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OCR for page 84
Bromine
Bromine (Br) is the only nonmetallic element that is a liquid at ambient
temperature and pressure. As summarized by Standen (1964), bromine
is widely distributed in nature but in relatively small proportions. Thus,
the earth's crust contains an average of 1.6 ppm bromine. Natural
minerals containing this element consist of certain rare silver halides
such as bromyrite, embolite, and iodobrom~te. The bromine available
for commercial exploitation occurs in the oceans, in water of closed
basins (salt lakes), and in brines or salt deposits. The bromine content
of ocean water averages 65 ppm, whereas the bromine content of the
other aqueous sources, such as salt lakes and brine wells, can be as high
as 5,600 ppm. In 1977, the domestic production of bromine amounted
to about 200 million kg (U.S. Department of the Interior, 1977~.
Bromine derivatives occur in gasoline, fumigation compounds, fire-
retardant materials, pharmaceutical preparations, dyes, and other
chemicals. Biological impacts of bromine could arise from its occur-
rence as a natural constituent of soils, plants, and animals and from its
use in fumigants and pharmaceutical preparations.
ESSENTIALITY
Literature evidence for the essentiality of bromine in animals is con-
flicting. Winnek and Smith (1937) did not observe a bromine deficiency
in rats fed purified diets containing about 0.5 ppm bromine. Bromine
84
OCR for page 85
Bromine
85
supplementation, as KBr, at levels of 20 ppm did not significantly affect
the rate of growth, feed intake, or the general appearance of the treated
rats. In a similarly conducted gestation study, no effects on reproduc-
tive parameters were observed that could be attributed to the various
dietary bromine treatments. Conversely, a nutritional requirement for
bromine in mice and chickens, respectively, was postulated by Huff et
al. (1956) and Bosshardt et al. (1956~. In the niece studies, bromine, as
KBr, at 3.75 ppm was effective in reversing the growth inhibition
caused by the dietary inclusion of 2 percent iodinated casein. In the
poultry studies, day-old chicks were reared for 31 days on diets supple-
mented with bromine, as NaBr, at ~ and 15 ppm. Improvements in
growth attributed to the supplemental bromine ranged from ~ to 10
percent. In swine, although the study was not designed to assess es-
sentiality, Barber et al. (1971) did not observe any improvement in
productive performance when bromine (200 ppm as an equimolar
mixture of NH4Br, KBr, and NaBr) was fed throughout the
growing~nishing period.
The status of bromine in animal nutrition is summarized best by
Mertz (1970) in that: "growth responses to bromine supplementation
have been observed in chickens and mice, but the essentiality, bio-
logical function, or mode of action of the element have not yet been
unequivocally proved."
METABOLISM
Excellent reviews on the metabolism of bromine in animals have been
published by Gross (1962) and Unclerwood (1977~.
Winnek and Smith (1937) measured the distribution of bromine in the
bodies of rats reared on diets containing either 0.S or 20.0 ppm of
bromine, as KBr. At the end of the 12~ to 200 day test period, the
tissues of the rats fed the 0.5 ppm diet contained bromine levels,
expressed on a dry weight basis, that varied from 3.5 ppm for liver to
32.0 ppm for spleen. Tissues from the rats treated with 20 ppm con-
tained more bromine than those from the rats fed the low-bromine diet
with corresponding values for liver and spleen being 120 and 190 ppm,
respectively. Cole and Patrick (1958) examined the uptake and excre-
tion of a radioactive isotope of bromine, as K82Br, in young rats that
had been reared for 2 weeks on a diet low in bromine. The radiotracer
was given intraperitoneally, and animals were sacrificed for tissue
analysis at various time intervals postinjection. After 24 hours, the
pancreas contained the highest relative amount of the radiotracer and
OCR for page 86
86 MINERAL TOLERANCE OF DOMESTIC ANIMALS
the brain contained the lowest. Overall differences were small with the
percentages of administered dose per gram of tissue (wet weight) vary-
ing from 0.5 for brain to 1.4 for spleen. All tissues were essentially
depleted of radiotracer by 72 hours postinjection. Bromine excretion,
as evidenced by the quantity of radiotracer in the urine, was found to
occur pr~ncipaBy through the kidney. Rauws (1975) has summarized the
pharmacokinetics of the bromide ion in animal systems by concluding
that it is completely absorbed in the gastrointestinal tract, it is distrib-
uted primarily in the extracellular fluid Dike chloride), it penetrates the
blood-brain barrier, and it is excreted mainly via the kidney.
SOURCES
Bromine is ubiquitous in nature, and consequently it is an ingredient of
all feedstuiis. Bowen (1966) has stated that the average bromine con-
tent of soils is 5 ppm and that this figure for land plants is 15 ppm. Other
dietary sources of bromine would include salt that has been prepared
from brines containing relatively high levels of bromine.
TOXICOSIS
LOW LEVELS
Bromine toxicity per se has not been studied in large animals. In a study
Of lactating dairy cows, Lynn et al. (1963) did not observe an adverse
effect on milk production when bromine, as NaBr, was fed in sequential
dosages of 9.5, 19.0, and 38.0 ppm for a 72-day penod. Likewise in
swine, Barber e' al. (1971) observed that 200 ppm of bromine, as a
mixture of inorganic bromides, did not adversely affect rate of gain,
feed conversion, dressing percentage, or several other carcass quality
parameters.
HIGH LEVELS
In chicks, Doberenz et al. (1965) noted that a dietary concentration of
bromine, as NaBr, of 20,000 ppm caused death by 2 weeks of age.
Dosages of S,000 and 10,000 ppm resulted in a reduced rate of gain,
while a dosage of 2,500 ppm was without effect on production param-
eters. In a series of studies in rats, Van Logten et al. (1973, 1974) noted
that at dietary levels of bromine, as NaBr, of 19,200 ppm the treated
OCR for page 87
Bromine
87
rats did not groom themselves normally and showed signs of motor
incoordination of the hind legs. At this level, relative kidney weights
were increased. No clear effects on growth rate, food intake, or
histology were observed.
FACTORS INFLUENCING TOXICITY
The primary factor that can influence bromine toxicity is chloride.
Winnek and Smith (1937) demonstrated, in rats, that the Br:C1 ratio of
the diet influenced the amount of bromine deposited in the tissues.
Czerw~nski (195X) showed that chloride administration to rabbits that
had induced acute and chronic brom~sm caused a threefold increase in
the rate of bromine excretion. In a similar manner, Rauws and Van
Logten (1975) showed that the biological half-life of bromine (assessed
by measuring blood levels) in rats pretreated with diets containing 2,000
ppm bromine and then treated with sodium chloride in the drinking
water approximated 25.1, 12.0, 6.9, and 2.5 days. The levels of salt
causing these decreases in half-life were, correspondingly, 0, 80, ADD,
and 600 ppm.
TISSUE LEVELS
Lynn et al. (1963) found that dairy cows fed 9.5 to 38.0 ppm of bromine,
as NaBr, resulted in milk residues that ranged from 1 to 12 ppm on a wet
weight basis.
In regard to humans, FAoJw~o (1966) has established an acceptable
daily intake of 1 me bromine, as inorganic bromides, per kg of body
weight. The Food and Drug Administration (1976) has established a
tolerance of 125 ppm in or on processed foods with certain exceptions
and when it occurs by use of certain specified chemicals.
MAXIMUM TOLERABLE LEVELS
Data on which to base a maximum tolerable level for bromine in animal
feeds are sparse. Growing pigs tolerated 200 ppm, growing chickens
tolerated 5,000 ppm, and growing rats tolerated 4,800 ppm without
adverse effects. Based on these data and the interrelationships of
bromine and chIonne, no adverse effects would be expected in poultry
consuming 2,500 ppm of bromine and in other animals consuming 200
ppm of bromine.
OCR for page 88
~ MINERAL TOLERANCE OF DOMESTIC ANIMALS
SUMMARY
Boone is Eddy ~s~buted in name ~~ land plants brim
Were cogent ~ Foul 15 ~m. Evidence lo support Rs -redone
essend~ty is inconclusive' Em_ ~ k~ Comers bee noted Cow
Facts Mom Beam suppleme on. Generally, bromine coheres
cologne in me-~sm, Ed i~esdon ~ Mosaic bm~des
muses a generalized ~s~don in me tissue ex~cenul~ Duid. It is
Wiry excreted, pdm~y ~ me ~dney$ so ~1 tissue concen-
_ons son dedlne ~ norm upon cession ~ Adams on.
OCR for page 89
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92 MINERAL TOLERANCE OF DOMESTIC ANIMALS
REFERENCES
Barber, R. S., R. Braude, and K. G. Mitchell. 1971. Arsanilic acid, sodium salicylate and
bromide salts as potential growth stimulants for pigs receiving diets with and without
copper sulfate. Br. J. Nutr. 25:381.
Bosshardt, D. K., 1. W. Huff, and R. H. Barnes. 1956. Effect of bromine on chick grown.
Proc. Sac. Exp. Biol. Med. 92:219.
Bowen, H. J. M. 1966. Trace Elements in Biochemistry. Academic Press, New York and
London.
Cole, B. T., and H. Patrick. 1958. Tissue uptake and excretion of bromine~2 by rats.
Arch. Biochem. Biophys. 74:357.
Czerwinski, A. L. 1958. Bromide excretion as affected by chloride administration. J. Am.
Pharm. Assoc. 47:467.
Doberenz, A. R., A. A. Kurnick, B. J. Hulett, and B. L. Reid. 196S. Bromide and fluoride
toxicities in the chick. Poult. Sci. 44:1500.
FAD/WHO. 1966. Evaluation of Some Pesticide Residues in Food, p. 115. FAO, Ply: ~/15
wHo/Food Add. 67.32.
Food and Drug Administration. 1976. Inorganic Bromide, Ch. I, p. 608. Title 21, Code of
Federal Regulations.
Gross, J. 1962. Iodine and Bromine. In C. L. Comar and F. Bronner (eds.). Mineral
Metabolism, vol. II, part B. pp. 221-285. Academic Press, New York and London.
Huff, J. W., D. K. Bosshardt, O. P. Miller, and R. H. Barnes. 1956. A nutritional
requirement for bromine. Proc. Soc. Exp. Biol. Med. 92:216.
Lynn, G. E., S. A. Shrader, O. H. Hammer, and C. A. Lassiter. 1963. Occurrence of
bromides in the milk of cows fed sodium bromide and grain fumigated with methyl
bromide. J. Agric. Food Chem. 11:87.
Mertz, W. 1970. Some aspects of nutritional trace element research. Fed. Proc. 29:1482.
Rauws, A. G. 1975. Bromide pharmacokinetics: A model for residue accumulation in
animals. Toxicology 4:195.
Rauws, A. G., and M. J. Van Logten. 1975. The influence of dietary chloride on bromide
excretion in the rat. Toxicology 3:29.
Standen, A. (ed.). 1964. Kirk-Othmer Encyclopedia of Chemical Technology, vol. 3.
John Wiley tic Sons, New York, London, Sydney.
Underwood, E. J. 1977. Trace Elements in Human and Animal Nutrition. Academic
Press, New York and London.
U.S. Department of the Interior. 1977. Bureau of Mines Minerals Yearbook, Bromine
chapter.
Van Logten, M. J., M. Wolthius, A. G. Rauws, and R. Kroes. 1973. Short-term toxicity
study on sodium bromide in rats. Toxicology 1:321.
Van Logten, M. J., M. Wolthius, A. G. Rauws, R. Kroes, E. M. Don Tonkelaar, H.
Berkvens, and G. J. Van Esch. 1974. Semichronic toxicity study of sodium bromide in
rats. Toxicology 2:2S7.
Winnek, P. S., and A. H. Smith. 1937. Studies on the role of bromide in nutrition. J. Biol.
Chem. 121:345.
Representative terms from entire chapter:
bromine content
