Rotenone – acts as a respiratory enzyme inhibitor. Used most to control aphids and caterpillars. Nicotine – mimics acetylcholine (Ach) in the central nervous system ganglia, causing twitching, convulsions and death. Pyrethrum – affects both the central and peripheral nervous systems, stimulating nerve cells to produce repetitive discharges and eventually leading to paralysis. Developing larvae exhibit rupture of the malformed cuticle or death by starvation not registered in U.S.ĭepending upon the type can have various effects: Interrupt mitochondrial electron transport at Site 1 mainly used as a miticide display toxicity to aquatic arthropods and fish.Īcts on the larval stages of most insect by inhibiting or blocking the synthesis of chitin in the exoskeleton. Results of testing on one type (fipronil) indicate no effects on the clams, oysters or fish, with marginal effects on shrimp. Effective against psylla, aphids, whitefly and thrips.
Inhibits mitochondrial electron transport at the NADH-CoQ reductase site leading to disruption of ATP formation. Regarded for its high level of specificity. Effective against caterpillars, lepidopteran larvae, leaf miners, thrips and termites. Generally have low toxicity to mammals, birds and fish.Īcts by disrupting binding of acetylcholine in nicotinic acetylcholine receptors at the postsynaptic cell. Used in the control of sucking insects, soil insects, whiteflies, termites, turf insects and the Colorado potato beetle. Effective against most agricultural insect pests extremely toxic to fish.Īct on the central nervous system causing irreversible blockage of the postsynaptic nicotinergic acetylcholine receptors. Symptoms include tremors, incoordination, hyperactivity and paralysis. Used extensively against mites on fruit trees and formerly used as an antifouling agent and molluscacide very toxic to aquatic life.Īcts by keeping open the sodium channels in neuronal membranes affecting both the peripheral and central nervous systems causing a hyper-excitable state. Inhibit phosphorylation at the site of dinitrophenol uncoupling, preventing the formation of ATP. Used in the control of OP and carbamate-resistant pests.Īct by uncoupling or inhibiting oxidative phosphorylation preventing the formation of adenosine triphosphate (ATP). Inhibit the enzyme monoamine oxidase that degrades neurotransmitters causing an accumulation of these compounds affected insects become quiescent and die. Has very broad spectrum toxicity and is highly toxic to fish. Used only against mites with very low toxicity to other organisms.Ĭause acetylcholinesterase (AChE) inhibition leading to central nervous system effects (i.e., rapid twitching of voluntary muscles and eventually paralysis). A broad-range insecticide, generally the most toxic of all pesticides to vertebrates.Įxhibit ovicidal activity (i.e., they kill the egg stage). Usually broad-spectrum insecticides that have been taken out of use.Ĭause acetylcholinesterase (AChE) inhibition and accumulation of acetylcholine at neuromuscular junctions causing rapid twitching of voluntary muscles and eventually paralysis. Some act on the GABA (γ-aminobutyric acid) receptor preventing chloride ions from entering the neurons causing a hyperexcitable state characterized by tremors and convulsions. Most act on neurons by causing a sodium/potassium imbalance preventing normal transmission of nerve impulses. Insecticide Types and Their Modes of Action Insecticide Type Many insecticides act upon the insect's nervous system (e.g., cholinesterase inhibition), while others act as growth regulators or endotoxins. They are classified based on their structure and mode of action. Insecticides are chemicals used to control insects by killing them or preventing them from engaging in undesirable or destructive behaviors. Consider Other Causes with Similar Evidence.Consider Contributing, Modifying and Related Factors.Consider Listing Insecticides as a Candidate Cause.Checklist of Sources, Site Evidence and Biological Effects.
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