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FLUORINE TOXICITY

(FLUOROSIS)
Fluorine: some initial comments
 In pure form, fluorine, is a very reactive gas (found in
exceedingly small amounts in nature)

 But fluoride also exists widely in minerals--bound to


metals as fluorides (e.g., sodium fluoride).

 Whether or not fluorine is a trace element essential to


human health is still debated, but in tiny amounts it protects
teeth from bacterial decay and promotes bone growth.

 Fluorides such as sodium fluoride (NaF), sodium


fluorophosphate (SMFP), and tin fluoride (SnF2),are common
ingredients in toothpaste.

 Dentists give their patients semiannual fluoride treatments


FLUORINE
• So reactive that it is found in combination with many
minerals/elements like aluminium, iron, calcium, silicates,
phosphates etc.
• An important constituent of many of the rocks and ores.
• Fluorides are emitted from industries involved in the
manufacture of aluminium, steel, phosphate fertilizers, brick
kilns, potteries, ferro-enamel, fused tricalcium phosphate etc.

• The fumes or effluents coming out of the industries/ gases or


smoke dust coming out of volcanic eruptions may settle on
fields, pastures or water reservoirs. -contamination of fields,
pastures or water, thus, fluorine is present in varying
concentrations in soil, water, atmosphere and plants.
FLUORINE …contd
• Humans and animals exposed to very low concentrations of
fluorine for prolonged periods result in accumulation of
fluorides in body particularly bones and teeth without
exhibiting any clinical signs in the beginning.
• The signs, become apparent after long periods when too
much damage has been produced in the target organs.
• Acute fluorine poisoning is not commonly observed except in
accidental ingestion/exposure to high quantity of fluorine.
• Chromic fluorine poisoning, also termed as fluorosis is a very
serious both in animals and human beings.
• Natural water always contain some amount of fluorine
• Concentration depend on the fluorine containing mineral
present
• Most fluorine containing mineral are soluble in water:
underground sources are more heavily laden with fluorine
Mechanism of toxicity:
• Fluorides, being strongly irritant produce
gastroenteritis.
• Fluoride-ions increase permeability of blood vessels
and cause coagulation defects, haemorrhages,
congestion and oedema of organs, particularly brain.
• Fluoride-ions inhibit a number of enzymes, namely-
preglycolytic, phosphatases and cholinesterase and,
thus inhibit glycolysis and increase sensitivity of the
body system to acetylcholine.
• Produce too much gastric irritation and vomitions.
However, probability of toxicity is more in those
species where vomit ion reflex is absent.
Acute Fluorine Poisoning:
• accidental ingestion of large quantities of fluorine containing
salts e.g. sodium fluoride, sodium fluoroacetate, sodium
fluorosilicate
• excessively contaminated water, feeds and fodder.
• Sodium fluoride is used as a vermifuge for the control of
round worms in pigs and lice in poultry.
• Sodium fluoroacetate is used as a rodenticide.
• Accidental ingestion of the baits containing fluoroacetate or
the poisoned animals
• Excessive licking of phosphate rocks as mineral supplements
• Pigs are most commonly affected. (About 4-5 per cent
sodium fluoride in feed is lethal for pigs. Lethal dose of
fluorosilicate is 100 g for equines and 200 g for bovines)
Clinical signs:
• Vomition, anorexia, salivation, ruminal stasis,
• Abdominal pain, gastroenteritis, diarrhoea, urination,
weakness
• constant chewing, dyspnoea, excitability, muscular tremors,
• pupillary dilatation, tetany, clonic convulsions,
• sudden collapse, coma and death due to respiratory and
cardiac collapse.
Postmortem lesions:
• Haemorrhagic gastroenteritis.
• Congestion of viscera, particularly liver and kidneys.
• Bone and dental lesions are absent.
Diagnosis
History, clinical signs and circumstantial evidences
Differential diagnosis:
• Inorganic poisoning e.g. arsenic
• Cholinesterase inhibitors
• Warfarin poisoning
Treatment:
• No specific antidote is available.
• Prognosis of poisoning is poor
• Acutely exposed animals require calcium gluconate (IV) and oral
magnesium hydroxide or milk to bind fluoride before absorption.
• Pet owners must be made aware of the potential danger of human dental
products.
• Symptomatic treatment may be given.
(i) Gastrointestinal sedatives.
(ii) Intravenous infusion of calcium salts.
(iii) Intravenous infusion of glucose solution.
Chronic fluoride poisoning (Fluorosis):
• Observed after prolonged ingestion of small but toxic amounts of fluorine
in the diet/feed or fodder contaminated by industrial pollution trom
aluminium smelting factories, steel works, cement factories, brick kilns,
coal burning electric power stations, glass manufacturing and phosphate
processing units etc.
• Consumption of contaminated water or use of fluoride containing
minerals or phosphate rocks as feed supplements for animals may also be
responsible for flucrosis.
• Non-fatal syndrome, but productivity of the affected animals goes down.
• Animals normally ingest low levels of fluorine throughout the life as
fluoride is a normal constituent o fforages, especially legumes.
• Fluorine gets deposited in bones and teeth without any apparent signs of
toxicity.
• Long latent period probably due to gradual saturation of bones and teeth
with fluorine as these tissues act as sink for fluorine.
• Once these structures get saturated, fluorine ions start exerting general
toxic effects. Unabsorbed fluoride is eliminated through faeces.
Sources of poisoning:
• Feeds, fodder, water, mineral supplements rich in
fluorine
• top dressing of pastures with phosphate lime stone
• Areas adjoining industrial units emitting fluorine
containing gases or dusts or the areas in the vicinity
of volcanoes.
• Animals ingesting vegetation/crops or grazing on the
pastures where industrial effluents or the smoke and
gases coming out of industrial units or volcanoes
settle are also poisoned.
Factors affecting toxicity:
• Solubility of the compounds (e.g. sodium fluoride is more toxic than
calcium fluoride)
• sodium fluoride is the most toxic, and calcium fluoride the least toxic.
• Soluble fluorides originating from industrial fumes or dusts are more
toxic than fluoride in rock phosphate. Soluble fluoride is rapidly
absorbed; approximately half is rapidly excreted, and the rest remains
in bone and teeth.
• Amount ingested, Duration of exposure
• Rate of excretion
• Age of the animal, Nutritional status, general health conditions of the
animals
• Individual susceptibility and resistance,
• Stress factors, species variation etc.
• Degree of susceptibility : calves, dairy cows, beef cattle, sheep, horses,
pig and poultry.
• Compared to cattle, susceptibility of sheep is less because of
comparatively lower biological availability of fluoride ions in sheep.
Mechanism of toxicity:
• Fl ions interfere with excretion of calcium or osteoclast action
• Fluoride ions replace hydroxyl-radicals in the apatite crystals thus
resulting in abnormal osteoid which is further responsible for poor
bony matrix and irregular mineralizalisation
• Because of damage to blast cells, mineralization of pre-enamel,
predentine, precemer and preskeletal matrices may be delayed i.e.
fluoride ions by affecting osteoblasts
• Also inhibits enzymes invo, in bone and teeth formation.
• Deposition of fluoride in bones occur throughout the life but in
teeth onIy during the formative stages.
• Thus, affects only the developing teeth(most severe in young and
growing animals). Therefore, dental lesions may be absent even in
very severe fluorosis cases, if the animals are adult.
• produces degenerative changes in bl marrow, kidneys, liver, adrenal
glands, heart muscles and CNS.
• Generally, two forms - dental Fluorosis (mottling and abrasion of
teeth ) and osteo fluorosis (intermittent lameness)
• At high levels most fluorides are corrosive to tissue.
• Fluoride binds to Ca2+, Mg2+, and Mn2+, acting as a direct
cellular poison (including bacterial cells, hence its use in
dental hygiene).
• In bone, fluoride binds calcium and replaces hydroxyl groups,
thereby increasing density in the mineral part of bone, which
is mostly hydroxy-apatite.
• In teeth developed during appropriate levels of fluoride
ingestion, the enamel is less soluble (protective).
• If intake is excessive, however, the enamel becomes dense
(brittle).
• In addition, faulty mineralization of teeth and bones occurs
when excessive fluoride interferes with intracellular calcium
metabolism and damages ameloblasts and odontoblasts,
leading to osteofluorosis.
Clinical signs:
Dental fluorosis:
• Due to uneven surface or shedding of teeth, mastication
becomes difficult, even impossible in worst affected cases
• Poor growth in young ant growing animals and acetonaemia
in adults.
• Affected animals like to drink cold water tl avoid pain while
ingesting fodder.
• Other general signs are anorexia, dry and rough hai coat,
rumed fur or feathers, emaciation and reduced milk
production
Clinical signs:
Osteo fluorosis(Skeletal)
• Sudden onset of lameness, unthriftiness, stiffness, painful gait and posture
• It is moving and diagonal, observed first in one leg and then in other leg
• Bones are palpably and visibly enlarged and thickened- proximal third of
metatarsal bones followed by thickening and enlargement of mandible,
deformation of the jaw, Sternum, metacarpal, ribs and spine.
• Pressing of affected limb bones give indication of pain.
• Thickening of the periosteal layer-lateral exostoses of long bones of legs.
• Articular surfaces are not involved, there is spurring and bridging of joints
leading to rigidity of the spine.
• Enlargement, chalky white appearance and roughening with intermittent
limping. Bones become more prone to fractures.
• As the condition worsens, there is cachexia and death.
• Other general signs of : loss of weight, intermittent diarrhoea, polydipsia,
polyuria, poorly concentrated urine, aplastic anaemia
Mild/Moderate
Mild

Severe Extremely severe


Guizhou Province, China

Residents of Guizhou Province, China that have


been most severely affected by fluoridosis have
developed thick, bony overgrowths, skeletal
deformities, darkly mottled teeth and gastric
disorders.

It is also possible that fluoride toxicity affects the


pineal gland and kidneys
Post mortem lesions:
• Normal ivory colour of bones is changed to chalky white, surfaces of
bones are roughened, diameter enlarged and lateral exostoses of the
long bones.
• Mottling, cavities on teeth, which are unevenly broken.
• Bone marrow cavity is diminished, gelatinous degeneration, aplastic
anaemia.
Microscopically,
• bony trabeculae are thickened and have a dense appearance with
sharp heavy outlines.
• Degenerative changes are observed in kidneys, liver, adrenal glands,
heart muscles and central nervous system.
• In kidneys, degeneration and disintegration of the tubular epithelium,
slight glomerular changes, thickened arterioles and fibrosis are also
observed.
• Atrophy of spongiosa, defective and irregular calcification of newly
formed osseous tissue, hypoplasia of enamel and dentine.
Diagnosis:
• History.
• Clinical signs.
• Post mortem findings.
• X-ray examination -sclerosis, perosis, hyperostosis
,increased density of abnormal porosity, periosteal
feathering and thickening.
• Microscopically, thick cortex due to periosteal
hyperostosis, uneven mineralization, zones of immature
bone, excess of osteoid tissue and atrophy of spongIOsa.
• Fluoride assay of feed, water, blood, urine, bone, teeth and
faeces.
Differential diagnosis:
• Vitamin D deficiency.
• Deficiency of phosphorus and calcium
• Parathyroid disease.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, ssanimals are removed from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, sheep.
• Symptomatic or supportive treatment.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o IV glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
PHOSPHOROUS TOXICITY
PHOSPHOROUS TOXICITY
• Along with Ca, P is an integral constituent of the animal body and is
universally distributed in soil and plants.
• About 80% deposited in bones and teeth in combination with
calcium while rest is primarily in organic combinations.
• Functions of phosphorus is the transfer of biological energy,
particularly through ATP.
• Deficiency of phosphorus -rickets and osteomalacia
• Hyperphosphatemia is comparatively of less common occurrence.
• Feeding of excess of wheat bran which is very rich in phosphorus
and deficient in calcium causes bran disease in horses.
• Similarly, meat high in phosphorus anj low in calcium causes
hyperphosphatemia in dogs and cats. .
• Severe nephritis also results.Into secondary hyperphosphatemia as
it interferes with th excretion of phosphorus.
• Cattle, sheep, dogs and game birds are atlected but most cases of
poisoning occur in swine
Sources of poisoning:
 Accidental ingestion of fertilizer-still in sacks or immediately
after spreading (from clumps offertilizer on cultivated land).
 Fire works, Baits containing lumps of white phosphorus for rats,
pets or ants kept on the pastures or ingestion of rats poisoned
with rodent baits or grazing of animals on the battle fieIds where
certain explosives have been used.
 Sometimes in finely divided form, P is mixed with fats and oils to
promote their absorption: over consumption of such fats and
oils also results into phosphorus poisoning.
 Red phosphorus is inert and nontoxic
 White or yellow phosphorus is toxic. (LOW potential)
 These need to be ingested in considerable quantities before
toxicity signs appear
Mechanism of toxicity:
• Local caustic action, phosphorus causes severe irritation of the
gastrointestinal mucosa and induces gastroenteritis and
diarrhoea.
• Phosphorus is absorbed into the blood stream, circulates in the
blood First as element and ultimately oxidised to phosphate
which causes hepatic degeneration.
CLINICAL SIGNS:
• Per-acute : Animals die after showing intense abdominal pain,
violent convulsions, severe CNS depression and coma
• Acute poisoning : salivation, nausea, vomition, severe
diarrhoea with mild abdominal pain, fever, polydipsia and
polyuria
Clinical signs:
• Jaundice, haematuria, oliguria, followed by delirium,
convulsions, coma and death.
• Course of illness is 3-5 days depending on the severity
of toxicity
• Pigs: vomitus is luminous in dark and gives a
characteristic garlic odour.
• Professional hazard- inhalation of fumes containing
phosphorus in industrial plants, human beings are
commonly affected.
Diagnosis:
• History.
• Clinical symptoms particularly acute gastroenteritis.
• Garlic odour of the vomitus and intestinal contents.
• Post-mortem lesions.
– Liver is enlarged, pale and yellowish in colour. Spleen is
small and atrophied.
– Congestion and haemorrhagic inflammation of
gastrointestinal tract.
– hydrothorax and oedema of other parts of the body.
– fatty degenerative changes with centrilobular necrosis in
liver.
– Fatty changes in kidneys and heart.
• Lab estimation of phosphorus in the blood, vomitus, intestinal
contents and faeces.
Differential diagnosis:
• Inorganic poisonings (arsenic, lead, mercury) causing
gastroenteritis and diarrhoea.
• Organophosphate compounds.

Treatment:
 Activated charcoal, emetics or SALINE /BULK purgatives.
 Gastrointestinal demulcents and astringents to take care of
gastroenteritis
 Fluid therapy to replenish the lost body fluids and electrolytes.
 In conditions of shock, give cardiac stimulants and intravenous
glucose infusion.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.
Treatment and Control
• Prognosis is very poor as removal of fluorides from teeth and bones is
difficult. No specific antidote is available.
• In chronic exposure, control is difficult unless animals are removed
from affected areas.
• Suggested that these affected areas may be used for animals with a
relatively short production life, eg, pigs, poultry, or finishing cattle and
sheep.
• Symptomatic or supportive treatment.
o Remove the animal(s) from the contaminated pastures.
o Change the feed, mineral supplement and drinking water.
o Correct the mineral deficiency - Ca and P, vit. A and D in the feed.
o Symptomatic -steroids, analgesics, antibiotics, fluid therapy, vit C
o Intravenously give glucose and calcium fluid
• Feeding calcium carbonate, aluminum oxide, (30 glday) 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.