokers completed an online survey in March 2013. Participants viewed e-cigarette use as less likely to cause lung cancer, oral cancer, or heart disease compared to smoking regular cigarettes (all p < .001). This finding was robust for all demographic g...

  16. Exhaled CO, a predictor of lung function?

    Fabricius, Peder; Scharling, Henrik; Løkke, Anders

    2007-01-01

    and whether CO could provide additional information to usual measures of smoking regarding prediction of present lung function and decline in lung function over an extended period of time. METHOD: Cigarette smokers from the Copenhagen City Heart Study with valid measures of lung function and exhaled CO......; in total 3738 subjects, 2096 women and 1642 men. RESULTS: Subjects not inhaling had slightly lower exhaled CO values than those inhaling, but substantially higher values than non-smokers (PSmokers of plain cigarettes had slightly lower CO values than smokers of filter cigarettes (P...BACKGROUND: Smoking is associated with an accelerated loss of lung function and inhalation accelerates the decline further. Exhaled CO reflects the exposure of smoke to the lungs. AIM: To investigate whether self-reported inhalation and type of cigarette influenced the level of exhaled CO...

  17. Manage Emotions Without Cigarettes

    Maybe you used to reach for a cigarette after a tough day at the office. Or found comfort in the companionship of a cigarette on a lonely night. Maybe you used to have cigarettes available as one way to help you deal with uncomfortable emotions.

  18. Lung pathology and exposure to radon daughters

    Saccomanno, G.

    1980-01-01

    The data presented suggest that the primary carcinogen of lung cancer in uranium miners is cigarette smoking because the incidence of lung cancer in noncigarette smokers is insignificant. In cigarette-smoking uranium miners, however, the incidence of cancer in those exposed to significant amounts of radon daughters is higher than in the smoking, nonmining population. This suggests that radon is an additive carcinogen if the lung has been injured by the cigarette-smoking carcinogen. Preliminary studies measuring DNA, T cells, and rosette inhibition immunological studies indicate closer monitoring of uranium miners' health during this occupation may be justified

  19. E-Cigarettes: Use, Effects on Smoking, Risks, and Policy Implications.

    Glantz, Stanton A; Bareham, David W

    2018-04-01

    Since e-cigarettes appeared in the mid-2000s, some practitioners, researchers, and policy makers have embraced them as a safer alternative to conventional cigarettes and an effective way to stop smoking. While e-cigarettes deliver lower levels of carcinogens than do conventional cigarettes, they still expose users to high levels of ultrafine particles and other toxins that may substantially increase cardiovascular and noncancer lung disease risks, which account for more than half of all smoking-caused deaths, at rates similar to conventional cigarettes. Moreover, rather than stimulating smokers to switch from conventional cigarettes to less dangerous e-cigarettes or quitting altogether, e-cigarettes are reducing smoking cessation rates and expanding the nicotine market by attracting youth.

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

    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. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

  1. Are Cigarette Smokers', E-Cigarette Users', and Dual Users' Health-Risk Beliefs and Responses to Advertising Influenced by Addiction Warnings and Product Type?

    Berry, Christopher; Burton, Scot; Howlett, Elizabeth

    2017-10-01

    This research examines cigarette smokers' and e-cigarette users' product-related health-risk beliefs across tobacco products and considers the effects of addiction warnings on consumers' responses to persuasion attempts. Study 1 used a cross-sectional survey with a sample of 195 adult cigarette smokers, e-cigarette users, and dual users to examine health-risk beliefs associated with combustible cigarettes and e-cigarettes (cancer, lung disease, stroke, heart disease, harm to an unborn baby, and addiction). Using a sample of 265 adult cigarette smokers, e-cigarette users, and dual users, Study 2 used a between-subjects experiment to examine the effects of an addiction warning presented in an advertisement on health-risk beliefs and willingness to try the promoted product. Study 1 results reveal that health-risk beliefs for cigarettes are extremely high, whereas health-risk beliefs for e-cigarettes are lower and vary across specific health-risk beliefs; specifically, beliefs related to addiction and harm to an unborn baby are greater than other risk beliefs. Extending these findings, Study 2 results demonstrate that health-risk beliefs associated with cigarette smoking are not affected by an addiction warning in a cigarette advertisement. However, an addiction warning in an e-cigarette advertisement does modify e-cigarette-related risk beliefs, which, in turn, reduces consumers' willingness to try the promoted e-cigarette. Findings indicate that the addition of an addiction warning may be effective in changing consumers' risk beliefs associated with e-cigarettes and consumers' responses to e-cigarette persuasion attempts. By examining cigarette smokers' and e-cigarette users' product-related health-risk beliefs and considering the effects of an addiction warning on consumers' responses to persuasion attempts, this research contributes to the understanding of how warnings in tobacco promotion affect cigarette smokers', e-cigarette users', and dual users' health

  2. Anti-proline-glycine-proline or antielastin autoantibodies are not evident in chronic inflammatory lung disease.

    Greene, Catherine M

    2010-01-01

    In patients with chronic inflammatory lung disease, pulmonary proteases can generate neoantigens from elastin and collagen with the potential to fuel autoreactive immune responses. Antielastin peptide antibodies have been implicated in the pathogenesis of tobacco-smoke-induced emphysema. Collagen-derived peptides may also play a role.

  3. Acrolein in cigarette smoke inhibits T-cell responses.

    Lambert, Cherie; McCue, Jesica; Portas, Mary; Ouyang, Yanli; Li, JiMei; Rosano, Thomas G; Lazis, Alexander; Freed, Brian M

    2005-10-01

    Cigarette smoking inhibits T-cell responses in the lungs, but the immunosuppressive compounds have not been fully identified. Cigarette smoke extracts inhibit IL-2, IFN-gamma, and TNF-alpha production in stimulated lymphocytes obtained from peripheral blood, even when the extracts were diluted 100-fold to 1000-fold. The objective of these studies was to identify the immunosuppressive compounds found in cigarette smoke. Gas chromatography/mass spectroscopy and HPLC were used to identify and quantitate volatile compounds found in cigarette smoke extracts. Bioactivity was measured by viability and production of cytokine mRNA and protein levels in treated human lymphocytes. The vapor phase of the cigarette smoke extract inhibited cytokine production, indicating that the immunosuppressive compounds were volatile. Among the volatile compounds identified in cigarette smoke extracts, only the alpha,beta-unsaturated aldehydes, acrolein (inhibitory concentration of 50% [IC50] = 3 micromol/L) and crotonaldehyde (IC50 = 6 micromol/L), exhibited significant inhibition of cytokine production. Although the levels of aldehydes varied 10-fold between high-tar (Camel) and ultralow-tar (Carlton) extracts, even ultralow-tar cigarettes produced sufficient levels of acrolein (34 micromol/L) to suppress cytokine production by >95%. We determined that the cigarette smoke extract inhibited transcription of cytokine genes. The inhibitory effects of acrolein could be blocked with the thiol compound N-acetylcysteine. The vapor phase from cigarette smoke extracts potently suppresses cytokine production. The compound responsible for this inhibition appears to be acrolein.

  4. Electronic cigarettes: a survey of perceived patient use and attitudes among members of the British thoracic oncology group

    Sherratt, Frances C.; Newson, Lisa; Field, John K.

    2016-01-01

    BACKGROUND: Smoking cessation following lung cancer diagnosis has been found to improve several patient outcomes. Electronic cigarette (e-cigarette) use is now prevalent within Great Britain, however, use and practice among patients with lung cancer has not as yet been explored. The current study aims to explore e-cigarette use among patients and examine current practice among clinicians. The results have important implications for future policy and practice. METHODS: Members of The British T...

  5. E-Cigarette Toxicity?

    Tegin, Gulay; Mekala, Hema Madhuri; Sarai, Simrat Kaur; Lippmann, Steven

    2018-01-01

    Tobacco smoking is the most preventable cause of morbidity and mortality. In just a few short years, electronic cigarettes (e-cigarettes) have become increasingly popular, especially for younger individuals. Many people believe that e-cigarettes are safe. The inhaled aerosols of e-cigarettes contain numerous potential toxicities, some of which could be dangerous for health with long-term use. The safety of prolonged aerosol exposure is not known. The use of e-cigarettes as a harm-reduction tool at stopping tobacco smoking is not uniformly successful. E-cigarettes may be safer than tobacco products, but repeated prolonged exposure to their aerosols has its own considerable potential risk. The long-term health consequences of their use remain to be established. Physicians should vigorously discourage the use of e-cigarettes and tobacco products, with special emphasis on abstinence for younger people and during pregnancy or lactation.

  6. Smoking habits in lung cancer patients: a hospital based case ...

    This retrospective, hospital based case-control study was designed to investigate the cigarette smoking history, the relationship between cigarette smoking and the risk of lung cancer in KHMC-Jordan. Six hundred cases with lung cancer (576 males, 24 females) and 600 controls were included in the study. The majority of ...

  7. Decline and infiltrated lung

    Giraldo Estrada, Horacio; Arboleda Casas, Felipe; Duarte, Monica; Triana Harker, Ricardo

    2001-01-01

    The paper describes the decline and infiltrated lung in a patient of 45 years, with diagnosis of arthritis rheumatoid from the 43 years, asymptomatic, without treatment, married, of the 15 to the 35 years of 3 to 10 cigarettes daily, she refers of 7 months of evolution episodes of moderate dyspnoea with exercises and dry cough with occasional mucous expectoration between others

  8. Diagnostic Imaging of Lung Cancer

    Kemal Kara

    2012-12-01

    Full Text Available Lung cancer is the most common cause of cancer related death in men and women. It is frequently seen among men than in women and male-female ratio is 1.5:1. Common epidemiological factors that increase risk of lung cancer is smoking. Early age to start smoking, high number of smoking cigarettes per a day and depth of inhalation increase risk of lung cancer. 25% of patients with lung cancer are nonsmokers that passively exposed to cigarette smoke. Occupational exposure to substances such as asbestos, arsenic, nickel, beryllium, mustard gas increases the risk of lung cancer. The well defined risk factor is exposure to asbestos. In addition advanced age, diffuse pulmonary fibrosis, chronic obstructive pulmonary disease (COPD and genetic predisposition are the risk factors that increases lung cancer. [TAF Prev Med Bull 2012; 11(6.000: 749-756

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

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

    1978-02-01

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

  10. Chronic electronic cigarette exposure in mice induces features of COPD in a nicotine-dependent manner.

    Garcia-Arcos, Itsaso; Geraghty, Patrick; Baumlin, Nathalie; Campos, Michael; Dabo, Abdoulaye Jules; Jundi, Bakr; Cummins, Neville; Eden, Edward; Grosche, Astrid; Salathe, Matthias; Foronjy, Robert

    2016-12-01

    The use of electronic (e)-cigarettes is increasing rapidly, but their lung health effects are not established. Clinical studies examining the potential long-term impact of e-cigarette use on lung health will take decades. To address this gap in knowledge, this study investigated the effects of exposure to aerosolised nicotine-free and nicotine-containing e-cigarette fluid on mouse lungs and normal human airway epithelial cells. Mice were exposed to aerosolised phosphate-buffered saline, nicotine-free or nicotine-containing e-cigarette solution, 1-hour daily for 4 months. Normal human bronchial epithelial (NHBE) cells cultured at an air-liquid interface were exposed to e-cigarette vapours or nicotine solutions using a Vitrocell smoke exposure robot. Inhalation of nicotine-containing e-cigarettes increased airway hyper-reactivity, distal airspace enlargement, mucin production, cytokine and protease expression. Exposure to nicotine-free e-cigarettes did not affect these lung parameters. NHBE cells exposed to nicotine-containing e-cigarette vapour showed impaired ciliary beat frequency, airway surface liquid volume, cystic fibrosis transmembrane regulator and ATP-stimulated K+ ion conductance and decreased expression of FOXJ1 and KCNMA1. Exposure of NHBE cells to nicotine for 5 days increased interleukin (IL)-6 and IL-8 secretion. Exposure to inhaled nicotine-containing e-cigarette fluids triggered effects normally associated with the development of COPD including cytokine expression, airway hyper-reactivity and lung tissue destruction. These effects were nicotine-dependent both in the mouse lung and in human airway cells, suggesting that inhaled nicotine contributes to airway and lung disease in addition to its addictive properties. Thus, these findings highlight the potential dangers of nicotine inhalation during e-cigarette use. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

  11. Estimating mortality due to cigarette smoking

    Brønnum-Hansen, H; Juel, K

    2000-01-01

    We estimated the mortality from various diseases caused by cigarette smoking using two methods and compared the results. In one method, the "Prevent" model is used to simulate the effect on mortality of the prevalence of cigarette smoking derived retrospectively. The other method, suggested by R....... Peto et al (Lancet 1992;339:1268-1278), requires data on mortality from lung cancer among people who have never smoked and among smokers, but it does not require data on the prevalence of smoking. In the Prevent model, 33% of deaths among men and 23% of those among women in 1993 from lung cancer...... are small and appear to be explicable. The Prevent model can be used for more general scenarios of effective health promotion, but it requires more data than the Peto et al method, which can be used only to estimate mortality related to smoking....

  12. Asbestos exposure-cigarette smoking interactions among shipyard workers

    Blanc, P.D.; Golden, J.A.; Gamsu, G.; Aberle, D.R.; Gold, W.M.

    1988-01-01

    The authors studied the roentgenograms, pulmonary function tests, and physical findings of 294 shipyard workers to evaluate asbestos exposure-cigarette smoking interactions. Roentgenographic parenchymal opacities, decreased pulmonary diffusing capacity for carbon monoxide, decreased flow at low lung volume, rales, and clubbing were each significantly related to the number of years elapsed since first exposure to asbestos and cigarette smoking status when analyzed by logistic regression. A dose-dependent cigarette smoking response that was consistent with synergism was present only for parenchymal opacities and decreased flow at low lung volume. These findings suggest that decreased flow at low lung volume, possibly reflecting peribronchiolar fibrosis, may be a functional corollary to smoking-associated parenchymal roentgenographic opacities among some asbestos-exposed individuals

  13. Role of Nrf2 and protective effects of Metformin against tobacco smoke-induced cerebrovascular toxicity

    Shikha Prasad

    2017-08-01

    Full Text Available Cigarette smoking (CS is associated with vascular endothelial dysfunction in a causative way primarily related to the TS content of reactive oxygen species (ROS, nicotine, and inflammation. TS promotes glucose intolerance and increases the risk of developing type-2 diabetes mellitus (2DM with which it shares other pathogenic traits including the high risk of cerebrovascular and neurological disorders like stroke via ROS generation, inflammation, and blood-brain barrier (BBB impairment. Herein we provide evidence of the role played by nuclear factor erythroid 2-related factor (Nrf2 in CS-induced cerebrobvascular/BBB impairments and how these cerebrovascular harmful effects can be circumvented by the use of metformin (MF; a widely prescribed, firstline anti-diabetic drug treatment. Our data in fact revealed that MF activates counteractive mechanisms primarily associated with the Nrf2 pathway which drastically reduce CS toxicity at the cerebrovascular level. These include the suppression of tight junction (TJ protein downregulation and loss of BBB integrity induced by CS, reduction of inflammation and oxidative stress, renormalization of the expression levels of the major BBB glucose transporter Glut-1 and that of the anticoagulant factor thrombomodulin. Further, we provide additional insights on the controversial interplay between Nrf2 and AMPK. Keywords: Oxidative stress, Cigarette smoke, Metformin, Blood hemostasis, Blood brain barrier, Tight junctions, Nrf2, Glucose transporter

  14. Diet and lung cancer

    Fabricius, P; Lange, Peter

    2003-01-01

    Lung cancer is the leading cause of cancer-related deaths worldwide. While cigarette smoking is of key importance, factors such as diet also play a role in the development of lung cancer. MedLine and Embase were searched with diet and lung cancer as the key words. Recently published reviews...... and large well designed original articles were preferred to form the basis for the present article. A diet rich in fruit and vegetables reduces the incidence of lung cancer by approximately 25%. The reduction is of the same magnitude in current smokers, ex-smokers and never smokers. Supplementation...... with vitamins A, C and E and beta-carotene offers no protection against the development of lung cancer. On the contrary, beta-carotene supplementation has, in two major randomised intervention trials, resulted in an increased mortality. Smoking remains the leading cause of lung cancer. The adverse effects...

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

    Holden, W.E.; Maier, J.M.; Malinow, M.R.

    1989-01-01

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

  16. Use of Electronic Cigarettes Among U.S. Adults With Medical Comorbidities.

    Kruse, Gina R; Kalkhoran, Sara; Rigotti, Nancy A

    2017-06-01

    Electronic cigarette (e-cigarette) use is rising in the U.S. Smokers with comorbidities may increasingly use e-cigarettes if they believe e-cigarettes reduce smoking-related harm. This study examined e-cigarette use among adults with medical comorbidities. In 2016, this study analyzed 68,136 U.S. adults in the 2014 and 2015 National Health Interview Survey. Prevalent e-cigarette use by medical comorbidities and adjusted odds of e-cigarette use were calculated. Among current cigarette smokers, ever use of e-cigarettes was more often reported by adults with one or more medical comorbidity versus those without comorbidity (18-24 years: 73.5% vs 61.4%; 25-44 years: 60.6% vs 54.3%; 45-64 years: 46.5% vs 40.3%; ≥65 years: 35.2% vs 19.4%; all pe-cigarette use more often than those without comorbidity (25-44 years, 17.8% vs 14.3%, p=0.03; 45-64 years, 15.9% vs 11.5%, p=0.02). Current smokers with chronic obstructive pulmonary disease, asthma, and cardiovascular disease had higher odds of ever e-cigarette use versus those without comorbidity. Current smokers with asthma and cardiovascular disease had higher odds of current e-cigarette use. Former smokers with chronic obstructive pulmonary disease had higher odds of ever and current e-cigarette use and former smokers with cancer had lower odds of current e-cigarette use. E-cigarette use by current and former smokers with medical comorbidities is substantial, especially among individuals with chronic lung or cardiovascular disease. Clinicians should routinely ask these patients about e-cigarette use, actively consider all pathways to help their patients quit combustible cigarettes, and recommend evidence-based treatments. Copyright © 2017 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.

  17. Cigarette smoke and plutonium

    Filipy, R.E.

    1983-01-01

    The major objective of this project is to obtain experimental data that are directly applicable to resolving the question of whether cigarette smokers are at greater risk than nonsmokers to potential health effects of inhaled plutonium. Because cigarette smokers constitute a large fraction of the population, a synergistic effect of plutonium and cigarette smoke might influence estimates of the health risk for plutonium and other transuranics released to the environment

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

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

    2016-01-01

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

  19. The E-cigarette Social Environment, E-cigarette Use, and Susceptibility to Cigarette Smoking.

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

    2016-07-01

    One concern regarding the recent increase in adolescent e-cigarette use is the possibility that electronic (e-) cigarettes may be used by those who might not otherwise have used cigarettes, and that dual use, or transition to cigarette use alone, may follow. Questionnaire data were obtained in 2014 from 11th/12th grade students attending schools in 12 communities included in the Southern California Children's Health Study. We evaluated the cross-sectional association between e-cigarette use, the social environment (family and friends' use and approval of e-cigarettes and cigarettes), and susceptibility to future cigarette use among never cigarette smokers (N = 1,694), using previously validated measures based on reported absence of a definitive commitment not to smoke. Among adolescents who had never used cigarettes, 31.8% of past e-cigarette users and 34.6% of current (past 30-day) e-cigarette users indicated susceptibility to cigarette use, compared with 21.0% of never e-cigarette users. The odds of indicating susceptibility to cigarette use were two times higher for current e-cigarette users compared with never users (odds ratio = 1.97; 95% confidence interval: 1.21-3.22). A social environment favorable to e-cigarettes (friends' use of and positive attitudes toward the use of e-cigarettes) was also associated with greater likelihood of susceptibility to cigarette use, independent of an individual's e-cigarette use. E-cigarette use in adolescence, and a pro-e-cigarette social environment, may put adolescents at risk for future use of cigarettes. E-cigarettes may contribute to subsequent cigarette use via nicotine addiction or social normalization of smoking behaviors. Copyright © 2016 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved.

  20. Diet and lung cancer

    Fabricius, P; Lange, Peter

    2003-01-01

    Lung cancer is the leading cause of cancer-related deaths worldwide. While cigarette smoking is of key importance, factors such as diet also play a role in the development of lung cancer. MedLine and Embase were searched with diet and lung cancer as the key words. Recently published reviews and l...... are only ameliorated to a minor degree by a healthy diet.......Lung cancer is the leading cause of cancer-related deaths worldwide. While cigarette smoking is of key importance, factors such as diet also play a role in the development of lung cancer. MedLine and Embase were searched with diet and lung cancer as the key words. Recently published reviews...... and large well designed original articles were preferred to form the basis for the present article. A diet rich in fruit and vegetables reduces the incidence of lung cancer by approximately 25%. The reduction is of the same magnitude in current smokers, ex-smokers and never smokers. Supplementation...

  1. Cigarette smoking and pulmonary diffusion defects in rheumatoid arthritis.

    Westedt, M L; Hazes, J M; Breedveld, F C; Sterk, P J; Dijkman, J H

    1998-01-01

    The pathogenesis of lung disease in rheumatoid arthritis (RA) has still to be defined. Risk factors associated with lung involvement in RA were investigated by means of pulmonary function studies in 40 RA patients without apparent lung disease. A decreased carbon monoxide (CO) diffusion capacity indicative of interstitial lung disease (ILD) was the main pulmonary function defect found in the first 20 patients. The occurrence was associated with current cigarette smoking. This association was confirmed in a case control study performed subsequently. These data suggest that ILD in RA is stimulated by smoking and provide an additional argument that modification of smoking behaviour in RA patients might lead to less severe complications.

  2. Perceptions about e-cigarette safety may lead to e-smoking during pregnancy.

    Baeza-Loya, Selina; Viswanath, Humsini; Carter, Asasia; Molfese, David L; Velasquez, Kenia M; Baldwin, Philip R; Thompson-Lake, Daisy G Y; Sharp, Carla; Fowler, J Christopher; De La Garza, Richard; Salas, Ramiro

    2014-01-01

    Electronic cigarettes (e-cigarettes) are nicotine-delivery devices that are increasingly used, especially by young people. Because e-cigarettes lack many of the substances found in regular tobacco, they are often perceived as a safer smoking alternative, especially in high-risk situations such as pregnancy. However, studies suggest that it is exposure to nicotine that is most detrimental to prenatal development. The authors studied perceptions of tobacco and e-cigarette health risks using a multiple-choice survey. To study the perceived safety of e-cigarettes versus tobacco cigarettes, 184 modified Global Health Youth Surveys (WHO, http://www.who.int/tobacco/surveillance/gyts/en/ ) were completed electronically or on paper. Age range, smoking status, and perceptions about tobacco cigarettes and e-cigarettes were studied. The results verified that younger people use e-cigarettes more than older people. Tobacco cigarettes were perceived as more harmful than e-cigarettes to health in general, including lung cancer and pregnancy. Although more research is necessary, the authors postulate that the perception that e-cigarettes are safer during pregnancy may induce pregnant women to use these devices more freely. Given that nicotine is known to cause fetal harm, pregnant mothers who smoke e-cigarettes could cause even greater harm to the fetus because e-cigarettes are perceived as being safer than tobacco cigarettes. Until more data about the effects of nicotine during pregnancy are available, the authors advocate for labeling of e-cigarettes as potentially harmful, at least during pregnancy.

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

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

    2014-01-01

    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

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

    Camlin, Nicole J. [School of Environment and Life Sciences, University of Newcastle, Callaghan, NSW 2308 (Australia); McLaughlin, Eileen A., E-mail: eileen.mclaughlin@newcastle.edu.au [School of Environment and Life Sciences, University of Newcastle, Callaghan, NSW 2308 (Australia); Holt, Janet E. [School of Biomedical Sciences and Pharmacy, University of Newcastle, Callaghan, NSW 2308 (Australia)

    2014-12-15

    A finite number of oocytes are established within the mammalian ovary prior to birth to form a precious ovarian reserve. Damage to this limited pool of gametes by environmental factors such as cigarette smoke and its constituents therefore represents a significant risk to a woman's reproductive capacity. Although evidence from human studies to date implicates a detrimental effect of cigarette smoking on female fertility, these retrospective studies are limited and present conflicting results. In an effort to more clearly understand the effect of cigarette smoke, and its chemical constituents, on female fertility, a variety of in vivo and in vitro animal models have been developed. This article represents a systematic review of the literature regarding four of experimental model types: 1) direct exposure of ovarian cells and follicles to smoking constituents’ in vitro, 2) direct exposure of whole ovarian tissue with smoking constituents in vitro, 3) whole body exposure of animals to smoking constituents and 4) whole body exposure of animals to cigarette smoke. We summarise key findings and highlight the strengths and weaknesses of each model system, and link these to the molecular mechanisms identified in smoke-induced fertility changes. - Highlights: • In vivo exposure to individual cigarette smoke chemicals alters female fertility. • The use of in vitro models in determining molecular mechanisms • Whole cigarette smoke inhalation animal models negatively affect ovarian function.

  5. Lung volumes and emphysema in smokers with interstitial lung abnormalities.

    Washko, George R; Hunninghake, Gary M; Fernandez, Isis E; Nishino, Mizuki; Okajima, Yuka; Yamashiro, Tsuneo; Ross, James C; Estépar, Raúl San José; Lynch, David A; Brehm, John M; Andriole, Katherine P; Diaz, Alejandro A; Khorasani, Ramin; D'Aco, Katherine; Sciurba, Frank C; Silverman, Edwin K; Hatabu, Hiroto; Rosas, Ivan O

    2011-03-10

    Cigarette smoking is associated with emphysema and radiographic interstitial lung abnormalities. The degree to which interstitial lung abnormalities are associated with reduced total lung capacity and the extent of emphysema is not known. We looked for interstitial lung abnormalities in 2416 (96%) of 2508 high-resolution computed tomographic (HRCT) scans of the lung obtained from a cohort of smokers. We used linear and logistic regression to evaluate the associations between interstitial lung abnormalities and HRCT measurements of total lung capacity and emphysema. Interstitial lung abnormalities were present in 194 (8%) of the 2416 HRCT scans evaluated. In statistical models adjusting for relevant covariates, interstitial lung abnormalities were associated with reduced total lung capacity (-0.444 liters; 95% confidence interval [CI], -0.596 to -0.292; Ppulmonary disease (COPD) (odds ratio, 0.53; 95% CI, 0.37 to 0.76; P<0.001). The effect of interstitial lung abnormalities on total lung capacity and emphysema was dependent on COPD status (P<0.02 for the interactions). Interstitial lung abnormalities were positively associated with both greater exposure to tobacco smoke and current smoking. In smokers, interstitial lung abnormalities--which were present on about 1 of every 12 HRCT scans--were associated with reduced total lung capacity and a lesser amount of emphysema. (Funded by the National Institutes of Health and the Parker B. Francis Foundation; ClinicalTrials.gov number, NCT00608764.).

  6. Electronic cigarette liquid increases inflammation and virus infection in primary human airway epithelial cells.

    Wu, Qun; Jiang, Di; Minor, Maisha; Chu, Hong Wei

    2014-01-01

    The use of electronic cigarettes (e-cigarettes) is rapidly increasing in the United States, especially among young people since e-cigarettes have been perceived as a safer alternative to conventional tobacco cigarettes. However, the scientific evidence regarding the human health effects of e-cigarettes on the lung is extremely limited. The major goal of our current study is to determine if e-cigarette use alters human young subject airway epithelial functions such as inflammatory response and innate immune defense against respiratory viral (i.e., human rhinovirus, HRV) infection. We examined the effects of e-cigarette liquid (e-liquid) on pro-inflammatory cytokine (e.g., IL-6) production, HRV infection and host defense molecules (e.g., short palate, lung, and nasal epithelium clone 1, SPLUNC1) in primary human airway epithelial cells from young healthy non-smokers. Additionally, we examined the role of SPLUNC1 in lung defense against HRV infection using a SPLUNC1 knockout mouse model. We found that nicotine-free e-liquid promoted IL-6 production and HRV infection. Addition of nicotine into e-liquid further amplified the effects of nicotine-free e-liquid. Moreover, SPLUNC1 deficiency in mice significantly increased lung HRV loads. E-liquid inhibited SPLUNC1 expression in primary human airway epithelial cells. These findings strongly suggest the deleterious health effects of e-cigarettes in the airways of young people. Our data will guide future studies to evaluate the impact of e-cigarettes on lung health in human populations, and help inform the public about potential health risks of e-cigarettes.

  7. Electronic cigarette liquid increases inflammation and virus infection in primary human airway epithelial cells.

    Qun Wu

    Full Text Available The use of electronic cigarettes (e-cigarettes is rapidly increasing in the United States, especially among young people since e-cigarettes have been perceived as a safer alternative to conventional tobacco cigarettes. However, the scientific evidence regarding the human health effects of e-cigarettes on the lung is extremely limited. The major goal of our current study is to determine if e-cigarette use alters human young subject airway epithelial functions such as inflammatory response and innate immune defense against respiratory viral (i.e., human rhinovirus, HRV infection.We examined the effects of e-cigarette liquid (e-liquid on pro-inflammatory cytokine (e.g., IL-6 production, HRV infection and host defense molecules (e.g., short palate, lung, and nasal epithelium clone 1, SPLUNC1 in primary human airway epithelial cells from young healthy non-smokers. Additionally, we examined the role of SPLUNC1 in lung defense against HRV infection using a SPLUNC1 knockout mouse model. We found that nicotine-free e-liquid promoted IL-6 production and HRV infection. Addition of nicotine into e-liquid further amplified the effects of nicotine-free e-liquid. Moreover, SPLUNC1 deficiency in mice significantly increased lung HRV loads. E-liquid inhibited SPLUNC1 expression in primary human airway epithelial cells. These findings strongly suggest the deleterious health effects of e-cigarettes in the airways of young people. Our data will guide future studies to evaluate the impact of e-cigarettes on lung health in human populations, and help inform the public about potential health risks of e-cigarettes.

  8. E-Cigarettes (For Parents)

    ... Staying Safe Videos for Educators Search English Español E-Cigarettes KidsHealth / For Parents / E-Cigarettes What's in this ... Print en español Los cigarrillos electrónicos What Are E-Cigarettes? E-cigarettes are devices marketed as a safe ...

  9. Toxicological and analytical assessment of e-cigarette refill components on airway epithelia.

    Singh, Jasjot; Luquet, Emilie; Smith, David P T; Potgieter, Herman J; Ragazzon, Patricia

    2016-12-01

    There are over 2.6 million users of e-cigarettes in the United Kingdom alone as they have been promoted as a safer alternative to traditional cigarettes. The addition of flavours and aromas has also proven to be popular with younger generations. In this review, we survey the range of studies in the short timeframe since e-cigarettes reached the market to draw attention to the health associated risks and benefits of their introduction. We complement this review with a case study reporting on the composition of selected e-cigarette refills with particular emphasis on the toxicological activity of its components on lung cells.

  10. Experimental animal studies of radon and cigarette smoke

    Cross, F.T.; Dagle, G.E.; Gies, R.A.; Smith, L.G.; Buschbom, R.L.

    1992-01-01

    Cigarette-smoking is a dominant cause of lung cancer and confounds risk assessment of exposure to radon decay products. Evidence in humans on the interaction between cigarette-smoking and exposure to radon decay products, although limited, indicates a possible synergy. Experimental animal data, in addition to showing synergy, also show a decrease or no change in risk with added cigarette-smoke exposures. This article reviews previous animal data developed at Compagnie Generale des Matieres Nucleaires and Pacific Northwest Laboratory (PNL) on mixed exposures to radon and cigarette smoke, and highlights new initiation-promotion-initiation (IPI) studies at PNL that were designed within the framework of a two-mutation carcinogenesis model. Also presented are the PNL exposure system, experimental protocols, dosimetry, and biological data observed to date in IPI animals

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

    Filipy, R.E.; Pappin, J.L.; Stevens, D.L.; Irby, S.G.

    1980-01-01

    Groups of rats were exposed or sham exposed to cigarette smoke for 7 mo, at which time they were exposed to an aerosol of 239 PuO 2 . Rats were then subjected to whole-body counting (17-keV X-rays) periodically, beginning at day 4 after plutonium exposure, and smoke exposures or sham exposures were resumed on day 7. Clearance of plutonium from the lungs of cigarette-smoke-exposed rats was significantly slower than that from the sham-exposed rats' lungs. The difference between the two groups became significant 7 days after the resumption of cigarette-smoke exposures

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

    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 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.

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

    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. Copyright © 2014 the American Physiological Society.

  14. Peak Expiratory Flow Rate In Cigarette Smokers | Ukoli | Highland ...

    Objective: To compare lung function between smokers and non-smokers using Peak Expiratory Flow Rate (PEFR). Methods: This study examines the peak expiratory flow rate (PEFR) of three hundred and forty cigarette smokers, age and sex-matched with PEFR of equal number of non-smokers. Results: The mean PEFR of ...

  15. Induction of lung lesions in Wistar rats by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and its inhibition by aspirin and phenethyl isothiocyanate

    Ye, Bo; Zhang, Yu-Xia; Yang, Fei; Chen, Hong-Lei; Xia, Dong; Liu, Ming-Qiu; Lai, Bai-Tang

    2007-01-01

    The development of effective chemopreventive agents against cigarette smoke-induced lung cancer could be greatly facilitated by suitable laboratory animal models, such as animals treated with the tobacco-specific lung carcinogen 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK). In the current study, we established a novel lung cancer model in Wistar rats treated with NNK. Using this model, we assessed the effects of two chemopreventive agents, aspirin and phenethyl isothiocyanate (PEITC), on tumor progression. First, rats were treated with a single-dose of NNK by intratracheal instillation; control rats received iodized oil. The animals were then sacrificed on the indicated day after drug administration and examined for tumors in the target organs. PCNA, p63 and COX-2 expression were analyzed in the preneoplastic lung lesions. Second, rats were treated with a single-dose of NNK (25 mg/kg body weight) in the absence or presence of aspirin and/or PEITC in the daily diet. The control group received only the vehicle in the regular diet. The animals were sacrificed on day 91 after bronchial instillation of NNK. Lungs were collected and processed for histopathological and immunohistochemical assays. NNK induced preneoplastic lesions in lungs, including 33.3% alveolar hyperplasia and 55.6% alveolar atypical dysplasia. COX-2 expression increased similarly in alveolar hyperplasia and alveolar atypical dysplasia, while PCNA expression increased more significantly in the latter than the former. No p63 expression was detected in the preneoplastic lesions. In the second study, the incidences of alveolar atypical dysplasia were reduced to 10%, 10% and 0%, respectively, in the aspirin, PEITC and aspirin and PEITC groups, compared with 62.5% in the carcinogen-treated control group. COX-2 expression decreased after dietary aspirin or aspirin and PEITC treatment. PCNA expression was significantly reduced in the aspirin and PEITC group. (1) A single dose of 25 mg/kg body weight

  16. Smoking-induced dopamine release studied with [11C]raclopride PET

    Kim, Yu Kyeong; Cho, Sang Soo; Lee, Do Hoon

    2005-01-01

    It has been postulated that dopamine release in the striatum underlies the reinforcing properties of nicotine. Substantial evidence in the animal studies demonstrates that nicotine interacts with and regulates the activation of the dopaminergic neuron. The aim of this study was to visualize the dopamine release by smoking in human brain using PET scan with [ 11 C]raclopride. Four male non-smokers or ex-smokers with an abstinence period longer than 1 year (mean age of 24.3±2.6 years) were enrolled in this study. Dopamine D2 receptor radioligand, [ 11 C]raclopride was administrated with bolus-plus-constant infusion. Dynamic PET was performed during 120 minutes (3x20s, 2x60s, 2x120s, 1x180s and 22x300s). Following the 50 minute-scanning, subjects smoked a cigarette containing 1 mg of nicotine while in the scanner. Blood samples for the measurements of plasma nicotine levels were collected at 0, 5, 10, 15, 20, 25, 30, 45, 60, and 90 minute after smoking. Regions for striatal structures were drawn on the coronal summed PET images guided with co-registered MRI. Binding potential, calculated as striatal-cerebellar/cerebellar activity, was measured under equilibrium condition at baseline and smoking session. The mean change in binding potential between the baseline and smoking in caudate, Putamen and ventral striatum was 3.7 % , 4.0 % and 8.6 %, respectively. This indicated the striatal dopamine release by smoking. The reduction in binding potential in the ventral striatum was significantly correlated with the cumulated plasma level of the nicotine (r 2 =0.91, p=0.04). These data demonstrate that in vivo imaging with [ 11 C]raclopride PET could measure nicotine-induced dopamine release in the human brain, which has a significant positive correlation with the amount of nicotine administered by smoking

  17. Smoking-induced dopamine release studied with [{sup 11}C]raclopride PET

    Kim, Yu Kyeong; Cho, Sang Soo; Lee, Do Hoon [Seoul National University College of Medicine, Seoul (Korea, Republic of)] (and others)

    2005-07-01

    It has been postulated that dopamine release in the striatum underlies the reinforcing properties of nicotine. Substantial evidence in the animal studies demonstrates that nicotine interacts with and regulates the activation of the dopaminergic neuron. The aim of this study was to visualize the dopamine release by smoking in human brain using PET scan with [{sup 11}C]raclopride. Four male non-smokers or ex-smokers with an abstinence period longer than 1 year (mean age of 24.3{+-}2.6 years) were enrolled in this study. Dopamine D2 receptor radioligand, [{sup 11}C]raclopride was administrated with bolus-plus-constant infusion. Dynamic PET was performed during 120 minutes (3x20s, 2x60s, 2x120s, 1x180s and 22x300s). Following the 50 minute-scanning, subjects smoked a cigarette containing 1 mg of nicotine while in the scanner. Blood samples for the measurements of plasma nicotine levels were collected at 0, 5, 10, 15, 20, 25, 30, 45, 60, and 90 minute after smoking. Regions for striatal structures were drawn on the coronal summed PET images guided with co-registered MRI. Binding potential, calculated as striatal-cerebellar/cerebellar activity, was measured under equilibrium condition at baseline and smoking session. The mean change in binding potential between the baseline and smoking in caudate, Putamen and ventral striatum was 3.7 % , 4.0 % and 8.6 %, respectively. This indicated the striatal dopamine release by smoking. The reduction in binding potential in the ventral striatum was significantly correlated with the cumulated plasma level of the nicotine (r{sup 2}=0.91, p=0.04). These data demonstrate that in vivo imaging with [{sup 11}C]raclopride PET could measure nicotine-induced dopamine release in the human brain, which has a significant positive correlation with the amount of nicotine administered by smoking.

  18. Cigarette smoking and electronic cigarette vaping patterns as a function of e-cigarette flavourings.

    Litt, Mark D; Duffy, Valerie; Oncken, Cheryl

    2016-11-01

    The present study examined the influence of flavouring on the smoking and vaping behaviour of cigarette smokers asked to adopt e-cigarettes for a period of 6 weeks. Participants were 88 current male and female smokers with no intention to stop smoking, but who agreed to substitute e-cigarettes for their current cigarettes. On intake, participants were administered tests of taste and smell for e-cigarettes flavoured with tobacco, menthol, cherry and chocolate, and were given a refillable e-cigarette of their preferred flavour or a control flavour. Participants completed daily logs of cigarette and e-cigarette use and were followed each week. Analyses over days indicated that, during the 6-week e-cigarette period, cigarette smoking rates dropped from an average of about 16 to about 7 cigarettes/day. e-Cigarette flavour had a significant effect such that the largest drop in cigarette smoking occurred among those assigned menthol e-cigarettes, and the smallest drop in smoking occurred among those assigned chocolate and cherry flavours. e-Cigarette vaping rates also differed significantly by flavour assigned, with the highest vaping rates for tobacco- and cherry-flavoured e-cigarettes, and the lowest rates for those assigned to chocolate. The findings suggest that adoption of e-cigarettes in smokers may influence smoking rates and that e-cigarette flavourings can moderate this effect. e-Cigarette vaping rates are also influenced by flavourings. These findings may have implications for the utility of e-cigarettes as a nicotine replacement device and for the regulation of flavourings in e-cigarettes for harm reduction. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

  19. Aryl hydrocarbon receptor-dependent regulation of miR-196a expression controls lung fibroblast apoptosis but not proliferation

    Hecht, Emelia; Zago, Michela; Sarill, Miles; Rico de Souza, Angela; Gomez, Alvin; Matthews, Jason; Hamid, Qutayba; Eidelman, David H.; Baglole, Carolyn J.

    2014-01-01

    The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor implicated in the regulation of apoptosis and proliferation. Although activation of the AhR by xenobiotics such as dioxin inhibits the cell cycle and control apoptosis, paradoxically, AhR expression also promotes cell proliferation and survival independent of exogenous ligands. The microRNA (miRNA) miR-196a has also emerged as a regulator of proliferation and apoptosis but a relationship between the AhR and miR-196a is not known. Therefore, we hypothesized that AhR-dependent regulation of endogenous miR-196a expression would promote cell survival and proliferation. Utilizing lung fibroblasts from AhR deficient (AhR −/− ) and wild-type (AhR +/+ ) mice, we show that there is ligand-independent regulation of miRNA, including low miR-196a in AhR −/− cells. Validation by qRT-PCR revealed a significant decrease in basal expression of miR-196a in AhR −/− compared to AhR +/+ cells. Exposure to AhR agonists benzo[a]pyrene (B[a]P) and FICZ as well as AhR antagonist CH-223191 decreased miR-196a expression in AhR +/+ fibroblasts concomitant with decreased AhR protein levels. There was increased proliferation only in AhR +/+ lung fibroblasts in response to serum, corresponding to a decrease in p27 KIP1 protein, a cyclin-dependent kinase inhibitor. Increasing the cellular levels of miR-196a had no effect on proliferation or expression of p27 KIP1 in AhR −/− fibroblasts but attenuated cigarette smoke-induced apoptosis. This study provides the first evidence that AhR expression is essential for the physiological regulation of cellular miRNA levels- including miR-196a. Future experiments designed to elucidate the functional relationship between the AhR and miR-196a may delineate additional novel ligand-independent roles for the AhR. - Highlights: • The AhR controls proliferation and apoptosis in lung cells. • The AhR regulates the expression of the microRNA miR-196a independent of

  20. Aryl hydrocarbon receptor-dependent regulation of miR-196a expression controls lung fibroblast apoptosis but not proliferation

    Hecht, Emelia [Department of Medicine, McGill University, Montreal, Quebec (Canada); Zago, Michela [Research Institute of the McGill University Health Centre, McGill University, Montreal, Quebec (Canada); Sarill, Miles [Department of Medicine, McGill University, Montreal, Quebec (Canada); Rico de Souza, Angela [Research Institute of the McGill University Health Centre, McGill University, Montreal, Quebec (Canada); Gomez, Alvin; Matthews, Jason [Department of Pharmacology and Toxicology, University of Toronto, Toronto, ON (Canada); Hamid, Qutayba; Eidelman, David H. [Department of Medicine, McGill University, Montreal, Quebec (Canada); Research Institute of the McGill University Health Centre, McGill University, Montreal, Quebec (Canada); Baglole, Carolyn J., E-mail: Carolyn.baglole@McGill.ca [Department of Medicine, McGill University, Montreal, Quebec (Canada); Research Institute of the McGill University Health Centre, McGill University, Montreal, Quebec (Canada)

    2014-11-01

    The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor implicated in the regulation of apoptosis and proliferation. Although activation of the AhR by xenobiotics such as dioxin inhibits the cell cycle and control apoptosis, paradoxically, AhR expression also promotes cell proliferation and survival independent of exogenous ligands. The microRNA (miRNA) miR-196a has also emerged as a regulator of proliferation and apoptosis but a relationship between the AhR and miR-196a is not known. Therefore, we hypothesized that AhR-dependent regulation of endogenous miR-196a expression would promote cell survival and proliferation. Utilizing lung fibroblasts from AhR deficient (AhR{sup −/−}) and wild-type (AhR{sup +/+}) mice, we show that there is ligand-independent regulation of miRNA, including low miR-196a in AhR{sup −/−} cells. Validation by qRT-PCR revealed a significant decrease in basal expression of miR-196a in AhR{sup −/−} compared to AhR{sup +/+} cells. Exposure to AhR agonists benzo[a]pyrene (B[a]P) and FICZ as well as AhR antagonist CH-223191 decreased miR-196a expression in AhR{sup +/+} fibroblasts concomitant with decreased AhR protein levels. There was increased proliferation only in AhR{sup +/+} lung fibroblasts in response to serum, corresponding to a decrease in p27{sup KIP1} protein, a cyclin-dependent kinase inhibitor. Increasing the cellular levels of miR-196a had no effect on proliferation or expression of p27{sup KIP1} in AhR{sup −/−} fibroblasts but attenuated cigarette smoke-induced apoptosis. This study provides the first evidence that AhR expression is essential for the physiological regulation of cellular miRNA levels- including miR-196a. Future experiments designed to elucidate the functional relationship between the AhR and miR-196a may delineate additional novel ligand-independent roles for the AhR. - Highlights: • The AhR controls proliferation and apoptosis in lung cells. • The AhR regulates the

  1. Beliefs and behavior regarding e-cigarettes in a large cross-sectional survey

    Sébastien Couraud

    2018-06-01

    Full Text Available Although e-cigarette use is increasing dramatically, numerous concerns persist regarding toxicity and their role in smoking cessation. We assessed beliefs and behavior regarding e-cigarettes in an adult French population.The 4th French nationwide observational survey, EDIFICE 4, was conducted among representative samples of 1602 laypersons (age, 40–75 years from 12 June-10 July 2014, using the quota method. Profile, beliefs and behavior were assessed by phone interviews of the participating lay population with no history of cancer (N = 1463. Tobacco use, nicotine dependence (Fagerström test and e-cigarette use were assessed.E-cigarette users represented 6% of the study lay population. E-cigarette users regarded e-cigarettes as helpful for quitting tobacco smoking and reducing the risk of lung cancer. Current dual users (e-cigarettes + cigarettes were more likely to attempt to quit than current exclusively cigarette smokers (odds ratio, 3.15 [1.74–5.70], and to consider themselves at higher risk for lung cancer (OR 3.85 [2.47–5.99]. They also considered e-cigarette vapor to be less toxic than tobacco smoke in terms of both active and passive exposure.Dual users typically consider themselves at higher risk for cancer and intend to quit smoking. Physicians should be made aware of this specific sub-population for whom e-cigarettes may be a useful trigger in the smoking cessation process. Keywords: Electronic cigarettes, Smoking cessation, Tobacco use, Lung neoplasms, Pulmonary disease, Risk factors, Smoke

  2. Cigarette Ads and Youth.

    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)

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

    2011-08-01

    at Tyler, Laboratory C-6, Routes 271 and 155, Tyler, TX 75708. E -mail: steven.idell@uthct.edu. This study was supported by the National Institutes of...sequential filtration over 100 and 40 2m cell strainers (Fisher Scientific, Freemont , Calif ). Filtrates were then centrifuged at 250g, 10-C for 20...stained with hematoxylin eosin (H& E ), and cover slipped H& E scores were interpreted as previously described (17). One hun dred high power fields per

  4. Hospitalized Smokers’ Expectancies for Electronic Cigarettes versus Tobacco Cigarettes

    Hendricks, Peter S.; Cases, Mallory G.; Thorne, Christopher B.; Cheong, JeeWon; Harrington, Kathleen F.; Kohler, Connie L.; Bailey, William C.

    2016-01-01

    Introduction To compare hospitalized smokers’ expectancies for electronic cigarettes (e-cigarettes) against their expectancies for tobacco cigarettes and evaluate relationships between e-cigarette expectancies and intention to use e-cigarettes. Methods Analysis of baseline data from a one-year longitudinal observational study. The setting was a tertiary care academic center hospital in the Southeastern U.S. Participants were 958 hospitalized tobacco cigarette smokers. A questionnaire of e-cigarette expectancies based on the Brief Smoking Consequences Questionnaire-Adult (BSCQ-A) was developed and administered along with the original, tobacco-specific, BSCQ-A. Intention to use e-cigarettes was assessed with a single 10-point Likert scale item. Results Participants reported significantly weaker expectancies for e-cigarettes relative to tobacco cigarettes on all 10 BSCQ-A scales. Participants held sizably weaker expectancies for the health risks of e-cigarettes (p < .001, Cohen's d = −2.07) as well as the ability of e-cigarettes to relieve negative affect (p < .001, Cohen's d = −1.01), satisfy the desire for nicotine (p < .001, Cohen's d = −.83), and taste pleasant (p < .001, Cohen's d = −.73). Among the strongest predictors of intention to use e-cigarettes were greater expectancies that e-cigarettes taste pleasant (p < .001, adjusted β = .34), relieve negative affect (p < .001, adjusted β = .32), and satisfy the desire for nicotine (p < .001, adjusted β = .31). Conclusions Hospitalizedtobacco smokers expect fewer negative and positive outcomes from e-cigarettes versus tobacco cigarettes. This suggests that e-cigarettes might be viable though imperfect substitutes for tobacco cigarettes. PMID:25452052

  5. Smoking-induced dopamine release studied with [{sup 11}C]Raclopride PET

    Kim, Yu Kyeong; Cho, Sang Soo [Seoul National University College of Medicine, Seoul (Korea, Republic of); Lee, Do Hoon [Center for Clinical Services, National Cancer Certer, Goyang (Korea, Republic of)] (and others)

    2005-10-15

    It has been postulated that dopamine release in the striatum underlies the reinforcing properties of nicotine. Substantial evidence in the animal studies demonstrates that nicotine interacts with dopaminergic neuron and regulates the activation of the dopaminergic system. The aim of this study was to visualize the dopamine release by smoking in human brain using PET scan with [{sup 11}C]raclopride. Five male non-smokers or ex-smokers with an abstinence period longer than 1 year (mean age of 24.4 {+-} 1.7 years) were enrolled in this study. [{sup 1C}]raclopride, a dopamine D2 receptor radioligand, was administrated with bolus-plus-constant infusion. Dynamic PET was performed during 120 minutes (3 x 20s, 2 x 60s, 2 x 120s, 1 x 180s and 22 x 300s). Following the 50 minute-scanning, subjects smoked a cigarette containing 1 mg of nicotine while in the scanner. Blood samples for the measurement of plasma nicotine level were collected at 0, 5, 10, 15, 20, 25, 30, 45, 60, and 90 minute after smoking. Regions for striatal structures were drawn on the coronal summed PET images guided with co-registered MRI. Binding potential, calculated as (striatal-cerebellar)/cerebellar activity, was measured under equilibrium condition at baseline and smoking session. The mean decrease in binding potential of [{sup 1C}]raclopride between the baseline and smoking in caudate head, anterior putamen and ventral striatum was 4.7%, 4.0% and 7.8%, respectively. This indicated the striatal dopamine release by smoking. Of these, the reduction in binding potential in the ventral striatum was significantly correlated with the cumulated plasma level of the nicotine (Spearman's rho=0.9, {rho} =0.4). These data demonstrate that in vivo imaging with [{sup 11}C]raclopride PET could measure nicotine-induced dopamine release in the human brain, which has a significant positive correlation with the amount of nicotine administered by smoking.

  6. Induction of Metallothionein Expression After Exposure to Conventional Cigarette Smoke but Not Electronic Cigarette (ECIG-Generated Aerosol in Caenorhabditis elegans

    Eric Cobb

    2018-04-01

    , conventional cigarette smoke induced the production of mtl-1 in a manner that correlates with the induction of stress-induced sleep suggesting a stress response to damage. The lack of cellular stress response to ECIG aerosol suggests it may be a safer alternative to conventional cigarettes.

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

    Ibrahim, N.K.; Abd-EL Aziz, N.; El-Deghidy, E.A.

    2010-01-01

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

  8. Myofibroblast differentiation and its functional properties are inhibited by nicotine and e-cigarette via mitochondrial OXPHOS complex III

    Lei, Wei; Lerner, Chad; Sundar, Isaac K.; Rahman, Irfan

    2017-01-01

    Nicotine is the major stimulant in tobacco products including e-cigarettes. Fibroblast to myofibroblast differentiation is a key process during wound healing and is dysregulated in lung diseases. The role of nicotine and e-cigarette derived nicotine on cellular functions including profibrotic response and other functional aspects is not known. We hypothesized that nicotine and e-cigarettes affect myofibroblast differentiation, gel contraction, and wound healing via mitochondria stress through...

  9. Rho-kinase inhibitor and nicotinamide adenine dinucleotide phosphate oxidase inhibitor prevent impairment of endothelium-dependent cerebral vasodilation by acute cigarette smoking in rats.

    Iida, Hiroki; Iida, Mami; Takenaka, Motoyasu; Fukuoka, Naokazu; Dohi, Shuji

    2008-06-01

    We previously reported that acute cigarette smoking can cause a dysfunction of endothelium-dependent vasodilation in cerebral vessels, and that blocking the angiotensin II (Ang II) type 1 (AT1) receptor with valsartan prevented this impairment. Our aim was to investigate the effects of a Rho-kinase inhibitor (fasudil) and a Nicotinamide Adenine Dinucleotide PHosphate (NADPH) oxidase inhibitor (apocynin) on smoking-induced endothelial dysfunction in cerebral arterioles. In Sprague-Dawley rats, we used a closed cranial window preparation to measure changes in pial vessel diameters following topical acetylcholine (ACh) before smoking. After one-minute smoking, we again examined the arteriolar responses to ACh. Finally, after intravenous fasudil or apocynin pre-treatment we re-examined the vasodilator responses to topical ACh (before and after cigarette smoking). Under control conditions, cerebral arterioles were dose-dependently dilated by topical ACh (10(-6) M and 10(-5) M). One hour after a one-minute smoking (1 mg-nicotine cigarette), 10(-5) M ACh constricted cerebral arterioles. However, one hour after a one-minute smoking, 10(-5) M ACh dilated cerebral pial arteries both in the fasudil pre-treatment and the apocynin pre-treatment groups, responses that were significantly different from those obtained without fasudil or apocynin pre-treatment. Thus, inhibition of Rho-kinase and NADPH oxidase activities may prevent the above smoking-induced impairment of endothelium-dependent vasodilation.

  10. Commonly used air filters fail to eliminate secondhand smoke induced oxidative stress and inflammatory responses.

    Muthumalage, Thivanka; Pritsos, Karen; Hunter, Kenneth; Pritsos, Chris

    2017-07-01

    Secondhand smoke (SHS) causes approximately 50,000 deaths per year. Despite all the health warnings, smoking is still allowed indoors in many states exposing both workers and patrons to SHS on a daily basis. The opponents of smoking bans suggest that present day air filtration systems remove the health hazards of exposure to SHS. In this study, using an acute SHS exposure model, we looked at the impact of commonly used air filters (MERV-8 pleated and MERV-8 pleated activated charcoal) on SHS by assessing the inflammatory response and the oxidative stress response in C57BL/6 mice. In order to assess the inflammatory response, we looked at the tumor necrosis factor alpha (TNF-α) cytokine production by alveolar macrophages (AMs), and for the oxidative response, we quantified the products of lipid peroxidation and the total glutathione (tGSH) production in lung homogenates. Our results showed that SHS caused significant immune and oxidative stress responses. The tested filters resulted in only a modest alleviation of inflammatory and oxidative responses due to SHS exposure. Our data show that these air filters cannot eliminate the risk of SHS exposure and that a short-term exposure to SHS is sufficient to alter the inflammatory cytokine response and to initiate a complex oxidative stress response. Our results are consistent with the statement made by the Surgeon General's reports that there is no risk free level of exposure to SHS.

  11. Does e-cigarette consumption cause passive vaping?

    Schripp, T; Markewitz, D; Uhde, E; Salthammer, T

    2013-02-01

    Electronic cigarette consumption ('vaping') is marketed as an alternative to conventional tobacco smoking. Technically, a mixture of chemicals containing carrier liquids, flavors, and optionally nicotine is vaporized and inhaled. The present study aims at the determination of the release of volatile organic compounds (VOC) and (ultra)fine particles (FP/UFP) from an e-cigarette under near-to-real-use conditions in an 8-m(3) emission test chamber. Furthermore, the inhaled mixture is analyzed in small chambers. An increase in FP/UFP and VOC could be determined after the use of the e-cigarette. Prominent components in the gas-phase are 1,2-propanediol, 1,2,3-propanetriol, diacetin, flavorings, and traces of nicotine. As a consequence, 'passive vaping' must be expected from the consumption of e-cigarettes. Furthermore, the inhaled aerosol undergoes changes in the human lung that is assumed to be attributed to deposition and evaporation. The consumption of e-cigarettes marks a new source for chemical and aerosol exposure in the indoor environment. To evaluate the impact of e-cigarettes on indoor air quality and to estimate the possible effect of passive vaping, information about the chemical characteristics of the released vapor is needed. © 2012 John Wiley & Sons A/S.

  12. College Students' Perceptions of Risk and Addictiveness of E-Cigarettes and Cigarettes

    Cooper, Maria; Loukas, Alexandra; Harrell, Melissa B.; Perry, Cheryl L.

    2017-01-01

    Background: As conventional cigarette use is declining, electronic cigarette ("e-cigarette") use is rising and is especially high among college students. Few studies examine dual use of e-cigarettes and cigarettes among this population. This study explores the relationship between dual and exclusive e-cigarette / cigarette use and…

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

    Ohnishi, Takamasa; Arnold, Lora L.; He, Jun; Clark, Nicole M.; Kawasaki, Shin; Rennard, Stephen I.; Boyer, Craig W.; Cohen, Samuel M.

    2007-01-01

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

  14. Electronic cigarettes: human health effects

    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 ae...

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

    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 0.05) 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 smoking-induced endothelial dysfunction. © The Author 2015. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

  16. Reduced nicotine content cigarettes, e-cigarettes and the cigarette end game

    Benowitz, Neal L.; Donny, Eric C.; Hatsukami, Dorothy K.

    2017-01-01

    The reduced nicotine content cigarette and the emergence of non-combusted nicotine products like e-cigarettes should be viewed not as alternatives but as complementary components of regulatory interventions that could virtually end combusted tobacco use. PMID:27555354

  17. Tobacco, e-cigarettes, and child health.

    Peterson, Lisa A; Hecht, Stephen S

    2017-04-01

    The availability of the Children's Health Exposure Assessment Resource funded by the National Institute of Environmental Health Sciences provides new opportunities for exploring the role of tobacco smoke exposure in causing harm to children. Children of smokers are exposed to nicotine and other harmful tobacco smoke chemicals in utero as well as in their environment. This passive exposure to tobacco smoke has a variety of negative effects on children. In-utero exposure to tobacco smoke causes poor birth outcomes and influences lung, cardiovascular, and brain development, placing children at increased risk of a number of adverse health outcomes later in life, such as obesity, behavioral problems, and cardiovascular disease. Furthermore, most smokers start in their adolescence, an age of increased nicotine addiction risk. Biomarkers of tobacco exposure helps clarify the role tobacco chemicals play in influencing health both in childhood and beyond. Although electronic cigarettes (e-cigarettes) appear to be a nicotine delivery device of reduced harm, it appears to be a gateway to the use of combustible cigarette smoking in adolescents. Pediatric researchers interested in elucidating the role of tobacco smoke exposure in adverse outcomes in children should incorporate biomarkers of tobacco exposure in their studies.

  18. Cigarette smoke and plutonium

    Filipy, R.E.

    1982-01-01

    The major objective of this project is to obtain experimental data that are directly applicable to resolving the question of whether cigarette smokers are at greater risk than nonsmokers to potential health effects of inhaled plutonium. Progress was made on two fronts during the past year. The autoradiographic technique developed from detection of plutonium on the interior surface of pulmonary airways (Annual Report, 1978) has been adapted to routine use in examining tracheas and bronchi of rats. Also, dogs exposed to cigarette smoke for over a year after inhalation of plutonium were killed and necropsied

  19. Changes in neutrophil morphology and morphometry following exposure to cigarette smoke.

    Lannan, S.; McLean, A.; Drost, E.; Gillooly, M.; Donaldson, K.; Lamb, D.; MacNee, W.

    1992-01-01

    Acute cigarette smoking delays neutrophils within the pulmonary circulation in some smokers. Evidence from an in-vitro Micropore filter model of the pulmonary capillaries indicates that this may be due to a smoke induced decrease in cell deformability. In order to determine whether changes in cell shape are associated with the observed decrease in neutrophil deformability following smoke exposure, cell morphology, using scanning electron microscopy, and morphometric measurements, made using transmission electron microscopy, were performed on aliquots of neutrophils harvested from whole blood in non-smoking subjects before and after exposure in vitro to cigarette smoke. Smoke exposure increased the maximum diameter and circumference of neutrophils, without changing their area. There was also a change in the maximum to minimum cell diameter ratio, which indicated that the cells had become less spherical. Scanning electron microscopy showed that smoke exposed cells had developed blebbing of their surface membranes, suggestive of an oxidative injury to the cell membrane rather than the shape changes associated with cell activation. These changes in the morphology and morphometry of smoke exposed neutrophils may contribute to the reduction in cell deformability induced by cigarette smoke. Images Fig. 3 Fig. 4 Fig. 5 PMID:1571278

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

    Gaur Dushyant

    2010-01-01

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

  1. Exercise Prevents Diaphragm Wasting Induced by Cigarette Smoke through Modulation of Antioxidant Genes and Metalloproteinases

    Gracielle Vieira Ramos

    2018-01-01

    Full Text Available Background. The present study aimed to analyze the effects of physical training on an antioxidant canonical pathway and metalloproteinases activity in diaphragm muscle in a model of cigarette smoke-induced chronic obstructive pulmonary disease (COPD. Methods. Male mice were randomized into control, smoke, exercise, and exercise + smoke groups, which were maintained in trial period of 24 weeks. Gene expression of kelch-like ECH-associated protein 1; nuclear factor erythroid-2 like 2; and heme-oxygenase1 by polymerase chain reaction was performed. Metalloproteinases 2 and 9 activities were analyzed by zymography. Exercise capacity was evaluated by treadmill exercise test before and after the protocol. Results. Aerobic training inhibited diaphragm muscle wasting induced by cigarette smoke exposure. This inhibition was associated with improved aerobic capacity in those animals that were submitted to 24 weeks of aerobic training, when compared to the control and smoke groups, which were not submitted to training. The aerobic training also downregulated the increase of matrix metalloproteinases (MMP-2 and MMP-9 and upregulated antioxidant genes, such as nuclear factor erythroid-2 like 2 (NRF2 and heme-oxygenase1 (HMOX1, in exercise + smoke group compared to smoke group. Conclusions. Treadmill aerobic training protects diaphragm muscle wasting induced by cigarette smoke exposure involving upregulation of antioxidant genes and downregulation of matrix metalloproteinases.

  2. Adolescent perceptions of cigarette appearance.

    Ford, Allison; Moodie, Crawford; MacKintosh, Anne M; Hastings, Gerard

    2014-06-01

    To reduce the possibility of cigarette appearance misleading consumers about harm caused by the product, the European Commission's draft Tobacco Products Directive proposed banning cigarettes implied a more pleasant and palatable smoke for young smokers. A long brown cigarette was viewed as particularly unattractive and communicated a stronger and more harmful product. This exploratory study provides some support that standardising cigarette appearance could reduce the appeal of cigarettes in adolescents and reduce the opportunity for stick design to mislead young smokers in terms of harm. © The Author 2013. Published by Oxford University Press on behalf of the European Public Health Association. All rights reserved.

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

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

    2001-07-01

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

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

    Skwarzec, B.; Ulatowski, J.; Struminska, D.I.; Borylo, A.

    2001-01-01

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

  5. Electronic Cigarettes on Hospital Campuses

    Clare Meernik

    2015-12-01

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

  6. Electronic Cigarettes on Hospital Campuses.

    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.

  7. Cigarette weight control systems

    Powell, G.F.W.; Bolt, R.C.; Simmons, A.

    1980-01-01

    A system is described for monitoring the weight of a continuous wrapped rod of tobacco formed by a cigarette-making machine. A scanner unit can be used which passes beta-rays from a primary radiation source through the rod. The absorption is measured by comparison of the intensity at a detector on the opposite side of the rod with that at a detector facing another smaller source, the balance unit. This is pre-set so that when the rod weight is correct the detected intensities from the two sources will be equal. It is essential that the scanning station is kept clean otherwise the dust is included in the weight reading and the cigarettes manufactured would be underweight. This can be checked using an artificial cigarette of known weight as a calibration check. In this device a test circuit can be connected to the scanner head and this opens the shutter over the radioactive source when the test is initiated. A warning device is initiated if the reading is beyond predetermined limits and can be made to prevent operation of the cigarette machine if a satisfactory test is not obtained. (U.K.)

  8. [Focus on electronic cigarettes].

    Tinghino, Biagio; Pacifici, Roberta; Di Pucchio, Alessandra; Palmi, Ilaria; Solimini, Renata; Faggiano, Fabrizio; Gorini, Giuseppe

    2013-01-01

    There is no clear regulation on electronic cigarettes (e-cig); their health effects are not yet fully investigated and there is insufficient standardisation and quality control of the product. Moreover, the e-cig could be a gateway for young people to nicotine addiction and traditional cigarette smoking. In Italy, the Ministry of Health banned the sale of e-cig with nicotine firstly to adolescents aged marketing of e-cigs, to make them less attractive, to forbid their use in enclosed areas, and prevent them from being promoted. E-cigs, however, seem to be much less dangerous than traditional cigarettes, although the few studies conducted are not sufficient to demonstrate either a clear therapeutic efficacy of e-cig or their total harmlessness. If e-cig had a known content, were made according to clear rules and in certified laboratories, without toxic substances, it could be used to help heavy smokers to quit, or at least to reduce smoking habits. There is a large proportion of smokers who are unable to quit. The revision of the European Directive (the proposal is being evaluated and we are waiting for its final approval) on tobacco recommends free sale for a minority of e-cigs only, those with a nicotine content e-cig and the much more dangerous tobacco cigarettes are still sold without any restriction.

  9. Advertising media and cigarette demand.

    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.

  10. Alpha-emitting radionuclides in cigarette tobacco

    Neton, James W.; Ibrahim, Shawki Amin

    1978-01-01

    As part of general studies of the concentration of 239/240 Pu, 238 Pu and 228,230,232 Th in the tissues of non-occupationally exposed individuals, it became evident that there was little or no information on their content in cigarette tobacco. To better understand this possible route of intake and its potential for lung exposure we have measured these nuclides in tobacco samples, from the U.S. Department of Agriculture (USDA), which have a well-known growing history, and in brand name cigarettes purchased commercially. The concentration of 239/240 Pu in both USDA and brand name tobacco has a range of 0.4-0.7 pCi/kg of tobacco while the 238 Pu concentration was ≤ 0.05 pCi/kg. The 228 Th concentration for USDA tobacco was 200 pCi/kg tobacco while the 232 Th was only 14 pCi/kg. The high 228/232 Th ratio may result from a lower uptake of 232 Th compared to that of 228 Ra. By comparing the concentration of these measured nuclides to other alpha emitters in tobacco that have been reported in the literature, i.e. 210 Po (400 pCi/kg) and 226 Ra (150 pCi/kg), it is apparent that 228 Th represents a significant fraction of the total alpha activity. It is also evident there is a much greater potential for exposure of the lung to radiation from 228 Th than from 239/240 Pu as a result of cigarette smoking. (author)

  11. Effect of epimedium pubescen flavonoid on bone mineral status and bone turnover in male rats chronically exposed to cigarette smoke.

    Gao, Shu-guang; Cheng, Ling; Li, Kang-hua; Liu, Wen-He; Xu, Mai; Jiang, Wei; Wei, Li-Cheng; Zhang, Fang-jie; Xiao, Wen-feng; Xiong, Yi-lin; Tian, Jian; Zeng, Chao; Sun, Jin-peng; Xie, Qiang; Lei, Guang-hua

    2012-06-19

    Epimedii herba is one of the most frequently used herbs in formulas that are prescribed for the treatment of osteoporosis in China and its main constituent is Epimedium pubescen flavonoid (EPF). However, it is unclear whether EPF during chronic exposure to cigarette smoke may have a protective influence on the skeleton. The present study investigated the effect of EPF on bone mineral status and bone turnover in a rat model of human relatively high exposure to cigarette smoke. Fifty male Wistar rats were randomized into five groups: controls, passive smoking groups and passive smoking rats administered EPF at three dosage levels (75, 150 or 300 mg/kg/day) in drinking water for 4 months. A rat model of passive smoking was prepared by breeding male rats in a cigarette-smoking box. Bone mineral content (BMC), bone mineral density (BMD), bone turnover markers, bone histomorphometric parameters and biomechanical properties were examined. Smoke exposure decreased BMC and BMD, increased bone turnover (inhibited bone formation and stimulated its resorption), affected bone histomorphometry (increased trabecular separation and osteoclast surface per bone surface; decreased trabecular bone volume, trabecular thickness, trabecular number, cortical thickness, bone formation rate and osteoblast surface per bone surface), and reduced mechanical properties. EPF supplementation during cigarette smoke exposure prevented smoke-induced changes in bone mineral status and bone turnover. The results suggest that EPF can prevent the adverse effects of smoke exposure on bone by stimulating bone formation and inhibiting bone turnover and bone resorption.

  12. 210Po in cigarette and the radiation dose inhaled by smoker

    Wang Xin; Chen Xingan; Pan Yingdong

    2000-01-01

    The contents of Polonium-210 in 16 brands of cigarettes from China and 4 brands of cigarettes from abroad were reported. The method that the authors used for separating Polonium-210 was electrochemical deposition method. The 210 Po contents were analyzed in whole cigarettes from freshly opened packs. The 210 Po contents of the China-made cigarettes ranged from 13.7 to 43.4 mBq/cig, from 18.0 to 67.3 mBq/g respectively, the mean values were 26.5 mBq/cig and 33.7 mBq/g respectively. The content of 210 Po in cigarettes from China is higher than that from abroad. The polonium contents of the ash, butt and main stream smoke were reported. The cigarettes were smoked with the eight-channel smoking machine for determining the concentration of the radionuclides in main stream smoke. ('Main Stream' means smoke taken into the mouth). About 15% of 210 Po contained in a cigarette was transferred into the main stream smoke, 40% of the whole 210 Po content remained in the ash and butt for filter cigarette, 60% for non-filter. The daily intake of the 210 Po from cigarette was 80 mBq, the annual dose equivalent to the lung tissue of human body was 0.46 mSv. In view of present knowledge, it is improbable that this dose is significant for the higher incidence of lung tissue of human body was 0.46 mSv. In view of present knowledge, it is improbable that this dose is significant for the higher incidence of lung cancer in smokers

  13. 2015 Legislative update of e-cigarette youth access and exposure laws.

    Dobbs, Page Daniel; Hammig, Bart; Sudduth, Abbie

    2016-07-01

    As of November 15, 2013, 22 states had passed laws explicitly addressing youth access to electronic cigarettes (e-cigarettes); by 2014, this increased to 41 states. Also in 2014, more than 13.4% of youth in the U.S. reported using e-cigarettes, making e-cigarette use more prevalent than conventional cigarette use (9.2%). We examined 221 bills addressing youth access and exposure to e-cigarettes between January 1 and November 1, 2015. Text searches on individual state general assembly websites and secondary sources were employed for data collection. Laws were analyzed using seven measures identified to protect adolescents from nicotine initiation and use. Two states (MI, PA) and Washington D.C. do not regulate the sale or distribution of e-cigarettes to youth as of November 1, 2015. Additionally, seventeen states have passed laws requiring e-cigarettes to use child-safety packaging to minimize unintended poisoning. As of July 1, 2016, four states (KS, LA, MN, and NC) will tax e-cigarettes. Oregon prohibits the use of e-cigarettes in cars with children under 18years of age, and Wyoming requires the public health department to develop educational campaigns to better educate the state on the risks of nicotine and tobacco products. While states are closing the gap of youth nicotine exposure, there remains a need to protect youth from e-cigarettes access, which can cause adverse health effects of brain development, lung function and potentially lead to addiction. Recommendation for the FDA to regulate e-cigarettes federally would close this regulation gap and protect youth across the U.S. Copyright © 2016 Elsevier Inc. All rights reserved.

  14. Adolescent Sports Participation, E-cigarette Use, and Cigarette Smoking.

    Veliz, Phil; McCabe, Sean Esteban; McCabe, Vita V; Boyd, Carol J

    2017-11-01

    Although sport participation among adolescents has been found to lower the risk of traditional cigarette smoking, no studies to date have assessed if this type of physical activity lowers the risk of e-cigarette use among adolescents. National data from the 2014 and 2015 Monitoring the Future study of 12th-grade students were used and analyses were conducted in 2016. Measures for past 30-day e-cigarette use and traditional cigarette smoking were used to assess differences between adolescents who participated in at least one competitive sport during the past year and adolescents who did not. Differences in e-cigarette use and traditional cigarette smoking were assessed between 13 different sports to determine which sports were associated with a greater or lower risk of these behaviors. Adolescents who participated in at least one competitive sport were less likely to engage in past 30-day traditional cigarette smoking (AOR=0.73, 95% CI=0.538, 0.973) and past 30-day dual use of traditional cigarettes and e-cigarettes (AOR=0.66, 95% CI=0.438, 0.982) when compared with their nonparticipating peers. Adolescents who participated in baseball/softball and wrestling were at greatest risk of e-cigarette use. Of the 13 assessed sports, none were found to lower the odds of e-cigarette use. No significant evidence was found that participation in a sport was a protective factor against e-cigarette use. Certain types of athletes are at an elevated risk of e-cigarette use, and prevention efforts targeted at these specific sports should be considered by school administrators. Copyright © 2017 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.

  15. E-Cigarette Use Among Adolescents Not Susceptible to Using Cigarettes

    Kowitt, Sarah D.; Osman, Amira; Ranney, Leah M.; Heck, Courtney; Goldstein, Adam O.

    2018-01-01

    Introduction Research suggests that adolescents who use electronic cigarettes (e-cigarettes), including adolescents not susceptible to smoking cigarettes (ie, those who have never smoked cigarettes and are not attitudinally susceptible to using cigarettes), are more likely to initiate using cigarettes or other combustible tobacco products than adolescents who do not use e-cigarettes. In this study, we examined correlates of e-cigarette use and susceptibility among adolescents not susceptible ...

  16. Contexts of cigarette and e-cigarette use among dual users: a qualitative study

    Pokhrel, Pallav; Herzog, Thaddeus A.; Muranaka, Nicholas; Regmi, Sakshi; Fagan, Pebbles

    2015-01-01

    Background Not much is currently understood regarding the contexts of cigarette and e-cigarette use among dual users. Proper application of e-cigarettes to smoking cessation or tobacco harm reduction would require an understanding of when and why dual users use cigarettes versus e-cigarettes. This study sought to elucidate the contexts of cigarette versus e-cigarette use among dual users. Methods Twelve focus group discussions were conducted with 62 young adult current daily e-cigarette users...

  17. 27 CFR 40.351 - Cigarette papers.

    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. Cigarette...

  18. Multielement determination in a Chinese cigarette brand

    Iskander, F.Y.

    1992-01-01

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

  19. Electronic cigarettes: human health effects

    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

  20. Electronic cigarettes: human health effects.

    Callahan-Lyon, Priscilla

    2014-05-01

    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. Literature searches were conducted through September 2013 using multiple electronic databases. 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. 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.

  1. E-Cigarettes and the Use of Conventional Cigarettes.

    Morgenstern, Matthis; Nies, Alina; Goecke, Michaela; Hanewinkel, Reiner

    2018-04-06

    In 2015, 12.1% of 12- to 17-year-olds in Germany had reportedly already tried e-cigarette smoking at least once. We carried out a study of the "gateway" hypothesis, according to which the use of e-cigarettes can motivate adolescents to start smoking conventional cigarettes. During the 2015/2016 school year, 2186 tenth-graders in the German states of Lower Saxony and Schleswig-Holstein who had never smoked conventional cigarettes before took part in a survey over a 6-month period (mean age 15.5 years, standard deviation 0.65; 53.6% female). 14.3% of the survey population (313 adolescents) said at the start of the survey period that they had already tried e-cigarettes at least once. By the end of the survey period, 12.3% (268) of those who had never smoked before had begun to experiment with conventional cigarettes. The risk of beginning such experimentation was 2.2 times higher among e-cigarette users. This association remained (relative risk = 2.18 [1.65; 2.83]) after statistical control for age, sex, state, immigrant background, type of school, socioeconomic status, various personality traits (sensation-seeking, impulsivity, anxiety, hopelessness, extraversion, agreeableness, conscientiousness, neuroticism, openness), and the use of alcohol, cannabis, and other illicit drugs. Further analysis revealed that the association between the use of e-cigarettes and the onset of conventional cigarette smoking was stronger among adolescents with low sensation-seeking scores and without any experience of alcohol intoxication. Among adolescents who have never smoked, experimentation with conventional cigarettes is more common in those who have used e-cigarettes. This effect seems to be stronger among adolescents who, in general, have a lower risk of starting to smoke. The 6-month observation period of this study is too short to allow any inference regarding a connection between e-cigarette use and the development of tobacco dependence.

  2. Chemical evaluation of electronic cigarettes

    Cheng, Tianrong

    2014-01-01

    Objective To review the available evidence evaluating the chemicals in refill solutions, cartridges, aerosols and environmental emissions of electronic cigarettes (e-cigarettes). Methods Systematic literature searches were conducted to identify research related to e-cigarettes and chemistry using 5 reference databases and 11 search terms. The search date range was January 2007 to September 2013. The search yielded 36 articles, of which 29 were deemed relevant for analysis. Results The levels ...

  3. Role of aberrant WNT signalling in the airway epithelial response to cigarette smoke in chronic obstructive pulmonary disease

    Heijink, Hilde; de Bruin, Harold G.; van den Berge, Maarten; Bennink, Lisa J. C.; Brandenburg, Simone M.; Gosens, Reinoud; van Oosterhout, Antoon J.; Postma, Dirkje S.

    Background WNT signalling is activated during lung tissue damage and inflammation. We investigated whether lung epithelial expression of WNT ligands, receptors (frizzled; FZD) or target genes is dysregulated on cigarette smoking and/or in chronic obstructive pulmonary disease (COPD). Methods We

  4. E-cigarettes and E-hookahs

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

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

    Woodman, G.; Newman, S.P.; Paiva, D.; Clarke, S.W.

    1987-01-01

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

  6. Exposure of F344 rats to aerosols of 239PuO2 and chronically inhaled cigarette smoke

    Finch, G.L.; Nikula, K.J.; Barr, E.B.; Bechtold, W.E.; Chen, B.T.; Griffith, W.C.; Hobbs, C.H.; Hoover, M.D.; Mauderly, J.L.

    1994-01-01

    Nuclear workers may be accidently exposed to radioactive materials such as 239 PuO 2 by inhalation, and thus have increased risk for lung cancer compared to the general population. Of additional concern is the possibility that interactions between radionuclides and other carcinogens may increase the risk of cancer induction. An important and common lung carcinogen is cigarette smoke. This study is being conducted to better determine the combined effects of inhaled 239 PuO 2 and cigarette smoke on the induction of lung cancer in rats

  7. E-cigarette use, perceptions, and cigarette smoking intentions in a community sample of young adult nondaily cigarette smokers.

    Brikmanis, Kristin; Petersen, Angela; Doran, Neal

    2017-05-01

    E-cigarettes have been suggested as a strategy for reducing harm from cigarettes. Although e-cigarettes could be a less-harmful alternative to cigarettes for those trying to quit, there may also be costs that outweigh any benefits of reduction. The purpose of the present study was to prospectively investigate perceptions of e-cigarettes, cigarette smoking intentions, and their associations with e-cigarette use over time. Community participants (N = 348, 57% male) aged 18 to 24 years were recruited for a longitudinal study of tobacco use. Inclusion criteria included nondaily cigarette smoking for ≥ 6 months with no history of daily smoking. Participants reported e-cigarette use over the past 14 days at baseline, and for the past 9 days at 3, 6, and 9 months. Assessments were completed online or via mobile phone. Across the 4 assessments, 22% to 33% of participants reported recent e-cigarette use. Intent to quit smoking cigarettes and intent to maintain smoking were unrelated to e-cigarette frequency. E-cigarette frequency was positively associated with perceiving e-cigarettes as less harmful than cigarettes and more positive e-cigarette expectancies (ps E-cigarette use was also more frequent among those who smoked cigarettes frequently and who used e-cigarettes to circumvent cigarette bans more often (ps e-cigarette use more than harm reduction. Findings instead seem consistent with the hypothesis that e-cigarettes are more often used to complement ongoing cigarette smoking. (PsycINFO Database Record (c) 2017 APA, all rights reserved).

  8. Lung cancer

    Aisner, J.

    1985-01-01

    This book contains 13 chapters. Some of the chapter titles are: The Pathology of Lung Cancer; Radiotherapy for Non-Small-Cell Cancer of the Lung; Chemotherapy for Non-Small-Cell Lung Cancer; Immunotherapy in the Management of Lung Cancer; Preoperative Staging and Surgery for Non-Small-Cell Lung Cancer; and Prognostic Factors in Lung Cancer

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

    Yuen-Shan Ho

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

  10. Cigarette smoke causes caspase-independent apoptosis of bronchial epithelial cells from asthmatic donors.

    Fabio Bucchieri

    Full Text Available Epidemiologic studies have demonstrated important links between air pollution and asthma. Amongst these pollutants, environmental cigarette smoke is a risk factor both for asthma pathogenesis and exacerbation. As the barrier to the inhaled environment, the bronchial epithelium is a key structure that is exposed to cigarette smoke.Since primary bronchial epithelial cells (PBECs from asthmatic donors are more susceptible to oxidant-induced apoptosis, we hypothesized that they would be susceptible to cigarette smoke-induced cell death.PBECs from normal and asthmatic donors were exposed to cigarette smoke extract (CSE; cell survival and apoptosis were assessed by fluorescence-activated cell sorting, and protective effects of antioxidants evaluated. The mechanism of cell death was evaluated using caspase inhibitors and immunofluorescent staining for apoptosis-inducing factor (AIF.Exposure of PBEC cultures to CSE resulted in a dose-dependent increase in cell death. At 20% CSE, PBECs from asthmatic donors exhibited significantly more apoptosis than cells from non-asthmatic controls. Reduced glutathione (GSH, but not ascorbic acid (AA, protected against CSE-induced apoptosis. To investigate mechanisms of CSE-induced apoptosis, caspase-3 or -9 inhibitors were tested, but these failed to prevent apoptosis; in contrast, CSE promoted nuclear translocation of AIF from the mitochondria. GSH reduced the number of nuclear-AIF positive cells whereas AA was ineffective.Our results show that PBECs from asthmatic donors are more susceptible to CSE-induced apoptosis. This response involves AIF, which has been implicated in DNA damage and ROS-mediated cell-death. Epithelial susceptibility to CSE may contribute to the impact of environmental tobacco smoke in asthma.

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

    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

  12. Chronic cigarette smoke causes oxidative damage and apoptosis to retinal pigmented epithelial cells in mice.

    Masashi Fujihara

    2008-09-01

    mechanism of smoke induced changes during early AMD.

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

    Brigido Flores, O.; Montalvan Estrada, A.; Fabelo Bonet, O.; Barreras Caballero, A.

    2015-01-01

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

  14. Chemical evaluation of electronic cigarettes.

    Cheng, Tianrong

    2014-05-01

    To review the available evidence evaluating the chemicals in refill solutions, cartridges, aerosols and environmental emissions of electronic cigarettes (e-cigarettes). Systematic literature searches were conducted to identify research related to e-cigarettes and chemistry using 5 reference databases and 11 search terms. The search date range was January 2007 to September 2013. The search yielded 36 articles, of which 29 were deemed relevant for analysis. The levels of nicotine, tobacco-specific nitrosamines (TSNAs), aldehydes, metals, volatile organic compounds (VOCs), flavours, solvent carriers and tobacco alkaloids in e-cigarette refill solutions, cartridges, aerosols and environmental emissions vary considerably. The delivery of nicotine and the release of TSNAs, aldehydes and metals are not consistent across products. Furthermore, the nicotine level listed on the labels of e-cigarette cartridges and refill solutions is often significantly different from measured values. Phenolic compounds, polycyclic aromatic hydrocarbons and drugs have also been reported in e-cigarette refill solutions, cartridges and aerosols. Varying results in particle size distributions of particular matter emissions from e-cigarettes across studies have been observed. Methods applied for the generation and chemical analyses of aerosols differ across studies. Performance characteristics of e-cigarette devices also vary across and within brands. Additional studies based on knowledge of e-cigarette user behaviours and scientifically validated aerosol generation and chemical analysis methods would be helpful in generating reliable measures of chemical quantities. This would allow comparisons of e-cigarette aerosol and traditional smoke constituent levels and would inform an evaluation of the toxicity potential of e-cigarettes.

  15. Chemical evaluation of electronic cigarettes

    Cheng, Tianrong

    2014-01-01

    Objective To review the available evidence evaluating the chemicals in refill solutions, cartridges, aerosols and environmental emissions of electronic cigarettes (e-cigarettes). Methods Systematic literature searches were conducted to identify research related to e-cigarettes and chemistry using 5 reference databases and 11 search terms. The search date range was January 2007 to September 2013. The search yielded 36 articles, of which 29 were deemed relevant for analysis. Results The levels of nicotine, tobacco-specific nitrosamines (TSNAs), aldehydes, metals, volatile organic compounds (VOCs), flavours, solvent carriers and tobacco alkaloids in e-cigarette refill solutions, cartridges, aerosols and environmental emissions vary considerably. The delivery of nicotine and the release of TSNAs, aldehydes and metals are not consistent across products. Furthermore, the nicotine level listed on the labels of e-cigarette cartridges and refill solutions is often significantly different from measured values. Phenolic compounds, polycyclic aromatic hydrocarbons and drugs have also been reported in e-cigarette refill solutions, cartridges and aerosols. Varying results in particle size distributions of particular matter emissions from e-cigarettes across studies have been observed. Methods applied for the generation and chemical analyses of aerosols differ across studies. Performance characteristics of e-cigarette devices also vary across and within brands. Conclusions Additional studies based on knowledge of e-cigarette user behaviours and scientifically validated aerosol generation and chemical analysis methods would be helpful in generating reliable measures of chemical quantities. This would allow comparisons of e-cigarette aerosol and traditional smoke constituent levels and would inform an evaluation of the toxicity potential of e-cigarettes. PMID:24732157

  16. Tobacco cigarette use versus electronic cigarette use: determinants of smoking and vaping behavior

    Kim Romijnders; Marlieke Beijaert; Liesbeth van Osch; Hein de Vries; Reinskje Talhout

    2018-01-01

    Background It is important to know why individuals use electronic cigarettes (e-cigarettes) compared to tobacco cigarettes. This comparison provides policy makers with opportunities to target different types of users. This study examined behavioral determinants associated with both tobacco and e-cigarette use. Differences between non-users (neither e-cigarette users nor smokers), smokers, e-cigarette users, and dual users were assessed for tobacco use versus e-cigarette u...

  17. The availability of electronic cigarettes in U.S. retail outlets, 2012: results of two national studies.

    Rose, Shyanika W; Barker, Dianne C; D'Angelo, Heather; Khan, Tamkeen; Huang, Jidong; Chaloupka, Frank J; Ribisl, Kurt M

    2014-07-01

    Since their introduction in 2007, electronic cigarette ('e-cigarette') awareness and use has grown rapidly. Little is known about variation in e-cigarette availability across areas with different levels of tobacco taxes and smoke-free air policies. This paper looks at US retail availability of e-cigarettes and factors at the store, neighbourhood and policy levels associated with it. In-person store audit data collected in 2012 came from two national samples of tobacco retailers in the contiguous US. Study 1 collected data from a nationally representative sample of tobacco retailers (n=2165). Study 2 collected data from tobacco retailers located in school enrolment zones for nationally representative samples of 8th, 10th and 12th grade public school students (n=2526). In 2012, e-cigarette retail availability was 34% in study 1 and 31% in study 2. Tobacco, pharmacy and gas/convenience stores were more likely to sell e-cigarettes than beer/wine/liquor stores. Retail availability of e-cigarettes was more likely in neighbourhoods with higher median household income (study 1), and lower percent of African-American (studies 1 and 2) and Hispanic residents (study 2). Price of traditional cigarettes was inversely related to e-cigarette availability. Stores in states with an American Lung Association Smoke-Free Air grade of F (study 1) or D (study 2) compared with A had increased likelihood of having e-cigarettes. Currently, e-cigarette availability appears more likely in areas with weak tax and smoke-free air policies. Given the substantial availability of e-cigarettes at tobacco retailers nationwide, states and localities should monitor the sales and marketing of e-cigarettes at point of sale (POS). Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

  18. France acts on electronic cigarettes.

    Cahn, Zachary

    2013-11-01

    France is deciding how to regulate electronic cigarettes. I first consider the French approach and how it contrasts with other attempts at electronic cigarette regulation globally. Next, I critique the individual elements of the French proposal. The overall approach taken by France is a positive development, but banning indoor use appears unnecessary and banning advertising may be counterproductive.

  19. Know More About Menthol Cigarettes

    ... to Quit Why Do You Want to Quit? Health Effects Benefits of Quitting How Much Will You Save How Smoking Affects Your Workout Secondhand Smoke Quiz: How Bad is Secondhand Smoke? E-Cigs, Menthol & Dip What We Know About E-Cigarettes Know More About Menthol Cigarettes Quitting Dip Stay ...

  20. Cigarette smoking habits among schoolchildren

    Branski, D; Knol, K; Kerem, E; Meijer, B.C

    1996-01-01

    Study objective: Cigarette smoking is a major preventable cause of morbidity and mortality worldwide. Most adult smokers start smoking regularly some time before 18 years of age. The aim of this study was to determine the age at which children begin cigarette smoking, to study the environmental

  1. Bidi smoking and lung cancer.

    Prasad, Rajendra; Singhal, Sanjay; Garg, Rajiv

    2009-04-01

    This article discusses the role of bidi smoking as a risk factor for lung cancer. A review of the documented evidence is presented. The literature from Pubmed has been searched using the key words 'beedi smoking', 'bidi smoking' and 'lung cancer'. The bibliographies of all papers found were further searched for additional relevant articles. After this thorough search, eight studies were found. The evidence suggests that bidi smoking poses a higher risk for lung cancer than cigarette smoking and risk further increases with both the length of time and amount of bidi smoking. The focus of tobacco control programs should be expanded to all types of tobacco use, including bidis, to reduce the increasing problem of lung cancer.

  2. Tobacco, E-Cigarettes and Child Health

    Peterson, Lisa A.; Hecht, Stephen S.

    2017-01-01

    Purpose of the review The availability of the Children’s Health Exposure Assessment Resource funded by the National Institute of Environmental Health Sciences provides new opportunities for exploring the role of tobacco smoke exposure in causing harm to children. Findings Children of smokers are exposed to nicotine and other harmful tobacco smoke chemicals in utero as well as in their environment. This passive exposure to tobacco smoke has a variety of negative effects on children. In utero exposure to tobacco smoke causes poor birth outcomes and influences lung, cardiovascular and brain development, placing children at increased risk of a number of adverse health outcomes later in life such as obesity, behavioral problems and cardiovascular disease. Furthermore, most smokers start in their adolescence, an age of increased nicotine addiction risk. Biomarkers of tobacco exposure helps clarify the role tobacco chemicals play in influencing health both in childhood and beyond. While e-cigarettes appear to be a nicotine delivery device of reduced harm, it appears to be a gateway to the use of combustible cigarette smoking in adolescents. Summary Pediatric researchers interested in elucidating the role of tobacco smoke exposure in adverse outcomes in children should incorporate biomarkers of tobacco exposure in their studies. PMID:28059903

  3. Perceptions of the Harm and Addictiveness of Conventional Cigarette Smoking Among Adolescent E-Cigarette Users.

    Owotomo, Olusegun; Maslowsky, Julie; Loukas, Alexandra

    2018-01-01

    Although existing evidence indicates that e-cigarette use is a risk factor for cigarette smoking initiation, mechanisms of this association are not yet known. E-cigarette users perceive e-cigarette use to be less harmful relative to conventional cigarettes, but their absolute perceptions of addictiveness of conventional cigarette smoking are unknown. This study examines how e-cigarette users compare with nonusers (non-e-cigarette users/nonconventional cigarette smokers), conventional cigarette smokers, and dual users on perceptions of harm and the addictiveness of conventional cigarette smoking and on other known predictors of cigarette smoking such as peer smoking, influence of antismoking ads, and risk-taking propensity. National samples of 8th- and 10th-grade students from 2014 and 2015 (N = 14,151) were obtained from the Monitoring the Future Study. Multivariate logistic regression models were used to examine relationships between adolescent smoking status and perceptions of harm and the addictiveness of conventional cigarette smoking while controlling for potential confounders. E-cigarette users had lower perceptions of the addictiveness of conventional cigarette smoking compared with nonusers but higher than cigarette smokers and dual users. E-cigarette users reported lower influence by antismoking ads, more conventional cigarette-smoking peers, and greater risk-taking propensity than nonusers. E-cigarette users and cigarette smokers did not differ in their perceived harm of conventional cigarette smoking or in their risk-taking propensity. E-cigarette users' attitudes and perceptions regarding conventional cigarette smoking may leave them vulnerable to becoming conventional cigarette smokers. Future studies should explore the prospective relationship between smoking-related perceptions of conventional cigarette smoking among e-cigarette users and the onset of cigarette smoking. Copyright © 2017 The Society for Adolescent Health and Medicine. Published

  4. Maternal smoking and the retinoid pathway in the developing lung

    Manoli Sara E

    2012-06-01

    Full Text Available Abstract Background Maternal smoking is a risk factor for pediatric lung disease, including asthma. Animal models suggest that maternal smoking causes defective alveolarization in the offspring. Retinoic acid signaling modulates both lung development and postnatal immune function. Thus, abnormalities in this pathway could mediate maternal smoking effects. We tested whether maternal smoking disrupts retinoic acid pathway expression and functioning in a murine model. Methods Female C57Bl/6 mice with/without mainstream cigarette smoke exposure (3 research cigarettes a day, 5 days a week were mated to nonsmoking males. Cigarette smoke exposure continued throughout the pregnancy and after parturition. Lung tissue from the offspring was examined by mean linear intercept analysis and by quantitative PCR. Cell culture experiments using the type II cell-like cell line, A549, tested whether lipid-soluble cigarette smoke components affected binding and activation of retinoic acid response elements in vitro. Results Compared to tobacco-naïve mice, juvenile mice with tobacco toxin exposure had significantly (P  Conclusions A murine model of maternal cigarette smoking causes abnormal alveolarization in association with altered retinoic acid pathway element expression in the offspring. An in vitro cell culture model shows that lipid-soluble components of cigarette smoke decrease retinoic acid response element activation. It is feasible that disruption of retinoic acid signaling contributes to the pediatric lung dysfunction caused by maternal smoking.

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

    Chen, Huaqun; Wang, Lijuan; Gong, Tao; Yu, Yang; Zhu, Chunhua; Li, Fen; Wang, Li; Li, Chaojun

    2010-01-01

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

  6. African-American smokers and cancers of the lung and of the upper respiratory and digestive tracts. Is menthol part of the puzzle?

    Richardson, T L

    1997-01-01

    The prevalence of cigarette smoking is higher among African Americans than among whites. African Americans have higher rates of lung cancer than whites, although they smoke fewer cigarettes. To explore this black-white difference in lung cancer rates, I examine various aspects of tobacco use in African-American smokers, including the age of initiation of smoking, quantity of cigarettes smoked, quit rates, level of nicotine dependence, biochemical differences, and brand preferences, specifical...

  7. The comparative in vitro assessment of e-cigarette and cigarette smoke aerosols using the γH2AX assay and applied dose measurements.

    Thorne, David; Larard, Sophie; Baxter, Andrew; Meredith, Clive; Gaҫa, Marianna

    2017-01-04

    DNA damage can be caused by a variety of external and internal factors and together with cellular responses, can establish genomic instability through multiple pathways. DNA damage therefore, is considered to play an important role in the aetiology and early stages of carcinogenesis. The DNA-damage inducing potential of tobacco smoke aerosols in vitro has been extensively investigated; however, the ability of e-cigarette aerosols to induce DNA damage has not been extensively investigated. E-cigarette use has grown globally in recent years and the health implications of long term e-cigarette use are still unclear. Therefore, this study has assessed the induction of double-strand DNA damage in vitro using human lung epithelial cells to e-cigarette aerosols from two different product variants (a "cigalike" and a closed "modular" system) and cigarette smoke. A Vitrocell ® VC 10 aerosol exposure system was used to generate and dilute cigarette smoke and e-cigarette aerosols, which were delivered to human bronchial epithelial cells (BEAS-2Bs) housed at the air-liquid-interface (ALI) for up to 120min exposure (diluting airflow, 0.25-1L/min). Following exposure, cells were immediately fixed, incubated with primary (0.1% γH2AX antibody in PBS) and secondary antibodies (DyLight™ 549 conjugated goat anti-mouse IgG) containing Hoechst dye DNA staining solution (0.2% secondary antibody and 0.01% Hoechst in PBS), and finally screened using the Cellomics Arrayscan VTI platform. The results from this study demonstrate a clear DNA damage-induced dose response with increasing smoke concentrations up to cytotoxic levels. In contrast, e-cigarette aerosols from two product variants did not induce DNA damage at equivalent to or greater than doses of cigarette smoke aerosol. In this study dosimetry approaches were used to contextualize exposure, define exposure conditions and facilitate comparisons between cigarette smoke and e-cigarette aerosols. Quartz crystal microbalance (QCM

  8. Receptivity to e-cigarette marketing, harm perceptions, and e-cigarette use.

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

    2015-01-01

    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. 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]. 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. 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.

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

    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

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

    Meng Wang

    2016-01-01

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

  11. Combustible cigarettes cost less to use than e-cigarettes: global evidence and tax policy implications.

    Liber, Alex C; Drope, Jeffrey M; Stoklosa, Michal

    2017-03-01

    Some scholars suggest that price differences between combustible cigarettes and e-cigarettes could be effective in moving current combustible smokers to e-cigarettes, which could reduce tobacco-related death and disease. Currently, in most jurisdictions, e-cigarettes are not subject to the same excise taxes as combustible cigarettes, potentially providing the category with a price advantage over combustible cigarettes. This paper tests whether e-cigarettes tax advantage has translated into a price advantage. In a sample of 45 countries, the price of combustible cigarettes, disposable e-cigarettes and rechargeable cigarettes were compared. Comparable units of combustible cigarettes cost less than disposable e-cigarettes in almost every country in the sample. While the e-liquids consumed in rechargeable e-cigarettes might cost less per comparable unit than combustible cigarettes, the initial cost to purchase a rechargeable e-cigarette presents a significant cost barrier to switching from smoking to vaping. Existing prices of e-cigarettes are generally much higher than of combustible cigarettes. If policymakers wish to tax e-cigarettes less than combustibles, forceful policy action-almost certainly through excise taxation-must raise the price of combustible cigarettes beyond the price of using e-cigarettes. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

  12. 27 CFR 41.34 - Cigarette papers.

    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 following...

  13. Electronic Cigarettes for Smoking Cessation.

    Orellana-Barrios, Menfil A; Payne, Drew; Medrano-Juarez, Rita M; Yang, Shengping; Nugent, Kenneth

    2016-10-01

    The use of electronic cigarettes (e-cigarettes) is increasing, but their use as a smoking-cessation aid is controversial. The reporting of e-cigarette studies on cessation is variable and inconsistent. To date, only 1 randomized clinical trial has included an arm with other cessation methods (nicotine patches). The cessation rates for available clinical trials are difficult to compare given differing follow-up periods and broad ranges (4% at 12 months with non-nicotine e-cigarettes to 68% at 4 weeks with concomitant nicotine e-cigarettes and other cessation methods). The average combined abstinence rate for included prospective studies was 29.1% (combination of 6-18 months׳ rates). There are few comparable clinical trials and prospective studies related to e-cigarettes use for smoking cessation, despite an increasing number of citations. Larger randomized clinical trials are essential to determine whether e-cigarettes are effective smoking-cessation devices. Copyright © 2016 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

  14. Acute effects of cigarette smoke on inflammation and oxidative stress : a review

    van der Vaart, H; Postma, DS; Timens, W; Ten Hacken, NHT

    Compared with the effects of chronic smoke exposure on lung function and airway inflammation, there are few data on the acute effects of smoking. A review of the literature identified 123 studies investigating the acute effects of cigarette smoking on inflammation and oxidative stress in human,

  15. Characterisation of mainstream and passive vapours emitted by selected electronic cigarettes.

    Geiss, Otmar; Bianchi, Ivana; Barahona, Francisco; Barrero-Moreno, Josefa

    2015-01-01

    Electronic cigarettes have achieved growing popularity since their introduction onto the European market. They are promoted by manufacturers as healthier alternatives to tobacco cigarettes, however debate among scientists and public health experts about their possible impact on health and indoor air quality means further research into the product is required to ensure decisions of policymakers, health care providers and consumers are based on sound science. This study investigated and characterised the impact of 'vaping' (using electronic cigarettes) on indoor environments under controlled conditions using a 30m(3) emission chamber. The study determined the composition of e-cigarette mainstream vapour in terms of propylene glycol, glycerol, carbonyls and nicotine emissions using a smoking machine with adapted smoking parameters. Two different base recipes for refill liquids, with three different amounts of nicotine each, were tested using two models of e-cigarettes. Refill liquids were analysed on their content of propylene glycol, glycerol, nicotine and qualitatively on their principal flavourings. Possible health effects of e-cigarette use are not discussed in this work. Electronic cigarettes tested in this study proved to be sources for propylene glycol, glycerol, nicotine, carbonyls and aerosol particulates. The extent of exposure differs significantly for active and passive 'vapers' (users of electronic cigarettes). Extrapolating from the average amounts of propylene glycol and glycerol condensed on the smoking machine filter pad to the resulting lung-concentration, estimated lung concentrations of 160 and 220mgm(-3) for propylene glycol and glycerol were obtained, respectively. Vaping refill liquids with nicotine concentrations of 9mgmL(-1) led to vapour condensate nicotine amounts comparable to those of low-nicotine regular cigarettes (0.15-0.2mg). In chamber studies, peak concentrations of 2200μgm(-3) for propylene glycol, 136μgm(-3) for glycerol and 0.6

  16. Electronic cigarettes: a survey of perceived patient use and attitudes among members of the British thoracic oncology group.

    Sherratt, Frances C; Newson, Lisa; Field, John K

    2016-05-17

    Smoking cessation following lung cancer diagnosis has been found to improve several patient outcomes. Electronic cigarette (e-cigarette) use is now prevalent within Great Britain, however, use and practice among patients with lung cancer has not as yet been explored. The current study aims to explore e-cigarette use among patients and examine current practice among clinicians. The results have important implications for future policy and practice. Members of The British Thoracic Oncology Group (BTOG) were contacted via several e-circulations (N = 2,009), requesting them to complete an online survey. Of these, 7.7 % (N = 154) completed the survey, which explored participant demographics and smoking history, perceptions of patient e-cigarette use, practitioner knowledge regarding sources of guidance pertaining to e-cigarettes, and practitioner advice. Practitioners frequently observed e-cigarette use among patients with lung cancer. The majority of practitioners (81.4 %) reported responding to patient queries pertaining to e-cigarettes within the past year; however, far fewer (21.0 %) felt confident providing patients with e-cigarette advice. Practitioner confidence was found to differentiate by gender (p = 0.012) and employment speciality (p = 0.030), with nurses reporting particularly low levels of confidence in advising. The results also demonstrate extensive variability regarding the practitioner advice content. The results demonstrate that patients refer to practitioners as a source of e-cigarette guidance, yet few practitioners feel confident advising. The absence of evidence-based guidance may have contributed towards the exhibited inconsistencies in practitioner advice. The findings highlight that training should be delivered to equip practitioners with the knowledge and confidence to advise patients effectively; this could subsequently improve smoking cessation rates and patient outcomes.

  17. Electronic Cigarette Use among Mississippi Adults, 2015

    Mendy, Vincent L.; Vargas, Rodolfo; Cannon-Smith, Gerri; Payton, Marinelle; Byambaa, Enkhmaa; Zhang, Lei

    2017-01-01

    Electronic cigarettes (e-cigarettes) are battery-powered devices that deliver nicotine in the form of aerosol. We identify differences and associations in e-cigarette use by sociodemographic characteristics and describe the reported reasons for initiating use among Mississippi adults. We used the 2015 Mississippi Behavioral Risk Factor Surveillance System, which collected information on e-cigarette use from 6,035 respondents. The prevalence of current e-cigarette use and having ever tried an ...

  18. Electronic Cigarettes on Hospital Campuses

    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 w...

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

    Manigrasso, Maurizio; Buonanno, Giorgio; Stabile, Luca; Morawska, Lidia; Avino, Pasquale

    2015-01-01

    The main aim of the present study was to estimate size segregated doses from e-cigarette aerosols as a function of the airway generation number in lung lobes. After a 2-second puff, 7.7 × 10 10 particles (D Tot ) with a surface area of 3.6 × 10 3  mm 2 (S Tot ), and 3.3 × 10 10 particles with a surface area of 4.2 × 10 3  mm 2 were deposited in the respiratory system for the electronic and conventional cigarettes, respectively. Alveolar and tracheobronchial deposited doses were compared to the ones received by non-smoking individuals in Western countries, showing a similar order of magnitude. Total regional doses (D R ), in head and lobar tracheobronchial and alveolar regions, ranged from 2.7 × 10 9 to 1.3 × 10 10 particles and 1.1 × 10 9 to 5.3 × 10 10 particles, for the electronic and conventional cigarettes, respectively. D R in the right-upper lung lobe was about twice that found in left-upper lobe and 20% greater in right-lower lobe than the left-lower lobe. - Highlights: • Lobar doses were compared for mainstreams of electronic and conventional cigarettes. • Aerosol doses from e-cigarettes were more than double that from conventional ones. • Doses from a 2-s puff exceed the daily doses of a no smoking Australian subject. • Highest deposition densities occurred at the lobar bronchi. • Aerosol deposition was greater in the right than in the left lung lobes. - Lobar bronchi and right lung lobes represent sites where effects of the aerosol from e-cigarette smoke may be more likely to occur

  20. E-Cigarette Marketing and Communication: How E-Cigarette Companies Market E-Cigarettes and the Public Engages with E-cigarette Information.

    Collins, Lauren; Glasser, Allison M; Abudayyeh, Haneen; Pearson, Jennifer L; Villanti, Andrea C

    2018-01-05

    Given the lack of regulation on marketing of electronic cigarettes (e-cigarettes) in the U.S. and the increasing exchange of e-cigarette-related information online, it is critical to understand how e-cigarette companies market e-cigarettes and how the public engages with e-cigarette information. Results are from a systematic review of peer-reviewed literature on e-cigarettes via a PubMed search through June 1, 2017. Search terms included: "e-cigarette*" OR "electronic cigarette" OR "electronic cigarettes" OR "electronic nicotine delivery" OR "vape" OR "vaping." Experimental studies, quasi-experimental studies, observational studies, qualitative studies, and mixed methods studies providing empirical findings on e-cigarette marketing and communication (i.e., non-marketing communication in the public) were included. One hundred twenty-four publications on e-cigarette marketing and communication were identified. They covered topics including e-cigarette advertisement claims/promotions and exposure/receptivity, the effect of e-cigarette advertisements on e-cigarette and cigarette use, public engagement with e-cigarette information, and the public's portrayal of e-cigarettes. Studies show increases in e-cigarette marketing expenditures and online engagement through social media over time, that e-cigarettes are often framed as an alternative to combustible cigarettes, and that e-cigarette advertisement exposure may be associated with e-cigarette trial in adolescents and young adults. Few studies examine the effects of e-cigarette marketing on perceptions and e-cigarette and cigarette use. Evidence suggests that exposure to e-cigarette advertisements affects perceptions and trial of e-cigarettes, but there is no evidence that exposure affects cigarette use. No studies examined how exposure to e-cigarette communication, particularly misleading or inaccurate information, impacts e-cigarette and tobacco use behaviors. The present article provides a comprehensive review of e-cigarette

  1. Lung Emergencies

    ... The Marfan Foundation Marfan & Related Disorders What is Marfan Syndrome? What are Related Disorders? What are the Signs? ... Emergencies Lung Emergencies Surgeries Lung Emergencies People with Marfan syndrome can be at increased risk of sudden lung ...

  2. Chemoprevention of Lung Cancer

    Szabo, Eva; Mao, Jenny T.; Lam, Stephen; Reid, Mary E.

    2013-01-01

    Background: Lung cancer is the most common cause of cancer death in men and women in the United States. Cigarette smoking is the main risk factor. Former smokers are at a substantially increased risk of developing lung cancer compared with lifetime never smokers. Chemoprevention refers to the use of specific agents to reverse, suppress, or prevent the process of carcinogenesis. This article reviews the major agents that have been studied for chemoprevention. Methods: Articles of primary, secondary, and tertiary prevention trials were reviewed and summarized to obtain recommendations. Results: None of the phase 3 trials with the agents β-carotene, retinol, 13-cis-retinoic acid, α-tocopherol, N-acetylcysteine, acetylsalicylic acid, or selenium has demonstrated beneficial and reproducible results. To facilitate the evaluation of promising agents and to lessen the need for a large sample size, extensive time commitment, and expense, surrogate end point biomarker trials are being conducted to assist in identifying the most promising agents for later-stage chemoprevention trials. With the understanding of important cellular signaling pathways and the expansion of potentially important targets, agents (many of which target inflammation and the arachidonic acid pathway) are being developed and tested which may prevent or reverse lung carcinogenesis. Conclusions: By integrating biologic knowledge, additional early-phase trials can be performed in a reasonable time frame. The future of lung cancer chemoprevention should entail the evaluation of single agents or combinations that target various pathways while working toward identification and validation of intermediate end points. PMID:23649449

  3. Association between menthol cigarette smoking and current use of electronic cigarettes among us adolescents.

    Israel Agaku

    2017-05-01

    Current e-cigarette use was significantly higher among menthol than nonmenthol cigarette smokers. These findings underscore the importance of efforts to reduce all forms of tobacco product use, including e-cigarettes, among youth.

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

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

    2014-07-01

    Despite the recent popularity of e-cigarettes, to date only limited data is available on their safety for both users and secondhand smokers. The present study reports a comprehensive inner and outer exposure assessment of e-cigarette emissions in terms of particulate matter (PM), particle number concentrations (PNC), volatile organic compounds (VOC), polycyclic aromatic hydrocarbons (PAH), carbonyls, and metals. In six vaping sessions nine volunteers consumed e-cigarettes with and without nicotine in a thoroughly ventilated room for two hours. We analyzed the levels of e-cigarette pollutants in indoor air and monitored effects on FeNO release and urinary metabolite profile of the subjects. For comparison, the components of the e-cigarette solutions (liquids) were additionally analyzed. During the vaping sessions substantial amounts of 1,2-propanediol, glycerine and nicotine were found in the gas-phase, as well as high concentrations of PM2.5 (mean 197 μg/m(3)). The concentration of putative carcinogenic PAH in indoor air increased by 20% to 147 ng/m(3), and aluminum showed a 2.4-fold increase. PNC ranged from 48,620 to 88,386 particles/cm(3) (median), with peaks at diameters 24-36 nm. FeNO increased in 7 of 9 individuals. The nicotine content of the liquids varied and was 1.2-fold higher than claimed by the manufacturer. Our data confirm that e-cigarettes are not emission-free and their pollutants could be of health concern for users and secondhand smokers. In particular, ultrafine particles formed from supersaturated 1,2-propanediol vapor can be deposited in the lung, and aerosolized nicotine seems capable of increasing the release of the inflammatory signaling molecule NO upon inhalation. In view of consumer safety, e-cigarettes and nicotine liquids should be officially regulated and labeled with appropriate warnings of potential health effects, particularly of toxicity risk in children. Copyright © 2013 Elsevier GmbH. All rights reserved.

  5. Endoplasmic reticulum stress in lung disease

    Stefan J. Marciniak

    2017-06-01

    Full Text Available Exposure to inhaled pollutants, including fine particulates and cigarette smoke is a major cause of lung disease in Europe. While it is established that inhaled pollutants have devastating effects on the genome, it is now recognised that additional effects on protein folding also drive the development of lung disease. Protein misfolding in the endoplasmic reticulum affects the pathogenesis of many diseases, ranging from pulmonary fibrosis to cancer. It is therefore important to understand how cells respond to endoplasmic reticulum stress and how this affects pulmonary tissues in disease. These insights may offer opportunities to manipulate such endoplasmic reticulum stress pathways and thereby cure lung disease.

  6. Nutrition for Lung Cancer

    ... Become An Advocate Volunteer Ways To Give Lung Cancer www.lung.org > Lung Health and Diseases > Lung Disease Lookup > ... Cancer Learn About Lung Cancer What Is Lung Cancer Lung Cancer Basics Causes & Risk Factors Lung Cancer Staging ...

  7. Menthol Cigarettes, Time to First Cigarette, and Smoking Cessation

    Sanders Edward

    2017-01-01

    Full Text Available The goal of the present work is to determine if menthol and non-menthol cigarette smokers differ with respect to time to first cigarette (TTFC and successful smoking cessation via a meta-analysis of published results. For 13 independent estimates, menthol smokers were slightly but statistically significantly more likely to exhibit TTFC ≤ 5 min (random-effects odds ratio (OR = 1.12; 95% confidence interval (CI, 1.04–1.21, while 17 independent estimates provided a non-significant difference for TTFC ≤ 30 min (random-effects OR = 1.06; 95% CI, 0.96–1.16. For cessation studies, meta-analysis of 30 published estimates indicated a decreased likelihood for menthol cigarette smokers to quit (random-effects OR = 0.87; 95% CI, 0.80–0.96. There was no difference between cessation rates for Caucasian menthol and non-menthol cigarette smokers, but the results support that African American menthol cigarette smokers find it more difficult to quit. Adjustment of cessation for socioeconomic status eliminated any statistically significant advantage for smoking cessation in non-menthol smokers. In conclusion, these results suggest that the observed differences in cessation rates between menthol and non-menthol cigarette smokers are likely explained by differences in socioeconomic status and also suggest that TTFC may not be a robust predictor of successful smoking cessation.

  8. Flavoured cigarettes, sensation seeking and adolescents' perceptions of cigarette brands.

    Manning, K C; Kelly, K J; Comello, M L

    2009-12-01

    This study examined the interactive effects of cigarette package flavour descriptors and sensation seeking on adolescents' brand perceptions. High school students (n = 253) were randomly assigned to one of two experimental conditions and sequentially exposed to cigarette package illustrations for three different brands. In the flavour descriptor condition, the packages included a description of the cigarettes as "cherry", while in the traditional descriptor condition the cigarette brands were described with common phrases found on tobacco packages such as "domestic blend." Following exposure to each package participants' hedonic beliefs, brand attitudes and trial intentions were assessed. Sensation seeking was also measured, and participants were categorised as lower or higher sensation seekers. Across hedonic belief, brand attitude and trial intention measures, there were interactions between package descriptor condition and sensation seeking. These interactions revealed that among high (but not low) sensation seekers, exposure to cigarette packages including sweet flavour descriptors led to more favourable brand impressions than did exposure to packages with traditional descriptors. Among high sensation seeking youths, the appeal of cigarette brands is enhanced through the use of flavours and associated descriptions on product packaging.

  9. Health care professional and cigarette cessation volunteers knowledge, attitude and practice on e-cigarettes

    Hooman Sharifi

    2018-01-01

    Background Electronic cigarettes (e-cigarette) are new phenomenon that has been widely accepted. E- Cigarettes are more popular that has become one of the preferable rout of smoking cessation in patients. Further researches are required for future advice on e-cigarette use.To determine Health Care Professional and Cigarette Cessation Volunteers Knowledge, Attitude and Practice on e-Cigarettes Methods In a cross-sectional description study, 147 medical professional ...

  10. EAMJ April Cigarette.indd

    2009-04-04

    Apr 4, 2009 ... associated with smoking compared to their non- smoking ... CIGARETTE SMOKING AND ORAL HEALTH AMONG HEALTHCARE STUDENTS. P. Komu, BDS (Nbi), ..... Ashwin, A. P., Hill, K., Balras, V., et al.A comparison.

  11. cigarette smoking and adolescent health

    2013-02-15

    Feb 15, 2013 ... CI (95%) = 0.22 – 0.96). Conclusively, the prevalence of smoking was high among in-school adolescents in the ... The link between cigarette smoking and many non- ..... potential. Epidemiologic Perspectives & Innovations;.

  12. Cigarette, alcohol, and caffeine consumption

    Rasch, Vibeke

    2003-01-01

    OBJECTIVE: To study the association between cigarette, alcohol, and caffeine consumption and the occurrence of spontaneous abortion. METHODS: The study population consisted of 330 women with spontaneous abortion and 1168 pregnant women receiving antenatal care. A case-control design was utilized;...... units alcohol per week and 375 mg or more caffeine per day during pregnancy may increase the risk of spontaneous abortion.......OBJECTIVE: To study the association between cigarette, alcohol, and caffeine consumption and the occurrence of spontaneous abortion. METHODS: The study population consisted of 330 women with spontaneous abortion and 1168 pregnant women receiving antenatal care. A case-control design was utilized......; cases were defined as women with a spontaneous abortion in gestational week 6-16 and controls as women with a live fetus in gestational week 6-16. The variables studied comprise age, parity, occupational situation, cigarette, alcohol, and caffeine consumption. The association between cigarette, alcohol...

  13. Cardiology Patient Page: Electronic Cigarettes

    ... products come in kid-friendly flavors (including grape, chocolate, bubble gum, and gummy bear). E-cigarette advertising ... a tobacco telephone quit line), approved nicotine replacement therapies (eg, patch, gum, or inhaler), and oral nonnicotine ...

  14. Symptoms during Adolescents’ First Use of Cigarettes and E-Cigarettes: A Pilot Study

    May S. Chen

    2017-10-01

    Full Text Available Symptoms adolescents experience during their first time using a cigarette predict their current use, but little is known regarding the symptoms experienced during first e-cigarette use. We conducted a pilot study to understand the symptoms adolescents experience when they first tried cigarettes and e-cigarettes and the associations between these symptoms and current use. Participants were 41 adolescents in two U.S. cities who had tried cigarettes or e-cigarettes. We asked adolescents to recall the symptoms they experienced during their first cigarette or e-cigarette and categorized symptoms as negative (felt bad, coughing/chest pain, bad taste, upset stomach, dizzy/lightheaded or positive (felt relaxed, rush/buzz. Adolescents reported fewer negative symptoms for first e-cigarette than first cigarette use (all p < 0.05. Current cigarette smoking was associated with endorsing fewer negative symptoms (OR = 0.49, 95% CI = [0.25, 0.95] and more positive symptoms (OR = 7.11, 95% CI = [1.47, 34.33] at first cigarette use. First e-cigarette use symptoms were not associated with current e-cigarette use. Adolescents reported fewer negative symptoms from first e-cigarette than from first cigarette, and e-cigarette symptoms did not influence use as they do for cigarettes. Additional research is needed to confirm these findings in longitudinal studies.

  15. Symptoms during Adolescents’ First Use of Cigarettes and E-Cigarettes: A Pilot Study

    Chen, May S.; Hall, Marissa G.; Parada, Humberto; Peebles, Kathryn; Brodar, Kaitlyn E.; Brewer, Noel T.

    2017-01-01

    Symptoms adolescents experience during their first time using a cigarette predict their current use, but little is known regarding the symptoms experienced during first e-cigarette use. We conducted a pilot study to understand the symptoms adolescents experience when they first tried cigarettes and e-cigarettes and the associations between these symptoms and current use. Participants were 41 adolescents in two U.S. cities who had tried cigarettes or e-cigarettes. We asked adolescents to recall the symptoms they experienced during their first cigarette or e-cigarette and categorized symptoms as negative (felt bad, coughing/chest pain, bad taste, upset stomach, dizzy/lightheaded) or positive (felt relaxed, rush/buzz). Adolescents reported fewer negative symptoms for first e-cigarette than first cigarette use (all p < 0.05). Current cigarette smoking was associated with endorsing fewer negative symptoms (OR = 0.49, 95% CI = [0.25, 0.95]) and more positive symptoms (OR = 7.11, 95% CI = [1.47, 34.33]) at first cigarette use. First e-cigarette use symptoms were not associated with current e-cigarette use. Adolescents reported fewer negative symptoms from first e-cigarette than from first cigarette, and e-cigarette symptoms did not influence use as they do for cigarettes. Additional research is needed to confirm these findings in longitudinal studies. PMID:29053574

  16. Cigarette smoking decreases global microRNA expression in human alveolar macrophages.

    Joel W Graff

    Full Text Available Human alveolar macrophages are critical components of the innate immune system. Cigarette smoking-induced changes in alveolar macrophage gene expression are linked to reduced resistance to pulmonary infections and to the development of emphysema/COPD. We hypothesized that microRNAs (miRNAs could control, in part, the unique messenger RNA (mRNA expression profiles found in alveolar macrophages of cigarette smokers. Activation of macrophages with different stimuli in vitro leads to a diverse range of M1 (inflammatory and M2 (anti-inflammatory polarized phenotypes that are thought to mimic activated macrophages in distinct tissue environments. Microarray mRNA data indicated that smoking promoted an "inverse" M1 mRNA expression program, defined by decreased expression of M1-induced transcripts and increased expression of M1-repressed transcripts with few changes in M2-regulated transcripts. RT-PCR arrays identified altered expression of many miRNAs in alveolar macrophages of smokers and a decrease in global miRNA abundance. Stratification of human subjects suggested that the magnitude of the global decrease in miRNA abundance was associated with smoking history. We found that many of the miRNAs with reduced expression in alveolar macrophages of smokers were predicted to target mRNAs upregulated in alveolar macrophages of smokers. For example, miR-452 is predicted to target the transcript encoding MMP12, an important effector of smoking-related diseases. Experimental antagonism of miR-452 in differentiated monocytic cells resulted in increased expression of MMP12. The comprehensive mRNA and miRNA expression profiles described here provide insight into gene expression regulation that may underlie the adverse effects cigarette smoking has on alveolar macrophages.

  17. Chemical composition of cigarette smoke

    Guerin, M. R.

    1979-01-01

    Cigarette smoke is a concentrated aerosol of liquid particles suspended in an atmosphere consisting mainly of nitrogen, oxygen, and carbon dioxide. While the precise chemical composition of the particulate and gaseous phases is dependent on the characteristics of the cigarette and the manner in which it is smoked, both phases contain tens of hundreds of individual constitutents. Notable among potentially hazardous constituents of smoke are tar, nicotine, carbon monoxide, nitric oxide, hydrogen cyanide, acrolein, benzo(a)pyrene, and N-nitrosamines.

  18. Cigarette tax avoidance and evasion.

    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.

  19. E-Cigarette Use, Perceptions, and Cigarette Smoking Intentions in a Community Sample of Young Adult Non-Daily Cigarette Smokers

    Brikmanis, Kristin; Petersen, Angela; Doran, Neal

    2017-01-01

    E-cigarettes have been suggested as a strategy for reducing harm from cigarettes. While e-cigarettes could be a less-harmful alternative to cigarettes for those trying to quit, there may also be costs that outweigh any benefits of reduction. The purpose of the present study was to prospectively investigate perceptions of e-cigarettes, cigarette smoking intentions and their associations with e-cigarette use over time. Community participants (n = 348, 57% male) aged 18–24 were recruited for a longitudinal study of tobacco use. Inclusion criteria included non-daily cigarette smoking for ≥ 6 months with no history of daily smoking. Participants reported e-cigarette use over the past 14 days at baseline and for the past 9 days at 3, 6, and 9 months. Assessments were completed online or via mobile phone. Across the 4 assessments, 22–33% of participants reported recent e-cigarette use. Intent to quit smoking cigarettes and intent to maintain smoking were unrelated to e-cigarette frequency. E-cigarette frequency was positively associated with perceiving e-cigarettes as less harmful than cigarettes and more positive e-cigarette expectancies (ps E-cigarette use was also more frequent among those who smoked cigarettes frequently and who used e-cigarettes to circumvent cigarette bans more often (ps e-cigarette use more than harm reduction. Findings instead seem consistent with the hypothesis that e-cigarettes are more often used to complement ongoing cigarette smoking. PMID:28125242

  20. Electronic Cigarette Use among Mississippi Adults, 2015.

    Mendy, Vincent L; Vargas, Rodolfo; Cannon-Smith, Gerri; Payton, Marinelle; Byambaa, Enkhmaa; Zhang, Lei

    2017-01-01

    Electronic cigarettes (e-cigarettes) are battery-powered devices that deliver nicotine in the form of aerosol. We identify differences and associations in e-cigarette use by sociodemographic characteristics and describe the reported reasons for initiating use among Mississippi adults. We used the 2015 Mississippi Behavioral Risk Factor Surveillance System, which collected information on e-cigarette use from 6,035 respondents. The prevalence of current e-cigarette use and having ever tried an e-cigarette was determined overall and by sociodemographic characteristics. Weighted prevalences and 95% confidence intervals were calculated, and prevalences for subgroups were compared using the X 2 tests and associations were assessed using logistic regression. In 2015, 4.7% of Mississippi adults currently used e-cigarettes, while 20.5% had ever tried an e-cigarette. The prevalence of current e-cigarette use was significantly higher for young adults, whites, men, individuals unable to work, those with income $35,000-$49,999, and current smokers compared to their counterparts. Similar results were observed for having ever tried an e-cigarette. E-cigarette use was associated with age, race, income, and smoking status. Most (71.2%) of current e-cigarette users and over half (52.1%) of those who have ever tried e-cigarettes reported that a main reason for trying or using e-cigarettes was "to cut down or quit smoking."

  1. Electronic Cigarette Use among Mississippi Adults, 2015

    Vincent L. Mendy

    2017-01-01

    Full Text Available Electronic cigarettes (e-cigarettes are battery-powered devices that deliver nicotine in the form of aerosol. We identify differences and associations in e-cigarette use by sociodemographic characteristics and describe the reported reasons for initiating use among Mississippi adults. We used the 2015 Mississippi Behavioral Risk Factor Surveillance System, which collected information on e-cigarette use from 6,035 respondents. The prevalence of current e-cigarette use and having ever tried an e-cigarette was determined overall and by sociodemographic characteristics. Weighted prevalences and 95% confidence intervals were calculated, and prevalences for subgroups were compared using the X2 tests and associations were assessed using logistic regression. In 2015, 4.7% of Mississippi adults currently used e-cigarettes, while 20.5% had ever tried an e-cigarette. The prevalence of current e-cigarette use was significantly higher for young adults, whites, men, individuals unable to work, those with income $35,000–$49,999, and current smokers compared to their counterparts. Similar results were observed for having ever tried an e-cigarette. E-cigarette use was associated with age, race, income, and smoking status. Most (71.2% of current e-cigarette users and over half (52.1% of those who have ever tried e-cigarettes reported that a main reason for trying or using e-cigarettes was “to cut down or quit smoking.”

  2. Cigarette smoking: knowledge and attitudes among Mexican physicians

    TAPIA-CONYER ROBERTO

    1997-01-01

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

  3. Flavoring Chemicals in E-Cigarettes: Diacetyl, 2,3-Pentanedione, and Acetoin in a Sample of 51 Products, Including Fruit-, Candy-, and Cocktail-Flavored E-Cigarettes.

    Allen, Joseph G; Flanigan, Skye S; LeBlanc, Mallory; Vallarino, Jose; MacNaughton, Piers; Stewart, James H; Christiani, David C

    2016-06-01

    There are > 7,000 e-cigarette flavors currently marketed. Flavoring chemicals gained notoriety in the early 2000s when inhalation exposure of the flavoring chemical diacetyl was found to be associated with a disease that became known as "popcorn lung." There has been limited research on flavoring chemicals in e-cigarettes. We aimed to determine if the flavoring chemical diacetyl and two other high-priority flavoring chemicals, 2,3-pentanedione and acetoin, are present in a convenience sample of flavored e-cigarettes. We selected 51 types of flavored e-cigarettes sold by leading e-cigarette brands and flavors we deemed were appealing to youth. E-cigarette contents were fully discharged and the air stream was captured and analyzed for total mass of diacetyl, 2,3-pentanedione, and acetoin, according to OSHA method 1012. At least one flavoring chemical was detected in 47 of 51 unique flavors tested. Diacetyl was detected above the laboratory limit of detection in 39 of the 51 flavors tested, ranging from below the limit of quantification to 239 μg/e-cigarette. 2,3-Pentanedione and acetoin were detected in 23 and 46 of the 51 flavors tested at concentrations up to 64 and 529 μg/e-cigarette, respectively. Because of the associations between diacetyl and bronchiolitis obliterans and other severe respiratory diseases observed in workers, urgent action is recommended to further evaluate this potentially widespread exposure via flavored e-cigarettes. Allen JG, Flanigan SS, LeBlanc M, Vallarino J, MacNaughton P, Stewart JH, Christiani DC. 2016. Flavoring chemicals in e-cigarettes: diacetyl, 2,3-pentanedione, and acetoin in a sample of 51 products, including fruit-, candy-, and cocktail-flavored e-cigarettes. Environ Health Perspect 124:733-739; http://dx.doi.org/10.1289/ehp.1510185.

  4. Expectancies for cigarettes, e-cigarettes, and nicotine replacement therapies among e-cigarette users (aka vapers).

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

    2015-02-01

    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. 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. 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. 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. © The Author 2014. Published by Oxford University Press on behalf of the Society for Research on Nicotine and Tobacco. All rights reserved

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

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

    1995-12-01

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

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

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

    1995-01-01

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

  7. E-cigarette Use and Cigarette Smoking Cessation among Texas College Students.

    Mantey, Dale S; Cooper, Maria R; Loukas, Alexandra; Perry, Cheryl L

    2017-11-01

    We examined the relationships between e-cigarette use and subsequent cigarette smoking behaviors at 6- and 12-month follow-ups among young adults. Participants were 18-29 year-old current and former cigarette smokers (N = 627) at 24 Texas colleges, participating in a 3-wave study. Multi-level, multivariable logistic regression models, accounting for school clustering, examined the impact of self-reported use of e-cigarettes on cigarette smoking status at 6- and 12-month follow-ups. Two mutually-exclusive groups of e-cigarette users were examined: those that used for cigarette smoking cessation and those that used for reasons other than cessation. Baseline covariates included socio-demographics, past quit attempts, nicotine dependence, cigarettes per day, and other tobacco use. Use of e-cigarettes for cigarette smoking cessation was associated with increased odds of cigarette smoking cessation at 6- and 12-month follow-ups, while using e-cigarettes for other reasons was not, when adjusting for covariates. Use of e-cigarettes for cigarette smoking cessation may reduce cigarette smoking rates in young adult college students. Additional research is needed examining e-cigarettes as a complement to evidence-based cessation resources that are associated with cigarette smoking cessation among young adults.

  8. A New Area to Fight: Electronic Cigarette

    Şermin Börekçi

    2015-08-01

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

  9. 210Po and 210Pb concentration of cigarettes traded in Hungary and their estimated dose contribution due to smoking

    Kovacs, Tibor; Somlai, Janos; Nagy, Katalin; Szeiler, Gabor

    2007-01-01

    It is known that tobacco leaves may contain 210 Pb and 210 Po in significant concentrations. The cumulative alpha-radiation dose due to the radioactive content of inhaled cigarette smoke and the increasing number of lung cancer cases explain the importance of the investigation. The present study investigated the activity concentrations of these two radionuclides in 29 Hungarian cigarette samples. The relation between 210 Po/ 210 Pb activity and nicotine/tar content of these cigarettes was also examined. 210 Po was determined by alpha spectrometry using a PIPS detector after chemical leaching and spontaneous deposition of 210 Po on a high nickel-content (25%) stainless steel disk. The 210 Pb activity was calculated from the 210 Po originated from the decay of 210 Pb after a waiting period of eight months. The 210 Po activity concentrations of the measured types of cigarettes ranged from 10.0 to 33.5 mBq/cigarette, and the activity of 210 Pb varied from 9.6 to 32.5 mBq/cigarette. The average annual committed effective dose is estimated to be 185.6±70.6μSv/y and 58.7±22.7μSv/y due to cigarette smoking (20 cigarettes/day) for 210 Po and 210 Pb, respectively

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

    Valenca, Samuel S; Lima, Elaine AC; Dire, Gláucio F; Bernardo-Filho, Mário; Porto, Luís Cristóvão

    2005-01-01

    The biological effects of cigarette smoke are not fully known. To improve our understanding of the action of various chemical agents, we investigated the biodistribution of sodium pertechnetate (Na 99m TcO 4 ) in mice exposed to cigarette smoke. Fifteen BALB/c male mice were exposed to the smoke of nine whole commercial cigarettes per day, 3 times/day, for up to 10 days to whole body exposure in a chamber. A control group of 5 BALB/c male mice was sham-smoked. One day later, the exposed and control groups of mice received (7.4 MBq/0.3 ml) of Na 99m TcO 4 before being killed at 30 min. Bones, brain, heart, intestine, kidney, liver, lungs, muscle, pancreas, spleen, stomach, testis and thyroid were weighed and these organs and blood radioactivity recorded with a gamma counter. The percentage per gram of tissue of injected dose (%ID/g) was determined for each organ. Cigarette smoke significantly decreased (p < 0.05) the %ID/g in red blood cells, bone, kidney, lung, spleen, stomach, testis and thyroid of the exposed mice. The toxic effects of cigarette smoke reduced the Na 99m TcO 4 biodistribution

  11. Contexts of cigarette and e-cigarette use among dual users: a qualitative study.

    Pokhrel, Pallav; Herzog, Thaddeus A; Muranaka, Nicholas; Regmi, Sakshi; Fagan, Pebbles

    2015-09-04

    Not much is currently understood regarding the contexts of cigarette and e-cigarette use among dual users. Proper application of e-cigarettes to smoking cessation or tobacco harm reduction would require an understanding of when and why dual users use cigarettes versus e-cigarettes. This study sought to elucidate the contexts of cigarette versus e-cigarette use among dual users. Twelve focus group discussions were conducted with 62 young adult current daily e-cigarette users [63% men; mean age = 25.1 (Standard Deviation = 5.5)]. Almost all participants either concurrently smoked cigarettes or had been recent dual users. Data were analyzed following principles of inductive deduction. Results indicated that dual users' use of cigarettes is influenced by particular activities (e.g., before/after eating), strong craving or need for stimulation (e.g., in response to stress), places/situations (e.g., when cigarette smokers are nearby; outdoors), use of other substances (alcohol, coffee), and unavailability of an e-cigarette when needed. In addition to particular activities and places/situations that are conducive to e-cigarette use, use of e-cigarette when cigarette is not available or where cigarette smoking is not permitted emerged as contexts specific to e-cigarette use. For habitual cigarette smokers wanting to quit tobacco smoking, switching over completely to e-cigarettes may require skills of cognitive-behavioral management. Future research needs to ascertain the characteristics of dual users who use e-cigarettes as cessation aids versus as cigarette alternative when cigarette is unavailable or smoking is not permitted.

  12. Short-term effects of a nicotine-free e-cigarette compared to a traditional cigarette in smokers and non-smokers.

    Ferrari, Marco; Zanasi, Alessandro; Nardi, Elena; Morselli Labate, Antonio Maria; Ceriana, Piero; Balestrino, Antonella; Pisani, Lara; Corcione, Nadia; Nava, Stefano

    2015-10-12

    A few studies have assessed the short-term effects of low-dose nicotine e-cigarettes, while data about nicotine-free e-cigarettes (NF e-cigarettes) are scanty. Concerns have been expressed about the use of NF e-cigarettes, because of the high concentrations of propylene glycol and other compounds in the e-cigarette vapor. This laboratory-based study was aimed to compare the effects of ad libitum use of a NF e-cigarette or and a traditional cigarette for 5 min in healthy adult smokers (n = 10) and non-smokers (n = 10). The main outcome measures were pulmonary function tests, fraction of exhaled nitric oxide (FeNO) and fractional concentration of carbon monoxide (FeCO) in exhaled breath. The traditional cigarette induced statistically significant increases in FeCO in both smokers and non-smokers, while no significant changes were observed in FeNO. In non-smokers, the traditional cigarette induced a significant decrease from baseline in FEF75 (81 % ± 35 % vs 70.2 % ± 28.2 %, P = 0.013), while in smokers significant decreases were observed in FEF25 (101.3 % ± 16.4 % vs 93.5 % ± 31.7 %, P = 0.037), FEV1 (102.2 % ± 9.5 % vs 98.3 % ± 10 %, P = 0.037) and PEF (109.5 % ± 14.6 % vs 99.2 % ± 17.5 %, P = 0.009). In contrast, the only statistically significant effects induced by the NF e-cigarette in smokers were reductions in FEV1 (102.2 % ± 9.5 % vs 99.5 ± 7.6 %, P = 0.041) and FEF25 (103.4 % ± 16.4 % vs 94.2 % ± 16.2 %, P =  .014). The present study demonstrated that the specific brand of NF e-cigarette utilized did not induce any majoracute effects. In contrast, several studies have shown that both traditional cigarettes and nicotine-containing e-cigarettes have acute effects on lung function. Our study expands on previous observations on the effects of NF e-cigarettes, but also for the first time describes the changes induced by smoking one traditional cigarette in a group of never smokers. The short-term use of the specific brand of NF e-cigarette assessed

  13. Cigarette advertising and adolescent smoking.

    Hanewinkel, Reiner; Isensee, Barbara; Sargent, James D; Morgenstern, Matthis

    2010-04-01

    Although most agree that the association between tobacco marketing and youth smoking is causal, few studies have assessed the specificity of this association. This study aims to examine the specificity of the association between cigarette advertising and teen smoking. A cross-sectional survey of 3415 German schoolchildren aged 10-17 years was conducted using masked images of six cigarette brands and eight other commercial products in 2008. The exposure variable was a combination of contact frequency (recognition) and brand names (cued recall). Sample quartile (Q) exposure to advertisement exposure was calculated in 2009. Outcome variables were ever tried and current (monthly) smoking, and susceptibility to smoking among never smokers. The prevalence of ever smoking was 31.1% and that of current smoking was 7.4%, and 35.3% of never smokers were susceptible to smoking. Ad recognition rates ranged from 15% for a regionally advertised cigarette brand to 99% for a sweet. Lucky Strike and Marlboro were the most highly recognized cigarette brands (with ad recognition rates of 55% and 34%, respectively). After controlling for a range of established influences on smoking behaviors, the adjusted ORs for having tried smoking were 1.97 (95% CI=1.40, 2.77) for Q4 exposure to cigarette ads compared with adolescents in Q1, 2.90 (95% CI=1.48, 5.66) for current smoking, and 1.79 (95% CI=1.32, 2.43) for susceptibility to smoking among never smokers. Exposure to ads for commercial products other than cigarettes was significantly associated with smoking in crude but not multivariate models. This study underlines the specificity of the relationship between tobacco marketing and youth smoking, with exposure to cigarette ads, but not other ads, being associated with smoking behavior and intentions to smoke. This finding suggests a content-related effect of tobacco advertisements. 2010 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.

  14. "Tobacco Truths": Health Magazine, Clinical Epidemiology, and the Cigarette Connection.

    Wilmshurst, Sara

    2015-01-01

    In the 1950s, Health, a magazine published by the Health League of Canada, was nonchalant about the risks of smoking and largely ignored early epidemiological studies of lung cancer. In the 1960s the magazine stopped accepting cigarette advertising and began to oppose smoking. Health's writers adjusted to new knowledge; the magazine gradually accepted clinical epidemiology as a source of medical knowledge and recognized smoking as a public health risk. As Canada's only devoted health publication for a lay audience at the time, Health provides a unique window into ways that smoking and health were portrayed to its readers.

  15. Effect of epimedium pubescen flavonoid on bone mineral status and bone turnover in male rats chronically exposed to cigarette smoke

    Gao Shu-guang

    2012-06-01

    Full Text Available Abstract Background Epimedii herba is one of the most frequently used herbs in formulas that are prescribed for the treatment of osteoporosis in China and its main constituent is Epimedium pubescen flavonoid (EPF. However, it is unclear whether EPF during chronic exposure to cigarette smoke may have a protective influence on the skeleton. The present study investigated the effect of EPF on bone mineral status and bone turnover in a rat model of human relatively high exposure to cigarette smoke. Methods Fifty male Wistar rats were randomized into five groups: controls, passive smoking groups and passive smoking rats administered EPF at three dosage levels (75, 150 or 300 mg/kg/day in drinking water for 4 months. A rat model of passive smoking was prepared by breeding male rats in a cigarette-smoking box. Bone mineral content (BMC, bone mineral density (BMD, bone turnover markers, bone histomorphometric parameters and biomechanical properties were examined. Results Smoke exposure decreased BMC and BMD, increased bone turnover (inhibited bone formation and stimulated its resorption, affected bone histomorphometry (increased trabecular separation and osteoclast surface per bone surface; decreased trabecular bone volume, trabecular thickness, trabecular number, cortical thickness, bone formation rate and osteoblast surface per bone surface, and reduced mechanical properties. EPF supplementation during cigarette smoke exposure prevented smoke-induced changes in bone mineral status and bone turnover. Conclusion The results suggest that EPF can prevent the adverse effects of smoke exposure on bone by stimulating bone formation and inhibiting bone turnover and bone resorption.

  16. Cigarette packaging and health warnings: the impact of plain packaging and message framing on young smokers.

    Mays, Darren; Niaura, Raymond S; Evans, W Douglas; Hammond, David; Luta, George; Tercyak, Kenneth P

    2015-03-01

    This study examined the impact of pictorial cigarette-warning labels, warning-label message framing and plain cigarette packaging, on young adult smokers' motivation to quit. Smokers aged 18-30 years (n=740) from a consumer research panel were randomised to one of four experimental conditions where they viewed online images of four cigarette packs with warnings about lung disease, cancer, stroke/heart disease and death, respectively. Packs differed across conditions by warning-message framing (gain vs loss) and packaging (branded vs plain). Measures captured demographics, smoking behaviour, covariates and motivation to quit in response to cigarette packs. Pictorial warnings about lung disease and cancer generated the strongest motivation to quit across conditions. Adjusting for pretest motivation and covariates, a message framing by packaging interaction revealed gain-framed warnings on plain packs generated greater motivation to quit for lung disease, cancer and mortality warnings (ppackaging regulations. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.

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

    Johnson, R.H. Jr.; Rosario, A. Jr.

    1990-01-01

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

  18. Changes in use of cigarettes and non-cigarette alternative products among college students.

    Loukas, Alexandra; Batanova, Milena; Fernandez, Alejandra; Agarwal, Deepti

    2015-10-01

    The present study examined change in use of various smoked and smokeless non-cigarette alternative products in a sample of college students, stratified by current, or past 30-day, cigarette smoking status. Participants were 698 students from seven four-year colleges in Texas. Participants completed two waves of online surveys regarding tobacco use, knowledge, and attitudes, with 14 months between each wave. The most prevalent products used by the entire sample at Wave 1 were cigarettes, followed by hookah, cigars/cigarillos/little cigars, and electronic cigarettes (e-cigarettes). At Wave 2, prevalence of e-cigarette use surpassed use of cigars/cigarillos/little cigars. Snus and chew/snuff/dip were relatively uncommon at both waves. Examination of change in use indicated that e-cigarette use increased across time among both current cigarette smokers and non-cigarette smokers. Prevalence of current e-cigarette use doubled across the 14-month period to 25% among current smokers and tripled to 3% among non-cigarette smokers. Hookah use also increased across time, but only among non-cigarette smokers, whereas it decreased among current cigarette smokers. Use of all other non-cigarette alternatives remained unchanged across time. Logistic regression analysis was used to examine the socio-demographic predictors of Wave 2 e-cigarette use, the only product that increased in use among both current cigarette smokers and non-cigarette smokers. Results indicated that Wave 1 current cigarette use and Wave 1 current e-cigarette use, but not gender, age, or race/ethnicity, were significantly associated with Wave 2 e-cigarette use. Findings underscore the need to track changes in the use of non-cigarette alternatives and call for additional research examining the factors contributing to change in use. Copyright © 2015 Elsevier Ltd. All rights reserved.

  19. Dependence levels in users of electronic cigarettes, nicotine gums and tobacco cigarettes.

    Etter, Jean-François; Eissenberg, Thomas

    2015-02-01

    To assess dependence levels in users of e-cigarettes, and compare them with dependence levels in users of nicotine gums and tobacco cigarettes. Self-reports from cross-sectional Internet and mail surveys. Comparisons of: (a) 766 daily users of nicotine-containing e-cigarettes with 30 daily users of nicotine-free e-cigarettes; (b) 911 former smokers who used the e-cigarette daily with 451 former smokers who used the nicotine gum daily (but no e-cigarette); (c) 125 daily e-cigarette users who smoked daily (dual users) with two samples of daily smokers who did not use e-cigarettes (2206 enrolled on the Internet and 292 enrolled by mail from the general population of Geneva). We used the Fagerström test for nicotine dependence, the nicotine dependence syndrome scale, the cigarette dependence scale and versions of these scales adapted for e-cigarettes and nicotine gums. Dependence ratings were slightly higher in users of nicotine-containing e-cigarettes than in users of nicotine-free e-cigarettes. In former smokers, long-term (>3 months) users of e-cigarettes were less dependent on e-cigarettes than long-term users of the nicotine gum were dependent on the gum. There were few differences in dependence ratings between short-term (≤3 months) users of gums or e-cigarettes. Dependence on e-cigarettes was generally lower in dual users than dependence on tobacco cigarettes in the two other samples of daily smokers. Some e-cigarette users were dependent on nicotine-containing e-cigarettes, but these products were less addictive than tobacco cigarettes. E-cigarettes may be as or less addictive than nicotine gums, which themselves are not very addictive. Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.

  20. Toxic metals distribution in different components of Pakistani and imported cigarettes by electrothermal atomic absorption spectrometer

    Kazi, T.G.; Jalbani, N.; Arain, M.B.; Jamali, M.K.; Afridi, H.I.; Sarfraz, R.A.; Shah, A.Q.

    2009-01-01

    It was extensively investigated that a significant flux of toxic metals, along with other toxins, reaches the lungs through smoking. In present study toxic metals (TMs) (Al, Cd, Ni and Pb) were determined in different components of Pakistani local branded and imported cigarettes, including filler tobacco (FT), filter (before and after normal smoking by a single volunteer) and ash by electrothermal atomic absorption spectrometer (ETAAS). Microwave-assisted digestion method was employed. The validity and accuracy of methodology were checked by using certified sample of Virginia tobacco leaves (ICHTJ-cta-VTL-2). The percentages (%) of TMs in different components of cigarette were calculated with respect to their total contents in FT of all branded cigarettes before smoking, while smoke concentration has been calculated by subtracting the filter and ash contents from the filler tobacco content of each branded cigarette. The highest percentage (%) of Al was observed in ash of all cigarettes, with range 97.3-99.0%, while in the case of Cd, a reverse behaviour was observed, as a range of 15.0-31.3% of total contents were left in the ash of all branded cigarettes understudy

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

    Fromme, Hermann; Schober, Wolfgang

    2015-04-01

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

  2. Benzene formation in electronic cigarettes.

    James F Pankow

    Full Text Available The heating of the fluids used in electronic cigarettes ("e-cigarettes" used to create "vaping" aerosols is capable of causing a wide range of degradation reaction products. We investigated formation of benzene (an important human carcinogen from e-cigarette fluids containing propylene glycol (PG, glycerol (GL, benzoic acid, the flavor chemical benzaldehyde, and nicotine.Three e-cigarette devices were used: the JUULTM "pod" system (provides no user accessible settings other than flavor cartridge choice, and two refill tank systems that allowed a range of user accessible power settings. Benzene in the e-cigarette aerosols was determined by gas chromatography/mass spectrometry. Benzene formation was ND (not detected in the JUUL system. In the two tank systems benzene was found to form from propylene glycol (PG and glycerol (GL, and from the additives benzoic acid and benzaldehyde, especially at high power settings. With 50:50 PG+GL, for tank device 1 at 6W and 13W, the formed benzene concentrations were 1.9 and 750 μg/m3. For tank device 2, at 6W and 25W, the formed concentrations were ND and 1.8 μg/m3. With benzoic acid and benzaldehyde at ~10 mg/mL, for tank device 1, values at 13W were as high as 5000 μg/m3. For tank device 2 at 25W, all values were ≤~100 μg/m3. These values may be compared with what can be expected in a conventional (tobacco cigarette, namely 200,000 μg/m3. Thus, the risks from benzene will be lower from e-cigarettes than from conventional cigarettes. However, ambient benzene air concentrations in the U.S. have typically been 1 μg/m3, so that benzene has been named the largest single known cancer-risk air toxic in the U.S. For non-smokers, chronically repeated exposure to benzene from e-cigarettes at levels such as 100 or higher μg/m3 will not be of negligible risk.

  3. Effects of e-Cigarette Advertisements on Adolescents' Perceptions of Cigarettes.

    Kim, Minji; Popova, Lucy; Halpern-Felsher, Bonnie; Ling, Pamela M

    2017-12-13

    This study examined the effect of exposure to "cigalike" (products resembling cigarettes) e-cigarette advertisements on adolescents' perceptions of cigarettes. A nationally representative sample of 802 adolescents (13-17 years old) was randomly assigned to watch three e-cigarette or three control advertisements. Never-smokers who saw the e-cigarette advertisements (n = 352) reported significantly lower perceived risks of smoking than those in the control condition (n = 320). Ever-smokers (n = 130) did not show significant differences across the conditions. In subgroup analyses, current smokers (reported smoking in the past 30 days, n = 31) in the e-cigarette condition reported significantly lower perceived benefits of smoking than those in the control condition. E-cigarette advertisements can affect adolescents' perceptions of cigarettes. Many advertisements, especially the ones promoting "cigalikes," depict e-cigarettes as being similar to cigarettes (e.g., look, flavor) but also as a solution for cigarettes' shortcomings (e.g., bad smell). While the advertisements include messages about problems posed by cigarettes, proposing e-cigarettes as a solution may decrease the perceived risks of smoking among never-smokers. It may also not be clear to adolescents whether advertisements are for cigarettes or e-cigarettes. Regulating e-cigarette advertisements to minimize adolescents' exposure may prevent potential harmful effects on never-smokers' perception of smoking.

  4. Short-term effects of electronic and tobacco cigarettes on exhaled nitric oxide

    Marini, Sara; Buonanno, Giorgio; Stabile, Luca; Ficco, Giorgio

    2014-01-01

    The objective of this study was to compare the short-term respiratory effects due to the inhalation of electronic and conventional tobacco cigarette-generated mainstream aerosols through the measurement of the exhaled nitric oxide (eNO). To this purpose, twenty-five smokers were asked to smoke a conventional cigarette and to vape an electronic cigarette (with and without nicotine), and an electronic cigarette without liquid (control session). Electronic and tobacco cigarette mainstream aerosols were characterized in terms of total particle number concentrations and size distributions. On the basis of the measured total particle number concentrations and size distributions, the average particle doses deposited in alveolar and tracheobronchial regions of the lungs for a single 2-s puff were also estimated considering a subject performing resting (sitting) activity. Total particle number concentrations in the mainstream resulted equal to 3.5 ± 0.4 × 10 9 , 5.1 ± 0.1 × 10 9 , and 3.1 ± 0.6 × 10 9 part. cm −3 for electronic cigarettes without nicotine, with nicotine, and for conventional cigarettes, respectively. The corresponding alveolar doses for a resting subject were estimated equal to 3.8 × 10 10 , 5.2 × 10 10 and 2.3 × 10 10 particles. The mean eNO variations measured after each smoking/vaping session were equal to 3.2 ppb, 2.7 ppb and 2.8 ppb for electronic cigarettes without nicotine, with nicotine, and for conventional cigarettes, respectively; whereas, negligible eNO changes were measured in the control session. Statistical tests performed on eNO data showed statistically significant differences between smoking/vaping sessions and the control session, thus confirming a similar effect on human airways whatever the cigarette smoked/vaped, the nicotine content, and the particle dose received. - Highlights: • Electronic cigarettes (with and without nicotine) mainstream aerosols were analyzed; • Particle number concentrations and size distributions

  5. Short-term effects of electronic and tobacco cigarettes on exhaled nitric oxide

    Marini, Sara, E-mail: s.marini@unicas.it [Department of Civil and Mechanical Engineering, University of Cassino and Southern Lazio, Cassino (Italy); Buonanno, Giorgio [Department of Civil and Mechanical Engineering, University of Cassino and Southern Lazio, Cassino (Italy); Queensland University of Technology, Brisbane (Australia); Stabile, Luca; Ficco, Giorgio [Department of Civil and Mechanical Engineering, University of Cassino and Southern Lazio, Cassino (Italy)

    2014-07-01

    The objective of this study was to compare the short-term respiratory effects due to the inhalation of electronic and conventional tobacco cigarette-generated mainstream aerosols through the measurement of the exhaled nitric oxide (eNO). To this purpose, twenty-five smokers were asked to smoke a conventional cigarette and to vape an electronic cigarette (with and without nicotine), and an electronic cigarette without liquid (control session). Electronic and tobacco cigarette mainstream aerosols were characterized in terms of total particle number concentrations and size distributions. On the basis of the measured total particle number concentrations and size distributions, the average particle doses deposited in alveolar and tracheobronchial regions of the lungs for a single 2-s puff were also estimated considering a subject performing resting (sitting) activity. Total particle number concentrations in the mainstream resulted equal to 3.5 ± 0.4 × 10{sup 9}, 5.1 ± 0.1 × 10{sup 9}, and 3.1 ± 0.6 × 10{sup 9} part. cm{sup −3} for electronic cigarettes without nicotine, with nicotine, and for conventional cigarettes, respectively. The corresponding alveolar doses for a resting subject were estimated equal to 3.8 × 10{sup 10}, 5.2 × 10{sup 10} and 2.3 × 10{sup 10} particles. The mean eNO variations measured after each smoking/vaping session were equal to 3.2 ppb, 2.7 ppb and 2.8 ppb for electronic cigarettes without nicotine, with nicotine, and for conventional cigarettes, respectively; whereas, negligible eNO changes were measured in the control session. Statistical tests performed on eNO data showed statistically significant differences between smoking/vaping sessions and the control session, thus confirming a similar effect on human airways whatever the cigarette smoked/vaped, the nicotine content, and the particle dose received. - Highlights: • Electronic cigarettes (with and without nicotine) mainstream aerosols were analyzed; • Particle number

  6. Patient–physician communication regarding electronic cigarettes

    Michael B. Steinberg

    2015-01-01

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

  7. Electronic cigarette explosions involving the oral cavity.

    Harrison, Rebecca; Hicklin, David

    2016-11-01

    The use of electronic cigarettes (e-cigarettes) is a rapidly growing trend throughout the United States. E-cigarettes have been linked to the risk of causing explosion and fire. Data are limited on the associated health hazards of e-cigarette use, particularly long-term effects, and available information often presents conflicting conclusions. In addition, an e-cigarette explosion and fire can pose a unique treatment challenge to the dental care provider because the oral cavity may be affected heavily. In this particular case, the patient's injuries included intraoral burns, luxation injuries, and alveolar fractures. This case report aims to help clinicians gain an increased knowledge about e-cigarette design, use, and risks; discuss the risk of spontaneous failure and explosion of e-cigarettes with patients; and understand the treatment challenges posed by an e-cigarette explosion. Copyright © 2016 American Dental Association. Published by Elsevier Inc. All rights reserved.

  8. Dual Use of E-Cigarettes and Traditional Cigarettes Among Adolescents in Taiwan, 2014-2016.

    Chen, Pei-Ching; Chang, Li-Chuan; Hsu, Chieh; Lee, Yue-Chune

    2018-02-02

    We investigated the use of electronic cigarettes (e-cigarettes) with traditional cigarettes among adolescents during 2014 to 2016 to identify risk factors for using e-cigarettes only, traditional cigarettes only, or both products. We used cross-sectional data from the Taiwan Global Youth Tobacco Survey, (conducted over a 3-year period by the Health Promotion Administration, Ministry of Health and Welfare, Taiwan), which is representative of tobacco use among adolescents aged 12-18 years. The outcome variable was smoking behavior. Dependent variables included gender, grade, monthly income/allowance, parents' educational level, parents' smoking status, close friends' smoking status, use of other tobacco products, contact with cigarette/e-cigarette advertisements, and access to free cigarettes/e-cigarettes. Multinomial regression identify factors influencing the smoking behaviors of adolescents, as manifested in the use of traditional cigarettes only, e-cigarettes only, e-cigarettes with traditional cigarettes, and nonsmoking. When weighted to the population, the sample included 1723150 adolescents in 2014, 1691568 adolescents in 2015, and 1627216 adolescents in 2016. The rates averaged over three years were as follows: nonsmoking (91.6%), traditional cigarettes only (5.4%), e-cigarettes only (1.5%), and dual usage (1.6%). Among adolescents in Taiwan, the following were risk factors for dual use: male, older, high monthly allowance, smoking parents, smoking friends, use of other tobacco products, contact with cigarette advertisements, and access to free cigarettes. Our results revealed an increase in the number of adolescents using e-cigarettes with traditional cigarettes. We recommend that the government continue smoking cessation programs while maintaining control over advertisements and promotions for tobacco products. This is the first study to examine the dual use of e-cigarettes and traditional cigarettes among adolescents in Taiwan. This study identified the

  9. [Smoking fewer cigarettes per day may determine a significant risk reduction in developing smoking attributable diseases? Is there a risk reduction for e-cigarette users?].

    Pieri, Luca; Chellini, Elisabetta; Gorini, Giuseppe

    2014-01-01

    Among Italian smokers--about 10 millions in 2013--about 600,000 began using electronic cigarettes (e-cigs) in last years. About 10% of e-cig users quitted smoking tobacco, whereas the 90% was dual users. Among them, about three out of four decreased the number of cigarettes smoked per day (cig/day), but did not quit. How many fewer cigarettes a smoker has to smoke to obtain significant health benefits? Is there a threshold? In order to observe a significant 27% reduction in the risk of developing lung cancer, a smoker must reduce the number of cig/day by at least 50%, while for the other smoking-related diseases (acute myocardial infarction - AMI, stroke, chronic obstructive pulmonary diseases), halving the number of cig/day did not drive to a significant risk reduction. Even smoking 5 cig/day increases the risk of AMI, whereas it significantly lowers the risk of lung cancer. Obviously, quitting smoking is the best choice to highly reduce risks for all smoking-related diseases. Therefore, in order to achieve significant risk reductions, e-cig users should quit smoking as first choice, or, if they feel it is impossible to them, reduce the consumption of traditional cigarettes to less than 5 cig/day.

  10. E-cigarettes also contain detrimental chemicals

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

    2014-01-01

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

  11. E-Cigarettes and Cancer Patients

    Cummings, K. Michael; Dresler, Carolyn M.; Field, John K.; Fox, Jesme; Gritz, Ellen R.; Hanna, Nasser H.; Ikeda, Norihiko; Jassem, Jacek; Mulshine, James L.; Peters, Matthew J.; Yamaguchi, Nise H.; Warren, Graham; Zhou, Caicun

    2014-01-01

    The increasing popularity and availability of electronic cigarettes (i.e., e-cigarettes) in many countries have promoted debate among health professionals as to what to recommend to their patients who might be struggling to stop smoking or asking about e-cigarettes. In the absence of evidence-based guidelines for using e-cigarettes for smoking cessation, some health professionals have urged caution about recommending them due to the limited evidence of their safety and efficacy, while others ...

  12. Emergence of electronic cigarette use in US adolescents and the link to traditional cigarette use.

    Lanza, Stephanie T; Russell, Michael A; Braymiller, Jessica L

    2017-04-01

    Electronic cigarettes (e-cigarettes) are increasingly used by US adolescents and may be a gateway to traditional cigarette use. We examine rates of both products by age and examine differences in age-varying rates by sex and race/ethnicity. Data are from the 2014 National Youth Tobacco Survey, a national sample of US middle and high school students (n=22.007); students ages 11-19 were included. Past 30-day e-cigarette and traditional cigarette use were examined as a function of age; sex and race/ethnicity were included as moderators. The age-varying association between e-cigarette and traditional cigarette use was also examined. Rates of e-cigarette use increase faster than traditional cigarette use from ages 13-16. Compared to females, males had higher rates of e-cigarette use from ages 14-17.5 and traditional cigarette use from ages 15-18. Between ages 12-14, more Hispanic adolescents used e-cigarettes compared to White or Black adolescents; after age 14 Hispanics and Whites reported similar rates, peaking at twice the rate for Blacks. Hispanic adolescents report greater traditional cigarette use versus Whites between ages 12-13, but lower rates between ages 15-18. E-cigarette use was strongly associated with traditional cigarette use, particularly during early adolescence [OR>40 before age 12]. Young Hispanic adolescents are at elevated risk for use of e-cigarettes and traditional cigarettes during early adolescence. During early adolescence, youth using e-cigarettes are more likely to smoke traditional cigarettes compared to youth not using e-cigarettes. The study of age-varying effects holds promise for advancing understanding of disparities in health risk behaviors. Copyright © 2016 Elsevier Ltd. All rights reserved.

  13. Electronic cigarettes and nicotine clinical pharmacology.

    Schroeder, Megan J; Hoffman, Allison C

    2014-05-01

    To review the available literature evaluating electronic cigarette (e-cigarette) nicotine clinical pharmacology in order to understand the potential impact of e-cigarettes on individual users, nicotine dependence and public health. Literature searches were conducted between 1 October 2012 and 30 September 2013 using key terms in five electronic databases. Studies were included in the review if they were in English and publicly available; non-clinical studies, conference abstracts and studies exclusively measuring nicotine content in e-cigarette cartridges were excluded from the review. Nicotine yields from automated smoking machines suggest that e-cigarettes deliver less nicotine per puff than traditional cigarettes, and clinical studies indicate that e-cigarettes deliver only modest nicotine concentrations to the inexperienced e-cigarette user. However, current e-cigarette smokers are able to achieve systemic nicotine and/or cotinine concentrations similar to those produced from traditional cigarettes. Therefore, user experience is critically important for nicotine exposure, and may contribute to the products' ability to support and maintain nicotine dependence. Knowledge about e-cigarette nicotine pharmacology remains limited. Because a user's e-cigarette experience may significantly impact nicotine delivery, future nicotine pharmacokinetic and pharmacodynamic studies should be conducted in experienced users to accurately assess the products' impact on public health.

  14. Electronic cigarettes and nicotine clinical pharmacology

    Schroeder, Megan J; Hoffman, Allison C

    2014-01-01

    Objective To review the available literature evaluating electronic cigarette (e-cigarette) nicotine clinical pharmacology in order to understand the potential impact of e-cigarettes on individual users, nicotine dependence and public health. Methods Literature searches were conducted between 1 October 2012 and 30 September 2013 using key terms in five electronic databases. Studies were included in the review if they were in English and publicly available; non-clinical studies, conference abstracts and studies exclusively measuring nicotine content in e-cigarette cartridges were excluded from the review. Results Nicotine yields from automated smoking machines suggest that e-cigarettes deliver less nicotine per puff than traditional cigarettes, and clinical studies indicate that e-cigarettes deliver only modest nicotine concentrations to the inexperienced e-cigarette user. However, current e-cigarette smokers are able to achieve systemic nicotine and/or cotinine concentrations similar to those produced from traditional cigarettes. Therefore, user experience is critically important for nicotine exposure, and may contribute to the products’ ability to support and maintain nicotine dependence. Conclusions Knowledge about e-cigarette nicotine pharmacology remains limited. Because a user's e-cigarette experience may significantly impact nicotine delivery, future nicotine pharmacokinetic and pharmacodynamic studies should be conducted in experienced users to accurately assess the products’ impact on public health. PMID:24732160

  15. Acute cigarette smoke exposure increases alveolar permeability in rabbits

    Witten, M.L.; Lemen, R.J.; Quan, S.F.; Sobonya, R.E.; Roseberry, H.; Stevenson, J.L.; Clayton, J.

    1985-01-01

    The authors measured lung clearance of aerosolized technetium-labeled diethylenetriamine pentaacetic acid (/sup 99m/TcDTPA) as an index of alveolar epithelial permeability in rabbits exposed to cigarette smoke. Eighteen rabbits were randomly assigned to 3 equal-size groups: control, all smoke exposure (ASE), and limited smoke exposure (LSE). Cigarette or sham smoke was delivered by syringe in a series of 5, 10, 20, and 30 tidal volume breaths with a 20-min counting period between each subset of breaths to determine /sup 99m/TcDTPA biologic half-life (T 1 / 2 ). Mean T 1 / 2 minimum was significantly lower for ASE and LSE rabbits than by control rabbits. They observed a significant difference at 20 and 30 breath exposures between the control and ASE group mean values for T 1 / 2 , arterial blood pressure, and peak airway pressure. A combination of light and electron microscopy showed focal alveolar edema and hemorrhage in the ASE and LSE groups but no alveolar-capillary membrane damage. In summary, acute cigarette smoke exposure increases alveolar permeability as measured by /sup 99m/TcDTPA clearance, but there was no detectable ultrastructural alteration of the alveolar-capillary membrane

  16. Radioactivity levels in jurak and moasel, comparison with cigarette tobacco

    Abdul-Majid, S.; Kutbi, I.I.; Basabrain, M.

    1994-01-01

    Jurak and moasel are tobacco products that contain, in addition to tobacco, juice of sugar cane, fruits, spices, tar and nicotine. These products are smoked by hubble-bubble, a popular smoking habit in the Middle Eastern and North African countries. Charcoal is put directly on these products during smoking and the smoke passes through water for cooling purpose before it goes to the lung, without filtering. Radioactivity levels were measured in these products, tobacco leaves, charcoal and in cigarette tobacco of most well known brand names by gamma spectrometry system consisting of HPGe detector coupled to a PC-based 8192 channel multichannel analyzer. The average 226 Ra concentrations in jurak, moasel, tobacco leaves, charcoal and cigarette tobacco in Bq/kg were:3.4, 1.8, 3.2, 2.9 and 7 respectively; that of 232 Th were: 3.8, 2.6, 3.5, 2.2 and 7.8 respectively; that of 40 K were 620, 445, 511, 163 and 876 respectively. It is expected that a jurak smoker inhales 10 times the radioactivity and a moasel smoker twice that compared to a 25 cigarette/d smoker. (author). 18 refs., 2 figs., 4 tabs

  17. Th17/Treg immunoregulation and implications in treatment of sulfur mustard gas-induced lung diseases.

    Iman, Maryam; Rezaei, Ramazan; Azimzadeh Jamalkandi, Sadegh; Shariati, Parvin; Kheradmand, Farrah; Salimian, Jafar

    2017-12-01

    Sulfur mustard (SM) is an extremely toxic gas used in chemical warfare to cause massive lung injury and death. Victims exposed to SM gas acutely present with inhalational lung injury, but among those who survive, some develop obstructive airway diseases referred to as SM-lung syndrome. Pathophysiologically, SM-lung shares many characteristics with smoking-induced chronic obstructive pulmonary disease (COPD), including airway remodeling, goblet cell metaplasia, and obstructive ventilation defect. Some of the hallmarks of COPD pathogenesis, which include dysregulated lung inflammation, neutrophilia, recruitment of interleukin 17A (IL -17A) expressing CD4 + T cells (Th17), and the paucity of lung regulatory T cells (Tregs), have also been described in SM-lung. Areas covered: A literature search was performed using the MEDLINE, EMBASE, and Web of Science databases inclusive of all literature prior to and including May 2017. Expert commentary: Here we review some of the recent findings that suggest a role for Th17 cell-mediated inflammatory changes associated with pulmonary complications in SM-lung and suggest new therapeutic approaches that could potentially alter disease progression with immune modulating biologics that can restore the lung Th17/Treg balance.

  18. Have combustible cigarettes met their match? The nicotine delivery profiles and harmful constituent exposures of second-generation and third-generation electronic cigarette users.

    Wagener, Theodore L; Floyd, Evan L; Stepanov, Irina; Driskill, Leslie M; Frank, Summer G; Meier, Ellen; Leavens, Eleanor L; Tackett, Alayna P; Molina, Neil; Queimado, Lurdes

    2017-03-01

    Electronic cigarettes' (e-cigarettes) viability as a public health strategy to end smoking will likely be determined by their ability to mimic the pharmacokinetic profile of a cigarette while also exposing users to significantly lower levels of harmful/potentially harmful constituents (HPHCs). The present study examined the nicotine delivery profile of third- (G3) versus second-generation (G2) e-cigarette devices and their users' exposure to nicotine and select HPHCs compared with cigarette smokers. 30 participants (10 smokers, 9 G2 and 11 G3 users) completed baseline questionnaires and provided exhaled carbon monoxide (eCO), saliva and urine samples. Following a 12-hour nicotine abstinence, G2 and G3 users completed a 2-hour vaping session (ie, 5 min, 10-puff bout followed by ad libitum puffing for 115 min). Blood samples, subjective effects, device characteristics and e-liquid consumption were assessed. Smokers, G2 and G3 users had similar baseline levels of cotinine, but smokers had 4 and 7 times higher levels of eCO (pe-cigarette liquids with significantly lower nicotine concentrations. During the vaping session, G3 users achieved significantly higher plasma nicotine concentrations than G2 users following the first 10 puffs (17.5 vs 7.3 ng/mL, respectively) and at 25 and 40 min of ad libitum use. G3 users consumed significantly more e-liquid than G2 users. Vaping urges/withdrawal were reduced following 10 puffs, with no significant differences between device groups. Under normal use conditions, both G2 and G3 devices deliver cigarette-like amounts of nicotine, but G3 devices matched the amount and speed of nicotine delivery of a conventional cigarette. Compared with cigarettes, G2 and G3 e-cigarettes resulted in significantly lower levels of exposure to a potent lung carcinogen and cardiovascular toxicant. These findings have significant implications for understanding the addiction potential of these devices and their viability/suitability as aids to

  19. Electronic Cigarettes: Their Constituents and Potential Links to Asthma.

    Clapp, Phillip W; Jaspers, Ilona

    2017-10-05

    Vaping is gaining popularity in the USA, particularly among teens and young adults. While e-cigs are commonly represented as safer alternatives to tobacco cigarettes, little is known regarding the health effects of their short- or long-term use, especially in individuals with pre-existing respiratory diseases such as asthma. Flavored e-cig liquids (e-liquids) and e-cig aerosols contain airway irritants and toxicants that have been implicated in the pathogenesis and worsening of lung diseases. In this review, we will summarize existing data on potential health effects of components present in e-cig aerosols, such as propylene glycol, vegetable glycerin, nicotine, and flavorings, and discuss their relevance in the context of asthma. Recent survey data indicate that adolescents with asthma had a higher prevalence of current e-cig use (12.4%) compared to their non-asthmatics peers (10.2%) and conveyed positive beliefs about tobacco products, especially e-cigs. Similarly, a study conducted among high school students from Ontario, Canada, indicated a greater likelihood of e-cig use in asthmatics as compared to their non-asthmatic peers. Availability of different flavorings is often cited as the main reason among youth/adolescents for trying e-cigs or switching from cigarettes to e-cigs. Occupational inhalation of some common food-safe flavoring agents is reported to cause occupational asthma and worsen asthmatic symptoms. Moreover, workplace inhalation exposures to the flavoring agent diacetyl have caused irreversible obstructive airway disease in healthy workers. Additionally, recent studies report that thermal decomposition of propylene glycol (PG) and vegetable glycerin (VG), the base constituents of e-liquids, produces reactive carbonyls, including acrolein, formaldehyde, and acetaldehyde, which have known respiratory toxicities. Furthermore, recent nicotine studies in rodents reveal that prenatal nicotine exposures lead to epigenetic reprogramming in the offspring

  20. Cigarette smokers' classification of tobacco products.

    Casseus, M; Garmon, J; Hrywna, M; Delnevo, C D

    2016-11-01

    Cigarette consumption has declined in the USA. However, cigar consumption has increased. This may be due in part to some cigarette smokers switching to filtered cigars as a less expensive substitute for cigarettes. Additionally, some cigarette smokers may perceive and consume little filtered cigars as cigarettes. The purpose of this study was to determine how cigarette smokers classify tobacco products when presented with photographs of those products. An online survey was conducted with a sample of 344 self-identified cigarette smokers. Respondents were presented with pictures of various types of tobacco products, both with and without packaging, and then asked to categorise them as either a cigarette, little cigar, cigarillo, cigar or machine-injected roll-your-own cigarette (RYO). Respondents were also asked about their tobacco use and purchasing behaviour. Overall, respondents had difficulty distinguishing between cigarettes, little cigars, cigarillos and RYO. When presented with images of the products without packaging, 93% of respondents identified RYO as a cigarette, while 42% identified a little cigar as a cigarette. Additionally, respondents stated that they would consider purchasing little cigars as substitutes for cigarettes because of the price advantage. The results of this survey suggest that when presented with photographs of tobacco products, large proportions of current smokers were unable to differentiate between cigarettes, little cigars, cigarillos, RYO and cigars. Findings have implications for existing public health efforts targeting cigarette smokers, and underscore the need to review current definitions of tobacco products and federal excise taxes on such products. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/.

  1. Cigarette and e-liquid demand and substitution in e-cigarette-naïve smokers.

    Stein, Jeffrey S; Koffarnus, Mikhail N; Stepanov, Irina; Hatsukami, Dorothy K; Bickel, Warren K

    2018-06-01

    Behavioral economic methods allow experimental manipulation of price and examination of its effects on tobacco product purchasing. These methods may be used to examine tobacco product abuse liability and to prospectively model possible effects of price regulation. In the present study, we examined multiple measures of behavioral economic demand for cigarettes and e-liquid for use in a second-generation electronic cigarette (e-cigarette) in e-cigarette-naïve cigarette smokers. Twenty-five smokers received an e-cigarette (eGo ONE CT), sampled study e-liquid (24 mg/mL nicotine), and completed recurring sessions in which they used an experimental income to purchase real-world supplies of cigarettes and/or e-liquid. Participants also completed self-report measures of drug effects/liking. When products were available alone, we observed lower demand for e-liquid than for cigarettes. This effect was magnified when cigarettes and e-liquid were available concurrently. In additional assessments, e-liquid served as a partial substitute for cigarettes, but cigarettes did not serve as a substitute for e-liquid. Finally, participants rated e-liquid more poorly than cigarettes on several dimensions of drug effects/liking (any effects, liking, desire, and probability of continued use). We conclude that e-cigarette-naïve smokers value cigarettes more highly than e-liquid across multiple contexts and measurements. Nonetheless, participants still valued e-liquid positively and purchased it frequently, both as a substitute for cigarettes and independently of cigarettes. To understand the variables that influence transitions from exclusive smoking to either dual cigarette/e-cigarette use or exclusive e-cigarette use, future work should systematically examine the role of duration of e-liquid exposure. (PsycINFO Database Record (c) 2018 APA, all rights reserved).

  2. The impact of cigarette taxes and advertising on the demand for cigarettes in Ukraine.

    Peng, Limin; Ross, Hana

    2009-06-01

    Cigarette consumption in Ukraine is increasing while the cigarettes are becoming more affordable due to low taxes and raising income. The impact of cigarette prices and taxes on cigarette consumption is unclear due to the limited research evidence using the local data. This study estimates the sensitivity of Ukraine population to cigarette prices and the affordability of cigarettes using the macro level data in order to predict the effectiveness of cigarette tax policy. Monthly time-series data available from 1997 to 2006 in Ukraine were used to estimate the generalized least square model with an AR(1) process to investigate the impact of cigarette price/tax, household income, the affordability of cigarettes and the volume of tobacco advertising on Ukraine domestic cigarette sales while controlling for other factors. Our analyses demonstrate a strong positive association between cigarette sales and household income as well as a strong positive association between cigarette sales and tobacco advertising activity. The population is found to have relatively low sensitivity to cigarette prices and cigarette taxes, but the impact of cigarettes' affordability is statistically significant, even though also of low magnitude. We speculate that the lower sensitivity to cigarette prices among Ukraine population is caused by wide price variation allowing smokers to avoid a price increase by brand substitution as well as by low costs of cigarettes, high social acceptance of smoking and limited effort to control tobacco use in Ukraine. Narrowing the cigarette price choices and increasing cigarette prices above the level of inflation and income growth by adopting the appropriate tax policy would likely increase the effectiveness of this tool for controlling the smoking rate in Ukraine as well as yield additional budget revenue gains. In addition, imposing advertising restriction may further help reducing the smoking prevalence.

  3. How do minimum cigarette price laws affect cigarette prices at the retail level?

    Feighery, E C; Ribisl, K M; Schleicher, N C; Zellers, L; Wellington, N

    2005-04-01

    Half of US states have minimum cigarette price laws that were originally passed to protect small independent retailers from unfair price competition with larger retailers. These laws prohibit cigarettes from being sold below a minimum price that is set by a formula. Many of these laws allow cigarette company promotional incentives offered to retailers, such as buydowns and master-type programmes, to be calculated into the formula. Allowing this provision has the potential to lower the allowable minimum price. This study assesses whether stores in states with minimum price laws have higher cigarette prices and lower rates of retailer participation in cigarette company promotional incentive programmes. Retail cigarette prices and retailer participation in cigarette company incentive programmes in 2001 were compared in eight states with minimum price laws and seven states without them. New York State had the most stringent minimum price law at the time of the study because it excluded promotional incentive programmes in its price setting formula; cigarette prices in New York were compared to all other states included in the study. Cigarette prices were not significantly different in our sample of US states with and without cigarette minimum price laws. Cigarette prices were significantly higher in New York stores than in the 14 other states combined. Most existing minimum cigarette price laws appear to have little impact on the retail price of cigarettes. This may be because they allow the use of promotional programmes, which are used by manufacturers to reduce cigarette prices. New York's strategy to disallow these types of incentive programmes may result in higher minimum cigarette prices, and should also be explored as a potential policy strategy to control cigarette company marketing practices in stores. Strict cigarette minimum price laws may have the potential to reduce cigarette consumption by decreasing demand through increased cigarette prices and reduced

  4. Avoidance of cigarette pack health warnings among regular cigarette smokers.

    Maynard, Olivia M; Attwood, Angela; O'Brien, Laura; Brooks, Sabrina; Hedge, Craig; Leonards, Ute; Munafò, Marcus R

    2014-03-01

    Previous research with adults and adolescents indicates that plain cigarette packs increase visual attention to health warnings among non-smokers and non-regular smokers, but not among regular smokers. This may be because regular smokers: (1) are familiar with the health warnings, (2) preferentially attend to branding, or (3) actively avoid health warnings. We sought to distinguish between these explanations using eye-tracking technology. A convenience sample of 30 adult dependent smokers participated in an eye-tracking study. Participants viewed branded, plain and blank packs of cigarettes with familiar and unfamiliar health warnings. The number of fixations to health warnings and branding on the different pack types were recorded. Analysis of variance indicated that regular smokers were biased towards fixating the branding rather than the health warning on all three pack types. This bias was smaller, but still evident, for blank packs, where smokers preferentially attended the blank region over the health warnings. Time-course analysis showed that for branded and plain packs, attention was preferentially directed to the branding location for the entire 10s of the stimulus presentation, while for blank packs this occurred for the last 8s of the stimulus presentation. Familiarity with health warnings had no effect on eye gaze location. Smokers actively avoid cigarette pack health warnings, and this remains the case even in the absence of salient branding information. Smokers may have learned to divert their attention away from cigarette pack health warnings. These findings have implications for cigarette packaging and health warning policy. Copyright © 2014 The Authors. Published by Elsevier Ireland Ltd.. All rights reserved.

  5. Shelter and indoor air in the twenty-first century: Radon, smoking and lung cancer risks

    Fabrikant, J.I.

    1988-04-01

    This document describes the relationship between indoor radon exposure, cigarette smoking, and lung cancer. The author explains the sources of radon, the tissues at risk, the human populations most likely to be affected, and the estimates of lung cancer in the population. 6 refs., 2 tabs

  6. Lung scintigraphy

    Dalenz, Roberto.

    1994-01-01

    A review of lung scintigraphy, perfusion scintigraphy with SPECT, lung ventilation SPECT, blood pool SPECT. The procedure of lung perfusion studies, radiopharmaceutical, administration and clinical applications, imaging processing .Results encountered and evaluation criteria after Biello and Pioped. Recommendations and general considerations have been studied about relation of this radiopharmaceutical with other pathologies

  7. Carbonyl Compounds Generated from Electronic Cigarettes

    Kanae Bekki

    2014-10-01

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

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

    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.

  9. Cigarette Cue Attentional Bias in Cocaine-Smoking and Non-Cocaine-Using Cigarette Smokers.

    Marks, Katherine R; Alcorn, Joseph L; Stoops, William W; Rush, Craig R

    2016-09-01

    Cigarette smoking in cocaine users is nearly four times higher than the national prevalence and cocaine use increases cigarette smoking. The mechanisms underlying cigarette smoking in cocaine-using individuals need to be identified to promote cigarette and cocaine abstinence. Previous studies have examined the salience of cigarette and cocaine cues separately. The present aim was to determine whether cigarette attentional bias (AB) is higher in cigarettes smokers who smoke cocaine relative to individuals who only smoke cigarettes. Twenty cigarette smokers who smoke cocaine and 20 non-cocaine-using cigarette smokers completed a visual probe task with eye-tracking technology. During this task, the magnitude of cigarette and cocaine AB was assessed through orienting bias, fixation time, and response time. Cocaine users displayed an orienting bias towards cigarette cues. Cocaine users also endorsed a more urgent desire to smoke to relieve negative affect associated with cigarette craving than non-cocaine users (g = 0.6). Neither group displayed a cigarette AB, as measured by fixation time. Cocaine users, but not non-cocaine users, displayed a cocaine AB as measured by orienting bias (g = 2.0) and fixation time (g = 1.2). There were no significant effects for response time data. Cocaine-smoking cigarettes smokers display an initial orienting bias toward cigarette cues, but not sustained cigarette AB. The incentive motivation underlying cigarette smoking also differs. Cocaine smokers report more urgent desire to smoke to relieve negative affect. Identifying differences in motivation to smoke cigarettes may provide new treatment targets for cigarette and cocaine use disorders. These results suggest that cocaine-smoking cigarette smokers display an initial orienting bias towards cigarette cues, but not sustained attention towards cigarette cues, relative to non-cocaine-using smokers. Smoked cocaine users also report a more urgent desire to smoke to relieve negative affect

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

    Marli Maria Knorst

    2014-10-01

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

  11. Multicentric cohort study on the long-term efficacy and safety of electronic cigarettes: study design and methodology.

    Manzoli, Lamberto; La Vecchia, Carlo; Flacco, Maria Elena; Capasso, Lorenzo; Simonetti, Valentina; Boccia, Stefania; Di Baldassarre, Angela; Villari, Paolo; Mezzetti, Andrea; Cicolini, Giancarlo

    2013-09-24

    While electronic cigarettes are forbidden in several countries, their sales are exploding in many others. Although e-cigarettes have been proposed as long-term substitutes for traditional smoking or as a tool for smoking cessation, very scarce data are available on their efficacy and safety.We describe the protocol of a 5-year multicentric prospective study aimed to evaluate short- and long-term adherence to e-cigarette smoking and the efficacy of e-cigarettes in reducing and/or quitting traditional cigarette smoking. The study will also compare the health effects of electronic vs traditional vs mixed cigarette smoking. From June to December 2013, we will enroll adult smokers of: (EC) e-cigarettes (self-reported inhaling ≥ 50 puffs per week since ≥ 6 months); (TC) traditional cigarettes (≥ 1 per day since ≥ 6 m); (Mixed) both electronic and traditional cigarettes (≥ 1 per day since ≥ 6 m). Eligible subjects will be requested participation through newspaper advertisements and direct contact at the shops. Each subject will have to compile a structured questionnaire at enrolment and after 6, 12, 24, 36 and 60 months. The level of carbon monoxide in expired after breath will be evaluated in all subjects declaring no traditional cigarette smoking in any follow-up phase, using portable carbon monoxide analyzers. The primary outcomes are traditional smoking cessation rates and number of smoked cigarettes. Secondary outcomes include adherence to e-cigarettes, self-reported adverse events, quality of life, and time to hospital admission for one among cardiovascular diseases, chronic obstructive pulmonary diseases, cancer of the lung, esophagus, larynx, oral cavity, bladder, pancreas, kidney, stomach, cervix, and myeloid leukemia. Admissions will be checked using official discharge data of the Abruzzo Region. A minimum of 500 subjects in each group will be enrolled, for a total of 1500 participants. Cox proportional hazards analysis will be used to calculate

  12. Behavioral economic substitutability of e-cigarettes, tobacco cigarettes, and nicotine gum.

    Johnson, Matthew W; Johnson, Patrick S; Rass, Olga; Pacek, Lauren R

    2017-07-01

    The public health impact of e-cigarettes may depend on their substitutability for tobacco cigarettes. Dual users of e-cigarettes and tobacco cigarettes completed purchasing tasks in which they specified daily use levels under hypothetical conditions that varied the availability and price of e-cigarettes, tobacco cigarettes, and nicotine gum (for those with nicotine gum experience). When either e-cigarettes or tobacco cigarettes were the only available commodity, as price per puff increased, purchasing decreased, revealing similar reinforcement profiles. When available concurrently, as the price of tobacco puffs increased, purchasing of tobacco puffs decreased while purchasing of fixed-price e-cigarette puffs increased. Among those with nicotine gum experience, when the price of tobacco puffs was closest to the actual market value of tobacco puffs, e-cigarette availability decreased median tobacco puff purchases by 44% compared to when tobacco was available alone. In contrast, nicotine gum availability caused no decrease in tobacco puff purchases. E-cigarettes may serve as a behavioral economic substitute for tobacco cigarettes, and may be a superior substitute compared to nicotine gum in their ability to decrease tobacco use. Although important questions remain regarding the health impacts of e-cigarettes, these data are consistent with the possibility that e-cigarettes may serve as smoking cessation/reduction aids.

  13. Do current and former cigarette smokers have an attentional bias for e-cigarette cues?

    Lochbuehler, Kirsten; Wileyto, E Paul; Tang, Kathy Z; Mercincavage, Melissa; Cappella, Joseph N; Strasser, Andrew A

    2018-03-01

    The similarity of e-cigarettes to tobacco cigarettes with regard to shape and usage raises the question of whether e-cigarette cues have the same incentive motivational properties as tobacco cigarette cues. The objective of the present study was to examine whether e-cigarette cues capture and hold smokers' and former smokers' attention and whether the attentional focus is associated with subsequent craving for tobacco cigarettes. It was also examined whether device type (cigalike or mod) moderated this relationship. Participants (46 current daily smokers, 38 former smokers, 48 non-smokers) were randomly assigned to a device type condition in which their eye-movements were assessed while completing a visual probe task. Craving was assessed before and after the task. Smokers, but not former or non-smokers, maintained their gaze longer on e-cigarette than on neutral pictures ( p = 0.004). No difference in dwell time was found between device type. None of the smoking status groups showed faster initial fixations or faster reaction times to e-cigarette compared with neutral cues. Baseline craving was associated with dwell time on e-cigarette cues ( p = 0.004). Longer dwell time on e-cigarette cues was associated with more favorable attitudes towards e-cigarettes. These findings indicate that e-cigarette cues may contribute to craving for tobacco cigarettes and suggest the potential regulation of e-cigarette marketing.

  14. E-Cigarette Marketing Exposure Is Associated With E-Cigarette Use Among US Youth.

    Mantey, Dale S; Cooper, Maria R; Clendennen, Stephanie L; Pasch, Keryn E; Perry, Cheryl L

    2016-06-01

    E-cigarettes are currently the most commonly used tobacco product among US youth. However, unlike conventional cigarettes, e-cigarettes are not subject to marketing restrictions. This study investigates the association between exposure to e-cigarette marketing and susceptibility and use of e-cigarettes in youth. Data were obtained from the 2014 National Youth Tobacco Survey. Participants were 22,007 US middle and high school students. Multivariate logistic regression models assessed the relationship between e-cigarette marketing (internet, print, retail, and TV/movies) and current and ever use as well as susceptibility to use e-cigarettes among never e-cigarette users. Exposure to each type of e-cigarette marketing was significantly associated with increased likelihood of ever and current use of e-cigarettes among middle and high school students. Exposure was also associated with susceptibility to use of e-cigarettes among current nonusers. In multivariate models, as the number of channels of e-cigarette marketing exposure increased, the likelihood of use and susceptibility also increased. Findings highlight the significant associations between e-cigarette marketing and e-cigarette use among youth and the need for longitudinal research on these relationships. Copyright © 2016 The Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved.

  15. The Impact of Trying Electronic Cigarettes on Cigarette Smoking by College Students: A Prospective Analysis.

    Sutfin, Erin L; Reboussin, Beth A; Debinski, Beata; Wagoner, Kimberly G; Spangler, John; Wolfson, Mark

    2015-08-01

    We assessed the impact of trying electronic cigarettes (e-cigarettes) on future cigarette smoking in a sample of smokers enrolled in college. In this longitudinal study, first-semester college students at 7 colleges in North Carolina and 4 in Virginia completed a baseline survey and 5 follow-up surveys between fall 2010 and fall 2013. Current cigarette smoking at wave 6 was the primary outcome. Participants (n = 271) reported current cigarette smoking at baseline and no history of e-cigarette use. We measured trying e-cigarettes at each wave, defined as use in the past 6 months. By wave 5, 43.5% had tried e-cigarettes. Even after controlling for other variables associated with cigarette smoking, trying e-cigarettes was a significant predictor of cigarette smoking at wave 6 (adjusted odds ratio [AOR] = 2.48; 95% confidence interval [CI] = 1.32, 4.66), as were friends' cigarette smoking (AOR = 4.20; 95% CI = 2.22, 7.96) and lifetime use of other tobacco products (AOR = 1.63; 95% CI = 1.22, 2.17). Trying e-cigarettes during college did not deter cigarette smoking and may have contributed to continued smoking.

  16. Impact of E-Cigarette Minimum Legal Sale Age Laws on Current Cigarette Smoking.

    Dutra, Lauren M; Glantz, Stanton A; Arrazola, René A; King, Brian A

    2018-05-01

    The purpose of this study was to use individual-level data to examine the relationship between e-cigarette minimum legal sale age (MLSA) laws and cigarette smoking among U.S. adolescents, adjusting for e-cigarette use. In 2016 and 2017, we regressed (logistic) current (past 30-day) cigarette smoking (from 2009-2014 National Youth Tobacco Surveys [NYTS]) on lagged (laws enacted each year counted for the following year) and unlagged (laws enacted January-June counted for that year) state e-cigarette MLSA laws prohibiting sales to youth aged e-cigarette and other tobacco use, sex, race/ethnicity, and age) and state-level (smoke-free laws, cigarette taxes, medical marijuana legalization, income, and unemployment) covariates. Cigarette smoking was not significantly associated with lagged MLSA laws after adjusting for year (odds ratio [OR] = .87, 95% confidence interval [CI]: .73-1.03; p = .10) and covariates (OR = .85, .69-1.03; p = .10). Unlagged laws were significantly and negatively associated with cigarette smoking (OR = .84, .71-.98, p = .02), but not after adjusting for covariates (OR = .84, .70-1.01, p = .07). E-cigarette and other tobacco use, sex, race/ethnicity, age, and smoke-free laws were associated with cigarette smoking (p e-cigarette use and other tobacco use yielded a significant negative association between e-cigarette MLSA laws and cigarette smoking (lagged: OR = .78, .64-.93, p = .01; unlagged: OR = .80, .68-.95, p = .01). After adjusting for covariates, state e-cigarette MLSA laws did not affect youth cigarette smoking. Unadjusted for e-cigarette and other tobacco use, these laws were associated with lower cigarette smoking. Copyright © 2017 The Society for Adolescent Health and Medicine. All rights reserved.

  17. E-cigarettes and National Adolescent Cigarette Use: 2004-2014.

    Dutra, Lauren M; Glantz, Stanton A

    2017-02-01

    E-cigarette use is rapidly increasing among adolescents in the United States, with some suggesting that e-cigarettes are the cause of declining youth cigarette smoking. We hypothesized that the decline in youth smoking changed after e-cigarettes arrived on the US market in 2007. Data were collected by using cross-sectional, nationally representative school-based samples of sixth- through 12th-graders from 2004-2014 National Youth Tobacco Surveys (samples ranged from 16 614 in 2013 to 25 324 in 2004). Analyses were conducted by using interrupted time series of ever (≥1 puff) and current (last 30 days) cigarette smoking. Logistic regression was used to identify psychosocial risk factors associated with cigarette smoking in the 2004-2009 samples; this model was then applied to estimate the probability of cigarette smoking among cigarette smokers and e-cigarette users in the 2011-2014 samples. Youth cigarette smoking decreased linearly between 2004 and 2014 (P = .009 for ever smoking and P = .05 for current smoking), with no significant change in this trend after 2009 (P = .57 and .23). Based on the psychosocial model of smoking, including demographic characteristics, willingness to wear clothing with a tobacco logo, living with a smoker, likelihood of smoking in the next year, likelihood of smoking cigarettes from a friend, and use of tobacco products other than cigarettes or e-cigarettes, the model categorized e-cigarette-only users (between 11.0% in 2012 and 23.1% in 2013) as current smokers. The introduction of e-cigarettes was not associated with a change in the linear decline in cigarette smoking among youth. E-cigarette-only users would be unlikely to have initiated tobacco product use with cigarettes. Copyright © 2017 by the American Academy of Pediatrics.

  18. A dual role for the immune response in a mouse model of inflammation-associated lung cancer

    Dougan, Michael; Li, Danan; Neuberg, Donna; Mihm, Martin; Googe, Paul; Wong, Kwok-Kin; Dranoff, Glenn

    2011-01-01

    Lung cancer is the leading cause of cancer death worldwide. Both principal factors known to cause lung cancer, cigarette smoke and asbestos, induce pulmonary inflammation, and pulmonary inflammation has recently been implicated in several murine models of lung cancer. To further investigate the role of inflammation in the development of lung cancer, we generated mice with combined loss of IFN-γ and the β-common cytokines GM-CSF and IL-3. These immunodeficient mice develop chronic pulmonary in...

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

    Martell, E.A.; Sweder, K.S.

    1984-01-01

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

  20. Lung density

    Garnett, E S; Webber, C E; Coates, G

    1977-01-01

    The density of a defined volume of the human lung can be measured in vivo by a new noninvasive technique. A beam of gamma-rays is directed at the lung and, by measuring the scattered gamma-rays, lung density is calculated. The density in the lower lobe of the right lung in normal man during quiet...... breathing in the sitting position ranged from 0.25 to 0.37 g.cm-3. Subnormal values were found in patients with emphsema. In patients with pulmonary congestion and edema, lung density values ranged from 0.33 to 0.93 g.cm-3. The lung density measurement correlated well with the findings in chest radiographs...... but the lung density values were more sensitive indices. This was particularly evident in serial observations of individual patients....

  1. What Is Lung Cancer?

    ... Shareable Graphics Infographics “African-American Men and Lung Cancer” “Lung Cancer Is the Biggest Cancer Killer in Both ... starts in the lungs, it is called lung cancer. Lung cancer begins in the lungs and may spread ...

  2. Abscess in the Lungs

    ... Home Lung and Airway Disorders Abscess in the Lungs Abscess in the Lungs Causes Symptoms Diagnosis Treatment Resources ... here for the Professional Version Abscess in the Lungs Abscess in the Lungs A lung abscess is a ...