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Sample records for active cigarette smoking

  1. Analyzing Cigarette Smoke.

    ERIC Educational Resources Information Center

    Jaffe, Dan; Griffin, Dale; Ricker, Janet

    1997-01-01

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

  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. 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.

  4. 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

  5. Cigarette smoking: health effects and control strategies.

    PubMed

    Alberg, Anthony J

    2008-12-01

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

  6. 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.

  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. Active and Passive Cigarette Smoking and the Risk of Cervical Neoplasia

    PubMed Central

    Trimble, Cornelia L.; Genkinger, Jeanine M.; Burke, Alyce E.; Hoffman, Sandra C.; Helzlsouer, Kathy J.; Diener-West, Marie; Comstock, George W.; Alberg, Anthony J.

    2011-01-01

    OBJECTIVE Evidence links active cigarette smoking to cervical neoplasia, but much less is known about the role of passive smoking. Using a prospective cohort design, we examined personal cigarette smoking and household passive smoke exposure in relation to the risk of cervical neoplasia. METHODS Cohorts were established based on data collected on the smoking status of all household members during private censuses of Washington County, Maryland in 1963 (n = 24,792) and 1975 (n = 26,381). Using the Washington County Cancer Registry, the occurrence of cervical neoplasia in the two cohorts was ascertained from 1963–1978 and from 1975–1994. Poisson regression models were fitted to estimate the relative risk of developing cervical neoplasia associated with active and passive smoking in both cohorts. The referent category for all comparisons was never smokers not exposed to passive smoking. RESULTS The adjusted relative risk and 95% confidence limits for passive smoking was 2.1 (1.3, 3.3) in the 1963 cohort and 1.4 (0.8, 2.4) in the 1975 cohort. The adjusted relative risk and 95% confidence limits for current smoking were 2.6 (1.7, 4.1) and 1.7 (1.1, 2.6) in the 1963 and 1975 cohort, respectively. CONCLUSION The associations were in the direction of increased risk for both passive smoking and current active smoking in both the 1963 and 1975 cohorts, but were stronger in the 1963 cohort. The results of this long-term, prospective cohort study corroborate the association between active cigarette smoking and cervical neoplasia and provide evidence that passive smoking is a risk factor for cervical neoplasia. PMID:15625160

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

    PubMed Central

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

    2013-01-01

    Background and Purpose Cigarette smoke is a major cause for chronic obstructive pulmonary disease (COPD). Andrographolide is an active biomolecule isolated from the plant Andrographis paniculata. Andrographolide has been shown to activate nuclear factor erythroid-2-related factor 2 (Nrf2), a redox-sensitive antioxidant transcription factor. As Nrf2 activity is reduced in COPD, we hypothesize that andrographolide may have therapeutic value for COPD. Experimental Approach Andrographolide was given i.p. to BALB/c mice daily 2 h before 4% cigarette smoke exposure for 1 h over five consecutive days. Bronchoalveolar lavage fluid and lungs were collected for analyses of cytokines, oxidative damage markers and antioxidant activities. BEAS-2B bronchial epithelial cells were exposed to cigarette smoke extract (CSE) and used to study the antioxidant mechanism of action of andrographolide. Key Results Andrographolide suppressed cigarette smoke-induced increases in lavage fluid cell counts; levels of IL-1β, MCP-1, IP-10 and KC; and levels of oxidative biomarkers 8-isoprostane, 8-OHdG and 3-nitrotyrosine in a dose-dependent manner. Andrographolide promoted inductions of glutathione peroxidase (GPx) and glutathione reductase (GR) activities in lungs from cigarette smoke-exposed mice. In BEAS-2B cells, andrographolide markedly increased nuclear Nrf2 accumulation, promoted binding to antioxidant response element (ARE) and total cellular glutathione level in response to CSE. Andrographolide up-regulated ARE-regulated gene targets including glutamate-cysteine ligase catalytic (GCLC) subunit, GCL modifier (GCLM) subunit, GPx, GR and heme oxygenase-1 in BEAS-2B cells in response to CSE. Conclusions Andrographolide possesses antioxidative properties against cigarette smoke-induced lung injury probably via augmentation of Nrf2 activity and may have therapeutic potential for treating COPD. PMID:23146110

  10. 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…

  11. 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...

  12. A Distinctive Alveolar Macrophage Activation State Induced by Cigarette Smoking

    PubMed Central

    Woodruff, Prescott G.; Koth, Laura L.; Yang, Yee Hwa; Rodriguez, Madeleine W.; Favoreto, Silvio; Dolganov, Gregory M.; Paquet, Agnes C.; Erle, David J.

    2005-01-01

    Rationale: Macrophages are believed to play a central role in emphysema based largely on data from mouse models. However, the relevance of these models to smoking-related lung disease in humans is uncertain. Objectives: We sought to comprehensively characterize the effects of smoking on gene expression in human alveolar macrophages and to compare these with effects seen in transgenic mouse models of emphysema. Methods: We used DNA microarrays with genomewide coverage to analyze alveolar macrophages from 15 smokers, 15 nonsmokers, and 15 subjects with asthma (disease control). Selected gene expression changes were validated by polymerase chain reaction and ELISA. Expression changes were compared with those identified by microarray analysis of interleukin-13–overexpressing and integrin-β6–deficient mice, which both develop emphysema. Measurements and Main Results: All 15 smokers shared a common pattern of macrophage gene expression that distinguished them from nonsmokers, a finding not observed in subjects with asthma. We identified 110 genes as differentially expressed in smokers despite using conservative statistical methods. Matrix metalloproteinase 12, a proteinase that plays a critical role in mouse models, was the third most highly induced gene in smokers (ninefold, p < 0.0001). However, most changes in smokers were not reflected in mouse models. One such finding was increased osteopontin expression in smokers (fourfold, p = 0.006), which was confirmed at the protein level and correlated with the degree of airway obstruction. Conclusions: Smoking induces a remarkably consistent and distinctive pattern of alveolar macrophage activation. These studies identify aspects of mouse models that are directly relevant to human smokers and also reveal novel potential mediators of smoking-related diseases. PMID:16166618

  13. Cigarette Smoke Induces Cellular Senescence

    PubMed Central

    Nyunoya, Toru; Monick, Martha M.; Klingelhutz, Aloysius; Yarovinsky, Timur O.; Cagley, Jeffrey R.; Hunninghake, Gary W.

    2006-01-01

    Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States, and cigarette smoking is the major risk factor for COPD. Fibroblasts play an important role in repair and lung homeostasis. Recent studies have demonstrated a reduced growth rate for lung fibroblasts in patients with COPD. In this study we examined the effect of cigarette smoke extract (CSE) on fibroblast proliferative capacity. We found that cigarette smoke stopped proliferation of lung fibroblasts and upregulated two pathways linked to cell senescence (a biological process associated with cell longevity and an inability to replicate), p53 and p16-retinoblastoma protein pathways. We compared a single exposure of CSE to multiple exposures over an extended time course. A single exposure to CSE led to cell growth inhibition at multiple phases of the cell cycle without killing the cells. The decrease in proliferation was accompanied by increased ATM, p53, and p21 activity. However, several important senescent markers were not present in the cells at an earlier time point. When we examined multiple exposures to CSE, we found that the cells had profound growth arrest, a flat and enlarged morphology, upregulated p16, and senescence-associated β-galactosidase activity, which is consistent with a classic senescent phenotype. These observations suggest that while a single exposure to cigarette smoke inhibits normal fibroblast proliferation (required for lung repair), multiple exposures to cigarette smoke move cells into an irreversible state of senescence. This inability to repair lung injury may be an essential feature of emphysema. PMID:16840774

  14. Effects of cigarette smoke on aerobic capacity and serum MDA content and SOD activity of animal

    PubMed Central

    Hu, Jian-Ping; Zhao, Xin-Ping; Ma, Xiao-Zhi; Wang, Yi; Zheng, Li-Jun

    2014-01-01

    Objective: Study the effects of cigarette smoke on aerobic capacity, serum MDA content and SOD activity of animal. Methods: 60 male mice are randomly divided into mild smoking group, heavy smoking group, and control group, and the exhausted swimming time, serum SOD activity and MDA content of the three groups of mice are respectively measured before and after the experiment. Results: After the experiment, the exhausted swimming time for the control group, mild smoking and heavy smoking groups is respectively 276.57 min, 215.57 min and 176.54 min, and the serum SOD activities for the three objects are 216.46 U/mL, 169.16 U/mL and 154.91 U/mL, and the MDA contents are respectively 16.41 mol/mL, 22.31 mol/mL and 23.55 mol/mL. According to the comparison, it is found that compared with the control group and pre-intervention, the exhausted swimming time and serum SOD activity of the smoking group decreases obviously, and its MDA content rises sharply, and the difference has significance (P < 0.05), moreover, the heavy smoking group has more obvious changes than the mild group. Conclusion: Cigarette smoke can significantly weaken the aerobic capacity and fatigue resistance of mice, and the more the smoking time is longer, the more the harmful effect is more serious, this is related to the SOD activity drops and MDA content rises due to smoking. PMID:25550969

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

    PubMed

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

    2014-03-01

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

  16. 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.

  17. 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.

  18. Comparison of dermal tumor promotion activity of cigarette smoke condensate from prototype (heated) cigarette and reference (combusted) cigarette in SENCAR mice.

    PubMed

    Tsuji, Hiroyuki; Okubo, Chigusa; Fujimoto, Hitoshi; Fukuda, Ichiro; Nishino, Tomoki; Lee, K Monica; Yoshimura, Hiroyuki

    2014-10-01

    Test cigarette (prototype "heated" cigarette) was evaluated on its dermal tumor promotion activity in SENCAR mice relative to conventional 3R4F cigarette. Mainstream cigarette smoke was generated under the modified Health Canada Intensive Regimen, and smoke condensate (CSCs) were collected using cold traps and extracted with acetone. Female mice received a topical application of 7,12-dimehtylbenz(a)anthracene (DMBA) as the tumor initiator on the back skin during Week 1. Subsequently, CSC was repeatedly applied as the tumor promoter at 5 doses, up to 30 mg tar/application, three times per week for 30 weeks. Test groups showed a clearly longer latency at lower doses (⩽15 mg), but the difference was less clear at higher doses (⩾22.5 mg), while mortalities were not affected throughout the study. Test groups also had consistently lower incidence and multiplicity of neoplasms, as well as lower incidences of non-neoplastic changes (e.g., inflammations and squamous epithelial hyperplasia on the site of application). The group without DMBA initiation did not induce any neoplasm but the respective Reference group showed an increase in tumorigenicity. In conclusion, the study demonstrated significant reduction in dermal irritancy and tumorigenicity of Test CSC compared to Reference CSC. PMID:25047211

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

    PubMed Central

    Geraghty, Patrick; Hardigan, Andrew

    2014-01-01

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

  20. 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.

  1. 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. PMID:26924598

  2. Alteration of human hepatic drug transporter activity and expression by cigarette smoke condensate.

    PubMed

    Sayyed, Katia; Vee, Marc Le; Abdel-Razzak, Ziad; Jouan, Elodie; Stieger, Bruno; Denizot, Claire; Parmentier, Yannick; Fardel, Olivier

    2016-07-01

    Smoking is well-known to impair pharmacokinetics, through inducing expression of drug metabolizing enzymes. In the present study, we demonstrated that cigarette smoke condensate (CSC) also alters activity and expression of hepatic drug transporters, which are now recognized as major actors of hepatobiliary elimination of drugs. CSC thus directly inhibited activities of sinusoidal transporters such as OATP1B1, OATP1B3, OCT1 and NTCP as well as those of canalicular transporters like P-glycoprotein, MRP2, BCRP and MATE1, in hepatic transporters-overexpressing cells. CSC similarly counteracted constitutive OATP, NTCP and OCT1 activities in human highly-differentiated hepatic HepaRG cells. In parallel, CSC induced expression of BCRP at both mRNA and protein level in HepaRG cells, whereas it concomitantly repressed mRNA expression of various transporters, including OATP1B1, OATP2B1, OAT2, NTCP, OCT1 and BSEP, and enhanced that of MRP4. Such changes in transporter gene expression were found to be highly correlated to those caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin, a reference activator of the aryl hydrocarbon receptor (AhR) pathway, and were counteracted, for some of them, by siRNA-mediated AhR silencing. This suggests that CSC alters hepatic drug transporter levels via activation of the AhR cascade. Importantly, drug transporter expression regulations as well as some transporter activity inhibitions occurred for a range of CSC concentrations similar to those required for inducing drug metabolizing enzymes and may therefore be hypothesized to be relevant for smokers. Taken together, these data established human hepatic transporters as targets of cigarette smoke, which could contribute to known alteration of pharmacokinetics and some liver adverse effects caused by smoking. PMID:27450509

  3. In vitro model of platelet-endothelial activation due to cigarette smoke under cardiovascular circulation conditions.

    PubMed

    Girdhar, Gaurav; Xu, Sulan; Jesty, Jolyon; Bluestein, Danny

    2008-07-01

    Cigarette smoke has been shown to increase platelet activation and endothelial cell (EC) adhesion molecule expression. In the present study, we utilized a hemodynamic shearing device (HSD) to investigate the above effects in vitro in a combined system of platelets and cultured HUVECs (Human Umblical Vein ECs) under physiological shear stress. We investigated the alteration of E-selectin expression on ECs upon exposure to: (1) platelets and nicotine-free smoke extract (NFE), (2) platelets alone, (3) NFE alone, under physiological shear stress. We additionally confirmed the protective effect of nicotine on platelet activation. We found that: (i) surface expression of E-selectin on ECs was significantly increased upon simultaneous exposure of ECs and platelets to NFE relative to exposure of ECs to either platelets or NFE alone (p < 0.05). (ii) Platelet activation was significantly increased in the presence of NFE (p < 0.05). (iii) Nicotine (200 nM) when added to NFE, significantly reduced platelet activation due to NFE (p < 0.05), an effect additionally confirmed by conventional cigarette extracts which contain nicotine (p < 0.05). We therefore conclude that: (a) NFE and platelets additively increase EC E-selectin surface expression, and (b) nicotine modulates platelet activation regardless of ECs. PMID:18452059

  4. Selective increase of antioxidant enzyme activity in the alveolar macrophages from cigarette smokers and smoke-exposed hamsters.

    PubMed

    McCusker, K; Hoidal, J

    1990-03-01

    Oxidants from cigarette smoke or those produced by phagocytes are implicated in the pathogenesis of emphysema. We reasoned that augmentation of antioxidant enzymes in cigarette smokers may be important in restricting direct and indirect oxidant damage to alveolar structures. Accordingly, we studied the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSHPx), in alveolar macrophages (AM) from cigarette smokers and from smoke-exposed hamsters. The activities of these antioxidant enzymes were compared with the activities found in AM from nonsmoking control subjects. The activities of SOD and CAT from AM of smokers and smoke-exposed hamsters were twice that found in control subjects (p less than 0.01), but there was no change in the activity of GSHPx. Using the hamster model, we found that filtration of smoke attenuated the increase in antioxidant activities, and that after smoking cessation, the increased activities had returned to those found with control subjects. An adaptive response was further suggested by prolonged survival of smoke-exposed hamsters in normobaric hyperoxia (O2 greater than 95%). Chronic smoke exposure in humans or hamsters causes increased SOD and CAT activities in AM. This augmented activity may serve as a mechanism to limit oxidant-mediated damage to alveolar structures. PMID:2310098

  5. Brain Activity in Cigarette Smokers Performing a Working Memory Task: Effect of Smoking Abstinence

    PubMed Central

    Xu, Jiansong; Mendrek, Adrianna; Cohen, Mark S.; Monterosso, John; Rodriguez, Paul; Simon, Sara L.; Brody, Arthur; Jarvik, Murray; Domier, Catherine P.; Olmstead, Richard; Ernst, Monique; London, Edythe D.

    2009-01-01

    Background When nicotine-dependent human subjects abstain from cigarette smoking, they exhibit deficits in working memory. An understanding of the neural substrates of such impairments may help to understand how nicotine affects cognition. Our aim, therefore, was to identify abnormalities in the circuitry that mediates working memory in nicotine-dependent subjects after they initiate abstinence from smoking. Methods We used blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI) to study eight smokers while they performed a letter version of the N-Back working memory task under satiety (≤1.5 hours abstinence) and abstinence (≥14 hours abstinence) conditions. Results Task-related activity in the left dorsal lateral prefrontal cortex (DLPFC) showed a significant interaction between test session (satiety, abstinence) and task load (1-back, 2-back, and 3-back). This interaction reflected the fact that task-related activity in the satiety condition was relatively low during performance of the 1-back task but greater at the more difficult task levels, whereas task-related activity in the abstinence condition was relatively high at the 1-back level and did not increase at the more difficult task levels. Conclusions We conclude that neural processing related to working memory in the left DLPFC is less efficient during acute abstinence from smoking than at smoking satiety. PMID:16038685

  6. The biology behind the atherothrombotic effects of cigarette smoke.

    PubMed

    Csordas, Adam; Bernhard, David

    2013-04-01

    Cigarette smoke is an aerosol that contains >4,000 chemicals, including nicotine, carbon monoxide, acrolein, and oxidant compounds. Exposure to cigarette smoke induces multiple pathological effects in the endothelium, several of which are the result of oxidative stress initiated by reactive oxygen species, reactive nitrogen species, and other oxidant constituents of cigarette smoke. Cigarette-smoke exposure interferes adversely with the control of all stages of plaque formation and development and pathological thrombus formation. The reactive oxygen species in cigarette smoke contribute to oxidative stress, upregulation of inflammatory cytokines, and endothelial dysfunction, by reducing the bioavailability of nitric oxide. Plaque formation and the development of vulnerable plaques also result from exposure to cigarette smoke via the enhancement of inflammatory processes and the activation of matrix metalloproteases. Moreover, exposure to cigarette smoke results in platelet activation, stimulation of the coagulation cascade, and impairment of anticoagulative fibrinolysis. Many cigarette-smoke-mediated prothrombotic changes are quickly reversible upon smoking cessation. Public health efforts should urgently promote our understanding of current cigarette-smoke-induced cardiovascular pathology to encourage individuals to reduce their exposure to cigarette smoke and, therefore, the detrimental consequences of associated atherothrombotic disease. PMID:23380975

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

    PubMed Central

    Kitamura, S

    1987-01-01

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

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

    PubMed

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

    2015-08-01

    The urokinase plasminogen activator receptor (uPAR) gene (PLAUR) has been identified as an asthma susceptibility gene, with polymorphisms within that gene being associated with baseline lung function, lung function decline, and lung function in a smoking population. Soluble cleaved uPAR (scuPAR), a molecule identified as a marker of increased morbidity and mortality in a number of diseases, has been shown to be elevated in the airways of patients with asthma and in patients with chronic obstructive pulmonary disease. However, the functionality of soluble receptor isoforms and their relationship with an important initiator for obstructive lung disease, cigarette smoke, remains undefined. In this study, we set out to determine the effect of cigarette smoke on soluble uPAR isoforms, its regulatory pathway and the resultant effect on bronchial epithelial cell function. We identified a positive association between cigarette pack-years and uPAR expression in the airway bronchial epithelium of biopsies from patients with asthma (n = 27; P = 0.0485). In vitro, cigarette smoke promoted cleavage of uPAR from the surface of bronchial epithelial cells (1.5× induction; P < 0.0001) and induced the soluble spliced isoform through changes in messenger RNA expression (∼2× change; P < 0.001), driven by loss of endogenous 3' untranslated region suppression. Elevated expression of the soluble isoforms resulted in a proremodeling cell phenotype, characterized by increased proliferation and matrix metalloproteinase-9 expression in primary bronchial epithelial cells. This suggests that cigarette smoke elevates soluble receptor isoforms in bronchial epithelial cells through direct (cleavage) and indirect (messenger RNA expression) means. These findings provide further insight into how cigarette smoke may influence changes in the airways of importance to airway remodeling and obstructive lung disease progression. PMID:25490122

  9. Assessing the mutagenic activities of smoke from different cigarettes in direct exposure experiments using the modified Ames Salmonella assay.

    PubMed

    Ishikawa, Shinkichi; Kanemaru, Yuki; Nara, Hidenori; Erami, Kazuo; Nagata, Yasufumi

    2016-06-01

    The Ames assay is useful for evaluating the mutagenic potentials of chemicals, and it has been used to evaluate the mutagenic potential of cigarette smoke (CS). In vitro direct exposure systems have been developed to mimic CS exposure in the human respiratory tract, and the Ames assay has been used with such systems. Ames tests were performed using the Vitrocell(®) direct exposure system in this study. The mutagenic potentials of whole mainstream CS and gas/vapor phase fractions produced by conventional combustible cigarettes under two smoking regimens were compared. Salmonella Typhimurium TA98 and TA100 were used with and without metabolic activation, and the number of revertants induced by exposure to each CS was determined. The amount of smoke particles to which cells were exposed were also determined, and dose-response curves describing the relationships between exposure to smoke particles and the number of revertants induced were plotted. The slopes of linear regressions of the dose-response curves were determined, and the slope for each CS was used as a mutagenic activity index for that CS. A new heated cigarette was also tested and smoke from the heated cigarette had a lower mutagenic activity in TA98 and TA100 with metabolic activation than did the conventional CS. The results indicate that the direct exposure system and the Ames test can be used to determine the mutagenic potentials of CS produced by different cigarettes under different conditions (i.e., using different Salmonella Typhimurium strains with and without metabolic activation, and using different smoking conditions). PMID:27265375

  10. CIGARETTE SMOKE AND LUNG CANCER

    EPA Science Inventory

    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 speci...

  11. Estimating cotinine associations and a saliva cotinine level to identify active cigarette smoking in alaska native pregnant women.

    PubMed

    Smith, Julia J; Robinson, Renee F; Khan, Burhan A; Sosnoff, Connie S; Dillard, Denise A

    2014-01-01

    Studies indicate nicotine metabolism varies by race and can change during pregnancy. Given high rates of tobacco use and limited studies among Alaska Native (AN) women, we estimated associations of saliva cotinine levels with cigarette use and second-hand smoke (SHS) exposure and estimated a saliva cotinine cutoff to distinguish smoking from non-smoking pregnant AN women. Using questionnaire data and saliva cotinine, we utilized multi-variable linear regression (n = 370) to estimate cotinine associations with tobacco use, SHS exposure, demographic, and pregnancy-related factors. Additionally, we estimated an optimal saliva cotinine cutoff for indication of active cigarette use in AN pregnant women using receiver operating characteristic (ROC) curve analysis (n = 377). Saliva cotinine significantly decreased with maternal age and significantly increased with cigarettes smoked per day, SHS exposure, and number of previous full term pregnancies. Using self-reported cigarette use in the past 7 days as indication of active smoking, the area under the ROC curve was 0.975 (95 % CI: 0.960-0.990). The point closest to 100 % specificity and sensitivity occurred with a cotinine concentration of 1.07 ng/mL, which corresponded to sensitivity of 94 % and specificity of 94 %. We recommend using a saliva cotinine cutoff of 1 ng/mL to distinguish active smoking in pregnant AN women. This cutoff is lower than used in other studies with pregnant women, most likely due to high prevalence of light or intermittent smoking in the AN population. Continued study of cotinine levels in diverse populations is needed. PMID:23423858

  12. Microcirculatory dysfunction induced by cigarette smoking.

    PubMed

    Lehr, H A

    2000-12-01

    This review deals with the deleterious effects of cigarette smroking on the microcirculation, both in terms of morphological (i.e., vessel wall injury, capillary loss) and functional aspects. The latter concerns predominantly changes in tissue perfusion and its regullatory mechanisms (i.e., reactive hyperemia, sequestration of blood cells in the microcirculation). The mechanisms of action of cigarette smoking on the microcirculation include compromised endothelial-dependent voasorelaxation, platelet aggregation, emdothelial cell dysfunction and the activation of circulating leukocytes. Through these mechanisms, cigarette smoking elicits the aggregation and adhesion of leukocytes and/or platelets to the microvascular endothelium in venules and arterioles, as assessed by intravital fluorescence microscopy in the hamster skinfold chamber model. This model has allowed us to learn more about the participation of reactive oxygen species, inflammatory mediators, and adhesion molecules in the orchestration of microcirculatory dysfunction after cigarette smoking. In the final part of this review, the clinical consequences of microcirculatory dysfunction are discussed and an outlook is offered on potential prophylactic interventions (i.e., antioxidant vitamins) aimed at abrogating the deleterious action of cigarette smoking on the microcirculation. PMID:11142334

  13. Histochemical evidence for generation of active oxygen species on the apical surface of cigarette-smoke-exposed tracheal explants.

    PubMed Central

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

    1991-01-01

    Cigarette smoke is known to contain many types of free radicals, and solutions of smoke tar have been shown to liberate hydrogen peroxide as well as superoxide radical. To further investigate the relationship of smoke exposure and generation of active oxygen species, the authors exposed rat tracheal explants to varying amounts of smoke for 10 minutes in a humidified chamber. After smoke exposure was completed, tracheal segments were incubated in a modification of the ultrastructural cerium chloride technique that was devised by Briggs et al. to demonstrate hydrogen peroxide production. Smoke dose-dependent deposition of cerium-containing reaction product was found on the cilia and the apical membranes; with low-dose smoke, the reaction product appeared as individual dots along the apical surface, but with greater amounts of smoke, heavy linear deposits of reaction product were found along the apical membranes. Smoke produced focal dose-related cell damage with blebbing of the apical membranes, loss of cilia, and focal cell necrosis. Catalase prevented both the positive histochemical reaction and the cell damage; if the catalase was first boiled, its protective effect was destroyed. Similarly, after smoke exposure was completed, tracheal segments were covered with a solution of nitroblue tetrazolium to demonstrate production of superoxide anion. A positive reaction was observed by light microscopy on the surface of tracheas that was exposed to smoke but not that exposed to air; the reaction could be prevented by addition of superoxide dismutase. The authors conclude that exposure of tracheal explants to cigarette smoke in vitro is associated with histochemical evidence of continuing production of both hydrogen peroxide and superoxide anion at the apical cell membrane. Images Figure 1 Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 PMID:1653519

  14. Cigarette smoke exposure triggers the autophagic cascade via activation of the AMPK pathway in mice.

    PubMed

    Furlong, Hayley C; Stämpfli, Martin R; Gannon, Anne M; Foster, Warren G

    2015-10-01

    We previously demonstrated that cigarette smoke (CS) exposure decreases primordial follicle counts and induces autophagy in ovarian granulosa cells in preference to apoptosis. Therefore, the objective of this study was to investigate molecular targets underlying smoke-induced activation of the reparative autophagy pathway in the ovary. Briefly, ovarian homogenates were prepared from adult female mice exposed to mainstream CS twice daily for 8 wk, using a whole-body exposure system. A gene array revealed that CS exposure induced a greater than 2-fold significant increase in the expression of proautophagic genes Cdkn1b, Map1lc3a, Bad, and Sqstm1/p62. A significant increase in Prkaa2, Pik3c3, and Maplc31b expression, as well as a significant decrease in Akt1 and Mtor expression, was detected by quantitative PCR. The 5'-AMP-activated protein kinase catalytic subunit (AMPK) alpha1 + alpha2 and ATG7 protein expression was significantly increased, whereas AKT1, mTOR, CDKN1B/p27, and CXCR4 proteins were significantly decreased in CS exposed versus control ovaries. Up-regulation of AMPK alpha1 + alpha2, a known initiator of autophagic signaling, and ATG7 further suggests activation of the autophagy cascade. Two prosurvival factors, AKT and mTOR, were decreased in expression, an outcome that favors induction of the autophagy pathway, whereas decreased levels of CDKN1B is suggestive of cell cycle dysregulation. In summary, our data suggest that CS exposure induces ovarian follicle loss through induction of the autophagic cascade via the AMPK pathway together with inhibition of antiautophagic markers AKT and mTOR. We further postulate that toxicant-induced dysregulation of reparative autophagy is a novel pathway central to impaired follicle development and subfertility. PMID:26377221

  15. TIME SERIES MODEL FOR CIGARETTE SMOKING ACTIVITY PATTERNS: MODEL VALIDATION FOR CARBON MONOXIDE AND RESPIRABLE PARTICLES IN A CHAMBER AND AN AUTOMOBILE

    EPA Science Inventory

    Human activity pattern-exposure models require accurate submodels for the exposures in microenvironments that people occupy, including those containing environmental tobacco smoke (ETS). his paper describes the Sequential Cigarette Exposure Model (SCEM), a general-purpose mathema...

  16. 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

  17. 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.

  18. 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.

  19. 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

  20. Cigarette smoking behavior in conjoined twins.

    PubMed

    Jarvik, M E; Gritz, E R; Rose, J E

    1983-01-01

    A study of cigarette smoking was undertaken in a pair of craniopagus twins to determine how a transfer of products of smoking is occurring between the twins. Alternately and independently, one twin smoked a nicotine-free cigarette, then the second twin smoked a nicotine-containing cigarette. The procedure enabled the investigators to study the migration of nicotine and carbon monoxide from one twin to the other. Salivary determination provided a noninvasive method of measuring cross circulation in conjoined twins. Measurements of salivary nicotine, however, indicated that, although the nicotine levels rose following smoking, there was relatively little transfer from one twin to the other through the circulation. PMID:6673459

  1. Analysis of complex mixtures--cigarette smoke.

    PubMed

    Borgerding, Michael; Klus, Hubert

    2005-07-01

    Mainstream cigarette smoke is a complex mixture that is inhaled into the respiratory system. The physical characteristics and chemical composition of mainstream smoke are reviewed and briefly compared with that of sidestream smoke. Special attention is paid to ageing effects and artifact formation during the sampling and testing of cigarette smoke, with specific examples of artifact formation during sampling discussed (nitrogen dioxide, methyl nitrite, etc.). Historically, the generation of cigarette smoke for chemical and biological testing has been based on standard smoke generation procedures that are intended for product comparisons. More recently, emerging global regulations have called for alternative smoke generation methods, with emphasis on results relevant to conditions of product use, e.g., estimates of maximum smoke emissions. Strategies for establishing such alternative smoke generation methods are discussed and the potential effects of alternative smoking conditions on analytical accuracy and precision are addressed. Current regulatory requirements that include Hoffmann analyte analysis (i.e., constituents reported to be associated with the risks of cigarette smoking) are also summarized and the potential effect of alternative smoke generation methods on individual constituent yields considered. Finally, a limited critique of emerging regulation that relates to mainstream cigarette smoke measurements, including a discussion of recent WHO recommendations, is offered. PMID:16092717

  2. Alcohol drinking and cigarette smoking: a "partner" for gastric ulceration.

    PubMed

    Ko, J K; Cho, C H

    2000-12-01

    Alcohol consumption and cigarette smoking are two etiologic factors that have a close relationship with peptic ulcer diseases. Chronic active gastritis is reportedly associated with chronic alcohol ingestion. Nonetheless, the inflammatory changes are likely to be related to concurrent Helicobacter pylori infection that is common among alcoholics. Moreover, chronic alcoholism is also correlated with the presence of gastric metaplasia. Both clinically and experimentally, alcohol had been shown to affect the mucosal barrier and histology. These ulcerogenic effects play a crucial role in altering gastric mucosal defense mechanisms. Cigarette smoking is coupled with the initiation and prolongation of gastric ulcers. Epidemiologic data show that cigarette smoking increases both the incidence and relapse rate of peptic ulcer diseases and also delays ulcer healing in humans. Retrospective studies also indicate that cigarette smoking is a key factor in inducing ulcer diseases rather than a linked behavior. The general detrimental effects of cigarette smoking in the gastric mucosa include reduction of circulating epidermal growth factor, increase in tissue free radical production and the presence of free radicals in smoke, together with reduction of mucosal constitutive nitric oxide synthase activity. Furthermore, the alteration of normal gastric mucosal blood flow and angiogenesis and the suppression of cell proliferation contribute largely to the delay in ulcer healing in cigarette smokers. Concurrent consumption of alcohol and cigarette smoking significantly increases the risk of gastric ulcers. In animal experiments, cigarette smoking potentiated ethanol-induced gastric mucosal damage. The reduction of mucus secretion, increase in leukotriene B4 level, increased activities of inducible nitric oxide synthase, xanthine oxidase and myeloperoxidase, and the expression of adhesion molecules in the gastric mucosa accompanied such potentiating effects. Substances other than

  3. Candy cigarettes: do they encourage children's smoking?

    PubMed

    Klein, J D; Forehand, B; Oliveri, J; Patterson, C J; Kupersmidt, J B; Strecher, V

    1992-01-01

    Candy and bubble gum cigarettes are packaged to resemble cigarette brands, and so they may encourage young children to smoke. Two studies of the role of these products in the development of children's attitudes and behaviors toward smoking were conducted. In the first study, six focus group interviews were conducted with 25 children in three age groups (4 through 5, 6 through 8, and 9 through 11 years old). Children in each group were shown five candy and snack foods and asked about their opinions and experiences with each item. In the second study, 195 seventh-grade students in a southeastern city school system were surveyed about their cigarette smoking and candy cigarette use. In the focus groups, candy cigarettes were recognized by most children. Young children played with the candy cigarettes more than with other candy or snack items and made general references to smoking behaviors. Older children made favorable references to smoking behavior; most knew which stores sold candy cigarettes, and many had chosen to buy and use these items, despite parental disapproval. Candy cigarettes may play a role in the development of children's attitudes toward smoking as an acceptable, favorable, or normative behavior. Elimination of these products should be part of efforts to prevent initiation of smoking by children. PMID:1728016

  4. 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.

  5. [Smoking history worldwide--cigarette smoking, passive smoking and smoke free environment in Switzerland].

    PubMed

    Brändli, Otto

    2010-08-01

    After the invention of the cigarette 1881 the health consequences of active smoking were fully known only in 1964. Since 1986 research findings allow increasingly stronger conclusions about the impact of passive smoking on health, especially for lung cancer, cardiovascular and respiratory disease in adults and children and the sudden infant death syndrome. On the basis of current consumption patterns, approximately 450 million adults will be killed by smoking between 2000 and 2050. At least half of these adults will die between age 30 and 69. Cancer and total deaths due to smoking have fallen so far only in men in high-income countries but will rise globally unless current smokers stop smoking before or during middle age. Higher taxes, regulations on smoking, including 100 % smoke free indoor spaces, and information for consumers could avoid smoking-associated deaths. Irland was 2004 the first country worldwide introducing smoke free bars and restaurants with positive effects on compliance, health of employees and business. In the first year after the introduction these policies have resulted in a 10 - 20 % reduction of acute coronary events. In Switzerland smoke free regulations have been accepted by popular vote first in the canton of Ticino in 2006 and since then in 15 more cantons. The smoking rate dropped from 33 to 27 % since 2001. PMID:20687040

  6. 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.

  7. 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.

  8. 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.

  9. Quercetin protects primary human osteoblasts exposed to cigarette smoke through activation of the antioxidative enzymes HO-1 and SOD-1.

    PubMed

    Braun, Karl F; Ehnert, Sabrina; Freude, Thomas; Egaña, José T; Schenck, Thilo L; Buchholz, Arne; Schmitt, Andreas; Siebenlist, Sebastian; Schyschka, Lilianna; Neumaier, Markus; Stöckle, Ulrich; Nussler, Andreas K

    2011-01-01

    Smokers frequently suffer from impaired fracture healing often due to poor bone quality and stability. Cigarette smoking harms bone cells and their homeostasis by increased formation of reactive oxygen species (ROS). The aim of this study was to investigate whether Quercetin, a naturally occurring antioxidant, can protect osteoblasts from the toxic effects of smoking. Human osteoblasts exposed to cigarette smoke medium (CSM) rapidly produced ROS and their viability decreased concentration- and time-dependently. Co-, pre- and postincubation with Quercetin dose-dependently improved their viability. Quercetin increased the expression of the anti-oxidative enzymes heme-oxygenase- (HO-) 1 and superoxide-dismutase- (SOD-) 1. Inhibiting HO-1 activity abolished the protective effect of Quercetin. Our results demonstrate that CSM damages human osteoblasts by accumulation of ROS. Quercetin can diminish this damage by scavenging the radicals and by upregulating the expression of HO-1 and SOD-1. Thus, a dietary supplementation with Quercetin could improve bone matter, stability and even fracture healing in smokers. PMID:22203790

  10. 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.

  11. BEHAVIOR OF CIGARETTE SMOKE IN HUMAN AIRWAYS

    EPA Science Inventory

    Experimental deposition patterns of cigarette smoke in surrogate human airway systems are very heterogeneous. article deposits are enhanced at predictable, well-defined morphological regions; most specifically, carinal ridges within bifurcation zones, and along posterior sections...

  12. An Ecological View of Cigarette Smoking

    ERIC Educational Resources Information Center

    Mausner, Bernard

    1973-01-01

    Evidence indicates many smokers use cigarettes as an important aid to coping and as an ego-enhancer. Paper read at the American Cancer Society Conference on Smoking in Tucson, Arizona, on March 30 and 31, 1972. (DS)

  13. 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.

  14. E-Cigarettes a Gateway to Smoking for Teens

    MedlinePlus

    ... page: https://medlineplus.gov/news/fullstory_159340.html E-Cigarettes a Gateway to Smoking for Teens: Study ... who had never smoked, but who had used e-cigarettes, were substantially more likely to begin smoking ...

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

    PubMed

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

    2015-03-01

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

  16. Cigarette smoke induces proinflammatory cytokine release by activation of NF-kappaB and posttranslational modifications of histone deacetylase in macrophages.

    PubMed

    Yang, Se-Ran; Chida, Asiya S; Bauter, Mark R; Shafiq, Nusrat; Seweryniak, Kathryn; Maggirwar, Sanjay B; Kilty, Iain; Rahman, Irfan

    2006-07-01

    Cigarette smoke-mediated oxidative stress induces an inflammatory response in the lungs by stimulating the release of proinflammatory cytokines. Chromatin remodeling due to histone acetylation and deacetylation is known to play an important role in transcriptional regulation of proinflammatory genes. The aim of this study was to investigate the molecular mechanism(s) of inflammatory responses caused by cigarette smoke extract (CSE) in the human macrophage-like cell line MonoMac6 and whether the treatment of these cells with the antioxidant glutathione (GSH) monoethyl ester, or modulation of the thioredoxin redox system, can attenuate cigarette smoke-mediated IL-8 release. Exposure of MonoMac6 cells to CSE (1% and 2.5%) increased IL-8 and TNF-alpha production vs. control at 24 h and was associated with significant depletion of GSH levels associated with increased reactive oxygen species release in addition to activation of NF-kappaB. Inhibition of IKK ablated the CSE-mediated IL-8 release, suggesting that this process is dependent on the NF-kappaB pathway. CSE also reduced histone deacetylase (HDAC) activity and HDAC1, HDAC2, and HDAC3 protein levels. This was associated with posttranslational modification of HDAC1, HDAC2, and HDAC3 protein by nitrotyrosine and aldehyde-adduct formation. Pretreatment of cells with GSH monoethyl ester, but not thioredoxin/thioredoxin reductase, reversed cigarette smoke-induced reduction in HDAC levels and significantly inhibited IL-8 release. Thus cigarette smoke-induced release of IL-8 is associated with activation of NF-kappaB via IKK and reduction in HDAC levels/activity in macrophages. Moreover, cigarette smoke-mediated proinflammatory events are regulated by the redox status of the cells. PMID:16473865

  17. Naloxone does not affect cigarette smoking.

    PubMed

    Nemeth-Coslett, R; Griffiths, R R

    1986-01-01

    In order to provide information about the hypothesis that endogenous opioids mediate the reinforcing properties of cigarette smoking, the present study examined the effects of naloxone, an opioid antagonist, on cigarette smoking in seven normal volunteers. The study used experimental procedures that had previously been shown sensitive for detecting the effects of other drugs, (including a nicotine antagonist) on smoking. Isolated subjects smoked their regular brand of cigarettes freely in a naturalistic laboratory environment while watching television or reading. Sixty minutes before each 2 h smoking session subjects received an IM injection of naloxone HCl (0.0625, 0.25, 1.0, or 4.0 mg/kg) or placebo. Each subject received each treatment three times in a mixed order across days. Naloxone did not significantly affect any measure of cigarette smoking including number of cigarettes, number of puffs, or expired air carbon monoxide level. Naloxone did, however, produce significant dose-related increases in subject ratings of yawning, stretching, and relaxation. The results of the present study provide no support for the endogenous opioid theory of smoking reinforcement. PMID:3088648

  18. Active Cigarette Smoking in Cognitively-Normal Elders and Probable Alzheimer's Disease is Associated with Elevated Cerebrospinal Fluid Oxidative Stress Biomarkers.

    PubMed

    Durazzo, Timothy C; Korecka, Magdalena; Trojanowski, John Q; Weiner, Michael W; O' Hara, Ruth; Ashford, John W; Shaw, Leslie M

    2016-07-25

    Neurodegenerative diseases and chronic cigarette smoking are associated with increased cerebral oxidative stress (OxS). Elevated F2-isoprostane levels in biological fluid is a recognized marker of OxS. This study assessed the association of active cigarette smoking with F2-isoprostane in concentrations in cognitively-normal elders (CN), and those with mild cognitive impairment (MCI) and probable Alzheimer's disease (AD). Smoking and non-smoking CN (n = 83), MCI (n = 164), and probable AD (n = 101) were compared on cerebrospinal fluid (CSF) iPF2α-III and 8,12, iso-iPF2α-VI F2-isoprostane concentrations. Associations between F2-isoprostane levels and hippocampal volumes were also evaluated. In CN and AD, smokers had higher iPF2α-III concentration; overall, smoking AD showed the highest iPF2α-III concentration across groups. Smoking and non-smoking MCI did not differ on iPF2α-III concentration. No group differences were apparent on 8,12, iso-iPF2α-VI concentration, but across AD, higher 8,12, iso-iPF2α-VI level was related to smaller left and total hippocampal volumes. Results indicate that active cigarette smoking in CN and probable AD is associated with increased central nervous system OxS. Further investigation of factors mediating/moderating the absence of smoking effects on CSF F2-isoprostane levels in MCI is warranted. In AD, increasing magnitude of OxS appeared to be related to smaller hippocampal volume. This study contributes additional novel information to the mounting body of evidence that cigarette smoking is associated with adverse effects on the human central nervous system across the lifespan. PMID:27472882

  19. 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

  20. Menthol attenuates respiratory irritation responses to multiple cigarette smoke irritants

    PubMed Central

    Willis, Daniel N.; Liu, Boyi; Ha, Michael A.; Jordt, Sven-Eric; Morris, John B.

    2011-01-01

    Menthol, the cooling agent in peppermint, is added to almost all commercially available cigarettes. Menthol stimulates olfactory sensations, and interacts with transient receptor potential melastatin 8 (TRPM8) ion channels in cold-sensitive sensory neurons, and transient receptor potential ankyrin 1 (TRPA1), an irritant-sensing channel. It is highly controversial whether menthol in cigarette smoke exerts pharmacological actions affecting smoking behavior. Using plethysmography, we investigated the effects of menthol on the respiratory sensory irritation response in mice elicited by smoke irritants (acrolein, acetic acid, and cyclohexanone). Menthol, at a concentration (16 ppm) lower than in smoke of mentholated cigarettes, immediately abolished the irritation response to acrolein, an agonist of TRPA1, as did eucalyptol (460 ppm), another TRPM8 agonist. Menthol's effects were reversed by a TRPM8 antagonist, AMTB. Menthol's effects were not specific to acrolein, as menthol also attenuated irritation responses to acetic acid, and cyclohexanone, an agonist of the capsaicin receptor, TRPV1. Menthol was efficiently absorbed in the respiratory tract, reaching local concentrations sufficient for activation of sensory TRP channels. These experiments demonstrate that menthol and eucalyptol, through activation of TRPM8, act as potent counterirritants against a broad spectrum of smoke constituents. Through suppression of respiratory irritation, menthol may facilitate smoke inhalation and promote nicotine addiction and smoking-related morbidities.— Willis, D. N., Liu, B., Ha, M. A., Jordt, S.-E., Morris, J. B. Menthol attenuates respiratory irritation responses to multiple cigarette smoke irritants. PMID:21903934

  1. 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

  2. Cigarette smoking, nicotine dependence, and treatment.

    PubMed Central

    Sees, K L

    1990-01-01

    Since the 1988 Surgeon General's report on nicotine addiction, more attention is being given to nicotine dependence as a substantial contributing factor in cigarette smokers' inability to quit. Many new medications are being investigated for treating nicotine withdrawal and for assisting in long-term smoking abstinence. Medications alone probably will not be helpful; they should be used as adjuncts in comprehensive smoking abstinence programs that address not only the physical dependence on nicotine but also the psychological dependence on cigarette smoking. PMID:2190425

  3. Activation of the UPR Protects against Cigarette Smoke-induced RPE Apoptosis through Up-Regulation of Nrf2*

    PubMed Central

    Huang, Chuangxin; Wang, Joshua J.; Ma, Jacey H.; Jin, Chenjin; Yu, Qiang; Zhang, Sarah X.

    2015-01-01

    Recent studies have revealed a role of endoplasmic reticulum (ER) stress-induced unfolded protein response (UPR) in the regulation of RPE cell activity and survival. Herein, we examined the mechanisms by which the UPR modulates apoptotic signaling in human RPE cells challenged with cigarette smoking extract (CSE). Our results show that CSE exposure induced a dose- and time-dependent increase in ER stress markers, enhanced reactive oxygen species (ROS), mitochondrial fragmentation, and apoptosis of RPE cells. These changes were prevented by the anti-oxidant NAC or chemical chaperone TMAO, suggesting a close interaction between oxidative and ER stress in CSE-induced apoptosis. To decipher the role of the UPR, overexpression or down-regulation of XBP1 and CHOP genes was manipulated by adenovirus or siRNA. Overexpressing XBP1 protected against CSE-induced apoptosis by reducing CHOP, p-p38, and caspase-3 activation. In contrast, XBP1 knockdown sensitized the cells to CSE-induced apoptosis, which is likely through a CHOP-independent pathway. Surprisingly, knockdown of CHOP reduced p-eIF2α and Nrf2 resulting in a marked increase in caspase-3 activation and apoptosis. Furthermore, Nrf2 inhibition increased ER stress and exacerbated cell apoptosis, while Nrf2 overexpression reduced CHOP and protected RPE cells. Our data suggest that although CHOP may function as a pro-apoptotic gene during ER stress, it is also required for Nrf2 up-regulation and RPE cell survival. In addition, enhancing Nrf2 and XBP1 activity may help reduce oxidative and ER stress and protect RPE cells from cigarette smoke-induced damage. PMID:25568320

  4. Prostate cancer risk and diet, recreational physical activity and cigarette smoking.

    PubMed

    Darlington, Gerarda Ann; Kreiger, Nancy; Lightfoot, Nancy; Purdham, James; Sass-Kortsak, Andrea

    2007-01-01

    Associations between prostate cancer and dietary factors, physical activity and smoking were assessed based on data from a population-based case-control study. The study was conducted among residents of northeastern Ontario. Cases were identified from the Ontario Cancer Registry and diagnosed between 1995 and 1998 at ages 50 to 84 years (N=752). Male controls were identified from telephone listings and were frequency matched to cases on age (N=1,613). Logistic regression analyses investigated history of diet, physical activity and smoking as potential risk factors. Tomato intake had a significant positive association with prostate cancer risk for highest versus lowest quartiles (OR=1.6; 95 percent CI: 1.2-2.0). Associations were observed for tomato or vegetable juices and ketchup (OR=1.5; 95 percent CI: 1.2-1.9; OR=1.2; 95 percent CI: 1.0-1.5, respectively). Neither other dietary variables nor smoking were associated with prostate cancer risk. Strenuous physical activity by men in their early 50s was associated with reduced risk (OR=0.8; 95 percent CI: 0.6-0.9). While the recreational physical activity association was consistent with results from previous studies, the tomato products association was not. PMID:17623560

  5. Youth smoking, cigarette prices, and anti-smoking sentiment.

    PubMed

    Decicca, Philip; Kenkel, Donald; Mathios, Alan; Shin, Yoon-Jeong; Lim, Jae-Young

    2008-06-01

    In this paper, we develop a new direct measure of state anti-smoking sentiment and merge it with micro-data on youth smoking in 1992 and 2000. The empirical results from the cross-sectional models show two consistent patterns: after controlling for differences in state anti-smoking sentiment, the price of cigarettes has a weak and statistically, insignificant influence on smoking participation, and state anti-smoking sentiment appears to have a potentially important influence on youth smoking participation. The cross-sectional results are corroborated by results from the discrete time hazard models of smoking initiation that include state-fixed effects. However, there is evidence of price-responsiveness in the conditional cigarette demand by youth and young adult smokers. PMID:17935201

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

    PubMed Central

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

    2015-01-01

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

  7. Cigarette smoke-induced kinin B1 receptor promotes NADPH oxidase activity in cultured human alveolar epithelial cells.

    PubMed

    Talbot, Sébastien; Lin, James Chi-Jen; Lahjouji, Karim; Roy, Jean-Philippe; Sénécal, Jacques; Morin, André; Couture, Réjean

    2011-07-01

    Pulmonary inflammation is an important pathological feature of tobacco smoke-related lung diseases. Kinin B1 receptor (B1R) is up-regulated in the rat trachea chronically exposed to cigarette-smoke. This study aimed at determining (1) whether exposure to total particulate matter of the cigarette smoke (TPM) can induce B1R in human alveolar epithelial A549 cells, (2) the mechanism of B1R induction, (3) the functionality of de novo synthesized B1R, and (4) the role of B1R in TPM-induced increase of superoxide anion (O₂(●⁻)) level. Results show that A549 cells exposed to 10 μg/ml TPM increased O₂(●⁻) level along with B1R (protein and mRNA) and IL-1β mRNA. In contrast, B2R and TNF-α mRNA were not affected by TPM. The increasing effect of TPM on O₂(●⁻) level was not significantly affected by the B1R antagonist SSR240612. TPM-increased B1R mRNA was prevented by co-treatments with N-acetyl-l-cysteine (potent antioxidant), diphenyleneiodonium (NADPH oxidase inhibitor), IL-1Ra (interleukin-1R antagonist) and SN-50 (specific inhibitor of NF-kB activation) but not by pentoxifylline (TNF-α release inhibitor), indomethacin and niflumic acid (COX-1 and -2 inhibitors). Stimulation of B1R with a selective agonist (des-Arg⁹-BK, 10 μM; 30 min) increased O₂(●⁻)production which was prevented by apocynin and diphenyleneiodonium (NADPH oxidase inhibitors). Data suggest that the increased expression of B1R by TPM in A549 cells is mediated by oxidative stress, IL-1β and NF-kB but not by cyclooxygenases or TNF-α. The amplification of O₂(●⁻) levels via the activation of B1R-NADPH oxidase may exacerbate pulmonary inflammation and contribute to the chronicity of tobacco smoke-related lung diseases. PMID:21600945

  8. The Effects of Cigarette Smoke Condensate and Nicotine on Periodontal Tissue in a Periodontitis Model Mouse

    PubMed Central

    Mori, Kenta; Hasegawa, Shiori; Yamashita, Motozo; Yamada, Satoru; Kitamura, Masahiro; Murakami, Shinya

    2016-01-01

    Cigarette smoking is a major lifestyle-related risk factor for periodontal diseases. However, the pathophysiological role of cigarette smoking in periodontal disease has yet to be fully elucidated. Here we report that the systemic administration of cigarette smoke condensate or nicotine, which is the major ingredient of cigarette smoke, augmented alveolar bone loss. Concomitantly, the number of osteoclasts in periodontal tissues increased and the expression of receptor activator of nuclear factor κB ligand was upregulated at the ligated side in mice with periodontitis. Nicotine also attenuated alveolar bone repair after ligature removal. These observations highlight the destruction of periodontal tissue by smoking and the unfavorable clinical course of periodontal disease in patients with a cigarette smoking habit. The present study demonstrates that periodontal disease models are useful for elucidating the pathogenesis of cigarette smoking-related periodontal diseases. PMID:27203240

  9. 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...

  10. Percentage of U.S. Adults Who Smoke Cigarettes

    MedlinePlus

    ... Coverage Percentage of Adults Who Smoke Cigarettes by Medicaid Coverage 6mph-3zwu Download these data » Click on ... Coverage Percentage of Adults Who Smoke Cigarettes by Medicare Coverage 5pgf-ueam Download these data » Click on ...

  11. Percentage of U.S. Adolescents Who Smoke Cigarettes

    MedlinePlus

    ... U.S. Adolescents Who Smoke Cigarettes Percentage of U.S. Adolescents Who Smoke Cigarettes Tobacco use is the leading ... This measure is calculated by the Division of Adolescent and School Health, National Center for Chronic Disease ...

  12. Cigarette smoke extract affects mitochondrial function in alveolar epithelial cells.

    PubMed

    Ballweg, Korbinian; Mutze, Kathrin; Königshoff, Melanie; Eickelberg, Oliver; Meiners, Silke

    2014-12-01

    Cigarette smoke is the main risk factor for chronic obstructive pulmonary disease (COPD). Exposure of cells to cigarette smoke induces an initial adaptive cellular stress response involving increased oxidative stress and induction of inflammatory signaling pathways. Exposure of mitochondria to cellular stress alters their fusion/fission dynamics. Whereas mild stress induces a prosurvival response termed stress-induced mitochondrial hyperfusion, severe stress results in mitochondrial fragmentation and mitophagy. In the present study, we analyzed the mitochondrial response to mild and nontoxic doses of cigarette smoke extract (CSE) in alveolar epithelial cells. We characterized mitochondrial morphology, expression of mitochondrial fusion and fission genes, markers of mitochondrial proteostasis, as well as mitochondrial functions such as membrane potential and oxygen consumption. Murine lung epithelial (MLE)12 and primary mouse alveolar epithelial cells revealed pronounced mitochondrial hyperfusion upon treatment with CSE, accompanied by increased expression of the mitochondrial fusion protein mitofusin 2 and increased metabolic activity. We did not observe any alterations in mitochondrial proteostasis, i.e., induction of the mitochondrial unfolded protein response or mitophagy. Therefore, our data indicate an adaptive prosurvival response of mitochondria of alveolar epithelial cells to nontoxic concentrations of CSE. A hyperfused mitochondrial network, however, renders the cell more vulnerable to additional stress, such as sustained cigarette smoke exposure. As such, cigarette smoke-induced mitochondrial hyperfusion, although part of a beneficial adaptive stress response in the first place, may contribute to the pathogenesis of COPD. PMID:25326581

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

    PubMed

    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

  14. 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

  15. Alpha radioactivity in cigarette smoke. [/sup 210/Po

    SciTech Connect

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

    1980-07-01

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

  16. Cigarette smoke, asbestos, and small irregular opacities

    SciTech Connect

    Weiss, W.

    1984-08-01

    The long-term inhalation of cigarette smoke is associated with the appearance of diffuse small irregular opacities of mild profusion on chest roentogenograms of some subjects in a limited number of reports. Human histologic and experimental animal studies have shown the presence of pulmonary interstitial fibrosis. The radiographic abnormalities may be explained by interstitial fibrosis, although bronchiolar wall thickening may also be involved. Because asbestos causes diffuse pulmonary fibrosis, the literature was reviewed for evidence concerning an interaction between cigarette smoke and asbestos in the frequency of pulmonary asbestosis. A majority of 14 prevalence studies and 7 cohort studies of asbestos workers with information on smoking habits have shown a positive interaction between the 2 agents. The interaction appears to be additive rather than synergistic. Smoking may exert an effect on the frequency of pulmonary asbestosis by increasing the effective fiber dose retained in the lungs through interference with clearance.

  17. Determinants of Cigarette Smoking Initiation in Jordanian Schoolchildren: Longitudinal Analysis

    PubMed Central

    Attonito, Jennifer; Madhivanan, Purnima; Yi, Qilong; Mzayek, Fawaz; Maziak, Wasim

    2015-01-01

    Objective: To identify determinants of cigarette smoking initiation, by gender, among schoolchildren in Irbid, Jordan. Methods: Between 2008 and 2011, data were collected annually using self-reported questionnaires over 4-years in a prospective cohort of 1,781 students recruited from all 7th grade classes in 19 secondary schools, selected out of a total 60, using probability-proportionate-to-size method. Independent predictors of smoking initiation were identified among the cigarette naïve participants (N = 1,454) with mixed-effect multivariable logistic regression. Results: Participants were 12.6 years of age on average at baseline. 29.8% of the 1,454 students (37.2% of boys and 23.7% of girls) initiated cigarette smoking by 10th grade. Of those who initiated (n = 498), 47.2% of boys and 37.2% of girls initiated smoking in the 8th grade. Determinants of cigarette smoking initiation included ever smoking a waterpipe, low cigarette refusal self-efficacy, intention to start smoking cigarettes, and having friends who smoked. For girls, familial smoking was also predictive of cigarette initiation. Conclusion: This study shows that many Jordanian youth have an intention to initiate cigarette smoking and are susceptible to cigarette smoking modeled by peers and that girls are influenced as well by familial cigarette smoking. Prevention efforts should be tailored to address culturally relevant gender norms, help strengthen adolescents’ self-efficacy to refuse cigarettes, and foster strong non-smoking social norms. PMID:25143297

  18. Vegetative effects of Stroop-test solving and cigarette smoking.

    PubMed

    Suter, T W; Bättig, K

    1982-01-01

    The vegetative effects of cigarette smoking were investigated in 28 male smokers required to answer STROOP stimuli and in 16 smokers tested under yoked conditions. The smoking effects were considerably more pronounced in the yoked group than in the task solving groups. Psychophysiological reactivity to solving the STROOP task only tented to be influenced by smoking. A possible role for the reinforcing effects of smoking in this type of experiment can therefore be seen more in the vegetative activation preparatory to coping with the task than in the modulation of the task-induced vegetative responses. PMID:7183087

  19. 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

    2016-01-01

    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

  20. 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

  1. Menthol attenuates respiratory irritation responses to multiple cigarette smoke irritants.

    PubMed

    Willis, Daniel N; Liu, Boyi; Ha, Michael A; Jordt, Sven-Eric; Morris, John B

    2011-12-01

    Menthol, the cooling agent in peppermint, is added to almost all commercially available cigarettes. Menthol stimulates olfactory sensations, and interacts with transient receptor potential melastatin 8 (TRPM8) ion channels in cold-sensitive sensory neurons, and transient receptor potential ankyrin 1 (TRPA1), an irritant-sensing channel. It is highly controversial whether menthol in cigarette smoke exerts pharmacological actions affecting smoking behavior. Using plethysmography, we investigated the effects of menthol on the respiratory sensory irritation response in mice elicited by smoke irritants (acrolein, acetic acid, and cyclohexanone). Menthol, at a concentration (16 ppm) lower than in smoke of mentholated cigarettes, immediately abolished the irritation response to acrolein, an agonist of TRPA1, as did eucalyptol (460 ppm), another TRPM8 agonist. Menthol's effects were reversed by a TRPM8 antagonist, AMTB. Menthol's effects were not specific to acrolein, as menthol also attenuated irritation responses to acetic acid, and cyclohexanone, an agonist of the capsaicin receptor, TRPV1. Menthol was efficiently absorbed in the respiratory tract, reaching local concentrations sufficient for activation of sensory TRP channels. These experiments demonstrate that menthol and eucalyptol, through activation of TRPM8, act as potent counterirritants against a broad spectrum of smoke constituents. Through suppression of respiratory irritation, menthol may facilitate smoke inhalation and promote nicotine addiction and smoking-related morbidities. PMID:21903934

  2. Metabolic activation of organic extracts from diesel, coke oven, roofing tar, and cigarette smoke emissions in the Ames Assay

    SciTech Connect

    Williams, K.; Lewtas, J.

    1985-01-01

    Four environmental emissions samples were ranked by their genotoxic potency in several bioassays. Although the relative potency of a series of automotive emissions (diesel and gasoline) in the Ames assay correlated well with the relative potency in mammalian cell and mouse skin, this was not the case for the coke oven, roofing tar, and cigarette smoke condensate (CSC) emissions. This study examines the role of metabolic activation in determining the difference between a microbial and a mammalian bioassay in ranking the genotoxic potency of these environmental emissions. Uninduced and Aroclor 1254-induced S9 from both rat and hamster liver were compared as the metabolic activator in the Ames assay with Salmonella typhimurium TA98. The diesel emissions sample was direct-acting while the other samples required activation. The standard S9 concentration also produced the maximum mutagenic activity. The relative potency of these four samples was not significantly different between the microbial (Ames), mammalian cell (mouse lymphoma), and tumor initiation (mouse skin) assays. These results suggest that the differences observed between the relative mutagenic activity of these emissions in the mammalian cell and microbial assays was not due to a lack of optimization of the S9 system but may be inherent in the different response of the indicator cells to different chemical classes.

  3. Metabolic activation of organic extracts from diesel, coke oven, roofing tar, and cigarette smoke emissions in the Ames assay

    SciTech Connect

    Williams, K.; Lewtas, J.

    1985-01-01

    The role of metabolic activation in the difference between a microbial and mammalian bioassays in the ranking of genotoxic potency of several environmental emissions was investigated. Although the relative potency in the Ames assay correlated well with the relative potency in mammalian cell and mouse skin for a series of automotive emissions (diesel and gasoline), this was not the case for the coke oven, roofing tar, and cigarette smoke condensate (CSC) emissions. The study examined several parameters of the metabolic activation with Salmonella typhimurium TA98 including S9 concentration and a comparison of Aroclor-1254 induced with uninduced S9 from both rat and hamster liver. The diesel-emissions sample was direct acting while the other samples required activation. The standard S9 concentration (approximately 1.25 mg protein/plate) also produced the maximum mutagenic activity. Induced S9s produced higher mutagenic activity than uninduced. The hamster S9 gave significantly higher mutagenic activies than rat S9 for the coke oven and CSC.

  4. 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.

  5. 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…

  6. Cigarette smoke induces cell motility via platelet-activating factor accumulation in breast cancer cells: a potential mechanism for metastatic disease

    PubMed Central

    Kispert, Shannon; Marentette, John; McHowat, Jane

    2015-01-01

    Most cancer deaths are a result of metastasis rather than the primary tumor. Although cigarette smoking has been determined as a risk factor for several cancers, its role in metastasis has not been studied in detail. We propose that cigarette smoking contributes to metastatic disease via inhibition of breast cancer cell platelet-activating factor acetylhydrolase (PAF-AH), resulting in PAF accumulation and a subsequent increase in cell motility. We studied several breast cell lines, including immortalized mammary epithelial cells (MCF-10A), luminal A hormone positive MCF-7, basal-like triple negative MDA-MB-468, and claudin-low triple-negative highly metastatic MDA-MB-231 breast tumor cells. We exposed cells to cigarette smoke extract (CSE) for up to 48 h. CSE inhibited PAF-AH activity, increased PAF accumulation, and increased cell motility in MDA-MB-231 metastatic triple negative breast cancer cells. The calcium-independent phospholipase A2 (iPLA2) inhibitor, (S) bromoenol lactone ((S)-BEL) was used to prevent the accumulation of PAF and further prevented the increase in cell motility seen previously when cells were exposed to CSE. Thus, iPLA2 or PAF may represent a therapeutic target to manage metastatic disease, particularly in triple-negative breast cancer patients who smoke. PMID:25802360

  7. 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

  8. 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

    2016-03-01

    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. PMID:27007390

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

    PubMed Central

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

    2016-01-01

    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. PMID:27007390

  10. Menthol pharmacology and its potential impact on cigarette smoking behavior.

    PubMed

    Ahijevych, Karen; Garrett, Bridgette E

    2004-02-01

    Menthol is the only tobacco additive promoted and advertised by the tobacco industry. Although a considerable body of research has examined the effects of menthol when it is administered alone and unburned, the effects of menthol when burned in cigarette smoke are more complex because it is administered in a matrix of more than 4,000 substances. Therefore, it is difficult to isolate potential pharmacological and toxic effects of menthol when it is administered in a smoke mixture. Menthol properties include cooling and local anesthesia, as well as effects on drug absorption and metabolism, bronchodilation and respiration changes, and electrophysiology. Subjective effects of smoothness and less harshness have been identified as reasons for menthol cigarette smoking, but findings have been inconclusive regarding the effect of menthol on carbon monoxide exposure and smoking topography parameters. Gaps in the research literature and future research areas include the following: (a) What is the role of menthol in tobacco reinforcement and addiction? (b) In the absence of nicotine, is menthol reinforcing? (c) Are the pharmacological and physiological effects of menthol mediated by a menthol-specific receptor or some other central nervous system-mediated action? (d) What are the influences of menthol and menthol metabolism on the metabolic activation and detoxification of carcinogens in tobacco smoke? and (e) Do differences exist in cigarette smoking topography in relation to the interaction of ethnicity, gender, and menthol cigarette preference? Answers to these questions will help to elucidate the function of menthol in cigarettes and its impact on smoking behavior. PMID:14982706

  11. Inhibition of immunological function mediated DNA damage of alveolar macrophages caused by cigarette smoke in mice.

    PubMed

    Ishida, Takahiro; Hirono, Yuriko; Yoshikawa, Kenichi; Hutei, Yoshimi; Miyagawa, Mayuko; Sakaguchi, Ikuyo; Pinkerton, Kent E; Takeuchi, Minoru

    2009-12-01

    Exposure to cigarette smoke impairs the pulmonary immune system, including alveolar macrophage function, although the mechanisms by which this occurs are not fully elucidated. This study investigates the effect of cigarette smoke exposure on the antigen-presenting activity of alveolar macrophages, which is required for antigen-specific response to T cells. C57BL/6 mice were exposed to cigarette smoke for 10 days using a Hamburg II smoking machine, and alveolar macrophages were obtained by bronchoalveolar lavage. The antigen-presenting activity of alveolar macrophages was significantly inhibited in mice exposed to cigarette smoke compared with mice not exposed to cigarette smoke. Major histocompatibility complex class II cell surface molecule-positive cells, B7-1 molecule-positive cells, and interleukin-1beta messenger RNA gene expression in alveolar macrophages were significantly decreased in mice exposed to cigarette smoke compared with mice not exposed to cigarette smoke. In contrast, DNA damage and generation of superoxide and hydrogen peroxide in alveolar macrophages were significantly increased by cigarette smoke exposure. These results suggest that inhibition of the antigen-presenting activity of alveolar macrophages may result from decreased expression of major histocompatibility complex class II and B7-1 molecules and interleukin-1beta messenger RNA gene expression following cigarette smoke exposure. Furthermore, inhibition of antigen presentation in alveolar macrophage may result from DNA damage induced by excessive amounts of reactive oxygen species being generated by alveolar macrophages following cigarette smoke exposure. These findings suggest that cigarette smoke impairs the immunological function of alveolar macrophages and, as a result, increases the risk for pulmonary infection. PMID:19922407

  12. 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. PMID:26700672

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

    PubMed Central

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

    2016-01-01

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

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

    SciTech Connect

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

    2013-09-01

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

  15. 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.

  16. Determinants of first puff and daily cigarette smoking in adolescents.

    PubMed

    O'Loughlin, Jennifer; Karp, Igor; Koulis, Theodoro; Paradis, Gilles; Difranza, Joseph

    2009-09-01

    Few prospective studies of smoking initiation have investigated a wide range of time-varying and invariant predictor variables at the individual and contextual levels concurrently. In this study (1999-2005), 877 Canadian students (mean age = 12.7 years) who had never smoked at baseline completed self-report questionnaires on cigarette smoking and 32 predictor variables in 20 survey cycles during secondary school. Height and weight were measured in survey cycles 1, 12, and 19. School administrators completed questionnaires on school tobacco control policies/activities, and trained observers collected data on access to tobacco products in commercial establishments near schools. Younger age, single-parent family status, smoking by parents, siblings, friends, and school staff, stress, impulsivity, lower self-esteem, feeling a need to smoke, not doing well at school, susceptibility to tobacco advertising, alcohol use, use of other tobacco products, and attending a smoking-tolerant school were independent determinants of smoking initiation. Independent determinants of daily smoking onset among initiators of nondaily smoking included smoking by siblings and friends, feeling a need to smoke, susceptibility to tobacco advertising, use of other tobacco products, and self-perceived mental and physical addiction. Adolescent tobacco control programs should address multiple individual and contextual-level risk factors. Strategies that address nicotine dependence symptoms are also needed for adolescents who have already initiated smoking. PMID:19635735

  17. 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...

  18. 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.

  19. Alpha 1-proteinase inhibitor is more sensitive to inactivation by cigarette smoke than is leukocyte elastase

    SciTech Connect

    Janoff, A.; Dearing, R.

    1982-10-01

    Aqueous solutions of gas phase cigarette smoke were incubated with pure human leukocyte elastase or with crude human leukocyte granule extract, and the effects on enzyme activity were determined using a synthetic amide substrate. Simultaneously, the same smoke solutions were incubated with 10% human serum under identical conditions, and the effects on serum inhibition of purified or crude leukocyte elastase were similarly measured. In addition, aqueous solutions of unfractionated cigarette smoke were incubated with leukocyte elastase or serum, and the abilities of the smoke-treated enzyme to digest elastin and of the smoke-treated serum to inhibit elastin digestion were determined. Both experimental protocols showed that serum elastase-inhibiting capacity (primarily caused by alpha 1-proteinase inhibitor) is more susceptible to inactivation by aqueous solutions of cigarette smoke than is leukocyte elastase, suggesting that elastase inhibition (rather than elastase activity) may be predominantly suppressed by cigarette smoke inhalation in vivo.

  20. 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.

  1. The Implications of Sidestream Cigarette Smoke for Cardiovascular Health.

    ERIC Educational Resources Information Center

    Hurshman, Larry G.; And Others

    1978-01-01

    Non-smokers exposed to emissions from a burning cigarette in ambient air demonstrate measureable physiological responses. The study showed that work capacity was reduced as a result of exposure to their sidestream cigarette smoke. (RE)

  2. The effects of cigarette smoking on human sexual potency.

    PubMed

    Gilbert, D G; Hagen, R L; D'Agostino, J A

    1986-01-01

    Forty-two male cigarette smokers, age 18 to 44, were randomly assigned to high-nicotine, low-nicotine, or control groups in a study relating cigarette smoking to sexual response. Subjects watched erotic film segments while their penile diameters, heart rates, and finger pulse amplitudes were continuously recorded by a polygraph. Subjects in the smoking groups smoked relatively high-nicotine (.9 mg) or very low-nicotine (.002 mg) cigarettes prior to watching the last two films, while control subjects ate candy. Smoking two high-nicotine cigarettes in immediate succession significantly decreased the rate of penile diameter change relative to the other conditions. These effects were not seen after a single cigarette was smoked. High-nicotine cigarettes caused significantly more vasoconstriction and heart rate increase than did low-nicotine cigarettes, which did not differ from control conditions. PMID:3812052

  3. Cigarette smoke alters the proteomic profile of lung fibroblasts.

    PubMed

    D'Anna, Claudia; Cigna, Diego; Costanzo, Giorgia; Bruno, Andreina; Ferraro, Maria; Di Vincenzo, Serena; Bianchi, Laura; Bini, Luca; Gjomarkaj, Mark; Pace, Elisabetta

    2015-06-01

    Smoking is strongly associated with diseases such as lung cancer and chronic obstructive pulmonary disease (COPD). Lung fibroblasts are crucial for the integrity of alveolar structure by producing extracellular matrix proteins which are required for attachment, structure, and function of alveolar epithelial cells. Despite the well-known association between cigarette smoke exposure and pulmonary and cardiovascular diseases, many questions remain regarding the mechanisms by which smoking induces diseases. The aim of this study is to detect differentially expressed proteins in human foetal lung cells (HFL-1) after 5 and 10% doses of cigarette smoke extract (CSE) exposure, combining two-dimensional electrophoresis (2DE) and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). In order to evaluate cellular ability to recover as well as lasting damage, we analysed the proteomic pattern 24 hours after the CSE removal (release). Eleven proteins had significant changes at various experimental points. Among these, 7 were up-regulated after CSE-treatments and 4 were down-regulated. Some spots seemed to be modified permanently or in a transient manner, in fact they returned to baseline levels after CSE-removal (normalisation after CSE release) and others were modified by selective CSE concentrations or only after release. MS identified, differentially expressed proteins are involved in stress response, mitochondrial activity, and aging. These findings may improve our understanding about molecular mechanisms underlying CSE caused damage and they may also integrate the comprehension of cigarette smoke effects on human health. PMID:25900673

  4. Safety Assessment of Mainstream Smoke of Herbal Cigarette

    PubMed Central

    Lee, Seung Min; Lim, Heung Bin

    2015-01-01

    Owing to the increase in price of cigarettes in Korea, herbal cigarettes have received increasing attention as a non-smoking aid; however, its safety has hardly been studied. We analyzed some of the toxic components in the mainstream smoke of herbal cigarettes, performed a mutagenicity test on smoke condensates for safety assessment, and compared the results with the corresponding values of a general cigarette with the same tar content. Herbal cigarette “A” was smoked using automatic smoking machine under ISO conditions in a manner similar to general cigarette “T”. The tar content measured was higher than that inscribed on the outside of a package. The mainstream smoke of herbal cigarette “A” did not contain detectable levels of tobacco-specific nitrosamines and nicotine. Carbon monoxide and benzo(α)pyrene contents in herbal cigarette “A” were higher than those in the general cigarette “T”. The phenolic contents such as hydroquinone, resorcinol, and catechol in herbal cigarette “A” were higher than those in the general cigarette “T”, but cresol contents in herbal cigarette “A” were lower than those in the general cigarette “T”. The content of aromatic amines such as 4-aminobiphenyl in herbal cigarette “A” was higher than that in the general cigarette “T”; however, this difference was not statistically significant. On the other hand, 1-aminonaphthalene, 2-aminonaphthalene, and 3-aminobiphenyl contents in herbal cigarette “A” were lower than those in the general cigarette “T”. The smoke condensates of herbal cigarette “A” exhibited a higher mutagenic potential than the condensates from the general cigarette “T” at the same concentration. We concluded that the mainstream smoke of herbal cigarette contains some toxic components, the smoke condensates of herbal cigarettes are mutagenic similar to general cigarette because of combustion products, and that the evaluation of the chemical and biological safety of

  5. 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. PMID:25505336

  6. Deposition of sidestream cigarette smoke in the human respiratory tract

    SciTech Connect

    Hiller, F.C.; McCusker, K.T.; Mazumder, M.K.; Wilson, J.D.; Bone, R.C.

    1982-04-01

    Measurement of deposition of sidestream cigarette smoke in the human respiratory tract is important for assessing the health effects of sidestream cigarette smoke. We measured the deposition fraction of sidestream cigarette smoke in 5 normal adult male volunteers using sidestream smoke at a concentration similar to that encountered indoors with smokers present. The mean deposition was 11%. These data indicate that the deposition fraction of sidestream smoke is similar to other previously studied aerosols in the same size range and is much less than mainstream smoke.

  7. Waterpipe Tobacco and Cigarette Smoking Among University Students in Jordan

    PubMed Central

    Khabour, Omar F.; Alzoubi, Karem H.; Eissenberg, Thomas; Mehrotra, Purnima; Azab, Mohammed; Carroll, Mary; Afifi, Rema A.; Primack, Brian A.

    2013-01-01

    Setting While waterpipe and cigarette smoking are well studied in Syria and Lebanon, data from Jordan are sparse. Objectives To characterize the relative prevalence of waterpipe tobacco and cigarette smoking among university students in Jordan, and to compare the demographic and environmental factors associated with each form of tobacco use. Design We surveyed 1845 students randomly recruited from four universities in Jordan. We used multivariable logistic regression controlling for clustering of individuals within universities to determine associations between demographic and environmental covariates and waterpipe tobacco and cigarette use. Results Waterpipe tobacco smoking rates were 30% in the past 30 days and 56% ever, and cigarette smoking rates were 29% in the past 30 days and 57% ever. Past 30-day waterpipe tobacco smoking rates were 59% for males and 13% for females. Compared with males, females had substantially lower odds of being current waterpipe (OR=0.12, 95% CI=0.10–0.15) or cigarette (OR=0.08, 95% CI=0.05–0.14) smokers. Compared with waterpipe tobacco smoking, current cigarette smoking was more significantly associated with markers of high socioeconomic status. Conclusion Waterpipe tobacco smoking is as common as cigarette smoking among Jordanian university students. While cigarette smoking is consistently associated with high socioeconomic status, waterpipe tobacco smoking is more evenly distributed across various populations. PMID:22525279

  8. Determination of toxic carbonyl compounds in cigarette smoke.

    PubMed

    Fujioka, Kazutoshi; Shibamoto, Takayuki

    2006-02-01

    Toxic carbonyl compounds, including formaldehyde, malonaldehyde, and glyoxal, formed in mainstream cigarette smoke were quantified by derivatization-solid phase extraction-gas chromatography methods. Cigarette smoke from 14 commercial brands and one reference (2R1F) was drawn into a separatory funnel containing aqueous phosphate-buffered saline. Reactive carbonyl compounds trapped in the buffer solution were derivatized into stable nitrogen containing compounds (pyrazoles for beta-dicarbonyl and alpha,beta-unsaturated aldehyde; quinoxalines for alpha-dicarbonyls; and thiazolidines for alkanals). After derivatives were recovered using C(18) solid phase extraction cartridges, they were analyzed quantitatively by a gas chromatograph with a nitrogen phosphorus detector. The total carbonyl compounds recovered from regular size cigarettes ranged from 1.92 mg/cigarette(-1) to 3.14 mg/cigarette(-1). The total carbonyl compounds recovered from a reference cigarette and a king size cigarette were 3.23 mg/cigarette(-1) and 3.39 mg/cigarette(-1), respectively. The general decreasing order of the carbonyl compounds yielded was acetaldehyde (1110-2101 microg/cigarette(-1)) > diacetyl (301-433 microg/cigarette(-1)), acrolein (238-468 microg/cigarette(-1)) > formaldehyde (87.0-243 microg/cigarette(-1)), propanal (87.0-176 microg/cigarette(-1)) > malonaldehyde (18.9-36.0 microg/cigarette(-1)), methylglyoxal (13.4-59.6 microg/cigarette(-1)) > glyoxal (1.93-6.98 microg/cigarette(-1)). PMID:16463255

  9. The effects of physical exercise on the cigarette smoke-induced pulmonary oxidative response.

    PubMed

    Menegali, Bruno T; Nesi, Renata T; Souza, Priscila S; Silva, Luciano A; Silveira, Paulo C L; Valença, Samuel S; Pinho, Ricardo A

    2009-12-01

    Studies have shown that the oxidative power of cigarettes is related to the pathogenesis of several pulmonary diseases and that regular physical exercise contributes significantly to reducing the deleterious effects of cigarettes. The objective of the present study was to investigate the therapeutic effects of physical exercise on histological and oxidative stress markers in animals exposed to cigarette smoke. Thirty-six male, eight-week-old C57BL-6 mice were divided into four groups (n = 9 for each group): control, exercise, cigarette smoke, and cigarette smoke plus exercise. The cigarette smoke (CS) groups were exposed to cigarette smoke 3 times/day (4 cigarettes/session) for 60 consecutive days. The exercise groups were submitted to swimming physical training 5 days/week for eight weeks. Forty-eight hours after the last exercise and cigarette exposure, the animals were sacrificed using cervical traction. The right lung was removed, processed, and stored for future analysis. In addition to the analysis of collagen content (hydroxyproline), oxidant production (anion superoxide), antioxidant enzyme activity (SOD and CAT), and lipid and protein oxidative damage (TBARS and Carbonylation), histological and morphological studies were performed. The results revealed that the animals exposed to cigarette smoke showed enlargement and destruction of the alveolar septum and increases in the numbers of macrophages and neutrophils, as well as in the amount of collagen. Our results also showed a decrease in the volume density of elastic fibers and an increase in the volume density of airspaces. However, physical exercise partially improved these markers. Additionally, physical exercise decreased oxidant production and increased the activity of the enzymatic antioxidant defense system, but did not reverse lipid and protein oxidative damage induced by cigarette smoke. These results suggest that physical training partially improves histological and oxidative stress parameters in

  10. 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. PMID:24908261

  11. 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

  12. Teen Smoking Down, E-Cigarette Use Up

    MedlinePlus

    ... nih.gov/medlineplus/news/fullstory_159286.html Teen Smoking Down, E-Cigarette Use Up CDC survey finds ... are getting some health messages loud and clear. Smoking among high school students is at an all- ...

  13. 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…

  14. 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.

  15. EFFECT OF CIGARETTE SMOKING IN EPIDEMIOLOGICAL STUDIES OF LUNG CANCER

    EPA Science Inventory

    This paper describes a method for adjusting the analysis of occupational-environmental lung cancer risks for the effects of cigarette smoking in cohort and case control studies. he method uses a function that relates an individual's death rate to his age and cigarette smoking his...

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

    PubMed Central

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

    2016-01-01

    The deleterious role of cigarette smoke has long been documented in various human diseases including periodontal complications. In this report, we examined this adverse effect of cigarette smoke on human gingival fibroblasts (HGFs) which are critical not only in maintaining gingival tissue architecture but also in mediating immune responses. As well documented in other cell types, we also observed that cigarette smoke promoted cellular reactive oxygen species in HGFs. And we found that this cigarette smoke-induced oxidative stress reduced HGF viability through inducing apoptosis. Our results indicated that an increased Bax/Bcl-xL ratio and resulting caspase activation underlie the apoptotic death in HGFs exposed to cigarette smoke. Furthermore, we detected that cigarette smoke also triggered autophagy, an integrated cellular stress response. Interesting, a pharmacological suppression of the cigarette smoke-induced autophagy led to a further reduction in HGF viability while a pharmacological promotion of autophagy increased the viability of HGFs with cigarette smoke exposures. These findings suggest a protective role for autophagy in HGFs stressed with cigarette smoke, highlighting that modulation of autophagy can be a novel therapeutic target in periodontal complications with cigarette smoke. PMID:27226776

  17. 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. PMID:25620659

  18. 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

  19. Cigarette smoke inhalation and the acute airway response.

    PubMed Central

    Higenbottam, T; Feyeraband, C; Clark, T J

    1980-01-01

    The acute airway response to smoking varying numbers (one to four) of identical cigarettes in rapid succession and smoking single cigarettes of differing tar/nicotine yields was assessed repeatedly in 13 healthy smokers. The airway response was variable, indicating airway narrowing consistently in only three subjects. There appeared no difference between forced spirometry and measurement of airway resistance in detecting the airway response. No relationship was observed between the airway response and amount of smoke inhaled into the lungs as measured either by changes in venous blood nicotine or percentage carboxyhaemoglobin. When five smokers inhaled smoke directly from a cigarette acute airway narrowing was consistently observed. A normal smoking pattern consisting of an initial drag of smoke into the mouth, followed after a pause by inhalation of smoke diluted with air, did not consistently cause airway narrowing although similar amounts of smoke as the direct drag were inhaled as assessed by changes in venous blood nicotine. The manner of smoke inhalation affects the relative concentrations of the different constituents of smoke reaching the lungs and also appears to be the main determinant of the acute airway response to smoking, which was unrelated to the number of cigarettes smoked or the tar content of the smoke. This suggests that patterns of smoke inhalation may influence the pathogenesis of bronchial disease associated with smoking. PMID:7434266

  20. Acute effects of cigarette smoking on microcirculation of the thumb.

    PubMed

    van Adrichem, L N; Hovius, S E; van Strik, R; van der Meulen, J C

    1992-01-01

    The acute effect of smoking on the microcirculation of the skin of the thumb was investigated in healthy volunteers. Twenty-two were smokers and 10 were non-smokers. The flow was assessed by means of laser Doppler flowmetry. The smokers inhaled 2 cigarettes. During smoking of their first and second cigarette respectively, a mean decrease in laser Doppler flow of 23.8% and 29.0% was seen (p = 0.03; p = 0.01). Ten minutes after smoking this decrease was recovered by half. This experiment confirms that one should prohibit smoking of cigarettes pre- and postoperatively for optimal wound healing conditions. PMID:1737221

  1. 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. PMID:18951229

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

    PubMed

    Pokhrel, Pallav; Herzog, Thaddeus A

    2015-03-01

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

  3. 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

  4. 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…

  5. Lipidomics of tobacco leaf and cigarette smoke.

    PubMed

    Dunkle, Melissa N; Yoshimura, Yuta; t'Kindt, Ruben; Ortiz, Alexia; Masugi, Eri; Mitsui, Kazuhisa; David, Frank; Sandra, Pat; Sandra, Koen

    2016-03-25

    Detailed lipidomics experiments were performed on the extracts of cured tobacco leaf and of cigarette smoke condensate (CSC) using high-resolution liquid chromatography coupled to quadrupole time-of-flight mass spectrometry (LC-Q-TOF MS). Following automated solid-phase extraction (SPE) fractionation of the lipid extracts, over 350 lipids could be annotated. From a large-scale study on 22 different leaf samples, it was determined that differentiation based on curing type was possible for both the tobacco leaf and the CSC extracts. Lipids responsible for the classification were identified and the findings were correlated to proteomics data acquired from the same tobacco leaf samples. Prediction models were constructed based on the lipid profiles observed in the 22 leaf samples and successfully allowed for curing type classification of new tobacco leaves. A comparison of the leaf and CSC data provided insight into the lipidome changes that occur during the smoking process. It was determined that lipids which survive the smoking process retain the same curing type trends in both the tobacco leaf and CSC data. PMID:26585203

  6. Mechanisms of acid reflux associated with cigarette smoking.

    PubMed Central

    Kahrilas, P J; Gupta, R R

    1990-01-01

    Studies were done to evaluate the lower oesophageal sphincter function of chronic smokers compared with non-smokers and to ascertain the acute effects of smoking on the sphincter and the occurrence of acid reflux. All subjects (non-smokers, asymptomatic cigarette smokers, and smokers with oesophagitis) were studied postprandially with a lower oesophageal sphincter sleeve assembly, distal oesophageal pH electrode, and submental electromyographic electrodes. The two groups of cigarette smokers then smoked three cigarettes in succession before being recorded for an additional hour. As a group, the cigarette smokers had significantly lower lower oesophageal sphincter pressure compared with non-smokers but the sphincter was not further compromised by acutely smoking cigarettes. Cigarette smoking did, however, acutely increase the rate at which acid reflux events occurred. The mechanisms of acid reflux during cigarette smoking were mainly dependent upon the coexistence of diminished lower oesophageal sphincter pressure. Fewer than half of reflux events occurred by transient lower oesophageal sphincter relaxations. The majority of acid reflux occurred with coughing or deep inspiration during which abrupt increases in intra-abdominal pressure overpowered a feeble sphincter. We conclude that cigarette smoking probably exacerbates reflux disease by directly provoking acid reflux and perhaps by a long lasting reduction of lower oesophageal sphincter pressure. PMID:2318431

  7. A Simple and Rapid Method for Standard Preparation of Gas Phase Extract of Cigarette Smoke

    PubMed Central

    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. PMID:25229830

  8. Psychosocial determinants of cigarette smoking among college students.

    PubMed

    Kear, Mavra E

    2002-01-01

    Although the prevalence of cigarette smoking among adolescents and adults consistently declined in the past decade, smoking among college students rose sharply. To reduce the morbidity and premature mortality caused by smoking, antismoking interventions need to target this vulnerable population. Anonymous self-report data were collected from a convenience sample of 224 college students who voluntarily completed a Web-based survey developed to assess the relation of risk-taking tendency, depression, social normative beliefs, and smoking resistance self-efficacy to cigarette smoking behavior. Employing structural analysis using LISREL (Jöreskog & Sörbom, 1996), all 4 factors were confirmed as determinants of smoking. Resistance self-efficacy, the only direct antecedent, mediated the link to risk-taking tendency, depression, and social normative beliefs. Antismoking interventions that focus on enhancing refusal skills and are delivered to homogeneous groups are proposed as an effective approach to reducing cigarette smoking among college students. PMID:12494745

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

    PubMed Central

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

    2016-01-01

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

  10. Cigarette smoke condensate activates nuclear transcription factor-kappaB through phosphorylation and degradation of IkappaB(alpha): correlation with induction of cyclooxygenase-2.

    PubMed

    Anto, Ruby John; Mukhopadhyay, Asok; Shishodia, Shishir; Gairola, C Gary; Aggarwal, Bharat B

    2002-09-01

    Cigarette smoke (CS) contains several carcinogens known to initiate and promote tumorigenesis and metastasis. Because various genes that mediate carcinogenesis and tumorigenesis are regulated by nuclear factor-kappaB (NF-kappaB), we postulated that the effects of CS must be mediated through activation of this transcription factor. Therefore, in the present report we investigated whether cigarette smoke condensate (CSC) activates NF-kappaB, and whether the pathway employed for activation is similar to that of TNF, one of the potent activators of NF-kappaB. Our results show that the treatment of human histiocytic lymphoma U-937 cells with CSC activated NF-kappaB in a dose- and time-dependent manner. The kinetics of NF-kappaB activation by CSC was comparable with that of TNF. CSC-induced NF-kappaB activation was not cell type-specific, as it also activated NF-kappaB in T cells (Jurkat), lung cells (H1299), and head and neck squamous cell lines (1483 and 14B). Activation of NF-kappaB by CSC correlated with time-dependent degradation of IkappaB(alpha), an inhibitor of NF-kappaB. Further studies revealed that CSC induced phosphorylation of the serine residue at position 32 in IkappaB(alpha). In vitro immunocomplex kinase assays showed that CSC activated IkappaB(alpha) kinase (IKK). The suppression of CSC-activated NF-kappaB-dependent reporter gene expression by dominant negative form of IkappaB(alpha), TRAF2, NIK and IKK suggests a similarity to the TNF-induced pathway for NF-kappaB. CSC also induced the expression of cyclooxygenase-2, an NF-kappaB regulated gene product. Overall, our results indicate that through phosphorylation and degradation of IkappaB(alpha), CSC can activate NF-kappaB in a wide a variety of cells, and this may play a role in CS-induced carcinogenesis. PMID:12189195

  11. 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.

  12. The biologic effects of cigarette smoke on cancer cells.

    PubMed

    Sobus, Samantha L; Warren, Graham W

    2014-12-01

    Smoking is one of the largest preventable risk factors for developing cancer, and continued smoking by cancer patients is associated with increased toxicity, recurrence, risk of second primary cancer, and mortality. Cigarette smoke (CS) contains thousands of chemicals, including many known carcinogens. The carcinogenic effects of CS are well established, but relatively little work has been done to evaluate the effects of CS on cancer cells. In this review of the literature, the authors demonstrate that CS induces a more malignant tumor phenotype by increasing proliferation, migration, invasion, and angiogenesis and by activating prosurvival cellular pathways. Significant work is needed to understand the biologic effect of CS on cancer biology, including the development of model systems and the identification of critical biologic mediators of CS-induced changes in cancer cell physiology. PMID:25043526

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

    SciTech Connect

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

    1989-01-01

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

  14. Cigarette smoking and lung destruction. Accumulation of neutrophils in the lungs of cigarette smokers.

    PubMed

    Hunninghake, G W; Crystal, R G

    1983-11-01

    It has been hypothesized that lung destruction in persons with emphysema associated with cigarette smoking is mediated by elastase released by neutrophils that have migrated to the alveolar structures in response to cigarette smoke. To directly evaluate this hypothesis, cell suspensions, isolated from bronchoalveolar lavage fluid and from open lung biopsies of nonsmokers and cigarette smokers with normal lung parenchyma and from open lung biopsies of nonsmokers and cigarette smokers who have sarcoidosis were evaluated for the presence of neutrophils. A significantly increased number of neutrophils was present in the cell suspensions isolated from bronchoalveolar lavage fluid and from open lung biopsies of both normal and sarcoid cigarette smokers compared with that in the nonsmokers (p less than 0.01, each comparison). Evaluation of the alveolar macrophages present in lavage fluid suggested a mechanism by which neutrophils may be attracted to the lungs of cigarette smokers: alveolar macrophages of cigarette smokers release a chemotactic factor for neutrophils, whereas alveolar macrophages of nonsmokers do not. In addition, alveolar macrophages of nonsmokers, after exposure to cigarette smoke, in vitro, are stimulated to release this chemotactic factor. These studies demonstrate that an increased number of neutrophils are present in the lungs of cigarette smokers compared with that in nonsmokers and suggest that cigarette smoke may attract neutrophils to the lung by stimulating alveolar macrophages to release a potent chemotactic factor for neutrophils. PMID:6556892

  15. 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,…

  16. 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…

  17. 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. PMID:17450995

  18. 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

  19. Exposure to smoking cues during an emotion recognition task can modulate limbic fMRI activation in cigarette smokers.

    PubMed

    Artiges, Eric; Ricalens, Emmanuel; Berthoz, Sylvie; Krebs, Marie-Odile; Penttilä, Jani; Trichard, Christian; Martinot, Jean-Luc

    2009-09-01

    Smoking cues (SCs) refer to smoking-associated environmental stimuli that may trigger craving and withdrawal symptoms, and predispose to relapse in smokers. Although previous brain imaging studies have explored neural responses to SCs, no study has characterized the effects of SCs on cerebral activity in smokers engaged in an attention-demanding cognitive task that is unrelated to smoking. Thirteen tobacco smokers and a demographically matched group of 13 healthy non-smokers participated in a fast event-related functional magnetic resonance imaging (fMRI) study that involved a visual task integrating SCs and neutral cues (NCs) during emotion recognition trials requiring a high level of attention. No significant SC-induced alterations were detected in smokers' behavioural performance. fMRI results show that non-smokers exhibited no difference between SC and NC trials; in contrast, smokers showed SC-induced widespread deactivations in a limbic, paralimbic and striatal network classically involved in addiction, and activation in the right dorsolateral prefrontal cortex. In addition, a correlation between deactivation of the right insula and the severity of smoking dependence (Fagerström test) was detected in smokers. These results suggest that the neural reactivity of smokers to SCs can be modified in the context of a cognitive challenge. This could reflect smokers' ability to inhibit cue-induced craving and may help in smoking cessation. PMID:19650816

  20. 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

  1. Cigarette smoking, physical activity, and alcohol consumption as predictors of cancer incidence among women at high risk of breast cancer in the NSABP P-1 Trial

    PubMed Central

    Land, Stephanie R.; Liu, Qing; Wickerham, D. Lawrence; Costantino, Joseph P.; Ganz, Patricia A.

    2014-01-01

    Background NSABP P-1 provides an opportunity to examine the association of behavioral factors with prospectively monitored cancer incidence and interactions with tamoxifen. Methods From 1992–1997, 13,388 women with estimated 5-year breast cancer (BC) risk greater than 1.66% or a history of lobular carcinoma in situ (87% under age 65; 67% post-menopausal) were randomly assigned to tamoxifen versus placebo. Invasive BC, lung (LC), colon (CC), and endometrial cancers (EC) were analyzed with Cox regression. Predictors were baseline cigarette smoking, leisure-time physical activity, alcohol consumption, and established risk factors. Results At median 7 years follow-up, we observed 395, 66, 35, and 74 BC, LC, CC, and EC, respectively. Women who had smoked were at increased risk of BC (P=.007; hazard ratio (HR)=1.3 for 15–35 years smoking, HR=1.6 for ≥35 years), LC (P<.001; HR=3.9 for 15–35 years; HR=18.4 for ≥35 years), and CC (P<.001; HR=5.1 for ≥35 years) versus never-smokers. Low activity predicted increased BC risk only among women assigned to placebo (P=.021 activity main effect, P=.013 activity-treatment interaction; HR=1.4 for placebo group) and EC among all women (P=.026, HR=1.7). Moderate alcohol (>0–1 drink/day) was associated with decreased risk of CC (P=.019; HR=.35) versus no alcohol. There were no other significant associations between these behaviors and cancer risk. Conclusion Among women with elevated risk of BC, smoking has an even greater impact on BC risk than observed in past studies in the general population. Impact Women who smoke or are inactive should be informed of the increased risk of multiple types of cancer. PMID:24569437

  2. Waterpipe Tobacco and Cigarette Smoking Direct Comparison of Toxicant Exposure

    PubMed Central

    Eissenberg, Thomas; Shihadeh, Alan

    2009-01-01

    Background Waterpipe (hookah, shisha) tobacco smoking has spread worldwide. Many waterpipe smokers believe that, relative to cigarettes, waterpipes are associated with lower smoke toxicant levels and fewer health risks. For physicians to address these beliefs credibly, waterpipe and cigarette must be compared directly. Purpose The purpose of this study is to provide the first controlled, direct laboratory comparison of the toxicant exposure associated with waterpipe tobacco and cigarette smoking Methods Participants (N=31; mean=21.4 years, SD=2.3) reporting monthly waterpipe use (mean 5.2 uses/month, SD=4.0) and weekly cigarette smoking (mean= 9.9 cigarettes/day, SD=6.4) completed a crossover study in which they each smoked a waterpipe for a maximum of 45 minutes or a single cigarette. Outcomes included expired air carbon monoxide (CO) 5 minutes after session’s end, and blood carboxyhemoglobin (COHb), plasma nicotine, heart rate, and puff topography. Data were collected in 2008–2009 and analyzed in 2009. Results CO increased, on average, by 23.9 ppm for waterpipe (SD=19.8) and 2.7 ppm for cigarette (SD=1.8) while peak waterpipe COHb levels (mean=3.9%, SD=2.5) were three times those observed for the cigarette (mean=1.3%, SD=0.5; Ps<0.001). Peak nicotine levels did not differ (mean ng/ml waterpipe=10.2, SD=7.0; cigarette=10.6, SD=7.7). Significant heart rate increases relative to pre-smoking were observed 5, 10, 15, 20, 25, and 35 minutes during the cigarette session and at every 5-minute interval during the waterpipe session (Ps<0.001). Mean total puff volume was 48.6 liters for waterpipe as compared to 1.0 liters for cigarette (P<0.001). Conclusions Relative to a cigarette, waterpipe use is associated with greater CO, similar nicotine, and dramatically more smoke exposure. Physicians should consider advising their patients that waterpipe tobacco smoking exposes them to some of the same toxicants as cigarette smoking and therefore the two tobacco smoking methods

  3. Decreasing prevalence of cigarette smoking in the middle income country of Mauritius: questionnaire survey

    PubMed Central

    Cox, Helen S; Williams, Joanne W; de Courten, Maximilian P; Chitson, Pierrot; Tuomilehto, Jaakko; Zimmet, Paul Z

    2000-01-01

    Objectives To describe changes in the prevalence of cigarette smoking in the middle income country of Mauritius from 1987 to 1998, and to relate these changes to legislative and health promotion efforts over the same period. Design Questionnaire survey. Setting Mauritius, an island in the Indian Ocean with a population of about 1.2 million (about 70% south Asian, 2% Chinese, and 28% Creole). Participants Data were obtained from 5072 participants in 1987, 6573 in 1992, and 6281 in 1998. Main outcome measures Prevalence of current smoking in 1987, 1992, and 1998, sales of cigarettes in Mauritius, and information on activities for control of tobacco. Results Self reported cigarette smoking has been decreasing in Mauritius since 1987, with the largest decrease between 1987 and 1992. From 1987 to 1998 smoking prevalence decreased by 23% in men and 61% in women. Smoking decreased across all age and ethnic groups and across different levels of income and education. Sales of cigarettes also decreased in line with smoking prevalence. Conclusions The introduction of cigarette taxes, a limited health promotion programme, and the absence of massive promotional campaigns by the sole tobacco company on Mauritius have led to a striking and continued decrease in smoking prevalence and cigarette consumption on the island. PMID:10926592

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

    PubMed

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

    2016-04-01

    The objective of this experiment was to evaluate the comparative value of cigarettes versus high dose e-cigarettes among nicotine-dependent cigarette smokers when compared with money or use of their usual cigarette brand. The experiment used a within-subject design with four sessions. After baseline assessment, participants attended two 15-min unrestricted smoking sessions: one cigarette smoking session and one e-cigarette smoking session. Participants then attended two multiple-choice procedure (MCP) sessions: a session comparing cigarettes and money and a session comparing e-cigarettes and money. Participants (n=27) had used cigarettes regularly, had never used e-cigarettes, and were not currently attempting to quit smoking. The sample consisted primarily of males (72%), with a mean age of 34 years. When given the opportunity to choose between smoking a cigarette or an e-cigarette, participants chose the cigarette 73.9% of the time. Findings from the MCP demonstrated that after the first e-cigarette exposure sessions, the crossover value for cigarettes ($3.45) was significantly higher compared with the crossover value for e-cigarettes ($2.73). The higher participant preference, self-reported smoking effects, and higher MCP crossover points indicate that cigarettes have a higher comparative value than high dose e-cigarettes among e-cigarette naive smokers. PMID:26886210

  5. Cigarette smoking prevalence in US counties: 1996-2012

    PubMed Central

    2014-01-01

    Background Cigarette smoking is a leading risk factor for morbidity and premature mortality in the United States, yet information about smoking prevalence and trends is not routinely available below the state level, impeding local-level action. Methods We used data on 4.7 million adults age 18 and older from the Behavioral Risk Factor Surveillance System (BRFSS) from 1996 to 2012. We derived cigarette smoking status from self-reported data in the BRFSS and applied validated small area estimation methods to generate estimates of current total cigarette smoking prevalence and current daily cigarette smoking prevalence for 3,127 counties and county equivalents annually from 1996 to 2012. We applied a novel method to correct for bias resulting from the exclusion of the wireless-only population in the BRFSS prior to 2011. Results Total cigarette smoking prevalence varies dramatically between counties, even within states, ranging from 9.9% to 41.5% for males and from 5.8% to 40.8% for females in 2012. Counties in the South, particularly in Kentucky, Tennessee, and West Virginia, as well as those with large Native American populations, have the highest rates of total cigarette smoking, while counties in Utah and other Western states have the lowest. Overall, total cigarette smoking prevalence declined between 1996 and 2012 with a median decline across counties of 0.9% per year for males and 0.6% per year for females, and rates of decline for males and females in some counties exceeded 3% per year. Statistically significant declines were concentrated in a relatively small number of counties, however, and more counties saw statistically significant declines in male cigarette smoking prevalence (39.8% of counties) than in female cigarette smoking prevalence (16.2%). Rates of decline varied by income level: counties in the top quintile in terms of income experienced noticeably faster declines than those in the bottom quintile. Conclusions County-level estimates of cigarette

  6. Associations Between Cigarette Smoking and Pain Among Veterans

    PubMed Central

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

    2015-01-01

    Individuals with chronic pain often report using cigarettes to cope, and smoking and chronic pain appear prevalent among US veterans. Pain may be a barrier to cigarette cessation and abstinence in this population. Because of physiological effects, smoking cigarettes may also interfere with pain management. A better understanding of how cigarette use relates to pain may assist in veteran cigarette cessation and pain management efforts. To assist these efforts, we searched the literature using keywords, such as “pain,” “smoking,” and “veteran,” to identify 23 journal articles published from 1993 to 2013 that reported on studies examining pain and smoking variables among military or veteran populations. Studies found that veterans reported using cigarettes to cope with pain, there was greater occurrence of pain and disability among smokers in the military, and smoking increased the odds of veterans receiving an opioid prescription for pain and misusing opioids. Studies also found increased odds of pain and smoking among Veterans Health Administration patients with post-traumatic stress disorder when compared with those without post-traumatic stress disorder. Studies support an interaction between pain and smoking among veterans. However, the mechanisms underlying this relationship remain unclear. Future studies focused on this interaction would benefit veteran populations. PMID:25595170

  7. 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.

  8. Teen Smoking Down, E-Cigarette Use Up

    MedlinePlus

    ... specialist at Lenox Hill Hospital in New York City, said, "While cigarette smoking in high school students ... D., pulmonary specialist, Lenox Hill Hospital, New York City; Dana Angelo White, M.S., R.D., clinical assistant ...

  9. Mutagenicity of smoke condensates from Canadian cigarettes with different design features.

    PubMed

    Mladjenovic, Nemanja; Maertens, Rebecca M; White, Paul A; Soo, Evelyn C

    2014-01-01

    There is currently limited knowledge regarding the impact of different cigarette designs on the toxicological properties of cigarette smoke condensate (CSC). This study used the Salmonella Mutagenicity Assay to examine the mutagenic activity of mainstream CSCs from 11 commercial Canadian cigarette brands with different design features or tobacco blend. The brands were selected to include design features that are common for cigarettes sold in the Canadian market, as well as cigarettes with alternate filters (charcoal or MicroBlue™), the super slim design, and cigarettes containing mixed blends of different tobacco types. CSCs were obtained using the International Organization for Standardization (ISO) and Health Canada Intense (HCI) smoking regimes, and mutagenic activity was assessed using Salmonella strains TA98, YG1041 and YG5185. Comparisons of the commercial brands to the Kentucky 3R4F, the Canadian Monitor 8 reference and a Canadian best seller revealed no significant reduction in CSC mutagenicity for cigarettes with alternate filters. However, the super slim design did afford some reduction in mutagenic potency. Nevertheless, since the study did not attempt to evaluate the impact of the cigarette designs on human health at the individual or population level, the super slim cigarettes cannot be considered 'reduced-harm' cigarettes. PMID:24321849

  10. Cigarette smoking and survival after ovarian cancer diagnosis.

    PubMed

    Nagle, Christina M; Bain, Christopher J; Webb, Penelope M

    2006-12-01

    We have examined the association between cigarette smoking and ovarian cancer survival in 676 women with invasive epithelial ovarian cancer, recruited into a case-control study in the early 1990s. Information about cigarette smoking and other personal and reproductive factors was obtained from a personal interview at the time of diagnosis. Cox proportional hazards models were used to evaluate the association between cigarette smoking and time to ovarian cancer death. Current smokers at diagnosis were more likely to die early than women who had never smoked [adjusted hazard ratio (HR), 1.36; 95% confidence interval (95% CI), 1.01-1.84]. Increased risks of dying were greater among those who had accumulated more pack-years of smoking (HR for 30+ pack-years compared with never smokers, 1.94; 95% CI, 1.41-2.66) and smoked more cigarettes per day (HR, 1.93; 95% CI, 1.37-2.73). All these associations were stronger among women with late-stage disease (HR for current versus never smokers, 1.58; 95% CI, 1.15-2.18). Time since quitting had little effect on survival after adjusting for lifetime smoking exposure. These results validate and extend recent findings and suggest that premorbid cigarette smoking is related to worse outcome in ovarian cancer patients. PMID:17164386

  11. 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)…

  12. Is the Exhaled Breath Temperature Sensitive to Cigarette Smoking?

    PubMed

    Carpagnano, Giovanna E; Ruggieri, Cinzia; Scioscia, Giulia; Storto, Maria Maddalena Lo; Zoppo, Luigi; Foschino-Barbaro, Maria P

    2016-10-01

    The smoking habit is accompanied by an acute inflammatory response which follows tissue injury. It would be desirable to find a non-invasive inflammatory marker that would simplify the task of studying and monitoring smokers more simply and allow us to identify populations at risk of contracting Chronic Obstructive Pulmonary Disease (COPD). Today's expectations regarding research focus on issues ranging from inflammatory markers to those of exhaled breath temperature (EBT) are considerable. That said, although the EBT has been largely studied in asthma and COPD, there have not been any studies thus far that have analysed the effect of cigarette smoking on the EBT.  Bearing this in mind, in this longitudinal study we aim to analyse the EBT in current smokers, monitor the effects both of cigarette smoking on EBT and of what happens after smoking cessation. Twenty-five (25) smokers (59.5 ± 3.1 yrs, 12 M) who participated in a multi-disciplinary smoking cessation programme and 25 healthy never-smokers (58.7 ± 2.9, 13 M) underwent EBT measurement. EBT values were higher in smokers before smoking (T0) than in never-smokers [34.6 (34.2-35) vs 33.2 (32.4-33.7)°C, p < 0.001. The smokers repeated measurement 5 minutes after smoking a cigarette (T1) and 2 hours after (T2). They repeated EBC measurement after 1 week (T3) and then after 3 months (T4) from smoking cessation. EBT is higher in smokers compared to controls. EBT increases after cigarette smoking and progressively decreases with the increase of time from when the last cigarette was smoked.  Thus, we can conclude that EBT is increased in smokers and also sensitive to the acute effect of cigarette smoke. PMID:26934668

  13. PAF mediates cigarette smoke-induced goblet cell metaplasia in guinea pig airways.

    PubMed

    Komori, M; Inoue, H; Matsumoto, K; Koto, H; Fukuyama, S; Aizawa, H; Hara, N

    2001-03-01

    Goblet cell metaplasia is an important morphological feature in the airways of patients with chronic airway diseases; however, the precise mechanisms that cause this feature are unknown. We investigated the role of endogenous platelet-activating factor (PAF) in airway goblet cell metaplasia induced by cigarette smoke in vivo. Guinea pigs were exposed repeatedly to cigarette smoke for 14 consecutive days. The number of goblet cells in each trachea was determined with Alcian blue-periodic acid-Schiff staining. Differential cell counts and PAF levels in bronchoalveolar lavage fluid were also evaluated. Cigarette smoke exposure significantly increased the number of goblet cells. Eosinophils, neutrophils, and PAF levels in bronchoalveolar lavage fluid were also significantly increased after cigarette smoke. Treatment with a specific PAF receptor antagonist, E-6123, significantly attenuated the increases in the number of airway goblet cells, eosinophils, and neutrophils observed after cigarette smoke exposure. These results suggest that endogenous PAF may play a key role in goblet cell metaplasia induced by cigarette smoke and that potential roles exist for inhibitors of PAF receptor in the treatment of hypersecretory airway diseases. PMID:11159026

  14. 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. PMID:26562061

  15. 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.…

  16. 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.

  17. The Effect of Cigarette Smoking on Bladder Carcinogens in Man

    PubMed Central

    Kerr, W. K.; Barkin, M.; Levers, P. E.; Woo, S. K.-C.; Menczyk, Z.

    1965-01-01

    In the metabolism of the amino acid, tryptophan, certain products with the orthoaminophenol configuration are believed to act as topical carcinogens in the urinary bladder. In addition, a statistical relationship between cigarette smoking and bladder cancer has been established in recent years. Thirty metabolic studies are reported on six healthy male subjects when smoking and not smoking. Results revealed a consistent rise in carcinogenic metabolites of tryptophan when smoking (+ 50%), with a reciprocal fall in the end product, N'-methylnicotinamide (- 34%). Carcinogens fell and N'-methylnicotinamide rose when subjects stopped smoking. These metabolic studies confirm the statistical relationship between smoking and bladder cancer, and suggest that cigarette smoking blocks the normal metabolism of tryptophan, leading to the accumulation of carcinogenic metabolites. PMID:14306113

  18. The effects of cigarette smoking on male fertility.

    PubMed

    Kovac, Jason R; Khanna, Abhinav; Lipshultz, Larry I

    2015-04-01

    Cigarette smoking, one of the main causes of preventable morbidity and mortality, has a multitude of well-known side effects. The relationship between cigarette smoking and infertility has been studied for decades; however, large-scale, population-wide prospective studies are lacking. The majority of the current literature is in the form of retrospective studies focused on the effects of smoking on semen analyses. This article discusses the results of these studies and reviews the postulated mechanisms. The effects of smoking on assisted reproduction and in vitro fertilization outcomes are noted. The consequences of smoking while pregnant on future fertility as well as the outcomes of second-hand smoke are analyzed. The current evidence suggests that men should be advised to abstain from smoking in order to improve reproductive outcomes. PMID:25697426

  19. Electronic cigarettes: do they have a role in smoking cessation?

    PubMed

    Odum, Lauren E; O'Dell, Katie A; Schepers, Jacqueline S

    2012-12-01

    Electronic cigarettes have gained popularity among patients as a smoking cessation aid despite not being approved or supported for this purpose by the United States Food and Drug Administration due to concerns with poor manufacturing practices and the presence of known carcinogens in the limited products that they tested. A few studies have evaluated the effects of electronic cigarettes on plasma nicotine levels and heart rate but found negligible effects. Safety data are mainly limited to surveys in which patients report only minor side effects, such as mouth and throat irritation, headache, vertigo, and nausea. The efficacy of electronic cigarettes has been evaluated in studies in which patients report great success with being able to cut back or stop tobacco cigarette consumption. However, many of these studies introduce bias due to recruiting on e-cigarette Web sites and having tobacco cigarette use self-reported by the participant rather than objectively tested. A few studies have formally evaluated nicotine craving when using electronic cigarettes with mixed results. Although patients support the use of electronic cigarettes in smoking cessation, more formal studies on safety and efficacy should be completed in order to determine whether these products have a role in smoking cessation. PMID:22797832

  20. 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

  1. 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.

  2. A Comparative Analysis of Teenagers Who Smoke Different Cigarette Brands.

    ERIC Educational Resources Information Center

    Enomoto, Carl E.

    2000-01-01

    Analyzes and compares the survey responses of teenagers who smoke different cigarette brands, specifically Marlboro, Camel, and Newport. Differences were seen across brands but teen smokers had similar opinions about quitting. Given the differences across brands, more flexible approaches may be needed to address teenage smoking. (Author/MKA)

  3. 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…

  4. 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…

  5. Peer Influences on Adolescent Cigarette Smoking: A Prospective Sibling Analysis.

    ERIC Educational Resources Information Center

    Rose, Jennifer S.; Chassin, Laurie; Presson, Clark C.; Sherman, Steven J.

    1999-01-01

    Studied role of nonshared parent and peer influences on siblings as predictors of adolescent cigarette smoking onset. Found peer influences were predictors of smoking onset when shared influences were controlled. Nonshared peer influences on siblings were stronger in educated families. Findings highlight utility of controlling for shared…

  6. The pathophysiological mechanisms underlying mucus hypersecretion induced by cold temperatures in cigarette smoke-exposed rats.

    PubMed

    Li, Min-Chao; Yang, Gang; Zhou, Xiang-Dong; Tselluyko, Sergey; Perelman, Juliy M

    2014-01-01

    In a recent study, we demonstrated that transient receptor potential melastatin 8 (TRPM8), a calcium-permeable cation channel that is activated by cold temperatures, is localized in the bronchial epithelium and is upregulated in subjects with chronic obstructive pulmonary disease, which causes them to be more sensitive to cold air. In the present study, we found that exposure to cold temperatures induced ciliary ultrastructural anomalies and mucus accumulation on the epithelial surface. Male Sprague-Dawley rats were exposed to cold temperatures to determine the effects of cold air on ultrastructural changes in cilia and the airway epithelial surface. The rats were also exposed to cigarette smoke and/or cold temperatures to determine the effects of smoke and cold air on TRPM8 expression and the role of cold air in cigarette smoke-induced mucus hypersecretion. Following real-time RT-PCR and western blot analysis, we observed a high expression of TRPM8 mRNA and protein in the bronchial tissue following cigarette smoke inhalation. As shown by ELISA, concurrent cold air enhanced the levels of mucin 5AC (MUC5AC) protein, as well as those of inflammatory factors [tumor necrosis factor (TNF)-α and interleukin (IL)-8] that were induced by cigarette smoke inhalation to a greater extent than stimulation with separate stimuli (cold air and cigarette smoke separately). The results suggest that cold air stimuli are responsible for the ultrastructural abnormalities of bronchial cilia, which contribute to abnormal mucus clearance. In addition, cold air synergistically amplifies cigarette smoke-induced mucus hypersecretion and the production of inflammatory factors through the elevated expression of the TRPM8 channel that is initiated by cigarette smoke inhalation. PMID:24154796

  7. Intentions to Smoke Cigarettes Among Never-Smoking US Middle and High School Electronic Cigarette Users: National Youth Tobacco Survey, 2011–2013

    PubMed Central

    Agaku, Israel T.; Arrazola, René A.; Apelberg, Benjamin J.; Caraballo, Ralph S.; Corey, Catherine G.; Coleman, Blair N.; Dube, Shanta R.; King, Brian A.

    2015-01-01

    Introduction: Electronic cigarette (e-cigarette) use is increasing rapidly, and the impact on youth is unknown. We assessed associations between e-cigarette use and smoking intentions among US youth who had never smoked conventional cigarettes. Methods: We analyzed data from the nationally representative 2011, 2012, and 2013 National Youth Tobacco Surveys of students in grades 6–12. Youth reporting they would definitely not smoke in the next year or if offered a cigarette by a friend were defined as not having an intention to smoke; all others were classified as having positive intention to smoke conventional cigarettes. Demographics, pro-tobacco advertisement exposure, ever use of e-cigarettes, and ever use of other combustibles (cigars, hookah, bidis, kreteks, and pipes) and noncombustibles (chewing tobacco, snuff, dip, snus, and dissolvables) were included in multivariate analyses that assessed associations with smoking intentions among never-cigarette-smoking youth. Results: Between 2011 and 2013, the number of never-smoking youth who used e-cigarettes increased 3-fold, from 79,000 to more than 263,000. Intention to smoke conventional cigarettes was 43.9% among ever e-cigarette users and 21.5% among never users. Ever e-cigarette users had higher adjusted odds for having smoking intentions than never users (adjusted odds ratio = 1.70, 95% confidence interval = 1.24–2.32). Those who ever used other combustibles, ever used noncombustibles, or reported pro-tobacco advertisement exposure also had increased odds for smoking intentions. Conclusion: In 2013, more than a quarter million never-smoking youth used e-cigarettes. E-cigarette use is associated with increased intentions to smoke cigarettes, and enhanced prevention efforts for youth are important for all forms of tobacco, including e-cigarettes. PMID:25143298

  8. 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.

  9. 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

  10. Cigarette smoking and gastrointestinal diseases: the causal relationship and underlying molecular mechanisms (review).

    PubMed

    Li, L F; Chan, R L Y; Lu, L; Shen, J; Zhang, L; Wu, W K K; Wang, L; Hu, T; Li, M X; Cho, C H

    2014-08-01

    Cigarette smoking is an important risk factor for gastrointestinal (GI) disorders, including peptic ulcers, inflammatory bowel diseases, such as Crohn's disease and cancer. In this review, the relationship between smoking and GI disorders and the underlying mechanisms are discussed. It has been demonstrated that cigarette smoking is positively associated with the pathogenesis of peptic ulcers and the delay of ulcer healing. Mechanistic studies have shown that cigarette smoke and its active ingredients can cause mucosal cell death, inhibit cell renewal, decrease blood flow in the GI mucosa and interfere with the mucosal immune system. Cigarette smoking is also an independent risk factor for various types of cancer of the GI tract. In this review, we also summarize the mechanisms through which cigarette smoking induces tumorigenesis and promotes the development of cancer in various sections of the GI tract. These mechanisms include the activation of nicotinic acetylcholine receptors, the formation of DNA adducts, the stimulation of tumor angiogenesis and the modulation of immune responses in the GI mucosa. A full understanding of these pathogenic mechanisms may help us to develop more effective therapies for GI disorders in the future. PMID:24859303

  11. Cigarette smoking and thinning of the brain's cortex.

    PubMed

    Karama, S; Ducharme, S; Corley, J; Chouinard-Decorte, F; Starr, J M; Wardlaw, J M; Bastin, M E; Deary, I J

    2015-06-01

    Cigarette smoking is associated with cognitive decline and dementia, but the extent of the association between smoking and structural brain changes remains unclear. Importantly, it is unknown whether smoking-related brain changes are reversible after smoking cessation. We analyzed data on 504 subjects with recall of lifetime smoking data and a structural brain magnetic resonance imaging at age 73 years from which measures of cortical thickness were extracted. Multiple regression analyses were performed controlling for gender and exact age at scanning. To determine dose-response relationships, the association between smoking pack-years and cortical thickness was tested and then repeated, while controlling for a comprehensive list of covariates including, among others, cognitive ability before starting smoking. Further, we tested associations between cortical thickness and number of years since last cigarette, while controlling for lifetime smoking. There was a diffuse dose-dependent negative association between smoking and cortical thickness. Some negative dose-dependent cortical associations persisted after controlling for all covariates. Accounting for total amount of lifetime smoking, the cortex of subjects who stopped smoking seems to have partially recovered for each year without smoking. However, it took ~25 years for complete cortical recovery in affected areas for those at the mean pack-years value in this sample. As the cortex thins with normal aging, our data suggest that smoking is associated with diffuse accelerated cortical thinning, a biomarker of cognitive decline in adults. Although partial recovery appears possible, it can be a long process. PMID:25666755

  12. 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.

  13. Occluded Cigarette Smoke Exposure Causing Localized Chloracne-Like Comedones.

    PubMed

    Patterson, Andrew T; Tian, Frances T; Elston, Dirk M; Kaffenberger, Benjamin H

    2015-01-01

    Many environmental acne disorders, including chloracne and oil acne, were previously thought to occur predominantly in occupational settings following polycyclic aromatic hydrocarbon exposure. Cigarette smoke has also been shown to contain a large number of these toxic polycyclic aromatic hydrocarbon components and strictly correlates with noninflammatory acneiform lesion development in postadolescent patients. We report a case of localized open comedones associated with occluded cigarette smoke exposure near the nasal cavity due to infrequently changed gauze following rhinectomy. The dermal uptake of polycyclic aromatic hydrocarbon components in cigarette smoke has the potential to function as a contributing factor in chloracne development. Several of these environmental and noninflammatory acne subtypes may share a common molecular propensity for enhanced comedogenesis originating from aryl hydrocarbon receptor pathway effects in the skin. Additional studies are needed to further elucidate the exact mechanistic pathways through which tobacco smoke impacts the integumentary system. PMID:26360246

  14. 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.

  15. 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. PMID:18639603

  16. 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

  17. Children's hedonic judgments of cigarette smoke odor: effects of parental smoking and maternal mood.

    PubMed

    Forestell, Catherine A; Mennella, Julie A

    2005-12-01

    Age-appropriate tasks were used to assess 3- to 8-year-old children's liking, identification, and preference for a variety of odors, including that of exhaled cigarette smoke. Children whose parents smoke took longer to decide whether they liked the cigarette odor and were significantly more likely to prefer the odor of cigarette to the neutral and unfamiliar odor of green tea compared with children of nonsmokers. Among children of smokers, relative preferences for the cigarette odor were related to maternal mood disturbance and depression scores. These findings suggest that some early learning about cigarette smoke odor is based on sensory experiences at home and anchors it to the emotional context in which their mothers smoke. PMID:16366814

  18. Children’s Hedonic Judgments of Cigarette Smoke Odor: Effects of Parental Smoking and Maternal Mood

    PubMed Central

    Forestell, Catherine A.; Monell, Julie A. Mennella

    2006-01-01

    Age-appropriate tasks were used to assess 3-to 8-year-old children’s liking, identification, and preference for a variety of odors, including that of exhaled cigarette smoke. Children whose parents smoke took longer to decide whether they liked the cigarette odor and were significantly more likely to prefer the odor of cigarette to the neutral and unfamiliar odor of green tea compared with children of nonsmokers. Among children of smokers, relative preferences for the cigarette odor were related to maternal mood disturbance and depression scores. These findings suggest that some early learning about cigarette smoke odor is based on sensory experiences at home and anchors it to the emotional context in which their mothers smoke. PMID:16366814

  19. Measuring environmental emissions from tobacco combustion: sidestream cigarette smoke review

    SciTech Connect

    Guerin, M.R.; Higgins, C.E.; Jenkins, R.A.

    1985-01-01

    The tobacco-derived environmental emission of most common concern is the smoke issuing from cigarettes between puffs. A review of smoke formation mechanisms, sampling methods, and selected emission factors suggests that sidestream deliveries are actually much less variable than is commonly thought. Examples of devices used to generate and collect sidestream smoke for analysis are described. Emissions computed as is common practice from sidestream/mainstream ratios are compared to those determined directly. 36 refs., 3 figs., 2 tabs.

  20. 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.

  1. 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.

  2. 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.

  3. Acetyl Radical Generation in Cigarette Smoke: Quantification and Simulations

    PubMed Central

    Hu, Na; Green, Sarah A.

    2014-01-01

    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 commerial 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 filber 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 acealdehyde 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. PMID:25253993

  4. 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. PMID:26469671

  5. Effect of subchronic administration of antioxidants against cigarette smoke exposure in rats.

    PubMed

    Sohn, H O; Lim, H B; Lee, Y G; Lee, D W; Kim, Y T

    1993-01-01

    Effects of subchronic administration of antioxidants against pulmonary damage mediated by cigarette smoke were investigated in rats. Rats were continuously received ascorbic acid, N-acetylcysteine and ginseng extract together drinking water from day 25 after birth. After 30 days of antioxidant supplementation, rats were exposed to cigarette smoke generated from six cigarettes (11 mg tar) for 20 min per day throughout 30 days, and then several biochemical markers related to the redox status in vivo were analyzed in the respiratory system. The cigarette smoke induced mild histological changes in trachea and lungs. The activity of superoxide dismutase (SOD) in the lung was significantly increased, and catalase and glutathione peroxidase activities were increased less than SOD, but total sulfhydryl compounds (Total-SH) content was decreased by cigarette smoking. In spite of the increase in activities of antioxidant enzymes, the inhibitory capacity of lung preparations on in vitro lipid peroxidation using ox brain homogenates was decreased and the change in the capacity was not related to the changes of these intracellular enzymes activities, but with the content of Total-SH. On the other hand, the content of thiobarbituric acid reactive substances and the ratio of elastase to anti-protease in the lung homogenates were significantly increased. Supplementation of antioxidants, however, effectively attenuated all of such alterations induced by cigarette smoke. These results indicate that although cigarette smoking induces antioxidant enzymes in the lung as a self defense mechanism, it seems to be not sufficient to protect the pulmonary system, and that chronic antioxidant feeding could be effective to reduce pulmonary damage induced by free radicals. PMID:8135656

  6. 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.

  7. Waterpipe Tobacco Smoking and Cigarette Smoking: A Direct Comparison of Toxicant Exposure and Subjective Effects

    PubMed Central

    Cobb, Caroline O.; Shihadeh, Alan; Weaver, Michael F.

    2011-01-01

    Introduction: Waterpipe tobacco smoking is increasing worldwide and is believed by many users to be less harmful and addictive than cigarette smoking. In fact, waterpipe tobacco and cigarette smoke contain many of the same chemicals, and users are exposed to the dependence-producing drug nicotine as well as other smoke toxicants. The subjective effect profile of these 2 tobacco use methods has not been compared directly, though this information is relevant to understanding the risk of dependence development. Methods: Fifty-four participants who reported waterpipe and cigarette smoking completed 2, 45-min, counter-balanced sessions in which they completed a waterpipe use episode (mean smoking time = 43.3 min) or a cigarette (mean = 6.1 min). Outcome measures included plasma nicotine, carboxyhemoglobin (COHb), and subjective effects, including those relevant to predicting dependence potential. Results: Mean (±SEM) peak plasma nicotine concentration did not differ by session (waterpipe = 9.8 ± 1.0 ng/ml; cigarette = 9.4 ± 1.0 ng/ml). Mean peak COHb concentration differed significantly (waterpipe = 4.5% ± 0.3%; cigarette = 1.2% ± 0.1%). Subjective effect changes for waterpipe and cigarette were comparable in magnitude but often longer lived for waterpipe. Conclusions: Relative to a cigarette, waterpipe tobacco smoking was associated with similar peak nicotine exposure, 3.75-fold greater COHb, and 56-fold greater inhaled smoke volume. Waterpipe and cigarette influenced many of the same subjective effect measures. These findings are consistent with the conclusion that waterpipe tobacco smoking presents substantial risk of dependence, disease, and death, and they can be incorporated into prevention interventions that might help deter more adolescents and young adults from experimenting with an almost certainly lethal method of tobacco use. PMID:21127030

  8. 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…

  9. 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

  10. Opinions of Turkish University Students on Cigarette Smoking at Schools

    NASA Astrophysics Data System (ADS)

    Keloglu-Isler, Esra; Erdogan, Irfan

    Cigarette smoking among college students is a critical public health problem with serious personal and social consequences. This study examined college student opinions about smoking in the student cafeteria, hallways and offices, considering smoking as freedom of choice, complying with the cigarette law and policy of universities on smoking. A sample of 1527 students (53.9% female, 46.1% male) attending to the six prestigious universities in Ankara, Turkey, completed a ten-item questionnaire. Results of the study showed that nonsmoking students reported the most favorable opinions toward the issues questioned, whereas occasional smokers and regular smokers reported the least favorable opinions. The highest level of disagreement by smokers and nonsmokers was provided for banning cigarette smoking in the cafeteria. Students generally agreed on that teachers should not smoke in the classrooms and in their offices with doors open. Recommended actions include campus-wide no-smoking policies embracing indoors and outdoors and identification and use of new ways of providing smoking prevention and cessation programs and services.

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

    PubMed

    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

  12. 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.

  13. Comparison of select analytes in aerosol from e-cigarettes with smoke from conventional cigarettes and with ambient air.

    PubMed

    Tayyarah, Rana; Long, Gerald A

    2014-12-01

    Leading commercial electronic cigarettes were tested to determine bulk composition. The e-cigarettes and conventional cigarettes were evaluated using machine-puffing to compare nicotine delivery and relative yields of chemical constituents. The e-liquids tested were found to contain humectants, glycerin and/or propylene glycol, (⩾75% content); water (<20%); nicotine (approximately 2%); and flavor (<10%). The aerosol collected mass (ACM) of the e-cigarette samples was similar in composition to the e-liquids. Aerosol nicotine for the e-cigarette samples was 85% lower than nicotine yield for the conventional cigarettes. Analysis of the smoke from conventional cigarettes showed that the mainstream cigarette smoke delivered approximately 1500times more harmful and potentially harmful constituents (HPHCs) tested when compared to e-cigarette aerosol or to puffing room air. The deliveries of HPHCs tested for these e-cigarette products were similar to the study air blanks rather than to deliveries from conventional cigarettes; no significant contribution of cigarette smoke HPHCs from any of the compound classes tested was found for the e-cigarettes. Thus, the results of this study support previous researchers' discussion of e-cigarette products' potential for reduced exposure compared to cigarette smoke. PMID:25444997

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

    PubMed

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

    1985-11-01

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

  15. 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

  16. 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

  17. Macrophage Elastase Suppresses White Adipose Tissue Expansion with Cigarette Smoking

    PubMed Central

    Tsuji, Takao; Kelly, Neil J.; Takahashi, Saeko; Leme, Adriana S.; McGarry Houghton, A.

    2014-01-01

    Macrophage elastase (MMP12) is a key mediator of cigarette smoke (CS)-induced emphysema, yet its role in other smoking related pathologies remains unclear. The weight suppressing effects of smoking are a major hindrance to cessation efforts, and MMP12 is known to suppress the vascularization on which adipose tissue growth depends by catalyzing the formation of antiangiogenic peptides endostatin and angiostatin. The goal of this study was to determine the role of MMP12 in adipose tissue growth and smoking-related suppression of weight gain. Whole body weights and white adipose depots from wild-type and Mmp12-deficient mice were collected during early postnatal development and after chronic CS exposure. Adipose tissue specimens were analyzed for angiogenic and adipocytic markers and for content of the antiangiogenic peptides endostatin and angiostatin. Cultured 3T3-L1 adipocytes were treated with adipose tissue homogenate to examine its effects on vascular endothelial growth factor (VEGF) expression and secretion. MMP12 content and activity were increased in the adipose tissue of wild-type mice at 2 weeks of age, leading to elevated endostatin production, inhibition of VEGF secretion, and decreased adipose tissue vascularity. By 8 weeks of age, adipose MMP12 levels subsided, and the protein was no longer detectable. However, chronic CS exposure led to macrophage accumulation and restored adipose MMP12 activity, thereby suppressing adipose tissue mass and vascularity. Our results reveal a novel systemic role for MMP12 in postnatal adipose tissue expansion and smoking-associated weight loss by suppressing vascularity within the white adipose tissue depots. PMID:24914890

  18. Measuring the impact of cigarette smoke on the UPR.

    PubMed

    Zhao, Hong; Yang, Jin; Shan, Lin; Jorgensen, Ellen D

    2011-01-01

    The unfolded protein response (UPR) is a set of pathways activated by the accumulation of improperly folded proteins. It can be triggered by a broad range of stressful conditions which disrupt successful maturation of proteins in the endoplasmic reticulum (ER) by interfering with proper folding, assembly, and posttranslational modification. Recent studies have demonstrated the induction of ER stress and activation of elements of the UPR in human lung cells exposed to diesel exhaust particles, airborne particulate matter, and tobacco smoke. ER stress has been found to play a role in a variety of lung maladies, including cancer, infections, idiopathic pulmonary fibrosis, and chronic obstructive pulmonary disease. Lung cancer is one of the few diseases where the etiological agent, cigarette smoke (CS), is well known. It is, therefore, desirable to measure dysregulation of the UPR pathway in samples representing both the earliest events (cells exposed to CS in vitro) and in clinical samples from healthy smokers and individuals with smoking-related lung diseases. We hereby provide a detailed description of methods for assessing the degree and timing of cellular response to CS with respect to the three major UPR pathways. PMID:21266229

  19. Menthol cigarettes and smoking initiation: a tobacco industry perspective

    PubMed Central

    2011-01-01

    Objectives To determine what the tobacco industry knew about menthol cigarettes and the initiation of smoking. Methods Based on Food and Drug Administration staff-supplied research questions we used a snowball sampling strategy to search the Legacy Tobacco Documents Library (http://legacy.library.ucsf.edu) between February and April 2010. Of the approximately 11 million documents available in the LTDL, the iterative searches returned tens of thousands of results. Researchers reviewed 2634 documents and 128 were deemed relevant to one or more of the research questions. Results The documents show that menthol is added to cigarettes in part because it is known to be an attractive feature to inexperienced smokers who perceive menthol cigarettes as less harsh and easier to smoke and because of their availability from friends and family. Second, the tobacco industry found that some youths smoke menthols because they perceive them to be less harmful than non-menthol cigarettes. A key product design issue concerns whether to increase brand menthol levels to appeal to the taste preferences of long-term menthol smokers or keep menthol levels lower to appeal to inexperienced smokers. Marketing studies showed that the companies carefully researched the menthol segment of the market in order to recruit younger smokers to their brands. The industry tracked menthol cigarette usage by age, gender and race to inform product development and marketing decisions. Conclusions Menthol is a prominent design feature used by cigarette manufacturers to attract and retain new, younger smokers. PMID:21504927

  20. Psycho-social study of cigarette smoking.

    PubMed

    Tandon, A K; Chaturvedi, P K; Dubey, A L; Narang, R K; Singh, S K; Chandra, S

    1990-04-01

    The present study has been carried out to assess the smoking habit among medical students and its relationship to demographic, social and psychological characteristics. Prevalence of smoking was found to be 30.79% in 854 students who responded to the questionnaire adequately. Smoking habit was more common among student who were married hailed from rural areas and the intensity of smoking increased with advancement in the career in medical profession. A strong association was observed between the habit and family history of smoking. The psychological factors associated with smoking were worry about examination unhappiness without justified cause and failure in friendship. PMID:21927445

  1. Effects of Low and High Nicotine Cigarette Smoking on Mood States and the HPA Axis in Men

    PubMed Central

    Mendelson, Jack H.; Sholar, Michelle B.; Goletiani, Nathalie; Siegel, Arthur J.; Mello, Nancy K.

    2005-01-01

    The acute effects of smoking a low or high nicotine cigarette on hypothalamic-pituitary-adrenal (HPA) hormones, subjective responses and cardiovascular measures were studied in 20 healthy men who met DSM-IV criteria for nicotine dependence. Within 4 puffs (or 2 min) after cigarette smoking began, plasma nicotine levels and heart rate increased significantly (P<0.01), and peak ratings of “high” and “rush” on a Visual Analogue Scale (VAS) were reported. Reports of “high”, “rush” and “liking” and reduction of “craving” were significantly greater after smoking a high nicotine cigarette than a low nicotine cigarette (P<0.05). Peak plasma nicotine levels after high nicotine cigarette smoking (23.9 ± 2.6 ng/ml) were significantly greater than after low nicotine cigarette smoking (3.63 ± 0.59 ng/ml) (P<0.001). After smoking a low nicotine cigarette, ACTH, cortisol, DHEA and epinephrine did not change significantly from baseline. After high nicotine cigarette smoking began, plasma ACTH levels increased significantly above baseline within 12 min and reached peak levels of 21.88 ± 5.34 pmol/L within 20 min. ACTH increases were significantly correlated with increases in plasma nicotine (r=0.85; P<0.0001), DHEA (r=0.66; P=0.002), and epinephrine (r=0.86; P<0.0001). Cortisol and DHEA increased significantly within 20 min (P<0.05) and reached peak levels of 424 ± 48 nmol/L and 21.13 ± 2.55 ng/ml within 60 and 30 min, respectively. Thus cigarette smoking produced nicotine dose-related effects on HPA hormones, subjective and cardiovascular measures. These data suggest that activation of the HPA axis may contribute to the abuse-related effects of cigarette smoking. PMID:15870834

  2. 210Po and 210Pb inhalation by cigarette smoking in Italy.

    PubMed

    Desideri, Donatella; Meli, Maria Assunta; Feduzi, Laura; Roselli, Carla

    2007-01-01

    210Po and its precursor 210Pb in cigarette smoke contribute a significant radiation dose to the lungs of smokers. In this work, the concentration of 210Po was determined in 17 of the most frequently smoked cigarette brands in Italy. Samples of tobacco, fresh filters, ash, and post-smoking filters were analyzed; 210Po was determined by alpha spectrometry after its spontaneous deposition on a silver disk. To verify the radioactive equilibrium between 210Po and 210Pb, lead was determined in one tobacco sample by counting the beta activity of its decay product 210Bi with a gas flow proportional detector after separation. The results of the present study show 210Po concentrations ranged from 6.84 to 17.49 mBq per cigarette. Based on these results, smokers who smoke 20 cigarettes per day inhale, on average, 79.53 +/- 28.65 mBq d(-1) of 210Po and 210Pb each. The mean value of the annual committed effective dose for Italian smokers, calculated by applying the dose conversion factor for adults of 4.3 microSv Bq(-1) for 210Po and 5.6 microSv Bq(-1) for 210Pb, was estimated to be 124.8 and 162.6 microSv y(-1) for 210Po and 210Pb, respectively. The lung dose from inhalation of cigarette smoke is much higher than the lung dose from inhalation of atmospheric 210Po and 210Pb. PMID:17164600

  3. 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

  4. 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.

  5. 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.

  6. Smoke chemistry, in vitro and in vivo toxicology evaluations of the electrically heated cigarette smoking system series K.

    PubMed

    Werley, Michael S; Freelin, Susan A; Wrenn, Susan E; Gerstenberg, Birgit; Roemer, Ewald; Schramke, Heike; Van Miert, Erik; Vanscheeuwijck, Patrick; Weber, Susanne; Coggins, Christopher R E

    2008-11-01

    The Electrically Heated Cigarette Smoking System Series K (EHCSS) produces smoke through the controlled electrical heating of tobacco. Evaluation of the EHCSS was accomplished by comparison with commercial and reference cigarettes, using International Organization for Standardization (ISO) and alternative puffing regimens based on nicotine exposures measured in a short-term clinical study. Using the alternative puffing regimen and compared with conventional cigarettes on a per cigarette basis, the EHCSS had 50-60% reductions in tar and nicotine; at least 90% reductions in carbon monoxide, nitrogen oxides, 1,3-butadiene, isoprene, acrylonitrile, polyaromatic hydrocarbons, hydrogen cyanide, aromatic amines, tobacco specific nitrosamines, and phenol; and least a 40% reduction in 2-nitropropane. Other important smoke constituents in EHCSS smoke were reduced as well. The in vitro studies showed similar large reductions in biological activity. Ames mutagenicity of total particulate matter (TPM) from the EHCSS was reduced by 70-90%; cytotoxicity of the TPM was reduced by approximately 82% and 65% for the gas-vapor phase. In vivo testing under ISO smoking conditions in the mouse skin painting assay demonstrated later dermal tumor onset, lower dermal tumor incidence, reduced dermal tumor multiplicity, and a lower proportion of malignant dermal tumors in EHCSS smoke condensate-exposed mice. Thirty-five day and 90-day nose-only inhalation studies in rats showed reductions in pulmonary inflammation and other biological activity, including histopathological endpoints. We conclude that under the conditions of these in vitro and in vivo studies, the EHCSS demonstrated significantly lower biological activity compared to conventional cigarettes, and may suggest the potential for reductions in human smokers. PMID:18590791

  7. Trends in major risk factors. Cigarette smoking.

    PubMed Central

    Simpson, D.

    1984-01-01

    The object of this paper is to examine the role of smoking as a risk factor in coronary heart disease, starting with a brief history of smoking in the U.K. and a reminder of the epidemiological evidence linking smoking and cardiovascular disease. This is followed by a more detailed look at the trends in consumption of tobacco and the major factors influencing those trends, together with an outline of the main components of a smoking control policy designed to combat our epidemic of smoking-induced disease. PMID:6694941

  8. Make Your Own Cigarettes: Toxicant Exposure, Smoking Topography, and Subjective Effects

    PubMed Central

    Koszowski, Bartosz; Rosenberry, Zachary R.; Viray, Lauren C.; Potts, Jennifer L.; Pickworth, Wallace B.

    2014-01-01

    Background Despite considerable use of make your own (MYO) cigarettes worldwide and increasing use in the United States, relatively little is known about how these cigarettes are smoked and the resultant toxicant exposure. Methods In a laboratory study, we compared two types of MYO cigarettes – roll your own (RYO) and personal machine made (PMM) – with factory made (FM) cigarettes in three groups of smokers who exclusively used RYO (n=34), PMM (n=23) or FM (n=20). Within each group, cigarettes were smoked in three conditions: 1) after confirmed overnight tobacco abstinence; 2) in an intense smoking paradigm; 3) and without restrictions. All cigarettes were smoked ad lib through a smoking topography unit. Results Plasma nicotine significantly increased after cigarettes in all conditions except PMM in the intense smoking paradigm. Puff volume, puff duration, total puff volume and puff velocity did not differ between cigarette types but the puffs per cigarette and time to smoke were significantly smaller for RYO compared to PMM and FM. Regardless of the cigarette, participants consumed the first three puffs more vigorously than the last three puffs. Conclusions Despite the belief of many of their consumers smoking MYO cigarettes are not a safe alternative to consumption of FM cigarettes. Like FM, MYO cigarettes expose their users to harmful constituents of tobacco smoke and despite differences in size and design their puffing profiles are remarkably similar. Impact These data are relevant to health and regulatory considerations on the MYO cigarettes. PMID:24925675

  9. 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. PMID:23314114

  10. Cigarette smoke detection from captured image sequences

    NASA Astrophysics Data System (ADS)

    Iwamoto, Kentaro; Inoue, Hironori; Matsubara, Toru; Tanaka, Toshihisa

    2010-01-01

    We investigate a detection of smoke from captured image sequences. We propose to address the following two problems in order to attain this goal. The first problem is to estimate candidate areas of smoke. The second problem is to judge if smoke exists in the scene. To solve the first problem, we apply the previously proposed framework where image sequences are divided into some small blocks and the smoke detection is done in each small block. In this framework, we propose to use color and edge information of the scene. To solve the second problem, we propose a method for judging if smoke exists in the scene by using the areas of smoke obtained in the last step part. We propose some feature values for judging if smoke exists in the scene. Then, by simulation we find the best combination of feature values. In addition, we study the effect of normalization, which provide better performance in recognition.

  11. Alteration of sperm protein profile induced by cigarette smoking.

    PubMed

    Chen, Xiaohui; Xu, Wangjie; Miao, Maohua; Zhu, Zijue; Dai, Jingbo; Chen, Zhong; Fang, Peng; Wu, Junqing; Nie, Dongsheng; Wang, Lianyun; Wang, Zhaoxia; Qiao, Zhongdong; Shi, Huijuan

    2015-07-01

    Cigarette smoking is associated with lower semen quality, but how cigarette smoking changes the semen quality remains unclear. The aim of this study was to screen the differentially expressed proteins in the sperm of mice with daily exposure to cigarette smoke. The 2D gel electrophoresis (2DE) and mass spectrometry (MS) analyses results showed that the mouse sperm protein profile was altered by cigarette smoking. And 22 of the most abundant proteins that correspond to differentially expressed spots in 2DE gels of the sperm samples were identified. These proteins were classified into different groups based on their functions, such as energy metabolism, reproduction, and structural molecules. Furthermore, the 2DE and MS results of five proteins (Aldoa, ATP5a1, Gpx4, Cs, and Spatc1) were validated by western blot analysis and reverse transcriptase-polymerase chain reaction. Results showed that except Spatc1 the other four proteins showed statistically significant different protein levels between the smoking group and the control group (P < 0.05). The expressions of three genes (Aldoa, Gpx4, and Spatc1) were significantly different (P < 0.05) at transcription level between the smoking group and the control group. In addition, five proteins (Aldoa, ATP5a1, Spatc1, Cs, and Gpx4) in human sperm samples from 30 male smokers and 30 non-smokers were detected by western blot analysis. Two proteins (Aldoa and Cs) that are associated with energy production were found to be significantly altered, suggesting that these proteins may be potential diagnostic markers for evaluation of smoking risk in sperm. Further study of these proteins may provide insight into the pathogenic mechanisms underlying infertility in smoking persons. PMID:26063603

  12. 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. PMID:26800860

  13. Interrelationships of cigarette smoking, testicular varicoceles, and seminal fluid indexes.

    PubMed

    Klaiber, E L; Broverman, D M; Pokoly, T B; Albert, A J; Howard, P J; Sherer, J F

    1987-03-01

    Data on cigarette smoking, testicular varicoceles, seminal fluid indexes, and oligospermia were examined in 160 young men without known disease and in 94 husbands in infertile couples. The combination of smoking and testicular varicoceles is strongly related to the incidence of oligospermia, defined as sperm count less than or equal to 20 X 10(6)/ml, in each sample. Smokers with testicular varicoceles, in each sample, had a disproportionately high incidence of oligospermia. In the combined sample of 254 men, the smokers with testicular varicoceles had an incidence of oligospermia approximately ten times greater than that in nonsmokers with testicular varicoceles and approximately five times greater than that in men who smoked but were without testicular varicoceles. This relationship of cigarette smoking and testicular varicoceles to oligospermia has not been previously reported. The pathophysiologic basis of the interaction between smoking and varicoceles was theorized to be due to an increased secretion of catecholamines from the adrenal medulla, induced by cigarette smoking. The elevated catecholamine concentrations in the renal vein would then reach the testes via retrograde flow down the internal spermatic vein in men with testicular varicoceles, resulting in seminiferous tubule damage. PMID:3556626

  14. 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

  15. 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.

  16. 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

  17. Smoking Norms and the Regulation of E-Cigarettes.

    PubMed

    Voigt, Kristin

    2015-10-01

    Electronic nicotine delivery systems (ENDS)-commonly called e-cigarettes-are at the center of a polarized debate. How should they be regulated? Central to this debate is the concern that e-cigarettes could lead to the renormalization of smoking and that the regulation of ENDS should therefore be modeled on the regulation of conventional cigarettes. I argue that arguments based on the renormalization of smoking can lend support to restrictions on marketing of ENDS, but that such arguments are problematic when used to justify restrictions on where ENDS can be used. The debate has been insufficiently sensitive to the ethical complexities of attempts to manipulate social norms to change health behaviors; these complexities must also inform the debate about ENDS and their regulation. PMID:26270285

  18. Perlite filtration of phenolic compounds from cigarette smoke.

    PubMed

    Rostami-Charati, Faramarz; Robati, Gholamreza Moradi; Naghizadeh, Farhad; Hosseini, Shahnaz; Chaichi, Mohammad Javad

    2013-01-01

    Adsorption of phenolic compounds and chemical analysis of them from a local production cigarette (named by Farvardin cigarette) smoke have been investigated by using perlite filtration. In this research, the mainstream smoke was tested by three filtration methods: Perlite filter, Cambridge filter and general cigarette filter. Then the used filter was extracted by pure methanol as solvent. After that, the extracted solution was analysed by GC-MS. By this consideration, the phenolic derivatives such as phenol, hydroquinone, resorcinol, pyrocatechol, m-cresol, p-cresol and o-cresol were detected. The structure of the perlite filtration after absorption was studied by SEM. In addition, its chemical structure was investigated by XRD and XRF. PMID:23190556

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

    PubMed Central

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

    2013-01-01

    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 safety (46.1%), exhibited greater comprehension of the health risks of smoking and were more likely (48.5%) than other participants (33.6%) to report quit intentions. Risk perceptions partially mediated the relationship between FDA evaluation belief and quit intentions. Conclusions These findings highlight the need for proactive, effective communication to the public about the aims of new tobacco product regulations. PMID:22251767

  20. Assessing the Validity of Self-Reported Adolescent Cigarette Smoking.

    ERIC Educational Resources Information Center

    Martin, Gary L.; Newman, Ian M.

    1988-01-01

    Compared adolescent cigarette smoking rates determined by traditional questionnaire, random response questionnaire, and carbon monoxide test. Results from 1,160 ninth graders in 40 classrooms in 7 schools indicated that random response questionnaire elicited statistically larger proportion of smokers than did traditional questionnaire. Neither…

  1. 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…

  2. Teenage Cigarette Smoking Self Test and Discussion Leader's Guide. Guide.

    ERIC Educational Resources Information Center

    Public Health Service (DHHS), Rockville, MD.

    This self test was designed to help teenagers understand their feelings about cigarette smoking. The book contains a leader's guide which describes how the test can be used as a self-administered, self-scored tool; as a basis for group discussion; or for research purposes. Also included are six duplicating masters which are perforated for easy…

  3. Preventing Relapse to Cigarette Smoking by Behavioral Skill Training.

    ERIC Educational Resources Information Center

    Hall, Sharon M.; And Others

    1984-01-01

    Crossed two relapse prevention conditions (skills training-vs-discussion control) with two levels of aversive smoking in volunteer subjects (N=123). Results indicated that relapse-prevention skill training did prevent relapse among cigarette smokers. Lighter smokers were more favorably influenced. (LLL)

  4. 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…

  5. 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

  6. [Oral hygiene in pregnant women versus cigarette smoking].

    PubMed

    Nakonieczna-Rudnicka, Marta; Gogacz, Małgorzata; Kobyłecka, Elzbieta; Bachanek, Teresa

    2013-01-01

    Proper oral hygiene is an essential element of dental caries prophylaxis and periodontitis. The aim of the study was evaluation of the oral health state and the state of periodontal in pregnant women in relation to the status of cigarette smoking. Survey and clinical studies were conducted in the group of 100 women--80% pregnant women and 20% in the first week of puerperium remaining at the gynaecological and obstetric hospital wards in Lublin and its region. The mean age of the investigated was 27.94. Study results revealed no correlation between the frequency of pregnant women tooth-brushing and the status of cigarette smoking or non-smoking. The average oral hygiene evaluated on the basis of API index was stated essentially more frequently in the group of non-smoking women (50%) in comparison with the smoking women (24.14%),, whereas improper oral hygiene was stated essentially more frequently in the group of smoking women (31.03%) in comparison with non-smokers (11.29%) (chi = 7.82, p < 0.05). No correlation was stated between the state of periodontal in smoking and non-smoking pregnant women. PMID:24501798

  7. 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

  8. Cigarette smoking and bone healing: implications in foot and ankle surgery.

    PubMed

    Haverstock, B D; Mandracchia, V J

    1998-01-01

    Despite the known health risks associated with cigarettes, millions of Americans continue to smoke. Much has been reported on the adverse effects of cigarette smoke on wound healing. Recent experimental work and clinical observation have demonstrated the risk of impaired bone healing associated with cigarette smoking. The authors review the biological aspects of bone healing and analyze how the chemical components of cigarette smoke affect the bone healing process. Laboratory and clinical data are also reviewed. Cessation of cigarette smoking before foot and ankle surgery is recommended by the authors. PMID:9470121

  9. Cigarette Smoking Among Students at the University of Tuzla

    PubMed Central

    Ibisevic, Merima; Avdic, Azra; Osmanovic, Enes; Kadric, Nedzad; Avdic, Sevleta

    2015-01-01

    Introduction: Cigarette smoking among students is greatly widespread. Smoking prevalence ranges from 28% to 67% for students, respectively, from 19% to 34% for female students. Aim: The aim of this survey was to investigate the smoking habits of students, who are studying at three faculties at the University of Tuzla in academic Year 2012/2013 and to investigate whether there is a difference in smoking habits of students from different faculties and observed by gender. Patients and Methods: The study included a total of 254 students, 170 females (66.93%) and 84 male patients (33.07%). A representative sample consisted of students of three faculties of the University of Tuzla. Results: The conducted analyzes have shown that in this sample 22.8% of current smokers, and 7.8% are former smokers who now no longer smoke. Due to the adopted smoking habits, which some students began to adopt in the age of 13, in 47.5% part of students occasionally was observed some symptoms (cough, etc.) which are attributed to smoking. The analysis showed no statistically significant gender difference in smoking habits. Although the trend of smoking in the population students progression, one and the same quantity was well as male colleagues. We did not find any statistically significant difference in onset of adopting smoking habits. Conclusion: The analyzes have shown that in this sample 22.8% of current smokers, and 7.8% were former smokers who now no longer smoke. The analysis showed no statistically significant gender difference in smoking habits of all students. There were no statistically significant differences in the daily consumption of cigarettes between faculty. PMID:26005265

  10. Cigarette smoking, illicit drug use, and routes of administration among heroin and cocaine users

    PubMed Central

    Harrell, PT; Trenz, RC; Scherer, M; Ropelewski, LR; Latimer, WW

    2012-01-01

    Cigarette smoking is ubiquitous among illicit drug users. Some have speculated that this may be partially due to similarities in the route of administration. However, research examining the relationship between cigarette smoking and routes of administration of illicit drugs is limited. To address this gap, we investigated sociodemographic and drug use factors associated with cigarette smoking among cocaine and heroin users in the Baltimore, Maryland community (N=576). Regular and heavy cigarette smokers were more likely to be White, have a history of a prior marriage, and have a lower education level. Regular smoking of marijuana and crack was associated with cigarette smoking, but not heavy cigarette smoking. Injection use was more common among heavy cigarette smokers. In particular, regular cigarette smokers were more likely to have a lifetime history of regularly injecting heroin. Optimal prevention and treatment outcomes can only occur through a comprehensive understanding of the interrelations between different substances of abuse. PMID:22305644

  11. 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

    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

  12. 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

  13. 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…

  14. Reductions in cigarette smoking and acute myocardial infarction mortality in Jefferson County, Texas.

    PubMed

    McAlister, Alfred L; Huang, Philip; Ramirez, Amelie G; Harrist, Ronald B; Fonseca, Vincent P

    2010-12-01

    After litigation against the tobacco industry ended in a settlement, the Texas legislature funded pilot projects to reduce tobacco use in selected areas of the state. Subsequent telephone surveys showed that well-funded activities were successful in reducing population rates of self-reported cigarette smoking. We present evidence that the reduction in smoking promptly led to lower rates of death from acute myocardial infarctions. PMID:20966365

  15. Mood Variability and Cigarette Smoking Escalation among Adolescents

    PubMed Central

    Weinstein, Sally M.; Mermelstein, Robin; Shiffman, Saul; Flay, Brian

    2008-01-01

    The current study examined how affect dysregulation, as indexed via within-person negative mood variability, related to longitudinal patterns of smoking among adolescents. Eighth and 10th grade students (N = 517; 56% girls) provided data on cigarette use at baseline, six-, and twelve-month waves, and also provided ecological momentary assessments of negative moods via palmtop computers for one week at each wave. Mood variability was examined via the intraindividual standard deviations of negative mood reports at each wave. As predicted, high levels of negative mood variability at baseline significantly differentiated adolescents who escalated in their smoking behavior over time from those who never progressed beyond low levels of experimentation during the course of the study. Mixed-effects regression models revealed that adolescents who escalated in their smoking experienced a reduction in mood variability as smoking increased, whereas mood variability levels were more stable among those with consistently high or low levels of cigarette use. Results suggest that high negative mood variability is a risk factor for future smoking escalation, and mood stabilizing effects may reinforce and maintain daily cigarette use among youth. PMID:19071975

  16. Comparison of the behavioral effects of cigarette smoke and pure nicotine in rats

    PubMed Central

    Harris, Andrew C.; Mattson, Christina; LeSage, Mark G.; Keyler, Daniel E.; Pentel, Paul R.

    2010-01-01

    Animal models of tobacco dependence typically rely on parenteral administration of pure nicotine. Models using cigarette smoke inhalation might more accurately simulate nicotine exposure in smokers. The primary goal of this study was to validate methods for administering cigarette smoke to rats using exposure conditions that were clinically relevant and also produced brain nicotine levels similar to those produced by behaviorally active doses of pure nicotine. A secondary goal was to begin examining the behavioral effects of smoke. Nose-only exposure (NOE) to smoke for 10–45 min or whole-body exposure (WBE) to smoke for 1–4 hr produced serum nicotine concentrations similar to those in smokers (14–55 ng/ml), without excessive carbon monoxide exposure. Daily nicotine (0.1 mg/kg, s.c.) induced locomotor sensitization whereas 45-min NOE producing brain nicotine levels within the same range did not. Nicotine 0.125 mg/kg s.c. reversed withdrawal from a chronic nicotine infusion as measured by elevations in intracranial self-stimulation thresholds whereas 4-hr WBE producing similar brain nicotine levels did not. These data demonstrate the feasibility of delivering cigarette smoke to rats at clinically relevant doses, and provide preliminary evidence that the behavioral effects of nicotine delivered in smoke may differ from those of pure nicotine. PMID:20494826

  17. Cigarette Smoke Induces Systemic Defects in Cystic Fibrosis Transmembrane Conductance Regulator Function

    PubMed Central

    Raju, S. Vamsee; Jackson, Patricia L.; Courville, Clifford A.; McNicholas, Carmel M.; Sloane, Peter A.; Sabbatini, Gina; Tidwell, Sherry; Tang, Li Ping; Liu, Bo; Fortenberry, James A.; Jones, Caleb W.; Boydston, Jeremy A.; Clancy, J. P.; Bowen, Larry E.; Accurso, Frank J.; Blalock, J. Edwin; Dransfield, Mark T.

    2013-01-01

    Rationale: Several extrapulmonary disorders have been linked to cigarette smoking. Smoking is reported to cause cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction in the airway, and is also associated with pancreatitis, male infertility, and cachexia, features characteristic of cystic fibrosis and suggestive of an etiological role for CFTR. Objectives: To study the effect of cigarette smoke on extrapulmonary CFTR function. Methods: Demographics, spirometry, exercise tolerance, symptom questionnaires, CFTR genetics, and sweat chloride analysis were obtained in smokers with and without chronic obstructive pulmonary disease (COPD). CFTR activity was measured by nasal potential difference in mice and by Ussing chamber electrophysiology in vitro. Serum acrolein levels were estimated with mass spectroscopy. Measurements and Main Results: Healthy smokers (29.45 ± 13.90 mEq), smokers with COPD (31.89 ± 13.9 mEq), and former smokers with COPD (25.07 ± 10.92 mEq) had elevated sweat chloride levels compared with normal control subjects (14.5 ± 7.77 mEq), indicating reduced CFTR activity in a nonrespiratory organ. Intestinal current measurements also demonstrated a 65% decrease in CFTR function in smokers compared with never smokers. CFTR activity was decreased by 68% in normal human bronchial epithelial cells exposed to plasma from smokers, suggesting that one or more circulating agents could confer CFTR dysfunction. Cigarette smoke–exposed mice had decreased CFTR activity in intestinal epithelium (84.3 and 45%, after 5 and 17 wk, respectively). Acrolein, a component of cigarette smoke, was higher in smokers, blocked CFTR by inhibiting channel gating, and was attenuated by antioxidant N-acetylcysteine, a known scavenger of acrolein. Conclusions: Smoking causes systemic CFTR dysfunction. Acrolein present in cigarette smoke mediates CFTR defects in extrapulmonary tissues in smokers. PMID:24040746

  18. Associations of cigarette smoking with rheumatoid arthritis in African Americans

    PubMed Central

    Mikuls, Ted R.; Sayles, Harlan; Yu, Fang; LeVan, Tricia; Gould, Karen A.; Thiele, Geoffrey M.; Conn, Doyt; Jonas, Beth L.; Callahan, Leigh F.; Smith, Edwin; Brasington, Richard; Moreland, Larry W.; Reynolds, Richard; Bridges, S. Louis

    2010-01-01

    Objective To examine the associations of cigarette smoking with rheumatoid arthritis (RA) in African Americans and to determine to whether this association is impacted by HLA-DRB1 shared epitope (SE). Methods Smoking status, cumulative smoking exposure, and SE status were measured in African American patients with RA and in healthy controls. Associations of smoking with RA were examined using age- and gender-adjusted logistic regression. Additive and multiplicative SE-smoking interactions were examined. Results After adjusting for age and gender, ever (OR = 1.45; 95% CI 1.07 to 1.97) and current smoking (OR = 1.56; 95% CI 1.07 to 2.26) were more common in African American RA cases (n = 605) than in controls (n = 255). The association of smoking with RA was limited to those with a cumulative exposure exceeding 10 pack-years, associations that were evident in both autoantibody positive and negative disease. There was evidence of a significant additive interaction between SE status and heavy smoking (≥ 10 pack-years) in RA risk (attributable proportion due to interaction [AP] of 0.58, p = 0.007) with an AP of 0.47 (p = 0.006) between SE status and ever smoking. There was no evidence of multiplicative interactions. Conclusion Among African Americans, cigarette smoking is associated not only with the risk of autoantibody positive RA but also with the risk of autoantibody negative disease. RA risk attributable to smoking is limited to African Americans with more than 10 pack-years of exposure and is more pronounced among individuals positive for HLA-DRB1 SE. PMID:20722010

  19. Cigarette smoking among psychiatric patients in Brazil.

    PubMed

    Barros, Fabiana Cristina Ribeiro de; Melo, Ana Paula Souto; Cournos, Francine; Cherchiglia, Mariângela Leal; Peixoto, Eliane Rezende de Morais; Guimarães, Mark Drew Crosland

    2014-06-01

    The aim of this study was to estimate tobacco smoking prevalence among psychiatric patients attended in care facilities in Brazil and assess associated factors. A cross-sectional multicenter study was conducted of psychiatric patients (N = 2,475) selected from 26 care facilities. Current and ex-smokers were compared to those who had never smoked. Odds ratios were estimated using logistic regression. The current and past smoking prevalence rates were 52.7% and 18.9%, respectively. Being male, aged 40 years or over, drug and alcohol use, unprotected sex and a history of physical violence were factors associated with both current and past smoking, while a low education level (≤ 8 years of schooling), history of homelessness, not practicing a religion, current or previous psychiatric hospitalization, and main psychiatric diagnosis substance use disorders, were factors only associated with current smoking. Tobacco smoking prevalence among this population was high and was higher than the rate in the general population. Appropriate interventions and smoking prevention policies should be incorporated into mental health services. PMID:25099043

  20. 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. PMID:23372073

  1. 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.

  2. Cigarette smoking and brain regulation of energy homeostasis.

    PubMed

    Chen, Hui; Saad, Sonia; Sandow, Shaun L; Bertrand, Paul P

    2012-01-01

    Cigarette smoking is an addictive behavior, and is the primary cause of cardiovascular and pulmonary disease, and cancer (among other diseases). Cigarette smoke contains thousands of components that may affect caloric intake and energy expenditure, although nicotine is the major addictive substance present, and has the best described actions. Nicotine exposure from cigarette smoke can change brain feeding regulation to reduce appetite via both energy homeostatic and reward mechanisms, causing a negative energy state which is characterized by reduced energy intake and increased energy expenditure that are linked to low body weight. These findings have led to the public perception that smoking is associated with weight loss. However, its effects at reducing abdominal fat mass (a predisposing factor for glucose intolerance and insulin resistance) are marginal, and its promotion of lean body mass loss in animal studies suggests a limited potential for treatment in obesity. Smoking during pregnancy puts pressure on the mother's metabolic system and is a significant contributor to adverse pregnancy outcomes. Smoking is a predictor of future risk for respiratory dysfunction, social behavioral problems, cardiovascular disease, obesity, and type-2 diabetes. Catch-up growth is normally observed in children exposed to intrauterine smoke, which has been linked to subsequent childhood obesity. Nicotine can have a profound impact on the developing fetal brain, via its ability to rapidly and fully pass the placenta. In animal studies this has been linked with abnormal hypothalamic gene expression of appetite regulators such as downregulation of NPY and POMC in the arcuate nucleus of the hypothalamus. Maternal smoking or nicotine replacement leads to unhealthy eating habits (such as junk food addiction) and other behavioral disorders in the offspring. PMID:22848202

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

    PubMed

    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

  4. 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

  5. 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

  6. Cigarette smoking among Chinese PLWHA: An exploration of changes in smoking after being tested HIV positive.

    PubMed

    Wang, Yuanhui; Chen, Xinguang; Li, Xiaoming; Wang, Yan; Shan, Qiao; Zhou, Yuejiao; Shen, Zhiyong

    2016-03-01

    Prevention and cessation of Tobacco use among persons living with HIV/AIDS (PLWHA) represents a significant challenge for HIV/AIDS patient care in China and across the globe. Awareness of HIV-positive status may alter the likelihood for PLWHA smokers to change their smoking habit. In this study, we tested the risk enhancement and risk reduction hypotheses by assessing changes in cigarette smoking behavior among PLWHA after they received the positive results of their HIV tests. Cross-sectional survey data collected from a random sample of 2973 PLWHA in care in Guangxi, China were analyzed. Changes in cigarette smoking after receiving the HIV-positive test results, as well as the current levels of cigarette smoking were measured. Among the total participants, 1529 (51.7%) were self-identified as cigarette smokers, of whom 436 (28.9%) reduced smoking and 286 (19.0%) quit after receiving their HIV-positive test results. Among the quitters, 210 (73.9%) remained abstinent for a median duration of two years. There were also 124 (8.2%) who increased cigarette smoking. Older age, female gender, more education, and receiving antiretroviral therapy were associated with quitting. In conclusion, our study findings support the risk reduction and risk enhancement hypotheses. A large proportion of smoking PLWHA reduced or quit smoking, while a small proportion increased smoking. Findings of this study suggest that the timing when a person receives his or her HIV-positive test result may be an ideal opportunity for care providers to deliver tobacco cessation interventions. Longitudinal studies are indicated to verify the findings of this study and to support smoking cessation intervention among PLWHA in the future. PMID:26457812

  7. Sleep disturbances associated with cigarette smoking.

    PubMed

    McNamara, Joseph P H; Wang, Jiantong; Holiday, David B; Warren, Jessica Young; Paradoa, Marilyn; Balkhi, Amanda Marie; Fernandez-Baca, Jeannette; McCrae, Christina S

    2014-01-01

    Sleep disturbances resulting in insufficient sleep have been linked to negative physical, cognitive, and public health outcomes. Despite this, there has yet a study that examines the impact of smoking on sleep in a US based national sample. The current study sought to observe sleep disturbances associated with smoking status. Sleep disturbances in adults aged 20 years and above, from the 2005-2006 National Health and Nutrition Examination Survey, were measured among current, former, and never smokers (NS). Current smokers (CS) reported significantly less total sleep time, longer sleep onset latency, increased difficulty falling asleep, maintaining sleep, and waking up earlier than desired when compared to NS. Former smokers reported disturbances similar to NS and CS experienced poorer sleep than nonsmokers. Our study is the first to observe sleep difficulty by smoking status in a large, population-based, nationally representative sample. Recommendations for smoking cessation programs are discussed. PMID:24040938

  8. Haemorheological consequences of chronic cigarette smoking.

    PubMed

    Ernst, E

    1995-10-01

    Smoking is a universally accepted major cardiovascular risk factor, but the mechanisms by which it promotes ischaemic vascular disease are not fully understood. The changes that chronic smoking exerts on the flow properties of blood might contribute to an explanation. It is well documented that smoking leads to a rise in haematocrit. It also alters the rheological behaviour of red blood cells and increases both plasma viscosity and fibrinogen levels. Finally, it increases the total white cell count and modifies leukocyte function. Together these changes cumulate in a significant deterioration of the flow properties of blood, as evidenced by a steep increase in whole blood viscosity. Alterations of blood rheology in turn can promote atherothrombogenesis in several ways. It seems possible, therefore, that one mechanism by which smoking increases the risk of vascular diseases operates through its complex effects on blood rheology. PMID:8749271

  9. Smoking

    MedlinePlus

    ... Smoking harms nearly every organ of the body. Cigarette smoking causes 87 percent of lung cancer deaths. ... of the same problems as smokers do. E-cigarettes often look like cigarettes, but they work differently. ...

  10. Functional neuroimaging study in identical twin pairs discordant for regular cigarette smoking.

    PubMed

    Lessov-Schlaggar, Christina N; Lepore, Rebecca L; Kristjansson, Sean D; Schlaggar, Bradley L; Barnes, Kelly Anne; Petersen, Steven E; Madden, Pamela A F; Heath, Andrew C; Barch, Deanna M

    2013-01-01

    Despite the tremendous public health and financial burden of cigarette smoking, relatively little is understood about brain mechanisms that subserve smoking behavior. This study investigated the effect of lifetime regular smoking on brain processing in a reward guessing task using functional magnetic resonance imaging and a co-twin control study design in monozygotic (MZ) twin pairs that maximally controls for genetic and family background factors. Young adult (24-34 years) MZ female twin pairs (n = 15 pairs), discordant for regular smoking defined using Centers for Disease Control criteria as having smoked ≥100 cigarettes in their lifetime, were recruited from an ongoing genetic epidemiological longitudinal study of substance use and psychopathology. We applied hypothesis-driven region of interest (ROI) and whole-brain analyses to investigate the effect of regular smoking on reward processing. Reduced response to reward and punishment in regular compared with never-regular smokers was seen in hypothesis-driven ROI analysis of bilateral ventral striatum. Whole-brain analysis identified bilateral reward-processing regions that showed activation differences in response to winning or losing money but no effect of regular smoking; and frontal/parietal regions, predominantly in the right hemisphere, that showed robust effect of regular smoking but no effect of winning or losing money. Altogether, using a study design that maximally controls for group differences, we found that regular smoking had modest effects on striatal reward processing regions but robust effects on cognitive control/attentional systems. PMID:22340136

  11. Cigarette smoking and drug use in schoolchildren: IV--factors associated with changes in smoking behaviour.

    PubMed

    Alexander, H M; Callcott, R; Dobson, A J; Hardes, G R; Lloyd, D M; O'Connell, D L; Leeder, S R

    1983-03-01

    Factors associated with changes in the smoking behaviour of approximately 6000 schoolchildren (two cohorts aged between 10 and 12 years in 1979) over 12 months are described. They were measured twice as part of a randomized controlled trial of a smoking prevention programme. Four groups were defined: (a) those who became smokers (adopters); (b) those who remained non-smokers; (c) those who became non-smokers (quitters), and, (d) those who remained smokers. Personal and social variables were ordered using a logistic regression model according to the strength of their association with adopting and quitting smoking. Factors distinguishing adopters from children who remained nonsmokers were, being a member of the older cohort, having friends who smoke, having siblings who smoke, approving of cigarette advertising and having a relatively large amount of money to spend each week. Factors distinguishing quitters from children who continued to smoke were, having siblings who do not smoke, being a member of the younger cohort, disapproving of cigarette advertising and having a relatively small amount of money to spend each week. Initial attitude scores were indicative of future smoking behaviour and where smoking behaviour changed, attitudes also changed so that the two remained congruent. The younger cohort improved their knowledge of smoking hazards over the year irrespective of their smoking behaviour. The older cohort showed significant differences in knowledge which were dependent upon smoking category, with 1980 smokers having lower knowledge scores than non-smokers and showing an apparent decrement in their previous knowledge. PMID:6341272

  12. Cigarette smoke potentiates asbestos-induced airflow abnormalities

    SciTech Connect

    Wright, J.L.; Tron, V.; Wiggs, B.; Churg, A.

    1988-01-01

    It has been suggested that exposure to both asbestos and cigarette smoke can produce worse parenchymal lung disease than exposure to asbestos alone. Using a guinea pig model of asbestos administration that produces primarily airway disease and associated airflow abnormalities, we showed previously that the combination of asbestos and smoke acts synergistically to produce more marked increases in tissue collagen, fibrosis of airway walls, and early interstitial fibrosis than are seen with asbestos alone. To investigate the functional effects of these morphological and biochemical abnormalities, pulmonary function tests for volumes and flows, including lung volumes, pressure-volume curves, and flow-volume curves, were performed. By themselves, both smoke and asbestos produced increases in total lung capacity (TLC), residual volume (RV), and functional residual capacity (FRC); the two agents together made all these changes worse than either one alone. Both smoking and asbestos moved the pressure-volume curve upward, and the effects of the two agents together were again greater than either alone. Similarly, both smoke and asbestos decreased flows, and the two agents produced more severe impairment than either one by itself. The changes in volumes, pressure-volume curve, and flows correlated with both increased thickness of small airway walls and increases in airspace size. These observations indicate that, at least in this guinea pig model, cigarette smoke can potentiate the functional consequences of asbestos exposure.

  13. Cigarette Smoke Modulates Vascular Smooth Muscle Phenotype: Implications for Carotid and Cerebrovascular Disease

    PubMed Central

    Jabbour, Pascal M.; Tjoumakaris, Stavropoula I.; Gonzalez, Fernando; Hasan, David M.; Rosenwasser, Robert H.; Owens, Gary K.; Koch, Walter J.; Dumont, Aaron S.

    2013-01-01

    Background The role of smooth muscle cell (SMC) phenotypic modulation in the cerebral circulation and pathogenesis of stroke has not been determined. Cigarette smoke is a major risk factor for atherosclerosis, but potential mechanisms are unclear, and its role in SMC phenotypic modulation has not been established. Methods and Results In cultured cerebral vascular SMCs, exposure to cigarette smoke extract (CSE) resulted in decreased promoter activity and mRNA expression of key SMC contractile genes (SM-α-actin, SM-22α, SM-MHC) and the transcription factor myocardin in a dose-dependent manner. CSE also induced pro-inflammatory/matrix remodeling genes (MCP-1, MMPs, TNF-α, IL-1β, NF-κB). CSE increased expression of KLF4, a known regulator of SMC differentiation, and siKLF4 inhibited CSE induced suppression of SMC contractile genes and myocardin and activation of inflammatory genes. These mechanisms were confirmed in vivo following exposure of rat carotid arteries to CSE. Chromatin immune-precipitation assays in vivo and in vitro demonstrated that CSE promotes epigenetic changes with binding of KLF4 to the promoter regions of myocardin and SMC marker genes and alterations in promoter acetylation and methylation. Conclusion CSE exposure results in phenotypic modulation of cerebral SMC through myocardin and KLF4 dependent mechanisms. These results provides a mechanism by which cigarette smoke induces a pro-inflammatory/matrix remodeling phenotype in SMC and an important pathway for cigarette smoke to contribute to atherosclerosis and stroke. PMID:23967268

  14. Carbonyl Compounds in the Gas Phase of Cigarette Mainstream Smoke and Their Pharmacological Properties.

    PubMed

    Horinouchi, Takahiro; Higashi, Tsunehito; Mazaki, Yuichi; Miwa, Soichi

    2016-01-01

    Cigarette mainstream smoke is composed of gas and tar phases and contains >4000 chemical constituents, including nicotine and tar. The substances in the gas phase but not in the tar phase can pass through the airway epithelial barrier, enter the systemic circulation via the pulmonary circulation, and increase systemic oxidative damage, leading to the development of cigarette smoking-related diseases such as atherosclerosis. Recently, we identified some stable carbonyl compounds, including acrolein (ACR) and methyl vinyl ketone (MVK), as major cytotoxic factors in nicotine- and tar-free cigarette smoke extract (CSE) of the gas phase. CSE, ACR, and MVK induce protein kinase C (PKC)-dependent activation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) and subsequent generation of reactive oxygen species (ROS) via NOX, causing plasma membrane damage and cell apoptosis. CSE, ACR, and MVK also trigger carbonylation of PKC, which is an irreversible oxidative modification. Cell damage and PKC carbonylation in response to treatment with CSE, ACR, or MVK are abolished by thiol-containing antioxidants such as N-acetyl-L-cysteine and reduced glutathione. Thus pharmacological modulation of PKC and NOX activities and the trapping of ROS are potential strategies for the prevention of diseases related to cigarette smoking. PMID:27251492

  15. 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...

  16. 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...

  17. 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. PMID:25808744

  18. Cigarette Smoking among Adolescents aged 13-15 in Viet Nam and Correlates of Current Cigarette Smoking: Results from GYTS 2014 Data.

    PubMed

    Huong, Le Thi; Vu, Nga Thi Thu; Dung, Nguyen Ngoc; Xuan, Le Thi Thanh; Giang, Kim Bao; Hai, Phan Thi; Huyen, Doan Thu; Khue, Luong Ngoc; Lam, Nguyen Tuan; Minh, Hoang Van; Nga, Pham Thi Quynh

    2016-01-01

    The aim of this paper is to report the rate of current and ever cigarette smoking and explore correlates of current cigarette smoking among adolescents aged 13-15 in Viet Nam. This analysis was derived from GYTS survey, which comprised of 3,430 adolescents aged 13-15, conducted in 2014 in 13 cities and provinces of Viet Nam. We calculated the weighted rates of current and ever cigarette smoking and reported patterns of smoking behavior. We also performed logistic regression to explore correlates of current cigarette smoking behavior. The weighted rate of ever cigarette smoking was 9.5% (95% confidence interval (CI): 8.5 %-10.5%), in which the weighted rate among males (15.4%; 95% CI: 13.6%-17.0%) was higher than that among females (4.2%; 95% CI: 3.3%-5.1%). The weighted rate of current cigarette smoking was relatively low at 2.5% (95%CI: 2.0%- 3.0%) with higher weighted rate among males (4.9%; 95% CI: 3.8%-5.9%) compared to the corresponding figure among females (0.2%; 95% CI: 0.0 %-0.5%). Current cigarette smoking was significantly higher among males than females, in students aged 15 versus 13 years old, and in students who had several or all close friends smoking and students with daily observation of smoking at school. For greater smoking reduction outcomes, we recommend that tobacco interventions for adolescents should consider targeting more male students at older ages, establish stricter adherence to school-based banning of cigarette smoking, engage both smoking and nonsmoking adolescents and empower adolescents to resist peer smoking influence as well as changing their norms or beliefs towards smoking benefits. PMID:27087178

  19. 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. PMID:27351343

  20. 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.

  1. 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

  2. Antioxidant activity of pomegranate juice reduces emphysematous changes and injury secondary to cigarette smoke in an animal model and human alveolar cells

    PubMed Central

    Husari, Ahmad; Hashem, Yasmine; Bitar, Hala; Dbaibo, Ghassan; Zaatari, Ghazi; El Sabban, Marwan

    2016-01-01

    Background Cigarette smoke (CS) increases oxidative stress (OS) in the lungs. Pomegranate juice (PJ) possesses potent antioxidant activities, attributed to its polyphenols. This study investigates the effects of PJ on the damaging effects of CS in an animal model and on cultured human alveolar cells (A549). Methods Male C57BL/6J mice were divided into the following groups: Control, CS, CS + PJ, and PJ. Acute CS exposure was for 3 days, while chronic exposure was for 1 and 3 months (5 days of exposure/week). PJ groups received daily 80 μmol/kg via bottle, while other groups received distilled water. At the end of the experiments, different parameters were studied: 1) expression levels of inflammatory markers, 2) apoptosis, 3) OS, and 4) histopathological changes. In vitro, A549 cells were pretreated for 48 hours with either PJ (0.5 μM) or vehicle. Cells were then exposed to increasing concentrations of CS extracted from collected filters. Cell viability was assessed by counting of live and dead cells with trypan blue staining. Results Acutely, a significant increase in interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α expression, apoptosis, and OS was noted in CS when compared to Control. PJ significantly attenuated the expression of inflammatory mediators, apoptosis, and OS. Chronically (at 1 and 3 months), increased expression of TNF-α was observed, and lung sections demonstrated emphysematous changes when compared to Control. PJ supplementation to CS animals attenuated the increased expression of TNF-α and normalized lung cytoarchitecture. At the cellular level, CS extract reduced cellular proliferation and triggered cellular death. Pretreatment with PJ attenuated the damaging effects of CS extract on cultured human alveolar cells. Conclusion The expression of inflammatory mediators associated with CS exposure and the emphysematous changes noted with chronic CS exposure were reduced with PJ supplementation. In vitro, PJ attenuated the damaging

  3. Characterization of Nrf2 activation and heme oxygenase-1 expression in NIH3T3 cells exposed to aqueous extracts of cigarette smoke.

    PubMed

    Knörr-Wittmann, Constanze; Hengstermann, Arnd; Gebel, Stephan; Alam, Jawed; Müller, Thomas

    2005-12-01

    Cigarette smoke (CS) is a complex chemical mixture estimated to be composed of up to 5000 different chemicals, many of which are prooxidant. Here we show that, at least in vitro, the cellular response designed to combat oxidative stress resulting from CS exposure is primarily controlled by the transcription factor Nrf2, a principal inducer of antioxidant and phase II-related genes. The prominent role of Nrf2 in the cellular response to CS is substantiated by the following observations: In NIH3T3 cells exposed to aqueous extracts of CS (i) Nrf2 is strongly stabilized and becomes detectable in nuclear extracts. (ii) Nuclear localization of Nrf2 coincides with increased DNA binding of a putative Nrf2/MafK heterodimer to its cognate cis-regulatory site, i.e., the antioxidant-responsive element (ARE). (iii) Studies on the regulatory elements of the oxidative stress-inducible gene heme oxygenase-1 (hmox1) using various hmox1 promoter/luciferase reporter constructs revealed that the strong CS-dependent expression of this gene is primarily governed by the distal enhancers 1 ("E1") and 2 ("E2"), which both contain three canonical ARE-like stress-responsive elements (StREs). Notably, depletion of Nrf2 levels caused by RNA interference significantly compromised CS-induced hmox1 promoter activation, based on the distinct Nrf2 sensitivity exhibited by E1 and E2. Finally, (iv) siRNA-dependent knock-down of Nrf2 completely abrogated CS-induced expression of phase II-related genes. Taken together, these results confirm the outstanding role of Nrf2 both in sensing (oxidant) stress and in orchestrating an efficient transcriptional response aimed at resolving the stressing conditions. PMID:16274879

  4. 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. PMID:18927347

  5. Smoking Norms and the Regulation of E-Cigarettes

    PubMed Central

    2015-01-01

    Electronic nicotine delivery systems (ENDS)—commonly called e-cigarettes—are at the center of a polarized debate. How should they be regulated? Central to this debate is the concern that e-cigarettes could lead to the renormalization of smoking and that the regulation of ENDS should therefore be modeled on the regulation of conventional cigarettes. I argue that arguments based on the renormalization of smoking can lend support to restrictions on marketing of ENDS, but that such arguments are problematic when used to justify restrictions on where ENDS can be used. The debate has been insufficiently sensitive to the ethical complexities of attempts to manipulate social norms to change health behaviors; these complexities must also inform the debate about ENDS and their regulation. PMID:26270285

  6. 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

  7. 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.

  8. Self-Reported Maternal Cigarette Smoke Exposure during the Periconceptional Period and the Risk for Omphalocoele

    PubMed Central

    Feldkamp, Marcia L.; Srisukhumbowornchai, Sivithee; Romitti, Paul A.; Olney, Richard S.; Richardson, Sandra D.; Botto, Lorenzo D.

    2015-01-01

    Background We investigated whether maternal exposure to cigarette smoke was associated with omphalocoele and whether periconceptional folic acid modified the association. Methods We analysed data from the National Birth Defects Prevention Study on omphalocoele case (n = 301) and control (n = 8135) mothers for infants born from 1997 through 2007. Mothers who reported active smoking or exposure to second-hand smoke during the periconceptional period (1 month before conception to 3 months after) were considered exposed. Those who reported use of folic acid supplements during the same period were considered supplement users. Odds ratios and 95% confidence intervals were estimated using multivariable logistic regression adjusted for alcohol use, preconception body mass index, and race/ethnicity. Results One hundred fifteen (38.2%) case and 2592 (31.9%) control mothers reported exposure to cigarette smoke during the periconceptional period. Adjusted odds ratios [95% confidence intervals] were 1.19 [0.94, 1.53] for any smoke exposure, 0.87 [0.54, 1.40] for active smoking, 1.38 [1.00, 1.90] for second-hand smoke exposure, and 1.16 [0.80, 1.67] for both exposures combined. No dose-response relationship was observed. Folic acid-containing supplements did not reduce the risk for omphalocoele among women with active or second-hand smoke exposure. Conclusions Self-reported active maternal smoking, with or without exposure to second-hand smoke, during the periconceptional period was not associated with omphalocoele. In contrast, there was a possible association with periconceptional exposure to second-hand smoke. PMID:24313669

  9. Cigarette Smoke Delays Regeneration of the Olfactory Epithelium in Mice.

    PubMed

    Ueha, Rumi; Ueha, Satoshi; Sakamoto, Takashi; Kanaya, Kaori; Suzukawa, Keigo; Nishijima, Hironobu; Kikuta, Shu; Kondo, Kenji; Matsushima, Kouji; Yamasoba, Tatsuya

    2016-08-01

    The olfactory system is a unique part of the mammalian nervous system due to its capacity for neurogenesis and the replacement of degenerating receptor neurons. Cigarette smoking is a major cause of olfactory dysfunction. However, the mechanisms by which cigarette smoke impairs the regenerative olfactory receptor neurons (ORNs) remain unclear. Here, we investigated the influence of cigarette smoke on ORN regeneration following methimazole-induced ORN injury. Administration of methimazole caused detachment of the olfactory epithelium from the basement membrane and induced olfactory dysfunction, thus enabling us to analyze the process of ORN regeneration. We found that intranasal administration of cigarette smoke solution (CSS) suppressed the recovery of ORNs and olfaction following ORN injury. Defective ORN recovery in CSS-treated mice was not associated with any change in the number of SOX2(+) ORN progenitor cells in the basal layer of the OE, but was associated with impaired recovery of GAP43(+) immature ORNs. In the nasal mucosa, mRNA expression levels of neurotrophic factors such as brain-derived neurotrophic factor, neurotrophin-3, neurotrophin-5, glial cell-derived neurotrophic factor, and insulin-like growth factor-1 (IGF-1) were increased following OE injury, whereas CSS administration decreased the ORN injury-induced IGF-1 expression. Administration of recombinant human IGF-1 prevented the CSS-induced suppression of ORN recovery following injury. These results suggest that CSS impairs regeneration of ORNs by suppressing the development of immature ORNs from ORN progenitors, at least partly by reducing IGF-1 in the nasal mucosa. PMID:27003941

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

    PubMed

    Warner, K E

    1985-02-01

    In the US, media coverage of the health hazards of cigarette smoking is consored by the tobacco industry. Tobacco companies, which in 1983 alone spent US$2.5 billion on smoking promtion, are a major source of advertising revenue for many media organizations. As a result media organizations frequently refuse to publish antismoking information, tent to tone down coverage of antismoking news events, and often refuse to accept antismoking advertisements. In a 1983 "Newsweek" supplement on personal health, prepared by the American Medical Association, only 4 sentences were devoted to the negative effects of smoking. A spokesman for the association reported that "Newsweek" editors refused to allow the association to use the forum to present a strong antismoking message. In 1984 a similar type of health supplement, published by "Time," failed to mention smoking at all. An examination of 10 major women's magazines revealed that between 1967-79, 4 of the magazines published no articles about the hazards of smoking and only 8 such articles appeared in the other 6 magazines. All of these magazines carried smoking advertisements. During the same time period, 2 magazines, which refused to publish cigarette ads, published a total of 16 articles on the hazards of smoking. Small magazines which publish antismoking articles are especially vulnerable to pressure from the tobacco industry. For example, the tobacco industry canceled all its ads in "Mother Jones" after the magazine printed 2 antismoking articles. 22 out of 36 magazines refused to run antismoking advertisements when they were requested to do so. Due to poor media coverage, th public's knowledge of the hazards of smoking is deficient. Recent surveys found that 2/3 of the public did not know that smoking could cause heart attacks, and 1/2 of the respondents did not know that smoking is the major cause of lung cancer. An analysis of time trends in cigarette smoking indicates that the public does respond to antismoking

  11. Lung glutathione adaptive responses to cigarette smoke exposure

    PubMed Central

    2011-01-01

    Background Smoking tobacco is a leading cause of chronic obstructive pulmonary disease (COPD), but although the majority of COPD cases can be directly related to smoking, only a quarter of smokers actually develop the disease. A potential reason for the disparity between smoking and COPD may involve an individual's ability to mount a protective adaptive response to cigarette smoke (CS). Glutathione (GSH) is highly concentrated in the lung epithelial lining fluid (ELF) and protects against many inhaled oxidants. The changes in GSH that occur with CS are not well investigated; therefore the GSH adaptive response that occurs with a commonly utilized CS exposure was examined in mice. Methods Mice were exposed to CS for 5 h after which they were rested in filtered air for up to 16 h. GSH levels were measured in the ELF, bronchoalveolar lavage cells, plasma, and tissues. GSH synthesis was assessed by measuring γ-glutamylcysteine ligase (GCL) activity in lung and liver tissue. Results GSH levels in the ELF, plasma, and liver were decreased by as much as 50% during the 5 h CS exposure period whereas the lung GSH levels were unchanged. Next, the time course of rebound in GSH levels after the CS exposure was examined. CS exposure initially decreased ELF GSH levels by 50% but within 2 h GSH levels rebound to about 3 times basal levels and peaked at 16 h with a 6-fold increase and over repeat exposures were maintained at a 3-fold elevation for up to 2 months. Similar changes were observed in tissue GCL activity which is the rate limiting step in GSH synthesis. Furthermore, elevation in ELF GSH levels was not arbitrary since the CS induced GSH adaptive response after a 3d exposure period prevented GSH levels from dropping below basal levels. Conclusions CS exposures evoke a powerful GSH adaptive response in the lung and systemically. These data suggests there may be a sensor that sets the ELF GSH adaptive response to prevent GSH levels from dipping below basal levels. Factors

  12. Teens Using E-cigarettes May Be More Likely to Start Smoking Tobacco

    MedlinePlus

    ... are more likely than others to start smoking traditional cigarettes and other combustible tobacco products within the ... regular cigarettes, they do carry a risk of addiction.” Data were collected as part of a longitudinal ...

  13. Intellectual Impairment in Children of Women Who Smoke Cigarettes during Pregnancy.

    ERIC Educational Resources Information Center

    Olds, David L.; And Others

    1994-01-01

    Examined the relationship between maternal cigarette smoking during pregnancy and children's intellectual functioning through age four. Found that children whose mothers smoked 10 or more cigarettes per day during pregnancy had Stanford-Binet scores 4 points lower than those whose mothers did not smoke during pregnancy. (HTH)

  14. Waterpipe a gateway to cigarette smoking initiation among adolescents in Irbid, Jordan: a longitudinal study

    PubMed Central

    Jaber, R.; Madhivanan, P.; Veledar, E.; Khader, Y.; Mzayek, F.; Maziak, W.

    2015-01-01

    SETTING According to anecdotal evidence, waterpipe smoking may lead to the initiation of cigarette smoking among young people. This hypothesis is yet to be examined using an appropriate study design and a theoretical model for behavioral change. OBJECTIVE To compare the risk of cigarette smoking initiation among waterpipe-only smokers and never smokers in a school-based sample of adolescents from Irbid, Jordan. METHODS A total of 1454 cigarette-naïve participants were drawn from a longitudinal study on smoking behavior conducted in Irbid among 1781 seventh graders who were enrolled at baseline (2008) and completed the study questionnaire on smoking behavior annually until 2011. Grouped time-survival analysis was used to compare the risk of subsequent initiation of cigarette smoking between waterpipe smokers (n = 298) and never smokers (n = 1156) using adjusted hazard ratios (aHRs) and 95% confidence intervals (95%CI). RESULTS Risk of initiation of cigarette smoking among waterpipe smokers was significantly higher than among never smokers after adjusting for potential confounders (aHR 1.67, 95%CI 1.46–1.92). The association between waterpipe and cigarette smoking initiation was dose-dependent. The risk of initiating cigarette smoking increased with increase in the frequency of waterpipe smoking (P for linear trend < 0.001). CONCLUSIONS Waterpipe smoking led to the initiation of cigarette smoking among this cohort of Jordanian adolescents; the effect was dose-dependent. PMID:25860006

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

    SciTech Connect

    Bond, J.A.; Chen, B.T.; Griffith, W.C.; Mauderly, J.L.

    1989-06-01

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

  16. Educational attainment and cigarette smoking: a causal association?†

    PubMed Central

    Gilman, Stephen E; Martin, Laurie T; Abrams, David B; Kawachi, Ichiro; Kubzansky, Laura; Loucks, Eric B; Rende, Richard; Rudd, Rima; Buka, Stephen L

    2016-01-01

    Background Despite abundant evidence that lower education is associated with a higher risk of smoking, whether the association is causal has not been convincingly established. Methods We investigated the association between education and lifetime smoking patterns in a birth cohort established in 1959 and followed through adulthood (n = 1311). We controlled for a wide range of potential confounders that were measured prior to school entry, and also estimated sibling fixed effects models to control for unmeasured familial vulnerability to smoking. Results In the full sample of participants, regression analyses adjusting for multiple childhood factors (including socioeconomic status, IQ, behavioural problems, and medical conditions) indicated that the number of pack-years smoked was higher among individuals with less than high school education [rate ratio (RR) = 1.58, confidence interval (CI) = 1.31, 1.91]. However, in the sibling fixed effects analysis the RR was 1.23 (CI = 0.80, 1.93). Similarly, adjusted models estimated in the full sample showed that individuals with less than high school education had fewer short-term (RR = 0.40; CI = 0.23, 0.69) and long-term (RR = 0.59; CI = 0.42, 0.83) quit attempts, and were less likely to quit smoking (odds ratio = 0.34; CI = 0.19, 0.62). The effects of education on quitting smoking were attenuated in the sibling fixed effects models that controlled for familial vulnerability to smoking. Conclusions A substantial portion of the education differential in smoking that has been repeatedly observed is attributable to factors shared by siblings that contribute to shortened educational careers and to lifetime smoking trajectories. Reducing disparities in cigarette smoking, including educational disparities, may therefore require approaches that focus on factors early in life that influence smoking risk over the adult life span. PMID:18180240

  17. 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. PMID:26942842

  18. Relationship between cigarette smoking and radiographic knee osteoarthritis in Chinese population: a cross-sectional study.

    PubMed

    Zhang, Yi; Zeng, Chao; Li, Hui; Yang, Tuo; Deng, Zhen-Han; Yang, Ye; Ding, Xiang; Xie, Dong-Xing; Wang, Yi-Lun; Lei, Guang-Hua

    2015-07-01

    The purpose of this paper was to estimate the cross-sectional association between cigarette smoking and radiographic knee Osteoarthritis (OA) in Chinese population. A total of 3,789 subjects (1,796 females and 1,993 males) participated in this study. A subject was diagnosed with radiographic knee OA if Kellgren-Lawrence (K-L) grade ≥2 in at least one leg. The smoking status was classified into four levels based on the daily smoking habit: (1) 0/day; (2) 1-10/day; (3) 11-20/day; and (4) >20/day. Linear trend and multivariable logistic regression were conducted for statistical analysis. The prevalence of radiographic knee OA was 28.4 % among the subjects of this study. An inverse association was observed between cigarette smoking and radiographic knee OA in the linear trend test. Such association remained valid after adjusting the factors of age, gender, body mass index, betel quilt chewing status, physical activity, alcohol drinking status, mean total energy intake and educational level in the multivariable logistic regression. This study suggested a negative association between cigarette smoking and radiographic knee OA in the Chinese population. The findings of this study need to be confirmed by further prospective research. PMID:25588371

  19. Heterogeneity studies of hamster calcitonin following acute exposure to cigarette smoke: evidence for monomeric secretion.

    PubMed

    Tabassian, A R; Snider, R H; Nylen, E S; Cassidy, M; Becker, K L

    1993-05-01

    Various acute stimuli, including cigarette smoke, induce hypercalcitonemia in man and hamsters. We have shown that this occurs also in thyroidectomized subjects. In the present study we have further explored this phenomenon of secretion from the lungs by studying, simultaneously, the HPLC characteristics of pulmonary tissue and serum in control hamsters and in animals immediately following short-term exposure to cigarette smoke. In addition, we have studied the immunoheterogeneity of lung calcitonin 24 hours following the acute exposure. Control lungs contained monomeric immunoreactive calcitonin (M-iCT), high molecular mass iCT (H-iCT), and CT fragments. Immediately following smoke exposure, there was an acute decrease of lung iCT by radioimmunoassay (RIA) which consisted primarily of a decrease in M-iCT by HPLC. Simultaneously, the iCT increase in the serum by RIA was shown by HPLC to involve M-iCT. Twenty-four hours after smoke inhalation, the lung iCT by RIA and M-iCT by HPLC had returned towards control levels. These findings document the molecular characteristics of lung iCT following acute cigarette smoke stimulation, and suggest that under certain circumstances M-iCT may be actively secreted by the lung. It remains to be determined whether this type of secretion reflects hemocrine or paracrine release and what the physiological role for such a secretion may be. PMID:8507014

  20. 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. PMID

  1. Cigarette smoking and the development of premenstrual syndrome.

    PubMed

    Bertone-Johnson, Elizabeth R; Hankinson, Susan E; Johnson, Susan R; Manson, Joann E

    2008-10-15

    Moderate to severe premenstrual syndrome (PMS) affects as many as 20% of premenopausal women. Although smoking may be more common in women with PMS, it is unknown whether smoking is involved in PMS etiology. In 1991-2001, the authors conducted a case-control study nested within the prospective Nurses' Health Study II. Participants were US women aged 27-44 years and free of PMS at baseline, including 1,057 who developed PMS over 10 years and 1,968 reporting no diagnosis of PMS and only minimal menstrual symptoms during this time. Smoking at various ages was assessed by questionnaires. After adjustment for oral contraceptives and other factors, current smokers were 2.1 times as likely as never smokers to develop PMS over the next 2-4 years (95% confidence interval: 1.56, 2.83). Total pack-years and smoking during adolescence and young adulthood were also independently associated with a higher risk of PMS. For example, the relative risk for women who started smoking before age 15 years, compared with never smokers, was 2.53 (95% confidence interval: 1.70, 3.76). Results suggest that smoking, especially in adolescence and young adulthood, may increase risk of moderate to severe PMS. These findings may provide an additional incentive for young women to avoid cigarette smoking. PMID:18701443

  2. 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

  3. Psychosocial correlates of cigarette smoking among Asian American and Pacific Islander adolescents.

    PubMed

    Yang, Fang; Cheng, Wendy J Y; Ho, Moon-Ho R; Pooh, Karen

    2013-04-01

    Despite the growing body of research in adolescent cigarette smoking, there is a lack of research on Asian American and Pacific Islander (AAPI) adolescents. This study examined the prevalence and psychosocial correlates of the past 30-day cigarette smoking in Asian American (AA) and Pacific Islander (PI) adolescents by utilizing a multi-systemic theory-the problem behavior theory. Using the 2006-07 High School Questionnaire of California Healthy Kids Survey, variables such as cigarette smoking, individual characteristics and external influences were assessed. Chi-square tests and generalized estimating equations were used in the analyses. PIs had higher past 30-day cigarette smoking rates than AAs. In the whole AAPI population, significant correlates of cigarette smoking included: positive and negative attitudes toward cigarettes, perceived harm of cigarettes, perceived prevalence of peer cigarette smoking, friend disapproval of cigarette use, previous drug use, truancy, and academic performance. Interaction results showed that truancy increased the odds of cigarette use for AAs only. The study found differential prevalence and correlate of cigarette smoking in addition to common psychosocial correlates in AAs and PIs. It sheds light on the importance of studying AAs and PIs separately and further exploring other potential variables that contribute to the prevalence discrepancy. PMID:23380485

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

    PubMed

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

    2009-01-01

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

  5. 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.

  6. Evaluation of E-Cigarette Liquid Vapor and Mainstream Cigarette Smoke after Direct Exposure of Primary Human Bronchial Epithelial Cells

    PubMed Central

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

    2015-01-01

    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. PMID:25856554

  7. 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

  8. METABOLIC ACTIVATION OF ORGANIC EXTRACTS FROM DIESEL, COKE OVEN, ROOFING TAR, AND CIGARETTE SMOKE EMISSIONS IN THE AMES ASSAY

    EPA Science Inventory

    The role of metabolic activation in the difference between a microbial and mammalian bioassays in the ranking of genotoxic potency of several environmental emissions was investigated. Although the relative potency in the Ames assay correlated well with the relative potency in mam...

  9. Parent involvement in cigarette smoking prevention: two pilot evaluations of the "Unpuffables Program".

    PubMed

    Perry, C L; Pirie, P; Holder, W; Halper, A; Dudovitz, B

    1990-11-01

    Efforts to prevent the onset of cigarette smoking with young adolescents have been primarily successful in delaying onset, particularly with classroom curricula that emphasize social competencies. Maintenance of these reductions has been difficult to sustain into later adolescence, suggesting the need for programs to complement and supplement curricula. Since one group of adolescents more difficult to influence are those whose parents smoke, parental involvement in smoking prevention may be a powerful enhancer. This paper describes the "Unpuffables Program," an activity package program around smoking, for preadolescents and their parents. Two pilot evaluation studies in Minnesota and Massachusetts focus on the feasibility of and receptivity to the "Unpuffables Program." High awareness and participation rates were found in both settings. The program appears to provide an opportunity for smoking to be discussed at home, motivating smokers to consider cessation, and reinforcing nonsmoking parents' attitudes and behaviors. PMID:2283873

  10. 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.

  11. 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…

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

    PubMed

    Cobb, Nathan K; Sonti, Rajiv

    2016-08-01

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

  13. Relation between cigarette smoking and sarcopenia: meta-analysis.

    PubMed

    Steffl, M; Bohannon, R W; Petr, M; Kohlikova, E; Holmerova, I

    2015-01-01

    Cigarette smoking is a risk factor for many diseases. It could be associated with sarcopenia. The aim of this meta-analysis was to determine whether smoking is an isolated risk factor for sarcopenia. We searched PubMed, Web of Science, EBSCO, and Science Direct for articles addressing the relationship between cigarette smoking and sarcopenia. A total of 12 studies containing information on 22,515 participants were included in this meta-analysis. Odds ratio (OR) was calculated for each study group and for all studies together. An OR was also calculated separately for each sex. We used a fixed-effect model in overall estimation and in males, because results of small studies were significantly different from the results of large studies in those cases and in females where the estimation showed only moderate heterogeneity we used a random-effect model. According to proposes of the Cochrane Handbook for Systematic Reviews. The resulting OR in the fixed-effect model was 1.12 (95 % CI 1.03-1.21), OR for each sex was in the fixed-effect model 1.20 (95 % CI 1.06-1.35) in males and in the random-effect model 1.21 (95 % CI 0.92-1.59) in females. The results of this meta-analysis indicate that cigarette smoking as an isolated factor may contribute to the development of sarcopenia. However, the results of the individual studies were largely inconsistent due to different approaches of measuring the main variables which affected the results. PMID:25536323

  14. MUTATION SPECTRUM OF CIGARETTE SMOKE CONDENSATE IN SALMONELLA: COMPARISON TO MUTATIONS IN SMOKING-ASSOCIATED TUMORS

    EPA Science Inventory

    We used colony probe hybridization and polymerase chain reaction/DNA sequence analysis to determine the mutations in 1,600 revertants of salmonella induced by cigarette smoke condensate (CSC) in the presence of S9.CSC induced 80% G.C T-A transversions and 20% G.C A-T transitions ...

  15. 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

  16. 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. PMID:6617614

  17. [Cigarette smoking in medical personnel and evaluation of this problem by smoking and non-smoking patients].

    PubMed

    Pirogowicz, Iwona; Szerszeń, Małgorzata; Gwiazda, Elzbieta; Steciwko, Andrzej

    2008-01-01

    Cigarette smoking is a problem in all environments, including health service workers. It increases the number of ill people and accelerates death. The aim of this study was to diagnose the problem of smoking in medical staff and evaluation of this problem by patients. Research was made in hospitals and out-patient clinics in Opole by using an anonimous questionnaire. Along years there has been a decrease of smoking initiation age: 60-years-old-women had their first cigarette in 70% after them finished 18 years old, while most 30-year-old-women had it before. Every year the level of education in medical staff grows up, but the number of smokers in them does not fall down. It is still common to smoke in non-smokers and pregnant woman presence in spite of knowledge about passive smoking. Also pregnancy is not always strong argument to complete quit smoking, among medical staff as well. Smoking medical personnel has definitely negative evaluation by non-smoking patients (70%), a bit less negative it is seen by smoking patients. As the research showed, promotion of nonsmoking workers by employers could be a motivation to quit smoking. PMID:19189557

  18. Cigarette smoking and smoking cessation in relation to risk of rheumatoid arthritis in women

    PubMed Central

    2013-01-01

    Introduction Whereas the overall association between smoking and rheumatoid arthritis (RA) must be regarded as established, considerably less is known about how much smoking is needed to increase the risk of RA, that is, the effect of smoking intensity, duration and cessation. Methods The Swedish Mammography Cohort, including 34,101 women aged 54 to 89 years, was followed up from January 1, 2003 through December 31, 2010 (219 RA cases identified). Relative risks (RR) and their 95% confidence intervals (CI) were estimated as rate ratios using Cox proportional hazards model. Results There was a statistically significant association between smoking intensity (RR comparing 1 to 7 cigarettes/day vs never smoking 2.31 (95% CI: 1.59, 3.36)) as well as duration of smoking (comparing 1 to 25 years vs never smoking RR = 1.60 (95% CI: 1.07, 2.38)) and risk of RA. Compared to never smokers, the risk was still significantly elevated 15 years after smoking cessation (RR = 1.99 (95% CI: 1.23, 3.20)). However, among former smokers, the risk of RA seemed to be decreasing over time since stopping smoking: women who stopped smoking 15 years before the start of the follow-up had 30% lower risk of RA compared to those who stopped only a year before start of the follow-up (RR = 0.70 (95% CI: 0.24,2.02)). Conclusions This prospective study highlights that even light cigarette smoking is associated with increased risk of RA in women and that smoking cessation may reduce, though not remove, this risk. PMID:23607815

  19. 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

  20. 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.

  1. Prevalence of Cigarette Smoking among Adult Cancer Survivors in Korea

    PubMed Central

    Park, Jin Joo

    2015-01-01

    Purpose Cigarette smoking is associated not only with increased risk of cancer incidence, but also influences prognosis, and the quality of life of the cancer survivors. Thus, smoking cessation after cancer diagnosis is necessary. However, smoking behavior among Korean cancer-survivors is yet unknown. Materials and Methods We investigated the smoking status of 23770 adults, aged 18 years or older, who participated in the Health Interview Survey of the Korea National Health and Nutrition Examination Survey from 2007 to 2010. Data on the cancer diagnosis and smoking history were obtained from an interview conducted by trained personals. "Cancer-survivor" was defined as anyone who has been diagnosed with cancer by a physician regardless of time duration since diagnosis. Smoking status was classified into "never-smoker", "former-smoker", and "current-smoker". Former-smoker was further divided into "cessation before diagnosis" and "cessation after diagnosis". Results Overall, 2.1% of Korean adults were cancer-survivors. The smoking rate of Korean cancer-survivors was lower than that of non-cancer controls (7.8±1.3% vs. 26.4±0.4%, p<0.001). However, 53.4% of the cancer-survivors continued to smoke after their cancer diagnosis. In multivariate analysis, male gender [odds ratio (OR), 6.34; 95% confidence interval (CI), 2.62-15.31], middle-aged group (OR, 2.74; 95% CI, 1.12-6.72), the lowest income (OR, 4.10; 95% CI, 1.19-14.15), living with smoking family member(s) (OR, 5.49; 95% CI, 2.42-12.48), and the poor self-perceived health status (OR, 2.78; 95% CI, 1.01-7.71) were independently associated with persistent smoking among Korean cancer-survivors. Conclusion The smoking rate among Korean cancer survivors is low. However, the smoking cessation rate after the cancer diagnosis is also low. This mandates comprehensive and systematic intervention for smoking cessation among cancer-survivors. PMID:25684009

  2. Menthol attenuates respiratory irritation and elevates blood cotinine in cigarette smoke exposed mice.

    PubMed

    Ha, Michael A; Smith, Gregory J; Cichocki, Joseph A; Fan, Lu; Liu, Yi-Shiuan; Caceres, Ana I; Jordt, Sven Eric; Morris, John B

    2015-01-01

    Addition of menthol to cigarettes may be associated with increased initiation of smoking. The potential mechanisms underlying this association are not known. Menthol, likely due to its effects on cold-sensing peripheral sensory neurons, is known to inhibit the sensation of irritation elicited by respiratory irritants. However, it remains unclear whether menthol modulates cigarette smoke irritancy and nicotine absorption during initial exposures to cigarettes, thereby facilitating smoking initiation. Using plethysmography in a C57Bl/6J mouse model, we examined the effects of L-menthol, the menthol isomer added to cigarettes, on the respiratory sensory irritation response to primary smoke irritants (acrolein and cyclohexanone) and smoke of Kentucky reference 2R4 cigarettes. We also studied L-menthol's effect on blood levels of the nicotine metabolite, cotinine, immediately after exposure to cigarette smoke. L-menthol suppressed the irritation response to acrolein with an apparent IC₅₀ of 4 ppm. Suppression was observed even at acrolein levels well above those necessary to produce a maximal response. Cigarette smoke, at exposure levels of 10 mg/m³ or higher, caused an immediate and marked sensory irritation response in mice. This response was significantly suppressed by L-menthol even at smoke concentrations as high as 300 mg/m³. Counterirritation by L-menthol was abolished by treatment with a selective inhibitor of Transient Receptor Potential Melastatin 8 (TRPM8), the neuronal cold/menthol receptor. Inclusion of menthol in the cigarette smoke resulted in roughly a 1.5-fold increase in plasma cotinine levels over those observed in mice exposed to smoke without added menthol. These findings document that, L-menthol, through TRPM8, is a strong suppressor of respiratory irritation responses, even during highly noxious exposures to cigarette smoke or smoke irritants, and increases blood cotinine. Therefore, L-menthol, as a cigarette additive, may promote smoking

  3. Menthol Attenuates Respiratory Irritation and Elevates Blood Cotinine in Cigarette Smoke Exposed Mice

    PubMed Central

    Ha, Michael A.; Smith, Gregory J.; Cichocki, Joseph A.; Fan, Lu; Liu, Yi-Shiuan; Caceres, Ana I.; Jordt, Sven Eric; Morris, John B.

    2015-01-01

    Addition of menthol to cigarettes may be associated with increased initiation of smoking. The potential mechanisms underlying this association are not known. Menthol, likely due to its effects on cold-sensing peripheral sensory neurons, is known to inhibit the sensation of irritation elicited by respiratory irritants. However, it remains unclear whether menthol modulates cigarette smoke irritancy and nicotine absorption during initial exposures to cigarettes, thereby facilitating smoking initiation. Using plethysmography in a C57Bl/6J mouse model, we examined the effects of L-menthol, the menthol isomer added to cigarettes, on the respiratory sensory irritation response to primary smoke irritants (acrolein and cyclohexanone) and smoke of Kentucky reference 2R4 cigarettes. We also studied L-menthol’s effect on blood levels of the nicotine metabolite, cotinine, immediately after exposure to cigarette smoke. L-menthol suppressed the irritation response to acrolein with an apparent IC₅₀ of 4 ppm. Suppression was observed even at acrolein levels well above those necessary to produce a maximal response. Cigarette smoke, at exposure levels of 10 mg/m³ or higher, caused an immediate and marked sensory irritation response in mice. This response was significantly suppressed by L-menthol even at smoke concentrations as high as 300 mg/m³. Counterirritation by L-menthol was abolished by treatment with a selective inhibitor of Transient Receptor Potential Melastatin 8 (TRPM8), the neuronal cold/menthol receptor. Inclusion of menthol in the cigarette smoke resulted in roughly a 1.5-fold increase in plasma cotinine levels over those observed in mice exposed to smoke without added menthol. These findings document that, L-menthol, through TRPM8, is a strong suppressor of respiratory irritation responses, even during highly noxious exposures to cigarette smoke or smoke irritants, and increases blood cotinine. Therefore, L-menthol, as a cigarette additive, may promote smoking

  4. Exposure to Cigarette Smoke Reduces Vitamin D3 in the Blood Stream and Respiratory Tract

    MedlinePlus

    ... respiratory tract Share | Exposure to cigarette smoke reduces vitamin D3 in the blood stream and respiratory tract ... be understood as to how smoke causes inflammation. Vitamin D3 has anti-inflammatory and anti-bacterial effects. ...

  5. Cigarette smoking causes hearing impairment among Bangladeshi population.

    PubMed

    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

  6. 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

  7. Investigating Group Contingencies to Promote Brief Abstinence from Cigarette Smoking

    PubMed Central

    Meredith, Steven E.; Dallery, Jesse

    2013-01-01

    In contingency management (CM), monetary incentives are contingent on evidence of drug abstinence. Typically, incentives (e.g., “vouchers” exchangeable for goods or services) are contingent on individual performance. We programmed vouchers contingent on group performance to investigate whether these contingencies would promote brief abstinence from cigarette smoking. Thirty-two participants were divided into small teams (n = 3 per team). During three 5-day within-subject experimental conditions, participants submitted video recordings of breath carbon monoxide (CO) measures twice daily via Mōtiv8 Systems™, an Internet-based remote monitoring application. During the interdependent contingency condition, participants earned vouchers each time they and their teammates submitted breath CO samples indicative of abstinence (i.e., negative samples). During the independent contingency condition, participants earned vouchers each time they submitted negative samples, regardless of their teammates' performance. During the no vouchers condition, no monetary incentives were contingent on abstinence. In addition, half of the participants (n = 16) could communicate with their teammates through an online peer support forum. Although forum access did not appear to promote smoking abstinence, monetary incentives did promote brief abstinence. Significantly more negative samples were submitted when vouchers were contingent on individual performance (56%) or team performance (53%) relative to when no vouchers were available (35%; F = 6.9, p = 0.002). The results show that interdependent contingencies can promote brief abstinence from cigarette smoking. Moreover, the results suggest that these contingencies may help lower treatment costs and promote social support. PMID:23421358

  8. 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.

  9. A perspective on cigarette smoking during alcohol and substance use treatment

    PubMed Central

    Grigsby, Timothy J.; Forster, Myriam; Sussman, Steve

    2016-01-01

    Individuals in treatment for substance use continue to smoke at higher rates than the general population of the United States. This editorial presents a different perspective on cigarette smoking that might reflect aspects of the subculture of individuals who, representing a heterogeneous population, smoke while recovering from substance use associated problems. We discuss factors that independently and, in combination, influence cigarette smoking during treatment and recovery from substance use. We conclude that more qualitative research is needed to understand which factors, not typically emphasized in standard tobacco cessation programming, may contribute to cigarette smoking cessation for this population. PMID:25774483

  10. 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

  11. Inactivation of bronchial mucous proteinase inhibitor by cigarette smoke and phagocyte-derived oxidants

    SciTech Connect

    Carp, H.; Janoff, A.

    1980-08-01

    Freshly prepared aqueous solutions of cigarette smoke suppressed the elastase inhibitory capacity (EIC) of the acid-stable proteinase inhibitor present in bronchial mucus (BMPi) and human seminal plasma (HUSI-I). Thin-layer gel-immunofiltration analysis of mixtures of smoke-treated BMPi and human leukocyte elastase showed decreased elastase: BMPi complexes, increased uncomplexed BMPi and increased free elastase. Phenolic antioxidants prevented the suppression of the EIC of BMPi or HUSI-I by cigarette smoke. In addition, treatment of BMPi or HUSI-I with chemical oxidants caused a similar suppression of EIC. Furthermore, treatment of BMPi or HUSI-I with the phagocyte-derived oxidizing system, myeloperoxidase + H2O2 + Cl-, suppressed EIC. Finally, the functional activity of BMPi was significantly reduced in tracheal aspirates of human smokers compared to that of nonsmokers. These results support the hypothesis that local inactivation of BMPi in the conducting airways of the lung by inhaled cigarette smoke or by phagocyte-derived oxidants may play a role in the pathogenesis of obstructive lung disease in smokers.

  12. 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.

  13. 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.

  14. Abstention from chronic cigarette smoking normalizes blood rheology.

    PubMed

    Ernst, E; Matrai, A

    1987-03-01

    Smokers differ in terms of blood rheology from non-smokers. Ex-smokers differ from smokers but not from non-smokers. When investigated while abstaining from nicotine for 8 weeks, chronic cigarette smokers show a gradual normalization of blood and plasma viscosities, haematocrit, blood cell filterability, plasma fibrinogen levels as well as total white cell count. Those smokers who did not manage to abstain, reveal no such changes. The findings suggest that haemorheological alterations caused by smoking are reversible. This might play a role in the reduction of cardiovascular risk and in the elevation of tissue perfusion. PMID:3593464

  15. Adverse effects of cigarette and noncigarette smoke exposure on the autonomic nervous system: mechanisms and implications for cardiovascular risk.

    PubMed

    Middlekauff, Holly R; Park, Jeanie; Moheimani, Roya S

    2014-10-21

    This review summarizes the detrimental effects of cigarette and noncigarette emission exposure on autonomic function, with particular emphasis on the mechanisms of acute and chronic modulation of the sympathetic nervous system. We propose that the nicotine and fine particulate matter in tobacco smoke lead to increased sympathetic nerve activity, which becomes persistent via a positive feedback loop between sympathetic nerve activity and reactive oxidative species. Furthermore, we propose that baroreflex suppression of sympathetic activation is attenuated in habitual smokers; that is, the baroreflex plays a permissive role, allowing sympathoexcitation to occur without restraint in the setting of increased pressor response. This model is also applicable to other nontobacco cigarette emission exposures (e.g., marijuana, waterpipes [hookahs], electronic cigarettes, and even air pollution). Fortunately, emerging data suggest that baroreflex sensitivity and autonomic function may be restored after smoking cessation, providing further evidence in support of the health benefits of smoking cessation. PMID:25323263

  16. [Gender signs on female smoking: a sociological approach to women's cigarette smoking].

    PubMed

    Borges, Marcia Terezinha Trotta; Barbosa, Regina Helena Simões

    2009-01-01

    Based on an extensive review of specialized literature about woman smoking, this essay aims to promote a better understanding of this issue, proposing the adoption of Social Sciences concepts, particularly at gender category, to support more comprehensive and encompassing approaches towards prevention and health assistance of tobacco smoking women. Analyzing the epidemiologic scenario of woman smoking, three tendencies could be identified--pauperization, feminilization and juvenilization--confirming that many of women disease are related to social and gender inequalities. Gender dimension is associated to woman smoking through women's protest pathologies which historically express dissatisfactions and social contradictions experienced by women. The essay concludes that the meaning attributed to cigarette by women has strong connections with the ways gender relations are organized in current society, as well as with their relationships with health services, demanding broader and integral approaches of women's health, including woman smoking. PMID:19721953

  17. MAINSTREAM AND SIDESTREAM CIGARETTE SMOKE-INDUCED DNA ADDUCTS IN C7B1 AND DNA MICE

    EPA Science Inventory

    Exposure to environmentally tobacco smoke (ETS), which is largely composed of the sidestream cigarette smoke, has been implicated in increased incidence of cancer among nonsmokers. he present study was conducted to compare the potential of mainstream and sidestream cigarette smok...

  18. Paeonol attenuates cigarette smoke-induced lung inflammation by inhibiting ROS-sensitive inflammatory signaling.

    PubMed

    Liu, Meng-Han; Lin, An-Hsuan; Lee, Hung-Fu; Ko, Hsin-Kuo; Lee, Tzong-Shyuan; Kou, Yu Ru

    2014-01-01

    Cigarette smoking causes persistent lung inflammation that is mainly regulated by redox-sensitive pathways. We have previously reported that cigarette smoke (CS) activates reactive oxygen species- (ROS-) sensitive mitogen-activated protein kinases (MAPKs)/nuclear factor-κB (NF-κB) signaling leading to induction of lung inflammation. Paeonol, the main phenolic compound present in the Chinese herb Paeonia suffruticosa, has antioxidant and anti-inflammatory properties. However, whether paeonol has similar beneficial effects against CS-induced lung inflammation remains unclear. Using a murine model, we showed that chronic CS exposure for 4 weeks caused pulmonary inflammatory infiltration, increased lung vascular permeability, elevated lung levels of chemokines, cytokines, and 4-hydroxynonenal (an oxidative stress biomarker), and induced lung inflammation; all of these CS-induced events were suppressed by chronic treatment with paeonol. Using human bronchial epithelial cells (HBECs), we demonstrated that cigarette smoke extract (CSE) sequentially increased extracellular and intracellular levels of ROS, activated the MAPKs/NF-κB signaling, and induced interleukin-8 (IL-8); all these CSE-induced events were inhibited by paeonol pretreatment. Our findings suggest a novel role for paeonol in alleviating the oxidative stress and lung inflammation induced by chronic CS exposure in vivo and in suppressing CSE-induced IL-8 in vitro via its antioxidant function and an inhibition of the MAPKs/NF-κB signaling. PMID:25165413

  19. 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.

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

    PubMed Central

    Liu, Chun; Bronson, Roderick T.; Russell, Robert M.; Wang, Xiang-Dong

    2011-01-01

    In epidemiologic studies, high intake of β-cryptoxanthin has been associated with a decreased risk of lung cancer, particularly among current smokers. However, data are not available from well-controlled animal studies to examine the effects of β-cryptoxanthin on cigarette smoke-induced lung lesions, and the biological mechanisms by which β-cryptoxanthin might affect lung carcinogenesis. We evaluated the effects of β-cryptoxanthin supplementation on cigarette smoke-induced squamous metaplasia, inflammation, and changes in protein levels of pro-inflammatory cytokine [tumor necrosis factor alpha (TNFα)] and transcription factors [nuclear factor kappa B (NF-κB) and activator protein-1 (AP-1)], as well as on smoke-induced oxidative DNA damage [8-hydroxy-2′-deoxyguanosine (8-OHdG)] in the lung tissue of ferrets. Thirty six male ferrets were assigned to cigarette smoke exposure or no exposure and to low-dose, or high-dose β-cryptoxanthin, or no dose (2 × 3 factorial design) for 3 months. β-Cryptoxanthin supplementation dose-dependently increased plasma and lung β-cryptoxanthin levels in ferrets, whereas cigarette smoke exposure lowered plasma and lung β-cryptoxanthin levels. β-Cryptoxanthin at both doses significantly decreased smoke-induced lung squamous metaplasia and inflammation. β-Cryptoxanthin also substantially reduced smoke-elevated TNFα levels in alveolar, bronchial, bronchiolar and bronchial serous/mucous gland epithelial cells and in lung macrophages. Moreover, β-cryptoxanthin decreased smoke-induced activation of NF-κB, expression of AP-1 and levels of 8-OHdG. The beneficial effects of β-cryptoxanthin were stronger for high-dose β-cryptoxanthin than for low-dose β-cryptoxanthin. Data from this study indicate that β-cryptoxanthin provides a beneficial effect against cigarette smoke-induced inflammation, oxidative DNA damage and squamous metaplasia in the lungs. PMID:21421799

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

    PubMed

    Liu, Chun; Bronson, Roderick T; Russell, Robert M; Wang, Xiang-Dong

    2011-08-01

    In epidemiologic studies, high intake of β-cryptoxanthin has been associated with a decreased risk of lung cancer, particularly among current smokers. However, data are not available from well-controlled animal studies to examine the effects of β-cryptoxanthin on cigarette smoke-induced lung lesions, and the biological mechanisms by which β-cryptoxanthin might affect lung carcinogenesis. We evaluated the effects of β-cryptoxanthin supplementation on cigarette smoke-induced squamous metaplasia, inflammation, and changes in protein levels of proinflammatory cytokine [tumor necrosis factor alpha (TNFα)] and transcription factors [nuclear factor kappa B (NF-κB) and activator protein-1 (AP-1)], as well as on smoke-induced oxidative DNA damage [8-hydroxy-2'-deoxyguanosine (8-OHdG)] in the lung tissue of ferrets. Thirty-six male ferrets were assigned to cigarette smoke exposure or no exposure and to low-dose, or high-dose β-cryptoxanthin, or no dose (2 × 3 factorial design) for 3 months. β-Cryptoxanthin supplementation dose-dependently increased plasma and lung β-cryptoxanthin levels in ferrets, whereas cigarette smoke exposure lowered plasma and lung β-cryptoxanthin levels. β-Cryptoxanthin at both doses significantly decreased smoke-induced lung squamous metaplasia and inflammation. β-Cryptoxanthin also substantially reduced smoke-elevated TNFα levels in alveolar, bronchial, bronchiolar, and bronchial serous/mucous gland epithelial cells and in lung macrophages. Moreover, β-cryptoxanthin decreased smoke-induced activation of NF-κB, expression of AP-1 and levels of 8-OHdG. The beneficial effects of β-cryptoxanthin were stronger for high-dose β-cryptoxanthin than for low-dose β-cryptoxanthin. Data from this study indicate that β-cryptoxanthin provides a beneficial effect against cigarette smoke-induced inflammation, oxidative DNA damage and squamous metaplasia in the lungs. PMID:21421799

  2. 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.

  3. Use of a Visual Prompt To Reduce Public Cigarette Smoking on a College Campus.

    ERIC Educational Resources Information Center

    Hodges, Jilda; Srebro, Karen; Kane, Jeanette; Fruhwirth, Mary; Chambliss, Catherine

    Although there has been a substantial decline in cigarette consumption among the adult population in the United States, use of cigarettes among the adolescent population has continued to grow. Since 1993, a disturbing increase in smoking among college students has been observed. This study attempts to reduce public smoking outside classroom…

  4. 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)

  5. 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)

  6. 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…

  7. 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…

  8. 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…

  9. 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.

  10. Tobacco Industry Strategies to Minimize or Mask Cigarette Smoke: Opportunities for Tobacco Product Regulation

    PubMed Central

    Rees, Vaughan W.

    2013-01-01

    Introduction: The tobacco industry has developed technologies to reduce the aversive qualities of cigarette smoke, including secondhand smoke (SHS). While these product design changes may lessen concerns about SHS, they may not reduce health risks associated with SHS exposure. Tobacco industry patents were reviewed to understand recent industry strategies to mask or minimize cigarette smoke from traditional cigarettes. Methods: Patent records published between 1997 and 2008 that related to cigarette smoke were conducted using key word searches. The U.S. Patent and Trademark Office web site was used to obtain patent awards, and the World Intellectual Property Organization’s Patentscope and Free Patents Online web sites were used to search international patents. Results: The search identified 106 relevant patents published by Japan Tobacco Incorporated, British America Tobacco, Philip Morris International, and other tobacco manufacturers or suppliers. The patents were classified by their intended purpose, including reduced smoke constituents or quantity of smoke emitted by cigarettes (58%, n = 62), improved smoke odor (25%, n = 26), and reduced visibility of smoke (16%, n = 18). Innovations used a variety of strategies including trapping or filtering smoke constituents, chemically converting gases, adding perfumes, or altering paper to improve combustion. Conclusions: The tobacco industry continues to research and develop strategies to reduce perceptions of cigarette smoke, including the use of additives to improve smoke odor. Surveillance and regulatory response to industry strategies to reduce perceptions of SHS should be implemented to ensure that the public health is adequately protected. PMID:22949571

  11. Simvastatin inhibits induction of matrix metalloproteinase-9 in rat alveolar macrophages exposed to cigarette smoke extract

    PubMed Central

    Kim, Sang-Eun; Thuy, Tran Thi Thanh; Lee, Ji-Hyun; Ro, Jai Youl; Bae, Young-An; Kong, Yoon; Ahn, Jee-Yin; Lee, Dong-Soon; Oh, Yeon-Mock; Lee, Sang-Do

    2009-01-01

    Matrix metalloproteinase-9 (MMP-9) may play an important role in emphysematous change in chronic obstructive pulmonary disease (COPD), one of the leading causes of mortality and morbidity worldwide. We previously reported that simvastatin, an inhibitor of HMG-CoA reductase, attenuates emphysematous change and MMP-9 induction in the lungs of rats exposed to cigarette smoke. However, it remained uncertain how cigarette smoke induced MMP-9 and how simvastatin inhibited cigarette smoke-induced MMP-9 expression in alveolar macrophages (AMs), a major source of MMP-9 in the lungs of COPD patients. Presently, we examined the related signaling for MMP-9 induction and the inhibitory mechanism of simvastatin on MMP-9 induction in AMs exposed to cigarette smoke extract (CSE). In isolated rat AMs, CSE induced MMP-9 expression and phosphorylation of ERK and Akt. A chemical inhibitor of MEK1/2 or PI3K reduced phosphorylation of ERK or Akt, respectively, and also inhibited CSE-mediated MMP-9 induction. Simvastatin reduced CSE-mediated MMP-9 induction, and simvastatin-mediated inhibition was reversed by farnesyl pyrophosphate (FPP) or geranylgeranyl pyrophosphate (GGPP). Similar to simvastatin, inhibition of FPP transferase or GGPP transferase suppressed CSE-mediated MMP-9 induction. Simvastatin attenuated CSE-mediated activation of RAS and phosphorylation of ERK, Akt, p65, IκB, and nuclear AP-1 or NF-κB activity. Taken together, these results suggest that simvastatin may inhibit CSE-mediated MMP-9 induction, primarily by blocking prenylation of RAS in the signaling pathways, in which Raf-MEK-ERK, PI3K/Akt, AP-1, and IκB-NF-κB are involved. PMID:19299917

  12. 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…

  13. Big five personality factors and cigarette smoking: a 10-year study among US adults.

    PubMed

    Zvolensky, Michael J; Taha, Farah; Bono, Amanda; Goodwin, Renee D

    2015-04-01

    The present study examined the relation between the big five personality traits and any lifetime cigarette use, progression to daily smoking, and smoking persistence among adults in the United States (US) over a ten-year period. Data were drawn from the Midlife Development in the US (MIDUS) I and II (N = 2101). Logistic regression was used to examine the relationship between continuously measured personality factors and any lifetime cigarette use, smoking progression, and smoking persistence at baseline (1995-1996) and at follow-up (2004-2006). The results revealed that higher levels of openness to experience and neuroticism were each significantly associated with increased risk of any lifetime cigarette use. Neuroticism also was associated with increased risk of progression from ever smoking to daily smoking and persistent daily smoking over a ten-year period. In contrast, conscientiousness was associated with decreased risk of lifetime cigarette use, progression to daily smoking, and smoking persistence. Most, but not all, associations between smoking and personality persisted after adjusting for demographic characteristics, depression, anxiety disorders, and substance use problems. The findings suggest that openness to experience and neuroticism may be involved in any lifetime cigarette use and smoking progression, and that conscientiousness appears to protect against smoking progression and persistence. These data add to a growing literature suggesting that certain personality factors--most consistently neuroticism--are important to assess and perhaps target during intervention programs for smoking behavior. PMID:25799395

  14. Big five personality factors and cigarette smoking: A 10-year study among US adults

    PubMed Central

    Zvolensky, Michael J.; Taha, Farah; Bono, Amanda; Goodwin, Renee D.

    2015-01-01

    The present study examined the relation between the big five personality traits and any lifetime cigarette use, progression to daily smoking, and smoking persistence among adults in the United States (US) over a ten-year period. Data were drawn from the Midlife Development in the US (MIDUS) I and II (N=2,101). Logistic regression was used to examine the relationship between continuously measured personality factors and any lifetime cigarette use, smoking progression, and smoking persistence at baseline (1995–1996) and at follow-up (2004–2006). The results revealed that higher levels of openness to experience and neuroticism were each significantly associated with increased risk of any lifetime cigarette use. Neuroticism also was associated with increased risk of progression from ever smoking to daily smoking and persistent daily smoking over a ten-year period. In contrast, conscientiousness was associated with decreased risk of lifetime cigarette use, progression to daily smoking, and smoking persistence. Most, but not all, associations between smoking and personality persisted after adjusting for demographic characteristics, depression, anxiety disorders, and substance use problems. The findings suggest that openness to experience and neuroticism may be involved in any lifetime cigarette use and smoking progression, and that conscientiousness appears to protect against smoking progression and persistence. These data add to a growing literature suggesting that certain personality factors—most consistently neuroticism—are important to assess and perhaps target during intervention programs for smoking behavior. PMID:25799395

  15. 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

  16. Mainstream smoke chemistry analysis of samples from the 2009 US cigarette market.

    PubMed

    Bodnar, J A; Morgan, W T; Murphy, P A; Ogden, M W

    2012-10-01

    A survey of selected mainstream smoke constituents from commercially marketed US cigarettes was conducted in 2009. The US cigarette market was segmented into thirteen (13) strata based on Cambridge Filter Method (CFM) "tar" category and cigarette design parameters. Menthol and non-menthol cigarettes were included. Sixty-one (61) cigarette brand styles were chosen to represent the market. Another thirty-four (34) brand styles of interest were included in the survey along with a Kentucky 3R4F reference cigarette. Twenty mainstream smoke constituents were evaluated using the Health Canada smoking regimen. By weighting the results of the 61 brand styles using the number of brand styles represented by each stratum, the mainstream smoke constituent means and medians of the US cigarette market were estimated. For nicotine, catechol, hydroquinone, benzo(a)pyrene and formaldehyde the mean yields increased with increasing "tar" yields. Constituent yields for the ultra-low "tar" and low "tar" cigarettes were not significantly different for most other analytes as ventilation blocking defeated any filter air dilution design features. In contrast, normalization per mg nicotine provided an inverse ranking of cigarette yields per CFM "tar" categories. Menthol cigarette mean constituent yields were observed to be within the range of the non-menthol cigarettes of similar "tar" categories. PMID:22683394

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

    PubMed Central

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

    2013-01-01

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

  18. Development trends of first cigarette smoking experience of children: the Bogalusa heart study.

    PubMed Central

    Baugh, J G; Hunter, S M; Webber, L S; Berenson, G S

    1982-01-01

    During one school year a health habits survey investigated cigarette smoking behavior in a total biracial population of children, ages 8 to 17 years old. Information was collected concerning each child's first smoking experience. Over 60 per cent of the children reported they were given their first cigarettes. Half of those starting before age 12 smoked their first cigarettes with a family member or an older fried. The smoking habit appears to have become established by age 14, with a two-year gap between initiation and maintenance. PMID:7114342

  19. 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.

  20. Selenium in mainstream and sidestream smoke of cigarettes containing fly ash-grown tobacco.

    PubMed

    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. PMID:3428180

  1. Cigarette Smoking and Quit Attempts Among Injection Drug Users in Tijuana, Mexico

    PubMed Central

    2013-01-01

    Introduction: Injection drug use and cigarette smoking are major global health concerns. Limited data exist regarding cigarette smoking behavior and quit attempts among injection drug users (IDUs) in low- and middle-income countries to inform the development of cigarette smoking interventions. We conducted a cross-sectional study to describe cigarette smoking behavior and quit attempts among IDUs in Tijuana, Mexico. Methods: IDUs were recruited through community outreach and administered in-person interviews. Multivariable Poisson regression models were constructed to determine prevalence ratios (PRs) for quit attempts. Results: Of the 670 participants interviewed, 601 (89.7%) were current smokers. Of these, median number of cigarettes smoked daily was 10; 190 (31.6%) contemplated quitting smoking in the next 6 months; 132 (22.0%) had previously quit for ≥1 year; and 124 (20.6%) had made a recent quit attempt (lasting ≥1 day during the previous 6 months). In multivariable analysis, recent quit attempts were positively associated with average monthly income (≥3,500 pesos [US$280] vs. <1,500 pesos [US$120]; PR = 2.30; 95% CI = 1.57–3.36), smoking marijuana (PR = 1.38; 95% CI = 1.01–2.90), and smoking heroin (PR = 1.85; 95% CI = 1.23–2.78), and they were negatively associated with number of cigarettes smoked daily (PR = 0.96; 95% CI = 0.94–0.98). Conclusions: One out of 5 IDUs attempted to quit cigarette smoking during the previous 6 months. Additional research is needed to improve the understanding of the association between drug use patterns and cigarette smoking quit attempts, including the higher rate of quit attempts observed among IDUs who smoke marijuana or heroin compared with IDUs who do not smoke these substances. PMID:23873979

  2. 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

  3. Cigarette smoke enhances proliferation and extracellular matrix deposition by human fetal airway smooth muscle

    PubMed Central

    Vogel, Elizabeth R.; VanOosten, Sarah K.; Holman, Michelle A.; Hohbein, Danielle D.; Thompson, Michael A.; Vassallo, Robert; Pandya, Hitesh C.; Prakash, Y. S.

    2014-01-01

    Cigarette smoke is a common environmental insult associated with increased risk of developing airway diseases such as wheezing and asthma in neonates and children. In adults, asthma involves airway remodeling characterized by increased airway smooth muscle (ASM) cell proliferation and increased extracellular matrix (ECM) deposition, as well as airway hyperreactivity. The effects of cigarette smoke on remodeling and contractility in the developing airway are not well-elucidated. In this study, we used canalicular-stage (18–20 wk gestational age) human fetal airway smooth muscle (fASM) cells as an in vitro model of the immature airway. fASM cells were exposed to cigarette smoke extract (CSE; 0.5–1.5% for 24–72 h), and cell proliferation, ECM deposition, and intracellular calcium ([Ca2+]i) responses to agonist (histamine 10 μM) were used to evaluate effects on remodeling and hyperreactivity. CSE significantly increased cell proliferation and deposition of ECM molecules collagen I, collagen III, and fibronectin. In contrast, [Ca2+]i responses were not significantly affected by CSE. Analysis of key signaling pathways demonstrated significant increase in extracellular signal-related kinase (ERK) and p38 activation with CSE. Inhibition of ERK or p38 signaling prevented CSE-mediated changes in proliferation, whereas only ERK inhibition attenuated the CSE-mediated increase in ECM deposition. Overall, these results demonstrate that cigarette smoke may enhance remodeling in developing human ASM through hyperplasia and ECM production, thus contributing to development of neonatal and pediatric airway disease. PMID:25344066

  4. Interactions of several lipid-related gene polymorphisms and cigarette smoking on blood pressure levels.

    PubMed

    Yin, Rui-Xing; Wu, Dong-Feng; Wu, Jin-Zhen; Cao, Xiao-Li; Aung, Lynn Htet Htet; Miao, Lin; Long, Xing-Jiang; Liu, Wan-Ying; Zhang, Lin; Li, Meng

    2012-01-01

    The interactions of single nucleotide polymorphisms (SNPs) and cigarette smoking on blood pressure levels are limited. The present study was undertaken to detect nine lipid-related SNPs and their interactions with cigarette smoking on blood pressure levels. Genotyping of ATP-binding cassette transporter A1 (ABCA-1) V825I, acyl-CoA:cholesterol acyltransferase-1 (ACAT-1) rs1044925, low density lipoprotein receptor (LDL-R) AvaⅡ, hepatic lipase gene (LIPC) -250G>A, endothelial lipase gene (LIPG) 584C>T, methylenetetrahydrofolate reductase (MTHFR) 677C>T, proprotein convertase subtilisin-like kexin type 9 (PCSK9) E670G, peroxisome proliferator-activated receptor delta (PPARD) +294T>C, and Scavenger receptor class B type 1 (SCARB1) rs5888 was performed in 935 nonsmokers and 845 smokers. The interactions were detected by factorial regression analysis. The frequencies of genotypes (ACAT-1 and LIPG), alleles (ABCA-1), and both genotypes and alleles (LDL-R, LIPC, PPARD and SCARB1) were different between nonsmokers and smokers (P < 0.05-0.001). The levels of pulse pressure (PP, ABCA-1), and systolic, diastolic blood pressure (SBP, DBP) and PP (LIPC) in nonsmokers were different among the genotypes (P < 0.01-0.001). The levels of SBP (ABCA-1, ACAT-1, LIPG and PCSK9), DBP (ACAT-1, LDL-R, LIPC, PCSK9 and PPARD), and PP (LIPC, LIPG, MTHFR and PCSK9) in smokers were different among the genotypes (P < 0.01-0.001). The SNPs of ABCA-1, ACAT-1 and PCSK9; ACAT-1, LDL-R, MTHFR and PCSK9; and ABCA-1, LIPC, PCSK9 and PPARD were shown interactions with cigarette smoking to influence SBP, DBP and PP levels (P < 0.05-0.001); respectively. The differences in blood pressure levels between the nonsmokers and smokers might partly result from different interactions of several SNPs and cigarette smoking. PMID:22606049

  5. Tracheal Morphologic and Protein Alterations FollowingShort-Term Cigarette Mainstream Smoke Exposure to Rats.

    PubMed

    Carter, Charleata A; Misra, Manoj; Maronpot, Robert R

    2012-09-01

    A short-term 5-day nose-only cigarette smoke exposure study was conducted in Fisher 344 rats to identify smoke-induced tracheal protein changes. Groups of 10 male and female 5 week old rats were assigned to 1 of 4 exposure groups. Animals received filtered air, or 75, 200 or 400 mg total particulate matter (TPM)/m(3) of diluted 3R4F Kentucky reference cigarette mainstream smoke. Exposures were conducted for 3 hrs/day, for 5 consecutive days. Tracheas from half the rats were processed for pathology, and tracheas from the other half of the rats frozen immediately for proteomics. We hypothesized that smoke will activate tracheal inflammatory, apoptotic, proliferative, and stress-induced pathways. Mucosal epithelial toxicity from the inhaled material was evidenced by cilia shortening and loss of tracheal mucosal epithelium in smoke-exposed animals. Mucosal thinning occurred in all smoke-exposed groups with hyperplastic reparative responses in the 200 and 400 mg TPM/m(3) groups. Tracheal lysates from control vs. treated animals were screened for 800 proteins using antibody-based microarray technology and subsequently the most changed proteins evaluated by Western blot. Tracheal proteins expressed at high levels that were markedly increased or decreased by smoke exposure depended on dose and gender and included caspase 5, ERK 1/2 and p38. Signaling pathways common between the morphologic and protein changes were stress, apoptosis, cell cycle control, cell proliferation and survival. Changes in identified proteins affected by smoke exposure were associated with tracheal mucosal pathology, may induce functional tracheal changes, and could serve as early indicators of tracheal damage and associated disease. PMID:22988338

  6. Effect of Graphic Cigarette Warnings on Smoking Intentions in Young Adults

    PubMed Central

    Blanton, Hart; Snyder, Leslie B.; Strauts, Erin; Larson, Joy G.

    2014-01-01

    Introduction Graphic warnings (GWs) on cigarette packs are widely used internationally and perhaps will be in the US but their impact is not well understood. This study tested support for competing hypotheses in different subgroups of young adults defined by their history of cigarette smoking and individual difference variables (e.g., psychological reactance). One hypothesis predicted adaptive responding (GWs would lower smoking-related intentions) and another predicted defensive responding (GWs would raise smoking-related intentions). Methods Participants were an online sample of 1,169 Americans ages 18–24, who were randomly assigned either to view nine GWs designed by the FDA or to a no-label control. Both the intention to smoke in the future and the intention to quit smoking (among smokers) were assessed before and after message exposure. Results GWs lowered intention to smoke in the future among those with a moderate lifetime smoking history (between 1 and 100 cigarettes), and they increased intention to quit smoking among those with a heavy lifetime smoking history (more than 100 cigarettes). Both effects were limited to individuals who had smoked in some but not all of the prior 30 days (i.e., occasional smokers). No evidence of defensive “boomerang effects” on intention was observed in any subgroup. Conclusion Graphic warnings can reduce interest in smoking among occasional smokers, a finding that supports the adaptive-change hypothesis. GWs that target occasional smokers might be more effective at reducing cigarette smoking in young adults. PMID:24806481

  7. DNA replication and unscheduled DNA synthesis in lungs of mice exposed to cigarette smoke

    SciTech Connect

    Rasmussen, R.E.; Boyd, C.H.; Dansie, D.R.; Kouri, R.E.; Henry, C.J.

    1981-07-01

    Mice of the hybrid strain BC3F1/Cum (C57BL/Cum X C3H/AnfCum) were chronically exposed to measured amounts of machine-generated whole Kentucky reference 2A1 cigarette smoke. DNA replication and unscheduled DNA synthesis (UDS) were measured in lung tissue in vitro using a short-term organ culture method. Within one week of beginning smoke exposure, DNA replicative activity, as indicated by incorporation of (3H)-thymidine into total lung DNA, was increased more than two-fold over sham-exposed controls and remained elevated as long as smoke exposure was continued. Treatment of lung tissues in vitro with either the lung carcinogen 4-nitroquinoline-1-oxide or methylmethane sulfonate stimulated UDS, measured as incorporation of (3H)thymidine into lung DNA in the presence of hydroxyurea, presumably as the result of DNA repair activity. Until the 10th to 12th week of smoke exposure, at which time the accumulated deposition of total particulate material in the lung was approximately 40 mg, the level of UDS stimulated by the alkylating chemicals declined to approximately 50% of that seen in lung tissue from sham-exposed control mice. If the mice were removed from smoke exposure, DNA replicative activity returned to normal levels within one week, but the UDS response to DNA damage remained depressed up to five months after ending smoke exposure. The results show that both transient and apparently permanent changes are produced in mouse lung as the result of exposure to cigarette smoke. The role of these changes in lung neoplasia is under investigation.

  8. The feasibility of using a photoelectric cigarette smoke detector for energy-efficient air quality control

    SciTech Connect

    Nelson, R.M.; Alevantis, L.E.

    1985-01-01

    The object of this study was to determine the feasibility of using a smoke sensor to monitor and control cigarette smoke levels in occupied spaces and also to determine whether the use of such a detector could result in energy savings. A smoke detector was built and tested. The experimental results show that the smoke sensor output is a function of cigarette smoke concentration and that the smoke sensor gives a rapid and continuous response. In addition, a computer program that simulates the transient mass and energy interactions in buildings was modified so that the impact of ventilation strategies on indoor air quality and energy consumption could be studied when smokers are present. The results of the numerical modeling for an arbitrary test case show that the use of a smoke sensor to detect cigarette smoke particulates and to control ventilation can allow indoor air quality to be continuously maintained at acceptable levels while minimizing energy consumption.

  9. Prenatal exposure to cigarette smoke and childhood externalizing behavioral problems: a propensity score matching approach.

    PubMed

    Boutwell, Brian B; Beaver, Kevin M; Gibson, Chris L; Ward, Jeffrey T

    2011-08-01

    We examined the possibility that the association between maternal smoking during pregnancy and childhood behavioral problems is the result of confounding. Data from the first three waves of the Fragile Families and Child Wellbeing Study were analyzed. We estimated the association between maternal smoking during pregnancy and externalizing problems in three-year olds using a propensity score matching approach. After successfully matching children based on their mother's propensities to smoke during pregnancy, the results indicate that maternal cigarette smoking is related to childhood externalizing behavioral problems, but only among mothers who smoked more than a pack per day while pregnant. At lower levels of exposure, the association between exposure to cigarette smoke in utero and externalizing behavioral problems in childhood can be explained by confounding. The results of this study support prevention efforts intended to reduce prenatal exposure to cigarette smoke, especially by mothers who smoke heavily. PMID:21598153

  10. Assay of lapatinib in murine models of cigarette smoke carcinogenesis

    PubMed Central

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

    2014-01-01

    Lapatinib, a dual tyrosine kinase inhibitor targeting the epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER-2), is prescribed for the treatment of patients with metastatic breast cancer overexpressing HER-2. Involvement of this drug in pulmonary carcinogenesis has been poorly investigated. We used murine models suitable to evaluate cigarette smoke-related molecular and histopathological alterations. A total of 481 Swiss H mice were used. The mice were exposed to mainstream cigarette smoke (MCS) during the first four months of life. After 10 weeks, MCS caused an elevation of bulky DNA adducts, oxidative DNA damage and an extensive downregulation of microRNAs in lung. After four months, an increase in micronucleus frequency was observed in peripheral blood erythrocytes. After 7.5 months, histopathological alterations were detected in the lung, also including benign tumors and malignant tumors, and in the urinary tract. A subchronic toxicity study assessed the non-toxic doses of lapatinib, administered daily with the diet after weaning. After 10 weeks, lapatinib significantly attenuated the MCS-related nucleotide changes and upregulated several low-intensity microRNAs in lung. The drug poorly affected the MCS systemic genotoxicity and had modest protective effects on MCS-induced preneoplastic lesions in lung and kidney, when administered under conditions that temporarily mimicked interventions either in current smokers or ex-smokers. On the other hand, it caused some toxicity to the liver. Thus, on the whole, lapatinib appears to have a low impact in the smoke-related lung carcinogenesis models used, especially in terms of tumorigenic response. PMID:25053627

  11. 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.

  12. 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

  13. Chronic cigarette smoke exposure induces microbial and inflammatory shifts and mucin changes in the murine gut.

    PubMed

    Allais, Liesbeth; Kerckhof, Frederiek-Maarten; Verschuere, Stephanie; Bracke, Ken R; De Smet, Rebecca; Laukens, Debby; Van den Abbeele, Pieter; De Vos, Martine; Boon, Nico; Brusselle, Guy G; Cuvelier, Claude A; Van de Wiele, Tom

    2016-05-01

    Inflammatory bowel diseases (IBD) are complex multifactorial diseases characterized by an inappropriate host response to an altered commensal microbiome and dysfunctional mucus barrier. Cigarette smoking is the best known environmental risk factor in IBD. Here, we studied the influence of chronic smoke exposure on the gut microbiome, mucus layer composition and immune factors in conventional mice. We compared smoke-exposed with air-exposed mice (n = 12) after a smoke exposure of 24 weeks. Both Illumina sequencing (n = 6) and denaturing gradient gel electrophoresis (n = 12) showed that bacterial activity and community structure were significantly altered in the colon due to smoke exposure. Interestingly, an increase of Lachnospiraceae sp. activity in the colon was observed. Also, the mRNA expression of Muc2 and Muc3 increased in the ileum, whereas Muc4 increased in the distal colon of smoke-exposed mice (n = 6). Furthermore, we observed increased Cxcl2 and decreased Ifn-γ in the ileum, and increased Il-6 and decreased Tgf-β in the proximal colon. Tight junction gene expression remained unchanged. We infer that the modulating role of chronic smoke exposure as a latently present risk factor in the gut may be driven by the altered epithelial mucus profiles and changes in microbiome composition and immune factors. PMID:26033517

  14. Cigarette Smoke Amplifies Inflammatory Response and Atherosclerosis Progression Through Activation of the H1R-TLR2/4-COX2 Axis

    PubMed Central

    Barua, Rajat S.; Sharma, Mukut; Dileepan, Kottarappat N.

    2015-01-01

    Emerging evidence suggests that infection and persistent inflammation are key players in the pathogenesis of atherosclerotic cardiovascular disease (CVD). Although it is well established that cigarette smoke (CS) promotes atherosclerotic CVD, very little is known about the potential impact of the collective effects of CS and intermittent or chronic subclinical infection on atherosclerosis. Our previous studies demonstrated that mast cell-derived histamine and lipopolysaccharide (LPS) synergistically enhance endothelial cell inflammatory response. We further noted that the synergy between histamine and LPS was due to reciprocal upregulation of histamine receptor and Toll-like receptor 4 (TLR4) expression and functions. These results suggest that the combined and persistent effects of mast cell mediators and bacterial agents on the vasculature are risk factors of CVD. Our recent data demonstrated that CS extract enhances histamine- and LPS-induced expression of cyclooxygenase-2 (COX-2) in endothelial cells, suggesting that CS and mast cell mediators may collectively amplify inflammatory response in the vessel wall. We hypothesize that CS enhances histamine-mediated upregulation of TLR2/TLR4 signaling in the endothelium and promotes progression of atherosclerosis. This article presents our perspective on the modulatory effects of CS and nicotine on the “histamine-TLR-COX-2 axis.” PMID:26617606

  15. 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.)

  16. 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

  17. 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. PMID:23479305

  18. 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

  19. 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

  20. 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. PMID:22830488

  1. Do cigarette smoking and alcohol consumption associate with cannabis use and problem gambling among Spanish adolescents?

    PubMed

    Míguez Varela, M Del Carmen; Becoña, Elisardo

    2015-01-01

    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. PMID:25879473

  2. 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

  3. 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. PMID:26934369

  4. [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. PMID:26964200

  5. Nicotine-specific and non-specific effects of cigarette smoking on endogenous opioid mechanisms.

    PubMed

    Nuechterlein, Emily B; Ni, Lisong; Domino, Edward F; Zubieta, Jon-Kar

    2016-08-01

    This study investigates differences in μ-opioid receptor mediated neurotransmission in healthy controls and overnight-abstinent smokers, and potential effects of the OPRM1 A118G genotype. It also examines the effects of smoking denicotinized (DN) and average nicotine (N) cigarettes on the μ-opioid system. Positron emission tomography with (11)C-carfentanil was used to determine regional brain μ-opioid receptor (MOR) availability (non-displaceable binding potential, BPND) in a sample of 19 male smokers and 22 nonsmoking control subjects. Nonsmokers showed greater MOR BPND than overnight abstinent smokers in the basal ganglia and thalamus. BPND in the basal ganglia was negatively correlated with baseline craving levels and Fagerström scores. Interactions between group and genotype were seen in the nucleus accumbens bilaterally and the amygdala, with G-allele carriers demonstrating lower BPND in these regions, but only among smokers. After smoking the DN cigarette, smokers showed evidence of MOR activation in the thalamus and nucleus accumbens. No additional activation was observed after the N cigarette, with a mean effect of increases in MOR BPND (i.e., deactivation) with respect to the DN cigarette effects in the thalamus and left amygdala. Changes in MOR BPND were related to both Fagerström scores and changes in craving. This study showed that overnight-abstinent smokers have lower concentrations of available MORs than controls, an effect that was related to both craving and the severity of addiction. It also suggests that nicotine non-specific elements of the smoking experience have an important role in regulating MOR-mediated neurotransmission, and in turn modulating withdrawal-induced craving ratings. PMID:27095017

  6. 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

  7. The political obstacles to the control of cigarette smoking in the United States.

    PubMed

    Sapolsky, H M

    1980-01-01

    The opportunity to affect significantly the consumption of cigarettes in the United States through government action appears quite limited. Fifty million Americans smoke cigarettes. The United States is a leading producer of tobacco leaf and utilizes a price support system which is designed to protect tobacco growers. The industry is profitable and politicaly well connected. Several states are important producers of tobacco while others benefit from the excise tax imposed on cigarettes. The opposition to smoking is relatively weak and divided. Nevertheless, the tobacco industry worries about the future market for cigarettes. PMID:7419892

  8. 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

  9. Weak ventral striatal responses to monetary outcomes predict an unwillingness to resist cigarette smoking.

    PubMed

    Wilson, Stephen J; Delgado, Mauricio R; McKee, Sherry A; Grigson, Patricia S; MacLean, R Ross; Nichols, Travis T; Henry, Shannon L

    2014-12-01

    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, since 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

  10. The Effect of Cigarette Smoke Exposure on Spinal Cord Injury in Rats

    PubMed Central

    Cao, Yang; Lv, Gang; Wang, Yan-song; Guo, Zhan-peng

    2013-01-01

    Abstract 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. PMID:23234244

  11. 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…

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

    SciTech Connect

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

    1983-02-01

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

  13. Neutrophil Priming by Cigarette Smoke Condensate and a Tobacco Anti-Idiotypic Antibody

    PubMed Central

    Koethe, Susan M.; Kuhnmuench, John R.; Becker, Carl G.

    2000-01-01

    A polyphenol-rich reagent, referred to as CSC, was isolated from cigarette smoke condensate and shown to prime purified human neutrophils. A mouse monoclonal anti-idiotypic antibody directed against the polyphenol-reactive determinants on a rabbit polyclonal anti-tobacco glycoprotein antibody was generated and shown to also prime neutrophils. After priming by CSC or tobacco anti-idiotypic antibody, there was a 2.5-fold to threefold increase in CD11b/18 expression and doubling of the number of formyl-methionyl-leucyl-phenylalanine receptors on the cells. The primed cells showed a twofold increase, compared with unprimed cells, in production of superoxide and release of neutrophil elastase after stimulation with formyl-methionyl-leucyl-phenylalanine. Neutrophils in peripheral blood of cigarette smokers have been shown to be primed and more responsive to activating agents. The priming effects attributed to whole cigarette smoke have been demonstrated in these studies using purified neutrophils and CSC or tobacco anti-idiotypic antibody. These studies are a first step in testing the hypothesis that the inflammatory process contributing to progression of chronic obstructive pulmonary disease in ex-smokers may be driven, in part, by tobacco anti-idiotypic antibodies. This hypothesis is novel and carries with it the implication of a heretofore unrecognized autoimmune component in the disease process manifested through production of anti-idiotypic antibodies with tobacco-like activity. PMID:11073832

  14. New insights into the formation of volatile compounds in mainstream cigarette smoke

    PubMed Central

    Feng, S.; van Heemst, J.; McAdam, K. G.

    2010-01-01

    A sampling system has been set up to monitor a group of volatile smoke analytes (nitric oxide, acetaldehyde, acetone, benzene, toluene, 1,3 butadiene, isoprene and carbon dioxide) from mainstream cigarette smoke on a puff-resolved basis. The system was able to record gas evolution profiles during puffing and interpuff periods without interruption (e.g. taking clearing puffs). Gas phase smoke analytes were sampled as close to the mouth end of the cigarette filter as possible in order to minimise any dead volume effect. The results revealed that, for some volatile species, a significant fraction (e.g. up to 30% for benzene) in the cigarette mainstream smoke had been generated during the preceding smoulder period. These species were trapped or absorbed within the cigarette rod and then subsequently eluted during the puff. The identification of the two sources of the mainstream smoke, a smouldering source and a puffing source, has not been reported before. The observation contributes to the fundamental knowledge of the cigarette smoke formation and may have implications on wider smoke chemistry and associated effects. Figure A cross-sectional schematic of a burning cigarette, illustrating the main chemical and physical processes involved in the smoke formation PMID:20101495

  15. 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.

  16. Method for the Determination of Ammonia in Mainstream Cigarette Smoke Using Ion Chromatography.

    PubMed

    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

  17. 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…

  18. 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

  19. 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…

  20. Covariates of Current Cigarette Smoking among Secondary School Students in Budapest, Hungary, 1999

    ERIC Educational Resources Information Center

    Easton, Alyssa; Kiss, Eva

    2005-01-01

    To date, few studies have examined the relationship between health behavior risk factors and cigarette smoking in Hungary. From 1995 to 1999, the prevalence of current smoking increased from 35.9 to 46.0% among secondary students in Budapest, Hungary. The objective of the present study was to examine the association between smoking and other…

  1. Cigarette Taxes and Smoking Participation: Evidence from Recent Tax Increases in Canada

    PubMed Central

    Azagba, Sunday; Sharaf, Mesbah

    2011-01-01

    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. PMID:21655139

  2. 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

  3. 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.

  4. Sex differences in prevalence rates and predictors of cigarette smoking among in-school adolescents in Kilimanjaro, Tanzania.

    PubMed

    Siziya, S; Ntata, P R T; Rudatsikira, E; Makupe, C M; Umar, E; Muula, A S

    2007-09-01

    An analysis of the Global Youth Tobacco Survey for Kilimanjaro, Tanzania was carried out to assess sex differences in the prevalence rates and predictors of current cigarette smoking among in-school adolescents. A total of 2323 adolescents participated in the study of whom 53% were females and 47% males. The prevalence of current cigarette smoking was 3.0% and 1.4% among males and females, respectively. The common factors that were significantly positively associated with cigarette smoking between sexes were: having more pocket money, closest friend smoked cigarettes, seeing actors smoke on TV, videos or movies, and seeing advertisements for cigarettes at social gatherings. Seeing anti-smoking messages at social gatherings were negatively associated with smoking among both sexes. While having had something such as a t-shirt or pen with a cigarette brand logo on it was positively associated with cigarette smoking among males, it was negatively associated with cigarette smoking among females. Male adolescents older than 15 years, those in their 9th year of schooling, and those who had seen cigarette brand names on TV were more likely to smoke. Meanwhile, male respondents who were in their 8th year of schooling, had seen anti-smoking media messages, and advertisements for cigarettes in newspapers or magazines were less likely to smoke. Among female adolescents, those who had parents who smoked, and surprisingly those who perceived that cigarette smoking as harmful were more likely to smoke. Interestingly, seeing advertisement for cigarettes on billboards was negatively associated with smoking among female adolescents. Interventions aimed to reduce adolescent smoking need to be designed and implemented with due consideration of sex differences in these associated factors. PMID:18087898

  5. Comparative evaluation of the mutagenicity and genotoxicity of smoke condensate derived from Korean cigarettes

    PubMed Central

    2015-01-01

    Objectives Cigarette smoking is associated with carcinogenesis owing to the mutagenic and genotoxic effects of cigarette smoke. The aim of this study was to evaluate the mutagenic and genotoxic effects of Korean cigarettes using in vitro assays. Methods We selected 2 types of cigarettes (TL and TW) as benchmark Korean cigarettes for this study, because they represent the greatest level of nicotine and tar contents among Korean cigarettes. Mutagenic potency was expressed as the number of revertants per μg of cigarette smoke condensate (CSC) total particulate matter whereas genotoxic potency was expressed as a concentration-dependent induction factor. The CSC was prepared by the International Organization for Standardization 3308 smoking method. CHO-K1 cells were used in vitro micronucleus (MNvit) and comet assays. Two strains of Salmonella typhimurium (Salmonella enterica subsp.enterica; TA98 and TA1537) were employed in Ames tests. Results All CSCs showed mutagenicity in the TA98 and TA1537 strains. In addition, DNA damage and micronuclei formation were observed in the comet and MNvit assays owing to CSC exposure. The CSC from the 3R4F Kentucky reference (3R4F) cigarette produced the most severe mutagenic and genotoxic potencies, followed by the CSC from the TL cigarette, whereas the CSC from the TW cigarette produced the least severe mutagenic and genotoxic potencies. Conclusions The results of this study suggest that the mutagenic and genotoxic potencies of the TL and TW cigarettes were weaker than those of the 3R4F cigarette. Further study on standardized concepts of toxic equivalents for cigarettes needs to be conducted for more extensive use of in vitro tests. PMID:26796893

  6. 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

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

    PubMed

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

    1986-01-01

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

  8. Are The Predictors of Hookah Smoking Differ From Those of Cigarette Smoking? Report of a population-based study in Shiraz, Iran, 2010

    PubMed Central

    Abdollahifard, Gholamreza; Vakili, Veda; Danaei, Mina; Askarian, Mehrdad; Romito, Laura; Palenik, Charles J

    2013-01-01

    Background: The aim of this study was to determine the prevalence of tobacco use and effect of lifestyle factors on cigarette and hookah use among adult residents of Shiraz, Iran. Methods: In 2010, 1,000 participants were recruited in a multistage, random sampling cross-sectional population-based survey. Results: Response rate was 98%. Prevalence of cigarette smoking was 9.7%. Among cigarette users, 12.6% reported smoking <1 year; 13.4% smoked 1-2 years and 73.9% smoked>2 years. Almost half of those surveyed (48.9%) smoked <10 cigarettes per day (cpd); 28.4% smoked 10-15 cpd; 14.8% smoked 16-19 cpd, and 8%>20 cpd. Almost a quarter (20.4%) of the cigarette smokers tried to quit in the past year. Being male, married, aged 37-54, having higher perceived levels of stress, a non-manual occupation, and sedentary lifestyle were positively associated with cigarette smoking. Manual labor occupations, housewife/jobless status, and going frequently to restaurants were positive predictors of hookah smoking. Conclusions: Compared to cigarettes, hookah smoking was more prevalent among Iranian adults. Approximately, the prevalence of hookah smoking in women is the same as men, whereas cigarette use was 31 times more common in men. Cigarette and hookah smoking were associated with less healthy lifestyle habits in both men and women. PMID:23671779

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

    PubMed

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

    2015-11-01

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

  10. Prenatal Cigarette Smoke Exposure Causes Hyperactivity and Agressive Behavior: Role of Altered Catcholamines and BDNF

    PubMed Central

    Yochum, Carrie; Doherty-Lyon, Shannon; Hoffman, Carol; Hossain, Muhammad M.; Zellikoff, Judith T.; Richardson, Jason R.

    2014-01-01

    Smoking during pregnancy is associated with a variety of untoward effects on the offspring. However, recent epidemiological studies have brought into question whether the association between neurobehavioral deficits and maternal smoking is causal. We utilized an animal model of maternal smoking to determine the effects of prenatal cigarette smoke (CS) exposure on neurobehavioral development. Pregnant mice were exposed to either filtered air or mainstream CS from gestation day (GD) 4 to parturition for 4 hr/d and 5 d/wk, with each exposure producing maternal plasma concentration of cotinine equivalent to smoking <1 pack of cigarettes per day (25 ng/ml plasma cotinine level). Pups were weaned at postnatal day (PND) 21 and behavior assessed on at 4 weeks of age and again at 4–6 months of age. Male, but not female, offspring of CS-exposed dams demonstrated a significant increase in locomotor activity during adolescence and adulthood that was ameliorated by methylphenidate treatment. Additionally, male offspring exhibited increased aggression, as evidenced by decreased latency to attack and number of attacks in a resident intruder task. These behavioral abnormalities were accompanied by a significant decrease in striatal and cortical dopamine and serotonin and a significant reduction in brain-derived neurotrophic factor (BDNF) mRNA and protein. Taken in concert, these data demonstrate that prenatal exposure to CS produces behavioral alterations in mice that are similar to those observed in epidemiological studies linking maternal smoking to neurodevelopmental disorders and suggest a role for monoaminergic and BDNF alterations in these effects. PMID:24486851

  11. Prenatal cigarette smoke exposure causes hyperactivity and aggressive behavior: role of altered catecholamines and BDNF.

    PubMed

    Yochum, Carrie; Doherty-Lyon, Shannon; Hoffman, Carol; Hossain, Muhammad M; Zelikoff, Judith T; Richardson, Jason R

    2014-04-01

    Smoking during pregnancy is associated with a variety of untoward effects on the offspring. However, recent epidemiological studies have brought into question whether the association between neurobehavioral deficits and maternal smoking is causal. We utilized an animal model of maternal smoking to determine the effects of prenatal cigarette smoke (CS) exposure on neurobehavioral development. Pregnant mice were exposed to either filtered air or mainstream CS from gestation day (GD) 4 to parturition for 4h/d and 5d/wk, with each exposure producing maternal plasma concentration of cotinine equivalent to smoking <1 pack of cigarettes per day (25ng/ml plasma cotinine level). Pups were weaned at postnatal day (PND) 21 and behavior was assessed at 4weeks of age and again at 4-6months of age. Male, but not female, offspring of CS-exposed dams demonstrated a significant increase in locomotor activity during adolescence and adulthood that was ameliorated by methylphenidate treatment. Additionally, male offspring exhibited increased aggression, as evidenced by decreased latency to attack and number of attacks in a resident-intruder task. These behavioral abnormalities were accompanied by a significant decrease in striatal and cortical dopamine and serotonin and a significant reduction in brain-derived neurotrophic factor (BDNF) mRNA and protein. Taken in concert, these data demonstrate that prenatal exposure to CS produces behavioral alterations in mice that are similar to those observed in epidemiological studies linking maternal smoking to neurodevelopmental disorders. Further, these data also suggest a role for monaminergic and BDNF alterations in these effects. PMID:24486851

  12. 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

  13. E-cigarette use and intentions to smoke among 10-11-year-old never-smokers in Wales

    PubMed Central

    Moore, Graham F; Littlecott, Hannah J; Moore, Laurence; Ahmed, Nilufar; Holliday, Jo

    2016-01-01

    Background E-cigarettes are seen by some as offering harm reduction potential, where used effectively as smoking cessation devices. However, there is emerging international evidence of growing use among young people, amid concerns that this may increase tobacco uptake. Few UK studies examine the prevalence of e-cigarette use in non-smoking children or associations with intentions to smoke. Methods A cross-sectional survey of year 6 (10–11-year-old) children in Wales. Approximately 1500 children completed questions on e-cigarette use, parental and peer smoking, and intentions to smoke. Logistic regression analyses among never smoking children, adjusted for school-level clustering, examined associations of smoking norms with e-cigarette use, and of e-cigarette use with intentions to smoke tobacco within the next 2 years. Results Approximately 6% of year 6 children, including 5% of never smokers, reported having used an e-cigarette. By comparison to children whose parents neither smoked nor used e-cigarettes, children were most likely to have used an e-cigarette if parents used both tobacco and e-cigarettes (OR=3.40; 95% CI 1.73 to 6.69). Having used an e-cigarette was associated with intentions to smoke (OR=3.21; 95% CI 1.66 to 6.23). While few children reported that they would smoke in 2 years’ time, children who had used an e-cigarette were less likely to report that they definitely would not smoke tobacco in 2 years’ time and were more likely to say that they might. Conclusions E-cigarettes represent a new form of childhood experimentation with nicotine. Findings are consistent with a hypothesis that children use e-cigarettes to imitate parental and peer smoking behaviours, and that e-cigarette use is associated with weaker antismoking intentions. PMID:25535293

  14. 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. PMID:22392377

  15. Low-Dose Oxygen Enhances Macrophage-Derived Bacterial Clearance following Cigarette Smoke Exposure

    PubMed Central

    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. PMID:27403445

  16. 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. PMID:24157424

  17. Cigarette Smoking Is Associated with a Lower Concentration of CD105+ Bone Marrow Progenitor Cells

    PubMed Central

    Beyth, Shaul; Mosheiff, Rami; Safran, Ori; Daskal, Anat; Liebergall, Meir

    2015-01-01

    Cigarette smoking is associated with musculoskeletal degenerative disorders, delayed fracture healing, and nonunion. Bone marrow progenitor cells (BMPCs), known to express CD105, are important in local trophic and immunomodulatory activity and central to musculoskeletal healing/regeneration. We hypothesized that smoking is associated with lower levels of BMPC. Iliac bone marrow samples were collected from individuals aged 18–65 years during the first steps of pelvic surgery, under IRB approval with informed consent. Patients with active infectious or neoplastic disease, a history of cytotoxic or radiation therapy, primary or secondary metabolic bone disease, or bone marrow dysfunction were excluded. Separation process purity and the number of BMPCs recovered were assessed with FACS. BMPC populations in self-reported smokers and nonsmokers were compared using the two-tailed t-test. 13 smokers and 13 nonsmokers of comparable age and gender were included. The average concentration of BMPCs was 3.52 × 105/mL ± 2.45 × 105/mL for nonsmokers versus 1.31 × 105/mL ± 1.61 × 105/mL for smokers (t = 3.2,  P = 0.004). This suggests that cigarette smoking is linked to a significant decrease in the concentration of BMPCs, which may contribute to the reduced regenerative capacity of smokers, with implications for musculoskeletal maintenance and repair. PMID:26346476

  18. Cigarette Smoking Is Associated with a Lower Concentration of CD105(+) Bone Marrow Progenitor Cells.

    PubMed

    Beyth, Shaul; Mosheiff, Rami; Safran, Ori; Daskal, Anat; Liebergall, Meir

    2015-01-01

    Cigarette smoking is associated with musculoskeletal degenerative disorders, delayed fracture healing, and nonunion. Bone marrow progenitor cells (BMPCs), known to express CD105, are important in local trophic and immunomodulatory activity and central to musculoskeletal healing/regeneration. We hypothesized that smoking is associated with lower levels of BMPC. Iliac bone marrow samples were collected from individuals aged 18-65 years during the first steps of pelvic surgery, under IRB approval with informed consent. Patients with active infectious or neoplastic disease, a history of cytotoxic or radiation therapy, primary or secondary metabolic bone disease, or bone marrow dysfunction were excluded. Separation process purity and the number of BMPCs recovered were assessed with FACS. BMPC populations in self-reported smokers and nonsmokers were compared using the two-tailed t-test. 13 smokers and 13 nonsmokers of comparable age and gender were included. The average concentration of BMPCs was 3.52 × 10(5)/mL ± 2.45 × 10(5)/mL for nonsmokers versus 1.31 × 10(5)/mL ± 1.61 × 10(5)/mL for smokers (t = 3.2,  P = 0.004). This suggests that cigarette smoking is linked to a significant decrease in the concentration of BMPCs, which may contribute to the reduced regenerative capacity of smokers, with implications for musculoskeletal maintenance and repair. PMID:26346476

  19. 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…

  20. Biological responses in rats exposed to mainstream smoke from a heated cigarette compared to a conventional reference cigarette.

    PubMed

    Fujimoto, Hitoshi; Tsuji, Hiroyuki; Okubo, Chigusa; Fukuda, Ichiro; Nishino, Tomoki; Lee, K Monica; Renne, Roger; Yoshimura, Hiroyuki

    2015-03-01

    The heated cigarette (HC) generates mainstream smoke by vaporizing the components of the tobacco rod using a carbon heat source at the cigarette tip. Mainstream smoke of HC contains markedly less chemical constituents compared to combusted cigarettes. Mainstream smoke from HC was generated under Health Canada Intense regimen and its biological effects were compared to those of Reference (3R4F) cigarettes, using nose-only 5-week and 13-week inhalation studies. In the 13-week study, SD rats were necropsied following exposure to mainstream smoke from each cigarette at 200, 600 or 1000 µg wet total particulate matter/L for 1 h/day, 7 days/week or following a 13-week recovery period. Histopathological changes in the respiratory tract were significantly lesser in HC groups; e.g. respiratory epithelial hyperplasia in the nasal cavity and accumulation of pigmented macrophages in alveoli. After a 13-week recovery, the lesions were completely or partially regressed, except for accumulation of pigmented macrophages in alveoli, in both HC and 3R4F groups. In the 5-week study, SD rats were necropsied following exposure to mainstream smoke of either cigarette at 600 or 1000 µg/L for 1 h, two times/day (with 30 min interval), 7 days/week or following a 4-week recovery period. Bronchoalveolar lavage fluid (BALF) analysis of neutrophil percentages and enzyme levels like γ-GT, ALP and LDH indicated that pulmonary inflammation was significantly less in HC groups compared to 3R4F groups. In conclusion, HC demonstrated significantly lower biological effects compared to 3R4F, based on the BALF parameters and histopathology. PMID:25969858

  1. DOSIMETRY OF LOCALIZED ACCUMULATIONS OF CIGARETTE SMOKE AND RADON PROGENY AT BIFURCATIONS

    EPA Science Inventory

    Inhalation risk assessment protocols are frequently based upon assumptions of uniform particle deposition patterns and homogenous clearance processes within human lung airways. owever, experiments conducted with cigarette smoke and surrogate airway systems reveal "hot spots" at u...

  2. State Estimates of Adolescent Cigarette Use and Perceptions of Risk of Smoking: 2012 and 2013

    MedlinePlus

    ... 2015 STATE ESTIMATES OF ADOLESCENT CIGARETTE USE AND PERCEPTIONS OF RISK OF SMOKING: 2012 AND 2013 AUTHORS ... with an inverse association between use and risk perceptions (i.e., the prevalence of use is lower ...

  3. Maternal cigarette smoking during pregnancy and life-course-persistent offending.

    PubMed

    Piquero, Alex R; Gibson, Chris L; Tibbetts, Stephen G; Turner, Michael G; Katz, Solomon H

    2002-04-01

    Evidence exists documenting the relationship between maternal cigarette smoking and offspring criminal behavior. Although efforts to understand this relationship in a theoretical framework have only recently emerged, attempts made have been grounded in Moffitt's developmental taxonomy of antisocial behavior. Specifically, maternal cigarette smoking is generally viewed as a potential disruption in the offspring's neuropsychological development, which is subsequently associated with life-course-persistent offending. Using a birth cohort of 987 African Americans, the authors extend previous research by empirically assessing, prospectively, the link between maternal cigarette smoking and life-course-persistent offending while using different operationalizations of Moffitt's offending categorization. The authors' findings offer some support for the relationship between maternal cigarette smoking and life-course-persistent offending, which is dependent on how this concept is operationalized. PMID:12113165

  4. Determination of pyrethroid residues in tobacco and cigarette smoke by capillary gas chromatography.

    PubMed

    Cai, Jibao; Liu, Baizhan; Zhu, Xiaolan; Su, Qingde

    2002-07-26

    The extraction of fenpropathrin, cyhalothrin, cypermethrin, fenvalerate and deltamethrin from tobacco (Nicotina tobaccum) and cigarette smoke condensate with acetone, followed by partition of resulting acetone mixture with petroleum ether, was investigated and found suitable for capillary gas chromatography (GC) residue analysis. Florisil column clean-up was found to provide clean-up procedure for tobacco and cigarette smoke condensate permitting analysis to < or = 0.01 microgram.g-1 for most of the pyrethroids by GC with a 63Ni electron capture detector (GC-ECD). Quantitative determination was obtained by the method of external standards. Cigarettes made from flue-cured tobacco spiked with different amounts of pyrethroids were used and the pyrethroid levels in mainstream smoke were determined. For all the pyrethroid residues, 1.51-15.50% were transferred from tobacco into cigarette smoke. PMID:12198849

  5. Cigarette smoke induces alterations in the drug-binding properties of human serum albumin.

    PubMed

    Clerici, Marco; Colombo, Graziano; Secundo, Francesco; Gagliano, Nicoletta; Colombo, Roberto; Portinaro, Nicola; Giustarini, Daniela; Milzani, Aldo; Rossi, Ranieri; Dalle-Donne, Isabella

    2014-04-01

    Albumin is the most abundant plasma protein and serves as a transport and depot protein for numerous endogenous and exogenous compounds. Earlier we had shown that cigarette smoke induces carbonylation of human serum albumin (HSA) and alters its redox state. Here, the effect of whole-phase cigarette smoke on HSA ligand-binding properties was evaluated by equilibrium dialysis and size-exclusion HPLC or tryptophan fluorescence. The binding of salicylic acid and naproxen to cigarette smoke-oxidized HSA resulted to be impaired, unlike that of curcumin and genistein, chosen as representative ligands. Binding of the hydrophobic fluorescent probe 4,4'-bis(1-anilino-8-naphtalenesulfonic acid) (bis-ANS), intrinsic tryptophan fluorescence, and susceptibility to enzymatic proteolysis revealed slight changes in albumin conformation. These findings suggest that cigarette smoke-induced modifications of HSA may affect the binding, transport and bioavailability of specific ligands in smokers. PMID:24388826

  6. The Impact of Menthol Cigarettes on Smoking Initiation among Non-Smoking Young Females in Japan

    PubMed Central

    Connolly, Gregory N.; Behm, Ilan; Osaki, Yoneatsu; Wayne, Geoffrey F.

    2011-01-01

    Japan presents an excellent case-study of a nation with low female smoking rates and a negligible menthol market which changed after the cigarette market was opened to foreign competition. Internal tobacco industry documents demonstrate the intent of tobacco manufacturers to increase initiation among young females through development and marketing of menthol brands. Japanese menthol market share rose rapidly from less than 1% in 1980 to 20% in 2008. Menthol brand use was dominated by younger and female smokers, in contrast with non-menthol brands which were used primarily by male smokers. Nationally representative surveys confirm industry surveys of brand use and provide further evidence of the end results of the tobacco industry’s actions—increased female smoking in Japan. These findings suggest that female populations may be encouraged to initiate into smoking, particularly in developing nations or where female smoking rates remain low, if the tobacco industry can successfully tailor brands to them. The Japanese experience provides a warning to public health officials who wish to prevent smoking initiation among young females. PMID:21318010

  7. Self-Monitoring and Reactivity in the Modification of Cigarette Smoking.

    ERIC Educational Resources Information Center

    Abrams, David B.; Wilson, G. Terence

    1979-01-01

    Subjects were assigned to conditions based on smoking rates: self-monitoring nicotine plus health hazard information; self-monitoring cigarettes plus health information; and self-monitoring cigarettes with no health information. Nicotine self-monitoring groups showed greater reactivity. Exposure to health hazard information had no effect. (Author)

  8. Protobacco Media Exposure and Youth Susceptibility to Smoking Cigarettes, Cigarette Experimentation, and Current Tobacco Use among US Youth

    PubMed Central

    Fulmer, Erika B.; Neilands, Torsten B.; Dube, Shanta R.; Kuiper, Nicole M.; Arrazola, Rene A.; Glantz, Stanton A.

    2015-01-01

    Purpose Youth are exposed to many types of protobacco influences, including smoking in movies, which has been shown to cause initiation. This study investigates associations between different channels of protobacco media and susceptibility to smoking cigarettes, cigarette experimentation, and current tobacco use among US middle and high school students. Methods By using data from the 2012 National Youth Tobacco Survey, structural equation modeling was performed in 2013. The analyses examined exposure to tobacco use in different channels of protobacco media on smoking susceptibility, experimentation, and current tobacco use, accounting for perceived peer tobacco use. Results In 2012, 27.9% of respondents were never-smokers who reported being susceptible to trying cigarette smoking. Cigarette experimentation increased from 6.3% in 6th grade to 37.1% in 12th grade. Likewise, current tobacco use increased from 5.2% in 6th grade to 33.2% in 12th grade. Structural equation modeling supported a model in which current tobacco use is associated with exposure to static advertising through perception of peer use, and by exposure to tobacco use depicted on TV and in movies, both directly and through perception of peer use. Exposure to static advertising appears to directly increase smoking susceptibility but indirectly (through increased perceptions of peer use) to increase cigarette experimentation. Models that explicitly incorporate peer use as a mediator can better discern the direct and indirect effects of exposure to static advertising on youth tobacco use initiation. Conclusions These findings underscore the importance of reducing youth exposure to smoking in TV, movies, and static advertising. PMID:26308217

  9. E-Cigarettes for Immediate Smoking Substitution in Women Diagnosed with Cervical Dysplasia and Associated Disorders

    PubMed Central

    James, Shirley A.; Meier, Ellen M.; Wagener, Theodore L.; Smith, Katherine M.; Neas, Barbara R.; Beebe, Laura A.

    2016-01-01

    The aim of this study was to determine if 31 women with cervical dysplasia and associated conditions exacerbated by smoking would be successful substituting cigarettes with their choice of either nicotine replacement therapy (NRT) or electronic cigarettes (EC). Women received motivational interviewing and tried both NRT and ECs, choosing one method to use during a six-week intervention period. Daily cigarette consumption was measured at baseline, six, and 12 weeks, with differences analyzed by the Wilcoxon signed-rank test. Study analysis consisted only of women choosing to use ECs (29/31), as only two chose NRT. At the 12-week follow-up, the seven day point prevalence abstinence from smoking was 28.6%, and the median number of cigarettes smoked daily decreased from 18.5 to 5.5 (p < 0.0001). The median number of e-cigarette cartridges used dropped from 21 at the six-week follow-up to 12.5 at the 12-week follow-up. After initiating EC use, women at risk for cervical cancer were able to either quit smoking or reduce the number of cigarettes smoked per day. Although a controlled trial with a larger sample size is needed to confirm these initial results, this study suggests that using ECs during quit attempts may reduce cigarette consumption. PMID:26959042

  10. E-Cigarettes for Immediate Smoking Substitution in Women Diagnosed with Cervical Dysplasia and Associated Disorders.

    PubMed

    James, Shirley A; Meier, Ellen M; Wagener, Theodore L; Smith, Katherine M; Neas, Barbara R; Beebe, Laura A

    2016-03-01

    The aim of this study was to determine if 31 women with cervical dysplasia and associated conditions exacerbated by smoking would be successful substituting cigarettes with their choice of either nicotine replacement therapy (NRT) or electronic cigarettes (EC). Women received motivational interviewing and tried both NRT and ECs, choosing one method to use during a six-week intervention period. Daily cigarette consumption was measured at baseline, six, and 12 weeks, with differences analyzed by the Wilcoxon signed-rank test. Study analysis consisted only of women choosing to use ECs (29/31), as only two chose NRT. At the 12-week follow-up, the seven day point prevalence abstinence from smoking was 28.6%, and the median number of cigarettes smoked daily decreased from 18.5 to 5.5 (p < 0.0001). The median number of e-cigarette cartridges used dropped from 21 at the six-week follow-up to 12.5 at the 12-week follow-up. After initiating EC use, women at risk for cervical cancer were able to either quit smoking or reduce the number of cigarettes smoked per day. Although a controlled trial with a larger sample size is needed to confirm these initial results, this study suggests that using ECs during quit attempts may reduce cigarette consumption. PMID:26959042

  11. Dosimetry of localized accumulations of cigarette smoke and radon progeny at bifurcations

    SciTech Connect

    Martonen, T.B.; Hofmann, W.

    1991-01-01

    The work focuses upon deposition and clearance processes affecting cigarette smoke particles and radon progeny within surrogate airway models, replica casts and the human lung. As shall be demonstrated, 'cloud motion' for mainstream cigarette smoke can produce locations of enhanced deposition not experienced with dilute aerosols composed of like-sized particles. These sites of concentrated deposits occur at airway bifurcations, especially at the inclusive carinal ridges.

  12. Examining the relationships between posttraumatic stress disorder symptoms, positive smoking outcome expectancies, and cigarette smoking in people with substance use disorders: a multiple mediator model.

    PubMed

    Hruska, Bryce; Bernier, Jennifer; Kenner, Frank; Kenne, Deric R; Boros, Alec P; Richardson, Christopher J; Delahanty, Douglas L

    2014-01-01

    Cigarette smoking is highly prevalent in people with substance use disorders (SUDs) and is associated with significant physical health problems. Posttraumatic stress disorder (PTSD) is also highly associated with both SUDs and cigarette smoking and may serve as a barrier to smoking cessation efforts. In addition, people with PTSD are more likely to hold positive smoking outcome expectancies (i.e., beliefs that smoking cigarettes results in positive outcomes); these beliefs may contribute to cigarette smoking in people with SUDs experiencing PTSD symptoms. The present study examined the relationship between PTSD symptoms and typical daily cigarette smoking/cigarette dependence symptoms in a sample of 227 trauma-exposed current smokers with SUDs (59.9% male, 89.4% Caucasian) seeking detoxification treatment services. Additionally, the indirect effects of multiple types of positive smoking outcome expectancies on these relationships were examined. Participants completed questionnaires assessing PTSD symptoms, positive smoking outcome expectancies, cigarette consumption, and cigarette dependence symptoms. Results indicated that PTSD symptoms were not directly related to cigarette consumption or cigarette dependence symptoms. However, negative affect reduction outcome expectancies were shown to have a significant indirect effect between PTSD symptoms and cigarette consumption, while negative affect reduction, boredom reduction, and taste-sensorimotor manipulation outcome expectancies were all found to have significant indirect effects between PTSD symptoms and cigarette dependence symptoms. The indirect effect involving negative affect reduction outcome expectancies was statistically larger than that of taste sensorimotor manipulation outcome expectancies, while negative affect reduction and boredom reduction outcome expectancies were comparable in magnitude. These results suggest that expectancies that smoking can manage negative affective experiences are related to

  13. Adsorption of nicotine and tar from the mainstream smoke of cigarettes by oxidized carbon nanotubes

    NASA Astrophysics Data System (ADS)

    Chen, Zhigang; Zhang, Lisha; Tang, Yiwen; Jia, Zhijie

    2006-02-01

    The adsorption of nicotine and tar from the mainstream smoke (MS) by the filter tips filled respectively with oxidized carbon nanotubes (O-CNTs), activated carbon and zeolite (NaY) has been investigated. O-CNTs show exceptional removal efficiency and their adsorption mechanism is investigated. Capillary condensation of some ingredients from MS in the inner hole of O-CNTs is observed and may be the primary reason for their superior removal efficiency. The effect of O-CNTs mass on the removal efficiencies is also studied and the results show that about 20-30 mg O-CNTs per cigarette can effectively remove most of nicotine and tar.

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

    PubMed Central

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

    2012-01-01

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

  15. Analysis of hydrogen peroxide in an aqueous extract of cigarette smoke and effect of pH on the yield.

    PubMed

    Takanami, Yuichiro; Moriyama, Takako; Kosaka, Yasutaka; Nakayama, Tsutomu

    2009-10-01

    An analysis of hydrogen peroxide in an aqueous extract of cigarette smoke, which contains many redox-active compounds, requires a method with high selectivity. An aqueous extract of the particulate phase of cigarette smoke was analyzed by HPLC with an electrochemical detector (ECD). Samples were prepared by collecting the particulate phase of the cigarette smoke on a glass fiber filter and extracting it with a phosphate buffer. The obtained solution was purified by using a Waters Oasis MCX cation-exchange cartridge, and then analyzed by an HPLC-ECD system with a Shodex KS-801 mixed-mode resin column. Pre-injecting hydrogen peroxide at a high concentration into the HPLC instrument stabilized the analytical results. The recovery of hydrogen peroxide by using an extract of the particulate phase of the cigarette smoke was more than 80%. An increase in the amount of hydrogen peroxide was observed during extraction with the phosphate buffer at higher pH values. In contrast, extraction with phosphoric acid did not increase the amount of hydrogen peroxide during extraction. PMID:19809177

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

    PubMed

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

    2016-06-01

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

  17. Effect of Cigarette Smoke on Surface Roughness of Different Denture Base Materials

    PubMed Central

    Mahross, Hamada Zaki; Mohamed, Mahmoud Darwish; Hassan, Ahmed Mohammed

    2015-01-01

    Background Surface roughness is an important property of denture bases since denture bases are in contact with oral tissues and a rough surface may affect tissues health due to microorganism accumulation. Therefore, the effect of cigarette smoke on the surface roughness of two commercially available denture base materials was evaluated to emphasize which type has superior properties for clinical use. Materials and Methods A total numbers of 40 specimens were constructed from two commercially available denture base materials; heat-cured PMMA and visible light cured UDMA resins (20 for each). The specimens for each type were randomly divided into: Group I: Heat cured resin control group; Group II: Heat cured acrylic resin specimens exposed to cigarette smoking; Group III: Light cured resin control group; Group IV: Light cured resin specimens exposed to cigarette smoking. The control groups used for immersion in distilled water and the smoke test groups used for exposure to cigarette smoking. The smoke test groups specimens were exposed to smoking in a custom made smoking chamber by using 20 cigarettes for each specimen. The surface roughness was measured by using Pocket SurfPS1 profilometer and the measurements considered as the difference between the initial and final roughness measured before and after smoking. Results The t-test for paired observation of test specimens after exposure to smoking was indicated significant change in surface roughness for Group II (p< 0.05) but has no significance with Group IV. Otherwise, there were no significant differences with control groups (Group I and III). Conclusion The surface roughness of the dentures constructed from heat cured acrylic resin had been increased after exposure to cigarette smoke but had no impact on the dentures constructed from visible light cured resin. PMID:26501010

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

    PubMed Central

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

    2015-01-01

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

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

    PubMed

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

    2015-04-15

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

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

    SciTech Connect

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

    1983-08-08

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

  1. Nativity and Cigarette Smoking among Lower Income Blacks:Results from the Healthy Directions Study

    PubMed Central

    Wolin, Kathleen Y.; Okechukwu, Cassandra A.; Arthur, Carlotta M.; Askew, Sandy; Sorensen, Glorian; Emmons, Karen M.

    2009-01-01

    Blacks in the United States bear the greatest disease burden associated with cigarette smoking. Previous studies have shown that the rapidly increasing population of foreign-born Blacks has lower smoking rates compared to their native-born counterparts. However, less is known about whether cigarette smoking among Blacks varies by region of birth (US, Africa, or the Caribbean), generational status, or acculturation. We examined the association between nativity and cigarette smoking among 667 Black adult men and women enrolled in the Harvard Cancer Prevention Program project. In multi-variable analyses, US-born Blacks were more likely to be smokers compared to those born in the Caribbean (OR = 0.16, 95% CI 0.08, and 0.34) or in Africa (OR = 0.24, 95% CI 0.08, and 0.74). Language acculturation was positively associated with cigarette smoking (OR = 2.62, 95% CI 1.17, and 5.85). We found that US-born Blacks were more likely to be current cigarette smokers than those born in either Caribbean or African countries. Our findings highlight the importance of intervening early new Black immigrants to stem the uptake of cigarette smoking behaviors as individuals become acculturated. PMID:17924192

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

    PubMed

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

    2016-01-01

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

  3. Views from the Coalface: What Do English Stop Smoking Service Personnel Think about E-Cigarettes?

    PubMed Central

    Hiscock, Rosemary; Bauld, Linda; Arnott, Deborah; Dockrell, Martin; Ross, Louise; McEwen, Andy

    2015-01-01

    The UK Stop Smoking Services (SSS) are a source of information and advice on e-cigarettes for smokers and thus it is important to understand the knowledge of, and attitudes towards, e-cigarettes held by stop smoking practitioners. The datasets were English SSS quarterly monitoring returns (n = 207,883) and an online survey of English SSS practitioners, managers, and commissioners between 26th November and 15th December 2014 (n = 1801). SSS monitoring data suggested 2% of clients were using e-cigarettes to quit with SSS and that clients using e-cigarettes had similar quit rates to clients using Varenicline. Most SSS personnel are waiting for licenced e-cigarettes to become available before they will recommend them to clients. However, less than a quarter view e-cigarettes as “a good thing”. Managers and commissioners were more positive than practitioners. SSS personnel working for the NHS (hospitals and GP surgeries) were less positive about e-cigarettes than those employed elsewhere. E-cigarettes were cited as the most important reason for the recent decline in service footfall. Thus dissemination of information about e-cigarettes needs to be examined and services should address their stance on e-cigarettes with some urgency. PMID:26703638

  4. Views from the Coalface: What Do English Stop Smoking Service Personnel Think about E-Cigarettes?

    PubMed

    Hiscock, Rosemary; Bauld, Linda; Arnott, Deborah; Dockrell, Martin; Ross, Louise; McEwen, Andy

    2015-12-01

    The UK Stop Smoking Services (SSS) are a source of information and advice on e-cigarettes for smokers and thus it is important to understand the knowledge of, and attitudes towards, e-cigarettes held by stop smoking practitioners. The datasets were English SSS quarterly monitoring returns (n = 207,883) and an online survey of English SSS practitioners, managers, and commissioners between 26th November and 15th December 2014 (n = 1801). SSS monitoring data suggested 2% of clients were using e-cigarettes to quit with SSS and that clients using e-cigarettes had similar quit rates to clients using Varenicline. Most SSS personnel are waiting for licenced e-cigarettes to become available before they will recommend them to clients. However, less than a quarter view e-cigarettes as "a good thing". Managers and commissioners were more positive than practitioners. SSS personnel working for the NHS (hospitals and GP surgeries) were less positive about e-cigarettes than those employed elsewhere. E-cigarettes were cited as the most important reason for the recent decline in service footfall. Thus dissemination of information about e-cigarettes needs to be examined and services should address their stance on e-cigarettes with some urgency. PMID:26703638

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

    PubMed

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

    2016-01-01

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

  6. Cigarette smoke condensate increases cathepsin-mediated invasiveness of oral carcinoma cells

    PubMed Central

    Nagaraj, Nagathihalli S.; Zacharias, Wolfgang

    2007-01-01

    Cigarette smoke, which contains several carcinogens known to initiate and promote tumorigenesis and metastasis, is the major cause of oral cancer. Lysosomal cathepsin proteases play important roles in tumor progression, invasion and metastasis. In the present work we investigated the effects of cigarette smoke condensate (CSC) on cathepsin (B, D and L) expression and protease-mediated invasiveness in human oral squamous cell carcinoma (OSCC) cells. Our results show that treatment of OSCC cells (686Tu and 101A) with CSC activated cathepsins B, D and L in a dose-dependent manner. Both expression and activity of these cathepsins were up-regulated in CSC-exposed versus non-exposed cells. Although cathepsin L had the lowest basal level, it had the highest induction in exposed cells compared to cathepsins B and D. Suppression of CSC-induced cathepsin B and L activities by specific chemical inhibitors decreased the invasion process, suggesting that these proteases are involved in the invasion process. Overall, our results indicate that CSC activates cathepsin B and L proteolytic activity and enhances invasiveness in OSCC cells, a response that may play a role in CSC-mediated tumor progression and metastasis dissemination. PMID:17399918

  7. Cigarette smoking and its risk factors among elementary school students in Beijing.

    PubMed Central

    Zhu, B P; Liu, M; Shelton, D; Liu, S; Giovino, G A

    1996-01-01

    OBJECTIVES. This study investigated patterns of and risk factors for smoking among elementary school children in Beijing, China. METHODS. In 1988, anonymous questionnaires were administered to a multistage stratified cluster sample of 16996 students, aged mostly 10 to 12, in 479 fourth- to sixth-grade classes from 122 Beijing elementary schools. RESULTS. Approximately 28% of boys and 3% of girls had smoked cigarettes. The most frequently cited reasons for smoking initiation were "to imitate others' behavior" and "to see what it was like." Girls were more likely to get cigarettes from home than to purchase their own. Having close friends who smoked and being encouraged by close friends to smoke were strong risk factors for smoking. Smoking was also associated with lower parental socioeconomic status; having parents, siblings, or teachers who smoked; buying cigarettes for parents; performing poorly in school; and not believing that smoking is harmful to health. CONCLUSIONS. Gender differences in smoking prevalence among adolescents in China are larger than those among US teenagers, whereas the proximal risk factors for smoking are similar. Major efforts are needed to monitor and prevent smoking initiation among Chinese adolescents, particularly girls. PMID:8604762

  8. Determination of 10 carcinogenic polycyclic aromatic hydrocarbons in mainstream cigarette smoke.

    PubMed

    Ding, Yan S; Ashley, David L; Watson, Clifford H

    2007-07-25

    Polycyclic aromatic hydrocarbons (PAHs) are one class of chemical compounds that (1) are present at low to trace levels in unburned cigarette filler, and (2) are predominantly generated during combustion. According to a recent report of the International Agency for Research on Cancer, 10 carcinogenic PAHs together with 53 other known carcinogens are present in cigarette smoke. Accurate quantification of these chemicals helps assess public health risk to both smokers and nonsmokers exposed to second-hand smoke. We have developed and validated a specific and sensitive method for measuring these 10 carcinogenic PAHs in the particulate phase of mainstream tobacco smoke. Cigarette smoke particulate, produced using standard machine smoking protocols, was collected on glass fiber Cambridge filter pads. The particulate matter was solvent extracted, purified by solid-phase extraction, and analyzed by liquid chromatography/atmospheric pressure photoionization tandem mass spectrometry using isotopically labeled analogues as internal standards. Our method's limits of detection ranged from 11 to 166 pg and achieved sufficient reproducibility and accuracy to provide useful information on a range of cigarettes having dramatically different machine-smoked tar and nicotine deliveries. The identity of each PAH analyte was established from chromatographic retention time, analyte-specific fragmentation patterns, and relative peak area ratios of the product/precursor ion pairs. This new method provides higher sensitivity, specificity, and throughput than did earlier methods. We found relatively consistent PAH levels among a selection of domestic full-flavor cigarettes. The PAH levels in smoke from highly ventilated light and ultralight cigarettes were low when smoked using ISO (International Organization for Standardization) conditions. However, if highly ventilated cigarettes were smoked under more intense conditions (e.g., larger or more frequent puffs, vents blocked), their PAH

  9. Cigarette Smoking among HIV+ Men and Women: Examining Health, Substance Use, and Psychosocial Correlates across the Smoking Spectrum

    PubMed Central

    Webb, Monica S.; Vanable, Peter A.; Carey, Michael P.; Blair, Donald C.

    2008-01-01

    The prevalence of cigarette smoking among HIV+ individuals is greater than that found in the general population. However, factors related to smoking within this population are not well understood. This study examined the associations between smoking and demographic, medical, substance use, and psychosocial factors in a clinic-based sample of HIV+ men and women. Two hundred twelve participants completed self-report measures of tobacco use, HIV-related symptoms, viral load, CD4, alcohol and illicit drug use, depression, and social support. Multinomial logistic regression analyses modeled the independent associations of the cross-sectional set of predictors with smoking status. Results indicated that 74% of the sample smoked at least one cigarette per day; using standard definitions, 23% of the sample were light smokers, 22% were moderate smokers, and 29% smoked heavily. Smoking was associated with more HIV-related symptoms, greater alcohol and marijuana use, and less social support. Light smoking was related to minority race/ethnicity and less income; moderate smoking was associated with less education; and heavy smoking was related to less education and younger age. Viral load, CD4 count, and depression were not associated with smoking status. Psychosocial interventions targeting this population should consider the relationships between biopsychosocial factors and smoking behavior. PMID:17570050

  10. Prevalence and determinants of cigarette smoking among adolescents in Blantyre City, Malawi.

    PubMed

    Muula, A S

    2007-01-01

    Tobacco smoking is a major risk factor for non-communicable diseases such as ischaemic heart disease, stroke, chronic obstructive airways disease and several cancers. There is little data about the prevalence and determinants of smoking among adolescents in southern Africa. This study aimed to determine the prevalence and determinants of cigarette smoking among adolescents in Blantyre City, Malawi. Cross-sectional data were obtained from school-going adolescents in Blantyre in 2001 using the Global Youth Tobacco Survey data collection instrument. Data were analysed to determine prevalence of current and ever cigarette smoking, and predictors of smoking. The prevalence of current smoking and ever smoking were 3.0% and 15.6%, respectively. Predictors of current tobacco smoking included male gender, having friends or parents who smoked, having been exposed to advertisements about tobacco brands on television and having seen a lot of advertisements in newspapers and magazines. School programmes that included being taught about smoking in class and a class discussion on the dangers of tobacco were not associated with reduced current smoking. Intervention programmes aiming to curb tobacco smoking among adolescents should focus on dealing also with parental smoking, peer influence and pay special attention toward male gender. School-based programmes to prevent smoking should be evaluated as some may have little impact in influencing current smoking status. PMID:17547101

  11. [Cigarette smoking among the unemployed registered with Poznan District Employment Office].

    PubMed

    Gromadecka-Sutkiewicz, Małgorzata; Kłos, Jan

    2009-01-01

    The aim of this paper was to present the incidence and causes of smoking among those currently unemployed, and to show changes, if any, resulting from their continued joblessness. The analysis was based on the results of 1,068 surveys taken in 2007 among the unemployed registered with the District Employment Office in Poznan. It was found that cigarette smoking among the unemployed remains high and is associated with the respondents' gender, educational background, economic status and duration of unemployment. Severity of smoking increased more often for those unemployed on a short-term basis, with a number of smoked cigarettes per day more likely to decrease for those in medium- and long-term unemployment. Respondents quoted two equivalent reasons for smoking: wanting to have a cigarette and frustration. PMID:20301930

  12. A method for assessment of the genotoxicity of mainstream cigarette-smoke by use of the bacterial reverse-mutation assay and an aerosol-based exposure system.

    PubMed

    Kilford, Joanne; Thorne, David; Payne, Rebecca; Dalrymple, Annette; Clements, Julie; Meredith, Clive; Dillon, Debbie

    2014-07-15

    To date there are no widely accepted methods for the toxicological testing of complex gaseous mixtures and aerosols, such as cigarette smoke, although some modifications to the standard regulatory methods have been developed and used. Historically, routine testing of cigarettes has primarily focused on the particulate fraction of cigarette smoke. However, this fraction may not accurately reflect the full toxicity and mutagenicity of the smoke aerosol as a whole, which contains semi-volatiles and short-lived products of combustion. In this study we have used a modified version of the bacterial reverse-mutation (Ames) assay for the testing of mainstream smoke generated from 3R4F reference cigarettes with a Vitrocell(®) VC 10 exposure system. This method has been evaluated in four strains of Salmonella typhimurium (TA98, TA100, YG1024 and YG1042) and one strain of Escherichia coli (WP2 uvrA pKM101) in the absence and presence of a metabolic activation system. Following exposure at four concentrations of diluted mainstream cigarette-smoke, concentration-related and reproducible increases in the number of revertants were observed in all four Salmonella strains. E. coli strain WP2 uvrA pKM101 was unresponsive at the four concentrations tested. To quantify the exposure dose and to enable biological response to be plotted as a function of deposited mass, quartz-crystal microbalances were included in situ in the smoke-exposure set-up. This methodology was further assessed by comparing the responses of strain YG1042 to mainstream cigarette-smoke on a second VC 10 Smoking Robot. In summary, the Ames assay can be successfully modified to assess the toxicological impact of mainstream cigarette-smoke. PMID:25344108

  13. Changes in the structure and mechanical properties of pulmonary arteries of rats exposed to cigarette smoke.

    PubMed

    Liu, S Q; Fung, Y C

    1993-09-01

    The effect of cigarette smoke on the structure and mechanical properties of pulmonary arteries was studied in 2- and 3-month smoke-exposed rats. The animals were exposed to cigarette smoke in a smoke-generating system 10 times per day with one cigarette each time. The smoke density and the puffing duration and frequency of the system were regulated in accordance with reference values measured from human smokers. The volume fractions of the cells, including smooth muscle cells and fibroblasts, and extracellular matrix components, including collagen, elastin, and remainder (components not specified in this study), of the pulmonary arteries of approximately 450 microns in external diameter (at zero pressure) were determined in smoke-exposed and control rats by using an electron microscopic method. It was found that the volume fractions of the fibroblasts, the collagenous bundles, and the elastic laminae of the pulmonary arteries were increased significantly, whereas those of the smooth muscle cells and the remainder were decreased significantly in both the 2- and 3-month smoke-exposed rats in comparison with those of the corresponding control rats. The mechanical properties of the pulmonary arteries were determined based on the in vitro dimensional measurement of the vessels at various inflation pressures and zero-stress state. An increase in the stiffness of the pulmonary arteries was found in both the 2- and 3-month smoke-exposed rats. We conclude that cigarette smoke can induce structural and mechanical remodeling in the pulmonary arteries of rats. PMID:8368648

  14. Comparison of the Cytotoxic Potential of Cigarette Smoke and Electronic Cigarette Vapour Extract on Cultured Myocardial Cells

    PubMed Central

    Farsalinos, Konstantinos E.; Romagna, Giorgio; Allifranchini, Elena; Ripamonti, Emiliano; Bocchietto, Elena; Todeschi, Stefano; Tsiapras, Dimitris; Kyrzopoulos, Stamatis; Voudris, Vassilis

    2013-01-01

    Background: Electronic cigarettes (ECs) have been marketed as an alternative-to-smoking habit. Besides chemical studies of the content of EC liquids or vapour, little research has been conducted on their in vitro effects. Smoking is an important risk factor for cardiovascular disease and cigarette smoke (CS) has well-established cytotoxic effects on myocardial cells. The purpose of this study was to evaluate the cytotoxic potential of the vapour of 20 EC liquid samples and a “base” liquid sample (50% glycerol and 50% propylene glycol, with no nicotine or flavourings) on cultured myocardial cells. Included were 4 samples produced by using cured tobacco leaves in order to extract the tobacco flavour. Methods: Cytotoxicity was tested according to the ISO 10993-5 standard. By activating an EC device at 3.7 volts (6.2 watts—all samples, including the “base” liquid) and at 4.5 volts (9.2 watts—four randomly selected samples), 200 mg of liquid evaporated and was extracted in 20 mL of culture medium. Cigarette smoke (CS) extract from three tobacco cigarettes was produced according to ISO 3308 method (2 s puffs of 35 mL volume, one puff every 60 s). The extracts, undiluted (100%) and in four dilutions (50%, 25%, 12.5%, and 6.25%), were applied to myocardial cells (H9c2); percent-viability was measured after 24 h incubation. According to ISO 10993-5, viability of <70% was considered cytotoxic. Results: CS extract was cytotoxic at extract concentrations >6.25% (viability: 76.9 ± 2.0% at 6.25%, 38.2 ± 0.5% at 12.5%, 3.1 ± 0.2% at 25%, 5.2 ± 0.8% at 50%, and 3.9 ± 0.2% at 100% extract concentration). Three EC extracts (produced by tobacco leaves) were cytotoxic at 100% and 50% extract concentrations (viability range: 2.2%–39.1% and 7.4%–66.9% respectively) and one (“Cinnamon-Cookies” flavour) was cytotoxic at 100% concentration only (viability: 64.8 ± 2.5%). Inhibitory concentration 50 was >3 times lower in CS extract compared to the worst

  15. Cigarette smoke ventilation decreases prostaglandin inactivation in rat and hamster lungs

    SciTech Connect

    Maennistoe, J.; Uotila, P.

    1982-06-01

    The effects of cigarette smoke on the metabolism of exogenous PGE2 and PGF2 alpha were investigated in isolated rat and hamster lungs. When isolated lungs from animals were ventilated with cigarette smoke during pulmonary infusion of 100 nmol of PGE2 or PGF2 alpha, the amounts of the 15-keto-metabolites in the perfusion effluent were decreased. Pre-exposure of animals to cigarette smoke daily for 3 weeks did not change the metabolism of PGE2 when the lungs were ventilated with air. Cigarette smoke ventilation of lungs from pre-exposed animals caused, however, a similar decrease in the metabolism of PGE2 as in animals not previously exposed to smoke. After pulmonary injection of 10 nmol of /sup 14/C-PGE2 the radioactivity appeared more rapidly in the effluent during cigarette smoke ventilation suggesting inhibition of the PGE2 uptake mechanism. In rat lungs pulmonary vascular pressor responses to PGE2 and PGF2 alpha were inhibited by smoke ventilation.

  16. Exposure to cigarette smoke causes DNA damage in oropharyngeal tissue in dogs.

    PubMed

    Pérez, Natalia; Berrío, Alina; Jaramillo, Jairo Enrique; Urrego, Rodrigo; Arias, María Patricia

    2014-07-15

    More than 40 mutagenic and carcinogenic agents present in cigarette smoke have been identified as causative factors of human cancer, but no relation has been clearly documented in companion animals. In dogs, in addition to smoke inhalation and transdermic absorption, exposure to smoke includes oral ingestion of particles adhered to the animal's fur. This study evaluates the presence and type of histological alterations and DNA integrity in oropharyngeal tissue in dogs exposed and non-exposed to household cigarette smoke by means of histopathology and comet assay studies on biopsy and swab samples. A non-probabilistic convenience sample of 12 dogs were selected and classified in two groups: exposed and non-exposed to cigarette smoke. Non-parametric Kruskal-Wallis test was carried out on biopsy and swab data and a Chi(2) test was performed on the information obtained by histopathology. A significance level was set at P<0.05. Statistically significant differences were found between groups in comet assays carried out on biopsy samples. No differences (P>0.05) were found between groups based on comet assays swab samples and histopathology assessment. In conclusion, exposure to cigarette smoke causes DNA damage in dog oropharyngeal tissue. The use of dogs as sentinels for early DNA damage caused by exposure to environmental genotoxic agents like cigarette smoke is reported for the first time. PMID:25344107

  17. Summary of the Findings from a Study About Cigarette Smoking Among Teen-Age Girls and Young Women.

    ERIC Educational Resources Information Center

    Yankelovich, Skelly and White, Inc., New York, NY.

    This paper presents the major results of a study for the American Cancer Society on cigarette smoking among teen-age girls and young women, and findings relevant to the prevention and quitting of smoking. The four major trends found in this study are: (1) a dramatic increase in cigarette smoking among females; (2) an intellectual awareness of the…

  18. Electronic Cigarettes: Smoke-Free Laws, Sale Restrictions, and the Public Health

    PubMed Central

    2014-01-01

    Consumer use of e-cigarettes is rising despite a lack of rigorous safety testing, manufacturing controls, and a well-understood risk profile. Many states and municipalities have prohibited e-cigarette sale to minors or amended their smoke-free laws to restrict public use. I discuss the public health impact of e-cigarettes and the current lack of Food and Drug Administration regulation, and advocate that states and localities reexamine their smoke-free laws and sale restrictions to appropriately regulate public use and youth access. PMID:24825224

  19. Cigarette smoking among college students attending a historically Black college and university.

    PubMed

    Laws, Michelle A; Huang, Chien Ju; Brown, Roderick F; Richmond, Al; Conerly, Rhonda C

    2006-02-01

    Very little is known about the prevalence, patterns, social norms, and trends of smoking among students attending historically Black colleges and universities (HBCUs). The current study assessed the prevalence, patterns, and norms associated with cigarette smoking among a cross-sectional random sample of 371 undergraduate college students at a historically Black university in North Carolina. Eighty-seven percent of the respondents were non-smokers. Eighty-six percent of the students reported that smoking was discouraged among their peers and 45% responded that they preferred associating with peers who did not smoke cigarettes. Seventy-one percent of the students responded that they did not smoke before the age of 18 and 55% reported that, while they were growing up, neither of their parents smoked. Preliminary findings of this study indicate that smoking is not widely practiced and has not become a socially acceptable or encouraged norm among college students attending an HBCU. PMID:16520524

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

    PubMed Central

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

    2015-01-01

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

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

    PubMed Central

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

    2016-01-01

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

  2. Cigarette advertising and children's smoking: why Reg was withdrawn.

    PubMed Central

    Hastings, G. B.; Ryan, H.; Teer, P.; MacKintosh, A. M.

    1994-01-01

    OBJECTIVE--To examine the appeal of the Embassy Regal "Reg" campaign to young people. DESIGN--Three quantitative surveys and one piece of qualitative research: (a) self completion questionnaire administered in classrooms, (b) questionnaire led interviews with children, (c) questionnaire led interviews with adults, and (d) group discussions with children and adults. SETTINGS--(a) Secondary and middle schools in England; (b) north of England, Scotland, and Wales; (c) north of England, Scotland, and Wales; and (d) Glasgow. SUBJECTS--(a) 5451 schoolchildren aged 11-15 recruited by stratified random sampling; (b) 437 children aged 5-10 recruited by quota sampling; (c) 814 adults aged 15-65 recruited by quota sampling; and (d) 12 groups of children aged 10-15, three groups of adults aged 18-24, and three groups of adults aged 35-55. RESULTS--Children were familiar with cigarette advertising and in particular the Reg campaign. Although younger children struggled to understand the creative content of the adverts, older and smoking children could understand and appreciate the humour. They considered Reg to be amusing and could relate to the type of joke used in the advert. In addition Reg's flippant attitude towards serious issues appealed to the children. While adults aged 18-24 understood the campaign they did not identify with it, and 35-55 year olds (the campaign's supposed target) were unappreciative of the campaign. CONCLUSIONS--The Reg campaign was getting through to children more effectively than it was to adults and held most appeal for teenagers, particularly 14-15 year old smokers. It clearly contravened the code governing tobacco advertising, which states that advertising must not appeal to children more than it does to adults, and it may have had a direct impact on teenage smoking. In view of these findings the Advertising Standards Authority's decision to withdraw the Reg campaign seems appropriate. Images p935-a PMID:7950668

  3. Intracellular Metabolism of α,β-Unsaturated Carbonyl Compounds, Acrolein, Crotonaldehyde and Methyl Vinyl Ketone, Active Toxicants in Cigarette Smoke: Participation of Glutathione Conjugation Ability and Aldehyde-Ketone Sensitive Reductase Activity.

    PubMed

    Horiyama, Shizuyo; Hatai, Mayuko; Takahashi, Yuta; Date, Sachiko; Masujima, Tsutomu; Honda, Chie; Ichikawa, Atsushi; Yoshikawa, Noriko; Nakamura, Kazuki; Kunitomo, Masaru; Takayama, Mitsuo

    2016-01-01

    The major toxicants in cigarette smoke, α,β-unsaturated aldehydes, such as acrolein (ACR) and crotonaldehyde (CA), and α,β-unsaturated ketone, methyl vinyl ketone (MVK), are known to form Michael-type adducts with glutathione (GSH) and consequently cause intracellular GSH depletion, which is involved in cigarette smoke-induced cytotoxicity. We have previously clarified that exposure to cigarette smoke extract (CSE) of a mouse melanoma cell culture medium causes rapid reduction of intracellular GSH levels, and that the GSH-MVK adduct can be detected by LC/MS analysis while the GSH-CA adduct is hardly detected. In the present study, to clarify why the GSH-CA adduct is difficult to detect in the cell medium, we conducted detailed investigation of the structures of the reaction products of ACR, CA, MVK and CSE in the GSH solution or the cell culture medium. The mass spectra indicated that in the presence of the cells, the GSH-CA and GSH-ACR adducts were almost not detected while their corresponding alcohols were detected. On the other hand, both the GSH-MVK adducts and their reduced products were detected. In the absence of the cells, the reaction of GSH with all α,β-unsaturated carbonyls produced only their corresponding adducts. These results show that the GSH adducts of α,β-unsaturated aldehydes, CA and ACR, are quickly reduced by certain intracellular carbonyl reductase(s) and excreted from the cells, unlike the GSH adduct of α,β-unsaturated ketone, MVK. Such a difference in reactivity to the carbonyl reductase might be related to differences in the cytotoxicity of α,β-unsaturated aldehydes and ketones. PMID:27250793

  4. Exposure to Peers who Smoke Moderates the Association between Sports Participation and Cigarette Smoking Behavior among Non-White Adolescents

    PubMed Central

    Mays, Darren; Luta, George; Walker, Leslie R.; Tercyak, Kenneth P.

    2012-01-01

    Adolescent sports participants are less likely to smoke cigarettes, and sports participation may prevent young people from smoking. Research suggests that the relationship between sports participation and smoking may vary by race/ethnicity and is also possibly moderated by exposure to peer smoking. We investigated these relationships in a sample of 311 adolescents ages 13 – 21 presenting for well-visit medical appointments. Participants completed valid assessments of demographics, sports participation, exposure to peer smoking, and smoking behavior. The primary outcome was smoking status (never smoked, tried smoking, experimental/current smoker). Ordinal logistic regression was used separately for non-Hispanic White (n = 122) and non-White (n = 189; 70.4% Black, 14.3% Hispanic, and 15.3% other) adolescents. Among White adolescents, sports participants had significantly lower odds of smoking than non-sports participants, independent of age, gender, and peer smoking. For non-Whites, the adjusted effect of sports participation on smoking depended upon exposure to peers who smoke. Compared with non-sport participants with no exposure to peer smoking, sports participants with no exposure to peer smoking had significantly lower odds of smoking, whereas sports participants with exposure to peer smoking had significantly higher odds of smoking. Sports appear to be protective against smoking among non-Hispanic White adolescents, but among non-White adolescents exposure to peer smoking influences this protection. Interventions incorporating sports to prevent smoking should consider these racial/ethnic differences to address disparities in smoking-related disease. PMID:22698897

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

    PubMed

    Stinn, Walter; Arts, Josje H E; Buettner, Ansgar; Duistermaat, Evert; Janssens, Kris; Kuper, C Frieke; Haussmann, Hans-Juergen

    2010-09-10

    Knowledge on mechanisms of smoking-induced tumorigenesis and on active smoke constituents may improve the development and evaluation of chemopreventive and therapeutic interventions, early diagnostic markers, and new and potentially reduced-risk tobacco products. A suitable laboratory animal disease model of mainstream cigarette smoke inhalation is needed for this purpose. In order to develop such a model, A/J and Swiss SWR/J mouse strains, with a genetic susceptibility to developing lung adenocarcinoma, were whole-body exposed to diluted cigarette mainstream smoke at 0, 120, and 240 mg total particulate matter per m(3) for 6h per day, 5 days per week. Mainstream smoke is the smoke actively inhaled by the smoker. For etiological reasons, parallel exposures to whole smoke fractions (enriched for particulate or gas/vapor phase) were performed at the higher concentration level. After 5 months of smoke inhalation and an additional 4-month post-inhalation period, both mouse strains responded similarly: no increase in lung tumor multiplicity was seen at the end of the inhalation period; however, there was a concentration-dependent tumorigenic response at the end of the post-inhalation period (up to 2-fold beyond control) in mice exposed to the whole smoke or the particulate phase. Tumors were characterized mainly as pulmonary adenomas. At the end of the inhalation period, epithelial hyperplasia, atrophy, and metaplasia were found in the nasal passages and larynx, and cellular and molecular markers of inflammation were found in the bronchoalveolar lavage fluid. These inflammatory effects were mostly resolved by the end of the post-inhalation period. In summary, these mouse strains responded to mainstream smoke inhalation with enhanced pulmonary adenoma formation. The major tumorigenic potency resided in the particulate phase, which is contrary to the findings published for environmental tobacco smoke surrogate inhalation in these mouse models. PMID:20594951

  6. Effects of cigarette smoke on the Meckel's cartilage of rat fetus: morphologic, morphometric and stereologic study.

    PubMed

    Brandini, Daniela Atili; Sala, Miguel Angel; Lopes, Ruberval Armando; Semprini, Marisa; Contrera, Mary Garcia Duarte

    2005-01-01

    The purpose of this study was to investigate the effects of cigarette smoke on the development of the embryo mandible (Meckel's) cartilage in rat fetuses. When inhaled by female Wistar rats between the 9th and the 12th day of pregnancy, cigarette smoke (5 cigarettes a day) caused intrauterine growth retardation, providing smaller fetuses and placentas. In fetuses from the experimental group, the histopathologic examination revealed a poorly developed Meckel's cartilage with smaller chondroblasts showing a scanty cytoplasm with spherical and paler central nuclei, as well as more abundant cartilage matrix. Morphometric analysis revealed that Meckel's cartilage lacunae were smaller in the fetuses from the experimental group, although not showing any remarkable alteration in shape. The results suggested that inhalation of cigarette smoke by pregnant rats during the organogenic period induced growth retardation and delayed cellular differentiation in rat fetal Meckel's cartilage. PMID:16113936

  7. Effect of cigarette smoke, nicotine, and carbon monoxide on the permeability of the arterial wall

    SciTech Connect

    Allen, D.R.; Browse, N.L.; Rutt, D.L.; Butler, L.; Fletcher, C.

    1988-01-01

    The association between cigarette smoking and the development of atherosclerosis is well established, but the mechanism that makes cigarettes such a potent risk factor is not understood. There is normally a constant insudation of plasma macromolecules into the arterial wall. Fibrinogen and lipids are two of the large molecules involved in atherosclerosis. Therefore, we studied the effect of cigarette smoke, nicotine, and carbon monoxide on the permeability of the canine arterial wall to /sup 125/I-labeled fibrinogen. The results show that inhaled cigarette smoke significantly and rapidly increases the permeability of the arterial wall to fibrinogen and that this effect can be produced with carbon monoxide alone but not with intravenous nicotine.

  8. Lung matrix metalloproteinase-9 correlates with cigarette smoking and obstruction of airflow.

    PubMed Central

    Kang, Min Jong; Oh, Yeon-Mok; Lee, Jae Cheol; Kim, Dong Gyu; Park, Myung Jae; Lee, Myung Goo; Hyun, In Gyu; Han, Sung Koo; Shim, Young-Soo; Jung, Ki-Suck

    2003-01-01

    Cigarette smoking is the most important risk factor for obstruction of airflow in chronic obstructive pulmonary disease (COPD). Matrix metalloproteinases (MMPs) or an imbalance between MMPs and their inhibitors, the tissue inhibitors of MMP (TIMPs), is considered to play a role in the pathogenesis of COPD. We investigated whether the MMPs expression or the imbalance between MMPs and TIMP-1 is associated with the amount of cigarette smoking and the FEV1 value, in the lung parenchyma of 26 subjects (6 non-smokers and 20 cigarette smokers). First, we performed zymographic analysis to identify the profile of the MMPs, which revealed gelatinolytic bands mainly equivalent to MMP-9 in the smokers. We then measured, using enzyme immunoassay, the concentrations of MMP-9 and its inhibitor, TIMP-1. Correlation analysis revealed that both the MMP-9 concentrations and the molar ratios of MMP-9 to TIMP-1 (MMP-9/TIMP-1) were correlated with the amount of cigarette smoking. Furthermore, MMP-9 concentrations were inversely correlated with FEV1. In conclusion, this study shows that MMP-9 expression in human lung parenchyma is associated with cigarette smoking and also with the obstruction of airflow, suggesting that MMP-9 may play a role in the pathogenesis of the cigarette smoke-induced obstruction of airflow known as the characteristic of COPD. PMID:14676438

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

    SciTech Connect

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

    2012-03-15

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

  10. Social and Psychological Predictors of Initial Cigarette Smoking Experience: A Survey in Male College Students.

    PubMed

    Menati, Walieh; Nazarzadeh, Milad; Bidel, Zeinab; Würtz, Morten; Menati, Rostam; Hemati, Rohollah; Yaghoubi, Maryam; Zareimanesh, Elham; Mohammadi, Mohammad Sabour; Akhlaghi Ardekani, Farzad; Tazval, Jafar; Delpisheh, Ali

    2016-01-01

    Knowledge about social and psychological risk factors for initial cigarette smoking experience (ICSE) is sparse. The present study aimed to estimate the prevalence of ICSE and to examine the psychological and social factors related to ICSE. In a cross-sectional survey, 1,511 male college students were recruited using multistage sampling techniques from four universities located within the city of Ilam, Iran. Self-administered multiple-choice questionnaires were distributed to students from March to June 2013. Risk factors for ICSE were evaluated using logistic regression models. Participants were 22.3 ± 2.4 years of age. ICSE prevalence was 30.6%. In multivariable adjusted analysis, risk taking behavior (odds ratio [OR] = 1.61; 95% confidence interval [CI] = 1.11-2.33), perceived peer smoking prevalence (OR = 2.48; 95% CI = 1.03-5.97), positive thoughts about smoking (OR = 1.06; 95% CI = 1.02-1.10), high self-efficacy (OR = 0.95, 95% CI [0.93, 0.98]), presence in smokers' gathering (OR = 4.45; 95% CI = 2.88-6.81), comity of smokers (OR = 2.56; 95% CI = 1.66, 3.92), very hard access to cigarettes (OR = 2.20; 95% CI = 1.16-4.16), close friends' medium reaction toward smoking (OR = 1.38; 95% CI = 1.02-1.88), and sporting activity (OR = 0.74; 95% CI = 0.56-0.98) were significantly associated with ICSE. This study identified that a combination of psychological and social variables account for up to 78% of the probability of ICSE. The most important protective factor against ICSE was physical activity, whereas the most important risk factor for ICSE was frequent gathering in the presence of smokers. PMID:25326133

  11. Comparison of the Reinforcing Properties of Nicotine and Cigarette Smoke Extract in Rats

    PubMed Central

    Costello, Matthew R; Reynaga, Daisy D; Mojica, Celina Y; Zaveri, Nurulain T; Belluzzi, James D; Leslie, Frances M

    2014-01-01

    Tobacco dependence is difficult to treat, with the vast majority of those who try to quit relapsing within the first year. Improvements in smoking cessation therapies may be achieved by improving current preclinical research methods. However, most experimental tests in animals use nicotine alone, ignoring the 8000 other constituents found in tobacco smoke. To improve on this model, we have used self-administration to test the reinforcing properties of aqueous cigarette smoke extract (CSE) in rats, made by bubbling cigarette smoke through a saline solution. CSE is more potent than nicotine alone in both the acquisition and maintenance of self-administration, but did not exhibit higher progressive ratio responding. Mecamylamine and varenicline had similar potencies to block nicotine and CSE self-administration, indicating the involvement of nicotinic receptors in CSE reinforcement. Following extinction of responding, reinstatement was triggered by exposing animals to a pharmacological stressor, yohimbine (2.5 mg/kg, i.p.), alone and in combination with cues. Animals that self-administered CSE were significantly more sensitive to stress-induced reinstatement than those that self-administered nicotine. Ligand binding autoradiography studies showed nicotine and CSE to have similar affinities for different nicotinic receptor types. CSE significantly reduced MAO-A and MAO-B activities in vitro, whereas nicotine did not. Although CSE inhibition of MAO-A activity in vitro was found to be partially irreversible, irreversible inhibition was not observed in vivo. These experiments show that CSE is an effective reinforcer acting via nicotinic receptors. Furthermore, it better models MAO inhibition and is more sensitive to stress-induced reinstatement than nicotine alone, which is a potent trigger for relapse in smokers. PMID:24513971

  12. A longitudinal study of smokers' exposure to cigarette smoke and the effects of spontaneous product switching.

    PubMed

    Cunningham, Anthony; Sommarström, Johan; Camacho, Oscar M; Sisodiya, Ajit S; Prasad, Krishna

    2015-06-01

    A challenge in investigating the effect of public health policies on cigarette consumption and exposure arises from variation in a smoker's exposure from cigarette to cigarette and the considerable differences between smokers. In addition, limited data are available on the effects of spontaneous product switching on a smoker's cigarette consumption and exposure to smoke constituents. Over 1000 adult smokers of the same commercial 10mg International Organization for Standardization (ISO) tar yield cigarette were recruited into the non-residential, longitudinal study across 10 cities in Germany. Cigarette consumption, mouth level exposure to tar and nicotine and biomarkers of exposure to nicotine and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone were measured every 6months over a 3 and a half year period. Cigarette consumption remained stable through the study period and did not vary significantly when smokers spontaneously switched products. Mouth level exposure decreased for smokers (n=111) who switched to cigarettes of 7mg ISO tar yield or lower. In addition, downward trends in mouth level exposure estimates were observed for smokers who did not switch cigarettes. Data from this study illustrate some of the challenges in measuring smokers' long-term exposure to smoke constituents in their everyday environment. PMID:25777840

  13. Current manufactured cigarette smoking and roll-your-own cigarette smoking in Thailand: findings from the 2009 Global Adult Tobacco Survey

    PubMed Central

    2013-01-01

    Background Current smoking prevalence in Thailand decreased from 1991 to 2004 and since that time the prevalence has remained flat. It has been suggested that one of the reasons that the prevalence of current smoking in Thailand has stopped decreasing is due to the use of RYO cigarettes. The aim of this study was to examine characteristics of users of manufactured and RYO cigarettes and dual users in Thailand, in order to determine whether there are differences in the characteristics of users of the different products. Methods The 2009 Global Adult Tobacco Survey (GATS Thailand) provides detailed information on current smoking patterns. GATS Thailand used a nationally and regionally representative probability sample of 20,566 adults (ages 15 years and above) who were chosen through stratified three-stage cluster sampling and then interviewed face-to-face. Results The prevalence of current smoking among Thai adults was 45.6% for men and 3.1% for women. In all, 18.4% of men and 1.0% of women were current users of manufactured cigarettes only, while 15.8% of men and 1.7% of women were current users of RYO cigarettes only. 11.2% of men and 0.1% of women used both RYO and manufactured cigarettes. Users of manufactured cigarettes were younger and users of RYO were older. RYO smokers were more likely to live in rural areas. Smokers of manufactured cigarettes appeared to be more knowledge