Järup L, Persson B, Elinder C G
Department of Environmental Health and Infectious Diseases Control, Karolinska Hospital, Stockholm, Sweden.
Occup Environ Med. 1995 Dec;52(12):818-22. doi: 10.1136/oem.52.12.818.
to evaluate the degree of cadmium induced glomerular impairment and to assess the dose-response relation between cadmium dose and the prevalence of glomerular dysfunction.
A comparison of glomerular filtration rates (GFR) assessed by Cr-EDTA clearance was made in 42 solderers previously exposed to cadmium for at least five years. Blood and urine data were collected at health examinations in 1984, 1989, and 1993. Individual doses of cadmium were estimated by analysing cadmium in blood.
Glomerular lesions induced by cadmium are irreversible and the GFR decreases with the degree of tubular damage. The GFR also decreases with cadmium dose and there is a dose-response relation between blood cadmium and prevalence of glomerular damage with 3.4% prevalence at blood cadmium concentrations below 50 nmol/l, 33% at blood cadmium concentrations between 50 and 75 nmol/l and 100% prevalence of glomerular damage when cadmium in blood exceeds 75 nmol/l.
The kidney lesions induced by cadmium are irreversible and the prevalence of those lesions are dose dependent. There is also evidence of a dose related decrease in GFR even a long time after the end of exposure. Exposure to cadmium should therefore be minimised and workers exposed to cadmium should be examined regularly for many years after the end of exposure.
评估镉诱导的肾小球损伤程度,并评估镉剂量与肾小球功能障碍患病率之间的剂量反应关系。
对42名曾接触镉至少五年的焊工进行了比较,通过铬-乙二胺四乙酸清除率评估肾小球滤过率(GFR)。在1984年、1989年和1993年的健康检查中收集血液和尿液数据。通过分析血液中的镉来估算个体镉剂量。
镉诱导的肾小球病变是不可逆的,GFR随肾小管损伤程度而降低。GFR也随镉剂量降低,血液镉与肾小球损伤患病率之间存在剂量反应关系,血液镉浓度低于50 nmol/l时患病率为3.4%,血液镉浓度在50至75 nmol/l之间时为33%,血液镉超过75 nmol/l时肾小球损伤患病率为100%。
镉诱导的肾脏病变是不可逆的,这些病变的患病率与剂量有关。即使在接触结束很长时间后,也有证据表明GFR与剂量相关下降。因此,应尽量减少镉暴露,接触镉的工人在接触结束后应多年定期接受检查。