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The greatest industrial disaster of India; was it man-made?

Summary of background and causes:

Health effects:
Short term health effects:

Reversible reaction of glutathione (top) with methyl isocyanate (MIC, middle) allows the MIC to be transported into the body

The leakage caused many short term health effects in the surrounding areas. Apart from MIC, the gas cloud may have contained phosgene, hydrogen cyanide, carbon monoxide, hydrogen chloride, oxides of nitrogen, monomethyl amine (MMA) and carbon dioxide, either produced in the storage tank or in the atmosphere.

The gas cloud was composed mainly of materials denser than the surrounding air, stayed close to the ground and spread outwards through the surrounding community. The initial effects of exposure were coughing, vomiting, severe eye irritation and a feeling of suffocation. People awakened by these symptoms fled away from the plant. Those who ran inhaled more than those who had a vehicle to ride. Owing to their height, children and other people of shorter stature inhaled higher concentrations. Many people were trampled trying to escape.

Thousands of people had succumbed by the morning hours. There were mass funerals and mass cremations as well as disposal of bodies in the Narmada river. 170,000 people were treated at hospitals and temporary dispensaries. 2,000 buffalo, goats, and other animals were collected and buried. Within a few days, leaves on trees yellowed and fell off. Supplies, including food, became scarce owing to suppliers' safety fears. Fishing was prohibited as well, which caused further supply shortages.

A total of 36 wards were marked by the authorities as being "gas affected", affecting a population of 520,000. Of these, 200,000 were below 15 years of age, and 3,000 were pregnant women. In 1991, 3,928 deaths had been certified. Independent organizations recorded 8,000 dead in the first days. Other estimations vary between 10,000 and 30,000. Another 100,000 to 200,000 people are estimated to have permanent injuries of different degrees.

The acute symptoms were burning in the respiratory tract and eyes, blepharospasm, breathlessness, stomach pains and vomiting. The causes of deaths were choking, reflexogenic circulatory collapse and pulmonary oedema. Findings during autopsies revealed changes not only in the lungs but also cerebral oedema, tubular necrosis of the kidneys, fatty degeneration of the liver and necrotising enteritis. The stillbirth rate increased by up to 300% and neonatal mortality rate by 200%.

Hydrogen cyanide debate:

Whether hydrogen cyanide was present in the gas mixture is still a controversy. Exposed at higher temperatures, MIC breaks down to hydrogen cyanide (HCN). According to Kulling and Lorin, at +200 °C, 3% of the gas is HCN. However, according to another scientific publication, MIC when heated in the gas-phase starts breaks down to hydrogen cyanide (HCN) and other products above 400 °C. Concentrations of 300 ppm can lead to immediate collapse.

Laboratory replication studies by CSIR and UCC scientists failed to detect any HCN or HCN-derived side products. Chemically, HCN is known to be very reactive with MIC. HCN is also known to react with hydrochloric acid, ammonia, and methylamine (also produced in tank 610 during the vigorous reaction with water and choloroform) and also with itself under acidic conditions to form trimers of HCN called triazenes. None of the HCN-derived side products were detected in the tank residue.

The non-toxic antidote sodium thiosulfate (Na2S2O3) in intravenous injections increases the rate of conversion from cyanide to non-toxic thiocyanate. Treatment was suggested early, but because of confusion within the medical establishments, it was not used on larger scale until June 1985. .....more

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