Methyl mercury pollution in Minamata Bay and the Agano River in Japan

How it happened
After the second world war Japan was devastated, and during reconstruction there were little or no zoning laws, safety laws were ignored, and pollution laws were few. Everything was geared towards increasing output and trade.
The Chisso Chemical Company in southwestern Kyushu used mercuric sulphide and chloride as catalysts to convert acetylene into acetaldehyde and vinyl chloride, but in addition to this there was a side reaction where mercury was methylated, and highly poisonous methylmercury chloride was discharged with waste water into a drainage channel and then into Minamata Bay.
Minamata Bay is small, the only input from the land into the bay is a small drainage canal. The bay is in the Yatsushiro Sea, which is almost land-locked. For many centuries it has been a good fishing ground and a natural harbour. Historically the population have lived exclusively on fishing as the surrounding land is too steep for agriculture. As recently as 1973 there were still 144 ommercial fishermen in the area (fishing is prohibited only in the bay itself).
In Niigata Prefecture the Showa Electric Company in Kanose had been producing acetaldehyde using a similar method to Chisso since before 1951 and discharging its waste into the Agano River.
Minamata disease
Before the discovery of Minamata disease very few cases of organic mercury poisoning had been documented, and all of these had been caused by direct exposure to the mercury, either in chemical plants or from mercury-treated seeds or timber. There had been no recorded cases of mercury poisoning where the mercury had contaminated the environment and had subsequently passed up the food chain.
The disease manifests itself via a food chain of contaminated marine products. Manifestation requires the following: 1) the presence of mercury compounds in the water. 2) bioconcentration of mercury compounds in fish and shellfish. 3) a continuous daily intake of contaminated fish and/or shellfish in large quantities. The disease first occurred in 1953 in a fishing village on Minamata Bay, although when umbilical cords of the local population were examined they showed that contamination had occurred as far back as 1947(Japanese keep the umbilical cords as they symbolise the link between mother and child). For the first death infantile paralysis was entered as the cause. The main symptoms of the disease are sensory disturbances, ataxia, hearing loss, and constriction of the visual field.
There were also cases where mothers had eaten contaminated fish or shellfish and did not develop symptoms, but the mercury was transferred to the fetus. In such cases the symptoms usually appeared about three months after birth. One girl developed the disease at the age of five and survived unconscious for eighteen years, her older sister and parents were also victims. In one particular village overlooking the bay 15% of a ÿpopulation of 1100 were either killed or permanently paralysed by the disease.
Pathological examination shows damage to the visual areas of the occipital cortex, the cerebellum, and changes in the white matter of the brain. There is no effective treatment for the disease, though mercury eliminating drugs are prescribed.
Identifying the cause
At the time of the first outbreak rumours of mad cats in the areas around the victims' homes began to spread. However since 1950 unusual things had been happening in the bay; dead fish had been found floating on the surface; crows and seagulls were observed falling into the water, not dead but unable to fly; and octopus and cuttlefish were weakened, floated to the surface and were caught by the local children using only their bare hands. As well as cats going mad some pigs and dogs were also reported to be behaving strangely.
It was noticed that the incidence of disease in humans increased in summer and decreased in winter. The number of cases showed a good correlation, with a time lag of two months, with the local fish catch, and the consumption of fish and shellfish was greater in families of victims than in a control group, so ÿfish and shellfish in the bay were suspected.
The mercury compounds were absorbed by marine vegetation and plankton which were eaten by small fish and shellfish, which in turn were eaten by larger fish, man and domestic animals. However studies of fish and shellfish which had accumulated what had been presumed to be lethal doses of methylmercury showed that they had no abnormalities whatsoever. This was one of the major delays in finding the real cause of the disease.
The amounts of mercury in the organs of sufferers varied considerably, and dropped in a short time if they stopped eating contaminated fish, and did not appear to show a correlation with amount of mercury ingested, or the progress of disease. It is now recognised that the best indices of exposure to methylmercury are the levels in the hair, urine and blood. Levels of total mercury in the hair of a person with no known occupational exposure to mercury, and with low consumption of fish is usually below 5 ug g, those with Minamata disease can have 40 - 200 times this amount, and onset of the disease may occur at 10 times the normal level.
In 1965 an outbreak of poisoning similar to that of Minamata was reported in villages from the mouth of the Agano River to about 6 km upstream. In this outbreak there was a clear relationship between the amount of river fish eaten and the mercury content of the hair. Fishing was restricted in the river, and about one year later there were no new cases.
After the outbreak of Minamata disease in Niigata 1965 the government issued a statement saying that there were two possible pollution sources, the mercurial content in agricultural chemicals stored in a pier warehouse destroyed in the 1964 earthquake, and effluent from the Showa Electric Company, but there was insufficient data to ascribe the direct cause of the disease.
Further investigation revealed that at the time of the earthquake there were only 487 tons of agricultural chemicals stored in the warehouse, and the risk of it reaching the Agano river then polluting it was discounted. Moss from the river bottom was analysed and no mercury compounds were found until the mouth of the drain serving the Showa Electric company was reached. When the waste materials were analysed they showed a methylmercury content of 11.8 mg g, the waste was kept in piles at six different locations around the factory. It is now known that while methylmercury content of the river water was 1 ug the content in fish (especially nigoi, a popular local fish) was around 10 ug g, considerable concentration had occurred in the food chain.
The progress of the pollution.
The pollution began before 1953, probably in 1946 when Chisso factory started production, and continued until 1971. By 1959 it was realised that the cause of what would come to be known as Minamata disease was probably an organomercurial compound.
Investigations showed that sediments near the drainage channel serving the Chisso company contained as much as 400ppm mercury, and that concentrations dropped off as distance from the drainage channel increased. Concentrations of mercury in fish and shellfish were also found to decrease further away from the drainage channel.
After 1958 the effluent was dumped at the mouth of the Minamata river (which flows into Yatsushiro Sea), then in 1959 waste water was stored in a pool, and after 1960 was passed through a treatment plant where the pH was adjusted to 10 by adding lime, treated with coagulants then discharged into the original drainage channel. In 1966 there was further modification to the treatment system, and from 1968-1969 waste was stored in the pool again. In 1969 a new plant to remove mercury was installed and the effluent discharged into another pool. In 1971 a new plant opened which did not use mercury as a catalyst.
In 1975 the amount of mercury in sediments in Minamata Bay was estimated to be around 150 tons. The average tidal difference is 2.23 m, the surface water velocity of inflow caused by tidal action is 5 cm s-1, and outflow is 4 cm s-1, this amount has been found to be too low for sediment transport by tidal action. The maximum surface water velocity at the edge of the Yatsushiro Sea and the unpolluted water outside can reach 200 cm s, this is high enough to transport sediment.
In the four ears from 1975 mercury concentrations of bed sediments were sampled at 24 sites in the Yatsushiro Sea, and although the concentrations increased every year, all apart from the two closest to Minamata Bay showed amounts less than 1 ppm. So transport of mercury was occurring slowly, but not by tidal action. Using figures from the monitoring sites it was calculated that in 1975 13.43 tons of mercury existed in the Yatsushiro sea, and in 1978 the amount had increased to 30.26 tons. So the movement of mercury was accelerating.
Unfortunately the study did not measure methylmercury, which is more toxic to man than mercury, but it has been found in other studies in Canada that the proportion of methylmercury usually varies from 0.2% to 12% of the total mercury.
The dispersal of mercury form Minamata Bay to Yatsushiro Sea could not be by tidal action, and in the laboratory, experiments showed that desorption into the water was too slow to account for the measured rate of dispersal from bay to sea. The only other force strong enough is the movement of ships in and out of the bay. The number and size of ships had increased over the years of study, so this might be the cause for the dispersal of the mercury.
From 1980 to 1989 Kumamoto Prefecture tried to dredge up sediment that contained more than 25 ppm mercury. The contamination spread over at least 2110 km2, and the volume of mud involved was 1500km3. The cost of this operation was 48,388,200,000 yen.
The law, recognition and compensation
In 1956 "Minamata Disease" was recognised by doctors. In 1967 a lawsuit was brought against the Showa Electric Company in the Niigata District Court. In 1968 the Ministry of Health and Welfare officially recognised methylmercury poisoning in Minamata and Niigata as diseases caused by environmental pollution and granted compensation to the victims, and provided medical care. In 1968 annual surveys and monitoring was started in the Agano River Basin, and fishing was banned from the lower reaches of the river from 1965 till 1969. In 1969 the Factory Effluent Control Law set limits for methylmercury. In 1971 a judgement was issued ordering Chisso to pay damages to the victims. In 1973 an agreement between Chisso and the victims, or their families, on the amount of compensation was reached, however to receive compensation the patient must be officially recognised as suffering from the disease, recognition is decided by the prefectural governor or mayor. A few years later the government changed the standards by which Minamata disease was recognised and many cases were refused compensation. In 1981 in Kumamoto Prefecture there were 1483 verified cases of Minamata disease, and 439 deaths had occurred, a fatality rate of 29.6%. In 1982 the victims brought a case against the government. In 1986 in Kumamoto Prefecture the number of applications being processed in order to be recognised as a Minamata disease sufferer was 4630, in Kagoshima prefecture it was 738, and in Niigata Prefecture it was 63, applicants were often verified post-mortem. In 1992 the court ruled that the Chisso Chemical Company should pay 4 million yen (about £16,000) to 42 people claiming damages. In 1992 2252 people were recognised as "Minamata disease victims" by the government, of these 1228 had already died. In 1993 some of the victims won a suit at a court in Tokyo. The course of Japanese justice is tortuously slow, expensive and biased against the individual.