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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