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OCR for page 71
Boron
Boron (B) is an amorphous, dark brown nonmetal. A native sodium
tetraborate is found in California, Nevada, Oregon, and Asia Minor
from which borax (Na2B4O7 · lOH2O) is prepared and from which boron
can be isolated. Boron also occurs in nature as colemanite
(Ca2B6O', 5H2O), boronatrocalcite (CaB4O7NaBO2 8H2O), and bo-
racite (Mg7Ci2B~60301. A small amount (0.003 percent) of boron in steel
increases its hardness and improves its mechanical properties when
quenched or drawn. Boron also strongly absorbs neutrons, and boron
steel is used in shielding and in controlling the operating rate of atomic
power plants. Calcium boride is used in deoxidation of copper-brass
bronze. Borax is used in the manufacture of glass, enamels, soap, sizing
for paper, and as a preservative for wood and meats. Boron carbide is
used as an abrasive, and boron hydrides (boranes) are used as high-
energy fuels. Borax and boric acid solutions have long been used as
mild antiseptics, and fused borax containing colored metal oxides may
be used for artificial gems or, when ground, as pigments.
ESSENTIALITY
Boron has been established as essential for higher plants for over 50
years, and this element is added frequently to fertilizers for plants with
high requirements such as alfalfa, apples, and certain root and cruci-
ferous crops (rutabaga, turnips, red beets, sugar beets, cabbage, and
71
OCR for page 72
72 MINERAL TOLERANCE OF DOMESTIC ANIMALS
cauliflower). Boron deficiencies in plants most often occur on light-
colored sands and silt loams in humid regions. Liming may somewhat
decrease boron bioavailability in soils, but this decrease is probably
related to the need by plant tissues of a specific calciu~boron ratio.
Purified diets containing 0.15 to 0.16 ppm boron have been used in an
attempt to induce boron deficiency in rats, but they grew and repro-
duced as wed as those receiving supplemental boron (Hove et al., 1939;
Orent-Keiles, 1941; Teresi et al., 19441. Earlier suggestions that
potassium-deficient rats would benefit from boron supplementation
were not supported by later investigations (Folks, 19471. If boron is
required by rats, dietary need must be below 0.15 ppm. In rats fed a diet
containing not more than 0.001 ppm boron, hepatic RNA synthesis was
stimulated by an intraperitoneal injection of 20 ,uM borate as boric acid
(Weser, 1967~.
METABOLISM
Boron in food or administered as soluble borate or boric acid is rapidly
and almost completely absorbed from the gastrointestinal tract. Ochs-
ner (1917) and Kahlenberg (1924) indicated that boron can be absorbed
through intact skin, but the amounts are apparently too slight to pro-
duce systemic toxicosis. However, toxic amounts can be absorbed
through damaged skin (Pfeiffer et al., 1945~. The application of a 5
percent solution of boric acid to normal skin of human subjects pro-
duced barely detectable levels of boron in the urine, while application
to granulated wounds or burns produced prompt urinary boron excre-
tion. Cope (1943) found 2.0 to 2.5 g of boron at necropsy in some
patients treated for severe burns with saturated boric acid solution, and
there have been reports of toxicosis and death following absorption
from open skin lesions (Witthaus, 19111. The boron hydrides (boranes)
may be absorbed from the lungs and are highly toxic.
The main excretory pathway for boron is via the urine (Kent and
McCance, 1941; Owen, 1944; Tipton et al., 1966~.
SOURCES
The average boron concentration in the earth's crust is about 10 ppm,
with most soils ranging from 7 to 80 ppm (Krauskopf, 1972~. Among
plants, monocotyledons generally contain less boron than dicotyle-
dons. Boron deficiency is seen in a wide variety of plants when vegeta-
OCR for page 73
Boron
73
tive dry matter boron concentrations are less than 15 ppm. Adequate
but not excessive boron concentrations range from 20 to 100 ppm in the
dry matter. Boron toxicosis in plants occurs usually when dry tissue
concentrations of boron exceed 200 ppm. Neubert et al. (1969) have
published boron values for 24 crops and Bradford (1966) for 55 crops.
Zook and Lehmann (1968) analyzed tropical and subtropical fruits and
found that avocados had the highest boron concentration (7-10 ppm,
fresh basis), followed by stone fruits (1.~3.5 ppm), and pome and
citrus fruits and berries (0.~2.4 ppm). Cereal grains contain about 1 to
5 ppm boron (Beeson, 1941~. Animal muscle and organ concentrations
range mostly between 0.5 and 1.5 ppm (dry basis). Bone concentrations
are several times higher (Underwood, 1977~. Cow's milk normally con-
tains 0.5 to 1.0 ppm boron when fed diets containing 16 to 34
ppm boron with little variation associated with breed or stage of lacta-
tion (Hove et al., 1939; Owen, 19441. The World Health Organization
(1973) has calculated daily boron intakes of Aus~ian infants (0 6 mo)
from cow's milk to be 0.4 to 0.85 ma. A representative U.S. diet for
adults was calculated to provide 3 mg of boron per day, although
estimated boron intakes of adult humans around the world vary from
0.3 to 41.0 mg due to geographical differences (Schiettwein-Gsell and
Mommsen-Straub, 1973~.
The U.S. Department of the Interior has established an upper limit
for boron in public water supplies at 1 ppm (Bradford, 1971), and the
Environmental Protection Agency (1973) has proposed 5 ppm boron as
the allowable maximum in water for livestock. However, Green and
Weeth (1977) have found water boron concentrations in Nevada rang-
ing from 0.2 ppm in the Humboldt River to 80 ppm at Borax Flat. Most
water samples were above 1 ppm, and a number exceeded 5 ppm.
A child consuming milk containing approximately 0.7 g boric acid per
liter developed coeliac diseaselike symptoms (Forsyth, 19191. Human
burn patients who were treated topically wad saturated bone acid
solution accumulated up to 2.~2.5 g boron in their bodies (Cope, 19431.
Industrial poisoning from the "oxygen-bonded'' salts of boron has not
been reported. However, the boron hydrides (boranes) are highly toxic
and constitute a significant industrial hazard. Diborane, decaborane,
and pentaborane are most frequently encountered. These are used
chiefly as high-energy fuels, and decaborane has also been used as a
vulcanizer of rubber instead of sulfur (Browning, 1969~. Diborane
(B2H6) is a gas with a nauseating odor; decaborane (B,~H,4) is a solid
with an intense, bitter, chocolatelike odor; and pentaborane (B5Hg) is
a volatile liquid with a sweetish odor.
OCR for page 74
74 MINERAL TOLERANCE OF DOMESTIC ANIMALS
TOXICOSIS
LOW LEVELS
Oral
Little quantitative information defining chronic intake limits for boron
is available. Browning (1969) stated that 0.25 percent boric acid (437
ppm boron) in drinking water inhibited growth in animals but produced
no detected changes in the blood nor observable lesions at necropsy.
Green and Weeth (1977) conducted a study with Hereford heifers fed
grass hay (38 ppm boron) and water to which boron (as borax) had been
added at venous concentrations. They suggested that water containing
less than 29 ppm boron would not be discnm~nated against, while in the
range of 29 to 95 ppm, cattle would show preference for water win
lower boron concentrations. Consumption of 150 or 300 ppm boron in
water for 30 days produced inflammation and edema in the legs and
around the dew claws and decreased hay consumption, gain, hematm
cnt, and hemoglobin concentrations. Lethargy and occasional diarrhea
was seen in heifers consuming the higher level. Plasma boron concen-
trations were 0.53 ppm on control water (0.S ppm boron) and 11.2 and
18.9 ppm on water containing 150 and 300 ppm boron, respectively.
Dirty, 67, and 69 percent of the total daily boron intake on these three
respective treatments was excreted in Me urine. GIomerular filtration
rate and osmolal clearance were unaffected by the high boron levels,
but a relative diuresis was indicated by modifications in free water
clearance. Unnary phosphate excretion was decreased.
Green et al. (1973) concluded that 75 ppm boron in drinking water did
not affect growth or reproduction in rats. When boron concentrations
exceeded 150 ppm, these workers reported reduced body size, con-
tinued prepubescent fur, lack of incisor pigmentation, asperses, and
impaired ovarian development.
Prolonged consumption of small amounts of boric acid by human
beings has been reported by Browning (1969) to lead to maid gastro-
intestina] imtation, anorexia, disturbed digestion, nausea, emesis, and
an erythematous rash. As in the case reported by Sanders (1912), this
rash may be firm to the touch with a tendency to become purpunc. One
case of coeliac diseaselike symptoms has been reported (Forsyth, 1919)
in a child fed milk containing about 0.7 g of bone acid per liter. Medic-
inal use of bone acid and borax for babies has resulted in anorexia,
nausea, emesis, diarrhea, marked cardiac weakness, and a red papular
eruption over the entire body (British Medical Association, 1966~.
OCR for page 75
Boron
75
Inhalafion
Repeated exposure of rats to 20 ppm of decaborane in air for 6 hours
a day, 5 days a week, produced nervousness, restlessness, loss of
weight, unsteadiness, a tendency to belligerency, tremors of the head,
and convulsions (Svirbely, 1954b). Repeated exposure of rats and mice
to about 3 ppm of pentaborane in air procluced a similar but more
marked neurological effect, particularly with respect to belligerency.
The symptoms of human exposure to diborane (Lowe and Freeman,
1957; Cardasco et al., 1962) included pulmonary imitation, chest tight-
ness, dyspnea, nonproductive cough and wheezing, pneumonia, head-
ache, vertigo, chills, fatigue, and muscular weakness. Increased blood
nonprotein nitrogen concentrations and positive cephalin flocculation
tests were also seen.
Mild exposure to decaborane resulted in headache, nausea, dizzi-
ness, and drowsiness (Lowe and Freeman, 1957~. Exposure to penta-
borane produced headache, dizziness, often hiccups, and nervousness.
Drowsiness and nausea were sometimes experienced initially. Muscu-
lar pain and cramps were common. Liver and kidney damage were
evident as illustrated by abno~al liver function tests and elevated
blood nonprotein nitrogen and urea levels.
Maximum allowable air concentrations have been set at 0.1 ppm for
diborane, 0.5 ppm for decaborane, and 0.01 ppm for pentaborane
(Browning, 1969~.
HIGH LEVELS
Oral
The lethal dose of boric acid varies according to the species. In animals
it has been reported (Pfeifferet al., 1945) to range from 1.2 to 3.45 g (210
to 603 mg boron) per kilogram of body weight, and death is due to
central nervous paralysis and gastrointestinal irritation (Buzzo and
Ceratola, 1932~. In human adults, the single toxic dose of boric acid has
been reported to vary from 20 to 45 g (Potter, 1921~. Infant deaths have
been reported from single feedings of saturated boric acid solutions
containing 1 to 6 g (McNally and Rust, 1928; Young e! al., 1949~. Initial
symptoms include nausea, emesis (sometimes with blood), abdominal
pain, and diarrhea. A generalized erythematous rash, or even exfolia-
tion, may follow. In severe cases, shock with low blood pressure,
tachycardia, and cyanosis may be seen. Death appears due to central
nervous system depression. Necropsy signs include cloudy swelling of
the kidneys, centrolobular hepatic necrosis, and hemorrhagic enteritis.
OCR for page 76
76 MINERAL TOLERANCE OF DOMESTIC ANIMALS
Inhalation
The ~D50 of diborane for rats is about 50 ppm (WilIs, 1953~. Earliest signs
of nonlethal exposure include respiratory embarrassment, followed by
a slight fall in blood pressure, increased intestinal contraction, initial
stimulation, and subsequent depression of the cerebral cortex, brady-
cardia, and ventricular fibrillation. Stumpe (1960) exposed golden
hamsters to 5~00 ppm of diborane and found mean survival time
decreased with increasing concentration. .
The LD50 of decaborane for mice (exposed 4 hours) was about 36 ppm
(Svirbely, 1954a). Rats were initially resistant to this level, but upon
further exposure the ~D50 was found to range from 32 to 84 ppm. Prin-
cipal signs included restlessness, depressed respiration, incoordina-
tion, weakness, spasmodic movements, convulsions, and corneal
opacities. Decaborane inhaled by dogs led to bradycardia and periods
of moderate hypertension preceding the terminal fall in blood pressure
(Walton et al., 1955~.
The Ado of pentaborane for mice (exposed 4 hours) was about 11 ppm
and about 18 ppm for rats. Acute neurotoxicosis was evident, and signs
included restlessness, tremors, spasms, and convulsions. Corneal
opacities were seen at necropsy.
Acute human intoxication following exposure to boron hydrides was
first reported by Rozendaal (1951~. At that time it was not known which
compounds were responsible, and some affected individuals were ex-
posed to at least diborane and pentaborane. Symptoms reported in-
cluded generalized muscular cramps, mental confusion, disorientation,
loss of memory, exhaustion, shortness of breath, chills, fever, and
· -
spasmoc 1C SelZUreS.
injection
Walton et al. (1955) administered decaborane to dogs by subcutaneous,
intraperitoneal, or intravenous injection and produced toxicosis. Intra-
venous injection produced an epinephrinelike response, while all routes
of administration resulted in signs like those from high-level inhalation.
Decaborane (30 mg/kg of body weight) in corn oil was injected intra-
peritoneally into rabbits by Merritt et al. (1964~. Increased irritability,
then lethargy, and f~nally loss of response to sensory stimuli developed
over a 3- to ~hour interval. All rabbits died in less than 24 hours. Cole
et al. (1954) found that mice injected with suspensions of decaborane in
alcohol or gelatin, or with aqueous sodium bicarbonate solutions of
decaborane, were most severely affected by the alcohol suspension.
OCR for page 77
Boron
TOPICAL ABSORPTION
77
Pfeiffer et al. (1945) reported that the application of a 5 percent solution
of boric acid to damaged skin can result in systemic toxicosis. As much
as 2.0 to 2.5 g were found at necropsy by Cope (1943) in patients treated
for severe burns with saturated boric acid solution.
FACTORS INFLUENCING TOXICITY
Boric acid applied to intact skin will not be absorbed sufficiently to
cause systemic toxicosis, while such application to damaged skin may
result in intoxication and death. The boranes are appreciably more
toxic than boric acid or soluble berates, and pentaborane is the most
hazardous of all. The central nervous system toxicosis of decabotane
was most pronounced in rabbits, intermediate in rats, and least in dogs.
THERAPY
Removal from exposure is important. Hill and Svirbely (1954) found
that protection from decaborane vapors could be sustained for several
hours by a conventional chemical cartridge respirator filled with silica
gel. Acute diborane intoxication has been treated by Cardasco et al.
(1962) by oxygen or intermittent positive pressure breathing. Chronic
cases were also treated with bronco-dilators and expectorants. Merritt
(1965) has recommended methylene blue for decaborane poisoning on
the basis of its oxidizing effect, which counters the reducing potential
of boron hydrides. Cole et al. (195.4) reported a favorable response to
methylene blue when a bicarbonate solution of decaborane had been
administered intravenously to mice. However, the toxicosis resulting
from intravenous administration of an alcoholic suspension of deca-
borane yielded best to a combination of atrolactam'4e and sodium
lactate.
TISSUE LEVELS
Boron concentrations in most soft animal tissues range from 0.5 to 1.5
ppm (dry basis) and severalfold higher in bones. Hamilton et al.
(1972/1973) reported the following mean boron concentrations (parts
per million wet basis) in human tissues: blood, 0.4; liver, 0.2; kidney,
0.6; muscle, 0.1; brain, 0.06; testis, 0.09; lung, 0.6; and lymph nodes,
0.6. Human ribs from hard water areas in England contained 10.2 ppm
OCR for page 78
78 MINERAL TOLERANCE OF DOMESTIC ANIMALS
boron in the ash, while ribs from soft water areas contained 6.2 ppm
boron in the ash. Human dental enamel contained 0.5 to 69.0 ppm boron
(dry basis) with a mean of 18.2 ppm (Losee et al., 19731. Ingestion of
large amounts of bone acid increased tissue boron levels, particularly
those in the brain (Pfeiffer e' al., 1945~.
The boron concentration of cow's milk normally ranges from 0.5 to
1.0 ppm (Hove et al., 1939; Owen, 1944), but these values can be
altered by dietary boron intake. Owen (1944) increased Nick boron
concentration from 0.7 to over 3.0 ppm by adding 20.0 g of borax (3.5
g boron) daily to the cow's diet.
Green and Weeth (1977) fed Hereford heifers grass hay containing
38.3 ppm boron and water containing 0.S ppm boron, or water contain-
ing 150 or 300 ppm boron (added as borax). The three levels of boron
in water produced the following respective levels of boron in plasma
(milligrams per deciliter): 0.05, 1.12, or 1.89. Total daily boron intakes
were 0.7, 15.3, or 26.0 mg/kg of body weight, respectively. Daily un-
nary boron excretion was 0.2, 10.3, or 17.9 mg/kg of body weight,
respectively.
MAXIMUM TOLERABLE LEVELS
Boron has been added to lactating dairy cattle diets at 145 to 157 ppm
(in the form of borax) with no adverse effects (Owen, 1944~. Additions
of 150 ppm to water consumed by yearling cattle decreased feed con-
sumption and produced weight loss, edema, and inflammation of the
legs (Green and Weeth, 1977~. Both studies were short term (42 and 30
d, respectively). Based on these limited experimental data with cattle
and field experience with high-boron water, a maximum tolerable level
of 150 ppm boron (as borax) in the dry diet of cattle is suggested.
Extrapolation of this level to other species seems reasonable, based on
data with laboratory animals.
SUMMARY
Boron is a dark brown, nonmetal that occurs in nature as borax, cole-
man~te, boronatrocalcite, and boracite. It is used (in a variety of forms)
to harden steel, to absorb neutrons in atomic energy plants, in deoxida-
tion of bronze, in the manufacture of glass and porcelain enamels, as a
fire-proofing agent, in pharmaceuticals, and as high-energy fuel. Ani-
mal toxicosis is primarily an experimental phenomenon, although live-
OCR for page 79
Boron 79
stock in certain regions may be exposed to high-boron water (up to 80
ppm) that has not been shown to be toxic. Toxicosis in humans has
resulted from ingestion of boric acid or borax solutions, topical applica-
tion of boric acid solutions to burn-damaged skin, and inhalation of
boranes. Symptoms of illness include anorexia, nausea, emesis, diar-
rhea, cardiac weakness, and an erythematous rash when the toxicosis
results from bone acid or borax. Borane toxicosis by inhalation causes
pulmonary initation, dyspnea, pneumonia, headache, vertigo, nausea,
muscular pain, impaired cardiac function, and central nervous system
depression.
Boron is required by plants, but it has no known function in animals.
OCR for page 80
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OCR for page 82
82 MINERAL TOLERANCE OF DOMESTIC ANIMALS
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t
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OCR for page 83
Boron
83
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Representative terms from entire chapter:
ppm boron
