Renal, biliary, pulmonary and faecal excretion experiments were carried out with labelled hexachloro-1,3butadiene ([I4C]HCBD) in male Sprague-Dawley rats, given orally (p.0.) and intravenously (i.v.) in doses of 1 and 100 mg kg-' as a solution in polyethylene glycol. The radioactivity excreted over 72 h was determined in rats fitted with exteriorized biliary cannulae and in rats whose bile ducts remained fully functional, respectively. In addition, bile duct-duodenum cannula-linked rats, of which the donor was given 100 mg kg-I ["CIHCBD orally and the recipient had also a bile fistula, were examined within 30 h for radioactivity in the excreta, the kidney, the liver and the plasma. In non-cannulated rats, fractional urinary excretion decreased when the dosage increased and amounted to 23% and 8.6% after i.v. injection or 18.5% and 8.9% after p.0. administration of 1 and 100 mg kg-', respectively. Pulmonary excretion of radioactivity was < 9% and was not affected by the increase in dosage. In bile duct-cannulated rats, fractional urinary excretions were similar irrespective of the dose and the route of administration and amounted to ca. 7.5% of the dose. Decrease in fractional biliary excretion occurred with increase in dosage (88.7% vs 72%) after i.v. injection and (66.8% vs 58%) after gavage. In cannulated rats, faecal excretion was < 0.5% after i.v. injection and accounted for 3% and 16% of the dose after p.0. administration of 1 and 100 mg kg-I, respectively. In rats linked in a cascade fashion, the donors excreted 3%, 45% and 19.5% of the dose in the urine, the bile and the faeces versus 2%, 16.8% and 8.4% for the recipients, respectively. Renal, hepatic and plasma radioactivity concentrations represented 0.26, 0.11 and 0.013% g-' of the dose in the donors versus 0.15, 0.07 and 0.009% g-' of the dose in the recipients. Biliary decline may result from a saturation of the hepatobiliary mechanism after i.v. injection and/or a saturation of gastrointestinal HCBD absorption after p.0. administration. The results indicate that at least 80% of the biliary metabolites of HCBD undergo biliary recycling and constitutes about 40% of renal excretion and tissue uptake of [I4C]HCBD at the high dose level. They also support the assumption that decline in fractional urinary excretion with increase in HCBD dosage was unlikely to be due to renal saturation but was probably the result of hepatobiliary saturation and/or defective enterohepatic circulation of HCBD metabolites.