Cárdenas A, Roels H, Bernard A M, Barbon R, Buchet J P, Lauwerys R R, Roselló J, Hotter G, Mutti A, Franchini I
Unité de Toxicologie Industrielle et Médecine du Travail, Faculté de Médecine, Université Catholique de Louvain.
Br J Ind Med. 1993 Jan;50(1):17-27. doi: 10.1136/oem.50.1.17.
Several markers of renal changes have been measured in a cohort of 50 workers exposed to elemental mercury (Hg) and in 50 control workers. After application of selection criteria 44 exposed and 49 control workers were retained for the final statistical analysis. Exposed workers excreted on average 22 micrograms Hg/g creatinine and their mean duration of exposure was 11 years. Three types of renal markers were studied--namely, functional markers (creatinine and beta 2-microglobulin in serum, urinary proteins of low or high molecular weight); cytotoxicity markers (tubular antigens and enzymes in urine), and biochemical markers (eicosanoids, thromboxane, fibronectin, kallikrein, sialic acid, glycosaminoglycans in urine, red blood cell membrane negative charges). Several bloodborne indicators of polyclonal activation were also measured to test the hypothesis that an immune mechanism might be involved in the renal toxicity of elemental Hg. The main renal changes associated with exposure to Hg were indicative of tubular cytotoxicity (increased leakage of tubular antigens and enzymes in urine) and biochemical alterations (decreased urinary excretion of some eicosanoids and glycosaminoglycans and lowering of urinary pH). The concentrations of anti-DNA antibodies and total immunoglobulin E in serum were also positively associated with the concentration of Hg in urine and in blood respectively. The renal effects were mainly found in workers excreting more than 50 micrograms Hg/g creatinine, which corroborates our previous estimate of the biological threshold of Hg in urine. As these effects, however, were unrelated to the duration of exposure and not accompanied by functional changes (for example, microproteinuria), they may not necessarily represent clinically significant alterations of renal function.
在一组50名接触元素汞(Hg)的工人和50名对照工人中,对几种肾脏变化标志物进行了测量。应用选择标准后,44名接触汞的工人和49名对照工人被保留用于最终统计分析。接触汞的工人平均肌酐中汞排泄量为22微克/克,平均接触时间为11年。研究了三种类型的肾脏标志物,即功能标志物(血清中的肌酐和β2-微球蛋白、低分子量或高分子量尿蛋白);细胞毒性标志物(尿中的肾小管抗原和酶)以及生化标志物(尿液中的类花生酸、血栓素、纤连蛋白、激肽释放酶、唾液酸、糖胺聚糖、红细胞膜负电荷)。还测量了几种多克隆激活的血源指标,以检验免疫机制可能参与元素汞肾脏毒性的假设。与接触汞相关的主要肾脏变化表明存在肾小管细胞毒性(尿中肾小管抗原和酶泄漏增加)和生化改变(一些类花生酸和糖胺聚糖的尿排泄减少以及尿pH值降低)。血清中抗DNA抗体和总免疫球蛋白E的浓度也分别与尿汞和血汞浓度呈正相关。肾脏效应主要见于肌酐中汞排泄量超过50微克/克的工人,这证实了我们先前对尿汞生物阈值的估计。然而,由于这些效应与接触时间无关且未伴有功能变化(例如微量蛋白尿),它们不一定代表临床上显著的肾功能改变。