U. S. DEPARTMENT OF THE INTERIOR

FISH AND WILDLIFE SERVICE

Evaluation of the Toxicity of Selenium

to

White and Green Sturgeon

Prepared by

Dr. William N. Beckon

Sacramento, California 

March 2012
ACKNOWLEDGEMENTS

I would like to gratefully acknowledge the assistance and support of the following people in the 

preparation of this document: Theresa Presser and Sam Luoma both with the U.S. Geological 

Survey, as well as Joe Skorupa with the U.S. Fish and Wildlife Service, provided insightful 

discussions and input over the years on selenium bioaccumulation. Diane Fleck and Eugenia 

McNaughton both with the U.S. Environmental Protection Agency and Thomas Maurer with the 

U. S. Fish and Wildlife Service provided kind and patient support and guidance throughout the 

preparation of this report. Robin Stewart with the U.S. Geological Survey provided clam data. 

Regina Linville, Barbara Osmundson, Javier Linares-Casenave, Serge Doroshov, and Dennis 

Lemly provided invaluable reviews of early drafts of the report. None of the above is 

responsible for the final interpretation and conclusions in this report.

Literature citation should read as follows:

U. S. Fish and Wildlife Service. 2012. Evaluation of the Toxicity of Selenium to White and 

Green Sturgeon. U.S. Fish and Wildlife Service, Sacramento Fish and Wildlife Office, 

Environmental Contaminants Division. Sacramento, California. March 2012. 48 pp.
Evaluation of the Toxicity of Selenium to White and Green Sturgeon

Table of Contents

Abstract 1

Summary Table of Sturgeon Selenium Benchmarks 2

Introduction 3

White Sturgeon Exposure by Microinjection 5

White Sturgeon Exposure by Maternal Exposure 11

Green Sturgeon Exposure by Microinjection 13

Green Sturgeon Exposure by Maternal Exposure 15

Discussion 18

References 23

Appendix I 27

Appendix II 41
BLANK PAGE
1

U. S. DEPARTMENT OF THE INTERIOR

FISH AND WILDLIFE SERVICE

Sacramento Fish and Wildlife Office

2800 Cottage Way, Rm W-2605

Sacramento, California 95825

Evaluation of the Toxicity of Selenium to White and Green Sturgeon

Prepared by

Dr. WILLIAM N. BECKON

Environmental Contaminants Division

william_beckon@fws.gov

March 2012

Abstract

Fish of the genus Acipenser (sturgeon) are likely to be among the most vulnerable to selenium 

exposure in the San Francisco Estuary because these fish feed predominantly on benthic 

invertebrates, including the Asian clam, Corbula amurensis. This clam is an efficient 

bioaccumulator of selenium. The best data available for the most sensitive endpoint for sturgeon 

come from studies in which the survival of larvae was monitored following micro-injection of 

organic selenium (L-selenomethionine) into the yolk sacs of newly hatched larvae. Benchmark 

larval selenium concentrations from these studies were translated, by means of regressions, to 

selenium concentrations in the tissue and diet of adult white and green sturgeon. This analysis

indicates that white and green sturgeon are among the most sensitive of fish to adverse effects of 

selenium, with the listed green sturgeon being the more sensitive of these two species. These 

levels of sensitivity evidently put sturgeon at substantial risk at current levels of exposure in the 

San Francisco Bay area. Selenium concentrations in food items of sturgeon in the San Francisco 

Bay area are almost always high enough that they may cause at least 10 percent mortality in 

hatchling green sturgeon (≥3.58 μg/g), and they are frequently high enough that they may cause 

at least 10 percent mortality among hatchling white sturgeon (≥10.8 μg/g) as well. Below is a 

summary of benchmark concentrations of selenium derived here for the diets, whole body, 

muscle, and eggs of these two sturgeon species. 
2

Summary Table of Selenium Benchmarks

Concentration of selenium (μg/g dry wt.) 

corresponding to effect level (proportion affected)

Effect 

Level 5% 10% 5% 10% 5% 10% 5% 10%

Species

Se in diet 

of sturgeon

Se in 

sturgeon 

(whole 

body)

Se in 

sturgeon 

muscle

Se in 

sturgeon 

eggs Effect Form of selenium Exposure Data source

White 

sturgeon 5.45 10.8 2.55 3.86 3.55 5.56 4.67 6.83 larval 

mortality L-selenomethionine microinjection of larvae Linville 2006

39.3 48.4 8.51 9.65 13.1 15.0 14.0 15.8 larval 

abnormalities selenized yeast maternal diet Linville 2006

Green 

sturgeon 2.51 3.58 1.59 1.97 2.13 2.69 3.03 3.70 larval 

mortality L-selenomethionine microinjection of larvae

Linares-Casenave et al. 

2010

8.22 10.1 3.27 3.71 4.65 5.33 5.87 6.59 larval 

abnormalities selenized yeast maternal diet* Linares-Casenave et al. 2010, Linville 2006

*Green sturgeon maternal diet effect levels were calculated from white surgeon maternal dietary exposure larval developmental 

defects (Linville 2006) adjusted for relative species sensitivity using the ratio of EC10s for peak larval abnormalities from the white 

and green sturgeon microinjection experiments of Linares-Casenave et al. (2010).

Benchmark values listed in this table are shown in boldface type in the following text and graphs where the derivations are explained 

and illustrated.
3

Introduction

The San Francisco Bay, San Pablo Bay, and Suisun Bay are listed as impaired by selenium under 

303(d) of the Clean Water Act. Of the wildlife that live in, pass through, or are dependent on, 

these bays, benthic (bottom-dwelling) fish of the genus Acipenser (sturgeon) are likely to be 

among the most vulnerable to selenium. This is because these large, long-lived fish feed 

predominantly on benthic invertebrates (McKechnie and Fenner 1971; Radtke 1966; Ritz 2010), 

and since 1986 the San Francisco Bay benthic community has experienced a massive invasion of 

an Asian clam, Corbula amurensis, (Carlton et al. 1990; Nichols et al. 1990) that is a particularly 

efficient bioaccumulator of selenium (Linville et al. 2002). 

Two species of sturgeon are found in the San Francisco Bay estuary: white sturgeon (Acipenser 

transmontanus) and green sturgeon (Acipenser medirostris). White sturgeon in the San Francisco 

Bay estuary congregate in Suisun and San Pablo Bays where they remain year-round except for a 

small fraction of the population that moves up the Sacramento River, and to a lesser extent the 

San Joaquin River, to spawn in late winter and early spring (Kohlhorst et al. 1991). Thus, many 

individuals of this species remain year-round in a region of the San Francisco Bay estuary where 

they are exposed to dietary items (Corbula amurensis) that exceed selenium concentrations of 10 

μg/g (dry weight) much of the time (Linville et al. 2002, Kleckner et al. 2010). Linares et al. 

(2004) found concentrations of selenium as high as 46.7 μg/g in gonads of 39 white sturgeon 

captured in the San Francisco Bay. Kroll and Doroshov (1991) reported that developing ovaries 

of white sturgeon from San Francisco Bay contained as much as 71.8 μg/g selenium (dry 

weight); several times the concentration in fish eggs (20 μg/g dry weight) that Lemly (1996) 

suggested would cause a high level of hazard from reproductive impairment. 

Green sturgeon are more marine-oriented than white sturgeon, but also congregate in coastal 

bays and estuaries (Adams et al. 2007). Furthermore, green sturgeon in this area are federally 

listed as threatened under the Endangered Species Act. 

Therefore, in view of their status as well as their particular vulnerability to selenium, sturgeons 

must be pivotal species in establishing regulatory guidelines that would be broadly protective of 

wildlife in the San Francisco Bay area. The purpose of this report is to provide an analysis of 

recent sturgeon data that may be relevant to developing such guidelines. 

This analysis focuses on the “most sensitive endpoint”, the ecologically relevant adverse effect 

that occurs at the lowest concentrations of selenium, relative to the concentrations at which other 

effects or “endpoints” start to occur. This focus is consistent with the approach used by the 

USEPA Region 9 Biological Technical Assistance Group for establishing toxicity reference 

values (CDTSC HERD 2002). It also conforms with prudence and reason; the most sensitive 

endpoint should trump other effects levels in developing protective guidelines. 

Key studies by Linville (2006), Linares-Casenave et al. (2010), Silvestre et al. (2010), and 

Tashjian et al. (2006) provide white and green sturgeon larval and egg toxicity data. Linville 

(2006) also provides dietary, female muscle and maternal transfer data for white sturgeon while 

Tashjian et al. (2006) provides whole body and muscle data for white sturgeon. However, data 

on green sturgeon dietary, muscle and whole body is not currently available. To the best of our 
4

knowledge, the best data available for the most sensitive endpoint for sturgeon come from 

studies in which the survival of larvae was monitored following micro-injection of organic 

selenium (L-selenomethionine) into the yolk sacs of newly hatched larvae (Linville 2006,

Linares-Casenave et al. 2010, Silvestre et al. 2010). Benchmark larval selenium concentrations 

from these studies can be translated, by means of regressions, to selenium concentrations in the 

tissue and diet of adult sturgeon that deposit eggs from which the larvae with those 

concentrations would hatch. For rarer species, such as green sturgeon, for which there are 

insufficient data to derive species-specific regressions, regressions from a surrogate species of 

the same genus (i.e. white sturgeon) can be used (USEPA 1995). Use of such surrogates and 

regressions is a protective approach based on best available information. It is an approach that 

EPA employs extensively in setting water quality standards (e.g. USEPA 2004). 

The following flow diagram is provided to show the relationship of the larval effect levels and 

their translations to selenium in sturgeon diet and tissue. 

Flow Diagram of Translation Procedures. White and green sturgeon 5% and 10% larval 

effect values are determined from microinjection and maternal transfer studies. These are then 

translated to selenium concentrations in egg, muscle, whole body, and diet using regressions 

presented in each of the figures noted.

Diet

Whole 

body

Eggs

Muscle

Larvae

Trophic transfer

Maternal transfer

Effects: larval survival 

and deformities

Hatch

Fig. 3

Figs. 1,2,7,8,9,11

Figs. 6,10

Fig. 4

Fig. 5

Key

Direction of selenium

transfer/partitioning 

Direction of 

benchmark translation 
5

White Sturgeon (Acipenser transmontanus)

At the University of California, Davis, Linville (2006) studied several effects of selenium on 

white sturgeon, including the toxicity of selenium to larvae after hatching and before the larvae 

begin to actively feed. During this period of about two weeks, the larval fish obtain nutrition 

(and toxicants) from a yolk sac. Linville (2006) exposed these larvae to elevated selenium in 

two ways: (1) by microinjection of L-selenomethionine into the yolk sacs just after hatch and (2) 

by exposing mother fish to dietary selenium (selenized yeast) for up to six months before they 

deposited the eggs, thereby transferring selenium from the mother to the larvae mainly via the 

yolk sac (“maternal transfer”). We first provide a larval toxicity regression to determine 5% and 

10% effect levels for white sturgeon based on the Linville (2006) microinjection study. These 

effect levels are then translated to egg, muscle, whole body, and diet using other Linville (2006) 

data and Tashjian et al. (2006). Then we use results from the Linville (2006) maternal transfer 

study to determine 5% and 10% effect levels via maternal transfer and then perform similar 

translation of those effect levels to egg, muscle, whole body and diet.

White Sturgeon Exposure by Microinjection

Linville’s (2006) analysis focused mainly on developmental defects in the larvae, but the data 

she provided show that larval mortality in the microinjection treatments was the most sensitive 

endpoint of those she investigated (at the 5% and 10% effect levels, mortality occurs at lower 

selenium concentrations than defects; compare Figures 1 and 2). 

Figure 1. Mortality of white sturgeon larvae microinjected with L-selenomethionine in the yolk sac just after 

hatching (developmental stage 36). Selenium was measured in a subsample of larvae one day after injection. 

Mortality is the proportion that died by the time of yolk depletion, when the fish is ready to start eating (stage 

45). The data are from Table 3-15 in Linville (2006). Dashed lines indicate 95% confidence boundaries. 

LC05 and LC10 are the concentrations of selenium at which 5 and 10 percent (respectively) mortality is 

expected.

0%

50%

100%

1 10 100

Larval mortality

Selenium in larvae (μg/g dry wt.)

LC10 = 6.77 μg/g

White Sturgeon

regression:

y=1/(1+(20.0/x)2.02)

LC05 = 4.68 μg/g
6

Figure 2. Incidence of larval edema and/or skeletal deformities among white sturgeon larvae microinjected 

with L-selenomethionine in the yolk sac just after hatching. Data are from Tables 3-11 and 3-13 in Linville 

(2006). EC05 and EC10 are the concentrations of selenium at which 5 and 10 percent (respectively) rates of 

adverse effects are expected.

This agrees with the relative sensitivities of bird eggs to selenium, because bird egg hatchability 

is a more sensitive endpoint than teratogenesis (embryonic deformities) (Ohlendorf 2003), and 

bird egg hatchability is the avian equivalent of larval mortality (death by the time the yolk is 

fully depleted and feeding begins) in fish. 

White Sturgeon Larval Benchmarks – Microinjection

A standard log-logistic model (Beckon et al. 2008; Ritz 2010) of the larval mortality data yield 

LC05 and LC10 (the concentrations of selenium in larvae corresponding to 5% and 10% 

mortality) of 4.68 μg/g and 6.77 μg/g, respectively (Figure 1). As far as we know, field data on 

larval concentrations of selenium are not available; therefore, these larval benchmark 

concentrations are shown here only for the purpose of anchoring the following calculations of 

more useful benchmarks in eggs, muscle, whole body, and diet.

0%

50%

100%

1 10 100

Larval developmental defects

Selenium in larvae (μg/g dry wt.)

EC10 = 8.65 μg/g

White Sturgeon

regression:

y=1/(1+(13.5/x)4.92)

EC05 = 7.43 μg/g
7

White Sturgeon Egg Benchmarks – Microinjection

In another experiment, Linville (2006) fed gravid female white sturgeon selenized yeast for up to 

six months before they deposited their eggs, and she measured selenium in the eggs and in the 

larvae that hatched from those eggs. Therefore, the larval benchmark selenium concentrations 

from Figure 1 (from microinjection experiments) can be translated into corresponding egg 

concentrations (Figure 3). This translation indicates that selenium concentrations of 4.67 μg/g 

and 6.83 μg/g in white sturgeon eggs correspond to 5% and 10% mortality rates (respectively) in 

the larvae that hatch from those eggs.

Figure 3. Relationship between selenium in white sturgeon eggs and in the larvae (stage 36) that hatch from 

the eggs. The data are from Tables 3-18 in Linville (2006).

1

10

1 10

Selenium in eggs (

μg/g dry wt.)

Selenium in larvae (μg/g dry wt.)

White Sturgeon

regression:

log10y=-0.019+1.028*log10x

R-squared: 0.997

LC10 = 6.77 μg/g

LC05 = 4.68 μg/g

6.83 μg/g

4.67 μg/g
8

White Sturgeon Muscle Benchmarks – Microinjection

The benchmark larval selenium concentrations from Figure 1 translate into maternal muscle 

selenium concentrations of 3.55 μg/g (5% mortality) and 5.56 μg/g (10% mortality) using a 

conversion equation based on data from Linville’s (2006) work (Figure 4). Evidently, white 

sturgeon in the San Francisco estuary commonly exceed these benchmarks. In 46 white sturgeon 

(ages 4-18 years) caught in the San Francisco estuary from 2002 to 2004 (Linares et al. 2004), 

mean selenium concentration in muscle was 6.59 μg/g dry wt., above the 10% mortality 

benchmark. Among these sturgeon, selenium concentrations increased with age; therefore, it is 

likely that individuals older than 18 years (the age at which reproduction was beginning to occur 

in these wildcaught sturgeon) have even higher concentrations of selenium. This suggests that 

among white sturgeon in the San Fransico estuary, there may be more than 10% risk of mortality 

due to selenium.

Figure 4. Conversion from larval (stage 36) selenium to selenium in muscle tissue of the mother before 

depositing eggs. The data are from Table 3-18 in Linville (2006)

1

10

1 10

Selenium in maternal muscle (

μg/g dry wt.)

Selenium in larvae (μg/g dry wt.)

White sturgeon

regression:

log10y=-0.2644+1.2157*log10x

R-squared: 0.940

LC10 = 6.77 μg/g

LC05 = 4.68 μg/g

5.56 μg/g

3.55 μg/g
9

White Sturgeon Whole Body Benchmarks – Microinjection

These muscle concentrations (above) translate into maternal whole body selenium concentrations 

of 2.55 μg/g (LC05) and 3.86 μg/g (LC10) using a conversion equation based on data from a 

Tashjian et al. (2006) study (Figure 5). See the Discussion section for more details on this 

conversion step.

Figure 5. Relationship between muscle and whole-body concentrations of selenium in young white sturgeon 

(initially weighing about 30 g) exposed for 56 days to dietary selenium in the form of L-selenomethionine. 

Data are from Tables 2 and 3 in Tashjian et al. (2006).

1

10

100

1 10 100

Selenium in whole body (

μg/g dry wt.) 

Selenium in muscle (μg/g dry wt.)

White Sturgeon

regression:

y=exp(-0.238+0.926*ln(x))

R-squared: 0.981

EC10 = 5.56 μg/g

EC05 = 3.55 μg/g

3.86 μg/g

2.55 μg/g
10

White Sturgeon Dietary Benchmarks – Microinjection

The larval benchmark selenium concentrations from the microinjection experiment shown in 

Figure 1 can be translated directly into maternal dietary selenium concentrations by using data 

from the study by Linville (2006). In this study, she fed gravid female white sturgeon selenized 

yeast for up to six months before they deposited their eggs. She then measured selenium in the 

larvae that hatched from those eggs. These data indicate that selenium concentrations of 5.45 

μg/g and 10.8 μg/g in the food of adult female sturgeon correspond to 5% and 10% mortality 

rates (respectively) in the larvae they produce (Figure 6). See the Discussion section for more 

information on this translation. Diet items (i.e. Corbula amurensis) in the San Francisco Bay 

estuary exceed selenium concentrations of 10.8 μg/g (dry weight) much of the time (Linville et 

al. 2002, Kleckner et al. 2010) indicating that these selenium benchmarks are environmentally 

relevant in this system. 

 

1

10

100

1 10 100

Selenium in larvae (stage 36, μg/g 

dry wt.) 

Selenium in maternal diet (μg/g dry wt.)

fitted model:

log10y=0.271+0.542*log10x

LC10 = 6.77 μg/g

10.8 μg/g

LC05 = 4.68 μg/g

5.45 μg/g

White sturgeon

Figure 6. Relationship between selenium in the diet (selenized yeast) of gravid female white sturgeon 

and selenium in the larvae (stage 36) that hatch from the eggs that these females produced. Data for the 

fitted model are from Tables 3-1 and 3-5 in Linville (2006). Whiskers indicate standard error bars. 

Larval effect levels (LC05 and LC10) are from Figure 1.
11

White Sturgeon Exposure by Maternal Transfer

In the experiments of Linville (2006), adverse effects of selenium on larval white sturgeon 

occurred at lower concentrations in microinjection treatments than in experiments in which 

larvae were exposed to elevated selenium solely by “maternal transfer” (selenium deposited in 

the yolk of developing eggs by mother fish that had been exposed to dietary selenium) (compare 

Figures 2 and 7). However, although the most sensitive known endpoint is the “controlling” 

endpoint for protection of the species, here we include analysis of the maternal transfer 

experiment, because this appears to be a more natural mode of exposure (but see Discussion). 

In Linville’s (2006) maternal transfer experiment, the most sensitive endpoint for larvae was 

developmental abnormality rather than mortality (compare Figures 7 and 8). Developmental 

abnormalities are an equally valid determination of adverse effect or “take” in endangered 

species management decisions; therefore, in this experiment we focus on these developmental 

defects. 

 

White Sturgeon Larval Benchmarks – Maternal Transfer

The EC05 and EC10 (the concentrations of selenium in larvae corresponding to 5% and 10% 

abnormalities, that is, edema and/or spinal curvature) are 13.7 μg/g and 15.3 μg/g, respectively 

(Figure 7). 

0%

50%

100%

1 10 100

Developmental defects

Selenium in larvae (μg/g dry wt.)

EC10 = 15.3 μg/g

White Sturgeon

regression:

y=1/(1+(21.2/x)6.67)

EC05 = 13.7 μg/g

Figure 7. Incidence of larval edema and/or skeletal deformities among larvae from eggs of female white 

sturgeon exposed to dietary selenium in the form of selenized yeast. The data are from Table 3-18 in 

Linville (2006).
12

White Sturgeon Egg Benchmarks – Maternal Transfer

These larval selenium concentrations translate into egg concentrations of 14.0 μg/g (EC05) and 

15.8 μg/g (EC10), using the equation of Figure 3.

White Sturgeon Muscle Benchmarks – Maternal Transfer

The above larval concentrations translate into maternal muscle concentrations of 13.1 μg/g 

(EC05) and 15.0 μg/g (EC10), using the conversion equation of Figure 4. Of the 46 white 

sturgeon (ages 4-18 years) caught in the San Francisco estuary from 2002 to 2004 (Linares et al.

2004) some individuals approached, but none exceeded the EC05 benchmark (maximum 

selenium concentration in muscle: 12.4 μg/g), but see the discussion under White Sturgeon

Muscle Benchmarks – Microinjection above. 

White Sturgeon Whole Body Benchmarks – Maternal Transfer

These muscle concentrations translate into whole body selenium benchmark concentrations of 

8.51 μg/g (EC05) and 9.65 μg/g (EC10), using the equation of Figure 5.

White Sturgeon Dietary Benchmarks – Maternal Transfer

The larval benchmarks (above) translate into maternal diet selenium concentrations of 39.3 μg/g 

(EC05) and 48.4 μg/g (EC10) using the equation of Figure 6. These benchmarks are above the 

maximum concentrations of selenium in diet items (Corbula amurensis) collected in San 

Francisco estuary from 1995 to 2010 (22 μg/g), but see White Sturgeon Dietary Benchmarks –

Microinjection above.

0%

50%

100%

1 10 100

Larval mortality (stage 45)

Selenium in egg (μg/g dry wt.)

LC10 = 22.8 μg/g

White sturgeon

regression:

y=1/(1+(79.0/x)1.77)

LC05 = 15.0 μg/g

Figure 8. Mortality among larvae (Stage 45) from eggs of female white sturgeon exposed to dietary 

selenium as selenized yeast. The data are from Table 3-14 in Linville (2006).
13

Green Sturgeon (Acipenser medirostris)

Since 2006, green sturgeon in the San Francisco Bay-Delta area have been federally listed under 

the Endangered Species Act as threatened (71 FR 17757). Therefore, any regulatory benchmark 

established by a federal agency, such as the U. S. Environmental Protection Agency, must be 

reviewed by the National Oceanic and Atmospheric Administration (NOAA) to determine 

whether that benchmark is protective of the species.

Recently, groups of researchers at the University of California, Davis, have investigated the 

effects of selenium and methylmercury on both green and white sturgeon in various conditions of 

salinity and temperature (Kaufman et al. 2008; Linares-Casenave et al. 2010; Silvestre et al. 

2010; Walker 2009). Dietary exposure experiments showed that green sturgeon are “much more 

sensitive to selenium” than white sturgeon at environmentally relevant concentrations of 

selenium (Kaufman et al. 2008), but data from these experiments are not yet publicly available. 

However, data from selenium micro-injection experiments are available: in tabular form in the 

poster of Linares-Casenave et al. (2010) and in graphical form in the published paper of Silvestre 

et al. (2010). The data from these microinjection experiments confirm that the yolk sac larvae of 

green sturgeon are more sensitive to selenium than those of white sturgeon (compare Figures 1 

and 9).

0%

50%

100%

1 10 100

Larval mortality

Selenium in larvae (μg/g dry wt.)

LC10 = 3.73 μg/g

Green Sturgeon

regression:

y=1/(1+(6.57/x)3.88)

LC05 = 3.07 μg/g

Figure 9. Mortality of green sturgeon larvae microinjected with L-selenomethionine in the yolk sac 

just after hatching (developmental stage 36). Selenium was measured one day after injection. 

Mortality is the proportion that died by the time of yolk depletion, when the fish is ready to start

eating (stage 45). The data are from Tables 1 and 2 in Linares-Casenave et al. (2010), also shown in 

Table 1 and Figure 1 in Silvestre et al. (2010).
14

We first provide a larval toxicity regression to determine 5% and 10% effect levels for green 

sturgeon based on the Linares-Casenave et al. (2010) microinjection study. These effect levels 

are then translated to egg, muscle, whole body, and diet using the white sturgeon data from 

Linville (2006) and Tashjian et al. (2006) as a surogate. Then we use results from the LinaresCasenave et al. (2010) green and white sturgeon microinjection study to determine a sensitivity 

ratio and apply it to the Linville (2006) maternal transfer study to calculate green sturgeon 5% 

and 10% effect levels via maternal transfer. As for the white sturgeon we then perform similar 

translation of those effect levels to egg, muscle, whole body and diet for the green sturgeon.

Green Sturgeon Larval Benchmarks – Microinjection

A standard log-logistic model of the green sturgeon microinjection data yield larval LC05 and 

LC10 (the concentrations of selenium in larvae corresponding to 5% and 10% mortality) of 3.07 

μg/g and 3.73 μg/g, respectively (Figure 9). 

Green Sturgeon Egg Benchmarks – Microinjection

To the best of our knowledge, as yet there are no data relating selenium in eggs and larvae for 

green sturgeon. Therefore, we use the equation for white sturgeon (Figure 3) to translate larval 

benchmark selenium concentrations to corresponding selenium concentrations in the eggs from 

which the larvae hatch. Accordingly, selenium concentrations of 3.03 μg/g and 3.70 μg/g in 

green sturgeon eggs correspond to 5% and 10% mortality rates (respectively) in the larvae that 

hatch from those eggs.

Green Sturgeon Muscle Benchmarks – Microinjection

To the best of our knowledge, no data specific to green sturgeon are yet available to translate 

these larval selenium concentrations into concentrations in the muscle of the mother that 

produced the larvae. Therefore, we use the white sturgeon data referenced above (Figure 4) for 

the best available approximations of these translations in green sturgeon. Accordingly, the 5% 

and 10% larval benchmarks translate into maternal muscle selenium concentrations of 

approximately 2.13 μg/g and 2.69 μg/g, respectively.

Green Sturgeon Whole Body Benchmarks – Microinjection

To the best of our knowledge, no data specific to green sturgeon are yet available to translate the 

above muscle selenium concentrations into concentrations in the whole body of the mother that 

produced the larvae. Therefore, we use the white sturgeon data referenced above (Figure 5) for 

the best available approximations of these translations in green sturgeon. Accordingly, the 

muscle benchmarks translate into maternal whole body (dry weight) selenium concentrations of 

about 1.59 μg/g (LC05) and 1.97 μg/g (LC10).
15

Green Sturgeon Dietary Benchmarks – Microinjection

To the best of our knowledge, no trophic transfer data specific to green sturgeon are yet available 

to translate larval selenium concentrations or maternal tissue concentrations into concentrations 

in the diet of the mother that produced the eggs from which the larvae hatched. Therefore, we 

use the white sturgeon data referenced above (Figure 6) for the best available approximation of 

the appropriate translation. Accordingly, the green sturgeon larval benchmark selenium 

concentrations from Figure 9 translate into selenium concentrations of approximately 2.51 μg/g 

(EC05) and 3.58 μg/g (EC10) in the food of adult female green sturgeon (Figure 10). Almost all 

of the diet items (Corbula amurensis) collected in the San Francisco Bay estuary from 1995 to 

2010 exceeded these benchmark concentrations (Kleckner et al. 2010). 

Green Sturgeon Exposure by Maternal Transfer – calculated from relative sensitivity

As far as we know, for green sturgeon there has been no maternal transfer selenium toxicity 

experiment comparable to Linville’s (2006) experiment with white sturgeon (Figures 7 and 8). 

However, if we assume that the relative sensitivity of green and white sturgeon would be the 

same for naturally transferred selenium as for micro-injected selenium, then we can calculate a 

larval selenium sensitivity ratio for green and white sturgeon, and use this ratio to estimate, for 

green sturgeon, selenium benchmarks that correspond to those for maternally transferred 

selenium in white sturgeon. Such a ratio can be obtained from the micro-injection experiments 

1

10

100

1 10 100

Selenium in larvae (stage 36, μg/g 

dry wt.) 

Selenium in maternal diet (μg/g dry wt.)

fitted model:

log10y=0.271+0.542*log10x

LC10 = 3.73 μg/g

3.58 μg/g

LC05 = 3.07 μg/g

2.51 μg/g

Figure 10. Translation of selenium effect levels for larval green sturgeon (from Figure 9) into 

corresponding selenium concentrations in maternal diet using trophic and maternal transfer data for 

white sturgeon are from Linville (2006) (see Figure 6).
16

of Linares-Casenave et al. (2010) on both green and white sturgeon (Figure 11). The ratio of 

EC10’s (the sensitivy ratio, white to green) is 10.49/4.49 = 2.34. 

0%

50%

100%

1 10 100

Peak abnormalities

Selenium in larvae (μg/g dry wt.)

LC10 = 10.49 μg/g

White Sturgeon

regression:

y=1/(1+(62.06/x)1.24)

LC05 = 5.73 μg/g

0%

50%

100%

1 10 100

Peak abnormalities

Selenium in larvae (μg/g dry wt.)

LC10 = 4.49 μg/g

Green Sturgeon

regression:

y=1/(1+(8.53/x)3.42)

LC05 = 3.61 μg/g

Figure 11. Incidence of larval abnormalities among larvae from eggs of (A) white sturgeon and (B) 

green sturgeon microinjected with L-selenomethionine in the yolk sac just after hatching. Data are 

from Tables 1 and 2 in Linares-Casenave et al. (2010).

A

B
17

In Figure 11, the effect or “endpoint” used is the peak incidence of abnormalities rather than the

incidence of abnormalities at the end of the experiment. This is because transient abnormalities 

effectively immobilize developing larvae (Serge Doroshov pers.com.). This may cause adverse 

effects during larval development that are not represented by the incidence of abnormalities at 

the end of larval development. In the wild, transient abnormalities resulting in immobilization 

are likely to result in mortality due to predation or the inability to escape from poor habitat 

conditions. Even the peak incidence of abnormalities may not fully represent the full 

consequences of transient abnormalities, because some individual larvae may be affected by 

transient abnormalities only at some time other than the time of peak abnormalities in the group 

of larvae. Any adverse effects on those larvae are not counted in the analysis presented here. 

Full accounting of these adverse effects would require tagging and tracking the condition of each 

individual larva.

Green Sturgeon Larval Benchmarks – Maternal Transfer

The above sensitivity ratio applied to the white sturgeon maternal transfer benchmark selenium 

concentrations in larvae (Figure 7) yield the following corresponding green sturgeon benchmark 

larval selenium concentrations: larval EC05 = 5.84 μg/g (= 13.7 μg/g /2.34) and EC10= 6.54 

μg/g (=15.3 μg/g /2.34). 

Green Sturgeon Egg Benchmarks – Maternal Transfer

Corresponding benchmark selenium concentrations for green sturgeon eggs are calculated from 

the larval concentrations as they were for the injection experiment above using Figure 3. The 

resulting egg benchmarks are EC05 = 5.87 μg/g and the EC10 = 6.59 μg/g. 

Green Sturgeon Muscle Benchmarks – Maternal Transfer

Corresponding benchmark selenium concentrations for green sturgeon muscle are calculated 

from the larval concentrations as they were for the injection experiment above using Figure 4. 

These translations yield maternal muscle benchmarks of EC05 = 4.65 μg/g and EC10 = 5.33

μg/g.

Green Sturgeon Whole Body Benchmarks – Maternal Transfer

Corresponding benchmark selenium concentrations for green sturgeon whole body are calculated 

from the larval concentrations as they were for the injection experiment above using Figure 5. 

These translations yield maternal whole body benchmarks of EC05 = 3.27 μg/g and EC10 = 3.71

μg/g.

Green Sturgeon Dietary Benchmarks – Maternal Transfer

Corresponding benchmark selenium concentrations for the diet of green sturgeon are calculated 

from the larval concentrations as they were for the injection experiment above using Figure 10. 

This translation produces green sturgeon maternal diet benchmarks of EC05 = 8.22 μg/g and 

EC10= 10.1 μg/g.
18

Discussion

The whole-body LC10 selenium concentration derived here for white sturgeon (3.86 μg/g) is 

similar to the toxicity threshold of 4 μg/g suggested by Lemly (1996) and used by the U. S. Fish 

and Wildlife service for warmwater fish (Beckon et al. 2010). Green sturgeon are more 

susceptible to selenium toxicity; they appear to be about as sensitive to selenium as the more 

sensitive coldwater fish (Salmonids). The whole-body LC10 derived here for green sturgeon 

(1.97 μg/g) is close to the LC10 of 1.84 μg/g for juvenile Chinook salmon, and the EC10 of 2.19 

μg/g for juvenile rainbow trout (Beckon et al. 2010). The dietary LC05 and LC10 derived here 

for green sturgeon (2.51 μg/g and 3.58 μg/g respectively) bracket the concern threshold of 3 μg/g 

used by the U. S. Fish and Wildlife service (Beckon et al. 2010).

Because adult sturgeon are very large, it is difficult to analyze their tissue for selenium on a 

whole-body basis (requiring homogenization of the entire body). Therefore, as far as we know, 

data are not available for muscle/whole-body selenium regressions in adults of these species. 

The best available data for such a regression (Figure 5) came from only juvenile white sturgeon 

data (Tashjian et al. 2006). However, this regression is in good agreement with a generic 

muscle/whole-body relationship based on a much larger data set comprising several different fish 

families (Figure 12). Furthermore, the relationship is fairly robust regardless of the gender or 

reproductive condition of the fish (Figure 13) despite the suggestion (Osmundson & Skorupa 

2011) that selenium is differently partitioned among tissues depending on reproductive status. 

Therefore, it is likely that the juvenile muscle/whole-body relationship adequately represents the 

muscle/whole-body relationship of adult white and green sturgeon, and that the modest 

extrapolation of this relationship in this analysis (Figure 5) is reasonable.

Because of the meager data available to translate from larval selenium concentrations to maternal 

dietary concentrations of selenium (Figures 6 and 10), the choice of model is critical for 

interpolating between the data points. This translation incorporates two stages: trophic transfer 

(from maternal diet to maternal tissue) and maternal transfer (from maternal tissue to larval 

tissue). The exponential model (straight line on a log-log graph) used here for the combined 

transfer is valid if both transfer stages are adequately represented by exponential models. As far 

as we know, no one has questioned the applicability of such a model to maternal transfer, but it 

has been suggested that organisms actively, homeostatically regulate their internal concentrations 

of selenium (Brix et al. 2005). Such homeostatic regulation would result in trophic transfer 

functions that are better represented by “hockey stick” models, which include a plateau region in 

which internal tissue concentrations are purportedly held constant as exposure increases. If such 

regulation occurs, it would invalidate the straight-line exponential model, enabling mother 

sturgeon to consume more selenium without elevating their internal selenium concentrations or 

those of their eggs and larvae. However, a broad survey of field and laboratory bioaccumulation 

and trophic transfer data offers no support for such homeostatic regulation (for other 

bioaccumulative metals as well as for selenium). Rather the data strongly support continuous, 

non-homeostatic regulation, with trophic transfer functions that are well described by 

exponential models (Beckon 2010, Appendix II). Therefore, it is likely that the fitted straight 

line in Figures 6 and 10 (describing an exponential model) is suitable for translations of 

concentrations of selenium between maternal diet and larvae. Because only two data points are 

available in the published literature for this relationship (Linville 2006), regression is not 
19

possible; instead, the model was fitted manually so as to pass through those two points. The 

resulting model should be reasonably stable because each of the data points represents the 

average of three replicates (different cohorts from three different females) of 60 to 90 individual 

larvae per replicate. 

1

10

100

1 10 100

Selenium in whole body (

μg/g dry wt.) 

Selenium in muscle (μg/g dry wt.)

white sucker (Osmundson)

green sunfish (Osmundson)

other sp (Osmundson)

regression (all Osmundson)

white sturgeon (Tashjian 2006)

white sturgeon regression

y=exp(0.1004+0.833*ln(x))

R-squared: 0.91

n=189

y=exp(-0.238+0.926*ln(x))

R-squared: 0.98

n=6

Figure 12. Relationship between muscle and whole-body concentrations of selenium in young white 

sturgeon (Tashjian et al. 2006) compared with the relationship between muscle plug and whole-body 

concentrations of selenium in representatives of several families of fish caught in the Gunnison and 

Colorado Rivers and associated tributaries (data from Osmundson et al. 2007, Osmundson & 

Skorupa 2011).
20

For comparisons of the sensitivities of different species and endpoints to selenium, here we use 

EC10s rather than the more traditional EC50s. This is because EC10 is an effect level that is 

closer to levels that may be protective of species. When concentration-response curves have 

substantially different slopes (as in Figures 1 and 2, and Figure 11), then sensitivity comparisons 

based on EC50s would poorly represent relative sensitivities at effect levels of EC10 or below.

It should be noted that the green sturgeon experiment analyzed here (Linares-Casenave et al.

2010, Silvestre et al. 2010) was performed on the projeny of a single individual (Obtaining 

multiple individuals for experimentation was not practical because the species is listed as 

threatened in this area). Therefore, this analysis may underestimate or overestimate the 

sensitiviy of the population of green sturgeon from which this individual came. However, these 

are the best data available for green sturgeon at this time.

1

10

100

1 10 100

Selenium in whole body (

μg/g dry wt.) 

Selenium in muscle (μg/g dry wt.)

white sucker females w/ mature eggs

white sucker females w/ immature eggs, small ovaries

white sucker males

white sturgeon juveniles (Tashjian 2006)

white sturgeon regression

y=exp(-0.238+0.926*ln(x))

R-squared: 0.98

n=6

Figure 13. Relationship between muscle and whole-body concentrations of selenium in young white 

sturgeon (Tashjian et al. 2006) compared with the relationship between muscle plug and whole-body 

concentrations of selenium in white suckers (Catastomus commersoni) segregated by gender and 

reproductive condition (data from Appendix I in Osmundson & Skorupa 2011).
21

In the experiments of Linville (2006), adverse effects of selenium on larval white sturgeon 

occurred at lower concentrations in microinjection treatments than in experiments in which 

larvae were exposed to elevated selenium solely by maternal transfer. If this apparent difference 

is real, it may be related to the fact that in the microinjection experiments, the selenium is 

introduced suddenly as a free amino acid (L-selenomethionine) that is readily available for 

assimilation by the developing larvae, whereas maternally transferred selenium is incorporated 

into proteins that must be digested by the larvae before assimilation (Linville 2006). Heinz et al.

(2011) offered a similar explanation for his observation that methylmercury chloride injected 

into mallard eggs is more terratogenic than the same concentration of methylmercury maternally 

deposited in the egg. However, at the present time, for selenium in white sturgeon larvae, 

maternal transfer data are more limited (one experiment, two treatments) than microinjection 

data (multiple experiments, each with several treatments). Additionally, although the maternal 

transfer mode of exposure may seem to be more natural than injection of selenomethionine into 

larvae, in the maternal transfer experiments of Linville (2006), the mother fish were fed selenium 

in the form of selenized yeast. Sturgeon do not feed on selenized yeast in the wild, and there are 

indications that experiments based on exposure to dietary selenized yeast may underestimate 

selenium assimilation and toxicity (Heinz et al. 1996). For these reasons, until more data 

confirm the apparent difference in sensitivity to these two modes of exposure, and clarify reasons 

for it, prudence and caution impel us to use the data from the microinjection experiments as the 

basis for protective guidelines.

It may be that our analysis of the maternal transfer experiment of Linville (2006) underestimates 

the potential hazard of trophic and maternal transfer of selenium because of the relative youth of 

the captive-reared female sturgeon used in that experiment. White sturgeon captured in the wild 

from the San Francisco Bay/Estuary region exhibit a clear pattern of increasing selenium 

bioaccumulation with increasing age (Linares et al. 2004); individuals just beginning to 

reproduce in the wild (17 years old) had more than twice the selenium concentrations in muscle 

than the concentrations in the age class (6 years old) that were used in the Linville (2006) 

experiment. Still older (>17 years), fully reproductive individuals in the wild are likely to 

accumulate even higher levels of selenium.

It may be that the most sensitive endpoint for selenium effects on sturgeon is neither larval 

mortality nor larval abnormalities. Possibly these fish are even more sensitive to selenium after 

the larvae have finished yolk sac absorption and begin exogenous feeding, as seems to be the 

case for at least some salmonids (Beckon 2007, Beckon et al. 2010). To the best of our 

knowledge, sturgeon at this very sensitive stage have not yet been tested; Tashjian et al. (2006) 

tested a later, potentially less sensitive juvenile stage. Fish such as sturgeon could also be very 

sensitive to selenium effects on behavior, which could be important in the wild for predator 

avoidance, foraging, or reproductive success. For example, Hopkins et al. (2003) documented a 

substantial reduction in swimming speed, probably at least partly attributable to selenium, in 

benthic lake chubsucker (Erimyzon sucetta) exposed to coal ash. In green and white sturgeon, 

the effects of selenium on metabolic rates, growth, swimming performance, and avoidance of 

predators have been studied (Kaufman et al. 2008; Walker 2009), but the data have not yet been 

published. Until data on sublethal reproductive and behavioral effects such as these are 

published, to the best of our knowledge, the data used here are the best available for the most 

sensitive endpoint currently known for these fish.
22

The analysis presented here focuses only on the single most sensitive known endpoint. In 

reality, mortality and non-lethal endpoints are additive. That is, in addition to the mortality of 

developing embryos directly caused by selenium, a further proportion of surviving individuals 

suffers from other adverse effects of selenium: non-lethal effects (such as spinal deformities and 

impaired growth), indirect lethal effects (such as elevated vulnerability to predation due to 

mobility impairment caused by transitory edema, or other behavioral impairment), and later 

lethal effects (such as mortality among early stage juveniles). For these reasons, the analysis 

presented here probably underestimates the full extent of adverse effects of selenium on 

sturgeon. Therefore, benchmarks based on all adverse effects would likely be lower (more 

stringent) than those derived here on the basis of the most sensitive endpoint only.

Although uncertainty in data analysis has been viewed as an argument for relaxing protective 

standards, in reality, uncertainty may require greater stringency. Agencies that implement the 

Endangered Species Act are expected to “provide the benefit of the doubt” to listed species 

(USFWS & NOAA 2004). 

A strict interpretation of the “benefit of the doubt” guidance would suggest that, in modeling 

dose-response relationships, rather than a central-tendency model (least squares regression: solid 

line in Figures 1 and 2), some lower (more stringent) confidence bound should be used for 

deriving a protective guideline. Alternatively, a “safety factor”, “uncertainty factor”, “modifying 

factor” (USEPA 1993), and/or “margin of safety” could be included in the analysis (“Margins of 

safety are essential to any health related environmental standards if a reasonable degree of 

protection is to be provided against hazards which research has not yet identified.” [Senate 

Committee on Public Works, Report No.91-1196 (1970), pp.9-10]). However, in the case of 

selenium, care must be exercised in implementing any such factor or margin of safety, because 

selenium is essential at low concentrations, and there is a very narrow range between essentiality 

and toxic excess (e.g., Figures 3B and 5B in Beckon et al. (2008)). Larval mortality in sturgeon 

may be caused by deficiency of selenium as well as by toxic excess of selenium. An excessively 

large uncertainty factor could push a benchmark concentration into the zone of deficiency. No 

factor providing any margin of safety is included in the derivation of benchmark selenium 

concentrations presented here. However, the above analysis, based on the more sensitive 

microinjection route of exposure (rather than the maternal transfer route of exposure), provides 

conservative benchmarks founded on the best information currently available.

If selenium deficiency can occur in larval sturgeon, then data spanning a full range of 

concentrations from deficiency to toxic excess would best be represented by a biphasic model 

(Beckon et al. 2008). We know of no data as yet available relating larval survival of sturgeon to 

selenium in the zone of tissue concentrations that are likely to cause deficiency—probably < 1 

μg/g (whole body dry weight), based on experiments with juveniles of other species (Beckon et 

al. 2010). Therefore, for the available data, the simple log-logistic model used here (Figures 1, 

2, 7, 8, 9 and 11) should be adequate.
23

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27

Appendix I

Data and Methods

Log-logistic models were fitted to dose-response relationships by least squares non-linear 

regression, using the “nls” and “nls2” functions in the “R” statistical program. Confidence 

(95%) bounds were determined for non linear models using the “nls2”, “predict”, and “as.lm.nls” 

functions in “R”. Linear models for translations of tissue concentrations were determined using 

the “lm” function in “R” (except for Figures 11 and 12, as noted below). 

White sturgeon (Acipenser transmontanus)

Figure 1

Selenium effect on mortality of microinjected white sturgeon larvae. Data source: Table 3-15 in 

Linville (2006).

Treatment

Selenium 

in larvae 

(μg/g dry 

wt.)

Larval 

mortality

Study 1 non inj 2.6 0

Study 1 sham inj 2.54 0

Study 1 low 15.8 0.41

Study 1 medium 21.7 0.467

Study 1 high 46.6 0.676

Study 2 non inj 6.36 0

Study 2 sham inj 5.89 0.0167

Study 2 low 8.74 0.1

Study 2 medium 8.97 0.0334

Study 2 high 16.56 0.7

Formula: y ~ 1/(1 + (e/x)^b)

Parameters:

 Estimate Std. Error t value Pr(>|t|) 

e 20.0490 3.0848 6.499 0.000188 ***

b 2.0233 0.6224 3.251 0.011683 * 

---

Signif. codes: 0 '***' 0.001 '**' 0.01 '*' 0.05 '.' 0.1 ' ' 1 

Residual standard error: 0.1392 on 8 degrees of freedom

Number of iterations to convergence: 9 

Achieved convergence tolerance: 4.346e-06
28

Figure 2

Selenium effect on defects of microinjected white sturgeon larvae. Data source: Tables 3-11 and 

3-13 in Linville (2006).

Treatment

Selenium 

in larvae 

(μg/g dry 

wt.)

Edema 

and/or 

spinal 

curvature

Study 1 non inj 2.6 0

Study 1 sham inj 2.54 0.0395

Study 1 low 15.8 0.7669

Study 1 medium 21.7 0.8366

Study 1 high 46.6 0.7821

Study 2 low 8.74 0.1273

Study 2 medium 8.97 0.0508

Study 2 high 16.56 0.6949

Study 2 non/sham inj 6 0.0085

Formula: y ~ 1/(1 + (e/x)^b)

Parameters:

 Estimate Std. Error t value Pr(>|t|) 

e 13.5260 0.8507 15.900 9.44e-07 ***

b 4.9174 1.1663 4.216 0.00395 ** 

---

Signif. codes: 0 '***' 0.001 '**' 0.01 '*' 0.05 '.' 0.1 ' ' 1 

Residual standard error: 0.09781 on 7 degrees of freedom

Number of iterations to convergence: 9 

Achieved convergence tolerance: 7.008e-06

Figure 3

Selenium in white sturgeon eggs and larvae. Data source: Table 3-18 in Linville (2006). 

Call:

lm(formula = log10(egg) ~ log10(larva), data = WhiteSturgeonLinvile3_18)

Residuals:

 1 2 3 4 5 6 

0.013976 -0.008056 0.009141 -0.033171 0.031295 -0.013184 
29

Coefficients:

 Estimate Std. Error t value Pr(>|t|) 

(Intercept) -0.01930 0.02187 -0.882 0.427 

log10(larva) 1.02763 0.02711 37.909 2.89e-06 ***

---

Signif. codes: 0 '***' 0.001 '**' 0.01 '*' 0.05 '.' 0.1 ' ' 1 

Residual standard error: 0.02548 on 4 degrees of freedom

Multiple R-squared: 0.9972, Adjusted R-squared: 0.9965 

F-statistic: 1437 on 1 and 4 DF, p-value: 2.892e-06

Figure 4

Maternal transfer of selenium in white sturgeon. Data source: Tables 3-18 in Linville (2006).

Treatment

Selenium 

in 

maternal 

muscle 

(μg/g dry 

wt.)

Selenium 

in larvae 

(μg/g dry 

wt.)

Control C3 1.28 2.43

Control C4 1.22 1.69

Control C5 1.48 2.67

Treatment T1 9.93 11.6

Treatment T2 15.3 18.4

Treatment T3 11.1 7.75

Call:

lm(formula = log10(muscSe) ~ log10(larvaeSe), data = WhiteSturgeonLinville3_18)

Residuals:

 1 2 3 4 5 6 

-0.09717 0.07372 -0.08385 -0.03273 -0.08856 0.22859 

Coefficients:

 Estimate Std. Error t value Pr(>|t|) 

(Intercept) -0.2644 0.1237 -2.137 0.09937 . 

log10(larvaeSe) 1.2157 0.1533 7.930 0.00137 **

---

Signif. codes: 0 '***' 0.001 '**' 0.01 '*' 0.05 '.' 0.1 ' ' 1 

Residual standard error: 0.1441 on 4 degrees of freedom

Multiple R-squared: 0.9402, Adjusted R-squared: 0.9252 

F-statistic: 62.88 on 1 and 4 DF, p-value: 0.001369
30

Figure 5

Selenium in muscle and whole body in young white sturgeon. Data source: Tables 2 and 3 in 

Tashjian et al. (2006).

Selenium 

in 

muscle 

(μg/g dry 

wt.)

Selenium 

in whole 

body 

(μg/g 

dry wt.) 

8.2 5.2

17.2 11.8

22.9 14.7

36.8 22.5

52.9 34.4

54.8 27.5

Call:

lm(formula = log(WB) ~ log(musc), data = WhiteSturgeonTTF)

Residuals:

 1 2 3 4 5 6 

-0.06139 0.07235 0.02715 0.01373 0.10234 -0.15419 

Coefficients:

 Estimate Std. Error t value Pr(>|t|) 

(Intercept) -0.23765 0.21398 -1.111 0.328997 

log(musc) 0.92565 0.06399 14.467 0.000133 ***

---

Signif. codes: 0 '***' 0.001 '**' 0.01 '*' 0.05 '.' 0.1 ' ' 1 

Residual standard error: 0.1051 on 4 degrees of freedom

Multiple R-squared: 0.9812, Adjusted R-squared: 0.9766 

F-statistic: 209.3 on 1 and 4 DF, p-value: 0.0001327
31

Figure 6

Trophic and maternal transfer in white sturgeon. Data source: Tables 3-1 and 3-5 in

Linville (2006). 

Selenium 

in 

maternal 

diet 

(μg/g dry 

wt.)

Selenium 

in larvae 

(stage 

36, μg/g 

dry wt.) 

1.42 2.26

34.04 12.58

Figure 7

Developmental defects in white sturgeon larvae exposed to selenium via maternal diet. Data 

source: Table 3-18 in Linville (2006). 

Treatment

Selenium 

in larvae 

(μg/g dry 

wt.)

Developmental 

defects

Control C3 2.43 0

Control C4 1.69 0

Control C5 2.67 0

Treatment T1 11.6 0

Treatment T2 18.4 0.2778

Treatment T3 7.75 0.1333

Formula: defects ~ 1/(1 + (e/larvaeSe)^b)

Parameters:

 Estimate Std. Error t value Pr(>|t|) 

e 21.246 4.084 5.202 0.00651 **

b 6.666 8.410 0.793 0.47230 

---

Signif. codes: 0 '***' 0.001 '**' 0.01 '*' 0.05 '.' 0.1 ' ' 1 

Residual standard error: 0.06662 on 4 degrees of freedom

Number of iterations to convergence: 65 

Achieved convergence tolerance: 9.34e-06
32

Figure 8

Mortality in white sturgeon larvae exposed to selenium via maternal diet. Data source: Table 3-

14 in Linville (2006). 

Grouped 

exposure 

category

Selenium in egg 

(μg/g dry wt.)

Larval mortality 

(stage 45)

low 2.15 0.0027

med 9.31 0.022

high 20.5 0.0842

Formula: Mortality ~ 1/(1 + (e/SeEggs)^b)

Parameters:

 Estimate Std. Error t value Pr(>|t|) 

e 78.98147 3.86639 20.43 0.0311 *

b 1.76984 0.06086 29.08 0.0219 *

---

Signif. codes: 0 '***' 0.001 '**' 0.01 '*' 0.05 '.' 0.1 ' ' 1 

Residual standard error: 0.00103 on 1 degrees of freedom

Number of iterations to convergence: 3 

Achieved convergence tolerance: 7.521e-06
33

Green sturgeon (Acipenser medirostris)

Figure 9

Selenium effect on mortality of microinjected green sturgeon larvae. Data source: Javier 

Linares-Casenave, et al. poster (2010).

Treatment

Selenium in 

larvae (μg/g 

dry wt.)

Larval 

mortality

Se-L-Met 7.3 0.6

L-Met 3.5 0.12

Non-Inj 3.2 0.01

Formula: y ~ 1/(1 + (e/x)^b)

Parameters:

 Estimate Std. Error t value Pr(>|t|) 

e 6.5661 0.4116 15.952 0.0399 *

b 3.8791 0.9478 4.093 0.1526 

---

Signif. codes: 0 '***' 0.001 '**' 0.01 '*' 0.05 '.' 0.1 ' ' 1 

Residual standard error: 0.06239 on 1 degrees of freedom

Number of iterations to convergence: 5 

Achieved convergence tolerance: 6.219e-06

Figure 10

Data and fitted model are the same as in Figure 5

Figure 11A

Selenium effect on peak abnormalities of microinjected green sturgeon larvae. Data are from 

Tables 1 and 2 in Linares-Casenave et al. 2010.

Treatment

Selenium 

in larvae 

(μg/g dry 

wt.)

Peak 

abnormalities

Se-L-Met 8.6 0.08

L-Met 2.1 0.02

Non-Inj 2.1 0.01
34

S-PLUS 6 analysis:

Formula: Abnorm ~ 1/(1 + (e/SeLarvae)^b)

Parameters:

 Value Std. Error t value 

e 62.06060 26.492800 2.34255

b 1.23579 0.249522 4.95262

Residual standard error: 0.00707107 on 1 degrees of 

freedom

Correlation of Parameter Estimates:

 e 

b -0.985

Figure 11B

Selenium effect on peak abnormalities of microinjected white sturgeon larvae. Data are from 

Tables 1 and 2 in Linares-Casenave et al. 2010.

Treatment

Selenium 

in larvae 

(μg/g dry 

wt.)

Peak 

abnormalities

Se-L-Met 7.3 0.37

L-Met 3.5 0.04

Non-Inj 3.2 0.04

S-PLUS 6 analysis:

Formula: Abnorm ~ 1/(1 + (e/SeLarvae)^b)

Parameters:

 Value Std. Error t value 

e 8.52964 0.130246 65.4887
35

b 3.42169 0.202209 16.9216

Residual standard error: 0.00820243 on 1 

degrees of freedom

Correlation of Parameter Estimates:

 e 

b -0.755

Figure 12

Selenium in muscle and whole body in representatives of several families of fish caught in the 

Gunnison and Colorado Rivers and associated tributaries. Data sources: Barbara Osmundson 

pers. com., Osmundson et al. (2007), Osmundson & Skorupa (2011). For comparison, the white 

sturgeon data and regression from Figure 5 are also shown (orange color).

ID Species

Selenium in 

whole body 

(μg/g dry 

wt.)

Selenium in 

muscle (μg/g 

dry wt.)

BSW-WS3 WS 3.81 2.88

BSW-WS4 WS 4.21 4.83

BSW-WS7 WS 3.33 3.7

BSW-WS8 WS 4.51 3.7

2PW-WS1 WS 6.32 8.42

2PW-WS2 WS 6.77 9.36

2PW-WS3 WS 10.99 15.5

2PW-WS4 WS 12.65 23.6

MWB-WS2 WS 5.72 9.37

MWB-WS1 WS 8.32 11.5

2MW-WS1 WS 3.92 6.07

2MW-WS2 WS 3.79 4.56

2FL-WS1 WS 9.92 12.3

2FL-WS3 WS 5.28 9.23

WS-FL-1 WS 10.72 9.44

WS-FL-2 WS 5.92 9.44

WS-FL-3 WS 7.03 10.5

WS-FL-4 WS 6.4 11.4

WS-FL-5 WS 6.27 9.57
36

WS-FL-6 WS 5.33 9.29

WS-FL-8 WS 6.15 9.75

WS-FL-9 WS 5.59 10.5

AC-WSWB1 WS 8.8 11.1

AC-WSWB2 WS 8.71 12.1

MW-WS2 WS 11.37 12.8

MW-WS6 WS 10.7 16

MW-WS7 WS 8.44 12.1

PS2-WS1 WS 6.95 8.99

PS2-WS3 WS 7.49 10.6

PS2-WS4 WS 10.28 12.6

PS2-WS5 WS 6.73 11.6

GV1-WS1 WS 2.09 2.81

GV1-WS4 WS 1.78 2.53

GV1-WS6 WS 3.21 4.31

GV1-WS8 WS 2.27 3.52

GV1-WS9 WS 3.08 4.27

GV1-WS10 WS 3.04 3.14

GV1-WS13 WS 2.79 3.58

GV1-WS14 WS 2.51 2.95

GV1WS15 WS 3.43 4.09

GV1WS16 WS 2.83 3.59

WS-FL-7 WS 3.1 5.58

WS-FL-10 WS 5.51 6.29

2FL-WS2 WS 7.02 9.13

2FL-WS4 WS 7.3 8.47

2FL-WS5 WS 2.41 3.04

BSW-WS1 WS 2.72 4.39

BSW-WS6 WS 2.7 3.23

BSW-WS10 WS 2.55 1.63

2HW-WS1 WS 19.6 28.1

AC-WS2 WS 9.8 12.1

MW-WS1 WS 8.69 11.8

MW-WS4 WS 8.73 12.6

MW-WS5 WS 9.08 12.3

AC-WSWB3 WS 13.4 18

GV1-WS2 WS 3.12 2.81

GV1-WS5 WS 2.43 3.15

GV1-WS7 WS 2.14 3.14

GV1WS11 WS 3.18 4.32

GV1WS12 WS 2.75 3.4

AC-GS1 GS 10.8 14.7

ACOGS1 GS 22.8 28.1

ACO-GS3 GS 8.79 12.9

RW-GS1 GS 15.37 21.9

LW-GS2 GS 4.75 4.95

LW-GS4 GS 5.74 6.11

LW-GS6 GS 4.43 5.19

2MW-GS2 GS 3.75 5.14

BSW-GS2 GS 11.9 15.7
37

2PW-GS1 GS 6.43 10.1

2HW-GS1 GS 9.51 11.5

FL-GS-1 GS 9.13 10.5

GS-FL-8 GS 6.24 7.2

GS-FL-9 GS 7.04 9.26

GS-FL10 GS 7.72 7.65

FL-GS11 GS 6.19 5.99

FL-GS12 GS 10.2 12

FL-GS14 GS 9.71 12.1

FL-GS16 GS 9.88 12.5

SW-GS2 GS 7.18 7.49

MW-GSF5 GS 8.99 11.3

MW-GSF6 GS 9.7 13.6

MW-GSF7 GS 8.89 13.2

MW-GSF8 GS 9.81 12.4

MW-GSF9 GS 9.87 12.5

HW-GS1 GS 10.27 8.59

PS2-GS1 GS 5.34 5.34

PS2-GS2 GS 10.14 11.9

PS2-GS3 GS 11.83 13.6

GV1GS1 GS 3.26 3.79

GV1GS2 GS 3.95 4.22

GV1GS3 GS 4.33 4.08

GV2GS1 GS 3.65 4.23

GV2GS2 GS 6.22 5.74

GV2GS3 GS 3.46 4.41

GV3-GS1 GS 4.38 3.52

GV3-GS2 GS 5.59 5.45

GV3-GS6 GS 4.87 4.95

GV3-GS9 GS 4.44 4.32

BSW-GS1 GS 7.96 10.1

ACO-GS2 GS 7.87 11.9

MWB-GS1 GS 6.36 11.1

MWB-GS2 GS 8.67 11.8

MWB-GS3 GS 8.34 11

GS-FL-1 GS 6.08 7.08

GS-FL-2 GS 5.62 6.65

GS-FL-3 GS 18.1 26.4

FL-GS-5 GS 9.4 9.62

GS-FL-6 GS 12.2 16.7

SW-GS1 GS 5.29 8.12

SW-GS3 GS 7.3 10.6

MW-GSF1 GS 9.28 14.2

MW-GSF2 GS 6.82 11.3

MW-GSF4 GS 7.5 12.8

SC-FMS1 FMS 3.1 4.09

SC-FMS2 FMS 2.63 3.79

FL-FMS1 FMS 4.48 7.28

FL-FMS2 FMS 3.5 5.23

FL-FMS3 FMS 2.95 3.56
38

FL-FMS4 FMS 4.42 6.15

FL-FMS5 FMS 3.12 4.63

32-FMS1 FMS 2.19 4.23

32-FMS5 FMS 1.95 4.28

UCS-FMS1 FMS 2.76 3.57

RP-FM3 FMS 4.22 5.72

RP-FM4 FMS 4.55 5.6

FL-BHS3 BHS 1.97 2.3

FL-BHS4 BHS 1.3 1.47

FL-BHS5 BHS 2.42 3.07

PW3-BHS1 BHS 5.62 8.57

FL-BHS11 BHS 3.91 5.16

FL-BHS1 BHS 2.11 2.52

FL-BHS2 BHS 2.18 2.72

RP-BH1 BHS 2.11 2.76

RP-BH2 BHS 2.43 3.04

UCS-BHS1 BHS 2.13 3.64

PW3-CP1 CCP 11.7 20

PW3-CP2 CCP 4.78 8.24

PW3-CP3 CCP 4.1 6.56

PW3-CP4 CCP 6.29 7.81

CL-CP1 CCP 23.12 24.2

RP-CC1 CCP 6.32 6.1

32-C-1 CCP 4.01 5.06

FL-CP-1 CCP 5.91 10.2

FL-CP-2 CCP 9.02 11.5

FL-BT2 BT 5.02 4.01

RFL-BT1 BT 4.55 3.17

FL-BT1 BT 5.52 6.27

FL-BT11 BT 4.3 3.64

CR-RTC5 RTC 6.44 6.22

CR-RTC6 RTC 6.83 6.87

CR-RTC7 RTC 8.4 9.84

CR-RTC9 RTC 4.08 4.34

CRRTC10 RTC 5.275

FL-RTC1 RTC 6.55 7.29

JARVRTC RTC 5.51 6.96

RP-RT1 RTC 7.23 7.42

UCS-RTC3 RTC 3.84 5.74

UCS-RTC4 RTC 3.63 5.56

CR-BG-1 8.78 12.9

FL-BH3 BBH 7.31 7.49

FL-BH4 BBH 4.83 3.94

FL-BH1 BBH 5.47 4.26

FL-BH2 BBH 7.64 7.42

FL-BH8 BBH 8.59 7.82

FL-BH9 BBH 9.61 5.7

RFL-BH1 BBH 6.61 7.77

RFL-BH2 BBH 2.03 9.22

HW-BH1 BBH 4.92 4.67
39

HW-BH2 BBH 5.3 3.35

LCBH-1 BBH 2.9 2.04

BH-FL2 BBH 3.94 4.63

BH-FL-3 BBH 4.57 3.91

2PW-BH1 BBH 4.99 4.36

FL-CCF1 CCF 3.97 5.31

PW3-CC1 CCF 3.34 3.58

FL-CCF2 CCF 3.41 3.41

RFL-CF1 CCF 2.63 3.67

UCS-CC1 CCF 2.04 3.95

? CCF 1.88 1.95

CRCF-1 CCF 3.35 3.7

32 CCF 2.35 1.49

CL-LMB1 7.03 8.45

CL-SMB1 5.42 6.93

CL-SMB2 4.19 3.67

GVICSMB3 5.07 5.48

GVICSMB5 4.9 7.7

CRRSMB1 5.51 6.45

CRRSMB7 7.82 11

Linear least squares regression performed on natural-log-transformed data using Microsoft 

Excel:

SUMMARY OUTPUT

muscle to WB

Regression Statistics

Multiple R 0.908382

R Square 0.8251578

Adjusted R 

Square 0.8242229

Standard Error 0.2307081

Observations 189

ANOVA

df SS MS F

Significance 

F

Regression 1 46.97407909 46.97408 882.5361 9.86504E-73

Residual 187 9.953306565 0.053226

Total 188 56.92738565

Coefficients

Standard 

Error t Stat P-value Lower 95%

Upper 

95%

Intercept 0.1003801 0.055508758 1.808365 0.072156

-

0.009123739 0.209884

X Variable 1 0.8326865 0.028029496 29.70751 9.87E-73 0.77739187 0.887981
40

Figure 13

Selenium in muscle and whole body in white sucker caught in the Gunnison and Colorado Rivers 

and associated tributaries. Data source: Osmundson & Skorupa (2011). The white sucker data 

are the same as in Figure 12, but here separated by gender and reproductive condition of females. 

For comparison, the white sturgeon data and regression from Figure 5 are also shown (orange 

color).
41

Appendix II

It has been suggested that homeostatic regulation of selenium in food chains can be discerned in 

bioaccumulation across several steps of trophic transfer (Brix et al. 2005), requiring that at least 

one trophic transfer exhibit a “hockey stick” function. If such homeostatic regulation occurs, it 

would invalidate the exponential model (straight line on a log-log graph) used in Figures 6 and 

10. Below are five examples of the best species-specific and location-specific bioaccumulation 

relationships currently available. All these examples show field data from Beckon et al. (2010), 

incorporating estimates of lag time; all are well characterized by exponential models, and exhibit 

no evidence of homeostatic regulation at any link in the food chain. These results are consistent 

with the model used in Figures 6 and 10.

0.1

1

10

100

Selenium in tissue (μg/g whole 

0.1 1 10 100

body dry wt)

Selenium in water (μg/L)

Largemouth bass
42

0.11

10

100

Selenium in tissue (μg/g whole 

0.11 10 100

body dry wt)

Selenium in water (μg/L)

Fathead minnow

0.11

10

100

Selenium in tissue (μg/g whole 

0.11 10 100

body dry wt)

Selenium in water (μg/L)

Red shiner
43

0.1

1

10

100

0.1 1 10 100

Selenium in tissue (μg/g whole 

body dry wt)

Selenium in water (μg/L)

Waterboatman

0.1

1

10

100

0.1 1 10 100

Selenium in tissue (μg/g whole 

body dry wt)

Selenium in water (μg/L)

Siberian freshwater shrimp
44

The following four graphs show the best available data from laboratory studies of trophic 

transfer of selenium across a single link in the food chain. All support the conclusion that 

trophic transfer of selenium does not involve homeostatic regulation but is well represented by 

exponential functions (straight lines on log-log graphs), consistent with the model used in 

Figures 6 and 10.

0.1

1

10

100

0.1 1 10 100

Selenium in tissue 

(μg/g whole body dry wt)

Selenium in diet (μg/g dry wt)

White sturgeon

Tashjian et al. 2006

0.1

1

10

100

0.1 1 10 100

Selenium in tissue 

(μg/g whole body dry wt)

Selenium in diet (μg/g dry wt)

Bluegill

Cleveland et al. 1993
45

0.1

1

10

100

0.1 1 10 100

Selenium in tissue 

(μg/g whole body dry wt)

Selenium in diet (μg/g dry wt)

Fathead minnow

Ogle and Knight 1989

0.1

1

10

100

0.1 1 10 100

Selenium in tissue 

(μg/g whole body dry wt)

Selenium in diet (μg/g dry wt)

Daphnia magna

Besser et al. 1993
46

The following four graphs show the best available data on trophic transfer functions for metals, 

both essential (copper and zinc) and nonessential (cadmium). These data suggest that the above 

conclusion for selenium is generalizable to trophic transfer of metals: there is no evidence of 

homeostatic regulation of these elements anywhere in the food chain; trophic transfer functions 

are well represented by exponential models.

1

10

100

1000

10 100 1000 10000

Copper in tissue 

(μg/g whole body dry wt)

Copper in diet (μg/g dry wt)

Rainbow trout

Mount et al. 1994 

10

100

1000

10000

1 10 100 1000

Zn in tissue 

(μg/g dry wt)

Zn in water nominal (μg/L)

Algae

Chlamydomonas reinhardtii

Guan & Wang. 2004
47

0.01

0.1

1

10

100

0.01 0.1 1 10

Cd in tissue 

(μg/g whole body dry wt)

Cd in diet (μg/g dry wt)

Mayfly

Centroptilum triangulifer

Xie et al. 2009

Aug

Nov

Jan

0.01

0.1

1

10

0.1 1 10 100 1000

Cd in tissue 

(μg/g whole body dry wt)

Cd in water (ng/L)

Periphyton

Xie et al. 2009

Aug

Nov

Jan
48

References (Appendix II only)

Beckon WN, Gordus A, Eacock MCS. 2010. Biological effects. Ch. 7 in Grassland Bypass 

Project.

Besser JM, Canfield TJ, La Point TW. 1993. Bioaccumulation of organic and inorganic 

selenium in a laboratory food chain. Environ Toxicol Chem 12:57–72.

Brix KV, Toll JE, Tear LM,. DeForest DK, Adams WJ. 2005. Setting site-specific water quality 

standards by using tissue residue thresholds and bioaccumulation data. Part 2. Calculating 

site-specific selenium water quality standards for protecting fish and birds. Environ 

Toxicol Chem 24:231–237.

Cleveland L, Little EE, Buckler DR, Weidmeyer RH. 1993. Toxicity and bioaccumulation of 

waterborne and dietary selenium in juvenile bluegill (Lepomis macrochirus). Aquatic 

Toxicology 27:265-280.

Guan R, Wang WX. 2004. Dietary assimilation and elimination of Cd, Se, and Zn by Daphnia 

magna at different metal concentrations. Environ Toxicol Chem 23:2689–2698.

Kleckner, A.E., Stewart, A.R., Elrick, K., and Luoma, S.N., 2010, Selenium and stable isotopes 

of carbon and nitrogen in the benthic clam Corbula amurensis from Northern San 

Francisco Bay, California: May 1995–February 2010: U.S. Geological Survey Open-File 

Report 2010-1252, 34 p.

Mount DR, Barth AK, Garrison TD, Barten KA, Hockett JR. 1994. Dietary and waterborne 

exposure of rainbow trout (Oncorhynchus mykiss) to copper, cadmium, lead and zinc 

using a live diet. Environ Toxicol Chem 13(12): 2031-2041.

Ogle RS, Knight AW. 1989. Effects of elevated foodborne selenium on growth and reproduction 

of the fathead minnow (Pimephales promelas). Arch Environ Contam Toxicol 18:795–

803.

Tashjian DH, Teh SJ, Sogomonyan A, Hung SSO. 2006. Bioaccumulation and chronic toxicity 

of dietary L-selenomethionine in juvenile white sturgeon (Acipenser transmontanus). 

Aquatic Toxicology 79:401-409.

Xie L, Funk DH, Buchwalter DB. 2009. Trophic transfer of Cd from natural periphyton to the 

grazing mayfly Centroptilum triangulifer in a life cycle test.