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Copper sulfate

Sulfuric acid copper(2+) salt (1:1);Copper(2+) sulfate (1:1);Blue stone;Blue vitriol;Cupric sulfate;Cupric sulfate anhydrous;Cupric sulphate;Roman vitriol;Copper sulfate (CuSO4);Copper(II) sulfate;Copper sulfate;Copper monosulfate;Copper sulfate (1:1);Copper(2+) sulfate;Blue Copper;Incracide E 51;Incracide 10A;Hylinec;Monocopper sulfate;MAC 570;Cuivrol;Delcup;Bluestone;EarthTec;Sulfuric acid,copper(2+) salt (1:1);Mastercop;Upinorg;Reducer Cu;Baijunling;Black blue stone;Sulfuric acid,monocopper(1+) salt;XWHGS 005;131540-94-8;139939-69-8

7758-98-7

CuSO4

ARUVKPQLZAKDPS-UHFFFAOYSA-L

159.61

248.934158

231-847-6

KUW2Q3U1VV

0751

3288|3077

DTXSID6034479

Grayish-white to greenish-white rhombic crystals or amorphous powder /SRP: somewhat wet/; White when dehydrated; Gray to white and has rhombic crystals

V - Various

2833250000

Inorganic Bases

88.6

Cupric sulfate appears as a white or off-white solid. Melting point 200 °C with decomposition. Non-combustible.; Dry Powder; Large Crystals; Liquid; Liquid; Other Solid; Dry Powder; Wet Solid; Large Crystals; Dry Powder; Wet Solid; CBI; Grayish-white to greenish-white solid; Hygroscopic; Soluble in water; [Merck Index] White odorless crystalline solid; Soluble in water (316 g/L at 20 deg C); [MSDSonline]; WHITE HYGROSCOPIC CRYSTALS.

-0.25970

Slightly greenish to gray powder

2.29 at 59 °F (USCG, 1999) - Denser than water; will sink; 3.6; 3.6 g/cm³; 3.6 @25 °C

590; 590 °C decomp

650; 650 °C (decomp to cupric oxide)

INDICES OF REFRACTION: 1.733, 1.724, 1.739

Very soluble in hot water, soluble cold water; Soluble in methanol (1.1 g/100 ml), but insoluble in ethanol; it readily dissolves in aqueous ammonia and excess alkali metal cyanides, with the formation of complexes; In water, 243 g/l @ 0 °C.; 75.4 g/100 cc water @ 100 °C; 1.04 g/100 cc methanol @ 18 °C; Solubility in water, g/l at 20 °C: 203 (freely soluble)

KEEP TIGHTLY CLOSED.

7.3 mm Hg ( 25 °C)

For healthy, non-occupationally-exposed humans the major route of exposure to copper is oral. The mean daily dietary intake of copper in adults ranges between 0.9 and 2.2 mg. ... In some cases, drinking water may make a substantial additional contribution to the total daily intake of copper, particularly in households where corrosive waters have stood in copper pipes. ... All other intakes of copper (inhalation and dermal) are insignificant in comparison to the oral route. Inhalation adds 0.3-2.0 ug/day from dusts and smoke. Women using copper IUDs are exposed to only 80ug or less of copper per day from this source. The homeostasis of copper involves the dual essentiality and toxicity of the element. Its essentiality arises from its specific incorporation into a large number of proteins for catalytic and structural purposes. The cellular pathways of uptake, incorporation into protein and export of copper are conserved in mammals and modulated by the metal itself. Copper is mainly absorbed through the gastrointestinal tract. From 20 to 60% of the dietary copper is absorbed, with the rest being excreted through the feces. Once the metal passes through the basolateral membrane it is transported to the liver bound to serum albumin. The liver is the critical organ for copper homeostatis. The copper is partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The primary route of excretion is through the bile. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular weight complexes. ... The biochemical toxicity of copper, when it exceeds homeostatic control, is derived from its effects on the structure and function of biomolecules, such as DNA, membranes and proteins directly or through oxygen-radical mechanisms. The toxicity of a single oral dose of copper varies widely between species. ... The major soluble salts (copper(II) sulfate, copper(II) chloride) are generally more toxic than the less soluble salts (copper(II) hydroxide, copper (II) oxide). Death is preceded by gastric hemorrhage, tachycardia, hypotension, hemolytic crisis, convulsions and paralysis. ... Long-term exposure in rats and mice showed no overt signs of toxicity other than a dose-related reduction in growth after ingestion ... The effects included inflammation of the liver and degeneration of kidney tubule epithelium. ... Some testicular degeneration and reduced neonatal body and organ weights were seen in rats ... and fetotoxic effects and malformations were seen at high dose levels. ... Neurochemical changes have been reported after oral administration ... A limited number of immunotoxicity studies showed humoral and cell-mediated immune function impairment in mice after oral intakes in drinking-water ... Copper is an essential element and adverse health effects /in humans/ are related to deficiency as well as excess. Copper deficiency is associated with anemia, neutropenia and bone abnormalities but clinically evident deficiency is relatively infrequent in humans. .. Except for occasional acute incidents of copper poisoning, few effects are noted in normal /human/ populations. Effects of single exposure following suicidal or accidental oral exposure have been reported as metallic taste, epigastric pain, headache, nausea, dizziness, vomiting and diarrhea, tachycardia, respiratory difficulty, hemolytic anemia, hematuria, massive gastrointestinal bleeding, liver and kidney failure, and death. Gastrointestinal effects have also resulted from single and repeated ingestion of drinking-water containing high copper concentrations, and liver failure has been reported following chronic ingestion of copper. Dermal exposure has not been associated with systemic toxicity but copper may induce allergic responses in sensitive individuals. Metal fume fever from inhalation of high concentrations in the air in occupational settings have been reported ... A number of groups are described where apparent disorders in copper homeostasis result in greater sensitivity to copper deficit or excess than the general population. Some disorders have a well-defined genetic basis. These include Menkes disease, a generally fatal manifestation of copper deficiency; Wilson disease (hepatolenticular degeneration), a condition leading to progressive accumulation of copper; and hereditary aceruloplasminemia, with clinical symptoms of copper overload. Indian childhood cirrhosis and idiopathic copper toxicosis are conditions related to excess copper which may be associated with genetically based copper sensitivity ... These are fatal conditions in early childhood where copper accumulates in the liver. ... Other groups potentially sensitive to copper excess are hemodialysis patients and subjects with chronic liver disease. Groups at risk of copper deficiency include infants (particularly low birth weight/preterm babies, children recovering from malnutrition, and babies fed exclusively with cow's milk), people with maladsorption syndrome (e.g., celiac disease, sprue, cystic fibrosis), and patients on total parenteral nutrition. Copper deficiency has been implicated in the pathogenesis of cardiovascular disease. The adverse effects of copper must be balanced against its essentiality. Copper is an essential element for all biota ... At least 12 major proteins require copper as an integral part of their structure. It is essential for the utilization of iron in the formation of hemoglobin, and most crustaceans and molluscs possess the copper-containing hemocyanin as their main oxygen-carrying blood protein. ... A critical factor in assessing the hazard of copper is its bioavailablity. Adsorption of copper to particles and complexation by organic matter can greatly limit the degree to which copper will be accumulated ... At many sites, physiochemical factors limiting bioavailability will warrant higher copper limits. ... Excess copper is sequestered within hepatocyte lysosomes, where it is complexed with metallothionein. Copper hepatotoxicity is believed to occur when the lysosomes become saturated and copper accumulates in the nucleus, causing nuclear damage. This damage is possibly a result of oxidative damage, including lipid peroxidation. Copper inhibits the sulfhydryl group enzymes such as glucose-6-phosphate 1-dehydrogenase, glutathione reductase, and paraoxonases, which protect the cell from free oxygen radicals. It also influences gene expression and is a co-factor for oxidative enzymes such as cytochrome C oxidase and lysyl oxidase. In addition, the oxidative stress induced by copper is thought to activate acid sphingomyelinase, which lead to the production of ceramide, an apoptotic signal, as well as cause hemolytic anemia. Copper-induced emesis results from stimulation of the vagus nerve. (L277, T49, A174, L280) No indication of carcinogenicity to humans (not listed by IARC). People must absorb small amounts of copper every day because copper is essential for good health, however, high levels of copper can be harmful. Very-high doses of copper can cause damage to your liver and kidneys, and can even cause death. Copper may induce allergic responses in sensitive individuals. (L278, L279) The substance can be absorbed into the body by inhalation of its aerosol and by ingestion. Oral (L277) ; inhalation (L277) ; dermal (L277) Cough. Sore throat. Redness. Pain. Redness. Pain. Blurred vision. Abdominal pain. Burning sensation. Nausea. Vomiting. Diarrhoea. Shock or collapse. Breathing high levels of copper can cause irritation of the nose and throat. Ingesting high levels of copper can cause nausea, vomiting, diarrhea, headache, dizziness, and respiratory difficulty. (L278, L279) Chemical: COPPER SULFATE Occupational hepatotoxin - Secondary hepatotoxins: the potential for toxic effect in the occupational setting is based on cases of poisoning by human ingestion or animal experimentation. Methemo

Pleasant odor

On heating dec above 560 degree|Hydroscopic, with conversion to the pentahydrate in moist air below 30 °C|Dielectric constant: 10.3 @ 17 to 22 °C

Soluble in water.

Salts, Acidic

Anhydrous CUPRIC SULFATE serves as a weak oxidizing agent. Causes hydroxylamine to ignite. Gains water readily. The hydrated salt is vigorously reduced by hydroxylamine [Mellor 8:292(1946-1947)]. Both forms are incompatible with finely powdered metals. Both are incompatible with magnesium, corrode steel and iron, may react with alkalis, phosphates, acetylene gas, hydrazine, or nitromethane, and may react with beta-naphthol, propylene glycol, sulphathiazole and triethanolamine if the pH exceeds 7 (NTP, 1992). Both act as acidic salts, corrode metals and irritate tissues.

Not flammable (USCG, 1999)