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
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.
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).
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.
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
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.
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.
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
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
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
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.
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.
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.
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.
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
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
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.