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Harriet L. Hardy, M.D.; Hervey B. Elkins, Ph.D.; Benjamin P. W. Ruotolo, M.D.; John Quinby, M.D.; William H. Baker, M.D.
JAMA. 1954;154(14):1171-1175. doi:10.1001/jama.1954.02940480023007.
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The ideal clinical management of lead intoxication in human beings has not yet been achieved. Aub's original studies,1 demonstrating that calcium and lead behave much the same way in the body, have provided successful therapeutic leads. During episodes of acute intoxication, calcium has been used to force lead from the circulating blood to the skeleton, where it is deposited as a harmless tertiary phosphate. Since such lead can be mobilized, many attempts have been made with varying success to remove small amounts of lead slowly from the body in cases of chronic intoxication. Acid salts, low calcium diet, high phosphorus diet with magnesium sulfate, and potassium iodide have all been used in attempts to de-lead adults with chronic lead poisoning. Because in dilute solutions sodium citrate dissolves the tertiary lead phosphate, the form in which lead is stored, Kety and Letonoff2 suggested that the soluble complex of lead


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