Organophosphate Pesticides – These pesticides affect the nervous system by disrupting the enzyme that regulates acetylcholine, a neurotransmitter. Most organophosphates are insecticides. They were developed during the early 19th century, but their effects on insects, which are similar to their effects on humans, were discovered in 1932. Some are very poisonous (they were used in World War II as nerve agents). However, they usually are not persistent in the environment.
Carbamate Pesticides affect the nervous system by disrupting an enzyme that regulates acetylcholine, a neurotransmitter. The enzyme effects are usually reversible. There are several subgroups within the carbamates.
“The carbamate pesticides represent a class of food use pesticides that have been given high priority by Office of Pesticide Programs for the reassessment of tolerances in accordance with the mandates Food Quality Protection Act. Within the class, there are three distinct subgroups: N-methyl carbamates, thiocarbamates, and dithiocarbamates.” (from “Thiocarbamates: A Determination of the Existence of a Common Mechanism of Toxicity and A Screening Level Cumulative Food Risk Assessment,” 2001, EPA’s Office of Pesticide Programs)
Organochlorine Insecticides were commonly used in the past, but many have been removed from the market due to their health and environmental effects and their persistence (e.g. DDT and chlordane).
Pyrethroid Pesticides were developed as a synthetic version of the naturally occurring pesticide pyrethrin, which is found in chrysanthemums. They have been modified to increase their stability in the environment. Some synthetic pyrethroids are toxic to the nervous system.
“Pyrethrins are insecticides that are derived from the extract of chrysanthemum flowers (pyrethrum) (1). • The plant extract, called pyrethrum contains pyrethrin I and pyrethrin II collectively, called pyrethrins. • Pyrethrins are widely used for control of various insect pests. Pyrethroids are synthetic (human-made) forms of pyrethrins. There are two types that differ in chemical structure and symptoms of exposure. Type I pyrethroids include allethrin, tetramethrin, resmethrin, d-phenothrin, bioresmethrin, and permethrin (1, 2). Some examples of type II pyrethroids are cypermethrin, cyfluthrin, deltamethrin, cyphenothrin, fenvalerate, and fluvalinate (1, 2). Both type I and II pyrethroids inhibit the nervous system of insects. This occurs at the sodium ion channels in the nerve cell membrane. Some type II pyrethroids also affect the action of a neurotransmitter called GABA (3). How do pyrethrins (and pyrethroids) work? Nerve cell membranes have a specific electrical charge. Altering the amount of ions (charged atoms) passing through ion channels causes the membrane to depolarize which, in turn, causes a neurotransmitter to be released. Neurotransmitters help nerve cells communicate. Electrical messages sent between nerve cells allow them to generate a response, like a movement in an animal or insect. Pyrethrins affect the nervous system of insects by causing multiple action potentials in the nerve cells by delaying the closing of an ion channel (3). Pyrethrins and pyrethroids act as contact poisons, affecting the insect’s nervous system (1, 4). Even though pyrethrins and pyrethroids are nerve poisons, they are not cholinesterase inhibitors like organophosphate or carbamate insecticides. Pesticide products containing pyrethrins usually contain a synergist (such as piperonyl butoxide). Synergists work by restricting an enzyme that insects use to detoxify the pyrethrins. A synergist allows the insecticide to be more effective (4).” (from “The National Pesticide Information Center (NPIC) is a cooperative effort between Oregon State University and the United States Environmental Protection Agency”) http://npic.orst.edu/index.html
Neonicotinoids (NN) The neonicotinoids are a class of insecticides with a common mode of action that affects the central nervous system of insects, causing paralysis and death. All of the neonicotinoids were registered after 1984 and were not subject to reregistration. Some uncertainties have been identified since their initial registration regarding the potential environmental fate and effects of neonicotinoid pesticides, particularly as they relate to pollinators. Data suggest that neonicotinic residues can accumulate in pollen and nectar of treated plants and may represent a potential exposure to pollinators. Adverse effects data as well as beekill incidents have also been reported, highlighting the potential direct and/or indirect effects of neonicotinic pesticides. Therefore, among other refinements to ecological risk assessment during registration review, the Agency will consider potential effects of the neonicotinoids to honeybees and other pollinating insects. (from www.epa.gov Other examples are available in sources such as Recognition and Management of Pesticide Poisonings.)
Insect growth regulators are chemicals that mimic juvenile growth hormones in insects. They work by either altering the production of chitin (the compound insects use to make their exoskeleton) or by altering an insect’s development into adulthood. Some growth regulators force the insect to develop too rapidly, while others stop development. Because these biopesticides work on hormone pathways in insects, they are less likely to have effects on other organisms, including people. (from www.npic.orst.edu)
Protecting Honey bees from pesticides: Purdue extension LIST OF BEE TOXIC PESTICIDES
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