My discussion concerns several possible susceptibility factors to heavy metals that need further investigation.1-3 These metals, once assimilated, are only slowly excreted. For example, the biological half-life of mercury in rats is estimated at 70 to 100 days, and for cadmium, at 200 to 300 days-a considerable portion of the life span of these animals. In adult man, the half-life of lead in bone is estimated at 11 years. Human autopsy data likewise indicate a progressive increase in the total body burden with age, particularly for cadmium and lead. For example, the cadmium content of the human fetus is estimated at 1µg; by the age of 50 years, the "normal" body burden of cadmium for the American "standard man" has increased to 30 mg with concentrations in the kidney which may approach the critical level for toxic renal effects.2 Clearly, we must consider the extent to which pediatric exposure contributes to the body burden, whose effects may not be apparent until adult life. It is probably unwise to consider each metal by itself. Instead, one must think of metal-metal relationships. For example, the enzyme metallocarboxypeptidase has both esterase and peptidase functions.1 The normal metallic cofactor is zinc, which can be displaced from the enzyme by mercury, cadmium, or lead. The displacement produces metalloenzymes that have esterase, but not peptidase function. In fact, the cadmium metalloenzyme has somewhat greater in vitro activity in partially purified preparations than does the zinc metalloenzyme. Thus, these metals have the capacity to alter enzyme specificity and efficiency.
J. Julian Chisolm (Wed,) studied this question.