-------
AIR POLLUTION ASPECTS
OF
SELENIUM AND ITS COMPOUNDS
Prepared for the
National Air Pollution Control Administration
Consumer Protection & Environmental Health Service
Department of Health, Education, and Welfare
(Contract No. PH-22-68-25)
Compiled by Quade R. Stahl, Ph.D,
Litton Systems, Inc.
Environmental Systems Division
7300 Pearl Street
Bethesda, Maryland 20014
September 1969
-------
FOREWORD
As the concern for air quality grows, so does the con-
cern over the less ubiquitous but potentially harmful contami-
nants that are in our atmosphere. Thirty such pollutants have
been identified, and available information has been summarized
in a series of reports describing their sources, distribution,
effects, and control technology for their abatement.
A total of 27 reports have been prepared covering the
30 pollutants. These reports were developed under contract
for the National Air Pollution Control Administration (NAPCA) by
Litton Systems, Inc. The complete listing is as follows:
Aeroallergens (pollens) Ethylene
Aldehydes (includes acrolein Hydrochloric Acid
and formaldehyde) Hydrogen Sulfide
Ammonia Iron and Its Compounds
Arsenic and Its Compounds Manganese and Its Compounds
Asbestos Mercury and Its Compounds
Barium and Its Compounds Nickel and Its Compounds
Beryllium and Its Compounds Odorous Compounds
Biological Aerosols Organic Carcinogens
(microorganisms) Pesticides
Boron and Its Compounds Phosphorus and Its Compounds
Cadmium and Its Compounds Radioactive Substances
Chlorine Gas Selenium and Its Compounds
Chromium and Its Compounds Vanadium and Its Compounds
(includes chromic acid) Zinc and Its Compounds
These reports represent current state-of-the-art
literature reviews supplemented by discussions with selected
knowledgeable individuals both within and outside the Federal
Government. They do not however presume to be a synthesis of
available information but rather a summary without an attempt
to interpret or reconcile conflicting data. The reports are
-------
necessarily limited in their discussion of health effects for
some pollutants to descriptions of occupational health expo-
sures and animal laboratory studies since only a few epidemio-
logic studies were available.
Initially these reports were generally intended as
internal documents within NAPCA to provide a basis for sound
decision-making on program guidance for future research
activities and to allow ranking of future activities relating
to the development of criteria and control technology docu-
ments. However, it is apparent that these reports may also
be of significant value to many others in air pollution control,
such as State or local air pollution control officials, as a
library of information on which to base informed decisions on
pollutants to be controlled in their geographic areas. Addi-
tionally, these reports may stimulate scientific investigators
to pursue research in needed areas. They also provide for the
interested citizen readily available information about a given
pollutant. Therefore, they are being given wide distribution
with the assumption that they will be used with full knowledge
of their value and limitations.
This series of reports was compiled and prepared by the
Litton personnel listed below:
Ralph J. Sullivan
Quade R. Stahl, Ph.D.
Norman L. Durocher
Yanis C. Athanassiadis
Sydney Miner
Harold Finkelstein, Ph.D.
Douglas A. Olsen, Ph0D.
James L. Haynes
-------
The NAPCA project officer for the contract was Ronald C.
Campbell, assisted by Dr. Emanuel Landau and Gerald Chapman.
Appreciation is expressed to the many individuals both
outside and within NAPCA who provided information and reviewed
draft copies of these reports. Appreciation is also expressed
to the NAPCA Office of Technical Information and Publications
for their support in providing a significant portion of the
technical literature.
-------
ABSTRACT
Selenium compounds in the atmosphere are known to cause
irritation of the eyes, nose, throat, and respiratory tract in
humans, and und.er conditions of prolonged, exposure, gastroin-
testinal disorders result. In animals there are indications
that selenium ingestion may cause cancer of the liver, and it
is known to prod.uce pneumonia and. degeneration of liver and
kidneys.
Sources of atmospheric selenium includ.e combustion of
industrial and. residential fuels, refinery waste gases and. fumes,
and incineration of wastes including paper products which contain
as much as 6 ppm selenium. Little data is available on concen-
trations of selenium in the air; one report indicated an average
value of 0.001 |ag/m3 in the vicinity of Boston, Mass.
Electrostatic precipitators and. water scrubbers are effec-
tive in controlling emissions of selenium in industrial opera-
tions. No information has been found, on the economic costs of
selenium air pollution, or on the costs of its abatement.
Method.s are available for the analysis of selenium in the atmo-
sphere.
-------
CONTENTS
FOREWORD
ABSTRACT
1. INTRODUCTION 1
2. EFFECTS 2
2.1 Effects on Humans 2
2.1.1 Chronic Effects 2
2.1.2 Acute Poisoning 4
2.1.3 Retention and Elimination 5
2.1.4 Detoxification 7
2.1.5 Selenium in Nutrition 8
2.1.6 Elemental Selenium . 8
2.1.7 Selenium Dioxide, Selenites, Selenates . 9
2.1.8 Hydrogen Selenide 10
2.1.9 Selenium Oxychloride 11
2.1.10 Organoselenium Compounds 11
2.2 Effects on Animals 12
2.2.1 Livestock 12
2.2.2 Experimental Animals 15
2.2.2.1 Selenium, Selenites, Selenates. 15
2.2.2.2 Hydrogen Selenide 16
2.2.2.3 Organoselenium Compounds ... 18
2.2.3 Carcinogenesis 18
2.3 Effects on Plants 21
2.3.1 Selenium Indicator Plants 21
2.3.2 Secondary Selenium Absorbers 23
2.3.3 Grains, Vegetables, Grasses, and
Other Vegetation 25
2.4 Effects on Materials 27
2.5 Environmental Air Standards 27
3. SOURCES 28
3.1 Natural Occurrence 28
3.2 Production Sources 30
3.3 Product Sources 32
3.4 Other Sources 35
3.5 Environmental Air Concentrations 37
-------
4. ABATEMENT 42
5. ECONOMICS - 44
6. METHODS OF ANALYSIS 45
6.1 Sampling Methods 45
6.2 Qualitative Determination Methods 46
6.3 Quantitative Determination Methods 47
7. SUMMARY AND CONCLUSIONS 49
REFERENCES
APPENDIX
-------
LIST OF FIGURES
1. Selenium Content of Plants in Certain Counties in
the United States 22
2. Distribution of Seleniferous Vegetation 24
-------
LIST OF TABLES
1. Symptoms and Gross Pathology of Chronic Selenium
Poisoning in Livestock 14
2. Minimum Doses Fatal to Rats of Compounds of
Selenium, Tellurium, Arsenic, Vanadium, and
Molybdenum 17
3. Selenium Content of Coals 37
4. Atmospheric Selenium (1964-65) 38
5. Selenium Content of Particulates in Ambient Air,
1965 40
6. Mortality of Guinea Pigs from Inhalation of Hydrogen
Selenide 63
7. Producers of Selenium in the United States (1967) . 64
8. Salient Selenium Statistics, 1965-67 65
9. List of Merchandisers and Consumers of Selenium and
Its Compounds 66
10. Properties, Toxicity, and Uses of Some Selenium
Compounds 69
11. Selenium Content of Dust from Air-Conditioning
Filters, 1941 78
-------
1. INTRODUCTION
Selenium poisoning of humans and animals from ingestion
of foods containing toxic amounts of selenium has been and still
is a problem of great concern in the United States. Many plants
used as food by humans and animals can accumulate high concen-
trations of selenium from the soil. The soils of the Midwest
are particularly high in selenium. Extensive studies have been
made of the people, animals, food prod.ucts, and soils of the
high seleniferous areas. Selenium has also been found to be an
essential nutrient for animals and may be necessary for humans.
Selenium compounds, although toxic, have seldom present-
ed a serious problem in ind.ustry. Inhalation of the dust, fumes,
or vapors of selenium compounds can irritate the eyes, nose, and
throat, causing lacrimation, palpebral ed.ema, conjunctivitis,
sneezing, nasal congestion, anosmia, and coughing.
A study made in Boston, Mass, showed that there was ap-
proximately 0.001 |_ig/m3 of selenium in samples of rain, snow,
and air analyzed.. The sources of atmospheric selenium are be-
lieved to be terrestrial, such as fuels and. ores used by indus-
try, or possibly the burning of trash, particularly paper.
-------
2 . EFFECTS
2.1 Effects on Humans
Little information is available on the toxicity of sele-
nium through inhalation by humans. This is partly due to the
infrequent occurrence of serious intoxication during the indus-
trial use of selenium and its compound.s, and. also to the fact
that human exposure is largely through the consumption of food.
Ind.ustrial exposures are commonly a result of inhalation
of the dust, fumes, and vapors of selenium and its compounds,
although ingestion and skin contact are also important. The
effects of ind.us trial exposure have been reported, by Hamilton, 51 > 52
Dud.ley,26'27 Amor and Pringle,2 Clinton,16 and Glover.44 Dis-
cussion of these effects can be found in Trelease and. Beath, 119
Cerwenka and Cooper,12 Patty,89 and Cooper.19
The effects of selenium and. its compound.s on humans ap-
pear to differ somewhat from those observed in animals. Thus,
although animals can d,isplay d.efinite d.isease responses to the
amount of selenium ingested, (see Section 2.2), there have been
no chronic diseases in man attributable to selenium or its com-
pound.s .4
2.1.1 Chronic Effects
In general, chronic selenium intoxication in man prod.uces
the following symptoms: depression, marked, pallor, coated, tongue,
-------
languor, nervousness, occasional dermatitis, gastrointestinal
disturbances, gid.d.iness, and. garlic od.or of the breath and.
sweat .12,19,51 Moxon and Rhian°^ also noted, small local hemor-
rhages, severe ascites, liver and splenic d.amage, emaciation,
apathy, and progressive anemia. Hamilton^ mentioned irritation
of nose, throat, and bronchi; pain in the lumbar region; nasal
inflammation resembling that accompanying a cold; and night
sweats. The above authors believe that garlic odor of the
breath is one of the earliest and most characteristic symptoms
of selenium intoxication. '43 Although there has been some
question whether trace impurities of tellurium may give the gar-
lic odor,89 this odor has been found in workers exposed to 99.999
percent pure selenium.^4 other authors believe that symptoms of
respiratory ailments and. gastrointestinal disturbances are of ma-
jor significance in the diagnosis of selenium poisoning.
Rosenfeld. and. Beath^ stated, that the possible long-term
effects of selenium may be kidney and. liver d.amage. Also fibro-
sis of the lung may d.evelop following continued, exposure to dust
and gases in the air.
The studies of Had.jimarkos^ and. the data from earlier
investigatorslO^/HI suggest that selenium can increase the sus-
ceptibility of humans to d.ental caries. However, Cad.ell and
CousinsH founcg no changes in primary, d.ecayed, missing, and
-------
4
filled teeth that would ind.icate dependence on selenium intake.
Apparently the toxicity of selenium to humans may be
somewhat dependent on certain physical characteristics. Dudley
noted that mature men of dark complexion and stocky build had
less tendency to develop the symptoms of selenium poisoning
than did younger men with smaller build, and fair complexion.
Wands-^a indicated that this effect might more reasonably be d.ue
to dietary habits of ethnic or nationality groups, such as the
high level of wheat protein in Italian diets.
Besides the more obvious irritation effects of selenium
and its compound.s, it appears that some toxic action results
from the blocking of several enzyme systems. '
2.1.2 Acute Poisoning
The intense irritation prod.uced by d.usts and. fumes of se-
lenium and. its compounds normally prevents excessive exposure to
high concentrations of selenium, and. hence acute poisoning is
uncommon. Moxon and Rhian^4 noted, that the early signs of acute
poisoning are nervousness and fever, followed, by vomiting, then
quietness and somnolence. Difficult breathing develops, fol-
lowed by opisthotonos (tetanic spasm), clonic spasm, and falling
blood pressure. Death may occur from respiratory failure, or
convulsions resulting from action on the nervous system.
-------
2.1.3 Retention and Elimination
Studies of Glover^4 and others12'19 indicate that there
are no apparent long-term systemic effects in humans as a re-
sult of chronic exposures to selenium and its compounds. Thus
the body must have mechanisms for* the effective removal of se-
lenium so that accumulation of toxic amounts do not occur.
Animal experiments suggest that, at least at low concentrations,
the urinary and fecal excretion rates attain a steady state
during long periods of exposure to selenium. Results of studies
by Smith et aj^.112 indicate that cats administered. d.aily oral
doses of selenite (equivalent to 20 and. 100 (J.g of selenium per
kilogram of body weight) excreted, approximately 75 percent of
the selenium in the urine and. feces. When a toxic dose rate
(equivalent to 250 |_ig/kg of selenium) was ad.ministered., the
average excretion d.ropped. to approximately 64 percent of the
total intake.
The selenium not accounted for in the urine and. fecal
excretion may be (1) retained in the body, (2) excreted as a
volatile compound in the breath and. sweat, or (3) deposited, in
the hair. The importance of the first possibility d.epend.s on
the amounts excreted, by the latter routes. No experimental data
are available for direct comparison of the contribution of each
of the possible excretion routes. However, some d.ata indicate
-------
6
that excretion of volatile selenium compounds in the breath and
sweat is a significant excretion route. Schultz and Lewis"
found that when sodium selenate was administered subcutaneously
to cats as sod.ium selenite in a dose equivalent to 2,500 to
3,500 |j.g of selenium per kilogram of body weight, 17 to 52 per-
cent of the selenium was eliminated, as a volatile compound with-
in 8 hours. In a similar experiment McConnell^ found that 3
to 10 percent of the initial subcutaneously administered sele-
nite (equivalent to 3,000 to 4,000 U-g of selenium per kilogram
of body weight) was exhaled in 24 hours—-half, moreover,- in the
first 3 hours. Selenium is also deposited, in the hair in amounts
dependent on the selenium concentration and duration of the
exposure.^
According to Cerwenka and Cooper, ^ "Animal experiments
indicate that as soon as a certain state of saturation is reached
the excretion holds pace with the intake." If correct, this
means that the maximum amount of selenium retained, in the body
is dependent upon the level of exposure and not the d.uration of
the exposure. This may not be true of ingested organic selenium
compound.s. -*--*-^
The selenium that is retained is widely distributed in
the body- Ermakov^l found, that selenium was wid.ely distributed
in human organs and. tissues, and. that there was a significant
-------
difference in the distribution pattern among individuals.
Animals chronically exposed to toxic amounts of selenite are
found to retain most of the selenium in the liver, kidney,
spleen, pancreas, heart, and lungs.^9 Once removed from expo-
sure to selenium, the animals rapidly eliminated almost all the
selenium in the body, mainly in the urine within about 2
o ] 1 9
weeks. ' After this period elimination rapidly decreases to
a very slow rate that continues for a month or longer. Ingested
organic selenium appears to be retained, in the body longer than
the inorganic selenium compound.s. H-^
2.1.4 Detoxification
In the human body natural detoxification occurs through
reduction of selenium compounds to elemental selenium, which is
apparently not toxic1^ and is excreted, through the kidneys and
liver-->3/108 Elemental selenium is also converted to a volatile
compound., ->3 probably dimethyl selenide, ^ which is eliminated
through the breath and sweat.
There are several method.s of artificial d.etoxification
or prevention of selenium poisoning, at least for animals.
Animal stud.ies have shown that protein, particularly casein,
can help prevent intoxication from small amounts of ingested
selenium.46'70'107 Thus a high protein diet may be an impor-
tant factor in protecting humans against chronic selenium
-------
8
poisoning. Several studies have shown that arsenic can coun-
teract the toxicity of selenium in rats, 5/88 c|OgSf94 an<^ p£gS<_1
9
Amor and Pringle suggested the use of an arsenic tonic for pro-
tection of selenium workers, but it has never been tried. Bromo
benzene has been used to accelerate the excretion of selenium in
the urine.^7 However, some investigators^ found that this com-
pound, administered orally, produced no effect on the selenium
content of the body.
2.1.5 Selenium in Nutrition
Preliminary findings ind.icate that selenium may be a bene
ficial element to humans. In Jamaica the protein-d.eficiency
disease kwashiorkor, which is characterized, by an inability to
gain weight, appears to respond favorably to a d.iet supplement
of 25 ng of selenium as ft, ^"-d is el enodivaleric acid.. It has al-
ready been demonstrated, that selenium is an essential d.ietary
nutrient for animals.-'-'-'0/135 Selenium is prescribed for such
animal diseases as congenital white muscle d.isease, selenium-
responsive unthriftiness in cattle, exudative diathesis in poul-
try, and hepatosis diaetetica in pigs, as well as for barrenness
in ewes.
2.1.6 Elemental Selenium
Stud.ies to date ind.icate that elemental selenium is rela-
tively nontoxic. However, d.ust or fumes of selenium cause
-------
irritation of mucous membranes when inhaled. The selenium par-
ticulates are collected in the upper nasal passages and cause
catarrh, nosebleed., and loss of the sense of smell.^ Dermatitis
can also occur when sufficient amounts come in contact with the
skin.^
A d.etailed. description of an industrial exposure to red
selenium fumes is related by Clint on.-^ Exposure to the fumes,
which have an unpleasant, sour, garlic-like odor, resulted in
immediate and intense irritation of the eyes, nose, and throat.
Heavily exposed, workers noted, a severe burning sensation of the
nostrils, immediate sneezing, coughing, nasal congestion, dizzi-
ness, and red.ness of the eyes. Two to four hours after the ex-
posure, severe head.aches, mainly in the frontal region, were
experienced., and. lasted, until the following day. The most
heavily exposed, workers had edema of the uvula and. slight dif-
ficulty in breathing, while more pronounced dyspnea was noted
in one case. No selenium could, be found, in the urine, and af-
ter 3 d.ays all workers were entirely well and suffered no per-
sistent aftereffects.
2.1.7 Selenium Dioxide, Selenites, Selenates
Selenium d.ioxid.e (SeO2) and. selenite salts (SeO3 2)
read.ily form selenious acid, in the presence of moisture. Se-
lenious acid. and. its precursors are among the more toxic and
-------
10
irritating compounds of selenium. Exposure to selenium dioxide
has been reported to cause severe dermatitis^ an<3 burning of
the eyes, with intense pain, lacrimation, and congestion of the
conjunctiva. 6 Glover43 noted that some people, particularly
fair-haired workers, appear to become allergic to selenium di-
oxide; thus, on walking into a room where selenium dioxide is
present their eyes will puff up, while others in the room ex-
hibit no ill effect.
In general, susceptibility to the toxicity of selenium
compound.s varies wid.ely from one individ.ua! to another.
2.1.8 Hyd.roqen Selenide
Hyd.rogen selenid.e (H3Se) at room temperature is a gas
with a very offensive odor.-^ This selenid.e, probably the most
toxic and irritating of selenium derivatives, can be formed, by
the reaction of selenium with organic matter or certain other
elements, as well as from selenid.es by acid.s or in some cases
by water.
The symptoms of hyd.rogen selenid.e poisoning include nau-
sea, vomiting, metallic taste, garlic od.or of the breath, dizzi-
ness, extreme lassitud.e, and. fatigability. ' /2° These symptoms
were observed, in one case from exposure to 800 |ag/m3 (0.2 ppm)
of hyd.rogen selenide for less than 1 month. The symptoms of
acute hydrogen selenid.e poisoning were d.escribed. by Symanski
-------
11
as acute irritation of the mucous membrane of the respiratory
tract, pulmonary edema, severe bronchitis, and bronchial pneu-
monia.
Dudley and. Miller29 noted that a person rapid.ly loses
his ability to detect the od.or of hydrogen selenide because of
olfactory fatigue. These authors also mention that 5,000 |ag/m3
of this substance was intolerable to man and. caused, ocular and
nasal irritation.
2.1.9 Selenium Oxvchlorid.e
Selenium oxychlorid.e is a liquid, which is used, as a sol-
vent for paints and varnishes, as a chlorinating agent, and as
a resin plasticizer. Although it is strongly vesicant2? and
the vapors toxic, the danger of poisoning is not as great as
might be supposed, since the oxychloride has a low vapor pres-
sure and readily d.ecomposes in air.
2.1.10 Organoselenium Compound.s
There is a very limited, amount of data on the organic
selenium compound.s.
Motley _et_ aJL.. ^ reported acute sore throats in three
laboratory workers following exposure to dimethyl selenide or
combined organoselenium from hand.ling d.ogs injected, with sele-
nium. One worker contracted pneumonitis.
-------
12
2.2 Effects on Animals
Most reported, cases of animal poisoning result from the
ingestion of plants or foods containing toxic amounts of sele-
nium, usually bound with organic compounds. Cases involving
cattle, sheep, horses, and hogs have been described.^7 Numerous
animal experiments involving selenium and its compounds have
been reported. The results of some of the experiments have al-
ready been discussed in the sections concerned with Effects on
Humans. Selenium from different sources produces different
clinical and pathological symptoms in animals because of the
various selenium compounds present in the sources. For example,
Rosenfeld and Beath"' give the following order of toxicity from
equivalent amounts of selenium from different sources: wheat >
corn > barley > selenite > selenate. However, in animals, sub-
acute poisoning from selenium in general produces pneumonia,
fatty degeneration of the liver, and. degeneration of kidney
cells and. these symptoms clear up without resid.ual pathology
when exposure is discontinued. There is also evid.ence suggesting
that selenium may cause cancer of the liver in rats.
Studies have shown that selenium is a necessary dietary
0-7
element for many animals, including mammals and bird.s.
2.2.1 Livestock
Acute poisoning of livestock occurs from the consumption
-------
13
of highly seleniferous weeds-—usually in a single feeding—-in
many cases resulting in d.eath in a few hours . When the acute
poisoning begins to take effect, the movement and posture of
the animal become abnormal. Diarrhea usually follows, the tem-
perature rises, and the pulse becomes rapid and weak. Respira-
tion becomes labored, with mucous rales and possible blood froth
from the air passages. Bloating is usually pronounced, accom-
panied by abdominal pain, and urine excretion increases greatly-
Pupils dilate. Complete prostration and. apparent lethargy occur
just before death from respiratory failure. Emesis, diarrhea,
apathy, and paresis have been noted in pigs suffering from se-
lenium poisoning.
Chronic poisoning can be d.ivided into three types, de-
pending on the source of selenium: (1) blind, staggers, caused
by organic selenium compound.s (with or without small amounts of
selenate), which can be read.ily extracted, with water from native
selenium-bearing plants; (2) alkali d.isease, produced, from con-
sumption of plants or grains containing protein-bound, selenium
which is insoluble in water; and (3) chronic selenium poisoning,
prod.uced. experimentally from pure inorganic selenium compounds.
A summary of the three diseases is given in Table 1, which has
97
been compiled from the studies cited by Rosenfeld and Beath.
(See paragraphs under Section 2.3 for a d.iscussion of plants
containing selenium.)
-------
TABLE 1
SYMPTOMS AND GROSS PATHOLOGY OF CHRONIC SELENIUM POISONING IN LIVESTOCK
97
Blind Staqqers
Alkali Disease
Experimental Selenosis
Selenium source
Symptoms
Gross pathology
Certain selenium
"indicator1' plants
1st stage: increased
desire to eat, animal
staggers
2nd stage: increased
loss of muscular
control, front legs
become very weak,
does not eat or drink
3rd stage: paralysis,
nearly blind, abdominal
pain, body temperature
drops, emaciation, eyes
swollen and inflamed,
cornea cloudy, death
usually occurs in 3rd
stage
Necrosis (with cirrho-
sis) of liver, nephritis
(subacute and chronic),
enlarged gall bladder,
soft and flabby heart,
impacted intestinal
tract with irritation
Seleniferous grains
and grasses
Lameness, loss of
vitality, elongated
and hardened hoofs,
loss of hair
from mane and tail,
anemia, stiffness of
joints, roughened
coat
Atrophy and cirrhosis
of liver; chronic
nephritis; soft,
flabby, and atrophied
heart; edema of lungs
Selenite and selenate
inorganic salts
Emaciation, some loss
of muscle control,
trembling of skeletal
muscles, anorexia
Necrosis with occasional
cirrhosis of liver,
acute nephritis,
ulceration and gangrene
of intestinal tract
-------
15
2.2.2 Experimental Animals
Selenium poisoning in animals from administration of
selenium and its compounds may be acute, subacute, or chronic,
depending on the compound, dose, and duration of the exposure.
Acute symptoms in animals are garlicky od,or, nervousness,
fear, vomiting, and diarrhea.97 This is followed by quietness
and somnolence, difficult respiration, and. decreased reflexes.
Opisthotonos (tetanic spasm in muscles) follows. The blood
pressure continually drops until d.eath results from respiration
failure.
In rats, subacute and chronic selenosis produce loss in
body weight and. anorexia, followed, by cachexia, while ascites
edema may also develop. '
Smith et aj...-'••'-^ noted that among the common laboratory
animals the cat showed the greatest susceptibility and the rat
the greatest resistance to selenium poisoning.
2.2.2.1 Selenium, Selenites, Selenates
Hall _et_ aj.,.50 exposed, cats, guinea pigs, and. rabbits to
elemental selenium dust (which may have been contaminated with
selenium d.ioxide) at the concentration of 30,000 |ag/m3 for 16
hours. This exposure prod.uced. mild, interstitial pneumonitis
in the animals. Selenium fumes via vacuum evaporation cause
acute toxic reactions in rats.
-------
16
The susceptibility of animals to the toxicity of sodium
selenite and selenate has been stud.ied. by Franke and, Moxon, ^»40
Heinrich and MacCanon,60 and. Painter.87 Sodium selenite appears
to be more toxic to rats than sodium selenate by a factor of 1.5
to 1.6. A comparison of the toxicity of selenium compounds with
that for compounds of tellurium, arsenic, molybdenum, and. vana-
d.ium is given in Table 2.
2.2.2.2 Hydrogen Selenide
Dudley and Miller^°'^^ investigated, the effect of inhala-
tion of hyd.rogen selenid.e (H3Se) on guinea pigs. All guinea
pigs exposed, to H2Se in the concentration of 20,000 Hg/m3 for
60 minutes d.ied within 25 d.ays; 93 percent of the guinea pigs
inhaling 43,000 [ag/m3 for 30 minutes d.ied. within 30 d.ays; and
after 570,000 |Jg/m3 for only 10 minutes, all guinea pigs d.ied
within 5 days.28 Ad.d.itional stud.ies were cond.ucted. on guinea
pigs with various concentrations ranging from 1,000 to 45,000
[jg/m3 of H2Se and. for period.s of 2, 4, and. 8 hours. Table 6
in the Appendix summarizes the reported data. The major cause
of the d.eaths seemed to be pneumonitis caused, by irritation of
the respiratory tract. In ad.dition, damage to the liver and
spleen was observed.. At concentrations of 7,000 [ig/m3 and less
no response was observable in the guinea pigs during the expo-
sure period.s. In one experiment (8 hours at 42,000 |Jg/m3 ) it
-------
17
TABLE 2
MINIMUM DOSES FATAL TO RATS OF COMPOUNDS OF
SELENIUM, TELLURIUM, ARSENIC, VANADIUM, AND MOLYBDENUM
Compound MFD 75/48 hr*
Sodium selenite (Na2SeO3) 3,250 - 3,500
Sodium selenate (Na2SeO4) 5,250 - 5,750
Sodium tellurite (Na2Te03) 2,250 - 2,500
Sodium tellurate (Na2TeO4) 20,000 -30,000
Sodium arsenite (Na2HAsO3) 4,250 - 4,750
Sodium arsenate (Na2HAsO4) 14,000 -18,000
Sodium vanadate (NaVOs) 4,000 - 5,000
Ammonium molybdate ((NH4)6MO7O24) >160,000
*Minimum fatal dose to at least 75 percent of the
rats in 48 hours (in micrograms of compound per kilogram
of weight) via intraperitoneal injection.
-------
18
was noted that the guinea pigs spread selenium-containing exu-
date over their bodies which caused irritation of eyes and nose.
2.2.2.3 Organoselenium Compounds
Q o Q *3
Moxon and co-workers ^' found that in general the or-
ganic compounds are retained by the tissues to a greater extent,
and for a longer period, of time, than are the inorganic com-
pounds. However, there is a wid.e variation in the toxicity of
different organoselenium compounds. The lethal d.oses for some
organic compounds for rats via intraperitoneal injection are:
for selenocystine, the equivalent of 4,000 |_ig of selenium per
kilogram of body weight; for n-propylseleninic acid., 20,000 to
25,000 ng selenium; for B-selenodipropionic acid, and for B, B -
diselenodipropionic acid, 25,000 to 30,000 ug selenium.®^,83
Animal experiments with dimethyl selenid.e indicate that
this compound has a low degree of toxicity in mice and. rats7^
when injected intraperitoneally.
2.2.3 Carcinocfenesis
There are d.ata which ind.icate that selenium may be car-
cinogenic to animals, and therefore possibly to man. However,
further investigations are need.ed. to clarify the point. In
studies mad.e by Nelson _e_t aJ^.85 and. Fitzhugh et_ al_. ,3S 126 rats
were fed. selenium in organic combination with corn and wheat
(containing 5 to 10 ppm selenium) and. also inorganic selenid.es
-------
19
(10 to 50 ppm). Of the 53 rats that lived, over 18 months, 11
developed hepatic neoplasms of low malignancy, and, four devel-
oped microscopic ad.enomatoid hyperplasias. None of the neo-
plasms metastatized.. Rats that died before 18 months did not
exhibit neoplasms. On the basis of these early tests, the Food
Additive Amendment of 1958 included selenium in the cancer
clause.'*-'- Concern for the carcinogenic hazard of selenium in
foods was also shown by the National Acad.emy of Sciences ^ and
the World Health Organization.^2
However, it was thought by some people that the d.ata were
insufficient to prove the carcinogenic hazard.s of selenium, and
they urged a careful reevaluation of the problem. Some suggested
that the d.iet in the experiments of Nelson et. al_. -* was inad.e-
quate in protein. Pearce failed, to ind.uce cancer in rats by
sodium selenite feed.ing, but the experiment was terminated be-
fore 18 months, the time that the Nelson experiments began pro-
d.ucing "cancer." Clayton and. Baumann 5 found, that 5 ppm of
sodium selenate appeared to d.ecrease the susceptibility to azo-
dye-induced cancer of the liver. Furthermore, although the
hepatotoxicity of excess selenium is well known, no report of
liver cancer resulting from chronic selenium poisoning in farm
animals has been found, in the literature.
-------
20
cited the work of Tsuzuki .et. aj._. ,-^23 W]1O studied
rabbits and mice under conditions simulating industrial exposure
to selenium vapor and exposure to selenium metal dust. The au-
thors reported, that tumors formed in the subcutaneous tissue of
the d.orsal neck in some of the mice after unusual exposures to
selenium. The tumors were considered, to be ad.enomas, similar
histologically to cylindromas. The tumors apparently did not
metastasize.
191 199 1 9 A
Tscherkes and co-workers ^'-L^^'±^H: studied rats fed
mixtures of sod.ium selenate (430 and. 860 jag Se/100,000 u.g of
diet) and casein (12 to 30 percent). To some mixtures other
ingredients were ad.d.ed, including riboflavin, cystine, chlorine,
and. nicotinic acid. The overall tumor incid.ence was 8.5 per-
cent of the 200 rats. Four rats developed, hepatoma neoplasms,
two of which had. pulmonary metastasis. Sarcomas were found, in
seven rats, one sarcoma in the liver and the others in the me-
senteric lymph nod.es. There were four rats with adenomas and.
the same number with precancerous tumor forms.
Harr .et. ai_. -*7 also stud.ied. rats fed. selenites and sele-
nates (from 0.5 to 16.0 ppm Se) with 12 or 22 percent casein
added. No neoplasms were found, that could be attributed to the
selenium in the diet. However, three types of lesions were
found.: (1) acute toxic hepatitis associated, with osteodystrophy,
-------
21
icterus, and fluid imbalance; (2) chronic toxic hepatitis as-
sociated with chronic passive congestion, reticulosis, myocar-
ditis, productive pancreatic duct hyperplasia, hepatocyte
hyperplasia, and. hepatic necrosis; and (3) hepatic hyperplasia
associated with abnormal hepatic foci.
2.3 Effects on Plants
No studies were found concerning the effects of atmo-
spheric selenium on plants. However, it has been well established
that certain types of plants require selenium to grow, that they
can accumulate high concentrations of selenium from seleniferous
soils, and that some will even emit volatile selenium compounds
into the air. Furthermore, while some plants can store up very
high concentrations of selenium (up to 10,000 ppm), others (e.g.,
corn and wheat) can be damaged by the accumulation of small a-
mounts (300 ppm). Kubota _et_ _al_. summarized their work and
others on the selenium content of plants in the United. States.
Figure 1 shows the average selenium content of plants for 480
counties in 46 of the States.
2.3.1 Selenium Ind.icator Plants
Plants that can grow only in soil containing selenium and
can accumulate large amounts of selenium are referred, to as
"Death's selenium indicators."^'97 A number of these plants'
blossoms emit an offensive, garlic-like odor caused by the
-------
+ Counties in which greater than one-half of the plants contained less than 0.1 p.p.m.
e Counties in which greater than one-half of the plants contained more than 0.1 p.p.m.
• Counties were more than 50 p.p.m. of selenium was found in selenium-accumulator
plants but no data available in selenium content of forages or grains.
FIGURE 1
Selenium Content of Plants in Certain
Counties in the United States6^
to
-------
23
production of volatile selenium compounds. To an experienced
person the intensity of the odor provides an indication as to
the amount of selenium in the plant, which is related to the
amount in the soil.
These "primary" indicators normally grow in the soil of
arid and semiarid regions and are generally found in the Mid-
western and Western parts of the United. States. Includ.ed. in
the list of indicator plants are 24 species and varieties of
Astragalus (milk vetch, with pea-like flowers), section Xylo-
rhiza (woody aster) of Machaeranthera, section Oonopsis (gol-
denweed) of Haplopappus, and Stanleya (princes plume). The
geographical distribution of these plants is shown in Figure 2.
These plants contain large amounts of selenium, generally
1,000 to 10,000 ppm. The consumption of these plants by live-
stock prod.uces the disease synd.rome of blind staggers or acute
selenium poisoning discussed in Section 2.2.1.
2.3.2 Secondary Selenium Absorbers
Other types of plants also accumulate substantial amounts
of selenium (generally 50 to 500 ppm), but less than the "indi-
cator plants." However, they do not require selenium in the
soil for growth. These secondary selenium absorbers includ.e
species of Aster.- Atriplex, Castilleja, Camand.ra, Grayia, Gren-
d.elia, Gutierrezia, Machaeranthera, and. Mentzella. They can be
-------
FIGURE 2
Distribution of Seleniferous Vegetation
-------
25
used to indicate seleniferous soils through analysis of their
selenium content.
These secondary absorbers can accumulate only water-
soluble selenium from the soil. This is in contrast to the in-
dicator plants which can accumulate selenium from the soil
regardless of the form of selenium present. The second.ary se-
lenium absorbers may produce acute or chronic selenium poisoning
when consumed by livestock.
2.3.3 Grains, Vegetables, Grasses, and. Other Vegetation
Most grains, vegetables, and grasses could also be clas-
sified as secondary selenium absorbers in that they may simi-
larly absorb and accumulate water-soluble selenium compounds
from the soil. However, the maximum amount of selenium that is
accumulated by these plants is generally less than 30 ppm.
Wheat, barley, corn, oats, and rye that have been grown in a
seleniferous soil contain 0.1 to 30 ppm selenium. ^ vege-
tables normally accumulate less than 1 ppm in selenium-
containing soils, but values as high as 18 ppm have been noted.
The content of selenium in native grasses is quite variable.
They sometimes contain as much as 84 ppm selenium. ' Consump-
tion of plants that contain high amounts of selenium usually
prod.uces alkali disease in livestock.
-------
26
Crop plants are damaged by accumulation of large amounts
of selenium (30 to 300 ppm). The most common symptom of sele-
nium poisoning in plants is inhibition of growth. Some crops,
particularly wheat, barley, and. rye, will exhibit chlorosis.
Younger plants are more susceptible, and their growth inhibition
is greater than that of mature plants.
Hamilton and Beath-^' 55,56 have recently studied a large
number of plants for their uptake and. distribution of various
forms of selenium. These plants, includ.ing 20 range plants, 17
crop plants, and 18 vegetables, were stud.ied. while growing in
an artificially selenized. soil und.er greenhouse cond.itions. It
was found that the distribution of selenium within a plant var-
ied, widely and. that all the plants could, accumulate toxic a-
mounts of selenium.
Other vegetation, including tobacco, also can accumulate
selenium. However, because these types of vegetation accumulate
only small amounts of selenium and have not poisoned animals,
they have not been as well studied.. Dye _et_ aj^. 0 determined
the selenium content of some plants as follows :
-------
27
Se Content
Plant ppm (aver. )
Pear leaves 0.45
Apple leaves 0.53
Radish leaves 0.28
Lettuce leaves 0.60
Corn 0.32
Wheat 0.29
2.4 Effects on Materials
There is no information at present indicating that at-
mospheric selenium would have any detrimental effect on materi-
als .
2 . 5 Environmental Air 5tand.ard.s
The American Conference of Governmental Ind.ustrial Hy-
gienists (ACGIH) has set the threshold limit values for occu-
pational exposure during 40-hour weeks with 8-hour days at 200
f-ig/m3 for selenium compounds, except in 1967 when the limit for
selenium hexafluorid.e was set at 400 |jg/m3 . In 1962, the
value was lower, 100 |ag/m3 for selenium compounds.^4
No country has yet established, a 24-hour threshold, limit
value.
-------
28
3. SOURCES
3.1 Natural Occurrence
Selenium is widely distributed in the earth's crust at a
concentration of about 0.09 pptn.45 However, it is mainly con-
centrated in sulfide minerals and in the soil of the dry plains
of the Midwestern United States. Furthermore, some plants can
absorb and accumulate selenium in large amounts from the soil.
(See Section 2.3 for a discussion of these plants.)
Despite its wide distribution in nature, selenium is not
an essential constituent of any common rock-forming mineral.
However, it is recognized as a major constituent in at least 22
selenides, 6 sulfosalts, 1 oxid.e, 4 selenites, and. 1 selenate,
and as a minor constituent of 24 sulfides and. tellurid,es, 5
sulfosalts, and 1 tellurite. The important selenium minerals
are berzelionite (Cu2Se), tiemannite (HgSe), and. naumannite
(AgsSe). Selenium is associated, mainly with copper, iron,
lead, silver, gold, and uranium, and. is often found with pyrite,
chalcopyrite, bornite, and, other sulfide minerals. y Weathering
releases much of the selenium from these minerals; it may remain
as native selenium or, more often, be redeposited. as ferric se-
lenite in secondary iron minerals such as limonite. Luttrell ^
has prepared a partial list of selenium-bearing minerals.
-------
29
Selenium can be found in coal (see Section 3.4), igneous
rocks, hydrothermal deposits, and sedimentary rocks.67 In ig-
neous rocks and in sulfide ores probably most of the selenium
is wid.ely distributed, as selenid.es. Volcanic rocks in various
parts of the Western United. States contain as much as 120 ppm
22 34
selenium, ' and still higher concentrations are present in
some volcanic sulfur d.eposits.10 Hyd.rothermal ore deposits
containing high concentrations of selenium are widespread.
Some of the more common are those associated, with epithermal
gold and. silver deposits, as well as with antimony and. mercury
epithermal d.eposits. Large amounts of selenium in small con-
centrations are found, in copper deposits of the porphyry type
and in massive sulfide deposits, such as those in the Southern
Appalachians.
Several studies have been made of sed.imentary rock for-
mations (particularly in the Western United. States67), many of
which support poisonous seleniferous vegetation. Beath et al.
found that sand.stone from the Poison Butte area of Wyoming con-
tains 112 ppm selenium, that carbonaceous siltstone in western
Wyoming contains 680 ppm, and. that phosphate rock contains as
much as 212 ppm selenium. The Pierre Shale of the Western
United States, a carbonate rock, contains as much as 26 ppm
selenium. Carbonate rock from the Phosphoria Formation in
-------
30
Idaho, Montana, Utah, and. Wyoming contains selenium ranging
from 1 to 100 ppm, with an average of 19 ppm.67
Highly concentrated deposits of selenium have also been
found in the volcanic tuff of the Wind River formation of Wyo-
ming,34'120 and in sandstone-type uranium deposits, particularly
in the Gas Hills area of Wyoming and the Ambrosia Lake district
of New Mexico.
Selenium cannot be mined, profitably, with the present
method.s of technology, because of the low concentration of se-
lenium in mineral d.eposits. Therefore, selenium must be d.e-
rived as a by-product in the refining of other ores.
3.2 Production Sources
Quantities of selenium in mineral deposits are not suf-
ficient to make its extraction alone profitable. It therefore
is obtained, as a by-prod.uct from other processes.
The principal source of selenium is as a by-product from
the copper refineries; smaller amounts are obtained from lead
smelters and from the selenium-containing sulfur residues from
the chemical ind.ustry-67 Other sources are the refining of
various sulfid.e ores (gold, silver, nickel) and. uranium ores,
as well as the making of paper (when pyrites are used, as the
source of sulfur in the manufacturing process).
-------
31
In the smelting of copper ores, part of the selenium
remains with the crude or blister copper (about 0.05 percent
selenium), and part is carried through the flues as fumes and
dust which are collected and. returned to the reverberatory
2 0
furnaces. Dust from the lead, smelters is also add.ed to this
circulating stream of flue gases. In the electropurification
of the copper, the selenium precipitates with other metallic
products in the mud or slime that collects beneath the anode.
This anode mud., ranging from about 0.05 to 10 percent selenium,
is usually refined, by one of the following fundamental processes:
smelting with soda ash, roasting with soda ash, and roasting with
sulfuric acid to yield, about 98 to 99 percent pure selenium met-
al, with arsenic as the major impurity. ^
High-purity selenium, used in electronics, is made by
several method.s such as fractional d.istillation, zone refining,
and. catalytic oxid.ation to selenium dioxide followed by either
gaseous or wet red.uction.
The United. States is the major producer and consumer of
selenium. In 1967, six companies in the United States produced
selenium.9 They are listed, in Table 7 in the Appendix. Of
these, the Kawecki Chemical Company is a metal and alloy manu-
facturing company. The remaining companies prod.uce selenium
as a by-prod.uct in the copper refining process. Table 8 in
-------
32
the Appendix summarizes the production, apparent consumption,
and price of selenium for 1956 through 1967 in the United States,
3 . 3 Prod.uct Sources
Selenium has a variety of applications, but most require
only small quantities of the metal. The major users are the
electronic and electrical industries, in which 90 percent of
the selenium is used, in the manufacture of d.ry plate rectifiers,
while the rest is used mostly in photoelectric cells.20 The
chemical industry is the next largest user, accounting for over
one-third, of the total consumption. The glass ind.ustry and
xerography manufacturing also use significant amounts.
The major uses of selenium and its compound.s are as fol-
lows :
Rectifiers: These are used, extensively in electroplating,
welding, d.irect-current motor operation, and. ind.uction braking,
and in battery chargers, magnetic coils, arc lamps, and voltage
regulators. About 0.5 to 25 g of selenium are used, per recti-
fier, depending on cell size.
Photoelectric cells; These cells, which require about the same
amount of selenium as rectifiers, are used in photographic ex-
posure meters, d.etectors, electric eyes, colorimeters, and. py-
rometers .
Pigments: The largest use of selenium by chemical industries
-------
33
is for pigments. Selenium is compounded with cad.mium sulfide
to prepare the orange, red, and maroon cadmium sulfoselenide
pigments used to color plastics, paints, enamels, inks, and
rubber.
Glass : Selenium, sod.ium selenate, barium selenite, and sodium
selenite are ad.ded (0.02 to 0.3 Ib/ton of glass) to neutralize
green tint from iron impurities in glass. A slightly larger
amount is add.ed to prod.uce a pink tinge for such prod.ucts as
milk bottles and other food containers. Ruby-red glass (used
in tableware, vehicular taillights, traffic and. signal lights,
light filters, and. infrared, equipment) requires about 1 to 50
pounds of selenium per ton of glass. Selenides of the arsenic
groups are used, to make low-melting-temperature glasses, pri-
marily for research purposes.
Lubricants ; Tungsten diselenid.e (WSe2 ) and. columbium diselenid.e
(CbSes) powders are used as solid, lubricants directly applied to
rubbing surfaces or mixed, with other greases and with various
metals, ceramics, and. plastics to form self-lubricating parts.
Applications include the vacuum, rad.iation, aerospace, electro-
mechanical, and instrumentation fields.
Blasting caps; Selenium, with barium peroxide and tellurium,
is used, for variable, delayed.-action, gasless fuse powder in
blasting caps. Almost 10,000 pounds of selenium and tellurium
mixture are used, annually in this capacity.
-------
34
Chromium plating; Selenate solutions, ranging from 0.012 to
0.020 g/liter, are used in chromium-plating solutions which im-
part a superior corrosion-resistant property and a dull luster
(for prevention of glare) to the plated, material.
Stainless steel: Selenium improves the casting, forging, and
machinability of stainless steel without reducing its corrosion
resistance or hot-forging and cold-working properties. Selenium
content varies from 0.01 to 0.35 percent.
Medicines: In the form of sod.ium selenate solution, selenium is
used to control certain animal diseases49 such as congenital
white muscle disease in sheep, selenium-responsive unthriftiness
in cattle, exudative diathesis in poultry, and. hepatosis diaete-
tica in pigs. This solution is also used to overcome sterility
in ewes.
Photocopiers: Amorphorus selenium is used in the xerography
process.
There are many minor uses of selenium and. its compounds,
such as: in preparation of Pharmaceuticals (e.g., niacin and
cortisone); in deodorants; as accelerating and vulcanizing
agent in rubber products; as catalysts for oxidizing, dehydro-
genating, and. hardening of fats used in soaps, waxes, edible
fats, and plastics; in printing inks, transformer oils, mineral
oils, and. vegetable oils as an antioxid.ant; in linseed., oiticica,
-------
35
and tung oils for nondrying properties; in insecticides, para-
siticid.es, bactericid.es, and herbicid.es; in photographic photo-
sensitizers and toners; in mercury vapor detectors; as fire-
proofing agents for textiles and wire cable coverings; as insect
repellants; as phosphorescents and. luminescents. Selenium oxy-
chlorid.e is a powerful solvent used, as a paint and. varnish re-
mover and. for rubber resins, glue, and. other organic substances.
Applications which appear to be increasing are xerography
copying; steel prod.uction; preparation of red color television
phosphor (ZnSe), electrolytic manganese, and colored anodized.
aluminum; and. use in solid lubricants. There are new applica-
tions of selenium in animal health and nutrition.
No recent figures could, be found, provid.ing a breakdown
by uses of the consumption of selenium and. its compounds; how-
Q Q
ever, Minerals Yearbook includes a breakdown of the consump-
tion for 1955. A list of merchandisers and consumers of
selenium and its compounds is given in Table 9 in the Appendix,
while Table 10 in the Appendix lists some selenium compound.s
and their uses, and. Append.ix Table 8 includ.es consumption and
price statistics.
3.4 Other Sources
Selenium air pollution may occur from the heating or
burning of materials that contain selenium. Thus incineration
-------
36
of manufactured selenium products (see Section 3.3) may be a
pollution source if not properly controlled.. In addition, the
burning of coal and other natural materials that contain sulfur
can also be a source of selenium pollution. Normally where sul-
fur is found., selenium can also be found. Materials from ter-
restial sources such as fuels and. ores generally have a selenium-
to-sulfur ratio of approximately 1 x 10~4. "
Little information is available on the selenium content
of the various materials and products that are incinerated
every d.ay. Some possible sources of selenium include natural
fuels/ leather good.s, cloth materials, wood, prod.ucts, etc.
West-^O has found, selenium in paper products including ciga-
rette paper, newspaper, etc. (see Section 3.5). Lakin and
Davidson*^ summarized, the data on the selenium content of dif-
ferent coals. As can be seen from Table 3, the selenium con-
tent has been found as high as 7.38 ppm selenium in lignite
coal.
-------
37
TABLE 3
SELENIUM CONTENT OF COALS
66
Type of
Sample Location Coal
Western Wyoming Lignite
Montezuma County,
Colo.
Sand oval County,
N. Mex.
Morley, Alberta,
Canada
No. of Selenium Content (ppm)
Samples Ranqe
3 1.96-7.38
2 2.0-2.4
1
1
Average
3.88
2.2
0.1
2.0
3.5 Environmental Air Concentrations
Only one published report was found, relating to the at-
mospheric concentration of selenium in the United. States.
Hashimoto and Winchester-^ in 1964-1965 measured the selenium
content in samples of rain, snow, and air collected, on the cam-
pus of the Massachusetts Institute of Technology (Cambridge,
Mass.), in the semirural areas of Topsfield and Boxford, Mass.,
and in the smaller city of New Haven, Conn. The d.ata are shown
in Table 4. In Cambridge, the average selenium concentration
was 0.21 \J.g per liter of precipitation, which on the basis of
air samples is approximately equivalent to 0.001 |-ig/m3 of air
or 1 nanogram per cubic meter. Air samples (100 m3 ) were
taken by passing air (1 m3/hr) either through an aqueous bub-
bler or through a 1-micron pore diameter Millipore filter.
-------
38
TABLE 4
ATMOSPHERIC SELENIUM (1964-65 J59
Location3
Date
1964-65
Se in
, ,~b
Remarks
1
2
1
2
1
2
1
2
1
2
3
2
3
2
3
1
2
Mean
4
5
5
6
6
1
5
1
1
1
1
1
1
1
Dec. 18
Dec. 18
Jan. 3
Jan. 3
Jan. 10
Jan. 10
Jan. 16
Jan. 16
Jan. 24
Jan. 24
Feb. 22
Feb. 25
Mar. 20
Mar. 20
Mar. 29
Mar. 29
Mar. 29
Jan. 31
Feb. 27
Mar. 20
Mar. 20
Mar. 20
Feb. 27
May 11
May 20
May 20
May 27
May 27
June 1
June 1
0.15
0.09
1.40C
0.70
0.13
0.16
0.53
0.52
0.14
0.16
0.25
0.10
0.08
0.06
0.10
0.09
0.10
0.21
0.08
0.03
0.12
0.04
0.10
0.11
0.09
0.03
0.03
0.11
0.13
0.16
0.06
0.10
Falling
Falling
Rain +
Rain +
Falling
Falling
Falling
Falling
Falling
Falling
Falling
Rain
Ground
Falling
Ground
Falling
Falling
snow
snow
ice
ice
snow
snow
snow
snow
snow
snow
snow
snow
snow
snow
snow
snow
Ground snow
Ground snow
Ground snow
Ground snow
Ground snow
Tap water
Well water
Air, bubbler
Air, bubbler
Air, filter
Air, bubbler
Air, filter
Air.- bubbler
Air, filter
aSampling locations: 1. MIT campus, roof of earth
science building. 2. Ground location near 1.
3. Cambridge, near Central Square. 4. Topsfield,
Mass. 5. Boxford, Mass. 6. New Haven, Conn., Yale
University campus.
Micrograms of selenium per liter of water or 100 m
of air. One liter of water is roughly equivalent to
200 m3 of air.
GExcluded from mean.
-------
39
The rain or snow melt water (1 liter) was collected on poly-
ethylene, filtered on filter paper to remove particulates,
acidified, evaporated to a final volume of 0.1 ml, and analyzed
by neutron activation. The bubbler solutions were processed
similarly, while the Millipore filters were irradiated directly.
Based, on the selenium-to-sulfur ratio (1 x 10~4 ) , which
is similar to that found for geochemical materials, these au-
thors conclud.ed that the source of the selenium was probably
from terrestrial sources, including fuels and ores used by in-
dustry. The authors also suggested that a study of the sele-
nium-to-sulf ur ratio in different locations may give some
information about the length of time the selenium has been in
the air and. the sources of pollution.
Some unpublished, results on the selenium content of
particulates for various cities in the United. States is given
in Table 5. The particulate matter was collected from am-
bient air. The analytic procedure involved, extraction of the
samples with hydrochloric acid and. analysis of the extract by
atomic absorption spectrophotometry.
A study is presently being conducted, by Dr. Philip W.
West-^O to determine the selenium content of air in Baton Rouge,
La., and possibly in other areas. The preliminary investigation
shows that there is a d.etectable amount of selenium in Baton
-------
40
TABLE 5
SELENIUM CONTENT OF PARTICULATES IN AMBIENT AIR, 1965
Location Selenium Content ( ug/m3 ) *
California (Los Angeles) <0.06
Colorado (Denver) <0.05
Arizona (Phoenix) <0.04
California (Long Beach and San Francisco) "
Connecticut (Norwich) "
Delaware (Newark and Wilmington) "
District of Columbia "
Hawaii (Honolulu) "
Illinois (Chicago and East St. Louis) "
Indiana (Dunes State Park, East Chicago, "
Indianapolis, Ogden Dunes)
Kentucky (Lexington) "
Louisiana (New Orleans) "
Maine (Portland) "
Massachusetts (Lawrence) "
Michigan (Grand Rapids) "
Minnesota (St. Paul) "
Missouri (St. Louis) "
Montana (Helena) "
Nevada (Las Vegas) "
New Jersey (Glassboro, Marlton, "
Pemberton, Trenton)
*Values given are averages of 1965 quarterly composite of
5 to 7 samples; an air volume of 2,000 m (25°C) is assumed.
-------
41
Rouge, and that the probable source is trash burning. It was
found that paper and other prod.ucts of vegetation had. a high
concentration of selenium; for example, newsprint was found, to
contain up to 6 ppm selenium. The selenium content was thought
to be a result of the accumulation of selenium in the initial
tree or plant. However, Cole thought that selenium could be
introduced into paper from the pulping chemicals (e.g., the
use of pyrites for the source of sulfur).
Lakin and Davidson reported the results of analysis
of particulate matter for selenium in 1941. The samples were
collected from air-cond.itioner filters in various locations,
as shown in Table 11 in the Appendix. The selenium content
ranged from 0.05 to 10 ppm.
-------
42
4 . AB AT EMENT
No study has been made of the methods for control of se-
lenium and its compounds. However, based on the properties and
on the methods of recovery and. purification of selenium, wet
scrubbers and high-voltage electrostatic precipitators should
be effective. The common selenium atmospheric pollutants are
probably selenium dioxide (or selenious acid, in moist environ-
ments) and., to a lesser extent, hyd.rogen selenid.e. These com-
pounds are all soluble in water, the former a solid and the
latter a gas at ambient temperatures. Selenium metal, except
for the red. allotrope form, is insoluble in water. However, it
is soluble in strong bases, forming selenium compound.s, and it
will burn in air, producing selenium dioxide.
In the recovery and. purification processes of selenium,^
wet scrubbers and. electrostatic precipitators are used to col-
lect selenium dioxide fumes given off d.uring the smelting or
roasting, as well as to collect red selenium. Furthermore,
selenium emissions from trash burning are controlled by the
i "3 o
use of wet scrubbers.
At the present time, the chief industrial control methods
are the use of a good, ventilation system and. personal pro-
tective equipment, includ.ing safety goggles and. a respirator
when working in a low airborne concentration, and a supplied-air
-------
43
\ .
respirator in heavily contaminated areas. ^ Selenium-containing
liquid wastes are disposed, of by washing them down the drain,
while solid wastes are buried.
-------
44
5. ECONOMICS
No information has been found on the economic costs of
selenium air pollution or on the costs of its abatement. Data
on the production and. consumption of selenium are presented in
Section 3.
-------
45
6. METHODS OF ANALYSIS
6.1 Sampling Methods
Air samples have been collected by means of electrostatic
precipitators,89 filters,59 and liquid impingers.59'63'89 All
of these methods can be used for selenium dusts and fumes, while
only the last can be used for collection of vapors or gaseous
compounds.
The use of filters and. liquid impingers are the most
commonly used sampling method.s tod.ay. Some air samples were
taken by passing 100 m3 of air at the rate of 1 m3/hr through
a 1-micron pore d.iameter Millipore filter. Because selenium
is found, in many filter papers, Millipore filters or other
selenium-free collection med.ia (e.g., glass fibers) should be
used. However, some filter papers can be washed, with sodium
sulfid.e and water to remove traces of selenium. The liquid
used in the impingers has been water59'63 an(3 a solution of 40
to 48 percent hydrobromic acid with 5 to 10 percent bromine.
The water can be used, with nonvolatile water-soluble compound.s
such as selenium d.ioxide. The ad.vantage of the hydrobromic
acid.-bromine solution is that it converts selenium and. most of
its compounds to the soluble selenium tetrabromid.e. This solu-
tion, after collection, can be analyzed directly after decolori-
zation and neutralization,63 or the selenium may be separated by
d.istillation.
-------
46
It has also been suggested, that soda lime or silica gel
could be used, to collect vapors of selenium compounds.89
6 .2 Qualitative Determination Method.s
A quick qualitative estimation of selenium can be made
by taking advantage of the reaction of aromatic 1,2-diamines
with selenious acid, (or Se(IV) cation) to form colored, piasele-
noles. Elemental selenium and selenides readily oxidize in ni-
tric acid or hydrogen peroxide to selenious acid. Selenate
salts—or Se(Vl) cations—give only weak colors. The most com-
mon diamine employed is 3, 3 '-d.iaminobenzidine, which forms a
yellow dipiaselenole in acid and is sensitive to 10 ppm. The
4-dimethylamino and 4-methylthio derivatives of 1,2-phenyl-
enediamine will also react with selenious acid, to give stable
bright red and. blue-purple colors, respectively- Reaction with
2,3-diaminonaphthalene has been used as a spot test.35 other
ions—particularly copper, iron, tellurium, chromium, nickel,
and cobalt—may cause interference in high concentration, but
some may be masked, by complexing agents such as EDTA. Other
methods of detection of selenious acid that have been reported
are reaction with (1) iodides,91 (2) thiourea,23 (3) diphenyl-
hyd.razine, 36 and. (4) pyrrole,114 as well as the catalytic ef-
fect on the reaction of methylene blue with alkali sulfide.
-------
47
6.3 Quantitative Determination Methods
Several quantitative methods of analyzing selenium are
based on the reaction of selenious ion with 3,3'-d.iaminobenzi-
dine. West and Cimerman used, this reagent in connection with
the ring-oven technique. This colorimetric method is basically
free from interferences when masking reagents are used; limit of
identification is 0.08 p.g, is applicable in the range of 0.1 to
0.5 lag.129'131 Kawamura and Matsumoto63 spectrophotometrically
determined the selenium in air samples collected in impingers
by measuring the absorbance of the solutions treated, with this
reagent. The benzid.ine reagent has also been used, in fluoro-
metric determination of selenium in biological materials. '
Detection in these method.s was in the ord.er of 10 to 50 ppb
selenium.
Walk ins on, •*- as well as Allaway and Gary,-*- found, that
the product from 2,3-diaminonaphthalene and selenium showed a
fluorescence sensitivity in the neighborhood of 0.5 to 5 ppb
selenium—a sensitivity greater than that with the benzid.ine
prod.uct.
Neutron activation methods have been used, to determine
selenium from air samples (via filters and. aqueous bubbler) and
from samples of snow and. rain.59 A sensitivity of 0.01 |j.g of
selenium was obtained, when gamma rad.iation was measured, with a
-------
48
scintillation spectrometer. This technique has also been used
to determine traces of selenium in biological materials and in
metals,18
Recently West and Ramakrishna-*-^ have developed a method
for determining trace amounts of selenium based, on its catalytic
effect in the red.uction of methylene blue by sodium sulfite.
Color comparisons are mad.e in the range of 0.1 to 1.0 |~ig of se-
lenium. There is serious interference from copper if present
in an excess of 10 [ig. Kawashima and Tanaka64 also developed
a catalytic method based, on the reduction of 1,4,6,11-tetraaza-
naphthacene; this method is subject to interference from several
ions.
Walkinson-^? has d.iscussed some of the newer methods that
are used, in the analysis of selenium in biological material, in-
cluding polarography, X-ray fluorescence, and. atomic absorption
spectrophotometry-
-------
49
7. SUMMARY AND CONCLUSIONS
Selenium compounds, particularly the water-soluble com-
pounds, are toxic to humans and animals. In humans, mild, in-
halation of selenium d,usts, fumes, or vapors irritate the
membranes of the eyes, nose, throat, and. respiratory tract,
causing lacrimation, sneezing, nasal congestion, coughing, etc.
Prolonged exposure through inhalation can cause marked pallor,
coated tongue, gastrointestinal disorders, nervousness, and a
garlicky odor of breath and. sweat. In animals, subacute sele-
nium poisoning prod.uces pneumonia and degeneration of the liver
and kidneys. Furthermore, experiments with rats ind.icate that
selenium may cause cancer of the liver.
The biochemical effects of elemental selenium and. its
compounds on humans is not as yet thoroughly understood. The
selenium deficiency diseases found in animal species, as well
as some of the frank selenium poisoning, have not been observed
in man. Similarly, the carcinogenic hazard of selenium and. the
antagonistic effect of arsenic for selenium seen in animals are
yet to be shown in humans. These are important factors that
need clarification to properly evaluate the role of selenium
and its compounds in air pollution.
There is no information ind.icating that atmospheric se-
lenium has any detrimental effect on plants or materials. Some
-------
50
plants contain large amounts of selenium that can be toxic to
the plants themselves, as well as to humans and animals who in-
gest the plants.
Samples of snow/ rain, and. air taken in Boston, Mass.,
(1964-1965) show that the selenium content of the air is aver-
aging 0.001 |ag/m3 . Based, on the selenium-to-sulfur ratio in
these samples, the atmospheric selenium was probably from ter-
restrial sources, including the fuels and. ores used by ind.ustry.
Another source may be the burning of trash containing paper
products. Some papers when analyzed contain as much as 6 ppm
selenium. Selenium in paper may come from accumulation by the
original tree or plant, or possibly from the manufacturing of
the paper (from the use of pyrites in the process). Any vege-
tation which is burned, may be a possible source of atmospheric
selenium. Another source could be the refining of sulfide ores,
particularly copper and. lead ores.
Emissions of selenium and its compounds can be effectively
controlled by use of electrostatic precipitators and. water scrub-
bers .
No information has been found, on the economic costs of
selenium air pollution or on the costs of its abatement. Method.s
of analysis are available that can measure quantitatively in
the parts per billion or submicrogram region. However none
-------
51
of the methods is simple, rapid, or applicable to continuous
monitoring, and many of the method.s are not specific for sele-
nium. A rough estimate as to the magnitude of selenium in the
atmosphere might be made from the concentration of sulfur in
the atmosphere. This method would, be valid, if the sources of
these two pollutants are sulfid.e ores, fossil fuels, or igneous
and. sed.imentary rocks, since in these materials the average
weight ratio of selenium to sulfur is 1 x 10~4.
Based on the material presented in this report, further
studies are suggested, in the following areas:
(1) Further determination of the atmospheric concentra-
tion of selenium compounds in the cities of the United States,
particularly near copper refiners and other sulfide ore re-
finers, and near trash-burning sites.
(2) Determination of the long-term exposure effects on
humans and animals, particularly in the concentration range
found in the atmosphere.
(3) Determination of the amount of selenium in particu-
lates.
(4) Investigation of the possibility of antagonistic,
synergistic, or catalytic effect of selenium or its compounds
with other substances in the environmental air.
-------
52
REFERENCES
1. Allaway, W.H., and E.E. Gary, Determination of Submicrogram
Amounts of Selenium in Biological Materials, Anal. Chem. 36:
1359 (1964).
2. Amor, A.J., and P. Pringle, A Review of Selenium as an Indus-
trial Hazard, Bull. Hvo. 20;239 (1945).
3. Anderson, H.D., and A.L. Moxon, The Excretion of Selenium by
Rats on a Seleniferous Wheat Ration, J. Nutr. 22:103 (1941).
4. Death, O.A., H.F. Eppson, and C.S. Gilbert, Selenium and
Other Toxic Minerals in Soils and Vegetation, Wyoming Agr.
Expt. Sta. Bull. 206:1 (1935).
5. Death, O.A., C.S. Gilbert, and H.F. Eppson, The Use of Indi-
cator Plants in Locating Seleniferous Areas in the Western
United States. IV. Progress Report, Am. J. Dotany 28 ;887
(1941).
6. Death, O.A. , A.L. Hagner, and C.S. Gilbert, Some Rocks and
Soils of High Selenium Content, Geol. Surv. Wyoming Dull. 36;
23 (1946).
7. Dowen, H.J.M., and P.A. Cawse, The Determination of Selenium
in Diological Material by Radioactivation, Analyst 88:721
(1963).
8. Duchan, R.F., Industrial Selenosis, Occupational Med. 3:439
(1947).
9. Dutterfield, J.A. Selenium - 1967, Eng. & Mining J. 169:131
(1968).
10. Dyers, H.G., Selenium Occurence in Certain Soils in the
United States, with a Discussion of Related Topics, U.S.
Dept. Agr. Tech. Dull. 482:48 (1935).
11. Cadell, P.D., and F.C. Cousins, Urinary Selenium and Dental
Caries, Nature 185:846 (1960).
12. Cerwenka, E.A., Jr., and W.C. Cooper, Toxicology of Selenium
and Tellurium and Their Compounds, Arch. Environ. Health 3_:
189 (1961).
13. Challenger, F., Diological Methylation, Chem. Rev. 36:316
(1945).
-------
53
14. Cheng, K.L., Determination of Traces of Selenium, 3,3'-Di~
aminobenzidine as Selenium(IV) Organic Reagent, Anal. Chem.
18:1738 (1956). '
15. Clayton, C.C., and C.A. Baumann, Diet and Azo Dye Tumors:
Effect of Diet During a Period When the Dye is Not Fed,
Cancer Res. 9 ;575 (1949).
16. Clinton, M. , Jr., Selenium Fume Exposure, J. Ind. Hyg. Tox-
icol. 29:225 (1947).
17. Cole, J.W., Bureau of Mines, personal communication (Dec.
1968).
18. Conrad, F.J., and B.T. Kenna, Determination of Selenium by
Activation Analysis and Dry Volatilization, Anal. Chem. 39:
1001 (1967).
19. Cooper, W.C., "Selenium Toxicity in Man," in Symposium:
Selenium in Biomedicine, O.K. Muth Ed. (Westport, Conn.:
AVI Pub. Co., 1967) .
20. Grouse, W.H., "Selenium," in McGraw-Hill Encyclopedia of
Science and Technology, vol. 12 (New York: McGraw-Hill, p.
163, 1966).
21. Cummins, L.M., ^t a_l. , A Rapid Method for Determination of
Selenium in Biological Material, Anal. Chem. 36:382 (1964).
22. Davidson, D.F. , and H.A. Powers, Sel.enium Content of Some
Volcanic Rocks From Western United States and Hawaiian Is-
lands, U.S. Geol. Surv. Bull. 1084-C;69 (1959).
23. Deniges, G. , Detection of Selenium, Application to Natural
Waters," Bull. Soc. Pharm. Bordeaux 75:197 (1937).
24. Documentation of Threshold Limit Values, American Conference
of Governmental Industrial Hygienists, Committee on Threshold
Limit Values, Cincinnati, Ohio (1962).
25. Dubois, K.P-, A.L. Moxon, and O.E. Olson, Further Studies on
the Effectiveness of Arsenic in Preventing Selenium Poison-
ing, J. Nutr. 19:477 (1940).
26. Dudley, H.C., Toxicology of Selenium. II. The Urinary Excre-
tion of Selenium, Am. J. Hyg. 23:181 (1936).
27. Dudley, H.C., Selenium as a Potential Industrial Hazard,
Public Health Kept. (U.S.) 53:94 (1938).
-------
54
28. Dudley, H.C., and J.W. Miller, Toxicology of Selenium. IV.
Effects of Exposure to Hydrogen Selenide, Public Health
Rept. (U.S.) 52:1217 (1937).
29. Dudley, H.C., and J.W. Miller, Toxicology of Selenium. VI.
Effect of Subacute Exposure to Hydrogen Selenide, _J. Ind.
Hyg. Toxicol. 23:470 (1941).
30. Dye, W.B., _et al_. , Fluorometric Determination of Selenium in
Plants and Animals with 3,3"-Diaminobenzidine, Anal. Chem.
35_:1687 (1963).
31. Ermakov, V.V., Materials on the Distribution of Selenium in
Human Organs and Tissues, Byul. Eksperim. Biol. i Med. 59
(3):61 (1965).
32. Evaluation of the Carcinogenic Hazards of Food Additives,
World Health Organ., Tech. Rept. Ser. 220, Geneva (1961).
33. Evans, C.S., and C.M. Johnson, The Separation of Some Alkyl
Selenium Compounds, J. Chromatog. 21:202 (1966).
34. Everett, F.D., and L.C. Bauerle, Investigation of Tuffs Near
Lysite, Wyoming for Selenium, Bur. Mines Rept. of Inv. 5296:
30 (1957).
35. Feigl, F., Qualitative Analysis by Spot Tests, 3rd ed.
(New York: Elsevier, p. 266, 1946).
36. Feigl, F., and V- Demant, Microchemical Detection of Selenium,
Mikrochim. Acta, 1:322 (1937).
37. Feigl, F., and P.W. West, Test for Selenium, Based on a
Catalytic Effect, Anal. Chem. 19,:351 (1947).
38. Fitzhugh, O.G., A.A. Nelson, and C.I. Bliss, The Chronic
Oral Toxicity of Selenium, J. Pharmacol. 80:289 (1944).
39. Franke, R.W., and A.L. Moxon, The Minimum Fatal Dose of Sel-
enium, Tellurium, Arsenic, and Vanadium, J. Pharmacol. Exp.
Therap. 58 :454 (1936).
40. Franke, R.W., and A.L. Moxon, The Toxicity of Orally Ingested
Arsenic, Selenium, Tellurium, Vanadium and Molybdenum, J.
Pharmacol. EXP. Therap. 61:89 (1937).
-------
55
41. Frost, D.V., Arsenic and Selenium in Relation to the Food
Additive Law of 1958, Nutr. Rev. 18:129 (1960).
42. Frost, D.V., "Significance of the Symposium," in Symposium;
Selenium in Biomedicine, O.H. Muth, Ed. (Westport, Conn.:
AVI Pub. Co., 1967).
43. Glover, J.R., Some Medical Problems Concerning Selenium in
Industry, Trans. Assoc. Ind. Med. Officers 4:94 (1954).
44. Glover, J.R., Selenium in Human Urine: A Tentative Maximum
Allowable Concentration for Industrial Populations, Ann.
Occupational Hyq. (London), 10:1 (1967).
45. Goldschmidt, V.M., Geochemistry, Oxford, England: Clarendon
Press, p. 730, 1954.
46. Gortner, R.A., Chronic Selenium Poisoning of Rats as Influ-
enced by Dietary Protein, J. Nutr. 1J3:105 (1940).
47. Hadjimarkos, D.M., Effect of Selenium on Dental Caries, Arch.
Environ. Health 10:893 (1965).
48. Hadjimarkos, D.M., and C.W. Bonhurst, Selenium Content of
Eggs, Milk and Water in Relation to Dental Caries in Children,
J. Pediat. _59_:256 (1961).
49. Hadjimarkos, D.M., C.W. Bonhurst, and J.J. Mattice, Selenium
Concentration in Placental Tissue and Fetal Cord Blood, _J.
Pediat. 54:296 (1959).
50. Hall, R.H., _ejt al._. , Preliminary Observations on the Toxicity
of Elemental Selenium, Arch. Ind. Hyg. Occupational Med. _4:
458 (1951).
51. Hamilton, A., Industrial Poisons in the United States. (New
York: MacMillan, 1925).
52. Hamilton, A., Industrial Toxicology, (New York: Harper, 1934).
53. Hamilton, A., and H.L. Hardy, Industrial Toxicology, (New
York: Hoeber-Harper, 1949).
54. Hamilton, J.W., and O.A. Beath, Selenium Uptake and Conver-
sion by Certain Crop Plants, Agr. J. J55_:528 (1963).
55. Hamilton, J.W., and O.A. Beath, Uptake of Available Selenium
by Certain Range Plants, J. Range Management 6:261 (1963).
-------
56
56. Hamilton, J.W., and O.A. Beath, Amount and Chemical Form of
Selenium in Vegetable Plants, J. Aqr. Food C'hem. J2:37l (1964)-
57. Harr, J.R., "Selenium Toxicity in Rats. II. Histopathology,"
in Symposium: Selenium in Biomedicine, O.K. Muth, Ed. (West-
port, Conn.: AVI Pub. Co., 1967).
58. Hartley, W.J., Selenium Treatment of Animal Diseases and
Unthriftiness, New Zealand J. Aqr. 103;475 (1961).
59. Hashimoto, Y., and J.W. Winchester, Selenium in the Atmos-
phere, Environ, Sci. Technol. ^:338 (1967).
60. Heinrich, M., and D.M. MacCanon, Toxicity of Intravenous
Sodium Selenite in Dogs, Proc. S. Dakota Acad. Sci. 36:173
(1957).
61. Hoste, J., Diaminobenzidene as a Reagent for Vanadium and
Selenium, Anal. Chim. Acta. _30_:1504 (1952).
62. Jones, G.B., and K.O. Godwin, Studies on the Nutritional
Role of Selenium. I. Distribution of Radioactive Selenium in
Mice, Aust. J. Aqr. Res. .14:716 (1963).
63. Kawamura, M., and K. Matsumoto, Determination of Small
Amounts of Hydrogen Selenide in Air, Japan Analyst (Tokyo)
14(9):789 (1965).
64. Kawashima, T., and M. Tanaka, Determination of Submicrogram
Amounts of Selenium(IV) by Means of Catalytic Reduction of
1,4,6,11-Tetraazanaphthalene, Anal, Chim, Acta. 40:137 (1968).
65. Kubota, J. , _e_t al_. , Selenium in Crops in the United States
in Relation to Selenium—Responsive Diseases of Chemicals
J. Aqr. Food Chem. ,15.:448 (1967).
66. Lakin, H.W., and D.F. Davidson, "The Relation of Geochemistry
of Selenium to its Occurrence in Soils," in Symposium:
Selenium in Biomedicine, O.K. Muth, Ed. (Westport, Conn.:
AVI Pub. Co., 1967) .
67. Lansche, A.M., Selenium and Tellurium—A Materials Survey,
U.S. Bur. Mines Inform. Cir. 8340 (1967).
68. Lemley, R.E., Selenium Poisoning in the Human, J. Lancet
.60:528 (1940).
69. Lemley, R.E., and M.M. Merryman, Selenium Poisoning in the
Human, J. Lancet 61:435 (1941).
-------
57
70. Lewis, H.B., J. Schultz, and R.A. Gortner, Dietary Protein
and the Toxicity of Sodium Selenite in the White Rat, J.
Pharmacol. _68:292 (1940).
71. Luttrell, G.W., Annotated Bibliography on the Geology of
Selenium, U.S. Geol. Surv. Bull. 1019-M;867 (1959).
72. McConnell, K.P., Respiratory Excretion of Selenium Studied
with the Radioactive Isotope, J. Biol. Chem. 145:55 (1942).
73. McConnell, K.P., Passage of Selenium Through Mammary Glands
of White Rat and Distribution of Selenium in Milk Proteins
After Subcutaneous Injection of Sodium Selenate, J. Biol.
Chem. 173:653 (1948).
74. McConnell, K.P-, and O.W. Portman, "Toxicity of Dimethyl
Selenide in Rat and Mouse," Proc. Soc. Exptl. Biol. Med.
79_:230 (1952).
75. The Merck Index, 8th ed. (Rahway, N.J.: Merck, 1968).
76. Middleton, J.M., Selenium Burn of the Eye, A.M.A. Arch.
Ophthalmol. 38;806 (1947).
77. Mineral Facts and Problems, Staff, Bureau of Mines, Bur.
Mines Bull. 630:1118 U.S. Govt. Printing Office, Washington,
D.C. (1965).
78. Minerals Yearbook, Bureau of Mines, U.S. Govt. Printing
Office, Washington, D.C. (1960,1965).
79. Minerals Yearbook, Bureau of Mines, U.S. Govt,, Printing Off-
ice, Washington, D.C. (1966).
80. Minerals Yearbook, Bureau of Mines, U.S. Govt. Printing Off-
ice, Washington, D.C. (1967).
81. Motley, H.L., M.M. Ellis, and M.D. Ellis, Acute Sore Throats
Following Exposure to Selenium, J. Amer. Med. Assoc. 109
(1937).
82. Moxon, A.L., H.D. Anderson, and E.P. Painter, Toxicity of
Some Organic Selenium Compounds, J. Am. Pharm. Assoc. 29:
249 (1940). ~
83. Moxon, A.L., Toxicity of Selenium-Cystine and Some Other
Organic Compounds, J. Am. Pharm. Assoc. 63:357 (1935).
84. Moxon, A.L., and M. Rhian, Selenium Poisoning, Physiol.
Rev. 23:305 (1943).
-------
58
85. Nelson, A.A., O.G. Fitzhugh, and H.O. Calvery, Liver Tumours
Following Cirrhosis Caused by Selenium in Rats, Cancer
Res. 1:220 (1943).
86. Orstadius, K., Toxicity of a Single Subcutaneous Dose of
Sodium Selenite in Pigs, Nature 188 :1117 (1960).
87. Painter, E.P., The Chemistry and Toxicity of Selenium Com-
pounds, with Special Reference to the Selenium Problem,
Chem. Rev. 28:179 (1941).
88. Palmer, I.S., and C.W. Bonhurst, Modification of Selenite
Metabolism by Arsenite, J. Agr. Food Chem. 5:928 (1957).
89. Patty, F.A., (Ed.), Industrial Hygiene and Toxicology, vol.
II, 2nd ed. (New York: Interscience, p. 887, 1963).
90. Pearce, E.L., Dietary Factors Affecting the Resistance of
Rats to Selenium, M.S. Thesis, University of Wisconsin (1947)
91. Poluektov, N.S., Detection of Selenium and Tellurium in the
Presence of One Another,- Mikrochemie 15:32 (1934).
92. Pringle, P., Occupational Dermatitis Following Exposure to
Inorganic Selenium Compounds, Brit. J. Dermatol. Syphilis
.54:54 (1942).
93. Problems in the Evaluation of Carcinogenic Hazard from Use
of Food Additives, National Academy of Sciences-National
Research Council, Publ. 749, Washington, D.C. (1960), Cancer
Res., 21:429 (1961).
94. Rhian, M., and A.L. Moxon, Chronic Selenium Poisoning in
Dogs and Its Prevention by Arsenic. J. Pharmacol. 78:249
(1943).
95. Robinson, W.O., ^t _al_. , Determination of Selenium and Arsen-
ic by Distillation, Ind. Eng. Chem. Anal. Ed. 6 (1934).
96. Rosenfeld, I., Metabolic Effects and Metabolism of Se in
Animals, Agr. Exp. Sta. Univ. Wyoming Bull. 414 (1964).
97. Rosenfeld, I., and O.A. Death, Selenium, (New York: Academic
Press, 1964).
98. Sawicki, E. , New Color Test for Selenium, Anal. Chem. 29;
1376 (1957).
-------
59
99. Schultz, J., and H.B. Lewis, The Excretion of Volatile Sel-
enium Compounds After the Administration of Sodium Selenite
to White Rats, J. Biol. Chem. 133:199 (1940).
100. Schwarz, K. , Factor 3, Selenium and Vitamin E, Nutr. Rev.
_18:19-3 (1960). ~~ ~~
101. Schwatz, K., Development and Status of Experimental Work
on Factor-3-Selenium, Federation Proc. (Pt. I) 20:666
(1961). ~~
102. Selenium and Its Compounds, Nat. Safety News, 93:5 (1966).
103. Selenium and Sheep Losses Reduced in New Zealand, Fertiliser
Feeding Stuffs (London), 52(5):216 (i960).
104. Selenium in Animal Nutrition, Chem. Ind. (London) 33 :1042
(1959).
105. Selenium in Animal Nutrition, Chem. Ind. (London) ^1:170
(1962).
106. Sessa, T., Enzymes and Industrial Pathology II. Clinical
and Therapeutic Application, Folia Med. (Naples) 35:572
(1953). ~ ~
107. Smith, M.I., The Influence of Diet on the Chronic Toxicity
of Selenium, Public Health Rept. (U.S. ) .54:1441 (1939).
108. Smith, M.I., Chronic Endemic Selenium Poisoning, J. Am. Med.
Assoc. 116:562 (1941).
109. Smith, M.I., K.W. Franke, and B.B. Westfall, Selenium Prob-
lem in Relation to Public Health, Public Health Rept. (U.S. )
(1936).
110. Smith, M.I., E.F. Stohlman, and R.P- Lillie, The Toxicity
and Pathology of Selenium, J. Pharmacol . Exptl . Therap. 60 :
449 (1937).
111. Smith, M.I., and B.B. Westfall, Further Field Studies on
Selenium Problems in Relation to Public Health, Public Health
Rept. (U.S. ) _52.:1375 (1937).
112. Smith, M.I., B.B. Westfall, and E.F. Stohlman, The Elimina-
tion of Selenium and its Distribution in the Tissues, Public
Health Rept. (U.S.) J52_:1171 (1937).
-------
60
113. Smith, M.I., B.B. Westfall, and E.P. Stohlman, Studies of
the Fate of Selenium in the Organism, Public Health Rept.
(U.S.) 53:1199 (1938).
114. Suzuki, M. , Colorimetric Method for Determining Selenium
in Crude Copper, J. Chem. Soc. Japan 56:323 (1953).
115. Symanski, H., A Case of Hydrogen Selenide Poisoning, Peut.
Med. Wochschr. 75:1730 (1950).
116. Thomas Register of American Manufacturers, (New York: Thomas
Pub. Co., 1968).
117. Thompson, R.J., Acting Chief, Laboratory Services Section,
Division of Air Quality and Emission Data, National Air
Pollution Control Administration, Cincinnati, Ohio, personal
communication, (June 1969).
118. Threshold Limit Values for 1967, Adopted at the 29th Annual
Meeting of the American Conference of Governmental Industrial
Hygienists, Chicago, 111., (May 1-2, 1967)
119. Trelease, S.F., and O.A. Beath, Selenium, (New York: Colum-
bia University Press, 1949).
120. Trelease, S.F., and O.A. Beath, Selenium; Its Geological Oc-
currence and Its Biological Effects in Relation to Botany,
Chemistry, Agriculture/ Nutrition and Medicine (New York:
Published by the authors, 1949).
121. Tscherkes, L.A., S.G., Aptekar, and M.N. Volgarev, Hepatic
Tumors Induced by Selenium, Text in Russian. Byul. Eksperim.
Biol. i Medi. 53:78 (1961).
122. Tscherkes, L.A., M.N. Volgarev, and S.G. Aptekar, Acta.
Univ. Intern. Contra.. Cancrum. 19:632 (1963).
123. Tsuzuke, H., K. Okawa, and T. Hosoya, Experimental Selenium
Poisoning, Yokohama Med. Bull. 11:368 (1960).
124. Volgarev, M.N., and L.A., Tscherkes, "Further Studies in
Tissue Changes Associated with Sodium Selenate," in Symposium;
Selenium in Biomedicine, O.H. Muth, Ed. (Westport, Conn.:
AVI Pub. Co., 1967).
125. Wahlstrom, R.C., L.D. Rainstra, and O.E. Olson, "The Effect
of Arsenilic Acid and 3-Nitro-4-Hydroxybenzenearsonic acid,"
J. Animal Sci. 14:105 (1955).
-------
61
126. Walkinson, J.H./ Fluorometric Determination of Selenium in
Biological Material with 2,3-Diaminonaphthalene, Anal. Chem.
.38:92 (1966).
127. Walkinson, J.H., "Analytical Methods for Selenium in Biolog-
ical Material," in Symposium; Selenium in Biomedicine, O.K.
Muth, Ed. (Westport, Conn.: AVI Pub. Co., 1967).
128. Wands, R.C., Director, Advisory Center on Toxicology. Divi-
sion of Chemistry and Chemical Technology, National Research
Council, Washington, D.C., personal communication (June 1969)
129. West, P.W., "Chemical Analysis of Inorganic Pollutants,"
Air Pollution 11:163 (1968).
130. West, P.W., Louisiana State University, Baton Rouge, Louisi-
ana, personal communication (Dec. 1968).
131. West, P.W., and C. Cimerman, "Microdetermination of Selenium
with 3,3'-Diaminobenzidine by the Ring Oven Technique and
Its Application to Air Pollution Studies," Anal. Chem., 36;
2013 (1964).
132. West, P.W.> and T.V. Ramakrishna, A Catalytic Method for
Determining Traces of Selenium, Anal. Chem. 40:966 (1968).
133. Westfall, B.B., E.F. Stohlman, and M.I. Smith, Placental
Transmission of Selenium, J. Pharm. Expl. Therap. 64:55
(1938).
134. Williams, K.T., H.W. Lakin, and H.G. Byers, "Selenium Oc-
currence in Certain Soils in the United States, with a dis-
cussion of Related Topics, Fifth Report," U.S. Dept. Agr.
Tech. Bull. 758:1 (1941).
135. Wolf, E., V. Kollonitsch, and C.H. Kline, Survey of Selenium
Treatment in Livestock Production, J. Agr. Food Chem., JL1_:
355 (1963).
-------
APPENDIX
-------
APPENDIX
TABLE 6
MDRTALITY OF GUINEA PIGS FROM INHALATION OF HYDROGEN SELENIDE
29
Number
of
Concentration Guinea
(ufj/m )* Piqs
Days
1-5
Days
6-10
Days
11-15
Days
16-20
Days
21-25
.Days
26-30
% Dead Within
30 Days
2-hour exposure:
6,
12,
13,
21,
34,
36,
000
000
000
000
000
000
16
16
16
16
16
16
0
3
1
4
5
11
0
2
6
2
0
3
1
2
0
5
3
0
1
1
2
2
3
1
0
0
1
1
0
0
0
0
0
0
0
0
12
50
62
87
68
93
.5
.0
.5
.5
.8
.7
4-hour exposure:
6,
7,
12,
15,
45,
000
000
000
000
000
16
16
16
16
16
1
2
2
8
15
2
0
6
5
1
0
1
3
1
0
1
1
1
0
0
0
1
0
0
0
18
25
75
100
100
.8
.0
.0
.0
.0
8-hour exposure:
1,
1,
1,
6,
6,
7,
42,
000
000
000
000
000
000
000
Controls
16
16
16
16
16
16
16
32
0
1
0
15
7
5
14
1
2
3
7
3
3
2
2
1
4
1
2
2
0
5
0
0
1
0
2
3
1
1
1
0
0
1
1
1
0
1
2
0
0
0
0
0
50
50
56
81
87
87
100
9
.0
.0
.3
.3
.5
.5
.0
.4
co
*1 (ag/m3 = 0.000302 ppm.
-------
64
APPENDIX
TABLE 7
80
PRODUCERS OF SELENIUM IN THE UNITED STATES (1967)
Company Location
American Metal Climax, Inc. Carteret, N.J.
American Smelting and Refining Co. Baltimore, Md.
International Smelting and
Refining Co. Perth Amboy, N.J.
Kawecki Chemical Co. Boyertown, Pa.
Kennecott Copper Corp. Magna, Utah
Kennecott Refining Corp. Anne Arundel County, Md.
-------
APPENDIX
TABLE 8
SALIENT SELENIUM STATISTICS, 1956-6778'79'80
(Thousands of pounds of contained selenium)
ited States
Production3
Shipments to
consumers
Imports for
consumption
Consumption,
apparent*5
Producers '
stocks,
Dec. 31
Price per
1956
928
1,035
235
1,270
191
1957
1,077
625
148
773
651
1958
727
737
184
920
551
1959
799
1,011
224
1,234
339
1960
620
650
160
810
290
1961
1,022
787
117
904
515
1962
999
741
159
900
773
1963
928
679
339
1,018
1,022
1964
929
646
293
939
1,305
1965
540
824
251
1,075
1,021
1966
620
845
286
1,131
797
1967
598
659
301
960
736
pound, commer-
cial grade
World produc-
tion
$9.00-
15.00
1,923
$7.50-
12.00
1,940
$7.00-
7.50
1,507
$7.00
1,719
$6.50-
7.00
1,777
$5.75-
6.25
2,097
$5.75-
6.25
2,091
$4.50-
5.75
2,015
$4.50-
6.00
2,163
$4.50-
6.00
1,789
$4.50-
6.00
1,951
$4.50'
6.00
2,069
^Includes small quantity of secondary selenium for 1956-61.
Total of shipment and imports to consumers.
CFi
-------
APPENDIX
66
TABLE 9
LIST OF MERCHANDISERS AND CONSUMERS
OF SELENIUM AND ITS COMPOUNDS116
Accurate Electronics Co.
Alliance Industrial Products Co.
Allied International Co.
Allis-Chalmers Manufacturing Co.
Alloy chem Inc.
Alloys Unlimited Inc.
American Metal Climax Inc.
American-Orient Products Corp.
American Rectifier Corp.
American Smelting and Refining Co.
Amplex Chemical Co. Inc.
Anaconda Sales Company
Anchor Alloy Inc.
Anglo-American Metal & Ferro Alloy
Corp.
Atomergic Chemicals Co.
B & B Engineering Corp.
B & B Motor and Control Corp.
J. T. Baker .Chemical Co.
Belmont Smelting and Refining
Works Inc.
Bogue Electric Manufacturing Co.
Bradley Laboratories Inc.
Bradley Semiconductor Corp.
Cadillac Electric Products
Ceramic Color and Chemical
Manufacturing Co.
Christie Electric Corp.
City Chemical Corp.
Clinton Supply Co. Inc.
Darby Co. Ltd.
Davidson Aluminum & Metal Corp.
B. F. Drakenfield & Co.
E. I. du Pont de Nemours & Co. Inc.
Baling Corporation
Edal Industries, Inc.
Electron Equipment Corp.
Electronic Devices Inc.
Electronic Devices Inc.
Electronic Rectifier Co. Inc.
Electro-Seal Corp.
Electronic Space Products
Fansteel Metallurgical Corp.
Franklin Fibre-Lamitex Corp.
Gates Electronic Co. Inc.
Chicago, 111.
Chicago, 111.
New York, N.Y.
Milwaukee, Wis.
New York, N.Y.
Long Island City, N.Y.
New York, N.Y.
Rochester, N.Y.
College Point, N.Y.
New York, N.Y.
New York, N.Y.
New York, N.Y.
Brooklyn, N.Y.
New York, N.Y.
Carle Place, N.Y.
Norwood, La.
New York, N.Y.
North Phillipsburg, N.J.
Brooklyn, N.Y.
Paterson, N.J.
New Haven, Conn.
New Haven, Conn.
New Rochelle, N.Y.
New Brighton, Pa.
Los Angeles, Calif.
New York, N.Y.
Chicago, 111.
Pittsburgh, Pa.
Brooklyn, N.Y.
New York, N.Y.
Wilmington, Del.
Cambridge, Mass.
East Haven, Conn.
South Pasadena, Calif.
Brooklyn, N.Y.
Yonkers, N.Y.
Rochester, N.Y.
Des Plaines, 111.
Los Angeles, Calif.
North Chicago, 111.
Wilmington, Del.
Bronx, N.Y.
(continued)
-------
67
APPENDIX
TABLE 9
LIST OF MERCHANDISERS AND CONSUMERS
OF SELENIUM AND ITS COMPOUNDS116
General Electric Co.
General Instrument Corp.
Green Electric Co. Inc.
Industrial Metals Improvement Co.
Industrial Rectifier Co.
Insulation Products Co.
International Rectifier Corp.
IRC Inc., Boone Div.
ITT Components Div.
Kawecki Chemical Co. Inc.
Kennecott Sales Corp.
Kneisley Electric Co.
La Marche Bros.
Lambda Electronics Corp.
Ledex Div., Ledex Inc.
Lorain Products Corp.
Macarr Inc.
McKesson & Robbins, Inc.
Meaker Co.
Meaker Co.
Mellaphone Corp.
Metallurgical Products Co.
Metropolitan Metal Co.
Miller Sanford Corp.
Model Rectifier Corp.
Ohio Semiconductors Division
Opad Electric Co. Inc.
Pancoast International Corp.
Phelps Dodge Refining Corp.
Power Designs Inc.
Radio Receptor Co. Inc.
Ramm Rectifier Co. Inc.
Ramyr Manufacturing Co.
Rapid Electric Co. Inc.
Rectico Inc.
Rectifier Engineering & Supply Co.
Republic Chemical Corp.
J. E. Robin Inc.
J. A. Samuel & Co.
Sarkes Tarzian Inc.
Schauer Manufacturing Co.
Semi Alloys Inc.
Seneca Electric Co.
Siegel Chemical Co. Inc.
Strong Electric Corp.
Schenectady, N.Y.
Hicksville, L.I., N.Y.
Fair Lawn, N.J.
Pittsburgh, Pa.
New York, N.Y.
Pittsburgh, Pa.
El Segundo, Calif.
Boone, N.C.
Clifton, N.J.
New York, N.Y.
New York, N.Y.
Toledo, Ohio
Chicago, 111.
Plainview, N.Y.
Dayton, Ohio
Lorain, Ohio
New York, N.Y.
New York, N.Y.
Chicago, 111.
Nut ley, N.J.
Rochester, N.Y.
Philadelphia, Pa.
Detroit, Mich.
Brooklyn,
Brooklyn ,
Columbus,
New York,
New York,
New York,
Westbury,
N.Y.
N.Y.
Ohio
N.Y.
N.Y.
N.Y.
N.Y.
New York, N.Y.
New York, N.Y.
Los Angeles, Calif.
Bronx, N.Y.
Cedar Grove, N.J.
St. Louis, Mo.
New York, N.Y.
East Orange, N.J.
New York, N.Y.
Bloomington, Ind.
Cincinnati, Ohio
Mt. Vernon, N.Y.
Detroit, Mich.
Brooklyn, N.Y.
Toledo, Ohio
(continued)
-------
68
APPENDIX
TABLE 9
LIST OF MERCHANDISERS AND CONSUMERS
OF SELENIUM AND ITS COMPOUNDS116
Sylvan Chemical Corp.
Syntron Co.
Technical Apparatus Builders
C. Tennant Sons & Co. Inc.
Ther Electric & Machine Works Inc.
Trojan Rectifier and Equipment Co,
United Mineral & Chemical Corp.
R. T. Vanderbilt Co. Inc.
Westinghouse Electric Corp.
Zenitherm Alloys Corp.
Max Zuckerman & Sons
Englewood Cliffs,
Homer City, Pa.
New York, N.Y.
New York, N.Y.
Chicago, 111.
Inc. Lancaster, N.Y.
New York, N.Y.
New York, N.Y.
Pittsburgh, Pa.
Elizabeth, N.J.
Owings Mills, Md.
N.J,
-------
APPENDIX
TABLE 10 PROPERTIES, TOXICITY, AND USES OF SOME SELENIUM COMPOUNDS
75
Compound
Properties
Toxicity
Uses
Aluminum selenide
Al2Se3
Decomposes in
water
May be irritating
to eyes, mucous
membranes. Causes
garlic odor of
breath^ dizziness,
nausea
In preparation of
hydrogen selenide;
in semiconductor
research
Ammonium
hydroselenate
NH„(HSeO )
4 4
Ammonium magnesium
selenate
Mg(NH4)Ss04
Decomposes
Ammonium selenate
(NH4)2Se03
Decomposes
Ammonium selenite
Decomposed by
heat
Occupational
exposure has
caused pallor,
nervousness,
depression, garlic
odor of breath,
gastrointestinal
disturbances, and
dermatitis
In manufacture of red
glass as reagent for
alkaloids
Antimony
triselenide
o.
mp 605 C
Occupational
exposure has caused
pallor, nervousness,
depression, garlic
odor of breath, G.I.
disturbances, and
dermatitis
(continued)
-------
APPENDIX
TABLE 1.0 PROPERTIES, TOXICITY, AND USES OF SOME SELENIUM COMPOUNDS (Continued)
Compound
Arsenic hemiselenide
As2Se
Arsenic
pentaselenide
As2Se5
Arsenic
triselenide
As2Se3
Beryllium
selenate
BeSeO^,
4
Bismuth selenide
Bi2Se3
Properties
Decomposes in
boiling alkali
hydroxide
Decomposes
when heated
in air
mp 260°C
mp 170UC
Toxicity
Highly toxic.
Causes pallor,
nervousness ,
depression,
garlic odor of breath
and sweat, and
G.I. disturbances
Highly toxic.
Causes pallor,
nervousness,
depression, garlic
odor of breath and
sweat, and G.I.
disturbances
Highly toxic.
Causes pallor,
nervousness,
depression, garlic
odor of breath and
sweat, and G.I.
disturbances
Death may result
from short
exposure to
incredibly low
concentrations of
element and its
salts
Uses
In manufacture of
glass
In semiconductor
research
(continued)
-------
APPENDIX
TABLE 10 PROPERTIES, TOXICITY, AND USES OF SOME SELENIUM COMPOUNDS (Continued)
Compound
Cadmium selenate
CdSe04
Cadmium selenide
CdSe
Calcium selenide
CaSe
Cesium selenate
Cs2Se04
Chloroselenic acid
HClSe03
Cupric hydroselenite
Cu(HSe03)2
Cupric selenate
CuSeO
4
Cupric selenide
CuSe
Cupric selenite
CuSeO-,
Gold selenate
Au2(Se04)3
Properties
Decomposes at
100°C
mp 1350°C
mp 46°C
Decomposes in
light
Toxicity
Low toxic ity
because of
insolubility
Uses
In photoconductors,
semiconductors ,
photoelectric cells,
and rectifiers; in
phosphors
In electron emitters
In coloring Cu or Cu
alloys black
As catalyst in
Kjeldahl digestions;
in semiconductors
(continued)
-------
APPENDIX TABLE 1Q PROPERTIES, TOXICITY, AND USES OF SOME SELENIUM COMPOUNDS (Continued)
Compound
Gold selenide
Au2Se3
Hydrogen selenide
H Se
2
Indium selenide
InSe
Lead selenate
PbSeO4
Lead selenite
PbSeO3
Lithium selenate
LiSeO4
Lithium selenite
LiSe03
Manganese selenate
MnSeO4 • 2H O
Manganese selenide
MnSe
Manganese selenite
MnSeO3'2H2O
Properties
Decomposed by
heat
mp -64°C
mp 660°C
Decomposes
Melts at about
500 C
Toxicity
May be irritating to
eyes, mucous
membranes. Causes
garlic odor of breath,
dizziness, nausea
Uses
In semiconductor
research
to
(continued)
-------
APPENDIX
TABLE 10 PROPERTIES, TOXICITY, AND USES OF SOME SELENIUM COMPOUNDS (Continued)
Compound
Properties
Toxicity
Uses
Phosphorus
pentaselenide
Decomposes
Phosphorus
triselenide
P4Se3
mp 242 C
Potassium
biselenite
Potassium cobaltus
selenate
K2Co(Se04)2
Potassium selenate
As reagent
Potassium selenide
K2Se
Rubidium selenate
Selenic acid
H2SeO4
bp 26 (PC
mp 58°C
Selenium bromide
Decomposes at
227°C
mp -46°C
Occupational exposure
has caused pallor,
nervousness,
depression, garlic
odor of breath, G.I.
disturbances, and
dermatitis
(continued)
-------
APPENDIX
TABLE 10 PROPERTIES, TOXICITY, AND USES OF SOME SELENIUM COMPOUNDS (Continued)
Compound
Properties
Toxicity
Uses
Selenium chloride
Se2Cl2
Decomposes at
100°C
bp 130°C
mp -85°C
Can cause pallor,
nervousness,
depression, garlic
odor of breath,
depression, G.I.
disturbances, and
dermatitis
Selenium disulfide
SeS_
mp 100UC
Occupational exposure
has caused pallor,
nervousness,
depression, garlic
odor of breath, G.I.
disturbances, and
dermatitis
In eczemas and fungus
infections in dogs
and cats
Selenium
hexafluoride
mp -39UC
bp -34.5°C
sublimes at
-46.6°C
Occupational exposure
has caused pallor,
nervousness,
depression, garlic
odor of breath, G.I.
disturbances, and
dermatitis
As gaseous electric
insulator
Selenium
monosulfide
SeS
Decomposes at
118-9DC
Occupational
exposure has caused
pallor, nervousness,
depression, garlic
odor of breath and
sweat, G.I.
disturbances, and
dermatitis
Vet use: topically
against eczemas,
fungus infections,
demodectic mange, flea
bites in small animals
(continued)
-------
APPENDIX
TABLE 10 PROPERTIES, TOXICITY, AND USES OF SOME SELENIUM COMPOUNDS (Continued)
Compound
Properties
Toxicity
Uses
Selenium oxide
'2
mp 340 C
Occupational exposure
has caused pallor,
nervousness,
depression, garlic
odor of breath and
sweat, G.I.
disturbances, and
dermatitis
In the manufacture of
other selenium
compounds; as a reagent
for alkaloids
Selenium
oxychloride
SeOCl0
top 180 C
Strong irritant,
vesicant. Can cause
fatal pulmonary edema
Selenium
oxyfluoride
l
2
bp 124QC
mp 4.6 C
Strong irritant,
vesicant. Can cause
fatal pulmonary edema
Selenium
tetrabromide
Decomposes at
70-80°C
Occupational exposure
has caused pallor,
nervousness,
depression, garlic
odor of breath, G.I.
disturbances, and
dermatitis
Selenium
tetrachloride
SeCl,
mp 305 C
Sublimes at
170-196 C
Can cause pallor,
nervousness,
depression, garlic
odor of breath, G.I.
disturbances, and
dermatitis
Silver selenide
Ag2Se
mp 880 C
(continued)
-------
APPENDIX
TABLE 10 PROPERTIES, TOXICITY, AND USES OF SOME SELENIUM COMPOUNDS (Continued)
Compound
Silver selenite
Ag SeO
2 3
Sodium hydroselenite
NaHSeO3
Sodium selenate
Na2SeO4
Sodium selenide
Na2Se
Sodium selenite
Na2Se°3
Stannic selenide
SnSe2
Stannic selenite
Sn(Se03)2
Stannous selenide
SnSe
Strontium selenate
SrSeO
Properties
Decomposed by
heat to
selenium oxide
mp 875°C
mp 650°C
mp 861°C
Toxicity
Uses
As insecticide in
some horticultural
applications
In removing green
color from glass
during its
manufacture as
alkaloidal reagent
(continued)
-------
APPENDIX
TABLE 10 PROPERTIES, TOXICITY, AND USES OF SOME SELENIUM COMPOUNDS (Continued)
Compound
Properties
Toxicity
Uses
Strontium selenide
SrSe
Thallium selenate
Tl SeO,.
mp 400 C
Thallium selenide
mp 340°C
Zinc selenate
ZnSeO.
mp 50 C
Decomposes
Zinc selenide
ZnSe
o,
mp HOO^C
Occupational exposure
has caused pallor,
nervousness,
depression, garlic
odor of breath, G.I.
disturbances, and
dermatitis
-------
APPENDIX
78
TABLE 11
SELENIUM CONTENT OF DUST FROM
AIR-CONDITIONING FILTERS, 1941
66
Type of Building Where
Sample Was Collected
Location
Se (ppm)
Industrial
Dry goods store
Industrial
Residence
Residence
Residence
Office building
Unknown
Residence
Unknown
Office building
Los Angeles, Calif. 0.8
San Francisco, Calif. 0.05
San Francisco, Calif. 0.6
Grand Forks, N.Dak. 6
Houston, Tex. 3
University City, Mo. 2.5
(suburb of St. Louis)
St. Louis, Mo. 10
Chicago, 111. 2.5
Shaker Heights, Ohio 2.5
(suburb of Cleveland)
Philadelphia, Pa. 1.5
Washington, D.C. 5
------- |