Removal of noxious oxidants and carcinogenic volatile nitrosocom

Tobacco – Smoke separator or treater

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131334, A24B 1500

Patent

active

059097361

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BRIEF SUMMARY
The present invention establishes a methodology for withholding the noxious compounds, ie. nitrogen oxides, free radicals, aldehydes, hydrogen peroxide, carbon monoxide, trace elements and carcinogenic volatile nitrosocompounds from being inhaled during cigarette smoking, substances which until today are insufficiently retained by the use of conventional cigarette filters.


THEORETICAL BACKGROUND-LEVEL OF PREVIOUS TECHNOLOGY

A plethora of publications in international journals suggests that cigarette smoke is separated into two phases: a) a solid phase (tar); and b) a gas phase. This separation occurs with the use of a typical Cambridge-glass-fiber filter which withholds 99.9% of the particles which are greater in size than 0.1 .mu.m. The tar of the cigarette contains dramatically high concentrations of very stable free radicals which can be classified into at least four different categories. Semiquinones in equilibrium with quinone and hydroxyquinones are considered to be free radicals with most interesting chemical properties. The quinone system reduces the molecular oxygen to form superoxide (0.sub.2.sup.-) which then upon spontaneous dismutation forms hydrogen peroxide (H.sub.2 O.sub.2). In the gas phase, there are more than 10.sup.15 organic radicals per puff with half-lives of less than 1 second that are inhaled. It is paradoxical however that despite their minute half life these radicals can maintain high levels of activity for more than 10 minutes in the gas phase. In fact the concentration of these radicals is considerably increased as we approach the filter-end of the cigarette. An explanation for this paradox is to be found in the maintenance of a steady state situation; due to the ongoing production of free radicals (Pryor, W. A., Stone, K., Ann. N.Y. Acad. Sci. 686: 12-28, 1993).
Nitric oxide (NO) is the most important free radical in the gas phase of the cigarette smoke which, during smoking, participates in a sequence of reactions through which nitrogen dioxide, isoprene radicals, peroxyl radicals and alkoxyl radicals are formed. Cigarette smoke also contains a considerable number of aldehydes which contribute to its damaging toxic effects. It has been shown that minute amounts of aldehydes extracted from the cigarette smoke cause both protein catabolism and oxidation of thiol groups of the plasma proteins. These properties attributed to the aldehydes are the result of the reactions between the carbonyl group of the aldehydes and the --SH and --NH2 groups of the plasma proteins. For example, acroleine, from the cigarette smoke, reacts quickly with the --SH groups to form carbonyl compounds (Alving, K., Forhem, C., and Lundberg, J. M., Br. J. Pharmacol. 110: 739-746, 1993). In the tar of the cigarette smoke there are trace elements of, for example, iron, copper, manganese and cadmium which are implicated in many free radical producing reactions and lead to the formation of very active secondary radicals (e.g. peroxy radicals, alkoxy radicals, superoxide, cytotoxic aldehydes etc.). The introduction of the trace elements into the lung during cigarette smoking leads to a series of redox reactions both in lung fluids and alveolar macrophages which result in the formation of the very active hydroxyl radicals (OH--). These hydroxyl radicals are mainly formed in the presence of iron via the Fenton reaction. Copper can also form hydroxyl radicals by reacting with the hydrogen peroxide in the lung. Manganese, in low concentrations (10.sup.-7 M), stimulates the soluble guanylate cyclase of the endothelial cells of the lung causing the production of nitric oxide and superoxide through a positive feedback mechanism (Youn, Y. K., Lalonde, C., and Demling, R., Free Rad. Biol. Med. 12: 409-415, 1992). Carbon monoxide is produced during tobacco burning. A quantity of CO is retained in the lung even after exhaling, resulting in the stimulation of the soluble guanylate cyclase after its interaction with the heme moiety of the enzymes of the endothelial cells and other cells of the lung tissue. The increased

REFERENCES:
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patent: 4049673 (1977-09-01), Scheinberg
patent: 4612333 (1986-09-01), Vassileff
Bednarcyk, Norman E., "Tobacco Smoke Filters", pp. 252-264 (Noyes Data Corporation, Park Ridge, New Jersey 1972).
Derwent Publications, Ltd., London, GB, AN 82-84398E & JP, A, 57 138 375 (KOWA KK) (Aug. 26, 1982) (abstract).
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Patent Abstracts of Japan 14 (118) (Mar. 6, 1990) & JP, A, 01 317 538 (Asahi Chem. Ind. Co. Ltd.) (Dec. 22, 1989) (abstract).
Baumgartner pamphlet: "Baumgartner's Current Range of Cigarette Filters" (available before Jun. 27, 1993).

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