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Sample records for cigarette smoke-induced lung

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

    International Nuclear Information System (INIS)

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

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

    International Nuclear Information System (INIS)

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

  3. Protection from Cigarette Smoke-Induced Lung Dysfunction and Damage by H2 Relaxin (Serelaxin).

    Science.gov (United States)

    Pini, Alessandro; Boccalini, Giulia; Lucarini, Laura; Catarinicchia, Stefano; Guasti, Daniele; Masini, Emanuela; Bani, Daniele; Nistri, Silvia

    2016-06-01

    Cigarette smoke (CS) is the major etiologic factor of chronic obstructive pulmonary disease (COPD), which is characterized by airway remodeling, lung inflammation and fibrosis, emphysema, and respiratory failure. The current therapies can improve COPD management but cannot arrest its progression and reduce mortality. Hence, there is a major interest in identifying molecules susceptible of development into new drugs to prevent or reduce CS-induced lung injury. Serelaxin (RLX), or recombinant human relaxin-2, is a promising candidate because of its anti-inflammatory and antifibrotic properties highlighted in lung disease models. Here, we used a guinea pig model of CS-induced lung inflammation, and remodeling reproducing some of the hallmarks of COPD. Animals exposed chronically to CS (8 weeks) were treated with vehicle or RLX, delivered by osmotic pumps (1 or 10 μg/day) or aerosol (10 μg/ml/day) during CS treatment. Controls were nonsmoking animals. RLX maintained airway compliance to a control-like pattern, likely because of its capability to counteract lung inflammation and bronchial remodeling. In fact, treatment of CS-exposed animals with RLX reduced the inflammatory recruitment of leukocytes, accompanied by a significant reduction of the release of proinflammatory cytokines (tumor necrosis factor α and interleukin-1β). Moreover, RLX was able to counteract the adverse bronchial remodeling and emphysema induced by CS exposure by reducing goblet cell hyperplasia, smooth muscle thickening, and fibrosis. Of note, RLX delivered by aerosol has shown a comparable efficacy to systemic administration in reducing CS-induced lung dysfunction and damage. In conclusion, RLX emerges as a new molecule to counteract CS-induced inflammatory lung diseases. PMID:27048661

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

    OpenAIRE

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

    2013-01-01

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

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

    OpenAIRE

    BARLAS, FIRAT BARIŞ; ERDOGAN, SUAT

    2015-01-01

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

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

    NARCIS (Netherlands)

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

    2007-01-01

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

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

    OpenAIRE

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

    2015-01-01

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

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

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    Botelho Fernando M

    2012-09-01

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

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

    Science.gov (United States)

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

    2015-07-01

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

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

    Science.gov (United States)

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

    2016-05-27

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

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

    International Nuclear Information System (INIS)

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

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

    Directory of Open Access Journals (Sweden)

    Yang Jin

    2008-08-01

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

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

    Science.gov (United States)

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

    2015-11-01

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

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

    Directory of Open Access Journals (Sweden)

    Sichuan Xi

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

  15. Tobacco smoke-induced lung fibrosis and emphysema.

    Science.gov (United States)

    Morse, Danielle; Rosas, Ivan O

    2014-01-01

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

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

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    Zhi-Hua Chen

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

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

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    G. Vani

    2015-01-01

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

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

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    RobertForonjy

    2013-10-01

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

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

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

    2016-07-01

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

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

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

    2016-06-01

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

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

    OpenAIRE

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

    2016-01-01

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

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

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    Basyigit Ilknur

    2010-04-01

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

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

    Institute of Scientific and Technical Information of China (English)

    ZOU Ni; HONG Jiang; DAI Qiu-yan

    2009-01-01

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

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

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

    2016-01-01

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

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

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    Mardi A. Crane-Godreau

    2013-06-01

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

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

    Science.gov (United States)

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

    2015-01-01

    Cigarette smoke-induced chronic obstructive pulmonary disease is a very debilitating disease, with a very high prevalence worldwide, which results in a expressive economic and social burden. Therefore, new therapeutic approaches to treat these patients are of unquestionable relevance. The use of mesenchymal stromal cells (MSCs) is an innovative and yet accessible approach for pulmonary acute and chronic diseases, mainly due to its important immunoregulatory, anti-fibrogenic, anti-apoptotic and pro-angiogenic. Besides, the use of adjuvant therapies, whose aim is to boost or synergize with their function should be tested. Low level laser (LLL) therapy is a relatively new and promising approach, with very low cost, no invasiveness and no side effects. Here, we aimed to study the effectiveness of human tube derived MSCs (htMSCs) cell therapy associated with a 30mW/3J-660 nm LLL irradiation in experimental cigarette smoke-induced chronic obstructive pulmonary disease. Thus, C57BL/6 mice were exposed to cigarette smoke for 75 days (twice a day) and all experiments were performed on day 76. Experimental groups receive htMSCS either intraperitoneally or intranasally and/or LLL irradiation either alone or in association. We show that co-therapy greatly reduces lung inflammation, lowering the cellular infiltrate and pro-inflammatory cytokine secretion (IL-1β, IL-6, TNF-α and KC), which were followed by decreased mucus production, collagen accumulation and tissue damage. These findings seemed to be secondary to the reduction of both NF-κB and NF-AT activation in lung tissues with a concomitant increase in IL-10. In summary, our data suggests that the concomitant use of MSCs + LLLT may be a promising therapeutic approach for lung inflammatory diseases as COPD. PMID:26322981

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

    Directory of Open Access Journals (Sweden)

    Jean Pierre Schatzmann Peron

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

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

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    Nesi RT

    2016-03-01

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

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

    Institute of Scientific and Technical Information of China (English)

    张劲农; 陶晓南; 谢建敏; 向敏; 付薇

    2003-01-01

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

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

    Science.gov (United States)

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

    2016-01-01

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

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

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    Victoria L Palmer

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1983-02-01

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

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

    Science.gov (United States)

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

    2016-01-01

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

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

    International Nuclear Information System (INIS)

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

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

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    Yunye Ning

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

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

    Science.gov (United States)

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

    2015-08-01

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

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

    Science.gov (United States)

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

    2016-06-01

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

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

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    Alexander Salskov

    2011-01-01

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

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

    OpenAIRE

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

    2011-01-01

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

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

    Science.gov (United States)

    Rogers, D F; Jeffery, P K

    1986-01-01

    Specific pathogen-free rats were exposed to the cigarette smoke (CS) of 25 cigarettes daily for 14 days and concurrently given N-acetylcysteine (Nac) as 1% of their drinking water (average daily dose 973 mg/kg). The thickness of the epithelium was measured at four airway levels and the numbers of mucus-containing secretory cells, stained for neutral or acidic glycoprotein (NGP or AGP respectively), were counted in surface epithelium at eight airway levels. Cigarette smoke increased the thickness of the epithelium at three of the airway levels studied by between 37 and 72%. The number of secretory cells was increased at all airway levels distal to the upper trachea by between 102 and 421%. Secretory cells containing NGP were reduced in number but this was more than offset by a large increase in the number of secretory cells containing AGP at all airway levels. N-acetylcysteine inhibited CS-induced epithelial thickening. Nac also inhibited the CS-induced increase in the number of secretory cells with AGP, but had little effect on the CS-induced reduction in the number of cells with NGP. Thus, prophylactic oral N-acetylcysteine led to an overall inhibition of CS-induced mucous cell hyperplasia and epithelial hypertrophy. The results suggest a novel anti-inflammatory action for a drug with known mucolytic effects. PMID:3698928

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

    NARCIS (Netherlands)

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

    2014-01-01

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

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

    Science.gov (United States)

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

    1994-08-01

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

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

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    Min-Chao Duan

    2013-01-01

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

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

    Science.gov (United States)

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

    2013-01-01

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

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

    Science.gov (United States)

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

    2009-04-01

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

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

    Directory of Open Access Journals (Sweden)

    Mathieu C Morissette

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

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

    Science.gov (United States)

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

    2015-03-01

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

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

    International Nuclear Information System (INIS)

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

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

    Science.gov (United States)

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

    2016-01-01

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

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

    Directory of Open Access Journals (Sweden)

    John M. Hartney

    2012-07-01

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

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

    Science.gov (United States)

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

    2014-03-01

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

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

    International Nuclear Information System (INIS)

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

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

    Science.gov (United States)

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

    2014-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Lulu Li

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

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

    Institute of Scientific and Technical Information of China (English)

    姚懿雯; 吴军录; 权文强; 周宏; 张宇; 万海英; 李冬

    2014-01-01

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

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

    Science.gov (United States)

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

    2002-01-01

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

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

    OpenAIRE

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

    2016-01-01

    Abstract Many laboratories are working to develop in vitro models that will replace in vivo tests, but occasionally there remains a regulatory expectation of some in vivo testing. Historically, cigarettes have been tested in vivo for 90 days. Recently, methods to reduce and refine animal use have been explored. This study investigated the potential of reducing animal cigarette smoke (CS) exposure to 3 or 6 weeks, and the feasibility of separate lung lobes for histopathology or the Comet assay...

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

    Directory of Open Access Journals (Sweden)

    Mok Joanie

    2010-09-01

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

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

    Science.gov (United States)

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

    2011-03-01

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

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

    Science.gov (United States)

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

    2015-11-01

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

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

    OpenAIRE

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

    2013-01-01

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

  2. 32P-postlabeling DNA adduct assay: cigarette smoke-induced dna adducts in the respiratory and nonrespiratory rat tissues. Book chapter

    International Nuclear Information System (INIS)

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

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

    Science.gov (United States)

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

    2016-06-01

    Many laboratories are working to develop in vitro models that will replace in vivo tests, but occasionally there remains a regulatory expectation of some in vivo testing. Historically, cigarettes have been tested in vivo for 90 days. Recently, methods to reduce and refine animal use have been explored. This study investigated the potential of reducing animal cigarette smoke (CS) exposure to 3 or 6 weeks, and the feasibility of separate lung lobes for histopathology or the Comet assay. Rats were exposed to sham air or CS (1 or 2 h) for 3 or 6 weeks. Respiratory tissues were processed for histopathological evaluation, and Alveolar type II cells (AEC II) isolated for the Comet assay. Blood was collected for Pig-a and micronucleus quantification. Histopathological analyses demonstrated exposure effects, which were generally dependent on CS dose (1 or 2 h, 5 days/week). Comet analysis identified that DNA damage increased in AEC II following 3 or 6 weeks CS exposure, and the level at 6 weeks was higher than 3 weeks. Pig-a mutation or micronucleus levels were not increased. In conclusion, this study showed that 3 weeks of CS exposure was sufficient to observe respiratory tract pathology and DNA damage in isolated AEC II. Differences between the 3 and 6 week data imply that DNA damage in the lung is cumulative. Reducing exposure time, plus analyzing separate lung lobes for DNA damage or histopathology, supports a strategy to reduce and refine animal use in tobacco product testing and is aligned to the 3Rs (replacement, reduction and refinement). PMID:27160659

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

    OpenAIRE

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

    2014-01-01

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

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

    International Nuclear Information System (INIS)

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

  6. Polonium in cigarette smoke and radiation exposure of lungs

    International Nuclear Information System (INIS)

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

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

    Directory of Open Access Journals (Sweden)

    Dowling Nicole

    2010-05-01

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

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

    Science.gov (United States)

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

    2014-06-01

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

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

    International Nuclear Information System (INIS)

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

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

    OpenAIRE

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

    2014-01-01

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

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

    Energy Technology Data Exchange (ETDEWEB)

    Kim, Sang-In [Department of Cancer Biology, Beckman Research Institute of the City of Hope, 1500 East Duarte Road, Duarte, CA 91010 (United States); Arlt, Volker M. [Section of Molecular Carcinogenesis, Institute of Cancer Research, Brookes Lawley Building, Sutton, Surrey SM2 5NG (United Kingdom); Yoon, Jae-In [Department of Cancer Biology, Beckman Research Institute of the City of Hope, 1500 East Duarte Road, Duarte, CA 91010 (United States); Cole, Kathleen J. [Section of Molecular Carcinogenesis, Institute of Cancer Research, Brookes Lawley Building, Sutton, Surrey SM2 5NG (United Kingdom); Pfeifer, Gerd P. [Department of Cancer Biology, Beckman Research Institute of the City of Hope, 1500 East Duarte Road, Duarte, CA 91010 (United States); Phillips, David H. [Section of Molecular Carcinogenesis, Institute of Cancer Research, Brookes Lawley Building, Sutton, Surrey SM2 5NG (United Kingdom); Besaratinia, Ahmad, E-mail: ania@coh.org [Department of Cancer Biology, Beckman Research Institute of the City of Hope, 1500 East Duarte Road, Duarte, CA 91010 (United States)

    2011-11-01

    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 {sup 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.

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

    International Nuclear Information System (INIS)

    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 32P-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.

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

    Institute of Scientific and Technical Information of China (English)

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

    2014-01-01

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

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

    Science.gov (United States)

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

    1989-11-01

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

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

    OpenAIRE

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

    2014-01-01

    Cigarette smoke is well known for its adverse effects on human health, especially on the lungs. Basic research is essential to identify the mechanisms involved in the development of cigarette smoke-related diseases, but translation of new findings from pre-clinical models to the clinic remains difficult. In the present study, we aimed at comparing the gene expression signature between the lungs of human smokers and mice exposed to cigarette smoke to identify the similarities and differences. ...

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

    Science.gov (United States)

    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, ...

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

    OpenAIRE

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

    1993-01-01

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

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

    Science.gov (United States)

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

    2016-01-01

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

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

    NARCIS (Netherlands)

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

    2014-01-01

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

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

    International Nuclear Information System (INIS)

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

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

    International Nuclear Information System (INIS)

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

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

    OpenAIRE

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

    2014-01-01

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

  3. The history of the discovery of the cigarette-lung cancer link: evidentiary traditions, corporate denial, global toll.

    Science.gov (United States)

    Proctor, Robert N

    2012-03-01

    Lung cancer was once a very rare disease, so rare that doctors took special notice when confronted with a case, thinking it a once-in-a-lifetime oddity. Mechanisation and mass marketing towards the end of the 19th century popularised the cigarette habit, however, causing a global lung cancer epidemic. Cigarettes were recognised as the cause of the epidemic in the 1940s and 1950s, with the confluence of studies from epidemiology, animal experiments, cellular pathology and chemical analytics. Cigarette manufacturers disputed this evidence, as part of an orchestrated conspiracy to salvage cigarette sales. Propagandising the public proved successful, judging from secret tobacco industry measurements of the impact of denialist propaganda. As late as 1960 only one-third of all US doctors believed that the case against cigarettes had been established. The cigarette is the deadliest artefact in the history of human civilisation. Cigarettes cause about 1 lung cancer death per 3 or 4 million smoked, which explains why the scale of the epidemic is so large today. Cigarettes cause about 1.5 million deaths from lung cancer per year, a number that will rise to nearly 2 million per year by the 2020s or 2030s, even if consumption rates decline in the interim. Part of the ease of cigarette manufacturing stems from the ubiquity of high-speed cigarette making machines, which crank out 20,000 cigarettes per min. Cigarette makers make about a penny in profit for every cigarette sold, which means that the value of a life to a cigarette maker is about US$10,000. PMID:22345227

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

    Institute of Scientific and Technical Information of China (English)

    段敏超; 钟小宁; 黄颖; 何志义; 唐海娟

    2011-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Nagai A

    2003-09-01

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

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

    OpenAIRE

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

    2013-01-01

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

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

    OpenAIRE

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

    2011-01-01

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

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

    Science.gov (United States)

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

    1985-11-01

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

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

    International Nuclear Information System (INIS)

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

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

    International Nuclear Information System (INIS)

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

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

    International Nuclear Information System (INIS)

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

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

    OpenAIRE

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

    2012-01-01

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

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

    OpenAIRE

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

    2005-01-01

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

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

    OpenAIRE

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

    1991-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Trung Vu

    2016-04-01

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

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

    International Nuclear Information System (INIS)

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

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

    Directory of Open Access Journals (Sweden)

    Alvaro Camilo Dias Faria

    2010-01-01

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

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

    Science.gov (United States)

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

    2014-03-01

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

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

    OpenAIRE

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

    2007-01-01

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

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

    Science.gov (United States)

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

    2016-05-01

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

  1. SIRT1 pathway dysregulation in the smoke-exposed airway epithelium and lung tumor tissue

    OpenAIRE

    Beane, Jennifer; Cheng, Luis; Soldi, Raffaella; Zhang, Xiaohui; Liu, Gang; Anderlind, Christina; Lenburg, Marc E.; Spira, Avrum; Bild, Andrea H

    2012-01-01

    Cigarette smoke produces a molecular “field of injury” in epithelial cells lining the respiratory tract. However, the specific signaling pathways that are altered in the airway of smokers and the signaling processes responsible for the transition from smoking-induced airway damage to lung cancer remain unknown. In this study, we use a genomic approach to study the signaling processes associated with tobacco smoke exposure and lung cancer. First, we developed and validated pathway-specific gen...

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

    Directory of Open Access Journals (Sweden)

    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.

  3. In Utero Cigarette Smoke Affects Allergic Airway Disease But Does Not Alter the Lung Methylome.

    Directory of Open Access Journals (Sweden)

    Kenneth R Eyring

    Full Text Available Prenatal and postnatal cigarette smoke exposure enhances the risk of developing asthma. Despite this as well as other smoking related risks, 11% of women still smoke during pregnancy. We hypothesized that cigarette smoke exposure during prenatal development generates long lasting differential methylation altering transcriptional activity that correlates with disease. In a house dust mite (HDM model of allergic airway disease, we measured airway hyperresponsiveness (AHR and airway inflammation between mice exposed prenatally to cigarette smoke (CS or filtered air (FA. DNA methylation and gene expression were then measured in lung tissue. We demonstrate that HDM-treated CS mice develop a more severe allergic airway disease compared to HDM-treated FA mice including increased AHR and airway inflammation. While DNA methylation changes between the two HDM-treated groups failed to reach genome-wide significance, 99 DMRs had an uncorrected p-value < 0.001. 6 of these 99 DMRs were selected for validation, based on the immune function of adjacent genes, and only 2 of the 6 DMRs confirmed the bisulfite sequencing data. Additionally, genes near these 6 DMRs (Lif, Il27ra, Tle4, Ptk7, Nfatc2, and Runx3 are differentially expressed between HDM-treated CS mice and HDM-treated FA mice. Our findings confirm that prenatal exposure to cigarette smoke is sufficient to modify allergic airway disease; however, it is unlikely that specific methylation changes account for the exposure-response relationship. These findings highlight the important role in utero cigarette smoke exposure plays in the development of allergic airway disease.

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

    Directory of Open Access Journals (Sweden)

    Xiang Zhou

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

  5. 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.

    Science.gov (United States)

    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. PMID:26756937

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

    Directory of Open Access Journals (Sweden)

    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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1990-04-01

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

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

    International Nuclear Information System (INIS)

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

  9. [Lung cancer and cigarette smoking in women. (Results of a case control study)].

    Science.gov (United States)

    Vutuc, C

    1982-08-01

    Smoking habits of 297 female lung cancer patients (Kreyberg I: 202, Kreyberg II: 95) and 580 controls were analyzed. In addition tar exposures (TE) were calculated. Calculation of TE includes amount of consumptions, duration and the tar yields of all cigarette brands ever smoked. These are significant more smokers among patients (63%) and patients with a K I tumor (80%) compared to the controls (21%); K II: 29%. All patients and patients with a K I tumor had a significant longer smoking career (39.3 years; 39.6 years) and a higher tar exposure (TE = 1767; TE - 1810) compared to the controls (31.9 years, TE = 1146). K II: 37.4 years, TE = 1508. Lung cancer risks (adj. for TE) and population attributable risks (PAR) were: all age groups R = 7.3*, PAR = 54%; less than 40 years R = 1.1, PAR = 3%; 41-50 years R = 4.2*, PAR = 42% ; 51-60 years R = 7.6*, PAR = 62%; 61-70 years R = 7.8*, PAR = 54%; greater than 71 years R = 8.0*, PAR = 55%. Lung cancer risks (adj. for age) in relation to tar exposure and attributable risks (AR) were: TE less than 500: all cases R = 1.5, AT = 34% (KIR = 2.9, K II R = 0.8); TE 501-1000: all cases R = 4.2*, AR = 76% (KIR = 9.9*, K II R - 1.1): TE 1001-2000: all cases R = 12.1*, AR = 92% (KIR = 27.2*, K II R = 2.6**); TE 2001-3000: all cases R = 11.1*, AR = 91% (KIR = 25.2*, K II R = 2.0); TE greater than 3001: all cases R = 13.0*, AR = 92% (KIR = 29.3*, K II R = 3.3). These is a significant increase of risk of cigarette smokers beyond a TE of 501, which could be identified as a sort of critical exposure. There is a pronounced dose response relationship between cigarette smoking in relation to TE and lung cancer risk as concerning K I tumors but not KII tumors. Lung cancer risks in relation to age began smoking: less than 19 years R = 7.8*; 19 years and above R = 6.5*. *P less than 1%, **P less than 5%. PMID:7148206

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

    Directory of Open Access Journals (Sweden)

    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

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

    Indian Academy of Sciences (India)

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

    2010-06-01

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

  12. Cigarette smoke effects on TSPO and VDAC expression in a cellular lung cancer model.

    Science.gov (United States)

    Gavish, Moshe; Cohen, Shiri; Nagler, Rafael

    2016-09-01

    As redox iron and copper ions are found in lung pleural fluid and parenchyma, we aimed to examine the effect of cigarette smoke (CS) alone and the combined effects of CS and redox metals, iron and copper ions, containing medium (saliva), on epithelial H1299 lung cancer cells. We also examined the expression levels of the anticarcinogenic and proapoptotic 18 kDa translocator protein (TSPO) and its closely associated protein voltage-dependent anion channel (VDAC). H1299 cells were subjected to western blot analysis using anti-TSPO and anti-VDAC antibodies. With the former, the 18 kDa band appeared as expected and a 72 kDa band also appeared. It may be assumed that in H1299 lung cancer cells, an additional form of TSPO protein appears as a four-unit tetrameric complex, which is affected by CS exposure. A significant decrease in the expression level of the 72 kDa protein occurred following only 60 min of CS exposure, whereas VDAC protein levels were increased following only 30 min of CS exposure. These results, together with our previous related studies, suggest a comprehensive two-arm novel paradigm for lung cancer induced by CS, and mediated by an altered TSPO protein, possibly resulting from both the 72 kDa TSPO degradation and redox metal ion-induced enhancement of free radical attack. We suggest that both of the most important proapoptotic and anticancer proteins, p53 and TSPO, are damaged by CS, paving the way for lung cancer initiation and progression. PMID:26378498

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

    Science.gov (United States)

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

    2011-12-01

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

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

    Science.gov (United States)

    Nagler, Rafael; Cohen, Shiri; Gavish, Moshe

    2015-12-01

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

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

    International Nuclear Information System (INIS)

    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

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

    Science.gov (United States)

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

    2016-09-01

    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. PMID:27343559

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

    Science.gov (United States)

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

    1986-01-01

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

  18. Invited Commentary: The Etiology of Lung Cancer in Men Compared With Women

    OpenAIRE

    Alberg, Anthony J; Wallace, Kristin; Silvestri, Gerard A.; Brock, Malcolm V.

    2013-01-01

    Lung cancer is the leading cause of cancer death among women in the United States and other Western nations. The predominant cause of lung cancer in women is active cigarette smoking. Secondhand exposure to tobacco smoke is another important cause. The hypothesis that women are more susceptible than men to smoking-induced lung cancer has not been supported by the preponderance of current data, as noted by De Matteis et al. (Am J Epidemiol. 2013;177(7):601–612) in the accompanying article. How...

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

    Science.gov (United States)

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

    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’ 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. Objective 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. Methods This is a prospective, randomized, placebo-controlled, double-blind, three-parallel group study. The study is organized as a nested randomized

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

    Science.gov (United States)

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

    2016-01-01

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

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

    International Nuclear Information System (INIS)

    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 14C-arachidonic acid than rings from sham rats. Platelets from smoke-exposed rats synthesized more thromboxane (TXA2) from 14C-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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1985-01-01

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

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

    International Nuclear Information System (INIS)

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

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

    Directory of Open Access Journals (Sweden)

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

    2013-11-01

    Full Text Available In contrast to the problematic health and economic effects of acute and chronic smoke exposure on lung function and airway inflammation, there are still few data dealing with the effects of smoking. Smoke exposure can result in aberrant cell growth. In our experiments, pyrolyzed components of cigarettes have been shown to induce a strong stress response in cultured cells. We used human embryonic lung (HEL cells, which respond with an altered expression of a broad spectrum of genes. Therefore we performed a systematic analysis of the genetic expression behaviour, using the established whole genome microarray-technology which should be able to reveal the cellular effects. With these data we aim to generate a qualitative spectrum of cellular stress response activity. It is noticeable that after cells’ exposure to pyrolyzed tobacco smoke components the products of the most affected genes, e.g. ID1, inhibitor of DNA binding, are up-regulated as a rapid response after 2 h with a factor 3.8 and RPS2, ribosomal protein S2, is down-regulated to nearly 50 % after 24 hours. In databases they are documented as still uncharacterized and hypothetical proteins. The DDIT4 gene, encoding the DNA-damage-inducible transcript 4, associated with regulation and development of DNA processes after damage by ionizing radiation and in p53 mediated apoptotic processes, is up-regulated. The exposure leads to a rapid cellular stress response of genes like induction of the ID1, ID2, and ID3 genes, located on different chromosomes, already after two hours. They interact normally with DNA binding proteins under heterodimer formation and are considered as negative regulators of transcription. After 24 hours, a return back to normal was not observed and the genes remained stably down-regulated. The suppression of the GADD45B gene which is involved in the cell cycle regulation and after DNA damage a cell cycle arrest is mediated by the gene product. The C14orf4 gene (IRF2BPL

  5. Distribution of cigarette smoking in the lungs and its efect upon 99mTc DTPA clearance

    International Nuclear Information System (INIS)

    The distribution of submicronic particles during cigarette smoking was demonstrated by means of an insoluble (sup(99m)Tc sulfur colloid) aerosol in eleven habitual smokers with no evidence of impaired lung function. Considerable pains were taken to simulate precisely the conditions of their usual smoking. The distribution of aerosol during smoking was compared with that during normal tidal breathing in the same subjects. All subjects showed a shift towards greater apical and central (tracheo bronchial) deposition during smoking as compared with quiet respiration. These findings may be relevant to the apical predominance of centrilobular emphysema and bronchial carcinoma. In a second study the differential clearance of a submicronic sup(99m)Tc DTPA aerosol was studied in a population of habitual smokers immediately after smoking two cigarettes and in a control population. Differential clearance was studied continuously for a period of 60 minutes at several peripheral sites in both lung fields. In non smokers the clearance curve was monoexponential over the study period. In smokers the curve was biexponential and clearance overall was more rapid than in non smokers as expected. No difference in clearance was seen between the apices and the bases in smokers to correspond to the predominent apical distribution of cigarette smoke particles in either the erect or the supine position. The biexponential clearance curve in smokers may be due to diffusion of the aerosol from both alveoli and bronchi reflecting the greater central deposition in smokers even though this may not be evident on visual inspection of the aerosol lung scan. (Author)

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

    OpenAIRE

    Trung Vu; Lin Jin; Datta, Pran K.

    2016-01-01

    Epithelial to mesenchymal transition (EMT) is a process that allows an epithelial cell to acquire a mesenchymal phenotype through multiple biochemical changes resulting in an increased migratory capacity. During cancer progression, EMT is found to be associated with an invasive or metastatic phenotype. In this review, we focus on the discussion of recent studies about the regulation of EMT by cigarette smoking. Various groups of active compounds found in cigarette smoke such as polycyclic aro...

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

    Directory of Open Access Journals (Sweden)

    Abdessalem Koubaa

    2015-02-01

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

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

    Science.gov (United States)

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

    2014-01-01

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2005-02-01

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

  10. Lysyl Oxidase, A Critical Intra- and Extra-Cellular Target in the Lung for Cigarette Smoke Pathogenesis

    Directory of Open Access Journals (Sweden)

    Lijun Chen

    2011-01-01

    Full Text Available Cigarette smoke (CS, a complex chemical mixture, contains more than 4,800 different compounds, including oxidants, heavy metals, and carcinogens, that individually or in combination initiate or promote pathogenesis in the lung accounting for 82% of chronic obstructive pulmonary disease (COPD deaths and 87% of lung cancer deaths. Lysyl oxidase (LO, a Cu-dependent enzyme, oxidizes peptidyl lysine residues in collagen, elastin and histone H1, essential for stabilization of the extracellular matrix and cell nucleus. Considerable evidences have shown that LO is a tumor suppressor as exemplified by inhibiting transforming activity of ras, a proto oncogene. CS condensate (CSC, 4-(methylnitrosamino-1-(3-pyridyl-1-butanone (NNK and cadmium (Cd, major components of CS, down-regulate LO expression at such multiple levels as mRNA, protein and catalytic activity in lung cells in vitro and in vivo indicating LO as a critical intra- and extracellular target for CS pathogenesis in the lung. In view of multiple biological functions and regulation characteristics of the LO gene, molecular mechanisms for CS damage to lung LO and its role in emphysema and cancer pathogenesis are discussed in this review.

  11. HDAC3 mediates smoking-induced pancreatic cancer

    Science.gov (United States)

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

    2016-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Ximena M. Muresan

    2015-01-01

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

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

    International Nuclear Information System (INIS)

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1998-10-01

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

  15. Electronic Cigarettes

    Science.gov (United States)

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

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

    International Nuclear Information System (INIS)

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

  17. Lung Cancer

    Science.gov (United States)

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

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

    Institute of Scientific and Technical Information of China (English)

    赵华; 吴铁

    2009-01-01

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

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

    Science.gov (United States)

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

    2016-01-01

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1981-12-01

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

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

    Directory of Open Access Journals (Sweden)

    Shieh Ching Yang

    2002-10-01

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

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

    Science.gov (United States)

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

    2016-07-01

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

  3. The Roles of Cigarette Smoking and the Lung in the Transitions Between Phases of Preclinical Rheumatoid Arthritis.

    Science.gov (United States)

    Sparks, Jeffrey A; Karlson, Elizabeth W

    2016-03-01

    While the etiology of rheumatoid arthritis (RA) remains to be fully elucidated, recent research has advanced the understanding of RA pathogenesis to the point where clinical trials for RA prevention are underway. The current paradigm for RA pathogenesis is that individuals progress through distinct preclinical phases prior to the onset of clinically apparent RA. These preclinical RA phases consist of genetic risk, local inflammation, presence of RA-related autoantibodies, asymptomatic systemic inflammation, and early non-specific symptoms prior to clinical seropositive RA. Epidemiologic studies have been important in forming hypotheses related to the biology occurring in preclinical RA. Specifically, studies associating cigarette smoking with overall RA risk as well as transitions between phases of preclinical RA were vital in helping to establish the lung as a potential important initiating site in the pathogenesis of seropositive RA. Herein, we review the epidemiology associating smoking with transitions in preclinical phases of RA as well as the recent literature supporting the lung as a critical site in RA pathogenesis. PMID:26951253

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

    International Nuclear Information System (INIS)

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2013-09-01

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

  6. 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.

    Directory of Open Access Journals (Sweden)

    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

  7. 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.

    Science.gov (United States)

    Lerner, Chad A; Sundar, Isaac K; Yao, Hongwei; Gerloff, Janice; Ossip, Deborah J; McIntosh, Scott; Robinson, Risa; Rahman, Irfan

    2015-01-01

    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 could lead to

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

    Science.gov (United States)

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

    2015-04-15

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

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

    International Nuclear Information System (INIS)

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

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

    Directory of Open Access Journals (Sweden)

    Rahel eBirru

    2012-08-01

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

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

    OpenAIRE

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

    2012-01-01

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

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

    OpenAIRE

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

    2015-01-01

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

  13. Metabolites of the Polycyclic Aromatic Hydrocarbon Phenanthrene in the Urine of Cigarette Smokers from Five Ethnic Groups with Differing Risks for Lung Cancer

    Science.gov (United States)

    Patel, Yesha M.; Park, Sungshim L.; Carmella, Steven G.; Paiano, Viviana; Olvera, Natalie; Stram, Daniel O.; Haiman, Christopher A.; Le Marchand, Loic

    2016-01-01

    Results from the Multiethnic Cohort Study demonstrated significant differences in lung cancer risk among cigarette smokers from five different ethnic/racial groups. For the same number of cigarettes smoked, and particularly among light smokers, African Americans and Native Hawaiians had the highest risk for lung cancer, Whites had intermediate risk, while Latinos and Japanese Americans had the lowest risk. We analyzed urine samples from 331–709 participants from each ethnic group in this study for metabolites of phenanthrene, a surrogate for carcinogenic polycyclic aromatic hydrocarbon exposure. Consistent with their lung cancer risk and our previous studies of several other carcinogens and toxicants of cigarette smoke, African Americans had significantly (p<0.0001) higher median levels of the two phenanthrene metabolites 3-hydroxyphenanthrene (3-PheOH, 0.931 pmol/ml) and phenanthrene tetraol (PheT, 1.13 pmol/ml) than Whites (3-PheOH, 0.697 pmol/ml; PheT, 0.853 pmol/ml) while Japanese-Americans had significantly (p = 0.002) lower levels of 3-PheOH (0.621 pmol/ml) than Whites. PheT levels (0.838 pmol/ml) in Japanese-Americans were not different from those of Whites. These results are mainly consistent with the lung cancer risk of these three groups, but the results for Native Hawaiians and Latinos were more complex. We also carried out a genome wide association study in search of factors that could influence PheT and 3-PheOH levels. Deletion of GSTT1 explained 2.2% of the variability in PheT, while the strongest association, rs5751777 (p = 1.8x10-62) in the GSTT2 gene, explained 7.7% of the variability in PheT. These GWAS results suggested a possible protective effect of lower GSTT1 copy number variants on the diol epoxide pathway, which was an unexpected result. Collectively, the results of this study provide further evidence that different patterns of cigarette smoking are responsible for the higher lung cancer risk of African Americans than of Whites and the

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

    International Nuclear Information System (INIS)

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

  15. Menthol Cigarettes

    Science.gov (United States)

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

  16. Emphysema is associated with increased inflammation in lungs of atherosclerosis-prone mice by cigarette smoke: implications in comorbidities of COPD

    Directory of Open Access Journals (Sweden)

    Yao Hongwei

    2010-07-01

    Full Text Available Abstract Background Chronic obstructive pulmonary disease is associated with numerous vascular effects including endothelial dysfunction, arterial stiffness and atherogenesis. It is also known that a decline in lung function is associated with increased cardiovascular comorbidity in smokers. The mechanism of this cardiopulmonary dual risk by cigarette smoke (CS is not known. We studied the molecular mechanisms involved in development of emphysema in atherosclerosis-prone apolipoprotein E-deficient (ApoE-/- mice in response to CS exposure. Methods Adult male and female wild-type (WT mice of genetic background C57BL/6J and ApoE-/- mice were exposed to CS, and lung inflammatory responses, oxidative stress (lipid peroxidation products, mechanical properties as well as airspace enlargement were assessed. Results and Discussion The lungs of ApoE-/- mice showed augmented inflammatory response and increased oxidative stress with development of distal airspace enlargement which was accompanied with decline in lung function. Interestingly, the levels and activities of matrix metalloproteinases (MMP-9 and MMP-12 were increased, whereas the level of eNOS was decreased in lungs of CS-exposed ApoE-/- mice as compared to air-exposed ApoE-/- mice or CS-exposed WT mice. Conclusion These findings suggest that CS causes premature emphysema and a decline of lung function in mice susceptible to cardiovascular abnormalities via abnormal lung inflammation, increased oxidative stress and alterations in levels of MMPs and eNOS.

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

    International Nuclear Information System (INIS)

    Our previous studies demonstrated that exposure to cigarette smoke (CS), either mainstream or environmental, results in a remarkable downregulation of microRNA expression in the lung of both mice and rats. The goals of the present study were to evaluate the dose responsiveness to CS and the persistence of microRNA alterations after smoking cessation. ICR (CD-1) neonatal mice were exposed whole-body to mainstream CS, at the doses of 119, 292, 438, and 631 mg/m3 of total particulate matter. Exposure started within 12 h after birth and continued daily for 4 weeks. The levels of bulky DNA adducts and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodGuo) were measured by 32P postlabeling procedures, and the expression of 697 mouse microRNAs was analyzed by microarray. The highest CS dose was lethal. Exposure to CS caused a dose-dependent increase of DNA alterations. DNA adducts and, even more sharply, 8-oxodGuo were reverted 1 and 4 weeks after smoking cessation. Exposure to CS resulted in an evident dysregulation of microRNA expression profiles, mainly in the sense of downregulation. The two lowest doses were not particularly effective, while the highest nonlethal dose produced extensive microRNA alterations. The expression of most downregulated microRNAs, including among others 7 members of the let-7 family, was restored one week after smoking cessation. However, the recovery was incomplete for a limited array of microRNAs, including mir-34b, mir-345, mir-421, mir-450b, mir-466, and mir-469. Thus, it appears that microRNAs mainly behave as biomarkers of effect and that exposure to high-dose, lasting for an adequate period of time, is needed to trigger the CS-related carcinogenesis process in the experimental animal model used.

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2011-12-01

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

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

    International Nuclear Information System (INIS)

    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

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

    Science.gov (United States)

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

    2015-10-20

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

  1. Pyrazine, 2-ethylpyridine, and 3-ethylpyridine are cigarette smoke components that alter the growth of normal and malignant human lung cells, and play a role in multidrug resistance development.

    Science.gov (United States)

    Liu, Min; Poo, Wak-Kim; Lin, Yu-Ling

    2015-02-01

    Lung cancer is one of the few human diseases for which the primary etiological agent, cigarette smoke (CS), has been described; however, the precise role of individual cigarette smoke toxicant in tumor development and progression remains to be elusive. The purpose of this study was to assess in vitro the effects of previously identified cigarette smoke components, pyrazine, 2-ethylpyridine, and 3-ethylpyridine, on non-tumorigenic (MRC5) and adenocarcinomic (A549) human lung cell lines. Our data showed that the administration of three cigarette smoke components in combination perturbed the proliferation of both normal and adenocarcinomic cells. Study of malignant cells revealed that CS components were cytotoxic at high concentration (10(-6) M) and stimulatory in a dose-dependent manner at lower concentrations (10(-8) M to 10(-10) M). This adverse effect was enhanced when adenocarcinomic cells were maintained in hypoxia resembling intratumoral environment. Furthermore, exposure to pyrazine, 2-ethylpyridine, and 3-ethylpyridine induced oxidative stress in both normal and malignant cells. Finally, assessment of P-gp activity revealed that multidrug resistance was induced in CS component exposed adenocarcinomic lung cells and the induction was augmented in hypoxia. Taken together, pyrazine, 2-ethylpyridine, and 3-ethylpyridine adversely altered both normal and diseased lung cells in vitro and data collected from this study may help lung cancer patients to understand the importance of quitting smoking during lung cancer treatment. PMID:25449333

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1997-09-01

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

  3. Mechanisms of protein misfolding in conformational lung diseases.

    LENUS (Irish Health Repository)

    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.

  4. Cigarette smoke and plutonium

    International Nuclear Information System (INIS)

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

  5. 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

    Science.gov (United States)

    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<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. PMID:26053186

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

    DEFF Research Database (Denmark)

    Shaker, Saher B; Stavngaard, Trine; Laursen, Lars Christian; Stoel, Berend C; Dirksen, Asger

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

    Science.gov (United States)

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

    2016-01-01

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

  8. Modulation by aspirin and naproxen of nucleotide alterations and tumors in the lung of mice exposed to environmental cigarette smoke since birth.

    Science.gov (United States)

    La Maestra, Sebastiano; D'Agostini, Francesco; Izzotti, Alberto; Micale, Rosanna T; Mastracci, Luca; Camoirano, Anna; Balansky, Roumen; Trosko, James E; Steele, Vernon E; De Flora, Silvio

    2015-12-01

    Chemoprevention provides an important strategy for cancer control in passive smokers. Due to the crucial role played by smoke-related chronic inflammation in lung carcinogenesis, of special interest are extensively used pharmacological agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs). We evaluated the ability of aspirin and naproxen, inhibitors of both cyclooxygenase-1 and cyclooxygenase -2, to modulate environmental cigarette smoke (ECS)-induced lung carcinogenesis in A/J mice of both genders. Based on a subchronic toxicity study in 180 postweaning mice, we used 1600 mg/kg diet aspirin and 320 mg/kg diet naproxen. In the tumor chemoprevention study, using 320 mice, exposure to ECS started soon after birth and administration of NSAIDs started after weaning. At 10 weeks of life, the NSAIDs did not affect the presence of occult blood in feces. As assessed in a subset of 40 mice, bulky DNA adducts and 8-hydroxy-2'-deoxyguanosine levels were considerably increased in ECS-exposed mice and, irrespective of gender, both NSAIDs remarkably inhibited these nucleotide alterations. After exposure for 4 months followed by 5 months in filtered air, ECS induced a significant increase in the yield of surface lung tumors, the 43.7% of which were adenomas and the 56.3% were adenocarcinomas. Oct-4 (octamer-binding transcription factor 4), a marker of cell stemness, was detected in some adenocarcinoma cells. The NAIDs attenuated the yield of lung tumors, but prevention of ECS-induced lung adenomas was statistically significant only in female mice treated with aspirin, which supports a role for estrogens in ECS-related lung carcinogenesis and highlights the antiestrogenic properties of NSAIDs. PMID:26464196

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

    Directory of Open Access Journals (Sweden)

    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.

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

    Directory of Open Access Journals (Sweden)

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

    2011-01-01

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

  11. RelB is differentially regulated by IkappaB Kinase-alpha in B cells and mouse lung by cigarette smoke.

    Science.gov (United States)

    Yang, Se-Ran; Yao, Hongwei; Rajendrasozhan, Saravanan; Chung, Sangwoon; Edirisinghe, Indika; Valvo, Samantha; Fromm, George; McCabe, Michael J; Sime, Patricia J; Phipps, Richard P; Li, Jian-Dong; Bulger, Michael; Rahman, Irfan

    2009-02-01

    The activation of transcription factor NF-kappaB is controlled by two main pathways: the classical canonical (RelA/p65-p50)- and the alternative noncanonical (RelB/p52)-NF-kappaB pathways. RelB has been shown to play a protective role in RelA/p65-mediated proinflammatory cytokine release in immune-inflammatory lymphoid cells. Increased infiltration of macrophages and lymphoid cells occurs in lungs of patients with chronic obstructive pulmonary disease, leading to abnormal inflammation. We hypothesized that RelB, and its signaling pathway, is differentially regulated in macrophages and B cells and in lung cells, leading to differential regulation of proinflammatory cytokines in response to cigarette smoke (CS). CS exposure increased the levels of RelB and NF-kappaB-inducing kinase associated with recruitment of RelB on promoters of the IL-6 and macrophage inflammatory protein-2 genes in mouse lung. Treatment of macrophage cell line, MonoMac6, with CS extract showed activation of RelB. In contrast, RelB was degraded by a proteasome-dependent mechanism in B lymphocytes (human Ramos, mouse WEHI-231, and primary mouse spleen B cells), suggesting that RelB is differentially regulated in lung inflammatory and lymphoid cells in response to CS exposure. Transient transfection of dominant negative IkappaB-kinase-alpha and double mutants of NF-kappaB-inducing kinase partially attenuated the CS extract-mediated loss of RelB in B cells and normalized the increased RelB level in macrophages. Taken together, these data suggest that RelB is differentially regulated in response to CS exposure in macrophages, B cells, and in lung cells by IkappaB-kinase-alpha-dependent mechanism. Rapid degradation of RelB signals for RelA/p65 activation and loss of its protective ability to suppress the proinflammatory cytokine release in lymphoid B cells. PMID:18688039

  12. Lung Cancer

    Science.gov (United States)

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

    Institute of Scientific and Technical Information of China (English)

    林纯意

    2012-01-01

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

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

    OpenAIRE

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

    2014-01-01

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

  15. Smoke-induced seed germination in California chaparral

    Science.gov (United States)

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

    1998-01-01

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

  16. DO CHILDREN BENEFIT FROM INCREASING CIGARETTE TAXES? ACCOUNTING FOR THE ENDOGENEITY OF LUNG HEALTH AND ENVIRONMENTAL TOBACCO SMOKE EXPOSURE

    Science.gov (United States)

    My research investigates the relationship between environmental tobacco smoke (ETS) exposure and lung function in children. I use detailed individual health data from the Third National Health and Nutrition Survey (NHANES III) to measure the effect of environmental tobacco smoke ...

  17. Early onset lung cancer, cigarette smoking and the SNP309 of the murine double minute-2 (MDM2) gene

    International Nuclear Information System (INIS)

    The polymorphism SNP309 (rs2279744) in the promoter region of the MDM2 gene has been shown to alter protein expression and may play a role in the susceptibility to lung cancer. The MDM2 protein is a key inhibitor of p53 and several mechanisms of MDM2/p53 interactions are presently known: modulating DNA-repair, cell-cycle control, cell growth and apoptosis. We used 635 Caucasian patients diagnosed with lung cancer before 51 years of age and 1300 healthy gender and age frequency matched population Caucasian controls to investigate the association between the MDM2 SNP309 and the risk of developing early onset lung cancer. Conditional logistic models were applied to assess the genotype-phenotype association, adjusted for smoking. Compared to the GG genotype, the adjusted ORs for the TG and TT genotype were 0.9 (95% CI: 0.7–1.5) and 1.0 (95% CI: 0.7–1.5), respectively. Also no association was found for histological subtypes of lung cancer. The strength of this study is that within young cases the genetic component to develop lung cancer may be greater. Our results indicate that the MDM2 SNP309 is not significantly associated with lung carcinogenesis but point towards gender-specific differences

  18. Altered expression of the CCN genes in the lungs of mice in response to cigarette smoke exposure and viral and bacterial infections.

    Science.gov (United States)

    Gueugnon, Fabien; Thibault, Virginie C; Kearley, Jennifer; Petit-Courty, Agnès; Vallet, Amandine; Guillon, Antoine; Si-Tahar, Mustapha; Humbles, Alison A; Courty, Yves

    2016-07-15

    The CCN proteins are key signaling and regulatory molecules involved in many biological functions and contribute to malignant and non-malignant lung diseases. Despite the high morbidity and mortality of the lung respiratory infectious diseases, there is very little data related to the expression of the CCNs during infection. We investigated in mice the pulmonary mRNA expression levels of five CCNs (1 to 5) in response to influenza A virus (IAV) and bacterial agents (Nontypeable Haemophilus influenzae (NTHi), lipopolysaccharide (LPS) and lipoteichoic acid (LTA)). IAV, NTHi, LPS or LTA were instilled intranasally into mice. Mice were also exposed for 4days or 8weeks to cigarette smoke alone or prior infection to IAV in order to determine if CS modifies the CCN response to a viral infection. All challenges induced a robust inflammation. The mRNA expression of CCN1, CCN2 and CCN3 was decreased after short exposure to CS whereas prolonged exposure altered the expression of CCN1, CCN3 and CCN4. Influenza A virus infection increased CCN1, 2, 4 and 5 mRNA levels but expression of CCN3 was significantly decreased. Acute CS exposure prior infection had little effect on the expression of CCN genes but prolonged exposure abolished the IAV-dependent induction. Treatment with LPS or LTA and infection with NTHi revealed that both Gram-positive and Gram-negative bacteria rapidly modulate the expression of the CCN genes. Our findings reveal that several triggers of lung inflammation influence differently the CCN genes. CCN3 deserves special attention since its mRNA expression is decreased by all the triggers studied. PMID:27080955

  19. Cigarette smoking and K-ras mutations in pancreas, lung and colorectal adenocarcinomas: Etiopathogenic similarities, differences and paradoxes

    NARCIS (Netherlands)

    Porta, M.; Crous-Bou, M.; Wark, P.A.; Vineis, P.; Real, F.X.; Malats, N.; Kampman, E.

    2009-01-01

    Surprisingly different frequencies and patterns of K-ras mutations are observed in human adenocarcinomas of the pancreas, colorectum and lung. Their respective relationships with smoking are apparently paradoxical. We evaluated all the available types of clinical and epidemiological studies on the r

  20. Cigarette smoking and K-ras mutations in pancreas, lung and colorectal adenocarcinomas: etiopathogenic similarities, differences and paradoxes.

    NARCIS (Netherlands)

    Porta, M.; Crous-Bou, M.; Wark, P.A.; Vineis, P.; Real, F.X.; Malats, N.; Kampman, E.

    2009-01-01

    Surprisingly different frequencies and patterns of K-ras mutations are observed in human adenocarcinomas of the pancreas, colorectum and lung. Their respective relationships with smoking are apparently paradoxical. We evaluated all the available types of clinical and epidemiological studies on the r

  1. Lethal impacts of cigarette smoke in cultured tobacco cells

    Directory of Open Access Journals (Sweden)

    Kawano Tomonori

    2011-07-01

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

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

    Science.gov (United States)

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

    2016-06-15

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

  3. Role of CXCL5 in leukocyte recruitment to the lungs during secondhand smoke exposure.

    Science.gov (United States)

    Balamayooran, Gayathriy; Batra, Sanjay; Cai, Shanshan; Mei, Junjie; Worthen, G Scott; Penn, Arthur L; Jeyaseelan, Samithamby

    2012-07-01

    Chronic obstructive pulmonary disease (COPD) is the third leading cause of mortality in the United States. The major cause of COPD is cigarette smoking. Extensive leukocyte influx into the lungs, mediated by chemokines, is a critical event leading to COPD. Although both resident and myeloid cells secrete chemokines in response to inflammatory stimuli, little is known about the role of epithelial-derived chemokines, such as CXC chemokine ligand (CXCL)5, in the pathogenesis of cigarette smoke-induced inflammation. To explore the role of CXCL5, we generated CXCL5 gene-deficient mice and exposed them to secondhand smoke (SHS) for 5 hours/day for 5 days/week up to 3 weeks (subacute exposure). We observed a reduced recruitment of leukocytes to the lungs of CXCL5(-/-) mice compared with their wild-type (WT) counterparts, and noted that macrophages comprised the predominant leukocytes recruited to the lungs. Irradiation experiments performed on CXCL5(-/-) or WT mice transplanted with WT or CXCL5(-/-) bone marrow revealed that resident but not hematopoietic cell-driven CXCL5 is important for mediating SHS-induced lung inflammation. Interestingly, we observed a significant reduction of monocyte chemotactic protein-1 (MCP-1/CC chemokine ligand 2) concentrations in the lungs of CXCL5(-/-) mice. The instillation of recombinant MCP-1 in CXCL5(-/-) mice reversed macrophage recruitment. Our results also show the reduced activation of NF-κB/p65 in the lungs, as well as the attenuated activation of C-Jun N-terminal kinase, p42/44, and p38 mitogen-activated protein kinases and the expression of intercellular adhesion molecule-1 in the lungs of SHS-exposed CXCL5(-/-) mice. Our findings suggest an important role for CXCL5 in augmenting leukocyte recruitment in SHS-induced lung inflammation, and provide novel insights into CXCL5-driven pathogenesis. PMID:22362385

  4. Lung endothelial monocyte-activating protein 2 is a mediator of cigarette smoke–induced emphysema in mice

    OpenAIRE

    Clauss, Matthias; Voswinckel, Robert; Rajashekhar, Gangaraju; Sigua, Ninotchka L.; Fehrenbach, Heinz; Rush, Natalia I.; Schweitzer, Kelly S.; Yildirim, Ali Ö.; Kamocki, Krzysztof; Fisher, Amanda J.; Gu, Yuan; Safadi, Bilal; Nikam, Sandeep; Hubbard, Walter C.; Tuder, Rubin M

    2011-01-01

    Pulmonary emphysema is a disease characterized by alveolar cellular loss and inflammation. Recently, excessive apoptosis of structural alveolar cells has emerged as a major mechanism in the development of emphysema. Here, we investigated the proapoptotic and monocyte chemoattractant cytokine endothelial monocyte-activating protein 2 (EMAPII). Lung-specific overexpression of EMAPII in mice caused simplification of alveolar structures, apoptosis, and macrophage accumulation, compared with that ...

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

    International Nuclear Information System (INIS)

    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

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

    Energy Technology Data Exchange (ETDEWEB)

    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.

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

    OpenAIRE

    Rahel eBirru; Y. Peter eDi

    2012-01-01

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

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

    Science.gov (United States)

    Pfaff, Miles; Shah, Ajul; Steinbacher, Derek

    2014-02-01

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

  9. Cigarette smoking: health effects and control strategies.

    Science.gov (United States)

    Alberg, Anthony J

    2008-12-01

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

  10. Estimating mortality due to cigarette smoking

    DEFF Research Database (Denmark)

    Brønnum-Hansen, Henrik; Juel, K

    2000-01-01

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

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

    DEFF Research Database (Denmark)

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

    2012-01-01

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

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

    Science.gov (United States)

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

    2016-08-01

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

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

    Science.gov (United States)

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

    2009-01-01

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

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

    Science.gov (United States)

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

    2016-01-01

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2013-07-01

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

  16. Estimating mortality due to cigarette smoking

    DEFF Research Database (Denmark)

    Brønnum-Hansen, H; Juel, K

    2000-01-01

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

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

    OpenAIRE

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

    2015-01-01

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

  18. Gene by Environment Interaction Linking the Chromosome 15q25 Locus With Cigarette Consumption and Lung Cancer Susceptibility — Are African American Affected Differently?

    OpenAIRE

    Hopkins, R.J.; R. P. Young

    2016-01-01

    The majority of lung cancer cases result from complex interactions between smoking exposure, genetic susceptibility and a person's immune response to chronic inflammation or lung remodelling. Epidemiological studies confirm that susceptibility to developing chronic obstructive pulmonary disease (COPD), especially emphysema, is also closely linked to lung cancer susceptibility. Genetic epidemiology studies have consistently reported associations between the chromosome 15q25 locus with lung can...

  19. Integrative pathway genomics of lung function and airflow obstruction.

    Science.gov (United States)

    Gharib, Sina A; Loth, Daan W; Soler Artigas, María; Birkland, Timothy P; Wilk, Jemma B; Wain, Louise V; Brody, Jennifer A; Obeidat, Ma'en; Hancock, Dana B; Tang, Wenbo; Rawal, Rajesh; Boezen, H Marike; Imboden, Medea; Huffman, Jennifer E; Lahousse, Lies; Alves, Alexessander C; Manichaikul, Ani; Hui, Jennie; Morrison, Alanna C; Ramasamy, Adaikalavan; Smith, Albert Vernon; Gudnason, Vilmundur; Surakka, Ida; Vitart, Veronique; Evans, David M; Strachan, David P; Deary, Ian J; Hofman, Albert; Gläser, Sven; Wilson, James F; North, Kari E; Zhao, Jing Hua; Heckbert, Susan R; Jarvis, Deborah L; Probst-Hensch, Nicole; Schulz, Holger; Barr, R Graham; Jarvelin, Marjo-Riitta; O'Connor, George T; Kähönen, Mika; Cassano, Patricia A; Hysi, Pirro G; Dupuis, Josée; Hayward, Caroline; Psaty, Bruce M; Hall, Ian P; Parks, William C; Tobin, Martin D; London, Stephanie J

    2015-12-01

    Chronic respiratory disorders are important contributors to the global burden of disease. Genome-wide association studies (GWASs) of lung function measures have identified several trait-associated loci, but explain only a modest portion of the phenotypic variability. We postulated that integrating pathway-based methods with GWASs of pulmonary function and airflow obstruction would identify a broader repertoire of genes and processes influencing these traits. We performed two independent GWASs of lung function and applied gene set enrichment analysis to one of the studies and validated the results using the second GWAS. We identified 131 significantly enriched gene sets associated with lung function and clustered them into larger biological modules involved in diverse processes including development, immunity, cell signaling, proliferation and arachidonic acid. We found that enrichment of gene sets was not driven by GWAS-significant variants or loci, but instead by those with less stringent association P-values. Next, we applied pathway enrichment analysis to a meta-analyzed GWAS of airflow obstruction. We identified several biologic modules that functionally overlapped with those associated with pulmonary function. However, differences were also noted, including enrichment of extracellular matrix (ECM) processes specifically in the airflow obstruction study. Network analysis of the ECM module implicated a candidate gene, matrix metalloproteinase 10 (MMP10), as a putative disease target. We used a knockout mouse model to functionally validate MMP10's role in influencing lung's susceptibility to cigarette smoke-induced emphysema. By integrating pathway analysis with population-based genomics, we unraveled biologic processes underlying pulmonary function traits and identified a candidate gene for obstructive lung disease. PMID:26395457

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

    OpenAIRE

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

    2012-01-01

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

  1. 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

    International Nuclear Information System (INIS)

    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

  2. DrugFacts: Electronic Cigarettes (e-Cigarettes)

    Science.gov (United States)

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

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

    Directory of Open Access Journals (Sweden)

    Nohra Chalouhi

    2012-01-01

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

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

    Science.gov (United States)

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

    2015-01-01

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

  5. 1α,25-dihydroxyvitamin D₃ counteracts the effects of cigarette smoke in airway epithelial cells.

    Science.gov (United States)

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

    2015-06-01

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

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

    Science.gov (United States)

    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 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

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

    Directory of Open Access Journals (Sweden)

    Abdel-Sater Khaled A.

    2008-06-01

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

  8. [The challenge of electronic cigarettes].

    Science.gov (United States)

    Córdoba García, Rodrigo

    2014-01-01

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

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

    Science.gov (United States)

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

    2016-08-01

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

  10. Cigarette use, Cigarette Consumption and Price of Cigarette

    Institute of Scientific and Technical Information of China (English)

    JingMing Li

    2016-01-01

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

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

    Directory of Open Access Journals (Sweden)

    N. P. Lareau

    2015-07-01

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

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

    OpenAIRE

    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 parameters: NH4 level, NO emission and the declared tar and nicotine values. These correlations can be used to support the postulated hypotheses. In this report the NH4 amount in cigarettes was determined ...

  13. Associations Between Anthropometry, Cigarette Smoking, Alcohol Consumption, and Non-Hodgkin Lymphoma in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial

    OpenAIRE

    Troy, Jesse D.; Hartge, Patricia; Weissfeld, Joel L.; Oken, Martin M.; Colditz, Graham A.; MECHANIC, LEAH E.; Lindsay M. Morton

    2010-01-01

    Prospective studies of lifestyle and non-Hodgkin lymphoma (NHL) are conflicting, and some are inconsistent with case-control studies. The Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial was used to evaluate risk of NHL and its subtypes in association with anthropometric factors, smoking, and alcohol consumption in a prospective cohort study. Lifestyle was assessed via questionnaire among 142,982 male and female participants aged 55–74 years enrolled in the PLCO Trial dur...

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1978-02-01

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

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

    International Nuclear Information System (INIS)

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

  16. E-Cigarettes (For Parents)

    Science.gov (United States)

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

  17. E-Cigarettes (For Teens)

    Science.gov (United States)

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

  18. Women and lung cancer.

    OpenAIRE

    Itri, L

    1987-01-01

    Lung cancer has now surpassed breast cancer as the leading cause of cancer deaths in American women. In 1986, 49,000 women were diagnosed as having lung cancer; only 16 percent of them will survive 5 years or more. Cigarette smoking is unquestionably the leading contributing factor. Large numbers of women took up cigarette smoking during and after World War II. The grim aftermath has taken 20 years to surface--between 1950 and 1985, lung cancer deaths in women increased 500 percent. Even wors...

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

    Science.gov (United States)

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

    2010-11-01

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

  20. Repeated observation of immune gene sets enrichment in women with non-small cell lung cancer

    Science.gov (United States)

    Araujo, Jhajaira M.; Prado, Alexandra; Cardenas, Nadezhda K.; Zaharia, Mayer; Dyer, Richard; Doimi, Franco; Bravo, Leny; Pinillos, Luis; Morante, Zaida; Aguilar, Alfredo; Mas, Luis A.; Gomez, Henry L.; Vallejos, Carlos S.; Rolfo, Christian; Pinto, Joseph A.

    2016-01-01

    There are different biological and clinical patterns of lung cancer between genders indicating intrinsic differences leading to increased sensitivity to cigarette smoke-induced DNA damage, mutational patterns of KRAS and better clinical outcomes in women while differences between genders at gene-expression levels was not previously reported. Here we show an enrichment of immune genes in NSCLC in women compared to men. We found in a GSEA analysis (by biological processes annotated from Gene Ontology) of six public datasets a repeated observation of immune gene sets enrichment in women. “Immune system process”, “immune response”, “defense response”, “cellular defense response” and “regulation of immune system process” were the gene sets most over-represented while APOBEC3G, APOBEC3F, LAT, CD1D and CCL5 represented the top-five core genes. Characterization of immune cell composition with the platform CIBERSORT showed no differences between genders; however, there were differences when tumor tissues were compared to normal tissues. Our results suggest different immune responses in NSCLC between genders that could be related with the different clinical outcome. PMID:26958810

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

    International Nuclear Information System (INIS)

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2014-12-15

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

  3. Associations between anthropometry, cigarette smoking, alcohol consumption, and non-Hodgkin lymphoma in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial.

    Science.gov (United States)

    Troy, Jesse D; Hartge, Patricia; Weissfeld, Joel L; Oken, Martin M; Colditz, Graham A; Mechanic, Leah E; Morton, Lindsay M

    2010-06-15

    Prospective studies of lifestyle and non-Hodgkin lymphoma (NHL) are conflicting, and some are inconsistent with case-control studies. The Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial was used to evaluate risk of NHL and its subtypes in association with anthropometric factors, smoking, and alcohol consumption in a prospective cohort study. Lifestyle was assessed via questionnaire among 142,982 male and female participants aged 55-74 years enrolled in the PLCO Trial during 1993-2001. Hazard ratios and 95% confidence intervals were calculated using Cox proportional hazards regression. During 1,201,074 person-years of follow-up through 2006, 1,264 histologically confirmed NHL cases were identified. Higher body mass index (BMI; weight (kg)/height (m)(2)) at ages 20 and 50 years and at baseline was associated with increased NHL risk (P(trend) or =30 vs. 18.5-24.9, hazard ratio = 1.32, 95% confidence interval: 1.13, 1.54). Smoking was not associated with NHL overall but was inversely associated with follicular lymphoma (ever smoking vs. never: hazard ratio = 0.62, 95% confidence interval: 0.45, 0.85). Alcohol consumption was unrelated to NHL (drinks/week: P(trend) = 0.187). These data support previous studies suggesting that BMI is positively associated with NHL, show an inverse association between smoking and follicular lymphoma (perhaps due to residual confounding), and do not support a causal association between alcohol and NHL. PMID:20494998

  4. Cigarette Ads and Youth.

    Science.gov (United States)

    Carol, Julia

    1988-01-01

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

  5. Lung

    International Nuclear Information System (INIS)

    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 133Xe 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

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

    OpenAIRE

    Aoshiba K; Nagai A

    2003-01-01

    Abstract Cigarette smoking is a major risk factor in the development of various lung diseases, including pulmonary emphysema, pulmonary fibrosis, and lung cancer. The mechanisms of these diseases include alterations in alveolar epithelial cells, which are essential in the maintenance of normal alveolar architecture and function. Following cigarette smoking, alterations in alveolar epithelial cells induce an increase in epithelial permeability, a decrease in surfactant production, the inapprop...

  7. Lung cancer

    International Nuclear Information System (INIS)

    There will be over 160,000 cases of lung cancer diagnosed in the US in 1991, and deaths from this disease account for a quarter of all cancer deaths in this country. The incidence of lung cancer has continued to increase, especially among women. With 31% of American men and 25% of American women identified in the 1985 census as cigarette smokers, it is likely that this trend will continue well into the next century. Unfortunately, the majority of patients present with locally advanced tumors or distant metastatic disease. Presently, most patients with lung cancer will receive radiation therapy either in an attempt to control inoperable or locally advanced disease, or for palliation of symptomatic intrathoracic or metastatic disease. Because of the poor prognosis of all patients excepting those with early stage resectable lesions, lung cancer is appropriately the subject of intense clinical investigation and controversy throughout the world

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

    Institute of Scientific and Technical Information of China (English)

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

    2016-01-01

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

  9. Diagnostic Imaging of Lung Cancer

    OpenAIRE

    Kemal Kara; Ersin Ozturk

    2012-01-01

    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 as...

  10. Epidemiology of Lung Cancer.

    Science.gov (United States)

    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. PMID:26667337

  11. Cigarette Smoke Alters the Hematopoietic Stem Cell Niche

    Directory of Open Access Journals (Sweden)

    Robert W. Siggins

    2014-02-01

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

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

    International Nuclear Information System (INIS)

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

  13. Cardiology Patient Page: Electronic Cigarettes

    Science.gov (United States)

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

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

    International Nuclear Information System (INIS)

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

  15. Tobacco flakes on cigarette filters grow bacteria: a potential health risk to the smoker?

    Science.gov (United States)

    Pauly, J L; Waight, J D; Paszkiewicz, G M

    2008-09-01

    Bacterial growth from a single flake of tobacco was documented for cigarettes that had been purchased recently from local vendors and from cigarettes that had been stored for more than six years in a warehouse. In a novel tobacco flake assay, a pack of cigarettes was opened within the sterile environment of a laminar flow hood. A single flake of tobacco was collected randomly and aseptically from the middle of the cigarette column and placed onto the surface of a blood agar plate. The test cigarettes included eight different popular US brands, and these were from three different tobacco companies. After 24 hours of incubation at 37 degrees C, the plates showed bacterial growth for tobacco from all brands of cigarettes. Further, more than 90% of the individual tobacco flakes of a given brand grew bacteria. Likewise, bacteria grew from microparticulate tobacco that had been sieved from cigarettes. Tobacco flakes were observed lying loosely on the cut surface of the filter of cigarettes in newly opened packs, and bacteria grew from cigarette filters that had been touched to the surface of a blood agar plate. In conclusion, the results of these studies predict that diverse microbes and microbial toxins are carried by tobacco microparticulates that are released from the cigarette during smoking, and carried into mainstream smoke that is sucked deep into the lung. PMID:18768459

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

    International Nuclear Information System (INIS)

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

  17. Lung pathology and exposure to radon daughters

    International Nuclear Information System (INIS)

    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

  18. Electronic Cigarettes on Hospital Campuses

    Directory of Open Access Journals (Sweden)

    Clare Meernik

    2015-12-01

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

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

    LENUS (Irish Health Repository)

    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.

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

    OpenAIRE

    Savela, K; Hemminki, K

    1993-01-01

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

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

    Science.gov (United States)

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

    2014-07-01

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

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

    NARCIS (Netherlands)

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

    2013-01-01

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

  3. Smoking water pipe is injurious to lungs

    DEFF Research Database (Denmark)

    Sivapalan, Pradeesh; Ringbæk, Thomas; Lange, Peter

    2014-01-01

    This review describes the pulmonary consequences of water pipe smoking. Smoking water pipe affects the lung function negatively, is significantly associated with chronic obstructive pulmonary disease and increases the risk of lung infections. Case reports suggest that regular smokers of water pipe...... have a higher risk of developing malignancies, particularly lung cancer than cigarette smokers....

  4. Exhaled CO, a predictor of lung function?

    DEFF Research Database (Denmark)

    Fabricius, Peder; Scharling, Henrik; Løkke, Anders;

    2007-01-01

    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...

  5. Multielement determination in a Chinese cigarette brand

    International Nuclear Information System (INIS)

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

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

    International Nuclear Information System (INIS)

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

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

    Directory of Open Access Journals (Sweden)

    Gaur Dushyant

    2010-01-01

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

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

    Science.gov (United States)

    Gardi, Concetta; Valacchi, Giuseppe

    2012-07-01

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

  9. Imaging-based assessment of dyspnea in cigarette smokers

    Science.gov (United States)

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

    1994-05-01

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

  10. Exhaled CO, a predictor of lung function?

    DEFF Research Database (Denmark)

    Fabricius, P; Scharling, H; Lokke, A;

    2007-01-01

    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 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.......001). Increasing CO levels were correlated to a lower FEV(1)%pred and to an accelerated decline in lung function. However, in multiple linear regression analyses these correlations were not significant. CONCLUSION: Inhalation and type of cigarette affects exhaled CO levels. CO measures have no predictive value...

  11. Diagnostic Imaging of Lung Cancer

    Directory of Open Access Journals (Sweden)

    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

  12. Smoking-related lung disease.

    Science.gov (United States)

    Galvin, Jeffrey R; Franks, Teri J

    2009-11-01

    Dyspneic smokers who come to clinical attention demonstrate varying combinations of emphysema, airway inflammation, and fibrosis in addition to the changes of pulmonary Langerhans' cell histiocytosis. There is also growing acceptance of a link between cigarette smoke and alveolar wall fibrosis. Acute eosinophilic pneumonia is a dramatic response to recent-onset smoking seen in a small number of individuals. The interconnected pathways that lead to lung inflammation and fibrosis in cigarette smokers are slowly coming into focus. PMID:19935224

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

    OpenAIRE

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

    2013-01-01

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

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

    OpenAIRE

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

    2013-01-01

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

  15. Electronic cigarettes in the media.

    Science.gov (United States)

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

    2016-07-01

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

  16. Electronic cigarettes in the media

    Science.gov (United States)

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

    2016-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Senaida Bišanović

    2012-01-01

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

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

    International Nuclear Information System (INIS)

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

  19. Diet and lung cancer

    DEFF Research Database (Denmark)

    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 are...

  20. Diet and lung cancer

    DEFF Research Database (Denmark)

    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...

  1. Role of Lung Maintenance Program in the Heterogeneity of Lung Destruction in Emphysema

    OpenAIRE

    Tuder, Rubin M.; Yoshida, Toshinori; Fijalkowka, Iwona; Biswal, Shyam; Petrache, Irina

    2006-01-01

    Centrilobular emphysema caused by chronic cigarette smoking is a heterogeneous disease with a predominance of upper lobe involvement. It is presumed that this heterogeneity indicates a particular susceptibility to cigarette smoke or the fact that the inhaled smoke distributes preferentially to upper lung zones. The less involved areas might therefore retain the capacity for lung regeneration and gain of pulmonary function in terminally ill patients. We propose that the interplay between molec...

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

    Science.gov (United States)

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

    2015-08-01

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

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

    Science.gov (United States)

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

    2009-04-01

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

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

    Science.gov (United States)

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

    2016-01-01

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

  5. What's in a Cigarette?

    Science.gov (United States)

    ... Association's 'Tobacco 21' Initiative to Save Lives of Millennials, Future Generations by Raising Tobacco Sales Age to ... generous support Make a difference by delivering research, education and advocacy to those impacted by lung disease. ...

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

    Science.gov (United States)

    2010-04-01

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

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

    Energy Technology Data Exchange (ETDEWEB)

    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

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

    International Nuclear Information System (INIS)

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

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

    International Nuclear Information System (INIS)

    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

  10. Youths' understandings of cigarette advertisements.

    Science.gov (United States)

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

    2009-01-01

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

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

    International Nuclear Information System (INIS)

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

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

    OpenAIRE

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

    2014-01-01

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

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

    Science.gov (United States)

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

    2015-11-01

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

  14. Smoking and Other Interstitial Lung Diseases

    OpenAIRE

    Carpio Carlos; Gómez-Carrera Luis; Álvarez-Sala Rodolfo

    2011-01-01

    Cigarette smoking has been implicated in the development of some uncommon respiratory interstitial diseases. Desquamative interstitial pneumonia and respiratory bronchiolitis-associated interstitial lung diseases are characterized by a diffuse alveolar and peribronchiolar filling with macrophages, respectively. Pulmonary Langerhans' cell histiocytosis is a rare interstitial lung disorder characterized by the proliferation of Langerhans' cell forming interstitial infiltrates and nodules that c...

  15. Cigarette Smoking and Dyspnea Perception

    Directory of Open Access Journals (Sweden)

    Scano Giorgio

    2004-03-01

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

  16. Marketing of menthol cigarettes and consumer perceptions

    Directory of Open Access Journals (Sweden)

    Rising Joshua

    2011-05-01

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

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

    OpenAIRE

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

    2015-01-01

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

  18. Cigarette smoking index and K-ras gene mutation in bronchoalveolar lavage fluid in patients with lung cancer%吸烟指数与肺癌患者支气管肺泡灌洗液中的K-ras基因突变

    Institute of Scientific and Technical Information of China (English)

    李建祥; 陈锐; 童建

    2005-01-01

    背景:肺癌的高发与许多因素有关,吸烟是重要原因之一,及早诊断对肺癌治疗尤其重要.目的:探讨肺癌患者吸烟与支气管肺泡灌洗液中细胞K-ras基因突变的关系.设计:以患者为研究对象的随机对照实验研究.单位:一所大学放射医学与公共卫生学院卫生毒理学教研室,一所大学医院呼吸内科.对象:选择在苏州大学第二附属医院1999-07/2001-09住院及门诊接受经纤维支气管镜行支气管肺泡灌洗术并取得细胞学或病理学确诊的肺癌、良性疾病患者.方法:应用聚合酶链反应结合限制性片段长度多态性分析法,检测37例吸烟肺癌患者、25例非吸烟肺癌患者以及20例肺良性疾病患者支气管肺泡灌洗液中细胞K-ras基因第12位密码子突变的情况.主要观察指标:K-ras基因第12位密码子突变.结果:肺癌患者K-ras基因突变率为36%(22/62),肺良性疾病患者中未发现K-ras基因突变.重度吸烟者的突变率(69%)显著高于中度(31%)和轻度吸烟者(25%),以及非吸烟者(20%).突变的发生与患者的年龄及吸烟史相关,而与性别、TNM分型无关.结论:吸烟可能是导致K-ras基因突变的诱因之一;支气管肺泡灌洗液中K-ras基因突变的检测对预测吸烟者肺癌的发生和早期诊断,具有重要的临床价值.%BACKGROUND: Cigarette smoking has been recognized as one of the high risk factors in carcinogenesis of lung cancer. Early diagnosis of lung cancer may be of clinical therapy value.OBJECTIVE: To explore the mutation of K-ras oncogene in bronchoalveolar lavage fluid(BALF) in order to reveal its relationship with cigarette smoking in lung cancer patients.DESIGN: Randomized controlled trial based on the patients.SETTING: Department of Toxicology, College of Radiology and Public Health of a university, and Department of Respiratory Medicine of a university hospital.PARTICIPANTS: The out-patients and inpatients in the Second Affiliated Hospital of

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

    International Nuclear Information System (INIS)

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

  20. A New Area to Fight: Electronic Cigarette

    Directory of Open Access Journals (Sweden)

    Şermin Börekçi

    2015-08-01

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

  1. A Cancer That Went Up in Smoke: Pulmonary Reaction to e-Cigarettes Imitating Metastatic Cancer

    DEFF Research Database (Denmark)

    Madsen, Lene Margrethe Ring; Vinther Krarup, Niels Henrik; Bergmann, Troels Korshøj;

    2016-01-01

    e-Cigarettes have gained worldwide popularity as a substitute for smoking, but concern has been raised regarding the long-term effects associated with their use. We report a case of a 45-year-old female consumer of e-cigarettes who presented with 4 months of abdominal pain and fever. Initial imag....... Upon cessation of e-cigarette use (known as vaping), the lung nodules disappeared, and the liver lesions regressed. Our case report suggests that vaping can induce an inflammatory reaction mimicking metastatic cancer....... imaging discovered multiple pulmonary nodules and liver lesions suspicious of widespread metastases; however, an extensive evaluation found no evidence of malignancy. Results of a lung biopsy revealed an area with multinucleated giant cells suggestive of a foreign body reaction to a lipophilic material...

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

    Institute of Scientific and Technical Information of China (English)

    郭轶; 卢小刚; 代远斌

    2015-01-01

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

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

    Institute of Scientific and Technical Information of China (English)

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

    2010-01-01

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

  4. The Epithelial Cell in Lung Health and Emphysema Pathogenesis

    OpenAIRE

    Mercer, Becky A; Lemaître, Vincent; Powell, Charles A.; D’Armiento, Jeanine

    2006-01-01

    Cigarette smoking is the primary cause of the irreversible lung disease emphysema. Historically, inflammatory cells such as macrophages and neutrophils have been studied for their role in emphysema pathology. However, recent studies indicate that the lung epithelium is an active participant in emphysema pathogenesis and plays a critical role in the lung’s response to cigarette smoke. Tobacco smoke increases protease production and alters cytokine expression in isolated epithelial cells, sugge...

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

    International Nuclear Information System (INIS)

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

  6. Toxicological assessment of kretek cigarettes Part 5: mechanistic investigations, inhalation toxicity.

    Science.gov (United States)

    Roemer, E; Dempsey, R; Van Overveld, F J; Berges, A; Pype, J; Weiler, H; Vanscheeuwijck, P; Schorp, M K

    2014-12-01

    The biological effects of mainstream smoke (MS) from Indonesian-blended cigarettes with and without added cloves, cloves extracted with hot ethanol, and extracted cloves replenished with eugenol or clove oil were assessed in a 90-day inhalation study in rats. A separate 35-day inhalation study in rats was performed with MS from American-blended cigarettes with 0%, 2.5%, 5% or 10% added eugenol. Effects commonly seen in inhalation studies with MS were observed. These included histopathological changes indicative of irritation in the entire respiratory tract and inflammatory responses in the lung. Adding cloves to American- or Indonesian-blended cigarettes reduced the inflammatory response in the lung but with no difference between the two blend types. When the clove oil was extracted (∼ 75% reduction of eugenol achieved) from cloves, the inflammatory response in the lung was still reduced similarly to whole cloves but the severity of histopathological changes in the upper respiratory tract was less reduced. Add back of clove oil or pure eugenol reduced this response to a level similar to what was seen with whole cloves. When eugenol was added to American-blended cigarettes, similar findings of reduced lung inflammation and severity of histopathological changes in respiratory the tract was confirmed. These studies demonstrate a clear effect of cloves, and in particular eugenol, in explaining these findings. PMID:25455231

  7. Cigarette smoking: knowledge and attitudes among Mexican physicians

    Directory of Open Access Journals (Sweden)

    TAPIA-CONYER ROBERTO

    1997-01-01

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

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

    OpenAIRE

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

    2015-01-01

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

  9. Patient–physician communication regarding electronic cigarettes

    Directory of Open Access Journals (Sweden)

    Michael B. Steinberg

    2015-01-01

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

  10. E-Cigarettes Emit Toxic Vapors

    Science.gov (United States)

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

  11. E-Cigarettes 'In' At Some Schools

    Science.gov (United States)

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

  12. Why Teens Choose E-Cigarettes

    Science.gov (United States)

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

  13. E-Cigarettes 'In' At Some Schools

    Science.gov (United States)

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

  14. Lung cancer risk factors among women

    OpenAIRE

    Papadopoulos, Alexandra

    2012-01-01

    The incidence of female lung cancer in developed countries has been increasing since 1950 and particularly in France where the cigarettes consumption has also increased. Since 1980, a growing number of epidemiological surveys have pinpointed the risk of female lung cancer related to smoking. Consecutively, a debate on gender differences in lung cancer risk has appeared, but still in progress nowadays. The reproductive factors could explain these differences. In order to have recent and reliab...

  15. E-cigarettes also contain detrimental chemicals

    DEFF Research Database (Denmark)

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

    2014-01-01

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

  16. Flavour chemicals in electronic cigarette fluids

    OpenAIRE

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

    2015-01-01

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

  17. Electronic Cigarettes: Market Entry in Iceland?

    OpenAIRE

    Hinrik Hinriksson 1990

    2015-01-01

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

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

    Science.gov (United States)

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

    2016-05-01

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

  19. Electronic cigarettes: a short review.

    Science.gov (United States)

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

    2013-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Yun-Ching Huang

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

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

    Science.gov (United States)

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

    2015-01-01

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

  2. E-cigarettes also contain detrimental chemicals

    DEFF Research Database (Denmark)

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

    2014-01-01

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

  3. Wif1 Hypermethylation as Unfavorable Prognosis of Non-Small Cell Lung Cancers with EGFR Mutation

    OpenAIRE

    Lee, Su Man; Park, Jae Yong; Kim, Dong Sun

    2013-01-01

    Lung cancer is a leading cause of cancer-related mortality across the world and tobacco smoking is the major risk factor. The Wnt signaling pathway is known to be involved in smoke-induced tumorigenesis in the lung. Promoter hypermethylation of Wnt inhibitory factor 1 (Wif1) has become a common event in a number of human tumors. Using a methylation-specific PCR, hypermethylation of the Wif1 gene promoter was evaluated in 139 primary non-small cell lung cancers (NSCLCs) and its correlation wit...

  4. Corrective Taxes and Cigarette Characteristics.

    Science.gov (United States)

    Calcott, Paul; Petkov, Vladimir

    2016-07-01

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

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

    International Nuclear Information System (INIS)

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

  6. Short-term effects of electronic and tobacco cigarettes on exhaled nitric oxide

    International Nuclear Information System (INIS)

    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 × 109, 5.1 ± 0.1 × 109, and 3.1 ± 0.6 × 109 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 × 1010, 5.2 × 1010 and 2.3 × 1010 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 were

  7. Short-term effects of electronic and tobacco cigarettes on exhaled nitric oxide

    Energy Technology Data Exchange (ETDEWEB)

    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

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

    Directory of Open Access Journals (Sweden)

    Gao Shu-guang

    2012-06-01

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

  9. E-cigarettes: promise or peril?

    Science.gov (United States)

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

    2012-03-01

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

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

    Science.gov (United States)

    Fromme, Hermann; Schober, Wolfgang

    2015-04-01

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

  11. Toxic metals distribution in different components of Pakistani and imported cigarettes by electrothermal atomic absorption spectrometer.

    Science.gov (United States)

    Kazi, T G; Jalbani, N; Arain, M B; Jamali, M K; Afridi, H I; Sarfraz, R A; Shah, A Q

    2009-04-15

    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. PMID:18657905

  12. Toxic metals distribution in different components of Pakistani and imported cigarettes by electrothermal atomic absorption spectrometer

    International Nuclear Information System (INIS)

    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

  13. Carbonyl Compounds Generated from Electronic Cigarettes

    Directory of Open Access Journals (Sweden)

    Kanae Bekki

    2014-10-01

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

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

    Directory of Open Access Journals (Sweden)

    Marli Maria Knorst

    2014-10-01

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

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

    International Nuclear Information System (INIS)

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    1995-12-01

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

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

    International Nuclear Information System (INIS)

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

  18. Radioactivity levels in jurak and moasel, comparison with cigarette tobacco

    International Nuclear Information System (INIS)

    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 226Ra 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 232Th were: 3.8, 2.6, 3.5, 2.2 and 7.8 respectively; that of 40K 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

  19. Immediate response to cigarette smoke

    Energy Technology Data Exchange (ETDEWEB)

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

    1982-06-01

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

  20. Lung Cancer and Interstitial Lung Diseases: A Systematic Review

    Directory of Open Access Journals (Sweden)

    Kostas Archontogeorgis

    2012-01-01

    Full Text Available Interstitial lung diseases (ILDs represent a heterogeneous group of more than two hundred diseases of either known or unknown etiology with different pathogenesis and prognosis. Lung cancer, which is the major cause of cancer death in the developed countries, is mainly attributed to cigarette smoking and exposure to inhaled carcinogens. Different studies suggest a link between ILDs and lung cancer, through different pathogenetic mechanisms, such as inflammation, coagulation, dysregulated apoptosis, focal hypoxia, activation, and accumulation of myofibroblasts as well as extracellular matrix accumulation. This paper reviews current evidence on the association between lung cancer and interstitial lung diseases such as idiopathic pulmonary fibrosis, sarcoidosis, systemic sclerosis, dermatomyositis/polymyositis, rheumatoid arthritis, systemic lupus erythematosus, and pneumoconiosis.

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

    Science.gov (United States)

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

    2014-07-18

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

  2. Lung carcinoma signaling pathways activated by smoking

    Institute of Scientific and Technical Information of China (English)

    Jing Wen; Jian-Hua Fu; Wei Zhang; Ming Guo

    2011-01-01

    Lung cancer is the leading cause of cancer death in men and women worldwide, with over a million deaths annually. Tobacco smoke is the major etiologic risk factor for lung cancer in current or previous smokers and has been strongly related to certain types of lung cancer, such as small cell lung carcinoma and squamous cell lung carcinoma. In recent years, there has been an increased incidence of lung adenocarcinoma. This change is strongly associated with changes in smoking behavior and cigarette design. Carcinogens present in tobacco products and their intermediate metabolites can activate multiple signaling pathways that contribute to lung cancer carcinogenesis. In this review, we summarize the smoking-activated signaling pathways involved in lung cancer.

  3. Reducing the addictiveness of cigarettes

    OpenAIRE

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

    1998-01-01

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

  4. Menthol Cigarettes | Smokefree.gov

    Science.gov (United States)

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

  5. Cigarette Taxes and the Social Market

    OpenAIRE

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

    2011-01-01

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

  6. Cigarettes and Alcohol: Substitutes or Complements?

    OpenAIRE

    Decker, Sandra L.; Amy Ellen Schwartz

    2000-01-01

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

  7. Cigarette package design: opportunities for disease prevention

    OpenAIRE

    Pollay RW; DiFranza JR; Clark DM

    2002-01-01

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

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

    Science.gov (United States)

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

    2008-01-01

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

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

    International Nuclear Information System (INIS)

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

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

    Science.gov (United States)

    Sinzinger, H; Kaliman, J; Oguogho, A

    2000-03-01

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

  11. Heme-related gene expression signatures of meat intakes in lung cancer tissues

    OpenAIRE

    Lam, Tram Kim; Rotunno, Melissa; Ryan, Brid M.; Pesatori, Angela C.; Bertazzi, Pier Alberto; Spitz, Margaret; Caporaso, Neil E; Landi, Maria Teresa

    2013-01-01

    Lung cancer causes more deaths worldwide than any other cancer. In addition to cigarette smoking, dietary factors may contribute to lung carcinogenesis. Epidemiologic studies, including the Environment and Genetics in Lung cancer Etiology (EAGLE), have reported increased consumption of red/processed meats to be associated with higher risk of lung cancer. Heme-iron toxicity may link meat intake with cancer. We investigated this hypothesis in meat-related lung carcinogenesis using whole genome ...

  12. Updates and Controversies in the Rapidly Evolving Field of Lung Cancer Screening, Early Detection, and Chemoprevention

    OpenAIRE

    Hasmeena Kathuria; Yaron Gesthalter; Avrum Spira; Brody, Jerome S.; Katrina Steiling

    2014-01-01

    Lung cancer remains the leading cause of cancer-related death in the United States. Cigarette smoking is a well-recognized risk factor for lung cancer, and a sustained elevation of lung cancer risk persists even after smoking cessation. Despite identifiable risk factors, there has been minimal improvement in mortality for patients with lung cancer primarily stemming from diagnosis at a late stage when there are few effective therapeutic options. Early detection of lung cancer and effective sc...

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

    Science.gov (United States)

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

    2016-03-01

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

  14. Prospective study of effect of switching from cigarettes to pipes or cigars on mortality from three smoking related diseases.

    OpenAIRE

    Wald, N J; Watt, H C

    1997-01-01

    OBJECTIVE: To estimate the extent to which cigarette smokers who switch to cigars or pipes alter their risk of dying of three-smoking related diseases-lung cancer, ischaemic heart disease, and chronic obstructive lung disease. DESIGN: A prospective study of 21520 men aged 35-64 years when recruited in 1975-82 with detailed history of smoking and measurement of carboxyhaemoglobin. MAIN OUTCOME MEASURES: Notification of deaths (to 1993) classified by cause. RESULTS: Pipe and cigar smokers who h...

  15. Cigarette Litter: Smokers’ Attitudes and Behaviors

    Directory of Open Access Journals (Sweden)

    Julia C. Cartwright

    2012-06-01

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

  16. Hazardous waste status of discarded electronic cigarettes

    Energy Technology Data Exchange (ETDEWEB)

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

    2015-05-15

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

  17. Do cigarette and alcohol affect semen analysis?

    Directory of Open Access Journals (Sweden)

    Mehmet Zeynel Keskin

    2016-03-01

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

  18. Hazardous waste status of discarded electronic cigarettes

    International Nuclear Information System (INIS)

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

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

    Directory of Open Access Journals (Sweden)

    Olivia A. Wackowski

    2016-06-01

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

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

    Science.gov (United States)

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

    2016-01-01

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

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

    Science.gov (United States)

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

    2016-01-01

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

  2. Lung Disease

    Science.gov (United States)

    ... ePublications > Our ePublications > Lung disease fact sheet ePublications Lung disease fact sheet This information in Spanish (en ... disease? More information on lung disease What is lung disease? Lung disease refers to disorders that affect ...

  3. INDONESIAN YOUTH AND CIGARETTE SMOKING

    Directory of Open Access Journals (Sweden)

    Dwi Susilowati

    2012-11-01

    Full Text Available Background: The increasing number of children and young adults exposed to tobacco usage in the world is alarming. Indonesia is the third biggest tobacco consumer in the world after China and India. Smoking harms nearly every organ of the body, it reduce quality of life and life expectancy. Smoking causes illnesses, big economic lost and premature death. Tobacco use was the leading cause of preventable death. Smokers began at early age; they became the target of massive tobacco campaigns. Youth were vulnerable to tobacco advertising, once they began to smoke, it was difficult to quit. The Objectives of this paper is to identify tobacco usage among the Indonesian youth, to explore health problems, regulations related to tobacco consumption and efforts to implement the WHO Framework Convention on Tobacco Control. Methods: Method used is by reviewing studies and campaign information provided by researchers and practitioners in tobacco control programs. Result: Data shows that among people aged 10 to 24 years in Indonesia the current smokers were 23.7% daily smokers, 5.5% occasional smokers while the average cigarettes consumed daily were 12.2. Among lndonesian aged 13-15 years, there were 41% boys and 3.5% girls that were current cigarette smoking and 10.3% boys and 3,1% girls that had current tobacco other than cigarette. It is important that this preventable epidemic becomes a top public health issue in all countries. A complete ban on all tobacco advertising, promotion and sponsorship is a powerful tool to protect the world's youth and Indonesia should ratify tobacco ban. Key words: Indonesia, tobacco, youth, advertisement

  4. E-Cigarettes | Smokefree.gov

    Science.gov (United States)

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

  5. Cigarette Smoking and Urinary Organic Sulfides 

    Institute of Scientific and Technical Information of China (English)

    JIANLE; CAOWEN-JUN

    2000-01-01

    In order to observe how cigarette smoking influences levels of thio-thiazolidine-4-carboxylic acid(TTCA),high performance liquid chromatography(HPLC) was used to detect TTCA in urine from 18 healthy male volunteers.At the sme time,the total amout of urinary organic sulfides was determined by the iodine azide test(IAT).Nine of the volunteers had smoking higtories(5 to 10 cigarettes per day,as the smoking group),and the rest only occasionally smoke (1 to 2 cigarettes per month,as the control group).Samples were collected in the early morning (limosis)and 90 minutes after smoking a cigarette.Results showed that smoking a single cigaretter could elevate the level of urinary organic sulfides both in the smoking and control groups,while a smoking habit appeared to have no significant influence on the urinary organic sulfide level.No significant cumulative effect of cigarette smoking on urinary organic sulfides was found,The influence of cigarette on uinary organic sulfides was temporary.The results suggest that cigaretter smoking might be a confounding factor in biomontoring the levels of carbon disulfide in exposed workers.

  6. Cigarette smoking and risk of ovarian cancer

    DEFF Research Database (Denmark)

    Faber, Mette T; Kjær, Susanne K; Dehlendorff, Christian;

    2013-01-01

    The majority of previous studies have observed an increased risk of mucinous ovarian tumors associated with cigarette smoking, but the association with other histological types is unclear. In a large pooled analysis, we examined the risk of epithelial ovarian cancer associated with multiple...... measures of cigarette smoking with a focus on characterizing risks according to tumor behavior and histology....

  7. 47 CFR 73.4055 - Cigarette advertising.

    Science.gov (United States)

    2010-10-01

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

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

    Science.gov (United States)

    2012-03-30

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

  9. Electronic Cigarettes: Ambiguity and Controversies of Usage

    International Nuclear Information System (INIS)

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

  10. On the interaction between radon progeny and particles generated by electronic and traditional cigarettes

    Science.gov (United States)

    Vargas Trassierra, C.; Cardellini, F.; Buonanno, G.; De Felice, P.

    2015-04-01

    During their entire lives, people are exposed to the pollutants present in indoor air. Recently, Electronic Nicotine Delivery Systems, mainly known as electronic cigarettes, have been widely commercialized: they deliver particles into the lungs of the users but a "second-hand smoke" has yet to be associated to this indoor source. On the other hand, the naturally-occurring radioactive gas, i.e. radon, represents a significant risk for lung cancer, and the cumulative action of these two agents could be worse than the agents separately would. In order to deepen the interaction between radon progeny and second-hand aerosol from different types of cigarettes, a designed experimental study was carried out by generating aerosol from e-cigarette vaping as well as from second-hand traditional smoke inside a walk-in radon chamber at the National Institute of Ionizing Radiation Metrology (INMRI) of Italy. In this chamber, the radon present in air comes naturally from the floor and ambient conditions are controlled. To characterize the sidestream smoke emitted by cigarettes, condensation particle counters and scanning mobility particle sizer were used. Radon concentration in the air was measured through an Alphaguard ionization chamber, whereas the measurement of radon decay product in the air was performed with the Tracelab BWLM Plus-2S Radon daughter Monitor. It was found an increase of the Potential Alpha-Energy Concentration (PAEC) due to the radon decay products attached to aerosol for higher particle number concentrations. This varied from 7.47 ± 0.34 MeV L-1 to 12.6 ± 0.26 MeV L-1 (69%) for the e-cigarette. In the case of traditional cigarette and at the same radon concentration, the increase was from 14.1 ± 0.43 MeV L-1 to 18.6 ± 0.19 MeV L-1 (31%). The equilibrium factor increases, varying from 23.4% ± 1.11% to 29.5% ± 0.26% and from 30.9% ± 1.0% to 38.1 ± 0.88 for the e-cigarette and traditional cigarette, respectively. These growths still continue for long

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

    Science.gov (United States)

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

    2015-01-01

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

  12. Promotion of lung tumor growth by interleukin-17

    OpenAIRE

    Xu, Beibei; Guenther, James F.; Pociask, Derek A.; Wang, Yu; Kolls, Jay K.; You, Zongbing; Chandrasekar, Bysani; Shan, Bin; Sullivan, Deborah E.; Morris, Gilbert F.

    2014-01-01

    Recent findings demonstrate that inhaled cigarette smoke, the predominant lung carcinogen, elicits a T helper 17 (Th17) inflammatory phenotype. Interleukin-17A (IL-17), the hallmark cytokine of Th17 inflammation, displays pro- and antitumorigenic properties in a manner that varies according to tumor type and assay system. To investigate the role of IL-17 in lung tumor growth, we used an autochthonous tumor model (K-RasLA1 mice) with lung delivery of a recombinant adenovirus that expresses IL-...

  13. NNK-Induced Lung Tumors: A Review of Animal Model

    OpenAIRE

    Hua-Chuan Zheng; Yasuo Takano

    2011-01-01

    The incidence of lung adenocarcinoma has been remarkably increasing in recent years due to the introduction of filter cigarettes and secondary-hand smoking because the people are more exposed to higher amounts of nitrogen oxides, especially 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK), which is widely applied in animal model of lung tumors. In NNK-induced lung tumors, genetic mutation, chromosome instability, gene methylation, and activation of oncogenes have been found so as to disrup...

  14. Endothelial disruptive proinflammatory effects of nicotine and e-cigarette vapor exposures

    Science.gov (United States)

    Schweitzer, Kelly S.; Chen, Steven X.; Law, Sarah; Van Demark, Mary; Poirier, Christophe; Justice, Matthew J.; Hubbard, Walter C.; Kim, Elena S.; Lai, Xianyin; Wang, Mu; Kranz, William D.; Carroll, Clinton J.; Ray, Bruce D.; Bittman, Robert; Goodpaster, John

    2015-01-01

    The increased use of inhaled nicotine via e-cigarettes has unknown risks to lung health. Having previously shown that cigarette smoke (CS) extract disrupts the lung microvasculature barrier function by endothelial cell activation and cytoskeletal rearrangement, we investigated the contribution of nicotine in CS or e-cigarettes (e-Cig) to lung endothelial injury. Primary lung microvascular endothelial cells were exposed to nicotine, e-Cig solution, or condensed e-Cig vapor (1–20 mM nicotine) or to nicotine-free CS extract or e-Cig solutions. Compared with nicotine-containing extract, nicotine free-CS extract (10–20%) caused significantly less endothelial permeability as measured with electric cell-substrate impedance sensing. Nicotine exposures triggered dose-dependent loss of endothelial barrier in cultured cell monolayers and rapidly increased lung inflammation and oxidative stress in mice. The endothelial barrier disruptive effects were associated with increased intracellular ceramides, p38 MAPK activation, and myosin light chain (MLC) phosphorylation, and was critically mediated by Rho-activated kinase via inhibition of MLC-phosphatase unit MYPT1. Although nicotine at sufficient concentrations to cause endothelial barrier loss did not trigger cell necrosis, it markedly inhibited cell proliferation. Augmentation of sphingosine-1-phosphate (S1P) signaling via S1P1 improved both endothelial cell proliferation and barrier function during nicotine exposures. Nicotine-independent effects of e-Cig solutions were noted, which may be attributable to acrolein, detected along with propylene glycol, glycerol, and nicotine by NMR, mass spectrometry, and gas chromatography, in both e-Cig solutions and vapor. These results suggest that soluble components of e-Cig, including nicotine, cause dose-dependent loss of lung endothelial barrier function, which is associated with oxidative stress and brisk inflammation. PMID:25979079

  15. Radiation dose from cigarette tobacco

    International Nuclear Information System (INIS)

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

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

    Directory of Open Access Journals (Sweden)

    Gang Chen

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

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

    Science.gov (United States)

    Pokhrel, Pallav; Herzog, Thaddeus A

    2015-03-01

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

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

    International Nuclear Information System (INIS)

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

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

    Science.gov (United States)

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

    2015-03-01

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

  20. Nicotine-induced survival signaling in lung cancer cells is dependent on their p53 status while its down-regulation by curcumin is independent

    OpenAIRE

    Puliyappadamba Vineshkumar T; Cheriyan Vino T; Thulasidasan Arun Kumar T; Bava Smitha V; Vinod Balachandran S; Prabhu Priya R; Varghese Ranji; Bevin Arathy; Venugopal Shalini; Anto Ruby

    2010-01-01

    Abstract Background Lung cancer is the most lethal cancer and almost 90% of lung cancer is due to cigarette smoking. Even though nicotine, one of the major ingredients of cigarette smoke and the causative agent for addiction, is not a carcinogen by itself, several investigators have shown that nicotine can induce cell proliferation and angiogenesis. We observed that the proliferative index of nicotine is different in the lung cancer cell lines H1299 (p53-/-) and A549 (p53+/+) which indicates ...

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

    International Nuclear Information System (INIS)

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

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

    International Nuclear Information System (INIS)

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

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

    International Nuclear Information System (INIS)

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

  4. Folate and alcohol consumption and the risk of lung cancer

    Energy Technology Data Exchange (ETDEWEB)

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

    1991-03-11

    Because both folate deficiency and alcohol intake have been hypothesized to be lung cancer risk factors, the authors examined the effect of folate and alcohol consumption on risk of lung cancer in a case-control study conducted 1980-1984. Usual dietary intake of 450 histologically confirmed lung cancer cases and 902 controls, all Western New York residents, was ascertained using a modified food frequency questionnaire. Folate intake was not associated with lung cancer risk. After adjusting for age, cigarette smoking, education, and carotene intake, the odds ratio (OR) for the highest category of folate intake was 1.59 in males and 1.34 in females. There was some indication of a protective effect of folate only among women who never smoked. There was a suggestion of a positive association of alcohol intake with lung cancer risk in males, independent of age, education, cigarette smoking, and carotene. Consumers of more than 9 beers per month had an OR of 1.51 compared to non-drinkers. In both sexes, there was an indication of an interaction between beer ingestion and cigarette smoking. While folate intake did not appear to affect risk of lung cancer, the association of alcohol intake with risk independent of cigarette smoking deserves further inquiry.

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

    OpenAIRE

    Anderson, Stacey J

    2010-01-01

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

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

    OpenAIRE

    Ahmed, Sadeq Mohamed; Vaziri, Kamran

    2014-01-01

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

  7. Public opinion regarding earmarked cigarette tax in Taiwan

    OpenAIRE

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

    2003-01-01

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

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

    OpenAIRE

    Farsalinos, Konstantinos E; Polosa, Riccardo

    2014-01-01

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

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

    Science.gov (United States)

    Cobb, Nathan K; Sonti, Rajiv

    2016-08-01

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

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

    Science.gov (United States)

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

    2015-02-01

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

  11. Chronic smoker lung dosimetry of radon progeny

    International Nuclear Information System (INIS)

    The purpose of this study is to determine how cigarette smoking affects the dose of radon progeny in the lungs. An extensive survey of the medical literature suggests that about six physiological parameters may influence deposition as well as clearance of radon progeny and thus, affecting the resulting doses received by sensitive bronchial target cells. The calculations reflect a difference between the dose of a nonsmoker lung and the lung of the heavy long-term smoker, of a multiplicative factor 1,8. (authors)

  12. Lung Emergencies

    Science.gov (United States)

    ... Emergencies Cardiac Emergencies Eye Emergencies Lung Emergencies Surgeries Lung Emergencies People with Marfan syndrome can be at ... should be considered an emergency. Symptoms of sudden lung collapse (pneumothorax) Symptoms of a sudden lung collapse ...

  13. Lung metastases

    Science.gov (United States)

    Metastases to the lung; Metastatic cancer to the lung ... Metastatic tumors in the lungs are cancers that developed at other places in the body (or other parts of the lungs) and spread through the ...

  14. E-cigarettes and E-hookahs

    Science.gov (United States)

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

  15. Oxidative Stress and Exhaled Breath Analysis: A Promising Tool for Detection of Lung Cancer

    OpenAIRE

    Thomas, Paul S.; Craig Lewis; Hiang Ping Chan

    2010-01-01

    Lung cancer is one of the few neoplasia in which the principal aetiology is known, with cigarette smoke donating a considerable oxidative burden to the lungs. This may be part of the aetiology of lung cancer, but the neoplastic process is also associated with increased oxidative stress. Nonetheless, it is difficult to study the mechanisms behind the induction of lung cancer in smokers, but newer techniques of breath analysis targeting markers of oxidative stress and anti-oxidant capacity show...

  16. Cigarette smuggling in Europe: who really benefits?

    OpenAIRE

    Joossens, L.; Raw, M.

    1998-01-01

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

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

    OpenAIRE

    Escudero Diaz, Paula

    2016-01-01

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

  18. Nicotine and the Developing Human: A Neglected Element in the Electronic Cigarette Debate.

    Science.gov (United States)

    England, Lucinda J; Bunnell, Rebecca E; Pechacek, Terry F; Tong, Van T; McAfee, Tim A

    2015-08-01

    The elimination of cigarettes and other combusted tobacco products in the U.S. would prevent tens of millions of tobacco-related deaths. It has been suggested that the introduction of less harmful nicotine delivery devices, such as electronic cigarettes or other electronic nicotine delivery systems, will accelerate progress toward ending combustible cigarette use. However, careful consideration of the potential adverse health effects from nicotine itself is often absent from public health debates. Human and animal data support that nicotine exposure during periods of developmental vulnerability (fetal through adolescent stages) has multiple adverse health consequences, including impaired fetal brain and lung development, and altered development of cerebral cortex and hippocampus in adolescents. Measures to protect the health of pregnant women and children are needed and could include (1) strong prohibitions on marketing that increase youth uptake; (2) youth access laws similar to those in effect for other tobacco products; (3) appropriate health warnings for vulnerable populations; (4) packaging to prevent accidental poisonings; (5) protection of non-users from exposure to secondhand electronic cigarette aerosol; (6) pricing that helps minimize youth initiation and use; (7) regulations to reduce product addiction potential and appeal for youth; and (8) the age of legal sale. PMID:25794473

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

    Science.gov (United States)

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

    2007-02-01

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

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

    Directory of Open Access Journals (Sweden)

    Lee Jie-Min

    2007-06-01

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

  1. Cigarette purchasing behaviors when prices are high.

    Science.gov (United States)

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

    2004-01-01

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

  2. Beta-cryptoxanthin restores nicotine-reduced lung SIRT1 to normal levels and inhibits nicotine-promoted lung tumorigenesis and emphysema in A/J mice

    Science.gov (United States)

    Nicotine, a large constituent of cigarette smoke, is associated with an increased risk of lung cancer, but the data supporting this relationship are inconsistent. Here, we found that nicotine treatment not only induced emphysema but also increased both lung tumor multiplicity and volume in 4-nitrosa...

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

    Science.gov (United States)

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

    2016-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Ye Chun-Yuan

    2004-12-01

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

  5. Testing of human papillomavirus in lung cancer and non-tumor lung tissue

    International Nuclear Information System (INIS)

    Risk factors for lung cancer, such as cigarette smoking, environmental pollution, asbestos, and genetic determinants, are well-known, whereas involvement of the human papillomavirus (HPV) is still unclear. We examined a series of 100 lung cancer patients from Italy and the UK for the presence of HPV DNA in both lung tumor specimens and adjacent non-tumoral specimens from the same patients. Thirty-five of the most clinically relevant HPV types were assayed using PCR amplification of the highly conserved L1 region of the viral genome followed by hybridization with specific probes. No HPV was detected in tumor specimens nor in normal lung tissue of any patient. These data indicate that, in this Western series, HPV is not associated with the risk of lung cancer. Our findings will help refine estimates of lung cancer risk in patients affected by a common viral infection involved in other types of human cancer

  6. Electronic cigarette use outcome expectancies among college students

    Science.gov (United States)

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

    2016-01-01

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

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

    OpenAIRE

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

    2008-01-01

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

  8. Shelter and indoor air in the twenty-first century: Radon, smoking and lung cancer risks

    International Nuclear Information System (INIS)

    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

  9. Lung cancer induced in hamsters by low doses of alpha radiation from 210Po

    International Nuclear Information System (INIS)

    Lung cancers have been induced in 9 to 53 percent of hamsters given multiple intratracheal instillations of polonium-210 in amounts yielding lifetime exposures of 15 to 300 rads to the lungs. Cigarette smokers have previously been estimated to receive 20 rads to areas of the bronchial epithelium from deposited polonium-210. This finding thus supports the hypothesis that alpha radiation resulting from the polonium-210 or lead-210 present in cigarette smoke may be a significant causative factor in human lung cancer. (U.S.)

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

    International Nuclear Information System (INIS)

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

  11. Analysis of complex mixtures--cigarette smoke.

    Science.gov (United States)

    Borgerding, Michael; Klus, Hubert

    2005-07-01

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

  12. Naloxone does not affect cigarette smoking.

    Science.gov (United States)

    Nemeth-Coslett, R; Griffiths, R R

    1986-01-01

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

  13. Alpha-1 Antitrypsin and Lung Cell Apoptosis.

    Science.gov (United States)

    Serban, Karina A; Petrache, Irina

    2016-04-01

    Discovery of alpha-1 antitrypsin (A1AT) as the principal circulating inhibitor of neutrophil elastase was critical to the appreciation of protease/antiprotease imbalance involvement in the pathogenesis of emphysema. Additional targets of A1AT have been uncovered, along with their contribution to alveolar wall destruction induced by cigarette smoke exposure. We highlight in this report mechanisms of A1AT antiapoptotic effects on structural lung endothelial cells. This function was largely dependent on uptake of the protein from the circulation via clathrin- and, in part, caveolae-mediated endocytosis and on specific interactions with cysteine proteases such as capsase-3, -6, and -7. Exposures to cigarette smoke diminished A1AT intracellular uptake and its anticaspase action, suggesting that even in A1AT-suficient individuals, cigarette smoke may weaken the serpin's endothelial prosurvival effect. In addition, cigarette smoke exposure or genetic mutations known to induce posttranslational modifications such as oxidation or polymerization may alter A1AT bidirectional intracellular traffic in endothelial cells and thus determine its functional bioavailability in certain lung compartments. Uncovering and harnessing the A1AT canonical and noncanonical mechanisms will advance our understanding of the pathogenesis of emphysema and may provide means to improve the effectiveness of therapies in both A1AT-sufficient and A1AT-deficient individuals. PMID:27115949

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

    Science.gov (United States)

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

    2016-02-01

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

  15. Trends in Lung Cancer Incidence Rates, Oklahoma 2005–2010

    OpenAIRE

    Mowls, Dana S.; McCaffree, D. Robert; Beebe, Laura A.

    2015-01-01

    Purpose Lung cancer is the second most frequently diagnosed cancer among men and women in the United States. With cigarette smoking causing the majority of cases, patterns in lung cancer are often monitored to understand the impact of anti-tobacco efforts. The purpose of this research was to investigate trends in lung cancer incidence rates for the period 2005–2010 in Oklahoma. Methods Data on Oklahoma’s incident cases of lung cancer (2005–2010) were obtained from the Centers for Disease Cont...

  16. E-Cigarettes a Gateway to Smoking for Teens

    Science.gov (United States)

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

  17. E-Cigarette Poisonings Skyrocket Among Young Kids

    Science.gov (United States)

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

  18. E-Cigarettes a Gateway to Smoking for Teens

    Science.gov (United States)

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

  19. Doctors Divided on Safety, Use of Electronic Cigarettes

    Science.gov (United States)

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

  20. E-Cigarette Poisonings Skyrocket Among Young Kids

    Science.gov (United States)

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

  1. Teen Smoking Down, E-Cigarette Use Up

    Science.gov (United States)

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

  2. 15q12 Variants, Sputum Gene Promoter Hypermethylation, and Lung Cancer Risk: A GWAS in Smokers

    Science.gov (United States)

    Leng, Shuguang; Liu, Yushi; Weissfeld, Joel L.; Thomas, Cynthia L.; Han, Younghun; Picchi, Maria A.; Edlund, Christopher K.; Willink, Randall P.; Gaither Davis, Autumn L.; Do, Kieu C.; Nukui, Tomoko; Zhang, Xiequn; Burki, Elizabeth A.; Van Den Berg, David; Romkes, Marjorie; Gauderman, W. James; Crowell, Richard E.; Tesfaigzi, Yohannes; Stidley, Christine A.; Amos, Christopher I.; Siegfried, Jill M.; Gilliland, Frank D.

    2015-01-01

    Background: Lung cancer is the leading cause of cancer-related mortality worldwide. Detection of promoter hypermethylation of tumor suppressor genes in exfoliated cells from the lung provides an assessment of field cancerization that in turn predicts lung cancer. The identification of genetic determinants for this validated cancer biomarker should provide novel insights into mechanisms underlying epigenetic reprogramming during lung carcinogenesis. Methods: A genome-wide association study using generalized estimating equations and logistic regression models was conducted in two geographically independent smoker cohorts to identify loci affecting the propensity for cancer-related gene methylation that was assessed by a 12-gene panel interrogated in sputum. All statistical tests were two-sided. Results: Two single nucleotide polymorphisms (SNPs) at 15q12 (rs73371737 and rs7179575) that drove gene methylation were discovered and replicated with rs73371737 reaching genome-wide significance (P = 3.3×10–8). A haplotype carrying risk alleles from the two 15q12 SNPs conferred 57% increased risk for gene methylation (P = 2.5×10–9). Rs73371737 reduced GABRB3 expression in lung cells and increased risk for smoking-induced chronic mucous hypersecretion. Furthermore, subjects with variant homozygote of rs73371737 had a two-fold increase in risk for lung cancer (P = .0043). Pathway analysis identified DNA double-strand break repair by homologous recombination (DSBR-HR) as a major pathway affecting susceptibility for gene methylation that was validated by measuring chromatid breaks in lymphocytes challenged by bleomycin. Conclusions: A functional 15q12 variant was identified as a risk factor for gene methylation and lung cancer. The associations could be mediated by GABAergic signaling that drives the smoking-induced mucous cell metaplasia. Our findings also substantiate DSBR-HR as a critical pathway driving epigenetic gene silencing. PMID:25713168

  3. Biological effects of inhaled cigarette smoke in beagle dogs

    International Nuclear Information System (INIS)

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

  4. Tobacco and cigarette butt consumption in humans and animals

    OpenAIRE

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

    2011-01-01

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

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

    Science.gov (United States)

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

    2016-12-01

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

  6. Another Risk From Cigarette Smoking: Corneal Burn

    Directory of Open Access Journals (Sweden)

    Volkan Hürmeriç

    2012-12-01

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

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

    Science.gov (United States)

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

    2000-01-01

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

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

    Science.gov (United States)

    Warner, K E

    1985-02-01

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

  9. Collapsed Lung

    Science.gov (United States)

    A collapsed lung happens when air enters the pleural space, the area between the lung and the chest wall. If it is a ... is called pneumothorax. If only part of the lung is affected, it is called atelectasis. Causes of ...

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

    OpenAIRE

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

    2014-01-01

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

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

    OpenAIRE

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

    2005-01-01

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

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

    OpenAIRE

    Adioetomo, Sri Moertiningsih; Djutaharta, Triasih; Hendratno

    2005-01-01

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

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

    Science.gov (United States)

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

    2011-01-01

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

  14. 75 FR 69523 - Required Warnings for Cigarette Packages and Advertisements

    Science.gov (United States)

    2010-11-12

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

  15. Family History of Lung Cancer and Contemplation of Smoking Cessation

    OpenAIRE

    Madlensky, Lisa; Bousman, Chad A.

    2010-01-01

    Introduction The prevalence of cigarette smoking in the United States has decreased, but current rates remain above nationally set objectives. A family history of lung cancer may motivate adult smokers to quit and contribute to further reductions in smoking prevalence. Methods We surveyed adult smokers (N = 838) interviewed as part of the 2005 Health Information National Trends Survey. We examined the association between family history of lung cancer and smoking cessation precontemplation (no...

  16. Can Higher Cigarette Taxes Improve Birth Outcomes?

    OpenAIRE

    Evans, William N.; Ringel, Jeanne S

    1997-01-01

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

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

    OpenAIRE

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

    2012-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Venkatachalem Sathish

    2015-06-01

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

  19. Incidence and etiology of lung cancer in the Pacific Basin.

    Science.gov (United States)

    Hirohata, T; Fukuda, K

    1979-11-01

    Incidence of lung cancer in the Pacific Basin was either compiled from published reports or computed by the authors. The results showed a great variation in age-standardized annual incidence rates of lung cancer among 10 countries and 17 areas in the Pacific Basin where tumor registry statistics are available. For males the incidence rates ranged from 10 to over 70 and for females from less than 5 to over 30/100,000 population. The reason(s) for the great variation is unclear. Ionizing radiation, carcinogenic chemical substances (e.g., chromium, arsenic compounds, asbestos, etc.), or air pollution are unlikely to be responsible. Because cigarette smoking is known to be a major cause of lung cancer, the authors have suggested that surveys on cigarette smoking be conducted among various populations in the Pacific Basin so that etiologic significance of cigarette smoking for the noted variation can be assessed. In Hawaii such a survey is underway, and a preliminary analysis was made to examine the association between lung cancer and cigarette smoking among five races. PMID:537621

  20. The Alteration and Significance of Surfactant Protein A in Rats Chronically Exposed to Cigarette Smoke

    Institute of Scientific and Technical Information of China (English)

    Qiongjie HU; Huilan ZHANG; Shengdao XIONG; Xuemei SHI; Yongjian XU; Zhenxiang ZHANG; Guohua ZHEN; Jianping ZHAO

    2008-01-01

    In order to confirm the alteration and significance of cigarette smoke exposure on SP-A in rats, 20 Wistar rats were assigned randomly to two groups: an N group (n=10), and an S group (n=10). The ultra-structural change was observed by electron microscopy. The number of cells positive for SPA was by immunohistochemically measured. The mRNA expression in the lung tissues was deter-mined by reverse transcription polymerase chain reaction (RT-PCR). The number of cells positive for SPA of the S group (0.52±0.05) was lower than that of the N group (0.72±0.06) (P<0.05). The lev-els of mRNA of SPA in the lung tissues of the S group (0.3522±0.0512) was significantly lower than that of the N group (0.4432±0.05628) (P<0.05). It is concluded that cigarette smoke alone decreased the level of SP-A and that might have an important effect on surfactant metabolism and the host deense functions of surfactant in the peripheral airways, which might play a crucial role in the devel-opment of chronic obstructive lung disease.

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

    Directory of Open Access Journals (Sweden)

    Postma Dirkje S

    2007-07-01

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

  2. Effect of Trace and Toxic Elements of Different Brands of Cigarettes on the Essential Elemental Status of Irish Referent and Diabetic Mellitus Consumers.

    Science.gov (United States)

    Afridi, Hassan Imran; Talpur, Farah Naz; Kazi, Tasneem Gul; Brabazon, Dermot

    2015-10-01

    Cigarette smoking interferes with the metal homeostasis of the human body, which plays a crucial role for maintaining the health. A significant flux of heavy metals, among other toxins, reaches the lungs through smoking. In the present study, the relationship between toxic element (TE) exposure via cigarette smoking and diabetic mellitus incidence in population living in Dublin, Ireland is investigated. The trace [zinc (Zn) and selenium (Se)] and toxic elements arsenic (As), aluminum (Al), cadmium (Cd), nickel (Ni), mercury (Hg), and lead (Pb) were determined in biological (scalp hair and blood) samples of patients diagnosed with diabetic mellitus, who are smokers living in Dublin, Ireland. These results were compared with age- and sex-matched healthy, nonsmokers controls. The different brands of cigarette (filler tobacco, filter, and ash) consumed by the studied population were also analyzed for As, Al, Cd, Ni, Hg, and Pb. The concentrations of TEs in biological samples and different components of cigarette were measured by inductively coupled plasma atomic emission spectrophotometer after microwave-assisted acid digestion. The validity and accuracy of the methodology were checked using certified reference materials (CRM). The recovery of all the studied elements was found to be in the range of 96.4-99.7% in certified reference materials. The filler tobacco of different branded cigarettes contains Hg, As, Al, Cd, Ni, and Pb concentrations in the ranges of 9.55-12.4 ng/cigarette, 0.432-0.727 μg/cigarette, 360-496 μg/cigarette, 1.70-2.12 μg/cigarette, 0.715-1.52 μg/cigarette, and 0.378-1.16 μg/cigarette, respectively. The results of this study showed that the mean values of Al, As, Cd, Hg, Ni, and Pb were significantly higher in scalp hair and blood samples of diabetic mellitus patients in relation to healthy controls, while the difference was significant in the case of smoker patients (p < 0.001). The levels of all six toxic elements were twofolds to

  3. Analysis of trace metals in various brands of cigarettes

    International Nuclear Information System (INIS)

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

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

    Science.gov (United States)

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

    2013-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Richard Barnes

    2009-05-01

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

  6. Role of CXCL5 in Leukocyte Recruitment to the Lungs during Secondhand Smoke Exposure

    OpenAIRE

    Balamayooran, Gayathriy; Batra, Sanjay; Cai, Shanshan; Mei, Junjie; Worthen, G. Scott; Penn, Arthur L.; Jeyaseelan, Samithamby

    2012-01-01

    Chronic obstructive pulmonary disease (COPD) is the third leading cause of mortality in the United States. The major cause of COPD is cigarette smoking. Extensive leukocyte influx into the lungs, mediated by chemokines, is a critical event leading to COPD. Although both resident and myeloid cells secrete chemokines in response to inflammatory stimuli, little is known about the role of epithelial-derived chemokines, such as CXC chemokine ligand (CXCL)5, in the pathogenesis of cigarette smoke–i...

  7. Cigarette smoking and progression in multiple sclerosis

    NARCIS (Netherlands)

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

    2007-01-01

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

  8. Role of Interleukin 17 in Lung Carcinogenesis and Lung Cancer Progression

    Directory of Open Access Journals (Sweden)

    Jiandong MEI

    2016-01-01

    Full Text Available Interleukin 17 (IL-17 is an important pro-inflammatory cytokine. It plays a critical role in mediating pathogen defense reactions, and the pathological inflammation of autoimmune diseases. IL-17 is also involved in various inflammation-related carcinogenesis. Cigarette smoking is one of the most important risk factors of lung cancer. Chronic inflammation caused by smoking and other factors is accompanied with overexpression of IL-17 within the airway, which reveals a potential relationship between IL-17 and lung carcinogenesis. Furthermore, IL-17 also plays a role in lung cancer progression via different mechanisms. In this paper, we summarized the results of current studies on IL-17 and lung carcinogenesis, as well as lung cancer progression.

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

    Science.gov (United States)

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

    2015-01-01

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

  10. Reasons for Starting and Stopping Electronic Cigarette Use

    Directory of Open Access Journals (Sweden)

    Jessica K. Pepper

    2014-10-01

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

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

    Science.gov (United States)

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

    2015-01-01

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

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

    Science.gov (United States)

    Ahern, Nancy R; Mechling, Brandy

    2014-06-01

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

  13. Asbestos and lung cancer in Glasgow and the west of Scotland.

    OpenAIRE

    De Vos Irvine, H; Lamont, D W; Hole, D J; Gillis, C R

    1993-01-01

    OBJECTIVE--To quantify the relation between lung cancer and exposure to asbestos in men in west Scotland and to estimate the proportion of lung cancer which may be attributed to exposure to asbestos. DESIGN--An ecological correlation study of the incidence of lung cancer in men and past asbestos exposure. The unit of analysis was the postcode sector. Correction was made for past cigarette smoking, air pollution, and deprivation. SETTING--The region covered by the west of Scotland cancer regis...

  14. The Role of DNA Methylation in the Development and Progression of Lung Adenocarcinoma

    OpenAIRE

    Kerr, Keith M.; Galler, Janice S; Hagen, Jeffrey A.; Laird, Peter W; Laird-Offringa, Ite A.

    2007-01-01

    Lung cancer, caused by smoking in ∼87% of cases, is the leading cause of cancer death in the United States and Western Europe. Adenocarcinoma is now the most common type of lung cancer in men and women in the United States, and the histological subtype most frequently seen in never-smokers and former smokers. The increasing frequency of adenocarcinoma, which occurs more peripherally in the lung, is thought to be at least partially related to modifications in cigarette manufacturing that have ...

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

    OpenAIRE

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

    2014-01-01

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

  16. Lung density

    DEFF Research Database (Denmark)

    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...

  17. Lung Cancer

    Science.gov (United States)

    ... spreads in different ways, and each is treated differently. Non-small cell lung cancer is more common than small cell lung cancer. Small cell lung cancer grows more quickly and is more likely to spread to other organs in the body. Learn more about non-small cell lung cancer. Learn ...

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

    OpenAIRE

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

    2005-01-01

    The effect of raising cigarette taxes to reduce smoking has been the subject of several studies, which often treat the price of cigarettes as an exogenous factor given to smokers who respond to it by adjusting their smoking behavior. However, cigarette prices vary with brand and quality, and smokers can and do switch to lower-priced brands to reduce the impact of the tax on the cost of cigarettes as they try to consume the same number of cigarettes as they had before a tax hike. Using data fr...

  19. Association between cigarette smoking and pulmonary tuberculosis

    International Nuclear Information System (INIS)

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

  20. Lung cancer in the Indian subcontinent.

    Science.gov (United States)

    Noronha, Vanita; Pinninti, Rakesh; Patil, Vijay M; Joshi, Amit; Prabhash, Kumar

    2016-01-01

    Smoking tobacco, both cigarettes and beedis, is the principal risk factor for causation of lung cancer in Indian men; however, among Indian women, the association with smoking is not strong, suggesting that there could be other risk factors besides smoking. Despite numerous advances in recent years in terms of diagnostic methods, molecular changes, and therapeutic interventions, the outcomes of the lung cancer patients remain poor; hence, a better understanding of the risk factors may impact the preventive measures to be implemented at the community level. There is a lack of comprehensive data on lung cancer in India. In this review, we attempt to collate the available data on lung cancer from India. PMID:27606290

  1. From cellular doses to average lung dose

    International Nuclear Information System (INIS)

    Sensitive basal and secretory cells receive a wide range of doses in human bronchial and bronchiolar airways. Variations of cellular doses arise from the location of target cells in the bronchial epithelium of a given airway and the asymmetry and variability of airway dimensions of the lung among airways in a given airway generation and among bronchial and bronchiolar airway generations. To derive a single value for the average lung dose which can be related to epidemiologically observed lung cancer risk, appropriate weighting scenarios have to be applied. Potential biological weighting parameters are the relative frequency of target cells, the number of progenitor cells, the contribution of dose enhancement at airway bifurcations, the promotional effect of cigarette smoking and, finally, the application of appropriate regional apportionment factors. Depending on the choice of weighting parameters, detriment-weighted average lung doses can vary by a factor of up to 4 for given radon progeny exposure conditions. (authors)

  2. Aerosol deposition doses in the human respiratory tree of electronic cigarette smokers.

    Science.gov (United States)

    Manigrasso, Maurizio; Buonanno, Giorgio; Fuoco, Fernanda Carmen; Stabile, Luca; Avino, Pasquale

    2015-01-01

    Aerosols from eight e-cigarettes at different nicotine levels and flavoring were characterized as particle number size distributions in the range 5.6-560 nm by FMPS and CPC. Results were used to provided osimetry estimates applying the MMPD model.Particle number concentrations varied between 3.26 x 10(9) and 4.09 x 10(9) part cm(-3) for e-liquids without nicotine and between 5.08 x 10(9) and 5.29 x 10(9) part cm(-3) for e-liquids with nicotine. No flavor effects were detected on particle concentration data. Particle size distributions were unimodal with modes between 107-165 nm and 165-255 nm, for number and volume metrics, respectively. Averagely, 6.25 x 10(10) particles were deposited in respiratory tree after a single puff. Highest deposition densities and mean layer thickness of e-cigarette liquid on the lung epithelium were estimated at lobar bronchi. Our study shows that e-cigarette aerosol is source of high particle dose in respiratory system, from 23%to 35% of the daily dose of a no-smoking individual. PMID:25463721

  3. Neuronal Acetylcholine Nicotinic Receptors as New Targets for Lung Cancer Treatment.

    Science.gov (United States)

    Mucchietto, Vanessa; Crespi, Arianna; Fasoli, Francesca; Clementi, Francesco; Gotti, Cecilia

    2016-01-01

    Lung cancer is the leading cause of cancer-related deaths worldwide. Smoking accounts for approximately 70% of the cases of non- small cell lung cancer (NSCLC) and 90% of the cases of small-cell lung cancer (SCLC), although some patients develop lung cancer without a history of smoking. Nicotine is the most active addictive component of tobacco smoke. It does not initiate tumorigenesis in humans and rodents, but it alters the pathophysiology of lung cells by inducing the secretion of growth factors, neurotransmitters and cytokines, and promotes tumour growth and metastases by inducing cell cycle progression, migration, invasion, angiogenesis and the evasion of apoptosis. Most of these effects are a result of nicotine binding and activation of cell-surface neuronal nicotinic acetylcholine receptors (nAChRs) and downstream intracellular signalling cascades, and many are blocked by nAChR subtype-selective antagonists. Recent genome-wide association studies have revealed single nucleotide polymorphisms of nAChR subunits that influence nicotine dependence and lung cancer. This review describes the molecular basis of nAChR structural and functional diversity in normal and cancer lung cells, and the genetic alterations facilitating smoking-induced lung cancers. It also summarises current knowledge concerning the intracellular pathways activated by nicotine and other compounds present in tobacco smoke. PMID:26845123

  4. Controlling the level of radioactivity of cigarettes sold in Kinshasa: Case Tumbaco light and Embassy

    International Nuclear Information System (INIS)

    At the anti-smoking, which continues to grow now in the world with positive results on the chemical vectors: tar and nicotine, as we know the harm in North America and Europe, nowadays, radioactivity is added. This second vector radiation-induced lung cancer, radon is hazardous and radioactive daughters 210Pb and 210Po that Big Tobacco had hid the truth for 40 years. The surgeon C. Everett Ko op, a pioneer of Modern Pediatrics (Philadelphia, USA) showed that the radioactivity found in many tobacco 210Po, and that rather than derivatives of tar and nicotine, account for 90% of all lung cancers of smokers recounted. These assertions have prompted the current authors to control the level of alpha and beta radioactivity in cigarettes Tumbaco Embassy and light manufactured by Tabac Congo. These products are commonly consumed in the Democratic Republic of the Congo, particularly in the city of Kinshasa. Following this study, we present quantitative data related to lead the health authorities of the Democratic Republic of Congo to take necessary measures or to enact laws prohibiting smoking in public places and for monitoring production these cigarettes. Thus, the mean mass activities for gross alpha and beta measured for the cigarette lighter Tumbaco and Embassy appear respectively as follows: 11.32Bq/kg and 7.08Bq/kg for alpha cons 38.34Bq/kg and 29.5Bq/kg (Table 10). In addition, the estimated average effective dose for an annual consumption of cigarettes one pack per year worth 0.0726 mSv/ year (0.05 mSv/ hour) and light Tumbaco 0.04574 mSv/ year (0.02μSv/hour) for Embassy. These values are lower than the hourly limit or permissible annual dose for members of the public (or 1mSv/an 0.5μSv/hour) following radiation protection standards of the international Commission on Radiological Protection (ICRP 60, 1990). This means that these dose rates are below the threshold for non-stochastic effects, and these limits do not apply to stochastic or random effects (Tables 11

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

    Science.gov (United States)

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

    2016-01-01

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

  6. Epidemiologic studies of lung disease among miners exposed to increased levels of radon daughters

    International Nuclear Information System (INIS)

    The mortality of uranium miners from both lung cancer and other respiratory diseases is strongly dependent on exposure to radon daughters, cigarette smoking, and height. Lung cancer among 15 different mining groups was analyzed to determine what factors influence incidence and the induction-latent period. At low exposures or at low exposure rates, alpha radiation is more efficient in inducing lung cancer, producing an upward convex exposure-response curve. The induction-latent period is shortened by an increased age at the start of mining, by cigarette smoking, and by high exposure rates. For follow-up periods of 20 to 25 years, the incidence increases with age at the start of mining, with the magnitude of exposure, and with the amount of cigarette smoking. Instead of extrapolating downward from high exposures to estimate risk at low levels, it might be more appropriate to use cancer rates associated with background radiation as the lowest point on the exposure-response curve

  7. Role of Interleukin 17 in Lung Carcinogenesis and Lung Cancer Progression

    OpenAIRE

    Mei, Jiandong; Liu, Lunxu

    2016-01-01

    Interleukin 17 (IL-17) is an important pro-inflammatory cytokine. It plays a critical role in mediating pathogen defense reactions, and the pathological inflammation of autoimmune diseases. IL-17 is also involved in various inflammation-related carcinogenesis. Cigarette smoking is one of the most important risk factors of lung cancer. Chronic inflammation caused by smoking and other factors is accompanied with overexpression of IL-17 within the airway, which reveals a potential relationship b...

  8. Uranium mining and lung cancer in Navajo men

    International Nuclear Information System (INIS)

    We performed a population-based case-control study to examine the association between uranium mining and lung cancer in Navajo men, a predominantly nonsmoking population. The 32 cases included all those occurring among Navajo men between 1969 and 1982, as ascertained by the New Mexico Tumor Registry. For each case in a Navajo man, two controls with nonrespiratory cancer were selected. Of the 32 Navajo patients, 72 per cent had been employed as uranium miners, whereas no controls had documented experience in this industry. The lower 95 per cent confidence limit for the relative risk of lung cancer associated with uranium mining was 14.4. Information on cigarette smoking was available for 21 of the 23 affected uranium miners; eight were nonsmokers and median consumption by the remainder was one to three cigarettes daily. These results demonstrate that in a rural nonsmoking population most of the lung cancer may be attributable to one hazardous occupation

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

    Directory of Open Access Journals (Sweden)

    Maria Schulz

    2016-04-01

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

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

    Science.gov (United States)

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

    2016-01-01

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

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

    Directory of Open Access Journals (Sweden)

    Marianne Lund

    2015-01-01

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

  12. Evaluation of E-Cigarette Liquid Vapor and Mainstream Cigarette Smoke after Direct Exposure of Primary Human Bronchial Epithelial Cells

    Directory of Open Access Journals (Sweden)

    Stefanie Scheffler

    2015-04-01

    Full Text Available E-cigarettes are emerging products, often described as “reduced-risk” nicotine products or alternatives to combustible cigarettes. Many smokers switch to e-cigarettes to quit or significantly reduce smoking. However, no regulations for e-cigarettes are currently into force, so that the quality and safety of e-liquids is not necessarily guaranteed. We exposed primary human bronchial epithelial cells of two different donors to vapor of e-cigarette liquid with or without nicotine, vapor of the carrier substances propylene glycol and glycerol as well as to mainstream smoke of K3R4F research cigarettes. The exposure was done in a CULTEX® RFS compact  module, allowing the exposure of the cells at the air-liquid interface. 24 h post-exposure, cell viability and oxidative stress levels in the cells were analyzed. We found toxicological effects of e-cigarette vapor and the pure carrier substances, whereas the nicotine concentration did not have an effect on the cell viability. The viability of mainstream smoke cigarette exposed cells was 4.5–8 times lower and the oxidative stress levels 4.5–5 times higher than those of e-cigarette vapor exposed cells, depending on the donor. Our experimental setup delivered reproducible data and thus provides the opportunity for routine testing of e-cigarette liquids to ensure safety and quality for the user.

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

    Science.gov (United States)

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

    2005-06-01

    The effect of raising cigarette taxes to reduce smoking has been the subject of several studies, which often treat the price of cigarettes as an exogenous factor given to smokers who respond to it by adjusting their smoking behavior. However, cigarette prices vary with brand and quality, and smokers can and do switch to lower-priced brands to reduce the impact of the tax on the cost of cigarettes as they try to consume the same number of cigarettes as they had before a tax hike. Using data from a two-year follow-up interview survey conducted before and after a new cigarette tax scheme was imposed in Taiwan in 2002, this study examines three behavioral changes smokers may make to respond to tax-induced cigarette price increase: brand-switching, amount consumed, and amount spent on smoking. These changes were studied in relation to smoker income, before-tax cigarette price, level of addiction, exposure to advertizing, and consumer loyalty. We found that smokers, depending upon exposure to advertizing, level of consumer loyalty and initial price of cigarettes, switched brands to maintain current smoking habits and control costs. We also found that the initial amount smoked and level of addiction, not price, at least not at the current levels in Taiwan, determined whether a smoker reduced the number of cigarettes he consumed. PMID:15791675

  14. H2180 - cigarette smoke gas phase interaction

    International Nuclear Information System (INIS)

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

  15. Cigarette Cravings, Impulsivity, and the Brain.

    Science.gov (United States)

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

    2015-01-01

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

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

    Science.gov (United States)

    Etter, J F; Cornuz, J

    2009-07-01

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

  17. Cigarette cravings, impulsivity and the brain

    Directory of Open Access Journals (Sweden)

    Stéphane Potvin

    2015-09-01

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

  18. Longitudinal Trajectories of Cigarette Smoking Following Rape

    OpenAIRE

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

    2009-01-01

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

  19. Efficient Excise Taxation: The Evidence from Cigarettes.

    OpenAIRE

    Benjamin, Daniel K; William R. Dougan

    1997-01-01

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

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

    Science.gov (United States)

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

    2009-02-01

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

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

    International Nuclear Information System (INIS)

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

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

    Directory of Open Access Journals (Sweden)

    Rahman Irfan

    2009-05-01

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

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

    International Nuclear Information System (INIS)

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2009-07-01

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

  5. Exploring Cigarette Use among Male Migrant Workers in Nigeria

    Directory of Open Access Journals (Sweden)

    Olanrewaju Olusola Onigbogi

    2015-04-01

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

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

    Science.gov (United States)

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

    2010-04-01

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

  7. Electronic cigarettes: a survey of users

    Directory of Open Access Journals (Sweden)

    Etter Jean-François

    2010-05-01

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

  8. Cigarette package design: opportunities for disease prevention

    Directory of Open Access Journals (Sweden)

    Pollay RW

    2003-01-01

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

  9. [Respiratory bronchiolitis-associated interstitial lung disease (RB-ILD)].

    Science.gov (United States)

    Goeckenjan, G

    2003-05-01

    prognosis. After smoking cessation lung changes are reversible. Corticosteroid therapy is not necessary. A fatal outcome of RB-ILD has not been reported. Follow-up examinations are advisable in order to preclude other interstitial lung diseases. RB-ILD seems to be more frequent than it is assumed at present. The clinical picture is masked in most cases by the concomitant smoking induced chronic bronchitis. Thus only pronounced cases with structural changes and resulting differential diagnostic problems are diagnosed. PMID:12784181

  10. Lung transplant

    Science.gov (United States)

    ... lung transplants are done at the same time (heart-lung transplant) if the heart is also diseased. ... people develop cancers or have problems with the heart. For most ... transplant. They have better exercise endurance and are able ...

  11. Lung transplant

    Science.gov (United States)

    ... diseases that may require a lung transplant are: Cystic fibrosis Damage to the arteries of the lung because ... BC; Clinical Practice Guidelines for Pulmonary Therapies Committee; Cystic Fibrosis Foundation Pulmonary Therapies Committee. Cystic fibrosis pulmonary guidelines: ...

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

    OpenAIRE

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

    2005-01-01

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

  13. Temperature distribution in a cigarette oven during baking

    OpenAIRE

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

    2015-01-01

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

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

    OpenAIRE

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

    2015-01-01

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

  15. Cigarette Smoking and Brain Regulation of Energy Homeostasis

    OpenAIRE

    HuiChen; SoniaSaad; ShaunSandow

    2012-01-01

    Cigarette smoking is an addictive behavior, and is the primary cause of cardiovascular and pulmonary disease, and cancer (among other diseases). Cigarette smoke contains thousands of components that may affect caloric intake and energy expenditure, although nicotine is the major addictive substance present, and has the best described actions. Nicotine exposure from cigarette smoke can change brain feeding regulation to reduce appetite via both energy homeostatic and reward mechanisms, causing...

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

    OpenAIRE

    Etter, Jean-François

    2015-01-01

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

  17. Recent Advances in Cigarette Ignition Propensity Research and Development

    OpenAIRE

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

    2010-01-01

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

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

    OpenAIRE

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

    2014-01-01

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

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

    OpenAIRE

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

    2015-01-01

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

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

    International Nuclear Information System (INIS)

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

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

    International Nuclear Information System (INIS)

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

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

    Energy Technology Data Exchange (ETDEWEB)

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

    2014-10-24

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

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

    Science.gov (United States)

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

    2015-09-01

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

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

    DEFF Research Database (Denmark)

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

    2013-01-01

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

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

    Centers for Disease Control (CDC) Podcasts

    2016-01-05

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

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

    Centers for Disease Control (CDC) Podcasts

    2016-01-05

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

  7. Lung scintigraphy

    International Nuclear Information System (INIS)

    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

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

    Science.gov (United States)

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

    2016-06-01

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

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

    OpenAIRE

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

    2015-01-01

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

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

    Science.gov (United States)

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

    2015-12-01

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

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

    OpenAIRE

    New York State Department of Health; ,

    2006-01-01

    Executive Summary Raising the price of cigarettes is one of the most effective interventions to prevent and reduce cigarette use. Local, state, and federal governments can change the price of cigarettes by raising or lowering cigarette excise taxes and by implementing and enforcing minimum price laws. Smokers can also adjust their behavior by choosing discount or “bargain” brands, buying fewer cigarettes, and avoiding paying cigarette taxes by purchasing from retailers that do not le...

  12. E-Cigarette Prevalence and Correlates of Use among Adolescents versus Adults: A Review and Comparison

    OpenAIRE

    Chapman, Shawna L. Carroll; Wu, Li-Tzy

    2014-01-01

    Perceived safer than tobacco cigarettes, prevalence of electronic cigarette (e-cigarette) use is increasing. Analyses of cartridges suggest that e-cigarettes may pose health risks. In light of increased use and the potential for consequences, we searched Google Scholar and Pubmed in July of 2013 using keywords, such as e-cigarette and vaping, to compare differences and similarities in prevalence and correlates of e-cigarette use among adolescents (grades 6-12) versus adults (aged ≥18 years). ...

  13. Protective effects of anisodamine on cigarette smoke extract-induced airway smooth muscle cell proliferation and tracheal contractility

    International Nuclear Information System (INIS)

    Anisodamine, an antagonist of muscarinic acetylcholine receptors (mAChRs), has been used therapeutically to improve smooth muscle function, including microvascular, intestinal and airway spasms. Our previous studies have revealed that airway hyper-reactivity could be prevented by anisodamine. However, whether anisodamine prevents smoking-induced airway smooth muscle (ASM) cell proliferation remained unclear. In this study, a primary culture of rat ASM cells was used to evaluate an ASM phenotype through the ability of the cells to proliferate and express contractile proteins in response to cigarette smoke extract (CSE) and intervention of anisodamine. Our results showed that CSE resulted in an increase in cyclin D1 expression concomitant with the G0/G1-to-S phase transition, and high expression of M2 and M3. Functional studies showed that tracheal hyper-contractility accompanied contractile marker α-SMA high-expression. These changes, which occur only after CSE stimulation, were prevented and reversed by anisodamine, and CSE-induced cyclin D1 expression was significantly inhibited by anisodamine and the specific inhibitor U0126, BAY11-7082 and LY294002. Thus, we concluded that the protective and reversal effects and mechanism of anisodamine on CSE-induced events might involve, at least partially, the ERK, Akt and NF-κB signaling pathways associated with cyclin D1 via mAChRs. Our study validated that anisodamine intervention on ASM cells may contribute to anti-remodeling properties other than bronchodilation. -- Highlights: ► CSE induces tracheal cell proliferation, hyper-contractility and α-SMA expression. ► Anisodamine reverses CSE-induced tracheal hyper-contractility and cell proliferation. ► ERK, PI3K, and NF-κB pathways and cyclin D1 contribute to the reversal effect.

  14. Protective effects of anisodamine on cigarette smoke extract-induced airway smooth muscle cell proliferation and tracheal contractility

    Energy Technology Data Exchange (ETDEWEB)

    Xu, Guang-Ni; Yang, Kai; Xu, Zu-Peng; Zhu, Liang; Hou, Li-Na; Qi, Hong; Chen, Hong-Zhuan, E-mail: hongzhuan_chen@hotmail.com; Cui, Yong-Yao, E-mail: yongyaocui@yahoo.com.cn

    2012-07-01

    Anisodamine, an antagonist of muscarinic acetylcholine receptors (mAChRs), has been used therapeutically to improve smooth muscle function, including microvascular, intestinal and airway spasms. Our previous studies have revealed that airway hyper-reactivity could be prevented by anisodamine. However, whether anisodamine prevents smoking-induced airway smooth muscle (ASM) cell proliferation remained unclear. In this study, a primary culture of rat ASM cells was used to evaluate an ASM phenotype through the ability of the cells to proliferate and express contractile proteins in response to cigarette smoke extract (CSE) and intervention of anisodamine. Our results showed that CSE resulted in an increase in cyclin D1 expression concomitant with the G0/G1-to-S phase transition, and high expression of M2 and M3. Functional studies showed that tracheal hyper-contractility accompanied contractile marker α-SMA high-expression. These changes, which occur only after CSE stimulation, were prevented and reversed by anisodamine, and CSE-induced cyclin D1 expression was significantly inhibited by anisodamine and the specific inhibitor U0126, BAY11-7082 and LY294002. Thus, we concluded that the protective and reversal effects and mechanism of anisodamine on CSE-induced events might involve, at least partially, the ERK, Akt and NF-κB signaling pathways associated with cyclin D1 via mAChRs. Our study validated that anisodamine intervention on ASM cells may contribute to anti-remodeling properties other than bronchodilation. -- Highlights: ► CSE induces tracheal cell proliferation, hyper-contractility and α-SMA expression. ► Anisodamine reverses CSE-induced tracheal hyper-contractility and cell proliferation. ► ERK, PI3K, and NF-κB pathways and cyclin D1 contribute to the reversal effect.

  15. Lung function

    Institute of Scientific and Technical Information of China (English)

    2005-01-01

    2005200 The effect of body position changes on lung function, lung CT imaging and pathology in an oleic acid induced acute lung injury model. JI Xin-ping (戢新平), et al. Dept Emergency, 1st Affili Hosp, China Med Univ, Shenyang 110001. Chin J Tuberc Respir Dis, 2005;28(1) :33-36. Objective: To study the effect of body position changes on lung mechanics, oxygenation, CT images and pathology in an oleic acid-induced acute lung injury (ALl) model. Methods: The study groups con-

  16. Diet and obstructive lung diseases.

    Science.gov (United States)

    Romieu, I; Trenga, C

    2001-01-01

    The results presented in this review suggest that the impact of nutrition on obstructive lung disease is most evident for antioxidant vitamins, particularly vitamin C and, to a lesser extent, vitamin E. By decreasing oxidant insults to the lung, antioxidants could modulate the development of chronic lung diseases and lung function decrement. Antioxidant vitamins could also play an important role in gene-environment interactions in complex lung diseases such as childhood asthma. Data also suggest that omega-3 fatty acids may have a potentially protective effect against airway hyperreactivity and lung function decrements; however, relevant data are still sparse. Although epidemiologic data suggest that consumption of fresh fruit may reduce risk of noncarcinogenic airway limitation, there are no clear data on which nutrients might be most relevant. While some studies evaluate daily intake of vitamin C, other studies use fruit consumption as a surrogate for antioxidant intake. Given the dietary intercorrelations among antioxidant vitamins, particularly vitamin C, beta-carotene, and flavonoids, as well as other micronutrients, it may be difficult to isolate a specific effect. Some population subgroups with higher levels of oxidative stress, such as cigarette smokers, may be more likely to benefit from dietary supplementation, since some studies have suggested that antioxidant intake may have a greater impact in this group. Studies of lung function decrement and COPD in adults suggest that daily intake of vitamin C at levels slightly exceeding the current Recommended Dietary Allowance (60 mg/day among nonsmokers and 100 mg/day among smokers) may have a protective effect (20). In the Schwartz and Weiss (85) and Britton et al. (87) studies, an increase of 40 mg/day in vitamin C intake led to an approximate 20-ml increase in FEV1. Daily mean vitamin C intakes in these studies were 66 mg and 99.2 mg, respectively, and the highest intake level (178 mg/day) was approximately

  17. What Is Lung Cancer?

    Science.gov (United States)

    ... starts in the lungs, it is called lung cancer. Lung cancer begins in the lungs and may spread ... lung cancer. For more information, visit the National Cancer Institute’s Lung Cancer. Previous Basic Information Basic Information Basic Information ...

  18. Radon and lung cancer in Spain

    International Nuclear Information System (INIS)

    It is known that the incidence of lung cancer is related to inhalation of radon and radon daughters. However, the magnitude of the risk and its dependence upon physiological and environmental factors are still not well defined either experimentally or epidemiologically. Occupational studies of underground miners are the only available human epidemiological information to estimate the risk of exposure to radon daughters in the indoor environment. The results are shown of a study carried out to determine whether lung cancer mortality rates in Spain are significantly correlated with the average indoor radon levels. For this purpose, we have used indoor radon data generated from the national survey carried out in 1989. Lung cancer distribution by cities and deaths, by year of death and sex, were retrieved for each of the different provinces of Spain for the period 1960-1985, showing the evolution and changes in the incidence of lung cancer in the population. Data referring to the evolution of lung cancer for males and females from 1940 until 1985 are also shown. Since cigarette smoking has been linked to lung cancer the effect of smoking habits in the Spanish population was also considered in this analysis. The first results of this study establish no clear evidence of any substantial association between lung cancer mortality rates and indoor radon for males. However, a relationship was evident for females. (author)

  19. Support for Indoor Bans on Electronic Cigarettes among Current and Former Smokers

    Directory of Open Access Journals (Sweden)

    Stephanie K. Kolar

    2014-11-01

    Full Text Available Objectives: Electronic cigarette (e-cigarette use is increasing in the U.S. Although marketed as a safer alternative for cigarettes, initial evidence suggests that e-cigarettes may pose a secondhand exposure risk. The current study explored the prevalence and correlates of support for e-cigarette bans. Methods: A sample of 265 current/former smokers completed a cross-sectional telephone survey from June–September 2014; 45% Black, 31% White, 21% Hispanic. Items assessed support for home and workplace bans for cigarettes and e-cigarettes and associated risk perceptions. Results: Most participants were aware of e-cigarettes (99%. Results demonstrated less support for complete e-cigarette bans in homes and workplaces compared to cigarettes. Support for complete e-cigarette bans was strongest among older, higher income, married respondents, and former smokers. Complete e-cigarette bans were most strongly endorsed when perceptions of addictiveness and health risks were high. While both e-cigarette lifetime and never-users strongly supported cigarette smoking bans, endorsement for e-cigarette bans varied by lifetime use and intentions to use e-cigarettes. Conclusions: Support for indoor e-cigarette bans is relatively low among individuals with a smoking history. Support for e-cigarette bans may change as evidence regarding their use emerges. These findings have implications for public health policy.

  20. No sisyphean task: how the FDA can regulate electronic cigarettes.

    Science.gov (United States)

    Paradise, Jordan

    2013-01-01

    The adverse effects of smoking have fostered a natural market for smoking cessation and smoking reduction products. Smokers attempting to quit or reduce consumption have tried everything: "low" or "light" cigarettes; nicotine-infused chewing gum, lozenges, and lollipops; dermal patches; and even hypnosis. The latest craze in the quest to find a safer source of nicotine is the electronic cigarette. Electronic cigarettes (e-cigarettes) have swept the market, reaching a rapidly expanding international consumer base. Boasting nicotine delivery and the tactile feel of a traditional cigarette without the dozens of other chemical constituents that contribute to carcinogenicity, e-cigarettes are often portrayed as less risky, as a smoking reduction or even a complete smoking cessation product, and perhaps most troubling for its appeal to youth, as a flavorful, trendy, and convenient accessory. The sensationalism associated with e-cigarettes has spurred outcry from health and medical professional groups, as well as the Food and Drug Administration (FDA), because of the unknown effects on public health. Inhabiting a realm of products deemed "tobacco products" under recent 2009 legislation, e-cigarettes pose new challenges to FDA regulation because of their novel method of nicotine delivery, various mechanical and electrical parts, and nearly nonexistent safety data. Consumer use, marketing and promotional claims, and technological characteristics of e-cigarettes have also raised decades old questions of when the FDA can assert authority over products as drugs or medical devices. Recent case law restricting FDA enforcement efforts against e-cigarettes further confounds the distinction among drugs and medical devices, emerging e-cigarette products, and traditional tobacco products such as cigarettes, cigars, and smokeless tobacco. This Article investigates the e-cigarette phenomenon in the wake of the recently enacted Family Smoking Prevention and Tobacco Control Act of 2009