ENVIRONMENTAL CONTAMINANTS ENCYCLOPEDIA

SELENIUM ENTRY

July 1, 1997

COMPILERS/EDITORS: 

ROY J. IRWIN, NATIONAL PARK SERVICE

WITH ASSISTANCE FROM COLORADO STATE UNIVERSITY

STUDENT ASSISTANT CONTAMINANTS SPECIALISTS:

MARK VAN MOUWERIK

LYNETTE STEVENS

MARION DUBLER SEESE

WENDY BASHAM

NATIONAL PARK SERVICE 

WATER RESOURCES DIVISIONS, WATER OPERATIONS BRANCH

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HOW TO CITE THIS DOCUMENT: As mentioned above, for

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applications, this document may be cited as:

Irwin, R.J., M. VanMouwerik, L. Stevens, M.D.

Seese, and W. Basham. 1997. Environmental

Contaminants Encyclopedia. National Park Service,

Water Resources Division, Fort Collins, Colorado.

Distributed within the Federal Government as an

Electronic Document (Projected public availability
on the internet or NTIS: 1998).
Selenium (Se, CAS number 7782-49-2)

NOTE: This entry contains information on both elemental

selenium and selenium compounds.

Brief Introduction:

Br.Class: General Introduction and Classification Information:

Selenium is a naturally occurring, solid substance [953].

It is widely, but unevenly, distributed in the earth's

crust. It is commonly found in rocks and soil.

Selenium, in its pure form of metallic gray to black

hexagonal crystals, is often referred to as elemental

selenium or selenium dust. However, in the environment,

selenium is not often found in its pure form. It is

usually combined in rocks with other substances, such as

sulfide minerals, silver, copper, lead, and nickel

minerals [953].

Selenium chemistry is complex, as selenium can be in

several oxidation states. The most important oxidation

states are + 4 and + 6 [291]. The chemical reactions of

selenium resemble those of sulfur and are typically

nonmetallic in nature [291]. Selenium is a nonmetallic element [190,492] which has

tended to be a bigger environmental problem for fish and

wildlife in the Western United States, where selenium is

more abundant and more bioavailable (mostly due to

natural geological circumstances), than in the eastern

United States [463]. Exceptions in the Eastern U.S. tend

to be circumstances where there is highly contaminated

runoff from coal-fired power plant ash piles or other

unusual scenarios. 

NOTE: Other references refer to selenium as

"metallic" [953,672,697,940] or "semimetallic"

[445]).

Selenium is an essential nutrient for humans and animals,

and both can use inorganic as well as organic selenium

compounds [953]. In the body, selenium helps prevent

damage to tissues done by oxygen. Selenium, however,

harms people and animals when consumed in amounts not

much higher than those needed for good nutrition [953].

See the below Br.Haz section for a detailed discussion of

beneficial vs. detrimental effects of selenium.

Selenium is listed by the Environmental Protection Agency

as one of 129 priority pollutants [58]. Selenium is a

toxic pollutant designated pursuant to section 307(a)(1)
of the Clean Water Act and is subject to effluent

limitations [366, 40 CFR 401.15 (7/1/87)]. Selenium

received special attention in studies of subsurface

agricultural irrigation drainage waters of the San

Joaquin Valley of California because it was determined to

be a "substance of definite concern" [445].

Br.Haz: General Hazard/Toxicity Summary:

Selenium is one of the most fascinating and challenging

of all elements involved in poisoning of fish [488]. In

spite of its useful functions at very low concentrations,

selenium has many toxic impacts upon fish and wildlife at

high concentrations [37]. 

Plant and animal uptake and accumulation of selenium from

the environment is influenced by, among other factors:

the species of plant or animal; the concentrations and

chemical forms of selenium; the medium in which it/they

occur(s) (e.g., water and/or diet); the period of

exposure; and, in water, the chemical and other

characteristics of the water (e.g., dissolved oxygen

content, hardness, pH, redox state, salinity, and

temperature), including the presence of other chemicals

(e.g., sulfate or cadmium) [445]. Hardness is thought to

be an important co-factor related to toxicity and

bioavailability of many metals, but alkalinity is

sometimes a more important co-factor than is generally

realized (Pat Davies, Colorado Division of Wildlife,

personal communication, 1997).

A look at the detailed information presented below

reveals that selenium impacts have most often been

documented for birds, fish, and wildlife, while severe

impacts have rarely been documented for effects on

humans. As detailed further below, selenium in the

correct (low) doses and forms has many benefits to

humans, including its role as part of glutathione

peroxidase, an enzyme involved in cellular defense

against oxidative damage [893].

Although concentrations of trace amounts of the essential

element selenium is desirable, excess levels of selenium

are more poisonous than either arsenic or mercury [488].

Excess selenium, even as low as 3-8 ppb in the water) can

cause numerous life-threatening changes in feral fresh

water fish [488].

Assessment of risk of selenium toxicity to aquatic

organisms is complicated by the differential toxicity of

different selenium species and by biogeochemical

transformations of selenium species (see detailed

discussion in the Forms/Preparations/Formulations section
below under the subheading "Common Forms of Selenium")

[481].

Text in paragraph above reprinted with permission

from Environmental Toxicology and Chemistry, Volume

12, J.M. Besser, T.J. Canfield and T.W. La Point,

"Bioaccumulation of organic and inorganic selenium

in a laboratory food chain." Copyright 1993 SETAC].

The toxic potential and availability of selenium

compounds is related to chemical form, and most

importantly, solubility. Like sulfates, selenates (Se

+6) are relatively soluble and are readily taken up by

biologic systems [491]. By contrast, selenites (Se +4),

selenides (Se -2), and elemental selenium are relatively

insoluble. Selenides are so insoluble that in vivo

formation of mercury selenide by dietary administration

of selenite has been proposed as a method of

detoxification of methyl mercury [491].

Although not true in all cases, the relative toxicity of

various chemical forms of selenium is generally as

follows (from most to least toxic): hydrogen selenide ~

selenomethionine (in diet) > selenite ~ selenomethionine

(in water) > selenate > elemental selenium ~ metal

selenides ~ methylated selenium compounds [445]. 

Selenium is a striking example of a contaminant which is

predominantly (there are exceptions) referred to as a

potentially hazardous contaminant in the fish, wildlife,

and environmental toxicology literature but seems to be

given the benefit of the doubt as a beneficial element in

the human health literature [484,486]. Different species

do vary in sensitivity to individual contaminants, but

perhaps human health researchers should be looking more

closely at fish and wildlife literature and perhaps fish

and wildlife researchers should be looking more closely

at the human health literature. Is one group (human

health investigators) looking harder for positive effects

and the other group (wildlife investigators) looking

harder for negative effects? 

A few summarizations do treat the potential impacts and

benefits somewhat more evenly [487,488], but as of 1993,

most individual (specialized) research papers and reports

still seem to looking at selenium from either in a

somewhat negative or positive perspective. 

This contrast is partly explained by the fact that the

range between insufficient and too much selenium in the

diet of animals and humans is unusually narrow [445,488].

Thus, probably one of the most important reasons selenium

is treated as a totally positive element in so many

papers at the same time it is being treated as a totally
negative hazard in so many other papers has to do with

dose. Those looking at very low concentrations of

dietary selenium (this group seems to include most

researchers working on human health issues) are looking

for and finding benefits, while those looking at higher

concentrations of dietary selenium (this group includes

many researchers working on fish and wildlife issues) are

looking for and finding hazards. It is known that

different species of living things have different

sensitivities to selenium [445], but in the case of

selenium in humans versus selenium in fish and wildlife,

the difference may partly have to do dose and food chain

factors. Many of the most dramatic reports of selenium

poisoning have occurred in fish and wildlife resources in

ecosystems where elevated selenium levels are

biomagnified up through the food chain. 

Selenium nevertheless remains somewhat unusual and

interesting due to the sheer number of seemingly

contradictory literature references to selenium as a

contaminant which (depending on dose, form, and numerous

other details) can either help cause or help protect

against such things as liver damage, cancer, immune

system problems, and a host of other potential hazards.

Although Se is an essential micronutrient for various

immune mechanisms, an excess of Se may have a deleterious

effect on certain immunological functions. As these

activities are considered to be important defense

mechanisms against tumors and virus infections, a

nutritional imbalance of Se could result in an increased

risk of these disorders (Nair MP; Schwartz SA. 1990.

Immunoregulation of natural and lymphokine-activated

killer cells by selenium. Immunopharmacology; 1990 MayJun; 19(3); P 177-83, Author: Department of Pediatrics,

University of Michigan, Ann Arbor 48109-2029).

In the environmental toxicology literature, beneficial

aspects of selenium are most often mentioned as the

exception rather than the rule. Again, the reason for

this most likely has to do with dose and bioconcentration

through the food chain; documented problems related to

selenium are particularly common in higher food chain

levels in western areas which have elevated selenium

levels.

 

NOTE: One of the paradoxes of the widely publicized

selenium toxicity problems at Kesterson National

Wildlife Refuge was that selenium deficient soils

have been reported near Kesterson [486, (Biol.

Trace Element Res., Vol 20 (1-2), 1989]; at

Kesterson concentration of selenium from subsurface

agricultural drainage water, further concentrated

by evaporation, helped produce a buildup of
selenium. 

By contrast, if one looks through the human health

literature [484,486], one finds reference after reference

to the potential benefits of selenium. Selenium is

described [484,486] using such glowing phrases as: 

An anti-carcinogenic nutrient, a versatile

anticarcinogenic agent, an essential trace element

necessary for man, an element with numerous

protective functions, a redox switch which helps

prevent the malignant transformation of cells, an

inhibitor of the replication of tumor viruses, an

inhibitor of activation of oncogenes, possibly a

modification agent in carcinogen metabolism which

protects DNA against carcinogen-induced damage, an

anti-carcinogen which accepts biogenic methyl

groups, a detoxifying agent for certain metals and

xenobiotics, an immuno-potentiating agent, an agent

which can bind mercury and cadmium compounds to

make them more biologically inert, a part of the

anti-oxidative defence system, a protective agent

against mercury induced lipid peroxidation, a

defence against free radicals, an element

indispensable to appropriate immune response, an

element which can detoxify various metals by

chelating them, a risk factor for cancer in humans

which do not get enough of it, helpful in

preventing colon and breast cancer, and an element

which is possibly helpful in preventing skin,

liver, and pancreas cancer. 

In the human health literature the potentially harmful

aspects of selenium are most often treated as the

exception rather than the rule. Most of the documented

cases of selenium poisoning seem to be in response to

high selenium intake in certain areas of China [893]:

Yang, G., S. Wang, R. Zhou and S. Sun. 1983.

Endemic selenium intoxication of humans in China.

Am. J. Clin. Nutr. 37: 872-881. Yang, G., R.

Zhou, S. Yin, et al. 1989a. Studies of safe

maximal daily dietary selenium intake in a

seleniferous area in China. I. Selenium intake and

tissue levels of the inhabitants. J. Trace Elem.

Electrolytes Health Dis. 3(2): 77-87. Yang, G., S.

Yin, R. Zhou, et al. 1989b. Studies of safe

maximal daily dietary Se-intake in a seleniferous

area in China. II. Relation between Se-intake and

the manifestation of clinical signs and certain

biochemical alterations in blood and urine. J.

Trace Elem. Electrolytes Health Dis. 3(2): 123-

130. Although there is sometimes anecdotal

information given on harmful effects (like sodium
selenite causing deficits in mammalian limb

development if allowed to reach developing tissue),

there are more frequently just blanket statements

that selenium toxicity in humans is very rare in

the U.S. [484,486].

In a summary of beneficial aspects, Moore et al. [445]

stated that: 

Although it is yet to be proven that selenium is an

essential micronutrient for plants, it has been

shown to be essential for algae, bacteria, and fish

and other animals, including humans. Selenium

plays important biochemical and physiological roles

in animals, including: participating in protein

synthesis (e.g., of immunoglobulin and ubiquinone);

assisting in the mitochondrial transport of

electrons in muscles; facilitating an essential

metabolic union of oxygen and hydrogen; and in

enzymes containing selenium, such as glutathione

peroxidase, playing an important role in catalyzing

reactions that protect cell membranes from

oxidation damage, thereby complementing the

functions of vitamin E. Findings of human health

studies suggest that selenium may also play

important roles in preventing cardiovascular

diseases, arthritis, and certain types of cancer

(e.g., breast [female], colon, leukemia, liver,

lung [male], ovarian, prostrate, rectal, and skin

cancers) [445]. Signs of selenium deficiency in

animals include: loss of feathers or hair; reduced

growth; degeneration of the liver, pancreas, and

heart; myopathy (white muscle disease); periodontal

disorders; reproductive impairment; lameness;

steatitis; exudative diathesis; immunosuppression;

and gastroesophageal ulcers [445]. The difference

between essential and toxic doses of selenium is

quite narrow. Demayo et al. in 1979 estimated

there to be only a fifty-fold safety margin between

recommended and toxic dietary concentrations of

selenium for animals. Maier et al. (1987) suggest

that the safety margin for aquatic life may be

approximately 10-fold [445].

 

Humans require minute quantities of selenium to maintain

tissue elasticity and prevent premature aging, muscle

pain, and heart disease [173].

So, although excess selenium in certain forms can have

dramatic impacts of living things, selenium in certain

forms and small quantities often has benefits. Unlike

heavy metals such as cadmium, mercury, and lead, selenium

in small quantities in the diet of vertebrates and many

other living things does have redeeming qualities. 
Some contaminants specialists who have looked at some of

the human health and animal husbandry literature have

wondered whether or not slight elevations of some forms

of selenium in fish tissues may possibly be acting partly

in a protective manner (to a greater degree than is

commonly recognized) to humans and fish and wildlife

predators consuming fish contaminated with harmful

concentrations of heavy metals such as cadmium, mercury,

and lead (Jerry Miller, U.S. Bureau of Reclamation, Salt

Lake City, personal communication, 1994). However, care

should be taken in generalizing, and the many risks

associated with bioconcentration, reproductive risk, and

other potential risks of selenium cannot be ignored. See

also the Interactions section below for more details on

interactions between selenium and mercury.

The benefits, potential impacts, and food web fate of

selenium vary not only by the form of selenium involved,

but also by the type of organism. For example,

monogastric (non-ruminant) animals more readily absorb

dietary selenium+4 (selenite) than do ruminants [445]. 

The range between insufficient selenium in the diet of

animals and too much is narrow, and the effects of either

problem can be serious [63]. In humans, too much

selenium has also reportedly caused baldness, loss of

nails and teeth, fatigue, and death [173]. 

The toxicity to an animal of selenium exposure is

influenced by numerous factors, including: the species,

sex, lifestage, nutritional status, and health of the

organism; the chemical form(s) of selenium; previous

exposure history; environmental stresses, including

weather; and the presence of other, interactive chemicals

[445]. Selenium is more toxic to coho salmon that to

chinook salmon and more toxic to trout than to bluegills

[445]. Younger animals (especially fish fry and bird

embryos) and those consuming low-protein diets are very

sensitive to selenium's toxic effects [445]. Waterfowl

feeding on zooplankton or on algae may be more sensitive

to selenium contamination than those feeding on seeds

[222]. Mallards, cinnamon teal, and pintails, which

consume large amounts of seeds are therefore less at risk

than gadwalls and Norther shovelers, which consume

primarily algae and zooplankton [222]. Using the same

criteria, green winged teal and widgeon would be at

intermediate risk [222]. Chickens and Japanese quail are

more sensitive to selenium toxicity than are mallard

ducks, which are more sensitive than screech owls and

black-crowned night-herons [445]. 

A comprehensive toxicological profile for selenium and

its compounds, especially as it relates to human health,

is available from ATSDR [953]. Due to lack of time,
important highlights from this ATSDR document have not

yet been completely incorporated into this entry. A

synoptic review of selenium hazards to fish, wildlife,

and invertebrates was provided by Eisler in 1985 [37].

A more recent summary on selenium issues related to fish

was provided by Sorenson in 1991 [488]. However, a

tremendous amount of selenium research has been done

since then, partially as a result of the widely

publicized and dramatic impacts of high selenium levels

upon birds and other biota at Kesterson National Wildlife

Refuge in California. 

Br.Car: Brief Summary of Carcinogenicity/Cancer Information:

EPA 1996 IRIS database information [893]:

Evidence for classification as to human

carcinogenicity: weight-of-evidence classification

Classification: D; not classifiable as to

human carcinogenicity 

BASIS: Based on inadequate human data and

inadequate evidence of carcinogenicity in

animals. The evidence for various selenium

compounds in animal and mutagenicity studies

is conflicting and difficult to interpret;

however, evidence for selenium sulfide is

sufficient for a B2 (probable human

carcinogen) classification. 

Human carcinogenicity data: Inadequate. Data

on the potential carcinogenicity of selenium

and various selenium compounds in humans are

inadequate. 

Animal carcinogenicity data: Inadequate. The

carcinogenicity of selenium compounds has been

evaluated in several animal studies. However, the

data are conflicting and difficult to interpret

because of apparent anticarcinogenic activity and

high toxicity of some selenium salts.

Available data provide no suggestion that selenium is

carcinogenic in man, & evidence for neg correlation

between regional cancer death rates & selenium is not

convincing (IARC. Monographs on the Evaluation of the

Carcinogenic Risk of Chemicals to Man. Geneva: World

Health Organization, International Agency for Research on

Cancer, 1972-1985, Multivolume work.,p. V9 256, 1975)

[940].

There are many references in the literature to the
ability of selenium to inhibit carcinogenic processes.

For example, selenium has been shown to inhibit

carcinogenesis in several animal systems. Results show

that cadmium stimulates the growth of human prostatic

epithelium in vitro between 10(-9) M and 10(-7) M

concentrations. Selenium, at concentrations between 10(-

12) M and 10(-7) shows no growth stimulatory or

inhibitory effects on these cells. However, when present

at 10(-8) M level, selenium inhibits the growth

stimulation induced by cadmium (Webber MM; Biochem

Biophys Res Commun 127, 3: 871-7 (1985) [940]. Some of

the literature on inhibition of cancer by selenium is

summarized in IRIS [893]. See also: Br.Haz section above.

Although selenium can act as a protective anti-carcinogen

[484,486,488,491; see also Br.Haz above for details]

there are some references in the literature to selenium

as a potential carcinogen: 

Some salts of selenium are carcinogenic [168].

Selenium sulfide produced an increase in

hepatocellular carcinomas and adenomas [491].

Br.Dev: Brief Summary of Developmental, Reproductive,

Endocrine, and Genotoxicity Information:

Selenium is considered embryotoxic and teratogenic on the

basis of animal experiments [37,491]. 

Excess selenium has been documented to cause the

following problems [445]:

Excess selenium in plants can adversely affect seed

germination and growth. In animals, excess

selenium can cause: embryo malpositions and

deformities (teratogenesis), including

hydrocephaly, and malformed beak, eyes, face,

feet/hooves and toes, jaws, legs, nose and nasal

pits, spinal column, tail, and wings; abnormal

development of and damage to/degeneration of

internal organs, including the heart, liver, and

kidneys; edema; mutagenesis; reproductive

impairment, including reduced production, weight,

and hatchability of eggs; feed aversion,

emaciation, and reduced growth; skin lesions;

dullness, roughness, and loss of hair/feathers;

cracked, deformed, sore, and sloughed hoofs or

nails; stiffness and lameness (perhaps as a result

of joint erosion); respiratory failure; paralysis;

immune system suppression; a range of behavioral,

physiological, biochemical, and histopathological

changes; and death [445]. 
Effects of too much selenium in the diet of animals

include birth defects, sterility, and death [63]. 

There is no evidence from experimental animals

administered selenium compounds via the oral route or via

injection that selenium compounds are teratogenic in

mammals [953].

In human placenta in vitro studies, inorganic selenium

compounds reduce the toxicity of human placental

toxicants such as cadmium; however, neither the kinetics

nor the developmental toxicity of selenium is known for

humans [484,485]. 

Looking through the fish and wildlife literature, one

finds reference after reference to potential

environmental hazards of excess selenium (toxicity to

fish and wildlife, reproductive failures, birds and fish

born with birth defects, and all of the well-publicized

problems at Kesterson National Wildlife Refuge in

California, etc.). In fish, selenium tends to build up

in the ova [488]. This may relate to the fact that

selenium problems tend to be important in egg bearers

(Joe Hunn, NBS, Columbia, MO, personal communication,

1993).

Daily intraperitoneal injections of male rats with

selenium dioxide caused changes in the testes with

significant testicular degeneration and atrophy at the

highest dose tested [953]. On the other hand, selenium

deficiency has been reported to cause infertility in

livestock and decreased sperm production and motility in

selenium-deficient rats [953]. The relevance of these

reproductive effects in animals to potential reproductive

effects in humans is not known. In samples from more

than 200 men, no correlation between seminal plasma

selenium and sperm count or mobility was detected [953].

Selenium accumulates in the gonads of bass and bluegills

[36]. 

Impairment of reproduction (including development and

survival of embryos) is one of the most sensitive

indicators of selenium toxicity among birds (Heinz, Oct

1989; Heinz et al., 1989). Reproduction among fishes can

be significantly reduced or even eliminated with little

or no adult mortality (Lemly, 1986).

Inorganic selenium compounds have been observed to have

both genotoxic and antigenotoxic effects. The

antigenotoxic effects generally occur at lower selenium

exposure levels than the genotoxic effects [953].

In general, sodium selenite and sodium selenate have
produced mixed results in bacterial mutagenicity test

systems [953]. Results with mammalian cell systems are

mixed, although sodium selenite is more consistently

genotoxic in these systems [953]. At high

concentrations, sodium selenite induces unscheduled DNA

synthesis and chromosome aberrations in cultured human

fibroblasts [953].

Br.Fate: Brief Summary of Key Bioconcentration, Fate,

Transport, Persistence, Pathway, and Chemical/Physical

Information:

In the environment, selenium combines with oxygen to form

several substances. The most common are sodium selenite

and sodium selenate [953]. See the

Forms/Preparations/Formulations section below for more

details.

Preliminary data suggests the potential for

bioaccumulation or bioconcentration of selenium is

moderate for the following biota: mammals, birds, and

fish. It appears to be high to very high for higher

plants and low or limited for mollusks, crustacea, lower

animals, mosses, lichens, and algae [83].

Daphnids in aqueous selenium exposures may be

accumulating a portion of their selenium body burdens via

ingestion of selenium enriched algae [481].

The concentrations and chemical forms of selenium in

water are influenced by, among other factors, pH and

redox conditions. Although dissolved selenium in most

natural waters is dominated by the inorganic selenate and

selenite forms, substantial concentrations of selenium in

+6, +4, and -2 oxidation states can occur simultaneously

in natural aerobic surface waters of pH 6.5-9.0 [445]. 

Selenium concentrations in the soils, how tightly the

selenium is bound to soils, and man's activities (such as

irrigation practices and mining) can all play a role in

determining whether or not selenium becomes an

environmental problem in a given area. See also the

Bio.Detail section below for details on selenium

bioavailability and fate in soils.

As is the case for mercury, microorganisms in sediments

or sewage are capable of methylation or demethylation of

selenium [488]. Selenium is methylated and probably

demethylated in the environment and cycled through a

number of components of the food web, complicating

chemical determination of the chemical forms available to

fish [488]. Dimethylselenide is generated slowly from

raw sewage [488]. 
Selenium, like mercury, has many interactions with sulfur

compounds. This affinity for sulfur compounds may

account for some of the many synergistic and antagonistic

interactions between mercury and selenium (see the

Interactions section below for details). Also like

mercury, selenium chemistry, transformations, and

interactions with other contaminants are complex. In

fact, selenium is one of the most complex elements in

these regards. Due to these complexities,

generalizations about selenium should be approached with

caution.

Recent news media, human health, cattle and sheep

grazing, wildlife, rangeland, and geological

controversies about selenium were summarized by Tom

Harris in the February 10, 1992 issue of the High Country

News (Western U.S. paper published in Paonia, Colorado).

According to Harris, more research needs to be done to

better define: 1) the role of deep-rooted, seleniumtolerant plants such as Astragalus bisulcatus and woody

asters of the genus Xylorrhiza as "converter plants"

which draw relatively inert forms of selenium up from the

soil and metabolize them into water-soluble selenate--so

that when the converter plants die they deposit an

enriched halo of water soluble organic selenium compounds

that can be taken up by other plants and other biota (the

methylated daughter compounds are more bioavailable and

more potent than the parent compounds), 2) the role of

widespread trucking of cattle and hay in transporting

seeds of these "converter plants" into new areas, 3)

spreading selenium into new areas through applications of

phosphate fertilizers contaminated with selenium, 4) the

impact on hunters of consuming selenium contaminated

wildlife, including antelope, 5) the extent of selenium

contaminated meat (especially the liver, kidney and

heart) consumed by humans and wildlife.

Synonyms/Substance Identification:

Metallic Selenium [953]

CI 77805 [940]

ELEMENTAL SELENIUM [940]

SELEN (POLISH) [940]

SELENIUM (COLLOIDAL) [940]

SELENIUM ALLOY [940]

SELENIUM BASE [940]

SELENIUM DUST [940]

SELENIUM ELEMENTAL [940]

SELENIUM HOMOPOLYMER [940]

CASWELL NO. 732 [940]

EPA Pesticide Chemical Code 072001 [940]

Gray selenium [940] 
 Molecular Formula:

Se [940]

Associated Chemicals or Topics (Includes Transformation Products):

Relationships between this metal versus indicator plants,

other metals, and various rock types was summarized by Brooks

in 1972 [951]. Some of the same Astragalus plants which are

indicators for high selenium are also indicators for uranium

prospecting [951].

Certain uranium deposits contain appreciable quantities of

selenium [951]. Concentrations of vanadium in selenium rich

soils tends to be high [951]. Certain contaminants, such as

selenium, thorium 230, and vanadium, tend to occur together in

and leach out of uranium mining tailing piles in the U.S.;

thorium is quite dangerous and is often leached out of acid

process uranium piles (Ward Whicker, Colorado State

University, personal communication, 1996).

Site Assessment-Related Information Provided by Shineldecker

(Potential Site-Specific Contaminants that May be Associated

with a Property Based on Current or Historical Use of the

Property) [490]:

Other Associated Materials:

& Carbon disulfide

Metabolism/Metabolites [366]:

In the liver, many selenium compounds are biotransformed

to excretable metabolites. Identified metabolites are

trimethylselenide in urine and dimethylselenide in breath

(Friberg, L., Nordberg, G.F., Kessler, E. and Vouk, V.B.

(eds). Handbook of the Toxicology of Metals. 2nd ed.

Vols I, II.: Amsterdam: Elsevier Science Publishers

B.V., 1986.,p. V2).

Impurities [940]:

Commercial grade contains a min of 99% selenium & may

contain max 0.2% Tellurium, 0.1% Iron, 0.005% Lead &

0.005% Copper as impurities. The high purity grade ...

Is reported to contain a min of 99.99% Selenium.

Impurities which may be present @ concn no greater than

1-2 mg/kg each are mercury, tellurium, iron, arsenic &

other non-ferrous metals undesirable in electronic &

electrostatic applications. Higher concn of "inert"

contaminants such as sodium, magnesium, calcium, aluminum

& silicon can be tolerated. The ultra high purity grade,

prepared only on a laboratory scale, is reported to

contain 0.0001-0.001% Impurities. [IARC. Monographs on
the Evaluation of the Carcinogenic Risk of Chemicals to

Man. Geneva: World Health Organization, International

Agency for Research on Cancer,1972-PRESENT. (Multivolume

work).,p. V9 246 (1975)].

Water Data Interpretation, Concentrations and Toxicity (All Water

Data Subsections Start with "W."):

W.Low (Water Concentrations Considered Low):

No information found.

W.High (Water Concentrations Considered High):

Selenium concentrations in waters of the San Luis Drain

and Kesterson Reservoir were 170-420 ug/l (ppb) and 24-

430 ug/l, respectively [445].

W.Typical (Water Concentrations Considered Typical):

Typical Ocean Concentrations: EPA 1981: 0.00009 mg/l

[83]. 

Selenium concentrations in the world's oceans range from

0.000052 to 0.00013 mg/l (0.052 to 0.13 ppb) and average

0.09 ug/l (ppb) [445].

Typical Freshwater Concentrations:

EPA 1981: 0.02 mg/l [83]. 

1971: The average stream concentration was 0.2

ug/L and concentrations rarely exceed 1.0 ug/L

[190].

USGS 1974-1981: the 50th percentile of 161 (not

especially clean) NASQWAN and NWQSS river sites in

the U.S. was <1 ug/l; the 25th percentile was <1

ug/l, and the 75th percentile was 1 ug/l, with

concentrations trending downward more often than

upward [219]. These riverine sites in the USGS

study were mostly in (or downstream of)

agricultural and urban areas [219].

Concentrations of selenium in freshwater rivers

around the world range from <0.0001 to 0.4 mg/l

(<0.1 to 400 ppb) and average 0.2 ppb [445].

California, 1986: Ambient background level for

water was 0.2 ug/l [222].

W.Concern Levels, Water Quality Criteria, LC50 Values, Water

Quality Standards, Screening Levels, Dose/Response Data, and
Other Water Benchmarks:

W.General (General Water Quality Standards, Criteria, and

Benchmarks Related to Protection of Aquatic Biota in

General; Includes Water Concentrations Versus Mixed or

General Aquatic Biota):

Notes on total vs. acid soluble vs. dissolved

metals:

Although most of the lab tests done to develop

water quality criteria and other benchmarks

were originally based on "total" values rather

than "dissolved" values, and many original

criteria for selenium were specifically for

"total recoverable selenium [38], some

regulatory authorities nevertheless recommend

comparing criteria with dissolved or acid

soluble metals concentrations. For detailed

discussion, see the Laboratory and/or Field

Analyses section (far below).

EPA 1996 Great Lakes Guidance:

On November 14, 1996, EPA proposed in the

Federal Register that the acute toxicities of

selenate, selenite, and one form of

organoselenium are additive. They further

proposed that all forms be added together to

obtain a total for comparison with water

quality criteria and that total selenium can

be converted to dissolved by multiplying total

by 0.996. Further details: EPA suggested in

November of 1996 (Federal Register Vol 61, no.

221,pages 5844 to 58449) that:

1) A new acute aquatic life criterion be

used in the Great Lakes based on an

equation of the presence of selenium 4

(selenite) vs selenium 6 (selenate) vs

other forms; 

2) the acute toxicity of selenite

(Selenium IV) is 12.83 ug/L and that of

selenate (Selenium VI) is 185.9 ug/L. 

3) all forms of selenium tend to convert

back and forth into the other, and the

effects are basically additive.

4) Criterion Maximum Concentrations are

in total selenium, but the following

conversions may be used: A factor to
0.996 may be used to convert to convert

total (recoverable) acute criteria for

selenite to a dissolved criteria for

selenite.

Note: Another conversion factor

which is sometimes given: Selenium

(+4) conversion for acute and

chronic criteria: 0.922 (for

example, total recoverable selenium

(+4) criteria x 0.922 = dissolved

selenium (+4) criteria) [672]. 

The conversion factors recommended

by EPA for converting total

recoverable selenium to dissolved

concentrations in the January 1997

draft EPA Guidelines for 5 year

305(B) assessments was also 0.922.

Note: None of these generic

conversion factors are

universal. Both total and

dissolved concentrations should

be checked at new locations

before relying on generic

conversion factors (Pat Davies,

Colorado Division of Wildlife,

personal communication, 1997).

5) Depending on the relative proportions

of various selenium species, the acute

criterion for the Great Lakes is between

13 to 186 ug/L.

EPA 1996 IRIS Database [893]:

Ambient Water Quality Criteria for Aquatic

Organisms for Total Selenium [446,689,893]:

Acute Freshwater: 2E+1 ug/l 1-hour avg.

Chronic Freshwater: 5E+0 4-hour avg.

Marine Acute: 3.0E+2 ug/L 1-hour avg.

Marine Chronic: 7.1E+1 ug/L 4-hour avg. 

Contact: Criteria and Standards

Division / OWRS / (202)260-1315 

Discussion: Criterion were derived

from a minimum database consisting

of acute tests on a variety of

species. Requirements and methods
are covered in the reference to the

Federal Register. The agency

recommends an exceedance frequency

of no more than 3 years. 

Note: Before citing a concentration as

EPA's water quality criteria, it is

prudent to make sure you have the latest

one. Work on the replacement for the

Gold Book [302] was underway in March of

1996, and IRIS is updated monthly [893].

Oak Ridge National Lab, 1994: Ecological Risk

Assessment Freshwater Screening Benchmarks for

concentrations of contaminants in water [649]. To

be considered unlikely to represent an ecological

risk, field concentrations should be below all of

the following benchmarks [649]:

For selenium (CAS 7782-49-2, ug/L):

NATIONAL AMBIENT WATER QUALITY CRITERION

- ACUTE: 260

NATIONAL AMBIENT WATER QUALITY CRITERION

- CHRONIC: 35

SECONDARY ACUTE VALUE: No information

found.

SECONDARY CHRONIC VALUE: No information

found.

LOWEST CHRONIC VALUE - FISH: 88.32

LOWEST CHRONIC VALUE - DAPHNIDS: 91.65

LOWEST CHRONIC VALUE - NON-DAPHNID

INVERTEBRATES: No information found.

LOWEST CHRONIC VALUE - AQUATIC PLANTS:

100

LOWEST TEST EC20 - FISH: 40

LOWEST TEST EC20 - DAPHNIDS: 25

SENSITIVE SPECIES TEST EC20: 2.60

POPULATION EC2O: No information found.

Other Concern Levels for Water Concentrations:

EPA 1987: EPA freshwater criteria suggests
that selenium concentrations for a four-day

average should not exceed 5.0 ug/L, nor a onehour average above 20.0 ug/L (Dennis Lemly,

Fish and Wildlife Service, National Fisheries

Contaminant Research Center, personal

communication, 1991). 

A State of California recommendation based on

direct toxicity was that the 2.6 ug/L;

however, the water quality criteria based on

protection of human health was lower, 0.8 ug/L

for impounded waters (versus 10 ug/L for

flowing waters), due to bioconcentration

concerns [222]. The water quality criteria

based on protection of aquatic organisms in

the food chain was also quite low, only 0.9

ug/L for impounded waters (versus 11 ug/L for

flowing waters), due to bioconcentration

concerns [222].

Joseph Skorupa (Fish and Wildlife Service) has

suggested that selenium from agricultural

irrigation return waters may contribute to

problems in various areas throughout the

Western United States, and that the long-term

safety of aquatic systems containing 2 to 5

ppb of total waterborne selenium can be

questioned [463].

A June, 1992, Federal Register discussion of

issues related to selenium supplements in

animal feed included the following items of

interest on selenium toxicity in water [463]:

Dennis Lemly (Fish and Wildlife Service)

commented that although the forms of

selenium excreted by animals may not be

bioavailable to terrestrial ecosystems,

they may be bioavailable in aquatic

ecosystems. He suggested that certain

areas of the United States, where soil

selenium levels are relatively high and

bioavailable, are incapable of sustaining

even small increases of selenium in the

aqueous environment. Joseph Skorupa

(Fish and Wildlife Service) suggested

that selenium from agricultural

irrigation return waters may contribute

to problems in various areas throughout

the Western United States, and that the

long-term safety of aquatic systems

containing 2 to 5 ppb of total waterborne

selenium can be questioned. Marc

Sylvester (Geological Survey) suggested
that selenium in manure spread on farm

land in semiarid and arid areas in the

Western United States would most likely

be oxidized to the selenate form, which

is very mobile. Therefore, he indicated

that the assumption used in the worstcase analysis that a maximum of 10

percent of the selenium in waste-amended

soil will be lost to runoff is

unreasonable [463].

CVM met with the scientists from the

Department of Interior on May 31, 1990,

to discuss their concerns. These

scientists stated that research in

progress indicates that the specific form

of selenium is critical in determining

the potential for the occurrence of

selenium toxicity because amino forms of

selenium may bioconcentrate to toxic

levels in fish and birds even when

concentrations in water are less than 1

microgram per liter (ppb). For this

reason, according to the scientists,

information, as opposed to the

assumptions used in the worst-case

analysis, is needed on the specific forms

of selenium entering the environment

through animal waste and the fate of

these forms [463].

More recently, CVM learned that the

Environmental Protection Agency (EPA) is

developing a threshold value for

dissolved waterborne selenium to protect

wildlife using aquatic environments

because it appears that the current

ambient water quality criteria for

selenium of 5 ppb established for aquatic

species may not be adequate to protect

wildlife [463].

Information from Moore [445]:

See Moore for details on citations: In a

review of selenium cycling in aquatic

ecosystems, Lemly and Smith (1987) stated

that, "...selenium at concentrations greater

than 2 to 5 ug/L (ppb) in water can be

bioconcentrated in food chains and cause

toxicity and reproductive failure in fish."

Using his energy-based selenium

bioaccumulation model for aquatic birds,

DuBowy (1989) determined that the water
quality criterion for selenium would need to

be less than 2.8 ppb to protect waterfowl

reproduction. A University of California

Committee of Consultants formed to evaluate

the water quality objectives for the San

Joaquin River Basin originally proposed by the

CSWRCB (CSWRCB, Aug 1987), recommended a

criterion range between 1 and 1.5 ppb

waterborne selenium as a "...highly

conservative estimate of no adverse

effect...[which]...may account for the

possible deleterious effect of

bioaccumulation" (UC Committee of Consultants

on San Joaquin River Water Quality Objectives,

Feb 1988). This last range of concentrations

is the same as that recommended by scientists

from the University of California, Davis,

using data from their selenium toxicity

research and other scientific literature.

They stated that a "...conservative water

quality goal for the protection of aquatic

organisms, a level where no adverse effects

should occur, appears to be between 1.0 and

1.5 ppb" (Davis et al., Jan-Feb 1988).

Finally, taking bioaccumulation into effect,

the CSWRCB determined that a waterborne

concentration of 0.9 ug/l (ppb) selenium would

be necessary to ensure no adverse effects on

aquatic life (CSWRCB, Mar 1988).

The CCVRWQCB has adopted (CCVRWQCB, Dec 1988)

and CSWRCB subsequently approved (CSWRCB, Sep

1989) chronic water quality objectives for

selenium of 2-10 ug/l (ppb) (monthly means)

for wetlands in the Grasslands area, the San

Joaquin River, and Salt and Mud (North)

sloughs. The USEPA recently disapproved

several of the CCVRWQCB's drainage-related

water quality objectives, including some of

the selenium objectives. The USEPA stated

that the objectives did not satisfy Federal

legal requirements because they did not

protect designated water uses and they were

based, in part, on consideration of economic

factors (McGovern, Apr 1990).

In 1986, the U.S. Fish and Wildlife Service

evaluated the findings of toxicity research,

accounted for known biomagnification through

the food chain and associated reproductive

toxicity, and recommended the following total

recoverable selenium concentrations as target

safe levels (MATC's) for cleanup of Kesterson

Reservoir and the San Luis Drain: (1) water -
2 ppb, (2) sediment - 4 ppm dry weight, (3)

food for warmwater fishes - 5 ppm dry weight,

and (4) food for waterfowl - 3 ppm dry weight.

They also noted, that in order to protect fish

reproduction, their skeletal muscles should

not contain more than 5 ppm and their organs

(liver and gonads) should not contain more

than 10 ppm selenium (both concentrations are

for total selenium, dry weight) (Wallenstrom,

Aug 1986). Hamilton et al. (1990) suggest

that, in order to be safe for fish, dietary

concentrations of selenium should be less than

3 ug/g (ppm, dry weight).

Skorupa et al. (Mar 1989) evaluated data

developed in both laboratory and field studies

and estimated that the maximum acceptable

toxicant concentration of dietary selenium for

aquatic birds was 5.6 ppm, dry weight.

Recently, in an attempt to reduce wildlife

contamination hazards, the California

Department of Fish and Game adopted a selenium

standard for subsurface agricultural drainage

water evaporation ponds in the San Joaquin

Valley. The CDFG standard requires initiation

of special management actions (e.g., hazing)

when the selenium concentration in a composite

sample of aquatic invertebrates from a pond

equals or exceeds 4 ppm, dry weight. Other

than CDFG's evaporation pond-specific

standard, no regulatory standards currently

exist for the protection of fish and wildlife

from dietary exposure to selenium."

W.Plants (Water Concentrations vs. Plants):

Shallow Groundwater Ecological Risk Assessment

Screening Benchmark for Terrestrial Plants Listed

by Oak Ridge National Lab, 1994 [651]:

NOTE: To be considered unlikely to represent

an ecological risk, field concentrations in

shallow groundwater or porewater should be

below the following benchmark for any aqueous

solution in contact with terrestrial plants.

Toxicity of groundwater to plants may be

affected by many variables (pH, Eh, cation

exchange capacity, moisture content, organic

content of soil, clay content of soil,

differing sensitivities of various plants, and

various other factors). Thus, the following

solution benchmark is a rough screening

benchmark only, and site specific tests would
be necessary to develop a more rigorous

benchmark for various combinations of specific

soils and plant species [651]:

For CAS 7782-49-2, SELENIUM, the

benchmark is 0.7 mg/L (groundwater or

porewater).

Algal dry weight and chlorophyll-a concentrations

were both reduced in the test waters containing >75

ppb selenium+4. Algal cell replication was reduced

in the 100 ppb selenium+4 test waters and ceased in

the >125 ppb selenium+4 test waters. Algal

selenium depuration mechanisms were overwhelmed in

waters with >100 ppb selenium+4. After 10 days, no

significantly different effects on growth,

reproduction, or survival were observed among

daphnia fed high-, mixed-, or low-selenium diets.

The authors suggested that the algal selenium fed

to the daphnia might have been in a methylated

form, thereby explaining the unexpected results of

the daphnia toxicity experiment [445].

W.Invertebrates (Water Concentrations vs. Invertebrates):

LC50s for Brachionus calyciflorus and B. plicatilis

(both rotifers) were 16.0 and 17.0 mg/L (ppm),

respectively, for 24-hr exposures [998].

LC50s for Daphnia magna (water flea) were 0.66,

0.71, 0.43 and 0.43 mg/L for 24-, 48-, 96-hr and

14-day exposures, respectively [998].

LC50 for Mysidopsis bahia (Opossum shrimp) was

0.600 mg/L for a 96-hr exposure [998].

Daphnia mortality was concentration-related in the

waterborne selenium+6 experiments. Animals exposed

to 1.0 mg/l (1,000 ppb) water experienced 100%

mortality. Daphnia exposed to waterborne

selenium+6, but fed selenium-laden diets,

experienced decreased mortality, except in the 1.0

mg/l (1,000 ppb) water. The effects on growth rate

and production of young were similar. With the

exception of animals in the 1.0 mg/l (1,000 ppb)

water, daphnia receiving selenium-laden algae had a

higher growth rate and produced more offspring than

those fed the control diet. Radiotracer

experiments revealed that uptake of waterborne

selenate and depuration of selenate were reduced in

the presence of selenium in the diet and waterborne

seleno-DL-methionine. Results with waterborne

seleno-L-methionine were unclear [445]. 
The USFWS-NFCRC (Dec 1988) determined the 48-hour

LC50's for the cladoceran Daphnia magna and midge

Chironomus riparius (animals <1-day-old) exposed to

waterborne selenium. Two general test waters,

reconstituted freshwater (containing hardness of

134 mg/L [ppm] as calcium carbonate [CaCO3],

alkalinity of 60-65 mg/L as calcium carbonate, and

72 mg/L sulfate) or standard ASTM soft water

(containing hardness of 40-48 mg/L as calcium

carbonate, alkalinity of 30-35 mg/L as calcium

carbonate, and 54 mg/L sulfate); were supplemented

with selenium+6 (as sodium selenate), selenium+4

(as sodium selenite), a 6:1 mixture of sodium

selenate and sodium selenite, or seleno-Lmethionine. Mortality for these tests was defined

as cessation of mobility [445].

The daphnids did not respond to seleno-Lmethionine in a dose-responsive manner;

therefore, an LC50 could not be calculated.

LC50's for midge exposed to seleno-Lmethionine were 5.78 mg/L in hard freshwater

and 6.88 mg/L in ASTM soft water. Forty

eight-hour LC50's (in mg/L) for the daphnids

and midge, respectively, exposed to inorganic

selenium were as follows: 4.07 and 16.2 for

sodium selenate in hard freshwater and 2.56

and 10.5 in ASTM soft water; 3.02 and 7.95 for

sodium selenite in hard freshwater and 0.700

and 14.6 in ASTM soft water; and 2.62 and 9.34

for the 6:1 selenate:selenite mixture in hard

freshwater and 1.79 and 14.3 in ASTM soft

water [445].

The USFWS-NFCRC (Dec 1988; Dec 1987) also determined the

effects of chronic exposures to a 6:1 mixture of sodium

selenate:sodium selenite in reconstituted, hard

freshwater (same water chemistry as in acute tests) on

growth, reproduction, and survival of the same species

and age of daphnia and midge used in the acute tests.

Daphnia were exposed for 21 days to the following nominal

concentrations of waterborne selenium (in ug/L [ppb]): 4

(control), 85, 156, 348, 718, or 1,410. Midge were

exposed for 30 days to the following nominal

concentrations of waterborne selenium (in ug/L): 10

(control), 303, 837, 1,384, 2,953, or 6,050 [445].

Results:

In the daphnid study, percent survival was

significantly reduced at 1,410 ug/L. Both 348 and

718 ug/L caused significant reductions in total

young produced, young produced per surviving adult

reproductive day, intrinsic rate of natural

increase, and adult weight. Exposure to 156 ug/L
caused a significant reduction in adult daphnid

weight, but significantly increased length of

newborn daphnia. Exposure to 85 ug/L also

significantly increased length of newborn daphnia

[445].

In the midge study, percent emergence was

significantly reduced only at 6,050 ug/L.

Emergence time and day of first emergence both

increased significantly at all concentrations

greater than or equal to 837 ug/L. The authors

calculated the no observable effect concentrations

for daphnia and midge (for the 6:1

selenate:selenite mixture) to be 85 and 303 ug/L,

respectively [445].

W.Fish (Water Concentrations vs. Fish):

Excess selenium, even as low as 3-8 ppb (0.003-

0.008 ppm) in the water, can cause numerous lifethreatening changes in feral fresh water fish

[488].

The Environmental Protection Agency (EPA) 1987

update of the ambient water quality document for

selenium [update of reference 38] gives acute (96

hour LC50) values for teleost fish as typically

ranging from 620 to 66000 ppb (0.620 to 66.0 ppm);

however, where biomagnification is allowed to

occur, toxic effects are seen at concentrations as

low as 12 ppb in the lab and 2.5 ppb in the field

(Heidi Bestgen, Colorado State University, personal

communication). Repeated studies have shown that

concentrations in water between 2 and 10 ppb can

result in reproductive failure and mortality in

fish (Will Clements, Colorado State University,

personal communication).

LC50s for Cyprinodon variegatus (sheepshead minnow)

were 56.0, 26.0, 13.0 and 6.7 mg/L (ppm) for 24-,

48-, 72- and 96-hr exposures, respectively. The

no-observed-effect-concentration (NOEC) for death

was 2.0 mg/L for a 96-hr exposure [998].

The no-observed-effect-concentrations (NOEC) for

death in Lepomis macrochirus (bluegill) ranged from

0.33 to 0.64 mg/L for a 60-day exposure [998].

LC50s for Oncorhynchus kisutch (Coho salmon, silver

salmon) ranged from 16.9 to 38.0 mg/L for 96-hr

exposures, with most values between 21 and 28 mg/L

[998].
LC50s for Oncorhynchus tshawytscha (Chinook salmon)

ranged from 46.6 to 96.8 mg/L for 96-hr exposures,

with values falling over this entire range [998].

LC50s for Pimephales promelas (fathead minnow) were

1.00 and 0.60 mg/L for 96-hr and 14-day exposures,

respectively [998].

Fish toxicity information from Moore [445]:

See Moore [445] for citation details:

Pyron and Beitinger (1989) studied the acute

effects of waterborne selenium on fathead

minnows (Pimephales promelas). Six-month-old

minnows were exposed to <1 (control), 20, 36,

or 66 mg/l (ppm) selenium+6 (as sodium

selenate) for 24 hours following which mating

behavior, reproductive success, and larval

survival were monitored. Fish were fed clean

brine shrimp (Artemia sp.) plus commercial

flake food diets and exposed to the selenium

in reconstituted hard water.

All minnows exposed to 66 ppm selenium+6

waters died within 24 hours of exposure.

Surviving fishes in the test and control

waters exhibited similar mating behaviors and

experienced normal reproduction and hatching

success. However, almost all larvae of fish in

the 20 and 36 ppm selenium+6 waters exhibited

"...gross morphological abnormalities, in

particular general edema..." At seven days

post hatching, all edamatous larvae had died.

Ogle and Knight (1989) studied the effects of

dietary selenium on growth and reproduction of

fathead minnows. Beginning at least 105 days

prior to egg laying, fish were fed a purified

control diet (0.4 ppm) or one of five purified

diets to which a mixture of inorganic and

organic selenium was added to achieve the

following final dietary concentrations: 5.2,

10.2, 15.2, 20.3, or 29.5 ppm (all

concentrations in total selenium, dry weight).

Proportions of the various selenium forms

added to the diet were 25% selenium+6 (as

sodium selenate), 50% selenium+4 (as sodium

selenite), and 25% selenium-2 (as seleno-Lmethionine). Larval progeny were fed newly

hatched brine shrimp (ad libitum) and

maintained for 14 days. Average water

chemistry in the test waters included hardness

of 139.4 mg/l (ppm, as calcium carbonate), pH
of 8.19, and 0.8 ug/l (ppb) total selenium.

None of the test diets significantly affected

minnow reproduction (including number of

spawns per pair, number of eggs per spawn,

percent hatch, or percent survival after 14-

days). However, beginning on day 56 and

thereafter, growth of adult minnows was

significantly reduced by the 20.3 and 29.5 ppm

mixed selenium diets. The authors suggested

that reduced growth may have been caused by a

reduction in feeding. The lack of effects on

fish reproduction was attributed to reduced

bioaccumulation of selenium, possibly as a

result of unusual morphology and physiology of

the gastrointestinal tract of fathead minnows

compared with some other fish species.

The effects of dietary and waterborne selenium

on bluegill sunfish (Lepomis macrochirus) were

studied by Woock et al. (1987). Adult

bluegills were exposed for 323 days (260 days

prior to initiation of spawning experiments)

to: control trout chow diets (with 8.0%

moisture); trout chow diets containing

selenium+4 (as sodium selenite, nominal

dietary concentrations were 13 or 30 ug/g

[ppm]); or trout chow diets containing

selenium-2 (as dl- selenomethionine, nominal

dietary concentrations were 3, 13, or 30 ug/g

[ppm]). In one additional test, fish were

exposed to both a selenomethionine diet of 13

ppm and water containing 10 ug/l (ppb)

selenium+4 (as sodium selenite). Controls

contained <1 ug/g (ppm) selenium in the diet

and <1 ug/l (ppb) selenium in water. Average

water chemistry in the test waters included:

hardness of 16 mg/l (ppm, as calcium

carbonate); pH of 6.5; 46 mg/l (ppm) dissolved

solids; and 5.2 mg/l (ppm) sulfate. Biological

endpoints measured included: weight, lens

cataracts, and mortalities of adults; and

hatching rate, survival, and teratogenesis

among larvae.

Mortalities of adults were significant in both

30 ppm diet groups. Dying fish exhibited:

food aversion; edema; lethargy; melanism;

tetany; and erratic, spiral, or circular

swimming. Fish in the 30 ppm selenium+4 diet

group were significantly shorter and lighter

than fish in other treatment groups. Thirty

seven percent of the fish in the 30 ppm

selenium-2 diet group developed true lens
cataracts. Neither fish in the control nor

any of the other treatment groups had

cataracts. 

Hatching success was unaffected by selenium

exposure. However, larvae borne to adults fed

30 ppm selenium+4, 30 ppm selenium-2, or 13

ppm selenium-2 in the 10 ppb selenium+4 water

experienced significant mortality and high

frequencies of teratogenesis (including edema,

lordosis, and lower jaw gape). Offspring of

parents fed the selenium-2 diets experienced

significantly greater effects than those of

parents fed the selenium+4 diets. The authors

also noted that their findings may

underestimate the toxic effects of selenium in

natural fish diets, because the diets in their

study contained high protein levels which

could have ameliorated selenium's adverse

effects.

The USFWS-NFCRC (Dec 1988) conducted three

sets of acute and chronic toxicity tests

exposing bluegill to various waterborne and/or

dietary concentrations of selenium. In the

first set of tests, bluegill were exposed for

96 hours in a generic, hard freshwater or ASTM

soft water to various concentrations of

selenium+6 (as sodium selenate), selenium+4

(as sodium selenite), a 6:1 mixture of sodium

selenate and sodium selenite, selenium-2 (as

seleno-L-methionine), or selenium-2 (as

seleno-DL- methionine). Water chemistry in

this set of tests included: 134 mg/L (ppm)

hardness as calcium carbonate, 60-65 mg/L

alkalinity as calcium carbonate, and pH of 8.1

in the generic, hard freshwater; and 40-48

mg/L hardness as calcium carbonate, 30-35 mg/L

alkalinity as calcium carbonate, and pH of

7.2-7.6 in the ASTM soft water.

The second set of tests consisted of three

chronic toxicity experiments. In the first,

3-month-old bluegill were exposed for 30 days

in hard freshwater (water chemistry as just

described) to a 6:1 waterborne mixture of

sodium selenate and sodium selenite at the

following nominal, total selenium

concentrations (in mg/L [ppm]): 0 (control),

1.4, 2.7, 5.4, 10.9, or 21.7. In the second

experiment, 5-month-old bluegill were exposed

for 60 days in hard freshwater to the same 6:1

selenate:selenite mixture at the following

nominal, total selenium concentrations (in
mg/L): 0 (control), 0.171, 0.341, 0.683,

1.38, or 2.73. Fish surviving this 60-day

experiment were placed in selenium-free water

for 28 days to study depuration rates. In the

third experiment, 3-month-old bluegill were

exposed for 90 days to a seleno- L-methionineenriched diet containing the following nominal

concentrations g/Kg [ppm], wet weight): 0

(control), 1.6, 3.3, 6.5, 13.0, or 26.0. 

In the third set of tests, 2-year-old bluegill

were exposed for a total of 140 days (60 days

- pre-spawning phase and 80 days - spawning

phase) to 10 ug/L (ppb) selenium (as mixture

of selenate and selenite) and to dietary

selenium-2 (as seleno-L-methionine) in five

concentrations from 0 through 33.3 ug/g (ppm,

dry weight), except for one control group

which received no dietary selenium. Fry

produced during this study were exposed to the

same waterborne and, beginning 15 days post

hatch, the same dietary concentrations and

forms of selenium as their parents for a total

of 30 days. Water used in this set of tests

was the same hard freshwater described

earlier.

Ninety six-hour LC50's (in mg/L [ppm])

produced by the first set of tests for the

hard freshwater and ASTM soft water,

respectively, were as follows 72-120 and 98

for selenate, 7.8-13.0 and 7.8-13.0 for

selenite, 0.009 aneleno-L-methionine, and

0.010 and 0.013 for seleno-DL-methionine.

Preliminary findings from the 30-day

experiment revealed that bluegill experienced

significant mortality in all treatment waters.

Findings of the 60-day experiment revealed

that percent survival of bluegills was

significantly reduced in all treatments

containing greater than or equal to 0.683 mg/L

selenium. Findings of the third, 90-day

dietary experiment revealed no significant

dose-related effects on survival, although

overall condition of bluegills was reduced at

the highest two selenium concentrations.

In the third set of tests, preliminary

findings reveal that none of the treatments

affected adult bluegills, neither was percent

hatch of eggs spawned or growth of surviving

fry affected. However, after 30 days, fry in

the treatment group receiving the greatest

waterborne and dietary concentrations of
selenium had experienced a high rate of

mortality.

The USFWS-NFCRC (Dec 1989) conducted acute

(96-hour) and chronic (90-day) toxicity

studies with juvenile striped bass (Morone

saxatilis) exposed to waterborne selenium. In

the acute tests, fish were exposed to

selenium+6 (as sodium selenate), selenium+4

(as sodium selenite), a 6:1 mixture of sodium

selenate and sodium selenite, or seleno-Lmethionine. In the chronic test, 80-day-old

fish were exposed to the 6:1 mixture of sodium

selenate and sodium selenite. Test waters

included standard ASTM soft water (containing

hardness of 40-48 mg/L [ppm] as calcium

carbonate, alkalinity of 30-35 mg/L as calcium

carbonate, and pH of 7.2-7.6) or 1.2 g/L

(ppth) saline water with an alkalinity of 70-

75 mL as calcium carbonate.

96-hour LC50's for ASTM the saline water,

respectively, were as follows: selenate -39

and 34 mg/L, selenite 1.0 and 6.0 mg/L, 6:1

selenate:selenite mixture - 15.0 and 18.0 mg

and selenomethionine - 0.004 and 0.003 mg/L.

Concentrations of the 6:1 selenate:selenite

mixture up to 3.0 mg/l did not affect growth

or survival of fish after 90 days in the

chronic toxicity study.

Hunn et al. (1987) studied the chronic effects

of selenium+4 on rainbow trout (Salmo

gairdneri). Trout sac fry were fed (ad

libitum) a clean Rangen's salmon starter diet

supplemented with brine shrimp and exposed for

90 days to the following concentrations of

waterborne selenium+4 (as sodium selenite):

less than detection (control), 7.8, 12.4,

21.0, 47.2, or 99.5 ug/l (ppb). Water

chemistry of test waters included pH of 7.4,

272 mg/l hardness (ppm, as calcium carbonate),

and 237 mg/l alkalinity (ppm, as calcium

carbonate). Biological endpoints measured

during the study included survival, growth

(length and weight), and chemical composition

and mechanical properties of vertebral bones.

After 90 days, fish exposed to test waters

containing the highest selenium+4

concentration experienced significant

reductions in growth and survival. Fish

exposed to 47.2 ug/l (ppb) selenium+4 also

experienced significant mortality, but had an
increase in bone toughness. Bone calcium

concentrations were significantly reduced in

fish exposed to >12.4 ug/l (ppb) selenium+4.

Hunn et al. (1987) also conducted a 96-hour

acute toxicity study using rainbow trout and

waterborne sodium selenite. Water chemistry

during that study included hardness of 40 mg/l

(ppm) and pH of 7.2. The LC50 value

determined by that study was 1.80 mg/l (ppm).

Hamilton and Buhl (1990) conducted three sets

of experiments to determine the 24- and 96-

hour LC50 for various life stages of fall-run

chinook salmon (Oncorhynchus tshawytscha) and

coho salmon (Oncorhynchus kisutch) exposed to

waterborne selenate (as sodium selenate),

selenite (as sodium selenite, Na2SeO3),

seleno-DL-methionine, boron (as boric acid),

and molybdenum (as sodium molybdate) in waters

of three different qualities. Up to four life

stages were tested in each set of experiments,

including eyed eggs, alevins, swim-up fry (8-

12 weeks old, post hatch), and advanced fry

(14-21 weeks old). The first test water was

simulated San Luis Drain effluent (containing

the major anions and cations, but not the

trace elements) diluted 10-fold in

standardized freshwater (SLD/freshwater).

Water chemistry in the SLD/freshwater included

total hardness of 211 mg/l (ppm, as calcium

carbonate), pH of 7.82, conductivity of 721

umhos/cm, and 185 mg/l (ppm) sulfate. The

second test water was simulated San Luis Drain

effluent diluted 22.5-fold in standardized

brackish water (SLD/brackish water). Water

chemistry the SLD/brackish water included

total hardness of 333 mg/l (ppm, as calcium

carbonate), pH of 7.79, conductivity of 2,887

umhos/cm, and 291 mg/l ( sulfate. The third

test water was standard soft water formulated

in accordance with USEPA recommendations.

Water chemistry in the soft water included

total hardness of 41.7 mg/l (ppm, as calcium

carbonate), pH of 7.57, conductivity of 157

umhos/cm, and 47 mg/l (ppm) sulfate.

The first set of experiments involved exposing

the two fry life stages of chinook and coho

salmon to individual trace elements in the

SLD/freshwater of tests consisted of exposing

the two fry life stages of chinook and coho

salmon to mixtures of trace elements in the

SLD/freshwater, SLD/brackish water, and soft
water. The third set of tests involved

exposing eyed eggs, alevins, and swim-up fry

life stages of chinook salmon to individual

trace elements in the soft water. Results

from single element tests with selenium and

all interactive tests are discussed herein.

Individual-effect results for boron and

molybdenum are presented in their respective

subsections.

The researchers found the intermediate life

stag salmon to be more sensitive to the

chemicals' toxic effects than the youngest

(eyed eggs and alevins) and oldest (advanced

fry) life stages. Coho salmon were more

sensitive than chinook salmon. Waterborne

selenite was more toxic than seleno-DLmethionine, which was more toxic than

selenate. The LC50 values for selenite and

selenate were not significantly different

among water qualities.

Pooled LC50 values (in mg/l [ppm] for 24- and

96 hour tests, respectively) for chinook

salmon exposed to selenium were as follows:

46.9 and 13.8 for selenite in SLD/freshwater

and 65.6 and 23.4 in SLD/brackish water, 475

and 115 for selenate in SLD/freshwater and 484

and 149 in SLD/brackish water, and >21.6 for

seleno-DL-methionine at both times and in both

SLD/freshwater and SLD/brackish water. Pooled

LC50 values (in mg/l [ppm] for 24- and 96-hour

tests, respectively) for coho salmon exposed

to selenium were as follows: 28.8 and 7.8 for

selenite in SLD/freshwater and 44.1 and 13.6

in SLD/brackish water, and 234 and 32.5 for

selenate in SLD/freshwater and >369 and 39.0

in SLD/brackish water. LC50 values (in mg/l

[ppm] for 24- and hour tests, respectively)

for chinook salmon exposed to selenate in soft

water were as follows: >1,000 and >1,000 for

eyed eggs, >320 and >320 for 4 for fry. LC50

values (in mg/l [ppm] for 24- and 96-hour

tests, respectively) for chinook salmon

exposed to selenite in soft water were as

follows: >560 and >560 for eyed eggs; 202 and

104 for alevins; and 100 and 65.8, and 27.3

and 13.1 for two different sizes/ages of fry.

The interactive toxicities of various selenium

mixtures, including those with added boron

and/or molybdenum, were found to be additive.

96-hour LC50 values for chinook salmon exposed

to various mixtures of selenate and selenite
ranged from 46.6 to 85.5 mg/l (ppm) in

SLD/freshwater and from 51.9 to 96.8 mg/l

(ppm) in SLD/brackish water. 96-hour LC50

values for coho salmon exposed to various

mixtures of selenate and selenite ranged from

16.9 to 25.8 mg/l (ppm) in SLD/freshwater and

from 26.2 to 38.0 mg/l (ppm) in SLD/brackish

water.

The USFWS-NFCRC (Dec 1989) studied the effects

of a 6:1 waterborne mixture of sodium selenate

to sodium selenite on fall-run chinook salmon

in 120-day toxicity tests. Swim-up life stage

(0.5 g) fish were tested in reconstituted

waters designed to mimic the major ionic

concentrations (without the trace elements) of

San Luis Drain effluent diluted 37-fold in

standardized freshwater. Advanced fry life

stage fish were tested in the same

reconstituted waters diluted 22.5-fold in

standardized brackish water (~1.2 ppth

salinity). Preliminary results from these

experiments reveal growth and survival of

swim-up life stage fish were unaffected by

selenium concentrations up to 140 ppb and

advanced fry life stage fish exposed to 280

ppb selenium experienced significant growth

reductions after 90 days and total mortality

after 100 days.

The USFWS-NFCRC (Dec 1989; Dec 1987) conducted

two sets of tests to evaluate effects upon

juvenile fall-run chinook salmon of exposure

to selenium in food or water. In the first

study, fish were exposed for 30 days in

freshwater to D,L-selenomethionine-enriched

Oregon Moist Pellet diets containing the

following concentrations of selenium (in ppm,

wet weight): 0 (control), 15, 30, or 60.

Twenty four-hour seawater (30 ppth salinity)

challenge tests were conducted weekly during

the 30-day period. Fish were then exposed to

a selenium-free diet in seawater for an

additional 90 days. In the second study, fish

were exposed for 7 weeks in freshwater to a

6:1 waterborne mixture of sodium selenate and

sodium selenite containing the following

concentrations (in ug/l [ppb]): 0 (control),

35, 70, 140, 280, or 560. As in the first

study, 24-hour seawater challenges were

conducted weekly and, following the initial

phase of the study, fish were exposed to

selenium-free seawater for an additional 90

days.
Preliminary results from the first (dietary)

study reveal that increasing dietary selenium

concentrations resulted in reduced survival

and reduced growth of fish in the fr the

study; however, cumulative mortality in all

treatment groups was less than 1%. Results of

the seawater challenges showed that fish fed

the 30 ppm selenium-2 diet experienced delayed

osmoregulatory development and that those

receiving the 60 ppm selenium-2 diet failed to

develop any osmoregulatory ability. This

latter group of fish also failed to exhibit

normal gill Na+/K+ ATPase activity. Both the

30 and 60 ppm selenium-2 test groups also

experienced increased mortality during the

seawater challenges. Migratory behavior of

fish from treatment groups was not

significantly different than controls. During

the 3-month seawater exposure, mortality of

fish fed seleniferous diets was approximately

2-7 times higher than controls; however,

growth of surviving fish was not different

between treatment groups and controls.

Preliminary findings from the second

(waterborne) study reveal that after 6 weeks

in the freshwater phase of the study, there

were no significant differences between

control fish and those exposed to waterborne

selenium in terms of histopathological

changes, growth, or mortality. Neither did

control and treatment fish (following 48 days

of freshwater exposure) differ in downstream

migration behavior, or in growth or survival

for up to 3 months in seawater. Following 7

weeks of freshwater exposure, gill

sodium/potassium ATPase activity was not

significantly different between control and

treatment groups exposed to seawater. The

only difference between control and treatment

groups noted in the study was a markedly

higher mortality rate, following 24-hour

seawater challenges, in fish exposed to all

concentrations of waterborne selenium.

W.Wildlife (Water Concentrations vs. Wildlife or Domestic

Animals):

Oak Ridge National Lab, 1994: Risk Assessment

Screening Benchmarks for Wildlife derived for NoObserved-Adverse-Effect (NOAEL) levels (see

Tis.Wildlife, B) for these). To be considered

unlikely to represent an ecological risk, water
concentrations should be below the following

benchmarks for each species present at the site

[650]:

 CAS 7782-49-2 SELENIUM (AS SELENATE)

 WATER CONCEN-

 SPECIES TRATION (ppm)

Mouse (test species) 0.00000

Short-tailed Shrew 0.42900

Little Brown Bat 0.74100

White-footed Mouse 0.27700

Meadow Vole 0.48500

Cottontail Rabbit 0.23000

Mink 0.23800

Red Fox 0.17000

Whitetail Deer 0.09500

Comment: Actually, the number of

significant figures for a benchmark value

should never be more than one; even if

these values have been taken directly

from another report, they should be

rounded; otherwise the impression is

given of a level of accuracy that is

simply unwarranted. The uncertainties are

too large to justify such a fine

distinction (Owen Hoffman, SENES Oak

Ridge, Personal Communication, 1997).

To protect livestock/cattle use, selenium levels

should be less than 0.01 mg/L [671].

The Environmental Protection Agency (EPA) is

developing a threshold value for dissolved

waterborne selenium to protect wildlife using

aquatic environments because it appears that the

current ambient water quality criteria for selenium

of 5 ppb established for aquatic species may not be

adequate to protect wildlife.

W.Human (Drinking Water and Other Human Concern Levels):

EPA 1995 Region 9 Tap Water Preliminary Remediation

Goal and Region 3 RBC for tap water: 180 ug/L

[868,903].

EPA 1996 IRIS Database [893]:

Maximum Contaminant Level Goal (MCLG)

MCLG Value: 0.05 mg/L total selenium

[893,952]. 
Status/Year: Final 1991 Econ/Tech?:

No, does not consider economic or

technical feasibility Reference: 56

FR 3526 (01/30/91) 

Contact: Health and Ecological Criteria

Division / (202)260-7571 Safe Drinking

Water Hotline / (800)426-4791 

Discussion: EPA has concluded that

selenium should be placed in Category III

and promulgates an MCLG of 0.05 mg/L

based on a no-effect level obtained from

a human study in China (Yang et al.,

1989). Yang suggests that 0.400 mg of

selenium/person/day is the maximum safe

daily intake of selenium and assuming a a

daily average consumption of 2 L drinking

water per person containing 0.05 mg/L

selenium, the resulting selenium

ingestion would be 0.1 mg/person/day.

The average daily dietary intake in this

country is 0.125 mg selenium/person/day.

A combined ingestion of water containing

0.05 mg/L and a typical U.S. diet would

result in a total daily exposure of 0.225

mg selenium/person/day, well below the

limit of 0.400 mg selenium that Yang et

al. suggests is safe [893]. 

Maximum Contaminant Level (MCL) [893]:

Value: 0.05 mg/L total selenium 

Status/Year: Final 1991 Econ/Tech?:

Yes, does consider economic or

technical feasibility Reference: 56

FR 3526 (01/30/91) 

Contact: Drinking Water Standards

Division / OGWDW / (202)260-7575 Safe

Drinking Water Hotline / (800)426-4791 

Discussion: EPA has promulgated an MCL

equal to the MCLG of 0.05 mg/L. 

Ambient Water Quality Criteria for Human

Health [893]:

Water & Fish or Fish only: see discussion

below. See also 45 FR 79318 (11/28/80);

NTIS No. PB81-117814 

Contact: Criteria and Standards
Division / OWRS / (202)260-1315 

Discussion: The ambient water

quality criterion for selenium is

recommended to be identical to the

existing water standard which is 10

ug/L [893]. 

Older Values for Water Quality

Criteria for Human Health (10-6 Risk

Level for Carcinogens) were the

same: 

Published Criteria for Water

and Organisms: 10 ug/L

[446,689].

For human health the ambient

water quality criterion for

selenium is recommended to be

identical to the existing water

standard which is 10 ug/l.

Analysis of the toxic effects

data resulted in the calculated

level which is protective of

human health against the

ingestion of contaminated water

and contaminated aquatic

organisms. The calculated value

is comparable to the present

standard. For this reason a

selective criterion based on

exposure solely from

consumption of 6.5 g of aquatic

organisms was not derived.

/Selenium and cmpd/ [366,

USEPA/OWRS; Quality Criteria

for Water 1986 (1986) EPA

440/5-86-001].

Criteria Federal Register

Notice Number: 53 FR 177

Note: Before citing a concentration as EPA's

water quality criteria, it is prudent to make

sure you have the latest one. Work on the

replacement for the Gold Book [302] was

underway in March of 1996, and IRIS is updated

monthyly [893].

State Drinking Water Standards [940]:

(AL) ALABAMA 10 ug/l [USEPA/Office of Water;

Federal-State Toxicology and Risk Analysis
Committee (FSTRAC). Summary of State and

Federal Drinking Water Standards and

Guidelines (11/93)].

(AZ) ARIZONA 10 ug/l [USEPA/Office of Water;

Federal-State Toxicology and Risk Analysis

Committee (FSTRAC). Summary of State and

Federal Drinking Water Standards and

Guidelines (11/93)].

State Drinking Water Guidelines [940]:

(AZ) ARIZONA 45 ug/l [USEPA/Office of Water;

Federal-State Toxicology and Risk Analysis

Committee (FSTRAC). Summary of State and

Federal Drinking Water Standards and

Guidelines (11/93)].

(ME) MAINE 10 ug/l [USEPA/Office of Water;

Federal-State Toxicology and Risk Analysis

Committee (FSTRAC). Summary of State and

Federal Drinking Water Standards and

Guidelines (11/93)].

(MN) MINNESOTA 20 ug/l [USEPA/Office of Water;

Federal-State Toxicology and Risk Analysis

Committee (FSTRAC). Summary of State and

Federal Drinking Water Standards and

Guidelines (11/93)].

Bureau of Land Management RMC Benchmarks, 1995:

Risk Management Criteria (RMC) were developed for

the mostly dry BLM lands in the western U.S. These

risk management criteria should be used by the land

manager as a cautionary signal that potential

health hazards are present and that natural

resource management or remedial actions are

indicated [715]. Exceedances of the criteria

should be interpreted as follows [715]:

Less than criteria: low risk

1-10 times the criteria: moderate risk

10-100 times the criteria: high risk

>100 times the criteria: extremely high

risk

Human RMC criteria for selenium in surface

waters. These categories of humans not

exposed to surface waters with concentrations

of selenium exceeding the below RMCs are not

expected to experience adverse toxic effects

[715]:

Camp host: 1548 ug/L
Child Camper: 1422 ug/L

Boater: 5530 ug/L

Swimmer: 2395 ug/L

Human RMC criteria for selenium in ground

water. These categories of humans not exposed

to ground waters with concentrations of

selenium exceeding the below RMCs are not

expected to experience adverse toxic effects

[715]:

Child resident (living on properties

adjacent to BLM lands): 2 ug/L

Camp host: 18 ug/L

Child Camper: 51 ug/L

Worker: 39 ug/L

Surveyor: 387 ug/L

W.Misc. (Other Non-concentration Water Information):

Phytormediation: Plants "are very effective at removing

selenium from contaminated soils," asserts Norman Terry

of the University of California, Berkeley [1023]. They

not only absorb the chemical, they also turn some of it

into the less toxic dimethyl selenide gas [1023].

Selenate, the common form of selenium in soil, is about

600 times more toxic than dimethyl selenide gas [1023].

The company originally constructed the wetland, which

features cattails and bulrushes, for its beauty [1023].

Now, the wetland is removing 70 to 75 percent of the

selenium from the 10 million liters of wastewater that

the company pumps through it every day, says Terry

[1023]. In central California, at least two farmers are

using Indian mustard and tall fescue to extract selenium

from irrigation water, reports Gary S. Banuelos of the

U.S. Department of Agricultures's Agricultural Research

Service in Fresno, Calif [1023]. He advises the farmers

on the phytoremediation technology [1023].

A potential complication in comparing contaminants data

is that different investigators have sometimes meant

different things when they put the words "dissolved" or

"total" in front of a reported measurement. In the case

of nutrients, the "dissolved" portion is usually simply

that portion which has passed through a 0.45-micrometer

membrane filter and the "total" measurements implies that

it was not filtered and includes both dissolved and other

forms of the nutrient [141]. However, usage of the words

dissolved and total has not been uniform in the past and

there is still considerable debate about which methods

should truly be considered "dissolved" or "total" (Merle

Schlockey, USGS, personal communication).
Water bodies are often marked by heterogeneity of the

distribution of undissolved materials [691]. The size of

any effects depends on the difference in density of the

undissolved materials and the water, the size of the

particles or bubbles of the materials, and various

hydrodynamic factors such as the degree of turbulence in

the water. Thus, undissolved inorganic materials in

rivers and other natural water-bodies tend to increase in

concentration with increasing depth because the particles

tend to settle [691]. On the other hand, certain

biological detritus may tend to rise towards the surface

of the water because its density is less than that of

water; oils also commonly demonstrate this effect

markedly [691]. The surface microlayer is usually higher

in concentration of many metallic and organic

contaminants than the water column further down. 

If the only change one makes is to use the prefix

"dissolved" rather than the prefix "total" in an

otherwise identical water quality standard, the effect

can be a weakening of the standard related to total

loading of a system. Many contaminants which are not

currently dissolved can become dissolved at a later time,

when encountering different conditions (perhaps

downstream), such as changes in pH, additions of

surfactants or humic substances, bioturbation,

methylating organisms, and various other physical,

chemical, or biological changes.

One problem with relying too heavily on dissolved

fractions of metals is that the dissolved fraction misses

the metals carried by colloids. Colloids were found to

carry toxic metals 140 miles downstream of mining sources

in Leadville, Colorado, to be repeatedly washed from

flood deposited lowlands back into the river year after

year in spring runoff (Briant Kimball, USGS Salt Lake

City, as quoted in U.S. Water News, April 5th, 1995).

See Laboratory section below for EPA generic

(guesstimate) conversion factors to convert total to

dissolved concentrations.

Some environmental toxicologists make the argument that

dissolved metals in surface water and porewaters

represent most of what is bioavailable and thus "total"

metals parameters are not good as a measure of potential

biological effects. This is mostly true in many

situations, but it should be kept in mind that fish and

other aquatic organisms do not typically live in filtered

water and that many fish and other aquatic organisms live

in the sediments and in other situations in which they

come in contact with toxic or otherwise harmful compounds

(as certain colloids, precipitates, oxides, adsorbed

metals), etc. Sometimes the effect of total metals is
partially related to physical or chemical aspects, such

as when ferric oxide coats or covers benthic organisms.

Another factor to consider: contaminants carried

downstream by erosion of bottom sediments or colloids can

be mobilized when they come in contact with different

physical/chemical environments downstream (for example,

a tributary bringing low pH into the system).

Misc. Notes on colloids (Briant Kimball, USGS, Salt

Lake City Office, Personal Communication, 1995):

There is no question that dissolved metals are

critical to fish and invertebrates, but less

well recognized is the potential impact and

movement of metals in colloids. The

possibility of having colloidal material

present means there is a readily available

supply of metals in a state in which the

metals can quickly be reduced and mobilized.

In river banks, reducing environments form

just under the surface quickly. Toxic metals

of concern would include zinc, lead, copper,

and cadmium.

Colloids do move in surface water (for

example, transport of metal in colloids 140

miles downstream of Leadville, CO), but also

in groundwater, especially related to

radionuclides. 

Colloidal metals may effect biota more than is

widely recognized. Brown trout are effected

by colloids which travel kind of like

dissolved fractions, don't settle out. There

may be little understood colloidal pathways of

metals to fish, for example. Colloidal metals

become part of the caddis cast which are

ingested, once part of acid gut, metals can be

released. On the Arkansas River of Colorado

below Leadville, the dissolved metals have

gone down with treatment, but Will Clements of

CSU has discovered the toxicity has not been

reduced to the same extent as have the

dissolved metals. Treatment has not

eliminated colloidal fractions loaded with

cadmium and copper, and this is possibly

impacting the fish. 

In rivers, there is annual flushing of the

colloids, loads are much greater during

runoff.

Sediment Data Interpretation, Concentrations and Toxicity (All
Sediment Data Subsections Start with "Sed."):

Sed.Low (Sediment Concentrations Considered Low):

Selenium concentrations in freshwater sediments range

from 0.20 to 2.00 mg/kg (ppm) [445].

Sed.High (Sediment Concentrations Considered High):

Texas: The statewide 90th percentile value for selenium

was 1.9 mg/kg dry weight [7].

Selenium concentrations in freshwater sediments range

from 0.20 to 2.00 mg/kg (ppm) [445].

Analyses of sewage sludges from 50 publicly owned

treatment works by the U.S. Environmental Protection

Agency (1985): The mean concentration of selenium was

2.6 ppm (dry weight) [347].

Analyses of 74 Missouri sludges (1985): The mean for

selenium was 3 ppm. The range was 1-25 ppm (dry weight)

[347].

Sed.Typical (Sediment Concentrations Considered Typical):

No information found.

Sed.Concern Levels, Sediment Quality Criteria, LC50 Values,

Sediment Quality Standards, Screening Levels, Dose/Response

Data and Other Sediment Benchmarks:

Sed.General (General Sediment Quality Standards,

Criteria, and Benchmarks Related to Protection of Aquatic

Biota in General; Includes Sediment Concentrations Versus

Mixed or General Aquatic Biota):

USFWS: The toxic threshold for selenium transferred

to consumer species of fish and wildlife is 3 mg/kg

[648].

Sed.Plants (Sediment Concentrations vs. Plants):

No information found.

Sed.Invertebrates (Sediment Concentrations vs.

Invertebrates):

Where sediments contain 6-15 ppm selenium (dry

weight), the invertebrates may have up to 50 ppm

selenium (dry weight) which is a concentration that

would be directly toxic to adult fish and waterfowl

(Dennis Lemly, Fish and Wildlife Service, National
Fisheries Contaminant Research Center, personal

communication, 1991). 

Aquatic sediments containing more than 3 ppm

selenium (dry weight) usually cause selenium levels

in benthic invertebrates to exceed safe

concentrations (3-5 ppm dry weight for fish and

wildlife that feed upon them (Dennis Lemly, Fish

and Wildlife Service, National Fisheries

Contaminant Research Center, personal

communication, 1991).

Sed.Fish (Sediment Concentrations vs. Fish):

Where sediments contain 6-15 ppm selenium (dry

weight), the invertebrates may have up to 50 ppm

selenium (dry weight) which is a concentration that

would be directly toxic to adult fish and waterfowl

(Dennis Lemly, Fish and Wildlife Service, National

Fisheries Contaminant Research Center, personal

communication, 1991). 

Aquatic sediments containing more than 3 ppm

selenium (dry weight) usually cause selenium levels

in benthic invertebrates to exceed safe

concentrations (3-5 ppm dry weight for fish and

wildlife that feed upon them (Dennis Lemly, Fish

and Wildlife Service, National Fisheries

Contaminant Research Center, personal

communication, 1991). 

Sed.Wildlife (Sediment Concentrations vs. Wildlife or

Domestic Animals):

Where sediments contain 6-15 ppm selenium (dry

weight), the invertebrates may have up to 50 ppm

selenium (dry weight) which is a concentration that

would be directly toxic to adult fish and waterfowl

(Dennis Lemly, Fish and Wildlife Service, National

Fisheries Contaminant Research Center, personal

communication, 1991). 

Aquatic sediments containing more than 3 ppm

selenium (dry weight) usually cause selenium levels

in benthic invertebrates to exceed safe

concentrations (3-5 ppm dry weight for fish and

wildlife that feed upon them (Dennis Lemly, Fish

and Wildlife Service, National Fisheries

Contaminant Research Center, personal

communication, 1991). 

USFWS: The toxic threshold for selenium transferred

to consumer species of fish and wildlife is 3 mg/kg
[648].

Sed.Human (Sediment Concentrations vs. Human):

Bureau of Land Management RMC Benchmarks, 1995:

Risk Management Criteria (RMC) were developed for

the mostly dry BLM lands in the western U.S. These

risk management criteria should be used by the land

manager as a cautionary signal that potential

health hazards are present and that natural

resource management or remedial actions are

indicated [715]. Exceedances of the criteria

should be interpreted as follows [715]:

Less than criteria: low risk

1-10 times the criteria: moderate risk

10-100 times the criteria: high risk

>100 times the criteria: extremely high

risk

Human RMC criteria for selenium in sediments.

These categories of humans not exposed to

sediments with concentrations of selenium

exceeding the below RMCs are not expected to

experience adverse toxic effects [715]:

 Camp host: 774 mg/kg

 Child Camper: 356 mg/kg

 Boater: 2765 mg/kg

 Swimmer: 1197 mg/kg

Sed.Misc. (Other Non-concentration Sediment Information):

No information found.

Soil Data Interpretation, Concentrations and Toxicity (All Soil

Data Subsections Start with "Soil."):

Soil.Low (Soil Concentrations Considered Low):

No information found.

Soil.High (Soil Concentrations Considered High):

Analyses of sewage sludges from 50 publicly owned

treatment works by the U.S. Environmental Protection

Agency (1985): The mean concentration of selenium was

2.6 ppm (dry weight) [347].

Analyses of 74 Missouri sludges (1985): The mean for

selenium was 3 ppm. The range was 1-25 ppm (dry weight)

[347].
Most seleniferous soils contain less than 2 ppm selenium

[953].

Soil.Typical (Soil Concentrations Considered Typical):

Selenium is more abundant and more bioavailable (mostly

due to natural geological circumstances), than in the

eastern United States [463].

Typical Igneous Rocks (Earth's Crust) Concentrations: EPA

1981: 0.05 mg/kg dry weight [83]. 

Typical Soil Concentrations: EPA 1981: 0.2 mg/kg dry

weight [83]. 

Selenium concentrations in soils around the world range

widely, from areas of selenium deficiency to those with

seleniferous soils (0.1-1,200 mg/kg [ppm], respectively),

and average 0.4 ppm [445].

Quebec considers 1 ppm as background [347].

The mean elemental concentration of this metal in plants

was 0.1 ppm in the same areas where rocks were 1 ppm

[951]. Concentration in soils is 0.5 ppm [951].

Selenium concentration in geological materials: Igneous

rocks 0.05 ppm; shales 0 - 0.6 ppm; sandstones 0.0 - 0.05

ppm; limestones 0.08 ppm; soils 0.2 ppm (Wilber CG; Clin

Toxicol 17 (2): 171-230, 1980) [366].

The earth's crust is said to have an average selenium

concentration of 0.03 of 0.08 ppm (Wilber CG; Clin

Toxicol 17 (2): 171-230, 1980) [366].

Soil.Concern Levels, Soil Quality Criteria, LC50 Values, Soil

Quality Standards, Screening Levels, Dose/Response Data and

Other Soil Benchmarks:

Soil.General (General Soil Quality Standards, Criteria,

and Benchmarks Related to Protection of Soil-dwelling

Biota in General; Includes Soil Concentrations Versus

Mixed or General Soil-dwelling Biota):

Other Maximum Allowable Concentration (MAC) levels

of selenium (ppm dry weight): 10 (Stuttgart), 3

(London) [719] 

Proposal of Ontario Ministry of Agriculture and

Food for MAC in soils treated with sewage sludge:

1.6 ppm dry weight (published in Tokyo; work done

for Ontario) [719].
The 1987 soil (clean up) criteria given by the New

Jersey Department of Environmental Protection for

selenium is 4 mg/kg dry weight [347,386]. Quebec

considers 1 ppm as background, 3 ppm as moderately

contaminated soils, and 10 ppm as a threshold that

requires immediate cleanup [347]. Ontario

considers 1.6 ppm selenium as the maximum for

proposed redevelopment as agriculture and 5 ppm as

the maximum for proposed redevelopment as

residential or parkland [347].

Quebec considers 3 ppm as moderately contaminated

soil, and 10 ppm as a threshold that requires

immediate cleanup [347].

Suggested safe applications (kg/ha) of trace

compounds to Missouri soils without further

investigations (1988): The maximum cumulative

addition of selenium should not exceed 18 kg/ha

[347].

Soil.Plants (Soil Concentrations vs. Plants):

Levels of selenium (ppm dry weight) considered

phytotoxic: 10 (Vienna), 10 (Warsaw), 10 (Warsaw),

5 (Ontario) [719].

Oak Ridge National Lab, 1994: Risk Assessment

Screening Benchmarks for Terrestrial Plants. To be

considered unlikely to represent an ecological risk

to terrestrial plants, field concentrations in soil

should be below the following dry weight benchmark

for soil [651]:

For CAS 007782-49-2 (SELENIUM), the benchmark

is 1 mg/kg in soil (WILL and SUTER, 1994).

Soil.Invertebrates (Soil Concentrations vs.

Invertebrates):

No information found.

Soil.Wildlife (Soil Concentrations vs. Wildlife or

Domestic Animals):

No information found.

Soil.Human (Soil Concentrations vs. Human):

EPA 1996 National Generic Soil Screening Level

(SSL) designed to be conservative and protective at

the majority of sites in the U.S. but not

necessarily protective of all known human exposure
pathways, land uses, or ecological threats [952]:

SSL = 390 mg/kg for ingestion pathway [952].

SSL = None given for inhalation pathway [952].

SSL = 0.3 to 5 mg/kg for protection from

migration to groundwater at 1 to 20 DilutionAttenuation Factor (DAF) [952].

 EPA 1995 Region 9 Preliminary remediation goals

(PRGs), 1995 [868]:

Residential Soil: 380 mg/kg wet wt.

Industrial Soil: 8500 mg/kg wet wt.

NOTE:

1) PRGs focus on the human exposure pathways

of ingestion, inhalation of particulates and

volatiles, and dermal absorption. Values do

not consider impact to groundwater or

ecological receptors.

2) Values are based on a non-carcinogenic

hazard quotient of one.

3) PRGs for residential and industrial

landuses are slightly lower concentrations

than EPA Region III RBCs, which consider fewer

aspects [903].

 EPA 1995 Region 3 Risk based concentration (RBC) to

protect from transfers to groundwater: 

None given [903].

Bureau of Land Management RMC Benchmarks, 1995:

Risk Management Criteria (RMC) were developed for

the mostly dry BLM lands in the western U.S. These

risk management criteria should be used by the land

manager as a cautionary signal that potential

health hazards are present and that natural

resource management or remedial actions are

indicated [715]. Exceedances of the criteria

should be interpreted as follows [715]:

 Less than criteria: low risk

 1-10 times the criteria: moderate risk

10-100 times the criteria: high risk

>100 times the criteria: extremely high

risk

Human RMC criteria for selenium in soil.

These categories of humans not exposed to soil

with concentrations of selenium exceeding the

below RMCs are not expected to experience
adverse toxic effects [715]:

 Child resident (living on properties

adjacent to BLM lands): 10 mg/kg

Camp host: 258 mg/kg

Child Camper: 178 mg/kg

ATV Driver: 3629 mg/kg

Worker: 387 mg/kg

Surveyor: 3871 mg/kg

Soil.Misc. (Other Non-concentration Soil Information):

Misc. Notes Related to Selenium Bioavailability in Soils

[463]:

In areas of the Western United States (states west

of and including North Dakota, South Dakota,

Nebraska, Kansas, Oklahoma, and Texas), where

geological sources of selenium are abundant in the

soil profile, selenium tends to be more

bioavailable to ecosystems.

A major feature of this area is the presence of

pedocal soils. Pedocals are alkaline soils of

semiarid and arid climates. Bacterial and chemical

processes in these highly oxidizing, alkaline soils

favor the formation of calcium and sodium

selenates, which are very mobile and water soluble,

and are readily available forms of selenium to

plants. In addition, many areas in the Western

United States are prone to selenium enrichment of

the soil because of leaching of underlying

seleniferous rocks, such as the shales and clays of

the Upper Cretaceous Pierre, Steele, and Niobrara

Shales.

Pedalfer soils found in the Eastern United States

are acid to neutral soils of humid and semihumid

climates. These acid soils favor the formation of

more reduced and complexed forms of selenium, such

as ferric selenite. These complexes are generally

insoluble so as to reduce selenium bioavailability

to the point that forages and feeds grown in the

Eastern United States contain insufficient selenium

for proper animal nutrition.

In short, in areas in the Western United States

where selenium is abundant and bioavailable, a more

detailed analysis may be required for selenium

toxicity than would be required in the east [463].

Phytormediation: Plants "are very effective at

removing selenium from contaminated soils," asserts
Norman Terry of the University of California,

Berkeley [1023]. They not only absorb the

chemical, they also turn some of it into the less

toxic dimethyl selenide gas [1023]. Selenate, the

common form of selenium in soil, is about 600 times

more toxic than dimethyl selenide gas [1023]. See

also additional detail in W.Misc. section above. 

See also Fate.Detail section below.

Tissue and Food Concentrations (All Tissue Data Interpretation

Subsections Start with "Tis."):

Tis.Plants:

A) As Food: Concentrations or Doses of Concern to Living

Things Which Eat Plants:

Selenium is found in livestock feeds [445]. The

toxic effects of selenium on livestock have been

known for some time [445]. Grazing in seleniferous

areas and/or on selenium-accumulator plants has

been associated with acute and chronic maladies

known as the blind staggers and alkali disease,

respectively (although there is some debate

regarding whether the blind staggers is actually

caused by excess intake of selenium or some other

toxic property[ies] of forage such as locoweed [a

plant of either the genera Oxytropis or Astragalus

which causes severe poisoning when eaten by

livestock]) [445].

Livestock foraging on plants containing about 25

ppm selenium suffer from alkali disease,

characterized by a lack of vitality, loss of hair,

sterility, atrophy of hooves, lameness, and anemia

[491].

B) Body Burden Residues in Plants: Typical, Elevated, or

of Concern Related to the Well-being of the Organism

Itself:

The mean elemental concentration of this metal in

plants was 0.1 ppm in the same areas where rocks

were 1 ppm [951].

See also Tis.Misc section below.

The contents of copper, molybdenum, sulphur, zinc,

selenium, iron, manganese, and the

copper/molybdenum ratio were determined in

different native plant species from a mountain

area of central southern Norway. The overall mean
values and ranges (mg/kg DM) were copper: 6.0, 0.9-

27.2; molybdenum: 0.25, 0.01-3.57; zinc: 77, 8-

320; selenium: 0.05, less than 0.01-0.32; iron:

208, 15-2245; manganese: 338, 31-3784; sulfur:

(g/100 g DM) 0.20, 0.03-0.56; copper/molybdenum:

79, 1-7955. Levels of the individual elements

showed considerable variability, both between and

within plant groups. Mineral contents were compared

with the established requirements for sheep and

cattle, the following conclusion being drawn. The

levels of zinc, sulphur, iron, and manganese were

found to be adequate for ruminants. [Garmo TH et

al; Acta Agric Scand 36 (2): 147-161 (1986)] [940].

Tis.Invertebrates:

A) As Food: Concentrations or Doses of Concern to Living

Things Which Eat Invertebrates:

The following text is quoted from the Trinity River

Report [201] for reference comparison with values

from other areas: 

Predator Protection Level: The 0.5 mg/kg

predator protection level [20] was exceeded in

6 of 77 Trinity River samples. Included in

this group were samples of Mississippi map

turtles, mosquitofish, carp, spiny softshell

turtles, and unionid clams, all from sites

downstream of Dallas except for the

mosquitofish, which were from site 20. 

B) Concentrations or Doses of Concern in Food Items

Eaten by Invertebrates:

No information found.

C) Body Burden Residues in Invertebrates: Typical,

Elevated, or of Concern Related to the Well-being of the

Organism Itself:

The following information summarizes data gathered

from the NOAA National Status and Trends (NS&T)

Program for the year 1990 [697]:

For selenium in mussels and oysters combined

(n=214), the Geometric Mean was 2.5 ug/g dry

and the "high" concentration was 3.5 ug/g dry

weight [697]. NOAA "high" concentrations are

equal to the geometric mean plus one standard

deviation on the log normal distribution

[696].
The following text is quoted from the Trinity River

Report [201] for reference comparison with values

from other areas:

Maximum Level: The highest selenium

concentration was 0.71 mg/kg. This

concentration was found in a composite sample

of unionid clam flesh from site 14.

USFWS: Aquatic sediments containing more than 3

ppm selenium (dry weight) usually cause selenium

levels in benthic invertebrates to exceed safe

concentrations (3-5 ppm dry weight for fish and

wildlife that feed upon them (Dennis Lemly, Fish

and Wildlife Service, National Fisheries

Contaminant Research Center, personal communication

to Roy Irwin, 1991). Where sediments contain 6-15

ppm selenium (dry weight), the invertebrates may

have up to 50 ppm selenium (dry weight) which is a

concentration that would be directly toxic to adult

fish and waterfowl (Dennis Lemly, Fish and Wildlife

Service, National Fisheries Contaminant Research

Center, personal communication, 1991).

Tis.Fish:

A) As Food: Concentrations or Doses of Concern to Living

Things Which Eat Fish (Includes FDA Action Levels for

Fish and Similar Benchmark Levels From Other Countries):

Legal Limits for Concentrations in Fish and Fishery

Products: The lowest legal limit was 0.05 mg/kg

(Chile) [216,418]. Three countries have limits

less than or equal to 2.0 mg/kg, but the U.S.

apparently has no limit [216,418].

The California Department of Health Services

recommended a maximum allowable residue level of

1.0 mg/kg wet weight for muscle (fillet) tissue of

edible fish [222]. It was from this that the water

concentration concern level of 0.8 ppm was derived

(through back calculation from the tissue concern

level) [222].

Region III EPA RBC value for fish tissue: 6.8 mg/kg

[903].

The following text is quoted from the Trinity River

Report [201] for reference comparison with values

from other areas): 

Predator Protection Level: The 0.5 mg/kg

predator protection level [20] was exceeded in
6 of 77 Trinity River samples. Included in

this group were samples of Mississippi map

turtles, mosquitofish, carp, spiny softshell

turtles, and unionid clams, all from sites

downstream of Dallas except for the

mosquitofish, which were from site 20. 

Bureau of Land Management RMC Benchmarks, 1995:

Risk Management Criteria (RMC) were developed for

the mostly dry BLM lands in the western U.S. These

risk management criteria should be used by the land

manager as a cautionary signal that potential

health hazards are present and that natural

resource management or remedial actions are

indicated [715]. Exceedances of the criteria

should be interpreted as follows [715]:

Less than criteria: low risk

1-10 times the criteria: moderate risk

10-100 times the criteria: high risk

>100 times the criteria: extremely high

risk

Human RMC criteria for selenium in fish

consumed by humans. These categories of

humans not exposed to fish with concentrations

of selenium exceeding the below RMCs are not

expected to experience adverse toxic effects

[715]:

Child resident (living on properties

adjacent to BLM lands): 392 ug/kg

Camp host: 807 ug/kg

Child Camper: 2222 ug/kg

B) Concentrations or Doses of Concern in Food Items

Eaten by Fish:

The effects of dietary and waterborne selenium on

bluegill sunfish (Lepomis macrochirus) were studied

by Woock et al. (1987) [445]. Mortalities of

adults were significant in both 30 ppm diet groups.

Toxic effects have been documented in fish

consuming diets containing 10 to 33 mg/kg selenium,

concentrations similar to those in prey organisms

from selenium impacted habitats [481]. Dietary Semethionine is more toxic to fish than dietary

inorganic selenium [481].

Text in paragraph above reprinted with

permission from Environmental Toxicology and

Chemistry, Volume 12, J.M. Besser, T.J.

Canfield and T.W. La Point, "Bioaccumulation
of oganic and inorganic selenium in a

laboratory food chain." Copyright 1993 SETAC].

Selenium whole-body levels above 0.5 mg/kg are

considered harmful to fish and predators [20].

However, some more recent researchers have

concluded that harmful effects of selenium on

predators has seldom been documented for

concentrations below 3 mg/kg and often been

documented for concentrations above 30 mg/kg (the

"3/30 guideline", Jerry Miller, U.S. Bureau of

Reclamation, Salt Lake City, personal

communication, 1994). For example: 

Hamilton et al. (1990) suggest that, in order

to be safe for fish, dietary concentrations of

selenium should be less than 3 ug/g (ppm, dry

weight) [445]. USFWS: The toxic threshold for

selenium transferred to consumer species of

fish and wildlife is 3 mg/kg (ppm) [648].

The effects of dietary and waterborne selenium

on bluegill sunfish (Lepomis macrochirus) were

studied by Woock et al. (1987) [445].

Mortalities of adults were significant in both

30 ppm diet groups. 

Toxic effects have been documented in fish

consuming diets containing 10 to 33 mg/kg selenium,

concentrations similar to those in prey organisms

from selenium impacted habitats [481]. Dietary Semethionine is more toxic to fish than dietary

inorganic selenium [481].

Text in paragraph above reprinted with

permission from Environmental Toxicology and

Chemistry, Volume 12, J.M. Besser, T.J.

Canfield and T.W. La Point, "Bioaccumulation

of oganic and inorganic selenium in a

laboratory food chain." Copyright 1993 SETAC].

Aquatic sediments containing more than 3 ppm

selenium (dry weight) usually cause selenium levels

in benthic invertebrates to exceed safe

concentrations (3-5 ppm dry weight for fish and

wildlife that feed upon them (Dennis Lemly, Fish

and Wildlife Service, National Fisheries

Contaminant Research Center, personal communication

to Roy Irwin, 1991).

Ninety day survival of fish was reduced in fish fed

a diet containing > or = 9.6 ug of Se/g, and

reduced growth was noted in a diet containing > or
= 5.3 ug/g (ppm) [195].

Text in paragraph above reprinted with

permission from Environmental Toxicology and

Chemistry, Volume 9, S.J. Hamilton, K.J. Buhl,

N.L. Faerber, R.H. Wiedmeyer and F.A. Bullard,

"Toxicity of organic selenium in the diet to

chinook salmon." Copyright 1990 SETAC].

Reduced fish growth, whole-body concentrations of

selenium and survival were strongly correlated to

concentrations of selenium in diets (Hamilton,

1990) [445].

C) Body Burden Residues in Fish: Typical, Elevated, or of

Concern Related to the Well-being of the Organism Itself:

The toxic effect threshold of selenium for health

and reproduction is 4 mg/kg dry weight, whole body

[648]. 

In order to protect fish reproduction, their

skeletal muscles should not contain more than 5 ppm

and their organs (liver and gonads) should not

contain more than 10 ppm selenium (both

concentrations are for total selenium, dry weight)

(Wallenstrom, Aug 1986) [445].

An estimate of a no effect selenium concentration

in fish was a whole-body concentration of 1.1 mg/kg

wet weight [222]. This was the no effect level for

the fish itself, not predators which might be

eating many fish of the same species. A predator

protection level based on this data would therefore

have to be well below 1.1 mg/kg wet weight.

The geometric mean of whole-body (wet weight)

concentrations of fish in a 1980-1981 national

survey was 0.47 mg/kg [23]. A more recent (1976-

1984) NCBP survey report gave the national

geometric mean level for selenium in whole-body

fish as 0.42 mg/kg, the maximum level as 2.3 mg/kg,

and the 85th percentile level as 0.73 mg/kg wet

weight [384]. 

Whole body levels above 1.0 are not unusual in some

areas [488]. At polluted sites, selenium wholebody levels are often above 4.28 mg/kg dry weight

and liver (hepatic) levels are often above 6.7

mg/kg dry weight [488]. Normally, muscle contains

between 0.6 and 0.6 ppm and ovaries vary between

5.9 and 12.1 ppm dry weight [488].

The range of concentrations of selenium in a
studies of edible fish tissues in Pennsylvania in

1977 (included sites which were not especially

clean) was from ND to 3.34 mg/kg wwt [57].

Whole body concentrations of selenium in

mosquitofish from highly contaminated areas of

California were twice as high as the highest

reported liver concentrations from the literature

[488]. A North Carolina study of several species

of fish suggested the highest concentrations of

selenium were in the liver [488]. A separate

literature review that the liver of seleniumexposed fish accumulates higher levels of selenium

than skeletal muscles. However, selenium

concentrations in the liver typically correlate

with selenium concentrations in other tissues, even

though the distribution patterns within tissues, as

well as absolute values of selenium, vary

considerably with the species considered [488].

Some references state that selenium accumulates in

the axial muscles of fish, so fillet levels are

typically closer to whole-body concentrations than

are most other contaminants [27,136]. A more

recent, and somewhat contrasting summary documents

the tendency of selenium to concentrate more highly

in the liver, gonads, and kidneys of fish than in

muscle [488]. Selenium accumulates in the gonads

of bass and bluegills [36]. 

Sunfish exposed to aqueous selenium accumulate

selenium in the liver (7-27 ppm, wet weight) and

skeletal muscle, although the levels in skeletal

muscle are about half of those in the liver [488].

Selenium concentrations in muscle samples from

trout and dace from the Pecos River near Pecos

National Monument & Historical Park were 1.9 and

13.6 mg/kg wwt (Milford Fletcher, National Park

Service, Personal Communication). These two

samples were had higher concentrations of selenium

concentrations than the concentrations (0.29 to

1.41 mg/kg wwt) reported for trout collected

upstream in the Fish and Wildlife Service 1991

study of the Terrero Mine waste study area [479].

Two other Pecos River fish muscle samples had

selenium concentrations of <1.0 mg/kg (Milford

Fletcher, National Park Service, Personal

Communication).

An extremely high mean of 197 ppm dry weight was

reported for whole-body samples of mosquito fish

from a polluted area in California, a level so high

is it twice as high as the highest liver
concentrations previously published [488]. Some of

the high concentrations in mosquitofish from

polluted areas in California prompted one wag to

joke that letting the contaminated mosquitofish dry

out on a sidewalk would be creating a material

classified as a "hazardous waste."

The following text is quoted from the Trinity River

Report [201] for reference comparison with values

from other areas): 

Due to cost, we analyzed selenium in only 50

Trinity River samples. Selenium was found

above the detection limit (0.09 mg/kg) in all

but one sample. 

Gradient Monitoring Levels: The highest

concentration of selenium in 24 samples of

Trinity River mosquitofish was 0.52 mg/kg

(site 20). For contrast, mosquitofish from a

pond severely contaminated by agricultural

drainage at Kesterson National Wildlife Refuge

in California had selenium concentrations

ranging from 26 to 98 mg/kg [77,139].

Tis.Wildlife: Terrestrial and Aquatic Wildlife, Domestic

Animals and all Birds Whether Aquatic or not:

A) As Food: Concentrations or Doses of Concern to Living

Things Which Eat Wildlife, Domestic Animals, or Birds:

The following text is quoted from the Trinity River

Report [201] for reference comparison with values

from other areas: 

Predator Protection Level: The 0.5 mg/kg

predator protection level [20] was exceeded in

6 of 77 Trinity River samples. Included in

this group were samples of Mississippi map

turtles, mosquitofish, carp, spiny softshell

turtles, and unionid clams, all from sites

downstream of Dallas except for the

mosquitofish, which were from site 20. 

B) Concentrations or Doses of Concern in Food Items

Eaten by Wildlife, Birds, or Domestic Animals (Includes

LD50 Values Which do not Fit Well into Other Categories,

Includes Oral Doses Administered in Laboratory

Experiments):

See also [201] information in Tis.Wildlife, A)

above.
Oak Ridge National Lab, 1994: Risk Assessment

Screening Benchmarks for Wildlife derived from NoObserved-Adverse-Effect (NOAEL) levels (mg

contaminant per kg body weight per day). To be

considered unlikely to represent an ecological

risk, wet-weight field concentrations should be

below the following (right column) benchmarks for

each species present at the site [650]:

For CAS 7782-49-2, SELENIUM (AS SELENATE):

 NOAEL FOOD CONCENSPECIES (mg/kg/day) TRATION (ppm)

Mouse 0.07500 0.00000

 (test species) 

Short-tailed Shrew 0.09400 0.15700

Little Brown Bat 0.11900 0.35600

White-footed Mouse 0.08300 0.53800

Meadow Vole 0.06600 0.58200

Cottontail Rabbit 0.02200 0.11200

Mink 0.02400 0.17200

Red Fox 0.01400 0.14400

Whitetail Deer 0.00600 0.20200

Comment: Actually, the number of

significant figures for a benchmark value

should never be more than one; even if

these values have been taken directly

from another report, they should be

rounded; otherwise the impression is

given of a level of accuracy that is

simply unwarranted. The uncertainties are

too large to justify such a fine

distinction (Owen Hoffman, SENES Oak

Ridge, Personal Communication, 1997).

Skorupa et al. (Mar 1989) evaluated data developed

in both laboratory and field studies and estimated

that the maximum acceptable toxicant concentration

of dietary selenium for aquatic birds was 5.6 ppm,

dry weight [445]. 

In an attempt to reduce wildlife contamination

hazards, the California Department of Fish and Game

adopted a selenium standard for subsurface

agricultural drainage water evaporation ponds in

the San Joaquin Valley. The CDFG standard requires

initiation of special management actions (e.g.,

hazing) when the selenium concentration in a

composite sample of aquatic invertebrates from a

pond equals or exceeds 4 ppm, dry weight [445].

Selenium whole-body levels above 0.5 mg/kg are

considered harmful to fish and predators [20]. 
However, some more recent researchers have

concluded that harmful effects of selenium on

predators has seldom been documented for

concentrations below 3 mg/kg and often been

documented for concentrations above 30 mg/kg (the

"3/30 guideline", Jerry Miller, U.S. Bureau of

Reclamation, Salt Lake City, personal

communication, 1994).

USFWS: The toxic threshold for selenium transferred

to consumer species of fish and wildlife is 3 mg/kg

[648].

The toxic effect threshold of selenium for health

and reproduction is 4 mg/kg dry weight, whole body

[648]. Aquatic sediments containing more than 3

ppm selenium (dry weight) usually cause selenium

levels in benthic invertebrates to exceed safe

concentrations (3-5 ppm dry weight for fish and

wildlife that feed upon them (Dennis Lemly, Fish

and Wildlife Service, National Fisheries

Contaminant Research Center, personal

communication to Roy Irwin, 1991).

An estimate of a no effect selenium concentration

in fish was a whole-body concentration of 1.1 mg/kg

wet weight [222]. This was the no effect level for

the fish itself, not predators which might be

eating many fish of the same species. A predator

protection level based on this data would therefore

have to be well below 1.1 mg/kg wet weight.

Livestock foraging on plants containing about 25

ppm selenium suffer from alkali disease,

characterized by a lack of vitality, loss of hair,

sterility, atrophy of hooves, lameness, and anemia

[491].

Information from Moore [445]:

See Moore [445] for details on citations:

Smith et al. (1988) studied the effects of

dietary selenium-2 (as seleno-DL- methionine)

on black-crowned night-herons (Nycticorax

nycticorax). Thirteen and 23 days,

respectively, prior to egg laying, pairs of

adult herons were placed on 10 or 30 ppm (dry

weight) selenium-2 commercial diets

(containing 7-10% moisture). Birds on control

diets received 0.1 ppm selenium (dry weight).

Adults were necropsied after an average of 92

days on the test diets and hatchlings were

euthanized at three days of age. Biological
endpoints measured during the study included:

weight loss; reproductive success; eggshell

thickness; hatchling survival; and various

morphological, hematological, and biochemical

parameters.

Organ weights, hemoglobin concentrations,

hematocrits, egg fertility, eggshell

thickness, the Ratcliffe Index of eggshell

quality, and 72-hour hatchling survival were

unaffected in adults receiving either the 10

or 30 ppm selenium-2 diet. However, adult

herons fed the 30 ppm selenium-2 diet lost

significantly more weight than herons fed

other diets. Hatching success was not

different from controls, and teratogenesis was

not observed and hematology was unaffected in

embryos/hatchlings produced by adults fed the

10 ppm selenium-2 diet, however their

hatchlings did have significantly shorter

femur and radius-ulna lengths and

significantly higher liver malondialdehyde

concentrations.

Martin (1988) conducted four experiments to

assess the effects of selenium and boron on

avian reproduction. One experiment involved

feeding <1-year- old Japanese quail (Coturnix

japonica) laying ration control diets or such

diets supplemented with selenium+4 (as sodium

selenite), selenium-2 (as selenomethionine),

or boron (as sodium borate) to achieve the

following dietary concentrations: 10, or 15

ppm selenite; 5 or 8 ppm selenomethionine; or

25, 50, or 100 ppm borate (all values in dry

weight). In another experiment, fresh, fertile

Pekin duck eggs were injected with 0.1 ml of

saline solutio of the following concentrations

of selenium+4 (as sodium selenite): 0.0, 0.3,

0.4, 0.6, 0.8, 1.0, 1.4, 1.8, or 2.2 ppm. The

remaining experiments involved Single Comb

White Leghorn chickens (Gallus domesticus) in

dietary and egg-injection exposures to

selenium+4 (as sodium selenite), selenium-2

(as selenomethionine), and/or boron (as sodium

borate). In the chicken dietary study, hens

were fed either clean laying ration (control)

diets or such diets supplemented with selenium

and/or boron to achieve one of the following

concentrations: 12 ppm selenite, 12 ppm

selenite plus 500 ppm borate, 10 ppm

selenomethionine, or 10 ppm selenomethionine

plus 500 ppm borate (all values in dry

weight). In the chicken egg-injection study,
fresh, fertile eggs injected with one of the

following concentrations of selenium and/or

boron: 0.0, 0.6, 0.8, 1.0, 1.2, 1.4, 1.6, or

1.8 ppm selenite; 0.3, 0.5, or 1.0 ppm

selenomethionine; 0.0, 11.3, 15.8, 16, or 18.1

ppm borate; 1.8 ppm selenite plus 16 ppm

borate; or 0.5 ppm selenomethionine plus 16

ppm borate. Food and water were provided ad

libitum in all studies.

The results of the selenium tests, both singly

and in combination with boron, are discussed

herein. The independent results of boron are

discussed in boron subsection.

In the quail study, all concentrations of both

forms of selenium- supplemented diets resulted

in abnormal embryos, significantly reduced

hatchability of fertile eggs, and possibly

increased mortality. The percent hatchability

of eggs and the percent of abnormal embryos,

respectively, at each dietary concentration

were as follows: 15 ppm selenite, 25.6% and

70.3%; 10 ppm selenite, 10.2% and 83.9%; 7.5

ppm selenite, 65.6% and 8.8%; 8 ppm

selenomethionine, 10.4% and 66%; and 5 ppm

selenomethionine, 56.4% and 14%.

In the duck study, hatchability of fertile

eggs was significantly reduced at injected

selenite concentrations of >0.6 ppm. No

abnormal embryos were found in the control

eggs, however abnormal embryos were discovered

in all but one (0.4 ppm) of the selenite

treatment groups. Embryo abnormality and

mortality generally increased with increasing

concentrations of injected selenite.

In the dietary chicken study, egg production

generally decreased when birds were placed on

the treatment diets. Egg hatchability was

significantly reduced and abnormal embryos

were produced by all the treatment diets

except the selenite diet. The percent

hatchability of eggs and the percent of

abnormal embryos, respectively, at each

dietary concentration were as follows: 12 ppm

selenite, 84.9% and 0%; 12 ppm selenite plus

500 ppm borate, 51.9% and 14.9%; 10 ppm

selenomethionine, 23.2% and 33.8%; and 10 ppm

selenomethionine plus 500 ppm borate, 27.7%

and 25%. 

In the chicken egg-injection study, no
abnormal embryos were found in the control

groups; however, abnormal embryos were

produced by injecting >0.8 ppm

selenomethionine. Egg hatchability was

significantly reduced by injecting >1.8 ppm

selenite or >0.5 ppm selenomethionine.

Injections of borate with either selenite or

selenomethionine produced both abnormal

embryos and significantly reduced egg

hatchability.

Hoffman and Heinz (1988) reviewed the effects

on plasma biochemistry of dietary sodium

selenite and selenomethionine on mallard (Anas

platyrhynchos) hatchlings (see study by Heinz

et al., 1987). Plasma glutathionine

peroxidase activity was significantly

increased in mallards fed 5, 10, and 25 ppm

sodium selenite and those fed 10 ppm

selenomethionine. Mallards fed 25 ppm sodium

selenite also experienced increased

concentrations of plasma uric acid (an

indication of altered renal function) and

sorbitol dehydrogenase activity (an indication

of liver toxicity) was increased in birds fed

10 ppm selenomethionine.

Hoffman et al. (1989) studied the effects of

dietary selenium on the physiology of mallard

ducklings, specifically hepatic glutathione

metabolism and lipid peroxidation. One-dayold ducklings were provided with duck mash

diets (containing 7-9% moisture) with added

vitamin E and zinc, and supplemented with

selenium+4 (as sodium selenite) or selenium-2

(as seleno-ethionine), creating final dietary

selenium concentrations of 0.1, 10, 20, and 40

ppm. After six weeks, selenomethionine

accumulated to higher concentrations in the

liver and more strongly affected hepatic

glutathione metabolism and lipid peroxidation

than did selenite. The 20 and 40 ppm

selenomethionine diets significantly increased

the ratio of oxidized to reduced hepatic

glutathione and significantly increased

hepatic lipid peroxidation (as estimated by

malondialdehyde concentrations). The ratio of

oxidized to reduced hepatic glutathionine was

unaffected by the selenite diets; however, the

40 ppm selenite diet significantly increased

hepatic lipid peroxidation.

Heinz and Gold (1987) studied the behavior of

6-lard ducklings whose parents were fed diets
supplemented with selenium-2. Pairs of adult

mallards were fed a control diet or diets

supplemented with selenium-2 (as seleno-DLmethionine) to achieve final dry weight

concentrations of 1, 2, 4, or 8 ppm. The

adults received these diets beginning at least

four weeks prior to egg laying and ducklings

were fed untreated commercial duck starter

mash. Six days after hatching, ducklings were

exposed to a fright stimulus. The authors

determined that there were no significant

differences in response to the fright stimulus

among ducklings whose parents were fed the

control or selenium-laden diets.

Heinz et al. (1987) and Hoffman and Heinz

(1988) studied the effects of dietary

selenium+4 (as sodium selenite) and selenium-2

(as seleno-DL-methionine) on adult mallards

and their young. Beginning at least four

weeks prior to the laying of the first eggs,

mallard pairs were fed commercial duck mash

diets (with 7-10% moisture) nominally

containing: 0 ppm selenium (the control

diet); 1, 5, 10, 25, or 100 ppm selenium+4; or

10 ppm selenium-2. Ducklings were reared on

duck mash diets containing the same selenium

concentrations as in their parents' diets.

Most adults were killed following laying of

all 31 eggs needed for the study and surviving

ducklings were killed at three weeks of age.

Biological endpoints measured during the study

included: adult survival; weights of adults,

eggs, and hatchlings; eggshell quality; egg

fertility; hatching success of fertile eggs;

and number of 21-day-old hatchlings produced

and hatchling survival to 21 days.

Percent fertility, hatching success of fertile

eggs, and weights of eggs laid were not

significantly different among treatment

groups. Adults fed 100 ppm selenium+4

experienced significant weight loss and

mortality and produced eggs prior to death.

Adults fed 25 ppm selenium+4: experienced

significant weight loss; produced 44% fewer

eggs that hatched; produced smaller embryos

and ducklings, and a significantly lower

percentage and number of ducklings that

survived to 21 days of age; produced a

significant percentage of abnormal embryos

(22.2%); and produced poorer quality

eggshells. Adults fed 10 ppm selenium+4

produced a significant percentage of abnormal
embryos (11.2%). Adults fed 10 ppm

selenomethionine: produced 40% fewer eggs

that hatched; produced a significantly lower

percentage and number of ducklings that

survived to 21 days of age; and produced a

significant percentage of abnormal embryos

(18.3%), many more of which (a total of 13.1%)

were teratogenic than those abnormalities

produced in the selenite treatment groups.

The effects of two seleno-amino acids in the

diets of mallard ducks were studied by Heinz

et al. (1989) and Hoffman and Heinz (1988).

Beginning three weeks prior to pairing and

continuing through egg laying, adult mallards

were fed duck mash diets (containing ~10%

moisture) supplemented with seleno-DLmethionine or seleno-DL-cystine to achieve

final dietary concentrations of 0.1-0.2, 1, 2,

4, 8, or 16 ppm selenomethionine or 16 ppm

selenocystine. Adult ducks were sacrificed

after laying all eggs needed for the study.

Hatchlings were fed clean duck mash diets for

six days, after which they were sacrificed.

Adult mallards on the test diets experienced

no mortality nor did they show other signs of

selenium toxicity. Neither did the test diets

affect the initiation or rate of egg laying,

the fertility of eggs, egg weights or eggshell

thickness, or hatchling weights or sex ratio.

However, after three weeks on both of the 16

ppm diets (at the time of pairing), adult

females experienced significant, temporary

weight loss, and hatching success of fertile

eggs produced by hens on the 16 ppm

selenomethionine diet was significantly

reduced. Hens fed the 8 or 16 ppm

selenomethionine diets produced a

significantly higher percentage of malformed

embryos (6.8% and 67.9%, respectively),

produced fewer eggs that hatched (totals of

64% and 11%, respectively), and significantly

lower numbers and percent survival (81% and

0%, respectively) among 6-day-old ducklings.

Weights of surviving 6-day-old ducklings were

also significantly less in the 8 ppm

selenomethionine dietary group.

In review of the embryotoxic effects found in

the above-two studies, Hoffman and Heinz

(1988) noted that although the percent of

abnormal embryos (including those exhibiting

edema and/or stunted growth) was similar, the

frequency of teratogenesis (including multiple
malformations) among mallards fed

selenomethionine was significantly higher than

among those fed sodium selenite. The authors

suggested that the increased embryotoxic

effects associated with selenomethionine might

have been related to its much greater

accumulation in mallard eggs.

Heinz et al. (1988) also studied the toxicity

of dietary selenium+4 and selenium-2 to

mallard ducklings. For six weeks, one-day-old

ducklings were provided with duck mash diets

(containing 7-9% moisture) supplemented with

selenium+4 (as sodium selenite) or selenium-2

(as selenomethionine), creating final dietary

selenium concentrations of 0.1, 10, 20, 40,

and 80 ppm. Variables measured during the

study included food consumption, accumulation

of selenium in the liver, organ and body

weights, primary feather and tarsus lengths,

and mortality. Other than enlarged livers

associated with the selenite diet, neither of

the 10 ppm diets produced significant effects.

All of the 20, 40, and 80 ppm diets

significantly reduced food consumption and

growth. Mortality was 25% and 12.5% in the 40

ppm selenite and selenomethionine diets,

respectively, and equaled or approached 100%

in both of the 80 ppm diets. The authors

noted that mortality may have been influenced

by reduced consumption of food. There

appeared to be little relationship between

liver selenium concentrations and mortality.

The authors also noted that survival and

growth of ducklings were less sensitive to

dietary selenium than was reproduction among

mallards.

The USFWS-PWRC (Jan 1989) conducted two sets

of dietary selenium-2 studies with mallards to

assess the effects of overwintering in a

selenium- contaminated environment. Adult

male mallards were fed selenomethionineenriched mash diets (containing the following

nominal selenium concentrations: 0 [control],

10, 20, 40, or 80 ppm) for 16 weeks, followed

by 16 weeks on selenium-free diets. Adult

female mallards were exposed to 15 ppm

selenomethionine diets for 21 weeks.

Preliminary results of the male dietary study

reveal that: weight and survival were

unaffected in birds receiving the 10 ppm diet,

the 20 ppm diet caused some mortality, and all
birds exposed to the 80 ppm diet died. Once

removed from the seleniferous diet, weights of

surviving birds returned to normal. In the

female dietary study, preliminary results

reveal that reproductive impairment was

experienced by birds laying eggs within two

weeks after cessation of the seleniferous

diet. No such effects were evident after that

time.

The USFWS-PWRC (Jan 1990; Jan 1989; Jan 1988)

studied the interactive effects of three trace

elements and nutrition on mallard ducklings.

Various concentrations of arsenic+5 (as sodium

arsenate), boron (as boric acid), and/or

selenium-2 (as seleno-DL-methionine) were

added to ducklings' diets containing low (7%)

or normal (21%) amounts of protein. Two

separate sets of tests were conducted over 4

weeks. In the first, six groups of ducklings

were fed diets containing both levels of

protein, and arsenic+5 and selenium-2, singly

and in combination. In the second experiment,

six groups of ducklings were fed diets

containing both levels of protein, and boron

and selenium-2, singly and in combination.

The effects of selenium and both dietary

levels of protein are discussed here. The

interactive effects of selenium with arsenic

and selenium with boron are discussed in

subsections 3.5 ("Arsenic") and 3.6 ("Boron"),

respectively. Ducklings exposed to the lowprotein diet or the diet containing 60 ppm

selenium-2 experienced a reduced growth rate.

The combination of these diets caused hepatic

histological lesions and 100% mortality. When

exposed to a diet containing a normal level of

protein and 60 ppm selenium-2, ducklings

experienced hepatic histological lesions and

40% or 50% mortality. Ducklings were not

killed, but their growth was reduced when they

were fed diets containing 15 ppm selenium-2

and the low level of protein. These

preliminary results suggest that low-protein

diets can exacerbate the toxic effects on

mallard ducklings of dietary exposure to

selenium-2.

In another study, independent and interactive

effects of dietary boron and selenium-2 on

mallard reproduction were tested using a 3x3

replicated factorial design (Smith and Heinz,

Mar 1990; USFWS-PWRC, Jan 1988). The 9 diets

contained either no boron or selenium
(control), or boron (as boric acid) in

concentrations of 450 or 900 ppm, and/or

selenium-2 (as seleno-DL- methionine) in

concentrations of 3.5 or 7.0 ppm (all dry

weight concentrations). Adults were provided

the test diets prior to pairing and were

maintained on those diets until sacrificed.

Ducklings received the same dietary

concentrations of boron and/or selenium-2 as

their parents. All birds were sacrificed 14

days post hatch. The independent effects of

selenium-2 are discussed here and its effects

in combination with boron in subsection 3.6

("Boron").

None of the selenium-2 test diets had any

effects on egg size or weight. Hatching

success of fertile eggs was decreased to ~60%

of the control value by the 7.0 ppm selenium-2

diet. Early embryonic survival (0-7 days) was

not affected by dietary selenium-2

concentrations in this study; however, late

embryonic survival (day 8 to hatch) was

different among treatment groups. Embryo

mortality was 49% in the group receiving 7.0

ppm selenium-2.

Raabe et al. (Sep 1988) studied the acute

biological effects of inhaled dimethyl

selenide, about which very little is known.

Young-adult male Fisher-344 rats were exposed

to one of four airborne concentrations (0,

1,607, 4,499, or 8,034 ppm) of dimethyl

selenide for one hour. Significant changes

occurring one day following exposure to the

selenium gas included: inflammation of lungs

and/or liver; and changes in protein, RNA,

and/or DNA content in lungs and/or liver.

Spleen protein and RNA content of rats exposed

to the highest concentration of dimethyl

selenide were significantly elevated one week

following exposure. No other adverse effects

were observed during the 7-day study and, with

the exception of biochemical changes in the

spleen of rats exposed to 8,034 ppm selenium

gas, all organs of all rats recovered

completely by seven days post exposure. The

authors determined that (in acute exposures),

"...inhaled dimethylselenide vapor is

relatively nontoxic in rats."

C) Body Burden Residues in Wildlife, Birds, or Domestic

Animals: Typical, Elevated, or of Concern Related to the

Well-being of the Organism Itself:
The following text is quoted from the Trinity River

Report [201] for reference comparison with values

from other areas: 

The selenium level in one composite sample of

softshell turtles from the Rio Grande River at

Big Bend National Park was 0.64 mg/kg [65].

This level is somewhat higher than those (0.26

to 0.43 mg/kg) found in softshell turtles from

three sites (1, 15, 18) on the upper Trinity

River. However, it is about the same (0.67

mg/kg) as the concentration recorded for a

sample from highly polluted site 11 just

downstream of Dallas.

Tis.Human:

A) Typical Concentrations in Human Food Survey Items:

No information found.

B) Concentrations or Doses of Concern in Food Items

Eaten by Humans (Includes Allowable Tolerances in Human

Food, FDA, State and Standards of Other Countries):

Crit. Dose: 0.015 mg/kg-day [Study 1 NOAEL] UF: 3

MF: 1 [893].

RfD: 5E-3 mg/kg-day Confidence: High [893,952]. 

C) Body Burden Residues in Humans: Typical, Elevated, or

of Concern Related to the Well-being of Humans:

 Milk Concentrations [940]:

The mean value for selenium in human milk has been

reported to be 0.018 ppm with a range of 0.007 to

0.033 ppm. [Wilber CG; Clin Toxicol 17 (2): 171-

230 (1980)].

Tis.Misc. (Other Tissue Information):

A number of plants have been described as indicators of

higher-than-normal concentrations of this element in the

soil [951]. Toxicity to plants is moderate [951].

Monogastric (non-ruminant) animals more readily absorb

dietary selenium+4 than do ruminants [445].

 Liver References to Selenium: 

NOTE: many of these references are listed elsewhere

in this document as well, but are split out here
separately for those just interested in liver

issues. 

Whole body concentrations of selenium in

mosquitofish from highly contaminated areas of

California were twice as high as the highest

reported liver concentrations from the literature

[488]. A North Carolina study of several species

of fish suggested the highest concentrations of

selenium were in the liver [488]. A separate

literature review that the liver of seleniumexposed fish accumulates higher levels of selenium

than skeletal muscles. However, selenium

concentrations in the liver typically correlate

with selenium concentrations in other tissues, even

though the distribution patterns within tissues, as

well as absolute values of selenium, vary

considerably with the species considered [488].

Sunfish exposed to aqueous selenium accumulate

selenium in the liver (7-27 ppm, wet weight) and

skeletal muscle, although the levels in skeletal

muscle are about half of those in the liver [488].

Those fish accumulating the highest levels of

selenium in the liver have the lowest hematocrits,

lowest hemoglobin levels, lowest erythrocyte

numbers, abnormally small and irregularly shaped

erythrocytes, and reductions in both mean

corpuscular volumes and mean corpuscular hemoglobin

concentrations [488]. Green sunfish with the

highest levels of selenium in the liver have

pericarditis and myocarditis [488].

Se can either help cause or help protect against

such things as liver damage [445,484.486,488].

Selenium has been associated with abnormal

development of and damage to/degeneration of

internal organs, including the heart, liver, and

kidneys [445].

Se...possibly helpful in preventing skin, liver,

and pancreas cancer [484,486].

Some references state that selenium accumulates in

the axial muscles of fish, so fillet levels are

typically closer to whole-body concentrations than

are most other contaminants [27,136]. A more

recent, and somewhat contrasting summary documents

the tendency of selenium to concentrate more highly

in the liver, gonads, and kidneys of fish than in

muscle [488]. Selenium accumulates in the gonads

of bass and bluegills [36]. 
At Kesterson NWR, in order to protect fish

reproduction, their skeletal muscles should not

contain more than 5 ppm and their organs (liver and

gonads) should not contain more than 10 ppm

selenium (both concentrations are for total

selenium, dry weight) (Wallenstrom, Aug 1986)

[445]. 

The rate of absorption as elemental selenium ... Is

low. ... Liver & kidney are principal sites of

deposition. Excretion of selenium is by urine,

feces, sweat, & breath. [Clayton, G. D. and F. E.

Clayton (eds.). Patty's Industrial Hygiene and

Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed.

New York: John Wiley Sons, 1981-1982. 2130][366]

 Liver and kidney contained the highest

concentrations of most metals (in rats) [366].

In the liver, many selenium compounds are

biotransformed to excretable metabolites.

Identified metabolites are trimethylselenide in

urine and dimethylselenide in breath. /Selenium

compounds/[Friberg, L., Nordberg, G.F., Kessler, E.

and Vouk, V.B. (eds). Handbook of the Toxicology of

Metals. 2nd ed. Vols I, II.: Amsterdam: Elsevier

Science Publishers B.V., 1986.,p. V2

Heinz et al. (1990) calculated that mallards fed

selenium- enriched diets (10 ppm seleno-DLmethionine) accumulated 95% of peak selenium

concentrations in liver and breast muscle in 7.8

and 81 days, respectively [445].

Selenium in living tissue is often found associated

with protein. This is because some proteins

(including enzymes) require selenium and selenium

can readily substitute for sulfur in some sulfuramino acids such as cysteine, cystine, and

methionine (amino acids are the building blocks of

proteins). In plants, selenium accumulates in seeds

(Burau, Jul-Aug 1985). Chronic exposure of animals

to selenium causes accumulation in the following

tissues: liver, kidneys, pancreas, spleen, heart,

lungs, ovaries, testes, gills, brain, and blood

(NRC-Subcommittee on Selenium, 1976; Eisler, Oct

1985; Gillespie et al., 1988; Maier et al., 1987;

Ogle et al., 1988; USEPA, Sep 1987) [445].

In studies with mallards first fed then removed

from highly selenium- enriched diets (up to 160 ppm

seleno-DL-methionine), Heinz et al. (1990) found

that one-half of the selenium was lost from blood

and breast muscle tissues in 9.8 and 23.9 days,
respectively. In the liver, selenium was initially

lost rapidly and then more slowly. Selenium

concentrations in blood, breast muscle, and liver

tissues were predicted to return to background

levels in 58.4, 120.4, and 161.8 days, respectively

[445].

There appeared to be little relationship between

liver selenium concentrations and mortality. The

authors also noted that survival and growth of

ducklings were less sensitive to dietary selenium

than was reproduction among mallards [445].

Hamilton et al. (1990) suggest that, in order to be

safe for fish, dietary concentrations of selenium

should be less than 3 ug/g (ppm, dry weight) [445].

Liver enlargement was noted for many species of

fish exposed to selenium [488].

Bio.Detail: Detailed Information on Bioconcentration,

Biomagnification, or Bioavailability:

Preliminary data suggests the potential for bioaccumulation or

bioconcentration of selenium is moderate for the following biota:

mammals, birds, and fish. It appears to be high to very high for

higher plants and low or limited for mollusks, crustacea, lower

animals, mosses, lichens, and algae [83]. The best potential

mediums for biological monitoring (including gradient monitoring)

appear to include higher plants [83].

Plants easily take up selenate compounds from water and change

them to organic selenium compounds such as selenomethionine (a

transparent solid in pure form) [953]. 

Bioaccumulation of selenate can be diminished in the presence

of chromate, molybdate, sulfate, and selenomethionine [445]. One

rodent study suggested that more selenium is accumulated if methyl

mercury is present. Selenium accumulation in all organs (especially

the kidney) was accelerated (8-fold increase in 41 days in the

kidneys) in rats treated with mercury and selenium [488].

Some references state that selenium accumulates in the axial

muscles of fish, so fillet levels are typically closer to wholebody concentrations than are most other contaminants [27,136]. A

more recent, and somewhat contrasting summary documents the

tendency of selenium to concentrate more highly in the liver,

gonads, and kidneys of fish than in muscle [488]. Selenium

accumulates in the gonads of bass and bluegills [36]. 

A nationwide study of selenium in bivalves showed less

variation in levels from various stations than was found for most

other contaminants [62].

Laboratory aquatic microcosm experiments have clearly

demonstrated that the bioconcentration potential of selected

organic selenium compounds, including selenomethionine, is much

greater than for common inorganic selenium forms such as selenate
and selenite [445]. This is especially true at very low

waterborne concentrations [445]. Specifically, the USFWS-NFCRC

(Dec 1989) conducted microcosm experiments with algae

(Chlamydomonas reinhardtii) and daphnids (Daphnia magna) and

discovered that bioconcentration factors for dissolved

selenomethionine were much greater than for selenite, which were

greater than for selenate [445]. Besser et al. (1989) discovered

that algae and daphnia exposed to waterborne selenomethionine in

microcosms for 28 days accumulated tissue concentrations of

selenium tens of thousands of times greater than those in the water

[445]. In light of the high toxicity of dietary selenomethionine

to fish and wildlife, the speciation of waterborne selenium may be

more important in determining safe levels than the concentration of

total selenium [445].

Research in progress indicates that the specific form of

selenium is critical in determining the potential for the

occurrence of selenium toxicity because amino forms of selenium may

bioconcentrate to toxic levels in fish and birds even when

concentrations in water are less than 1 microgram per liter (ppb)

[463]. 

Due to bioconcentration concerns, the State of California

water quality criteria based on protection of aquatic organisms in

the food chain was quite low, only 0.9 ug/L for impounded waters

(versus 11 ug/L for flowing waters) [222].

The mean elemental concentration of this metal in plants was

0.1 ppm in the same areas where rocks were 1 ppm [951].

Bioconcentration factors (BCFs) estimated from 1 ug/L (ppb)

selenium as Se-methionine exposures were approximately 16,000 for

algae, 200,000 for daphnids, and 5,000 for bluegills [481]. Algae

and daphnids concentrated Se more strongly from selenite (BCFs of

220 to 3,600) than selenate (BCFs 65 to 500), while bluegills

concentrate se about equally from both species [481]. Daphnids in

aqueous selenium exposures may be accumulating a portion of their

selenium body burdens via ingestion of selenium enriched algae

[481]. Bluegills in Se-contaminated systems accumulate inorganic

Se species primarily via food chain uptake, although organoselenium

compounds such as Se-methionine may contribute significantly to Se

bioaccumulation by bluegills via both aqueous and food-chain uptake

[481].

Text in paragraph above reprinted with permission from

Environmental Toxicology and Chemistry, Volume 12, J.M.

Besser, T.J. Canfield and T.W. La Point, "Bioaccumulation of

oganic and inorganic selenium in a laboratory food chain."

Copyright 1993 SETAC].

 Misc. Notes Related to Selenium Bioavailability in Soils:

In areas of acid or neutral soils, the amount of biologically

available selenium should steadily decline. The decline may be

accelerated by active agricultural or industrial practices. In

dry areas with alkaline soils and oxidizing conditions,

elemental selenium and selenides in rocks and volcanic soils

may oxidize sufficiently to maintain the availability of
biologically active selenium. 

In areas of the Western United States (states west of and

including North Dakota, South Dakota, Nebraska, Kansas,

Oklahoma, and Texas), where geological sources of selenium are

abundant in the soil profile, selenium tends to be more

bioavailable to ecosystems [463]:

A major feature of this area is the presence of pedocal

soils. Pedocals are alkaline soils of semiarid and arid

climates. Bacterial and chemical processes in these

highly oxidizing, alkaline soils favor the formation of

calcium and sodium selenates, which are very mobile and

water soluble, and are readily available forms of

selenium to plants. In addition, many areas in the

Western United States are prone to selenium enrichment of

the soil because of leaching of underlying seleniferous

rocks, such as the shales and clays of the Upper

Cretaceous Pierre, Steele, and Niobrara Shales [463].

Pedalfer soils found in the Eastern United States are

acid to neutral soils of humid and semihumid climates.

These acid soils favor the formation of more reduced and

complexed forms of selenium, such as ferric selenite.

These complexes are generally insoluble so as to reduce

selenium bioavailability to the point that forages and

feeds grown in the Eastern United States contain

insufficient selenium for proper animal nutrition [463].

In short, in areas in the Western United States where

selenium is abundant and bioavailable, a more detailed

analysis may be required for selenium toxicity than would

be required in the east [463].

Bioaccumulation [445]: 

See Moore et al. [445] for literature citation details:

Selenate is readily accumulated by terrestrial plants.

In contrast, many aquatic organisms more readily take up,

accumulate, and metabolize selenomethionine and selenite

(Besser et al., 1989; Ogle et al., 1988). Within these

organisms, selenium is biochemically reduced to elemental

selenium and selenide forms, including methylated

selenium compounds and seleno-amino acids.

Bioaccumulation of selenate can be diminished in the

presence of chromate, molybdate, sulfate, and

selenomethionine.

Some plants, selenium accumulators, can take up and

accumulate very high concentrations of selenium in their

tissues (over 1,000 ppm) without injurious effects.

Primary or obligate selenium accumulators grow only where

soil selenium concentrations are high enough to satisfy
metabolic needs and include many species of Astragalus

and some species of Brassica, Haplopappus,

Machaeranthera, Oonopsis, and Stanleya, and Zylorhiza.

Secondary or facultative selenium accumulators can

tolerate, but do not require elevated soil selenium

concentrations. Facultative selenium accumulators

include many species of Aster and some species of

Astragalus, Atriplex, Castelleja, Comandra, Grayia,

Grindelia, Gutierrezia, Machaeranthera, and Mentzelia.

Selenium can also be bioconcentrated by a large number of

aquatic plants and animals that form the bases for

important fish and wildlife food chains. Hamilton et al.

(1990) note that algae and zooplankton can accumulate

selenium in tissues to concentrations several-hundred

times those found in water. The USFWS-NFCRC (Dec 1989)

conducted microcosm experiments with algae (Chlamydomonas

reinhardtii) and daphnids (Daphnia magna) and discovered

that bioconcentration factors for dissolved

selenomethionine were much greater than for selenite,

which were greater than for selenate. Besser et al.

(1989) discovered that algae and daphnia exposed to

waterborne selenomethionine in microcosms for 28 days

accumulated tissue concentrations of selenium tens of

thousands of times greater than those in the water.

According to Lemly (1989), bioconcentration factors for

aquatic plants and animals exposed to 5-30 ug/l (ppb)

waterborne selenium typically range from 500 to 35,000.

Using both field-collected and laboratory data, DuBowy

(1989) developed an energy-based selenium bioaccumulation

model for aquatic birds that he used to calculate a

bioaccumulation factor of 1,430 for waterfowl (ratio of

wet weight concentration of selenium in breast muscle

tissue to selenium concentration in water).

Bioconcentration factors in aquatic systems are

especially high when selenium occurs at very low

waterborne concentrations.

Although opinions are mixed, there is some evidence that

selenium can also biomagnify through the food chain Lemly

(1989) noted that biomagnification factors (between foodchain trophic levels) for 5-30 ug/l (ppb) waterborne

selenium in aquatic systems typically range from 3 to 7

times.

Selenium in the diet constitutes the most important

source for uptake in animals (Lemly, 1986; Lemly and

Smith, 1987). Although data are lacking, selenium in

natural diets most likely occurs primarily in organic

forms (Demayo et al., 1979b; Maier et al., 1987; NRCSubcommittee on Selenium, 1976). Selenomethionine may be

the dominant form of selenium in plant tissues and

selenocysteine may dominant in animal tissues (USFWSPWRC, Jan 1990). Dietary and possibly waterborne organic
selenium compounds (such as selenomethionine) are more

effectively and quickly taken up, accumulate to higher

concentrations, and are retained longer by animals than

are inorganic forms of selenium (Besser et al., 1989;

Burau, Jul-Aug 1985; Davis et al., Jan-Feb 1988; Heinz et

al., 1988; NRC-Subcommittee on Selenium, 1976; Ogle et

al., 1988). Heinz et al. (1990) calculated that mallards

fed selenium- enriched diets (10 ppm seleno-DLmethionine) accumulated 95% of peak selenium

concentrations in liver and breast muscle in 7.8 and 81

days, respectively.

Selenium absorption in the gastrointestinal tract is

dependent on a variety of factors, including: its

chemical form(s) (e.g., fish take up selenomethionine

through the gastrointestinal tract more readily than

either selenium+4 or selenium+6 [USEPA, Sep 1987]); the

animal's nutritional (protein) status; and whether or not

the animal is a ruminant (monogastric [nonruminant]

animals more readily absorb dietary selenium+4 than do

ruminants) (NRC-Subcommittee on Selenium, 1976). In

dietary selenium studies with Atlantic salmon smolts

(Salmo salar), Bell and Cowey (1989) found the

digestibility of DL-selenomethionine to be better than

selenium+4 (as sodium selenite), which was more easily

digested than was DL- selenocystine.

Selenium in living tissue is often found associated with

protein. This is because some proteins (including

enzymes) require selenium and selenium can readily

substitute for sulfur in some sulfur-amino acids such as

cysteine, cystine, and methionine (amino acids are the

building blocks of proteins). In plants, selenium

accumulates in seeds (Burau, Jul-Aug 1985). Chronic

exposure of animals to selenium causes accumulation in

the following tissues: liver, kidneys, pancreas, spleen,

heart, lungs, ovaries, testes, gills, brain, and blood

(NRC-Subcommittee on Selenium, 1976; Eisler, Oct 1985;

Gillespie et al., 1988; Maier et al., 1987; Ogle et al.,

1988; USEPA, Sep 1987).

Selenium loss (depuration) in animals occurs through

urination, exhalation, perspiration, and with feces and

milk. Urination is commonly the most important

depuration mechanism; however, at higher selenium

intakes, large quantities of volatile selenium can also

be lost through exhalation (Demayo et al., 1979b).

Selenium is excreted in urine as the trimethyl selenonium

ion and in feces as either elemental selenium or a metal

selenide (NRC- Subcommittee on Selenium, 1976).

Inorganic selenium is lost more rapidly by some species

than is organic selenium (Maier et al., 1987).

In studies with mallards first fed then removed from
highly selenium- enriched diets (up to 160 ppm seleno-DLmethionine), Heinz et al. (1990) found that one-half of

the selenium was lost from blood and breast muscle

tissues in 9.8 and 23.9 days, respectively. In the

liver, selenium was initially lost rapidly and then more

slowly. Selenium concentrations in blood, breast muscle,

and liver tissues were predicted to return to background

levels in 58.4, 120.4, and 161.8 days, respectively.

Eisler (Oct 1985) and Ohlendorf and Skorupa (1989)

provide tissue selenium concentrations for fish and

wildlife collected from both seleniferous and

uncontaminated environments.

Williams (Dec 1988) conducted a 96-hour study of the

effects of various concentrations of waterborne

selenium+6 (as sodium selenate [Na2SeO4]) and sulfate (as

sodium sulfate [Na2SO4]) on bioaccumulation and growth of

green algae (Selenastrum capricornutum). Selenium in the

test solutions also included modest amounts of selenite

and organoselenium (~4% and <6%, respectively). Test

solutions contained the following average concentrations

and approximate molar ratios (in parentheses) of selenate

(in ug/l [ppb]) and sulfate-sulfur ([SO4-S] in mg/l

[ppm]), respectively: 107 and 3.34 (1:75), 11.3 and 3.34

(1:750), 107 and 33.2 (1:750), and 11.3 and 33.2

(1:7,000). Separate algal growth tests (controls) were

conducted in waters containing 3.34 or 33.2 mg/l (ppm)

sulfate-sulfur with no additions of selenium. Algae were

cultured in modified Woods Hole media, with reduced

concentrations of magnesium sulfate (MgSO4; to 3.34 mg/l

S [ppm]), increased concentrations of magnesium carbonate

(MgCO3; to 3.65 mg/l Mg [ppm]), and no tris buffer or

EDTA [445]. More detail:

Increasing concentrations of sulfate, while

maintaining concentrations of selenate and

increasing ratios of sulfate to selenate

concentrations, both resulted in reduced

bioaccumulation of selenium by the algae. Algal

growth was reduced over the two controls in all

four selenium test waters and growth reductions

increased with increasing concentrations of

selenium in tissues. Of the four test waters, the

greatest growth occurred in the high sulfate - low

selenate solutions [445].

Interactions:

Under some circumstances, selenium may interact in an

antagonistic or protective manner with arsenic, cadmium, copper,

lead, mercury, silver, thallium, zinc, and the herbicide paraquat

[445]. Another reference stated that selenium can serve as an
antidote to the toxic effects of metals such as arsenic, mercury,

cadmium, copper, and thallium [491].

Bioaccumulation of selenate can be diminished in the presence

of chromate, molybdate, sulfate, and selenomethionine [445]. It

has also been noted that selenium toxicity can be reduced through

the administration of methionine and vitamin E [445]. These

interactions, however, are dependent upon the specific forms of the

chemicals involved, and mixing different forms of the same

chemicals can sometimes have the opposite effects [445]. For

example, dietary sulfate, which can have a protective effect on

selenate toxicity, does not affect the toxicity of selenite or

organoselenium. Dimethyl selenide (normally not very toxic) has a

synergistic effect with some mercuric salts, and although drinking

water containing arsenic can ameliorate the toxic effects of

dietary selenium, their toxic effects can be additive when provided

together in drinking water [445].

One study revealed the inhibitory effect of sodium selenite on

induction of bladder cancer by butylbutanolnitrosamine in rats. The

incidence of carcinoma in the control group was 87.5% whereas in

the sodium selenite group--50% (P less than 0.01) (Frolov AG, 1990.

The effect of sodium selenite on the butyl butanol nitrosamine

induction of bladder tumors in rats. Original title: Vliianie

natriia selenita na induktsiiu butilbutanolnitrozaminom opukholei

mochevogo puzyria u krys. Vopr-Onkol; 1990; 36(6); P 697-700

(Russian).

Interactions between Selenium and Mercury:

NOTE: Some of the interactions between selenium

and mercury were mentioned in the Brief

Introduction above. These are important enough

that they are repeated here with additional

information:

Selenium, like mercury, has many interactions with sulfur

compounds. This affinity for sulfur compounds may

account for some of the many synergistic and antagonistic

interactions between mercury and selenium (see details

below). Also like mercury, selenium chemistry,

transformations, and interactions with other contaminants

are complex. In fact, selenium is one of the most

complex elements in these regards. Due to these

complexities, generalizations about selenium should be

approached with caution.

Antagonism/Synergism: Four studies have suggested that

the presence of selenium reduces the toxicity of (is

antagonistic to) mercury (Hg), cadmium (Cd), arsenic

(As), and silver (Ag) [488]. The exact mechanism of

action for selenium induced protective effects of

vertebrates has not been elucidated [488]. Sorenson

(1991) suggested caution in attempting to use selenium

supplementation to decrease the severity of point-source

mercury contamination, since synergistic interactions
have also been observed, and since synergistic

interactions on even a single life stage (as demonstrated

on carp by Huckabee and Griffith) have a potential of

eliminating an entire population of fish [488]. Although

selenium and mercury interacted synergistically rather

than in an antagonistic (protective) fashion, the author

of the study which showed synergistic effects cautions

that it was an early lab study and should not totally

override all later field studies (John Huckabee, Electric

Power Institute, personal communication, 1994). 

Nevertheless, most mercury and selenium experts suggest

caution in using selenium to treat surface waters in an

effort to reduce mercury problems, since there is such a

small safety window between too little and too much

selenium. Interactions are known to be concentration

(dose) dependent [488]. Interactions between Se and

mercury can be synergistic at low aqueous mercury

concentrations (< or = 0.07 ppm) and antagonistic at high

mercury levels (> or = 0.10 ppm) and high selenium levels

[488]. In Sweden, selenium supplementation was tried as

a remedy for mercury problems in lakes and some reduced

mercury concentrations seemed to be the result; however,

too much selenium was eventually used and negative

effects on fish reproduction was eventually seen (John

Rudd, Freshwater Research Institute, Winnipeg, Manitoba,

personal communication, 1994). Moderate selenium

toxicity to adult fish may be irrelevant if the larval

fish are much more sensitive to selenium toxicity and

thus the fish do not make it to adulthood.

One rodent study suggested that more selenium is

accumulated if methyl mercury is present. Selenium

accumulation in all organs (especially the kidney) was

accelerated (8-fold increase in 41 days in the kidneys)

in rats treated with mercury and selenium [488].

Selenium has been referred to as an agent which can bind

mercury and cadmium compounds to make them more

biologically inert, as a protective agent against mercury

induced lipid peroxidation, as an element which can

detoxify various metals by chelating them [484,486].

Under some circumstances, selenium may interact in an

antagonistic or protective manner with mercury and

several other contaminants [445]. Some contaminants

specialists who have looked at some of the human health

and animal husbandry literature have wondered whether or

not slight elevations of some forms of selenium in fish

tissues may possibly be acting partly in a protective

manner (to a greater degree than is commonly recognized)

to humans and fish and wildlife predators consuming fish

contaminated with harmful concentrations of heavy metals

such as cadmium, mercury, and lead (Jerry Miller, U.S.
Bureau of Reclamation, Salt Lake City, personal

communication, 1994). However, care should be taken in

generalizing, and the many risks associated with

bioconcentration, reproductive risk, and other potential

risks of selenium cannot be ignored.

Dietary sulfate, which can have a protective effect on

selenate toxicity, does not affect the toxicity of

selenite or organoselenium; dimethyl selenide (normally

not very toxic) has a synergistic effect with some

mercuric salts; and although drinking water containing

arsenic can ameliorate the toxic effects of dietary

selenium, their toxic effects can be additive when

provided together in drinking water [445].

Metal selenides are formed with cadmium, copper, and

mercury. Many organic selenides also are common [445].

Gary Heinz and Dave Hoffman of the Patuxent Fish and

Wildlife Research Center in Laurel, MD, believe that, as

of November 1993, there is usually not enough data

available to tell exactly what various combinations of

various forms of selenium and mercury mean as body

burdens in various life stages of waterfowl. Organic

selenium (typically organoselenium compounds such as Semethionine) combined with organic mercury (typically

methyl mercury) appears to be the most dangerous

combination, but not all research has used these two.

Some workers have suggested that a ratio of one mole of

selenium/one mole of mercury can have protective effects

for certain adult organisms, but ratios found in nature

seldom work out to this exact ratio. Some preliminary

experimental data from Patuxent seems to hint that

certain doses of organic selenium combined with certain

doses of organic mercury can have "more than additive"

effects (deformities and death) on mallard duck embryos;

however, the reverse (antagonism) may be true for adult

ducks and the complexity of potential combinations of

forms and concentrations of the two compounds makes

generalizations difficult (Gary Heinz and Dave Hoffman,

Patuxent Fish and Wildlife Research Center, National

Biological Survey, personal communication, 1994). 

Interactions between Selenium and Sulfur:

Ratios of Se/S have been used to evaluate Se mobility and

sources of atmospheric pollutants; it Boston, the Se/S

ratios helped determine that a considerable portion of

the air pollution is due to petroleum combustion [488].

Selenium, like mercury. has many interactions with sulfur

compounds. This affinity for sulfur compounds may

account for some of the many synergistic and antagonistic

interactions between mercury and selenium.
Dietary sulfate, which can have a protective effect on

selenate toxicity, does not affect the toxicity of

selenite or organoselenium; dimethyl selenide (normally

not very toxic) has a synergistic effect with some

mercuric salts; and although drinking water containing

arsenic can ameliorate the toxic effects of dietary

selenium, their toxic effects can be additive when

provided together in drinking water [445].

Uses/Sources:

Selenium is a rare element forming only 9E-06 percent (9 X 10

to the power of - 6%) of the Earth's crust [291]. Selenium is an

essential nutrient for humans and animals, and both can use

inorganic as well as organic selenium compounds [953]. In the

body, selenium helps prevent damage to tissues done by oxygen

[953]. 

Plants take up selenium from soil, groundwater, sewage sludge,

and air pollution [83]. A number of plants have been described as

indicators of higher-than-normal concentrations of this element in

the soil [951]. Animals take up selenium from industrial sources,

contaminated air, contaminated water, and contaminated food [83].

Other than areas impacted by agricultural drainage, very high

concentrations of selenium in fish and wildlife occur primarily in

areas where selenium is naturally high in the soils, where there is

an influence of sewage sludge, or where coal fired power plants are

present [37,44]. 

Man's uses of selenium include photocopying, glass

manufacturing, the production of stainless steel, fungicides,

lubricants, electronic devices, pigments, dyes, insecticides, and

veterinary medicine [38,61]. Selenium is used in the production of

photocells, exposure meters, and solar cells [291]. Selenium also

finds extensive application in rectifiers, a result of its ability

to convert alternating electric current to direct current [291].

Other applications of the element include its use in the glass

industry to de-colorize glass, as a photographic toner, as an

additive in steel production, and in xerographic reproduction

[291]. Selenium dioxide is a good oxidizing agent and is used in

certain organic syntheses [291].

Used in electrodes [490].

 Major Uses [940]:

In the glass industry as a decolorizing agent. [Friberg, L.,

Nordberg, G.F., Kessler, E. and Vouk, V.B. (eds). Handbook of

the Toxicology of Metals. 2nd ed. Vols I, II.: Amsterdam:

Elsevier Science Publishers B.V., 1986.,p. V2 485].

As ingredient of toning baths in photography; as pigment in

mfr ruby-, pink-, orange-, or red-colored glass; as metallic

base in making electrodes for arc lights, electrical

instruments & apparatus; as rectifier in radio & television

sets; in selenium photocells, in semiconductor fusion
mixtures, selenium cells [The Merck Index. 10th ed. Rahway,

New Jersey: Merck Co., Inc., 1983. 1212].

In telephotographic apparatus; as vulcanizing agent in

processing of rubber; as catalyst in determination of

nitrogen by kjeldahl method; for dehydrogenation of organic

compounds [The Merck Index. 10th ed. Rahway, New Jersey:

Merck Co., Inc., 1983. 1212].

In steel & copper (degasifier & machineability improver)

[Sax, N.I. and R.J. Lewis, Sr. (eds.). Hawley's Condensed

Chemical Dictionary. 11th ed. New York: Van Nostrand Reinhold

Co., 1987. 1032].

Selenium is used extensively in the manufacture and

production of glass, pigments, rubber, metal alloys,

textiles, petroleum, medical therapeutic agents, and

photographic emulsions. [US Dept of Interior/Fish & Wildlife

Service Contaminant Reviews; Selenium Hazards to Fish,

Wildlife, and Invertebrates: A Synoptic Review Biol Rept No

(85)1.5 p.5 (1985)].

 Natural Sources [366]:

There are no true deposits of selenium anywhere and it cannot

economically be recovered from the earth directly.

[International Labour Office. Encyclopedia of Occupational

Health and Safety. Vols. I&II. Geneva, Switzerland:

International Labour Office, 1983. 2018].

Constitutes about 0.09 Ppm of the earth's crust. Occurs in

nature usually in the sulfide ores of the heavy metals; found

in small quantities in pyrite; in the minerals clausthalite

(PBSE), naumannite ((Ag,Pb)Se), tiemannite (HgSe); in

selenosulfur. [The Merck Index. 10th ed. Rahway, New Jersey:

Merck Co., Inc., 1983. 1212].

Present in the major oceans and in inland waters resulting in

the presence of selenium in drinking water. **PEER REVIEWED**

[IARC. Monographs on the Evaluation of the Carcinogenic Risk

of Chemicals to Man. Geneva: World Health Organization,

International Agency for Research on Cancer, 1972-1985.

(Multivolume work).,p. V2 248 (1973)].

Selenium accompanies sulfur in volcanic effluents. Soils in

the neighborhood of volcanos tend to have enriched amounts of

selenium. [Wilber CG; Clin Toxicol 17 (2): 171-230 (1980)].

Selenium concentration in geological materials: Igneous rocks

0.05 ppm; shales 0 - 0.6 ppm; sandstones 0.0 - 0.05 ppm;

limestones 0.08 ppm; soils 0.2 ppm. [Wilber CG; Clin Toxicol

17 (2): 171-230 (1980)].

The earth's crust is said to have an average selenium
concentration of 0.03 of 0.08 ppm. [Wilber CG; Clin Toxicol

17 (2): 171-230 (1980)].

Selenium is the most strongly enriched element in coal, being

present as an organoselenium compound, a chelated species, or

as an adsorbed element. [US Dept of Interior/Fish & Wildlife

Service Contaminant Reviews; Selenium Hazards to Fish,

Wildlife, and Invertebrates: A Synoptic Review Biol Rept No

(85)1.5 p.3 (1985)].

 Artificial Sources [940]:

Various industries discharge small amounts of selenium into

the air, water, and soil of the immediate vicinity. [Wilber

CG; Clin Toxicol 17 (2): 174 (1980)].

Forms/Preparations/Formulations:

 Common Forms of Selenium (Selenium Species):

The concentrations and chemical forms of selenium in

water are influenced by, among other factors, pH and

redox conditions. Although dissolved selenium in most

natural waters is dominated by the inorganic selenate and

selenite forms, substantial concentrations of selenium in

+6, +4, and -2 oxidation states can occur simultaneously

in natural aerobic surface waters of pH 6.5-9.0 [445].

One author found the following six forms of dissolved

selenium in water samples taken from three California

water bodies (Kesterson Reservoir, the San Joaquin River,

and the Salton Sea), all of which have received

subsurface agricultural drainage water: selenate,

selenite, seleno-amino acids, dimethyl selenonium ion

((CH3)2Se+1), dimethyl selenide, and dimethyl diselenide

[445].

In the environment, selenium naturally occurs in four

valence states, +6, +4, 0, and -2. Selenium dioxide

(SeO2), a selenium+2 form, does not occur naturally in

the environment, but is produced through the combustion

of fossil fuels [445]. Selenium in the +6 oxidation

state (as the selenate ion [SeO4-2]) is very common,

soluble, and stable in alkaline, oxidized waters and

soils. Selenate is the most common form of selenium in

subsurface agricultural drainage waters of the San

Joaquin Valley and in the San Joaquin River [445].

Selenium+4 (as the selenite ion [SeO3-2]) is somewhat

less soluble than selenate and forms under slightly less

oxidized conditions. Formation of the insoluble, inert,

and stable selenium (elemental or "metallic" selenium, a

mineral) is favored in acidic and reducing conditions.

Further chemical reduction leads to the formation of

selenium-2 (selenide), which is the basis of: inorganic
metal selenides (which are generally insoluble); many

organic selenium compounds, including amino acids (very

soluble) and methylated, volatile selenium forms

(relatively insoluble); and hydrogen selenide. Metal

selenides are formed, for example, with cadmium, copper,

and mercury. Examples of organoselenium compounds

include: the seleno- amino acids, selenocysteine

(C3H7NO2Se), selenocystine (C6H12N2O4Se2), and

selenomethionine (C5H11NO2Se); and the common methylated

selenide compounds dimethyl selenide ((CH3)2Se) and

dimethyl diselenide ((CH3)2Se2). Hydrogen selenide

(H2Se) is a highly toxic, volatile, and relatively

insoluble inorganic compound that is formed in some

industrial settings, but is not found in the natural

environment [445].

For a discussion of various forms of selenium see W.General

section above and Federal Register Vol 61, no. 221,pages 5844

to 58449.

Radionuclides:

The symbol for Selenium-75 is 75Se, the atomic number is

34, the half-life is 118 days, and X-ray emission is the

major form of decay [674].

Various forms of selenium commonly referred to in the

environmental toxicology literature under different names and

classification categories include:

Inorganic Selenium Compounds and Species: Bluegill

sunfish tend to take inorganic selenium primarily through

the food chain [481]. The most important oxidation

states are +4 and +6 [291]. Inorganic compounds include:

1. Selenates (selenium+6): Selenium in the +6

oxidation state (as the selenate ion [SeO4-2]) is

very common, soluble, and stable in alkaline,

oxidized waters and soils [445]. Selenate is the

most common form of selenium in subsurface

agricultural drainage waters of the San Joaquin

Valley and in the San Joaquin River [445]. 

2. Selenites (such as selenium +4 as sodium

selenite): Monogastric (non-ruminant) animals more

readily absorb dietary selenium +4 than do

ruminants [445]. The low waterborne concentrations

in the ocean may be due to precipitation of

selenium +4 with iron and manganese oxides [445].

Selenium +4 (as the selenite ion [SeO3-2]) is

somewhat less soluble than selenate and forms under

slightly less oxidized conditions. Formation of

the insoluble, inert, and stable selenium

(elemental or "metallic" selenium, a mineral) is
favored in acidic and reducing conditions [445].

3. Selenium dioxide (SeO2), a selenium +2 form,

does not occur naturally in the environment, but is

produced through the combustion of fossil fuels

[37].

4. Selenides (selenium -2): Further chemical

reduction leads to the formation of selenium -2,

which is the basis of:

A. Hydrogen selenide. Hydrogen selenide

(H2Se) is a highly toxic, volatile, and

relatively insoluble inorganic compound that

is formed in some industrial settings, but is

not found in the natural environment [445]. 

B. Various inorganic metal selenides (which

are generally insoluble). Metal selenides are

formed with cadmium, copper, and mercury.

Many organic selenides also are common (see

summary below) [445].

Organic Selenium (organoselenium) Compounds and Species:

There are numerous references in the literature

documenting that certain organic forms of selenium are

more bioavailable, more easily bioconcentrated, or more

toxic than are certain inorganic forms of selenium.

Organoselenium compounds can constitute 30-60% of the

selenium in some fresh and marine waters [445]. Organic

selenium includes:

1. Amino acids (very soluble) and methylated,

volatile selenium forms (relatively insoluble)

[445]: Examples of organoselenium compounds

include the seleno-amino acids, selenocysteine

(C3H7NO2Se), selenocystine (C6H12N2O4Se2); and the

common methylated selenide compounds dimethyl

selenide ((CH3)2Se) and dimethyl diselenide

((CH3)2Se2) [445].

NOTE: Dimethylselenide is generated slowly

from raw sewage [488]. Selenium is methylated

and probably demethylated in the environment

and cycled through a number of components of

the food web, complicating chemical

determination of the chemical forms available

to fish [488]. 

2. Selenomethionine (C5H11NO2Se):

Selenomethionines (Se-methionines, such as

selenium-2 as selenomethionine) are organoselenium

forms which are so prominent in the environmental

toxicology literature that they are discussed
separately. 

Selenomethionine may be the dominant form of

selenium in plant tissues and selenocysteine

may dominant in animal tissues (USFWS-PWRC,

Jan 1990) [445]. Dietary and possibly

waterborne organic selenium compounds (such as

selenomethionine) are more effectively and

quickly taken up, accumulate to higher

concentrations, and are retained longer by

animals than are inorganic forms of selenium

(Besser et al., 1989; Burau, Jul-Aug 1985;

Davis et al., Jan-Feb 1988; Heinz et al.,

1988; NRC-Subcommittee on Selenium, 1976; Ogle

et al., 1988) [445].

Although not true in all cases, the relative toxicity of

various chemical forms of selenium is generally as follows

(from most to least toxic): hydrogen selenide ~

selenomethionine (in diet) > selenite ~ selenomethionine (in

water) > selenate > elemental selenium ~ metal selenides ~

methylated selenium compounds [445]. The toxicity of dietary

selenocystine to mallard ducks was much less than

selenomethionine and may be somewhat less than selenite (Heinz

et al, 1989; Heinz et al., 1987) [445].

Differential Toxicity and Food Chain Characteristics of

Different Forms of Selenium:

Fish take up selenomethionine through the

gastrointestinal tract more readily than either selenium

+4 or selenium +6 [445]. 

Organoselenium compounds such as Se-methionine may

contribute significantly to Se bioaccumulation by

bluegills via both aqueous and food-chain uptake, whereas

inorganic compounds are accumulated mostly through the

food chain [481]. Dietary organic selenium in the form

of Se-methionine is more toxic to fish than dietary

inorganic selenium [481].

Text in paragraph above reprinted with permission

from Environmental Toxicology and Chemistry, Volume

12, J.M. Besser, T.J. Canfield and T.W. La Point,

"Bioaccumulation of oganic and inorganic selenium

in a laboratory food chain." Copyright 1993 SETAC].

Selenite is 10 times for toxic to fish than selenate, and

organic forms are even more toxic than selenite (Denny

Buckler, FWS Columbia, personal communication). The

USFWS-NFCRC (Dec 1989) conducted microcosm experiments

with algae (Chlamydomonas reinhardtii) and daphnids

(Daphnia magna) and discovered that bioconcentration

factors for dissolved selenomethionine were much greater
than for selenite, which were greater than for selenate

[445].

Selenium absorption in the gastrointestinal tract is

dependent on a variety of factors, including: its

chemical form(s) (e.g., fish take up selenomethionine

through the gastrointestinal tract more readily than

either selenium+4 or selenium+6 [USEPA, Sep 1987]); the

animal's nutritional (protein) status; and whether or not

the animal is a ruminant (monogastric [non-ruminant]

animals more readily absorb dietary selenium +4 than do

ruminants)[445].

Information from HSDB [940]:

The forms of selenium in soil depend on soil pH and

redox. At equilibrium, most soil selenium should be

elemental selenium. [Parr, J.F., P.B. Marsh, and J.M. Kla

(eds.). Land Treatment of Hazardous Wastes. Park Ridge,

New Jersey: Noyes Data Corporation, 1983. 186].

In areas of acid or neutral soils, the amount of

biologically available selenium should steadily decline.

The decline may be accelerated by active agricultural or

industrial practices. In dry areas with alkaline soils

and oxidizing conditions, elemental selenium and

selenides in rocks and volcanic soils may oxidize

sufficiently to maintain the availability of biologically

active selenium. [US Dept of Interior/Fish & Wildlife

Service Contaminant Reviews; Selenium Hazards to Fish,

Wildlife, and Invertebrates: A Synoptic Review Biol Rept

No (85)1.5 p.4 (1985)].

Chem.Detail: Detailed Information on Chemical/Physical Properties:

 Solubilities [940]:

Sol in aq potassium cyanide soln, potassium sulfite soln,

dilute aqueous caustic alkali soln [The Merck Index. 10th ed.

Rahway, New Jersey: Merck Co., Inc., 1983. 1212].

INSOL (sic, actually "relatively insoluble") IN WATER; SOL IN

SULFURIC ACID [Weast, R.C. (ed.) Handbook of Chemistry and

Physics, 68th ed. Boca Raton, Florida: CRC Press Inc., 1987-

1988.,p. B-125].

 Density/Specific Gravity [940]:

4.26-4.81 [Weast, R.C. (ed.) Handbook of Chemistry and

Physics, 68th ed. Boca Raton, Florida: CRC Press Inc., 1987-

1988.,p. B-125].

 Vapor Pressure [940]:
> 0.001 mm Hg at 20 deg C [Mackison, F. W., R. S. Stricoff,

and L. J. Partridge, Jr. (eds.). NIOSH/OSHA - Occupational

Health Guidelines for Chemical Hazards. DHHS(NIOSH)

PublicationNo. 81-123 (3 VOLS). Washington, DC: U.S.

Government Printing Office, Jan. 1981. 2].

 Boiling Point [940]:

690 deg C [Sax, N.I. Dangerous Properties of Industrial

Materials. 6th ed. New York, NY: Van Nostrand Reinhold, 1984.

2390].

 Melting Point [940]:

170-217 deg C [Weast, R.C. (ed.) Handbook of Chemistry and

Physics, 68th ed. Boca Raton, Florida: CRC Press Inc., 1987-

1988.,p. B-125].

 Molecular Weight [940]:

78.96 +/- 3 [Weast, R.C. (ed.) Handbook of Chemistry and

Physics, 68th ed. Boca Raton, Florida: CRC Press Inc., 1987-

1988.,p. B-125].

 Color/Form [940]:

LIQUID IS A BROWNISH RED [The Merck Index. 10th ed. Rahway,

New Jersey: Merck Co., Inc., 1983. 1212].

Selenium exists in several allotropic forms. 3 Are generally

recognized ... Selenium can be prepd with either amorphous or

crystalline structure. ... Amorphous is either red, in powder

form or black, in vitreous form. Crystalline monoclinic prism

is deep red; crystalline hexagonal form, the most stable

variety, is a metallic gray. [Weast, R.C. (ed.) Handbook of

Chemistry and Physics, 68th ed. Boca Raton, Florida: CRC

Press Inc., 1987-1988.,p. B-34].

 Odor [940]:

Odorless [Mackison, F. W., R. S. Stricoff, and L. J.

Partridge, Jr. (eds.). NIOSH/OSHA - Occupational Health

Guidelines for Chemical Hazards. DHHS(NIOSH) PublicationNo.

81-123 (3 VOLS). Washington, DC: U.S. Government Printing

Office, Jan. 1981. 1].

 Other Chemical/Physical Properties [940]:

Combines directly with hydrogen, with the halogens (excluding

iodine); oxidized to selenious acid by nitric acid, to

selenic acid by sulfuric acid; reduces hot aqueous soln of

silver and gold salts with formation of silver selenide and

metallic gold, respectively [The Merck Index. 10th ed. Rahway,

New Jersey: Merck Co., Inc., 1983. 1212].
Dark red-brown to bluish-black solid; sol in carbon

disulfide, methylene iodide, benzene or quinoline; density:

4.28; Softens @ 50-60 deg c & becomes elastic @ 70 deg c;

formed when molten selenium is cooled rapidly; when freshly

precipitated, reacts with water @ 50 deg c forming selenious

acid & hydrogen /amorphous selenium/ [The Merck Index. 10th

ed. Rahway, New Jersey: Merck Co., Inc., 1983. 1212].

Dark red, transparent crystals; two monoclinic forms: both

forms are metastable & change into gray form on heating;

melting point: below 200 deg c; density (alpha-form) 4.46

/Red selenium/ [The Merck Index. 10th ed. Rahway, New Jersey:

Merck Co., Inc., 1983. 1212].

Soluble in concentrated nitric acid; crystalline selenium is

a p-type semiconductor /red selenium/ [Sax, N.I. and R.J.

Lewis, Sr. (eds.). Hawley's Condensed Chemical Dictionary.

11th ed. New York: Van Nostrand Reinhold Co., 1987. 1032].

Lustrous gray to black hexagonal crystals; insol (sic,

actually "relatively insoluble") in alcohol; very slightly

sol in carbon disulfide (2 mg/100 ml); sol in ether; conducts

electricity & rectifies alternating current; conductivity

increases up to 1000 times on exposure to light; density 4.81

@ 20 deg C/4 deg C; melting point 217 deg C; Mohs' hardness:

2.0; Latent heat of fusion 16.4 cal/g; Latent heat of

vaporization 20.6 kcal/mol; Linear coefficient of thermal

expansion per degree C= 37X10-6; Specific heat (28 deg C):

0.084 cal/g/deg C; Surface tension (217 deg C): 92.5

dynes/cm; Thermal conductivity (25 deg C): 0.0007-0.00183

cal/(cm)(deg C)/sec. /Gray selenium/ [The Merck Index. 10th

ed. Rahway, New Jersey: Merck Co., Inc., 1983. 1212].

Melting point: transition point to hexagonal: 60-80 deg c

/amorphous selenium/ [Weast, R.C. (ed.) Handbook of Chemistry

and Physics, 68th ed. Boca Raton, Florida: CRC Press Inc.,

1987-1988.,p. B-125].

Exhibits both photovoltaic action, where light is converted

directly to electricity; exhibits photoconductive action,

where electrical resistance decreases with increased

illumination [Weast, R.C. (ed.) Handbook of Chemistry and

Physics, 68th ed. Boca Raton, Florida: CRC Press Inc., 1987-

1988.,p. B-34].

Soluble in chloroform /gray selenium/ [Weast, R.C. (ed.)

Handbook of Chemistry and Physics, 68th ed. Boca Raton,

Florida: CRC Press Inc., 1987-1988.,p. B-125].

Sol in carbon disulfide: 0.1 G/100 cc @ 46.6 Deg c /red

selenium/ [Weast, R.C. (ed.) Handbook of Chemistry and

Physics, 68th ed. Boca Raton, Florida: CRC Press Inc., 1987-

1988.,p. B-125].
BP: 684.9 +/- 1 deg C /Gray selenium/ [Weast, R.C. (ed.)

Handbook of Chemistry and Physics, 68th ed. Boca Raton,

Florida: CRC Press Inc., 1987-1988.,p. B-34].

Fate.Detail: Detailed Information on Fate, Transport, Persistence,

and/or Pathways:

See also: Information in Bio.Detail above for fate of

selenium in soils; and information in

Forms/Preparations/Formulations above.

Microorganisms in sediments and/or sewage are capable of

elemental methylation [488]. This process is well publicized for

mercury. Not so well known is the fact that selenium is methylated

and probably demethylated in the environment and cycled through a

number of components of the food web, complicating chemical

determination of the chemical forms available to fish [488].

Dimethylselenide is generated slowly from raw sewage [488]. 

Biogeochemical Cycling: In terrestrial environments,

insoluble (biologically unavailable) selenium in soils may be

oxidized by weathering and converted into soluble and bioavailable

forms like selenate and selenite [445]. In soil water, selenate

and, to a lesser extent selenite and possibly water-soluble

organoselenium, are bioavailable and readily taken up through plant

roots. Plants chemically reduce a portion to selenium-2 and

incorporate it into tissues in soluble and/or protein-bound amino

acids such as selenocystine, selenocysteine, and selenomethionine

[445]. Animals, including humans, then consume plants and other

animals containing selenium. Plants, animals, and microorganisms

release volatile forms of selenium (primarily dimethyl selenide and

to a lesser extent dimethyl diselenide) into the atmosphere where

it is oxidized, converted to elemental selenium, and returned to

the earth with rain, snow, or precipitating particulate matter. In

arid environments with alkaline soils (like the San Joaquin

Valley), selenium returned to soils in plant and animal wastes is

readily oxidized to selenate and once again becomes available for

biological uptake and cycling [445].

Selenium cycling in aquatic systems is somewhat different than

in terrestrial environments [445]. Waterborne selenium can remain

in a dissolved form, or be removed from solution through biological

uptake, precipitation, or volatilization [445].

As in terrestrial systems, selenium can be taken up through

the roots of higher aquatic plants. Many other aquatic organisms

(e.g., some bacteria, fungi, algae, and invertebrates that form

important components in aquatic food chains) also readily take up

waterborne selenate, selenite, and/or selenomethionine.

Selenium is also removed from the water column through

adsorption and complexation onto clay and particulates, and through

reaction and precipitation with some metals (e.g., selenite readily

reacts with iron to form ferric selenite [Fe2(SeO3)3] or

ferroselite [FeSe2]). As a result of these processes and

deposition of dead plant and animal tissue, a substantial portion

of the selenium in aquatic systems builds up in sediments, becomes
buried through subsequent sedimentation and/or is exposed to

further chemical and microbial reduction. This reduction leads to

the formation of insoluble elemental selenium, metal selenides, and

organic selenium-2, including methylated selenium-2 forms.

Selenium builds up most in sediments and tissues of plants, fish,

and wildlife in slow-moving or still, biologically productive

aquatic systems such as sloughs, wetlands, and some evaporation

ponds. Microcosm studies revealed that selenium more readily

accumulated in fine-textured, highly organic pond sediments than in

sandy riverine sediments [445].

Several mechanisms exist in aquatic sediments to return

(remobilize) selenium out of the sediments and back into the water

column and/or atmosphere. Such mechanisms include: oxidation and

methylation by plant roots and microorganisms, mixing and oxidation

as a result of feeding by fish and wildlife or burrowing by benthic

organisms, mixing and oxidation associated with water movements,

and oxidation by plant photosynthesis. Additionally, plant roots,

bottom-feeding fish and wildlife, and benthic invertebrates can all

take up selenium directly from sediments. Selenium can also be

released into the water and/or atmosphere in volatile, methylated

forms by plants, animals, algae, and as a result of microbial

activity. Although there is general agreement regarding the

various biogeochemical cycles involving selenium, little

quantitative information is available regarding process rates or

the specific roles of biota in these cycles [445].

 Notes on Selenium in Soil [366]:

The forms of selenium in soil depend on soil pH and redox. At

equilibrium, most soil selenium should be elemental selenium.

[Parr, J.F., P.B. Marsh, and J.M. Kla (eds.). Land Treatment

of Hazardous Wastes. Park Ridge, New Jersey: Noyes Data

Corporation, 1983. 186]. 

In areas of acid or neutral soils, the amount of biologically

available selenium should steadily decline. The decline may be

accelerated by active agricultural or industrial practices. In

dry areas with alkaline soils and oxidizing conditions,

elemental selenium and selenides in rocks and volcanic soils

may oxidize sufficiently to maintain the availablity of

biologically active selenium. [US Dept of Interior/Fish &

Wildlife Service Contaminant Reviews; Selenium Hazards to

Fish, Wildlife, and Invertebrates: A Synoptic Review Biol Rept

No (85)1.5 p.4 (1985)].

 Absorption, Distribution and Excretion [366]:

The rate of absorption as elemental selenium ... Is low. ...

Liver & kidney are principal sites of deposition. Excretion of

selenium is by urine, feces, sweat, & breath. [Clayton, G. D.

and F. E. Clayton (eds.). Patty's Industrial Hygiene and

Toxicology: Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York:

John Wiley Sons, 1981-1982. 2130].
Nonradioactive and radioactive metal salts were administered

intravenously to Sprague Dawley rats. The highest amount of

each metal approached the maximum tolerated dose. Cobalt (Co),

silver (Ag), and manganese (Mn) were eliminated rapidly. The

elimination of 20 to 50% of the dosage was observed for copper

(Cu), thallium (Tl), bismuth (Bi), lead (Pb), cesium (Cs),

gold (Au), zinc (Zn), mercury (Hg), selenium (Se), and

chromium (Cr). The slowest excretion rate was measured for

arsenic (As), cadmium (Cd), iron (Fe), methyl mercury (MeHg),

and tin (Sn). No substantial elimination rate decline was

observed for MeHg and Fe, and the decline was small for Tl,

Cs, Hg, Sn, Co, Ag, Zn, Cr, and As. Elimination of Ag and Mn

via feces was fast, with more than 70% eliminated on the first

day. Cu, Tl, Pb, and Zn were excreted at a slower rate, with

30.6 to 38.3% excreted on the first day. The rest of the

metals were eliminated slowly by the intestinal route. Co was

removed rapidly via urine, while Pb, Sn, Zn, MeHg, Ag, Fe, Mn,

and Cd were eliminated slowly. The biliary excretion of Ag,

As, and Mn was fast, with 25.5, 30.2 and 16.2% eliminated in

two hours. Cu, Se, Cd, Pb, Bi, and Co were eliminated at an

intermediate rate via the biliary route. Ag, As, Mn, Cu, Se,

Cd, Pb, Bi, and MeHg were highly concentrated in bile relative

to plasma. Liver and kidney contained the highest

concentrations of most metals. The intestinal route was the

major path of elimination for Ag, Mn, Cu, Tl, Pb, Zn, Cd, Fe,

and MeHg. Co, Cs, Au, Se, and Cr, were removed predominantly

by urine. For Bi, Hg, As, and Sn the two routes were similar.

[Gregus Z, Klaassen CO; Toxicol Appl Pharm 85 (1): 24-38

(1986)].

Laboratory and/or Field Analyses:

Many methods have been used to monitor for selenium [861,

953,1001,1003,1004,1005,1006]. EPA methods recommended depend on

the application: whether for drinking water [40 CFR Part 141 and

1005,1006,1008], NPDES discharge permits [40 CFR 136 and

1005,1006], CERCLA [861,1005,1006], RCRA [861,1005,1006], or lowdetection-limit water-quality based permitting [1001,1003,1004].

Other agencies (USGS, APHA, ASTM, NOAA, etc. also publish different

"standard methods." If one simply wants to know whether or not the

concentration exceeds EPA criteria or various low concentration

benchmarks for humans, fish, or wildlife, it is not always too

clear which "standard method" is optimum, although some might argue

that for water, the 1996 EPA methods 1639 (lab method) and 1669

(field method, see details below) should apply.

 Acceptable containers (after proper cleaning per EPA

protocols) for Antimony, Arsenic, Cadmium, Copper, Lead, Nickel,

Selenium, Silver, Thallium, and Zinc: 500-mL or 1-L fluoropolymer,

conventional or linear polyethylene, polycarbonate, or

polypropylene containers with lid [1003]. 

 Low concentration criteria or benchmarks require relatively

rigorous analyses using either hydride generation or graphite

furnace Atomic Absorption rather than ICP methods. Detection
limits should be no higher than comparison benchmarks or criteria

for various media (water, sediments, soil, tissues, etc), some of

which are low (see sections above). Unless required to be even

lower for comparisons with lower benchmarks, the detection limits

should usually not exceed the following default concentrations

often recommended by the National Park Service (Roy Irwin, National

Park Service, Personal Communication, 1996): 

0.50 ppm dry weight in tissues, 

Detection Limits as low as 0.05 ppb are possible if

required by lower benchmarks or criteria [953]

1.0 ppm dry weight in sediments and soils, 

Note: for certain soils, detection levels may need to be

as low as 0.3 mg/kg for protection from migration to

groundwater, depending upon the exact DilutionAttenuation Factor (DAF) [952]. Solids detection Limits

below 1 ppb are possible if required by lower benchmarks

or criteria [953]

0.001 ppm (mg/L) in water 

Note: water detection limits may need to be this low when

considering risk to aquatic organisms, since:

1) Long term safety of 2 to 5 ppb of total

waterborne selenium to fish and other aquatic

organisms can be questioned [463]. 

2) Excess selenium, even as low as 3-8 ppb in the

water) can cause numerous life-threatening changes

in feral fresh water fish [488].

Detection Limits as low as 0.001 ppb are possible if

required by lower benchmarks or criteria [953]. In some

situations (as when background concentrations are low),

water detection limits of 0.83 ug/L may be appropriate,

using EPA method 1639, since EPA Water Quality Criteria

are as low as 5 ug/L [1001,1003]. EPA Method 1638 allows

a detection limit of 1.2 ug/L [1003,1003]. 

Need to Analyze for Separate Selenium Species and then Add

Them before Comparison with Certain Benchmarks:

On November 14, 1996, EPA proposed in the Federal

Register that the acute toxicities of selenate, selenite,

and one form of organoselenium are additive. They

further proposed that all forms be added together to

obtain a total for comparison with water quality criteria

and that total selenium can be converted to dissolved by

multiplying total by 0.996 (Federal Register Vol 61, no.

221,pages 5844 to 58449):
Dissolved vs. Total vs. Acid Soluble:

Although most of the lab tests done to develop water

quality criteria and other benchmarks were originally

based on "total" values rather than "dissolved" values,

the lab settings were typically fairly clean and the

numbers generated by the lab tests are therefore often

even more comparable to field "dissolved" values than to

field "total" values (Glen Suter, Oak Ridge National Lab,

Personal Communication, 1995). 

As of January 1995, the U.S. EPA was recommending that

states use dissolved measurements in water quality

standards for metals, in concert with recommendations EPA

previously made for the Great Lakes [672]. The

conversion factors recommended by EPA for converting

total recoverable metals criteria to dissolved metal

criteria were given as follows [672]:

Selenium (+4) conversion for acute and chronic

criteria: 0.922 (for example, total recoverable

selenium (+4) criteria x 0.922 = dissolved selenium

(+4) criteria). EPA 1996 Great Lakes: EPA

suggested in November of 1996 (Federal Register Vol

61, no. 221,pages 5844 to 58449) that: the

following conversion may be used: A factor to 0.996

may be used to convert to convert total

(recoverable) acute criteria for selenite to a

dissolved criteria for selenite.

The conversion factors recommended by EPA for converting

total recoverable selenium to dissolved concentrations in

the January 1997 draft EPA Guidelines for 5 year 305(B)

assessments was also 0.922.

Note: None of these generic conversion factors

are universal. Both total and dissolved

concentrations should be checked at new

locations before relying on generic conversion

factors (Pat Davies, Colorado Division of

Wildlife, personal communication, 1997).

Filtration and Acidification of Water Samples:

For ICP water samples for metals, EPA recommends the

following (40 CFR Part 136, Appendix C, pertaining to ICP

analyses using method 200.7, 1994 edition of CFR Part

40):

1) For samples of "total or total recoverable

elements," samples should be acidified to a pH of

two or less at the time of collection or as soon as

possible thereafter.
Note: In more recent (1996) guidance related

to the more rigorous method 1669, EPA

clarified (some would say confused or added

data variability) the issue of when to acidify

by stating:

"Preservation recommendations for

Antimony, Arsenic, Cadmium, Copper, Lead,

Nickel, Selenium, Silver, Thallium, and

Zinc: Add 5 mL of 10% HN03 to 1-L sample;

preserve on-site or immediately upon

laboratory receipt" [1003]. 

Note: the nitric acid (triple

distilled or not?) and dilution

water (contaminated or not?) and

containers (proper type, cleaned

correctly or not?) used are all

potential sources of contamination

(see more detailed note below

related to data variation factors).

2) For determination of dissolved elements, the

samples must be filtered through a 0.45 micron

membrane filter as soon as soon as practical after

collection, using the first 50-100 ml to rinse the

filter flask. Acidify the filtrate with nitric

acid to a pH of 2 or less. Normally 3 mL of (1+1)

of nitric acid per liter should be sufficient to

preserve the sample.

3) For determination of suspended elements, the

samples must be filtered through a 0.45 micron

membrane filter as soon as soon as practical after

collection. The filter is then transferred to a

suitable container for storage and shipment, with

no preservation required.

Contaminants data from different labs, different states, and

different agencies, collected by different people, are often not

very comparable (see also, discussion in the disclaimer section at

the top of this entry).

As of 1997, the problem of lack of data comparability (not

only for water methods but also for soil, sediment, and tissue

methods) between different "standard methods" recommended by

different agencies seemed to be getting worse, if anything, rather

than better. The trend in quality assurance seemed to be for

various agencies, including the EPA and others, to insist on

quality assurance plans for each project. In addition to quality

control steps (blanks, duplicates, spikes, etc.), these quality

assurance plans call for a step of insuring data comparability

[1015,1017]. However, the data comparability step is often not

given sufficient consideration. The tendency of agency guidance

(such as EPA SW-846 methods and some other new EPA methods for bio-
concentratable substances) to allow more and more flexibility to

select options at various points along the way, makes it harder in

insure data comparability or method validity. Even volunteer

monitoring programs are now strongly encouraged to develop and use

quality assurance project plans [1015,1017]. 

At minimum, before using contaminants data from diverse

sources, one should determine that field collection methods,

detection limits, and lab quality control techniques were

acceptable and comparable. The goal is that the analysis in the

concentration range of the comparison benchmark concentration

should be very precise and accurate. 

It should be kept in mind that quality control field and lab

blanks and duplicates will not help in the data quality assurance

goal as well as intended if one is using a method prone to false

negatives. Methods may be prone to false negatives due to the use

of detection limits that are too high, the loss of contaminants

through inappropriate handling, or the use of inappropriate

methods. 

Other more detailed information on sources of potential

variation in contaminants data:

Variation in concentrations of contaminants may sometimes

be due to differences in how individual investigators

treat samples in the field and lab rather than true

differences in environmental concentrations. It was

recognition that collectors and labs often contaminate

samples that led EPA to develop the 1600 series of water

protocols for low detection limit applications

[1001,1002,1003,1004]. In comparing contaminants data

from different labs, different states, and different

agencies, one should keep in mind that they are often not

very comparable. They may be as different as apples and

oranges since:

1) Different Agencies (EPA, USGS, NOAA, and various

State Agencies) publish different lab and field

protocols. Each of these protocols is different

and has typically changed over time.

Note: Even "Standard EPA Methods" which are

supposedly widely used by consultants,

industry, and academia, have been variable

over time and between application category

(Drinking Water vs. NPDES, vs. RCRA, vs.

CERCLA, vs. Water-Quality Based permits,

etc.). 

Preservation and other details of various EPA

lab and field protocols have changed over the

years, just as they have at USGS and various

States and other agencies. USGS data from 30

years ago may be different than USGS data

today due to differences (drift) in lab and
field protocols rather than differences in

environmental concentrations.

2) Independent labs and field investigators are not

always using "the latest and greatest methods,"

and it is difficult for them to keep up with all

the changes from various agencies in the midst of

their "real world" busy lives. Updates are not

always convenient to obtain. For example, EPA

changes are scattered through various proposed

Federal Register Notices, various updates of CFRs,

and numerous publications originating in many

different parts of EPA and their contractors. The

wording is sometimes imprecise and is often

inconsistent between EPA methods for different

applications. 

3) The details of the way one person collects,

filters, and acidifies water samples in the field

may be different than the way another does it.

Sources of potential variation include the

following:

A) The protocol phrases "As soon as practical

or as soon as possible." Different situations

can change the elapsed time considered by the

field collector to be "as soon as practical."

It may take different amounts of time to get

to a safe or otherwise optimum place to filter

and/or acidify and cool the samples. In one

case precipitation and other changes could be

going on in the collection bottle while the

bottle is on the way to filtration and

acidification. In other cases, the field

collector filters and acidifies the samples

within minutes. Weather, safety concerns, and

many other factors could play a role.

B) Differences in numerous other details of

the method used can drastically change the

results. Some cold, wet, hurried, or fire

ant-bitten collectors might decide that it is

not "practical" to filter and acidify quite so

immediately in the field, and may decide the

shore, a vehicle, a motel room, or even a

remote lab are more "practical" locations.

Filtering and acidifying in the field

immediately has been thought of as a better

option for consistency (see copper and silver

entries for examples of what can happen if

there is a delay). However, in recent

methodology designed to prevent some the

contamination and variability listed above,

EPA has recently suggested that waiting until
the sample arrives at the lab before

acidifying is OK [1003]. 

C) What kind of .45 micron filter was used?

The flat plate filters that were used for

years tended to filter .45 micron sizes at

first and then smaller and smaller sizes as

the filtering proceeded and the filter loaded

up with particulate matter. As the filter

clogged, the openings grew smaller and

colloids and smaller diameter matter began to

be trapped on the filter. For this reason,

both the USGS and EPA 1600 series protocols

have gone to tortuous-path capsule filters

that tend to filter .45 micron sizes more

reliably over time. Example of specifications

from EPA method 1669:

Filter—0.45-um, 15-mm diameter or larger,

tortuous-path capsule filters, Gelman

Supor 12175, or equivalent [1003].

D) "Normally 3 mL of (1+1) of nitric acid per

liter should be sufficient to preserve the

(water) sample" (40 CFR Part 136, Appendix C,

pertaining to ICP analyses using method 200.7,

1994 edition of CFR Part 40). Sometimes it is

not, depending on alkalinity and other

factors. What field collectors sometimes

(often?) do is just use pop tabs of 3 mL of

nitric acid and hope for the best rather than

checking to see that the acidity has been

lowered to below a pH of two. EPA CFR

guidelines just call for a pH of below two,

whereas samples meant to be "acid soluble"

metals call for a pH of 1.5 to 2.0 [25]. See

also, various USEPA 1984 to 1985 Ambient Water

Quality Criteria Documents for individual

metals.

Note: Some shippers will not accept

samples with a pH of less than 1 for

standard shipping (John Benham, National

Parks Service Personal Communication,

1997).

E) One person might use triple distilled

concentrated nitric acid rather than reagent

grades of acid to avoid possible contamination

in the acid, while another may not. When

using very low detection limits, some types of

acid may introduce contamination and influence

the results. Using a 10% dilution of nitric

acid as called for by EPA [1003] is another
potential source of contamination, since the

dilution water and/or containers may be

contaminated. Sometimes people may be

incorrectly determining that background

concentrations are high due to contamination

sources such as these (Pat Davies, Colorado

Division of Wildlife, personal communication,

1997).

Note: Just using triple distilled nitric

acid may not be the total answer to

potential contamination. The key issue

to be sure that the acid used is free of

the metals being analyzed. In guidance

for EPA method 1669, the use of

"ultrapure nitric acid; or Nitric acid,

dilute, trace-metal grade" is specified

[1003]. In guidance for EPA method 1638,

the use of "Nitric acid—concentrated (sp

gr 1.41), Seastar or equivalent" is

specified [1003].

F) Holding times can strongly influence the

results and there can be quite a bit of

variation even within EPA recommended 6 month

limits (see Silver entry for details).

Holding times recommended for EPA for water

samples of metals other than mercury or

chromium VI have usually been listed as 6

months (Federal Register, Volume 49, No. 209,

Friday, October 28, 1984, page 43260). In the

1994 version of the CFR, NPDES holding times

for mercury and Chromium VI are the same ones

listed in 1984, but no EPA holding times are

given for other metals (40 CFR, Part 136.3,

Table 2, page 397, 1994). EPA sources stated

this was a typo, that no one else brought it

to their attention in the last 3 years, that 6

months is still an operable holding time for

"other metals" including this one, and that 6

months is actually an artifact from the days

when 6 month composite samples were used for

NPDES permits rather than having been

originally scientifically derived. 

Counterpoint: Although some information

suggests that 6 months is probably too

long for some contaminants in some

scenarios (see silver and copper

entries), not all of the information in

the literature casts the 6 month metals

holding time in such questionable light.

In one study, two EPA research chemists

found that preservation under certain
conditions of drinking water (EPA Method

200.8) metals samples to a pH of less

than 2 effectively stabilized the metal

concentrations for 6 months. They found

that trace metal standards in the 10 to

50 ug/L concentration could be held in 1%

nitric acid if a 5% change of

concentration was acceptable [1009].

Some metal concentrations changed more

than 5% (Zinc up to 24%, Selenium up to

23%) [1009]. Vanadium, Manganese and

Arsenic changed up to 5-7% [1009]. In

some of the trials, metals were higher

after 6 months due to leaching from

containers, while in some they were lower

[1009]. The changes were nevertheless

considered not of great consequence

related to drinking water MCLs and EPA

method 200.8 [1009]. However, it is not

clear that the careful measures utilized

(like rechecking to make sure the pH was

less than 2, the use of particular kinds

of water samples, the use of particular

acids, etc.) in this one study replicates

what goes on in day to day ("real world")

contaminants lab work around the country.

Some EPA sources state that 6 months

should be OK if the sample bottle is

vigorously shaken and re-acidified in the

lab prior to lab analyses, a practice not

universally or even particularly commonly

done in labs today. The degree to which

a water sample is re-acidified, rechecked for pH, shaken before analysis,

and the length of time it sits before and

after these steps, seems to vary a lot

between laboratories, and EPA guidance

for various methods is not consistent.

Some labs recheck pH, some don't. Some

shake, some don't, etc. For drinking

water, preservation is considered

complete after the sample is held in pH

of less than 2 for at least 16 hours

[1007]. New EPA Method 1638 specifies: 

"Store the preserved sample for a

minimum of 48 h at 0–4(C to allow

the acid to completely dissolve the

metal(s) adsorbed on the container

walls. The sample pH should be

verified as <2 immediately before

withdrawing an aliquot for

processing or direct analysis. If,
for some reason such as high

alkalinity, the sample pH is

verified to be >2, more acid must be

added and the sample held for

sixteen hours until verified to be

pH <2" [1003].

For many other methods, the minimum

holding time in acid is not stated or is

different (see various EPA and other

Agency methods). 

G) If present, air in head space can cause

changes in water sample concentrations (Roy

Irwin, National Park Service, Personal

Communication, based on several discussions

with EPA employees and various lab managers in

February 1997).

Note: air from the atmosphere or in

headspace can cause oxidation of

anaerobic groundwater or anaerobic

sediment samples. This oxidation can

cause changes in chemical oxidation

states of contaminants in the sample, so

that the results are not typical of the

anaerobic conditions which were present

in the environment prior to sampling

(John Benham, National Park Service,

Personal Communication, 1997). 

H) When is the sample shaken in the lab or the

field? If the filter is acidified in the

field, it will be shaken on the way back to

the lab. If lab acidified, how much and when

is the sample shaken and then allowed to sit

again for various times periods before

analyses? Many methods treat this

differently, and what many field collectors

and labs actually do before analyzing samples

is different as well. For EPA method 1638,

the word shake appears in the "Alternate total

recoverable digestion procedure": 

"..Tightly recap the container and shake

thoroughly" [1003].

I) If one field filters and acidifies, one

often changes metal concentrations and

colloidal content compared to samples not

treated in this manner. Acidifying effects

microbial changes. If one holds the samples a

while before filtering and acidifying, the

situation changes. In collection bottles,
there are potential aging effects: temperature

changes, changes in basic water chemistry as

oxygen and other dissolved gasses move from

the water into the headspace of air at the

top, potential aggregation of colloidal

materials, precipitation of greater sizes over

time, development of bigger and more colloids,

and more sorption (Roy Irwin, National Park

Service, personal communication, 1997). 

4) The guidance of exactly where to take water

samples varies between various state and federal

protocols. Taking water samples at the surface

microlayer tends to increase concentrations of

various contaminants including metals. Other areas

of the water column tend to produce different

concentrations. Large quantities of anthropogenic

substances frequently occur in the surface

microlayer at concentrations ranging from 100 to

10,000 times greater than those in the water column

[593]. These anthropogenic substances can include

plastics, tar lumps, PAHs, chlorinated

hydrocarbons, as well as lead, copper, zinc, and

nickel [593]. Sometimes a perceived trend can be

more the result of the details of the sample microlocation rather than real changes in environmental

concentrations (Roy Irwin, National Park Service,

personal communication, 1997). The new EPA method

1669 mentions the microlayer, and states that one

can use a fluoropolymer closing mechanism, threaded

onto the bottle, to open and close a certain type

of bottle under water, thereby avoiding surface

microlayer contamination [1003]. However, even

this relatively new EPA method 1669 also gives

recommendations for ways to sample directly at the

surface, and does not discourage the use of surface

samples.

5) Although the above examples are mostly related

to water samples, variability in field and lab

methods can also greatly impact contaminant

concentrations in tissues, soil, and sediments.

Sediment samples from different microhabitats in a

river (backwater eddy pools vs. attached bars, vs.

detached bars, vs. high gradient riffles vs. low

gradient riffles, vs. glides, etc.) tend to have

drastically different concentrations of metals as

well as very different data variances (Andrew

Marcus, Montana State University, personal

communication, 1995). Thus, data is only optimally

comparable if both data collectors were studying

the same mix of microhabitats, a stratified

sampling approach which would be unusual when

comparing random data from different investigators.
6) Just as there are numerous ways to contaminate,

store, ship, and handle water samples, so are there

different agency protocols and many different ways

to handle samples from other media. One

investigator may use dry ice in the field, another

may bury the samples in a large amount of regular

ice immediately after collection in the field,

while a third might place samples on top of a small

amount of ice in a large ice chest. The speed with

which samples are chilled can result in different

results not only for concentrations of organics,

but also for the different chemical species (forms)

of metals (Roy Irwin, National Park Service,

personal communication, 1997). 

7) In comparing contaminants metals data, soil and

sediment contaminant concentrations should usually

be (but seldom has been) normalized for grain size,

total organic carbon, and/or acid volatile sulfides

before biologically-meaningful or trend-meaningful

comparisons are possible (Roy Irwin, National Park

Service, Personal Communication, 1997).

8) There has been tremendous variability in the

precautions various investigators have utilized to

avoid sample contamination. Contamination from

collecting gear, clothes, collecting vehicles,

skin, hair, collector's breath, improper or

inadequately cleaned sample containers, and

countless other sources must carefully be avoided

when using methods with very low detection limits

[1003]. The EPA 1600 series method, some of which

are described below, are designed to minimize some

the common sources of contamination.

Highlights from EPA Method 1639: Determination of trace

elements in ambient waters by stabilized temperature graphite

furnace atomic absorption:

This 1996 proposed EPA method provides procedures to

determine dissolved elements in ambient waters at EPA

water quality criteria (WQC) levels using stabilized

temperature graphite furnace atomic absorption (GFAA)

[1003]. It may also be used to determine total

recoverable element concentrations in these waters

[1003]. 

As of March 1997, the EPA 1600 series methods had not yet

been officially approved in 40 CFR for use in NPDES

permits, but the improvements in these methods were

suggested by EPA staff to be wise practice when

attempting low detection limit analyses for metals.
This method was developed by integrating the analytical

procedures contained in EPA Method 200.9 with the

stringent quality control (QC) and sample handling

procedures necessary to avoid contamination and ensure

the validity of analytical results during sampling and

analysis for metals at EPA WQC levels [1003]. This

method contains QC procedures that will ensure that

contamination will be detected when blanks accompanying

samples are analyzed [1003]. This method is accompanied

by Method 1669: Sampling Ambient Water for Determination

of Trace Metals at EPA Water Quality Criteria Levels (the

"Sampling Method") [1003]. The Sampling Method is

necessary to ensure that contamination will not

compromise trace metals determinations during the

sampling process [1003].

Many of the requirements for this method are similar to

those for other EPA 1600 series methods [1003].

This method may be used with the following metals [1003]:

Antimony (Sb), CAS 7440-36-0

Cadmium (Cd), CAS 7440-43-9

Trivalent Chromium, CAS 16065-83-1 

Nickel (Ni), CAS 7440-02-0

Selenium (Se), CAS 7782-49-2

Zinc (Zn), CAS 7440-66-6

For dissolved metal determinations, samples must be

filtered through a 0.45-um capsule filter at the field

site [1003]. The filtering procedures are described in

the Sampling Method [1003]. Except for trivalent

chromium, the filtered samples may be preserved in the

field or transported to the laboratory for preservation

[1003]. Procedures for field preservation are detailed

in the Sampling Method; procedures for laboratory

preservation are provided in this method [1003]. To

determine trivalent chromium, a field preparation step,

which is described in the Sampling Method, is used to

isolate the trivalent chromium [1003].

To determine total recoverable analytes in ambient water

samples, a digestion/extraction is required before

analysis when the elements are not in solution (e.g.,

aqueous samples that may contain particulate and

suspended solids) [1003].

Construction materials—Only the following materials

should come in contact with samples: fluoropolymer (FEP,

PTFE), conventional or linear polyethylene,

polycarbonate, polypropylene, polysulfone, or ultrapure

quartz [1003]. PTFE is less desirable than FEP because

the sintered material in PTFE may contain contaminates

and is susceptible to serious memory contamination
[1003]. Fluoropolymer or glass containers should be used

for samples that will be analyzed for mercury because

mercury vapors can diffuse in or out of the other

materials resulting either in contamination or low-biased

results [1003]. All materials, regardless of

construction, that will directly or indirectly contact

the sample must be cleaned using EPA procedures and must

be known to be clean and metal free before proceeding

[1003].

The following materials have been found to contain trace

metals and must not be used to hold liquids that come in

contact with the sample or must not contact the sample

itself, unless these materials have been shown to be free

of the metals of interest at the desired level: Pyrex,

Kimax, methacrylate, polyvinylchloride, nylon, and Vycor

[1003]. In addition, highly colored plastics, paper cap

liners, pigments used to mark increments on plastics, and

rubber all contain trace levels of metals and must be

avoided [1003].

Serialization—It is recommended that serial numbers be

indelibly marked or etched on each piece of Apparatus so

that contamination can be traced, and logbooks should be

maintained to track the sample from the container through

the labware to injection into the instrument [1003]. It

may be useful to dedicate separate sets of labware to

different sample types; e.g., receiving waters vs.

effluents [1003]. However, the Apparatus used for

processing blanks and standards must be mixed with the

Apparatus used to process samples so that contamination

of all labware can be detected [1003].

Do not dip pH paper or a pH meter into the sample; remove

a small aliquot with a clean pipet and test the aliquot

[1003]. When the nature of the sample is either unknown

or known to be hazardous, acidification should be done in

a fume hood [1003].

Store the preserved sample for a minimum of 48 h at 0–4(C

to allow the acid to completely dissolve the metal(s)

adsorbed on the container walls [1003]. The sample

should then verified to be pH < 2 just before withdrawing

an aliquot for processing or direct analysis [1003]. If

for some reason such as high alkalinity the sample pH is

verified to be > 2, more acid must be added and the

sample held for 16 h until verified to be pH < 2 [1003].

One of the requirements for the alternate total

recoverable digestion procedure is to tightly recap the

container and shake thoroughly [1003]. 

Highlights from EPA Method 1669 for Sampling Ambient Water for

Trace Metals at EPA Water Quality Criteria Levels [1003]:
As of March 1997, the 1600 series methods had not yet

been officially approved in 40 CFR for use in NPDES

permits, but the improvements in these methods were

suggested by EPA staff to be wise practice when

attempting low detection limit analyses for metals.

This "field method details" protocol is for the

collection and filtration of ambient water samples for

subsequent determination of total and dissolved Antimony,

Arsenic, Cadmium, Copper, Chromium III, Chromium VI,

Lead, Mercury, Nickel, Selenium, Silver, Thallium, and

Zinc, at low (Water Quality Criteria Range)

concentrations [1003]. It is designed to support the

implementation of water quality monitoring and permitting

programs administered under the Clean Water Act [1003].

This method is not intended for determination of metals

at concentrations normally found in treated and untreated

discharges from industrial facilities [1003]. Existing

regulations (40 CFR Parts 400–500) typically limit

concentrations in industrial discharges to the mid to

high part-per-billion (ppb) range, whereas ambient metals

concentrations are normally in the low part-per-trillion

(ppt) to low ppb range [1003]. This guidance is

therefore directed at the collection of samples to be

measured at or near the water quality criteria levels

[1003]. Often these methods will be necessary in a water

quality criteria-based approach to EPA permitting [1001].

Actual concentration ranges to which this guidance is

applicable will be dependent on the sample matrix,

dilution levels, and other laboratory operating

conditions [1003].

The ease of contaminating ambient water samples with the

metal(s) of interest and interfering substances cannot be

overemphasized [1003]. This method includes sampling

techniques that should maximize the ability of the

sampling team to collect samples reliably and eliminate

sample contamination [1003].

Clean and ultraclean—The terms "clean" and "ultraclean"

have been used in other Agency guidance [1004] to

describe the techniques needed to reduce or eliminate

contamination in trace metals determinations [1003].

These terms are not used in this sampling method due to

a lack of exact definitions [1003]. However, the

information provided in this method is consistent with

summary guidance on clean and ultraclean techniques

[1004].

Preventing ambient water samples from becoming

contaminated during the sampling and analytical process

is the greatest challenge faced in trace metals

determinations [1003]. In recent years, it has been
shown that much of the historical trace metals data

collected in ambient water are erroneously high because

the concentrations reflect contamination from sampling

and analysis rather than ambient levels [1003].

Therefore, it is imperative that extreme care be taken to

avoid contamination when collecting and analyzing ambient

water samples for trace metals [1003].

There are numerous routes by which samples may become

contaminated [1003]. Potential sources of trace metals

contamination during sampling include metallic or metalcontaining sampling equipment, containers, labware (e.g.

talc gloves that contain high levels of zinc), reagents,

and deionized water; improperly cleaned and stored

equipment, labware, and reagents; and atmospheric inputs

such as dirt and dust from automobile exhaust, cigarette

smoke, nearby roads, bridges, wires, and poles [1003].

Even human contact can be a source of trace metals

contamination [1003]. For example, it has been

demonstrated that dental work (e.g., mercury amalgam

fillings) in the mouths of laboratory personnel can

contaminate samples that are directly exposed to

exhalation [1003].

For dissolved metal determinations, samples must be

filtered through a 0.45-um capsule filter at the field

site [1003]. The filtering procedures are described in

this method [1003]. The filtered samples may be

preserved in the field or transported to the laboratory

for preservation [1003]. 

This document is intended as guidance only [1003].

Use of the terms "must," "may," and "should" are

included to mean that EPA believes that these

procedures must, may, or should be followed in

order to produce the desired results when using

this guidance [1003]. In addition, the guidance is

intended to be performance-based, in that the use

of less stringent procedures may be used so long as

neither samples nor blanks are contaminated when

following those modified procedures [1003].

Because the only way to measure the performance of

the modified procedures is through the collection

and analysis of uncontaminated blank samples in

accordance with this guidance and the referenced

methods, it is highly recommended that any

modifications be thoroughly evaluated and

demonstrated to be effective before field samples

are collected [1003].

The method includes a great many details regarding

prevention of field contamination of samples, including

clothing needed, clean hands vs. dirty hands operations,

and numerous other details [1003]. 
Surface sampling devices—Surface samples are collected

using a grab sampling technique [1003]. Samples may be

collected manually by direct submersion of the bottle

into the water or by using a grab sampling device [1003].

Grab samplers may be used at sites where depth profiling

is neither practical nor necessary [1003].

An alternate grab sampler design is available [1003].

This grab sampler is used for discrete water samples and

is constructed so that a capped clean bottle can be

submerged, the cap removed, sample collected, and bottle

recapped at a selected depth [1003]. This device

eliminates sample contact with conventional samplers

(e.g., Niskin bottles), thereby reducing the risk of

extraneous contamination [1003]. Because a fresh bottle

is used for each sample, carryover from previous samples

is eliminated [1003].

Subsurface sampling devices—Subsurface sample collection

may be appropriate in lakes and sluggish deep river

environments or where depth profiling is determined to be

necessary [1003]. Subsurface samples are collected by

pumping the sample into a sample bottle [1003]. Examples

of subsurface collection systems include the jar system

device or the continuous-flow apparatus [1003]. 

Advantages of the jar sampler for depth sampling are (1)

all wetted surfaces are fluoropolymer and can be

rigorously cleaned; (2) the sample is collected into a

sample jar from which the sample is readily recovered,

and the jar can be easily recleaned; (3) the suction

device (a peristaltic or rotary vacuum pump, is located

in the boat, isolated from the sampling jar; (4) the

sampling jar can be continuously flushed with sample, at

sampling depth, to equilibrate the system; and (5) the

sample does not travel through long lengths of tubing

that are more difficult to clean and keep clean [1003].

In addition, the device is designed to eliminate

atmospheric contact with the sample during collection

[1003].

Selection of a representative site for surface water

sampling is based on many factors including: study

objectives, water use, point source discharges, non-point

source discharges, tributaries, changes in stream

characteristics, types of stream bed, stream depth,

turbulence, and the presence of structures (bridges,

dams, etc.) [1003]. When collecting samples to determine

ambient levels of trace metals, the presence of potential

sources of metal contamination are of extreme importance

in site selection [1003].

Ideally, the selected sampling site will exhibit a high

degree of cross-sectional homogeneity [1003]. It may be
possible to use previously collected data to identify

locations for samples that are well mixed or are

vertically or horizontally stratified [1003]. Since

mixing is principally governed by turbulence and water

velocity, the selection of a site immediately downstream

of a riffle area will ensure good vertical mixing [1003].

Horizontal mixing occurs in constrictions in the channel

[1003]. In the absence of turbulent areas, the selection

of a site that is clear of immediate point sources, such

as industrial effluents, is preferred for the collection

of ambient water samples) [1003].

To minimize contamination from trace metals in the

atmosphere, ambient water samples should be collected

from sites that are as far as possible (e.g., at least

several hundred feet) from any metal supports, bridges,

wires or poles [1003]. Similarly, samples should be

collected as far as possible from regularly or heavily

traveled roads [1003]. If it is not possible to avoid

collection near roadways, it is advisable to study

traffic patterns and plan sampling events during lowest

traffic flow [1003].

The sampling activity should be planned to collect

samples known or suspected to contain the lowest

concentrations of trace metals first, finishing with the

samples known or suspected to contain the highest

concentrations [1003]. For example, if samples are

collected from a flowing river or stream near an

industrial or municipal discharge, the upstream sample

should be collected first, the downstream sample

collected second, and the sample nearest the discharge

collected last [1003]. If the concentrations of

pollutants is not known and cannot be estimated, it is

necessary to use precleaned sampling equipment at each

sampling location [1003].

One grab sampler consists of a heavy fluoropolymer collar

fastened to the end of a 2-m-long polyethylene pole,

which serves to remove the sampling personnel from the

immediate vicinity of the sampling point [1003]. The

collar holds the sample bottle [1003]. A fluoropolymer

closing mechanism, threaded onto the bottle, enables the

sampler to open and close the bottle under water, thereby

avoiding surface microlayer contamination [1003].

Polyethylene, polycarbonate, and polypropylene are also

acceptable construction materials unless mercury is a

target analyte [1003]. Assembly of the cleaned sampling

device is as follows:

Sample collection procedure—Before collecting ambient

water samples, consideration should be given to the type

of sample to be collected, the amount of sample needed,

and the devices to be used (grab, surface, or subsurface
samplers) [1003]. Sufficient sample volume should be

collected to allow for necessary quality control

analyses, such as matrix spike/ matrix spike duplicate

analyses [1003].

Highlights from EPA Method 1638: Determination of Trace

Elements in Ambient Waters by Inductively Coupled Plasma —

Mass Spectrometry:

This 1996 proposed EPA method is for the determination of

dissolved elements in ambient waters at EPA water quality

criteria (WQC) levels using inductively coupled plasmamass spectrometry (ICP-MS) [1003]. It may also be used

for determination of total recoverable element

concentrations in these waters [1003]. This method was

developed by integrating the analytical procedures in EPA

Method 200.8 with the quality control (QC) and sample

handling procedures necessary to avoid contamination and

ensure the validity of analytical results during sampling

and analysis for metals at EPA WQC levels [1003]. This

method contains QC procedures that will assure that

contamination will be detected when blanks accompanying

samples are analyzed [1003]. This method is accompanied

by Method 1669: Sampling Ambient Water for Determination

of Trace Metals at EPA Water Quality Criteria Levels

("Sampling Method") [1003]. The Sampling Method is

necessary to assure that trace metals determinations will

not be compromised by contamination during the sampling

process [1003].

This method may be used with the following metals:

Antimony (Sb), CAS 7440-36-0

Cadmium (Cd), CAS 7440-43-9

Copper (Cu), CAS 7440-50-8

Lead (Pb), CAS 7439-92-1

Nickel (Ni), CAS 7440-02-0

Selenium (Se), CAS 7782-49-2

Silver (Ag), CAS 7440-22-4

Thallium (Tl), CAS 7440-28-0

Zinc (Zn), CAS 7440-66-6

As of March 1997, the EPA 1600 series methods had not yet

been officially approved in 40 CFR for use in NPDES

permits, but the improvements in these methods were

suggested by EPA staff to be wise practice when

attempting low detection limit analyses for metals

[1003].

This method is not intended for determination of metals

at concentrations normally found in treated and untreated

discharges from industrial facilities [1003]. Existing

regulations (40 CFR Parts 400–500) typically limit

concentrations in industrial discharges to the mid to
high part-per-billion (ppb) range, whereas ambient metals

concentrations are normally in the low part-per-trillion

(ppt) to low ppb range [1003].

The ease of contaminating ambient water samples with the

metal(s) of interest and interfering substances cannot be

overemphasized [1003]. This method includes suggestions

for improvements in facilities and analytical techniques

that should maximize the ability of the laboratory to

make reliable trace metals determinations and minimize

contamination [1003]. These suggestions are ...based on

findings of researchers performing trace metals analyses

[1003]. Additional suggestions for improvement of

existing facilities may be found in EPA's Guidance for

Establishing Trace Metals Clean Rooms in Existing

Facilities, which is available from the National Center

for Environmental Publications and Information (NCEPI) at

the address listed in the introduction to this document

[1003].

Clean and ultraclean—The terms "clean" and "ultraclean"

have been applied to the techniques needed to reduce or

eliminate contamination in trace metals determinations

[1003]. These terms are not used in this method because

of their lack of an exact definition [1003]. However,

the information provided in this method is consistent

with the summary guidance on clean and ultraclean

techniques [1003].

The procedure given in this method for digestion of total

recoverable metals is suitable for the determination of

silver in aqueous samples containing concentrations up to

0.1 mg/L [1003]. For the analysis of samples containing

higher concentrations of silver, succeedingly smaller

volume, well-mixed sample aliquots must be prepared until

the analysis solution contains <0.1 mg/L silver [1003].

Sample preservation—Preservation of samples and field

blanks for both dissolved and total recoverable elements

may be performed in the field at time of collection or in

the laboratory [1003]. However, to avoid the hazards of

strong acids in the field and transport restrictions, to

minimize the potential for sample contamination, and to

expedite field operations, the sampling team may prefer

to ship the samples to the laboratory within two weeks of

collection [1003]. Samples and field blanks should be

preserved at the laboratory immediately upon receipt

[1003]. For all metals, preservation involves the

addition of 10% HNO3 to bring the sample to pH <2 [1003].

For samples received at neutral pH, approx 5 mL of 10%

HNO3 per liter will be required [1003].

Do not dip pH paper or a pH meter into the sample; remove

a small aliquot with a clean pipet and test the aliquot
[1003]. When the nature of the sample is either unknown

or known to be hazardous, acidification should be done in

a fume hood [1003]. 

Store the preserved sample for a minimum of 48 h at 0–4(C

to allow the acid to completely dissolve the metal(s)

adsorbed on the container walls [1003]. The sample pH

should be verified as <2 immediately before withdrawing

an aliquot for processing or direct analysis [1003]. If,

for some reason such as high alkalinity, the sample pH is

verified to be >2, more acid must be added and the sample

held for sixteen hours until verified to be pH <2 [1003].

In some situations (as when background concentrations are

low), water detection limits as low as 0.029 ug/L may be

necessary for silver, using EPA method 1638, since EPA

Water Quality Criteria are as low as 0.31 ug/L [1001].

In some situations (as when background concentrations are

low), water detection limits as low as 0.0097 ug/L may be

necessary for antimony, using EPA method 1638, since EPA

Water Quality Criteria are as low as 14 ug/L [1001]

[1003].

In some situations (as when background concentrations are

low), water detection limits as low as 0.0079 ug/L may be

necessary for thallium, using EPA method 1638, since EPA

Water Quality Criteria are as low as 1.7 ug/L [1001]

[1003].

In some situations (as when background concentrations are

low), water detection limits as low as 0.14 ug/L may be

necessary for zinc, using EPA methods 1638 or 1639, since

EPA Water Quality Criteria are as low as 28 ug/L [1001]

[1003].

EPA 1996 IRIS Database, information related to older methods

for drinking water [893]:

 Monitoring Requirements: Ground water systems monitored

every 3 years; surface water systems monitored annually;

systems out of compliance must begin monitoring quarterly

until system is reliably and consistently below MCL. 

 Analytical Methods: Atomic absorption/furnace technique

(EPA 270.2; SM 304): Previous PQL= 0.01 mg/L. 

See also: EPA EMMI database [861].