Piscator M
Environ Health Perspect. 1981 Aug;40:107-20. doi: 10.1289/ehp.8140107.
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.
动物实验表明，注射大量镉会导致注射部位出现肉瘤或睾丸损伤，并最终引发睾丸肿瘤。长期低剂量接触镉在实验动物中并未引发睾丸或前列腺肿瘤。对接触镉的工人进行的流行病学研究显示，至少在三项独立调查中发现前列腺癌导致的死亡人数过多。所有报告的病例可能在数十年前就有大量接触史，但没有足够的数据进行任何剂量反应计算。在任何一项研究中都没有考虑前列腺癌的总体流行病学情况。对近期前列腺癌流行病学文献的综述揭示了一些基本事实。已表明，在前列腺癌死亡率低的地区，小的潜伏性前列腺癌与死亡率高的地区一样常见。在美国，黑人前列腺癌死亡率远高于白人。婚姻状况也被认为是前列腺癌发展的一个因素。非洲的黑人人口死亡率远低于美国的黑人，这可能取决于饮食习惯的巨大差异。因此，种族、性别和营养因素可能对前列腺癌的发展很重要，因为它们可能影响激素状态。在大量接触期间，睾丸和前列腺中的镉浓度会增加，并且已经表明，接触镉的动物睾丸激素合成会减少。过度接触可能会干扰前列腺中锌与激素的关系，这可能是大量接触镉的个体患前列腺癌的一个可能解释。镉对细胞的直接作用不太可能，低水平接触镉也不太可能是前列腺癌的致病因素。
