Methylmercury 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.

Angiosperm diversity

Angiosperms appeared in the fossil record around 120MYA, now they occupy every freshwater and terrestrial habitat in the world, except the arctic tundra and coniferous forests. Some have even returned to the marine habitat that plants originated from, to compete with their distant ancestors the green algae. Angiosperms have great diversity and are still rapidly diversifying and expanding their range.
Origins.
There are a few theories, some say they originated from the Gnetales, some say from the Benettitales, others say they may have a polyphyletic origin. A polyphyletic origin seems unlikely as this would mean that their unique features, double fertilization etc. would have arisen independently more than once. So their origin is still unknown and still remains the "abominable mystery" that perplexed Darwin.
Early angiosperms were simple shrubby flowers, rather like magnolias, and were pollinated by the beetles and flies that already existed and lived off the gymnosperms. Spread and diversification was aided, perhaps triggered, by the break up of Pangea and the climatic changes which followed. Angiosperms germinate quicker than gymnosperms and with insect pollination were genetically diverse - great advantages in time of change. Fossilised remains of the early magnolia type flowers are to be found from one end of Laurasia to the other.
After the Cretaceous extinctions, around 60MYA, there was an explosion of new species, as there usually is after massive extinctions. Angiosperms diversified rapidly along with new forms of insects, bees, moths and butterflies. These insects had special mouthparts, pollen cages etc. that were suited to their particular type of flower. And the flowers became more specialised in shape so that they could only be pollinated by specific insects, they also had UV patterns, landing platforms, special odours, and long tubular corollas etc. This mutualism triggered an escalating process of specialization which culminates in one species of flower becoming totally dependant on one species of insect, and vice versa, as is the case with the yucca and yucca moth.
On the arid plains of America and Asia grasses evolved. One species would predominate over miles and miles of flat ground. They did not need insects to pollinate them, the wind did it, and their flowers became reduced and dull coloured, but pollen production increased.
The most recent trend in diversification is seen in the Compositae, the largest, and perhaps most widespread family. The flowers are gathered together, sometimes in groups of 100's or more, the nectar is relatively easy to get at, so they are pollinated by quite a wide range of insects.
Man has had a hand in diversification too. Ever since he stopped being a hunter/gatherer and started farming he has bred plants to try to enhance the qualities he desired, and to minimize what he did not want. Until recently his efforts were rather simple, and were confined to compatible crosses, but with the advent of genetic engineering he can change things at the gene level, producing hybrids that would never have occurred naturally. As farming has become an international business, the diversity of cereals etc. has actually lessened, and many countries now have seed banks, in an effort to preserve the varieties that have lower yields, but may be of use in the future. In the wild too diversity may be decreasing because so much land is being used for human needs, and less is left wild each year.

Symbiosis in plants

The past.
It is believed that symbiosis first occurred 1900-1200 MYA when an anaerobic heterotroph injested , but did not digest an aerobic heterotroph. The early atmosphere of the earth had litle or no oxygen, but gradually the oxygen content increased. As this happened the anaerobic organisms would find conditions increasingly toxic, ingesting an aeriobic oganism would enable them to survive. It is believed that this ingested orgnism was like a mitochondrion.
Symbiosis is the organisation of two or more organisms for the mutual benefit - though the only benefit the mitichondrion-like organism got was a controlled environment inside its host. This is believed to be the way eukaryotes evolved.
The next evolutionary step is believed to have been the aquisition of mobility. This could have happened when an amoeboflagellate ancestor joined the anaerobic/aerobic organism. Similar organisms exist today e.g. slime moulds and fungi. When an autotrophic organism joins the above symbiotic trio you have the origin of green plants. This is known as the Serial Endosymbiotic Theory, and accounts for the origin of animals too. Today mitochondrion still have their own DNA, and divide by binary fission, though they depend on the nucleus for instructions and cannot exist on their own.
Symbiotic relationships today.
Anabena and Nostoc (blue green algae) have the ability to fix nitrogen, and are often found living symbiotically; Anabena in the chambers of the fronds of Azolla (an aquatic, floating fern); and Nostoc in hornworts and liverworts.
Perhaps the best known symbiotic relationship is that between some algae and fungi that grow to form a plant body of consistently recognizable structure and apperance - lichen. They can inhabit extreme environments e.g. some grow inside sandstone formations in Antartica, others can actively photosynthesize at -18.5oC. Some say that the relationship is parasitic with the fungus as the parasite, but the fungus surrounds the alga, protecting it, the hyphae absorb and adsorb water and minerals from the substrate enabling the alga to extend its habitat range.
Legumes have a symbiotic relationship with nitrogen fixing bacteria that live in their roots. Mycorrhizal associations with the roots of vascular plants are widespread, the fungi play a vital role in phosphorus absorption. Some of these relationships are highly specific with only one spaecies of fungus associating with one plant species, e.g. the larch and Boletus elegens. There are also symbiotic relationships between plant and insect. Ants inhabit the thorns of Acacia trees, the ants gain food from the Beltian bodies (small nutritive organs located at the tip of each leaflet) and in return protect the Acacia from herbivores by killing or biting them, and keep other plants at bay by attacking them if they get too close.