Abstract

The relationship between blood lead concentration and nerve conduction velocity has been examined, using the cynomolgus monkey as a model for human lead poisoning, with lead dose and blood lead concentration maintained under controlled conditions, to determine whether nerve conduction velocity could be used as an objective measure of the effects of lead on the nervous system at subclinical concentrations. Five cynomolgus monkeys were maintained at a blood lead concentration of 90-100 micrograms Pb/100 ml for nine months by daily oral dosing with lead acetate (12-15 mg Pb/kg body weight). Motor nerve conduction velocity in the ulnar nerve was measured, together with blood lead concentrations. Blood lead concentrations were proportional to lead intake, reaching a stable level within one to two weeks. Lead did not accumulate in the blood, and blood lead concentrations were found to decrease to a maintained plateau from initial high concentrations during the first seven days of dosing. The animals showed no clinical or behavioural evidence of lead poisoning at any time during the study, although there was a progressive decrease in blood packed cell volume, haemoglobin concentration, and erythrocyte concentration. The maximal motor nerve conduction velocity of the ulnar nerve remained constant throughout the study, although changes were observed in the conduction velocity of slowly conducting nerve fibres. At termination, intranuclear inclusions were found in the renal tubular cells of all animals as were focal areas of myelin degeneration in the ulnar and sciatic nerves.