Effect of Dietary Calcium and Phosphorus on Toxicity of Lead in the Rat

Abstract

Since the introduction of calcium salts or calcium containing foods, by Aub and his associates, 1 in the treatment of lead poisoning, numerous papers have appeared in the literature advocating such therapy. The rationale of the procedure was based on the following facts: First, the solubility of lead phosphate was found to be analogous to that of calcium phosphate; hence Aub and his associates believed that lead might be deposited in the bones in the same manner that lime salts are and thus be removed from the circulation. Second, when diets low in calcium were fed to cats, the trabeculae of the bones of the animals were diminished in size and in number as compared to those of animals fed diets to which calcium had been added. This was interpreted to mean that the addition of calcium salts to diets in general results in an increased storage of lime salts in the trabeculae; and since lead was supposed to behave like calcium, its deposition in the bones could be hastened or increased by furthering the process of calcification through the administration of calcium. Third, the fact that lead colic may be alleviated, almost instantly, by the intravenous administration of calcium chloride was thought to add additional evidence that calcium “drives” lead into the bones. However, the later studies of Aub and coworkers 2 discredit such an assumption since the alleviation of pain is too rapid to be due to precipitation of lead in the osseous tissue. Aub and his .coworkers are, therefore, now inclined to believe that the action of calcium in this instance is to relax the intestinal musculature.

That the administration of calcium salts does not always result in improved calcification unless the phosphorus in the diet is controlled, may be inferred from the experiments of McCollum, Shipley and Park 3 on the production of rickets in rats.