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Deaths Due to Asphyxiant Gases
Published in Sudhir K. Gupta, Forensic Pathology of Asphyxial Deaths, 2022
Fatality of a case is decided by blood concentration of thiosulphate. Its presence in the blood together with the analysis of sulfide are suggestive of fatal cases. Thiosulfate in urine is the only indicator to prove H2S poisoning in nonfatal cases11. And its nondetectability in urine is suggestive of acute death.12 Radiologically on X-ray and CT scan, pleural effusion and consolidation can easily be appreciated.
CBRN and the Trauma Victim
Published in Ian Greaves, Keith Porter, Jeff Garner, Trauma Care Manual, 2021
Ian Greaves, Keith Porter, Jeff Garner
These include oxygen, respiratory support and, where appropriate, cyanide antidotes including sodium nitrite/thiosulphate and cobalt-chelation therapy (including hydroxocobalamin). The management of hydrogen sulphide (H2S) poisoning is sodium nitrite and oxygen. Sodium nitrite for cyanide and H2S poisoning is used with the intention of causing a MetHb level of ~30% in order to dissociate the poison from the mitochondria and back into the intravascular compartment. It should, however, be avoided in cases of trauma (haemorrhage) or carbon mon-oxide (CO) poisoning.
Asphyxia
Published in Kevin L. Erskine, Erica J. Armstrong, Water-Related Death Investigation, 2021
Hydrogen sulfide is a gas originating from the natural environment, organic decomposition, and industry. Specific sources include sewers, septic tanks, the manufacture of petroleum-containing products and paper, natural gas, and volcanoes.8 It is commonly described as having a rotten egg odor. At higher concentrations in the ambient environment and with prolonged inhalation, its odor becomes undetectable due to paralysis of the olfactory nerves, and respiratory impairment and unconsciousness may ensue.8 Due to the occupational hazards and past reports of deaths, OSHA regulations restrict the amount of exposure and require training, equipment for detection of the gas, and the use of respiratory protective equipment.13,14 The action of H2S is at the cellular level, similar to cyanide. During the scene investigation, blackening of metal objects, including coins, may be noted. At autopsy, a greenish discoloration of the tissues, in addition to the characteristic odor, may be noted. Prompt toxicological testing may reveal elevated sulfate ion or thiosulfate levels.8
Descriptive epidemiology of clinically significant occupational poisonings, United States, 2008–2018
Published in Clinical Toxicology, 2021
John W. Downs, Brandon K. Wills, Kirk L. Cumpston, S. Rutherfoord Rose
Whereas intentional poisonings are more frequently ingestions, unintended occupational poisonings are frequently inhalational or dermal in nature. An occupational inhalational fatality was recently widely publicized following the accidental creation of chlorine gas in a restaurant [11]. In our study, the primary route of exposure reported in fatal poisoning was inhalational in over 80% of cases. This reinforces the need for employers and worksites to educate workers on the chemical risks associated with their workplace, particularly inhalational risks, and to emphasize the use of proper personal respiratory protection and safety measures. Although the annual number of deaths attributable to hydrogen sulfide is small, it has remained a killer of workers despite the passage of 30 years, suggesting that occupations and industries with risk for hydrogen sulfide exposure, such as the natural gas and sewage processing industries may need to improve their safety efforts. Similarly, carbon monoxide killed on average 1 worker per year during the study period. While this number is small, it is still disheartening when one considers that these deaths were uniformly preventable with proper education about carbon monoxide sources and the use of appropriate exposure controls to include respiratory protection when necessary.
Intramuscular cobinamide versus saline for treatment of severe hydrogen sulfide toxicity in swine
Published in Clinical Toxicology, 2019
Patrick C. Ng, Tara B. Hendry-Hofer, Norma Garrett, Matthew Brenner, Sari B. Mahon, Joseph K. Maddry, Philippe Haouzi, Gerry R. Boss, Thomas F. Gibbons, Allyson A. Araña, Vikhyat S. Bebarta
Intramuscular cobinamide was effective in improving survival in this large swine model of severe hydrogen sulfide toxicity. Sulfide is a potentially deadly toxin. Currently, there are no established antidotes. Given the potential exposures in industry, in mass casualty settings, and by terrorists as described by national organizations like the Department of Homeland Security, an ideal antidote would be one that can be administered easily in the prehospital setting. An antidote that can be administered intramuscularly, in small volumes, is ideal. Cobinamide is a promising agent that can potentially fill this need [16] . Future studies will be directed at further understanding cobinamide in various doses and its effects on sulfide toxicity. Additionally, our group is developing an inhalational model for sulfide toxicity. We plan to study the efficacy of cobinamide in this model.
Bulk phase resource ratio alters carbon steel corrosion rates and endogenously produced extracellular electron transfer mediators in a sulfate-reducing biofilm
Published in Biofouling, 2019
Gregory P. Krantz, Kilean Lucas, Erica L.- Wunderlich, Linh T. Hoang, Recep Avci, Gary Siuzdak, Matthew W. Fields
Protein concentrations were measured with a Qubit Protein Assay Kit (Life Technologies, Carlsbad, CA, USA). Carbohydrate concentration was measured as previously described (Clark et al. 2006). Lactate and acetate were quantified using an Ultimate 3000 high performance liquid chromatography instrument with a 300 mm × 7.8 mm HPLC Organic Acid Analysis Aminex HPX-87H Ion Exclusion Column (Thermo Scientific, Dionex Germering, Germany). Sulfate and hydrogen sulfide concentrations were measured using a Hach Colorimeter (Hach, Co., Loveland, CO, USA) with the associated sulfate assay (Method 10248) and sulfide assay (Method 8131).