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Sample records for activity cigarette smoking

  1. Influence of cigarette circumference on smoke chemistry, biological activity, and smoking behaviour.

    PubMed

    McAdam, Kevin; Eldridge, Alison; Fearon, Ian M; Liu, Chuan; Manson, Andrew; Murphy, James; Porter, Andrew

    2016-12-01

    Cigarettes with reduced circumference are increasingly popular in some countries, hence it is important to understand the effects of circumference reduction on their burning behaviour, smoke chemistry and bioactivity. Reducing circumference reduces tobacco mass burn rate, puff count and static burn time, and increases draw resistance and rod length burned during puff and smoulder periods. Smoulder temperature increases with decreasing circumference, but with no discernible effect on cigarette ignition propensity during a standard test. At constant packing density, mainstream (MS) and sidestream (SS) tar and nicotine yields decrease approximately linearly with decreasing circumference, as do the majority of smoke toxicants. However, volatile aldehydes, particularly formaldehyde, show a distinctly non-linear relationship with circumference and increases in the ratios of aldehydes to tar and nicotine have been observed as the circumference decreases. Mutagenic, cytotoxic and tumorigenic specific activities of smoke condensates (i.e. per unit weight of condensate) decrease as circumference decreases. Recent studies suggest that there is no statistical difference in mouth-level exposure to tar and nicotine among smokers of cigarettes with different circumferences. Commercially available slim cigarettes usually have changes in other cigarette design features compared with cigarettes with standard circumference, so it is difficult to isolate the effect of circumference on the properties of commercial products. However, available data shows that changes in cigarette circumference offer no discernible change to the harm associated with smoking.

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

    SciTech Connect

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

    1987-08-01

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

  3. Effect of filtration by activated charcoal on the toxicological activity of cigarette mainstream smoke from experimental cigarettes.

    PubMed

    Gaworski, Charles L; Schramke, Heike; Diekmann, Joerg; Meisgen, Thomas J; Tewes, Franz J; Veltel, Detlef J; Vanscheeuwijck, Patrick M; Rajendran, Narayanan; Muzzio, Miguel; Haussmann, Hans-Juergen

    2009-07-01

    Activated charcoal (AC) filtration reportedly decreases the yields of smoke vapor phase constituents including some identified as human carcinogens and respiratory irritants. Non-clinical studies including chemical smoke analysis, in vitro cytotoxicity and mutagenicity (bacterial and mammalian cells), and in vivo subchronic rat inhalation studies were carried out using machine smoking at ISO conditions with lit-end research cigarettes containing AC filters. The objective was to assess whether AC filter technology would alter the established toxicity profile of mainstream smoke by increasing or decreasing any known toxicological properties, or elicit new ones. The reduced yield of vapor phase irritants from AC filter cigarettes correlated with markedly decreased in vitro cytotoxicity and in vivo morphology of the nose and lower respiratory tract. Increased yields of particulate phase constituents (e.g. polycyclic aromatic hydrocarbons) in AC filtered smoke were noted in comparison to controls in some studies. The in vitro bacterial mutagenicity of AC filtered smoke particulate preparations was occasionally increased over control levels. Laryngeal epithelial thickness was increased in some rats inhaling AC filtered smoke in comparison to controls, an effect perhaps related to higher inspiratory flow. When tested under more intense Massachusetts Department of Public Health smoking conditions, AC filter associated reductions in vapor phase constituent yields were smaller than those seen with ISO conditions, but the effect on in vitro cytotoxicity remained.

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

    SciTech Connect

    Sorak-Pokrajac, M.; Dermelj, M.; Slejkovec, Z.

    1994-01-01

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

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

    PubMed Central

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

    2014-01-01

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

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

    PubMed

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

    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 μg/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.

  7. Cigarette Consumption and Cigarette Smoking Prevalence Among Adults in Kansas

    PubMed Central

    Lai, Sue Min

    2015-01-01

    Introduction Recent tobacco prevention and cessation activities have focused on nonsmoking ordinances and behavioral changes, and in Kansas, the overall prevalence of cigarette smoking among adults has decreased. The objective of this study was to determine whether overall cigarette consumption (mean annual number of cigarettes smoked) in Kansas also decreased. Methods Data on cigarette smoking prevalence for 91,465 adult Kansans were obtained from the Behavioral Risk Factor Surveillance System survey for 1999 through 2010. Data on annual cigarette consumption were obtained from the 2002 and 2006 Kansas Adult Tobacco Survey and analyzed by totals, by sex, and by smoking some days or smoking every day. Linear regression was used to evaluate rate changes over time. Results Among men, but not women, cigarette smoking prevalence decreased significantly over time. The prevalence of smoking every day decreased significantly among both men and women, whereas the prevalence of smoking on some days increased significantly for women but not men. For current smokers, the mean annual number of cigarettes consumed remained the same. Conclusion The decline in overall smoking prevalence coupled with the lack of change in mean annual cigarette consumption may have resulted in a more intense exposure to cigarettes for the smoking population. The significant increase in some day use among women indicates a need for additional prevention and education activities; the impact on future lung cancer incidence rates needs further investigation. PMID:26068414

  8. Dioxins in cigarette smoke

    SciTech Connect

    Muto, H.; Takizawa, Y.

    1989-05-01

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

  9. p38 mitogen-activated protein kinase mediates sidestream cigarette smoke-induced endothelial permeability.

    PubMed

    Low, Brad; Liang, Mei; Fu, Jian

    2007-07-01

    Second-hand smoke is associated with increased risk of cardiovascular diseases. So far, little is known about the signaling mechanisms of second-hand smoke-induced vascular dysfunction. Endothelial junctions are fundamental structures important for maintaining endothelial barrier function. Our study showed that sidestream cigarette smoke (SCS), a major component of second-hand smoke, was able to disrupt endothelial junctions and increase endothelial permeability. Sidestream cigarette smoke stimulated the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and myosin light chain (MLC). A selective inhibitor of p38 MAPK (SB203580) prevented SCS-induced loss of endothelial barrier integrity as evidenced by transendothelial resistance measurements. Resveratrol, an antioxidant that was able to inhibit SCS-induced p38 MAPK and MLC phosphorylation, also protected endothelial cells from the damage. Thus, p38 MAPK mediates SCS-induced endothelial permeability. Inhibition of p38 MAPK may have therapeutic potential for second-hand smoke-induced vascular injury.

  10. Reduced toxicological activity of cigarette smoke by the addition of ammonia magnesium phosphate to the paper of an electrically heated cigarette: subchronic inhalation toxicology.

    PubMed

    Moennikes, O; Vanscheeuwijck, P M; Friedrichs, B; Anskeit, E; Patskan, G J

    2008-05-01

    Cigarette smoke is a complex chemical mixture that causes a variety of diseases, such as lung cancer. With the electrically heated cigarette smoking system (EHCSS), temperatures are applied to the tobacco below those found in conventional cigarettes, resulting in less combustion, reduced yields of some smoke constituents, and decreased activity in some standard toxicological tests. The first generation of electrically heated cigarettes (EHC) also resulted in increased formaldehyde yields; therefore, a second generation of EHC was developed with ammonium magnesium phosphate (AMP) in the cigarette paper in part to address this increase. The toxicological activity of mainstream smoke from these two generations of EHC and of a conventional reference cigarette was investigated in two studies in rats: a standard 90-day inhalation toxicity study and a 35-day inhalation study focusing on lung inflammation. Many of the typical smoke exposure-related changes were found to be less pronounced after exposure to smoke from the second-generation EHC with AMP than to smoke from the first-generation EHC or the conventional reference cigarette, when compared on a particulate matter or nicotine basis. Differences between the EHC without AMP and the conventional reference cigarette were not as prominent. Overall, AMP incorporated in the EHC cigarette paper reduced the inhalation toxicity of the EHCSS more than expected based on the observed reduction in aldehyde yields.

  11. Cigarette Smoking in Iran

    PubMed Central

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

    2012-01-01

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

  12. Cigarette smoking augments sympathetic nerve activity in patients with coronary heart disease.

    PubMed

    Shinozaki, Norihiko; Yuasa, Toyoshi; Takata, Shigeo

    2008-05-01

    It has been shown that cigarette smoking increases blood pressure (BP) and heart rate (HR), and decreases muscle sympathetic nerve activity (MSNA) in healthy young smokers. The decrease in MSNA might be secondary to baroreflex responses to the pressor effect. We tested the hypothesis that cigarette smoking increases MSNA in smokers with impaired baroreflex function. The effects of cigarette smoking on BP, HR, forearm blood flow (FBF), forearm vascular resistance (FVR), and MSNA were examined in 14 patients with stable effort angina (59+/-3 years, group CAD) and 10 healthy smokers (23+/-1 years, group C). In group CAD, the arterial baroreflex sensitivity (BRS) was significantly lower than in group C (4.7+/-0.8 versus 15.1+/-2.2 msec/mmHg, P<0.01). In both groups, cigarette smoking increased the plasma concentration of nicotine, systolic and diastolic BP, HR, and FVR significantly (P<0.01), but decreased FBF significantly (P<0.01). After smoking, MSNA was decreased significantly in group C (from 35.2+/-3.5 to 23.5+/-3.2 bursts/100 beats, P<0.01), but increased significantly in group CAD (from 48.8+/-5.4 to 57.3+/-5.5 bursts/100 beats, P<0.01). There was significant correlation between BRS and changes in MSNA (r= -0.62, P<0.01). Cigarette smoking increased MSNA in smokers with impaired baroreflex function. This demonstrates that cigarette smoking stimulates sympathetic nerve activity by both a direct peripheral effect and a centrally mediated effect.

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

    PubMed Central

    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 (C3−/−) mice develop less emphysema and have fewer CD11b+CD11c+ mDCs infiltrating the lungs as compared to wild type mice. Proteolytic cleavage of C3 by neutrophil elastase releases C3a, which in turn increases expression of its receptor (C3aR) on lung mDCs. Mice deficient in the C3aR (C3ar−/−) partially phenocopy the attenuated responses to chronic smoke observed in C3−/− mice. Consistent with a role for C3 in emphysema C3 and its active fragments are deposited on the lung tissue of smokers with emphysema, and smoke exposed mice. Together, these findings suggest a critical role for C3a through autocrine/paracrine induction of C3aR in the pathogenesis of cigarette smoke induced sterile inflammation and provide new therapeutic targets for the treatment of emphysema. PMID:25465103

  14. Vitamin C blocks inflammatory platelet-activating factor mimetics created by cigarette smoking.

    PubMed Central

    Lehr, H A; Weyrich, A S; Saetzler, R K; Jurek, A; Arfors, K E; Zimmerman, G A; Prescott, S M; McIntyre, T M

    1997-01-01

    Cigarette smoking within minutes induces leukocyte adhesion to the vascular wall and formation of intravascular leukocyte-platelet aggregates. We find this is inhibited by platelet-activating factor (PAF) receptor antagonists, and correlates with the accumulation of PAF-like mediators in the blood of cigarette smoke-exposed hamsters. These mediators were PAF-like lipids, formed by nonenzymatic oxidative modification of existing phospholipids, that were distinct from biosynthetic PAF. These PAF-like lipids induced isolated human monocytes and platelets to aggregate, which greatly increased their secretion of IL-8 and macrophage inflammatory protein-1alpha. Both events were blocked by a PAF receptor antagonist. Similarly, blocking the PAF receptor in vivo blocked smoke-induced leukocyte aggregation and pavementing along the vascular wall. Dietary supplementation with the antioxidant vitamin C prevented the accumulation of PAF-like lipids, and it prevented cigarette smoke-induced leukocyte adhesion to the vascular wall and formation of leukocyte-platelet aggregates. This is the first in vivo demonstration of inflammatory phospholipid oxidation products and it suggests a molecular mechanism coupling cigarette smoke with rapid inflammatory changes. Inhibition of PAF-like lipid formation and their intravascular sequela by vitamin C suggests a simple dietary means to reduce smoking-related cardiovascular disease. PMID:9153277

  15. Physical Activity, Body Mass Index, Alcohol Consumption and Cigarette Smoking among East Asian College Students

    ERIC Educational Resources Information Center

    Seo, Dong-Chul; Torabi, Mohammad R.; Chin, Ming-Kai; Lee, Chung Gun; Kim, Nayoung; Huang, Sen-Fang; Chen, Chee Keong; Mok, Magdalena Mo Ching; Wong, Patricia; Chia, Michael; Park, Bock-Hee

    2014-01-01

    Objective: To identify levels of moderate-intensity physical activity (MPA) and vigorous-intensity physical activity (VPA) in a representative sample of college students in six East Asian economies and examine their relationship with weight, alcohol consumption and cigarette smoking. Design: Cross-sectional survey. Setting: College students…

  16. Dietary behaviors, physical activity, and cigarette smoking among pregnant Puerto Rican women

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Few studies have examined predictors of meeting health guidelines in pregnancy among Latina women. We assessed dietary behaviors, physical activity, and cigarette smoking in the Latina Gestational Diabetes Mellitus Study, a prospective cohort of 1231 prenatal care patients. Self-reported information...

  17. The Effect of Active and Passive Household Cigarette Smoke Exposure on Pregnant Women With Asthma

    PubMed Central

    Momirova, Valerija; Dombrowski, Mitchell P.; Schatz, Michael; Wise, Robert; Landon, Mark; Rouse, Dwight J.; Lindheimer, Marshall; Caritis, Steve N.; Sheffield, Jeanne; Miodovnik, Menachem; Wapner, Ronald J.; Varner, Michael W.; O’Sullivan, Mary Jo; Conway, Deborah L.

    2010-01-01

    Background: The article was designed to estimate the effect of active and passive household cigarette smoke exposure on asthma severity and obstetric and neonatal outcomes in pregnant women with asthma. Methods: We used a secondary observational analysis of pregnant women with mild and moderate-severe asthma enrolled in a prospective observational cohort study of asthma in pregnancy and a randomized clinical trial (RCT) comparing inhaled beclomethasone and oral theophylline. A baseline questionnaire detailing smoking history and passive household smoke exposure was given to each patient. Smoking status was confirmed in the RCT using cotinine levels. Data on asthma severity and obstetric and neonatal outcomes were collected and analyzed with respect to self-reported tobacco smoke exposure. Kruskal-Wallis and Pearson χ2 statistics were used to test for significance. Results: A total of 2,210 women were enrolled: 1,812 in the observational study and 398 in the RCT. Four hundred and eight (18%) women reported current active smoking. Of the nonsmokers, 790 (36%) women reported passive household smoke exposure. Active smoking was associated with more total symptomatic days (P < .001) and nights of sleep disturbance (P < .001). Among the newborns of active smokers, there was a greater risk of small for gestational age < 10th percentile (P < .001), and a lower mean birth weight (P < .001). There were no differences in symptom exacerbation or outcome between nonsmokers with and without passive household cigarette smoke exposure. Conclusions: Among pregnant women with asthma, active but not passive smoking is associated with increased asthma symptoms and fetal growth abnormalities. PMID:19820079

  18. Active and passive smoking - New insights on the molecular composition of different cigarette smoke aerosols by LDI-FTICRMS

    NASA Astrophysics Data System (ADS)

    Schramm, Sébastien; Carré, Vincent; Scheffler, Jean-Luc; Aubriet, Frédéric

    2014-08-01

    The aerosol generated when a cigarette is smoked is a significant indoor contaminant. Both smokers and non-smokers can be exposed to this class of pollutants. Nevertheless, they are not exposed to the same kind of smoke. The active smoker breathes in the mainstream smoke (MSS) during a puff, whereas the passive smoker inhales not only the smoke generated by the lit cigarette between two puffs (SSS) but also the smoke exhaled by active smokers (EXS). The aerosol fraction of EXS has until now been poorly documented; its composition is expected to be different from MSS. This study aims to investigate the complex composition of aerosol from EXS to better understand the difference in exposure between active and passive smokers. To address this, the in-situ laser desorption ionisation Fourier transform ion cyclotron mass spectrometry (LDI-FTICRMS) was used to characterise the aerosol composition of EXS from two different smokers. Results clearly indicated many similarities between EXS samples but also significant differences with MSS and SSS aerosol. The comparison of MSS and EXS aerosol allowed the chemicals retained by the active smoker's lungs to be identified, whereas the convolution of the EXS and SSS aerosol compositions were considered relevant to the exposition of a passive smoker. As a consequence, active smokers are thought to be mainly exposed to polar and poorly unsaturated oxygenated and nitrogenated organics, compared with poorly oxygenated but highly unsaturated compounds in passive smokers.

  19. Irritants in cigarette smoke plumes

    SciTech Connect

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

    1982-11-01

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

  20. Health Education and Cigarette Smoking

    PubMed Central

    Morison, James B.; Medovy, Herry; MacDonell, Gordon T.

    1964-01-01

    The smoking habits of Winnipeg school students were surveyed before and after a three-year program of health education on the hazards of smoking, directed to 8300 out of 48,000 students. The program consisted of informal approaches to students in elementary schools and a formal program of talks, lectures, films, and student participation for older students. There were fewer students at all ages who had never smoked a cigarette at the time of the second survey. There was a slight decrease in the number of regular smokers in high school, most marked in the school where the program was enthusiastically received and student participation was most active. A direct relationship between parental smoking and that of the student, and an inverse relationship between academic achievement and student smoking, were shown on both surveys. The majority of students believed that smoking caused lung cancer and other hazards to health, although this was less marked among smokers. The results indicated that an intensive program of health education directed to the teenagers in school was a potentially useful approach to the problem of cigarette smoking. PMID:14154295

  1. Cigarette smoke induces aberrant EGF receptor activation that mediates lung cancer development and resistance to tyrosine kinase inhibitors.

    PubMed

    Filosto, Simone; Becker, Cathleen R; Goldkorn, Tzipora

    2012-04-01

    The EGF receptor (EGFR) and its downstream signaling are implicated in lung cancer development. Therefore, much effort was spent in developing specific tyrosine kinase inhibitors (TKI) that bind to the EGFR ATP-pocket, blocking EGFR phosphorylation/signaling. Clinical use of TKIs is effective in a subset of lung cancers with mutations in the EGFR kinase domain, rendering the receptor highly susceptible to TKIs. However, these benefits are limited, and emergence of additional EGFR mutations usually results in TKI resistance and disease progression. Previously, we showed one mechanism linking cigarette smoke to EGFR-driven lung cancer. Specifically, exposure of lung epithelial cells to cigarette smoke-induced oxidative stress stimulates aberrant EGFR phosphorylation/activation with impaired receptor ubiquitination/degradation. The abnormal stabilization of the activated receptor leads to uncontrolled cell growth and tumorigenesis. Here, we describe for the first time a novel posttranslational mechanism of EGFR resistance to TKIs. Exposure of airway epithelial cells to cigarette smoke causes aberrant phosphorylation/activation of EGFR, resulting in a conformation that is different from that induced by the ligand EGF. Unlike EGF-activated EGFR, cigarette smoke-activated EGFR binds c-Src and caveolin-1 and does not undergo canonical dimerization. Importantly, the cigarette smoke-activated EGFR is not inhibited by TKIs (AG1478; erlotinib; gefitinib); in fact, the cigarette smoke exposure induces TKI-resistance even in the TKI-sensitive EGFR mutants. Our findings show that cigarette smoke exposure stimulates not only aberrant EGFR phosphorylation impairing receptor degradation, but also induces a different EGFR conformation and signaling that are resistant to TKIs. Together, these findings offer new insights into cigarette smoke-induced lung cancer development and TKI resistance.

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

    PubMed

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

    2015-09-01

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

  3. Cigarette smoke activates human monocytes by an oxidant-AP-1 signaling pathway: implications for steroid resistance.

    PubMed

    Walters, Matthew J; Paul-Clark, Mark J; McMaster, Shaun K; Ito, Kazuhiro; Adcock, Ian M; Mitchell, Jane A

    2005-11-01

    Smoking cigarettes is a major risk factor for the development of cardiovascular and respiratory disease. Moreover, smoking-induced pathophysiology is often resistant to the anti-inflammatory effects of glucocorticoids. The nature of cigarette smoke-induced inflammation is still not defined, although neutrophil recruitment and activation seem to be consistent features. In the current study, we have used a range of approaches to demonstrate that cigarette smoke activates human monocytes and macrophages to release the CXC chemokine CXCL8 [(interleukin-8 (IL-8)]. Furthermore, we show for the first time that cigarette smoke synergizes with proinflammatory cytokines IL-1beta and tumor necrosis factor-alpha, and it is this interaction that confers steroid resistance to smoke-induced CXCL8 release. We go on to show that smoke-induced activation of human cells is an oxidant-mediated phenomenon acting through activator protein-1, but not nuclear factor kappaB, pathway. These observations add significantly to our understanding of smoke as an inflammatory stimulus that has implications for potential the development of treatments of smoking or related disease.

  4. Cigarette smoke can activate the alternative pathway of complement in vitro by modifying the third component of complement.

    PubMed Central

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

    1985-01-01

    Cigarette smoking is associated with significant increases in the number of pulmonary mononuclear phagocytes and neutrophils. A potent chemoattractant for these cells is C5a, a peptide generated during complement (C) activation. We, therefore, investigated the possibility that cigarette smoke could activate the complement system in vitro. Our results show that factor(s) (mol wt less than 1,000) present in an aqueous solution of whole, unfiltered cigarette smoke can deplete the hemolytic capacity of whole human serum in a dose-dependent manner. The particle-free, filtered gas phase of cigarette smoke is inactive. The smoke factor(s) do not activate serum C1, but do deplete serum C4 activity. Treatment of purified human C3 with whole smoke solution modifies the molecule such that its subsequent addition to serum (containing Mg/EGTA to block the classical pathway) results in consumption of hemolytic complement by activation of the alternative pathway. Smoke-modified C3 shows increased anodal migration in agarose electrophoresis, but this is not due to proteolytic cleavage of the molecule as evidenced by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. In contrast to methylamine-treated C3, C3 treated with smoke is only partially susceptible to the action of the complement regulatory proteins Factors H and I. In addition, smoke-modified C3 has diminished binding to Factor H as compared with methylamine-treated C3. Finally, smoke-modified C3 incorporates [14C]methylamine which suggests that the thiolester bond may be intact. These data indicate that aqueous whole cigarette smoke solution can modify C3 and activate the alternative pathway of complement, perhaps by a previously unrecognized mechanism. Should this occur in vivo, complement activation might partly account for the extensive pulmonary leukocyte recruitment observed in smokers. Images PMID:3156879

  5. Reducing the inhibitory effect of cigarette smoke on the activity of oral peroxidase by the addition of berberine in cigarette filter.

    PubMed

    Wu, Jinfeng; Ye, Xiaoli; Cui, Xuelong; Li, Xuegang; Zheng, Lifeng; Chen, Zhu

    2013-05-01

    This study was carried out to evaluate the effect of cigarette smoke (CS) on the activity of oral peroxidase (OPO) after berberine was added to the cigarette filter. Activated carbon fiber (ACF) was chosen to load berberine as a part of the cellulose acetate (CA) filter to obtain the modified B-ACF cigarette filter. Then the effects of CS from the testing cigarettes on the activity of OPO were investigated in vitro by the 2-nitrobenzoic acid assay, and the smoke chemistry was also analyzed, especially the content of hydrogen cyanide (HCN) in the CS. The results indicated that the loss of activity of OPO in B-ACF filter cigarette group decreased by 20% and 25%, compared with those of ACF and CA filter cigarette groups, respectively. The relative residual activity of OPO in B-ACF filter group was increased with the increase of berberine in the filter compared with the CA filter group. It could be observed that the reduction in HCN might be related to the berberine in the cigarette filter, reducing the inhibition of CS on the activity of OPO.

  6. 210Po and 210Pb Activity Concentrations in Cigarettes Produced in Vietnam and Their Estimated Dose Contribution Due to Smoking

    NASA Astrophysics Data System (ADS)

    Tran, Thuy-Ngan N.; Le, Cong-Hao; Chau, Van-Tao

    Smoking cigarettes contributes significantly to the increase of radiation in human body because 210Po and 210Pb exist relatively high in tobacco leaves. Therefore, these two radioisotopes in eighteen of the most frequently sold cigarette brands produced in Vietnam were examined in this study. 210Po was determined by alpha spectroscopy using a passivated implanted planar silicon (PIPS) detector after a procedure including radiochemical separation and spontaneous deposition of polonium on a copper disc (the deposition efficiency of 210Po on a copper disc was approximately 94%). Sequentially, 210Pb was determined through the ingrowth of 210Po after storing the sample solutions for approximately six months. The activity concentrations of 210Po in cigarettes ranged from 13.8 to 82.6 mBq/cigarette (the mean value was 26.4 mBq/cigarette) and the activity concentrations of 210Pb in cigarettes ranged from 13.9 to 78.8 mBq/cigarette (the mean value was 25.8 mBq/cigarette). The annual committed effective dose for smokers who smoke one pack per day was also estimated to be 295.4 µSv/year (223.0 µSv/year and 72.4 µSv/year from 210Po and 210Pb, respectively). These indicated that smoking increased the risk of developing lung cancer was approximately 60 times greater for smokers than for non-smokers.

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

    PubMed

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

    2016-04-01

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

  8. Cigarette smoke extract affects functional activity of MRP1 in bronchial epithelial cells.

    PubMed

    van der Deen, Margaretha; de Vries, Elisabeth G E; Visserman, Hylke; Zandbergen, Wouter; Postma, Dirkje S; Timens, Wim; Timmer-Bosscha, Hetty

    2007-01-01

    Cigarette smoke is the principal risk factor for development of chronic obstructive pulmonary disease (COPD). Multidrug resistance-associated protein 1 (MRP1) is a member of the ATP-binding cassette (ABC) superfamily of transporters, which transport physiologic and toxic substrates across cell membranes. MRP1 is highly expressed in lung epithelium. This study aims to analyze the effect of cigarette smoke extract (CSE) on MRP1 activity. In the human bronchial epithelial cell line 16HBE14o-, MRP1 function was studied flow cytometrically by cellular retention of carboxyfluorescein (CF) after CSE incubation and MRP1 downregulation by RNA interference (siRNA). Cell survival was measured by the MTT assay. Immunocytochemically, it was shown that 16HBE14o(-) expressed MRP1 and breast cancer resistance protein. Coincubation of CSE IC50 (1.53% +/- 0.22%) with MK571 further decreased cell survival 31% (p, = 0.018). CSE increased cellular CF retention dose dependently from 1.7-fold at 5% CSE to 10.3-fold at 40% CSE (both p < 0.05). siRNA reduced MRP1 RNA expression with 49% and increased CF accumulation 67% versus control transfected cells. CSE exposure further increased CF retention 24% (p = 0.031). A linear positive relation between MRP1 function and CSE-modulating effects (r = 0.99, p =0.089) was shown in untransfected, control transfected, and MRP1 downregulated 16HBE14o- cells analogous to blocking effects with MRP1 inhibitor MK571 (r = 0.99, p = 0.034). In conclusion, cigarette smoke extract affects MRP1 activity probably competitively in bronchial epithelial cells. Inhibition of MRP1 in turn results in higher CSE toxicity. We propose that MRP1 may be a protective protein for COPD development.

  9. Cigarette smoking impairs Na+-K+-ATPase activity in the human coronary microcirculation.

    PubMed

    Miura, Hiroto; Toyama, Kazuyoshi; Pratt, Phillip F; Gutterman, David D

    2011-01-01

    The extracellular K(+) concentration ([K(+)](o)) has been proposed to link cardiac metabolism with coronary perfusion and arrhythmogenesis, particularly during ischemia. Several animal studies have also supported K(+) as an EDHF that activates Na(+)-K(+)-ATPase and/or inwardly rectifying K(+) (K(ir)) channels. Therefore, we examined the vascular reactivity of human coronary arterioles (HCAs) to small elevations in [K(+)](o), the influence of risk factors for coronary disease, and the role of K(+) as an EDHF. Changes in the internal diameter of HCAs were recorded with videomicroscopy. Most vessels dilated to increases in [K(+)](o) with a maximal dilation of 55 ± 6% primarily at 12.5-20.0 mM KCl (n = 38, average: 16 ± 1 mM). Ouabain, a Na(+)-K(+)-ATPase inhibitor, alone reduced the dilation, and the addition of Ba(2+), a K(ir) channel blocker, abolished the remaining dilation, whereas neither endothelial denudation nor Ba(2+) alone reduced the dilation. Multivariate analysis revealed that cigarette smoking was the only risk factor associated with impaired dilation to K(+). Ouabain significantly reduced the vasodilation in HCAs from subjects without cigarette smoking but not in those with smoking. Cigarette smoking downregulated the expression of the Na(+)-K(+)-ATPase catalytic α(1)-subunit but not Kir2.1 in the vessels. Ouabain abolished the dilation in endothelium-denuded vessels to a same extent to that with the combination of ouabain and Ba(2+) in endothelium-intact vessels, whereas neither ouabain nor ouabain plus Ba(2+) reduced EDHF-mediated dilations to bradykinin and ADP. A rise in [K(+)](o) dilates HCAs primarily via the activation of Na(+)-K(+)-ATPase in vascular smooth muscle cells with a considerable contribution of K(ir) channels in the endothelium, indicating that [K(+)](o) may modify coronary microvascular resistance in humans. Na(+)-K(+)-ATPase activity is impaired in subjects who smoke, possibly contributing to dysregulation of the coronary

  10. Cigarette smoking, physical activity, and alcohol consumption: relationship to blood lipids and lipoproteins in premenopausal females.

    PubMed

    Stamford, B A; Matter, S; Fell, R D; Sady, S; Cresanta, M K; Papanek, P

    1984-07-01

    A total of 164 premenopausal female subjects were randomly selected for evaluation from a much larger pool of volunteers. The relationships between blood lipid and lipoprotein levels as dependent variables and cigarette smoking, physical activity, and alcohol consumption were determined from partial regression coefficients. A lower HDL-C level (10.1 mg/dL) was seen in smokers v nonsmokers. For each ounce of alcohol consumed, HDL-C level was higher by 2.8 mg/dL, and greater physical activity was associated with a higher HDL-C level of 8.6 mg/dL. An analysis of covariance with covariance adjustments for age and body fat revealed that smokers who regularly exercise or consume alcohol had significantly lower HDL-C levels than nonsmokers with similar habits. Subjects who both exercise and consume alcohol demonstrated higher HDL-C levels than those who indulge in one or the other separately. Results suggest that cigarette smoking may attenuate the effects of chronic exercise or alcohol consumption, or of both, to raise HDL-C levels. Also, chronic exercise and alcohol consumption may exert an additive effect, raising HDL-C level.

  11. Sleep deprivation increases cigarette smoking.

    PubMed

    Hamidovic, Ajna; de Wit, Harriet

    2009-09-01

    Loss of sleep may impair the ability to abstain from drug use, through any of a number of mechanisms. Sleep loss may increase drug use by impairing attention and inhibitory control, increasing the value of drug rewards over other rewards, or by inducing mood states that facilitate use of a drug. In the present study, we examined whether sleep deprivation (SD) would increase smoking in cigarette smokers, and whether it would do so by impairing attention or inhibitory control. Healthy cigarette smokers (N=14) were tested in a two-session within subject study, after overnight SD or after a normal night's sleep. Subjects were tested in both conditions in randomized order, after abstaining from cigarettes for 48 hours. The procedure was designed to model the human relapse situation. On each 6-h laboratory session after sleep or no sleep, subjects completed mood and craving questionnaires, tasks measuring behavioral inhibition and attention, and a choice procedure in which they chose between money and smoking cigarettes. SD increased self-reported fatigue and decreased arousal, it increased the number of cigarettes subjects chose to smoke, impaired behavioral inhibition and attention. However, the impairments in inhibition or attention were not related to the increase in smoking. It is possible that SD increases smoking because smokers expect that it will reduce sleepiness. Thus, the findings suggest that sleep loss may increase the likelihood of smoking during abstinence not through inhibitory or attentional mechanisms but because of the potential of nicotine to reduce subjective sleepiness.

  12. Cigarette smoke and lung cancer

    SciTech Connect

    Martonen, T.B.; Hofmann, W.; Lowe, J.E.

    1987-01-01

    Cigarette smoke has been implicated in a causal relationship with carcinoma of the lung. An intriguing feature of the disease is the site-selectivity with which bronchogenic cancer manifests itself; most cancers are detected in the main, lobar and segmental bronchi, perhaps specifically at airway bifurcations. The elevated risk of lung cancer to smokers may result from a complex interplay between smoking and exposure to ambient Rn progeny, including the promotional-effect role (as opposed to being the initiating event) of cigarette smoke in tumor development. It has been determined that smokers exposed to average indoor Rn progency levels receive surprisingly high doses at hot spots within bronchial bifurcations.

  13. Tiotropium bromide exerts anti-inflammatory activity in a cigarette smoke mouse model of COPD.

    PubMed

    Wollin, L; Pieper, M P

    2010-08-01

    Tiotropium bromide is a long acting muscarinic antagonist (LAMA), marketed under the brand name Spiriva, for the treatment of chronic obstructive pulmonary disease (COPD). Besides its proven direct bronchodilatory activity, recent clinical studies demonstrated that tiotropium is able to reduce the exacerbation rate and impact the clinical course of COPD. One significant pathological feature believed to be causative for the progressive nature of COPD is chronic pulmonary inflammation. The aim of the present study was to investigate the anti-inflammatory activity of tiotropium on cigarette smoke-induced pulmonary inflammation in mice. C57Bl/6 mice were exposed to cigarette smoke (CS) for four days with increasing exposure time for up to 6h per day to elicit pulmonary inflammation and mediator release. One hour before smoke exposure, animals were treated with tiotropium by inhalation (0.01-0.3mg/mL) for 5 min; 18h after the last CS exposure a bronchoalveolar lavage was performed. Tiotropium concentration-dependently inhibited pulmonary neutrophilic inflammation with an IC(50) of 0.058 mg/mL and a maximum inhibition of 60% at 0.3mg/mL. Furthermore, the CS-induced pulmonary release of leukotriene B(4), interleukin-6, keratinocyte-derived chemokine, monocyte chemotactic protein-1, macrophage inflammatory protein-1 alpha and -2, and tumor necrosis factor alpha was dose-dependently reduced. The bronchodilatory activity of tiotropium against acetycholine-induced bronchoconstriction was found to be in the same dose range as the anti-inflammatory activity with an IC(50) of 0.045 mg/mL and a maximum bronchodilation of 90% at 0.3mg/mL. Our data suggest that the beneficial effects of tiotropium on the course of COPD shown in patients may be associated with an anti-inflammatory activity.

  14. The Association Between Mental Health and Cigarette Smoking in Active Duty Military Members

    DTIC Science & Technology

    2011-02-01

    2.1.2 General Tobacco Use Costs ...................................................................... 1 2.1.3 Cigarette Smoking in Adolescents...Characteristics and Impact . Tobacco use is the single most preventable cause of death and disease in the United States. Approximately 21% of the U.S... pack of 20 cigarettes sold in the U.S. (low estimate) are $10.28. The average retail price per pack in the U.S. (including sales tax) is $4.20 (Ref

  15. Cigarette smoking and leukocyte subpopulations in men.

    PubMed

    Freedman, D S; Flanders, W D; Barboriak, J J; Malarcher, A M; Gates, L

    1996-07-01

    Because of previously reported associations among the total leukocyte count, cigarette smoking, and risk of cardiovascular disease, we examined the relation of cigarette smoking to various leukocyte subpopulations among 3467 men aged 31 to 45 years. The median total leukocyte count was 36% higher (7840 vs. 5760 cells/mL) among current cigarette smokers than among men who had never smoked, and both stratification and regression analyses were used to examine independent associations with leukocyte subpopulations. At equivalent counts of other subpopulations, CD4+ lymphocytes and neutrophils were the cell types most strongly associated with cigarette smoking; each standard deviation change in counts of these subpopulations increased the odds of current (vs. never) smoking by approximately threefold. Furthermore, whereas 15% of the 238 men with relatively low (< 25 percentile) counts of both neutrophils and CD4+ lymphocytes were cigarette smokers, 96% of the 249 men with relatively high counts of both subpopulations were current smokers. Counts of T lymphocytes also tended to be higher among the 32 men with self-reported ischemic heart disease than among other men. These results, along with previous reports of immunologically active T lymphocytes in atherosclerotic plaques, suggest that this subpopulation may be of particular interest in studies examining the relation of leukocytes to cardiovascular disease.

  16. Cigarette smoking and breast cancer.

    PubMed

    Baron, J A; Newcomb, P A; Longnecker, M P; Mittendorf, R; Storer, B E; Clapp, R W; Bogdan, G; Yuen, J

    1996-05-01

    A priori hypotheses suggest that cigarette smoking could either increase or decrease breast cancer incidence. To clarify these competing hypotheses, we used data from a very large population-based breast cancer case-control study to investigate the impact of smoking on breast cancer risk. Breast cancer patients less than 75 years old were identified from statewide tumor registries in Wisconsin, Massachusetts, Maine, and New Hampshire; controls were randomly selected from driver's license lists (age less than 65) or lists of Medicare beneficiaries (age 65-74). Information on reproductive history, medical history, and personal habits including cigarette smoking was obtained by telephone interview. A total of 6,888 cases and 9,529 controls were interviewed. There was virtually no relationship between current smoking and breast cancer risk (multivariate odds ratio, 1.00; 95% confidence interval, 0.92-1.09), and former smokers had a barely increased risk (odds ratio, 1.10; 95% confidence interval, 1.01-1.19). Similar results were observed among both premenopausal and postmenopausal women. There was no suggestion that heavy or long-term smoking increased or decreased risk, nor were there indications that women who began smoking at an early age were at increased risk, as has been hypothesized. The results of this large population-based study indicate that smoking does not influence the risk of breast cancer, even among heavy smokers who began smoking at an early age.

  17. Activation of transcription factors in human bronchial epithelial cells exposed to aqueous extracts of mainstream cigarette smoke in vitro.

    PubMed

    Sekine, Takashi; Hirata, Tadashi; Mine, Toshiki; Fukano, Yasuo

    2016-01-01

    This study aimed to identify the most sensitive transcription factor activated by cigarette smoke extract (CSE) and to explore cigarette smoke components that have high biological activities in a cell-base assay. Previously, we found evidence that implicated 10 different transcription factors as having a high biological activity to CSE in vitro, based on the results of a comprehensive gene expression profile. For this study, luciferase reporter assays for each transcription factor were developed in two types of human bronchial epithelial cells: NCI-H292 and BEAS-2B cells. The results demonstrated that the nuclear factor erythroid 2-related factor 2 (NRF2)/anti-oxidant response element (ARE) pathway was the most sensitive in response to CSE. Consistently, hemo oxygenase-1 (HO-1), a downstream target gene of NRF2, was effectively up-regulated in BEAS-2B cells exposed to CSE. Moreover, among 1395 cigarette smoke components, naphthoquinones including 9,10-phenaotrenquinone, quinones, benzenediols and α, β-unsaturated carbonyls, were identified as major smoke components that contribute to activating the NRF2/ARE pathway, as indicated by the ARE-reporter assay in BEAS-2B cells. Taken together, NRF2 appears to be a key molecule in the CSE-induced cellular response, and the employed methodology is helpful for the analysis of molecular and cellular effects by CSE.

  18. Cigarette access and pupil smoking rates: a circular relationship?

    PubMed

    Turner, Katrina M; Gordon, Jacki; Young, Robert

    2004-12-01

    Adolescents obtain cigarettes from both commercial and social sources. While the relationship between commercial access and adolescent smoking has been researched, no one has considered in detail whether rates of peer smoking affect cigarette availability. In two relatively deprived Scottish schools that differed in their pupil smoking rates, we assess pupil access to cigarettes. 896 13 and 15 year olds were surveyed, and 25 single-sex discussion groups held with a sub-sample of the 13 year olds. Smokers in both schools obtained cigarettes from shops, food vans and other pupils. However, pupils in the 'high' smoking school perceived greater access to both commercial and social sources, and had access to an active 'peer market'. These findings suggest that variations in cigarette access may contribute to school differences in pupil smoking rates, and that the relationship between access and adolescent smoking is circular, with greater availability increasing rates, and higher rates enhancing access.

  19. p38 mitogen-activated protein kinase determines the susceptibility to cigarette smoke-induced emphysema in mice

    PubMed Central

    2014-01-01

    Background There is a need for agents that suppress inflammation and progression of chronic obstructive pulmonary disease. p38 mitogen-activated protein kinase (p38 MAPK) has been associated with this disorder, and several inhibitors of this cascade are in clinical trials for its treatment, but their efficacy and utility are unknown. This study evaluated the relationship between p38 MAPK activation and susceptibility to cigarette smoke (CS)-induced emphysema, and whether its inhibition ameliorated the lung inflammation and injury in murine models of cigarette smoke exposure. Methods In acute and chronic CS exposure, the activation and expression of p38 MAPK in the lungs, as well as lung inflammation and injury (proteinase production, apoptosis, and oxidative DNA damage), were compared between two mouse strains: C57BL/6 (emphysema-susceptible) and NZW (emphysema-resistant). The selective p38 MAPK inhibitor SB203580 (45 mg/kg) was administrated intra-peritoneally to C57BL/6 mice, to examine whether it ameliorated cigarette smoke-induced lung inflammation and injury. Results Acute CS-induced lung inflammation (neutrophil infiltration, mRNA expressions of TNF-α and MIP-2), proteinase expression (MMP-12 mRNA), apoptosis, and oxidative DNA damage were significantly lower in NZW than C57BL/6 mice. p38 MAPK was significantly activated and up-regulated by both acute and chronic CS exposure in C57BL/6 but not NZW mice. mRNA expression of p38 MAPK was also upregulated in C57BL/6 by chronic CS exposure and tended to be constitutively suppressed in NZW mice. SB203580 significantly attenuated lung inflammation (neutrophil infiltration, mRNA expressions of TNF-α and MIP-2, protein levels of KC, MIP-1α, IL-1β, and IL-6), proteinase expression (MMP-12 mRNA), oxidative DNA damage, and apoptosis caused by acute CS exposure. Conclusions Cigarette smoke activated p38 MAPK only in mice that were susceptible to cigarette smoke-induced emphysema. Its selective inhibition ameliorated

  20. Cigarette Smoke inhibits ROCK2 activation in T cells and modulates IL-22 production

    PubMed Central

    Weng, Chien-Huan; Gupta, Sanjay; Geraghty, Patrick; Foronjy, Robert

    2016-01-01

    Gene-environment interactions are known to play a key role in the development of rheumatoid arthritis (RA). Exposure to cigarette smoke (CS) is one of the strongest environmental risk factors associated with RA and has been shown to mediate a range of complex immunomodulatory effects from decreased T and B cell activation to depressed phagocytic function. The effects of CS on the function of TH17 cells, one of the key TH effector subsets implicated in RA pathogenesis, are not fully understood. IRF4 is one of the crucial transcription factors involved in TH-17 differentiation and is absolutely required for the production of IL-17 and IL-21 but, interestingly, inhibits the synthesis of IL-22. The production of IL-17 and IL-21 by IRF4 can be augmented by its phosphorylation by the serine-threonine kinase ROCK2. Given that CS has been reported to increase ROCK activity in endothelial cells, here we investigated the effects of CS on the ROCK2-IRF4 axis in T cells. Surprisingly, we found that CS leads to decreased ROCK2 activation and IRF4 phosphorylation in T cells. This effect was associated with increased IL-22 production. Using a GEF pull-down assay we furthermore identify ARHGEF1 as a key upstream regulator of ROCK2 whose activity in T cells is inhibited by CS. Thus CS can inhibit the ROCK2-IRF4 axis and modulate T cell production of IL-22. PMID:26882474

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

    PubMed

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

    2015-12-01

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

  2. Effects of Cigarette Smoke on the Activation of Oxidative Stress-Related Transcription Factors in Female A/J Mouse Lung

    PubMed Central

    Tharappel, Job C.; Cholewa, Jill; Espandiari, Parvaneh; Spear, Brett T.; Gairola, C. Gary; Glauert, Howard P.

    2010-01-01

    Cigarette smoke contains a high concentration of free radicals and induces oxidative stress in the lung and other tissues. Several transcription factors are known to be activated by oxidative stress, including nuclear factor-κB (NF-κB), activator protein-1 (AP-1), and hypoxia-inducible factor (HIF). Studies were therefore undertaken to examine if cigarette smoke could activate these transcription factors, as well as other transcription factors that may be important in lung carcinogenesis. Female A/J mice were exposed to cigarette smoke for 2, 5, 10, 15, 20, 42, or 56 days (6 hr/day, 5 days/wk). Cigarette smoke did not increase NF-κB activation at any of these times, but NF-κB DNA binding activity was lower after 15 days and 56 days of smoke exposure. The DNA binding activity of AP-1 was lower after 10 days and 56 days but was not changed after 42 days of smoke exposure. The DNA binding activity of HIF was quantitatively increased after 42 days of smoke exposure but decreased after 56 days. Whether the activation of other transcription factors in the lung could be altered after exposure to cigarette smoke was subsequently examined. The DNA binding activities of FoxF2, myc-CF1, RORE, and p53 were examined after 10 days of smoke exposure. The DNA binding activities of FoxF2 and p53 were quantitatively increased, but those of myc-CF1 and RORE were unaffected. These studies show that cigarette smoke exposure leads to quantitative increases in DNA binding activities of FoxF2 and p53, while the activations of NF-κB, AP-1, and HIF are largely unaffected or reduced. PMID:20711931

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

    SciTech Connect

    Welsh, M.J.

    1983-06-01

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

  4. Infrared spectroscopy study of the influence of inhaled vapors/smoke produced by cigarettes of active smokers

    NASA Astrophysics Data System (ADS)

    Popa, Cristina

    2015-05-01

    While much is known about the effect of smoke and vapors on the composition of blood, little is known about their impact on the composition of breath. When tobacco from traditional cigarettes (T) is burned, it produces harmful smoke compared with the vapor produced when using electronic cigarettes (E). Using a noninvasive, safe, and rapid CO2 laser-photoacoustic method, this study aimed to examine the ethylene changes at different time intervals in the exhaled breath composition of E-cigarette smokers and T-cigarette smokers, before and after the consecutive exposures to cigarettes. Oxidative stress from exposure to tobacco smoke has a role in the pathogenic process, leading to chronic obstructive pulmonary disease. The evidence on the mechanisms by which T-smoking causes damage indicates that there is no risk-free level of exposure to tobacco smoke. The study revealed that the ethylene level (in the E-cigarette smoker's case) was found to be in smaller concentrations (compared with T-cigarette smoker's case) and that E-cigarettes may provide an alternative to T-cigarette smoking.

  5. Infrared spectroscopy study of the influence of inhaled vapors/smoke produced by cigarettes of active smokers.

    PubMed

    Popa, Cristina

    2015-05-01

    While much is known about the effect of smoke and vapors on the composition of blood, little is known about their impact on the composition of breath. When tobacco from traditional cigarettes (T) is burned, it produces harmful smoke compared with the vapor produced when using electronic cigarettes (E). Using a noninvasive, safe, and rapid CO2 laser-photoacoustic method, this study aimed to examine the ethylene changes at different time intervals in the exhaled breath composition of E-cigarette smokers and T-cigarette smokers, before and after the consecutive exposures to cigarettes. Oxidative stress from exposure to tobacco smoke has a role in the pathogenic process, leading to chronic obstructive pulmonary disease. The evidence on the mechanisms by which T-smoking causes damage indicates that there is no risk-free level of exposure to tobacco smoke. The study revealed that the ethylene level (in the E-cigarette smoker's case) was found to be in smaller concentrations (compared with T-cigarette smoker's case) and that E-cigarettes may provide an alternative to T-cigarette smoking.

  6. The Influence of Second-Hand Cigarette Smoke Exposure during Childhood and Active Cigarette Smoking on Crohn’s Disease Phenotype Defined by the Montreal Classification Scheme in a Western Cape Population, South Africa

    PubMed Central

    Chivese, Tawanda; Esterhuizen, Tonya M.; Basson, Abigail Raffner

    2015-01-01

    Background Smoking may worsen the disease outcomes in patients with Crohn’s disease (CD), however the effect of exposure to second-hand cigarette smoke during childhood is unclear. In South Africa, no such literature exists. The aim of this study was to investigate whether disease phenotype, at time of diagnosis of CD, was associated with exposure to second-hand cigarette during childhood and active cigarette smoking habits. Methods A cross sectional examination of all consecutive CD patients seen during the period September 2011-January 2013 at 2 large inflammatory bowel disease centers in the Western Cape, South Africa was performed. Data were collected via review of patient case notes, interviewer-administered questionnaire and clinical examination by the attending gastroenterologist. Disease phenotype (behavior and location) was evaluated at time of diagnosis, according to the Montreal Classification scheme. In addition, disease behavior was stratified as ‘complicated’ or ‘uncomplicated’, using predefined definitions. Passive cigarette smoke exposure was evaluated during 3 age intervals: 0–5, 6–10, and 11–18 years. Results One hundred and ninety four CD patients were identified. Cigarette smoking during the 6 months prior to, or at time of diagnosis was significantly associated with ileo-colonic (L3) disease (RRR = 3.63; 95%CI, 1.32–9.98, p = 0.012) and ileal (L1) disease (RRR = 3.54; 95%CI, 1.06–11.83, p = 0.040) compared with colonic disease. In smokers, childhood passive cigarette smoke exposure during the 0–5 years age interval was significantly associated with ileo-colonic CD location (RRR = 21.3; 95%CI, 1.16–391.55, p = 0.040). No significant association between smoking habits and disease behavior at diagnosis, whether defined by the Montreal scheme, or stratified as ‘complicated’ vs ‘uncomplicated’, was observed. Conclusion Smoking habits were associated with ileo-colonic (L3) and ileal (L1) disease at time of diagnosis in

  7. Active cigarette smoking, variants in carcinogen metabolism genes and breast cancer risk among pre- and postmenopausal women in Ontario, Canada.

    PubMed

    Cotterchio, Michelle; Mirea, Lucia; Ozcelik, Hilmi; Kreiger, Nancy

    2014-01-01

    Cigarette smoking is strongly associated with various diseases including many cancers; however, evidence regarding breast cancer risk remains inconclusive with some studies reporting no association, and others an increased risk with long duration and early initiation of smoking. Genetic variation in carcinogen-metabolizing enzymes may modify these associations. Breast cancer cases were identified from the Ontario Cancer Registry (OCR) during 2003-2004 and population controls through random digit dialing methods. All subjects completed self-administered questionnaires. Subsequently, saliva samples were obtained from cases (N = 1,776) and controls (N = 1,839) for deoxyribonucleic acid (DNA) extraction. Multivariate logistic regression was used to estimate odds ratio (OR) and 95% confidence intervals (CI) for active smoking variables, and interactions were assessed between smoking and 36 carcinogen-metabolizing candidate gene variants. No statistically significant association was found between active smoking and breast cancer risk among all women nor when stratified by menopausal status; however, nonsignificant increased premenopausal breast cancer risk was observed among current smokers and women smoking before first pregnancy. Several statistically significant interactions were observed between smoking and genetic variants (CYP1A2 1548C>T, CYP1A1 3801T>C, CYP1B1 4326G>C, NAT1 c.-85-1014T>A, UGT1A7 W208R 622T>C, SOD2 c.47T>C, GSTT1 deletion). However, in analyses stratified by these genotypes, smoking ORs had wide confidence intervals (and with few exceptions included 1.0) making interpretations difficult. Active smoking was not associated with breast cancer risk, although several significant interactions were observed between smoking, carcinogen-metabolizing genetic variants, and breast cancer risk.

  8. Genetic effects of fresh cigarette smoke in Saccharomyces cerevisiae.

    PubMed

    Gairola, C

    1982-09-01

    Ability of fresh cigarette smoke from University of Kentucky reference cigarette 2R1 to induce gene conversion, reverse mutation and mitotic crossing-over in strain D7 of Saccharomyces cerevisiae was examined. A closed cell suspension-recycle system using 2 peristaltic pumps interconnected to a single-port reverse-phase smoking machine was developed to provide complete exposure of cells to smoke within 0.2--10 sec of its generation. The exposed cells showed a dose-dependent increase in the frequency of all the 3 genetic endpoints examined. Cell age was an important factor with younger cells being more sensitive than older. Filtration studies showed that the gas phase possessed as much as 25% of the total whole-smoke activity. Activated charcoal reduced the activity of smoke in direct proportion to its amount in the filter. Acetate filter did not appreciably alter the activity. A comparison of whole smoke from various cigarettes showed that: (1) the nicotine content of a cigarette does not affect the genetic activity of smoke; (2) burley and flue-cured tobaccos have differential activity in gene conversion and reverse mutation systems; and (3) the genetic effects of whole smoke are not peculiar to tobacco pyrolysis because similar effects are produced by smokes from lettuce and other non-tobacco cigarettes. It is concluded that the yeast D7 system can be used effectively for the quantitative evaluation of genetic effects of smoke from different cigarettes, and both whole cigarette smoke and its gas phase possess mutagenic as well as recombinogenic activity that can be modified by the use of filters.

  9. Chronic exposure to cigarette smoke leads to activation of p21 (RAC1)-activated kinase 6 (PAK6) in non-small cell lung cancer cells

    PubMed Central

    Syed, Nazia; Solanki, Hitendra S.; Puttamallesh, Vinuth N.; Balaji, Sai A.; Nanjappa, Vishalakshi; Datta, Keshava K.; Babu, Niraj; Renuse, Santosh; Patil, Arun H.; Izumchenko, Evgeny; Prasad, T.S. Keshava; Chang, Xiaofei; Rangarajan, Annapoorni; Sidransky, David; Pandey, Akhilesh; Gowda, Harsha; Chatterjee, Aditi

    2016-01-01

    Epidemiological data clearly establishes cigarette smoking as one of the major cause for lung cancer worldwide. Recently, targeted therapy has become one of the most preferred modes of treatment for cancer. Though certain targeted therapies such as anti-EGFR are in clinical practice, they have shown limited success in lung cancer patients who are smokers. This demands discovery of alternative drug targets through systematic investigation of cigarette smoke-induced signaling mechanisms. To study the signaling events activated in response to cigarette smoke, we carried out SILAC-based phosphoproteomic analysis of H358 lung cancer cells chronically exposed to cigarette smoke. We identified 1,812 phosphosites, of which 278 phosphosites were hyperphosphorylated (≥ 3-fold) in H358 cells chronically exposed to cigarette smoke. Our data revealed hyperphosphorylation of S560 within the conserved kinase domain of PAK6. Activation of PAK6 is associated with various processes in cancer including metastasis. Mechanistic studies revealed that inhibition of PAK6 led to reduction in cell proliferation, migration and invasion of the cigarette smoke treated cells. Further, siRNA mediated silencing of PAK6 resulted in decreased invasive abilities in a panel of non-small cell lung cancer (NSCLC) cells. Consistently, mice bearing tumor xenograft showed reduced tumor growth upon treatment with PF-3758309 (group II PAK inhibitor). Immunohistochemical analysis revealed overexpression of PAK6 in 66.6% (52/78) of NSCLC cases in tissue microarrays. Taken together, our study indicates that PAK6 is a promising novel therapeutic target for NSCLC, especially in smokers. PMID:27542207

  10. Determination of Po-210 content in cigarette smoke using a smoking machine: A case study of Iranian cigarettes.

    PubMed

    Horváth, Mária; Shahrokhi, Amin; Bátor, Péter; Tóth-Bodrogi, Edit; Kovács, Tibor

    2017-02-06

    The Po-210 content of tobacco has been known for a long time, however, different results can be found about the estimated amount of Po-210 that is inhaled by humans as a result of smoking cigarettes. Because of the unique properties of Po-210, the smoking machines available on the market are not suitable because of their failure to quantitatively collect Po-210 for measurement. Therefore, to estimate precisely the amount of Po-210 entering the lungs as a result of smoking, a smoking machine and sampling protocol based on relevant ISO standards - ISO-3308, ISO-3402 and ISO-4387 - was developed. A 5% HCl solution was found to be the best absorber of Po-210 from smoke. Seventeen different brands of cigarettes distributed in Iran were used to validate the new machine and sampling protocol. The Po-210 concentration was determined by alpha spectrometry; the cigarette smoke solution underwent combined acid treatment after adding a Po-209 tracer. The Po-210 activity concentration of cigarettes sold in Iran was between 9.7 ± 1.2 and 26.5 ± 4.6 mBq/cigarette and it was determined that there was no relationship between the Po-210 and nicotine contents of cigarette smoke. Additionally, it was found that 15 ± 10% of the cigarette Po-210 was transferred to the mainstream smoke.

  11. Cigarette advertising and adolescent experimentation with smoking.

    PubMed

    Klitzner, M; Gruenewald, P J; Bamberger, E

    1991-03-01

    The extent to which cigarette advertising contributes to increases in smoking has been debated by public health professionals and the tobacco industry. One aspect of this debate has been the degree to which advertising influences smoking among adolescents. Previous research suggests that there are significant relationships between measures of advertising and smoking. However, potential simultaneous relationships between these measures have not been addressed. Observed correlations may arise from the effects of advertising on smoking or from smokers' selective exposure to advertisements. This study examined relationships between cigarette advertising and smoking experimentation. Using environmental and psychological measures of advertising exposure, it was demonstrated that adolescents who experimented with cigarettes were better able to recognize advertised products than those who had not, a selective exposure effect. Conversely, subjects who were better at recognizing advertised brands were more likely to have experimented with cigarettes, an effect due to their exposure to cigarette advertising.

  12. Do electronic cigarettes help with smoking cessation?

    PubMed

    2014-11-01

    Smoking causes around 100,000 deaths each year in the UK, and is the leading cause of preventable disease and early mortality. Smoking cessation remains difficult and existing licensed treatments have limited success. Nicotine addiction is thought to be one of the primary reasons that smokers find it so hard to give up, and earlier this year DTB reviewed the effects of nicotine on health. Electronic cigarettes (e-cigarettes) are nicotine delivery devices that aim to mimic the process of smoking but avoid exposing the user to some of the harmful components of traditional cigarettes. However, the increase in the use of e-cigarettes and their potential use as an aid to smoking cessation has been subject to much debate. In this article we consider the regulatory and safety issues associated with the use of e-cigarettes, and their efficacy in smoking cessation and reduction.

  13. Why Is Cigarette Smoking So Addicting? An Overview of Smoking as a Chemical and Process Addiction.

    ERIC Educational Resources Information Center

    Christen, Arden G.; Christen, Joan A.

    1994-01-01

    Reviews the addictive nature of cigarette smoking and the pharmacologic, psychological, and sociocultural parameters of tobacco use. The dynamic combination of related factors makes cigarette smoking extremely resistant to long-term extinction. The article suggests the use of active support systems during nicotine addiction recovery. (SM)

  14. Polonium in cigarette smoke and radiation exposure of lungs

    NASA Astrophysics Data System (ADS)

    Carvalho, Fernando P.; Oliveira, João M.

    2006-01-01

    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 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.

  15. A Wearable Sensor System for Monitoring Cigarette Smoking

    PubMed Central

    Sazonov, Edward; Lopez-Meyer, Paulo; Tiffany, Stephen

    2013-01-01

    Objective: Available methods of smoking assessment (e.g., self-report, portable puff-topography instruments) do not permit the collection of accurate measures of smoking behavior while minimizing reactivity to the assessment procedure. This article suggests a new method for monitoring cigarette smoking based on a wearable sensor system (Personal Automatic Cigarette Tracker [PACT]) that is completely transparent to the end user and does not require any conscious effort to achieve reliable monitoring of smoking in free-living individuals. Method: The proposed sensor system consists of a respiratory inductance plethysmograph for monitoring of breathing and a hand gesture sensor for detecting a cigarette at the mouth. The wearable sensor system was tested in a laboratory study of 20 individuals who performed 12 different activities including cigarette smoking. Signal processing was applied to evaluate the uniqueness of breathing patterns and their correlation with hand gestures. Results: The results indicate that smoking manifests unique breathing patterns that are highly correlated with hand-to-mouth cigarette gestures and suggest that these signals can potentially be used to identify and characterize individual smoke inhalations. Conclusions: With the future development of signal processing and pattern-recognition methods, PACT can be used to automatically assess the frequency of smoking and inhalation patterns (such as depth of inhalation and smoke holding) throughout the day and provide an objective method of assessing the effectiveness of behavioral and pharmacological smoking interventions. PMID:24172124

  16. Acute effects of electronic and tobacco cigarette smoking on complete blood count.

    PubMed

    Flouris, Andreas D; Poulianiti, Konstantina P; Chorti, Maria S; Jamurtas, Athanasios Z; Kouretas, Dimitrios; Owolabi, Emmanuel O; Tzatzarakis, Manolis N; Tsatsakis, Aristidis M; Koutedakis, Yiannis

    2012-10-01

    The World Health Organisation called for research assessing the safety of electronic cigarette (e-cigarette). We evaluated the acute effect of active and passive e-cigarette and tobacco cigarette smoking on complete blood count (CBC) markers in 15 smokers and 15 never-smokers, respectively. Smokers underwent a control session, an active tobacco cigarette smoking session, and an active e-cigarette smoking session. Never-smokers underwent a control session, a passive tobacco cigarette smoking session, and a passive e-cigarette smoking session. The results demonstrated that CBC indices remained unchanged during the control session and the active and passive e-cigarette smoking sessions (P>0.05). Active and passive tobacco cigarette smoking increased white blood cell, lymphocyte, and granulocyte counts for at least one hour in smokers and never smokers (P<0.05). It is concluded that acute active and passive smoking using the e-cigarettes tested in the current study does not influence CBC indices in smokers and never smokers, respectively. In contrast, acute active and passive tobacco cigarette smoking increase the secondary proteins of acute inflammatory load for at least one hour. More research is needed to evaluate chemical safety issues and other areas of consumer product safety of e-cigarettes, because the nicotine content in the liquids used may vary considerably.

  17. Influence of cigarette smoking on thyroid gland--an update.

    PubMed

    Sawicka-Gutaj, Nadia; Gutaj, Paweł; Sowiński, Jerzy; Wender-Ożegowska, Ewa; Czarnywojtek, Agata; Brązert, Jacek; Ruchała, Marek

    2014-01-01

    Many studies have shown that cigarette smoking exerts multiple effects on the thyroid gland. Smoking seems to induce changes in thyroid function tests, like decrease in TSH and increase in thyroid hormones. However, these alterations are usually mild. In addition, tobacco smoking may also play a role in thyroid autoimmunity. Many studies have confirmed a significant influence of smoking on Graves' hyperthyroidism and particularly on Graves' orbitopathy. Here, smoking may increase the risk of disease development, may reduce the effectiveness of treatment, and eventually induce relapse. The role of smoking in Hashimoto's thyroiditis is not as well established as in Graves' disease. Nonetheless, lower prevalence of thyroglobulin antibodies, thyroperoxidase antibodies and hypothyroidism were found in smokers. These findings contrast with a study that reported increased risk of hypothyroidism in smokers with Hashimoto's thyroiditis. Moreover, cigarette smoking increases the incidence of multinodular goitre, especially in iodine-deficient areas. Some studies have examined cigarette smoking in relation to the risk of thyroid cancer. Interestingly, many of them have shown that smoking may reduce the risk of differentiated thyroid cancer. Furthermore, both active and passive smoking during pregnancy might modify maternal and foetal thyroid function. This review evaluates the current data concerning the influence of cigarette smoking on thyroid gland, including hormonal changes, autoimmunity and selected diseases. These findings, however, in our opinion, should be carefully evaluated and some of them are not totally evidence-based. Further studies are required to explain the effects of smoking upon thyroid pathophysiology.

  18. Carbon monoxide kinetics following simulated cigarette smoking

    SciTech Connect

    Karnik, A.S.; Coin, E.J.

    1980-05-01

    Carbon monoxide kinetics were measured in the blood (% carboxyhemoglobin) and alveolar phase (ppM carbon monoxide) after simulated cigarette smoking. Cigarette smoking was siumlated using the same amount of carbon monoxide that 2R1F cigarettes manufactured by the Tobacco Research Institute would contain. Ten boluses of air containing carbon monoxide equivalent to smoking one cigarette were inhaled by six healthy nonsmoker volunteers. Carbon monoxide in the air phase was measured by an Ecolyzer and carboxyhemoglobin was measured by a CO-Oximeter. The mean rise in alveolar carbon monoxide immediately and 20 min after inhaling the last bolus was 3.3 and 3.1 ppM, respectively (p<.005). The mean rise in carboxyhemoglobin immediately and 20 min after inhalation of the last bolus was 0.8 and 0.5% respectively (P<.005). The changes in carboxyhemoglobin were found to be similar to changes that occur when one cigarette is actually smoked.

  19. Relative sensitivities of plasma lecithin:cholesterol acyltransferase, platelet-activating factor acetylhydrolase, and paraoxonase to in vitro gas-phase cigarette smoke exposure.

    PubMed

    Bielicki, J K; Knoff, L J; Tribble, D L; Forte, T M

    2001-03-01

    In order to identify potential atherogenic properties of gas-phase cigarette smoke, we utilized an in vitro exposure model to determine whether the activities of several putative anti-atherogenic enzymes associated with plasma lipoproteins were compromised. Exposure of heparinized human plasma to gas-phase cigarette smoke produced a dose-dependent reduction in the activity of platelet-activating factor acetylhydrolase (PAF-AH). Reductions of nearly 50% in PAF-AH activity were observed following exposure to gas-phase smoke from four cigarettes over an 8-h period. During this time of exposure, lecithin:cholesterol acyltransferase (LCAT) was rendered almost completely inactive (>80%). In contrast, paraoxonase was totally unaffected by cigarette smoke. Supplementation of plasma with 1 mM reduced glutathione was found to protect both PAF-AH and LCAT from cigarette smoke, suggesting that cysteine modifications may have contributed to the inhibition of these two enzymes. To evaluate this possibility, we blocked the free cysteine residues of these enzymes with the reversible thiol-modifying reagent dithiobisnitrobenzoic acid (DTNB). Reversal of the DTNB-cysteine adducts following cigarette smoke exposures revealed that LCAT, but not PAF-AH, was protected. Moreover, high doses (1.0-10 mM) of acrolein and 4-hydroxynonenal, reactive aldehydic species associated with cigarette smoke, completely inhibited plasma LCAT activity, whereas PAF-AH was resistant to such exposures. Taken together, these results indicate a divergence regarding the underlying mechanism of PAF-AH and LCAT inhibition upon exposure to gas-phase cigarette smoke. While LCAT was sensitive to exposure to volatile aldehydic products involving, in part, cysteine and/or active site modifications, the enzyme PAF-AH exhibited an apparent resistance. The latter suggests that the active site of PAF-AH is in a microenvironment that lacks free cysteine residues and/or is shielded from volatile aldehydic combustion

  20. Organ specificity of aryl hydrocarbon hydroxylase induction by cigarette smoke

    SciTech Connect

    Yoshikawa, M.; Arashidani, K.; Kawamoto, T.; Kodama, Y. )

    1990-06-01

    Biotransformation of many chemicals found in cigarette smoke, such as PAHs and nitrosamines, is generally considered essential for the mutagenic, carcinogenic effects of these xenobiotics. In fact, the genotic action of these premutagens or precarcinogens is dependent on metabolic activation catalyzed by microsomal monooxygenases. The first enzymatic reaction of the PAHs metabolic pathway is catalyzed by a cytochrome P-450-dependent monooxygenase, the aryl hydrocarbon hydroxylase (AHH). AHH leads to the formation of reactive arene oxides, which are further metabolized by enzymatic and non-enzymatic reaction into many metabolites. AHH induction in laboratory animals exposed to cigarette smoke has also been reported, and the data show that this response is highly dependent on species and tissues. Exposure of small laboratory animals to cigarette smoke generally induces AHH in the kidney and lung, while the effect of cigarette smoke on the hepatic AHH activity appears variable.

  1. Cigarette smoking and invasive cervical cancer

    SciTech Connect

    Brinton, L.A.; Schairer, C.; Haenszel, W.; Stolley, P.; Lehman, H.F.; Levine, R.; Savitz, D.A.

    1986-06-20

    A case-control study of 480 patients with invasive cervical cancer and 797 population controls, conducted in five geographic areas in the United States, included an evaluation of the relationship of several cigarette smoking variables to cervical cancer risk. Although smoking was correlated with both age at first intercourse and number of sexual partners, a significant smoking-related risk persisted for squamous cell carcinoma after adjustment for these factors (relative risk, 1.5). Twofold excess risks were seen for those smoking 40 or more cigarettes per day and those smoking for 40 or more years. Increased risks, however, were observed only among recent and continuous smokers. In contrast to squamous cell cancer, no relationship was observed between smoking and risk of adenocarcinoma or adenosquamous carcinoma. These results suggest a causal relationship between cigarette smoking and invasive squamous cell cervical cancer, perhaps through a late-stage or promotional event, although the mechanisms of action require further elucidation.

  2. Cigarette smoke inhibits brain mitochondrial adaptations of exercised mice.

    PubMed

    Speck, Ana Elisa; Fraga, Daiane; Soares, Priscila; Scheffer, Débora L; Silva, Luciano A; Aguiar, Aderbal S; Estreck, Emílio L; Pinho, Ricardo A

    2011-06-01

    Physical exercise and smoking are environmental factors that generally cause opposite health-promoting adaptations. Both physical exercise and smoking converge on mitochondrial adaptations in various tissues, including the pro-oxidant nervous system. Here, we analyzed the impact of cigarette smoking on exercise-induced brain mitochondrial adaptations in the hippocampus and pre-frontal cortex of adult mice. The animals were exposed to chronic cigarette smoke followed by 8 weeks of moderate-intensity physical exercise that increased mitochondrial activity in the hippocampus and pre-frontal cortex in the non-smoker mice. However, mice previously exposed to cigarette smoke did not present these exercise-induced mitochondrial adaptations. Our results suggest that smoking can inhibit some brain health-promoting changes induced by physical exercise.

  3. Impact of cigarette smoking in type 2 diabetes development.

    PubMed

    Xie, Xi-tao; Liu, Qiang; Wu, Jie; Wakui, Makoto

    2009-06-01

    Many patients with type 2 diabetes mellitus (DM2) are at risk for micro and macro vascular complications, which could be observed in heavy smokers. Cigarette smoking increases the risk for type 2 diabetes incidence. Nicotine, acknowledged as the major pharmacologically active chemical in tobacco, is responsible for the association between cigarette smoking and development of diabetes. This minireview summarized recent studies on nicotine effects on insulin action and insulin secretion, indicating the impact of nicotine on type 2 diabetes development.

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

    PubMed

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

    2012-01-01

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

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

    SciTech Connect

    Kitamura, S.

    1987-06-01

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

  6. Women, smoking, cigarette advertising and cancer.

    PubMed

    Ernster, V L

    1986-01-01

    Cigarette smoking is a major cause of cancer in women, accounting for about one-fourth of their estimated 219,000 cancer deaths per year. Cigarette smoking specifically increases a woman's risk of developing cancer of the lung, larynx, esophagus, oral cavity, pancreas, kidney, bladder, and possibly uterine cervix. During the past twenty years, concerted efforts have been made by the tobacco industry to increase sales to women. Strategies have included development of "feminine" brands such as Virginia Slims, slick media campaigns portraying smoking as elegant and glamorous, and sponsorship of fashion, women's sports events, and even medical programs. Reversal of these alarming trends requires that women as well as men recognize the role of cigarette smoking in cancer causation, and support programs which promote non-smoking as well as combat the influence of the tobacco industry on women's smoking behavior.

  7. Effect of solvent and extraction methods on the bacterial mutagenicity of sidestream cigarette smoke

    SciTech Connect

    Morin, R.S.; Tulis, J.J.; Claxton, L.D.

    1987-01-01

    The mutagenic activity of sidestream cigarette-smoke particles was estimated by testing sidestream cigarette-smoke particles that had been collected under controlled burning conditions in the laboratory. Two different extraction methods (Soxhlet and ultrasonic agitation) and 3 different solvents (dichloromethane, methanol, and acetone) were compared for their efficiencies in the extraction of compounds from sidestream cigarette-smoke particles that are mutagenic in the Ames test. The mutagenic activity of the sidestream smoke particles was estimated to be 15,000-20,000 revertants per cigarette in TA98 with metabolic activation and 12,000-17,000 revertants per cigarette in TA100 without metabolic activation.

  8. Light cigarette smoke-induced emphysema and NFκB activation in mouse lung

    PubMed Central

    Santos Valenca, Samuel; Castro, Paulo; Alves Pimenta, Wagner; Lanzetti, Manuella; Vargas Silva, Simone; Barja-Fidalgo, Cristina; Gonçalves Koatz, Vera Lúcia; Porto, Luís Cristóvão

    2006-01-01

    Light cigarette (LC) exposure is supposed to be less hazardous with a decreased incidence of cancer and tobacco-associated diseases. C57BL/6 mouse groups were subjected to smoke from 3, 6 or 12 LC for 60 days and compared with mice exposed to ambient air (EAA) in order to study lung injury by morphometrical and biochemical methods. Bronchoalveolar lavage (BAL) analysis and histology and stereology were performed. Tissue from the right lung was used for measuring thiobarbituric acid reactive substances (TBARS) and Western blot analysis. One way anova was performed followed by the Student–Newman Keuls post-test (P < 0.05). The cellular content of BAL was 95% alveolar macrophages in all groups except in mice exposed to 3 LC, where 23% neutrophils were observed. Emphysema was not observed in three and 6 LC, but it was found in 12 LC parallel to increased volume density (Vv) of airspaces from 61.0 ± 0.6 (EAA) to 80.9 ± 1.0 (12 LC) and decreased Vv of elastic fibres from 17.8 ± 0.9 (EAA) to 11.8 ± 0.6 (12 LC). All exposed groups to LC showed low TBARS levels compared with mice EAA. Lung tissue from animals exposed to 12 LC showed decreased tissue inhibitor of metalloprotease-2 and increased matrix metalloprotease-12 detection, which suggests an imbalance in extracellular matrix (ECM). Increased tumour necrosis factor-α and nuclear factor-κB detection were observed in exposed groups to LC when compared with mice EAA. The data suggest that LC is so dangerous to lungs as full-flavour cigarettes inducing ECM imbalance and emphysema. PMID:16965565

  9. "Smoking wet": respiratory failure related to smoking tainted marijuana cigarettes.

    PubMed

    Gilbert, Christopher R; Baram, Michael; Cavarocchi, Nicholas C

    2013-01-01

    Reports have suggested that the use of a dangerously tainted form of marijuana, referred to in the vernacular as "wet" or "fry," has increased. Marijuana cigarettes are dipped into or laced with other substances, typically formaldehyde, phencyclidine, or both. Inhaling smoke from these cigarettes can cause lung injuries. We report the cases of 2 young adults who presented at our hospital with respiratory failure soon after they had smoked "wet" marijuana cigarettes. In both patients, progressive hypoxemic respiratory failure necessitated rescue therapy with extracorporeal membrane oxygenation. After lengthy hospitalizations, both patients recovered with only mild pulmonary function abnormalities. To our knowledge, this is the first 2-patient report of severe respiratory failure and rescue therapy with extracorporeal oxygenation after the smoking of marijuana cigarettes thus tainted. We believe that, in young adults with an unexplained presentation of severe respiratory failure, the possibility of exposure to tainted marijuana cigarettes should be considered.

  10. Lung injury after cigarette smoking is particle related.

    PubMed

    Sangani, Rahul G; Ghio, Andrew J

    2011-01-01

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

  11. Does environmental cigarette smoke affect breastfeeding behavior?

    PubMed Central

    Firouzbakht, Mozhgan; Hajian-Tilaki, Karimallah; Nikpour, Maryam; Banihosseini, Zahra

    2017-01-01

    BACKGROUND: Exposure of lactating women to environmental cigarette smoke may increase cotinine in breast milk, which in turn may reduce the volume of milk and the duration of breastfeeding. OBJECTIVES: To assess the relationship between exposure to environmental cigarette smoke and breastfeeding behavior. MATERIALS AND METHODS: This prospective cohort study was conducted on 290 mothers in Babol - Iran, who had been breastfeeding for 3–5 days after delivery. The lactating mothers were divided into two groups: those exposed to environmental cigarette smoke, and those free from smoke exposure. The study questionnaire included demographic data, information on environmental cigarette smoke, and breastfeeding behavior. Data was collected through telephone interviews at 2, 4, and 6 months of follow-up. Statistical analysis included descriptive statistics, and test of significance using Chi-square test, t-test, log-rank test, and Cox proportional hazards model. RESULTS: The continuation of breastfeeding for the group of exposed mothers and the unexposed group was (mean ± standard deviation) 5.57 ± 0.098 and 5.58 ± 0.109, respectively in 6 months of follow-up. There was no significant difference between the two groups (P = 0.93). The percentage of exclusive breastfeeding at 6 months in the group exposed to cigarette smoke was 65% compared to 76% of the nonexposed group. However, the difference was not statistically significant (P = 0.149). CONCLUSIONS: In this study, no significant association was observed between the group exposed to environmental cigarette smoke and the nonexposed group in breastfeeding behavior, although the percentage of exclusive breastfeeding at 6 months was less in the group exposed to environmental cigarette smoke. Further exploratory studies are needed. PMID:28163575

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

    PubMed

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

    2016-01-12

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

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

    PubMed Central

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

    2016-01-01

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

  14. Cigarette Smoking Onset among High School Students.

    ERIC Educational Resources Information Center

    Hansen, William B.; And Others

    While data on the onset of cigarette smoking among younger adolescents has been investigated extensively, it is less clear whether the same social factors influence older adolescents. To examine these social factors, as well as the influence of personality and beliefs, 1,977 high school participants in an anti-smoking study completed a…

  15. Adolescents' leisure activities, parental monitoring and cigarette smoking - a cross-sectional study

    PubMed Central

    2011-01-01

    Background Adolescent participation in leisure activities is developmentally beneficial, but certain activities may increase health compromising behaviours, such as tobacco smoking. A limited range of leisure activities has been studied, with little research on out-of-school settings where parental supervision is a potential protective factor. Tobacco smoking is an important, potentially modifiable health determinant, so understanding associations between adolescent leisure activities, parental monitoring, demographic factors and daily smoking may inform preventive strategies. These associations are reported for a New Zealand adolescent sample. Methods Randomly selected schools (n = 145) participated in the 2006 Youth In-depth Survey, a national, biennial study of Year 10 students (predominantly 14-15 years). School classes were randomly selected and students completed a self-report questionnaire in class time. Adjustment for clustering at the school level was included in all analyses. Since parental monitoring and demographic variables potentially confound relations between adolescent leisure activities and smoking, variables were screened before multivariable modelling. Given prior indications of demographic differences, gender and ethnic specific regression models were built. Results and Discussion Overall, 8.5% of the 3,161 students were daily smokers, including more females (10.5%) than males (6.5%). In gender and ethnic specific multivariate analysis of associations with daily smoking (adjusted for age, school socioeconomic decile rating, leisure activities and ethnicity or gender, respectively), parental monitoring exhibited a consistently protective, dose response effect, although less strongly among Māori. Attending a place of worship and going to the movies were protective for non-Māori, as was watching sports, whereas playing team sport was protective for all, except males. Attending a skate park was a risk factor for females and Māori which

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

    PubMed

    Coggins, Christopher R E; Gaworski, Charles L

    2008-04-01

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

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

    PubMed Central

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

    2015-01-01

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

  18. Overview of the pharmacogenomics of cigarette smoking.

    PubMed

    Ho, M K; Tyndale, R F

    2007-04-01

    Cigarette smoking increases the risk of numerous health problems, including cancer, cardiovascular and pulmonary disorders, making smoking the leading cause of preventable death in the world. Nicotine is primarily responsible for the highly addictive properties of cigarettes. Although the majority of smokers express a desire to quit, few are successful in doing so. Twin and family studies have indicated substantial genetic contributions to smoking behaviors. One major research focus has been to elucidate the specific genes involved; this has been accomplished primarily through genome-wide linkage analyses and candidate gene association studies. Much attention has focused on genes involved in the neurotransmitter pathways for the brain reward system and genes altering nicotine metabolism. This paper reviews the current state of knowledge for genetic factors implicated in smoking behaviors, and examines how genetic variations may affect therapeutic outcomes for drugs used to assist smoking cessation.

  19. Smoking bans, cigarette prices and life satisfaction.

    PubMed

    Odermatt, Reto; Stutzer, Alois

    2015-12-01

    The consequences of tobacco control policies for individual welfare are difficult to assess, even more so when related consumption choices challenge people's willpower. We therefore evaluate the impact of smoking bans and cigarette prices on subjective well-being by analyzing data for 40 European countries and regions between 1990 and 2011. We exploit the staggered introduction of bans and apply an imputation strategy to study the effect of anti-smoking policies on people with different propensities to smoke. We find that higher cigarette prices reduce the life satisfaction of likely smokers. Overall, smoking bans are barely related to subjective well-being, but increase the life satisfaction of smokers who would like to quit smoking. The latter finding is consistent with cue-triggered models of addiction and the idea of bans as self-control devices.

  20. Cigarette smoke reversibly activates hypoxia-inducible factor 1 in a reactive oxygen species-dependent manner

    PubMed Central

    Daijo, Hiroki; Hoshino, Yuma; Kai, Shinichi; Suzuki, Kengo; Nishi, Kenichiro; Matsuo, Yoshiyuki; Harada, Hiroshi; Hirota, Kiichi

    2016-01-01

    Cigarette smoke (CS) is a major contributor to the development of a large number of fatal and debilitating disorders. However, the precise molecular mechanisms underlying the effects of CS in lung disease are largely unknown. To elucidate these pathophysiological processes, we examined the in vitro and in vivo effects of CS extract (CSE) and CS on the transcription factor, hypoxia-inducible factor 1 (HIF-1). CSE induced concentration- and time-dependent accumulation of HIF-1α protein in human lung epithelial-like cells under non-hypoxic conditions. Genes upregulated by HIF-1, including vascular endothelial growth factor and regulated in development and DNA damage response 1, both of which are involved in smoking-induced emphysematous changes, were increased by CSE treatment under non-hypoxic conditions in vitro and in vivo. Further investigation revealed that reactive oxygen species were generated in cells exposed to CSE and were required for CSE-mediated induction of HIF-1α protein, as was activation of phosphoinositide 3-kinase and mitogen-activated protein kinase pathways. In conclusion, we demonstrated that CSE and CS induced HIF-1 activation in vitro and in vivo, respectively. The evidence warrants further investigation to indicate that HIF-1 plays an important role in CS-induced gene expression, which is deeply involved in pulmonary cellular stress and small airway remodelling. PMID:27680676

  1. Lung injury after cigarette smoking is particle-related

    EPA Science Inventory

    That specific component responsible and the mechanistic pathway for increased human morbidity and mortality after cigarette smoking have yet to be delineated. We propose that 1) injury and disease following cigarette smoking are associated with exposure and retention of particles...

  2. Cigarette smoke extract-induced p120-mediated NF-κB activation in human epithelial cells is dependent on the RhoA/ROCK pathway

    PubMed Central

    Zhang, Chao; Qin, Shenghui; Qin, Lingzhi; Liu, Liwei; Sun, Wenjia; Li, Xiyu; Li, Naping; Wu, Renliang; Wang, Xi

    2016-01-01

    Cigarette smoke exposure is a major cause of chronic obstructive pulmonary disease (COPD), but the underlying molecular inflammatory mechanisms remain poorly understood. Previous studies have found that smoke disrupts cell-cell adhesion by inducing epithelial barrier damage to the adherens junction proteins, primarily E-cadherin (E-cad) and p120-catenin (p120). Recently, the anti-inflammatory role of p120 has drawn increasing attention. In this study, we demonstrate that p120 has a role in the cigarette smoke extract-induced inflammatory response, presumably by regulating NF-κB signaling activation. Mechanistically, we show that p120-mediated NF-κB signaling activation in airway epithelial inflammation is partially RhoA dependent and is independent of E-cad. These results provide novel evidence for the role of p120 in the anti-inflammatory response. PMID:27586697

  3. Cigarette smoking effect on human cochlea responses

    PubMed Central

    Rogha, Mehrdad; Hashemi, Mostafa; Askari, Narges; Abtahi, Seyed Hamidreza; Sepehrnejad, Mahsa; Nilforoush, Mohammad Hossein

    2015-01-01

    Background: Smoking is one of the most important risk factor in increasing of non-communicable disorders, especially chronic diseases such as cancer, stroke, heart and respiratory diseases. Cigarette smoking could damage the cochlea and causing hearing loss. The otoacoustic emission (OAE) is a source of information for determining cochlear responses to sound stimuli and how to change the response of the auditory system in some diseases. OAE test was sensitive to outer hair cells (OHCs) activity. Materials and Methods: In this study, tried to evaluate a hearing threshold of the smoker group versus non-smoker ones through pure tone audiometery, transient evoked otoacoustic emission (TEOAE) and distortion product otoacoustic emission (DPOAE) tests. Results: The results indicated that significant decrement of 8000 Hz threshold, reduced DPOAE/TEOAE amplitude in the smoker group than non-smoker one (P < 0.05). DPOAE amplitudes decline reflects the cochlear damage caused by smoking. Conclusion: OAEs test was clinically non-invasive, accurate, and objective evaluation of the performance of cochlear OHCs. PMID:26380233

  4. Transcriptome sequencing reveals e-cigarette vapor and mainstream-smoke from tobacco cigarettes activate different gene expression profiles in human bronchial epithelial cells

    PubMed Central

    Shen, Yifei; Wolkowicz, Michael J.; Kotova, Tatyana; Fan, Lonjiang; Timko, Michael P.

    2016-01-01

    Electronic cigarettes (e-cigarettes) generate an aerosol vapor (e-vapor) thought to represent a less risky alternative to main stream smoke (MSS) of conventional tobacco cigarettes. RNA-seq analysis was used to examine the transcriptomes of differentiated human bronchial epithelial (HBE) cells exposed to air, MSS from 1R5F tobacco reference cigarettes, and e-vapor with and without added nicotine in an in vitro air-liquid interface model for cellular exposure. Our results indicate that while e-vapor does not elicit many of the cell toxicity responses observed in MSS-exposed HBE cells, e-vapor exposure is not benign, but elicits discrete transcriptomic signatures with and without added nicotine. Among the cellular pathways with the most significantly enriched gene expression following e-vapor exposure are the phospholipid and fatty acid triacylglycerol metabolism pathways. Our data suggest that alterations in cellular glycerophopholipid biosynthesis are an important consequences of e-vapor exposure. Moreover, the presence of nicotine in e-vapor elicits a cellular response distinct from e-vapor alone including alterations of cytochrome P450 function, retinoid metabolism, and nicotine catabolism. These studies establish a baseline for future analysis of e-vapor and e-vapor additives that will better inform the FDA and other governmental bodies in discussions of the risks and future regulation of these products. PMID:27041137

  5. Transcriptome sequencing reveals e-cigarette vapor and mainstream-smoke from tobacco cigarettes activate different gene expression profiles in human bronchial epithelial cells.

    PubMed

    Shen, Yifei; Wolkowicz, Michael J; Kotova, Tatyana; Fan, Lonjiang; Timko, Michael P

    2016-04-04

    Electronic cigarettes (e-cigarettes) generate an aerosol vapor (e-vapor) thought to represent a less risky alternative to main stream smoke (MSS) of conventional tobacco cigarettes. RNA-seq analysis was used to examine the transcriptomes of differentiated human bronchial epithelial (HBE) cells exposed to air, MSS from 1R5F tobacco reference cigarettes, and e-vapor with and without added nicotine in an in vitro air-liquid interface model for cellular exposure. Our results indicate that while e-vapor does not elicit many of the cell toxicity responses observed in MSS-exposed HBE cells, e-vapor exposure is not benign, but elicits discrete transcriptomic signatures with and without added nicotine. Among the cellular pathways with the most significantly enriched gene expression following e-vapor exposure are the phospholipid and fatty acid triacylglycerol metabolism pathways. Our data suggest that alterations in cellular glycerophopholipid biosynthesis are an important consequences of e-vapor exposure. Moreover, the presence of nicotine in e-vapor elicits a cellular response distinct from e-vapor alone including alterations of cytochrome P450 function, retinoid metabolism, and nicotine catabolism. These studies establish a baseline for future analysis of e-vapor and e-vapor additives that will better inform the FDA and other governmental bodies in discussions of the risks and future regulation of these products.

  6. Development of nitroxide radicals-containing polymer for scavenging reactive oxygen species from cigarette smoke

    NASA Astrophysics Data System (ADS)

    Yoshitomi, Toru; Kuramochi, Kazuhiro; Binh Vong, Long; Nagasaki, Yukio

    2014-06-01

    We developed a nitroxide radicals-containing polymer (NRP), which is composed of poly(4-methylstyrene) possessing nitroxide radicals as a side chain via amine linkage, to scavenge reactive oxygen species (ROS) from cigarette smoke. In this study, the NRP was coated onto cigarette filters and its ROS-scavenging activity from streaming cigarette smoke was evaluated. The intensity of electron spin resonance signals of the NRP in the filter decreased after exposure to cigarette smoke, indicating consumption of nitroxide radicals. To evaluate the ROS-scavenging activity of the NRP-coated filter, the amount of peroxy radicals in an extract of cigarette smoke was measured using UV-visible spectrophotometry and 1,1-diphenyl-2-picrylhydrazyl (DPPH). The absorbance of DPPH at 517 nm decreased with exposure to cigarette smoke. When NRP-coated filters were used, the decrease in the absorbance of DPPH was prevented. In contrast, both poly[4-(cyclohexylamino)methylstyrene]- and poly(acrylic acid)-coated filters, which have no nitroxide radical, did not show any effect, indicating that the nitroxide radicals in the NRP scavenge the ROS in cigarette smoke. As a result, the extract of cigarette smoke passed through the NRP-coated filter has a lower cellular toxicity than smoke passed through poly[4-(cyclohexylamino)methylstyrene]- and poly(acrylic acid)-coated filters. Accordingly, NRP is a promising material for ROS scavenging from cigarette smoke.

  7. Development of nitroxide radicals-containing polymer for scavenging reactive oxygen species from cigarette smoke.

    PubMed

    Yoshitomi, Toru; Kuramochi, Kazuhiro; Binh Vong, Long; Nagasaki, Yukio

    2014-06-01

    We developed a nitroxide radicals-containing polymer (NRP), which is composed of poly(4-methylstyrene) possessing nitroxide radicals as a side chain via amine linkage, to scavenge reactive oxygen species (ROS) from cigarette smoke. In this study, the NRP was coated onto cigarette filters and its ROS-scavenging activity from streaming cigarette smoke was evaluated. The intensity of electron spin resonance signals of the NRP in the filter decreased after exposure to cigarette smoke, indicating consumption of nitroxide radicals. To evaluate the ROS-scavenging activity of the NRP-coated filter, the amount of peroxy radicals in an extract of cigarette smoke was measured using UV-visible spectrophotometry and 1,1-diphenyl-2-picrylhydrazyl (DPPH). The absorbance of DPPH at 517 nm decreased with exposure to cigarette smoke. When NRP-coated filters were used, the decrease in the absorbance of DPPH was prevented. In contrast, both poly[4-(cyclohexylamino)methylstyrene]- and poly(acrylic acid)-coated filters, which have no nitroxide radical, did not show any effect, indicating that the nitroxide radicals in the NRP scavenge the ROS in cigarette smoke. As a result, the extract of cigarette smoke passed through the NRP-coated filter has a lower cellular toxicity than smoke passed through poly[4-(cyclohexylamino)methylstyrene]- and poly(acrylic acid)-coated filters. Accordingly, NRP is a promising material for ROS scavenging from cigarette smoke.

  8. Association between Peer Cigarette Smoking and Electronic Cigarette Smoking among Adolescent Nonsmokers: A National Representative Survey

    PubMed Central

    Hwang, Jun Hyun; Park, Soon-Woo

    2016-01-01

    We assessed the association between electronic cigarette (e-cigarette) use and peer cigarette smoking, a major risk factor for the initiation of cigarette smoking in adolescents. Data from the 2013 Korea Youth Risk Behavior Web-based Survey of 65,753 nonsmokers aged 13–18 years were analyzed using multiple logistic regression. A total of 3.8% of the Korean adolescents were ‘ever e-cigarette’ users and 1.2% were current users. Adjusted odds ratios (ORs) for current and ever e-cigarette use compared to those whose closest friends were non-smokers ranged from 2.05 (95% confidence interval [CI], 1.82–2.30) to 5.50 (95% CI, 4.77–6.34), and from 2.23 (95% CI, 1.77–2.81) to 7.82 (95% CI, 5.97–10.25) for those who had ‘some’ close friends to ‘most/all’ friends who smoked, respectively. The slopes of the adjusted ORs for e-cigarette use in ‘never smokers’ were more than twice as steep as those in ‘former smokers’, showing a significant interaction effect between the proportion of smoking closest friends and cigarette smoking status (never or former smokers) (p<0.001 for interaction). Peer cigarette smoking had a significant association with e-cigarette use in adolescent nonsmokers, and this association was greater on never smokers than former smokers. PMID:27695093

  9. Depressive Symptoms and Cigarette Smoking in a College Sample

    ERIC Educational Resources Information Center

    Kenney, Brent A.; Holahan, Charles J.

    2008-01-01

    Objective and Participants: The authors examined (1) the relationship between depressive symptoms and cigarette smoking in a college sample and (2) the role of smoking self-efficacy (one's perceived ability to abstain from smoking) in explaining the relationship between depressive symptoms and cigarette smoking. Methods: Predominantly first-year…

  10. Predicting the Cytotoxic Potency of Cigarette Smoke by Assessing the Thioredoxin Reductase Inhibitory Capacity of Cigarette Smoke Extract.

    PubMed

    Zhang, Longjie; Ning, Min; Xu, Yingbo; Wang, Chenghui; Zhao, Guangshan; Cao, Qingqing; Zhang, Jinsong

    2016-03-21

    The present study investigated the influence of the cigarette smoke extract (CSE) on mammalian thioredoxin reductase (TrxR) activity. TrxR is a selenoenzyme with a selenocysteine (Sec) residue exposed on the enzyme's surface. This unique Sec residue is particularly susceptible to modification by numerous types of electrophiles, leading to inactivation of TrxR and consequent cytotoxicity. Cigarette smoke contains various electrophiles, and the present study showed that CSE could inhibit intracellular TrxR through causing crosslinking and alkylation of TrxR1. TrxR inhibitory capacities of various CSEs were evaluated by using mouse-liver homogenate. Among the CSEs prepared from 18 commercial cigarette brands, TrxR inhibitory capacities of the maximum and the minimum had a 2.5-fold difference. Importantly, CSE's inhibitory capacity greatly paralleled its cytotoxic potency in all cell lines used. Compared to cytotoxic assays, which have been widely used for evaluating cigarette toxicity but are not suitable for simultaneously examining a large number of cigarette samples, the present method was simple and rapid with a high-throughput feature and thus could be used as an auxiliary means to predict the cytotoxicity of a large number of cigarette samples, making it possible to extensively screen numerous agricultural and industrial measures that potentially affect cigarette safety.

  11. The Impact of Trying Electronic Cigarettes on Cigarette Smoking by College Students: A Prospective Analysis

    PubMed Central

    Reboussin, Beth A; Debinski, Beata; Wagoner, Kimberly G.; Spangler, John; Wolfson, Mark

    2015-01-01

    Objectives. We assessed the impact of trying electronic cigarettes (e-cigarettes) on future cigarette smoking in a sample of smokers enrolled in college. Methods. In this longitudinal study, first-semester college students at 7 colleges in North Carolina and 4 in Virginia completed a baseline survey and 5 follow-up surveys between fall 2010 and fall 2013. Current cigarette smoking at wave 6 was the primary outcome. Participants (n = 271) reported current cigarette smoking at baseline and no history of e-cigarette use. We measured trying e-cigarettes at each wave, defined as use in the past 6 months. Results. By wave 5, 43.5% had tried e-cigarettes. Even after controlling for other variables associated with cigarette smoking, trying e-cigarettes was a significant predictor of cigarette smoking at wave 6 (adjusted odds ratio [AOR] = 2.48; 95% confidence interval [CI] = 1.32, 4.66), as were friends’ cigarette smoking (AOR = 4.20; 95% CI = 2.22, 7.96) and lifetime use of other tobacco products (AOR = 1.63; 95% CI = 1.22, 2.17). Conclusions. Trying e-cigarettes during college did not deter cigarette smoking and may have contributed to continued smoking. PMID:26066954

  12. Proliferative Activity of Liver Growth Factor is Associated with an Improvement of Cigarette Smoke-Induced Emphysema in Mice

    PubMed Central

    Terrón-Expósito, Raúl; Díaz-Gil, Juan José; González-Mangado, Nicolás; Peces-Barba, Germán

    2014-01-01

    Cigarette smoke (CS)-induced emphysema is a major component of chronic obstructive pulmonary disease (COPD). COPD treatment is based on the administration of bronchodilators and corticosteroids to control symptoms and exacerbations, however, to date, there are no effective therapies to reverse disease progression. Liver growth factor (LGF) is an albumin-bilirubin complex with mitogenic properties, whose therapeutic effects have previously been reported in a model of emphysema and several rodent models of human disease. To approach the therapeutic effect of LGF in a model of previously established emphysema, morphometric and lung function parameters, matrix metalloproteinase (MMP) activity and the expression of several markers, such as VEGF, PCNA, 3NT and Nrf2, were assessed in air-exposed and CS-exposed C57BL/6J male mice with and without intraperitoneal (i.p.) injection of LGF. CS-exposed mice presented a significant enlargement of alveolar spaces, higher alveolar internal area and loss of lung function that correlated with higher MMP activity, higher expression of 3NT and lower expression of VEGF. CS-exposed mice injected with LGF, showed an amelioration of emphysema and improved lung function, which correlated with lower MMP activity and 3NT expression and higher levels of VEGF, PCNA and Nrf2. Taken together, this study suggests that LGF administration ameliorates CS-induced emphysema, highlights the ability of LGF to promote alveolar cell proliferation and may be a promising strategy to revert COPD progression. PMID:25401951

  13. Cigarette smoke extract induces epithelial-mesenchymal transition of human bladder cancer T24 cells through activation of ERK1/2 pathway.

    PubMed

    Sun, Xin; Deng, Qifei; Liang, Zhaofeng; Liu, Zhiqi; Geng, Hao; Zhao, Li; Zhou, Qirui; Liu, Jie; Ma, Jiaxing; Wang, Daming; Yu, Dexin; Zhong, Caiyun

    2017-02-01

    Bladder cancer is a common genitourinary malignant disease worldwide. Abundant evidence has shown that cigarette smoke (CS) is a crucial risk factor for bladder cancer. Nevertheless, the mechanism underlying the relationship between cigarette smoking and bladder cancer remains unclear. In the present study, we investigated the effects of cigarette smoke extract (CSE) on mitogen-activated protein kinase (MAPK) pathway activation and EMT alterations in human bladder cancer T24 cells, and the preventive effect of extracellular regulated protein kinases 1 and 2 (ERK1/2) inhibitor U0126 was further examined. Our results illustrated that CSE exposure induced morphological change of human bladder cancer T24 cells, enhanced migratory and invasive capacities, reduced epithelial marker expression and elevated mesenchymal marker expression. Meanwhile, exposure of T24 cells to CSE resulted in activation of ERK1/2 pathway as well as activator protein 1 (AP-1) proteins. Interestingly, treatment with ERK1/2 inhibitor U0126 effectively abrogated CSE-triggered EMT and ERK1/2/AP-1 activation. These findings provide novel insight into the molecular mechanisms of CS-associated bladder cancer and may open up new avenues in the search for potential target of bladder cancer intervention.

  14. [History of cigarette smoking. The effect of tobacco smoking on women's health].

    PubMed

    Zalewska, Marta; Jagielska, Iwona; Kazdepka-Ziemińska, Anita; Ludwikowski, Grzegorz; Szymański, Wiesław

    2009-01-01

    History of cigarette smoking started on XV century, when Columb imported tobacco to Europe. Popular using of tobacco we are indebted Jaen Nicot Villeman, the name of nicotine originate from his surname. Tobacco first was exploited like a drug, however now it is a very harmful stimulant. Cigarette smoking is still an actual problem and increased risk of many diseases. Very toxic components of smoke get inside all the organs and upsetting their activities and proper running of the life processes. It is common knowledge that smoking badly influences women's health. Nicotine makes the negative influence on function of ovaries metabolism of hormones and state of osseous tissue. Maternal smoking during pregnancy is associated with obstetrical and pediatrician complication with fetus, newborn and child. The aim of the article is to summarize the role of tobacco smoking on women's health.

  15. Active cigarette smoking and the risk of breast cancer at the level of N-acetyltransferase 2 (NAT2) gene polymorphisms.

    PubMed

    Kasajova, Petra; Holubekova, Veronika; Mendelova, Andrea; Lasabova, Zora; Zubor, Pavol; Kudela, Erik; Biskupska-Bodova, Kristina; Danko, Jan

    2016-06-01

    The aim of our study was to assess the correlation between the tobacco exposure and NAT2 gene (rs1041983 C/T, rs1801280 T/C, rs1799930 G/A) polymorphisms in association with breast cancer development. We wanted to determine the prognostic clinical importance of these polymorphisms in association with smoking and breast cancer. For the detection of possible association between smoking, NAT2 gene polymorphisms, and the risk of breast cancer, we designed a case-controlled study with 198 patients enrolled, 98 breast cancer patients and 100 healthy controls. Ten milliliters of peripheral blood from the cubital vein was withdrawn from every patient. The HRM (high resolution melting) analysis was used for the detection of three abovementioned NAT2 gene polymorphisms. When comparing a group of women smoking more than 5 cigarettes a day with the patients smoking fewer than 5 cigarettes a day, we found out that if women were the carriers of aberrant AA genotype for rs1799930, the first group of women had higher risk of breast carcinoma than the second group. If patients were the carriers of aberrant TT genotype for rs1041983, for rs1801280CC genotype, and rs1799930AA genotype and they smoked more than 5 cigarettes a day, they had higher risk of malignant breast disease than never-smoking women. Our results confirm the hypothesis that NAT2 gene polymorphisms (rs1041983 C/T, rs1801280 T/C, and rs1799930 G/A) in association with long-period active smoking could be the possible individual risk-predicting factors for breast cancer development in the population of Slovak women.

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

    SciTech Connect

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

    2013-09-01

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

  17. Cigarette smoking and health. American Thoracic Society.

    PubMed

    1996-02-01

    Cigarette smoking remains the primary cause of preventable death and morbidity in the United States. Smoking causes lung cancer, COPD, and CHD and contributes significantly to mortality from other conditions such as stroke. Maternal smoking during pregnancy causes low birthweight and perinatal mortality, and it may have lasting impact on the child's physical and cognitive growth. Passive exposure to ETS causes lung cancer and poses particular danger to the respiratory health of young children. Smoking cessation strategies are important, but the should be supplemented by community and policy-level interventions. Workplace or community smoking bans, statewide taxes on tobacco, and antismoking media campaigns may be effective adjuncts to individual cessation strategies. These strategies may be an even more important disincentive to smoking initiation. The expanding horizon of health consequences of smoking and its costs to American society should again challenge public health agencies to develop and implement effective strategies to prevent smoking acquisition by young people. These health effects should also motivate health professionals in other countries where smoking prevalence is increasing, rather than decreasing, to initiate more effective efforts to reverse this trend and minimize the excess morbidity and death that accompany this dangerous habit.

  18. NOS3 polymorphisms, cigarette smoking, and cardiovascular disease risk: The Atherosclerosis Risk in Communities study

    Technology Transfer Automated Retrieval System (TEKTRAN)

    Endothelial nitric oxide synthase (NOS3) activity and cigarette smoking significantly influence endothelial function. We sought to determine whether cigarette smoking modified the association between NOS3 polymorphisms and risk of coronary heart disease or stroke. All 1085 incident coronary heart di...

  19. Information management strategies within conversations about cigarette smoking: parenting correlates and longitudinal associations with teen smoking.

    PubMed

    Metzger, Aaron; Wakschlag, Lauren S; Anderson, Ryan; Darfler, Anne; Price, Juliette; Flores, Zujeil; Mermelstein, Robin

    2013-08-01

    The present study examined smoking-specific and general parenting predictors of in vivo observed patterns of parent-adolescent discussion concerning adolescents' cigarette smoking experiences and associations between these observed patterns and 24-month longitudinal trajectories of teen cigarette smoking behavior (nonsmokers, current experimenters, escalators). Parental solicitation, adolescent disclosure, and adolescent information management were coded from direct observations of 528 video-recorded parent-adolescent discussions about cigarette smoking with 344 teens (M age = 15.62 years) with a history of smoking experimentation (321 interactions with mothers, 207 interactions with fathers). Adolescent initiation of discussions concerning their own smoking behavior (21% of interactions) was predicted by lower levels of maternal observed disapproval of cigarette smoking and fewer teen-reported communication problems with mothers. Maternal initiation in discussions (35% of interactions) was associated with higher levels of family rules about illicit substance use. Three categories of adolescent information management (full disclosure, active secrecy, incomplete strategies) were coded by matching adolescents' confidential self-reported smoking status with their observed spontaneous disclosures and responses to parental solicitations. Fully disclosing teens reported higher quality communication with their mothers (more open, less problematic). Teens engaged in active secrecy with their mothers when families had high levels of parental rules about illicit substance use and when mothers expressed lower levels of expectancies that their teen would smoke in the future. Adolescents were more likely to escalate their smoking over 2 years if their parents initiated the discussion of adolescent smoking behavior (solicited) and if adolescents engaged in active secrecy.

  20. Influence of cigarette smoking on human autonomic function

    NASA Technical Reports Server (NTRS)

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

    1993-01-01

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

  1. Selenium-mediated reduction in the mutagenicity of cigarette smoke

    SciTech Connect

    Chortyk, O.T.; Baker, J.L.; Chamberlain, W.J.

    1988-01-01

    Cigarette smoke contains carcinogens and mutagens and affects the health of smokers. Recently, increased research has proven the potentially protective activity of selenium (Se) against heavy metal toxicity, cancer, and other health disorders. Accordingly, we have proposed the fortification of tobacco with Se to develop safer cigarettes. As a start in evaluating any biological effects of added Se, we have determined the mutagenicity of inhaled, mainstream (MS) cigarette smoke condensate (CSC), with and without Se, in the preincubation assay of the Ames test. Initially, it was shown that Se, as sodium selenite, was not mutagenic at high concentrations (up to 80 micrograms/plate) with strains TA1538 and TA1978. Subsequently, the effects of different levels of Se, added to MS CSC, were examined with TA98, TA100, and TA1538. On the average, addition of 10 micrograms Se produced mutagenicity reductions of about 50%. Higher levels of added Se yielded further reductions. Cigarette sidestream (SS) smoke, collected between puffs, was also tested. Again, Se added to SS-CSC gave similar reductions, confirming its antimutagenic effect for both mainstream and sidestream smoke.

  2. Total particulate matter concentration skews cigarette smoke's gene expression profile.

    PubMed

    Dvorkin-Gheva, Anna; Vanderstocken, Gilles; Yildirim, Ali Önder; Brandsma, Corry-Anke; Obeidat, Ma'en; Bossé, Yohan; Hassell, John A; Stampfli, Martin R

    2016-10-01

    Exposure of small animals to cigarette smoke is widely used as a model to study the pathogenesis of chronic obstructive pulmonary disease. However, protocols and exposure systems utilised vary substantially and it is unclear how these different systems compare. We analysed the gene expression profile of six publically available murine datasets from different cigarette smoke-exposure systems and related the gene signatures to three clinical cohorts. 234 genes significantly regulated by cigarette smoke in at least one model were used to construct a 55-gene network containing 17 clusters. Increasing numbers of differentially regulated clusters were associated with higher total particulate matter concentrations in the different datasets. Low total particulate matter-induced genes mainly related to xenobiotic/detoxification responses, while higher total particulate matter activated immune/inflammatory processes in addition to xenobiotic/detoxification responses. To translate these observations to the clinic, we analysed the regulation of the revealed network in three human cohorts. Similar to mice, we observed marked differences in the number of regulated clusters between the cohorts. These differences were not determined by pack-year. Although none of the experimental models exhibited a complete alignment with any of the human cohorts, some exposure systems showed higher resemblance. Thus, depending on the cohort, clinically observed changes in gene expression may be mirrored more closely by specific cigarette smoke exposure systems. This study emphasises the need for careful validation of animal models.

  3. Total particulate matter concentration skews cigarette smoke's gene expression profile

    PubMed Central

    Dvorkin-Gheva, Anna; Vanderstocken, Gilles; Yildirim, Ali Önder; Brandsma, Corry-Anke; Obeidat, Ma'en; Bossé, Yohan; Hassell, John A.

    2016-01-01

    Exposure of small animals to cigarette smoke is widely used as a model to study the pathogenesis of chronic obstructive pulmonary disease. However, protocols and exposure systems utilised vary substantially and it is unclear how these different systems compare. We analysed the gene expression profile of six publically available murine datasets from different cigarette smoke-exposure systems and related the gene signatures to three clinical cohorts. 234 genes significantly regulated by cigarette smoke in at least one model were used to construct a 55-gene network containing 17 clusters. Increasing numbers of differentially regulated clusters were associated with higher total particulate matter concentrations in the different datasets. Low total particulate matter-induced genes mainly related to xenobiotic/detoxification responses, while higher total particulate matter activated immune/inflammatory processes in addition to xenobiotic/detoxification responses. To translate these observations to the clinic, we analysed the regulation of the revealed network in three human cohorts. Similar to mice, we observed marked differences in the number of regulated clusters between the cohorts. These differences were not determined by pack-year. Although none of the experimental models exhibited a complete alignment with any of the human cohorts, some exposure systems showed higher resemblance. Thus, depending on the cohort, clinically observed changes in gene expression may be mirrored more closely by specific cigarette smoke exposure systems. This study emphasises the need for careful validation of animal models. PMID:27995131

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

    PubMed

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

    2012-01-02

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

  5. Cigarette Smoking is Associated with Unhealthy Patterns of Food Consumption, Physical Activity, Sleep Impairment, and Alcohol Drinking in Chinese Male Adults

    PubMed Central

    Cappelli, Christopher; Li, Yawen; Tanenbaum, Hilary; Chou, Chih-Ping; Spruijt-Metz, Donna; Palmer, Paula H.; Johnson, C. Anderson

    2015-01-01

    Objectives According to a recent national survey, tobacco use is a critical public health issue in China, with more than two thirds of Chinese males smoking. Findings in Western populations suggest that smoking may cluster with other health-risk behaviors. To explore these relationships in Chinese male adults, we utilized baseline data from the China Seven Cities Study (CSCS). Methods Male adults (N=12,122) were included. Smoking status was defined as never smokers, ex-smokers, current smokers, and current heavy smokers. Logistic regression was employed to investigate the association of cigarette smoking and patterns of food consumption, physical activity, and alcohol drinking. Results After controlling for age, socioeconomic status, and city residence, heavy smokers consumed significantly less vegetables, fruits, milk and other dairy products, spent significantly more time watching television, slept and exercised less, and got drunk or engaged in binge drinking more frequently compared to never, ex, or current smokers (p<0.05). Conclusion Findings suggest significant associations of heavy cigarette smoking with other health-risk behaviors in Chinese male adults, underscoring the need for tobacco control interventions for Chinese males. PMID:26321106

  6. Determination of Formaldehyde in Cigarette Smoke

    NASA Astrophysics Data System (ADS)

    Wong, Jon W.; Ngim, Kenley K.; Eiserich, Jason P.; Yeo, Helen C. H.; Shibamoto, Takayuki; Mabury, Scott A.

    1997-09-01

    Formaldehdye is considered a hazardous air pollutant with numerous sources that include environmental tobacco smoke (ETS). With the increasing interest regarding ETS and public health the measurement of formaldehyde readily lends itself to a laboratory experiment comparing methods of analysis. This experiment involves the collection, derivatization, extraction, and analysis of formaldehyde from cigarette smoke using two methods. Formaldehyde is extracted from smoke and derivitized with a solution of 2,4-DNPH with subsequent cleanup by solid-phase extraction and analysis of the hydrazone by HPLC with UV detection; additionally a solution of cysteamine yields the corresponding thiazolidine derivative that is liquid/liquid extracted and subsequently analyzed by either GC with NPD or FPD (sulfur mode). Reasonable agreement among the methods was obtained by lab demonstrators with spike recoveries yielding 94.7 + 6.8 (n=5) and 89.2 (n = 4) % for NPD and FPD, respectively while HPLC spiked recoveries were 83.6 + 3.2 (n = 5) %; mean class spike recoveries ranged from 80-100%. Student results (in mg/cigarette) from smoke samples were similar to literature values with 163.2 + 69.2 (n = 7) and 149.4 (n = 7) % for NPD and FPD, respectively; the HPLC result was significantly lower at 45.1 + 23.7(n = 7) with losses presumably due to hydrazone precipitating from the smoke extracted solution. Students particularly benefited from the "real world" nature of the analysis and the experience evaluating disparate methods of determining a common analyte.

  7. Cigarette Smoking and Pancreatic Cancer Survival.

    PubMed

    Yuan, Chen; Morales-Oyarvide, Vicente; Babic, Ana; Clish, Clary B; Kraft, Peter; Bao, Ying; Qian, Zhi Rong; Rubinson, Douglas A; Ng, Kimmie; Giovannucci, Edward L; Ogino, Shuji; Stampfer, Meir J; Gaziano, John Michael; Sesso, Howard D; Cochrane, Barbara B; Manson, JoAnn E; Fuchs, Charles S; Wolpin, Brian M

    2017-03-30

    Purpose Cigarette smoking is associated with increased incidence of pancreatic cancer. However, few studies have prospectively evaluated the association of smoking with patient survival. Patients and Methods We analyzed survival by smoking status among 1,037 patients from two large US prospective cohort studies diagnosed from 1986 to 2013. Among 485 patients from four prospective US cohorts, we also evaluated survival by prediagnostic circulating levels of cotinine, a metabolite of nicotine that is proportional to tobacco smoke exposure. On the basis of prediagnosis cotinine levels, we classified patients as nonsmokers (< 3.1 ng/mL), light smokers (3.1-20.9 ng/mL), or heavy smokers (≥ 21.0 ng/mL). We estimated hazard ratios (HRs) for death by using Cox proportional hazards models, with adjustment for age, sex, race/ethnicity, body mass index, diabetes status, diagnosis year, and cancer stage. Results The multivariable-adjusted HR for death was 1.37 (95% CI, 1.11 to 1.69) comparing current smokers with never smokers ( P = .003). A statistically significant negative trend in survival was observed for increasing pack-years of smoking ( Ptrend = .008), with HR for death of 1.49 (95% CI, 1.05 to 2.10) for > 60 pack-years of smoking versus never smoking. Survival among former smokers was similar to that for never smokers, regardless of time since quitting. Heavy smokers defined by prediagnostic circulating cotinine levels had a multivariable-adjusted HR for death of 1.76 (95% CI, 1.23 to 2.51) compared with nonsmokers. Among patients with circulating cotinine levels measured within 5 years before diagnosis, heavy smokers had a multivariable-adjusted HR for death of 2.47 (95% CI, 1.24 to 4.92) compared with nonsmokers. Conclusion Cigarette smoking was associated with a reduction in survival among patients with pancreatic cancer.

  8. How does electronic cigarette access affect adolescent smoking?

    PubMed

    Friedman, Abigail S

    2015-12-01

    Understanding electronic cigarettes' effect on tobacco smoking is a central economic and policy issue. This paper examines the causal impact of e-cigarette access on conventional cigarette use by adolescents. Regression analyses consider how state bans on e-cigarette sales to minors influence smoking rates among 12 to 17 year olds. Such bans yield a statistically significant 0.9 percentage point increase in recent smoking in this age group, relative to states without such bans. Results are robust to multiple specifications as well as several falsification and placebo checks. This effect is both consistent with e-cigarette access reducing smoking among minors, and large: banning electronic cigarette sales to minors counteracts 70 percent of the downward pre-trend in teen cigarette smoking for a given two-year period.

  9. Cigarette Smoking among Korean Adolescents: Prevalence and Correlates.

    ERIC Educational Resources Information Center

    Juon, Hee-Soon; And Others

    1995-01-01

    Examines prevalence of cigarette smoking and explores its relationship with individual, family, school, and psychological factors among Korean adolescents. Current prevalence of cigarette smoking was 8.45 percent. Smoking prevalence increased with age among boys. Perceived peer use, academic stress, grade, and type of school were associated with…

  10. Effects of exposure to cigarette smoke on intestinal propulsion in rats.

    PubMed

    Furuno, K; Okazaki, M; Eto, K; Kawasaki, H; Gomita, Y

    1995-08-01

    The effects of acute exposure to cigarette smoke and systemic administration of nicotine on intestinal propulsion were investigated in rats. The propulsive activity was measured as migration of charcoal powder in the intestine. This activity was suppressed by acute exposure (10 min) to cigarette smoke and by nicotine (0.5 mg/kg x 2, s.c.) administration. This intestinal suppression was more marked in the rats given nicotine than in those exposed to cigarette smoke, whereas the plasma concentrations of nicotine in both rats were similar. These results suggest that acute exposure to cigarette smoke and nicotine administration delay gastric emptying and/or suppress intestinal propulsion, and that some components other than nicotine contained in cigarette smoke may attenuate the suppression of intestinal propulsion induced by nicotine.

  11. Sex differences in the brain's dopamine signature of cigarette smoking.

    PubMed

    Cosgrove, Kelly P; Wang, Shuo; Kim, Su-Jin; McGovern, Erin; Nabulsi, Nabeel; Gao, Hong; Labaree, David; Tagare, Hemant D; Sullivan, Jenna M; Morris, Evan D

    2014-12-10

    Cigarette smoking is a major public health danger. Women and men smoke for different reasons and cessation treatments, such as the nicotine patch, are preferentially beneficial to men. The biological substrates of these sex differences are unknown. Earlier PET studies reported conflicting findings but were each hampered by experimental and/or analytical limitations. Our new image analysis technique, lp-ntPET (Normandin et al., 2012; Morris et al., 2013; Kim et al., 2014), has been optimized for capturing brief (lasting only minutes) and highly localized dopaminergic events in dynamic PET data. We coupled our analysis technique with high-resolution brain scanning and high-frequency motion correction to create the optimal experiment for capturing and characterizing the effects of smoking on the mesolimbic dopamine system in humans. Our main finding is that male smokers smoking in the PET scanner activate dopamine in the right ventral striatum during smoking but female smokers do not. This finding-men activating more ventrally than women-is consistent with the established notion that men smoke for the reinforcing drug effect of cigarettes whereas women smoke for other reasons, such as mood regulation and cue reactivity. lp-ntPET analysis produces a novel multidimensional endpoint: voxel-level temporal patterns of neurotransmitter release ("DA movies") in individual subjects. By examining these endpoints quantitatively, we demonstrate that the timing of dopaminergic responses to cigarette smoking differs between men and women. Men respond consistently and rapidly in the ventral striatum whereas women respond faster in a discrete subregion of the dorsal putamen.

  12. Nicotine Replacement, Topography, and Smoking Phenotypes of E-cigarettes

    PubMed Central

    Strasser, Andrew A.; Souprountchouk, Valentina; Kaufmann, Amanda; Blazekovic, Sonja; Leone, Frank; Benowitz, Neal L.; Schnoll, Robert A.

    2016-01-01

    Objectives Little is known about the degree of nicotine replacement across first-generation e-cigarette brands, how e-cigarettes are used, and if there is variation across brands in relevant smoking phenotypes. The objective of this project was to collect data that are critical to better understanding, use, and exposure when using e-cigarettes, which may then inform clinical trials and tobacco regulatory policy. Methods Twenty-eight cigarette smokers were randomized to use one of 5 popular brands of e-cigarettes for a 10-day study. Day 1 (own cigarette brand) data established baseline levels for cotinine, carbon monoxide (CO), topography, cigarette liking, withdrawal, and craving. Participants returned on Days 5 and 10 to reassess these measures while exclusively using e-cigarettes. Results Compared to cigarette smoking, e-cigarettes provided significantly lower nicotine levels (25%-50%), reduced CO exposure, and lower ratings of liking (p < .05). Topography significantly differed between cigarette and e-cigarette sessions (p < .05). All brands significantly reduced withdrawal and craving (p < .05). There were no significant brand differences in outcome measures associated with exposure or use. Conclusions E-cigarettes are not liked as much as cigarettes, provide significantly lower nicotine replacement, reduce CO exposure, and mitigate withdrawal and craving. The patterns of use significantly differ compared to cigarette smoking. PMID:27942543

  13. Cigarette smoke exposure facilitates allergic sensitization in mice

    PubMed Central

    Moerloose, Katrien B; Robays, Lander J; Maes, Tania; Brusselle, Guy G; Tournoy, Kurt G; Joos, Guy F

    2006-01-01

    Background Active and passive smoking are considered as risk factors for asthma development. The mechanisms involved are currently unexplained. Objective The aim of this study was to determine if cigarette smoke exposure could facilitate primary allergic sensitization. Methods BALB/c mice were exposed to aerosolized ovalbumin (OVA) combined with air or tobacco smoke (4 exposures/day) daily for three weeks. Serology, lung cytopathology, cytokine profiles in bronchoalveolar lavage fluid (BALF) and on mediastinal lymph node cultures as well as lung function tests were performed after the last exposure. The natural history and the immune memory of allergic sensitization were studied with in vivo recall experiments. Results Exposure to OVA induced a small increase in OVA-specific serum IgE as compared with exposure to PBS (P < 0.05), while no inflammatory reaction was observed in the airways. Exposure to cigarette smoke did not induce IgE, but was characterized by a small but significant neutrophilic inflammatory reaction. Combining OVA with cigarette smoke not only induced a significant increase in OVA-specific IgE but also a distinct eosinophil and goblet cell enriched airway inflammation albeit that airway hyperresponsiveness was not evidenced. FACS analysis showed in these mice increases in dendritic cells (DC) and CD4+ T-lymphocytes along with a marked increase in IL-5 measured in the supernatant of lymph node cell cultures. Immune memory experiments evidenced the transient nature of these phenomena. Conclusion In this study we show that mainstream cigarette smoke temporary disrupts the normal lung homeostatic tolerance to innocuous inhaled allergens, thereby inducing primary allergic sensitization. This is characterized not only by the development of persistent IgE, but also by the emergence of an eosinophil rich pulmonary inflammatory reaction. PMID:16571114

  14. [Smoking and electronic cigarettes in France].

    PubMed

    Berlin, Ivan

    2016-12-01

    France is one of the developed countries where the prevalence of tobacco use is the highest. The reduction of incidence and prevalence of tobacco use in the near future would considerably decrease tobacco associated mortality and morbidity. The electronic cigarette, a consumer product that delivers pharmacologically active substances, is used by several millions of persons in France. The benefit-risk ratio of electronic cigarette use is unknown, as of today.

  15. Pattern of inhalation of tobacco smoke in pipe, cigarette, and never smokers.

    PubMed

    Rodenstein, D O; Stănescu, D C

    1985-09-01

    There is controversy on whether both primary and secondary pipe smokers do inhale tobacco smoke. We studied inhalation of tobacco smoke in 6 primary and 6 secondary pipe smokers and compared it with that in 20 cigarette smokers and 11 never smokers. Respiratory movements were assessed with inductive plethysmography, nasal flow through measurements of nasal pressure, oral flow with an oral thermistor, puffing through pressure measurements in the cigarette holder or the pipe, and upper airways by fluoroscopy. In all pipe smokers except 1, breathing and smoking appeared as independent activities. The former was exclusively nasal, whereas the latter was exclusively oral. Smoke was sucked and puffed by a to-and-fro movement of the tongue sliding along the soft palate. The oropharyngeal isthmus was closed (or only intermittently opened) by the apposition of the soft palate and the tongue, thus preventing overt inhalation of smoke. In most cigarette smokers, smoking interfered with the breathing route. Once smoke was sucked into the mouth, the oropharyngeal isthmus opened and inspiration proceeded through both mouth (with inhalation of smoke) and nose. Cigarette smoking interfered also with the evenness of ventilation. Never smokers avoided inhalation by oropharyngeal closure followed by oral expiration. We conclude that the oropharyngeal isthmus is the essential gate controlling smoke inhalation. Most secondary pipe smokers are able to change their smoking pattern and avoid overt inhalation when switching from cigarette to pipe smoking. The inhalation pattern appears to be acquired in the course of the smoking history.

  16. Analysis of the smoke of cigarettes containing Salvia divinorum.

    PubMed

    Krstenansky, John L; Muzzio, Miguel

    2014-09-01

    Salvia divinorum is a hallucinogen sold over the internet in several forms. Perhaps the most common method of use is smoking the dried leaf material. The sole presumed active constituent, salvinorin A, is a selective kappa-opioid receptor agonist. Upon smoking of the dried leaf material, some of the salvinorin A is destroyed or converted to other materials, leaving in question the actual amount of salvinorin A delivered that leads to the psychotomimetic effect. On average, 133 μg of salvinorin A was delivered in the smoke from an 830 mg per cigarette, which contained ∼2.7 mg of salvinorin A. Hence, only ∼5% of the salvinorin A available in the dried plant material was delivered in the smoke. Upon smoking, hydrolysis of salvinorin A to salvinorin B, an inactive and minor component of the leaf material, also occurs as evidenced by a higher delivered amount of salvinorin B vs salvinorin A (217 vs 133 μg per cigarette). Since smoking is an effective means of achieving the hallucinogenic effect and salvinorin A is the presumed sole active ingredient in the plant, the estimated effective dose of salvinorin A by inhalation is <133 μg per person. Considering the reported rapid metabolism of salvinorin A in vivo, the dose reaching the brain would be substantially less.

  17. Structural and functional alteration of blood vessels caused by cigarette smoking: an overview of molecular mechanisms.

    PubMed

    Rahman, Mohammad M; Laher, Ismail

    2007-10-01

    Smoking is a significant independent risk factor for cardiovascular disease and is a leading cause of structural and functional alterations of the cardiovascular system. Most clinical and experimental investigations of the pathophysiology of cigarette smoking have studied the effects of smoke as a whole, while a few studies focused on specific components of cigarette smoke, e.g. nicotine and carbon monoxide, which are only 2 of the more than 4,000 different chemicals present in cigarette smoke. The findings point to some discrepancies when the effects of whole smoke are compared to nicotine alone, while there is almost uniform agreement that both active and passive smoking have detrimental effects on the cardiovascular system, although a milder effect was suggested for the latter. This review focuses on findings from clinical and experimental studies on the vascular effects of active and passive cigarette smoking and nicotine exposure. The findings are discussed in terms of tissue (conduit vs. resistance arteries and veins), species, age, gender and dosage. Although the exact pathophysiology of cigarette smoking has not been unveiled, cigarette smoking causes injury to the vascular endothelium, produces superoxide anions, reduces production and bioavailability of nitric oxide (NO), increases production and release of endothelin, causes endothelial dysfunction, thrombosis, atherosclerosis, infarction, coronary artery disease (CAD), stroke and death.

  18. Cigarette smoking, binge drinking, physical activity, and diet in 138 Asian American and Pacific Islander community college students in Brooklyn, New York.

    PubMed

    Arliss, Rebecca M

    2007-02-01

    Assessment of cigarette smoking, alcohol consumption, physical activity, and diet in the Asian American and Pacific Islander (AAPI) community has been neglected. A questionnaire was used to investigate these health risk behaviors in 466 students at an urban community college and results for the 138 AAPI study participants were compared to the 328 non-Asians. Results for AAPI study participants showed that twenty percent (20.3%) were current cigarette smokers and 7.7% smoked eleven or more cigarettes per day. Ten percent (10.7%) reported binge drinking on one to two days per month and 17.3% reported binge drinking on three or more days per month. With regard to physical activity, 28.8% participated in stretching, 23.6% in strength and toning, 29.4% in moderate exercise, and 25.4% in vigorous exercise. Results indicated that on the day preceding the survey, only 11.9% consumed five or more servings of fruits and vegetables, 88.4% ate no more than two servings of high-fat foods, and 37.6% consumed tofu, soymilk, or other soy food. AAPI study participants were more likely to frequently binge drink (p < .05), less likely to participate in strength and toning exercises (p < .05), and more likely to consume soy foods daily (p < .01) than non-Asian study participants. Recommendations are presented for health promotion program planning.

  19. Do smokers crave cigarettes in some smoking situations more than others? Situational correlates of craving when smoking

    PubMed Central

    Scharf, Deborah; Kirchner, Thomas; Shiffman, Saul

    2010-01-01

    Introduction: Smokers tend to smoke when experiencing craving, but even within smoking occasions, craving may vary. We examine variations in craving when people were smoking in various real-world situations. Methods: Using Ecological Momentary Assessment, 394 smokers recorded smoking, craving, and smoking context in real time on electronic diaries over 2 weeks of ad libitum smoking. Assessments occurred immediately prior to smoking. Mixed modeling was used to analyze associations between craving and situational variables. Results: Craving varied across smoking situations, but the differences were small (<1 on a 0–10 scale). Specifically, craving was higher in smoking situations where smoking was restricted, likely because high craving leads smokers to violate restrictions. Controlling for restrictions, craving was higher when cigarettes were smoked while eating or drinking, were with other people (vs. alone), were in a group of people (vs. other people simply in view), during work (vs. leisure), and during activity (vs. inactivity). In addition, craving was higher for cigarettes smoked early in the day. No differences in craving were observed in relation to drinking alcohol or caffeine (vs. doing anything else), being at work (vs. home), being at a bar or restaurant (vs. all other locations), interacting with others (vs. not interacting), or other people smoking (vs. no others smoking). Discussion: Even though most craving reports prior to smoking were high, and situations were thus expected to have little influence on craving, results suggest that some cigarettes are craved more than others across different smoking situations, but differences are small. PMID:20133379

  20. Inhibitory effect of Chinese green tea on cigarette smoke-induced up-regulation of airway neutrophil elastase and matrix metalloproteinase-12 via antioxidant activity.

    PubMed

    Chan, Ka Ho; Chan, Stanley Chi Hang; Yeung, Sze Chun; Man, Ricky Ying Keung; Ip, Mary Sau Man; Mak, Judith Choi Wo

    2012-09-01

    Our recent study has indicated that Chinese green tea (Lung Chen), in which epigallocatechin-3-gallate (EGCG) accounts for 60% of catechins, protected cigarette smoke-induced lung injury. We now hypothesized that Lung Chen tea may also have potential effect on lung oxidative stress and proteases/anti-proteases in a smoking rat model. Sprague-Dawley rats were exposed to either sham air (SA) or 4% cigarette smoke (CS) plus 2% Lung Chen tea or water by oral gavage. Serine proteases, matrix metalloproteinases (MMPs) and their respective endogenous inhibitors were determined in bronchoalveolar lavage (BAL) and lung tissues by gelatin/casein zymography and biochemical assays. Green tea consumption significantly decreased CS-induced elevation of lung lipid peroxidation marker, malondialdehyde (MDA), and CS-induced up-regulation of neutrophil elastase (NE) concentration and activity along with that of α(1)-antitrypsin (α(1)-AT) and secretory leukoproteinase inhibitor (SLPI) in BAL and lung. In parallel, significant elevation of MMP-12 activity was found in BAL and lung of the CS-exposed group, which returned to the levels of SA-exposed group after green tea consumption but not CS-induced reduction of tissue inhibitor of metalloproteinase (TIMP)-1 activity, which was not reversed by green tea consumption. Taken together, our data supported the presence of local oxidative stress and protease/anti-protease imbalance in the airways after CS exposure, which might be alleviated by green tea consumption through its biological antioxidant activity.

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

    PubMed Central

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

    2015-01-01

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

  2. Chronic exposure to cigarette smoke during gestation results in altered cholinesterase enzyme activity and behavioral deficits in adult rat offspring: potential relevance to schizophrenia.

    PubMed

    Zugno, Alexandra I; Fraga, Daiane B; De Luca, Renata D; Ghedim, Fernando V; Deroza, Pedro F; Cipriano, Andreza L; Oliveira, Mariana B; Heylmann, Alexandra S A; Budni, Josiane; Souza, Renan P; Quevedo, João

    2013-06-01

    Prenatal cigarette smoke exposure (PCSE) has been associated with physiological and developmental changes that may be related to an increased risk for childhood and adult neuropsychiatric diseases. The present study investigated locomotor activity and cholinesterase enzyme activity in rats, following PCSE and/or ketamine treatment in adulthood. Pregnant female Wistar rats were exposed to 12 commercially filtered cigarettes per day for a period of 28 days. We evaluated motor activity and cholinesterase activity in the brain and serum of adult male offspring that were administered acute subanesthetic doses of ketamine (5, 15 and 25 mg/kg), which serves as an animal model of schizophrenia. To determine locomotor activity, we used the open field test. Cholinesterase activity was assessed by hydrolysis monitored spectrophotometrically. Our results show that both PCSE and ketamine treatment in the adult offspring induced increase of locomotor activity. Additionally, it was observed increase of acetylcholinesterase and butyrylcholinesterase activity in the brain and serum, respectively. We demonstrated that animals exposed to cigarettes in the prenatal period had increased the risk for psychotic symptoms in adulthood. This also occurs in a dose-dependent manner. These changes provoke molecular events that are not completely understood and may result in abnormal behavioral responses found in neuropsychiatric disorders, such as schizophrenia.

  3. Smoke of cigarettes and little cigars: an analytical comparison.

    PubMed

    Hoffmann, D; Wynder, E L

    1972-12-15

    Chemical data are presented from a comparison study of the smoke of cigarettes and little cigars. The tobacco products and their mainstream smokes were analyzed for a number of toxic constituents in an effort to define "smoke inhalability." This issue has particular public health importance because the difference in the inhalability of cigar and cigarette smoke is generally assumed to account for the differences in the health risk to the individual smoker.

  4. Green tea polyphenol EGCG suppresses cigarette smoke condensate-induced NF-kappaB activation in normal human bronchial epithelial cells.

    PubMed

    Syed, D N; Afaq, F; Kweon, M-H; Hadi, N; Bhatia, N; Spiegelman, V S; Mukhtar, H

    2007-02-01

    Cigarette smoke is a powerful inducer of inflammatory responses resulting in disruption of major cellular pathways with transcriptional and genomic alterations driving the cells towards carcinogenesis. Cell culture and animal model studies indicate that (-)-epigallocatechin-3-gallate (EGCG), the major polyphenol present in green tea, possesses potent anti-inflammatory and antiproliferative activity capable of selectively inhibiting cell growth and inducing apoptosis in cancer cells without adversely affecting normal cells. Here, we demonstrate that EGCG pretreatment (20-80 microM) of normal human bronchial epithelial cells (NHBE) resulted in significant inhibition of cigarette smoke condensate (CSC)-induced cell proliferation. Nuclear factor-kappaB (NF-kappaB) controls the transcription of genes involved in immune and inflammatory responses. In most cells, NF-kappaB prevents apoptosis by mediating cell survival signals. Pretreatment of NHBE cells with EGCG suppressed CSC-induced phosphorylation of IkappaBalpha, and activation and nuclear translocation of NF-kappaB/p65. NHBE cells transfected with a luciferase reporter plasmid containing an NF-kappaB-inducible promoter sequence showed an increased reporter activity after CSC exposure that was specifically inhibited by EGCG pretreatment. Immunoblot analysis showed that pretreatment of NHBE cells with EGCG resulted in a significant downregulation of NF-kappaB-regulated proteins cyclin D1, MMP-9, IL-8 and iNOS. EGCG pretreatment further inhibited CSC-induced phosphorylation of ERK1/2, JNK and p38 MAPKs and resulted in a decreased expression of PI3K, AKT and mTOR signaling molecules. Taken together, our data indicate that EGCG can suppress NF-kappaB activation as well as other pro-survival pathways such as PI3K/AKT/mTOR and MAPKs in NHBE cells, which may contribute to its ability to suppress inflammation, proliferation and angiogenesis induced by cigarette smoke.

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

    ERIC Educational Resources Information Center

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

    2011-01-01

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

  6. Erythrocyte Antioxidant Defenses Against Cigarette Smoking in Ischemic Heart Disease

    PubMed Central

    Basalingappa, Doddamani R; Uppala, Satyanarayana; Mitta, Geeta

    2015-01-01

    Background Cigarette smoke promotes atherogenesis by producing oxygen-derived free radicals. Aim The present study was conducted to determine the effect of cigarette smoking on lipid peroxidation and erythrocyte antioxidant status in ischemic heart disease (IHD). Materials and Methods A total of 327 male subjects were enrolled for this study, divided into two groups consisting of 200 patients, who were consecutively admitted for IHD in the intensive cardiac care unit (ICCU) of a Government Hospital and 127 age matched male healthy subjects. Both the groups were subsequently categorised into smokers and non smokers sub groups depending upon the smoking history {>/= 20 pack years of smoking; (20 cigarettes per day for one year constitutes one pack year)}. All 327 subjects were investigated for lipid profile, malondialdehyde (MDA) levels and the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPX). Statistical Analysis The differences in the parameters between the groups were tested for significance by one way ANOVA using the SPSS software version 19. A p-value of < 0.001 was considered to be significant statistically. Multiple comparisons were made between all the four groups by Post Hoc Tukey test. Results There was highly significant difference (p<0.001) observed in GPX activity, in comparison to CAT and SOD (p=0.032, p=0.009) between smokers vs non smokers in control group as well as patient group. The plasma MDA levels were found to be increased significantly (p<0.001) in IHD patients, who smoked as compared to those who did not. Conclusion Chronic smoking enhances erythrocyte lipid peroxidation in IHD patients with concomitant failure of both plasma and erythrocyte antioxidant defense mechanisms. Along with conventional lipid markers and plasma MDA levels, the erythrocyte GPX activity was observed to be a better marker of oxidative stress, in chronic smokers, who are at risk of developing IHD. PMID:26266112

  7. [Electronic Cigarettes: Lifestyle Gadget or Smoking Cessation Aid?].

    PubMed

    Schuurmans, Macé M

    2015-07-01

    Electronic cigarettes (e-cigarettes) are vaporisers of liquids often containing nicotine. In the inhaled aerosol carcinogens, ultrafine and metal particles are detected usually in concentrations below those measured in tobacco smoke. Therefore, these products are expected to be less harmful. This has not yet been proven. The long-term safety of e-cigarettes is unknown. Short duration use leads to airway irritation and increased diastolic blood pressure. So far only two randomised controlled trials have investigated efficacy and safety of e-cigarettes for smoking cessation: No clear advantage was shown in comparison to smoking cessation medication. Due to insufficient evidence, e-cigarettes cannot be recommended for smoking cessation. Problematic are the lack of regulation and standardisation of e-cigarette products, which makes general conclusions impossible.

  8. The contribution of low tar cigarettes to environmental tobacco smoke

    SciTech Connect

    Chortyk, O.T.; Schlotzhauer, W.S. )

    1989-05-01

    A series of low tar cigarettes (LTC) were smoked and the quantities of condensable mainstream (inhaled) and sidestream (between puffs) smoke compounds were determined and compared to those produced by a high tar, nonfilter cigarette. It was found that the LTC produced large quantities of sidestream smoke condensates, about equal to the high tar cigarette, and contained very high levels of toxic or cocarcinogenic phenols. On an equal weight basis, the LTC emitted more of these hazardous compounds into sidestream and environmental tobacco smoke. Higher smoke yields of a flavor additive and a sugar degradation product indicated addition of such compounds during the manufacture of LTC. It was concluded that, compared to a high tar cigarette, smoking LTC may be better for the smoker, but not for the nearby nonsmoker. Information should be developed to allow smokers to choose LTC that produce lower levels of hazardous compounds in their environmentally emitted sidestream smoke.

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

    PubMed

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

    2015-08-01

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

  10. A Symbolic Interaction Approach to Cigarette Smoking: Smoking Frequency and the Desire to Quit Smoking

    PubMed Central

    Reitzes, Donald C.; DePadilla, Lara; Sterk, Claire E.; Elifson, Kirk W.

    2013-01-01

    This study applies a symbolic interaction perspective to the investigation of smoking frequency and a person’s desire to quit smoking cigarettes. Data derived from 485 Atlanta area adult smokers provide a diverse, community-based sample of married and single men and women, aged 18 to 70 years old with a range of income, education, and occupational experiences. Multiple regression was used to analyze the data in order to explore the influence of social demographic characteristics, social interaction, subjective assessments of health, self conceptions, and smoker identity on smoking frequency and quitting smoking. Findings include: (1) the relationship with a non-smoker and hiding smoking negatively impacted smoking frequency, while perceiving positive consequences from smoking has a positive effect on smoking frequency; and (2) perceiving positive consequences of smoking was negatively related to the desire to quit smoking, while a negative smoker identity has a positive influence on the desire to quit. Taken as a whole, the symbolic interaction-inspired variables exerted strong and independent effects on both smoking frequency and quitting smoking. Future smoking interventions should focus on meanings and perceived consequences of smoking in general, and on the smoker identity in the development of campaigns to encourage quitting cigarette smoking. PMID:23869112

  11. Cigarette smoking and mechanisms of susceptibility to infections of the respiratory tract and other organ systems.

    PubMed

    Feldman, Charles; Anderson, Ronald

    2013-09-01

    The predisposition of cigarette smokers for development of oral and respiratory infections caused by microbial pathogens is well recognised, with those infected with the human immunodeficiency virus (HIV) at particularly high risk. Smoking cigarettes has a suppressive effect on the protective functions of airway epithelium, alveolar macrophages, dendritic cells, natural killer (NK) cells and adaptive immune mechanisms, in the setting of chronic systemic activation of neutrophils. Cigarette smoke also has a direct effect on microbial pathogens to promote the likelihood of infective disease, specifically promotion of microbial virulence and antibiotic resistance. In addition to interactions between smoking and HIV infection, a number of specific infections/clinical syndromes have been associated epidemiologically with cigarette smoking, including those of the upper and lower respiratory tract, gastrointestinal tract, central nervous and other organ systems. Smoking cessation benefits patients in many ways, including reduction of the risk of infectious disease.

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

    PubMed

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

    2015-03-01

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

  13. Comparison of environmental tobacco smoke (ETS) concentrations generated by an electrically heated cigarette smoking system and a conventional cigarette.

    PubMed

    Tricker, Anthony R; Schorp, Matthias K; Urban, Hans-Jörg; Leyden, Donald; Hagedorn, Heinz-Werner; Engl, Johannes; Urban, Michael; Riedel, Kirsten; Gilch, Gerhard; Janket, Dinamis; Scherer, Gerhard

    2009-01-01

    Smoking conventional lit-end cigarettes results in exposure of nonsmokers to potentially harmful cigarette smoke constituents present in environmental tobacco smoke (ETS) generated by sidestream smoke emissions and exhaled mainstream smoke. ETS constituent concentrations generated by a conventional lit-end cigarette and a newly developed electrically heated cigarette smoking system (EHCSS) that produces only mainstream smoke and no sidestream smoke emissions were investigated in simulated "office" and "hospitality" environments with different levels of baseline indoor air quality. Smoking the EHCSS (International Organisation for Standardization yields: 5 mg tar, 0.3 mg nicotine, and 0.6 mg carbon monoxide) in simulated indoor environments resulted in significant reductions in ETS constituent concentrations compared to when smoking a representative lit-end cigarette (Marlboro: 6 mg tar, 0.5 mg nicotine, and 7 mg carbon monoxide). In direct comparisons, 24 of 29 measured smoke constituents (83%) showed mean reductions of greater than 90%, and 5 smoke constituents (17%) showed mean reductions between 80% and 90%. Gas-vapor phase ETS markers (nicotine and 3-ethenylpyridine) were reduced by an average of 97% (range 94-99%). Total respirable suspended particles, determined by online particle measurements and as gravimetric respirable suspended particles, were reduced by 90% (range 82-100%). The mean and standard deviation of the reduction of all constituents was 94 +/- 4%, indicating that smoking the new EHCSS in simulated "office" and "hospitality" indoor environments resulted in substantial reductions of ETS constituents in indoor air.

  14. Electronic Cigarettes Use and Intention to Cigarette Smoking among Never-Smoking Adolescents and Young Adults: A Meta-Analysis

    PubMed Central

    Zhong, Jieming; Cao, Shuangshuang; Gong, Weiwei; Fei, Fangrong; Wang, Meng

    2016-01-01

    Electronic cigarettes (e-cigarettes) use is becoming increasingly common, especially among adolescents and young adults, and there is little evidence on the impact of e-cigarettes use on never-smokers. With a meta-analysis method, we explore the association between e-cigarettes use and smoking intention that predicts future cigarette smoking. Studies were identified by searching three databases up to January 2016. The meta-analysis results were presented as pooled odds ratio (OR) with 95% confidence interval (CI) calculated by a fixed-effects model. A total of six studies (91,051 participants, including 1452 with ever e-cigarettes use) were included in this meta-analysis study. We found that never-smoking adolescents and young adults who used e-cigarettes have more than 2 times increased odds of intention to cigarette smoking (OR = 2.21, 95% CI: 1.86–2.61) compared to those who never used, with low evidence of between-study heterogeneity (p = 0.28, I2 = 20.1%). Among never-smoking adolescents and young adults, e-cigarettes use was associated with increased smoking intention. PMID:27153077

  15. Cigarette smoke metabolically promotes cancer, via autophagy and premature aging in the host stromal microenvironment

    PubMed Central

    Salem, Ahmed F.; Al-Zoubi, Mazhar Salim; Whitaker-Menezes, Diana; Martinez-Outschoorn, Ubaldo E.; Lamb, Rebecca; Hulit, James; Howell, Anthony; Gandara, Ricardo; Sartini, Marina; Galbiati, Ferruccio; Bevilacqua, Generoso; Sotgia, Federica; Lisanti, Michael P.

    2013-01-01

    Cigarette smoke has been directly implicated in the disease pathogenesis of a plethora of different human cancer subtypes, including breast cancers. The prevailing view is that cigarette smoke acts as a mutagen and DNA damaging agent in normal epithelial cells, driving tumor initiation. However, its potential negative metabolic effects on the normal stromal microenvironment have been largely ignored. Here, we propose a new mechanism by which carcinogen-rich cigarette smoke may promote cancer growth, by metabolically “fertilizing” the host microenvironment. More specifically, we show that cigarette smoke exposure is indeed sufficient to drive the onset of the cancer-associated fibroblast phenotype via the induction of DNA damage, autophagy and mitophagy in the tumor stroma. In turn, cigarette smoke exposure induces premature aging and mitochondrial dysfunction in stromal fibroblasts, leading to the secretion of high-energy mitochondrial fuels, such as L-lactate and ketone bodies. Hence, cigarette smoke induces catabolism in the local microenvironment, directly fueling oxidative mitochondrial metabolism (OXPHOS) in neighboring epithelial cancer cells, actively promoting anabolic tumor growth. Remarkably, these autophagic-senescent fibroblasts increased breast cancer tumor growth in vivo by up to 4-fold. Importantly, we show that cigarette smoke-induced metabolic reprogramming of the fibroblastic stroma occurs independently of tumor neo-angiogenesis. We discuss the possible implications of our current findings for the prevention of aging-associated human diseases and, especially, common epithelial cancers, as we show that cigarette smoke can systemically accelerate aging in the host microenvironment. Finally, our current findings are consistent with the idea that cigarette smoke induces the “reverse Warburg effect,” thereby fueling “two-compartment tumor metabolism” and oxidative mitochondrial metabolism in epithelial cancer cells. PMID:23388463

  16. Information Management Strategies within Conversations about Cigarette Smoking: Parenting Correlates and Longitudinal Associations with Teen Smoking

    ERIC Educational Resources Information Center

    Metzger, Aaron; Wakschlag, Lauren S.; Anderson, Ryan; Darfler, Anne; Price, Juliette; Flores, Zujeil; Mermelstein, Robin

    2013-01-01

    The present study examined smoking-specific and general parenting predictors of in vivo observed patterns of parent-adolescent discussion concerning adolescents' cigarette smoking experiences and associations between these observed patterns and 24-month longitudinal trajectories of teen cigarette smoking behavior (nonsmokers, current…

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

    PubMed

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

    2014-11-15

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

  18. Cigarette smoking, exercise and high density lipoprotein cholesterol.

    PubMed

    Stamford, B A; Matter, S; Fell, R D; Sady, S; Papanek, P; Cresanta, M

    1984-07-01

    Cigarette smoking is associated with depressed levels of HDL-C, whereas exercise is associated with elevated levels of HDL-C. The purpose was to determine effects of smoking and exercise on blood lipids and lipoproteins in middle-aged males. It was hypothesized that smoking may attenuate the effects of exercise to elevate HDL-C. A total of 269 males (70 smokers) met all criteria for inclusion in the study population. Age, height, weight, body fatness via hydrostatic weighing, daily caloric consumption and alcohol intake, and smoking habits and history were determined. Interviews concerning physical activity patterns were conducted and cardiovascular responses to treadmill exercise were determined. Subjects were grouped as sedentary (low activity), participants in vigorous recreational activities (moderate activity) and joggers/runners (high activity). Analysis of covariance with adjustments for factors which may affect blood lipids and lipoproteins was employed. Smokers demonstrated lower HDL-C and higher total cholesterol levels than nonsmokers. High activity subjects demonstrated significantly higher HDL-C levels than the low and moderate groups which did not differ. High activity smokers did not differ from low activity nonsmokers with respect to HDL-C. This supports the proposed hypothesis. Nonsmokers were higher in weight and body fatness than smokers even though smokers consumed 288 more calories per day on the average. This suggests that smoking may account for a significant number of calories through altered metabolism or some other means.

  19. A simple and rapid method for standard preparation of gas phase extract of cigarette smoke.

    PubMed

    Higashi, Tsunehito; Mai, Yosuke; Noya, Yoichi; Horinouchi, Takahiro; Terada, Koji; Hoshi, Akimasa; Nepal, Prabha; Harada, Takuya; Horiguchi, Mika; Hatate, Chizuru; Kuge, Yuji; Miwa, Soichi

    2014-01-01

    Cigarette smoke consists of tar and gas phase: the latter is toxicologically important because it can pass through lung alveolar epithelium to enter the circulation. Here we attempt to establish a standard method for preparation of gas phase extract of cigarette smoke (CSE). CSE was prepared by continuously sucking cigarette smoke through a Cambridge filter to remove tar, followed by bubbling it into phosphate-buffered saline (PBS). An increase in dry weight of the filter was defined as tar weight. Characteristically, concentrations of CSEs were represented as virtual tar concentrations, assuming that tar on the filter was dissolved in PBS. CSEs prepared from smaller numbers of cigarettes (original tar concentrations ≤ 15 mg/ml) showed similar concentration-response curves for cytotoxicity versus virtual tar concentrations, but with CSEs from larger numbers (tar ≥ 20 mg/ml), the curves were shifted rightward. Accordingly, the cytotoxic activity was detected in PBS of the second reservoir downstream of the first one with larger numbers of cigarettes. CSEs prepared from various cigarette brands showed comparable concentration-response curves for cytotoxicity. Two types of CSEs prepared by continuous and puff smoking protocols were similar regarding concentration-response curves for cytotoxicity, pharmacology of their cytotoxicity, and concentrations of cytotoxic compounds. These data show that concentrations of CSEs expressed by virtual tar concentrations can be a reference value to normalize their cytotoxicity, irrespective of numbers of combusted cigarettes, cigarette brands and smoking protocols, if original tar concentrations are ≤15 mg/ml.

  20. Snuffing out cigarette sales and the smoking deaths epidemic.

    PubMed

    Laugesen, Murray

    2007-06-15

    Smokers need new products and policies to escape smoking's risks. And the next generation needs policies that will better protect them from becoming smokers. Low-nitrosamine tobacco snuff (hereafter termed 'snuff') is 20 times less dangerous than cigarette smoking. Its sale as nasal snuff raises the question as to how long cigarettes, including cigars and pipe tobacco, should continue to be sold and allowed to hasten the deaths of 4000 New Zealanders annually. Oral snuff has helped to reduce smoking to unusually low levels in Swedish men, is much less dangerous than smoking, and does not cause lung or mouth cancer. Moreover, smokeless tobacco (which includes snuff) could reduce smoking-caused health inequity for Maori. Snuff can improve population health, and more so if more smokers switch to it. Continued bans on snuff are now regarded by some experts as unsound public policy. Added to the mountain of evidence against cigarettes, sufficient evidence now exists for Government to use snuff to create safer tobacco choices for smokers, end cigarette sales altogether, and thus end the cigarette smoking deaths epidemic--in which 200,000 New Zealanders have died so far. The New Zealand Government can: Fund media campaigns to inform smokers of their new choices, and to urge them to quit smoking. (The 2007 Budget commits an extra $11 million per year for 4 years, an excellent start.) Regulate for warnings on snuff cans stating that snuff is "addictive but much safer than smoking", and regulate imports to only permit reduced-risk low-nitrosamine products. Tax each class of tobacco products proportionate to the respective risks of each. (Tax cigarettes at 20 times the snuff rate, instead of at the same rate.) Legislate, to expand the Smoke-free Environments Act's aims to include ending the sale of cigarettes and ending smoking deaths--i.e: Allow oral snuff to compete with cigarettes for market share (and for the smoker's nicotine receptors). Reduce addiction to smoking, by

  1. CSEO – the Cigarette Smoke Exposure Ontology

    PubMed Central

    2014-01-01

    Background In the past years, significant progress has been made to develop and use experimental settings for extensive data collection on tobacco smoke exposure and tobacco smoke exposure-associated diseases. Due to the growing number of such data, there is a need for domain-specific standard ontologies to facilitate the integration of tobacco exposure data. Results The CSEO (version 1.0) is composed of 20091 concepts. The ontology in its current form is able to capture a wide range of cigarette smoke exposure concepts within the knowledge domain of exposure science with a reasonable sensitivity and specificity. Moreover, it showed a promising performance when used to answer domain expert questions. The CSEO complies with standard upper-level ontologies and is freely accessible to the scientific community through a dedicated wiki at https://publicwiki-01.fraunhofer.de/CSEO-Wiki/index.php/Main_Page. Conclusions The CSEO has potential to become a widely used standard within the academic and industrial community. Mainly because of the emerging need of systems toxicology to controlled vocabularies and also the lack of suitable ontologies for this domain, the CSEO prepares the ground for integrative systems-based research in the exposure science. PMID:25093069

  2. Effect of cigarette smoke on human serum trypsin inhibitory capacity and antitrypsin concentration

    SciTech Connect

    Chowdhury, P.; Bone, R.C.; Louria, D.B.; Rayford, P.L.

    1982-07-01

    Investigation of the effect of cigarette smoke on the serum trypsin inhibitory capacity (TIC) and antitrypsin content in 89 smokers compared with 37 nonsmokers revealed that cigarette smoking is associated with a significantly lower level of TIC. No alteration in serum antitrypsin content was found because of cigarette smoking. Further analysis of the data indicated a correlation between the magnitude of smoking and the reduction in serum TIC. The reduction of TIC in cigarette smokers is consistent with the recent findings of decreased alpha 1-antitrypsin activity in rat lung and the reduced elastase inhibitory capacity per mg of alpha 1-antitrypsin found in the serum of smokers. The decrease in TIC in the serum of smokers, in addition to the reported decrease in elastolytic activity, may be useful in explaining the pathogenesis of emphysema frequently found in smokers.

  3. Effect of cigarette smoke extract on the polymorphonuclear leukocytes chemiluminescence: influence of a filter containing glutathione.

    PubMed

    Zappacosta, B; Persichilli, S; Minucci, A; Fasanella, S; Scribano, D; Giardina, B; De Sole, P

    2005-01-01

    Cigarette smoking is known to be a risk factor for several chronic and neoplastic diseases. Many compounds formed by cigarette burning, ranging from particulate materials to water solutes and gaseous extracts, are considered to be noxious agents, and many biochemical and molecular mechanisms have been proposed for the toxic effects of cigarette smoke. The oral cavity and the upper respiratory tract represent the first contact areas for smoke compounds; even a single cigarette can produce marked effects on some components of the oral cavity, either chemical compounds, such as glutathione and enzymes, or cellular elements, such as polymorphonuclear leukocytes. Several studies suggest a protective role of glutathione against the noxious effects of tobacco smoke; the sulphydril groups of glutathione, in fact, could react with some smoke products, such as unsaturated aldehydes, leading to the formation of harmless intermediate compounds and simultaneously preventing the inactivation of metabolically essential molecules, such as some enzymes. In this paper we analyse the effect of a filter containing glutathione on the respiratory burst of polymorphonuclear leukocytes exposed to aqueous extract of cigarette smoke, measuring their chemiluminescence activity. The results of this paper indicate that the GSH-containing filter has a likely protective effect against the inhibition of cigarette smoke extract on polymorphonuclear leukocyte activity.

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

    PubMed

    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.

  5. Menthol vs nonmenthol cigarettes: effects on smoking behavior.

    PubMed Central

    McCarthy, W J; Caskey, N H; Jarvik, M E; Gross, T M; Rosenblatt, M R; Carpenter, C

    1995-01-01

    OBJECTIVES. The purpose of this study was to examine intraindividual differences in smoking behavior between smoking regular and mentholated cigarettes. METHODS. Healthy male smokers (n = 29) smoked either a regular or a mentholated cigarette in two separate sessions 1 week apart. Commercial brands with comparable tar, nicotine, and CO content were used. Smoking behavior was constrained by fixed 15-second interpuff intervals, but puff volume and number of puffs were unconstrained. RESULTS. When smoking the non-mentholated brand of cigarettes, participants smoked 22% more puffs and had 13% higher mean volumes per puff than they did when smoking the mentholated brand of cigarettes. The aggregate 39% excess exposure to cigarette smoke in the regular-cigarette condition was not accompanied by commensurate excesses in expired carbon monoxide or in physiological measures normally correlated with nicotine exposure. CONCLUSIONS. These findings parallel differences in physiological correlates of exposure to nicotine found in cross-sectional comparisons of African-American and White smokers and are consistent with the results of emerging laboratory investigations. PMID:7832264

  6. Upregulation of contractile endothelin type B receptors by lipid-soluble cigarette smoking particles in rat cerebral arteries via activation of MAPK

    SciTech Connect

    Sandhu, Hardip; Xu, Cang Bao; Edvinsson, Lars

    2010-11-15

    Cigarette smoke exposure increases the risk of stroke. However, the underlying molecular mechanisms are poorly understood. Endothelin system plays key roles in the pathogenesis of stroke. The present study was designed to examine if lipid-soluble (dimethyl sulfoxide-soluble) cigarette smoke particles (DSP) induces upregulation of contractile endothelin type B (ET{sub B}) receptors in rat cerebral arteries and if activation of mitogen activated protein kinase (MAPK) and nuclear factor-kappaB (NF-{kappa}B) mediate the upregulation of contractile endothelin receptors in the cerebral arteries. Rat middle cerebral arteries were isolated and organ cultured in serum free medium for 24 h in the presence of DSP with or without specific inhibitors: MEK specific (U0126), p38 specific (SB202190), JNK specific (SP600125), NF-{kappa}B specific (BMS-345541) or (IMD-0354), transcription inhibitor (actinomycin D), or translation blocker (cycloheximide). Contractile responses to the ET{sub B} receptor agonist sarafotoxin 6c were investigated by a sensitive myograph. The expression of the ET{sub B} receptors were studied at mRNA and protein levels using quantitative real time PCR and immunohistochemistry, respectively. Results show that organ culture per se induced transcriptional upregulation of contractile ET{sub B} receptors in the cerebral vascular smooth muscle cells. This upregulation was further increased at the translational level by addition of DSP to the organ culture, but this increase was not seen by addition of nicotine or water-soluble cigarette smoke particles to the organ culture. The increased upregulation of contractile ET{sub B} receptors by DSP was abrogated by U0126, SP600125, actinomycin D, and cycloheximide, suggesting that the underlying molecular mechanisms involved in this process include activation of MEK and JNK MAPK-mediated transcription and translation of new contractile ET{sub B} receptors. Thus, the MAPK-mediated upregulation of contractile ET{sub B

  7. Cigarette Smoking by Adolescent Females: Implications for Health and Behavior.

    ERIC Educational Resources Information Center

    Gritz, Ellen R.

    Cigarette smoking is a behavior with profound biomedical and psychosocial consequences across the life span. Although it is advertised in terms of youth, beauty, sexual appeal, success and independence, smoking is intimately linked with addiction, disease and death. Smoking has been shown to be a leading contributer to several kinds of cancer,…

  8. Can cigarette warnings counterbalance effects of smoking scenes in movies?

    PubMed

    Golmier, Isabelle; Chebat, Jean-Charles; Gélinas-Chebat, Claire

    2007-02-01

    Scenes in movies where smoking occurs have been empirically shown to influence teenagers to smoke cigarettes. The capacity of a Canadian warning label on cigarette packages to decrease the effects of smoking scenes in popular movies has been investigated. A 2 x 3 factorial design was used to test the effects of the same movie scene with or without electronic manipulation of all elements related to smoking, and cigarette pack warnings, i.e., no warning, text-only warning, and text+picture warning. Smoking-related stereotypes and intent to smoke of teenagers were measured. It was found that, in the absence of warning, and in the presence of smoking scenes, teenagers showed positive smoking-related stereotypes. However, these effects were not observed if the teenagers were first exposed to a picture and text warning. Also, smoking-related stereotypes mediated the relationship of the combined presentation of a text and picture warning and a smoking scene on teenagers' intent to smoke. Effectiveness of Canadian warning labels to prevent or to decrease cigarette smoking among teenagers is discussed, and areas of research are proposed.

  9. Behavioral Control of Cigarette Smoking: A Comprehensive Program

    ERIC Educational Resources Information Center

    Hackett, Gail; Horan, John

    1977-01-01

    Cigarette smoking has been a behavioral enigma. Single treatment techniques, when successful, are usually plagued by high recidivism rates and "practical" insignificance. Two recent developments, rapid smoking and comprehensive behavioral programming, hold promise for the eventual behavioral control of smoking. This study describes one such…

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

    PubMed Central

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

    2016-01-01

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

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

    PubMed

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

    2016-07-01

    Electronic cigarettes (E-cigarettes) are a potential means of addressing the harm to public health caused by tobacco smoking by offering smokers a less harmful means of receiving nicotine. As e-cigarettes are a relatively new phenomenon, there are limited scientific data on the longer-term health effects of their use. This study describes a robust in vitro method for assessing the cytotoxic response of e-cigarette aerosols that can be effectively compared with conventional cigarette smoke. This was measured using the regulatory accepted Neutral Red Uptake assay modified for air-liquid interface (ALI) exposures. An exposure system, comprising a smoking machine, traditionally used for in vitro tobacco smoke exposure assessments, was adapted for use with e-cigarettes to expose human lung epithelial cells at the ALI. Dosimetric analysis methods using real-time quartz crystal microbalances for mass, and post-exposure chemical analysis for nicotine, were employed to detect/distinguish aerosol dilutions from a reference Kentucky 3R4F cigarette and two commercially available e-cigarettes (Vype eStick and ePen). ePen aerosol induced 97%, 94% and 70% less cytotoxicity than 3R4F cigarette smoke based on matched EC50 values at different dilutions (1:5 vs. 1:153 vol:vol), mass (52.1 vs. 3.1 μg/cm(2)) and nicotine (0.89 vs. 0.27 μg/cm(2)), respectively. Test doses where cigarette smoke and e-cigarette aerosol cytotoxicity were observed are comparable with calculated daily doses in consumers. Such experiments could form the basis of a larger package of work including chemical analyses, in vitro toxicology tests and clinical studies, to help assess the safety of current and next generation nicotine and tobacco products.

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

    PubMed Central

    Pokhrel, Pallav; Herzog, Thaddeus A.

    2015-01-01

    Despite the lack of clarity regarding their safety and efficacy as smoking cessation aids, electronic or 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 to 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 multiethnic 1988 current daily smokers [M age = 45.1 (SD = 13.0); 51.3% Women] who had made an average lifetime quit attempts of 8.5 (SD = 18.7) but were not currently engaged in a cessation attempt. Reasons for wanting to quit smoking were assessed by using the Reasons for Quitting (RFQ) 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

  13. Evaluation of the genotoxic and cytotoxic potential of mainstream whole smoke and smoke condensate from a cigarette containing a novel carbon filter.

    PubMed

    Bombick, D W; Bombick, B R; Ayres, P H; Putnam, K; Avalos, J; Borgerding, M F; Doolittle, D J

    1997-09-01

    A novel carbon filter has been developed which primarily reduces the amount of certain vapor phase constituents of tobacco smoke with greater efficiency than the charcoal filters of cigarettes currently in the market. In vitro indicators of genotoxic and cytotoxic potential were used to compare the cigarette smoke condensate (particulate phase) or whole cigarette smoke (vapor phase and particulate phase) from cigarettes containing the novel carbon filter with smoke condensate or whole smoke from commercial or prototype cigarettes not containing the novel carbon filter. Ames bacterial mutagenicity, sister chromatid exchange (SCE) in Chinese hamster ovary (CHO) cells, and neutral red cytotoxicity assays in CHO cells were utilized to assess the genotoxic and cytotoxic potential of the cigarette smoke condensates. SCE and neutral red cytotoxicity assays were utilized to assess the genotoxic and cytotoxic potential of the whole smoke. As expected, the novel carbon filter did not significantly affect the genotoxic or cytotoxic activity of the smoke condensate, although we did observe that the use of low-nitrogen tobacco reduced the mutagenicity of the condensate in Salmonella typhimurium strain TA98. However, the whole smoke from cigarettes containing the novel carbon filter demonstrated significant reductions in genotoxic and cytotoxic potential compared to cigarettes without the novel carbon filter. The toxicity of the smoke was correlated (r = 0.7662 for cytotoxicity and r = 0.7562 for SCE induction) to the aggregate mass of several vapor phase components (acetone, acetaldehyde, acrolein, acrylonitrile, 1,3-butadiene, ammonia, NOx, HCN, benzene, isoprene, and formaldehyde) in the smoke of the cigarettes utilized in this study. In conclusion, this novel carbon filter, which significantly reduced the amount of carbonyls and other volatiles in mainstream cigarette smoke, resulted in significant reductions in the genotoxic and cytotoxic activity of the smoke as measured

  14. Cigarette Smoke Attenuates the Nasal Host Response to Streptococcus pneumoniae and Predisposes to Invasive Pneumococcal Disease in Mice

    PubMed Central

    Shen, Pamela; Morissette, Mathieu C.; Vanderstocken, Gilles; Gao, Yang; Hassan, Muhammad; Roos, Abraham; Thayaparan, Danya; Merlano, Maria; Dorrington, Michael G.; Nikota, Jake K.; Bauer, Carla M. T.; Kwiecien, Jacek M.; Labiris, Renee; Bowdish, Dawn M. E.; Stevenson, Christopher S.

    2016-01-01

    Streptococcus pneumoniae is a leading cause of invasive bacterial infections, with nasal colonization an important first step in disease. While cigarette smoking is a strong risk factor for invasive pneumococcal disease, the underlying mechanisms remain unknown. This is partly due to a lack of clinically relevant animal models investigating nasal pneumococcal colonization in the context of cigarette smoke exposure. We present a model of nasal pneumococcal colonization in cigarette smoke-exposed mice and document, for the first time, that cigarette smoke predisposes to invasive pneumococcal infection and mortality in an animal model. Cigarette smoke increased the risk of bacteremia and meningitis without prior lung infection. Mechanistically, deficiency in interleukin 1α (IL-1α) or platelet-activating factor receptor (PAFR), an important host receptor thought to bind and facilitate pneumococcal invasiveness, did not rescue cigarette smoke-exposed mice from invasive pneumococcal disease. Importantly, we observed cigarette smoke to attenuate nasal inflammatory mediator expression, particularly that of neutrophil-recruiting chemokines, normally elicited by pneumococcal colonization. Smoking cessation during nasal pneumococcal colonization rescued nasal neutrophil recruitment and prevented invasive disease in mice. We propose that cigarette smoke predisposes to invasive pneumococcal disease by suppressing inflammatory processes of the upper respiratory tract. Given that smoking prevalence remains high worldwide, these findings are relevant to the continued efforts to reduce the invasive pneumococcal disease burden. PMID:26930709

  15. Smoking behaviors and intentions among current e-cigarette users, cigarette smokers, and dual users: A national survey of U.S. high school seniors.

    PubMed

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

    2017-03-01

    E-cigarette use among adolescents has increased significantly in recent years, but it remains unclear whether cigarette smoking behaviors and intentions for future cigarette smoking differ among current (i.e., 30-day) non-users, only e-cigarette users, only cigarette smokers, and dual users. A nationally representative sample of 4385 U.S. high school seniors were surveyed during the spring of their senior year via self-administered questionnaires in 2014. An estimated 9.6% of U.S. high school seniors reported current e-cigarette use only, 6.3% reported current cigarette smoking only, and 7.2% reported current dual use of e-cigarettes and cigarette smoking. There were no significant differences between current only cigarette smokers and dual users in the odds of early onset of cigarette smoking, daily cigarette smoking, intentions for future cigarette smoking, friends' cigarette smoking behaviors, attempts to quit cigarette smoking, or the inability to quit cigarette smoking. Adolescents who only used e-cigarettes had higher odds of intentions for future cigarette smoking in the next 5years (AOR=2.57, 95% CI: 1.21-5.24) than current non-users. Dual users and only cigarette smokers had higher odds of cigarette smoking behaviors and intentions for future cigarette smoking than non-users or only e-cigarette users. Adolescents who engage in current dual use have cigarette smoking behaviors and intentions for future cigarette smoking that more closely resemble cigarette smokers than e-cigarette users. Adolescents who only use e-cigarettes have higher intentions to engage in future cigarette smoking relative to their peers who do not engage in e-cigarette use or cigarette smoking.

  16. Cigarette smoking and radiographic progression in rheumatoid arthritis

    PubMed Central

    Finckh, A; Dehler, S; Costenbader, K H; Gabay, C

    2007-01-01

    Background Smoking is a well‐established environmental risk factor for the development of rheumatoid arthritis (RA). However, it remains unclear whether smoking influences RA disease progression and whether smokers have more radiographic damage progression than non‐smokers over time. Objective To compare the rates of radiographic damage progression in current smokers and non‐smokers in a large prospective RA cohort. Methods The SCQM‐RA is a population‐based registry monitoring disease activity, radiographic damage and symptoms at regular intervals. All patients in the SCQM‐RA database with sequential plain radiographs were included. Joint erosions were assessed in 38 hand and foot joints with a validated scoring method. The rate of erosion progression was analysed using multivariate longitudinal regression models and adjusted for potential confounders. Results 2004 RA patients with a mean of 3.6 sequential radiographs and 3.1 years of follow‐up were included. The 545 (27%) current smokers smoked on average 16 cigarettes per day and had a mean past smoking exposure of 20.6 pack‐years. Radiographic joint damage progressed at a similar rate in current smokers and non‐smokers (p = 0.26). However, smoking intensity was associated with a significant inverse dose–response; heavy smokers (>1 pack‐day) progressed significantly less than non‐smokers or moderate smokers (p<0.001). Conclusion Radiographic joint damage progressed at an equivalent rate in smokers and non‐smokers. Furthermore, a significant trend was observed for reduced radiographic progression and generally more favourable functional scores among heavy smokers, suggesting that cigarette smoke does not accelerate RA disease progression. PMID:17237117

  17. Cigarette smoking and short-term addiction treatment outcome.

    PubMed

    Harrell, P T; Montoya, I D; Preston, K L; Juliano, L M; Gorelick, D A

    2011-06-01

    Cigarette smoking is common among patients in cocaine and opioid dependence treatment, and may influence treatment outcome. We addressed this issue in a secondary analysis of data from an outpatient clinical trial of buprenorphine treatment for concurrent cocaine and opioid dependence (13 weeks, N=200). The association between cigarette smoking (lifetime cigarette smoking status, number of cigarettes smoked per day prior to study entry) and short-term treatment outcome (% of urine samples positive for cocaine or opioids, treatment retention) was evaluated with analysis of covariance, bivariate correlations, and multivariate linear regression. Nicotine-dependent smokers (66% of participants) had a significantly higher percentage of cocaine-positive urine samples than non-smokers (12% of participants) (76% vs. 62%), but did not differ in percentage of opioid-positive urine samples or treatment retention. Number of cigarettes smoked per day at baseline was positively associated with percentage of cocaine-positive urine samples, even after controlling for baseline sociodemographic and drug use characteristics, but was not significantly associated with percentage of opioid-positive urine samples or treatment retention. These results suggest that cigarette smoking is associated with poorer short-term outcome of outpatient treatment for cocaine dependence, but perhaps not of concurrent opioid dependence, and support the importance of offering smoking cessation treatment to cocaine-dependent patients.

  18. Experimental animal studies of radon and cigarette smoke

    SciTech Connect

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

    1992-12-31

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

  19. Conditioning arbitrary stimuli to cigarette smoke intake: a preliminary study.

    PubMed

    Payne, T J; Etscheidt, M; Corrigan, S A

    1990-01-01

    This study represents an attempt to classically condition arbitrary stimuli to cigarette smoke intake. A smoker either smoked or mock-smoked a cigarette in two discriminative contexts for 20 sessions. The contingencies were reversed during an additional last two sessions. Measures of heart rate, skin temperature, and puff duration were monitored during all sessions. Results suggested that both manipulations of smoke delivery and context cues were related to puff duration. The pattern of psychophysiological reactivity was mixed and not easily interpreted. This experimental paradigm may be useful in the investigation of conditioning factors underlying addictive behaviors.

  20. Cigarette smoking: an independent risk factor in alcoholic pancreatitis.

    PubMed

    Talamini, G; Bassi, C; Falconi, M; Frulloni, L; Di Francesco, V; Vaona, B; Bovo, P; Rigo, L; Castagnini, A; Angelini, G; Vantini, I; Pederzoli, P; Cavallini, G

    1996-03-01

    It is not known whether cigarette smoking plays a role as a risk factor in alcoholic pancreatitis. The aim of this study was to compare drinking and smoking habits in three groups of male subjects with an alcohol intake in excess of 40 g/day: (i) 67 patients with acute alcoholic pancreatitis, without other known potential causative agents; (ii) 396 patients with chronic alcoholic pancreatitis; and (iii) 265 control subjects randomly selected from the Verona polling lists and submitted to a complete medical checkup. The variables considered were age at onset of disease, years of drinking and smoking, daily alcohol intake in grams, number of cigarettes smoked daily, and body mass index (BMI). Cases differed from controls in daily grams of alcohol, number of cigarettes smoked and BMI (Mann-Whitney U test, p < 0.00001 for each comparison). Multivariate logistic regression analysis, comparing acute and chronic cases, respectively, versus controls, revealed an increased relative risk of pancreatitis in the two comparisons, associated in both cases with a higher alcohol intake (p < 0.00001) and cigarette smoking (p < 0.00001). No significant interaction between alcohol and smoking was noted, indicating that the two risks are independent. In conclusion, in males a higher number of cigarettes smoked daily seems to be a distinct risk factor in acute and chronic alcoholic pancreatitis.

  1. Microbiological components in mainstream and sidestream cigarette smoke

    PubMed Central

    2012-01-01

    Background Research has shown that tobacco smoke contains substances of microbiological origin such as ergosterol (a fungal membrane lipid) and lipopolysaccharide (LPS) (in the outer membrane of Gram-negative bacteria). The aim of the present study was to compare the amounts of ergosterol and LPS in the tobacco and mainstream (MS) and sidestream (SS) smoke of some popular US cigarettes. Methods We measured LPS 3-hydroxy fatty acids and fungal biomass biomarker ergosterol in the tobacco and smoke from cigarettes of 11 popular brands purchased in the US. University of Kentucky reference cigarettes were also included for comparison. Results The cigarette tobacco of the different brands contained 6.88-16.17 (mean 10.64) pmol LPS and 8.27-21.00 (mean 14.05) ng ergosterol/mg. There was a direct correlation between the amounts of ergosterol and LPS in cigarette tobacco and in MS smoke collected using continuous suction; the MS smoke contained 3.65-8.23% (ergosterol) and 10.02-20.13% (LPS) of the amounts in the tobacco. Corresponding percentages were 0.30-0.82% (ergosterol) and 0.42-1.10% (LPS) for SS smoke collected without any ongoing suction, and 2.18% and 2.56% for MS smoke collected from eight two-second puffs. Conclusions Tobacco smoke is a bioaerosol likely to contain a wide range of potentially harmful bacterial and fungal components. PMID:22898193

  2. A Study of Cigarett Smoking Among Adults.

    ERIC Educational Resources Information Center

    Mausner, Bernard

    The various activities carried out under a grant from the Cancer Society are discussed, including preparatory work, pilot and exploratory studies, the conduct of the major study, and additional activities. The bulk of the report, however, is devoted to the major study in which measures were obtained of: 1) patterns of support for smoking; 2)…

  3. Current Cigarette Smoking Among Adults - United States, 2005-2015.

    PubMed

    Jamal, Ahmed; King, Brian A; Neff, Linda J; Whitmill, Jennifer; Babb, Stephen D; Graffunder, Corinne M

    2016-11-11

    Tobacco use is the leading cause of preventable disease and death in the United States, and cigarettes are the most commonly used tobacco product among U.S. adults (1,2). To assess progress toward achieving the Healthy People 2020 target of reducing the proportion of U.S. adults who smoke cigarettes to ≤12.0% (objective TU1.1),* CDC assessed the most recent national estimates of cigarette smoking prevalence among adults aged ≥18 years using data from the 2015 National Health Interview Survey (NHIS). The proportion of U.S. adults who smoke cigarettes declined from 20.9% in 2005 to 15.1% in 2015, and the proportion of daily smokers declined from 16.9% to 11.4%. However, disparities in cigarette smoking persist. In 2015, prevalence of cigarette smoking was higher among adults who were male; were aged 25-44 years; were American Indian/Alaska Native; had a General Education Development certificate (GED); lived below the federal poverty level; lived in the Midwest; were insured through Medicaid or were uninsured; had a disability/limitation; were lesbian, gay, or bisexual; or who had serious psychological distress. Proven population-based interventions, including tobacco price increases, comprehensive smoke-free laws, anti-tobacco mass media campaigns, and barrier-free access to tobacco cessation counseling and medications, are critical to reducing cigarette smoking and smoking-related disease and death among U.S. adults, particularly among subpopulations with the highest smoking prevalences (3).

  4. Current cigarette smoking among adults - United States, 2005-2014.

    PubMed

    Jamal, Ahmed; Homa, David M; O'Connor, Erin; Babb, Stephen D; Caraballo, Ralph S; Singh, Tushar; Hu, S Sean; King, Brian A

    2015-11-13

    Tobacco smoking is the leading cause of preventable disease and death in the United States, resulting in approximately 480,000 premature deaths and more than $300 billion in direct health care expenditures and productivity losses each year (1). To assess progress toward achieving the Healthy People 2020 objective of reducing the percentage of U.S. adults who smoke cigarettes to ≤12.0%,* CDC assessed the most recent national estimates of smoking prevalence among adults aged ≥18 years using data from the 2014 National Health Interview Survey (NHIS). The percentage of U.S. adults who smoke cigarettes declined from 20.9% in 2005 to 16.8% in 2014. Among daily cigarette smokers, declines were observed in the percentage who smoked 20–29 cigarettes per day (from 34.9% to 27.4%) or ≥30 cigarettes per day (from 12.7% to 6.9%). In 2014, prevalence of cigarette smoking was higher among males, adults aged 25–44 years, multiracial persons and American Indian/Alaska Natives, persons who have a General Education Development certificate, live below the federal poverty level, live in the Midwest, are insured through Medicaid or are uninsured, have a disability or limitation, or are lesbian, gay, or bisexual. Proven population-based interventions, including tobacco price increases, comprehensive smoke-free laws, high impact mass media campaigns, and barrier-free access to quitting assistance, are critical to reduce cigarette smoking and smoking-related disease and death among U.S. adults.

  5. Selenium mediated reduction of the toxicity expression of cigarette smoke condensate in Photobacterium phosphoreum

    SciTech Connect

    Yates, I.E.; Chortyk, O.T.; Lanier, J.L.

    1986-02-01

    Recently, attention has focused on the potential protective activity of selenium against heavy metal toxicity, cancer and other health disorders. Currently, cigarette smoke affects the health of more people than any other environmental pollutant. Producing cigarettes fortified with selenium has been proposed as a possible method to develop a safer tobacco product. Consequently, it would be informative to determine if the presence of selenium in cigarette smoke leads to increased or decreased toxicity. Luminescent assays have been developed for a wide variety of applications ranging from measuring enzyme activities to monitoring water purity. The purpose of this study was to evaluate the effect of selenium on the toxicity of cigarette smoke condensate using in vivo bacterial bioluminescence assays.

  6. Differential Effects between Cigarette Total Particulate Matter and Cigarette Smoke Extract on Blood and Blood Vessel

    PubMed Central

    Park, Jung-Min; Chang, Kyung-Hwa; Park, Kwang-Hoon; Choi, Seong-Jin; Lee, Kyuhong; Lee, Jin-Yong; Satoh, Masahiko; Song, Seong-Yu; Lee, Moo-Yeol

    2016-01-01

    The generation and collection of cigarette smoke (CS) is a prerequisite for any toxicology study on smoking, especially an in vitro CS exposure study. In this study, the effects on blood and vascular function were tested with two widely used CS preparations to compare the biological effects of CS with respect to the CS preparation used. CS was prepared in the form of total particulate matter (TPM), which is CS trapped in a Cambridge filter pad, and cigarette smoke extract (CSE), which is CS trapped in phosphate-buffered saline. TPM potentiated platelet reactivity to thrombin and thus increased aggregation at a concentration of 25~100 μg/mL, whereas 2.5~10% CSE decreased platelet aggregation by thrombin. Both TPM and CSE inhibited vascular contraction by phenylephrine at 50~100 μg/mL and 10%, respectively. TPM inhibited acetylcholine-induced vasorelaxation at 10~100 μg/mL, but CSE exhibited a minimal effect on relaxation at the concentration that affects vasoconstriction. Neither TPM nor CSE induced hemolysis of erythrocytes or influenced plasma coagulation, as assessed by prothrombin time (PT) and activated partial thromboplastin time (aPTT). Taken together, CS affects platelet activity and deteriorates vasomotor functions in vitro. However, the effect on blood and blood vessels may vary depending on the CS preparation. Therefore, the results of experiments conducted with CS preparations should be interpreted with caution. PMID:27818738

  7. A Period of Increased Susceptibility to Cigarette Smoking among High School Students.

    ERIC Educational Resources Information Center

    Filice, Gregory A.; Hannan, Peter J.; Lando, Harry A.; Joseph, Ann M.

    2003-01-01

    Assessed susceptibility to cigarette smoking among high school students who never smoked. Students participated in voluntary extracurricular anti-tobacco activities throughout the school year. Pre- and post-intervention surveys indicated that among 9th grade nonsmokers, susceptibility increased over the year, while it decreased for 10th-12th grade…

  8. Cigarette Smoking and Anti-Smoking Counseling Practices among Physicians in Wuhan, China

    ERIC Educational Resources Information Center

    Gong, Jie; Zhang, Zhifeng; Zhu, Zhaoyang; Wan, Jun; Yang, Niannian; Li, Fang; Sun, Huiling; Li, Weiping; Xia, Jiang; Zhou, Dunjin; Chen, Xinguang

    2012-01-01

    Purpose: The paper seeks to report data on cigarette smoking, anti-smoking practices, physicians' receipt of anti-smoking training, and the association between receipt of the training and anti-smoking practice among physicians in Wuhan, China. Design/methodology/approach: Participants were selected through the stratified random sampling method.…

  9. Does Switching to Reduced Ignition Propensity Cigarettes Alter Smoking Behavior or Exposure to Tobacco Smoke Constituents?

    PubMed Central

    Rees, Vaughan W.; Norton, Kaila J.; Cummings, K. Michael; Connolly, Gregory N.; Alpert, Hillel R.; Sjödin, Andreas; Romanoff, Lovisa; Li, Zheng; June, Kristie M.; Giovino, Gary A.

    2010-01-01

    Introduction: Since 2004, several jurisdictions have mandated that cigarettes show reduced ignition propensity (RIP) in laboratory testing. RIP cigarettes may limit fires caused by smoldering cigarettes, reducing fire-related deaths and injury. However, some evidence suggests that RIP cigarettes emit more carbon monoxide and polycyclic aromatic hydrocarbons, and smokers may alter their smoking patterns in response to RIP cigarettes. Both of these could increase smokers’ exposures to harmful constituents in cigarettes. Methods: An 18-day switching study with a comparison group was conducted in Boston, MA (N = 77), and Buffalo, NY (N = 83), in 2006–2007. Current daily smokers completed 4 laboratory visits and two 48-hr field data collections. After a 4-day baseline, Boston participants switched to RIP cigarettes for 14 days, whereas Buffalo participants smoked RIP cigarettes throughout. Outcome measures included cigarettes smoked per day; smoking topography; salivary cotinine; breath CO; and hydroxylated metabolites of pyrene, naphthalene, phenanthrene, and fluorene. Because the groups differed demographically, analyses adjusted for race, age, and sex. Results: We observed no significant changes in smoking topography or CO exposure among participants who switched to RIP cigarettes. Cigarette use decreased significantly in the switched group (37.7 cigarettes/48 hr vs. 32.6 cigarettes/48 hr, p = .031), while hydroxyphenanthrenes increased significantly (555 ng/g creatinine vs. 669 ng/g creatinine, p = .007). No other biomarkers were significantly affected. Discussion: Small increases in exposure to phenanthrene among smokers who switched to RIP versions were observed, while other exposures and smoking topography were not significantly affected. Toxicological implications of these findings are unclear. These findings should be weighed against the potential public health benefits of adopting RIP design standards for cigarette products. PMID:20805292

  10. Urinary pH, cigarette smoking and bladder cancer risk

    PubMed Central

    Alguacil, Juan; Kogevinas, Manolis; Silverman, Debra T.; Malats, Núria; Real, Francisco X.; García-Closas, Montserrat; Tardón, Adonina; Rivas, Manuel; Torà, Montserrat; García-Closas, Reina; Serra, Consol; Carrato, Alfredo; Pfeiffer, Ruth M.; Fortuny, Joan; Samanic, Claudine; Rothman, Nathaniel

    2011-01-01

    Glucuronide conjugates of 4-aminobiphenyl and its N-hydroxy metabolite can be rapidly hydrolyzed in acidic urine to undergo further metabolic activation and form DNA adducts in the urothelium. We conducted a large multicenter case–control study in Spain to explore the etiology of bladder cancer and evaluated the association between urine pH and bladder cancer risk, alone and in combination with cigarette smoking. In total, 712 incident urothelial cell carcinoma cases and 611 hospital controls directly measured their urine pH with dipsticks twice a day (first void in the morning and early in the evening) during four consecutive days 2 weeks after hospital discharge. We found that a consistently acidic urine pH ≤6.0 was associated with an increased risk of bladder cancer [odds ratio (OR) = 1.5, 95% confidence interval (CI): 1.2–1.9] compared with all other subjects. Furthermore, risk estimates for smoking intensity and risk of bladder cancer among current smokers tended to be higher for those with a consistently acidic urine (OR = 8.8, 11.5 and 23.8) compared with those without (OR = 4.3, 7.7 and 5.8, respectively, for 1–19, 20–29 and 30+ cigarettes per day; Pinteraction for 30+ cigarettes per day = 0.024). These results suggest that urine pH, which is determined primarily by diet and body surface area, may be an important modifier of smoking and risk of bladder cancer. PMID:21402590

  11. Comparative 13-week inhalation study of cigarette smoke from cigarettes containing cast sheet tobacco.

    PubMed

    Potts, Ryan J; Meckley, Daniel R; Shreve, W Keith; Pence, Deborah H; Ayres, Paul H; Doolittle, David; Swauger, James E; Sagartz, John W

    2007-06-01

    A subchronic, nose-only inhalation study was conducted to compare the effects of mainstream smoke from a reference cigarette containing conventional reconstituted tobacco sheet at 30% of the finished blend to mainstream smoke from cigarettes containing 10% or 15% cast sheet (a specific type of reconstituted tobacco sheet) substituted for part of the conventional reconstituted tobacco. Male and female Sprague-Dawley rats were exposed for 1 h/day, 5 d/wk, for 13 wk to mainstream smoke at 0, 0.06, 0.20, or 0.80 mg wet total particulate matter per liter of air. Clinical signs, body and organ weights, clinical chemistry, hematology, carboxyhemoglobin (COHb), serum nicotine, plethysmography, gross pathology, and histopathology were determined. Exposure to cigarette smoke induced a number of changes in respiratory physiology, histopathology, and serum nicotine and COHb levels when compared to sham animals. When corresponding dose groups of reference and cast sheet mainstream smokes were compared, no biological differences were noted. At the end of the exposure period, subsets of rats from each group were maintained without smoke exposures for an additional 13 wk (recovery period). At the end of the recovery period, there were no statistically significant differences in histopathological findings observed between the reference and either cast sheet cigarette. Substitution of 10% or 15% cast sheet tobacco for conventional reconstituted tobacco sheet does not alter the inhalation toxicology of the mainstream smoke when compared to mainstream smoke from a reference cigarette containing conventional reconstituted tobacco sheet.

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

    SciTech Connect

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

    1989-01-01

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

  13. Exposure of bronchial epithelial cells to whole cigarette smoke: assessment of cellular responses.

    PubMed

    Phillips, Jeremy; Kluss, Bruno; Richter, Audrey; Massey, Eian

    2005-06-01

    Cigarette smoke is composed of approximately 5% particulate phase and 95% vapour phase by weight. However, routine in vitro toxicological testing of smoke normally only measures the activity of the particulate phase. This study describes a new system for exposing cells at an air-liquid interface to serial dilutions of gaseous smoke. Confluent monolayers of NCI-H292 human lung epithelial cells on semipermeable membranes were placed in a purpose-designed Perspex chamber at an air-liquid interface. The cells were exposed to dilute whole mainstream cigarette smoke for 30 minutes, followed by a 20-hour recovery period. Firstly, high and low delivery cigarettes were compared, and cytotoxicity was determined by using the neutral red uptake assay. Clear differential cytotoxic responses were observed with the two cigarette types, which correlated positively with the concentrations of components in smoke, and particularly compounds in the vapour phase, such as aldehydes. Secondly, low doses of smoke were found to up-regulate mRNA levels of the secreted mucin, MUC5AC, and to stimulate the production of interleukin (IL)-6, IL-8 and matrix-metalloprotease-1, but had no effect on growth-related oncogene alpha. This system will facilitate further investigations into the toxicological mechanisms of cigarette smoke components, and may be useful for studying other gaseous mixtures or aerosols.

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

    PubMed

    Vu, Trung; Jin, Lin; Datta, Pran K

    2016-04-11

    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.

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

    PubMed Central

    Vu, Trung; Jin, Lin; 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 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. PMID:27077888

  16. Adolescent Consumption of Sports and Energy Drinks: Linkages to Higher Physical Activity, Unhealthy Beverage Patterns, Cigarette Smoking, and Screen Media Use

    PubMed Central

    Larson, Nicole; DeWolfe, Jessica; Story, Mary; Neumark-Sztainer, Dianne

    2014-01-01

    Objective To examine patterns of adolescent sports and energy drink (SED) consumption and identify behavioral correlates. Design Data were drawn from EAT 2010 (Eating and Activity in Teens), a population-based study. Setting Adolescents from 20 middle and high schools in Minneapolis/St. Paul, Minnesota completed classroom-administered surveys. Participants 2,793 adolescents (53.2% girls) in grades 6–12. Variables Measured Beverage patterns; breakfast frequency; moderate-to-vigorous physical activity (MVPA); media use; sleep; and cigarette smoking. Analysis Linear and logistic regression models were used to estimate associations between health behaviors and SED consumption, adjusting for demographics. Results Over a third of adolescents consumed sports drinks and 14.7% consumed energy drinks at least once a week. Among boys and girls, both sports and energy drink consumption were related to higher video game use; sugar-sweetened beverage and fruit juice intake; and smoking (P<0.05). Sports drink consumption was also significantly related to higher MVPA and organized sport participation for both genders (P<0.01). Conclusions and Implications Although sports drink consumption was associated with higher MVPA, adolescents should be reminded of recommendations to consume these beverages only following vigorous, prolonged activity. There is also a need for future interventions designed to reduce SED consumption to address the clustering of unhealthy behaviors. PMID:24809865

  17. Counseling Chinese Patients about Cigarette Smoking: The Role of Nurses

    ERIC Educational Resources Information Center

    Li, Han Zao; Zhang, Yu; MacDonell, Karen; Li, Xiao Ping; Chen, Xinguang

    2012-01-01

    Purpose: The main purpose of this study is to determine the cigarette smoking rate and smoking cessation counseling frequency in a sample of Chinese nurses. Design/methodology/approach: At the time of data collection, the hospital had 260 nurses, 255 females and five males. The 200 nurses working on the two daytime shifts were given the…

  18. Psychosocial Correlates of Cigarette Smoking among College Students in China

    ERIC Educational Resources Information Center

    Mao, Rong; Li, Xiaoming; Stanton, Bonita; Wang, Jing; Hong, Yan; Zhang, Hongshia; Chen, Xinguang

    2009-01-01

    The objectives are to examine the smoking practice and intention among Chinese college students and to explore the association between cigarette smoking and individual and psychosocial factors. Cross-sectional data were collected from 1874 students from 19 college campuses in Jiangsu province, China. Both bivariate and multivariate analyses were…

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

    PubMed Central

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

    2012-01-01

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

  20. Training and cardiovascular responses from cigarette smoke exposure.

    PubMed

    de Sá, Felipe Gonçalves Dos Santos; da Mota, Gustavo Ribeiro; Sant'Ana, Paula Grippa; da Cunha, Márcia Regina Holanda; Marocolo, Moacir; Castardeli, Edson

    2014-12-31

    The aim of this study was to evaluate the early effect of the endurance training (ET) on systolic blood pressure (SBP), heart rate (HR) and rate pressure-product (RPP) after acute cigarette smoke exposure. Twenty male Wistar rats were randomly allocated into two groups: trained (TEx; n = 10) and control (CEx; n = 10), exposed to smoke. TEx rats undertook ET during 2 weeks (swimming, 5 days/week; 1 h/session) and CEx group was kept in sedentary lifestyle. After ET protocol both groups were exposed to cigarette smoke only once (total 1 h; 2 × 30 min with interval of 10 min between exposures; rate of 10 cigarettes/30 min). SBP, HR and RPP were measured after 2 weeks and just after (5 min) acute cigarette smoke (tail plethysmograph). All parameters did not differ (P > 0.05) between TEx (RPP = 45018 ± 1970 mmHg/bpm) and CEx (43695 ± 2579 mmHg/bpm) after ET protocol. However, all cardiovascular parameters increased (P < 0.05) only for CEx just after the cigarette smoke exposure. We concluded that ET can attenuate the aggression from acute smoking to cardiovascular system, with a few days of training and even with no chronic effect on these parameters at basal condition.

  1. Cigarette smoking and its possible effects on sperm

    SciTech Connect

    Kulikauskas, V.; Blaustein, D.; Ablin, R.J.

    1985-10-01

    The possible effects of cigarette smoking on sperm were evaluated by comparison of the quality of sperm from 103 smokers and 135 nonsmokers in a blind study. Smokers were found to possess significantly decreased density (number) and motility of their sperm than nonsmokers. Morphologic abnormalities, particularly bicephalia, although prevalent among individual smokers, did not differ significantly when a comparison of smokers versus nonsmokers was made as a whole. Based on these observations and those of others demonstrating the presence of the mutagenic properties of smoke condensates, the authors suggest that decreases in sperm density and motility in cigarette smokers may be reflective of smoke condensate-induced mutagenic spermatogenital alterations.

  2. E-cigarette aerosols induce lower oxidative stress in vitro when compared to tobacco smoke.

    PubMed

    Taylor, Mark; Carr, Tony; Oke, Oluwatobiloba; Jaunky, Tomasz; Breheny, Damien; Lowe, Frazer; Gaça, Marianna

    2016-07-01

    Tobacco smoking is a risk factor for various diseases. The underlying cellular mechanisms are not fully characterized, but include oxidative stress, apoptosis, and necrosis. Electronic-cigarettes (e-cigarettes) have emerged as an alternative to and a possible means to reduce harm from tobacco smoking. E-cigarette vapor contains significantly lower levels of toxicants than cigarette smoke, but standardized methods to assess cellular responses to exposure are not well established. We investigated whether an in vitro model of the airway epithelium (human bronchial epithelial cells) and commercially available assays could differentiate cellular stress responses to aqueous aerosol extracts (AqE) generated from cigarette smoke and e-cigarette aerosols. After exposure to AqE concentrations of 0.063-0.500 puffs/mL, we measured the intracellular glutathione ratio (GSH:GSSG), intracellular generation of oxidant species, and activation of the nuclear factor erythroid-related factor 2 (Nrf2)-controlled antioxidant response elements (ARE) to characterize oxidative stress. Apoptotic and necrotic responses were characterized by increases in caspase 3/7 activity and reductions in viable cell protease activities. Concentration-dependent responses indicative of oxidative stress were obtained for all endpoints following exposure to cigarette smoke AqE: intracellular generation of oxidant species increased by up to 83%, GSH:GSSG reduced by 98.6% and transcriptional activation of ARE increased by up to 335%. Caspase 3/7 activity was increased by up to 37% and the viable cell population declined by up to 76%. No cellular stress responses were detected following exposure to e-cigarette AqE. The methods used were suitably sensitive to be employed for comparative studies of tobacco and nicotine products.

  3. Tunable Diode Laser Applications To Cigarette Smoke Analysis

    NASA Astrophysics Data System (ADS)

    Vilcins, Gunars; Harward, Charles N.; Parrish, Milton E.; Forrest, Gary T.

    1983-11-01

    High resolution infrared tunable diode laser spectroscopy (TDL) has been applied to the study of cigarette smoke for qualitative and quantitative determinations involved in tobacco blend and cigarette filter developments. As examples of the different types of application of this work, several TDL studies are presented. The measurements of smoke components on a puff-by-puff basis in confined sample chambers and flowing streams were used to study the smoke component deliveries and the effects of filter dilution. The study of isotopes generated during combustion of chemically treated tobaccos was another application of the TDL system to complex gas mixtures without prior separation of compo-nents. The application of the TDL to the study of cigarette filters and smoke delivery simultaneously was demonstrated by using two well resolved absorption lines of two different gases which occur on a single TDL wavelength scan.

  4. Asbestos exposure-cigarette smoking interactions among shipyard workers

    SciTech Connect

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

    1988-01-15

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

  5. Asbestos exposure-cigarette smoking interactions among shipyard workers.

    PubMed

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

    1988-01-15

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

  6. E-cigarette Use and Willingness to Smoke in a Sample of Adolescent Nonsmokers

    PubMed Central

    Wills, Thomas A.; Sargent, James D.; Knight, Rebecca; Pagano, Ian; Gibbons, Frederick X.

    2016-01-01

    Objective There is little evidence on the consequences of electronic cigarette (e-cigarette) use in adolescence. With a multiethnic sample of nonsmokers, we assessed the relation between e-cigarette use and social-cognitive factors that predict smoking combustible cigarettes (cigarettes). Methods School-based cross-sectional survey of 2,309 high school students (M age 14.7 years). Participants reported on e-cigarette use and cigarette use; on smoking-related cognitions (smoking expectancies, prototypes of smokers) and peer smoker affiliations; and on willingness to smoke cigarettes. Regression analyses conducted for non-cigarette smokers tested the association between e-cigarette use and willingness to smoke cigarettes, controlling for demographics, parenting, academic and social competence, and personality variables. Structural equation modeling (SEM) analyses tested whether the relation between e-cigarette use and willingness was mediated through any of the three smoking-related variables. Results Nonsmokers who had used e-cigarettes (18% of the total sample) showed more willingness to smoke cigarettes compared to those who had never used any tobacco product; the adjusted odds ratio was 2.35 (95% confidence interval 1.73 – 3.19). Additionally, willingness prospectively predicted smoking onset. SEM showed that the relation between e-cigarette use and willingness to smoke was partly mediated through more positive expectancies about smoking but there was also a direct path from e-cigarette use to willingness. Conclusions Among adolescent nonsmokers, e-cigarette use is associated with willingness to smoke, a predictor of future cigarette smoking. The results suggest that use of e-cigarettes by adolescents is not without attitudinal risk for cigarette smoking. These findings have implications for formulation of policy about access to e-cigarettes by adolescents. PMID:26261237

  7. Polonium in size fractionated mainstream cigarette smoke, predicted deposition and associated internal radiation dose.

    PubMed

    Tiwari, M; Sahu, S K; Bhangare, R C; Pandit, G G

    2016-10-01

    In this study, size fractionated mass and (210)Po activity concentrations in mainstream cigarette smoke (MCS) were monitored for three popular cigarette brands. Size segregated collection of MCS was carried out using a cascade type impactor, while mass and (210)Po activity concentration were analyzed gravimetrically and alpha spectrometry (following the radiochemical separation) respectively. Multiple-Path Particle Dosimetry (MPPD V2.11) model is used for prediction of deposition fraction calculations for the MCS deposition in different compartment of human respiratory tract. The activity concentration of (210)Po is founds 10.56 ± 2.46 mBq per cigarette for the tested cigarette brands. (210)Po size distribution indicates most of this associates with fine fraction (Dp < 2.23 μm) of cigarette smoke. The committed annual effective dose to smokers (smoking on an average 20 cigarette a day), considering the (210)Po and (210)Pb concentrations (assuming it is in secular equilibrium with (210)Po) in MCS, was estimated between 0.22 and 0.40 mSv, with mean value of 0.30 mSv for tested cigarette brands. Considering the risk factor of fatal cancer due to radiation exposure of lung (exposure time of 30 years); the average collective estimated fatal cancer risk is estimated as 1.5 × 10(-4) due to (210)Po and (210)Pb exposure to smokers.

  8. [Smoking cigarettes and pain--implications for the postoperative period].

    PubMed

    Billert, Hanna; Gaca, Michał; Adamski, Dariusz

    2007-01-01

    Smoking cigarettes poses a number of relevant medical and social problems. Impact of smoking on pain threshold and tolerance may be of significance for surgical patients, who are prompted to abstain from cigarettes before operation. Association between smoking and pain perception is complex. Experimental data bring evidence for analgesic action of nicotine and tobacco smoke acting via nicotinic acetylochline receptors (nAChR). However, clinical studies are unequivocal. Smoking is connected with some pain syndromes. Smokers take much more analgesics than non-smokers and probability of developing opioid dependence is increased in this group of patients. Smokers also present with altered mechanism of stress-induced analgesia and both gender and pain modalities influence their pain perception. Some studies demonstrate increased requirements for postoperative opioid analgesia in smoking patients. Strategies for postoperative pain treatment in smokers should involve regional techniques and clonidine.

  9. Epidemiologic link between tuberculosis and cigarette/biomass smoke exposure: Limitations despite the vast literature.

    PubMed

    Bishwakarma, Raju; Kinney, William H; Honda, Jennifer R; Mya, Jenny; Strand, Matthew J; Gangavelli, Avani; Bai, Xiyuan; Ordway, Diane J; Iseman, Michael D; Chan, Edward D

    2015-05-01

    The geographic overlap between the prevalence of cigarette smoke (CS) exposure and tuberculosis (TB) in the world is striking. In recent years, relatively large number of studies has linked cigarette or biomass fuel smoke exposure and various aspects of TB. Our goals are to summarize the significance of the known published studies, graphically represent reports that quantified the association and discuss their potential limitations. PubMed searches were performed using the key words 'tuberculosis' with 'cigarette', 'tobacco', 'smoke' or 'biomass fuel smoke.' The references of relevant articles were examined for additional pertinent papers. A large number of mostly case-control and cross-sectional studies significantly associate both direct and second-hand smoke exposure with tuberculous infection, active TB, and/or more severe and lethal TB. Fewer link biomass fuel smoke exposure and TB. While a number of studies interpreted the association with multivariate analysis, other confounders are often not accounted for in these analyses. It is also important to emphasize that these retrospective studies can only show an association and not any causal link. We further explored the possibility that even if CS exposure is a risk factor for TB, several mechanisms may be responsible. Numerous studies associate cigarette and biomass smoke exposure with TB but the mechanism(s) remains largely unknown. While the associative link of these two health maladies is well established, more definitive, mechanistic studies are needed to cement the effect of smoke exposure on TB pathogenesis and to utilize this knowledge in empowering public health policies.

  10. Environmental tobacco smoke (ETS) evaluation of a third-generation electrically heated cigarette smoking system (EHCSS).

    PubMed

    Frost-Pineda, Kimberly; Zedler, Barbara K; Liang, Qiwei; Roethig, Hans J

    2008-11-01

    This sub-study of a randomized, controlled, forced-switching, open-label, parallel-group, clinical study compared environmental tobacco smoke (ETS) produced when 60 male and female adult smokers switched to a third-generation electrically heated cigarette smoking system (EHCSS), continued to smoke a conventional cigarette (CC), or stopped smoking (No-smoking). Concentrations of air constituents including respirable suspended particulate (RSP), carbon monoxide (CO), ammonia and total volatile organic compounds (TVOCs) and ETS markers including solanesol-related particulate matter (Sol-PM), ultraviolet absorbing particulate matter (UVPM), fluorescent particulate matter (FPM), nicotine and 3-ethenyl pyridine (3-EP) were measured in a ventilated, furnished conference room over a 2-h period on separate occasions for each smoking condition. When the EHCSS was used, concentrations of CO and most ETS markers were in the same range as during no-smoking. Concentrations of ammonia were reduced by 41% and concentrations of other selected constituents of ETS were reduced by 87-99% in the air of a room in which EHCSS cigarettes were smoked as compared to concentrations in the same room when conventional cigarettes were smoked. Switching from conventional cigarette smoking to the EHCSS resulted in substantial reductions in concentrations of several markers of environmental tobacco smoke.

  11. Cigarette Smoking, Field-Dependence and Contrast Sensitivity,

    DTIC Science & Technology

    1986-01-01

    This study examined the separate and combined effects of cigarette smoking and field- dependence on contrast sensitivity. No previous research on...smokers were tested for field- dependence and measured for contrast sensitivity (Nicolet CS 20000 Testing System) under carefully controlled...deprived of smoking for at least 90 min. Habitual smoking and field- dependence were found to be separately and interactively related to contrast

  12. Cigarette Smoking and Oxidative Stress in Patients with Coronary Artery Disease

    PubMed Central

    Kamceva, Gordana; Arsova-Sarafinovska, Zorica; Ruskovska, Tatjana; Zdravkovska, Milka; Kamceva-Panova, Lidija; Stikova, Elisaveta

    2016-01-01

    AIM: To determine whether cigarette smoking, as a risk factor for CAD, affects (anti)oxidant status. MATERIAL AND METHODS: The study included patients with CAD, divided according to their smoking status and the number of cigarettes smoked during a day. Biological markers of oxidative stress (concentration of oxidants and activity of antioxidant enzymes) were measured in all subjects. RESULTS: The study included 300 patients with CAD, (average age of 63 ± 11 years), predominantly males. Of the total, 34.0% were active smokers, 23.0% were former smokers, and 43.0% were non-smokers. Most of the active smokers smoked 1-20 cigarettes/day. In terms of concentration of oxidants (MDA and HP) there was not a significant difference between smokers versus non-smokers. As for the activity of antioxidant enzymes (SOD, CAT and GPX), a statistically significant difference was found in the activity of GPX among the active smokers with CAD and the non-smokers with CAD (p = 0.039). CONCLUSION: Smoking as a risk factor for CAD is closely associated with increased oxidative stress, and the number of cigarettes smoked plays an important role in increasing the level of oxidative damage and reducing antioxidant defence. PMID:28028404

  13. Betulin inhibited cigarette smoke-induced COPD in mice.

    PubMed

    Chunhua, Ma; Long, Hongyan; Zhu, Weina; Liu, Zheng; Jie, Ruan; Zhang, Yajie; Wang, Yarui

    2017-01-01

    The purpose of the present study was to evaluate the protective effect of betulin (BE) on CS (cigarette smoke)-induced COPD in mice and explore its underlying mechanisms. 60 male ICR mice were randomly assigned to five groups: control group, model group, dexamethasone (2mg/kg) group, BE (20mg/kg) group and BE (40mg/kg) group. The COPD mice were induced by cigarette smoke exposure for 8 weeks. The result of H&E staining demonstrated that BE inhibited CS-induced pathological injury in lung tissue. Besides, BE could restore the activities of superoxide dismutase (SOD) in serum and in lung, catalase (CAT) in serum and reduce the content of malondialdehyde (MDA) in serum and in lung. BE also inhibited the overproductions of pro-inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interleukin-1β (IL-1β). Furthermore, the administration of BE significantly inhibited the protein expression of ROCK/NF-κB pathway in CS-induced mice. Our findings suggested that BE might effectively ameliorate the progression of COPD via ROCK/NF-κB pathway in mice.

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

    SciTech Connect

    Chen, Huaqun; Wang, Lijuan; Gong, Tao; Yu, Yang; Zhu, Chunhua; Li, Fen; Wang, Li; Li, Chaojun

    2010-05-28

    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{sup -/-} 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.

  15. Acetyl radical generation in cigarette smoke: Quantification and simulations

    NASA Astrophysics Data System (ADS)

    Hu, Na; Green, Sarah A.

    2014-10-01

    Free radicals are present in cigarette smoke and can have a negative effect on human health. However, little is known about their formation mechanisms. Acetyl radicals were quantified in tobacco smoke and mechanisms for their generation were investigated by computer simulations. Acetyl radicals were trapped from the gas phase using 3-amino-2, 2, 5, 5-tetramethyl-proxyl (3AP) on solid support to form stable 3AP adducts for later analysis by high-performance liquid chromatography (HPLC), mass spectrometry/tandem mass spectrometry (MS-MS/MS) and liquid chromatography-mass spectrometry (LC-MS). Simulations were performed using the Master Chemical Mechanism (MCM). A range of 10-150 nmol/cigarette of acetyl radical was measured from gas phase tobacco smoke of both commercial and research cigarettes under several different smoking conditions. More radicals were detected from the puff smoking method compared to continuous flow sampling. Approximately twice as many acetyl radicals were trapped when a glass fiber particle filter (GF/F specifications) was placed before the trapping zone. Simulations showed that NO/NO2 reacts with isoprene, initiating chain reactions to produce hydroxyl radical, which abstracts hydrogen from acetaldehyde to generate acetyl radical. These mechanisms can account for the full amount of acetyl radical detected experimentally from cigarette smoke. Similar mechanisms may generate radicals in second hand smoke.

  16. Vascular effects of cigarette smoke in isolated pig lungs

    SciTech Connect

    Gilman, M.J.; Sylvester, J.T.; Kennedy, T.P.; Menkes, H.A.; Traystman, R.J.

    1981-11-01

    To determine the local effects of cigarette smoke on the pulmonary vasculature, we measured pulmonary artery pressure--flow curves in isolated, blood-perfused pig lungs before and after 4 exposures to cigarette smoke. During each exposure, smoke was administered into the trachea for 3 to 4 min at a rate of 20 to 25 puffs/min and a puff volume of 35 to 50 ml with a smoking machine. During hypoxia (inspired PO2, 50 mmHg), when baseline vasomotor tone was high, cigarette smoke caused an acute transient vasodilation. During control (inspired PO2, 200 mmHg), when baseline tone was low, no significant effect was observed. In addition to this acute effect, cigarette smoke caused a depression of the pulmonary pressor response to hypoxia, which developed gradually during the course of the experiment. Indomethacin, at perfusate concentrations of 20 and 100 micrograms/ml, did not significantly alter the acute vasodilating effect of smoking, suggesting that prostaglandins synthesized by cyclooxygenase were not the mediators of this response. Indomethacin did, however, prevent the gradual depression of the pulmonary vasoconstrictor response to hypoxia.

  17. E-Cigarette Use Among Never-Smoking California Students.

    PubMed

    Bostean, Georgiana; Trinidad, Dennis R; McCarthy, William J

    2015-12-01

    We determined the extent to which adolescents who have never used tobacco try e-cigarettes. Data on the prevalence and correlates of e-cigarette use among 482,179 California middle and high school students are from the 2013-2014 California Healthy Kids Survey. Overall, 24.4% had ever used e-cigarettes (13.4% have never used tobacco and 11.0% have used tobacco), and 12.9% were current e-cigarette users (5.9% have never used tobacco). Among those who have never used tobacco, males and older students were more likely to use e-cigarettes than females and younger students. Hispanics (odds ratio [OR] = 1.60; confidence interval [CI] = 1.53, 1.67) and those of other races (OR = 1.24; CI = 1.19, 1.29) were more likely than Whites to have ever used e-cigarettes, but only among those who had never used smokeless tobacco and never smoked a whole cigarette. E-cigarette use is very prevalent among California students who have never smoked tobacco, especially among Hispanic and other race students, males, and older students.

  18. Cigarette smoking causes epigenetic changes associated with cardiorenal fibrosis.

    PubMed

    Drummond, Christopher A; Crotty Alexander, Laura E; Haller, Steven T; Fan, Xiaoming; Xie, Jeffrey X; Kennedy, David J; Liu, Jiang; Yan, Yanling; Hernandez, Dawn-Alita; Mathew, Denzil P; Cooper, Christopher J; Shapiro, Joseph I; Tian, Jiang

    2016-12-01

    Clinical studies indicate that smoking combustible cigarettes promotes progression of renal and cardiac injury, leading to functional decline in the setting of chronic kidney disease (CKD). However, basic studies using in vivo small animal models that mimic clinical pathology of CKD are lacking. To address this issue, we evaluated renal and cardiac injury progression and functional changes induced by 4 wk of daily combustible cigarette smoke exposure in the 5/6th partial nephrectomy (PNx) CKD model. Molecular evaluations revealed that cigarette smoke significantly (P < 0.05) decreased renal and cardiac expression of the antifibrotic microRNA miR-29b-3 and increased expression of molecular fibrosis markers. In terms of cardiac and renal organ structure and function, exposure to cigarette smoke led to significantly increased systolic blood pressure, cardiac hypertrophy, cardiac and renal fibrosis, and decreased renal function. These data indicate that decreased expression of miR-29b-3p is a novel mechanism wherein cigarette smoke promotes accelerated cardiac and renal tissue injury in CKD. (155 words).

  19. ISE Analysis of Hydrogen Sulfide in Cigarette Smoke

    NASA Astrophysics Data System (ADS)

    Li, Guofeng; Polk, Brian J.; Meazell, Liz A.; Hatchett, David W.

    2000-08-01

    Many advanced undergraduate analytical laboratory courses focus on exposing students to various modern instruments. However, students rarely have the opportunity to construct their own analytical tools for solving practical problems. We designed an experiment in which students are required to build their own analytical module, a potentiometric device composed of a Ag/AgCl reference electrode, a Ag/Ag2S ion selective electrode (ISE), and a pH meter used as voltmeter, to determine the amount of hydrogen sulfide in cigarette smoke. Very simple techniques were developed for constructing these electrodes. Cigarette smoke is collected by a gas washing bottle into a 0.1 M NaOH solution. The amount of sulfide in the cigarette smoke solution is analyzed by standard addition of sulfide solution while monitoring the response of the Ag/Ag2S ISE. The collected data are further evaluated using the Gran plot technique to determine the concentration of sulfide in the cigarette smoke solution. The experiment has been successfully incorporated into the lab course Instrumental Analysis at Georgia Institute of Technology. Students enjoy the idea of constructing an analytical tool themselves and applying their classroom knowledge to solve real-life problems. And while learning electrochemistry they also get a chance to visualize the health hazard imposed by cigarette smoking.

  20. Factors Associated with American Indian Cigarette Smoking in Rural Settings

    PubMed Central

    Hodge, Felicia; Nandy, Karabi

    2011-01-01

    Introduction: This paper reports on the prevalence, factors and patterns of cigarette smoking among rural California American Indian (AI) adults. Methods: Thirteen Indian health clinic registries formed the random household survey sampling frame (N = 457). Measures included socio-demographics, age at smoking initiation, intention to quit, smoking usage, smoking during pregnancy, health effects of smoking, suicide attempts or ideation, history of physical abuse, neglect and the role of the environment (smoking at home and at work). Statistical tests included Chi Square and Fisher’s Exact test, as well as multiple logistic regression analysis among never, former, and current smokers. Results: Findings confirm high smoking prevalence among male and female participants (44% and 37% respectively). American Indians begin smoking in early adolescence (age 14.7). Also, 65% of current smokers are less than 50% Indian blood and 76% of current smokers have no intention to quit smoking. Current and former smokers are statistically more likely to report having suicidal ideation than those who never smoked. Current smokers also report being neglected and physically abused in childhood and adolescence, are statistically more likely to smoke ½ pack or less (39% vs. 10% who smoke 1+ pack), smoke during pregnancy, and have others who smoke in the house compared with former and never smokers. Conclusion: Understanding the factors associated with smoking will help to bring about policy changes and more effective programs to address the problem of high smoking rates among American Indians. PMID:21695023

  1. The Relation between Frequency of E-Cigarette Use and Frequency and Intensity of Cigarette Smoking among South Korean Adolescents

    PubMed Central

    Lee, Jung Ah; Lee, Sungkyu; Cho, Hong-Jun

    2017-01-01

    Introduction: The prevalence of adolescent electronic cigarette (e-cigarette) use has increased in most countries. This study aims to determine the relation between the frequency of e-cigarette use and the frequency and intensity of cigarette smoking. Additionally, the study evaluates the association between the reasons for e-cigarette use and the frequency of its use. Materials and Methods: Using the 2015 Korean Youth Risk Behavior Web-Based Survey, we included 6655 adolescents with an experience of e-cigarette use who were middle and high school students aged 13–18 years. We compared smoking experience, the frequency and intensity of cigarette smoking, and the relation between the reasons for e-cigarette uses and the frequency of e-cigarette use. Results: The prevalence of e-cigarette ever and current (past 30 days) users were 10.1% and 3.9%, respectively. Of the ever users, approximately 60% used e-cigarettes not within 1 month. On the other hand, 8.1% used e-cigarettes daily. The frequent and intensive cigarette smoking was associated with frequent e-cigarette uses. The percentage of frequent e-cigarette users (≥10 days/month) was 3.5% in adolescents who did not smoke within a month, but 28.7% among daily smokers. Additionally, it was 9.1% in smokers who smoked less than 1 cigarette/month, but 55.1% in smokers who smoked ≥20 cigarettes/day. The most common reason for e-cigarette use was curiosity (22.9%), followed by the belief that they are less harmful than conventional cigarettes (18.9%), the desire to quit smoking (13.1%), and the capacity for indoor use (10.7%). Curiosity was the most common reason among less frequent e-cigarette users; however, the desire to quit smoking and the capacity for indoor use were the most common reasons among more frequent users. Conclusions: Results showed a positive relation between frequency or intensity of conventional cigarette smoking and the frequency of e-cigarette use among Korean adolescents, and frequency of e-cigarette

  2. Effects of exposure to cigarette smoke prior to pregnancy in diabetic rats

    PubMed Central

    2011-01-01

    Background The purpose of this study was to evaluate the effects of cigarette smoke exposure before pregnancy on diabetic rats and their offspring development. Methods Diabetes was induced by streptozotocin and cigarette smoke exposure was conducted by mainstream smoke generated by a mechanical smoking device and delivered into a chamber. Diabetic female Wistar rats were randomly distributed in four experimental groups (n minimum = 13/group): nondiabetic (ND) and diabetic rats exposed to filtered air (D), diabetic rats exposed to cigarette smoke prior to and into the pregnancy period (DS) and diabetic rats exposed to cigarette smoke prior to pregnancy period (DSPP). At day 21 of pregnancy, rats were killed for maternal biochemical determination and reproductive outcomes. Results The association of diabetes and cigarette smoke in DSPP group caused altered glycemia at term, reduced number of implantation and live fetuses, decreased litter and maternal weight, increased pre and postimplantation loss rates, reduced triglyceride and VLDL-c concentrations, increased levels of thiol groups and MDA. Besides, these dams presented increased SOD and GSH-Px activities. However, the increased antioxidant status was not sufficient to prevent the lipid peroxidation observed in these animals. Conclusion Despite the benefits stemming from smoking interruption during the pregnancy of diabetic rats, such improvement was insufficient to avoid metabolic alterations and provide an adequate intrauterine environment for embryofetal development. Therefore, these results suggest that it is necessary to cease smoking extensive time before planning pregnancy, since stopping smoking only when pregnancy is detected may not contribute effectively to fully adequate embryofetal development. PMID:21851636

  3. Medicalisation, smoking and e-cigarettes: evidence and implications.

    PubMed

    Morphett, Kylie; Carter, Adrian; Hall, Wayne; Gartner, Coral

    2016-11-30

    There is debate in the tobacco control literature about the value of a medical model in reducing smoking-related harm. The variety of medical treatments for smoking cessation has increased, health professionals are encouraged to use them to assist smoking cessation and tobacco dependence is being described as a 'chronic disease'. Some critics suggest that the medicalisation of smoking undermines the tobacco industry's responsibility for the harms of smoking. Others worry that it will lead smokers to deny personal responsibility for cessation, create beliefs in 'magic bullets' for smoking cessation, or erode smokers' confidence in their ability to quit. We argue that the medicalisation of smoking will have limited impact due to the emphasis on population-based interventions in tobacco control, the ambiguous place of nicotine among other drugs and the modest efficacy of current pharmacotherapies. These factors, as well as lay understandings of smoking that emphasise willpower, personal choice and responsibility, have contributed to the limited success of medical approaches to smoking cessation. While the rapid uptake of e-cigarettes in some countries has provided an option for those who reject medical treatments for smoking cessation, current regulatory developments could limit the potential of e-cigarettes to provide non-therapeutic nicotine for those who currently smoke tobacco.

  4. Acute effects of cigarette smoking on pattern electroretinogram.

    PubMed

    Gundogan, Fatih C; Durukan, A Hakan; Mumcuoglu, Tarkan; Sobaci, Gungor; Bayraktar, M Zeki

    2006-09-01

    In this study, acute effects of cigarette smoking on the pattern electroretinogram (PERG) were investigated. First, variability of the PERG was studied in a group of young male smokers (26 right eyes of 26 subjects). Then PERGs were investigated in a group of habitual smokers (17 right eyes of 17 subjects) in separate real smoking and sham smoking sessions. On each session PERGs were recorded pre-smoking (PS), immediately after smoking (IAS) and 5 min after smoking (5th) conditions. Real smoking significantly increased P50 amplitudes and decreased N95 latencies. Regarding P50 amplitudes in the real smoking sessions, the differences were significant between PS and IAS (PS: 3.3 +/- 0.5 muV, IAS: 3.7 +/- 0.7microV, P = 0.015) and between PS-5th (PS: 3.3 +/- 0.5microV, 5th: 4.1 +/- 0.9microV, P = 0.039). There was significant difference (P = 0.024) between N95 latencies of PS (98.5 +/- 6.9 ms) and IAS (94.7 +/- 5.1 ms) in the real smoking sessions. No statistically significant difference was observed in sham smoking sessions. Our results indicated, for the first time, that cigarette smoking may influence PERG amplitude and latency significantly in habitual smokers.

  5. Iron pentacarbonyl detection limits in the cigarette smoke matrix using FT-IR spectroscopy

    NASA Astrophysics Data System (ADS)

    Parrish, Milton E.; Plunkett, Susan E.; Harward, Charles N.

    2005-11-01

    Endogenous metals present in tobacco from agricultural practices have been purported to generate metal carbonyls in cigarette smoke. Transition metal catalysts, such as iron oxide, have been investigated for the reduction of carbon monoxide (CO) in cigarette smoke. These studies motivated the development of an analytical method to determine if iron pentacarbonyl [Fe(CO) 5] is present in mainstream smoke from cigarette models having cigarette paper made with iron oxide. An FT-IR puff-by-puff method was developed and the detection limit was determined using two primary reference spectra from different sources to estimate the amount of Fe(CO) 5 present in a high-pressure steel cylinder of CO. We do not detect Fe(CO) 5 in a single 35 mL puff from reference cigarettes or from those cigarette models having cigarette paper made with iron oxide, with a 30-ppbV limit of detection (LOD). Also, it was shown that a filter containing activated carbon would remove Fe(CO) 5.

  6. Carbon monoxide fractions in cigarette and hookah (hubble bubble) smoke.

    PubMed

    Sajid, K M; Akhter, M; Malik, G Q

    1993-09-01

    We studied the carbon monoxide (CO) fractions in hookah and cigarette smoke, using a carbon monoxide micro smokerlyzer (model EC50, BEDFONT, U.K.). Mean carbon monoxide fractions (% by volume) of hookah smoke, using domestic charcoal were 0.38 +/- 0.07 (large hookah; unfiltered); 1.40 +/- 0.43 (small hookah; unfiltered); 0.34 +/- 0.06 (large hookah; filtered); 1.36 +/- 0.35 (small hookah; filtered) and 0.41 +/- 0.08 (cigarette smoke). The highest fractions were obtained with small size hookah and increase in size of hookah (i.e., volume of air in water base, fire bowl volume, pipe length, etc.) reduced the CO fraction significantly (P < 0.001). The fractions of cigarette lie between large and small hookah. The fractions vary slightly with different varieties of tobacco, e.g., CO fractions with Dera wala tobacco are significantly low (P < 0.05). Use of commercial charcoal gives significant rise in CO fractions (P < 0.001). Comparison of filtered and unfiltered smoke shows no significant difference in values. We conclude that the CO hazard is as high with hookah smoking as with cigarette smoking.

  7. Comparison of Biological Responses in Rats Under Various Cigarette Smoke Exposure Conditions

    PubMed Central

    Tsuji, Hiroyuki; Fujimoto, Hitoshi; Matsuura, Daiki; Nishino, Tomoki; Lee, K Monica; Yoshimura, Hiroyuki

    2013-01-01

    A variety of exposure regimens of cigarette smoke have been used in animal models of lung diseases. In this study, we compared biological responses of smoke exposure in rats, using different smoke concentrations (wet total particulate matter [WTPM]), daily exposure durations, and total days of exposure. As a range-finding acute study, we first compared pulmonary responses between SD and F344 strains after a single nose-only exposure to mainstream cigarette smoke or LPS. Secondly, F344 rats were exposed to cigarette smoke for 2 or 13 weeks under the comparable daily exposure dose (WTPM concentration x daily exposure duration; according to Haber’s rule) but at a different WTPM concentration or daily exposure duration. Blood carboxylhemoglobin was increased linearly to the WTPM concentration, while urinary nicotine plus cotinine value was higher for the longer daily exposure than the corresponding shorter exposure groups. Gamma glutamyl transferase activity in bronchoalveolar lavage fluid (BALF) was increased dose dependently after 2 and 13 weeks of cigarette smoke exposure, while the neutrophil content in BALF was not increased notably. Smoke-exposed groups showed reduced body weight gain and increased relative lung and heart weights. While BALF parameters and the relative lung weights suggest pulmonary responses, histopathological examination showed epithelial lesions mainly in the upper respiratory organs (nose and larynx). Collectively, the results indicate that, under the employed study design, the equivalent daily exposure dose (exposure concentration x duration) induces equivalent pulmonary responses in rats. PMID:23914058

  8. Cigarette smoking and adolescents: messages they see and hear.

    PubMed Central

    Crawford, M. A.

    2001-01-01

    Cigarette smoking is the primary preventable cause of mortality and morbidity in the US. But in the mid-1990s, more than one-third of US teenagers were smokers, despite their awareness of the health risks and negative consequences of tobacco use. In 1996, as part of a three-year qualitative study to explore differences in adolescent smoking by gender and ethnicity, members of the Tobacco Control Network examined messages that teens receive about cigarette smoking. Consisting of 178 focus groups with 1,175 teenagers covering all levels of smoking experience, the study included teens from five ethnic groups, stratified by gender and ethnicity, from urban and rural areas across the US. The authors reviewed the sources and content of messages that teens reported were most influential in their decisions to smoke or not smoke cigarettes. Family and peers, school, television, and movies were the primary sources for both pro- and anti-smoking messages. The authors conclude that a lack of clear, consistent antismoking messages leaves teens vulnerable to the influences of pro-smoking messages from a variety of sources. Interventions need to be culture- and gender-specific. Family-based interventions appear to be needed and efficacious, but resource intensive. Building self-esteem may prove to be a promising intervention. PMID:11889286

  9. The Effect of Cigarette Smoking on Gingival Crevicular Fluid Flow.

    DTIC Science & Technology

    1986-01-01

    Medical Electronics, Inc., Irvine, CA) has been marketed that electronically measures and quantitates the amount of fluid on a paper strip. The...during illness; brand smoked (nicotine content); and inhalation tendencies. Each question is scored, ith higher scores given for responses indicating...the depth of inhalation, the number and volume of puffs taken per cigarette, the 1 38 brand name of the cigarette (CO content varies between brands

  10. Social Psychological Factors in Adolescent Cigarette Smoking.

    ERIC Educational Resources Information Center

    Sherman, Steven J.; And Others

    Results emanating from smoking cessation programs suggest the necessity for a greater commitment to research for primary smoking prevention. Because of the early onset of smoking, more research must focus on adolescents and preadolescents who have not yet begun to smoke regularly. Three areas of concentrated study are proposed: (1) the initiation…

  11. Cigarette smoke, bacteria, mold, microbial toxins, and chronic lung inflammation.

    PubMed

    Pauly, John L; Paszkiewicz, Geraldine

    2011-01-01

    Chronic inflammation associated with cigarette smoke fosters malignant transformation and tumor cell proliferation and promotes certain nonneoplastic pulmonary diseases. The question arises as to whether chronic inflammation and/or colonization of the airway can be attributed, at least in part, to tobacco-associated microbes (bacteria, fungi, and spores) and/or microbial toxins (endotoxins and mycotoxins) in tobacco. To address this question, a literature search of documents in various databases was performed. The databases included PubMed, Legacy Tobacco Documents Library, and US Patents. This investigation documents that tobacco companies have identified and quantified bacteria, fungi, and microbial toxins at harvest, throughout fermentation, and during storage. Also characterized was the microbial flora of diverse smoking and smokeless tobacco articles. Evidence-based health concerns expressed in investigations of microbes and microbial toxins in cigarettes, cigarette smoke, and smokeless tobacco products are reasonable; they warrant review by regulatory authorities and, if necessary, additional investigation to address scientific gaps.

  12. Cigarette Smoke, Bacteria, Mold, Microbial Toxins, and Chronic Lung Inflammation

    PubMed Central

    Pauly, John L.; Paszkiewicz, Geraldine

    2011-01-01

    Chronic inflammation associated with cigarette smoke fosters malignant transformation and tumor cell proliferation and promotes certain nonneoplastic pulmonary diseases. The question arises as to whether chronic inflammation and/or colonization of the airway can be attributed, at least in part, to tobacco-associated microbes (bacteria, fungi, and spores) and/or microbial toxins (endotoxins and mycotoxins) in tobacco. To address this question, a literature search of documents in various databases was performed. The databases included PubMed, Legacy Tobacco Documents Library, and US Patents. This investigation documents that tobacco companies have identified and quantified bacteria, fungi, and microbial toxins at harvest, throughout fermentation, and during storage. Also characterized was the microbial flora of diverse smoking and smokeless tobacco articles. Evidence-based health concerns expressed in investigations of microbes and microbial toxins in cigarettes, cigarette smoke, and smokeless tobacco products are reasonable; they warrant review by regulatory authorities and, if necessary, additional investigation to address scientific gaps. PMID:21772847

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

    PubMed

    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.

  14. The involvement of serotonin metabolism in cigarette smoke-induced oxidative stress in rat lung in vivo.

    PubMed

    Lau, Way Kwok-Wai; Li, Xiang; Yeung, Dave Sze-Chun; Chan, Ka-Ho; Ip, Mary Sau-Man; Mak, Judith Choi-Wo

    2012-11-01

    Recently, we have reported the dysregulation of circulating serotonin (5-hydroxytryptamine, 5-HT) homeostasis in patients with chronic obstructive pulmonary disease (COPD). An increase in metabolism of 5-HT has been reported to induce oxidative stress via monoamine oxidase (MAO)-dependent pathway. The present study aimed at investigating the effect of cigarette smoke exposure on the systemic circulation and local airway 5-HT levels as well as MAO-mediated oxidative pathway using a cigarette smoke-exposed rat model. Male Sprague-Dawley rats (150-200 g) were exposed to either sham air or 4% (v/v, smoke/air) cigarette smoke for 1 hour daily for 56 consecutive days. Sera, bronchoalveolar larvage (BAL) and lung tissues were collected 24 hours after the last exposure. We found a significant reduction in the reduced glutathione (rGSH) and an elevation in advanced oxidation protein products (AOPP), a protein oxidation marker, in the lung of cigarette smoke-exposed group (p < 0.05). A significant increase in 5-HT was found in serum (p < 0.05), but not in the BAL or lung, after cigarette smoke exposure. MAO-A activity was significantly elevated in the lung of cigarette smoke-exposed group (p < 0.05). Furthermore, increased superoxide anion levels were found in lung homogenates of cigarette smoke-exposed rats after incubation with 5-HT (p < 0.05), which was positively associated with the increase in MAO-A activity (r = 0.639, p < 0.05). Our findings supported the presence of GSH disruption and protein oxidation in the lung after cigarette smoke exposure. The metabolism of 5-HT by MAO-A in the lung enhanced cigarette smoke-induced superoxides, which might contribute to the pathogenesis of COPD.

  15. Effect of cigarette menthol content on mainstream smoke emissions.

    PubMed

    Gordon, S M; Brinkman, M C; Meng, R Q; Anderson, G M; Chuang, J C; Kroeger, R R; Reyes, I L; Clark, P I

    2011-10-17

    The 2009 Family Smoking Prevention and Tobacco Control Act empowered the U.S. Food and Drug Administration to study "the impact of the use of menthol in cigarettes on the public health, including such use among children, African Americans, Hispanics and other racial and ethnic minorities," and develop recommendations. Current scientific evidence comparing human exposures between menthol and nonmenthol smokers shows mixed results. This is largely because of the many differences between commercial menthol and nonmenthol cigarettes other than their menthol content. We conducted an innovative study using two types of test cigarettes: a commercial nonmenthol brand that we mentholated at four different levels, and Camel Crush, a commercial cigarette containing a small capsule in the filter that releases menthol solution into the filter when crushed. Cigarettes were machine-smoked at each of the menthol levels investigated, and the total particulate matter (TPM) was collected on a quartz fiber filter pad and analyzed by gas chromatography/mass spectrometry for menthol, nicotine, tobacco-specific nitrosamines (TSNAs), polycyclic aromatic hydrocarbons (PAHs), cotinine, and quinoline. The mainstream smoke was also monitored continuously in real time on a puff-by-puff basis for seven gas-phase constituents (acetaldehyde, acetonitrile, acrylonitrile, benzene, 1,3-butadiene, isoprene, and 2,5-dimethylfuran), using a proton transfer reaction-mass spectrometer. Average yields (in micrograms/cigarette) for the analytes were determined. Menthol in the TPM samples increased linearly with applied menthol concentration, but the amounts of nicotine along with the target TSNAs, PAHs, cotinine, and quinoline in the cigarettes remained essentially unchanged. Similarly, yields of the targeted volatile organic compounds (VOCs) in whole smoke from the mentholated nonmenthol cigarettes that were measured in real-time were largely unaffected by their menthol levels. In the Camel Crush

  16. Effect of Cigarette Smoke on Acrylic Resin Teeth

    PubMed Central

    Patil, Seema S.; M.R., Dhakshaini; Gujjari, Anil Kumar

    2013-01-01

    Background: The discolouration of artificial teeth, which hampers aesthetics, is one of the negative effects of cigarette smoking. Therefore, the effect of cigarette smoke on the colour stability of commercially available acrylic resin teeth needs to be evaluated for clinical success and to ascertain as to which brand has superior properties. Material and Methods: Three commercially available acrylic teeth were evaluated, after division into Group A (Premadent), Group B (Astra), and Group C (Sanyo- Dent). Selected brands were subdivided as study group and control group. Each set of acrylic resin teeth were stored in artificial saliva at 37±1°C for 24 hours. After 24 hours of immersion, the colour measurement of each tooth (T0) was performed. Second colour measurements were done after 21 days (T21) of exposure to cigarette smoke for study group and after immersion in artificial saliva for control group. All data was statistically analyzed by using Repeated Measures ANOVA and Two-way ANOVA (p<0.05). Results: Group A showed least total colour change on exposure to cigarette smoke, followed by Group B and Group C had the highest total colour change. In control group, after immersion in artificial saliva, a slight increase in total colour change was observed for all groups, which was clinically acceptable. Conclusion: Group A (crosslinked acrylic resin teeth) was more colour stable and more resistant to the discolouration which was caused by cigarette smoke, followed by Group B (crosslinked acrylic resin teeth). Group C (Non-crosslinked acrylic resin teeth) was least colour stable and most susceptible to discolouration which was caused by cigarette smoke. PMID:24179942

  17. Silymarin attenuates airway inflammation induced by cigarette smoke in mice.

    PubMed

    Li, Diandian; Xu, Dan; Wang, Tao; Shen, Yongchun; Guo, Shujin; Zhang, Xue; Guo, Lingli; Li, Xiaoou; Liu, Lian; Wen, Fuqiang

    2015-04-01

    Cigarette smoke (CS), which increases inflammation and oxidative stress, is a major risk factor for the development of COPD. In this study, we investigated the effects of silymarin, a polyphenolic flavonoid isolated from the seeds and fruits of milk thistle, on CS-induced airway inflammation and oxidative stress in mice and the possible mechanisms. BALB/c mice were exposed to CS for 2 h twice daily, 6 days per week for 4 weeks. Silymarin (25, 50 mg/kg·day) was administered intraperitoneally 1 h before CS exposure. Bronchoalveolar lavage fluid (BALF) was acquired for cell counting and the detection of pro-inflammatory cytokine levels. Lung tissue was collected for histological examination, myeloperoxidase (MPO) activity assay, superoxide dismutase (SOD) activities, and malondialdehyde (MDA) levels. The phosphorylation of ERK and p38 was evaluated by Western blotting. Pretreatment with silymarin significantly attenuated CS-induced thickening of the airway epithelium, peribronchial inflammatory cell infiltration, and lumen obstruction. The numbers of total cells, macrophages, and neutrophils, along with the MPO activity (a marker of neutrophil accumulation) in BALF, were remarkably decreased by silymarin in CS-exposed mice (all p<0.05). In addition, silymarin pretreatment dampened the secretion of TNF-α, IL-1β, and IL-8 in BALF. High-dose silymarin (50 mg/kg·day) administration also prevented CS-induced elevation in MDA levels and decrease in SOD activities (p<0.05). Furthermore, the CS-induced phosphorylation of ERK and p38 was also attenuated by silymarin (p<0.05). These results suggest that silymarin attenuated inflammation and oxidative stress induced by cigarette smoke. The anti-inflammatory effect might partly act through the mitogen-activated protein kinases (MAPK) pathway.

  18. Analysis of the Effects of Cigarette Smoke on Staphylococcal Virulence Phenotypes

    PubMed Central

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

    2015-01-01

    Cigarette smoking is the leading preventable cause of death, disease, and disability worldwide. It is well established that cigarette smoke provokes inflammatory activation and impairs antimicrobial functions of human immune cells. Here we explore whether cigarette smoke likewise affects the virulence properties of an important human pathogen, Staphylococcus aureus, and in particular methicillin-resistant S. aureus (MRSA), one of the leading causes of invasive bacterial infections. MRSA colonizes the nasopharynx and is thus exposed to inhalants, including cigarette smoke. MRSA exposed to cigarette smoke extract (CSE-MRSA) was more resistant to macrophage killing (4-fold higher survival; P < 0.0001). CSE-MRSA demonstrated reduced susceptibility to cell lysis (1.78-fold; P = 0.032) and antimicrobial peptide (AMP) (LL-37) killing (MIC, 8 μM versus 4 μM). CSE modified the surface charge of MRSA in a dose-dependent fashion, impairing the binding of particles with charge similar to that of AMPs by 90% (P < 0.0001). These changes persisted for 24 h postexposure, suggesting heritable modifications. CSE exposure increased hydrophobicity by 55% (P < 0.0001), which complemented findings of increased MRSA adherence and invasion of epithelial cells. CSE induced upregulation of mprF, consistent with increased MRSA AMP resistance. S. aureus without mprF had no change in surface charge upon exposure to CSE. In vivo, CSE-MRSA pneumonia induced higher mouse mortality (40% versus 10%) and increased bacterial burden at 8 and 20 h postinfection compared to control MRSA-infected mice (P < 0.01). We conclude that cigarette smoke-induced immune resistance phenotypes in MRSA may be an additional factor contributing to susceptibility to infectious disease in cigarette smokers. PMID:25824841

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

    PubMed

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

    2015-06-01

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

  20. Cigarette smoke extract (CSE) induces transient receptor potential ankyrin 1(TRPA1) expression via activation of HIF1αin A549 cells.

    PubMed

    Nie, Yichu; Huang, Chuqin; Zhong, Shan; Wortley, Michael A; Luo, Yulong; Luo, Wei; Xie, Yanqing; Lai, Kefang; Zhong, Nanshan

    2016-10-01

    We previously found that transient receptor potential ankyrin 1 (TRPA1) in guinea pig tracheal epithelial cells was elevated after 14 days of cigarette smoke (CS) exposure. However, the mechanism underlying CS-induced TRPA1 expression remains unknown. Here, we explored whether cigarette smoke extract (CSE)-induced TRPA1 expression is related with modulation of HIF1α in A549 cells. Our results showed that CSE increased TRPA1 expression in A549 cells, decreased Iκ B, PHD2, and HDAC2, and increased ROS release and nuclear translocation of NF-κ B and HIF1α. Moreover, HIF1α siRNA and/or MG132 (a proteasome inhibitor) pretreatment significantly inhibited CSE-induced TRPA1 expression and HIF1α nuclear translocation in A549 cells. However, HIF1α siRNA pretreatment did not affect CSE-induced NF-κ B nuclear translocation, suggesting that CSE-induced TRPA1 expression in A549 cells is directly mediated by HIF1α, but not by NF-κ B. Similar to CSE treatment, treatment of A549 cells with LPS caused significant increases in nuclear translocation of NF-κ B and HIF1α mRNA expression, but did not alter TRPA1 mRNA expression. However, pretreatment with PHD2 siRNA did result in increased TRPA1 mRNA expression in LPS-treated A549 cells; an effect that was inhibited by SN50 (a NF-κ B inhibitor). It suggests a role for NF-κ B to indirectly regulate TRPA1 mRNA expression via modulating HIF1α mRNA transcription. In addition, treatment cells with HDAC2 siRNA plus 2%CSE resulted in increased HIF1α nuclear translocation and TRPA1 expression, which was significantly inhibited by MG132 and HIF1α siRNA. These results suggest that HDAC2 indirectly modulates TRPA1 expression by promoting the DNA-binding activity of HIF1α. These findings show that CSE increases TRPA1 expression in airway epithelial cells by directly activating HIF1α, and that this increase in TRPA1 expression is indirectly regulated via NF-κ B, PHD2 and HDAC2 modulation of HIF1α activity.

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

    SciTech Connect

    Archer, V.E.

    1985-01-01

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

  2. Clearance of polonium-210-enriched cigarette smoke from the rat trachea and lung

    SciTech Connect

    Cohen, B.S.; Harley, N.H.; Tso, T.C.

    1985-06-30

    The distribution and clearance of alpha radioactivity in the lungs of rats were measured after inhalation of smoke from cigarettes highly enriched in /sup 210/Po. Female Fischer rats were exposed daily for 6 months to smoke from cigarettes with 500 times the normal content of /sup 210/Po. Control rats were exposed to standard cigarette smoke. Animals were serially withdrawn and killed. After necropsy the trachea, major bronchi, larynx, and nasopharynx were examined for surface alpha activity by an etched track technique utilizing cellulose nitrate detectors. Areas of accumulated activity were seen on samples of larynx from rats exposed to the /sup 210/Po-enriched cigarettes. No other local accumulations were seen on the airways. The lower lungs were analyzed radiochemically for /sup 210/Po. Both radiochemical analysis and track measurements showed highly elevated activity concentrations in rats exposed to the /sup 210/Po-enriched cigarettes. Following withdrawal from smoking, both short- and long-term clearance components were seen. The parameters which fit the postexposure data for clearance of the lung burden cannot fit the buildup during the exposure period.

  3. [Cigarette smoking is the most important causal factor for developing chronic obstructive pulmonary disease (COPD)].

    PubMed

    Muro, Shigeo

    2011-10-01

    Cigarette smoking is the most important causal factor for developing chronic obstructive pulmonary disease(COPD). On the other hand, a substantial proportion of COPD cases suffer from obstructive disorder by other causes than smoking, especially among younger persons, females, and residents of developing countries. There are evidences that several rare genetic syndromes(such as alpha 1-antitrypsin deficiency) and occupational exposures as causes of COPD. Environmental tobacco smoke, biomass smoke, and dietary factors are likely causes of COPD, although their contribution is much less compared to active smoking. Smoking during pregnancy may also pose a risk for the fetus, by affecting lung growth and development in uterus. The quicker the smoking cessation is achieved, the more improvements in the lung functions the COPD patients can obtain. Smoking should be avoided as soon as possible in all the COPD subjects and those who are at risk for developing COPD.

  4. Protein kinase CK2-mediated phosphorylation of HDAC2 regulates co-repressor formation, deacetylase activity and acetylation of HDAC2 by cigarette smoke and aldehydes.

    PubMed

    Adenuga, David; Rahman, Irfan

    2010-06-01

    Histone deacetylase 2 (HDAC2) mediates the repression of pro-inflammatory genes by deacetylating core histones, RelA/p65 and the glucocorticoid receptor. Reduced level of HDAC2 is associated with steroid resistant inflammation caused by cigarette smoke (CS)-derived oxidants and aldehydes. However, the molecular mechanisms regulating HDAC2 in response to CS and aldehydes is not known. Here, we report that CS extract, and aldehyde acrolein induced phosphorylation of HDAC2 which was abolished by mutations at serine sites S(394), S(411), S(422) and S(424). HDAC2 phosphorylation required direct interaction with serine-phosphorylated protein kinase CK2alpha and involved reduced HDAC2 deacetylase activity. Furthermore, HDAC2 phosphorylation was required for HDAC2 interaction with transcription factors, co-repressor complex formation, CBP recruitment, acetylation on lysine residues and modulates transrepression activity. Thus, phospho-acetylation of HDAC2 negatively regulates its deacetylase activity which has implications in steroid resistance in chronic inflammatory conditions.

  5. Impulsivity and the reinforcing value of cigarette smoking.

    PubMed

    Doran, Neal; McChargue, Dennis; Cohen, Lee

    2007-01-01

    The present study tested the hypothesis that impulsivity would predict perceptions of positive and negative reinforcement from smoking. The secondary hypothesis was that the relationship between impulsivity and smoking reinforcement expectations would be mediated by the character trait of self-directedness. College students (n=202) who reported smoking cigarettes participated in the survey study. Hierarchical regression analyses confirmed that impulsivity predicted expectations about positive (beta=.22, p=.001) and negative (beta=.25, p=.001) reinforcement from smoking. These relationships were also mediated by self-directedness. Results suggest that impulsive smokers in the early stages of dependence may smoke because they expect smoking to be extremely pleasurable as well as to help dispel bouts with negative affect. Furthermore, their elevated expectations about smoking may be related to difficulties adapting to challenging environments and working toward long-term goals.

  6. A comparison of in vitro toxicities of cigarette smoke condensate from Eclipse cigarettes and four commercially available ultra low-"tar" cigarettes.

    PubMed

    Foy, J W D; Bombick, B R; Bombick, D W; Doolittle, D J; Mosberg, A T; Swauger, J E

    2004-02-01

    Eclipse is a cigarette that primarily heats rather than burns tobacco. R.J. Reynolds Tobacco Company (RJRT) has previously reported the results of in vitro toxicity studies comparing Eclipse with University of Kentucky 1R5F and 1R4F reference cigarettes. To characterize the differences between Eclipse and very low yielding/ultra low-"tar" (vULT) tobacco-burning cigarettes, RJRT conducted a comparative evaluation of the genotoxicity and cytotoxicity of mainstream cigarette smoke condensate (CSC) from Eclipse and three vULT tobacco-burning cigarettes (Now 83 Box, Merit Ultima and Carlton Soft Pack) as well as the leading ultra low-"tar" (ULT) brandstyle (Marlboro Ultra Lights) under four smoking regimens: (1) FTC-35 ml puff volume every 60 s for a 2 s duration (35/60/2); (2) 50/30/2, 0% vents blocked; (3) Massachusetts-45/30/2, 50% vents blocked; (4) Canadian-55/30/2, 100% vents blocked. Ames testing indicated that Eclipse CSC was less (P<0.05) mutagenic than CSC from the four cigarettes under all smoking regimens when compared on a revertants per mg Total Particulate Matter (TPM) basis. When mutagenicity was calculated on a revertants per cigarette basis the mutagenicity of Eclipse CSC was lower (P<0.05) than the mutagenicity of Merit Ultima, Carlton Soft Pack, and Marlboro Ultra Lights, regardless of the puffing regimen. On a per cigarette basis, the calculated mutagenicity of Eclipse was higher (P<0.05) than Now 83 Box cigarettes in the FTC and 50/30/2 regimens but lower (P<0.05) in the Massachusetts and Canadian regimens. Eclipse CSC was less (P<0.05) cytotoxic as measured in the neutral red assay (based on EC(50) values-microg TPM/ml media) than the CSC from the four test cigarettes regardless of the regimen used. Collectively, these data demonstrate that the toxicity of CSC from Eclipse is significantly reduced relative to the activity of CSC from the tested vULT cigarettes and the Marlboro Ultra Lights.

  7. Detection of Hand-to-Mouth Gestures Using a RF Operated Proximity Sensor for Monitoring Cigarette Smoking

    PubMed Central

    Lopez-Meyer, Paulo; Patil, Yogendra; Tiffany, Tiffany; Sazonov, Edward

    2013-01-01

    Common methods for monitoring of cigarette smoking, such as portable puff-topography instruments or self-report questionnaires, tend to be biased due to conscious or unconscious underreporting. Additionally, these methods may change the natural smoking behavior of individuals. Our long term objective is the development of a wearable non-invasive monitoring system (Personal Automatic Cigarette Tracker – PACT) to reliably monitor cigarette smoking behavior under free living conditions. PACT monitors smoking by observing characteristic breathing patterns of smoke inhalations that follow a cigarette-to-mouth hand gesture. As envisioned, PACT does not rely on self-report or require any conscious effort from the user. A major element of the PACT is a proximity sensor that detects typical cigarette-to-mouth gesture during cigarette smoking. This study describes the design and validation of a prototype RF proximity sensor that captures hand-to-mouth gestures with a high sensitivity (0.90), and a methodology that can reject up to 68% of artifacts gestures originating from activities other than cigarette smoking. PMID:23723954

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

    PubMed

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

    2013-01-01

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

  9. Triple Quad-ICP-MS Measurement of Toxic Metals in Mainstream Cigarette Smoke from Spectrum Research Cigarettes.

    PubMed

    Pappas, R Steven; Gray, Naudia; Gonzalez-Jimenez, Nathalie; Fresquez, Mark; Watson, Clifford H

    2016-01-01

    We previously reported toxic metal concentrations in the mainstream smoke from 50 varieties of commercial cigarettes available in the USA using quadrupole inductively coupled plasma-mass spectrometry (ICP-MS). However, efforts to continue producing high quality data on select mainstream cigarette smoke constituents demand continued improvements in instrumentation and methodology and application of the methodology to cigarettes that differ in design or construction. Here we report a new application of 'triple quad'-ICP-MS instrumentation to analyze seven toxic metals in mainstream cigarette smoke from the Spectrum variable nicotine research cigarettes. The Spectrum cigarettes are available for research purposes in different configurations of low or conventional levels of nicotine, mentholated or nonmentholated, and tar delivery ranges described as 'low tar' or 'high tar'. Detailed characterizations of specific harmful or potentially harmful constituents delivered by these research cigarettes will help inform researchers using these cigarettes in exposure studies, cessation studies and studies related to nicotine addiction or compensation.

  10. Expression of a constitutively active nitrate reductase variant in tobacco reduces tobacco-specific nitrosamine accumulation in cured leaves and cigarette smoke.

    PubMed

    Lu, Jianli; Zhang, Leichen; Lewis, Ramsey S; Bovet, Lucien; Goepfert, Simon; Jack, Anne M; Crutchfield, James D; Ji, Huihua; Dewey, Ralph E

    2016-07-01

    Burley tobaccos (Nicotiana tabacum) display a nitrogen-use-deficiency phenotype that is associated with the accumulation of high levels of nitrate within the leaf, a trait correlated with production of a class of compounds referred to as tobacco-specific nitrosamines (TSNAs). Two TSNA species, 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) and N-nitrosonornicotine (NNN), have been shown to be strong carcinogens in numerous animal studies. We investigated the potential of molecular genetic strategies to lower nitrate levels in burley tobaccos by overexpressing genes encoding key enzymes of the nitrogen-assimilation pathway. Of the various constructs tested, only the expression of a constitutively active nitrate reductase (NR) dramatically decreased free nitrate levels in the leaves. Field-grown tobacco plants expressing this NR variant exhibited greatly reduced levels of TSNAs in both cured leaves and mainstream smoke of cigarettes made from these materials. Decreasing leaf nitrate levels via expression of a constitutively active NR enzyme represents an exceptionally promising means for reducing the production of NNN and NNK, two of the most well-documented animal carcinogens found in tobacco products.

  11. Smoking Revolution” A Content Analysis of Electronic Cigarette Retail Websites

    PubMed Central

    Grana, Rachel A.; Ling, Pamela M.

    2014-01-01

    Background Electronic cigarettes (e-cigarettes) have been increasingly available and marketed in the U.S. since 2007. As patterns of product adoption are frequently driven and reinforced by marketing, it is important to understand the marketing claims encountered by consumers. Purpose To describe the main advertising claims made on branded e-cigarette retail websites. Methods Websites were retrieved from two major search engines in 2011 using iterative searches with the following terms: electronic cigarette, e-cigarette, e-cig, and personal vaporizer. Fifty-nine websites met inclusion criteria, and 13 marketing claims were coded for main marketing messages in 2012. Results Ninety-five percent of the websites made explicit or implicit health-related claims, 64% had a smoking cessation-related claim, 22% featured doctors, and 76% claimed that the product does not produce secondhand smoke. Comparisons to cigarettes included claims that e-cigarettes were cleaner (95%) and cheaper (93%). Eighty-eight percent stated that the product could be smoked anywhere and 71% mentioned using the product to circumvent clean air policies. Candy, fruit, and coffee flavors were offered on most sites. Youthful appeals included images or claims of modernity (73%), increased social status (44%), enhanced social activity (32%), romance (31%), and use by celebrities (22%). Conclusions Health claims and smoking cessation messages that are unsupported by current scientific evidence are frequently used to sell e-cigarettes. Implied and overt health claims, the presence of doctors on websites, celebrity endorsements, and the use of characterizing flavors should be prohibited. PMID:24650842

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

    PubMed Central

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

    2013-01-01

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

  13. Urine Menthol as a Biomarker of Mentholated Cigarette Smoking

    PubMed Central

    Benowitz, Neal L; Dains, Katherine M.; Dempsey, Delia; Havel, Christopher; Wilson, Margaret; Jacob, Peyton

    2010-01-01

    Objectives Menthol cigarettes are smoked by 27% of U.S. smokers, and there are concerns that menthol might enhance toxicity of cigarette smoking by increasing systemic absorption of smoke toxins. We measured urine menthol concentrations in relation to biomarkers of exposure to nicotine and tobacco carcinogens. Methods Concentrations of menthol glucuronide (using a novel analytical method), nicotine plus metabolites (nicotine equivalents, NE), 4-(methylnitrosamino)-1-(3)pyridyl-1-butanol (NNAL) and polycyclic aromatic hydrocarbon (PAH) metabolites were measured in the urine of 60 menthol and 67 regular cigarette smokers. Results Urine menthol was measurable in 82% of menthol and 54% in regular cigarette smokers. Among menthol smokers urine menthol was highly correlated with NE, NNAL and PAHs. In a multiple regression model NE but not menthol was significantly associated with NNAL and PAHs. Conclusions Urine menthol concentration is a novel biomarker of exposure in menthol cigarette smokers, and is highly correlated with exposure to nicotine and carcinogens. Menthol is not independently associated with carcinogen exposure when nicotine intake is considered. PMID:20962297

  14. Associations between posttraumatic stress disorder symptom clusters and cigarette smoking.

    PubMed

    Greenberg, Jodie B; Ameringer, Katherine J; Trujillo, Michael A; Sun, Ping; Sussman, Steve; Brightman, Molly; Pitts, Stephanie R; Leventhal, Adam M

    2012-03-01

    Understanding the relationship between Posttraumatic stress disorder (PTSD) and cigarette smoking has been difficult because of PTSD's symptomatic heterogeneity. This study examined common and unique lifetime cross-sectional relationships between PTSD symptom clusters [Re-experiencing (intrusive thoughts and nightmares about the trauma), Avoidance (avoidance of trauma-associated memories or stimuli), Emotional Numbing (loss of interest, interpersonal detachment, restricted positive affect), and Hyperarousal (irritability, difficulty concentrating, hypervigilance, insomnia)] and three indicators of smoking behavior: (1) smoking status; (2) cigarettes per day; and (3) nicotine dependence. Participants were adult respondents in the National Epidemiologic Survey of Alcohol and Related Conditions with a trauma history (n = 23,635). All four symptom clusters associated with each smoking outcome in single-predictor models (ps <. 0001). In multivariate models including all of the symptom clusters as simultaneous predictors, Emotional Numbing was the only cluster to retain a significant association with lifetime smoking over and above the other clusters, demographics, and Axis-I comorbidity (OR = 1.30, p < .01). While Avoidance uniquely associated with smoking status and nicotine dependence in multivariate models, these relations fell below significance after adjusting for demographics and comorbidity. No clusters uniquely associated with cigarettes per day. Hyperarousal uniquely related with nicotine dependence over and above the other clusters, demographics, and Axis-I comorbidity (OR = 1.51, p < .001). These results suggest the following: (a) common variance across PTSD symptom clusters contribute to PTSD's linkage with smoking in the American population; and (b) certain PTSD symptom clusters may uniquely associate with particular indicators of smoking behavior. These findings may clarify the underpinnings of PTSD-smoking comorbidity and inform smoking interventions for

  15. Adolescents’ and Young Adults’ Perceptions of Electronic Cigarettes for Smoking Cessation: A Focus Group Study

    PubMed Central

    Camenga, Deepa R.; Cavallo, Dana A.; Kong, Grace; Morean, Meghan E.; Connell, Christian M.; Simon, Patricia; Bulmer, Sandra M.

    2015-01-01

    Introduction: Research has shown that adults perceive that electronic cigarettes (e-cigarettes) are effective for smoking cessation, yet little is known about adolescents and young adults’ perceptions of e-cigarettes for quitting cigarette smoking. This study describes middle, high school, and college students’ beliefs about, and experiences with, e-cigarettes for cigarette smoking cessation. Methods: We conducted 18 focus groups (n = 127) with male and female cigarette smokers and nonsmokers in 2 public colleges, 2 high schools, and 1 middle school in Connecticut between November 2012 and April 2013. Participants discussed cigarette smoking cessation in relation to e-cigarettes. Verbatim transcripts were analyzed using thematic analysis. Results: All participants, regardless of age and smoking status, were aware that e-cigarettes could be used for smoking cessation. College and high school participants described different methods of how e-cigarettes could be used for smoking cessation: (a) nicotine reduction followed by cessation; (b) cigarette reduction/dual use; and (c) long-term exclusive e-cigarette use. However, overall, participants did not perceive that e-cigarette use led to successful quitting experiences. Participants described positive attributes (maintenance of smoking actions, “healthier” alternative to cigarettes, and parental approval) and negative attributes (persistence of craving, maintenance of addiction) of e-cigarettes for cessation. Some college students expressed distrust of marketing of e-cigarettes for smoking cessation. Conclusions: Adolescent and young adult smokers and nonsmokers perceive that there are several methods of using e-cigarettes for quitting and are aware of both positive and negative aspects of the product. Future research is needed to determine the role of e-cigarettes for smoking cessation in this population. PMID:25646346

  16. Biological effects of cigarette smoke, wood smoke, and the smoke from plastics: The use of electron spin resonance

    SciTech Connect

    Pryor, W.A. )

    1992-12-01

    This review compares and contrasts the chemistry of cigarette smoke, wood smoke, and the smoke from plastics and building materials that is inhaled by persons trapped in fires. Cigarette smoke produces cancer, emphysema, and other diseases after a delay of years. Acute exposure to smoke in a fire can produce a loss of lung function and death after a delay of days or weeks. Tobacco smoke and the smoke inhaled in a burning building have some similarities from a chemical viewpoint. For example, both contain high concentrations of CO and other combustion products. In addition, both contain high concentrations of free radicals, and our laboratory has studied these free radicals, largely by electron spin resonance (ESR) methods, for about 15 years. This article reviews what is known about the radicals present in these different types of smokes and soots and tars and summarizes the evidence that suggests these radicals could be involved in cigarette-induced pathology and smoke-inhalation deaths. The combustion of all organic materials produces radicals, but (with the exception of the smoke from perfluoropolymers) the radicals that are detected by ESR methods (and thus the radicals that would reach the lungs) are not those that arise in the combustion process. Rather they arise from chemical reactions that occur in the smoke itself. Thus, a knowledge of the chemistry of the smoke is necessary to understand the nature of the radicals formed. Even materials as similar as cigarettes and wood (cellulose) produce smoke that contains radicals with very different lifetimes and chemical characteristics, and mechanistic rationales for this are discussed. Cigarette tar contains a semiquinone radical that is infinitely stable and can be directly observed by ESR. Aqueous extracts of cigarette tar, which contain this radical, reduce oxygen to superoxide and thus produce both hydrogen peroxide and the hydroxyl radical.

  17. Cellular mechanisms of mainstream cigarette smoke-induced lung epithelial tight junction permeability changes in vitro.

    PubMed

    Olivera, Dorian S; Boggs, Susan E; Beenhouwer, Chris; Aden, James; Knall, Cindy

    2007-01-01

    Mainstream cigarette smoke increases the permeability of human airways; however, the mechanism for this increased permeability is poorly defined. Tight junctions between adjacent epithelial cells constitute the physiological barrier to fluid and macromolecules in epithelium. These structures are highly regulated by phosphorylation and their association with the cytoskeleton. The goal of these studies was to identify the signal transduction pathways that regulate smoke-induced permeability. Using a physiologically relevant air-liquid interface exposure system, electrically tight monolayers of the human bronchial epithelial cell-line Calu-3 were exposed to fresh, whole mainstream cigarette smoke. This exposure results in a regulated, dose-dependent loss of epithelial barrier function in the lung epithelial monolayers. With cigarette smoke exposure, transepithelial electrical resistance (TER) is decreased and albumin flux is increased, indicating a loss in barrier function to ions and macromolecules, respectively; however, both largely recover in 30 min. Smoke-induced losses of macromolecular barrier function are the result of multicellular junctional reorganization, resulting in increased leak volume rather than leak frequency. Inhibiting Rho kinase (ROCK) significantly reduces the smoke-induced permeability to both ions and macromolecules, while inhibiting protein tyrosine kinases (PTK) only reduces smoke-induced macromolecular permeability. Interestingly, inhibiting myosin light chain kinase (MLCK) exacerbates smoke-induced permeability, indicating that MLCK and ROCK have opposing regulatory roles. Our results demonstrate that the smoke-induced loss of epithelial barrier function in human bronchial epithelium is a regulated process rather than a cytotoxic response. Additionally, our results indicate that activation of PTK and ROCK and inactivation of MLCK contribute to the increased airway permeability caused by mainstream cigarette smoke.

  18. Role of cigarette smoking in urological malignancies and clinical interventions for smoking cessation

    PubMed Central

    Bjurlin, Marc A.; Verze, Paolo; De Nunzio, Cosimo; Shariat, Shahrokh F.; Brausi, Maurizio; Donin, Nicholas M.

    2016-01-01

    Introduction Cigarette smoking is the single greatest preventable cause of disease and death. Our literature review highlights the increased risk of cigarette smoking and kidney cancer, bladder cancer and prostate cancer. Material and methods Smoking cessation improves outcomes at all stages of these disease processes, where patients who quit for 10–20 years appear to obtain a similar risk as those who have never smoked, even after diagnosis of disease. Results Urologists, however, very seldom provide smoking cessation assistance. By applying brief smoking cessation intervention techniques, physicians’ posses an effective means of providing quitting advice. Conclusions Patients who receive smoking cessation advice from their urologist are 2.3 times more likely to attempt to quit. Urologists are well-positioned to screen, counsel, and promote cessation at regular intervals, which may improve quit rates, and ultimately improve our patients’ outcomes. PMID:28127452

  19. Extended Treatment with Bupropion SR for Cigarette Smoking Cessation

    ERIC Educational Resources Information Center

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

    2006-01-01

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

  20. Retail Food Availability, Obesity, and Cigarette Smoking in Rural Communities

    ERIC Educational Resources Information Center

    Hosler, Akiko S.

    2009-01-01

    Context: Disparities in the availability of nutritionally important foods and their influence on health have been studied in US urban communities. Purpose: To assess the availability of selected retail foods and cigarettes, and explore ecologic relationships of the availability with obesity and smoking in rural communities. Methods: Inventories of…

  1. Cigarette Smoke Cadmium Breakthrough from Traditional Filters: Implications for Exposure

    PubMed Central

    Pappas, R. Steven; Fresquez, Mark R.; Watson, Clifford H.

    2015-01-01

    Cadmium, a carcinogenic metal, is highly toxic to renal, skeletal, nervous, respiratory, and cardiovascular systems. Accurate and precise quantification of mainstream smoke cadmium levels in cigarette smoke is important because of exposure concerns. The two most common trapping techniques for collecting mainstream tobacco smoke particulate for analysis are glass fiber filters and electrostatic precipitators. We observed that a significant portion of total cadmium passed through standard glass fiber filters that are used to trap particulate matter. We therefore developed platinum traps to collect the cadmium that passed through the filters and tested a variety of cigarettes with different physical parameters for quantities of cadmium that passed though the filters. We found less than 1% cadmium passed through electrostatic precipitators. In contrast, cadmium that passed through 92 mm glass fiber filters on a rotary smoking machine was significantly higher, ranging from 3.5% to 22.9% of total smoke cadmium deliveries. Cadmium passed through 44 mm filters typically used on linear smoking machines to an even greater degree, ranging from 13.6% to 30.4% of the total smoke cadmium deliveries. Differences in the cadmium that passed through from the glass fiber filters and electrostatic precipitator could be explained in part if cadmium resides in the smaller mainstream smoke aerosol particle sizes. Differences in particle size distribution could have toxicological implications and could help explain the pulmonary and cardiovascular cadmium uptake in smokers. PMID:25313385

  2. Cigarette smoke cadmium breakthrough from traditional filters: implications for exposure.

    PubMed

    Pappas, R Steven; Fresquez, Mark R; Watson, Clifford H

    2015-01-01

    Cadmium, a carcinogenic metal, is highly toxic to renal, skeletal, nervous, respiratory and cardiovascular systems. Accurate and precise quantification of mainstream smoke cadmium levels in cigarette smoke is important because of exposure concerns. The two most common trapping techniques for collecting mainstream tobacco smoke particulate for analysis are glass fiber filters and electrostatic precipitators. We observed that a significant portion of total cadmium passed through standard glass fiber filters that are used to trap particulate matter. We therefore developed platinum traps to collect the cadmium that passed through the filters and tested a variety of cigarettes with different physical parameters for quantities of cadmium that passed though the filters. We found <1% cadmium passed through electrostatic precipitators. In contrast, cadmium that passed through 92 mm glass fiber filters on a rotary smoking machine was significantly higher, ranging from 3.5 to 22.9% of total smoke cadmium deliveries. Cadmium passed through 44 mm filters typically used on linear smoking machines to an even greater degree, ranging from 13.6 to 30.4% of the total smoke cadmium deliveries. Differences in the cadmium that passed through from the glass fiber filters and electrostatic precipitator could be explained in part if cadmium resides in the smaller mainstream smoke aerosol particle sizes. Differences in particle size distribution could have toxicological implications and could help explain the pulmonary and cardiovascular cadmium uptake in smokers.

  3. Methods for Quantification of Exposure to Cigarette Smoking and Environmental Tobacco Smoke: Focus on Developmental Toxicology

    PubMed Central

    Florescu, Ana; Ferrence, Roberta; Einarson, Tom; Selby, Peter; Soldin, Offie; Koren, Gideon

    2013-01-01

    Active and passive smoking have been associated with an array of adverse effects on health. The development of valid and accurate scales of measurement for exposures associated with health risks constitutes an active area of research. Tobacco smoke exposure still lacks an ideal method of measurement. A valid estimation of the risks associated with tobacco exposure depends on accurate measurement. However, some groups of people are more reluctant than others to disclose their smoking status and exposure to tobacco. This is particularly true for pregnant women and parents of young children, whose smoking is often regarded as socially unacceptable. For others, recall of tobacco exposure may also prove difficult. Because relying on self-report and the various biases it introduces may lead to inaccurate measures of nicotine exposure, more objective solutions have been suggested. Biomarkers constitute the most commonly used objective method of ascertaining nicotine exposure. Of those available, cotinine has gained supremacy as the biomarker of choice. Traditionally, cotinine has been measured in blood, saliva, and urine. Cotinine collection and analysis from these sources has posed some difficulties, which have motivated the search for a more consistent and reliable source of this biomarker. Hair analysis is a novel, noninvasive technique used to detect the presence of drugs and metabolites in the hair shaft. Because cotinine accumulates in hair during hair growth, it is a unique measure of long-term, cumulative exposure to tobacco smoke. Although hair analysis of cotinine holds great promise, a detailed evaluation of its potential as a biomarker of nicotine exposure, is needed. No studies have been published that address this issue. Because the levels of cotinine in the body are dependent on nicotine metabolism, which in turn is affected by factors such as age and pregnancy, the characterization of hair cotinine should be population specific. This review aims at

  4. Socioeconomic Distinction, Cultural Tastes, and Cigarette Smoking.

    PubMed

    Pampel, Fred C

    2006-03-01

    OBJECTIVES: The inverse relationship between socioeconomic status (SES) and smoking is typically seen in terms of the greater economic and social resources of advantaged groups, but it may also relate to cultural resources. This study aims to test theories of symbolic distinction by examining relationships between smoking and ostensibly unrelated cultural preferences. METHODS: Using the 1993 General Social Survey, ordinal logistic regression models, and a three-category dependent variable (never, former, and current smoker), the analysis estimates relationships of musical likes and dislikes with smoking while controlling for SES and social strain. RESULTS: Preferences for classical music are associated with lower smoking, while preferences for bluegrass, jazz, and heavy metal music are associated with higher smoking. CONCLUSIONS: The results suggest that SES groups may use smoking, like other cultural tastes, to distinguish their lifestyles from those of others.

  5. Socioeconomic Distinction, Cultural Tastes, and Cigarette Smoking*

    PubMed Central

    Pampel, Fred C.

    2011-01-01

    Objectives The inverse relationship between socioeconomic status (SES) and smoking is typically seen in terms of the greater economic and social resources of advantaged groups, but it may also relate to cultural resources. This study aims to test theories of symbolic distinction by examining relationships between smoking and ostensibly unrelated cultural preferences. Methods Using the 1993 General Social Survey, ordinal logistic regression models, and a three-category dependent variable (never, former, and current smoker), the analysis estimates relationships of musical likes and dislikes with smoking while controlling for SES and social strain. Results Preferences for classical music are associated with lower smoking, while preferences for bluegrass, jazz, and heavy metal music are associated with higher smoking. Conclusions The results suggest that SES groups may use smoking, like other cultural tastes, to distinguish their lifestyles from those of others. PMID:21874073

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

    PubMed

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

    2013-08-01

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

  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

    PubMed Central

    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. Different physiological and behavioural effects of e-cigarette vapour and cigarette smoke in mice.

    PubMed

    Ponzoni, L; Moretti, M; Sala, M; Fasoli, F; Mucchietto, V; Lucini, V; Cannazza, G; Gallesi, G; Castellana, C N; Clementi, F; Zoli, M; Gotti, C; Braida, D

    2015-10-01

    Nicotine is the primary addictive substance in tobacco smoke and electronic cigarette (e-cig) vapour. Methodological limitations have made it difficult to compare the role of the nicotine and non-nicotine constituents of tobacco smoke. The aim of this study was to compare the effects of traditional cigarette smoke and e-cig vapour containing the same amount of nicotine in male BALB/c mice exposed to the smoke of 21 cigarettes or e-cig vapour containing 16.8 mg of nicotine delivered by means of a mechanical ventilator for three 30-min sessions/day for seven weeks. One hour after the last session, half of the animals were sacrificed for neurochemical analysis, and the others underwent mecamylamine-precipitated or spontaneous withdrawal for the purposes of behavioural analysis. Chronic intermittent non-contingent, second-hand exposure to cigarette smoke or e-cig vapour led to similar brain cotinine and nicotine levels, similar urine cotinine levels and the similar up-regulation of α4β2 nicotinic acetylcholine receptors in different brain areas, but had different effects on body weight, food intake, and the signs of mecamylamine-precipitated and spontaneous withdrawal episodic memory and emotional responses. The findings of this study demonstrate for the first time that e-cig vapour induces addiction-related neurochemical, physiological and behavioural alterations. The fact that inhaled cigarette smoke and e-cig vapour have partially different dependence-related effects indicates that compounds other than nicotine contribute to tobacco dependence.

  9. The use of a novel tobacco-substitute sheet and smoke dilution to reduce toxicant yields in cigarette smoke.

    PubMed

    McAdam, K G; Gregg, E O; Liu, C; Dittrich, D J; Duke, M G; Proctor, C J

    2011-08-01

    The Institute of Medicine encouraged the pursuit and development of potential reduced-exposure products, tobacco products that substantially reduce exposure to one or more tobacco toxicants and can reasonably be expected to reduce the risk of one or more specific diseases or other adverse health effects. One approach to reducing smoke toxicant yields is to dilute the smoke with glycerol. We report chemical, biological and human exposure data related to experimental cigarettes containing up to 60% of a novel glycerol containing "tobacco-substitute" sheet. Analysis of mainstream smoke from experimental cigarettes showed reductions in yields of most measured constituents, other than some volatile species. In vitro toxicological tests showed reductions in the activity of smoke particulates in proportion to their glycerol content. Human exposure to nicotine was reduced by a mean of 18% as determined by filter studies and by 14% using 24h urinary biomarker analysis. Smoke particulate exposures were reduced by a mean of 29% in filter studies and NNK exposure by similar amounts based on urinary 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol concentrations. These results show that reducing exposure to some smoke toxicants is possible using a tobacco-substitute sheet, although some smoke toxicants, and the sensory attributes of the smoke, remain as technical challenges.

  10. Attitudes toward Cigarette Smoking among College Students

    ERIC Educational Resources Information Center

    Van Volkom, Michele

    2008-01-01

    The purpose of the current study was to gather data on the attitudes and smoking habits of university students. Data were collected from 250 undergraduates dealing with various aspects of smoking behavior. There were 80 smokers and 170 nonsmokers, including 21 former smokers. In addition to demographic information, participants were assessed with…

  11. Cigarette smoking among Beijing (Peking) high schoolers.

    PubMed

    Ye, G S; Lin, W S

    1984-01-01

    Students smoking at 2 key middle schools and 6 ordinary middle schools in Beijing, China were surveyed to determine the form in which high schoolers start smoking, and how long they have smoked. The patterns and causes of smoking were analyzed. The investigation was made from March to May 1981. 430 boys and 423 girls were selected from key schools and 1396 boys and 1394 girls from ordinary schools. Ages ranged from 13-17. All subjects completed a questionnaire in the classroom. To increase the reliability of the survey, names were kept secret. The students surveyed were classified into groups according to their smoking status: current regular smokers; occasional smokers; ex-smokers; and nonsmokers. In the key schools, there were only 4 smokers among 430 students, accounting for 0.9% of the total. Of these, 1 was Senior Class 2, 2 Senior Class 1, and 1 Junior Class 3. In the ordinary schools, 10% were smokers. 19.7% of the boys and 0.4% of the girls smoked. Among the boys, the higher the class, the more numerous the smokers. The smoking rate was 8.2% in the 1st year of junior high but rose to 34% in senior class 2; the difference was statistically significant. "Special occasion" smokers were few, only 5.5% of the students. In junior class, the number of regular smokers was about 2/3 to 4/5 that of occasional smokers. And by senior class 2 the number of regular smokers had risen to about 3 times that of the occasional smokers. In every grade, there were students who had given up smoking. Most had been occasional smokers. Some high schoolers had started to smoke in primary school and had a 4-5 year history of smoking, but most had only picked up smoking for 1-2 years after announcement of the Rules for High School Students prohibiting smoking. There were 3 smoking patterns: smoking without inhaling; inhaling the smoke deeply into the lungs, then expiring through the mouth or nostrils; and combining patterns 1 and 2. Of 265 students, 128 used the 1st pattern, 121 the

  12. Effects of whole cigarette smoke on human gingival fibroblast adhesion, growth, and migration.

    PubMed

    Semlali, Abdelhabib; Chakir, Jamila; Rouabhia, Mahmoud

    2011-01-01

    The aim of this study was to investigate the effects of a single exposure to whole cigarette smoke on human gingival fibroblast behavior. Normal oral mucosa fibroblasts were exposed once to whole cigarette smoke for 5, 15, or 30 min, and then were used to analyze cell adhesion, β1-integrin expression, cell growth and viability, cell capacity to contract collagen gel, and cell migration following wound infliction. Our findings showed that when gingival fibroblasts were exposed once to whole cigarette smoke, this resulted in a significant inhibition of cell adhesion, a decrease in the number of β1-integrin-positive cells, increased LDH activity in the target cells, and reduced growth. The smoke-exposed fibroblasts were also not able to contract collagen gel matrix and migrate following insult. Overall results demonstrate that a single exposure to whole cigarette smoke produced significant morphological and functional deregulation in gingival fibroblasts. This may explain the higher predisposition of tobacco users to oral infections and diseases such as cancer.

  13. Monitoring of cigarette smoking using wearable sensors and support vector machines.

    PubMed

    Lopez-Meyer, Paulo; Tiffany, Stephen; Patil, Yogendra; Sazonov, Edward

    2013-07-01

    Cigarette smoking is a serious risk factor for cancer, cardiovascular, and pulmonary diseases. Current methods of monitoring of cigarette smoking habits rely on various forms of self-report that are prone to errors and under reporting. This paper presents a first step in the development of a methodology for accurate and objective assessment of smoking using noninvasive wearable sensors (Personal Automatic Cigarette Tracker-PACT) by demonstrating feasibility of automatic recognition of smoke inhalations from signals arising from continuous monitoring of breathing and hand-to-mouth gestures by support vector machine classifiers. The performance of subject-dependent (individually calibrated) models was compared to performance of subject-independent (group) classification models. The models were trained and validated on a dataset collected from 20 subjects performing 12 different activities representative of everyday living (total duration 19.5 h or 21,411 breath cycles). Precision and recall were used as the accuracy metrics. Group models obtained 87% and 80% of average precision and recall, respectively. Individual models resulted in 90% of average precision and recall, indicating a significant presence of individual traits in signal patterns. These results suggest the feasibility of monitoring cigarette smoking by means of a wearable and noninvasive sensor system in free living conditions.

  14. Effects of type of smoking (pipe, cigars or cigarettes) on biological indices of tobacco exposure and toxicity.

    PubMed

    Funck-Brentano, Christian; Raphaël, Mathilde; Lafontaine, Michel; Arnould, Jean-Pierre; Verstuyft, Céline; Lebot, Martine; Costagliola, Dominique; Roussel, Ronan

    2006-10-01

    Although all forms of smoking are harmful, smoking pipes or cigars is associated with lower exposure to the lethal products of tobacco products and lower levels of morbidity and mortality than smoking cigarettes. Cytochrome P-450-1A (CYP1A) is a major pathway activating carcinogens from tobacco smoke. Our primary aim was to compare CYP1A2 activity in individuals smoking pipes or cigars only, cigarettes only and in non-smokers. We studied 30 smokers of pipes or cigars only, 28 smokers of cigarettes only, and 30 non-smokers male subjects matched for age. CYP1A2 activity was assessed as the caffeine metabolic ratio in plasma. One-day urine collection was used for determining exposure to products of tobacco metabolism. Nitrosamine and benzo[a]pyrene DNA adducts were measured in lymphocytes. CYP1A2 activity was greater (p<0.0001) in cigarette smokers (median: 0.61; interquartile range: 0.52-0.76) than in pipe or cigar smokers (0.27; 0.21-0.37) and non-smokers (0.34; 0.25-0.42) who did not differ significantly. Urinary cotinine and 1-hydroxypyrene levels were higher in cigarette smokers than in pipe or cigar smokers and higher in the later than in non-smokers. DNA adducts levels were significantly lower in pipe or cigar smokers than in cigarette smokers. In multivariate analysis, cigarette smoking was the only independent predictor of CYP1A2 activity (p<0.0001) and of 1-hydroxypyrene excretion in urine (p=0.0012). In this study, pipe or cigar smoking was associated with lower exposure to products of tobacco metabolism than cigarette smoking and to an absence of CYP1A2 induction. Cigarette smoking was the only independent predictor of CYP1A2 activity in smokers. However, inhalation behaviour, rather than the type of tobacco smoked, may be the key factor linked to the extent of tobacco exposure and CYP1A2 induction. Our results provide a reasonable explanation for the results of epidemiological studies showing pipe or cigar smoking to present fewer health hazards than

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

    PubMed Central

    Eyring, Kenneth R.; Pedersen, Brent S.; Yang, Ivana V.; Schwartz, David A.

    2015-01-01

    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. PMID:26642056

  16. Attachment of radon progeny to cigarette-smoke aerosols

    SciTech Connect

    Biermann, A.H.; Sawyer, S.R.

    1995-05-01

    The daughter products of radon gas are now recognized as a significant contributor to radiation exposure to the general public. It is also suspected that a synergistic effect exists with the combination cigarette smoking and radon exposure. We have conducted an experimental investigation to determine the physical nature of radon progeny interactions with cigarette smoke aerosols. The size distributions of the aerosols are characterized and attachment rates of radon progeny to cigarette-smoke aerosols are determined. Both the mainstream and sidestream portions of the smoke aerosol are investigated. Unattached radon progeny are very mobile and, in the presence of aerosols, readily attach to the particle surfaces. In this study, an aerosol chamber is used to contain the radon gas, progeny and aerosol mixture while allowing the attachment process to occur. The rate of attachment is dependent on the size distribution, or diffusion coefficient, of the radon progeny as well as the aerosol size distribution. The size distribution of the radon daughter products is monitored using a graded-screen diffusion battery. The diffusion battery also enables separation of the unattached radon progeny from those attached to the aerosol particles. Analysis of the radon decay products is accomplished using alpha spectrometry. The aerosols of interest are size fractionated with the aid of a differential mobility analyzer and cascade impactor. The measured attachment rates of progeny to the cigarette smoke are compared to those found in similar experiments using an ambient aerosol. The lowest attachment coefficients observed, {approximately}10{sup {minus}6} cm{sup 3}/s, occurred for the ambient aerosol. The sidestream and mainstream smoke aerosols exhibited higher attachment rates in that order. The results compared favorably with theories describing the coagulation process of aerosols.

  17. Mecamylamine pretreatment counteracts cigarette smoke induced changes in hypothalamic catecholamine neuron systems and in anterior pituitary function.

    PubMed

    Andersson, K

    1985-11-01

    We have studied the effects of acute, intermittent exposure to tobacco smoke on discrete hypothalamic CA nerve terminal networks and on neuroendocrine function by means of quantitative histofluorimetrical determinations of catecholamine (CA) fluorescence in sections of rat brain and by radioimmunoassay procedures for hormones. Acute intermittent exposure to cigarette smoke induced a lowering of NA levels and increased NA turnover in discrete hypothalamic nerve terminal regions. This exposure also induced increases in DA turnover in the median eminence. The cigarette smoke lowered TSH, prolactin, LH and FSH serum levels, but induced an increase in serum corticosterone concentrations. To determine if the above mentioned changes in neuroendocrine function were nicotine mediated, a cholinergic nicotine-like blocking agent, mecamylamine, was administered prior to exposure to cigarette smoke. Pretreatment with mecamylamine (1.0 mg kg-1) counteracted the cigarette smoke induced changes in CA levels and turnover in all hypothalamic CA nerve terminal regions as well as the changes in serum levels of the pituitary hormones and corticosterone. It is suggested that acute intermittent exposure to cigarette smoke, via its nicotine component, lowers TSH, prolactin, LH and FSH secretion at least in part through activation of the tubero-infundibular DA neurons. Furthermore, the nicotine component of the cigarette smoke is suggested to induce the increase in corticosterone serum levels via increasing NA turnover in the paraventricular hypothalamic nucleus.

  18. Determination of methyl-, 2-hydroxyethyl- and 2-cyanoethylmercapturic acids as biomarkers of exposure to alkylating agents in cigarette smoke.

    PubMed

    Scherer, Gerhard; Urban, Michael; Hagedorn, Heinz-Werner; Serafin, Richard; Feng, Shixia; Kapur, Sunil; Muhammad, Raheema; Jin, Yan; Sarkar, Mohamadi; Roethig, Hans-Juergen

    2010-10-01

    Alkylating agents occur in the environment and are formed endogenously. Tobacco smoke contains a variety of alkylating agents or precursors including, among others, N-nitrosodimethylamine (NDMA), 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), acrylonitrile and ethylene oxide. We developed and validated a method for the simultaneous determination of methylmercapturic acid (MMA, biomarker for methylating agents such as NDMA and NNK), 2-hydroxyethylmercapturic acid (HEMA, biomarker for ethylene oxide) and 2-cyanoethylmercapturic acid (CEMA, biomarker for acrylonitrile) in human urine using deuterated internal standards of each compound. The method involves liquid/liquid extraction of the urine sample, solid phase extraction on anion exchange cartridges, derivatization with pentafluorobenzyl bromide (PFBBr), liquid/liquid extraction of the reaction mixture and LC-MS/MS analysis with positive electrospray ionization. The method was linear in the ranges of 5.00-600, 1.00-50.0 and 1.50-900 ng/ml for MMA, HEMA and CEMA, respectively. The method was applied to two clinical studies in adult smokers of conventional cigarettes who either continued smoking conventional cigarettes, were switched to test cigarettes consisting of either an electrically heated cigarette smoking system (EHCSS) or having a highly activated carbon granule filter that were shown to have reduced exposure to specific smoke constituents, or stopped smoking. Urinary excretion of MMA was found to be unaffected by switching to the test cigarettes or stop smoking. Urinary HEMA excretion decreased by 46 to 54% after switching to test cigarettes and by approximately 74% when stopping smoking. Urinary CEMA excretion decreased by 74-77% when switching to test cigarettes and by approximately 90% when stopping smoking. This validated method for urinary alkylmercapturic acids is suitable to distinguish differences in exposure not only between smokers and nonsmokers but also between smoking of conventional and

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

    PubMed

    Wang, Wei; Li, Xiaoguang; Xu, Jie

    2015-01-01

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

  20. [Genome-wide associations for cigarette smoking behavior].

    PubMed

    Strauss, Ewa

    2013-01-01

    Diseases related to tobacco smoking are the second leading cause of death in the world. Despite increasing evidence of genetic determination, the susceptibility genes and loci underlying various aspects of smoking behavior are largely unknown. Genome-wide association studies (GWASs) provided a new conceptual framework in the search for variants underlying common traits/disorders. A massive scan of the genome and a "hypothesis-free" approach enable discovery of new aspects of genetics of complex traits. In this paper the results of GWASs and GWAS meta-analyzes of cigarette smoking behavior and nicotine dependence are reviewed with the particular attention to smoking cessation success and the replacement therapy. The results of these studies are discussed in the context of the results of the candidate gene association studies. Studies on the role of the genomic regions, identified in GWASs, in the development of smoking-related diseases are also discussed.

  1. Nicotine yield and measures of cigarette smoke exposure in a large population: are lower-yield cigarettes safer?

    PubMed Central

    Maron, D J; Fortmann, S P

    1987-01-01

    We examined the relationship of machine-estimated nicotine yield by cigarette brand with the level of cigarette consumption and two biochemical measures of smoke exposure (expired-air carbon monoxide and plasma thiocyanate) in a large, population-based sample of smokers (N = 713). The lower the nicotine yield of the cigarette, the greater the number of cigarettes smoked per day. Prior to adjusting for number of cigarettes smoked per day, nicotine yield was not related to the actual measures of smoke exposure. Smokers of ultralow-yield cigarettes had laboratory tests of smoke exposure which were not significantly different from those of smokers of higher-yield brands. Only after adjustment for number of cigarettes smoked per day did nicotine yield become significantly related to expired-air carbon monoxide and to plasma thiocyanate. In multivariate analysis, the number of cigarettes smoked per day accounted for 28 per cent and 22 per cent of the variance in observed expired-air carbon monoxide and plasma thiocyanate levels, respectively, whereas nicotine yield accounted for only 1 per cent and 2 per cent of the variance, respectively. The relative lack of an effect of nicotine yield on the biochemical measure appears to be due to the fact that smokers of lower nicotine brands smoked more cigarettes per day, thereby compensating for reduced delivery of smoke products. Our data do not support the concept that ultralow-yield cigarettes are less hazardous than others. Machine estimates suggesting low nicotine yield underrepresent actual human consumption of harmful cigarette constituents. PMID:3565645

  2. Cigarette smoke exposure aggravates air space enlargement and alveolar cell apoptosis in Smad3 knockout mice.

    PubMed

    Farkas, Laszlo; Farkas, Daniela; Warburton, David; Gauldie, Jack; Shi, Wei; Stampfli, Martin R; Voelkel, Norbert F; Kolb, Martin

    2011-10-01

    The concept of genetic susceptibility factors predisposing cigarette smokers to develop emphysema stems from the clinical observation that only a fraction of smokers develop clinically significant chronic obstructive pulmonary disease. We investigated whether Smad3 knockout mice, which develop spontaneous air space enlargement after birth because of a defect in transforming growth factor-β (TGF-β) signaling, develop enhanced alveolar cell apoptosis and air space enlargement following cigarette smoke exposure. We investigated Smad3(-/-) and Smad3(+/+) mice at different adult ages and determined air space enlargement, alveolar cell proliferation, and apoptosis. Furthermore, laser-capture microdissection and real-time PCR were used to measure compartment-specific gene expression. We then compared the effects of cigarette smoke exposure on Smad3(-/-) and littermate controls. Smad3 knockout resulted in the development of air space enlargement in the adult mouse and was associated with decreased alveolar VEGF levels and activity and increased alveolar cell apoptosis. Cigarette smoke exposure aggravated air space enlargement and alveolar cell apoptosis. We also found increased Smad2 protein expression and phosphorylation, which was enhanced following cigarette smoke exposure, in Smad3-knockout animals. Double immunofluorescence analysis revealed that endothelial apoptosis started before epithelial apoptosis. Our data indicate that balanced TGF-β signaling is not only important for regulation of extracellular matrix turnover, but also for alveolar cell homeostasis. Impaired signaling via the Smad3 pathway results in alveolar cell apoptosis and alveolar destruction, likely via increased Smad2 and reduced VEGF expression and might represent a predisposition for accelerated development of emphysema due to cigarette smoke exposure.

  3. GENOTOXICITY OF TEN CIGARETTE SMOKE CONDENSATES IN FOUR TEST SYSTEMS: COMPARISONS AMONG ASSAYS AND CONDENSATES

    EPA Science Inventory

    The particulate fraction of cigarette smoke, cigarette smoke condensate (CSC), is genotoxic in many short-term in vitro tests and carcinogenic in rodents. However, no study has evaluatedd a set of CSCs prepared from a diverse set of cigarettes in a variety of short-term genotoxic...

  4. GENOTOXICITY OF TEN CIGARETTE SMOKE CONDENSATES IN FOUR TEST SYSTEMS: COMPARISONS BETWEEN ASSAYS AND CONDENSATES

    EPA Science Inventory

    What is the study?
    This the first assessment of a set of cigarette smoke condensates from a range of cigarette types in a variety (4) of short-term genotoxicity assays.
    Why was it done?
    No such comparative study of cigarette smoke condensates has been reported. H...

  5. The interaction between anxiety sensitivity and cigarette smoking level in relation to sleep onset latency among adolescent cigarette smokers.

    PubMed

    Bilsky, Sarah A; Feldner, Matthew T; Knapp, Ashley A; Babson, Kimberly A; Leen-Feldner, Ellen W

    2016-08-01

    Cigarette smoking during adolescence is linked to a number of sleep disturbances and has been consistently linked to sleep onset latency among adults. However, little research has examined factors that may influence the relation between cigarette smoking level and sleep onset latency among adolescents. One factor that may be particularly important in this regard is anxiety sensitivity (AS). The current study examined whether cigarette smoking level interacted with AS in its association with sleep onset latency among 94 adolescent (Mage = 15.72) cigarette smokers. As hypothesized, AS interacted with smoking level to relate to sleep onset latency, even after controlling for age and gender. This relation was specific to sleep onset latency as opposed to other types of sleep disturbances, and that adolescents who smoked at higher levels tended to go to sleep later and wake up later than adolescents who smoked at relatively lower levels.

  6. RelB attenuates cigarette smoke extract-induced apoptosis in association with transcriptional regulation of the aryl hydrocarbon receptor.

    PubMed

    Iu, Matthew; Zago, Michela; de Souza, Angela Rico; Bouttier, Manuella; Pareek, Swati; White, John H; Hamid, Qutayba; Eidelman, David H; Baglole, Carolyn J

    2017-02-27

    Chronic obstructive pulmonary disease (COPD) is a chronic and prevalent respiratory disease caused primarily by long term inhalation of cigarette smoke. A major hallmark of COPD is elevated apoptosis of structural lung cells including fibroblasts. The NF-κB member RelB may suppress apoptosis in response to cigarette smoke, but its role in lung cell survival is not known. RelB may act as a pro-survival factor by controlling the expression of superoxide dismutase 2 (SOD2). SOD2 is also regulated by the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor that suppresses cigarette smoke-induced apoptosis. As the AhR is also a binding partner for RelB, we speculate that RelB suppresses cigarette smoke-induced apoptosis by regulating the AhR. Using an in vitro model of cigarette smoke exposure (cigarette smoke extract [CSE]), we found that CSE down-regulated RelB expression in mouse lung fibroblasts, which was associated with elevated levels of cleaved PARP. Genetic ablation of RelB elevated CSE-induced apoptosis, including chromatin condensation, and reduced mitochondrial function. There was also more reactive oxygen species production in RelB(-/-) cells exposed to CSE. While there was no alteration in Nrf2 expression or localization between RelB(-/-) and wild type cells in response to CSE, RelB(-/-) cells displayed significantly decreased AhR mRNA and protein expression, concomitant with loss of AhR target gene expression (Cyp1a1, Cyp1b1, Nqo1). Finally, we found that RelB binds to the Ahr gene at 3 sites to potentially increase its expression via transcriptional induction. These data support that RelB suppresses cigarette smoke-induced apoptosis, potentially by increasing the AhR. Together, these two proteins may comprise an important cell survival signalling pathway that reduces apoptosis upon cigarette smoke exposure.

  7. Waterpipe Tobacco Smoking and Susceptibility to Cigarette Smoking Among Young Adults in the United States, 2012–2013

    PubMed Central

    Haider, M. Rifat; Barnett, Tracey E.; Guo, Yi; Getz, Kayla R.; Thrasher, James F.; Maziak, Wasim

    2016-01-01

    Introduction Waterpipe tobacco smoking, also known as hookah and shisha, has surged in popularity among young people in the United States. Waterpipe is also increasingly becoming the first tobacco product that young people try. Given the limited access to and limited portability of waterpipes, waterpipe smokers who become more nicotine dependent over time may be more likely to turn to cigarettes. This study examined the relationship between waterpipe tobacco smoking and susceptibility to cigarette smoking among young adults in the United States. Methods Using data from the 2012–2013 National Adult Tobacco Survey, a nationally representative sample of US adults, we reported rates of current waterpipe smoking and susceptibility to cigarette smoking by demographic characteristics and by use of other tobacco products among survey participants aged 18 to 24 years. Multivariable logistic regression was used to examine the relationship between current waterpipe smoking and susceptibility to cigarette smoking, defined as the lack of a firm intention not to smoke soon or within the next year. Results Of 2,528 young adults who had never established cigarette smoking, 15.7% (n = 398) reported being waterpipe smokers (every day or some days [n = 97; 3.8%] or rarely [n = 301; 11.9%]); 44.2% (176/398) of waterpipe smokers reported being susceptible to cigarette smoking. Those who smoked waterpipe rarely were 2.3 times as susceptible to cigarette smoking as those who were not current waterpipe smokers (OR = 2.3; 95% CI, 1.6–3.4). Conclusion Current waterpipe smoking is associated with susceptibility to cigarette smoking among young adults in the United States. Longitudinal studies are needed to demonstrate causality between waterpipe smoking and initiation of cigarette smoking. PMID:26890407

  8. Cigarette smoking and lead levels in occupationally exposed lead workers

    SciTech Connect

    Brown, C.P.; Spivey, G.H.; Valentine, J.L.; Browdy, B.L.

    1980-07-01

    One hundred eleven workers at a secondary Pb smelter were surveyed to determine smoking and personal hygiene habits. Fifty-three percent of the smokers had blood Pb levels in excess of 60 ..mu..g/dl, compared to 31% of nonsmokers (p = 0.02). Among smokers, 66% of heavy smokers (greater than or equal to 1 pack a day) had blood Pb levels over 60 ..mu..g/dl, compared to 39% of the light smokers (p = O.05). Those who kept their cigarettes on their person had a higher proportion of blood Pb greater than 60 ..mu..g/dl than workers who kept their cigarettes elsewhere (63 vs 36%, respectively; p = 0.08). The difference in blood Pb levels between smokers and nonsmokers may be due in part to direct environmental contamination of cigarettes or impaired lung clearance mechanisms, and could be important in workers with already elevated blood Pb levels.

  9. Bone marrow cells repair cigarette smoke-induced emphysema in rats.

    PubMed

    Huh, Jin Won; Kim, Sun-Yong; Lee, Ji Hyun; Lee, Jin-Seok; Van Ta, Quang; Kim, Mijung; Oh, Yeon-Mok; Lee, Yun-Song; Lee, Sang-Do

    2011-09-01

    The therapeutic potential of stem cells in chronic obstructive pulmonary disease is not well known although stem cell therapy is effective in models of other pulmonary diseases. We tested the capacities of bone marrow cells (BMCs), mesenchymal stem cells (MSCs), and conditioned media of MSCs (MSC-CM) to repair cigarette smoke-induced emphysema. Inbred female Lewis rats were exposed to cigarette smoke for 6 mo and then received BMCs, MSCs, or MSC-CM from male Lewis rats. For 2 mo after injection, the BMC treatment gradually alleviated the cigarette smoke-induced emphysema and restored the increased mean linear intercept. The BMC treatment significantly increased cell proliferation and the number of small pulmonary vessels, reduced apoptotic cell death, attenuated the mean pulmonary arterial pressure, and inhibited muscularization in small pulmonary vessels. However, only a few male donor cells were detected from 1 day to 1 mo after BMC administration. The MSCs and cell-free MSC-CM also induced the repair of emphysema and increased the number of small pulmonary vessels. Our data show that BMC, MSCs, and MSC-CM treatment repaired cigarette smoke-induced emphysema. The repair activity of these treatments is consistent with a paracrine effect rather than stem cell engraftment because most of the donor cells disappeared and because cell-free MSC-CM also induced the repair.

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

    PubMed

    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.

  11. Cigarette smoke induces genetic instability in airway epithelial cells by suppressing FANCD2 expression

    PubMed Central

    Hays, L E; Zodrow, D M; Yates, J E; Deffebach, M E; Jacoby, D B; Olson, S B; Pankow, J F; Bagby, G C

    2008-01-01

    Chromosomal abnormalities are commonly found in bronchogenic carcinoma cells, but the molecular causes of chromosomal instability (CIN) and their relationship to cigarette smoke has not been defined. Because the Fanconi anaemia (FA)/BRCA pathway is essential for maintenance of chromosomal stability, we tested the hypothesis that cigarette smoke suppresses that activity of this pathway. Here, we show that cigarette smoke condensate (CSC) inhibited translation of FANCD2 mRNA (but not FANCC or FANCG) in normal airway epithelial cells and that this suppression of FANCD2 expression was sufficient to induce both genetic instability and programmed cell death in the exposed cell population. Cigarette smoke condensate also suppressed FANCD2 function and induced CIN in bronchogenic carcinoma cells, but these cells were resistant to CSC-induced apoptosis relative to normal airway epithelial cells. We, therefore, suggest that CSC exerts pressure on airway epithelial cells that results in selection and emergence of genetically unstable somatic mutant clones that may have lost the capacity to effectively execute an apoptotic programme. Carcinogen-mediated suppression of FANCD2 gene expression provides a plausible molecular mechanism for CIN in bronchogenic carcinogenesis. PMID:18475298

  12. Attitudes toward E-Cigarettes, Reasons for Initiating E-Cigarette Use, and Changes in Smoking Behavior after Initiation: A Pilot Longitudinal Study of Regular Cigarette Smokers

    PubMed Central

    Barr, Dana Boyd; Stratton, Erin; Escoffery, Cam; Kegler, Michelle

    2015-01-01

    Objectives We examined 1) changes in smoking and vaping behavior and associated cotinine levels and health status among regular smokers who were first-time e-cigarette purchasers and 2) attitudes, intentions, and restrictions regarding e-cigarettes. Methods We conducted a pilot longitudinal study with assessments of the aforementioned factors and salivary cotinine at weeks 0, 4, and 8. Eligibility criteria included being ≥18 years old, smoking ≥25 of the last 30 days, smoking ≥5 cigarettes per day (cpd), smoking regularly ≥1 year, and not having started using e-cigarettes. Of 72 individuals screened, 40 consented, 36 completed the baseline survey, and 83.3% and 72.2% were retained at weeks 4 and 8, respectively. Results Participants reduced cigarette consumption from baseline to week 4 and 8 (p’s < 0.001); 23.1% reported no cigarette use in the past month at week 8. There was no significant decrease in cotinine from baseline to week 4 or 8 (p’s = ns). At week 8, the majority reported improved health (65.4%), reduced smoker’s cough (57.7%), and improved sense of smell (53.8%) and taste (50.0%). The majority believed that e-cigarettes versus regular cigarettes have fewer health risks (97.2%) and that e-cigarettes have been shown to help smokers quit (80.6%) and reduce cigarette consumption (97.2%). In addition, the majority intended to use e-cigarettes as a complete replacement for regular cigarettes (69.4%) and reported no restriction on e-cigarette use in the home (63.9%) or car (80.6%). Conclusions Future research is needed to document the long-term impact on smoking behavior and health among cigarette smokers who initiate use of e-cigarettes. PMID:25621193

  13. Smoking and symbolism: children, communication and cigarettes.

    PubMed

    Rugkåsa, J; Kennedy, O; Barton, M; Abaunza, P S; Treacy, M P; Knox, B

    2001-04-01

    Health promotion, with its concern with empowerment and autonomy, must recognize the agency of its target population. Based on 85 in-depth interviews with 10- to 11-year-old children throughout Northern Ireland, this paper argues that it is necessary to focus on the social relations of children if we are to understand and prevent childhood smoking. Addressing the complex issue of childhood agency, it is argued that regardless of various restrictions to their choices, children can act intentionally in constructing their identities. Instead of viewing the smoking children as communicating with the adult world, we focus on smoking as negotiation of status within the children's culture. Such negotiations utilize symbolism derived from and shared with the 'adult world'. It is important that those analyzing children's lives understand children's ideas and behaviour on their own terms. We must make sure that the very concepts in which the children's experiences are put are appropriate ones. It is suggested that the metaphor 'rite of passage' and terminology such as peer 'pressure' versus adult 'influence', commonly used to analyse the children's smoking behaviour, may actually conceal important aspects of childhood agency.

  14. Adolescent Cigarette Smoking as Compensatory Behavior.

    ERIC Educational Resources Information Center

    Newman, Ian M.

    The extent to which smokers as compared to non-smokers recognize their failure to achieve was studied. The subjects were 80 ninth grade pupils, half of whom smoked. A nine point self-anchoring Expectation scale was developed to determine how closely the subjects came to meeting the perceived expectations of their parents, their school, their…

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

    SciTech Connect

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

    1985-04-01

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

  16. [Cigarette smoking--threat from first days of life].

    PubMed

    Gajewska, Ewa; Malak, Roksana; Mojs, Ewa; Samborski, Włodzimierz

    2008-01-01

    It is obvious that smoking is harmful. It is especially dramatic that it may cause a lot of dysfunctions among newborns who without their free will are expose to toxic tobacco components. The consequences are as serious when mother smoke as when she is exposed to environmental tobacco smoke (ETS). Exposure to cigarette smoke during pregnancy is directly correlated to premature rupture of the membranes, premature birth, intrauterine growth retardatyion--IURG, low birth weight, smaller body length of newborn, reduced lung function--hypoxia, delayed development of respiratory and nervous system, sudden infant death syndrome--SIDS, obesity, allergy, arterial hypertension or even tumors. That is why the prophylactic of above illnesses is important since first days of life.

  17. Effects of prenatal exposure to cigarette smoke on offspring tumor susceptibility and associated immune mechanisms.

    PubMed

    Ng, Sheung P; Silverstone, Allen E; Lai, Zhi-Wei; Zelikoff, Judith T

    2006-01-01

    Epidemiologic evidence suggests that prenatal exposure to intact (unfractionated) cigarette smoke (CS) increases the incidence of cancer in the offspring. A toxicology study was carried out to examine the effects and underlying mechanisms of prenatal exposure to mainstream cigarette smoke (MCS) on offspring resistance to tumor challenge and surveillance mechanisms critical for the recognition and destruction of tumors. Pregnant B6C3F1 mice were exposed by inhalation to MCS for 5 days/week (4 h/day from gestational day 4 to parturition). Smoke-induced effects on offspring-host resistance to transplanted tumor cells; natural killer (NK) cell and cytotoxic T-lymphocyte (CTL) activity; cytokine levels; lymphoid organ immune cell subpopulations; and histology-were examined in 5-, 10- and 20-week-old male and female offspring. At a concentration of smoke roughly equivalent to smoking <1 pack of cigarettes/day, prenatally exposed male offspring challenged at 5 week of age with EL4 lymphoma cells demonstrated a greater than two-fold increase in tumor incidence (relative to age-/gender-matched air-exposed offspring); tumors in prenatally smoke-exposed pups also grew significantly faster. Cytotoxic T-lymphocyte activity in the smoke-exposed 5- and 10-week-old male pups was significantly less than that of the age- and gender-matched controls. No effects of prenatal CS exposure were observed on offspring NK activity, cytokine levels, lymphoid organ histology, or immune cell subpopulations. Results demonstrated that exposure of pregnant mice to a relevant dose of MCS decreased offspring resistance against transplanted tumor cells and persistently reduced CTL activity in prenatally exposed pups. This study provides biological plausibility for the epidemiologic data indicating that children of mothers who smoke during pregnancy have a greater risk of developing cancer in later life.

  18. Relative importance of cigarette smoking in occupational lung disease.

    PubMed Central

    Elmes, P C

    1981-01-01

    Since 1900 respiratory disease has remained a constant serious cause of chronic ill health and premature death in Britain. The falling importance of tuberculosis and pneumonia has been off-set by the rise in lung cancer. Bronchitis morbidity and mortality have fallen only slightly since 1935. To produce any real improvement in the future existing information as to cause must be studied. The relative contribution of occupational exposure is compared with the importance of cigarette smoking. Relevant information is scanty and has been produced to emphasise the existence of occupational diseases rather than assess their importance to the community as whole. In Britain the evidence is that within the coal mining and iron and steel industries conditions are now such that dust exposure contributes little to the morbidity or mortality compared with the workers' smoking habits. Similar results have been shown by a cross-sectional survey of many dusty occupations in Western Germany. Only in the disappearing Welsh slate industry has dust disease been at least as important as smoking. Until the current regulations were introduced conditions existed among asbestos workers such that the combined effect of cigarette smoking and dust exposure led to a loss of life expectation of over 10 years in moderate smokers. Since the new regulations were introduced the risk for asbestos workers should approximate to that for other industrial workers. While control of occupational exposure to respiratory hazards remains important, a far greater improvement to respiratory health would be produced by controlling tobacco smoking. PMID:7470398

  19. Oxidative damage in keratinocytes exposed to cigarette smoke and aldehydes.

    PubMed

    Avezov, Katia; Reznick, Abraham Z; Aizenbud, Dror

    2014-06-01

    Cigarette smoke (CS) is a significant environmental source of human exposure to chemically active saturated (acetaldehyde) and α,β-unsaturated aldehydes (acrolein) inducing protein carbonylation and dysfunction. The exposure of oral tissues to environmental hazards is immense, especially in smokers. The objectives of the current study were to examine the effect of aldehydes originating from CS on intracellular proteins of oral keratinocytes and to observe the antioxidant response in these cells. Intracellular protein carbonyl modification under CS, acrolein and acetaldehyde exposure in the HaCaT keratinocyte cell line, representing oral keratinocytes was examined by Western blot. Possible intracellular enzymatic dysfunction under the above conditions was examined by lactate dehydrogenase (LDH) activity assay. Oxidative stress response was investigated, by DCF (2,7-dichlorodihydrofluorescein) assay and GSH (glutathione) oxidation. Intracellular protein carbonyls increased 5.2 times after CS exposure and 2.7 times after exposure to 1 μmol of acrolein. DCF assay revealed an increase of fluorescence intensity 3.2 and 3.1 times after CS and acrolein exposure, respectively. CS caused a 72.5% decrease in intracellular GSH levels compared to controls. Activity of intracellular LDH was preserved. α,β-Unsaturated aldehydes from CS are capable of intracellular protein carbonylation and have a role in intracellular oxidative stress elevation in keratinocytes, probably due to the reduction in GSH levels.

  20. The use of bupropion SR in cigarette smoking cessation

    PubMed Central

    Wilkes, Scott

    2008-01-01

    Cigarette smoking remains the largest preventable cause of premature death in developed countries. Until recently nicotine replacement therapy (NRT) has been the only recognised form of treatment for smoking cessation. Bupropion, the first non-nicotine based drug for smoking cessation was licensed in the United States of America (US) in 1997 and in the United Kingdom (UK) in 2000 for smoking cessation in people aged 18 years and over. Bupropion exerts its effect primarily through the inhibition of dopamine reuptake into neuronal synaptic vesicles. It is also a weak noradrenalin reuptake inhibitor and has no effect on the serotonin system. Bupropion has proven efficacy for smoking cessation in a number of clinical trials, helping approximately one in five smokers to stop smoking. Up to a half of patients taking bupropion experience side effects, mainly insomnia and a dry mouth, which are closely linked to the nicotine withdrawal syndrome. Bupropion is rarely associated with seizures however care must be taken when co-prescribing with drugs that can lower seizure threshold. Also, bupropion is a potent enzyme inhibitor and can raise plasma levels of some drugs including antidepressants, antiarrhythmics and antipsychotics. Bupropion has been shown to be a safe and cost effective smoking cessation agent. Despite this, NRT remains the dominant pharmacotherapy to aid smoking cessation. PMID:18488428

  1. Cigarette advertising and media coverage of smoking and health.

    PubMed

    Warner, K E

    1985-02-07

    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

  2. Cigarette smoking among students and the influence of legal regulations on passive smoking.

    PubMed

    Gawlikowska-Sroka, A; Dzieciolowska-Baran, E; Szczurowski, J; Teul, I; Poziomkowska-Gesicka, I; Kamienska, E

    2013-01-01

    Research suggests that reducing the degree of nicotine addiction in the population cannot be achieved only by prevention programs. Legislative measures are necessary to be taken by the state. The aim of this study was to assess the degree of tobacco abuse in three groups of students. It also assesses the influence of ban on smoking in public places on passive contact of students with tobacco. A customized survey made up of open and closed questions was conducted among 102 students of electrical faculty, 109 medical students, and 71 students of animal husbandry faculty. The results showed that significantly more women from the electrical faculty smoked. Among the students of animal husbandry, men smoke significantly more cigarettes than women. Women studying animal husbandry start smoking significantly earlier (by about 2 years) than women from other faculties. They are also significantly less likely to smoke cigarettes at school and at home. According to the study, the Polish law to ban smoking in public places, in force since the 15th of November 2010, did not make students quit smoking, although the rate of smoking students decreased. Students did not observe restrictions on smoking in their environment. The study indicates a positive influence of the anti-nicotine legislation on passive smoking, just after 3 months from its introduction.

  3. Toxicological assessment of kretek cigarettes Part 6: the impact of ingredients added to kretek cigarettes on smoke chemistry and in vitro toxicity.

    PubMed

    Roemer, E; Dempsey, R; Hirter, J; Deger Evans, A; Weber, S; Ode, A; Wittke, S; Schorp, M K

    2014-12-01

    Mainstream smoke (MS) from experimental kretek cigarettes with three ingredient mixes at low (typical use level) and high (2.5 or 3 times that level) inclusion rates was compared to a control kretek cigarette of identical construction (cloves and humectants), but without the addition of ingredients. 350 ingredients, commonly used in various combinations and in a limited number in a given brand in the manufacture of marketed kretek cigarettes were assessed. The MS composition of the kretek cigarettes was characterized by a comprehensive set of analytes (55 smoke constituents). Furthermore, the smoke was assessed in vitro for its cytotoxicity in the Neutral Red Uptake assay (particle phase and gas/vapor phase separately) in mouse embryo BALB/c 3T3 cells, and for mutagenicity/genotoxicity in the Salmonella typhimurium reverse mutation assay and the mammalian cell mouse lymphoma TK assay in L5178Y cells, the latter with and without metabolic activation. There were some statistically significant differences in the yield of smoke constituents (increases as well as decreases, nearly all of them less than ± 20%) as a result of the addition of the ingredient mixes. However, the addition of the three different mixes of ingredients to the experimental kreteks did not change the in vitro cytotoxicity and mutagenicity/genotoxicity of the smoke, when compared to the control kretek cigarette.

  4. Synergistic effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor by alveolar macrophages of rats.

    PubMed

    Morimoto, Y; Kido, M; Tanaka, I; Fujino, A; Higashi, T; Yokosaki, Y

    1993-10-01

    The objective of this study was to evaluate the combined effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor (TNF) by alveolar macrophages. Rats were exposed to cigarette smoke in vivo, and production of TNF by alveolar macrophages was measured in the presence of mineral fibres in vitro. For smoke exposure, rats were divided into two groups. Five were exposed to a daily concentration of 10 mg/m3 of cigarette smoke for an eight hour period, and five rats (controls) were not exposed to smoke. Bronchoalveolar lavage was performed after exposure to smoke and the recovered alveolar macrophages were incubated with either chrysotile or ceramic fibres on a microplate for 24 hours. Activity of TNF in the supernatant was determined by the L-929 fibroblast cell bioassay. When alveolar macrophages were not stimulated by mineral fibres, production of TNF by rats exposed to smoke and unexposed rats was essentially the same. When alveolar macrophages were stimulated in vitro by chrysotile or ceramic fibres, production of TNF by alveolar macrophages from rats exposed to smoke was higher than that by alveolar macrophages from unexposed rats. The findings suggest that cigarette smoke and mineral fibres have a synergistic effect on TNF production by alveolar macrophages.

  5. Synergistic effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor by alveolar macrophages of rats.

    PubMed Central

    Morimoto, Y; Kido, M; Tanaka, I; Fujino, A; Higashi, T; Yokosaki, Y

    1993-01-01

    The objective of this study was to evaluate the combined effects of mineral fibres and cigarette smoke on the production of tumour necrosis factor (TNF) by alveolar macrophages. Rats were exposed to cigarette smoke in vivo, and production of TNF by alveolar macrophages was measured in the presence of mineral fibres in vitro. For smoke exposure, rats were divided into two groups. Five were exposed to a daily concentration of 10 mg/m3 of cigarette smoke for an eight hour period, and five rats (controls) were not exposed to smoke. Bronchoalveolar lavage was performed after exposure to smoke and the recovered alveolar macrophages were incubated with either chrysotile or ceramic fibres on a microplate for 24 hours. Activity of TNF in the supernatant was determined by the L-929 fibroblast cell bioassay. When alveolar macrophages were not stimulated by mineral fibres, production of TNF by rats exposed to smoke and unexposed rats was essentially the same. When alveolar macrophages were stimulated in vitro by chrysotile or ceramic fibres, production of TNF by alveolar macrophages from rats exposed to smoke was higher than that by alveolar macrophages from unexposed rats. The findings suggest that cigarette smoke and mineral fibres have a synergistic effect on TNF production by alveolar macrophages. Images PMID:8217857

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

    PubMed

    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.

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

    PubMed

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

    2015-10-15

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

  8. Cigarette smoke-induced lung emphysema in mice is associated with prolyl endopeptidase, an enzyme involved in collagen breakdown

    PubMed Central

    Koelink, Pim J.; Henricks, Paul A. J.; Jackson, Patricia L.; Nijkamp, Frans P.; Garssen, Johan; Kraneveld, Aletta D.; Blalock, J. Edwin; Folkerts, Gert

    2011-01-01

    There is increasing evidence that the neutrophil chemoattractant proline-glycine-proline (PGP), derived from the breakdown of the extracellular matrix, plays an important role in neutrophil recruitment to the lung. PGP formation is a multistep process involving neutrophils, metalloproteinases (MMPs), and prolyl endopeptidase (PE). This cascade of events is now investigated in the development of lung emphysema. A/J mice were whole body exposed to cigarette smoke for 20 wk. After 20 wk or 8 wk after smoking cessation, animals were killed, and bronchoalveolar lavage fluid and lung tissue were collected to analyze the neutrophilic airway inflammation, the MMP-8 and MMP-9 levels, the PE activity, and the PGP levels. Lung tissue degradation was assessed by measuring the mean linear intercept. Additionally, we investigated the effect of the peptide l-arginine-threonine-arginine (RTR), which binds to PGP sequences, on the smoke-induced neutrophil influx in the lung after 5 days of smoke exposure. Neutrophilic airway inflammation was induced by cigarette smoke exposure. MMP-8 and MMP-9 levels, PE activity, and PGP levels were elevated in the lungs of cigarette smoke-exposed mice. PE was highly expressed in epithelial and inflammatory cells (macrophages and neutrophils) in lung tissue of cigarette smoke-exposed mice. After smoking cessation, the neutrophil influx, the MMP-8 and MMP-9 levels, the PE activity, and the PGP levels were decreased or reduced to normal levels. Moreover, RTR inhibited the smoke-induced neutrophil influx in the lung after 5 days' smoke exposure. In the present murine model of cigarette smoke-induced lung emphysema, it is demonstrated for the first time that all relevant components (neutrophils, MMP-8, MMP-9, PE) involved in PGP formation from collagen are upregulated in the airways. Together with MMPs, PE may play an important role in the formation of PGP and thus in the pathophysiology of lung emphysema. PMID:21112944

  9. The mutagenic assessment of mainstream cigarette smoke using the Ames assay: a multi-strain approach.

    PubMed

    Thorne, David; Kilford, Joanne; Hollings, Michael; Dalrymple, Annette; Ballantyne, Mark; Meredith, Clive; Dillon, Deborah

    2015-04-01

    Salmonella typhimurium strains TA1535, TA1537, TA97, TA102 and TA104 were assessed for their suitability and use in conjunction with a Vitrocell(®) VC 10 Smoking Robot and 3R4F reference mainstream cigarette smoke. Little information exists on TA97, TA104, TA1535, TA1537 and TA102 using an aerosol 35mm spread-plate format. In this study, TA1535 and TA1537 were considered sub-optimal for use with a scaled-down format, due to low spontaneous revertant numbers (0-5 revertants/plate). In the context of a regulatory environment, TA97 is deemed an acceptable alternative for TA1537 and was therefore selected for whole smoke exposure in this study. However, there is no acceptable alternative for TA1535, therefore this strain was included for whole smoke exposure. TA1535, TA97, TA102 and TA104 were assessed for mutagenic responses following exposure to cigarette smoke at varying concentrations (using diluting airflow rates of 1.0, 4.0, 8.0 and 12.0L/min), and exposure times of 24 and 64min. A positive mutagenic response to cigarette smoke was observed in strain TA104 at both the 24 and 64min time points, in the presence of S-9, at the highest smoke concentration tested (1.0L/min diluting airflow). The three remaining strains were found to be unresponsive to cigarette smoke at all concentrations tested, in the presence and absence of metabolic activation. Cigarette smoke particulate deposition was quantified in situ of exposure using quartz crystal microbalance technology, enabling data to be presented against an associated gravimetric mass (μg/cm(2)). Finally, data obtained in this study were combined with previously published Ames data for TA98, TA100, YG1024, YG1042 and Escherichia coli (WP2 uvrA pKM101), generated using the same 35mm methodology. The combined data-set was used to propose an aerosol testing strategy, based on strain compatibility with the whole smoke aerosol, whilst maintaining the essence of the regulatory guidelines for the standard Ames assay.

  10. Cigarette smoke chemistry market maps under Massachusetts Department of Public Health smoking conditions.

    PubMed

    Morton, Michael J; Laffoon, Susan W

    2008-06-01

    This study extends the market mapping concept introduced by Counts et al. (Counts, M.E., Hsu, F.S., Tewes, F.J., 2006. Development of a commercial cigarette "market map" comparison methodology for evaluating new or non-conventional cigarettes. Regul. Toxicol. Pharmacol. 46, 225-242) to include both temporal cigarette and testing variation and also machine smoking with more intense puffing parameters, as defined by the Massachusetts Department of Public Health (MDPH). The study was conducted over a two year period and involved a total of 23 different commercial cigarette brands from the U.S. marketplace. Market mapping prediction intervals were developed for 40 mainstream cigarette smoke constituents and the potential utility of the market map as a comparison tool for new brands was demonstrated. The over-time character of the data allowed for the variance structure of the smoke constituents to be more completely characterized than is possible with one-time sample data. The variance was partitioned among brand-to-brand differences, temporal differences, and the remaining residual variation using a mixed random and fixed effects model. It was shown that a conventional weighted least squares model typically gave similar prediction intervals to those of the more complicated mixed model. For most constituents there was less difference in the prediction intervals calculated from over-time samples and those calculated from one-time samples than had been anticipated. One-time sample maps may be adequate for many purposes if the user is aware of their limitations. Cigarette tobacco fillers were analyzed for nitrate, nicotine, tobacco-specific nitrosamines, ammonia, chlorogenic acid, and reducing sugars. The filler information was used to improve predicting relationships for several of the smoke constituents, and it was concluded that the effects of filler chemistry on smoke chemistry were partial explanations of the observed brand-to-brand variation.

  11. Patch testing for allergic contact dermatitis to cigarettes: smoked/unsmoked components and formaldehyde factors.

    PubMed

    Carew, Benjamin; Muir, Jim

    2014-08-01

    A patient with hand dermatitis reported that switching her smoking hand resulted in reduced symptoms. When allergy to cigarettes is suspected the literature supports standard allergy testing as well as testing the individual components of cigarettes. Initial standard patch testing revealed an allergy to formaldehyde and the formaldehyde releasing agent, quaternium-15. The patient did not react to her usual roll-your-own cigarette components but reacted to the smoked filter paper of a particular brand of cigarette she frequently borrowed from a friend. Possible explanations include either a variation of ingredients between cigarettes that alters the formaldehyde concentration or another unidentified allergen in the branded cigarette causing allergic contact dermatitis.

  12. Induction of alopecia in mice exposed to cigarette smoke.

    PubMed

    D'Agostini, F; Balansky, R; Pesce, C; Fiallo, P; Lubet, R A; Kelloff, G J; De Flora, S

    2000-04-03

    Besides being responsible for a high proportion of those chronic degenerative diseases that are the leading causes of death in the population, tobacco smoking has been associated with skin diseases. Smoke genotoxicants are metabolized in hair follicle cells, where they form DNA adducts and cause DNA damage. The suspicion was raised that, in humans, a link may exist between smoking and both premature grey hair and hair loss. In order to check this hypothesis, we carried out a study in C57BL/6 mice exposed whole-body to a mixture of sidestream and mainstream cigarette smoke. After 3 months exposure, most mice developed areas of alopecia and grey hair, while no such lesions occurred either in sham-exposed mice or in smoke-exposed mice receiving the chemopreventive agent N-acetylcysteine with drinking water. Cell apoptosis occurred massively in the hair bulbs at the edge of alopecia areas. Smoke-exposed mice had extensive atrophy of the epidermis, reduced thickness of the subcutaneous tissue, and scarcity of hair follicles. On the whole, exposure to smoke genotoxic components appears to alter the hair cycle with a dystrophic anagen pattern. Although this mechanism is different from that of genotoxic cytostatic drugs, N-acetylcysteine appears to exert protective effects in both conditions.

  13. Evaluation of E-cigarette liquid vapor and mainstream cigarette smoke after direct exposure of primary human bronchial epithelial cells.

    PubMed

    Scheffler, Stefanie; Dieken, Hauke; Krischenowski, Olaf; Förster, Christine; Branscheid, Detlev; Aufderheide, Michaela

    2015-04-08

    E-cigarettes are emerging products, often described as "reduced-risk" nicotine products or alternatives to combustible cigarettes. Many smokers switch to e-cigarettes to quit or significantly reduce smoking. However, no regulations for e-cigarettes are currently into force, so that the quality and safety of e-liquids is not necessarily guaranteed. We exposed primary human bronchial epithelial cells of two different donors to vapor of e-cigarette liquid with or without nicotine, vapor of the carrier substances propylene glycol and glycerol as well as to mainstream smoke of K3R4F research cigarettes. The exposure was done in a CULTEX® RFS compact  module, allowing the exposure of the cells at the air-liquid interface. 24 h post-exposure, cell viability and oxidative stress levels in the cells were analyzed. We found toxicological effects of e-cigarette vapor and the pure carrier substances, whereas the nicotine concentration did not have an effect on the cell viability. The viability of mainstream smoke cigarette exposed cells was 4.5-8 times lower and the oxidative stress levels 4.5-5 times higher than those of e-cigarette vapor exposed cells, depending on the donor. Our experimental setup delivered reproducible data and thus provides the opportunity for routine testing of e-cigarette liquids to ensure safety and quality for the user.

  14. Chitosan removes toxic heavy metal ions from cigarette mainstream smoke

    NASA Astrophysics Data System (ADS)

    Zhou, Wen; Xu, Ying; Wang, Dongfeng; Zhou, Shilu

    2013-09-01

    This study investigated the removal of heavy metal ions from cigarette mainstream smoke using chitosan. Chitosan of various deacetylation degrees and molecular weights were manually added to cigarette filters in different dosages. The mainstream smoke particulate matter was collected by a Cambridge filter pad, digested by a microwave digestor, and then analyzed for contents of heavy metal ions, including As(III/V), Pb(II), Cd(II), Cr(III/VI) and Ni(II), by graphite furnace atomic absorption spectrometry (GFAAS). The results showed that chitosan had a removal effect on Pb(II), Cd(II), Cr(III/VI) and Ni(II). Of these, the percent removal of Ni(II) was elevated with an increasing dosage of chitosan. Chitosan of a high deace tylation degree exhibited good binding performance toward Cd(II), Cr(III/VI) and Ni(II), though with poor efficiency for Pb(II). Except As(III/V), all the tested metal ions showed similar tendencies in the growing contents with an increasing chitosan molecular weight. Nonetheless, the percent removal of Cr(III/VI) peaked with a chitosan molecular weight of 200 kDa, followed by a dramatic decrease with an increasing chitosan molecular weight. Generally, chitosan had different removal effects on four out of five tested metal ions, and the percent removal of Cd(II), Pb(II), Cr(III/VI) and Ni(II) was approximately 55%, 45%, 50%, and 16%, respectively. In a word, chitosan used in cigarette filter can remove toxic heavy metal ions in the mainstream smoke, improve cigarette safety, and reduce the harm to smokers.

  15. Correlates of Cigarette Smoking among Male Chinese College Students in China--A Preliminary Study

    ERIC Educational Resources Information Center

    Li, Kaigang; Kay, Noy S.

    2009-01-01

    The main purpose of this preliminary study was to examine the association between four constructs of the Health Belief Model (HBM) (i.e. perceived severity of smoking-related health problems, perceived susceptibility to smoking-health related problems, perceived barriers to non-smoking and perceived benefits of non-smoking) and cigarette smoking

  16. Latino cigarette smoking patterns by gender in a US national sample

    PubMed Central

    Kristman-Valente, Allison; Flaherty, Brian P.

    2015-01-01

    Background Latino smokers are a rising public health concern who experience elevated tobacco related health disparities. Purpose Additional information on Latino smoking is needed to inform screening and treatment. Analysis Latent class analysis using smoking frequency, cigarette preferences, onset, smoking duration, cigarettes per day and minutes to first cigarette were used to create multivariate latent smoking profiles for Latino men and women. Results Final models found seven classes for Latinas and nine classes for Latinos. Despite a common finding in the literature that Latino smokers are more likely to be low-risk, intermittent smokers, the majority of classes, for both males and females, described patterns of high-risk, daily smoking. Gender variations in smoking classes were noted. Conclusions Several markers of smoking risk were identified among both male and female Latino smokers including long durations of smoking, daily smoking and preference for specialty cigarettes, all factors associated with long-term health consequences. PMID:26304857

  17. Time-course of cigarette smoke contamination of clinical hydrogen breath-analysis tests.

    PubMed

    Rosenthal, A; Solomons, N W

    1983-11-01

    The time-course of the contamination of exogenous hydrogen from cigarette smoke on postprandial breath hydrogen concentration was evaluated in 10 subjects, six regular smokers and four occasional smokers. Breath hydrogen values were determined by gas chromatography 10 min, 5 min, and immediately prior to smoking a filter cigarette; during smoking from a sample of exhaled air containing smoke; and 5, 10, and 15 min after extinguishing the cigarette. A three- to 137-fold increase above basal hydrogen concentrations was produced by exhaled cigarette smoke, but most subjects had re-equilibrated to baseline values within 10 to 15 min after the cigarette. If subjects undergoing clinical hydrogen breath tests cannot refrain from smoking during the duration of the test, one should allow an interval of at least 15 min from the end of smoking to the collection of a breath sample.

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

    SciTech Connect

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

    1989-01-01

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

  19. Cigarette Smoking Practice and Attitudes, and Proposed Effective Smoking Cessation Measures among College Student Smokers in China

    ERIC Educational Resources Information Center

    Cui, Yanping; Ying, Mao; Fan, Hongqi

    2012-01-01

    Purpose: This paper aims to investigate the average daily consumption of cigarettes and its correlates, attitudes toward smoking, and suggestions for anti-smoking measures in a sample of Chinese college student smokers. Design/methodology/approach: A sample of 150 college student cigarette smokers in Baoding, a city near Beijing, filled out a…

  20. Effect of cigarette smoke exposure in vivo on bronchial smooth muscle contractility in vitro in rats.

    PubMed

    Chiba, Yoshihiko; Murata, Masahiko; Ushikubo, Hiroko; Yoshikawa, Yuji; Saitoh, Akiyoshi; Sakai, Hiroyasu; Kamei, Junzo; Misawa, Miwa

    2005-12-01

    Cigarette smoking is a risk factor for the development of airway hyperresponsiveness and chronic obstructive pulmonary disease. Little is known concerning the effect of cigarette smoking on the contractility of airway smooth muscle. The current study was performed to determine the responsiveness of bronchial smooth muscles isolated from rats that were subacutely exposed to mainstream cigarette smoke in vivo. Male Wistar rats were exposed to diluted mainstream cigarette smoke for 2 h/d every day for 2 wk. Twenty-four hours after the last cigarette smoke exposure, a marked airway inflammation (i.e., increases in numbers of neutrophils, lymphocytes, and macrophages in bronchoalveolar lavage fluid and peribronchial tissues) was observed. In these subacutely cigarette smoke-exposed animals, the responsiveness of isolated intact (nonpermeabilized) bronchial smooth muscle to acetylcholine, but not to high K+ -depolarization, was significantly augmented when compared with the air-exposed control group. In alpha-toxin-permeabilized bronchial smooth muscle strips, the acetylcholine-induced Ca2+ sensitization of contraction was significantly augmented in rats exposed to cigarette smoke, although the contraction induced by Ca2+ was control level. Immunoblot analyses revealed an increased expression of RhoA protein in the bronchial smooth muscle of rats that were exposed to cigarette smoke. Taken together, these findings suggest that the augmented agonist-induced, RhoA-mediated Ca2+ sensitization may be responsible for the enhanced bronchial smooth muscle contraction induced by cigarette smoking, which has relevance to airway hyperresponsiveness in patients with chronic obstructive pulmonary disease.

  1. Effect of Menthol on Nicotine Pharmacokinetics in Rats After Cigarette Smoke Inhalation

    PubMed Central

    2012-01-01

    Introduction: The effect of menthol on nicotine disposition is important in understanding smoking behaviors among different racial groups. The present study was to evaluate whether menthol affects the pharmacokinetics of nicotine after cigarette smoke inhalation. Methods: Rats were exposed to mainstream smoke from either a nonmentholated or mentholated cigarette (1 puff/min for 10 min) using a smoke inhalation apparatus. For the multiple-cigarette smoke inhalation, rats received the smoke from either nonmentholated or mentholated cigarette (10 puffs) every 12 hr for a total of 17 cigarettes. Serial blood samples were collected during the 10-min inhalation phase for the single-cigarette smoke or the 17th cigarette inhalation and for 30 hr thereafter. Nicotine and its major metabolite cotinine were assayed by radioimmunoassay methods. Results: Following single-cigarette smoke inhalation, mentholated cigarettes significantly decreased the mean peak concentrations of nicotine in plasma (Cmax) from 27.1 to 9.61 ng/ml and the total area under the plasma concentration–time curves (AUC) from 977 to 391 ng min/ml as compared with those after nonmentholated cigarette smoke inhalation. Cmax and AUC values for cotinine were also significantly reduced by menthol. Similarly after multiple smoke inhalation, Cmax, AUC, and the mean average steady-state plasma concentration of nicotine as well as cotinine were significantly lower in mentholated cigarette inhalation. Interestingly, there was a significant increase in the cotinine to nicotine AUC ratio from 13.8 for the nonmentholated to 21.1 for the mentholated cigarette. Conclusions: These results suggest that menthol in mentholated cigarettes can substantially decrease the absorption and/or increase the clearance of nicotine. PMID:22311961

  2. Reduction of aldehydes and hydrogen cyanide yields in mainstream cigarette smoke using an amine functionalised ion exchange resin

    PubMed Central

    2011-01-01

    Background Cigarette smoking is a well recognized cause of diseases such as lung cancer, chronic obstructive pulmonary disease and cardiovascular disease. Of the more than 5000 identified species in cigarette smoke, at least 150 have toxicological activity. For example, formaldehyde and acetaldehyde have been assigned as Group 1 and Group 2B carcinogens by IARC, and hydrogen cyanide has been identified as a respiratory and cardiovascular toxicant. Active carbon has been shown to be an effective material for the physical adsorption of many of the smoke volatile species. However, physical adsorption of acetaldehyde, formaldehyde and also hydrogen cyanide from smoke is less effective using carbon. Alternative methods for the removal of these species from cigarette smoke are therefore of interest. A macroporous, polystyrene based ion-exchange resin (Diaion®CR20) with surface amine group functionality has been investigated for its ability to react with aldehydes and HCN in an aerosol stream, and thus selectively reduce the yields of these compounds (in particular formaldehyde) in mainstream cigarette smoke. Results Resin surface chemistry was characterized using vapour sorption, XPS, TOF-SIMS and 15N NMR. Diaion®CR20 was found to have structural characteristics indicating weak physisorption properties, but sufficient surface functionalities to selectively remove aldehydes and HCN from cigarette smoke. Using 60 mg of Diaion®CR20 in a cigarette cavity filter gave reductions in smoke formaldehyde greater than 50% (estimated to be equivalent to >80% of the formaldehyde present in the smoke vapour phase) independent of a range of flow rates. Substantial removal of HCN (>80%) and acetaldehyde (>60%) was also observed. The performance of Diaion®CR20 was found to be consistent over a test period of 6 months. The overall adsorption for the majority of smoke compounds measured appeared to follow a pseudo-first order approximation to second order kinetics. Conclusions This

  3. Cadmium exposure from smoking cigarettes: variations with time and country where purchased.

    PubMed

    Elinder, C G; Kjellström, T; Lind, B; Linnman, L; Piscator, M; Sundstedt, K

    1983-10-01

    Cadmium has been determined in 26 brands of cigarettes purchased in eight different countries throughout the world and in 16 different samples of cigarettes produced in Sweden between 1918 and 1968. In addition the amount of cadmium released from smoking one cigarette to the particulate phase collected from a smoking simulation machine, corresponding to the amount actually inhaled by a smoker, has been determined. The cadmium concentration in different brands of cigarettes ranged from 0.19 to 3.0 micrograms Cd/g dry wt, with a general tendency toward lower values in cigarettes from developing countries. No systematic change in the cadmium concentration of cigarettes with time could be revealed. The amount of cadmium inhaled from smoking one cigarette containing about 1.7 microgram Cd was estimated to be 0.14 to 0.19 microgram, corresponding to about 10% of the total cadmium content in the cigarette.

  4. Cigarette smoke exposure reveals a novel role for the MEK/ERK1/2 MAPK pathway in regulation of CFTR

    PubMed Central

    Xu, Xiaohua; Balsiger, Robert; Tyrrell, Jean; Boyaka, Prosper N.; Tarran, Robert; Cormet-Boyaka, Estelle

    2015-01-01

    Background CFTR plays a key role in maintenance of lung fluid homeostasis. Cigarette smoke decreases CFTR expression in the lung but neither the mechanisms leading to CFTR loss, nor potential ways to prevent its loss have been identified to date. Methods The molecular mechanisms leading to down-regulation of CFTR by cigarette smoke were determined using pharmacologic inhibitors and silencing RNAs. Results Using human bronchial epithelial cells, here we show that cigarette smoke induces degradation of CFTR that is attenuated by the lysosomal inhibitors, but not proteasome inhibitors. Cigarette smoke can activate multiple signaling pathways in airway epithelial cells, including the MEK/Erk1/2 MAPK pathway regulating cell survival. Interestingly, pharmacological inhibition of the MEK/Erk1/2 MAPK pathway prevented the loss of plasma membrane CFTR upon cigarette smoke exposure. Similarly, decreased expression of Erk1/2 using silencing RNAs prevented the suppression of CFTR protein by cigarette smoke. Conversely, specific inhibitors of the JNK or p38 MAPK pathways had no effect on CFTR decrease after cigarette smoke exposure. In addition, inhibition of the MEK/Erk1/2 MAPK pathway prevented the reduction of the airway surface liquid observed upon cigarette smoke exposure of primary human airway epithelial cells. Finally, addition of the antioxidant NAC inhibited activation of Erk1/2 by cigarette smoke and precluded the cigarette smoke-induced decrease of CFTR. Conclusions These results show that the MEK/Erk1/2 MAPK pathway regulates plasma membrane CFTR in human airway cells. General Significance The MEK/Erk1/2 MAPK pathway should be considered as a target for strategies to maintain/restore CFTR expression in the lung of smokers. PMID:25697727

  5. Cigarette Smoking and Risk of Meningioma: The Effect of Gender

    PubMed Central

    Claus, Elizabeth B.; Walsh, Kyle M.; Calvocoressi, Lisa; Bondy, Melissa L.; Schildkraut, Joellen M.; Wrensch, Margaret; Wiemels, Joseph L.

    2013-01-01

    Background A number of studies have reported on the association between smoking and meningioma risk, with inconsistent findings. We examined the effect of gender on the association between cigarette smoking and risk of intra-cranial meningioma in a large population-based, case-control study. Methods The data includes 1433 intra-cranial meningioma cases aged 29–79 years diagnosed among residents of the states of Connecticut, Massachusetts, North Carolina, the San Francisco Bay Area and eight Texas counties between May 1, 2006 and April 28, 2011 and 1349 controls that were frequency-matched on age, sex and geography. The data are analyzed separately and in a meta-analysis with six previously reported studies. Results Female cases who reported having ever smoked were at significantly decreased risk of intra-cranial meningioma (Odds ratio (OR) = 0.8, 95% confidence interval (CI), 0.7–0.9) in contrast to male cases who were at increased risk (OR:1.3, 95%CI: 1.0–1.7). Similar findings were noted for current and past smokers. Smoking-induced risk for females did not vary by menopausal status. For males, increased duration of use (p = 0.04) as well as increasing number of pack-years (p = 0.02) was associated with elevated risk. A meta-analysis including 2614 cases and 1,179,686 controls resulted in an OR for ever smoking of 0.82 (95%CI: 0.68–0.98) for women and 1.39 (95%CI: 1.08–1.79) for men. Conclusion The association of cigarette smoking and meningioma case status varies significantly by gender with women at reduced risk and men at greater risk. Impact Whether the observed differences are associated with a hormonal etiology will require additional investigation. PMID:22473761

  6. Electronic Cigarette Use and Smoking Abstinence in Japan: A Cross-Sectional Study of Quitting Methods

    PubMed Central

    Hirano, Tomoyasu; Tabuchi, Takahiro; Nakahara, Rika; Kunugita, Naoki; Mochizuki-Kobayashi, Yumiko

    2017-01-01

    The benefit of electronic cigarettes (e-cigarettes) in smoking cessation remains controversial. Recently, e-cigarettes have been gaining popularity in Japan, without evidence of efficacy on quitting cigarettes. We conducted an online survey to collect information on tobacco use, difficulties in smoking cessation, socio-demographic factors, and health-related factors in Japan. Among the total participants (n = 9055), 798 eligible persons aged 20–69 years who smoked within the previous five years were analyzed to assess the relationship between the outcome of smoking cessation and quitting methods used, including e-cigarettes, smoking cessation therapy, and unassisted. E-cigarette use was negatively associated with smoking cessation (odds ratio (OR) = 0.632; 95% confidence interval (CI) = 0.414–0.964) after adjusting for gender, age, health-related factors, and other quitting methods. Conversely, smoking cessation therapy (i.e., varenicline) was significantly associated with smoking cessation (OR = 1.885; 95% CI = 1.018–3.492) in the same model. For effective smoking cessation, e-cigarette use appears to have low efficacy among smokers in Japan. Allowing for the fact that this study is limited by its cross-sectional design, follow-up studies are needed to assess the prospective association between e-cigarette use and smoking cessation. PMID:28218695

  7. Cigarette smoke extracts induce overexpression of the proto-oncogenic gene interleukin-13 receptor α2 through activation of the PKA-CREB signaling pathway to trigger malignant transformation of lung vascular endothelial cells and angiogenesis.

    PubMed

    Meng, Mei; Liao, Huaidong; Zhang, Bin; Pan, Yanyan; Kong, Ying; Liu, Wenming; Yang, Ping; Huo, Zihe; Cao, Zhifei; Zhou, Quansheng

    2017-02-01

    Cigarette smoking is a major cause of lung cancer. Tumor-associated endothelial cells (TAECs) play important roles in tumor angiogenesis and metastasis. However, whether cigarette smoking can trigger genesis of lung TAECs has not been reported yet. In the current study, we used lung endothelial cell (EC) lines as a model to study the pathological effect of cigarette smoke extracts (CSEs) on human lung ECs, and found that a lower dose of 4% CSEs obviously caused abnormal morphological changes in ECs, increased the permeability of endothelial monolayer, while a higher concentration of 8% CSEs caused EC apoptosis. Strikingly, CSEs induced a 117-fold overexpression of a pro-tumorigenic interleukin-13 receptor α2 gene (IL-13Rα2, also named as CT-19) through activation of the protein kinase A (PKA) and cAMP response element-binding protein (CREB) signaling pathway. A PKA specific inhibitor H89 completely abolished CSEs-induced IL-13Rα2 overexpression. The overexpression of IL-13Rα2 in lung ECs significantly increased the tumorigenic, migratory, and angiogenic capabilities of the cells, suggesting that IL-13Rα2 promotes genesis of lung TAECs. Together, our data show that CSEs activate the PKA, CREB, and IL-13Rα2 axis in lung ECs, and IL-13Rα2 promotes the malignant transformation of lung ECs and genesis of TAECs with robust angiogenic and oncogenic capabilities. Our study provides new insight into the mechanism of CSEs-triggered lung cancer angiogenesis and tumorigenesis, suggesting that the PKA-CREB-IL-13Rα2 axis is a potential target for novel anti-lung tumor angiogenesis and anti-lung cancer drug discovery.

  8. Natural killer cell activity in cigarette smokers and asbestos workers

    SciTech Connect

    Ginns, L.C.; Ryu, J.H.; Rogol, P.R.; Sprince, N.L.; Oliver, L.C.; Larsson, C.J.

    1985-06-01

    In order to evaluate the effects of cigarette smoking and asbestos exposure on cellular immunity, the authors tested a group of cigarette smokers and asbestos workers for natural killer (NK) activity in the peripheral blood. The mean NK activity in cigarette smokers was lower than in normal subjects (13.7 +/- 1.6 versus 29.0 +/- 3%; p less than 0.05). As a group, the mean NK activity for the asbestos-exposed group was also reduced compared with that of the nonsmoking control group (22.6 +/- 3.2%; p less than 0.05). When divided according to the smoking status, the asbestos workers who were nonsmokers or ex-smokers showed similar decreases in NK activity compared with normal subjects (19.5 +/- 6.2 and 21.2 +/- 4.5%, respectively; p less than 0.05). A subgroup of asbestos-exposed subjects who currently smoked showed no decrease in NK activity. The data show that NK activity is reduced in the peripheral blood of cigarette smokers and asbestos workers. The relatively normal NK activity found in asbestos workers who also smoked is unexplained. Impairment of NK activity is a potential mechanism for the increased incidence of infection and cancer in smokers and neoplasia in asbestos workers.

  9. Associations Between Initial Water Pipe Tobacco Smoking and Snus Use and Subsequent Cigarette Smoking Results From a Longitudinal Study of US Adolescents and Young Adults

    PubMed Central

    Soneji, Samir; Sargent, James D.; Tanski, Susanne E.; Primack, Brian A.

    2015-01-01

    IMPORTANCE Many adolescents and young adults use alternative tobacco products, such as water pipes and snus, instead of cigarettes. OBJECTIVE To assess whether prior water pipe tobacco smoking and snus use among never smokers are risk factors for subsequent cigarette smoking. DESIGN, SETTING, AND PARTICIPANTS We conducted a 2-wave national longitudinal study in the United States among 2541 individuals aged 15 to 23 years old. At baseline (October 25, 2010, through June 11, 2011), we ascertained whether respondents had smoked cigarettes, smoked water pipe tobacco, or used snus. At the 2-year follow-up (October 27, 2012, through March 31, 2013), we determined whether baseline non–cigarette smokers had subsequently tried cigarette smoking, were current (past 30 days) cigarette smokers, or were high-intensity cigarette smokers. We fit multivariable logistic regression models among baseline non–cigarette smokers to assess whether baseline water pipe tobacco smoking and baseline snus use were associated with subsequent cigarette smoking initiation and current cigarette smoking, accounting for established sociodemographic and behavioral risk factors. We fit similarly specified multivariable ordinal logistic regression models to assess whether baseline water pipe tobacco smoking and baseline snus use were associated with high-intensity cigarette smoking at follow-up. EXPOSURES Water pipe tobacco smoking and the use of snus at baseline. MAIN OUTCOMES AND MEASURES Among baseline non–cigarette smokers, cigarette smoking initiation, current (past 30 days) cigarette smoking at follow-up, and the intensity of cigarette smoking at follow-up. RESULTS Among 1596 respondents, 1048 had never smoked cigarettes at baseline, of whom 71 had smoked water pipe tobacco and 20 had used snus at baseline. At follow-up, accounting for behavioral and sociodemographic risk factors, baseline water pipe tobacco smoking and snus use were independently associated with cigarette smoking

  10. Direct enhancement by cigarette smoke of asbestos fiber penetration and asbestos-induced epithelial proliferation in rat tracheal explants

    SciTech Connect

    Hobson, J.; Gilks, B.; Wright, J.; Churg, A.

    1988-06-01

    Tracheal explants from Sprague-Dawley rats were briefly exposed to cigarette smoke or air (control) and then to amosite asbestos. Asbestos fibers in or under the tracheal epithelium were counted and extent of hyperplastic lesions was ascertained at 24 hours, 72 hours, and 1 week after exposure. Smoke-exposed cultures showed significantly greater numbers of fibers in the epithelium and greater proliferative activity compared to findings in cultures not exposed to smoke. These observations indicate that very short exposure to cigarette smoke can directly affect the response of the epithelium to asbestos fibers and that smoke exposure need not be concurrent with asbestos exposure for such event to occur. These reactions may play a role in the greater incidences of lung cancer and asbestosis seen in asbestos-exposed workers who smoke.

  11. Toxicological assessment of kretek cigarettes: Part 2: kretek and American-blended cigarettes, smoke chemistry and in vitro toxicity.

    PubMed

    Piadé, J-J; Roemer, E; Dempsey, R; Hornig, G; Deger Evans, A; Völkel, H; Schramke, H; Trelles-Sticken, E; Wittke, S; Weber, S; Schorp, M K

    2014-12-01

    Two commercial kretek cigarettes typical for the Indonesian market and a reference kretek cigarette were compared to the American-blended reference cigarette 2R4F by smoke chemistry characterization and in vitro cytotoxicity and mutagenicity assessments. Despite the widely diverse designs and deliveries of the selected kretek cigarettes, their smoke composition and in vitro toxicity data present a consistent pattern when data were normalized to total particulate matter (TPM) deliveries. This confirms the applicability of the studies' conclusions to a wide range of kretek cigarette products. After normalization to TPM delivery, nicotine smoke yields of kretek cigarettes were 29-46% lower than that of the 2R4F. The yields of other nitrogenous compounds were also much lower, less than would be expected from the mere substitution of one third of the tobacco filler by clove material. Yields of light molecular weight pyrolytic compounds, notably aldehydes and hydrocarbons, were reduced, while yields of polycyclic aromatic hydrocarbons were unchanged and phenol yield was increased. The normalized in vitro toxicity was lowered accordingly, reflecting the yield reductions in gas-phase cytotoxic compounds and some particulate-phase mutagenic compounds. These results do not support a higher toxicity of the smoke of kretek cigarettes compared to American-blended cigarettes.

  12. Cigarette smoke condensate increases C. albicans adhesion, growth, biofilm formation, and EAP1, HWP1 and SAP2 gene expression

    PubMed Central

    2014-01-01

    Background Smokers are more prone to oral infections than are non-smokers. Cigarette smoke reaches the host cells but also microorganisms present in the oral cavity. The contact between cigarette smoke and oral bacteria promotes such oral diseases as periodontitis. Cigarette smoke can also modulate C. albicans activities that promote oral candidiasis. The goal of this study was to investigate the effect of cigarette smoke condensate on C. albicans adhesion, growth, and biofilm formation as well as the activation of EAP1, HWP1 and secreted aspartic protease 2. Results Cigarette smoke condensate (CSC) increased C. albicans adhesion and growth, as well as biofilm formation. These features may be supported by the activation of certain important genes. Using quantitative RT-PCR, we demonstrated that CSC-exposed C. albicans expressed high levels of EAP1, HWP1 and SAP2 mRNA and that this gene expression increased with increasing concentrations of CSC. Conclusion CSC induction of C. albicans adhesion, growth, and biofilm formation may explain the increased persistence of this pathogen in smokers. These findings may also be relevant to other biofilm-induced oral diseases. PMID:24618025

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

    SciTech Connect

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

    2014-12-15

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

  14. Smoking and reproduction: The oviduct as a target of cigarette smoke

    PubMed Central

    Talbot, Prue; Riveles, Karen

    2005-01-01

    The oviduct is an exquisitely designed organ that functions in picking-up ovulated oocytes, transporting gametes in opposite directions to the site of fertilization, providing a suitable environment for fertilization and early development, and transporting preimplantation embryos to the uterus. A variety of biological processes can be studied in oviducts making them an excellent model for toxicological studies. This review considers the role of the oviduct in oocyte pick-up and embryo transport and the evidence that chemicals in both mainstream and sidestream cigarette smoke impair these oviductal functions. Epidemiological data have repeatedly shown that women who smoke are at increased risk for a variety of reproductive problems, including ectopic pregnancy, delay to conception, and infertility. In vivo and in vitro studies indicate the oviduct is targeted by smoke components in a manner that could explain some of the epidemiological data. Comparisons between the toxicity of smoke from different types of cigarettes, including harm reduction cigarettes, are discussed, and the chemicals in smoke that impair oviductal functioning are reviewed. PMID:16191196

  15. Cigarette smoke toxicants as substrates and inhibitors for human cytosolic SULTs

    SciTech Connect

    Yasuda, Shin; Idell, Steven; Fu Jian; Carter, Glendora; Snow, Rhodora; Liu, M.-C. . E-mail: ming.liu@uthct.edu

    2007-05-15

    The current study was designed to examine the role of sulfation in the metabolism of cigarette smoke toxicants and clarify whether these toxicants, by serving as substrates for the cytosolic sulfotransferases (SULTs), may interfere with the sulfation of key endogenous compounds. By metabolic labeling, [{sup 35}S]sulfated species were found to be generated and released into the media of HepG2 human hepatoma cells and primary human lung endothelial cells labeled with [{sup 35}S]sulfate in the presence of cigarette smoke extract (CSE). Concomitantly, several [{sup 35}S]sulfated metabolites observed in the medium in the absence of CSE either decreased or disappeared. Eleven previously prepared human cytosolic SULTs were tested for sulfating activity with CSE and known cigarette smoke toxicants as substrates. Activity data revealed SULT1A1, SULT1A2, SULT1A3, and SULT1C2 as major enzymes responsible for their sulfation. To examine their inhibitory effects on the sulfation of 17{beta}-estradiol by SULT1A1, enzymatic assays were performed in the presence of three representative toxicant compounds, namely N-hydroxy-4-aminobiphenyl (N-OH-4-ABP), 4-aminobiphenyl (4-ABP) and 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP). IC{sub 50} values determined for the sulfation of 17{beta}-estradiol by SULT1A1 were 11.8 {mu}M, 28.2 {mu}M, and 500 {mu}M, respectively, for N-OH-4-ABP, 4-ABP and PhIP. Kinetic analyses indicated that the mechanism underlying the inhibition of 17{beta}-estradiol sulfation by these cigarette smoke toxicants is of a mixed competitive-noncompetitive type. Metabolic labeling experiments clearly showed inhibition of the production of [{sup 35}S]sulfated 17{beta}-estradiol by N-OH-4-ABP in a concentration-dependent manner in HepG2 cells. Taken together, these results suggest that sulfation plays a significant role in the metabolism of cigarette smoke compounds. By serving as substrates for SULTs, cigarette smoke toxicants may interfere with the metabolism

  16. Cigarette Smoking Causes Hearing Impairment among Bangladeshi Population

    PubMed Central

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

    2015-01-01

    Lifestyle including smoking, noise exposure with MP3 player and drinking alcohol are considered as risk factors for affecting hearing synergistically. However, little is known about the association of cigarette smoking with hearing impairment among subjects who carry a lifestyle without using MP3 player and drinking alcohol. We showed here the influence of smoking on hearing among Bangladeshi subjects who maintain a lifestyle devoid of using MP3 player and drinking alcohol. A total of 184 subjects (smokers: 90; non-smokers: 94) were included considering their duration and frequency of smoking for conducting this study. The mean hearing thresholds of non-smoker subjects at 1, 4, 8 and 12 kHz frequencies were 5.63±2.10, 8.56±5.75, 21.06±11.06, 40.79±20.36 decibel (dB), respectively and that of the smokers were 7±3.8, 13.27±8.4, 30.66±12.50 and 56.88±21.58 dB, respectively. The hearing thresholds of the smokers at 4, 8 and 12 kHz frequencies were significantly (p<0.05) higher than those of the non-smokers, while no significant differences were observed at 1 kHz frequency. We also observed no significant difference in auditory thresholds among smoker subgroups based on smoking frequency. In contrast, subjects smoked for longer duration (>5 years) showed higher level of auditory threshold (62.16±19.87 dB) at 12 kHz frequency compared with that (41.52±19.21 dB) of the subjects smoked for 1-5 years and the difference in auditory thresholds was statistically significant (p<0.0002). In this study, the Brinkman Index (BI) of smokers was from 6 to 440 and the adjusted odds ratio showed a positive correlation between hearing loss and smoking when adjusted for age and body mass index (BMI). In addition, age, but not BMI, also played positive role on hearing impairment at all frequencies. Thus, these findings suggested that cigarette smoking affects hearing level at all the frequencies tested but most significantly at extra higher frequencies. PMID:25781179

  17. Toxicological effects of cigarette smoke on Ana-1 macrophages in vitro.

    PubMed

    Yuan, Fengjiao; Dong, Ping; Wang, Xiang; Fu, Xiao; Dai, Mingjun; Zhang, Weiyun

    2013-11-01

    Cigarette smoke exposure is associated with increased risk of different disorders. Immunological dysfunction especially in macrophages is one of important reasons in the initiation, progression and exacerbation of smoke-related pulmonary illnesses. However, it is still obscure how cigarette smoke impacts the vitality and functions of macrophages. In the present study, we examined the effects of cigarette smoke extract (CSE) on mouse Ana-1 macrophages and tried to elucidate the involved mechanism. The results showed CSE induced cell apoptosis accompanied by increased releasing of lactate dehydrogenase (LDH), mitochondrial injury and oxidative stress. It also inhibited anti-apoptosis protein Bcl-2 expression and promoted pro-apoptosis protein Bax and Bad expressions. Moreover, low-dose CSE increased nuclear NF-κB levels of macrophages; on the contrary, high-dose CSE or long-time treatment decreased it. These observations were in correspondence with changes of intracellular ROS level and antioxidant enzymes' activity. Furthermore, pretreatment with 10μM of NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) for 1h significantly enhanced macrophage apoptosis. Taken together, these data implied that mitochondrial dysfunction and oxidative stress played important roles in the injury of Ana-1 cells caused by CSE, which was related to NF-κB pathway; an anti-apoptotic program played a dominant role at low doses/short-term exposure to CSE, whereas a pro-apoptotic program was initiated at high doses/long-term exposure.

  18. Oxidative stress and innate immunity responses in cigarette smoke stimulated nasal epithelial cells.

    PubMed

    Pace, Elisabetta; Ferraro, Maria; Di Vincenzo, Serena; Gerbino, Stefania; Bruno, Andreina; Lanata, Luigi; Gjomarkaj, Mark

    2014-03-01

    Cigarette smoke extracts (CSE) may play a significant role in diseases of the upper airway including chronic rhinosinusitis. Even short term exposure of cigarette smoke has adverse effects on mitochondrial functions and redox homeostasis in tissues which may progress to further complications associated with chronic smoking. Cigarette smoke alters toll-like receptor 4 (TLR4) expression and activation in bronchial epithelial cells. Carbocysteine is an anti-oxidant and mucolytic agent. The effects of carbocysteine on CSE induced oxidative stress and on associated innate immune and inflammatory responses in nasal epithelial cells are largely unknown. The present study was aimed to assess in CSE stimulated nasal epithelial cells (RPMI 2650) the effects of carbocysteine (10(-4)M) on: cell survival, intracellular reactive oxygen species (ROS) production, TLR4 expression, LPS binding and neutrophil chemotaxis (actin reorganization). We found that CSE increased ROS production, TLR4 expression, LPS binding and neutrophil chemotaxis and all these events were counteracted by pre-incubating CSE stimulated RPMI 2650 cells with carbocysteine. In conclusion, the present study provides compelling evidence that carbocysteine may be considered a promising therapeutic strategy in chronic inflammatory nasal diseases.

  19. USP17-mediated deubiquitination and stabilization of HDAC2 in cigarette smoke extract-induced inflammation.

    PubMed

    Song, Huihui; Tao, Lianqin; Chen, Chen; Pan, Lina; Hao, Jimin; Ni, Yingmeng; Li, Dan; Li, Bin; Shi, Guochao

    2015-01-01

    Histone deacetylase HDAC2 regulates genes transcription via removing the acetyl group from histones. Glucocorticoids, the most potent anti-inflammatory treatment available for inflammatory diseases, inhibit the expression of inflammatory genes by recruiting HDAC2 to activated genes. In the lungs of patients who smoke and have chronic obstructive pulmonary disease (COPD) or asthma, glucocorticoids are not effective enough to suppress airway inflammation, which is so called "glucocorticoid resistance", due to decreased HDAC2 level caused by cigarette smoke. We report that the ubiquitin-specific protease USP17 interacts with HDAC2. USP17 deubiquitinates and stabilizes the protein level of HDAC2. In cigarette smoke extract-exposed airway epithelial cells and macrophages, HDAC2 is excessively ubiquitinated and degraded in the proteasome attributed to low expression of USP17. Furthermore, over-expression of USP17 blocks the destruction of HDAC2 induced by cigarette smoke extract. These results provide a new insight into the mechanisms of glucocorticoid resistance in airway inflammatory disease. Small molecules which can specifically induce the expression of USP17 might be useful in reversing glucocorticoid resistance.

  20. Associations between phenylthiocarbamide gene polymorphisms and cigarette smoking.

    PubMed

    Cannon, Dale S; Baker, Timothy B; Piper, Megan E; Scholand, Mary Beth; Lawrence, Daniel L; Drayna, Dennis T; McMahon, William M; Villegas, G Martin; Caton, Trace C; Coon, Hilary; Leppert, Mark F

    2005-12-01

    Phenotypic evidence indicates that the ability to taste the bitter compounds phenylthiocarbamide (PTC) and 6-n-propylthiouracil (PROP) may protect against cigarette smoking. In this study, PTC gene haplotypes were found to be associated with both the odds of being a smoker and the importance of cigarette taste as a smoking motive. Smokers (n = 384) and nonsmokers (n = 183) were genotyped for polymorphisms that affect taste sensitivity to PTC and PROP. The "taster" PAV haplotype, relative to the "nontaster" AVI haplotype, was predicted to be associated with reduced odds of being a smoker and lower taste motivation as measured by the Wisconsin Inventory of Smoking Dependence Motives-68 taste/sensory processes scale. The results did not support the predicted association between the PAV and AVI haplotypes and smoker odds, but the AAV haplotype, which confers intermediate PTC/PROP taste sensitivity, was associated with reduced smoker prevalence (49% vs. 70%), chi(2)(1, N = 567) = 10.392, p = .001. The predicted relationship between PAV and AVI and taste motivation was found, F(2, 348) = 3.303, p = .038. The results encourage further exploration of the role of taste/sensory processes in tobacco dependence.

  1. [Cigarette as "companion": a critical gender approach to women's smoking].

    PubMed

    Borges, Márcia Terezinha Trotta; Simões-Barbosa, Regina Helena

    2008-12-01

    This article presents the main results of a study that examined the symbolic and material meanings of women's smoking, adopting a critical and qualitative gender approach. Semi-structured interviews were held with 14 women smokers in different stages of the smoking cessation process. The research locus was a tobacco treatment program located in a public hospital in Rio de Janeiro, Brazil. The findings showed how deeply smoking is interwoven in these women's social and gender trajectories, playing a decisive support role when they have to deal with various difficulties in life. The cigarette as a "companion" emerged as the main empirical category, as something always available to quell anxiety and loneliness, as well as a source of pleasure and relaxation. The critical gender approach evidenced how women's reproductive and productive work overload reinforces their tobacco dependency. In health care, in order to attain women smokers' adherence to the arduous cessation process, it is crucial to consider the complex relations between social and gender dimensions when cigarettes are viewed as a "companion".

  2. Brand differences of free-base nicotine delivery in cigarette smoke: the view of the tobacco industry documents.

    PubMed

    Ferris Wayne, G; Connolly, G N; Henningfield, J E

    2006-06-01

    The recent availability of internal tobacco industry documents provides significant insight into industry knowledge and manipulation of tobacco smoke delivery. One critical area of research is the role of smoke chemistry in determining the absorption and effects of smoke constituents, especially harm producing or pharmacologically active compounds. Independent scientific research has suggested that the nicotine dosing characteristics, hence the addiction potential of cigarettes, may be determined in part by the amount of free-base nicotine in cigarette smoke and its effects on the location, route, and speed of absorption in the body and on the sensory perception effects of the inhaled smoke. Tobacco industry documents describe the use of a number of methods internally for measuring free-base nicotine delivery. These include the common use of cigarette "smoke pH" as a means to estimate the fraction of free-base nicotine in the particulate matter (PM) in cigarette smoke, as well as efforts to measure free-base nicotine directly. Although these methods do not provide accurate absolute measures of free-base nicotine in smoke, consistencies observed in the findings across the various manufacturers indicate: (1) real relative differences in the acid/base chemistry of the smoke from different brands of cigarettes; (2) a connection between differences in free-base levels and brand-dependent differences in sensory perception and smoke "impact"; and (3) levels of free-base nicotine that are greater than have typically been publicly discussed by the industry. Furthermore, the results of these methods are generally consistent with those of a recent study from the Centers for Disease Control and Prevention which directly measured the free-base fraction of nicotine across a range of cigarette types. Consideration of the likely fundamental importance of free-base nicotine levels in cigarette smoke, together with the efforts discussed in the tobacco industry documents to measure

  3. Sampling and analysis of cigarette smoke using the solid adsorbent Tenax

    SciTech Connect

    Higgins, C.E.; Griest, W.H.; Guerin, M.R.

    1984-05-01

    The commercial introduction of ultra-low-tar delivery cigarette products has posed challenges in the analysis of their smoke constituents. The application of solid sorbent trapping and thermal desorption, programmed-temperature glass-capillary-column gas chromatography has proven useful for both gas phase and particulate matter analyses. In gas phase analysis the cigarette is smoked directly through a Cambridge filter and Tenax trap, and in whole smoke analysis through the Tenax trap alone. For cigarettes having deliveries of < 1 mg tar/cigarette the entire trap content, or a fraction thereof, is desorbed at 250/sup 0/C in the injection port of the gas chromatograph, and the cryothermally trapped organic desorbate is separated by programmed temperature gas chromatography. Tenax used to trap smoke from higher tar delivery cigarettes is duluted with clean Tenax and homogenized before analysis. Quantitation is made by the method of external standards, the RSD for smoke components averaging generally +-20%. Higher RSD's of +-60% in the case of some ultra-low cigarette smoke components may be influenced by mainstream enrichment by sidestream smoke drifting near the air dilution vents in the filter rod. This method of analysis when applied to whole smoke can determine the entire cigarette delivery of many gas phase and particulate matter components, and has sufficient sensitivity that flavor related components in cigarette smoke are analyzable. The distribution of some semivolatile components between gas and particulate phases has been determined by application of this method and is reported.

  4. Molecular mechanism of reduction in pregnenolone synthesis by cigarette smoke

    SciTech Connect

    Bose, Mahuya; Whittal, Randy M.; Gairola, C. Gary; Bose, Himangshu S.

    2008-05-15

    Steroidogenic acute regulatory protein (StAR) facilitates the movement of cholesterol from the outer to inner mitochondrial membrane for the synthesis of pregnenolone. Here, we investigated the molecular mechanism of the reduction of pregnenolone synthesis by cigarette smoke condensate (CSC). Pre-exposure or post-exposure of cells with CSC led to reduced pregnenolone synthesis, in a fashion similar to its effect on isolated mitochondria. However, there was no difference in the expression of 30 kDa StAR in cells treated with moderately concentrated CSC by either regimen. The active form of 37 kDa StAR is degraded easily suggesting that the continuous presence of CSC reduces StAR expression. Mitochondrial import of {sup 35}S-methionine-labeled StAR followed by extraction of the StAR-mitochondrial complex with 1% digitonin showed similarly sized complexes in the CSC-treated and untreated mitochondria. Further analysis by sucrose density gradient centrifugation showed a specific complex, 'complex 2', in the untreated mitochondria but absent in the CSC-treated mitochondria. Mass spectrometric analysis revealed that complex 2 is the outer mitochondrial protein, VDAC1. Knockdown of VDAC1 expression by siRNA followed by co-transfection with StAR resulted in a lack of pregnenolone synthesis and 37 kDa StAR expression with reduced expression of the intermediate, 32 kDa StAR. Taken together, these results suggest that in the absence of VDAC1, active StAR expression is reduced indicating that VDAC1 expression is essential for StAR activity. In the absence of VDAC1-StAR interaction, cholesterol cannot be transported into mitochondria; thus the interaction with VDAC1 is a mandatory step for initiating steroidogenesis.

  5. Impact of State Cigarette Taxes on Disparities in Maternal Smoking During Pregnancy

    PubMed Central

    Baum, Christopher F.

    2014-01-01

    Objectives. We evaluated the impact of state tobacco control policies on disparities in maternal smoking during pregnancy. Methods. We analyzed 2000–2010 National Vital Statistics System natality files with 17 699 534 births from 28 states and the District of Columbia that used the 1989 revision of the birth certificate. We conducted differences-in-differences regression models to assess whether changes in cigarette taxes and smoke-free legislation were associated with changes in maternal smoking during pregnancy and number of cigarettes smoked. To evaluate disparities, we included interaction terms between maternal race/ethnicity, education, and cigarette taxes. Results. Although maternal smoking decreased from 11.6% to 8.9%, White and Black women without a high school degree had some of the highest rates of smoking (39.7% and 16.4%, respectively). These same women were the most responsive to cigarette tax increases, but not to smoke-free legislation. For every $1.00 cigarette tax increase, low-educated White and Black mothers decreased smoking by nearly 2 percentage points and smoked between 14 and 22 fewer cigarettes per month. Conclusions. State cigarette taxes may be an effective population-level intervention to decrease racial/ethnic and socioeconomic disparities in maternal smoking during pregnancy. PMID:24922149

  6. Artifact formation during smoke trapping: An improved method for determination of N-nitrosamines in cigarette smoke

    SciTech Connect

    Caldwell, W.S.; Conner, J.M. )

    1990-09-01

    Studies in our laboratory revealed artifactual formation of N-nitrosamines during trapping of mainstream and sidestream tobacco smoke by the method of Hoffmann and coworkers. Both volatile and tobacco-specific N-nitrosamines were produced. This artifact formation took place on the Cambridge filter, which is part of the collection train used in the previously published procedure. When the filter was treated with ascorbic acid before smoke collection, artifact formation was inhibited. The improved method resulting from these studies was applied to a comparative analysis of N-nitrosamines in smoke from cigarettes that heat, but do not burn, tobacco (the test cigarette) and several reference cigarettes. Concentrations of volatile and tobacco-specific N-nitrosamines in both mainstream and sidestream smoke from the test cigarette were substantially lower than in the reference cigarettes.

  7. Effect of Cigarette Smoke Exposure and Structural Modifications on the α-1 Antitrypsin Interaction with Caspases

    PubMed Central

    Lockett, Angelia D; Van Demark, Mary; Gu, Yuan; Schweitzer, Kelly S; Sigua, Ninotchka; Kamocki, Krzysztof; Fijalkowska, Iwona; Garrison, Jana; Fisher, Amanda J; Serban, Karina; Wise, Robert A; Flotte, Terence R; Mueller, Christian; Presson, Robert G; Petrache, Horia I; Tuder, Rubin M; Petrache, Irina

    2012-01-01

    α-1 Antitrypsin (A1AT) is a serpin with a major protective effect against cigarette smoke–induced emphysema development, and patients with mutations of the A1AT gene display a markedly increased risk for developing emphysema. We reported that A1AT protects lung endothelial cells from apoptosis and inhibits caspase-3 activity. It is not clear if cigarette smoking or A1AT mutations alter the caspase-3 inhibitory activity of A1AT and if this serpin alters the function of other caspases. We tested the hypothesis that the caspase-3 inhibitory activity of A1AT is impaired by cigarette smoking and that the A1AT RCL, the key antiprotease domain of the serpin, is required for its interaction with the caspase. We examined the caspase-3 inhibitory activity of human A1AT purified from plasma of actively smoking and nonsmoking individuals, either affected or unaffected with chronic obstructive pulmonary disease. We also tested the caspase inhibitory activity of two mutant forms of A1AT, the recombinant human piZZ and the RCL–deleted (RCL-null) A1AT forms. A1AT purified from the blood of active smokers exhibited marked attenuation in its caspase-3 inhibitory activity, independent of disease status. In vitro exposure of the normal (MM) form of A1AT to cigarette smoke extract reduced its ability to interact with caspase-3, measured by isothermal titration calorimetry, as did the deletion of the RCL, but not the ZZ point mutation. In cell-free assays A1AT was capable of inhibiting all executioner caspases, -3, -7 and especially -6, but not the initiator or inflammatory caspases. The inhibitory effect of A1AT against caspase-6 was tested in vivo, where overexpression of both human MM and ZZ-A1AT via adeno-associated virus transduction significantly protected against apoptosis and against airspace damage induced by intratracheal instillation of caspase-6 in mice. These data indicate a specific inhibitory effect of A1AT on executioner caspases, which is profoundly attenuated by

  8. How people think about the chemicals in cigarette smoke: a systematic review.

    PubMed

    Morgan, Jennifer C; Byron, M Justin; Baig, Sabeeh A; Stepanov, Irina; Brewer, Noel T

    2017-02-21

    Laws and treaties compel countries to inform the public about harmful chemicals (constituents) in cigarette smoke. To encourage relevant research by behavioral scientists, we provide a primer on cigarette smoke toxicology and summarize research on how the public thinks about cigarette smoke chemicals. We systematically searched PubMed in July 2016 and reviewed citations from included articles. Four central findings emerged across 46 articles that met inclusion criteria. First, people were familiar with very few chemicals in cigarette smoke. Second, people knew little about cigarette additives, assumed harmful chemicals are added during manufacturing, and perceived cigarettes without additives to be less harmful. Third, people wanted more information about constituents. Finally, well-presented chemical information increased knowledge and awareness and may change behavior. This research area is in urgent need of behavioral science. Future research should investigate whether educating the public about these chemicals increases risk perceptions and quitting.

  9. Anxiety, depression, and cigarette smoking: a transdiagnostic vulnerability framework to understanding emotion-smoking comorbidity.

    PubMed

    Leventhal, Adam M; Zvolensky, Michael J

    2015-01-01

    Research into the comorbidity between emotional psychopathology and cigarette smoking has often focused upon anxiety and depression's manifest symptoms and syndromes, with limited theoretical and clinical advancement. This article presents a novel framework to understanding emotion-smoking comorbidity. We propose that transdiagnostic emotional vulnerabilities-core biobehavioral traits reflecting maladaptive responses to emotional states that underpin multiple types of emotional psychopathology-link various anxiety and depressive psychopathologies to smoking. This framework is applied in a review and synthesis of the empirical literature on 3 transdiagnostic emotional vulnerabilities implicated in smoking: (a) anhedonia (Anh; diminished pleasure/interest in response to rewards), (b) anxiety sensitivity (AS; fear of anxiety-related sensations), and (c) distress tolerance (DT; ability to withstand distressing states). We conclude that Anh, AS, and DT collectively (a) underpin multiple emotional psychopathologies, (b) amplify smoking's anticipated and actual affect-enhancing properties and other mechanisms underlying smoking, (c) promote progression across the smoking trajectory (i.e., initiation, escalation/progression, maintenance, cessation/relapse), and (d) are promising targets for smoking intervention. After existing gaps are identified, an integrative model of transdiagnostic processes linking emotional psychopathology to smoking is proposed. The model's key premise is that Anh amplifies smoking's anticipated and actual pleasure-enhancing effects, AS amplifies smoking's anxiolytic effects, and poor DT amplifies smoking's distress terminating effects. Collectively, these processes augment the reinforcing properties of smoking for individuals with emotional psychopathology to heighten risk of smoking initiation, progression, maintenance, cessation avoidance, and relapse. We conclude by drawing clinical and scientific implications from this framework that may

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

    PubMed Central

    Chen, Song; Jiang, Wei

    2015-01-01

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

  11. Attributions for Smoking Behavior: Comparing Smokers with Nonsmokers and Predicting Smokers' Cigarette Consumption.

    ERIC Educational Resources Information Center

    Kleinke, Chris L.; And Others

    1983-01-01

    Compared smokers' (214) and nonsmokers' (220) explanations for cigarette smoking behavior to determine predictors of cigarette consumption. Results showed addiction and affective smoking were the most important motives predicting consumption. Presented at the meeting of the Southeastern Psychological Association, Washington, DC, 1980. (WAS)

  12. Evaluation of Nationwide Health Costs of Air Pollution and Cigarette Smoking

    ERIC Educational Resources Information Center

    Williams, J. R.; Justus, C. G.

    1974-01-01

    The findings of this study indicate cigarette smoking causes more respiratory diseases than does air pollution. The 1970 nationwide health cost of respiratory diseases is estimated at $6.22 billion. The effect of air pollution accounts for between 1 and 5 percent of this total cost while cigarette smoking represents 68 percent. (MLB)

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

    ERIC Educational Resources Information Center

    Klesges, Robert C.; And Others

    1991-01-01

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

  14. Mechanisms of clearance of nontypeable Haemophilus influenzae from cigarette smoke-exposed mouse lungs.

    PubMed

    Gaschler, G J; Zavitz, C C J; Bauer, C M T; Stämpfli, M R

    2010-11-01

    Inflammation is prevalent in all stages of chronic obstructive pulmonary disease, and, furthermore, individuals undergo periods of exacerbation, during which pulmonary inflammation increases, often a result of bacterial infection. The present study investigates the in vivo consequences of cigarette smoke exposure on bacterial challenge with nontypeable Haemophilus influenzae (NTHi). BALB/c and C57 black 6 (C57BL/6) mice were exposed to cigarette smoke once or twice daily for a total period of 8 weeks. Exacerbated inflammation was observed in cigarette smoke-exposed compared to room-air-exposed mice following challenge with live or heat-inactivated NTHi. Accelerated clearance of live NTHi from cigarette smoke-exposed mice was independent of the establishment of chronic inflammation or direct toxic effects of cigarette smoke components on bacteria. Mechanistically, a cell-free factor in the bronchoalveolar lavage fluid contributed to accelerated clearance following passive transfer to naive mice. Further investigation demonstrated increased titres of immunoglobulin A in the bronchoalveolar lavage fluid, but not the blood, of cigarette smoke-exposed mice, including increased titres of NTHi-specific immunoglobulin A, whereas heavy chain joining element (J(H))(-/-) B-cell-deficient cigarette smoke-exposed mice did not demonstrate decreased bacterial burden following challenge. The present results demonstrate that cigarette smoke exposure results in exacerbated inflammation following challenge with NTHi, as well as increased titres of antibodies that contribute to bacterial clearance.

  15. Reconsidering the legality of cigarette smoking advertisements on television public health and the law.

    PubMed

    Hodge, James G; Collmer, Veda; Orenstein, Daniel G; Millea, Chase; Van Buren, Laura

    2013-01-01

    Television advertisements depicting the use of electronic cigarettes have recently exposed minors to images of smoking behaviors. While these advertisements are currently legal, existing laws should be interpreted or expanded to ban the commercial depiction of smoking behaviors with any product that resembles a cigarette to shield minors from potentially influential advertising.

  16. Cadmium in smoke particulates of regular and filter cigarettes containing low and high cadmium concentrations

    SciTech Connect

    Bache, C.A.; Reid, C.M.; Hoffman, D.; Adams, J.D.; Lisk, D.J.

    1986-03-01

    In the work reported, filter and nonfilter cigarettes were prepared from high-cadmium tobacco grown on a municipal sludge-amended soil or a low-cadmium tobacco grown on untreated soil alone. These were smoked by machine to determine the effectiveness of the cigarette filters in possibly reducing the quantities of cadmium in the mainstream smoke particulates.

  17. An Integrated Framework for the Analysis of Adolescent Cigarette Smoking in Middle School Latino Youth

    ERIC Educational Resources Information Center

    Guilamo-Ramos, Vincent; Dittus, Patricia; Holloway, Ian; Bouris, Alida; Crossett, Linda

    2011-01-01

    A framework based on five major theories of health behavior was used to identify the correlates of adolescent cigarette smoking. The framework emphasizes intentions to smoke cigarettes, factors that influence these intentions, and factors that moderate the intention-behavior relationship. Five hundred sixteen randomly selected Latino middle school…

  18. Examining Demographic Factors Related to Cigarette Smoking among Undergraduate Students at a Turkish University

    ERIC Educational Resources Information Center

    Oktay, Erkan; Çelik, Ali Kemal; Akbaba, Ahmet Ilker

    2013-01-01

    Cigarette smoking is the leading global preventable health risk, and it is associated with well-known health risks such as morbidity, mortality, cancer, cardiovascular disease, and nicotine addiction. When analyzed by age group, cigarette smoking in Turkey is the most prevalent among younger adult populations. The college years appear to be a time…

  19. Role of activin-A in cigarette smoke-induced inflammation and COPD.

    PubMed

    Verhamme, Fien M; Bracke, Ken R; Amatngalim, Gimano D; Verleden, Geert M; Van Pottelberge, Geert R; Hiemstra, Pieter S; Joos, Guy F; Brusselle, Guy G

    2014-04-01

    Activin-A is a pleiotropic cytokine belonging to the transforming growth factor-β superfamily and has been implicated in asthma and pulmonary fibrosis. However, the role of activin-A and its endogenous inhibitor, follistatin, in the pathogenesis of chronic obstructive pulmonary disease (COPD) is unknown. We first quantified activin-A and follistatin in the lungs of air- or cigarette smoke-exposed mice and in the lungs of patients with COPD by immunohistochemistry, ELISA and quantitative real-time PCR. We subsequently studied the effect of cigarette smoke on primary human bronchial epithelial cells in vitro. Next, activin-A signalling was antagonised in vivo by administration of follistatin in mice exposed to air or cigarette smoke for 4 weeks. Protein levels of activin-A were increased in the airway epithelium of patients with COPD compared with never-smokers and smokers. Cigarette smoke-exposed human bronchial epithelial cells expressed higher levels of activin-A and lower levels of follistatin. Both mRNA and protein levels of activin-A were increased in the lungs of cigarette smoke-exposed mice, whereas follistatin levels were reduced upon cigarette smoke exposure. Importantly, administration of follistatin attenuated the cigarette smoke-induced increase of inflammatory cells and mediators in the bronchoalveolar lavage fluid in mice. These results suggest that an imbalance between activin-A and follistatin contributes to the pathogenesis of cigarette smoke-induced inflammation and COPD.

  20. Community and Individual Factors Associated with Cigarette Smoking among Young Men Who Have Sex with Men

    ERIC Educational Resources Information Center

    Holloway, Ian W.; Traube, Dorian E.; Rice, Eric; Schrager, Sheree M.; Palinkas, Lawrence A.; Richardson, Jean; Kipke, Michele D.

    2012-01-01

    Young men who have sex with men (YMSM) have higher rates of cigarette smoking than their heterosexual counterparts, yet few studies have examined factors associated with cigarette smoking among YMSM. The present study sought to understand how different types of gay community connection (i.e., gay community identification and involvement, gay bar…

  1. Short cigarette smoke exposure facilitates sensitisation and asthma development in mice.

    PubMed

    Lanckacker, Ellen A; Tournoy, Kurt G; Hammad, Hamida; Holtappels, Gabriele; Lambrecht, Bart N; Joos, Guy F; Maes, Tania

    2013-05-01

    Epidemiological studies indicate that cigarette smoke exposure is a risk factor for increased sensitisation and asthma development. The aim of this study was to examine the impact of cigarette smoke on sensitisation and allergic airway inflammation in response to a low dose of house dust mite (HDM), and to obtain potential mechanistic insights. Mice were exposed to low doses of HDM extract combined with air or cigarette smoke exposure, either during allergen sensitisation or during the development of allergic airway disease. Mice concomitantly exposed to low-dose HDM, combined with cigarette smoke for 3 weeks, demonstrated an asthmatic phenotype with significantly increased airway eosinophilia, goblet cell metaplasia, airway hyperresponsiveness and a rise in HDM-specific serum immunoglobulin G1, compared to sole HDM or cigarette smoke exposure. In addition, short cigarette smoke inhalation, during the initial contact with HDM allergens, was sufficient to facilitate sensitisation and development of a complete asthmatic phenotype after rechallenge with HDM. Mechanistically, short cigarette smoke exposure amplified dendritic cell-mediated transport of fluorescein isothiocyanate-labelled HDM allergens to the intrathoracic lymph nodes and generated a local T-helper cell type 2 response. Short cigarette smoke exposure is sufficient to facilitate allergic sensitisation and the development of low-dose HDM-induced allergic asthma, possibly by affecting dendritic cell function.

  2. Pharmacokinetics of nicotine in rats after multiple-cigarette smoke exposure

    SciTech Connect

    Rotenberg, K.S.; Adir, J.

    1983-06-15

    The pharmacokinetics of nicotine and its major metabolites was evaluated in male rats after multiple-cigarette smoke exposure. A smoke-exposure apparatus was used to deliver cigarette smoke to the exposure chamber. The rats were exposed to smoke from a single cigarette every 8 hr for 14 days and to the smoke of a cigarette spiked with radiolabeled nicotine on the 15th day. Blood and urine samples were collected at timed intervals during the 10-min smoke-exposure period of the last cigarette and up to 48 hr thereafter. Nicotine, cotinine, and other polar metabolites were separated by thin-layer chromatography and quantified by liquid scintillation counting. The data were analyzed by computer fitting, and the derived pharmacokinetic parameters were compared to those observed after a single iv injection of nicotine and after a single-cigarette smoke exposure. The results indicated that the amount of nicotine absorbed from multiple-cigarette smoke was approximately 10-fold greater than that absorbed from a single cigarette. Also, unlike the single-cigarette smoke exposure experiment, nicotine plasma levels did not decay monotonically but increased after the 5th hr, and high plasma concentrations persisted for 30 hr. The rate and extent of the formation of cotinine, the major metabolite of nicotine, were decreased as compared with their values following a single-cigarette smoke exposure. It was concluded that nicotine or a constituent of tobacco smoke inhibits the formation of cotinine and may affect the biotransformation of other metabolites. Urinary excretion tended to support the conclusions that the pharmacokinetic parameters of nicotine and its metabolites were altered upon multiple as compared to single dose exposure.

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

    PubMed

    Janković Mandić, Ljiljana; Đolić, Maja; Marković, Dragana; Todorović, Dragana; Onjia, Antonije; Dragović, Snežana

    2016-01-01

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

  4. Vertical Equity Consequences of Very High Cigarette Tax Increases: If the Poor Are the Ones Smoking, How Could Cigarette Tax Increases Be Progressive?

    ERIC Educational Resources Information Center

    Colman, Gregory J.; Remler, Dahlia K.

    2008-01-01

    Cigarette smoking is concentrated among low-income groups. Consequently, cigarette taxes are considered regressive. However, if poorer individuals are much more price sensitive than richer individuals, then tax increases would reduce smoking much more among the poor and their cigarette tax expenditures as a share of income would rise by much less…

  5. Nontypeable Haemophilus influenzae clearance by alveolar macrophages is impaired by exposure to cigarette smoke.

    PubMed

    Martí-Lliteras, Pau; Regueiro, Verónica; Morey, Pau; Hood, Derek W; Saus, Carles; Sauleda, Jaume; Agustí, Alvar G N; Bengoechea, José Antonio; Garmendia, Junkal

    2009-10-01

    Nontypeable Haemophilus influenzae (NTHI) is an opportunistic gram-negative pathogen that causes respiratory infections and is associated with progression of respiratory diseases. Cigarette smoke is a main risk factor for development of respiratory infections and chronic respiratory diseases. Glucocorticoids, which are anti-inflammatory drugs, are still the most common therapy for these diseases. Alveolar macrophages are professional phagocytes that reside in the lung and are responsible for clearing infections by the action of their phagolysosomal machinery and promotion of local inflammation. In this study, we dissected the interaction between NTHI and alveolar macrophages and the effect of cigarette smoke on this interaction. We showed that alveolar macrophages clear NTHI infections by adhesion, phagocytosis, and phagolysosomal processing of the pathogen. Bacterial uptake requires host actin polymerization, the integrity of plasma membrane lipid rafts, and activation of the phosphatidylinositol 3-kinase (PI3K) signaling cascade. Parallel to bacterial clearance, macrophages secrete tumor necrosis factor alpha (TNF-alpha) upon NTHI infection. In contrast, exposure to cigarette smoke extract (CSE) impaired alveolar macrophage phagocytosis, although NTHI-induced TNF-alpha secretion was not abrogated. Mechanistically, our data showed that CSE reduced PI3K signaling activation triggered by NTHI. Treatment of CSE-exposed cells with the glucocorticoid dexamethasone reduced the amount of TNF-alpha secreted upon NTHI infection but did not compensate for CSE-dependent phagocytic impairment. The deleterious effect of cigarette smoke was observed in macrophage cell lines and in human alveolar macrophages obtained from smokers and from patients with chronic obstructive pulmonary disease.

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

    PubMed

    Choi, Damee; Ota, Shotaro; Watanuki, Shigeki

    2015-12-01

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

  7. Deteriorating effect on bone metabolism and microstructure by passive cigarette smoking through dual actions on osteoblast and osteoclast.

    PubMed

    Ko, Chun Hay; Chan, Ruby Lok Yi; Siu, Wing Sum; Shum, Wai Ting; Leung, Ping Chung; Zhang, Lin; Cho, Chi Hin

    2015-05-01

    There is no clear evidence to show the direct causal relationship between passive cigarette smoking and osteoporosis. Furthermore, the underlying mechanism is unknown. The objective of this study is to demonstrate the effects of long-term passive cigarette smoking on bone metabolism and microstructure by a mouse model and cell culture systems. BALB/c mice were exposed to 2 or 4 % cigarette smoke for 14 weeks. The bone turnover biochemical markers in urine and serum and also the bone micro-architecture by micro-CT were compared with the control group exposed to normal ambient air. In the cell culture experiments, mouse MC3T3-E1 and RAW264.7 cell lines to be employed as osteoblast and osteoclast, respectively, were treated with the sera obtained from 4 % smoking or control mice. Their actions on cell viability, differentiation, and function on these bone cells were assessed. The urinary mineral and deoxypyridinoline (DPD) levels, and also the serum alkaline phosphatase activity, were significantly higher in the 4 % smoking group when compared with the control group, indicating an elevated bone metabolism after cigarette smoking. In addition, femoral osteopenic condition was observed in the 4 % smoking group, as shown by the decrease of relative bone volume and trabecular thickness. In isolated cell studies, osteoblast differentiation and bone formation were inhibited while osteoclast differentiation was increased. The current mouse smoking model and the isolated cell studies demonstrate that passive cigarette smoke could induce osteopenia by exerting a direct detrimental effect on bone cells differentiation and further on bone remodeling process.

  8. [The phenomenon of spreading smoking cigarettes among the students in Institute of Cosmetology and Heath Care in Bialystok].

    PubMed

    Kleszczewska, Ewa

    2007-01-01

    Tobacco smoking is one of the principal public Heath problems. The Word Heath Organization declared the addiction of tobacco smoking as a separate disease, International Classification of Diseases, ICD number F17. The health service workers play a huge part in establishing pro-health attitudes. They are expected to participate in campaigns promoting a tobacco-free lifestyle. It is important that the persons mentioned were nonsmokers. The main goal of the study was to estimate the phenomenon of spreading smoking cigarettes among the students and accomplishing their knowledge and awareness about threats resulting from tobacco smoking. The study was performed among 501 students. They answered questions concerning smoking and knowledge about nicotine dependence. The research touched such questions as conviction about damage caused by smoking, the source of information, causes and effects of smoking, about environment whether they are, the interviewee's smoking preventive activities.

  9. Desquamative interstitial pneumonia in a child related to cigarette smoke.

    PubMed

    Ischander, Mariam; Fan, Leland L; Farahmand, Vanda; Langston, Claire; Yazdani, Shahram

    2014-03-01

    An 8-year-old white male was referred to our clinic for a 1-year history of decreased appetite and no weight gain. His entire workup failed to demonstrate cystic fibrosis, or any infectious or immune-related diseases. Chest imaging and clinical picture suggested parenchymal lung disease. Histopathology examination of the video-assisted thoracoscopic biopsy of his lungs showed a desquamative interstitial pneumonia (DIP)-like pattern that resembled that of adult smokers with the same disease. Genes for surfactant proteins B and C and the transporter ABCA3 were all negative. Furthermore, lack of any genetic disorder for surfactant proteins, along with his history of heavy exposure to 10 pack-years of indoor secondhand smoke suggests that this child's DIP is due to secondhand cigarette exposure. He had nearly complete resolution of his symptoms after a year of treatments with pulse steroid and hydroxycholoroquine. To the best of our knowledge this is the first case of cigarette smoke-related DIP reported in a child.

  10. Cigarette smoke and CFTR: implications in the pathogenesis of COPD

    PubMed Central

    Rowe, Steven M.; Raju, S. Vamsee; Bebok, Zsuzsa; Matalon, Sadis; Collawn, James F.

    2013-01-01

    Chronic obstructive pulmonary disease (COPD) is a progressive respiratory disorder consisting of chronic bronchitis and/or emphysema. COPD patients suffer from chronic infections and display exaggerated inflammatory responses and a progressive decline in respiratory function. The respiratory symptoms of COPD are similar to those seen in cystic fibrosis (CF), although the molecular basis of the two disorders differs. CF is a genetic disease caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene encoding a chloride and bicarbonate channel (CFTR), leading to CFTR dysfunction. The majority of COPD cases result from chronic oxidative insults such as cigarette smoke. Interestingly, environmental stresses including cigarette smoke, hypoxia, and chronic inflammation have also been implicated in reduced CFTR function, and this suggests a common mechanism that may contribute to both the CF and COPD. Therefore, improving CFTR function may offer an excellent opportunity for the development of a common treatment for CF and COPD. In this article, we review what is known about the CF respiratory phenotype and discuss how diminished CFTR expression-associated ion transport defects may contribute to some of the pathological changes seen in COPD. PMID:23934925

  11. Effect of Tocopheryl Acetate on Maternal Cigarette Smoke Exposed Swiss Albino Mice Inbred Fetus

    PubMed Central

    Chaudhary, Janardan; Shamal, SN; Supriya, K; Srivastava, Mona; More, RS

    2016-01-01

    Introduction Cigarette smoking is worldwide problem which can be correlated with teratogenicity. Tocopheryl acetate plays as an antioxidant against the oxidative stress evolved by cigarette smoke exposure during pregnancy. Aim To study the effect of maternal exposure to cigarette smoke and Tocopheryl acetate on fetuses of mice. Materials and Methods Pregnant mice randomly assigned to different groups (Group I (control), Group II (Tocopheryl acetate), Group III(soyabean oil used as vehicle for Tocopheryl acetate), Group IV (Cigarette smoke Exposed), Group V (Cigarette smoke exposed plus Tocopheryl acetate) and Group VI(Cigarette smoke exposed plus soyabean oil) were exposed to cigarette smoke 3 times a day for 20 minutes each time and Tocopheryl acetate with dose of 200mg/kg/day in 0.3ml of soyabean oil as vehicle orally through oral gavage from the 5th day of gestation to 15th day. Results Cigarette smoke exposed mice showed significant fetal weight loss, resorption, placental anomalies, severe growth retardation, venous congestion, haemorrhage, limbs defects and enphalocele. Negligible abnormalities were seen among the control and Tocopheryl acetate group. Cigarette smoke exposed group with Tocopheryl acetate exhibited weight gain among the fetus as well as no gross abnormalities. The oxidative stress was significantly increased by increasing Malondialdehyde (MDA) 293±81.57 μmol/mg (p<0.0001) and decreasing Superoxide Dismutase (SOD) 1.43 ± 0.23mg/ml, (p<0.0001) Reduced Glutathione (GR) 0.017±0.002mg/ml, (p<0.01) and Catalase (CAT) 0.248±0.005mg/ml, (p<0.0001). Tocopheryl acetate induced group significantly maintained the oxidative stress with all p <0.0001. Conclusion It can be concluded that Tocopheryl acetate may have an ameliorating effect on the cigarette smoke during pregnancy on fetus. PMID:27891325

  12. Selenium in mainstream and sidestream smoke of cigarettes containing fly ash-grown tobacco

    SciTech Connect

    Gutenmann, W.H.; Lisk, D.J.; Shane, B.S.; Hoffmann, D.; Adams, J.D.

    1987-01-01

    The quantities of selenium, tar and nicotine present in mainstream (MS) and sidestream (SS) smoke of machine-smoked cigarettes was studied. The cigarettes were prepared from tobacco purposely cultured on fly ash-amended soil so as to increase its selenium concentration. Selenium concentration was found to be the same in the gaseous phase of both MS and SS smoke, but its concentration was significantly higher (p less than 0.05) in the particulate matter of the MS smoke. Tar was higher in MS smoke and nicotine in SS smoke. Factors affecting selenium concentrations in tobacco and its possible environmental significance are discussed.

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

    PubMed Central

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

    2014-01-01

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

  14. Influence of filter ventilation on the chemical composition of cigarette mainstream smoke.

    PubMed

    Adam, Thomas; McAughey, John; Mocker, Christoph; McGrath, Conor; Zimmermann, Ralf

    2010-01-04

    Total yields of cigarette smoke constituents are greatly influenced by smoking behaviour, the tobacco blend as well as a variety of cigarette design parameters. Thereby, filter ventilation, i.e. diluting the smoke by providing a zone of microscopic holes around the circumference of the filter is one method to reduce the yield of 'tar' and other smoke compounds. However, little is known how these design variations influence the combustion conditions, and therefore, the overall chemical pattern of the smoke. In this paper single photon ionization-time-of-flight mass spectrometry (SPI-TOFMS) is used to characterize and compare cigarettes on a puff-by-puff basis, which differ only in filter ventilation magnitude. The research cigarettes investigated were made from Virginia tobacco and featured filter ventilations of 0% (no ventilation), 35%, and 70%. The cigarettes were smoked under two different puffing regimes, one using the puffing parameters of the conventional International Organization for Standardization (ISO) smoking regime and a more intense smoking condition. Results show that every variation entails a change of the chemical pattern, whereby, in general, cigarettes with 0% filter ventilation as well as the intense smoking regime lead to a more complete combustion compared to the ISO smoking conditions and the high ventilated cigarettes. Changes in the overall patterns can also be observed during the smoking for individual puffs. Some substances dominate the first puff, some species are more pronounced in the middle puffs, whereas others are preferably formed in the last puffs. This demonstrates the high complexity of the occurring processes. Results might help to understand the formation and decomposition reactions taking place when a cigarette is smoked and offer scope for targeted reduction strategies for specific toxicants or groups of toxicants in the smoke.

  15. Cigarette smoke impairs airway epithelial barrier function and cell-cell contact recovery.

    PubMed

    Heijink, I H; Brandenburg, S M; Postma, D S; van Oosterhout, A J M

    2012-02-01

    Cigarette smoking, the major cause of chronic obstructive pulmonary disease (COPD), induces aberrant airway epithelial structure and function. The underlying mechanisms are unresolved so far. We studied effects of cigarette smoke extract (CSE) on epithelial barrier function and wound regeneration in human bronchial epithelial 16HBE cells and primary bronchial epithelial cells (PBECs) from COPD patients, nonsmokers and healthy smokers. We demonstrate that CSE rapidly and transiently impairs 16HBE barrier function, largely due to disruption of cell-cell contacts. CSE induced a similar, but stronger and more sustained, defect in PBECs. Application of the specific epidermal growth factor receptor (EGFR) inhibitor AG1478 showed that EGFR activation contributes to the CSE-induced defects in both 16HBE cells and PBECs. Furthermore, our data indicate that the endogenous protease calpain mediates these defects through tight junction protein degradation. CSE also delayed the reconstitution of 16HBE intercellular contacts during wound healing and attenuated PBEC barrier function upon wound regeneration. These findings were comparable between PBECs from smokers, healthy smokers and COPD patients. In conclusion, we demonstrate for the first time that CSE reduces epithelial integrity, probably by EGFR and calpain-dependent disruption of intercellular contacts. This may increase susceptibility to environmental insults, e.g. inhaled pathogens. Thus, EGFR may be a promising target for therapeutic strategies to improve mucosal barrier function in cigarette smoking-related disease.

  16. Periostin mediates cigarette smoke extract-induced proliferation and migration in pulmonary arterial smooth muscle cells.

    PubMed

    Wang, Xiao-Dong; Li, Fang; Ma, Dong-Bo; Deng, Xiang; Zhang, Hui; Gao, Jia; Hao, Li; Liu, Dan-Dan; Wang, Jing

    2016-10-01

    Cigarette smoking is an important risk factor for pulmonary arterial hypertension (PAH). Pulmonary arterial smooth muscle cells (PASMCs) play a critical role in the pathogenesis of PAH-associated arterial remodeling. This study was done to explore the expression and biological roles of periostin in PASMCs following exposure to cigarette smoke extract (CSE). PASMCs were exposed to different concentrations of CSE and tested for gene expression and reactive oxygen species (ROS) production. PASMCs were incubated with recombinant periostin protein or transfected with small interfering RNA targeting periostin before CSE exposure and then examined for cell proliferation and migration. Compared to control cells, exposure to CSE led to a significant upregulation of periostin. Pretreatment with 5mM N-acetyl-l-cysteine (an inhibitor of ROS formation) or 10μM U0126 (an inhibitor of ERK1/2) significantly prevented the induction of periostin in CSE-treated PASMCs. The addition of recombinant periostin protein significantly enhanced the proliferation and migration of PASMCs. In contrast, knockdown of endogenous periostin counteracted the proliferation and migration of PASMCs induced by CSE treatment. In conclusion, CSE induces the expression of periostin in PASMCs via promotion of ROS and activation of ERK1/2. Periostin mediates the effects of CSE on PASMC proliferation and migration. These findings warrant further exploration of the roles of periostin in cigarette smoking-associated pulmonary arterial remodeling.

  17. Comparison of Nicotine and Carcinogen Exposure with Water pipe and Cigarette Smoking

    PubMed Central

    Jacob, Peyton; Abu Raddaha, Ahmad H.; Dempsey, Delia; Havel, Christopher; Peng, Margaret; Yu, Lisa; Benowitz, Neal L.

    2013-01-01

    Background Smoking tobacco preparations in a water pipe (hookah) is widespread in many places of the world and is perceived by many as relatively safe. We investigated biomarkers of toxicant exposure with water pipe compared to cigarette smoking. Methods We conducted a cross-over study to assess daily nicotine and carcinogen exposure with water pipe and cigarette smoking in 13 people who were experienced in using both products. Results While smoking an average of 3 water pipe sessions compared to smoking 11 cigarettes per day, water pipe use was associated with a significantly lower intake of nicotine, greater exposure to carbon monoxide and a different pattern of carcinogen exposure compared to cigarette smoking, with greater exposure to benzene and high molecular weight PAHs, but less exposure to tobacco-specific nitrosamines, 1,3-butadiene and acrolein, acrylonitrile, propylene oxide, ethylene oxide, and low molecular weight PAHs. Conclusions A different pattern of carcinogen exposure might result in a different cancer risk profile between cigarette and water pipe smoking. Of particular concern is the risk of leukemia related to high levels of benzene exposure with water pipe use. Impact Smoking tobacco in water pipes has gained popularity in the United States and around the world. Many believe that water pipe smoking is not addictive and less harmful than cigarette smoking. We provide data on toxicant exposure that will help guide regulation and public education regarding water pipe health risk. PMID:23462922

  18. Impacts of cigarette smoking on immune responsiveness: Up and down or upside down?

    PubMed Central

    Qiu, Feifei; Liang, Chun-Ling; Liu, Huazhen; Zeng, Yu-Qun; Hou, Shaozhen; Huang, Song; Lai, Xiaoping; Dai, Zhenhua

    2017-01-01

    Cigarette smoking is associated with numerous diseases and poses a serious challenge to the current healthcare system worldwide. Smoking impacts both innate and adaptive immunity and plays dual roles in regulating immunity by either exacerbation of pathogenic immune responses or attenuation of defensive immunity. Adaptive immune cells affected by smoking mainly include T helper cells (Th1/Th2/Th17), CD4+CD25+ regulatory T cells, CD8+ T cells, B cells and memory T/B lymphocytes while innate immune cells impacted by smoking are mostly DCs, macrophages and NK cells. Complex roles of cigarette smoke have resulted in numerous diseases, including cardiovascular, respiratory and autoimmune diseases, allergies, cancers and transplant rejection etc. Although previous reviews have described the effects of smoking on various diseases and regional immunity associated with specific diseases, a comprehensive and updated review is rarely seen to demonstrate impacts of smoking on general immunity and, especially on major components of immune cells. Here, we aim to systematically and objectively review the influence of smoking on major components of both innate and adaptive immune cells, and summarize cellular and molecular mechanisms underlying effects of cigarette smoking on the immune system. The molecular pathways impacted by cigarette smoking involve NFκB, MAP kinases and histone modification. Further investigations are warranted to understand the exact mechanisms responsible for smoking-mediated immunopathology and to answer lingering questions over why cigarette smoking is always harmful rather than beneficial even though it exerts dual effects on immune responses. PMID:27902485

  19. The menthol smoker: tobacco industry research on consumer sensory perception of menthol cigarettes and its role in smoking behavior.

    PubMed

    Kreslake, Jennifer M; Wayne, Geoffrey Ferris; Connolly, Gregory N

    2008-04-01

    The use of menthol in cigarettes is actively promoted by the tobacco industry for its perceived sensory benefits, and smokers of menthol cigarettes commonly differ from nonmenthol smokers in markers of smoking behavior and addiction. In this study, we analyzed internal tobacco industry documents to describe the relationships between sensory perception and the attitudes, preferences, and patterns of cigarette use among menthol smokers. Two unique types of menthol smoker emerged from this analysis: those who cannot tolerate the harshness and irritation associated with smoking nonmenthol cigarettes, and those who seek out the specific menthol flavor and associated physical sensation. Among the first segment of menthol smokers, menthol reduces negative sensory characteristics associated with smoking. This segment of smokers may include a large proportion of occasional smokers or young people, as well as smokers who have "traded down" to a less strong cigarette because of perceived harshness or negative health effects. Some established menthol smokers, on the other hand, appear to be tolerant of and even actively seek stronger sensory attributes, including higher menthol levels. Smokers of these "stronger" menthols have traditionally been disproportionately Black and male. Some beginning or occasional smokers may adopt menthols for their mild properties and to cover up the taste of tobacco, but then develop a stronger desire for the menthol taste over time. Future research measuring smoking behavior and evaluating cessation outcomes of menthol smokers should consider the duration of menthol use and differentiate smokers according to their reasons for using menthols.

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

    SciTech Connect

    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.

  1. Is there a relation between school smoking policies and youth cigarette smoking knowledge and behaviors?

    PubMed

    Darling, Helen; Reeder, Anthony I; Williams, Sheila; McGee, Rob

    2006-02-01

    To comply with workplace legislation, New Zealand schools are required to have policies regarding tobacco smoking. Many schools also have policies to prevent tobacco use by students, including education programmes, cessation support and punishment for students found smoking. This paper investigated the associations between school policies and the prevalence of students' cigarette smoking. Furthermore, we investigated the association between school policy and students' tobacco purchasing behavior, knowledge of health effects from tobacco use and likelihood of influencing others not to smoke. Data were obtained from a self-report survey administered to 2,658 New Zealand secondary school students and staff from 63 schools selected using a multi-stage sampling procedure. Components of school policy were not significantly associated with smoking outcomes, health knowledge or health behavior, and weakly related to a punishment emphasis and students advising others to not smoke. Similarly, weak associations were found between not advising others to not smoke and policies with a punishment emphasis as well as smoke-free environments. The results suggest that having a school tobacco policy was unrelated to the prevalence of tobacco use among students, tobacco purchasing behavior and knowledge of the negative health effects of tobacco.

  2. Behavioral filter vent blocking on the first cigarette of the day predicts which smokers of light cigarettes will increase smoke exposure from blocked vents.

    PubMed

    Strasser, Andrew A; Tang, Kathy Z; Sanborn, Paul M; Zhou, Jon Y; Kozlowski, Lynn T

    2009-12-01

    Filter vent blocking on best-selling light cigarettes increases smoke yield during standard machine testing but not in clinical investigations of smokers. The purpose of the study was to investigate the effect of (a) manipulating cigarette filter vent blocking and (b) blocking status of first cigarette of the day on carbon monoxide (CO) boost. Participants (n = 25; Marlboro Lights nonmenthol cigarette smokers, age range 21-60 years, minimum 15 daily cigarettes, and daily smoking for a minimum 5 years) completed the laboratory-based, within-subject, double-blind, cross-over design of 2 smoking sessions, one utilizing a smoking topography device, one without. Each session consisted of smoking 4 cigarettes; 2 with filter vents blocked and 2 with filter vents unblocked. Spent first daily cigarette filters collected between sessions were scored for evidence of filter vent blocking. Smoking cigarettes with blocked filter vents significantly increased CO boost in both laboratory sessions (p < .001). Those who blocked their first cigarette of the day (n = 10) had significantly greater CO boost when smoking a blocked cigarette, in relation to smoking an unblocked cigarette and in comparison with nonblockers (p = .04). Total puff volume was a significant predictor of CO boost when smoking unblocked and blocked cigarettes (ps < .04). Blocking filter vents significantly increased smoke exposure in relation to when filter vents are not blocked, particularly for those who block filter vents on their first cigarette of the day. Total puff volume predicted CO boost, and results suggest that smokers adjust their smoking behavior by cigarette blocking status. Those smokers who block filter vents may be increasing their exposure by 30%.

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

    PubMed

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

    2012-01-01

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

  4. Environmental Smoking Restrictions and Light Cigarette Adoption Among Chinese Urban Smokers.

    PubMed

    Yang, Tingzhong; Jiang, Shuhan; Oliffe, John L; Feng, Xueying; Zheng, Jianzhong

    2015-08-01

    Light cigarette adoption involves complex psychological and behavioral processes with many underlying factors. While numerous studies have shown that environmental restrictions on smoking are associated with higher probability of smoking cessation, it is also possible that some smokers may switch from regular to light cigarettes due to environmental pressures. The current study evaluates whether smoking restrictions in households, workplaces, and public places were respectively associated with light cigarette adoption. A cross-sectional multistage sampling process was used to recruit participants and collect data about demographics and smoking characteristics and environmental restriction variables. Multiple logistic models were employed to examine the association between environmental smoking restrictions and light cigarette adoption. Of 4735 respondents, 1592 (30.3 %) were current smokers, and 69.7 % (N = 1141) of the smokers were identified as light cigarette adopters. In a multivariate model, smoking restrictions in households, workplaces, and public places were significantly associated with higher light cigarette adoption. Under environmental smoking restrictions, which pose unique challenges to tobacco control efforts, light cigarette adoption may increase. The study findings are essential for health policy makers in designing and implementing targeted smoking cessation interventions and health education programs.

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

    PubMed Central

    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 lung function though high prevalence is reported in Andhra Pradesh, India. Objectives: The purpose of this study was to examine whether PEFR differs between cigarette and cigar smokers compared to non-smokers and also to estimate the intensity of cigarette and cigar smoking on PEFR. Methods: PEFR was recorded in cigarette smokers (n=49) and cigar smokers (n=10) as well as in non-smokers (n=64) using Wright’s mini Peak Flow Meter. Results: PEFR is decreased in both cigarette as well in cigar smokers compared to non-smokers and the magnitude of decline was higher in cigar smoking elderly individuals. Conclusion: The intensity of cigarette and cigar smoking (pack-years) emerged as the main variable to influence airway obstruction in smokers that caused greater reduction in PEFR. PMID:24179889

  6. Cigarette smoking. January 1970-February 1989 (Citations from the NTIS data base). Report for January 1970-February 1989

    SciTech Connect

    Not Available

    1989-03-01

    This bibliography contains citations concerning the health consequences and social impact of cigarette smoking. Cigarette dependence, laws and legislation, chemical analysis of cigarettes, studies of persons apt to become smokers, behaviors associated with smoking, smoking-cessation programs, medical costs incurred from smoking, and complications from smoking when other diseases are present are explored. (This updated bibliography contains 357 citations, 58 of which are new entries to the previous edition.)

  7. Consistency of daily cigarette smoking amount in dependent adults.

    PubMed

    Perkins, Kenneth A; Jao, Nancy C; Karelitz, Joshua L

    2013-09-01

    Self-reported cigarettes per day (CPD) is a very common screening as well as dependent or independent measure in clinical and nonclinical research on smoking, but the consistency of CPD across days in dependent smokers is uncertain. Adult dependent smokers (N = 357; 170 men, 187 women) retrospectively reported "usual" CPD at screening and then prospectively self-monitored CPD on 3 consecutive days of 1 week during an ad libitum baseline period. Participants were those recruited for later tests of brief medication effects in those with high (n = 170) versus low (n = 187) interest in quitting smoking soon (within 3 months). Consistency was determined by intraclass correlation (ICC). Prospective daily CPD was generally consistent (ICC = 0.78, 95% CI of 0.74-0.81), but CPD changed (increased or decreased) by 5 cigarettes/day or more in 40% of participants and by at least 10/day in 10%. Consistency in CPD was greater in higher dependent smokers and in women with low (vs. high) quit interest, but consistency tended to be greater in men with high (vs. low) quit interest. Although retrospectively reported CPD at screening was consistent with the overall mean for prospectively monitored daily CPD, 15% of participants differed by at least 5/day between methods, and digit bias was twice as likely with retrospective versus prospective CPD, which was at chance levels. Understanding variability in CPD may improve knowledge of dependence and factors that foster or discourage daily smoking amount, but precise assessment of daily CPD likely requires prospective monitoring.

  8. Implicit attitudes toward smoking: how the smell of cigarettes influences responses of college-age smokers and nonsmokers.

    PubMed

    Glock, Sabine; Kovacs, Carrie; Unz, Dagmar

    2014-05-01

    The habit of smoking may have automatic behavioral components guided by implicit attitudes. Smokers' attitudes toward smoking should thus be less negative than nonsmokers', so that a salient smoking cue (smell) is able to activate positive aspects of these attitudes. An affective priming task was used to explore this hypothesis. Unexpectedly, smokers and nonsmokers showed equally negative implicit attitudes, irrespective of smell. Smokers exposed to the cigarette smell did, however, display generally slower responses than nonsmokers, suggesting attentional bias. This could have implications for smoking policies in contexts where attentional factors affect performance.

  9. Plain packaging of cigarettes and smoking behavior: study protocol for a randomized controlled study

    PubMed Central

    2014-01-01

    Background Previous research on the effects of plain packaging has largely relied on self-report measures. Here we describe the protocol of a randomized controlled trial investigating the effect of the plain packaging of cigarettes on smoking behavior in a real-world setting. Methods/Design In a parallel group randomization design, 128 daily cigarette smokers (50% male, 50% female) will attend an initial screening session and be assigned plain or branded packs of cigarettes to smoke for a full day. Plain packs will be those currently used in Australia where plain packaging has been introduced, while branded packs will be those currently used in the United Kingdom. Our primary study outcomes will be smoking behavior (self-reported number of cigarettes smoked and volume of smoke inhaled per cigarette as measured using a smoking topography device). Secondary outcomes measured pre- and post-intervention will be smoking urges, motivation to quit smoking, and perceived taste of the cigarettes. Secondary outcomes measured post-intervention only will be experience of smoking from the cigarette pack, overall experience of smoking, attributes of the cigarette pack, perceptions of the on-packet health warnings, behavior changes, views on plain packaging, and the rewarding value of smoking. Sex differences will be explored for all analyses. Discussion This study is novel in its approach to assessing the impact of plain packaging on actual smoking behavior. This research will help inform policymakers about the effectiveness of plain packaging as a tobacco control measure. Trial registration Current Controlled Trials ISRCTN52982308 (registered 27 June 2013). PMID:24965551

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

    PubMed

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

    2015-10-01

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

  11. Is there a role for e-cigarettes in smoking cessation?

    PubMed

    Leduc, Charlotte; Quoix, Elisabeth

    2016-04-01

    The use of e-cigarettes has dramatically increased over the past few years and their role in smoking cessation remains controversial. Several clinical studies have evaluated their efficacy in smoking cessation but most of them are prospective cohort studies. Only two randomized, controlled trials have compared e-cigarettes versus placebo or patches. A meta-analysis of these two randomized, controlled trials has been performed. Nicotine-containing e-cigarettes appear to help smokers unable to stop smoking altogether to reduce their cigarette consumption when compared with placebo. However, these results are rated 'low' by GRADE standards. Many cohort studies have been conducted, with contradictory results. For some, e-cigarettes could increase the risk of nonsmokers developing nicotine dependence and of current smokers maintaining their dependence. The debate remains open and more randomized trials are needed with long-term data about the efficacy and safety of e-cigarettes.

  12. Estimating fetal morbidity and mortality resulting from cigarette smoke exposure by measuring cotinine levels in maternal serum.

    PubMed

    Haddow, J E; Knight, G J; Palomaki, G E; Haddow, P K

    1988-01-01

    An essay for cotinine levels in maternal serum was used to define cigarette smoking exposure level and fetal morbidity and mortality. Cotinine, a metabolite of nicotine, has a circulating half-life of about a day, making it more reliable than nicotine as an indicator or active and passive smoke exposure. Maternal smoking has been linked in previous studies with low Apgar scores, low birthweight, decreased placental blood flow, fetal activity, fetal breathing movements, depressed prostacyclin synthesis in umbilical artery, increased perinatal mortality and spontaneous abortion. In this study, 8063 2nd trimester pregnant women whose serum had been collected and frozen in 1979-1983 were analyzed for smoking habit determined from intake questionnaires. Cotinine levels correlated with 95% of those reporting no smoking, and 93% of those reporting smoking. Smokers with cotinine 10 ng/ml was higher than expected, possible because some women quit before blood was drawn. Cotinine levels did not correlate as well as number of cigarettes per day reported. There was a significant association between serum cotinine and birthweight at the 10 and 20 cigarette/day level, and a trend toward a link between cotinine and fetal deaths in 2nd and 3rd trimesters. Among infants of the 30% of women exposed to passive smoke whose serum cotinine levels were 1 ng/ml, the average birth weight was 107 g lower than those of non-exposed women, a difference remaining after controlling for maternal weight and height, infant's sex, maternal age, gravidity and education.

  13. Ambivalence about smoking and cue-elicited neural activity in quitting-motivated smokers faced with an opportunity to smoke.

    PubMed

    Wilson, Stephen J; Creswell, Kasey G; Sayette, Michael A; Fiez, Julie A

    2013-02-01

    Many cigarette smokers appear to experience ambivalence about smoking, defined as the simultaneous co-occurrence of a strong desire to smoke and a strong wish to quit smoking. Research suggests that this ambivalence about smoking affects how smokers respond to cigarette-related stimuli, but many important questions remain about precisely how smoking ambivalence influences cognitive and affective processing during cigarette cue exposure. We used functional magnetic resonance imaging (fMRI) to address this knowledge gap by examining the relation between self-reported ambivalence about smoking and cue-reactivity in quitting-motivated smokers presented with an opportunity to smoke. Eighty-two quitting-motivated cigarette smokers completed a measure assessing their ambivalence about smoking. Subsequently, participants initiated an attempt to quit smoking and underwent an fMRI session, during which they were asked to hold and view a cigarette. Consistent with hypotheses, results indicated that self-reported smoking ambivalence was negatively correlated with cigarette-related activation in brain areas linked to reward-related processing, motivation, and attention (i.e., rostral anterior cingulate and medial prefrontal cortex, caudate nucleus, visual cortex). Self-reported ambivalence was not, however, correlated with activation in brain regions related to conflict processing. This pattern of results is discussed with respect to the process of change for those attempting to quit smoking.

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

    PubMed Central

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

    2013-01-01

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

  15. Cigarette Smoke Toxins Deposited on Surfaces: Implications for Human Health

    PubMed Central

    Martins-Green, Manuela; Adhami, Neema; Frankos, Michael; Valdez, Mathew; Goodwin, Benjamin; Lyubovitsky, Julia; Dhall, Sandeep; Garcia, Monika; Egiebor, Ivie; Martinez, Bethanne; Green, Harry W.; Havel, Christopher; Yu, Lisa; Liles, Sandy; Matt, Georg; Destaillats, Hugo; Sleiman, Mohammed; Gundel, Laura A.; Benowitz, Neal; Jacob, Peyton; Hovell, Melbourne; Winickoff, Jonathan P.; Curras-Collazo, Margarita

    2014-01-01

    Cigarette smoking remains a significant health threat for smokers and nonsmokers alike. Secondhand smoke (SHS) is intrinsically more toxic than directly inhaled smoke. Recently, a new threat has been discovered – Thirdhand smoke (THS) – the accumulation of SHS on surfaces that ages with time, becoming progressively more toxic. THS is a potential health threat to children, spouses of smokers and workers in environments where smoking is or has been allowed. The goal of this study is to investigate the effects of THS on liver, lung, skin healing, and behavior, using an animal model exposed to THS under conditions that mimic exposure of humans. THS-exposed mice show alterations in multiple organ systems and excrete levels of NNAL (a tobacco-specific carcinogen biomarker) similar to those found in children exposed to SHS (and consequently to THS). In liver, THS leads to increased lipid levels and non-alcoholic fatty liver disease, a precursor to cirrhosis and cancer and a potential contributor to cardiovascular disease. In lung, THS stimulates excess collagen production and high levels of inflammatory cytokines, suggesting propensity for fibrosis with implications for inflammation-induced diseases such as chronic obstructive pulmonary disease and asthma. In wounded skin, healing in THS-exposed mice has many characteristics of the poor healing of surgical incisions observed in human smokers. Lastly, behavioral tests show that THS-exposed mice become hyperactive. The latter data, combined with emerging associated behavioral problems in children exposed to SHS/THS, suggest that, with prolonged exposure, they may be at significant risk for developing more severe neurological disorders. These results provide a basis for studies on the toxic effects of THS in humans and inform potential regulatory policies to prevent involuntary exposure to THS. PMID:24489722

  16. Do cigarette smoking and alcohol consumption associate with cannabis use and problem gambling among Spanish adolescents?

    PubMed

    Míguez Varela, M Del Carmen; Becoña, Elisardo

    2015-03-01

    This article examined the relationship between cigarette smoking or alcohol consumption and cannabis use and problem gambling among a random and representative sample of 1447 Spanish adolescents (797 males and 650 females with an average of 12.8 years). An ad-hoc questionnaire was used to assess cigarette smoking, alcohol consumption (beer, wine and spirits) and cannabis use. Gambling was assessed with the South Oaks Gambling Screen Revised for Adolescents (SOGS-RA). Results indicated a positive and significant association between cigarette smoking and alcohol consumption and the two aforementioned variables. A larger percentage of cigarette smokers and drinkers was found among those participants who had consumed cannabis before or scored significantly in problem gambling. Additionally, multiple regression analysis confirmed that both cigarette smoking and alcohol consumption (beer and wine) were the most determinant variables for cannabis use and problem gambling.

  17. Plasma neuropeptide Y levels relate cigarette smoking and smoking cessation to body weight regulation.

    PubMed

    Hussain, Tajamul; Al-Daghri, Nasser M; Al-Attas, Omar S; Draz, Hossam M; Abd Al-Rahman, Sherif H; Yakout, Sobhy M

    2012-06-10

    Loss and disproportionate gain of body weight often seen respectively in smokers and quitters are believed to be due to disrupted energy homeostasis induced by nicotine, the major constituent of cigarette smoke. Energy homeostasis is suggested to be regulated by the coordinated actions of peripheral adipose tissue derived leptin and the brain hypothalamic orexigenic neuropeptide Y (NPY). While the studies probing the role of leptin and NPY in weight modulating effect of nicotine have so far been inconsistent and based largely on animal systems, there is a paucity of data involving human subjects. Here we measured the plasma levels of orexigenic neuropeptide Y (NPY) and leptin in 35 non-smokers and 31 cigarette smokers before and three months after smoking cessation. Compared to non-smokers, smokers were leaner and had reduced NPY and leptin levels. Smoking cessation resulted in a significant weight gain and increased waist circumference accompanied by increased leptin and NPY levels. NPY levels were significantly correlated with body weight (r=0.43, p<0.05), BMI (r=0.41, p<0.05), and waist circumference (r=0.37, p<0.05), while leptin correlated with BMI (r=0.42, p<0.05) and waist circumference (r=0.39, p<0.05). Association of leptin with smoking status, but not that of NPY, was lost after controlling for anthropometric parameters. Weight modulating effect of cigarette smoke may thus involve its direct action on NPY, independent of leptin. Altered leptin levels in smokers and quitters may merely reflect changes in body weight or precisely fat mass.

  18. Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells.

    PubMed

    Checa, Marco; Hagood, James S; Velazquez-Cruz, Rafael; Ruiz, Victor; García-De-Alba, Carolina; Rangel-Escareño, Claudia; Urrea, Francisco; Becerril, Carina; Montaño, Martha; García-Trejo, Semiramis; Cisneros Lira, José; Aquino-Gálvez, Arnoldo; Pardo, Annie; Selman, Moisés

    2016-01-01

    Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disease of unknown etiology. A growing body of evidence indicates that it may result from an aberrant activation of alveolar epithelium, which induces the expansion of the fibroblast population, their differentiation to myofibroblasts and the excessive accumulation of extracellular matrix. The mechanisms that activate the alveolar epithelium are unknown, but several studies indicate that smoking is the main environmental risk factor for the development of IPF. In this study we explored the effect of cigarette smoke on the gene expression profile and signaling pathways in alveolar epithelial cells. Lung epithelial cell line from human (A549), was exposed to cigarette smoke extract (CSE) for 1, 3, and 5 weeks at 1, 5 and 10% and gene expression was evaluated by complete transcriptome microarrays. Signaling networks were analyzed with the Ingenuity Pathway Analysis software. At 5 weeks of exposure, alveolar epithelial cells acquired a fibroblast-like phenotype. At this time, gene expression profile revealed a significant increase of more than 1000 genes and deregulation of canonical signaling pathways such as TGF-β and Wnt. Several profibrotic genes involved in EMT were over-expressed, and incomplete EMT was observed in these cells, and corroborated in mouse (MLE-12) and rat (RLE-6TN) epithelial cells. The secretion of activated TGF-β1 increased in cells exposed to cigarette smoke, which decreased when the integrin alpha v gene was silenced. These findings suggest that the exposure of alveolar epithelial cells to CSE induces the expression and release of a variety of profibrotic genes, and the activation of TGF-β1, which may explain at least partially, the increased risk of developing IPF in smokers.

  19. Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells

    PubMed Central

    Checa, Marco; Hagood, James S.; Velazquez-Cruz, Rafael; Ruiz, Victor; García-De-Alba, Carolina; Rangel-Escareño, Claudia; Urrea, Francisco; Becerril, Carina; Montaño, Martha; García-Trejo, Semiramis; Cisneros Lira, José; Aquino-Gálvez, Arnoldo; Pardo, Annie; Selman, Moisés

    2016-01-01

    Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disease of unknown etiology. A growing body of evidence indicates that it may result from an aberrant activation of alveolar epithelium, which induces the expansion of the fibroblast population, their differentiation to myofibroblasts and the excessive accumulation of extracellular matrix. The mechanisms that activate the alveolar epithelium are unknown, but several studies indicate that smoking is the main environmental risk factor for the development of IPF. In this study we explored the effect of cigarette smoke on the gene expression profile and signaling pathways in alveolar epithelial cells. Lung epithelial cell line from human (A549), was exposed to cigarette smoke extract (CSE) for 1, 3, and 5 weeks at 1, 5 and 10% and gene expression was evaluated by complete transcriptome microarrays. Signaling networks were analyzed with the Ingenuity Pathway Analysis software. At 5 weeks of exposure, alveolar epithelial cells acquired a fibroblast-like phenotype. At this time, gene expression profile revealed a significant increase of more than 1000 genes and deregulation of canonical signaling pathways such as TGF-β and Wnt. Several profibrotic genes involved in EMT were over-expressed, and incomplete EMT was observed in these cells, and corroborated in mouse (MLE-12) and rat (RLE-6TN) epithelial cells. The secretion of activated TGF-β1 increased in cells exposed to cigarette smoke, which decreased when the integrin alpha v gene was silenced. These findings suggest that the exposure of alveolar epithelial cells to CSE induces the expression and release of a variety of profibrotic genes, and the activation of TGF-β1, which may explain at least partially, the increased risk of developing IPF in smokers. PMID:26934369

  20. [Methane Concentration Detection System for Cigarette Smoke Based on TDLAS Technology].

    PubMed

    Yang, Ke; Zhang, Long; Wu, Xiao-song; Li, Zhi-gang; Wang, An; Liu, Yong; Ji, Min

    2015-12-01

    Rapid and real-time analysis of cigarette smoke is of great significance to study the puff-by-puff transfer rules in the suction process and to explore the relationship between smoking and health. By combining with the modified commercial smoking machine herein, cigarette smoke online analysis system was established based on the TDLAS technology. The puff-by-puff stability of this system was verified by simulated cigarette composed of a pocket containing CH₄ (volume fraction of 0.4), of which the second harmonic peaks are near 1.39. Using this system, the concentration of CH₄ in four different kinds of cigarettes was analyzed puff-by-puff by a semiconductor laser, of which center wavelength was at 1 653.72 nm. The results showed that the CH₄ concentration of cigarette smoke increased puff-by-puff. CH₄ concentration in the flue-cured cigarette is obviously higher than that of blended cigarette by comparing the content of all and puff-by-puff concentration. The puff-by-puff concentration of flue-cured cigarette increased from 400 to 900 ppm, however, the puff-by-puff concentration of blended cigarette increased from 200 to 600 ppm. Simultaneously, there was significant difference between different kinds of the flue-cured. Comparing to tradi- tional analysis methods, this system can effectively avoid the interference of other gases in the smoke cigarette as a result of its strong anti-interference. At the same time, it can finish analysis between suction interval without sample pretreatment. The technology has a good prospect in the online puff-by-puff analysis of cigarette smoke.

  1. Electronic cigarettes and thirdhand tobacco smoke: two emerging health care challenges for the primary care provider.

    PubMed

    Kuschner, Ware G; Reddy, Sunayana; Mehrotra, Nidhi; Paintal, Harman S

    2011-02-01

    PRIMARY CARE PROVIDERS SHOULD BE AWARE OF TWO NEW DEVELOPMENTS IN NICOTINE ADDICTION AND SMOKING CESSATION: 1) the emergence of a novel nicotine delivery system known as the electronic (e-) cigarette; and 2) new reports of residual environmental nicotine and other biopersistent toxicants found in cigarette smoke, recently described as "thirdhand smoke". The purpose of this article is to provide a clinician-friendly introduction to these two emerging issues so that clinicians are well prepared to counsel smokers about newly recognized health concerns relevant to tobacco use. E-cigarettes are battery powered devices that convert nicotine into a vapor that can be inhaled. The World Health Organization has termed these devices electronic nicotine delivery systems (ENDS). The vapors from ENDS are complex mixtures of chemicals, not pure nicotine. It is unknown whether inhalation of the complex mixture of chemicals found in ENDS vapors is safe. There is no evidence that e-cigarettes are effective treatment for nicotine addiction. ENDS are not approved as smoking cessation devices. Primary care givers should anticipate being questioned by patients about the advisability of using e-cigarettes as a smoking cessation device. The term thirdhand smoke first appeared in the medical literature in 2009 when investigators introduced the term to describe residual tobacco smoke contamination that remains after the cigarette is extinguished. Thirdhand smoke is a hazardous exposure resulting from cigarette smoke residue that accumulates in cars, homes, and other indoor spaces. Tobacco-derived toxicants can react to form potent cancer causing compounds. Exposure to thirdhand smoke can occur through the skin, by breathing, and by ingestion long after smoke has cleared from a room. Counseling patients about the hazards of thirdhand smoke may provide additional motivation to quit smoking.

  2. Adolescent elite athletes' cigarette smoking, use of snus, and alcohol.

    PubMed

    Martinsen, M; Sundgot-Borgen, J

    2014-04-01

    The purpose was to examine cigarette smoking, use of snus, alcohol, and performance-enhancing illicit drugs among adolescent elite athletes and controls, and possible gender and sport group differences. First-year students at 16 Norwegian Elite Sport High Schools (n = 677) and two randomly selected high schools (controls, n = 421) were invited to participate. Totally, 602 athletes (89%) and 354 (84%) controls completed the questionnaire. More controls than athletes were smoking, using snus, and drinking alcohol. Competing in team sports was associated with use of snus [odds ratio = 2.8, 95% confidence interval (CI) 1.6 to 4.7] and a similar percentage of male and female handball (22.2% vs 18.8%) and soccer players (15.7% vs 15.0%) reported using snus. For controls, not participating in organized sport was a predictor for smoking (odds ratio = 4.9, 95% CI 2.2 to 10.9). Female athletes were more prone to drink alcohol than males (46.3% vs 31.0%, P < 0.001). Only, 1.2% athletes and 2.8% controls reported use of performance-enhancing illicit drugs. In conclusion, use of legal drugs is less common among athletes, but this relationship depends on type of sport and competition level. The association between team sports and use of snus suggests that sport subcultures play a role.

  3. The human laryngeal microbiome: effects of cigarette smoke and reflux

    PubMed Central

    Jetté, Marie E.; Dill-McFarland, Kimberly A.; Hanshew, Alissa S.; Suen, Garret; Thibeault, Susan L.

    2016-01-01

    Prolonged diffuse laryngeal inflammation from smoking and/or reflux is commonly diagnosed as chronic laryngitis and treated empirically with expensive drugs that have not proven effective. Shifts in microbiota have been associated with many inflammatory diseases, though little is known about how resident microbes may contribute to chronic laryngitis. We sought to characterize the core microbiota of disease-free human laryngeal tissue and to investigate shifts in microbial community membership associated with exposure to cigarette smoke and reflux. Using 454 pyrosequencing of the 16S rRNA gene, we compared bacterial communities of laryngeal tissue biopsies collected from 97 non-treatment-seeking volunteers based on reflux and smoking status. The core community was characterized by a highly abundant OTU within the family Comamonadaceae found in all laryngeal tissues. Smokers demonstrated less microbial diversity than nonsmokers, with differences in relative abundances of OTUs classified as Streptococcus, unclassified Comamonadaceae, Cloacibacterium, and Helicobacter. Reflux status did not affect microbial diversity nor community structure nor composition. Comparison of healthy laryngeal microbial communities to benign vocal fold disease samples revealed greater abundance of Streptococcus in benign vocal fold disease suggesting that mucosal dominance by Streptococcus may be a factor in disease etiology. PMID:27775059

  4. The Synergistic Impact of Excessive Alcohol Drinking and Cigarette Smoking upon Prospective Memory

    PubMed Central

    Marshall, Anna-Marie; Heffernan, Thomas; Hamilton, Colin

    2016-01-01

    The independent use of excessive amounts of alcohol or persistent cigarette smoking have been found to have a deleterious impact upon Prospective Memory (PM: remembering future intentions and activities), although to date, the effect of their concurrent use upon PM is yet to be explored. The present study investigated the impact of the concurrent use of drinking excessive amounts of alcohol and smoking cigarettes (a “Polydrug” group) in comparison to the combined effect of the single use of these substances upon PM. The study adopted a single factorial independent groups design. The Cambridge Prospective Memory Test (CAMPROMPT) is a test of both time-based and event-based PM and was used here to measure PM. The CAMPROMPT was administered to 125 adults; an excessive alcohol user group (n = 40), a group of smokers who drink very little alcohol (n = 20), a combined user group (the “Polydrug” group) who drink excessively and smoke cigarettes (n = 40) and a non-drinker/low alcohol consumption control group (n = 25). The main findings revealed that the Polydrug users recalled significantly fewer time-based PM tasks than both excessive alcohol users p < 0.001 and smokers p = 0.013. Polydrug users (mean = 11.47) also remembered significantly fewer event-based PM tasks than excessive alcohol users p < 0.001 and smokers p = 0.013. With regards to the main aim of the study, the polydrug users exhibited significantly greater impaired time-based PM than the combined effect of single excessive alcohol users and cigarette smokers p = 0.033. However, no difference was observed between polydrug users and the combined effect of single excessive alcohol users and cigarette smokers in event-based PM p = 0.757. These results provide evidence that concurrent (polydrug) use of these two substances has a synergistic effect in terms of deficits upon time-based PM. The observation that combined excessive drinking and cigarette smoking

  5. Association between Family and Friend Smoking Status and Adolescent Smoking Behavior and E-Cigarette Use in Korea

    PubMed Central

    Joung, Myoung Jin; Han, Mi Ah; Park, Jong; Ryu, So Yeon

    2016-01-01

    Smoking is harmful to the health of adolescents because their bodies are still growing. The aim of this study was to analyze the association between the smoking status of Korean adolescents’ parents and friends and their own smoking behavior. The study assessed a nationwide sample of 72,060 middle and high students from the 10th Korea Youth Risk Behavior Web-based Survey (2014). Descriptive analysis, chi-square tests, and multiple logistic regression analysis were used to probe the association between family and friend smoking status and adolescent smoking behavior. The current cigarette smoking rates were 13.3% of boys and 4.1% of girls. The corresponding rates for electronic cigarette smoking were 4.1% and 1.5%, respectively. Higher exposure to secondhand smoke, smoking by any family member, more friends smoking, and witnessed smoking at school were associated with current smoking and electronic smoking. The smoking status of family and friends was significantly related to adolescent smoking behavior. These results should be considered in designing programs to control adolescent smoking. PMID:27898019

  6. Acculturation and cigarette smoking in Hispanic women: A meta-analysis.

    PubMed

    Kondo, Karli K; Rossi, Joseph S; Schwartz, Seth J; Zamboanga, Byron L; Scalf, Carissa D

    2016-01-01

    The present study was a random-effects model meta-analysis of 26 studies published between 1990 and 2010 (k = 32; n = 39,777) that (a) examined the association between acculturation and cigarette smoking in Hispanic women and (b) evaluated age, national origin, and measure and dimensionality (unidimensional vs. bidimensional) of acculturation as moderating variables. Results indicate a strong positive relationship and suggest larger effects of acculturation on cigarette smoking in women of Mexican descent as compared with women originating from other Latin American countries for current and lifetime smoking, as well as smoking overall. The effect of acculturation on cigarette smoking was larger in adults as compared with adolescents for current smoking and smoking overall. Few differences in effect size by measure or dimensionality of acculturation emerged. Results are discussed with regard to implications for future research and the measurement of acculturation.

  7. Acculturation and Cigarette Smoking in Hispanic Women: A Meta-Analysis

    PubMed Central

    Kondo, Karli K.; Rossi, Joseph S.; Schwartz, Seth J.; Zamboanga, Byron L.; Scalf, Carissa D.

    2015-01-01

    The present study was a random-effects model meta-analysis of 26 studies published between 1990 and 2010 (k = 32; n = 39,777) that (a) examined the association between acculturation and cigarette smoking in Hispanic women and (b) evaluated age, national origin, and measure and dimensionality (unidimensional vs. bidimensional) of acculturation as moderating variables. Results indicate a strong positive relationship and suggest larger effects of acculturation on cigarette smoking in women of Mexican descent as compared with women originating from other Latin American countries for current and lifetime smoking, as well as smoking overall. The effect of acculturation on cigarette smoking was larger in adults as compared with adolescents for current smoking and smoking overall. Few differences in effect size by measure or dimensionality of acculturation emerged. Results are discussed with regard to implications for future research and the measurement of acculturation. PMID:26114872

  8. Determination of Carbon Dioxide, Carbon Monoxide, and Methane Concentrations in Cigarette Smoke by Fourier Transform Infrared Spectroscopy

    ERIC Educational Resources Information Center

    Tan, T. L.; Lebron, G. B.

    2012-01-01

    The integrated absorbance areas of vibrational bands of CO[subscript 2], CO, and CH[subscript 4] gases in cigarette smoke were measured from Fourier transform infrared (FTIR) spectra to derive the partial pressures of these gases at different smoke times. The quantity of the three gas-phase components of cigarette smoke at different smoke times…

  9. Genomic impact of cigarette smoke, with application to three smoking-related diseases

    PubMed Central

    2012-01-01

    There is considerable evidence that inhaled toxicants such as cigarette smoke can cause both irreversible changes to the genetic material (DNA mutations) and putatively reversible changes to the epigenetic landscape (changes in the DNA methylation and chromatin modification state). The diseases that are believed to involve genetic and epigenetic perturbations include lung cancer, chronic obstructive pulmonary disease (COPD), and cardiovascular disease (CVD), all of which are strongly linked epidemiologically to cigarette smoking. In this review, we highlight the significance of genomics and epigenomics in these major smoking-related diseases. We also summarize the in vitro and in vivo findings on the specific perturbations that smoke and its constituent compounds can inflict upon the genome, particularly on the pulmonary system. Finally, we review state-of-the-art genomics and new techniques such as high-throughput sequencing and genome-wide chromatin assays, rapidly evolving techniques which have allowed epigenetic changes to be characterized at the genome level. These techniques have the potential to significantly improve our understanding of the specific mechanisms by which exposure to environmental chemicals causes disease. Such mechanistic knowledge provides a variety of opportunities for enhanced product safety assessment and the discovery of novel therapeutic interventions. PMID:22989067

  10. The effect of cigarette smoke exposure on spinal cord injury in rats.

    PubMed

    Fan, Zhong-kai; Cao, Yang; Lv, Gang; Wang, Yan-song; Guo, Zhan-peng

    2013-03-15

    In this study, we examined whether cigarette smoke has neuroprotective or toxic effects on spinal cord injury (SCI). Male Sprague-Dawley rats were included in the study and received either cigarette smoke exposure or fresh air exposure. Twenty-four hours after the last cigarette smoke or fresh air exposure, all rats were injured at thoracic level 12 (T12), using an established static compression model. Our data showed that the cigarette smoke group had higher water content; higher permeability of the blood-spinal cord barrier (BSCB); higher malondialdehyde (MDA) levels, aquaporin-4 (AQP4) and hypoxia-inducible factor 1-alpha (HIF-1α) protein expression, and mRNA levels; and lower glutathione (GSH) levels than the control group values at 12 h, 24 h, and 48 h after SCI. There was no significant difference in these between the cigarette smoke group and the control group at 0 h after SCI. The results of the Basso, Beattie, and Bresnahan (BBB) hindlimb locomotor rating scale showed that rats in the cigarette smoke group had greater dysfunction in hindlimb movement than did rats in control group from 2 to day 6 after SCI. The extent of recovery did not make any difference from day 7 to day 10 after SCI between the cigarette smoke group and the control group. These results suggested that cigarette smoke can reinforce the oxidative stress injury via HIF-1α and AQP4 in the early stage after SCI. It is possible that cigarette smoke exposure does not affect SCI recovery in the long term; however, it can aggravate the edema and deteriorate BSCB disruption via HIF-1α and AQP4 in the early stage after SCI. More studies will be essential to consider this hypothesis and elucidate the mechanisms involved.

  11. Weak Ventral Striatal Responses to Monetary Outcomes Predict an Unwillingness to Resist Cigarette Smoking

    PubMed Central

    Wilson, Stephen J.; Delgado, Mauricio R.; McKee, Sherry A.; Grigson, Patricia S.; MacLean, R. Ross; Nichols, Travis T.; Henry, Shannon L.

    2014-01-01

    As a group, cigarette smokers exhibit blunted subjective, behavioral, and neurobiological responses to nondrug incentives and rewards relative to nonsmokers. Findings from recent studies suggest, however, that there are large individual differences in the devaluation of nondrug rewards among smokers. Moreover, this variability appears to have significant clinical implications, as reduced sensitivity to nondrug rewards is associated with poorer smoking cessation outcomes. Currently, little is known about the neurobiological mechanisms that underlie these individual differences in the responsiveness to nondrug rewards. Here, we tested the hypothesis that individual variability in reward devaluation among smokers is linked to the functioning of the striatum. Specifically, functional magnetic resonance imaging was used to examine variability in the neural response to monetary outcomes in nicotine-deprived smokers anticipating an opportunity to smoke – circumstances found to heighten the devaluation of nondrug rewards by smokers in prior work. We also investigated whether individual differences in reward-related brain activity in those expecting to have access to cigarettes were associated with the degree to which the same individuals subsequently were willing to resist smoking in order to earn additional money. Our key finding was that deprived smokers who exhibited the weakest response to rewards (i.e., monetary gains) in the ventral striatum were least willing to refrain from smoking for monetary reinforcement. These results provide evidence that outcome-related signals in the ventral striatum serve as a marker for clinically meaningful individual differences in reward-motivated behavior among nicotine-deprived smokers. PMID:24777394

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

    PubMed

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

    2010-11-01

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

  13. Anxiety, Depression, and Cigarette Smoking: A Transdiagnostic Vulnerability Framework to Understanding Emotion-Smoking Comorbidity

    PubMed Central

    Leventhal, Adam M.; Zvolensky, Michael J.

    2014-01-01

    Research into the comorbidity between emotional psychopathology and cigarette smoking has often focused upon anxiety and depression’s manifest symptoms and syndromes, with limited theoretical and clinical advancement. This paper presents a novel framework to understanding emotion-smoking comorbidity. We propose that transdiagnostic emotional vulnerabilities—core biobehavioral traits reflecting maladaptive responses to emotional states that underpin multiple types of emotional psychopathology—link various anxiety and depressive psychopathologies to smoking. This framework is applied in a review and synthesis of the empirical literature on three trandiagnostic emotional vulnerabilities implicated in smoking: (1) anhedonia (Anh; diminished pleasure/interest in response to rewards); (2) anxiety sensitivity (AS; fear of anxiety-related sensations); and (3) distress tolerance (DT; ability to withstand distressing states). We conclude that Anh, AS, and DT collectively: (a) underpin multiple emotional psychopathologies; (b) amplify smoking’s anticipated and actual affect enhancing properties and other mechanisms underlying smoking; (c) promote progression across the smoking trajectory (i.e., initiation, escalation/progression, maintenance, cessation/relapse); and (d) are promising targets for smoking intervention. After existing gaps are identified, an integrative model of transdiagnostic processes linking emotional psychopathology to smoking is proposed. The model’s key premise is that Anh amplifies smoking’s anticipated and actual pleasure-enhancing effects, AS amplifies smoking’s anxiolytic effects, and poor DT amplifies smoking’s distress terminating effects. Collectively, these processes augment the reinforcing properties of smoking for individuals with emotional psychopathology to heighten risk of smoking initiation, progression, maintenance, cessation avoidance, and relapse. We conclude by drawing clinical and scientific implications from this

  14. Effect of charcoal-containing cigarette filters on gas phase volatile organic compounds in mainstream cigarette smoke.

    PubMed

    Polzin, G M; Zhang, L; Hearn, B A; Tavakoli, A D; Vaughan, C; Ding, Y S; Ashley, D L; Watson, C H

    2008-09-01

    Of the chemicals identified to date in mainstream cigarette smoke with known toxicological properties, the volatile organic compounds (VOCs) are considered the most hazardous group owing to their high abundance and toxicity. In this research we evaluate a recently introduced line of cigarettes that contain charcoal in their filters. The amount of charcoal in these filters ranged from 45 mg to 180 mg and were either dispersed among the filter material or contained in a small cavity in the filter segment. Charcoal has long been used for removing VOCs from both water and air. Our findings indicate that these cigarettes reduce machine generated mainstream smoke deliveries of a wide range of VOCs compared to a similar, non-charcoal filtered, cigarette. However, this reduction is dependent not only on the amount of charcoal present but also on the volume of smoke being drawn through the filter. While a brand with 45 mg charcoal reduces VOC delivery under ISO smoking conditions, charcoal saturation and breakthrough occur under more intense smoking conditions. Breakthrough is minimised for brands with the most charcoal. Overall, the brands with the most charcoal are effective at reducing VOC deliveries under even intense smoking conditions.

  15. Growth of fetuses of rats exposed to ethanol and cigarette smoke during gestation.

    PubMed

    Leichter, J

    1989-01-01

    Pregnant rats were exposed to cigarette smoke and ethanol separately and in combination in order to determine the interactive effects of these two drugs on outcome of pregnancy. The animals were exposed to cigarette smoke daily for a 2-hour period from day 1 to 20 of pregnancy. The ethanol was given in the drinking water in progressively higher concentrations. It was 10% for the first week and 20% during the next three weeks before mating, and 30% from day 1 to 20 of pregnancy. Exposure to cigarette smoke alone significantly reduced fetal weight when compared to pair-fed and ad libitum controls. The combination of ethanol plus smoke caused a significantly greater reduction in fetal weight than did ethanol alone. These findings indicate that prenatal exposure to the combination of alcohol and cigarette smoke exerts a synergistic rather than an additive effect on fetal growth.

  16. Comparison of cigarette and water pipe smoking among female university students in Egypt.

    PubMed

    Labib, Nargis; Radwan, Ghada; Mikhail, Nabiel; Mohamed, Mostafa K; Setouhy, Maged El; Loffredo, Christopher; Israel, Ebenezer

    2007-05-01

    This study investigated behavioral and sociodemographic factors associated with tobacco use among female university students patronizing water pipe cafes in Cairo, Egypt. We interviewed two groups of female university student smokers (100 and 96 students from a public and a private university, respectively). The interviews took place in nine water pipe cafes near the two universities. A logistic regression model was developed to analyze the relationship between tobacco-related knowledge and beliefs and the choice between smoking water pipe or cigarettes. Among these smokers, 27% smoked cigarettes only, 37.8% smoked water pipe only, and 35.2% smoked both types of tobacco. Most of the water pipe smokers (74.1%) preferred this method because they believe it to be less harmful than smoking cigarettes. More than half of the subjects were encouraged to start smoking by other females (56.6%). Curiosity was a significant factor for initiation (OR = 2.8, 95% CI = 1.3-6.2, p<.01). We found no significant differences between water pipe and cigarette smokers regarding current age, age at initiation, quit attempts, knowledge about the hazards of smoking, wanting to be fashionable, or smoking with friends. About one in four (23.7%) attempted to quit, with health cited as a major reason. An urgent need exists for correction of the misperception among this study population that water pipe smoking is safe and less harmful than cigarette smoking.

  17. Smoking among construction workers: The nonlinear influence of the economy, cigarette prices, and antismoking sentiment

    PubMed Central

    Okechukwu, Cassandra; Bacic, Janine; Cheng, Kai-Wen; Catalano, Ralph

    2012-01-01

    Little research has been conducted on the influence of macroeconomic environments on smoking among blue-collar workers, a group with high smoking prevalence and that is especially vulnerable to the effects of changing economic circumstances. Using data from 52,418 construction workers in the Tobacco Use Supplement to the United States Current Population Survey, we examined the association of labor market shock, cigarette prices, and state antismoking sentiments with smoking status and average number of cigarettes smoked daily. Data analysis included the use of multiple linear and logistic regressions, which employed the sampling and replicate weights to account for sampling design. Unemployed, American-Indian, lower-educated and lower-income workers had higher smoking rates. Labor market shock had a quadratic association, which was non-significant for smoking status and significant for number of cigarettes. The association of cigarette prices with smoking status became non-significant after adjusting for state-level antismoking sentiment. State-level antismoking sentiment had significant quadratic association with smoking status among employed workers and significant quadratic association with number of cigarettes for all smokers. The study highlights how both workplace-based smoking cessation interventions and antismoking sentiments could further contribute to disparities in smoking by employment status. PMID:22795358

  18. Smoking among construction workers: the nonlinear influence of the economy, cigarette prices, and antismoking sentiment.

    PubMed

    Okechukwu, Cassandra; Bacic, Janine; Cheng, Kai-Wen; Catalano, Ralph

    2012-10-01

    Little research has been conducted on the influence of macroeconomic environments on smoking among blue-collar workers, a group with high smoking prevalence and that is especially vulnerable to the effects of changing economic circumstances. Using data from 52,418 construction workers in the Tobacco Use Supplement to the United States Current Population Survey, we examined the association of labor market shock, cigarette prices, and state antismoking sentiments with smoking status and average number of cigarettes smoked daily. Data analysis included the use of multiple linear and logistic regressions, which employed the sampling and replicate weights to account for sampling design. Unemployed, American-Indian, lower-educated and lower-income workers had higher smoking rates. Labor market shock had a quadratic association, which was non-significant for smoking status and significant for number of cigarettes. The association of cigarette prices with smoking status became non-significant after adjusting for state-level antismoking sentiment. State-level antismoking sentiment had significant quadratic association with smoking status among employed workers and significant quadratic association with number of cigarettes for all smokers. The study highlights how both workplace-based smoking cessation interventions and antismoking sentiments could further contribute to disparities in smoking by employment status.

  19. Cigarette smoking and human papillomavirus in patients with reported cervical cytological abnormality.

    PubMed Central

    Burger, M P; Hollema, H; Gouw, A S; Pieters, W J; Quint, W G

    1993-01-01

    OBJECTIVE--To assess the relation between two risk factors for cervical neoplasia: smoking and infection with oncogenic human papillomavirus. It has been suggested that smoking causes a local immunological defect, which could facilitate the infection and persistence of human papillomavirus. DESIGN--Cross sectional epidemiological study. Completion of a structured questionnaire by the patients, analysis of cervical scrapes for human papillomavirus, and morphological examination of biopsy specimens. SETTING--Outpatient gynaecological clinic. SUBJECTS--181 women with a report of cervical cytological abnormality. MAIN OUTCOME MEASURES--Prevalence of infection with oncogenic human papillomavirus and smoking habits. RESULTS--Oncogenic human papillomavirus was found in the cervix of 26 (41%) of the 63 women who did not smoke, 22 (58%) of the 38 who smoked 1-10 cigarettes a day, 28 (61%) of the 46 who smoked 11-20 cigarettes a day, and 26 (76%) of the 34 who smoked > or = 21 cigarettes a day. The prevalence of the virus thus increased in accordance with the number of cigarettes smoked (p = 0.001). This relation remained after adjustment for age at first intercourse and lifetime number of sexual partners. Of the 63 non-smokers, 23 had previously smoked at least 10 cigarettes a day at some time. Of these 23 women, 14 (61%) had oncogenic human papillomavirus in their cervix. Of the 40 women who had never smoked at least 10 cigarettes a day, 12 (30%) had the virus. The prevalence of oncogenic human papillomavirus in non-smokers therefore depended on previous smoking habits (p = 0.03). CONCLUSION--The dose dependent effect of cigarette smoking on the occurrence of oncogenic human papillomavirus favours a causal relation between these risk factors for cervical neoplasia. PMID:8387842

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

    NASA Astrophysics Data System (ADS)

    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.

  1. Effects of Internet-Based Voucher Reinforcement and a Transdermal Nicotine Patch on Cigarette Smoking

    ERIC Educational Resources Information Center

    Glenn, Irene M.; Dallery, Jesse

    2007-01-01

    Nicotine replacement products are commonly used to promote smoking cessation, but alternative and complementary methods may increase cessation rates. The current experiment compared the short-term effects of a transdermal nicotine patch to voucher-based reinforcement of smoking abstinence on cigarette smoking. Fourteen heavy smokers (7 men and 7…

  2. Psychological Satisfactions Derived from Smoking Cigarettes in Fifty-Seven Dental Patients.

    ERIC Educational Resources Information Center

    Christen, Arden G.; Glover, Elbert D.

    1983-01-01

    Studied factors to help dentists understand smoking in patients. Dental patients (N=57) attended "quit smoking" clinics and were given the Horn Smoker's Self-Test which elicits information on factors relating to smoking. The most important functions cigarettes serve, according to smokers, were to satisfy craving, act as a crutch, and provide…

  3. Method for the Determination of Ammonia in Mainstream Cigarette Smoke Using Ion Chromatography

    PubMed Central

    Watson, Christina Vaughan; Feng, June; Valentin-Blasini, Liza; Stanelle, Rayman; Watson, Clifford H.

    2016-01-01

    Ammonia in mainstream smoke is present in both the particulate and vapor phases. The presence of ammonia in the cigarette filler material and smoke is of significance because of the potential role ammonia could have in raising the “smoke pH.” An increased smoke pH could shift a fraction of total nicotine to free-base nicotine, which is reportedly more rapidly absorbed by the smoker. Methods measuring ammonia in smoke typically employ acid filled impingers to trap the smoke. We developed a fast, reliable method to measure ammonia in mainstream smoke without the use of costly and time consuming impingers to examine differences in ammonia delivery. The method uses both a Cambridge filter pad and a Tedlar bag to capture particulate and vapor phases of the smoke. We quantified ammonia levels in the mainstream smoke of 50 cigarette brands from 5 manufacturers. Ammonia levels ranged from approximately 1μg to 23μg per cigarette for ISO smoking conditions and 38μg to 67μg per cigarette for Canadian intense smoking conditions and statistically significance differences were observed between brands and manufacturers. Our findings suggest that ammonia levels vary by brand and are higher under Canadian intense smoking conditions. PMID:27415766

  4. Cigarette Smoking among Korean International College Students in the United States

    ERIC Educational Resources Information Center

    Sa, Jaesin; Seo, Dong-Chul; Nelson, Toben F.; Lohrmann, David K.

    2013-01-01

    Objective and Participants: This study explored (1) the prevalence of cigarette smoking among South Korean international college students in the United States, (2) differences in smoking between on- and off-campus living arrangements, and (3) predictors of an increase in smoking over time in the United States Methods: An online survey was…

  5. Depressive Mood, the Single-Parent Home, and Adolescent Cigarette Smoking.

    ERIC Educational Resources Information Center

    Covey, Lirio S.; Tam, Debbie

    1990-01-01

    Examines the relationship between depressive mood and cigarette smoking among a sample of 123 adolescent males and 82 adolescent females. Finds an independent relation of depressive mood, friends' smoking behavior, and living in a single-parent home. Concludes that depressive mood and stress may contribute to the onset of smoking. (FMW)

  6. Addressing a Threat to the Healthfulness of Tomorrow's Generation: The Case of Cigarette Smoking in Nigeria

    ERIC Educational Resources Information Center

    Egbe, Catherine O.; Petersen, Inge; Meyer-Weitz, Anna

    2014-01-01

    Cigarette smoking has widely received the attention of international and local health bodies. Efforts are being made towards curbing smoking prevalence globally with a view to reduce the health, economic and social effects of smoking in the society. While some developed countries are recording success in this effort mainly through stringent…

  7. Cigarette taxes and smoking participation: evidence from recent tax increases in Canada.

    PubMed

    Azagba, Sunday; Sharaf, Mesbah

    2011-05-01

    Using the Canadian National Population Health Survey and the recent tax variation across Canadian provinces, this paper examines the impact of cigarette taxes on smoking participation. Consistent with the literature, we find evidence of a heterogeneous response to cigarette taxes among different groups of smokers. Contrary to most studies, we find that the middle age group-which constitutes the largest fraction of smokers in our sample-is largely unresponsive to taxes. While cigarette taxes remain popular with policy makers as an anti-smoking measure, identifying the socio-demographic characteristics of smokers who respond differentially to tax increase will help in designing appropriate supplementary measures to reduce smoking.

  8. Is Smokeless Tobacco Use an Appropriate Public Health Strategy for Reducing Societal Harm from Cigarette Smoking?

    PubMed Central

    Tomar, Scott L.; Fox, Brion J.; Severson, Herbert H.

    2009-01-01

    Four arguments have been used to support smokeless tobacco (ST) for harm reduction: (1) Switching from cigarettes to ST would reduce health risks; (2) ST is effective for smoking cessation; (3) ST is an effective nicotine maintenance product; and (4) ST is not a “gateway” for cigarette smoking. There is little evidence to support the first three arguments and most evidence suggests that ST is a gateway for cigarette smoking. There are ethical challenges to promoting ST use. Based on the precautionary principle, the burden of proof is on proponents to provide evidence to support their position; such evidence is lacking. PMID:19440266

  9. Cigarette smoke promotes drug resistance and expansion of cancer stem cell-like side population.

    PubMed

    An, Yi; Kiang, Alan; Lopez, Jay Patrick; Kuo, Selena Z; Yu, Michael Andrew; Abhold, Eric L; Chen, Jocelyn S; Wang-Rodriguez, Jessica; Ongkeko, Weg M

    2012-01-01

    It is well known that many patients continue to smoke cigarettes after being diagnosed with cancer. Although smoking cessation has typically been presumed to possess little therapeutic value for cancer, a growing body of evidence suggests that continued smoking is associated with reduced efficacy of treatment and a higher incidence of recurrence. We therefore investigated the effect of cigarette smoke condensate (CSC) on drug resistance in the lung cancer and head and neck cancer cell lines A549 and UMSCC-10B, respectively. Our results showed that CSC significantly increased the cellular efflux of doxorubicin and mitoxantrone. This was accompanied by membrane localization and increased expression of the multi-drug transporter ABCG2. The induced efflux of doxorubicin was reversed upon addition of the specific ABCG2 inhibitor Fumitremorgin C, confirming the role of ABCG2. Treatment with CSC increased the concentration of phosphorylated Akt, while addition of the PI3K inhibitor LY294002 blocked doxorubicin extrusion, suggesting that Akt activation is required for CSC-induced drug efflux. In addition, CSC was found to promote resistance to doxorubicin as determined by MTS assays. This CSC-induced doxurbicin-resistance was mitigated by mecamylamine, a nicotinic acetylcholine receptor inhibitor, suggesting that nicotine is at least partially responsible for the effect of CSC. Lastly, CSC increased the size of the side population (SP), which has been linked to a cancer stem cell-like phenotype. In summary, CSC promotes chemoresistance via Akt-mediated regulation of ABCG2 activity, and may also increase the proportion of cancer stem-like cells, contributing to tumor resilience. These findings underscore the importance of smoking cessation following a diagnosis of cancer, and elucidate the mechanisms of continued smoking that may be detrimental to treatment.

  10. Reduced tar, nicotine, and carbon monoxide exposure while smoking ultralow- but not low-yield cigarettes

    SciTech Connect

    Benowitz, N.L.; Jacob, P. III; Yu, L.; Talcott, R.; Hall, S.; Jones, R.T.

    1986-07-11

    An unresolved public health issue is whether some modern cigarettes are less hazardous than other and whether patients who cannot stop smoking should be advised to switch to lower-yield cigarettes. The authors studied tar (estimated by urine mutagenicity), nicotine, and carbon monoxide exposure in habitual smokers switched from their usual brand to high- (15 mg of tar), low- (5 mg of tar), or ultralow-yield (1 mg of tar) cigarettes. There were no differences in exposure comparing high- or low-yield cigarettes, but tar and nicotine exposures were reduced by 49% and 56%, respectively, and carbon monoxide exposure by 36% while smoking ultralow-yield cigarettes. Similarly, in 248 subjects smoking their self-selected brand, nicotine intake, estimated by blood concentrations of its metabolite continine, was 40% lower in those who smoked ultralow but no different in those smoking higher yields of cigarettes. The data indicate that ultralow-yield cigarettes do deliver substantial doses of tar, nicotine, and carbon monoxide, but that exposure are considerably less than for other cigarettes.

  11. A comparative study by electron paramagnetic resonance of free radical species in the mainstream and sidestream smoke of cigarettes with conventional acetate filters and 'bio-filters'.

    PubMed

    Valavanidis, A; Haralambous, E

    2001-01-01

    Tobacco smoking is the most important extrinsic cause, after the diet, for increasing morbidity and mortality in humans. Unless current tobacco smoking patterns in industrialised and non-industrialised countries change, cigarettes will kill prematurely 10 million people a year by 2025. Greece is at the top of the list of European countries in cigarette consumption. In 1997, a Greek tobacco company introduced a new 'bio-filter' (BF) claiming that it reduces substantially the risks of smoking. In a recent publication [Deliconstantinos G, Villiotou V, Stavrides J. Scavenging effects of hemoglobin and related heme containing compounds on nitric oxide, reactive oxidants and carcinogenic volatile nitrosocompounds of cigarette smoke. A new method for protection against the dangerous cigarette constituents. Anticancer Res 1994; 14: 2717-2726] it was claimed that the new 'bio-filter' (activated carbon impregnated with dry hemoglobin) reduces certain toxic substances and oxidants (like NO, CO, NOx, H2O2, aldehydes, trace elements and nitroso-compounds) in the gas-phase of the mainstream smoke. We have investigated by electron paramagnetic resonance (EPR) the mainstream and sidestream smoke of the BF cigarette, in comparison with three other cigarettes with similar tar and nicotine contents, that have conventional acetate filters. We found that BF cigarette smoke has similar tar radical species with the same intensity EPR signals to those of the other cigarettes. The ability of the aqueous cigarette tar extracts to produce hydroxyl radicals (HO*), which were spin trapped by DMPO, was very similar to, or even higher than, the other 3 brands. The gas-phase of the mainstream smoke of the BF cigarette showed a 30-35% reduction in the production of oxygen-centered radicals (spin trapped with PBN). In the case of the sidestream smoke, BF cigarettes produced substantially higher concentrations of gas-phase radicals, compared to the other brands. These results suggest that BF is

  12. Estimating the Smoking Ban Effects on Smoking Prevalence, Quitting and Cigarette Consumption in a Population Study of Apprentices in Italy

    PubMed Central

    Pieroni, Luca; Muzi, Giacomo; Quercia, Augusto; Lanari, Donatella; Rundo, Carmen; Minelli, Liliana; Salmasi, Luca; dell’Omo, Marco

    2015-01-01

    Objectives: We evaluated the effects of the Italian 2005 smoking ban in public places on the prevalence of smoking, quitting and cigarette consumption of young workers. Data and Methods: The dataset was obtained from non-computerized registers of medical examinations for a population of workers with apprenticeship contracts residing in the province of Viterbo, Italy, in the period 1996–2007. To estimate the effects of the ban, a segmented regression approach was used, exploiting the discontinuity introduced by the application of the law on apprentices’ smoking behavior. Results: It is estimated that the Italian smoking ban generally had no effect on smoking prevalence, quitting ratio, or cigarette consumption of apprentices. However, when the estimates were applied to subpopulations, significant effects were found: −1% in smoking prevalence, +2% in quitting, and −3% in smoking intensity of apprentices with at least a diploma. PMID:26287220

  13. Influence of smoking charcoal filter tipped cigarettes on various biomarkers of exposure.

    PubMed

    Scherer, Gerhard; Urban, Michael; Engl, Johannes; Hagedorn, Heinz-Werner; Riedel, Kirsten

    2006-09-01

    Charcoal (CC) filters of cigarettes are known to significantly reduce a series of volatile constituents in mainstream smoke, including reactive alpha,beta-unsaturated aldehydes such as acrolein and crotonaldehyde. We performed a randomized, crossover, 2-wk brand-switching study with 39 smokers. Twenty of the subjects smoked cellulose acetate (CA) filter tipped cigarettes during wk 1 of the study; the remaining 19 subjects smoked CC filter tipped cigarettes during wk 1. In wk 2, the subjects switched to the corresponding brand with the other filter type, with similar smoking machine-derived tar and nicotine yields. Daily cigarette consumption, carbon monoxide in exhaled breath, salivary cotinine, and urinary nicotine equivalents (molar sum of nicotine plus five major metabolites) did not change significantly when switching to the cigarettes with the other filter type. Urinary excretion rates of 3-hydroxy-1-methylpropylmercapturic acid (metabolite of crotonaldehyde), monohydroxybutenylmercapturic acid (metabolite of 1,3-butadiene), and S-phenylmercapturic acid (metabolite of benzene) were significantly lower when smoking CC compared to CA filter tipped cigarettes. The reduction in amount of 3-hydroxypropylmercapturic acid (metabolite of acrolein) was of borderline significance. Other mercapturic acids and thioethers (the latter is a summary parameter that indicates the exposure to electrophilic compounds) were not or were only slightly reduced upon smoking CC filter tipped cigarettes. We conclude that smoking CC filter tipped cigarettes does not change the uptake of carbon monoxide and nicotine when compared to CA filter tipped cigarettes with similar tar and nicotine yields, but significantly reduces the exposure to toxicologically relevant smoke constituents such as acrolein, crotonaldehyde, 1,3-butadiene, and benzene.

  14. Atorvastatin and Simvastatin Promoted Mouse Lung Repair After Cigarette Smoke-Induced Emphysema.

    PubMed

    Pinho-Ribeiro, Vanessa; Melo, Adriana Correa; Kennedy-Feitosa, Emanuel; Graca-Reis, Adriane; Barroso, Marina Valente; Cattani-Cavalieri, Isabella; Carvalho, Giovanna Marcella Cavalcante; Zin, Walter Araújo; Porto, Luis Cristóvão; Gitirana, Lycia Brito; Lanzetti, Manuella; Valença, Samuel Santos

    2017-03-01

    Cigarette smoke (CS) induces pulmonary emphysema by inflammation, oxidative stress, and metalloproteinase (MMP) activation. Pharmacological research studies have not focused on tissue repair after the establishment of emphysema but have instead focused on inflammatory stimulation. The aim of our study was to analyze the effects of atorvastatin and simvastatin on mouse lung repair after emphysema caused by CS. Male mice (C57BL/6, n = 45) were divided into the following groups: control (sham-exposed), CSr (mice exposed to 12 cigarettes a day for 60 days and then treated for another 60 days with the vehicle), CSr+A (CSr mice treated with atorvastatin for 60 days), and CSr+S (CSr mice treated with simvastatin for 60 days). The treatment with atorvastatin and simvastatin was administered via inhalation (15 min with 1 mg/mL once a day). Mice were sacrificed 24 h after the completion of the 120-day experimental procedure. We performed biochemical, morphological, and physiological analyses. We observed decreased levels of leukocytes and cytokines in statin-treated mice, accompanied by a reduction in oxidative stress markers. We also observed a morphological improvement confirmed by a mean linear intercept counting in statin-treated mice. Finally, statins also ameliorated lung function. We conclude that inhaled atorvastatin and simvastatin improved lung repair after cigarette smoke-induced emphysema in mice.

  15. Plasmacytoid dendritic cells prevent cigarette smoke and Chlamydophila pneumoniae-induced Th2 inflammatory responses.

    PubMed

    Sorrentino, Rosalinda; Gray, Pearl; Chen, Shuang; Shimada, Kenichi; Crother, Timothy R; Arditi, Moshe

    2010-10-01

    Smoking promotes the development of allergic asthma and pneumonia. Chlamydophila pneumoniae lung infection is associated with an increased risk for asthma, inducing an immune response regulated by dendritic cells (DCs). This study sought to determine whether exposure to cigarette smoke modulates the functional activity of CD11c-positive DCs in the lung, with and without concomitant C. pneumoniae infection. Bone marrow-derived DCs (BMDCs) were exposed in vitro to cigarette smoke extract (CSE) and/or live C. pneumoniae (Cpn), and then adoptively transferred intratracheally into wild-type mice. Although CSE plus Cpn appeared to exert an additive effect on the production of Th2 cytokines in vitro, we did not see this effect in vivo. However, the adoptive transfer of DCs pulsed with both CSE and C. pneumoniae into the lungs of naive mice led to an influx of plasmacytoid DCs (pDCs) that suppressed the Th2 skewing ability of the transferred BMDCs. The depletion of pDCs by antibody restored the Th2 skewing ability of the BMDCs. The expression of indoleamine-2,3-dioxygenase in the lung was reduced after the depletion of pDCs, and blocking IFN-α in vitro prevented the ability of pDCs to inhibit the Th2 responses induced by myeloid DCs (mDCs), suggesting their potential involvement in the mechanism of altered polarization. In conclusion, exposure to cigarette smoke skews C. pneumoniae-induced mDCs responses toward a Th2 bias in the lung, which is prevented by pDCs. We propose that pDCs may play a major role in the immunosuppressive lung environment in smokers with C. pneumoniae infection.

  16. Effectiveness of a Mobile Phone App for Adults That Uses Physical Activity as a Tool to Manage Cigarette Craving After Smoking Cessation: A Study Protocol for a Randomized Controlled Trial

    PubMed Central

    Lintunen, Taru; Kettunen, Tarja; Vanhala, Mauno; Toivonen, Hanna-Mari; Kinnunen, Kimmo; Heikkinen, Risto

    2015-01-01

    Background Results from studies on the effects of exercise on smoking-related variables have provided strong evidence that physical activity acutely reduces cigarette cravings. Mobile technology may provide some valuable tools to move from explanatory randomized controlled trials to pragmatic randomized controlled trials by testing the acute effectiveness of exercise on quitters under real-life conditions. An mHealth app was developed to be used as a support tool for quitters to manage their cigarette cravings. Objective The primary aim of this paper is to present the protocol of a study examining the effectiveness of the Physical over smoking app (Ph.o.S) by comparing the point prevalence abstinence rate of a group of users to a comparator group during a 6-month follow-up period. Methods After initial Web-based screening, eligible participants are recruited to attend a smoking cessation program for 3 weeks to set a quit smoking date. Fifty participants who succeed in quitting will be randomly allocated to the comparator and experimental groups. Both groups will separately have 1 more counseling session on how to manage cravings. In this fourth session, the only difference in treatment between the groups is that the experimental group will have an extra 10-15 minutes of guidance on how to use the fully automated Ph.o.S app to manage cravings during the follow-up period. Data will be collected at baseline, as well as before and after the quit day, and follow-up Web-based measures will be collected for a period of 6 months. The primary efficacy outcome is the 7-day point prevalence abstinence rate, and secondary efficacy outcomes are number of relapses and cravings, self-efficacy of being aware of craving experience, self-efficacy in managing cravings, and power of control in managing cravings. Results Recruitment for this project commenced in December 2014, and proceeded until May 2015. Follow-up data collection has commenced and will be completed by the end of

  17. Effect of cigarette smoking on copper, lead, and cadmium accumulation in human lens

    PubMed Central

    Cekic, O.

    1998-01-01

    AIM—To identify cigarette smoking as a risk factor for development of cataract, to determine the importance of copper, lead, and cadmium in cataractogenesis, and to learn about any relation between those elements.
METHODS—Copper, lead, and cadmium concentrations were measured by atomic absorption spectrophotometry in 37 cataractous and nine normal human lenses.
RESULTS—All three element accumulations in lenses with cataract were statistically meaningful. Lenticular copper, lead, and cadmium were increased significantly with cigarette smoking. Cadmium had a positive correlation both with lead and copper in cataractous lenses.
CONCLUSION—The accumulation of copper, lead, and cadmium occurs in cataract. The probable source of cadmium in humans is cigarettes. Lenticular cadmium accumulation also increases copper and lead precipitation in the lens. Cigarette smoking might be cataractogenic.

 Keywords: cigarettes; cataract; copper; lead; cadmium PMID:9613387

  18. Low-Dose Oxygen Enhances Macrophage-Derived Bacterial Clearance following Cigarette Smoke Exposure.

    PubMed

    Bain, William G; Tripathi, Ashutosh; Mandke, Pooja; Gans, Jonathan H; D'Alessio, Franco R; Sidhaye, Venkataramana K; Aggarwal, Neil R

    2016-01-01

    Background. Chronic obstructive pulmonary disease (COPD) is a common, smoking-related lung disease. Patients with COPD frequently suffer disease exacerbations induced by bacterial respiratory infections, suggestive of impaired innate immunity. Low-dose oxygen is a mainstay of therapy during COPD exacerbations; yet we understand little about whether oxygen can modulate the effects of cigarette smoke on lung immunity. Methods. Wild-type mice were exposed to cigarette smoke for 5 weeks, followed by intratracheal instillation of Pseudomonas aeruginosa (PAO1) and 21% or 35-40% oxygen. After two days, lungs were harvested for PAO1 CFUs, and bronchoalveolar fluid was sampled for inflammatory markers. In culture, macrophages were exposed to cigarette smoke and oxygen (40%) for 24 hours and then incubated with PAO1, followed by quantification of bacterial phagocytosis and inflammatory markers. Results. Mice exposed to 35-40% oxygen after cigarette smoke and PAO1 had improved survival and reduced lung CFUs and inflammation. Macrophages from these mice expressed less TNF-α and more scavenger receptors. In culture, macrophages exposed to cigarette smoke and oxygen also demonstrated decreased TNF-α secretion and enhanced phagocytosis of PAO1 bacteria. Conclusions. Our findings demonstrate a novel, protective role for low-dose oxygen following cigarette smoke and bacteria exposure that may be mediated by enhanced macrophage phagocytosis.

  19. Pyrolysis and combustion of tobacco in a cigarette smoking simulator under air and nitrogen atmosphere.

    PubMed

    Busch, Christian; Streibel, Thorsten; Liu, Chuan; McAdam, Kevin G; Zimmermann, Ralf

    2012-04-01

    A coupling between a cigarette smoking simulator and a time-of-flight mass spectrometer was constructed to allow investigation of tobacco smoke formation under simulated burning conditions. The cigarette smoking simulator is designed to burn a sample in close approximation to the conditions experienced by a lit cigarette. The apparatus also permits conditions outside those of normal cigarette burning to be investigated for mechanistic understanding purposes. It allows control of parameters such as smouldering and puff temperatures, as well as combustion rate and puffing volume. In this study, the system enabled examination of the effects of "smoking" a cigarette under a nitrogen atmosphere. Time-of-flight mass spectrometry combined with a soft ionisation technique is expedient to analyse complex mixtures such as tobacco smoke with a high time resolution. The objective of the study was to separate pyrolysis from combustion processes to reveal the formation mechanism of several selected toxicants. A purposely designed adapter, with no measurable dead volume or memory effects, enables the analysis of pyrolysis and combustion gases from tobacco and tobacco products (e.g. 3R4F reference cigarette) with minimum aging. The combined system demonstrates clear distinctions between smoke composition found under air and nitrogen smoking atmospheres based on the corresponding mass spectra and visualisations using principal component analysis.

  20. Cigarette sidestream smoke induces phosphorylated histone H2AX.

    PubMed

    Toyooka, Tatsushi; Ibuki, Yuko

    2009-05-31

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

  1. Effect of Cigarette Smoke on Salivary Total Antioxidant Capacity

    PubMed Central

    Bakhtiari, Sedigheh; Azimi, Somayyeh; Mehdipour, Masoumeh; Amini, Somayyeh; Elmi, Zahra; Namazi, Zahra

    2015-01-01

    Background and aims. Cigarette smoke can induce oral cancer by its free radicals and oxidative damage. Salivary anti-oxidants system is believed to have an important role in defense mechanisms against oxidative stress. This study was compared total antioxidant capacity (TAoC) of saliva in smokers and nonsmokers. Materials and methods. In this cross-sectional study, 30 male smokers with mean age of 45.23 years and 30 nonsmokers with mean age of 45.30 years participated. Unstimulated whole saliva samples were collected in the morning in two groups by spitting method. TAoC of saliva was measured with the special kit in two groups at the same time. Statistical analysis was performed by covariance test. Results. The mean salivary TAoC in nonsmokers (0.741±0.123 U/ml) was higher than that in smokers (0.529±0.167 U/ml). This difference was statistically significant (P<0.001). Conclusion. Smoking can alter salivary antioxidant capacity. PMID:26889367

  2. How cigarette additives are used to mask environmental tobacco smoke

    PubMed Central

    Connolly, G.; Wayne, G.; Lymperis, D.; Doherty, M.

    2000-01-01

    OBJECTIVE—To understand the tobacco industry's research on and use of cigarette additives that alter the perception of exposure to environmental tobacco smoke (ETS).
DATA SOURCES—Internal documents from four websites maintained by the major US tobacco manufacturers and company patents pertaining to the use of ETS altering additives obtained from the US Patent and Trademark Office online database.
STUDY SELECTION—Electronic searches of the four industry websites and the US patent database were conducted using keywords to identify relevant data.
DATA EXTRACTION—Industry documents and patents obtained using an exploratory snowball sampling method were reviewed and grouped into four general categories according to whether the additive(s) described affected ETS visibility, odour, irritation, or emissions. Accuracy of isolated findings was validated through cross comparison of the data sources.
DATA SYNTHESIS—Results of this preliminary study provide evidence that tobacco manufacturers have conducted extensive research on the use of chemical additives to reduce, mask, or otherwise alter the visibility, odour, irritation, or emission of ETS.
CONCLUSIONS—Findings suggest that the tobacco industry uses additives to reduce the perception of ETS. To protect the public, appropriate regulation of tobacco additives should be mandated.


Keywords: environmental tobacco smoke; tobacco industry; additives; masking PMID:10982572

  3. Acculturation, Gender, Depression, and Cigarette Smoking among U.S. Hispanic Youth: The Mediating Role of Perceived Discrimination

    ERIC Educational Resources Information Center

    Lorenzo-Blanco, Elma I.; Unger, Jennifer B.; Ritt-Olson, Anamara; Soto, Daniel; Baezconde-Garbanati, Lourdes

    2011-01-01

    Hispanic youth are at risk for experiencing depressive symptoms and smoking cigarettes, and risk for depressive symptoms and cigarette use increase as Hispanic youth acculturate to U.S. culture. The mechanism by which acculturation leads to symptoms of depression and cigarette smoking is not well understood. The present study examined whether…

  4. Application of the protection motivation theory in predicting cigarette smoking among adolescents in China.

    PubMed

    Yan, Yaqiong; Jacques-Tiura, Angela J; Chen, Xinguang; Xie, Nianhua; Chen, Jing; Yang, Niannian; Gong, Jie; Macdonell, Karen Kolmodin

    2014-01-01

    Reducing tobacco use among adolescents in China represents a significant challenge for global tobacco control. Existing behavioral theories developed in the West - such as the Protection Motivation Theory (PMT) - may be useful tools to help tackle this challenge. We examined the relationships between PMT factors and self-reported cigarette smoking behavior and intention among a random sample of vocational high school students (N=553) in Wuhan, China. Tobacco-related perceptions were assessed using the PMT Scale for Adolescent Smoking. Among the total sample, 45% had initiated cigarette smoking, and 25% smoked in the past month. Among those who never smoked, 15% indicated being likely or very likely to smoke in a year. Multiple regression modeling analysis indicated the significance of the seven PMT constructs, the four PMT perceptions and the two PMT pathways in predicting intention to smoke and actual smoking behavior. Overall, perceived rewards of smoking, especially intrinsic rewards, were consistently positively related to smoking intentions and behavior, and self-efficacy to avoid smoking was negatively related to smoking. The current study suggests the utility of PMT for further research examining adolescent smoking. PMT-based smoking prevention and clinical smoking cessation intervention programs should focus more on adolescents' perceived rewards from smoking and perceived efficacy of not smoking to reduce their intention to and actual use of tobacco.

  5. Limitations in the characterisation of cigarette products using different machine smoking regimes.

    PubMed

    Purkis, Stephen W; Troude, Valerie; Duputié, Gerald; Tessier, Christian

    2010-12-01

    It is recognised that no single machine smoking regime can represent the different behaviours of individual human smokers. It has been argued that the current ISO standard regime provides machine yields that are somewhat low for certain cigarette designs compared to human intake. Various cigarette machine smoking regimes have been proposed as options for regulatory use to provide data that reflect "average" or "maximum" yields as related to human intake. Some public health representatives have proposed that the intense regime mandated for testing in Canada with 100% of the ventilation holes in the cigarette filter blocked, should be used for product characterisation and that it is not necessary that it should reflect general human smoking behaviour. We believe that this is a flawed approach because our studies and those of other workers demonstrate that the conditions generated in the cigarette when using this intense machine smoking regime are extreme in comparison to th