Overt clinical disease from undue lead exposure has become a relatively rare phenomenon in adult populations. However, exposure situations that may result in subclinical disease are not uncommon in various occupational settings. Five demolition workers, dismantling an old iron structure covered with lead‐content paint, were studied. The use of cutting torches resulted in lead fumes, with significant exposure, albeit without gross “lead poisoning.” All five workers showed biochemical manifestations of chronic lead intoxication‐that is, elevated blood lead level, inhibition of δ‐aminolevulinic acid dehydratase (ALA‐D), and elevated erythrocytic protoporphyrin concentration (PROTO). The effect of lead on the biosynthesis of heme was assessed by investigating the functional capacity of the cytochrome P‐450 system of the liver, through drug metabolism studies. The plasma elimination rates (half‐lives) of antipyrine and phenylbutazone—drugs primarily metabolized by the hemeprotein P‐450 dependent hepatic microsomaf enzyme system—were measured before and after chelation therapy. Prior to chelation therapy all half‐lives were within the normal range. A slight decrease in the half‐life of antipyrine was found after treatment. These studies show that chronic exposure to lead has only a minimal effect on hepatic cytochrome P‐450 dependent enzymatic activities in adult males.
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