Copper carbonate

FCS -> FDA Cumulative Estimated Daily Intake (CEDI)

FCS -> FDA Inventory of Food Contact Substances Listed in 21 CFR

Other Solid

Blue-green powder; Insoluble in water; [Redox Pty MSDS]

This chemical does not meet GHS hazard criteria for 1.3% (2 of 151) of reports.

Warning

H302 (98.7%): Harmful if swallowed [Warning Acute toxicity, oral]

P261, P264, P264+P265, P270, P271, P273, P280, P301+P317, P302+P352, P304+P340, P305+P351+P338, P319, P321, P330, P332+P317, P337+P317, P362+P364, P391, P403+P233, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 151 reports by companies from 8 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Chemical: Carbonic acid, copper(2+) salt (1:1)

Carbonic acid, copper(2+) salt (1:1) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Carbonic acid, copper(2+) salt (1:1) are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

Copper carbonate: Does not have an individual approval but may be used under an appropriate group standard

Acute copper poisoning after ingestion can cause liver injury, methemoglobinemia, and hemolytic anemia. Acute renal failure may result, secondary to massive hemoglobinuria. [Goldfrank, p. 1259] An irritant that may cause transient eye injury; Harmful by ingestion; [Redox Pty MSDS] See Copper.

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 carbonate. (All substances listed may be in anhydrous or hydrated form.)

Verdigris, formed by atmospheric corrosion of the surface of metallic copper presumably composed of copper carbonates & oxides, causes immediate irritation & conjunctival inflammation when accidentally dropped or dusted on the eyes of patients but the reaction subsides without permanent damage soon after the eye is cleaned by irrigation. ... /Verdigris/

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.

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.

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.

1.0 [mg/m3], as Cu

8 hr Time Weighted Avg (TWA): 1 mg/cu m /Copper dusts and mists, as Cu/

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed 3 times the TLV-TWA for no more than a total of 30 minutes during a work day, and under no circumstances should they exceed 5 times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Copper dusts and mists, as Cu/

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)

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)

Verdigris, formed by atmospheric corrosion of the surface of metallic copper presumably composed of copper carbonates & oxides, causes immediate irritation & conjunctival inflammation when accidentally dropped or dusted on the eyes of patients, but the reaction subsides without permanent damage soon after the eye is cleaned by irrigation. /Verdigris/

Pigs maintained on diets supplemented with copper carbonate (600-750 ppm) or copper sulfate (250-425 ppm) for 48-79 days exhibited a variety of toxic effects including the gradual development of anemia, jaundice, hepatic necrosis, gastrointestinal hemorrhage, and decreased weight gain.

Groups of six female large white pigs /were maintained/ on maize meal diets supplemented with 600 ppm basic copper carbonate to which soybean meal, dried skim milk, or white fish meal protein supplements were added. The treatment lasted for 48 days and the pigs in the soya, milk, and fish fed groups received 6.4, 11.0, and 15.4 mg copper(+2)/kg/day, respectively. Gradual development of anemia was observed in all treatment groups, but the fish fed group had signs of toxicity. It was presumed that the high calcium levels in the fish meal diet adversely affected the zinc availability, and thus led to toxicity.

The activities of delta-aminolevulinic acid synthase, delta-aminolevulinic acid dehydratase and porphobilinogen deaminase among heme biosynthetic enzymes were determined in bone marrow cells and peripheral blood of rats administered basic cupric carbonate at doses of 0, 70, 220, 670, and 2,000 ppm in the diet for 12 months. The activities were all significantly increased in male rats at doses of 670 and 2,000 ppm, but not in female rats. The result shows that there are sex differences in the toxicological effects of basic cupric carbonate on the heme biosynthetic pathway in erythropoietic tissues.

The oral acute toxicity and 12 months chronic toxicity of basic cupric carbonate, were tested in Slc: Wistar rats. In the acute toxicity test, seven groups consisting of 10 five week old rats of each sex were orally given basic cupric carbonate in doses of 764-2281 mg/kg. Three or 4 days after administration, hematuria was noted in some male and female rats that received doses of 1,100 mg/kg or more. The necrospy of dead animals revealed hemorrhage of the glandular stomach mucosa and hematuria in the urinary bladder in the same groups. The calculated LD50 values were 1350 mg/kg in males and 1495 mg/kg in females. In the chronic toxicity test, five groups consisting of 42 five week old rats of each sex were fed on diets containing basic cupric carbonate at level of 0 (control), 70, 220, 670, and 2,000 ppm for 12 months. Depression of body weight gain was noted in the 2,000 ppm group of both sexes, but no dead animal was observed throughout the test period. There were marked increases of serum GOT, GPT and LDH activities in the male 2,000 ppm group at 1, 3, 6 and 12 months. Histologically, the incidences of single cell necrosis in the liver was increased significantly in the 2,000 ppm group of both sexes. The results suggest that the diet containing basic cupric carbonate at a level of 2,000 ppm was toxic to rats, and that 670 ppm is the maximum no effect dose under the conditions used.

For more Non-Human Toxicity Excerpts (Complete) data for COPPER(II) CARBONATE (6 total), please visit the HSDB record page.

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 carbonate. (All substances listed may be in anhydrous or hydrated form.)

Copper is mainly absorbed through the gastrointestinal tract, but it can also be inhalated and absorbed dermally. It passes through the basolateral membrane, possibly via regulatory copper transporters, and is transported to the liver and kidney bound to serum albumin. The liver is the critical organ for copper homoeostasis. In the liver and other tissues, copper is stored bound to metallothionein, amino acids, and in association with copper-dependent enzymes, then partitioned for excretion through the bile or incorporation into intra- and extracellular proteins. The transport of copper to the peripheral tissues is accomplished through the plasma attached to serum albumin, ceruloplasmin or low-molecular-weight complexes. Copper may induce the production of metallothionein and ceruloplasmin. The membrane-bound copper transporting adenosine triphosphatase (Cu-ATPase) transports copper ions into and out of cells. Physiologically normal levels of copper in the body are held constant by alterations in the rate and amount of copper absorption, compartmental distribution, and excretion. (L277, L279)

Rats were fed a diet contain basic cupric carbonate, at doses of 0, 70, 220, 670 and 2,000 ppm as cupric hydroxide and 12 months, the levels of copper in the blood and tissues were determined by atomic absorption analysis. At the same time, fluctuations in the levels of iron and zinc, which are essential elements, were determined in the tissues. Levels of copper, iron and zinc in blood were practically unchanged after feeding for 12 months at the highest dose, 2000 ppm. Copper in the liver increased markedly at doses of 670 and 2000 ppm from 1 month, and the level reached about 50 times that of the control group. The level of copper in the kidney significantly increased at larger doses than 670 ppm. Iron concentration in the kidney did not change at smaller doses than 220 ppm, but significantly decreased at higher doses than 670 ppm. The level of copper in the kidney increased only at the highest dose. /Basic cupric carbonate/

Used in pigments, pyrotechnics, insecticides, to make other copper salts, for coloring brass black, as an astringent in pomade preparations, as an antidote for phosphorus poisoning, smut preventive, fungicide for seed treatment, in animal and poultry feeds as readily absorbable source of copper, and as a veterinary medication (anthelmintic aid in sheep); [HSDB]

Farming (Feed Additives) [Category: Industry]

For Copper(II) carbonate (USEPA/OPP Pesticide Code: 022901) ACTIVE products with label matches. /SRP: Registered for use in the U.S. but approved pesticide uses may change periodically and so federal, state and local authorities must be consulted for currently approved uses./

MEDICATION

MEDICATION (VET)

IN ANIMAL & POULTRY FEEDS AS READILY ABSORBABLE SOURCE OF COPPER

USEPA/OPP Pesticide Code 022901; Trade Names: Malachite; Bremen green; Bremen blue.

Grade: Technical, CP /Basic/

All Other Basic Inorganic Chemical Manufacturing

Carbonic acid, copper(2+) salt (1:1): ACTIVE