Environmental and toxicological aspects of insect growth regulators.

Abstract

Insect growth regulators (IGRs) are a class of new chemicals that interfere with maturation and reproduction in insects. Proposed hypotheses on the biochemical mechanism of action are presented herein. The environmental aspects as metabolism in soils, plants, insects, and animals suggest strongly that these chemicals undergo rapid degradation and metabolism to innocuous metabolites. The toxicological properties determined for registration of the IGR methoprene, isopropyl (E,E)-11-methoxy-3,7,11-trimethyl-2,4-dodecadienoate, reflected no significant effects against any of the species tested. Toxicological evaluations in swine, sheep, hamsters, rats, dogs, rabbits, guinea pigs, and cattle revealed no clinical signs of toxicosis. Additionally, teratological studies in swine, sheep, hamsters, rats, and rabbits also resulted in no observable effects in the animals at the levels administered.

Sterilization Effects of Adult-targeted Baits Containing Insect Growth Regulators on Delia antiqua

“…There would be many advantages if these chemicals were used as chemosterilants for onion flies. First, as IGRs specifically interfere with chitin deposition which was only discovered in insect cuticle or work as specific hormones influence insect maturity and reproduction mediation 54 , they are of great safety to mammal and human as IGRs act specifically on arthropods. This makes them optimized chemicals to be used in baits for onion flies.…”

Beyond brood: the potential impacts of insect growth disruptors on the long-term health and performance of honey bee colonies

“…The term IGD refers to a broad class of chemicals that disrupt insect growth, development, and reproduction (Pener and Dhadialla 2012) by acting on the insect endocrine system to interfere with metamorphosis and developmental processes (Williams 1967;Hoffmann and Lorenz 1998;Jindra and Bittova 2020) or by acting as chitin synthesis inhibitors to impair the formation of new cuticle (Grosscurt 1978;Cutler and Scott-Dupree 2007;Matsumura 2010). Because of their selectively lethal activity towards immature insects and their low lethality to beneficial adult insects such as pollinators, IGDs are often considered lower risk relative to other more traditional chemistries such as neurotoxins (Wright 1976), and they are frequently preferred over other insecticides in agricultural settings where beneficial insects are present. One particularly high-profile example of this use pattern is in blooming almond orchards in California (Mullin et al 2016;CalDPR 2019;Wade et al 2019).…”

“…Insect hormone mimics (IHM) are compounds that act on the insect endocrine system to disrupt the process of insect metamorphosis (Wright 1976;Hoffmann and Lorenz 1998;Jindra and Bittova 2020). Like CSIs, IHMs result in the mortality of immature insects by interfering with the hormone balance required for successful ecdysis, often blocking molting or triggering it prematurely, resulting in death (Dhadialla et al 1998;Retnakaran et al 2003;Jindra and Bittova 2020).…”

“…This review will address exposure to agrochemicals, focusing on insect growth disruptors (IGDs), a pesticide class that is known to affect pathways associated with insect growth and development (Pener and Dhadialla 2012). While the effects of IGDs on immature insects are fairly well understood (Wright 1976;Dhadialla et al 1998;Tunaz and Uygun 2004), effects on adult insects are discussed less frequently. This review will cover two broad categories of IGDs, chitin synthesis inhibitors (CSI), and insect hormone mimics (IHM), examining their effects on honey bees and discussing gaps in the current literature relating to the effects of IGDs on honey bee reproduction and colony performance.…”

Control of Cacopsylla (Psylla) pyri (L.) (Stenorhyncha, Psyllidae) by juvenile hormone analogues

“…JHAs are specific in their effects on the class Insecta and only in the defined life period. The toxicity of JHAs (methoprene) to vertebrates is very low, 34 500 ppm for mice (SIDDAL and SLADE, 1974) and they have almost no teratogenic effect on mammals (SIDDAL, 1976;WRIGHT, 1976). Only a weak mutagenicity was observed in Drosophila, but it can coincide with the morphogenic activity of the tested juvenoids (SOCHA et al, 1988).…”