By Dr Senani Wijesena 29/07/2016

PART 1 – Introduction

Fluoride is an element widely distributed in the environment, occurring in the air, soils, rocks, and water from natural and chemical sources. It occurs naturally at low levels (0.11mg/L) in water derived from ground water, as calcium fluoride and other forms in Australia and the USA (N.B 1mg/L = 1ppm).

Over the past 100 years, the levels of fluoride in foods in general purchased at the grocery store have increased. The reasons for the increase include, the mass fluoridation of water supplies in some countries, the introduction of fluoride–based pesticides, the mechanical deboning processes (of chicken/meats) and the use of Teflon. Foods such as seafood, fluoridated milk, fruits and vegetables sprayed with pesticides and processed beverages contain between 0.5-0.8ppm of fluoride. Tea contains a high level on average 3ppm of fluoride.

Fluoride is not considered an essential nutrient for human health hence no recommended dietary allowance has been calculated.

Although fluoride is used industrially as a fluorine compound in the manufacture of ceramics, pesticides, aerosol propellants, refrigerants, glassware, and Teflon cookware, it is a generally unwanted byproduct of electricity generation, aluminium, coal, fertilizer, and iron ore manufacture. Fluoride, hence, contaminates our atmosphere and water supply as a pollutant. In addition to these sources, many countries, including Australia and the USA add fluoride to the public water supply increasing exposure and adverse health effects.

The fluoride that is used for industrial purposes as well as for water fluoridation is not the naturally occurring calcium fluoride that occurs in ground water but is fluorosilicic acid or sodium silicofluoride which is a by-product of the phosphate fertiliser industry. Fluorosilicic acid from this source is also contaminated with heavy metals such as lead, arsenic, aluminum, chromium, mercury, beryllium, cadmium, hydrogen fluoride and barium which then enters the public water supply. Fluorosilicic acid comes under many different names, all are classified by the Standard for the Uniform Scheduling of Drugs and Poisons (SUDP) as S7 poisons (others are arsenic, cyanide); and as health, physicochemical and eco-toxicological (environmental) hazards, according to Australia’s National Occupational Health and Safety Commission (NOHSC).

In 2014, the total Industry Emission of fluoride in Australia was calculated at 8.8 million kg for that year by the National Pollutant Inventory. The EPA (environment protection authority) in Australia has been alerted to the death and illness (fluorosis) leading to severe deformity of kangaroos in close proximity to smelters in Portland and Craigburn, Victoria and the high fluoride emission levels since 2005.  In 1952, a peer-reviewed study on Merino sheep in QLD by a senior government chemist J.M. Harvey was published detailing the fluoride poisoning of sheep due to drinking artesian water that contained naturally high fluoride levels. Similarly, cattle and horses exposed to high fluoride levels have experienced skeletal deformity, underactive thyroid, impaired fertility and dental fluorosis according to several reports and studies undertaken in Australia and world-wide over the last 60 years. The EPA has been investigating these emissions and levels, and states humans ‘may’ not be affected by these exposures, however further follow up studies have not been done.

To date, the Australian government has not undertaken any formal studies to evaluate the safety and adverse effects of water fluoridation on human health, despite many observational and epidemiological studies in humans world-wide and in Australia indicating a positive correlation between fluoride intake and disease.

How did water fluoridation begin?

The medicinal use of fluorides world-wide began in January 1945 when community water supplies in Grand Rapids, United States were fluoridated to a level of 1 ppm as a dental caries prevention measure. This was based on earlier observations of mottled teeth enamel (fluorosis) occurring in areas of the United States such as Colorado where fluoride levels were naturally high and the investigation into the cause being fluoride and the perceived association with reduced levels of dental caries.

It is now known that these earlier studies were inaccurate and flawed and that dental caries rates were no different between areas of high natural water fluoridation and low.  In fact, recent reviews of National data, world-wide, since the 1930’s, including New Zealand, USA and Australia, show that tooth decay had started to decline well before the first implementation of water fluoridation due to improved nutrition and public health. Despite early objection to fluoridate public water, water fluoridation was accepted into legislation.

Australia adopted the policy of fluoridating drinking water in the 1960’s and 1970’s, also despite flawed and conflicted studies. The Australian drinking water guidelines currently recommend a maximum concentration of fluoride of 1.5mg/L or 1.5 ppm that mirrors the WHO guidelines for drinking water quality 2006. Currently, Sydney Water fluoridates its water supply at 1ppm or 1mg/L with industrial fluorosilicic acid or sodium silicofluoride. An individual drinking 2 L of water per day for example will accumulate 2 mg per day of fluoride due to drinking water alone in Australia. The daily ingestion of fluoride varies, however, depending on amount of water consumed and also exposure from other sources such as food, beverages, pollution etc.

The maximum safe dosage of fluoride from ALL sources had been previously considered to be 8mg per day or 0.14 mg/kg. On March 22, 2006, the prestigious National Research Council of the National Academies of Science USA released a 450-page review of fluoride toxicity. The report, which was three years in the making, concluded that the safe drinking water standard for fluoride of 4 ppm or 4mg/L (8mg/day for a 2L daily water intake) causes significant damage to teeth, and places consumers at elevated risk for bone damage, including bone fracture and joint pain. Because of this, the NRC recommended that the fluoride safety standard be reduced to 2ppm, which is marginally higher than the amount of fluoride currently in the public water supply in the USA and Australia. In 2011, the U.S. Department of Health and Human Services and the U.S. Environmental Protection Agency (EPA) lowered the recommended level of water fluoride in the USA to 0.7 mg/L due to the observation of dental fluorosis (mottled teeth) in individuals exposed to fluoride from 1ppm/L. In addition to its concerns about tooth and bone damage, the NRC identified a range of other health effects that may be associated with fluoride exposure, including damage to the brain, disruption of the endocrine system (thyroid gland, pineal gland, and glucose metabolism), infertility and bone cancer. These will be discussed further later in this article.

Some countries around the world have naturally high levels of fluoride (>1.5mg/L) in its ground water and include parts of India, Sri Lanka, China, California, and certain parts of Africa (Zimbabwe, Gabon) and South America. Many studies from India and China have confirmed skeletal fluorosis/deformity and hypothyroidism (underactive thyroid) in a significant proportion of the population in highly fluoridated areas. India, in fact as a result of these findings has implemented a reverse osmosis filtration process to remove fluoride from the water supply. Bottled water and tap water from these countries may contain high amounts of fluoride if they are not previously filtered, despite not formally fluoridating their water supply.

Further discussion on world-wide water fluoridation

The United States’ lead in instituting artificial water fluoridation in the 1940’s led to its acceptance by the World Health Organization as an effective oral health intervention. At least 30 nations have instituted artificial water fluoridation policies as a result. However, a number of countries including Sweden, The Netherlands, Germany, Israel and Switzerland stopped fluoridating their water supplies due to concerns about safety and effectiveness. Community water fluoridation is rare in continental Europe with 98% choosing not to fluoridate drinking water. According to the Danish Ministry of Environment and Energy, “toxic fluorides have never been added to the public water supplies” therefore Denmark does not practice artificial water fluoridation. Near the end of 2015, Ireland was the only country in the European Union with a nationwide mandate for water fluoridation. In a 2002 public survey in Ireland, however, 45% of respondents expressed some concern about fluoridation.

Currently, only about 5% of the world’s population—350 million people—(including 200 million Americans) consume artificially fluoridated water globally. Only eight countries— Malaysia, Australia, USA, New Zealand, Singapore, Chile, Hong Kong and Brazil, have more than 50% of the water supply artificially fluoridated. Over the past two decades many small communities in Canada, the USA, Australia, and New Zealand have stopped fluoridating their water supplies and in Israel the Minister for Health announced in April 2013 the end of mandatory water fluoridation. However, public health authorities continue to try and develop new community water fluoridation schemes.

Water fluoridation world-wide and dental caries

The 1999 US Centers for Disease Control and Prevention (CDC) report states that despite the substantial decline in the prevalence and severity of dental caries in the United States during the 20^th Century (which occurred in both fluoridated and non-fluoridated areas in the USA and all western countries), this largely preventable disease is still common with national data indicating that 67% of persons aged 12-17 years and 94% of persons aged greater than 18 years have experienced caries in their permanent teeth. According to World Health Organization (WHO) data, the US, which fluoridates about two-thirds of public water supplies, actually has higher rates of tooth decay than many countries that do not fluoridate their water, including Denmark, the Netherlands, Japan, Belgium, and Sweden. Furthermore, if fluoride were effective in preventing caries, you would expect to see an increase in tooth decay when fluoridation is stopped. However, this is not the case.

So why fluoridate and in what form?

The only demonstrated positive impact of fluoride on human health is its contribution to prevention of dental caries (infection of teeth enamel) and this has only been shown consistently with TOPICAL fluoride application e.g. use of fluoridated toothpaste, gels, mouth washes, rinses and not with ingested fluoride from treated water, according to studies world wide including Australia, USA and Sweden.

Hydroxyapatite in teeth enamel is made up of calcium, magnesium, and phosphate compounds and is susceptible to decay induced by acid-producing bacteria. Fluoride interacts with hydroxyapatite to form fluoroapatite, which is less susceptible to erosion by acid-producing oral bacteria.

It is known that when fluoride from water is ingested, a large proportion of the fluoride is excreted in the urine, some deposits in bone and teeth and only a small amount reaches the tooth enamel via salivary secretions. Fluoride that is ingested is known to reach the teeth to exert its anti-caries effect via saliva only. However as only small amounts reach the tooth via this delivery method, unlike topical applications such as toothpaste, ingested fluoride via water has very little effect. Recent studies have shown that the differences in fluoride concentration in surface enamel between permanent teeth from areas with no or low water fluoride levels and fluoridated areas were minimal and that no difference in dental caries rates in children were detected. This supports the fact that effect of fluoride is almost exclusively post-eruptive (after teething) and topical rather than systemic, challenging claims made for water fluoridation’s efficacy.

Topical application of fluoride in the oral cavity has two advantages: a) application at the site of action; and b) reducing the systemic exposure since in subjects with an adequate spitting response, only a percentage (adults 10%, young children 40%) of the fluoride applied becomes inadvertently swallowed and systemically available. The effectiveness of topical fluoride treatments, i.e. fluoride varnish, gel, mouth rinse, or toothpaste on dental health have been compared in numerous studies. Results are clearly in favour of a beneficial effect of topical fluoride treatment. There was no evidence of adverse effects of topical fluoride treatments in these studies. However, Long-term studies in age groups other than children and adolescents are still lacking and it is recommended they be undertaken.

Topical fluoride and health cautions – click on link for article

Causes of dental caries and the role of fluoride – click on link for article

PART 2 – Adverse effects of fluoride on human health

No fluoride deficiency disease has ever been documented for humans. However, several adverse health effects of fluoride excess have been documented and warrant concern. A review by the National Research Council in the USA for the Environmental Protection Agency examined toxicological and physiological effects of fluoride on human health in 2006. This review and many other studies have identified a number of potential and established adverse effects and health problems associated with fluoride excess including cognitive (mental) impairment/low IQ in children, hypothyroidism, dental and skeletal fluorosis, hip fractures, enzyme and electrolyte (blood biochemistry) derangement, and cancer (including osteosarcoma, uterine cancer). Evidence in general suggests that fluoride has potential to cause major adverse human health problems while having only a modest dental caries prevention effect (topical fluoride only) leading to advice by those in the scientific community to cease water fluoridation in countries that practice it.

Fluoride and dental fluorosis

The adverse impact of fluoride in producing brittle teeth has been recognized in laboratory animals since 1933, and fluoride-induced brittle teeth were demonstrated to be worse with industrial fluorides compared with naturally occurring calcium fluoride. Since the 1980s numerous studies have identified that adults and children are exceeding the agreed limits for maximum fluoride intake, contributing to a rapid rise in dental fluorosis (mottled, brittle teeth due to low mineralisation)—the first sign of fluoride toxicity. There is no safe limit for fluoride ingestion in relation to dental fluorosis, but fluoridated levels exceeding 0.3 ppm have been associated with teeth mottling and discolouration.

Dental fluorosis remains highly prevalent world-wide. Currently, about 41-50% of children in Australia and the United States, where water has been fluoridated at an average level of 1 ppm, have varying degrees of dental fluorosis—with levels of over 50% occurring in some fluoridated areas. Excess fluoride exposure during the first 8 years of a child’s life when teeth are developing (i.e. prior to tooth eruption) is the cause of dental fluorosis and manifests as white spots, streaks, brown stains, pitting and other defects in the tooth enamel. Although fluorosis can be cosmetically treated, the damage to the enamel is permanent and can psychologically affect the individual. Common causes of fluorosis include: fluoridated drinking water (particularly during infancy), ingestion of fluoride toothpaste, use of fluoride tablets, and consumption of processed foods made with fluoridated water. The safe level for aesthetic or cosmetic effects such as dental fluorosis has been set lower by the National Research Council USA at 2mg/L fluoride.

Fluoride and IQ of children and thyroid function

As early as 1928, Stocks observed that children consuming well water (contains naturally high fluoride) in the village of Somerset, England exhibited both goiter (enlarged thyroid) and mottled enamel teeth (dental fluorosis). Some years later, Wilson (1941) found dental fluorosis associated with goiter and cretinism among children living in areas of Punjab where fluoride was recognized geologically to be significantly high. In a 2005 study, it was found that 47% of children living in a New Delhi neighbourhood with average water fluoride levels of 4.37 ppm had evidence of clinical hypothyroidism (underactive thyroid) attributable to fluoride.

In a recent meta-analysis of 27 studies of fluoride and neurotoxicity, mostly in China, a loss of 7 points in IQ was noted in children on average and a significant decline in cognitive function attributed to fluoride ingestion at 2.5 to 4 mg/L in drinking water. On review of these studies by the NRC in the USA, they state “although the studies lacked sufficient detail for the committee to fully assess their quality and relevance to U.S. populations, the consistency of the results appears significant enough to warrant additional research on the effects of fluoride on intelligence.”

It is well known that low IQ and brain dysfunction/cretinism and degenerative changes in the central nervous system can occur in children exposed to low thyroid function in their pregnant mothers and during early childhood. In fact, several authors have reported an association between endemic goiter and fluoride exposure in human populations in India, Nepal, England, South Africa and Kenya. Although endemic goiter is generally attributed to iodine deficiency, some of the goitrogenic areas associated with fluoride exposure were not considered to be iodine deficient.

The mechanisms through which fluoride exacerbates hypothyroidism include competitive binding with iodine, decreased uptake by cells of the thyroid hormones, as well as synthesis obstruction of thyroid hormones T3 and T4. Fluoride is known to interfere with the activity of the enzyme, deiodinase that converts T4 to the active T3 in the periphery and in humans is associated with elevated TSH concentrations (a laboratory sign of low thyroid function).

Fluoride-induced hypothyroidism is likely to be more common in iodine- deficient settings. Australian surveys indicate that the general Australian population is mildly deficient in iodine. Iodine-deficient children ingesting fluoridated water have been found to demonstrate intellectual deficits even at water fluoride levels of 0.9 ppm.

After taking account of influential factors such as gender and age, both of which are linked to increased risk of hypothyroidism, a 2012 cross-sectional observational study in the U.K (where 10% of the population receives fluoridated water) found areas with fluoride levels above 0.3mg/L had higher than expected rates of hypothyroidism than in areas with levels below this dilution. In the conclusion, the researchers stated their concern about the validity of community fluoridation as a safe public health measure and recommended that public dental health interventions should ‘stop those reliant on ingested fluoride and switch to topical fluoride base and non-fluoride based interventions’.

The above findings have been reiterated by the 2006 NRC official report in the USA on Fluoride and its effect on human health, further noting that in humans, effects on thyroid function were associated with fluoride exposures of 0.05-0.13 mg/kg/day when iodine intake was adequate and 0.01-0.03 mg/kg/day when iodine intake was inadequate. The effects of fluoride on thyroid function, for instance (as noted by this report), might depend on whether iodine intake is low, adequate or high, or whether dietary selenium is adequate” The NRC noted that the effect on the thyroid gland can occur at 10 times lower levels than the purported safe dosage (0.114mg/kg/day) which are exceeded by millions of children and adults in the USA and Australia drinking water fluoridated at 1ppm.

Fluoride and Skeletal Fluorosis

Skeletal fluorosis is a chronic metabolic bone disease caused by ingestion or inhalation of large amounts of fluoride. Skeletal fluorosis is common (>20% prevalence) in those ingesting fluoride >2 ppm and manifests as joint pain in both upper and lower limbs, numbing and tingling of the extremities, back pains, and knock-knees. Clinical complications of skeletal fluorosis include arthritis, radiculomyelopathy (disease of the spinal cord and spinal nerve roots), quadriparesis, and pathological bone fractures.

Clinical studies have shown that fluoride intake (via systemic exposure) rapidly enters mineralized tissues like bone and developing teeth and forms a complex known as fluorapatite. By competing with magnesium and calcium in teeth and bones, fluoride deranges the delicate bone formation and bone resorption processes. It causes a delay in mineralization of bone. More recently, fluoride has been shown to induce osteoclastogenesis (bone breaking down) in mice. Fluoride is also known to be mitogenic (induce cell replication) at low concentrations and can inhibit enzyme function. While fluoride may increase bone mass (its predominantly anabolic effect), the newly formed bone appears to lack normal structure and strength according to human and animal studies. These effects cause a change in bone matrix and its crystalline structure and to a reduction in mechanical strength properties leading to increased susceptibility to fractures and cancer.

High systemic fluoride exposure can lead to skeletal sclerosis (excess hardening of bone), ligament calcifications, and often osteoporosis, osteomalacia or osteopenia (low bone density). An increased incidence of hip fracture associated with systemic fluoride intake has been noted in many studies as well as an increased risk of developing osteosarcoma (bone cancer).

Fluoride and bone fractures

A summary of 33 studies since 1991 was done by the National Health and MRC (medical research council) of Australia on the effects of fluoride on bone. One of two cohort studies showed an increase in fracture incidence at fluoride levels four times greater than optimal water fluoridation and the other showed no effect after 20 years optimal fluoridation. Analysis of these studies also led to the conclusion that fluoride up to 1mg/L does not have an adverse effect on bone strength, bone mineral density or incidence of fracture. Several studies world-wide, however, have shown an increased risk of hip fracture in both men and women exposed to artificial fluoridation at 1ppm, suggesting that low levels of fluoride may increase the risk of hip fracture in the elderly. A report by the NRC in 2006 USA concluded that the EPA’s (Environmental protection agency) maximum safe drinking water fluoride standard (4mg/L) is too high and does not protect against adverse health effects such a skeletal fluorosis and bone fractures for a lifetime exposure. According to the 2006 NRC report, hip fractures in the elderly were observed (a) in Finland at water levels at or greater than 1.5ppm (b) increasing in what appears a linear fashion between 1ppm and 4.3ppm in China while (c) bone fracture (of any type) were found to increase between 1.5 and 5.5 in Mexico. Based on available evidence, the NRC concluded that fluoride increases the rate of bone fracture at 4 ppm (the level currently considered “safe” by the EPA), and noted that fluoride may increase the fracture risk at levels lower than 4 ppm, however, it failed to state what level is considered to be safe. Considering humans are exposed to other sources of fluoride such as industrial and food sources, caution must be taken when considering overall daily fluoride intake.

Since the integrity of cortical bone is critical to hip strength, fluoride’s ability to reduce cortical (compact) bone density has been posited as a key mechanism explaining the link between fluoride and hip fractures. Even when fluoride increases bone density, as it often does with trabecular (spongy) bone, it can simultaneously make your bone more brittle and subject to fracture due to the reduced strength of the bone that is laid down.

Fluoride and Brain

Histopathological changes similar to those associated with Alzheimer’s disease in people have been seen in rats chronically exposed to fluoride, according to the 2006 NRC report. Fluorides increase the production of free radicals in the brain and oxidative stress is known to be the underlying pathological mechanism for development of Alzheimer’s disease. In these animal studies, following fluoride exposure, oxidative stress increased significantly, estimated by increased lipid peroxidation and a decrease in the activity of the antioxidant enzyme, superoxide dismutase. The neurotransmitter (e.g., dopamine, norepinephrine, and serotonin) content was also altered. However, these aspects were more pronounced in animals given fluoride and aluminum together.

The NRC recommended further research needed to be undertaken to clarify fluoride’s biochemical effects on the brain, including studies of populations exposed to different concentrations of fluoride in drinking water should include measurements of reasoning ability, problem solving, IQ and short and long term memory.

Fluoride and Cancer

There have also been a number of studies that link fluoride and cancer. Most of these studies conclude that the evidence has been inadequate to draw conclusions one way or another and that the evidence linking fluorides with cancer was deemed “inadequate”. Some population-based-studies, however, strongly suggest that chronic fluoride ingestion is a possible cause of uterine cancer and bladder cancer and that there may be a link with osteosarcoma (rare malignant bone tumor occurring mostly in individuals between 10-24 years old). Some studies have also linked high incidence of bone cancer to fluoridation in drinking water and animal studies show mitogenic effects of fluoride on bone cells. On the other hand, a few reports have also indicated that fluoride exposure has no role in osteosarcoma. Further research, hence is required.

The 2006 NRC report has made several statements regarding the link between fluoride and cancer and include; Fluoride appears to have the potential to initiate or promote cancers, particularly of the bone, but the evidence is tentative and mixed. Osteosarcoma is of particular concern as a potential effect of fluoride because of (1) fluoride deposition in bone (2) the mitogenic effect of fluoride on bone cells (stimulates osteoblasts/bone cells causing proliferation) (3) a pre-1993 publication of some positive as well as negative, epidemiological reports on association of fluoride exposure with osteosarcoma risk.

Fluoride tends to accumulate in parts of bones where they are growing: these areas, known as growth plates are where osteosarcomas typically develop. During periods of rapid skeleton growth, fluoride uptake in bone increases and fluoride has been reported to increase calcium absorption in the intestine. A recent study also found high serum (blood) fluoride levels in osteosarcoma patients along with high drinking water fluoride level in these patients suggesting a link between water fluoride and osteosarcoma.

The NRC 2006 report also recommended further research be undertaken to assess the possible risk of fluoride on bladder cancer risk. An ecological study from Taiwan found a high incidence of bladder cancer in women in areas where natural fluoride content in water is high. The link between fluoride exposure as a cause of bladder cancer in this study however was difficult to confirm according to the authors due to other confounding variable factors, however, the finding is a cause for concern. Industrial fluoride exposure and its association with excess incidences of primary cancer of the lungs and urinary bladder have been observed in workers at the cryolite mill in Copenhagen, Denmark between the years 1943 to 1987 who were employed at the mill for more than 6 months from 1924 to 1961. The study had been extended a further 12 years to 1999 and confirms the initial observations.

Other effects of fluoride on human health

The single animal study of pineal function indicates that fluoride exposure results in altered melatonin production and altered timing of sexual maturity (early menarche age/onset of periods) with the later being supported by two human studies. Whether fluoride affects pineal function in humans remains to be demonstrated. Recent data on pineal organ function in humans suggests that altered pineal gland function could affect not just sexual maturation, but also calcium metabolism, parathyroid function, postmenopausal osteoporosis, cancer and psychiatric disease.

The 2006 NRC report states in regards to Diabetes Mellitus-“The conclusion from the available studies is that sufficient fluoride exposure appears to bring about increases in blood glucose or impaired glucose tolerance in some individuals and to increase the severity of some types of diabetes. In general, impaired glucose metabolism appears to be associated with serum or plasma fluoride concentrations of about 0.1 mg/L or greater in both animals and humans. In addition, diabetic individuals will often have higher than normal water intake, and consequently, will have higher than normal fluoride intake for a given concentration of fluoride in drinking water. An estimated 16-20 million people in the U.S. (and over 1 million people in Australia) have been diagnosed with diabetes mellitus; therefore, any role of fluoride exposure in the development of impaired glucose metabolism or diabetes is potentially significant.”

As the human kidneys concentrate fluoride as much as 50-fold from plasma to urine the effect of low doses of fluoride on kidney and liver enzyme functions in humans needs to be carefully documented in communities exposed to different concentrations of fluoride in drinking water. It has also been suggested by the NRC and scientists that as fluoride accumulates in high concentration in bone and bone marrow is where the progenitors of the immune system cells are found, the effect of fluoride on immune function needs to be further assessed particularly up to water fluoridation levels of 4mg/L and in immune-compromised individuals.

Conclusion

In an extensive review of fluoride and human health published in 2011, the European Commission’s Scientific Committee on Health and Environmental Risks concluded that fluoride is not essential for human growth and development. However, despite widespread recognition of the nonessential nature of fluoride, the Australian National Health and Medical Research Council and the New Zealand Health Ministry currently regard fluoride as a nutrient and have provided nutrient reference values for fluoride and the European Union is currently consulting on whether to set recommended levels for adequate daily intake.

Fluoride has modest benefit in terms of reduction of dental caries but significant costs in relation to cognitive impairment, hypothyroidism, dental and skeletal fluorosis, enzyme and electrolyte derangement, and uterine cancer. Given that most of the toxic effects of fluoride are due to ingestion, whereas its predominant beneficial effect is obtained via topical application, ingestion or inhalation of fluoride predominantly in any form constitutes an unacceptable risk with virtually no proven benefit.

Of all sources of fluoride, artificially fluoridated water is the most practical source to eliminate in order to reduce its human hazards at population levels. Indeed, the abundance of fluoride sources ingested by humans, from tea to cereals and condiments, suggest that the prime public health priority in relation to fluoride is how to reduce ingestion from multiple sources, rather than adding this abundant and toxic chemical to water or food.

Dental caries is essentially the outcome of bacterial infection of teeth enamel. Newer non-fluoride approaches such as probiotics, Xylitol/stevia (natural sweetener), improved diet and biofilms show increasing promise in caries prevention with a strong safety profile in relation to human health.

References

1. Sugars and Dental Caries. The American journal of clinical Mutrition, October 2003, Vol 78, No 4, 881S-892S
2. health.nsw.gov.au/oralhealth/pages/water-fluoridation-fact-sheet.aspx
3. Yonsei Med J.1997 Apr; 38(2):101-10. Relationship between nutritional intake and dental caries experience of junior high students. Kwon HK1, Suh I, Kim YO, Kim HJ, Nam CM, Jun KM, Kim HG.
4. http://ec.europa.eu/health/scientific_committees/opinions_layman/fluoridation/en/l-3/5.htm
5. J Epidemiol Community Health.2015 Jul;69(7):619-24. doi: 10.1136/jech-2014-204971. Epub 2015 Feb 24. Are fluoride levels in drinking water associated with hypothyroidism prevalence in England? A large observational study of GP practice data and fluoride levels in drinking water. Peckham S1, Lowery D1, Spencer S
6. npi.gov.au
7. Kaste LM, Selwitz RH et al. Coronal Caries in the primary and permanent dentition of children and adolescents 1-17 years of age: United States, 1988-91. J Dent Res 1996; 75:631-41
8. Winn DM, Brunelle JA, Selwitz RH, et al. Coronal and root caries in the dentition of adults in the United States, 1988-91. J Dent Res 1996; 75:642-51
9. Brunelle JA, Carlos JP. Recent trends in dental caries in US children and the effect of water fluoridation. J Dent Res 1990:69:723-727
10. Newbrun E. Effectiveness of water fluoridation . J Public Health Den 1996;65:253-258
11. John Colquhoun DDS PhD, Why I changed my mind about water fluoridation. Perspectives in Biology and Medicine Volume 41, page 29-44 1997.
12. Oral Manifstation of thyroid disorders and its management. Shalu Chandna and Manish Bathla. Indian J Endocrinol Metab 2011 July; 15 (suppl2): S113-S116
13. Navneet Singh et al. A comparative study of fluoride ingestion levels, serum thyroid hormone and TSH level derangements, dental fluorosis status among school children from endemic and non-endemic fluorosis areas. Springerplus, 2014:3:7
14. Susheela et al Excess fluoride ingestion and thyroid hormone derangements in children living in Delhi India. Fluoride. 2005;38:151-161
15. Wu et al. Effects on fluoride and arsenic on serum thyroid hormone in rats. J Herbal Medic Toxico. 2008;2:39-43
16. Xiang et al. Fluoride and thyroid function in two villages in China. J Toxicol Environ Health Sci. 2009;1:54-59
17. Dagmar et al. Fluorine in the aetiology of endemic goiter. The Lancet. 1941; Vol 237 (6129): 211-212
18. Bobek S. Kahl S. Ewy Z. Effect of long term fluoride administration on thyroid hormone level blood in rats. Endocrinol Exp. 1976; 10 (4). 289-95
19. Zhao et al. Long term effects of various iodine and fluorine doses on the thyroid and fluorosis in mice. Endocr Regul 1998 June; 32 (2) 63-70
20. Wang et al. Fluoride-induced thyroid dysfunction in rats: roles of dietary protein and calcium levels. Toxico Ind Health. 2009 Feb; 25(1) 49-57
21. Jiang et al. Effects of excess fluoride and Iodide on thyroid function and morphology. Biol Trace Elem Res. 2016 April; 170 (2) 382-9
22. Siddiqui A H . Fluorosis in Nalgonda district, Hypederabad. Br Med J. 1955;2:1408-13
23. Desai MP. Disorders of the thyroid gland in India. Indian J Pediatr. 1997;64:11-20
24. Day TK. Powell-Jackson PR. Fluoride water hardness and endemic goiter. Lancet. 1972;1:113-8
25. Steyn DG. Reinach Endemic goiter in the union of South Africa and some neighbouring territories. Dept Nutr. 1955:7:18-24
26. Jooste PL. Weight MJ et al. Endemic goiter in the absence of iodine deficiency in schoolchildren of the northern cape province of South Africa. Eur J Clin Nutr. 1999; 53: 8-12
27. Sudhir et al. Assessment of skeletal and non skeletal fluorosis in endemic fluoridated areas of Vidharbha Region, India: A survey. Indianjournal of community medicine: Official publication of Indian association of preventive and social medicine. 2010 April; 35 (2): 298-301
28. ET Everett. J Dent Res 2011 May; 90(5): 552-560
29. SR Grobler et al. The relationships between two different drinking water fluoride levels, dental fluorosis and bone mineral density in children. The open dentistry journal. 2009; 3: 48-54
30. Christa Danielson et al. Hip fractures and fluoridation in Utah’s elderly population. JAMA 1992; 268 (6). 746-748
31. L Rune Hedlund and JC Gallagher. Increased incidence of hip fracture in osteoporotic women treated with sodium fluoride. Journal of bone and mineral research. 1989; Volume 4; Issue 2; 223-225
32. Drug Chem Toxicol.2009;32(3):215-21. Effect of concurrent chronic exposure of fluoride and aluminum on rat brain. Kaur T1, Bijarnia RK, Nehru B.
33. K Cheng. Adding fluoride to water supplies to prevent dental caries is controversial. BMJ 2007 Oct 6; 335 (7622): 699-702
34. Philippe Grandjean. Extended follow up of cancer incidence in fluoride exposed workers. J Natl Cancer Inst (2004) 96 (10) ;802-802
35. Turner et al. Calcif Tissue Int. 1993 Feb;52(2):130-8. A mathematical model for fluoride uptake by the skeleton.
36. Elise B Bassin et al. Age specific fluoride exposure in drinking water and osteosarcoma (USA). Cancer causes and control. May 2006, Volume 17, pp 421-428
37. Caverzasio J, Palmer G, Suzuki A, Bonjour JP. Mechanism of the mitogenic effect of fluoride on osteoblast-like cells; evidence for a G-protein dependent tyrosine phosphorylation process. J Bone Miner Res. 1997;12:1975–83.
38. Sandhu R, Lal H, Kundu ZS, Kharb S. Serum fluoride and sialic acid levels in osteosarcoma. Biol Trace Elem Res. 2011;144:1–5 (accepted).
39. Pasquini GM, Davey RA, Michelangeli VP, Grill V, Kaczmarczyk SJ, Zajac JD. Local secretion of parathyroid hormone related protein by an osteoblastic osteosarcoma (UMR 106-01) cell line results in growth inhibition. Bone. 2002;31:598–605.
40. Xiang QY, Liang YX, Chen BH, Wang CS, Zhen LQ, Chan LS, et al. Study on the application of benchmark dose and biological monitoring indexes of fluoride in drinking water. Zhonghua Yu Fang Yi Xue Za Zhi. 2004;38:261–4.
41. Wergedal JE, Lau K-HW, Baylink DJ. Fluoride and bovine bone extract influence cell proliferation and phosphatase activities in human bone cell cultures. Clin Orthop Relat Res. 1988;233:274–82.
42. Ramesh N, Vuayaraghavan AS, Desai BS, Natarajan M, Murthy PB, Pillai KS. Low levels of p53 mutations in Indian patients with osteosarcoma and the correlation with fluoride levels in bone. J Environ Pathol Toxicol Oncol. 2001;20:237–43.
43. REPORT OF THE FORUM on Fluoridation, 2002, pg 37)
44. Dr Mercola website.