Fluorosis

Fluorosis

Fluorosis is a chronic disease caused by the continued ingestion of small but toxic amounts of fluorine in the diet or drinking water over a long duration leading to the cumulative effect, while acute poisoning occurs due to inhalation of fluorine containing gases by smoke, vapours, dust from industries of aluminium, copper, glass, enamel, iron, steel and super phosphate. Dusts from volcanic eruptions also contain large amount of fluorine. Accidental administration of large amount of fluorine leads to 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 ppm in animal rations is considered adequate. The maximal tolerable level varies with the species, e.g., 40-50 ppm for cattle and horses, and 200 ppm for chickens.

Etiology

Toxic quantities of fluorides occur naturally, e.g., certain rock phosphates, 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.

           

In general, there is a correlation between solubility of a fluoride and its toxicity. For example, of the common fluorides, sodium fluoride is the most toxic, and calcium fluoride / sodium fluorosilicate 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.

            The toxic effects of fluorine depend on the amount ingested into the body, the solubility and bioavailability of it. When level exceeds 100 ppm of fluorine in ration utilizing the source of fluorine as rock phosphate or cryolite likely to cause diseases in cattle. calcium fluoride / sodium fluorosilicate is relatively non-toxic and an intake of 400 mg to 2 gm/kg of body weight is necessary to have fatal effects. Sodium fluoride is nearly twice toxic and general level of 50 ppm of dry ration should not be executed, otherwise induces Fluorosis. Mottling of tooth enamel occurs at 27 ppm, moderate effects at 49 ppm level. Whereas bony light lesions are observed at 27 ppm, moderate at 49 ppm level and marked at 93 ppm. Milk production in dairy cows is not affected at 50 ppm of fluorine in the diet up to fourth lactation. Fluorine in excess of 2 ppm in water is toxic to animals. Minor tooth lesions occurs at 5 ppm, while when the level exceeds of 10 ppm the excessive wear and tear of tooth occurs. More systemic effects occur when the water contains 30 ppm of fluorine. Chronic intoxication occurs when bore water contains 12 – 19 ppm fluorine. When daily intake of fluorine is 0.5 – 1.7 mg / kg body wt. in the form of sodium fluoride produces dental lesions in growing animals without affecting general health, whereas the adult animals can tolerate double the dose of the above intake i.e. 1 – 3.58 mg/kg body wt. per day is sufficient to cause severe dental Fluorosis without affecting growth rate or reproductive function. An intake of 1 mg/kg body wt. is the maximum safe limit for ruminants. An intake of 2 mg/kg body wt. produces clinical signs after continued ingestion. In case of pregnant cows the fluorine content of bones of new born calves depends on the dam’s intake of fluorine in the last 3-4 months of pregnancy.

Epidemiology

            The common cause are drinking water from deep wells, artesian bores, industrial contamination of pasture and the feeding of fluorine from phosphatic rock supplements / limestone usually occurs in animals suffering from phosphorus deficiency. Death loses are rare and restricted largely to acute poisoning. But the major losses are due to the unthriftiness caused by chronic fluorosis.

Pathogenesis

           

Fluoride has a high affinity for 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.

            Normally two forms of Fluorosis are recognized: Dental Fluorosis and osteofluorosis. Fluoride inhibits the enzymes that participate in the formation of bones and teeth (proteolytic enzymes and phosphatases). The teeth defects are due to increased osteoblstic activity. In the presence of fluorine, hydroxyapettie is replaced by fluoroapatite. The cortex of the long bones is thickened with subsequent developments of exostoses and calcification of ligaments and tendons. Fluoride also inhibits the utilization of ascorbate for bone and teeth formation. It also inhibits AChE.

Clinical Findings

Acute poisoning from inhalation of fluorine-containing gases or from ingestion of rodenticides or ascaricides containing fluoride is rare. Clinically, gastroenteritis, para sympathetic signs (salivation, frequent urination, vomition and diarrhoea) and nervous signs (characteristic and include tremers, weakness, papillary dilation, hyperaesthesia, constant chewing and convulsions) are followed within a few hours by collapse and death due to respiratory and cardiac failure. In case of ruminants, there is ruminal stasis, constipation / gastroenteritis occurs due to irritation of stomach witht the formation of hydrofluoric acid.

           

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. The teeth of animals exposed after the teeth are developed remain normal even if severe skeletal fluorosis develops. Clinical signs, apart from mild tooth lesions, occur in many animals when bone fluoride reaches 4000 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 all 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.

            In dental form: deciduous as well as permanent teeth that have grown prior to poisoning are free from lesions. In cattle lateral incisors show most pronounced changes. The earliest and mildest sign is mottling of tooth enamel, erosion of teeth, with the appearance of pigmented spots, opaque chalk like areas, very light yellow, green, brown or black coloured spots having inner pigmented streaks and pits or bands arranged horizontally across the teeth. Presence of multiple carries is a constant feature of this poisoning. If the period of intoxication exposure is for alimited period then there is bi-lateral affection of teeth, improper mastication, reduced appetite, poor growth in young ones and acetonaemia in adults. In chronic poisoning anaemia is observed due to suppression of haemopoietic activity of the bone marrow and interference with mineralization process. Reduced milk yield is observed when fluorine intake level is ranged between 150 – 200 ppm.

            Adverse effect on reproduction, significant increase in post calving anoestrus, decline in fertility is observed in cows receiving a diet containing 8 – 12 ppm fluorine for a year.

Lesions

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. Degenerative changes in the kidneys, liver, and several endocrine organs have been reported, as has anemia, but are not pathognomonic.

Diagnosis

Casual observation of affected animals may suggest chronic debilitating arthritis; osteoporosis; or deficiency of calcium, phosphorus, or vitamin D. The lameness, in advanced cases, may be wrongly attributed to an accident. The 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 3000-4000 ppm fluorine and levels of <4500 ppm in compact bones from cattle are considered innocuous. In cattle, toxicosis is associated with levels of >5500 ppm in compact bone and >7000 ppm in cancellous bone; in sheep, levels are believed to be lower (2000-3000 ppm in compact bone and 4000-6000 ppm in cancellous bone).

Treatment and Control

            No specific antidotal therapy. Supplementation of diet with calcium, phosphates and vitamin D. 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. Supportive therapy consists of administration of corticosteroids and analgesics.

Control, other than by removal of animals from affected areas, is difficult. It has been suggested that affected areas may be used for animals having a relatively short production life, e.g., pigs, poultry, or finishing cattle and sheep. However, no treatment has been shown to cure the chronic effects of fluorine toxicity.