Plumbism developed in a 17 year old boy while he was working in an indoor firing range. Diagnosis was delayed because a blood lead level was initially reported to be within normal limits and because acute intermittent porphyria was suspected. Subsequently, lead poisoning was clearly documented by characteristic abnormalities of the heme biosynthetic pathway in erythrocytes (inhibited δ-aminolevulinic acid dehydratase activity, increased protoporphyrin-IX), increased urinary excretion of δ-aminolevulinic acid and coproporphyrin, and elevated levels of lead in blood and urine. These abnormalities as well as decreased nerve conduction velocity and reduced hepatic cytochrome P-450 function, as assessed by metabolism of antipyrine, returned towards normal with chelation therapy. Investigation of the firing range showed airborne lead to be markedly increased during firing; a co-worker was also found to have asymptomatic lead poisoning. This experience shows that exposure to heavy metals can occur by mechanisms which are unusual and not widely recognized, and illustrates the importance of testing erythrocytes and urine for distinct biochemical abnormalities related to the heme synthetic pathway when differentiating hereditary hepatic porphyria from plumbism.
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