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Learn Toxicology with Ranjana
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Fluorine

Sources : 

  • Toxic quantities of fluorides occur naturally in some feed products like raw rock phosphates, produced from them, partially defluorinated phosphates and the phosphatic limestones.
  •  In certain areas the drinking water usually from deep wells contains high levels of fluorides.
  • Factory contamination also adds to increased fluorides in water. Sodium fluoride is  more toxic than calcium fluoride.

Mode of transmission:

No evidence of transmission of toxicity from animal to animal.

Mechanism of action:

  • Excessive fluoride results in delayed and impaired mineralization of teeth and skeleton.
  • In the teeth, fluoride damages the ameloblasts and odontoblasts. This leads to abnormalities  on developing teeth.
  • In fully developed teeth, enamel formation does not occur and this leads to rapid and excessive wear of molars and incisors.
  • Oxidation of organic material in the areas of wear results in brown or black discolouration.
  • In the bones fluorides disrupt osteogenesis, causes acceleration of bone remodelling with  production of abnormal bones.
  • Occasionally osteoporosis may also be caused.
  • Fluoride acts as anticoagulant because it precipitates calcium in the form of calcium fluoride.
    In acute intoxication, large amounts of soluble inorganic fluoride form hydrofluoric acid in acidic medium of the stomach .This causes gastrointestinal irritation.

 

Clinical Signs:

  • In acute cases the symptoms include excitement, clonic convulsions, bladder and bowel incontinence, stiffness and weakness, weight loss, decreased milk production,  excessive salivation, nausea and vomiting, cardiac failure and death.
  • In chronic cases the symptoms include mottled and pitted enamel, unevenly worn teeth, apendicular lameness, unnatural posture, generalised stiffness, cachexia, poor performance and dull hair coat. Lapping of water indicates dental pain. Exostosis of long bone extremities which are painful.

 

Lesions:

  • The teeth of affected animals will have periodic radiolucent areas.
  • The affected bones will be enlarged and chalky white in colour with no lustre.
  • The periosteal surface will be rough.
  • Bone marrow cavity is diminished and shows gelatinous degeneration and aplastic anaemia.

Diagnosis:

History

Clinical signs

Post-mortem lesions

Estimation of fluoride in plasma,bone ,urine and dental tissues.

Urine may contain 15-20ppm of fluoride as compared to 2-6ppm in normal urine.


Treatment:
Acute toxicity:There is no specific treatment for acute fluoride toxicity.Symptomatic treatment may save some animals.These includes GI sedatives and intravenous calcium salts till disappearance of tetany and hyperesthesia.

Chronictoxicity:
Tolerance to fluoride can be increased by balanced intake of calcium, phosphorus and vitamin D.
Aluminium salts ,calcium carbonate and defluorinated phosphate can be administered orally to from insoluble compounds with fluoride in the gut.The feed or water containing excess fluoride can be diluted with feed or roughage that is low in fluoride.
Supportive therapy might include steroids ,antibiotics, analgesics and fluid therapy.
 

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