Toxicity by Methyl-Mercury on Human Fitness

It is a bio accumulative environmental toxicant. Methyl-mercury is formed from inorganic mercury by the act of anaerobic organisms that live in aquatic systems comprising of lakes, rivers, wetlands, sediments, soils and the open ocean. This methylation procedure transforms inorganic mercury to methyl-mercury in the natural environment. Methyl-mercury is formed in aquatic systems and because it is not voluntarily eliminated from organisms it is bio-magnified in aquatic food chains from bacteria, to plankton, through macro invertebrates, to herbivorous fish and to piscivorous fish. At apiece step in the food chain, the concentration of methyl-mercury in the organism upturns. 

The concentration of methyl-mercury in the topmost level aquatic predators can touch a level a million times developed than the level in the water. This is because methyl-mercury has a half-life of about 72 days in aquatic organisms’ follow-on in its bio-accumulation within these food chains. Organisms, including humans, fish-eating birds, and fish-eating mammals such as otters and whales that consume fish from the top of the aquatic food chain receive the methyl-mercury that has accumulated through this procedure. Fish and other aquatic species are the only significant source of human methyl-mercury exposure. Ingested methyl-mercury is enthusiastically and entirely absorbed by the gastrointestinal tract. 

Several studies indicate that methyl-mercury is related to subtle developmental deficits in children exposed in-utero such as loss of intelligence quotient points, and declined performance in tests of language skills, memory function and attention deficits. Methyl-mercury exposure in adults has also been related to increased risk of cardiovascular disease including heart attack. Some evidence also suggests that methyl-mercury can cause autoimmune effects in sensitive individuals. Recent evidence suggests that the developmental and cardiovascular toxicity of methyl-mercury may be mediated 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 sternly poisoned by food contaminated with high levels of methyl-mercury, conspicuously the dumping of industrial waste that resulted in the pollution in the 1960s and 1970s in which wheat treated with methyl-mercury as a preservative and intended as seed grain was fed to animals and directly consumed by people. These resulted in neurological symptoms including loss of physical coordination, and difficulty in speech, narrowing of the visual field, hearing impairment, blindness, and death. 

At present, exposures of this scale are rarely seen and are confined to isolated incidents. Accordingly, concern over methyl-mercury pollution is currently focused on more subtle effects that may be related to levels of exposure presently seen in populations with high to moderate levels of dietary fish consumption. These effects are not necessarily identifiable on an individual level or may not be uniquely recognizable as due to methyl-mercury. However, such effects may be detected by comparing populations with different levels of exposure. There are isolated reports of various clinical health effects in individuals who consume large amounts of fish; however, the specific health effects and exposure patterns have not been verified with larger, controlled studies.