Buchet J P, Roels H, Bernard A, Lauwerys R
J Occup Med. 1980 Nov;22(11):741-50.
The renal function of workers occupationally exposed to cadmium (n = 148), to mercury vapor (n = 63) or to inorganic lead (n = 25) has been compared with that of workers with no occupational exposure to heavy metals (n = 88). A moderate exposure to lead (Pb-B < 62 microgram/100 ml) does not seem to alter renal function. Excessive exposure to cadmium increases the urinary excretion of both low- and high-molecular-weight proteins and of tubular enzymes. These changes are mainly observed in workers excreting more than 10 microgram Cd/g creatinine or with Cd-B above 1 microgram Cd/100 ml whole blood. Occupational exposure to mercury vapor induces glomerular dysfunction as evidenced by an increased urinary excretion of high-molecular-weight proteins and a slightly increased prevalence of higher beta 2-microglobulin concentration in plasma without concomitant change in urinary beta 2-microglobulin concentration. beta-galactosidase activity in blood and in urine is also increased. The likelihood of these findings is greater in workers with Hg-B and Hg-U exceeding 3 microgram/100 ml whole blood and 50 microgram/g creatinine, respectively. The hypothesis is put forward that the glomerular dysfunction induced by cadmium and mercury might result from an autoimmune mechanism.
已将职业性接触镉(n = 148)、汞蒸气(n = 63)或无机铅(n = 25)的工人的肾功能与无重金属职业接触的工人(n = 88)的肾功能进行了比较。中度铅接触(Pb-B < 62微克/100毫升)似乎不会改变肾功能。过度接触镉会增加低分子量和高分子量蛋白质以及肾小管酶的尿排泄量。这些变化主要见于肌酐排泄量超过10微克镉/克或全血镉含量超过1微克镉/100毫升的工人。职业性接触汞蒸气会导致肾小球功能障碍,表现为高分子量蛋白质的尿排泄量增加,血浆中β2-微球蛋白浓度略有升高,而尿中β2-微球蛋白浓度无相应变化。血液和尿液中的β-半乳糖苷酶活性也会增加。汞含量(Hg-B)超过3微克/100毫升全血且汞排泄量(Hg-U)超过50微克/克肌酐的工人出现这些结果的可能性更大。有人提出假设,镉和汞引起的肾小球功能障碍可能是由自身免疫机制导致的。