United States FINAL DRAFT
Environmental Protection ECAO-CIN-G058
A°encv September, 1989
4>EPA Research and
Development
HEALTH AND ENVIRONMENTAL EFFECTS DOCUMENT
FOR SELENIUM AND COMPOUNDS
Prepared for
OFFICE OF SOLID WASTE AND
EMERGENCY RESPONSE
Prepared by
Environmental Criteria and Assessment Office
Office of Health and Environmental Assessment
U.S. Environmental Protection Agency
Cincinnati, OH 45268
DRAFT: DO NOT CITE OR QUOTE
NOTICE
document 1s a preliminary draft. It has not been formally released
.S. Environmental Protection Agency and should not at this stage be
I to represent Agency policy. It 1s being circulated for comments
ichnlcal accuracy and policy Implications.
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DISCLAIMER
This report Is an external draft for review purposes only and does not
constitute Agency policy. Mention of trade names or commercial products
does not constitute endorsement or recommendation for use.
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PREFACE
Health and Environmental Effects Documents (HEEOs) are prepared for the
Office of Solid Waste and Emergency Response (OSWER). This document series
1s Intended to support listings under the Resource Conservation and Recovery
Act (RCRA) as well as to provide health-related limits and goals for emer-
gency and remedial actions under the Comprehensive Environmental Response,
Compensation and Liability Act (CERCLA). Both published literature and
Information obtained for Agency Program Office files are evaluated as they
pertain to potential human health, aquatic life and environmental effects of
hazardous waste constituents. The literature searched for In this document
and the dates searched are Included In "Appendix: Literature Searched."
Literature search material Is current up to 8 months previous to the final
draft date listed on the front cover. Final draft document dates (front
cover) reflect the date the document 1s sent to the Program Officer (OSWER).
Several quantitative estimates are presented provided sufficient data
are available. For systemic toxicants, these Include Reference doses (RfDs)
for chronic and subchronlc exposures for both the Inhalation and oral
exposures. The subchronlc or partial lifetime RfO, 1s an estimate of an
exposure level that would not be expected to cause adverse effects when
exposure occurs during a limited time Interval I.e., for an Interval that
does not constitute a significant portion of the Hfespan. This type of
exposure estimate has not been extensively used, or rigorously defined as
previous risk assessment efforts have focused primarily on lifetime exposure
scenarios. Animal data used for subchronlc estimates generally reflect
exposure durations of 30-90 days. The general methodology for estimating
subchronlc RfDs 1s the same as traditionally employed for chronic estimates,
except that subchronlc data are utilized when available.
In the case of suspected carcinogens, RfDs are not estimated. Instead,
a carcinogenic potency factor, or q-|* (U.S. EPA, 1980b), 1s provided.
These potency estimates are derived for both oral and Inhalation exposures
where possible. In addition, unit risk estimates for air and drinking water
are presented based on Inhalation and oral data, respectively.
Reportable quantities (RQs) based on both chronic toxlclty and carclno-
genldty are derived. The RQ Is used to determine the quantity of a hazard-
ous substance for which notification 1s required In the event of a release
as specified under the Comprehensive Environmental Response, Compensation
and Liability Act (CERCLA). These two RQs (chronic toxldty and carclno-
genldty) represent two of six scores developed (the remaining four reflect
1gn1tab1lHy, reactivity, aquatic toxlclty, and acute mammalian toxldty).
Chemical-specific RQs reflect the lowest of these six primary criteria. The
methodology for chronic toxldty and cancer based RQs are defined In U.S.
EPA, 1984 and 1986b, respectively.
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EXECUTIVE SUMMARY
In the United States, selenium Is produced by recovering 1t from
by-products generated during the electrolytic refining of copper ore (Elkln,
1982; U.S. Department of Interior, 1982, 1988). In 1984, 559,078 pounds of
selenium were recovered from these by-products by three domestic producers.
Also, selenium Is recovered domestically from previously manufactured xero-
graphic drums and selenium rectifiers (USDI, 1982). Approximately 1 million
pounds of selenium were Imported 1n 1987 (USDI). The following are esti-
mates of selenium consumption by end-use categories In 1987 (USDI, 1988):
electronic and photocopier components, 43%; glass manufacturing, 20%; chemi-
cals and pigments, 20%; other (Including agriculture and metallurgy), 17%.
Because of Us photoelectric and semiconducting properties, selenium 1s used
primarily In the production of photocopying components, photoelectric cells,
photovoltaic cells and semiconducting rectifiers (Elkln, 1982).
Selenium Is an element; therefore, It does not degrade In the environ-
ment, It simply changes from one form to another. The ma.lor features of
selenium chemistry that affect Its fate and transport 1n the environment are
associated with changes In Us oxidation state and the resulting differences
1n chemical properties (Callahan et al., 1979). Because selenium only
changes form and does not degrade In nature, 1t undergoes an environmental
cycling process Involving soil, rocks, plants, animals, water and air (NAS,
1976). When released to the atmosphere In partlculate-phase, selenium 1s
removed by physical processes such as rainfall and settling (NAS, 1976).
Volatile selenium compounds are released to air by plant and mlcroblal
transformations (Zleve and Peterson, 1984; Chau et al., 1976), where they
react with sunlight-formed HO radical to form selenium dioxide and other
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compounds that can be transported physically to water and soil. In both
water and soil, the blomethylatlon of selenium to release volatile selenium
to air 1s an Important part of the environmental cycling process (Cooke and
Bruland, 1987; Z1eve and Peterson, 1984). Selenium In oxidation state +6
(selenate) 1s the most soluble and mobile selenium species In the soil and
water environments (Gruebel et al., 1987; Callahan et al., 1979). Because of
the solubility, stability and ability of selenate to be taken up by plants,
1t 1s considered the most dangerous form of selenium 1n relation to environ-
mental pollution 1s (NAS, 1976; Callahan et al., 1979).
Selenium Is distributed widely 1n the earth's crust, and with suffi-
ciently sensitive analytical techniques, selenium can be detected In
virtually all rocks and soil on the earth's surface (NAS, 1976). Because of
this ubiquitous distribution 1n the environment, the detection of selenium
1n air, water, soil, food and vegetation 1s expected (IARC, 1975). Selenium
1s released to the environment from natural sources such as volcanoes, rock
and soil erosion, sea sprays and volatile emissions from plants and micro-
flora (NAS, 1976; Arlmoto et al., 1985). Humans release selenium to the
environment through Incineration of coal, fuel oil and solid waste, from
emissions and waste streams generated through mining, refining and Indus-
trial applications (NAS, 1976; U.S. EPA, 1987a). More than half of the
human releases are attributed to the combustion of coal (NAS, 1976). Based
upon available monitoring data, the average selenium content of drinking
water Is ~0.2 ppb and the mean concentration In urban air 1s ~3 ng/m3
(Bennett, 1986). These concentrations can be used to estimate average dally
Intakes of 400 ng/day for water and 60 ng/day for Inhalation. The average
dally Intakes for water and Inhalation are small 1n comparison to the esti-
mated average dally Intake of 139 yg/day for food (Gartrell et al., 1986a).
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Acute toxldty data for selenium 1n aquatic vertebrates were available
for 21 species of fish and 1 amphibian. Among freshwater species, the
96-hour LCcgS for selenium as sodium selenlte ranged from 0.62 mg/l for
the fathead minnow, Plmephales promelas (Elsler, 1985) to 35 mg/l for the
common carp, CypMnus carplo (Etnler et al., 1987). Fathead minnows were
also the least tolerant vertebrate species to selenate-selenlum, with a
96-hour LC5Q of 2 mg/l 1n a flowthrough test (Etnler et al., 1987).
Zebraflsh, Brachyodanlo rerlo. and juvenile striped bass, Morone saxatnis.
were the most tolerant of exposure to selenate-selenlum, with 96-hour
LC5Qs of 82 and 85.8 mg/l, respectively (N11m1 and Laham, 1976; Klauda,
1986). The toxldty of selenium as selenium dioxide ranged from a 96-hour
LC5Q of 7.3 mg/l for fathead minnows to 20 mg/l for zebraflsh
(Cardwell et al., 1976; N11m1 and Laham, 1976).
Fathead minnows were equally sensitive to the sodium salts of selenlte
and selenate, while zebraflsh were equally sensitive to the potassium and
sodium salts of selenlte and selenate. The toxlclty of selenium as sodium
selenate to striped bass decreased nearly 10-fold as fish developed from the
prolarva to juvenile stage {Klauda, 1986). Toxldty values for saltwater
fish ranged from a 96-hour LC5Q of 0.6 mg/l for haddock larvae, Helano-
grammus aegHflnus. to 96-hour LC5_s of 14.2-15.1 mg/l for winter
flounder larvae, Pseudopleuronectes ameMcanus. exposed to unidentified
forms of selenium (Elsler, 1985).
In a series of behavioral and physiological studies, goldfish, Carasslus
auratus. exhibited behavioral Impairment at 0.25 ppm (Weir and Mine, 1970),
while fathead minnows, Plmephales promelas. did not avoid selenate at
concentrations of 0.3-11.2 mg Se/l (Watenpaugh and BeHlnger, 1985).
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Oxygen consumption by fathead minnows was not affected by exposure to 60 mg
Se/8, for 24 hours (Watenpaugh and BeHlner, 1985). Oxygen consumption by
the hermit crab.Cllbanarlus vlttatus. exposed to 100 ppm selenium was
depressed at 16°C 1n 10 o/oo salinity test medium, although oxygen consump-
tion rates were generally elevated at lower salinities and higher tempera-
tures (Wolfenberger, 1987).
Acute toxldty data for selenium In aquatic Invertebrates were available
for a total of 22 species, Including 3 cladocerans, 2 copepods, 4 amphlpods,
4 decapods, 1 mysld, 3 Insects and 5 molluscs. The 48-hour LC5Qs of
selenlte-selenlum to daphnlds ranged from 0.098-3.87 mg/a, (Etnler et al.,
1987; Reading and Bulkema, 1983). The 48-hour EC^s for unfed and fed
daphnlds exposed to sodium selenlte were 0.47 and 1.5 mg/l, repsectlvely.
The 48-hour NOEC for unfed daphnlds was 1.0 mg/8. (Adams and Heldolph,
1985). The 96-hour LC5Qs for amphlpods ranged from 2.88-6.17 mg/8,
(Etnler et al., 1987). The toxldty of selenlte-selenlum to Daphnla magna
was 4-fold lower when assays were conducted In soft water; no significant
differences were observed for Chlronomus plumosus. based on water hardness
(Mayer and Ellersleck, 1986).
The toxldty of selenium as sodium selenate to 5th Instar Daphnla magna
(48-hour LC,-ns of 0.55 and 0.75 ppm) was comparable to that observed for
sodium selenlte (Johnston, 1987). In contrast, the toxldty of selenate-
selenlum to Hyallela azteca (96-hour LC5Q of 0.76 mg/l) was 4- to 8-fold
greater than that observed with sodium selenlte (Etnler et al., 1987). The
toxldty of selenium as selenium dioxide was represented by 96-hour LC s
of 33, 1.90 and 0.25 mg/8. for the crab, Scylla serrata. bay scallop,
Arqopecten 1rrad1ans. and surf clam, Splsula sol1d1ss1ma. respectively
(KMshnaja, 1987; Nelson et al., 1988). The 96-hour LC5Q of selenium as
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selenium dioxide to crabs, oysters and mussels was >10 mg/a (Martin et
al.t 1981). The 96-hour LC5Q for the midge, Tanytarsus d1ss1m111s. was
42.4 mg/a (Elsler, 1985). Exposure of embryos of the zebraflsh, Brachy-
danlo rerlo, to <10 mg/a selenium as selenium dioxide for 168 hours did
not affect hatching and mortality. Exposure of zebraflsh larvae resulted In
significantly higher levels of mortality at concentrations >3 mg/a after
168 hours and at 10 mg/a after 96 hours (N11m1 and Laham, 1975).
The 168-hour LC5Q for fathead minnows, Plmephales promelas. was 2.9 mg
Se/a. The 336-hour LC5Qs for goldfish, Carrasslus auratus. and blue-
gills, Lepomls macrochlrus, were 8.8 and 17.6 mg Se/a, respectively
(Cardwell et al., 1976). The 113-hour LC™ for embryos and the 7-day
LC5Q for tadpoles of the frog, Xenopus laevls. were 2.0 and 1.5 mg Se/a,
respectively (Elsler, 1985). The 48-day LC5Qs for bluegllls, L. macro-
chlrus. and fathead minnow, P. promelas. were 0.4-2.0 and 1.1 mg Se/a,
respectively. The 10-day LC™ for perch, Perca flavescens. was 4.8
mg/a, while the 43-day LC,n for coho salmon, Oncorhynchus klsutch. was
0.16 mg/a. The 96-day LC5Q for rainbow trout, Salmo qalrdnerl. was 0.29
mg Se/a (Elsler, 1985).
Exposure of Daphnla maqna to 0.2-0.8 mg selen1te-selen1um/a for 28
days did not affect total eggs per daphnld or live young per daphnld;
however, mean brood size was affected at 0.8 mg Se/a (Reading and Bulkema,
1983). In another study, the 7-, 14- and 21-day EC5Qs for D. maqna
exposed to selenlte-selenlum were 0.38, 0.38 and 0.35 mg/a, respectively.
The NOEC based on survival and reproduction was 0.24 and >0.24 mg/a,
respectively. The 28-day LC,. for D. maqna 1n a third study was 0.24 mg
Se/a (Adams and Heldolph, 1985).
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Exposure of the amphlpod Allorchestes compressa to 44 yg selenlte-
selenlum/i did not significantly affect growth or survival of treated
Individuals after 4 weeks. Animals exposed to 93 yg Se/8, experienced
reduced growth and a significant level of mortality over the same period
(Ahsanullah and Brand, 1985). The 14-day LC5Q for another scud, Hyallela
azteca. was 0.07 mg Se/8. (Elsler, 1985).
Fathead minnow larvae, Plmephales promelas, experienced significant
reductions In final dry weight when larvae were fed rotifers cultured on
selenium-contaminated algae. The mean selenium concentrations In minnows
were 43 and 51.7 yg/g In two experiments (Bennett et al., 1986). High
tissue concentrations of selenium 1n blueglll sunflsh, Lepomls macrochlrus.
resulted 1n significant differences In percent fertilization and hatch when
the ovaries of females contained from 5.79-8.0 mg Se/kg. These levels were
16-21 times higher than those 1n uncontamlnated sunflsh (Glllesple and
Baumann, 1986).
Exposure of early life stages of the striped bass, Morone saxatllls. to
low (0.089-0.099 mg Se/l) and high (1.217-1.360 mg Se/i) concentrations
of selenate-selenlum resulted 1n a significant reduction In exponential
growth rates for fish 1n both treatments for days 3-15. There were no
differences In growth rates between days 19 and 60 but there was a signifi-
cant Incidence 1n developmental abnormalities of the lower jaw and severe
blood cytopathology (Klauda, 1986). Exposure of rainbow trout fry, Sal mo
galrdnerl, to >47 yg selenlte selenium/a resulted 1n significant reduc-
tions 1n survival and fry weight and length after 90 days. Survival and
growth were not affected at <21 yg Se/l. BCFs were Inversely related to
exposure concentrations but did not exceed 200. Exposure of fry to >12 yg
Se/a resulted 1n significant reductions 1n the calcium concentrations 1n
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bone (Hunn et al., 1987). Percent hatch of sheepshead minnows, CypMnodon
varlegatus. was <4X at concentrations of <3.6 mg selenlte-selenlum/i.
Juveniles experienced 4, 24 and 90X reductions In survival at 0.47, 0.97 and
>0.97 mg Se/l, respectively. Growth of juvenile sheepshead minnows was
reduced by 8X at 0.47 and 0.97 mg/l (U.S. EPA, 1987).
Exposure of four consecutive generations of Cer1odaphn1a afflnls to
sodium selenlte resulted 1n a reduction 1n the tolerance of C. afflnls over
succeeding generations. The NOEL was reduced from 0.2-0.1 mg/l after two
generations (Owsley and McCauley, 1986). There were no significant differ-
ences 1n growth of Daphnla maqna exposed to <0.05 ppm selenlte-selenlum or
In mean numbers of eggs produced, the percent maturation or mortality levels
for daphnlds exposed to <0.025 ppm selenlte-selenlum (U.S. EPA, 1987). The
number of offspring produced and survival of first generation myslds,
Mysldopsls bahla. exposed to selenlte-selenlum was significantly reduced at
0.32 mg/i. No statistically significant differences were observed In
myslds exposed to 0.14 mg/l (U.S. EPA, 1987).
The no-effect level for dietary selenium as either sodium selenlte or
selenomethlonlne In blueglll sunflsh, Lepomls macrochlrus. over 324 days Is
-13-30 yg Se/g. The maximum BCF for blueglll sunflsh, L. macrochlrus.
exposed to 120 yg Se (as selenous add)/l for 28 days was 20 and the
tissue half-life during a 7-day depuration period was between 1 and 7 (Woock
et al., 1987). BCFs for rainbow trout, Salmo qa1rdner1. exposed to <10 yg
selen1te-selen1um/kg ranged from 3.1 1n embryos to 104 1n livers of
juveniles. BCFs for trout exposed to ~100 yg selen1te-selen1um/kg ranged
from 1.6 1n sac-fry to 31.6 1n livers of Juveniles after 96 hours (Hodson et
al., 1986). The BCF for selenium as sodium selenlte In carp, Cvprlnus
carplo, for an unspecified exposure duration and selenium concentration was
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0.6-6.0. The BCF for selenlte-selenlum 1n minnows, Plmephales promelas.
exposed to 83 yg/8. for 28 days was 4443 (Etnler et al.. 1987).
Exposure of fathead minnows, Plmephales promelas. to waterborne
selenate-selenlum (10-40 ng Se/ml) resulted In a maximum body burden level
of -0.5-0.8 yg Se/g fish after 20-30 days. Selenium was depurated to ~3
yg/g after 30 days. Exposure of minnows to selenium-contaminated daphnlds
(1.33-7.32 yg Se/g) resulted In selenium body burden levels of -0.3-1.2
yg Se/g fish after 80 days. Depuration of selenium was slower than that
observed 1n fish exposed to waterborne selenium. Fish exposed to both
sources of selenium had body-burden levels of selenium that did not plateau
during the 56-day exposure phase, reaching 0.4-2.0 yg Se/g fish. Depura-
tion of selenium from these fish was slow (Bertram and Brooks, 1986). Fed
and starved juveniles of the striped bass, Horone saxat111s. exposed to 1.29
mg selenate-selen1um/a for 60 days accumulated selenium at comparable
rates, producing BCFs of 0.68 and 0.69. Fed juveniles exposed to 90 yg
Se/a showed no Increase 1n whole body levels of selenium, while starved
juveniles had a BCF of 11.78 (Klauda, 1986). The half-lives In days for
selenate, selenlte and selenometh1on1ne administered orally via gavage at a
level of 20 ng Se/g to fathead minnows, £. promelas. ranged from 3.9 (liver)
to 487 (adipose tissue), 2.2 (liver) to 64 (heart) and 1.0 (liver) to 69
(adipose tissue) (Klelnow and Brooks, 1986).
Mussels exposed to 50 yg selenium/4 for 15-50 days accumulated
selenlte-selenlum at a rate of 0.12 ng Se/g/day. The presence of Inorganic
(30 yg Hg/a) and organic (3 yg Hg/a) mercury Increased the uptake of
selenlte-selenlum to 0.24 and 0.40 ng Se/g/day, respectively. Organic
selenium (CQH,00Se)0 accumulated at a rate of 0.15 ng Se/g/day In
Old C
the presence of mercury (Pelletler, 1986).
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There were no apparent effects observed In growth of natural assemblages
of phytoplankton or In growth of a species Isolated from field samples
Thalassloslra aestevalls exposed to <1000 nM selenium (Holllbaugh et al.,
1980). There were no effects on growth of either the green or red algae,
Dunallella pMmolecta and Porphyr1d1um cruentum. exposed to 10 ppm
selenHe-selenlum (Gennlty et al., 1985). The 48-hour LC5Q for Oedogonlum
cardlacum was <0.1 mg/a, while the 96-hour LC™ for Anabaena var1ab111s
was 15-17 mg/l (Elsler, 1985). The 96-hour EC5Q for duckweed, Lemna
minor, exposed to selenium was 2.4 mg/B, (Wang, 1986).
Population growth of Tetrahymena pyMformls was Inhibited by 1.4 ppm
selenium and stopped completely at 140 ppm (Tang et al., 1985). T.
pyrlformls also experienced a dose-dependent Inhibition 1n division of
synchronized cells exposed to 10, 20, 50 and 100 ppm selenium (as SeO?)
(Cao and Tang, 1985). Growth of cultures of the algae, Chlorella vulgarls
and Phorm1d1um foveolarum. was reduced by -40% In the presence of 0.25 ppm
selenate-selenlum. Growth of £. vulgarls 1n a 4.0 ppm solution of selenium
was 97% of that observed 1n controls and completely Inhibited 1n P. foveo-
larum (Trlpathl and Pandey, 1985). Selenium retarded growth of the marine
dlnoflagellate, Prorocentrum mlcans. 1n cultures Incubated with 100 and 1000
ppm selenium. Growth was slightly enhanced at 10 and 50 ppm selenium for
the first 15 days of treatment but was Increasingly Inhibited compared with
controls after 15 days. Growth of the marine dlnoflagellate, Crypthecodln-
1um cohnll. was severely Inhibited by selenium at >10 ppm selenium within
1.5 days of the Initiation of treatment (Prevot and Soyer-Goblllard, 1986).
Concentrations of selenium 1n soil and earthworms ranged from trace
levels to 1.3 mg/kg at an Industrial site and from trace quantities to 7.6
mg/kg, respectively (Bayer and Cromartle, 1987). In an experimental field
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study, the concentration of selenium 1n earthworms, Aporrectodea tubercu-
lata. Aporrectodea turglda. and Lumbrlcus rubellus. from control plots (<0.1
mg Se/kg soil) was 16 mg/kg, while concentrations of selenium 1n worms from
treated plots were 36, 43, 51, 36 and 78 mg/kg. Uptake of selenium by worms
was not Influenced by pH or other soil variables (organic matter content,
phosphorous, potassium or magnesium) (Beyer et al., 1987). The 8-hour
LD5Qs for selenlte and selenate In earthworms, Lumbrlcus terrestMs.
treated Intraperltoneally were 31 and 60 mg/kg, respectively (Serda and
Furst, 1987).
Exposure of American coot, Fullca amerlcana, mallard, Anas platy-
rhynchos. northern pintail, Anas acuta. cinnamon teal, Anas cyanoptera.
gadwall, Anas strepera. black-necked stilt, Hlmantropus mexlcanus. American
avocet, Recurvlrostra amerlcana. and eared grebe, Podlceps nlgrlcolHs. to
selenium-contaminated Irrigation dralnwater ponds (~300 ppb Se) resulted 1n
an Increase 1n reproductive Impairment. Frequency of dead and abnormal
embryos ranged from 2.5 (ducks) to 31.7% (grebes) and 4.0 (ducks) to 8.8%
(coots), respectively. Overall, 19.6% of the 347 nests monitored produced
at least one embryo or chick with an abnormality. There were no abnormali-
ties In embryos of birds from 92 nests 1n an uncomtamlnated area over a
2-year period. Average selenium concentrations In bird livers and eggs from
nests 1n contaminated areas ranged from 9.1-81.4 ppm dry weight, compared
with 4.1-6.1 ppm 1n livers of birds from an uncontamlnated area. The
no-effect level for dietary selenium as sodium selenlte or selenometh1on1ne
1n mallard ducklings, Anas platyrhynchos. 1s ~10 ppm (Ohlendorf et al.,
1986).
Concentrations of selenium In water and sediment from two bays on the
Gulf Coast of Texas were 0.11 and 1.44 mg/kg. Concentrations of selenium 1n
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barnacle, Balanus aburneus. crab, CalUnectes sapldus. oyster, Crassosstrea
v1rq1n1ca. clam, Ranqla cuneata. and polychaete, Nereis sp., from those bays
were 0.77, 0.08, 0.14, 0.54 and 0.49 mg/kg wet weight, respectively (Guthrle
et al., 1979). The level of selenium In algae, Euglena sp., from tailing
areas of the Elliot Lake mining district, Canada, was 2700 ng/g dry weight,
compared to a concentration of 0.2 ng/g 1n world river water (Mann et al.,
1988). Selenium concentrations 1n water, sediment, and clam valves and
viscera of Asiatic clams, Corblcula flumlnea. from a control site In the New
River, Virginia, were 0.11, 0.88, 0.29 and 3.90 ppm, respectively. Selenium
concentrations In samples from sites receiving thermal effluent discharges
were 0.10, 0.60, 0.50 and 16.5 ppm, respectively (Rodgers et al., 1980).
The concentrations of selenium In water and sediment 1n the upper
Mississippi River were below detection (1 yg/i and ~0.2 yg/g, respec-
tively) but concentrations of selenium In fillets, livers and kidneys of
common carp ranged from 0.161-0.356, 0.858-2.17 and 0.943-1.62 yg/g wet
weight, respectively. Concentrations of selenium 1n fillets from smallmouth
bass and sauger ranged from 0.36-0.425 and 0.284-0.369 yg/g wet weight,
respectively. Concentration factors for the edible tissue of common carp
ranged from 322-712 (Boyer, 1984).
Concentrations of selenium 1n surface and bottom waters of a cooling
water reservoir ranged from
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levels >5 yg/g wet weight after 20 weeks (Woock and Summers, 1984). In a
separate study, concentrations of selenium 1n the water column of a power
plant cooling reservoir were 20-30 times higher than background levels with
a mean value of 10 yg/l, while concentrations 1n flora and fauna were
10-15 times background levels. Concentrations of selenium 1n surface sedi-
ments were ~4 yg Se/g wet weight. Selenium was 519- and 3975-fold higher
1n perlphyton and fish, respectively, than 1n water (Lemly, 1985a).
Concentrations of selenium 1n water from utility wastewater treatment
basins were 7.0, 3.0, <2.0, <2.0 and <2.0 yg/l. Concentrations of
selenium In black crapple, Pomoxls nlgromaculatus. pumpklnseed, Lepomls
aurltus. brown bullhead, Ictalurus nebulosus. and carp, Cyprlnus carplo.
from these basins ranged from 2.7-37.6 mg/kg (Skinner, 1985). Concentra-
tions of selenium 1n carcasses of bluegllls, Lepomls macrochlrus. and large-
mouth bass, Mlcropterus salmoldes from cooling water reservoirs that receive
ash pond effluent ranged from 4-9 ppm. Selenium concentrations 1n gonads
varied between sexes within reservoirs with significantly higher levels
(<2-fold) In ovaries (<1 to -12 ppm) than In testes (<1 to ~7 ppm).
Selenium concentrations In carcasses of bluegllls and bass from a cooling
water reservoir that did not receive ash pond effluent was ~1 ppm. Selenium
concentrations 1n carcasses of bluegllls and bass from a municipal water
reservoir were <0.5 ppm (Baumann and Glllesple, 1986).
Concentrations of selenium 1n oysters, Crassostrea vlrqlnlca. and
sediment from a site In Lake Pontchartraln, Louisiana, were 0.013 and 0.007
yg/g dry weight, respectively. Concentrations of selenium In clams,
Rangla cuneata. and sediment from a second site were 0.032 and 0.031 yg/g
dry weight, respectively. Concentrations of selenium 1n clam tissue and
sediment from a third site were 0.041 and 0.05 yg/g dry weight, respec-
tively (Byrne and DeLeon, 1986).
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A selenium concentration of 14 yg/g was measured at the northern end
of Lake Macquarle, New South Wales, but the concentration decreased rapidly
to a plateau level of 4 yg/g. Concentrations of selenium In seagrass,
Zostera capMcornl. from the northern and southern sections of the lake were
~3.9 and ~0.6 yg/g, respectively. Concentrations of selenium 1n algae
Enteromorpha sp. were higher In samples collected from the northern section
of the lake, ranging from 0.3-1.6 yg/g. Whole body concentrations of
selenium In mussels, Trlchomya hlrsuta. and cockles, Anadara trapezia, from
the northern end of the lake were 3.3 and 6.4 yg Se/g, respectively
(Bailey, 1987).
Phytoplankton from Xiamen Bay, Fujlan Province, China contained 1.24 ppm
selenium, while seaweed concentrations ranged from 0.08-0.61 ppm. The
concentration of selenium 1n zooplankton ranged from 2.16-6.30 ppm. Concen-
trations of selenium In other Invertebrates and fish were approximately
equal to those found In zooplankton on a dry weight basis but concentrations
were dependent on the tissue analyzed (L1u et al., 1987).
Selenium concentrations 1n the top 10 cm of sediment from 14 Ontario
lakes ranged from <1-16 yg/g. Concentrations of selenium 1n tissues of
lake trout, whHeflsh, common sucker, yellow perch, northern pike and
walleye from the study lakes were 0.78, 0.84, 0.55, 0.38, 0.37 and 0.25 yg
wet we1ght/g, respectively (Johnston, 1987).
Concentration ranges for selenium 1n water and sediment from the San
Luis Drain, Kesterson ponds and Volta waterways In California were 0.29-0.33
and 65-100, 0.009-0.32 and 1.8-67, and 0.0002-0.0014 and <0.2-0.5, respec-
tively. Concentration ranges for selenium In algae and net plankton In
these systems were 63-72 and not measured, 12-330 and 58-120, and below
detection-!.4 and 1.4-2.8, respectively. Concentration ranges for selenium
xvl
-------
In all aquatic Insects and mosquHoflsh In these systems were 170-330 and
140-370, 16-290 and 104-290, and 0.68-3.0 and 1.2-1.4, respectively. The
Investigators noted that selenium concentrations generally Increased from
water to sediments to plants to animals (Salkl and Lowe, 1987).
Mean selenium concentrations In kidney, liver and muscle of dolphins,
Laqenorhynchus alblrostrls. were 5.85, 8.15 and 1.91 mg/kg dry weight,
respectively. Selenium concentrations 1n blubber, kidney, liver and muscle
of pilot whales, Globlcephala melaena, from two different collection sites
were 0.49 and 0.59 (mg/kg wet weight), 13.0 and 11.3, 50.5 and 31.4, and
1.22 and 2.94 mg/kg dry weight, respectively (Mulr et al., 1988).
BCFs for phytoplankton, perlphyton and plants exposed to selenium 1n the
field ranged from 237-1320, 158-1070, and 166-24,400, respectively. BCFs
for zooplankton, Insects, annelids, crustaceans and molluscs exposed to
combined waterborne and dietary sources of selenium under natural conditions
1n the field ranged from 176-2080, 371-5200, 770-1320, 420-1975 and
600-2550, respectively. BCFs for carnivorous, planktlvorous and omnivorous
fish 1n the field ranged from 590-35,675, 445-27,000 and 364-23,000,
respectively (Lemly, 1985b).
Addition of selenium to field mesocosms resulted 1n a replacement of
chrysophytes by chlorophytes In low dose enclosures and cyanophytes 1n the
high dose enclosure. There were no significant differences between zoo-
plankton communities among 1, 10 and 100 yg selenlte-selenlum treatments
(Salkl et al., 1985).
Studies 1n dogs (Welssman et al., 1983) and rats (MecMnsky et al., 1981)
Indicate that selenium metal and selenlous add are absorbed readily follow-
ing Inhalation exposure. Gastrointestinal absorption and b1oava1lab1l1ty of
selenium Is greater with organic selenium compounds (e.g., SeMet) compared
xv11
-------
to Inorganic compounds. Among Inorganic selenium compounds, selenltes and
selenates are absorbed more readily than metal selenldes and elemental
selenium (Venugopal and Luckey, 1978).
Following absorption, selenium Is distributed throughout the body, with
higher levels found In the liver and kidneys. McAdam and Levander (1987)
found higher muscle selenium levels In rats fed diets with organic selenium
compounds (D- or L-SeHet) compared to rats fed sodium selenate or selenlte.
Reduction of selenium compounds to hydrogen selenlde followed by
methylatlon Is the major transformation pathway leading to the excretion of
selenium (Mushak, 1983). Methylatlon occurs predominantly In the liver.
Tr1methylselenon1um, excreted 1n the urine, 1s the major excretory product
at low doses of selenium. At higher doses of selenium, larger amounts of
dlmethylselenlde are produced. Olmethylselenlde Is exhaled through the
lungs. Metal selenldes and metal-protein selenlde compounds may also be
formed from hydrogen selenlde.
Selenium 1s an essential element that 1s a part of glutathlone peroxl-
dase. The dally safe and adequate level of selenium Intake for adults 1s
considered to be 50-200 yg (0.05-0.2 mg) (NAS, 1980). Selenium 1s also
quite toxic, with selenosls (brlttleness of nails, loss of nails and hair,
dermatitis, nervous symptoms) reported In humans following chronic dietary
Intake of 3.2-6.69 mg/day (Yang et al., 1983).
Adverse effects reported 1n animals treated orally with selenium
compounds Include effects on growth, reduced survival, hlstopathologk
changes 1n the liver and testes and Immune system effects. Subchronlc NOELs
that have been Identified In laboratory animals are 0.16 mg Se/kg/day of
sodium selenlte or selenlferous wheat 1n rats (Halverson et al., 1966) and
0.63 mg Se/kg/day of sodium selenlte 1n hamsters (Beems and van Beek, 1985).
Limited chronic studies of selenium compounds do not Identify NOELs.
XV111
-------
Selenium toxlclty following Inhalation exposure has not been studied In
animals. Symptoms reported In humans following occupational exposure to
selenium Include a strong garlic odor 1n the breath, sweat and urine, acute
sore throats and cold-Uke symptoms, gastrointestinal Irritation, lacrlma-
tlon, and a metallic taste In the mouth (Hamilton and Hardy, 1974). The
development of garlic breath and cold-Uke symptoms Is thought to result
from the hepatic production of dlmethylselenlde which 1s exhaled through the
lungs (01sk1n et al., 1979).
CarclnogenlcHy studies of selenium are not conclusive. Selenium
sulflde has tested positive for cardnogenlclty In rats and female mice In
an NCI/NTP (1980a) bloassay. However, the Identify of the test compound 1s
unclear and thus the study Is judged Inadequate for derivation of a cancer
potency factor for selenium sulflde. Nelson et al. (1943) reported
Increased tumor Incidences In rats treated orally with selenlferous corn and
wheat (diets were suboptlmal In protein). Schroeder and MHchener (1971a)
also reported tumor Incidences 1n rats treated with sodium selenate; how-
ever, because treated rats lived longer than controls, the tumor Incidence
may not be related to the cardnogenlclty of the compound. Negative results
were reported 1n rats treated with sodium selenate or selenlte (Harr et al.,
1967; Tlnsley et al., 1967) and 1n mice treated with sodium selenate or
selenlte (Schroeder and MHchener, 1972).
Epidemiology studies (Wlllett and Stampfer, 1986; Salonen et al., 1984,
1985; Kok et al., 1987) and studies 1n animals (Shamberger, 1985) suggest
that selenium has antlcardnogenlc activity. This effect may be due to the
ability of selenium to protect against cellular damage by peroxldatlon of
fat (Shamberger, 1985), or 1t may be a result of the effect of selenium on
the Immune system (Koller et al., 1986).
x1x
-------
Selenium 1s teratogenlc to livestock (Barlow and Sullivan, 1982), but
developmental effects reported 1n laboratory rodents are limited to
decreased fetal body weight (Nobunaga et al., 1979). A limited multi-
generation study (Schroeder and Kitchener, 1971b) found that by the third
generation, CD-I mice treated with selenate In the drinking water at 0.57
mg/kg/day failed to breed, or produced a large proportion of runts.
The evidence that selenium Is an animal carcinogen 1s conflicting.
Ep1dem1olog1cal data did not suggest that selenium 1s a carcinogen to
humans. Mutagenldty data were mixed, but there Is evidence that certain
compounds of selenium are mutagenlc and clastogenlc.
There were no data regarding the cardnogfenldty of selenium compounds
In humans and the data In laboratory animals for selenium are considered
Inadequate. Therefore, selenium, based on U.S. EPA classification scheme,
1s considered a Group D substance: not classifiable as to cardnogenldty
In humans (U.S. EPA, 1986b). Neither cancer potency estimates nor a
cancer-based RQ were derived for selenium. However, because of positive
evidence of cardnogenldty 1n both rats and female mice (NCI/NTP, 1980a),
selenium sulflde, based on the U.S. EPA (1986b) classification scheme, could
be considered as Group B2 - probably carcinogenic to humans.
Inhalation data were Inadequate for derivation of RfD values for sub-
chronic or chronic Inhalation exposure. An oral RfD of 0.003 mg Se/kg/day
was derived by applying an uncertainty factor of 10 and a modifying factor
of 1.5 to the LOAEL of 3.2 mg/day associated with selenosls In a high-
selenium region 1n the Peoples Republic of China (Yang et al., 1983). This
derivation conforms to the derivation of verified RfD values for selenourea
and selenlous acid available on IRIS (U.S. EPA, 1985c,d). The RfD for
xx
-------
selenium of 0.003 mg/kg/day was adopted for both subchronlc and chronic oral
exposure. An RQ of 10 for chronic (noncancer) toxldty was based on
selenosls (severe CNS disturbances) 1n humans In the Yang et al. (1983)
study.
xxl
-------
TABLE OF CONTENTS
Page
1. INTRODUCTION 1-1
1.1. STRUCTURE AND CAS NUMBER 1-1
1.2. PHYSICAL AND CHEMICAL PROPERTIES 1-1
1.3. PRODUCTION DATA 1-1
1.4. USE DATA 1-6
1.5. SUMMARY 1-13
2. ENVIRONMENTAL FATE AND TRANSPORT 2-1
2.1. AIR 2-1
2.2. WATER 2-3
2.2.1. Chemical Speclatlon 2-3
2.2.2. Photolysis 2-4
2.2.3. Blomethylatlon and Volatilization 2-4
2.2.4. Sorptlon 2-5
2.2.5. B1oconcentrat1on 2-5
2.3. SOIL 2-6
2.3.1. Leaching 2-6
2.3.2. Blotransformatlon 2-6
2.4. SUMMARY 2-7
3. EXPOSURE 3-1
3.1. WATER 3-2
3.2. FOOD 3-4
3.3. INHALATION 3-9
3.4. DERMAL 3-10
3.5. SUMMARY 3-10
4. ENVIRONMENTAL TOXICOLOGY 4-1
4.1. AQUATIC TOXICOLOGY 4-1
4.1.1. Acute Effects on Fauna 4-1
4.1.2. Chronic Effects on Fauna 4-12
4.1.3. Effects on Flora 4-25
4.1.4. Effects on Bacteria 4-27
4.2. TERRESTRIAL TOXICOLOGY 4-27
4.2.1. Effects on Fauna 4-27
4.2.2. Effects on Flora 4-36
4.3. FIELD STUDIES 4-36
4.4. AQUATIC RISK ASSESSMENT 4-43
4.5. SUMMARY 4-44
xx11
-------
TABLE OF CONTENTS (cont.)
Page
5. PHARMACOKINETCS 5-1
5.1. ABSORPTION 5-1
5.2. DISTRIBUTION 5-7
5.3. METABOLISM 5-10
5.4. EXCRETION 5-12
5.5. SUMMARY 5-14
6. EFFECTS 6-1
6.1. SYSTEMIC TOXICITY 6-1
6.1.1. Inhalation Exposure 6-1
6.1.2. Oral Exposure 6-2
6.1.3. Other Relevant Information 6-11
6.2. CARCINOGENICITY 6-14
6.2.1. Inhalation 6-14
6.2.2. Oral 6-14
6.2.3. Other Relevant Information 6-16
6.3. MUTAGENICITY 6-20
6.4. TERATOGENICITY 6-20
6.5. OTHER REPRODUCTIVE EFFECTS 6-25
6.6. SUMMARY 6-26
7. EXISTING GUIDELINES AND STANDARDS 7-1
7.1. HUMAN 7-1
7.2. AQUATIC 7-2
8. RISK ASSESSMENT 8-1
8.1. CARCINOGENICITY 8-1
8.1.1. Inhalation 8-1
8.1.2. Oral 8-1
8.1.3. Other Routes 8-2
8.1.4. Weight of Evidence 8-2
8.1.5. Quantitative Risk Estimates 8-3
8.2. SYSTEMIC TOXICITY 8-4
8.2.1. Inhalation Exposure 8-4
8.2.2. Oral Exposure 8-5
XX111
-------
TABLE OF CONTENTS (cont.)
Page
9. REPORTABLE QUANTITIES 9-1
9.1. BASED ON SYSTEMIC TOXICITY 9-1
9.2. BASED ON CARCINOGENICITY 9-6
10. REFERENCES 10-1
APPENDIX A: LITERATURE SEARCHED A-l
APPENDIX B: SUMMARY TABLE FOR CROTONALDEHYDE B-l
xxlv
-------
LIST OF TABLES
No. Title Page
1-1 Synonyms, CAS Numbers, Molecular Heights, Empirical
Formulas and Structures of Selenium and Compounds 1-2
1-2 Physical Properties of Selenium and Compounds 1-4
1-3 1977 Production Data for Selenium and Compounds 1-7
3-1 Average Dally Intake (yg/day) of Selenium 1n Fiscal
Years 1978-1981/1982 3-3
3-2 Selenium 1n the Adult American Diet for Fiscal Years
1981-1982 3-5
3-3 Selenium 1n the Infant American Diet for Fiscal Years
1981-1982 3-6
3-4 Selenium In the Toddler American Diet for Fiscal Years
1981-1982 3-7
3-5 Average Selenium Content of Some Foods In the American
Diet 3-8
4-1 Median Response Concentration for Aquatic Vertebrates
Exposed to Selenium 4-2
4-2 Median Response Concentration for Aquatic Invertebrates
Exposed to Selenium 4-7
4-3 Metal Concentration 1n Soil and Earthworms from
Contaminated and Natural Sites 4-28
5-1 Calculated Internal Absorption of 75Se 1n Rats Expressed
as Fraction of Administered Dose 5-3
5-2 Calculated Internal Absorption of 7SSe 1n Rats Expressed
as Fraction of Administered Dose 5-4
5-3 Concentrations of Selenium In Tissues from Rats Fed Diets
Containing Added D-Selenometh1on1ne (SeMET), L-SeMet,
Selenlte or Selenate 5-9
6-1 Selenium Levels In Hair, Blood and Urine of Residents of
High- and Adequate-Se Areas of China 6-8
6-2 Safe and Adequate Ranges of Dally Selenium Intake 6-12
6-3 Acute Oral Toxlclty of Selenium Compounds 6-13
xxv
-------
LIST OF TABLES (cont.)
No. Title Page
6-4 Incidence of Tumors 1n F344 Rats and 86C3F1 Mice Treated
by Gavage with Selenium Sulflde for 103 Weeks 6-17
6-5 Mutagenldty Testing of Selenium Compounds 6-21
9-1 Toxldty Summary for Oral Exposure to Selenium 9-2
9-2 Composite Scores for Selenium 9-5
9-3 Selenium: Minimum Effective Dose (MED) and Reportable
Quantity (RQ) 9-7
xxvl
-------
LIST OF ABBREVIATIONS
AADI Adjusted acceptable dally Intake
AIC Acceptable Intake chronic
ATP Adenoslne tMphosphate
AWQC Ambient Water Quality CMtlera
BCF Bloconcentratlon factor
B-G Beta glucuronldase
CAS Chemical Abstract Service
CMC Carboxymethylcellulose
CS Composite score
DNA Deoxyrlbonuclelc acid
ECso Concentration effective to 50% of recipients
(and all other subscripted concentration levels)
ECG Electrocardiogram
GGT Gamma-glutamyl transpepsldase
Concentration lethal to 50% of recipients
(and all other subscripted dose levels)
Dose lethal to 50% of recipients
LDH Lactate dehydrogenase
LOAEL Lowest-observed-adverse-effect level
LTso Exposure time lethal to 50% of recipients
MATC Maximum allowable toxicant concentration
MED Minimum effective dose
NK Natural killer
NOAEL No-observed-adverse-effect level
NOEC No-observed-effect concentration
NOEL No-observed-effect level
xxvll
-------
LIST OF ABBREVIATIONS (cent.)
PEL Permissible exposure limit
ppb Parts per billion
ppm Parts per million
RBC Red blood cell chollnesterase
RfD Reference dose
RMCL Recommended maximum contaminant level
RQ Reportable quantity
RV(j Dose-rating value
RVe Effect-rating value
SDH SorbHol dehydrogenase
TLV Threshold limit value
TWA Time-weighted average
XXV111
-------
1. INTRODUCTION
1.1. STRUCTURE AND CAS NUMBER
The CAS Registry numbers, molecular weights, empirical formulas,
structures and common synonyms for selenium and Us compounds are presented
In Table 1-1.
1.2. PHYSICAL AND CHEMICAL PROPERTIES
The physical properties of selenium and selected selenium compounds are
listed 1n Table 1-2. The Important oxidation states of selenium are -2, 0,
+2, +4 and +6. There 1s no evidence that the +2 state occurs In nature
(Elkln, 1982).
Selenium 1s positioned between sulfur and .tellurium 1n group 6A on the
periodic table of elements. The chemical properties of selenium salts
resemble 1n behavior those of the corresponding sulfur and tellurium salts
(Elkln, 1982). Selenium can act as both an oxldant and reductant In many
reactions because of Us variable oxidation states. Strong oxldants can
convert selenium dioxide (+4 oxidation state) and Us derivatives to the
hexavalent (*6) state (Elkln, 1982).
The selenium halldes and oxyhalldes hydrolyze upon contact with water,
and are therefore not stable 1n moist environments (Elkln, 1982). The
organic selenium compounds are frequently susceptible to photolysis or
oxidation when exposed to light or air. This Instability 1n light or air Is
characterized by the selenium compound turning red (Elkln, 1982).
1.3. PRODUCTION DATA
In the United States, selenium Is produced by recovering It from
by-products generated during the electrolytic refining of copper ore (Elkln,
1982; USDI, 1982, 1988). Copper refinery anode slimes contain selenium,
0141d 1-1 03/30/89
-------
TABLE 1-1
Synonyms. CAS Numbers. Holecular Heights, Empirical Formulas and Structures of Selenium and Compounds
Chemical/Synonyms
Selenium (Element)
Hydrogen selenlde
selenium hydride
Selenlc acid
Selenlous acid
monohydrated selenium dioxide
selenous acid
Selenium bromide
dlselenlum dlbromlde
Selenium chloride
dlselenlum dlchlorlde
Selenium dlethyldlthlocarbamate
CAS Number
7782-49-2
7783-07-5
7783-08-6
7783-00-8
7789-52-8
10025-68-0
5456-28-0
Holecular
Weight
78.96
80.98
144.98
128.98
317.73
228.83
672.08
Empirical Formula
Se
H2Se
H204Se
•
H203Se
Br2Se2
Cl2Se2
CpOHiONiSeSft
Structure
Se
H-Se-H
0
II
HO-Se-OH
II
0
0
II
HO-Se-OH
Br-Se-Se-Br
Cl-Se-Se-Cl
CHpCHi
tetrakls(dlethyldlthlocarbamato)
selenium ethyl selenac
GO
CO
o
oo
Se-Sc-N
\
CH2CH3
-------
TABLE 1-1 (cont.)
Chemical/Synonyms
Selenium dioxide
selenium oxide
selenium anhydride
selenium (IV) dioxide
selenlous acid anhydlrlde
Selenium dlsulflde
Selenium oxychlorlde
selenlnyl chloride
_, selenlnyl dlchlorlde
^ selenium chloride oxide
selenium oxydlchlorlde
Sodium selenate
selenlc acid, sodium salt
Sodium selenlte
selenlous acid, sodium salt
CAS Number Molecular Empirical Formula
Weight
7446-08-4 110.96 02Se
7488-56-4 143.08 SeSe2
7791-23-3 165.87 Cl2OSe
13410-01-0 188.94 Na2Se04
10102-18-8 172.95 Na2Se03
Structure
0=Se=0
0=Se=S
Cl-Se-Cl
II
0
0
II
Na-0-Se-O-Na
II
0
0
II
Na-0-Se-O-Na
o
CO
CO
o
CD
-------
TABLE 1-2
Physical Properties of Selenium and Compounds
Chemical
Selenium
(element)
Hydrogen
selenlde
Selenlc
acid
Selenlous
acid
Selenium
bromide
Selenium
chloride
Selenium
dlethyl-
dlthlo
carbamate
Selenlous
dioxide
Selenium
dlsulflde
Selenium
oxychlorlde
Description
red amorphous powder or
colloidal crystal to
gray-black crystal*-'*
gas with a disagreeable
odor6
white hygroscopic
solid5
deliquescent prisms6
dark red liquid with
unpleasant odor6
deep red oily liquid6
orange-yellow powder b
lustrous tetragonal
needles6
bright red-yellow
compound
nearly colorless or
yellow compound*1
Neltlng
Point
217"Ca
-65.73°CC
58"CC
decomposes
at 70°Cd
NA
-85-C*:
63-71 °Cb
340°CC
<100°Cd
5eCe
Boiling
Point
685°C
-41.3eCe
260°C
decomposes*1
NA
227
decomposes*1
127°C
decomposes0
(733 mm Hg)
NA
NA
decomposes
180°C6
Density
4.81 (red 20°C)C
2.2(-42°C)c
2.9508 (15/4°C)6
3.004 (15/4"C)6
3.604
(15/4°C)e
2.7741 (25/4"C)6
1.32 (20/20°C)b
3.95 (15/15°C)d
NA
2.44(16/4eC)e
Water
Solubility
Insoluble*1
270 mg/100 tag/i
567 ml/100
mlc (20°C)
167 g/100 ccd
(20°C)
decomposes*1
decomposes*1
Insoluble5
38.4 g/100 cc
(14'C)
Insoluble In
cold water*1
decomposes*1
Nonaqueous Solubility
soluble In H2S04d
soluble 1n CS2 and
COC2
soluble In H2S04e
decomposes In alcohol
very slightly soluble
In alcohol
decomposes In alcohol,
soluble 1n CS2d
soluble In benzene,
chloroform. CS2C
soluble 1n benzene,
chloroform. CS2
soluble In benzene;
66.7 g/100 cc alcohol
(14°C)d
decomposes Vti aqua regla
and HN03d
mlsclble In CC14,
chloroform, CS2
Vapor Pressure
1 mm Hg (343.7°C)a
4.5 atm (0.2°C)e
12.0 atm (30.8°C)e
NA
2 mm Hg (150C)6
4.5 mm Hg (35°C)
NA
NA
NA
NA
NA
NA
benzene and toluene6
00
CD
-------
1ABLE 1-2 (cont.)
Chemical
Selenium
selenate
Selenium
selenlte
Description
white crystals6
white crystals'*
Melting
Point
NA
NA
Boiling Density Water
Point Solubility
NA 3.213 (17.4T.)*1 43.5 g/100 cc
(20°C)d.f
NA NA soluble4
Nonaqueous Solubility Vapor Pressure
NA NA
Insoluble In alcohold NA
(1982)
"Hawley (1981)
'Dean (1985)
<*Ueast (1985)
ewindholz (1983)
fHater solubility for the decahydrate
NA = Not available
o
CO
i
00
vO
-------
tellurium, gold and silver. The selenium recovered from these slimes (known
as primary selenium) Is recovered by various soda smelting or soda roasting
operations.
In 1983 and 1984, U.S. production of primary selenium amounted to
780,115 and 559,078 pounds, respectively (USDI, 1988). Production volumes
of primary selenium for 1985-1987 were withheld by the Department of
Interior to avoid disclosing company proprietary data. During 1987, the
U.S. producers of primary selenium were Asarco at Amarlllo, TX, Phelps Dodge
Refining Corp., at El Paso, TX, and BP Minerals America Corp. (formerly
Kennecott Corp.) at Magna, UT (USDI, 1988).
Secondary selenium Is selenium recovered from products previously
manufactured from selenium. In 1981, -100,000 pounds of secondary selenium
was recovered (USDI, 1982). Xerox Corporation 1n Webster, NY, recovered
secondary selenium from used xerographic drums and Selenium Inc., 1n
Maplevllle, RI, recovered 1t from both xerographic drums and used selenium
rectifiers (USDI, 1982). More recent production volumes of secondary
selenium were not available from the USDI (1988).
U.S. Imports and exports of selenium 1n 1987 amounted to 1,093,170 and
357,621 pounds, respectively (USDI, 1988).
Available production data for the selenium salts are presented 1n
Table 1-3.
1.4. USE DATA
The following are estimates of selenium consumption by end-use cate-
gories 1n 1987 (USDI, 1988): electronic and photocopier components, 43%;
glass manufacturing, 20%; chemicals and pigments, 20%; other (Including
agricultural and metallurgy), 17%.
0141d 1-6 06/15/89
-------
TABLE 1-3
1977 Production Data for Selenium and Compounds*
Company/Location
Selenium (Element)
Asarco Inc.,
Amarlllo, TX
Denver, CO
Kennecott,
Salt Lake CHy, UT
U.S. Metals Refining Co.,
Carteret, NJ
Cerac, Inc.,
Milwaukee, MI
United Mineral & Chemical Corp.,
New York, NY
Robeco Chemical,
New York
Leonard 0 Buck & Co Inc. ,
Morris town, NJ
Comlnco American Inc.,
Spokane, WA
Henley & Co. , Inc.,
New York, NY
North American Minerals Co.,
PHtsburg, PA
Owens-Illinois Inc.,
Toledo, OH
IMC,
Llbertyvllle, IL
Copalco International Ltd.,
New York
Manufacturer/
Importer
manufacturer
manufacturer
manufacturer
manufacturer
manufacturer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Production Range
(Ibs/year)
10,000-100,000
<1,000
100,000-1,000,000
100,000-1,000,000
confidential
<1000
none
10,000-100,000
<1000
confidential
10,000-100,000
10,000-100,000
none
1000-10,000
0141d
1-7
03/30/89
-------
TABLE 1-3 (cont.)
Company/Location
Selenium (Element) (cont.)
Alloychem, Inc.,
New York, NY
Brandels Goldschmldt & Co.,
New York, NY
NL Industries Inc.,
New York, NY
Phillips Brothers Division of
Engelhard Minerals & Chem.,
New York, NY
Hercules Inc.,
Wilmington, DE
Holtrachem Inc. ,
Natlck, MA
Xerox Corp. ,
Rochester, NY
Degussa Corporation,
Theodore, AL
Indussa-D1v1s1on of African
Metals, New York, NY
Kaweckl Berylco Ind., Inc.,
Reading, PA
Ametalco Inc.,
New York, NY
Manufacturer/
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Importer
Production Range
(Ibs/year)
1000-10,000
none
10,000-100,000
confidential
confidential
none
10,000-100,000
none
10,000-100,000
1000-10,000
confidential
Hydrogen Selenlde
Synthatron Corp.,
Parslppany, NJ
Scientific Gas Products Inc.,
South Pla1nf1eld, NJ
manufacturer
manufacturer
1000-10,000
1000-10,000
0141d
1-8
03/30/89
-------
TABLE 1-3 (cont.)
Company/Location
Manufacturer/
Importer
Production Range
(Ibs/year)
Hydrogen Selenlde (cont.)
II-VI Inc.,
Saxonburg, PA
manufacturer
<1000
Selenlc Add
Engelhard Industries D1v.,
Union, NJ
manufacturer
confidential
Selenlous Add
Chemical Products Plant,
Cleveland, OH
United Mineral & Chemical,
New York, NY
Falrmount Chemical Co., Inc.,
Newark, NJ
The Harshaw Chemical Co.,
Cleveland, OH
manufacturer
Importer
Importer
Importer
<1000
1,000-10,000
<1000
<1000
Selenium Chloride
Cerac, Inc.,
Milwaukee, WI
Falrmount Chemical Co., Inc.,
Newark, NJ
United Mineral & Chemical,
New York
manufacturer
manufacturer
Importer
confidential
<1000
<1000
Selenium Dioxide
Cerac, Inc.,
Milwaukee, WI
manufacturer
confidential
0141d
1-9
03/30/89
-------
TABLE 1-3 (cont.)
Company/Location
Selenium Dioxide (cont.)
United Mineral & Chemical,
New York, NY
Henley & Co., Inc.,
New York, NY
Alloychem., Inc.,
New York, NY
SST Corp.,
Clifton, NJ
Manufacturer/
Importer
Importer
Importer
Importer
Importer
Production Range
(Ibs/year)
<1000
confidential
1000-10,000
<1000
Selenium Dlsulflde
Robeco Chemicals, Inc.,
New York, NY
ICD Group, Inc.,
New York, NY
Importer
Importer
confidential
none
Sodium Selenate
Cerac, Inc.,
Milwaukee, WI
Falrmount Chemical Co. Inc.,
Newark, NJ
manufacturer
Importer
confidential
<1000
Sodium Selenlte
Cerac, Inc.,
Milwaukee, WI
United Mineral & Chemical Corp.,
New York, NY
Falrmount Chemical Co. Inc.,
Newark, NJ
manufacturer
Importer
Importer
confidential
1000-10,000
<1000
0141d
1-10
03/30/89
-------
TABLE 1-3 (cont.)
Company/Location
Manufacturer/
Importer
Production Range
(Ibs/year)
Sodium Selenlte (cont.)
EM Laboratories, Inc.,
Elmsford, NY
Deka Minerals, Inc.,
New York, NY
Importer
Importer
1000-10,000
none
*Source: U.S. EPA, 1977
OUld
1-11
03/30/89
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The photoelectric and semiconducting properties of selenium are respon-
sible for Us primary use In the electronics and optical Industry (Elkln,
1982). The electrical conductivity of selenium Is ~3 orders of magnitude
higher during exposure to light than In the dark. Because of these prop-
erties, selenium Is used 1n photovoltaic cells, photoelectric cells and
semiconducting rectifiers. Xerography 1s the most highly developed form of
electrophotography or photocopying and Is a primary application of the
photoconductlve properties of selenium (Elkln, 1982).
The glass manufacturing Industry uses selenium to Impart various tints,
such as red and bronze, and to neutralize or de-colorize greenish tints
caused by Iron Impurities (IARC, 1975; Elkln, 1982). The ceramics, paint
and plastics Industries use a variety of selenium pigments to produce colors
ranging from yellow to maroon.
Selenium 1s used In metallurgy as a property modifier to form alloys
with Iron, copper, nickel, cobalt and lead (Elkln, 1982).
Sodium selenate and selenlc add have been added to chrome-plating baths
since 1959 to Improve corrosion protection from pitting, blistering and
rusting (Elkln, 1982). An Important application of this Is the plating of
automobile parts exposed to road salt In the snow belts.
Selenium dlethyldHhlocarbamate Is used by the rubber Industry as a
vulcanization accelerator, antloxldant and UV stabilizer (Elkln, 1982).
Selenium dioxide 1s an Important oxidizing agent and catalyst for the
synthesis of organic chemicals and drug products (Elkln, 1982). Selenium
sulflde 1s used 1n topical pharmaceutical products (such as Selsun from
Abbott Laboratories) to control seborrhelc dermatitis of the scalp (Elkln,
1982). Sodium selenlte and various organoselenlum compounds are used In
photographic printing solutions and bleach fixing baths (Elkln, 1982).
0141d 1-12 03/30/89
-------
Tablets containing several mlcrograms of sodium selenlte are sold without a
prescription In the United States as dietary supplements (Elkln, 1982).
In agriculture, selenium (sodium selenate and selenlte) 1s used as a
feed additive to compensate for animal feed grown 1n selenium-deficient soil
(USOI, 1988). In April 1988, the U.S. Food and Drug Administration
\
published new regulations allowing the level of selenium In animal feed to
be Increased from 0.1-0.3 ppm (USOI, 1988).
1.5. SUMMARY
In the United States, selenium Is produced by recovering H from
by-products generated during the electrolytic refining of copper ore (Elkln,
1982; USOI, 1982, 1988). In 1984, 559,078 pounds of selenium were recovered
from these by-products by three domestic producers. Also, selenium 1s
recovered domestically from previously manufactured xerographic drums and
selenium rectifiers (USOI, 1982). Approximately 1 million pounds of
selenium were Imported 1n 1987 (USDI). The following are estimates of
selenium consumption by end-use categories In 1987 (USDI, 1988): electronic
and photocopier components, 43%; glass manufacturing, 20%; chemicals and
pigments, 20%; other (Including agriculture and metallurgy), 17%. Because
of Us photoelectric and semiconducting properties, selenium 1s used
primarily In the production of photocopying components, photoelectric cells,
photovoltaic cells and semiconducting rectifiers (Elkln, 1982).
0141d 1-13 03/30/89
-------
2. ENVIRONMENTAL FATE AND TRANSPORT
Selenium 1s an element; therefore, 1t does not degrade In the environ-
ment, but simply changes from one form to another. The major features of
selenium chemistry that affect Its fate and transport 1n the environment are
associated with changes 1n Us oxidation state and the resulting differences
1n chemical properties (Callahan et al., 1979). The chemical speclatlon of
selenium Is discussed In more detail 1n Section 2.2. Because of the chang-
ing forms of selenium compounds 1n nature, selenium undergoes an environ-
mental cycling process that Involves soil, rocks, plants, animals, water
(oceans, lakes, etc.) and the atmosphere (NAS, 1976). Figure 2-1 1s a
simplified diagram of the cycling of selenium 1n nature.
2.1. AIR
Selenium can exist In the atmosphere 1n both the partlculate and the
vapor phase. Partlculate-phase selenium enters the atmosphere from sources
such as wind-blown dusts (from soil and rock erosion), fly ash from coal
combustion, and volcanic emissions (Chapter 3). No data are available to
suggest that chemical transformation processes are Important to the fate of
partlculate-phase selenium In air. Removal of partlculate-phase selenium
from air occurs physically by wet and dry deposition processes, such as
rainfall and settling (NAS, 1976). A mean selenium concentration of 210
ng/i was detected In rain and snow collected In Cambridge, MA, from
December 1964 to March 1965 (Stahl, 1969). Lower mean levels of 11-21
ng/i were detected 1n rainfall collected at the Enewetak Atoll (Marshall
Islands) 1n 1979 (Arlmoto et al., 1985).
Vapor-phase selenium enters the atmosphere by volatile emissions from
mlcroflora and plants. Important selenium compounds emitted to air from
0142d 2-1 06/15/89
-------
SEDIMENTS l>
SEDIMENTARY
MOCKS
EARTH'S
CORE
FIGURE 2-1
The Cycling of Selenium 1n Nature. (For simplicity, microorganisms are
not Included 1n the above scheme, although they are Important to many of the
processes Involved 1n the cycle.)
Source: NAS (1976)
0142d
2-2
03/30/89
-------
mlcroflora Include dimethyl selenlde and dimethyl dlselenlde (Callahan et
al., 1979; Olson et al., 1983; Cooke and Bruland, 1987). These selenium
compounds are expected to react with sunlight-produced hydroxyl radicals In
air, assuming their atmospheric chemistry Is similar to that of dimethyl
sulflde and dimethyl dlsulflde. Based upon experimentally measured reaction
rate constants of the sulfldes with H0» and an average concentration of
5xlOf5 HO*/cm3 1n air (Atkinson, 1985), the half-lives of dimethyl
selenlde and dimethyl dlselenlde In air can be estimated to be 3.75 days and
1.9 hours, respectively. Based upon observed sulflde reactions (Atkinson,
1985), the major products of hydroxyl reaction will Include selenium dioxide
and methyl hydrogen selenlte. These selenium degradation products are
probably susceptible to physical removal from air.
2.2. WATER
2.2.1. Chemical Spedatlon. Selenium Is stable In four valence states
(-2, 0, +4, +6), which are discussed Individually below (Callahan et al.,
1979; NAS, 1976). In aerobic water conditions, selenium can exist In the
form of the selenate, selenlte or hydrogen selenlte anlons (Callahan et al.,
1979; NAS, 1976).
Selenate selenium (+6 oxidation state): the selenates are rela-
tively soluble 1n water, stable over the environmental pH range,
and readily taken up by plants. Because of this solubility,
stability and plant uptake potential, selenate appears to be the
most dangerous form of selenium In relation to environmental
pollution.
Selenlte selenium (+4 oxidation state): most selenlte salts are
less soluble than the corresponding selenates; especially relevant
to the aquatic environment Is the very low solubility of ferric
selenltes. Another characteristic (Important to environmental
cycling) 1s the property of selenlte to rapidly become reduced to
elemental selenium under addle conditions by mild reducing agents,
such as ascorbic add or sulfur dioxide. The probability that
selenlte will form Insoluble compounds, absorbates with ferric
oxides, or be reduced to Insoluble elemental selenium minimizes the
possibility for Its transport 1n the aquatic environment.
0142d 2-3 03/30/89
-------
Elemental selenium (0 oxidation state); because of Us extreme
Insolubility 1n water, elemental selenium appears to be a major
sink for selenium that can be considered to be Inert 1n the aquatic
environment. Elemental selenium burns 1n air to form selenium
dioxide. In the combustion of fossil fuels or solid wastes
containing selenium, the selenium 1s converted to selenium dioxide,
which can then be reduced to elemental selenium by the sulfur
dioxide that 1s also present. This mechanism can be responsible
for the occurrence of elemental selenium 1n fly ash from coal
combustion.
Selenlde selenium (oxidation state -2): the metal selenldes are
relatively Insoluble 1n water and do not appear to be taken up
readily by plants. Thus, the metal selenldes (and elemental
selenium) may represent a useful Inert sink for the detoxification
of selenium In areas where these compounds occur or are deposited.
In semlarld and arid regions, selenlde-selenlum appears to have
been oxidized, over geologic time, to selenate. Hydrogen selenlde
decomposes rapidly to form elemental selenium and 1s of minor
Importance to the overall fate of selenium 1n aquatic environments.
Organic selenium (oxidation state -2): essentially all of the
relevant organic selenium compounds In the aquatic environment
contain selenium 1n the -2 oxidation state. These compounds will
decompose 1n the environment to eventually form elemental selenium.
2.2.2. Photolysis. Although selenium exhibits photo-conductive prop-
erties, no data are available to suggest that photolysis Is Important In
determining the environmental fate of selenium 1n the aquatic environment
(Callahan et al., 1979).
2.2.3. Blomethylatlon and Volatilization. The blomethylatlon and
volatilization of selenium are considered together because the products of
blomethylatlon Include the volatile dimethyl selenldes. Chau et al. (1976)
demonstrated 1n laboratory studies that microbes present 1n lake sediments
(from Sudsbury, Ontario) could methylate organic and Inorganic selenium
compounds with the formation of gaseous dimethyl selenlde and dimethyl
dlselenlde. In addition, Chau et al. (1976) found that 4 of 12 sediment
samples were able to evolve methylated selenldes without the addition of any
selenium compounds; the naturally occurring selenium content of the
sediments ranged from 0.48-20.48 mg/kg.
0142d 2-4 03/30/89
-------
Cooke and Bruland (1987) examined surface water from three sites In
California to determine the chemical species of selenium that were present
In the natural waters. Six dissolved species were Identified: Inorganic
selenates and selenltes, nonvolatile organic selenldes (Including seleno
ami no adds and a d1methylselenon1um Ion), and volatile dimethyl selenlde
and dimethyl dlselenlde. The presence of the volatile methylated selenldes
was considered Important In the environmental cycling of selenium and a
major process by which selenium Is removed from the aquatic environment.
2.2.4. Sorptlon. The sorptlon of selenium to aquatic sediments and
suspended matter depends on a variety of factors, such as the chemical
species of selenium that Is present, the pH of the water, and the presence
of minerals and clays (Callahan et al., 1979; Gruebel et al., 1987;
BarYosef, 1987). The mobility of selenium 1n both surface water and ground-
water has been found to depend strongly upon oxidation state (Gruebel et
al., 1987). Mobility 1n groundwater 1s associated with oxidation state +6,
while mobility 1n surface waters may be associated with both the *4 and +6
oxidation states. This seems reasonable, since the f6 oxidation state
refers to the selenates, which are the most soluble of the selenium
compounds. Apparently, selenium can undergo an adsorptlon-desorptlon cycle
In the aquatic environment, which 1s determined primarily by the changes In
the oxidation states of the selenium species that are present. Partitioning
to sediments Is likely to occur as the oxidation state 1s reduced from +6-0;
desorptlon (with subsequent dissolution 1n the water column) Is likely to
occur when the oxidation state reaches +6.
2.2.5. B1oconcentrat1on. Data pertaining to the bloconcentratlon of
selenium In aquatic organisms has been compiled by U.S. EPA (1987a). F1sh
(fathead minnow, striped bass) exposed to sodium selenate (oxidation state
0142d 2-5 09/20/89
-------
+6) were reported to exhibit BCFs ranging from 0.68-52. Fish (rainbow trout,
fathead minnow, blueglll, largemouth bass) exposed to sodium selenlte or
selenlous acid (oxidation state +4) were reported to exhibit BCFs ranging
from 2-470.
2.3. SOIL
2.3.1. Leaching. Data specific to the leaching of selenium 1n soil were
not located 1n the available literature; however, mobility 1n soil Is
probably analogous to movement In groundwater and surface water as discussed
1n Section 2.2.4. It Is expected that selenium In oxidation state +6
(selenate) will be the most mobile of the selenium species 1n soil, while
selenium 1n oxidation state 0 will be generally Immobile.
2.3.2. Blotransformatlon. Selenates and selenltes are taken up by plants
and are generally reduced within the plant to oxidation state -2 In the form
of soluble amlno adds or protein-bound ami no adds (Callahan et al., 1979).
As plants decay, the selenium 1n the plant tissue 1s returned to the soil
where It can be oxidized to other oxidation states. It has also been shown
that living plants can release volatile selenium compounds Into the
atmosphere (Z1eve and Peterson, 1984). Z1eve and Peterson (1984) suggested
that plants, 1n addition to soil microorganisms, play an Important role 1n
selenium volatilization to the atmosphere as part of the environmental
cycling process.
The mlcroblal formation of volatile selenium compounds (principally
dimethyl selenlde) has been reported to be widespread (Z1eve and Peterson,
1984). Reamer and Zoller (1980) demonstrated that microorganisms 1n soil
and sewage sludge converted Inorganic selenium compounds to volatile
methylated spedes. These volatile species Included dimethyl selenlde,
dimethyl dlselenlde, dimethyl selenone and methyl methylselenlte.
0142d 2-6 03/30/89
-------
2.4. SUMMARY
Selenium Is an element; therefore, It does not degrade In the environ-
ment, 1t simply changes from one form to another. The major features of
selenium chemistry that affect Its fate and transport 1n the environment are
associated with changes In Its oxidation state and the resulting differences
1n chemical properties (Callahan et al., 1979). Because selenium only
changes form and does not degrade In nature, It undergoes an environmental
cycling process Involving soil, rocks, plants, animals, water and air (NAS,
1976). When released to the atmosphere In partlculate-phase, selenium 1s
removed by physical processes such as rainfall and settling (NAS, 1976).
Volatile selenium compounds are released to air by plant and mlcroblal
transformations (Z1eve and Peterson, 1984; Chau et al., 1976), where they
react with sunlight-formed H0« to form selenium dioxide and other
compounds that can be transported physically to water and soil. In both
water and soil, the blomethylatlon of selenium to release volatile selenium
to air 1s an Important part of the environmental cycling process (Cooke and
Bruland, 1987; Z1eve and Peterson, 1984). Selenium 1n oxidation state *6
(selenate) Is the most soluble and mobile selenium species In the soil and
water environments (Gruebel et al., 1987; Callahan et al., 1979). Because of
the solubility, stability and ability of selenate to be taken up by plants,
It 1s considered the most dangerous form of selenium 1n relation to environ-
mental pollution (NAS, 1976; Callahan et al., 1979).
0142d 2-7 06/15/89
-------
3. EXPOSURE
Selenium 1s widely distributed 1n the earth's crust, and with suffi-
ciently sensitive analytical techniques, selenium can be detected In
virtually all rocks and soil on the earth's surface (NAS, 1976). Host
estimates of Us average concentration 1n the earth's crust range from
0.03-0.8 ppm; several fall around 0.1 ppm (NAS, 1976). Because of this
ubiquitous distribution 1n the environment, the detection of selenium 1n
air, water, soil, food and vegetation Is expected (IARC, 1975).
Distribution of selenium to the air and water environments occurs from
both natural and anthropogenic sources. Natural sources of release to the
atmosphere Include volcanic emissions, wind-blown dusts, sea sprays from the
oceans, and release of volatile selenium compounds from both plants and
animals as a result of biological processes (NAS, 1976; AMmoto et al.,
1985). Anthropogenic sources of release to the atmosphere Include the
mining, smelting and refining of selenium-containing ores, the processing of
Industrial products from refined selenium, and the Incineration of coal,
fuel oil and solid waste (NAS, 1976; U.S. EPA, 1987a). More than half of
the anthropogenic releases are attributed to coal combustion (NAS, 1976).
The average selenium content 1n U.S. coal 1s ~2-3 ppm; the selenium content
of fuel oil or crude oil may range from 0.006-2.2 ppm (NAS, 1976). Combus-
tion sources release selenium In fly ash particles and as vapors (flue-gas),
which will primarily become partlculate material.
Selenium Is released naturally to the water environment by weathering
and erosion of rocks and soil (U.S. EPA, 1987a). Man releases selenium to
water by wastewater discharges from mining, refining and Industrial appli-
cations processing. In addition, selenium Is released to water through
0143d 3-1 06/15/89
-------
physical removal (wet and dry deposition) of participate matter from the
atmosphere (U.S. EPA, 1987a).
3.1. WATER
Based upon available monitoring data, 1t has been estimated that the
average selenium content of drinking water 1s ~0.2 ppb (Bennett, 1986). It
1s possible, however, that some drinking waters may contain much higher
selenium levels at various geographical locations where the content of
naturally occurring selenium 1s high. For example, In a high selenlferous
area of South Dakota, selenium levels of 50-330 ppb were found 1n 10 of 44
drinking waters from sampled wells (U.S. EPA, 1980a). A study of home tap
water samples collected from 3676 residences -located 1n 35 geographically
dispersed areas found 9.96X of the samples with selenium levels above the
detection limit of 1 ppb and a maximum positive detection of 36.8 ppb (U.S.
EPA, 1980a).
Assuming an average drinking water selenium concentration of 0.2 ppb
(200 ng/a,) (Bennett, 1986) and an adult consumption of 2 I/day, the
average dally Intake from drinking water can be estimated to be 400 ng,
which 1s much lower than the average dally Intake from food (Table 3-1).
An analysis of monitoring data from 211 sampling stations 1n the
National American Stream Quality Accounting Network and National Water
Quality Surveillance System found mean selenium concentrations of <1 ppb 1n
river water from throughout the United States (Smith et al., 1987); monitor-
Ing was conducting between 1974 and 1981 with a detection limit of 1 ppb.
An analysis of 1062 groundwaters and 590 surface waters from New Jersey
found selenium In all water samples, with a median concentration of 2.0 ppb
In both groundwater and surface water (Page, 1981). Preliminary results
from the U.S. EPA's Nationwide Urban Runoff Program detected selenium levels
of 2-77 ppb 1n stormwater runoff from three U.S. cities (Cole et al., 1984).
0143d 3-2 06/15/89
-------
TABLE 3-1
Average Dally Intake (yg/day) of Selenium 1n Fiscal Years 1978-1981/1982*
Fiscal Year
1981/1982
1980
1979
1978
Adult
139
141
152
156
Toddler
54
58
45
52
Infant
22
19
15
18
*Source: Gartrell et al.. 1986a,b
0143d
3-3
03/31/89
-------
It has been estimated that the average selenium concentration of waters from
the open oceans (not affected by localized contamination) Is -0.09 ppb (NAS,
1976; Elkln, 1982). The principal species In the ocean 1s the selenate 1on
(Elkln, 1982).
3.2. FOOD
The U.S. Food and Drug Administration has conducted the Total Diet
Studies (also referred to as Market Basket Programs) since the early 1960s
(Gartrell et al., 1986a). These studies survey the American food supply and
measure dietary Intake of selected pesticides, Industrial chemicals and
elements. The Adult Total Diet Study monitors the market food supply 1n the
diets of 16- to 19-year-old males, who generally consume more food than
other age groups. The results of the most recent study with respect to
selenium are presented In Table 3-2. For this study, 27 market basket
samples (consisting of -120 Individual food Hems) were collected from
retail markets from the northeast, south, west and north central regions of
the United States. Collection occurred between October 1980 and March 1982,
referred to as Fiscal Years 1981/82. The collected food Hems were
separated Into the various food groups and were then blended Into
homogeneous composites for analysis by food group. Tables 3-3 and 3-4 11st
similar results for the Infant (6 months old) and Toddler (2 years old)
Total Diet Studies. The average dally Intake of selenium for the American
adult, toddler and Infant (see Table 3-1) Is based upon results of the Total
Diet Studies for Fiscal Years 1978 to 1981/82.
Table 3-5 lists reported selenium levels 1n various staple food Hems of
the American diet. The selenium content of food grown In high-selenium vs.
low-selenium soils, however, may vary by up to three orders of magnitude
(U.S. EPA, 1980a).
0143d 3-4 06/15/89
-------
TABLE 3-2
Selenium 1n the Adult American Diet for Fiscal Years 1981-19823
Food Group
Dairy products
Meat, fish, poultry
Grain and cereal
products
Potatoes
Leafy vegetables
Legume vegetables
Root vegetables
Garden fruits
Fruits
011s and fats
Sugar and adjuncts
Beverages
TOTAL
Average
Concentration0
(ppm)
0.008
0.209
0.183
0.004
0.002
0.003
0
0.001
0
0.002
0
<0.001
NA
Number
Positive0
11
27
27
5
5
8
0
3
0
2
0
1
89e
Concentration
Range0"
trace-0.02
0.14-0.30
0.10-0.34
trace
trace
trace
0
trace
0
trace
0
trace
trace-0.34
Average
Intake
Ug/day)
6.17
54.9
77.0
0.590
0.114
0.245
0
0.071
0
0.106
'0
0.272
139
^source: Gartrell et al. (1986a)
DBased on all composites analyzed
C0ut of 27 composites for the Individual food group
dTrace Indicates at the detection limit
eOut of 324 composites
NA = Not applicable
0143d
3-5
03/31/89
-------
TABLE 3-3
Selenium In the Infant American Diet for Fiscal Years 1981-19823
Food Group
Whole milk
Other dairy products
Meat, fish, poultry
Grain and cereal
products
Potatoes
Vegetables
Fruits and fruit
juices
011s and fats
Sugar and adjuncts
Beverages
Drinking Water
TOTAL
Average
Concentration13
(ppm)
0.009
0.015
0.112
0.192
0.002
0.007
0
0.005
0
0
0
NA
Number
Positive0
8
7
13
13
1
7
0
2
0
0
0
51e
Concentration
Ranged
trace
trace-0.09
0.05-0.20
0.12-0.34
trace
trace
0
trace
0
0
0
trace-0.34
Average
Intake
(yg/day)
5
2
5
6
0
0
0
0
0
0
0
21
.63
.94
.34
.80
.021
.690
.110
.5
aSource: Gartrell et al., 1986b
bBased on all composites analyzed
C0ut of 13 composites for each Individual food group
dTrace Indicates at the detection limit
eOut of 143 composites
NA = Not applicable
0143d
3-6
03/31/89
-------
TABLE 3-4
Selenium In the Toddler American Diet for Fiscal Years 1981-19823
Average
Food Group Concentration1*
(ppm)
Whole M1lk
Other dairy products
Meat, fish, poultry
Grain and cereal products
Potatoes
Vegetables
Fruits and fruit juices
011s and fats
Sugar and adjuncts
Beverages
Drinking Water
TOTAL
0.009
0.022
0.208
0.189
0.003
0.003
0
0.036
0.005
0
0
NA
Number
Positive0
8
11
13
13
1
3
0
9
4
0
0
62e
Concentration
Ranged
trace
trace
0.06-0.33
0.12-0.31
trace
trace
0
trace-0.17
trace
0
0
trace-0.33
Average
Intake
(vg/day)
4.63
1.51
24.8
22.1
0.138
0.199
0
0.605
0.153
0
0
54.1
aSource: Gartrell et al., 1986b
bBased on all composites analyzed
C0ut of 13 composites for each Individual food group
dTrace Indicates at the detection limit
eOut of 143 composites
NA = Not applicable
0143d
3-7
03/31/89
-------
TABLE 3-5
Average Selenium Content of Some Foods 1n the American D1eta
Food
Selenium Content
(vg/g wet wt.)
Vegetables, canned and freshb
Fresh garlic
Mushrooms, canned and fresh
Fruits, canned and fresh
Cereal products0
Corn flakes
Rice cereal
Egg white
Egg yolk
Brown sugar
White sugar
Cheeses
Table cream
Whole milk
Meat (excluding kidney)
Seafood
0.010 (0.004-0.039)
0.249
0.118
0.006 (<0.002-0.013)
0.387 (0-0266-0.665)
0.026
0.028
0.051
0.183
0.011
0.003
0.082 (0.052-0.105)
0.006
0.012
0.224 (0.116-0.432)
0.532 (0.337-0.658)
aSource: U.S. EPA, 1980a
bMean excluding mushrooms and garlic
cMean excluding corn flakes and rice cereal
0143d
3-8
06/15/89
-------
3.3. INHALATION
A review of available data concerning the concentration of trace
elements 1n ambient atmospheric participate matter has found selenium
concentrations of 0.0056-0.19, 0.01-3.0 and 0.2-30 ng/m3 In the air from
remote locations, rural locations and U.S. urban locations, respectively
(Schroeder et al., 1987). The mean selenium concentration 1n air from urban
locations 1s ~3 ng/m3 (Bennett, 1986). A concentration of 1.07 ng/m3
was detected In air near the Delaware coast In August, 1982; this was higher
than levels of 0.16-0.43 ng/m3 detected In air near the coast of Bermuda
(Gibson et al., 1986). The 5-year (1978-1982) average selenium concentra-
tion 1n the air of El Paso, TX, has been reported to be 1 ng/m3, with
highest levels reaching 205 ng/m3 (Wlersema et al., 1984). Selenium
levels of 2.9-4.3 ng/m3 have been monitored Inside of automobiles travel-
Ing the California freeways (WHz et al., 1986); these levels may be higher
than the outdoor ambient levels by a factor of 2 or 3.
A major use of selenium Is 1n the manufacture of photocopier components
(USDI, 1988). Measurement of selenium 1n the air near working photocopiers
has been reported to range from 10-600 ng/m3 (Hansen and Andersen, 1986).
The level of selenium In various tobacco, leaves has been reported to range
from 0.03-2.28 mg/kg, with the selenium content of associated cigarette
smoke ranging from 7.7-63 ng/clgarette (Jenkins, 1986).
Assuming an average atmospheric selenium concentration of 3 ng/m3
(Bennett, 1986) and an adult air Inhalation of 20 mVday, the average
dally Intake from Inhalation can be estimated to be 60 ng, which Is much
lower than the average dally Intake from food (see Table 3-4).
0143d 3-9 06/15/89
-------
3.4. DERMAL
Selenium sulfldes are used In various anti-dandruff shampoos (concentra-
tion of 1-2.5%) and topical pharmaceutical products to control seborrhek
dermatitis of the scalp (U.S. EPA, 1980a; Elkln, 1982). It has been
reported that ordinary application of selenium-containing shampoo does not
significantly elevate selenium levels 1n blood when compared with controls
(U.S. EPA, 1980a).
Selenium has many Industrial uses, and most significant dermal exposure
would be confined primarily to occupational settings (U.S. EPA, 1980a). Eye
Irritations and skin burns have occurred from direct contact with selenium
dioxide at a plant refining copper by the electrolytic method (Robin, 1984).
3.5. SUMMARY
Selenium 1s distributed widely 1n the earth's crust, and with suffi-
ciently sensitive analytical techniques, selenium can be detected In
virtually all rocks and soil on the earth's surface (NAS, 1976). Because of
this ubiquitous distribution In the environment, the detection of selenium
1n air, water, soil, food and vegetation Is expected (IARC, 1975). Selenium
1s released to the environment from natural sources such as volcanoes, rock
and soil erosion, sea sprays and volatile emissions from plants and micro-
flora (NAS, 1976; AMmoto et al., 1985). Humans release selenium to the
environment through Incineration of coal, fuel oil and solid waste, from
emissions and waste streams generated through mining, refining and Indus-
trial applications (NAS, 1976; U.S. EPA, 1987a). More than half of the
human releases are attributed to the combustion of coal (NAS, 1976). Based
upon available monitoring data, the average selenium content of drinking
water 1s ~0.2 ppb and the mean concentration 1n urban air 1s ~3 ng/m3
(Bennett, 1986). These concentrations can be used to estimate average dally
0143d 3-10 03/31/89
-------
Intakes of 400 ng/day for water and 60 ng/day for Inhalation. The average
dally Intakes for water and Inhalation are small In comparison with the
estimated average dally Intake of 139 ug/day for food (Gartrell et al.,
1986a).
0143d 3-11 06/15/89
-------
4. ENVIRONMENTAL TOXICOLOGY
4.1. AQUATIC TOXICOLOGY
4.1.1. Acute Toxic Effects on Fauna. The acute toxldty of selenium to
aquatic vertebrates as expressed by the LC™ 1s presented 1n Table 4-1.
LC5Qs were reported for numerous species of freshwater and marine
vertebrates exposed to selenium dioxide, sodium and potassium selenlte, and
sodium and potassium selenate. Exposure of rainbow trout, Salmo qalrdnerl.
to selenium as sodium selenlte produced the lowest 96-hour LC™ (1.80
mg/l) Identified In this review for a freshwater vertebrate (Hunn et al.,
1987). Carp, Cyprlnus carplo. zebraflsh, Brachyodanlo rerlo. and white
sucker, Catostomus commersonl. were among the least sensitive freshwater
vertebrates, with 96-hour LC50S ranging from 23-35 mg/l (N11m1 and
Laham, 1976; Etnler et al., 1987). U.S. EPA (1987a) reported the results of
additional studies 1n which the toxldty of selenium as selenlte ranged from
0.620 mg/l for fathead minnows to 35 mg/l for the common carp.
Fathead minnows, Plmephales promelas. appeared to be the most sensitive
freshwater species to selenium as sodium selenate (96-hour LC50 of 2.0
mg/l under flowthrough conditions) but there were no studies reported 1n
which the sensitivity of rainbow trout to selenium as sodium selenate was
assessed. Zebraflsh, Brachyodanlo rerlo. and juvenile striped bass, Horone
saxatms. were the most tolerant of exposure to selenium as sodium
selenate, with 96-hour LC5Qs of 82 and 85.8 mg/l, respectively (N11m1
and Laham, 1976; Klauda, 1986).
The toxldty of selenium as selenium dioxide ranged from a 96-hour
LCcQ of 7.3 mg/l for fathead minnows, Plmephales promelas (Cardwell et
al., 1976) to 20 mg/l for zebraflsh, Brachyodanlo rerlo (N11m1 and Laham,
1976). The sensitivity of fathead minnows to selenium either as sodium
0144d 4-1 04/01/89
-------
TABLE 4-1
Median Response Concentration for Aquatic Vertebrates Exposed to Selenium
Oi — —
a. Median Response Concentration
i
o
^^
o
oo
Species
Rainbow trout
Rainbow trout
Salmo qalrdnerl
Salmo qalrdnerl
Salmo qalrdnerl
Salmo qalrdnerl
Salmo qalrdnerl
Rainbow trout
Salmo qalrdnerl
Brook trout
Salvellnus fontanalls
Northern pike
' Esox luclus
Northern pike
Esox luclus
Goldfish
Carasslus auratus
Goldfish
Carraslus auratus
Carp
Cvprlnus carplo
Cvprlnus carplo
Chemical
Se
Se
Se
Se
Se
Na2Se03
Na2Se03
Na2Se03
Na2Se03
Na2Se03
Se02
Se
Na2Se03
Se02
Se02
Se
Na2Se03
Test
Method
S
NR
NR
NR
NR
FT.M
FT.H
S.M
FT.H
FT
FT
NR
FT.H
S
FT
NR
S
24-Hour
NR
NR
NR
NR
NR
NR
NR
NR
NR
NR
36.3 mg/l
NR
NR
NR
71.3 mg/t
(65.8-77.2)
72 mg/t
NR
48 -Hour
NR
NR
NR
NR
NR
NR
NR
NR
NR
NR
23.8 mg/l
NR
NR
12 ppm
(7.9-17.0)
46.5 mg/l
(42.6-50.7)
NR
NR
96 -Hour
1.8 mg/l
8.1 mg/l
4.2-4.5 mg/l
12.5 mg/l
7.2-8.8 mg/l
8.8 mg/l
8.2 mg/l
4.35 mg/l
7.2 mg/l
1.80 mg/l
(1.29-2.51)
14.3 mg/l
NR
NR
NR
36.6 mg/l
(26.7-50.2)
35 mg/l
35 mg/l
Comments
LC5Q. hardness = 40 yg/l
"50
"50
"50
"50
LC5Q. fish not fed
LCso. fish fed every other
day
"50
LC50. fish fed dally
LC5o, temperature = 12°C
LC5Q. temperature = 15.5°C
75-hour LC50 =11.1 mg/l
75. 5 -hour LC50 =11.1 mg/l
LC5Q based on mortality after
a 7-day recovery period
LC5Q. temperature = 25.4°C
"50
"50
Reference
Palawskl et al.. 1985
Elsler. 1985
Elsler. 1985
Hsler. 1985
Elsler. 1985
Etnler et al., 1987
Etnler et al.. 1987
Etnler et al.. 1987
Etnler et al.. 1987
Hunn et al.. 1987
Cardwell et al.. 1976
Klaverkamp et al..
1983
Etnler et al.. 1987
Weir and Nine, 1970
Cardwell et al.. 1976
Elsler. 1985
Etnler et al.. 1987
-------
TABLE 4-1 (cont.)
o
o.
i
04/01/8
Species
Fathead minnow
Plmephales promelas
Fathead minnow
Plmephales promelas
Fathead minnow
Fathead minnow
Plmephales promelas
(Juveniles)
Plmcphales promelas
Fathead minnow
Plmcphales promelas
Fathead minnow
Zebraflsh
Brachyodanla rerlo
(larvae)
White sucker
Catostomus coonersonl
Chemical
Se
Se
Se
Se02
45. 7X
Na2Se04
Na2Se04
Na2Se04
Na2Se03
Na2Se03
Na2Se03
Se02
Na2Se03-5H20
(selenlte)
Na2Se04
(selenate)
(selenlte)
K2Se04
(selenate)
Se
Test
Method
NR
NR
S
FT
S
S
S.M
FT.H
S.H
S.H
S.H
S
S
S
S
S
NR
Median
24 -Hour
NR
NR
NR
24.3 mg/l
(16.4-36)
NR
82 mg/t
(76-89)
NR
NR
NR
NR
NR
NR
NR
NR
NR
NR
NR
Response Concentration
48 -Hour
NR
NR
NR
NR
NR
NR
NR
NR
«R
NR
NR
NR
NR
NR
NR
NR
48.6 mg/t
96-Hour
0.62-0.97
mg/l
2.2-12.5
mg/l
10 mg/l
7.3 mg/l
(5.7-9.2)
10 mg/t
(5.9-17)
NR
11.8 mg/t
2.0 mg/l
10.9 mg/l
6.7 mg/t
2.8 mg/t
20 mg/l
23 mg/l
82 mg/l
15 mg/l
81 rag/I
31.4 mg/l
Comments Reference
LC50 Elsler. 1985
LCso Elsler. 1985
LCso, hardness = 40 mg/t Palawskl et al., 1985
LCso, temperature = 24.7°C Cardwell et al.. 1976
LC$o Mayer and E Hers leek,
1986
LC5Q Watenpaugh and
Bellinger. 1985a
LCso Etnler et al.. 1987
LCso Etnler et al.. 1987
LCSO Etnler et al.. 1987
LCso Etnler et al.. 1987
LCso Etnler et al.. 1987
LCso Nllml and Laham. 1976
LCso Nllml and Laham. 1976
LCso Nllml and Laham. 1976
LCso Nllml and Laham. 1976
LCso Nllml and Laham. 1976
LCso Elsler. 1985
-------
TABLE 4-1 (cent.)
2 Median Response Concentration
*fc
Q.
4*
O
O
00
Species
White sucker
Catostomus c earner son 1
Catostomus comersonl
Channel catfish
Ictalurus punctatus
Mosqultof Ish
Gambusla afflnls
Striped bass
Ttorone saxltllls
Striped Bass
Moronc saxatllls
(prolarva)
Horone saxatllls
(larva)
Horone saxatllls
(juvenile)
Blueglll sunflsh
Blueglll
Lepoals macrochlrus
Frog
Xenopus laevls
(embyro)
Xenopus laevls
(tadpole)
Chemical
Na2Se03
Na2Se03
Se02
45. 7X
Se
Se
Se
Se
Na2Se04
Na2Se04
Na2Se04
Se
Se02
Se
Se
Test
Method
Fl
Fl.H
FT
S
NR
S
S
S
FT
FT
FT
S
FT
NR
NR
24-Hour
NR
NR
46.7 mg/t
(42.1-51.8)
NR
NR
NR
NR
NR
NR
NR
NR
NR
77.3 mg/t
(72.1-82.8)
NR
NR
48 -Hour
NR
NR
NR
NR
>6 mg/t
NR
NR
NR
NR
NR
NR
NR
NR
NR
NR
96 -Hour
31.4 mg/l
29 mg/t
19.1 mg/t
(17.1-21.4)
6.1 mg/t
(4.1-9.0)
12.6 mg/t
1.32 mg/t
(1.09-1.69)
2.40 mg/t
(2.89-3.05)
1.55 mg/t
(0.97-2.47)
9.8 mg/t
(8.3-11.3)
13.0 mg/t
(11.6-14.5)
85.8 mg/t
(81.6-90.0)
4.5 mg/t
NR
4.0 mg/t
NR
Comments
"50
"50
LC5Q temperature = 24.9°C
"50
"50
LCjQ, hardness = 40 mg/t
LC50, hardness = 285 mg/t
LC50. salinity = 1°/00
hardness = 455 mg/t
"50
"50
"50
LC5Q. hardness = 40 mg/t
LC50, temperature = 24.9°C
"50
72-hour. LC5o = 8 mg/t
Reference
Etnler et al.. 1987
Klaverkamp et al
1983
Cardwell et al..
• •
1976
Mayer and E Hers leek,
1986
Elsler. 1985
Palawskl et al.,
Palawskl et al.,
Palawskl et al.,
Klauda. 1986
Klauda. 1986
Klauda. 1986
Palawskl et al..
Cardwell et al..
Elsler. 1985
Elsler. 1985
1985
1985
1985
1985
1976
-------
TABLE 4-1 (cont.)
I
en
Species Chemical
Haddock Se
Melanoqrammus
aegllflnus (larvae)
Sheepshead minnow Se
Cyprlnodon varlegatus
Atlanta stlverslde Se
Menldla menldla
Four spine stickleback Se
Apeltes quaduacus
Plnftsh Se
Laqodon rhomb lodes
Mullet Wa2Se03
Mug 11 auratus
(larvae)
Summer flounder Se
Parallchthys dentatus
(larvae)
Winter flounder Se
Pseudopleuronectes
amerlcanus
(larvae)
Striped gouraml SeOp
Collsa fasclatus
Median
Test
Method 24-Hour
NR NR
NR NR
NR NR
NR NR
NR NR
S NR
NR NR
NR NR
S 9.99 mg/t
Response Concentration
48-Hour 96-Hour
NR 0.6 rog/t
NR 7.4-67.1 mg/t
NR 9.72 mg/t
NR 17.4 mg/t
NR 4.4 mg/t
(2.9-6.7)
6.2 ppm NR
(±1.08)
NR 3.5 mg/t
NR 14.2-15.1
mg/t
5.77 mg/t 2.65 mg/t
Comments
1050
LC50
LCso
LC50
LC50
LC50, temperature = 18°C
LCSO
LCSO
LCjQt temperature = 25°C
120 -hour LCso =2.25 mg/t
Reference
Elsler. 1985
Elsler. 1985
Elsler. 1985
Elsler. 1985
Elsler. 1985
Unsal. 1987
Elsler. 1985
Elsler. 1985
Srlvastava and
Tyagl. 1985
FT = Flowthrough; N = measured; NR = not reported; S = static
oo
lO
-------
selenlte or selenate was comparable (Etnler et al., 1987) and zebraflsh were
equally sensitive to the potassium and sodium salts of selenlte and selenate
(N11m1 and Laham, 1976). Klauda (1986) reported a nearly 10-fold Increase
1n tolerance of striped bass, Horone saxatlHs. to sodium selenate as fish
developed from the prolarva to juvenile stages.
Studies assessing the toxldty of selenium to saltwater vertebrates were
less numerous than those dealing with freshwater vertebrates. Toxldty
values ranged from a 96-hour LC5Q of 0.6 mg/ft, for haddock larvae,
Melanogrammus aegllflnus. to 96-hour LC5Qs of 14.2-15.1 mg/i for winter
flounder larvae, Pseudopleuronectes amerlcanus. exposed to unidentified
forms of selenium (Elsler, 1985).
In another study, Hlraoka et al. (1985) assessed the toxldty of
selenium as sodium selenlte to red medaka, Oryzlas latlpes. Investigators
exposed 8-day-old fry to 1, 10 and 100 ppm selenium for 24 hours at 25°C.
Test solutions were prepared In a 50:50 mix of tap and delonlzed water.
Observed mortality levels In the test solutions were 0, 30 and 100%,
respectively.
Klauda (1986) assessed the toxldty of selenate as the sodium salt to
embryos of the striped bass, Morone saxatllls. Embryos were exposed to a
series of selenium concentrations ranging from 6-2000 mg/i 1n 1 1
volumes. Solutions were aerated and renewed dally during the 96-hour test.
The Investigator reported a 93.3X hatch and survival for eggs exposed to
2000 mg Se/l for 4 days.
The acute toxldty of selenium to aquatic Invertebrates as expressed by
the LC5Q 1s presented 1n Table 4-2. Ninety-six hour LC5Qs of 33, 1.90
and 0.25 mg/a were reported for the crab, Scylla serrata. bay scallop,
Argopecten Irradlans. and surf clam, Splsula so11d1ss1ma, respectively,
0144d 4-6 04/01/89
-------
TABLE 4-2
Nedtan Response Concentration For Aquatic Invertebrates Exposed to Selenium
Species
Water flea
Daphnla magna
Daphnta magna
Oaphnla magna
Water flea
Oaphnla magna
(5th Instar)
Water flea
Daphnla magna
(5th Instar)
Water flea
Oaphnla magna
(juveniles)
Oaphnla magna
Oaphnla magna
Daphnla pulex
Daphnla pulex
Daphnla pulex
Daphnla pulex
Cladocera
Cerlodaphnla afflnls
Copepod
Acartta clausl
Acartla tonsa
Chemical
Se
Se
Na2Se03
Ma2Se03
Na2Se04
Na2Se04
45. 7X
Na2Se03
45. 7X
Na2Se03
Ma2Se03
Na2Se03
Na2Se03
Na2Se03
Na2Se03
Se
Se
Test
Method
S
NR
FT
SR
SR
SR
S
S
NR
S
S
S
S
NR
NR
Median
24 -Hour
0.66 mg/t
(0.53-0.87)
NR
NR
1.65 ppn
1.51 ppm
NR
NR
NR
NR
NR
NR
NR
0.76 mg/t
(0.64-0.90)
NR
NR
Response Concentration
48-Hour
0.43 ng/t
(0.35-0.57)
<0.25 mg/t
0.71 mg/t
0.68 ppn
0.75 ppm
0.55 ppm
(0.50-0.60)
4 mg/t
(3.0-5.2)
1 mg/t
(0.5-1.9)
3.87 mg/t
(3.5-4.46)
1.37 mg/t
0.61 mg/t
0.098 mg/t
0.60 mg/t
(0.51-0.71)
NR
NR
96-Hour
NR
0.71 mg/t
NR
0.44 ppm
0.58 ppm
NR
NR
NR
NR
NR
NR
NR
NR
1.74 mg/t
0.80 mg/t
Comments
"50
"50
"50
"50
"50
"50
EC5Q, temperature = 18°C
hardness = 280 mg/t
EC5Q, temperature = 18°C
hardness = 40 mg/t
"50
"50
"50
"50
LC5Q. temperature = 23°C
"50
"50
Reference
LeBlanc. 1980
Elsler. 1985
Etnler et al.. 1987
Johnston. 1987
Johnston. 1987
Johnston, 1987
Mayer and
Ellersleck. 1986
Mayer and
Ellersleck. 1986
Reading and Bulkema,
1983
Etnler et al.. 1987
Etnler et al.. 1987
Etnler et al.. 1987
Owsley and McCauley.
1986
Elsler. 1985
Elsler. 1985
O9
-------
TABLE 4-2 (cont.)
o
— ' Median Response Concentration
^
Q.
4*
00
04/01/89
Species
Copepod (cont.)
Hyallela azteca
Hayallela azteca
Notocalllsta sg.
Allorchestes
compressa
Allorchestes
compressa
Cyclaspts usltata
Scud
Hyallela azteca
Blue crab
Calllnectes sapldus
Dungeness crab
Cancer maglster
(larvae)
Crab
Cancer maglster
(zoeae)
Crab
Scylla serrata
Shrimp
Hysldopsls bah la
(adult)
Hysldopsls bahla
(juvenile)
Brown-shrimp
Penaeus aztecus
Chlronomus plumosus
Chemical
Se
Na2Se03
Na2Se03
Na2Se03
Na2Se03
Na2Se03
Na2Se04
Se
Se
Se02
SeOp
Se
Se
Se
45. 7X
Na2Se03
Test
Hethod
NR
FT
FT.H
FT.H
FT.H
FT.H
FT.H
NR
NR
S
S
NR
NR
NR
S
24 -Hour
NR
NR
NR
NR
NR
NR
NR
NR
NR
NR
68 mg/t
NR
NR
NR
NR
48 -Hour
NR
0.94 mg/t
NR
NR
NR
NR
NR
NR
NR
NR
46 mg/t
(39.5-52)
NR
NR
NR
50 mg/t
(41-61)
96-Hour
0.34 mg/t
NR
2.88 mg/t
6.17 mg/t
4.77 mg/t
6.12 mg/t
0.76 mg/t
4.6 mg/t
(2.7-7.8)
1.04 mg/t
>10 mg/t
33 mg/t
(28.4-38.3)
1.5 mg/l
0.6 mg/t
1.2 mg/t
(0.8-1.8)
NR
Comments Reference
IC50 Elsler. 1985
LC5Q Etnler et al..
LC5Q Etnler et al. .
LCso Etnler et al. ,
LC5Q Etnler et al..
LC5Q Etnler et al..
LC§o Etnler et al..
lC5o Elsler. 1985
LC$o Elsler. 1985
LC5Q. temperature = 15°C Martin et al..
LCso Krlshnaja et al
1987
LCso Elsler. 1985
LC50 Elsler. 1985
LCso Elsler. 1985
ECso, temperature = 22*C Mayer and
hardness - 280 mg/t Ellersteck. 198
1987
1987
1987
1987
1987
1987
1981
••
6
-------
TABLE 4-2 (cont.)
Median Response Concentration
Species Chemical Test
Method 24-Hour 48-Hour 96-Hour
Brown-shrimp (cont.)
Chlronomus plumosus 45. 7X S NR
Mosquito larvae Se NR NR
Culex fatlgans
Nidge Se NR NR
Tanytarsus dlsslmllls
Snail Se NR NR
Physa
Oyster SeO? S NR
Crassostrea glgas
(embryos)
Mussel Se02 S NR
Mvtllus edulls
(embryos)
Bay scallops SeOp S NR
Argopecten Irradlans
(juvenile)
Surf clam SeOp S NR
Splsula solldlsslma
(Juvenile)
36.5 mg/t NR
(25.2-52.9)
<3.10 mg/t NR
NR 42.4 mg/t
>10 mg/t 24 mg/t
>10 mg/t NR
>10 mg/t NR
NR 0.25 mg/t
(0.23-0.28)
NR 1.90 mg/t
(1.79-2.01)
Comments Reference
ECjQ, temperature = 22°C Mayer and
hardness = 39 mg/t Ellersleck. 1986
LC50 Elsler. 1985
LCso Elsler. 1985
LCso Elsler. 1985
EC50. temperature = 20°C Martin et al.. 1981
EC50. temperature = 14°C Martin et al.. 1981
LC50. temperature = 20°C Nelson et al.. 1988
LC5Q. temperature = 20°C Nelson et al.. 1988
FT = Flowthrough; H = measured; NR = not reported; S = static; SR = static renewal
o
03
-------
exposed to selenium as selenium dioxide (Krlshnaja et al., 1987; Nelson et
al., 1988). Martin et al. (1981) reported that the 96-hour LC5Q of
selenium when derived from selenium dioxide for crabs, oysters and mussels
was >10 mg/l.
The toxldty of selenium as sodium selenlte was reported for water fleas
and amphlpods (Reading and Bulkema, 1983; Owsley and McCauley, 1986; Etnler
et al., 1987; Johnston, 1987). The 48-hour LC5Qs for Daphnla magna were
0.68 and 0.71 mg/l, while those for Daphnla pulex ranged from 0.098-3.87
mg/i. The 48-hour LC,. of selenium as sodium selenlte to another
cladoceran, Cerlodaphnla afflnls. was comparable with that for species of
Daphnla (0.60 mg/l). Amphlpods were slVghtly less sensitive than
cladocerans to selenium as sodium selenlte. The 96-hour LC5Qs for several
species ranged from 2.88-6.17 mg/a. Mayer and Ellersleck (1986) reported
a 48-hour EC5Q that was 4-fold lower for D. magna when assays were
conducted 1n soft water, but no significant differences for Chlronomus
plumosus when assays were conducted In hard and soft water. U.S. EPA
(1987a) reported the results of additional studies 1n which the toxldty of
selenium as selenlte ranged from 0.21 mg/l for D_. magna to 203 mg/a for
the leech, Nephelopsls obscura.
The toxldty of selenium as sodium selenate to 5th Instar Daphnla magna
was comparable to that observed for sodium selenlte (Johnston, 1987). The
48-hour LC s for selenium as sodium selenate were 0.55 and 0.75 ppm. In
contrast, the toxldty of selenium as sodium selenate to Hyallela azteca was
4- to 8-fold greater than that observed with sodium selenlte (Etnler et al.,
1987). The 96-hour LC5Q was 0.76 mg/i.
Some Investigators did not Identify the form of selenium to which
aquatic Invertebrates were exposed (LeBlanc, 1980; Elsler, 1985). The
0144d 4-10 06/15/89
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amphlpod, Hyallela azteca. was the most sensitive Invertebrate Identified 1n
this category, with a 96-hour LC5Q of 0.34 mg/i. The midge, Tanytarsus
d1ss1m111s. was the most tolerant Invertebrate Identified, with a 96-hour
LC5Q of 42.4 mg/1.
In other studies, Adams and Heldolph (1985) conducted static tests
exposing fed and unfed Daphnla magna to selenium as sodium selenlte. The
48-hour EC5_s for unfed and fed daphnlds were 0.47 and 1.5 mg/a, respec-
tively. The 48-hour NOEC for unfed daphnlds was 1.0 mg/l.
Pagano et al. (1986) assessed the toxlclty of selenium to embryos of the
sea urchin, Paracentrotus 11v1dus. Gametes were collected from sacrificed
adults. Fertilized embryos were exposed for the duration of their develop-
ment. Investigators observed a blockage of development at the gastrula
stage for embryos exposed to 55.3 ppm selenium.
Wolfenberger (1986) assessed the survival of the hermit crab, CUban-
arlus vlttatus. after a 24-hour period of exposure to 100 ppm selenium under
varying conditions of salinity and temperature. Mean survival time was
greatest In 20 °/ salinity (~80 and 140 hours for two populations)
when assays were conducted at 16°C. At 20 and 24°C, mean survival time was
greatest for crabs exposed to selenium 1n 10 / salinity solutions
(~80 and 215 hours, and 130 and 70 hours, respectively).
Johnston (1987) reported LT5Qs for the water flea, Daphnla magna.
exposed to selenium as sodium selenlte and selenate. LT5_s for daphnlds
exposed to 3.0, 1.0, 0.8, 0.6 and 0.5 ppm selenium as sodium selenate were
17, 31, 55, 86 and 150 hours, respectively. LT5Qs for daphnlds exposed to
the same concentrations of selenium, but as sodium selenlte, were 9.5, 26.5,
50, 74 and 99 hours, respectively. The IT™ for daphnlds exposed to 0.4
ppm selenium as sodium selenlte was 130 hours. The Investigators reported
0144d 4-11 04/01/89
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that sodium selenlte was 1.42 times more toxic to daphnlds than sodium
selenate based on the Incipient LC s of 0.31 and 0.44 ppm selenium,
respectively.
In a series of behavioral and physiological studies, several groups of
Investigators assessed the effects of selenium on avoidance responses by
fish and respiration by crabs and fish. Weir and H1ne (1970) reported that
goldfish, Carasslus auratus, exhibited behavioral Impairment at 0.25 ppm.
Watenpaugh and Beltlnger (1985a) reported that fathead minnows, Plmephales
promelas. did not avoid selenate at concentrations of 0.3-11.2 mg Se/l.
Watenpaugh and Beltlnger (1985b) reported that oxygen consumption by fathead
minnows was not affected by exposure to 60 mg. Se/l for 24 hours, although
minnows at this level may have physiologically compensated to maintain
oxygen consumption rates. Wolfenberger (1987) reported that oxygen consump-
tion by the hermit crab, C11banar1us vlttatus. exposed to 100 ppm selenium
was depressed at 16°C 1n 10 / salinity test medium, although oxygen
consumption rates were generally elevated at lower salinities and higher
temperatures.
4.1.2. Chronic Effects on Fauna.
4.1.2.1. TOXICITY — N11m1 and Laham (1975) assessed the toxlclty of
selenium as selenium dioxide to embryos and larvae of the zebraflsh,
Brachydanlo rerlo. Embryos and larvae were exposed to selenium at 26°C 1n
covered petrl dishes 1, 2.5, 7 and 27 hours after fertilization (correspond-
ing to Stages 3-5, 10, 15 and 21 of normal embryonic development). Exposure
media were renewed dally. Hatching and mortality of zebraflsh embryos was
unaffected by exposure to <10 mg/8, for 168 hours of treatment for any of
the embryonic stages. Mortality of larvae after hatching was significantly
affected by selenium at concentrations >3 mg/a after 168 hours of
treatment and at 10 mg/i after 96 hours of treatment.
0144d 4-12 04/01/89
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Cardwell et al. (1976) assessed the toxlclty of selenium as selenium
dioxide to fathead minnow, Plmephales promelas. goldfish, Carrasslus
auratus. bluegUl sunflsh, Lepomls macrochlrus. and flagflsh, Jordanella
florldae. Fish were exposed to selenium under Intermittent flow conditions
at 24-25°C for 120-336 hours. The 120-, 144- and 168-hour LC5 s for
fathead minnows were 4.5, 3.2 and 2.9 mg Se/l, respectively. The 120-,
216-, 144-, 168-, 264- and 336-hour LC5()s for goldfish were 32.7, 22.3,
17.2, 13.0, 11.5 and 8.8 mg/l, respectively. The 168-, 192-, 240-,
288- and 336-hour LC5Qs for bluegllls were 30.7, 27.7, 23.6, 20.5 and 17.6
mg Se/a, respectively. Investigators reported LT,. s (1n Heu of
LC5Qs) of 83, 67, 68, 55 and 44 hours for flagflsh exposed to 11.2, 16.9,
21.8, 27.9 and 37.6 mg Se/l, respectively. Cardwell et al. (1976) also
examined the latent effects of exposure to selenium 1n fathead minnows and
flagflsh. Fish exposed to <33.2 mg Se/a for 24 hours were then monitored
1n uncontamlnated water for 28 days. No effects on survival or growth of
any of the treated groups of fish were reported.
Klaverkamp et al. (1983) assessed the toxlclty of selenlte selenium to
yellow perch, Perca flavescens. 1n an Intermittent flowthrough exposure
study. Perch were collected by beach seine from a mercury-polluted lake 1n
northwestern Ontario. A 240-hour LC-n of 4.8 mg Se/J. was reported.
Reading and Bulkema (1983) assessed the chronic toxlclty of selenium as
sodium selenlte to Daphnla magna In a 28-day static-renewal test. Exposure
concentrations were 0.2, 0.4, 0.6 and 0.8 mg Se/i. Daphnlds were fed dally
a 50,000 cells/mi, algal suspension. No effects on total eggs per daphnld,
live young per daphnld and mean brood size were reported, except at 0.8 mg
Se/l.
0144d 4-13 04/01/89
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Adams and Heldolph (1985) assessed the toxldty of selenium as sodium
selenlte to Daphnla magna 1n 21-day static-renewal tests. Selenium concen-
trations were measured throughout the study. Daphnlds were fed trout chow
at a concentration of 30 mg/8. and test solutions were renewed 3 times/
week. The Investigators reported 7-, 14- and 21-day EC^_s of 0.38, 0.38
and 0.35 mg/l, respectively. The NOEC based on survival for all observa-
tion periods was 0.24 mg/l. The NOEC based on reproduction for all
observation periods was >0.24 mg/l.
Ahsanullah and Brand (1985) assessed the toxldty of selenium as sodium
selenlte to the amphlpod, Allorchestes compressa. First Instar juveniles
were exposed to a continuous flow of sodium selenlte stock solutions mixed
with seawater (32-35 °/00) for 4 weeks. Exposure to 44 yg Se/8. did
not significantly affect either growth or survival of treated Individuals.
Amphlpods exposed to 193 yg Se/8. experienced 100% mortality by the end
of the study, while animals exposed to 93 yg Se/B. experienced reduced
growth and a significant level of mortality over the 4-week study. The
estimated MATC for Allorchestes compressa juveniles exposed to sodium
selenlte 1s 44-93 yg Se/l.
Elsler (1985) reported the results of studies assessing the toxldty of
selenium to several aquatic Invertebrates. The 14- and 28-day LC s for
the waterflea, Daphnla magna. exposed to selenium were 0.43 and 0.24 mg
Se/i, respectively. The 14-day LC5Q for scud, Hyallela azteca. exposed
to selenium was 0.07 mg Se/l. Elsler (1985) also reported the results of
studies assessing the toxldty of selenium to aquatic vertebrates. The
113-hour LC5Q of selenium to embryos and the 5- and 7-day LC s Of
selenium to tadpoles of the frog, Xenopus laevls. were 2.0, 2.6 and 1.5 mg
Se/l, respectively. The 48-day LC5Qs for selenium 1n blueglll sunflsh.
0144d 4-14 04/01/89
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Lepomls macrochlrus. and fathead minnow, Plmephales promelas. were 0.4-2.0
and 1.1 mg Se/a, respectively. The 10-day LC5Q In perch, Perca flaves-
cens, was 4.8 mg/a, while the 43-day LC™ In coho salmon, Oncorhynchus
klsutch. was 0.16 mg/a. The 9-, 21- and 96-day LC5Qs for rainbow trout,
Sal mo qalrdneM. exposed to selenium were 5.4-7.0, 0.46 and 0.29 mg Se/a,
respectively.
Bennett et al. (1986) assessed the uptake and transfer of selenium
through an aquatic food chain (algae, Chlorella pyrenoldosa. to rotifers,
Brachlonus calydflorus) and Its effects on fathead minnow larvae,
Plmephales promelas. Algae were cultured 1n the presence of selenium for 3
days, with a maximum concentration of selenium 1n the culture media of 2.5
mg Se/a. Rotifers were permitted to feed for 5 hours In selenium-laden
algae before harvesting. The algae:rot1fer ratio (yg algae/maiyg
rotifer/ma) was 25:50. The concentration of selenium 1n rotifers reached
a plateau at ~40 yg Se/g rotifer. Three feeding experiments were con-
ducted with larval fathead minnows. The first experiment entailed feeding
minnows contaminated rotifers for 7 days commencing 4 days posthatch,
followed by 19 days on a control diet. The second experiment entailed
control diets for 8 days posthatch, followed by a selenium-contaminated diet
for 9 days. The third experiment entailed control diets for 2 days
posthatch and a selenium-contaminated rotifer diet for 7 days. No
mortalUes among larval fish could be attributed to dietary selenium, but
there were significant reductions In final dry weight of treated larvae In
the first and second experiments. The mean final larval selenium
concentrations 1n these two experiments were 43 and 51.7 yg/g,
respectively.
G11lesp1e and Baumann (1986) assessed the effect of high tissue
concentrations of selenium on the reproductive success of blueglll sunflsh,
0144d 4-15 06/15/89
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Lepomls macrochlrus. Adult bluegllls were collected by electroshocklng from
a cooling water Impoundment and a municipal water supply lake In North
Carolina. Males and females were mated with fish both from their own lake
and the other water body. Fertilization success was determined by stripping
eggs from females and combining with sperm J[n vitro. Percent fertilization
was determined from the proportion of mltotlcally active zygotes 2-3 hours
after fertilization. Hatching success was estimated by holding fertilized
eggs In closed aquaria with redrculatlng dty lake water at 22-25°C. The
Investigators reported significant differences 1n percent fertilization or
hatch among parent combinations. Larvae from crosses Involving selenium-
contaminated females had gross abnormal morphologies characterized by
general edema. Concentrations of selenium 1n the ovaries of the females
ranged from 5.79-8.0 mg/kg wet weight; these levels were 16-21 times higher
than those 1n uncontamlnated fish.
Klauda (1986) assessed the effects of exposure of early life stages of
the striped bass, Morone saxatllls. to selenium as sodium selenate.
Prolarvae, postlarvae and Juveniles were exposed to low (0.089-0.099 mg
Se/8.) and high (1.217-1.360 mg Se/l) concentrations of selenium under
constant flow conditions for 60 days. A significant reduction In expo-
nential growth rates as determined by total length was reported for both
selenium treatments for days 3-15 compared with controls, but no significant
difference based on dry weight. There were no differences observed between
days 19 and 60. A significant Incidence In developmental abnormalities of
the lower jaw and severe blood cytopathology were also reported.
Owsley and McCauley (1986) assessed the toxldty of sodium selenlte to
four consecutive generations of CeModaphnla afflnls. Treatments consisted
of exposure to 0.0, 0.05, 0.1, 0.2, 0.4 and 0.8 mg Se/l until three broods
0144d 4-16 06/15/89
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were produced In the controls (~8 days). Test solutions were renewed and
organisms were fed every other day. The assays demonstrated a reduction 1n
the tolerance of Cer1odaphn1a aff1n1s In succeeding generations. The NOEL
was reduced from 0.2 to 0.1 mg/a after two generations of exposure to
selenium.
Hunn et al. (1987) assessed the chronic toxldty of selenium as sodium
selenlte to rainbow trout fry, Salmo galrdnerl. 1n partial life-cycle
studies. Fry were exposed to selenium under flowthrough conditions at 12°C
for 90 days. F1sh were fed dally a commercial diet supplemented with live
naupl11 of brine shrimp. Concentrations of selenium 1n exposure vessels
were determined by hydride generation atomic absorption. Exposure of fry to
>47 yg Se/a significantly reduced survival and fry length after 90 days.
Survival and growth were not affected at <21 yg Se/a. Weight was
significantly reduced at 100 yg Se/a by the end of the study. The
highest body burden levels of selenium were achieved after 30 days of
treatment and declined thereafter. BCFs were Inversely related to exposure
concentrations but did not exceed 200 yg/a. Exposure of fry to >12 yg
Se/a significantly reduced the calcium concentrations 1n bone. The
Investigators suggested that 12 yg Se/a represents a NOEL for Inorganic
selenium 1n rainbow trout.
Johnston (1987) assessed the subacute toxldty of selenium as sodium
selenate In daphnlds (12±6 hours old neonates) exposed to selenium at 22°C
for 15 days. Test medium was renewed dally. Daphnlds were provided with
cultures of Chlorella pyrenoldosa (108 cells/ma) as a food source.
Daphnlds demonstrated a concentration-response relationship between
Increasing concentrations of selenium (0.025-0.5 ppm) and reductions In the
percent Increase In Initial length and mean numbers of eggs produced. There
0144d 4-17 04/01/89
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were no significant differences regarding growth between groups at <0.05 ppm
or regarding mean numbers of eggs produced at <0.025 ppm. There were also
no differences observed In the percent maturation or mortality levels for
daphnlds exposed to 0.025 ppm selenium compared with control daphnlds.
U.S. EPA (1987a) reported the results of chronic studies with myslds,
Mys1dops1s bahla. and sheepshead minnows, CypMnodon vaMegatus, exposed to
selenlte selenium. Number of offspring produced and survival of first
generation myslds were reduced significantly at 0.32 mg/a. Nonstatlstl-
cally significant reductions 1n survival (18%) and reproduction (22%) were
observed In myslds exposed to 0.14 mg/a. Percent hatch of sheepshead
minnows was <4% at concentrations of 0.97, 1.9 and 3.6 mg/a. Juveniles
experienced 4, 24 and 90% reductions In survival at 0.47, 0.97 and >0.97 mg
Se/a, respectively. Growth of juvenile sheepshead minnows was reduced by
8% at 0.47 and 0.97 mg/a.
Woock et al. (1987) assessed the effects of dietary selenium as either
sodium selenlte or selenomethlonlne to blueglll sunflsh, Lepomls macro-
chlrus. Effects of dietary selenium on fish were also assessed In conjunc-
tion with waterborne selenium as sodium selenlte. Treatments consisted of
dietary selenium as selenomethlonlne at concentrations of 3, 13 and 30 yg
Se/g, dietary selenium as sodium selenlte at 13 and 30 yg Se/g, and a
combined treatment of dietary selenomethlonlne at 13 yg Se/g and a water-
borne concentration of sodium selenlte of 10 yg Se/a. Selenium 1n water
and food was determined by hydride generation atomic absorption spectro-
scopy. Exposure of adult bluegllls to these treatments for 260 days
resulted 1n significantly higher levels of mortality and significantly lower
final body weights and lengths among fish fed a diet supplemented with 30
yg Se/g. Exposure of adult bluegllls to selenium for 287-324 days
0144d 4-18 04/01/89
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resulted In reproductive Impairment manifested by a reduction In larval
survival and the percent of larvae with teratogenlc conditions. Larval
survival was reduced In groups that received a diet supplemented with 30
yg Se/g 1n either form and adults fed a diet containing 13 yg Se/g as
sodium selenlte combined with a waterborne exposure of 10 yg Se/l as
sodium selenlte. Exposure of larvae to the dletary/waterborne selenium
treatment and 30 yg/g dietary selenium as selenomethlonlne produced 50 and
100% of larvae with terata, respectively. There were no effects on the
percentage hatch for eggs from adults treated as described above. The NOEL
for dietary selenium 1n either form In blueglll sunflsh appears to be
between 13 and 30 yg Se/g.
Boyum and Brooks (1988) assessed the effects of selenium In water and
diet on Daphnla magna. Oaphnlds were exposed to 0.05, 0.1, 0.5 and 1.0 mg
Se/l as sodium selenate In culture water at 23°C for 28 days. Test
solutions were renewed twice weekly. Daphnlds were fed Chlamydomonas reln-
hardtH dally. In another part of the experiment, algae exposed to sodium
selenate at the concentrations listed above were fed to daphnlds for the
28-day treatment period. In daphnlds exposed to 1.0 mg dissolved Se/l or
fed algae exposed to 1.0 mg Se/l 10054 mortality occurred In 16 and 7 days,
respectively. Daphnlds given algae exposed to 0.75 mg Se/l experienced
100% mortality after 18 days. Mortality was 80-90% 1n daphnlds exposed to
0.05, 0.1 and 0.5 mg dissolved Se/l for 28 days. Daphnlds given algae
exposed to 0.05-0.5 mg Se/l experienced 30-50% mortality during the 28-day
study. Control mortality 1n both studies ranged from 10-20%. There were no
significant differences 1n numbers of offspring produced among controls.
Total number of offspring produced by daphnlds fed selenium-laden algae
exceeded that of control daphnlds In all treatment groups except for the 1.0
0144d 4-19 04/01/89
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mg Se/8, treatment groups. The Intrinsic growth rate for daphnlds was
always significantly greater In daphnlds fed selenium-laden algae and
declined with an Increase 1n the concentration of selenium 1n which the
algae were cultured.
4.1.2.2. BIOACCUMULATION/BIOCONCENTRATION — Barrows et al. (1980)
assessed the bloconcentratlon and elimination of selenium (as selenous add)
by blueglll sunflsh, Lepomls macrochlrus. F1sh were exposed In open aquaria
under flowthrough conditions with a 5-6 volume turnover/day. Sample size
for the 28-day exposure portion of the study was 100 fish. Fish remaining
at the end of the exposure phase were transferred to clean systems for a
7-day depuration phase. The mean water concentration for selenium 1n this
study was 120 yg/l. The maximum BCF was 20 and the tissue half-life was
between 1 and 7 days.
Flnley (1985) assessed the uptake of selenium by blueglll sunflsh,
Lepomls macrochlrus. fed mayfly nymphs, Hexagenla llmbata. collected from a
selenium-contaminated lake. Control sunflsh were fed a low-selenium diet
consisting of mealworms. F1sh were fed to satiation twice dally for 44
days. There were four fish In each treatment group. F1sh were held In
glass aquaria at 21PC under constant flow conditions. Three of four
bluegllls fed selenium-contaminated mayflys died on days 17, 35 and 44.
Selenium concentrations 1n skeletal muscle of those fish were 5.1, 5.4 and
7.9 yg Se/g wet weight, respectively. Liver concentrations were 8.5, 15.1
and 86 yg Se/g, respectively. Concentrations of selenium 1n muscle and
liver of the remaining fish were 7.5 and 69 yg/g, respectively. Concen-
trations of selenium 1n muscle of control fish ranged from 1.8-2.1 vg/g.
Concentrations 1n the livers of two fish were 5 and 7 yg/g. The Investi-
gators also reported that treated fish had a variety of hlstopathologlcal
abnormalities.
0144d 4-20 04/01/89
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Bertram and Brooks (1986) assessed the accumulation of selenium from
food and water by fathead minnows, Plmephales promelas. F1sh were either
exposed to waterborne selenium (as sodium selenate), offered daphnlds raised
on selenium-contaminated algae, Chlamydomonas, or subjected to both treat-
ments under flowthrough conditions at 25°C. Selenium water concentrations
were 10, 20 and 40 ng Se/ml. Concentrations of selenium 1n the food
supply were 1.33, 3.66 and 7.32 jjg Se/g. F1sh were exposed to waterborne
selenium and both treatments simultaneously for 8 weeks. Duration of
treatment for fish fed a selenium-contaminated diet was 11 weeks. A minimum
depuration period of 2 weeks followed the termination of treatment 1n all
cases. Uptake of selenium by minnows exposed ,to 10 and 20 ng/mi reached a
plateau at a body burden level of -0.5 vg Se/g fish after 25-30 days.
Uptake of selenium by minnows exposed to 40 ng/mi reached a plateau at a
body burden level of ~0.8 ^g Se/g fish after 20 days. All groups demon-
strated a linear decrease 1n body burden levels of selenium to ~3 yg/g
after a 30-day depuration period. Whole body burden levels of selenium 1n
fish offered a selenium-contaminated diet demonstrated a linear Increase
over the course of the treatment period for all treatments reaching ~0.3,
0.5 and 1.2 jjg Se/g fish for the low, moderate and high treatments,
respectively, after 80 days. Depuration of selenium was observed following
the conclusion of the exposure phase but at a slower rate than that observed
1n fish exposed to waterborne selenium. Fish exposed to both sources of
selenium also demonstrated a linear Increase 1n body burden levels of
selenium without reaching a plateau during the 56-day exposure phase,
reaching 0.4, 0.9 and 2.0 pg Se/g fish for the low, moderate and high
treatments, respectively. Depuration of selenium from these fish was slow.
0144d 4-21 04/01/89
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Hodson et al. (1986) assessed the accumulation of waterborne radio-
labeled selenlte by rainbow trout, Salmo galrdnerl. eggs, fry and juveniles.
Fertilized eggs were obtained from a laboratory brood stock and Incubated at
10-12°C. Eggs were exposed to selenium In cylindrical mesh-bottomed
containers In 30 i tanks. Eggs were collected each day for 4 days.
Sac-fry were held In the same containers as described for the eggs, while
sw1m-up fry swam freely through the 30 l tanks. Fry were collected dally
for 4 days. Eggs and fry were exposed to 0.4 and 45.6 yg Se/a.
Juvenile trout were fed a caseln-torula diet supplemented with 0.4 yg Se/g
of dry feed. After 12 weeks on this diet, fish were held without feeding
for 4 days and exposed to the low and high treatments as described above.
Fish were subsequently sampled over the ensuing 96 hours. Eggs exposed to
the high-dose treatment accumulated 10-100 times more selenium (~100
yg/kg) than eggs 1n the low-dose treatment (<10 yg/kg). The majority of
the uptake occurred In the Initial 24 hours. Swim-up fry accumulated more
selenium than sac-fry. Fry experienced a linear Increase In the concentra-
tion of selenium over the 96-hour exposure period with no Indication of an
approaching plateau. Concentrations of selenium 1n sw1m-up fry from the
high dose approached 1000 yg/kg by the end of the study. Concentrations
of selenium In juveniles Increased as a function of both exposure concentra-
tion and time. Concentrations 1n liver were the highest (-1000 yg/kg)
among tissues examined (liver, viscera, gill, muscle and gill) after 96
hours. BCFs for the low-dose fish ranged from 3.1 1n embryos to 104 In
livers of juveniles. BCFs for the high-dose fish ranged from 1.6 1n sac-fry
to 31.6 1n livers of juveniles.
Klauda (1986) measured the uptake of selenium by prolarvae, postlarvae
and juveniles of striped bass, Horone saxatlHs. exposed to sodium selenate
0144d 4-22 06/15/89
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for 60 days under flowthrough conditions. Fed and starved Juveniles exposed
to 1.29 mg/l accumulated selenium at comparable rates, producing BCFs of
0.68 and 0.69. Fed juveniles exposed to 90 jig Se/l showed no Increase
In whole body levels of selenium, while starved juveniles had a BCF of 11.78.
Klelnow and Brooks (1986) assessed the uptake, distribution and elimi-
nation of orally administered selenium as the radlolabeled [75Se] sodium
salts of selenate and selenlte, and l-selenometh1on1ne In the fathead
minnow, Plmephales promelas. A single oral dose of test solution was
administered to fish by gavage at a level of 20 ng Se/g tissue wet weight.
Fish were held In flowthrough aquaria at 25°C and collected at various times
over a 40-day period. Selenium accumulated to a greater degree 1n liver and
kidney compared with muscle, adipose tissue or gonads. The pattern of
accumulation was generally similar for each of the compounds tested,
although selenate preferentially accumulated 1n the blood and
selenomethlonlne 1n the heart. Other significant differences 1n magnitude
of uptake during the absorption and early distribution phases were observed
for the liver, bile, kidney, spleen and gill. The half-lives In days for
selenate, selenlte and selenomethlonlne ranged from 3.9 (liver) to 487
(adipose tissue), 2.2 (liver) to 64 (heart) and 1.0 (liver) to 69 (adipose
tissue), respectively.
Pelletler (1986) assessed the accumulation of selenium by the mussel,
HytHus edulls. In the absence and presence of Inorganic and organic
mercury. Forms of selenium to which mussels were exposed Included Inorganic
dissolved selenlte Na2SeO~ and adsorbed organic selenium
(CghLOpSe)-. Mussels were exposed to 50 yg selenlum/l for 15-50
days In tanks provided with continuously circulating seawater. Mussels
accumulated Inorganic selenium but not organic selenium at a rate of 0.12 ng
Se/g/day In the absence of mercury. The presence of Inorganic (30 ^g
0144d 4-23 06/15/89
-------
Hg/a) and organic (3 yg Hg/1) mercury Increased the uptake of
Inorganic selenium to 0.24 and 0.40 ng Se/g/day, respectively. Organic
selenium became available to the mussels 1n the presence of methyl mercury,
and accumulated at a rate of 0.15 ng Se/g/day.
Etnler et al. (1987) reported the results of studies assessing the
accumulation of selenium In carp, Cyprlnus carplo, and fathead minnows,
Plmephales promelas. The BCF for selenium as sodium selenlte 1n carp for an
unspecified exposure duration and selenium concentration was 0.6-6.0. The
BCF for selenium as sodium selenlte 1n minnows exposed to 83 yg/ft, for 28
days was 4443.
Boyum and Brooks (1988) assessed the uptake of selenium as sodium
selenate by Daphnla magna. Daphnlds were exposed to radioactive selenium at
a concentration of 0.5 mg/8, In algae-free water and 1n solutions with
selenium-laden algae. A 72-hour duration exposure phase was followed by a
96-hour depuration phase. The rates of uptake and depuration and total
amount of selenium Incorporated by the daphnlds were reduced In the presence
of selenium-laden algae. There were no significant differences among three
treatments of selenium-laden algae In terms of uptake and depuration, except
for a single sample period for algae with the lowest ratio of selenium to
algae.
Boyum and Brooks (1988) also assessed the uptake of selenium as sodium
selenate by Daphnla magna In the presence of selenomethlonlne. Daphnlds
were exposed to selenium at a concentration of 0.50 mg/8. In one treatment
augmented with 1 and 2 mg Se-methlonlne/i In two other treatments. The
results Indicated that the uptake and depuration of selenium were decreased
by the presence of Increasing concentrations of selenomethlonlne.
0144d 4-24 04/01/89
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4.1.3. Effects on Flora.
4.1.3.1. TOXICITY — HolUbaugh et al. (1980) assessed the effects of
selenium on growth of natural assemblages of phytoplankton In enriched
seawater. Water samples from Sanlch Inlet, B.C., Canada, were collected by
peristaltic pump and augmented with N, P and SI. Water was then filtered
through a 102 ym pore mesh and transferred to experimental vessels.
Samples were held 1n an outdoor waterbath maintained at 12-16°C. Growth was
monitored dally as changes In the In vivo fluorescence of chlorophyll a.
There were no apparent effects observed 1n growth of natural assemblages of
phytoplankton or 1n growth of a species Isolated from field samples of
Tha1ass1os1ra aestevalls exposed to <1000 nM selenium.
Elsler (1985) reported the results of studies assessing the toxlclty of
selenium to algae. The 48-hour LC5Q for Oedogonlum cardlacum was <0.1
mg/a, while the 96-hour LC_. for Anabaena var1ab111s was 15-17 mg/a.
Gennlty et al. (1985) assessed the effects of selenium on the I1p1d
content of green and red algae, Dunallella pMmolecta and Porphyr1d1um
cruentum. respectively. Axenlc cultures of these species were grown 1n
artlflcal seawater at 22°C. Selenium as Na9SeO_ was added to achieve a
L. 0
concentration of 10 ppm. Growth was not affected 1n either of these species
at this concentration. No selen1te-1nduced changes were observed 1n
cultures of £_._ cruentum after 35 days of treatment. Significantly lower
levels of certain fatty adds of polar llplds were observed 1n cultures of
£. pMmolecta exposed to 10 ppm selenium after 35 days of treatment.
Tang et al. (1985) reported that 1.4 ppm selenium (as the sodium salt)
Inhibited population growth of Tetrahymena pyrlformls. A concentration of
140 ppm selenium completely stopped growth. Cao and Tang (1985) reported a
dose-dependent Inhibition In division of synchronized T. pyrlformls cells
exposed to 10, 20, 50 and 100 ppm selenium (as SeO?).
0144d 4-25 04/01/89
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TMpathl and Pandey (1985) assessed the effects of selenium (as sodium
selenate) on growth of the algae, Chlorella vulgaMs and Phormldlum
foveolarum. Tests were conducted 1n 150 ma of culture solution 1n 250
ma conical flasks. Assays were conducted for 30 days at temperatures
ranging from 25-29°C. Growth was determined by fresh and dry weight of
algae. Growth of cultures In the presence of the lowest concentration of
selenium tested (0.25 ppm) was only 60-61% of that observed In control
cultures. Growth of cultures In higher concentrations of selenium demon-
strated a concentration-dependent response. Growth of C. vulqaMs 1n a 4.0
ppm solution of selenium was 97% of that observed In controls and completely
Inhibited 1n P. foveolarum.
Prevot and Soyer-Goblllard (1986) assessed the effects of selenium on
growth of two marine dlnoflagellates, Prorocentrum mlcans and Crypthecodln-
1um cohnll. Investigators reported that selenium retarded growth of P.
mlcans 1n culture Incubated with 100 and 1000 ppm selenium. Growth was
slightly enhanced at 10 and 50 ppm selenium for the first 15 days of
treatment, but was Increasingly Inhibited compared with controls beyond that
point 1n time. Growth of C. cohn11 was severely Inhibited by selenium at
all test concentrations (10, 100, 1000 ppm) within 1.5 days of the Initia-
tion of treatment. A variety of ultrastructural changes were noted by the
Investigators In cells exposed to selenium.
Wang (1986) assessed the toxldty of selenium to duckweed, Lemna minor.
Tests were conducted In 200 ma fruit Jars with 200 ma of plant nutrient
solution and 20 colonies or 40 fronds of duckweed 1n each jar. Assays were
conducted for 4 days at 27°C. The test endpolnt was a reduction 1n the
number of fronds In comparison with control samples. Frond numbers were
determined dally. The 96-hour EC™ for duckweed exposed to selenium as
determined by this assay was 2.4 mg/a.
0144d 4-26 04/01/89
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4.1.3.2. BIOCONCENTRATION — Mann et al. (1988) measured the level of
selenium In algae, Euglena sp., from tailing areas of the Elliot Lake mining
district, Canada. A concentration of 2700 ng/g dry weight was reported In
algae from this area. The Investigators cited a concentration of 0.2 ng/g
1n world river water for comparison.
4.1.4. Effects on Bacteria. Pertinent data regarding the effects of
exposure of aquatic bacteria to selenium were not located 1n the available
literature cited 1n Appendix A.
4.2. TERRESTRIAL TOXICOLOGY
4.2.1. Effects on Fauna. Beyer and Cromartle (1987) surveyed the
concentrations of selenium In earthworms and soil from a variety of sites.
Their findings are presented In Table 4-3. Concentrations 1n soil ranged
from trace levels to 1.3 mg/kg at an Industrial site. Concentrations 1n
worms ranged from trace quantities to 7.6 mg/kg.
Beyer et al. (1987) assessed the potential for earthworms, Aporrectodea
tuberculata. Aporrectodea turglda and LumbMcus rubellus. to concentrate
selenium. A moderately eroded plowed field was divided Into 9 m2 plots.
Five plots were treated with selenous acid 1n the autumn of 1980 to achieve
concentrations of 0.44, 0.64, 0.89, 3.9 and 6.7 mg selenium/kg of soil.
Clltellate earthworms were collected 19 months after treatment of the plots.
Earthworms were refrigerated on moist paper towels for 3 days and then
sacrificed by Immersion Into boiling water. Worms were cut Into 1-3 cm
sections before alimentary canals were flushed with distilled water. The
concentration of selenium In worms from control plots (<0.1 mg Se/kg soil)
was 16 mg/kg. Concentrations of selenium 1n worms from treated plots were
36, 43, 51, 36 and 78 mg/kg, respectively. The uptake of selenium by worms
was reportedly not Influenced by pH or other soil variables (organic matter
content, phosphorous, potassium or magnesium).
0144d 4-27 04/01/89
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TABLE 4-3
Metal Concentration In Soil and Earthworms from Contaminated and Natural Sites*
Site
Species
Selenium
mg kg"1 (dry weight)
Earthworms
Soil
Comments
OO
Natural
Natural A
Natural B
Natural B
Natural C
Natural D
Natural E
Natural F
Elsenoldes carollnenls (c)
£. loennbergl (c)
Lumbrlcus rubellus (c)
E_. loennbergl (c)
£. loennbergl (c)
Aporretodea turglda (c)
£. loennbergl (c)
1.4
2.5
1.0
t
1.8
OO
us
Hell drained soil on
Patuxent Wildlife Res. Ctr.,
Laurel, ND
Moderately well drained soil
on Patuxent Wildlife Res.
Ctr., Laurel, MD
Moderately well drained soil
on Patuxent Wildlife Res.
Ctr., Laurel, MD
Poorly drained soil on
Patuxent Wildlife Res. Ctr..
Laurel, MD
Stream bed on Patuxent Wild-
life Res. Ctr., Laurel, MD
Mountalntop In Shenandoah
National Park, Skyland VA
Beach Swamp by Pocomoke
River, Whaleysvllle, MD
-------
TABLE 4-3 (cont.)
rvj
10
o
0
^
GO
Site
Natural
Natural F
Natural G
Mining
Mining A
Mining B
Mining B
Mining Cl
Mining C2
Mining C2
Selenium
mg kg"1 (dry weight)
Species Comments
Earthworms Soil
E. loennbergl (a) 1.5 t Beach Swamp by Pocomoke
River. Whaleysvllle, MD
Sparganophllas elsenl (c) 0.48 t Border of Potomac River.
Me lean. VA
L. terrestrls (a) t 0.58 Soil near Mineral mil
copper mine, Louisville, MD
A. tuberculata (c) 2.1 t Soil near New Galena lead
mine. New Galena, PA
A. Tonga (c) 0.48 t Soil near New Galena lead
mine, New Galena, PA
Pheretlma sp. (c) 0.19 t Dump near Ecton lead-copper-
zinc mine. Audobon, PA
L. terrestrls (c) t t Dump near Ecton lead-copper-
zinc mine, Audobon, PA
A tuberculata (ate) 0 60 t Dumo near Ecton Ip^rl-ronnpr
zinc mine Audobon, PA
-------
TABLE 4-3 (cont.)
OJ
o
Site Species
Mining
Mlnlnq C3 L. terrestrls (a*c)
M1n1nq C4 L. terrestrls (a)
Industrial
Industrial A Apporrectodea spp. (c)
Industrial B L. terrestrls (a)
Industrial C A. Tonga (c)
Industrial D A. trapezoldes (c)
Industrial D A. trapezoldes (a)
Selenium
mg kg"1 (dry weight)
Comments
Earthworms Soil
t t Dump near Ecton lead-copper-
zinc mine Audobon, PA
t t Dump near Ecton lead-copper-
zinc mine Audobon, PA
4.0 1.3 Cherry Hill Park, near city
Incinerator. Baltimore. MD
t t Greening Park, In an Indus-
trial area. Baltimore. MD
1.1 t Park near Wagners Point,
In an Industrial area,
Baltimore. ND
2.0 t Fort Arml stead mineral pig-
ments plant, Baltimore, MD
t t Fort Arml stead Park, near
o
-p-
^x
O
oo
vO
mineral pigments plant,
Baltimore, MD
-------
TABLE 4-3 (cont.)
SHe
Species
Selenium
m«j kg"1 (dry weight)
Earthworms Soil
Comments
Industrial
Industrial E
Industrial E
Industrial Fl
Industrial F2
Industrial F2
Industrial G
Industrial G
A. trapezoldes (c)
A. trapezoldes (a)
A. Tonga (c)
A. Tonga (c)
A. tuberculata (c)
1^. rubellus (c)
A. trapezoldes (c)
0.50
0.83
1.6
1.7
CD
10
t Park on Caroline Street,
In an Industrial area.
Baltimore. ND
t Park on Caroline Street.
In an Industrial area,
Baltimore. MD
0.39 Brldesburg Recreation
Center, In an Industrial
area, Philadelphia, PA
t - Brldesburg Recreation
Center. In an Industrial
area. Philadelphia. PA
t Brldesburg Recreation
Center, In an Industrial
area, Pylladelphla, PA
t Soil from road right-of-way,
near mineral pigments plnnl.,
Beltsvllle. MD
t Soil from road right-of-way.
near mineral pigments plant,
Beltsvllle. ND
-------
TABLE 4-3 (cont.)
Site
Species
Selenium
mg kg"1 (dry weight)
Earthworms Soil
Comments
Industrial
Industrial HI A. trapczoides (c)
Industrial H2
CO
ro
A. trapezoides (c)
*Source: Beyer and Cromartle, 1987
t = trace, c = clltellate, a = aclltellate
1.8
2.7
0.20
Soli ft oni grounds of coal-
fired power plant, Vienna.
MD
Soi I f i om yi /ids of can I -
fired power plant, Vienna,
MD
Galvanized Towers
Tower A
Con. A
Tower B
Con. B
E_. loennbergl
E. loennbergl
E. loennbergl
E. loennbergl
(a)
(a)
(c)
(a)
2.6 t Soil from beneath power 1
tower. Laurel, MD
7.6 t Soil 20 m from power line
tower. Laurel, MD
5.5 t Soil from beneath power 1
tower. Laurel, MD
2.5 t Soil 20 m from power line
tower. Laurel, MD
Ine
Ine
-------
Serda and Furst (1987) assessed the toxldty of the sodium salts of
selenlte and selenate to the earthworm, LumbMcus terrestMs. Worms were
Injected with doses ranging from 40-160 mg/kg behind the clHellum Into the
hemocoel and observed for 24 hours. The 8-hour LO-.s for selenlte and
selenate 1n worms treated Intraperltoneally were 31 and 60 mg/kg,
respectively.
Ohlendorf et al. (1986) monitored the reproductive efforts of American
coot, Fullca amerlcana. mallard, Anas platyrhynchos. northern pintail, Anas
acuta, cinnamon teal, Anas cyanoptera. gadwall, Anas strepera. black-necked
stilt, Hlmantropus mexlcanus. American avocet, Recurvlrostra amerlcana. and
eared grebe, Podlceps nlgrlcollls. from Irrigation dralnwater ponds contami-
nated with high levels of selenium for a 4-month period. Nests were checked
weekly during the Incubation periods. Eggs were periodically examined to
determine the condition of the embryo. Frequency of dead and abnormal
embryos ranged from 2.5-31.7% 1n ducks and grebes, respectively, and
4.0-8.8% 1n ducks and coots, respectively. There was some evidence to
Indicate that mortality of hatchllngs was high. Overall, 19.6% of the 347
nests monitored 1n this study produced at least one embryo or chick with an
abnormality. There were no abnormalities In embryos of birds from 92 nests
In an uncontamlnated area over a 2-year period. Average selenium concentra-
tions 1n bird livers and eggs from nests 1n contaminated areas ranged from
9.1-81.4 ppm dry weight compared with 4.1-6.1 ppm In livers of birds from an
uncontamlnated area. Concentrations of other heavy metals (Ag, As, Cd, Hg,
Pb and Zn) In livers and embryos of birds from the contaminated site were
equal to or less than levels 1n birds from uncontamlnated sites. Levels of
selenium measured 1n the water column were reported to be -300 ppb. Most of
0144d 4-33 04/01/89
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the selenium 1n plants, Invertebrates and fish 1s 1n organic forms such as
selenomethlonlne and selenocystlne, which have a greater potential for
toxlclty to birds.
Heinz et al. (1987) assessed the effects of selenium on reproduction 1n
mallard ducks, Anas platyrhynchos. Ducks of both sexes were fed selenium-
contaminated duck mash at concentrations of selenium ranging from 1-100 ppm.
Sources of selenium Included the sodium salt and seleno-DL-meth1on1ne.
Females were offered treated mash for a total of 4 weeks and prevented from
laying eggs during that time until paired with males offered the same
contaminated diet for that period. Eggs were held 1n an Incubator at
37.6°C. All but one bird offered mash contaminated with 100 ppm selenium
died before the end of the study (16-39 days) without producing any eggs.
One male died after 57 days on a diet containing 25 ppm selenium. Percent
fertility of adults or hatchabllHy of eggs was not affected among groups
treated with selenium as the sodium salt. Eggs from females fed seleno-DL-
methlonlne (10 ppm selenium) exhibited very low hatching success. Survival
of ducklings from groups fed 25 ppm (as sodium salt) and 10 ppm (as
seleno-DL-meth1on1ne) was lower than In other groups. Incidence of abnormal
embryos was significantly higher 1n ducks fed mash contaminated with >10 ppm
selenium (from either source). Abnormal embryos from sodium selenlte
treated ducks exhibited embryotoxlc manifestations rather than the terato-
genlc abnormalities exhibited by embryos from ducks treated with seleno-OL-
methlonlne. Duckling weights were lower In 25 ppm (as sodium salt) and 10
ppm (as seleno-DL-meth1on1ne) groups. Eggs from ducks fed seleno-DL-
methlonlne exhibited a 5- to 10-fold higher level of selenium than eggs from
ducks fed selenium as the sodium salt.
0144d 4-34 04/01/89
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Heinz and Gold (1987) assessed the behavior of mallard ducklings, Anas
platyrhynchos. produced by adults treated with selenium (as seleno-DL-
methlonlne). Birds were treated for 4 weeks with 1, 2, 4 or 8 ppm of
selenium as part of their dally feed. Of the 95 females treated, 10 did not
produce any ducklings for testing. Ducklings were maintained at 21-25°C for
6 days after hatching. Behavior was assessed by frightening the ducklings
with a rotating alternating black and white paddle. The distance traversed
by a duckling for 2 seconds after experiencing the stimulus was compared
among ducklings from different groups. There were no significant differ-
ences 1n behavior of surviving ducklings from different groups despite the
fact that ducklings from the 8 ppm selenium group experienced teratogenlc
effects, embryo mortality, and death and reduced growth of hatchllngs.
Heinz et al. (1988) assessed the toxldty of selenomethlonlne and sodium
selenlte to mallard ducklings, Anas platyrhynchos. Groups of 10 ducklings
were randomly assigned to each of 20 pens. Birds In 4 pens each received
dietary additions of 0, 10, 20, 40 and 80 ppm selenium mixed Into commercial
duck starter mash. Treatments continued for ~6 weeks. Birds receiving the
80 ppm selenium treatment 1n either form experienced significant levels of
mortality (60-80X) during the first 2 weeks of treatment and 100X mortality
by the end of the study. Significant mortality was observed In birds
treated with 40 ppm selenium as sodium selenlte after 2 weeks (~10X) and as
selenomethlonlne after 3 weeks (~5X). There were no mortalities among birds
offered diets containing 0, 10 and 20 ppm selenium. Sodium selenlte at >20
ppm selenium reduced food consumption after 1 week; treatment with seleno-
methlonlne at >40 ppm selenium also resulted 1n a reduction 1n food consump-
tion after 1 week. For the most part, food consumption by birds treated
with 10 ppm selenium did not differ from that of controls. Body weights of
0144d 4-35 04/01/89
-------
ducklings treated with >20 ppm were significantly lower than those of
controls, while body weights of birds treated with 10 ppm selenium were not
significantly lower than those for control birds, except for one observation
period. Ducklings fed 10 ppm selenium as sodium selenlte had larger livers
than control birds. This effect was not observed 1n birds fed 10 ppm
selenium as selenomethlonlne. Selenium accumulated more rapidly 1n the
livers of birds treated with selenomethlonlne than those treated with sodium
selenlte. The Investigators concluded that 10 ppm dietary selenium as
sodium selenlte or selenomethlonlne appeared to be close to a no-effect
level In mallard ducklings.
4.2.2. Effects on Flora. Pertinent data ' regarding the effects of
exposure of terrestrial flora to selenium were not located In the available
literature cited 1n Appendix A.
4.3. FIELD STUDIES
GuthMe et al. (1979) determined the concentrations of selenium 1n
water, sediment and biota from two bays on the Gulf Coast of Texas. Samples
were analyzed by neutron activation. Concentrations of selenium 1n water
and sediment were 0.11 and 1.44 mg/kg, respectively. Concentrations of
selenium 1n barnacle, Balanus aburneus. crab, CalUnectes sapldus. oyster,
Crassosstrea vlrglnlca. clam, Rangla cuneata. and polychaete, Nereis sp.
were 0.77, 0.08, 0.14, 0.54 and 0.49 mg/kg wet weight, respectively.
Rodgers et al. (1980) determined the concentrations of selenium In the
shells and viscera of Asiatic clams, Corblcula flumlnea. from two sites 1n
the New River, Virginia, and the water and sediment from those sites. Clams
were collected from one site that received the thermal effluent from a coal-
fired electric generating plant and a second site that was not Influenced by
thermal effluents. Selenium concentrations were determined by neutron
0144d 4-36 04/01/89
-------
activation. Selenium concentrations 1n water, sediment, and clam valves and
viscera from a control site were 0.11, 0.88, 0.29 and 3.90 ppm, respec-
tively. Selenium concentrations 1n samples from sites receiving thermal
effluent discharges were 0.10, 0.60, 0.50 and 16.5 ppm, respectively.
Boyer (1984) determined the concentrations of selenium 1n the water,
sediment and fish of the upper Mississippi River. The concentrations of
selenium 1n water and sediment were below detection limits (1 yg/i and
-0.2 yg/g, respectively). Concentrations of selenium In fillets, livers
and kidneys of common carp ranged from 0.161-0.356, 0.858-2.17 and
0.943-1.62 yg/g wet weight, respectively. Concentrations of selenium In
fillets from smallmouth bass and sauger .ranged from 0.36-0.425 and
0.284-0.369 yg/g wet weight, respectively. Concentration factors for the
edible tissue of common carp collected from the upper reaches of the
Mississippi River reportedly ranged from 322-712.
Sorensen et al. (1984) assessed a variety of factors relating to changes
associated with selenium accumulation 1n green sunflsh, Lepomls cyanellus,
from Belews Lake, North Carolina. Selenium concentrations 1n tissues ranged
from 2.3-22.3 ppm from contaminated fish and 1.3 ppm 1n reference fish.
Investigators reported capillary changes and resultant edema 1n hepato-
pancreas and skeletal muscle, swollen and vacuolated gill lamellae, signifi-
cantly Increased hepatopancreas weight-to-body weight ratios, and signifi-
cantly lower hematocrlts. Additional hlstopathologlcal effects that were
not observed 1n reference fish were noted 1n hepatopancreas, kidney, heart
and ovaries.
Woock and Summers (1984) monitored the levels of selenium 1n the water,
sediments and biota from a North Carolina reservoir and assessed the uptake
of selenium by caged golden shiners, Notemlqonus crysoleucas. In the same
0144d 4-37 04/01/89
-------
reservoir. Concentrations of selenium In surface and bottom waters over a
2-year period ranged from 5 yg/g wet
weight after 20 weeks of exposure.
Lemly (1985a) determined the concentrations of selenium In water, sedi-
ment and biota of a North Carolina power plant cooling reservoir. Selenium
concentrations were determined by differential pulse polarography or by
flameless atomic absorption spectrophotometry. Concentrations of selenium
In the water column were 20-30 times higher than background levels with a
mean value of 10 yg/t, while concentrations In flora and fauna were
10-15 times background levels. Concentrations of selenium 1n surface
sediments were ~4 yg Se/g wet weight. Selenium concentration was 519- and
3975-fold higher In perlphyton and fish, respectively, than In water. Fish
were exposed to dietary concentrations of selenium that were 519-1395 times
the concentration of selenium In water.
0144d 4-38 06/15/89
-------
Lemly (1985b) summarized the results of several field studies assessing
the Impact of selenium on the endemic fauna. Durations of exposure ranged
from 56 days to 8 years. Concentrations of selenium In water and sediment
ranged from 1-360 and 0.2-17.1 yg Se/l, respectively. The highest
concentrations of selenium In the biota of these systems was generally found
1n fish. Observed effects Included reproductive failure, teratogenlc
effects and high levels of mortality.
Lemly (1985b) also assembled the results of a series of studies address-
Ing the concentration of selenium In aquatic fauna and wildlife following
exposure to combined waterborne and dietary sources under natural conditions
In the field. BCFs for phytoplankton, perlphyton and plants ranged from
237-1320, 158-1070 and 166-24,400, respectively. BCFs for zooplankton
ranged from 176-2080. BCFs for Insects, annelids, crustaceans and molluscs
ranged from 371-5200, 770-1320, 420-1975 and 600-2550, respectively. BCFs
for carnivorous, planktlvorous and omnivorous fish ranged from 590-35,675,
445-27,000 and 364-23,000, respectively.
Salkl et al. (1985) examined the Influence of selenium on the flora and
fauna of field mesocosms. Mesocosms (10 m diameter) consisted of poly-
ethylene-walled experimental enclosures set Into a sheltered bay In Clay
Lake, Ontario. The mesocosms enclosed -79 m2 of sediment and 130 m3 of
water. Radlolabeled sodium selenlte was added to the enclosures to achieve
concentrations of 1, 10 and 100 yg Se/a. The study duration was ~6
weeks. Among phytoplankton, chrysophytes Initially dominated all communi-
ties. By the end of the study, chlorophytes dominated 1n control and low-
dose enclosures, chrysophytes were the dominant group 1n the 10 yg Se/ft,
enclosure, and cyanophytes dominated 1n the high-dose enclosure. There were
no significant differences among zooplankton communities within the
0144d 4-39 06/15/89
-------
enclosures 2 days after the addition of selenium to the enclosures. Changes
In total abundance and blomass of zooplankton were similar among enclosures
through the course of the experiment.
Skinner (1985) determined the concentrations of selenium In black
crapple, Pomoxls nlgromaculatus. pumpklnseed, Lepomls aurUus. brown bull-
head, Ictalurus nebulosus. and carp, CypMnus carplo. collected from utility
wastewater treatment basins. F1sh were collected by electro-shocking and
sacrificed within 1 hour of collection. F1sh tissues were held on dry 1ce
enroute to the laboratory and stored at 0°C until analysis. Concentrations
of selenium 1n water from basins A, B, C, D and E were 7.0, 3.0, <2.0f <2.0
and <2.0 iig/8,, respectively. Carp and crapple from basin A had tissue
levels of selenium ranging from 11.2-15.8 mg/kg. The concentration of
selenium 1n carp from basin B was 22.7 mg/kg. The concentration of selenium
1n a male and a female carp from basin C was 33.1 and 37.6 mg/kg, respec-
tively. The concentration of selenium In carp, bullhead and pumpklnseed
from basin D ranged from 2.7-8.9 mg/kg and 1n carp from basin E ranged from
2.9-3.7 mg/kg. The highest-levels of selenium 1n fish tissue were found In
fish collected 1n basins receiving fly ash water.
Baumann and G1llesp1e (1986) assessed the accumulation of selenium by
largemouth bass, Hlcropterus salmoldes. and bluegllls, Lepomls macrochlrus.
from one municipal and three power plant cooling water reservoirs. Selenium
concentrations 1n carcasses of bluegllls and bass from a municipal reservoir
were <0.5 ppm. Selenium concentrations In carcasses of bluegllls and bass
from a cooling water reservoir that did not receive ash pond effluent was ~1
ppm. Concentrations of selenium 1n carcasses of bluegllls and bass from
cooling water reservoirs that did receive ash pond effluent ranged from 4-9
ppm. There were no apparent differences 1n selenium levels of carcasses
0144d 4-40 06/15/89
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between sexes or species, except for a 2-fold difference 1n species from a
reservoir receiving ash pond effluent. Selenium concentrations In gonads
varied between sexes within reservoirs, with significantly higher levels
(<2-fold) 1n ovaries (<1 to ~12 ppm) than In testes (<1 to ~7 ppm).
Byrne and DeLeon (1986) determined the concentration of selenium In
oysters, Crassostrea v1rg1n1ca. clams, Rangla cuneata. and sediments from
three sites 1n Lake Pontchartraln, Louisiana. The concentration of selenium
In mollusc tissue and sediment was determined by gas hydride-atomic absorp-
tion spectrophotometry. Selenium was not concentrated from sediment by
these organisms. Concentrations of selenium In oyster tissue and sediment
from one site were 0.013 and 0.007 yg/g dry weight, respectively.
Concentrations of selenium 1n clam tissue and sediment from a second site
were 0.032 and 0.031 yg/g dry weight, respectively. Concentrations of
selenium 1n clam tissue and sediment from a third site were 0.041 and 0.05
yg/g dry weight, respectively.
Batley (1987) determined the concentrations of selenium In sediment,
seagrass, Zostera capMcornl. green algae, Enteromorpha sp., the hairy
mussel, TMchomya hlrsuta. and the cockle, Anadara trapezia, from Lake
MacquaMe, New South Wales. Selenium concentrations 1n sediment and biota
were determined by neutron activation analysis. A selenium concentration of
14 yg/g was measured at the northern end of the lake, but the concentra-
tion decreased rapidly to a plateau level of 4 yg/g. Concentrations of
selenium 1n seagrass from the northern and southern sections of the lake
were ~3.9 and ~0.6 yg/g, respectively. Concentrations of selenium In
algae were higher 1n samples collected from the northern section of the
lake, ranging from 0.3-1.6 yg/g. Whole body concentrations of selenium 1n
mussels and cockles from the northern end of the lake were 3.3 and 6.4 yg
Se/g, respectively.
0144d 4-41 04/01/89
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L1u et al. (1987) determined the concentrations of selenium 1n phyto-
plankton, seaweed, zooplankton, other Invertebrates and fish from Xiamen
Bay, Fujlan Province, China. Flora concentrated selenium 3-4 orders of
magnitude above the ambient concentration In seawater. Phytoplankton con-
tained 1.24 ppm selenium, while seaweed concentrations ranged from 0.08-0.61
ppm. The concentration of selenium 1n zooplankton was 3- to 4-fold higher
than that found In marine flora. Concentrations ranged from 2.16-6.30 ppm.
Concentrations of selenium In other Invertebrates and fish were approxi-
mately equal to those found In zooplankton on a dry weight basis, but
concentrations were dependent on the tissue analyzed.
Johnson (1987) determined the concentrations of selenium In sediments
and fish from 14 Ontario lakes. Sediment was collected from the deepest
part of each lake. Selenium concentrations In sediment and fish samples
were determined by coloMmetrlc techniques. Selenium concentrations In the
top 10 cm of sediment ranged from <1-16 yg/g. Concentrations of selenium
In tissues of lake trout, whlteflsh, common sucker, yellow perch, northern
pike and walleye from the study lakes were 0.78, 0.84, 0.55, 0.38, 0.37 and
0.25 vg wet welght/g, respectively.
Sa1k1 and Lowe (1987) determined the concentrations of selenium In
water, sediment and biota from the San Luis Drain, Kesterson Reservoir and
the Volta Wildlife Area of California. Samples were analyzed for total
selenium by hydride generation-atomic absorption spectrophotometry. The
detection limits for selenium 1n water, sediments and tissues were 0.00017
mg/a, 0.2 vg/g wet weight and 0.05 yg/g, respectively. Concentration
ranges for selenium 1n water and sediment from the San Luis Drain, Kesterson
reservoir and Volta waterways were 0.29-0.33 mg/i and 65-100 vg/g,
0.009-0.32 mg/8, and 1.8-67 yg/g, and 0.0002-0.0014 mg/l and O.2-0.5
0144d 4-42 04/01/89
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yg/g, respectively. Concentration ranges for selenium In algae and net
plankton 1n these systems were 63-72 yg/g and not measured, 12-330 yg/g
and 58-120 yg/g, and below detectlon-1.4 yg/g and 1.4-2.8 wg/g,
respectively. Concentration ranges for selenium In all aquatic Insects and
mosqultoflsh In these systems were 170-330 yg/g and 140-370 yg/g, 16-290
yg/g and 104-290 yg/g, and 0.68-3.0 yg/g and 1.2-1.4 yg/g, respec-
tively. The Investigators noted that selenium concentrations generally
Increased from water to sediments to plants to animals.
Mulr et al. (1988) determined the concentration of selenium In dolphins,
Lagenorhynchus alblrostMs. and pilot whales, Globlcephala melaena. from the
coast of Newfoundland, Canada. Dolphin tissues were obtained from dolphins
killed by entrapment 1n 1ce and whale tissues were obtained from whales
stranded on beaches In Newfoundland. Processed tissue samples were analyzed
for their selenium content by flameless atomic absorption spectrophotometry.
Mean selenium concentrations 1n kidney, liver and muscle of dolphins were
5.85, 8.15 and 1.91 mg/kg dry weight, respectively. Selenium concentrations
1n blubber, kidney, liver and muscle of whales from two different collection
sites were 0.49 and 0.59 (mg/kg wet weight), 13.0 and 11.3, 50.5 and 31.4,
and 1.22 and 2.94 mg/kg dry weight, respectively.
4.4. AQUATIC RISK ASSESSMENT
There were no significant studies Identified during the compilation of
this document to refute the conclusions reached or the criteria generated 1n
U.S. EPA (1987a). Since the National Water Quality Criteria Approach used
by U.S. EPA (1987a) to generate fresh and saltwater criteria for selenium Is
the approach that has been adopted for analysis of aquatic toxldty data 1n
HEEDs, an analysis of the data presented 1n this document will not be
conducted.
0144d 4-43 04/01/89
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4.5. SUMMARY
Acute toxIcHy data for selenium 1n aquatic vertebrates were available
for 21 species of fish and 1 amphibian. Among freshwater species, the
96-hour LC5Qs for selenium as sodium selenlte ranged from 0.62 mg/l for
the fathead minnow, Plmephales promelas (Elsler, 1985) to 35 mg/l for the
common carp, Cyprlnus carplo (Etnler et al., 1987). Fathead minnows were
also the least tolerant vertebrate species to selenate-selenlum, with a
96-hour LC5Q of 2 mg/l In a flowthrough test (Etnler et al., 1987).
Zebraflsh, Brachyodanlo rerlo. and juvenile striped bass, Horone saxatlHs.
were the most tolerant of exposure to selenate-selenlum, with 96-hour
LC5Qs of 82 and 85.8 mg/l, respectively (N1tm1 and Laham, 1976; Klauda,
1986). The toxldty of selenium as selenium dioxide ranged from a 96-hour
LC50 of 7.3 mg/l for fathead minnows to 20 mg/8. for zebraflsh
(Cardwell et al., 1976; N11m1 and Laham, 1976).
Fathead minnows were equally sensitive to the sodium salts of selenlte
and selenate, while zebraflsh were equally sensitive to the potassium and
sodium salts of selenlte and selenate. The toxldty of selenium as sodium
selenate to striped bass decreased nearly 10-fold as fish developed from the
prolarva to juvenile stage (Klauda, 1986). Toxldty values for saltwater
fish ranged from a 96-hour LC5Q of 0.6 mg/l for haddock larvae,
Melanogrammus aegl1f1nus. to 96-hour LC5Qs of 14.2-15.1 mg/l for winter
flounder larvae, Pseudopleuronectes amerkanus. exposed to unidentified
forms of selenium (Elsler, 1985).
In a series of behavioral and physiological studies, goldfish, Carasslus
auratus. exhibited behavioral Impairment at 0.25 ppm (Weir and H1ne, 1970),
while fathead minnows, Plmephales promelas. did not avoid selenate at
concentrations of 0.3-11.2 mg Se/l (Watenpaugh and Beltlnger, 1985).
0144d 4-44 04/01/89
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Oxygen consumption by fathead minnows was not affected by exposure to 60 mg
Se/8, for 24 hours (Watenpaugh and Beltlner, 1985). Oxygen consumption by
the hermit crab, CllbanaMus vlttatus. exposed to 100 ppm selenium was
depressed at 16°C 1n 10 °/ salinity test medium, although oxygen
consumption rates were generally elevated at lower salinities and higher
temperatures (Wolfenberger, 1987).
Acute toxldty data for selenium 1n aquatic Invertebrates were available
for a total of 22 species, Including 3 cladocerans, 2 copepods, 4 amphlpods,
4 decapods, 1 mysld, 3 Insects and 5 molluscs. The 48-hour LC5Qs of
selenlte-selenlum to daphnlds ranged from 0.098-3.87 mg/a, (Etnler et al.,
1987; Reading and Bulkema, 1983). The 48-hour EC5-s for unfed and fed
daphnlds exposed to sodium selenlte were 0.47 and 1.5 mg/a, repsectlvely.
The 48-hour NOEC for unfed daphnlds was 1.0 mg/8, (Adams and Heldolph,
1985). The 96-hour LC5Qs for amphlpods ranged from 2.88-6.17 mg/8.
(Etnler et al., 1987). The toxldty of selenlte-selenlum to Daphnla magna
was 4-fold lower when assays were conducted In soft water; no significant
differences were observed for Chlronomus plumosus. based on water hardness
(Mayer and Ellersleck, 1986).
The toxldty of selenium as sodium selenate to 5th Instar Daphnla maqna
(48-hour LC5Qs of 0.55 and 0.75 ppm) was comparable with that observed for
sodium selenlte (Johnston, 1987). In contrast, the toxldty of selenate-
selenlum to Hyallela azteca (96-hour LC™ of 0.76 mg/l) was 4- to 8-fold
greater than that observed with sodium selenlte (Etnler et al., 1987). The
toxldty of selenium as selenium dioxide was represented by 96-hour LC5Qs
of 33, 1.90 and 0.25 mg/l for the crab, Scylla serrata. bay scallop,
Arqopecten Irradlans. and surf clam, Splsula solldlsslma. respectively
(Krlshnaja, 1987; Nelson et al., 1988). The 96-hour LC™ of selenium as
0144d 4-45 06/15/89
-------
selenium dioxide to crabs, oysters and mussels was >10 mg/l (Martin et
al., 1981). The 96-hour LC,.- for the midge, Tanytarsus dlsslmHls. was
42.4 mg/l (Elsler, 1985). Exposure of embryos of the zebraflsh, Brachy-
danlo reMo, to <10 mg/l selenium as selenium dioxide for 168 hours did
not affect hatching and mortality. Exposure of zebraflsh larvae resulted 1n
significantly higher levels of mortality at concentrations >3 mg/l after
168 hours and at 10 mg/l after 96 hours (N11m1 and Laham, 1975).
The 168-hour LC5_ for fathead minnows, Plmephales promelas. was 2.9 mg
Se/l. The 336-hour LC5Qs for goldfish, Carrasslus auratus. and
bluegllls, Lepomls macrochlrus. were 8.8 and 17.6 mg Se/l, respectively
(Cardwell et al., 1976). The 113-hour LC • for embryos and the 7-day
LC5_ for tadpoles of the frog, Xenopus laevls. were 2.0 and 1.5 mg Se/l,
respectively (Elsler, 1985). The 48-day LC s for bluegllls, L. macro-
chlrus. and fathead minnow, £. promelas. were 0.4-2.0 and 1.1 mg Se/l,
respectively. The 10-day LCcn for perch, Perca flavescens. was 4.8
5U
mg/l, while the 43-day LC5Q for coho salmon, Oncorhynchus klsutch. was
0.16 mg/l. The 96-day LC5Q for rainbow trout, Salmo galrdnerl. was 0.29
mg Se/l (Elsler, 1985).
Exposure of Daphnla magna to 0.2-0.8 mg selen1te-selen1um/l for 28
days did not affect total eggs per daphnld or live young per daphnld;
however, mean brood size was affected at 0.8 mg Se/l (Reading and Bulkema,
1983). In another study, the 7-p 14- and 21-day EC5Qs for D. maqna
exposed to selenlte-selenlum were 0.38, 0.38 and 0.35 mg/l, respectively.
The NOEC based on survival and reproduction was 0.24 and >0.24 mg/l,
respectively. The 28-day LC™ for ]). magna 1n a third study was 0.24 mg
Se/l (Adams and Heldolph, 1985).
0144d 4-46 04/01/89
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Exposure of the amphlpod Allorchestes compressa to 44 yg selenlte-
selenlum/a. did not significantly affect growth or survival of treated
Individuals after 4 weeks. Animals exposed to 93 yg Se/8. experienced
reduced growth and a significant level of mortality over the same period
(Ahsanullah and Brand, 1985). The 14-day LC5 for another scud, Hyallela
azteca. was 0.07 mg Se/a, (Elsler, 1985).
Fathead minnow larvae, Plmephales promelas. experienced significant
reductions 1n final dry weight when larvae were fed rotifers cultured on
selenium-contaminated algae. The mean selenium concentrations 1n minnows
were 43 and 51.7 yg/g In two experiments (Bennett et al., 1986). High
tissue concentrations of selenium 1n blueglll sunflsh, Lepomls macrochlrus.
resulted 1n significant differences 1n percent fertilization and hatch when
the ovaries of females contained from 5.79-8.0 mg Se/kg. These levels were
16-21 times higher than those In uncontamlnated sunflsh (Glllesple and
Bauamann, 1986).
Exposure of early life stages of the striped bass, Horone saxatllls. to
low (0.089-0.099 mg Se/a) and high (1.217-1.360 mg Se/a) concentralons
of selenate-selenlum resulted In a significant reduction In exponential
growth rates for fish 1n both treatments for days 3-15. There were no
differences 1n growth rates between days 19 and 60 but there was a signifi-
cant Incidence 1n developmental abnormalities of the lower jaw and severe
blood cytopathology (Klauda, 1986). Exposure of rainbow trout fry, Salmo
qalrdnerl. to >47 yg selenlte selenium/a resulted 1n significant reduc-
tions 1n survival and fry weight and length after 90 days. Survival and
growth were not affected at <21 yg Se/a. BCFs were Inversely related to
exposure concentrations but did not exceed 200. Exposure of fry to >12 yg
Se/8. resulted 1n significant reductions 1n the calcium concentrations 1n
0144d 4-47 04/01/89
-------
bone (Hunn et al., 1987). Percent hatch of sheepshead minnows, Cyprlnodon
varlegatus. was <4% at concentrations of <3.6 mg selenlte-selenlum/i.
Juveniles experienced 4, 24 and 90% reductions In survival at 0.47, 0.97 and
>0.97 mg Se/i, respectively. Growth of juvenile sheepshead minnows was
reduced by 8% at 0.47 and 0.97 mg/s, (U.S. EPA, 1987a).
Exposure of four consecutive generations of CeModaphnla affInls to
sodium selenlte resulted In a reduction 1n the tolerance of C. afflnls over
succeeding generations. The NOEL was reduced from 0.2-0.1 mg/B, after two
generations (Owsley and McCauley, 1986). There were no significant differ-
ences In growth of Daphnla magna exposed to <0.05 ppm selenHe-selenlum or
1n mean numbers of eggs produced, the percent maturation or mortality levels
for daphnlds exposed to <0.025 ppm selenHe-selenlum (U.S. EPA, 1987a). The
number of offspring produced and survival of first generation myslds,
Mysldopsls bahla. exposed to selenlte-selenlum was significantly reduced at
0.32 mg/a. No statistically significant differences were observed In
myslds exposed to 0.14 mg/i (U.S. EPA, 1987a).
The no-effect level for dietary selenium as either sodium selenlte or
selenomethlonlne In blueglll sunflsh, Lepomls macrochlrus. over 324 days Is
-13-30 yg Se/g. The maximum BCF for blueglll sunflsh, L. macrochlrus.
exposed to 120 yg Se (as selenous add)/ft. for 28 days was 20 and the
tissue half-life during a 7-day depuration period was between 1 and 7 (Woock
et al., 1987). BCFs for rainbow trout, Salmo qalrdnerl. exposed to <10 yg
selen1te-selen1um/kg ranged from 3.1 In embryos to 104 1n livers of
Juveniles. BCFs for trout exposed to -100 yg selenlte-selenlum/kg ranged
from 1.6 In sac-fry to 31.6 In livers of juveniles after 96 hours (Hodson et
al., 1986). The BCF for selenium as sodium selenlte 1n carp, Cyprlnus
carplo. for an unspecified exposure duration and selenium concentration was
0144d 4-48 06/15/89
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0.6-6.0. The BCF for selenlte-selenlum 1n minnows, Plmephales promelas.
exposed to 83 yg/a for 28 days was 4443 (Etnler et al., 1987).
Exposure of fathead minnows, Plmephales promelas. to waterborne
selenate-selenlum (10-40 ng Se/ma) resulted In a maximum body burden level
of -0.5-0.8 yg Se/g fish after 20-30 days. Selenium was depurated to ~3
yg/g after 30 days. Exposure of minnows to selenium-contaminated daphnlds
(1.33-7.32 yg Se/g) resulted 1n selenium body burden levels of -0.3-1.2
yg Se/g fish after 80 days. Depuration of selenium was slower than that
observed 1n fish exposed to waterborne selenium. Fish exposed to both
sources of selenium had body-burden levels of selenium that did not plateau
during the 56-day exposure phase, reaching 0.4-2.0 yg Se/g fish. Depura-
tion of selenium from these fish was slow (Bertram and Brooks, 1986). Fed
and starved juveniles of the striped bass, Horone saxatllls. exposed to 1.29
mg selenate-selenlum/ 8. for 60 days accumulated selenium at comparable
rates, producing BCFs of 0.68 and 0.69. Fed Juveniles exposed to 90 yg
Se/8. showed no Increase 1n whole body levels of selenium, while starved
juveniles had a BCF of 11.78 (Klauda, 1986). The half-lives In days for
selenate, selenlte and selenomethlonlne administered orally via gavage at a
level of 20 ng Se/g to fathead minnows, P. promelas. ranged from 3.9 (liver)
to 487 (adipose tissue), 2.2 (liver) to 64 (heart) and 1.0 (liver) to 69
(adipose tissue) (Klelnow and Brooks, 1986).
Mussels exposed to 50 yg selenium/8, for 15-50 days accumulated
selenlte-selenlum at a rate of 0.12 ng Se/g/day. The presence of Inorganic
(30 yg Hg/l) and organic (3 yg Hg/a) mercury Increased the uptake of
selenlte-selenlum to 0.24 and 0.40 ng Se/g/day, respectively. Organic
selenium (CQH,00Se)0 accumulated at a rate of 0.15 ng Se/g/day 1n
o / c e.
the presence of mercury (Pelletler, 1986).
0144d 4-49 04/01/89
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There were no apparent effects observed In growth of natural assemblages
of phytoplankton or In growth of a species Isolated from field samples
Thalassloslra aestevalls exposed to <1000 nM selenium (HolUbaugh et al.,
1980). There were no effects on growth of either the green or red algae,
Dunallella prlmolecta and Porphyrldlum cruentum. exposed to 10 ppm
selenlte-selenlum (Gennlty et al., 1985). The 48-hour LC5Q for Oedoqonlum
cardlacum was <0.1 mg/l, while the 96-hour LC5Q for Anabaena var1ab111s
was 15-17 mg/8. (Elsler, 1985). The 96-hour EC5Q for duckweed, Lemna
minor, exposed to selenium was 2.4 mg/SL (Wang, 1986).
Population growth of Tetrahymena pyrlformls was Inhibited by 1.4 ppm
selenium and stopped completely at 140 ppm- (Tang et al., 1985). T.
pyrlformls also experienced a dose-dependent Inhibition 1n division of
synchronized cells exposed to 10, 20, 50 and 100 ppm selenium (as SeOp)
(Cao and Tang, 1985). Growth of cultures of the algae, Chlorella vulqarls
and Phormldlum foveolarum, was reduced by ~40% 1n the presence of 0.25 ppm
selenate-selenlum. Growth of C_. vulgarls 1n a 4.0 ppm solution of selenium
was 97% of that observed 1n controls and completely Inhibited 1n P_.
foveolarum (TMpathl and Pandey, 1985). Selenium retarded growth of the
marine dlnoflagellate, Prorocentrum mlcans. 1n cultures Incubated with 100
and 1000 ppm selenium. Growth was slightly enhanced at 10 and 50 ppm
selenium for the first 15 days of treatment but was Increasingly Inhibited
compared with controls after 15 days. Growth of the marine dlnoflagellate,
Crypthecod1n1um cohnll. was severely Inhibited by selenium at >10 ppm
selenium within 1.5 days of the Initiation of treatment (Prevot and
Soyer-Goblllard, 1986).
Concentrations of selenium 1n soil and earthworms ranged from trace
levels to 1.3 mg/kg at an Industrial site and from trace quantities to 7.6
0144d 4-50 04/01/89
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mg/kg, respectively (Beyer and Cromartle, 1987). In an experimental field
study, the concentration of selenium In earthworms, Aporrectodea tubercu-
lata. Aporrectodea turglda. and Lumbrlcus rubellus. from control plots (<0.1
mg Se/kg soil) was 16 mg/kg, while concentrations of selenium 1n worms from
treated plots were 36, 43, 51, 36 and 78 mg/kg. Uptake of selenium by worms
was not Influenced by pH or other soil variables (organic matter content,
phosphorous, potassium or magnesium) (Beyer et al., 1987). The 8-hour
LD5Qs for selenlte and selenate In earthworms, Lumbrlcus terrestMs.
treated Intraperltoneally were 31 and 60 mg/kg, respectively (Serda and
Furst, 1987).
Exposure of American coot, FuUca americana. mallard, Anas platy-
rhynchos. northern pintail, Anas acuta, cinnamon teal, Anas cyanoptera.
gadwall, Anas strepera. black-necked stilt, Hlmantropus mexlcanus. American
avocet, Recurvlrostra americana. and eared grebe, Podlceps nlgrlcolHs. to
selenium-contaminated Irrigation dralnwater ponds (-300 ppb Se) resulted In
an Increase In reproductive Impairment. Frequency of dead and abnormal
embryos ranged from 2.5 (ducks) to 31.7% (grebes) and 4.0 (ducks) to 8.8%
(coots), respectively. Overall, 19.6% of the 347 nests monitored produced
at least one embryo or chick with an abnormality. There were no abnormali-
ties 1n embryos of birds from 92 nests In an uncomtamlnated area over a
2-year period. Average selenium concentrations 1n bird livers and eggs from
nests 1n contaminated areas ranged from 9.1-81.4 ppm dry weight, compared
with 4.1-6.1 ppm In Hvers of birds from an uncontamlnated area. The
no-effect level for dietary selenium as sodium selenlte or selenomethlonlne
1n mallard ducklings, Anas platyrhynchos. 1s ~10 ppm (Ohlendorf et al.,
1986).
0144d 4-51 06/15/89
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Concentrations of selenium 1n water and sediment from two bays on the
Gulf Coast of Texas were 0.11 and 1.44 mg/kg. Concentrations of selenium In
barnacle, Balanus aburneus. crab, CalUnectes sapldus. oyster, Crassosstrea
v1rg1n1ca. clam, Rangla cuneata. and polychaete, Nereis sp., from those bays
were 0.77, 0.08, 0.14, 0.54 and 0.49 mg/kg wet weight, respectively (Guthrle
et al., 1979). The level of selenium 1n algae, Euglena sp., from tailing
areas of the Elliot Lake mining district, Canada, was 2700 ng/g dry weight,
compared to a concentration of 0.2 ng/g In world river water (Mann et al.,
1988). Selenium concentrations In water, sediment, and clam valves and
viscera of Asiatic clams, Corblcula flumlnea. from a control site 1n the New
River, Virginia, were 0.11, 0.88, 0.29 and 3.90 ppm, respectively. Selenium
concentrations 1n samples from sites receiving thermal effluent discharges
were 0.10, 0.60, 0.50 and 16.5 ppm, respectively (Rodgers et al., 1980).
The concentrations of selenium 1n water and sediment 1n the upper
Mississippi River were below detection (1 yg/8. and ~0.2 yg/g, respec-
tively) but concentrations of selenium 1n fillets, livers and kidneys of
common carp ranged from 0.161-0.356, 0.858-2.17 and 0.943-1.62 yg/g wet
weight, respectively. Concentrations of selenium In fillets from smallmouth
bass and sauger ranged from 0.36-0.425 and 0.284-0.369 yg/g wet weight,
respectively. Concentration factors for the edible tissue of common carp
ranged from 322-712 (Boyer, 1984).
Concentrations of selenium 1n surface and bottom waters of a cooling
water reservoir ranged from
-------
Selenium concentrations 1n shad, catfish and blueglll ranged from 3.6-28.8
yg/g wet weight. Selenium concentrations In shad and blueglll from an
uncontamlnated site were 35- to 50-fold lower. Exposure of golden shiners,
Notemlqonus crysoleucas. to 5-15 yg Se/8, Insltu resulted In tissue
levels >5 yg/g wet weight after 20 weeks (Woock and Summers, 1984). In a
separate study, concentrations of selenium 1n the water column of a power
plant cooling reservoir were 20-30 times higher than background levels with
a mean value of 10 yg/a, while concentrations 1n flora and fauna were
10-15 times background levels. Concentrations of selenium In surface
sediments were ~4 yg Se/g wet weight. Selenium was 519- and 3975-fold
higher 1n perlphyton and fish, respectively, than 1n water (Lemly, 1985a).
Concentrations of selenium In water from utility wastewater treatment
basins were 7.0, 3.0, <2.0, <2.0 and <2.0 yg/SL. Concentrations of sele-
nium In black crapple, Pomoxls nlgromaculatus. pumpklnseed, Lepomls aurUus.
brown bullhead, Ictalurus nebulosus. and carp, CypMnus carplo, from these
basins ranged from 2.7-37.6 mg/kg (Skinner, 1985). Concentrations of
selenium 1n carcasses of bluegllls, Lepomls macrochlrus. and largemouth
bass, Hlcropterus salmoldes from cooling water reservoirs that receive ash
pond effluent ranged from 4-9 ppm. Selenium concentrations In gonads varied
between sexes within reservoirs with significantly higher levels (<2-fold)
1n ovaries (<1 to -12 ppm) than 1n testes (<1 to ~7 ppm). Selenium concen-
trations 1n carcasses of bluegllls and bass from a cooling water reservoir
that did not receive ash pond effluent was ~1 ppm. Selenium concentrations
In carcasses of bluegllls and bass from a municipal water reservoir were
<0.5 ppm (Baumann and Glllesple, 1986).
Concentrations of selenium 1n oysters, Crassostrea v1rg1n1ca. and
sediment from a site In Lake Pontchartraln, Louisiana, were 0.013 and 0.007
0144d 4-53 04/01/89
-------
yg/g dry weight, respectively. Concentrations of selenium In clams,
Rangla cuneata. and sediment from a second site were 0.032 and 0.031 yg/g
dry weight, respectively. Concentrations of selenium 1n clam tissue and
sediment from a third site were 0.041 and 0.05 yg/g dry weight, respec-
tively (Byrne and DeLeon, 1986).
A selenium concentration of 14 yg/g was measured at the northern end
of Lake Macquarle, New South Wales, but the concentration decreased rapidly
to a plateau level of 4 yg/g. Concentrations of selenium 1n seagrass,
Zostera caprlcornl. from the northern and southern sections of the lake were
-3.9 and ~0.6 yg/g, respectively. Concentrations of selenium 1n algae
Enteromorpha sp. were higher In samples collected from the northern section
of the lake, ranging from 0.3-1.6 yg/g. Whole body concentrations of
selenium 1n mussels, TMchomya hlrsuta. and cockles, Anadara trapezia, from
the northern end of the lake were 3.3 and 6.4 yg Se/g, respectively
(Batley, 1987).
Phytoplankton from Xiamen Bay, Fujlan Province, China contained 1.24 ppm
selenium, while seaweed concentrations ranged from 0.08-0.61 ppm. The
concentration of selenium 1n zooplankton ranged from 2.16-6.30 ppm. Concen-
trations of selenium 1n other Invertebrates and fish were approximately
equal to those found In zooplankton on a dry weight basis but concentrations
were dependent on the tissue analyzed (Liu et al., 1987).
Selenium concentrations In the top 10 cm of sediment from 14 Ontario
lakes ranged from <1-16 yg/g. Concentrations of selenium 1n tissues of
lake trout, whHeflsh, common sucker, yellow perch, northern pike and
walleye from the study lakes were 0.78, 0.84, 0.55, 0.38, 0.37 and 0.25 yg
wet welght/g, respectively (Johnston, 1987).
0144d 4-54 06/15/89
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Concentration ranges for selenium 1n water and sediment from the San
Luis Drain, Kesterson ponds and Volta waterways In California were 0.29-0.33
and 65-100, 0.009-0.32 and 1.8-67, and 0.0002-0.0014 and <0.2-0.5, respec-
tively. Concentration ranges for selenium In algae and net plankton 1n
these systems were 63-72 and not measured, 12-330 and 58-120, and below
detectlon-1.4 and 1.4-2.8, respectively. Concentration ranges for selenium
1n all aquatic Insects and mosqultoflsh 1n these systems were 170-330 and
140-370, 16-290 and 104-290, and 0.68-3.0 and 1.2-1.4, respectively. The
Investigators noted that selenium concentrations generally Increased from
water to sediments to plants to animals (Salkl and Lowe, 1987).
Mean selenium concentrations In kidney, liver and muscle of dolphins,
Lagenorhynchus alb1rostr1s. were 5.85, 8.15 and 1.91 mg/kg dry weight,
respectively. Selenium concentrations In blubber, kidney, liver and muscle
of pilot whales, Globlcephala melaena. from two different collection sites
were 0.49 and 0.59 (mg/kg wet weight), 13.0 and 11.3, 50.5 and 31.4, and
1.22 and 2.94 mg/kg dry weight, respectively (Mu1r et al., 1988).
BCFs for phytoplankton, peMphyton and plants exposed to selenium In the
field ranged from 237-1320, 158-1070, and 166-24,400, respectively. BCFs
for zooplankton, Insects, annelids, crustaceans and molluscs exposed to
combined waterborne and dietary sources of selenium under natural conditions
In the field ranged from 176-2080, 371-5200, 770-1320, 420-1975 and
600-2550, respectively. BCFs for carnivorous, planktlvorous and omnivorous
fish 1n the field ranged from 590-35,675, 445-27,000 and 364-23,000,
respectively (Lemly, 1985b).
Addition of selenium to field mesocosms resulted 1n a replacement of
chrysophytes by chlorophytes In low-dose enclosures and cyanophytes 1n the
0144d 4-55 04/01/89
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high-dose enclosure. There were no significant differences between zoo-
plankton communities among 1, 10 and 100 yg selenlte-selenlum treatments
(Salkl et a!., 1985).
0144d 4-56 04/01/89
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5. PHARMACOKINETICS
5.1. ABSORPTION
Rhoads and Sanders (1985) found rapid clearance of 75Se-selenate (0.35
yg) and 75Se-selen1te (0.21 yg) from the lungs of female rats treated
by Intratracheal Instillation. For both compounds, -50J4 of the dose was
cleared 1n 44 minutes.
In a study by Welssman et al. (1983), 10 beagle dogs of each sex
(sedated with sodium phenobarbHal and trlflupromazlne hydrochloMde) were
exposed (nose-only) for 10-40 minutes to aerosols of 75Se-selen1ous add
or 75Se-selen1um. Particle sizes were .0.5+^2.4 ym for selenlous add and
0.7+K5 ym for selenium. Two dogs were sacrificed 2 hours and 2, 4, 8,
16, 32, 64, 128, 194 and 256 days after exposure. The Initial amounts of
selenium deposited were 28+12 yg/kg following exposure to selenlous add
and 22^9 yg/kg following exposure to selenium. Determination of radio-
activity 1n the tissues of dogs sacrificed at 2 hours Indicated that -97 and
80% of the deposited selenium was absorbed following exposure to selenlous
add and selenium, respectively. Welssman et al. (1983) also exposed dogs
to radlolabeled selenlous acid or selenium (2-30 yg Se/kg) by Intravenous
Injection, nasal Instillation, gavage or 1n the diet. The dogs were sacri-
ficed 4 days after dosing and the amount of selenium 1n muscle following
oral or nasal Instillation compared with Intravenous exposure was used to
estimate absorption. Absorption was estimated at 73+13.7, 95.8+16.4 and
49.5+9.9X of the administered dose following nasal Instillation, gavage and
feeding of selenlous add, respectively, and 52.U59, 72.7*04.2 and 9.5+1.7X
following nasal Instillation, gavage and feeding of selenium, respectively.
0145d 5-1 06/15/89
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Medlnsky et al. (1981) studied the absorption of selenium In anesthe-
tized male and female F344 rats exposed for 10 minutes to resplrable
particles of 7SSe-selen1um (1.3^0.7 yg/rat) or 75Se-selen1ous add
(3.6^2.4 yg Se/rat) by nose-only Inhalation. Additional groups of rats
were treated with 75Se-selen1ous add or 75Se-selen1um by gavage (<20
yg/rat) or nasal Instillation (<20 yg/rat). The dermal absorption of
selenlous add was also determined. The Investigators estimated absorption
by comparing tissue levels of selenium following Inhalation, oral, nasal or
dermal exposure to tissue levels of selenium following Intravenous exposure.
The nasal absorption of selenium was determined In anesthetized rats 1n
which the stomach was surgically exposed and Ugated at the pyloHc
sphincter to trap material cleared Into the stomach. The calculated absorp-
tion of selenium following exposure to selenlous add or selenium by various
routes Is shown In Table 5-1. The absorption of selenium from selenlous
add and selenium metal was similar following nasal exposure, but alveolar
and gastrointestinal absorption of selenlous add was greater than the
absorption of selenium metal.
Based on studies of acute Inhalation exposure of rats (Medlnsky et al.,
1981) and dogs (Welssman et al., 1983) to selenium and selenlous add,
Medlnsky et al. (1985) developed a model to project steady-state tissue
selenium concentrations 1n humans exposed by Inhalation to selenium. The
results, shown In Table 5-2, Indicate that exposure to selenium In urban air
(1 ng Se/m3) for a lifetime would contribute little to the selenium burden
1n human tissues, while exposure at the TLV (0.2 mg Se/m3), 8 hours/day, 5
days/week for a lifetime would greatly Increase the lung and liver burden of
selenium compared with the range of selenium levels generally found In these
tissues.
0145d 5-2 06/15/89
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TABLE 5-1
Calculated Internal Absorption of 75Se 1n Rats Expressed
as Fraction of Administered Dose3
Total Absorption^
Chemical
Form Nasalc
Selenlous 0.18+0.092
acid
Elemental 0.16+0.037
selenium
Gastro- Alveolar6
1ntest1nald
0.87+0.094 0.94+0.029
0.504-0.28 0.57+0.17
Cutaneous^
0. QUO. 01
NR
aSource: Medlnsky et al., 1981
bMean +. SD
cRats were sacrificed 4 hours after dosing.
dRats were sacrificed 24 hours after dosing.
eFract1on absorbed per day for 9 days
NR * Not reported
0145d 5-3 04/01/89
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TABLE 5-2
Projected Steady-State Concentrations of Selenium In Organs
and Tissues of People Exposed to Selenium 1n Urban Atmosphere or In
the Workplace and Measured Selenium Concentrations 1n Human Tissues3*^
Organ
Lung
Liver
Blood
Other tissues
Inhaled
Atmosphere0
0.4
0.02
0.01
0.002
Selenium
In the Workplace at
TLV Concentrations'1
22,000
1,200
440
78
Selenium In
Human Tissues6
100-300
70-680
100-340f
60-370
aSource: Medlnsky et al.. 1985
bng Se/g blood-free tissue wet weight
cAssumes 23 mVday Inhaled, 1 ng Se/m3
^Assumes 0.2 mg Se/m3 Inhaled 8 hours/day, 5 days/week
eCasey et al. (1982). Measured concentrations for numbers Indicate range
of values reported.
fAllaway et al. (1968)
0145d 5-4 04/01/89
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Venugopal and Luckey (1978) stated that gastrointestinal absorption of
selenium 1n the form of selenltes, selenates and selenlferous compounds 1n
mammals 1s rapid and efficient, but metal selenldes and elemental selenium
are absorbed poorly.
Thomson and Stewart (1974) treated three fasting women orally with
7SSe-selen1te at a dose of <10 yg Se. Absorption of selenium was calcu-
lated to be 70, 64 and 44% 1n the three Individuals, Indicating variation In
the gastrointestinal absorption of selenlte-selenlum.
Young et al. (1982) fed volunteers chicken meat Intrinsically enriched
with the 74Se Isotope (chickens were treated by gavage with
74Se032~), and a simultaneous dose of 76Se selenlte. Examination of
fecal excretion of 74Se and 76Se Indicated a lower absorption of
selenium from selenlte than from selenium Incorporated In chicken meat.
Selenium 1s an essential element for humans. The element 1s a part of
the enzyme glutathlone peroxldase, which Is Important 1n the cellular
defense against oxldatlve damage. Because selenium Is essential, the
concept of bloavallabllHy Is discussed often. Factors that affect the
bloavallabllHy of selenium, as reviewed by Young et al. (1982), Include
Intake levels of the element and Us chemical form; the presence or absence
of promoters or Inhibitors such as ascorbic acid, phytate, fiber, sugars,
fats and proteins; mineral-mineral Interactions; type and degree of food
processing; and the 1ngest1on of certain drugs. Young et al. (1982) also
suggested that nutritional state, physiological states (such as growth and
pregnancy) and pathological states can Influence selenium utilization.
Levander et al. (1983) studied the bloavallabllHy of selenium In groups
of 10 Finnish men provided with selenium supplementation (200 yg Se/day)
1n the form of Se-r1ch wheat, Se-r1ch yeast or sodium selenate for 11 weeks,
0145d 5-5 04/01/89
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followed by a 10-week posttreatment period. Twenty men treated wHh
placebos served as controls. All subjects In the study had low prestudy
plasma selenium levels (-70 ng/mi). Selenium b1oava1labH1ty was assessed
by the determination of platelet glutathlone peroxldase activity, and the
determination of plasma and erythrocyte selenium levels. Treatment with
selenate resulted 1n a 43 ng/ma Increase 1n plasma selenium at 11 weeks,
when plasma concentration appeared to plateau. Supplementation with Se-Mch
wheat or yeast resulted 1n plasma selenium Increases of 102 and 97 ng/mi
at 11 weeks, respectively, and these levels appeared to be Increasing.
Erythrocyte selenium levels did not appear to Increase following treatment
with selenate, while treatment with wheat and yeast more than doubled eryth-
rocyte selenium levels without signs of a plateau. Platelet glutathlone
peroxldase activity following treatment with selenate or Se-r1ch wheat
Increased to 170 and 162% of control activity, respectively, following 4
weeks of treatment, and appeared to plateau. Treatment with Se-rlch yeast
resulted In a slow Increase In platelet glutathlone peroxldase activity,
approaching the activity of the other treatment groups by week 11. During a
10-week posttreatment period, plasma selenium levels and platelet gluta-
thlone peroxldase activity returned to control levels 1n the selenate group,
but remained elevated 1n the Se-r1ch wheat and yeast groups. The response
of plasma glutathlone peroxldase activity to selenium supplementation (all
forms) was found to be very poor. The Investigators stated that seleno-
methlonlne (SeMet) Is the major form of selenium In Se-r1ch wheat, and H Is
also thought to be a major component of yeast selenium.
In a similar study 1n New Zealand, where selenium levels are low,
Thomson et al. (1982) treated 16 volunteers with dally supplements of SeMet
or sodium selenlte (100 yg Se) for at least 11 weeks. Treatment with
0145d 5-6 06/15/89
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SeMet resulted 1n a greater Increase In whole blood, erythrocyte and plasma
selenium compared with treatment with selenlte. Increases In whole blood
glutathlone peroxldase were similar following treatment with the two
compounds.
5.2. DISTRIBUTION
Following nose-only Inhalation exposure of beagle dogs to aerosols of
7SSe-selen1ous add or selenium, most of the selenium was found 1n the
lung, liver, kidneys, spleen, heart and blood (Welssman et al., 1983). The
percent of the Initially deposited selenium retained 1n these tissues during
the first 90 days postdoslng ranged from -0.1-0.2% In the liver to 0.0002-
0.001% 1n the blood. Concentrations of 7SSe 1n the liver peaked 2 hours
after exposure, while concentrations 1n other tissues did not peak until 2-4
days after exposure. Elimination half-lives of selenium, estimated
graphically, were -42-46 days for the liver and 30 days for other organs.
Two weeks after Fisher rats were given Intratracheal Instillations of
7sSe-selenate (0.35 vq) or 75Se-selen1te (0.21 vg), ~20X of the
administered activity was found In the carcass, 5% of the dose was found 1n
the liver and 5% of the dose 1n the skeleton (Rhoads and Sanders, 1985).
Results for the two compounds were similar.
Thomson and Stewart (1974) treated three fasting women orally with
7SSe-selen1te at a dose of <10 yg Se. Based on urinary and fecal
excretion, the Investigators estimated that 53, 51 and 35% of the dose was
retained by the three subjects 14 days after dosing.
McAdam and Levander (1987) fed purified Torula yeast-based diets con-
taining 2.5 or 5.0 yg Se/g as D-SeMet, L-SeMet, sodium selenlte or sodium
selenate to groups of eight male weanling Sprague-Dawley rats for 6 weeks.
0145d 5-7 06/15/89
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Although Inorganic selenium appeared to be more toxic based on mortality and
body weight gain (Section 6.1.2.1.), skeletal muscle selenium levels were
higher following exposure to organic selenium compounds. Plasma, red blood
cell, liver, heart and skeletal muscle selenium levels are presented In
Table 5-3, which Indicates that higher muscle selenium levels were not
reflected consistently by proportionate Increases 1n plasma or red blood
cell selenium; therefore, monitoring of whole blood selenium may not
adequately reflect selenium body burden.
Using light and electron microscopic visualization, a series of studies
Indicated that selenium can accumulate In the anterior pituitary
(Thorladus-Usslng and Danscher, 1985), adrenal gland (Thorladus-Usslng and
Rasmussen, 1986) and oocyte {Thorladus-Usslng et al., 1986) of rats treated
with sodium selenlte orally or by 1ntraper1toneal Injection. The selenium
found was reported to be In the form of selenlte or a selenlde bound to an
endogenous metal (possibly zinc). In the adrenal gland and anterior
pituitary, selenium located 1n secretory cells and In the ovary; selenium
accumulated 1n secondary and mature Graaflan follicles. The amount of
selenium located 1n the tissues of concern In relation to administered dose
was not provided.
Gregus and Klaassen (1986) examined tissue selenium levels 4 hours after
4-6 urethane-anesthetlzed, bile duct-cannulated male Sprague-Dawley rats
were given an Intravenous Injection of selenium (sodium selenlte and
[75Se]selen1ous add) at doses of 0.03, 0.1, 0.3 or 1.0 mg/kg. The
distribution of selenium was found to be Independent of dose within the dose
range examined. Selenium levels were highest In the liver and kidney,
accounting for 7.42-12.6 and 4.34-7.52% of the dose/10 g of tissue, respec-
tively. Blood levels of selenium accounted for 0.621-1.78% of the dose per
10 ml.
0145d 5-8 06/15/89
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tn
o.
TABLE 5-3
Concentrations of Selenium 1n Tissues from Rats Fed Diets Containing Added D-Selenomethlonlne (SeMet),
L-SeMet, Selenlte or Selenatea»b
tn
i
us
Dietary Se
Level
(vg/g)
Control
2.5
2.5
2.5
2.5
5.0
5.0
5.0
5.0
Form
D-SeMet
L -SeMet
selenlte
selenate
D-SeMet
L -SeMet
selenlte
selenate
Plasma
(vg Se/ml)
0.6H0.03b
0.56+0.06b
0.43+0.04b
0.42+0. Olb
0.8U0.043
0.58+0.08b
0.64+0.04b
0.56+0.05b
RBC
(yg Se/g)
2.05+0.12b
1.6H0.10b
1.07^0.04C
0.85±0.12C
3.07*0.11a
3.02+0.38a
1.92f0.34b
1.64+0.21b
Liver
(vg Se/g)
2.83+0.20b
1.86+0.12d
1.35f0.07e
1.34±0.14e
3.40+0.223
3.49+0.20a
2.39+0.15c
1.8H0.15d
Heart
fug Se/g)
2.20+0.20a
1.15+0.23b
0.28+0.02C
0.47+0.10°
1.94+0.05a
2.0H0.10a
0.50+0.06C
0.44*0.03C
Skeletal Muscle
(yg Se/g)
1.27+0.31b
0.84+0.06C
0.12+0.01d
0.14±0.01d
1.57+0.113
1.69+0.073
0.17*0. 03d
0.17+0.01d
aSource: McAdam and Levander, 1987
bMean + SEM, n=5 except In 5.0 vg/g selenlte
common superscript letter differ p<0.05.
group In which n=3. Means In a column not sharing a
CD
-------
5.3. METABOLISM
Reviews of the metabolism of selenium (Mushak, 1983; Ganther, 1986)
Indicate that reduction 1s a major pathway of selenium blotransformatlon In
mammals. The reduction pathway of selenium metabolism 1s shown In Figure
5-1. In the presence of ATP, sulfurylase enzyme and glutathlone, selenate
(+6) 1s reduced to selenlte (+4). Selenlte Is further reduced by reducing
agents, Including thlols and ascorbic add, to form selenotMsulfldes. The
reaction of selenlte with glutathlone, the major cellular thlol, results 1n
the formation of GSSeSG, which 1s further reduced to hydrogen selenlde (-2)
by the glutathlone reductase pathway. The formation of hydrogen selenlde
occurs 1n the liver and the erythrocytes (Ganther, 1986).
Elemental selenium can be formed by the spontaneous decomposition of the
selenopersulf1de Intermediate In the glutathlone reductase pathway or by the
spontaneous oxidation of hydrogen selenlde (Ganther, 1986). Elemental
selenium formed 1n the tissues may be biologically active; H Is hydrophoblc
and can bind tightly to proteins, and may bind to nucleic adds and Uplds.
The major elimination pathway of selenium 1s by the methylatlon of
hydrogen selenlde to dlmethylselenlde or tr1methylselenon1um. The formation
of tr1methylselenon1um, which 1s excreted In the urine, predominates when
selenium levels are low, while at higher levels dlmethylselenlde accumulates
and 1s exhaled through the lungs (Mushak, 1983).
Hydrogen selenlde 1s converted to methylated selenium by at least two
methyl transferases: the most active transferase, found 1n the cytosol of
the liver, and a transferase found 1n liver mlcrosomes (Mushak, 1983). The
methyl donor for both enzymes 1s S-adenosylmeth1on1ne. Increased selenium
Intake results In the enhancement of mlcrosomal transferase activity.
0145d 5-10 04/01/89
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Se04*~ •» RTP » Rdenosine Selenophosphate + PPt
(•tl«n*ti> tulfurylui, Hje*
SSSeOj*' * RHP » SeO,*' + 6SSG
ISH (Illtnltl)
4 RSH (69. 6SH) t> H,SeOj > 6SSeS6 + 3H20
((•l«nep*riul'
GSSeSS »• 6SSeH »• HzSe
MPOPH, flutcthlen* KSDPM, (lutathlen*
nductu* p«dutt»n
HzSe »> CH3SeH » CH3-Se-CH3 •> (CHj), Se*
(dl*«thyli«loniun> (triitthylstlonlun)
FIGURE 5-1
Metabolism of Selenium
Source: Muschak, 1983; Ganther, 1986
0145d 5-11 04/01/89
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Hydrogen selenlde may also react with metal Ions to form metal
selenldes, or with protein and metal Ions to form a protein-metal selenlde
complex (Garberg and Hogberg, 1986). These pathways may help prevent toxic
effects of heavy metals (e.g., cadmium, mercury).
Selenocyanate has been Identified as a minor urinary metabolite 1n rats
treated with selenium at relatively high doses (Vadhanav1k1t et al., 1987).
A study of the metabolism of selenocyanate 1n rats (VadhanavIkH et al.,
1987) Indicates that H also 1s methylated, with 61% of a subcutaneous dose
of 75SeCN recovered as tr1methylselenon1um In the urine of rats.
5.4. EXCRETION
Welssman et al. (1983) reported that fallowing nose-only Inhalation
exposure of beagle dogs to 7SSe-selen1ous add (28^9 ygSe/kg) or
7sSe-selen1um (22+.9 pg Se/kg), urinary excretion accounted for 70-80% of
the excreted dose, presumably during the first 32 days after dosing, the
period during which urine and feces were collected. Exhalation of 73Se
accounted for only 0.6% of the excreted dose during the first 10 days after
exposure; the remainder of the excreted dose appeared In the feces.
Determination of urinary and fecal excretion of selenium after male and
female F344 rats were treated by Intravenous Injection, nose-only Inhalation
exposure or gavage with low doses (<20 yg Se/rat) of 7SSe-selen1ous add
or 75Se-selen1um Indicated similar distributions of Se 1n the excreta 24
hours after dosing (Medlnsky et al., 1981). Following Intravenous, Inhala-
tion and gavage treatment, 27-52, 20-28 and 14-45% of the dose appeared 1n
the urine, respectively, while 5-11, 6-8 and 12-28% of the dose appeared In
the feces, respectively.
During a 2-week period following an Intratracheal Instillation of
7SSe-selenate (0.35 jig) or 75Se-selen1te (0.21 pg), rats excreted
-40% of the dose 1n the urine and feces (Rhoads and Sanders, 1985).
0145d 5-12 04/01/89
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Thomson and Stewart (1974) treated three fasting women orally with
7SSe-selen1te at a dose of not more than 10 jag Se. Fourteen days after
treatment ~14, 9 and 7% of the dose was excreted In the urine, with 33, 40
and 58% of the dose excreted 1n the feces.
Gregus and Klaassen (1986) reported that 4 days following an Intravenous
dose of selenium given to male Sprague-Dawley rats (0.3 mg Se/kg as sodium
selenlte and [75Se]selen1ous add), 17.6+3.6 and 4.34^0.34% of the dose
was excreted 1n the urine and feces, respectively.
McConnell and Roth (1966) studied the excretion of selenium In young
male rats given subcutaneous Injections of varying doses of 7SSe-selen1te
or 75Se-L-SeMet. Following treatment with selenlte at a dose of 0.005 or
0.913 mg Se/kg, 0.2 and 10.6% of the dose was exhaled In 24 hours, with 32.9
and 23.2% of the dose excreted 1n the urine, respectively. Treatment with
selenlte at doses >2.146 mg Se/kg resulted 1n the exhalation of at least 41%
of the dose, with 2-20% of the dose excreted 1n the urine. L-SeMet treat-
ment resulted 1n the exhalation of 1.3 and 6.1% of the dose 1n 24 hours,
with 27.1 and 35.8% of the dose excreted In the urine at doses of 0.001 and
1.065 mg Se/kg, respectively. At doses of L-SeMet >2.45 mg Se/kg, >17.1% of
the dose was exhaled, while -7-22% of the dose was excreted In the urine.
Following treatment with either selenlte or L-SeMet, exhalation of selenium
was greatest during the first 6 hours after treatment. The Investigators
noted that larger amounts of selenium were excreted following treatment with
selenlte compared to treatment with L-SeMet.
Calabrese (1985) stated that the renal excretion of tr1methylselenon1um
1s slower In male rats compared with female rats. This difference 1n secre-
tion was eliminated 1n castrated male rats, Indicating that the excretion of
tr1methylselenon1um In male rats Is androgen-dependent. Selenium and
0145d 5-13 06/15/89
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methylated selenium compounds have been shown to be more toxic to male rats
than to female rats. This Increased toxldty to male rats was not
eliminated 1n castrated male rats, suggesting an additional mechanism of
Increased sensitivity of male rats to selenium.
5.5. SUMMARY
Studies in dogs (Welssman et al., 1983) and rats (Medlnsky et al., 1981}
Indicate that selenium metal and selenlous add are absorbed readily follow-
ing Inhalation exposure. Gastrointestinal absorption and bloavallabllUy of
selenium Is greater with organic selenium compounds such as SeMet compared
with Inorganic compounds. Among Inorganic selenium compounds, selenltes and
selenates are absorbed more readily than metal selenldes and elemental
selenium (Venugopal and Luckey, 1978).
Following absorption, selenium 1s distributed throughout the body, with
higher levels found 1n the liver and kidneys. McAdam and Levander (1987)
found higher muscle selenium levels In rats fed diets with organic selenium
compounds (0- or L-SeMet) compared to rats fed sodium selenate or selenlte.
Reduction of selenium compounds to hydrogen selenlde followed by
methylatlon 1s the major transformation pathway leading to the excretion of
selenium (Mushak, 1983). Methylatlon occurs predominantly 1n the liver.
Trlmethylselenonlum, excreted 1n the urine, Is the major excretory product
at low doses of selenium. At higher doses of selenium, larger amounts of
dlmethylselenlde are produced. Olmethylselenlde 1s exhaled through the
lungs. Metal selenldes and metal-protein selenlde compounds may also be
formed from hydrogen selenlde.
0145d 5-14 06/15/89
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6. EFFECTS
6.1. SYSTEMIC TOXICITY
6.1.1. Inhalation Exposure.
6.1.1.1. SUBCHRONIC -- Pertinent data regarding the toxldty of
selenium following subchronlc Inhalation exposure were not located In the
available literature dted In Appendix A.
6.1.1.2. CHRONIC -- Hamilton and Hardy (1974) reviewed symptoms that
have been reported 1n chronic Industrial selenium poisoning. The symptoms
reported most frequently Include a strong garlic odor 1n the breath, sweat
and urine, acute sore throats and cold-Uke symptoms, gastrointestinal Irri-
tation, lacrlmatlon, and a metallic taste 1n the mouth. Exposure concentra-
tions resulting In these effects were not provided. The development of
garlic breath and cold-Uke symptoms Is thought to be a result of the
hepatic production of dlmethylselenlde, which 1s exhaled through the lungs
(Dlskln et al., 1979).
Dlskln et al. (1979) described a case of a 71-year-old man who had been
employed 1n selenium refining for 50 years. The man was admitted to the
hospital with chest pain and ECG evidence of cardiac Infarction. The
patient had reddish orange hair and red fingernails, a result of high
selenium exposure. The patient developed cardlogenlc shock and died 8 days
after admission. At autopsy, sections of the lungs showed numerous perl-
vascular noncaseatlng granulomas that varied In age. Analysis of tissues
for selenium revealed abnormally high levels In the lungs (109 ppm, normal
levels 0.15-0.21 ppm), perlbronchlal lymph nodes (26 ppm, normal levels 0.1
ppm), and hair (213 ppm, normal levels 0.36-0.74 ppm), but not In other
tissues, Including the trachea (0.33 ppm, normal levels not reported) and
0146d 6-1 04/03/89
-------
liver (0.47 ppm, normal levels 0.43-0.53 ppm). The Investigators stated
that the perlvascular location of the granulomas suggested a blood-borne
toxin, presumably d1methylselen1de.
Glover (1967) measured urinary selenium concentration of workers at a
selenium rectifier plant over a 5-year period. A1r concentrations, measured
sporadically, appeared to correlate with urinary selenium concentrations.
Glover (1967) recommended a maximum allowable urinary concentration of 0.1
mg Se/i, which he believed corresponded to an air concentration of 0.1 mg
Se/m3. Glover (1967) did not believe that garlic odor of the breath was a
reliable guide to selenium absorption. Garlic breath was absent In men
excreting as much as 0.1 mg Se/a, 1n the urine, while 1t was present In
workers with urinary selenium concentrations of 0.5-1.0 mg/i. Glover
(1967) reported that the cause of death of 17 selenium workers was not found
to differ from expected values. The duration of exposure for these workers
was not provided.
6.1.2. Oral Exposure.
6.1.2.1. SUBCHRONIC -- Halverson et a'i. (1966) fed groups of 8 or 10
young male Sprague-Dawley rats sodium selenlte or selenlferous wheat at
dietary levels of 1.6, 3.2, 4.8, 6.4, 8.0 or 9.6 ppm selenium for 6 weeks.
Assuming rats eat food equivalent to 5% of their body weight/day (U.S. EPA,
1986a), these diets provided selenium doses of 0.08, 0.16, 0.24, 0.32, 0.4
or 0.48 mg/kg/day. An additional group of rats was fed selenlferous wheat
at a dietary level of 11.2 ppm selenium (0.56 mg/kg/day). Control rats were
fed the basal diet, which contained 0.7 ppm Se (0.04 mg/kg/day). All rats
treated with selenlferous wheat at 11.2 ppm died, while 5/8 and 1/8 rats
treated with selenlferous wheat at 9.6 and 8.0 ppm died. In rats treated
with sodium selenlte, 1/10 and 1/8 died at 9.6 and 8.0 ppm, respectively.
0146d 6-2 04/03/89
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All deaths occurred after the fourth week of the study. Treatment of rats
with either form of selenium at >6.4 ppm resulted In significant (p<0.01)
growth depression. A small growth depression was also observed 1n rats
treated with selenlte (but not selenlferous wheat) at 4.8 ppm. Rats treated
with selenlferous wheat at >6.4 ppm Se had significantly (p<0.05) enlarged
spleens, while at >8.0 ppm a significant (p<0.05) reduction In hemoglobin
and an enlargement of the pancreas was observed. Liver weights of rats
treated at 6.4-11.2 ppm Se were reduced significantly (p<0.01) and livers of
rats treated at >6.4 ppm Se showed varying degrees of mottling, roughness
and discoloration. It Is not clear 1f the liver effects were observed 1n
selenlferous wheat or selenlte treated rats, or In both groups of rats. The
dietary level of 3.2 ppm Se (0.16 mg/kg/day) 1s considered a NOEL (U.S. EPA,
1984a).
NCI/NTP (1980a) treated groups of 10 male and 10 female F344 rats and
B6C3F1 mice by gavage with selenium sulflde 1n CMC 7 days/week for 13 weeks,
followed by 1 week of observation. Rats were treated at doses of 0 (vehicle
control), 3.2, 5.6, 10, 17.8 or 31.8 mg/kg/day, and mice were treated at
doses of 0 (vehicle control), 21.6, 46.4, 100, 216 or 464 mg/kg/day. Doses
were not calculated 1n terms of selenium because the substance under study
was not defined clearly; analysis Indicated that the substance was primarily
selenium monosulflde with selenium dlsulflde, selenium and sulfur also
present. All rats survived the treatment, and no effect on growth rate was
noted. The only hlstologlcal change noted In rats was focal coagulation
necrosis with Infiltration by Inflammatory cells 1n the livers of rats
treated at 31.8 mg/kg/day. In mice, 464 mg/kg/day was clearly an effect
level; four females and one male died, body weight gain was suppressed 1n
females, and from week 3 to the end of the study, both sexes appeared thin
0146d 6-3 06/15/89
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or showed hunched posture on both. An Increased Incidence and severity of
microscopic Interstitial nephritis was also observed 1n mice treated at 464
mg/kg/day. Except for the death of one female mouse treated at 216
mg/kg/day, compound-related effects were not observed 1n mice at lower doses.
Beems and van Beek (1985) fed groups of eight male and eight female
weanling Syrian hamsters sodium selenlte 1n the diet at concentrations of
0.1 (unsupplemented control), 1, 5, 10 or 20 ppm Se for 42 days. Based on
food Intake data, the Investigators calculated that the selenium Intake was
0.007, 0.1, 0.31, 0.61 or 1.21 mg/kg/day for males and 0.007, 0.1, 0.3, 0.63
and 1.26 mg/kg/day for female hamsters fed at 0.1, 1, 5, 10 or 20 ppm,
respectively. No effects on survival or behavior were noted. Body weight
gain was reduced 1n males at all doses compared with unsupplemented
controls, but the reduction was found to correspond to differences 1n food
Intake. No changes 1n body weights were noted In females. At necropsy, no
gross treatment-related abnormalities were noted. The only microscopic
changes observed were lesions In the liver of most hamsters treated at 20
ppm, Including necrosis, oval-cell proliferation 1n the perlportal areas,
enlargement of hepatocytes, and hepatocellular nuclei mainly In the centrl-
lobular areas, and accumulation of brown pigment 1n macrophages In the perl-
portal region. This study Identifies a subchronlc LOAEL of 1.21 mg/kg/day
1n hamsters, and a NOEL of 0.63 mg/kg/day.
In a 60-day study, McAdam and Levander (1987) fed groups of eight male
weanling Sprague-Dawley rats Torula yeast-based purified diets (<0.02 yg
Se/g) with 2.5, 5 or 10 vg/g (ppm) added selenium as D-SeMet, L-SeMet,
sodium selenlte or sodium selenate. Assuming rats eat food equivalent to 5%
of their body weight/day, these diets provided selenium at doses of 0.125,
0.25 or 0.5 mg/kg/day. All rats provided with diets containing selenium
(all forms) at 10 yg/g died within 29 days. At 5.0 yg/g, 5 selenlte-,
0146d 6-4 06/15/89
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3 L-SeMet-, 1 D-SeMET- and 1 selenate-fed rat died. At 2.5 yg/g all rats
survived except two rats fed selenate. Body weight gain was decreased
significantly 1n rats fed Inorganic selenium at 5.0 jig/g, but not In rats
fed organic selenium. Little difference 1n body weight gain was observed 1n
rats fed 2.5 yg Se/g. Determination of muscle selenium levels at the end
of the study Indicated a greater accumulation of selenium following organic
selenium exposure compared with exposure to Inorganic compounds (see Section
5.2.). Hlstopathologlcal examinations were not completed.
In a study by Keller et al. (1986), the Immune responses of female
Sprague-Dawley rats (12/group) provided with drinking water containing
sodium selenlte at 0, 0.5, 2.0 or 5.0 ppm Se for 10 weeks were examined.
Based on an estimated water consumption of 0.02 a/day for a 0.25 kg rat
(U.S. EPA, 1980b), the rats were treated with additional selenium at doses
of ~0, 0.04, 0.16 or 0.4 mg/kg/day. Determination of NK activity Indicated
significantly enhanced cytoxlclty against YAC-1 tumor cells at 0.5 and 2.0
ppm, with NK activity similar to controls at 5 ppm. Humoral antibody
production against keyhole limpet hemocyanln was reduced In all selenium-
treated rats, with a statistically significant (p<0.05) decrease observed
only at 5.0 ppm. Selenium treatment significantly (p<0.01) reduced delayed-
type hypersensltWHy response at all doses. Additional effects noted were
a significant (p<0.05) decrease 1n prostaglandln synthesis, an Increase 1n
relative thymus weight at 5.0 ppm, and a dose-related Increase 1n relative
liver weights. The only microscopic lesions noted were mild hepatocyte
hypertrophy and mild congestion of renal cortical veins. The dose at which
these effects occurred was not stated. From their results, the Investi-
gators suggested that the effect of selenium on the Immune system may be the
underlying mechanism of the antlcarclnogenlc and carcinogenic properties of
selenium.
0146d 6-5 04/03/89
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6.1.2.2. CHRONIC -- Smith et al. (1936) conducted an epidemlologic
study of the chronic toxlclty of selenium 1n humans on farms 1n South
Dakota, Wyoming and Nebraska where animals were known to be suffering from
alkali disease. Clinical signs 1n farm workers that were attributed to
selenium Included bad teeth, jaundice, chloasma, vertigo, chronic gastro-
intestinal disease, dermatitis, nail changes, arthritis, edema, lassitude
and fatigue. Analyses of food resulted In an estimation of dally selenium
Intake of 0.1-0.2 mg/kg. Of the urine samples analyzed for selenium, 45X
contained 0.2-1.33 yg/mi,. The observed symptoms appeared to correlate
with a urinary selenium concentration >0.2 yg/mi.
U.S. EPA (1980a) summarized a number of studies that show an association
between high selenium Intake and an Increase 1n dental carles 1n humans. No
exposure data were provided. Increased Incidences 1n dental carles have
also been produced In rats fed high levels of dietary selenium (Buttner,
1963), and In monkeys, Hacaca 1rus. provided with selenium In the drinking
water at 1 ppm (Bowen, 1972).
Beath (1962) reported symptoms of lassitude, alopecia, discoloration of
the skin and loss of fingernails In persons exposed to well water containing
9 mg/ft, selenium. Assuming a 70 kg person consumes 2 t of water/day,
this water concentration corresponds to a dose of -0.26 mg/kg/day. Discon-
tinuation of the use of selenium-contaminated water resulted 1n regrowth of
hair and nails and Increased mental alertness.
Yang et al. (1983) reported outbreaks of selenium Intoxication In the
Hubel province of the People's Republic of China. Dietary selenium Intake
1n this region was compared with a region of high selenium Intake without
selenium Intoxication. In five villages In the Hubel Province, severe out-
breaks of selenosls occurred, affecting an average of 49.2X of the popula-
tion, with 85.5% of the population affected 1n one village. Evacuation and
0146d 6-6 06/15/89
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change 1n the diet resulted 1n recovery. The Investigators Indicated that
the selenium source appeared to be high levels of selenium 1n surface coal
that leached Into the soil and became available to uptake by vegetable
crops. Apparently, the outbreak was caused by an Increase In the consump-
tion of selenium-accumulating vegetables, Including corn and turnip greens,
as a result of a drought that led to failure of the rice crop. The contri-
bution of selenium In drinking water was considered negligible, compared
with dietary selenium.
The symptoms reported Included bMttleness of nails, loss of nails and
hair, pruritus of the scalp, dermatitis characterized by hyperemla, edema
and eruptive blistering, and nervous symptoms such as peripheral anesthesia,
acroparesthesla and pain In the limbs. In more severe cases, exaggerated
tendon reflexes, numbness, convulsions, motor dysfunction progressing to
paralysis, and hemlplegla developed. Mottled teeth and Increased tooth
decay were also found, but because fluoride levels were high 1n the area,
these observations are difficult to Interpret. The above symptoms were
associated with dally selenium Intake ranging from 3.2-6.69 mg/day, with an
average Intake of 4.99 mg/day, estimated from analysis of components from
the diets of six persons. Analysis of the diets of three persons from an
area with high selenium without selenosls, showed a dally selenium Intake
ranging from 0.24-1.51 mg/day with an average Intake of 0.75 mg/day. Hair,
blood and urine selenium levels found 1n high selenium areas with and with-
out selenosls and 1n areas with adequate selenium are presented In Table 6-1.
Yang et al. (1983) also reported the case of a male worker who consumed
one tablet of sodium selenlte dally (-0.9 mg Se) for >2 years. Effects
observed were garlic odor In his dermal excretions and thickened, fragile
nails. After stopping selenium Intake, his nails became smooth. The
0146d 6-7 04/03/89
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CD
TABLE 6-1
Selenium Levels 1n Hair, Blood and Urine of Residents of High- and Adequate-Se Areas of China3
Area Sampled
H1gh-Se area where chronic
selenosls was observed
H1gh-Se area where chronic
selenosls was observed
H1gh-Se area where chronic
selenosls was not observed
Se-adequate area
Hair
n vq Se/g
1745 (1.9-8.2)
65 32.2
(4.1-100)b
14 3.7
(1.9-8.2)
1745 0.36
(±0.17)
Blood
n pg Se/ma.
Ill (0.35-0.58)
72 3.2
(1.3-7.5)
14 0.44
(0.35-0.58)
111 0.095
(±0.091)
Urine
n pg Se/mH
19 (0.88-6.63)
17 2.68
(0.88-6.63)
14 0.14
(0.04-0.33)
19 0.026
(±0.012)
aSource: Young et al., 1982
bF1gures 1n parentheses are range or standard deviation.
CD
IO
-------
authors suggested that a dally Intake of 1.0 mg selenium over a long period
may be toxic to humans. Blood (0.179 ppm) and hair selenium (0.828 ppm)
concentrations were well below those associated with selenosls 1n the high
selenium area. The authors suggested that tissue levels alone are not
sufficient to predict selenium Intoxication; the form of selenium Ingested
must also be known because organic selenium accumulates In the tissues to a
greater extent than Inorganic selenium.
Longnecker et al. (1987) found no evidence of selenium toxldty among 77
South Dakotans with high dietary selenium Intake (up to 590 yg/day). The
ranges of selenium levels 1n plasma, whole blood and toenalls were 118-295
ng/ml, 176-521 ng/ma and 0.67-2.00 yg/g, respectively.
Chronic exposure of livestock to high levels of selenium can result In
alkali disease. The symptoms observed Include emaciation, lack of vitality,
loss of hair, separation of the hoof, atrophy and decompensation of the
heart, cirrhosis of the liver, anemia, glomerulonephrltis and erosion 1n the
joints of the long bones (U.S. EPA, 1980a).
In the chronic NCI/NTP (1980a) gavage study, groups of 50 F344 rats/sex
and 50 B6C3F1 mice/sex were treated by gavage with selenium sulflde 1n CMC
(see Section 6.1.2.1. for description of the test material) dally for 103
weeks at dosages of 3 or 15 mg/kg/day (rats) or 20 or 100 mg/kg/day (mice).
Equal sized groups of untreated and vehicle-treated controls were main-
tained. High-dose rats of both sexes had reduced rate of body weight gain
that became evident after -16 weeks of treatment and resulted 1n lower body
weights at termination. Exposure to selenium had no apparent effect on
survival of rats. Nonneoplastlc hlstopathologlc lesions In rats Included
focal hepatocellular changes 1n high-dose males and Increased lung pigmenta-
tion In high-dose males and In low- and high-dose females. Exposure to
0146d 6-9 06/15/89
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selenium had no effects on body weights or survival of mice. There was no
mention of nonneoplastlc hlstopathologk lesions 1n mice.
FHzhugh et al. (1944) found decreased growth rate, a restriction of
food Intake and liver lesions In female Osborne-Mendel rats (18/group) fed
selenium In the diet In the form of selenlferous wheat or corn at 5, 7 or 10
ppm [0.25, 0.35 or 0.5 mg/kg/day assuming a rat food Intake equivalent to 5%
of body weight (U.S. EPA, 1986a)] for up to 24 months. Additional groups of
rats were fed Inorganic selenlde (ammonium potassium selenlde) at 10, 20 or
40 ppm Se (0.5, 1 or 2 mg/kg/day). The basal diet used 1n this study was
suboptlmal 1n the level of protein. Mortality was Increased In rats fed at
>10 ppm selenium. Cirrhosis of the liver, found at all treatment levels,
was observed 1n 71/100 treated rats surviving for >3 months. Further
Information concerning the protocol and carcinogenic effects observed In
this study (described 1n Nelson et al., 1943) are presented 1n Section 6.2.2.
Schroeder and Mltchener (1971a) treated groups of -50 male and 50 female
Long-Evans BLU:LE rats with sodium selenlte or sodium selenate 1n the drink-
Ing water at a concentration of 2-3 mg Se/l [0.28-0.42 mg/kg/day assuming
a 0.35 kg rat body weight and a 0.049 a/day drinking water Intake (U.S.
EPA, 1986a)]. Similar groups of rats provided with drinking water with no
added selenium served as controls. The experiment was Intended to continue
throughout the Hfespan of the treated animals as a carclnogenlcHy
bloassay. Male rats were especially sensitive to sodium selenlte, with 50%
dying within 2 months. Male rats surviving selenlte-treatment were given
sodium selenate for the remainder of the experiment. Similar effects on
survival were not observed In female sodium selenlte-treated rats. No other
parameters of toxldty were reported.
0146d 6-10 04/03/89
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6.1.3. Other Relevant Information. Selenium, an essential element for
humans, Is a part of glutathlone peroxldase. Additional proteins that
contain selenium Include selenoproteln of muscle and Se-transport protein.
Other selenoprotelns and selenoamlno acids have been found but have not been
defined further (Koller and Exon, 1986). The dally safe and adequate level
of selenium Intake for adults 1s considered to be 50-200 yg (NAS, 1980).
This level, along with safe and adequate dally selenium Intake levels for
Infants and children, Is presented In Table 6-2.
Selenium deficiency 1n humans 1n China has been associated with Keshan
disease, a cardlomyopathlc condition characterized by cardiac enlargement,
ECG abnormalities, heart failure, gallop rhythm and cardiac shock (Koller
and Exon, 1986). In persons In low selenium areas In New Zealand, stress
seems to result In the expression of selenium-deficiency syndromes, which
Include Intermittent muscle tenderness and pain and white fingernail beds.
Epidemiology studies 1n low selenium areas 1n the United States and Finland
appear to show an association between low selenium and cardiovascular
disease (Koller ana Exon, 1986).
Carter (1966) reported a fatal case of selenium Intoxication 1n a child
who drank gun-bluing compound containing 1.8% selenlous add. The clinical
signs of toxldty observed Included peripheral vascular collapse, pulmonary
edema and coma. Autopsy revealed pulmonary congestion, hemorrhage and edema.
Oral I.DCQ values for selenium compounds 1n animals are summarized In
Table 6-3. The lowest LD5Q was 1.8 mg Se/kg for sodium selenate 1n
rabbits (Muehlberger and Schrenk, 1928), while the highest oral LD5Q, 6700
mg Se/kg 1n rats, Is for selenium metal (Cummins and Klmura, 1971).
Interactions of selenium have been reviewed by Dlplock (1976) and U.S.
EPA (1980a). Selenium has been shown to be antagonistic to the toxic
0146d 6-11 04/03/89
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TABLE 6-2
Safe and Adequate Ranges of Dally Selenium Intake*
Group
Infants
Children
Adults
Age
(years)
0.0-0.5
0.5-1
1-3
4-6
7 +
NA
Dally Selenium Intake
(yg)
10-40
20-60
20-80
30-120
50-200
50-200
*Source: U.S. EPA, 1980a; NAS, 1980
NA = Not applicable
0146d 6-12 04/03/89
-------
0
-p.
o.
s
o
-p.
0
oo
Species/Strain Sex
Hlce/CD-1 F
Rats/Sprague- M
Dawley
Rats/Sprague- M
Dawley
Rats/Sprague- M
Dawley
Rats/Sprague- M
Dawley
Rabbi ts/NR NR
RabbHs/NR NR
NR = Not reported
TABLE 6-3
Acute Oral Toxlclty of Selenium Compounds
Compound LD5Q 10 ^Q
(mg/kg compound) (mg/kg selenium)
sodium selenlte 8.4 3.8
sodium selenlte 7 3.2
selenourea 50 32.1
selenium sulflde 138 76.2
elemental selenium 6700 6700
sodium selenlte NR 2.85
sodium selenate NR 1.8
Reference
Plasterer
et al., 1985
Cummins and
Klmura. 1971
Cummins and
Klmura. 1971
Cummins and
Klmura, 1971
Cummins and
Kumura, 1971
Muehlberger and
Schrenck, 1928
Muehlberger and
Schrenck. 1928
-------
effects of silver, cadmium, Inorganic mercury and thallium. Rats provided
with a selenium supplemented diet were protected from paraquat toxlclty
compared with selenium deficient rats (Omaye et al., 1978).
Sodium arsenlte 1n drinking water (5 mg/8.) has been shown to alleviate
chronic and acute toxlclty 1n rats fed selenlferous grains (Moxon, 1938).
Arsenic appears to alleviate the toxlclty of selenium by enhancing the
biliary excretion of selenium.
Dietary sulfate partially restores the growth of rats treated with sele-
nlte or selenate 1n the diet (Halverson and Monty, 1960). Sodium sulfate In
the diet protected against liver necrosis 1n rats fed selenate (10 mg Se/kg)
but not selenlte or selenlferous wheat (Halverson et al., 1962).
6.2. CARCINOGENICITY
6.2.1. Inhalation. Pertinent data regarding the carclnogenlclty of
selenium following Inhalation exposure were not located 1n the available
literature dted 1n Appendix A.
6.2.2. Oral. Nelson et al. (1943) (see Section 6.1.2.2. for noncarclno-
genlc effects In this study that were reported by FHzhugh et al., 1944)
treated groups of 18 female Osborne-Mendel rats with diets containing
selenium at 5, 7 or 10 ppm In the form of selenlferous corn or wheat for 2
years. An additional group of rats was fed selenium at 10 ppm In the diet
1n the form of a solution of ammonium potassium selenlde and ammonium
potassium sulflde. Eighteen rats were maintained as controls. The basal
diet used 1n this study was suboptlmal 1n the level of protein. Mortality
was high and tended to be proportional to selenium Intake; only four rats
treated with selenlferous corn and wheat and six rats treated with selenlde
survived for 2 years. At all doses, cirrhosis of the liver was observed.
0146d 6-14 06/15/89
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Cirrhosis was found 1n rats that died or were killed as early as 3 months,
and 1n 43/53 rats surviving 2 years. Liver tumors were observed only In
rats with cirrhosis. Of the 53 rats surviving 2 years, 11 developed hepato-
cellular "adenomas or low grade carcinomas." The 14 control rats that
survived to 18 months showed no evidence of neoplasla. No discussion of the
statistical significance of these findings was presented.
Schroeder and Mltchener (1971a) reported a statistically significant
Increase In the number of tumors 1n rats treated with sodium selenate In
drinking water at 2-3 ppm Se. IARC (1975) noted that "an evaluation of
these results was not possible because not all autopsled animals were
examined hlstologlcally and because treated, animals lived longer than
controls." Further details concerning methods and effects on survival are
presented 1n Section 6.1.2.2.
Harr et al. (1967) and Tlnsley et al. (1967) did not find a carcinogenic
effect 1n male and female Wlstar rats (1437 rats used In the studies)
provided with sodium selenlte or sodium selenate at 0.5-16 ppm Se In the
diet throughout their lifetimes. Liver effects (accentuated lobular
pattern, hyperemla, cellular degeneration, mildly prol1ferat.1ve hepatocytes,
blnucleatlon and multiple nucleoll) were observed 1n rats treated at 4, 6, 8
or 16 vg/g (4, 6, 8 or 16 ppm) 1n the diet.
Schroeder and MHchener (1972) treated groups of -50 male and 50 female
Swiss mice with selenate or selenlte 1n double delonlzed drinking water at a
dose of 0 or 3 ppm. Treatment began at weaning and was continued until all
mice were dead. Under the conditions of the study, selenium did not
significantly Increase the Incidence of tumors.
In an NCI/NTP (1980a) bloassay, groups of 50 male and 50 female F344
rats and B6C3F1 mice were treated by gavage 7 days/week with selenium
0146d 6-15 04/03/89
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sulflde 1n CMC. Rats were treated at doses of 3 or 15 mg/kg/day and mice
were treated at doses of 20 or 100 mg/kg/day. Similar groups of rats and
mice treated with the vehicle or left untreated served as controls. Doses
were not calculated 1n terms of selenium because the substance under study
was not defined clearly; analysis Indicated that the substance was primarily
selenium monosulflde with selenium dlsulflde, elemental selenium and sulfur
also present. Survival of rats and mice was not affected by selenium
sulflde treatment. Tumor Incidence data, presented In Table 6-4, Indicated
that primary liver tumors were Increased significantly (p<0.001) 1n male and
female rats and female mice (p<0.001) at the high dose, and lung tumors were
Increased significantly (p<0.001) In female mice. NCI/NTP (1980a) concluded
that under the conditions of the study, selenium sulflde was carcinogenic 1n
male and female F344 rats and female B6C3F1 mice, but was not carcinogenic
1n male B6C3F1 mice, although male mice may have been able to tolerate
higher doses.
6.2.3. Other Relevant Information. The NCI/NTP has conducted dermal
cardnogenlclty studies of selenium sulflde (NCI/NTP, 1980b) and Selsun*
(antldandruff shampoo containing 2.5% selenium sulflde) (NCI/NTP, 1980c) In
ICR Swiss mice. In these studies, groups of 50 mice/sex were treated
dermally 3 times/week for 86 weeks with selenium sulflde at 0.5 or 1 mg, or
with 0.05 mi. of a 25 or 50% Selsun* solution. Similar groups of vehicle
controls were maintained. The studies were terminated at 86 weeks because
of poor survival. Amyloldosls, a known cause of death 1n Swiss mice,
contributed to the deaths of most mice after 1 year. Dermal application of
selenium sulflde or Selsun* did not result 1n treatment-related Increases
In tumor Incidences. Both studies were limited by the relatively short
llfespan of ICR mice.
0146d 6-16 09/15/89
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TABLE 6-4
Incidence of Tumors In F344 Rats and B6C3F1 Mice Treated by Gavage
with Selenium Sulflde for 103 Weeks8
Species/Strain Sex Dose
(mg/kg/day)
Rat/F344 H 0 (vehicle)
3
15
F 0 (vehicle)
3
15
Mouse/B6C3Fl N 0 (vehicle)
20
100
F 0 (vehicle)
20
100
M 0 (vehicle)
20
100
F 0 (vehicle)
20
100
Duration
of Study
(weeks)
104
104
104-105
104
104
104-105
104
104-105
104-105
104
104-105
104-105
104
104-105
104-105
104
104-105
104-105
Tumor Type
hepatocellular carcinoma
or neoplastlc nodule
hepatocellular carcinoma
or neoplastlc nodule
lung alveolar/bronchlolar
carcinoma or ademona
lung alevolar/bronchlolar
carcinoma or adenoma
hepatocellular carcinoma
or adenoma
hepatocellular carcinoma
or adenoma
Tumor Incidence
(p value)
1/50 (p<0.001)b
0/50 (NS)
24/49 (p<0.001)c
1/50 (p<0.001)°
0/50 (NS)
37/50 (p<0.001)c
4/40 (p=0.022)b
10/50 (NS)
13/50 (p=0.016)c
0/49 (p<0.001)b
3/50 (NS)
12/49 (p<0.001)c
15/50 (p<0.026)b
14/50 (NS)
23/50 (NS)
0/49 (p<0.001)b
2/50 (NS)
25/49 (p<0.001)c
o
CO
OD
IO
-------
TABLE 6-4 (cont.)
.*»
en
a.
Quality of Evidence
The compound was administered to adequate numbers of animals of both sexes by a
relevant route of exposure at two dose levels.
The substance under study was not clearly defined - analysis Indicated that the
substance was primarily selenium monosulflde with selenium dlsulflde. elemental
selenium and sulfur also present. The amounts of the Individual compounds were not
determined. Hale mice may not have been treated at the maximum tolerated dose.
Strengths of Study:
Weakness of Study:
Overall Adequacy: Adequate
aSource: NCI/NTP. 1980a
?] bCochran-Arm1tage Test
co
cF1sher Exact
NS = Not significant
o
CO
oo
lO
-------
Further evaluation of the data, however, failed to Identify the specific
selenium salt associated with neoplastlc lesions; therefore the NCI/NTP
(1980) study 1s considered Inconclusive.
Selenium, an essential element, has been extolled as an antlcardnogen.
Several epidemiology studies reviewed by Wlllett and Stampfer (1986) have
reported lower blood selenium levels 1n cancer patients compared with
cancer-free subjects. Wlllett and Stampfer (1986) Indicated that these
studies have limited significance because the effect of cancer on blood
selenium level was not distinguished from an effect of selenium on cancer.
Several more recent studies (Wlllett et al., 1983; Salonen et al., 1984,
1985; Kok et al., 1987) examined selenium levels of serum samples collected
before the diagnosis of cancer. These studies have also shown a relation-
ship between low serum selenium levels and cancer. Kok et al. (1987)
observed a significant association between cancer and low selenium levels In
men but not women, and Indicated that similar results were found 1n the
studies by Wlllett et al. (1983) and Salonen et al. (1985).
Numerous studies 1n animals have also reported antlcardnogenlc effects
of selenium against carcinogen-Induced carcinomas. Animal studies reviewed
by Shamberger (1985) have found that selenium treatment reduces the Inci-
dence of skin tumors Induced by 3-methylcholanthrene and benzopyrene, liver
tumors Induced by 3-methyl-4-d1methyl-am1noazobenzene, 2-acetylam1nofluorene
and aflatoxln B,, tracheal tumors Induced by 1-methyl-l-nltrosourea,
mammary gland tumors Induced by 7,12-dlmethyl-benzanthracene, anthracene and
N-methyl-N-nltrosurea, tumors of the colon and large and small bowel Induced
by 1,2-d1methylhydraz1ne and azoxymethane, and lung and large and small
bowel tumors Induced by b1s(2-oxopropyl)n1trosam1ne. Mice, rats or hamsters
were treated In these studies with selenium In the diet at 0.1-6 ppm, 1n the
0146d 6-19 09/15/89
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drinking water at 1-4 ppm, or dermally with a 0.005X selenium solution. The
observation that selenium protects against fat-sensitive types of cancers
may Indicate that selenium protects against cellular damage caused by
peroxldatlon of fat (Shamberger, 1985).
In a study of the effect of selenium on the Immune system In rats,
Koller et al. (1986) found that selenium In the diet at 0.5 and 5.0 ppm
enhanced NK activity, while treatment at 10 ppm resulted In NK activity
similar to controls (see Section 6.1.2.1.). From these results, the
Investigators postulated that enhancement of NK activity may be a mechanism
of the antlcarclnogenlc activity of selenium, suggesting that neoplasms that
are NK sensitive may be prevented or are responsive to selenium therapy.
6.3. MUTAGENICITY
Hutagenlclty data for selenium compounds are summarized 1n Table 6-5.
The results were mixed, with both positive and negative results reported.
The most frequently tested compounds were sodium selenlte and sodium
selenate. Shamberger (1985) reviewed mutagen1c1ty data for selenium and
concluded that 1n general, sodium selenlte (+4) was more mutagenlc 1n
mutation systems than sodium selenate (+6). The only study of selenium
metal found that the metal was more active 1n Inducing sister chromatld
exchange 1n human whole blood cultures than selenium dioxide, sodium
selenlde or sodium selenlte (Ray and Altenburg, 1980).
6.4. TERATOGENICITY
Robertson (1970) reported that during a 5-year period, all but one of
four certain pregnancies and one probable pregnancy among eight women
exposed to selenium 1n the preparation of medium for Salmonella culture
ended In miscarriage (clinical factors may have accounted for two
miscarriages). In the single pregnancy that went to term, the Infant had
0146d 6-20 09/15/89
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IflDLC O-D
Hutagenlclty Testing of Selenium Compounds
^
°- Assay
Reverse
mutation
Reverse
mutation
Rec assay
DNA damage
Rec assay
, ONA damage
rsj
Chromosome
aberrations
Chromosome
aberrations
Chromosome
aberrations
Indicator/
Organism
Salmonella
typhlmurlum
TA98. TA100
and 1A1537
S. typhlmurlum
(specific
strains not
stated)
Bacillus
subtllls
17A (rec».
45T (rec-)
B. subtllls
17A (rec»)
457 (rec-)
rat lymphocytes
In vitro
Chinese hamster
ovary cells
human lympho-
cytes Jin vitro
Compound
Na2Se03.
Na2Se04
selentte.
selenate
sodium
selenlte
(Na2Se03).
selentous acid
(H2Se03) (M)
selenlc acid
(H2Se04) (»6)
Na2Se03
Na2Se03.
Na2Se04
Na2Se03.
H2Se03.
Application
plate
Incorporation
plate
Incorporation
spot test
spot test
added to
cultures
added to
cultures
added to
cultures
Concentration Activating Response
or Dose System
0.12 |iN none «•
NR none - selenlte
«• selenate
0.8-10 mg none «•
1 or 10 mg none
1. 5, 7.5, 1 none »
and 2.5xlO"«
H
-
10~* to » glutathlone »
10~« N thlone »
6.5. 13. 26 none all » except
or 53xlO~» N Na2Se04
Comment
Heakly * only In TA100
Selenate resulted In an
Increase In base-pair
substitutions
None
NaOH was added to raise
the pH
Significant Increase of
abnormal metaphases at
1xlO~» N (p<0.01) and
2.5xlO~» N (p<0.001)
Selenate was more active
In Inducing aberrations
without glutathlone;
glutathlone enhanced the
activity of selenlte
Efficiency of chromosome -
breaking activity was In
Reference
Noda et al..
1979
Lofroth and
Ames. 1978
Nakamuro
et al.. 1976
Nakamuro
et al.. 1976
Newton and
Lilly. 1986
Whiting
et al.. 1980
Nakamuro
et al.. 1976
H2Se04,
sodium selenate
(Na2Se04).
selenium oxide
(Se02)
the following order:
H2Se03 > Na2Se03 > Se02 »
H2Se04 > Na2Se04; activity
of the M compounds was
greater than the +6
compounds
00
IO
-------
TABLE 6-5 (cont.)
o<
I
rsj
Assay
Cloning
efficiency
Nick transla-
tion assay -
DNA damage
(strand breaks)
Sister
chromatld
exchange
Indicator/
Organism
human dlplold
flbroblasts
human dlplold
flbroblasts
human whole
blood cultures
Compound Application
Na2Se03 added to
cultures
Na?Se03 added to
cultures
sodium selenlde added to
(Se^-); cultures
selenium
Concentration Activating Response
or Dose System
0.1-1.0 raM «• glutathlone *
1 S-9 «•
50-500 tiN _f glutathlone <•
1.12x10"* to none «•
8.0xlO~> N
Comment Reference
S-9 and reduced glutathlone Snyder, 1987
Induced similar enhancement
of cloning ability
Reduced glutathlone In- Snyder. 1987
creased DNA damage; HO-
scavenger, mannltol and
peroxide scavenger, catalase
had no effect on strand
break formation, suggesting
that the breaks most likely
do not arise via free oxygen
radical formation
SCE Inducing abilities of Ray and
Se In decreasing order of Altenburg.
effectiveness; selenium > 1980
dioxide (Se4*);
selenium (Se°).
sodium selenlte
(Se**)
selenium dioxide > sodium
selenlde > sodium selenlte
Sister
chromatld
exchange
Crossing over
Chromosome
aberrations
human whole
blood cultures
Drosophlla
aelanoqaster
rat lymphocytes
and bone marrow
cells
sodium
selenate
selenocystlne.
seleno-
oethlonlne
Na2Se03
added to
cultures
added to
media
In vivo expo-
sure of rats
(Intravenous)
1.12x10'* to none
8.00xlO's H
1.63. 5.22. NA
16.3. 81.6
iiH seleno-
cystlne; 1.63,
5.22. 16.3 vH
selenomethlonlne
1.5. 2, 2.5, NA
6. 5 mg/kg for
2 treatments
or 6 tag/kg for
1 treatment
None
reduction In None
recombination
combination
- lymphocytes; Doses of 5 or 6 mg/kg were
<• bone marrow near lethal doses
at 5 or 6 mg/kg
for 2 treatments
Ray and
Altenburg,
1986
Ting and
Walker, 1969
Newton and
Lilly. 1986
NR = Not reported; NA = not applicable
u>
CO
-------
bilateral club-foot. Urinary selenium levels of these women toward the end
of the 5-year period were similar to controls living 1n the same area.
In a review of the reproductive effects of selenium, Barlow and Sullivan
(1982) Indicated that hoof abnormalities have been noted 1n foals, calves
and lambs born to animals grazing on selenlferous pastures. Rosenfeld and
Beath (1947, 1964) described other malformations In lambs born 1n selenlf-
erous areas. The majority (85%) of lambs born In the area had abnormal eyes
and limbs and died at birth or shortly after birth. In survivors, limb
deformities Impaired locomotion. Eye deformities Included large cysts
protruding through the Hds, sclera fused to bone preventing rotation,
colobomas, and abnormal or absent lens, cornea or Iris. Some lambs were
mkrophthalmlc with multiple ocular cysts. Hlstologlc examination of the
eyes revealed bizarre structural arrangement resulting from arrested growth
and poor differentiation. Hypoplasla of reproductive organs was also noted
1n lambs that survived. Estimates of selenium doses resulting 1n these
effects were not provided.
Numerous studies reviewed by U.S. EPA (1980a) Indicate that In hens,
selenHe In the diet at 8-10 mg/kg can result 1n fetal deaths and extensive
malformations of the central nervous system, extremities and beak. Because
these studies are not useful for risk assessment, they will not be discussed
further.
Fetotoxlc effects of selenium 1n rodents appear to be less dramatic than
those 1n domestic animals (Barlow and Sullivan, 1982), predominantly result-
Ing In a decrease In fetal body weight. Nobunaga et al. (1979) treated
groups of 14 female IVCS mice with selenium as sodium selenHe In the
drinking water at 0, 3 or 6 ppm Se for 30 days before mating with untreated
males. Selenium treatment was continued until gestation day 18 when the
mice were sacrificed and the fetuses were examined. No effects on the
0146d 6-23 09/15/89
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number of Implants/dam, the number of dead fetuses, the number of resorp-
tlons, or the number of malformed fetuses were noted. Fetal body weight was
decreased significantly (p<0.05) at 6 ppm, but not at 3 ppm.
Plasterer et al. (1985) treated groups of 45 pregnant CD-I mice by
gavage with distilled water or with sodium selenlte 1n distilled water at a
dose of 7 mg/kg/day on gestation days 7-14. Shortly after birth, Individual
pups were examined for gross structural abnormalities, and Utters were
weighed on both the day of birth and 48 hours later. Under the conditions
of the study, sodium selenlte did not result In any maternal or fetal
effects.
Holmberg and Perm (1969) did not find any teratogenk effects In
hamsters given an Intravenous Injection of sodium selenlte at 2 mg/kg on
gestation day 8. Pretreatment with sodium selenlte markedly reduced the
teratogenlc effects of Intravenous Injections of cadmium sulfate and sodium
arsenate.
Lee et al. (1979) studied the effects of selenium treatment and simulta-
neous selenium and methylmercury treatment on the Induction of cleft palate
In mice. Pregnant ICR mice were treated with single subcutaneous Injections
of selenium or selenium and methylmercury on gestation day 10, or multiple
Injections on gestation days 9-12 or 7-12. Treatment with selenium at 2
mg/kg/day had no effect on mean Utter size, mean fetal weight or the
percent of mice with cleft palate. At 3.5 mg Se/kg/day, the only effect
noted was a significant decrease In mean fetal body weight. Treatment of
mice with methylmercury and selenium simultaneously appeared to potentiate
the ability of methylmercury to Induce cleft palates when treatment was
administered on gestation days 9-12.
OH6d 6-24 09/15/89
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6.5. OTHER REPRODUCTIVE EFFECTS
Schroeder and MHchener (1971b) completed a multi-generation study 1n
which five pairs of CD-I mice were fed a purified diet containing minimal
(0.056 ppm) selenium, and were provided with drinking water containing
selenate at a concentration of 3 ppm Se [0.57 mg/kg/day, assuming a 0.03 kg
mouse body weight and a 0.0057 l/day drinking water Intake (U.S. EPA,
1986a)]. Treatment was Initiated at weaning. Control mice were provided
with the same diet. Pairs of mice were allowed to breed up to 6 months of
age. The second generation was bred from Fl , F,. and F, offspring,
a ID 1C
and the third generation was obtained from F. and F. offspring. The
parameters of toxlclty evaluated Included Intervals between Utters, age at
which first litter was produced, number of runts, number of stillborn,
failure to breed successfully, congenital abnormalities and maternal death.
By these criteria, selenium at 3 ppm 1n the drinking water was toxic to
mice. The strain began to die out at the third generation; seven pairs
failed to breed, Including 16 runts among 23 mice born to three pairs. For
all generations, selenium treatment resulted 1n 93 runts of 389 live-born
offspring, 1 stillborn Utter, the death of 23 offspring shortly after birth
and 1 maternal death. The Increase In the number of runts was statistically
significant for all generations, while deaths of offspring were only sig-
nificant In the F, generation. Congenital malformations were not reported.
In a study concerning the effects of selenium on the testes, Nebbla et
al. (1987) treated groups of 7-12 male Wlstar rats with sodium selenlte In
the drinking water at a concentration of 4, 8 or 16 ppm (1.8, 3.7 or 7.3 ppm
Se) for 240 days. Assuming that a 0.35 kg rat drinks 0.049 l/day (U.S.
EPA, 1986a), the 1.8, 3.7 and 7.3 ppm Se concentrations correspond to doses
of 0.25, 0.52 and 1.0 mg/kg/day, respectively. Control rats were provided
with tap water. Body weights of rats treated at 7.3 ppm were significantly
0146d 6-25 09/15/89
-------
lower than controls, and testes weight and testes-to-body weight ratio were
Increased significantly compared with controls. Microscopic examination of
the testes revealed damaged tubules 1n rats treated at 7.3 ppm, exhibiting
ol1gosperm1a and vacuollzatlon of spermatlds without multlnucleated cells.
Moderate Intertubular edema was also observed. Similar but less severe
effects were noted at 3.7 ppm; no effects were noted at 1.8 ppm. Measure-
ment of testlcular enzyme activities compared with controls Indicated a
significant decrease 1n SDH activity at 3.7 and 7.3 ppm, a significant
Increase 1n GGT activity at 7.3 ppm, significant decreases 1n B-G activity
at 1.8 and 3.7 ppm and a significant Increase 1n B-G activity at 7.3 ppm.
Testlcular LDH activity was found to be Increased significantly at all dose
levels. The significance of the changes 1n enzyme activity are not clear.
The reproductive capacity of these rats was not determined.
6.6. SUMMARY
Selenium Is an essential element that Is a part of glutathlone peroxl-
dase. The dally safe and adequate level of selenium Intake for adults 1s
considered to be 50-200 v9 (0.05-0.2 mg) (NAS, 1980). Selenium 1s also
quite toxic, with selenosls (brlttleness of nails, loss of nails and hair,
dermatitis, nervous symptoms) reported In humans following chronic dietary
Intake of 3.2-6.69 mg/day (Yang et al., 1983).
Adverse effects reported In animals treated orally with selenium com-
pounds Include effects on growth, reduced survival, hlstopathologlc changes
In the liver and testes and Immune system effects. Subchronlc NOELs that
have been Identified In laboratory animals are 0.16 mg Se/kg/day of sodium
selenlte or selenlferous wheat In rats (Halverson et al., 1966) and 0.63 mg
Se/kg/day of sodium selenlte 1n hamsters (Beems and van Beek, 1985).
Limited chronic studies of selenium compounds do not Identify NOELs.
0146d 6-26 09/15/89
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Selenium toxldty following Inhalation exposure has not been studied In
animals. Symptoms reported 1n humans following occupational exposure to
selenium Include a strong garlic odor 1n the breath, sweat and urine, acute
sore throats and cold-like symptoms, gastrointestinal Irritation, lacrlma-
tlon, and a metallic taste In the mouth (Hamilton and Hardy, 1974). The
development of garlic breath and cold-Uke symptoms 1s thought to result
from the hepatic production of dlmethylselenlde, which Is exhaled through
the lungs (D1sk1n et al., 1979).
Carclnogenlclty studies of selenium are not conclusive. Selenium
sulflde has tested positive for cardnogenldty 1n rats and female mice 1n
an NCI/NTP (1980a) bloassay. Increased tumor Incidences were also reported
by Nelson et al. (1943) In rats treated orally with selenlferous corn and
wheat (diets were suboptlmal 1n protein), and In rats treated with sodium
selenate (Schroeder and MHchener, 1971a). Negative results were reported
1n rats treated with sodium selenate or selenlte (Harr et al., 1967; Tlnsley
et al., 1967) and In mice treated with sodium selenate or selenlte
(Schroeder and MHchener, 1972).
Epidemiology studies (WHlett and Stampfer, 1986; Salonen et al., 1984,
1985; Kok et al., 1987) and studies using animals (Shamberger, 1985) suggest
that selenium has antlcarclnogenlc activity. This effect may be due to the
ability of selenium to protect against cellular damage by peroxldatlon of
fat (Shamberger, 1985), or 1t may be a result of the effect of selenium on
the Immune system (Koller et al., 1986).
The available evidence suggests that selenium Is fetotoxlc and
teratogenlc. A study by Roberts (1970) weakly associates miscarriage and
birth of Infants with bilateral club foot to occupational exposure to
selenium.
0146d 6-27 09/15/89
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Selenium 1s teratogenlc to livestock (Barlow and Sullivan, 1982), but
developmental effects reported 1n laboratory rodents are limited to
decreased fetal body weight (Nobunaga et al., 1979). A limited multi-
generation study (Schroeder and MHchener, 1971b) found that by the third
generation, CD-I mice treated with selenate In the drinking water at 0.57
mg/kg/day failed to breed, or produced a large proportion of runts.
Testlcular degeneration and ol1gosperm1a were reported 1n rats treated with
selenium at 1 mg/kg/day 1n drinking water for 240 days (Nebbla et al., 1987).
0146d 6-28 09/15/89
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7. EXISTING GUIDELINES AND STANDARDS
7.1. HUMAN
The WHO (1984) maximum guideline for selenium 1n drinking water 1s 0.01
mg/l.
The AWQC for selenium 1s 0.01 mg/st (U.S. EPA, 1980a, 1982), which Is
also the current drinking water standard (see below). The value was chosen
with the consideration that only 5-10% of dally exposure to selenium should
come from water-related sources, for example drinking water and aquatic
organisms.
U.S. EPA (19855) recommended 10-day health advisories of 0.041 and 0.144
mg/8. for a 10 kg child and a 70 kg adult, respectively. These values are
based on the subchronlc rat study by Halverson et al. (1966). The AADI
(U.S. EPA, 1985b) for a 70 kg adult 1s 0.106 mg/i based on the human study
by Yang et al. (1983).
U.S. EPA (1985a) has proposed an RMCL of 0.045 mg/i. The RMCL 1s a
nonenforceable health goal that would result 1n no known or anticipated
health effects. The current enforceable MCL for selenium, based on the WHO
(1984) guidelines, 1s 0.01 mg/il (U.S. EPA, 1985c).
The verified oral RfDs for selenlous acid and selenourea are 0.003 and
0.005 mg/kg/day (U.S. EPA, 1985c,d), respectively. Both values are based on
the human ep1dem1olog1cal study by Yang et al. (1983), which reported
selenosls 1n persons exposed to selenium at 0.046 mg/kg/day.
Final RQs for selenium compounds are 1000 for selenourea, 100 for
selenium [(a release of selenium does not need to be reported If the
diameter of the metal Is >100 ym (0.004 Inches)] and sodium selenlte, and
10 for selenlous add and selenium oxide (U.S. EPA, 1986b). The proposed RQ
for selenium dlsulflde Is 10 pounds (U.S. EPA, 1987b).
0147d 7-1 06/15/89
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The OSHA PEL for selenium compounds (as Se) 1s 0.2 mg/m3 (OSHA, 1985).
ACGIH (1987) has also recommended a TLV-TWA of 0.2 mg Se/m3 for selenium
compounds to protect against systemic toxlclty and Irritation (ACGIH, 1986).
U.S. FDA (1987) has ruled that feed for major food producing animals may
be supplemented with sodium selenlte or selenate at a level not to exceed
0.3 ppm Se. Feed supplements for limited feeding may also be supplemented
with selenium at a rate not to exceed an Intake of 0.7 mg/head/day for sheep
and 3 mg/head/day for beef cattle.
7.2. AQUATIC
Adams and Johnson (1981) proposed a criterion for selenium 1n freshwater
systems of 52 yg/a based on data demonstrating that the amphlpod,
Hyallela azteca. was the most sensitive species tested. The criterion was
calculated from the product of the 14-day LC5Q of 0.07 mg/l for this
species and an average application factor of 0.74 derived from the ratio of
time-Independent LCrQ values to the geometric means of MATCs for rainbow
trout and Daphnla magna.
Lemly (1985b) recommended a maximum permissible level of selenium In
warm water lakes and reservoirs of 5 yg Se/l as a long-term average (>30
days). The author suggested that 10 yg Se/8. was a reasonable criterion
for selenium In rivers and streams containing centrarchlds and 50 yg
Se/a. 1n rivers containing only salmonlds. A criterion for selenium 1n
cold water lakes and reservoirs of 50 yg Se/i was recommended 1f only
salmonlds were present, but a criterion of 5 yg Se/8, was recommended If
centrarchlds were present. Lemly (1985b) apparently based these criteria on
data collected from field studies rather than from calculations or extrapo-
lation from laboratory-derived toxlclty data.
0147d 7-2 04/03/89
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U.S. EPA (1987a) reported that "The procedures described 1n the
'Guidelines for Deriving Numerical National Water Quality Criteria1 for the
Protection of Aquatic Organisms and Their Uses Indicate that, except
possibly where a locally Important species 1s very sensitive, freshwater
aquatic organisms and their uses should not be affected unacceptably 1f the
4-day average concentration of selenium does not exceed 5.0 yg/t more
than once every 3 years on the average and If the 1-hour average concen-
tration does not exceed 20 yg/l more than once every 3 years on the
average."
U.S. EPA (1987a) also reported that "The procedures described 1n the
'Guidelines for Deriving Numerical National Water Quality Criteria for the
Protection of Aquatic Organisms and Their Uses' Indicate that, except
possibly where a locally Important species 1s very sensitive, saltwater
aquatic organisms and their uses should not be affected unacceptably 1f the
4-day average concentration of selenium does not exceed 71 ^g/i more
than once every 3 years on the average and 1f the 1-hour average concen-
tration does not exceed 300 vq/i more than once every 3 years on the
average." Despite these criteria for marine systems, U.S. EPA (1987a)
recommended that the status of marine fish communities be monitored whenever
the concentration of selenium 1n saltwater was >5.0
0147d 7-3 04/03/89
-------
8. RISK ASSESSMENT
Statements concerning available literature 1n this document refer to
published, quotable sources and are In no way meant to Imply that confiden-
tial business Information (CBI), which this document could not address, are
not In existence. From examination of the bibliographies of the CBI data,
however, 1t was determined that CBI data that would alter the approach to
risk assessment or the risk assessment values presented herein do not exist.
8.1. CARCINOGENICITY
8.1.1. Inhalation. Pertinent data regarding the carclnogenldty of
selenium compounds following Inhalation exposure were not located 1n the
available literature cited In Appendix A.
8.1.2. Oral. Oral carclnogenldty studies of selenium compounds have
been Inconclusive. Nelson et al. (1943) found Increased tumor Incidences 1n
rats fed selenlferous corn or wheat In a basal diet that was suboptlmal 1n
protein. Schroeder and MHchener (1971a) reported a significant Increase 1n
tumor Incidences In rats treated with selenate 1n the drinking water at 2-3
ppm Se. An evaluation of this study 1s not possible, however, because not
all autopsled rats were examined h1stolog1cally, and treated rats lived
longer than controls (IARC, 1975). Positive results were also reported 1n
male and female rats and female mice treated by gavage with selenium sulflde
(NCI/NTP, 1980a). However, the Identity of the compound associated with
neoplastlc evidence Is unclear; therefore the study Is considered
Inconclusive.
In contrast, Harr et al. (1967) and "Mnsley et al. (1967) did not find a
carcinogenic effect In male and female Wlstar rats provided with sodium
selenlte or sodium selenate 1n the diet at 0.5-16 yg Se/g diet throughout
0148d 8-1 09/15/89
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their lifetimes. Negative results were also reported In mice treated with
selenate or selenlte In the drinking water at 3 ppm (Schroeder and
MHchener, 1972).
Numerous studies, reviewed by Shamberger (1985), 1n which animals were
treated with a known carcinogen and selenium In the diet (0.1-6 ppm) or
drinking water (1-4 ppm), Indicate that selenium has antlcardnogenlc
activity. In addition, epidemiology studies reviewed by Wlllet and Stampfer
(1986) have reported an association between lower selenium blood levels and
cancer. It has been suggested that selenium may protect against cellular
damage caused by peroxldatlon of fat (Shamberger, 1985). From results of a
study concerning the effect of selenium on the Immune system In rats, Koller
et al. (1986) suggested that selenium may act as an antlcardnogen by
enhancing NK activity.
8.1.3. Other Routes. Dermal carclnogenldty bloassays of selenium
sulflde (NCI/NTP, 1980b) and Selsun® (antldandruff shampoo containing 2.5X
selenium sulflde) (NCI/NTP, 1980c) 1n mice have not resulted 1n Increased
tumor Incidences.
8.1.4. Weight of Evidence. After reviewing available carclnogenldty
data, IARC (1975) concluded that animal data were Insufficient to evaluate
the carclnogenldty of selenium compounds, and that human data did not
suggest that selenium was carcinogenic.
U.S. EPA (1980a) Indicated that the carclnogenldty of selenium
compounds Is a complex Issue for the following reasons: 1) there 1s
evidence that selenates, selenltes and selenldes at nontoxlc levels have
antlcardnogenlc activity 1n animals; 2) even at moderate dietary
concentrations (5-10 ppm) of selenates and selenltes, the chronic toxldty
1s high, and this toxldty Interferes with tumor development because of
0148d . 8-2 09/15/89
-------
early deaths; 3) the solubility and, therefore, the availability of
different selenium compounds Is highly variable; 4) low concentrations of
selenium are essential; and 5) the chronic toxldty studies are difficult to
compare because of the large number of different selenium compounds studied,
the dependence of tumor Induction on changes 1n protein and selenium levels
1n the diet, and Incomplete hlstopathologkal examinations In a number of
studies.
There are no data regarding the carclnogenlclty of selenium to humans.
Because the animal evidence 1s conflicting and difficult to Interpret, 1t
can be considered Inadequate evidence of a carcinogenic effect. Therefore,
based on no human carclnogenlclty data and Inadequate animal data, selenium
can be considered, according to U.S. EPA classification scheme, as Group D
carcinogen - not classifiable as to human carclnogenlclty (U.S. EPA, 1986b).
However, because of positive evidence of carclnogenlclty 1n both rats and
female mice (NCI/NTP, 1980a), selenium sulflde, based on U.S. EPA (1986b)
classification scheme, could be considered as Group B2 - probably carcino-
genic to humans.
8.1.5. Quantitative Risk Estimates.
8.1.5.1. INHALATION ~ The lack of data concerning the carclnogen-
lclty of selenium following Inhalation exposure precludes the derivation of
an Inhalation potency factor.
8.1.5.2. ORAL — According to U.S. EPA (1986b) guidelines, quantita-
tive risk assessments are not appropriate for agents that are Judged to be
1n Group D. Therefore, a potency factor for oral exposure to selenium will
not be derived. Since H Is unclear regarding the chemical species of
selenium associated with carclnogenlclty In the NCI/NTP (1980a) study, H Is
Inappropriate to estimate a potency factor for oral exposure to selenium
sulflde.
0148d 8-3 09/21/89
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8.2. SYSTEMIC TOXICITY
8.2.1. Inhalation Exposure.
8.2.1.1. LESS THAN LIFETIME EXPOSURE (SUBCHRONIC) -- Pertinent data
regarding the toxlclty of selenium following subchronlc Inhalation exposure
were not located 1n the available literature, precluding the derivation of a
subchronlc Inhalation RfD.
8.2.1.2. CHRONIC EXPOSURE -- Data regarding the toxlclty of selenium
compounds following chronic Inhalation exposure are limited to reports of
occupational exposure that are not sufficient for RfD derivation. Symptoms
reported following occupational exposure to selenium compounds (concentra-
tions not specified) Include garlic odor In the breath, sweat and urine,
acute sore throats and cold-Uke symptoms, gastrointestinal Irritation,
lacrlmatlon and a metallic taste 1n the mouth (Hamilton and Hardy, 1974).
Dlskln et al. (1979) described a case of a selenium worker who had peMvas-
cular noncaseatlng granulomas 1n the lungs at autopsy that were suggestive
of a blood-borne toxin. Dlskln et al. (1979) suggested that the lung
effects observed 1n this case and other effects of occupational exposure to
selenium may result from the hepatic production of dlmethylselenlde, which
1s exhaled through the lungs.
Pharmacoklnetlc studies using dogs (Welssman et al., 1983) and rats
(Medlnsky et al., 1981) Indicate that selenium and selenlous acid are
absorbed readily following Inhalation exposure. Based on these studies,
Medlnsky et al. (1985) developed a model to project steady-state tissue
selenium concentrations In humans exposed to selenium by Inhalation.
Results from the model suggest that exposure to selenium 1n urban air (1 ng
Se/m3) for a lifetime would contribute little to the selenium burden 1n
human tissues compared with oral exposure, while exposure at the TLV (0.2 mg
0148d 8-4 09/21/89
-------
Se/m3), 8 hours/day, 5 days/week for a lifetime may result 1n liver
burdens 2-17 and lung burdens 73-220 times greater than selenium levels
normally found 1n these tissues. Although lung and liver burdens of
selenium associated with adverse effects are not known, Medlnsky et al.
(1985) concluded that chronic exposure to selenium near the TLV may be a
hazard to some Individuals.
8.2.2. Oral Exposure.
8.2.2.1. LESS THAN LIFETIME EXPOSURE (SUBCHRONIC) — Selenium 1s an
essential element that 1s also very toxic. The safe and adequate Intake for
adults 1s estimated at 50-200 yg/day (0.71-2.9 yg/kg/day) (NAS, 1980).
Selenosls has been reported 1n humans chronically exposed to dietary
selenium at a dose as low as 3.2 mg/day (46 yg/kg/day) (Yang et al., 1983).
The available subchronlc animal studies of selenium are difficult to
evaluate because of the various selenium compounds studied. The results of
the subchronlc studies Indicate that death occurs In rats at a dose of -0.5
mg/kg/day (MeAdam and Levander, 1987; Halverson et al., 1966). Additional
effects reported 1n rats and hamsters treated at >0.24 mg/kg/day Included
hlstopathologlc changes In the liver and changes In body weight (MeAdam and
Levander, 1987; Halverson et al., 1966; Beems and van Beek, 1985). The
highest NOEL below the LOAEL 1n a subchronlc animal study 1s 0.16 mg/kg/day
1n rats reported by Halverson et al. (1966).
Because of the narrow range between a dose considered safe and adequate
for humans and a dose resulting 1n effects In humans, greater confidence can
be placed 1n an RfO based on human rather than animal data. Therefore, the
chronic oral RfD of 4.6 yg/kg/day or 3.2 mg/day for a 70 kg human Is
recommended as the subchronlc RfD for selenium. The derivation of this RfO,
based on the study by Yang et al. (1983), 1s described In Section 8.2.2.2.
0148d 8-5 09/21/89
-------
Confidence In this RfD Is high based on low confidence In the study and high
confidence In the data base.
8.2.2.2. CHRONIC EXPOSURE — Chronic oral studies In animals
(Fltzhugh et al., 1944; Schroeder and MHchener, 1971a,b) have used doses
that resulted 1n Increased mortality, and did not Identify LOAELs, NOAELs or
NOELs potentially useful for risk assessment.
The toxldty of selenium depends on numerous factors Including the
selenium and nutritional status of the Individual, b1oava1labH1ty of
different forms of selenium and Interactions with heavy metals. Because of
these factors, the limited number of human studies reporting selenium doses
resulting 1n effects are difficult to compare. An epidemiology study In
selenlferous areas In South Dakota (Smith et al., 1936) reported symptoms of
selenosls In persons with a dietary selenium Intake of 0.1-0.2 mg/kg/day
(7-14 mg/day for a 70 kg human). Beath (1962) found symptoms of selenosls
1n persons drinking well water containing 9 mg selenium/a. (18 mg/day
assuming a drinking water Intake of 2 a/day). In a single case, selenosls
was observed In a man who consumed one sodium selenHe tablet dally (0.9
mg/day) for 2 years (Yang et al., 1983). The verified chronic oral RfDs for
selenlous add (U.S. EPA, 1985c) and selenourea (U.S. EPA, 1985d), and the
AIC for selenium (U.S. EPA, 1984a) are based on the study by Yang et al.
(1983), which reported outbreaks of selenosls 1n China among persons consum-
ing selenium In the diet at 3.2-6.69 mg/day (based on the diets of six
persons). Selenosls was not observed 1n areas with selenium Intakes averag-
ing 0.75 mg/day (based on the diets of three persons). The RfDs and AIC are
based on the 3.2 mg/kg LOAEL. The values were derived by dividing the LOAEL
by an uncertainty factor of 10 to extrapolate from a LOAEL, and a modifying
factor of 1.5 because of Information suggesting that selenium 1n drinking
0148d 8-6 09/21/89
-------
water Is absorbed more efficiently than selenium In food. An uncertainty
factor of 10 to account for human variability was not considered necessary
because the LOAEL was from a large population of humans (248 Inhabitants of
the 5 most heavily affected villages, although estimates of dietary Intake
were based on the diets of 6 persons, and the LOAEL, 3.2 mg/day, 1s a value
for 1 person). The RfDs, 0.21 mg/day for selenlous acid (U.S. EPA, 1985d)
and 0.35 for selenourea (U.S. EPA, 1985c), and the RfD and AIC of 0.21
mg/day for selenium are at the upper end of the range of a safe and adequate
dally Intake of 50-200 vq Se/day (0.05-0.2 mg/day) (NAS, 1980).
Confidence In the Yang et al. (1983) study 1s low because the range of
doses resulting 1n effects was based on the analysis of the diets of only
six people. Confidence In the data base Is considered high based on
additional supporting epidemiology studies and reviews of the toxldty of
selenium resulting 1n long-term selenium Intake levels similar to or higher
than the RfO. Reflecting confidence 1n the data base, confidence 1n the RfD
of 0.32 mg/day (0.05 mg/kg/day) 1s high.
0148d 8-7 09/21/89
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9. REPORTABLE QUANTITIES
9.1. BASED ON SYSTEMIC TOXICITY
The toxlclty of selenium was discussed 1n Chapter 6. Data considered
for RQ derivation are presented In Table 9-1. Data from the NCI/NTP (1980a)
gavage study using rats and mice are not Included because the Identity of
the test material was not reported sufficiently to allow estimation of
dosages of selenium. In the study by Beems and van Beek (1985), hlstologk
changes 1n the liver were observed 1n hamsters treated with sodium selenlte
1n the diet at a dose of 1.21 mg Se/kg/day for 42 days. Halverson et al.
(1966) reported deaths of rats fed selenlferous wheat at 0.56 mg Se/kg/day
for 6 weeks, while liver effects were noted 1n rats at 0.32 mg Se/kg/day; 1t
1s possible that deaths from exposure to selenium 1n this study occurred at
lower dosages as well. Death occurred 1n rats treated with sodium selenlte
1n the diet at a dose of 0.5 mg Se/kg/day for 29 days (MeAdam and Levander,
1987), and In rats treated with sodium selenlte In the diet 0.28 mg Se/kg
day for 2 months (Schroeder and MHchener, 1971a). In a chronic study In
rats (FHzhugh et al., 1944), Increased mortality anc! cirrhosis of the liver
were observed 1n rats treated with ammonium potassium selenlde 1n the diet
at a dose of 0.5 mg Se/kg/day. Reduced food Intake and growth and the
presence of liver lesions were observed at 0.25 mg/kg/day. Schroeder and
MHchener (1971b) reported Increased mortality of offspring and an Increase
1n the number of runts from mice treated with sodium selenate In the
drinking water at a dose of 0.57 mg Se/kg/day for 3 generations. In an
epidemiology study (Yang et al., 1983), selenosls was observed In persons
consuming diets containing selenium that provided doses of 3.2-6.69 mg/day
(based on analysis of the diets of six persons). The symptoms reported
Included brlttleness of nails, loss of nails and hair, prurltls of the
scalp, dermatitis characterized by
0149d 9-1 06/15/89
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TABLE 9-1
Toxlctty Summary for Oral Exposure to Selenium
VO
o.
Species/Strain Sex
Hamsters/ N
Syrian
Rats/Sprague- N
Dawley
Rats/Sprague- N
Dawley
Rats/Sprague- N
Dawley
i
*«» Rats /Os borne- F
Nendel
Rats/Osborne- F
Nendel
Rats/Long- N.F
Evans RLV:LE
Nice/CD-I N.F
o
o
00
Ifi
Average
No. at Body
Start Height
(kg)
8 0.14b
8-10 0.35b
8-10 0.35b
8 0.35b
18 0.35b
18 0.35b
50/sex 0.35b
5/sex 0.03b
Vehicle Compound
diet sodium selentte
diet selenlferous
wheat
diet selenlferous
wheat or sodium
selenlte
diet D-SeNet. L-Se
Net. selenlte
or selenate
diet ammonium potas-
sium selenlde
diet selenlferous
grain
drinking sodium selenlte
water
drinking sodium selenate
water
Exposure
20 ppm sodium
selenlte In
the diet for
42 days
11.2 ppro Se
for 6 weeks
6.4 ppm Se
for 6 weeks
10 v9/g Se In
the diet for
29 days
10 ppm Se for
up to 24 months
5 ppm selenium
In the diet
for 24 months
2 mg Se/l for
2 months
3 ppm for 3
generations,
parental gen-
eration treated
for 6 months
Transformed Equivalent
Animal Dose Human Dosea
(mg/kg/day) (ng/kg/day)
1.21C 0.15
0.56d 0.10
0.32d 0.055
0.5d 0.09
0.5d 0.09
0.25d 0.043
0.28* 0.048
0.57f 0.043
Response
Hlstopathologtc changes In
the liver (oval cell pro-
liferation, necrosis of
cells and foci of cells)
Death after 4 weeks of
treatment
Reduced liver weights.
mottling, roughness and
discoloration of the liver
Death
Increased mortality.
cirrhosis of the liver
Reduced feed Intake and
growth; liver lesions
Increased mortality of
offspring before weaning.
an Increase In the number
of runts
Increased mortality at
2 months
Reference
Beems and van
Beek. 1985
Halverson
et al.. 1966
Halverson
et al.. 1966
NcAdam and
Levander.
1987
Fltzhugh
et al.. 1944
Fltzhugh
et al.. 1944
Schroeder and
Nltchener,
1971a
Schroeder and
Nltchener,
1971a
-------
TABLE 9-1 (cent.)
No. at
Species/Strain Sex Start
Humans N.F NR
Average
Body
Height Vehicle
(kg)
70b diet
Compound
dietary
selenium
Transformed
Exposure Animal Dose
(mg/kg/day)
3.21 mg/day NA
average sele-
nium Intake
Equivalent
Human Dose8
(mg/kg/day)
0.046
Response Reference
Selenosls: brlttleness and Vang et al..
loss of nails, loss of 1983
hair, dermatitis, nervous
symptoms
Calculated by multiplying the animal transformed dose by the cube root of the ratio of the animal body weight to the human body weight
bReference body weights (0.14 kg hamster; 0.35 kg rat; 0.03 kg mouse; 70 kg human) (U.S. EPA. 1986c)
C0ose provided by Investigators
Calculated assuming a rat eats food equivalent to 5X of Its body weight/day (U.S. EPA. 1986c)
Calculated assuming a 0.35 kg rat drinks 0.049 ft of water/day (U.S. EPA. 1986c)
vo 'Calculated assuming a 0.03 kg mouse drinks 0.0057 ft of water/day (U.S. EPA. 1986c)
i
" NR = Not reported; NA = not applicable
o
CO
-------
hyperemla, edema and eruptive blistering, and nervous system effects Includ-
ing peripheral anesthesia, acroparesthesla, pain In the limbs, and numbness,
convulsions and motor dysfunction progressing to paralysis 1n more severe
cases.
The derivations of candidate CS and RQ values are presented 1n Table
9-2. Candidate CSs were not computed for data from the studies by Beems and
van Beek (1985), Halverson et al. (1966), McAdam and Levander (1987) and
Schroeder and MHchener (1971a) because adequate chronic data were avail-
able. In the epidemiology study (Yang et al., 1983), the syndrome of
selenosls was observed In persons consuming selenium 1n the diet at a dose
as low as 3.2 mg/day. This dose corresponds to an RVd of 4.7. It 1s not
clear what specific effects were observed at the reported dose. The con-
servative approach 1s to assume that the most severe effects, nervous system
effects Including convulsions and paralysis, occurred at the lowest reported
dose. The effects on the nervous system correspond to an RV of 9.
Multiplying the RVg by the RVrf yields a CS of 42.3.
Mortality, corresponding to an RV of 10, was reported In both the
Fltzhugh et al. (1944) chronic rat study and the Schroeder and MHchener
(1971b) 3-generat1on study using mice. Mortality occurred In the FHhzhugh
et al. (1944) rat study at a human MED of 6.3 mg/kg, which corresponds to an
RVd of 4.3, while In the Schroeder and MHchener (1971b) 3-generat1on
study, Increased mortality of offspring occurred at a human MED of 2.8
mg/kg, corresponding to an RV. of 4.8. Multiplying the RV s by the
RV s yields CSs of 43 and 48 for the FHzhugh et al. (1944) and Schroeder
and MHchener (1971b) studies, respectively.
U.S. EPA (1983) also derived an RQ of 10 based on a CS of 49 calculated
from the Schroeder and MHchener (1971b) 3-generat1on study using mice.
0149d 9-4 06/15/89
-------
VO
o.
TABLE 9-2
Composite Scores for Selenium
10
1
en
Species
Rats
Mice
Animal Dose
(mg/kg/day)
0.5
0.57
Chronic
Human MED
(mg/day)
5.9
3.01
RVd
4.3
6.3
Effect
Increased mortality,
cirrhosis of the liver
Increased mortality
RVe
10
10
CS
43
62.8
RQ
10
10
Reference
Mtzhugh et al .,
1944
Schroeder and
Humans
NA
3.21
of offspring before
weaning
4.7 Selenosls (effects
on the nervous system,
Including convulsions
and paralysis)
MHchener, 1971b
42.6 10 Yang et al.,
1983
NA = Not applicable
CO
10
-------
The CS reported In U.S. EPA (1983) differs slightly from the CS derived 1n
Table 9-2 because different assumptions were used to estimate dosage from
the 3 ppm drinking water concentration. U.S. EPA (1983) calculated the dose
assuming mice drink water equivalent to 17X of their body weight/day,
resulting In a dose of 0.51 mg/kg/day, while the CS derived above was
calculated assuming a 0.03 kg mouse drinks 0.0057 l water/day (U.S. EPA,
1986c), resulting In a dose of 0.57 mg/kg/day.
The CSs computed for mortality 1n rats (FHzhugh et al., 1944), mortal-
ity In offspring of mice (Schroeder and HHchener, 1971b) and severe nervous
effects 1n humans (Yang et al., 1983) range from 42.3-48, and all correspond
to an RQ of 10. The CS of 42.3 and RQ: of 10.computed for the Yang et al.
(1983) study 1s chosen over either of the slightly higher CSs calculated
from the animal data because the uncertainty associated with extrapolation
from animals to humans 1s eliminated. This CS and RQ are presented 1n Table
9-3.
9.2. BASED ON CARCINOGENICITY
Oral studies of the carclnogenlcHy of selenium compounds In animals
have not been conclusive. Nelson et al. (1943) found Increased tumor
Incidences In rats treated with selenlferous corn or wheat. This study Is
limited because the basal diet was suboptlmal 1n protein. Positive results
were also reported In male and female rats and female mice treated by gavage
with sodium selenlde (NCI/NTP, 1980a). This study Is limited because the
compound under study was not defined clearly. Schroeder and MHchener
(1971a) reported a significant Increase 1n the Incidences of tumors 1n rats
treated with selenate 1n the drinking water at 2-3 ppm Se. An evaluation of
these data 1s not possible because not all autopsled rats were examined
hlstologlcally and treated rats lived longer than controls (IARC, 1975).
0149d 9-6 06/15/89
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TABLE 9-3
Selenium and Compounds
Minimum Effective Dose (MED) and Reportable Quantity (RQ)
Route: oral
Dose*: 3.2 mg Se/day
Effect: severe nervous symptoms: convulsions, paralysis
RVd: 4.7
RVe: 9
Composite Score: 42.6
RQ: 10
Reference: Yang et al., 1983
*Equ1valent human dose
0149d 9-7 06/15/89
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Harr et al. (1967) and Tlnsley et al. (1967) did not find a carcinogenic
effect In male and female Wlstar rats provided with sodium selenlte or
sodium selenate 1n the diet at 0.5-16 yg Se/g diet throughout their life-
times. Negative results were also reported In mice treated with selenate or
selenlte at 3 ppm (Schroeder and Kitchener, 1972).
Determining the carcinogenic potential of selenium 1s further compli-
cated by the essentiality of selenium and numerous studies reporting anti-
carcinogenic activity. Human epidemiology studies also tend to show an
Inverse relationship between blood selenium levels and cancer. Based on the
lack of human cardnogenldty data and Inadequate animal evidence, selenium
can be considered, according to EPA classification scheme, as Group 0
substance - not classifiable as to human cardnogenlclty. Substances with
an EPA Group D classification are not given a hazard ranking; therefore, an
RQ based on cardnogenlclty cannot be assigned. Evaluation of the NCI/NTP
(1980a) study failed to demonstrate the association of a chemical species of
selenium with cardnogenlclty. Therefore, 1t Is Inappropriate to estimate
an RQ based on cardnogenldty of selenium sulflde. However, because of the
evidence of cardnogenldty In both rats and female mice 1n this study,
selenium sulflde may be classified as a Group D substance based on the U.S.
EPA (1986b) classification scheme.
0149d 9-8 09/21/89
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0150d 10-2 04/03/89
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Beath, O.A. 1962. The story of selenium In Wyoming. University of
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and Se 1n earthworms and soil from diverse sites. Environ. Monlt. Assess.
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0150d 10-21 04/03/89
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0150d 10-22 04/03/89
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0150d 10-23 04/03/89
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0150d 10-24 04/03/89
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0150d 10-25 04/03/89
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0150d 10-26 04/03/89
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0150d 10-27 04/03/89
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0150d 10-28 04/03/89
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Woock, S.E. and P.B. Summers, Jr. 1984. Selenium monitoring 1n Hyco
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abllHy with reference to human nutrition. Am. J. CUn. Nutr. 35(5):
1076-1088.
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and soils. Sd. Total Environ. 32: 197-202.
0150d 10-29 04/03/89
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APPENDIX A
LITERATURE SEARCHED
This HEED 1s based on data Identified by computerized literature
searches of the following:
CHEMLINE
TSCATS
CASR online (U.S. EPA Chemical Activities Status Report)
TOXLINE
TOXLIT
TOXLIT 65
RTECS
OHM TADS
STORET
SRC Environmental Fate Data Bases
SANSS
AQUIRE
TSCAPP
NTIS
Federal Register
CAS ONLINE (Chemistry and Aquatic)
HSDB
SCISEARCH
Federal Research 1n Progress
These searches were conducted In May, 1988, and the following secondary
sources were reviewed:
ACGIH (American Conference of Governmental Industrial Hyglenlsts).
1986. Documentation of the Threshold Limit Values and Biological
Exposure Indices, 5th ed. Cincinnati, OH.
ACGIH (American Conference of Governmental Industrial Hyglenlsts).
1987. TLVs: Threshold Limit Values for Chemical Substances 1n the
Work Environment adopted by ACGIH with Intended Changes for
1987-1988. Cincinnati, OH. 114 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2A. John Wiley and
Sons, NY. 2878 p.
Clayton, G.D. and F.E. Clayton, Ed. 1981. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2B. John Wiley and
Sons, NY. p. 2879-3816.
0151d A-l 04/03/89
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Clayton, G.D. and F.E. Clayton, Ed. 1982. Patty's Industrial
Hygiene and Toxicology, 3rd rev. ed., Vol. 2C. John Wiley and
Sons, NY. p. 3817-5112.
Grayson, M. and D. Eckroth, Ed. 1978-1984. Klrk-Othmer Encyclo-
pedia of Chemical Technology, 3rd ed. John Wiley and Sons, NY. 23
Volumes.
Hamilton, A. and H.L. Hardy. 1974. Industrial Toxicology, 3rd ed.
Publishing Sciences Group, Inc., Littleton, MA. 575 p.
IARC (International Agency for Research on Cancer). IARC Mono-
graphs on the Evaluation of Carcinogenic Risk of Chemicals to
Humans. IARC, WHO, Lyons, France.
Jaber, H.M., W.R. Mabey, A.T. L1eu, T.W. Chou and H.L. Johnson.
1984. Data acquisition for environmental transport and fate
screening for compounds of Interest to the Office of Solid Waste.
EPA 600/6-84-010. NTIS PB84-243906. SRI International, Menlo
Park, CA.
NTP (National Toxicology Program). 1987. Toxicology Research and
Testing Program. Chemicals on Standard Protocol. Management
Status.
Ouellette, R.P. and J.A. King. 1977. Chemical Week Pesticide
Register. McGraw-Hill Book Co., NY.
Sax, I.N. 1984. Dangerous Properties of Industrial Materials, 6th
ed. Van Nostrand Relnhold Co., NY.
SRI (Stanford Research Institute). 1987. Directory of Chemical
Producers. Menlo Park, CA.
U.S. EPA. 1986. Report on Status Report 1n the Special Review
Program, Registration Standards Program and the Data Call In
Programs. Registration Standards and the Data Call 1n Programs.
Office of Pesticide Programs, Washington, DC.
USITC (U.S. International Trade Commission). 1986. Synthetic
Organic Chemicals. U.S. Production and Sales, 1985, USITC Publ.
1892, Washington, DC.
Verschueren, K. 1983. Handbook of Environmental Data on Organic
Chemicals, 2nd ed. Van Nostrand Relnhold Co., NY.
Wlndholz, M., Ed. 1983. The Merck Index, 10th ed. Merck and Co.,
Inc., Rahway, NJ.
Worthing, C.R. and S.B. Walker, Ed. 1983. The Pesticide Manual.
British Crop Protection Council. 695 p.
0151d A-2 04/03/89
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In addition, approximately 30 compendia of aquatic toxUUy data were
reviewed, Including the following:
Battelle's Columbus Laboratories. 1971. Water Quality Criteria
Data Book. Volume 3. Effects of Chemicals on Aquatic Life.
Selected Data from the Literature through 1968. Prepared for the
U.S. EPA under Contract No. 68-01-0007. Washington, DC.
Johnson, W.W. and M.T. Flnley. 1980. Handbook of Acute Toxldty
of Chemicals to F1sh and Aquatic Invertebrates. Summaries of
Toxldty Tests Conducted at Columbia National Fisheries Research
Laboratory. 1965-1978. U.S. Dept. Interior, Fish and Wildlife
Serv. Res. Publ. 137, Washington, DC.
McKee, J.E. and H.W. Wolf. 1963. Water Quality Criteria, 2nd ed.
Prepared for the Resources Agency of California, State Water
Quality Control Board. Publ. No. 3-A.
Plmental, D. 1971. Ecological Effects of -Pesticides on Non-Target
Species. Prepared for the U.S. EPA, Washington, DC. PB-269605.
Schneider, B.A. 1979. Toxicology Handbook. Mammalian and Aquatic
Data. Book 1: Toxicology Data. Office of Pesticide Programs, U.S.
EPA, Washington, DC. EPA 540/9-79-003. NTIS PB 80-196876.
0151d A-3 04/03/89
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APPENDIX B
Summary Table for Selenium and Compounds
oo
CT>
00
Species
Inhalation Exposure
Subchronlc ID
Chronic ID
Carc1nogen1c1ty ID
Oral Exposure
Subchronlc human
Chronic human
Carc1nogen1c1ty ID
REPORTABLE QUANTITIES
Based on Chronic Toxlclty:
Based on Carc1nogen1c1ty:
Exposure Effect RfD or qi* Reference
ID ID ID NA
ID ID ID NA
ID ID ID NA
3.2 mg/day selenosls 0.21 mg/day Yang et al., 1983
3.2 mg/day selenosls 0.21 mg/day Yang et al., 1983
ID ID ID NA
10 Yang et al., 1983
ID
ID = Insufficient Data
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