1. Latha Chandran, MD, MPH* 2. Rosa Cataldo, DO† 1. *Editorial Board. 2. †Assistant Clinical Instructor, Department of Pediatrics, Stony Brook University Medical Center, Stony Brook, NY. After completing this article, readers should be able to: 1. Delineate the disparities of pediatric lead poisoning among socioeconomic and racial groups. 2. List three common sources of lead. 3. Describe the emerging data on immediate and long-term neurotoxic effects of lead on the developing brain. 4. Discuss two chelating agents and their common adverse effects. 5. Employ a multipronged, multidisciplinary approach in the overall management of pediatric lead poisoning. For many centuries, starting as early as 4000 BC, lead has been used for a variety of purposes. Ancient Romans used lead for glazing pottery, piping, cooking utensils, and sweetening of wine. Lead toxicities were well documented in Egyptian papyrus rolls, describing its use for homicidal purposes. Over the centuries, lead poisoning was noted by different terms such as “the miner's disease,” “lead blindness,” “lead colic,” “lead gout,” and “plumbism.” It was a common cause of morbidity and mortality among shipbuilders, wine drinkers, and potters. Lead encephalopathy and lead psychosis also were recognized early in human history, when potters were described as “paralytic, splenetic, lethargic, cachectic, and toothless.” The use of lead became widespread during the industrial revolution. Use of lead-based paints, gasoline, and food containers resulted in profound environmental contamination. The toxic clinical effects of lead poisoning in children were linked to lead-based paint used in the early 20th century. More than half of the homes built in the United States before 1950 contained lead paint. Lead-based paints were banned in the United States in 1977 (the maximum allowable amount is now 0.07 mg/cm2), and the United States Environmental Protection Agency phased out lead from gasoline between 1975 and 1986. Due to measures such …