[Cadmium toxicity: summary of personal studies].

R Lauwerys, J P Buchet, H Roels, A Bernard
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Abstract

Occupational and environmental exposure to cadmium leads to a progressive and almost irreversible accumulation of the metal in the body. The epidemiological and experimental studies carried out by the authors allow them to draw the following conclusions: 1) the kidney is usually the critical organ i.e. the organ exhibiting the first signs of adverse effects following long term moderate exposure to cadmium by inhalation or by ingestion. 2) Cadmium interferes not only with the tubular reabsorption process(es) for low molecular weight proteins (e.g. beta 2 . microglobulin, retinol binding protein) but also with the glomerular or tubular mechanism determining the excretion of high molecular weight proteins (e.g. albumin, transferrin). Both types of proteinuria may occur independently. 3) The renal functional disturbances induced by cadmium and compatible not only with a tubular dysfunction but also a glomerular dysfunction. 4) The early detection of renal disturbances induced by cadmium should not rely only on the determination of total proteinuria but necessitates the analysis in urine of at least one low molecular weight protein (beta 2-microglobulin or retinol binding protein) and one high molecular weight protein (albumin). 5) Before the occurrence of renal dysfunction and providing the intensity of exposure to cadmium is moderate, urinary cadmium reflects mainly the body burden whereas blood cadmium reflects mainly the last few months exposure. 6) In adult male workers occupationally exposed to cadmium, the critical concentration of cadmium in the renal cortex is in the order of 200 ppm. The corresponding critical urinary level is approximately 10 micrograms/g creatinine. The critical level of cadmium in the renal cortex is not reached if the exposure is kept at a level where cadmium in blood does no exceed 1 microgram/100 ml. 7) Comparison of literature data on current exposure of the general population to cadmium and the critical exposure level indicates that some groups of the general population absorb daily amounts of cadmium closed to the critical level. 8) The critical biological levels indicated under (6) do not necessarily prevent an exacerbation of the age-related decline in renal function. 9) A preliminary study performed in Belgium suggests that cadmium might play a role in the increased mortality by renal diseases in a population living in an area polluted by cadmium. More detailed studies are necessary to confirm this hypothesis.

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[镉毒性:个人研究综述]。
职业性和环境性镉暴露会导致镉在体内逐渐且几乎不可逆地积累。作者进行的流行病学和实验研究使他们得出以下结论:1)肾脏通常是关键器官,即在长期吸入或摄入适量接触镉后最先出现不良反应迹象的器官。2)镉不仅会干扰低分子量蛋白质(如β 2)的管状重吸收过程。微球蛋白,视黄醇结合蛋白),但也与肾小球或小管机制决定高分子量蛋白质(如白蛋白,转铁蛋白)的排泄。两种类型的蛋白尿可能独立发生。3)镉所致的肾功能障碍不仅与肾小管功能障碍相容,还与肾小球功能障碍相容。4)早期发现镉引起的肾功能紊乱不应仅仅依靠尿总蛋白的测定,而必须分析尿中至少一种低分子量蛋白(β 2-微球蛋白或视黄醇结合蛋白)和一种高分子量蛋白(白蛋白)。5)在出现肾功能障碍之前,在镉暴露强度适中的情况下,尿镉主要反映机体负荷,血镉主要反映最近几个月的暴露。6)职业接触镉的成年男性工人,肾皮质镉的临界浓度约为200 ppm。相应的尿临界水平约为10微克/克肌酐。如果暴露量保持在血液中镉不超过1微克/100毫升的水平,则不会达到肾皮质镉的临界水平。7)一般人群当前镉暴露量与临界暴露水平的文献数据比较表明,一般人群中某些群体的镉日吸收量接近临界水平。8)(6)项中指出的临界生物学水平并不一定能防止与年龄相关的肾功能衰退加剧。9)在比利时进行的一项初步研究表明,在镉污染地区生活的人群中,镉可能在肾脏疾病死亡率增加中起作用。需要更详细的研究来证实这一假设。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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