Fluoride Poisoning: Introduction
(Fluorosis) |  |
| 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 ppm to prevent dental caries. Fluorine at 1-2 mg/kg in animal rations is considered adequate. The maximal tolerable level varies by species, eg, 40-50 ppm for cattle and horses, and 200 mg/kg for chickens. (The terms “fluorine” and “fluoride” are used interchangeably.) |
| Etiology: |
| 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 may contain high levels of fluorides. Volcanic ash may be high in fluoride. 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 certain enamelling processes may contaminate forage crops. Contamination of the surrounding area, particularly in the direction of the prevailing wind, may extend 5-6 miles. Forage crops grown on high-fluorine soils have increased levels due to mechanical contamination with soil particles. 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. |
| Fluoride binds to Ca2+, Mg2+, and Mn2+, acting as a direct cellular poison (including bacterial cells, hence its use in dental hygiene). At high levels most fluorides are corrosive to tissue. In bone, fluoride binds calcium and replaces the hydroxyl groups in the mineral part of bone, which is mostly hydroxyapatite. In teeth developed during fluoride ingestion, the enamel is less soluble
(protective) and more dense (brittle, if excessive). In addition, faulty mineralization of teeth and bones occurs when excessive fluoride interferes with intracellular calcium metabolism and damages ameloblasts and odontoblasts. |
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| Clinical Findings: |
| 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, gastroenteritis and cardiac (ventricular tachycardia and 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. Clinical signs, apart from mild tooth lesions, occur in many animals when bone fluoride reaches 4,000
ppm. Skeletal fluorosis results in accelerated bone resorption and remodeling with production of exostoses and sclerosis. Metabolically active bones (ribs, mandible, and long 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 diseased cattle may move around on their knees due to spurring and bridging of the joints in the late stages. When the skeleton becomes saturated (30-40 times
normal bone content), “flooding” of the soft tissue occurs, which causes a rise in plasma fluorides and metabolic breakdown evidenced by a loss of appetite and listlessness. |
Lesions:
| Acute ingestion of high levels of fluoride causes inflammation of the gut and degenerative changes in the lungs, liver, and kidneys. In chronic cases, mottling, staining, and excessive wearing occur in teeth that develop during the time of excessive fluoride ingestion. A more advanced stage of fluorosis is marked by skeletal abnormalities; the bones become chalky white, soft, thickened, and in the extreme, develop exostoses that may be palpated, especially along the long
bones and on the mandible in animals exposed at any age. |
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| Diagnosis: |
| 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 animals exposed at time of permanent teeth development; 3) lameness, as the result of fluoride accumulation in bone; and 4) systemic evidence as reflected by anorexia, inanition, and cachexia. |
| The normal levels of fluorine in livestock are considered to be <0.2 ppm in plasma, 1-8 in urine, 200-600 in bones, and 200-500 in teeth. Normal bovine urine contains <5 ppm fluorine; in borderline toxicity, urine contains 20-30 ppm, and in cattle with systemic signs, >35 ppm. In pigs, bones appear normal with 3,000-4,000 ppm fluorine, and levels of <4,500 ppm in compact bones from cattle are considered innocuous. In cattle, toxicosis is associated with levels of
>5,500 ppm in compact bone and >7,000 ppm in cancellous bone; in sheep, levels are believed to be lower (2,000-3,000 ppm in compact bone and 4,000-6,000 ppm in cancellous bone). |
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| Treatment and Control: |
| Acutely exposed animals require calcium gluconate (IV) and oral magnesium hydroxide or milk to bind fluoride before absorption. In chronic exposure, control is difficult unless animals are removed from affected areas. It has been suggested that 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. |
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