Hydrogen cyanide lethality

The use of black cyanide as a fumigant and rodenticide makes use of the atmospheric humidity action that Hberates hydrogen cyanide gas. It can only be used effectively ia confined spaces where hydrogen cyanide builds up to lethal concentrations for the particular appHcation. Black cyanide is also used ia limited quantities ia the production of pmssiates or ferrocyanides (see Iron compounds). 

Samples of smoke during fires have indicated that hydrogen cyanide is not of concern in fire deaths because the levels found were much below lethal levels. 

It is well known that hydrogen cyanide can be liberated during combustion of nitrogen containing polymers such as wool, silk, polyacrylonitrile, or nylons (1, 2). Several investigators have reported cyanide levels in smoke from a variety of fires (3, 4, 5). The levels reported are much below the lethal levels. Thus the role of cyanide in fire deaths would seem to be quite low. However, as early as 1966 the occurence of cyanide in the blood (above normal values) of fire victims was reported (6). Since then many investigators have reported elevated cyanide levels in fire victims (7-13). However, it has been difficult to arrive at a cyanide blood level which can be considered lethal in humans. In this report the results of cyanide analysis in blood of fire victims are reported as well as the possibility that cyanide may, in some cases, be more important than carbon monoxide as the principal toxicant in fire smoke. 

Lethal human toxicity values have not been established or have not been published. However, based on available information, this agent appears to be approximately half as toxic as Hydrogen cyanide (C07-A001). 

CK in liquid or gas form is highly irritating to the eyes and upper respiratory tract. Inside the body, it converts to hydrogen cyanide, which inactivates certain enzyme systems that prevent cells from utilizing oxygen. Impacted skin may appear flushed. Low levels of exposure often cause weakness, headache, disorientation, nausea, and vomiting. Higher levels of exposure will result in loss of consciousness, terminate respiration, and cause death within 15 minutes. An immediate lethal dose often causes violent contractions of blood vessels accompanied by severe shock. This reaction may cause death prior to asphyxiation.1 ... 

Bd Wt = body weight Cardio = cardiovascular d = day(s) DC so = concentration that resulted in 50% decrease in average respiratory rate EEG = electroencephalogram Endocr = endocrine F = female Gastro = gastrointestinal HCN = hydrogen cyanide Hemato = hematological LCso = lethal concentration, 50% kill LOAEL = lowest-observed-adverse-effect level M = male min = minutes NaCN = sodium cyanide NOAEL = no-observed-adverse-effect level NS = not specified (occup) = occupational Resp = respiratory sec = second(s) yr = year(s) x time(s)... 

When comparing the available acute lethal toxicity information for cyanide compounds, it was concluded that, for oral exposure, the molar lethal toxicities of hydrogen cyanide, sodium cyanide, and potassium cyanide are similar. Rabbits appeared to be more susceptible to the lethal toxicity of these three compounds than rats (Ballantyne 1988). 

Absorption. Absorption of cyanide across the gastrointestinal mucosa depends on the pH of the gut and the pKa and lipid solubility of the particular cyanide compound. Hydrogen cyanide is a weak acid with a pKa of 9.2 at 25 °C. The acidic environment in the stomach favors the non-ionized form of hydrogen cyanide and facilitates absorption. Information regarding the rapid lethal effects following oral intake of cyanide in humans (Gosselin et al. 1976) indicates that cyanide is rapidly absorbed from the gastrointestinal tract. 

Respiratory Effects. Respiratory effects commonly occur after inorganic cyanide poisoning by any route of exposure. Following inhalation, the first breath of a lethal concentration of hydrogen cyanide causes hyperpnea (Rieders 1971). The victims experience shortness of breath that may be rapidly (>1 minute) followed by apnea. Dyspnea was reported in patients who survived acute inhalation exposure to cyanide... 

Hydrogen cyanide is extremely toxic hy ingestion, inhalation, skin absorption, and all routes of exposure. An oral dose of 50 mg could be lethal to humans (Patnaik, P. 1999. A Comprehensive Guide to the Hazardous Properties of Chemical Substances, 2nd ed.. New York John Wiley). Symptoms from acute poisoning include labored breathing, shortness of breath, paralysis, unconsciousness, and respiratory failure. Lower doses can cause headache, nausea and vomiting. Oral LDsoin mice is 3.7 mg/kg. Amyl nitrite is an effective antidote. 

Kondrltzer et al.,130 n searching for a salt of 2-PAM that would be more soluble than 2-PAM I in water, made a number of other salts. Most of these were considerably more soluble in water than 2-PAM I. One of the most soluble was the lactate, with a solubility of 1 g/ml. Unfortunately, this salt was found to be quite unstable in aqueous solution with respect to heat. I was less soluble in water than the lactate, but more than 13 times as soluble as the iodide. Furthermore, solutions of I at a pH of 3.5-4.3 could be autoclaved at 120°C for 15 min with only a 4% loss. Solutions of this salt stored at 50-70°C for 1-3 mo contained at least 78% of the original oxime and no more than 0.1% of hydrogen cyanide. When the aged solutions were examined for lethality to experimental animals, their lethal activities were exactly those expected on the basis of their oxime concent rat ions. 

AC- Hydrogen Cyanide or Prussic Acid(Fr Vincennite or Manganite),HCN col liq with odor of bitter almonds, bp ca 78°F(25.6°) lethal when inhaled one of the "blood gases (Group B, nonpersistant chem agents)(Ref 16,p 242 Ref 36,p 29-27)... 

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