In the United States, this disease has been identified most often in 1to 3-year-old children who inhabit urban slum areas where old, deteriorated housing prevails. (Lead paint was used in most houses built before 1940 and in many built before 1960.) The chewing of leaded paint is promoted by compulsive ingestion (pica) from windowsills and painted plaster walls. The development of an acute encephalopathy is the most serious complication, resulting in death in 5 to 20 percent of cases and in permanent neurologic and mental deficits in more than 25 percent of survivors.
Clinical manifestations These develop over a period of 3 to 6 weeks. The child becomes anorectic, less playful and less alert, and more irritable. These symptoms may be misinterpreted as a behavior disorder or a manifestation of mental retardation. Intermittent vomiting, vague abdominal pain, clumsiness, and ataxia may be added. If these early signs of intoxication are not recognized and the child continues to ingest lead, more flagrant signs of acute encephalopathy may develop—most frequently in the summer months, for reasons that are not understood. Vomiting becomes more persistent, apathy progresses to drowsiness and stupor interspersed with periods of hyperirritability, and, finally, seizures and coma supervene. This syndrome may evolve in a period of a week or less, most rapidly in children younger than 2 years of age; in older children, it is more likely to develop in recurrent and less severe episodes. This clinical syndrome must be distinguished from tuberculous meningitis, viral meningoencephalitis, and the various conditions causing acute increased intracranial pressure. Usually, in lead encephalopathy, the CSF is under increased pressure with manifest papilledema, and there may be a slight lymphocytic pleocytosis and elevated protein but normal glucose values. It follows that lumbar puncture should be done with caution and only if it is essential for diagnosis.
Diagnosis Because the symptoms of plumbism are nonspecific, the diagnosis depends on an appreciation of the potential causative factors and the results of certain laboratory tests. Lead lines at the metaphyses of long bones and basophilic stippling of red cells are seen but are too inconstant to be relied on, but basophilic stippling of bone marrow erythroblasts is uniformly increased. Impairment of hemoglobin synthesis, which is exquisitely sensitive to the toxic effects of lead, results in the increased excretion of urinary coproporphyrin (UCP) and of Δ-aminolevulinic acid (ALA). These urinary indices and the lead concentrations in the serum bear an imperfect relationship to the clinical manifestations. In the test for UCP, which is readily performed in the clinic and emergency department, a few milliliters of urine are acidified with acetic acid and shaken with an equal volume of ether; if coproporphyrin is present, the ether layer will reveal a reddish fluorescence under a Wood lamp. This test is strongly positive when the whole blood concentration of lead exceeds 80 mcg/dL. The diagnosis can be confirmed by promoting lead excretion with calcium disodium edetate (CaNa2 ethylenediaminetetraacetic acid [EDTA]), given in three doses (25 mg/kg) at 8-h intervals. Excretion of over 500 mg in 24 h is indicative of plumbism. The measurement of zinc protoporphyrin (ZPP) in the blood is another reliable means of determining the presence and degree of lead exposure. The binding of erythrocyte protoporphyrin to zinc occurs when lead impairs the normal binding of erythrocyte protoporphyrin to iron. Elevated ZPP can also be induced when access to iron is limited by other conditions, such as iron deficiency anemia.