Lead Poisoning in Adults

Lead causes injury by behaving like useful divalent cations, especially calcium and zinc. It can occupy calcium- and zinc-dependent binding sites, altering intracellular signalling, mitochondrial activity, and antioxidant defenses. No blood lead concentration has been established as completely free of adverse effects. The hematologic pattern comes from two blocked steps in heme synthesis. Lead inhibits delta-aminolevulinic acid dehydratase in the cytoplasm and ferrochelatase in the mitochondrion. Iron can no longer be incorporated efficiently into protoporphyrin IX, so heme production falls. The anemia may be normocytic or progress toward microcytosis. Zinc then substitutes for iron in the porphyrin ring, raising erythrocyte zinc protoporphyrin. Lead also affects the kidney, vascular system, reproductive system, and nervous system. Chronic exposure is associated with chronic interstitial nephropathy, hyperuricemia and saturnine gout, hypertension, reduced fertility, adverse reproductive outcomes, and cognitive or behavioural impairment. These effects can develop gradually, without a dramatic acute poisoning episode.