Copper Toxicity In Food

 

Copper 

            Copper is a metallic element that occurs naturally as the free metal, or associated with other elements in compounds that comprise various minerals. Most copper compounds occur in +1 Cu(I) and +2 Cu(II) valence states. Copper is primarily used as a metal or an alloy (e.g., brass, bronze, gun metal). Copper sulfate is used as a fungicide, algicide, and nutritional supplement.

Sources of exposure

          Copper particulates are released into the atmosphere by windblown dust; volcanic eruptions; and anthropogenic sources, primarily copper smelters and ore processing facilities. Copper particles in the atmosphere will settle out or be removed by precipitation, but can be resuspended into the atmosphere in the form of dust.

Copper is released into waterways by natural weathering of soil and rocks, disturbances of soil, or anthropogenic sources (e.g., effluent from sewage treatment plants).

The general population is exposed to copper through inhalation, consumption of food and water, and dermal contact with air, water, and soil that contains copper. The estimated daily intake of copper from food is 1.0–1.3 mg/day for adults.

Drinking water is the primary source of excess copper. Populations living near sources of copper emissions, such as copper smelters and refineries and workers in these and other industries may also be exposed to high levels of copper in dust by inhalation. Copper concentrations in soils near copper emission sources could be sufficiently high to result in significantly high intakes of copper in young children who ingest soil. For example, copper concentrations of 2,480–6,912 ppm have been measured near copper smelters. These levels of copper in soils would result in the intake of 0.74– 2.1 mg copper per day in a child ingesting 300 mg of soil.

Health effects

          Copper is an essential nutrient that is incorporated into a number of metalloenzymes involved in hemoglobin formation, drug/xenobiotic metabolism, carbohydrate metabolism, catecholamine biosynthesis, the cross-linking of collagen, elastin, and hair keratin, and the antioxidant defence mechanism.

            Copper-dependent enzymes, such as cytochrome c oxidase, superoxide dismutase, ferroxidases, monoamine oxidase, and dopamine β-monooxygenase, function to reduce activated oxygen species or molecular oxygen. Symptoms associated with copper deficiency in humans include normocytic, hypochromic anemia, leukopenia, and osteoporosis.

            Copper homeostasis plays an important role in the prevention of copper toxicity, exposure to excessive levels of copper can result in a number of adverse health effects including liver and kidney damage, anemia, immunotoxicity, and developmental toxicity. Many of these effects are consistent with oxidative damage to membranes or macromolecules. Copper can bind to the sulfhydryl groups of several enzymes, such as glucose-6-phosphatase and glutathione reductase, thus interfering with their protection of cells from free radical damage.

One of the most commonly reported adverse health effect of copper is gastrointestinal distress. Nausea, vomiting, and/or abdominal pain in humans ingesting beverages contaminated with copper or water containing copper sulfate.

Copper is also irritating to the respiratory tract. Coughing, sneezing, runny nose, pulmonary fibrosis, and increased vascularity of the nasal mucosa have been reported in workers exposed to copper dust.

The liver is also a sensitive target of toxicity. Liver damage (necrosis, fibrosis, abnormal biomarkers of liver damage) have been reported in individuals ingesting lethal doses of copper sulfate. Liver effects have also been observed in individuals diagnosed with Wilson’s disease, Indian childhood cirrhosis, or idiopathic copper toxicosis (which includes Tyrollean infantile cirrhosis). These syndromes are genetic disorders that result in an accumulation of copper in the liver; the latter two syndromes are associated with excessive copper exposure.

There is some evidence from animal studies to suggest that exposure to airborne copper or high levels of copper in drinking water can damage the immune system. Impaired cell-mediated and humoral-mediated immune function have been observed in mice. Studies in rats, mice, and mink suggest that exposure to high levels of copper in the diet can result in decreased embryo and fetal growth.

Prevention and control

People can prevent copper toxicity by:           

Limiting exposure to copper from contaminated food and drinks, avoiding the use of corroded or rusted copper cookware, dishes, and utensils.

Installing filters in the house that remove unwanted minerals from water sources

 Reference:

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2. Tapiero H, Townsend DM, Tew KD. Trace elements in human physiology and pathology. Copper. Biomed Pharmacother. 2003 Nov; 57(9):386-98.
3. Gamakaranage CS, Rodrigo C, Weerasinghe S, Gnanathasan A, Puvanaraj V, Fernando H. Complications and management of acute copper sulphate poisoning; a case discussion. J Occup Med Toxicol. 2011 Dec 19; 6(1): 34.
4. Fuentealba IC, Aburto EM. Animal models of copper-associated liver disease. Comp Hepatol. 2003 Apr 03; 2(1):5.
5. Sinkovic A, Strdin A, Svensek F. Severe acute copper sulphate poisoning: a case report. Arh Hig Rada Toksikol. 2008 Mar; 59(1): 31-5