U.S. DEPARTMENT OF COMMERCE
National Technical Information Service
PB-245 987
PRELIMINARY INVESTIGATION OF EFFECTS ON THE ENVIRONMENT
OF BORON, INDIUM NICKEL, SELENIUM, TIN, VANADIUM AND
THEIR COMPOUNDS
VOLUME IV - SELENIUM
VERSAR, INCORPORATED
PREPARED FOR
ENVIRONMENTAL PROTECTION AGENCY
AUGUST 1975
-------
KEEP UP TO DATE
Between the time you ordered this report—
which is only one of the hundreds of thou-
sands in the NTIS information collection avail-
able to you—and the time you are reading
this message, several new reports relevant to
your interests probably have entered the col-
lection.
Subscribe to the Weekly Government
Abstracts series that wil! bring you sum-
maries of new reports as soon as they are
received by NTIS from the originators of the
research. The WGA's are an NTIS weekly
newsletter service covering the most recent
research findings in 25 areas of industrial,
technological, and sociological interest—
invaluable information for executives and
professionals who must keep up to date.
The executive and professional informa-
tion service provided by NTIS in the Weekly
Government Abstracts newsletters will give
you thorough and comprehensive coverage
of government-conducted or sponsored re-
search activities. And you'll get this impor-
tant information within two weeks of the time
it's released by originating agencies.
WGA newsletters are computer produced
and electronically photocomposed to slash
the time gap between the release of a report
and its availability. You can learn about
technical innovations immediately—and use
them in the most meaningful and productive
ways possible for your organization. Please
request NTIS-PR-205/PCW for more infor-
mation.
The weekly newsletter series will keep you
current. But learn what you have missed in
the past by ordering a computer NTISearch
of all the research reports in your area of
interest, dating as far back as 1964, if you
wish. Please request NTIS-PR-186/PCN for
more information.
WRITE: Managing Editor
5285 Port Royal Road
Springfield, VA 22161
Keep Up To Date With SRIWI
SRIM (Selected Research in Microfiche)
provides you with regular, automatic distri-
bution of the complete texts of NTIS research
reports only in the subject areas you select.
SRIM covers almost all Government re-
search reports by subject area and/or the
originating Federal or local government
agency. You may subscribe by any category
or subcategory of our WGA (Weekly Govern-
ment Abstracts) or Government Reports
Announcements and Index categories, or to
the reports issued by a particular agency
such as the Department of Defense, Federal
Energy Administration, or Environmental
Protection Agency. Other options that will
give you greater selectivity are available on
request.
The cost of SRIM service is only 45f#
domestic (60£ foreign) for each complete
microfiched report. Your SRIM service begins
as soon as your order is received and proc-
essed and you will receive biweekly ship-
ments thereafter. If you wish, your service
will be backdated to furnish you microfiche
of reports issued earlier.
Because of contractual arrangements with
several Special Technology Groups, not all
NTIS reports are distributed in the SRIM
program. You will receive a notice in your
microfiche shipments identifying the excep-
tionally priced reports not available through
SRIM.
A deposit account with NTIS is required
before this service can be initiated. If you
have specific questions concerning this serv-
ice, please call (703) 451-1558, or write NTIS,
attention SRIM Product Manager.
This information product distributed by
us. DEPARTMENT OF COMMERCE
National Technical Information Service
5285 Port Royal Road
Springfield, Virginia 22161
-------
ffA-sto/2-7S-ooso PB 245 987
PRELIMINARY INVESTIGATION OF
EFFECTS ON THE ENVIRONMENT Of BORON.
INDIUM NICKEL. SELENIUM. TIN.
AND THEIR
VOLUMC IV
SCLEHIUU
Reproduced by
NATIONAL TECHNICAL
INFORMATION SERVICE
US Department of Commerce
Springfield, VA. 22151
OFFICE OF TOXIC SUBSTANCES
ENVIRONMENTAL PROTECTION AGENCY
WASHINGTON, D.C. 20490
AUGUST. 197S
-------
-------
-------
SELENIUM
TABLE OF CONTENTS
Page
FOREWORD .... . IV-1
I. PRODUCERS, SITES AND COSTS ...... i ..... . . ±V-2
A. Producers and Sites . . .............. IV-2
B. Costs ............... * ...... TV-5
C. Physical Properties ..... . ......... IV-5
II. PRODUCTION . ... . . . .; . . . IV-6
A. Producers ........... . . . . . . . . . IV-6
B. Quantities . ... ... . ... . . IV-6
1. Production .................. IV-6
2. Production Trends . . . . ... . . ... . . IV-6
C. Process. .... . . . . . . . . *v 3V-7
1. Selenium Recovery .............. IV-7
2. Selenium Oorrpounds . . . . . . . .... ... IV-8
III. USES ... . . . . . IV-10
A. Selenium and its Compounds . . ... . . . . ... IV-10
B. Future and Potential Uses .......... . •. IV-10
IV. CURRENT PRACTICE IV-13
A. Handling and Transportation . . . . . . . . . . . IV-13
B. Disposal ..................... IV-13
V. ENVIRONMENTAL C^rtAMlNATION . . . * . • i . . . . . . . IV-14
A. From Use ...*........... IV-14
B. From Production ............... . . IV-15
C. From Inadvertent Sources ..........••• TV-16
VI. MCNITORiNG AND ANALYSIS ............... TV-18
A. Monitoring .................... IV-18
B. Analysis of Selenium ............... IV-18
C. Analysis of Selenium In Urine .......... IV-18
D. Analysis of Selenous Acid . . . ... . . . ... IV-18
E. Detection of Selenium in 10 part per billion
ranges . . . . . . . . . IV-19
VII. CHEMICAL REACTIVITY . * _ IV-20
A. Environmental and Use Associated Reactions . . . . IV-20
B. Aspects with Biological Implications . . . . . . . IV-20
-------
-------
VERfAR
INC
TABLE OF CONTENTS
(Ooh't)
Page
C. Fish ............ ..'.. . , . .... . . IV-81
D. Invertebrates ................... IV-81
E. Plants . .......... IV-81
F. Microorganisms .................. IV-81
G. Results of Personal Contacts with Medical Personnel IV-82
XI, CURRENT REGUIATIONS ........... . . . . . . W-83
XII. SEMOARDS. ...................... IV-84
XIII. SUMMAFY AND OONOJUSIONS ......... . ..... IV-85
A. Sumtary . . . . . . . . . . . . . IV-85
B. Conclusions ................... IV-86
C. Recotmendations ...... . . . . IV-87
iii.
-------
LIST OF TABLES
1. Selenium Products and Producers: . . . ... . . . . . . IV-2
2. Physical Properties . . . . . . . . . ... . . ... . . 17-5
3. Selerdum and Import Trends, metric tons selenium .... IV-7
4. Table of Uses. . .............. IV-12
5. Relation of Urinary Selenium to Pood Selenium IV-22
6. Selenium Lewis in Various Species of Plants IV-26
7. Selenium Content in Human Organs and Tissues IV-29
8. Effects of Selenium Supplements on Tissue Levels of
Selenium in Yearling Ewes IV-32
9. Effects of Selenium Supplementation on Tissue Selenium
Levels in Swine IV-33
10. Endogenous Levels of Selenium in the Tissues of Male
. White Leghorn Chickens IV-34
11. Endogenous Selenium Levels in the Tissues of the Mature
Females of Three Avian Species IV-35
12. Effects of Selenium Supplementation on Tissue Selenium
Levels in Broiler Chickens IV-37
13. Effect of Selenium Supplements on Selenium Content of
Hens' Eggs IV-38
14. Distribution of Selenium in Tops and Roots of Selenium
Accumulators IV-40
15. Distribution of Se Between Roots and Tops IV-41
16. Selenium Content of Mature Com Grown in Sand Cultures . IV-42
17. Effect of Selenium Compounds on Growth of Microorganisms IV-46
18. Organic Selenium and Selenate in Native Plants ..... IV-51
19. Metabolic Reactions Inhabited by Selenium Compounds . . IV-52
20. Noninhibitory Metabolic Actions of Selenium . IV-53
21. Selenium in Sea Water IV-59
22. Selenium in Coal IV-59
IV.
-------
LIST OF TABLES
(Ooh't)
Page
23. Selenium Content of Atmospheric Dust from Air-
oonditioning Filters ........ .... .... . . . IV-60
24. The Selenium Content of Water, Milk, Eggs, Meat, and
Bread. W-60
25. Selenium: Sulfur Ratio of Sore Possible Sources of Air
Pollution and Sore Environmental Samples . . . . . . . IV-61
26. Selenium Content of Vegetables and Fruits . . ... . . IV-62
27. Selenium Content of Grains and Cereal Products . . . . . 3V-63
28. Selenium Content of Miscellaneous Products ....... IV-65
29. Selenium Content of Dairy Products ........... IV-65
30. Selenium Content of Meats and Seafoods .... . . . . . IV-65
31. Selenium Content of Strained Baby Foods ........ IV-66
32. Minimum lethal Dose of Selenium Compounds . . . . . . . IV-75
33. ID5() for Some Selenium Conpounda^Administered by Intra-
peritoneal Injection. . . . . . . / . . . . . . , . . IV-76
v.
-------
-------
•151-V
Volume IV
Preliminary tovestigatiai of Effects
on Environment of1 Selenium and Its Cbnpounds
Ihis is Volute IV of a series of six reports on the environmental
effects of boron, indium, nickel, selenium, tin, and vanadium and their
compounds. The information is based on literature reviews, direct con-
tact with representatives of companies involved in the production or
use of the materials, and consultation with knowledgeable individuals
from industry, academic institutions and the Federal Government.
-------
IV-2
I. PRODUCERS, SITES AND COSTS
A. Producers and Sites
Table 1 lists commercially significant chemical_produqts -
and the companies involved. For this study significant is defined
as production exceeding 1/2 metric ton or $1,000 value. Other mater-
ials may also be included in the discussion because of their unu-
sual properties, such as toxicity, or their anticipated future sig-
nificance. .
Selenium Products and Producers
Table 1.
7172)
Producer
Chemical
Ammonium aele-
nite
Barium selenate
Barium selenite
Cadmium reds
(cadmium sele-
nide lithopone)
Company, subordination
City Chem. Corp.
City Chem. Corp.
Fairmont Chem. Co., Inc.
Filo Color and Chem. Corp.
Hercules Inc., Coatings &
Specialty Products Dept.
H. Kohnstamm & Co., Inc., Gen.
Color Co.
SCM Corp.,
Glidden-^Durkee Div., Pigments
and Color Group
Smith Chem. & Color Co., Inc.
City Chem. Corp.
Allied Chem. Corp.
Specialty Ch^ems. Div.
:*'' '
Kewanee Oil Co.,
Barshaw Chem.. Co.,
Crystal & Electronic Prod. Dept,
/*:
Calcium selenate City Chem. Corp.
Carbon diselenide Strem Chems. Inc.
Chromium selenium Kawecki Bsrylco: Indust., Inc.
Cadmium selenate
Cadmium selenide
Location
Jersey City, N.J.
Jersey City, N.J.
Newark, N.J.
Newark, N.J.
Glen Falls, N.Y.
Newark, N.J.
Baltimore, Md.
Jamaica, N.Y
Jersey City, N.J.
Marcus Hook, Pa.
Solon, Ohio
Jersey City, N.J.
Danvers, Mass.
Boyertown, Pa.
-------
IV-3
Chemical
Cobaltous sele-
nate
Cobaltous sele-
nite
Cupric selenite
Cuprous selenide
Hydrogen selenide
Potassium sele-
nocyanate
Selenic acid
Selenium (Metal)
Selenium Products and Producers
Table 1. (cont).
Producer
Company, subordination
City Chem. Corp.
City Chem. Corp.
City Chem. Corp.
Fairmont Chem. Co., Inc.
The Shepherd Chem. Co.
G.D. Searle & Co., Will Ross,
Inc.
Matheson Gas Products
City Chem. Corp.
Filo Color and Chem. Corp.
City Chem. Corp.
Alloychem, Inc.
American Smelting & Refining
Co.
Atomergic Chemetals Co.
Gallard-Sch.lesinger
Bram Metallurgical Chem. Co.
City Chem. Corp.
Electronic Space Products, Inc.
Fairmont Chem. Co.', Inc.
Goldsmith, DF Chem. & Metal Corp,
Kewanee Oil Co.,
Harshaw Chem. Co.
Hercules Inc., Drakenfeld Colors
Induss'a Corp.
Location
Jersey City, N.J.
Jersey City, N.J.
Jersey City, N.J.
Newark, N.J.
Cincinnati, Ohio
Cucamonga, Calif.
East Rutherford,
N.J.
Gloucester, Mass.
Joliet, 111.
La Porta, Tex.
Morrow, Ga.
Newark, Calif.
Jersey City, N.J.
Newark, N.J.
Jersey City, N-J.
New York, N.Y.'
New York, N.Y.
Carle Place, N.Y.
Los Angeles, Cal.
Philadelphia, Pa.
New York, N.Y.
Los Angeles, Cal.
Newark, N.J.
Evanston, 111.
Cleveland, Ohio
Washington, Pa.
New York, N.Y.
-------
IV-4
Selenium Products and Producers
Table 1. (cont).
Producer
Chemical
Selenium (Metal)
(contj
Company, subordination
Kawecki Berylco Ind., Inc.
Phelps Dodge Refining Corp.
Robecko Chems. Inc.
Sylvan Chem. Corp.
Var-'Lac-Oid Chem. Co.
Ventron Corp., Alfa Products
Apache Chems.i Inc.
Fairmont Chem. Co., Inc.
Filo Color and Chem. Corp.
Kawecki Berylco Indust., Inc.
Seleium mono- City Chem. Corp.
chloride
Salenium oxychlor- Fairmont Chem. Co*, Inc.
ide ; ..'•".•
Selenium dioxide
Selenious acid
Sodium selenate
Sodium selenite
Zinc selenide
Zinc selenite
City Chem. Corp.
Fairmont Chem. Co., Inc.
Filo Color-and Chem. Corp..
City Chem. Corp.
Fairmont Chem. Co., Inc.
City Chem. Corp.
Fairmont Chem. Co., Inc.
Filo Color and Chem. Corp.
City Chem. Corp.
Kewanee Pil Co.,
Harshaw Ghem. Co.
City Chem. Corp.
Fairmont Chem. Co., Inc.
Filo Color and Chem. Corp,
The Shepherd Chem. Co.
Location
New York, N.Y.
New York, N.Y.
New York, N.Y.
Englewood Cliffs,
N.J.
Elizabeth, N.J.
Beverly, Mass.
Rockfield, 111.
Newark, N.J.
Newark, N.J.
Boyertown, Pa0
Jersey City, N.J»
Newark, N.J.
Jersey City, N.J.
Newark, N0J.
Newark, N.J.
Jersey City, N.J.
Newark, N.J.
Jersey City, N.J.
Newark, N.J.
Newark, N.J.
Jersey City, N.J
Solon, Ohio
Jersey City, N.J.
Newark, N.J.
Newark, N.J.
Cincinnati, Ohio
-------
IV-5
B. Costs
The 1972 producers' price for commercial and high-purity
selenium was $19.80 and $25.30 per kilogram. The dealers' price for
commercial grade selenium was $19.80 to $20.50 in the beginning of
the year, slumped below $19.50 in August, and was back to $19.80 at
(3)
the year's end.
Since most of the commercial selenium compounds are pro-
duced from selenium metal, their prices are primarily based oh the
selenium prices above plus processing costs.
C. Physical Properties
The major materials covered in this report are selenium
metal and selenium dioxide. Physical properties of these materials
are presented in Table 2. ,
Table 2
Physical Properties of Selenium and Selenium Dioxide
Solubility
in water
g/100oc @j °C
Seleniun 4.82 220 688 insoluble
Se02
Specific
Gravity
4.82
3.95
Melting
Point
°C
220
340-350
Boiling
Point
•C
688
sublimes
3i7
-------
VER/A
fAR INC
II. PRODUCTION
A. Producers
1. In 1972 primary selenium production was at four major
electrolytic copper refiners:
U.S. Metals Refining Co. Carteret, N.J.
American Metal-Climax
American Smelting & Refining Co. Baltimore, Md.
International Smelting &Ref. Co. Perth Amboy, N.J.
Anaconda Co.
Kennecott Copper Corp. Garfield, ut.
The Inspiration Consolidated Copper Co., Magna Cop-
per Co., and Phelps Dodge Corp. transferred crude materials con-
taining primary selenium from their copper refineries to the above
plants.
2. Selenium is recovered by domestic secondary refiner-
ies from purchased electronic scrap.
B. Quantities
1. Production
i • . In 1972, 335,000 kilograms of primary selenium were
.1
produced; secondary selenium production is estimated at 13,500
kilograms. Considerable selenium domestic scrap was reused by man-
ufacturers after outside reprocessing. Some selenium-containing
material was also shipped to foreign plants for recovery.
In August, 1971, Congress authorized the disposal of
210,000 kilograms of selenium held in national stockpile. In
1972, 7,290 kilograms of selenium from the stockpile were sold or
exchanged.
2. Production trends
Table 3 shows a trend in the U.S. production of sel-
enium together with the amounts imported for domestic consumption.
The variations are caused in part by trends in the copper indus-
try, on which selenium production depends. In fact, the United
States was the world's leading selenium producer prior to the
-------
IV-7
1967-68 copper strike, the imports fot consumption do not off-
set production changes.
Selenium and Import Trends, metric tons selenium
1968
287
210
1969
565
248
1970
455
205
1971
298
179
1972
348
195
Production
Imports
C. Process
1. Selenium recovery
Copper refinery anode slimes contain from 3 to 28 per
cent selenium. They provide the greater part of the U.S. and
world production of selenium. The sludge is aerated with dilute
sulfuric acid to separate the copper. In one process for recover-
ing the selenium, the slime residue is heated with soda ash and
silica and oxidized to the dioxide by blowing air through the melt.
Some of the selenium dioxide sublimes and is collected in water or
aqueous alkali in a *»et scrubber system, then sodium hydroxide
or mixed with sodium nitrate is added to the selenium dioxide to
form sodium selenite. The melt solidifies on cooling, and is
crushed. At this point the selenium salt is leached with cold wat-
er. Up to this point, tellurium, which is present in the anode
slimes ;.ilong with selenium, is carried along with the selenium in
the processing. The alkaline leach liquor is neutralized with sul-
furic acid, precipitating the bulk of the tellurium. The hydra-
feed dioxide with selenous acid remains in solution. Fairly pure
(99.5%) selenium is precipitated with sulfur dioxide. The treat-
ment followed next depends on the impurities.
An alternative procedure is to evaporate the leach
liquor from the roasted slime to dryness. Coke reduces the sele-
nium salts (selenites or selenates) to the selenide. The sodium
-------
IV-8
selenide is dissolved in water and treated with air to precipitate
, • (6)
pure selenium:
~— » Se .+ 2NaOH
The details of the process used by industry are not
available because of proprietary considerations. Industrial proces-
ses are complicated and generally tailored to a special mix of
recoverable valuable components. The components include copper, sil-
ver, gold, tellurium, and metals of the platinum group. Some infor-
mation has been published about the Kerinecott Copper Corporation
operation at Gar field, including qualitative information of result-
ing environmental contamination from this operation.
In the process used by the Kennecott Copper Corp. the
decopperized slimes are smelted in a rotary kiln with sodium bisul-
fate, or a mixture of sodium sulfate and sulfuric acid. The selen-
ium dioxide formed is volatized and recovered in a scrubber-Cottrell
system* The selenium-free residue, a fluid soda slag, is discharged
into water or granulated and water-leached. The crude selenium is
dissolved in aqueous sodium sulfite, and the product treated with
sulfuric acid.
Na2SeS03 + H2S04— »Na2S04 + Se + S02 + H20
The selenium formed is distilled several times, discarding the first
and last fractions. It is then formed into a shot and sold as the
high-purity grade.
2 . Selenium compounds
a« Ferroselenium
Ferroselenium is prepared from a fused mixture
of powdered iron and powdered selenium.
b. Selenium dioxide
. Selenium dioxide is an intermediate in the extrac-
tion of selenium from anode slimes. Commercial selenium dioxide is
prepared either by the catalytic oxidation of selenium with air or
treatment with nitric acid and evaporation.
-------
IV-9
c. Selenium oxychloride
Selenium oxychloride may be prepared by chlor-
inating a mixture of selenium and selenium dioxide dry or suspend-
ed in carbon tetrachioride.:
-------
IV-10
INC.
III. USES
; \. . • • . ' . • •. ' .
A. Selenium and its Compounds
A breakdown of the estimated use pattern for selenium in 1972 is
shorn in Figure 1. Selenium consumption in 1972 increased about 10 per cent
over that of the previous year. A detailed summary of current selenium usage
is presented in Table 4.
B. Future and Potential Uses
There are suitable substitutes for selenium in many of its applications.
For many electronic applications germanium or silicon can be used. In the chemical,
rubber, and steel industries, sulfur and tellurium are possible substitutes. In
copying devices, zinc oxide and certain dyes and organic materials can serve
as photo conductors. Under current technology, however, only selenium is
suitable in reusable photosensitive plates. '
-------
25%
PHOTOCOPYING
35%
GLASS MANUFACTURE
20
ELECTRONIC DEVICE
I
Selenium uses
-------
IBable 4.
Table of Uses
(31
Qonpound
Selenium
and
its
Compounds
Use
Glass manufacture
Photocopy Machines
Electronic devices
Pigments
Other
Purpose
Small amounts of selenium added to
glass melts to neutralize the green
color caused by iron »
Large amounts used to produce gray
and bronze window glass that re-
duces glare and heat transmission
Used in manufacture of red and
amber-colored glass for signals
and decorative uses
Comments '
Amount of selenium used for this
purpose increased 15% from 1971
to 1972
Bulk of pigment was required for
production of "cadmium red" (cadmium
sulfoselenides)
to
Small amounts ire*^ as additive
poultry and swine feed
greater use of copying machines
caused only slight increase in
selenium usage from 1971 to 1972 due
to more efficient use of selenium
and the reclaiming of domestic scrap
Industry expansion was offset by
more efficient use of selenium compoun<
Amount of selenium used for this
purpose increased appreciably from
1971 to 1972
Produces significant beneficial
effects
-------
IV-13
IV. CURRENT PRMTICE
A. Handling and Transportation
Commercial elenental selenium is relatively inert and may be
handled without special precaution. This is also true for stable metal
selenides, such as copper and lead. All other selenium compounds should be
treated with caution since some of these compounds can enter through the lungs
or skin and nay affect the body organs. This includes the reactive selenides,
the volatile and soluble conpounds, and particularly hydrogen selenide and
organics.
• •
Selenic acid with a melting point of 580, is classified as a
corrosive liquid, and transport containers must carry a white label. Cargo
aircraft cannot accept more than 25 liters of selehic acid and passenger air-
craft transport is prohibited. Vften handled as a solid, selenic acid requires
a poison label. Quantities of solid selenic acid up to 25 kilograms can be
(8)
shipped in passenger aircraft and 95 kilograms can be shipped in cargo planes.
(9)
One manufacturer uses the following containers to ship selenium:
(a) Selenium (commercial grade, powder of 80, 140, 200 and 325 mesh,
selenium analysis - 99.7%) - packaged in 45 kg pail.
(b) Selenium (high-purity, pellets of 1/8" diameter, analysis
99.99% selenium minimum) - packaged in 55 kg fiber drum con-
taining four 13.5 kg fiJaer polyethylene-iined containers.
B. Disposal
containers.
Selenium metal and selenium compounds must be disposed of in closed
(10)
-------
f- r IV-14
fAR INC.
V. QJVZRDNMEMTAL CONTAMINATION
A. Fran Use
a. Glass
Selenium, or in some cases sodium selenate, sodium selenite,
or barium selenite is added to glass in small amounts to decolor it or in
larger amounts to color it. Material may be lost to the environment when the
raw materials are handled. Salts of selenium, which are soluble, serve as an
example of this. Mixing ingredients for glass making, especially in batch pro-
cessing, is done with dry materials causing some loss by dusting. A large
amount of the elemental selenium used is volatized during melting as was con-
firmed by stack analysis. The glass industry estimates that 184 metric tons
of selenium were emitted into the atmosphere in 1969. ' Except for possible
local concern, this should not pose an environmental problem. Data is not
available oh selenium loss to the environment via other channels. Considering
the nature of the processes involved, however, this figure should be insignifi-
cant.
b. Photocopying
For the most part the photocopy processes of charging, exposure,
image development, image transfer, linage fixing, and photoceptor cleaning
take place in an enclosed environment, presenting little chance for contamination.
The exception is in the manufacture of photocopy equipment, where selenium is
jost to the atmosphere in the vacuum plating operation. The industry estimates
that about one kilogram per metric ton of selenium processed or around 135
kilograms in 1972 escaped into the atmosphere.
c. Pigments, Chemicals and Miscellaneous
The pigments are dispersed in liquid madia, applied by painting,
spraying, screen printing or dipping, and fired at 480 to 870 C. Bag filters
are used to control emission to the atmosphere, and losses to the environment
via other routes are very small. Among other uses of selenium, its use as an
insecticide, particularly for carnations and crysanthemums, allows small
amounts to get into the environment. *
-------
VER/A.
IV-15
'ER/AR //yfc
B. Fran Production
Selenium recovery in the United States is principally a by-product of
copper refining. The environmental contamination from selenium is closely re-
lated to the mining and milling of copper-bearing ores during the recovery of
selenium, unfortunately, analyses of the wastes are not available.
A major producer of selenium and precious metals by recovery
from the copper-bearing ore has recently started analyzing waste streams. The
analyses cover a long list of elements including selenium and is complicated
by the extremely small concentration levels. Sore qualitative information is
provided on losses of selenium to the environment. Selenium was found in a
number of waste streams within the operation. The precious metals recovery is
4 probable source of loss of selenium. In the selenium recovery process there
ale several points where selenium vapor may be lost. Besides the melting
operation and drying oven, which represent small potential losses of selenium,
the bisulfate fusion is of great concern. In the original installation a wet
scrubber was installed on the exhaust Side followed by a electrostatbr pre-
dpitator. In 1971 new hooding and wet scrubbers followed by electrostatic
precipitators were installed at all vapor discharge points. This eliminated
visual emissions to the atmosphere, but no analyses of the exhausts are avail-
able.
Selenium is also present in the very hot exhaust gases from the reverber-
atory furnaces and converters in the copper smelter. This is revealed by chemical
analysis of particulate matter collected in the balloon flues and electrostatic
precipitators through which the exhaust gases flow. Selenium is also found in
waste water stream from the selenium recovery plant and from the wet scrubbers
ahead of the sulfuric acid plant. Selenium may appear in the water used in
leaching metal values from waste dumps.
-------
IV-16
(AR INC.
C. From Inadvertent Sources
A survey was made in a representative U.S. town of the amount of
selenium in solid waste. The objective was to determine the extent to which
the handling/ processing/ and disposal of solid waste contributed selenium
to the environment. Emphasis was placed on emission of selenium as a result
of incinerating solid waste. The highest concentration observed was 14»5
micrograms per gram of participate matter collected in a stack emission sample.
Maximum values of 0.014 and 0.023 milligrams per liter were observed for an
incinerator residue quench water and an incinerator fly ash quench water
Q.8)
sample/ respectively.
During 1971 coal samples were analyzed for several elements including
selenium. The average selenium content was 8 ppm for 15 samples of coal taken
from various parts of the United States. During the combustion of coal/ the
selenium is discharged with the ash, of which fly ash averages about 65 per cent
of the total. In 1969 the total consumption of bituminous and anthracite coal
consumed was 469/000/000 metric tons. Based on this figure/ 90 per cent
application of controls, and 85 per cent efficiency of controls/ the selenium
emissions were calculated to be 573 metric tons.* '
Until recently, data on the selenium content of oil was almost non-
existent. Since 1971, however, analyses have been made for the Office of Air
Programs of the Environmental Protection Agency. The average selenium content
was 0.4 ppm for 10 samples of foreign and domestic crude oil. Assuming the above
figure and tile oonfoustion of 76 x 106 cubic meters of residual fuel oil, the
selenium emissions to the atmosphere amounted to 30 metric tons for 1969.* '
D. Amount Entering the Environment
Probably the major source of selenium in the environment is the
weathering of natural rocks. This apparently introduces much more selenium
into the waters and the atmosphere than the total of sources attributed to man.
m addition, selenium enters food chains directly through plants grown on seleniferous
soil. These factors are discussed in detail in Section IX.
-------
IV-17
Sources attributed to the activities of nan, as described earlier
in Section V, can account for approximately 3,500 metric tons of selenium
per year entering the atmosphere (about 900 metric tons per year) and landfills
or dumps (about 2,600 ire trie tons per year), based on:
Source Amount Entering Environment per Year
Glass Manufacture 200. kkg (mostly ataobsphere)
Fuel Oil Combustion 30 kkg (atmosphere)
Cbal Combustion 573 kkg - to^atmosphere
2,500 kkg -to land
Other 200 kkg
Total 3,503 kkg
-------
IV-18
VI. MDNTTOPING AND ANALYSIS
A. Monitoring
There are no data available en the monitoring for selenium of
air or water.
B. Analysis of Selenium
In most methods used for the analysis of selenium, the selenium
must be in solution as the quadrivalent ion. It is then either reduced and
precipitated as the element or measured volunetrically by oxidation to the
hexivalent state, or by iodimetry. Selenium can also be determined polaro-
graphically. The only specific spot test for selenium depends on its catalytic
action on the reduction and decoloration of methylene blue by alkali sulf ides.
A drop of the solution to be tested is added to a few crystals of sodium sulfite,
followed by a little sodium sulfide solution, and then the methylene blue. The
(19)
sensitivity is 0.08 micrograms.
C. Analysis of Selenium in Urine
Urine is digested in a sulfuric-nitric acid mixture followed by
distillation with HBr-Br2 solution which separates selenium as SeBr..
Sulfur dioxide precipitates selenium which is filtered off and estimated by
an iodine thiosulfate titration. * .
D. Analysis of Selenous Acid
, Ihis spectrophotonetric method for the determination of sufcroicrai
quantities of selenous acid was developed in 1971. The procedure is based
on the oxidation of hydroxylamine hydrochloride to nitrous acid by selenous
acid followed by tiie subsequent coupling of the diazonium salt with
N(l-naphthyl)^thylenediamine dihydrochloride. Optimum conditions have
been established. The range of determination is 0.01 to 0.20 mg Se17 per liter.
The method is simple, sensitive, and reproducible with no common interferences
which cannot be easily obviated.
-------
IV-19
E. Detection of Seleniun in 10 part per billion range
The current level of selenium tolerated in Illinois public waters
is 10 parts per billion (0.01 mg/1) which is beyond the capability Qf classical
analytical methods due to limitations of volume of sample, time of analysis,
or removal of interfering substances. A fluorometric method was developed to
analyze the selenium by the Analytical Research Department of Abbott laboratories,
North Chicago, Illinois. Elemental selenium is converted to selenious acid
by the action of a bromine-bromide redox buffer. Selenious acid reacts with
2, 3-diaminonaphthalene in acid solution to form the strongly fluorescent
naphtho-[2,3-d]-2-seleno-l,3-diaaole. Selenates axe not reduced to seleriites
under these conditions, hence the method is specific for elemental selenium
and selenium in the four valance state. Plots of fluorescent intensity vs
concentration in the region of 0.005 to 0.2 ug selenium (IV) axe linear and
practically free from reagent interference at excitation frequency of 366 nm
and a fluorescent emission minimum of 522 nm.
-------
IV-20
VII, CHEMICAL REACTIVITY
A. Environmental and Use Associated Reactions
The bulk of the uses of selenium are of non-chemical nature, so
chemical reactivity plays a limited role.
B. Aspects with Biological Implications
The exhalation of volatile selenium compounds by plants, animals,
and ndcroorganisma is a minute source of selenium to the atmosphere. Selenium
may be acted on by bacteria in nature to produce highly poisonous compounds, '
such as dimethyl diselenide, given off by certain plants, and dimethyl selenide,
(24)
given off by microorganisms and animals.
-------
IV-21
VIII. BIOLOGY
A. Absorption and Excretion
1. Humans
Selenium is absorbed through the lung, alimentary tract, and
hands. Excretion is via respiration, urine, feces, milk, and perspiration.
The concentration of selenium in the urine may reflect selenium exposure. The
normal range for selenium concentration in the urine of healthy male adults
125)
is 0.10 to 1.50 ppm. One study of farm families attempted to correlate
urinary selenium with selenium levels in the diet. Table 5 shows a trend of
increased selenium in the urine of individuals consuming foods high in selenium
content. Except for one individual, all the urinary selenium concentrations
/•j5\
fall within the normal range.v '
A study of Oregon school children gave good correlation between
'•••'..": '• ' '....' : ' • •'•'..' '-•' '•'.'' • ; • (12)
selenium in foods, urinary selenium excretion, and prevalence of dental canes.
2. Other Mammals
Orally ingested selenium is absorbed by the small intestine. Ex-
cretion, is mainly through the urine, but also in the feoes, perspiration, and
exhaled air. The solubility of the selenium compound and the ratio of sulfur
(26)
to selenium determine the rate of selenium absorption. Intestinal transport
of sulfur-35 methicnine and selenium-75-selenatethionine apparently proceed via
the sane active mechanism in everted hamster intestinal sacs. Selenite and
selenocystine are absorbed by a different mechanism. Their sulfur analogs do
not affect their absorption.*28*
Orally administered selenium was not absorbed from the rumen or
abomasum (gastric stomach) of sheep or from the stomach of swine. In both
species, selenium was secreted into the duodenum, due to its presence in
(29)
pancreatic juice bile, and intestinal secretions. Only 35 per cent of
ingested selenium was absorbed by the sheep, compared with 85 per cent of the
same dose absorbed by swine when rations containing 0.35 and 0.50 ppm selenium,
respectively, were consumed. Monogastrics absorb selenium with a higher efficiency
than ruminants, perhaps because ingested selenite could be converted to in-
-------
IV-22
Table 5
Halation of Urinary Selenium to Food Selenium
Family Urinary selenium
Food selenium
No.
97
51
22
113
52
83
27
76
107
47
74
78
16
19
(ppm)
0
0
0
0
0
0
0
0
0
0
1
1
1
1
.25,
.20,
.20,
.20,
.26
.13,
.29,
.43,
.94
.70,
.03,
.00,
.05,
.24,
0
0
0
0
0
0
0
0
1
1
b
1
.27, 0.32
.27
.21
.20, 0.24
.38, 0.40
.56
.73
.80, 0.98
.10
.14
.36, 1.33
.98
Milk
Trace
0.
0-
0.
0.
0,
0.
0.
0.
—
36
25
25
34
22
35
39
57
Trace
0.
1.
1,
36
14
27
Eggs
0
1
1
1
0
•MI
4
3
3
4
5
.57
.35
.40
.45
.32
••
••
.08
.65
.08
.12
.04
•»
Meat \fegetables
— Trace
1.60 0.36
— 0.41-0.74
— 0.30-0.82
— Traoe-0.58
2.19 —
2.22 — .
3.30 0.27-1.05
— Traoe-0.18
— 0.23-2.04
Cereal grains
*
Trace
1.90
Trace
0
—
—
—
—
3.30
— ' — 0.45-1.00
— 1.03-17.80
— 2.42
8.00 1.26
3.60
2.50-18
4.20-10
.80
.00
-------
IV-23
soluble fonts by rumen microorganisms. Elenental selenium is footed from
both selenite and seleno-amino acids in the gastrointestinal tract of ruminants,
: (28)
indicating both reductive and oxidative reactions taking place.
Selenium intake, retention, and excretion were studied in rats
(nonogastrics) fed different forms and concentrations of selenium for 70 days
in a corn torula yeast diet. The apparent absorption of selenium averaged
about 80 per cent of intake for all diets. The selenium balance in the rats
was examined at day eight (trial I) and day 50 (trial II). The daily selenium
intake in micrograms increased from day eight to day 50, but the 72 hour
selenium retention at day 50 was reduced to less than half the retention at
day eight. The percentage of fecal excretion of the selenium intake did not
change from day eight to day 50.
At both times, selenite-fed rats excreted a higher percentage
of selenium in the feces than selenomethionine-fed rats. The percentage of
urinary excretion of selenium intake was more than doubled at day 50 compared
with day eight. In rats fed 0.146 ppm selenium as selenite, the percentage
of selenium excreted in the urine increased from 6.4 per cent to 32.5 per cent
from day eight to day 50. The selenium intake in this latter group of rats
was highest of all groups. The increased urinary excretion and decreased
selenium retention indicate that perhaps selenium equilibrium was reached.
In lambs (ruminants) fed torula yeast diets containing 0.014 to
5.014 ppm selenium as sodium selenite for 97 days, the excretion of either
intravenously or orally administered selenium-75-sodium selenite in the feoas,
urine, and respiration was determined during a 12-day period. The fecal
excretion, expressed as a percentage of administered dose of radioactivity,
was about five per cent in lambs intravenously dosed, and about 20 to 25 per
cent in orally-dosed lambs. (This latter is comparable to the percentage of
oral selenium intake excreted in the feces of rats). The percentage of fecal
excretion was unaffected by dietary levels of selenium indicating that the
amount absorbed depends upon the amount taken in. Both urinary and volatile
-------
IV-24
selenium excretion increased with increasing dietary level of selenium.
•flre effect on urinary excretion was most prounounosd, ranging from less than
10 per cent of the orally or intravenously administered radioactivity in rats
fed 0.14 ppm selenium to more than 40 per cent of the oral dosef and 60 per
cent of the intravenous dose,in rats fed 5.014 ppm selenium. Radioactive
selenium retention was progressively reduced in all tissues of animals fed
higher concentrations of selenium.
The respiratory excretion of labelled selenium compounds was
investigated in rats. A significantly higher percentage of radioactivity was
excreted by respiration, and a lower percentage in the urine, in animals in-
(32)
jected with selenite than with selenate.1 Excretion by exhalation was
essentially complete six hours after injection. Animals receiving low doses
(0.08 rag selenium per kg) of selenate retained significantly more and exhaled
significantly less selenium than animals receiving 1.40 mg selenium per kg.
Urinary and fecal excretion percentages* vere unchanged. Rats injected with non-
radioactive selenite two hours before receiving radioactive selenite showsd no
differences in exhaled selenium compared with rats receiving both simultaneously.
If the cold selenite was administered 12 to 48 hours prior to the radioactive
selenite, respiratory excretion of selenium was reduced to levels close to those
observed when no carrier was given.
Selenium oxychloride (4 and 12 mg) .applied to the skin of rabbits
was absorbed. A liver concentration of 2.0 to 4.3 ppm and blood level of 0.6
H2^
to 2.2 ppm resulted. '
5
3. Nbnmammalian Vertebrates
Orally administered selenium-75 was used to study the absorption
and excretion of selenium by hens (Gall us domestica). Selenium was absorbed at
the level of tiie small and large intestine, and excreted by the liver, intestine,
kidney, and lung as in mammals. Selenium-75 was still present in all tissues
(33)
examined even 30 days after its administration.
-------
'KR/AR INC.
IV-25
Carp contained 19 ppm selenium after a month in a 10 ppm
solution of selenious acid. The mudsnail contained 90 ppm selenium after
.: ' •• ' .• •.:•• ••'•• ' . :-. .•' •"• (34 \ • .•''.•••••
the same treatment. Duckweed contained 698 ppm.l '
4. Plants
The accumulation of selenium by plants depends upon several factors:
the species of plant, environmental conditions, age and phase of plant growth,
(12V
and the nature of the selenium compounds. The selenium content of plants
grown in the sane soil reflects the differing abilities of plants to accumu-
late selenium, as shown in Table 6.
Plants may be classified into three groups, based on their
(12)
selenium absorption. ' Primary selenium indicators or accumulators or
"fifeath's indicators" or converter plants contain large amounts of selenium
(iOOO to 10,000 ppm), which is mostly present in water soluble, low molecular
weight, organic compounds. Secondary selenium absorbers rarely contain more
than a few hundred ppm selenium oh a dry weight basis, and a large percentage
of the selenium is in the form of selenate. Most cultivated crop plants, grains,
and grasses accumulate low concentrations of selenium (up to 30 ppm). The
selenium is associated with the plant protein mainly as selenarethionine.
Seasonal variations in selenium accumulation occur in indicator
plants, but generally not in crop plants. Selenium concentrations are highest
during periods of initial growth. Selenium accumulation depends upon the
(12)
amount of selenium available to the plant in both indicator and crop plants.
Studies on the availability of different forms of selenium compounds showed that
calcium selenate was more readily absorbed than sodium selenate, and plants
absorbed more selenium as selenate than selenite. Iron (III) hydroxide selenite
and sodium selenite were readily absorbed by indicator plants, but uptake by
crop plants was slow. Iron (II) selenide was not absorbed by crop plants and only
limited amounts were absorbed by young indicator plants. Organic selenium
(extract of Astragalus racemoSus) was more readily absorbed than inorganic
forms as shown in Figure, 2.
-------
IV-26
Table 6
Selenium Levels in Various Species of Plants
(12)
Species Selenium Content (ppm)
Astragalus bisulcatus 5,530
Stanlaya pinnata 1,190
Atriplex nuttallii 300
Grasses 23
-------
IV-27
8000
• Nots*6, SEMES
• PLANT EXTRACT SERIES
5 10 15 20 25 30 35 40
SELENIUM IN CULTURE SOLUTION (PPM)
Figure 2
Comparison of the ability of corn and A. rocemosus
to accumulate selenium from selenite and
from organic selenium in Astragalus extract
-------
IV-28
The addition of sulfate to the nutrient medium depressed
selenate absorption by wheat and com, but not the absorption of other forms
(12)
of selenium. ' Apparently sulfate and selenate compete for the sane site
of active uptake. Selenite is absorbed at a different site. During absorption
selenite is reduced to what appears to be elemental selenium. ' The initial
step in the absorption of selenium may involve ion exchange between the plant
roots and the medium. Uptake of selenium-75-labelled selenite by excised
Astragalus preussii roots showed that after an initial rapid absorption of ions,
an equilibrium was established between incoming and outgoing ions after five
minutes. Neither an increase in time nor isotope concentration affected the
percentage of selenium-75 absorption. Eighty-seven per cent of the absorbed
selenium was present in the sap in the dissolved state, and the remainder was
/12\
bound to the root skeleton. ^'
3ii some species, such as white clover, selenite was readily ab-
sorbed by the leaves and translocated to the stolons and roots. Tracer
studies in indicator plants have revealed that selenium absorbed by the roots
is translocated to areas of active growth and metabolic activity. Selenium
apparently is not stored in the plants, as aged leaves showed a loss of
(12)
selenium from the nesophyll as chloride was lost.
Selenium is volatilized from the leaves of intact plants and
also from drying crop plants. Several volatile selenium compounds have
been identified, with dimethyl diselenide comprising the largest fraction.
; B. Distribution
1. Human
The selenium content in human organs and tissues from subjects of
various ages is shown in Table 7. In children, pancreatic selenium is extremely
high compared with other tissues. In the adolescent and adults, liver and
(25)
kidney tend to contain the highest levels of selenium. '
-------
Selenium Content in Human Organs and Tissues
(25)
Organ and
Tissue
Heart
Lungs
Spleen
Liver
Kidneys
Pancreas
Muscles
Skin
Bone
Child
Seven
Months,
Extreme
Pre-
maturity
0.0083
0.0020
0.0140
0.0072
0.0037
0.0260
0.0021
0,0036
0.0105
Child
Nine
Months,
Intra-
uferine
Asphyxia
0.0040
0.0016
0.0071
0.0026
0.0028
0.0240
0.0021
0.0021
0.0090
Child
Nine
Months,
Intra-
uterine
Asphyxia
0.0006
0.0006
0.0079
0.0011
0.0031
0.0261
0.0024
0.0025
0.0064
Child
Six
Months,
Extrene
Pre-
maturity
0.0204
0.0011
0.0046
0.0019
0.0014
0.0260
0.0016
0.0028
0.0984
Girl
15 Years,
Food
Poisoning
0.0004
0.0024
0.0018
0.0079
0.0080
0.0032
0.0014
C.0012
0.0021
Man
29 Years,
Skull
Fracture
(Trauma)
0.0072
0.0138
0.0076
0.0058
0.0271
0.0026
0.0028
0.0028
0.0031
Man
64 Years,
Mechanical
Asphyxia
0.0114
t
0.0100
0.0078
0.0161
0.0161
0.0100
0.0226
0.0i24
0.0243
Man
75 Years,
General
Athero-
sclerosis
0.0024
0,0024
0.0014
6.0072
0.0016
0.0021
0.0020
0.0032
. ___
to
vo
-------
VER/A
IV-30
fAR INC.
2. Other Manuals
The highest oonoentraticns of selenium in rats fed experimental
diets for 70 days occurred in the kidneys in all the groups. The liver con-
tained the next highest concentration, followed by the spleen and blood, the
skin, hair, and ^muscles. In lambs fed varying selenium intakes, the highest
retention of oral or intravenous selenium-75 was in the pelt and "whole blood,
followed by the kidney, liver, and lung. The percentage of the radioactive dose
retained was much greater in all tissues of animals fed low selenium diets.
Mipose tissue retained much less selenium-75 than muscle or bone.
The distribution of selenium-75 injected as selenate in the blood of
rats varied with the amount of selenium injected. The fraction of injected dose
per ml appearing in the red blood cells increased almost tenfold as the selenium
dose was increased from 0.08 to 1.4 mg selenium per kg. The total serum lipo-
protein selenium content more than doubled as the selenium dosage was increased,
and most of this effect could be attributed to a tenfold increase in the
(32)
selenium content of the ether-acetone extractable lipid fraction.v ' The alpha-
2-globulin fraction of serum proteins contained the highest amounts of injected
selenium.
In animals receiving very low dietary levels of selenium, the highest
selenium concentrations usually occur in the kidney, followed by the liver and
muscle. The selenium level in the liver rises more rapidly than in the kidney
(28)
as the level of dietary selenium is increased.
Selenium-75 appears in the milk of dogs injected with radioactive
selenite 278 days previously. Owes fed a high selenium diet for six months,
followed by a low selenium diet may transmit protective levels of selenium to their
(28)
lambs bom nearly one year after the ewes ware placed on the low selenium diet.
The pups of female rats maintained on selenium-supplemented diets
for 70 days before mating contained more than four times as much selenium on
day one as the pups of dams continuously maintained on low selenium diets. The
birth weights of the pups were not significantly different, but at 55 days of
age, weights of pups of selenium-supplemented dams were double the weights of
pups of low selenium dams. The selenium levels of all groups of pups were
not significantly different on day 55 in the surviving pups. The kidneys had
the highest selenium levels. Mortality data indicate that pups of dams fed
-------
IV-31
0.078 to 0.093 ppm selenium supplements prior to breeding had a higher
survival value than pups of dams fed low (0.024 ppm) or higher (0.120 to
(30)
0.146 ppm) selenium for the same period.
The effects of dietary intake of selenium on the distribution of
(35)
selenium in the organs of yearling ewes are shown in Table 8. High
selenium intake resulted in high selenium in the liver; high levels also
occurred in the kidneys. Selenium apparently cleared from the animal tissues
to some extent once the selenium supplements were withheld, but organ selenium
was still higher than for animals fed basal diet. The liver and kidneys can
accumulate quite high levels of selenium if dietary selenium is high. No
significant differences in muscle, heart/ or liver selenium levels were observed
•..•'••' (38)
between swine receiving dietary selenium supplements of 0.1 ppm or 1.0 ppm. St
Table 9
The apparent differences in tissue accumulation of selenium between
the ruminant sheep and the nonogastric swine may be due to excretion differences,
basal diet selenium levels, absorption differences, or other species differences.
3. Nonmammalian Vertebrates
Endogenous selenium distributed in the tissues of three avian species
(39)
receiving chicken breeder pellets containing 0.27 ppm selenium was studied.
Leghorn chickens is shown in Table 10 for two ages. The pineal concentration
was extraordinarily higher than in the other tissues, especially in the 24-week
old males. The liver and kidney accumulated the largest concentrations of in-
jected selenium-75, and the older birds accumulated twice as much as did the
young birds.
The tissue distribution of endogenous selenium is shown in Table 11
for.female chickens, turkeys, and Japanese quail (Ooturnix coturnix japonica)
at the laying stage. The pineal selenium in all species is much less than
that observed in the male chickens. The pituitary and kidney of all species
contained high selenium concentrations. The pancreas of Ooturnix also con-
tained quite high selenium. The fecal and crop selenium concentrations were
about the same. Egg yolks had a much higher selenium content than the whites
or shells.
-------
IV-32
Table 8.
Effects of Selenium Supplements on Tissue
Levels of Selenium in Yearling Ewes (35)
Selenium Content (ppm)
Diet Kidney Liver Muscle Heart Fat
Basal Clew Se) 0.5 0.75 0 — 0
8 rag Se per day-44 days
64 days-basal diet 1.57 1.85 0 0.57 0
10 mg Se daily€4 days 6.87 9.10 0.8 1.90 0
20 mg Se daily-44 days
61 days-basal diet 1.47 1.33 0 Q.99 0
17 mg Se daily-116 days 3.95 29.21 0.8 1.75 0
-------
IV-33
Table 9.
Effects of Selenium Supplementation on Tissue
Selenium levels in Swine
(38)
Selenium Level (pgn)
Tissue Basal diet + 0.1 ppm Se Basal diet + 1.0 ppm Se
muscle 0.16 0.15
heart 0.21 0.17
0.56 0.52
-------
IV-34
Table 10.
Endogenous Levels of Selenium in the
Tissues of Male White Leghorn Chickens
(39)
Selenium Content (ppm)
Tissue 24-Week Old Year-Old
Blood 0.329 0.634
Pireal 18.85 4.04
Liver 0.737 0.499
Kidney 0.934 0.681
Cerebellun 0.278 0.277
-------
IV-35
Table 11.
Endogenous Selenium Levels in the Tissues
of the Mature Females of three Avian Species
(39)
Part
Blood
Pineal
Pituitary
Eye
Kidney
Spleen
liver
Pancreas
Magnum
Cerebrum
Dienoephalon
Cerebellum
Ovary
Pectoral
Feoes
Crop contents
Egg yolk
Egg albumin
Eggshell
Ration
Chicken
0.182
1.27
. 1.16
0.095
0.649
0.539
0.475
0.364
0.295
0.230
0.222
0.214
0.182
0.174
0.079
0.071
0.531
0.103
0.067
0.271
Selenium Content (ppm)
Turkey
0.166
0.364
0.982
0.072
1.077
0.705
0.800
0.499
0.182
0.230
0.190
0.301
0.364
0.190
0.127
0.127
-—
— .
' •. — ;
0.337
Coturnix
0.459
0.380
1.11
0.120
1.50
0.950
0.887
1.259
0.348
0.356
0.309
0.372
0.491
0.301
0.198
' —
0.626
0.135
0.143
0 ,337
-------
IV-36
In 14- and 20-week oM turkeys, the addition of 0.1 or 0.2 ppm
selenium to the diets produced no significant differences in the seleniun
(38)
levels in the breast muscle, liver muscle, liver, or blood. In broiler
chickens, the addition of 0.1 to 0.4 ppm selenium to a basal diet containing
0.07 ppm selenium resulted in some effects on tissue seleniunflevels as
shown in Table 12. Dietary levels of 0.2 ppm selenium caused increases in
both muscle and kidney selenium content. Skin selenium was alao somewhat
increased by the supplementation. Dietary selenium at 0.1 ppm apparently in-
creased liver selenium content, but higher levels reduced it. In another
study, no changes in thigh or breast muscle selenium in chickens were pro-
duced by the addition of 2.0 ppm selenium to the diet. Liver, kidney, and
(38)
heart selenium were increased by this supplementation. Dietary supple-
mentation of organic selenium more effectively increases tissue concentra-
(26)
tions of selenium than inorganic supplements.
The addition of 0.1 ppm of sodium selenite to the diet of
laying hens increased laying capacity by 10 per cent and increased the selenium
content of liver, ovary, heart, pectoral muscle, blood cells, and kidney. '
Selenium accumulation was greater in the kidneys of nonlayers and less distinct
in the kidneys of layers, presumably due to the increased selenium deposition
(47)
in the eggs of layers. The selenium content in the eggs of hens fed 0.1
ppm selenium supplements was higher than in nonsupplenentad hens' eggs as
ahown in Table 13.
The incubating eggs of hens receiving 36 micrograms of selenium
daily in their diets showed steadily increasing amounts of selenium in their
yolk sac and in the liver, blood, and proteins, but not in the heart, of
(43)
developing embryos.
Studies with radioactive oonpounds revealed that injected selenite,
but not selenate, becomes bound to the serum proteins of chicks. At low levels,
binding is predominantly to the alpha and gamma globulins, but at higher con-
centrations, albumin binding also takes place. Treatment of the serum proteins
from chicks injected with both radioactive selenate and selenite with dilute
i released 85 per cent of the bound selenium-75 from the protein of which
(44)
note than half was selenite.
-------
IV-37
Table 12.
Effects of Selenium Supplementation on Tissue
Selenium Levels in Broiler Chickens
' . /• , .. ' ", •• . . • '(38). ' . ;. ;. .' ' .;'••• = •'; :
Selenium Content (ppn)
Basal Basal Basal
Tissue Basal + 0.1 ppm Se + 0.2 ppm Se -f 0.4.ppn Se
muscle
liver
kidwsy
skin
0.061
0.25
0.39
0.09
0.071
0.48
0.34
0.13
0.103
0.34
0.80
0.16
0.114
0.13
0.56
0.13
-------
IV-38
Table 13.
Effect of Selenium Supplements on Selenium
Content of Hens' Eggs
(42)
Selenium Content (micrograras)
Diet Albumin YoUc
Basal 1.9 3.14
Basal + 0.1 ppm 3e 2.34 3.64
-------
IV-39
/AR INC.
4. Plants
The distribution of selenium in plants is quite different for
indicator plants compared with crop plants. Table 14 shows that in most
indicator species, higher selenium concentrations occur in the tops of the
plants then in the roots; for crop plants, the opposite is true; the roots
have a higher selenium content than the leaves and stems as shown in Table 15.
The distribution of selenium in the parts of mature com grown in sand culture
with various concentrations of selenium added as either selenite or organic
selenium is 'shown in Table 16. Supplemental organic selenium (2.5 and 5.0
ppm) produces much higher selenium accumulation in all parts of the corn than
the selenite.
C. Growth and Nutrition
1. Humans
Selenium has been demonstrated to be a definite nutritional re-
quirement in animals. Some preliminary findings suggest the necessity of
selenium in human nutrition as well.
In children treated for Jcwashiorkor in Jamaica, satisfactory
weight gain responses were not achieved until the diets were supplemented daily
IAC\
with 0.25 mg of selenium as y, Y-diseleno-di-n-valeric acid. Similar effects
were observed in infants suffering from malnutrition in Jordan. Oral
administration of 0.30 mg of selenium as sodium selenite daily in milk stimu-
lated weight gains. Selenium is reduced in the whole blood, plasma, formed
elements and plasma proteins of victims of kwashiorkor compared with healthy
adults or children recovered from kwashiorkor. '
2. Mammals
Selenium deficiency diseases are not uncommon in ruminants and
nonruminahts, mammals, and avians. In rodents, hepatic necrosis accompanied by
renal necrosis, pancreatic dystrophy, and skeletal and heart muscle degeneration
are the symptoms of severe selenium deficiency. MitDchondrial and cytoplasmic
changes in the liver can be detected by electron microscopy before gross necrosis
is evident. Death may occur in four to six weeks unless selenium supplements
are supplied. Vitamin E is also effective in alleviating symptoms.
-------
IV-40
Table 14.
Distribution of Selenium in Tops and Roots
of Selenium Accumulators
(12)
Plant
Astragalus crotalariae
A, beathii
A. pattersoni var. praelongus
A. argillosus
A. blsulcatus
A. preussii
A. beathii (greenhouse, selenate)
A. pattersoni
A. raoemosus (greenhouse, selenite)
Haplopappus fremontii
Stanleya pinnata
Selenium
Tops
2,000
1,963
583
385
1,180
313
524
730
1,256
4,800
125
(ppm)
Roots
45
66
26
27
130
40
213
296
659
4,800
429
Ratio
Tops/roots
44
30
22
14
9
8
2.5
2.5
1.8
1.0
0.3
-------
IV-41
Table 15.
i Roots and
(36)
Distribution of Se Between Roots and 7bps
Se Oondentration
(1000's of 0>HAJn. Dry Wt.)
Species
Spinach
Perennial ryegrass
Tomato
Mustard
Barley
Sunflower
Wheat
Annual ryegrass
Alfalfa
Subterranean clover
Fhalaris tuberosa
Oiion
Boots
2578
1802
1753
1760
1886
2507
1774
2194
1561
3979
1635
650
Tops
110
115
138
163
176
262
195
256
207
538
229
246
Concentration
Ratio
Roots
Tops
23.4
15.6
12.7
10.8
10.7
9.6
9.1
8.6
7.5
7.4
7.1
2.6
-------
IV-42
Table 16.
SeleniumContent of Mature Corn Grown in Sand Cultures
(12)
oej.cau.uni
adted
(ppn)
0.5
1.0
2.5
5.0
Roots
Aa &
135
155
209
321
121
218
817
1,820
Steins
Aa £
60
105
147
182
78
138
393
1,228
leaves
Aa
58
76
141
134
B*
86
153
359
890
Grain
A3
77
107
209
308
#
55
99
325
694
Selenium added to culture solutions:
®A: sodium selenite
selenium as aqueous extract of A. bisulpatus
-------
'ER/AR INC.
In swine, hepatosis diaetetica is characterized by liver
necrosis, degeneration of the muscles and heart, massive transudaticns, and
ceroid pignents in the adipose tissue. Nutritional muscular dystrophy is
accompanied by increased lewis of serum glutamate oxaloacetate trans-
aminase. Death results in 22 to 45 days. Diets containing 0.5 ppm selenium
as sodium selenite or 100 ppm vitamin E, or both, reduced the incidence of
mortality. Cystine was ineffective.
In horses in New Zealand, neonatal myopathy could be relieved
by injections of sodium selenate at birth and at 10 days of age. Hie
syndrome is characterized by watery, chalky white, degenerating musculature,
• ' -.'.-•.''• ' • • ' .•••••'••."'..: (35) . .'
loss of hair, and abnormally thick, firm layers of yellow-brown fat.
3. Other Mammals
White muscle disease (HMD) occurs in lambs and calves whose dams
have been fed diets containing less than 0.02 ppm selenium in the dry matter.
The symptoms are severe bleaching and calcification of skeletal and heart
muscles, resulting in a loss of normal motor function and deformed linbs.
High levels of serum glutamate oxaloacetate transaminase and creatinuria
accompany the syndrome.
WMD can be prevented by feeding ewes 0.1 ppm selenium in the diet.
One hundred mg of sodium selenite per 30 kg body weight administered orally
to cows prevents VMD in calves. Lambs and calves can also be treated pro-
phylactically with selenium compounds. Vitamin E alone was ineffective.
Selenium is required for normal reproduction and growth of off-
spring. In New Zealand, the percentage of lambing in certain areas was in-
creased from 62 per cent to 94 per cent by the oral dosing of ewes with 5 mg
of selenium as sodium selenite prior to breeding.
Selenium-depleted rats were obtained by feeding a purified low
/47\
selenium diet containing vitamin E to weanling rats.v ' After twenty weeks,
selenium levels in the blood, liver, and skeletal muscles had been reduced from
0.32, 0.60 and 0.23 ppm to 0.05, 0.04 and 0.02 ppm, respectively. Seventy per
cent of these declines occurred within the first six weeks. Improved growth
and increases in liver and blood selenium were observed 20 weeks after be-
ginning a dietary supplement of 0.5 ppm selenium as seleno-nisthionine. Females
-------
IV-44
maintained on the lew selenium diet reproduced normally through three litters,
but the offspring had reduced growth and little hair compared with offspring
fed a selenium-supplemented diet or born to dams on a supplemented diet.
4. Birds
Exudative diasthesis in chicks apparently develops due to a lack
of ability to absorb sufficient vitamin E. The symptoms include edema,
hemorrhage, anemia, degeneration of hemoglobin, and decrease in albumin. The
abdominal wall takes on a greenish-blue appearance . Symptoms appear two to
three weeks after chicks are placed on a diet deficient in both selenium and
vitamin E. The absence of selenium produces flbrotic pancreatic degeneration
with an acratpanying decrease in lipase. As a result, lipid digestion is
severely impaired. Undigested lipids cannot be absorbed and the absorption
of fat-soluble vitamin E is extremely reduced. Relief can be obtained by
supplemanting the diet with large amounts of vitamin E, so that enough is
absorbed, or with selenium to restore normal pancreatic function. The amount
of selenium necessary is directly related to the amount of vitamin E provided
in the diet. Only 0.01 ppn selenium as sodium selenite is needed if 100 Inter-
national Units of vitamin E per kg are present. With only 10 to 15 units, 0.02
to 0.04 ppm of dietary selenium is necessary for relief of the synptoms.
In turkeys, selenium deficiency is manifested by severe degener-
ation of the gizzard musculature. Exudative diasthesis may be present, but is
not as severe as in chicks. Anemia and generalized myopathy are accompanying
(35)
•
Poor feathering and wasting of the entire body are symptoms of
selenium deficiency in Japanese quail. Extremely frail young are produced by
females fed very low selenium diets (0.002 to 0.005 ppm) . If the young are
maintained on the same low-selenium diets, death occurs by day 25. Vitamin
E supplementation dees not relieve the condition.
5. Plants
In indicator plants, growth effects of selenium are not always
the same. The growth of Astragalus racemosus was greatly stimulated by
the presence of selenite or selenate in the medium. The growth of other
-------
IV-45
species in the same genus was actually inhibited by the presence of high
selenium, although selenium uptake was pronounced. The growth of Astragalus
racemosus was reduced when the selenium source was Astragalus extract.
Selenium accumulation occurred at a higher level than with inorganic
selenium, however.
In the crop plants alfalfa and white clover, no beneficial
effect of selenium on plant growth was observed at even very low concentrations
of selenium (0.099 ppb). Apparently these crop plants have no nutritional re-
quirement for selenium.
6. Microorganisms
The micronutrient requirement of selenium for microorganisms
has not been investigated. However, the induction of formic acid dehydrogenase
•.-••'• ••'.'.' - ' .• ' —fl
in Eacherichia coli in a highly purified medium requires tie addition of 10
. IA6\
molar selenite. HB'
Compounds of selenium have different affects on the growth of
microorganisms as shown in Table 17.
-------
IV-46
Table 17.
Effect of Selenium Conpounds on Growth
of Microorganisms
Organism
Chlorella vulgaris
cased
Saccharoryces cerevisiae
Escherichia coli
Yeast
Paramecium .caudatum
Neurospora crassa
Aspergillus niger
Effect on Growth
Increase in cell size
Inhibition
Inhibition
Inhibition
Stimulate cell division
Inhibition
Inhibition
Inhibition
Selenium Ccnpound
selencnethionine
selenopurine, seleno-
quanine
selenate
selenate
selenite
selenite
selenate
selenate
-------
IV-47
D. Biochemistry
1. Animals
a. Fate of inorganic selenium compounds
Selenite and selenate axe rapidly incorporated into similar
protein fractions of the blood and other organs soon after administration to
animals. The initial plasma binding is to albumin, but the bulk of the selenium
remaining in the blood is bound to the alpha globulin fraction, from which it
is slowly excreted. Inorganic selenium detaches from albumin and enters various
other cells of the body where it can catalyze the oxidation of sulfhydryl groups.
The body attempts to detoxify selenite in the liver by reductive methylation
to the trimethylselenonium ion, which can be excreted by the kidney, or dimethyl
(49)
selenide which can be excreted by the lungs.
Originally, inorganic selenium compounds were thought to under-
go conversion to selenoamino acids, followed by their incorporation into proteins.
This hypothesis is contradicted by a number of experimental findings: the
rapidity with which selenium appears in the protein; the ease with which it is
removed by dialysis with dilute alkali or treatment with sulfhydryl reagents
or urea; and the concentration of selenium in a limited number of protein
fractions as demonstrated by gel filtration, electrophoresis, and autoradiography.
Apparently selenite and selenate bind to the sulfhydryl bridges of proteins
directly or as other inorganic ions such as selenotrisulf ide.
In vitro studies indicate that mammalian tissues are able
to reduce selenite to elemental selenium. Fresh tissue homogenates reduced
both selenate and selenite to elemental selenium. Selenite was reduced more
(12)
readily. Ihe amount of reduction varied from tissue to tissue.
b. Fate of organoselenium compounds
Selenomethionine is actively transported across cell mem-
branes by the same mechanism as msthionine, but selendcystine is apparently not
(12)
accumulated by the cystine mechanism. •
-------
IV-48
Selenium amino acids apparently undergo the sane metabolic
(49)
reactions a? their sulfur analogs. Selenonethionine and selenocystine are
incorporated into proteins, and converted into selenium analogs of sulfur
metabolites. Thus selenoglutathione, selenotaurine, seleuocysteic acid and
selenpcystathicnine are produced from selenonethionine and selenocystine
in the rat and chick.
Radioactive seleno amino acid analogs are often used in
studies of protein synthesis.
c. Antioxidant function
Selenium compounds apparently have the capacity to act as
biochemical redox agents and to function as biological antioxidants.
Highly reactive free radicals and peroxides may form in the body as a result
of antioxidant deficiency, radiation damage, the aging process and oxygen
toxicity. Free radical products of lipid peroxidation, for example, in the
absence of sufficient antioxidants such as vitanin E and ascorbic acid, can cause
significant alterations in the structural and functional components of the
cell by initiating chain reactions. Comparative studies on in vitro peroxida-
tion inhibition by proteins from control and selenium-supplemented animals
indicated that selenoproteins are the superior antioxidants, inhibiting
peroxidation 20 to 500 per cent better than control proteins and 50 to 500
tines more efficiently than vitamin E.
Selenium compounds were more efficient peroxide decomposers.
Selenocystine consumed up to three moles of peroxide oxygen per mole compared
with riethionine, which consumed one mole of peroxide per mole of amino acid.
Free radicals in tissues produced by gamma irradiation with cobalt-60 damage
proteins and amino acids! Selencmethionine was a more effective protector
of both labile and stable amino acids against radiation damage than nethionine.
Presumably functioning as a free radical scavenger, selenonethionine also had
5.2 and 3.3 times the protective activity as nethionine, and selenocystine had
3.2 and 1.9 tines the protective activity of cystine for alcohol dehydrogenase
and ribonuclease, respectively. Selenocystine was also a more effective pro-
tector of enzymes against loss of activity by peroxidation.
-------
VER/AR
IV-49
INC.
Selenocystine promotes the oxidation of low molecular
weight thiols such as reduced glutathione and cysteine while protecting
sensitive sulfhydryl groups on enzymes.
Recently selenium was found to be a required oof actor for
glutathione peroxidase in rats. Glutathione peroxidase protects hemoglobin
from peroxidation by destroying hydrogen peroxide by reacting it with reduced
glutathione. Selenium is apparently an integral part of the enzyme required
for its activity. The precise role of the selenium in the mechanism of the
reaction has not as yet been elucidated. Purified ovine glutathione peroxidase
contains at least two atoms of selenium per molecule of enzyme.
2. Plants
Of the total seleniun in the tops of non-accumulator plants, 70 to
90 per cent is usually found in the insoluble fraction; most of this can be solu-
bilized by proteolytic enzymes. In contrast, in indicator plants, soluble
/28)
selenium compounds are present in the largest amounts.
Selenomsthicnine in protein is the dominant form of selenium in
non-accumulator plants. Selenomethylselenocysteine in the soluble fraction was
the dominant form of selenium in some indicator species.
The reduction of selenate to selenite may be the rate limiting
step in the utilization of selenium by plants. In the roots, selenite is con-
verted to elemental selenium. Selenocysteine is formed from selenite by an
unknown mechanism. Selenocysteine is converted to selenoglutathione, Selen-
omethylselenocysteine in indicator plants, selenocystathione in non-accumulator
plants, and incorporated into protein in non-accumulators, and to a small extent,
in indicators. In non-accumulators, selenocystathione is converted to seleno-
nethionine, which is mostly incorporated into protein, but may be converted to
(28) • •
selenomsthylselenomethionine.
-------
IV-50
The forms of seleniun present in a number of native plant
species are summarized in Table 18. Inorganic selenium was present as selenate,
but no selenite was found. Plants containing the highest percentages of in-
Q2\
organic selenium are usually the most toxic to livestock.v '
Presumably, organoselenium compounds can be absorbed directly
by the plant, and, therefore, can be more quickly metabolized than selenate,
which must first be converted to selenite.
3. Inhibition of Metabolic Reactions by Selenium Compounds
Selenium corpounds apparently inhibit enzymatic reactions in
(25)
two ways: inorganic selenite and selenate interfere with sulfhydryl
(12)
groups on the enzyme surface; • organic and inorganic selenium compounds
oonpete with their sulfur analogs. Some reactions inhibited by selenium
oorpounds appear in Table 19.
4. Miscellaneous Actions
Selenium may replace sulfur in some reactions and stimulate
others. Table 20 summarizes some of these effects.
-------
VER/AR
INC.
IV-51
Table 18.
Organic Selenium and Selenate in Native Plants
(12)
Plants
(arranged in
order of decreasing
% organic Se)
Castilleja chronosa
Tl ,.._.,. .--LI-. _. ..IT 1 t. f { /fc&«-ii \
Acjropyron smiunxi iwyo . j
Agropyron smithii (Wyo.)
Oryzopsis hymenoides (Utah)
Ocnandra palllxia
Haplopappus frenontii
TVj juu-MunMruvi £*«M«4*K4 4 fM4>aW\
Agropyron snutinii tutan;
Gutierrezia sarothrae
Haplopappus engelroanii
Castilleja angustifblia
Grindelia squarrosa
Haplopappus £remontii
subsp. wardii
Gutierrezia diversifolia
Aster oomnutatis
Machaeranthera venusta
Machaeranthera glabriuscula
Aster occidentalis
Atriplex canescens
Hynenoxys f loribunda
Machaeranthera rarnosa
Atriplex confertifblia
Aster caerulesoens
Atriplex nuttallii
Ototal Se
in plant
(ppn)
1,812
98
41
93
140
680
202
120
101
250
102
932
723
325
3,486
1,431
284
477
575
1,345
1,734
560 -..,'
502 \
Forms
Organic
C%)
95
91
85
78
74
70
51
50
47
46
45
42
37
25
24
23
23
19
16
15
10
9
8
of Se
Selenate
(%)
5
9
15
22
26
30
49
50
53
54
55
58
63
75
76
77
77
81
84
85
90
91
92
Water-soluble
Se
(%)
57
63
51
57
41
79
78
67
74
84
78
67
71
92
89
91
99
84
94
98
98
98
95
-------
IV-52
•••.:..-•. ; Table 19.
MetaJx>lic Reactions Inhibited by Selenium Compounds
. (12,48)
Inhibited
Reaction or EnzynE
Trananethylation
Glycolysis (nitrogen
atmosphere)
Sucxanic dehydrogenase
DNA depolymerization by
DNAse
Respiration
Succinbxidase
Purified I>-aminq acid oxidase
Purified B-amylase
Purified urease
Inspiration
Oiondroitin sulfate
synthesis
Cell division
Jteimentaticn
Glycolysis
Respiration
Oxygen intake
Triose phosphate dehydrogenase
Isocitrate dehydrogenasis
B-galactosidase synthesis
Sulfate reduction
Growth
Oxygen consunption
Chlorophyll synthesis
Iteaction Site
Liver honogenate
Rat liver honogenate
Muscle powder
Pancreas
Tissue slices
Chick entoryonic cartilage
Chick enbryonic cartilage
Chlorella vulgaris
Yeast
Yeast
Yeast
Yeast
Yeast
Yeast
Jfethionine-reguiring
Escherichia coli
Desulfovibrio desulfuricans
Mouse leukemia cells
Paramecium caudatum
Crop plants
Selenium Compound
selenite, selenate
selenite
selenite
selenite
selenite
selenite
selenite (0.001M)
selenite (0.001M)
selenite (0.001M)
selenate
selenate
selenonethionine
selenate, selenite,
selenide
selenite
selenite
selenite
selenite
selenite
selenomethioniitE
selenate
selenopurine
selenite
selenate
-------
IV-53
Table 20.
Noninhibitory Metabolic Actions of Selenium
(12,48,51)
Action
Fumarase activation
Methylation substrate
Methyl donor
Formate dehydrogenase induction
incorporation into protein
ATP sulfhydrylase substrate
Glutathione peroxidase
oonponent ; .
Organism
Pig (heart)
Fungi
Yeast
Escherichia cbli
Azotobacter aerogenes
E. opli
rary^idg albicans
Yeast
Rat '
Selenium Oonpound
selenate (0.025M)
selenite, selenate
selencnethionine
selenite
selenahethiohine >
selenite
selenate
-------
IV-54
IX;
A. Environmental Content, Transport, Contamination
The natural content of selenium in the soil and rocks is the
(12)
largest source of selenium in most environments. ' Both the presence and
absence of selenium can provide biological hazards.
Soil selenium enters the food chain by plant accumulation. In
selfiniferous soils, certain species of plants prevail which easily accumulate
selenium levels toxic to livestock. In fact, the presence of certain plant
species is steadfast evidence of a selaniferous zone. Crop plants grown on
such soils, if they themselves survive, may also contain selenium levels poisonous
to livestock. The distribution of some seleniferous areas in the western United
States is reflected in Figure 3, which shows the distribution of seleniferous
(12)
vegetation in that area.
In areas where soil selenium is extremely low, forage plants contain
very little selenium. Livestock ingesting food raised in these areas produce
offspring which exhibit severe deficiency diseases. The symptoms depend upon
the species. Figure 4 illustrates the lack of overlap between areas in the
United States where white muscle disease, a selenium deficiency syndrome, occurs,
(12)
and areas supporting seleniferous vegetation. The map in Figure 5 shows
the distribution of the selenium content of forages in the Pacific Northwest. ^13'
The coincidence of high WMD areas shown in Figure 4 with forages containing very low
selenium as shown in Figure 5 is evident. Areas with adequate forage selenium
show no incidence of WMD.
Waters in seleniferous areas may contain toxic selenium levels. •- .
Drainage from irrigation and soil leaching are principal sources of selenium
in waters. In Nebraska, water from 42 per cent of all wells sampled and
from one quarter of all surface water locations contained selenium in greater
concentrations than the U.S. Public Health Service standard (10 yg/1).
The amount of selenium which is carried to sea water is great enough to cause
serious poisoning of the ocean had there been-no mechanism for the removal of
(12)
selenium from sea water. Selenium is removed from aqueous solution by
-------
PLANT SPBOMEN
COLLECTION PONT
O 6O-50O PPM SELEMUM
• OVER 900 PPM SELENIUM
Figure 3
Distribution of seleniferous vegetation in the western United States
-------
• SELEMFBROUS VULIMUH
\ WHITE MUSCLE DISEASE OCCURRENCE
Figure 4
Distribution of vegetation containing more than 50 ppm selenium,
in relation to distribution of occurrence of white muscle disease in livestock
-------
IV-57
VERY LOW S« -LESS THAN 0.10 PPM IN MORE THAN 90%
OF SAMPLES AND LESS THAN 0.09 PPM
W MORE THAN 80% OF SAMPLES
LOW Se - LESS THAN 0.10 PPM IN MORE THAN
80% OF SAMPLES AND LESS THAN
0.05 PPM IN MORE THAN 60% OF
SAMPLES
VARIABLE $• ~ LESS THAN OM PPM IN 50% OF
SAMPLES
ADEQUATE S« - MORE THAN O.fO PPM IN 90% OR
—~—— MORE OF SAMPLES
Figure 5
Selenium content of forages in the Pacific Northwest
-------
IV-58
adsorption on precipitated hydroxides of iron and manganese, organic matter
"•'"•• ' ' (12) ''••"••' ' -':.'•.•
and iron sulfides. Nearly all sea floor samples analyzed contain
selenium. Values reported range fron 0.03 to 2.0 ppm selenium. *12*
(See Table 21)
Coal contains variable amounts of selenium. Table 22 shows
some reported values. The burning of fuels containing selenium may represent
a significant source of the element in the environment. The selenium content
of atmospheric dust collected on air conditioning filters in various industrial
areas in the United States are presented in Table 23. The range of selenium
contents found in some foods which are ingested by humans are presented in
(12)
Table 24. Animal products contain considerable amounts of selenium.v
In one study, an attempt is made to identify the source of atmospheric
selenium pollutions by comparing the selenium: sulfur ratio of various fuels
with that ratio in air particulates and in top soils. The data are presented in
Table 25. Selenium: sulfur ratios for petroleum samples are of the sane order
of magnitude as the air samples collected.
Most fresh vegetables and fruits for human consumption contain quite
low amounts of selenium as shown in Table 26. Starchy vegetable products con-
tain much higher selenium concentrations as shown in Table 27. Table 28 presents
the selenium content of meats and seafoods. Kidneys have notably high selenium
content. Seafood has generally higher selenium content than meat. The selenium
contents of dairy products are, in general, lower than for meats, and higher
than for fruits and vegetables. (Table 29) Table 30 shows the variable
selenium content of eggs and some sweeteners. The content of baby foods appears
in Table 31. The lover selenium content in baby foods compared with fresh
may be due to volatilization of selenium during the cooking. All food samples
analyzed were purchased in Beltsville, Maryland, northeast of Washington,
D.C.(17)
-------
IV-59
Table 21.
Selenium in Sea Water
(15)
No. of
Area Samples
Caribbean 4
Western North Atlantic 8
Eastern North Atlantic 7
Western South Atlantic 2
Eastern Pacific 6
Antarctic 1
Long Island Sound 8
Selenium
fcange
0.095-0.14
0.069-0.13
0.076-0.11
0,070-0.080
0.061-6.12
0.052
0. 10 -0.13
(Mog./l)
Average
0.11
0.096
0.088
0.075
0.087
0.052
o.ii
Table 22.
Selenium in Ooal
(15)
Area
No. of
Samples
Selenium (ppm)
Range
Average
Lignite
Western Wyoming
Mantezuma County,
Qolorado
3
2
1.96-7.38
2.0 -2.4
3.88
2.2
Coal
Morley, Alberta,
Canada
Sandoval County,
New Mexico
Kladno, Czechoslovakia
Liege, Belgium
1
1
Present
Present
2.0
0.1
-------
IV-60
Table 23.
Selenium Content of Atmospheric Dust From Air-Condi tioning
Filters
(15)
Type of Building
Where Sample Was
Collected
industrial
Dry goods store
Industrial
Residence
Residence
Residence
Office Building
Unknown
Residence
i
Unknown
Office Building
Location
Los Angeles, California
San Francisco, California
San Leandro, California
Grand Forks, North Dakota
Houston, Texas
University City, suburb of
St Louis, Missouri
St. Louis, Missouri
Chicago, Illinois
Shaker Heights, suburb of
Cleveland, Ohio
Philadelphia, Pennsylvania
Washington, D.C.
Selenium
(ppra)
0.8
0.05
0.6
6.0
• 3.0
2.5
10.0
2.5
2.5
1.5
0.5
Table 24.
The Selenium Content of Water, Milk, Eggs, Meat, and Bread
(12)
Material
Water
Milk
Egos
Meats
Bread
Total
Nunber of
Samples
44
50
32
6
11
Nunfcer of sanplas showing:
No Selenium
20
0
0
0
0
Traces
14
6
0
0
5
Positive
10
44
32
6
6
Selenium (ppm)
Mininum*
0.05
0.16
0.25
1.17
0.25
Maximum
0.33
1.27
9.14
8.00
1.00
•Positive samples only
-------
iv-ei
Table 25.
Selenium: Sulfur Ratio of Some Possible Sources
of Air Pollution and Some Environmental Samples
(16)
Sample
Raw petroleum
Heavy petroleum A
Heavy petroleum B
Heavy petroleum C
Rubber tires
Goal .
Soot (mechanical collection)
Soot (electrical collection)
Soil
Soil extract
Selenium
(wg/g)
0.92
1.10
0.75
1.12
1.33
1.18
4.30
0.50
1.14
0.50
Sulfur
(mg/g)
18.4
10.9
16.9
19.3
13.0
2.44
138.00
30.00
1.76
0.11
Se/S Ratio
(xlO")
0.42
1.03
0.55
0.58
1.01
4.85
0.31
0.17
6.84
0.48
-------
IV-62
Table 26.
Selenium Content of Vegetables and Fruits
'Products
•-••'•' . .' . • ' •
Carrots
Fresh
Canned
Cabbage, fresh
Cauliflower, fresh
Corn
Fresh
Canned
Garlic, fresh
Green pepper, fresh
Green beans
Fresh
Canned
Lettuce, fresh
Mushroom
Fresh
Canned
Qnicn, white, fresh
Potatoes
Sweet, fresh
White, fresh
White, canned
Radish, fresh
Tomatoes
Fresh
Canned
Turnips, fresh
Mean excluding mushroom
and garlic
-,•'.' • '•'•'.
Apple, fresh, peeled
Applesauce, canned
Banana, fresh, peeled
Orange, fresh, peeled
Peach •
Fresh, peeled
Canned
•Pear". '••
Fresh, peeled
Canned
Pineapple
Fresh
Canned •
i*//.
vg
Vegetables
0.022,
0.013,
0.022,
0.006,
0.004,
0.003
0.276,
0.006,
0.006,
0.009,
0.009,
0.122,
0.109,
0.015,
0.007,
0.003,
0.007,
0.042,
0.005,
0.010,
0.006,
j ••
Se/gran
0.022
0.013
0.023
00.007
0.004
0.005
0.222
0.008
0.006
0.009
0.007
0.141
0.100
0.015
0.006
0.006
0.011
0.036
r
0.005
0.009
0.008
0.010
Fruits
0.003,
0.002,
0.010,
0.014,
0.004,
0.004,
0.006,
<0.002,
0.006,
0.008,
Mean
• . ••••': :•
0.006
0.002
0.009
0.012
0.004
0.002
0.006
<0.002
0.005
0.012
0.006
-------
W-63
Table 27.
Selenium Content of Grains and Cereal Products
(17J :
Product yg Se/gram
Barley cereal 0.643, 0.676
Bread
White 0.280, 0.274
Wholewheat 6.676, 0.654
Com flakes 0.024, 0.028
Flour
White 0.187, 0.197
Wholewheat 0.627, 0.645
Noodles, egg 0.662, 0.583
Oat breakfast oereal, prepared 0.451, 0.406
Oats, quick 0.114, 0.105
Rice ' ••';'" ".-. • -.••.•:•:-•
Polished 0.334, 0.303
Brown 0.383, 0.394
Rioa breakfast cereal,
puffed, prepared 0.026, 0.031
Wheat oereal 0.241, 0.241
Wheat breakfast cereal,
prepared O.llO, 0.100
Mean excluding corn flakes
and rice oereal 0.387
-------
IV-64
Table 28.
Selenium Content of Miscellaneous Products
(17)
Product yg Se/gram
• Egg • ' • •• '- : •
YolMl 0.174, 0.193
Yolk #2 0.192, 0.174
White II 0.057, 0.057
White #2 0.046, 0.043
Saccharin 0.005, 0.005
Sugar
Brown 0.012, 0.010
White 0.003, 0.003
Table 29.
Selenium Content of Dairy Products
(17)
Product
Cheese •/• '•••'• • .' '' •
Cottage
Swiss
Cream/ table
Cream substitute
Milk
Evaporated, canned
Skim
t~t t—, ,, i-_ . An ••>-, il i1..1 n ft JIO
Skim, powdered, axled tz
Whole hortogeniaed
yg Se/gram
0.090,
0.054,
0.101,
0.005,
0.034,
0.012,
P.045,
0 098
V • v^ w f
0.243,
0.013,
0.090
0.050
0.108
0.006
0.033
0.013
0.050
0 094
w * v^~
0.238
0.011
Mean 0.069
-------
IV-65
'AR INC.
Table 30. :
Selenium Content of Meats and Seafoods
(17)
Meat
Product
Mean excluding kidneys
yg Se/grain
Beef
Bound steak
Ground
Liver
Kidney
Pork
Chop
Kidney
Latrib
Chop
Kidney
Chidcen
Breast
Leg
Skin
0.363,
0.208,
0.454,
1.41,
0.217,
1.89,
0,172,
1.38,
0.106,
0,121,
6.154,
0.318
0.189
0.409
1.69
0.261
1.90
0.184
1-47
0.125
0.151
0.146
0.224
Seafoods
Lobster tail
Shriitp, shelled, deveined
Cod, fillet
Flounder, fillet
Oysters
0.634,
0.572,
0.465,
0.335,
0.646,
0.681
0.604
0.390
0.338
0.659
Maan
0.532
-------
IV-66
Table 31.
Selenium Content of strained Baby Raods
(17)
Product
Beef
Chicken
Lanf?
Liver
Pork
Carrots
Green beans
Peaches
Pears
Oatmeal cereal with applesauce
and bananas
Rice cereal with applesauce
and bananas
Vanilla custard pudding
PgSe/gram
0.118
0.112,
0.123,
0.247,
0.114,
0.002,
0.005,
0.003,
0.002,
0.113
0.101
0.138
0.269
0.133
0.002
0.004
0.004
0.005
0.026, 0.033
0.019,
0.016,
0.023
0.015
Mean
0.068
-------
IV-67
B. Persistence and Degradation
The weathering of sedimentary rock is thought to have created
seleniferous soil. The deposition of selenium in sediments may be a pro-
duct of volcanic ash, which contains significant levels of selenium.
Accumulation and deposition of selenium by marine organisms also con-
tributed. ' The cycling of selenium in nature is summarized in
Figure 6. '• ; ' •
The selenium in young soils occurs predominantly in an inorganic
form not utilizable by crop plants. Selenium aoctrnulator (indicator) plants
and sore bacteria can function as selenium converters, removing the selenium
from the soil and returning it in an organic form, which can be absorbed by
other plants. The established biological valence transformations of selenium
are reduction reactions. Selenate, and selenite can be converted to elementary
selenium and selenoorganics by plants and microorganisms. Evidence for microbial
oxidation of selenium is the lack of buildup of organic selenium compounds in
nonsterile soils. However, the oxidative stages in the selenium cycle may be
abiotic, as about 80 per cent of elementary selenium as dust in moist air is
converted to selenium dioxide, which reacts with water to form selenious acid.
Selenite is the most unstable form of selenium, and may be readily oxidized
to selenate.'12'B>
Organic selenium and some selenium salts are easily leached from
soils, and the selenium content of irrigation waters, springs, and shallow
pools may be quite high in seleniferous regions. In alkaline soils, much of
the selenium may be trapped by reaction with iron oxides. Iron-selenium
compounds are quite insoluble under basic conditions, and the selenium available
to indicator plants and microorganisms, but not crop plants. Acidification
of the soil by microbe action can cause the conversion of insoluble inorganic
selenium to soluble forms. ''
Selenium may enter animals in several ways. The predominant route
is through ingestion of vegetation containing high levels of selenium.
Carnivores obtain selenium by eating prey fed on seleniferous forage. Selenium
-------
-LV-bB
GROUND AND
RUNMNt WKTW
MAIN AND
Cycling of excessive levels of selenium in nature
-------
IV-69
rAR INC.
in drinking water is another possible source. Small amounts of selenium
may be inhaled, as animals, plants, and microorganisms all produce volatile
selenium compounds. Animals excrete selenium in the feces, urine, perspiration,
as well as in the breath.
A feeding experiment in sheep was designed to determine the movement
of physiological levels of selenium from the soil through plants into animals
(52)
and their offspring using two groups of ewes fed alfalfa. One group
was fed alfalfa grown on untreated soil, and the other group ate alfalfa
raised on selenium-treated soil. The physiogical effect on the animals was
measured by examining the incidence of white muscle disease (WMD) in the
offspring of both groups. No incidence of WMD was observed in the lambs of
ewes fed the alfalfa grown in selenium-treated soil. (This alfalfa contained
2.6-2.7 ppm selenium compared with 0.01 to 0.04 ppm selenium in the untreated).
In the other group, 25 per cent of the offspring died of WMD during the first
six weeks of life. Almost 70 per cent of the lambs surviving to six weeks of
age showed WMD lesions. The lambs in the former group had extremely higher
levels of selenium in their tissues than the lambs with the high incidence of
WMD.
The ewes fed on the high-selenium alfalfa were detained and main-
tained on low-selenium alfalfa (<0.01 ppm) for the next year. Of the lambs
born to these ewes at the end of that time, only one out of thirteen surviving
to six weeks of age exhibited symptoms of WM). This was not evident until
microscopic examination of the muscle was carried out. In a new group of ewes
fed on the low-selenium alfalfa, over 50 per cent of the surviving six-veek
old lambs had WMD. The protection afforded the lambs of the former group of
ewes even a year after the removal of selenium from the diet indicates a long
retention time for the element. This experiment also illustrates soil retention
of selenium in an indirect way as measured by selenium content of the alfalfa.
The alfalfa from the selenium-treated plot (1 ppm selenium applied) contained
2.6 to 2.7 ppm selenium. Alfalfa grown the following year, without another .
selenium addition to the soil, contained 0.43 to 0.57 ppm selenium. Since the
same strain of alfalfa was used in both years, environmental factors must have
been responsible for the differences in selenium accumulation. Uhfortunately,
soil selenium levels were not determined.
-------
IV-70
'ER/AR INC.
C. Bioaccunulation
As discussed in Section VIII under absorption and excretion, higher
plants tend to accumulate selenium from the soil, depending upon the species,
form of selenium, and other environmental conditions. ^^ Certain species
of plants thrive on soils containing levels of selenium toxic to most other
plants, these selenium indicator plants may accumulate thousands of parts
per million selenium, absorbing both organic and inorganic forms. Secondary
indicator plants, which grow well on both seleniferous and nonseleniferous
soils, can accumulate several hundred ppm selenium without adverse effects.
Crop plants accumulate selenium readily, depending upon the chemical form, but
concentrations over 30 ppm are toxic to most plants.
Animals readily absorb inorganic and organic selenium through the
/io 2R^ *™3*
small intestine. ' Jfonogastric absorption is more efficient than ruminant.
Mast of the selenium (70 to 80 per cent) is quickly excreted in the urine, breath,
perspiration, and bile. The remaining selenium beccnes bound or incorporated
into blood and tissue proteins and is only slowly eliminated. The offspring of
parents maintained on very low selenium diets for long periods of time show
severe deficiency symptoms unless selenium supplementations are given, although
the parents do not exhibit illness. The experiment with sheep discussed in
Section DCB illustrates that the effective retention tine of selenium is at
(52)
least a year in sheep.
if
Fresh water plankton accumulate selenium. Large amounts of selenium
were found in the zcoplarikton in Lake Michigan downwind of Chicago. The range of
the selenium concentration was 0.1 to 1.2 ppm.' '
-------
VKR/A.ft
IV-71
INC,
X. TOXICiTY . ;
A. Humans
1. Occupational Exposures
Workers exposed to fine elemental selenium dust collect the dust
in the upper nasal passages, producing catarrh, nose bleeding, and loss of
smell. A few cases of selenium dermatitis have occurred. Exposure to fumes
of elemental selenium produces frontal headache, intense irritation of the
eyes and nasopharyngeal passages, slight difficulty in breathing, and uvular
(25)
edema. Exposed workers recovered within three days and no ill effects persisted.
Most of the workers in a Japanese factory making selenium rectifiers ,
are minors and children. Hypochromic anemia and drastic leuoopenia were pre-
valent in workers who had been employed in the factory for a long time. Finger-
nails were damaged from regular contact with selenium, and increasing numbers
(12)
of female workers reported irregular menses or menostasis. '
Selenium dioxide readily dissolves in water producing selenious
acid. Intense local irritation and inflammation of the skin and mucous mem-
branes occur upon contact. Selenium dioxide, selenious acid, and selenite may
be absorbed through the skin, resultijig in internal accumulation. Allergic
dermatitis to selenium dioxide may desvelop, especially in fairheaded pe»ople.
(25)
Sodium thiosulfate solution is used to treat exposure.
Hydrogen selenide fumes, from an etching and imprinting operation
on a steel strip using a selenious acid bath induced nausea, vomiting, metallic
taste in the mouth, extreme lassitude, and fatigability. Olfactory fati
-------
/AR INC.
IV-72
2. Epidemiolpgical Exposures
Acute dermatitis which proved to be selenium poisoning was
observed in a rancher in South Dakota. Appreciable quantities of selenium
were found in the water, neat, vegetables, and dairy products fron his ranch.
The patient was treated with bromobenzene to eliminate selenium from his
system.
Many other cases of selenium dermatitis have been reported from
North Dakota, South Dakota, Montana, Wyoming, and Nebraska. Symptoms included
various degrees of skin rash, follicular rashes over the hairy parts of the
body, extreme fatigue, and dizziness. The selenium sources were home-grown
farm oroducts in the diet. Recovery was achieved by removal of selenium from
. ..
Well water from the Wasatch geological formation in Utah contained
9 ppm selenium. Chronic selenosis occurred in the children, parents, and dog
drinking the water. No selenium was found in the food. Lassitude, total or
partial loss of hair, discoloration and loss of fingernails were symptoms of
the condition. A halt in the use of the water brought regrowth of -the hair
(25)
and nails and increased mental alertness. '
People living in seleniferous regions should be conscious of
(12 25)
the possible danger of selenium in foods and water. ' •
Chronic selenosis has been known in an area of Colombia, South
America since the 1600 's. The black "peladero" soi} in the area contains ex-
tremely high levels of selenium, which accumulate in the corn and other crops,
and forage plants and are present in the streams in the area. Loss of hair
and nails, and the birth of malformed babies have been symptoms of the selenosis
in Indians living in the area. Animals grazing there lost hair and hoofs, showed
malformations of lips and legs, a number of animals aborted, and eggs failed
to hatch. (12)
B. Mammals
1. Acute Toxicity
Injected doses of selenium compounds at levels of 200 microgranis
selenium per kg body weight usually produce toxic effects in cattle, horses,
-------
IV-73
fAR INC.
and pigs. Ccnsunpticn of plant materials containing 400 to 800 ppm selenium
proved fatal to sheep, hogs, and calves. Table 32 indicates rninimum lethal
doses of selenium compounds for both livestock and laboratory animals. Table
33 lists the LDenia for some intraperitoneally administered selenium compounds
5U S
in the mouse and rat.
Symptoms of acute selenosis in livestock include uncertain gait
and stance, rapid, weak pulse (90 to 300) elevated body temperature (103 to !
105 F) labored respiration with mucous rales, bloody froth from the air passages,
bloating accompanied by abdominal pain, and diuresis. The mucous membranes are
pale or bluish, and the pupils dilated. Lethargy and prostration precede death.
Death is due to respiratory failure. The urine may contain 0.1 to 20 ppm,
and the bile 1 to 6 ppm selenium. Highest selenium concentrations are found
in the liver (22 ppm), blood .(5 to 15 ppm), kidney (10 ppm), spleen (8 ppm),
and brain.(12)
Gross and microscopic pathology showed evident systemic damage,
(12)
especially hemorrhage, congestion and necrosis of the parenchymatbus organs.
Acute selenite selenosis in laboratory animals was manifested by
initial signs of nervousness and fear, vomiting, diarrhea, and respiratory
difficulty. Quietness and somnolence were followed by opisthotonos, tetanic
spasms in the muscles of the extremities, clonic spasm, and death. The heart
rate remained normal, and a gradual fall in blood pressure began 15 to 30 minutes
• -' "••'•• • •-•:'•••' (12) ' ' • • • '•••'•
after injection and continued until death. .
2. Subacute and Chronic Poisonino
a. The blind-staggers type of chronic selenosis appears in
cattle ingesting large amounts of indicator plants, which contain a moderate
or high concentration of water-soluble organic selenium. Severity of the toxicity
depends upon the type of plant ingested, stage of growth, and soil type. In
the first stages of poisoning, the animal may walk in circles, stumble over
objects in his path and exhibit little desire to eat or drink. In the second
stage, the manifestations of the first stage become more severe, and the front
legs become weak and seem unable to support the animal. Loss of desire to eat
or drink occurs, although no paralysis is exhibited by the tongue.and throat
-------
JV-74
muscles involved in swallowing. The final stage prior to death is a paralytic
stage. The tongue and throat muscles are paralyzed. The animal is nearly
blind, respiration is labored and accelerated, and there is evidence of great
abdominal pain, which causes constant grating of the teeth and salivation. A
subnormal body temperature, swollen and inflamed eyelids, and cloudy corneas
are evident. The mucous membrane of the mouth is pale. The animal may appear
emaciated. The onset of the third stage is sudden, and death usually occurs
within a few hours.
Impaction of the rumen, and stasis in the omasum are patho-
logical findings characteristic of blind staggers. If the syndrome is re-
cognized during the first or second stage, some relief may be afforded by
drenching the animal with warm water. Small doses of strychnine sulfate may
be injected. No laxative should be administered during the initial stages of
treatment to minimize the irritation to the stomach.
b. Chronic poisoning of the alkali disease type results from
the ingestion of feedstuffs (com, wheat, barley, oats, grasses and hay) con-
taining 10 to 30 ppm selenium. The selenium is predominantly present in the
proteins of these feeds. The amount of selenium is related to the availability
of soil selenium.
The general symptoms of alkali disease include lack of vitality,
anemia, stiffness of joints, lameness, roughened coat, loss of hair, and hoof
lesions and deformities. Death may occur within two months after a horse is
placed on a seleniferous pasture.
In alkali disease higher concentrations of selenium appear in
the hair and hoofs than the other parts of the body. The heart and liver ex-
hiiit the most damage. The heart becomes soft, flabby and atrophied. Fibrosis
is evident in the liver and kidneys.
The only certain treatment is to discontinue feeding seleni-
n 2)
ferous grain and forage.
-------
-------
IV-76
Table 33.
LD5Q for Some Seleniun Compounds
Administered by Intraperitoneal Injection
(12)
^50
Selenium Compound Animal (mg Se/kg)
isoselenourea sulfate rat 3.0 ± 0.3
sel^nohoncystine rat 3.5 ±0.4
d/-l, or d,l-weso~selenocystine rat 4.0 ± 0.2
selenomethionine rat 4.5 ± 0.3
selenotetraglutathione rat 6.0 ± 0.3
dimethyl selenide nouse 1300
dimethyl selenide rat 1600
6-selenopurine mouse 160 ± 37
-------
r W-77
VER/AR INC.
c. Chronic Selenosis by Inorganic Selenium
Selenite administration produced symptoms similar to
those seen in alkali disease. Inappetence was the most pronounced symptom.
Some lesions characteristic of alkali disease were produced in equines and
pigs after repeated small doses of selenite. In equines emaciation, drowsiness,
and loss of appetite preceded death; loss of hair and separation of the hoof
occurred in pigs. Peculiar trembling of the skeletal muscles, shivering during
exercise, anorexia and inability to rise were noted in cattle.
d. Subacute and Chronic Selenium Tbxicity in Laboratory
Animals &2>
. i
Considerable species and individual variation to the toxic
effects of selenium exists. In subacute and acute selenosis, when fractions of
a minimum lethal dose are given, the effect is cumulative. A continued increase
in the manifestations of toxicity upon repeated administrations suggests that
no altered susceptibility or acquired tolerance develops. Young animals are
more susceptible to selenium intoxication than older animals; female rats are
more susceptible than males. Pats are apparently able to distinguish betwaen
various concentrations of selenium in the diet even when the increments were
small.
In general, concentrations in diets of less than 5 ppm
selenium as seleniferous grain prevented normal growth, 9 ppm resulted in death
of young animals, and 10 ppm produced restricted food intake in adult rats. Food
which contains 40 to 50 ppm of selenium even when consumed in small amounts
is more toxic than food which contains 10 to 12 grams per day.
The toxic manifestations of inorganic selenium compounds
and seleniferous grains are almost identical under similar experimental con-
ditions. The addition of 7.2 ppm selenium as seleniferous wheat or 10 ppm as
selenite to the diet was toxic to dogs.
-------
IV-78
Chronic selenosis may be produced in various experimental
animals with concentrations of 10 to 16 ppn of selenium in the diet or drinking
water. If the selenium concentration is between 20 and 30 ppm, subacute
selenosis may develop. Intraperitoneal, oral or subcutaneous administration
of selenite or selenate produces chronic or subacute selenosis in rats when
the dose is 1.5 to 2;2 mg per kg body weight. •
Subacute and chronic selenosis are characterized by marked
loss of body weight, anorexia followed by cachexia, ascites and edema, anemia,
intermittent vomitting and decreased hepatic function.
3. Teratogenicity
Plaoental transmission of selenium has been shown to occur.
Offspring of selenized parents tended to be underweight, and malformations were
evident in lambs bom to ewes grazed on seleniferous pastures. Congenital
alkal i disease appeared in a 14-day-old colt born of a mare in which symptoms
appeared during gestation.
Gross abnormalities were observed in chick embryos from eggs
laid by selenium-fed hens. Ch farms in seleniferous regions the failure of
eggs to hatch may be due to deformities which prevent hatching, and not to
infertility. Deformities in embryos were produced by injecting eggs with
(54)
selenite before incubation.
4. Carcinogenicity
Conflicting data has been presented on the role of selenium as
a carcinogen.* Three studies exist which implicate the carcinogenic nature
of selenium, but it has been argued that low-protein diets, the inability of
the liver tumors to metastasize and the lack of controls in one study render
the data inconclusive. In the most recent study young.rats were given 20 ppm
selenate, selenite and tellurite in drinking water. The selenite produced
markedly toxic effects, particularly in the males. The selenate level was
increased to 3 ppm at the end of one year, and the experiment continued for
the lifetime of the rats. At death, 42 per cent of the selenate<-fed rats
exhibited benign or malignant tumors compared with 17 per cent of the controls,
18 par cent in the tellurite-fed animals, and 13 per cent in the selenite-fed
-------
IV-79
iJAR INC,
ones. All of the tutors in the controls and 91 per cent in the selenate-fed
rats developed after two years. (Selenite-fed rats were all sacrificed by
the end of 23 months because of the high mortality and toxicity of the compound.)
5. Anticarcinogenicity
A growing number of apparent antitumor actions of selenium
compounds have appeared. ' Male rats receiving m'-metiiyl-p-dimethyl-
aminoazobenzene (m'-DAB) had an incidence of 93 per cent liver tumors compared
with 31 per cent present in animals also receiving 5 ppm selenium as sodium
selenite.
Intraperitoneal injection of selenocystine (1 mg/kg) into rats
injected with Murphy lymphosarcoma cells inhibited tumor growth. Rats not
2
receiving selenocystine treatment had tumors approximately 30 on in area
after 21 days compared with tumors 8 on in rats receiving selenocystine. The
inhibition was quite specific to selenocystine, since benzyl-selenium alanine
did not inhibit tumor growth.
In human patients > two with acute leukemia and two with chronic
myeloid leukemia, daily doses of 100 mg selenocystine administered in capsules
for 10 to 57 days produced a marked reduction in the immature leukocytes
circulating in the blood. Therapy had to be discontinued despite promising
effects because the patients experienced nausea and vomiting.
The addition of sodium selenide to crpton oil, which was painted
on to the skin of mice, reduced tumor incidence from 132 tumors in mice painted
without selenide to nine tumors.
In mice, 6-selenopurine was as effective as 6-nErcaptopurine in
inhibiting the growth of lymphomas. Intraperitoneal 2-aiitinoHS-selenopurine
also inhibited tumor growth, but oral doses were ineffective.
A very high negative correlation between blood selenium levels
in human males and "human cancer death rates" has been reported. (R = 0.96;
P<0.001). Studies with microorganisms indicate that selenium interferes with
itudi<
(25)
cell division processes. More complete studies are necessary to ascertain
the exact interactions of selenium compounds.
-------
IV-80
IAR INC
6. Factors Affecting Selenium Tbxicity
Arsenite and arsenate, but not arsenic sulfides, are equally affective
in preventing the toxic action of selenium in seleniferous wheat, ' sodiu*
selenite and selenocystine . Organic arsenicals have been found to give
partial protection against chronic selenosis in rats. Arsenic increases
biliary excretion of selenium.
The presence of sulfide in an injection to rats reduces the toxic
effects of selenite. Dietary sulfate reduced selenium-produced gtwth de-
pression, but not liver damage. Sulfate modified chronic selenosis produced
by selenate, was less effective against selenite, and ineffective against
(12)
seleniferous wheat. ., • *-
/.. .
-------
IV-81
C. Fish
Selenium poisoning has been produced in goldfish and catfish. The
catfish died within 48 hours after receiving a single intraperitoneal injection
of 0.15 mg or more selenium as sodium selenite. An injection of 0.05 mg
selenium produced no iirerediate effects, but exophthalmus, ascites, tissue
edema, and death occurred within 12 to 15 days. Marked reductions in blood
(12)
specific gravity, red blood cells, and hemoglobin were noted.
D. Invertebrates
Selenium has been effectively used to control aphids, mites, and
red spiders in greenhouses. Surprisingly, larvae and adults of some species
of insects are apparently immune to selenium poisoningi Larvae of Oecanthos-
celides fraterculus, a bruchid, and Bruchophagus mexicanus, a seed chalcid,
were capable of consuming seeds of Astragalus bisulcatus containing 1475 ppm
selenium. The insect bodies contained 67 ppm selenium. Flies containing
20 ppm selenium, fly larvae, containing 7.5 to 10 ppm selenium, Were found on
Astragalus pectinatus, whose roots contained 190 to 420 ppm selenium. Grass-
hoppers and blister beetles have also been found feeding on high-selenium
plants.(12)
Soil and leaf nematodes were effectively controlled by sodium
selenate. Selenium applications to soil may pose real health hazards to humans
and farm animals if used on garden or forage crops.
E. Plants
Organic selenium (as Astragalus extract) produced less growth in-
hibition and toxicity to crop plants than inorganic selenium. In order of
diminishing toxicity, some selenium compounds injurious to plants are:
selenious acid, selenic acid, selenite, selenate, and selenocyanate.
Selenate toxicity in crop plants appears as white chlorosis of the
leaves. Older leaves become yellowed. The roots become stunted, but are
otherwise normal in appearance.
Leaves injured by selenite are likely to be darker green than usual.
Older leaves wither and become brown. Extremely high concentrations of selenite
induced white chlorosis and premature death of wheat plants. Foots poisoned
-------
IV-82
by selenite haw a pinkish appearance, which, upon macroscopic examination,
is found to be due to zed granules within the roots. The red granules are
thought to be elemental selenium. The main roots axe thickened, with sup-
(12) '
pressed development of lateral roots.
P. Microorganisms
Although selenium inhibits growth of many microorganisms, some
strains of bacteria apparently can adapt to a high-selenium environment.
-4
Escherichia ooli grown in a medium containing 2 x 10 molar selenate exhibits
a lag in growth lasting for 24 to 48 hours. After that time, the growth
ultimately attained the same levels as control cultures. The adapted E. ooli
cultures maintained their resistance to selenate even after nine transfers on
(58)
selenate-free nutrient agar plants.v
Cultures of bacteria isolated from selenium-rich soils in Russia
were more resistant to high concentrations of the element than cultures
isolated from selenium-depleted soils. A Moscow-region strain of Bacillus
itegaterium could be acclimated to high selenium by growth on a medium con-
— (59)
taining 0.05 ppm selenium* '
G. Results of Personal Qantacts with Medical Personnel
A total of 74 toxioologists and toedioal examiners throughout the
United States were contacted by telephone or letter with regard to their pro-
fessional acquaintance with incidences of accidental poisoning of humans attri-
buted to selenium or its conpounds. Of the 31 responses, there were five
reported instances of selenium poisoning, none of which were fatal. These
are described as follows:
3 cases - accidental poisoning by "Selsun" dandruff treatment
preparation (three widely separated instances; two
children, one adult). Most serious symptom was alopecia.
2 cases - accidental poisoning of two families (parents and children)
in Alabama due to high selenium content of well water (8 and
12 ppm). Symptoms included skin lesions.
-------
IV-83
fAR INC.
XI. CURRENT REGUIATIONS
Fran public water supplies the permissible criterion for selenium
(2* ,4*.6*) is 0.01 mg/1. (10 ppb) .60
The State of Illinois has established the regulation for public
water that the "maximum allowable twelve-month average selenium concentration"
is 0.01 mg/1. No single analysis shall show a concentration at any tine of
more than 1.5 times this value. The justification given for this criterion is
is that "to maintain the rather narrow margin of safety imposed by the back-
ground ingestion of selenium from food, drinking water must not contain more than
0.01 mg/1 of selenium".(61)
A tentative allowable concentration of 1 mg/1 of selenium in urine was
reccranended for rural populations living on seleriiferous soil and for workers
exposed to selenium or its compounds.
American Peed Manufacturers Association, Inc., sent a petition to the
Pood and Drug Administration to amend the Pood Additive Regulations to permit
the safe use of selenium as a nutrient in the feed of chickens, turkeys, and
swine. The proposal provides that selenium as sodium selenite or selenate
may be added at a level not to exceed 0.1 ppm for chickens and swine and 0.2
ppm for turkeys. The status of the petition is dependent on the contents
(62)
arising from the publication of the proposed changes. '
-------
IV-84
XII. STANDARDS
(63)
Threshold Limit Values elementary selenium
and its common inorganic compounds:
U0S.S.R.:TLV (1959)
0.2 mg (as Se)/nf
O.lmg/m3
TLV for Hydrogen Selenide
TLG for Selenium hexafluoride (SeF,)
b
0.05 ppm (equivalent to,
approximately 0.2 mg/m )
0.05 ppn or approximately
0.4
-------
IV-85
.XIII; SUMMARY AND CONCLUSIONS '
A. Sunnary
Selenium is a paradoxical element, beneficial or essential in
amounts varying from trace to parts per million concentrations for humans>
animals and plants and quite toxic to animals at concentrations which may
exist in the environment. Also, the sensitivity to selenium and its compounds
is extremely variable in all classes.
Selenium production is a by-product of copper recovery both in the
U.S. and elsewhere. The United States has slipped from its position as the
world's leading selenium producer as a result of the 1967-1968 copper strikes.
However, the production of selenium does not present any economic or strategic
problems. At present, selenium imports amount to less than one-half of the
production, and less than sixty per cent of the selenium available to U.S. copper
refiners is recovered. In practically all the applications for selenium, the
chemically similar compounds of sulfur and tellurium can be substituted. However,
only selenium is suitable in reusable photosensitive plates considering current
technology.
Selenium is widely distributed in nature, but is found in greater con-
centrations associated with sulfide minerals of lead, iron, copper and other metals.
The concentration is certain "seleniferous" soils is great enough that specific
species of plants growing there pick up sufficient selenium to be toxic to
animals. This natural source of selenium entering the environment is significant
but less than that from the weathering of natural rock.
Selenium entering the environment from activities of man is estimated
at 3,500 metric tons per year, of which most is attributed to the combustion of
coal. These contributions appear to be snail in comparison to contributions from
natural sources.
Selenium and its compounds are only moderately toxic to man. The
effects disappear when the exposure ceases. Individual sensitivity seems to
be a big factor which is highlighted by instances of dermatitis among workers
handling selenium. A number of cases of' accidental human poisoning by selenium
in well water and by selenium sulfide (chndruff treatment) have been reported.
-------
IV-86
Selenium compounds are absorbed through the small Intestine and
excreted in the urine, feoes, exhaled air and perspiration. Inorganic
selenium salts become tightly bound to protein, binding with free sulfhydryl
groups „ Qrganoselenium compounds are metabolized like their sulfur analoos
75
Tracer studies with selenium amino acids, for example, have made use of
this property. Selenium is a growth requirement in livestock, poultry and
rodents. White muscle disease in sheep and exudative diasthesis in chickens
are selenium deficiency diseases prevalent in areas of the world with low-
selenium soils.
Plants are extremely efficient accumulators of selenium especially
organoselenium, but tolerance of plants to selenium varies greatly. Selenium
"indicator" plants may accumulate thousands of ppm selenium without ill effects.
and in these plants, selenium is a growth factor. The selenium is present in
small molecular weight organic compounds. Although crop plants accumulate
selenium, concentrations of 25 to 50 ppm may produce phytotoxicity. Selenium
is incorporated into protein in crop plants, but selenium does not appear to be
a necessary growth factor.
High selenium plants and waters are significant dangers to livestock
in seleniferous zones due to the extreme toxicity of the element. Chronic or
acute blind staggers or alkali disease may occur depending upon the type of
plant and amount ingested. Urinary selenium levels appear higher in humans
ingesting foods raised in seleniferous areas, and chronic and acute cases of
poisoning have been reported.
Selenium is transmitted from the mother to the fetus, teduced re-
production rates and weakened offspring occur in selenium-deficient mothers.
Excessive selenium may act as a teratogen. The majority of the evidence indicates
that selenium compounds can function as antitumor agents rather than carcinogens.
Selenium compounds function as growth inhibitors in many microorganisms. Animals,
plants and microorganisms reduce selenium, but metabolic oxidation has not
been clearly established in any species.
B. Conclusions
The following conclusions are based on the information contained in
this report:
(1) The major hazard to man from selenium arises from habitation
-------
VER/AR INC.
IV-87
of regions of the U.S. in which seleniferous soils exist. Dietary and water
intake high in selenium can produce severe toxic effects. Mild to moderate
occupational hazards from selenium also exist.
(2) Sources of selenium attribute! to the activities of man are
small in comparison to the natural sources (soil, plants, rock). However,
localized high concentrations may result from dumping of solid wastes from
coal and fuel oil coribusticn, fuel desulfurizatian, and from mining and pro-
cessing of a number of metallic ores.
(3) Hazards to plants and livestock from selenium exist in areas
of seleniferous soils,- but thsse are generally weJuLHknown and controlled.
C. Recommendations
The following reoonmandation is baaed on the stannary and conclusions
presented above;
(1) T&e amounts and fate of selenium entering the environment through
solid waste disposal from various activities of man should be more closely
studied. These solids arise from the desulfurization and combustion of selenium-
containing fuels (coal and fuel oil) and from various mining activities.
-------
IV-88
(1) Stanford Research Institute. U.S.A. Chemical Information Services.
1974 Directory of Chemical Products/ Selenium Chpt. Menlo Park,
California, 1974.
(2) Chemical Purchasing Chemicals Directory 1973-1974. Myers Publishing
Company. New York, New York (October, 1973). ...-•'*•
(3) Minerals Yearbook 1972, Minor Metals Chpt. Bureau of Mines, U.S. Depart-
ment of the Interior. Washington, D. C., 1974.
(4) Handbook of Chemistry and Physics 1971-1972, 52nd ed., Robert C. Weast,
ed. The Chemical Rubber Co., Cleveland, Ohio, 1971.
(5) Mineral Facts and Problems, 1970, Selenium Chpt. Bureau of Mines, U.S.
Department of the Interior. Washington, D.C. Bulletin 650.
(6) .Gagnell, K. W. The Chemistry of Selenium, Tellurium and Polonium.
Elsevier Publishing Company. AnBterdanv/Lcndon/New York, 1966.
(7) Encyclopedia of Chemical Technology, XVII, 2nd ed. R. Kirk and D. F.
Othner, eds. John Wiley & Sons, Inc., 1964.
(8) Sax, Irving N. Dangerous Properties of Industrial Materials, 3rd ed.
Van Nostrand Reinhold Co., New York, New York, 1968.
(9) Selenium. American Smelting and Refining Company. New York, New York.
pp. 51-52. (February, 1965).
(10) Workplace Standards Administration, Bureau of Labor Standards. Material
Safety Data Sheet. U.S. Department of Labor. (May, 1969).
(11) Davis, W. E. and Assoc. National Inventory of Sources and Emissions.
Barium, Boron, Copper, Selenium, and Zinc 1969. Section IV. Environ-
mental Protection Agency Contract No. 68-02^-0100. (NT IS - PB 210-679),
May, 1972.
(12) Rosenfeia, Irene and Orville A. Beath. Selenium: Geobotany, Biochemistry,
Toxicity, and Nutrition. Academic Press, New York, 1964.
(13) Carter, 0. L., M. J. Brown, W. H. Allaway, and E. E. Gary. Selenium
Content of Forage and Hay Crops in the Pacific Northwest. Agron. J.
60:532-534(1968).
f • • . . •
(14) Selenium in the resources of Nebraskaxdn comparison to public health
standards. American Water Resources Association Publications, Proceedings
Series No. 16, Urbana, Illinois, pp. 1-2, 1972.
(15) Lakin, H. W. & D. F. Davidson. The Relation of the Geochemistry of
Selenium to its Occurrence in Soils. In Symposium: Selenium in Bio-
nedicine, 0. H. Muth, ed. AVI Publishing Company, inc., Weatport,
Connecticut, pp. 27-56, 1967.
-------
IV-89
fAR INC.
References
(16) Hashimoto, Y., J. Y. Hwang, and S. Yanagisawa. Possible Source of
Atmospheric Pollution of Selenium.Gcnmunication. 4(2)157-158 (1970).
(17) Morris, W. D., and 0. A. Levander. Selenium Content of Poods. J.
Nutr. 100:1383-1388 (1970).
(18) Johnson, Henry. Determination of Selenium in Solid Waste. Environ-
mental Science and Technology. 4(10):850-853 (October; 1970).
(19) Gagnell, K. W. The Chemistry of Selenium, Tellurium and Polonium. ;
Elsevier Publishing Company. Amsterdam/Lcngcn/toew York, 1966.
(20) Glover, J. R. Selenium in Human Urine: A Tentative Maximum Allowable
Concentration for Industrial Populations. Ann. Occup. Hyg. (Loidon).
10(1):13-14 (January, 1967).
(21) Osbrun, Robert L., A. D. Shendrikar, and Phillip W. West. A New
SpectrophototBtric Method for Determination of Submicrogram Quantities
of Selenium. Analytical Oiemistry. 43 (4): 594-597 (April, 1971).
(22) Raihle, James A. Fluorometric Determination of Selenium in Effluent
Streams with 2,3 - dianencnaphthalene. Environmental Science and
Technology. 6(7):621-622 (July, 1972).
(23) Chemical Engineering News. 49(29):29-30,33 (July, 1971).
(24) Lakin, Herbert W. Selenium in Our Environment. Trace Elements in the
Environment, Adventures in Chemistry Series, no. 123. American Chemical
Society. Washington, D. C., 1973.
(25) Cooper, W. Charles. Selenium toxicity in man. In: Symposium: Selenium
in Biomedicine, 0. H. Muth, Editor. The AVI Publishing Company, Inc.
Westport, Connecticut, pp. 185-199, 1967.
(26) Scott, Milton L. Selenium. In: Mineral Metabolism. An Advanced
Treatise CL1. GxLmar, and Felix Bonner, Editors. Vol; 2 Pt. The
Elements. Academic Press, Inc.: New York 3. p. 543-558, 1962.
(27) McCbnnell, K. P. and G. J. Cho. Active Transport of Selenium in the
Everted Intestine of the Hamster. In: Symposium: Selenium in Bio-
medicine, 0. H. Muth, Editor. The AVT Publishing Company, Inc.
Westport, Connecticut, pp. 329-343, 1967.
(28) Allaway, W. H., E. E. Gary, and C. F. Ehlig. The Cycling of lew levels
of Selenium in soild, plants and animals. In: Symposium: Selenium in
Biomedicine, 0. H. Muth, Editor. The AVI Publishing Company, Inc.
Westport, Connecticut, p. 273-296, 1967.
Olson, 0. E. Soil, Plant, Animal Cycling of Excessive Levels of Selenium.
In: Symposium: Selenium in Biomedicine, 0. H. Muth, ed. The AVI Publish-
ing Company, Inc. Westport/ Connecticut, pp. 297-312, 1967.
-------
IV-90
References
(29) Wright, Paul L. The absorption and tissue distribution of selenium in
depleted animals. In: Synpoeium: SeleMum in Bicmadicine/0. H. Muth,
Editor. The AVI Publishing Company, Inc. Westport, Odnnecticut.
p. 313-328, 1967.
(30) Gary, E. E., W. H. Allaway and M. Miller. Utilization of Different Forms
of Dietary Selenium. J. Anim. Sci. 36:285-292(1973).
(31) Lopez, P. L., R. L. Preston and W. H. Pfander. Whole Body Retention, Tissue
Distribution and Exereticn of Selenium - 75 After Oral and Intravenous
Administration in Lambs Fed Varying Selenium Intakes. J. Nutr. 97:123-
132 (1968).
(32) Hirooka, T., and J. T. Galantoos. Selenium MBtabolism. I. Respiratory
Excretion. Biochim. Biophys. Acta (Anpterdam) 130:313-320 (1966).
(33) Poll, E. G., G. Dumitrae, and A. Feteanie. Contributions to the study of
the distribution of Se in the tissues of hens (Gassus dgrfeatica).
Lucrari Stiint. Agron. Balescu. (Bucuresti). Ser. C 10:249-256 (1967).
(34) Sakurayama, H. Studies on the selenium opisoning. 7. Experimental
studies en rearing of fishes, shells and duckweed in se.lenious acid
solution. Shikoku Acta. Med. 16:122-127 (1960).
(35) Selenium in Nutrition. National Academy of Sciences. Washington, D.C.,
1971.
(36) Johnson, C. M., C. J. Asher, and T. C. Broyer. Distribution of Selenium
in Plants. In: Symposium: Selenium in Biomedicine, 0. H. Muth, ed.,
The AVI Publishing Odmpany, Inc. Westport, Connecticut, pp. 57-75,
1967.
Harr, J. R., J. F. Bone, I. J. Tinsley, P. H. Weswig, and R. S. Yomanoto.
Selenium Toxicity in Rats II. Histopathology. In: Symposium: Selenium
in Bionedicine, O. H. Muth, ed. The AVI Publishing Ocnpany, Inc. Westport,
Connecticut, pp. 153-178, 1967.
Volgarev, M. N. and L. A. Tscherkes. Further Studies in Tissue Changes
Associated with Socium Selenate. In: Synpoeiun: Selenium in Bio-
medicine, O. H. Muth, ed. The AVI Publishing Company, Inc. Westport,
Connecticut, pp. 179-184, 1967. ' , '
(37) Hirooka, T. and J. T. Galambos. Selenium Metabolism. III. Serum Proteins,
Lipoproteins and Liver Injury. Biochim. Biophys. Acta (Amsterdam).
130:321-328 (1966).
(38) Van Houweling, C. D., Dir. Final Environmental Impact Statement - Rule
Making on Selenium in Animal Feeds, EJS-AA-74 0159 F, 1974.
(39) JfcFarland, L. Z., C. M. Winget, W. 0. Wilson, and C. M. Johnson. Role
of Selenium in Tissues of Chickens, Turkeys and Ooturnix. pp. 216-221
(1969).
-------
VER/A
IV-91
IAR INC.
References
(40) Cals, I. Selenium distribution in chicken tissues and organs. Veterinariya
(Moscow) 45:58-61 (1969).
(41) Cals, I. and Z. Pelekis. Age dynamics of the selenium concentration in
laying hens. Vestn. Sel'skckhoz. Nauki (Moscow). 16:23-29 (1971).
(42) Cals, I. Selenium concentration in chicken eggs as determined by its
content in the feed, vestn. Sel'skokhoz. Nauki (Moscow) 14:108-111
(1969).
(43) Cals. I. Distribution of selenium in chick organs. Veterinqriya (Moscow)
48:89-92 (1971).
(44) Jenkins, K. J., R. C. Dickscn and M. Hiridogeh. Intravascular Transport
of Selenium in the Chick. In: Trace Elem. Metab. Anim. Proc. WAPP
(World Ass. Anim. Prod)/IBP (int. Bibl. Progr.) Int. Symp. C. F. Mills,
ed. Livingstone: London, England, 1969.
(45) Schwarz, K. Developmental status of experimental work on Factor-3-
Selenium. Fed. Proc. 20:666-673 (1961).
(46) Hopkins, L. L., Jr., and A. G. Majaj. Selenium in Human Nutritian. In:
Symposium: Selenium in Bioredicine, 0. H. Muth, ed. The AVI Publishing
Catpany, Inc. Westport, Connecticut, pp. 203-214, 1967.
(47) Hurt, H. D., E. E. Gary, and W. J. Visek. Growth* Reproduction, and
Tissue Concentrations of Selenium in the Selenium-Depleted Rat. J. Nutr.
101:761-766 (1971).
(48) Shrift, A. Microbiol Research with Selenium. In: Synposium: Selenium
in Bianedicine, 0. H. Muth, ed. The AVI Publishing Company, Inc. West-
port, Connecticut, pp. 241-271t 1972.
(49) Martin, J. L., and M. L. Gerlach. Selenium Metabolism in Animals. Ann.
N. Y. Acad. Sci. pp. 193-199.
(50) Millar, K. R., M. A. Gardiner, and A. D. Sheppard. A comparison of the
metabolism of intravenously injected sodium selenite, sodium selenate,
and selencmethionine in rats. N.Z.J. Agric. Res. 16:115-127 (1972).
(51) Tappel, A. L., and K. A. Caldwell. Redox Properties of Selenium Ocnpounds
Related to Biochemical Function. In: Symposium: Selenium in Biomedicine,
0. H. Muth, ed. The AVI Publishing Company, Inc. Westport, Connecticut.
pp. 345-361, 1972.
Rotrudc, J. T., A. L. Pope, H. E. Ganther, A. B. Swanson, D. G. Hafeman,
and W. G. Holkstra. Selenium: Biochemical Pole as a ocnponent of
Glutathione Peroxidase. Science 179:588-590 (1973).
(52) Alloway, W. H., D. P. Moore, J. E. Oldfield and 0, H. Muth. Movement of
Physiological Levels of Selenium from Soils through Plants to Animals.
J. Nute. 88:411-418 (1966).
-------
IV-92
References
(53) Selenium in plankton. Marine Pollution Bulletin. 2(5):69 (May, 1971).
(54) Rosenfeld, Irene and Orville A. Beath. Selenium: Geobotany, Biochemis-
try, Otoocicity, and Nutrition. Academic Press, New York, 1964.
(55) The Selenium Paradox. Pd. Oosmet. Tbxical. 10:867-874 (1972).
(56) Shapiro, J. R. Selenium and Carcino genesis: A Review. Ann. N.Y.
Acad. Sci. pp. 215-219.
(57) Selenium and Cancer. Nutr, Rev. 28:75-80 (1970).
(58, Levander, 0. A. Metabolic Interrelationships and Adaptations in Selenium
59) ToxicLty. Ann. N.Y. Acad. Sci. pp. 181-192.
(60) Lund, Herbert E. Industrial Pollution Control Handbook. MoGraw Hill
Book Company. New York, New York. •
(61) Proposed Illinois Pollution Control Board Rules and Regulations, Ghpt VI.
Illinois Environmental Protection Agency. (October 24, 1973).
(62) Rule-Making on Selenium in Animal Feeds. Bureau of Vetinary Medicine.
The Food and Drug Administration, U.S. Department of Health, Education,
and Welfare. Rockville, Maryland, January 28, 1974.
(63) Documentation of the Threshold Limit Values for Substances in Workroom
Air, 3rd ed. American Conference of Government Industrial Hygienists,
1971.
------- |