neurons needs to be modified (Song and Narahashi, 1996); that is why pyrethroids are so potent.
Acute exposure to the type II pyrethroid deltamethrin induces apoptosis in the rat brain that might be associated with the neurodegeneration seen after exposure (Wu and Liu, 2000). Persistent increases in p53 and Bax expression and transient increases in Bcl-2 expression that were seen immunohistochemically after deltamethrin treatment of rats could contribute to the apoptotic cell death (Wu et al., 2000).
Pyrethroids are much more potent in insects than in mammals; the difference in LD50s is a factor of about 4500 (Elliott, 1976). The major factors underlying the selective toxicity of pyrethroids in insects are sodium-channel sensitivity and temperature dependence (Song and Narahashi, 1996). Insect sodium channels are 100–1000 times more sensitive to pyrethroids than are mammalian sodium channels (Narahashi, 2001; Warmke et al., 1997). Furthermore, the activity of pyrethroids is temperature-dependent; they have a greater effect on sodium channels at lower temperatures than at higher temperatures. For example, potency increases by a factor of 5 if temperature is lowered by 10°C (Song and Narahashi, 1996). Because insects have a lower body temperature (about 27°C) than mammals (about 37°C), temperature dependence contributes to the selective toxicity in insects. A difference (by a factor of about 3) in the rate of pyrethroid detoxification between mammals and insects also contributes to the selective toxicity.
Ray and Forshaw (2000) review pyrethroid poisonings. Accidental spilling of pyrethroids on the head, face, and eyes caused pain, lacrimation, photophobia, congestion, and edema of the conjunctiva and eyelids (He et al., 1988, 1989). Acute ingestion of pyrethroids was reported to cause epigastric pain, nausea, vomiting, headache, dizziness, anorexia, fatigue, tightness in the chest, blurred vision, paresthesia, palpitations, coarse muscular fasciculations, and disturbances of consciousness (He et al., 1988, 1989).
Cutaneous paresthesia is a general effect seen after exposure to all pyrethroids and pyrethrins. It is reversible and not accompanied by electrophysiologic, clinical, and persistent abnormalities. Type II pyrethroids tend to be more potent toxicants than type I pyrethroids (Aldridge, 1990; Flannigan and Tucker, 1985; He et al., 1988, 1989; Knox et al., 1984; Kolmodin-Hedman et al., 1982; LeQuesne et al., 1981; Litchfield, 1985; Tucker and Flannigan, 1983; Vijverberg and van den Bercken, 1990). There have been reports of contact dermatitis (Bainova, 1987; Tomova, 1982), but the dermal toxicity is not considered serious (Bradbury and Coats, 1989; Miyamoto, 1976).
Acute inhalation of type II pyrethroids has been reported to have irritating effects on the mucous membranes of respiratory passages (Vijverberg and van den Bercken, 1990). Asthma-like attacks and anaphylactic reactions with peripheral vascular collapse were reported after exposure to pyrethrins (ATSDR, 2001b).
Altenkirch and colleagues (1996) reported on the neurological examinations of 23 reported cases (out of 64) of pyrethroid poisoning. Exposures were to permethrin, deltamethrin, cyphenothrin, tetramethrin, and mixtures of various pesticides. In nine cases, severe somatic or psychiatric disorders were present that had no plausible relationship to the chemical exposure. Cullen (1987) reported that eight people developed multiple chemical sensitivity syndrome after exposure to pyrethroids. In six cases, a causal link between acute