Abstract
Lead is a divalent cation that affects many biochemical targets. Knowledge of its toxic effects extends back to antiquity. The most important target of this toxicant is the central nervous system. At high doses, encephalopathy is the most serious outcome. This is now a rare occurrence. At lesser doses, impaired cognition and behavior are seen. Knowledge of lead toxicity has passed through five stages. Initially it was thought to be a disease of adults: miners, printers, and painters. In 1892 the first cases of childhood lead poisoning were recognized. Initially it was thought that if a child did not die during the acute episode, he or she was left without any trace of the illness. Residua were then thought to occur only in those who displayed signs of encephalopathy in the acute phase. Over the past 35 years studies have demonstrated cognitive and behavioral deficits in those children who had elevated lead burdens but no clinical signs. As better methods were employed to study the disease, effects were found in lower and lower body burdens. Lead has many sources. The most important source of high-dose exposure in children is household paint. Airborne lead was a significant source, and with the removal of lead from gasoline and other interventions and greatly increased awareness of lead's hazards, the mean blood lead level of young children in the United States dropped from 15 μg dl−1 in the 1970s to less than 2 μg dl−1.