Cigarette tar

Volunteers smoked the labelled cigarettes. The activity deposited in the mouth, and the activity removed to the GI tract in the 15-min interval between smoking and measurement, were measured with collimated detectors. The clearance of activity from the lung was followed for 2 d to allow the deposit to be fractionated into TB and P components. Comparative tests were also done with subjects inhaling 2.5-jum polystyrene particles, which were also labelled with 123I. 

The polystyrene particles and the 1-IHD labelled tar were removed from the TB region with similar clearance half-lives of about 2 h (Fig. 7.5). The pulmonary removal of polystyrene was too slow to measure with the 123I label, but 1-IHD was removed from the P region with a half-life of 18 h, and this was attributed to absorption into the bloodstream. 

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Polycychc aromatic hydrocarbons (PAHs) are carcinogens produced by the thermal breakdown of organic materials. These are widely distributed in both food and the environment, and are some of the principal carcinogens in cigarette tar and air pollution. Of over 20 PAHs isolated, benzopyrene and quinoline compounds are the most commonly encountered in foods, particularly those which are broiled or fried (111). Shellfish living in petroleum contaminated waters may also contain PAHs (112). 

Evans M.D., Church D.F., and Pryor W.A. (1991), Aqueous cigarette tar extracts damage human al-proteinase inhibitor, Chem. Bio. Int. 79, 151-164. 

The radicals in PM2 5 have similar EPRg-values and line shapes to the radicals found in cigarette tar (12, 18, 31, 33, 37). The cigarette tar radicals produce DNA damage that is similar to that produced by PMj 5. The cigarette tar radicals are a family of semiquinone... 

The data shown in Figures 1-4 support the suggestion that PM2 5 contains radicals that, like those in cigarette tar, can reduce oxygen to superoxide, which then forms hydrogen peroxide and, ultimately, the hydroxyl radical, as shown in reactions 1-3. Iron and copper ions, which are the transition metals most frequently found in combustiongenerated particles (44) and also are ubiquitous in biological systems, could be involved in reaction 3 ... 

In conclusion, we have shown that PMj 5 contains stable radicals that can be detected by EPR. The EPR parameters, persistence in air, and DNA-damaging capacity of the PM2 5 radicals are similar to those of the radicals in cigarette tar. Therefore, we propose that the radicals associated with PMj 5 include semiquinone-type radicals that, like the... 

These pathways are thought to result in the production of superoxide (13) or in the release of superoxide directly from the particles themselves. Superoxide production leads to the formation of hydrogen peroxide, and metal ions such as Fe + react with hydrogen peroxide to produce the hydroxyl radical. It is well documented that the hydroxyl radical can damage DNA as well as lipids and proteins (18, 19). Some of the health effects of cigarette tar and smoke are attributed to free radicals that can initiate production of superoxide and hydroxyl radical (3, 10, 11, 20, 21). (Adapted from Dellinger et al., 2001)... 

Cyclo-oxygenase activity. Aqueous cigarette tar extracts, in rat pulmonary alveolar macrophages, increased cyclo-oxygenase activity threefold above the initial activity within 2 hours of incubation and gradually decreased below the initial activity after 8 hours of incubation. Accumulated levels of prostaglandin-2 increased dramatically after 12 hours of incubation . 

E-cadherin expression. Smoke extract, on pig airway epithelial cells and mouse trachea, produced a decrease of E-cadherin expression on membrane and an increase of cytoplasmic expression at 12 and 24 hours after exposure. The expression at 24 hours was higher than at 12 hours k Electron transport inhibition. Acetonitrile extracts of cigarette tar inhibited stage three and four respiration of intact mitochondria. Exposure of respiring submito-chondrial particles to the acetonitrile extracts of cigarette tar results in a dose-dependent inhibition of oxygen consumption... 

T-cells influence. SSTE and nicotine were incubated in splenic mononuclear cells at concentrations of 1 10 or 1 10 dilutions of STD, or 10 or 100 i.g/mL nicotine, during 4 days of stimulation with anti-CD3. The treatment sustained expression of IL-2, IFN-y, IL-10, and IL-4 cytokine mRNA at 100 i.g/mL nicotine. STD did not exhibit residual expression of cytokine mRNA. Restimulated STD exhibited maximum IL-2, IL-4, IFN- y, and IL-10 mRNA at 48 hours . STE, in splenic mononuclear cell culture at LlOHo 1 10 dilutions, increased IL-2 production and decreased IL-10 at 1 10 dilution. IFN-y production was decreased at all concentrations. STE did not alter IL-4 product ion k P-benzoquinone, a thiol-reactive benzene derivative from cigarette tar, was incubated in human peripheral blood mononuclear cells at a concentration of 10 xM. The treat-... 

Minnear, and B. M. Freed. The cigarette tar component p-benzoquinone blocks T lymphocyte activation by inhibiting interleukin-2 production, but not CD25, lCAM-1, or LFA-1 expression. Toxicol Appl Pharmacol 1997 143(1) 30-36. 

Randerath. Tissue distribution of covalent DNA damage in mice treated dermally with cigarette tar preference for lung and heart DNA. Carcinogenesis 1988 9(1) 75-80. 

NT145 Tanaka, T. and A. Rivenson. Mastocytoma induced by cigarette smoke particulates cigarette tar . Arch Dermatol Res 1986 279(2) 130-135. 

NT169 Ohmori, T., H. Mori, and A. Riven-son. A study of tobacco carcinogenesis XX mastocytoma induction in mice by cigarette smoke particulates ( cigarette tar ). Am J Pathol 1981 102(3) 381-387. 

Boudreau, K. H. Sohn, K. Stone, and W. A. Pryor. Activation and inactivation of cyclo-oxygenase in rat alveolar macrophages by aqueous cigarette tar extracts. Free Radic Biol Med 1999 27(5-6) 673-682. 

Li, Q., Aubrey, M.T., Christian, T. Freed, B.M. (1997) Differential inhibition of DNA synthesis in human T cells by the cigarette tar components hydroquinone and catechol. Fundam. appl. Toxicol., 38, 158-165... 

In a study on the immunotoxic effects of cigarette tar components, hydroquinone, at a concentration that did not affect the viability of the cells (50 pmol/L), decreased IL-2-dependent DNA synthesis and cell proliferation by > 90% in cultured human T lymphoblasts (Li et al., 1997). Hydroquinone inhibited Fc-receptor-mediated phagocytosis in mouse peritoneal macrophages only at rather high concentrations (100 pmol/L) (Manning et al., 1994). 

Fig. 7.5. Lung clearance curves of one subject O, polystyrene particles, 2.5-fim diameter A, 1-iodohexadecane in cigarette tar.

Young JC, Robinson JC, Rickert WS. 1981. How good are the numbers for cigarette tar at predicting deliveries of carbon monoxide, hydrogen cyanide and acrolein J Toxicol Environ Health 7 801-808. 

SYNS CIGARETTE TAR COLOMBIAN BLACK TOBACCO CIGARETTE REFINED TAR TAR, from tobacco TOBACCO REFINED TAR TOBACCO TAR U.S. BLENDED LIGHT TOBACCO CIGARETTE REFINED TAR... 

Yoshie Y, Ohshima H. Synergistic induction of DNA strand breakage by cigarette tar and nitric oxide. Carcinogenesis 1997 18(7) 1359-63. 

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