Ellis K J, Yuen K, Yasumura S, Cohn S H
Environ Res. 1984 Feb;33(1):216-26. doi: 10.1016/0013-9351(84)90018-5.
The primary objective of this study was to develop dose-response relationships of cadmium in human beings. In vivo measurements of kidney, liver, urine, and blood cadmium, and urinary levels of beta 2-microglobulin and total protein were obtained in 82 industrially exposed workers and 30 control subjects. The values of 200 micrograms/g creatinine for urinary beta 2-microglobulin and 250 mg/g creatinine for urinary total protein were used to define the upper limit for normal kidney function. Forty-one of the cadmium workers (18 active, 23 retired) were classified as having abnormal kidney function; all control subjects had normal kidney function. Most workers with Cd above 70 ppm in the liver were judged to have some evidence of kidney abnormalities. The dose-response relationship for liver cadmium for the actively employed workers could be described by a linear logistic regression model: (Formula: see text) where p is the individual's probability of having kidney dysfunction. The loss of cadmium from the kidney following dysfunction prohibited a direct logistic analysis of the kidney cadmium data. However, when the linear relationship between kidney and liver cadmium for the subjects with normal kidney function was combined with the logistic equation for the liver, a predicted-response curve was obtained for the kidney. The logistic models predict a 50% probability of having kidney dysfunction at 38.4 mg for the kidney and 42.3 ppm for the liver, respectively.
本研究的主要目的是建立人体镉的剂量-反应关系。对82名职业暴露工人和30名对照者进行了肾脏、肝脏、尿液和血液中镉的体内测量，以及尿液中β2-微球蛋白和总蛋白水平的检测。尿β2-微球蛋白200微克/克肌酐和尿总蛋白250毫克/克肌酐的值被用来定义正常肾功能的上限。41名镉作业工人（18名在职，23名退休）被判定为肾功能异常；所有对照者肾功能正常。肝脏中镉含量高于70 ppm的大多数工人被判定有一些肾脏异常的证据。在职工人肝脏镉的剂量-反应关系可用线性逻辑回归模型描述：（公式：见原文）其中p是个体出现肾功能障碍的概率。肾功能障碍后肾脏中镉的流失使得无法对肾脏镉数据进行直接的逻辑分析。然而，当将肾功能正常者肾脏和肝脏镉之间的线性关系与肝脏的逻辑方程相结合时，得到了肾脏的预测反应曲线。逻辑模型预测，肾脏镉含量为38.4毫克、肝脏镉含量为42.3 ppm时，出现肾功能障碍的概率分别为50%。
