Mercury is a very dangerous poison. One of the cobalamin compounds is methyl-cobalamin, and unfortunately this can react with less poisonous Hg(II) to generate [CH₃Hg]⁺ an even more poisonous ion.

Whilst man can exacerbate the problem greatly by releasing mercury and organomercurials into the environment, there is a natural level due to conversion of Hg(II) into [CH₃Hg]⁺ in sediments. (See Harrison) Unfortunately anyone eating fish is likely to have an increased level of methylmercurials in their body. The formation of methymercuriials from methylcobablamin was proposed by Wood in 1968 as a direct consequence of some model reactions with the [MeCo(CN)₅]³⁺ and Hg(II) by Halpern and Maher. The cyanocobaltates were one of the first cobalamin models, being discovered slightly before the discovery of the cobaloximes by Schrauzer.

The worst episode of methylmercury poisoning occured in Minamata Bay in Japan, with a devastating effect upon the local fishermen and their families.

From the 1930's to the 1960's, a chemical company dumped tons of mercury into Minamata Bay in Japan. Thousands of people living around the bay developed methylmercury poisoning through the consumption of contaminated fish. The victims suffered from severe neurological damage, which later became known as Minamata Disease. Symptoms of this disorder may include tingling sensations, muscle weakness, unsteady gait, tunnel vision, slurred speech, hearing loss, and abnormal behaviour, such as sudden fits of laughter. Jennifer Pepall