The mercury applied to lakes was found in young-of-the-year yellow perch within two months, whereas the mercury applied to wetlands and uplands had a slower but longer influx.Acute methylmercury poisoning can occur either directly from the release of methylmercury into the environment or indirectly from the release of inorganic mercury that is subsequently methylated in the environment. For example, methylmercury poisoning occurred at Grassy Narrows in Ontario, Canada (see Ontario Minamata disease) as a result of mercury released from the mercury-cell Chloralkali process, which uses liquid mercury as an electrode in a process that entails electrolytic decomposition of brine, followed by mercury methylation in the aquatic environment. An acute methylmercury poisoning tragedy occurred also in Minamata, Japan following release of methylmercury into Minamata Bay and its tributaries (see Minamata disease). In the Ontario case, inorganic mercury discharged into the environment was methylated in the environment; whereas, in Minamata, Japan, there was direct industrial discharge of methylmercury. Dietary sources
Because methylmercury is formed in aquatic systems, and because it is not readily eliminated from organisms, it is biomagnified in aquatic food chains from bacteria, to plankton, through macroinvertebrates, to herbivorous fish and to piscivorous (fish-eating) fish. At each step in the food chain, the concentration of methylmercury in the organism increases. The concentration of methylmercury in the top level aquatic predators can reach a level a million times higher than the level in the water. This is because methylmercury has a half-life of about 72 days in aquatic organisms resulting in its bioaccumulation within these food chains.
Methylmercury has a half-life in human blood of about 50 days.Several studies indicate that methylmercury is linked to subtle developmental deficits in children exposed in utero such as loss of IQ points, and decreased performance in tests of language skills, memory function and attention deficits. Methylmercury exposure in adults has also been linked to increased risk of cardiovascular disease including heart attack. Some evidence also suggests that methylmercury can cause autoimmune effects in sensitive individuals. Despite some concerns about the relationship between methylmercury exposure and autism, there are few data that support such a link. Although there is no doubt that methylmercury is toxic in several respects, including through exposure of the developing fetus, there is still some controversy as to the levels of methylmercury in the diet that can result in adverse effects. Recent evidence suggests that the developmental and cardiovascular toxicity of methylmercury may be mitigated by co-exposures to omega-3 fatty acids and perhaps selenium, both found in fish and elsewhere.There have been several episodes in which large numbers of people were severely poisoned by food contaminated with high levels of methylmercury, notably the dumping of industrial waste that resulted in the pollution and subsequent mass poisoning in Minamata and Niigata, Japan and the situation in Iraq in the 1960s and 1970s in which wheat treated with methylmercury as a preservative and intended as seed grain was fed to animals and directly consumed by people (see Basra poison grain disaster).