THE TAR FRACTION OF CIGARETTE-SMOKE DOES NOT PROMOTE ARTERIOSCLEROTICPLAQUE DEVELOPMENT

In addition to being the single greatest known environmental cause of cancer, cigarette smoke (CS) is also a major contributor to heart dise ase. We reported previously that 1) inhalation of either mainstream or sidestream CS promotes aortic arteriosclerotic plaque development; 2) 1,3 butadiene, a vapor-phase component of CS, promotes plaque develop ment at 20 ppm, which at the time was only 2 times higher than the thr eshold limit value; and 3) individual tar fraction carcinogens in CS, including polynuclear aromatic hydrocarbons (PAHs) and nitrosamines, e ither do not promote plaque development or do so only at high concentr ations. These results suggested that the tar fraction is not the prima ry source of plaque-promoting agents in CS. We asked whether repeated exposure to the tar fraction of CS, collected in a cold trap (TAR), pr omotes plaque development in an avian model of arteriosclerosis. Aceto ne extracts of mainstream CS tar from burning, unfiltered reference ci garettes were solubilized in dimethyl sulfoxide (DMSO) and injected we ekly into cockerels for 16 weeks (25 mg/kg/week). Positive controls we re injected weekly with the synthetic PAH carcinogen, 7,12 dimethylben z(a)anthracene (DMBA) dissolved in DMSO and negative controls were inj ected with DMSO. Plaque location and prevalence did not differ from gr oup to group. Morphometric analysis of plaque cross-sectional areas sh owed that plaque sizes, which are log-normally distributed, were signi ficantly larger in the DMBA cockerels compared to both the TAR and DMS O groups. There reported here, combined with other recent findings, su pport the conclusion that the primary arteriosclerotic plaque-promotin g components of CS are in the vapor phase.