Toxicity pyrethroids

Other cases of potentiation will be discussed in later chapters dealing with individual pollutants. These will include the synergism of pyrethroid toxicity to... 

The molecular basis for the evolution of distinct kdr mutations in different insects and arachnids remains unclear. Assuming that the pyrethroid binding site(s) (and/or the pyrethroid response domain) is composed of multiple amino acid residues, there are two ways by which different mutations can be selected in different insects and arachnids. First, the random mutation hypothesis mutation in any pyrethroid binding site/response domain affects pyrethroid toxicity without impacting normal sodium channel functional properties. Thus, selection of different mutations in different insects and arachnids is purely random. Second, the nonrandom mutation hypothesis mutation in any pyrethroid binding site/response domain affects pyrethroid toxicity, but some mutations also drastically alter normal sodium channel functional properties in one species, but not in another, presumably because of different sodium channel backbone sequences. That is, there may be severe fimess costs for some mutations, if placed out of their native protein context. 

Cypermethrin is practically nontoxic to birds but is highly toxic to bees. Fish and crustaceans are extremely sensitive to cypermethrin and pyrethroid compounds in laboratory settings. However, various factors (e.g., sediment binding) may reduce pyrethroid toxicity to these nontarget organisms in a natural environment. 

The mechanisms by which pyrethroids alone are toxic are complex and become more complicated when they are co-formulated with piperonyl butoxide, an organ-ophosphorus insecticide, or both, as these compounds inhibit pyrethroid metabolism. The main effects of p3rethroids are on sodium and chloride channels. As a result, excitable (nerve and muscle) cells are the principal targets of pyrethroid toxicity, which is manifested as disordered function rather than structural damage. In that way, the major toxic effect of dermal exposure is paresthesia, supposable also due to hyperactivity of cutaneous sensory nerve fibers [12]. 

Other possible mechanisms of pyrethroid toxicity have been investigated. Inhibition of Ca ", Mg -ATPase, and calcium-binding protein calmodulin has been observed with some pyrethroids. 

Pyrethroids from Chiysanthemic Acid. The unsaturated side chains of the aHethrolone alcohol moieties of the natural pyrethrins are readily epoxidized by microsomal oxidases and converted to diols, thus detoxifying the insecticides. Esterification of chrysanthemic acid (9), R = CH3, with substituted ben2yl alcohols produces usehil insecticides barthrin [70-43-9J, 2-chloro-3,4-methylenedioxyben2yl (+)-i7j ,/n7 j -chrysanthemate, and dimethrin [70-38-2] 2,4-dimethylben2yl (+)-i7j ,/n7 j -chrysanthemate. These have alimited spectmm of insecticidal activity but are of very low mammalian toxicity, ie, rat oralLD s >20,000 mg/kg. 

T. Cairns and J. Sherma, eds.. Comprehensive Analytical Profiles of Important Pesticides, CRC Press, Boca Raton, Fla., 1992, 304 pp. From the series ModemMethods for Pesticide Analysis, provides detailed information on properties and analytical methodology for nine prominent pesticides, pyrethroids, and fumigants in food. Includes formulations and uses, chemical and physical properties, toxicity data, and tolerances on various foods and feeds. Analytical information may be given in enough detail for methods to be carried out without having to consult additional Hterature sources. 

Since 1945 the use of synthetic pesticides in the United States has grown 33-fold. The amounts of herbicides, insecticides, and fungicides used have changed with time due, in large part, to changes in agricultural practices and cosmetic standards (14, 15). At the same time, the toxicity and biological effectiveness of these pesticides have increased at least 10-fold (15). For example, in 1945 DDT was applied at a rate of about 2 kg/ha. With the more potent insecticides available now, similar effective insect control is achieved with pyrethroids and aldicarb applied at 0.1 kg/ha and 0.05 kg/ha, respectively. 

Amweg EL, Weston DP, Ureda NM (2005) Use and toxicity of pyrethroid pesticides in the Central Valley, California, USA. Environ Toxicol Chem 24(4) 966-972... 

Weston DP, Holmes RW, You J, Lydy MJ (2005) Aquatic toxicity due to residential use of pyrethroid insecticides. Environ Sci Technol 39(24) 9778-9784... 

You J, Pehkonen S, Weston DP, Lydy MJ (2008) Chemical availability and sediment toxicity of pyrethroid insecticides to Hyalella azteca Application to field sediment with unexpectedly low toxicity. Environ Toxicol Chem 27(10) 2124—2130... 

Mechanism of action can be an important factor determining selectivity. In the extreme case, one group of organisms has a site of action that is not present in another group. Thus, most of the insecticides that are neurotoxic have very little phytotoxicity indeed, some of them (e.g., the OPs dimethoate, disyston, and demeton-5 -methyl) are good systemic insecticides. Most herbicides that act upon photosynthesis (e.g., triaz-ines and substituted ureas) have very low toxicity to animals (Table 2.7). The resistance of certain strains of insects to insecticides is due to their possessing a mutant form of the site of action, which is insensitive to the pesticide. Examples include certain strains of housefly with knockdown resistance (mutant form of Na+ channel that is insensitive to DDT and pyrethroids) and strains of several species of insects that are resistant to OPs because they have mutant forms of acetylcholinesterase. These... 

The organophosphorons insecticides dimethoate and diazinon are mnch more toxic to insects (e.g., housefly) than they are to the rat or other mammals. A major factor responsible for this is rapid detoxication of the active oxon forms of these insecticides by A-esterases of mammals. Insects in general appear to have no A-esterase activity or, at best, low A-esterase activity (some earlier stndies confnsed A-esterase activity with B-esterase activity) (Walker 1994b). Diazinon also shows marked selectivity between birds and mammals, which has been explained on the gronnds of rapid detoxication by A-esterase in mammals, an activity that is absent from the blood of most species of birds (see Section 23.23). The related OP insecticides pirimiphos methyl and pirimiphos ethyl show similar selectivity between birds and mammals. Pyrethroid insecticides are highly selective between insects and mammals, and this has been attributed to faster metabolic detoxication by mammals and greater sensitivity of target (Na+ channel) in insects. 

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