VPT-621 Assignment

Fluorine Toxicity
Submitted by
Aakanksha
P-2352
Very reactive and non metallic halogen
Inorganic or organic
Varying amounts (animals, bones & teeth)
Minerals (Fuorspar, Topaz, mica etc)
Soil, water, rocks-plants
Chronic- more common
Sources
Feed supplements & mineral mixture
 feed grade phosphates < 1% F
Drinking water
 deep wells, borewells
Contaminated forages
 stem/leaves>seeds/grains
Industries effluents and gases or dusts
Volcanic eruptions
Accidental ingestion
NaF, Na fluorosilicate, Na fluoroacetate
Factors affecting toxicity
Species
 Acute toxicosis in dogs
Calves>dairy>beef>sheep>horse>pig>poultry
Dose
 2-4ppm
Solubility
 NaF>CaF
Age
Young
Nutritional status
Stress
Toxicokinetics
Absorption:
75-90% from GIT; NaF
Distribution:
all parts, calcified tissue(bone/teeth)
96-99% incorporated into hydroxyapatite of bone (1000-1500ppm)
Excretion:
 50% kidney; unabsorbed in feces, milk
Cumulative action: constant or increasing amount ingested over
time
Fluorosis: F- = 2-3X of normal
Diet F- decreases, bone F- decrease after long period of time
Mechanism of Action (Acute)
Gastroenteritis
 NaF+HCl HF+NaCl
Disrupting ionic balance
 Hypocalcemia (neurotransmission), hyperkalemia
( inhibit Na+K+ATPase pump), hypomagnesemia
Enzyme inhibition
preglycolytic, phosphatase enzyme, AChE;
cardiotoxicity
Anticoagulant
 increase blood clotting time, acute
Mechanism of Action (Chronic)
Dental fluorosis
 damage osteoblast and odontoblast in developing tooth
 Delayed and impaired mineralization
 Malformation of enamel & dentine, stain
 Do not develop in adult tooth
Osteofluorosis
 interfere with osteoclast and damage osteoblast cells
 Replacement of OH- radicals in hydroxyapatite, abnormal
osteoid
 Osteoporosis, exostosis (periosteal), sclerosis
 Active bones (locomotion, chewing, breathing) affected more
Clinical signs and symptoms
Acute fluorine poisoning
 Within 30 min of exposure, ingestion of large amount of
soluble F
 Irritation, vomition, gastroenteritis, abdominal pain,
diarrhoea, muscle weakness; collapse and death
 Ruminants: ruminal stasis with constipation or
diarrhoea
 Nervous signs
 NaF: delayed blood clotting and fatal haemorrhages
 Respiratory paralysis, arrhythmia, cardiac failure- death
Bovine incisors illustrating changes associated with the 5 severity grades for
dental fluorosis. From left to right, tooth no. 1 is normal, no. 2 is slightly
discoloured, no. 3 is mottled with striated enamel, tooth no. 4 displays coarse
mottling with stained enamel, no. 5 shows moderate mottling,
hypomineralization, abrasions and hypoplasia and tooth no. 6 shows severe
mottling and erosions of enamel

Metatarsal bone from 2 cows of
the same breed, size and age.
Left: normal; Right: abnormal.
Note roughned, chalky white
irregular periosteal surface
Cross section of 2 metatarsal bones. Bone from point
of arrow outwards is flouride induced abnormal
bone. Note abnormal character of thickened cortical
bone.
Chronic fluorine poisoning
Dental fluorosis
 Mottling of teeth (incisors)
 Brittle and break
 Damage to gums, infection of
roots
 Tooth shedding
 Drink cold water
Skeletal fluorosis
Periodic and intermittent
lameness, moving and
diagonal
Increaded diameter of bones
Callus formation on ribs
Palpation of bone- pain
Post mortem findings
Acute toxicity:
Cyanosis, early rigor mortis, haemorrhagic
gastroenteritis (brain)
Bone and dental lesions are absent
Chronic toxicity
Mottling, staining and wearing of developing teeth
Bones- soft, chalky and thickened, exostosis
Aplastic anemia
Diagnosis
Circumstantial evidences
History
Clinical signs
X-ray
Serum electrolytes
Bones
Cattle : 3000ppm
Sheep: 5000ppm
Urine: 15-20 ppm
Treatment
Acute
Calcium compounds, aluminium salts or milk
Gastric aspiration and lavage
Quinidine
IV calcium salts
Dialysis
Chronic toxicity
Balanced Ca, P and Vit D
AL sulphates or chloride, CaCo3 and defluorinatedphosphate
Supportive therapy: steroids, antibiotic, analgesic and fluid
Treatment
Animals may be aided by good quality balanced nutrition and
avoidance of stresses
Inclusion of some aluminum (most often aluminum sulfate) or
calcium (calcium carbonate) compounds in the diet has lessened
the effects of a given amount of fluoride (NRC, 1974; Shupe, 1970)
Animals may be administered calcium gluconate (IV) and
magnesium hydroxide or milk orally to minimize fluoride
absorption or enhance excretion
If dental lesions are present, they are irreversible
 Osteofluorotic lesions may be prevented by reduction of the
total fluoride intake, so that normal bone is laid down over
previously induced osteofluorotic bone.
Treatment
Once chronic fluorosis develop, treatment is
ineffective
The primary objective should be directed toward
prevention
Livestock consume supplements and mineral mixes
containing <1% fluoride content
If it is impractical to limit fluoride exposure
Reducing fluoride exposure of young or pregnant
animals may limit the development of chronic fluorosis
Treatment
The minimum optimal dose likely to cause toxicity and requiring therapeutic
intervention has been set at 5 mg/kg of body weight
 Milk has a proven role in reducing the absorption of fluoride (Ca has a fluoride
binding effect)
Absorption can be minimized using, calcium gluconate, calcium lactate, or milk
of magnesia and aluminum, which form insoluble complexes that decrease the
absorption of fluoride
Gastric lavage is recommended instead of an emetic agent because of the danger
of aspiration of gastric contents and burning of the esophagus due to hydrofluoric
acid present in the stomach
Alkalization of the body fluids results in the faster removal of the ingested
fluoride from the body fluids because of the faster flux of fluoride out of the cells
and its elimination into the urine
Oxygen therapy, artificial respiration, and hemodialysis are recommended until
the stabilization of vital signs and serum chemistry
Prevention of Fluoride Toxicosis
Caution must be exercised to prevent the occurrence of fluoride
toxicosis in cattle
 No sources of feed and water should contain fluoride in excess
Pastures or rangelands should not be overgrazed, so that the chances of
ingestion of high fluoride soils will be decreased
Fluoride in mineral mixture should not exceed .20% for dairy and breeding
beef cattle or .30% for slaughter cattle (AAFCO, 1979)
One must also be aware of potential industrial pollution from new
industries in an area or from long-established industries that change
processes or methods of operation.
Sprinkler irrigation with geothermal waters may contain high levels of
fluoride (5 to 10 mg/liter)
 Steps should be taken to prevent exposure of cattle to as many sources of
excessive fluoride as practical
Thank you