Logo

National Pesticide Information Center

npic@ace.orst.edu

1.800.858.7378

Copper Sulfate

Technical Fact Sheet

NPIC Technical Fact Sheets provide information that is complex and intended for individuals with a scientific background and/or familiarity with toxicology and risk assessment. This document is intended to promote informed decision-making. Please refer to the General Fact Sheet for less technical information.

Molecular Structure -
Copper Sulfate

Chemical Class and Type:

  • Copper sulfate is an algaecide, bactericide, and fungicide. When it is mixed with calcium hydroxide it is known as Bordeaux mixture.1 The International Union of Pure and Applied Chemistry (IUPAC) name for this active ingredient is copper (2+) sulfate or copper (II) sulfate. Other names include copper (2+) tretraoxidosulfate or copper (II) tretraoxidosulfate.2
  • Formulations include basic copper sulfate, copper sulfate monohydrate, copper sulfate pentahydrate, and copper sulfate anhydrous. Their Chemical Abstracts Service (CAS) registry numbers are 1344-73-6, 1332-14-5, 7758-99-8, and 7758- 98-7, respectively. Pesticides containing copper sulfate monohydrate and/or copper sulfate anhydrous have been cancelled by the United States Environmental Protection Agency (U.S. EPA).3
  • Copper sulfate has been used in the United States since the 1700s, and it was first registered for use in the United States in 1956. The U.S. EPA completed the reregistration of copper sulfate in 2009.3 See the text box on Laboratory Testing.
  • Copper sulfate is an inorganic salt that is highly soluble in water.3,4 The copper ion is the component of copper sulfate with toxicological implications.3
  • Copper is an essential mineral, and the recommended dietary allowance of copper for human adults has been set at 900 µg/day.5
  • Copper is also a ubiquitous element. It can be found in the environment and in foods and water.3

Laboratory Testing: Before pesticides are registered by the U.S. EPA, they must undergo laboratory testing for short-term (acute) and long-term (chronic) health effects. Laboratory animals are purposely given high enough doses to cause toxic effects. These tests help scientists judge how these chemicals might affect humans, domestic animals, and wildlife in cases of overexposure.

Uses:

  • Copper sulfate is used as a fungicide, algaecide, root killer, and herbicide in both agriculture and non-agricultural settings. It is also used as an antimicrobial and molluscicide.3 Uses for individual products containing copper sulfate vary widely. Always read and follow the label when applying pesticide products.
  • Copper sulfate is used as a drying agent in the anhydrous form, as an additive for fertilizers and foods, and several industrial applications such as textiles, leather, wood, batteries, ink, petroleum, paint, and metal, among others.6 It is used also as an animal nutritional supplement.8
  • Some products containing copper sulfate can be used in organic agriculture.3
  • Signal words for products containing copper sulfate may range from Caution to Danger. The signal word reflects the combined toxicity of the active ingredient and other ingredients in the product. See the pesticide label on the product and refer to the NPIC fact sheets on Signal Words and Inert or "Other" Ingredients.
  • To find a list of products containing Copper Sulfate which are registered in your state, visit the website http://npic.orst.edu/reg/state_agencies.html and search by "active ingredient."

Physical / Chemical Properties:

  • Copper sulfate pentahydrate and basic copper sulfate are the only copper sulfate forms contained in currently registered pesticide products.3 Chemical properties for these two forms are summarized in the table below.
Active Ingredient CASRN3 Formula3 Copper (%Cu)3 Form6,7 Vapor pressure (mmHg at 25 °C)1 Molecular weight (g/mol)3 Specific gravity / density6,7 Solubility (water)1,7
Copper sulfate pentahydrate 7758-99-8 CuSO4 · 5H2O 25.4 Blue crystals,
granules or powder
Non-volatile 249.65 2.286 SG
(15.6 °C / 4 °C)
148g/kg (0 °C),
736g/kg (100 °C)
Basic copper sulfate 1344-73-6 3Cu(OH)2 · CuSO4 54.2 Light blue /
green fine powder
Not found 468.29 0.800-0.900 SG Insoluble (soluble in acids)

Mode of Action:

Target Organisms

  • The copper ion is the component of copper sulfate with toxicological implications. Copper ions appear to bind to functional groups of protein molecules in fungi and algae and cause protein denaturation, producing cell damage and leakage. Protein components that act as binding sites are sulfidal groups, phosphate (thiol), carboxyls, and imidazoles.3
  • In mollusks, copper sulfate disrupts surface epithelia function and peroxidase enzymes.3

Non-target Organisms

  • Copper is an essential nutrient. The acute toxicity of copper-containing pesticides is not attributed to systemic toxicity but to the efforts of the body to equilibrate copper concentrations.3
  • Copper plays a role in oxidative stress. It has the potential to act as a catalyst in the formation of free radicals but it also plays a role in reducing reactive oxygen species.9 Copper in the body primarily exists bound to proteins.10,11
  • Ingestion of copper sulfate irritates the digestive system and may cause emesis, which may limit toxicity.12 Tissue corrosion, shock and death may occur after exposure to large doses of copper sulfate. Damage to blood cells, liver and kidney has also been reported.13
  • Sheep can be particularly sensitive to products containing copper sulfate, possibly due to inefficient copper excretion.14

Acute Toxicity:

Oral

  • The acute oral LD50 in rats is 450 to 790 mg/kg. The U.S. EPA considered copper sulfate pentahydrate to be moderately toxic by ingestion.3 See the text boxes on Toxicity Classification and LD50/LC50.
  • Humans may be exposed to copper in drinking water. Volunteers drank purified water with copper at concentrations ranging from 0-12 mg/L. They reported nausea starting at 4 mg/L and vomiting at 6 mg/L. Solutions containing copper and orange flavor raised the NOEL to 6 mg/L for nausea and 12 mg/L for vomiting. Hence, flavored beverages contaminated with copper may lead to higher exposures.15 See the text box on NOEL.
  • Scientists measured total copper ion in people's blood serum after they ingested copper sulfate. Mean blood copper levels of 287 µg/L Cu were correlated with mild toxicosis and levels of 798 µg/L Cu to severe toxicosis.16
  • The toxic dose of copper sulfate for cattle is 200-880 mg/kg. Sheep are ten times more sensitive with a toxic dose of 20-110 mg/kg of copper sulfate.17
  • Adult roosters were exposed by intubation to copper sulfate doses of 200, 600, 800, 1200 and 1600 mg/kg body weight. The acute LD50 was determined to be 693 mg/kg. Treated animals developed diarrhea and died within 24 to 28 hours. Necropsies revealed bleeding of the kidneys and liver, necrosis in liver tissue, and testicular atrophy.18

LD50/LC50: A common measure of acute toxicity is the lethal dose (LD50) or lethal concentration (LC50) that causes death (resulting from a single or limited exposure) in 50 percent of the treated animals. LD50 is generally expressed as the dose in milligrams (mg) of chemical per kilogram (kg) of body weight. LC50 is often expressed as mg of chemical per volume (e.g., liter (L)) of medium (i.e., air or water) the organism is exposed to. Chemicals are considered highly toxic when the LD50/LC50 is small and practically non-toxic when the value is large. However, the LD50/LC50 does not reflect any effects from long-term exposure (i.e., cancer, birth defects or reproductive toxicity) that may occur at levels below those that cause death.

Dermal

  • Copper sulfate is not a skin irritant. It was classified by the U.S. EPA as very low in toxicity for dermal irritation. The dermal LD50 was greater than 2000 mg/kg in rats.3
  • Copper sulfate caused severe eye irritation from day 1 in rabbits that were exposed up to 21 days, and it was ranked as highly toxic by the U.S. EPA for primary eye irritation.3
  • No data were found regarding the potential for copper sulfate to cause dermal sensitization in any species.3

Inhalation

  • The inhalation LC50 for rats is 1.29 mg/L.19

Signs of Toxicity - Animals

  • Signs reported in cats and dogs after ingestion of copper pennies include diminished appetite, depression, vomiting, dehydration and abdominal pain.20,21 Some breeds of dogs are particularly sensitive to copper poisoning due to a genetic defect. These include dalmatians, bedlington, west highland white, and skye terriers, in which ingestion of copper results in weakness, anorexia and vomiting.22 Older dogs may develop liver damage and excess fluid in the peritoneal cavity.17
  • Signs of poisoning in livestock after acute ingestion include abdominal pain, diarrhea, vomiting, shock, decreased body temperature, increased heart rate, and death. Diarrhea and vomit may have a green to blue color.23
  • After ingestion of 20 to 100 mg/kg body weight of copper sulfate, sheep had diminished appetite, diarrhea, salivation, inflammation, corrosion, lesions in the stomach and intestines, and abdominal pain. These symptoms can lead to dehydration, shock and death.14,17
  • Anorexia, nasal discharge, recumbency, jaundice, and death are among the signs observed in cows.24 Reddish brown urine, accelerated respiration, and elevated copper concentrations in the blood, kidney, and liver have also been observed.25 Signs in goats include anorexia and recumbency.26
  • Pigs fed concentrations of 500 ppm Cu as copper sulfate pentahydrate showed less weight gain, reduced hemoglobin, lower hematocrit, lower plasma copper, and increased copper liver content. A dose of copper sulfate with 250 ppm Cu produced faster weight gain, and no changes in tested blood parameters.27
TOXICITY CLASSIFICATION - COPPER SULFATE
High Toxicity Moderate Toxicity Low Toxicity Very Low Toxicity
Acute Oral LD50 Up to and including 50 mg/kg
(≤ 50 mg/kg)
Greater than 50 through 500 mg/kg
(>50-500 mg/kg)
Greater than 500 through 5000 mg/kg
(>500-5000 mg/kg)
Greater than 5000 mg/kg
(>5000 mg/kg)
Inhalation LC50 Up to and including 0.05 mg/L
(≤0.05 mg/L)
Greater than 0.05 through 0.5 mg/L
(>0.05-0.5 mg/L)
Greater than 0.5 through 2.0 mg/L
(>0.5-2.0 mg/L)
Greater than 2.0 mg/L
(>2.0 mg/L)
Dermal LD50 Up to and including 200 mg/kg
(≤200 mg/kg)
Greater than 200 through 2000 mg/kg
(>200-2000 mg/kg)
Greater than 2000 through 5000 mg/kg
(>2000-5000 mg/kg)
Greater than 5000 mg/kg
(>5000 mg/kg)
Primary Eye Irritation Corrosive (irreversible destruction of ocular tissue) or corneal involvement or irritation persisting for more than 21 days Corneal involvement or other eye irritation clearing in 8 - 21 days Corneal involvement or other eye irritation clearing in 7 days or less Minimal effects clearing in less than 24 hours
Primary Skin Irritation Corrosive (tissue destruction into the dermis and/or scarring) Severe irritation at 72 hours (severe erythema or edema) Moderate irritation at 72 hours (moderate erythema) Mild or slight irritation at 72 hours (no irritation or erythema)
The highlighted boxes reflect the values in the "Acute Toxicity" section of this fact sheet. Modeled after the U.S. Environmental Protection Agency, Office of Pesticide Programs, Label Review Manual, Chapter 7: Precautionary Labeling. http://www.epa.gov/oppfead1/labeling/lrm/chap-07.pdf

Signs of Toxicity - Humans

  • Signs and symptoms from oral exposure include metallic taste, nausea, vomiting, diarrhea, and upper abdominal pain.28 Symptoms are affected by stomach acidity and content.3 Green or blue coloration of the vomit, stool, and saliva have been reported.29 Corrosion of the gastrointestinal epithelium may occur.3 Copper exposure may also cause failure of the liver, kidneys, and circulatory system.28
  • Additional signs including dark brown or red urine, decreased urine production, gastrointestinal bleeding, jaundice, bluish skin or mucous membranes, delirium, and coma have been reported in patients who ingested up to 50 g of copper sulfate.30
  • Symptoms of acute exposure to dust and powder formulations may include skin and eye irritation. Soluble copper sulfate in the eye may be corrosive to the cornea.28
  • Inhalation exposure may result in irritation of the respiratory tract, including corrosion of mucous membranes.28 Other signs and symptoms from inhalation exposure to copper salts include congestion of mucous membranes and ulceration of the nasal septum.31
  • Always follow label instructions and take steps to minimize exposure. If any exposure occurs, be sure to follow the First Aid instructions on the product label carefully. For additional treatment advice, contact the Poison Control Center at 1-800- 222-1222. If you wish to discuss an incident with the National Pesticide Information Center, please call 1-800-858-7378.

Chronic Toxicity:

Animals

  • Twelve rabbits inhaled sprayed Bordeaux mixture for 10 minutes, 3 times daily for 4 months. The concentration was increased gradually from 1% to 3%. All animals developed inflammation, copper deposits, and degenerative changes in the lung tissue. In contrast to other studies with longer exposure times, this research did not find granulomas or fibrosis in the lung tissue.32
  • Rats were fed ad libitum a diet containing 0, 500, 1000, 2000 or 4000 ppm of copper as copper sulfate for one month. Copper content increased in the blood, spleen, and liver for all groups. Growth and food intake decreased with higher concentrations. At the highest dose, rats died after the first week.33
  • Male rats were given 100 mg/kg/day of copper sulfate by gavage for 20 days. Signs included change of paw color from pink to white and reduced body weight. Further analysis showed destruction of red blood cells and copper deposition and necrosis in liver and kidney tissue.34
  • Pigs were fed copper sulfate pentahydrate at copper concentrations of 0, 250 and 425 ppm Cu for 48 to 79 days. Gastrointestinal hemorrhage, cirrhosis of the liver, and jaundice were observed at the highest dose.35
  • Sixteen lambs ate a diet containing copper sulfate pentahydrate at a concentration of 15 ppm Cu for 88 days. Two lambs died due to jaundice. The livers of the surviving lambs contained high concentrations of copper.27
  • Sheep fed mixtures containing 5.3-9.9% copper sulfate pentahydrate ingested 0.645-1.660 g copper sulfate daily for 28 to 113 days. Signs included lethargy, jaundice, hemoglobinuria, bloody nasal discharge, fast pulse, fast breathing, greenishblack stools, and recumbency before death.36
  • Laying hens were fed copper sulfate at concentrations of 78 ppm Cu and 1437 ppm Cu for 2 weeks. At the highest concentration, hens produced fewer eggs, consumed less feed, and developed ulcers in the gizzard and oral cavity.37 Other studies of chickens that were fed copper sulfate reported oral lesions proportional to the dose of copper, and conflicting effects on feeding rate and weight gain.38,39,40,41
  • Rats exposed by inhalation to copper sulfate for 1 hour/day for 10 days at a concentration of 330 g/L spray had increased concentrations of copper in the liver and plasma. Copper did not accumulate in the lung tissue.42

NOAEL: No Observable Adverse Effect Level

NOEL: No Observed Effect Level

LOAEL: Lowest Observable Adverse Effect Level

LOEL: Lowest Observed Effect Level

Humans

  • A group of 179 adults from Ireland, Chile, and the U.S. were exposed once weekly to a solution of copper sulfate (0, 2, 4, 6, and 8 mg Cu/L) for 5 weeks. Acute LOAEL and NOAEL were determined at 6 and 4 mg Cu/L. Nausea within 15 minutes after exposure was the most common observed effect. Vomiting, diarrhea, and abdominal pain were also reported to a lesser extent.43 These results were confirmed in two additional independent experiments involving a total of 1634 people from around the world.44,45 See the text box on NOAEL, NOEL, LOAEL, and LOEL.
  • Researchers administered copper sulfate dissolved in tap water at doses of 0, 1, 3, and 5 mg Cu/L for 2 weeks to groups of 15 healthy adult women. Subjects drank an average of 1.64 L per day. Reported symptoms include nausea, abdominal pain, and vomiting at exposure ≥3 mg Cu/L.46
  • "Vineyard sprayer's lung" is a condition reported after chronic inhalation of Bordeaux mixture by agricultural workers who may be exposed seasonally.47 It is characterized by particular lung tissue changes including lesions, blue coloration, scarring, and nodules.47,48 Symptoms include weakness, loss of appetite, decreased body weight, shortness of breath, and in some cases cough.47,48 See the text box on Exposure.

Exposure: Effects of copper sulfate on human health and the environment depend on how much copper sulfate is present and the length and frequency of exposure. Effects also depend on the health of a person and/or certain environmental factors.

Endocrine Disruption:

  • No data were found related to copper sulfate and endocrine disruption.3

Carcinogenicity:

Animals

  • Researchers orally dosed mice with 1.25, 2.50, 5.00, 7.50, 10.0 or 12.5 mg/kg body weight copper sulfate. Red blood cell DNA was damaged in a dose-dependent way.49 Mice given 8.25 mg/kg copper by gavage in the form of copper sulfate showed genotoxic and mutagenic responses in bone marrow and in whole blood.50
  • Newly hatched white leghorn chicks were orally dosed with copper sulfate at a concentration of 10 mg/kg body weight. Chicks were sacrificed after 24 hours, and bone marrow chromosome aberration tests demonstrated an increased incidence of micronuclei in exposed chicks, indicating DNA damage.51

Humans

  • The U.S. EPA did not evaluate copper sulfate for carcinogenic effects because there was no conclusive evidence linking copper or copper salts to cancer development in animals that can normally regulate copper in their bodies.3 See the text box on Cancer.

    Cancer: Government agencies in the United States and abroad have developed programs to evaluate the potential for a chemical to cause cancer. Testing guidelines and classification systems vary. To learn more about the meaning of various cancer classification descriptors listed in this fact sheet, please visit the appropriate reference, or call NPIC.

  • High levels of copper have been associated with carcinogenesis and a high risk of cancer mortality.9,52 Copper may affect cancer growth and cell proliferation and stimulate blood vessel formation.10,11 Decreasing copper levels may inhibit cancer growth.11
  • Increased incidence of renal cell cancer has been associated with exposure to copper sulfate when used as a pesticide in vineyards. Outpatient surveys found that people reporting chronic exposures to copper sulfate of greater than 10 years had an odds ratio of 2.7 (95% CI: 1.3-5.5) for increased risk of renal cancer.53 Exposure levels were not reported.
  • Cancer ratings for copper sulfate by the International Agency for Research on Cancer (IARC) or the National Toxicology Program (NTP) were not found.

Reproductive or Teratogenic Effects:

Animals

  • The teratogenic effect of copper sulfate was studied by injecting pregnant hamsters with copper on the eighth day of pregnancy in doses ranging from 2.13 to 10.0 mg Cu/kg in the form of copper sulfate. All concentrations resulted in embryocidal and teratogenic effects. Embryonic resorptions, severe heart malformations, hernias and other malformations were reported. Researchers concluded that the placentas were permeable to copper ions.54
  • Mice were fed copper sulfate at 0.5, 1.0, 1.5, 2.0, 3.0, and 4.0 g/kg food for a month, and then mated. Pregnant mice continued with the diet until day 19. Researchers noted greater fetal mortality, lower fetal weights, and abnormalities at the two highest doses.55
  • The U.S. EPA determined the chronic NOAEL for reproductive effects was 11.7 mg/kg body weight copper and the chronic LOAEL for reproductive effects was 15.1 mg/kg body weight of copper based on a study of mink.3
  • Adult chickens were exposed to copper sulfate by gavage at concentrations of 200, 600, 800, 1200, and 1600 mg/kg body weight. Researchers noted testicular atrophy and spermatogenic arrest proportional to the concentrations of copper sulfate.18
  • Rabbit sperm motility decreased when placed in solutions of copper sulfate pentahydrate ranging from 1:1 to 1:10 for 1-2 hours.56

Humans

  • Researchers exposed human spermatozoa to 8 x 10-8, 8 x 10-6, and 8 x 10-5 mol cupric ions in the form of CuCl2 for 30 minutes. Spermatozoa were immobilized after 20 minutes of exposure at the two highest concentrations; reduced motility was also noted in the low dose group.57
  • Wilson’s disease may provide insight into potential reproductive health effects of copper. Wilson’s disease is a rare genetic disorder in which the body retains too much copper. The effects include infertility, higher miscarriage rates, loss of menses and hormonal imbalances in women.58,59 In men, the testes don’t function properly. Exposure to copper sulfate does not cause Wilson’s disease.59

Fate in the Body:

Absorption

  • When humans eat ionic copper, it is absorbed by the small intestine and to a lesser extent by the stomach. It can be absorbed by passive diffusion or active transport mechanisms.5 Levels of copper in the bloodstream peaked between 1 and 3 hours after ingestion.29
  • The extent of copper absorption is dependent in part on copper dietary intake.5
  • Copper absorption can be enhanced by the presence of proteins and organic acids, such as citric acid and acetic acid, and inhibited by phytate, zinc, iron, molybdenum, calcium, and phosphorous.5
  • Levels of serum ionic copper in people following acute oral exposure were greatest within 12 hours of ingestion and decreased dramatically after 12 hours of ingestion. These results indicate that copper is absorbed rapidly to be incorporated in the blood.16
  • Women absorb more copper than men below the age of 60, but there were no differences in older people.60

Distribution

  • After inhalation of Bordeaux mixture, vineyard workers presented copper deposits not only in the lung tissue but also in the liver, spleen, kidney, and lymph nodes. Inhaled copper is absorbed by the respiratory tract and carried by the bloodstream and lymphatic system to other organs.61
  • In intestinal cells, copper is incorporated into metal-binding proteins. It can be stored for up to three days, used by the cell, or be transported by blood plasma to other organs while bound to some proteins. The copper is then deposited in the liver.5
  • The primary target organ of copper is the liver, where copper can be stored bound to proteins.5 Copper is also distributed to the bile, bone, brain, hair, heart, intestine, kidneys, muscle, nails, skin, and spleen.5,62
  • Copper in the body can exist bound to ceruloplasmin (85-95%) or as free copper which is bound to albumin (5-15%). The latter is responsible for the toxic effects.63

Metabolism

  • After copper is absorbed and bound to proteins, it is transported in blood throughout the body.5

Excretion

  • Excess copper is excreted and not often stored in the body.64
  • Copper is primarily excreted in the feces through the bile; it can also be excreted to a much smaller extent in the urine, sweat, and by normal sloughing of the skin. Women can also eliminate very small amounts of copper through menstruation and men can eliminate it in semen. Small amounts can also be eliminated in hair and nails.5
  • Subjects ate food dosed with radiolabeled copper and a whole-body scanner was used to measure retained copper levels. Half-lives ranged from 13 to 33 days in the body.65

Medical Tests and Monitoring:

  • Homeostatic regulation of copper makes it problematic to identify biomarkers for early changes in copper levels associated with deficiency or excess.45 Extreme copper imbalance can be indicated by tissue damage but due to homeostasis, high copper exposures may not always be detectable. Currently, biomarkers cannot reliably detect excess copper exposures even in cases when patients are symptomatic.65
  • Serum copper concentration and ceruloplasmin activity are traditional metabolic copper indicators good for detection of copper deficiency. Age, sex, pregnancy, hormone levels, and health conditions may affect them.65 Copper chaperone (CCS), which responds to copper deficiency and excess, has been recently identified as a potential biomarker but its significance is unknown.66 Liver aminotransferases have been traditionally used as indicator for high copper status.65
  • Scientists have used atomic absorption spectrophotometry to quantify copper in scalp hair, blood, and urine.67 This method has also been used to measure copper in fingernails.68 Some investigators have postulated the need for more research in hair analysis, stating it has potential as a bioindicator because hair can be easily obtained, but scientists have identified several factors associated with the unreliability of hair mineral analysis.69,70
  • Inductively coupled plasma emission spectroscopy has been used to measure copper in blood, urine, and sweat. Sampling and methodology limitations have been reported for sweat determination.71
  • Blood samples can be evaluated for indicators of copper status. Erythrocyte superoxidase dismutase (SOD1), platelet cytochrome-C oxidase (CCO), plasma diamine oxidase (DAO), and peptidylglycine-amidating monooxygenase (PAM) activity, all copper-containing enzymes in blood cells, have been considered good deficiency indicators of metabolically active copper and copper stores.65

Environmental Fate:

Soil

  • Copper sulfate can dissociate or dissolve in the environment releasing copper ions. This process is affected by its solubility, which in turn is affected by pH, redox potential, dissolved organic carbon, and ligands present in the soil. Copper in soil may originate from natural sources, pesticides, and other anthropogenic sources such as mining, industry, architectural material, and motor vehicles.3
  • Copper accumulates mainly at the surface of soils and it can persist because it has a tendency to bind to organic matter, minerals, and some metal oxides. It may leach from acidic or sandy soil.72,73
  • The more acidic the soil, less binding occurs. Researchers observed that 30% of copper was bound at pH 3.9 and 99% of copper was bound at pH 6.6.74
  • Researchers applied the equivalent of 18 kg/ha/yr of copper sulfate in irrigation water to experimental soil columns to measure copper buildup in the soil. Soil types were not specified. Nearly all of the applied copper remained in the top 3 cm of soil. The researchers concluded that irrigation water treated with copper sulfate as an algaecide could lead to soil levels that could damage crops.75
  • A study that evaluated leaching of copper from sandy soil to water revealed lower mobility at pH 5-7. Any pH outside of this range was correlated with higher mobility. The researchers reported that the presence of calcium ions decreased leaching of copper, increasing its binding capacity. The presence of sodium ions had the opposite effect and caused more copper to leach.76
  • Researchers spiked samples of sandy loam soil from a barley field with 0, 100, 200, 400, and 800 µmol/kg of copper. Copper became less bioavailable over the 220 days of the experiment. Soils that remained moist retained the most copper.77

Water

  • Copper sulfate is an inorganic salt that is highly soluble in water.3 The disassociated copper ions mainly bind to organic matter or remain dissolved in water.78
  • Researchers added 774 g copper sulfate pentahydrate to channel catfish ponds over 16 weeks. Researchers found that 90% of the copper was bound to the sediments within minutes of application and 99% of it was bound after 2 days. Nearly all of the copper remained in the top 16 cm of sediment.79
  • Researchers collected water and sediment samples from Lake Mathews, California, following an application of 2250 kg copper sulfate as an algaecide. Copper concentrations at the reservoir outflow peaked two days after the application at 17 µg/L and stabilized at approximately 3 µg/L after two weeks. Researchers calculated that 20% of the applied copper left the reservoir by day 70 and much of the remaining copper became bound in the upper layer of the sediment. Sediment concentrations were 10-600 µg/g.80
  • Comparable results were obtained after studying the fate of copper sulfate applied to the Saint Germain Les Belles reservoir in France after application of 50 kg copper sulfate. Researchers calculated that 17% of the added copper left the water body over a period of 70 days. Dissolved copper in the water column existed mainly in a colloidal form. Accumulation of copper was not significant.81

Air

  • No data were found regarding the fate of copper sulfate in the atmosphere.

Plants

  • Copper is an essential mineral for plant growth and its concentration is regulated by homeostatic mechanisms. However, copper can be toxic to plants by affecting electron transport in photosynthesis.82
  • Bioavailability depends on the amount of copper, soil pH, organic carbon, precipitation, and temperature.83
  • Researchers examined the toxicity of copper to citrus seedlings in three soil types with pH ranging from 5.7 to 8.2. Samples were spiked with fertilizer and copper sulfate pentahydrate, and incubated for 47 days. Citrus root stock seedlings (Swingle citrumelo) were then transplanted into the pots and allowed to grow for 330 days. In two of three soils, citrus seedlings had reduced leaf, stem, and root dry weights at greater copper application rates. Readily soluble copper increased with decreasing soil pH, but accounted for less than 10% of the total copper. Readily soluble copper is the most phytotoxic form.84
  • Researchers exposed onion (Allium cepa) bulbs and garden cress (Lepidium sativum) seeds to solutions of copper as copper sulfate. They calculated that the concentrations of copper required to inhibit 50% of growth (IC50) after 48 hours of exposure to be 0.00112 ± 0.00019 mmol/L (, SD) for A. cepa and 2.42917 ± 0.25897 mmol/L for L. sativum.85

Indoor

  • There are no registered indoor uses for copper sulfate. No data was available regarding indoor fate of copper sulfate.

Food Residue

  • Copper sulfate was not included in the list of pesticide residues in food to be monitored by the U.S. Department of Agriculture.86
  • Copper sulfate pentahydrate residues are exempt from the requirement for a tolerance in cattle products, eggs, goats, hogs, horses, milk, poultry, and sheep, and after harvest on raw agricultural commodities. Residues may be anticipated from its use as a fungicide in agriculture, and as a bactericide/fungicide in animal premises.87

Ecotoxicity Studies:

Birds

  • The U.S. EPA classified copper as moderately toxic to birds based on the acute oral LD50 for bobwhite quail (Colinus virginianus) of 384 mg/kg copper sulfate pentahydrate and 98 mg/kg metallic copper. The chronic LOAEL for bobwhite quail is 289 mg/kg metallic copper.3 An acute oral LD50 for bobwhite quail exposed to copper sulfate was also reported as 616 mg/kg. The dietary LC50 for bobwhite quail is 1369 mg/kg over 8 days.1
  • Researchers fed 450 mg/kg copper from copper sulfate to male chicks for 21 days. They noted reduced feeding and less weight gain in exposed birds.40
  • A flock of captive 3-week-old Canada geese (Branta canadensis) used a pond treated with copper sulfate. Ten of the geese died nine hours after ingestion of roughly 600 mg/kg copper sulfate.88
  • Limited data are available regarding copper sulfate toxicity to wild birds.89

Fish and Aquatic Life

  • The toxicity of copper to fish and other aquatic life depends on its bioavailability, which is strongly dependent on pH, the presence of dissolved organic carbon (DOC), and water chemistry such as the presence of calcium ions.90
  • Fish kills have been reported after copper sulfate applications for algae control in ponds and lakes. However, oxygen depletion and dead organisms clogging the gills have been cited as the cause of fish deaths, resulting from massive and sudden plant death and decomposition in the water body.91,92,93
  • Researchers exposed juvenile rainbow trout (Oncorhynchus mykiss) to either hard water or soft water spiked with copper for 30 days. The 96-hour LC50 value for fish exposed to soft water was the same as the controls. Fish in the hard-water, high dose (60 µg/L) treatment groups showed an increased sensitivity to copper; the 96-hour LC50 dropped to 91 µg/L Cu.94
  • The mean 96-hour LC50 (with 95% confidence limits) for copper exposure in alevin, swim-up, parr and smolt steel-head (Salmo gairdneri) are 28 (27-30), 17 (15-19), 18 (15-22), and 29 (>20) µg/L of copper respectively. The mean 96-hour LC50 for copper exposure in alevin, swim-up, parr and smolt Chinook salmon (Oncorhynchus tshawytscha) are 26 (24-33), 19 (18-21), 38 (35-44), and 26 (23-35) µg/L of copper respectively. The experiments were done by adding copper as CuCl2.95
  • Copper sulfate is toxic to shrimp due to damage of the gill epithelium and respiration disruption.96 Copper also disrupts olfaction in fish, possibly interfering with their ability to locate food, predators, and spawning streams.97,98
  • The toxicity of copper sulfate to blue tilapia (Oreochromis aureus) fingerlings was found to increase with the decrease in total alkalinity. The 96-hour LC50 for alkalinities of 225, 112, 57 and 16 mg CaCO3/L were 43.06, 6.61, 0.69 and 0.18 mg CuSO4/L respectively.99
  • The 48-hour LC50 for the fathead minnow (Pimephales promelas) is 19.2 ± 3.1 (mean ± SD) µg/L Cu.100 Other researchers determined that 96-hour LC50 values ranged from 5.3 to 169.5 µg/L Cu depending on DOC, pH, and calcium concentrations in soft water.90
  • The mean 24-hour, 48-hour, 72-hour, and 96-hour LC50 values for zebra fish (Danio rerio) were reported (with 95 % confidence intervals) as 0.349 (0.245-0.478), 0.158 (0.113-0.221), 0.134 (0.097-0.189), and 0.094 (0.069-0.137) mg/L Cu, respectively.101
  • The 48-hour LC50 for the non-biting midge (Chironomus tentans) is 1,136.5 ± 138.6 (mean ± SD) µg/L Cu.100

    EC50: The median effective concentration (EC50) may be reported for sublethal or ambiguously lethal effects. This measure is used in tests involving species such as aquatic invertebrates where death may be difficult to determine. This term is also used if sublethal events are being monitored.

    Newman, M.C.; Unger, M.A. Fundamentals of Ecotoxicology; CRC Press, LLC.: Boca Raton, FL, 2003; p 178.

  • Reported 48-hour LC50 concentrations for Daphnia magna include 0.00115 mmol CuSO4/L85 and 18.9 ± 2.3 (mean ± SD) µg/L Cu.100 The LC50 for Daphnia pulex was relatively constant at 24, 48, and 72 hours. Reported values were 21-31 µg/L, 20-31 µg/L, and 20-29 µg/L, respectively.102 The 24- and 48-hour EC50 (with 95% confidence intervals) for Daphnia similis was 0.035 (0.030-0.042) and 0.032 (0.026-0.039) mg/L Cu, respectively.101See the text box on EC50.
  • Researchers studied the effect of sediment on copper toxicity in three Daphnia species, D. similis, D. magna, and D. laevis. They reported that the toxicity is reduced in the presence of sediments because bioavailability of copper is decreased. For D. magna the 48-hour EC50 varied from 0.045 mg/L as copper sulfate without sediment to 0.347 mg/L as copper sulfate in the presence of sediment.103
  • The LC50 value for the juvenile freshwater prawn (Macrobrachium rosenbergii) was 0.53 ± 0.04 (mean ± SE) for 24 hours. The 48-, 72-, and 96-hour LC50 values were 0.45 ± 0.05 mg/L, 0.45 ± 0.04 mg/L, and 0.45 ± 0.04 mg/L.104
  • Aquatic snails (Biomphalaria glabrata) had a 24-hour and 48-hour LC50 (with 95% confidence intervals) of 1.868 (1.196- 3.068) and 0.477 (0.297-0.706) mg/L Cu, respectively.101
  • Researchers exposed 1-day-old freshwater snail eggs (Lymnaea luteda) to copper at concentrations from 1 to 320 µg/L of copper for 14 days at 21 °C in a semi-static embryo toxicity test. Embryos exposed to copper at 100 to 320 µg/L died within 168 hours. At lower doses from 3.2-10 µg/L, significant delays in hatching and increased mortality were noted. Snail embryos (Lymnaea luteda L.) had a 96-hour EC50 (with 95% confidence interval) of 28.31 (21.86 - 36.64) µg/L Cu.105
  • Researchers reported no observed effects concentrations (NOEC) of 8.2-103 mg/L copper in the freshwater rotifer (Brachionus calyciflorus). Toxicity increased with decreasing levels of DOC and decreasing pH.106

Terrestrial Invertebrates

  • The U.S. EPA considers copper to be practically nontoxic to bees. The acute oral LD50 is >100 µg/bee.3
  • The LD50 for Bordeaux mixture in bees was reported as 23.3 ?g/bee Cu by ingestion, and greater than 25.2 µg/bee Cu by contact. The 14-day LC50 for worms is higher than 195.5 mg/kg of Cu in soil.1

Regulatory Guidelines:

Reference Dose (RfD): The RfD is an estimate of the quantity of chemical that a person could be exposed to every day for the rest of their life with no appreciable risk of adverse health effects. The reference dose is typically measured in milligrams (mg) of chemical per kilogram (kg) of body weight per day.

U.S. Environmental Protection Agency, Technology Transfer Network, Air Toxics Health Effects Glossary, 2009. http://www.epa.gov/ttnatw01/hlthef/hapglossaryrev.html#RfD

  • There is no reference dose (RfD) established for copper sulfate. See the text box on Reference Dose (RfD).
  • The U.S. EPA has set an action level of 1.3 mg/L for copper in drinking water.107
  • The American Conference of Industrial Hygienists (ACGIH) has set both the Threshold Limit Value (TLV) and the Time- Weighted Average (TWA) as 1 mg/m3. Copper sulfate, both anhydrous and pentahydrate, and copper dusts and mists are considered as copper. The Maximale Arbeitsplatz-Konzentration or maximum workplace concentration (MAK) for copper sulfate has been set at 0.1 mg/m3 (inhalable fractions).108,109

    Maximum Contaminant Level (MCL): The MCL is the highest level of contaminant that is legally allowed in drinking water. The MCL is enforceable. The MCL is typically measured in milligrams (mg) of contaminant per liter (L) of water.

    U.S. Environmental Protection Agency, Region 5, Water, Underground Injection Control Terms, 2011. http://epa.gov/r5water/uic/glossary.htm#mcl

  • There is no Maximum Contaminant Level for copper. The Maximum Contaminant Level (MCL) Goal for copper is 1.3 mg/L. The National Secondary Drinking Water Regulations set a secondary standard of 1.0 mg/L for copper and 250 mg/L for sulfate. See the text box on Maximum Contaminant Level (MCL).
Date Reviewed: December 2012

Please cite as: Boone, C.; Jervais, G.; Luukinen, B.; Buhl, K.; Stone, D. 2012. Copper Sulfate Technical Fact Sheet; National Pesticide Information Center, Oregon State University Extension Services. http://npic.orst.edu/factsheets/cuso4tech.html.

References:

  1. Tomlin, C. D. S. The Pesticide Manual, A World Compendium, 15th ed.; British Crop Protection Council: Surrey, UK, 1997; pp 646-649.
  2. Connelly, N. G.; Damhus, T.; Hartshorn, R. M.; Hutton, A. T. Nomenclature of Inorganic Chemistry, IUPAC Recommendations 2005. International Union of Pure and Applied Chemistry and the Royal Society of Chemistry: Cambridge, 2005; p 366.
  3. Reregistration Eligibility Decision (RED) for Coppers; U.S. Environmental Protection Agency, Office of Prevention, Pesticides and Toxic Substances, Office of Pesticide Programs, U.S. Government Printing Office: Washington, DC, 2009.
  4. Pizarro, F.; Olivares, M.; Araya, M.; Gidi, V.; Uauy, R. Gastrointestinal effects associated with soluble and insoluble copper in drinking water. Environ. Health. Perspect. 2001, 109 (9), 949-52.
  5. Gropper, S. A. S.; Smith, J. L.; Groff, J. L. Advanced nutrition and human metabolism; Thomson/Wadsworh: Victoria, Australia, 2005; pp 446-456.
  6. O'Neil, M. J. The Merck index : an encyclopedia of chemicals, drugs, and biologicals; Merck: Whitehouse Station, NJ, 2001; p 2676.
  7. Goldschmidt, J. L. MSDS - Basic Copper Sulfate Material Safety Data Sheet; Old Bridge Chemicals, Inc. http://www.oldbridgechem.com/msds/basic-copper-sulfate.php (accessed Jan 2011), updated 1999.
  8. Hazardous Substances Data Bank; Copper (II) Sulfate, Pentahydrate, CASRN: 7758-99-8. http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~7rxy67:2 (accessed Dec 2009), updated 2007.
  9. Theophanides, T.; Anastassopoulou, J. Copper and carcinogenesis. Crit. Rev. Oncol. Hematol. 2002, 42 (1), 57-64.
  10. Daniel, K. G.; Harbach, R. H.; Guida, W. C.; Dou, Q. P. Copper storage diseases: Menkes, Wilsons, and cancer. Front Biosci. 2004, 9, 2652-62.
  11. Goodman, V. L.; Brewer, G. J.; Merajver, 11. S. D. Copper deficiency as an anti-cancer strategy. Endocr. Relat. Cancer 2004, 11 (2), 255-263.
  12. Kamrin, M. A., Pesticide Profiles: Toxicity, Environmental Impact, and Fate; Lewis Publishers: Boca Raton, FL, 1997; p 243-247.
  13. Krieger, R. I. Handbook of Pesticide Toxicology Agents, 2nd ed.; Academic Press, Inc.: San Diego, CA, 2001; Vol. 2, pp 1361-1362.
  14. Oruc, H. H.; Cengiz, M.; Beskaya, A. Chronic copper toxicosis in sheep following the use of copper sulfate as a fungicide on fruit trees. J. Vet. Diagn. Invest. 2009, 21 (4), 540-543.
  15. Olivares, M.; Araya, M.; Pizarro, F.; Uauy, R. Nausea Threshold in Apparently Healthy Individuals Who Drink Fluids Containing Graded Concentrations of Copper. Regul. Toxicol. Pharmacol. 2001, 33 (3), 271-275.
  16. Chuttani, H. K.; Gupta, P. S.; Gulati, S.; Gupta, D. N., Acute copper sulfate poisoning. Am. J. Med. 1965, 39 (5), 849-854.
  17. Thompson, L. J. Copper. Veterinary Toxicology, Basic and Clinical Principles; Gupta, R. C. Ed.; Academic Press: Oxford, England, 2007; pp 427-429.
  18. Shivanandappa, T.; Krishnakumari, M. K.; Majumder, S. K. Testicular atrophy in Gallus domesticus fed acute doses of copper fungicides. Poult. Sci. 1983, 62 (2), 405-8.
  19. Meister, R. T. Crop Protection Handbook; Meister Publishing Co.: Willoughby, OH, 2006; p D 104-D 105.
  20. Poortinga, E. W. Copper penny ingestion in a cat. Can. Vet. J. 1995, 36 (10), 634-634.
  21. Talcott, P. A. Copper. Small Animal Toxicology, 2nd ed.; Peterson, M. E., Ed.; Saunders Elsevier: St. Louis, 2006; pp 668-673.
  22. Webb, C. B.; Twedt, D. C.; Meyer, D. J. Copper-Associated Liver Disease in Dalmatians: A Review of 10 Dogs (1998-2001). J. Vet. Intern. Med. 2002, 16 (6), 665-668.
  23. Radostits, O. M.; Gay, C. C.; Hinchcliff, K. W.; Constable, P.D. Diseases associated with inorganic and farm chemicals - Primary Copper Poisoning. Veterinary Medicine: A Textbook of the Diseases of Cattle, Horses, Sheep, Pigs and Goats, 10th ed.; Saunders Elsevier: New York, 2007.
  24. Bradley, C. H. Copper poisoning in a dairy herd fed a mineral supplement. Can. Vet. J. 1993, 34 (5), 287-292.
  25. Banton, M. I.; Nicholson, S. S.; Jowett, P. L.; Brantley, M. B.; Boudreaux, C. L. Copper toxicosis in cattle fed chicken litter. J. Am. Vet. Med. Assoc. 1987, 191 (7), 827-8.
  26. Cornish, J.; Angelos, J.; Puschner, B.; Miller, G.; George, L. Copper toxicosis in a dairy goat herd. J. Am. Vet. Med. Assoc. 2007, 231 (4), 586-589.
  27. Kline, R. D.; Hays, V. W.; Cromwell, G. L. Effects of Copper, Molybdenum and Sulfate on Performance, Hematology and Copper Stores of Pigs and Lambs. J. Anim Sci. 1971, 33 (4), 771-779.
  28. Reigart, J. R.; Roberts, J. R. Copper Compounds. Recognition and Management of Pesticide Poisonings, 5th ed.; U.S. Environmental Protection Agency, Office of Prevention, Pesticides and Toxic Substances, Office of Pesticide Programs, U.S. Government Printing Office: Washington, DC, 1999; pp 145-146.
  29. Mason, K. E. A Conspectus of Research on Copper Metabolism and Requirements of Man. J. Nutr. 1979, 109 (11), 1979-2066.
  30. Chugh, K. S.; Sharma, B. K.; Singhal, P. C.; Das, K. C.; Datta, B. N. Acute renal failure following copper sulphate intoxication. Postgrad. Med. J. 1977, 53 (615), 18-23.
  31. Schienberg, H. I. Copper, alloys, and compounds. Encyclopedia of Occupational Health and Safety, 3rd ed.; Parmeggiani, L., Ed.; International Labour Office: Geneva, Switerzland, 1983; pp 546-548.
  32. Santic, Z.; Puvacic, S.; Radovic, S.; Puvacic, Z. Vineyard pesticide induced changes in the lungs: experimental studying on rabbits. Med. Arh. 2005, 59 (6), 343-5.
  33. Boyden, R.; Potter, V. R.; Elvehjem, C. A. Effect of Feeding High Levels of Copper to Albino Rats. J. Nutr. 1938, 15 (4), 397-402.
  34. Rana, S. V.; Kumar, A. Biological haematological and histological observations in copper poisoned rats. Ind. Health. 1980, 18 (1), 9-17.
  35. Suttle, N. F.; Mills, C. F. Studies of the toxicity of copper to pigs. Brit. J. Nutr. 1966, 20 (02), 149-161.
  36. Boughton, I. B.; Hardy, W. T. Chronic Copper Poisoning in Sheep. Texas AES Bull. 1934, 499, 5-32.
  37. Gilbert, R. W.; Sander, J. E.; Brown, T. P. Copper sulfate toxicosis in commercial laying hens. Avian Dis. 1996, 40 (1), 236-9.
  38. Jensen, L. S.; Dunn, P. A.; Dobson, K. N. Induction of oral lesions in broiler chicks by supplementing the diet with copper. Avian Dis. 1991, 35 (4), 969-73.
  39. Pesti, G. M.; Bakalli, R. I. Studies on the feeding of cupric sulfate pentahydrate and cupric citrate to broiler chickens. Poultry Sci. 1996, 75, 1086-1091.
  40. Luo, X. G.; Ji, F.; Lin, Y. X.; Steward, F. A.; Lu, L.; Liu, 40. B.; Yu, S. X. Effects of dietary supplementation with copper sulfate or tribasic copper chloride on broiler performance, relative copper bioavailability, and oxidation stability of vitamin E in feed. Poult Sci. 2005, 84 (6), 888-893.
  41. Idowu, O. M. O.; Laniyan, T. F.; Kuye, O. A.; Oladele-Ojo, V. O.; Eruvbetine, D. Effect of Copper Salts on Performance, Cholesterol, Residues in Liver, Eggs and Excreta Of Laying Hens. Arch. Zootec. 2006, 55 (212), 327-338.
  42. Romeu-Moreno, A.; Aguilar, C.; Arola, L.; Mas, A. Respiratory toxicity of copper. Environ. Health Perspect. Suppl 3 1994, 102, 339-40.
  43. Araya, M.; McGoldrick, M. C.; Klevay, L. M.; Strain, J. J.; Robson, P.; Nielsen, F.; Olivares, M.; Pizarro, F.; Johnson, L.; Poirier, K. A. Determination of an Acute No-Observed-Adverse-Effect Level (NOAEL) for Copper in Water. Regul. Toxicol. Pharm. 2001, 34 (2), 137-145.
  44. Araya, M.; Chen, B.; Klevay, L. M.; Strain, J. J.; Johnson, L.; Robson, P.; Shi, W.; Nielsen, F.; Zhu, H.; Olivares, M.; Pizarro, F.; Haber, L. T., Confirmation of an acute no-observed-adverse-effect and low-observed-adverse-effect level for copper in bottled drinking water in a multi-site international study. Regul. Toxicol. Pharm. 2003, 38 (3), 389-399.
  45. Araya, M.; Olivares, M.; Pizarro, F.; González, M.; Speisky, H.; Uauy, R. Copper exposure and potential biomarkers of copper metabolism. BioMetals 2003, 16 (1), 199-204.
  46. Pizarro, F.; Olivares, M.; Uauy, R.; Contreras, P.; Rebelo, A.; Gidi, V. Acute gastrointestinal effects of graded levels of copper in drinking water. Environ. Health Perspect. 1999, 107 (2), 117-21.
  47. Villar, T. G. Vineyard sprayer's lung, Clinical aspects. Am. Rev. Respir. Dis. 1974, 110 (5), 545-55.
  48. Pimentel, J. C.; Marques, F. "Vineyard sprayer's lung": a new occupational disease. Thorax 1969, 24 (6), 678-688.
  49. Saleha Banu, B.; Ishaq, M.; Danadevi, K.; Padmavathi, P.; Ahuja, Y. R. DNA damage in leukocytes of mice treated with copper sulfate. Food Chem. Toxicol. 2004, 42 (12), 1931-1936.
  50. Prá, D.; Franke, S.; Giulian, R.; Yoneama, M.; Dias, J.; Erdtmann, B.; Henriques, J. Genotoxicity and mutagenicity of iron and copper in mice. BioMetals 2008, 21 (3), 289-297.
  51. Bhunya, S. P.; Jena, G. B. Clastogenic effects of copper sulphate in chick in vivo test system. Mutat. Res. Genet. Toxicol. 1996, 367 (2), 57-63.
  52. Wu, T.; Sempos, C. T.; Freudenheim, J. L.; Muti, P.; Smit, E. Serum iron, copper and zinc concentrations and risk of cancer mortality in US adults. Ann. Epidemiol. 2004, 14 (3), 195-201.
  53. Buzio, L.; Tondel, M.; De Palma, G.; Buzio, C.; Franchini, I.; Mutti, A.; Axelson, O. Occupational risk factors for renal cell cancer. An Italian case-control study. Med. Lav. 2002, 93 (4), 303-9.
  54. Ferm, V. H.; Hanlon, D. P., Toxicity of Copper Salts in Hamster Embryonic Development. Biol. Reprod. 1974, 11 (1), 97-101.
  55. Lecyk, M. Toxicity of cupric sulfate in mice embryonic development. Zool. Poloniae 1980, 28 (2), 101-105.
  56. Roychoudhury, S.; Massanyi, P. In vitro copper inhibition of the rabbit spermatozoa motility. J. Environ. Sci. Health A Tox. Hazard Subst. Environ. Eng. 2008, 43 (6), 651-6.
  57. Araya, R.; Gomez-Mora, H.; Vera, R.; Bastidas, J. M. Human spermatozoa motility analysis in a Ringer's solution containing cupric ions. Contracept. 2003, 67 (2), 161-3.
  58. Keen, C. L.; Uriu-Hare, J. Y.; Hawk, S. N.; Jankowski, M. A.; Daston, G. P.; Kwik-Uribe, C. L.; Rucker, R. B. Effect of copper deficiency on prenatal development and pregnancy outcome. Am. J. Clin. Nutr. 1998, 67 (5 Suppl), 1003S-1011S.
  59. Tarnacka, B.; Rodo, M.; Cichy, S.; Czlonkowska, A. Procreation ability in Wilson's disease. Acta. Neurol. Scand. 2000, 101 (6), 395-8.
  60. Johnson, P. E.; Milne, D. B.; Lykken, G. I. Effects of age and sex on copper absorption, biological half-life, and status in humans. Am. J. Clin. Nutr. 1992, 56 (5), 917-25.
  61. Pimentel, J. C.; Menezes, A. P., Liver disease in vineyard sprayers. Gastroenterol. 1977, 72 (2), 275-83.
  62. Barceloux, D. G. Copper. J. Toxicol. Clin. Toxicol. 1999, 37 (2), 217 - 230.
  63. Brewer, G. J., Risks of Copper and Iron Toxicity during Aging in Humans. Chem. Res. Toxicol. 2009.
  64. Linder, M. C.; Hazegh-Azam, M. Copper biochemistry and molecular biology. Am. J. Clin. Nutr. 1996, 63 (5), 797S-811.
  65. Danzeisen, R.; Araya, M.; Harrison, B.; Keen, C.; Solioz, M.; Thiele, D.; McArdle, H. J. How reliable and robust are current biomarkers for copper status? Brit. J. Nutr. 2007, 98 (04), 676-683.
  66. Harvey, L. J.; McArdle, H. J., Biomarkers of copper status: a brief update. Brit. J. Nutr. Suppl. S3 2008, 99 , S10-S13.
  67. Shah, F.; Kazi, T. G.; Afridi, H. I.; Kazi, N.; Baig, J. A.; Shah, A. Q.; Khan, S.; Kolachi, N. F.; Wadhwa, S. K. Evaluation of status of trace and toxic metals in biological samples (scalp hair, blood, and urine) of normal and anemic children of two age groups. Biol. Trace Elem. Res. 2011, 141 (1-3), 131-49.
  68. Moses, M. F.; Prabakaran, J. J. Evaluation of Occupational Exposure to Toxic Metals using Fingernails as Biological Indicators. Res. J. Environ. Toxicol. 2011, 5 (1), 65-70.
  69. Kempson, I. M.; Skinner, W. M.; Kirkbride, K. P. The occurrence and incorporation of copper and zinc in hair and their potential role as bioindicators: a review. J. Toxicol. Environ. Health B Crit. Rev. 2007, 10 (8), 611-22.
  70. Seidel, S.; Kreutzer, R.; Smith, D.; McNeel, S.; Gilliss, D. Assessment of Commercial Laboratories Performing Hair Mineral Analysis. J. Am. Med. Assoc. 2001, 285 (1), 67-72.
  71. Genuis, S.; Birkholz, D.; Rodushkin, I.; Beesoon, S. Blood, Urine, and Sweat (BUS) Study: Monitoring and Elimination of Bioaccumulated Toxic Elements. Arch. Environ. Contam. Toxicol. 2011, 61 (2), 344-357.
  72. Flores-Vélez, L. M.; Ducaroir, J.; Jaunet, A. M.; Robert, M. Study of the distribution of copper in an acid sandy vineyard soil by three different methods. Eur. J. Soil Sci. 1996, 47 (4), 523-532.
  73. Copper Sulfate Crops for use as algicide and invertebrate pest control; Organic Materials Review Institute (OMRI); Eugene, OR, 2001; p 17.
  74. Temminghoff, E. J. M.; Van der Zee, S. E. A. T. M.; de Haan, F. A. M. Copper Mobility in a Copper-Contaminated Sandy Soil as Affected by pH and Solid and Dissolved Organic Matter. Environ. Sci. Technol. 1997, 31 (4), 1109-1115.
  75. Salam, D.; El-Fadel, M. Mobility and Availability of Copper in Agricultural Soils Irrigated from Water Treated with Copper Sulfate Algaecide. Water Air Soil Pollut. 2008, 195 (1), 3-13.
  76. He, Z. L.; Zhang, M.; Yang, X. E.; Stoffella, P. J. Release Behavior of Copper and Zinc from Sandy Soils. Soil Sci. Soc. Am. J. 2006, 70 (5), 1699-1707.
  77. Tom-Petersen, A.; Hansen, H. C. B.; Nybroe, O. Time and Moisture Effects on Total and Bioavailable Copper in Soil Water Extracts. J. Environ. Qual. 2004, 33 (2), 505-512.
  78. Saar, R. A.; Weber, J. H. Fulvic acid: modifier of metal-ion chemistry. Environ. Sci. Technol. 1982, 16 (9), 510A-517A.
  79. Liu, R.; Zhao, D.; Barnett, M. Fate and Transport of Copper Applied in Channel Catfish Ponds. Water Air Soil Pollut. 2006, 176 (1), 139-162.
  80. Haughey, M. A.; Anderson, M. A.; Whitney, R. D.; Taylor, W. D.; Losee, R. F. Forms and fate of Cu in a source drinking water reservoir following CuSO4 treatment. Water Res. 2000, 34 (13), 3440-3452.
  81. Hullebusch, E. V.; Chatenet, P.; Deluchat, V.; Chazal, P. M.; Froissard, D.; Lens, P. N. L.; Baudu, M. Fate and forms of Cu in a reservoir ecosystem following copper sulfate treatment (Saint Germain les Belles, France). J. Phys. IV France 2003, 107, 1333-1336.
  82. Yruela, I. Copper in plants. Braz. J. Plant. Physiol. 2005, 17 (1), 145-156.
  83. Gunkel, P.; Roth, E.; Fabre, B. Copper distribution in chemical soil fractions and relationships with maize crop yield. Environ. Chem. Lett. 2003, 1 (1), 92-97.
  84. Alva, A. K.; Huang, B.; Paramasivam, S. Soil pH Affects Copper Fractionation and Phytotoxicity. Soil Sci. Soc. Am. J. 2000, 64 (3), 955-962.
  85. Arambasic, M. B.; Bjelic, S.; Subakov, G. Acute toxicity of heavy metals (copper, lead, zinc), phenol and sodium on Allium cepa L., Lepidium sativum L. and Daphnia magna St.: Comparative investigations and the practical applications. Water Res. 1995, 29 (2), 497-503.
  86. Food and Drug Administration Pesticide Program Residue Monitoring 1993-2003; U.S Food and Drug Administration, Center for Food Safety and Applied Nutrition: Silver Spring, MD, 2008.
  87. Copper Sulfate Pentahydrate; Tolerance Exemption in or on Various Food and Feed Commodities. Fed. Regist. August 11, 2006, 71, 46106-46110.
  88. Henderson, B. M.; Winterfield, R. W. Acute copper toxicosis in the Canada goose. Avian Dis. 1975, 19 (2), 385-7.
  89. Eisler, R. Copper Hazards To Fish, Wildlife, and Invertebrates: A Synoptic Review. Biological Science Report USGS/BRD/BSR--1997-0002; U.S. Geological Survey, Patuxent Wildlife Research Center: Laurel, MD 20708, 1998; Report No. 33.
  90. Welsh, P. G.; Parrott, J. L.; Dixon, D.G.; Hodson, P. V.; Spry, D. J.; Mierle, G. Estimating acute copper toxicity to larval fathead minnow (Pimephales promelas) in soft water from measurements of dissolved organic carbon, calcium, and pH. Can. J. Fish. Aquat. Sci. 1996, 53, 1263-1271.
  91. Bartsch, A. F. Practical methods for control of algae and water weeds. Public Health Rep. 1954, 69 (8), 749-57.
  92. Hanson, M. J.; Stefan, H. G. Side effects of 58 years of copper sulfate treatement of the Fairmont Lakes, Minnesota1. J. Am. Water Resour. Assoc. 1984, 20 (6), 889-900.
  93. Masser, M. P.; Murphy , T. R.; Shelton, J. L. Aquatic Weed Management: Herbicides; Southern Regional Aquatic Center, U.S. Department of Agriculture, Cooperative State Research, Education, and Extension Service, U.S. Government Printing Office: Washington, DC, 2006.
  94. Taylor; L, N.; McGeer; J, C.; Wood; C, M.; McDonald; D, G. Physiological effects of chronic copper exposure to rainbow trout (Oncorhynchus mykiss) in hard and soft water : Evaluation of chronic indicators. Environ. Toxicol. Chem. 2000, 19 (9), 2298-2308.
  95. Chen, J.-C.; Lin, C.-H. Toxicity of copper sulfate for survival, growth, molting and feeding of juveniles of the tiger shrimp, Penaeus monodon. Aquacult. 2001, 192 (1), 55-65.
  96. Sandahl, J. F.; Miyasaka, G.; Koide, N.; Ueda, H. Olfactory inhibition and recovery in chum salmon (Oncorhynchus keta) following copper exposure. Can. J. Fish. Aquat. Sci. 2006, 63 (8), 1840-1847.
  97. Jaensson, A.; Olsén, K. H. Effects of copper on olfactory-mediated endocrine responses and reproductive behaviour in mature male brown trout Salmo trutta parr to conspecific females. J. Fish Biol. 2010, 76 (4), 800-817.
  98. Chapman, G. A. Toxicities of Cadmium, Copper, and Zinc to Four Juvenile Stages of Chinook Salmon and Steelhead. Trans. Am. Fish. Soc. 1978, 107 (6), 841-847.
  99. Straus, D. L. The acute toxicity of copper to blue tilapia in dilutions of settled pond water. Aquacult. 2003, 219 (1-4), 233-240.
  100. Mastin, B. J.; Rodgers, J. J. H. Toxicity and Bioavailability of Copper Herbicides (Clearigate, Cutrine-Plus, and Copper Sulfate) to Freshwater Animals. Arch. Environ. Contam. Toxicol. 2000, 39 (4), 445-451.
  101. de Oliveira-Filho, E. C.; Lopes, R. M.; Paumgartten, F. J. R. Comparative study on the susceptibility of freshwater species to copperbased pesticides. Chemosphere 2004, 56 (4), 369-374.
  102. Ingersoll, C. G.; Winner, R. W. Effect on Daphnia pulex (de geer) of daily pulse exposures to copper or cadmium. Environ. Toxicol. Chem. 1982, 1 (4), 321-327.
  103. Arauco, L. R. R.; Da Cruz, C.; Neto, J. G. M. Efito da presença de sedimento na toxicidade agua do sulfato de cobre e do triclorfon para três espécies de daphnia. Pestic. Rev. Ecotoxicol. e Meio Ambiente 2005, 15.
  104. Li, N.; Zhao, Y. L.; Yang, J. Accumulation, distribution, and toxicology of copper sulfate in juvenile giant freshwater prawns, Macrobrachium rosenbergii. Bull. Environ. Contam. Toxicol. 2005, 75 (3), 497-504.
  105. Khangarot, B. S.; Das, S. Effects of copper on the egg development and hatching of a freshwater pulmonate snail Lymnaea luteola L. J. Hazard. Mater. 2010, 179 (1-3), 665-675.
  106. De Schamphelaere, K. A.; Heijerick, D. G.; Janssen, C. R. Cross-phylum comparison of a chronic biotic ligand model to predict chronic toxicity of copper to a freshwater rotifer, Brachionus calyciflorus (Pallas). Ecotoxicol. Environ. Saf. 2006, 63 (2), 189-95.
  107. 2009 Edition of the Drinking Water Standards and Health Advisories; U.S. Environmental Protection Agency, U.S. Government Printing Office: Washington, DC, 2009.
  108. Chemical Safety Cards Copper Sulfate (anhydrous); Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health: Atlanta, GA, 2001.
  109. Chemical Safety Cards Copper (II) Sulfate, Pentahydrate; Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health: Atlanta, GA, 2001.

Related Topics: