Lead poisoning
Lead poisoning is chronic accumulation of inorganic lead, most often from lead paint dust in pre-1978 housing in children or occupational inhalation in adults, that inhibits heme synthesis and injures the developing brain and kidneys. Diagnosis rests on a venous blood lead level. Management is graded by that level: mandatory source removal at every threshold, oral succimer for 45 to 69 mcg/dL, and combined dimercaprol plus edetate calcium disodium for encephalopathy or levels of 70 mcg/dL or higher.
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What this article covers
- Overview
A chronic heavy-metal toxin, rarely a single ingestion: cumulative lead absorption from household dust, soil, imported cosmetics or folk remedies, lead-glazed pottery, or occupational sources such as…
- Epidemiology
Children under six years bear the burden, mostly from household dust from deteriorating lead-based paint in housing built before 1978, plus soil, imported cosmetics, folk or ayurvedic remedies, and lead-glazed pottery.
- Risk factors
Housing built before 1978, where deteriorating or disturbed lead paint generates household dust.
- Pathophysiology
Enzyme inhibition halts heme synthesis: lead inhibits ALAD early in the heme pathway and ferrochelatase at the final step, so erythrocyte protoporphyrin and delta-aminolevulinic acid accumulate and a sideroblastic, microcytic anemia results.
- Clinical features
Most children are asymptomatic at levels that still cause harm, which is why screening drives detection; impaired intelligence and neurodevelopmental outcomes appear at levels as low as 10 mcg/dL.
- Differential diagnosis
Iron deficiency anemia: microcytic and can coexist with lead poisoning, but lacks prominent stippling and shows low ferritin rather than an elevated lead level.
- Diagnosis
First, the diagnosis is confirmed by a venous blood lead level: a capillary fingerstick test screens at 12 and 24 months of age in high-risk children, but any elevated capillary result must then be…
- Management
First, for encephalopathy or a critically ill patient, secure airway, breathing, and circulation: treat seizures with a benzodiazepine, elevate the head of the bed, and admit to an intensive care…
- Complications
Irreversible neurocognitive injury in children, including intelligence deficits and learning disability persisting lifelong, correlating with peak blood lead level and age at exposure.
- Prognosis
Peak blood lead level and age at exposure predict neurologic outcome: higher levels and earlier exposure predict a larger, more permanent deficit; no threshold is harmless to the developing brain.
- Prevention
There is no safe blood lead level: effects on intelligence appear at levels as low as 10 mcg/dL, and the reference value for public health case management has fallen across revisions, from 10 to 5 to the current 3.5 mcg/dL.
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