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NAAMP III Archive - deformed frogs
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Are Increases in Ultraviolet Light a Plausible Factor Contributing toAmphibian Deformities?

Gerald T. Ankley

U.S. Environmental Protection Agency
National Health and Environmental Effects Research Laboratory
Mid-Continent Ecology Division
6201 Congdon Boulevard
Duluth, MN 55804

Several lines of circumstantial evidence compel consideration of increases in ultraviolet (UV)light as a possible contributing factor to the recent observations of developmental abnormalities(primarily limb deformities) in amphibian species. First, corresponding with seeming increasesin the incidence of deformities, there has been a clear documentation of recent increases in theintensity of UV light, particularly UVB (ca., 295-330 nm), at various locations around the world(e.g., Kerr et al. 1993). Moreover, some of the largest relative increases in UV have been shownto occur in late spring and early summer (Herman et al. 1996), a period which coincides withreproduction and critical windows of development of amphibian species in northern latitudes. Finally, changes in UV light offer an intriguing potential explanation from the perspective of theseemingly non-contiguous, somewhat random nature of locations where limb deformities havebeen observed. That is, observations of deformed frogs and toads have been made at locationsranging from agriculturally-impacted wetlands to state forests. This would not be consistent, forexample, with the use of a particular pesticide.

Ultraviolet light can cause direct biological damage through mechanisms ranging from oxidativestress, via the generation of free oxygen radicals, to direct damage of DNA through formation ofthymidine dimers. Also, there are a number of naturally-occurring and anthropogeniccompounds that can enhance UV-induced damage by acting as photosensitizers; foremost amongthese are a number of polycyclic aromatic hydrocarbons (PAHs). Unlike concentrations of mostother contaminants in the environment (e.g., organochlorine insecticides), PAH levels haveremained relatively constant (Simcik et al. 1996), presumably due to a relatively constant inputfrom non-point sources such as combustion of fossil fuels.

There have been a few published reports of the effects of UV, both with and withoutphotosensitizers, on survival and development of amphibians. For example, UV treatment hasbeen utilized as a standard technique by biologists to cause a host of specific developmentalabnormalities in amphibians (Kao and Danilchik 1991); however, the wavelengths used forinducing these types of abnormalities typically are too low to be of significance from anecological perspective. In other studies, Worrest and Kimeldorf (1975; 1976) reported thatexposure of toad embryos to environmentally-realistic levels of UVB resulted in a variety ofdevelopmental and morphological abnormalities including lordosis, epidermal hyperplasia andcorneal effects. Grant and Licht (1995) made similar observations with frog embryos which hadbeen exposed to relatively high levels of UVB for short periods of time. Blaustein et al. (1994;1995) reported a correlation between photolyase (a DNA repair enzyme) activity in frogs andsalamanders and their sensitivity (embryo survival) to UV in a field setting. In an evaluation ofthe role of multiple stressors on amphibian survival, Long et al. (1995) reported a synergisticinteraction between UVB exposure and low pH on survival/development of Rana pipiens. Instudies with photosensitizers, Kagan et al. (1984) reported that the toxicity of anthracene (aPAH) and alpha-terthienyl (a plant product) to R. pipiens could be increased by an order ofmagnitude upon exposure to UVA (ca., 330-400 nm) light. Similarly, Fernandez and L'Haridon(1992) reported that UVA significantly enhanced the genotoxicity of certain PAHs to newtembryos.

The preceeding literature review is not comprehensive, but it clearly demonstrates that UVA/Bexposure can causes significant effects on survival/development of amphibians in lab and fieldsettings. Further, these types of effects can be exacerbated by the presence of photosensitizerssuch as PAHs. However, the degree to which UV might be responsible for the specific limbdeformities under consideration is uncertain. There has been no direct demonstration that UVcan induce limb deformities in developing amphibians; however, few if any of the studiesperformed to date were designed in a fashion that would allow this hypothesis to be realisticallyassessed. Also, the mechanism of action via which UV could cause limb malformations is notcertain; for example, direct damage of DNA (i.e., mutations) would seem to be an unlikelyexplanation given the consistency in types of deformities within and among sites. One possiblelinkage of UV to limb deformities might be related to alterations in vitamin A/retinoic acidmetabolism. Vitamin A is a known antioxidant that can protect against UV-induced oxidativestress, and also is a precursor of retinoic acid, which is critical for normal limb bud formationand development (see previous presentation by K. Muneoka).

Given uncertainty concerning potential linkages between UV and developmental effects inamphibians, there is a need for further research in this area. This work should be conducted withenvironmentally-realistic UV (and visible) light exposure regimes, with careful attention to keydevelopmental processes throughout metamorphosis. Ideally, this research also would includeconsideration of endpoints of exposure/effects from a mechanistic perspective (e.g., thymidinedimerization, chromosomal damage, status of antioxidants, etc.). Finally, given their ubiquitousdistribution, it would seem prudent to consider the possible role of photosensitizers in terms ofpossible UV effects on amphibians.


Blaustein, A.R., P.D. Hoffman, D.G. Hokit, J.M. Kiesecker, S.C. Wells and J.B. Hays. 1994. UV repair and resistance to solar UVB in amphibian eggs: A link to population declines? Proc.Natl. Acad. Sci. 91:1791-1795.

Blaustein, A.R., B. Edmund, J.M. Kiesecker, J.J. Beatty and D.G. Hokit. 1995. Ambientultraviolet radiation causes mortality in salamander eggs. Ecol. Appl. 5:740-743.

Fernandez, M. And J. L'Haridan. 1992. Influence of lighting conditions on toxicity andgenotoxicity of various PAH in the newt in vivo. Mut. Res. 298:31-41.

Grant, K.P. and L.E. Licht. 1995. Effects of ultraviolet radiation on life-history stages ofanurans from Ontario, Canada. Can. J. Zool. 73:2292-2301.

Herman, J.R., P.K. Bhartia, J. Ziemke, Z. Ahmad and D. Larko. 1996. UV-B increases (1979-1992) from decreases in total ozone. Geophys. Res. Lett. 23:2117-2120.

Kagan, J., P.A. Kagan and H.E. Buhse. 1984. Light-dependent toxicity of alpha-terthienyl andanthracene toward late embryonic stages of Rana pipiens. J. Chem. Ecol. 10:1115-1122.

Kao, K. And M. Danilchik. 1991. Generation of body plan phenotypes in early embryogenesis. Meth. Cell Biol. 36:271-284.

Kerr, J.B. and C.T. McElroy. 1993. Evidence for large upward trends of ultraviolet-B radiationlinked to ozone depletion. Science 262:1032-1034.

Long, L.E., L.S. Saylor and M.E. Soule. 1995. A pH/UV-B synergism in amphibians. Conser.Biol. 9:1301-1303.

Simick, M.F., S.J. Eisenreich, K.A. Golden, S. -P.Liu, E. Lipiatou, D.L. Swackhamer and D.T.Long. 1996. Atmospheric loading of polycyclic aromatic hydrocarbons to Lake Michigan asrecorded in sediments. Environ. Sci. Technol. 30:3039-3046.

Worrest, R.C. and D.J. Kimeldorf. 1975. Photoreactivation of potentially lethal, UV-induceddamage to boreal toad (Bufo boreas boreas) tadpoles. Life Sci. 17:1545-1550.

Worrest, R.C. and D.J. Kimeldorf. 1976. Distortions in amphibian development induced byultraviolet-B enhancement (290-315 nm) of a simulated solar spectrum. Photochem. Photobiol.24:377-382.

U.S. Department of the Interior
U.S. Geological Survey
Patuxent Wildlife Research Center
Laurel, MD, USA 20708-4038
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Last Modified: June 2002