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Other field data in the area show avian concentration of selenium. For example, coots at Stewart Lake and Ouray National Wildlife Refuge (NWR) had liver selenium concentrations of 32 ug/g which, based on results from Kesterson, was sufficient to cause deformities. Indeed, deformed coots led to closure of Ouray NWR for a while. This investigation shows that selenium, zinc, and boron all were elevated in waterfowl and fish compared with mean concentrations elsewhere. Both the zinc and selenium in coot livers was similar to Kesterson (Stephens et al. 1992). Selenium in the 30 ug/g range was also found in mallard livers at Sweitzer Lake (Butler et al. 1991), but no nests were found to evaluate reproductive impairment. Concentrations of selenium in livers of ducks, grebes, and coots in wetlands of the Uncompahgre Project also had elevated (17 to 49 ug/g) selenium (Butler et al. 1994), but once again, direct evidence of reproductive failure or deformities was absent. An element of controversy with respect to avian toxicity is the natural rate of teratogenesis. Ohlend.orf (1997) assumes low (-0.5%) rates compared. with those of O'Toole and. Raisbeck (1998), who quote several references that indicate that the rate of normal teratogenesis in avian species is higher (0.6 to 4.2% in mallards). O'Toole and Raisbeck (1998) question much of the historical mammalian research on selenium. They note that there is little doubt that selenium was a problem at Kesterson and the Kendrick site in Wyoming, but they question the ubiquity of selenium poisoning. For example, O'Toole and Raisbeck state, "we do not consider that either numbers (concentrations of selenium in tissues) or lesions (morphological analysis) alone generate an assured diagnosis of selenosis." They also disagree that craniofacial abnormalities are a unique indicator of selenium poisoning, saying that a variety of chemicals, physical factors, and inherited defects cause the same problems in chickens and turkeys. Selenium is apparently not teratogenic to maminalian species. When toxicosis was induced, heart lesions were observed in mammals but not in birds. O'Toole and Raisbeck also do not believe that selenium causes central nervous system problems in mammals and note that none have been reported in birds. O'Toole and Raisbeck also take note of the prevailing theory of "oxidative stress as the pivotal biochemical lesion in selenosis." Although they cite several references supporting this statement, they believe that "the link between oxidant stress and epithelial lesions remains to be demonstrated." These investigators, however, cite some of their own data that are at least suggestive of the same hypothesis. O'Toole and Raisbeck (1998) believe that whole blood concentrations of selenium >10 ug/ml are suspicious for selenosis and note that "affected birds may have no lesions other than emaciation, a common nonspecific feature of many diseases of free-ranging waterfowl." O'Toole and Raisbeck also agree that egg concentrations of >3 ug/g are a probable indicator of selenois but question what they call a "focused necropsy approach" or just looking for selenium. Other analyses and better microbiology are needed. "What is missing in many field studies is a correlation between tissue concentrations and disease syndromes and/or lesions that match credible descriptions of selenosis in waterfowl." For example, they believe that teratogenesis should have been observed at Stillwater, yet it was not. Moreover, O'Toole and Raisbeck believe that one ought to be able to produce in the lab what is observed in the field-a belief disputed by Skorupa (1998). As with fish, effects of boron on avian species have been evaluated. Stephens and Waddell (1998) note that boron is not a problem for birds unless the diet contains 1000 ug/g. One study shows, however, that the combined toxicity of boron-selenium mixtures to ducklings was