The basic and applied toxicology of cyanides and cyanogens has widespread commercial, occupational, environmental, clinical, forensic, military, and public health implications. This book provides a detailed and updated reference describing the properties, uses, general and human toxicology, clinical recognition, diagnosis and medical management, and countermeasures is therefore required in academic, medical, occupational, environmental, medico-legal, regulatory, emergency response, and military arenas. Edited by a world-renowned team of experts from academia, defense and industry, this book will be an invaluable reference for professionals, researchers and students in cyanide and cyanogens.
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Yes, you can access Toxicology of Cyanides and Cyanogens by Alan H. Hall, Gary E. Isom, Gary A. Rockwood in PDF and/or ePUB format, as well as other popular books in Biological Sciences & Neuroscience. We have over one million books available in our catalogue for you to explore.
Andrea R. Allen,, Lamont Booker, and Gary A. Rockwood
Disclaimer: the views expressed in this chapter are those of the authors and do not reflect the official policy of the Department of the Army, Department of Defense, or the U.S. Government.
At a Glance
Cyanide intoxication can result from diet, fires, alternative and standard medical treatments, industrial exposure, and intentional exposure (e.g., suicide, homicide, terrorism).
Cyanide blocks the oxidative respiration pathway, impeding oxygen usage within tissues; the major metabolic pathway results in the formation of less toxic thiocyanate.
Across species, long-term effects of cyanide post-exposure include a range of behavioral and neurological dysfunction, such as Parkinsonism.
Antidotal treatments for acute cyanide toxicity may significantly reduce adverse sequelae and provide a better quality of life post-exposure.
1.1 Introduction
Cyanide (CN) is a potent toxicant with rapid onset of histotoxic anoxia through inhibition of mitochondrial oxidative phosphorylation (Way, 1984), inhibition of oxidative metabolism (cytochrome C oxidase (CcOX) inhibition), and alteration of critical cellular ion homeostasis (Gunasekar et al., 1996). CN exists in a variety of forms, including gaseous hydrogen cyanide (HCN), water-soluble potassium (K) and sodium (Na) salts, poorly water-soluble mercury (Hg), copper (Cu), gold (Au), and silver (Ag) CN salts (Leybell et al., 2011). Cyanogens, which are glycosides of sugar and CN-containing aglycon (Makkar et al., 2007), include complex nitrile-containing compounds that can generate free CN of toxicological significance (Rao et al., 2013). Within the liver, the enzyme rhodanese catalyzes the conversion of CN to thiocyanate (SCN), which is normally excreted through the kidneys. CN can bind to both the oxidized and reduced forms of CcOX, but it possesses a greater affinity for the oxidized form (Van Buuren et al., 1972).
Cyanogenic compounds, such as amygdalin, can be found in certain plants, particularly in the seeds and pits of members of the genus Prunus, which includes apricot pits, peach pits, cherry pits, apple seeds, and almond husks (Shepherd & Velez, 2008). Other sources of CN exposure include exposure from industrial products and processes. Worldwide industrial consumption of CN is estimated to be 1.5 million tons per year, and occupational exposures account for a significant number of CN poisonings (Cummings, 2004). CN is typically used as a poison (e.g., used during World War II in concentration camps; used as a chemical for pest control). CN is an ingredient in some jewelry cleaners, photographic solutions, metal polish, and is also a by-product of the manufacture of some synthetic products such as nylon, rayon, polyurethane foam, and insulation (Hamel, 2011). In industrialized countries, the most common cause of CN poisoning is fires (Megarbane et al., 2003). Toxicologic evaluation of passengers following the explosion in 1985 of a Boeing 737 during take-off in Manchester, England, revealed that 20% of the 137 victims who escaped had dangerously elevated blood levels of carbon monoxide, while 90% had dangerously elevated levels of CN (Walsh & Eckstein, 2004; Jameson, 1995). Lastly, CN exposure can also occur via acts of terrorism, murder, and suicide.
The intentional and unintentional use, or threat of use, of CN in domestic and foreign incidents has occurred in recent years. These include the 1995 Tokyo subway attack (Sauter & Keim, 2001), the 2002 recovery of stored CN in Paris, France, linked to Al-Qaeda operatives (Cloud, 2004), and the 2004 discovery by US forces of âcookbooksâ on how to make HCN. Some recent threats include images of a âchemical laboratoryâ in a house in Fallujah, Iraq, that was allegedly used by terrorists linked to Abu Musab al-Zarqawi (Gertz, 2004), contamination of smokeless tobacco products with CN from a local merchant (Lenart et al., 2010), and the 2012 London Olympic threat to distribute CN-adulterated lotions (Bromund et al., 2012; Ritz, 2012). The Centers for Disease Control and Prevention (CDC) and the Occupational Safety and Health Administration (OSHA) developed regulations for CN and set permissible exposure limits at 10 ppm and 4.7 ppm, respectively (www.cdc.gov/niosh; www.osha.gov). Because of the rapidly debilitating actions of CN, it is necessary to quickly diagnose the level of exposure and provide supportive treatment to counteract the effects from CN intoxication.
Acute toxicity can be defined as the antagonistic effects resulting from a single exposure to a chemical substance or repeated exposures within a short period of time (
h) (Andrew, 2009). The clinical features of acute CN poisoning are variable, and the major determinants of severity and mortality are the source of exposure (CN or CN compound), the route and magnitude of exposure (amount and duration), and the effects and the time of any treatments that may have been tried (Yen et al., 1995). Acute CN toxicity can take place through ingestion, membrane absorption, and inhalation. Since there are no pathognomonic clinical signs and symptoms for its toxicity, it is pertinent to acquire a full patient or epidemiologic history and consider ...
Table of contents
Cover
Title Page
Copyright
Table of Contents
Dedication
List of Contributors
Foreword
Chapter 1: Acute cyanide toxicity
Chapter 2: Chronic cyanide exposure: Case studies and animal models
Chapter 3: Physicochemical properties, synthesis, applications, and transport
Chapter 4: Cyanide metabolism and physiological disposition
Chapter 5: Biochemical mechanisms of cyanide toxicity
Chapter 6: Environmental toxicology of cyanide
Chapter 7: Cyanide in the production of long-term adverse health effects in humans
Chapter 8: Pediatric cyanide poisoning
Chapter 9: Sodium nitroprusside in intensive care medicine and issues of cyanide poisoning, cyanide poisoning prophylaxis, and thiocyanate poisoning
Chapter 10: Smoke inhalation
Chapter 11: Occupational exposure to cyanide
Chapter 12: Cyanogenic aliphatic nitriles
Chapter 13: The special case of acrylonitrile (CH2=CHâCâĄN)
Chapter 14: Cyanide in chemical warfare and terrorism
Chapter 15: Cyanide-induced neural dysfunction and neurodegeneration
Chapter 16: Cyanides and cardiotoxicity
Chapter 17: Respiratory effects of cyanide
Chapter 18: The analysis of cyanide in biological samples
Chapter 19: Postmortem pathological and biochemical diagnosis of cyanide poisoning
Chapter 20: Medicolegal and forensic factors in cyanide poisoning
Chapter 21: Brief overview of mechanisms of cyanide antagonism and cyanide antidotes in current clinical use
Chapter 22: Cyanide antidotes in clinical use: 4-dimethylaminophenol (4-DMAP)
Chapter 23: Cyanide antidotes in clinical use: dicobalt EDTA (KelocyanorÂŽ)
Chapter 24: Amyl nitrite, sodium nitrite, and sodium thiosulfate
Chapter 25: Cyanide antidotes in current clinical use: hydroxocobalamin
Chapter 26: Cyanide antidotes in development and new methods to monitor cyanide toxicity
Chapter 27: Recent perspectives on alpha-ketoglutarate: A potential cyanide antidote
