ABSTRACT
Lead is a nonessential element, a ubiquitous environmental contaminant of considerable general and cumulative toxicity, and a suspected human carcinogen. Having similar physicochemical properties, Pb2 competes with Ca2 inhibiting the release of neurotransmitters, interfering with the regulation of cell metabolism by binding to calcium receptors, and blocking calcium transport to protein binding sites and mitochondria (1). It effectively and functionally displaces or substitutes for Ca2 in calmodulin and other receptor proteins, with such interactions possibly representing a fundamental mechanism of Pb toxicity (2,3). Lead forms coordination complexes with sulfur, nitrogen, and oxygen, and it exerts its toxic action through inhibition of sulfhydryl dependent enzymes (4-6). It produces adverse effects in most tissues and organs of the body, particularly on the central nervous system (CNS), the kidneys, involving damage to proximal tubules, and on the hematopoietic system, with parallel effects on metabolic processes. The identification of causal relationships is complicated by the delay between the time of lead exposure and the onset of toxic manifestations.
