Fluoride and health

FLUORIDE AND HEALTH

Dr. Priyanka SharmaIII year MDSDept 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 20ppmDried sea foods also fluoride rich 84.5ppm (South East Asia)

Fluoride in beverages-Ranges from 0.05 to 1.05 ppm

Fluoride from food0.3 to 0.6 mg/dayFluoride intake in first 6months of life-bottle/breast fedBreast 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 AssessmentMarch 2010, Volume 162, Issue 1, pp 1-14

http://link.springer.com/journal/10661


http://link.springer.com/journal/10661/162/1/page/1

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,• HeadacheTreatment –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

http://www.fluoridealert.org/health/bone/fracture/index.html

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.

CONCLUSIONConc. Or dose of fluoride Effect 2ppm Injury to vegetation1ppm Dental caries reduction2ppm or more Mottled enamel5ppm No osteosclerosis8ppm osteosclerosis20-80mg/ day or more Crippling fluorosis50ppm Thyroid changes100ppm Growth retardationMore than 125ppm Kidney changes2.5-5.0gm 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/kgCLD – 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.



http://link.springer.com/journal/10661/162/1/page/1

• 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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