Sällsten G, Barregård L
Department of Occupational Medicine, Sahlgrenska University Hospital, Göteborg, Sweden.
Biometals. 1997 Oct;10(4):357-61. doi: 10.1023/a:1018392904399.
The excretion of mercury, copper and zinc in urine, and mercury in whole blood and plasma, was determined in 40 chloralkali workers exposed to mercury vapour and 40 age-matched referents. The Hg concentrations in whole blood, plasma and urine were higher in the exposed group (35 nmol l-1, 30 nmol l-1, and 11.5 nmol mmol-1 creatinine, respectively) in comparison with the reference group (15 nmol l-1, 6.3 nmol l-1, and 1.8 nmol mmol-1 creatinine, respectively). The urinary copper excretion was similar in the two groups, while U-Zn excretion was significantly higher (P = 0.04) in the exposed group, median 0.83 mumol mmol-1 creatinine versus 0.76 munmol mmol-1 creatinine in the reference group. In a subgroup of exposed workers with current U-Hg above 11.5 nmol l-1 mmol-1 creatinine (20 micrograms g-1 creatinine) the median U-Zn was 1.1 mumol mmol-1 creatinine. In both groups smokers had high U-Zn levels than non smokers. When both U-Hg and smoking were taken into account in a linear regression model, there was a significant association between U-Hg and U-Zn in the combined group of exposed and referents (P = 0.002). This study indicates that mercury exposure in humans, as in animals, causes increased urinary excretion of zinc. The mechanisms may be induced synthesis of metallothionein in the kidneys, displacement of Zn from preexisting metallothionein by Hg, or a decreased reabsorption of zinc in the kidneys owing to a slight tubular dysfunction.
对40名接触汞蒸气的氯碱工人及其40名年龄匹配的对照者,测定了他们尿液中汞、铜和锌以及全血和血浆中汞的排泄量。与对照组(全血、血浆和尿液中的汞浓度分别为15 nmol/L、6.3 nmol/L和1.8 nmol/mmol肌酐)相比,接触组的全血、血浆和尿液中的汞浓度更高(分别为35 nmol/L、30 nmol/L和11.5 nmol/mmol肌酐)。两组的尿铜排泄量相似,而接触组的尿锌排泄量显著更高(P = 0.04),中位数为0.83 μmol/mmol肌酐,对照组为0.76 μmol/mmol肌酐。在当前尿汞高于11.5 nmol/L mmol-1肌酐(20 μg/g肌酐)的接触工人亚组中,尿锌中位数为1.1 μmol/mmol肌酐。两组中吸烟者的尿锌水平均高于非吸烟者。当在一个线性回归模型中同时考虑尿汞和吸烟因素时,接触组和对照组的合并组中尿汞与尿锌之间存在显著关联(P = 0.002)。这项研究表明,与动物一样,人类接触汞会导致尿锌排泄增加。其机制可能是诱导肾脏中金属硫蛋白的合成、汞将锌从预先存在的金属硫蛋白中置换出来,或者由于轻微的肾小管功能障碍导致肾脏对锌的重吸收减少。