In the production process, both the Z and E isomers are formed in a ratio (Z:E) of 8.5:1. The technical grade material therefore contains over 92% chlorfenvinphos. Unfortunately, no data is available in the Toxics Release Inventory (TRI) database on total environment releases of this compound from facilities. This is mainly because chlorfenvinphos was not considered a dangerous toxin until the early 1990s. Therefore, chlorfenvinphos is not one of the compounds about which facilities were required to report to the Toxic Release Inventory. Toxicokinetics 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. However, as an organophosphorus compound, it does not accumulate well in tissues. 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., Excretion of chlorfenvinphos is fairly rapid. In rats, an administered dose is excreted in 4 days, mostly in urine. Mechanism of toxicity The toxicity of chlorfenvinphos is primarily caused by its inhibition of cholinesterase activity. Chlorfenvinphos reacts with the acetylcholine binding sites of enzymes that hydrolyze acetylcholine, thereby preventing their catalysis of this reaction. The reaction itself is a phosphorylation, which is reversible. The phosphorylated enzymes can undergo conformational changes and additional reactions however, which prevent the dephosporylation. This “aging” results in irreversible inhibition of the cholinesterase. Acetylcholine is a neurotransmitter in the nervous system, it targets muscarinic and nicotinic receptors and receptors in the central nervous system. These receptors are used to pass on an action potential across the synaptic cleft between neurons. Inhibition of acetylcholinesterase enzymes results in the accumulation of acetylcholine at its receptors. This leads to continuous or excessive stimulation of neurons that respond to acetylcholine. Cholinergic poisoning leads to different symptoms, depending on the part of the nervous system that is affected. The most likely cause of death in chlorfenvinphos is respiratory failure due to paralysis and bronchoconstriction. Toxicity Toxic effects The toxic effects of accumulation of acetylcholine can be divided