Keywords
hydrogen sulfide
acute poisoning
chronic poisoning
neurotoxicity
biochemical mechanisms
therapeutic treatment strategies
acute poisoning
chronic poisoning
neurotoxicity
biochemical mechanisms
therapeutic treatment strategies
Abstract
Hydrogen sulfide (H2S) poisoning remains a significant cause of occupational mortality and is the second most common cause of death due to toxic gas. There is a lack of understanding of the toxic mechanisms leading to acute death caused by H2S. Studies suggest different causes of death due to fatal H2S exposure at accident sites, and this issue needs to be resolved. The development of appropriate drugs requires further research to understand the mechanisms of life-threatening symptoms following acute H2S poisoning. This review presents and discusses the neurological symptoms and lesions observed in various animal models and in humans following acute and chronic exposure to sublethal or lethal levels of H2S.
The aim of the research was to conduct a systematic review of the available literature to investigate the toxic effects of acute and chronic H2S poisoning in humans and animals, current recommendations and therapeutic agents for the treatment of acute and chronic H2S poisoning, and to identify prospects for further research.
In acute H2S poisoning, the nervous, respiratory, and cardiovascular systems are the main targets, leading to respiratory failure, seizures, hypotension, and cardiac disorders. Some patients who survived acute poisoning develop long-term sequelae, especially from the central nervous system. Currently, treatment for hydrogen sulfide poisoning is mainly supportive, as there are no clearly recognized drugs with proven clinical efficacy. New potential drugs are in the preclinical stage, most of which are aimed at binding H2S. Therefore, additional research is needed to develop new drugs to prevent and treat the acute and chronic consequences of hydrogen sulfide poisoning.
References
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2. Abe K., Kimura H. The possible role of hydrogen sulfide as an endogenous neuromodulator. J. Neurosci. 1996. V. 16. P. 1066–1071.
3. Hosoki R., Matsuki N., Kimura H. The possible role of hydrogen sulfide as an endogenous smooth muscle relaxant in synergy with nitric oxide. Biochem. Biophys. Res. Commun. 1997. V. 237. P. 527–531. https://doi.org/10.1006/bbrc.1997.6878.
4. Worksafe New Zealand, Workplace exposure standard (WES) review: hydrogen sulphide (CAS NO: 7783-06-4). 2018. URL: https://worksafe.govt.nz/laws-and-regulations/consultations/proposed-changes-to-workplace-exposure-standards-and-biological-exposure-indices/.
5. Donham K. J. The concentration of swine production. Effects on swine health, productivity, human health, and the environment. Vet. Clin. North. Am. Food Anim. Pract. 2000. V. 16 (3). P. 559–597.
6. Hydrogen sulfide and traffic-related air pollutants in association with increased mortality: a case-cross over study in Reykjavik, Iceland. R. G. Finnbjornsdottir, A. Oudin, B. T. Elvarsson et al. BMJ Open. 2015. V. 5 (4). P. e007272.
7. Ramos A. K., Fuentes A., Carvajal-Suarez M. Self-reported occupational injuries and perceived occupational health problems among latino immigrant swine confinement workers in Missouri. J. Environ. Public Health. 2018. V. 2018. P. 1–8.
8. Elwood M. The scientific basis for occupational exposure limits for hydrogen sulphide – a critical commentary. Int. J. Environ. Res. Public Health. 2021. V. 18. P. 2866. https://doi.org/10.3390/ijerph18062866.
9. Toxicological investigations in a fatal and non-fatal accident due to hydrogen sulphide (H2S) poisoning. E. Ventura Spagnolo, G. Romano, P. Zuccarello et al. Forensic. Sci. Int. 2019. V. 300. P. e4–8. https://doi.org/10.1016/j.forsciint.2019.04.026.
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11. Case report: analysis of a case of hydrogensulfide poisoning in a waste treatment plant. A. Genjiafu, M. Shi, X. Zhang, X. Jian. Front. Public Health. 2023. V. 11. P. 1226282. https://doi.org/10.3389/fpubh.2023.1226282.
12. Metabolism of hydrogen sulfide (H2S) and production of reactive sulfur species (RSS) by superoxide dismutase. K. R. Olson, Y. Gao, F. Arif et al. Redox Biol. 2018. V. 15. P. 74–85.
13. Midazolam efficacy against acute hydrogen sulfide-induced mortality and neurotoxicity. P. Anantharam, D. S. Kim, E. M. Whitley et al. J. Med. Toxicol. 2018. V. 14. P. 79–90. https://doi.org/10.1007/s13181-017-0650-4.
14. Transcriptomic profile analysis of brain inferior colliculus following acute hydrogen sulfide exposure. D. S. Kim, P. Anantharam, P. Padhi et al. Toxicology. 2020. V. 430 (152345). P. 152345.
15. Determinants of lactic acidosis in acute cyanide poisonings. F. J. Baud, M. K. Haidar, R. Jouffroy et al. Crit. Care Med. 2018. V. 46 (6). P. e523–e529.
16. Are H2S-trapping compounds pertinent to the treatment of sulfide poisoning? P. Haouzi, B. Chenuel, T. Sonobe, C. M. Klingerman. Clin. Toxicol. 2014. V. 52. P. 566.
17. Methylene blue administration during and after life-threatening intoxication by hydrogen sulfide: efficacy studies in adult sheep and mechanisms of action. P. Haouzi, N. Tubbs, J. Cheung, A. Judenherc Haouzi. Toxicol. Sci. 2019. 168, 443–459.
18. Insights into the inhibitory mechanisms of NADH on the alpha gamma heterodimer of human NAD-dependent isocitrate dehydrogenase. Y. Liu, L. Hu, T. Ma et al. Sci. Rep. 2018. V. 8. P. 3146.
19. Kimura H. Hydrogen sulfide induces cyclic AMP and modulates the NMDA receptor. Biochem. Biophys. Res. Commun. 2000. V. 267. P. 129–133.
20. Guidotti Tee L. Hydrogen sulfide intoxication. Handb. Clin. Neurol. 2015. V. 131. P. 111–133. https://doi.org/10.1016/b978-0-444-62627-1.00008-1.
21. Transcriptomic profiling of control and thyroid-associated orbitopathy (TAO) orbital fat and TAO orbital fibroblasts under going adipogenesis. D. W. Kim, K. Taneja, T. Hoang et al. Invest. Ophthalmol. Vis. Sci. 2021. V. 62 (9). P. 24.
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23. Sahar Ali F., Nirmeen Adel K. Cognitive functions changes among Egyptian sewage network workers. Toxicol. Ind. Health. 2010. V. 26. P. 229–238.
24. Haouzi P., Sonobe T., Judenherc-Haouzi A. Hydrogen sulfide intoxication induced brain injury and methylene blue. Neurobiol Dis. 2020. V. 133. P. 104474.
25. Fisher R. S. An overview of the 2017 ILAE operational classification of seizure types. Epilepsy Behav. 2017. V. 70 (PtA). P. 271–273.
26. Sudden unexpected death in epilepsy: the neuro-cardio-respiratory connection. T. A. Manolis, A. A. Manolis, H. Melita, A. S. Manolis. Seizure. 2019. V. 64. P. 65–73.
27. Cobinamide is effective for treatment of hydrogen sulfide-induced neurological sequelae in a mouse model. P. Anantharam, E. M. Whitley, B. Mahama et al. Ann. N. Y. Acad. Sci. 2017.V. 1408 (1). P. 61–78.
28. Methylene blue counteracts H2S toxicity-induced cardiac depression by restoring L-type Ca channel activity. A. Judenherc-Haouzi, X. Q. Zhang, T. Sonobe et al. Am. J. Physiol. Regul. Integr. Comp. Physiol. 2016. V. 310. P. R1030–R1044.
29. On the efficacy of cardio-pulmonary resuscitation and epinephrine following cyanide- and H2S intoxication-induced cardiac asystole. A. Judenherc-Haouzi, T. Sonobe, V. S. Bebarta, P. Haouzi. Cardiovasc. Toxicol. 2018. V. 18 (5). P. 436–449.
30. Methylene blue counteracts H2S-induced cardiac Ion channel dysfunction and ATP reduction. J. Y. Cheung, J. Wang, X. Q. Zhang et al. Cardiovasc. Toxicol. 2018. V. 18 (5). P. 407–419.
31. Hydrogen sulfide toxicity in a thermal spring: a fatal outcome. H. Daldal, B. Beder, H. Serin, S. Sun- gurtekin. Clin. Toxicol (Phila). 2010. V. 48 (7). P. 755–776. https://doi.org/10.3109/15563650.2010.508044.
32. Treatment of life-threatening H2S intoxication: lessons from the trapping agent tetranitrocobinamide. P. Haouzi, M. MacCann, M. Brenner et al. Environ. Toxicol. Pharmacol. 2022. V. 96. P. 103998. https://doi.org/10.1016/j.etap.2022.103998.
33. Sonobe T., Haouzi P. Sulfide intoxication-induced circulatory failure is mediated by a depression in cardiac contractility. Cardiovasc. Toxicol. 2016. V. 16 (1). P. 67–78.
34. Immediate and long-term outcome of acute H2S intoxication induced coma in unanesthetized rats: effects of methylene blue. T. Sonobe, B. Chenuel, T. K. Cooper, P. Haouzi. PLoS One. 2015. V. 10. P. e0131340.
35. Baldelli R. J., Green F. H., Auer R. N. Sulfide toxicity: mechanical ventilation and hypotension determine survival rate and brain necrosis. J. Appl. Physiol. 1993. V. 75. P. 1348–1353.
36. Hydrogen sulfide specifically alters NAD(P)H quinone dehydrogenase 1 (NQO1) olfactory neurons in the rat. F. Imamura, T. K. Cooper, S. Hasegawa Ishii et al. Neuroscience. 2017. V. 366. P. 105–112.
37. Outcome after hydrogen sulphide intoxication. E. A. Q. Mooyaart, E. L. G. Gelderman, M. W. Nijsten et al. Resuscitation. 2016. V. 103. P. 1–6.
38. Price W. D., Price S. M., Johnston M. Novel treatment of dihydrogen sulfide inhalation using hyperbaric oxygen during mass casualty. Undersea Hyperb. Med. 2021. V. 48 (2). P. 153–156.
39. Intramuscular cobinamide versus saline for treatment of severe hydrogen sulfide toxicity in swine. P. C. Ng, T. B. Hendry-Hofer, N. Garrett et al. Clin. Toxicol. 2019. V. 57 (3). P. 189–196.
40. A sulfonyl azide-based sulfide scavenger rescues mice from lethal hydrogen sulfide intoxication. Y. Miyazaki, E. Marutani, T. Ikeda et al. Toxicol. Sci. 2021. V. 183 (2). P. 393–403.
41. De Nolf R. L., Kahwaji C. I. EMS mass casualty management. Treasure Island (FL): StatPearls. 2022.
42. IL-26 in the induced sputum is associated with the level of systemic inflammation, lung functions and body weight in COPD patients. L. Savchenko, M. Mykytiuk, M. Cinato et al. Int. J. Chron. Obstruct. Pulmon. Dis. 2018. V. 13. P. 2569–2575. https://doi.org/10.2147/COPD.S164833.