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Patterns of Injury
Published in Mansoor Khan, David Nott, Fundamentals of Frontline Surgery, 2021
Danyal Magnus, Katherine A. Brown, Mansoor Khan, William G. Proud
Bhopal in India is globally remembered due to pressure developing in a storage vessel, leading to an explosive gas release followed by further gas venting, in December 1984. The release of methyl isocyanate led to the immediate death of between 3,787 and 16,000. A few 500,000 are said to have suffered ill effects.
The Toxic Environment and Its Medical Implications with Special Emphasis on Smoke Inhalation
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Jacob Loke, Richard A. Matthay, G. J. Walker. Smith
Various physiological and pulmonary responses have been used to correlate these data from laboratory animals with those of human victims at the industrial plant methyl isocyanate accident in Bhopal, India. In Chapter 3, Alarie and Schaper correlate the obstructive ventilatory pattern in animals with the obstructive airway disease noted among surviving victims in Bhopal. Thus, besides establishing that methyl isocyanate is a potent sensory and pulmonary irritant, these animal studies are valuable in extrapolating “safe” amounts of exposure for humans (Ferguson et al., 1986).
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
The Bhopal disaster, also referred to as the Bhopal gas tragedy, was a gas leak incident in India, considered the world's worst industrial disaster.590 It occurred on the night of 2–3 December 1984 at the Union Carbide India Limited (UCIL) pesticide plant in Bhopal, Madhya Pradesh. Over 500,000 people were exposed to methyl isocyanate gas and other chemicals. The toxic substance made its way in and around the shantytowns located near the plant.591 Estimates vary on the death toll. The official immediate death toll was 2259. The government of Madhya Pradesh confirmed a total of 3787 deaths related to the gas release.592 Others estimate that 8000 died within two weeks and another 8000 or more have since died from gas-related diseases.593–595 A government affidavit in 2006 stated that the leak caused 558,125 injuries including 38,478 temporary partial injuries and approximately 3900 severely and permanently disabling injuries.596
Methyl isocyanate inhalation induces tissue factor-dependent activation of coagulation in rats
Published in Drug and Chemical Toxicology, 2019
Raymond C. Rancourt, Jacqueline S. Rioux, Livia A. Veress, Rhonda B. Garlick, Claire R. Croutch, Eric Peters, William Sosna, Carl W. White
The mechanisms of airway injury by toxic inhaled chemicals (TICs) are incompletely understood, and therapies for such injuries are often lacking, resulting in high morbidity and mortality in exposed individuals. Accidental discharge of TICs can be extremely hazardous as evidenced by the release of methyl isocyanate (MIC) at Bhopal, India, in 1984. During that incident, more than 500 people perished in the immediate vicinity before emergency response arrival. At least 2,000 additional individuals died in the immediate days after exposure (Dhara and Dhara 2002). Reports from the media indicated that many deaths occurred within minutes to a few hours after MIC had drifted into Bhopal (Dhara and Dhara 2002). Due to the emergent disaster, however, no systematic autopsy data has been published.
Employing in vitro metabolism to guide design of F-labelled PET probes of novel α-synuclein binding bifunctional compounds
Published in Xenobiotica, 2021
Chukwunonso K. Nwabufo, Omozojie P. Aigbogun, Kevin J.H Allen, Madeline N. Owens, Jeremy S. Lee, Christopher P. Phenix, Ed S. Krol
Metabolites M8A and M8B possess the same retention time and are both 14 Da less than the parent compound. This is consistent with the non-fluorinated C8-6-I in which M5A and M5B correspond to N1 and N3 demethylation (see Figure 5(C,D)). The MS/MS spectrum of the precursor ion (m/z 442.27) reveals three major diagnostic peaks: (M8A1) at m/z 326.26 corresponding to the loss of indene from the precursor ion, (M8A2) at m/z 306.37 corresponding to the loss of indene followed by loss of hydrogen fluoride and, (M8A3) at m/z 309.35 corresponding to the loss of indene followed by loss of terminal ammonia. Product ion M8A4 at m/z 295.33 is produced as a result of methyl amine loss from M8A1 and this product ion can further lose hydrogen fluoride to yield M8A6 (Figure S11(A,B)). Two product ions allowed us to determine that there are two demethylated metabolites and the position of demethylation. The first product ion is the loss of isocyanic acid (O = C=NH, 43 Da) from M8A2 at m/z 306.37 to M8A7 at m/z 263.36. The loss of isocyanic acid instead of methyl isocyanate indicates that N1 of the precursor ion lacks a methyl group (Figure S11(B)). Conversely, product ion M8B8 with m/z 249.36 corresponds to the loss of methyl isocyanate (O = C=NCH3, 57 Da) from M8B2 (Figure S11(C)). This indicates that the N1 of the precursor ion has a methyl group present, however the loss of 14 Da is as a result of the lack of methyl group on N3. Therefore, M8A and M8B are both N1 and N3 demethylated metabolites of the caffeine moiety of 19F-[C8-6-I].