The Tragedy of Minimata

Written by:  Dr Mike C • Edited by: Diana Cooper
Updated Apr 1, 2011
• Related Guides: Mercury | Symptoms

Ignorance kills, but not always quickly or in an obvious manner. Find out why discharges from chemical plants in the 1950s to rivers and the ocean led to frank mercury poisoning, birth defects and a range of neurological and physiological symptoms.

Today, in the developed world, waste discharges are subject to proper treatment and monitoring to ensure that they remain within tolerated concentrations such that the environment and the biosphere are properly protected. But this wasn't always so. There is a saying that out of sight is out of mind. This was the philosophy of the chemical industry in the past where toxic waste streams were concerned. By-products were conveniently dumped into river systems or directly to the sea with little or no processing. Two reasons governed this: ignorance and economics. The consequences can be tragic, as illustrated in the discharges of mercury compounds to Minimata Bay in Japan starting in the 1950s.

Mercury chloride is used as a catalyst (a substance that speeds up a reaction, but is left unchanged by it) in the manufacture of acetaldehyde. Acetaldehyde is a feedstock for other chemicals and finds use as a synthetic flavoring substance, food preservative and fragrances ingredient, amongst other things. Some of the catalyst was lost to the environment through waste streams. It has been known since antiquity that mercury is a neurotoxin — mercury vapor was used to steam the brims of hats in the millinery trade. After prolonged exposure, milliners often started to show neurological symptoms, hence the origin of the expression "as mad as a hatter." Ultimately, as with any heavy metal, chronic exposure can prove fatal.

In Minamata Bay, the mercury released into the marine environment became concentrated (bioaccumulated) within the food web. It was taken up by phytoplankton and in turn, the phytoplankton were consumed by zooplankton, in their turn they were eaten by small fish which were consumed by larger fish. In the end, the fish (and their mercury burden) were consumed by the top predator — humans. The first cases of people stricken with an unknown illness came to light in 1956. The patients were suffering from a range of symptoms including, severe convulsions, sensory disturbance in the hands and feet, impairment of vision and hearing, muscular weakness, periods of loss of consciousness, crazed behavior followed by coma and, ultimately death in 17 cases.

It took quite some time for it to be accepted that the causative agent was mercury; it was too politically and economically embarrassing. The severity of the poisoning was worse than one would have predicted from environmental measurements. This was due to the effects of bioaccumulation and that the form of mercury involved (methylmercury chloride) was able to cross the blood brain barrier more easily than the element itself. Tragically, methylmercury can also accumulate in the placenta and there have been children born with deformities and disabilities as a consequence of ingestion of the compound in utero. Officially, nearly 3000 victims were recognized as suffering from Minamata disease.

The Minamata Bay tragedy was one of the events that spawned a greater understanding of the role of chemical form in toxicity and the birth of a new discipline: trace metal speciation. Trace metal speciation seeks to determine the balance between various chemical forms of an element in a given sample, since it is these forms that dictate the nutritive, toxicolological or residence time behavior within a compartment of the biosphere.

Sources of further information

This article was drawn from lecture material that I have presented to students around the world. Should you wish to have further information on this topic, I'd recommend that you look at the following websites:

National Minamata Institute:

History and remediation efforts:

Medical symptoms:

Image bank:

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