Manifestations of Toxicity

Toxic manifestations of cadmium ingestion include renal dysfunction, osteoporosis and bone pain, abdominal pain, vomiting and diarrhea, anemia, and bone marrow involvement (Table 1).

Gastrointestinal toxicity The mechanisms for cadmium's effects on the gastrointestinal tract are not certain. Whether these toxicities stem from an irritative effect of the metal or whether there is cellular damage has not been resolved in animal or in vitro studies. One possibility is that in vitro studies of neural tissue suggest that cadmium blocks adrenergic and cholinergic synapses. Therefore, it is possible that cadmium interferes with autonomic nervous system influence on gastrointestinal motility.

Renal toxicity Renal tubular dysfunction is manifest in patients with itai itai disease as glycosuria and proteinuria, including excessive excretion of a- and ^-microglobulin. Approximately 50-75% of cadmium accumulation in the body occurs in the liver and kidneys. Urinary cadmium excretion of 200 mg (1.78 mmol)g-1 of renal cortical tissue has been associated with tubular dysfunction. In the kidney, cadmium is bound to metallothionein. When the amount of intracellular cadmium accumulation exceeds metallothionein binding capacity, this is the point at which renal toxicity is hypothesized to occur.

Bone marrow and bone In short-term accumulation of cadmium in the marrow, there is a proliferation of cells in the myeloid/monocyte category. However, with longer term burden, marrow hypo-plasia is reported, including decreased production of erythropoietin. Although a reduction in marrow cells may indicate that the osteogenic precursors in the marrow may also be reduced (Table 1), this is not borne out by studies both in humans and in rats. In these cases, biochemical markers of bone formation (osteocalcin) and resorption (deoxypyridino-line) are both increased, indicating a high turnover state. In rats, circulating parathyroid hormone levels are also elevated, suggesting that the high turnover is due to secondary hyperparathyroidism and subsequent inability of the bone matrix to mature and bind calcium and phosphate. Parenteral administration of 1,25-dihydroxyvitamin D has been reported to decrease circulating parathyroid hormone in the rat and to reduce bone turnover. Moreover, other animal studies report that cadmium interferes with hydroxyapatite nucleation and growth, thus making it difficult for bone matrix to bind to calcium.

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