Lead-containing paints were administered orally to 27 rhesus monkeys for periods of 18-667 days. Lead acetate was fed to nine monkeys of three different species for 9-156 days. Excretion of one week’s dose of lead in six primates ranged from 35 to 94 %. The animals incurred moderate to extreme elevations of lead in blood, most lost weight, or had depressed weight gains, and developed Burtonian lines, some died suddenly and unexpectedly, and many terminated in a moribund state with profound anemia. Only one neonate had obvious signs of lead encephalopathy. The monkeys’ ages, dose and source of lead, and possibly other factors, affected their response to lead.

Lead poisoning is most common among primates of the subfamily Cercopithecinae. Evidence is provided that indicates members of this subfamily may be predisposed to ingestion of lead-containing cage paint by virtue of their foraging and grooming habits. It is also noted that social stress and teething in immature primates is associated with gnawing leaded paint from cage bars.

Necropsies were performed on 25 rhesus monkeys, three cebus monkeys and three baboons which had been fed leaded paint or lead acetate at various doses up to 666 days. The 31 test primates and six controls ranged in age from five days to about eight years. In addition, the brains of 13 subadult squirrel monkeys fed lead oxide and two controls were studied grossly and microscopically. Lead content of liver, kidney and brain correlated with clinical outcome and typical histologic changes. Neuropathologie lesions, most severe in the young, occurred in 28 of 43 test primates despite a paucity of neurological signs. Brain lesions were similar to those occurring in human lead encephalopathy and included degenerative and proliferative changes of small vessels, ring hemorrhages, edema, perivascular hyalin droplets, rosette-like deposits of proteinaceous exudates, focal loss of myelin, astrogliosis and necrosis of hippocampal neurons.

Oral administration of lead-containing paint to rhesus monkeys induced anemia, more profound in older primates. Erythrocytes were microcytic and hypochromic, but tended to become macrocytic terminally. Stippled erythrocytes were increased in all poisoned monkeys, especially in those with high blood lead levels and anemia. Proteinuria, glycosuria, casts and sloughed tubular cells containing acid-fast inclusion bodies were found on urinalysis. Terminal elevations of blood urea nitrogen were associated with profound anemia and renal tubular damage. Repeated blood lead values over 200 μg/dl were associated with a moribund termination while monkeys which had levels under 100 μg/dl remained apparently healthy. Behavioral studies in a small number of subclinically poisoned juveniles and neonates failed to reveal deficiencies of visual acuity or cognitive ability, nor was there evidence of alterations in levels of activity.