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1990). The hypotheses proposed to explain local declines include disease and the introduction of exotic predators (Hayes and Jennings 1986; Carey and Bryant 1995), modification in exposure of eggs to ultraviolet light (Blaustein et al. 1994), and pathogens (Morell 1999). There also have been numerous reports of amphibian kills after chemical spills or agricultural spraying. Environmental contamination also might contribute to continuing declines by affecting the growth and development of young amphibians (Carey and Bryant 1995).

There have been reports of deformities, such as extra, missing, or malformed limbs, in wild populations of frogs in the United States and Canada (Schmidt 1997; Ouellet et al. 1997; Tietge 1997). The deformities could be caused by exposure to chemical pollutants, increased exposure to ultraviolet light, parasite infestations, or some combination of the three (Schmidt 1997). However, more recent studies indicate that the physical presence of parasitic trematode worms, which form cysts in the developing hind-limb regions of frogs, might be primarily responsible for supernumerary limbs in frogs (Sessions and Ruth 1990; Sessions 1997; Johnson et al. 1999; Sessions et al. 1999). The phenomenon seems to be caused by physical disturbances, because similar effects can be induced by implanting inert resin beads, similar in size to trematode cysts, into the developing limb buds of frogs (Sessions and Ruth 1990). However, results from studies conducted by the Minnesota Pollution Control Agency and the National Institutes of Environmental Health Sciences have linked gross deformities observed in frogs in northwestern Minnesota to biologically active agents in the water they inhabit (Burkhart et al. 1998). Specifically, water samples taken from ponds with high incidences of frog malformations (affected sites) were tested in FETAX assays, in which X. laevis embryos were exposed to pond water for 96 h and observed for mortality and malformations. The results of these assays were compared with those conducted with water samples taken from ponds with unaffected frog populations (reference sites). The water from affected sites induced mortality and malformations, whereas the water from reference sites did not. The observed malformations were dose dependent and reproducible. Research projects are under way to try to establish a plausible link between exposure to specific chemical contaminants and the appearance of specific deformities under laboratory conditions.

The role of hormones, such as estradiol, testosterone, and corticosterone, in the growth and metamorphosis of toads has been studied in the laboratory (Richards and Nace 1978; Gray and Janssens 1990; Hayes et al. 1993; Hayes 1995; Hayes and Wu 1995a,b). For example, the action of exogenous corticosterone on toads has been shown to closely resemble the effects of exogenous thyroid hormones, suggesting that steroids might interact with endogenous thyroid hormones (Hayes et al. 1993; Hayes 1997). In a study of DDT, male African clawed frogs were induced to synthesize the female yolk protein vitellogenin in the liver after intraperitoneal injection of 1.0 or 250.0 µg o,p'-DDT/g body weight for 7 d (Palmer and Palmer 1995). Vitellogenin synthesis is considered a hallmark of exposure to estrogens, but other studies involving DDT suggest that DDT might act as acontinue