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Choking Agent: CG

Description and Property Data Detection Symptoms and Effects
Medical Countermeasures Physical Countermeasures Decontamination
Selected Precursors Comments and Historical Notes ICD Codes

CHEMICAL PROTECTIVE ENSEMBLES ARE REQUIRED FOR PROTECTION!
Hazardous on
exposure by:
Ingestion
Inhalation
Injection
Skin contact

Masks, including self-contained breathing apparatus (SCBA) masks, provide limited protection.

Complete chemical protective ensembles should be worn to ensure protection.

Evacuate uphill and upwind without moving through the agent cloud.

Water contaminated by CG poses potential hazards.

Go to Table of Initial Isolation Distances

CA Index Name

Carbonic dichloride

CAS Registry Number

75-44-5

RTECS Number

SY5600000

An odor sometimes described as that of new mown hay may be detected (odor threshold 1.5 mg/m3); this odor may be rapidly replaced by an "irritating" or "toxic" odor (irritation threshold 4 mg/m3).

Synonyms: Phosgene
Carbon dichloride oxide
Carbon oxychloride
Carbonyl chloride
Carbonyl dichloride
Chloroformyl chloride
Dichloroformaldehyde

CHEMICAL AND PHYSICAL PROPERTIES

Structural Formula

Molecular
Formula
CCl2O Molecular
Weight
98.92

Boiling
Point

7.6° Melting
Point
-128°
Vapor
Density
3.4 Liquid
Density
1.37 at 20°
Vapor
Pressure
1418 mm Hg at 25°
1180 mm Hg at 20°
555 mm Hg at 0°
365 mm Hg at -10°
Volatility 4,300,000 mg/m3 at 7.6°
2,200,000 mg/m3 at -10°
528,000 mg/m3 at -40°
Nonflammable

USFA Hazard Ratings
FIRE
0
HEALTH
4
REACTIVITY
1
SPECIAL
UN 1076
EINECS 200-870-3
ICSC 0007

DETECTION

The M18A2 and ICAD chemical agent detectors may be used for detection. In addition, there are a variety of commercially available detection systems, including test papers and dosimeters.

SYMPTOMS AND EFFECTS

Depending on the degree of intoxication, symptoms may include:

eye irritation, usually accompanied by lacrimation (tearing) and blepharospasm
corneal opacification
dry throat
irritation in the nose and/or throat (“burning”)
smokers may report a metallic taste
cough (nonproductive initially; may progress to productive of a frothy sputum)
nausea
dyspnea
chest discomfort/tightness (“burning”); wheezes or rales may be heard
symptoms of hypoxemia, including headache, feeling “lightheaded” up to cyanosis
tachycardia
laryngospasm

Chest x-rays may show evidence for pulmonary edema with bilateral infiltrates (so-called “batwing infiltrates”). Note that x-rays will not usually be useful as predictive tools, as observable changes in the x-rays may lag behind changes in the condition of a victim.

Lactate dehydrogenase levels may be elevated.

Oxygen saturation should be monitored, especially in symptomatic patients. Arterial blood gas measurements may also be useful.

There is usually a latent period between exposure to phosgene and the onset of symptoms. This period may be as long as three days, but is usually less than a day. Individuals believed to have been exposed to phosgene should be held for observation for at least 8 hours. If, after the observation period, no symptoms have developed and a chest x-ray shows no signs of edema, the patient may be discharged but should be given instructions to be alert to symptoms of pulmonary edema and to be reevaluated if symptoms appear.

Exercise may induce the appearance of symptoms. Victims should be discouraged from exercise; if possible, all victims should be evacuated as litter cases.

Exposure to liquid phosgene, or to high concentrations of phosgene vapor, may produce skin and eye irritation. The eyes are at particular hazard in exposure to liquid phosgene.

Exposure to liquid phosgene, especially when it has been held under pressure, may result in cold injuries up to frostbite.

Historically, the effects of phosgene were attributed to the action of hydrochloric acid formed by its hydrolysis. It is now recognized that, while hydrochloric acid formation may play a role in some effects (especially in early irritation), the major mechanisms for damage are acylation of nucleophiles and lipid peroxidation by phosgene.

TOXICITY DATA
LCLo Route of
Administration
in
360 mg-m-3/30 min inhalation humans
LCt50 Route of
Administration
in
900 mg-m-3/min inhalation mice
LC50 Route of
Administration
in
3200 mg-m-3 inhalation humans

ACGIH TLV 0.1 ppm (0.40 mg/m3)
OSHA PEL 0.1 ppm (0.40 mg/m3)
IDLH 2 ppm

Exposure Time AEGL-2 AEGL-3
10 minutes 0.6 ppm (2.5 mg/m3) 3.6 ppm (15 mg/m3)
30 minutes 0.6 ppm (2.5 mg/m3) 1.5 ppm (6.2 mg/m 3)
1 hour 0.3 ppm (1.2 mg/m3) 0.75 ppm (3.1 mg/m3)
4 hours 0.08 ppm (0.33 mg/m3) 0.20 ppm (0.82 mg/m3)
8 hours 0.04 ppm (0.16 mg/m3) 0.09 ppm (0.34 mg/m3)

MEDICAL COUNTERMEASURES

Useful Drugs Bronchodilators Diuretics Ibuprofen (?) N-acetylcysteine (?) Oxygen

Prophylaxis

Hexamethylenetetramine administered prior to phosgene inhalation appears to offer significant protection against the effects of inhaled phosgene in animals. However, there appears to be no apparent benefit to administration after exposure.

Treatment

Victims should be removed from the area of the cloud and decontaminated as rapidly as possible. Victims should be discouraged from engaging in any activities that may increase their breathing rates or the depth of breathing.

Eyes should be lavaged with normal saline or water for at least 3 minutes if irritated or exposed to liquid phosgene.

Administration of oxygen should be initiated as rapidly as possible. Patients with pulmonary edema may require positive end expiratory pressure (PEEP) oxygen administration.

Diuretics (e.g., furosemide) and aerosolized bronchodilators (e.g., albuterol) may be useful for managing the effects of pulmonary edema.

There are no recognized antidotes for phosgene exposure. However, in a recent overview (J. Borak and W. F. Diller, Phosgene exposure: mechanisms of injury and treatment strategies, J. Occup. Environ. Med. 43(2): 110-9, Feb, 2001), the authors note that two materials, ibuprofen and N-acetylcysteine have shown some promise in preventing phosgene-induced pulmonary edema in animal models when administered during the latent phase. They note that, for ibuprofen, administration of 25 to 50 mg/kg by mouth would be expected to provide a level similar to that found effective in animals, and, for N-acetylcysteine, 20 mL of a 20% NAC solution administered by nebulizer would likewise provide a level similar to that found effective in animals. Neither treatment is currently approved, however.

PHYSICAL COUNTERMEASURES


Initial Isolation and Protective Action Distances

SMALL RELEASE

(small package/leaking container)

First
ISOLATE
in all directions
Then
PROTECT
persons downwind during
DAYNIGHT
150 m (500 ft)
[90 m (300ft)]
1.3 km (0.8 mi)
[0.9 km (0.6 mi)]
3.3 km (2.0 mi)
[4.1 km (2.6 mi)]

LARGE RELEASE

(large package/multiple small packages)

First
ISOLATE
in all directions
Then
PROTECT
persons downwind during
DAYNIGHT
800 m (2500 ft)
[800 m (2500 ft)]
7.3 km (4.5 mi)
[6.6 km (4.1 mi)]
11.0+ km (7.0+ mi)
[11.0+ km (7.0+ mi)]
Distances in square brackets [] are for accidental releases of this agent.

Breathing protection (self-contained breathing equipment or gas mask) must be used. Protective gear including breathing protection and gloves should be worn when treating casualties prior to decontamination. Casualties should be decontaminated as rapidly as possible (see the section on decontamination). Remove casualties from exposure as rapidly as possible. Casualties should be evacuated using stretchers, even if ambulatory, if possible to minimize exertion. Casualties must not be moved into clean treatment areas where unmasked/ungloved personnel are working until decontamination is complete.

The agent is nonflammable; however, both chlorine (decomposition product) and hydrochloric acid (as a result of reaction of the decomposition products) may be produced when the agent is heated.

The agent will react with water to produce hydrochloric acid and carbon dioxide.

Also refer to 2000 Emergency Response Guidebook (ERG2004) Guide 125.

DECONTAMINATION

Victims

At temperatures above its boiling point (7.6° C, 47° F), it is most likely that exposure will be solely to phosgene vapor. If there is no evidence of exposure to liquid phosgene, decontamination may simply require removing the victim from the contaminated area and removing outer clothing (which should be bagged and labeled for later return).

When the ambient temperature is below the boiling point of phosgene, or when there is evidence of exposure to liquid phosgene, decontamination of victims is accomplished by removing the victim from the contaminated area, removal of clothing, and removal or neutralization of agent present on the skin. Clothing should be bagged and labeled. While the low boiling point of CG makes it unlikely that small amounts of liquid will remain long on the skin, visible droplets may be blotted (not wiped) away using an absorbent material (e.g., paper towels, facial tissues, etc.). Soapy water should be used to clean the skin using a rinse, towel off, rinse process if liquid has been observed. Hair should be thoroughly cleaned using soap and water, with care being taken to prevent wash water from contacting eyes.

If the eyes have been exposed to liquid phosgene or if eye irritation is present, flush the eyes with saline or water for at least 3-5 minutes.

Property

The low boiling point of CG means that decontamination of property can usually be accomplished by simply allowing the agent to evaporate. If rapid decontamination is needed, steam can be used.

Phosgene is only slightly soluble in water at 20°.

COMMON PRECURSORS

COMMENTS

Phosgene is a major industrial chemical, employed as an intermediate in a variety of organic syntheses. About 1,950,000,000 kilograms (about 4.3 billion pounds) were produced in 1999.

Phosgene may be used as a chlorinating agent in the production of nerve agent precursors.

Phosgene is one of the combustion products of chlorinated plastics, and is also formed by thermal decomposition of chlorinated solvents such as carbon tetrachloride and chloroform. It is a significant hazard in smoke coming from fires in modern buildings. It is also believed that a significant number of mild-to-moderate exposures occur as a result of people using heat guns in combination with solvents such as methylene chloride (from which phosgene is a result of thermal decomposition) to remove paint.

A bit of trivia regarding the code designation for phosgene. It has been indicated that the reason no nerve agent was given the code GC is because there was concern that the similarity between the CG code used for phosgene and a GC code would cause confusion (although this is not the only explanation given for the lack of a GC code).

Historical Notes

The first reported synthesis of CG was in 1812 by John Davy, who obtained it by using sunlight to promote the reaction of carbon monoxide with chlorine in one of the earliest experiments in photochemistry. Its common name, phosgene, reflects this origin, being a combination of the Greek phos (light) and genes (born).

It became important in industry at the end of the 19th Century as an intermediate in the production of dyes.

World War I

While phosgene was occasionally used alone, it was much more common for it to be used in combinations, especially with chlorine (which helped eject the phosgene from containers) as was done by the Germans. The Germans were not alone – the British, for instance, favored a 1:1 chlorine:phosgene mixture they codenamed White Star.

Phosgene was used first by the Germans (along with chlorine) on 19 December, 1915 at Nieltje in Flanders. The attack was a cloud attack that required some 4000 cylinders containing around 88 tons of phosgene. The effect of the German phosgene attack was to some degree mitigated by the fact that the British had developed a “gas helmet,” a flannel hood (with a celluloid eyepiece) that could be impregnated with chemicals that would act to neutralize agents. This hood, impregnated with a phenolate solution and known as the P. helmet, was issued in the summer of 1915. Despite this, the first attack produced well over a thousand casualties, including 120 deaths.

In January, 1916, shortly after the first phosgene attack, the modified P.H. helmet – for which hexamethylenetetramine was added to the materials used to impregnate the hoods to give increased protection against phosgene (on advice from Russia) – began to be issued. In June of 1916 the British began to use the White Star phosgene mixture to support attacks in the Somme. While a massive release planned for right before the start of the offensive had to be cancelled due to unfavorable weather, almost 10,000 cylinders were used between June 26 and July1.

Phosgene was seen as particularly useful because of its latent period, which had the effect in some circumstances of making it necessary to send soldiers who were only suspected of having been exposed to the rear. This made it very valuable in disrupting units. At the same time, the relatively low persistence of phosgene made it suitable for use to soften up positions before an attack, since it would be less likely than agents like mustard gas to be a hazard to one’s own troops.

The Germans produced over 18,000 tons of phosgene during the war, followed closely by the French (with just under 16,000 tons). The Americans and the British, in contrast, produced relatively small amounts - about 1400 tons each – but were allowed to use French phosgene.

Towards the end of the war, the Germans also experimented with particulation of phosgene, adsorbing it on pumice granules, with the goal of producing a more persistent agent. The granules were incorporated in shells for a 158 mm gas projector. It is unclear if they were used in combat.

While phosgene never achieved the public notoriety of mustard gas, it was probably the most lethal gas fielded during the First World War. In one study of gas exposure cases, it was found that 17% of those exposed to phosgene died. Some estimates suggest that phosgene was responsible for over 85% of the deaths caused by chemical weapons during the war.

Post-World War I

The lethality of phosgene ensured that it had a place in the arsenals of essentially every nation with a chemical capability after the First World War. It was relied on to different degrees in different countries, however. As World War II loomed, the French had given it primacy of place (based on the variety of munitions they filled with it) even over mustard gas, while the Czechs (preferring mustard gas) had just enough on hand to test gas mask filters.

Phosgene would be little used during the Second World War, however. The Japanese appear to have employed some in China, but the general moratorium on the use of chemical weapons that held during this war meant it would remain in the arsenals. This is not to say there was no planning for its use, however, as it figured in the preparations of both the Allies and the Axis for retaliation should the other use chemical weapons first, and in plans to shorten the war or stave off defeat. Probably the most famous example of this planning is found in the British Joint Planning Staff report of 27 July, 1944, in which the use of “16 tons per square mile” of phosgene against 20 German cities (or 1000 tactical targets) was discussed (of course, the JPS also pointed out the drawbacks of using gas, especially with reference to possible retaliation, and recommended against its use in this same report). (A bit of trivia about Allied cooperation in the chemical field – had the Americans elected to use phosgene bombs in the European theater, they would have needed to get them from the British; the phosgene in the bombs might well have originated in the U.S., however, since the British had built up their stockpile in part with American phosgene.)

Phosgene has continued to be a feature of military chemical stockpiles well after the Second World War. There have also been occasional suggestions that some nations had moved beyond stockpiling it. For instance, Egypt was accused of using phosgene against Yemeni forces during their intervention in 1963-1967.

The simplicity of its production and relative lethality, coupled with the ability to use it for either nerve gas production or for legitimate industrial purposes, mean that it will likely always have a place, especially when it can be used against technically unsophisticated foes. However, its importance has declined rapidly as the more lethal and faster acting nerve agents entered stockpiles, and it is no longer considered a first line, or even second line, military agent by the major powers.

In 1969, the U.S. Army decided to eliminate its phosgene stocks. In what would prove to be a misguided attempt to be fiscally responsible, rather than destroying them, the Army decided to sell the phosgene to various chemical companies (mostly for use in the manufacture of plastics). Unfortunately for the Army, the Viet Nam war had ensured that almost anything it did was going to be unpopular, and when, on August 14, public attention was drawn to a rail shipment of the phosgene from the Rocky Mountain Arsenal to Jones Chemical in Caledonia, New York, the effort to save tax dollars turned into a public relations nightmare. Despite the fact that all the proper permits had been secured, the Army was accused of recklessly endangering the lives of those along the railroad by shipping a dangerous war gas, questions were asked in Congress, and (although the shipment that provoked the uproar was delivered) a final shipment was blocked, leaving the Army to store 1300 tons of phosgene at the arsenal.

More recently, questioning eyes have turned towards Iraq where the phosgene plant at the al-Qa’qa’ phosgene plant was reconstructed, giving rise to concerns that it might be part of an effort to reconstitute the chemical weapons capabilities of the country. In the same region, Iran, Iraq’s old adversary, built up its phosgene capacity with the construction of a phosgene generator with a capacity of about 1.5 tons/hour with the aid of Salzgitter Anlagenbau.

Significant Accidental Release

On May 20, 1928 an accidental release of phosgene from a factory in Hamburg, Germany produced a gas cloud that extended for 10 km, resulting in at least three hundred casualties, including ten deaths. The amount released was estimated at 11 metric tons.

Terrorist Use

The Aum Shinrikyo cult employed phosgene in an attack on a journalist, Shouko Egawa, in Yokohama, Japan on September 20, 1994. The gas was introduced into her apartment through the mail slot while she slept, resulting in her hospitalization for respiratory distress. She was awakened by pain caused by the gas. Ms. Egawa had angered Aum's leadership by her reporting on the cult.

An incident on 19 April, 1995 in which several hundred people at the main railway station in Yokohama, Japan were made ill by an unidentified gas identified in some sources as a phosgene attack did not, in fact, involve phosgene. Confusion seems to have arisen because of an initial misidentification of the agent by the authorities.

Related International Classification of Diseases Codes
Heading ICD-9-CM
Toxic effect of other specified gases, fumes, or vapors 987.8
Toxic effect of unspecified gases, fumes, or vapors 987.9
Accidental poisoning by other specified solid and liquid substances E866.8
Accidental poisoning by unspecified solid and liquid substances E866.9
Accidental poisoning by other specified gases and vapors E869.8
Accidental poisoning by unspecified gases and vapors E869.9
Suicide and self-inflicted poisoning using other and unspecified solid and liquid substances E950.9
Suicide and self-inflicted poisoning using other specified gases and vapors E952.8
Suicide and self-inflicted poisoning using unspecified gases and vapors E952.9
Assault by poisoning using other solid and liquid substances E962.1
Assault by poisoning using other gases and vapors E962.2
Injury due to terrorism involving chemical weapons E979.7
Injury due to war operations by gases, fumes, and chemicals E997.2
Death due to terrorism involving chemical weapons U01.7
Heading ICD-10
Accidental poisoning by and exposure to other and unspecified chemicals and noxious substances X49
Intentional self-poisoning (suicide) by and exposure to other gases and vapors X67
Assault (homicide) by gases and vapors X88
Assault (homicide) by other specified chemicals and noxious substances X89
Assault (homicide) by unspecified chemical or noxious substance X90
War operations involving chemical weapons and other forms of unconventional warfare Y36.7

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