Role of cadmium in carcinogenesis with special reference to cancer of the prostate

Abstract

It has been shown in animal experiments that injections of large amounts of cadmium cause sarcoma at injection sites or testicular damage and eventually testicular tumors. Long-term exposure with small doses of cadmium has not caused testicular or prostatic tumors in experimental animals. Epidemiological studies on cadmium-exposed workers have shown excess deaths due to prostatic cancer in at least three independent investigations. All reported cases probably had considerable exposure decades ago, but there are not enough data to permit any dose-response calculations. The general epidemiology of prostatic cancer was not taken into account in any of the studies. A review of recent literature on epidemiology of prostatic cancer has revealed some basic facts. Small latent prostatic cancer has been shown to be as common in areas with low mortality from prostatic cancer as in areas with high mortality. In the U.S. the black population has a much higher death rate from prostatic cancer than the white population. Marital status has also been implied as a factor in the development of prostatic cancer. Black populations in Africa have much lower death rates than blacks in the U.S., which may depend on large differences in dietary habits. Thus racial, sexual and nutritional factors might be important for the development of prostatic cancer, since they may influence hormonal status. Cadmium concentrations in testes and prostate increase during heavy exposure, and it has been shown that testosterone synthesis will decrease in cadmium-exposed animals. Excessive exposure may interfere with the zinc/hormone relationship in the prostate, which could be a possible explanation for the development of prostatic cancer in heavily exposed individuals. Direct action of cadmium on the cells is not likely, nor is it probable that low level exposure to cadmium can be a causative factor for prostatic cancer.