구리 염화물

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

Excerpt from ERG Guide 171 [Substances (Low to Moderate Hazard)]:

· CALL 911. Then call emergency response telephone number on shipping paper. If shipping paper not available or no answer, refer to appropriate telephone number listed on the inside back cover.

· ELIMINATE all ignition sources (no smoking, flares, sparks or flames) from immediate area.

INHALATION: move to fresh air.

Excerpt from ERG Guide 171 [Substances (Low to Moderate Hazard)]:

General First Aid:

· Wear positive pressure self-contained breathing apparatus (SCBA).

0.01 [mg/m3], respirable fraction (Cu, inorganic cmpnds)[German Research Foundation (DFG)]

... MATERIALS WHICH ARE TOXIC AS STORED OR WHICH CAN DECOMP INTO TOXIC COMPONENTS DUE TO CONTACT WITH HEAT, MOISTURE, ACIDS, OR ACID FUMES, SHOULD BE STORED IN COOL, WELL-VENTILATED PLACE, OUT OF DIRECT RAYS OF THE SUN, AWAY FROM AREAS OF HIGH FIRE HAZARD, & SHOULD BE PERIODICALLY INSPECTED AND MONITORED. INCOMPATIBLE MATERIALS SHOULD BE ISOLATED FROM EACH OTHER. /CHLORIDES/

Environmental consideration - land spill: Dig a pit, pond, 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 consideration - water spill: Neutralize with agricultural lime (calcium oxide), crushed limestone (calcium carbonate), or sodium bicarbonate (NaHCO3). Use mechanical dredges or lifts to remove immobilized masses of pollutants & precipitates.

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

Excerpt from ERG Guide 171 [Substances (Low to Moderate Hazard)]:

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.

If material not involved in fire: Keep material out of water sources & sewers. Build dikes to contain flow as necessary.

Personnel protection: Keep upwind. ... Avoid breathing vapors or dusts. Wash away any material which may have contacted the body with copious amt of water or soap & water.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

Excerpt from ERG Guide 154 [Substances - Toxic and/or Corrosive (Non-Combustible)]:

Excerpt from ERG Guide 171 [Substances (Low to Moderate Hazard)]:

Immediate precautionary measure

EYES: irrigate opened eyes for several minutes under running water. INGESTION: do not induce vomiting. Rinse mouth with water (never give anything by mouth to an unconscious person). Seek immediate medical advice. SKIN: should be treated immediately by rinsing the affected parts in cold running water for at least 15 minutes, followed by thorough washing with soap and water. If necessary, the person should shower and change contaminated clothing and shoes, and then must seek medical attention. INHALATION: supply fresh air. If required provide artificial respiration.

The effects of superoxide dismutase, catalase, copper(II) (3,5-diisopropylsalicylate)2 and other copper compounds on radiation transformation in vitro using C3H 10T1/2 cells have been studied. When present only during irradiation, cupric chloride and cuprous chloride inhibited the initiation phase of radiation transformation.

The ameliorating effects of copper(+2) and sulfate(2-) ions on concurrent selenite toxicity were compared in two factorial experiments in weanling rats. 0, 500 and 1,000 mg copper (as cupric chloride)/kg diet were fed in conjuction with 0, 5, 10 and 20 mg selenium (as Na2Se)3)/kg diet. Cupric(+2) ion, but not sulfate(2-) ion, prevented mortality among selenite intoxicated rats. There were significant copper-selenium interaction effects on feed intake, daily gain, packed cell volume, serum copper and iron, sperm counts, and weights of liver, kidney and testis. Sulfate increased liver copper concentrations.

Oral LD50 values (at 24 and 168 hr) for 8 metal salts were detected in female mice pretreated orally with small doses (1/10 of the challenge doses) of the same metal ions or with deionized water at 24 hr prior to the challenge doses. Pretreatment with copper(2+), had little effect on the lethality of the same ion. Pretreatment with copper(2+), mercury(2+), or zinc(2+) protected mice against the toxic action of cadmium(2+).

Salts of metals which are carcinogenic, noncarcinogenic, or of unknown carcinogenicity were assayed for their abilities to modulate ultraviolet induced mutagenesis in Escherichia coli WP2. Copper chloride acted as comutagen in E coli WP2, which has wild type DNA repair capability, but was much less comutagenic in the repair deficient strain WP2S (uvra). The survival of irradiated or unirradiated cells was not affected by the compound. The comutagenic effects might occur either via metal induced decreases in the fidelity of repair replication or via metal induced depurination.

For more Interactions (Complete) data for COPPER(II) CHLORIDE (6 total), please visit the HSDB record page.

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)

EC50 Selenastrum capricornatum (green alga) 85 ug/l/14 days /Cell volume bioassay/

EC50 Thalassiosira pseudonana (alga, saltwater) 5 ug/l/72 hr /Growth rate bioassay/

EC50 Nitschia closterium (alga, saltwater) 33 ug/l/96 hr /Growth rate bioassay/

EC50 Chlorella stigmatophora (alga, saltwater) 70 ug/l/21 days /Cell volume bioassay/

For more Ecotoxicity Values (Complete) data for COPPER(II) CHLORIDE (7 total), please visit the HSDB record page.

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. ...

Drug Induced Liver Injury Rank (DILIrank 2.0)

Cupric chloride

vNo-DILI-concern

0

No match

DOI:10.1016/j.drudis.2016.02.015

COPPER CHLORIDE APPLIED IN 0.08 TO 0.16 MOLAR SOLN TO CORNEAS OF RABBITS AFTER REMOVAL OF EPITHELIUM, OR INJECTED INTO STROMA, CAUSES SEVERE REACTION WITH PERMANENT OPACIFICATION.

... 25 MG OF COPPER CHLORIDE INJECTED SC IN 1% SOLN IN RABBITS CAUSED LOCAL NECROSIS & LOSS IN WT. ...

The freshwater teleost Tilapia mossambica was subjected to lethal (6.0 mg/l= LC50/48 hr) and sublethal (1.5 mg/l) copper treatment for 1, 7, and 14 days. The whole animal oxygen consumption and the activity levels of succinate dehydrogenase and lactate dehydrogenase in liver and muscle were studied. The decrease in oxygen consumption and succinate dehydrogenase activity and significant increase in lactate dehydrogenase activity suggest that the stressed fish is meeting its energy requirement through anaerobic oxidation and these enzymes can be used as indicators in monitoring metal induced toxicity in fish.

The role of lysosomes in the pathogenesis of copper induced hepatotoxicity was studied in mice. Two strains of female C57B1-mice (conventional and beige) were injected intraperitoneally with 0 or 8 milligrams per kilogram aqueous copper (II) chloride daily for up to 4 weeks. Macroscopically, the livers of mice treated for 1 week were similar to those of the controls. After 2 weeks, livers of treated animals were diffusely tan to red and the edges of the individual lobes were blunted. At 4 weeks, the livers were gray to tan, and their lobes were marked rounded. Hepatic lesions consisting of karyomegaly, accumulation of lipofuscin within hepatocytes, and Kupffer cells, acute necrosis of random hepatocytes, and aggregation of leukocytes within the sinusoids developed in both strains; however, they developed more quickly and were more severe in beige mice. In both strains, the onset of the hepatic lesions closely paralleled the appearance and distribution of copper within the leukocytes. Beige mice are more susceptible to copper mediated hepatotoxicity, suggesting that normal lysosomes have protective effects for hepatocytes by sequestering copper from other cytoplasmic components.

For more Non-Human Toxicity Excerpts (Complete) data for COPPER(II) CHLORIDE (13 total), please visit the HSDB record page.

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 4.54 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).

Cupric chloride 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.

Toxic pollutant designated pursuant to section 307(a)(1) of the Federal Water Pollution Control Act and is subject to effluent limitations. /Copper and cmpd/

Used as a catalyst, deodorizing and desulfurizing agent (petroleum industry), mordant (textiles industry), oxidizing agent (aniline dyestuffs); Also used in inks, metallurgy (refining copper, silver, and gold), tinting baths (iron and tin), electrotyping baths (plating copper or aluminum), photography (fixer), pyrotechnics, pigments for glass and ceramics, feed additives, wood preservatives, disinfectants, fungicides, and water purification; [HSDB]

Aluminum Producing [Category: Industry]

Ceramics making [Category: Hobbies]

As catalyst for org and inorg reactions; in petroleum industry as deodorizing, desulfurizing, purifying agent; as mordant for dyeing and printing textiles; as oxidizing agent for aniline dyestuffs; in indelible, invisible, and laundry marking inks; in metallurgy in wet process for recovering mercury from ores; in refining copper, silver, gold; in tinting baths for iron, tin; in electrotyping baths for plating copper or aluminum; in photography as fixer, desensitizer, and reagent; in producing color in pyrotechnic compositions; in manufacturing of acrylonitrile, fast black (melanin); in pigments for glass, ceramics; as feed additive, wood preservative, disinfectant.

Isomerization and cracking catalyst. Mordant in dyeing and printing fabrics, sympathetic ink, disinfectant, pyrotechnics, wood preservation, fungicides, metallurgy, preservation of pulpwood, deodorizing and desulfurizing petroleum distillates, photography, water purification, feed additive, electroplating baths, pigment for glass and ceramics, acrylonitrile manufacturing.

In the preparation of copper(II) oxychloride; as a catalyst in numerous organic chlorination reactions such as the production of vinyl chloride or 1,2-dichloroethane; mordant and in the petroleum industry to sweeten sulfidic crude oil; for platting copper on aluminum, and in tinning baths for tin and germanium; as a pigment in glass and ceramics; as a wood preservative; and in water treatment.

REACTION OF METALLIC COPPER WITH CHLORINE AT 400-500 DEGREES C.

Prepn: Pray, Inorg Syn 5: 153 (1957); Gmelin's, Copper (8th ed) 60b: 253-95 (1958); Glemser, Sauer in Handbook of Preparative Inorganic Chemistry, vol 2, G Brauer, ed (Academic Press, New York, 2nd ed, p 1008 (1965).

(1) By the union of copper and chlorine. (2) Copper carbonate is treated with hydrochloric acid and the product crystallized. /Dihydrate/

COPPER(II) CHLORIDE SOLN CAN BE PREPARED BY DIRECT METATHESIS USING, EG COPPER(II) SULFATE AND BARIUM CHLORIDE.

For more Methods of Manufacturing (Complete) data for COPPER(II) CHLORIDE (7 total), please visit the HSDB record page.

All Other Basic Inorganic Chemical Manufacturing

Copper chloride: ACTIVE

Copper chloride (CuCl2): ACTIVE

AS READILY AVAILABLE FORM OF COPPER IN FEEDING TRIALS. 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. ...

CONCENTRATED CUPRIC CHLORIDE SOLUTIONS ABSORB LARGE QUANTITIES OF NITROGEN GAS & HENCE ARE OF INTEREST IN POLLUTION CONTROL.