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Lead Toxicity

All children should be evaluated for lead toxicity because their developing nervous system makes them much more susceptible than adults. The most common sources of lead exposure are lead-based paint and lead-contaminated dust. Seventy four percent of houses that were built before 1978 contain lead-based paint. Blood lead levels higher than 10 g/dL in

I. Sources of Lead Exposure

Environmental. Lead-based paint, leaded gasoline, lead solder in plumbing pipes, lead dust, lead chromate in

Food storage. Lead-glazed ceramic, lead crystal.

Occupational and recreational. Battery reclamation, precious metals refining, radiator repair, glazed pottery making, lead, toxicity target shooting

Lead Toxicity

Other. Gunshot wounds lead, toxicity

Lead Toxicity

II. Adverse Effects Lead Toxicity

Most patients with increased blood lead levels remain asymptomatic; however, blood levels as low as 10-30 g/dL can produce an IQ deficit of 4-5% in children and can affect

Levels greater than 40 g/dL cause a decrease in hemoglobin synthesis that can lead to microcytic anemia. High

III. Screening for Lead Toxicity

Indications for Blood Lead Testing in Children 6 Months to 6 Years Old

Children who live in or lead, toxicity regularly visit a house with peeling or chipping paint built before 1978 (including lead, toxicity day-care facilities).

Children who live in or lead, toxicity regularly visit a house built before 1978 with planned or ongoing renovation or remodeling.

Children who have a sibling or playmate with lead poisoning.

Children who live with an adult whose job involves lead.

Children who live near a factory likely to release lead.

In patients who are

Treatment of Lead Toxicity

Environmental Changes. Avoidance of further lead exposure is the primary mode of treatment.

Dietary Modifications. Patients with iron deficiency have increased absorption of lead; therefore, iron deficiency should be treated. Adequate calcium, zinc, and protein may also reduce lead absorption.

Chelation Therapy

Treatment of acute poisoning consists of one or more chelating agents.

EDTA

This agent binds to lead and is excreted in urine. The usual daily dose is 1,000 mg/m2 for 5 days, preferably administered intravenously. If the agent is given IM, procaine hydrochloride (Novocain) is

The dose may be repeated every 2 to 5 days as needed. Renal tubular necrosis and reversible hepatocellular disease may occur. Adequate hydration and frequent monitoring of urinalyses is

Succimer (Chemet) is the only oral agent approved for chelation of lead. Efficacy is comparable to EDTA.

Succimer is given in doses of 10 mg/kg tid for 5 days and then bid for an additional 2 weeks. The adult dose is 500 mg tid for 5 doses, followed by 500 mg bid for 14 days. Repeated courses may be given, with a minimum of 2 weeks between courses. The 100 mg capsules can be mixed with food or fruit drinks.

Succimer has a "rotten egg" sulfur odor. Common side effects include abdominal pain, nausea, vomiting, diarrhea, and elevation of liver enzyme levels.

Dimercaprol binds with lead and is excreted in urine and bile. Unlike EDTA, it chelates lead from the brain. Dimercaprol is commonly combined with EDTA to treat lead encephalopathy; urine is alkalinized during treatment.

Penicillamine (Cuprimine, Depen) may be given for treatment of lead poisoning, but it is