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Dietary study <br />Discussion <br />Predicted thresholds for toxic effects in fish from exposure to selenium are 2µg/L in <br /> <br /> <br />1 <br /> <br />ii <br /> <br />water and 3µg/g in diet (Lemly 1993a; NIWQP 1998). In this study, the highest water and <br />dietary concentrations were 27.2 µg/L and 1.40 µg/g, respectively. Adverse effects due to <br />exposure to dissolved and dietary selenium were not observed over the concentration ranges <br />studied in this investigation. The most likely explanation for this outcome is that the magnitude <br />of bioaccumulation in the experimental food chain, and consequently, the level of dietary <br />exposure was not sufficient to produce a response. The general design of our bioaccumulation <br />food chain was based on Dobbs et al. (1996). They observed equilibrium bioconcentration <br />factors (selenium concentration in whole organism divided by water concentration) in algae and <br />rotifer of about 400 to 500. Bioconcentration factors in algae and rotifer in our investigation <br />ranged from 51 to 77. This result suggests that we observed only a fraction of the potential <br />bioaccumulation that can occur and explains why adverse effects were not observed even though <br />dissolved selenium exposure concentrations were above the 2 µg/L threshold. <br />Guidelines that present threshold values for interpretation of biological effects of <br />selenium are intended to be applied to natural systems where selenium may cycle between <br />biological organisms and the physical environment. Cycling of selenium in a complex <br />environment plays a major role in the potential for bioaccumulation (Lemly and Smith 1987). <br />For example, in aquatic habitats associated with the Colorado River near Grand Junction, <br />21 <br />