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OCR for page 364
Phosphorus
lthe element phosphorus (P), although widely distributed in nature,
never occurs in the free state. It combines spontaneously and vigor-
ously with oxygen, and even its pentoxide, P2O5, combines readily with
water to form orthophosphonc acid. It is found widely scattered in
igneous and sedimentary rocks and in all bodies of water, primarily as
salts of orthophosphor~c acid (Van Wazer, 1958~. Phosphorus was first
prepared in the free state by Brandt, an alchemist of Hamburg, Ger-
many, in 1669 and was first recognized as an essential constituent of
bones by Gahn, a Swedish chemist, in 1769 (Van Wazer, 19611. It
probably plays a more varied role in the chemistry of living organisms
than any other single element. This review is limited to naturally oc-
curr~ng phosphorus in feed ingredients and supplemental phosphate
compounds. It does not include the organophosphorus compounds,
such as certain pesticides, or elemental fonns of phosphorus that are
highly toxic (Goodman and Gilman, 19751.
ESSENTIALITY
From the time of its discovery by Brandt, phosphorus was thought to
be important in metabolism. In addition to being of major importance
as a constituent of bone, phosphorus is an essential component of
organic compounds involved in almost every aspect of metabolism.
Phosphorus plays an important part in muscle, energy, carbohydrate,
364
OCR for page 365
Phosphorus 365
amino acid, fat, and nerve tissue metabolism; in normal blood chemis-
try; and in skeletal growth. Phosphate is an important part of the
nucleic acids, DNA and RNA; it is a component of many coenzymes and
is found in compounds such as adenosine di- and tri-phosphate (Irving,
19641.
METABOLISM
Phosphorus has more known functions than any other mineral element
in the animal body. In addition to playing a major role, along with
calcium, in the formation of bones and teeth, it is located in every cell
of the body and is vitally concerned in many metabolic processes,
including the buffering of body fluids (White et al., l96X). Practically
every energy transfer inside living cells involves the forming or break-
~ng of chemical bonds that link oxides of phosphorus to carbon or to
carbon-nitrogen compounds. Since every biological event involves
gain or loss of energy, one can readily appreciate the great physiologi-
cal role of phosphorus in animal metabolism.
Phosphorus in the form of orthophosphate is absorbed chiefly in the
upper small intestine, the duodenum. The amount absorbed is depen-
dent on source, calcium to phosphorus ratio, intestinal pH, lactose
intake, and dietary levels of calcium, phosphorus, vitamin D, iron,
aluminum, manganese, potassium, magnesium, and fat (Irving, 19641.
As is the case for most nutrients, the greater the need, the more eff~-
cient the absorption. Phosphorus absorbed from the intestine is circu-
lated through the body and is readily withdrawn from the blood for use
by the bones and teeth during periods of growth. Some incorporation
into the bone occurs at all ages. It may be withdrawn from bones to
maintain normal blood plasma levels during periods of dietary depr~va-
tion. The plasma phosphorus level, along with calcium, is regulated by
the parathyroid hormone and thyrocalcitonin. The plasma phosphorus
level is inversely related to the blood calcium level; however, in partu-
rient paresis, both usually decline. Excess phosphorus is excreted pri-
mafily by the kidney (Bartter, 19641.
SOURCES
Phosphorus is present in variable amounts in almost all common feed-
stuffs (National Research Council, 1971~. The phosphorus levels are
dependent on the plant species, the level of soil fertility, and the stage
of maturity at the time of consumption. The biological availability of the
OCR for page 366
366 MINERAL TOLERANCE OF DOMESTIC ANIMALS
phosphorus in plant material is quite variable and is dependent upon the
phosphorus compounds present and the animal species consuming the
feedstuffs.
Most animal diets require supplemental sources of phosphorus in
addition to that present in the common feedstuffs. There are a number
of supplemental sources. The major types include: calcium phosphates
(dicalcium phosphate, monocalcium phosphate, defluorinated rock
phosphate, bone meal, Guano organ phosphates), ammonium phos-
phates (monoammonium phosphate, diammonium phosphate, ammo-
nium polyphosphate), sodium phosphates (monosodium phosphate,
disodium phosphate, sodium topolyphosphate), and phosphoric acid.
There is considerable variation in the biological availability of phos-
phorus from sources within these types, especially within the calcium
phosphates. A review on the biological availability of phosphorus to
livestock was prepared by Peeler (1972~.
TOXICOSIS
Phosphorus is involved in almost all aspects of metabolism. In addition,
it interacts with many of the other essential and nonessential mineral
elements making dietary levels of this element critical to optimum
animal performance (growth rate, feed efficiency, mink production, egg
production).
Optimum animal performance is linked very closely with optimum
calcium and phosphorus levels in the diet. Most animals require a fairly
narrow calcium to phosphorus ratio usually no wider than 2:1;
however, ruminants can tolerate wider ratios than monogastr~c
animals, providing the phosphorus level is adequate. If the calcium to
phosphorus ratio is balanced, the animal can tolerate wider ranges of
dietary phosphorus levels. The quantitative aspects of the dietary cal-
cium to phosphorus ratio and subsequent animal performance are dis-
cussed in several recent reviews (Hays, 1976; Preston et al., 1977;
Waibe! et al., 19771.
A relative excess of phosphorus in relation to calcium can result In
some very detrimental situations. One of these is a malady of ruminants
known as urolithiasis (urinary calculi). This is the formation of stones
or calculi in the kidney or bladder with resultant obstruction of urine
excretion. The blockage results in a buildup of urine in the bladder with
eventual rupture of the bladder or urethra. Bladder rupture results in
temporary relief, but this is followed by abdominal distention, depres-
sion, and death due to uremia (Blood and Henderson, 19681. The forma-
OCR for page 367
Phosphorus
367
lion of stones may be affected by several factors; however, a series of
papers from South Dakota (Emetics and Embry, 1962, 1963, 1964)
leaves little doubt regarding the importance of phosphorus level in the
ration and the accompanying calcium level upon the development of
urinary calculi in wether lambs. Feeding a high level of phosphorus (0.S
percent) resulted in a high incidence of urinary calculi (Table 27~. The
maximum dietary level of phosphorus that can be tolerated by sheep
without the development of calculi lies between 0.37 and 0.69 percent
of the diet dry matter. Increasing the calcium level in the ration seemed
to provide partial protection against the occurrence of calculi in sheep
receiving higher levels of phosphorus. Monosodium phosphate, diso-
dium phosphate, and sodium tripolyphosphate all appeared to be about
equal in calculi-producing ability; dicalcium phosphate contributed cal-
cium and significantly reduced the incidence of calculi (Bushman et al.,
19651.
Several workers (Singsen et al., 1962; Crowley et al., 1963; Harms et
al., 1965; Charles and Jensen, 1975) have observed that high dietary
levels of phosphorus (0.8 to 1.2 percent) depressed the performance of
laying hens (egg production alla egg shell quality). The level necessary
to depress performance of hens maintained on the floor was less than
for cage layers. It is postulated that this difference is due to the higher
dietary phosphorus requirement (approximately 0.2 percent greater) of
caged hens. McGillivray and Smidt (1974) investigated the effect of
excess phosphorus on broiler performance. They observed decreases
in weight gains and efficiency of feed utilization as dietary phosphorus
levels were increased above 0.S percent (calcium level at 1 percent).
Significant mortality was noted when the dietary phosphorus level was
raised to 2 percent (approximately 4 times requirements.
Another problem associated with a relative excess of phosphorus in
relation to calcium is a bone disorder (called osteodystrophia fibrosa,
nutritional secondary hyperparathyroidism, osteomalacia, osteopo-
rosis, big head disease) that has been observed in several species
(Bartter, 1964~. A high phosphorus intake causes an increased concen-
tration of serum phosphorus, which secondarily results in a lowering of
the serum calcium. This effect then stimulates the parathyroid gland to
increase serum calcium by resorption of the bone and to increase renal
phosphate excretion. Thus, pronounced bone loss in adult animals can
occur by feeding excess dietary phosphorus or insufficient dietary cal-
cium. In some instances, the demineralized skeleton is replaced by
fibrous connective tissue.
Nutritional secondary hyperparathyroidism occurs in horses fed high
levels of grain without calcium supplementation (Joyce et al., 19711. It
OCR for page 368
368 MINERAL TOLERANCE OF DOMESTIC ANIMALS
develops in 6 to 12 months when a diet with a calcium to phosphorus
ratio of 0.~: 1.0 is fed and progresses rapidly when the ratio is 0.6:1.0
(National Research Council, 1973~. Studies at Cornell (Schryver et al.,
1971; Argenzio et al., 1974) have shown that high phosphate diets (1.2
percent phosphorus, 0.4 percent calcium) depressed the intestinal ab-
sorption of calcium, the concentration of calcium in plasma, renal ex-
cretion, and calcium retention. The rate of deposition of calcium In
bone and the rate of removal of calcium from bone were elevated in
response to the high phosphate intake. Phosphate retention and the
plasma phosphate concentration increased when the horses were fed
the high-phosphate diet.
A purified diet containing 1.20 percent phosphorus and 0.12 percent
calcium fed to beagles produced rapid loss of bone and easily detached
incisor teeth. This did not occur with dogs fed the same diet containing
0.42 percent phosphorus and 0.54 percent calcium (Henrikson, 1968~.
Confirmation of the effects of high phosphate intakes on the integrity of
adult bone, and direct evidence for a parathyroid hormone-mediated
mechanism contributing to increased resorption of bone in dogs was
provided by Laflamme and Jowsey (1972) and Krook et al. (1971~.
In a series of papers, Draper and associates (Anderson and Draper,
1972; Draper et al., 1972; Sie et al., 1974) showed that excess dietary
phosphorus has an accelerating effect on bone resorption in aging rats
and mice by a mechanism involving the parathyroid hormone. When a
diet containing 0.6 percent calcium was fed with 0.3, 0.6, 1.2, or 1.S
percent phosphorus, calcium loss in the 0.6 percent phosphorus group
was 16 percent greater than in the 0.3 percent phosphorus group and
was 37 percent greater in the 1.2 percent phosphorus group. A similar
response was obtained with mice (Krishnarao and Draper, 1972~.
High phosphorus levels in laboratory animals have caused hyper-
trophy of the parathyroid glands. However, a more sensitive criterion
of excess phosphate is the appearance of metastatic calcification in soft
tissues, especially in the kidney, stomach, and aorta (WorId Health
Organization, 1964; Ellinger, 1972~. Kidney calcification may be ob-
served in a few weeks or months, depending on the dose level. The
highest levels of phosphorus in diets for rats that did not cause signifi-
cant kidney damage were 0.90 and 1.30 percent. It is difficult to indicate
a borderline between dose levels that do not produce nephrocalcinosis
and those that produce early signs of such changes, because the com-
position of the diet (amount of calcium, acid-base balance, vitamin D)
has an important influence on the appearance of renal calcification.
From a consideration of the experimental evidence, it is estimated that
diets containing 1 percent phosphorus or more may be nephrocalcino-
genic in rats. Diets containing 0.9 percent phosphorus and 0.S percent
OCR for page 369
Phosphorus
369
calcium or higher levels of phosphate produced calcification in the soft
tissues of guinea pigs (Hogan et al., 1950; House and Hogan, 1955~.
MAXIMUM TOLERABLE LEVELS
It is difficult, if not Impossible, to separate the effects of a dietary
calcium-phosphorus imbalance from that of excessive dietary phos-
phorus levels. Many of the studies conducted- with higher levels of
phosphorus have simultaneously used inadequate levels of calcium.
This accentuates the problem, and one cannot always tell whether the
observations are due to the -low calcium or the high phosphorus, or
both. There are enough studies in the literature, however, to indicate
that, even when calcium levels are at requirement or higher levels, high
levels of phosphorus can cause increased bone resorption especially
In adult animals. Supplemental phosphates are usually not considered
to be highly toxic, since single large oral doses can be tolerated with
only minor effects (mild diarrhea, abdominal distress). On the other
hand, long-term consumption of dietary levels 2 to 3 times the require-
ment level will cause severe problems due to induced changes in cal-
cium metabolism. This level is very dependent on the calcium level of
the diet, as wed as other factors such as vitamin D, aluminum, po-
tassium, and magnesium. Although the effects of excess dietary phos-
phorus can, to some extent, be counteracted by increasing dietary
calcium, the lower efficiency of calcium absorption limits the extent to
which the effect of a high phosphorus intake can be offset by increasing
the intake of calcium. When tolerance is expressed in terms of a multi-
ple of the requirement level, phosphorus has one of the lowest toler-
ance factors of any mineral element.
Assuming the presence of adequate levels of dietary calcium, the
folBowing phosphorus levels can be tolerated; however, depending on
the age and production status of the animal, even these levels may
reduce performance: cattle, 1 percent; sheep, 0.6 percent; swine, 1.5
percent; poultry, 1 percent; laying hen, 0.8 percent; horse, 1 percent;
rabbit, 1 percent. For the very young of some species, higher levels of
phosphorus are tolerate`] or needed for short periods of time.
SUMMARY
Phosphorus, although widely distributed in nature, never occurs in the
free state. It probably plays a more varied role in the chemistry of living
organisms than any other single element. In addition to being of major
OCR for page 370
370 MINERAL TOLERANCE OF DOMESTIC ANIMALS
importance as a constituent of bone, phosphorus is an essential compo-
nent of organic compounds involved in almost every aspect of metab-
olism. Animal performance is linked very closely with calcium and
phosphorus levels in the diet. Most animals require a fairly narrow
calcium to phosphorus ratiousually no wider than 2:1, however,
ruminants can tolerate wider ratios than monogastnc animals, provid-
ing the phosphorus level is adequate. A relative excess of phosphorus
in relation to calcium can result in some very detrimental situations,
and, even when calcium is at requirement or higher levels, high levels
of phosphorus can cause increased bone resorption in adult animals.
Long-term consumption of dietary levels 2 to 3 times the requirement
level wiD cause severe problems due to induced changes in calcium
metabolism.
OCR for page 371
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OCR for page 376
376 MINERAL TOLERANCE OF DOMESTIC ANIMALS
REFERENCES
Anderson, G. H., and H. H. Draper. 1972. Effect of dietary phosphorus on calcium
metabolism in intact and parathyroidectomized adult rats. J. Nutr. 102:1123.
Argenzio, R. A., J. E. Lowe, H. F. Hintz, and H. F. Schryver. 1974. Calcium and
phosphorus homeostasis in horses. J. Nutr. 104:18.
Bartter, F. C. 1964. Disturbances of phosphorus metabolism, pp. 315-339. In C. L.
Comar and F. Bronner, eds. Mineral Metabolism, vol. 2, part A. Academic Press,
New York.
Blood, D. C., and J. A. Henderson. 1968. Veterinary Medicine, 3rd ed. Williams &
Wilkins Co., Baltimore, Md.
Bushing, D. H., R. J. Emerick, and L. B. Embry. 1965. Incidence of urinary calculi in
sheep as affected by various dietary phosphates. J. Anim. Sci. 24:671.
Charles, O. W., and L. Jensen. 1975. Effect of phosphorus levels on laying hen perform-
ance. Poult. Sci. 54:1744.
Crowley, T. A., A. A. Kurnick, and B. L. Reid. 1963. Dietary phosphorus for laying
hens. Poult. Sci. 42:758.
Draper, H. H., Ten-Lin Sie, and J. G. Bergan. 1972. Osteoporosis in aging rats induced
by high phosphorus diets. J. Nutr. 102:1133.
Ellinger, R. H. 1972. Phosphates as Food Ingredients. CRC Press, Cleveland, Ohio.
Emerick, R. J., and L. B. Embry. 1962. Calcium and phosphorus levels related to urinary
calculi in sheep. J. Anim. Sci. 21:995.
Emerick, R. J., and L. B. Embry. 1963. Calcium and phosphorus levels related to the
development of phosphate urinary calculi in sheep. J. Anim. Sci. 22:510.
Emenck, R. J., and L. B. Embry. 1964. Effects of calcium and phosphorus levels and
diethylstilbestrol on urinary calculi incidence and feedlot performance of lambs. J.
Anim. Sci. 23:1079.
Goodman, L. S., and A. Gilman. 1975. The Pharmacological Basis of Therapeutics, 5th
ed. The Macmillan Company, New York.
Hanns, R. H., B. L. Damron, and P. W. Waldroup. 1965. Influence of high phosphorus
levels in caged layer diets. Poult. Sci. 44:1249.
Hays, V. W. 1976. Phosphorus in Swine Nutrition. National Feed Ingredients Associa-
tion, Des Moines, Iowa.
Henrikson, P. 1968. Periodontal disease and calcium deficiency. Acta Odont. Scandinav.
26(Suppl. 50):1.
Hogan, A. G., W. O. Regan, and W. B. House. 1950. Calcium phosphate deposits in
guinea pigs and the phosphorus content of the diet. J. Nutr. 41:203.
House, W. B.' and A. G. Hogan. 1955. Injury to guinea pigs that follows a high intake
of phosphates. J. Nutr. 55:507.
Irving, J. T. 1964. Dynamics and functions of phosphoms, pp. 24~313. In C. L. Comar
and F. Bronner, eds. Mineral Metabolism, vol. 2, part A. Academic Press, New York.
Joyce, J. R., K. R. Pierce, W. M. Romane, and J. M. Baker. 1971. Clinical study of
nutritional secondary hyperparathyroidism in horses. J. Am. Vet. Med. Assoc.
1 58:2033.
Krishnarao, G. V. G.. and H. H. Draper. 1972. Influence of dietary phosphate on bone
resorption in senescent mice. J. Nutr. 102:1 143.
Krook, L., L. Lutwak, P. Hendrikson, F. Kallfelz, C. Hirsch, B. Romanus, L. F.
Belanger, J. R. Marier, and B. E. Sheffy. 1971. Reversibility of nutritional osteo-
porosis: Physicochemical data on bones from an experimental study in dogs. J. Nutr.
101:233.
OCR for page 377
Phosphorus
377
Laflamme, G. H., and J. Jowsey. 1972. Bone and soft tissue changes with oral phosphate
supplements. J. Clin. Invest. 51:2834.
McGillivray, J. J., and M. J. Smidt. 1974. Monoarnmonium phosphate as a phosphorus
source for poultry. Poult. Sci. 53:1954. (Abstr.)
National Research Council. 1971. Atlas of Nutritional Data on United States and Cana-
dian Feeds. National Academy of Sciences, Washington, D.C.
National Research Council. 1973. Nutrient Requirements of Domestic Animals. Nutrient
Requirements of Horses. National Academy of Sciences, Washington, D.C.
Peeler, H. T. 1972. Biological availability of nutrients in feeds: Availability of major
mineral ions. J. Anim. Sci. 35:695.
Preston, R. L., N. L. Jacobson, K.D. Wiggers, M. H. Wiggers, and G. N. Jacobson.
1977. Phosphorus in Ruminant Nutrition. National Feed Ingredients Association, Des
Moines, Iowa.
Schryver, H. F., H. F. Hintz, and P. H. Craig. 1971. Calcium metabolism in ponies fed
a high phosphorus diet. J. Nutr. 101:259.
Sie, Ten-Lin, H. H. Draper, and R. R. Bell. 1974. Hypocalcemia, hyperparathyroidism
and bone resorption in rats induced by dietary phosphate. J. Nutr. 104:1195.
Singsen, E. P., A. H. Spandorf, L. D. Matterson, J. A. Serape, and J. J. Tlustohowicz.
1962. Phosphorus in the nutrition of the adult hen. 1. Minimum phosphorus require-
ments. Poult. Sci. 41:1401.
Van Wazer, J. R. 1958. Phosphorus and Its Compounds. vol. I: Chemistry. Interscience
Publishers, New York.
Van Wazer, J. R. 1961. Phosphorus and Its Compounds. vol. II: Technology, Biological
Functions and Applications. Interscience Publishers, New York.
Waibel, P. E., R. H. Harms, and B. L. Damron. 1977. Phosphorus in Poultry and Game
Bird Nutrition. National Feed Ingredients Association, Des Moines, Iowa.
White, A., P. Handler, and E. L. Smith. 1968. Principles of Biochemistry, 4th ed.
McGraw-Hill, New York.
World Health Organization Technical Report, Series No. 281. 1964. Specifications for the
Identity and Purity of Food Additives and Their Toxicological Evaluation: Emul-
sifiers, Stabilizers, Bleaching and Maturing Agents. World Health Organization,
Geneva.
Representative terms from entire chapter:
dietary phosphorus
