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Deaths Due to Asphyxiant Gases
Published in Sudhir K. Gupta, Forensic Pathology of Asphyxial Deaths, 2022
Postmortem Findings: No specific finding was identified during the autopsy. The entire body and clothes were smeared with marshy foul-smelling materials of the sewage. Conjunctivas were congested. Finger nailbeds were intensely bluish (Figure 11.2). Lungs in all three cases were congested and edematous. Sub pleural hemorrhages of different sizes were present in all three cases (Figure 11.3). All internal organs were congested. The stomach mucosa of all the cases showed congestion (Figure 11.4). Along with routine viscera, blood under paraffin wax layer seal was also sent for chemical analysis in view of identification of dissolved sewer gas if any. Chemical analysis confirmed the presence of H2S (Hydrogen Sulphide) in the blood sample of all three cases. All the cases showed the presence of Ethyl Alcohol in blood samples too.
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
Low level exposure to hydrogen sulfide: a review of emissions, community exposure, health effects, and exposure guidelines
Published in Critical Reviews in Toxicology, 2023
Stuart Batterman, Amelia Grant-Alfieri, Sung-Hee Seo
This report examines the recent literature pertaining to health effects caused by the inhalation of hydrogen sulfide (H2S) gas, focusing on effects at low exposure levels that are relevant to community exposure. We seek to gather and critically assess evidence of community exposure to H2S, identify culpable emission sources, and analyze human health effects associated with chronic exposure to H2S at low concentrations. We specifically focus on literature relevant to low-level community exposure to assess the minimum exposure levels associated with adverse health effects, although we also consider low-level occupational exposures given its relevance to understanding chronic health effects. We define low level exposures as H2S concentrations below 0.1 ppm, medium level as between 0.1 and 1 ppm, and high level exposures as above 1 ppm. These limits are flexible given the importance of exposure duration and the variation of concentrations that may be measured or estimated in any particular study. An important distinction, however, is that the low and medium-level categories are distinctly lower than current standards or guidelines for workplace settings, which mostly range from 1 to 50 ppm.
A comprehensive review of treatments for hydrogen sulfide poisoning: past, present, and future
Published in Toxicology Mechanisms and Methods, 2023
Cristina Santana Maldonado, Abigail Weir, Wilson K. Rumbeiha
Hydrogen sulfide (H2S) is a toxic gas with a distinctive smell of rotten egg. The discovery of endogenously produced H2S led to research aiming to understand its physiological roles and its potential applications for the treatment of several chronic diseases via multiple mechanisms including anti-inflammatory and cytoprotective effects in tissue injury, anti-oxidant properties, and vasodilation among others (Goodwin et al. 1989; Savage and Gould 1990; Wallace and Wang 2015). Endogenously, H2S is produced from the amino acids homocysteine and serine found in the mitochondria and cytosol (Kamoun 2004; Kimura 2011). Many have cited the effectiveness of treating patients with respiratory diseases with low concentrations of H2S. Wang et al. (2020) showed the successful use of 40 ppm H2S for 8 h daily to treat chronic obstructive pulmonary disease (COPD) in rats. The H2S donor sodium hydrosulfide (NaHS) has been cited to have a protective effect on pulmonary artery endothelial cells in rat models of COPD (Wang et al. 2020). Notably, however, genetic defects in the metabolism of endogenously produced H2S to nontoxic sulfate metabolite such as that caused by ETHE1 deficiency have been associated with chronic H2S poisoning (Beauchamp et al. 1984; Szabo 2007; Tiranti et al. 2009; Tiranti and Zeviani 2013; Di Meo et al. 2015). ETHE1 deficiency and similar genetic defects cause H2S-induced chronic neurodegeneration from accumulating H2S leading to death in the first decade of life (Tiranti et al. 2004).
The roles of hydrogen sulfide in renal physiology and disease states
Published in Renal Failure, 2022
Jianan Feng, Xiangxue Lu, Han Li, Shixiang Wang
Hydrogen sulfide (H2S) is a toxic, colorless gas with an odor of rotten eggs. It exists in nature and can be found in natural gas, volcanic emissions and petroleum [1]. In 1989, Warenycia and Goodwin [2] first demonstrated that the human body contains H2S, which mainly exists in the brain, and indicated that the brainstem is more sensitive to exogenous H2S than other parts of the brain. The physiological function of H2S has only recently been gradually recognized. High concentrations of H2S may lead to complete inhibition of cell respiration, mitochondrial membrane potential depolarization and superoxide generation [3]. Low levels of H2S can regulate homeostatic mechanisms such as blood pressure (BP) control and apoptosis and participate in pathological mechanisms including oxidative stress (OS) and inflammation [4,5]. In the kidneys, H2S is actively involved in renal regulation, and H2S production disorders are involved in the onset and development of many kidney diseases [6]. Although exogenous H2S has been shown to play key roles in alleviating various animal models of kidney damage, its specific molecular mechanism is unknown.