Chemistry International
Vol. 22, No.2, March 2000

2000, Vol. 22
No. 2 (March)
..News from IUPAC
..West Africa Chemical Society
..Reports from Symposia

..Awards and Prizes
..New Books
..Reports from Commissions
..Conference Announcements
..Conferences

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Chemistry International
Vol. 22, No. 2
March 2000

New Books and Publications

 

New Publication from the World Health Organization

Copper, Environmental Health Criteria No. 200

1998, xxii + 360 pages (English with summaries in French and Spanish), ISBN 92-4-157200-0, CHF 72.-/USD 64.80; In developing countries: CHF 50.40, Order No. 1160200. WHO Distribution and Sales, CH-1211 Geneva 27, Switzerland; E-mail: [email protected]; Tel.: +41 22 791 24 76; Fax: +41 22 791 48 57.

This book evaluates the risks to human health and the environment posed by exposure to copper, a malleable metal found naturally in a wide variety of mineral salts and organic compounds, and in the metallic form. Copper is an essential element for all biota. It is widely used in cooking utensils and water distribution systems, in fertilizers, bactericides, fungicides, algicides, and antifouling paints, and in animal feed additives and growth promoters. Industrial applications include use as an activator in froth flotation and sulfide ores, in the production of wood preservatives, in electroplating, and in the manufacturing of azo-dyes.

The report opens with a description of the array of sampling techniques, preparation, and analytical methods available for quantifying copper in environmental and biological samples. Section 2 covers sources of human and environmental exposure. Natural sources include windblown dust, volcanoes, decaying vegetation, forest fires, and sea spray. Anthropogenic emissions arise from smelters, iron foundries, power stations, and combustion sources such as municipal incinerators.

A section on environmental behavior discusses what is known about the fate of copper released to the atmosphere, water, and land. Data indicate that most copper is released to land; major sources are mining operations, agriculture, solid waste, and sludge from treatment works. Bioaccumulation, which occurs if the copper is biologically available, can lead to exceptionally high body burdens in animals and terrestrial plants. A review of levels detected in different environmental compartments supports the conclusion that, for healthy members of the general population, the major route of exposure is oral, with substantial exposure possible when drinking-water is contaminated with copper.

A section on kinetics and metabolism cites evidence that copper is mainly absorbed through the gastrointestinal tract, where part is excreted through the feces and the remainder is transported to the liver bound to serum albumin. The liver is the critical organ of copper homeostasis. When copper exceeds homeostatic control, its biological toxicity arises from its effects on the structure and function of biomolecules such as DNA, membranes, and proteins.

A review of abundant findings from studies in laboratory animals and in vitro test systems shows wide species variations in toxic effects. Rats exposed to single doses by the oral route showed alterations in blood biochemistry and hematology, and adverse effects on the liver, kidney, and lungs. Long-term exposure in rats and mice demonstrated no overt signs of toxicity other than a dose-related reduction in growth. Studies of chronic toxicity and carcinogenicity were judged inadequate for assessment. Limited data on immunotoxicity suggest some impairment of humoral and cell-mediated immune functions in mice. While studies of neurotoxicity have failed to demonstrate behavioral effects, some neurochemical changes have been reported after oral administration.

An assessment of health effects in humans draws on numerous investigations of copper's role as both an essential and a toxic element, and on abundant evidence that adverse effects may arise from both deficient and excessive intakes. Clinically evident deficiency, which is rare in the general population, is characterized by anemia, neutropenia, and bone abnormalities. Copper toxicity, likewise rare in the general population, usually arises following the consumption of contaminated beverages, including drinking-water, or from accidental or suicidal ingestion of high quantities of copper salts. Symptoms include vomiting, lethargy, acute hemolytic anemia, renal and liver damage, neurotoxicity, and increased blood pressure and respiratory rates.

The evaluation gives particular attention to the clinical features of population groups known to be especially sensitive to copper toxicity. These people include premature infants fed on cow's milk, infants recovering from severe malnutrition, hemodialysis patients, patients suffering from chronic liver disease, and patients with genetically determined disorders of copper homeostasis, such as Menkes disease, Wilson disease, and hereditary aceruloplasminemia. The report also cites evidence from several recent dietary surveys indicating suboptimal copper intake in the mean population. Health effects arising from insufficient copper intake, which may have a role in the pathogenesis of cardiovascular disease, were judged to be more important than adverse effects associated with excessive ingestion.

 

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