Fluoride and health

FLUORIDE AND
HEALTH
Dr. Priyanka Sharma
III year MDS
Dept of Public Health Dentistry

CONTENTS
• Introduction
• Indian scenario
• Places in India having high fluoride concentration
• Recommended fluoride ranges
• Health and fluorides
- Urban mortality
- Cancer mortality
-Congeital Anomalies
- Developmental defects
- Al-F Interaction
- Effect on RBCS

• Effect on skeletal muscles
• Effect on ligament and blood vessels
• Neurological manifestations
• Kidney
• GI system
• Endocrine
• Bone (arthritis and osteoporosis)
• Reproductive system
• Cardiovascular system

• Immunological and lymphoreticular system
• At molecular level
• Immune system
• Dental enamel
• Conclusion
• References

INTRODUCTION
• Fluorine is the ninth element of the periodic table.
Nevertheless, its applications and biological
significances were known only in the decades of
1920’s. It is the lightest member of the halogen
family and the most electronegative among all
chemical elements(Hodge and Smith, 1965).

• Fluorine has both notable chemical qualities and
physiological properties, which are of great
interest and significance to human health.
• Fluorine is rarely or never found free in the nature
in elemental form. It has strong affinity to combine
chemically with other elements to form compounds
called ‘fluoride’.

• The chemical activity of the fluoride ion (E0 = -2.8
Volts) makes it physiologically more active than other
elemental ion.
• Therefore, fluoride ions play an important role in human
physiology. Its presence in low concentration may either
inhibit or stimulates enzymatic process and its
interaction with other organic and inorganic body
components may cause disruption in normal
physiological functions of human body.

Fluoride in animal products-
Beef, pork and mutton-0.3ppm
Fish products- up to 20ppm
Dried sea foods also fluoride rich 84.5ppm
(South East Asia)
Fluoride in beverages-
Ranges from 0.05 to 1.05 ppm

Fluoride from food
0.3 to 0.6 mg/day
Fluoride intake in first 6months of life-bottle/breast
fed
Breast fed infant receives 0.003 to 0.004mg/day

Indian Scenario
• India is among the 23 nations around the globe
where health problems occur due to excess
ingestion of fluoride (>1.5 mg/l) by drinking
water.
Hussain J and Sharma KC. Environmental Monitoring and Assessment
March 2010, Volume 162, Issue 1, pp 1-14

Places with fluoride levels in
various parts in India
• 1.1-2.1 ppm : New Delhi to Sirsa and Hissar,
Sangrur Bhatinda, Faridkot, Firozpur of Punjab,
Suratgarh, Sirohi South of Jaipur in Rajasthan,
Kutch, and Western Jamnagar District in Gujrat.
• 4.0 – 8.0 ppm : Chandi and Betul areas of Madhya
Pradesh, Anantpur, Karimnagar, Krishna District (>
5.0 ppm) Nalgonda, Karnool, Hyderabad.
Textbook of community Dentistry, TR Gururaja Rao, 2004, Pg 310

• Between 1.5 – 5.0 ppm : Coimbatore,
Dharmapuri, North Arcot, Salem, Tiruchy,
Madurai in Tamilnadu.
• 9.5 ppm Gulabpur, 8.5 ppm Phag, Chirava,
19.0 ppm Sagalia in Western India.

Recommended Fluoride Ranges
• WHO in 1963 has recommended a range of 0.7-1.2 ppm
F in drinking water.
• This acts as an optimum limit of dental caries.
• Dental fluorosis occurs in human beings consuming
water containing 2.0mg/litre or more of fluoride
particularly during first 8 years of life and skeletal
fluorosis results if the water contains above 4.0ppm and
is consumed regularly over a long period of time.

• The acute lethal dose for an adult is 32-64 mg/kg body weight.
• That is, for an adult of 70kg weight, it could be around 2.2 gm of
fluoride and safety tolerated dose is 8-16 mg/kg body weight.
• Even if a child swallows the contents of family sized tooth paste
(270mg)., the child will ingest 270mg of fluoride which is below
certainly the lethal dose of 320 mg fluoride in a 2 yr old child.
• Moreover it is difficult for a child to swallow 270 gm toothpaste.

• However in 1971- US national academy of sciences- 1mg for
an adult and the fixed concentration must not be more
than 1mgF/lt of water.
Fluoridated tooth paste
• Not to be given for children < 3 years
• >3 yrs – 1/3 toothpaste, pea sized
• 75gm tube - 75mg F

Use of fluoridated toothpaste - Blood fluoride levels in children
Rajan et al 1987,1988- 5-10yr, 10-14yr old
Tested fluoride level in blood, before & after brushing with fluoridated toothpaste.
[ After confirming various animal trials found that on the salivary fluoride level
after brushing with fluoride-containing toothpaste, fluoride in saliva was enhanced;
the level of fluoride returned to normal within 60 min. indicating clearance of
salivary fluoride through the gastro-intestinal tract, highly vascularized oral mucosa
may also absorb fluoride and cause the circulatory fluoride level to rise following
use of fluoride-containing toothpaste for brushing].

American Academy of pediatric dentistry,1967, revised in 2014.

KNIFE WITH TWO EDGES
Hussain et al. Journal of Tissue Research Vol. 4 (2) 263-273 (2004)

Concentration of fluoride and
biological effects
Hussain et al. Journal of Tissue Research Vol. 4 (2) 263-273 (2004)

Health and Fluoridation
• It has been suggested over the years that many
different disorders can be caused or aggravated by
fluoridation. [ Table in next page ]
• Urban Mortality : Rogot et al (1978) sampled 473
urban areas of USA. Overall the findings clearly
showed no consistent relation between fluoridation
and observed changes in mortality over the 20
years of study period.
Murray et al, Fluorides in caries prevention, 3rd edit, chapter 17 page 337

CANCER MORTALITY
• Cancer Mortality : Yiamouyiannis and Burk (1977) studied age
dependence on cancer mortality related to artificial
fluoridation in USA.

• New Burn and also Royal Statistic society explained the
reason behind this result in 1977.
• US Census and San Francisco 20 year period study, 1970,
showed no trend in cancer mortality after age adjustment.
• Great Britain, Royal College of Physician 1976 conducted a
study and showed no tendency of ratio of greater cancer in
high fluoridated areas.

Congenital anomalies
Suggestion that fluoride is a cause of mongolism ( Down’s syndrome)
derives from two studies of Rapaport ( 1059, 1963) in USA.
 Berry 1958 did the similar study in 9 English towns, making the sort of
intensive enquiries that are needed for complete ascertainment.
Erickson et al (1976) very large study of 13,87,027 birthday using two
sources : the Metropolitan Atlanta Congenital Malformation Surveillance
Program and the National Cleft Lip and Palate Intelligence Service,
showing no association.

Developmental defects
• Fluoride crosses the placenta in limited amounts
and is found in fetal and placental tissue (Gedalia
et al., 1961; Theuer et al., 1971).
• The available human data suggest that fluoride has
the potential to be developmentally toxic at doses
associated with moderate to severe fluorosis.

• The human and animal data suggest that the
developing fetus is not a sensitive target of
fluoride toxicity.
• Exposure to high levels of fluoride has been
described together with an increased
incidence of spina bifida (Gupta et al., 1995).

• The occurrence of spina bifida was examined in a
group of 50 children aged 5–12 years living in an
area of India with high levels of fluoride in the
drinking water (4.5–8.5 ppm) and manifesting
either clinical (bone and joint pain, stiffness, and
rigidity), dental, or skeletal fluorosis.

• An age- and weight-matched group of children living in
areas with lower fluoride levels (#1.5 ppm) served as a
control group. Spina bifida was found in 22 (44%) of the
children in the high fluoride area and in six (12%)
children in the control group.
• This study did not examine the possible role of
potentially important nutrients such as folic acid,
however, and had other study design flaws.

Aluminium – Fluoride interaction
• Brudevold, Moreno and Bakhos in 1973 showed
that addition of 0.2 ppm Al to a solution of 1
ppm F reduces the ionic fluoride by 25-30%.
Weddle and Muhler 1957, in their animal trials
showed the complex formed probably AlF6
-3 was
not readily absorbed.

The evidence as a whole ( Tennakone et al 1987, Nicholson et al 1987,
Moody et al 1990) suggested one more finding that only a most unusual
combination of circumstances ( fluoridated water boiled to small bulk
in an aluminium vessel in the presence of citric acid) would lead to
undesirable high levels of Al (causing Alzheimer’s dementia).
Hence only a small proportion of Al salts are normally absorbed from
the gut, so even if an Al-F complex did form, it would be most unlikely
to be absorbed.

Effect on Red Blood Cells
• It is known that when fluoride is ingested, it accumulates on the erythrocyte
membrane, besides other cells, tissues and organs.
• The erythrocyte membrane in turn looses calcium content.
• The membrane which is deficient in Ca content, is pliable and is thrown into
folds.
• The RBCs attain the shape of an amoeba with pseudopodia like folds projecting in
different directions.
• Such RBCs are termed as Echinocytes.
Text book of community Dentistry. Vimal Sikri 2003, Chp 5, Pg 243

• The life span of RBCs is 120-130 days, the echinocytesundergo
phagocytosis and are eliminated from circulation quite clearly.
• This means that RBCs in individuals exposed to fluoride poisoning
do not live the entire life span, but are likely to be eliminated
as echinocytes.
• This leads to low hemoglobin levels.

Effect on Skeletal Muscles
• In a fluorosed muscles there are wide spread changes within a fibre
revealing destruction of the actin and myosin filaments.
• The mitochondria loses its structural integrity, thereby providing
evidence that muscle energy is likely to be depleted.
• Certain phosphokinase levels are high in serum of patients suffering from
skeletal fluorosis which is an indication that the muscle mitochondria is
destroyed and muscle membrane has become highly permeable.

Effect on ligaments and blood
vessels
• A unique feature of excess fluoridation is that
the soft tissues like ligaments and blood
vessels tend to harden and calcify.
• The blood vessels can be blocked by such
calcifications.

Neurological manifestations
• Nervousness, depression, tingling sensation in
finger and toes, excessive thirst (polydyspia)
and tendency to urinate frequency (polyuria)
are controlled by certain regions of the brain
and it appears to be adversely affected.

• The neurological manifestations have been
exclusively reported from India.
• Credit for the earliest description of
neurological complications in fluorosis must be
given to Shortt et al. (1937), who reported ten
such cases from Nellore district of Madras.

• A few sporadic cases have also been described from other parts
of India (Chuttani et al., 1962; Janardhanan and Venkaswamy,
1957; Murthi et al., 1953).
• Fluoride has been shown to interfere with glycolysis. Because
the central nervous system relies heavily on this energy source,
hypotheses have been advanced as to a mechanism for fluoride
effects on the central nervous system.

• Althoug effects on glycolytic enzymes could explain the neuromuscular
symptoms seen frequently in cases of fluoride poisoning (e.g., tetany,
paresthesia, paresis, convulsions), studies tend to indicate that hypocalcemia
caused by fluoride binding of calcium causes these symptoms (Eichler et al.,
1982).
• The decreases in intelligence were reported in children living in areas of China
with high levels of fluoride in the drinking water, as compared to matched
groups of children living in areas with lowl levels of fluoride in the drinking
water (Li et al., 1995; Lu et al., 2000), but these studies are weak in as much as
they do not address important confounding factors.

Effect on kidneys
• It is in literature that fluoridation is safe for persons with normal
kidney functions.
• There are remote possibilities that renal failure may cause
fluoride retention leading to higher tsuue fluoride concentration
and smaller margin of safety than for normal individuals.
• Roholm et al 2002, concluded in his study that cryolite produces
considerable changes in bone and ligament over long period of
exposure but not oral changes.

• No renal pathology in animal experimental studies is
been found with 50 ppm of fluoride or less.
• Certain species exhibited changes for abot 100ppm.
• Urine may be yellowish red in color and itching may
occur.

• Sometimes in acute conditions :
- Congestion and cloudy swelling of renal tubular cells
- Hyperemia and fatty degeneration of tubular
epithelium
- Not limited to kidney but widely distributed acyte
visceral hyperemia.
- If the individual survives, regeneration may occur
during recovery.

Effect on gastrointestinal
system
• The primary gastrointestinal effects following both acute and
chronic oral exposure to fluoride consist of nausea, vomiting,
and gastric pain. The irritation of the gastric mucosa is
attributed to fluoride (as sodium fluoride) forming hydrofluoric
acid in the acidic environment of the stomach (Hoffman et al.,
1980;Waldbott, 1981).
• The uncharged hydrogen fluoride molecule can then penetrate
cell membranes and enter the neutral environment of the
cytoplasm.

Non- ulcer dyspepsia due to excess intake of fluoride
• nausea
• loss of appetite
• pain in stomach
• gas formation & bloated feeling
• constipation followed by intermittent diarrhea,
• Headache
Treatment –drink safe water
(Susheela et al 1992, Das et al 1994, Dasarathy et al 1996)
• A study by Susheela et al. (1993) assessed the prevalence and severity of
gastrointestinal disturbance in an area of endemic skeletal and dental fluorosis
in India.

• The highest prevalence (52.4%) of non-ulcer dyspeptic symptoms
was found among 288 individuals (69 families) living in a village
where the mean fluoride concentration in the 36 separate water
sources was 3.2 ppm(range 0.25 to 8.0 ppm).
• Eleven of these water sources were defined by the authors as safe
(i.e., with fluoride levels of 1.0 ppm or less).
• The authors noted that in patients who reverted to safe water,
dyspeptic symptoms and complaints disappeared within 2-3
weeks.

Endocrine effects
• In the endocrine system where the intermediary
metabolism and synthesis of highly sensitive hormones
involves enzymatic action, it is expected that
interferences with the mechanism by chemical agents
would produce early and pronounced clinical effects.

• Considerable attention has consequently been given of
recent years to the behavior of fluoride in hormone
chemistry and to the possible and to the possible
clinical disturbances of endocrine function,
particularly the thyroid gland Robinson et al., 2002).

• Significant increases in serum thyroxin levels were observed
in residents of North Gujarat, India with high levels of
fluoride in the drinking water (range of 1.0–6.53 mg/L; mean
of 2.70 mg/L) (Michael et al., 1996).
• No significant changes in serum triiodothyronine or thyroid
stimulating hormone levels were found. Increases in serum
epinephrine and norepinephrine levels were also observed. It
is unclear if nutritional deficiencies played a contributing
role to the observed endocrine effects.

Effect on Thyroid
• It has been found that sometimes excessive
fluoridation effect does not exist for thyroid.
• The main facts behind this statement are:
- Fluorine does not accumulate in thyroid.
- Fluorine does not affect the uptake of iodine
by the thyroid tissues.
- Pathological changes in the thyroid shows no
increased frequency.

- The administration of fluorine does not
interfere with prophylactic action of iodine on
endemic goiter.
- The beneficial effect of iodine in threshold
dosage to experimental animals is not
inhibited by administration of fluorine even in
an excessive dose.

Fluoride and bone
• Animal studies- F effect on bone strength
• Human population – bone in children, hip in
elderly

Fluoride and arthritis (Eichmiller
– JADA 2005)
• 50yr old man- cancer –topical fluoride gel for a
long period
Gastric symptoms , leg muscle soreness and
knee joint soreness...
• Research from India – severe arthritic changes
& crippling neurologic complications

Osteoporosis
• Fluoride above 4 mg/l in drinking water may cause
a condition of dense and brittle bones known as
osteoporosis. It affects tens of million of people
worldwide and is responsible for as many as 75% of
all fractures in people over the age of 45.
• Costly and disabling fractures of spine, hip, wrist
and other bones can be preceded by years of
undetected bone loss. It is found that as many as
20% of those who suffer from osteoporosis related
hip fractures die within 6 months.
• Women are at four times greater risk of developing
osteoporosis than males (Bezerra et al., 2003).

Reproductive system
• There are limited data on the potential of
fluoride to induce reproductive effects in
humans following oral exposure.
• A metaanalysis found a statistically significant
association between decreasing total fertility
rate and increasing fluoride levels in municipal
drinking water (Freni, 1994).

• Annual county birth data (obtained from the
NationalCenter for Health Statistics) for over
525,000 women aged 10–49 years living in
areas with high fluoride levels in community
drinking water were compared to a control
population approximately 985,000 women)
living in adjacent counties with low fluoride
drinking water levels.

• The fluoride-exposed population lived in
counties reporting a fluoride level of 3 ppm or
higher in at least one system.
• The weighted mean fluoride concentration
(county mean fluoride level weighted by the
1980 size of the population served by the
water system) was 1.51 ppm (approximately
0.04mg fluoride/kg/day), and 10.40% of the
population was served by water systems with
at least 3 ppm fluoride.

• The mean weighted mean fluoride
concentration in the control population was
1.08 ppm (approximately 0.03 mg
fluoride/kg/day).
• However, this meta-analysis relied on a
comparison of two quite disparate data sets,
inasmuch as the fluoridation population often
did not correlate well with the population for
whom health statistics was available.

• Furthermore, other studies have not found a
similar correlation. Another study found
significantly decreased serum testosterone
levels in 30 men diagnosed with skeletal
fluorosis and in 16 men related to men with
fluorosis and living in the same house as the
patient (Susheela and Jethanandani, 1996).

• The mean drinking water fluoride levels were
3.9 ppm (approximately 0.11 mg
fluoride/kg/day), 4.5 ppm (0.13 mg
fluoride/kg/day), and 0.5 ppm (0.014 mg
fluoride/kg/day) in the patients with skeletal
fluorosis, related men, and a control group of
26 men living in areas with low endemic
fluoride levels.

• No correlations between serum testosterone
and urinary fluoride levels or serum
testosterone and serum fluoride levels were
found. One limitation of this study is that the
control men were younger (28.7 years) than
the men with skeletal fluorosis (39.6 years)
and the related men (38.7 years). In addition,
the groups are small and potentially
confounding factors are not well addressed
(Mychreest et al., 2002).

Cardiovascular effects
• The cardiovascular effects of fluoride have
been attributed to hypocalcemia and
hypercalemia caused by high fluoride levels.
• Fluoride can bind with serum calcium if the
dose is sufficient and cause hypocalcemia.
Calcium is necessary for the functional
integrity of the voluntary and autonomic
nervous systems.

• Hypocalcemia can cause tetany, decreased
myocardial contractility, and possibly
cardiovascular collapse (Bayless and Tinanoff,
1985).
• Hyperkalemia has been suggested as the cause
of the repeated episodes of ventricular
fibrillation and eventual death that are often
encountered in cases of fluoride poisoning
(Baltazar et al., 1980).

Immunological and
lymphoreticular effects
• A request to the American Academy of Allergy
was made by the U.S. Public Health Service for
an evaluation of suspected allergic reactions
to fluoride as used in the fluoridation of
community water supplies (Austen et al.,
1971).

• The response to this request included a review
of clinical reports and an opinion as to
whether these reports constituted valid
evidence of a hypersensitivity reaction to
fluoride exposure of types I, II, III, or IV
(Austen et al., 1971), which are, respectively,
anaphylactic or reaginic, cytotoxic, toxic
complex, and delayed-type reactivity.

• The Academy reviewed the wide variety of
symptoms presented (vomiting, abdominal pain,
headaches, scotomata [blind, or partially blind
areas in the visual field], personality change,
muscular weakness, painful numbness in
extremities, joint pain, migraine headaches,
dryness in the mouth, oral ulcers, convulsions,
mental deterioration, colitis, pelvic hemorrhages,
urticarial, nasal congestion, skin rashes, epigastric
distress, and hematemesis) and concluded that
none of these symptoms were likely to be
immunologically mediated reactions of types I–IV.

• No studies were located that investigated
alterations in immune response following
fluoride exposure in humans. No studies were
located that investigated alterations in
immune response following fluoride exposure
in human. In a study with rabbits administered
4.5 mg fluoride/kg/ day as sodium fluoride for
18 months, decreased antibody titers were
observed (Jain and Susheela, 1987).

• These results were observed after 6 months of
treatment; the authors hypothesized that a
threshold level is reached at which time the
immune system is impaired.
• However, as only one dose level (4.5 mg
fluoride/ kg/day) was tested, no dose-effect.

Effect at molecular level
• The acceleration of the aging process by
fluoride occurs at the bio-chemical level
through enzyme inhabitation, collagen break
down, genetic damage or disruption of the
immune system. Fluoride damage enzymes,
and results in a wide range of chronic disease.
• Fluoride as low as 1 mg/l causes breakdown of
collagen, the most abundant of the body
protein at 30%.

• It leads to irregular formation of collagen,
which serves as a major structural component
of skin, ligaments, tendons, muscles,
cartilage, bone and teeth. A number of studies
revealed that fluoride causes genetic damage.
• The mechanism cannot be exactly pinpointed
because fluoride interferes with a number of
physiological processes.

• Most evidence indicates that it acts on the
DNA Repair Enzyme system. It may also
interfere with DNA synthesis. If the
unprepared DNA damdamages occur in a cell,
producing a sperm or egg it will be replicated
in every cell of the offspring body and leads to
birth defects. Irreparable damage of a
segment of DNAis responsible for control of
cell growth and may cause tumors or cancer.

Effect on immune system
• Fluoride interacts with the bonds of protein
molecular required to maintain the normal shape
of proteins. The fluoride effect the immune system
by i) Damage the immune system by inhibiting the
migration rate of white blood cells to infected
means, ii) Interferes with phagcytosis (destruction
of bacteria and other foreign agents by white
blood cells or iii) Induces the release of super
oxide free radicals in resting white blood cell. The
fluoride induced interference leads to an increased
and more prolonged exposure of the body to
foreign materials and releases free radicals
damaging the body.

Effect on dental enamel
• Dental fluorosis is a condition that results from
the intake of excess levels of fluoride during
the period of tooth development, usually from
birth to approximately 6–8 years of age.
• It has been termed a hypoplasia or
hypomineralization of dental enamel and
dentine and is associated with the excessive
incorporation of fluoride into these structures.

• The severity of this condition, generally
characterized as ranging from very mild to
severe, is related to the extent of fluoride
exposure during the period of tooth
development.
• Mild dental fluorosis is usually typified by the
appearance of small white areas in the
enamel; individuals with severe dental
fluorosis have teeth that are stained and
pitted (“mottled”) in appearance.

• In human fluorotic teeth, the most prominent
feature is a hypomineralization of the enamel.
In contrast to many animal species, fluoride
induced enamel hypoplasia (indicating a
severe fluoride disturbance of enamel matrix
production) seems to be rare in affected
human enamel.

• The staining and pitting of fluorosed dental enamel
are both post eruptive phenomena (i.e., acquired
after tooth eruption and occur as a consequence of
the enamel hypomineralization).
• The incorporation of excessive amounts of fluoride
into enamel is believed to interfere with its normal
maturation, as a result of alterations in the
rheologic structure of the enamel matrix and/or
effects on cellular metabolic processes associated
with normal enamel development (WHO, 1984;
Aoba, 1997; Whitford, 1997). Experimental animal
studies suggest that this hypomineralization results
from fluoride disturbance of the process of enamel
maturation (Richards et al., 1986).

• In India, Viswanathan (1951) first reported a
disease similar to mottled enamel, which is
prevalent in human beings in Madras
presidency. Mahajan (1934) reported a similar
disease in cattle in certain parts of old
Hyderabad state. However, Shortt et al. (1937)
was the first to identify the disease as
fluorosis.
• Subsequent to these findings, cases of
fluorosis were reported from several other
parts of the country.

• Dental fluorosis is caused in human being consuming
water containing 1.5 mg/l or more of fluorides,
particularly frombirth to the age of eight.Mottled
enamel usually takes the shape of modification to
produce yellow brown stains or an unnatural opaque
chalky white appearance with occasional striations
patting.
• The incidence and severity of mottling was found to
increase with increasing concentration of fluoride in
drinking water. In extensive studies, Dean and
coworkers (Dean, 1942; Dean and Elvove, 1937) have
correlated the appearance and severity of dental
fluorosis to different fluoride levels in the drinking
water with the aid of a special classification and
weighing of severity of the lesion.

• Distribution of dental fluorosis at different
levels of fluoride in drinking water may be
assessed by a mottled enamel index of the
community, which is defined in terms of the
degree of severity of mottled enamel observed
clinically. Since no such data available in India
to evaluate community index of fluorosis and
in the absence of this permissive or excessive
limits of fluoride in drinking water are only
arbitrary.

CONCLUSION
Conc. Or dose of fluoride Effect
2ppm Injury to vegetation
1ppm Dental caries reduction
2ppm or more Mottled enamel
5ppm No osteosclerosis
8ppm osteosclerosis
20-80mg/day or more Crippling fluorosis
50ppm Thyroid changes
100ppm Growth retardation
More than 125ppm Kidney changes
2.5-5.0gm F Death

81
• Certainly Lethal dose (CLD) – 32 – 64mg/kg body weight
• Safety tolerated dose (STD) – 8 – 16mg/kg body weight
(1/4TH OF CLD)
• For Children - 15mg/kg
CLD – 5- 10 mg/kg of NaF

RECOMMENDATION
• Parental supervision of brushing or mouth
rinsing
• The use of small amounts of tooth paste
• The use of products with lower fluoride levels
• Teaching children not to swallow tooth paste
or mouth rinse
• Strict adherence to current recommendation
by professionals who prescribe fluoride dietary
supplement.

“TOO MUCH OF GOOD THING
SPOILS EVERYTHING”

• When used appropriately fluoride is a safe and effective
agent that can be used to prevent dental caries.
• In Indian Senario to ensure maximum results fluoridation
techniques should be used in combination.
• As majority of population reside in rural areas in india
water fluoridation may not be appropriate technique .
• Fluoride dentrifices and mouth rinses can be advised
for the general population.
• Introudction of school water fluoridation benefits the
children who are at higher risk.

References
• Hussain J and Sharma KC. Environmental Monitoring and
Assessment.March 2010, Volume 162, Issue 1, pp 1-14.
• Textbook of community Dentistry, TR Gururaja Rao. 2004
edi.
• Rajan et al 1987,1988, Use of fluoridated toothpaste -
Blood fluoride levels in children, International society of
fluoride research.
• American Academy of pediatric dentistry,1967, revised in
2014. Refernce manual , Vol 37 No.6.

• Murray et al, Fluorides in caries prevention, 3rd
edit, chapter 17 page 337.
• Hussain, I. Hussain, J., Sharma, K.C. and Ojha,
K.G.: In: Environmental Scenario of 21st Centaury,
APH Pub. Co.,NewDelhi, pp. 355 –374 (2002).
• Hussain, J., Sharma, K.C. andHussain, I.: Ind. J.
Environ. Health, (2004). Communicated.
• Connett, P.: Fluoride, 35(4): 245-24 (2002).
• Lavy, S.M.: J.Can. Dent.Associ., 69(5): 286-291
(2003).

• Lu,Y., Sun, Z.R. andWu,L.N.: Fluoride, 33(2):
74-78 (2000).
• Robinson, R.F., Griffith, J.R.,Wolowich,W.R.
andNahata, M.C.:Vet. Hum. Toxicol., 44(2):
93-95 (2002).

Fluoride and health

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