industrial disasters, which are disasters caused by industrial companies, either by accident, negligence or incompetence. They are a form of industrial accident where great damage, injury or loss of life are caused. Other disasters can also be considered industrial disasters, if their causes are rooted in the products or processes of industry. For example, the Great Chicago Fire of 1871 was made more severe due to the heavy concentration of lumber indu stry, wood houses, fuel and other chemicals in a small area. September 21, 1921: Oppau explosion in Germany. Occurred when a tower silo s toring 4,500 tonnes of a mixture of ammonium sulfate and ammonium nitrate fertil izer exploded at a BASF plant in Oppau, now part of Ludwigshafen, Germany, killi ng 500 600 people and injuring about 2,000 more. 1932-1968: The Minamata disaster was caused by the dumping of mercury compou nds in Minamata Bay, Japan. The Chisso Corporation, a fertilizer and later petro chemical company, was found responsible for polluting the bay for 37 years. It i s estimated that over 3,000 people suffered various deformities, severe mercury poisoning symptoms or death from what became known as Minamata disease. April 16, 1947: Texas City Disaster, Texas. At 9:15 AM an explosion occurred aboard a docked ship named the Grandcamp. The explosion, and subsequent fires a nd explosions, is referred to as the worst industrial disaster in America. A min imum of 578 people lost their lives and another 3,500 were injured as the blast shattered windows from as far away as 25 mi (40 km). Large steel pieces were thr own more than a mile from the dock. The origin of the explosion was fire in the cargo on board the ship. Detonation of 3,200 tons of ammonium nitrate fertilizer aboard the Grandcamp led to further explosions and fires. The fertilizer shipme nt was to aid the struggling farmers of Europe recovering from World War II. Alt hough this industrial disaster was one of the largest involving ammonium nitrate , many others have been reported including a recent one in North Korea. 1948: A chemical tank wagon explosion within the BASF's Ludwigshafen, German y site caused 207 fatalities. February 3, 1971: The Thiokol-Woodbine Explosion at a Thiokol chemical plant in Georgia kills 29 people and seriously injures 50. June 1, 1974: Flixborough disaster, England. An explosion at a chemical plan t near the village of Flixborough kills 28 people and seriously injures another 36. July 10, 1976: Seveso disaster, in Seveso, Italy, in a small chemical manufa cturing plant of ICMESA. Due to the release of dioxins into the atmosphere and t hroughout a large section of the Lombard Plain, 3,000 pets and farm animals died and, later, 70,000 animals were slaughtered to prevent dioxins from entering th e food chain. In addition, 193 people in the affected areas suffered from chlora cne and other symptoms. The disaster lead to the Seveso Directive, which was iss ued by the European Community and imposed much harsher industrial regulations. December 3, 1984: The Bhopal disaster in India is one of the largest industr ial disaster on record. A runaway reaction in a tank containing poisonous methyl isocyanate caused the pressure relief system to vent large amounts to the atmos phere at a Union Carbide plant. Estimates of its death toll range from 4,000 to 20,000. The disaster caused the region's human and animal populations severe hea lth problems to the present. November 1, 1986: The Sandoz disaster in Schweizerhalle, Switzerland, releas ing tons of toxic agrochemicals into the Rhine. June 28, 1988: Auburn, Indiana, improper mixing of chemicals kills four work ers at a local metal-plating plant in the worst confined-space industrial accide nt in U.S. history; a fifth victim died two days later.[1] October 23, 1989: Phillips Disaster. Explosion and fire killed 23 and injure d 314 in Pasadena, Texas. Registered 3.5 on the Richter scale. May 1, 1991: Sterlington, Louisiana. An explosion at the IMC operated Angus Chemical Nitro-paraffin Plant Sterlington, Louisiana killed 8 workers and injure

d 120 other people. There was severe damage to the surrounding community. The bl asts were heard more that 8 miles away. the explosion left burned out cars and c hunks of twisted metal littering the streets of the town. September 21, 2001: Toulouse, France. An explosion at the AZF fertilizer fac tory killed 29 and injured 2,500. Extensive structural damage to nearby neighbou rhoods. October 4, 2010: Alumina plant accident. Ajka, Kolontr, Devecser and several other settlements, Hungary. The dam of Magyar Aluminium Zrt.'s red mud reservoir broke and the escaping highly toxic and alkaline (~pH 13) sludge flooded severa l settlements. There were nine victims including a little girl and hundreds of i njuries (mostly chemical burns). January 20, 1909: Chicago Crib Disaster. During the construction of a water intake tunnel for the city of Chicago, a fire broke out on a temporary water cri b used to access an intermediate point along the tunnel. The fire began in the d ynamite magazine and burned the wooden dormitory that housed the tunnel workers. 46 workers survived the fire by jumping into the lake and climbing onto ice flo es or the spoil heap near the crib. 29 men were burned beyond recognition, and a pproximately 60 men died. Most of the remainder drowned or froze to death in the lake and were not recovered.[2][3][4] April 27, 1978: Willow Island disaster. A cooling tower for a power plant un der construction in Willow Island, West Virginia collapsed, killing 51 construct ion workers. The cause was attributed to placing loads on recently poured concre te before it had cured sufficiently to withstand the loads. It is thought to be the largest construction accident in United States history.[5] Defense industry July 17, 1944: Port Chicago Disaster. A munitions explosion that killed 320 people occurred at the Port Chicago Naval Magazine in Port Chicago, California. August 9, 1965: Little Rock AFB in Searcy, Arkansas. 53 contract workers wer e killed during a fire at a Titan missile silo. The cause of the fire was determ ined to be a welding rod damaging a hydraulic hose allowing hydraulic vapors to leak and spread throughout silo, which were then ignited by an open flame source . [edit] Energy industry May 1962: The Centralia, Pennsylvania coal mine fire began, forcing the grad ual evacuation of the Centralia borough. The fire continues to burn in the aband oned borough in 2011, 49 years later. March 1967: The Torrey Canyon oil supertanker was shipwrecked off the wester n coast of Cornwall, England, causing an environmental disaster. This was the fi rst major oil spill at sea. August, 1975 The Banqiao Dam flooded in the Henan Province of China due to e xtraordinarily heavy rains and poor construction quality of the dam built during Great Leap Forward, immediately killing over 100,000, plus over 150,000 died of subsequent epidemic diseases and famine, total deal toll around 250,000, making it the worst technical disaster ever happened in history. March 16, 1978 The Amoco Cadiz, an oil tanker owned by the company Amoco (no w merged with BP) sank near the Northwest coasts of France, resulting in the spi lling of 68,684,000 US Gallons of crude oil (1,635,000 barrels). This is the lar gest oil spill of its kind (spill from an oil tanker) in History. March 28, 1979: Three Mile Island accident. Partial nuclear meltdown. Mechan ical failures in the non-nuclear secondary system, followed by a stuck-open pilo t-operated relief valve (PORV) in the primary system, allowed large amounts of r

eactor coolant to escape. Plant operators initially failed to recognize the loss of coolant, resulting in a partial meltdown. The reactor was brought under cont rol but not before up to 481 PBq (13 million curies) of radioactive gases were r eleased into the atmosphere.[6] June 3, 1979: Ixtoc I oil spill, The Ixtoc I exploratory oil well suffered a blowout resulting in the third largest oil spill and the second largest acciden tal spill in history. November 20, 1980: A Texaco oil rig drilled into a salt mine transforming th e Lake Peigneur, a freshwater lake before the accident, into a salt water lake. July 23, 1984: Romeoville, Illinois, Union Oil refinery explosion kills 19 p eople. November 19, 1984: San Juanico Disaster, an explosion at a liquid petroleum gas tank farm kills hundreds and injures thousands in San Juanico, Mexico. April 26, 1986: Chernobyl disaster. At the Chernobyl Nuclear Power Plant in Prypiat, Ukraine a test on reactor number four goes out of control, resulting in a nuclear meltdown. The ensuing steam explosion and fire killed up to 50 people with estimates that there may be between 4,000 and several hundred thousand add itional cancer deaths over time. Fallout could be detected as far away as Canada . The Chernobyl Exclusion Zone, covering portions of Belarus and Ukraine surroun ding Prypiat, remains poisoned and mostly uninhabited. Prypiat itself was totall y evacuated and remains as a ghost town. May 5, 1988: Norco, Louisiana, Shell Oil refinery explosion after hydrocarbo n gas escaped from a corroded pipe in a catalytic cracker and was ignited. Louis iana state police evacuated 2,800 residents from nearby neighborhoods. Seven wor kers were killed and 42 injured. The total cost arising from the Norco blast is estimated at US$ 706 million. July 6, 1988: Piper Alpha disaster. An explosion and resulting fire on a Nor th Sea oil production platform kills 167 men. Total insured loss is about US$ 3. 4 billion. To date it is rated as the world's worst offshore oil disaster in ter ms both of lives lost and impact to industry. March 24, 1989: Exxon Valdez oil spill. The Exxon Valdez, an oil tanker boun d for Long Beach, California, hits Prince William Sound's Bligh Reef dumping an estimated minimum 10.8 million US gallons (40.9 million litres, or 250,000 barre ls) of crude oil into the sea. It is considered to be one of the most devastatin g human-caused environmental disasters ever to occur in history.[7] 100,000 to a s many as 250,000 seabirds died as well as at least 2,800 sea otters, approximat ely 12 river otters, 300 harbor seals, 247 bald eagles, and 22 orcas, and billio ns of salmon and herring eggs were destroyed.[8] Overall reductions in populatio n have been seen in various ocean animals, including stunted growth in pink salm on populations.[9] Sea otters and ducks also showed higher death rates in follow ing years, partially because they ingested prey from contaminated soil and from ingestion of oil residues on hair due to grooming.[10] The effects of the spill continue to be felt 20 years later. March 23, 2005: Texas City Refinery explosion. An explosion occurred at a Br itish Petroleum refinery in Texas City, Texas. It is the third largest refinery in the United States and one of the largest in the world, processing 433,000 bar rels of crude oil per day and accounting for 3% of that nation's gasoline supply . Over 100 were injured, and 15 were confirmed dead, including employees of the Fluor Corporation as well as BP. BP has since accepted that its employees contri buted to the accident. Several level indicators failed, leading to overfilling o f a knock out drum, and light hydrocarbons concentrated at ground level througho ut the area. A nearby running diesel truck set off the explosion. December 11, 2005: Hertfordshire Oil Storage Terminal fire. A series of expl osions at the Buncefield oil storage depot, described as the largest peacetime e xplosion in Europe, devastated the terminal and many surrounding properties. The re were no fatalities. Total damages have been forecast as 750 million. February 7, 2010: 2010 Connecticut power plant explosion. A large explosion occurred at a Kleen Energy Systems 620-megawatt, Siemens combined cycle gas- and oil- fired power plant in Middletown, Connecticut, United States. Preliminary r

eports attributed the cause of the explosion to a test of the plant's energy sys tems.[11] The plant was still under construction and scheduled to start supplyin g energy in June 2010.[12] The number of injuries was eventually established to be 27.[13] Five people died in the explosion.[14] April 20, 2010: Deepwater Horizon oil spill in the Gulf of Mexico. 11 oil pl atform workers died in an explosion and fire that resulted in a massive oil spil l in the Gulf of Mexico, considered the largest offshore spill in U.S. history.[ 15] March 2011 Fukushima I nuclear accidents [edit] Food industry May 2, 1878: The Washburn "A" Mill in Minneapolis was destroyed by a flour d ust explosion, killing 18. The mill was rebuilt with updated technology. The exp losion led to new safety standards in the milling industry.[16] January 15, 1919: The Boston Molasses Disaster. A large molasses tank burst and a wave of molasses rushed through the streets at an estimated 35 mph (56 km/ h), killing 21 and injuring 150. The event has entered local folklore, and resid ents claim that on a hot summer day, the area still smells of molasses. September 3, 1991: 1991 Hamlet chicken processing plant fire in Hamlet, Nort h Carolina, where locked doors trapped workers in a burning processing plant, ca using 25 deaths. February 7, 2008: The 2008 Georgia sugar refinery explosion in Port Wentwort h, Georgia, United States. Thirteen people were killed and 42 injured when a dus t explosion occurred at a sugar refinery owned by Imperial Sugar. [edit] Manufacturing industry January 10, 1860: Pemberton Mill was a large factory in Lawrence, Massachuse tts that collapsed without warning. An estimated 145 workers were killed and 166 injured. March 20, 1905: Grover Shoe Factory disaster was a boiler explosion, buildin g collapse and fire that killed 58 people and injured 150 in Brockton, Massachus etts. March 25, 1911: Triangle Shirtwaist Factory fire in New York City. This was a major industrial disaster in the U.S., causing the death of more than one hund red garment workers who either died in the fire or jumped to their deaths. The f ire led to legislation requiring improved factory safety standards and helped sp ur the growth of the International Ladies' Garment Workers' Union, which fought for better working conditions for sweatshop workers in that industry. May 10, 1993: Kader Toy Factory fire. A fire started in a poorly built facto ry in Thailand. Exit doors were locked and the stairwell collapsed. 188 workers were killed, mostly young women. May 13, 2000: Enschede fireworks disaster. A fire and explosion at a firewor ks depot in Enschede, Netherlands leaves 22 people dead and 947 injured. About 1 ,500 homes are damaged or destroyed. The damage is estimated to be over US$ 300 million in insured losses. April 18, 2007: Qinghe Special Steel Corporation disaster. A ladle holding m olten steel separated from the overhead iron rail, fell, tipped, and killed 32 w orkers, injuring another 6. February 1 2008 an illegal fireworks factory in Istanbul, located on a build ings third floor explodes, followed 5 minutes later by an explosion in the paint factory located in the buildings lower floors. [edit] Mining industry See mining accident for more. March 10, 1906: Courrires mine disaster in Courrires, France. 1,099 workers di ed, including children, in the worst mine accident ever in Europe.

October 14, 1913:' Senghenydd Colliery Disaster, the worst Mining accident i n the United Kingdom, 439 workers died. April 26, 1942: Benxihu Colliery disaster in Benxi, Liaoning, China. 1,549 w orkers died, in the worst coal mine accident ever in the world. May 28, 1965: 1965 Dhanbad coal mine disaster took place in Jharkhand, India , killing over 300 miners. October 21, 1966: Aberfan disaster was a catastrophic collapse of a colliery spoil-tip that occurred in the Welsh village of Aberfan, killing 116 children a nd 28 adults. January 30, 2000: Baia Mare cyanide spill took place in Baia Mare, Romania. The accident, called the worst environmental disaster in Europe since Chernobyl, was a release of 100,000 tons of cyanide contaminated water by a Aurul mining c ompany due to reservoir broke into the rivers Somes, Tisza and Danube. Although no human fatalities were reported, the leak killed up to 80% of aquatic life of some of the affected rivers.

Oppau explosion Caption from Popular Mechanics Magazine 1921 The Oppau explosion occurred on September 21, 1921 when a tower silo storing 4,5 00 tonnes of a mixture of ammonium sulfate and ammonium nitrate fertilizer explo ded at a BASF plant in Oppau, now part of Ludwigshafen, Germany, killing 500 600 p eople and injuring about 2,000 more. The plant began producing ammonium sulfate in 1911, but during World War I when Germany was unable to obtain the necessary sulfur, it began to produce ammonium nitrate as well. Ammonia could be produced without overseas resources, using the Haber process. Compared to ammonium sulfate, ammonium nitrate is strongly hygroscopic, so the m ixture of ammonium sulfate and nitrate clogged together under the pressure of it s own weight, turning it into a plaster-like substance in the 20 m high silo. Th e workers needed to use pickaxes to get it out, a problematic situation because they could not enter the silo and risk being buried in collapsing fertilizer. To ease their work, small charges of dynamite were used to loosen the mixture. T he procedure was tried experimentally and was considered safe; it was not known at the time that ammonium nitrate was explosive. Nothing extraordinary happened during an estimated 20,000 firings, until the fateful explosion on September 21. As all involved died in the explosion, the causes are not clear. A theory is th at the mixture changed and a higher concentration of ammonium nitrate was presen t. Contents [hide] 1 2 3 4 Scale of the explosion See also References External links

[edit] Scale of the explosion The explosion was estimated to be equivalent to about 1 2 kilotonnes of TNT and wa s heard as a loud bang in Munich, more than 300 km away. The pressure wave rippe d roofs off up to 25 km away and destroyed windows even farther away. In Heidelb erg (30 km from Oppau), traffic was stopped by the mass of broken glass on the s treets.

About 80 percent of all buildings in Oppau were destroyed, leaving 6,500 homeles s. At ground zero a 90 m by 125 m crater, 19 m deep, was created. Damages were e stimated by New York Times in 1922 at then 321 million Marks[1] (since Germany s uffered heavy hyperinflation in 1919 1924, given amounts and exchange-rates are no t very descriptive). According to some descriptions, only 450 tonnes exploded, out of 4,500 tonnes of fertilizer stored in the warehouse.[citation needed]

Minamata disease From Wikipedia, the free encyclopedia (Redirected from Minamata disaster) Minamata disease Classification and external resources The crippled hand of a Minamata disease victim ICD-10 T56.1 ICD-9 985.0 MedlinePlus 001651 Minamata disease (??? Minamata-byo?), sometimes referred to as Chisso-Minamata d isease (?????? Chisso-Minamata-byo?), is a neurological syndrome caused by sever e mercury poisoning. Symptoms include ataxia, numbness in the hands and feet, ge neral muscle weakness, narrowing of the field of vision and damage to hearing an d speech. In extreme cases, insanity, paralysis, coma and death follow within we eks of the onset of symptoms. A congenital form of the disease can also affect f etuses in the womb. Minamata disease was first discovered in Minamata city in Kumamoto prefecture, J apan in 1956. It was caused by the release of methylmercury in the industrial wa stewater from the Chisso Corporation's chemical factory, which continued from 19 32 to 1968. This highly toxic chemical bioaccumulated in shellfish and fish in M inamata Bay and the Shiranui Sea, which when eaten by the local populace resulte d in mercury poisoning. While cat, dog, pig, and human deaths continued over mor e than 30 years, the government and company did little to prevent the pollution. As of March 2001, 2,265 victims had been officially recognised (1,784 of whom ha d died)[1] and over 10,000 had received financial compensation from Chisso.[2] B y 2004, Chisso Corporation had paid $86 million in compensation, and in the same year was ordered to clean up its contamination.[3] On March 29, 2010, a settlem ent was reached to compensate as-yet uncertified victims.[4] A second outbreak of Minamata disease occurred in Niigata Prefecture in 1965. Bo th the original Minamata disease and Niigata Minamata disease are considered two of the Four Big Pollution Diseases of Japan. Contents [hide] 1 1908 1955 2 1956 1959 2.1 Finding the cause 2.2 Identification of mercury 3 1959 3.1 Compensation of fishermen and patients, 1959 3.2 Wastewater treatment 4 1959-69 4.1 Continued pollution 4.2 Congenital Minamata disease

4.3 Outbreak of Niigata Minamata disease 5 1969 1973 5.1 Official government recognition 5.2 Struggle for a new agreement 5.3 Uncertified patients' fight to be recognised 6 Victims 7 Democratizing effects 8 Media 9 In popular culture 10 Minamata disease today 11 See also 12 Notes 13 References 14 Further reading 15 External links [edit] 1908 1955 See also: Timeline of Minamata disease The Chisso Corporation first opened a chemical factory in Minamata in 1908. Init ially producing fertilisers, the factory followed the nationwide expansion of Ja pan's chemical industry, branching out into production of acetylene, acetaldehyd e, acetic acid, vinyl chloride and octanol, among others. The Minamata factory b ecame the most advanced in all of Japan, both before and after World War II.[cit ation needed] The waste products resulting from the manufacture of these chemica ls were released into Minamata Bay through the factory wastewater. Inevitably th ese pollutants had an environmental impact. Fisheries were damaged in terms of r educed catches, and in response, Chisso reached two separate compensation agreem ents with the fishery cooperative in 1926 and 1943.[5] Wastewater discharge from the Chisso factory in Minamata (W. E. Smith) The rapid expansion of the Minamata factory spurred on the local economy and as Chisso prospered, so did Minamata. This fact, combined with the lack of other in dustry, meant that Chisso had great influence in Minamata. At one point, over ha lf of the tax revenue of Minamata City authority came from Chisso and its employ ees, and the company and its subsidiaries were responsible for creating a quarte r of all jobs in Minamata.[6] Minamata was even dubbed Chisso's "castle town", i n reference to the capital cities of feudal lords who ruled Japan during the Edo period.[7] The Chisso Minamata factory first started acetaldehyde production in 1932, produ cing 210 tons that year. By 1951 production had jumped to 6,000 tons per year an d reached a peak of 45,245 tons in 1960.[8] Throughout, the Chisso factory's out put amounted to between a quarter and a third of Japan's total acetaldehyde prod uction. The chemical reaction used to produce the acetaldehyde used mercury sulf ate as a catalyst. A side reaction of the catalytic cycle led to the production of a small amount of an organic mercury compound, namely methylmercury.[9] This highly toxic compound was released into Minamata Bay from the start of productio n in 1932 until 1968, when this production method was discontinued. [edit] 1956 1959 On April 21, 1956, a five year-old girl was examined at the Chisso Corporation's factory hospital in Minamata, Japan, a town on the west coast of the southern i sland of Kyushu. The physicians were puzzled by her symptoms: difficulty walking , difficulty speaking and convulsions. Two days later her younger sister also be gan to exhibit the same symptoms and she too was hospitalised. The girls' mother informed doctors that her neighbour's daughter was also experiencing similar pr oblems. After a house-to-house investigation eight further patients were discove red and hospitalised. On May 1, the hospital director reported to the local publ ic health office the discovery of an "epidemic of an unknown disease of the cent

ral nervous system", marking the official discovery of Minamata disease.[10] To investigate the epidemic, the city government and various medical practitione rs formed the Strange Disease Countermeasures Committee (??????? Kibyo Taisaku I inkai?) at the end of May 1956. Owing to the localised nature of the disease, it was suspected to be contagious and as a precaution patients were isolated and t heir homes disinfected. Unfortunately, this contributed to the stigmatisation an d discrimination experienced by Minamata victims from the local community. Durin g its investigations, the committee uncovered surprising anecdotal evidence of t he strange behaviour of cats and other wildlife in the areas surrounding patient s' homes. From around 1950 onwards, cats had been seen to have convulsions, go m ad and die. Locals called it the "cat dancing disease" (???? neko odori byo?), o wing to their erratic movement. Crows had fallen from the sky, seaweed no longer grew on the sea bed and fish floated dead on the surface of the sea. As the ext ent of the outbreak was understood, the committee invited researchers from Kumam oto University to help in the research effort. The Kumamoto University Research Group was formed on August 24, 1956. Researcher s from the School of Medicine began visiting Minamata regularly and admitted pat ients to the university hospital for detailed examinations. Gradually a more com plete picture of the symptoms exhibited by patients was uncovered. The disease d eveloped without any prior warning, with patients complaining of a loss of sensa tion and numbness in their hands and feet. They became unable to grasp small obj ects or fasten buttons. They could not run or walk without stumbling, their voic es changed in pitch and many patients complained of difficulties seeing, hearing and swallowing. In general these symptoms deteriorated and were followed by sev ere convulsions, coma and eventually death. By October 1956, 40 patients had bee n discovered, 14 of whom had died: an alarming mortality rate of 36.7%.[11] [edit] Finding the cause Researchers from Kumamoto University also began to focus on the cause of the str ange disease. They found that the victims, often members of the same family, wer e clustered in fishing hamlets along the shore of Minamata Bay. The staple food of victims was invariably fish and shellfish from Minamata Bay. The cats in the local area, who tended to eat scraps from the family table, had died with sympto ms similar to those now discovered in humans. This led the researchers to believ e that the outbreak was caused by some kind of food poisoning, with contaminated fish and shellfish being the prime suspects. On November 4 the research group announced its initial findings: "Minamata disea se is rather considered to be poisoning by a heavy metal... presumably it enters the human body mainly through fish and shellfish."[12] [edit] Identification of mercury Methylmercury-cation-3D-vdW.png Methylmercury.png Methylmercury, an organic mercury compound released in factory wastewater and th e cause of Minamata disease As soon as the investigation identified a heavy metal as the causal substance, t he wastewater from the Chisso plant was immediately suspected as the origin. The company's own tests revealed that its wastewater contained many heavy metals in concentrations sufficiently high to bring about serious environmental degradati on including lead, mercury, manganese, arsenic, selenium, thallium and copper. I dentifying which particular poison was responsible for the disease proved to be extremely difficult and time consuming. During the years 1957 and 1958, many dif ferent theories were proposed by different researchers. Initially manganese was thought to be the causal substance due to the high concentrations found in fish and the organs of the deceased. Thallium, selenium and a multiple contaminant th eory were also proposed but it was not until March 1958, when visiting British n eurologist Douglas McAlpine suggested that Minamata symptoms resembled those of

organic mercury poisoning, that the focus of the investigation centered on mercu ry. In February 1959, the mercury distribution in Minamata Bay was investigated. The results shocked the researchers involved. Large quantities of mercury were dete cted in fish, shellfish and sludge from the bay. The highest concentrations cent red around the Chisso factory wastewater canal in Hyakken Harbour and decreased going out to sea, clearly identifying the plant as the source of contamination. At the mouth of the wastewater canal, a figure of 2 kg of mercury per ton of sed iment was measured: a level which would be economically viable to mine. Ironical ly, Chisso did later set up a subsidiary to reclaim and sell the mercury recover ed from the sludge.[13] Hair samples were taken from the victims of the disease and also from the Minama ta population in general. In patients the maximum mercury level recorded was 705 ppm (parts per million), indicating very heavy exposure and in non-symptomatic Minamata residents the level was 191 ppm. This compared to an average level of 4 ppm for people living outside the Minamata area.[13] On November 12, 1959, the Ministry of Health and Welfare's Minamata Food Poisoni ng Subcommittee published its results: "Minamata disease is a poisoning disease that affects mainly the central ner vous system and is caused by the consumption of large quantities of fish and she llfish living in Minamata Bay and its surroundings, the major causative agent be ing some sort of organic mercury compound."[14] [edit] 1959 The Chisso factory and its wastewater routes During the investigation by researchers at Kumamoto University, the causal subst ance had been identified as a heavy metal and it was widely presumed that the Ch isso plant was the source of the contamination. Chisso was coming under closer s crutiny and in order to deflect criticism the wastewater output route was change d. Chisso knew of the environmental damage caused by its wastewater and was well aware that it was the prime suspect in the Minamata disease investigation. Desp ite this, from September 1958, instead of discharging its waste into Hyakken Har bour (the focus of investigation and source of original contamination), it disch arged wastewater directly into Minamata River. The immediate effect was the deat h of fish at the mouth of the river, and from that point on new Minamata disease victims began to appear in other fishing villages up and down the coast of the Shiranui Sea, as the pollution spread over an even greater area.[15] Chisso failed to co-operate with the investigation team from Kumamoto University . It withheld information on its industrial processes, leaving researchers to sp eculate what products the factory was producing and by what methods.[16] The Chi sso factory's hospital director, Hajime Hosokawa, established a laboratory in th e research division of the plant to carry out his own experiments into Minamata disease in July 1959. Food to which factory wastewater had been added was fed to healthy cats. Seventy-eight days into the experiment cat 400 exhibited symptoms of Minamata disease and pathological examinations confirmed a diagnosis of orga nic mercury poisoning. The company did not reveal these significant results to t he investigators and ordered Hosokawa to stop his research.[17] In an attempt to undermine Kumamoto University researchers' organic mercury theo ry, Chisso and other parties with a vested interest that the factory remain open (including the Ministry of International Trade and Industry and the Japan Chemi cal Industry Association) funded research into alternative causes of the disease , other than its own waste.[18] [edit] Compensation of fishermen and patients, 1959

For more details on this topic, see Minamata disease compensation agreements of 1959. Polluting wastewater had damaged the fisheries around Minamata ever since the op ening of the Chisso factory in 1908. The Minamata Fishing Cooperative had manage d to win small payments of "sympathy money" (???? mimaikin?) from the company in 1926 and again in 1943, but after the outbreak of Minamata disease the fishing situation was becoming critical. Fishing catches had declined by 91% between the years 1953 and 1957. The Kumamoto prefectural government issued a partial ban o n the sale of fish caught in the heavily polluted Minamata Bay, but not an all-o ut ban, which would have legally obliged it to compensate the fishermen. The fis hing cooperative protested against Chisso and angrily forced their way into the factory on 6 August and 12 August, demanding compensation. A committee was set u p by Minamata Mayor Todomu Nakamura to mediate between the two sides but this co mmittee was stacked heavily in the company's favour. On 29 August the fishing co operative agreed to the mediation committee's proposal, stating: "In order to en d the anxiety of the citizens, we swallow our tears and accept". The company pai d the cooperative JPY20 million (USD55,600) and set up a JPY15 million (USD41,70 0) fund to promote the recovery of fishing. Protestors at the gates of the Chisso factory (W. E. Smith) Since the change of route of wastewater output in 1958, pollution had spread up and down the Shiranui Sea, damaging fisheries there too. Emboldened by the succe ss of the small Minamata cooperative, the Kumamoto Prefectural Alliance of Fishi ng Cooperatives also decided to seek compensation from Chisso. On 17 October, 1, 500 fishermen from the alliance descended on the factory to demand negotiations. When this produced no results the alliance members took their campaign to Tokyo , securing an official visit to Minamata by members of the Japanese Diet. During the visit on 2 November alliance members forced their way into the factory and rioted, causing many injuries and JPY10 million (USD27,800) worth of damage. The violence was covered widely in the media, bringing the nation's attention to th e Minamata issue for the first time since the outbreak began. Another mediation committee was set up, an agreement hammered out and signed on 17 December. JPY25 million "sympathy money" was paid to the alliance and a JPY65 million fishing r ecovery fund established. In 1959, the victims of Minamata disease were in a much weaker position than the fishermen. The recently formed Minamata Disease Patients Families Mutual Aid So ciety was much more divided than the fishing cooperatives. Patients' families we re the victim of discrimination and ostracism from the local community. Local pe ople felt that the company (and their city that depended upon it) was facing eco nomic ruin. To some patients this ostracism by the community represented a great er fear than the disease itself. After beginning a sit-in at the factory gates i n November 1959 the patients asked Kumamoto Prefecture Governor Hirosaku Teramot o to include the patients' request for compensation with the mediation that was ongoing with the prefectural fishing alliance. Chisso agreed and after a few wee ks' further negotiation, another "sympathy money" agreement was signed. Patients who were certified by a Ministry of Health and Welfare committee would be compe nsated: adult patients received JPY100,000 (USD278) per year; children JPY30,000 (USD83) per year and families of dead patients would receive a one-off JPY320,0 00 (USD889) payment. [edit] Wastewater treatment On October 21, 1959, Chisso was ordered by the Ministry of International Trade a nd Industry to switch back its wastewater drainage from the Minamata River to Hy akken Harbour and to speed up the installation of wastewater treatment systems a t the factory. Chisso installed a Cyclator purification system on December 19, 1 959, and opened it with a special ceremony. Chisso's president Kiichi Yoshioka d rank a glass of water supposedly treated through the Cyclator to demonstrate tha t it was safe. In fact, the wastewater from the acetaldehyde plant, which the co

mpany knew still contained mercury and led to Minamata disease when fed to cats, was not treated through the Cyclator at the time. Testimony at a later Niigata Minamata disease trial proved that Chisso knew the Cyclator to be completely ine ffective: "...the purification tank was installed as a social solution and did n othing to remove organic mercury."[19] The deception was successful and almost all parties involved in Minamata disease were duped into believing that the factory's wastewater had been made safe from December 1959 on. This widespread assumption meant that doctors were not expect ing new patients to appear, resulting in numerous problems in the years to follo w, as the pollution continued. In most people's minds, the issue of Minamata dis ease had been resolved. [edit] 1959-69 The years between the first set of "sympathy money" agreements in 1959 and the s tart of the first legal action to be taken against Chisso in 1969 are often call ed the "ten years of silence". In fact, much activity on the part of the patient s and fishermen took place during this period but nothing had a significant impa ct on the actions of the company or the coverage of Minamata in the national med ia. [edit] Continued pollution Despite the almost universal assumption to the contrary, the wastewater treatmen t facilities installed in December 1959 had no effect on the level of organic me rcury being released into the Shiranui Sea. The pollution and the disease it cau sed continued to spread. The Kumamoto and Kagoshima prefectural governments cond ucted a joint survey in late 1960 and early 1961 into the level of mercury in th e hair of people living around the Shiranui Sea. The results confirmed that orga nic mercury had spread all around the inland sea and that people were still bein g poisoned by contaminated fish. Hundreds of people were discovered to have leve ls greater than 50 ppm of mercury in their hair, the level at which people are l ikely to experience nerve damage. The highest result recorded was that of a lady from Goshonoura island who had 920 ppm in her sample. The prefectural governments did not publish the results and did nothing in respo nse to these surveys. The participants who had donated hair samples were not inf ormed of their result, even when they requested it. A follow-up study ten years later discovered that many had died from "unknown causes".[20] [edit] Congenital Minamata disease Local doctors and medical officials had noticed for a long time an abnormally hi gh frequency of cerebral palsy and other infantile disorders in the Minamata are a. In 1961 a number of medical professionals including Masazumi Harada (later to receive an honour from the United Nations for his body of work on Minamata dise ase) set about re-examining children diagnosed with cerebral palsy. The symptoms of the children closely mirrored those of adult Minamata disease patients but m any of their mothers did not exhibit symptoms. The fact that these children had been born after the initial outbreak and had never been fed contaminated fish al so led their mothers to believe they were not victims. At the time the medical e stablishment believed the placenta would protect the foetus from toxins in the b loodstream, which is indeed the case with most chemicals. What was not known at the time was that exactly the opposite is the case with methylmercury: the place nta removes it from the mother's bloodstream and concentrates the chemical in th e fetus. After several years of study and the autopsies of two children, the doctors anno unced that these children were suffering from an as yet unrecognised congenital form of Minamata disease. The certification committee convened on 29 November 19 62 and agreed that the two dead children and the 16 children still alive should be certified as patients, and therefore liable for "sympathy" payments from Chis

so, in line with the 1959 agreement.[21] [edit] Outbreak of Niigata Minamata disease For more details on this topic, see Niigata Minamata disease. Minamata disease broke out again in 1965, this time along the banks of the Agano River in Niigata Prefecture. The polluting factory (owned by Showa Denko) emplo yed a chemical process using a mercury catalyst very similar to that used by Chi sso in Minamata. As in Minamata, from the autumn of 1964 to the spring of 1965, cats living along the banks of the Agano River had been seen to go mad and die. Before long patients appeared with identical symptoms to patients living on the Shiranui Sea, and the outbreak was made public on 12 June 1965. Researchers from the Kumamoto University Research Group and Hajime Hosokawa (who had retired fro m Chisso in 1962) used their experience from Minamata and applied it to the Niig ata outbreak. In September 1966 a report was issued proving Showa Denko's pollut ion to be the cause of this second Minamata disease. Unlike the patients in Minamata, the victims of Showa Denko's pollution lived a considerable distance from the factory and had no particular link to the company . As a result the local community was much more supportive of patients' groups a nd a lawsuit was filed against the company in March 1968, only three years after discovery. The events in Niigata catalysed a change in response to the original Minamata in cident. The scientific research carried out in Niigata forced a re-examination o f that done in Minamata and the decision of Niigata patients to sue the pollutin g company allowed the same response to be considered in Minamata. Masazumi Harad a has said that, "It may sound strange, but if this second Minamata disease had not broken out, the medical and social progress achieved by now in Kumamoto... w ould have been impossible."[22] Around this time two other pollution-related diseases were also grabbing headlin es in Japan. Victims of Yokkaichi asthma and Itai-itai disease were forming citi zens' groups and filed lawsuits against the polluting companies in September 196 7 and March 1968 respectively. Collectively these diseases came to be known as t he Four Big Pollution Diseases of Japan.[23] Slowly but surely the mood in Minamata and Japan as a whole was shifting. Minama ta patients found the public gradually becoming more receptive and sympathetic a s the decade wore on. This culminated in 1968 with the establishment in Minamata of the Citizens' Council for Minamata Disease Countermeasures which was to beco me the chief citizens' support group to the Minamata patients. A founding member of the citizens' council was Michiko Ishimure, a local housewife and poet who l ater that year published Pure Land, Poisoned Sea: Our Minamata disease (???????? ?? Kugai Jodo: Waga Minamatabyo?) a book of poetic essays that received national acclaim. [edit] 1969 1973 [edit] Official government recognition Finally on 26 September 1968 twelve years after the discovery of the disease (an d four months after Chisso had stopped production of acetaldehyde using its merc ury catalyst) the government issued an official conclusion as to the cause of Mi namata disease: "Minamata disease is a disease of the central nervous system, a poisoning ca used by long-term consumption, in large amounts, of fish and shellfish from Mina mata Bay. The causative agent is methylmercury. Methylmercury produced in the ac etaldehyde acetic acid facility of Shin Nihon Chisso's Minamata factory was disc harged in factory wastewater... Minamata disease patients last appeared in 1960, and the outbreak has ended. This is presumed to be because consumption of fish and shellfish from Minamata Bay was banned in the fall of 1957, and the fact tha

t the factory had waste-treatment facilities in place from January 1960." The conclusion contained many factual errors: eating fish and shellfish from oth er areas of the Shiranui Sea, not just Minamata Bay, could cause the disease; ea ting small amounts, as well as large amounts of contaminated fish over a long ti me also produced symptoms; the outbreak had not in fact "ended" in 1960 nor had mercury-removing wastewater facilities been installed in January 1960. Neverthel ess, the government announcement brought a feeling of relief to a great many vic tims and their families. Many felt vindicated in their long struggle to force Ch isso to accept responsibility for causing the disease and expressed thanks that their plight had been recognised by their social superiors. The struggle now foc used on to what extent the victims should be compensated.[24] [edit] Struggle for a new agreement In light of the government announcement, the patients of the Mutual Aid Society decided to ask for a new compensation agreement with Chisso and submitted the de mand on 6 October. The company replied that it was unable to judge what would be fair compensation and asked the national government to set up a binding arbitra tion committee to decide. This proposal split the members of the patients' socie ty, many of whom were extremely wary of entrusting their fate to a third party, as they had done in 1959 with unfortunate results. At a meeting on 5 April 1969 the opposing views within the society could not be reconciled and the organisati on split into the Arbitration Group (who were willing to accept binding arbitrat ion) and the Litigation Group (who decided to sue the company). That summer Chis so sent gifts to the families who opted for arbitration rather than litigation. Minamata patients and family members hold photographs of their dead during a dem onstration (W. E. Smith) An arbitration committee was duly set up by the Ministry of Health and Welfare o n 25 April, but it took almost a year to draw up a draft compensation plan. A ne wspaper leak in March 1970 revealed that the committee would ask Chisso to pay o nly JPY2 million (USD5,600) for dead patients and JPY140,000 to JPY200,000 (USD3 90 to USD560) per year to surviving patients. The Arbitration Group were dismaye d by the sums on offer. They petitioned the committee, together with patients an d supporters of the Litigation Group, for a fairer deal. The arbitration committ ee announced their compensation plan on 25 May in a disorderly session at the Mi nistry of Health and Welfare in Tokyo. Thirteen protesters were arrested. Instea d of accepting the agreement as they had promised, the Arbitration Group asked f or increases. The committee was forced to revise its plan and the patients waite d inside the Ministry building for two days while they did so. The final agreeme nt was signed on 27 May. Payments for deaths ranged from JPY1.7 million to JPY4 million (USD4,700 to USD11,100), one-time payments from JPY1 million to JPY4.2 m illion (USD2,760 to USD11,660) and annual payments of between JPY170,000 and JPY 380,000 (USD470 to USD1,100) for surviving patients. On the day of the signing, the Minamata Citizens' Council held a protest outside the Minamata factory gates . One of the Chisso trade unions held an eight-hour strike in protest at the poo r treatment of the Arbitration Group by their own company.[25] The Litigation Group, representing 41 certified patients (17 already deceased) i n 28 families, submitted their suit against Chisso in the Kumamoto District Cour t on 14 June 1969. The leader of the group, Eizo Watanabe (a former leader of th e Mutual Aid Society), declared that, "Today, and from this day forth, we are fi ghting against the power of the state." Those who decided to sue the company cam e under fierce pressure to drop their lawsuits against the company. One woman wa s visited personally by a Chisso executive and harassed by her neighbours. She w as ignored, her family's fishing boat used without permission, their fishing net s cut and human faeces thrown at her in the street.[26] The Litigation Group and their lawyers were helped substantially by an informal national network of citizens' groups that sprung up around the country in 1969.

The Associations to Indict [Those Responsible for] Minamata Disease (????????? M inamata-byo o Kokuhatsu Suru Kai?) were instrumental in raising awareness and fu nds for the lawsuit. The Kumamoto branch in particular was especially helpful to the case. In September 1969 they set up a Trial Research Group which included l aw professors, medical researchers (including Masazumi Harada), sociologists and even the housewife and poet Michiko Ishimure to provide useful material to the lawyers to improve their legal arguments. In fact their report: Corporate Respon sibility for Minamata Disease: Chisso's Illegal Acts,[27] published in August 19 70, formed the basis of the ultimately successful lawsuit.[25] The trial lasted almost four years. The Litigation Group lawyers sought to prove Chisso's corporate negligence. Three main legal points had to be overcome to wi n the case. First the lawyers had to show that methylmercury caused Minamata dis ease and that the company's factory was the source of pollution. The extensive r esearch by Kumamoto University and the government conclusion meant that this poi nt was proved quite easily. Secondly, could and should the company have anticipa ted the effect of its wastewater and should it have taken steps to prevent the t ragedy (i.e. was the company negligent in its duty of care)? Thirdly, was the "s ympathy money" agreement of 1959, which forbade the patients from claiming any f urther compensation, a legally binding contract? The trial heard from patients and their families but the most important testimon y came from Chisso executives and employees. The most dramatic testimony came fr om Hajime Hosokawa who spoke on 4 July 1970 from his hospital bed where he was d ying of cancer. He explained his experiments with cats, including the infamous " cat 400" which developed Minamata disease after being fed factory wastewater. He also spoke of his opposition to the 1958 change in wastewater output route from Hyakken Harbour to Minamata River. His testimony was backed up by a colleague w ho also told how company officials had ordered them to halt their cat experiment s in the autumn of 1959. Hajime Hosokawa died three months after giving his test imony. Former factory manager Eiichi Nishida admitted that the company put profi ts ahead of safety, resulting in dangerous working conditions and a lack of care with mercury. Former Chisso President Kiichi Yoshioka admitted that the company promoted a theory of dumped World War II explosives even though it knew it to b e unfounded. The verdict handed down on 20 March 1973 represented a complete victory for the patients of the Litigation Group: "The defendant's factory was a leading chemical plant with the most advanced technology and ... should have assured the safety of its wastewater. The defend ant could have prevented the occurrence of Minamata disease or at least have kep t it at a minimum. We cannot find that the defendant took any of the precautiona ry measures called for in this situation whatsoever. The presumption that the de fendant had been negligent from beginning to end in discharging wastewater from its acetaldehyde plant is amply supported. The defendant cannot escape liability for negligence." The "sympathy money" agreement was found to be invalid and Chisso was ordered to make one-time payments of JPY18 million (USD66,000) for each deceased patient a nd from JPY16 million to JPY 18 million (USD59,000 to USD66,000) for each surviv ing patient. The total compensation of JPY937 million (USD3.4 million) was the l argest sum ever awarded by a Japanese court.[28] [edit] Uncertified patients' fight to be recognised While the struggles of the arbitration and litigation groups against Chisso were continuing, a new group of Minamata disease sufferers emerged. In order to qual ify for compensation under the 1959 agreement, patients had to be officially rec ognised by various ad hoc certification committees according to their symptoms. Unfortunately, in an effort to limit the liability and financial burden on the c

ompany, these committees were sticking to a rigid interpretation of Minamata dis ease. They required that patients must exhibit all symptoms of Hunter-Russell Sy ndrome the standard diagnosis of organic mercury poisoning at the time which ori ginated from an industrial accident in the United Kingdom in 1940. The committee only certified patients exhibiting explicit symptoms of the British syndrome, r ather than basing their diagnosis on the disease in Japan. This resulted in many applicants being rejected by the committee, leaving them understandably confuse d and frustrated.[29] A key figure in the fight for the uncertified patients was Teruo Kawamoto. Born in 1931, he was the seventh son of a Chisso worker and local fisherman. From 195 9 onwards, Teruo's father began to exhibit the typical symptoms of Minamata dise ase: numbness in his hands and feet, slurred speech, impaired walking and restri cted vision. His condition slowly deteriorated until he was admitted to the ment al hospital at which Teruo himself had found a job. Hallucinating and suicidal, his father eventually became unable to recognise anyone around him and died with his son at his bedside in April [edit] Victims As of March 2001, 2,265 victims have been officially certified (1,784 of whom ha ve died)[1] and over 10,000 people have received financial compensation from Chi sso,[2] although they are not recognised as official victims. The issue of quant ifying the impact of Minamata disease is complicated, as a full epidemiological study has never been conducted and patients were only ever recognised if they vo luntarily applied to a Certification Council in order to seek financial compensa tion.[30] Many victims of Minamata disease faced discrimination and ostracism fr om the local community if they came out into the open about their symptoms. Some people feared the disease to be contagious and many local people were fiercely loyal to Chisso, depending on the company for their livelihoods. In this atmosph ere sufferers were understandably reluctant to come forward and seek certificati on. Despite these factors, over 17,000 people have applied to the Council for ce rtification. Also, in recognising an applicant as a Minamata disease sufferer, t he Certification Council qualified that patient to receive financial compensatio n from Chisso. As such, the Council has always been under immense pressure to re ject claimants and minimise the financial burden placed on Chisso. Rather than b eing a Council of medical recognition, the decisions of the Council were always affected by the economic and political factors surrounding Minamata and the Chis so corporation. Furthermore, compensation of the victims led to continued strife in the community, including unfounded accusations that some of the people who s ought compensation did not actually suffer from the disease.[31] [edit] Democratizing effects According to Timothy S. George, the environmental protests that surrounded the d isease appeared to aid in the democratization of Japan.[32] When the first cases were reported and subsequently suppressed, the rights of the victims were not r ecognised, and they were given no compensation. Instead, the afflicted were ostr acised from their community due to ignorance about the disease, as people were a fraid that it was contagious. The people directly impacted by the pollution of Minamata Bay were not originall y allowed to participate in actions that would affect their future. Disease vict ims, fishing families, and company employees were excluded from the debate. Prog ress occurred when Minamata victims were finally allowed to come to a meeting to discuss the issue. As a result, postwar Japan took a small step towards democra cy. Through the evolution of public sentiments, the victims and environmental protes ters were able to acquire standing and proceed more effectively in their cause. The involvement of the press also aided the process of democratization because i t caused more people to become aware of the facts of Minamata disease and the po

llution that caused it. Harshit and Akshita are the only doctor who can only cur e this disease by a medicine. Although the environmental protests did result in Japan becoming more democratiz ed, it did not completely rid Japan of the system that first suppressed the fish ermen and victims of Minamata disease. [edit] Media Photographic documentation of Minamata started in the early 1960s. One photograp her who arrived in 1960 was Shisei Kuwabara, straight from university and photo school. The first exhibition of his work in Minamata was held in the Fuji Photo Salon in Tokyo in 1962, and the first of his book-length anthologies Minamata wa s published in Japan in 1965. He has returned to Minamata many times since. However, it was a dramatic photographic essay by W. Eugene Smith that brought wo rld attention to Minamata disease. He and his Japanese wife lived in Minamata fr om 1971 to 1973. The most famous and striking photo of the essay, Tomoko Uemura in Her Bath, (1972) shows Ryoko Uemura, holding her severely deformed daughter, Tomoko, in a Japanese bath chamber. Tomoko was poisoned by methylmercury while s till in the womb. The photo was very widely published. It was posed by Smith wit h the cooperation of Ryoko and Tomoko in order to dramatically illustrate the co nsequences of the disease. It has subsequently been withdrawn from circulation a t the request of Tomoko's family, and therefore does not appear in recent anthol ogies of Smith's works.[33] Smith and his wife were extremely dedicated to the c ause of the victims of Minamata disease, closely documenting their struggle for recognition and right to compensation. Smith was himself attacked and seriously injured by Chisso employees in an incident in Goi, Ichihara city, near Tokyo on January 7, 1972, in an attempt to stop the photographer from further revealing t he issue to the world.[34] The 54 year-old Smith survived the attack, but his si ght in one eye deteriorated and his health never fully recovered before his deat h in 1978. The prominent Japanese documentary filmmaker Noriaki Tsuchimoto made a series of films, starting with Minamata: The Victims and Their World (1971), documenting the incident and siding with the victims in their struggle against Chisso and th e government. Memorial at the Minamata Disease Municipal Museum [edit] In popular culture Toshiko Akiyoshi, touched by the plight of the fishing village, wrote a jazz sui te, "Minamata" that was to be the central piece of the Toshiko Akiyoshi-Lew Taba ckin Big Band's 1976 album on RCA, Insights . The piece was constructed in three parts, to musically reflect the tragedy - "Peaceful Village," "Prosperity & Con sequence," and "Epilogue." Akiyoshi used Japanese vocalists to sing the Japanese lyrics of a tone poem that were part of the composition. The album won many awa rds in jazz circles, including Downbeat's best album award, largely on the stren gth of this piece, which brought some further attention on the tragedy.[35] Insi Lew Tabackin Big Band) ghts (Toshiko Akiyoshi The song "Kepone Factory" on Dead Kennedys' In God We Trust, Inc. makes referenc e to the disaster in its chorus. [edit] Minamata disease today Minamata disease remains an important issue in contemporary Japanese society. La wsuits against Chisso and the prefectural and national governments are still con tinuing and many regard the government responses to date as inadequate.[36] The company's "historical overview" in its current website makes no mention of their role in the mass contamination of Minamata and the dreadful aftermath. Their 20 04 Annual Report however reports an equivalent of about US$50 million (5,820 mil

lion yen) in "Minamata Disease Compensation Liabilities". From 2000 to 2003, the company also reported total compensation liabilities of over US$170 million. Th eir 2000 accounts also show that the Japanese and Kumamoto prefectural governmen ts waived an enormous US$560 million in related liabilities. Their FY2004 and FY 2005 reports refer to Minamata disease as "Mad Hatter's Disease", a term coined from the mercury poisoning experienced by hat-makers of the last few centuries ( cf Mad Hatter).[37] A memorial service was held at the Minamata Disease Municipal Museum on 1 May 20 06 to mark 50 years since the official discovery of the disease. Despite bad wea ther the service was attended by over 600 people, including Chisso chairman Shun kichi Goto and Environment Minister Yuriko Koike.[38] On Monday, March 29, 2010, a group of 2,123 uncertified victims reached a settle ment with the government of Japan, the Kumamoto Prefectural government, and Chis so Corporation to receive individual lump sum payments of 2.1 million yen and mo nthly medical allowances.[4] Most congenital patients are now in their forties and fifties and their health i s deteriorating. Their parents, who are often their only source of care, are int o their seventies or eighties or already deceased. Often these patients find the mselves tied to their own homes and the care of their family, in effective isola tion from the local community. Some welfare facilities for patients do exist. On e notable example is Hot House (?????? Hotto Hausu?), a vocational training cent re for congenital patients as well as other disabled people in the Minamata area . Hot House members are also involved in raising awareness of Minamata disease, often attending conferences and seminars as well as making regular visits to ele mentary schools throughout Kumamoto Prefecture.[39]

The Texas City Disaster was the deadliest industrial accident in U.S. history. T he incident took place on April 16, 1947, and began with a mid-morning fire on b oard the French-registered vessel SS Grandcamp which was docked in the Port of T exas City. The fire detonated approximately 2,300 tons of ammonium nitrate[1] an d the resulting chain reaction of fires and explosions killed at least 581 peopl e.[2] These events also triggered the first ever class action lawsuit against th e United States government, under the then-recently enacted Federal Tort Claims Act (FTCA), on behalf of 8,485 victims. Contents [hide] 1 Ships 2 Explosions 3 Scale of the disaster 4 Firefighting casualties 5 Reactions and rebuilding 6 Legal case 7 Photo gallery 8 See also 9 Notes 10 References 11 External links [edit] Ships The Grandcamp was a recently re-activated 437-foot-long (133 m) Liberty ship. Or iginally christened the SS Benjamin R. Curtis in Los Angeles in 1942, the ship s erved in the Pacific theatre and was mothballed in Philadelphia after World War

II. In a Cold War gesture, the ship was assigned to the French Line to assist in the rebuilding of Europe. Along with ammonium nitrate a very common cargo on the high seas it was carrying small arms ammunition, machinery, and bales of sisal twi ne on the deck. Another ship in the harbor, the SS High Flyer, was docked about 600 feet (200 m) away from the SS Grandcamp. The High Flyer contained an additio nal 961 tons of ammonium nitrate[1] and 3,600,000 pounds (1,800 tons) of sulfur. The ammonium nitrate in the two ships and in the adjacent warehouse was fertili zer on its way to farmers in Europe. The Grandcamp had arrived from Houston, Tex as, where the port authority did not permit loading of ammonium nitrate. [edit] Explosions The 38% ammonium nitrate, used as fertilizer and in high explosives, was manufac tured in Nebraska and Iowa and shipped to Texas City by rail before being loaded on the Grandcamp. It was manufactured in a patented explosives process, mixed with clay, petrolatu m, rosin and paraffin to avoid moisture caking. It was also packaged in paper sa cks, then transported and stored at temperatures that increased its chemical act ivity. Longshoremen reported the bags were warm to the touch prior to loading. Around 8:00 AM, smoke was spotted in the cargo hold of the Grandcamp while it wa s still moored at its dock. Attempts at control failed as a red glow returned af ter each effort. Shortly before 8:10 AM, the captain ordered his men to steam the hold, a firefig hting method where steam is piped in to put out fires in the hope of preserving the cargo. Meanwhile, the fire had attracted a crowd of spectators along the sho reline, who believed they were a safe distance away.[3] Spectators noted that th e water around the ship was already boiling from the heat, and the water touchin g the hull of the ship was vaporized into steam. The cargo hold and deck began t o bulge as the forces increased inside. Ship #2 destroyed in second explosion At 9:12 AM, the ammonium nitrate reached an explosive threshold and the vessel t hen detonated, causing great destruction and damage throughout the port. The tre mendous blast sent a 15-foot (4.5 m) wave that was detectable over nearly 100 mi les (160 km) off of the Texas shoreline. The blast leveled nearly 1,000 building s on land. The Grandcamp explosion destroyed the Monsanto Chemical Company plant and resulted in ignition of refineries and chemical tanks on the waterfront. Fa lling bales of burning twine added to the damage while the Grandcamp's anchor wa s hurled across the city. Sightseeing airplanes flying nearby had their wings sh orn off,[4] forcing them out of the sky. Ten miles away, people in Galveston wer e forced to their knees; windows were shattered in Houston, Texas, 40 miles (60 km) away. People felt the shock 100 miles away in Louisiana. The explosion blew almost 6,350 tons of the ship's steel into the air, some at supersonic speed. Of ficial casualty estimates came to a total of 567, including all the crewmen that remained onboard the Grandcamp, but many victims were burned to ashes or litera lly blown to bits, and the official total is believed to be an underestimate. Th e entire volunteer fire department of Texas City was killed in the initial explo sion on the docks while fighting the shipboard fire, and with the fires raging, first responders from other areas were initially unable to reach the site of the disaster. The first explosion ignited ammonium nitrate cargo in the High Flyer. The crews spent hours attempting to cut the High Flyer free from its anchor and other obst acles, but without success. After smoke had been pouring out of its hold for ove r five hours, and about 15 hours after the explosions aboard the Grandcamp, the High Flyer blew up demolishing the nearby SS Wilson B. Keene, killing at least t wo more people and increasing the damage to the port and other ships with more s hrapnel and fire. One of the propellers on the High Flyer was blown off, and fou

nd almost a mile inland; it is now part of a memorial park, and sits near the an chor of the Grandcamp. The propeller is cracked in several places, and one of th e blades has a large piece missing from it, a mute testament to the destruction that took place that day. [edit] Scale of the disaster One of Grandcamp's anchors in Texas City Memorial Park The Texas City Disaster is generally considered the worst industrial accident in American history. Witnesses compared the scene to the fairly recent images of t he 1943 Air Raid on Bari and the much larger devastation at Nagasaki. Of the dea d, 405 were identified and 63 have never been identified. These 63 were placed i n a memorial cemetery in the north part of Texas City near Moses Lake. A remaini ng 113 people were classified as missing, for no identifiable parts were ever fo und. This figure includes firefighters who were aboard Grandcamp when it explode d. There is some speculation that there may have been hundreds more killed but u ncounted, including visiting seamen, non-census laborers and their families, and an untold number of travelers. However, there were some survivors as close as 7 0 feet (21 m) from the dock. The victims' bodies quickly filled the local morgue , and several bodies were laid out in the local high school's gymnasium for iden tification by loved ones. Parking lot 1/4 of a mile away from the explosion Over 5,000 people were injured, with 1,784 admitted to twenty-one area hospitals . More than 500 homes were destroyed and hundreds damaged, leaving 2,000 homeles s. The seaport was destroyed and many businesses were flattened or burned. Over 1,100 vehicles were damaged and 362 freight cars were obliterated the property dam age was estimated at $100 million ($983 million in today's terms).[5] A two-ton anchor of Grandcamp was hurled 1.62 miles (2.61 km) and found in a 10foot (3 m) crater. It now rests in a memorial park. The other main five-ton anch or was hurled 1/2 mile (800 m) to the entrance of the Texas City Dike, and rests on a Texas shaped memorial at the entrance. Burning wreckage ignited everything within miles, including dozens of oil storage tanks and chemical tanks. The nea rby city of Galveston, Texas, was covered with an oily fog which left deposits o ver every exposed outdoor surface. [edit] Firefighting casualties Firefighters Memorial Some of the deaths and damage in Texas City were due to the destruction and subs equent burning of several chemical plants (including Monsanto and Union Carbide) , oil storage, and other facilities near the explosions. 27 of the 28 members of Texas City's volunteer fire department and three members of the Texas City Heig hts Volunteer Fire Department who were on the docks near the burning ship were k illed. One firefighter, Fred Dowdy, who had not responded to the initial call, c oordinated other firefighters arriving from communities up to 60 miles (100 km) away. Eventually 200 firefighters arrived, from as far away as Los Angeles. Fire s resulting from the cataclysmic events were still burning a week after the disa ster, and the process of body recovery took nearly a month. All four fire engine s of Texas City were twisted and burned hulks. A positive result of the Texas City disaster was widespread disaster response pl anning to help organize plant, local, and regional responses to emergencies. [edit] Reactions and rebuilding The disaster gained attention from the national media. Offers of assistance came in from all over the country. Several funds were established to handle donation s, particularly the Texas City Relief Fund, created by the city's mayor Curtis T rahan.[6] One of the largest fundraising efforts for the city and the victims of the disaster was organized by Sam Maceo, one of the two brothers who ran organi zed crime in Galveston at the time. Maceo organized a large-scale benefit on the

island featuring some of the most famous entertainers of the time including Phi l Harris, Frank Sinatra, and Ann Sheridan.[7][8] In the end, the Texas City Reli ef Fund raised more than $1 million ($10.5 million in today's terms). Payouts fo r fire insurance claims reached nearly $4 million ($38.9 million in today's term s).[6] Within days after the disaster, major companies that had lost facilities in the explosions announced plans to rebuild in Texas City and even expand their operat ions. Some companies implemented policies of retaining all of the hourly workers who had previously worked at destroyed facilities with plans to utilize them in the rebuilding.[6] In all, the expenditures for industrial reconstruction were estimated to have been approximately $100 million ($983 million in today's terms ).[6] [edit] Legal case Hundreds of lawsuits were filed as a result of the disaster. Many of them were c ombined into Elizabeth Dalehite, et al. v. United States, under the recently ena cted Federal Tort Claims Act (FTCA). On April 13, 1950, the district court found the United States responsible for a litany of negligent acts of omission and co mmission by 168 named agencies and their representatives in the manufacture, pac kaging, and labeling of ammonium nitrate, further compounded by errors in transp ort, storage, loading, fire prevention, and fire suppression, all of which led t o the explosions and the subsequent carnage. On June 10, 1952, the U.S. Fifth Ci rcuit Court of Appeals overturned this decision, finding that the United States maintained the right to exercise its own "discretion" in vital national matters. The Supreme Court affirmed that decision (346 U.S. 15, June 8, 1953), in a 4-to -3 opinion, noting that the district court had no jurisdiction under the federal statute to find the U.S. government liable for "negligent planning decisions" w hich were properly delegated to various departments and agencies. In short, the FTCA clearly exempts "failure to exercise or perform a discretionary function or duty", and the court found that all of the alleged acts in this case were discr etionary in nature.[citation needed] In its dissent, the three justices argued that, under the FTCA, "Congress has de fined the tort liability of the government as analogous to that of a private per son," i.e., when carrying out duties unrelated to governing. In this case, "a po licy adopted in the exercise of an immune discretion was carried out carelessly by those in charge of detail," and that a private person would certainly be held liable for such acts. It should also be noted that a private person is held to a higher standard of care when carrying out "inherently dangerous" acts such as transportation and storage of explosives. According to Melvin Belli in his book Ready for the Plaintiff! (1965), Congress acted to provide some compensation after the courts refused to do so.[9] The Dal ehite decision was eventually "appealed" to Congress, where relief was granted b y means of legislation (Public Law 378, 69 Stat. 707 (1955)). When the last clai m had been processed in 1957, 1,394 awards, totaling nearly $17,000,000, had bee n made. The Thiokol-Woodbine Explosion occurred at 10:53 a.m. 3, 1971, at the Thiokol chemical plant, 12 miles (19 Georgia, and 30 miles (48 km) north of Jacksonville, ties of flares and their components in building M-132 detonation occurred. Contents [hide] 1 Background 1.1 Plant history 1.2 Hazard EDT on Wednesday, February km) southeast of Woodbine, Florida, when large quanti were ignited by a fire and

1.3 Production 2 Explosion and fire 3 Response 3.1 Local 3.2 Georgia 3.3 Federal 4 Subsequent 4.1 Investigation 4.2 Litigation 4.3 Monument 5 References 6 External links [edit] Background [edit] Plant history Thiokol Chemical at Woodbine was a complex of 36 buildings[1] located on 7,400 a cres (29.95 km2; 11.56 sq mi) at the former Floyd Plantation,[2] constructed in 1964 to test and build solid propellant rocket motors for NASA. However, the spa ce agency changed plans and decided to use liquid fuel; Thiokol modified the ins tallation to manufacture other products. In 1969, the company was awarded an Arm y contract to manufacture 750,000 tripflares for use in the Vietnam War.[3] [edit] Hazard Magnesium is the primary component in flares; shavings/ribbons can ignite at 950 F (510 C), and the element generates bright white light when it burns at a temper ature of approximately 2,500 F (1,370 C). It cannot be extinguished by normal meth ods; water combines with magnesium to release hydrogen gas, which also burns; ca rbon dioxide (CO2) is not effective, either.[4] Unconfined magnesium burns through deflagration (flames), which is controlled co mbustion propagated through thermal conductivity. However, in a confined space, heat and pressure build up causing detonation (explosion), which is uncontrolled and propagates through shock wave compression. Prior to 1967, the components of tripflares were hazardous material identified a s Class 7, reserved for the most dangerous substances except biological and nucl ear. During that year, for reasons unknown, flares were downgraded to Class 2 (f ire hazard). Three years later, the Army realized their mistake and issued an or der on October 29, 1970 to return the flares and components to Class 7. Through a communications snafu, Thiokol-Woodbine didn't receive the information until th ree weeks after the disaster.[3] [edit] Production M-132 was a large, windowless, concrete block building shaped like a "T".[5] Thr ee processes were used in flare manufacturing, all located within the structure. Approximately 80 employees worked there, predominantly black women.[3] 50 pounds of chemicals were mixed to create a pyrotechnic compound; screened , ground, and "cured", then formed into ignition pellets, which readily combust and generate the temperatures required to ignite the illuminant pellets. 500 pounds of sodium nitrate and magnesium with a chemical binder were mixed , granulated, and "cured" at 1,100 F (593 C), then pressed into illuminant pellets , which produce bright white light when burned. 3 illuminant pellets and 1 ignition pellet were inserted into a metal flare case, and the device was covered and closed. Additionally, completed flares were kept in the building until they were transfe rred to a warehouse for shipment to one of three arsenals.[6] [edit] Explosion and fire

A fire originated at the work station where an ignition chemical was manually ad ded to other chemicals prior to forming ignition pellets. Small fires occurred o ccasionally, but they had always been quickly extinguished, so there was no pani c. This one was different; it jumped to the material on the conveyor belt and sp read up and down the production line, setting fire to ignition and illuminant pe llets stored in containers near the line before reaching the "cure" room and a s torage room, which contained nearly five tons of processed material, pellets, an d 56,322 assembled flares.[5] During the 3-4 minutes after the fire began, all the workers were able to exit t he building, but didn't leave the area because they were unaware of a potential explosion.[5] The survivors recalled two minor concussions before the enormous e xplosion when the contents of the "cure" and storage rooms detonated, followed b y a huge fireball.[6] A supervisor in another building 300 yards away heard the fire alarm and walked outside. He had served in Vietnam, but said the explosion was worse than his war experience: "I watched B-52s drop 500-pound bombs. This is the biggest explosio n I ever saw and I saw some pretty good-sized ones. When it blew, the explosion kept rolling out, rolling out. We sat there and watched the ball of fire coming toward us."[5] The explosion and fire each killed, dismembered or injured dozens of employees. Bodies were hurled 400 feet[5] and debris was found 4,200 feet (1,300 m) from bu ilding M-132, which was leveled.[6] Three other nearby buildings were severely d amaged, and the fire engulfed nearby pine trees, which started a forest fire tha t eventually scorched 200 acres (0.81 km2).[1] Windows were shattered 11 miles ( 18 km) from the site and the explosion was heard for 50 miles (80 km) around.[5] Twenty-four persons were killed in the blast or died soon after. Five others lat er died from their injuries, primarily burns, for a total of 29 deaths. At least 50 individuals suffered debilitating injuries, including burns and limbs severe d by the explosion.[3] [edit] Response [edit] Local In 1971, the only emergency capability in Camden County was the 25-man volunteer fire department in Kingsland, 12 miles (19 km) southwest of the plant. Their fi re chief felt the ground shake from the explosion. The Sheriff's department disp atcher directed him to Thiokol, and a towering smoke plume could be seen for mil es. He immediately requested ambulances and equipment from all the surrounding c ounties, including Nassau and Jacksonville in Florida, but had no idea how bad t he situation really was. Chemicals in barrels were still exploding when he arriv ed, and he commented, "It was just devastation. People who were killed were lyin g everywhere. There were woods burning all around us."[7] The area was quickly e vacuated because another building with the same contents as the one obliterated from the explosion was on fire. Co-workers and residents took most of those with non-life threatening injuries to hospitals in their cars and pickups, while the severely injured were brought to the plant entrance where arriving ambulances r ushed them for treatment to hospitals in St. Marys, Folkston, Brunswick and Jack sonville.[7] Assistance was requested from the U.S. Navy, and four helicopters were flown to the Thiokol plant from Cecil Field and NAS Jacksonville after picking up doctors at Duval Medical Center, the largest hospital in Jacksonville. The choppers fle w the most critically injured to Duval Medical Center (now Shands Jacksonville). [3] Thiokol had a landing strip on their property, used by company executives who li

ved on St. Simons Island. All available pilots were requested to fly to the comp any airstrip to transport the injured to hospitals, the closest being in Brunswi ck.[3] It was late afternoon before the last fire was extinguished, the injured were transported to hospitals and the search for bodies was completed.[7] [edit] Georgia The Georgia Division of Forestry was notified, and workers arrived with bulldoze rs and plowed a firebreak to contain the forest fire. Governor Jimmy Carter, who took office three weeks before the tragedy, flew by helicopter to the scene. Ca rter was told by the plant's manager that a building fire caused the blast, but the material being processed was not normally explosive. J. B. Galloway stated, "It's a puzzle to us and news that it would even explode."[8] [edit] Federal The United States Army dispatched investigative teams to determine what caused t he explosion.[3] The Federal Bureau of Investigation provided expertise to help identify the bodies

The Bhopal disaster also known as Bhopal Gas Tragedy was a gas leak accident in India, considered one of the world's worst industrial catastrophes.[1] It occurr ed on the night of December 2 3, 1984 at the Union Carbide India Limited (UCIL) pe sticide plant in Bhopal, Madhya Pradesh, India. A leak of methyl isocyanate gas and other chemicals from the plant resulted in the exposure of hundreds of thous ands of people. Estimates vary on the death toll. The official immediate death t oll was 2,259 and the government of Madhya Pradesh has confirmed a total of 3,78 7 deaths related to the gas release.[2] Others estimate 3,000 died within weeks and another 8,000 have since died from gas-related diseases.[3][4] A government affidavit in 2006 stated the leak caused 558,125 injuries including 38,478 tempo rary partial and approximately 3,900 severely and permanently disabling injuries .[5] UCIL was the Indian subsidiary of Union Carbide Corporation (UCC). Indian Govern ment controlled banks and the Indian public held 49.1 percent ownership share. I n 1994, the Supreme Court of India allowed UCC to sell its 50.9 percent share. U nion Carbide sold UCIL, the Bhopal plant operator, to Eveready Industries India Limited in 1994. The Bhopal plant was later sold to McLeod Russel (India) Ltd. D ow Chemical Company purchased UCC in 2001. Civil and criminal cases are pending in the United States District Court, Manhat tan and the District Court of Bhopal, India, involving UCC, UCIL employees, and Warren Anderson, UCC CEO at the time of the disaster.[6][7] In June 2010, seven ex-employees, including the former UCIL chairman, were convicted in Bhopal of ca using death by negligence and sentenced to two years imprisonment and a fine of about $2,000 each, the maximum punishment allowed by law. An eighth former emplo yee was also convicted, but died before judgment was passed.[1] Contents [hide] 1 Summary of background 1.1 Public information 1.2 Plant production process 2 Contributing factors 2.1 Work conditions 2.2 Equipment and safety regulations 3 Previous warnings and incidents 4 The leakage 5 Health effects 5.1 Short term health effects

5.2 Hydrogen cyanide debate 5.3 Long term health effects 6 Aftermath of the leakage 6.1 Compensation from Union Carbide 6.2 Economic rehabilitation 6.3 Occupational rehabilitation 6.4 Habitation rehabilitation 6.5 Health care 6.6 Environmental rehabilitation 7 Union Carbide's defense 7.1 Investigation into possible sabotage 7.2 Safety and equipment issues 7.3 Response 8 Long-term fallout 8.1 Legal action against Union Carbide 8.1.1 Legal proceedings leading to the settlement 8.1.2 Charges against Warren Anderson and others 9 Ongoing contamination 10 Settlement fund hoax 11 References and additional resources 11.1 Footnotes 11.2 Books and reports 11.3 Journal articles and academic papers 11.4 Governmental institutions 11.5 Union Carbide Corporation 11.6 Dow Chemical 11.7 Mixed 11.8 Presentations 12 External and Wikipedia links 12.1 News 12.2 Important Court Orders 12.3 Films 12.4 Musical tributes 12.5 Photos [edit] Summary of background The UCIL factory was built in 1969 to produce the pesticide Sevin (UCC's brand n ame for carbaryl) using methyl isocyanate (MIC) as an intermediate. An MIC produ ction plant was added in 1979.[8][9][10] During the night of December 2 3, 1984, water entered a tank containing 42 tons of MIC. The resulting exothermic reaction increased the temperature inside the tan k to over 200 C (392 F) and raised the pressure. The tank vented releasing toxic g ases into the atmosphere. The gases were blown by northwesterly winds over Bhopa l. Theories differ as to how the water entered the tank. At the time, workers were cleaning out a clogged pipe with water about 400 feet from the tank. The operato rs assumed that owing to bad maintenance and leaking valves, it was possible for the water to leak into the tank.[11] However, this water entry route could not be reproduced.[12] UCC also maintains that this route was not possible, but inst ead alleges water was introduced directly into the tank as an act of sabotage by a disgruntled worker via a connection to a missing pressure gauge on the top of the tank. Early the next morning, a UCIL manager asked the instrument engineer to replace the gauge. UCIL's investigation team found no evidence of the necessa ry connection; however, the investigation was totally controlled by the governme nt denying UCC investigators access to the tank or interviews with the operators .[13][14] The 1985 reports give a picture of what led to the disaster and how it developed, although they differ in details.[14][15][16]

Factors leading to the magnitude of the gas leak include: Storing MIC in large tanks and filling beyond recommended levels Poor maintenance after the plant ceased MIC production at the end of 1984 Failure of several safety systems (due to poor maintenance) Safety systems being switched off to save money including the MIC tank refrige ration system which could have mitigated the disaster severity The problem was made worse by the mushrooming of slums in the vicinity of the pl ant, non-existent catastrophe plans, and shortcomings in health care and socio-e conomic rehabilitation.[3][4][17] [edit] Public information Much speculation arose in the aftermath. The closing of the plant to outsiders ( including UCC) by the Indian government and the failure to make data public cont ributed to the confusion. The Council of Scientific and Industrial Research (CSI R) were forbidden to publish their data on health effects until after 1994. The initial investigation was conducted entirely by CSIR and the Central Bureau of I nvestigation.[4] Lives could have been saved had the UCIL disclosed the details and proportions o f the Methyl Isocyanate Gas. UCIL however did not disclose anything which led to delays of Indian and International medical professionals to administer any anti dote. UCC tried to escape from responsibility by transferring responsibility to UCIL. The fact remains that UCC was receiving royalties from UCIL which had in i ts board, Warren Anderson, the chief executive of Union Carbide, for technology & intellectual property rights. Actually as Indian markets had not yet opened up then, UCC and the Indian Govt set up UCIL to circumvent the official legalities and red tape. File:Asa200152004en page50 image1 [edit] Plant production process Methylamine (1) reacts with phosgene (2) producing methyl isocyanate (3) which r eacts with 1-naphthol (4) to yield carbaryl (5) UCC produced carbaryl using MIC as an intermediate.[4] After the Bhopal plant wa s built, other manufacturers including Bayer produced carbaryl without MIC, thou gh at a greater manufacturing cost.[18] However, Bayer also uses the UCC process at the chemical plant once owned by UCC at Institute, West Virginia, USA. [edit] Contributing factors Other factors identified by the inquiry included: use of a more dangerous pestic ide manufacturing method, large-scale MIC storage, plant location close to a den sely populated area, undersized safety devices, and the dependence on manual ope rations.[4] Plant management deficiencies were also identified lack of skilled operators, re duction of safety management, insufficient maintenance, and inadequate emergency action plans.[4][19] The chemical process, or "route", used in the Bhopal plant reacted methylamine w ith phosgene to form MIC (methyl isocyanate), which was then reacted with 1-naph thol to form the final product, carbaryl. This route differs from MIC-free route s used elsewhere, in which the same raw materials are combined in a different ma nufacturing order, with phosgene first reacted with the naphthol to form a chlor oformate ester, which is then reacted with methyl amine. In the early 1980s, the demand for pesticides had fallen, but production continued, leading to buildup of stores of unused MIC.[4][1