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Cobalt intake

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. [Pg.412]

Human dietary cobalt intakes are in the order of 10-30 jg per day. A detailed dietary intake study in Canada by Dabeka and McKenzie (1995) resulted in an average intake of 11 Jg Co per day, equivalent to 0.18 J,g per day for a 60-kg adult. This agrees with UK estimates of 11 to 28 j,g per day (Steering Group of Food Surveillance 1985) and of 20 to 40 jg per day by Smith and Carson (1980). The almost tenfold higher older intake estimates of Schroeder et al. (1967) and of Snyder et al. [Pg.830]

In itself, however, the elevation of soil cobalt content normally associated with urban areas cannot be regarded as presenting any problems. The toxicity of cobalt for grazing stock is low and the uptake of cobalt from contaminated soils is so restricted that it could not possibly produce toxic levels of cobalt in herbage. Although cases of poisoning in both cattle and sheep have been reported [319, 320] when stock have been repeatedly dosed directly with cobalt salts over a long period of time, the levels of cobalt intake involved were of a different... [Pg.145]

Cobalt intake in average U.S. diet—Estimates of the average cobalt intake of adults in the United States range from 0.14 to 0.58 mg per day. [Pg.211]

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. [Pg.211]

The amount of each element required in daily dietary intake varies with the individual bioavailabihty of the mineral nutrient. BioavailabiUty depends both on body need as deterrnined by absorption and excretion patterns of the element and by general solubiUty, and on the absence of substances that may cause formation of iasoluble products, eg, calcium phosphate, Ca2(P0 2- some cases, additional requirements exist either for transport of substances or for uptake or binding. For example, calcium-binding proteias are iavolved ia calcium transport an intrinsic factor is needed for vitamin cobalt,... [Pg.374]

Dabeka RW. 1989. Survey of lead, cadmium, cobalt, and nickel in infant formulas and evaporated milks and estimation of dietary intakes of the elements by infants 0-12 months old. Sci Total Environ... [Pg.506]

These are classified as those with a requirement below one pg (microgram) per day. Elements in this class include boron, chromium, fluoride, iodine, molybdenum, nickel, selenium, cobalt and manganese. Cobalt is part of vitamin (see above). However, there appear to be no recommended dietary intakes for any of these except molybdenum. [Pg.347]

Cobalt in small amounts is an essential element associated with vitamin B12, but at high levels can be toxic. There are no daily recommended intake levels for cobalt. Intestinal bacteria use cobalt to produce cobalamin, which in turn is an essential component of vitamin B12. Industrially, cobalt is used in pigments, permanent magnets, and as an alloy to harden metals as in tungsten carbide blades or drills. [Pg.127]

R.W. Dabeka, A.D. McKenzie, Survey of lead, cadmium, fluoride, nickel, and cobalt in food composites and estimation of dietary intakes of these elements by Canadians in 1986-1988, J. AOAC Int. 78 (1995) 897-909. [Pg.545]

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. [Pg.281]

At normal levels of iron intake, absorption requires uptake from the intestinal lumen by the mucosa and transfer from the mucosa to the portal blood. Both events are inversely affected by the state of body iron stores. In iron deficiency states, nonferrous metals such as cobalt and manganese, which have an ionic radius similar to that of iron and form octahedral complexes with six-coordinate covalent bonds, also are absorbed at an increased rate. Oral administration of a large dose of iron reduces (or temporarily inhibits) the absorption of a second dose of iron by the absorptive enterocytes even in the presence of systemic iron deficiency. The mechanism of mucosal block, which resists acquiring additional iron by the en-teroeytes with high amounts of intracellular iron, is not yet understood. It probably involves set points established in the enterocytes for iron recently consumed in the diet (dietary regulator). [Pg.677]

Ruminants require cobalt for the bacterial biosynthesis of vitamin B12 in the first stomach. Cobalt-deficient sheep or cattle show diminished feed intakes and weight loss. In cows, milk production declines and the fre-... [Pg.830]

Thomson ABR and Valbeeg LS (1972) Intestinal intake of iron, cobalt and manganese in the iron-dficient rat. Am J Physiol 223(6) 1327—1329. [Pg.840]

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. [Pg.651]

Cobalt is an essential element. Its deficiency can result in pernicious anemia. It is present in vitamin B12. Excessive intake of this element may result in polycythemia or overproduction of erythrocytes and heart lesions. Exposure to its dusts can produce cough and respiratory irritation. Chronic inhalation of its dusts or fumes can decrease pulmonary functions and may cause diffuse nodular fibrosis and other pulmonary diseases. Skin contact may induce dermal hypersensitivity reactions, producing an allergy-type dermatitis. [Pg.663]

Cardiac disorders include various dysrhythmias associated with potassium and magnesium depletion and poor caloric intake ( Holiday heart ) and cardiomyopathy, which has been associated with long-term alcohol use as well as with ingestion of cobalt (which was once used to stabilize beer). [Pg.191]

It seems that the daily intake of cobalt by humans is about 5-45 ixg [5-7]. The recommended daily intake of vitamin B12 for adults is 3 ji.g (0.13 xg of Co) [5,8], taking into account that only 50% is absorbed in the intestine [9]. [Pg.334]

Samples such as hair, nails, blood, urine, and various tissues are analyzed by NAA for both essential and toxic trace elements (Bhandari et al. 1987, Lai et al. 1987). The analysis can be related to determine their effect on disease outcomes. These authors have reported that the diet and environment contribute largely towards the trace elements in the human body. It is has been demonstrated in other works that the selenium concentration in human nails is an accurate monitor of the dietary intake of selenium. As a consequence, the nail monitor has been extensively used to study the protective effect of dietary selenium against cancer and heart disease in numerous prospective case-control studies. In another study by Kanabrocki et al. (1979) on human thumbnails in USA, using thermal NAA technique, the average concentration of metals studied in clinically symptom-free adult female and male subjects were found to be zinc, 184 vs. 153 ppm chromium, 6.8 vs. 4.2 selenium, 0.9 vs. 0.6 gold, 2.6 vs. 0.4 mercury, 1.9 vs. 0.4 silver 0.7 vs. 0.3 cobalt, 0.07 vs. 0.04. In another study, the fluorine concentration in bone biopsy samples was... [Pg.263]


See other pages where Cobalt intake is mentioned: [Pg.830]    [Pg.833]    [Pg.830]    [Pg.833]    [Pg.388]    [Pg.334]    [Pg.1736]    [Pg.98]    [Pg.408]    [Pg.1782]    [Pg.379]    [Pg.412]    [Pg.1005]    [Pg.166]    [Pg.36]    [Pg.7]    [Pg.350]    [Pg.3193]    [Pg.314]    [Pg.231]    [Pg.2565]    [Pg.770]    [Pg.836]    [Pg.1214]    [Pg.3192]    [Pg.375]    [Pg.731]   
See also in sourсe #XX -- [ Pg.830 ]




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