Methyl mercury Minamata

Another major incident concerning methyl mercury was the severe pollution of Minamata bay in Japan (see Box 8.1). Here fish, fish-eating and scavenging birds, and humans feeding upon fish all died from organomercury poisoning. There may have been localized declines of marine species in this area due to methyl mercury, but there is no clear evidence of this. 

Methylmercury in the marine environment may originate from industrial discharges or be synthesised by natural methylation processes. Fish do not themselves methylate inorganic mercury [62,64], but can accumulate methyl mercury from sea water [63]. Methylmercury has been detected in sea water only from Minamata Bay, Japan, an area with a history of gross mercury pollution from industrial discharge. It has been found in some sediments but at very low concentrations, mainly from areas of known mercury pollution. It represents usually less than 1% of the total mercury in the sediment, and frequently less than 0.1% [65-67]. Microorganisms within the sediments are considered to be responsible for the methylation [65,68], and it has been suggested that methylmercury may be released by the sediments to the sea water, either in... 

Tokuyama Bay, Japan, received 6.6 metric tons of mercury wastes between 1952 and 1975 in wastewater from two chloralkali plants, although sediment analysis suggests that as much as 380 tons of mercury were released (Nakanishi et al. 1989). Unlike Minamata Bay, however, there were no human sicknesses reported, and the hair of residents contained 0 to 5 mg Hg/kg FW vs. 15 to 100 mg Hg/kg FW in Minamata residents. In 1970, a maximum concentration of 3.3 mg total Hg/kg FW was reported in tissues of Squilla, a crustacean. In 1973, a health safety limit was set of 0.4 mg total Hg/kg FW in edible fish and shellfish tissues with a maximum of 0.3 mg methyl-mercury/kg FW permitted at least five species of fish had more than 0.4 mg total Hg/kg FW, and fishing was prohibited. Contaminated sediments (>15 mg total Hg/kg) were removed by dredging and reclamation between 1974 and 1977. By 1979, the mercury content of all fish, except one species, was less than 0.4 mg total Hg/kg FW fishing was prohibited. By 1983, all fish and shellfish contained less than 0.4 mg Hg/kg FW and fishing was allowed (Nakanishi et al. 1989). 

An epidemic of intoxication from ingestion of fish contaminated with methyl mercury occurred in the Minamata district in Japan, and, as a result, methyl mercury intoxication is often referred to as Minamata disease." Infants born to mothers with exposure to large amounts of methyl mercury had microen-cephaly, mental retardation, and cerebral palsy with convulsions. In an incidence in Iraq, ingestion of wheat products contaminated with methyl mercury fungicide by pregnant women caused similar symptoms of neurological damage and mental retardation. The fetus is... 

In the late 1950s the subtle and serious consequences of methyl mercury exposure became evident in Minamata, Japan. Initially, early signs of uncoordinated movement and numbness around the lips and extremities, followed by constriction in visual fields in fishermen and their families, baffled health experts. Developmental effects were clearly evident in infants who exhibited subtle to severe disabilities. This spectrum of adverse effects was finally related to methyl mercury exposure from consumption of contaminated fish. Minamata Bay was contaminated with mercury and methyl mercury from a factory manufacturing the chemical acetaldehyde. Mercury was used in the manufacturing process, which also resulted in both mercury and methyl mercury being discharged into Minamata Bay. The fish in the bay accu-... 

A case of Minamata disease caused by the methyl mercury discharged by a chemical factory in Japan provides us with bitter lessons. Inappropriate treatments of toxic chemical substances for the duration of 1932 to 1968 resulted in creating and torturing more than 14,000 victims with a neurological syndrome by severe mercury poisoning. It has been fifty years since the disease was official discovered in 1956. The case is not yet fully solved and lawsuits and claims for compensations continue even to this day. 

Minamata is an industrial city on the Yatsushiro coast of Japan on the southernmost island (K5rushu). In the city there was a factory that manufactured the chemicals vinyl chloride (used to make the plastic PVC see pp. 168-71) and acetaldehyde for many years. The processes used inorganic mercury (mercuric oxide) as a catalyst. The effluent from the factory contained inorganic mercury and perhaps also some organic mercury (methyl mercury), produced as a by-product in the chemical reaction in the plant. This effluent was discharged into the waters of Minamata Bay. 

How mercury from a Japanese factory contaminated fish in Minamata Bay. The effluent, containing inorganic mercury and discharged into the bay from the factory, was not dispersed in the water, but formed sediment at the bottom where micro-organisms converted the mercury into the more toxic methyl-mercury. The methylmercury accumulated in fish and was consumed by people eating the fish. 

The Japanese diet contains a lot of fish, and the local fishermen and their families would eat more fish than most. The fishermen were catching fish and seafood in the waters of Minamata Bay, waters which proved to be heavily contaminated with methyl mercury. In 1956 the first case of what became known as Minamata disease was reported and then other people started to present themselves to doctors and at hospitals with various symptoms such as muscular incoordination and difficulties in speech. Their pet cats, which were also eating the fish, suffered similar symptoms. 

Dr Hosokawa, director of the Minamata City hospital was conducting his own experiments based on the theory from the university He fed cats waste effluent from the factory that was producing acetaldehyde and was able to produce similar symptoms in them, and he detected other changes by pathological examination at autopsy The company that owned the factory, the Chisso Minamata Chemical Company, was aware of his work and by 1959 knew that it was likely that Minamata disease was caused by the effluent from their factory In i960 methyl mercury was detected in seafood and in 1961 it was detected in sediments derived from the factory. In 1966 the factory installed a water circulation system which removed the mercury pollution. The factory eventually stopped the process in 1968 and in the same year the Japanese government announced its opinion that the disease was due to consumption of methyl mercury in contaminated fish and seafood. 

One of the particularly tragic aspects of the Minamata disaster was the effect methyl mercury exposure had on unborn children. Some of the mothers exposed to methyl mercury from the fish and seafood gave birth to babies who were severely affected with a disorder similar to infantile paralysis, suffering cerebral palsy and mental retardation. This occurred even in mothers who showed no symptoms themselves, a classic characteristic of a teratogen. Some babies were born completely paralysed. 

Organic forms of mercury, such as methyl mercury, which caused the Minamata disease, are different from the other two forms in that they are very soluble in fat and therefore readily able to enter the brain and nervous system (see p. i8). Again the interaction with natural sulphur-containing substances in the body is important. A product of this interaction mimics an amino acid for which a specific system of transport into the brain exists. So, rather like the Spartans in the Trojan horse, mercury enters the brain, and once there it can disrupt essential processes. 

Methyl mercury is toxic to humans causing CNS and peripheral nervous system injuries. 13 Those exposed suffer a degeneration of their nervous systems. Symptoms include numbness in lips and limbs, involuntary movement, constricted vision, slurred speech, and hallucinations. The most famous historic example of MeHg poisoning is the Minamata disease outbreak in Japan. 14 ... 

Matsumoto, H., G. Koya, and T. Takeuchi. 1965. Fet Minamata disease. A neiux)pathological study of two cases of inlrauterine intoxication by a methyl mercury compoimd. J. 

Minamata disease was first discovered in 1956 around Minamata Bay, Japan. A similar epidemic occurred in 1965 along the Agano river, Japan. Minamata disease is methyl mercury poisoning that occurred in humans who ingested fish contaminated with methylmercury discharged in waste water from a chemical plant. Methylmercury is also teratogenic (Ui 1992, Harada 1995, Eto 1997, Schardein 2000 see also Part III, Chapter 17). 

Akagi H, Grandjean P, Takizawa Y and Weihe P (1998) Methyl mercury dose estimation from umbilical cord concentrations in patients with Minamata disease. Environ Res 77 98—103. Akagi H, Malm O, Branghes FJP, Kinjo Y, Kashima Y, Guimaraes JRD, Oliveira RB, Haragughi K, Pfeiffer WC, Takizawa Y and Kato H (1995) Human exposure to mercury due to goldmining in the Tapajos River basin, Amazon, Brazil Speciation of mercury in human hair, blood and urine. Water Air Soil Pollut 80 85-94. 

Haeada M (1978) Congenital Minamata disease intrauterine methyl mercury poisoning. Teratology 18 285-288. 

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