Phosgene

PHOSGENE (COCl2), chlorocarbonic acid anhydride, which it converts into upon hydrolysis. The simplest method of obtaining Phosgene is the direct combination of chlorine with carbon monoxide in the presence of charcoal as a catalyst. The reaction proceeds according to the equation: Cl2 + CO = COCl2. Phosgene can also be obtained by oxidation of chloroform (CHCl3), carbon tetrachloride (CCl4), and chloropicrin (NO2CCl3). The reaction proceeds according to the equation: 2CHCl3 + 3O2 = 2COCl2 + H2O + CCl4. Phosgene is a colorless, transparent, easily volatile liquid, specific gravity 1.4, boiling point +8.2°, with the odor of stale hay. Upon very strong cooling, Phosgene solidifies into a crystalline mass; melting point -126°. The vapor density of Phosgene is 3.5 times that of air. Phosgene dissolves in water and itself is a good solvent for many chemical warfare agents, including mustard gas. Dissolving in water, Phosgene hydrolyzes into hydrochloric acid and carbon dioxide according to the equation: COCl2 + H2O = 2HCl + CO2. The hydrolysis of Phosgene proceeds more slowly than that of chlorine, but more rapidly than that of diphosgene (see). In the presence of moisture, Phosgene corrodes metal. Due to its great physical (volatility) and chemical (hydrolysis) activity, Phosgene belongs to the group of unstable chemical warfare agents. Phosgene for combat purposes is used in gas cylinders, artillery chemical shells, and mines. In industry, Phosgene is widely used for the production of paints. The specific reaction for determining Phosgene in air is the pumping of the test air through a 3% aqueous solution of aniline. A white crystalline precipitate of diphenylurea is formed. The reaction proceeds according to the equation: 2C6H5NH2 + COCl2 = C6H4NH-CO-C6H4NH + 2HCl. From a toxicological point of view, Phosgene belongs to the group of chemical warfare agents of asphyxiating action with delayed manifestation of poisoning symptoms. Phosgene enters the organism through the respiratory organs, primarily affecting lung tissue. Along with its local action, Phosgene also possesses a general action (resorption). It accumulates. The toxicity of Phosgene is very great (0.03 mg/l causes serious poisoning). According to literature data, the lethal dose for phosgene is 450 mg/kg. Phosgene in combat concentrations does not possess noticeable irritating properties. Because of this, the moment of exposure is often unnoticed or accompanied only by the sensation of the smell of stale hay, slight salivation, and slight coughing. The victim often attaches no significance to these weakly expressed symptoms. Upon leaving the contaminated zone, all these phenomena usually disappear and a period of so-called apparent well-being sets in. After the latent period (4–8 hours or more), signs of developing poisoning begin to appear in the form of a depressed state, mental depression, gradually increasing dyspnea, coughing, initially dry and then turning into a cough with massive expectoration of foamy sputum (up to 1 liter per day). Even slight physical exertion increases dyspnea and coughing, causing cyanosis. The patient's complaints consist of weakness, dyspnea, chest pain, and coughing with foamy sputum. In serious cases of poisoning, anoxemia and asphyxia (blue and gray types), pulmonary edema, emphysema, blood changes (thickening, increased viscosity, coagulability) develop; consequently, thromboses and embolisms are possible, a decrease in total and reserve alkalinity, and shifts in white blood cells. In the first hour, body temperature drops by 0.5–1.0°, then rises, reaching 38.0–38.5° and is maintained at this level throughout the pulmonary-asphyctic period (48–72 hours). In fatal, rapidly progressing cases, the temperature, having dropped in the first hour, does not rise but continues to decrease to 35.0° or lower. In cases of secondary infection, the temperature rises rapidly to 40.0–41.0° (the period of pulmonary inflammation—most often after 48 hours). The boundaries of the heart expand, the tones become impure, murmurs appear, accentuation on the second tone of the pulmonary artery, sometimes splitting of tones and even loss. Very rarely—asystole. The pulse is accelerated to 130, less often bradycardia; sometimes arrhythmia and alrorhythmia. Blood pressure is lowered. In the period of sharply expressed blue asphyxia, blood pressure is elevated. In the kidneys, glomerulonephritis phenomena are observed. The liver and spleen are enlarged, painful, and soft. Acute, moderately expressed gastroenteritis. On the part of the nervous system, neurosis phenomena are observed; shock is rare. Weak conjunctivitis, changes in the retina and choroid (secondary in nature due to blood changes and anoxemia)—hyperemia, hemorrhages, thromboses. Metabolism is disturbed; increased excretion of nitrogen-containing products, calcium salts, and phosphorus. There is accelerated breakdown of protein substance. The critical moment is the first 48–72 hours (development and conclusion of the pulmonary-asphyctic period). The total duration of the disease (without complications) is 2–4 weeks. Mortality fluctuates within 5–8% (depends on many causes: severity of intoxication, behavior at the moment and after poisoning, individual characteristics of the victim, time, nature, and quality of first aid). The maximum number of deaths (80%) falls on the first 72 hours. The remaining 20% fall on the period from 3 to 16 days and depend on complications: heart weakness, acute asphyxia, secondary infection. Autopsy in the pulmonary-asphyctic period shows an increase in the weight and volume of the lungs (4–5 times), a change in the character of the lung surface and color (mottling) due to the alternation of emphysema and atelectasis foci, hyperemia, edema, and often infarcts. The pleural cavities in most cases are free of fluid. The pleura is smooth, shiny, and moist. The heart cavities are stretched and filled with dark blood clots. Sometimes hemorrhages are found under the endocardium of the left ventricle. In other organs, mainly venous congestion phenomena, sometimes infarcts. Prevention—gas mask. First aid measures: removal from the contaminated atmosphere, removal of contaminated clothing, complete rest, warming of the body (hot water bottles), inhalation of oxygen (or other methods of introducing oxygen—under the skin, into a vein), bloodletting (400–700 cm3), administration of CaCl2 and a 25% solution of gum glucose; cardiac (camphor, strophanthin). In cases of collapse—injections (physiological saline, glucose solution, gum glucose, Ringer's solution). Careful nursing, hygienic conditions of maintenance, light, non-irritating food. Upon recovery, respiratory gymnastics.

A. Glebovich. Discovery. The object of investigation is air. Internal organs and other objects are unlikely to give a positive result upon investigation due to the decomposition of Phosgene. From the object, Phosgene is displaced by a current of air and absorbed by aniline solution: turbidity appears due to the formation of diphenylurea from Phosgene and aniline, which is poorly soluble in water. To absorb free chlorine, which may accompany phosgene, the air is first passed through a solution of potassium iodide and sodium sulfite. The second, less specific method is the absorption of phosgene by alcohol with subsequent cleavage of the halogen upon the action of metallic sodium, dilution with water, acidification with nitric acid, and detection of the chloride ion with silver nitrate. The reaction represents a general method for detecting volatile halogen compounds with carbon in the absence of hydrogen chloride, which is determined by a special test. Rapid (non-specific) detection of Phosgene using the Beilstein reaction: a heated copper wire or mesh (copper fabric) introduced into a colorless flame of a spirit lamp in air containing Phosgene imparts a green color to the flame.