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Chronic cadmium poisoning occurs after prolonged exposure to the dust or fumes of cadmium-containing compounds. This paper describes the case of a pigment worker exposed to cadmium carbonate dust who exhibited many of the characteristic features of chronic cadmium poisoning.
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A study was conducted to characterize the molecular species of retinol-binding protein (RBP) isolated from the urine of rabbits chronically poisoned with cadmium. The RBP species, identical with regard to both molecular size (approximately 20,000) and immunoreactivity, were separated into four fractions by means of polyacrylamide gel electrophoresis (PAGE), which yielded two holo-RBP (H2 and H1) and two apo-RBP (A2 and A1) species. The urinary excretion ratio of these fractions (H2 : H1 : A2 : A1) was found to be about 70 : 6 : 21 : 3. No distinct difference of amino acid composition between holo- and apo-RBP was observed. An additional species of apo-RBP (designated An) was also isolated from theaged holo-RBP (H2) by isoelectric focusing in gel. Using the separated molecular species of rabbit RBP as well as of human RBP, their interactions with human prealbumin (PA) were examined both by human PA-Sepharose affinity chromatography, and by gel filtration on Sephadex G-100 after in vitro incubation of the RBP with human PA. Purified rabbit holo-RBP exhibited almost the same binding ability to human PA as did human RBP. Retinol within RBP molecule enhanced the affinity to PA, resumably through the change of tertiary structure, although the presence of retinol was not essential for the protein-protein interaction.
In an attempt to elucidate the etiology and pathogenesis of 'Itai-Itai' disease, the relationship between bone and kidney lesions in cadmium-poisoned rats was determined using the standard renal clearance technique. Calcium and cadmium contents in the femur and kidney were also estimated. The severity of renal lesions was histologically evident both in the tubule and glomerulus, and paralleled the decrease in GFR and the increase in FF. There was no significant change in fractional excretion of phosphate, but fractional excretion of calcium increased in the cadmium-poisoned rats. The secondary hyperparathyroidism followed by uremic renal osteodystrophy did not result in an osteomalacia. Thus, it is apparent that disturbance in calcium reabsorption in the tubules plays a role in the loss of calcium, and cadmium associated with low levels of calcium has a direct effect on the bone-causing osteomalacia.
An examination has been made of the relative effectiveness of three chelating agents in reducing lethality in acute cadmium poisoning. The chelating agents used were sodium 2,3 dimercaptosulfonate (DMPS), N-Acetyl d,1 penicillamine (NAPA), and 2,3 dimercaptosuccinic acid (DMSA). For cadmium acetate administered ip at a level of 16.9 mg/kg, the oral administration of the chelating agents at a 20:1 mole ratio in three doses subsequent to the cadmium acetate at 20 minutes, 90 minutes, and 210 minutes resulted in a significant enhancement of the survival rate for all three compounds. At this level none of the control animals survived beyond 2 days. On the basis of the experiments carried out here the survival rates decreased in the order sodium 2,3 dimercaptopropane-sulfonate greater than 2,3 dimercaptosuccinic acid greater than N-Acetyl d,l penicillamine. In a study of the effect of the mole ratio of the chelating agent sodium 2,3 dimercaptopropanesulfonate to cadmium acetate on the survival rate, it was found that the survival rate attained a maximum for values between 20 and 60 and dropped off at both higher and lower values. It was also found that for at least one set of conditions, younger animals were better able to survive the administration of cadmium acetate and the antidote than older animals.
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