Abstract
The seriousness of cadmium as a toxic agent has been recognized for many years, but the nature of the toxicity has been obscure. As a divalent cation, cadmium has the potential for interaction with biochemical systems that normally interact with calcium, magnesium, and zinc. The symptoms of cadmiosis reflect such interactions. The testicular necrosis of cadmium poisoning suggests strongly that zinc metabolism in testicular tissue is disrupted (1, 2). The “itaiitai” disease which has been extensively investigated in Japan by Kobayashi (3) implicate cadmium interference with calcium metabolism. Unlike other divalent toxic agents such as cobalt or beryllium, cadmium is seldom the causative agent in acute poisoning (4). Cadmium is insidious in that long exposure to presumably “safe” amounts in the environment can lead to drastic and perhaps irreversible physiological consequences (5). The relative binding constants for cadmium by acetate, imidizole, amino, and sulfhydryl groups is some six to 10 times the constants for calcium, zinc, nickel, and cobalt (6). Such an affinity for biologically active groups leads to the problems of long-term cadmium exposure that have been documented by Schroeder and his coworkers (1). The influence of their work has focused attention on the possible association of cadmium with some form of hypertension. What is not clear is the immediate effect of cadmium on the cardiovascular system. Scattered data from several authors (7, 8, 9, 10) suggest that although hypertension may result ultimately, there is not a clear, direct development of hypertension as cadmium is accumulated. Among the most intriguing reports are those of an initial hypotension (7, 8) and electrocardiographic changes (9, 10) in cadmiosis.
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