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Beynen AC, 2019. Fluoride in dog food

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Abstract

Fluoride in dog food Fluorine is an elemental gas that occurs rarely in nature, but in ionic form as fluoride-containing compounds, it is widely distributed in the earth's crust and soil. Hydrogen fluoride is released to the air from volcanic eruptions and industrial high-temperature processing of mined resources. Various fluorides end up in land or water and may be taken up by plants. Animals eating those plants can accumulate fluoride in their bones. Fluoride is not intentionally added to petfood, but comes with bone residues in animal ingredients. Perhaps, fluoride is an essential nutrient for dogs in minute amounts, but high intakes are toxic, depending on the chemical form. European legislation has set a maximum for fluoride: 170 mg total fluoride per kg complete canned or kibbled dog food when completely dried (1, 2). Public, fluoridated drinking water, to help prevent human dental decay, has about 1 mg fluoride/kg. Excessive intake of absorbable fluoride during dental development causes chalk-like patches in tooth enamel. Such dental mottling was seen in puppies fed a diet with added sodium fluoride, but not with other fluoride sources; the diets contained 167 mg fluoride per kg dietary dry weight. It is likely that long-term feeding of a diet high in absorbable fluoride induces skeletal fluorosis in dogs, which is typified by bone outgrowth and stiffness. Fluoride is also called a bone-seeking element. Canine dental and skeletal fluorosis may still occur in areas with groundwater high in dissolved fluoride. The scant research data suggest that commercial dog food normally does not cause fluorosis. Food fluoride measured in 2009 (3) was much lower than the European maximum, while bone-derived fluoride is limitedly absorbed. There is no evidence that fluoride in dog foods imposes risk of diseases, including fluorosis.
Creature Companion 2019; May: 42-43.
Anton C. Beynen
Fluoride in dog food
Fluorine is an elemental gas that occurs rarely in nature, but in ionic form as fluoride-containing
compounds, it is widely distributed in the earth’s crust and soil. Hydrogen fluoride is released to
the air from volcanic eruptions and industrial high-temperature processing of mined resources.
Various fluorides end up in land or water and may be taken up by plants. Animals eating those
plants can accumulate fluoride in their bones.
Fluoride is not intentionally added to petfood, but comes with bone residues in animal ingredients.
Perhaps, fluoride is an essential nutrient for dogs in minute amounts, but high intakes are toxic,
depending on the chemical form. European legislation has set a maximum for fluoride: 170 mg
total fluoride per kg complete canned or kibbled dog food when completely dried (1, 2). Public,
fluoridated drinking water, to help prevent human dental decay, has about 1 mg fluoride/kg.
Excessive intake of absorbable fluoride during dental development causes chalk-like patches in
tooth enamel. Such dental mottling was seen in puppies fed a diet with added sodium fluoride, but
not with other fluoride sources; the diets contained 167 mg fluoride per kg dietary dry weight. It is
likely that long-term feeding of a diet high in absorbable fluoride induces skeletal fluorosis in dogs,
which is typified by bone outgrowth and stiffness. Fluoride is also called a bone-seeking element.
Canine dental and skeletal fluorosis may still occur in areas with groundwater high in dissolved
fluoride. The scant research data suggest that commercial dog food normally does not cause
fluorosis. Food fluoride measured in 2009 (3) was much lower than the European maximum, while
bone-derived fluoride is limitedly absorbed. There is no evidence that fluoride in dog foods imposes
risk of diseases, including fluorosis.
Dietary fluoride
The analysed concentrations of total fluoride (F) in dry and wet dog foods (3-9, Note 1) were
generally lower than 170 mg/kg dietary dry matter (ddm). One brand of dry dog food contained 460
mg/kg ddm, which was due to rock phosphate added as mineral source (6). A semi-moist dog food
with a fluoride-contaminated mineral ingredient had 573 mg F/kg ddm (9). Two foods (presumably
canned) carried 326 and 550 mg F/kg ddm (7). The four excessive levels were reported in 1984 (6),
1985 (7) and 1987 (9).
Mammalian bone meal may contain 200 to 600 mg total F/kg (4, 7). When its ash content is put at
40%, then animal meal with 20% ash has up to 300 mg F. Fish meal may hold 100 to 400 mg F/kg (7)
and feed phosphates can bring along 70 to 3860 mg/kg (10). There is only about 1 mg F/kg in grains
(11). Besides the ingredients, the water added during production also is a source of F in petfood.
Dental and skeletal fluorosis
Dogs living in areas endemic for fluorosis may display conditions featuring dental and/or skeletal
fluorosis. Such dogs, from locations in China (12), India (13) and Turkey (14), were subjected to
clinical studies. The occurrence of mottled teeth and bony exostoses in dogs at three kennels has
been attributed to the feeding of a commercial dry food containing 460 mg total F/kg ddm (6, 15). A
semi-moist food with 573 mg F/kg ddm was accused of having induced dental and skeletal fluorosis
in dogs (9).
Puppies and their mothers were fed one of four diets with similar calcium and phosphate levels (4).
The control diet contained pure calcium phosphate. Test diets had either calcium phosphate plus
NaF, bone meal or feed phosphate. Control and test diets provided 15 and 193 mg F/kg ddm. Only
the permanent teeth of puppies fed NaF (n = 4) developed dental fluorosis.
Dogs aged 7-14 weeks were fed a basal ration without (n = 2) or with (n = 6) 0.1-0.2 g NaF per day
(16), equivalent to about 500 mg F/kg ddm. Eruption of permanent teeth was considerably delayed
in all dogs fed F. Discolored hypoplasias of the premolars and molars were seen. Ten to 14 weeks
after F administration, bones were markedly thickened, due to periosteal bone formation, while the
original cortex was thin.
Absorption and metabolism
The concentration of soluble F in the intestinal content determines quantitative F absorption. The
hydroxyl group in hydroxyapatite can be replaced by F, so forming fluorapatite. The two premises
explain that young dogs fed iso-fluorous diets accumulated drastically more F in their femurs when
NaF was the F source instead of bone meal or feed phosphate (4, Note 2).
One hour after oral administration of 2 mg F to fasting Beagles, plasma F concentration was
markedly increased when using NaF, but was unchanged for MgF2 or CaF2 (17). The three F sources
were given with water. Administration of NaF together with milk reduced the peak concentration of
plasma F by 40%.
The addition of F-rich rock phosphate to dog chow markedly raised plasma F (15). Femur F increased
over time in growing dogs (4) and was directly related with NaF intake in weanling (18) and adult
dogs (5, Note 3). NaF feeding enhanced bone remodeling in adult dogs (19).
In young dogs dosed orally with NaF for three months (20), equivalent to 45 mg F/kg ddm, the
increase in urinary F excretion corresponded with 48% of the dose. Net intestinal F absorption was
higher than 48%, as there was body retention (20) and biliary excretion (21) of F.
Osteosarcoma
Fluoridated drinking water and high-fluoride food are considered potential causes of canine
osteosarcoma (3, 22, 23). A case-control study (24) found that dogs with osteosarcoma (n = 161)
were not exposed to community fluoridation more frequently than dogs with other types of cancer.
Rodenticide and mordant
Fluoroacetate was, and sodium fluoroacetamide is used as rodenticide. In 1979 it was reported that
one or both organofluorides were present in marketed frozen, minced poultry meat, causing acute,
mass poisoning in dogs (25). Three dogs living in a sawmill had dental fluorosis, which was put down
to steady contamination of their food with sawdust impregnated with chromium trifluoride (26, 27).
Note 1
Total fluoride in complete dog foods (mg/kg dietary dry matter)
Ref
Year
Ana
-
lysis
Wet
dog
Dry
dog foods
n
Mean
Range
n
Mean
Range
4
1946
a
1
19.6
5
1970
b
1
10
6
1984
nr
2
258
56, 460
7
1985
c
*
5
188
12.5
-
505
3
30.3
8.1
-
51.0
8
1986
b
13
29.
8
4.5
-
22
26.5
2.4
-
74.0
9
1987
b
1+
573
3
2009
a
*
10
7.9
<0.2
12.4
Overall mean/range
109
4.5
-
505
132
.
2
<0.2
-
573
Total fluoride in complete cat foods (mg/kg dietary dry matter)
Ref
Year
Ana
-
lysis
Wet cat
foods
Dry
cat foods
n
Mean
Range
n
Mean
Range
7
1985
c
*
7
62.5
8.2
-
173
5
43.7
4.7
-
89.7
8
1986
b
8
31.2
3.6
-
57.4
5
32.5
9.0
-
52.2
Ref, Year = reference and year of publication; nr = not reported; *Dry and wet foods were assumed
to contain 90 and 20% dry matter; + = semi-moist food
Analysis: a, fluoride was extracted from ashed samples with perchloric acid distillation and
determined by titration with thorium nitrate; b, after dry ashing the samples, the ash was dissolved
in hydrochloric acid and fluoride was determined using a specific fluoride ion electrode; c, fluoride
was extracted from the samples into hydrochloride acid, derivatized and determined by gas
chromatography and flame ionization detector
Note 2
In healthy human subjects, the bioavailability or F ingested with NaF and bone meals has been
compared (28, 29). Bioavailability was calculated from the area under the curve of the plasma F
concentration versus time. When the bioavailability of F from NaF was taken as 100%, the average,
relative availability of F from bone meals ranged from 4 to 40% (28, 29). Preparations tested were
bone-meal tablets, chicken- and fish-bone meal. The highest relative bioavailabilities were seen
when the F sources were taken at the end of breakfast rather than on a fasting stomach.
Note 3
In the enamel and dentine of teeth extracted from a two-year old dog, F was analysed before and at
various intervals after the addition of NaF to food and drinking water (30). The F content of dentine
rose in a time-dependent fashion, whereas that of enamel remained essentially constant.
Note 4
A report by the U.S. Department of Health and Human Services (31) has reviewed the toxicity of
fluorine and hydrogen fluoride in dogs.
Note 5
In weanling puppies fed (presumably ad libitum) a magnesium-deficient, semipurified dry diet (4.2
mg Mg/MJ metabolizable energy), the addition NaF to the diet (250 mg F/kg) caused a further
lowering of weight gain by about 60% (32, 33). In another experiment, weanling pups were given
free access to diets with 1.6 or 9.5 mg Mg/MJ, each without or with 200 mg F/kg (34). Magnesium
deficiency markedly lowered growth, while NaF only slightly lowered weight gain at both planes of
magnesium supply. Feed intake was not reported.
Puppies were pair-fed a magnesium-deficient diet (1.6 mg Mg/MJ) comparable with those having
free access to the same diet, but with added NaF (200 mg F/kg) (18). The two groups had similar
cumulative weight gain during the experimental period of six weeks. Thus, dietary F did not affect
metabolic efficiency of growth. Noteworthily, under ad libitum conditions in that same experiment
(18), magnesium deficiency (1.6 versus 10.5 mg/MJ) did not reduce weight gain. Feed intake was not
reported.
Note 6
Intravenous injection of a single dose of NaF (5 to 20 mg/kg body weight) had a pronounced diuretic
effect in dogs (35). For adult dogs fed once daily, the dose range is roughly equivalent to 150 to 600
mg F/kg dry food. In almost all NaF feeding studies, the impact of F on water consumption and/or
urine production was not reported (4, 5, 16, 18, 19, 32, 33). Contrary to what would be expected, in
young dogs dosed orally with NaF, equivalent to 45 mg F/kg ddm, water consumption and urine
production were decreased by 79 and 59% (20).
Note 7
Seven-day old, suckling pups underwent chronic acid-base disturbances or control treatment by
twice daily intragastric administration of NH4Cl (acidosis), NaHCO3 (alkalosis) or NaCl (control) (36,
37). Two pups in each group also received F (presumably as NaF), while one pup did not. After 30
days the pups were killed.
The acidotic animals had higher tooth fluoride concentrations than their alkalotic counterparts. The
enamel from the two acidotic pups supplemented with F showed disturbed mineralization, which
was less severe than for the unsupplemented acidotic pup, but more pronounced than in the
supplemented controls. The two F-supplemented alkalotic animals had minor changes in the enamel
mineralization pattern, but more recognizable than in the unsupplemented pup. It was advanced
that a decrease in urinary pH diminishes F excretion, thus increasing the likelihood of dental fluorosis
(37).
Note 8
Magnesium deficiency causes calcification of kidney tissue in dogs and so does excessive intake of
phosphorus. A decrease in dietary magnesium from 10.5 or 9.5 to 1.6 mg/MJ raised kidney calcium
in dogs, which was counteracted by the addition of NaF to the diet (18, 34). Most likely, phosphorus-
induced nephrocalcinosis in dogs (38, 39) is also prevented by supplemental dietary NaF (cf. 40).
Note 9
It has been reported that feeding dogs with 20-120 mg NaF/day for four months caused goiter
(Maumene E, 1854, cited by ref. 41). For a 20-kg dog, the lowest NaF challenge corresponds with
about 30 mg F/kg ddm. Addition of NaF to the incubation medium of dog thyroid slices mimicked
some of the actions of thyroid-stimulating hormone (42-45), which might lead to thyroid
enlargement.
Note 10
Note 1 also presents data on total F concentrations in cat foods. Little is known about metabolism
and toxicity of dietary F in cats. Clearance of intravenously administered F (presumably as NaF) from
extracellular fluids was two times faster in cats than in dogs (46).
Literature
1. European Commission. Directive 2002/32/EC of the European Parliament and of the Council of 7
May 2002 on undesirable substances in animal feed (OJ L 140, 30.5.2002, p. 10)
2. Commission Regulation(EU) 2015/186 of 6 February 2015 amending Annex 1 to Directive
2002/32/EC of the European Parliament and of the Council as regards maximum levels for arsenic,
fluorine, lead, mercury, endosulfan and Ambrosia seeds (OJ L 31/11 7.2.2015)
3. Environmental Working Group. Dog food comparison shows high fluoride levels. (June 26, 2009).
https://www.ewg.org/research/dog-food-comparison-shows-high-fluoride-levels
4. Greenwood DA, Blayney JR, Skinsnes OK, Hodges PC. Comparative studies of the feeding of
fluorides as they occur in purified bone meal powder, defluorinated phosphate and sodium fluoride,
in dogs. J Dental Res 1946; 25: 311-326.
5. Henrikson P-A, Luwak L, Krook L, Skogerboe R, Kallfelz F, Bélanger LF, Marier JR, Sheffy BE,
Romanus B, Hirsch C. Fluoride and nutritional osteoporosis: physicochemical data on bones from an
experimental study in dogs. J Nutr 1970; 100: 631-642.
6. Marks TA, Schellenberg D, Metzler CM, Oostveen J, Morey JM. Effect of dog food containing 460
ppm fluoride on rat reproduction. J Toxicol Environ Health 1984; 14: 707-714.
7. Siebert G, Trautner K. Fluoride content of selected human food, pet food and related materials. Z
Ernährungswiss 1985; 24: 54-66.
8. Mumma RO, Rashid KA, Shane BS, Scarlett-Kranz JM, Hotchkiss JH, Eckerlin RH, Maylin GA, Lee CY,
Rutzke M, Gutenmann WH, Bache CA, Lisk DJ. Toxic and protective constituents in pet foods. Am J
Vet Res 1986; 47: 1633-1637.
9. Grancher D, Jean-Blain C, Milhaud G. Fluorosis in the dog. In: Nutrition, Malnutrition and Dietetics
in the Dog and Cat. Proceedings of an International Symposium, Hannover, 1987, pp 108-109.
10. Synek O, Šucman E, Šucmanová M. Determination of fluorides in feeding phosphates. Acta Vet
Brno 1978; 47: 159-162.
11. Waldbott GL. Fluoride in food. Am J Clin Nutr 1963; 12: 455-462.
12. Xu J-C, Wang Y-Z, Xue D-M, Xin S-Z, Dai R-T, Zhang Z-L, Cheng X. X-ray findings and pathological
basis of bone fluorosis. Chinese Med J 1987; 100: 8-16.
13. Reddy DR, Murthy JMK, Rama Mohan S. Spinal cord studies in fluorotic dogs. Fluoride 1987; 20:
28-29.
14. Kilikalp D, Cinar A, Belge F. Effects of chronic fluorosis on electrocardiogram in dogs. Fluoride
2004; 37: 96-101.
15. Shellenberg D, Marks TA, Metzler CM, Oostveen JA, Mory MJ. Lack of effect of fluoride on
reproductive performance and development in Shetland Sheepdogs. Vet Human Toxicol 1990; 32:
309-314.
16. Bauer WH. Experimental chronic fluorine intoxication: effect on bones and teeth. Am J Orthod
Oral Surg 1945; 31: 700-719.
17. Patz J, Henschler D, Fickenscher. Bioverfügbarkeit von Fluorid aus verschiedenen Salzen und
unter dem Einfluβ verschiedener Nahrungsbestandteile. Dtsch zahnärztl Z 1977; 32: 482-486.
18. Chiemchaisri Y, Phillips PH. Certain factors including fluoride which affect magnesium calcinosis
in the dog and rat. J Nutr 1965; 86: 23-28.
19. Snow GR, Anderson C. Short-term chronic fluoride administration in Beagles: a pilot study. Bone
1985; 6: 365-367.
20. Khandare AL, Uday Kumar P, Lakshmaiah N. Beneficial effect of tamarind ingestion on fluoride
toxicity in dogs. Fluoride 2000; 33: 33-38.
21. Whitford GM. The physiological and toxicological characteristics of fluoride. J Dent Res 1990; 69
(Spec Iss): 5399-549.
22. Hannah H, Bachand A, Lana S, Reif J. Water fluoridation and canine osteosarcoma. Epidemiology
2004; 15: S83.
23. Henriques J. Fluoride: an unknown cause of disease in dogs.
https://www.dogsnaturallymagazine.com/fluoride/
24. Rebhun RB, Kass PH, Kent MS, Watson KD, Withers SS, Culp WTN, King AM. Evaluation of optimal
water fluoridation on the incidence and skeletal distribution of naturally arising osteosarcoma in pet
dogs. Vet Comp Oncol 2016. DOI: 10.1111/vco.12188
25. Egyed MN. Mass poisoning in dogs due to meat contaminated by sodium fluoroacetate or
fluoroacetamide (special reference to the differential diagnosis). Fluoride 1979; 12: 76-84.
26. Loeffler K, Brehm H. Zahnschmelzverfärbung infolge Kontamination mit fluorhaltigem Sägemehl.
Kleintierpraxis 1982; 27: 417.
27. Loeffler K, Brosi C, Oelschlager W, Freyler L. Fluorose beim Hund. Kleintierpraxis 1979: 24: 167-
171.
28. Trautner K, Siebert G. An experimental study of bio-availability of fluoride from dietary sources in
man. Arch Oral Biol 1986; 31: 223-228.
29. Trautner K, Einwag J. Factors influencing the bioavailability of fluoride from calcium-rich, health-
food products and CaF2 in man. Arch Oral Biol 1987; 32: 401-406.
30. McClure FJ. Fluorine acquired by mature dog’s teeth. Science 1942; 95: 256.
31. U.S. Department of Health and Human Services. Toxicological profile for fluorides, hydrogen
fluoride, and fluorine, 2003 update.
32. Bunce GE, Chiemchaisri Y, Phillips PH. The mineral requirements of the dog IV. Effect of certain
dietary and physiologic factors upon the magnesium deficiency syndrome. J Nutr 1962; 76: 23-29.
33. Bunce GE, Jenkins KJ, Phillips PH. The mineral requirements of the dog III. The magnesium
requirement. J Nutr 1962; 76: 17-22.
34. Chiemchaisri Y, Phillips PH. Effect of dietary fluoride upon the magnesium calcinosis syndrome. J
Nutr 1963; 81: 307-311.
35. Gottlieb L, Grant SB. Diuretic action of sodium fluoride. Proc Soc Exp Biol Med 1923; 29: 1293-
1294.
36. Angmar-Månsson B, Whitford GM. Effects of acid-base status and fluoride on developing canine
enamel. Caries Res 1986; 20: 159.
37. Angmar-Månsson B, Whitford GM. Environmental and physiological factors affecting dental
fluorosis. J Dent Res 1990; 69 (Spec Iss): 706-713.
38. Laflamme GH, Jowsey J. Bone and soft tissue changes with oral phosphate supplements. J Clin
Invest 1972; 51: 2834-2840.
39. Schneider P, Ober KM, Ueberberg H. Contribution to the phosphate-induced nephropathy in the
dog. Comparative light and electron microscopic investigations on the proximal tubule after oral
application of K2HPO4, NaHPO4, KCl and NaCl. Exp Path 1981; 53-65.
40. Grooten HNA, Ritskes-Hoitinga J, Mathot JNJJ, Lemmens AG, Beynen AC. Dietary fluoride
prevents phosphorus-induced nephrocalcinosis in rats. Biol Trace Elem Res 1991; 29: 147-155.
41. Susheela AK. Fluorosis and iodine deficiency disorders in India. Curr Sci 2018; 115: 860-867.
42. Kariya T, Kotani M, Field JB. Effects of sodium fluoride and other metabolic inhibitors on basal
and TSH-stimulated cyclic AMP and thyroid metabolism. Metabolism 1974; 23: 967-973.
43. Pastan I, Macchia V, Katzen R. Effect of fluoride on the metabolic activity of thyroid slices.
Endocrinol 1968; 83: 157-160.
44. Raspé E, Roger PP, Dumont JE. Carbamylcholine, TRH, PGF and fluoride enhance free
intracellular Ca++ and Ca++ translocation in dog thyroid cells. Biochem Biophys Res Commun 1986;
141: 569-577.
45. Yamashita K, Field JB. Elevation of cyclic guanosine 3, 5-monophosphate levels in dog thyroid
slices caused by acetylcholine and sodium fluoride. J Biol Chem 1972; 247: 7062-7066.
46. Whitford GM, Biles ED, Birdsong-Whitford NL. A comparative study of fluoride pharmacokinetics
in five species. J Dent Res 1991; 70: 948-951.
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