COPPER

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.

DESIGNATIONS

EPA PESTICIDE CHEMICAL CODE:022501

MOLECULAR FORMULA

ERG GUIDE NUMBER

151-SUBSTANCES - TOXIC (NON-COMBUSTIBLE)

SYNONYM REFERENCE

(RTECS , 2001; HSDB , 2001; NIOSH , 2001; OHM/TADS , 2001)

USES/FORMS/SOURCES

USES

Copper has excellent electrical conductivity, corrosion resistance, malleability and ductility, which make it very useful as an industrial metal (Baxter et al, 2000).
As much as 75 percent of the copper used in the USA is for electrical conductors such as wire and switches (Bingham et al, 2001a; ILO, 1998). Copper is widely used in applications for which high electrical and thermal conductivity are needed. Copper whiskers are used in thermal and electrical composites (ACGIH, 1996a; Lewis, 1997a).
Copper is used in important alloys such as bronze (copper alloyed with as much as 10 percent tin) and brasses (copper alloyed mainly with zinc). Monel metal, another copper alloys, is copper alloyed with nickel (Baxter et al, 2000; Lewis, 1997a).

Copper alloyed with cadmium is used in electrical conductors; with magnesium and aluminum, in resistance wire and heating wire; with nickel, for chemical equipment; and with beryllium, in electrical contacts, springs, dies, bellows and welding links (Ashford, 1994).
Brasses containing less than 58 percent copper have little application (Bingham et al, 2001a).

Copper is useful in electroplated coatings and undercoatings for products made from nickel, chromium, and zinc, and in cooking utensils. Copper is also made into corrosion-resistant plumbing pipes, used in heating and roofing materials for building construction, and has applications in industrial machinery and in automobiles (HSDB, 2002; ILO, 1998; Lewis, 1997a).
In agricultural applications, copper compounds (particularly copper sulfate) are used in insecticides, fungicides, herbicides, and algicides (Bingham et al, 2001a).
Copper's contraceptive effects (as a spermatocide) are exploited for intrauterine devices. Its contraceptive effects permit the use of a smaller device, resulting in fewer side effects such as pain and bleeding (Bingham et al, 2001a; Goldfrank, 1998; HSDB, 2002).
Copper and its compounds have many other miscellaneous uses:

They are used for chemical and pharmaceutical applications; in pollution control catalysts; in pigments, dyes and anti-fouling paints; in works of art; in coinage; in fabrics and textiles, glass and ceramics; in cement, nylon and paper products; for printing and photocopying; in pyrotechnics; as analytical reagents; and in wood preservatives.
They are also used in ammunition, flameproofing and fuel additives, and the flakes are used as insulation for liquid fuels (ACGIH, 1996a; Budavari, 2000; HSDB, 2002; ILO, 1998; Lewis, 1997a).
Copper naphthenate has been used as a coating material for hardwood floors, causing toxicity to residents (Kim & Chomchai, 1999).

COPPER COMPOUNDS (Copper I and Copper II compounds):

COPPER OXIDE: Cupric oxide (black copper oxide) (CuO) or Cuprous oxide (red copper oxide) (Cu2O). Copper oxide is used as a catalyst and a pigment for ceramic, glass, enamel, porcelain and artificial; it is used in copper metallurgy, pyrotechnics and welding and in the manufacture of rayon; it serves as a solvent for chromic iron ores; it is used as an optical glass polishing agent; and it is found in batteries, electrodes, desulfurizing oils, paints fungicides and insecticides (Bingham et al, 2001; Budavari, 2000; ILO, 1998).
COPPER ACETATE: Cupric acetate or cupric acetate, basic or Cuprous acetate (acetic acid copper (1+) salt). Copper acetate is used as a paint pigment, insecticide, fungicide, mordant and mildew preventive (Budavari, 2000).
COPPER CARBONATE: Cupric carbonate, basic (copper carbonate hydroxide). Copper carbonate is used in pigments, pyrotechnics, insecticides, fungicides and brass coloring (Clayton & Clayton, 1994).
COPPER CHLORIDE: Cupric chloride (CuCl2) or Cuprous chloride (CuCl). Copper chloride is used as a disinfectant, in metallurgy, for the preservation of wood pulp, for deodorizing and desulfurizing petroleum distillates, in photography, in water purification, and as a feed additive (Clayton & Clayton, 1994).
COPPER NITRATE: Cupric nitrate (CuN2O6). The nitrate shares many uses with copper chloride and, in addition, is used preferentially in pharmaceutical preparations and in paints, varnishes and enamels (Clayton & Clayton, 1994).
COPPER CYANIDE: Cuprous cyanide (CuCN). Its chief use is in the electroplating of copper on iron (Clayton & Clayton, 1994).
COPPER GLYCINATE - Copper glycinate is used in cattle to increase dairy yields (Oon et al, 2006).
COPPER SULFATE/SULFIDE: Cupric sulfate, basic (copper hydroxide sulfate) or Cupric sulfide(CuS) or Cuprous sulfide (Cu2S). It is used as a fungicide, molluscicide and wood preservative, for water treatment as a bactericide and algaecide, as a mordant, in electroplating, as a froth flotation agent, in leather tanning and hide preservation, in works of art, for animal nutrition, and in some fertilizers. It is also used medicinally as an emetic, and in several intrauterine contraceptive devices (Bingham et al, 2001; ILO, 1998; Kirk-Othmer, 1992).

FORMS

INDUSTRIAL

Industrially, copper is available as ingots, sheets, rods, wire, tubing, shot or powder, or in high purity (less than 10 ppm impurities) as single crystals or whiskers (HSDB , 2002; Lewis, 1997).
Commercial copper is available in the following purities (HSDB , 2002):
Electrolytic tough-pitch 99.90% Cu
Deoxidized 99.90% Cu
Oxygen-free 99.92% Cu
Silver-bearing 99.90% Cu
Arsenical 99.68% Cu
Free-cutting 99.40 to 99.50% Cu

SOURCES

ISOTOPES: Copper occurs naturally in its elemental state. There are two naturally occurring stable isotopes, atomic weights 63 (69.09 percent) and 65 (30.91 percent), and nine artificial isotopes (atomic weights 58-62, 64, 66-68). It has valences 1 and 2. It is present in the earth's crust at 70 ppm and in seawater at 0.001 to 0.02 ppm (Budavari, 2000). It is the 26th-most-abundant element in the earth's crust (Harbison, 1998).
ORE: Copper is also found in various ores including chalcopyrite, chalcocite, bornite, tetrahedrite, enargite, antlerite, azurite, azurmalachite, covellite, cuprite and malachite (Lewis, 1993; Budavari, 2000). The main ore is chalcopyrite (approximately 85 percent). Most copper mined today (about 85 percent) comes from ores containing 2 percent or less copper (Bingham et al, 2001). Copper is a noble metal, like silver and gold (Barceloux, 1999).
BIOLOGICAL: Copper is an essential trace element in the human and animal diets, with many metabolic functions not fully understood, and is involved in plant metabolism. It occurs in biological complexes such as pheophytin (an analog of chlorophyll), hemocyanin, tyrosinase and ceruloplasmin (Baselt, 2000; Budavari, 2000). Copper is the third-most-abundant trace element in the human body (Barceloux, 1999).

In humans, copper is found in many proteins (Bingham et al, 2001). It is essential for the function of many enzymes such as catalase and peroxidase, and is an important catalyst for heme synthesis and iron absorption (Barceloux, 1999; Goldfrank, 1998).
Copper influences gene expression and is a cofactor for oxidative enzymes such as superoxide dismutase, cytochrome C oxidase and lysyl oxidase, as well as for aminolevulonic acid (Baxter et al, 2000a).

-CLINICAL EFFECTS

GENERAL CLINICAL EFFECTS

WITH POISONING/EXPOSURE

ROUTES OF EXPOSURE: Copper compounds may be toxic by inhalation, ingestion, injection, and skin or eye exposure. Copper salts are particularly irritating.
INHALATION: Exposure to fumes or dust may cause irritation of the nose and upper respiratory tract, as well as sneezing and coughing. Perforation of the nasal septum can also occur. 'Metal fume fever,' with respiratory and flu-like symptoms such as chills and muscle aches, may result from exposure to fumes or fine dust. The incidence of copper-induced metal fume fever is low due to the high temperatures required to volatilize copper.
INGESTION: Acute ingestion of copper salts can cause irritation, severe nausea and vomiting, salivation, abdominal pain, epigastric burning, hemolysis, gastrointestinal bleeding with hemorrhagic gastritis, hematemesis and melena, anemia, hypotension, jaundice, seizures, coma, shock and death. Hepatic and renal failure may develop several days after acute ingestion. Methemoglobinemia may rarely occur. Copper may produce a metallic or sweet taste.
INJECTION: Subcutaneous injection of copper glycinate resulted in nausea and vomiting, acute renal failure, hemolytic anemia, acute hepatic failure, disseminated intravascular coagulation, and dermal necrosis at the injection site.
DERMAL: Skin exposure may cause irritation, itching, eczema, allergic contact dermatitis, hypersensitivity, and a greenish discoloration of the hair, teeth and skin.
EYE: Exposure of the eyes to copper fumes or dust can cause irritation, conjunctivitis, palpebral edema, ulceration and corneal turbidity. Eye irritation, uveitis, abscess and loss of the eye may also occur from the mechanical action of lodged copper particles. Penetration of the eye by fine fragments can result in severe ocular damage. Corneal discoloration (Kayser-Fleischer ring) is a hallmark of Wilson disease.

POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Highly toxic, may be fatal if inhaled, swallowed or absorbed through skin.
Avoid any skin contact.
Effects of contact or inhalation may be delayed.
Fire may produce irritating, corrosive and/or toxic gases.
Runoff from fire control or dilution water may be corrosive and/or toxic and cause pollution.

ACUTE CLINICAL EFFECTS

Metallic copper itself has little if any toxicity, in general (Budavari, 2000). Soluble salts of copper are poisonous, but usually only when ingested intentionally (as in a suicide) or used as a topical treatment (as for an extensive area of burned skin) (ILO , 1998).

Inhalation of high levels of copper dust or fume can cause respiratory tract irritation (ACGIH, 1991). It is not known how much copper is absorbed with inhalation exposure; however, people working in atmospheres heavily polluted with copper have had increased serum copper levels (Friberg, 1986). Chronic inhalation of copper-containing aerosols may cause pulmonary alveolar proteinosis (Likhaechev et al, 1975).

Metal fume fever has been reported in workers exposed to an extremely fine copper dust at concentrations of 0.075 to 0.12 mg/m(3), or to copper fume(Hathaway et al, 1996; Proctor & Hughes, 1978). Symptoms include upper respiratory irritation, chills and muscle aches (Baselt, 2000). Some authors have questioned this association (Borak et al, 2000).

Ingestion of sufficient concentrations of copper salts may result in a metallic taste, salivation, nausea, vomiting, burning in the epigastrium, diaphoresis, abdominal/gastric pain and bloody diarrhea, and may lead, rarely, to convulsions, coma and death. Copper sulfate has been reported to cause gastrointestinal bleeding (hemorrhagic gastritis), which may potentially occur with other irritating copper salts (ACGIH, 1996; Agarwal et al, 1975; ILO , 1998) Jantsch et al, 1984; (Sittig, 1991; Yang et al, 1997).

Reported cases of acute gastrointestinal 'upset' due to copper have been reviewed, and diagnostic criteria proposed (Eife et al, 1999a; Eife et al, 1999b).
Copper salts may induce a rapid onset of repeated vomiting (98% within 15 minutes of ingestion), with a range of two to ten episodes of vomiting following a single oral dose. The vomitus is characteristically greenish-blue (Gunay et al, 2006; Gulliver, 1991).
Acute gastrointestinal symptoms have occurred as a result of several incidents in which new copper piping was installed to supply domestic water (Knobeloch et al, 1998).
Headache, vomiting and abdominal pain immediately developed in an adult after ingestion of two mouthfuls of a fungicide containing copper 8-hydroxyquinolate; methemoglobinemia with hemolysis developed later (Yang et al, 1997).

Systemic effects can occur from high-level acute ingestion of copper salts, which can be absorbed from the stomach and produce hemolysis, anemia, and liver and kidney damage secondary to hemolysis (Friberg, 1986).

Jaundice appears in about 25% of patients on the second or third day after acute ingestion of copper salts and may be accompanied by hepatomegaly, increased levels of transaminase and liver tenderness, with biopsy showing centrilobular necrosis and biliary stasis (Baxter et al, 2000a; Zimmerman, 1978). Hepatic accumulation of copper is an essential feature of the development of copper toxicosis (Bremner, 1998).
Acute renal failure develops in 20% to 40% of patients with acute copper sulfate intoxication and is believed to be mainly due to intravascular hemolysis. This might also occur after ingestion of other copper salts. Anuria or oliguria may develop 24 to 48 hours after ingestion, accompanied by an increase in BUN (Wahl et al, 1963; Chugh et al, 1977; Chugh et al, 1977a).
Acute tubular necrosis follows by several hours the acute gastrointestinal symptoms of copper salt ingestion (Baxter et al, 2000a). Blood or protein in the urine can occur (Friberg, 1986).
Intravascular red cell hemolysis has been reported after acute ingestion (Chugh et al, 1977; ILO , 1998; Walsh et al, 1977; Yang et al, 1997; Gunay et al, 2006). Hemolytic anemia may follow several hours after the acute gastrointestinal symptoms of copper salt ingestion (Baxter et al, 2000a). Rarely, methemoglobinemia has been reported (Chugh et al, 1975; Eastwood et al, 1983; Kim & Chomchai, 1999; Matter et al, 1969; Todd & Thompson, 1961; Yang et al, 1997).

Skin contact with some copper salts may result in severe irritation, with itching, erythema and dermatitis, and may produce systemic toxicity (Holzman et al, 1966). The irritating effects of copper salts on the skin result in itching eczema (ACGIH, 1996).

Very high levels of exposure to copper dust or fume may result in symptomless greenish discoloration of the hair, tongue and teeth (ACGIH, 1996; Baxter et al, 2000a; Hathaway et al, 1991). Green pigmentation of blonde hair has been reported after exposure to copper-contaminated tap water, swimming pools containing copper-based algicides and application of copper contaminated henna (Mascaro et al, 1995; Person, 1985; Tosti et al, 1991).

Exposure to copper can result in conjunctivitis and corneal ulceration or turbidity as well as palpebral edema (ACGIH, 1996; Goldfrank, 1998; Sittig, 1991). The strong alkalinity of copper cyanide solutions used in plating baths can result in severe eye burns with corneal damage (Grant & Schuman, 1993).

Copper particles can lodge in and irritate the eyes (Friberg, 1986; Hathaway et al, 1991).

Copper or copper alloy foreign bodies lodged in the eye (chalcosis lentis) can result in uveitis, abscess, serious injury or loss of the eye; over time, the copper may dissolve and disseminate to the lens, cornea and iris, where it may produce a greenish-brown discoloration of the anterior capsule visible by slit-lamp microscope (Goldfrank, 1998; Grant & Schuman, 1993).
Retinal injury has been reported as a result of the intra-ocular retention of a copper foreign body. Electro-retinographic changes improved, but did not fully reverse, following removal of the object (Dayan et al, 1999).

Nasal mucous membranes may become irritated after inhalation exposure to the dusts and mists of copper salts; ulceration and perforation of the nasal septum may result in some cases, with atrophic changes of the nasal mucous membranes (ACGIH, 1996; Sittig, 1991).

Metabolic acidosis has been described in patients with hemodialysis-induced copper toxicity (Klein et al, 1972; Eastwood et al, 1983).

Copper is reportedly linked with toxin-induced seizures (Goldfrank, 1998).

Fever, hypotension, lethargy and coma have been reported with severe copper sulfate intoxication and might develop after ingestion of other copper salts (Agarwal et al, 1993; Akintonwa et al, 1989; Chuttani et al, 1965; Schwartz & Schmidt, 1986). Hemoglobinuria and hematuria have been reported after copper sulfate ingestion and might occur with intoxication from other copper salts (Walsh et al, 1977).

The toxicology of copper and its compounds has been the subject of several extensive reviews (Anon, 1998; Barceloux, 1999).

CHRONIC CLINICAL EFFECTS

Chronic copper poisoning has not generally been described in humans, except in individuals with Wilson disease, in which progressive copper toxicity results from a hereditary metabolic disorder involving deficiency in the copper-binding and transport protein ceruloplasmin. Generally, the effects of copper excess are reversible (Baselt, 2000; Friberg, 1986).

Patients with this disorder suffer endogenous copper poisoning if they fail to eat a copper-deficient diet. Decreased serum ceruloplasmin levels and increased deposition of copper in parenchymal tissue are hallmarks of this disorder; the resultant damage is fatal (Baselt, 2000; Friberg, 1986).
Discoloration of the peripheral parts of the corneas (Kayser-Fleischer rings) is a non-injurious hallmark feature of Wilson disease. A 'sunflower-like' discoloration of the most anterior layers of the lens has also been reported in these patients (Baselt, 2000; Grant & Schuman, 1993).

Indian childhood cirrhosis has been associated with increased hepatic copper concentrations, partly attributable to the use of copper or brass drinking vessels used to prepare animal milk or water. Milk apparently takes up copper more readily than water does, and thus milk copper contamination may be the cause (Bhave et al, 1987; Horslen et al, 1994; O'Neill & Tanner, 1989; Tanner et al, 1983; Tanner, 1998).

Multiple cases of childhood cirrhosis have been reported from various locations, but the involvement of copper in these cases is not entirely apparent (Rodec et al, 1999; (Walker, 1999; Walker-Smith, 1999) Trollman et al, 1999). The histological pattern of liver damage in a series of 12 German infants was noted to be variable (Muller-Hocker et al, 1998).
Various authors have suggested that at least some of these cases may be due to an inherited disorder or predisposition in conjunction with increased copper intake, or the result of copper in conjunction with some other environmental factor(s) (Anon, 1998; Horslen et al, 1994; Muller et al, 1998; Scheinberg & Sternlieb, 1994; Tanner, 1998; Tanner, 1998).
Severe liver disease involving massive accumulation of copper in the liver has been reported in a few cases not meeting the diagnostic criteria for either Wilson disease or Indian childhood cirrhosis (Horslen et al, 1994). Moreover, this so-called Indian childhood cirrhosis is becoming increasingly recognized in non-Indian children, and hepatic copper levels should be determined in all cases of childhood liver failure of unknown origin (Price et al, 1996).
Idiopathic copper toxicosis is related to abnormal hepatic copper accumulation with cirrhosis and cholestasis, not always due to an exogenous copper source, and is characterized by distinct clinical and pathologic features. This disorder is generally found in such pediatric liver diseases as Wilson disease, Indian childhood cirrhosis, the non-Indian disease called idiopathic copper toxicosis, and disorders associated with chronic cholestasis (Muller et al, 1998). These diseases usually result from a genetic predisposition to the hepatic accumulation of copper (Barceloux, 1999; Anon, 1998).

Lung damage after chronic exposure to fumes in industry has not been described. The higher incidence of respiratory cancer reported in copper smelters has been attributed to the presence of arsenic in the ore (Hathaway et al, 1991).

Repeated exposure to copper fume and fine dust (possibly cupric oxide) is known to cause metal fume fever, a flu-like condition involving fever, chills, sweats, muscle aches and pains, cough and general malaise. Symptoms begin within a few hours after exposure and subside within 24 to 48 hours, leaving no permanent effects (Baselt, 2000; Friberg, 1986).

Limited epidemiological data indicate that coronary heart disease is associated with modest (5%) increases in serum copper. It is not apparent whether copper is a cause of heart disease or simply serves as a marker of some other phenomenon (Ford, 2000).

Additional epidemiologic studies of copper and heart disease have been reviewed and do not provide convincing evidence of a causal relationship (Anon, 1998).
In a nested case-control study within a prospective population study, cardiovascular mortality was found to be significantly increased in a population of patients with high serum copper and low serum zinc levels (Reunanen et al, 1996).

Limited epidemiologic evidence associates the development of Parkinson disease with occupational exposure to copper for in excess of 20 years. Possible interactions with lead, iron and manganese have been suggested (Gorell et al, 1999).

More than 20 years of occupational exposure to lead-copper or iron-copper combinations was associated with Parkinson disease in one case-control study (Gorell et al, 1999).
Occupational copper exposure was somewhat more frequent in 34 patients with Parkinson disease than in controls in another study (Wechsler et al, 1991).

Chronic exposure to low levels of copper has been reported to induce anemia, probably from hemolytic effects (HSDB , 2002; ACGIH, 1991).

Allergic contact dermatitis has been reported with chronic copper exposure, but is extremely rare (Bockendahl, 1974; Bingham et al, 2001).

Copper DEFICIENCY has caused anemia, CNS symptoms and vascular damage (Friberg, 1986). However, clinically significant copper deficiency is reportedly rare, occurring only with substantial gastrointestinal malabsorption or reduced intake, or with the X-linked copper disorder known as Menke's disease, characterized by physical and mental retardation, brain degeneration, hypothermia, and death in the first few years of life (Bingham et al, 2001).

Some effects are the result of mixed chronic exposure:

Vineyard workers suffering from lung damage were exposed to a mixture of copper sulfate and lime, and were also possibly exposed to ARSENIC (Friberg, 1986).
Smelter workers could be exposed to other metals, as could miners, who might also be exposed to CRYSTALLINE SILICA. Although there have been reports of chronic copper poisoning in copper refinery workers, the noted effects were most likely due to contaminants such as arsenic, lead and selenium in the ore (Kirk-Othmer, 1992a).

-FIRST AID

FIRST AID AND PREHOSPITAL TREATMENT

SUMMARY

Vomiting is rapid and spontaneous in most patients following ingestion of copper salts.

ACTIVATED CHARCOAL

There are no studies demonstrating adsorption of copper to activated charcoal. Most highly charged metal ions are not well adsorbed to activated charcoal. Activated charcoal may obscure endoscopy findings after ingestion of corrosive copper salts as well as creating a risk of corrosive GI perforation with copper. Activated charcoal is NOT recommended in the pre-hospital setting.

-MEDICAL TREATMENT

LIFE SUPPORT

Support respiratory and cardiovascular function.

SUMMARY

FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Move victim to fresh air.
Call 911 or emergency medical service.
Give artificial respiration if victim is not breathing.
Do not use mouth-to-mouth method if victim ingested or inhaled the substance;give artificial respiration with the aid of a pocket mask equipped with a one-way valve or other proper respiratory medical device.
Administer oxygen if breathing is difficult.
Remove and isolate contaminated clothing and shoes.
In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes.
For minor skin contact, avoid spreading material on unaffected skin.
Keep victim warm and quiet.
Effects of exposure (inhalation, ingestion or skin contact) to substance may be delayed.
Ensure that medical personnel are aware of the material(s) involved and take precautions to protect themselves.

FIRST AID

FIRST AID (DUST/MIST)

The folling first aid measures are suggested for copper DUST or MIST exposure (National Institute for Occupational Safety and Health, 2007; OSHA, 2000):

Immediately wash the eyes with large amounts of water, occasionally lifting the lower and upper lids. Get medical attention immediately. Primary eye protection (spectacles or goggles), as defined by the Occupational Safety and Health Administration (OSHA), should be used when working with this chemical. Face shields should only be worn over primary eye protection.

Contact lens use is not recommended when working with this chemical. If contact lenses are worn, then appropriate eye and face protection devices must be used. OSHA emphasizes that dusty and/or chemical environments may represent an additional hazard to contact lens wearers.

DERMAL EXPOSURE - Promptly wash the contaminated skin with soap and water. If this chemical penetrates clothing, promptly remove the clothing and wash the skin with soap and water. Get medical attention promptly.
INHALATION EXPOSURE - Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attention as soon as possible.
ORAL EXPOSURE - If this chemical has been swallowed, get medical attention immediately.
TARGET ORGANS - Eyes, skin, respiratory system, liver and kidneys (increased risk with Wilson's disease).

FIRST AID (FUMES)

The following first aid measures are suggested for copper FUME exposure (National Institute for Occupational Safety and Health, 2007):

INHALATION EXPOSURE - Move the exposed person to fresh air at once. If breathing has stopped, perform artificial respiration. Keep the affected person warm and at rest. Get medical attentions as soon as possible.
TARGET ORGANS - Eyes, skin and respiratory system (increased risk with Wilson's disease).

INHALATION EXPOSURE

INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm.

DERMAL EXPOSURE

DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

EYE EXPOSURE

DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.

ORAL EXPOSURE

ACTIVATED CHARCOAL: Administer charcoal as a slurry (240 mL water/30 g charcoal). Usual dose: 25 to 100 g in adults/adolescents, 25 to 50 g in children (1 to 12 years), and 1 g/kg in infants less than 1 year old.

-RANGE OF TOXICITY

MINIMUM LETHAL EXPOSURE

The minimum lethal human dose to this agent has not been delineated.

Ingestion of 10 to 20 grams of a soluble copper salt is lethal, and death usually occurs 7 to 10 days after ingestion (Baselt, 2000).

In an untreated adult, an estimated lethal dose is reported to be about 10 to 20 grams of copper (Barceloux, 1999).

CASE REPORTS

Chronic ingestion of copper-containing coins by a mentally disturbed patient resulted in severe copper toxicity and death. At autopsy, 275 US coins were found in the stomach (Yelin et al, 1987).
Hasan et al (1995) reported the death of a mentally handicapped 46-year-old man due to chronic ingestion of British coins. At autopsy, over 700 coins were removed, mostly 1-pence and 2-pence, which were composed of 97 percent copper (Hasan et al, 1995).

MAXIMUM TOLERATED EXPOSURE

ROUTE OF EXPOSURE

ORAL

The lowest published toxic dose for humans via the oral route is 120 mcg/kg, with nausea and vomiting reported (RTECS , 2002). The ingestion of as little as one gram of copper may cause toxic serum concentrations (Barceloux, 1999). Ingestion of greater than 25 mg/L copper in beverages or foods has been associated with acute gastroenteritis (Barceloux, 1999).
Tap water copper concentrations of 1 to 2 mg/L have been tolerated by adults with no adverse effects, but are not as well tolerated by children (Nordberg et al, 1985).
Children developed severe liver disorders after ingestion of 10 mg of copper in contaminated milk (Bingham et al, 2001).
In studies of 61 healthy volunteers drinking single 200-mL volumes of copper sulfate, nausea developed at 4 mg/L (33 subjects, concentration as elemental copper) and vomiting developed at 6 mg/L (7 subjects). In this study, 2 mg/L seemed to be generally tolerated (Olivares et al, 2001).
In a study involving 1-week-long exposures to drinking water with varying copper concentrations in a Latin-squares design, no association of gastrointestinal symptoms with cumulative copper intake was noted at concentrations of 0 to 5 mg/L. However, exposure to concentrations of 3 mg/L or more was associated with nausea, abdominal pain and vomiting (Pizarro et al, 1999a; Pizarro et al, 1999b).
The taste threshold for copper in water in the Olivares (2001) study was separately reported to be 2.6 mg/L (Zacarias et al, 2001). Various authors have reported taste thresholds of 0.8 to 5 mg/L copper (Anon, 1998).
CASE REPORT: Two 6-year-old boys (fraternal twins) developed hepatotoxicity following consumption of an energy drink mixed with chocolate milk on a daily basis for the previous 8 months, as well as 2 multivitamins daily. Total amount of copper consumed was 9088 mcg/day, approximately 21 times the recommended daily allowance for their age. Both patients had elevated liver enzyme concentrations; however, a liver biopsy of one of the patients revealed extensive fibrosis with positive staining for copper and a dry copper weight of 1400 mcg/g of liver tissue. Despite chelation therapy with trientine and zinc, the patient developed liver failure within a week of presentation. He received a liver transplant within 72 hours and recovered uneventfully. The second patient's liver biopsy was negative despite a dry copper weight of 3020 mcg/g of liver tissue. He remained stable following chelation therapy with penicillamine. It is suspected that the first patient may have had either underlying liver disease or a possible unidentified defect of copper metabolism, resulting in liver failure despite a dry copper weight of less than half that of his brother (Bartlett & Erickson, 2012).

INHALATION

Inhalation of 60 to 100 mg/kg of copper dust caused gastrointestinal symptoms including vomiting and inflammation (ITI, 1995).

OCCUPATIONAL

Workers exposed to concentrations of one to three mg/m(3) for short periods experienced altered taste response but no nausea. Airborne levels from 0.02 to 0.4 mg/m(3) produced no complaints (Hathaway et al, 1996).
Studies on exposures from industrial copper welding and refining operations in Great Britain indicate that concentrations up to 0.4 mg/m(3) cause no ill effects (ACGIH, 1996).

However, another study reported symptoms similar to metal fume fever in workers exposed to metallic copper dust at an airborne concentration of 0.1 mg/m(3) (ACGIH, 1996).

OTHER

COPPER VESSELS: Preparation of food (particularly acidic foods) in copper vessels with loss of the tinned surface has produced gastroenteritis (Gill & Bhagat, 1999).

Indian childhood cirrhosis has been associated with increased hepatic copper concentrations, partly attributable to the use of copper or brass drinking vessels used to prepare animal milk (Bhave et al, 1987).
Beverages (especially those that are acidic) prepared or stored in brass containers may become contaminated by copper ions and cause poisoning when consumed. Symptoms are nausea and vomiting, which may occur within 10 minutes of consumption.

TAP WATER: Excessive copper in tap water may occur as a result of leaching of copper from pipes; acidity increases the leaching (Spitalny et al, 1984; Prociv, 1997).

Carcinogenicity Ratings for CAS7440-50-8 :

ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Copper, fume
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Copper, dusts and mists, as Cu
EPA (U.S. Environmental Protection Agency, 2011): D ; Listed as: Copper

D : Not classifiable as to human carcinogenicity.

IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed
NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Copper (dusts and mists, as Cu)
MAK (DFG, 2002): Not Listed
NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed

TOXICITY AND RISK ASSESSMENT VALUES

EPA IRIS

EPA Risk Assessment Values for CAS7440-50-8 (U.S. Environmental Protection Agency, 2011):

Oral:

Slope Factor:
RfD:

Inhalation:

Unit Risk:
RfC:

Drinking Water:

Unit Risk:

TOXICITY VALUES

References: RTECS, 2002 ITI, 1995
- LD50- (INTRAPERITONEAL)MOUSE:
- LDLo- (SUBCUTANEOUS)RABBIT:
- TDLo- (ORAL)HUMAN:
- TDLo- (INTRAVENOUS)RABBIT:
- TDLo- (ORAL)RABBIT:
- TDLo- (SUBCUTANEOUS)RABBIT:
- TDLo- (INTRAPERITONEAL)RAT:
- TDLo- (INTRAUTERINE)RAT:
- TDLo- (ORAL)RAT:

-STANDARDS AND LABELS

WORKPLACE STANDARDS

ACGIH TLV Values for CAS7440-50-8 (American Conference of Governmental Industrial Hygienists, 2010):

Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.

Adopted Value

Copper, fume

TLV:

TLV-TWA: 0.2 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: Not Listed
Codes: Not Listed
Definitions: Not Listed

TLV Basis - Critical Effect(s): Irritation; GI; metal fume fever
Molecular Weight: 63.55

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

Adopted Value

Copper, dusts and mists, as Cu

TLV:

TLV-TWA: 1 mg/m(3)
TLV-STEL:
TLV-Ceiling:

Notations and Endnotes:

Carcinogenicity Category: Not Listed
Codes: Not Listed
Definitions: Not Listed

TLV Basis - Critical Effect(s): Irritation; GI; metal fume fever
Molecular Weight: 63.55

For gases and vapors, to convert the TLV from ppm to mg/m(3):

[(TLV in ppm)(gram molecular weight of substance)]/24.45

For gases and vapors, to convert the TLV from mg/m(3) to ppm:

[(TLV in mg/m(3))(24.45)]/gram molecular weight of substance

AIHA WEEL Values for CAS7440-50-8 (AIHA, 2006):

Not Listed

NIOSH REL and IDLH Values for CAS7440-50-8 (National Institute for Occupational Safety and Health, 2007):

Listed as: Copper (dusts and mists, as Cu)
REL:

TWA: 1 mg/m(3)
STEL:
Ceiling:
Carcinogen Listing: (Not Listed) Not Listed
Skin Designation: Not Listed
Note(s): [*Note: The REL also applies to other copper compounds (as Cu) except Copper fume.]

IDLH:

IDLH: 100 mg Cu/m3 (as Cu)
Note(s): Not Listed

OSHA PEL Values for CAS7440-50-8 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):

Listed as: Copper Fume (as Cu)
Table Z-1 for Copper Fume (as Cu):

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3: 0.1

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: No
Notation(s): Not Listed

Listed as: Copper Dusts and mists (as Cu)
Table Z-1 for Copper Dusts and mists (as Cu):

8-hour TWA:

ppm:

Parts of vapor or gas per million parts of contaminated air by volume at 25 degrees C and 760 torr.

mg/m3: 1

Milligrams of substances per cubic meter of air. When entry is in this column only, the value is exact; when listed with a ppm entry, it is approximate.

Ceiling Value:
Skin Designation: No
Notation(s): Not Listed

OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS7440-50-8 (U.S. Occupational Safety and Health Administration, 2010):

Not Listed

ENVIRONMENTAL STANDARDS

EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS7440-50-8 (U.S. Environmental Protection Agency, 2010):

Listed as: Copper
Final Reportable Quantity, in pounds (kilograms):

5000 (2270)

Additional Information:
Listed as: Copper and compounds

Additional Information:

EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS7440-50-8 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA RCRA Hazardous Waste Number for CAS7440-50-8 (U.S. Environmental Protection Agency, 2010b):

Not Listed
Editor's Note: The D, F, and K series waste numbers and Appendix VIII to Part 261 -- Hazardous Constituents were not included. Please refer to 40 CFR Part 261.

EPA SARA Title III, Extremely Hazardous Substance List for CAS7440-50-8 (U.S. Environmental Protection Agency, 2010):

Not Listed

EPA SARA Title III, Community Right-to-Know for CAS7440-50-8 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):

Listed as: Copper Compounds: Includes any unique chemical substance that contains copper as part of that chemical's infrastructure (except for C.I. Pigment Blue 15 (PB-15, CAS No. 147-14-8), C.I. Pigment Green 7 (PG-7, CAS No. 1328-53-6), and C.I. Pigment Green 36 (PG-36, CAS No. 14302-13-7) except copper phthalocyanine compounds that are substituted with only hydrogen and/or bromine and/or chlorine that meet the following molecular structure definition: [graphic available only on GPO site].
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

Listed as: Copper
Effective Date for Reporting Under 40 CFR 372.30: 1/1/87
Lower Thresholds for Chemicals of Special Concern under 40 CFR 372.28:

DOT List of Marine Pollutants for CAS7440-50-8 (49 CFR 172.101 - App. B, 2005):

Listed as Copper metal powder
Severe Marine Pollutant: Yes

EPA TSCA Inventory for CAS7440-50-8 (EPA, 2005):

Listed as: Copper

SHIPPING REGULATIONS

SURFACE

DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):

Not Listed

ICAO International Shipping Name (ICAO, 2002):

Not Listed

LABELS

NFPA

NFPA Hazard Ratings for CAS7440-50-8 (NFPA, 2002):

Not Listed

-HANDLING AND STORAGE

SUMMARY

INDUSTRIAL CHEMICALS

The main industrial route of exposure to copper is inhalation of its dust or fumes. This should be avoided or minimized by use of appropriate respiratory protection with face masks (Harbison, 1998).
Copper dust inhalation causes irritation of the upper respiratory tract, and influenza-like symptoms (Hathaway et al, 1996). Eye, mouth and nose irritation as well as gastrointestinal and dermal effects are also likely with exposure (ACGIH, 1996).
In the case of copper dust or mists, wear appropriate clothing to prevent prolonged or repeated skin contact. Wear eye protection to reduce the probability of eye contact (Sittig, 1991).

HANDLING

Contact lenses should not be worn when working with copper (HSDB , 2001). Proper eye protection should be used to prevent eye contact (NIOSH , 2001).

When working in environments with copper dust or fume concentration above 1 mg/m(3), use NIOSH recommended respirator and eye protection (HSDB , 2001; NIOSH , 2001).

Clothing that becomes wet or significantly contaminated should be removed immediately and replaced. Any potentially contaminated clothing should be removed and replaced before leaving the work site (HSDB , 2001; NIOSH , 2001).

Skin contact should be avoided. Workers should wash skin immediately after contact with copper or its compounds (HSDB , 2001; NIOSH , 2001).

When working with copper's soluble salts, wear appropriate protective clothing, as they can be corrosive to skin (OHM/TADS , 2001).

When handling copper, wear gloves, goggles and overalls (ITI, 1995).

STORAGE

CONTAINER

Store as to avoid creation of fine copper dusts or fumes (Sittig, 1991).
In the presence of some complexing agents, copper can react with aqueous media to form hydrogen. Slow pressurization of the container results, which may cause containers to burst upon standing. Such an explosion occurred with a bottle of "cuprous solution" prepared by standing cupric oxide in strong hydrochloric acid over excess copper (Urben, 1999).
Store in a watertight container, as copper reacts with water, which can cause vapor explosion (Urben, 1999).
Copper will become dull when exposed to air; over time, it will become coated in green basic carbonate (Budavari, 2000).

ROOM/CABINET RECOMMENDATIONS

Proper local exhaust ventilation should exist in rooms where copper fumes are produced (HSDB , 2001).

INCOMPATIBILITIES

Separate from the following compounds, as Copper will react violently with all of them (Lewis, 2000):
- Acetylene (C2H2)
- Chlorine (Cl2) + oxygen difluoride (OF2)
- Hydrogen peroxide (H2O2)
- Hydrogen sulfide (H2S) + air
- Poatssium peroxide (K2O2)
- Lead azide (Pb(N3)2)
- Sodium azide (NaN3)
- Sodium peroxide (Na2O2)
- Bromates
- Chlorates
- Iodates
- Dimethyl sulfoxide + trichloroacetic acid
- Ethylene oxide
- Hydrazine mononitrate
- Hydrazoic acid
- Sulfuric acid
Liquid copper will explode on contact with water (Lewis, 2000).
Potentially explosive reactions may occur with acetylenic compounds, 3-bromopropyne, ethylene oxide, lead azide and ammonium nitrate. Copper will ignite on contact with chlorine, chlorine trifluoride, fluorine (above 121 degrees F) and hydrazine nitrate (above 70 degrees F) (Lewis, 2000).
Copper is incompatible with 1-bromo-2-propyne (Lewis, 2000).
It is also incompatible with acids (Pohanish & Greene, 1997).
In dust or mist form, copper is incompatible with magnesium metal (Sittig, 1991).
In the presence of wet acetylene and ammonia, copper and brasses (down to 60 percent copper) will form explosive acetylides (NFPA, 1997).
On long standing, a white precipitate may form which is a readily explodable peroxide (HSDB , 2001).
Finely divided copper mixed with chlorates or iodates explode on friction, percussion, shock or heating (HSDB , 2001; Urben, 1999).
Store to avoid contact with oxidizers and acids (Sittig, 1991).
Ignites on contact with chlorine, chlorine trifluoride, fluorine (above 121 degrees C) and hydrazinium nitrate (above 70 degrees C) (Lewis, 2000).

-PERSONAL PROTECTION

SUMMARY

RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Wear positive pressure self-contained breathing apparatus (SCBA).
Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.

EYE/FACE PROTECTION

Wear appropriate eye protection to prevent probability of eye contact with copper dusts or mist (HSDB , 2001).

Contact lenses should not be worn when working with copper (HSDB , 2001).

RESPIRATORY PROTECTION

Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.

PROTECTIVE CLOTHING

CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 7440-50-8.

Specific recommendations and test data for this chemical were not found in the available manufacturers' product literature. A complete list of consulted manufacturers and references is presented below.

-PHYSICAL HAZARDS

FIRE HAZARD

SUMMARY

Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- 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.
Copper is noncombustible, except in powder form (Lewis, 1997).
Copper is a hazardous fire danger in powdered form (OHM/TADS , 2001).
Copper ignites on contact with the following (Lewis, 2000):
- Chlorine
- Chlorine trifluoride
- Fluorine (above 121 degrees C)
- Hydrazinium nitrate (above 70 degrees C)
Copper foil burns spontaneously in the presence of gaseous chlorine (NFPA, 1997).

FLAMMABILITY CLASSIFICATION

NFPA Flammability Rating for CAS7440-50-8 (NFPA, 2002):

Not Listed

FIRE CONTROL/EXTINGUISHING AGENTS

SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Dry chemical, CO2 or water spray.

LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Water spray, fog or regular foam.
Move containers from fire area if you can do it without risk.
Dike fire control water for later disposal; do not scatter the material.
Use water spray or fog; do not use straight streams.

TANK OR CAR/TRAILER LOAD FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Fight fire from maximum distance or use unmanned hose holders or monitor nozzles.
Do not get water inside containers.
Cool containers with flooding quantities of water until well after fire is out.
Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank.
ALWAYS stay away from tanks engulfed in fire.
For massive fire, use unmanned hose holders or monitor nozzles; if this is impossible, withdraw from area and let fire burn.

NFPA Extinguishing Methods for CAS7440-50-8 (NFPA, 2002):

Not Listed

EXPLOSION HAZARD

Liquid copper explodes on contact with water (Lewis, 2000).

Copper forms potentially explosive reactions with the following (Lewis, 2000):

Acetylenic compounds
Ammonium nitrate
3-Bromopropyne
Ethylene oxide
Lead azide

Copper and brasses (down to 60 percent copper) react readily in the presence of wet acetylene and ammonia to form explosive acetylides (NFPA, 1997).

Unstable acetylides are also formed when acetylene comes in contact with copper that has been heated to form a tarnish of copper oxide (NFPA, 1997).

Heat, percussion, and sometimes light friction may cause combinations of finely divided copper and finely divided bromates (also chlorates or iodates) of barium, calcium, magnesium, potassium, sodium, or zinc to explode (NFPA, 1997).

A white deposit, which is a readily explosive peroxide, may form upon long standing (HSDB , 2001).

An explosion resulted from the corrosion of brass parts (on a vacuum gage and water jet vacuum pump) after prolonged exposure to hydrozoic acid vapors (NFPA, 1997).

Reactions involving copper solutions which release hydrogen can cause pressure build up in closed containers that may lead to explosions of the containers (NFPA, 1997).

DUST/VAPOR HAZARD

Copper dust and fumes cause irritation of the upper respiratory tract, and copper fumes will also irritate the eyes, nose, and throat (HSDB , 2001).

Inhalation, skin and/or eye contact can cause irritation to the eyes, nose, and pharynx, perforation of the nasal septum, dermatitis, lung, liver and kidney damage, and anemia (ITI, 1995; NIOSH , 2001).

Exposure to copper oxide fumes can cause "metal fume fever" (ACGIH, 1996; Budavari, 2000; ITI, 1995).

REACTIVITY HAZARD

Copper is noncombustible, except in powder form (Lewis, 2000).

Liquid copper explodes on contact with water (Lewis, 2000).

Copper forms potentially explosive reactions with the following (Lewis, 2000):

Acetylenic compounds
Ammonium nitrate
3-Bromopropyne
Ethylene oxide
Lead azide

Copper and brasses (down to 60 percent copper) react readily in the presence of wet acetylene and ammonia to form explosive acetylides (NFPA, 1997).

Unstable acetylides are also formed when acetylene comes in contact with copper that has been heated to form a tarnish of copper oxide (NFPA, 1997).

Heat, percussion, and sometimes light friction may cause combinations of finely divided copper and finely divided bromates (also chlorates or iodates) of barium, calcium, magnesium, potassium, sodium, or zinc to explode (NFPA, 1997).

A white deposit, which is a readily explosive peroxide, may form upon long standing (HSDB , 2002).

Copper forms an incandescent reaction with potassium oxide (Lewis, 2000).

The reacting mixture of phosphorus and copper, iron, nickel, or platinum can become incandescent when heated (NFPA, 1997).

Copper ignites on contact with the following (Lewis, 2000):

Chlorine
Chlorine trifluoride
Fluorine (above 121 degrees C)
Hydrazinium nitrate (above 70 degrees C)

Copper reacts violently with the following (Lewis, 2000):

Acetylene (C2H2)
Chlorine (Cl2) + oxygen difluoride (OF2)
Hydrogen peroxide (H2O2)
Hydrogen sulfide (H2S) + air
Poatssium peroxide (K2O2)
Lead azide (Pb(N3)2)
Sodium azide (NaN3)
Sodium peroxide (Na2O2)
Bromates
Chlorates
Iodates
Dimethyl sulfoxide + trichloroacetic acid
Ethylene oxide
Hydrazine mononitrate
Hydrazoic acid
Sulfuric acid

Copper is incompatible with 1-bromo-2-propyne (Lewis, 2000).

Copper becomes dull when exposed to air. In moist air, copper gradually becomes coated with green basic carbonate (Budavari, 2000).

A bluish-green precipitate of cupric hydroxide is formed when water-soluble cupric salts mix with sodium hydroxide. When warmed, the precipitate is changed to black cupric oxide (Budavari, 2000).

Potassium ferrocyanide produces a brownish-red precipitate of copper ferrocyanide (Budavari, 2000).

In acidic solutions, hydrogen sulfide produces a black precipitate of cupric sulfide which is soluble in a solution of sodium cyanide (Budavari, 1996).

Aluminum, iron, or zinc cause metallic copper to precipitate from its solutions (Budavari, 2000).

The explosion of copper azide produces metallic copper and nitrogen (Yinon & Zitrin, 1981).

EVACUATION PROCEDURES

SUMMARY

Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.

SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

Increase, in the downwind direction, as necessary, the isolation distance of at least 25 to 50 meters (80 to 160 feet) in all directions.

FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

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.

PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)

CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number:

MEXICO:

SETIQ:

01-800-00-214-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5559-1588;
For calls originating elsewhere, call: 011-52-555-559-1588.

CENACOM:

01-800-00-413-00 in the Mexican Republic;
For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885;
For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.

ARGENTINA:

CIQUIME:

0-800-222-2933 in the Republic of Argentina;
For calls originating elsewhere, call: +54-11-4613-1100.

BRAZIL:

PRÓ-QUÍMICA:

0-800-118270 (Toll-free in Brazil);
For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).

COLUMBIA:

CISPROQUIM:

01-800-091-6012 in Colombia;
For calls originating in Bogotá, Colombia, call: 288-6012;
For calls originating elsewhere, call: 011-57-1-288-6012.

CANADA:

CANUTEC:

613-996-6666 (Collect calls are accepted);
*666 cellular (in Canada only).

UNITED STATES:

CHEMTREC®:

1-800-424-9300 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
703-527-3887 for calls originating elsewhere (Collect calls are accepted).

CHEM-TEL, INC.:

1-800-255-3924 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
813-248-0585 for calls originating elsewhere (Collect calls are accepted).

INFOTRAC:

1-800-535-5053 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
352-323-3500 for calls originating elsewhere (Collect calls are accepted).

3E COMPANY:

1-800-451-8346 (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
760-602-8703 for calls originating elsewhere (Collect calls are accepted).

NATIONAL RESPONSE CENTER (NRC):

1-800-424-8802 - (24 hours) (Toll-free in the U.S., Canada, and the U.S. Virgin Islands);
202-267-2675 for calls in the District of Columbia.

MILITARY SHIPMENTS:

703-697-0218 - Explosives/ammunition incidents (Collect calls are accepted);
1-800-851-8061 - All other dangerous goods incidents.

NATIONWIDE POISON CONTROL CENTER (United States only):

1-800-222-1222 (Toll-free in the U.S.).

For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions.
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.
Keep unauthorized personnel away.
Stay upwind.
Keep out of low areas.

AIHA ERPG Values for CAS7440-50-8 (AIHA, 2006):

Not Listed

DOE TEEL Values for CAS7440-50-8 (U.S. Department of Energy, Office of Emergency Management, 2010):

Listed as Copper
TEEL-0 (units = mg/m3): 1
TEEL-1 (units = mg/m3): 3
TEEL-2 (units = mg/m3): 5
TEEL-3 (units = mg/m3): 100
Definitions:

TEEL-0: The threshold concentration below which most people will experience no adverse health effects.
TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure.
TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape.
TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.

AEGL Values for CAS7440-50-8 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):

Not Listed

NIOSH IDLH Values for CAS7440-50-8 (National Institute for Occupational Safety and Health, 2007):

IDLH: 100 mg Cu/m3 (as Cu)
Note(s): Not Listed

CONTAINMENT/WASTE TREATMENT OPTIONS

SUMMARY

SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- 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.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 151 (ERG, 2004)
- Wear positive pressure self-contained breathing apparatus (SCBA).
- Wear chemical protective clothing that is specifically recommended by the manufacturer. It may provide little or no thermal protection.
- Structural firefighters' protective clothing provides limited protection in fire situations ONLY; it is not effective in spill situations where direct contact with the substance is possible.
At the time of this 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 (HSDB , 2001).
- Copper dusts or mist, and copper compounds may be disposed of in sealed containers in a secured sanitary landfill (HSDB , 2001).
The following information is for COPPER CONCENTRATES CONTAINING LEAD SULFIDES (AAR, 2000):
- For land spills, liquid or solid material should be contained by digging a pit, pond, or lagoon holding area. Prevent solids from dissolving in rain or fire-fighting water by covering the material with plastic.
- For water spills, trap material at the bottom by using natural deep water pockets, excavated lagoons, or sand bag barriers. Trapped material may then be removed with suction hoses. Mechanical dredges or lifts may be employed to remove masses of pollutants and precipitates.

WASTE TREATMENT OPTIONS

RECYCLING/RECLAMATION

Electrolytic techniques are used to recover a variety of heavy metals from process streams or rinsewaters, including the recovery of copper from sulfuric acid solutions (Freeman, 1998).
Filter presses or sludge driers have been used to increase the concentration of copper in electroplating wastewater treatment sludge, making the sludge more useful for copper reclamation (Freeman, 1998).
Strong-acid cation-exchange resins can be used to remove copper from wastewater by exchanging hydrogen for the copper in a reversible reaction. Copper can then be removed from the resin to yield a more concentrated copper solution, using a moderately concentrated (about 10%) strong mineral acid such as sulfuric or hydrochloric acid. It may be possible to recycle the copper obtained by this method (Freeman, 1998).
Copper can be concentrated in waste streams using reverse osmosis, and it can then be electrolytically removed for reclamation (HSDB , 2001).
Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.

CHEMICAL TREATMENT

Chemical precipitation may be used to convert copper in aqueous solutions to an insoluble form (Freeman, 1998). This is the preferred method for removing toxic heavy metals such as copper from electroplating waters (HSDB , 2001).
Sodium borohydride is a reducing agent that can be used to convert copper in waste solutions to the insoluble elemental form. The most efficient conversion occurs with the process carried out in the pH range between 8 and 11 (Freeman, 1998).
Other precipitation processes for metal-bearing hazardous waste streams include hydroxide, lime, and/or sulfide treatment (HSDB , 2001).
Potassium ferricyanide (which is not very toxic), lime, or NaHCO3 can be used to precipitate copper. Metallic copper can be precipitated from salts with the addition of aluminum, iron, or zinc (OHM/TADS , 2001).
Various processes used in the textile industry to de-colorize effluent wastewaters from the dyeing process were studied. The results showed that the use of ozonation or advanced oxidation to remove color from the azo dye Direct Blue 80 readily releases inorganic copper and may significantly affect the toxicity of the treated wastewater (Adams et al, 1995).
DISPOSAL METHODS: Copper dust, mist, and copper compounds may be placed in sealed containers and disposed of in a secured sanitary landfill (HSDB , 2001).
If reclamation of copper is not feasible, the metal can be precipitated using caustics, and the resulting sludge deposited in a chemical waste landfill (HSDB , 2001).
Route wastes to metal salvage facility (HSDB , 2001).

BIOREMEDIATION

Rhizofiltration, the use of plant roots to absorb, concentrate, and precipitate heavy metals from polluted effluents, is an emerging remediation technology. Hydroponically grown Indian mustard (Brassica juncea) roots were shown to remove copper in solution. When grown hydroponically, large quantities of roots of this plant may be produced rapidly and economically (Dushenkov et al, 1995).
- Wetland ecosystems have also been used to remove heavy metal pollutants such as copper. For the most efficient removal, the pollutants must pass through the rooting zone. Floating areas of wetland vegetation may not act as a mechanism for heavy metal binding (Denny et al, 1995).
Up to 4 percent copper is incorporated by biological bodies in activated sludge or ripe sewage (OHM/TADS , 2001).
Banana pith (Musacea zingiberales) was shown to adsorb copper from electroplating waste and synthetic solutions. Optimum adsorption occurred at a pH of 4.5, and the data followed the Langmuir isotherm model with maximum capacities of 8.55 mg/g for copper in electroplating waste and 13.46 mg/g in synthetic solution (Low et al, 1995).

PHYSICAL TREATMENT

Peat was used as a substrate for adsorbing copper, nickel and zinc from wastewater. A contact time of two hours was needed to reach equilibrium and the reaction was exothermic. The adsorption follows both the Langmuir and Freundlick models (Viraraghavan & Dronamraju, 1993).
Adsorption onto activated carbon, activated alumina, or iron filings has shown potential for treating wastewaters contaminated with metals (HSDB , 2001).
- Iron oxide coated to quartz sand by a heating process was used in reusable packed bed designs to remove copper from water. Concentrations of 0.64 to 3.20 mg/L of copper were completely removed (Lai et al, 1994).

-ENVIRONMENTAL HAZARD MANAGEMENT

POLLUTION HAZARD

Copper is widely distributed in nature, where it exist in its elemental state, in sulfides, arsenites, chlorides and carbonates (HSDB , 2001).

Copper occurs naturally in all forms in the earth's crust and in water. It also occurs in combined forms in several minerals, such as chalcopyrite, chalcocite, bornite, tetrahedrite, enargite and antlerite. It is found in marked concentrations in igneous rock (55 ppm), sandstone (50 ppm) and shales (45 ppm), and in lower concentrations in limestone (4 ppm). In the continental crust, copper tends to exist in the highest concentration in the ferromagnesium minerals, such as basalt pyropene and biotite (HSDB, 2004).

Copper pollution in water sources or soils may be the result of operations at nearby copper mines and smelters. Municipal incineration, stack emissions from coal burning power plants, and tobacco smoke may be other sources (HSDB, 2004).

Globally, the atmospheric copper flux from human activities is approximately three times higher than from natural sources. Non-ferrous metal production is a significant source of atmospheric copper (HSDB , 2001).

The use of copper piping in household plumbing systems may also result in copper water pollution. Acidity increases the leaching of copper into tap water (Spitainy et al, 1984). Copper concentrations may also increase in soft and chlorinated water (NRC, 1988).

Preparation of food using copper and brass utensils or vessels may also be a source of copper contamination in water (NRC, 1988).

Preparation of acidic foods in copper vessels with loss of the tinned surface has produced gastroenteritis (Ross, 1955).
Indian childhood cirrhosis has been associated with elevated hepatic copper concentrations, partly attributable to the use of copper or brass drinking vessels used to prepare animal milk (Bhave et al, 1987).

Spiritual green water was administered to members of spiritual churches by church leaders. Preliminary analysis identified copper sulfate in this green water (Akintonwa et al, 1989).

ENVIRONMENTAL FATE AND KINETICS

Copper is not likely to build up in the atmosphere due to the short residence time for airborne copper aerosols. However, airborne copper may be transported over long distances as evidenced by increases in the copper levels found in polar ice cores (Alloway, 1990).

WATER

SURFACE WATER
- Biotransformation processes do not appear to have a significant bearing on the aquatic fate of copper, although some copper complexes may be metabolized (HSDB , 2001).
- Fluxes of copper from the sediments to the water column in response to the presence of dissolved organic matter were measured in field enclosures placed on the floor of Lake Anna, Virginia. Phytoplankton added to the chamber water did not cause a rise in dissolved copper, but the addition of sodium humate resulted in a persistent 500% increase in dissolved copper concentration. The results suggest that enhancement of the concentration of dissolved copper in the water column by the formation of soluble organometallic complexes may occur from long term (but not short term) products of decomposition processes (Lehman & Mills, 1994).
- Copper forms acidic solution in water, and will precipitate insoluble oxides (OHM/TADS , 2001).

SOIL

TERRESTRIAL
- The balance between copper in the parent rock and in the derivative soil is affected by numerous factors, including the degree of weathering, the nature and intensity of the soil formation, drainage, pH, oxidation-reduction potential, and the amount of organic matter in the soil (HSDB , 2001).
- The total copper content of soils is not an accurate indication of copper levels in plants because of the variety of conditions which influence copper availability (HSDB , 2001).
- Acidic rainfall will probably not result in significant mobilization of copper from organic soils unless the pH of the rainfall is less than 3. However, mobilization may be increased in urban areas because of the effects of land disruption and increased acid rainfall (HSDB, 2004).
- Copper and other metals have been found to inhibit mineralization of nitrogen and phosphorus in contaminated forest soils, and may disturb important microbial processes such as nutrient cycling. While other metals also cause these effects, high levels of copper may be the most toxic to soil microorganisms and may reduce fungal species diversity (HSDB , 2001).
- Copper retention in soil is influenced by pH of the soil, as well as organic content (OHM/TADS , 2001).

ABIOTIC DEGRADATION

Airborne copper aerosols have a short residence time, but also may be transported over long distances. In water, copper can form acidic solutions and precipitate insoluble oxides. In surface water and soil, acidic conditions enhance copper mobility, while alkaline conditions favor precipitation. In soils, copper adsorption is a fast process, while desorption is relatively slow. Soil pH and organic content influence copper retention (HSDB, 2004; OHM/TADS , 2001; Hogg et al, 1993; Alloway, 1990).

BIOACCUMULATION

HUMANS

Copper concentrations were studied in 10 human males (mean age 43 years) that died suddenly. The liver was found to contain the highest levels of copper. There was a positive relationship between the concentration of copper and the amount of metallothionein in the tissue (HSDB , 2001).

FISH

Copper accumulated in the gills and midgut glands but not in the muscle tissue of shore crabs (Carcinus maenas). The accumulation of copper in the gill tissues was positively correlated with the solution salinity (Weeks et al, 1993).
Trout were fed a diet containing 10 g of Cu and Cd per kg dry weight of food for 28 days. Cadmium was more toxic than copper, causing 14 mortalities compared to one in the case of copper. The copper accumulated in the gills, liver, kidney and muscle tissues (Handy, 1993).

PLANTS

AQUATIC
- Excessive copper accumulates in citrus plant roots and causes phytotoxicity, but the addition of calcium to the soil in the form of CaCO3 or CaSO4 reduces the phytotoxicity (Alva et al, 1993).

MAMMALS

Copper accumulated in the liver of moose in Finland. The copper concentration in the livers of newborn moose was as high as 1 mg/g fresh mass and was significantly higher than in other newborn mammals. Ingesting the moose liver posed a health risk to humans (Hyvarinen & Nygren, 1993).
The Japanese serow, a bovine-ruminant, was found to accumulate copper in the liver (with a mean Cu concentration of 66.4 mcg/g). There were significantly higher concentrations found in the male liver than the female. The copper uptake correlated with the concentration of Cu in food plants (HSDB , 2001).
Tissue concentrations of copper were measured in six male Wistar rats. The highest accumulation was found in the kidney (HSDB , 2001).

OTHER

INVERTEBRATES
- Oysters collected from a canal lined with wood treated with chromated copper arsenate had high levels of metals in their tissues. The copper body burden of snails (Thais haemastoma floridana) that consumed the oysters increased 4-fold in 8 weeks (Weis & Weis, 1993).

BIOCONCENTRATION FACTOR

MARINE AND FRESHWATER PLANTS: 1000 (OHM/TADS, 2001)
ALGAE: 1840 to 3040 (OHM/TADS, 2001)
SPHAEROTILUS: 3890 (OHM/TADS, 2001)
MARINE INVERTEBRATES: 1670 (OHM/TADS, 2001)
- In soft parts: 5000 (OHM/TADS, 2001)
MARINE FISH: 667 (OHM/TADS, 2001)
FRESHWATER INVERTEBRATES: 1000 (OHM/TADS, 2001)
MARINE BACTERIA: 990 (OHM/TADS, 2001)
FRESHWATER FISH: 200 (OHM/TADS, 2001)

ENVIRONMENTAL TOXICITY

ECOTOXICITY STUDIES

Acidic conditions promote the solubility of copper and increase the concentration of ionic copper. Depending on the tolerance for various levels of copper in solution, these conditions may affect microorganisms and other aquatic animal populations (HSDB , 2001).
The effect of calcium on the toxicity of copper toward the brown alga, Cystoseira barbata forma aurentia, was evaluated and showed calcium plays a protective role in the alga growth by blocking the action of copper on chlorophyll a (Pellegrini et al, 1993).
A concentration of 0.080 ppm of copper sulfate in solution void of fulvic acids produced 89.2% mortality to the rodifer Brachionus calyciflorus. At fulvic acids to copper ratios equal to or greater than 1, no rodifer mortality was observed, suggesting that fulvic acids adsorb and complex copper ions, reducing their toxic effects (Porta & Ronco, 1993).
Dissolved organic carbon (DOC) and pH had significant effects on the toxicity of copper toward the larval fathead minnow. The regression equation describing the relationship was LC50 = -0.308 + 0.192 pH + 0.136 (pH.log(10)DOC), over a pH range of 5.4 to 7.3 and DOC range of 0.2 to 16 mg/L (Welsh et al, 1993).
Marine mussels, Mytilus edulis (L.), were exposed to copper at a concentration of 50 mcg/L for six days. The mussels suffered lysosomal destabilization in the digestive cells. Transfer of the mussels to clean seawater restored the lysosomal function in all but the oldest samples (Hole et al, 1993).
Green oysters and blue mussels were collected from areas with heavy copper contamination. The oysters and mussels were transferred to clean seawater tanks and rate of copper removal (depuration) monitored. The half-life of copper in green oysters was 11.6 days and in blue mussels it was 6.4 days (Han et al, 1993).
The toxicity of five metals (cadmium, copper, nickel, lead, and zinc), as a function of pH (at pH 6 through 9), was tested against several benthic and epibenthic species. Copper and lead had their highest toxicity at pH 6.3 and least at pH 8.3 (Schubauerberigan et al, 1993).
Shore crabs, Carcinus maenas, were exposed to sublethal (0.5 mg/L) and lethal (2 mg/L) concentrations of waterborne copper. Thickening of the gill tissue was observed after 5 to 6 days of exposure and suggested tissue hypoxemia was the major toxic effect at the lethal concentrations (Nonnotte et al, 1993).
Copper concentrations of 5.0 mcg/L to 0.1 mg/L caused modification of electric organ discharge activity in two species of weakly electric fish, Gnathonemus petersi and G. tamandua (Family Mormyridae). The pattern of this response was variable (Lewis et al, 1994).
The growth rate of Rhine River water bacteria populations were found to be sensitive to low levels of copper in solution. The estimated EC50 value was 25 to 310 mcg/L (Tubbing et al, 1993).
The photosystem II activity of the blue green alga, Anabaena cylindrica, was inhibited 50% at a concentration of 10 mcM/L and completely blocked at 50 mcM/L (Mishra et al, 1993).
Rice plants were grown in nutrient solutions containing copper at concentrations between 0.002 and 6.25 g/m(3). The photosynthetic electron transport activity of the plants was inversely proportional to the growth media copper concentrations (Lidon & Henriques, 1993).

ECOTOXICITY VALUES FOR WATER

References: (Jacobson et al, 1993; Lin & Dunson, 1993; Welsh et al, 1993)
EC50 - (WATER) VILLOSA IRIS: 27 mcg/L for 24H
EC50 - (WATER) ANODONTA GRANDIS: 33 mcg/L for 24H
LC50 - (WATER) STRIPED BASS LARVAE: 0.1 ppm for 24H
LC50 - (WATER) STRIPED BASS LARVAE: 0.05 ppm for 48 to 96H
LC50 - (WATER) FATHEAD MINNOW: 2 mcg/L for 96H (pH 5.6, DOC 0.2 mg/L)
LC50 - (WATER) FATHEAD MINNOW: 182 mcg/L for 96H (pH 6.9, DOC 15.6 mg/L)
LC50 - (WATER) VILLOSA IRIS: 83 mcg/L for 24H
LC50 - (WATER) ANODONTA GRANDIS: 44 mcg/L for 24H
LC50 - (WATER) FUNDULUS HETEROCLITUS: 1.7 mg/L for 96H
LC50 - (WATER) RIVULUL MARMORATUS: 1.4 mg/L for 96H

FRESHWATER TOXICTY VALUES

References: (OHM/TADS, 2001)
TLm - (WATER) FATHEAD MINNOW: 0.14 to 0.24 ppm for 96H, soft flow-through
TLm - (WATER) BLUEGILL: 1.25 ppm for 96H, as Cu
TLm - (WATER) GAMMARUS PSEUDOLIMNAEUS: 0.02 ppm for 96H, as Cu
TLm - (WATER) RAINBOW TROUT: 0.8 ppm for 48H
TLm - (WATER) PHYSA INTEGRA: 0.039 ppm for 96H, as Cu
TLm - (WATER) CRAYFISH: 1.0 ppm for 24H
TLm - (WATER) CAMPELOMA DECISUM: 1.7 ppm for 96H, as Cu
TLm - (WATER) RAINBOW TROUT: 0.9 ppm for 48H
TLm - (WATER) BROOK TROUT: 0.1 ppm, as Cu
TLm - (WATER) FATHEAD MINNOW: 0.43 ppm for 96H, static
TLm - (WATER) FATHEAD MINNOW: 0.47 ppm for 96H, flow-through sulfate salt
TLm - (WATER) FATHEAD MINNOW: 0.13 to 0.22 ppm for 96H, soft flow-through
TLm - (WATER) BANDED KILLIFISH: 1.5 ppm for 24H, as Cu
TLm - (WATER) BANDED KILLIFISH: 0.92 ppm for 48H, as Cu
TLm - (WATER) BANDED KILLIFISH: 0.86 ppm for 96H, as Cu
TLm - (WATER) STRIPED BASS: 8.3 ppm for 24H, as Cu
TLm - (WATER) STRIPED BASS: 6.2 ppm for 48H, as Cu
TLm - (WATER) STRIPED BASS: 4.3 ppm for 96H, as Cu
TLm - (WATER) PUMPKIN SEED: 3.8 ppm for 24H, as Cu
TLm - (WATER) PUMPKIN SEED: 2.9 ppm for 48H, as Cu
TLm - (WATER) PUMPKIN SEED: 2.4 ppm for 96H, as Cu
TLm - (WATER) WHITE PERCH: 11.8 ppm for 24H, as Cu
TLm - (WATER) WHITE PERCH: 8.0 ppm for 48H, as Cu
TLm - (WATER) WHITE PERCH: 6.2 ppm for 96H, as Cu
TLm - (WATER) AMERICAN EEL: 10.6 ppm for 24H, as Cu
Lethal - (WATER) NERIES SP: 0.1 ppm for 48H
LC50 - (WATER) BLUEGILL: 1.25 ppm as Cu for 96H, static chloride salt
LC50 - (WATER) NITZCHMIA LINEARIS: 0.81 ppm as Cu for 120H, static chloride salt
LC50 - (WATER) ACRONEURIA: 8.3 ppm as Cu for 96H, static sulfate salt
LC50 - (WATER) EPHEMERELLA: 0.32 ppm as Cu for 48H, static sulfate salt
LC50 - (WATER) HYDROPSYCHE: 32 ppm as Cu for 336H, static sulfate salt
LC50 - (WATER) CAMPELOMA DECISUM: 1.7 ppm as Cu for 96H, flow through sulfate salt
LC50 - (WATER) PHYSA INTEGRA: 0.039 ppm as Cu for 96H, flow through sulfate salt
LC50 - (WATER) GAMMARUS PSEUDOLIMNAEUS: 0.02 ppm as Cu for 96H, flow through sulfate salt
LC50 - (WATER) BROOK TROUT, Adult: 0.01 ppm as Cu for 96H, chronic field study
LC50 - (WATER) RAINBOW TROUT: 0.75 ppm as Cu for 48H, static
LC50 - (WATER) STRIPED BASS, Larvae: 0.1 ppm as Cu for 24H, static
LC50 - (WATER) STRIPED BASS, Larvae: 0.05 ppm as Cu for 48 to 96H, static
LC50 - (WATER) STRIPED BASS, Fingerling: 0.1 ppm as Cu for 24H, static
LC50 - (WATER) STRIPED BASS, Fingerling: 0.08 ppm as Cu for 48H, static
LC50 - (WATER) STRIPED BASS, Fingerling: 0.05 ppm as Cu for 72 to 96H, static
LC100 - (WATER) STRIPED BASS, Fingerling: 0.25 ppm for 24H, as Cu
LC100 - (WATER) STRIPED BASS, Fingerling: 0.1 ppm for 48 to 96H, as Cu
LC100 - (WATER) STRIPED BASS, Larvae: 0.2 ppm for 24H
LC100 - (WATER) STRIPED BASS, Larvae: 0.1 ppm for 48 to 96H
LCLo - (WATER) ORCONECTES RUSTICUS, Adult: 2.5 ppm as Cu for 24H, all died within 15D
LCLo - (WATER) ORCONECTES RUSTICUS, Adult: 1.0 ppm for 384H
TC - (WATER) FISH: 0.015 ppm for 96H
TC - (WATER) CRUSTCEA: 0.015 ppm
TC - (WATER) MULLUSKS: 0.015 ppm
TC - (WATER) PHYTOPLANKTON: 0.015 ppm
TC - (WATER) ZOOPLANKTON: 0.015 ppm
TCLo - (WATER) DAPHNIA MAGNA: 0.56 ppm, continuous flow
TCLo - (WATER) ORCONECTES RUSTICUS, Immature: 0.06 to 0.125 ppm, acute toxicity threshold
TCLo - (WATER) ORCONECTESRUSTICUS, Immature: 0.015 ppm, as Cu -- growth retarded
TCLo - (WATER) RAINBOW TROUT, Eggs: 0.1 ppm, as Cu -- slowed hatching
TCLo - (WATER) CHLORELLA PYRENOIDOSA: 0.001 ppm for 24H, as Cu -- growth rate retarded
TCLo - (WATER) CHLORELLA PYRENOIDOSA: 0.005 ppm for 48H, as Cu -- growth rate retarded
TCLo - (WATER) NITZSCHIA PALEA: 0.005 ppm -- prevents growth
TCLo - (WATER) GREEN & BLUEGREEN ALGAE: 0.1 to 0.3 ppm, as Cu -- inhibits growth
TL50 - (WATER) BROWN BULLHEAD: 0.18 ppm for 96H, flow-through hard sulfate salt
TL50 - (WATER) RAINBOW TROUT: 1.25 ppm for 24H, as Cu, static, hard sufate salt
TL50 - (WATER) RAINBOW TROUT: 0.89 ppm for 96H, as Cu, static, hard sulfate salt

FRESHWATER TOXICITY VALUES

LC50 - RAINBOW TROUT (Oncorhynchus mykiss) (Taylor et al, 2003):

juvenile-5.6 g (mean wet wt): 1.05 mcmol/L for 96H -- in hard water, at 18 degrees C, pH 8, 120 mg/L as CaCO3 hardness, 95 mg/L alkalinity, 3 mg/L dissolved organic matter
juvenile-10.6 g (mean wet wt): approximately 0.10 mcmol/L for 96H -- in soft water, at 16 degrees C, pH 7.2, 20 mg/L as CaCO3 hardness, 15 mg/L alkalinity, 0.4 mg/L dissolved organic matter
juvenile-10.6 g (mean wet wt): 0.14 mcmol/L for 48H -- in soft water, at 16 degrees C, pH 7.2, 20 mg/L as CaCO3 hardness, 15 mg/L alkalinity, 0.4 mg/L dissolved organic matter
3H LA50 (amount of copper bound to gills at 96H LC50), juvenile-5.6 g (mean wet wt): 3.1 nmol/g for 96H -- measured value for hard water
3H LA50 (amount of copper bound to gills at 96H LC50), juvenile: 0.2 nmol/g --calculated value for soft water

LC50 - YELLOW PERCH (Perca flavescens) (Taylor et al, 2003):

juvenile-2.7 g (mean wet wt): 4.16 mcmol/L for 96H -- hard water, at 18 degrees C, pH 8, 120 mg/L as CaCO3 hardness, 95 mg/L alkalinity, 3 mg/L dissolved organic matter
juvenile-5.3 g (mean wet wt): 0.44 mcmol/L for 96H -- soft water, at 16 degrees C, pH 7.2, 20 mg/L as CaCO3 hardness, 15 mg/L alkalinity, 0.4 mg/L dissolved organic matter
juvenile-5.3 g (mean wet wt): 0.53 mcmol/L for 48H -- soft water, at 16 degrees C, pH 7.2, 20 mg/L as CaCO3 hardness, 15 mg/L alkalinity, 0.4 mg/L dissolved organic matter
3H LA50 (amount of copper bound to gills at 96H LC50), juvenile-2.7 g (mean wet wt): 27.8 nmol/g -- measured value for hard water
3H LA50 (amount of copper bound to gills at 96H LC50), juvenile: 1.7 nmol/g -- calculated value for soft water

SALTWATER TOXICTY VALUES

References: (OHM/TADS, 2001):

EC50 - (WATER) CRAB, Adult: 109 ppm for 48H (as Cu); static; sulfate
EC50 - (WATER) CRAB, Larvae: 0.6 ppm for 48H (as Cu); static; sulfate
EC50 - (WATER) PRAWN, Adult: 29.5 ppm for 48H (as Cu); static; sulfate
EC50 - (WATER) PRAWN, Larvae: 0.33 ppm for 48H (as Cu); static; sulfate
EC50 - (WATER) LOBSTER, Larvae: 0.1-0.3 ppm for 48H (as Cu); static; sulfate
TC - (WATER) ALGAE: 0.05 ppm -- 80% inhibited
THRESHOLD - (WATER) PRAWNS: 0.5 ppm
THRESHOLD - (WATER) SHORECRAB: 1-2 ppm
TLm - (WATER) OYSTERS: 1.9 ppm for 96H
LC - (WATER) BARNACLES: 10 ppm for 2H
LC - (WATER) BARNACLES: 0.22 ppm for 48H
LC - (WATER) MUSSEL: 0.55 ppm for 12H
LC - (WATER) SOFT CLAM: 0.5 ppm for 72H -- 100% deaths
LC - (WATER) POLYCHAETE WORM: 0.05 ppm for 96H

SALTWATER TOXICITY VALUES

Marine Mussels (Zuniga et al, 2003):

EC50 - MUSSEL (Aulacomya ater): 192 mcg/L for 24H; 132 mcg/L for 48H; 108 mcg/L for 72H; 97 mcg/L for 96H; 119 mcg/L for 144H -- byssal attachment (at 12 degrees C, pH 7.6-8, dissolved oxygen >5 mg/L, mean salinity 28 ppt)
EC50 - MUSSEL (Chromytilus chorus): 390 mcg/L for 24H; 415 mcg/L for 48H; 369 mcg/L for 72H; 321 mcg/L for 96H; 226 mcg/L for 144H -- byssal attachment (at 12 degrees C, pH 7.6-8, dissolved oxygen >5 mg/L, mean salinity 28 ppt)
EC50 - MUSSEL (Perumytilus purpuratus): 181 mcg/L for 24H; 76 mcg/L for 48H; 99 mcg/L for 72H; 93 mcg/L for 96H; 89 mcg/L for 144H -- byssal attachment (at 12 degrees C, pH 7.6-8, dissolved oxygen >5 mg/L, mean salinity 2 ppt)
EC50 - MUSSEL (Semimytilus algosus): 291 mcg/L for 24H; 298 mcg/L for 48H; 268 mcg/L for 72H; 234 mcg/L for 96H; 220 mcg/L for 144H -- byssal attachment (at 12 degrees C, pH 7.6-8, dissolved oxygen >5 mg/L, mean salinity 28ppt)
LC50 - MUSSEL (Aulacomya ater): 165 mcg/L for 72H; 147 mcg/L for 96H; 139 mcg/L for 144H -- at 12 degrees C, pH 7.6-8, dissolved oxygen >5 mg/L, mean salinity 28 ppt
LC50 - MUSSEL (Perumytilus purpuratus): 228 mcg/L for 72H; 122 mcg/L for 96H; 126 mcg/L for 144H -- at 12 degrees C, pH 7.6-8, dissolved oxygen >5 mg/L, mean salinity 28 ppt
LC50 - MUSSEL (Chromytilus chorus): <8000 mcg/L for 24H; <8000 mcg/L for 72H; <8000 mcg/L for 96H; <8000 mcg/L for 144H -- at 12 degrees C, pH 7.6-8, dissolved oxygen >5 mg/L, mean salinity 28 ppt
LC50 - MUSSEL (Semimytilus algosus): 1708 mcg/L for 72H; 479 mcg/L for 96H; 247 mcg/L for 144H -- at 12 degrees C, pH 7.6-8, dissolved oxygen >5 mg/L, mean salinity 28 ppt

AQUATIC AND SOIL TOXICITY VALUES

Soil Nematodes (Boyd & Williams, 2003):

EC50 - NEMATODE (Caenorhabditis elegans):

2.04 mg/L for 72H -- decreased reproduction; aquatic lab test using CuCl2 in K-medium
2.06 mg/L for 24H -- decreased movement; aquatic lab test using CuCl2 in K-medium

EC50 - NEMATODE (Pristionchus pacificus):

2.21 mg/L for 72H -- decreased reproduction; aquatic lab test using CuCl2 in K-medium
8.07 mg/L for 24H -- decreased movement; aquatic lab test using CuCl2 in K-medium

LC50 - NEMATODE (Caenorhabditis elegans) :

85.4 mg/L for 24H -- aquatic lab test using CuCl2 in K-medium
179 mg/L for 24H -- soil test using Cu metal salt in K-medium with sandy soil (at pH 6.1, organic matter content 1.4%)

LC50 - NEMATODE (Pristionchus pacificus):

18.9 mg/L for 24H -- aquatic lab test using CuCl2 in K-medium
48.2 mg/L for 24H -- soil test using Cu metal salt in K-medium with sandy soil (at pH 6.1, organic matter content 1.4%)

LC50 - NEMATODE (Panagrellus redivivus):

160 mg/L for 24H -- aquatic lab test using CuCl2 in K-medium
251 mg/L for 24H -- soil test using Cu metal salt in K-medium with sandy soil (at pH 6.1, organic matter content 1.4%)

-PHYSICAL/CHEMICAL PROPERTIES

MOLECULAR WEIGHT

63.546

DESCRIPTION/PHYSICAL STATE

Copper is a lustrous, ductile, malleable, odorless solid with a distinct golden-red or reddish-brown color (ACGIH, 1996; Budavari, 2000; Lewis, 2000; NIOSH , 2002).

In water, the color of copper is often blue or green (OHM/TADS , 2002).
When exposed to moist air, copper gradually develops a coating of green basic carbonate (Budavari, 2000).
Copper salts are usually blue or green in color (ACGIH, 1996).

Workers exposed to copper fume may note a metallic or sweet taste (Hathaway et al, 1991).

Copper has a face-centered cubic structure (Budavari, 2000).

VAPOR PRESSURE

1 mmHg (at 1628 degrees C) (Lewis, 2000)

20 mmHg (at 1970 degrees C) (OHM/TADS , 2001)

SPECIFIC GRAVITY

TEMPERATURE AND/OR PRESSURE NOT LISTED

SOLID: 8.94 (NIOSH , 2002)

DENSITY

TEMPERATURE AND/OR PRESSURE NOT LISTED

SOLID: 8.94 g/cm(3) (Budavari, 2000)
SOLID: 8.92 g/cm(3) (ACGIH, 1996; Lewis, 2000)

FREEZING/MELTING POINT

FREEZING POINT

1981 degrees F (NIOSH , 2001)

MELTING POINT

1083 degrees C (ACGIH, 1996; ITI, 1995; Lewis, 2000)

BOILING POINT

25 degrees C (at 2595 mmHg) (Lewis, 2000)

2567 degrees C (ACGIH, 1996)

2595 degrees C (Budavari, 2000; ITI, 1995)

4703 degrees F (NIOSH , 2001)

FLASH POINT

Not Applicable (NIOSH , 2001)

EXPLOSIVE LIMITS

LOWER

Not Applicable (NIOSH , 2001)

UPPER

Not Applicable (NIOSH , 2001)

SOLUBILITY

IN WATER

Copper is insoluble in hot and cold water (HSDB , 2002; NIOSH , 2002).

OTHER

Copper is slowly soluble in ammonia water (Budavari, 2000).
It is soluble in nitric acid and hot sulfuric acid, and is very slightly soluble in hydrochloric acid and ammonium hydroxide (HSDB , 2002; Sittig, 1991).
Copper is attacked very slowly by cold hydrochloric acid or dilute sulfuric acid when exposed to the atmosphere. It is readily attacked by alkalies, dilute nitric acid, and by both hot concentrated sulfuric acid (H2SO4) and bromic acid (HBr). It is also attacked by acetic and other organic acids (Budavari, 2000; Lewis, 1997).

OTHER/PHYSICAL

ODOR THRESHOLD

Odorless (HSDB , 2002)

HEAT OF FUSION

48.9 cal/g (Budavari, 2000)

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