Page 835 - The Toxicology of Fishes

Toxicology of Synthetic Pyrethroid Insecticides in Fish: A Case Study 815

• More rapid uptake? Not a factor.
• More efficient distribution to nervous system? Not a factor.
• Detoxification deficiencies? Important factor.
• Slow elimination? Probably a factor.
• Differential stereoselective toxicity? Not a factor.
• Secondary modes of action? Possibly a factor.
• Nervous system sensitivity? Important factor.

Extended persistence of residues in the sediments can result from their binding to particulates in an
aquatic system (Gan et al., 2005). California drainage systems are of special concern because of the
high usage of pyrethroids and persistence of the residues in sediments (Oros and Werner, 2005).
Foodchain exposures may result, and regeneration of bioavailable residues in water may result over time
if the compounds desorb off the sediment (Amweg et al., 2005; Maund et al., 2002; Weston et al., 2004).
A new emphasis on extraction and analytical methodologies (You et al., 2004) is contributing to a better
understanding of pyrethroid residue persistence and bioavailability. Microbial biodegradation of pyre-
throids in aquatic systems (in the sediment and the water column) has been acknowledged to play an
important role in the degradability and persistence of the residues (Lee et al., 2004). Probabilistic risk
assessments of pyrethroids in aquatic systems have been developed in hopes of understanding the
potential adverse impacts of the insecticides on aquatic species (Solomon et al., 2001). Ethofenprox
(Figure 20.2) is an example of a pyrethroid insecticide that is much less toxic to fish; notably, it is the
only one without a carboxylester in the molecule. It is hoped that a better understanding of the factors
that contribute to the highly potent toxicity of pyrethroids to fish will lead to the design and synthesis
of safer compounds and improved methods for using them safely.

Acknowledgments

The author is very appreciative of the work of numerous graduate students on the research discussed in
this chapter, especially Steve Bradbury, Scott Dyer, Dan Symonik, Patricia Rice, and David Featherstone.
Collaborators James McKim, Charlie Drewes, Gary Atchison, and John Clark are also much appreciated.
This is a publication of the Iowa Agriculture and Home Economics Experiment Station, Project 5075.

References
Amweg, E. L., Weston, D. P., and Ureda. U. M. (2005). Use and toxicity of pyrethroid pesticides in the Central
Valley, California, USA. Environ. Toxicol. Chem. 24, 966–972.
Bloomquist, J. R. (1985). Neurotoxic insecticides inhibit GABA-dependent chloride uptake by mouse brain
vesicles. Biochem. Biophys. Res. Commun., 133, 37–43.
Bloomquist, J. R. (1996). Ion channels as targets for insecticides. Annu. Rev. Entomol., 41, 163–190.
Bloomquist, J. R. and Soderlund, D. M. (1985). Neurotoxic insecticides inhibit GABA-dependent chloride
uptake by mouse brain vesicles. Biochem. Biophys. Res. Comm., 133, 37–43.
Bradbury, S. P. (1982). Toxicity and Excretion of Fenvalerate in Bobwhite Quail, Masters thesis, Iowa State
University, Ames.
Bradbury, S. P. and Coats, J. R. (1982). Toxicity of fenvalerate to bobwhite quail, including brain and liver
residues associated with mortality. J. Toxicol. Environ. Health, 10, 307–319.
Bradbury, S. P. and Coats, J. R. (1989a). Toxicokinetics and toxicodynamics of pyrethroid insecticides in fish.
Environ. Toxicol. Chem. 8, 373–380.
Bradbury, S. P. and Coats, J. R. (1989b). Comparative toxicology of the pyrethroid insecticides. Rev. Environ.
Contam. Toxicol., 18, 134–177.
Bradbury, S. P., Coats, J. R., and McKim, J. M. (1985). Differential toxicity and uptake of two fenvalerate
formulations in fathead minnows (Pimephales promelas). Environ. Toxicol. Chem., 4(4), 533–541.