Excessive concentrations of copper are toxic, and even lethal. Ingestion, inhalation, or skin absorption of large amounts ofcopper can cause a metallic taste in the mouth, abdominal pain, nausea and vomiting, diarrhea, headache, and shock. As little as 11 mg kg _ is regarded as a minimally toxic dose to humans. Large quantities have been lethal. Damage to brain, kidney, liver, and digestive tract may also result from acute toxicity. However, absorption of copper by mouth and skin is fairly low and vomiting frequently further limits absorption, so much of the damage from acute Cu exposure is a chemical 'burn' caused by its caustic nature and local protein damage.
Chronic toxicity to Cu is rarely observed in humans, but liver disease has been observed in vineyard workers after years of applying copper-based fungicides to grapes. A genetic defect causing excessive Cu accumulation is known as 'Wilson's disease'. This defect causes accumulation of Cu in the liver and kidneys up to 30 times normal concentrations. Early signs include a brown ring around the cornea of the eye (Kaiser-Fleisher ring), anemia, jaundice, and swelling. If untreated it can be fatal; however, it is readily treated using chelating agents to remove copper, dietary zinc supplementation to reduce copper absorption, and limiting copper in the diet. Wilson's disease is caused by an autosomal recessive. This means that both parents must carry at least one copy of the gene for the child to inherit it, and males and females are equally at risk.
While copper toxicity can be a problem with livestock (sheep in particular), it is largely caused by excessive concentrations added to feed as a supplement, rather than occurring naturally as a result of accumulation in forage from soil. Given the complex interactions between copper and other trace elements for absorption and effects, it is often difficult to regulate the supplementation correctly. Acute or chronic copper toxicity is rare in crop plants, and is usually traced to repeated or excessive use of copper based fungicides or livestock supplementation.
Copper is extremely toxic to many aquatic and marine organisms. Algae and phytoplankton are inhibited by copper in the water at part per billion (mg l_1) concentrations; copper is widely used as an algaecide. The toxicity of dissolved copper is determined in large part by its chemical speciation. Inorganic and most organic complexes reduce the uptake and toxicity of copper. Some selected results of toxicity tests with a wide variety of freshwater and marine organisms is shown in Table 1. Given the wide variation in methods used and species tested it is difficult to make direct comparisons but some of the more sensitive species are strongly inhibited or killed at concentrations that occur in polluted
Table 1 Selected results of copper toxicity tests on aquatic organisms
Toxicity threshold (pgl 1)
Freshwater plants Chlorella pyrenoidosa Anabaena flos-aquae Navicula incerta Lemna minor Nitzschia palea
Marine plants Prorocentrum micans Asterionella japonica Nitzschia closterium Thalassiosira pseudonana Macrocystis pyrifera
Freshwater animals Daphnia magna Limnodrilus hoffmeisterii Campeloma decisum Oronectes rusticus Oncorynchys gardeneri Lepomis macrochirus
Saltwater animals Acartia tonsa
Crassostrea virginica (embryo) Rangia cuneata Homarus americana Pseudopleuronectes americanus
Growth inhibition 75% Growth inhibition
4 day EC 50 (growth rate) 7 day EC 50 (growth rate) 100% Growth inhibition
5 day EC 50 (growth rate) 72 h EC 50 (growth rate) 96 h EC 50 (growth rate) 72 h EC 50 (growth rate)
96 h EC 50 (photosynthesis rate)
EC 50, estimated concentration of copper causing 50% of reported effect; LC 50, estimated concentration of copper causing 50% mortality in the experimental population in 96 h.
environments. Even within the same species, the results vary substantially, depending upon the water chemistry, the testing protocol, and the life stage of the test organisms.
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