BIOMEDICAL AND ENVIRONMESTAL SCIENCES 10. 415.435( 1997)

Environmental Implications of Excessive

Selenium: A Review

A. DENNIS LEMLY

United States Forest Service, Southern Research Station, Coldwater

Fisheries Research C’nit , Department of Fisheries and Wildlife

Sciences, Virginia Tech University, Blacksburg, VA

24061-0321, US A

Selenium is a naturally occurring trace element that is nutritionally required in small

amounts but it can become toxic at concentrations only twice those required. The narrow margin between beneficial and harmful levels has important implications for human activities that

increase the amount of selenium in the environment. Two of these activities, disposal of fossil

fuel wastes and agricultural irrigation of arid, seleniferous soils, have poisoned fish and

wildlife, and threatened public health at several locations in the United States. Research studies of these episodes have generated a data base that clearly illustrates the environmental hazard

of excessive selenium. It is strongly bioaccumulated by aquatic organisms and even slight increases in waterborne concentrations can quickly result in toxic effects such as deformed embryos and reproductive failure in wildlife. The selenium data base has been very beneficial in

developing hazard assessment procedures and establishing environmentally sound water quality

criteria. The two faces of selenium. required nutrient and potent toxin, make it a particularly

~ important trace element in the health of both animals and man. Because of this paradox, environmental selenium in relation to agriculture, fisheries, and wildlife will continue to raise important land and water-management issues for decades to come. If these issues are dealt with

using prudence and the available environmental selenium data base, adverse impacts to natural

resources an&public health can be avoided.

INTRODUCTION

Selenium is a trace element that is normally present in surface waters at concentrations of about 0.1-O. 3,ug/l (parts-per-billion; Lemly, 1985a). In slightly greater

amounts, i. e. , l-5pg/l, it can bioaccumulate in aquatic food chains and become a

concentrated dietary source of selenium that is highly toxic to fish and wildlife (Lemly

and Smith, 1987; Lemly, 1993a). Dietary selenium is passed from parents to offspring in the eggs, where it can be teratogenic to developing embryos and cause complete reproductive failure (Gillespie and Baumann, 1986; Heinz et al. , 1987, 1989;

Coyle et al. , 1993 ; Lemly, 1993b). This scenario of poisoning has occurred in

reservoirs contaminated by selenium leached from fly-ash at coal-fired electric generating stations in the eastern U. S. (Garrett and Inmann, 1984; Lemly, 1985b). and

in wetlands used to dispose subsurface agricultural irrigation drainage in the western

U.S. (Lemly, et al., 1993; Lemly 1994a, 199413). Public health may also be

threatened if humans consume selenium-contaminated fish and wildlife (Fan et al.,

1988).

0895-3988/97

CN 11-2816

Copyright 0 1997 by CAF’M

415
416 A. DENNIS LEMLY

Because of these and other episodes of contamination, the role and importance of

selenium as an environmental pollutant has gained widespread attention among research scientists, natural resource managers, and regulatory agencies in the U. S.

during the past decade. Although the basic toxicological symptoms and paradox of selenium (nutritionally required in small amounts by both animals and humans, but

highly toxic in slightly greater amounts) have been known for many years (Draize

and Beath, 1935; Ellis et al., 1937; Rosenfeld and Beath, 1946; Hartley and

Grant, 1961), it was not until the late 1970s and early 1980s that the potential for

widespread contamination of aquatic ecosystems due to human activities was recognized ( Andren et al. , 1975; Cherry and Guthrie, 1977; Evans et al., 1980; National Research Council, 1980a; Braunstein et al. , 1981). In fact, as recently as

1970 selenium was being called the “unknown pollutant” with respect to what was

known about its cycling and toxicity in the aquatic environment (Copeland, 1970).

Since that time much has been learned about the environmental implications of excessive selenium. This article is a concise review that gives a current perspective on major sources of selenium, impacts and threats to wildlife and humans, ways to assess

environmental hazard, and criteria for protecting environmental quality and public

health.

MAJOR SOURCES OF SELENIUM CONTAMINATION

Two factors stand apart as the major human-related causes of selenium mobilization and introduction into the environment. First is the procurement, processing, and

combustion of fossil fuels. Selenium is an important trace element present in coal,

crude oil, oil shale, coal conversion materials (liquefaction oils and synthetic gases),

and their waste by-products (Pillay et al. , 1969 ; American Petroleum Institute,

1978 ; Fruchter and Petersen, 1979; Schlinger and Richter, 1980; Clark et aL . ,

1980; U. S.EPA, 1980; Cowser and Richmond, 1980; Nystrom and Post, 1982).

Rain can leach selenium from coal and oil-shale mining, preparation, and storage

sites, where it may enter down-gradient streams and reservoirs through precipitation

runoff (Davis and Boegly, 1981; Heaton et al., 1982, Jones, 1990). More importantly, selenium is highly concentrated in the mineral fraction (fly-ash and bottom

ash) remaining after coal is burned ( Kaakinen et al. , 1975 ; Klein et al. , 1975).

Over 70 million tons of coal fly-ash are produced annually in the U. S. and most of it

is disposed by dumping into wet-slurry or dry ash basins (Murtha et al. , 1983). Selenium-laden leachate and overflow from these basins often makes its way into rivers,

streams, and impoundments. Selenium concentrations can rapidly increase in fish and

aquatic organisms in the receiving water, ultimately resulting in tissue damage, reproductive failure, and elimination of entire fish communities (Cumbie and Van

Horn, 1978; Garrett and Inmann, 1984; Lemly, 1985a, 1985b; Sorensen, 1986).

The second major factor is the irrigation of seleniferous soils for crop production

in arid and semi-arid regions. For example, deposits of Cretaceous marine shales have

weathered to produce high selenium soils in many areas of the western U. S. , notably

the San Joaquin Valley of California and certain parts of Wyoming, Colorado, Nevada, North and South Dakota, Montana, New Mexico, Arizona, Utah, Nebraska,

and Kansas (Kubota, 1980; Tanji et al., 1986; Allen and Wilson, 1990; Presser

and Ohlendorf, 1987; Presser et al., 1990; Severson et al., 1991) . These areas

usually require substantial irrigation for agricultural crop production. Excessive
SELENIUM IN THE ENVIRONMENT 417

amounts of irrigation water are necessary to leach away salts and prevent salinization

of soils. This can lead to the production of subsurface drainage that may be highly

contaminated with dissolved selenium and other soil trace elements that have been

leached from the soil along with salts ( Presser and Barnes, 1985; Saiki, 1986a;

Summers and Anderson, 1986; Fuji, 1988; Deverel et al., 1989). Selenium in

agricultural irrigation drainwater was responsible for massive poisoning of fish and

wildlife at Kesterson National Wildlife Refuge, California in the early to mid-1980s

(Marshall, 1985; Hoffman et al., 1986; Saiki, 1986a, 1986b; Saiki and Lowe,

1987; Ohlendorf et al., 1986, 1988a, 1988b). Subsequent studies have shown irrigation-related selenium contamination to be a threat to aquatic systems and wildlife

refuges in many western states (U. S. Fish and Wildlife Service, 1986; Summers and

Anderson, 1986; Ohlendorf et al. , 1987; Sylvester et al. , 1991).

AQUATIC CYCLING AND BIOACCUMULATION

The Selenium Cycle

Four primary pathways exist for selenium in aquatic systems: (i) it can be absorbed or ingested by organisms, (ii) it can bind or complex with particulate matter,

(iii) it can remain free in solution, or (iv) it can be released to the atmosphere

through volatilization. Over time, most selenium is either taken up by organisms or

bound to particulate matter. Through deposition of biologically incorporated selenium

and settling of particulate matter (sedimentation), most of it usually accumulates in

the top layer of sediment and detritus. However, sediments are only a temporary

repository for selenium because there are numerous biological, chemical, and physical

processes that can move it out of sediments as well. Aquatic systems are very dynamic

and selenium can be cycled from sediments into biota and remain at elevated levels for

years after waterborne inputs of selenium are stopped.

Immobilization and Removal Processes

Selenium can be removed from solution and sequestered in sediments through the

natural processes of chemical and microbial reduction of the selenate form (Se VI) to

the selenite form (Se IV), followed by absorption (binding and complexation) onto

clay and the organic carbon phase of particulates, reaction with iron species, and coprecipitation and settling. Regardless of the route, once selenium is in the sediments,

further chemical and microbial reduction may occur, resulting in insoluble organic,

mineral, elemental, or adsorbed selenium. Most selenium in animal and plant tissues

is eventually deposited as detritus and, over time , isolated through the process of sedimentation. In total, immobilization processes effectively remove selenium from the

soluble pool, especially in slow moving or still-water habitats and wetlands. Ninety

percent of the total selenium in an aquatic system may be in the upper few centimeters

of sediment and overlying detritus (Lemly and Smith, 1987).

Mobilization Processes

Selenium in sediments is particularly important to long-term habitat quality because mechanisms present in most aquatic systems effectively mobilize this selenium
418 A. DENNIS LEMLY

into food chains and thereby cause long-term dietary exposure of fish and wildlife. Selenium is made available for biological uptake by four chemical and/or biological processes. The first is the oxidation and methylation of inorganic and organic selenium by

plant roots and microorganisms (oxidation is the conversion of selenium in the reduced

organic, elemental, or selenite forms to the selenite or selenate forms; methylation is

the conversion of selenium to an organic form containing one or more methyl groups,

which usually results in a volatile form). The second process is the biological mixing

and associated oxidation of sediments that results from the burrowing of benthic invertebrates and feeding activities of fish and wildlife. The third process consists of

physical perturbation and chemical oxidation associated with water circulation and

mixing ( current, wind, stratification, precipitation, and upwelling). Finally, sediments may be oxidized by plant photosynthesis. Two additional pathways provide for

direct movement of selenium from sediments into food chains, even when the surface

water does not contain elevated concentrations of the element. These pathways are

uptake of selenium by rooted plants and uptake by bottom-dwelling invertebrates and

detrital-feeding fish and wildlife. These two pathways may be the most important in

the long-term cycling of potentially toxic concentrations of selenium. Thus, rooted

plants and the detrital food pathway can continue to be highly contaminated and expose fish and wildlife through dietary routes even though concentrations of selenium in

water are low ( Lemly and Smith, 1987) Some of the sedimentary and waterborne

selenium may be converted to volatile organic forms (e. g. , dimethyl selenide) by microbial activity in the water and sediments, and subsequently released (degassed) into

the atmosphere through the water-air interface or through direct release by plants.

Volatilization is an important mechanism by which selenium can be removed from

aquatic systems and, thereby, help alleviate the threat of selenium toxicosis to fish

and wildlife (Karlson and Frankenberger, 1989, 1990).

Bioaccumulation

The major environmental implications of excessive selenium are associated with

its propensity to bioaccumulate in aquatic food chains and, thereby, contaminate the

diet of fish and wildlife and, in some cases, humans. Aquatic organisms can accumulate this element to concentrations one or more orders of magnitude greater than the

concentrations in their water or food (Fig. 1) . The reason for this bioaccumulation

may be that selenium is chemically similar to sulfur, and it sometimes is an essential

micronutrient for animals. Over evolutionary time, aquatic animals may have evolved

mechanisms to retain and accumulate selenium under conditions of scarcity. Whatever

the reason, bioaccumulation has important implications for toxic effects. For example, where fish have experienced chronic toxicity, selenium in the water has been

concentrated from 100 to more than 30,000 times, depending on the species and tissue sampled. Selenium accumulation in the organisms eaten by fish and wildlife is

usually the major pathway leading to toxicity. Biomagnification of selenium (the accumulation of progressively greater concentrations by successive trophic levels of a

food chain) usually ranges from 2 to 6 times between the primary producers (algae

and plants) and the lower consumers (invertebrates and forage fish). For example,

fish that eat contaminated plankton or benthic invertebrates may accumulate selenium

to concentrations that are 4 times those of their food, which in turn, could contain

500 times the selenium concentration in the water. The food chain biomagnification
SELENIUM IN THE ENVIRONMEXT 419

factor would then be 4 and the total bioconcentration factor for the fish would be

2,000 (i. e. , 4 X 500). These relationships are important in natural systems because

they can cause top-level consumers, such as predatory fish, birds, and mammals, to

receive toxic selenium levels in the diet even though the concentration in water is low

(< lOpg/liter) Moreover, the risk of toxicity through the detrital food pathway will

conti-nue despite a loss of selenium from the water column, as long as contaminated

sediments are present (Lemly and Smith, 1987).

FIG. 1. A typical scenario for bioaccumulation of selenium in aquatic food chains.

In this example the bioaccumulation factor for fish relative to water is 3,750 for

the planktonic food pathway (750 X 5) , and 5,250 for the benthic food pathway

(350 X 3 X 5). The food-chain biomagnification factor for the invertebrate-to-fish

trophic step is 5 for both pathways.

Role of Habitat Variability

The processes regulating selenium cycling are very similar in all aquatic habitats

and wetlands. However, the relative importance of each process may vary from one

location to another depending on hydrologic factors that affect food chain bioaccumulation and exposure of wildlife. For example, in fast flowing waters, fine organic sediments ‘such as those produced by the deposition and decay of particulate matter and

plant and animal tissue may be rare because they are continually flushed out of the

system. In such waters there is little opportunity for a contaminated surface layer of

sediment to develop. Moreover, rooted plants and benthic invertebrates are often

scarce in this habitat type. The benthic-detrital component of the system and the associated food pathways thus play a smaller role in the selenium cycle in lotic (flowing)

waters than in lentic (slow water) habitats such as reservoirs and wetlands. Systems

that tend to accumulate selenium most efficiently are shallow wetlands and marshes,
420 A. DENNIS LEMLY

and reservoirs with low flushing rates. In these systems biological productivity is often high and selenium may be readily trapped through immobilization processes or

through direct uptake by organisms. Sediments often build up a high selenium concentration that is remobilized gradually and continually through detrital and planktonic organisms. These habitats are also typically some of the most important !peding and

breeding habitats for fish and wildlife, especially waterfowl and shorebirds. Several

habitat types often occur together in one aquatic system or wetland complex. For example, rivers may have fast flowing waters, slow moving pools, and shallow backwater marshes all within a few hundred meters of each other. The degree of fish and

wildlife exposure to selenium varies among habitats according to the intensity of use,

type of use ( e. g . , feeding vs. resting), and the relative contributions of the various

processes that regulate selenium cycling and bioaccumulation in food chains (Lemly

and Smith, 1987).

THREATS TO ECOSYSTEMS

Case Example 1. Toxic Impacts to Fish

Belews Lake, North Carolina was contaminated by selenium in wastewater released from a coal-fired electric generating facility. From 1974 through 1985, water

was withdrawn from the lake and mixed with bottom ash from the coal burners and

fly-ash collected by electrostatic precipitators. This slurry was pumped from the power plant and discharged into a 142 hectare ash basin, where suspended solids were collected by gravitational settling. Runoff water from the coal storage area and power

plant site was collected by sump units and also pumped into the ash basin. Seleniumladen (150-2OOpg/l) return flows from the ash basin entered the west side of Belews

Lake through an ash sluice water canal.

Selenium bioaccumulated in aquatic food chains and caused severe reproductive

failure and teratogenic deformities in fish (Cumbie and Van Horn, 1978; Lemly,

1985a, 1985b, 1993b). Congenital malformations consisted of missing fins, protruding eyes, and grossly deformed spines and heads (Fig. 2). Concentrations of selenium

in the lake water averaged only lO,ug/l, but were accumulated from 519 times (periphyton) to 3,975 times (visceral tissue of fish) in the biota. The pattern and degree

of accumulation was essentially complete within 2 years after the initial operation of

the power plant, and persisted throughout the period of selenium discharge into the

lake ( 1974-1985). Highest concentrations of selenium were found in fish, followed

by benthic macroinvertebrates, plankton, and periphyton. The planktonic and detrital food pathways exposed fishes to potential dietary concentrations of selenium that

were some 770 and 510-l) 395 times the waterborne exposure, respectively. Of the

20 species of fish originally present in the reservoir, 16 were eliminated (which included all of the important gamefish species) through a combination of dietary toxicity

and reproductive failure (Fig. 3). Two species were rendered sterile but persisted as

adults and one additional species was eliminated but managed to partially recolonize

from a relatively uncontaminated headwater area. Only one of the original resident

species, the selenium-tolerant mosquitofish ( Gambusia affiinis > survived, along with

two introduced cyprinids. The severe toxic impacts in Belews Lake occurred even

though concentrations of waterborne selenium were only lo-20 times those in nearby

uncontaminated reservoirs; the flora and fauna contained only about lo-15 times as
SELEKIUM IN THE ENVIRONMENT 421

FIG. 2. An example of selenium-induced teratogenic deformities in

fish. These are mosquitofish ( Gambusia affinis) collected from

Belews Lake, North Carolina during the period of selenium contamination. The top two individuals are deformed and have severe

kyphosis (convex curvature of the thoracic region of the spine,

Arrow 1) and lordosis (concave curvature of the lumbar region of

the spine, Arrow 2). They also are missing or have vestigial

pelvic fins (Arrow 3 ) The bottom individual is normal.

much selenium.

The findings from Belews Lake serve as a clear illustration of how selenium can

rapidly impact fish populations. Moreover, this case example highlights the fact that

selenium can accumulate and be biologically magnified to toxic levels even though waterborne concentrations are in the low microgram per liter range. Were it not for

bioaccumulation, these waterborne concentrations would pose little threat to aquatic

life. Information from the field studies of selenium toxicity in Belews Lake was instrumental in the U. S. Environmental Protection Agency’s decision to lower the national water quality criterion for selenium from 35pg/l to 5pg/l (U. S. EPA, 1987).

In response to concerns about the fishery problems in Belews Lake the electric utility company changed its ash disposal practices. This involved switching to a dry-ash

handling system that disposed the waste in a landfill rather than a wet-basin. By mid

1986, selenium-laden wastewater no longer entered the lake (North Carolina Department of Natural Resources and Community Development, 1986).

Follow-up studies were conducted in 1996 to assess recovery of the ecosystem in

Belews Lake (Lemly, 1997a). Selenium concentrations and associated impacts to fish

were measured and compared to pre-1986 conditions to determine how much change

occurred during the decade since selenium inputs stopped. Findings were also examined using a hazard assessment protocol ( Lemly, 1995) to determine if ecosystem-lev-
422 .A. DENNIS LEIMLY

Ictalurtdae

Cyprinidaa

Poaciliidae -

-_

Centrarchidae I

-Catortomidae

- Percichthyidae

\-

Ctupeidao

Percidao

t 1973

,\,‘I/., , , , , ,

75

f t

77 79 81 83

Unit I Unit 2

-e

-_)

FIG. 3. The pattern of poisoning of fish in Belews Lake, North Carolina due to selenium conramination. Selenium-laden wastewater (150-2OOpg/l) was discharged into the lake begining in 1974

and within three years most of the fish ( 16 species) had been eliminated due to dietary toxicity and

reproductive failure.

el hazards to fish and aquatic birds had changed as well. Results showed that waterborne selenium fell from a peak of 2Opg/l before 1986, to < lpg/l in 1996; concentrations in biota were 85-95 % lower in 1996. Hazard ratings indicated that high hazard existed prior to 1986 and that moderate hazard was still present in 1996, primarily due to selenium in the sediment-detrital food pathway. Concentrations of selenium

in sediments fell by about 65-75 96 during the period but remained sufficiently elevated (l-4pg/g) to contaminate benthic food organisms of fish and aquatic birds. Field

evidence confirmed the validity of the high hazard ratings. Developmental abnormalities in young fish persisted in 1996. This indicated that selenium-induced teratogenesis and reproductive impairment were still occurring. Moreover, the concentrations of

selenium in benthic food organisms were sufficient to cause mortality in young bluegill

and other centrarchids because of Winter Stress Syndrome (Lemly, 1993~ 1996a).

At the ecosystem level, recovery in Belews Lake has been slow. Toxic effects were

still evident ten years after selenium inputs were stopped. The sediment-associated selenium will likely continue to be a significant hazard to fish and aquatic birds for years

to come in this aquatic system.

Case Example 2. Toxic Impacts to Wildlife

In 1985, subsurface irrigation drainage was implicated as the cause of death and

deformities in thousands of waterfowl and shorebirds at Kesterson National Wildlife

Refuge in California (Ohlendorf et al. , 1986). Naturally occurring trace elements

and salts were leached from soils on the west side of the San Joaquin Valley and carried to the refuge in irrigation return flows that were used for wetland management

(Zahm, 1986). One of the trace elements, selenium, bioaccumulated in aquatic food

chains and contaminated 500 hectares of shallow marshes. Elevated selenium was

found in every animal group coming into contact with these wetlands -from fis h

and birds to insects, frogs, snakes, and mammals (Saiki and Lowe, 1987; Clark,

1987; Ohlendorf et al. , 1988a). Congenital malformations in young waterbirds were
SELENIUM IN THE ENVIRONMENT 423

severe, and included missing eyes and feet, protruding brains, and grossly deformed

beaks, legs, and wings (Ohlendorf et ul., 1986, 1988b; Hoffman et (IL., 1988).

Several species of fish were eliminated due to the combined effects of high salinity, elevated selenium, and other contaminants (Saiki et al., 1992). A high frequency

( 30 % ) of stillbirths occurred in the single remaining species, mosquitofish Gumbusiu

uffiniJ (Saiki et ul., 1991). Laboratory studies conducted by the U. S. Fish and

Wildlife Service confirmed the field assessment that selenium in irrigation drainage

was the cause of the fish and wildlife problem (Lemly et al. , 1993). The “poisoned”

refuge became highly publicized and sparked a great deal of political and scientific controversy (Marshall, 1985; Popkin, 1986; Harris, 1991).

The findings at Kesterson National Wildlife Refuge led to a new awareness of the

environmental hazards posed by selenium in agricultural irrigation drainage. In 1986,

the U.S. Department of the Interior, the Federal steward of more than 400 irrigation-drainage facilities and 200 wildlife refuges in the western states (U. S. Bureau of

Reclamation, 1981)) established a multi-agency program to investigate irrigation-related drainwater problems. This program conducted screening-level assessments in 13

states, including 20 national wildlife refuges (Table 1) . The western San Joaquin

Valley and Kesterson National Wildlife Refuge were used as models for identifying

and prioritizing potential study areas based on the occurrence of conditions known to

contribute to drainwater problems. Samples of water, sediment, and biota (invertebrates, whole-fish, bird liver, bird eggs) were analyzed for a variety of trace elements, heavy metals, and pesticides, and the results were compared to concentrations

known to be toxic to fish and wildlife in experimental studies. Geological and hydrological studies were’ conducted and, where possible, observations were made to document the occurrence of deformed embryos and hatchlings, which is a biomarker for

selenium poisoning in birds (Hoffman and Heinz, 1988).

By 1992 it was known that eleven of the sixteen study areas where biological

samples had been taken were seriously contaminated by selenium. The concentrations

present at these eleven sites exceeded toxicity thresholds for fish and wildlife (Presser

et ul., 1994) . These study areas are spread across nine states (Fig. 4) Overt selenium toxicosis -i. e. , deformities in bird embryos and hatchlings-was found in five

states; California, Utah, Wyoming, Nevada, and Montana (Fig. 4, Table 1). In

some cases, these teratogenic effects occurred even though the waterborne concentrations of selenium were below those recommended by the U. S EPA for the protection

of aquatic life (Lemly et al. , 1993).

The biogeochemical conditions leading to the production of subsurface irrigation

drainage, culminating in death and deformities in wildlife, have been termed the

“Kesterson Effect” (Presser, 1994). The Kesterson Effect is prevalent throughout

the western United States and consists of these key conditions: (i) a marine sedimentary basin that contains Cretaceous soils, which usually have relatively high concentrations of selenium; (ii) alkaline, oxidized soils that promote the formation of watersoluble forms of selenium and other trace elements; (iii) a dry climate in which evaporation greatly exceeds precipitation, leading to salt buildup in soils; (iv) subsurface

layers of clay that impede downward movement of irrigation water and cause waterlogging of the crop root zone; and ( v) subsurface drainage, by natural gradient or

buried tile drainage networks, into migratory bird refuges or other wetlands.
424 A. DESNIS LEMLY

TABLE 1

Study Areas and National Wildlife Refuges Investigated m the U.S. Department of the Interior’s

Irrigation Drainage Program ( Lemly er al. , 1993)

State and Study Area National Wildife Refuge (NWR)

- -Oregon

Malheurb

Oregon/California

Malheur NWR

California

Klamath Basin

Sacramento Complex

Tulare Lake Bed’

Salton Scab

California/Arizona

Lower Colorado River

Nevada

Utah

Montana

Colorado

Wyoming

Lower Klamath NWR

Sacramento NWR

Delevan NWR

Colusa NWR

Sutter NWR

Kern NWR

Pixley NWR

Tule Lake NWR

Salton Sea NWR

Havasu NWR

Cibola NWR

Imperial NWR

Stillwater’

Middle Green River’

Sun River’

Milk River Basin

Gunnison River Basinb

Pine River

Kendrick Project’

Riverton Projectb

Stillwater NWR

Ouray NWR

Benton Lake NWR

-

-

-

Bowdoin NWR

-

South Dakota

Belle Fourche Projectb

Angostura Project

Kansas

Middle Arkansas Riverb

Texas

Lower Rio Grande Valley

New Mexico

Middle Rio Grande Valley

Idaho

American Falls Reservoir

-

-

-

Laguna Atascosa NWR

Basque de1 Apache NWR

Minidaka NWR

’ Study areas where overt symptoms of selenium toxicosis (deformities) were found in young migratory birds.

’ Study areas where toxicity is predicted based on concentrations of selenium found in fish and bird tissues.
SELENIUM IN THE ENVIRONMENT 425

F1c.4. Locations in the western United States where selenium in subsurface agricultural irrigation drainage has poisoned fish and wildlife. 1 = Malhew National Wildlife Refuge (NWR) ; 2 = Stillwater NWR; 3 = Tulare

Lake Bed Area: 4 = Salton Sea Area; 5 = Benton Lake NWR; 6 = Belle

Fourche Reclamation Project; 7 = Bowdoin NWR; 8 = Riverton Reclamation Project; 9 = Ouray NWR; 10 = Gunnison River Basin: 11 = Middle

Arkansas River. Teratogenic deformities associated with selenium bioaccu-.

mulation in young birds were found at locations 2, 3. 5. 7, and 9.

The field studies conducted by U. S. Department of the Interior indicate that the

toxic threat of selenium-laden irrigation drainage to wetlands, fish, and wildlife is not

restricted to Kesterson National Wildlife Refuge, the San Joaquin Valley, or the State

of California. Contamination has proven to be pervasive throughout the western states

(Fig. 4 > and threatens waterfowl populations in the Central and Pacific flyways

(Presser et al. , 1994; Skorupa et al., in press). Managers of wetlands in the western U. S. and elsewhere must recognize selenium-laden irrigation drainage as a threat

with the potential to affect wildlife populations on an international scale.

THREATS TO HUMAN HEALTH

Excessive selenium in the environment can threaten public health in the same

way it threatens fish and wildlife, i.e. , by accumulating in potential food items. In

some locations soils that are naturally high in selenium may cause selenium concentrations in agricultural crops to be excessive, leading to chronic poisoning in humans
426 A. DENNIS LEMLY

(Yang et al., 1983). For situations in which human activities have led to contaminated aquatic systems, public health risks are associated with consumption of selenium-contaminated fish and wildlife. The U. S. National Academy of Sciences and the

U.S. Environmental Protection Agency recommend that a daily intake of 50.2OOvg

selenium should be adequate for nutritional requirements in adults (National Research

‘Council, 1980b; U.S. EPA, 1984). Th e dose necessary to cause chronic selenosis in

humans is not well defined but the threshold for toxicity appears to lie somewhere in

the range of GO-9OOpg per day (Yang et al., 1989a, 1989b; Longnecker et al.,

1991) . Thus, the margin of safety for selenium, i. e. , the difference between the dietary levels that are beneficial and those that are possibly harmful, is small-a factor

ranging from about 5 to 18.

In Case Example 2, public health agencies recognized the possibility that selenium poisoning could occur in humans that ate fish and wild game taken from contaminated sites. Federal land management authorities erected warning signs at these locations to alert the public to the health risks associated with selenium contamination and

guard against consumption of contaminated food (Fig. 5) . Dietary guidelines formulated by the California Department of Health stipulated that adults should eat no more

than one meal (4 ounces) of fish or wild game per 2 weeks (Moore et al. , 1990).

Children less than 15 years of age and women of childbearing age were advised not to

eat any fish or wild game due to concerns about potential reproductive and developmental effects. Advisories were issued when the selenium concentrations reached or

exceeded 2 pg/g wet weight (Fan et al. , 1988 > . The rationale for this threshold

concentration was as follows: By simple calculation, fish or game containing 1 ,ug/g

selenium contributes 113 pg per 4 oz serving. At 2 ,ug/g the single serving would contribute 226 pg, which exceeds the upper limit of the recommended daily intake

GOVERNMENT PROPERTY

NO TRESPASSING

Potential health risk from

selenium contamination

FI G. 5. An example of the signs used to

alert the public of the health risks from selenium contamination at Federally managed

wetlands in the western United States.
SELENIUM IN THE ENVIRONMENT 427

(200 pg) This exceedance would be due to a single meal, not including other daily

intake. Therefore, a concentration of 2 pg/g was designated as the action level for issuing consumption advisories. A complete ban on consumption was issued and posted

at sites where concentrations of selenium in fish or bird tissues exceeded 5 ,ug/g wet

weig_ht (a concentration of 5 ,ng/g would contribute 565 I-(g per serving, which is in

excess of the 500 pg/day chronic toxicity threshold suggested by Levander, 1987).

The risks to public health in Case Example 2 prompted the first widely publicized

consumption advisories and bans due to excessive environmental selenium in the United States. These advisories were issued in 1984-85 (Fan et al., 1988). Since that

time, several other advisories have been issued for selenium contaminated reservoirs

and wetlands. For example, the fishery of Belews Lake (Case Example 1) began to

recover after 1986 as selenium levels fell, but the concentrations in fish tissues were

still great enough (3-8pg/g) to pose a threat to human health. This threat was recognized and advisories were issued begining in 1989 (Lemly, 1997a). The stipulations

of those advisories paralleled the ones given above. Warnings have also been posted at

several wildlife refuges contaminated by seleniferous irrigation drainage in the western

U. S (e.g., Stephens et al., 1992; Butler et al., 1994). It is now widely recognized in the U. S. that excessive selenium in the environment can, and does, pose a

threat to human health as well as fish and wildife. In regard to the two case examples

discussed in this paper, timely intervention by public health agencies prevented what

could have otherwise developed into episodes of human poisoning. Other countries

would be well advised to take note of these examples.

HAZARD ASSESSMENT AND ENVIRONMENTAL QUALITY CRITERIA

It is important to monitor and evaluate environmental conditions as a way of predicting, detecting, and, hopefully, avoiding potential selenium problems before they

occur. A hazard assessment protocol (Protocol) for selenium has recently been developed and is now available for use in this regard (Lemly, 1995, 1997b). The Protocol

characterizes hazard in terms of the potential for food-chain bioaccumulation and reproductive impairment in fish and aquatic birds, which are the most sensitive biological responses for estimating ecosystem-level impacts of selenium contamination. Five

degrees of hazard are possible depending on where the highest concentrations of selenium measured in environmental samples fall on the corresponding hazard profile given in the Protocol (Fig. 6) . The degree of hazard is given a numerical score: 5 = high

hazard, 4 = moderate hazard, 3 = low hazard, 2 = minimal hazard, and 1~ no identifiable hazard. A separate hazard score is given to each of five ecosystem components;

water, sediments, benthic macroinvertebrates, fish eggs, and aquatic bird eggs. A

final hazard characterization is determined by adding individual scores and comparing

the total to the following evaluation criteria: 5 = no hazard, 6-8 = minimal hazard, 9-

11 = low hazard, 12-15 = moderate hazard, 16-25 = high hazard ( Fig. 6, Table 2 ;

Lemly, 1995, 1997b).

Selenium hazards to fish can vary seasonally because of a condition known as

Winter Stress Syndrome (WSS; Lemly, 1993~ 1996a, 1997~). WSS is severe lipid

depletion brought on by external stressors in combination with normal reductions in

feeding and activity during cold weather. Fish can develop this syndrome in response

to chemical stressors such as water pollutants, or biological stressors such as parasites. Substantial mortality can result, potentially changing year-class strength and
428 A. DENNIS LEIMLY

population structure of the affected species, and altering community-level ecological

interactions. Selenium hazards should be evaluated in the context of seasonal metabolic changes that normally occur in test organisms. WSS could be an important cause of

mortality in many circumstances. Wastewater discharges containing selenium may

pose a greater toxic threat to fish during winter than at other times of the year (Lemly;- 1997d). A comprehensive protocol for aquatic hazard assessment should include

testing for WSS. Because of the possibility of WSS, conservative estimates of hazard

are necessary and the role of season in aquatic hazard assessment must be accounted

for.

TABLE 2

Example Data Sets for Aquatic Hazard Assessment of Selenium Followmg the Protocol Method

(Lemly, 1995)

Site and Environmental Selenium Evaluation by

Component Concentration” Component Totals for the Site

Haaardb Score Score Hazard

Wetland X

Water

Sediments

Invertebrates

Fish eggs

Bird eggs

Reservoir X

Water

Sediments

Invertebrates

Fish eggs

Bird eggs

River X

Water

Sediments

Invertebrates

Fish eggs

Bird eggs

< 1-3

0.7-l

1-3

2-4

2-7

9-93 High

7-41 High

12-72 High

75-120 High

12-120 High

3-4 Moderate

0.6-3 Low

3-33 High

8-27 High

1-17 Moderate

Low

None

Minimal

Minimal

Low

Low

3

1

2

2

3

11 11

5

5

5

5

5

25 25

4

3

5

5

4

21 21 High

High

“Selenium concentrations in pg/l (parts per billion) for water; mg/g (parts per million) dry weight for sediments, invertebrates, and eggs.

b Hazard ratings were determined by comparing selenium concentrations to hazard profiles given in Fig. 6.

In addition to the Protocol, which predicts environmental hazard, there are also

recent guidelines for evaluating the toxicological significance of selenium residues in
SELENIUM IN THE ENVIRONMEST 429

aquatic organisms and recommendations for water quality criteria to protect fish and

wildlife (Lemly, 1993a, 1996b). Diagnostic selenium concentrations are available for

water, food-chain, predatory fish (consuming fish or invertebrate prey), and aquatic

birds. Waterborne selenium concentrations of 2 pg/l or greater (parts per billion; total recoverable basis in 0.45~ filtered samples) should be considered hazardous to the

health a-rid long-term survival of fish and wildlife populations due to the high potential

for food-chain bioaccumulation, dietary toxicity, and reproductive effects. In some

cases, ultratrace amounts of dissolved and particulate organic selenium may lead to

bioaccumulation and toxicity even when total waterborne concentrations are less than

l&l.

Food-chain organisms such as zooplankton, benthic invertebrates, and certain

forage fishes can accumulate up to 30 ,ug/g dry weight selenium (some taxa up to 370

,ug/g) with no apparent effect on survival or reproduction. However, the dietary toxicity threshold for fish and wildlife is only 3 pg/g; these food organisms would supply

a toxic dose of selenium while being unaffected themselves. Because of this, foodchain organisms containing 3 pg/g (parts per million) dry weight or more should be

viewed as potentially lethal to fish and aquatic birds that consume them.

Biological effects thresholds (dry weight) for the health and reproductive success

of freshwater and anadromous fish are: whole-body = 4pg/g; skeletal muscle = 8pg/

g; liver = 12pg/g; ovaries and eggs = lOpg/g. Effects thresholds for aquatic birds

are: liver = 10 ,ug/g; eggs = 3pg/g. The most precise way to evaluate potential reproductive impacts to adult fish and aquatic bird populations is to measure selenium concentrations in gravid ovaries and eggs. This single measure integrates waterborne and

dietary exposure, and allows an evaluation based on the most sensitive biological endpoint. If natural resource managers obtain measurements of selenium in water, foodchain organisms, and fish and wildlife tissues, and apply the preceeding guidelines

and assessment protocol, they can accurately determine the overall selenium status

and health of aquatic ecosystems.

CONCLUSIONS

There have been several cases of selenium contamination in the United States

that have resulted in severe poisoning of fish and wildlife. Research studies of these

episodes have generated a data base that clearly illustrates the environmental implications of excessive selenium and the associated threats to public health. Moreover, the

data base has been, and continues to be, used to benefit future generations of wildlife

and humans by providing guidance on what the acceptable and unacceptable concentrations of selenium are from waterborne and dietary routes of exposure. It is hoped

that this information will be useful for developing countries and nations around the

world because they too may soon have to deal with many of the same problems. The

two faces of selenium-required nutrient and potent toxin-make it a paricularly important trace element in the health of both animals and man. Because of this paradox,

environmental selenium in relation to agriculture, fisheries, and wildlife will continue

to raise important land and water management issues for decades to come. If these issues are dealt with in a timely, prudent manner guided by the environmental selenium

data base, adverse impacts to natural resources and public health can be avoided.
430 A. DENNIS LEMLY

-_

Hazard from

accumulation in

planktonic foodchain and dietary

toxicity to fish

and aquatic birds

Hazard from

accumulation in

benthic foodchain and dietary

toxicity to fish

and aquatic birds

Hazard from

dietary toxicity

and reproductive

impairment in

fish and aquatic

birds

High

Moderate

Minimal

None

Cl l-2 2-3 3-5 z-5

Selenium in Water &t/l)

High -

Moderate -

Low -

Minimal -

None -

b

Minimal

None

Cl 1-2 2-3 3 - 4 >4

Selenium in sediments @g/g dry weight)

High

Moderate

-1

c2 2-3 3-4 4-5 >5

Selenium in macroinvertebrates @g/g dry wt.)
SELENIUM IN THE ENVIRONMENT 431

High -

_ Hazard from

_ reproductive Moderate -

impairment

Low- -/-1.--1

Minimal

None

c3 3-5 5-10 1 O-20 >20

Selenium in fish eggs @g/g dry weight)

Hazard from

reproductive

impairment

Minimal -

None -

c3 3-5 5-12 12-20 >20

Selenium in aquatic bird eggs @g/g dry wt.)

Fro. 6. Guidelines for rating hazard and predicting the toxic threat of selenium to fish and aquatic

birds based on selenium concentrations. Numerical scores are assigned to each hazard rating and

added to derive a final hazard estimate for the site (see text for explanation) .

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