chapter 2 - literature review
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CHAPTER 2
LITERATURE REVIEW
2.1 Origin of Minamata Disease
Minamata disease, which is a typical example of the pollution related to health
damage in Japan, was first discovered in 1956, around Minamata Bay in Kumamoto
Prefecture, Japan. Since the discovery of the disease, investigation of the cause has been
made and finally in 1968, the government announced its opinion that Minamata disease
was caused by the consumption of fish and shellfish contaminated by methylmercury
compound discharged from a chemical plant.
It is known that Minamata disease is a disorder of the central nervous system and
shows various signs and symptoms including sensory disturbance in the distal portions of
four extremities, ataxia and concentric contraction of the visual field. At the end of March
2001, 2,955 Minamata disease patients have been certified, of which 2,265 patients have
been located on Yatsushiro Sea coast. Due to the clinical and protective measures taken
after the discovery of the disease, Minamata disease no longer seems to occur in Japan
(Minister of Environment Japan, 2001).
According to Yasuko Tanaka, Minamata disease started when the village cats
turned into demons. One year, they were sleepy pets and next, they were hyperactive
monsters which screeching, scratching and jumping around as if possessed. That was
when she drew the connection between Japan's worst case of industrial pollution in
nearby Minamata and the splitting headaches, tunnel vision and shaking hands that she
and several other villagers had been suffering (Watts, 2001).
2.2 Chronology of Minamata Disease
The first case identified to be Minamata disease was on 1956. The chronology of
the Minamata disease before and after the first outbreak was summarized in the Table
2.1, 2.2, 2.3 and 2.4.
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Table 2.1 Chronology of Minamata Disease from 1950s (as cited in Yorifuji et al., 2013).
Year Events
1953 The local cats which ate great quantities of fish from the Minamata bay were seen
behave strangely and went mad before they died (Harada, 2004).
1954 A few patients with neurological symptoms of unknown origin were detected.
(Nishigaki and Harada, 1975).
1956 First official notification of strange disease to the Minamata Public Health Centre
(Harada, 1995) and Minamata Strange Disease Countermeasures Committee was
formed (Harada, 2004).
1957 The local government of Kumamoto Prefecture considered applying the Food
Sanitation Act (Kumamoto Prefecture, 1996). However, Ministry of Health and
Welfare of Japan (MHWJ) decided that it is impossible to apply Food Sanitation Act
and ignored the applications (MHWJ, 1996).
1958 - Chisso factory changed the drainage route from Minamata bay to Minamata River
(Miyazawa, 1996).
- A neurologist from United Kingdom examined Minamata disease patients and
listed methylmercury as one of the metals which could induce Minamata disease.
However, the neurologist has been prevented from presenting his findings to the
Japanese Society of Neurology (Hunter et al., 1940).
1959 - Chisso Hospital director Hajime Hosokawa fed factory effluent to cats and induced
the symptoms of Minamata disease but this was suppressed (Harada, 2004).
- Minamata Food Poisoning Committee concluded that the etiological agent was
mercury. However, the committee has been suppressed as it was not 'scientifically'
proven (Kumamoto University, 1996).
1960 The investigation by Kumamoto Prefecture Institute for Health Research indicated that
the contamination had spread throughout the entire Shiranui Sea (Harada, 1995).
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Table 2.2 Chronology of Minamata Disease from 1960s (as cited in Yorifuji et al., 2013).
Year Events
1962 - A professor at Kumamoto University School of Medicine had succeeded in
extracting methylmercury chloride from the sludge of the acetaldehyde production
process in the factory (Irukayama et al., 1962). However, the finding was disclosed.
- An unusual occurrence of cerebral palsy infants was officially recognized as
congenital Minamata Disease.
1965 Methylmercury food poisoning occurred in Niigata, causing 'Niigata Minamata
disease'. The factory responsible which Showa Denko operated in the same way as
Chisso factory (Saito, 2009)
1967 A legal case relating to Niigata Minamata disease went on trial in 1967 (MHWJ, 1996).
1968 - On May, Chisso ended the manufacture of acetaldehyde which was responsible for
Minamata disease (Arima, 1979).
- On September, the government of Japan agreed that there was causal relationship
between waste water from Chisso and Showa Denko with Minamata disease
(MHWJ, 1996).
Table 2.3 Chronology of Minamata Disease from 1960s (as cited in Yorifuji et al., 2013).
Yea
r
Events
1972 Two Minamata disease patients were brought to the first global environmental conference,
United Nations Conference on the Human Environment which held in Stockholm
(Harada, 2004).
1977 A new and more rigid set of government accreditation criteria for Minamata disease
required a combination of neurological signs (Yorifuji et al., 2013).
1978 Kumamoto local government issues debt to help Chisso pay compensation (Ministry of
Environment, 2011).
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Table 2.4 Chronology of Minamata Disease from 2000s (as cited in Yorifuji et al., 2013).
Yea
r
Event
2004 The Japanese Supreme Court confirmed the liability of the national and Kumamoto
Prefecture governments for damage caused by methylmercury poisoning in the Minamata
area (McCurry, 2006)
2009 United Nations Environment Programme (UNEP) initiates a global mercury phase-out and
works to develop a global legally binding instrument on mercury which plan for signature
in Japan in 2013 (UNEP, 2010).
2013 In October, a new international convention named Minamata Convention to control
mercury emissions was opened for signing in Japan (National Institute for Minamata
Disease). The private law suits still continue until now (Yorifuji et al., 2013).
2.3 Symptoms
Minamata disease is neurological syndrome caused by severe mercury poisoning
and caused by the daily consumption of large quantities of fish and shellfish that were
heavily contaminated with the toxic chemical generated in chemical factories and then
discharged into the sea. Symptoms include ataxia, numbness in the hands and feet,
general muscle weakness, narrowing of the field of vision and damage to hearing and
speech. In extreme cases, insanity, paralysis, command death follow within weeks of the
onset of symptoms. A congenital form of the disease can also affect fetuses (Hachiya,
2006).
The symptoms of Minamata disease also include sensory disorders in the distal
portion of the four extremities which are loss of sensation in the hands and feet, ataxia
which is difficulty coordinating movement of hands and feet, concentric constriction of
the visual field which narrowing of the field of vision, hearing impairment,
disequilibrium which is impairment of faculties for maintaining balance, speech
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impediments where speech becomes slurred and unclear, tremors such trembling of the
hands and feet, and disorder of the ocular movement where eye movement becomes
erratic (Minamata Disease Municipal Museum, 2007).
In very severe cases, victims fall into a state of madness, lose consciousness, and
may even die. In relatively mild cases, the condition is barely distinguishable from other
ailments such as headache, chronic fatigue, and a generalized inability to distinguish taste
and smell. Most patients exhibit a full set of severe symptoms which, in 16 cases, the
patient died within 3 months of the onset of symptoms, and in 1965 the mortality rate was
44.3%. Since then a large number of incomplete or mild cases, displaying an incomplete
set of symptoms, have also been identified (MDMM, 2007).
Symptoms of spasms, blurred vision and hearing loss were first recognized in the
50s when the ailment was called "itaitabyo" (ouch ouch disease), but it was not until 1968
that the government blamed the nearby Chisso chemical corporation for pumping
mercury waste into the bay. More than 900 victims died in agony. Many babies in the
area were born with knarled limbs. Thousands of victims were ostracized, first out of a
mistaken fear that the disease might be contagious, and later, because their legal suits
drew unwanted attention to the invisible pollution in this picturesque region (Watts,
2001).
In August 1956, the Minamata Disease Research Group of the Kumamoto
University Medical School was formed to investigate the cause of the outbreaks. The
group was made the analysis report which described on Table 2.5, Table 2.6 and Table
2.7. The Table 2.5 shows the analysis of clinical symptoms in 34 cases of acute and sub-
acute Minamata disease. This analysis was showed that the symptoms gradually
increased and finally caused general paralysis, deformity, difficulty in swallowing,
convulsions and even death. Among the first 52 patients discovered, 21 died within one
year of the onset of the disease. Among them, 16 died within three month and 4 died
within six month.
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Next, the Table 2.6 shows the analysis of the comparison of clinical symptoms
and signs in congenital Minamata disease, exogenous idiocy and inflantile cerebral palsy.
It was found that in instances of exogenous idiocy caused by other factors, cerebellar
symptom and strabismus were rarely observed but pathological reflex was remarkable.
The other analysis described in Table 2.7 was show the frequency of symptoms in
congenital Minamata disease cases which the results showed three cases out of 29 have
died, 25 of the 29 cases were examined (Harada & Smith, 1975).
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Table 2.5 Clinical Symptoms in 34 Cases of Acute and Sub-Acute Minamata Disease
(Harada & Smith, 1975)
Symptoms Percentage (%)
Disturbance of sensation
Supertical
Deep
100
100
Constriction of the visual field 100
Dysarthia 88.2
Disturbances of coordination
Adiadochokinesis
Finger to finger and finger to nose
(dysmetria)
Ataxic gait
93.5
80.6
82.4
Romberg’s sign 42.9
Impairment of hearing 85.3
Tremor 75.8
Tendon reflex
Exaggerated
Weak
38.2
8.8
Pathological reflexes 11.8
Salivation 23.5
Mental disturbances 70.6
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Table 2.6 Comparison of Clinical Symptoms and Signs in Congenital Minamata Disease,
Exogenous Idiocy and Infantile Cerebral Palsy (Harada & Smith, 1975).
Symptom and Sign No. of Cases Congenital
Minamata
Disease
(%)
Exogenous
idiocy
(%)
Infantile
Cerebral
Palsy
(%)
Intelligence disturbance 17 100 100 25
Primitive reflex 17 100 61 31
Cerebellar abnormalities 17 100 33 18
Extraphyramidal
abnormalities such as chorea,
athetosis
16 94 72 100
Hypersalivation 16 94 32 68
Parnxysmal disorders 14 82 66 0
Strabismus 13 76 11 37
Pyramidal abnormalities
(spastic paralysis)
12 71 100 43
Asymmetry of symptoms and
signs
0 0 72 18
Causative factor present 0 0 50 62
Causative factors in the cases of exogenous idiocy and inflantile cerebral palsy:
Abnormal pregnancy, fever, and trauma.
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Table 2.7 Frequency of Symptoms in Congenital Minamata Disease Cases (Harada &
Smith, 1975).
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Symptom and Sign Number of Cases
Intelligence disturbance 25
Dysarthia 24
Extraphyramidal hyperkinesia and hypokinesia 23
Cerebellar symptom 19
Deformation of limbs 21
Primitive reflex 18
Strabismus 18
Hypersalivation 18
Parnxysmal disorder 9
Pathological reflex 12
Inhibited body growth 17
Note: 3 cases out of 29 have died, 25 of the 29 cases were examined
Figure 2.1 Crippled hand (Smith, 1971).
Figure 2.2 Inability to move (Smith, 1971)
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2.4 Chisso Factory
On 1908, the Nihon Carbide factory was merged with Sogi Electric to form Nihon
Chisso Hiryo Kabushiki Gaisha (Japan Nitrogenous Fertilizers). The firm initially used
carbide to produce ammonia for fertilizers. However, the factory had purchased a
German patent for producing ammonia without carbide in 1921; it began using carbide
and acetylene, which derived from carbide to manufacture a wider range of organic
synthetic compounds such as acetaldehyde.
On 1932, the factory began producing the acetaldehyde from acetylene gas which
used mercury as a catalyst. The process was developed by Hikoshichi Hashimoto, who
later became factory manager and served as Minamata's mayor. On 1951, the factory had
changed the oxidizer of acetaldehyde production from manganese to iron (Miyazawa,
1996) to increase production of acetaldehyde. The changes are considered to have
increased methylmercury waste from the factory (Miyazawa, 1996).
On 1952, the factory succeeded in producing octanol from acetaldehyde
(Miyazawa, 1996). Japan had previously relied on imports of octanol, an important
ingredient in plastics. As a result, the factory increased production of acetaldehyde and
methylmercury waste from the factory also increased. As the most advanced chemical
company during those decades, the Chisso factory clearly had an important economic
role where the Minamata city had grew with the factory. In May 1968, Chisso ended the
manufacture of acetaldehyde which was responsible for Minamata disease (Arima, 1979).
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Figure 2.3 Chemical waste discharge from Chisso factory (Smith, 1971)
2.5 Minamata Disease in Other Countries
2.5.1 Niigata Minamata Disease
On 31 May 1965, staffs of the University of Niigata reported to the Health
Department of the Niigata Prefectural Government that patients suspected to be
organomercury poisoning appeared in Niigata. In June 1965, the Niigata Prefectural
Government established the Research Headquarters for Mercury Poisoning in Niigata
Prefecture to address the situation (MEJ, 2011).
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2.5.1.1 Origin
There were factories and agricultural chemical plants on the basin of the Agano
River, where mercury is used. The epidemiological group of the Special Research Team
confirmed that the waste water from these plants did not flow into the Agano River, and
excluded them from the subjects as causative plants. As a result, only the Kanose plant of
Showa Denko remained to be the causative factory (MEJ, 2011).
The source of generation of the substance was believed came from to Kanose
plant of Showa Denko because total mercury of high concentrations was detected from
the mud collected in the vicinity of the outfall and the huge heaps of coal sludge in the
plant. The plant was located on the upper Agano River (MEJ, 2011).
2.5.1.2 Source of Mercury
Showa Denko is the factory that responsible in Niigata Minamata Diseases. On
April 7 1967, the Special Research Team had presented a report which concluded that the
methylmercury compound generated secondarily in the process of acetaldehyde
production at the Showa Denko Kanose plant flew into the Agano River and accumulated
in the river fishes. In the case of the Kanose plant of Showa Denko, the production of
acetaldehyde was closed down in January 1965 prior to the official acknowledgement of
Niigata Minamata Disease in May 1965 (MEJ, 2011).
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2.5.2 Canadian Minamata Disease
Canadian Minamata Disease is the third mercury pollution that came after
Minamata and Niigata. However, there are issues in naming the mercury pollution in
Canada. There is an opinion that it shall be named organic mercury poisoning rather than
Minamata disease because naming it as Minamata disease harbours a risk that it may be
interpreted as a disease endemic to the Minamata area (Harada et al., 2011).
Organic mercury poisoning were causes by direct poisoning through occupational
exposure or accidents while, Minamata disease is a form of organic mercury poisoning
which originated from environmental pollution and mediated by the food chain.
Therefore, it has been decided to name it as Canadian Minamata Disease because it is not
an occupational exposure or accident (Harada et al., 2011).
2.5.2.1Origin
Canadian mercury pollution had caused an issue due to the mercury pollution of
the Great Lakes in the USA. In 1969, Fimreit investigated the mercury pollution
throughout Canada and found that Wabigoon and English Rivers in Ontario as being
polluted. The mercury levels in the fish and waterfowls of these areas were shown to be
high too (Vermeer et al., 1973).
2.5.2.2 Source of Mercury
The pollution source was found to be Dryden Chemical’s caustic soda factory
upstream. The pulp industry is one of the main industries in Canada and caustic soda is
used to bleach the pulp. Mercury was used as a catalyst to purify the caustic soda (Harada
et al., 2011).
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2.6 Convention of Minamata Disease
Minamata disease is a serious health damage and environmental destruction, was
caused by improper management of mercury and delayed appropriate measures. In order
to prevent global environmental pollution and health damage caused by mercury, a new
convention named "Minamata Convention on Mercury" was agreed at the fifth session of
the Intergovernmental Negotiating Committee to prepare a global legally binding
instrument on mercury (INC5) held in Geneva, Switzerland in January 2013. The
Convention was adopted and opens for signature at the Conference of Plenipotentiaries
(Diplomatic Conference) which held on 9 to 11 October 2013 in Japan (Ministry of the
Environment Japan, 2011).
The convention was addressed specific manufacturing processes, notably phasing
out mercury in the production of acetaldehyde, the source of the contamination at
Minamata. The Japanese government pushed for the convention to be named after the
Minamata tragedy. Even so, nearly 60 years after that incident came to light, victims’
groups say the Chisso Corporation has not been held sufficiently accountable, and the
pollution has not been properly cleaned up. They said the Japanese government has
neither fully assessed the damage to human health and the environment nor adequately
compensated victims (Environmental Health Perspectives, 2013).
The government officially recognizes fewer than 3,000 patients from the Mina-
mata and Niigata incidents, more than half of whom are now dead. Those patients have
received some compensation and medical expense payments, while around 10,000 others
have received more modest compensation for having “applicable conditions.” Yet more
than 65,000 people have reportedly applied for compensation and medical expenses
under a new program (EHP, 2013)
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