Tobacco smoke is a complex mixture with over 8700 identified constituents. Smoking causes many diseases including lung cancer, cardiovascular disease, and chronic obstructive pulmonary disease. However, the mechanisms of how cigarette smoke impacts disease initiation or progression are not well understood and individual smoke constituents causing these effects are not generally agreed upon.
View Article and Find Full Text PDFActivated charcoal (AC) filtration reportedly decreases the yields of smoke vapor phase constituents including some identified as human carcinogens and respiratory irritants. Non-clinical studies including chemical smoke analysis, in vitro cytotoxicity and mutagenicity (bacterial and mammalian cells), and in vivo subchronic rat inhalation studies were carried out using machine smoking at ISO conditions with lit-end research cigarettes containing AC filters. The objective was to assess whether AC filter technology would alter the established toxicity profile of mainstream smoke by increasing or decreasing any known toxicological properties, or elicit new ones.
View Article and Find Full Text PDFToxicological comparisons were made of three commercial cigarettes, namely Marlboro full flavor, Marlboro Lights, and Marlboro Ultra Lights, with the 1R4F reference cigarette. The main comparison was a 90-d inhalation study with mainstream smoke at 150 mg total particulate matter per cubic meter, in Sprague-Dawley rats using 6 h/d and 7 d/w exposures. The principal endpoint was histopathology of the respiratory tract, along with examinations of free lung cell counts after broncho-alveolar lavage.
View Article and Find Full Text PDFFree radicals in cigarette smoke have attracted a great deal of attention because they are hypothesized to be responsible in part for several of the pathologies related to smoking. Hydroquinone, catechol, and their methyl-substituted derivatives are abundant in the particulate phase of cigarette smoke, and they are known precursors of semiquinone radicals. In this study, the in vitro cytotoxicity of these dihydroxybenzenes was determined using the neutral red uptake (NRU) assay, and their radical-forming capacity was determined by electron paramagnetic resonance (EPR).
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