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OCR for page 142
Chromium
The name for the element chromium (Cr) was derived from the Greek
designation for color because aB chromium compounds have color.
Chromium is a hard metal that takes a high polish. It is used in steel and
other alloys, in numerous industrial and chemical procedures, in paints
and dyes, and in the tanning industry. When electroplated, it pros
duces the hard, noncorrosive, lustrous surface commonly seen as
'~chrome" on many consumer items. Chromium is derived from the
ore, chromite (FeOCr2O3), by the reduction of the oxide with aluminum
(Chemical Rubber Co., 1971/19721. Use of this element in the United
States increased by 50 percent in the years 194~1968 and was esti-
mated at 1~/3 million tons in 1~8 (Knapp, 1971~. Reviews on chromium
include Underwood (1977) and the National Research Council (1974~.
ESSENTIALITY
Mertz (1967) and Schroeder (1968) have investigated the role of
chromium as an essential element for animals and concluded that chro-
mium (III) is required for normal carbohydrate and lipid metabolism, as
first suggested by Curran (1954~. In rats fed low-chromium diets in a
nearly chromium-free environment, severe impairment of glucose
tolerance was observed. The condition was particularly evident in older
breeding rats and was improved gradually by chromium supplemen-
tation (Mertz et al., 1965a,b). There was a higher requirement for
142
OCR for page 143
Chromium
143
chromium in human subjects with an impaired glucose tolerance test
(Mertz et al., 19771.
Life-term studies with mice and rats given 5 ppm chromium (III) in
drinking water showed increased growth over controls for both sexes
and decreased mortality of males (Schroeder et al., 1963a,b). Sub-
sequent life-term studies with mice, given 5 ppm chromium (VI) in
drinking water, showed slight weight decreases compared with
controls.
The inorganic salts of chromium also improve glucose tolerance
(Gurson and Saner, 19731. More information is needed on the biolog~-
cally active chem~c~ statefs) and physiological rolefs) of chromium. It
is possible that a deficiency, of this element may exist for species
ingesting highly purified diets and for animals in which stress has de-
pleted body stores. Supplementing laying hens with 10 ppm chromium
as CrCI3 for 28 days improved interior egg quality as measured by
Haugh units (Jensen et al., 19781.
METABOLISM
Chromium (III) is required for utilization of glucose in peripheral tis-
sues, acting in conjunction with insulin. The biologically active form of
chromium is called glucose tolerance factor (GTF). It is a small organic
molecule containing nicutin~c acid, glycine, glutamic acid, cysteine,
and chromium (Mertz et al., 1974; Mertz, l97S), but its exact structure
is not yet known. The content of chromium in the human body is known
to decrease throughout life (Schroeder et al., 1962), and evidence of
chromium (GTF) deficiency in adults has been obtained (Freund et al.,
1979~. The extent to which GTF deficiency occurs is unknown; however,
it is thought to be common in the elderly.
Absorption of orally administered chromium (III) is very low regard-
less of nutritional status and dosage (Mertz, 1967~; the major excretory
route of absorbed chromium is the urinary tract, although feces contain
some 5iCr activity following intravenous dosage with 5tCrCl3. Oral
administration of 5tCrCI3 to rats resulted in 5-10 percent absorption
within 5 minutes of stomach tubing, but chromium retained by the
animals decreased to less than 1 percent at 1 hour (Polansky and Ander-
son, 19781.
When Mertz et al. (1969) administered chromium (III) up to 250 ,uCi
as 5~CrCl3 · 6H2O to pregnant rats, either by stomach tube or intra-
venously, no activity was found in the young; but, with intragastric
administration of labeled chromic chloride incorporated into brewer's
OCR for page 144
144 MINERAL TOLERANCE OF DOMESTIC ANIMALS
yeast, the isotope was transported to the young at an average level of
20 percent of the dose administered to the mother. Diets high in natural
chromium also increased chromium levels in the young, while 2 ppm
chromium (IIT), as the acetate, in drinking water had no effect.
The greatest proportion of chromium QII) in tissues of rats 96 hours
after having been injected intravenously with 5~C<~3 was found in
kidney and spleen. Chromium QIT) was excreted mainly via urine
(Hopkins, 1965; Mathur and Doisy, 1972~. When Kraintz and Talmage
(1952) injected rats and rabbits with 5tC~3, the greatest concentration
was found in bone marrow. The chromium Q11) was associated closely
with ad serum proteins in rabbits 24 hours foBow~ng intravenous injec-
tion. Sukhacheva et al. (l 978) injected 0.05 mg of radioactive chromium
per rat as Na2Cr207 (chromium VI) and CrCI3 (chromium IlI). Chro-
m~um DII) and (VI) were accumulated in spleen but only the trivalent
form accumulated in liver. The blood clearance of chromium (VI) was
more rapid than that of chromium (IIT). Chromium (IlI) associated
closely with serum proteins, while chromium (VI) was bound to red
blood cells (Gray and Sterling, l9SO).
Chromium 0TI) as chromic oxide (Cr2O] has been used for several
decades as a fecal marker in digestibility and absorption studies in
many species: chicks (Dansky and Hill, 1952; Hill and Anderson, 1958),
rats (Schurch et al., 1950), sheep (Reid et al., 1950; Woolfolk et al.,
1950; Lassiter et al., 1966), and humans (Irwin and Crampton, 1951;
Whitby and Lang, 1960~. Fecal chromium recoveries have been vana-
ble, generally ranging between 90 and 100 percent. Radioactive
chromium has been a useful tagging agent in tracing the fate of river
waters to the sea, because it is not appreciably concentrated by river or
oceanic biota (Osterberg et al., 1965~.
SOURCES
Chromium is ubiquitous in water, soil, and living matter. Wide varia-
tion among concentrations reported may be due to differences in
analytical procedures, standards, and geographical locations. Values
for chromium in foods, flora, forage, and soil were given by Schroeder
et al. (1962), most of which were less than 100 ppb. The level of
chromium in feed grade phosphates ranged from 39 ppm in defluon-
nated phosphate to 128 ppm in dicalcium phosphate (unpublished data,
International Minerals and Chemical Corp., Libertyville, Ill.~.
Summarization of water analysis (National Research Council, 1974)
indicated a range of 1 to 112 ppb chromium with a mean of 8 ppb.
OCR for page 145
Chromium
145
Definition of the chemistry of naturally occurring chromium com-
plexes is incomplete, and information on the biological availability of
these compounds is limited. Naturally occurring complexed chromium,
however, appears to be better utilized than the inorganic salts (Mertz
e' al., 1%9~. The tnvalent and hexavalent forms of chromium are the
most stable and are encountered more commonly than is the divalent
state. Most of the chronic and dichromate compounds are soluble,
while chromates are highly insoluble. Of the three common valency
states IT, ITI, and VI—only the trivalent chromium forms octahedral
coordination complexes and polynuclear orated complexes by
hydrolysis in aqueous solution, decreasing solubility of the ion. Hexa-
valent chromium has acidic properties, does not form coordination
compounds, and is easily reduced to chromium (IlI); but it has also
been found in natural materials (Mertz, 1967~. Chromium (~) is also
rapidly converted to chromium QII).
TOXICOSIS
Because of their protein-precipitating and oxidizing properties,
chromium triox~de, chromates, and bichromates are potent proto-
plasm~c poisons, but chromic oxide, trivalent chromium salts, and
medic chromium are much less toxic (Pascale et at., 1952~. Chromium
toxicity has been reviewed by MacKenzie e' al. (1958~.
LOW LEVELS
Signs of chrome oral toxicosis of chromium ail, and chromium (VI)
differ among species. They consist primarily of skin contact dermatitis
and sores, irritation of respiratory passages, ulceration and perforation
of the nasal septum, and lung cancer.
The toxicity of chromium (III) when administered by the oral route
has been studied very little. No adverse effects (Table 14) were
observed in either mice or rats given 5 ppm chromium QII) as chromium
acetate in Winking water throughout their life (Schroeder et at., 1964,
196S). MacKenzie et al. (1958) gave both forms to rats in drinking water
for 1 year at levels up to 25 ppm. Tissue deposition of chromium
increased in liver, kidney, bone, and spleen, with the spleen con-
siderably higher in chromium content than the other three tissues when
chromium (VI) was administered. Physiological effects were not dif-
ferent at 0 to 11 ppm chromium. With an intake of 25 ppm, animals
receiving chromium (VI) showed tissue chromium contents 9 times
OCR for page 146
146 MINERAL TOLERANCE OF DOMESTIC ANIMALS
greater than those ingesting chromium (III) but with no adverse effects
on weight gain, food consumption, or pathology from either form of
chromium. Table 14 shows effects on young chicks of chromium in
poultry feeds. Chromium (III) at levels up to 500 ppm in water did not
adversely affect growth of rats and mice (Table 14), while 25 ppm
chromium (VI) decreased water consumption in rats. Growing rats fed
varying levels of Cr-nicotin~c acid complex up to 276 ppm chromium
exhibited no abnormalities after 20 weeks (Mertz, 1975; Mertz and
Rog~nski, 1975~.
HIGH LEVELS
-
Few cases of acute systemic intox~cation by chrom~um ingestion in man
or animals have been reported. The peso was 18 and 60 mg chromium
per kilogram of body weight, respectively, for chromium as chromalum
[KCr(SO4~2. 12H2O] and a chromium (III) nicotinic acid complex with
high GTF activity in rats injected intravenously (Mertz, l97S; Mertz and
Rog~nski, 1975~. The lethal single oral dose for chromium (VI) in young
rats was 130 mg/kg, while as much as 650 mg/kg body weight of chro-
m~um (III) produced no overt toxicosis (Sam~tz et al., 1962~. Garner's
Veterinary Toxicology (1967) has given the acute lethal dose of chro-
mate (VI) for mature cattle at around 700 mg/kg, while 30~0 mg/kg of
body weight produced chromium poisoning in young calves. Inflam-
mation and congestion of the stomach, ulceration of the rumen and
abomasum, and high blood and liver chromium levels were charac-
teristic findings. Chromium levels of 30 ppm in liver and 4 ppm in blood,
compared with normal levels of less than 2 ppm, were suggested as
indicative of chromium poisoning.
FACTORS AFFECI1NG TOXICITY
Hill and Matrone (1970) investigated the influence of CrCl3 6H2O,
chromium (ITI), in alleviating adverse effects of ammonium vanadate
fed to chicks at 0, 10, and 20 ppm added vanadium. At 20 ppm supple-
mentary vanadium, grown was depressed and morality was high.
Additions of chromium (III) at dietary levels of SOD, 1,000, and 2,000
ppm significantly alleviated both problems but did not completely over-
come vanadium toxicosis. Without added vanadium, 2,000 ppm chrm
mium (III) depressed growth, but mortality was unaffected. Levels of
500 and 1,000 ppm supplementary chromium (III) without added
vanadium produced no significant differences in chicks from those
receiving no added chromium or vanadium.
OCR for page 147
Chromium
. . .
TISSUE LEVELS
147
Generally, mammalian tissue concentrations range from 10 to several
hundred ppb (Mertz, 1967~. Chromium (VI) rarely occurs in biological
tissues. Schroeder et al. (1962) listed chromium concentrations on a
fresh weight basis of various animal and human tissues as 100 ppb or
less and found that tissue concentrations decrease with age except in
the lung. An intake of 25 ppm chromium (VI) increased tissue chro-
m~um levels 9 times that which was found when chromium (III) was fed.
MAXIMUM TOLERABLE LEVELS
Chromic oxide (Cr203) (III) has been used as a fecal marker in cattle
and sheep for periods of several weeks at levels as high as 3,000 ppm
chromium with no evidence of adverse effects. Chicks were fed 1,000
ppm chromium as chromic chloride (CrCl3) (III) without effect, but
2,000 ppm resulted in reduced growth.
Potassium chromate (K2CrO4) (VI) and sodium chromate (Na2CrO4)
(VI) have been fed to chicks at levels of 100 ppm with no adverse
effects. Tissue levels of chromium were increased in rats offered
7.7 ppm chromium in the water as potassium chromate, and decreased
water intake occurred with 25 ppm of the element in the water. Chromic
chloride had no effect on rats when offered as 25 ppm chromium in the
water.
Maximum tolerable dietary levels are set at 3,000 ppm chromium as
the oxide and 1,000 ppm as the chloride for domestic animals.
SUMMARY
Chromium (IIT) is essential in animal nutrition as a constituent of glu-
cose tolerance factor (GTF). The GTF organic complex is 50 times more
active biologically than inorganic chromium (III), while chromium (VI)
is rarely found in living systems. Chromium trioxide, chromates, and
bichromates are toxic due to their protein-precipitating and oxidizing
properties. Chronic chromium toxicosis results in skin contact derma-
titis, irritation of respiratory passages, ulceration and perforation of the
nasal septum, and lung cancer. Chromium (VI) compounds appear to
be more toxic than chromium (III) compounds. Acute systemic
chromium intoxication is rare but was produced with a single oral dose
OCR for page 148
148 MINERAL TOLERANCE OF DOMESTIC ANIMALS
of 700 mg~kg of body weight chromaum (VI) in mature cattle and 30~0
mg/lcg of body weight chromium (VI) in young calves. Signs of acute
toxicosis included inflammation and congestion of the stomach, ulcera-
don of the rumen and abomasum, and increased concentration of blood
and liver chromium.
OCR for page 149
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OCR for page 152
152 MINERAL TOLERANCE OF DOMESTIC ANIMALS
REFERENCES
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OCR for page 153
Chromium
153
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Schroeder, H. A., W. H. Vinton, Jr., and J. J. Balassa. 1963a. Effect of chromium,
cadmium and other trace metals on the growth and survival of mice. J. Nutr. 80:39.
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83:239.
Schroeder, H. A., J. J. Balassa, and W. H. Vinton, Jr. 1965. Chromium, cadmium and
lead in rats: Effects on life span, tumors and tissue levels. J. Nutr. 86:51.
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an index for detennining the digestibility of a diet. J. Nutr. 41:629.
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havior of trivalent and hexavalent chromium in rats. In M. Kirchgessner (ed.). Trace
Element Metabolism in Man and Animal 3, p. 268. Proc. 3rd. Int. Symp.
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demic Press, New York.
Whitby, L. G., and D. Lang. 1960. Experience w~th the chromic oxide method of fecal
marking in metabolic balance investigations on humans. J. Clin. Invest. 39:854.
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A comparison of fecal nitrogen excretion rate, chromium oxide and "chromagen(s)"
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Representative terms from entire chapter:
chromic oxide
