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Childhood lead poisoning: Clinical manifestations and diagnosis

Richard L Hurwitz, MD
Dean A Lee, MD, PhD
Section Editors
Donald H Mahoney, Jr, MD
Michele M Burns, MD, MPH
Jan E Drutz, MD
Deputy Editor
James F Wiley, II, MD, MPH


Lead (Pb), a stable metallic element with an atomic number of 82 and atomic weight of 207, was first smelted around 4000 BC as a by-product of silver processing. The consequences of lead toxicity have been recognized for millennia and are thought to have contributed to the fall of the Roman Empire [1]. Complications of lead poisoning were first acknowledged in the United States in the early 20th century. Despite this knowledge, lead was included as an ingredient of gasoline in the 1920s and continued to be used in paint until the 1970s [2,3].

As lead was removed from gasoline and paint, the average blood lead level (BLL) in children decreased from 16 mcg/dL (0.77 micromol/L) to less than 3 mcg/dL (0.14 micromol/L) [4,5]. Residual lead from these and other products remains in the environment because elemental lead cannot be degraded. In many parts of the developing world, lead continues to be used in gasoline, pigment (eg, in paint, cosmetics, and crayons), pottery glaze, solder, cooking vessels, and even medications. These products occasionally are imported into the United States and are potential sources of lead exposure.

The clinical manifestations and diagnosis of lead toxicity will be reviewed here. Prevention and treatment of lead poisoning are discussed separately. (See "Childhood lead poisoning: Exposure and prevention" and "Childhood lead poisoning: Management".)


The toxic lead level in the United States is determined by the Centers for Disease Control (CDC) based upon the current understanding of the complications caused by a given concentration of lead in the blood. Between 1970 and 2012, the toxic level or "reference value" was gradually decreased from 60 mcg/dL (2.9 micromol/L) to the 97.5th percentile of blood lead levels in US children (5 mcg/dL [0.24 micromol/L] as of 2012) (table 1). The decrease in 1991 was prompted by evidence of cognitive and behavioral effects of low-level lead toxicity [6,7] Changes in the definition of the toxic level have been accompanied by changes in policies for screening, treatment, and prevention [8]. Subsequently, a reference level corresponding to the 97.5th percentile of blood lead levels in US children (5 mcg/dL [0.24 micromol/L] as of 2012) has been adopted [9].

The prevalence of lead toxicity has decreased in the United States since the 1970s because of preschool screening programs, increased public awareness, and the removal of lead from gasoline and paint products. The prevalence of BLLs >10 mcg/dL (0.48 micromol/L) in American children between one and five years of age decreased from 88 to 4.4 percent between 1976 and 1994 [10], and to 0.8 percent for the period 2007 to 2010 [5,11]. Although the incidence and severity of lead poisoning in the United States are decreasing, an estimated 450,000 children in the United States were above the reference value of 5 mcg/dL (0.24 micromol/L) in 2012 [9].


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