Lauwerys R R, Roels H A, Buchet J P, Bernard A, Stanescu D
Environ Health Perspect. 1979 Feb;28:137-45. doi: 10.1289/ehp.7928137.
The kidney seems more sensitive to the chronic effect of cadmium than the lung. Only minor impairments of lung function (mild form of obstructive lung disease) were found after long-term occupational exposure (less than 20 yr) to moderate concentration of cadmium oxide dust and fume. This conclusion, cannot, however be extrapolated to acute or subacute inhalational exposure. The nephrotoxicity of cadmium consists in a tubular dysfunction characterized by an increased excretion of beta 2-microglobulin and giving rise to the classical tubular proteinuria and in a glomerular dysfunction evidenced by an increased excretion of high molecular weight proteins and increased levels of beta 2-microglobulin and creatinine in plasma and giving rise to a glomerular type proteinuria. These renal changes were mainly found in workers whose cadmium concentration at time of the survey exceeded 1 microgram Cd/100 ml in blood and 10 microgram Cd/g creatinine in urine. It should, however, be stressed that higher levels of Cd in blood and in urine are not necessarily associated with the presence of excessive proteinuria. In newly exposed workers, the Cd level in blood increases progressively to a plateau after several weeks. Cadmium level in urine fluctuates more. In workers exposed for several months to an airborne concentration exceeding 200 microgram/m3, Cd concentration in urine seems mainly influenced by recent exposure.
肾脏似乎比肺对镉的慢性影响更敏感。长期职业接触(少于20年)中等浓度的氧化镉粉尘和烟雾后,仅发现肺功能有轻微损害(轻度阻塞性肺病)。然而,这一结论不能外推至急性或亚急性吸入暴露。镉的肾毒性表现为肾小管功能障碍,其特征是β2-微球蛋白排泄增加,导致典型的肾小管蛋白尿;以及肾小球功能障碍,表现为高分子量蛋白质排泄增加,血浆中β2-微球蛋白和肌酐水平升高,导致肾小球型蛋白尿。这些肾脏变化主要见于调查时血镉浓度超过1微克镉/100毫升血液和尿镉浓度超过10微克镉/克肌酐的工人。然而,应该强调的是,血液和尿液中较高的镉水平不一定与蛋白尿过多有关。在新接触镉的工人中,血镉水平在几周后逐渐升高至稳定水平。尿镉水平波动更大。在接触空气中镉浓度超过200微克/立方米数月的工人中,尿镉浓度似乎主要受近期接触的影响。