Minamata Disease was discovered for
the first time in the world at Minamata City, Kumamoto Prefecture, Japan,
in 1956 (Minamata Disease Research Group;
1968, Harada M; 1995), and for the next
time at Niigata City, Niigata Prefecture, Japan, in 1965 (Tsubaki
T & Irukayama K; 1977). The both cases were attributed to the methyl
mercury that was generated in the process for producing acetaldehyde using
mercury as catalyst. Methyl mercury had accumulated in fishes and shellfishes
and those who ate them had been poisoned with it. These cases of the poisoning
with organic mercury poisoning were the first to take place in the world
through the food chain transfer of its environmental pollution. The cases
of organic mercury poisoning that had been known prior to Minamata Disease
occurred as the result of the direct poisoning of those who were engaged
in organic-mercury handling occupations or those who took it in accidentally
(Hunter D et al; 1940, Lundgren
KD et al; 1949).
The Shiranui Sea that caused the first
Minamata Disease i.e. that in Minamata has an area of 1,200 square kilometers
and once enjoyed abundance of fishes, shellfishes and so forth and then
a population of approximately 200,000 were engaged in fishery and other
relative jobs. The residents living there were accustomed to eat fishes
and shellfishes as main dishes throughout years. Some of them ate 500 grams
of them a day. On the other hand, the residents living along the Agano
River, Niigata, that caused the second Minamata disease also ate the fresh
water fishes caught in great quantities there (Harada
M; 1972, 1994).
According to Prof. Tokuomi, sensory
disturbance and constriction of the visual field were observed as an example
of the typical symptoms of Minamata Disease among 100% of its patients,
coordination disturbance among 93.5%, dysarthria among 88.2%, hearing disturbance
among 85.3% and tremor among 75.8%. Besides, the patients’ serious symptoms
were evidenced by the fact that 82.4% of them showed walking disturbance
(Tokuomi H; 1960). They are typical symptoms
of methyl mercury poisoning but, in fact, there are patients with various
combinations of symptoms and with various degrees of symptoms that range
from mild to serious cases. It can be said that the population of patients
with non-typical symptoms is greater than that with typical symptoms. Particularly,
glove and stocking type and perioral sensory disturbances were characteristically
observed with Minamata Disease (Harada M; 1995).
The Minamata Disease with such unique sensory disturbance alone has however
been found out so far. The pattern of such sensory disturbance is similar
to that of peripheral nervous disturbance. According to the study conducted
lately, there are great possibilities that they may belong to the category
of central nervous disturbance (Ninomiya T et
al; 1995). Some chronic period or mild cases of coordination disturbance
are difficult to identify. If this is the case, electroophthalmography
(EOG) and optokinetic nystagmus pattern (OKP) can conveniently be used
for obtaining referential data (Harada M; 1995).
Particularly, in new-developing case of Minamata Disease, the possibilities
of the occurrence of mild and non-typical symptoms are greater than those
of typical serious symptoms.
Table
1, Figure 1 shows the frequency of
clinical symptoms and the pattern of sensory disturbance of those suspected
of suffering from chronic Minamata Disease (Harada
M; 1995). The hair mercury value of the residents living around the
Shiranui Sea has come down at present as shown in Figure
2 but there still remain various symptoms (Harada
M; 1998).
In 1962, it was found that methyl
mercury causes unborn children’s poisoning via the placenta. It is called
congenital Minamata Disease (Minamata Disease
Research Group; 1968, Harada M; 1986). The
author has identified 64 cases of it so far. All its patients are such
that another member or other members of their family had also suffered
from Minamata Disease and their mothers ate much fishes and shellfishes
during pregnancy. The site and timing (1952-1963) of congenital Minamata
Disease agreed with those of acquired Minamata Disease. The handicapped
accounted for 9.0% of the children newly born in the settlements with the
highest density of the disease. Observed among its initial symptoms were
such ones as mental retardation with 100% of its patients, primitive reflexes
with 100%, coordination disturbance with 100%, dysarthria with 100%, limb
deformation with 100%, growth disorder with 100%, chorea-athetose with
95%, and hypersalivation with 95%. What a mercury value they showed soon
after their birth was not known because the disease was found out five
through eight years later (Harada M; 1986).
In Japan, it is an old custom that the umbilical cords of newly-born children
are preserved by their parents in memory of their birth. Noting it, the
author and others measured their methyl mercury value. As the result, the
high methyl mercury values of 1.0 ppm or so were detected from them (Harada
M; 1995). In addition, it became pathologically and experimentally
clear that it belonged to the category of viviparous methyl mercury poisoning.
The congenital Minamata Disease that occurred via the placenta was the
first that had ever been found out in the world. Besides, all its patients’
symptoms were serious and those with neither mild nor imperfect type symptoms
were not found out among them. The school children living in polluted areas
showed mild diskinesia and intellectual disturbance. The author and others
considered that they had occurred under the influence of methyl mercury.
Lately it has been suggested that an influence may be exerted on unborn
children although the hair mercury value of already-born children is up
to tentative safety criterion 50 ppm (Harada M;1996).
The Minamata Disease patients officially
recognized at Minamata or Niigata amount to a population of 2,200 or 800
respectively. In addition, those who are suspected of suffering from Minamata
Disease (with chronic and mild symptoms) amount to a population of 12,000.
The production of factories’ methyl mercury containing waste water was
discontinued after the processes that produced methyl mercury were disused
in 1968. The mercury discharged into the Minamata Bay still remained there
and, for its removal, reclamation and dredging were carried out so late
as 15 years after its discovery. If the discharge of methyl mercury containing
waste water is discontinued earlier, it was not considered that so many
patients were affected by serious Minamata Disease symptoms (Harada
M; 1994).
In Canada, mercury pollution was also
caused by a caustic soda factory and the methyl mercury produced through
the methylation of the inorganic mercury in the nature contaminated aborigines.
Cat’s Minamata Disease was also found out there (Takeuchi
et al; 1977). The hair mercury value of the residents living there
exceeded 50 ppm and some of them showed as high hair mercury as 100 ppm.
The author and others found out mild neurological symptoms among them (Harada
M et al; 1977). The Canadian Government recognized mercury pollution,
but denied the occurrence of Minamata Disease insisting that no serious
typical cases were found out. On the other hand, the environmental mercury
pollution by caustic soda factories brought on severe criticism not only
in Canada but also in Asia and Middle and South Americas. Japan has already
made switch-over to the caustic soda production processes that require
no mercury to be used. In the meanwhile, some other countries have notyet
accomplished such switch-over.
In Jirin City, China, methyl mercury
flew out of a chemical complex into a river. This pollution was the same
as that by Chisso Corporation, Minamata, in that it was caused by an acetaldehyde
factory. However, it caused the fishes living there to disappear entirely
so the occurrence of Minamata Disease was avoided fortunately. On the other
hand, Jirin and Heilong Provinces announced that some residents showed
hair mercury values more than 50 ppm and some of those living in the downstream
of the river showed the symptoms peculiar to Minamata Disease though being
mild. On the other hand, delayed Minamata Disease was observed there. Its
symptoms advance even after mercury intake is discontinued (Pan
Yun Zhon et al; 1988). According to Haerbin University’s investigation,
fishermen showed mean and maximum hair mercury values of 20 and 71.2 ppm
respectively and those with the hair mercury values more than 20 ppm showed
sensory disturbance with 44% and visual field constriction with 17% (Song
Zeng Ren et al; 1993).
The author and others started the
analysis of residents’ hair mercury values along the Amazon River, Brazil
in 1988, and in 1992 carried out joint research with Tokyo University,
Yokohama National University, and Para State University. Its results are
shown in Table 2. At Garimpo,
garimpeiros were confirmed to have caused inorganic mercury poisoning.
However, the fishermen living on the downstream side of Garimpo showed
high hair mercury values in 1994, those of some of them being confirmed
to exceed 100 ppm in 1994, and more than 90% of detected mercury was methylated
(Akagi H et al; 1995,
Harada
M; 1996, 1997, 1998). The maximum mercury value of 3.17 ppm was detected
form the fishes caught there so hair mercury contamination was considered
as attributable to fish eating (Akagi H et al; 1995).
It exceeded the tentative safety criterion of mercury value so it is feared
that fishermen’s health may be affected by it. Nevertheless, Minamata
Disease was not found out in the author and others’ clinical examination
carried out until 1994. The occurrence of Minamata Disease takes five steps
until becoming apparent (Table 3,
Fig. 3). It can be said that the Amazon
River has already come to the fourth step and it is feared that unborn
children may be affected because they are more sensitive than already-born
children and adults. The clinical epidemiological investigation carried
out in Canada, Iraq, New Zealand and Faeroes Islands revealed that even
mothers’ hair mercury values less than 50 ppm may affect their unborn
children (WHO; 1990, Grandjean
P et al; 1997). In the author and others’ examination of the conserved
umbilical cords of children, the mothers of congenital Minamata Disease
patients showed the minimum hair mercury value of 21.5 ppm (Harada
M; 1997).
Mercury is used for gold mining in
East Africa and the Philippines also (Ikingura
JR et al; 1996, Harada M et al; 1998).
In Tanzania and Kenya, there was a great concern that the Victoria Lake
may be contaminated with it. Nevertheless, garimpeiros and fishermen showed
low hair mercury values (Table 4)
because mercury is used at a lower rate there than in the Amazon River.
The fishes caught in the lake also showed the low mercury values of 0.0089
through 0.063 ppm. Nevertheless, some women showed extraordinarily high
mercury values up to 470 ppm. These cases of hair mercury did not considered
as attributable to their contamination through the food chain transfer
of mercury because it was confirmed to be almost inorganic mercury. Investigation
also revealed that women were using the cosmetic soaps with a mercury content
of 2% to whiten their skin and that their health was affected by them.
The Government had already prohibited their use but there is a possibility
that they may become a new source of mercury contamination.
Minamata Disease was discovered with
many cases of typical symptoms coming up in Minamata. At present, the mercury-polluted
areas of the world are in need of the data of its minimum requirements
and its influence on unborn children.