30
2. Interpreting Selenium Concentrations
and field studies show that the most sensitive indicator of selenium
impacts on centrarchid populations is reproductive success (Cumbie
and Van Horn 1978; Lemly 1985a; Gillespie and Baumann 1986; Woock
et al. 1987; Hermanutz et al. 1992; Coyle et al. 1993). This is also true
for fathead minnows (Pyron and Beitinger 1989; Schultz and Hermanutz
1990), and probably for salmonids and percichthyids as well, since the
residue levels at which tissue damage and mortality of fry and juveniles occurs is almost identical to that for centrarchids (Lemly 1985a;
Hamilton et al. 1986, 1989, 1990; Coughlan and Velte 1989). The most
precise way to assess selenium status and potential reproductive impairment of adult fish is to measure selenium levels in gravid ovaries.
This single measure integrates waterborne and dietary exposure and
allows evaluation of the most sensitive biological endpoint. Biologists
and natural resource managers should consider this when designing
aquatic monitoring studies to assess selenium contamination.
Aquatic Bird Tissues
Several publications provide detailed discussions of the interpretation
of tissue concentrations of selenium in waterfowl and other aquatic
birds (eg, Ohlendorf 1989; Skorupa and Ohlendorf 1991; Heinz 1996;
Skorupa et al. 1996). A brief summary of the conclusions of these reports is presented here.
Field and laboratory studies have shown that the most sensitive indicator of selenium toxicity in aquatic birds is reproductive failure.
Embryo mortality and teratogenic effects in hatchlings are markers for
selenium toxicity, and impacts begin to occur when tissue concentrations reach 7 J.1g Se/g in eggs and 10 J.1g Se/g in adult bird livers. However, not all species are affected at these concentrations, and follow-up
studies of reproductive performance are recommended to provide conclusive evidence of adverse effects. The levels of mortality and deformities increase markedly as concentrations rise, and 50% or more of
all birds may be affected when residues reach 10 J.1g Se/g in eggs and
30 J.1g Se/g in adult livers. Logistic response curves show that the pattern of selenium-induced teratogenesis is consistent between locations
for same-species exposures (Skorupa and Ohlendorf 1991), lending support for the premise that uniform environmental quality guidelines
can be applied across a range of habitat types and environmental conditions. Moreover, studies of aquatic birds show that there is agreement among thresholds at which waterborne selenium begins to
become a toxic hazard via food-chain bioaccumulation. For both fish
and wildlife, this threshold falls within the range of 2 to 5 J.1g SelL
(Skorupa 1998). Based on these findings, I recommend that 7 J.1g Se/g
in bird eggs and 10 J.1g Se/g in bird liver tissue be used as the thresholds for toxic effects for selenium impacts on avian reproduction. The
simplest and most accurate way to assess selenium status and potential
2. Interpreting Selenium Concentrations
and field studies show that the most sensitive indicator of selenium
impacts on centrarchid populations is reproductive success (Cumbie
and Van Horn 1978; Lemly 1985a; Gillespie and Baumann 1986; Woock
et al. 1987; Hermanutz et al. 1992; Coyle et al. 1993). This is also true
for fathead minnows (Pyron and Beitinger 1989; Schultz and Hermanutz
1990), and probably for salmonids and percichthyids as well, since the
residue levels at which tissue damage and mortality of fry and juveniles occurs is almost identical to that for centrarchids (Lemly 1985a;
Hamilton et al. 1986, 1989, 1990; Coughlan and Velte 1989). The most
precise way to assess selenium status and potential reproductive impairment of adult fish is to measure selenium levels in gravid ovaries.
This single measure integrates waterborne and dietary exposure and
allows evaluation of the most sensitive biological endpoint. Biologists
and natural resource managers should consider this when designing
aquatic monitoring studies to assess selenium contamination.
Aquatic Bird Tissues
Several publications provide detailed discussions of the interpretation
of tissue concentrations of selenium in waterfowl and other aquatic
birds (eg, Ohlendorf 1989; Skorupa and Ohlendorf 1991; Heinz 1996;
Skorupa et al. 1996). A brief summary of the conclusions of these reports is presented here.
Field and laboratory studies have shown that the most sensitive indicator of selenium toxicity in aquatic birds is reproductive failure.
Embryo mortality and teratogenic effects in hatchlings are markers for
selenium toxicity, and impacts begin to occur when tissue concentrations reach 7 J.1g Se/g in eggs and 10 J.1g Se/g in adult bird livers. However, not all species are affected at these concentrations, and follow-up
studies of reproductive performance are recommended to provide conclusive evidence of adverse effects. The levels of mortality and deformities increase markedly as concentrations rise, and 50% or more of
all birds may be affected when residues reach 10 J.1g Se/g in eggs and
30 J.1g Se/g in adult livers. Logistic response curves show that the pattern of selenium-induced teratogenesis is consistent between locations
for same-species exposures (Skorupa and Ohlendorf 1991), lending support for the premise that uniform environmental quality guidelines
can be applied across a range of habitat types and environmental conditions. Moreover, studies of aquatic birds show that there is agreement among thresholds at which waterborne selenium begins to
become a toxic hazard via food-chain bioaccumulation. For both fish
and wildlife, this threshold falls within the range of 2 to 5 J.1g SelL
(Skorupa 1998). Based on these findings, I recommend that 7 J.1g Se/g
in bird eggs and 10 J.1g Se/g in bird liver tissue be used as the thresholds for toxic effects for selenium impacts on avian reproduction. The
simplest and most accurate way to assess selenium status and potential