Vol. 22, No. 2
Books and Publications
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.