Phosgene MSDS

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This post was last edited by zhangyong6404 on 2009-10-22 at 14:53.
Overview:
Name: Phosgene; Carbonyl chloride
English names: Phosgene; Carbonyl chloride
Molecular formula: COCl2
Molecular weight: 98.92
Structure: See figure
CAS No.: 75-44-5
National standard code: 23038
Derivatives (related substances):
Similar substances: Diphosgene, Triphosgene, Formaldehyde, Dichloromethane
Upstream products: Carbon tetrachloride, Fuming sulfuric acid, Carbon monoxide, Chlorine
Downstream products: Methyl chloroacetate, Isocyanates, Benzene sulfonyl isocyanate, Methyl chloroformate, Ethyl chloroformate, 2-Ethylhexyl chloroformate, Diethyl carbonate, Dimethyl carbonate, Diphenyl carbonate, Chloroacetyl chloride, N,N’-Dimethyl-N,N’-diphenylurea, N-Chloromethyl-N-phenylcarbamoyl chloride, N,N’-Dissuccinimide carbonate, Tetraethylammonium chloride, Benzoyl chloride
Basic properties:
Appearance: Colorless or slightly yellow gas (industrial-grade material is usually a light yellow liquid); when concentrated, it has a strong irritating or asphyxiating odor. 　　Melting point: -127.84°C (-118°C) Boiling point: 7.48°C (8.2°C) Specific heat capacity: 8.2 J/W Relative density: 3.5 (air = 1) ； 1.37 (water = 1) Vapor pressure: 202.65 kPa (27.3°C) Volatility: 6652.25 mg/L Stability: Stable Hazard symbols: 6 (toxic gas), 20 (corrosive) Solubility: Slightly soluble in water; it undergoes gradual hydrolysis. Soluble in organic solvents such as aromatics, carbon tetrachloride, and chloroform. Other: Highly toxic! Non-flammable. Reaction with carbon dioxide to produce it/Source: In the laboratory, it can be produced by reacting carbon tetrachloride with hydrochloric acid. Heat carbon tetrachloride to 55–60°C and add fuming hydrochloric acid drop by drop; phosgene will then be released. If liquid phosgene is required, the phosgene generated is condensed. 　　Phosgene is typically produced industrially by the reaction of carbon monoxide with chlorine. This is a highly exothermic reaction; the reactor equipped with activated carbon should have a water-cooled jacket to maintain the reaction temperature at around 200°C. To obtain high-quality phosgene and reduce equipment corrosion, an appropriate excess of thoroughly dried carbon monoxide should be used when mixing it with chlorine. The mixture is fed from the upper part of the synthesizer; after passing through the activated carbon layer, it is quickly converted into phosgene. When a synthesizer with specifications of Ф700×2900 is used, each unit can produce 200 tons of phosgene per year. Raw material consumption quotas: chlorine (>99%) 925 kg/t, oxygen (under standard conditions) 268 (m3) kg/t, coke 400 kg/t. 　　Raw material consumption quota: Chlorine (>99%) 925 kg/t ； Oxygen (under standard conditions) 268 (m3) kg/t ； Coke 400 kg/t. 　　Direct reaction of chloroform with hydrogen peroxide: CHCl3 + H2O2 = HCl + H2O + COCl2 (phosgene) – Chloroform can be oxidized to produce phosgene if not stored properly. 　　Oxygen can also be produced using hydrogen peroxide and then reacted with chloroform: 2CHCl3 + O2 = 2HCl + 2COCl2 (phosgene). In the event of a phosgene leak, it should be absorbed using water mist; phosgene readily undergoes hydrolysis: COCl2 + H2O = 2HCl + CO2. Uses: Phosgene is an important organic intermediate in the production of pesticides ； Modern Medicine ； Engineering plastics ； Polyurethane materials have many uses, as does **. In pesticide production, it is used to synthesize the carbamate insecticide carbofuran ； Carbofuran ； Many varieties such as leafhopper powder are also used in the production of the fungicide carbendazim and various herbicides. China’s Linxiang Amino Chemicals Factory and Ningyang Pesticide Factory have become manufacturing bases for carbamate pesticides, with Ningyang Jiaoyao Factory capable of producing 43 different varieties. Isocyanate-based products produced from phosgene, such as TDI, MDI, and PAPI, are used in rigid polyurethane foams ； soft foam ； elastomer ； Important raw materials for synthetic leather ； Certain types of isocyanates are widely used in polyurethane coatings ； There are also special varieties used as adhesives, such as Lenox glue. It is used in the dye industry to produce dye intermediates such as alizarin acid, and in the defense industry to manufacture the fixing agent dimethyldiphenylurea as well as as a military poison gas. Chloroformates produced using phosgene are pesticides ； Pharmaceuticals ； Intermediates for organic synthesis such as polymerization initiators. When producing the engineering plastic polycarbonate by the direct phosgene method or the transesterification method, phosgene is required as a raw material. Phosgene is highly toxic and a strong irritant ； Asphyxiating gases. Inhalation of phosgene causes pulmonary edema ； Pneumonia and other conditions pose a risk of death. It was widely used in the Auschwitz concentration camp during World War II to kill prisoners of war, Jews, **criminals, and others. Toxicity Overview of poisoning This substance is a typical transient toxin. The semi-lethal dose LD50 for inhalation poisoning is 3200 mg·min/m3, and the semi-disabled dose is 1600 mg·min/m3. After inhalation, symptoms appear after a few hours of incubation, manifesting as difficulty breathing, chest pain, and decreased blood pressure; in severe cases, it can lead to coma and death. Gas masks provide effective protection and usually do not require disinfection. Antidotes include urotropine, among others. Artificial respiration is prohibited in patients showing symptoms of pulmonary edema. 　　Detailed Information I. Health Hazards Routes of exposure: Inhalation, dermal absorption. 　　Health hazards: It primarily damages the respiratory tract, causing chemical bronchitis, pneumonia, and pulmonary edema. 　　Acute poisoning: In mild cases, patients experience symptoms such as tearing, photophobia, throat discomfort, coughing, and chest tightness. In moderate cases, in addition to an exacerbation of these symptoms, patients suffer from mild breathing difficulties and slight cyanosis. In severe cases, pulmonary edema or adult respiratory distress syndrome occurs; patients have severe coughing, produce large amounts of frothy sputum, experience respiratory distress, and show significant cyanosis. There is a period of symptom relief before the onset of pulmonary edema (usually 1–24 hours). Mediastinal and subcutaneous emphysema can occur concurrently. 　　II. Toxicological data and environmental behavior Acute toxicity: LC50 = 1400 mg/m3, 1/2 hour (inhalation by rats); inhalation of 3200 mg/m3 by humans is fatal; an inhalation concentration of 25 ppm for 30 minutes represents the minimum lethal concentration. 　　Subacute and chronic toxicity: When animals inhaled 0.0008 mg/L for 5 hours (5 days), 40% developed emphysema. 　　Sources of pollution: Phosgene is used as a treatment agent for polyurethane products, a plasticizer, a raw material for polycarbonates, a fiber treatment agent, an herbicide, a **stabilizer, dyes, dye intermediates, and raw materials for pharmaceuticals. Leaks or accidental releases during production can lead to pollution.
Hazardous properties: Non-flammable. It has high chemical reactivity and is highly corrosive when in contact with water. 　　Combustion (decomposition) product: hydrogen chloride. 　　3. On-site emergency monitoring methods:
Rapid chemical analysis methods: Nitrobenzylpyridine detection tubes, diamine indicator paper method – from “Emergency Monitoring, Handling, and Disposal Techniques for Sudden Environmental Pollution Incidents”, edited by Man Benta.
Gas detection tubes (products from Beijing Labor Protection Institute and German company Dräger).

4. Laboratory monitoring methods:
Ultraviolet spectrophotometry (HJ/T31-1999, for exhaust gases from fixed pollution sources).
Iodometric method – from “Methods for Monitoring and Analyzing Air and Exhaust Gases”, compiled by the Environmental Protection Bureau.
Silver nitrate treated with nitric acid.

5. Environmental standards:
China (TJ36-79): Maximum allowable concentration of harmful substances in workshop air – 0.5 mg/m3.
China (GB16297-1996): Comprehensive emission standards for air pollutants.
① Maximum allowable emission concentrations (mg/m3):
5.0 (Table 1); 3.0 (Table 2).
② Maximum allowable emission rates (kg/h):
Level 2: 0.12–1.2 (Table 1); 0.10–1.0 (Table 2).
Level 3: 0.18–1.8 (Table 1); 0.15–1.5 (Table 2).
③ Monitoring limits for unorganized emissions (mg/m3):
0.080 (Table 2); 0.10 (Table 1).

6. Emergency handling and disposal methods:
I. Emergency response to leaks
Evacuate people from the area affected by the leak to an upwind location immediately, and isolate the area. For small leaks, isolate a distance of 150 meters; for large leaks, isolate a distance of 450 meters. Strict restrictions should be placed on access to the area. It is recommended that emergency responders wear self-contained positive-pressure breathing apparatus and protective clothing. Enter the site from the upwind side. Seal the source of leakage as much as possible. Ensure proper ventilation to accelerate diffusion. Neutralize by spraying ammonia water or other dilute alkaline solutions. Construct dikes or dig pits to contain the large amount of wastewater generated. Leaking containers must be properly handled, repaired, and inspected before being used again. 　　Phosgene is highly hydrolyzable; even in cold water, its hydrolysis occurs at a rapid rate. Water sources, water-containing foods, and substances that absorb water easily will not become contaminated. Phosgene reacts rapidly with ammonia to produce mainly non-toxic substances such as urea and ammonium chloride; therefore, concentrated ammonia can be used to disinfect phosgene. Phosgene reacts with organic amines to produce a white precipitate of diphenylurea and aniline hydrochloride. This reaction can be used to test phosgene. Phosgene is rapidly decomposed in an alkaline solution to form non-toxic substances. Various bases and alkaline substances can be used to disinfect phosgene. 　　II. Protective Measures Respiratory protection: During normal operations, a filtering gas mask (full-face mask) should be worn. It is recommended to wear an air respirator during emergency rescue or evacuation. 　　Eye protection: Protection is provided under respiratory protection. 　　Body protection: Wear a rubberized gas mask suit. 　　Hand protection: Wear rubber gloves. 　　Others: Smoking, eating, and drinking are prohibited at the work site. Conduct pre-employment and regular health checks. 　　III. First aid measures Skin contact: Remove contaminated clothing and rinse with flowing water. 　　Eye contact: Lift the eyelids and rinse with flowing water or saline. Seek medical attention. 　　Inhalation: Quickly move to an area with fresh air. Keep the airway clear. If there is difficulty breathing, administer oxygen. If breathing stops, perform artificial respiration immediately. Seek medical attention. 　　Fire extinguishing method: This product is non-flammable. Firefighters must wear filter-type gas masks (full-face masks) or self-contained breathing apparatus, as well as full-body fire and gas-resistant suits, to extinguish the fire from upwind. Cut off the gas supply. Use water spray to cool the container; if possible, move the container away from the fire to an open area. In the event of phosgene leakage, small amounts can be dispersed using steam, while larger amounts can be washed away with liquid ammonia spray. Extinguishing agents: fogged water, dry powder, carbon dioxide. 　　 Mechanism of poisoning The main pathological change following inhalation of phosgene poisoning is toxic pulmonary edema. Pulmonary edema is the result of increased permeability in the pulmonary capillaries. There are various theories regarding the causes of pulmonary edema, such as acylation, direct action, hydrochloric acid effect, neural reflex action, and changes in pulmonary hemodynamics, each of which has experimental support. However, no hypothesis can fully explain the occurrence and development of pulmonary edema. 　　It is currently generally believed that increased permeability of the pulmonary capillary wall is closely related to the acylation by phosgene. Phosgene is an acyl halide compound whose active functional group is the carbonyl group (O=C). It possesses highly reactive chemical properties; it undergoes acylation reactions with important functional groups such as amino groups, thiol groups, and hydroxyl groups in lung tissue proteins. This leads to widespread inhibition of the lung enzyme system, thereby affecting normal cellular metabolism and function. As a result, the air-blood barrier in the lungs is damaged, increasing the permeability of pulmonary capillaries and causing pulmonary edema. Furthermore, damage to alveolar surfactant is also one of the important factors in phosgene poisoning. Under normal conditions, the alveolar surface is covered with a layer of surfactant secreted by type II alveolar epithelial cells. This surfactant reduces the surface tension of the liquid in the alveoli, preventing them from collapsing during exhalation and helping to keep the alveoli dry. Dipalmitoyl phosphatidyl choline (DPPC) is one of the main components of pulmonary surfactant. Acyl-CoA ester transferase is involved in its biosynthesis. Following phosgene poisoning, the activity of this enzyme decreases, which leads to a reduction in the amount of DPPC in the alveolar walls. This diminishes the function of alveolar surfactant, resulting in an increase in the surface tension of the fluid within the alveoli and thus alveolar collapse. The alveolar pressure drops significantly, while the hydrostatic pressure in the pulmonary capillaries increases as a counteraction; this causes fluid to leak out from the blood vessels in large quantities, leading to the development of pulmonary edema. 　　Pathological changes: The pathophysiological changes associated with phosgene and diphosgene poisoning are primarily caused by pulmonary edema. 　　In the case of inhalation poisoning, breathing first slows down briefly, followed by shallow and rapid breathing. After the onset of early pulmonary edema, the reduced alveolar respiratory surface area and thickened alveolar walls impair gas exchange within the alveoli. Together with the accumulation of edematous fluid in the respiratory tract, bronchospasm, and bronchial narrowing caused by mucosal swelling, pulmonary ventilation is impaired, resulting in respiratory hypoxia. This leads to a decrease in blood oxygen levels and an increase in CO2 levels, causing the skin and mucous membranes to turn cyanotic. At this time, there are compensatory changes in respiratory and circulatory function, such as increased breathing rate, enhanced activity of the intercostal muscles, a rapid and strong heartbeat, and a slight rise in blood pressure. 　　In the late stage of edema, due to ① a large amount of fluid in the alveoli, lung pressure increases, thereby increasing the load on the right heart ； ②The massive infiltration of plasma into the lungs reduces the blood volume in the circulatory system, leading to blood concentration and increased viscosity. Increased peripheral resistance leads to an increased load on the left heart ； ③Prolonged severe hypoxia leads to muscular dystrophy, and as a result, symptoms of cardiac failure such as reduced cardiac contractility, arrhythmias, slowed circulation, and gradually decreasing blood pressure can occur. The latter can further exacerbate tissue hypoxia, increase the levels of incomplete oxidation products in the body, and lead to acidosis and electrolyte imbalances. The level of CO2 in the blood gradually decreases, the capillaries in the internal organs dilate while those in the periphery constrict; the skin and mucous membranes turn pale, blood pressure drops sharply, acute circulatory failure occurs, and shock sets in. In this phase, due to pulmonary edema combined with circulatory failure, the body loses its ability to compensate. 　　As pulmonary edema progresses, plasma leaks out in large quantities from the pulmonary capillaries, resulting in a decrease in plasma volume and blood concentration. This leads to a reduction in plasma proteins, while the numbers of red and white blood cells as well as hemoglobin levels increase, along with an elevation in the hematocrit. These changes are consistent with the degree of pulmonary edema. Due to thick blood, slow blood flow, and tissue damage, blood coagulability increases. As a result, thrombi and emboli can form. 　　The central nervous system is very sensitive to hypoxia. In the early stages of hypoxia, the cerebral cortex becomes excited, leading to restlessness, headaches, dizziness, and other symptoms ； In severe cases of hypoxia, the condition gradually shifts to a state of suppression, with symptoms such as apathy and fatigue. As hypoxia progresses further, the inhibition in the cerebral cortex deepens and spreads to subcortical areas. The respiratory and circulatory centers may shift from an excited state to an inhibited state, resulting in weakened breathing and heartbeat, and ultimately central paralysis that leads to the cessation of breathing and heartbeat and death. 　　Pathological examination reveals pale skin, an enlarged chest cavity, absent intercostal spaces, and pink frothy secretions coming from the mouth and nose, with more secretion flowing out when the chest cavity is compressed. The lungs appear \"marble-like\" due to the alternating presence of various lesions such as pulmonary edema, emphysema, pulmonary congestion, atelectasis, and mild bleeding. 　　 Clinical manifestations: Phosgene (diphosgene) poisoning can be classified clinically into four types based on the severity of the poisoning: mild, moderate, severe, and fulminant. Mild poisoning presents with very mild symptoms; the staging is not distinct, and it is only manifested as symptoms of indigestion and bronchitis, with recovery possible within a week. Lightning-type poisoning is extremely rare; it occurs mostly when a very high concentration of the poison is inhaled. Within a few minutes after exposure, death can result from reflexive cessation of breathing and heartbeat. In moderate to severe cases of poisoning, the condition progresses rapidly and severely. The typical clinical manifestations can be divided into four stages: (1) Irritation stage Irritation symptoms appear immediately upon inhaling phosgene. The main symptoms include early onset of irritation in the eyes and respiratory tract, such as eye pain, tearing, coughing, chest tightness and shortness of breath, changes in breathing rate, abnormal sense of smell or a persistent odor of phosgene, as well as pain in the throat and behind the sternum ； Symptoms of the autonomic and central nervous systems include headache, dizziness, fatigue, restlessness or reduced speech, apathy, nausea, vomiting, and upper abdominal pain. At equal doses of phosgene inhalation, poisoning at high concentrations for a short period results in severe irritation symptoms ； Symptoms of poisoning due to low concentrations over a long period are mild. However, when the inhalation dose is high, respiratory irritation symptoms are pronounced and last for a longer period of time. 　　(II) Incubation period: The symptomatic signs subside or lessen, and the subjective symptoms improve, but the pathological process continues to progress, with pulmonary edema gradually developing. The incubation period is generally 2 to 13 hours. Severe poisoning: 2–4 hours, or even 1 hour ； Moderate poisoning lasts 8 to 12 hours, and sometimes up to 24 hours. 　　(III) Pulmonary edema stage The transition from the incubation period to the pulmonary edema stage can occur suddenly or gradually, and this stage generally lasts 1–3 days. 　　Early symptoms of pulmonary edema (with interstitial pulmonary edema appearing first) include general fatigue, headache, chest tightness, rapid and shallow breathing, increased pulse rate, coughing, and restlessness. On auscultation, breath sounds are diminished, with fine moist rales or crackles at the lung bases. Chest imaging shows signs of pulmonary edema. Subsequently, the general condition deteriorated, and alveolar pulmonary edema developed rapidly. Typical symptoms and signs include wheezing, difficulty breathing, frequent coughing, the production of large amounts of pink frothy sputum, rapid pulse, nausea, vomiting, and upper abdominal pain. Tapping the chest reveals tympanic and dull sounds. The lower limit of the lungs is decreased, and the cardiac dullness boundary disappears ； On auscultation, the entire lungs were filled with dry and wet rales. Blood tests show signs of blood concentration, along with decreased arterial oxygen partial pressure and oxygen saturation. Alveolar pulmonary edema progresses rapidly, generally reaching its peak within 24 hours. The pulmonary edema stage can be further divided into two phases depending on the functionality of the circulatory system. 　　1. Cyanotic hypoxia stage: During this stage, blood oxygen levels decrease, causing cyanosis of the skin and mucous membranes, but circulatory function is still able to compensate. Blood pressure is normal or slightly high, with a fast and strong pulse. The patient is conscious, with a body temperature that can rise to 38–39°C. Due to pulmonary edema, which impairs the elimination of CO2, carbonic acid levels in the blood increase, leading to respiratory acidosis ； Excessive CO2 loss can also occur due to hyperventilation, leading to respiratory alkalosis. 　　2. Pale (or shock) hypoxia stage: The condition continues to worsen, with extreme difficulty breathing. In severe cases, all the respiratory auxiliary muscles become involved in the effort to breathe, and circulatory failure gradually sets in: the pulse becomes weak, rapid, and irregular; blood pressure drops; the skin and mucous membranes turn pale; cold sweats appear; and the patient gradually falls into a coma. At this point, the blood oxygen level is lower, and the amount of incomplete oxidation products increases, leading to metabolic acidosis. 　　The symptoms and signs of phosgene (diphosgene) poisoning reach their peak at 24–48 hours; without prompt treatment, death can occur within 1–3 days, while severe cases may lead to death within 5 days. Therefore, anyone who inhales phosgene must be under close observation for at least 3 to 4 days. 　　(IV) Recovery period: In cases of mild poisoning, or after treatment, the pulmonary edema fluid can be absorbed within 2 to 4 days after the onset of the illness, and the overall condition improves. Cough and shortness of breath decrease, sputum production reduces, body temperature drops, and lung rales lessen or disappear. The results of X-ray examinations, pulmonary function tests, and blood gas analyses gradually returned to normal. Generally, recovery is almost complete 5 to 7 days after poisoning, and full health is restored within 2 to 3 weeks. However, symptoms such as dizziness, dry throat, loss of appetite, and unstable respiratory and circulatory functions persisted for several weeks. 　　In the case of a secondary infection, the condition usually worsens on the 3rd to 4th day after poisoning. Body temperature continues to rise, and the absorption of pulmonary edema is slow; death may occur due to bronchopneumonia 8 to 15 days after poisoning. In addition, other complications may occur, such as pleurisy and bronchitis; occasionally, pulmonary embolism, lung gangrene, lung abscess, as well as embolisms in the lower extremities, brain, heart, retina, and other areas. 　　The main sequelae include chronic bronchitis, emphysema, bronchiectasis, advanced lung abscess, and a predisposition to tuberculosis. The prognosis of phosgene poisoning depends on the dose inhaled, the severity of the condition, the treatment received, and any complications that arise. It is difficult to determine the prognosis during the incubation period. Those with pallid asphyxia generally have a poor prognosis. The time of death is mostly within 1 to 2 days after poisoning. Those who survive more than 48 hours generally recover, though they may be left with sequelae. The main cause of death was severe hypoxia and circulatory failure resulting from pulmonary edema. In the late stage, most die from bronchopneumonia. 　　Additional note: Phosgene is highly toxic and a strong irritant ； Asphyxiating gases. Inhalation of phosgene causes pulmonary edema ； Pneumonia and other conditions pose a risk of death. 　　Emergency procedures for phosgene leaks: Evacuate people from the contaminated area promptly to an upwind location and isolate it immediately; for minor leaks, isolate a distance of 150 meters, and for major leaks, isolate a distance of 450 meters, strictly restricting access. It is recommended that emergency responders wear self-contained positive-pressure breathing apparatus and protective clothing. Enter the site from the upwind side. Seal the source of leakage as much as possible. Ensure proper ventilation to accelerate diffusion. Neutralize by spraying ammonia water or other dilute alkaline solutions. Construct dikes or dig pits to contain the large amount of wastewater generated. Leaking containers must be properly handled, repaired, and inspected before being used again. 　　Phosgene is highly hydrolyzable; even in cold water, its hydrolysis occurs at a rapid rate. Water sources, water-containing foods, and substances that absorb water easily will not become contaminated. Phosgene reacts rapidly with ammonia to produce mainly non-toxic substances such as urea and ammonium chloride; therefore, concentrated ammonia can be used to disinfect phosgene. Phosgene reacts with organic amines to produce a white precipitate of diphenylurea and aniline hydrochloride. This reaction can be used to test phosgene. Phosgene is rapidly decomposed in an alkaline solution to form non-toxic substances. Various bases and alkaline substances can be used to disinfect phosgene. 　　Additional note: Phosgene has an odor similar to that of green apples; it is highly toxic. Inhaling it causes liquefaction in the lungs, and excessive inhalation can lead to death from asphyxiation. 　　Long-term experiments on human exposure to trace amounts of phosgene have shown that this gas can cause weight gain; as a result, workers in factories that produce phosgene may experience weight gain, which is related to the inhalation of trace amounts of phosgene.