Investigations on the lung and kidney function in workers exposed to cadmium.
Investigations on the lung and kidney function in workers exposed to cadmium.
复制标题
暴露于镉的工人中对肺和肾功能的调查。
DOI：
10.1289/ehp.7928137
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发表时间：
1979-02
影响因子：
10.4
通讯作者：
中科院分区：
文献类型：
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作者：
肾脏似乎比肺对镉的慢性影响更敏感。长期(不到20年)接触中等浓度的氧化镉粉尘和烟雾后，仅发现轻微的肺功能损害(轻度阻塞性肺病)。然而，这一结论不能推断为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，表现为β2-微球蛋白排泄增加，出现典型的肾小管型蛋白尿；肾小球功能障碍，表现为大分子蛋白排泄增加，血浆中β2-微球蛋白和肌酐水平升高，导致肾小球型蛋白尿。这些肾脏改变主要见于调查时血镉浓度超过1微克Cd/100毫升、尿镉浓度超过10微克Cd/g肌酐的工人。然而，应该强调的是，血和尿中镉的水平较高并不一定与过量蛋白尿的存在有关。在新接触的工人中，血液中的镉水平在几周后逐渐上升到一个平台期。尿镉水平波动较大。在接触空气浓度超过200微克/立方米数月的工人中，尿镉浓度似乎主要受最近接触的影响。
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.