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OCR for page 40
Arsenic
Arsenic (As) is a solid, brittle nonmetal, tin-white to steel-gray in color,
with a metallic luster. It is found usually combined in the minerals
orpiment and realgar (natural sulfides), arsenolite, arsenopyrite, cobalt-
ite, and niccolite. Arsenic occurs in tri- or pentavalent states, with
arsenic trioxide (AS2O3) the most common compound. In the United
States arsenic trioxide or white arsenic is produced principally as a
by-product of copper and lead smelting and in the recovery of other
metals such as gold and silver. White arsenic is used for manufacturing
calcium and lead arsenate insecticides, wood preservatives, and herbi-
cides and is the starting material for almost all organic and inorganic
arsenic compounds (Lansche, 1965~. Arsenic is widely distributed in
the biosphere. In areas near smelters and refineries, arsenic contamina-
tion of soil and herbage is quite common (Lillie, 19701. Addition of 0.01
percent organic arsenic compounds to diets for growing swine has been
shown to increase average daily gain and improve feed efficiency
(Carpenter, 1951~. Several reviews on arsenic are available (Frost,
1953; NRC, 1977; Underwood, 19774.
ESSENTIALITY
Schroeder and Balassa (1966) fed arsenic to rats and mice at 0.053 ppm
over long periods and noted normal growth and development. They
concluded that if arsenic is an essential trace element for these animals,
40
OCR for page 41
Arsenic
41
requirements are of the order of 1.0 mg per rat daily or less. There have
been reports on the improved appearance of skin and hair of mice, rats,
and horses supplemented with arsenic (Sollman, 1953; Schroeder and
Balassa, 1966~. Nielsen et al. (1975) maintained rats on diets with 0.030
ppm (air dry basis) and found a rough hair coat, decreased growth,
decreased hematocrits, and enlarged spleens when compared to
controls receiving 4.5 ppm arsenic. Anke et al. (1977) observed defi-
ciency signs in goats and minipigs fed less than 50 ppb arsenic, in-
cluding impaired reproductive performance, decreased birth weights,
increased neonatal mortality, and lower weight gains in second-
generation animals.
Chicks fed 15 to 25 ppb arsenic for 4 weeks weighed less than con-
trols supplemented with 1 ppm additional arsenic (Nielsen and Shuler,
1978~. Neonatal mortality in rats was decreased with arsenic supple-
mentation (Nielsen e' al., 1977~.
The beneficial effects of various organic arsenicals on growth, health,
and feed efficiency of poultry and swine have been reviewed by Frost
(1953, 1967) and Frost et at. (1955~. Arsanilic acid, 4-nitrophenylarsonic
acid, 3-nitro-4-hydroxyphenylarsonic acid, and phenylarsenoxide have
been found to be valuable in animal production. The phenylarsenoxides
are more potent as coccidiostats than arsenic acids, but only the arson-
ic acids are recognized as growth stimulants for swine and poultry
(Frost et al., 19551. The precise mechanism of action is unknown but
closely resembles that of antibiotics and is to some extent comple-
mentary to them (Underwood, 19771. Addition of 0.01 percent
3-nitro-4-hydroxyphenylarsonic acid to the diet of growing swine
(12.7 kg) increased the average daily gain from 0.20 to 0.33 kg and
improved feed efficiency by 6.3 percent (Carpenter, 19511.
METABOLISM
Arsenic in the forms in which it usually occurs in foods is readily
absorbed and rapidly excreted, mainly via the urine (Coulson et al.,
1935~. Less than 10 percent of the usual soluble forms of arsenic appear
in the feces. Inorganic arsenic ingested as arsenic trioxide (As2O3) is
also well absorbed but has a longer retention period in tissues and is
excreted almost equally in the feces and urine in man and in the rat
(Coulson et al., 1935; Overby and Frederickson, 19631. Organic arsenic
compounds (arsanilic acid) are well absorbed and deposited in tissues
of swine and chickens at levels proportional to the dietary level. Organ-
ic arsenic is removed rapidly from tissues and excreted mostly in the
OCR for page 42
42 MINERAL TOLERANCE OF DOMESTIC ANIMALS
feces (Frost et al., 1955; Hanson et al., 1955; Overby and Frost, 1960;
Overby and Frederickson, 1963~.
The toxicity of arsenic varies with the species of animal, valence of
the compound, solubility, route of exposure, and absorption and excre-
tion rates. No forms of the element accumulate in tissues; some are
simply excreted more rapidly than others (Frost, 19671.
A recent report (Lakso and Peoples, 1975) showed that ingested
inorganic arsenate (Na2HAsO4 · 2H2O) and arsenite (HAs02) could be
methylated in vivo by both the ruminant (cow) and nonruminant (dog)
and that the methylated arsenic found in the urine is not necessarily due
to its ingestion as such in plant material.
An "organic" form of arsenic was found in muscle and liver of fish
following oral or parenteral administration of radioactive arsenic as
sodium arsenate. The conversion appeared to be endogenous and a
result of action by intestinal microflora (Penrose, 1975~. Biomethyla-
tion of metal ions capable of redox activity can occur by way of methyl
vitamin BE or methyl iodine (Wood, 1975~. Arsenicals appear to be
oxidized in vivo from trivalent to pentavalent, but the reverse does not
occur (Overby and Frederickson, 1963~.
Studies on tissue accumulation and excretion of 76As injected as
sodium arsenite have shown wide species differences (Hunter et al.,
1942; Ducoffet al., 19481. Greatest arsenic concentrations in all animals
were found generally in liver, kidney, spleen, and lung (Frost, 1953~. In
rats, unlike other species studied, arsenic was concentrated in the
blood and retained apparently in bound form.
SOURCES
Arsenic occurs in normal soils at levels ranging from 1 to 40 ppm, but
higher levels can result from the extensive use of arsenical sprays for
control of insects and weeds. Most fruits, vegetables, cereal grains,
meat, and dairy products contain less than 0.5 ppm and rarely exceed
1 ppm (fresh basis), but this level can increase due to contamination
(Underwood, 1977~.
The arsenic concentration in seawater ranges from 2 to 5 ppb
(Schroeder and Balassa, 1966~. The arsenic content of commercial fish-
meals used in livestock production ranged from 2.6 to 9.1 ppm (air dry
basis) (Lunde, 1968~. The arsenic contents of fish and crustaceans on
a fresh weight basis are as follows: freshwater fish, 0.75 ppm (average
for 15 species) (Ellis et ai., 1941~; cod, eel, and mackerel, 1.5~. 1 ppm
OCR for page 43
Arsenic
43
(Holmes and Remington, 1934~; shellfish and crustaceans, ~174 ppm
(Chapman, 1926~.
Sheep and cattle do not find arsenic distasteful and, in fact, may
develop a taste for it (Clarke and Clarke, 19751. Ruminants were re-
ported to graze selectively contaminated forage.
TOXICOSIS
Many reviews on arsenic toxicosis are available (Vallee et al., 1960;
Buchanan, 1962; Albert, 1965; Hammond, 1965; Schroeder and
Balassa, 1966; Fowler and Weissberg, 1974; Clarke and Clarke, 1975;
Ammerman et al., 19771. Arsenicals differ widely in their toxicity.
Trivalent arsenicals, which specifically block lipoate-dependent en-
zymes, are generally more toxic than pentavalent arsenicals (Frost,
1967).
Arsenic also appears to exert a toxic action by attachment to sulfhy-
dry! groups of protein. The attachment is loose enough that compounds
with sulfLydryl groups with greater affinity for arsenic can withdraw
the tissue arsenic for urinary excretion.
Generally, inorganic arsenicals are more toxic than the organic
forms. Factors such as absorption into cells, rate of oxidation, rate of
elimination, etc., vary with circumstances, and most generalizations
concerning arsenicals have important exceptions (Frost, 19671. Degree
of toxicity in ruminants is variable and may depend on route of expo-
sure, animal age, nutritional status, and duration of exposure (Case,
1974; Selby et al., 1974~.
LOW LEVELS
Chronic toxicosis due to arsenic is seldom reported, but Selby et-al.
(1974) noted that chronic arsenic administration resulted in an improve-
ment in the appearance of the hair of cattle. With arsenic withdrawal,
the improvement in hair coat was lost and animals appeared unthrifty,
lost weight, and had inflamed eyes. Other signs of arsenic intoxication
include inflamed mucous membranes of the upper respiratory tract,
diarrhea, cachexia, eczema, and incoordination of gait.
The recommended growth promotant level of arsanilic acid in the diet
for swine is about 100 ppm of the compound. When 10 times this level
was fed to swine for 20 days (Ledet et al., 1973), severe posterior
paresis or quadriplegic was observed in several animals by day 15. The
OCR for page 44
44 MINERAL TOLERANCE OF DOMESTIC ANIMALS
tissue arsenic levels were correlated with time on the diet, and periph-
eral nerve tissue had an affinity for arsenic. Carpenter (1951) reported
3-nitro-4-hydroxyphenylarsonic acid to be toxic to swine when fed at a
level of 0.02 percent of the tote] ration for 2 - weeks. This toxicosis was
characterized by stiffness of the hind legs.
In chronic studies with rats, Franke and Motion (1937) found 50 ppm
of dietary arsenic, as Na2HAs03, were slightly toxic. Arsanilic acid at
70 ppm arsenic was well tolerated by growing rats (Frost, 19531. Rats
had increased levels of tissue arsenic when fed diets containing 16 ppm
arsenic, as AS203, or protein-bound arsenic in turkey liver derived from
an organic pentavalent arsenical (Morgareidge, 1963~.
HIGH LEVELS
Arsenic poisoning is commonly an acute clinical syndrome and death
usually occurs so rapidly that preceding illness, if observed, is of a few
days' duration. The signs of inorganic arsenic toxicosis vary with the
quantity and method of administration. The usual signs displayed by
cattle that have been dipped in solutions containing excessive arsenic
include colicky pain, vomiting, diarrhea, marked depression, and der-
matitis usually due to increased capillary permeability and cellular ne-
crosis. The time until onset and severity are governed by the amount of
arsenic absorbed through the skin (Kinsley, 1929~. Signs of acute inges-
tion toxicosis are similar; however, skin lesions are rarely present. The
lesions at necropsy of acute cases include gastroenteritis, glomerular
nephritis, and, frequently, dermatitis. Acute signs in horses are cere-
bral involvement and signs of intense pain with head banging (Lillie,
1970).
Animals may survive a high single oral dose that can be toxic with a
short period of repeated exposures, although it has been suggested that
tolerances of low oral doses may be increased by repeated dosage
(Clarke and Clarke, 19751. Following a single oral dose, almost all of the
administered arsenic is excreted within a few days. Ruminants that
survive arsenic intoxication by a single dose should be withheld from
market for 2 weeks and for 6 weeks following multiple dosage (Selby et
al., 19741. Swine and poultry that have received arsenic as a growth
promotant must be held 5 days following withdrawal before slaughter
for market (AAFCO, 19781.
Most nonruminants are more susceptible to intoxication than are
ruminants or horses. Arsanilic acid is the least toxic of the arsenicals
investigated. The fatal dose for horses and cows was 300 grains
(approximately 40 mg/kg of body weight) arsenic per day, as contrasted
OCR for page 45
Arsenic
45
with 4 8 grains (approximately ~12 mg/l~g of body weight) for sheep.
Horses and cattle could ingest 2~30 grains (2.66 to 4 mg/kg of body
weight) arsenic daily continuously with no apparent ill effects (Reives,
1925~. The oral Also of arsanilic acid and 3-nitro~hydroxy-
phenylarsonic acid in rats was about 800 and 100 mg of arsenic per
kilogram of body weight, respectively (Frost, 19531.
FACTORS INFLUENCING TOXICITY
Arsenic salts were effective in counteracting selenium toxicity (see
section on selenium) in poultry (Thapar et al., 1969) and in rats (Hend-
rick et al., 1953; Olson et al., 19631. The latter authors measured ex-
haled selenide and concluded that arsenic had no effect, however, on
selenide excretion with low levels of selenium. Muth et al. (1971) re-
ported that 1 ppm dietary arsenic as sodium arsenate in selenium-
deficient diets for ewes reduced incidence of myopathy in the lambs but
that 0.1 ppm arsenic was not protective. Arsenic decreased the reten-
tion of selenium in the liver and also decreased the elimination of
selenium via the volatilization pathway thus increasing the excretion of
selenium into the gut (Levander, 1971~.
TISSUE LEVELS
A period of about 6 weeks is necessary to deplete body tissues of
arsenic when animals have been exposed repeatedly to excessive levels
of the element over a long period of time (Selby et al., 1974~. Arsenic
levels are higher in skin, hair, liver, kidney, and spleen than in other
tissues of intoxicated ruminants.
In cattle poisoned under field conditions (Reagor, 1973), liver levels
were 3.5 to 60.4 ppm (dry weight). Liver arsenic levels were 27 ppm
(dry weight) in dead steers that had consumed about 300 mg arsenic
per day as MSMA (monosodium acid methanearsonate) for 7 days
(Dickinson, 19721. Muscle arsenic averaged 8.8 ppm (dry weight) in
these acutely poisoned cattle. Cattle that had consumed 1.25 ppm die-
tary arsenic for 8 weeks had muscle arsenic levels of 0.2 ppm (dry
weight) and all tissue concentrations tested were 1 ppm arsenic or less
(Peoples, 19641.
Cows consuming 18 ppm arsenic (40 mg per head daily) as dried
manure from poultry that had received 3-nitro4-hydroxyphenylarsonic
acid had no arsenic residue in milk after 5 days on the diet (Calvert and
Smith, 19721. When arsanilic acid or the above arsenic compound was
OCR for page 46
46 MINERAL TOLERANCE OF DOMESTIC ANIMALS
administered by gelatin capsule in amounts of 0, 1.6, or 3.2 mg arsenic
per kilogram of body weight to cows for 5 days, milk arsenic increased
from 0.015 to 0.026 ppm for arsanilic acid only at the highest level. No
changes in milk were found with the other treatments. Jersey cows fed
0, 0.026, 0.015, or 0.103 mg arsenic per kilogram of body weight as lead
arsenate for 126 days all had milk arsenic levels below 0.0S ppm
(Marshall et al., 1963~.
Overby and Frederickson (1963) reported that muscle arsenic levels
were lower for animals that had received organic arsenic than for the
inorganic forties. The arsenic content of spleen, kidneys, and muscle of
cattle ranged between 2.4 to 9.3 ppm (dry weight) when exposed to
contaminated pasture containing 3 to 227 ppm arsenic on a dry weight
basis (Lillie, 1970~.
MAXIMUM TOLERABLE LEVELS
Arsenic-conta~ning compounds differ widely in their toxicity with the
inorganic forms being more toxic than the organic forms (Table 5~. This
has been observed more from the standpoint of acute arsenic toxicosis,
since chronic cases are seldom seen. Arsenic, as lead arsenate, at a
level of 4.68 mg/kg of body weight (approximately 200 ppm dietary
arsenic) was fed to cows without adverse effect. Potassium arsenite
was tolerated at a level of 285 ppm arsenic by swine but caused de-
creased feed consumption and weight loss at a level of 570 ppm.
Arsanilic acid has been fed to swine and poultry at 100 ppm to
increase animal performance, and 1,000 ppm of this compound have
been tolerated in several studies without adverse effect.
Although there are suggested differences in tolerance to arsenic
among species, the maximum tolerable dietary levels are set at 50 ppm
for inorganic forms and 100 ppm for organic forms of arsenic for do-
mestic animals.
SUMMARY
Arsenic is widely distributed in the biosphere and can be a major source
of contamination for livestock in areas surrounding smelters and where
arsenicals are used to control weeds and insects. Fish and crustaceans
have unusually high levels of arsenic and may represent a source of
increased intake of the element where fishmeal products are fed. Several
organic arsenicals are recognized as growth stimulants for swine and
OCR for page 47
Arsenic
47
poultry, and they also act as coccidiostats. Their mechanism of action
as a growth stimulant resembles that of the antibiotics. Organic arid
inorganic arsenicals differ greatly in their toxic level, metabolism, and
excretion. Trivalent arsenicals specifically block lipoate-dependent en-
zymes and are more toxic than pentavalent forms. Arsenic also appears
to exert a toxic action by attachment to sulihydry} groups of protein.
Arsenic poisoning is frequently an acute clinical syndrome, and death
usually occurs so rapidly that preceding illness is of only a few days
duration. The signs vary with quantity and method of administration
but usually include colicky pain, diarrhea, depression, gIomerular
nephritis, and dermatitis usually due to increased capillary permeability
and cellular necrosis.
TABLE 5 Largest Single Oral Dose of Organic
Arsenic Compounds Tolerated by Different Speciesa
Source
Phenylarsonic acid
Arsenosoaniline
Arsanilic acid
Dodecylamine p-chlorophenylarsonate c 100
3-Nitro~hydroxyphenylarsonic acid 20
~Nitrophenylarsonic acid 75
a Frost et al., 1955; dose expressed as milligrams of arsenic-
containing compound.
~ Doses resulting in no mortality or less than 10 percent mortality.
c Adult rats weighing 100 to 150 g were used.
~ Chickens weighing 1,130 to 1,360 g were used.
e Maximum tolerated single dose for ducks weighing approximately
1,130g.
Rat, Chicken, Duck,
m&Qcg6.c mg/kg. d mge
10 35
25 35
400 300~00 1,000
100
100 < 100
<100
OCR for page 48
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OCR for page 51
Arsenic
REFERENCES
51
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OCR for page 52
52 MINERAL TOLERANCE OF DOMESTIC ANIMALS
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Representative terms from entire chapter:
ppm arsenic
