CN
Chloroacetophenone (CN) C6H5COCH2Cl

yellow

Color Code: Red
Agent State: Micro-Particulate Solid
Classification: Lacrimator, Irritant
Chemical: Synthetic
  • Developed in 1923
  • LC50: 10,000 mg min/m3
  • ICt50: 20 mg min/m3
  • Takes effect in 5 to 10 seconds
  • Produces: Tearing, Burning sensation on the skin, Photophobia
    (sensitivity to light)
  • No effect on animals
    (Due to animals’ under developed tear-duct and protection by fur)
  • No effects on alcohol or drug intoxicated individuals
    (Pain Resistant)
  • Recovery within 10 minutes
  • Side or after effects: Has caused documented second degree burn and acute "vesicular dermatitis"
  • Has caused poisoning and documented incidents of death
  • Decontamination: Soda Ash or Alcoholic Caustic Soda
  • Shelf-life 3 years. Depends on humidity and packaging
  • CN is a Co-carcinogen (cancer promoting)

Early records reveal that German scientists discovered CN about 1870. This is a chemical compound that was first prepared for use in 1877 but was not subsequently used to any great extent. The French were the first to use it successfully in the late 1920’s to break up civil disorders in their colonies. It was then adopted practically all over the world for use by law enforcement agencies around 1930. During World War II (1941-45) CN was further developed and it was discovered that micro-pulverized CN (talc-sized particles) produced a longer lasting and greater irritation effect.

In 1923, the United States Government financed the development of chemical agents at Edgewood Arsenal. A great deal of time and expense went into the research of non-lethal irritants that could be successfully used in law enforcement. CN was successfully developed in a form very similar to what we have today in canisters. CN is the active ingredient of Chemical Mace, an aerosol irritant acquired by many U.S. police agencies around 1965.

CN in its pure form is a white crystalline solid resembling ordinary granulated sugar or salt. Since it is made of solid particles, it must be carried through the air by an agent or expelled in a fine dust. CN has an odor similar to apple blossoms.

CN causes tearing and irritation of the eyes, and a burning sensation on the skin. The primary effects of CN on the eyes is lachrymation (tearing) and photophobia (sensitivity to light).

There are certain subjects on which CN will have little effect. CN has little or no effect on animals. Tests reveal that if a dog is tied up where he cannot move freely, he will make very little attempt to get away from CN when it is present or sprayed on him. Any individual who is under the influence of narcotics or alcohol to the extent that he has lost his sense of feeling will not be affected by CN.

Decontamination of CN

Decontamination of CN requires a soda ash solution or alcoholic caustic soda. An individual subjected to CN should be taken out into the fresh air; he should not rub his face or eyes and should immediately proceed to wash his eyes and face. Most soaps contain an oil and should not be used to wash the area. Oil traps CN in the skin and can cause a severe rash or burn. Affected clothing should be changed. 

Health Hazard of CN Aerosol

In 1969 Doctor Penneys et al., writing in the prestigious New England Journal of Medicine, described several cases of contact dermatitis (abnormal congestion and redness of the skin) ascribed to CN aerosol (Chemical Mace). Two of the four cases were of the allergic contact variety, and the other two represented inadvertently acquired sensitivity to chloroacetophenone (CN).

CN or CS do not have any effect on those under the influence of narcotics, alcohol or on animals.

Case No. 1: A twenty seven year old male had been admitted to a hospital with a subsiding "erythematous, crusted eruption" on the left side of the face and eye. The dermatitis appeared about three hours after he had been sprayed with CN aerosol (Chemical Mace) in an incident that took place four days prior to admission.

Case No. 2: A thirty year old policeman’s exposure to CN aerosol (Chemical Mace) in the course of his work resulted in an acute "vesicular dermatitis" on the forearm.

The two remaining cases, one male and one female, had been exposed under occlusive patch for twenty four hours. Both displayed a scaly, pruritic eruption at the side of the application two weeks following exposure. These cases had been accidentally sensitized during the initial handling of Case No.1.

The fact that five out of eight subjects tested could be shown to have developed contact sensitivity suggested to Penneys et al., that a high percentage of people will show a sensitization to Chemical Mace. Since a one second spray from a squirt can of Mace will deliver a maximum of about 25 milligrams of CN, most of which will not reach the target, and since two of the four cases reported resulted from exposure during the evaluation of a Mace victim, medical examiners conclude that chloroacetophenone is a potent sensitizing agent. In this study, removal of the agent after one minute with soap and water eliminated the reaction: however, a delay in removal beyond one minute resulted in development of a dermatitis that typically occurred forty-eight hours after the exposure.

In a second report Penneys emphasized that those persons whose occupations result in frequent exposure to CN should bear in mind the propensity of chloroacetophenone to sensitize the human subject. The particular contact dermatitis that develops may result in itching, erythema, edema, vesiculation and, in the worst cases, purpura and necrosis (hemorrhage and death of cells).

The following photographs demonstrate the dermatitis caused by CN and is based on "Annales de Dermatologie, Accidents Cutanés Aux Bombes D’autodefense", by J.L. Rigon (Figure 1):

edema21.jpg (3226 bytes)    edema22.jpg (4821 bytes)
Figure 1: Edema caused by CN. 

(Click on image for larger view.)

Toxicology of CN

CN, the active ingredient in Chemical Mace, when applied directly to the skin produces extreme irritation with erythema and vesicles (a small sac or cyst filled with fluid such as a blister). The higher the degree of humidity, the more severe the lesions. In animals and in man, CN behaves as potential allergens on repeated exposures. CN may have two effects: it usually produces irritant dermatitis, but can also sometimes produce a genuine eczema (a disease of the skin attended with itching and secretion). In subjects exposed to CN sprays, lesions develop in two stages: first, redness and burning sensation on the face, which characteristically is only affected on one side, owing to the lateral projection of the tear gas. Then, on the following day, there appears an edema (secretion of fluid into cell tissues) with swelling of the eyelids. Oozing rapidly turns to crusts, and in the absence of treatment, infection is the rule. Cure requires as many as 10 to 15 days of treatment. Eczema may also affect those factory workers who become sensitized and develop an allergy. Therefore, CN causes dermatitis and is a sensitizer that may cause very serious allergic reactions upon repeated exposure.

CN as an aerosol, or at higher dosages, may cause more damage to the eyes and skin than either DM or CS (Ortho-chlorobenzalmalononitrile). The American Journal of Ophthalmology reports findings from a study of 14 eyes enucleated (removing the eye) following injury by CN tear gas weaponry. Five of the eyes were removed shortly after injury, revealing necrosis (death of a cell) of the anterior segment, an intense necrotizing keratitis (death of the tissue of the cornea) of varying degree, and an associated suppurative iridocyclitis (inflammation of the iris). Undoubtedly these changes represented the acute chemical damage of tear gas. The remaining nine eyes were enucleated up to 15 years following injury, and the findings in these chronic cases can be best attributed to the sequelae of neuroparalytic keratopathy (abnormal condition of nerve paralysis resulting in the degeneration of the eye), probably related to the neurotoxic effects of tear gas.

CN has also been implicated as a cancer "promoter" or "co-carcinogen." The tumors observed were benign papillomas of the skin. In these experiments a 1% solution of CN was painted on the skin of mice that had been pretreated with the known carcinogen 9,10-dimethyl-1,2-benzanthracene 1.

The Journal of Forensic Sciences, "Chloroacetophenone (Tear gas) Poisoning: by A.A. Stein, M.D. and William E. Kirwan," reports that on October 7, 1958 a 29-year old white single man had barricaded himself in his room. A single #112 tear gas grenade containing 128 gms of CN was then fired into this room. The subject was exposed to the gas in this room for approximately 30 minutes. He was then admitted to the emergency room of the Albany Medical Center Hospital. On admission to the hospital the patient was agitated and under restraints. His clothes and body smelled of tear gas. He remained in a semicomatose condition for approximately 12 hours and then suddenly developed pulmonary edema and died (Table 1).

1 "Harvest of Death", by J.B. Neilands & Gordon H. Orians. Published by "Collier-Macmillan Limited", London, 1972.

Table 1

THE FOLLOWING SUMMARIZES FINDINGS IN 4 CASES OF TEAR GAS (CN) POISONING 2

Doctor Age Race Sex Psychiatric Dx Size of Room Exposure Time Time of Death
After Admission
Davis 33 W M Psychotic Small Hours 4 Days
Mann 68 W M Alcoholic House ±12 hours 81/2 hours
Helpern 42 W M Alcoholic Moderate-Sized 10 Minutes 45 hours
Stein 29 W M Paranoid
Schizophrenia
9’1" x 9’1" x 8' 30 minutes 12 hours

Edgewood Arsenal reports that deaths associated with inhalation of CN reveal signs of rales, rhonchi (a coarse rattling noise in the bronchial tubes), dyspnea (difficult or labored breathing), chest pains, and shortness of breath. The pathological lesions were listed as edema, congestion, hemorrhage of lungs, pseudomembrane (falty tissue) formation, and pneumonia. All signs and lesions can be related to damage to the air passages and lungs.

2 Journal of Forensic Sciences, January 1964. Vol. 9. Page 380. "Chloroacetophene (Tear Gas) Poisoning: A Clinico-Pathologic Report", by A.A. Stein, M.D. and William E. Kirwan.

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