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  • Lead poisoning causes multisystem clinical effects: headache, abdominal pain, constipation, vomiting, clumsiness, irritability, and drowsiness.
  • Laboratory evaluation may demonstrate anemia, basophilic stippling, elevated erythrocyte protoporphyrins (EP), zinc protoporphyrins (ZPP), and elevated blood lead level (BLL).
  • Management requires identification and removal of the source of exposure.
  • Chelation with CaNa2EDTA, BAL, or succimer is dictated by BLL and severity of symptoms.

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The average blood lead level of American children has decreased by more than 80% since the 1970s because of early screening initiatives and environmental hazard reduction.1,2 In spite of this progress, it is estimated that almost 1 million children still have some degree of lead poisoning.3 Several long-term studies have shown an association of lead levels previously thought to be nontoxic with impaired growth and behavioral and neurocognitive development.4 Before 1970, the lead intervention level was 60 μg/dL, but the Centers for Disease Control and Prevention revised the action downward several times to its current level of 10 μg/dL in 1991.1 Lead poisoning affects people of all ages and classes, but the prevalence of lead poisoning remains highest in inner-city underprivileged children.5,6

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Despite frequent media reports of lead discovered in children's toys (mostly imported from overseas), ingestion of leaded household paint is the most common and clinically relevant source of lead poisoning in children.6,7 Most homes built before 1978 were painted with lead-based paint.8 A small paint chip containing 50% lead can produce acute lead poisoning in a toddler. Renovation of old buildings and poorly controlled lead abatement pose a risk for lead poisoning through inhalation and ingestion of contaminated dust and soil.9 Lead exposure can also occur through drinking water contaminated by lead in plumbing, from living in close proximity to stationary air pollution sources such as lead smelters, from lead brought home from a parent's workplace, drinking from improperly fired lead-glazed pottery, some folk remedies, bullets lodged in joint spaces, and other unusual sources. The phaseout of leaded gasoline has had a major impact in reducing exposure to lead.8

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Up to 50% of lead ingested can be absorbed by the gastrointestinal tract in infants and children.6 Iron deficiency and dietary calcium deficiency increase the absorption of lead in the gut. Up to 30% of lead dust and fumes can be absorbed through the respiratory tract, while percutaneous absorption of lead is less than 0.1% of the applied quantity. Lead readily crosses the placental barrier, and fetal exposure is cumulative until birth.10 Although distribution of absorbed lead in the body is complex, the emergency physician should think of lead using a three-compartment model: blood, soft tissue, and bone. Acutely 99% of the lead in blood is attached to red blood cells. Under chronic exposure conditions, the bone serves as a storage organ for 70% of the pediatric lead burden and can release lead back into the blood and soft ...

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