Copper sulfate

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

88.6

-0.25970

Slightly greenish to gray powder

3.6 g/cm³

590 °C (decomp)

650 deg C (decomp to cupric oxide)

INDICES OF REFRACTION: 1.733, 1.724, 1.739

H2O: 203 g/L (20 ºC)

Store at +5°C to +30°C.

7.3 mm Hg ( 25 °C)

Oral-Rat LD50: 300 mg/kg

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)

III

6.1

UN 3288 6.1/PG 3

2

36/38-50/53-22-51/53-36/37/38

24/25-36-60-61-22-26

GL8800000

Xn,N,Xi

Treasury is ventilated, low temperature and dry; store and transport separately from food

hygroscopic

P273-P501

H410

SRP: At the time of review, criteria for land treatment or burial (sanitary landfill) disposal practices are subject to significant revision. Prior to implementing land disposal of waste residue (including waste sludge), consult with environmental regulatory agencies for guidance on acceptable disposal practices.|Group III Containers (both combustible and non-combustible) that previously held organic mercury, lead, cadmium, arsenic, or inorganic pesticides should be triple rinsed, punctured and disposed of in a sanitary landfill. Non-rinsed containers should be encapsulated and buried at a specially designated landfill site. /Organic mercury, lead, cadmium, arsenic, or inorganic pesticides/|The following wastewater treatment technologies have been investigated for copper (II) sulfate: activated carbon.|Add slowly to a large container of water. Stir in slight excess of soda ash. Let stand for 24 hr. Decant or siphon into another container and neutralize with 6 M HCl. ... The sludge may be added to landfill. Recommendable methods: Precipitation, solidification, & landfill. Peer-review: ... Copper can be recovered by cation exchange. (Peer-review conclusions of an IRPTC expert consultation (May 1985))

Anhydrous copper sulfate causes hydroxylamine to ignite & the hydrated salt is vigorously reduced.|Solutions of sodium hypobromite are decomposed by powerful catalytic action of cupric ions, even as impurities. /Cupric salts/

In accordance with 21 CFR 184.1(b)(1), the ingredient is used in food with no limitation other than current good manufacturing practice. The affirmation of this ingredient as generally recognized as safe (GRAS) as a direct human food ingredient is based upon the following current good manufacturing practice conditions of use: 1) The ingredient is used as a nutrient supplement as defined in 21 CFR 170.3(o)(20) of this chapter and as a processing aid as defined in 21 CFR 170.3(o)(24) of this chapter. 2) The ingredient is used in food at levels not to exceed current good manufacturing practice. Copper sulfate may be used in infant formula in accordance with section 412(g) of the Federal Food, Drug, and Cosmetic Act (the act) or with regulations promulgated under section 412(a)(2) of the act. Prior sanctions for this ingredient different from the uses established in this section do not exist or have been waived.|Trace minerals added to animal feeds. These substances added to animal feeds as nutritional dietary supplements are generally recognized as safe when added are levels consistent with good feeding practice. Element: Copper; Source compound: copper sulfate. (All substances listed may be in anhydrous or hydrated form.)

Excerpt from ERG Guide 151 [Substances - Toxic (Non-combustible)]: Non-combustible, substance itself does not burn but may decompose upon heating to produce corrosive and/or toxic fumes. Containers may explode when heated. Runoff may pollute waterways. (ERG, 2016)|Not combustible. Gives off irritating or toxic fumes (or gases) in a fire.

|Warning|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P273, P280, P301+P312, P302+P352, P305+P351+P338, P321, P330, P332+P313, P337+P313, P362, P391, and P501|Danger|H302 (97.26%): Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P273, P280, P301+P312, P302+P352, P305+P351+P338, P310, P321, P330, P332+P313, P337+P313, P362, P391, and P501|Aggregated GHS information provided by 1180 companies from 35 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|Aggregated GHS information provided by 15 companies from 1 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.|H301: Toxic if swallowed [Danger Acute toxicity, oral]|P201, P202, P260, P261, P264, P270, P271, P272, P280, P281, P301+P310, P301+P330+P331, P302+P352, P303+P361+P353, P304+P340, P305+P351+P338, P307+P311, P308+P313, P310, P312, P314, P321, P330, P333+P313, P363, P403+P233, P405, and P501

Excerpt from ERG Guide 151 [Substances - Toxic (Non-combustible)]: As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. SPILL: Increase, in the downwind direction, as necessary, the isolation distance shown above. FIRE: If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions. (ERG, 2016)

Excerpt from ERG Guide 151 [Substances - Toxic (Non-combustible)]: Do not touch damaged containers or spilled material unless wearing appropriate protective clothing. Stop leak if you can do it without risk. Prevent entry into waterways, sewers, basements or confined areas. Cover with plastic sheet to prevent spreading. Absorb or cover with dry earth, sand or other non-combustible material and transfer to containers. DO NOT GET WATER INSIDE CONTAINERS. (ERG, 2016)

Filtering masks to minimize inhalation of dust. (USCG, 1999)|Personnel protection: ... Wear appropriate chemical protective gloves, boots and goggles.

If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire (material itself does not burn or burns with difficulty).

Environmental concerns - land spill: Dig a pit, lagoon,or holding area to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water.|Environmental concerns - water spill: Neutralize with agricultural lime (CaO), crushed limestone (CaCO3), or sodium bicarbonate (NaHCO3). Adjust pH to neutral (pH= 7). Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates.

Personnel protection: Keep upwind. ... Avoid breathing vapors or dusts. Wash away any material which may have contacted the body with copious amounts of water or soap and water.|If material not involved in fire: Keep material out of water sources & sewers. Build dikes to contain flow as necessary.|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants.|SRP: Contaminated protective clothing should be segregated in such a manner so that there is no direct personal contact by personnel who handle, dispose, or clean the clothing. Quality assurance to ascertain the completeness of the cleaning procedures should be implemented before the decontaminated protective clothing is returned for reuse by the workers.

A STRONG IRRITANT

Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 1 mg/cu m. /Copper (dusts and mists)/

Personal protection: particulate filter respirator adapted to the airborne concentration of the substance. Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Then store and dispose of according to local regulations.

Well closed. Dry.

Evaporation at 20 °C is negligible; a harmful concentration of airborne particles can, however, be reached quickly when dispersed, especially if powdered.

The substance is severely irritating to the eyes and skin. The aerosol is irritating to the respiratory tract. Corrosive on ingestion. Ingestion could cause effects on the blood, kidneys and liver. This may result in haemolytic anaemia, kidney impairment and liver impairment.

Repeated or prolonged inhalation of the aerosol may cause effects on the lungs. Ingestion may cause effects on the liver.

PREVENT DISPERSION OF DUST!

Use local exhaust or breathing protection.

Protective gloves.

Wear face shield or eye protection in combination with breathing protection.

Cupric sulfate is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 10 lb or 45.4 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

highly toxic

Acute oral toxicity (LD50): 300 mg/kg in rats [MSDS]. Copper sulfate ingestion (accidental or deliberate) is a rare form of poisoning usually limited to the Indian subcontinent. Though the rates are on the decline, it is essential that physicians are aware of its lethal complications and management strategies. The main complications of copper sulfate ingestion include intravascular hemolysis, methemoglobinaemia, acute kidney injury, and rhabdomyolysis. Severe gastrointestinal effects may occur with acute overdosage. In extreme or long-term overdosage, symptoms may be similar to those of Wilson's disease, a disease in which the liver does not filter copper adequately and copper accumulates in the liver, brain, eyes, and other organs. Gradually, high copper levels may cause life-threatening organ damage. Ingestion of more than 15 mg of copper has been reported to be toxic to humans. In a survey of human clinical case studies, 5.3 mg/day was the lowest oral dose at which local gastrointestinal irritation was seen. Ingestion of gram quantities of copper sulfate resulted in death by suicide, whereas less severe effects were reported from estimated copper doses of 40 to 50 mg from ingestion of carbonated beverages in contact with copper containers. Limited data are available on the chronic toxicity of copper. The hazard from dietary intakes of up to 5 mg/day appears to be low. Treatment of cupric sulfate toxicity is symptomatic and may involve the use of a chelating agent (e.g. penicillamine, trientine and zinc) to remove any excessive metal that has been absorbed. In addition, dialysis may be useful.|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. ...

Acute hepatotoxicity of copper is usually the result of ingestion of toxic amounts (1 to 10 g), often as a suicide attempt. In children, accidental poisoning can occur, particularly with ingestion of coins. Initial symptoms may be metallic taste and gastrointestinal distress due to gastric or small bowel erosions. Acute overdoses of copper can lead to early appearance of cardiovascular collapse, coma and death within hours. Liver injury tends to arise after 24 to 72 hours and is characterized by marked elevations in serum aminotransferase levels, minimal increases in alkaline phosphatase, early appearance of hepatic failure, and elevation in prothrombin time and ensuing jaundice. Shock and renal failure may also be present as well as rhabdomyolysis and severe hemolytic anemia. The overall clinical pattern of the liver injury is that of acute hepatic necrosis, and the hepatic manifestations resemble the acute toxicity of iron and zinc, and can be reproduced in animals. Shock and rhabdomyolysis may contribute to the serum enzyme elevations while hemolytic anemia may account for some of the increase in total bilirubin levels. Therapy of copper overdose includes gastric lavage, fluid replacement, dimercaprol (BAL) and penicillamine, with blood transfusions for hemolytic anemia and dialysis for acute renal failure.

THE IV INDUCED STIMULATION OF ALPHA-ADRENERGIC NERVOUS SYSTEM BY CUPRIC SULFATE WAS PARTIALLY ATTENUATED BY PRETREATMENT OF SHEEP WITH METHYSERGIDE. PHENOXYBENZAMINE COMPLETELY BLOCKED THE EFFECTS OF CUPRIC SULFATE & TREATMENT WITH PROPRANOLOL ENHANCED THE EFFECTS.|Acute copper (II) sulfate poisoning in the mouse induces renal tubular degeneration and necrosis. Administration of sodium 2,3-dimercaptopropane-sulfonate effectively prevented the development on the morphological sequelae of copper intoxication.|Pokeweed mitogen (PWM), a T cell-dependent polyclonal B cell activator, stimulates the differentiation of immunoglobin secreting cells from normal human peripheral blood mononuclear cells. ... Peripheral blood mononuclear cells failed to generate immunoglobin secreting cells in response to poke weed mitogen after brief exposure to D-penicillamine and copper sulfate; preincubation with either penicillamine or copper sulfate alone had no effect. Experiments utilizing purified populations of B and T cells indicated that penicillamine and copper sulfate markedly inhibited helper T cell activity but not B cell function.|Dimercaptosuccinic acid ... administered intragastrically to rabbits after sc administration of copper sulfate promoted urinary excretion.|For more Interactions (Complete) data for COPPER(II) SULFATE (10 total), please visit the HSDB record page.

LD50 Rat oral 300 mg/kg body weight LD50 Rabbit Oral 125 mg/kg body weight LD100 Mouse Oral 50 mg/kg body weight /from table/

About 80 percent of the absorbed copper is bound to liver metallothionein; the remainder is incorporated into cytochrome c oxidase or sequestered by lysosomes. The bioavailability of copper from the diet is about 65-70% depending on a variety of factors including chemical form, interaction with other metals, and dietary components.

Occurs in nature as mineral hydrocyanite.

... Copper sulfate ... may originate from mining and ore crushing and beneficiation processes. Smelting operations may /also/ produce /copper/ sulfate ... .

Terrestrial Fate: In soil, copper sulfate is partly washed down to lower levels, partly bound by soil components, and partly oxidatively transformed.|... Granular copper sulfate /was applied/ to the surface of Hoover Reservoir, Franklin County, Ohio. Soluble and particulate cupric copper concn at several depths were measured by atomic absorption spectrophotometry for four days after application. The soluble cupric copper concn decreased to near baseline values in 2 to 6 hr when 0.2 or 0.4 g of copper sulfate per square meter were added to the surface. Most of the copper sulfate was dissolved in the first 1.75 m of the water column, and only 2 percent of the total copper sulfate reached the depth of approx 4.5 m.

The milk of female vineyard workers, who were exposed to copper sulfate and a variety of other pesticides, contained 6.2 times as much copper as the milk of milkmaids who did equally hard work but not exposed to pesticides.

The milk of female vineyard workers, who were exposed to copper sulfate and a variety of other pesticides, contained 6.2 times as much copper as the milk of milkmaids who did equally hard work but not exposed to pesticides.

Elemental use in copper deficiency Copper and copper containing compounds are broadly used in medical practice. Metallic copper is used already for many years in dental fillings and in copper intrauterine devices (IUD) for reversible contraception. Ointments containing copper, which release copper ions that are absorbed by the skin in the management of cramps, disturbances of renal function, peripheral, venous hypostatic circulatory disturbances, rheumatic disease and swelling associated with trauma. There are also cosmetic facial creams containing copper as their main active ingredient.

Copper is an essential trace element that is included in some over-the-counter multivitamin and mineral supplements, even though copper deficiency is quite rare and supplementation is rarely needed. The amounts of copper found in typical supplements has not been associated with serum enzyme elevations or with clinically apparent liver injury. However, accidental or intentional copper overdose can cause an acute liver injury and chronic ingestion of excessive amounts of copper can result in copper overload and chronic liver injury.

Trace Elements and Metals

Antidotes; Emetics; Fungicides, Industrial|/SRP: EXTERNAL/ ANTIDOTE FOR WHITE PHOSPHORUS POISONING.|/SRP: FORMER USE/ A 0.1% soln of copper sulfate has been used for gastric lavage in phosphorus poisoning; it must be removed promptly to avoid copper poisoning. Topical application of a 1% soln is of value for phosphorus burns of the skin.|EXPT USE: IN EXPT WITH RATS TO FIND SIMPLE EFFICIENT ANTIDOTE FOR PHOSPHORUS BURNS, USE OF 5% COPPER SULFATE WAS HIGHLY TOXIC. SOLN OF 5% SODIUM BICARBONATE WITH 1% HYDROXYETHYL-CELLULOSE, 3% COPPER SULFATE & LAURYL SULFATE NEUTRALIZES PROCESS OF BURNING PHOSPHORUS.|For more Therapeutic Uses (Complete) data for COPPER(II) SULFATE (11 total), please visit the HSDB record page.

... Its routine use as an emetic is not recommended, because of the potential toxicity of improperly prepared soln and the hazards attending the use of large, corrosive doses.|Overdose may be poisonous (enteritis, hepatitis, nephritis).|MAY CAUSE DRAMATIC INCR IN MORTALITY OF TURKEYS GIVEN BLACKHEAD CONTROL DRUGS CONTAINING ARSENIC & EXPOSED TO BLACKHEAD.|CUPRIC ... SULFATE /AS EMETIC/ OFTEN IS EFFECTIVE, BUT POTENTIAL HEMOLYTIC & RENAL TOXICITY IS TOO GREAT TO RECOMMEND USE.

Copper is an essential mineral that plays a key role in many physiological processes, including angiogenesis, skin generation and expression and stabilization of skin proteins. Copper is found naturally in many food sources including meats, vegetables, and grains. Copper has potent biocidal properties and is used to eliminate bacteria, viruses and parasites,. Copper is one of the nine essential minerals for humans, as it plays an imperative role in various physiological pathways in basically all human tissue, as well as in the health of the dermis and epidermis. In addition to the above, copper is essential in wound healing, as it promotes angiogenesis and skin extracellular matrix formation and stabilization.

Agents counteracting or neutralizing the action of POISONS. (See all compounds classified as Antidotes.)|Agents that cause vomiting. They may act directly on the gastrointestinal tract, bringing about emesis through local irritant effects, or indirectly, through their effects on the chemoreceptor trigger zone in the postremal area near the medulla. (See all compounds classified as Emetics.)

Primarily absorbed in the small intestine. Based on studies with radioactive isotopes of copper, most copper is absorbed from the stomach and duodenum of the gastrointestinal tract. Maximum blood copper levels are observed within 1 to 3 hours following oral administration, and about 50 percent of ingested copper was absorbed. Copper absorption is proposed to occur by two mechanisms, one energy- dependent and the other enzymatic. Factors that can interfere with copper absorption include competition for binding sites with zinc, interactions with molybdenum and sulfates, chelation with phytates, and inhibition by ascorbic acid (vitamin C). Copper absorbed from the gastrointestinal tract is transported rapidly to blood serum and deposited in the liver bound to metallothionein. From 20 to 60% of the dietary copper is absorbed.|This drug is 80% eliminated via the liver in bile. Minimal excretion by the kidney. Metabolism studies show that persons with daily intakes of 2-5 mg of copper per day absorbed 0.6 to 1.6 mg (32%), excreted 0.5 to 1.3 mg in the bile, passed 0.1 to 0.3 mg directly into the bowel, and excreted 0.01 to 0.06 mg in the urine. As the data indicate, urinary excretion plays a negligible role in copper clearance, and the main route of excretion is in the bile. Other nonsignificant excretory routes include saliva, sweat, menstrual flow, and excretion into the intestine from the blood.|The body of a 70 kg healthy individual contains approximately 110 mg of copper, 50% of which is found in the bones and muscles, 15% in the skin, 15% in the bone marrow, 10% in the hepatic system, and 8% in the brain. The distribution of copper is affected by sex, age, and the amount of copper in the diet. Brain and liver have the highest tissue levels (about one-third of the total body burden), with lesser concentrations found in the heart, spleen, kidneys, and blood. The iris and choroid of the eye have very high copper levels. Erythrocyte copper levels are generally stable, however, plasma levels fluctuate widely in association with the synthesis and release of ceruloplasmin. Plasma copper levels during gestation may be 2-3 times levels measured before pregnancy, due to the increased synthesis of ceruloplasmin.|Effect of hydrogen ion (H+) concentration, water hardness, suspended solids, fish age, size, and species, acclimatization to copper, and levels of copper in food on poisoning of fish by copper sulfate used as a herbicide in freshwater ponds is discussed. Copper levels in muscle, kidney, and organs of rainbow trout were approximately 0.8-1.1, 2.0-2.3, and 115-150 mg/kg fresh weight, respectively, after 12 months intermittent exposure to various copper sulfate containing formulations 0.6, 2.0, and 100 mg/kg, respectively, in controls ... .|Male rats were orally administered for 2, 5, and 11 days with 0.5 mmol/kg of copper cmpd. ... In the case of cupric carbonate, copper was much more distributed in the tissues, especially in the liver, than for copper sulfate. The copper level increased progresively in mitochondria lysosomal fractions of the liver in proportion to the period of administration. In the 105,000 g supernatant fraction, copper was distributed in the metallothionein fraction rather than in the superoxide dismutase fraction. The administration of copper cmpd resulted in an increase in the zinc level in the liver, kidney and spleen, preferentially in the metallothionein fraction of the liver, but it seemed to have little effect on iron metabolism.

Maximum blood copper levels were observed within 1 to 3 hours following oral administration, and about 50 percent of ingested copper was absorbed. Copper absorption is believed to occur by two mechanisms, one energy- dependent and the other enzymatic. Factors that can interfere with copper absorption include competition for binding sites with zinc, interactions with molybdenum and sulfates, chelation with phytates, and inhibition by ascorbic acid. Copper absorbed from the intestine is transported quickly into blood serum and deposited in the liver bound to metallothionein. It is released and incorporated into ceruloplasmin, a copper-specific transport protein. The remaining copper in the serum binds to albumin or amino acids or is contained in the erythrocytes. About 80 percent of the absorbed copper is bound to liver metallothionein; the remainder is included into cytochrome c oxidase or sequestered by lysosomes.

The biological half-life of copper from the diet is 13-33 days with biliary excretion being the primary route of elimination.

This drug is an essential trace element for the functioning of many metalloenzymes including ceruloplasmin, ferroxidase II, lysyl oxidase, monoamine oxidase, Zn-copper superoxide dismutase, tyrosinase, dopamine-β-hydroxylase, and cytochrome-c-oxidase. It is involved in erythropoiesis & leukopoiesis, bone mineralization, elastin and collagen cross-linking, oxidative phosphorylation, catecholamine metabolism, melanin formation & antioxidant protection of cells. Cupric sulfate may also have a role in iron turnover, ascorbic acid metabolism, phospholipid metabolism, myelin formation, glucose homeostasis, and cellular immune defense. After the metal passes through the basolateral membrane it is transported to the liver, attached to serum albumin. The liver is the critical organ for the homeostasis of copper. The copper is then prepared for excretion through the bile or incorporation into various proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. In the dermis, copper promotes dermal fibroblasts proliferation, upregulates collagen (types I, II, and V) and elastin fiber components (elastin, fibrillins) production by fibroblasts, through the induction of TGF-β, promotes heat shock protein-47, important for collagen fibril formation, serves as a cofactor of LOX enzyme required for extracellular matrix protein cross-linking, stabilizes the skin ECM once formed, as increased crosslinking of collagen and elastin matrices occurs in a copper dose dependant manner, serves as a cofactor of superoxide dismutase, an antioxidant enzyme in the skin, essential for protection against free radicals, inhibits cellular oxidative effects such as membrane damage and lipid peroxidation, acts as a cofactor of tyrosinase, a melanin biosynthesis essential enzyme responsible for skin and hair pigmentation. In reference to its role as a biocide, copper is an essential nutrient for many organisms. It acts as a cofactor in respiration, and therefore copper is required for aerobic metabolism. Accumulation of copper ions or intracellular release of free copper ions from proteins lead to cell damage. Copper catalyzes reactions that result in the production of hydroxyl radicals through the Fenton and Haber-Weiss reactions. The highly reactive oxygen intermediates lead to lipid peroxidation and oxidation of proteins. Free copper ions oxidize sulfhydryl groups, such as cysteine, in proteins or the cellular redox buffer glutathione. In particular, copper ions inactivate proteins by damaging Fe-S clusters in cytoplasmic hydratases.|A significant drop in metabolic reserves was noted in cupric sulfate treated snails. Free amino acid levels dropped and the lactate level increased. The effects of copper treatment on rates of metabolite oxidation and ammonia production in the presence of exogenously added alpha-ketoglutarate were evaluated. A 92% drop in alpha-ketoglutarate dehydrogenase, a 33% drop in alanine aminotransferase, and a 78% rise in glucose 6-phosphatase were recorded. Molluscicidal activity of copper was due to a metabolic block in the tricarboxylic acid cycle at the alpha-ketoglutarate level.|ACUTE IV INFUSION OF 300 MG COPPER SULFATE IN CONSCIOUS SHEEP CAUSED AN INCREASE FROM 10.3 TO 22.5 TORR IN MEAN PULMONARY ARTERY PRESSURE & PULMONARY ARTERY WEDGE PRESSURE FROM 3.5 TO 7.6 TORR, WHEREAS SYSTEMIC ARTERIAL PRESSURE INCREASED FROM 95 TO 102 TORR. CARDIAC OUTPUT DECREASED FROM 4.7 TO 3.3 L/MIN. PULMONARY VASCULAR RESISTANCE & SYSTEMIC VASCULAR RESISTANCE INCREASED TO 320 & 160% OF BASE LINE, RESPECTIVELY. THIS PULMONARY HYPERTENSION WAS PRODUCED BY STIMULATION OF THE ALPHA-ADRENERGIC NERVOUS SYSTEM.

INGESTION: copper sulfate may induce severe gastroenteric distress (vomiting, gastroenteric pain, and local corrosion and hemorrhages), prostration, anuria, hematuria, anemia, increase in white blood cells, icterus, coma, respiratory difficulties, and circulatory failure. (USCG, 1999)

INGESTION: induce vomiting and administer gastric lavage; give a saline cathartic, fluid therapy, and transfusions if required; calcium disodium EDTA has been found moderately effective. SKIN AND EYES: wash affected tissues with water. (USCG, 1999)

Fresh air, rest.

Rinse skin with plenty of water or shower.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. Administer activated charcoal ... . /Copper and related compounds/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious. Start an IV with lactated Ringer's /SRP: "To keep open", minimal flow rate/. Watch for signs of fluid overload. For hypotension with signs of hypovolemia, administer fluid cautiously. Consider vasopressors if hypotensive with a normal fluid volume. Watch for signs of fluid overload ... . Use proparacaine, hydrochloride to assist eye irrigation ... . /Copper and related compounds/

A ... NUMBER OF CASES OF ACUTE POISONING IN MAN FROM INGESTING COPPER SULFATE, SOME OF THEM FATAL, HAVE BEEN REPORTED ... FROM NEW DELHI ... . THE REPORT CONCERNS 48 HOSPITALIZED PATIENTS & 5 AUTOPSY CASES, 2/3 MALE, MOSTLY BETWEEN THE AGES OF 16 & 25 YR. DOSAGE ESTIMATES RANGED FROM 1 TO 12 G ... SWALLOWED IN WATER. SYMPTOMS ... WERE ... METALLIC TASTE, BURNING IN EPIGASTRIUM, & REPEATED VOMITING. IN MORE SEVERE CASES, DIARRHEA (14 PATIENTS) APPEARED ON THE FIRST OR SECOND DAY & LASTED 24 HR; 20 ... SHOWED BLOOD IN GI TRACT FROM INJURY TO GASTRIC MUCOSA, LEADING TO ULCERATION IN SEVERE CASES. SUPPRESSION OF URINE FOLLOWED JAUNDICE ... . LIVER BIOPSY SHOWED CENTRILOBULAR NECROSIS & BILIARY STASIS. HYPERTENSION LEADING TO SHOCK ... CONSIDERED BAD PROGNOSTIC SIGN: 3 OF 4 DIED. COMA DEVELOPED IN 4, PRESUMABLY DUE TO UREMIA FROM RENAL INJURY, & DEATHS OCCURRED IN 7 (14.6%).|CONTACT OF SKIN WITH COPPER SULFATE CAN RESULT IN ITCHING ECZEMA ... CONTACT OF EYE WILL RESULT IN CONJUNCTIVITIS, EDEMA OF EYELIDS, & ULCERATION & TURBIDITY OF CORNEA.|A report of 11 patients who had ingested an estimated 1 to 50 g of copper sulfate; they suffered nausea & vomiting, with epigastric pain in 5, diarrhea in 5, hypotension in 2, hematemesis or melena in 10, pallor in 10, jaundice in 8, delirium in 3, & coma in 2. All had intravascular hemolysis & developed oliguria or anuria. Five patients died despite gastric lavage, intravenous fluids, mannitol, diuretics, and dialysis.|... Toxic blood levels can be seen after oral ingestion of as little as 1 g of copper sulfate in an adult. ... A patient ... ingested 250 gm of copper sulfate, developed transient hepatic dysfunction, and recovered after the prompt administration of chelation therapy.|For more Human Toxicity Excerpts (Complete) data for COPPER(II) SULFATE (23 total), please visit the HSDB record page.

Blue Vitriol

The substance can be absorbed into the body by inhalation of its aerosol and by ingestion.

Cough. Sore throat.

Redness. Pain.

Redness. Pain. Blurred vision.

Indust uses (froth flotation, wood preservative, chem manufacture), 52%; agricultural uses (pesticides, feed fertilizers, nutrients), 48% (1984)

USEPA/OPP Pesticide Code 024408; Trade Names: None listed.|Grade: Technical, CP, NF, also sold as monohydrate. Available as crystals or powder.|Crystals; wettable powder; suspension concentrate|Various crystal sizes: medium, large liquid, powder (snow) form, granular, water soluble|For more Formulations/Preparations (Complete) data for COPPER(II) SULFATE (17 total), please visit the HSDB record page.

Agriculture, forestry, fishing and hunting|Sulfuric acid copper(2+) salt (1:1): ACTIVE|Sulfuric acid, copper(2+) salt (1:?): INACTIVE|The cmpd, eg cupric sulfate, cupric chloride, cupric acetate and cupric nitrate, showed excellent preservation of mosses and lichens, and very good preservation of ferns and grasses.|... The highest utilized copper cmpd in the USA is copper sulfate.|COPPER(II) CHLORIDE IS A READILY AVAILABLE FORM OF COPPER IN FEEDING TRIALS WHICH COMPARES FAVORABLY WITH COPPER SULFATE IN CATTLE AND SWINE TRIALS.|... SALTS OF COPPER, INCLUDING THE SUBACETATE, OXYCHLORIDE, CHLORIDE AND OXIDE, HAVE FUNGICIDAL PROPERTIES AND OCCASIONALLY REPLACE THE SULFATE IN SPRAYS. ...

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients|Cosmetics -> Skin conditioning|ALGICIDES