Organophosphates insecticide toxicity

Lydy MJ, Linck SL. 2003. Assessing the impact of triazine herbicides on organophosphate insecticide toxicity to the earthworm Eisenia fetida. Arch Environ Contam Toxicol 45 343-349. 

Table 2.2 Effect of Piperonyl Butoxide and SKF 525A Pretreatment on Organophosphate Insecticides Toxicity in Mice...

Belden, J. and Lydy, M. 2000. Impact of atrazine on organophosphate insecticide toxicity. Environ. Toxicol. Chem., 19, 2266-2274. 

The variation in toxicity of common organophosphate insecticides is exemplified in Table 5.37. The range of chlorinated hydrocarbon insecticides (Table 5.38) have, with the exception of Endrin and Isodrin, somewhat lower oral and dermal toxicities. The toxicities of a range of oilier insecticides, fungicides, herbicides and rodenticides are summarized in Table 5.39. 

Murphy SD. 1980. Toxic interactions with dermal exposure to organophosphate insecticides [Abstract]. Toxicol Lett 5(Supplement 1) 34. 

Murphy SD. 1982. Toxicity of hepatic metabolism of organophosphate insecticides in developing rats. In Hunt VR, Smith MK, Worth D, eds. Banbury report, Vol. II. Environmental factors in hiunan growth and development symposium, November 1-4, 1981. Cold Spring Harbor, NY Cold Spring Harbor Laboratory, 125-136. 

Skinner CS, Kilgore WW. 1982a. Acute dermal toxicities of various organophosphate insecticides in mice. J Toxicol Environ Health 9 491-497. 

Uzokwu M. 1974. Comparative feto-toxicity of organophosphate insecticide in mice. Bulletin of Epizoot Dis Afr 22 161-166. 

Organophosphate insecticides also inhibit RBC-ACHE and PCHE. Inhibition of ACHE in erythrocytes is assumed to mirror inhibition of ACHE in the nervous system, which is the receptor of the toxic action, to some extent. Therefore, measurements of RBC-ACHE and PCHE are used for biological monitoring of exposure to OP insecticides (Maroni, 1986). Inhibitions of RBC-ACHE and PCHE activities are correlated with intensity and duration of exposure, although at different levels for each OP compound. Blood ACHE, being the same molecular target as that responsible for acute toxicity in the nervous system, is a true indicator of effect, while PCHE can only be used as an indicator of exposure. 

Signs of disulfoton toxicity, such as muscle tremors, fasciculations, lacrimation, and salivation, in animals are generally observed after a few daily doses, but begin to diminish in severity as exposure to dislllfoton continues (Bombinski and DuBois 1958). This phenomenon is known as tolerance. Tolerance appears to be a reproducible phenomenon that does not depend on the organophosphate insecticide used, the route of administration, or the animal species (Costa et al. 1982b). Several possible mechanisms have been proposed /explain this phenomenon. 

McCarty RT, Haufler M, Osborn MG, et al. 1969. Oral toxicity of four organophosphate insecticides to farm livestock. Am J Vet Res 1149-1153. 

Slotkin, T.A., Levin, E.D. and Seidler, F.J. (2006) Comparative developmental neurotoxicity of organophosphate insecticides effects on brain development are separable from systemic toxicity. Environ. Health Perspect., 114 (5), 746-751. 

Organophosphate insecticides are designed for nontoxicity to humans in that the S is relatively nontoxic. Toxicity is achieved by the host s oxidation of the S to 0 as well as the inability to detoxify by hydrolysis of the ester groups. 

Farm workers are especially susceptible to organophosphate insecticide poisoning. Unsafe spraying conditions can lead to accumulated toxicity and chronic symptoms. Since there are many enzymes in the body which are in the serine esterase family along with Achase and can complex... 

The term potentiation is then reserved for those cases where both compounds have appreciable intrinsic toxicity, such as in the case of malathion and EPN. Malathion has a low mammalian toxicity due primarily to its rapid hydrolysis by a carboxylesterase. EPN (Figure 9.6) another organophosphate insecticide, causes a dramatic increase in malathion toxicity to mammals at dose levels, which, given alone, cause essentially no inhibition of acetylcholinesterase. The increase in toxicity as a result of coadministration of these two toxicants is the result of the ability of EPN, at low concentrations, to inhibit the carboxylesterase responsible for malathion degradation. 

Pape-Lindstrom, P.A. and Lydy, M.J. (1997) Synergistic toxicity of atrazine and organophosphate insecticides contravenes the response addition mixture model, Environmental Toxicology and Chemistry 16 (11), 2415-2420. 

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