Roels H A, Boeckx M, Ceulemans E, Lauwerys R R
Industrial Toxicology and Occupational Medicine Unit, School of Medicine, Catholic University of Louvain, Brussels, Belgium.
Br J Ind Med. 1991 Apr;48(4):247-53. doi: 10.1136/oem.48.4.247.
The spontaneous and chelator mediated excretion of mercury in urine was investigated in male subjects occupationally exposed to mercury vapour (alkaline battery and chloralkali plants) who did not exhibit any sign of kidney damage. The time course of the spontaneous elimination of mercury in urine was examined in seven workers (age 22-40) who had been removed from exposure to mercury vapour (average duration of exposure 4.4 years) because their urinary mercury concentrations repeatedly exceeded 100 micrograms/g creatinine. The post exposure observation period started 10 to 29 days after the date of removal and lasted about 300 days (slow HgU elimination phase). For each worker, the kinetics of the spontaneous HgU decline followed a first order process; the biological half life ranged from 69 to 109 days (mean 90 days). The increased urinary excretion of mercury after a single oral administration of 2 g meso-2,3-dimercaptosuccinic acid (DMSA) was investigated in 16 control workers (group A; age 23 to 49), in 11 workers removed from exposure for at least two years (group B; age 27 to 41), and in 16 workers currently exposed to mercury vapour (group C; age 21 to 58). In group C, the DMSA experiment was repeated twice (three weeks before and three weeks after a holiday) after measures had been taken to reduce the mercury emission. The urinary mercury excretion was significantly higher during the 24 hours after DMSA administration in all groups compared with that in the 24 hours before. The bulk (50-70%) of the DMSA stimulated mercury excretion appeared within the first eight hours. In each group, the amount of mercury (microgram Hg/24h) excreted after DMSA was significantly correlated with that before administration of DMSA. The groups whose exposure had ceased, however, exhibited much higher correlation for coefficients (r=0.97 for group B and 0.86 for group C after three weeks of holiday) than those currently exposed to mercury vapour (r-0.66 for group C before and 9.58 after reduction of exposure). The data suggest that after a few days of cessation of occupational exposure to mercury vapour the HgU before and after administration of DMSA mainly reflects the amount of mercury stored in the kidney, which represents a mercury pool with a slow turnover.
对职业性接触汞蒸气（碱性电池厂和氯碱厂）且未表现出任何肾脏损伤迹象的男性受试者，研究了汞在尿液中的自发排泄及螯合剂介导的排泄情况。对7名工人（年龄22 - 40岁）进行了研究，他们因尿汞浓度多次超过100微克/克肌酐而被调离汞蒸气接触环境（平均接触时长4.4年），以此来考察尿液中汞自发消除的时间进程。接触后观察期在调离日期后的10至29天开始，持续约300天（汞尿缓慢消除阶段）。对于每名工人，汞尿自发下降的动力学遵循一级过程；生物半衰期在69至109天之间（平均90天）。在16名对照工人（A组；年龄23至49岁）、11名已调离接触环境至少两年的工人（B组；年龄27至41岁）和16名当前仍接触汞蒸气的工人（C组；年龄21至58岁）中，研究了单次口服2克内消旋 - 2,3 - 二巯基丁二酸（DMSA）后汞尿排泄的增加情况。在C组中，在采取措施减少汞排放后，DMSA实验重复了两次（假期前三周和假期后三周）。与给药前24小时相比，所有组在DMSA给药后24小时内尿汞排泄量均显著更高。DMSA刺激的汞排泄量的大部分（50 - 70%）在前8小时内出现。在每组中，DMSA给药后排泄的汞量（微克汞/24小时）与给药前显著相关。然而，已停止接触的组系数相关性更高（假期三周后B组r = 0.97，C组r = 0.86），高于当前仍接触汞蒸气的组（接触减少前C组r = 0.66，接触减少后r = 0.58）。数据表明，在停止职业性接触汞蒸气几天后，DMSA给药前后的汞尿主要反映了肾脏中储存的汞量，这代表了一个周转缓慢的汞池。
