Hydrocyanic Acid

HYDROCYANIC ACID (syn. hydrogen cyanide acid), a mobile, easily flammable, colorless liquid with a characteristic odor; boiling point 25.6°, melting point -14°; vapor density 0.93; mixes with water and alcohol in all proportions. It apparently consists of a mixture of the normal (H-CN) and isomeric forms (H-N=C), which easily transform into each other (the formula H-N≡C was also proposed). Mol. wt. 27, easily polymerizes, forming dimers and polymers. (For preparation, see S. k. as a disinfectant.) It is displaced from its salts, although slowly, even by atmospheric carbon dioxide (2 NaCN + H₂CO₃ = Na₂CO₃ + 2HCN). Hydrocyanic acid is widespread in the plant world, occurring in the form of glycosides such as amygdalin, vicinin, linamarin, gynocardin, lotusin, and others. The most studied and at the same time most important biological reaction of hydrocyanic acid (and all cyanides, otherwise called cyanogen compounds, capable of breaking down in the body to form hydrocyanic acid) is the inhibition of oxygen consumption it causes, and no theory of biological oxidation can avoid the question of the substrate of hydrocyanic acid's action. In Warburg's teaching, this substrate is considered to be an organic complex containing a heavy metal, usually iron, which plays the role of a catalyst for oxidation processes. According to the views of many authors [Abderhalden, Gellhorn (1923), Voegtlin (1926), etc.], the substrate of hydrocyanic acid's action are compounds characterized by a sulfhydryl group (R.SH), possessing the ability of self-oxidation (transition to RS-SR), probably through the intermediate formation of peroxide (RS-O-O-SR), such as cysteine, glutathione, etc.; according to these views, hydrocyanic acid reduces the disulfide and prevents oxidation. According to data from Warburg and his school (Toda and others), the reaction of the type 2R.SH → RS-SR is not spontaneous oxidation, but proceeds with the participation of the same iron as a catalyst. In Wieland's teaching, the substrate of hydrocyanic acid's action is catalase, whose ability to decompose peroxides is inhibited by hydrocyanic acid (Schoenbein, 1867). Since according to recent data [Euler (1930) and others], the carrier of catalase properties of plasma is a protein complex containing, like the 'respiratory pigment', a hemin-like substance, despite the differences in views on oxidative processes, there is apparently no doubt about the main substrate of hydrocyanic acid's action on these processes, and it must be considered an organic iron complex. Given the high reactivity of hydrocyanic acid, one cannot deny the possibility of other substrates of its action, although with less biological significance. Thus, Low several decades ago put forward the hypothesis about the significance of the aldehyde group (R.COH) of protoplasm as the substrate of action of many poisons, including hydrocyanic acid. When studying the inhibitory effect of hydrocyanic acid and its salts on the respiration of various objects (egg cells, avian erythrocytes, skeletal muscle, liver and nervous tissue, etc.), various authors [Battelli and Stern (1910), Meyerhof (1923), Warburg (1908-21), etc.] used different concentrations, varying by at least 200 times (0.01-2 millimoles, i.e., 0.2-50 per 1 million). These differences depend not only on the object but also on the difference in the duration of exposure of the concentrations used and on the degree of inhibition achieved by different authors. The average concentrations that reduce the respiration of various cells to 50% of normal are apparently 0.01-0.05 millimoles (Warburg). A significant difference in the susceptibility of individual functions is established by experiments of Weizsäcker (1912): 0.5 mg of hydrocyanic acid reduces oxygen consumption by an isolated frog heart to zero, while the work capacity of the cardiac muscle decreases only to 50-60%. The smell of diluted hydrocyanic acid is usually described as the smell of bitter almonds. Many people perceive it insufficiently clearly or not at all. Higher concentrations of hydrocyanic acid (used in disinsection) are characterized less by olfactory sensations but by irritation of mucous membranes and a metallic taste in the mouth [Skramlik (1919) and others]. The sensation of burning and scratching on the tongue and palate, as well as in the upper respiratory tract, is considered characteristic of these concentrations of hydrocyanic acid. Reflexively, some increase in secretion and hyperemia of mucous membranes occur. In poisoning with salts of alkali metals, for example potassium cyanide, in strong concentrations, the cauterizing action of alkalis, not inherent in hydrocyanic acid itself, may occur (the local action of cyanide alkalis on the skin is characterized by itching, and in the presence of abrasions leads to ulcers). The numbness and even loss of sensitivity that follow irritation when using sufficient concentrations of hydrocyanic acid led to its use for many years in small concentrations as a local anesthetic (gargles, etc.). The absorption of hydrocyanic acid, especially when inhaling its vapors, occurs so quickly that earlier researchers even assumed that it kills reflexively without being absorbed. It has been established (both in experiments on animals and in cases of poisoning in disinsection and in humans) that hydrocyanic acid can be absorbed through intact skin. This absorption can be facilitated by hyperemia and sweating of the skin when external temperature increases or during intense muscular work. The distribution of hydrocyanic acid in the body, according mainly to forensic medical studies, is not uniform, and the largest amount of it is usually found in the blood (in cases of poisoning per os, in the abdominal cavity). Unchanged hydrocyanic acid is excreted by the lungs, but most cyanides are excreted from the body in the form of less toxic thiocyanate compounds [up to 70-100%, according to Smith (1930) and others]. The formation of the latter occurs mainly in the liver (Bodansky, 1923), but according to Stuber (1933), also in the salivary glands, adrenal glands, thyroid gland, and other organs. The process of 'sulfuration' of hydrocyanic acid, according to Stuber, is enzymatic in nature (the enzyme rhodanese). Thiocyanates are excreted by the salivary glands (mainly submandibular) and kidneys and can be easily detected with ferric chloride, better after preliminary acidification (the appearance of ruby-red color of thiocyanate iron). This excretion also occurs in normal people due to small amounts of cyanides and thiocyanates introduced with plant food, but in smokers in larger quantities due to traces of hydrocyanic acid in tobacco smoke. Preliminary administration of preparations containing a sulfhydryl group and easily releasing sulfur (sodium hyposulfite, cysteine, etc.) increases the process of formation of thiocyanate compounds and can prevent or alleviate hydrocyanic acid poisoning. In addition to the formation of thiocyanates (KCNS), during the oxidation of hydrocyanic acid, small amounts of cyanates (KCNO) can also form, which are also significantly less toxic compared to hydrocyanic acid. The possibility of hydrocyanic acid turning into formic acid is less clear. In the detoxification of hydrocyanic acid, the process of forming cyanhydrins, i.e., compounds of hydrocyanic acid with carbohydrates having a free aldehyde or ketone group, may also be significant. These compounds, if they are formed in the body, gradually release hydrocyanic acid, which then turns into thiocyanate compounds (Forst). Thus, the formation of cyanhydrins can prevent or alleviate poisoning by reducing the concentration of hydrocyanic acid, which can be achieved by introducing various aldoses and ketoses into the body. In poisoning with hydrocyanic acid in humans and warm-blooded animals (dog, cat, rabbit, etc.), if it does not fatally proceed within a few seconds or minutes, the prodromal, dyspneic, convulsive, and paralytic stages are traditionally distinguished. The first stage is especially clear in humans. Initially, there are increasing sensations of irritation of mucous membranes (a peculiar metallic scratchy taste, burning on the tongue, scratching in the palate), rush of blood to the head, feeling of heaviness in the forehead, tearing headaches, nausea, dizziness, tightness in the chest and palpitations. As the sensation of lack of air intensifies, agonizing dyspnea develops, pupils dilate and eyeballs protrude, general tremor or individual jerks occur, and with a feeling of extreme fear, loss of consciousness occurs, and the poisoned person falls. Clonic and tonic convulsions appear, which, due to rapidly developing paralytic phenomena, are expressed to varying degrees in different cases and have different durations. Convulsive evacuation of feces and urine, as well as vomiting, are often observed. Visible mucous membranes are colored bright red (when a vein is exposed in an experimental animal, the venous blood shining through the vessel wall has an arterial color). This discoloration of venous blood usually coincides with the appearance of convulsions. The cessation of convulsions, disappearance of all movements (including reflex ones) except respiratory movements characterizes the paralytic stage. Sometimes only a few minutes after the cessation of respiratory movements, cardiac arrest occurs.

Autopsy of those who have died does not reveal data different from those observed in acute asphyxia: dark, poorly coagulating blood, filling the veins, dilation of cerebral vessels and small hemorrhages in the brain, and sometimes in the endocardium and other organs, and the smell of bitter almonds from the corpse. In poisoning with very large doses, venous blood retains its bright red color, mentioned above. In poisoning with non-lethal doses, recovery can occur relatively quickly, and during the recovery stage from paralysis, convulsions and shortness of breath may reappear. In a number of cases, however (including those not ending in death at later stages), the paralytic period can last for hours. Characteristic of poisoning with H. c. is the rapid development of the symptom complex and the change in the color of venous blood, making it similar to arterial blood, which has long attracted the attention of researchers. The origin of this symptom led to various hypotheses, until Geppert (1888) firmly established that it is associated with an increased content of O₂ in the venous blood, approaching its content in arterial blood. Geppert also showed that the blood of the poisoned subject easily gives up its oxygen when the partial pressure of O₂ in the environment is reduced, both in vitro and in vivo. In the latter case, by making the poisoned animal inhale H₂, he observed darkening of the arterial blood. Despite the fact that O₂ is in the blood in the form of its usual compound with Hb, the study of gas exchange conducted by Geppert showed that the consumption of O₂ and the release of carbon dioxide in poisoning with H. c. sharply decrease. The latter thus depends on the disruption of O₂ consumption by tissues poisoned with H. c. Due to the suppression of this consumption, blood containing oxy-Hb passes into the veins, retaining its arterial color. The significance of oxygen (resp. the formation of oxy-Hb) in the appearance of the symptom of brightening of venous blood is particularly clearly demonstrated in frogs, which easily tolerate oxygen starvation without impairment of circulation: 1. Under anaerobic conditions (in an atmosphere of N₂ or H₂) poisoning with H. c. does not lead to brightening of the blood, and when brightening has occurred, the blood darkens (Verbriigge), and due to the restoration of blood in the lesser circle, arterial blood darkens before venous blood (Karasik, 1928). 2. In experiments under aerobic conditions with pulmonary breathing excluded, when O₂ can enter the blood only through the skin, brightening occurs 3-4 times more slowly than in experiments with preserved pulmonary breathing (Karasik, 1928). 3. The O₂ consumption, suppressed by H. c., can be experimentally increased, and at the same time, darkening of the previously bright blood can be observed. The latter occurs: a) when heating the frog in water or in a thermostat at 26-32° [Zillessen (1891), Karasik (1928)] and b) when tetanizing the motor nerves or poisoning with convulsants (Karasik, 1928). These latter data show, on the one hand, that O₂ in the blood of the poisoned animal is in the form of easily reducible oxy-Hb, and, on the other hand, that H. c. does not completely paralyze oxidative processes. The previously recognized difference in the rate of postmortem darkening of blood in warm-blooded animals and frogs (Preyer, 1870) is a misunderstanding related to the fact that in frogs, arterialization of blood continues after paralysis of the respiratory center due to diffusion of oxygen through the skin. Thus, all available experimental data establish that the gas function of the blood in poisoning with H. c. is not impaired and that the brightening of venous blood is associated with its richer content of oxy-Hb. Spectroscopic examination of blood taken from a poisoned animal during life does not reveal changes in the blood pigment; however, blood taken from the corpse of an animal that died from large doses of H. c. may give spectral changes, previously attributed to the combination of H. c. with hemoglobin - cyan-Hb. The study of this compound showed that it is obviously obtained when H. c. acts on postmortem formed methemoglobin (by replacing hydroxyl groups in it with the CN group) and in connection with this it is now more often called cyan-methemoglobin. The reaction of MtHb with H. c. is so sensitive that it can be used to recognize each of the reagents [Schonbein (1868), Robert (1891-1900)]. The similarity in color of CNHb with oxy-Hb led at one time to a misconception about its composition and for a time it was called cyanoxige- 1U0 moglobin. Formed postmortem, oxygen-free cyanmethemoglobin has no significance in the pathogenesis of poisoning with H. c. Thus, the analysis of the most pathognomonic symptom of poisoning with H. c. - the brightening of venous blood - leads to the conclusion that it is a symptom of acute tissue oxygen starvation. The latter underlies most other symptoms of poisoning. Excitation of the centers of the medulla oblongata (respiratory, vasomotor and the center of the vagus nerve) according to experimental data does not differ from their excitation observed when the trachea is clamped and acute anemia of the medulla oblongata. However, according to the latest data (S. Heymans, 1931), in the initial excitation of respiration, the ability of H. c. (similar to nicotine, lobeline and other substances) to excite sensory nerve endings located in the carotid sinus is of importance. Denervation of the sinus in Heymans' experiments and his colleagues prevented excitation of the respiratory center by small doses of H. c., and an increase in doses caused only suppression and paralysis of respiration, no longer reflex but of central origin. The symptom complex of damage to the central nervous system coincides so much with that observed in asphyxia of other origin (see Asphyxia) that only the following feature has been noted so far: asphyxial convulsions and other manifestations of excitation of the central nervous system are not eliminated (or are eliminated with difficulty) by artificial respiration; this difference, as follows from the foregoing, is due to the fact that asphyxia in poisoning with H. c. is caused not by a lack of O₂ in the blood, but by 'internal suffocation of tissues'. The disruption of gas exchange in H. c. amounts to a sharp decrease in O₂ consumption and CO₂ release [Geppert, Kravkov (1903), Hess (1923), Messerle (1926) and others], with the oxygen content in venous blood almost reaching its content in arterial blood. (After the acute symptoms of poisoning have passed, O₂ consumption compared to normal may increase.) As in oxygen starvation of other origin, hyperglycemia (and sometimes glycosuria) and the appearance of lactic acid in the blood and urine are observed. The excretion of N in urine sharply increases (the excretion of uric acid increases by 2-3 times). The breakdown of nitrogenous substances, according to Mansfeld and Muller (Mans-feld, Miiller, 1911), is associated with oxygen starvation of the thyroid gland, the preliminary removal of which prevents this increase. The excretion of sulfur with urine (mainly neutral sulfur) increases significantly - up to 150% of normal. The total phosphorus content in urine is also increased. The body temperature, especially in severe poisoning, as would be expected with a sharp decrease in oxidative processes, falls; this decrease is particularly significant in the paralytic stage and at the beginning of recovery. In the decrease in body temperature, not only the reduction in heat production but also the increase in heat loss, caused by vasodilation, is of importance. In animals that died in convulsions, a postmortem increase in temperature may be observed. In humans, as in animals, besides lightning-fast and rapid deaths, cases of 'late' death from H. c. are observed. Pathological-histological findings found in these cases in the central nervous system, judging by the factual material of a number of authors (Edelmann, Schmorl, Snesarev, A. Meyer and others), resemble, and in part coincide with those found in poisoning with CO, and are apparently mainly associated with the severe disturbances of cerebral circulation and changes in the cerebral parenchyma characteristic of asphyxia. The more frequent localization of changes in the globus pallidus, observed in poisoning with H. c. and carbon monoxide, as shown by the latest experimental studies of Meyer (1933), is also found in poisoning with chloroform and ether and is obviously associated with the special sensitivity of these nerve structures to oxygen starvation (regardless of the factors causing it). In connection with the fact that H. c. is quite rapidly excreted (resp. detoxified) by the body, the possibility of its cumulation is difficult. Habituation to H. c. also does not develop, and the certain resistance found in a few experimental studies should obviously be explained by the acquisition of a certain tolerance to oxygen starvation. With repeated administration of sufficient doses, cumulation of the effect occurs, which in experiments on animals (Collins and Martland, 1908) led to paralytic phenomena.

In humans (Hasselmann, 1925), with many years of work with H. a. and cyanides, changes in the blood have been found resembling polycythemia rubra, obviously connected with the reaction of the blood-forming organs to prolonged oxygen starvation (see Mountain sickness). The endurance of various animals to H. a. varies, with those species characterized by more intense oxidative processes being more sensitive to it. According to Barcroft's data (1931), warm-blooded animals, in their ability to inhale indefinitely long concentrations of H. a., are arranged in the following series (in increasing resistance): dog, rat (0.1 mg/l), mouse (0.14 mg/l), rabbit, monkey, cat (0.18 mg/l), goat (0.24 mg/l), guinea pig (0.40 mg/l). Judging from one of Barcroft's experiments, humans are more resistant than dogs. Data from other authors for humans are different. According to Lehman and Hess, concentrations of 0.05 mg/l cause headache, nausea, vomiting, palpitations; 0.1 mg/l is already dangerous to life, and 0.3 mg/l causes death in a few minutes. The lethal dose of H. a. for humans is taken as 1 mg per 1 kg of body weight. For various warm-blooded animals it varies from 3 to 15 mg per 1 kg of body weight. Assistance in poisoning with H. a. should be as rapid as possible. In poisoning with vapors of H. a., the victim must be immediately removed from the poisoned atmosphere; in poisoning per os, vomiting must be induced (apomorphin subcutaneously), stomach lavage (lavage with 0.04% potassium permanganate or 1% hydrogen peroxide to oxidize H. a. is recommended), administration of substances that neutralize H. a. (activated charcoal, 0.5-1% potassium permanganate or 2% hydrogen peroxide by teaspoonfuls). In case of insufficient spontaneous respiration - artificial respiration, which has special importance because it promotes the elimination of hydrocyanic acid. It should be borne in mind that the state of oxygen starvation, in which the consumption of O₂ is sharply suppressed by H. a., can, due to a decrease in its concentration in the blood (elimination, neutralization), quickly change to one in which oxygen consumption by tissues is possible but is disrupted due to paralysis of the respiratory center. Along with artificial respiration, measures to stimulate the respiratory center are necessary, both reflexively (sniffing ammonia spirit, etc.) and by humoral means (inhaling a mixture of O₂ with CO₂, administration of lobeline, atropine, caffeine), with the preference being for administration of such agents that simultaneously stimulate the heart (caffeine). At the same time, intravenous administration of substances that promote the neutralization of H. a. is necessary. Of substances that promote the transformation of H. a. into thiocyanates, in humans only sodium thiosulfate (commonly though incorrectly called 'sodium hyposulfite') has been tested, administered in amounts of 5-10 cm³ and more of a 5-10% solution (preferably repeated). Good results from it in human practice were obtained by Feyerabend, Pique [Feyerabend (1928), Pique (1928)]. Great importance is attached to the use of substances that convert H. a. into cyanhydrins (glucose, etc.). Of these, diacetone ('oxantine'), which simultaneously stimulates the respiratory center, is preferable. Its significance, according to Forst, consists in its significantly faster penetration through the blood-brain barrier compared to other ketoses. The combination of aldoses and ketoses with sulfur compounds gives a much better effect. In experimental works, some authors have successfully combined the administration of glucose with insulin. Recently [Hug (1932-33) and others], a protective and therapeutic effect of substances that form methemoglobin (sodium nitrite, etc.) has been discovered. Their role obviously consists in the fact that the Mt Hb formed, easily passing into cyanmethemoglobin (see above), prevents the action of H. a. on tissues. Recently (Hug and others), a protective and therapeutic effect of substances that form methemoglobin has been discovered. Their role obviously consists in the fact that methemoglobin, binding H. a. and passing into cyanmethemoglobin (see above), prevents its action on tissues. The use of these substances has already passed the stage of experimental research and there are several cases of their use in human poisonings. This latter circumstance gave Hug (1934) reason to recommend the following method for neutralizing absorbed H. a.: 1) inhalation of amyl nitrite; 2) intravenous administration of 10-20 cm³ of 2% sodium nitrite (after which inhalation of amyl nitrite is stopped); 3) intravenous administration of 10-20 cm³ of 30% sodium thiosulfate. The last two measures should be repeatable. However, since sodium nitrite can lead to methemoglobinemia of a degree that is in itself dangerous to life, the total dose should not exceed 1.0. The rapid decrease in H. a. concentration in the blood achieved through the formation of cyanmethemoglobin allows the slower effect of thiosulfate to manifest itself (cyanmethemoglobin gradually releases H. a., which passes into thiocyanates). Poisonings with H. a. and cyanides, which for a long time occurred as accidental or as a result of suicide attempts, are also observed as industrial poisonings, especially due to the use of H. a. as a disinfectant (see Disinsection, Disinfection), and its use as a combat poison gas (see Combat poison gases) creates the danger of poisonings in war. The use of H. a. in medicine is very limited (see Bitter almond water, Bitter almond oil, Cherry laurel water). It has been proposed to test H. a. as a means of stimulating the respiratory center. H. a. is also used (0.3 cm³ of 2% sodium cyanide, i.e. 0.1-0.11 mg per 1 kg of body weight) intravenously to determine the speed of blood circulation in healthy people. The speed at which the salt reaches the capillary network was determined by them by the moment of onset of respiratory stimulation. This method causes the same concerns as the use of such a strong poison as a means of stimulating respiration.

Hydrocyanic acid as an industrial poison under certain conditions can pose a significant poisoning hazard, especially due to its use as an insecticide, deratizer, and disinfectant in agriculture and transport (see Disinfection). In the USA, Germany, and other countries, hydrocyanic acid is widely used for disinfecting granaries, warehouses, and elevators (especially when infested with flour moths), for disinfecting cotton, fruit trees, greenhouses, etc., as the best means due to its low cost, ease of application, and effectiveness. In industry, hydrocyanic acid can be released from its salts (cyanides) when used in various technical processes—in electroplating for copper plating, brass plating, gilding, and silvering, in metallurgy for extracting gold and silver, for ore flotation, hardening steel products, etc. As a by-product, hydrocyanic acid is formed during incomplete combustion of organic nitrogen-containing substances (for example, celluloid), is contained in small quantities in blast furnace gas, illuminating gas, in wastewater from textile factories using red blood salt for mordanting and dyeing, and may be encountered in small quantities in many other productions. The amount of cyanides (mainly HCN) used for cyanidation and other purposes is very significant: in Germany, for example, during the first 10 years after the introduction of cyanidation in 1917, about 10,000 tons of cyanides were consumed and over 40 million cubic meters were cyanidized. In the USA, by the early 1930s, annual consumption of cyanides reached 12,000 tons worth about 500 million dollars. In the USSR, where cyanidation was introduced relatively recently, the demand for sodium cyanide in 1932 for agricultural needs alone amounted to a relatively small figure of 100 tons. Professional poisonings from hydrocyanic acid were observed very rarely before the introduction of cyanidation. Only during and especially after the war do descriptions of professional poisonings appear, often of a mass nature, arising in connection with cyanidation. Baile described a case of poisoning of 100 soldiers caused by cyanidated ammunition issued without proper ventilation; there were no fatal cases in this instance. In 1927, near Düsseldorf, a mass poisoning occurred at a cyanidated factory-mill, in which about 200 people were poisoned by hydrocyanic acid adsorbed by special work clothing that remained in the premises during cyanidation and was not properly ventilated. In the USA, over 3 years (1920-23), 18 fatal poisonings were registered, of which 4 were for ticketless passengers on steamships, the rest were the result of violation of established instructions. The nature of professional poisonings from hydrocyanic acid is so distinctive that it allows speaking of an industrial type of poisoning, as opposed to the type of acute lightning-fast poisonings usually described in pharmacology and toxicology guides, which presumably occur extremely rarely in production. The industrial type of poisoning is characterized by a variety of nervous symptoms, mainly of the sensory-motor apparatus, appearing against a background of constantly increasing paralysis of the central nervous system: headache, dizziness and nausea, often accompanied by vomiting, unpleasant taste and burning sensation in the mouth, scratching in the nose and throat, irritation of the conjunctiva, feeling of tightness in the chest and lack of air, pain in the heart area and a strong feeling of fear, followed by general weakness and loss of consciousness. From the side of the motor apparatus—general weakness, disturbance of coordination of movements, unsteady gait, contraction of individual muscles and often clonic and tetanic convulsions; along with this, palpitations, difficulty breathing, shortness of breath, cyanosis, dilated pupils, comatose state. If death does not occur within the first hour after poisoning, a favorable outcome can be expected. Professional diseases associated with the use of cyanides are sometimes observed in electroplaters in the form of eczema of the hands and acne rosacea of the face. The toxicodynamics of industrial type poisonings is characterized by the fact that at certain (production) concentrations a stationary equilibrium is established, in which the inhaled HCN, due to insufficiently clarified transformations in the body, is neutralized and does not reach the concentration in the blood necessary for paralysis of the respiratory center, but remains at a level sufficient only to cause and maintain tissue anoxia (Fmry, Heubner). Poisoning prevention consists in as complete hermetization as possible of processes in which HCN is released, in the installation of local exhausts and sufficient general ventilation, in eliminating direct contact with cyanides through mechanization of production operations and individual protective devices, in maintaining thorough cleanliness of the premises and a number of general hygienic measures. Special preventive measures for cyanidation—thorough instruction, eviction of residents, protection zone, ventilation of the premises and testing of the air for the absence of HCN. It must be borne in mind that soft tissues—clothing, soft furniture, etc.—easily adsorb and retain HCN for a long time (which has repeatedly been the cause of poisonings) and that hydrocyanic acid can enter the body through the skin.

n.

Pravdin. Disinsective significance of HCN. Hydrocyanic acid for disinfection, in the direct sense of this word, is not applied, since it does not possess noticeable bactericidal action, but deserves attention as a very energetic insecticide and deratization agent. HCN for disinsective purposes is applied in the form of fumigations and can be obtained by the interaction of KCN, NaCN, KNa(CN)₂, K₄FeCN₆ with sulfuric acid: 2KCN+H₂SO₄=2HCN+K₂SO₄; K₄FeCN₆ + 3H₂SO₄=6HCN+FeSO₄ + 2K₂SO₄. In practice the first method of obtaining HCN is more often chosen. For disinsective purposes the content of HCN in the atmosphere is usually brought to one volume percent, corresponding approximately to 25 g NaCN or equivalent amounts of other cyanide compounds when calculated per 1 m³ of the space being fumigated (the cyanide salts must contain not less than 90% of the active substance). For the complete displacement of HCN from the indicated amount of NaCN (25 g) 32 g H₂SO₄ (according to Bome), diluted with three times its amount of water, is required. However, the content of HCN in the atmosphere can vary within wide limits without visible reduction of the disinsective effect, as is evident from the following formula of Teichmann: 1-JIT (unit-immediate result of action, N-content of HCN in volume percent, T-duration of fumigation). The product NT when calculated for achieving actual success in disinsective action must be not less than two. The actual content of HCN in the atmosphere is often considerably lower than the data of theoretical calculation; therefore with the indicated norms of interacting products it is necessary to prolong the exposure time to 6-8 hours (instead of two, provided for in Teichmann's formula). The application of HCN as an insecticidal agent leads to reliable results in disinsection, is very simple in technique and does not require special apparatus. (For the purpose of gas formation the cyanide product is mixed with sulfuric acid in a simple clay or oak vessel.) HCN does not spoil any objects being disinfected, nor does it require detailed preparation of the objects for fumigation; only the hermetic sealing of premises according to the rules accepted for gasification is necessary. The practical application of this method is very limited due to the exceptional toxicity of HCN and the danger to life associated with handling and also with staying in premises disinfected with HCN. The task of cyanization is also complicated by the absence of means for neutralizing HCN by chemical neutralization; the removal of residues of gas from the disinfected premises is possible only by ventilation, but even under this last condition HCN is sometimes detected in many adsorbents a month after fumigation. HCN finds application mainly for disinsection and deratization of railway cars and ship transport. Abroad it is also practiced for fighting moths (with the help of special chambers). Cyanization is also applied in the fight against agricultural pests. HCN is applied in practice in all these cases on the basis of special instructions and with the application of all necessary precautions against possible poisoning (gas masks, special clothing, control of completeness of degassing). For the latter purpose phenolphthalein test papers, prepared according to a special recipe, are most often used, which when air containing HCN is passed through them in a special apparatus are colored¹ pink. In rooms reliably ventilated after HCN these papers during 5 minutes of action either do not become colored at all or acquire only a pink tint. For the purpose of reducing the danger of poisoning derivatives of HCN are used along with it, known under the name of cyclones-A, B, C; cyclones represent a combination of HCN with various lacrimators (CH₂Cl₃;CH₃COOCl;C₂HBr₃COOCH₂CH₃), signaling the danger of poisoning; nevertheless this danger is not completely eliminated by this means (see also Disinsection, Disinfection, Deratization).

G. Chistyakov. Forensic medical significance belongs to hydrocyanic acid itself and its metallic salts. HCN is a component of bitter almond water (0.1%) and laurel cherry water (0.07-0.1%), as well as Aquae Cerasorum nigrae (0.04%). HCN in these preparations is formed from the glycoside amygdalin contained in plants, which in the presence of the enzyme emulsin and water breaks down into HCN, oil of bitter almonds (see Almond) and sugar. The lethal dose of anhydrous HCN is 0.05-0.06 g. Poisoning from eating a large number of plum pits has been observed. HCN is also found in some liqueurs, for example, peach, maraschino. Hydrocyanic acid is also contained in carbon monoxide and is formed in explosions of celluloid. Commercial bitter almond oil is very poisonous. Poisonings with HCN occur mostly as accidents in chemical laboratories due to inhalation of hydrocyanic acid, sometimes during disinsection. Poisonings (accident, murder, suicide) from bitter almond water, bitter almonds, beverages, etc. are rarely observed. In the investigation of a corpse signs of asphyxia are usually found, an inconsistently encountered smell of bitter almonds, predominantly from the brain and stomach contents. On the gastric mucosa, unlike potassium cyanide, only some signs of irritation are found: injection of vessels, ecchymoses. In subacute poisoning with HCN there are changes in the central nervous system in the form of noticeable macroscopically foci of softening in the lentiform nuclei. Due to the instability of HCN chemical examination of the internal organs must be carried out as soon as possible. In some cases HCN can be preserved in parts of the corpse for a long time, which should not be forgotten when deciding on exhumation. In the literature cases are described where the detection of HCN was possible 15-100 days after death, and in one observation even after 4 months the presence of hydrocyanic acid could still be proved in parts of the corpse. For diagnostic purposes during autopsy it is recommended to apply preliminary tests, in particular the fairly sensitive guaiac test of Schönbein. V. Vladimirsky. Detection in legal cases. Poisonings with salts of HCN are most often encountered: potassium cyanide and sodium cyanide, which is manifested by a sharply alkaline reaction of the stomach contents in fresh internal organs. The stomach together with the contents of internal organs is subjected to distillation with steam (see Poisons-isolation). Into the first receiver (flask) 2-5 cm³ of a solution of caustic soda is poured. When 2-5 cm³ of distillate has collected in the receiver, it is replaced with another, and the first portion is tested for HCN. To the first portion of distillation (and to portions from subsequent ones after adding caustic soda) 2-5 drops of a solution of ferrous sulfate (ferrous sulfate) and ferric chloride are added, the liquid is thoroughly shaken and acidified with dilute hydrochloric acid to a weakly acidic reaction. In the presence of HCN a blue precipitate or blue coloring of the liquid appears. With very small amounts the coloring and precipitate may appear after 24-48 hours. For the detection of HCN in the air, for example after disinsection of premises with hydrocyanic acid, paper strips moistened with guaiac tincture are placed in the air; after removing the alcohol with a 72% solution of copper sulfate the paper strips turn blue in the presence of hydrocyanic acid. It should be noted that bluing can be caused by other oxidizing agents (chlorine, nitrogen oxides, ozone). Therefore a negative result is significant. Some authors have proposed benzidine for such a reaction, which makes it possible to judge the amount of hydrocyanic acid in the air of premises after disinsection. Paper strips are soaked with a mixture of equal volumes of two solutions: 1) 2.86 g of copper acetate per 1 liter; 2) 475 cm³ of a saturated (at room temperature) solution of benzidine and 525 cm³ of water. The appearance of a strong blue coloring in 7 seconds indicates the presence of 0.077 mg of hydrocyanic acid per 1 liter (danger). If no coloring appears within 7 seconds the content cannot be more than 0.0077 mg per 1 liter (no danger).