Toxicity excessive cobalt

Cohall is present in vitamin Bi to Ihe extent of about 4ci-. Lack of cobalt in tlie soil and feedstuffs prevents tuniinants from synthesizing all of the vilamin B j for their needs. Thus, cobalt can be added to feedstuffs as the chloride, sulfate, oxide, nr carbonate. Excessive cobalt intakes are toxic, causing a reduction in feed intake and body weight, accompanied by emaciation, anemia, debility, and elevated levels of cobull in the liver. It is of interest to note that clinical coball tnxiciiy closely resembles clinical cobalt deficiency. 

At one time, cobalt chloride, a salt of the metal cobalt, was added to beer in the USA as a foam stabilizer. Such salts had been used to treat people with anaemia at doses of 300 mg per day without any apparent problems. However, heavy beer drinkers, who drank about 10 litres per day, suffered effects on the heart, known as cardiomyopathy, a degeneration of the heart muscle, which was eventually ascribed to the cobalt. It transpired that, while cobalt alone was apparently not toxic to the heart, even at single doses many times higher than the exposure from the additive in beer, in the exceptionally heavy drinkers the toxic effects of cobalt were greatly increased. It turned out that the victims were malnourished individuals and deficient in particular amino acids, which was an important factor in increasing the toxicity of the cobalt. Furthermore, the excessive alcohol intake was itself an additional factor. The potentiation of the toxicity of cobalt was unexpected and so had not been taken into account in the safety assessment. This illustrates the difficulty of anticipating all possible circumstances in safety evaluation. 

Although an excess of cobalt can be toxic to animals, there is a wide margin of safety between the nutritional requirement and the toxic level. Cobalt toxicosis is extremely unlikely to occur under practical farming conditions. Unlike copper, cobalt is poorly retained by the body tissues and an excess of the element is soon excreted. The toxic level of cobalt for cattle is 1 mg cobalt/kg body weight daily. Sheep are less susceptible to cobalt toxicosis than cattle and have been shown to tolerate levels up to 3.5 mg/kg. Excessive cobalt supplementation of ruminant diets can lead to the production of analogues of vitamin B12 and a reduction in the quantity of the true vitamin. Cobalt compounds pose a risk to human health as they cause cancer if inhaled and they irritate the skin for this reason, their use has been restricted in the... 

TOXICITY. Cobalt toxicity is not likely to result from the consumption of normal foods and beverages, because there is a very wide margin between essential and harmful levels. Excess cobalt intake in man results in an increase in the number of red blood cells, a disorder known as poly-cythemia. 

Cobalt is found in most natural foods. Although a necessary trace element, it is toxic to humans if ingested in large amounts. The human body does excrete in urine excessive amounts of cobalt compounds such as found in vitamin B ... 

Cobalt is an essential element that is part of vitamin B12, or cobalamin, a coenzyme that is essential in the formation of proteins, nucleic acids, and red blood cells. Although cobalt poisoning is not common, excessive levels can be harmful. Most cases of human exposure to toxic levels of cobalt have occurred through inhalation in the workplace. Many exposures have been suffered by workers working with hard metal alloys of cobalt and tungsten carbide, where very fine particles... 

The toxicity of excessive Co, in part, appears to be an interaction with anemia resulting from decreased iron absorption. In rats, the intestinal absorption of iron is reduced by almost two-thirds in the presence of the ten-fold higher cobalt absorption (Underwood 1984). 

Sulfur has an antagonistic effect on several essential trace elements. Excessive amounts of sulfur can induce a secondary deficiency of copper (mainly in animals), cobalt and selenium. Ho vever, not only the sulfur amino acid cysteine but also sulfate eliminates the adverse effects of copper-, cobalt-or selenium-based toxicities (Baker and Czarnecki-Maulden 1987). Sulfate increases the urinary loss of selenate, but not of selenite this explains the assumption that there is a direct antagonism between sulfate and selenate (Schrauzer 1998). 

Millikan, C. R. (1947). Effect of molybdenum on the severity of toxicity symptoms in flax induced by an excess of either manganese, zinc, copper, nickel, or cobalt in the nutrient solution. 7. Aust. Inst. Agric. Sci. 13 180-6. 

It may be noted that many toxic metals are also essential for the body, at trace levels. Their absence from the diet can produce various deficiency syndromes and adverse health effects. Such essential metals include selenium, copper, cobalt, zinc, and iron. On the other hand, excessive intake can produce serious adverse reactions. Also, a number of metals, such as aluminum, bismuth, lithium, gold, platinum, and thallium, have been used in medicine. Despite their beneficial effects, excessive intake of these metals and their salts can cause serious poisoning. 

Heavy metals ate potentially dangerous toxicants which are the destabilizing factor in the ecological system of established biocoenosis. lead, cadmium, meicuiy, cobalt, and other heavy metals may be inducers of the oxidative stress, which is based on formation of excessive quantity of free radicals [1, 2], Their reactivity is extremely high and initiates chain oxidation reaction. Free radicals become the reason for serious functional disorders, because various cell components are damaged [3]. Initiation of hpid peroxidation in biological membranes is an example and promotes disturbance of their structure and penetrability increase. Specialized enzymatic and nonenzymatic antioxidant systerrrs are protection against free radicals [4]. 

The excess of cobalt is toxic and leads to polycythemia, i ., an increase in the number of RBC in the blood. The deficiency of cobalt causes ... 

---