Lead Poisoning

Lead poisoning results from ingestion or inhalation of lead from paint (in homes built before leaded paint was banned), contaminated soil and dust, drinking water carried in lead pipes, battery recycling, smelting, glazed pottery, traditional remedies and cosmetics (kohl, surma), spent ammunition, and retained bullet fragments. Children under 6 years are the most vulnerable because they absorb up to 50% of ingested lead (adults about 10%), and hand-to-mouth behavior and iron deficiency raise uptake.

There is no safe blood lead level in children. A level of 3.5 micrograms/dL or higher is the current reference for action in children, and 45 micrograms/dL or higher meets the usual threshold for chelation. Lead is distributed to blood (half-life about 30 days), soft tissue and bone (half-life 20 to 30 years), and bone stores release lead during pregnancy, lactation and osteoporosis.

Mechanisms

• Inhibition of delta-aminolevulinic acid dehydratase and ferrochelatase, so heme synthesis is impaired
• Substitution for calcium in neuronal signalling, which disturbs synaptic function
• Oxidative stress, renal tubular damage and hypertension

Complications: encephalopathy with cerebral edema and seizures (usually over 100 micrograms/dL in children), permanent cognitive and behavioral impairment, anemia, chronic kidney disease, hypertension, gout, infertility and, in pregnancy, miscarriage and low birth weight.

• Children: irritability, anorexia, pallor, abdominal pain, constipation, pica, developmental delay and learning difficulty, hearing loss, short stature
• Adults: abdominal colic, constipation, fatigue, headache, memory and mood disturbance, myalgia, arthralgia, hypertension, motor neuropathy with wrist drop (radial) or foot drop (peroneal), a bluish gum line (Burton line)
• Severe: vomiting, ataxia, seizures, papilledema, coma (encephalopathy)
• Red flags: persistent vomiting, ataxia, seizures, altered consciousness, blood lead over 70 micrograms/dL in a child, and pregnancy

1. Venous whole-blood lead level (capillary samples need confirmation by venous sampling). It is the standard test.
2. Full blood count with film: microcytic or normocytic anemia and basophilic stippling.
3. Iron studies (ferritin), zinc protoporphyrin or free erythrocyte protoporphyrin (raised).
4. Renal function, urate, electrolytes, liver tests, blood pressure.
5. Abdominal radiograph: radio-opaque paint chips, glazes or fragments in a child with a high level or acute symptoms. Long bone radiographs: dense metaphyseal bands ("lead lines") in chronic childhood exposure.
6. Environmental assessment of the home, workplace, water, soil, hobbies, imported goods, ceramics and remedies, and testing of household members.
7. CT head for encephalopathy.

Differentials: iron deficiency anemia, acute intermittent porphyria, appendicitis, intussusception, other causes of encephalopathy, other neuropathies including arsenic and thallium.

Removal of the source is the most important intervention, and must come before and during chelation.

1. Source control: remove the child or worker from exposure, arrange certified home remediation, cleaning with wet methods and high-efficiency vacuum, hand washing, and screening of siblings and workplace colleagues.
2. Nutrition: iron sufficiency (ferrous sulfate 3 mg/kg of elemental iron daily orally for children with deficiency, adults 65 mg of elemental iron once or twice daily), calcium 1000 mg daily for adults (children by age) and a balanced diet with regular meals.
3. Blood lead under 45 micrograms/dL: source removal, nutrition, and repeat testing every 1 to 3 months until falling and under 5 micrograms/dL for 2 successive tests. No chelation.
4. Chelation for children with blood lead 45 to 69 micrograms/dL: succimer 10 mg/kg (or 350 mg/m2) orally every 8 hours for 5 days, then every 12 hours for 14 days. Monitor liver tests and blood count weekly. Adverse effects: nausea, rash, transient liver enzyme rise, neutropenia. Retest 1 to 2 weeks after finishing, since rebound occurs from bone.
5. Adults: chelation for symptomatic patients with blood lead over 50 micrograms/dL or any patient over 80 micrograms/dL, with succimer 10 mg/kg orally every 8 hours for 5 days, then every 12 hours for 14 days.
6. Severe poisoning (blood lead 70 micrograms/dL or higher, or any encephalopathy):
   • Admit to intensive care, with restricted fluids (about 1 to 1.5 L/m2 daily) to limit cerebral edema, and seizure control with lorazepam 4 mg IV (children 0.1 mg/kg, maximum 4 mg).
   • Dimercaprol 75 mg/m2 IM every 4 hours (about 3 to 5 mg/kg per dose) for 3 to 5 days. Do not give to patients with peanut allergy, and use with care in G6PD deficiency.
   • Start calcium disodium EDTA 4 hours after the first dimercaprol dose, at 1000 mg/m2 a day (adults up to 75 mg/kg a day, maximum 2 g) as a continuous IV infusion for 5 days, with careful monitoring of renal function, calcium, zinc and magnesium. Never give sodium EDTA, which causes fatal hypocalcemia. Do not give EDTA to an oliguric patient until urine flow is established.
   • Give a second 5-day course after at least 2 days apart if blood lead rebounds over 45 micrograms/dL.
7. Pregnancy: source removal, adequate calcium (1500 to 2000 mg daily), and chelation only for severe symptomatic poisoning because of limited data.
8. Gastrointestinal decontamination for ingested lead objects: whole bowel irrigation with polyethylene glycol 25 mL/kg/h for children (1 to 2 L/h for adults) until the radiograph is clear, and endoscopic or surgical removal of retained gastric objects.
9. Retained bullet fragment in a joint or disc space: surgical removal for symptomatic or high-level patients.

Follow-up: blood lead every 1 to 3 months until under 5 micrograms/dL, with developmental assessment and early educational support for children, and renal function and blood pressure checks for adults. Counsel on prevention, occupational hygiene and water safety.