Congenital lead encephalopathy in monkeys.

Thirty-one squirrel monkey fetuses were exposed to lead acetate given to the mothers perorally during the last three-fourths or two-thirds of pregnancy. The mean maternal blood lead concentration of the group was 37 micrograms/100 ml and the individual means ranged from 22-82 micrograms/100 ml. Examination of the central nervous system was performed in 15 of the offspring (one abortion, eight stillborns, three neonatal deaths, two killed fetuses and one killed newborn). The mean cerebral weight was reduced for the fetal age (about 10%). Three cerebra were paradoxically overweight for the fetal age as well as for the body weight, probably due to edema. Neurohistology revealed large numbers of characteristic perivascular, petechial hemorrhages in the white matter in six of the fifteen cerebra. In two of these cases, such hemorrhages were also found in the white matter of the cerebellum, brain stem and spinal cord. Examination of four recovered placentas (two after delivery and two at hysterotomies) indicated a lead dose-dependent weight reduction and revealed various pathological lesions. The extensive brain hemorrhages, as well as varying degrees of edema, were seen in stillborns and neonates, while prenatally sacrificed fetuses showed few or no petechial hemorrhages and no signs of edema. It is suggested that lead is involved in the parenchymal growth retardation and the endothelial changes in the prenatal brain, as well as the placental damage, and that prematurity, birth-associated mechanical stress and asphyxia contribute to or precipitate vascular lesions, which may form the basis of acute, or later apparent, neurobehavioral disturbances.