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.
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.
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).
Total fluoride in complete dog foods (mg/kg dietary dry matter)
Total fluoride in complete cat foods (mg/kg dietary dry matter)
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
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.
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.
A report by the U.S. Department of Health and Human Services (31) has reviewed the toxicity of
fluorine and hydrogen fluoride in dogs.
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
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).
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
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).
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
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).
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)
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