Occupational Asthma Reference

Sriramachari S, The Bhopal gas tragedy: An environmental disaster, Current Science, 2004;86:905-920,

Keywords: Bhopal, acute inhalation injury, methyl isocyanate, hydrogen cyanide, pm, histoligy, India

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Abstract

The multi-disciplinary study of histopathology and toxicology of Bhopal gas tragedy resolved several issues. First, the progression of severe pulmonary oedema to chronic fibrosis was confirmed experimentally, following a single exposure to MIC. Analysis of the residue in Tank 610 revealed over 21 chemicals. Apart from MIC and HCN, some of them were tracked down to the blood and viscera of dead and living ‘exposees’. The rationale of NaTS therapy was substantiated by elevated urinary NaSCN levels in Double Blind Clinical Trials as well as patients. Apart from cyanide, the ‘cherry red’ discolouration was also shown to result from binding of MIC to end-terminal valine residues of Hb, as shown by changes in 2–3DPG levels and blood gas profiles. The finding of Ncarbamoylation of several other end-terminal amino acids of tissue proteins confirmed the distribution of MIC within the body, although the underlying mechanism is not yet fully understood. Possibly, the much faster S-carbamoylated compounds of the blood like glutathione and other sulphydryl containing enzymes like rhodanese could be responsible for re-circulation of MIC and protracted cyanide toxicity. It is hoped that eventually the enigma of the ‘Bio-chemical Lesion’ of MIC toxicity will be unraveled.

Plain text: The multi-disciplinary study of histopathology and toxicology of Bhopal gas tragedy resolved several issues. First, the progression of severe pulmonary oedema to chronic fibrosis was confirmed experimentally, following a single exposure to MIC. Analysis of the residue in Tank 610 revealed over 21 chemicals. Apart from MIC and HCN, some of them were tracked down to the blood and viscera of dead and living 'exposees'. The rationale of NaTS therapy was substantiated by elevated urinary NaSCN levels in Double Blind Clinical Trials as well as patients. Apart from cyanide, the 'cherry red' discolouration was also shown to result from binding of MIC to end-terminal valine residues of Hb, as shown by changes in 2-3DPG levels and blood gas profiles. The finding of Ncarbamoylation of several other end-terminal amino acids of tissue proteins confirmed the distribution of MIC within the body, although the underlying mechanism is not yet fully understood. Possibly, the much faster S-carbamoylated compounds of the blood like glutathione and other sulphydryl containing enzymes like rhodanese could be responsible for re-circulation of MIC and protracted cyanide toxicity. It is hoped that eventually the enigma of the 'Bio-chemical Lesion' of MIC toxicity will be unraveled.

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