Salt and Trace Minerals for Livestock, Poultry and Other Animals
TRACE MINERALS AND CADMIUM TOXICITY
Traditionally cadmium toxicity was associated with the waste from mining and smelting of metals such as zinc and lead and with municipal sewage sludge. Recently cadmium has been detected at high levels in some phosphate and zinc sulfate fertilizers. Some researchers suspect that cadmium is being taken up by certain plants and thus plays a greater role in fescue toxicosis and grass tetany then previously believed. The concentrations of calcium, copper, zinc, iron, and selenium in the diet can have a dramatic effect on cadmium absorption and metabolism.
Cadmium toxicity and metabolism:
Cadmium has been shown to manifest its toxicity in animals by accumulating in most organs with the kidney being the main target organ. It causes the loss of proteins in the urine both from the blood and the kidney itself. Cadmium is also toxic to the central nervous system. It causes alterations of cellular functions in lungs. It affects both humoral and cell mediated immune response in animals.
Cadmium toxicity is directly related to cadmium absorption and retention because the half-life in some tissues, such as kidney, liver and gastrointestinal tract is measured in years. Trace mineral nutrition and calcium levels are the most important factors affecting cadmium absorption in most practical diets. When copper zinc, iron and selenium are adequate, less than 1% of the cadmium consumed ends up being absorbed in most ruminants (347). Adequately nourished cows only retained 0.75% of the oral dose after 14 days, but 0.13% was still present after 131 days (346).
Zinc and copper have similar electron configurations in the outer shell as cadmium. Thus these elements are often antagonistic in that exposure to cadmium will lower the copper status, and increasing zinc consumption will lower cadmium uptake and retention (341). Similarly, increasing selenium intake reduces the toxicity of cadmium by shifting the tissue distribution of cadmium from metallothionein to high-molecular-mass proteins that are more easily excreted.
High cadmium intakes (> 40 ppm in diet) cause symptoms similar to a zinc deficiency and were prevented by zinc supplementation (344). The symptoms include loss of appetite, poor growth, retarded testicular development, and parakeratosis in sheep. When lower concentrations of cadmium were given to sheep that were marginal in their copper status, the symptoms resembled those of a copper deficiency, such as anemia, impaired bone mineralization, loss of wool crimp, abortion and stillbirths (343). When pregnant ewes were fed 3.0-3.4 ppm cadmium in their diets, copper status was impaired to the point that the crimp in the wool was compromised. However, when excess zinc (750 ppm) was added to the diet, the effects on copper status were reduced (342).
In cattle, feeding 5 ppm cadmium during gestation reduced liver copper concentration in the newborn calves by 29%. Feeding 1 ppm cadmium to the gestating cows was sufficient to reduce liver copper stores by 40% (345). Because cattle are susceptible to copper deficiency, excess cadmium is more likely to be detected as a copper deficiency than in other species. Kidney and liver cadmium concentrations increased 5-8 fold when grazed pastures were fertilized with sewage sludge for eight years. However, no histological kidney damage was noted because maximal kidney concentrations were 32 ppm on a fresh weight basis, which is well under the 200 ppm in humans required to cause kidney damage (219).
Ammerman et al. (339) reported the interactions of cadmium and zinc in poultry. Turkey poults fed 2 ppm cadmium had hock and feather abnormalities on a low-zinc diet (10 ppm), but not on a high-zinc diet (60 ppm). However, when 20 ppm cadmium was fed, the 60 ppm zinc did not prevent deficiency symptoms. In poultry, diets containing 60-75 ppm cadmium will reduce egg production, delay testes development in males and cause kidney damage. When rats are fed low-zinc diets, as little as 1.5 ppm cadmium can reduce blood copper and inhibit bone mineralization. In rats, 6 ppm cadmium was found to have the same inhibitory affect on copper absorption as 1000 ppm zinc (342). Confirmation of cadmium toxicity in non-ruminants is best achieved by measuring kidney cadmium concentrations and the presences of histological kidney damage.
Dr. Swerczek a veterinary pathologist at the University of Kentucky has proposed the concept that cadmium may play a role in grass tetany and other induced mineral deficiencies (340). Some plants such as tobacco stalks appear to concentrate cadmium from phosphate fertilization and when these stalks are spread on pastures the cadmium leaches out and is taken up by the grass. Many of the signs associated with grass tetany are similar to cadmium toxicity. It is possible that cadmium, even in very low concentrations in the forages, may have a greater impact on animal health than previously recognized.
Traditionally cadmium toxicity was associated with mining of zinc and lead, and with the application of municipal sewage sludge to pasture. However, the detection of cadmium in some phosphate and zinc sulfate fertilizers means that livestock producers need to be aware of the possibility of cadmium toxicity in environments where it has not been a problem previously. Dietary copper, zinc, iron and selenium can have a major impact on cadmium absorption and retention. Feeding a well-fortified trace mineral salt is the first line of defense to minimize the risk of cadmium toxicity in livestock and poultry.
Copyright: 2006