Significance of cadmium levels in blood and urine during long‐term exposure of rats to cadmium

Abstract

Cadmium concentrations in blood, urine, kidney cortex, and liver were followed in female rats injected ip with J mg/kg Cd 5 times a week for 3 mo or receiving CdCl₂ in drinking water at 2 and 20 ppm Cd for 11 mo and 200 ppm Cd for 8 mo. Control rats were given deionized water or injected with physiological saline.

At low exposures (0, 2, and 20 ppm Cd po) the rate of Cd accumulation in liver was lower than that in kidney cortex, whereas at higher exposures it equaled (200 ppm Cd po) or even exceeded (1 mg/kg Cd ip) that in kidney cortex. In groups receiving 2, 20, and 200 ppm Cd, the Cd concentration in blood increased to a plateau value, which was reached after about 3 mo of treatment and was proportional to the Cd concentration in drinking water; this suggests that, at equilibrium, the blood Cd level mainly reflects current exposure. In rats injected with 1 mg/kg Cd ip no plateau level of Cd in blood was reached, although a tendency to level off seemed to occur after 2.5 mo. The Cd concentration in urine fluctuated more than that in blood. However, at all doses and before renal damage occurred, the amount of Cd excreted in urine tended to increase with duration of treatment. The significant correlation between the Cd level in renal cortex and that in urine confirms that the latter is mainly a reflection of the body burden. When renal dysfunction occurs, excretion of Cd in urine increases sharply.

The results of these experiments confirm previous conclusions derived from clinical investigations, that in the absence of Cd‐induced renal damage, Cd in blood mainly reflects recent exposure whereas Cd in urine is a satisfactory indicator of the amount of Cd stored in the kidney.