What are the affects of bhopal gas tradegy on government and people ??
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Reviewed the studies of human health effects that resulted from exposure to methyl isocyanate gas that leaked from the Union Carbide plant in Bhopal, India, in Dec. 1984. The studies were conducted during both the early and late recovery periods. The Bhopal gas tragedy is undoubtedly one of the worst industrial disasters in the history of mankind resulting in mortality of 2500-6000 and debilitating over 200 000 people. Inhabitants in the township were exposed to different degrees and there are more than 500 000 registered victims that survived the tragedy
The accident was apparently initiated by the introduction of water into the Methyl Iso Cyanate (MIC) storage tank resulting in an uncontrollable reaction with liberation of heat and escape of MIC in the form of a gas.
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 sulphydrylcontaining 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
The two ICMR projects on histopathology and toxicology have more than fulfilled the initial hopes and expectations. The sequence of pathological changes in the acute, sub-acute and chronic stages have been clearly delineated. Experimental studies with MIC and its aqueous derivatives have confirmed the pathogenesis and pulmonary changes after single exposure are comparable to human autopsy findings.
The accident was apparently initiated by the introduction of water into the Methyl Iso Cyanate (MIC) storage tank resulting in an uncontrollable reaction with liberation of heat and escape of MIC in the form of a gas.
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 sulphydrylcontaining 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
The two ICMR projects on histopathology and toxicology have more than fulfilled the initial hopes and expectations. The sequence of pathological changes in the acute, sub-acute and chronic stages have been clearly delineated. Experimental studies with MIC and its aqueous derivatives have confirmed the pathogenesis and pulmonary changes after single exposure are comparable to human autopsy findings.
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Reviewed the studies of human health effects that resulted from exposure to methyl isocyanate gas that leaked from the Union Carbide plant in Bhopal, India, in Dec. 1984. The studies were conducted during both the early and late recovery periods. The Bhopal gas tragedy is undoubtedly one of the worst industrial disasters in the history of mankind resulting in mortality of 2500-6000 and debilitating over 200 000 people. Inhabitants in the township were exposed to different degrees and there are more than 500 000 registered victims that survived the tragedy
The accident was apparently initiated by the introduction of water into the Methyl Iso Cyanate (MIC) storage tank resulting in an uncontrollable reaction with liberation of heat and escape of MIC in the form of a gas.
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 sulphydrylcontaining 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
The two ICMR projects on histopathology and toxicology have more than fulfilled the initial hopes and expectations. The sequence of pathological changes in the acute, sub-acute and chronic stages have been clearly delineated. Experimental studies with MIC and its aqueous derivatives have confirmed the pathogenesis and pulmonary changes after single exposure are comparable to human autopsy findings.In-depth molecular studies of ocular, respiratory, reproductive, immunological, genetic and psychological health carried out so far have helped to understand the extent and severity of long term effects associated with the disaster.Long-term monitoring of the affected community and use of appropriate methods of investigation that include well-designed cohort studies for such conditions, characterization of personal exposure and accident analysis have helped to determine several clinical and epidemiological inadequacies, including poor study design, bias and inaccurate exposure classification of studies conducted previously on victims of the tragedy.
The accident was apparently initiated by the introduction of water into the Methyl Iso Cyanate (MIC) storage tank resulting in an uncontrollable reaction with liberation of heat and escape of MIC in the form of a gas.
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 sulphydrylcontaining 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
The two ICMR projects on histopathology and toxicology have more than fulfilled the initial hopes and expectations. The sequence of pathological changes in the acute, sub-acute and chronic stages have been clearly delineated. Experimental studies with MIC and its aqueous derivatives have confirmed the pathogenesis and pulmonary changes after single exposure are comparable to human autopsy findings.In-depth molecular studies of ocular, respiratory, reproductive, immunological, genetic and psychological health carried out so far have helped to understand the extent and severity of long term effects associated with the disaster.Long-term monitoring of the affected community and use of appropriate methods of investigation that include well-designed cohort studies for such conditions, characterization of personal exposure and accident analysis have helped to determine several clinical and epidemiological inadequacies, including poor study design, bias and inaccurate exposure classification of studies conducted previously on victims of the tragedy.
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