The practice of science ought to be utterly dispassionate, driven only by a desire to discover the true nature of the world around us. But political correctness, having infected the rest of our society, has invaded science as well. In early December, four scientists managed to publish the results of an experiment that was far more political than scientific in one of our nation’s most prestigious scientific journals. Their thesis: that man‐made chemicals such as chlorofluorocarbons (CFCs) are the cause of deformed frogs, toads and salamanders. The chemicals cause the widely reported thinning of the earth’s ozone layer, and less ozone means more ultraviolet (UV) radiation gets through to the earth’s surface and causes deformities.
They base their conclusion on an experiment involving a particular kind of salamander, and neither their methodology nor their conclusion withstands scrutiny.
Long‐toed salamanders are about five inches long, gray‐black in color and slathered with bright mustard yellow splotches across the back and tail. Commonly called “mole salamanders,” they seldom see the light of day, spending their adult lives under forest litter or in burrows, venturing from those dark places mostly at night. They’re successful little beasts and live up to 20 years.
The salamanders have to hide from the sun because they have very low levels of photolyase, an enzyme that repairs DNA damage caused by UV radiation. The female salamander doesn’t know about that when she returns to a pond to mate and attaches her eggs to underwater surfaces, but that behavior keeps the eggs below water, and the water shields the eggs from UV radiation.
Given all that’s known about the biochemistry and behavior of the long‐toed salamander, dire consequences would be expected from exposing its eggs to sunlight.
That’s exactly what Professor Andrew R. Blaustein of Oregon State University and three colleagues found. They collected salamander eggs from an Oregon pond, placed 200 eggs in mylar‐covered containers and another 200 in acetate‐covered containers, and floated them on the pond’s surface. The mylar blocked 94 percent of the sun’s UV radiation; 90 percent of the sun’s UV radiation passed through the acetate.
The>Washington 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?
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?