Exposure to Tobacco Smoke

Conrad, André

doi:10.1002/9783527635320.ch5

Cited by 3 publications

(2 citation statements)

References 114 publications

(33 reference statements)

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“…Individual smoking behavior and intensity and the brand of cigarettes smoked further modulate the amount, number, and type of smoke chemicals to which an individual is exposed. 3 To date, apart from a handful of candidate compounds, the relevance of most compounds in cigarette smoke in CVD initiation, progression, and cardiovascular outcome has not been studied. Importantly, it is likely that it is not just a single compound or a compound class, such as oxidants, that are the CVD-relevant fraction of cigarette smoke but rather a highly complex and changing mixture of compounds that is responsible for disease initiation, progression, and cardiovascular outcome.…”

Section: This Article Accompanies the Atvb In Focusmentioning

confidence: 99%

Smoking and Cardiovascular Disease

Meßner

Bernhard

2014

ATVB

812

329

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Abstract-Smoking represents one of the most important preventable risk factors for the development of atherosclerosis. The present review aims at providing a comprehensive summary of published data from clinical and animal studies, as well as results of basic research on the proatherogenic effect of smoking. Extensive search and review of literature revealed a vast amount of data on the influence of cigarette smoke and its constituents on early atherogenesis, particularly on endothelial cells. Vascular dysfunction induced by smoking is initiated by reduced nitric oxide (NO) bioavailability and further by the increased expression of adhesion molecules and subsequent endothelial dysfunction. Smoking-induced increased adherence of platelets and macrophages provokes the development of a procoagulant and inflammatory environment. After transendothelial migration and activation, macrophages take up oxidized lipoproteins arising from oxidative modifications and transdifferentiate into foam cells. In addition to direct physical damage to endothelial cells, smoking induces tissue remodeling, and prothrombotic processes together with activation of systemic inflammatory signals, all of which contribute to atherogenic vessel wall changes. There are still great gaps in our knowledge about the effects of smoking on cardiovascular disease. However, we know that smoking cessation is the most effective measure for reversing damage that has already occurred and preventing fatal cardiovascular outcomes. Clinical DataEvidence for smoking-induced initial vascular damage and endothelial dysfunction stems from an array of clinical studies analyzing endothelial function using various techniques. 6 As mentioned above, in 1993, Celermajer et al 5 were able to show that continuous smoking impairs FMD of the brachial artery in a dose-dependent manner, shown by the strong association between FMD and pack years smoked. This was also found to be the case with coronary arteries in a study by Zeiher et al. 7 Interestingly, reduction of endothelium-dependent dilatation by smoking was reversible, and significant improvement of FMD 1 year after cessation has been reported. 8 Likewise, a recent study of Amato et al 9 revealed that smoking light cigarettes impairs FMD as much as smoking regular cigarettes, arguing against light cigarettes as a less harmful alternative.Measurement of FMD represents a useful tool to assess the effects of smoking on the vascular wall. Independent of its FMD reducing activity, smoking was shown to induce other proatherogenic alterations in the vascular wall (eg, by deposition of smoke chemicals). The time needed to restore interrupted functions of the vascular endothelium will depend on the specific process that has caused the endothelial damage; some alterations of the endothelial wall may vanish more rapidly than others, without these being reflected by improved FMD.Clinical studies assessing the interrelation of secondhand smoking and FMD reported strong correlations. Secondhand smoking was shown to impair endo...

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Section: This Article Accompanies the Atvb In Focusmentioning

confidence: 99%

Smoking and Cardiovascular Disease

Meßner

Bernhard

2014

ATVB

812

329

View full text Add to dashboard Cite

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“…It was preferred to focus on the MSS due to the capability of a smoking machine to repetitively obtain MSS . Moreover, active smoking (inhalation of the MSS by the smoker) is the main health issue relative to the consumption of tobacco products …”

Section: Introductionmentioning

confidence: 99%

Study of the mainstream cigarette smoke aerosols by Fourier transform ion cyclotron resonance mass spectrometry coupled to laser/desorption and electrospray ionization – Additional insights on the heteroaromatic components

Kamissoko

Carré

Schramm

et al. 2019

Rapid Comm Mass Spectrometry

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Rationale:The chemical composition of the particulate phase of cigarette smoke inhaled by the active smoker is still poorly known in spite of its importance from a health point of view. A non-targeted approach is applied to cigarette smoke particles collected on a quartz filter to obtain an as complete as possible description of this complex mixture.Methods: A home-made smoking machine including devices for volatile organic compounds (VOCs) and particle sampling was used. The validation of the cigarette smoking and cigarette smoke collection procedures was conducted by the quantification of some compounds by gas chromatography/mass spectrometry (GC/MS). The particles were investigated by Fourier transform ion cyclotron resonance mass spectrometry (FTICR-MS) directly after their collection on quartz filters by laser/desorption ionization (LDI) or after extraction with CH 2 Cl 2 by electrospray ionization (ESI). Results: The determination of the benzene, toluene, ethylbenzene and xylenes (from 2 to 35 μg/cigarette) and nicotine (0.68 ± 0.05 mg/cigarette) validated the used sampling method. The complementarity of the LDI and ESI sources for the cigarette smoke analysis was established. The ESI analyses evidenced polar compounds and components with a pyridine group and LDI ensured the detection of polycondensed heteroaromatic species. Finally, this methodology was employed to characterize particles from cigarettes with or without flavoring additives. Conclusions: Some insights into the composition of cigarette smoke inhaled by active smokers have been obtained. The~1750 observed features revealed the huge complexity of cigarette smoke particles and the diversity of the possible associated health issues. Both heteroaromatic and highly oxygenated compounds produced by combustion and pyrolysis have been highlighted.

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