It is well known that high
cadmium exposure causes renal damage,
osteoporosis and
osteomalacia, whereas the dose-response relationships at low-level exposure are less well established. WHO estimated (1992) that a urinary excretion of 10 nmol/mmol
creatinine would constitute a 'critical limit' below which kidney damage would not occur. Later, Belgian and Swedish studies have shown signs of
cadmium induced kidney dysfunction in the general population already at urinary
cadmium levels around 2-3 nmol/mmol
creatinine. The Swedish OSCAR (
OSteoporosis-
CAdmium as a Risk factor) study comprised 1021 individuals, exposed to
cadmium in the environment. Blood and urinary
cadmium were used as dose estimates.
Protein HC (alpha-1-microglobulin) was used as an
indicator of renal tubular damage. Forearm bone mineral density (BMD) was assessed with DXA (dual energy x-ray absorptiometry) technique. The study showed that tubular
proteinuria occurred at much lower levels of
cadmium dose than previously known. A negative dose-effect relationship was found between
cadmium dose and BMD for people at the age of 60 or older. In this age group, there was also a dose-response relationship, showing a three-fold increased risk of low BMD in the group with urinary
cadmium over 3 nmol/mol
creatinine, as compared to the lowest dose group. There was also evidence of an increased risk of forearm fractures with increasing
cadmium levels in the population 50 years of age or older. The potential public health consequences of low level
cadmium exposure should be recognized, and measures taken to reduce
cadmium exposure to an absolute minimum.