Endothelial damage and platelet activation may mediate increased cardiovascular morbidity and mortality in tobacco cigarette smokers. Our study was designed to determine whether acute effects of tobacco smoking on endothelium and platelets could be avoided by the substitution of non-tobacco cigarettes. Twenty healthy nonsmokers smoked two tobacco cigarettes in 20 minutes and on another occasion (separated by 1 week) smoked two cigarettes made from wheat, cocoa, and citrus plants. Mean endothelial cell counts from venous blood before and after smoking tobacco cigarettes were 2.3 and 4.8 and before and after smoking non-tobacco cigarettes counts were 2.5 and 3.0. Mean platelet aggregate ratios before and after smoking tobacco cigarettes were 0.80 and 0.65 and before and after smoking non-tobacco cigarettes they were 0.81 and 0.78. Much greater effects of tobacco smoking on endothelial cell counts and platelet aggregate ratios suggest the possibility that non-tobacco cigarette smoking may be less harmful to the cardiovascular system than is tobacco cigarette smoking.

The disposition of butylbenzyl phthalate (BBP), a widely used plasticizer, was evaluated after oral and iv administration to rats. Male Fischer-344 rats were dosed with [14C]BBP at 2, 20, 200, or 2000 mg/kg po or 20 mg/kg iv to determine the effects of dose on rates and routes of excretion. In 24 h, 61-74% of the dose was excreted in the urine and 13-19% in the feces at 2-200 mg/kg. At the 2000-mg/kg dose, 16% of the 14C was excreted in the urine and 57% in the feces. Urinary 14C was composed of monophthalate derivatives (MP: 10-42% of the dose) and glucuronides of these monophthalate derivatives (2-21% of the dose). At 4 h after iv administration of BBP (20 mg/kg), 53-58% of the dose was excreted in the bile of anesthetized rats. No parent compound was found in the bile, but monobutyl phthalate-glucuronide and monobenzyl phthalate-glucuronide (26% and 13% of the dose, respectively) and trace amounts of free monoesters (2% of the dose) and unidentified metabolites (14% of the dose) were present. Although BBP is an asymmetric diester with the potential of forming equal amounts of monobutyl phthalate (MBuP) and monobenzyl phthalate (MBeP), larger quantities of MBuP were formed (MBuP = 44% versus MBeP = 16% of the dose). The half-lives of BBP, MP, and total 14C in blood (20 mg/kg, iv) were 10 min, 5.9 h, and 6.3 h, respectively. This study indicates that BBP is rapidly metabolized and that the major route of excretion of metabolites is biliary. These metabolites are reabsorbed and ultimately eliminated in the urine.