Mercury poisoning - Minamata, Japán

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During the 1950's an acetaldehyde plant in Minamata began dumping heavy metals into the local bay, and ended up poisoning the local aquatic wildlife. After a while, poison symptoms began emerging in the local population, many of which lost basic motor controls and began to act very irregularly.

In the late 1950s Minimata Bay became contaminated with Mercury from a nearby factory manufacturing the chemical acetaldehyde. Mercury, used in the manufacturing process, was being discharged into the Bay. Due to mercury's bioaccumulative properties, the fish in the bay were being over exposed to methyl mercury. The fish passed on the Mercury built up in their bodies to the fish-consuming residents nearby. Scientists estimate that the Biomagnification of the Mercury was as great as a millionfold.

Minamata disease - sometimes referred to as Chisso-Minamata disease - is a neurological syndrome caused by severe mercury poisoning. Symptoms include ataxia, numbness in the hands and feet, general muscle weakness, narrowing of the field of vision, and damage to hearing and speech. In extreme cases, insanity, paralysis, coma, and death follow within weeks of the onset of symptoms. A congenital form of the disease can also affect foetuses in the womb.

Symptoms of mercury poisoning:

Initial symptoms included uncoordinated movement and numbness of the lips and extremities, followed by constricted vision. The effect upon the infants was even more severe as many were born with a wide range of disabilities. This was one of the first modern lessons of the dangers of methyl mercury.

The Japanese authorities were hesitant to publicize the issue and just over a year later a similar incident happened at Niigata, Japan where 13 people died and 330 were affected.

Mercury causes the most harmful effects when its vapor is inhaled (#Gilbert, 2004). When elemental mercury vapor enters the body, it is readily absorbed into the bloodstream and easily crosses the blood-brain barrier and the placenta. After entering the brain, mercury is oxidized and will not transfer back across the blood-brain barrier. When continuous exposure occurs, mercury accumulates in the nervous system, leading to potentially debilitating nervous system afflictions. Health effects include tremors, drowsiness, depression, and decreased performance on memory and verbal tests.

Adverse health effects from overexposure to methylmercury are much more common and have been observed through several tragic case studies (highlighted below in the #History of Use section). The first case of widespread methylmercury poisoning was in Minamata, Japan, where an abnormally high number of children experienced symptoms similar to cerebral palsy.

Mercury is a known human developmental toxicant. The U.S. National Research Council states, "60,000 newborns annually may be at risk for adverse neurodevelopmental effects from in utero exposure to methylmercury (MeHg)". Autopsies of the developing brains of those affected in the Minamata, Japan mercury tragedy show widespread damage to all areas of the brain. Tissues from fetuses killed in the Iraq Mercury Poisoning episode showed disrupted cellular patterns and underdeveloped tissues.

Symptoms of exposure arise only after a latency period during which no effects are observed. The length of the latency is indirectly proportional to the level of exposure: the higher the exposure, the less time it takes for the symptoms to be observed.

Source of description

Juliana P. DeCarvalho (2013) Minamata, Japan. Online available from: Accessed 04th August, 2013.

Gilbert, Steven G. A Small Dose of Toxicology. CRC Press, 2004.