The radiation was devastating. Only 29 of the 200 salamander eggs under acetate hatched, while 190 of those under mylar hatched. Twenty‐five of the 29 salamanders that hatched in the acetate‐topped containers were deformed; only one of the 190 salamanders that hatched under mylar was deformed.
In a report of their experiment, published in the December Proceedings of the National Academy of Sciences, Blaustein and his colleagues wrote, “Our results show that ambient levels of UV-B adversely affect the development and induce deformities in some amphibian species in their natural habitat.” The results show nothing of the sort, of course. In their “natural habitat,” long‐toed salamanders don’t float their eggs on the surface of ponds and expose them to sunlight. Neither do they have to be provided with mylar parasols to avoid the effects of the sun. Anchoring their eggs well below the surface of the water is sufficient.
Dr. Blaustein said that the results point to increasing UV levels as the probable cause of the deformities. But his results say nothing about UV levels or their effects. To do so, Dr. Blaustein would need to show differential effects between current, higher UV levels and past, lower UV levels. He doesn’t. In fact, the UV level in the acetate‐covered containers in the experiment he reported was about 90 percent of the level currently reaching the earth. That’s roughly equivalent to the UV level before CFCs began damaging the ozone layer. Under Dr. Blaustein’s experimental conditions, the old, low level of UV is devastating enough.
There is a biologically sound explanation for missing limbs and extra limbs in long‐toed salamanders, and there are two good reasons it has not been widely reported. For one thing, it’s not politically correct; for another, it’s biologically complicated. The first reason is probably more important.
Research done by Professor Stanley Sessions of Hartwick College, Oneonta, New York, reveals that the larvae of parasitic flatworms called trematodes, not UV radiation, causes deformities in long‐toed salamanders. The trematodes live in garter snakes, and their eggs are released in garter snake feces. Pond snails eat the eggs, and free‐swimming trematode larvae that hatch within the snails are released into the pond water. Those larvae bore into developing salamanders and cause the deformities. Dr. Sessions acknowledges that other factors may contribute to some deformities, but the occurrence of deformities in long‐toed salamanders “probably reflects a sporadic and localized natural phenomenon, especially fluctuations in pond snail populations.”
He’s on solid ground. In their summary of a workshop on causes of amphibian deformities, a scientist from the Environmental Protection Agency and two from universities concluded that trematodes “are particularly plausible causes.” They cite no other cause for which there is direct evidence from field studies.
TheWashington Post, USA Today, and ABC News all reported Dr. Blaustein’s conclusions about UV radiation. Don’t expect such publicity for Dr. Sessions’ work. How can “fluctuations in pond snail populations” compete with evil industry as the cause for deformities in amphibians?