oalib
Search Results: 1 - 10 of 100 matches for " "
All listed articles are free for downloading (OA Articles)
Page 1 /100
Display every page Item
Identification of bacterial and fungal components in tobacco and tobacco smoke
Lennart Larsson, Bogumila Szponar, Beston Ridha, Christina Pehrson, Jacek Dutkiewicz, Ewa Krysińska-Traczyk, Jolanta Sitkowska
Tobacco Induced Diseases , 2008, DOI: 10.1186/1617-9625-4-4
Abstract: Many hundreds of compounds known to contribute to disease development have been identified in tobacco smoke. Both active and second hand smoking causes cancer and a multitude of other diseases such as for example chronic bronchitis and asthma. Three studies [1-3] have revealed that tobacco smoke contains endotoxin (lipopolysaccharide, LPS), a family of inflammatory toxins from Gram-negative bacteria known to cause respiratory disease upon inhalation [4]. Hasday et al. [1] found that the amounts of endotoxin in tobacco were comparable with those of some other agricultural products. While Hasday et al. [1] used a Limulus method for measuring endotoxin, Larsson et al. [2] introduced gas chromatography-tandem mass spectrometry (GC-MSMS) for demonstrating 3-hydroxytetradecanoic acid, a unique LPS constituent [5], in cigarette tobacco and smoke. GC-MSMS is a very specific analysis method for unequivocal identification of LPS. Sebastian et al. [3], using the same GC-MSMS method, demonstrated a linear relationship between the number of cigarettes smoked over a 5-h period indoors and air concentrations of endotoxin. Whether bioactive microbial compounds other than LPS, such as for example peptidoglycan and various fungal components, are present in cigarette smoke is not known from the literature.An integrated method for characterizing microbial composition in environmental samples by GC-MSMS has been developed at our laboratory [6]. The method includes a protocol for preparation and analyzing samples for LPS markers 3-hydroxy fatty acids (3-OH FAs) of 10 – 18 carbon chain lengths, peptidoglycan marker muramic acid (MuAc), and fungal biomass marker ergosterol (Erg). In the present study a modified version [7] of this method was used for 1) measuring 3-OH FAs, MuAc, and Erg in tobacco from cigarettes of international as well as local brands purchased in different countries in Europe and Asia including "light" and "full flavor" cigarettes; 2) analysing the microbiological compo
Lethal impacts of cigarette smoke in cultured tobacco cells
Masaru Yukihiro, Takuya Hiramatsu, Tomonori Kawano
Tobacco Induced Diseases , 2011, DOI: 10.1186/1617-9625-9-8
Abstract: By employing the tobacco cells as model materials for cigarette smoke toxicity assay, the impacts of the combustion by-products such as nitrogen oxides could be highlighted as the toxic impacts of the plant-derived endogenous chemicals could be excluded in the plant cells.Cigarette smoke-induced cell death was assessed in tobacco cell suspension cultures in the presence and absence of pharmacological inhibitors.Cigarette smoke was effective in induction of cell death. The smoke-induced cell death could be partially prevented by addition of nitric oxide (NO) scavenger, suggesting the role for NO as the cell death mediator. Addition of NO donor to tobacco cells also resulted in development of partial cell death further confirming the role of NO as cell death mediator. Members of reactive oxygen species and calcium ion were shown to be protecting the cells from the toxic action of smoke-derived NO.In the United States, the toxic impacts of various chemicals to various organisms have been documented in the Ecotoxicology Database (ECOTOX) of the US EPA. The cigarette smoke is known to be toxic and thus harmful to human health [1], both at cellular [2] and genetic levels [3]. On the other hand, the impacts of cigarette smoke in various organisms including living plants have been poorly documented to date. In order to understand and generalize the toxic mechanism of cigarette smoke in living cells, comparison of the data between animal systems and other biological system such as microbial and plant systems is highly beneficial.Since the cigarette smoke is derived from combustion of tobacco leaves, the chemical components in the smoke must be the mixture of (i) chemical contents originally present in the tobacco leaves and (ii) the chemicals formed through combustion process (combustion by-products) [4]. Both former (such as nicotine, phenolics, etc.) and latter chemicals (such as hydrogen peroxide) are known to be harmful to human health [3]. However, it is natural to assu
Cigarette Smoke, Bacteria, Mold, Microbial Toxins, and Chronic Lung Inflammation  [PDF]
John L. Pauly,Geraldine Paszkiewicz
Journal of Oncology , 2011, DOI: 10.1155/2011/819129
Abstract: 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. 1. Introduction: Chemical and Biological Components of Tobacco and Smoke For many years, scientists have undertaken studies to define the chemical composition of green tobacco leaf, cured-fermented-stored tobacco leaf, and tobacco smoke with the intent of identifying chemicals that may pose a significant health risk [1–4]. An illustration has been prepared of the annual increase, from 1954 to 2005, in the total number of tobacco smoke chemicals that have been identified [4]. Today, there is a consensus of opinion that cigarette smoke consists of at least 5,300 different chemicals [4]. These chemicals are present in the complex aerosol that consists of a heterogeneous mixture of gas- (vapor-) phase and particulate- (“tar-”) phase components [1–4]. Detailed listings of the chemicals in mainstream and sidestream tobacco smoke are available, and an assessment of their propensity for harm has been presented; a partial listing of references is included [1–4]. Most of the chemicals, toxicants, and carcinogens in tobacco smoke arise from the burning (pyrolysis) of the tobacco [1, 2, 4]. The potential for harm has also been studied for chemicals that do not arise from the burning of tobacco. The chemicals include metallic and nonmetallic elements, isotopes, and salts [1, 2, 4]. In addition, pesticides and other intact agrochemicals have been identified in tobacco smoke [1, 2, 4]. Also included in this tabulation of chemicals
Hazardous Compounds in Tobacco Smoke  [PDF]
Reinskje Talhout,Thomas Schulz,Ewa Florek,Jan Van Benthem,Piet Wester,Antoon Opperhuizen
International Journal of Environmental Research and Public Health , 2011, DOI: 10.3390/ijerph8020613
Abstract: Tobacco smoke is a toxic and carcinogenic mixture of more than 5,000 chemicals. The present article provides a list of 98 hazardous smoke components, based on an extensive literature search for known smoke components and their human health inhalation risks. An electronic database of smoke components containing more than 2,200 entries was generated. Emission levels in mainstream smoke have been found for 542 of the components and a human inhalation risk value for 98 components. As components with potential carcinogenic, cardiovascular and respiratory effects have been included, the three major smoke-related causes of death are all covered by the list. Given that the currently used Hoffmann list of hazardous smoke components is based on data from the 1990s and only includes carcinogens, it is recommended that the current list of 98 hazardous components is used for regulatory purposes instead. To enable risk assessment of components not covered by this list, thresholds of toxicological concern (TTC) have been established from the inhalation risk values found: 0.0018 μg day ?1 for all risks, and 1.2 μg day ?1 for all risks excluding carcinogenicity, the latter being similar to previously reported inhalation TTCs.
Cannabis and tobacco smoke are not equally carcinogenic
Robert Melamede
Harm Reduction Journal , 2005, DOI: 10.1186/1477-7517-2-21
Abstract: Tobacco has dramatic negative consequences for those who smoke it. In addition to its high addiction potential [1], tobacco is causally associated with over 400,000 deaths yearly in the United States, and has a significant negative effect on health in general [2]. More specifically, over 140,000 lung-related deaths in 2001 were attributed to tobacco smoke [3]. Comparable consequences would naturally be expected from cannabis smoking since the burning of plant material in the form of cigarettes generates a large variety of compounds that possess numerous biological activities [4].While cannabis smoke has been implicated in respiratory dysfunction, including the conversion of respiratory cells to what appears to be a pre-cancerous state [5], it has not been causally linked with tobacco related cancers [6] such as lung, colon or rectal cancers. Recently, Hashibe et al [7] carried out an epidemiological analysis of marijuana smoking and cancer. A connection between marijuana smoking and lung or colorectal cancer was not observed. These conclusions are reinforced by the recent work of Tashkin and coworkers [8] who were unable to demonstrate a cannabis smoke and lung cancer link, despite clearly demonstrating cannabis smoke-induced cellular damage.Furthermore, compounds found in cannabis have been shown to kill numerous cancer types including: lung cancer [9], breast and prostate [10], leukemia and lymphoma [11], glioma [12], skin cancer [13], and pheochromocytoma [14]. The effects of cannabinoids are complex and sometimes contradicting, often exhibiting biphasic responses. For example, in contrast to the tumor killing properties mentioned above, low doses of THC may stimulate the growth of lung cancer cells in vitro [15].The genotoxic effects of partially oxidized hydrocarbons created by burning either cannabis or tobacco have been widely examined as the likely source of genetic changes that lead to the carcinogenic state [16]. As a result, the medical potential of canna
Are students exposed to tobacco smoke in German schools?
Thaqi, Agim,Merkel, Günter,Wichmann, H.-Erich,Heinrich, Joachim
GMS Medizinische Informatik, Biometrie und Epidemiologie , 2005,
Abstract: The aim of this study was to investigate to which extent 6th grade school children are exposed to tobacco smoke by others. As biomarker for the exposure to tobacco smoke nicotine and cotinine were measured in the urine. Our study population consisted of 771 schoolchildren aged 11-14 years who according to a questionnaire did not smoke. In addition we analysed the data of 459 school children who were not exposed to tobacco smoke at home. The nicotine and cotinine concentrations in the spontaneous urine sample were determined by HPLC methods.On average in about 20% of all non-smoking children, who were not exposed to tobacco smoke at home, biomarker (nicotine or cotinine) were detected in the urine. The percentage of the detected biomarker values (nicotine and/or cotinine) in the urine of the school children varied between 0% and 50% between schools. In addition we determined the proportion of smoking classmates per school. No positive association was found between the detected biomarker values of the non-smoking school children not exposed to tobacco smoke at home and the proportion of smokers per school. The concentration of biomarker depending on the time of day the urine samples were collected showed higher nicotine and cotinine values when the urine sample was collected between 10 and 12 o'clock in the morning compared to urine samples collected between 7 and 10 a.m.In spite of the limitations our study provides some evidence that children are exposed involuntarily to tobacco smoke by others at school. That is why our results support the requirement of a general legal ban on smoking for teachers, the school staff and students.
Pulmonary toxicity of chronic exposure to tobacco and biomass smoke in rats
Dogan, Omer Tamer;Elagoz, Sahande;Ozsahin, Sefa Levent;Epozturk, Kursat;Tuncer, Ersin;Akkurt, Ibrahim;
Clinics , 2011, DOI: 10.1590/S1807-59322011000600027
Abstract: objective: the objective of this study was to examine the separate and combined effects of tobacco and biomass smoke exposure on pulmonary histopathology in rats. introduction: in addition to smoking, indoor pollution in developing countries contributes to the development of respiratory diseases. methods: twenty-eight adult rats were divided into four groups as follows: control group (group i, no exposure to tobacco or biomass smoke), exposed to tobacco smoke (group ii), exposed to biomass smoke (group iii), and combined exposure to tobacco and biomass smoke (group iv). after six months the rats in all four groups were sacrificed. lung tissue samples were examined under light microscopy. the severity of pathological changes was scored. results: group ii differed from group i in all histopathological alterations except intraparenchymal vascular thrombosis. there was no statistically significant difference in histopathological changes between the subjects exposed exclusively to tobacco smoke (group ii) and those with combined exposure to tobacco and biomass smoke (group iv). the histopathological changes observed in group iv were found to be more severe than those in subjects exposed exclusively to biomass smoke (group iii). discussion: chronic exposure to tobacco and biomass smoke caused an increase in severity and types of lung injury. conclusion: exposure to cigarette smoke caused serious damage to the respiratory system, particularly with concomitant exposure to biomass smoke.
Microbial biofilms - part I: Ecological and genetical aspects  [PDF]
Ivanovi? Mirjana,Vu?eti? Mirjana
Stomatolo?ki Glasnik Srbije , 2006, DOI: 10.2298/sgs0601035i
Abstract: Relatively new advances in microscopy and molecular technology have made possible studying of bacterial communities in situ. Natural bacterial associations in biofilm matrix function as cooperative consortia in a complex but synchronized manner. Regardless of formation, biofilms are developing in a multicellular pattern. Microcolonies forming a biofilm can be populations of a single species or multi-species bacterial communities influenced by environmental parameters. Numerous conditions, such as characteristics of the surface and interactions, availability of nutrients, composition of microbial community and hydrodynamics may influence the structure of a biofilm. Implementation of molecular methods in understanding of oral flora and its features is making shifts in our dental plaque knowledge. .
Detrimental Effects of Environmental Tobacco Smoke in Relation to Asthma Severity  [PDF]
Suzy A. A. Comhair,Benjamin M. Gaston,Kristin S. Ricci,Jeffrey Hammel,Raed A. Dweik,W. Gerald Teague,Deborah Meyers,Elizabeth J. Ampleford,Eugene R. Bleecker,William W. Busse,William J. Calhoun,Mario Castro,Kian Fan Chung,Douglas Curran-Everett,Elliot Israel,W. Nizar Jarjour,Wendy Moore,Stephen P. Peters,Sally Wenzel,Stanley L. Hazen,Serpil C. Erzurum
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018574
Abstract: Environmental tobacco smoke (ETS) has adverse effects on the health of asthmatics, however the harmful consequences of ETS in relation to asthma severity are unknown.
Impact of the "Tobacco control law" on exposure to environmental tobacco smoke in Spain
I?aki Galán, Nelva Mata, Carmen Estrada, Lucía Díez-Ga?án, Luis Velázquez, Belén Zorrilla, Ana Gandarillas, Honorato Ortiz
BMC Public Health , 2007, DOI: 10.1186/1471-2458-7-224
Abstract: Cross-sectional, population-based study. The self-reported exposure to environmental tobacco smoke at home, at work, in bars and restaurants of the population aged 18 to 64 years in the Madrid Region during a period prior to the law (October and November 2005; n = 1750) was compared to that of the period immediately after the law came into force (January-July 2006; n = 1252). Adjusted odds ratios (OR) were calculated using logistic regression models.Passive exposure to tobacco smoke at home has hardly changed. However, at indoor workplaces there has been a considerable reduction: after the law came into force the OR for daily exposure > 0–3 hours versus non-exposure was 0.11 (95% CI: 0.07 to 0.17) and for more than 3 hours, 0.12 (95% CI: 0.09 to 0.18). For fairly high exposure in bars and restaurants versus non-exposure, the OR in the former was 0.30 (95% CI: 0.20 to 0.44) and in the latter was 0.24 (95% CI: 0.18 to 0.32); for very high exposure versus non-exposure they were 0.16 (95% CI: 0.10 to 0.24) and 0.11 (95% CI: 0.07 to 0.19), respectively. These results were similar for the smoking and non-smoking populations.A considerable reduction in exposure to environmental tobacco smoke in the workplace and, to a lesser extent, in bars and restaurants, is related to the implementation of the "Tobacco control law". Although only initial figures, these results already demonstrate the effectiveness of strategies that establish control measures to guarantee smoke-free places.In Spain, smoking is the main risk factor for morbidity and mortality, causing around 55,000 deaths annually [1]. The most recent data for prevalence, from the National Health Survey (2003), show that 31% of the adult population smoke regularly [2], a level that positions Spain at around the average for countries within the European Union [3].Second-hand smoke exposure causes disease and premature death in children and adults who do not smoke, and there is no risk-free level of exposure [4]. Policies
Page 1 /100
Display every page Item


Home
Copyright © 2008-2017 Open Access Library. All rights reserved.