CN
Chloroacetophenone (CN) C6H5COCH2Cl

|
|
| 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 1920s 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 policemans 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
Dautodefense", by J.L. Rigon (Figure 1):

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 |
91" x 91" 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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