Cobalt toxicity

Produced by Neurospora crassa on low iron medium or in cobalt-toxic media. Iron-deficient cells (mycelia) of N. crassa take up iron more rapidly from XFe59 than from Fe59Cl3 or Fe59 citrate. 

Padmanaban, G. and P. S. Sarnia An iron-binding compound from cobalt-toxic cultures of Neurospora crassa. Arch. Biochem. Biophys. 108, 362 (1965). 

Henretig F, Joffe M, Baffa G, etal. (1998) Elemental cobalt toxicity and effects of chelation therapy. Veterinary and Human Toxicology 30 372-378. 

Cobalt toxicity is occasionally found in high-Co soils formed from serpentinite and other ultrabasic rocks. Deficiency is most likely in coarse-textured, acid-leached soils alkaline or calcareous soils and humus-rich soils. Extractability by strong acids can range from very little (< 1%) to a large fraction (>30%) of the total Co, depending on the forms of Co in the soil. 

Symptoms of chronic cobalt toxicity in humans occurred in anemic persons undergoing therapy with iron supplements to which cobalt was added to promote iron absorption and to stimulate erythropoiesis. Depending on the degree of iron deficiency and the amount of iron supplement prescribed, patients thus treated could typically receive from 0.17 to 3.19 mg Co kg per day over periods of days to many months. 

Cobalt toxicity symptoms in these patients included anorexia, nausea, vomiting, diarrhea, substernal aches, erythema, skin rashes, tinnitus, and neurogenic deafness. In some of the cobalt-treated patients paresthesias, numbness and other neurological signs developed, while others suffered optic nerve damage (Herndon etal. 1980). Erythema and several of the other symptoms can be directly attributed to the cobalt-induced stimulation of erythropoie-sis, leading to polycythemia. 

Lock, K., K.A. De Schamphelaere, S. Becaus, et al. 2006. Development and validation of an acute biotic ligand model (BLM) predicting cobalt toxicity in soil to the potworm Enchytraeus albidus. Soil Biology and Biochemistry 38 1924—1932. 

A healthy 46-year-old patient developed progressively worsening symptoms of cobalt toxicity following 6 months of synovectomy and replacement of ceramic-on-ceramic hip bearing to a metal-on-polyethylene bearing. Blood cobalt concentration peaked at 6521 p /L. The patient died from cobalt-induced cardiomyopathy. Implant retrieval analysis confirmed a loss qf28.3g mass cfthe cobalt-chromium femoral head as a result of severe abrasive wear by ceramic particles embedded in the revision polyethylene liner [83 ]. 

Pregnancy The cobalt toxicity concerns become higher in the case of women posing a risk during pregnancy owing to transplacental metal transfer. 

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, copper, molybdenum, iodine, iron, manganese, nickel, selenium, and zinc are sometimes provided to mminants. Mineral deficiency or toxicity in sheep, especially copper and selenium, is a common example of dietary mineral imbalance (21). Other elements may be required for optimal mminant performance (22). ExceUent reviews of trace elements are available (5,22). 

Cobalt difluoride, used primarily for the manufacture of cobalt trifluoride, CoF, is available from Advance Research Chemicals, Inc., Aldrich Chemicals, and PCR in the United States, Fluorochem in the UK, and Schuhardt in Germany. The 1993 price varied from 60 to 200/kg depending on the quantity and the price of cobalt metal. C0F2 is shipped as a corrosive and toxic material in DOT-approved containers. 

Pentafluorobenzene. Pentafluoroben2ene has been prepared by several routes multistage saturation—rearomati2ation process based on fluorination of ben2ene with cobalt trifluoride reductive dechlorination of chloropentafluoroben2ene with 10% pabadium-on-carbon in 82% yield (226,227) and oxidation of penta uorophenylbydra2ine in aqueous copper sulfate at 80°C in 77% yield (228). Its ioni2ation potential is 9.37 V. One measure of toxicity is LD q = 710 mg/kg (oral, mouse) (127). 

Copper sulfate, in small amounts, activates the zinc dust by forming zinc—copper couples. Arsenic(III) and antimony(TTT) oxides are used to remove cobalt and nickel they activate the zinc and form intermetaUic compounds such as CoAs (49). Antimony is less toxic than arsenic and its hydride, stibine, is less stable than arsine and does not form as readily. Hydrogen, formed in the purification tanks, may give these hydrides and venting and surveillance is mandatory. The reverse antimony procedure gives a good separation of cadmium and cobalt. 

Fire Hazards - Flash Point Not flammable Flammable Limits in Air (%) Not flammable Fire Extinguishing Agents Not pertinent Fire Extinguishing Agents Not To Be Used Not pertinent Special Hazards of Combustion Products Toxic cobalt oxide fumes form during fires Behavior in Fire No data Ignition Temperature Not pertinent Electrical Hazard Not pertinent Burning Rate Not pertinent. 

The first major use of titanium dioxide was as a replacement for toxic lead compounds in paint It combines a brilliant white color with very high covering power. Addition of certain compounds of nickel changes the white color to yellow cobalt compounds give a green paint. 

Trace metals can serve as essential nutrients and as toxic substances (Sunda et al, 1991 Frausto da Silva and Williams, 1991). For example, cobalt is a component of vitamin B-12. This vitamin is essential for nitrogen fixing algae. In contrast, copper is toxic to marine phytoplankton at free ion concentrations similar to those found in seawater (Sunda and... 

In a different way, metallic-core nanoparticles [346-349] (prepared cf. Section 3.10) equipped with biocompatible coats such as L-cysteine or dextrane may be exploited for highly efficient and cell-specific cancer cell targeting, i.e., for improving diagnosis and therapy of human cancer. In a recent proof-of-principle experiment an unexpectedly low toxicity of the L-cysteine-covered cobalt nanoparticles was demonstrated [433] For diagnostic purposes, it is expected to use the advantageous magnetic properties of the metallic-core nanoparticles to obtain a contrast medium for MRI with considerably increased sensitivity, capable to detect micro-metastases in the environment of healthy tissues [434 37]. 

Potassium thiocyanate, cobalt(ll) chloride, and hydrochloric acid are toxic. 

Coprecipitation is a partitioning process whereby toxic heavy metals precipitate from the aqueous phase even if the equilibrium solubility has not been exceeded. This process occurs when heavy metals are incorporated into the structure of silicon, aluminum, and iron oxides when these latter compounds precipitate out of solution. Iron hydroxide collects more toxic heavy metals (chromium, nickel, arsenic, selenium, cadmium, and thorium) during precipitation than aluminum hydroxide.38 Coprecipitation is considered to effectively remove trace amounts of lead and chromium from solution in injected wastes at New Johnsonville, Tennessee.39 Coprecipitation with carbonate minerals may be an important mechanism for dealing with cobalt, lead, zinc, and cadmium. 

In July, 1970, 14 trace elements were known to be essential to human health. One of these is cobalt. Yet at least one researcher suggests that the addition of small amounts of cobalt to stabilize beer foam may have resulted in the deaths of a number of people in Minneapolis and Omaha. He theorizes that cobalt was necessary to activate the toxicity of selenium, which is naturally present in those areas. This is another example of a synergistic affect. Separately neither would have been harmful, but together they could cause fatalities. 

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