Amphibian Mortality Due To Ultraviolet Radiation, Researchers Find

Now, field experiments in the Oregon Cascade Mountains have confirmed what many scientists had suspected -- ambient levels of ultraviolet-B (UV-B) radiation from the sun can cause high rates of mortality and deformity in some species of frogs and other amphibians. The earth is shielded from UV radiation by the ozone layer, which is believed to be thinning because of the increased use of chlorofluorocarbons as refrigerants, solvents and cleaning agents.

"There has been a great deal of recent attention to the suspected increase in amphibian deformities. However, most reports have been anecdotal, and no experiment in the field under natural conditions had been performed previously," said Joseph M. Kiesecker of Yale University, who presented his findings Feb. 17 at the annual meeting of the American Association for the Advancement of Science in Philadelphia.

Kiesecker, along with Andrew R. Blaustein of Oregon State University, compared the embryos of long-toed salamanders shielded from UV-B radiation by mylar filters to unshielded embryos. They found that 95 percent of the shielded embryos hatched, compared to only 14.5 percent of the unshielded embryos. Even more striking, only 0.5 percent of the surviving shielded salamanders had deformities while 91.9 percent of the unshielded salamanders had deformities. Malformed tails, blisters and edema were the most frequent deformities.

"The recent thinning of the protective ozone layer in the upper atmosphere has been linked to increased risks of skin cancer and cataracts in humans as well as to the destruction of fragile plant life. Deformed and dying frogs may be linked to thinning ozone as well," said Kiesecker, who is studying other possible factors, such as water level and quality, which also can affect the amount of UV-B radiation reaching amphibians.

UV-B radiation also may impair disease defense mechanisms, making amphibians more susceptible to pathogens and parasites that may hamper normal development and increase mortality, Kiesecker said. For example, he found increased mortality associated with a pathogenic fungus (Saprolegnia ferax) infecting some embryos exposed to UV-B, while embryos under mylar filters were not infected. The UV-B may work synergistically with the fungus, said Kiesecker, who reports seeing an outbreak of fungal pathogens in a number of amphibian species in the last 10 years.

Amphibians are ideal species for the study of UV-B exposure, he noted. Many lay their eggs in open, shallow water where exposure to UV-B is high. Typically, a population of 200 breeding pairs of toads, for example, will produce as many as 1 million embryos. Furthermore, amphibian species have varying amounts of an enzyme called photolyase, which is the principal enzyme for repairing UV damage to DNA. Photolyase attacks a major UV photoproduct in DNA -- cyclobutane pyrimidine dimers -- which can cause mutations and cell death if left unchecked.

Kiesecker, a zoologist and postdoctoral fellow, reported that frog and toad species with the greatest photolyase activity had the lowest mortality rates in developing embryos. For example, he and his colleagues noted an increase in embryo mortality of 15 to 20 percent in the Western toad and the Cascade frog -- two species with low levels of photolyase -- while the Pacific tree frog, which has a high photolyase level, is thriving. All three species live in the same habitat in the Cascade Mountains.

The field studies, which were completed in May and June 1997, also are reported in part in the December issue of the Proceedings of the National Academy of Sciences. Funding was from the National Science Foundation and the Donnelley Fellowship sponsored by the Yale Institute for Biospheric Studies.