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Mercury in the Food Chain
Almost all mercury compounds are toxic and can be dangerous at very low levels in both aquatic and terrestrial ecosystems. Because mercury is a persistent substance, it can build up, or bioaccumulate, in living organisms, inflicting increasing levels of harm on higher order species such as predatory fish and fish eating birds and mammals through a process know as "biomagnification". Although the long-term effects of mercury on whole ecosystems are unclear, the survival of some affected populations and overall biodiversity are at risk.
In the environment, particularly lakes, waterways and wetlands, mercury can be converted to a highly toxic, organic compound called methylmercury through biogeochemical interactions. Methylmercury, which is absorbed into the body about six times more easily than inorganic mercury, can migrate through cells which normally form a barrier to toxins. It can cross the blood-brain and placental barriers, allowing it to react directly with brain and fetal cells. Mercury contamination causes a wide range of symptons in organisms, and affects the kidneys and neurological systems in particular. While low levels may not be directly lethal for individual organisms, toxicological effects like impaired reproduction, growth, neuro-development, and learning ability, in addition to behavioral changes, can lead to increases in mortality and the risk of predation for some wildlife.
The most important pathway for mercury bioaccumulation is through the food chain, as illustrated in the figure below. In the water, plants and small organisms like plankton take up mercury through passive surface absorption or through food intake. For "autotrophic" organisms (which do not eat other organisms), passive absorption is the only route of exposure. The amount of mercury that results in these species from even a lifetime of passive absorption is not generally harmful to the organism. On the other hand, heterotrophic organisms (animals which eat other life forms) may be exposed to dangerous concentrations via a second route. Methylmercury biomagnifies through the food chain as predators eat other organisms and absorb the contaminants that their food sources contained. Over time, an individual who consumes plants or prey contaminated with methylmercury will acquire levels greater than in either its habitat or its food. As a result, top predators acquire greater body burdens of mercury than the fish they consume.
(If the concentration of methylmercury in lake water is considered to have an absolute value of 1, then approximate bioaccumulation factors for microorganisms like phytoplankton are 105; for macroorganisms like zooplankton and planktivores are 106 ; and for piscivores like fish, birds and humans are 107. Reference: Metal Ions in Biological Systems)
Methylmercury in Fish
Methylmercury is held tightly to fish protein when absorbed through the gills or when contaminated food sources are eaten. In some cases, methylmercury levels in carnivorous fish, such as freshwater bass, walleye and pike, and marine shark and swordfish, bioaccumulate up to a million times greater than in the surrounding water. Although fish appear to be tolerant to large body burdens of methylmercury, there have been human deaths in cases of severe poisoining. For example, in the 1950s, the Chisso Corporation in Minamata, Japan, released untreated effluent containing methyl mercury chloride into Minamata Bay. Once in the bay's sediments, the mercury was readily absorbed by marine species, contaminating the entire ecosystem. Fish consumed by local residents resulted in the deaths of more than 1000 individuals and severely impacted the developing fetuses of pregnant women.
In general, levels of mercury increase with fish size and age, although not always. Levels also vary by species and location. Bioaccumulation in fish is influenced by the amount of methylmercury present, which is in turn affected by local biogeochemical processes and by mercury inputs from atmospheric pollution. In order to limit human exposure to mercury from contaminated fish, various government departments have issued fish consumption advisories for water bodies throughout Canada.
Methylmercury in Wildlife
Piscivorous (fish eating) predators such as loons, merganser ducks, osprey, eagles, herons, and kingfishers, generally have very high concentrations of mercury. Mercury has been detected in Common Loons from Alaska to Atlantic Canada, and blood concentrations have been correlated with levels in prey fish species. A recent survey of mercury in loons from five regions across the US and Canada has shown that blood mercury concentrations increased from west to east, with the highest levels in southeast Canada. High levels of mercury are suspected to impair the loon's reproductive success as well as cause growth related problems.These problems inevitably lead to an increased death rate and a decreased birth rate, resulting in a reduction in the abundance of natural populations.
In addition, mercury has been found in predatory mammals such as otters from south central Ontario. It is thought that elevated mercury levels in otters may cause early mortality due to toxicity and behavioral changes. While the reproduction and behavior of bird species is generally affected by exposure to methylmercury, mammals most often suffer neurological effects. The severity of the toxic effects will depend on the degree of exposure, and may range from a slight impairment to reproductive failure or death.
In the past, mercury risk reduction strategies focused on restricting human consumption of heavily contaminated fish in order to protect human health. Such a strategy is clearly not adequate for the protection of wildlife. Species such as otter and mink cannot heed warning notices or fish consumption advisories. Since mercury is so widely distributed in the Canadian environment, their risk is real and immediate, especially when effects such as impaired growth and reproduction, neurological damage, kidney damage, and weight loss, which occur at relatively low concentrations, are considered.
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