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Effects of azinphos‐methyl on northern bobwhite: A comparison of laboratory and field results
Author(s) -
Matz Angela C.,
Bennett Richard S.,
Landis Wayne G.
Publication year - 1998
Publication title -
environmental toxicology and chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.1
H-Index - 171
eISSN - 1552-8618
pISSN - 0730-7268
DOI - 10.1002/etc.5620170721
Subject(s) - colinus , aché , zoology , toxicity , bobwhite quail , toxicology , acetylcholinesterase , pesticide , biology , chemistry , agronomy , ecology , biochemistry , quail , organic chemistry , enzyme
Abstract The U.S. Environmental Protection Agency's (U.S. EPA's) ecological risk assessment process uses laboratory toxicity data in quotient indices to characterize risks to wildlife, but with poor understanding of the relationship between these data and actual field effects. To explore this relationship, we compared toxicity results from a controlled field study to those from a dietary toxicity (median lethal concentration) laboratory test. In the field test, northern bobwhite ( Colinus virginianus ) chicks were cross‐fostered to bantam chicken ( Gallus domesticus ) hens. Then, 12‐d‐old broods in enclosed alfalfa fields were exposed to sprayed azinphos‐methyl (Guthion® 2S) at three application rates (0 [control], 0.77, and 3.11 kg active ingredient/ha). Chick survival was significantly lower at 3.11 kg/ha 0 to 5 d postspray and at both application rates 6 to 10 d postspray compared to control ( p < 0.05). Chick brain acetylcholinesterase (AChE) activity, growth, and weight of crop contents were significantly reduced in treatments compared to control ( p < 0.05). In the laboratory test, 12‐d‐old bobwhite were exposed to dietary concentrations of 0 (control), 150, 240, 380, and 600 ppm azinphos‐methyl for 5 d. Survival was significantly lower at 600 ppm compared to control, and brain AChE activity and growth rates were significantly reduced from control for all concentrations ( p < 0.05). Chick survival, brain AChE activity, and growth in the field were significantly different from equivalent exposures in the laboratory ( p < 0.05), with equivalency determined by U.S. EPA's vegetation residue estimates, and temporal patterns of effects differed between field and laboratory. We conclude that the effects observed in the field differed from that predicted by risk quotients because the quotient method does not consider alternate routes of exposure, behavioral responses, influence of spatial and temporal environmental variability, or indirect effects.