scholarly journals Second-Hand Smoke Increases Bronchial Hyperreactivity and Eosinophilia in a Murine Model of Allergic Aspergillosis

2003 ◽  
Vol 10 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Brian W. P. Seymour ◽  
Edward S. Schelegle ◽  
Kent E. Pinkerton ◽  
Kathleen E. Friebertshauser ◽  
Janice L. Peake ◽  
...  
Keyword(s):  
Tobacco Smoke ◽  
Murine Model ◽  
Airway Hyperresponsiveness ◽  
Allergic Bronchopulmonary Aspergillosis ◽  
Ambient Air ◽  
Airway Hyperreactivity ◽  
Second Hand Smoke ◽  
Th2 Response ◽  
Allergic Lung Disease ◽  
Public Areas

Involuntary inhalation of tobacco smoke has been shown to aggravate the allergic response. Antibodies to fungal antigens such asAspergillus fumigatus(Af) cause an allergic lung disease in humans. This study was carried out to determine the effect of environmental tobacco smoke (ETS) on a murine model of allergic bronchopulmonary aspergillosis (ABPA). BALB/c mice were exposed to aged and diluted sidestream cigarette smoke to simulate 'second-hand smoke'. The concentration was consistent with that achieved in enclosed public areas or households where multiple people smoke. During exposure, mice were sensitized to Af antigen intranasally. Mice that were sensitized to Af antigen and exposed to ETS developed significantly greater airway hyperreactivity than did mice similarly sensitized to Af but housed in ambient air. The effective concentration of aerosolized acetylcholine needed to double pulmonary flow resistance was significantly lower in Af + ETS mice compared to the Af + AIR mice. Immunological data that supports this exacerbation of airway hyperresponsiveness being mediated by an enhanced type 1 hypersensitivity response include: eosinophilia in peripheral blood and lung sections. All Af sensitized mice produced elevated levels of IL4, IL5 and IL10 but no IFN-γ indicating a polarized Th2 response. Thus, ETS can cause exacerbation of asthma in ABPA as demonstrated by functional airway hyperresponsiveness and elevated levels of blood eosinophilia.

scholarly journals Second-hand Smoke Increases Nitric Oxide and Alters the IgE Response in a Murine Model of Allergic Aspergillosis

2005 ◽  
Vol 12 (2) ◽  
pp. 113-124 ◽  
Author(s):  
Brian W. P. Seymour ◽  
Janice L. Peake ◽  
Kent E. Pinkerton ◽  
Viswanath P. Kurup ◽  
Laurel J. Gershwin
Keyword(s):  
Nitric Oxide ◽  
Murine Model ◽  
Allergic Bronchopulmonary Aspergillosis ◽  
Ambient Air ◽  
Lung Parenchyma ◽  
Second Hand Smoke ◽  
No Production ◽  
Ifn Γ ◽  
Ige Response

This study was performed to determine the effects of environmental tobacco smoke (ETS) on nitric oxide (NO) and immunoglobulin (Ig) production in a murine model of allergic bronchopulmonary aspergillosis (ABPA). Adult BALB/c mice were exposed to aged and diluted sidestream cigarette smoke from day 0 through day 43 to simulate “second-hand smoke”. During exposure, mice were sensitized to solubleAspergillus fumigatus(Af) antigen intranasally between day 14 and 24. All Af sensitized mice in ambient air (Af + AIR) made elevated levels of IgE, IgG1, IgM, IgG2a and IgA. Af sensitized mice housed in ETS (Af + ETS) made similar levels of immunoglobulins except for IgE that was significantly reduced in the serum and bronchoalveolar lavage (BAL). However, immunohistochemical evaluation of the lung revealed a marked accumulation of IgE positive cells in the lung parenchyma of these Af + ETS mice. LPS stimulation of BAL cells revealed elevated levels of NO in the Af + AIR group, which was further enhanced in the Af+ETS group.In vitrorestimulation of the BAL cells on day 45 showed a TH0 response with elevated levels of IL3, 4, 5, 10 and IFN-γ. However, by day 28 the response shifted such that TH2 cytokines increased while IFN-γ decreased. The Af + ETS group showed markedly reduced levels in all cytokines tested, including the inflammatory cytokine IL6, when compared to the Af+AIR group. These results demonstrate that ETS affects ABPA by further enhancing the NO production and reduces the TH2 and the inflammatory cytokines while altering the pattern of IgE responses.

scholarly journals Effects of Involuntary Smoking and Vaping on the Cardiovascular System

2019 ◽  
Author(s):  
Manfred Neuberger
Keyword(s):  
Tobacco Smoke ◽  
Social Acceptance ◽  
Animal Experiments ◽  
Ambient Air ◽  
Air Pollutant ◽  
Ambient Air Pollution ◽  
Second Hand Smoke ◽  
Coronary Syndrome ◽  
Acute Changes ◽  
Tobacco Specific Nitrosamines

In deaths and diseases attributed to tobacco smoke cardiovascular events exceed cancer and respiratory diseases. Second hand smoke (SHS) promotes the development of arteriosclerosis and can also trigger acute changes of endothelial function and of blood coagulability. Indoor smoking bans reduced coronary syndrome and myocardial infarction 10-20% within one year and were followed by sustainable decreases of stroke and diabetes. With a smoke-free hospitality industry people recognized tobacco smoke as an air pollutant, smoking in public was denormalized and social acceptance of smoking in front of children and pregnant women decreased also in homes and in cars. Combined effects with ambient air pollution are proven for active smoking and suspected for SHS. Contamination with third hand smoke (THS, “cold smoke”)  persists for months in homes and cars, creating secondary pollutants that in some cases are more toxic (e.g., tobacco-specific nitrosamines).  Remnants found in air, dust, and on surfaces (carpets, wallpapers, upholstery, soft toys) were associated with their metabolites in saliva and urine of children and with elevated levels of nicotine on hands and cotinine in urine of nonsmokers residing in homes previously occupied by smokers. In animal experiments effects of THS were found on thrombogenesis, insulin resistance through oxidative stress, on the developing immune system, lipid metabolism and alterations in liver, lung, skin and behavior. Much less is known about health effects for bystanders from the aerosols exhaled during “vaping” of e-cigarettes, but nicotine and other toxins from e-cigarettes are certainly a hazard, which should be prevented by the use of dermal and oral nicotine products, which are safer for nicotine replacement and without risk for bystanders.

scholarly journals Recent Developments in the Determination of Biomarkers of Tobacco Smoke Exposure in Biological Specimens: A Review

2021 ◽  
Vol 18 (4) ◽  
pp. 1768
Author(s):  
Hernâni Marques ◽  
Pedro Cruz-Vicente ◽  
Tiago Rosado ◽  
Mário Barroso ◽  
Luís A. Passarinha ◽  
...  
Keyword(s):  
Tobacco Smoke ◽  
Solid Phase ◽  
Smoke Exposure ◽  
Tobacco Smoke Exposure ◽  
World Health ◽  
Second Hand Smoke ◽  
Tobacco Exposure ◽  
Wide Range ◽  
Recent Developments

Environmental tobacco smoke exposure (ETS) and smoking have been described as the most prevalent factors in the development of certain diseases worldwide. According to the World Health Organization, more than 8 million people die every year due to exposure to tobacco, around 7 million due to direct ETS and the remaining due to exposure to second-hand smoke. Both active and second-hand exposure can be measured and controlled using specific biomarkers of tobacco and its derivatives, allowing the development of more efficient public health policies. Exposure to these compounds can be measured using different methods (involving for instance liquid- or gas-chromatographic procedures) in a wide range of biological specimens to estimate the type and degree of tobacco exposure. In recent years, a lot of research has been carried out using different extraction methods and different analytical equipment; this way, liquid–liquid extraction, solid-phase extraction or even miniaturized procedures have been used, followed by chromatographic analysis coupled mainly to mass spectrometric detection. Through this type of methodologies, second-hand smokers can be distinguished from active smokers, and this is also valid for e-cigarettes and vapers, among others, using their specific biomarkers. This review will focus on recent developments in the determination of tobacco smoke biomarkers, including nicotine and other tobacco alkaloids, specific nitrosamines, polycyclic aromatic hydrocarbons, etc. The methods for their detection will be discussed in detail, as well as the potential use of threshold values to distinguish between types of exposure.

L -Selectin is required for the development of airway hyperresponsiveness but not airway inflammation in a murine model of asthma

2001 ◽  
Vol 107 (6) ◽  
pp. 1019-1024 ◽  
Author(s):  
Lynne C. Fiscus ◽  
Jenny Van Herpen ◽  
Douglas A. Steeber ◽  
Thomas F. Tedder ◽  
Mimi L.K. Tang
Keyword(s):  
Airway Inflammation ◽  
Murine Model ◽  
Airway Hyperresponsiveness

TACI-Ig prevents the development of airway hyperresponsiveness in a murine model of asthma

2008 ◽  
Vol 38 (12) ◽  
pp. 1959-1968 ◽  
Author(s):  
J. Bilsborough ◽  
E. Chadwick ◽  
S. Mudri ◽  
X. Ye ◽  
W. R. Henderson ◽  
...  
Keyword(s):  
Murine Model ◽  
Airway Hyperresponsiveness

Effect of prenatal waterpipe tobacco smoke on airway inflammation in murine model of asthma of adult offspring mice

2017 ◽  
Vol 29 (8) ◽  
pp. 366-373 ◽  
Author(s):  
Nour A. Al-Sawalha ◽  
Hanadi F. Al-Bo’ul ◽  
Karem H. Alzoubi ◽  
Omar F. Khabour ◽  
Vaidehi J. Thanawala
Keyword(s):  
Airway Inflammation ◽  
Tobacco Smoke ◽  
Murine Model ◽  
Adult Offspring

scholarly journals Deficiency in the Serum-Derived Hyaluronan-Associated Protein-Hyaluronan Complex Enhances Airway Hyperresponsiveness in a Murine Model of Asthma

2010 ◽  
Vol 153 (3) ◽  
pp. 223-233 ◽  
Author(s):  
Long Zhu ◽  
Lisheng Zhuo ◽  
Koji Kimata ◽  
Etsuro Yamaguchi ◽  
Hideto Watanabe ◽  
...  
Keyword(s):  
Murine Model ◽  
Airway Hyperresponsiveness

scholarly journals Preliminary evidence that high levels of nicotine on children’s hands may contribute to overall tobacco smoke exposure

2017 ◽  
Vol 27 (2) ◽  
pp. 217-219 ◽  
Author(s):  
E Melinda Mahabee-Gittens ◽  
Ashley L Merianos ◽  
Georg E Matt
Keyword(s):  
Young Children ◽  
Tobacco Smoke ◽  
Controlled Trial ◽  
Positive Association ◽  
Preliminary Evidence ◽  
Tobacco Smoke Exposure ◽  
Second Hand Smoke ◽  
Significant Positive Association ◽  
Convenience Sample ◽  
Salivary Cotinine

BackgroundDust and surfaces are important sources of lead and pesticide exposure in young children. The purpose of this pilot study was to investigate if third-hand smoke (THS) pollutants accumulate on the hands of children who live in environments where tobacco is used and if hand nicotine levels are associated with second-hand smoke (SHS), as measured by salivary cotinine.MethodsParticipants were parents and children (n=25; age mean (SD)=5.4 (5.3) years) presenting to the emergency department with a potentially SHS-related illness. A convenience sample of participants were recruited at baseline from an ongoing two-group, randomised controlled trial of a SHS reduction and tobacco cessation intervention. Parents were current smokers; thus, all children were at risk of SHS and THS exposure to varying extents. Primary outcome measures, which were assessed in child participants only, were hand nicotine and salivary cotinine. Parents reported sociodemographics and smoking patterns; children’s medical records were abstracted for chief complaint, medical history and discharge diagnosis.ResultsAll children had detectable hand nicotine (range=18.3–690.9 ng/wipe). All but one had detectable cotinine (range=1.2–28.8 ng/mL). Multiple linear regression results showed a significant positive association between hand nicotine and cotinine (p=0.009; semipartial r2=0.24), independent of child age.DiscussionThe higher-than-expected nicotine levels and significant association with cotinine indicate that THS may play a role in the overall exposure of young children to tobacco smoke toxicants and that hand wipes could be a useful marker of overall tobacco smoke pollution and a proxy for exposure.Trial registration numberClinicalTrials.gov Identifier: NCT02531594

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