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Hypoxia in Acute Chemical Emergencies: Toxicity, Mechanism, and Treatment

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Abstract

Hypoxia is a pathological condition in which the whole body or a particular region of the body suffers from oxygen deprivation. There are various kinds of hypoxia viz. hypoxemic hypoxia (e.g., high-altitude pulmonary edema, high-altitude cerebral edema, etc.), anemic hypoxia (e.g., chronic anemia, carbon monoxide (CO) poisoning, etc.), stagnant hypoxia (heart failure, vasodilatory shock, etc.), and histotoxic hypoxia. In histotoxic hypoxia, the quantity of oxygen reaching the cells is normal, but the cells are unable to utilize the oxygen efficiently. This is due to inactivation of enzymes involved in oxidative phosphorylation. This causes profound reduction in adenosine triphosphate production by the mitochondria, leading to various cellular perturbations, and possibly cell death. The gases considered as chemical asphyxiants act either by decreasing the oxygen-carrying capacity of the blood (CO) or by interfering with cellular utilization of oxygen (cyanide and hydrogen sulfide). Regardless of mode of action, chemical asphyxiants can cause severe hypoxia (chemical hypoxia), which is detrimental for the living organisms. Acute chemical emergencies can be encountered during industrial disasters, occupational exposures, accidents, use of chemical warfare agents, and acts of terrorism. This chapter discusses the toxicity, molecular mechanism(s) of action, and treatment modalities of chemical asphyxiants. Possible implication of organophosphorus compounds in producing chemical hypoxia is also addressed. This information will be useful for medical management of hypoxia-related chemical emergencies.

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Acknowledgements

Authors acknowledge Dr. B.K. Bhattacharya, Head, Division of Biochemistry and Biotechnology, and Dr. Pravin Kumar, Head, Division of Pharmacology and Toxicology, DRDE, Gwalior, for their valuable suggestions. Authors also thank Mr. Shiv Kumar Yadav and Ms. Poonam Singh, Research Scholars, Division of Pharmacology and Toxicology, DRDE, Gwalior, for their excellent technical support in preparation of this manuscript.

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  1. Defence Research and Development Establishment, Jhansi Road, Gwalior, 474 002, Madhya Pradesh, India

    Rahul Bhattacharya & M. P. Kaushik

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Correspondence to Rahul Bhattacharya .

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  1. Defence Institute of Physiology and Allied Sciences (DIPAS), New Delhi, Delhi, India

    Shashi Bala Singh

  2. Department of Medicine and Director for Systems, The University of Chicago, Chicago, USA

    Nanduri R. Prabhakar

  3. Department of Anaesthesiology, School of Medicine, State University of New York, Stony Brook, New York, USA

    Srinivas N Pentyala

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Bhattacharya, R., Kaushik, M.P. (2014). Hypoxia in Acute Chemical Emergencies: Toxicity, Mechanism, and Treatment. In: Singh, S., Prabhakar, N., Pentyala, S. (eds) Translational Research in Environmental and Occupational Stress. Springer, New Delhi. https://doi.org/10.1007/978-81-322-1928-6_19

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