|
Items in cart [1] |
Questions? Call 888-624-8373 |
| Copyright © 2009. National Academy of Sciences. All rights reserved. Terms of Use and Privacy Statement |
Below are the first 10 and last 10 pages of uncorrected machine-read text (when available) of this chapter, followed by the top 30 algorithmically extracted key phrases from the chapter as a whole.
Intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text on the opening pages of each chapter.
Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.
Do not use for reproduction, copying, pasting, or reading; exclusively for search engines.
OCR for page 24
Antimony
Antimony (Sb) is a lustrous, silver-white metal with a bluish tinge that
is classified with arsenic and bismuth as a Group VA metal in the
periodic table. Very little antimony occurs free in nature, and most is
derived from the principal antimony ore, stibnite (Sb2S3), which con-
tains 71 to 75 percent of this element when nearly pure. Abundant
deposits are found in China, Mexico, Bolivia, Algeria, Portugal, and
France. Other valuable antimony ores include cervantite (Sb2O4),
valentinite (S~03), and kermesite (Sb2S2O). Mean antimony concen-
tration in the earth's crust has been estimated to be 0.2 ppm (Schroeder,
1973~.
Metallic antimony was used in the manufacture and plating of vases
and household vessels as early as 4000 B.C. (Mellor, 1939) and as a
constituent of ancient bronzes in the fifth or sixth Egyptian Dynasty
(Fink and Kopp, i933~. Use of stibnite as a cosmetic (Kohl) is referred
to in the Old Testament and in early Chinese and Arabic writings.
Industrial uses are diverse, but a major portion serves as a constituent
of alloys with lead, tin, and copper. Lead-antimony alloys are used in
storage battery grids, pewter, printer's type, lead shot, lead electrodes,
cable coverings, foil, and solder. The trisulfide (Sb2S3) and pentasulfide
(Sb2Ss) are used in the compounding of rubber. Antimony trioxide
(Sb2O3) is used as a textile dye, and lead antimonate EPb3(SbO4 )2] as a
paint pigment. Oxides are used as opacifiers in enamels and as de-
colorizing and refining agents in glass maufacture. An important phar-
maceutical compound is tartar emetic, potassium antimony! tartrate
24
OCR for page 25
Antimony
25
(KSbC4H;O7-~/~H2O), which has been used for years in the treatment of
schistosomiasis.
ESSENTIALITY
Antimony has no known essential metabolic function in living or-
ganisms, and Liebscher and Smith (1968) have used this mineral as a
model for nonessential elements. Thiol-containing enzymes are inhib-
ited in vitro by antimony salts. The possibility of similar enzyme inhibi-
tions in vivo and the affinity of trivalent antimony for erythrocytes may
be significant for the effectiveness of antimony tartrates in treatment of
schistosomiasis.
METABOLISM
Soluble antimony compounds, such as antimonites and tartrates, are
slowly absorbed from the alimentary tract. Waitz et al. (1965) reported
that ingestion of potassium antimony! tartrate by monkeys, rats, and
mice led to greater fecal than urinary excretion, and these workers
concluded that gastrointestinal absorption was poor. Felicetti et al.
(1974) found that very little of either trivalent or pentavalent antimony
tartrate was absorbed by hamsters from a Savage. About 2 percent of
the initial body burden was present 4 days later, and nearly two-thirds
of this was found in the gastrointestinal tract. Antimony halides are
hydrolyzed to oxides in the alimentary tract and are apparently not
absorbed.
The metabolic behavior of antimony is affected by its valence state.
Trivalent antimony concentrates in the liver of all species studied
(Brady et al., 1945; Djuric et al., 1962; Gellhorn et al., 1946; Otto et al.,
1947; Otto and Maren, 1950; Rowland, 1968; Tarrant et al., 1971;
Thomas et al., 1973), in the thyroid and parathyroid of dogs (Brady et
al., 1945), and in the erythrocytes of many species, including man (Otto
and Maren, 1950; Otto et al., 1947~. Hair, skin, and skeletal accumula-
tions of trivalent antimony have been reported in mice (Molokhia and
Smith, 1969; Thomas et al., 1973) and hamsters (Felicetti e! al., 1974~.
Pentavalent antimony has a lesser affinity for the liver than does triva-
lent antimony and accumulates more in the spleen (Gellhorn et al.,
19461. Human erythrocytes do not concentrate antimony in the penta-
valent state (Otto et al., 19471. In most rodents, trivalent antimony is
excreted primarily in the feces and pentavalent primarily in the urine
OCR for page 26
26 MINERAL TOLERANCE OF DOMESTIC ANIMALS
(Otto and Maren, 1950), but in humans, both valence states of antimony
are excreted in the urine (Otto et al., 19471.
SOURCES
Potentially toxic exposures occur as a consequence of industrial pro-
cessing and use of antimony, preparation, or storage of food in con-
tainers improperly glazed with an antimony enamel and accidental
ingestion or parenteral administration of excessive doses of antimony
compounds. The most common industrial exposures to antimony are
during the mining, smelting, and refining of the ore; in the production
of alloys; in the manufacture of abrasives; and in type-setting
(Browning, 19691. Inhalation of antimony-containing dusts or fames
constitute the main hazard, and the American Conference of Industrial
Hygienists has set a threshold limit of 0.5 mg/m3 of air. Stibine (SbH3 ~
is a colorless gas evolved when certain antimony alloys are treated with
acid and subjected to electrolysis (e.g., during the charging of storage
batteries). Stibine is also released when some antimony compounds are
treated with steam, or when nascent hydrogen comes into contact with
metallic antimony or a soluble antimony compound. The threshold limit
for stibine in air for an 8-hour working day has been set at 0.1 mg per
liter. Antimony trioxide is frequently used as an opacif~er in vitreous
coatings. Enamel glazes of this type, particularly if low in silica, are
readily attacked by acids of foodstuffs. Monier-Williams (1925, 1934)
found that exposure of enamelled containers to a 1 percent solution of
citric acid dissolved 0.01 g of antimony per liter.
Published studies of antimony levels in foods or animal feedstuffs are
few. Murthy et al. (1971) analyzed the total diets for 7 days of institu-
tionalized children in 28 localities in the United States. Intakes varied
from 0.25 to 1.28 mg antimony per day, and dietary concentrations
ranged from 0.21 to 0.69 ppm. Hamilton and Minski (1972/1973) ana-
lyzed adult English diets and found a mean intake of 34 ,ug/day. These
workers also noted that the proportion of refined foods in the diet may
influence such values, since brown sugar contained 0.08 ppm antimony
and refined white sugar contained <0.002 ppm.
OCR for page 27
Antimony
TOXICOSIS
LOW LEVELS
Oral
27
The dietary concentration of antimony that induces toxicosis is depen-
dent upon valence state, pentavalent compounds being less irritating
than trivalent compounds (Goodwin, 19441. Bradley and Fredrick
(1941) reported that rats fed potassium antimony! tartrate in increasing
daily doses over 12 months grew normally on amounts up to 100 mg/kg
body weight (36.5 mg/kg antimony), but cardiac pathology was evident.
Antimony metal up to 1 g/kg body weight produced similar effects.
Pribyl (1927) fed rabbits 15 mg of potassium antimony! tartrate per
kilogram body weight (5.5 mg/kg antimony) and found increased con-
centrations of nonprotein nitrogen in blood and urine. After 5 to 20
days, icterus was noted and some individuals showed fatty degenera-
tion and parenchymal necrosis of the liver. Wieland (1937) found no
pathology in rabbits fed 2 to 6 mg potassium antimony! tartrate per kg
body weight (0.7 to 2.2 mg/kg antimony). Lifetime studies (Schroeder
et al., 1968) with mice showed that 5 ppm antimony as potassium
antimony! tartrate in drinking water reduced mean life span of females
slightly. No evidence of carcinogenesis or tumorigenesis was obtained.
Inhalation
Guinea pigs were exposed by Dernehl et al. (1945) to a dust concentra-
tion of antimony trioxide of 45.4 mg/m3 of air (19 mg/m3 antimony) for
2 hours daily, 7 days a week for 3 weeks, followed by 3 hours daily
exposure. All animals showed extensive interstitial pneumonitis, and 4
died. No electrocardiogram changes were evident, but 11 out of 15
guinea pigs having 138 or more hours of exposure showed fatty degen-
eration of the liver. There was also a leucocytopenia, a polymorpho-
nuclear neutrophilopenia, and a relative Iymphocytosis. Gross et al.
(1951) exposed rats to antimony trioxide for periods up to 14 months
and induced a chronic lipoid pneumonia. The lipoid deposits were
intra-alveolar with some perifocal fibrosis.
Briegeret al. (1954) exposed rabbits to the dust of antimony trisulfide
in a concentration of S.6 mg/m3 of air (2 mg/m3 antimony), 7 hours per
day, 5 days per week for 6 weeks. The lungs showed a mild degree of
venous congestion and areas of focal hemorrhage. Higher concentra-
tions of 27.8 mg/m3 of air (10 mg/m3 antimony) induced lung inflamma-
OCR for page 28
28 MINERAL TOLERANCE OF DOMESTIC ANIMALS
lion. Slight to moderate myocardial damage produced changes in the T
waves. In some rabbits the myocardium was flabby and dilated, with
swelling of the fibers and granular cytoplasmic inclusions. Dogs ex-
posed by Brieger et al. (1954) to 5.3 and 5.6 mg antimony trisulfide per
cubic meter of air (1.9 to 2.0 mg/m3 antimony) were not affected
adversely.
Industrial poisoning of humans by antimony may not be clear-cut,
since industrial antimony usually contains other substances, such as
arsenic, and toxic signs and symptoms are somewhat similar. Renes
(1953), in a study of mining, concentrating, and smelting stibnite, found
air concentrations of antimony to be 4.7 to 11.8 mg/m3, while arsenic
concentrations were 0.4 to 1.1 mg/m3. Early signs of arsenical poisoning
were absent, and he concluded that the illness observed was due to the
antimony. Renes (1953) suggested that apparent differences in the
toxicity of antimony in different industrial settings may be related to
particle size. In his study, particle size was usually less than 1 ,um.
Bulmer and Johnston (1948) found no ill health in humans working in a
laboratory where antimony tr~sulf~de was crushed and ground. Particles
were small but not as minute as in a fume. Two men were exposed for
a year to air antimony concentrations of 52 mg/m3. Schrumpf and Zabel
(1910) described a variety of symptoms in 15 to 20 percent of type-
setters, including irritability, fatigue, pains in the limbs, anorexia, and
gastrointestinal complaints. Gocher (1945) noted muscular pains, head-
ache, dizziness, and oppression in the chest. Fei! (1939) and Renes
(1953) recorded laryngitis and tracheitis in antimony smelters. The
latter researcher also observed abdominal cramps, diarrhea, vomiting,
dizziness, nerve tenderness and tingling, severe headaches, and pros-
tration. Acutely ill individuals showed pneumorutis but no peripheral
parenchymal pulmonary damage. Removal from exposure and treat-
ment with penicillin aerosols rapidly alleviated the symptoms. Fell
(1939) found a characteristic skin eruption in foundry workers in which
the eruption was pustular, sometimes covered with a crust (like the
lesions of chickenpox) and present on limbs, face, and chest. There was
also some irritation of eyes and throat, some gingivitis, and clinical
appearance of anemia. Briegeret al. (1954) studied men in a plant where
resinoid grinding wheels were manufactured and where antimony tri-
sulfide had replaced lead for the preceding 2 years. Air concentrations
of antimony varied between 0.6 and 5.5 mg/m3, with most above 3.0.
Several men had died of heart attacks, and 35 out of 75 men examined
electrocardiographically showed abnormalities, mostly in the T waves.
OCR for page 29
Antimony
HIGH LEVELS
Oral
29
Acute toxicosis in rabbits was studied by Oelkers (1937), who found
that a single oral dose of 125 mg of potassium antimony! tartrate per
kilogram of body weight (46 mg/kg antimony) was fatal in all cases; 120
mg/kg of body weight (44 mg/kg antimony) was almost certainly fatal in
24 to 36 hours; and 115 mg/kg of body weight (42 mg/kg antimony) killed
50 percent of the animals. In oral studies with rats, Bradley and Fred-
rick (1941) found the minimum lethal dose of potassium antimony!
tartrate expressed as antimony was 300 mg/kg of body weight. Franz
(1937) described centrolobular fatty degeneration of the liver and de-
generative changes in the kidneys of rats.
Monier-Williams (1934) reported that in 1928 there was an outbreak
of sickness in Newcastle-on-Tyne in 56 individuals who had drunk
lemonade made in white enamelled buckets. A drinking glass of lemon-
ade was found to contain the equivalent of about 100 mg potassium
antimony! tartrate (36.5 mg antimony). Symptoms reported included a
burning sensation in the stomach, colic, nausea, vomiting, and col-
lapse. The usual emetic dose of potassium antimony! tartrate is about
30 to 60 mg (11 to 22 mg antimony).
Injection
Bradley and Frednck (1941) established the ~D50 for antimony metal and
five antimony compounds administered intraperitoneally to the rat.
These values (per kilogram of body weight) were 100 mg of antimony
metal, 3,250 mg of antimony trioxide (1,360 mg antimony), 4,000 mg of
antimony pentoxide (1,500 mg antimony), 1,000 mg of antimony tnsul-
fide (360 mg antimony), 1,500 mg of antimony pentasulfide (450 mg
antimony), and 11 mg of potassium antimony! tartrate (4 mg antimony).
Animals dying within a few days showed loss of weight, general weak-
ness, loss of hair, dyspnea, and myocardial insufficiency. At necropsy,
myocardial congestion and dilatation of the nght heart were prominent.
There was little change in the lungs. The livers were congested and
showed some degeneration and polymoIphonuclear inf~ltration. Toxic
glomerular nephritis was present most markedly in rats receiving the
tartrate, while metallic antimony produced moderate splenic hyper-
plasia with some eosinophilia.
Seitz (1924) reported that subcutaneous injections of rabbits and
OCR for page 30
30 MINERAL TOLERANCE OF DOMESTIC ANIMALS
guinea pigs with 53 mg of metallic antimony per kilogram of body
weight produced a mild polycythemia and eosinophilia. The LD50 of a
single subcutaneous injection of antimony compounds in mice was
found (Ercoli, 1971) to be (per kilogram of body weight) 48 mg for
sodium antimony} tartrate (19 mg antimony), 55 mg for potassium
antimony! tartrate (20 mg antimony), 390 mg for a chelate of sodium
antimony! tartrate and 3-mercaptovaline (pen~cillam~ne) (57 mg
antimony), 2,000 mg for stibocaptate (500 mg antimony), and 670 mg for
stibophen (110 mg antimony). Cotton and Logan (1966) noted that
potassium antimony! tartrate injected intravenously into dogs at the
rate of 64 mg/kg of body weight (23.3 mg/kg antimony) depressed car-
diac contractile force and induced bradycardia.
Potassium antimony! tartrate has been administered frequently intra-
venously for treatment of human schistosom~asis and leishmaniasis.
Usual dosage has been 20 to 25 mg/kg of body weight (7 to 9 mg/kg
antimony) for 20 days. Symptoms of acute intoxication foliow~ng thera-
peutic intravenous injection have been occasionally reported. They
include headache, giddiness, sore throat, a metallic taste in the mouth,
cough, nausea, diarrhea, tachycardia, muscular stiffness and debility
(Strong, 1942~. Cardiac arrhythmias resulting in death have been re-
ported numerous times (Ming-Hsin et a]., 1958~. Khalil (1931) noted
bradycardia (both acute and of short duration, and chronic) during a
course of injections, returning to normal when they were discontinued.
Mainzer and Krause (1940) concluded that this is not due to vagal
stimulation, but to a direct toxic action of antimony on the heart mus-
cle. Ming-Hsin et al. (1958) suggested that the cardiac disturbance is a
combined effect of autonom~c system dysfunction caused by antimony
inhibiting the cerebral cortex and inducing hyperexcitability of the
myocardium. Gastrointestinal disturbances and mild jaundice com-
monly appear 2 to 3 weeks after a course of injections (Chopra, 1927~.
A frequent sequel of antimony administration is pneumonia (Cushny,
1941~. Papular skin eruptions are also sometimes seen following re-
peated injections.
Inhalation
Stibine (SbH3,) toxicity closely resembles that of arsine, death occurring
rapidly on exposure to concentrations of 1 percent in air. It is a power-
ful hemolytic poison. The lethal dose for white mice was estimated to
be 100 mg/1 (98 mg/1 antimony) for 1 hour and 40 niinutes (Stock and
Guttman, 1904), and for week-old chicks, 25 to 30 mg/1 (Steele et al.,
OCR for page 31
Antimony
31
1944~. The hemolytic effect has been described by Webster (1946) and
Dunn and Webster (19451. Webster (1946) found a single exposure to 40
to 45 mg/1 for 1 hour was dangerous for dogs and cats, death occurring
within a few hours to a day. These concentrations produced marked
hemoconcentration but no hemoglobinur~a. In guinea pigs, ery-
throcytes underwent morphological change (crenation) within a few
minutes after exposure. Exposure of guinea pigs to 65 mg/1 stibine (63
m&/1 antimony) for 1 hour produced hemogiobinuna, and anemia fol-
lowed in a few days. With 92 mg/1 (90 mg/1 antimony), animals died on
the second to sixth days with casts in the renal tubules.
Although the threshold Knot of stibine in ear for man has been set at
0.1 mg/1, no chronic stibine poisoning has been reported. Several cases
of toxicity have been reported (Dernehl et al., 1944; Nau et al., 1944)
from a mixture of gases including arsine, hydrogen sulfide, and stibine.
These were liberated when water was added to a hot dross containing
aluminum, compounds of arsenic and antimony, and an excess of free
sulfur. Affected individuals experienced severe headache, nausea,
weakness, abdominal and lumbar pain, hematuria, and profound hemo-
lytic anemia. Recovery followed hospitalization and treatment by
transfusion and intravenous injection of glucose.
FACTORS INFLUENCING TOXICITY
The seventy of antimony toxicosis is influenced by the form in which
it occurs, the animal species affected, and the route of administration.
In general, trivalent antimony is more toxic than pentavalent antimony.
Small particles (
OCR for page 32
32 MINERAL TOLERANCE OF DOMESTIC ANIMALS
TISSUE LEVELS
Using neutron activation, Smith (1967) found median antimony concen-
trations in human tissues between 0.05 and 0. 15 ppm (dry basis). High-
est levels were found in lungs (0.28 ppm) and hair (0.34 ppm). Liebscher
and Smith (1968), also using neutron activation, reported antimony
concentrations in 23 different human tissues. These were taken from
healthy adults who died as a result of violence and who had no known
direct industrial exposure to antimony dust or fumes. They lived and
worked in the area of Glascow, Scotland. On a dry basis, highest mean
concentrations were found in hair (0.69 ppm), lung (0.4X ppm), and
prostate (0.42 ppm). Lowest mean concentrations were found in spleen
(0.07 ppm) and ovary (0.07 ppm). However, great variation was evi-
dent, e.g., antimony concentration in teeth ranged from 0.005 to 0.665
ppm and in hair from 0.080 to 6.58 ppm. Molokhia and Smith (1967)
determined that the apex of the lungs had the highest concentrations
and the base of the lungs the lowest. These workers also found that the
lymph glands had relatively high antimony concentrations (0.3~0.43
ppm wet weight). Hamilton et al. (1972/1973) reported generally lower
antimony concentrations in human tissues than did Smith (1967) and
Liebscher and Smith (1968) but similar to those for mouse tissues
obtained by Molokhia and Smith (19691. Mean human blood antimony
concentrations were 0.005 ppm. Rib antimony was approximately 1.5
ppm in ash. Nixon et al. ( 1967) reported a mean of 0.034 ppm antimony
in dental enamel of Scottish subjects and 0.070 ppm for Egyptian sub-
jects treated with antimony for hilharzia. Smith (1947), studying the
excretion rate of potassium antimony! tartrate in man, found the 5()
percent excretion time to be approximately 500 hours.
MAXIMUM TOLERABLE LEVELS
Data are insufficient to set a dietary maximum tolerable level for anti-
mony with precision. Based on limited evidence, a level of 7~150 ppm
in the dry diet is suggested for the rabbit.
SUMMARY
Antimony is a lustrous, white metal classed with arsenic and bismuth
(Group VA) in the periodic table. It occurs in nature primarily as
OCR for page 33
Antimony
33
stibn~te (Sb2S3) and is extensively used in alloys with lead in storage
battery grids and printer's type, as the sulfide in compounding of rub-
ber, and as oxides in flame-retarding textiles and in enamel and glass
manufacture. Humans may be poisoned by industrial dusts and fumes
or by consuming acid food or drink prepared or stored in vessels coated
with antimony-containing enamel or glaze. Food and feeds seem gen-
erally low in antimony. Trivalent antimony appears to be more toxic
than pentavalent antimony, and toxicity from dusts is greater when
particle size is small (~1 ,um). Stibine (SbH3 ), released by treatment of
antimony with acid, is an extremely toxic hemolytic gas. Animal tox-
icity is primarily an experimental phenomenon.
Symptoms of illness in humans include anorexia, nausea, abdominal
cramps, diarrhea, emesis, muscular pains, nerve tenderness, head-
aches, oppression in the chest, pneumonitis, and pustular skin erup-
tions. Stibine induces hemolysis and anemia.
Antimony has no known essential metabolic function and inhibits
thiol-containing enzymes in vitro. Potassium antimony! tartrate has
been used extensively in treatment of human schistosomiasis.
OCR for page 34
I:
-
v
-
'e
·
·
o
· -
- ~
so
A,
· -
s:
· -
o
· -
~:
¢
an
o
cO
an
m
¢
o
C.
c
E
o
_
3 ~
o Soo
(~) ·O
~ 3
C: sit
~ ~ {'5
.E
Z ~
-
3
o
A:
o
._
Ct
3
r r _
u, 3 i;; o m u,
as _
Y ° ~ ~ ~ a ~ ~ 3 ~ ~ 5 5, ~ i, 3 ~ E
.' 8 ~
c ~ 0
~
._ ~ 3_ 3 3 ._
_ o ~
e ~ ~ e ~ Id, TO ~ :,0
_ ~ ~ lo, V'
- - -
~ E O E C E e c
_ ? ~ _ ~ W._ ~ ,,, E ~ E ~ _ E
v,
~ Y ~:
~ ~ ~ ~ ~ 0 ~
_1 _ `~)
-
o
c: ~
~ _ _
~ ._ ._
.C) ,D 9
~ Ct Ct
34
~,
_ ~ ~ _
._ ._ ._ ._
~D D D 9
D D eD ,;D
Ct Ct ~ Ct
OCR for page 35
c c
~ - - e"
o `'
_ 3
cry
— ~ Y ~ ~ ~
~ ~ . ^~0 `~O C
O A ID ~ ~ ~ ~ o
~ 3 m ~ lo
_ ~ ,~ ~ g .^ .~ .^
td Ce al ~s ~ ~ ~ ~ ~ V
~.~ 0 c c ~ c - e ~ e = ~ En. e
0 E · · y _ y D e D e D C Y D C C D Y D
Y D o o D _ ~ _ ~ ~ ~ ~ ~ ~ E ~
ct ~= ° o ~ t~ ~ .° ~> .0 c~ . c~ .0 c~ .78 ,0 .~ .0
e ~ :~, ~ E ~ E ~ E ° 9' ~ ° gY E ° 9s E ° 9x E ° 98 E ° =~,
~ ~ 0 c y E E E E
E c & -9_ ·e 0 E O E O
~ <: a c =. 8._ E c E.c i.c
E ~ e t, E 4, ~ ~ ~ ~ ~ ~ ~ E
E O E g E E Y 0 !E E E E E ~
o fi ~ ~ g ~ ~ ~ e E e ~ c Y c e ~ c c D
E E E E E E E E E E E
8 ~ ~ 8 ~ ° ~ ~ ~
~ ~ _ ~ _ ~ ~ ~ ~
0 . - _ ~
0 ~ ~
1 ~ _ ~
O O ~ C~~ a O
a
35
OCR for page 36
· -
-
m
Em
al
E
O _ ;5 =
~ _ _ L.
Ye ~ ED ~ ~ ~ Y =
~ US Cal C)
Y y.° E ° e s
.~ =.~ 8.~ a ~ E
~ i ~ 3 ~ ~ ~
0 os ~ ~ 3 3 0 ~ E
u~ u~ ~Q ~ _ ct
E ~ E a5 E 8 a5 ~ S e 5
E ._ ~ -_ t ~ -~5 e ~C =5 ~E ° ~s -_ ,° D 3
. ~ Y ~ Y y ~
5 O ~ ~ ~ib ~ ~ ~ ~ ~ ~ ~
' 1 ' E °' t~ ° 8 ~ `= ° 0 ~
o o`, ~ C,0 ~ ~5
E ° O i vl. u
Z E E E ~ 0 Z
36
OCR for page 37
Antimony
REFERENCES
37
Bradley, W. R., and W. G. Fredrick. 1941. Toxicity of antimony-animal studies. Ind.
Med. 2:15.
Brady, F. J., A. H. Lawton, D. B. Corvie, H. L. Andrews, A. T. Ness, and G. E. Ogden.
1945. Localisation of trivalent radioactive Sb following intravenous administration to
dogs infected with Diroflaria immitis. Am. J. Trop. Med. 25:103.
Brieger, H., C. W. Semisch, J. Stasney, and D. A. Piatnek. 1954. Industrial antimony
poisoning. Ind. Med. Surg. 23:521.
Browning, E. 1969. Toxicity of Industrial Metals, 2nd ed. Butterworth and Co., Ltd.,
London. 383 pp.
Bulmer, F. M. R., and J. H. Johnston. 1948. Antimony trisulphide. J. Ind. Hyg. 30:26.
Chopra, R. N. 1927. Experimental investigation into the action of organic compounds of
antimony. Indian J. Med. Res. 15:41.
Cotton, M. D., and M. E. Logan. 1966. Effects of Sb on the cardiovascular system and
intestinal smooth muscle. J. Pharmacol. 151:7.
Cushny, A. R. 1941. Antimony, Pharmacology and Therapeutics, p. 81. Churchill, Lon-
don.
Dernehl, C. U., F. M. Stead, and C. A. Nau. 1944. Arsine, stibine and H2S. Accidental
generation in a metal refinery. Ind. Med. Surg. 13:361.
Dernehl, C. U.' C. A. Nau, and H. H. Sweets. 1945. Animal studies on the toxicity of
inhaled antimony trioxide. J. Ind. Hyg. Toxicol. 27:256.
Djuric, D., R. G. Thomas, and R. Lie. 1962. The distribution and excretion of trivalent
antimony in the rat following inhalation. Int. Arch. Gewerbepathol. Gewerbehyg.
19:529.
Dunn, R. C., and S. H. Webster. 1945. Haemoglobinuria, crystals, casts and globules in
renal tubules of guinea-pigs following chemical analyses. Am. J. Pathol. 23:967.
Ercoli, N. 1971. Significance of the chemotherapeutic index in the treatment of schisto-
somiasis with antimony compounds. Bull. wHO 45:371.
Feil, A. 1939. Le role de l'antimonine en pathologic professionelle. Pr. Med. 47:1133.
Felicetti, S. A., R. G. Thomas, and R. O. McClellan. 1974. Metabolism of two valence
states of inhaled antimony in hamsters. Am. Ind. Hyg. Assoc. J. 35:292.
Fink, C. G., and A. H. Kopp. 1933. A rediscovered ancient Egyptian craft. Metrop. Mus.
Stud. 4:163.
Franz, G. 1937. Zur pathologischen Anatomie der Antimonvergiftung. Arch. Exp.
Pathol. Pharmakol. 186:661.
Gellhorn, A., N. A. Tupikova, and H. B. Van Dyke. 1946. Tissue distribution and
excretion of four organic antimonials after single or repeated administration to normal
hamsters. J. Pharmacol. 87:169.
Gocher, T. E. P. 1945. Antimony intoxication. Northwest Med., Seattle 44:92.
Goodwin, L. G. 1944. The toxicity and trypanocidal activity of some organic antimonials.
J. Pharmacol. 81:224.
Gross, P., J. H. Brown, and T. F. Hatch. l9S1. Experimental endogenous lipoid pneu-
monia. Am. J. Pathol. 57:690.
Hamilton, E. I., and M. J. Minski. 1972/1973. Abundance of the chemical elements in
man's diet and possible relations with environmental factors. Sci. Total Environ.
1:375.
Hamilton, E. I., M. J. Minski, and J. J. Cleary. 1972/1973. The concentration and
distribution of some stable elements in healthy human tissue from the United King-
dom (An environmental study). Sci. Total Environ. 1:341.
OCR for page 38
38 MINERAL TOLERANCE OF DOMESTIC ANIMALS
Khalil, B. M. 1931. The specific treatment of human schistosomiasis. Beih. Arch.
Schiffs-u. Trop. Hyg. 35:225.
Liebscher, K., and H. Smith. 1968. Essential and nonessential trace elements. A method
of determining whether an element is essential or nonessential in human tissue. Arch.
Environ. Health 17:881.
Mainzer, F., and M. Krause. 1940. Changes of the electrocardiogram during antimony
treatment. Trans. R. Soc. Trop. Med. Hyg. 33:405.
Mellor, J. W. 1939. Treatise on Inorganic and Theoretical Chemistry. vol. 9, p. 339.
Longmans Green, New York.
Ming-Hsin, H., C. Shaoh-Chi. P. Yu-Siu, and Y. Kuo-Yuei. 1958. Mechanism and treat-
ment of cardiac arrhythmias in tartar emetic intoxication. Chim. Med. 1. 76:103.
Molokhia, M. M., and H. Smith. 1967. Trace elements in the lung. Arch. Environ. Health
15:745.
Molokhia, M. M., and H. Smith. 1969. Tissue distribution of trivalent antimony in mice
infected with Schistosoma mansoni. Bull. WHO 40:123.
Monier-Williams, G. W. 1925. The solubility of glazes and enamels used in cooking
utensils. Analyst 50:133.
Monier-Williams, G. W. 1934. Antimony in Enamelled Hollow-Ware. Min. Health Rep.
Publ. Health Med. Subj. No. 73. H. M. Stationery Office, London.
Murthy, G. K., U. Rhea, and J. T. Peeler. 1971. Levels of antimony, cadmium, chro-
mium, cobalt, manganese, and zinc in institutional total diets. Environ. Sci. Technol.
5:436.
Nau, C. A., W. Andersen, and R. E. Cone. 1944. Arsine, stibine and HIS. Accidental
industrial poisoning by a mixture. Ind. Med. Surg. 13:308.
Nixon, G. S., H. D. Livingstone, and H. Smith. 1967. Estimation of antimony in human
enamel by activation analysis. Caries Res. 1:327.
Oelkers. H. A. 1937. Zur Pharmakologie des Antimons. Arch. Exp. Pathol. Pharmakol.
187:56.
Otto, G. F., T. H. Maren. and H. W. Brown. 1947. Blood levels and excretion rates of
antimony in persons receiving trivalent and pentavalent antimonials. Am. J. Hyg.
46:193.
Otto, G. F., and T. H. Maren. 1950. Studies on the chemotherapy of filariasis. VI. Studies
on the excretion and concentration of antimony in blood and other tissues following
the injection of trivalent and pentavalent antimonials into experimental animals. Am.
J.Hyg.51:370.
Pribyl, E. 1927. Nitrogen metabolism in experimental subacute arsenic and antimony
poisoning. J. Biol. Chem. 74:775.
Renes, L. E. 1953. Antimony poisoning in industry. Arch. Ind. Hyg. 7:99.
Rowland, H. A. K. 1968. StiJbokinetics I: Studies on mice with '24Sb-labelled sodium
antimony dimercaptosuccinate (astiban). Trans. R. Soc. Trop. Med. Hyg. 62:632.
Schroeder, H. A. 1973. Recondite toxicity of trace elements, pp. 107-199. In W. J.
Hayes, Jr., ed. Essays in Toxicology, vol. 4. Academic Press, New York.
Schroeder, H. A.' M. Mitchener. J. J. Balassa, M. Kanisawa, and A. P. Nason. 1968.
Zirconium, niobium, antimony and fluorine in mice: Effects on growth, survival and
tissue levels. J. Nutr. 95:95.
Schrumpf, P., and B. Zabel. 1910. Klinische und experimentelle Untersuchungen~uber
die Antimonvergiftung der Schriftsetzer. Arch. Exp. Pathol. Pharmakol. 63:242.
Seitz, A. 1924. Die Hygiene in Schrifftgiessereigewerbe. Arch. Hyg. 94:284.
Smith, H. 1967. ~e distribution of antimony, arsenic, copper and zinc in human tissue.
J. Forensic Sci. Soc. 7:97.
OCR for page 39
Antimony
39
Smith, R. E. 1947. Studies on the biological exchange of radio-antimony in animals and
man. Fed. Proc. 6:205.
Steele, J. M., F. J. Gerrard, and D. R. Matheson. 1!744. Gases as antimalarials. Effect of
stibine. U.S. Nav. Med. Res. Inst. Res. Prod. 10:150.
Stock, A., and O. Guttman. 1904. Uber den Antimonwassersto~und das gelbe Antimon.
Ber. Dtsch. Chem. Ges. 37:885.
Strong, R. P. 1942. In Still's Diagnosis, Prevention and Treatment of Tropical Diseases.
Blakiston, Philadelphia.
Tamnt, M. E., S. Wadley, and J. J. Woodage. 1971. The effect of penicillamine on the
treatment of experimental schistosomiasis with tartar emetic. Ann. Trop. Med. Para-
sitol. 6S:233.
Thomas, R. G., S. W. Felicetti, R. V. Lucchino, and R. O. McClellan. 1973. Retention
patterns of antimony in mice following inhalation of particles formed at different
temperatures. Proc. Sac. Exp. Biol. Med. 144:544.
Waitz, J. A., R. E. Ober, J. E. Musenhelder, and P. E. Thompson. 1965. Physiological
disposition of antimony after administration of i24Sb labelled tartar emetic to rats,
mice and monkeys and the effects of tris (p amino phenyl) carbonium palmoate on this
distribution. Bull. WHO 33:537.
Webster, S. H. 1946. Volatile hydrides of toxicological importance. J. Ind. Hyg. 28:167.
Wieland, M. 1937. Zur Pharmakologie des Antimons. Cited by Browning. 1969.
Representative terms from entire chapter:
antimony compounds
