Fluorides are widely distributed in the environment and originate naturally from rocks and soil or from industrial processes. Water supplies for human consumption have been adjusted to contain 1 mg/L to prevent dental caries. Fluorine at 1–2 mg/kg in animal rations is considered adequate. The maximal tolerable level in the feed (dry basis) varies by species, eg, 40–50 mg/kg for cattle, sheep, and horses, and 200 mg/kg for chickens. (The terms “fluorine” and “fluoride” are used interchangeably.)
Toxic quantities of fluorides occur naturally, eg, certain rock phosphates and the superphosphates produced from them, partially defluorinated phosphates, and the phosphatic limestones. In certain areas, drinking water from deep wells or volcanic ash may contain high levels of fluorides. Wastes from industrial processes, fertilizers, and mineral supplements are the most common causes of chronic fluorosis. The fluorine-containing gases and dusts from manufacturing of fertilizers, mineral supplements, metal ores (steel and aluminum), and enamelling processes may contaminate forage crops. Contamination of the surrounding area may extend 5–6 miles downwind. Forage crops grown on high-fluorine soils have increased levels due to mechanical contamination with soil particles, while plant uptake contributes little. Feed-grade phosphates must contain no more than 1 part of fluorine to 100 parts phosphorus. A 100-g tube of fluoride toothpaste may contain 75–500 mg of sodium fluoride, depending on the brand.
There is a general correlation between solubility of a fluoride and its toxicity. Of the common fluorides, sodium fluoride is the most toxic, and calcium fluoride the least toxic. The fluorides of rock phosphates and most cryolites are of intermediate toxicity. Soluble fluorides originating from industrial fumes or dusts are more toxic than fluoride in rock phosphate. Soluble fluoride is rapidly absorbed; approximately half is rapidly excreted, and the rest remains in bone and teeth.
At high levels most fluorides are corrosive to tissue. Fluoride binds to Ca2+, Mg2+, and Mn2+, acting as a direct cellular poison (including bacterial cells, hence its use in dental hygiene). In bone, fluoride binds calcium and replaces hydroxyl groups, thereby increasing density in the mineral part of bone, which is mostly hydroxy-apatite. In teeth developed during appropriate levels of fluoride ingestion, the enamel is less soluble (protective). If intake is excessive, however, the enamel becomes dense (brittle). In addition, faulty mineralization of teeth and bones occurs when excessive fluoride interferes with intracellular calcium metabolism and damages ameloblasts and odontoblasts, leading to osteofluorosis.
Acute poisoning from inhalation of fluorine-containing gases or from ingestion of rodenticides or ascaricides containing fluoride is rare. Oral cleaning products present a danger to pets, especially dogs. The fatal dose of sodium fluoride is 5–10 mg/kg and toxic effects occur below 1 mg/kg. Fluoride (75–90% absorbed by 90 min) lowers serum calcium and magnesium. Clinically, gastro-enteritis, ventricular tachycardia, ECG abnormalities, and nervous signs may be followed within a few hours by collapse and death.
The signs of fluorosis from chronic ingestion are the same regardless of the source of fluoride. Levels too low to produce skeletal signs can cause changes in the enamel of developing teeth, leading to chalkiness or mottling, staining, and rapid and irregular wear. When exposure occurs after dental development, the teeth remain normal even if severe skeletal fluorosis develops. Skeletal fluorosis results in accelerated bone resorption and remodeling with production of exostoses and sclerosis. Metabolically active bones and growing bones in the young are most affected. Affected animals are lame, and feed and water intake and weight gain are decreased. Severely affected cattle may move around on their knees due to spurring and bridging of the joints in the late stages. When the skeleton becomes saturated, “flooding” of the soft tissue causes a rise in plasma fluorides and metabolic breakdown evidenced by a loss of appetite and listlessness.
The cytotoxic effects of acute ingestion of fluoride are inflammation of the gut and degenerative changes in the lungs, liver, and kidneys. In animals exposed during dental development, teeth show mottling, staining, and increased wear. Animals with dental lesions have poor nutrition and poor health. In chronic cases, animals of all ages develop a severe form of skeletal fluorosis that is marked by bilateral and symmetric skeletal abnormalities; the bones become chalky white with abnormal periosteal surfaces and thickened cortex; in the extreme, exostoses develop along the long bones. In cattle, changes in the mandible, ribs, metacarpals, and metatarsals are common.
Urine fluoride levels are time dependent due to rapid elimination. In cases of known ingestion, serum calcium and magnesium levels are beneficial. Casual observation of affected animals may suggest chronic debilitating arthritis; osteoporosis; or deficiency of calcium, phosphorus, or vitamin D. Lameness in advanced cases may be wrongly attributed to an accident. Nonspecific staining seen in cattle teeth may be confused with incipient fluorosis. A developing fluoride toxicosis can be recognized by the following criteria (from most to least reliable): 1) chemical analyses to determine the amount of fluorine in the diet, urine, bones, and teeth; 2) tooth effects, in young animals; 3) lameness, as the result of bony changes; and 4) systemic evidence as reflected by anorexia, inanition, and cachexia.
The normal levels of fluorine in livestock are considered to be <0.2 mg/L in plasma, 1–8 mg/L in urine, 200–600 mg/kg in bones (dry basis), and 200–500 mg/kg in teeth. Urinary levels of fluoride >15 mg/L suggest recent intake of excessive fluoride or possible intoxication. Fluoride levels <4,500 mg/kg in compact bones may be innocuous. In cattle, toxicosis is associated with levels >5,500 mg/kg in compact bone and >7,000 mg/kg in cancellous bone, but these may be lower in some species. Fluoride levels must be interpreted along with history, clinical signs, and lesions.
Treatment and Control
Acutely exposed animals require calcium gluconate (IV) and oral magnesium hydroxide or milk to bind fluoride before absorption. Pet owners must be made aware of the potential danger of human dental products. In chronic exposure, control is difficult unless animals are removed from affected areas. It has been suggested that these affected areas may be used for animals with a relatively short production life, eg, pigs, poultry, or finishing cattle and sheep. Feeding calcium carbonate, aluminum oxide, aluminum sulfate, magnesium metasilicate, or boron has either decreased absorption or increased excretion of fluoride, and thus could offer some control of chronic fluorosis under some conditions. However, no treatment has been shown to cure the chronic effects of fluorine toxicity.
Last full review/revision March 2012 by Herman J. Boermans, DVM, MSc, PhD