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Simulation of cholinesterase inhibition caused by sublethal exposure of grassland birds to insecticides in Texas
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Although insecticide applications have killed wildlife, direct effects of insecticide exposure usually are sublethal. To evaluate factors that contribute to dietary insecticide exposure and to predict sublethal impact of insecticide applications on birds, I created a simulation model of bird foraging in an agricultural landscape. I obtained data to simulate applications of organophosphorus and carbamate insecticides typical for Texas, deposition and decay of insecticides in the environment, bird foraging, and subsequent cholinesterase (ChE) inhibition in birds. I evaluated the model's ability to predict ChE inhibition by (1) simulating field studies and comparing model predictions to field data, and (2) evaluating the relative sensitivity of ChE inhibition to foraging location, diet selection, and daily intake rate. Except for ChE inhibition caused by the insecticide chlorpyrifos, model predictions of ChE inhibition and insecticide decay reasonably approximated reality. Simulated ChE inhibition was most sensitive to foraging location; however, diet preferences and daily intake became more important when toxicities of residue concentrations among crop fields were more equal. Granivores experienced the greatest inhibition because simulated plants contained more residues than insects or mammals. Omnivores experienced slightly less inhibition, followed by insectivores. Carnivores barely experienced ChE inhibition because their mammalian'prey received few residues and the birds rapidly excreted ingested residues. Organophosphates caused greater ChE inhibition than carbamates. I used the model to predict ChE inhibition in I individual from each of 15 wild bird species over a 6-month period during which insecticides were applied at maximum recommended rates I or 2 times. In this worse-case scenario, mean ChE inhibition in most non-carnivorous bird species exceeded 20% at some point during the 6-month simulation, a sublethal level that denotes "significant" exposure and at which birds may experience nausea and/or may exhibit minor behavioral changes. Birds with greater ChE inhibition have a higher chance of more severe behavioral or physiological effects. The model may be useful to predict insecticide exposure of and sublethal ChE inhibition in grassland bird species, provided adequate knowledge of foraging behavior, diet, insecticide use, and compoundspecific ChE inhibition in different wild birds is available.
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Includes bibliographical references: p. 57-65.
Issued also on microfiche from Lange Micrographics.
Corson, Michael Scott (1996). Simulation of cholinesterase inhibition caused by sublethal exposure of grassland birds to insecticides in Texas. Master's thesis, Texas A&M University. Available electronically from
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