Page 828 - The Toxicology of Fishes

808 The Toxicology of Fishes

Na +

Cl – Cl –
K +
Cl –

Nerve Axon – Nerve Potential Propagation
Na +

PYR
Cl – Na + Cl –
K +
Na + Na + Cl – Na + Na +
Nerve Axon with Pyrethroid – Repeated
Nerve Impulses
FIGURE 20.2 The mechanism of neurotoxic action of a pyrethroid at the sodium channel of the nerve axon prevents
complete closing of the sodium gate, which allows constant leakage of Na ions, which leads to hyperexcitability in the
+
neuron.
Mammalian studies on the toxicodynamics of pyrethroids have shown that the type I pyrethroids cause
primarily hyperactivity and tremors, while type II pyrethroids cause writhing, seizures, and choreoathe-
tosis. Both types primarily affect the sodium channels and effect hyperpolarization of the axons, but the
type II compounds produce longer sodium currents and cause blocking of nerve conductance. In cock-
roaches, symptomological differences also exist between the two types of pyrethroids. Research on birds
and fish has not generally revealed distinct differences in toxic symptoms, but it is possible that they also
respond differently, at some level, to the two classes of pyrethroids. The structural differences between
type I and type II pyrethroids are simple; type II pyrethroids have an α-cyano group at the benzylic carbon
of the alcohol portion of the ester. In Figure 20.1, pyrethrin I, tefluthrin, and ethofenprox are type I
pyrethroids, and fenvalerate (and its commercially important resolved S,S-isomer) represents the type II
class. Soderlund et al. (2002) have provided a review of the toxic modes of action of pyrethroid insecticides.
Toxic symptoms in fish (fathead minnows) have been observed in acute toxicity tests with fenvalerate
(Bradbury et al., 1985). Swimming near the surface, darting, hyperactivity, and bursts of rapid swimming
eventually led to violent whole-body contractions. The toxic syndrome was investigated in considerable
physiological detail in adult rainbow trout (Bradbury et al., 1987a). Increases in cough rate and mucous
secretion by the gills were the first signs of toxicity noted. Fine tremors developed, with the tremors slowly
becoming more severe and eventually progressing to seizures with twisting and thrashing. Histopathology
of the gills after death revealed numerous aneurisms and necrotic cells. Major detrimental impacts on heart
rate, ventilation rate, and blood chemistry have also been described in the acute toxicosis phase for the trout.
Chronic toxicity and sublethal toxic effects have been demonstrated at concentrations much lower than
those that elicit acute toxic effects. Chronic toxicity endpoints such as growth and reproduction have
revealed very low no-observable-adverse-effect levels (NOAELs) for several pyrethroids, with the early
life stages showing great susceptibility to impaired growth rates. Behavioral toxicity has been reported
in the form of swimming abnormalities (hyperactivity, loss of equilibrium, abnormal lateral flexure)
(Glickman et al., 1982; Rice et al., 1997).

Factors Influencing Toxicity

The acute toxicity of pyrethroids to fish was traditionally measured in standardized water or in filtered
or purified water. Many studies have demonstrated the extraordinary toxicity of photostable synthetic
pyrethroids to fish; in many cases, they are as toxic as organochlorine insecticides such as DDT, dieldrin,