Overview of Fluoride Poisoning

Fluorides are found naturally in rock phosphates and limestone. Industrial wastes associated with fertilizer and mineral supplement production are frequent sources of fluoride exposure. Metal ores associated with steel and aluminum processing are common industrial sources. Fluoride dusts dispersed downwind from these sources may contaminate forage crops for many kilometers. Forage crops grown on contaminated soil may contain increased concentrations of fluoride associated with physical contamination with soil particulates. There is minimal direct uptake of fluoride by the plant. With the potential of fluoride contamination in many feed and water sources, it is recommended that feed-grade phosphates contain <1% fluoride. Acute fluoride exposure at high concentrations will cause corrosive damage to tissues. In contrast, chronic exposure, which is seen more frequently, causes delayed or impaired mineralization of bones and teeth. The solubility of fluoride correlates generally with the degree of toxicity. Fluoride is known to interact with various elements, including aluminum, calcium, phosphorus, and iodine. Fluoride is a cellular poison that interferes with the metabolism of essential metals such as magnesium, manganese, iron, copper, and zinc. Because bacterial metabolism may be affected in a similar manner, this attribute accounts for the use of fluoride in dental hygiene products. Soluble fluoride is rapidly absorbed; ~50% is excreted by glomerular filtration. More than 95% of the fluoride that is retained is deposited in the bones and teeth, forming hydroxyapatite after the interference with calcium metabolism and replacement of hydroxyl ions. At low levels of fluoride exposure, the solubility of the enamel is reduced, resulting in protection. At higher levels of exposure, the enamel becomes dense and brittle. If exposure occurs during pregnancy, developing bones and teeth are severely affected. Faulty, irregular mineralization of the matrix associated with altered ameloblastic, odontoblastic, or osteoblastic activity ultimately results in poor enamel formation, exostosis, sclerosis, and osteoporosis.

Acute poisoning associated with massive ingestion of ascaricides (sodium fluoride), rodenticides (sodium fluorosilicate), or oral dental products will produce clinical disease within 2 hr. The fatal dosage of sodium fluoride is ~5–10 mg/kg. Toxic manifestations may be evident after consumption of ~1 mg/kg. Serum calcium and magnesium concentrations decline rapidly after the onset of the clinical syndrome. Severe gastroenteritis, salivation, restlessness, sweating, anorexia, muscle weakness, stiffness, dyspnea, ventricular tachycardia, and clonic convulsions followed by depression and death are typically seen. Chronic fluorosis is characterized by unthrifty animals with skeletal and dental abnormalities. Reduced feed and water intake accompanied by poor weight gain and milk production reflect dental lesions and impaired mastication. Mottled, chalky, pitted and stained enamel, and uneven and excessive wear on the teeth are frequently seen. Dental pain manifested by lapping of drinking water may be apparent. Skeletal abnormalities associated with increased bone resorption and remodeling produces severe lameness, stiffness, abnormal hoof growth, and exostoses. In later stages of the syndrome, severely affected cattle may be forced to move on their knees because of spurring and bridging of joints. Periosteal hyperostosis is seen on ribs. Metabolically active and growing bones of young animals are more severely affected. Anemia and hypothyroidism manifested by reduced T₃ and T₄ levels plus reduced serum calcium concentrations are often present.

A diagnosis of acute fluoride poisoning should be based on a history of exposure and typical clinical or pathologic manifestations. Confirmation with urine or serum measurements should be interpreted with caution, because rapid, time-dependent elimination of fluoride occurs. The measurement of serum calcium and magnesium concentrations may provide supportive evidence. Chronic fluorosis may require many months to develop. Fluoride concentrations in tissues must be considered in association with history, clinical disease, and necropsy findings. Animals exhibiting skeletal and dental abnormalities manifested by lameness, osteoporosis, anorexia, or reduced productivity should be evaluated for chronic fluorosis. Other disease syndromes such as arthritis; calcium, phosphorous, or vitamin D deficiency; metal toxicities such as molybdenum, selenium, or arsenic; and ergotism may be confused with chronic poisoning. In addition to tissue analysis, radiographs and histologic evaluation may provide useful information. In livestock, normal fluoride concentrations in the diet range from ~20–50 mg/kg. Depending on the duration of exposure and species susceptibility, concentrations in the diet ranging from 100–300 mg/kg may produce chronic poisoning. Water concentrations >30 mg/L are considered toxic. In young dairy cattle with a lengthy lifetime production potential, tolerance levels should be reduced by at least 2-fold. Because fluoride does not accumulate in soft tissue, analysis of liver and kidney has limited usefulness. In livestock, normal plasma concentrations are <0.2 mg/L, whereas concentrations ranging from 0.7–1.9 mg/L are consistent with poisoning. Corresponding urinary concentrations <0.5 mg/L are normal. Toxic concentrations based on recent exposure range from 14–120 mg/L. Fluoride concentrations in bones and teeth may reach levels as high as 1,500 mg/kg and 1,000 mg/kg, respectively, without adverse effects. Concentrations ranging from 6,000–13,000 mg/kg and 7,500–11,000 mg/kg, respectively, are consistent with a diagnosis of chronic fluorosis in livestock. Plasma concentrations may rise substantially once the skeletal concentrations of fluoride approach saturation.

Animals developing acute poisoning may be administered calcium gluconate (IV) and magnesium hydroxide or milk orally to minimize fluoride absorption, although the prognosis may remain poor if massive amounts of fluoride were ingested. Once manifestations of chronic fluorosis develop, treatment is ineffective. The primary objective should be directed toward prevention. In many instances, it may be difficult or impractical to remove livestock from contaminated areas. Supplementation with calcium carbonate, aluminum salts, magnesium metasilicate, or boron will reduce absorption or enhance excretion. It is recommended that livestock consume supplements and mineral mixes containing <1% fluoride content. If it is impractical to limit fluoride exposure, raising species with a relatively short production life, such as poultry, pigs, or sheep, should be considered. Reducing fluoride exposure of young or pregnant animals may limit the development of chronic fluorosis.