Early records reveal that German scientists discovered CN (Chloroacetophenone) 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 was the active ingredient of Chemical Mace®, an aerosol irritant acquired by many U.S. police agencies in 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 effect 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 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 soap contains 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.
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. 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 report’s 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.
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.
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