Inorganic Chemical Pollutants
William J. Rea, Kalpana D. Patel in Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
Cyanides are formed as follows: NH3 and CH4 → N – CN + 3H2. Their economic importance is large, with 450,000 tons produced worldwide in 1970 and 180,000 tons in the United.States in 1977. Production of cyanides has increased over the past 14 years. They are hazardous when used in industry and in agricultural fumigation. In addition to the original use of salt (cyanides) for the extraction of gold, cyanide is mainly used in the production of plastics and synthetic fibers. Cyanides are used in plating or metal hardening operations. Cyanides are used in forming urethanes, polymethacrylates, polyacrylonitrile, and polyamides. Cyanides in the form of alkali cyanide result in epistaxis and nasal ulceration at 5-mg/m3 concentrations. If alkali cyanides are mixed with hydrochloric acid, HCN may be formed. HCN is directly produced in some chemical industrial plants, and exposures at 20 ppm (or even less) may produce serious symptoms, particularly of a neurological nature. Concentrations of 100 ppm (or larger) may be fatal. Over 3000 people died at Bhopal, India, after the noted leak of methylisocyanate, and an estimated 300,000 or more were adversely affected, some of whom may have become chemically sensitive. The TLV value for alkali cyanides is 5 mg/m3.894
Anti-Nutrients in Bamboo Shoots
Nirmala Chongtham, Madho Singh Bisht in Bamboo Shoot, 2020
Cyanogenic glycosides are amino acid–derived constituents of plants produced as secondary metabolites that release hydrogen cyanide when chewed or digested. Plants synthesize cyanogenic glycosides as a defence mechanism against the attack of herbivores, insects and pathogens. They occur in at least 2,500 plant species, represented within most plant families of which a number of species are used as food. There are approximately 25 known cyanogenic glycosides and these are generally found in the edible parts of plants, such as apples, apricots, cherries, peaches, plums, almonds, cassava, bamboo shoots, linseed/flaxseed, lima beans, chickpeas, cashews, etc. The toxicity of cyanogenic glycosides and their derivatives is dependent on the release of hydrogen cyanide. The act of chewing or digestion leads to the hydrolysis of the substances, causing cyanide to be released. Symptoms of cyanide toxicity in humans have been reported to include rapid respiration, low blood pressure, headache, dizziness, vomiting, stomachache, diarrhea, convulsion and in severe cases death.
Biomarkers of Chemical Warfare Agents
Anthony P. DeCaprio in Toxicologic Biomarkers, 2006
Cyanide is a rapidly acting, lethal agent capable of interacting with sulfur compounds and metallic complexes. It interferes with the body’s ability to utilize oxygen. With the interruption of aerobic processes, the tissues switch to anaerobic metabolism resulting in buildup of lactic acid and creation of metabolic acidosis. Death can occur within six to eight minutes following absorption of toxic levels of cyanide. Following acute exposure to low or moderate levels of cyanide, the victim can experience increased rate and depth of breathing, dizziness, nausea, vomiting, and headache. If exposure continues, the signs and symptoms can quickly progress to convulsions, cessation of respiration, cardiac effects, and death. Cyanide casualties may appear similar to nerve agent casualties but will not evidence miosis, copious secretions, or fasciculations. Immediate laboratory findings may include elevated blood cyanide levels, metabolic acidosis with high lactate levels, or elevated arterial oxygen levels. The latter two findings may reflect disease states other than cyanide poisoning.
Development of sodium tetrathionate as a cyanide and methanethiol antidote
Published in Clinical Toxicology, 2022
Adriano Chan, Jangwoen Lee, Subrata Bhadra, Nesta Bortey-Sam, Tara B. Hendry-Hofer, Vikhyat S. Bebarta, Sari B. Mahon, Matthew Brenner, Brian Logue, Renate B. Pilz, Gerry R. Boss
Cyanide is a well-known toxic chemical. It is generated as hydrogen cyanide gas in structural fires and is a major contributor to death by smoke inhalation [1]. It is used in a variety of industries, with over three billion pounds of cyanide salts produced annually worldwide [2]. It has the potential to be released by terrorists and is considered a high-priority chemical threat by the Center for Disease Control. Currently approved treatments for cyanide poisoning in the United States are hydroxocobalamin and the combination of sodium nitrite and sodium thiosulfate. Both treatments must be given intravenously over 10–15 min, which would not be practical in the setting of a major fire, industrial accident, or terrorist attack. A treatment is needed that can be given quickly, for example by intramuscular injection using an autoinjector. This requires that the drug is sufficiently potent and soluble that it can be administered in a small volume.
Cyanide poisoning in Thailand before and after establishment of the National Antidote Project*
Published in Clinical Toxicology, 2018
Sahaphume Srisuma, Aimon Pradoo, Panee Rittilert, Sunun Wongvisavakorn, Achara Tongpoo, Charuwan Sriapha, Wannapa Krairojananan, Netnapis Suchonwanich, Sumana Khomvilai, Winai Wananukul
There were 130 cases (37.9%) in the Before group and 213 cases (62.1%) in the Project group (Table 1). Median age was five years (interquartile range [IQR]: 3–29 years). Fifty-two percent of patients were male. Common sources of cyanide were cyanogenic glycosides (n = 245, 71.4%) including 243 from cassava, one from bitter almond, and one from bamboo shoot. There were 98 (28.6%) cyanide chemical exposures, 70 of which were exposed to gold or silver polishing solutions. Most exposures were unintentional (316, 92.1%). There were more cases with self-harm intent in the Project group (22, 10.3%) than in the Before group (five, 3.9%) (p value .038). Of the 27 self-harm cases, the majority involved ingestion of cyanide chemical (26; 96.3% of 27 cases), followed by cyanogenic glycoside (one, 3.7%). Most of the cases were symptomatic at presentation (338, 98.5%). Eighty patients (23.3%) had initial severe symptoms. There was no difference in initial severity between the two groups (Table 2).
Challenges in the diagnosis of acute cyanide poisoning
Published in Clinical Toxicology, 2018
J. L. Parker-Cote, J. Rizer, J. P. Vakkalanka, S. V. Rege, C. P. Holstege
The current medical literature contains inconsistencies concerning the expected clinical and laboratory findings after cyanide poisoning. Conventional reviews report that hydrogen cyanide has a bitter almond odor. Prior reports claim that only 20–40% and possibly 60–80% of individuals can discern the odor [17,18]. Cherry-red skin is another physical exam finding that is reported as characteristic of cyanide toxicity, due to increased venous hemoglobin oxygen saturation. However, there is not a predictable incidence in which cherry-red skin is present upon initial presentation. Patients may present after cardiovascular collapse with subsequent cyanosis rather than cherry-red skin [1]. In one case series of intentional cyanide ingestions pink lividity and a “bitter” almond smell were not prevailing signs [19]. Additional signs and symptoms associated with cyanide toxicity are dizziness, headache, nausea, vomiting, tachypnea, tachycardia, restlessness, seizures, and loss of consciousness. However, these signs and symptoms can occur from a multitude of medical conditions and are not specific to cyanide toxicity. Metabolic acidosis with associated hyperlactatemia has been a predominant laboratory finding in various reports.
Related Knowledge Centers
- Chemical Compound
- Chemistry
- Functional Group
- Inorganic Compound
- Nitrogen
- Cyanide Poisoning
- Potassium Cyanide
- Carbon
- Salt
- Sodium Cyanide