Cadmium uptake from feed and its distribution to food products of livestock.

Distribution of cadmium (Cd) into the edible products of three species of food-producing animals was investigated during long-term dietary administration of supplemental cadmium chloride. Cows were exposed to 0.2 (control), 2.4, and 11.3 ppm Cd on whole ration basis for a period of three months followed by a three-month period on control ration. No accumulation of Cd occurred in milk, muscle, or bone at any of the time periods. A dose-related increase of Cd was observed in liver and kidney. The Cd concentration in these organs showed a gradual rise even when the animals were given control ration for three months after an initial three-month exposure to Cd; this observation suggests a mobilization and redistribution of this metal from other tissues. Dietary Cd levels in swine rations were 0.2, 2.4, and 10.1 ppm. The highest level of Cd produced a slightly reduced growth rate in swine. No accumulation of Cd was observed in muscle, bone, or brain. Liver and kidney showed a treatment and time-related increase in cadmium values at 6 and 12 weeks on experiment. During a three-month depletion phase after an initial three months of Cd administration, no further change in liver and kidney Cd levels was observed. White Leghorn chickens were treated by administering 0.3, 1.9, and 13.1 ppm Cd in their diets for up to 6 months. No accumulation of Cd occurred in eggs or bones. A slight increase of Cd level was observed in chicken muscle after six months of exposure. Liver and kidney had the highest levels of Cd, which showed a dose and time-related increase in these organs. No depletion of liver and kidney Cd was seen during seven weeks following a six-week treatment period. In all three species, the kidney Cd levels were severalfold higher than those of liver at all dietary levels. In swine, the renal cortex and medulla had similar Cd concentration in control animals but in all animals exposed to supplemental Cd, a dramatic rise in Cd levels in renal cortex was observed. Medullary Cd did not show a proportional time and dose-related increase in Cd levels, although the levels showed some increase. In kidney and liver of all three species the Cd levels showed a positive correlation with the amount of Cd-binding protein in these tissues. Induced levels of this metal-binding protein may explain accumulation and persistence of Cd-residues in these organs. In all three species, the concentrations of renal Cd-binding protein increased at a rate greater than those in liver. Although the food-producing animals may act as an effective filter of Cd in the case of an environmental increase of this metal, consumption of visceral organs from such animals may pose a hazard. This is particularly critical since the daily intake of Cd in human diet is already estimated to exceed the tolerance limits suggested by WHO/FAO.