Page 834 - The Toxicology of Fishes

814 The Toxicology of Fishes

TABLE 20.2
Lethal Brain Concentrations of Pyrethroids
Concentration (µg/g)
Pyrethroid Mouse Quail Rainbow Trout
cis-Cypermethrin 1.7 a 4.0 a 0.2 a
Fenvalerate 1.0 b 1.3 c 0.16 d
cis-Permethrin 6.0 e Not tested 2.0 e
trans-Permethrin 36.4 e Not tested 2.0 e
a Data from Edwards et al. (1985) for the 1R,αS isomer only; aqueous
exposures to trout and p.o. exposures to the mouse and Japanese quail.
b Data from Lawrence and Casida (1982); intracerebral LC 50 value for the
2S,αS isomer.
c Data from Bradbury and Coats (1982); p.o. exposure to bobwhite quail
(Colinus virginianus).
d Data from Bradbury et al. (1987a); aqueous exposure.
e Data from Glickman and Lech (1982); i.v. and i.p. exposures.

interpreted due to limitations of the whole-body method of analysis of these three metabolic ions. There
was clear evidence that the pyrethroid disrupted osmoregulation, possibly contributing, as a secondary
factor, to the toxicity of this insecticide to fish.
An investigation of the effects of a pyrethroid and other toxic chemicals on behavior and morphology
(development) has revealed another possible secondary toxic impact on fish. Rice et al. (1997) showed
that permethrin not only was acutely toxic to juvenile medaka (at 10 µg/L and 40 µg/L) but also caused
sublethal behavioral effects long before death. Specifically, permethrin produced loss of equilibrium and
initial hyperactivity, followed by hypoactivity, excessive lateral flexure, and an underreactive startle
response.

Fish Nervous System Sensitivity
It is feasible that the nervous system of fish is more sensitive to pyrethroids than those in mammals and
birds. One possible way to investigate this possibility was to collect fish soon after death, dissect out
their brains, and conduct residue analysis on them to determine the concentration required in the brain
to induce mortality. Comparisons of the brain concentrations of synthetic pyrethroids at death were made
from several studies that utilized fish, birds, and mammals. Table 20.2 shows the results. For cis-
cypermethrin, the concentration required in the mouse brain for lethality is more than 8 times higher
than for trout, and the concentration required in the quail brain is 20-fold higher. For fenvalerate, the
amounts are 6-fold greater for mouse and 8-fold greater for quail. Higher quantities were also required
for permethrin isomers. These comparative data, drawing on work from several research laboratories,
indicate that the fish brain may be considerably more susceptible to pyrethroids than are mammal and
bird brains. Methods developed for the study of fish neurophysiology and toxicology may help improve
our understanding of their nervous system better and its susceptibility to certain classes of toxic chem-
icals. Noninvasive recording methods, using the startle response in Mauthner cells in larval medaka,
have shown promise (Featherstone et al., 1991). Studies on the differences in types of symptoms and
responses for different classes of toxic chemicals have also shown utility for the comparison of qualitative
and quantitative effects on the fish nervous system (Featherstone et al., 1993).

Conclusions
Several factors probably contribute to the enhanced toxicity of synthetic pyrethroids to fish, as compared
to higher vertebrate species. A summary of the factors examined here, with an assessment of their
possible involvement, follows: