Copper toxicity | |
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Other names | Copperiedus |
A Kayser-Fleischer ring, copper deposits found in the cornea, is an indication the body is not metabolizing copper properly. | |
Specialty | Toxicology |
Copper toxicity (or Copperiedus) is a type of metal poisoning caused by an excess of copper in the body. Copperiedus could occur from consuming excess copper salts, but most commonly it is the result of the genetic condition Wilson's disease and Menke's disease, which are associated with mismanaged transport and storage of copper ions. Copper is essential to human health as it is a component of many proteins. But hypercupremia (high copper level in the blood) can lead to copper toxicity if it persists and rises high enough.
Chronic toxicity by copper is rare. [1] The suggested safe level of copper in drinking water for humans varies depending on the source, but tends to be pegged at 1.3 mg/L. [2] So low is the toxicity of copper that copper(II) sulfate is a routine reagent in undergraduate chemistry laboratories. [3]
Acute symptoms of copper poisoning by ingestion include vomiting, hematemesis (vomiting of blood), hypotension (low blood pressure), melena (black "tarry" feces), coma, jaundice (yellowish pigmentation of the skin), and gastrointestinal distress. [4] Individuals with glucose-6-phosphate dehydrogenase deficiency may be at increased risk of hematologic effects of copper. [4] Hemolytic anemia resulting from the treatment of burns with copper compounds is infrequent. [4]
Chronic (long-term) copper exposure can damage the liver and kidneys. [5] Mammals have efficient mechanisms to regulate copper stores such that they are generally protected from excess dietary copper levels. [5] [6]
Those same protection mechanisms can cause milder symptoms, which are often misdiagnosed as psychiatric disorders. There is a lot of research on the function of the Cu/Zn ratio in neurological, endocrinological, and psychological conditions. [7] [8] [9] Many of the substances that protect humans from excess copper perform important functions in the neurological and endocrine systems, leading to diagnostic difficulties. When they are used to bind copper in the plasma, to prevent it from being absorbed in the tissues, their own function may go unfulfilled. Such symptoms often include mood swings, irritability, depression, fatigue, excitation, difficulty focusing, and feeling out of control. To further complicate diagnosis, some symptoms of excess copper are similar to those of a copper deficit.
The U.S. Environmental Protection Agency's Maximum Contaminant Level (MCL) in drinking water is 1.3 milligrams per liter. [4] [10] The MCL for copper is based on the expectation that a lifetime of consuming copper in water at this level is without adverse effect (gastrointestinal). The US EPA lists copper as a micronutrient and a toxin. [11] Toxicity in mammals includes a wide range of animals and effects such as liver cirrhosis, necrosis in kidneys and the brain, gastrointestinal distress, lesions, low blood pressure, and fetal mortality. [12] [13] [14] The Occupational Safety and Health Administration (OSHA) has set a limit of 0.1 mg/m3 for copper fumes (vapor generated from heating copper) and 1 mg/m3 for copper dusts (fine metallic copper particles) and mists (aerosol of soluble copper) in workroom air during an eight-hour work shift, 40-hour work week. [15] Toxicity to other species of plants and animals is noted to varying levels. [11]
The EPA lists no evidence for human cancer incidence connected with copper, and lists animal evidence linking copper to cancer as "inadequate". Two studies in mice have shown no increased incidence of cancer. One of these used regular injections of copper compounds, including cupric oxide. One study of two strains of mice fed copper compounds found a varying increased incidence of reticulum cell sarcoma in males of one strain, but not the other (there was a slightly increased incidence in females of both strains). These results have not been repeated. [16]
One manifestation of copper toxicity, cirrhosis of the liver in children (Indian childhood cirrhosis), has been linked to boiling milk in copper cookware. The Merck Manual states that recent studies suggest that a genetic defect is associated with this particular cirrhosis. [17]
An inherited condition called Wilson's disease causes the body to retain copper, since it is not excreted by the liver into the bile. This disease, if untreated, can lead to brain and liver damage, and bis-choline tetrathiomolybdate is under investigation as a therapy against Wilson's disease.
An X-linked recessive trait that is inherited named Menke's disease causes disruption of connective tissue due to mutations in genes. If severely affected the approximate span of life is three years. One treatment used to correct the mutation is copper-histidine treatment. [18]
Elevated free copper levels exist in Alzheimer's disease, [19] which has been hypothesized to be linked to inorganic copper consumption. [20] Copper and zinc are known to bind to amyloid beta proteins in Alzheimer's disease. [21] This bound form is thought to mediate the production of reactive oxygen species in the brain. [22]
ICD-9-CM code 985.8 Toxic effect of other specified metals includes acute and chronic copper poisoning (or other toxic effect) whether intentional, accidental, industrial etc.
In addition, it includes poisoning and toxic effects of other metals including tin, selenium, nickel, iron, heavy metals, thallium, silver, lithium, cobalt, aluminum and bismuth. Some poisonings, e.g. zinc phosphide, would/could also be included as well as under 989.4 Poisoning due to other pesticides, etc.
Excluded are toxic effects of mercury, arsenic, manganese, beryllium, antimony, cadmium, and chromium.
Code | Term |
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T56.4X1D | Toxic effect of copper and its compounds, accidental (unintentional), subsequent encounter |
T56.4X1S | Toxic effect of copper and its compounds, accidental (unintentional), sequela |
T56.4X2D | Toxic effect of copper and its compounds, intentional self-harm, subsequent encounter |
T56.4X2S | Toxic effect of copper and its compounds, intentional self-harm, sequela |
T56.4X3D | Toxic effect of copper and its compounds, assault, subsequent encounter |
T56.4X3S | Toxic effect of copper and its compounds, assault, sequela |
T56.4X4D | Toxic effect of copper and its compounds, undetermined, subsequent encounter |
T56.4X4S | Toxic effect of copper and its compounds, undetermined, sequela |
Concept ID | Term |
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46655005 | Copper |
43098002 | Copper fever |
49443005 | Phytogenous chronic copper poisoning |
50288007 | Chronic copper poisoning |
73475009 | Hepatogenous chronic copper poisoning |
875001 | Chalcosis of eye |
90632001 | Acute copper poisoning |
In cases of suspected copper poisoning, penicillamine is the drug of choice, and dimercaprol, a heavy metal chelating agent, is often administered. Vinegar is not recommended to be given, as it assists in solubilizing insoluble copper salts. The inflammatory symptoms are to be treated on general principles, as are the nervous ones. [23] Treatment can also look like ozone oxidation for environmental toxicity problems, as well as removing sediment in water areas because sediment can be a home for toxicants to reside. [24]
There is some evidence that alpha-lipoic acid (ALA) may work as a milder chelator of tissue-bound copper. [25] Alpha lipoic acid is also being researched for chelating other heavy metals, such as mercury. [26]
Too much copper in water may damage marine and freshwater organisms such as fish and molluscs. [27] Fish species vary in their sensitivity to copper, with the LD50 for 96-h exposure to copper sulphate reported to be in the order of 58 mg per litre for Tilapia ( Oreochromis niloticus ) and 70 mg per litre for catfish ( Clarias gariepinus ) [28] The chronic effect of sublethal concentrations of copper on fish and other creatures is damage to gills, liver, kidneys and the nervous system. It also interferes with the sense of smell in fish, thus preventing them from choosing good mates or finding their way to mating areas. [29]
Copper-based paint is a common marine antifouling agent. [30] In the United States, copper-based paint replaced tributyltin, which was banned due to its toxicity, as a way for boats to control organic growth on their hulls. In 2011, Washington state became the first U.S. state to ban the use of copper-based paint for boating, although it only applied to recreational boats. [31] California has also pursued initiatives to reduce the effect of copper leaching, with the U.S. EPA pursuing research. [32]
Copper is an essential elemental for metabolic processes in marine algae. It is required for electron transport in photosynthesis and by various enzyme systems. Too much copper can also affect phytoplankton or marine algae in both marine and freshwater ecosystems. It has been shown to inhibit photosynthesis, disrupt electron transport in photosystem 2, reduce pigment concentrations, restrict growth, reduce reproduction, etc. [33] The toxicity of copper is widely recognized and is used to help prevent algal blooms. The effect of copper is solely dependent on the free copper the water is receiving. It's determined by the relative solubility and the concentration of the copper binding ligands.
Studies have shown that copper concentrations are toxic when marine phytoplankton are confined to areas that are heavily impacted by anthropogenic emissions. [34] Some of the studies have used a marine amphipod to show how Copper affects it. This particular study said that the juveniles were 4.5 more times sensitive to the toxins than the adults. [35] Another study used 7 different algal species. They found that one species was more sensitive than the others, which was Synechococcus, and that another species was more sensitive in seawater, which wasThalassiosira weissflogii. [36]
One study used cyanobacteria, diatoms, coccolithophores, and dinoflagellates. This study showed that cyanobacteria was the most sensitive, diatoms were the least sensitive, and the coccolithophores and dinoflagellates were intermediate. They used copper ion in a buffer system and controlled it at different levels. They found that cyanobacteria reproduction rates were reduced while other algae had maximum reproduction rates. They found that Copper may influence seasonal successions of species. [37]
Copper and copper alloys such as brass have been found to be toxic to bacteria via the oligodynamic effect. The exact mechanism of action is unknown, but common to other heavy metals. Viruses are less susceptible to this effect than bacteria. Associated applications include the use of brass doorknobs in hospitals, which have been found to self-disinfect after eight hours, and mineral sanitizers, in which copper can act as an algicide. Overuse of copper sulfate as an algicide has been speculated to have caused a copper poisoning epidemic on Great Palm Island in 1979. [38]
Selenium is a chemical element; it has the symbol Se and atomic number 34. It is a nonmetal with properties that are intermediate between the elements above and below in the periodic table, sulfur and tellurium, and also has similarities to arsenic. It seldom occurs in its elemental state or as pure ore compounds in Earth's crust. Selenium was discovered in 1817 by Jöns Jacob Berzelius, who noted the similarity of the new element to the previously discovered tellurium.
A poison is any chemical substance that is harmful or lethal to living organisms. The term is used in a wide range of scientific fields and industries, where it is often specifically defined. It may also be applied colloquially or figuratively, with a broad sense.
Wilson's disease is a genetic disorder in which excess copper builds up in the body. Symptoms are typically related to the brain and liver. Liver-related symptoms include vomiting, weakness, fluid build-up in the abdomen, swelling of the legs, yellowish skin, and itchiness. Brain-related symptoms include tremors, muscle stiffness, trouble in speaking, personality changes, anxiety, and psychosis.
Arsenic poisoning is a medical condition that occurs due to elevated levels of arsenic in the body. If arsenic poisoning occurs over a brief period of time, symptoms may include vomiting, abdominal pain, encephalopathy, and watery diarrhea that contains blood. Long-term exposure can result in thickening of the skin, darker skin, abdominal pain, diarrhea, heart disease, numbness, and cancer.
Toxicity is the degree to which a chemical substance or a particular mixture of substances can damage an organism. Toxicity can refer to the effect on a whole organism, such as an animal, bacterium, or plant, as well as the effect on a substructure of the organism, such as a cell (cytotoxicity) or an organ such as the liver (hepatotoxicity). Sometimes the word is more or less synonymous with poisoning in everyday usage.
Mercury poisoning is a type of metal poisoning due to exposure to mercury. Symptoms depend upon the type, dose, method, and duration of exposure. They may include muscle weakness, poor coordination, numbness in the hands and feet, skin rashes, anxiety, memory problems, trouble speaking, trouble hearing, or trouble seeing. High-level exposure to methylmercury is known as Minamata disease. Methylmercury exposure in children may result in acrodynia in which the skin becomes pink and peels. Long-term complications may include kidney problems and decreased intelligence. The effects of long-term low-dose exposure to methylmercury are unclear.
Gyromitrin is a toxin and carcinogen present in several members of the fungal genus Gyromitra, like G. esculenta. Its formula is C4H8N2O. It is unstable and is easily hydrolyzed to the toxic compound monomethylhydrazine CH3NHNH2. Monomethylhydrazine acts on the central nervous system and interferes with the normal use and function of vitamin B6. Poisoning results in nausea, stomach cramps, and diarrhea, while severe poisoning can result in convulsions, jaundice, or even coma or death. Exposure to monomethylhydrazine has been shown to be carcinogenic in small mammals.
Liver disease, or hepatic disease, is any of many diseases of the liver. If long-lasting it is termed chronic liver disease. Although the diseases differ in detail, liver diseases often have features in common.
Ethion (C9H22O4P2S4) is an organophosphate insecticide. Ethion is known to affect a neural enzyme called acetylcholinesterase and prevent it from working.
Cyanotoxins are toxins produced by cyanobacteria. Cyanobacteria are found almost everywhere, but particularly in lakes and in the ocean where, under high concentration of phosphorus conditions, they reproduce exponentially to form blooms. Blooming cyanobacteria can produce cyanotoxins in such concentrations that they can poison and even kill animals and humans. Cyanotoxins can also accumulate in other animals such as fish and shellfish, and cause poisonings such as shellfish poisoning.
Manganism or manganese poisoning is a toxic condition resulting from chronic exposure to manganese. It was first identified in 1837 by James Couper.
Iodomethane, also called methyl iodide, and commonly abbreviated "MeI", is the chemical compound with the formula CH3I. It is a dense, colorless, volatile liquid. In terms of chemical structure, it is related to methane by replacement of one hydrogen atom by an atom of iodine. It is naturally emitted by rice plantations in small amounts. It is also produced in vast quantities estimated to be greater than 214,000 tons annually by algae and kelp in the world's temperate oceans, and in lesser amounts on land by terrestrial fungi and bacteria. It is used in organic synthesis as a source of methyl groups.
Endrin is an organochlorine compound with the chemical formula C12H8Cl6O that was first produced in 1950 by Shell and Velsicol Chemical Corporation. It was primarily used as an insecticide, as well as a rodenticide and piscicide. It is a colourless, odorless solid, although commercial samples are often off-white. Endrin was manufactured as an emulsifiable solution known commercially as Endrex. The compound became infamous as a persistent organic pollutant and for this reason it is banned in many countries.
Soil contamination, soil pollution, or land pollution as a part of land degradation is caused by the presence of xenobiotic (human-made) chemicals or other alteration in the natural soil environment. It is typically caused by industrial activity, agricultural chemicals or improper disposal of waste. The most common chemicals involved are petroleum hydrocarbons, polynuclear aromatic hydrocarbons, solvents, pesticides, lead, and other heavy metals. Contamination is correlated with the degree of industrialization and intensity of chemical substance. The concern over soil contamination stems primarily from health risks, from direct contact with the contaminated soil, vapour from the contaminants, or from secondary contamination of water supplies within and underlying the soil. Mapping of contaminated soil sites and the resulting clean ups are time-consuming and expensive tasks, and require expertise in geology, hydrology, chemistry, computer modelling, and GIS in Environmental Contamination, as well as an appreciation of the history of industrial chemistry.
Zinc toxicity is a medical condition involving an overdose on, or toxic overexposure to, zinc. Such toxicity levels have been seen to occur at ingestion of greater than 50 mg of zinc. Excessive absorption of zinc can suppress copper and iron absorption. The free zinc ion in solution is highly toxic to bacteria, plants, invertebrates, and even vertebrate fish. Zinc is an essential trace metal with very low toxicity in humans.
Cylindrospermopsin is a cyanotoxin produced by a variety of freshwater cyanobacteria. CYN is a polycyclic uracil derivative containing guanidino and sulfate groups. It is also zwitterionic, making it highly water soluble. CYN is toxic to liver and kidney tissue and is thought to inhibit protein synthesis and to covalently modify DNA and/or RNA. It is not known whether cylindrospermopsin is a carcinogen, but it appears to have no tumour initiating activity in mice.
Environmental toxicology is a multidisciplinary field of science concerned with the study of the harmful effects of various chemical, biological and physical agents on living organisms. Ecotoxicology is a subdiscipline of environmental toxicology concerned with studying the harmful effects of toxicants at the population and ecosystem levels.
Paracetamol poisoning, also known as acetaminophen poisoning, is caused by excessive use of the medication paracetamol (acetaminophen). Most people have few or non-specific symptoms in the first 24 hours following overdose. These symptoms include feeling tired, abdominal pain, or nausea. This is typically followed by absence of symptoms for a couple of days, after which yellowish skin, blood clotting problems, and confusion occurs as a result of liver failure. Additional complications may include kidney failure, pancreatitis, low blood sugar, and lactic acidosis. If death does not occur, people tend to recover fully over a couple of weeks. Without treatment, death from toxicity occurs 4 to 18 days later.
Senecionine is a toxic pyrrolizidine alkaloid isolated from various botanical sources. It takes its name from the Senecio genus and is produced by many different plants in that genus, including Jacobaea vulgaris. It has also been isolated from several other plants, including Brachyglottis repanda, Emilia, Erechtites hieraciifolius, Petasites, Syneilesis, Crotalaria, Caltha leptosepala, and Castilleja.
Copper is an essential trace element that is vital to the health of all living things. In humans, copper is essential to the proper functioning of organs and metabolic processes. The human body has complex homeostatic mechanisms which attempt to ensure a constant supply of available copper, while eliminating excess copper whenever this occurs. However, like all essential elements and nutrients, too much or too little nutritional ingestion of copper can result in a corresponding condition of copper excess or deficiency in the body, each of which has its own unique set of adverse health effects.
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