Chloroacetophenone(CN) was first synthesized in 1870 by the Germans. It is used as a riot control agent (RCA) due to its potency as a lachrymatory agent. It got its fame after World War I when it was given the trade name Mace, the first American manufacturer of CN devices and sold for personal and commercial protection. Generically, it is known as tear gas. It was used in US military systems until its replacement by CS (ochlorobenzylidene malononitrile) in 1959. However, CN is still sold commercially in the United States and is used by militaries and police all over the world.

Uses

Chloroacetophenone is used as a nonlethal or less-than-lethal chemical in riot control situations to distract, deter, incapacitate, disorient, or disable disorderly people; to clear facilities or areas; to deny areas; or for hostage rescue. It can also be used in peacekeeping operations. It is also used in military training as a confidence builder for the protective mask.

Environmental Fate

Chloroacetophenone has a half-life under aerobic conditions of 672 h and can be biodegraded in most moist, nutrient-rich soil.
Biodegradation in water is similar to degradation in soil. Howard et al. (1991) reports the same 672 h half-life for CN in aerobic surface water. This half-life is extended up to 2688 h for anaerobic aqueous degradation.
Volatile losses of CN from surface waters can be another significant process for CN disappearance in water. For instance, Olajos and Stopford (2004) calculated that CN contamination in a river would have a half-life of approximately 14 days, while CN contamination in a lake would have a half-life of approximately 110 days.

Mechanism of Toxicity 

Chloroacetophenone is considered less than lethal or nonlethal because it has a large safety ratio. That is, its effective dose or concentration ECt50 is low compared to its lethal dose or concentration (LCt50). In the body, CN is converted to an electrophilic metabolite. It is an SN2 alkylating agent that reacts with SH groups and other nucleophilic sites of biomolecules. Alkylation of SH-containing enzymes leads to enzyme inhibition with disruption of cellular processes. CN was found to inhibit human plasma cholinesterase via a non-SH interaction, and some of the toxic effects may be due to alkylation of SHcontaining enzymes.

Chloroacetophenone as well as CS is an SN2-alkylating agent with activated halogen groups that react readily at nucleophilic sites. The prime targets include sulfhydryl-containing enzymes such as lactic dehydrogenase. Alkylation of SH-containing enzymes leads to enzyme inhibition with disruption of cellular processes. It has been suggested that tissue injury may be related to inactivation of certain of these enzyme systems. The initial response to the inhalation of CN or other sensory irritants is consistent with the Kratschmer reflex and the Sherrington pseudoaffective response. These aerosols stimulate the pulmonary irritant receptors to produce bronchoconstriction and increased pulmonary blood volume by augmenting sympathetic tone. The chlorine atoms released from CN on contact with skin and mucous membranes are reduced to hydrochloride acid, which can cause local irritation and burns. CN was also found to inhibit human plasma cholinesterase via a non-SH interaction.