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ELSEVI ER Aquatic Toxicology 57 (2002) 39 49 AIJIIATIE TllKlClMlE www.elsevicr.com~locatc~ayuatox Symptoms and implications of selenium toxicity in fish: the Belews Lake case example A. Dennis Lemly * Abstract Belcws Lake, North Carolina was contwminated by selenium in wastewater from a coal-fired power plant during the mid-1970s. and toxic impacts to the resident fish community (20 species) were studied for over two decades. Symptoms of chronic selcnitun poisoning in Belews Lake fish included, (1) tclangiectasia (swelling) of gill lamellae; (2) elevated lymphocytes; (3) reduced hematocrit and hemoglobin (anemia); (4) cornea1 cataracts; (5) exopthalmus (popeye); (6) pathological alterations in liver, kidney, heart, and ovary (e.g. vacuolization of parenchymal hepato- cytes, intracapillary proliferative glomerulonephritis. severe pericarditis and myocarditis, necrotic and ruptured mature egg follicles); (7) reproductive failure (reduced production of viable eggs due to ovarian pathology, and post-hatch mortality due to bioaccumulation of selenium in eggs): and (8) teratogenic deformities of the spine, head, mouth, and fins. Important principles of selenium cycling and toxicity were documented in the Belews Lake studies. Selenium poisoning in fish can be ‘invisible’, because, the primary point of impact is the egg, which receives selenium from the female’s diet (whether consumed in organic or inorganic forms), anti stores it until hatching, whereupon it is metabolized by the developing fish. If concentrations in eggs are great enough (about 10 p&/g or greater) biochemical functions may be disrupted. and tcratogenic deformity and death may occur. Adult fish can survive and appear healthy despite the fact that extensive reproductive failure is occurring- 19 of the 20 species in Belews Lake were eliminated as a result of this insidious mode of toxicity. Bioaccumulation in aquatic food chains causes otherwise harmless concentrations of selenium to reach toxic levels, and the selenium in contaminated sediments can be cycled into food chains for ciecades. The ~CSSOIIS learned ii-0111 Belews Lake provide information useful for protecting aquatic ecosystems as new sclenitm~ issues etncrge. ‘0 2002 Elsevicr Science B.V. All rights reserved. 1. Introduction One of the most extensive and prolonged casts of selenium poisoning in freshwater fish occurred at Belews Lake, North Carolina, USA (Fig. 1).

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Page 1: AIJIIATIE TllKlClMlE - Southern Research · 3.3.2. Kidney At the ultrastructure level, the kidney of normal fish is quite similar to that of humans, and is made up of glomeruli, mesangial

ELSEVI ER Aquatic Toxicology 57 (2002) 39 49

AIJIIATIETllKlClMlE

www.elsevicr.com~locatc~ayuatox

Symptoms and implications of selenium toxicity in fish: theBelews Lake case example

A. Dennis Lemly *

Abstract

Belcws Lake, North Carolina was contwminated by selenium in wastewater from a coal-fired power plant duringthe mid-1970s. and toxic impacts to the resident fish community (20 species) were studied for over two decades.Symptoms of chronic selcnitun poisoning in Belews Lake fish included, (1) tclangiectasia (swelling) of gill lamellae; (2)elevated lymphocytes; (3) reduced hematocrit and hemoglobin (anemia); (4) cornea1 cataracts; (5) exopthalmus(popeye); (6) pathological alterations in liver, kidney, heart, and ovary (e.g. vacuolization of parenchymal hepato-cytes, intracapillary proliferative glomerulonephritis. severe pericarditis and myocarditis, necrotic and rupturedmature egg follicles); (7) reproductive failure (reduced production of viable eggs due to ovarian pathology, andpost-hatch mortality due to bioaccumulation of selenium in eggs): and (8) teratogenic deformities of the spine, head,mouth, and fins. Important principles of selenium cycling and toxicity were documented in the Belews Lake studies.Selenium poisoning in fish can be ‘invisible’, because, the primary point of impact is the egg, which receives seleniumfrom the female’s diet (whether consumed in organic or inorganic forms), anti stores it until hatching, whereupon itis metabolized by the developing fish. If concentrations in eggs are great enough (about 10 p&/g or greater)biochemical functions may be disrupted. and tcratogenic deformity and death may occur. Adult fish can survive andappear healthy despite the fact that extensive reproductive failure is occurring- 19 of the 20 species in Belews Lakewere eliminated as a result of this insidious mode of toxicity. Bioaccumulation in aquatic food chains causes otherwiseharmless concentrations of selenium to reach toxic levels, and the selenium in contaminated sediments can be cycledinto food chains for ciecades. The ~CSSOIIS learned ii-0111 Belews Lake provide information useful for protecting aquaticecosystems as new sclenitm~ issues etncrge. ‘0 2002 Elsevicr Science B.V. All rights reserved.

1. Introduction

One of the most extensive and prolonged castsof selenium poisoning in freshwater fish occurredat Belews Lake, North Carolina, USA (Fig. 1).

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Belews Lake was contaminated by selenium inwastewater released from a coal-fired electric gen-erating facility. From 1974 to 1986, water waswithdrawn from the lake and mixed with bottomash from the coal burners and fly-ash collected byelectrostatic precipitators. This slurry waspumped from the power plant and discharged intoa 142 Ha ash basin, where suspended solids werecollected by gravitational settling. Selenium-laden(150-200 1-1s Se per 1) return flows from the ashbasin entered the west side of Belews Lakethrough an ash sluice water canal (Lemly, 1985).

Selenium bioaccumulated in aquatic foodchains and caused severe tissue pathology andreproductive impairment in the resident fish com-munity (Lemly, 1985; Sorensen, 1986). In late19X6, the power plant stopped discharging sele-

I BELEWS LAKE /0 1 2

FORSYTI-ICOUNTY

COUNTY i COUNTY

nium-laden water into the lake, and a period ofnatural recovery began. However, monitoringstudies revealed that the rate of recovery wasslow-elevated selenium residues and associatedbiological effects in fish were still present a decadelater (Lemly, 1997).

The Belews Lake episode provides a wealth ofinformation on environmental cycling, long-termpersistence, and hazard of selenium to freshwaterbiota. It is an excellent case example for examin-ing the symptoms and biological consequences ofselenium toxicity. This paper utilizes that data-base to present a review of the pathology ofselenium poisoning in fish. It also discusses theecological lessons learned from Belews Lake andpoints out the need to evaluate new, emergingselenium issues that threaten aquatic habitats inthe USA and elsewhere.

2. Biochemical basis of selenium toxicity

The primary manifestations of selenium toxicityare due to a simple but important flaw in theprocess of protein synthesis. Sulfur is a key com-ponent of proteins, and sulfur-to-sulfur linkages(ionic disulfide bonds) between strands of aminoacids are necessary for protein molecules to coilinto their tertiary (helix) structure which, in turn,is necessary for proper functioning of proteins,either as components of cellular structure (tissuesynthesis) or as enzymes in cellular metabolism.Selenium is similar to sulfur with regard to itsbasic chemical and physical properties (has samevalence states and forms analogs of hydrogensulfide, thiosulfate, sulfite, and sulfate), and mam-malian studies show that cells do not discriminatewell between the two as proteins are being synthe-sized (it is assumed that the mechanistic featuresunderlying toxicity are essentially the same forfish, since the resulting pathology and teratogenicfeatures are the same). When present in excessiveamounts, selenium is erroneously substituted forsulfur, resulting in the formation of a triseleniumlinkage (Se-Se-Se) or a selenotrisulfide linkage(SSeeS), either of which prevent the formation ofthe necessary disulfide chemical bonds (S-S). Theend result is distorted, dysfunctional enzymes and

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protein molecules, which impairs normal cellularbiochemistry (Canther, 1974; Stadtman, 1974;Diplock and Hoekstra, 1976; Reddy and Mas-saro, 1983; Sunde, 1984). Thus, while selenium isa sulfur analog in some respects, its biochemistryand potential toxicity are quite different.

These selenium-induced errors in proteinbiosynthesis can have several outcomes. The mostwell documented overt toxic symptom in fish isreproductive teratogenesis. Selenium consumed inthe diet of adult fish is deposited in the eggs,where it is metabolized by larval fish after hatch-ing. A variety of lethal and sublethal deformitiescan occur in the developing fish, affecting bothhard and soft tissues (Lemly, 199322). Substitutionof selenium for sulfur can also impair properformation of proteins in juvenile and adult fish,and many internal organs and tissues can developpathological alterations that are symptomatic ofchronic selenosis (Sorensen, 1986). Studies inmammals and waterfowl show that acute toxicresponses may also involve tissue damage frombioreactive superoxides produced in response tohigh concentrations of selenium (O’Toole andRaisbeck, 1998).

3. Pathological effects in fish

3.1. Gills

The primary structure of adult teleost gills isthe semi-circular gill arch, usually four pairs.Each arch contains a double row of filaments, andeach filament has a row of microscopic lamellaeprojecting from each side (Fig. 2). The lamellaecontain the blood sinusoids and capillary beds,and are covered by a thin epithelial cell layer,typically two cells thick, underlain by supportingpillar cells which maintain patency of vascularlumina. Gill lamellae are normally thin, delicatestructures (Fig. 221). which are necessary for effec-tive gas exchange in respiration. Gills from greensunfish (Lqwn~i.s C~W~W/~US) exposed to seleniumcontamination in Belews Lake exhibited exten-sively dilated blood sinusoids and swollen lamel-lae (telangiectasia) packed with erythrocytes (Fig.2b; Sorensen et al., 1984). Hemorrhaging of the

gill tissue often occurred in association with thiscondition. Selenium-induced dilation of gill lamel-lae causes impaired blood flow, ineffective gasexchange (reduced respiratory capacity), andmetabolic stress response (increased respiratorydemand and oxygen consumption) that can leadto death (Lemly, 1993b).

Green sunfish from Belews Lake exhibited sig-nificantly reduced hematocrit values (packed ery-throcyte volumes) as compared with fish from anuncontaminated reference lake (33 vs. 39%). bulh a d significantly elevated numbers o flymphocytes. Thrombocytes constituted a higherpercentage of total leucocytes in Belews Lake fish,but hemoblasts were less numerous than in refer-ence fish (Sorensen et al., 1984). These shifts inhematological parameters reflect importantchanges in the overall health of fish. Reductionsin hematocrit are associated with anemia and

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lowered mean corpuscular hemoglobin concentra-tion (MCHC; Lemly, 1993b). Reduced MCHCcauses impaired respiratory capacity, because, se-lenium can bind to hemoglobin, rendering it inca-pable of carrying oxygen. A decrease inrespiratory capacity can quickly lead to metabolicstress, because, the fish must expend more energyto meet respiratory demands (Lemly, 1993b).Lower numbers of hemoblasts reflects reducederythropoiesis and delayed replacement of agingred cells in circulation, which also contributes toreduced respiratory capacity and metabolicstress (Lemly , 1 9 9 3 b ) . A n e l e v a t i o n i nlymphocytes signals a generalized immune re-sponse triggered by physiological stress and areduced state of health.

3.3.1. J!hP?The structural features of liver tissue from nor-

mal green sunfish consist of bilaminar arrays ofhepatocytes (liver plates) separated by small bloodsinusoids. Blood enters the liver from the hepaticartery and hepatic portal vein, moves between theliver plates in the sinusoids, and ultimately col-lects in central veins which empty into the hepaticveins. Parenchymal hepatocytes typically containnumerous mitochondria, rough endoplasmicreticulum, well developed nucleoli, and both cen-tral and peripheral chromatin islands (Sorensen,1986). Kupffer cells, (phagocytic tissue histocytes)are rarely present in healthy individuals, andlymphocytes are not numerous. Green sunfishfrom Belews Lake exhibited several histopatho-logical changes in l iver t issue. Lymphocyteinfiltration was apparent along with extensive vac-uolization of parenchymal hepatocytes aroundcentral veins. Increased numbers of Kupffer cellswere present and the central veins were distendedand swollen due to loss of surrounding parenchy-ma1 cells. Cell nuclei were often deformed andpleomorphic, and numerous perisinusoidal lipiddroplets (unmetabolized residues) were present(Sorensen et al., 1984). Collectively, these ultra-structural changes reflect a degeneration of tissuestructure that is sufficient to significantly alterliver function. This liver pathology syndrome is

characteristic of chronic selenosis in fish and othervertebrates (Sorensen, 1986).

3.3.2. KidneyAt the ultrastructure level, the kidney of normal

fish is quite similar to that of humans, and ismade up of glomeruli, mesangial cells, podocytes,endothelial and tubular cells, and both capillaryand central veins (which collect and transporturine). Belews Lake green sunfish that had accu-mulated high levels of selenium showed focal in-tracapillary proliferative glomerulonephritis(Sorensen et al., 1984). In this condition, excessivenumbers of mesangial cells are present along withan abnormally abundant matrix and periglomeru-lar fibrosis (which can lead to a hardening of thetissue). Numerous tubular casts were present, andtubular epithelium was desquamated, vacuolated,and often destroyed (which can render the tubularsystem of the mesonephros incapable of function-ing properly). These renal changes in Belews Lakefish were consistent with symptoms of chronicselenium poisoning in other vertebrates (Sorensenet al., 1984).

3.3.3. HeartA clear pathological pattern occurred in the

hearts of fish from Belews Lake. The pericardialspaces surrounding the heart were filled with infl-ammatory cells, which were not present in fishfrom reference locations. This condition was diag-nosed as severe pericarditis. Numerous inflamma-tory cells were also present within the ventricularmyocardial tissue, a condition known as my-ocarditis. The occurrence of pericarditis and my-ocarditis was attributed to the direct action ofselenium on heart tissue, coupled with indirecteffects of selenium on the kidney (inducedglomerulonephritis a n d associated uremia;Sorensen et al., 1984).

Ovaries of fish from Belews Lake containednumerous swollen, necrotic, and ruptured matureegg follicles, especially in gravid individuals. Nosuch pathology was observed in fish from refer-ence locations (Sorensen et al., 1984). These toxicsymptoms were a primary factor contributing to

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43

reproductive failure of fish in Belews Lake, whichaffected 19 species and totally altered the aquaticecosystem for over a decade (Lemly, 1985, 1997;see Section 41.

3.4. E,wr

One of the less well known symptoms of sele-nium poisoning in fish is the occurrence of sele-nium-induced cataracts. This condition can affectboth the lens and cornea, and has been inducedexperimentally in mammals by dietary exposureto selenite (Shearer et al., 1987). Fish from BelewsLake sometimes had cornea1 cataracts on theireyes (Fig. 3); none were found in fish from refer-ence lakes. Cataracts were present in up to 8.1%of fish examined in surveys conducted during1975- 1982, which was the period of maximumselenium concentrations in fish. By 1992, seleniumresidues had fallen in fish, commensurate withreduced selenium inputs to Belews Lake, and theprevalence of cataracts had also fallen, to about1% (Lemly, 1993a).

Another abnormality of the eyes that is associ-ated with selenium poisoning in fish is a conditionknown as edema-induced exopthahnus, or pro-truding eyeballs. One of the general physiologicalresponses of fish to high levels of selenium isedema, which is the accumulation of fluid in thebody cavity and head (Ellis et al., 1937). The fluid

results from tissue damage, specifically an upset incell permeability as a consequence of distortedselenoproteins in the membrane structure thatcauses internal organs to become ‘leaky’. Theexcess fluid can create pressure sufficient to swellthe abdomen and force the eyes to protrude fromtheir sockets (Fig. 4). Blood may be present in thefluid, resulting in noticeable hemorrhaging aroundthe eyes. Up to 21% of some fish species in BelewsLake exhibited exopthalmus, with the greatestprevalence occurring in crappie, Po~ri0si.v spp.(Lemly, 19932)).

Developmental malformations are among themost conspicuous and diagnostic symptoms of‘chronic selenium poisoning in fish. Terata arepermanent biomarkers of toxicity, and can beused to reliably identify and evaluate impacts ofselenium on fish populations (Lemly, 1997). De-

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formities in fish that affect feeding or respirationcan be lethal shortly after hatching (Fig. 5). Con-sequently, few individuals bearing terata will sur-vive to join the juvenile population. Terata thatare not directly lethal, but which distort the spineand fins, can reduce the swimming ability of fishand lead to increased susceptibility to preda-tion-an important indirect cause of mortality.These two factors generally prevent most de-formed individuals from surviving to adulthood.In Belews Lake, the reproductive impacts on pis-civorous species eliminated much of the predationpressure and allowed many of the deformed indi-viduals of non-piscivorous species to persist intothe juvenile and adult life stages (Lemly, 1985).

Several types of teratogenic deformities wereevident in Belews Lake fish, and many individualsexhibited multiple malformations. The most overtterata were spinal deformities consisting olkyphosis, lordosis, and scoliosis (Figs. 6-S). Lessobvious but no less common were terata involvingthe mouth and fins (Fig. 9; Lemly, 19933). Theprevalence of deformities varied among speciesand between years, reaching a high of 70’%1 ingreen sunfish during 1982. There was a closeparallel between levels of selenium in fish tissues

A

and frequency of deformities. Terata becamemore common as selenium increased from 1975 to1982, peaked in 19X2, and decreased in frequency

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Fig. 8. Outward appearance and X-ray image of selcnium-in-ciuccd tcratit in channel cat t ish (1~~rtrlwu.s /xrrwrtr/r/.r) fromBelews Lake. (A, Normal: 13. mild spinal deformity (kyphosisand lordosis); C, scvcr~’ deformities (kylhosis and scoliosis).

following the cessation of selenium inputs to thelake in 1986 (Lemly, 1993a). In 1996, seleniumresidues had fallen by 85 - 95’%, from their 1982high, and the prevalence of deformities was 6% orless (Lemly, 1997). An overall relationship be-tween tissue selenium burdens and incidence ofdeformities in the Belews Lake fish community isshown in Fig. 10 (Lemly, 1993a, 1997). BelewsLake was the first site to provide conclusive evi-dence that exposure to elevated selenium causesteratogenic deformities in natural populations offreshwater fish.

4. 1Scological implications

Selenium poisoning in fish can be ‘invisible’,because, the primary point of impact is the egg,which receives selenium from the female’s diet andstores it mntil hatching, whereupon teratogenicdeformity and death may occur. Adult fish cansurvive and appear healthy despite the fact thatmassive reproductive failure is occurring (Lemly,1985; Coyle et al., 1993). Consequently, fish popu-lations can decline or even disappear over thecourse of a few years for no apparent reason-unless one is cognizant of selenium’s insidiousmode of toxicity. In Belews Lake, fish populationsdisappeared over the course of 4 years (1974-1977), and by the time biologists documented

Fig. 9. Other teratogenic effects of selenium in Belews Lakefish, shown here in red shiners (Noriopis hdwd), includeddeformed mouth and jaws (top), and deformed upper llcadand vestigial pectoral tins (middle). Individual on bottom isnormal.

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46

Deformedfish(%I

60

5 0

4 0

3 0

2 0

1 0

0

0 10 20 30 40 50 60 70 80 90

Whole-body selenium concentration @g/g dry weight)

l-‘ig. IO. Relationship between whole-body concentrations of selenium and prevalence of tcratogenic deformities in the fishcommunity of Rclcws Lake, NC, during the period 1975 1996. Lines represent the best fit exponential function (cubic model,r’ = 0.881) for plots of data from all lish species combined.

changes in population structure associated withelevated selenium (Cumbie and Van Horn, l978),it was far too late to prevent the fishery fromcollapsing.

Selenium bioaccumulated in the aquatic foodchains of Mews Lake and caused severe repro-ductive failure in fish (Cumbie and V:m Horn,1978; Lemly, 1985). Concentrations of selenium inthe lake water averaged IO CL&/I (uncontaminatedreference locations had selenium concentrations< 1 @I), but were accumulated from 519 times(periphyton) to 3975 times (visceral tissue of fish)in the biota. The pattern and degree of accumula-tion were essentially complete within 2 years afterthe initial operation of the power plant, and per-sisted throughout the period of selenium dis-

charge into the lake (1974-1985). Highestconcentrations of selenium were found in fish,followed by benthic macroinvertebrates, plank-ton, and periphyton. The planktonic and detritalfood pathways exposed fish to potential dietaryconcentrations of selenium that were some 770and 510~- 1395 times the waterborne exposure,respectively.

Of the 20 species of fish originally present inBelews Lake, 19 were effectively rendered sterile,because of reproductive failure. Some persisted asadults for a few years, but eventually all 19 wereeliminated. Only one of the original resident spe-cies, the seieniurn-tolerant mosquitofish (Grzmlzl-sic/ cifj5ni.y Baird and Girard) survived relativelyunaffected, along with two introduced cyprinids.The fishery was decimated without massive fishkills, because of the subtle, yet lethal mechanism

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by which selenium impacts can occur. The severetoxic impacts in Belews Lake took place eventhough concentrations of waterborne seleniumwere only IO-20 times those in nearby uncontam-inated reservoirs; the flora and fauna containedabout lo-50 times as much selenium.

4.3. Persistence i7f impucts

In response to concerns about the fisheryproblems in Belews Lake the electric utilitycompany switched to a dry-ash handling systemthat disposed the waste in a landfill rather thana wet-basin. By late 1986, selenium-ladenwastewater no longer entered the lake (NCDN-RCD, 1986), and in subsequent years a stockingprogram was successful in re-establishing adultpopulations of sport fish (e.g. centrarchids suchas largemouth bass Micropterus salmoides Lace-pede, and bluegill Lepomis mcrcrochirzuRafinesque). Follow-up studies were conductedin 1996 to assess recovery of the ecosystem inBelews Lake (Lemly, 1997). Selenium concentra-tions and associated impacts to fish were mea-sured and compared with pre-1986 conditions todetermine how much change occurred duringthe decade since selenium inputs stopped. Find-ings were also examined using a hazard assess-ment protocol (Lemly, 1995) to determine ifecosystem-level hazards to fish and aquatic birdshad changed as well. Results showed that water-borne selenium fell from a peak of 20 pg/l be-fore 1986, to < 1 pg/l in 1996; concentrations inbiota were 85-95% lower in 1996. Hazard rat-ings indicated that high hazard existed prior to1986 and that moderate hazard was still presentin 1996, primarily due to selenium in the sedi-ment-detrital food pathway. Concentrations ofselenium in sediments fell by about 65.-75%during the period but remained sufficiently ele-vated (l-4 pg/g) to contaminate benthic foodorganisms of fish and aquatic birds. Field evi-dence confirmed the validity of the high hazardratings. Developmental abnormalities in youngfish persisted in 1996, indicating that selenium-induced teratogenesis and reproductive impair-ment were still occurring. Moreover, theconcentrations of selenium in benthic food or-

ganisms were sufficient to cause mortality inyoung bluegill and other centrarchids, becauseof Winter Stress Syndrome, which is a substan-tial (up to 33%) increase in the sensitivity of fishto selenium during cold weather (Lemly, 1993b,1996).At the ecosystem level, recovery in BelewsLake was very slow, with impacts on fish repro-duction evident 10 years after the input of sele-nium stopped (Lemly, 1997). The low inflow ofwater and long retention time (volume replace-ment time about 1500 days), combined with lowproductivity (oligotrophic), tend to reduce natu-ral flushing and enhance recycling of seleniumwithin the reservoir. Projections indicate thatseveral more decades may be necessary for theecosystem to fully recover (Lemly, 1997). Thelatent effects occurred, because, selenium per-sisted in sediments, where it was mobilizedthrough the food chain gradually, yet continu-ally, and accumulated to toxic levels in fisheggs. Impacts to reproduction persisted eventhough adult populations were re-establishedthrough a stocking program.

5. Conclusions

The findings from Belews Lake serve as clearevidence of how selenium can rapidly, yet insidi-ously, impact fish populations. Moreover, thiscase example demonstrates that selenium can ac-cumulate and be biologically magnified to toxiclevels when waterborne concentrations are only5- 10 pg/l. This information was instrumental inthe US Enviromnental Protection Agency’s deci-sion to lower the US national water qualitycriterion for selenium from 35 to 5 pg/l(USEPA, 1987).

In the United States, anthropogenic distur-bances have greatly increased the likelihood thataquatic ecosystems will experience elevated sele-nium. From the 1960s through the 198Os, twodisturbances stood apart as the major human-re-lated causes of selenium mobilization on a re-gional and national scale. These were, (1)combustion of fossil fuels; and (2) agriculturalirrigation of seleniferous soils in arid and semi-arid regions (Lemly, 1985; Lemly et al., 1993~).

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During the 199Os, other issues have emerged aspotentially important factors in the mobilizationand bioaccumulation of hazardous concentrationsof selenium, including, (1) phosphate mining; (2)use of constructed wetlands to treat selenium-laden wastewater; (3) accumulation of animalwaste at livestock feedlots and intensive rearingfacilities; and (4) landfill disposal of ash fromcoal-fired power plants. These new seleniumthreats may be sufficient to cause widespread,unihrseen impacts on fish populations (Lemly,1999). Lessons learned from Belews Lake regard-ill& the mode, rate, and persistence of seleniumtoxicity provide a foundation for protectingaquatic ecosystems as new selenium issues emergein the USA and elsewhere.

Acknowledgements

I am indebted to the Department of Biology atWake Forest University for facilities and technicalsupport that allowed me to investigate the land-mark selenium pollution event at Belews Lake,North Carolina. In particular, the assistance ofMichael Riggs and John Foil, Jr came at a pivotaltime and produced field data which became thecornerstone for understanding selenium bioaccu-mulation and toxicity in fish. The Media Produc-tion Service’s PhotoGraphics Lab at VirginiaTech University prepared illustrations.

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