The intraperitoneal administration of Pb acetate (5 x 20 mg Pb/kg per day) evokes a moderate and transient hypochromic anemia, a long-lasting enhanced urinary excretion of delta-aminolevulinic acid whereas the urinary excretion of alkaline phosphatase is not affected and that of lactic dehydrogenase only marginally. It is concluded that neither the hematologic response nor the slight nephrotoxicity are responsible for the lethal action of Pb. Chelate treatment started 3 days after the last Pb dose and was continued over 7 weeks. The daily intraperitoneal dose was 25, 50, and 100 mumol/kg, respectively. The efficacy in promoting the urinary excretion of Pb decreased in the following order: Ca diethylenetriaminepentaacetate greater than 2,3-dimercaptopropane-1-sulfonate greater than Zn diethylenetriaminepentaacetate greater than D-penicillamine. This effect was mainly due to the mobilization of skeletal Pb. The chelating agents also lowered the excretion of delta-aminolevulinic acid but failed to exert a beneficial influence on the anemia and the lethal action of Pb. These negative results raise questions about the usefulness of chelation therapy in cases of acute Pb poisoning.