However, because of its toxic effect as a cholinesterase inhibitor it has been banned in several countries, including the United States and the European Union.

It was introduced in the United States in 1963 and was used as an insecticide and acaricide for controlling fleas and ticks on domestic pets and other animals.

Because of these effects, chlorfenvinphos was often used on farms to control adult flies in dairy barns, milk rooms, poultry houses and yards, and in other animal buildings.

Furthermore, it was used to control larval flies in manure storage pits and piles and other refuse accumulation areas around dairies and feedlots.

Chlorfenvinphos was also used against Colorado beetles on potatoes and scale insects and mite eggs on citrus.

No international regulations exist for the use of chlorfenvinphos, although standards and guidelines have been set to protect people from the possible harmful effects of the toxin.

An exception is Switzerland, where chlorfenvinphos is still allowed for use in crops and certain vegetables under the brand name Birlane.

[6] Chlorfenvinphos is most commonly absorbed into the body through either ingestion of food products that have been treated with the pesticide, or through dermal absorption, though the latter is much less efficient.

Once absorbed, chlorfenvinphos is widely distributed throughout the body, and has been detected in a variety of bodily fluids.

The first and most important step of metabolism of chlorfenvinphos in humans is accomplished by the enzyme cytochrome P450 in liver microsomes.

This enzyme facilitates oxidative dealkylation of the compound to acetaldehyde and 2-chloro-1-(2,4-dichlorophenyl) vinylethylhydrogen phosphate, the latter of which quickly breaks down to acetophenone.

Acetophenone is then reduced to an alcohol and conjugated by glutathione transferases.,[12][13] Excretion of chlorfenvinphos is fairly rapid.

[4] The toxic effects of accumulation of acetylcholine can be divided into three categories, based upon its actions in different parts of the nervous system.

Muscarinic receptors that respond to acetylcholine are found in smooth muscles, the heart and exocrine glands.

The nicotinic symptoms of cholinergic poisoning are therefore fatigue, involuntary twitching, muscular weakness, hypertension and hyperglycemia.

Symptoms of accumulation of acetylcholine in the central nervous system are diverse and include tension, anxiety, ataxia, convulsions, depression of the respiratory and circulatory centers and coma.

These small amounts can be used to prove that chlorfenvinphos exposure has occurred and the method of analysis is non-invasive.

[18] Ingestion of chlorfenvinphos, either by accident or through suicidal intent, can be treated as with other acute organophosphate poisonings.