Copper ingestion

Non-Indian childhood cirrhosis This similar condition, found in other countries, is indistinguishable from Indian childhood cirrhosis. Therefore, it is also called copper-related liver disease. A genetic defect is probably involved. Any correlation with increased copper ingestion is unlikely. (398)... 

The homeostasis and analysis of copper (Cu) are discussed in Chapter 30. Copper ingestion has been foxmd to lead to... 

A lack of neurotoxicity from copper ingestion contrasts the psychiatric picture of Wilson s disease. Inhalation of copper particles by inhalant abusers who sniff metallic paint results in pulmonary deposits of copper but no apparent neurotoxicity (Wilde 1975). Acute poisoning causes nervous excitation followed by depression, but no other central nervous system symptoms appear, even after massive ingestions (Gosselin et al. 1984 Yelin et al. 1987). The same lack of neurotoxicity applies to chronic exposures (Gosselin et al. 1984). 

Klevay LM, Hyg SD. 1973. Hypercholesterolemia in rats produced by an increase in the ratio of zinc to copper ingested. Am J Clin Nutr 26 1060-1068. 

Copper ingestion causes nausea, vomiting, abdominal pain, metallic taste and diarrhea. Ingestion of large doses may cause stomach and intestine ulceration, jaundice and kidney and liver damage... 

Under unusual circumstances, toxicity may arise from ingestion of excess amounts of minerals. This is uncommon except in the cases of fluorine, molybdenum, selenium, copper, iron, vanadium, and arsenic. Toxicosis may also result from exposure to industrial compounds containing various chemical forms of some of the minerals. Aspects of toxicity of essential elements have been pubhshed (161). 

Lead nitrate and copper(ll) sulfate are moderately toxic by ingestion or inhalation. 

Light-amber to yellow-red, oily fuming liquid with a suffocating, pungent, and nauseating odor. This material is hazardous through inhalation and ingestion, and produces local skin/eye impacts. It is noncorrosive to carbon steel and iron when dry. However, when wet it will attack steel, cast iron, aluminum, stainless steel, copper and copper alloys, and many nickel based materials. 

Knobeloch, L., M. Ziarik, J. Howard, B. Theis, D. Farmer, H. Anderson, and M. Proctor. 1994. Gastrointestinal upsets associated with ingestion of copper-contaminated water. Environ. Health Perspect. 102 958-961. 

Di Giulio, R.T. and P.F. Scanlon. 1984. Effects of cadmium and lead ingestion on tissue concentrations of cadmium, lead, copper, and zinc in mallard ducks. Sci. Total Environ. 39 103-110. 

Fed diets containing up to 1000 mg Zn/kg ration for up to 1 year Pomeranian, 2.2 kg, 4-months old, ingested four copper-clad zinc pennies... 

Died from ingestion of 34 copper-clad zinc pennies... 

Ogden, L., W.C. Edwards, and N.A. Nail. 1988. Zinc intoxication in a dog from the ingestion of copper-clad zinc pennies. Veterin. Human Toxicol. 30 577-578. 

Oral exposure to cyanide usually results from accidental, homicidal, or suicidal ingestion of cyanide salts. Sodium cyanide and potassium cyanide are the most frequently studied cyanide compounds. Copper cyanide, potassium silver cyanide, silver cyanide, and calcium cyanide are other compounds that humans could encounter through oral or dermal exposure. Cassava roots and certain fruit pits contain compounds that can be broken down to form cyanide. Cassava roots form the staple diet of some populations in Africa, Central and South America, and Asia. However, it must be noted that cassava roots are notoriously deficient in protein and other nutrients and contain many other compounds, in addition to cyanide, that could be responsible for some of the observed toxic effects. Thiocyanate is a metabolite of cyanide that is formed in the body after exposure to cyanide compounds. When possible, all oral exposures are expressed as mg CN/kg/day. 

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