The road to primary prevention of lead toxicity in children.

Abstract

The clinical recognition of lead toxicity in children in the United States has changed drastically over the past 50 years. Accordingly, both medical management and public policy in such cases needs to be modernized in keeping with these changes. Fifty years ago lead poisoning in children was often only recognized in the severe acute phase (acute lead encephalopathy). Today this condition is rare, and children are detected in screening programs most often in the asymptomatic phase. The removal of lead additives from gasoline and the removal of lead solder from food and beverage cans has greatly reduced the background level of lead absorption during the past decade.1 The changes in exposure to lead and its clinical presentation mandate that we change the approach to the management of childhood lead toxicity. We must place reduced emphasis on chelation therapy and major emphasis on the environmental history to identify the source(s) of lead in the child's environment and steps to separate the child from these sources. The primary source of lead in childhood lead toxicity 50 years ago was deteriorating lead paint in old housing: it remains the primary source in the United States today. Reduction of exposure is the single most important modality of long-term management, as it has been for >50 years. When chelating agents first appeared—2,3-dimercapto-1-propanol (BAL)2 in 1946 and calcium disodium ethylenediaminetetraacetate (CaNa2EDTA)3 in 1950—childhood lead poisoning was recognized clinically only in the severe acute phase. These agents alone reduced the mortality of severe acute lead encephalopathy from 66% to approximately 25% to 30%.4Subsequently, it was found that these agents given in combination5 reduced mortality to about 1% to 2%. They were not effective in reducing the neurologic sequelae.6Ongoing prospective studies conducted now to at least 10½ years …