Miscellaneous Contaminants


Copper

Copper is a biologically necessary trace element, however increased levels in water or in tissues have detrimental effects. There are many data on acute lethal effects, usually obtained from experiments with high levels of copper, but relatively few data on chronic effects (National Research Council 1979b).

In general, copper enters the aquatic environment primarily from soils and mineral deposits by the erosional activity of water. Most natural waters are capable of removing copper from the water column. The chemical form of copper in water and, hence, its toxicity is related to pH, alkalinity, salinity, and cornplexation with ligands, clays, inorganic particulates, hardness (Ca++ and Mg++) and metal oxides. Certain chemical forms exhibit varying degrees of absorption and toxicity. Because of this, there is much uncertainty in identifying detrimental concentrations under different circumstances. Bottom-dwelling organisms that feed by particulate filtration may be especially susceptible to adsorbed copper. Whole body copper concentrations tend to decrease as the trophic levels increase, presumably because consuming organisms are capable of metabolic regulation.

In humans, copper is necessary for good health. However, very large single or daily intakes of copper can be harmful to health. Drinking water that contains higher than normal levels of copper may cause vomiting, diarrhea, stomach cramps, and nausea. Very young children are sensitive to copper, and long-term exposure to high levels of copper in food and water may cause liver damage and death. Copper is not known to cause cancer or birth defects in humans. The seriousness of the effects of copper can be expected to increase with both level and duration of exposure.

Polychlorinated-dibenzo-p-dioxins and furans (PCDD/PCDFs)

Polychlorinated-dibenzo-p-dioxins and furans (PCDD and PCDFs) are byproducts formed in the production of chlorinated substances, combustion processes and in direct chlorination reactions such as chlorine bleaching of paper pulp. The most significant sources are municipal waste and hospital incinerators, which combust wastes that include chlorinated products. An important additional source is motor vehicle fuel combustion in countries where leaded fuel containing chlorine scavengers is still used. Pulp and paper mills using chlorine in the bleaching process have been important sources to the aquatic environment of 2,3,7,8-substituted TCDD. PCDD/Fs are also trace contaminants in chlorophenoxy herbicides and chlorophenol wood preservatives. Tetrachlorinated dioxin (2,3,7,8-TeCDD) is the most toxic among this group of chemicals.

Dioxins and furans are very toxic to some animal species, but the evidence for corresponding toxicity in humans has not been established. The physiological effects of exposure to high levels are similar to PCBs (carcinogenisis in animal studies, immune suppression, hormonal disruption, and developmental impairment). The IARC considers dioxins and furans as possibly carcinogenic to humans.

Hexachlorobenzene (HBC or HCBZ)

HCB is produced as a by-product in the production of a large number of chlorinated compounds, particularly lower chlorinated benzenes, and in the production of several pesticides. It has been used in small amounts as a fungicide, and it has limited use as a pesticide. It is emitted to the atmosphere in flue gases and fly ash generated at waste incineration facilities. HCB has a relatively high bioaccumulation potential because of its high lipophilicity and long-half-life in biota (Niimi 1988). Other chlorobenzenes (tetra- and penta-substituted) are also relatively lipophilic, semi-volatile, and persistent especially in the abiotic environment (Mackay et al. 1992).

Animal studies show that ingestion of hexachlorobenzene on a long-term basis can harm the liver, immune system, kidneys, and blood and produce eruptions and pigmentations of the skin. These studies also suggest that ingestion of hexachlorobenzene on a long-term basis can lead to cancer of the liver and thyroid. There is weak evidence that marginal perturbations of porphyrin metabolism may occur with blood HCB levels in the 2-40 m g·L-1 range. Such subclinical effects are not expected in association with the blood levels (<2 m g·L-1) seen in the general population.

The International Agency for Research on Cancer (IARC) has classified HCB as a possible human carcinogen, based on sufficient evidence in animals, but inadequate evidence of carcinogenicity in humans.

Endosulfan

Endosulfan is a very toxic insecticide still widely used against a variety of insects, especially on high value crops and particularly in tropical countries. Isomers of endosulfan are detected as contaminants in air, water, sediments, soil, fish, other aquatic organisms, and food. It has been measured and detected in the Arctic in a limited number of studies. It is a concern mainly because of its high volume usage at more southern latitudes.

Little is known of the effects of long-term exposure to low levels of endosulfan in humans. Animal studies have shown effects on the kidneys, testes, developing fetus, and liver from long-term exposure to low levels of endosulfan. The ability of animals to fight infection was also lowered. Animal studies have not shown that endosulfan causes cancer, and no human studies are available. Neither the IARC nor the US EPA has classified endosulfan as a human carcinogen.

Chlorobornanes (CHBS)

The complex mixture of chlorobornanes (CHBs), known as toxaphene, was widely used in the US on cotton crops until the early 1980s. Use peaked between 1972 and 1975 and declined in the late 1970s and early 1980s. Manufacture was banned in the US in 1982; use was banned in 1986. Similar products are still used in Mexico, Central America, eastern Europe, and the former Soviet Union. Toxaphene has been globally dispersed by atmospheric transport to the same extent as DDT and PCBs.

Toxaphene is produced by the chlorination of bornane and can consist of over 300 compounds, substituted with 6 to 10 chlorines, with an average composition of C10H10Clg. Analysis is difficult because of the mixture's complexity, because it occurs in the presence of other interfering OCs (PCBs, DDTs, HCHs), and because of the lack of standards. For this reason, the levels and effects of toxaphene in the Arctic are not well studied even though it is a major concern.

Toxaphene is an insecticidal mixture consisting largely of chlorinated bornanes (CHBs) with a small proportion of chlorinated camphenes. Even though CHB mixtures have been banned or severely restricted in many countries, continued input to the environment may occur from regions outside the Arctic where use is still permitted and by volatilization from contaminated soils. CHBs, originating from long-range transport through the atmosphere, have been responsible for the closure of a commercial and sport fishery in Lake Laberge (Yukon). In winter, they are deposited mainly by precipitation and particle dry deposition, while in summer gas exchange with open water facilitates their movement. The food chain can amplify the effects of atmospheric deposition, leading to elevated levels of CHBs in top predator fish in some lakes and not in others. One of the great difficulties in making quantitative budget estimates of CHBs for lakes or the Arctic Ocean is the disparity in analytical methods of measuring this complex mixture of compounds. It is recommended that considerable effort be made to quality control and assure a variety of sampling and analytical methodologies used for measuring CHBs. A laboratory inter-comparison of analytical techniques that includes recognized international laboratories is highly desirable.

Toxaphene is one of the major contaminants detected in arctic biota (particularly fish and marine mammals) (Andersson et al. 1988, Kawano et al. 1988, Muir et al. 1988, Norstrom et al. 1988, Lockhart et al. 1989). Lockhart and co-workers noted that in some locations consumption of fish and their livers by native people could lead to an intake of CHBs that exceed the US National Academy of Sciences acceptable daily intake of 1.25 µg·kg-l·day-1 (Bidleman et al. 1989).

Exposure in humans from breathing, eating, or drinking high levels of toxaphene for brief periods has been reported to cause damage to the lungs, nervous system, liver, and kidneys and can result in death. Gastrointestinal discomfort and seizures as well as chromosomal aberrations have been reported in humans exposed occupationally to toxaphene. Limited data suggest that chronic exposure to low environmental levels of toxaphene may also result in some effects on the liver, kidneys, lungs, and nervous system.

There is no conclusive evidence available to link toxaphene exposure with cancer in humans. The IARC has classified toxaphene as possibly carcinogenic to humans. Based on animal studies (thyroid and hepatic carcinomas), toxaphene has been classified as a probable human carcinogen by the US EPA. Toxaphene has recently been observed to have estrogenic effects on human breast cancer estrogen-sensitive cells. Xenoestrogens have been hypothesized to have a role in human breast cancer. In addition to potential carcinogenic effects, toxaphene may also cause disruption of the endocrine system due to its estrogenic activity.

Mirex

Mirex is of interest because of its high Kow and its persistence. It was used as an insecticide and fire retardant, mainly in the US and Canada until it was banned in 1978. High levels of mirex were found in Lake Ontario and St. Lawrence River biota as a result of past industrial releases. In these areas, levels are declining in lake trout and coho salmon, but not in herring gulls and beluga whales. Its presence in Arctic biota at low levels is somewhat surprising, but may be explained by exposure of migratory species to this contaminant when feeding at southern latitudes.

Information on the human health effects of mirex are limited. Chronic exposure is related to renal effects, decreases in body weight or body weight gain greater than 10%, non-precancerous lesions of the liver, and cancer (an increased incidence of hepatocellular adenomas was noted, but only in animals having hepatotoxicity). The IARC has classified mirex as a possible human carcinogen, based on sufficient evidence in animals, but inadequate evidence of carcinogenicity in humans.