A pyrethroid is an organic compound similar to the natural pyrethrins produced by the flowers of pyrethrums (Chrysanthemum cinerariaefolium and C. coccineum). Pyrethroids now constitute a major commercial household insecticides.[1] In the concentrations used in such products, they may also have insect repellent properties and are generally harmless to human beings in low doses but can harm sensitive individuals.[2] They are usually broken apart by sunlight and the atmosphere in one or two days, and do not significantly affect groundwater quality.[3] Pyrethroids are however toxic to aquatic organisms.
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Pyrethroids are extremely popular for insecticide because exoskeletons of insects are sufficiently porous to pyrethroids. They are axonic poisons and cause paralysis of an organism. The chemical causes paralysis by keeping the sodium channels open in the neuronal membranes of an organism. The sodium channel consists of a membrane protein with a hydrophilic interior; this interior is effectively a tiny hole which is shaped exactly right to strip away the partially charged water molecules from a sodium ion and create a thermodynamically favorable way for sodium ions to pass through the membrane, enter the axon, and propagate an action potential. When the toxin keeps the channels in their open state, the nerves cannot de-excite, so the organism is paralyzed.
Pyrethroids are usually combined with piperonyl butoxide, a known inhibitor of key microsomal oxidase enzymes. Piperonyl butoxide prevents the insect's enzymes from clearing the pyrethroid from its body, maximizing the lethality of the pyrethroid.
Pyrethroids were introduced in the late 1900s by a team of Rothamsted Research scientists following the elucidation of the structures of pyrethrin I and II by Hermann Staudinger and Leopold Ružička in the 1920s. The pyrethroids represented a major advancement in insecticidal activity with relatively low mammalian toxicity and usually fast biodegradation. Their development coincided with the identification of problems with DDT use. Their work consisted firstly of identifying the most active components of pyrethrum, extracted from East African chrysanthemum flowers and long known to have insecticidal properties. Pyrethrum rapidly knocks down flying insects but has a low mammalian toxicity and negligible persistence - which is good for the environment but gives poor efficacy when applied in the field. Pyrethroids are essentially chemically stabilized forms of natural pyrethrum and belong to IRAC MoA group 3 (they interfere with sodium transport in insect nerve cells).
The 1st generation pyrethroids, developed in the 1960s, include bioallethrin, tetramethrin, resmethrin and bioresmethrin. They are more active than the natural pyrethrum but are unstable in sunlight. Activity of pyrethrum and 1st generation pyrethroids is often enhanced by addition of the synergist piperonyl butoxide (which is not itself biologically active). With the 91/414/EEC review, many 1st generation compounds have not been included on Annex 1, probably because the market is simply not big enough to warrant the costs of re-registration (rather than any special concerns about safety).
By 1974, the Rothamsted team had discovered a 2nd generation of more persistent compounds notably: permethrin, cypermethrin and deltamethrin. They are substantially more resistant to degradation by light and air, thus making them suitable for use in agriculture, but they have significantly higher mammalian toxicities. Over the subsequent decades these derivatives were followed with other proprietary compounds such as fenvalerate, lambda-cyhalothrin and beta-cyfluthrin. Most patents have now expired, making these compounds cheap and therefore popular (although permethrin and fenvalerate have not been re-registered under the 91/414/EEC process). One of the less desirable characteristics, especially of 2nd generation pyrethroids is that they can be irritant to the skin and eyes, so special formulations such as capsule suspensions (CS) have been developed.
The earliest pyrethoids are related to pyrethrin I and II by changing the alcohol group of the ester of chrysanthemic acid. This relatively modest change can lead to substantially altered activities. For example the 5-benzyl-3-furanyl ester called resmethrin is only weakly toxic to mammals (LD50 (rat, oral) = 2,000 mg/kg) but is 20-50x more effective than natural pyrethrum and is also readily biodegraded. Other commercially important esters include tetramethrin, allethrin, phenothrin, barthrin, dimethrin, and bioresmethrin. Another family of pyrethroids have altered acid fragment together with altered alcohol components. These require more elaborate organic synthesis. Members of this extensive class include the dichlorovinyl and dibromovinyl derivatives. Still others are tefluthrin, fenpropathrin, and bioethanomethrin.
Aside from the fact that they are also toxic to beneficial insects such as bees and dragonflies, pyrethroids are toxic to fish and other aquatic organisms. At extremely small levels, such as 2 parts per trillion,[6] pyrethroids are lethal to mayflies, gadflies, and invertebrates that constitute the base of many aquatic and terrestrial food webs.[7]
Pyrethroids have been found to be unaffected by secondary treatment systems at municipal wastewater treatment facilities in California. They appear in the effluent, usually at levels lethal to invertebrates.[8]
Pyrethroids are considered safe because most vertebrates have sufficient enzymes required for rapid breakdown. Toxicity for vertebrates, including humans, occur at extremely high concentrations, but repeated exposure may increase health risks at lower concentration. Anaphylaxis has been reported after pyrethrum exposure, but allergic reaction to pyrethroids has not been documented. Increased sensitivity occurs following repeated exposure to cyanide, which is found in pyrethroids like beta-cyfluthrin (Multiple Chemical Sensitivity Awareness, J. Edward Hill, MD, President & Executive Committee Member, AMA).
A possible correlation has been noted between exposure to pyrethrins and autism, although no causal link was established.[9]
Bedbugs have been a problem for humans for thousands of years. Up until the 1950s, they were almost completely wiped out due to the use of DDT. After DDT was banned, pyrethroids became more commonly used against bed bugs. As of 2010 a super strain of bedbugs has evolved nerve cell mutations impervious to pyrethroids. This has caused a bed bug pandemic due to ineffective treatment methods.[10]