Insect growth regulator
An insect growth regulator (IGR) is a substance (chemical) that inhibits the life cycle of an insect. IGRs are typically used as insecticides to control populations of harmful pests, such as cockroaches or fleas.[1]
Contents
Advantages
Many IGRs are labeled "reduced risk" by the Environmental Protection Agency, meaning that they target juvenile harmful insect populations while causing less detrimental effects to beneficial insects. Many beekeepers have reported IGR's negatively affecting brood and young bees . Unlike classic insecticides, IGRs do not affect an insect's nervous system and are thus more worker-friendly within closed environments.[2] IGRs are also more compatible with pest management systems that use biological controls. In addition, while insects can become resistant to insecticides, they are less likely to become resistant to IGRs.[3]
How IGRs work
As an insect grows, it undergoes a process called molting, where it grows a new exoskeleton under its old one and then sheds to allow the new one to swell to a new size and harden.[3] IGRs prevent an insect from reaching maturity by interfering with the molting process.[4] This in turn curbs infestations because immature insects cannot reproduce.[1] Because IGRs work by interfering with an insect's molting process, they take longer to kill than traditional insecticides. Death typically occurs within 3 to 10 days, depending on the product, the insect's life stage when the product is applied and how quickly the insect develops. Some IGRs cause insects to stop feeding long before they die.[4]
Hormonal IGRs
Hormonal IGRs typically work by mimicking or inhibiting the juvenile hormone (JH), one of the two major hormones involved in insect molting. IGRs can also inhibit the other hormone, ecdysone, large peaks of which trigger the insect to molt. If JH is present at the time of molting, the insect molts into a larger larval form; if absent, it molts into a pupa or adult.[4] IGRs that mimic JH can produce premature molting of young immature stages, disrupting larval development.[4] They can also act on eggs, causing sterility, disrupting behavior or disrupting diapause, the process that causes an insect to become dormant before winter.[3] IGRs that inhibit JH production can cause insects to prematurely molt into a nonfunctional adult.[3] IGRs that inhibit ecdysone can cause pupal mortality by interrupting the transformation of larval tissues into adult tissues during the pupal stage.[4]
Chitin synthesis inhibitors
Chitin synthesis inhibitors work by preventing the formation of chitin, a carbohydrate needed to form the insect's exoskeleton. With these inhibitors, an insect grows normally until it molts. The inhibitors prevent the new exoskeleton from forming properly, causing the insect to die. Death may be quick, or take up to several days depending on the insect. Chitin synthesis inhibitors can also kill eggs by disrupting normal embryonic development.[2][3] Chitin synthesis inhibitors affect insects for longer periods of time than hormonal IGRs. These are also quicker acting but can affect predaceous insects, arthropods and even fish.[2] Compounds include benzoylurea pesticides.
Examples
- Azadirachtin
- Hydroprene (Gentrol)
- Methoprene (Precor)
- Pyriproxyfen (Nyguard, Nylar, Sumilarv)
- Triflumuron (Starycide)
References
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