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AchE Inhibition leads to Decrease, Population growth rate
Key Event Relationship Overview
AOPs Referencing Relationship
|AOP Name||Adjacency||Weight of Evidence||Quantitative Understanding||Point of Contact||Author Status||OECD Status|
|Acetylcholinesterase inhibition leading to acute mortality||non-adjacent||Low||Low||Dan Villeneuve (send email)||Under Development: Contributions and Comments Welcome||Under Development|
Life Stage Applicability
Key Event Relationship Description
- AChE inhibition at the individual level may lead to a declining population trajectory.
Evidence Supporting this KER
- Wildlife studies including fish and birds have shown that exposure to AchE inhibitors can lead to physiological changes and behavioral alterations, which can make individuals more vulnerable to prey. It is biologically plausible that decreased survival and reproduction could decrease the population trajectory, if the scale of the changes were significant.
Uncertainties and Inconsistencies
In bluegill and largemouth bass, the principal mode of exposure was unclear. The relative uptake from pesticide-treated insects versus direct uptake from water was not quantifiable, although the data suggest that fish more readily metabolize insecticides introduced via diet than via oral exposure (Macek 1972).
Fish appeared to be more sensitive to exposure at a higher water temperature (Macek 1972).
Known modulating factors
Known Feedforward/Feedback loops influencing this KER
Domain of Applicability
Fish and aquatic invertebrates exposed to OP insecticides showing high AChE inhibition as compared to fish from untreated ponds, did not recover normal AChE activity for 28 days following exposure (Macek 1972).
Birds exposed to OP pesticides display behavioral changes (Eng 2017).
OP toxicity in birds and mammals is determined by multiple factors. Varying sensitivity within taxa is related to chemical affinity for binding with brain AChE, ability of hepatic and brain tissue to metabolize these compounds and activate latent inhibitors, and the affinity of parent compounds and their metabolites for nontarget esterases (Grue 1997).
Banaee,M., Sureda, A. Mirvaghefi, A.R. and K. Ahmadi. 2011. Effects of Diazinon on Biochemical Parameters of Blood in Rainbow Trout (Oncorhynchus mykiss). Pestic. Biochem. Physiol. 99(1): 1-6.
Calisi, A., Lionetto, M.G., Schettino, T. 2011. Biomarker response in the earthworm Lumbricus terrestris exposed to chemical pollutants. Science of the Total Environment. 409, 4456-4464.
Eng, M.L., Stutchbury, B.J.M. & Morrissey, C.A. 2017. Imidacloprid and chlorpyrifos insecticides impair migratory ability in a seed-eating songbird. Sci Rep 7, 15176.
Grue, C.E., Gibert, P.L., Seeley, M.E. 1997. Neurophysiological and Behavioral Changes in Non-Target Wildlife Exposed to Organophosphate and Carbamate Pesticides: Thermoregulation, Food Consumption, and Reproduction. Amer. Zool., 37:369-388.
Jarvinen AW, Nordling BR, Henry ME. 1983. Chronic toxicity of dursban (chlorpyrifos) to the fathead minnow (Pimephales promelas) and the resultant acetylcholinesterase inhibition. Ecotoxicol Environ Saf 7:423–434.
Khalil,F., I.J. Kang, S. Undap, R. Tasmin, X. Qiu, Y. Shimasaki, and Y. Oshima. 2013. Alterations in Social Behavior of Japanese Medaka (Oryzias latipes) in Response to Sublethal Chlorpyrifos Exposure. Chemosphere. 92(1): 125-130.
Macek, K.J., Walsh, D.F., Hogan, J.W., Holz, D.D. 1972. Toxicity of the Insecticide Dursban to Fish and Aquatic Invertebrates in Ponds. Trans. Am. Fish. Soc., 101(3): 420-427.
Pant, R., Katiyar, S.K. 1983. Effect of malathion and acetylcholine on the developing larvae of Philosamia ricini (Lepidoptera: Saturniidae). J. Biosci. 5(1), 89-95.
Yen,J., S. Donerly, E.D. Levin, and E.A. Linney. 2011. Differential Acetylcholinesterase Inhibition of Chlorpyrifos, Diazinon and Parathion in Larval Zebrafish. Neurotoxicol. Teratol. 33(6): 735-741.