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reference water and fed brine shrimp. Survival was near zero when the fish were fed site food that ranged in concentration from 4.5-37 ug/g. Larvae from broodstock that were fed food with 4.6 ug/g of selenium also showed much lower survival (approximately 20-80% survival in three trials}-a survival rate lower than for the larvae hatched from the high-selenium eggs and fed brine shrimp. The data are interesting because they suggest that the concentration in food is the determining factor in survival, not the concentration in the eggs and larvae. Of course, larval fish high in selenium would typically be exposed to high-selenium food sources as well. Nevertheless, the data have implications regarding both the toxicological mechanism and the setting of standards for protection of aquatic species. 3.2 Toxicity to Birds Serious deformities in aquatic birds at Kesterson led to the recognition of elevated selenium in western irrigation projects. As with fish, however, much is unknown regarding uptake and specific transformations within the various species. For example, Hoffinan and Heinz (1988) report that the mode of action of embryotoxicity and teratogenesis of selenium on mallards is uncertain. Evidence of increased lipid peroxidation and related glutathione peroxidase activity were found by Hoffman and Heinz (1988) and in coots from Kesterson by Ohlendorf et al. (1988). Selenium-caused oxidant-induced stress or damage and increased lipid peroxidation has been identified in mammals (Dougherty and Hoekstra 1982), and increases in organic solvent- soluble lipofuchsin pigments of the liver as well as glutathione peroxidase activity were identified in mice (Csallany et al. 1984). Hoffman and Heinz (1988) also demonstrate that selenomethionine was much more toxic than selenite, probably because uptake is much greater. Harmful effects were observed when feed of 10 and 25 ug/g of selenium as selenite or selenomethionine was provided. Similarly, Ohl endorf (1997) states that dietary concentrations of 6 ug/g and higher will affect sensitive species. Most studies do not report a water concentration that is considered harmful. Nolan and Clark (1997), however, state that irrigation drain water containing 3-20 gg/L selenium is hazardous to some aquatic birds under some conditions, but that greater than 20 gg/L is hazardous to most aquatic birds under most conditions. Concentrations greater than 20 gg/L are common in the Grand Valley, but as described in Sect. 1.5, obvious effects have not been identified. There are considerable differences in species' sensitivity to selenium. For example, ducks are more sensitive than stilts, which are more sensitive than avocets the latter being relatively insensitive to selenium (Ohlendorf 1997). Grebes also have less susceptibility than most other waterfowl (Hoffman et al. 1988). According to Ohlendorf (1997), ducks exhibit deformities at a 10% rate when egg concentrations are approximately 20 ug/g, stilts at 35 ug/g, and avocets at 75 ug/g. Concentrations in this range are found in the Grand Valley and in waters associated with the Uncompahgre Proicct. For example, mallard egg selenium concentrations were as high as 17 ug/g, but most were less than 10 ug/g. Five coot eggs, however, exceeded 20 ug/g of selenium (Butler et al. 1994). Another study in the Grand Valley also reports coot eggs with concentrations high enough to indicate risk from selenium (Butler et al. 1996). Only one incident of Kesterson- like deformities has been reported in the area. The low incidence of identified deformities may be the result of low overall reproduction (Osmundson, D.B., U.S. Fish and Wildlife Service, personal communication, June 25, 1999).