Passive Pb transport across the red cell membrane has been studied by measuring Pb uptake from Pb-buffered solutions into resealed ghosts containing EGTA. Over 90% of Pb uptake occurs by a pathway which is inhibited by drugs which block anion transport. The order of effectiveness is 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS) and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS) greater than phloretin greater than furosemide and bumetanide. Ouabain and cytochalasin B are ineffective. This implicates the anion-exchange mechanism in Pb uptake. The rate of Pb uptake by this route is directly proportional to external Pb2+ and HCO3- concentrations, and inversely proportional to the H+ concentration. These findings suggest that Pb transport depends on the formation of PbCO3 in solution. Pb transport depends upon the presence of a second anion. In the presence of HCO3-, the rate is stimulated in the order ClO4- less than NO3- and CH3CO2- less than F- less than Cl- less than Br- less than I-. The temperature dependence of Pb uptake is similar to that of HCO3-(-)Cl- exchange. Changes in membrane potential appear to influence Pb transport. The effects are small and somewhat variable, but in general a negative internal potential accelerates uptake and reduces exit. A positive internal potential reduces uptake and accelerates exit. These results suggest that Pb is transported on the anion exchanger. Exchange of PbCO3 for a monovalent anion best fits the experimental data, although transport of a ternary PbCO3(-)anion- complex is a possibility.