(Adapted for the UK from Fluoride Action Network’s compendium of 50 Reasons.)

In pharmaceutical medicines which possess marketing authorisations, fluoride is classified as a drug when used to prevent or mitigate disease. As a matter of basic logic, adding fluoride to water for the sole purpose of preventing tooth decay (a non-waterborne disease) is a form of medical treatment. This converts potable drinking water into a prophylactic medicine. All other water treatment chemicals are added to improve the water’s quality or safety, which fluoride does not do.

Three Courts of Law since 1958 have ruled that fluoridated water is a medicine. (The Supreme Court of Canada, 1958; Scotland, 1983; The Supreme Court of New Zealand, 2018). In England, a piece of Primary Law, the Medicines Act 1968 s.130, defines a medicine and although fluoridated water is not specifically mentioned, the definition of a medicine in the Act matches the physical state and intention of the compound created when an active substance (fluoride) is added to a carrier (drinking water). Shaw (2012) writes: “Water fluoridation is currently permitted [in England and Wales] by the Water Act 2003, but this appears to contradict legislation and regulations governing food and healthcare in the UK and the EU. It is concluded that the status quo rests on the legal fiction that fluoridated water does not constitute a medication.” 

Informed consent is standard practice for all medication, and one of the key reasons why most of Western Europe has ruled against fluoridation. With water fluoridation we are allowing governments to do to whole communities (forcing people to take a medicine irrespective of their consent) what individual doctors cannot do to individual patients. Put another way: Does one resident have the right to require that their resident neighbour ingests a certain medication even if it is against that neighbour’s will? (NHS Constitution; European Convention on Human Rights and Biomedicine, Article 5).  The UK Care Act 2014 in its preamble appears to place a responsibility on Local Authorities to respect their Constituents’ Human Rights. 

Once fluoride is put in the water it is impossible to control the dose each individual receives because people drink different amounts of water. Being able to control the dose a patient receives is critical in mainline medical practice. Some people (e.g., manual labourers, athletes, diabetics, pregnant women and people with kidney disease) drink substantially more water than others. 

According to Dr. Arvid Carlsson, the 2000 Nobel Laureate in Medicine and Physiology and one of the scientists who helped keep fluoridation out of Sweden: “Water fluoridation goes against leading principles of pharmacotherapy, which is progressing from a [universal] stereotyped medication — of the type “1 tablet containing 1mg of the active substance 3 times a day” — to a much more individualized therapy as regards both dosage, strength and selection of drugs. The addition of drugs to the drinking water means exactly the opposite of an individualized therapy” (Carlsson 1978). (See https://www.medicalprotection.org/uk/articles/consent-uk – a patients’ autonomy and right to withhold consent.)

Fluoridated water is not the only way people are exposed to fluoride. Other sources of fluoride include food and beverages processed with fluoridated water (Kiritsy 1996; Heilman 1999), fluoridated dental products (Bentley 1999; Levy 1999), mechanically deboned meat (Fein 2001), TEA (Levy 1999), and pesticide residues (e.g., from cryolite) on food (Stannard 1991; Burgstahler 1997). It is now widely acknowledged that exposure to non-water sources of fluoride has significantly increased since the water fluoridation programme first began (NRC 2006). The advice given by the World Health Organisation is that exposure to fluoride should be quantified before more fluoride is added to people’s environment.

The World Health Organisation’s recommendation

“In setting national standards or local guidelines for fluoride or in evaluating the possible health consequences of exposure to fluoride, it is essential to consider the intake of water by the population of interest and the intake of fluoride from other sources (e.g., from food and air). Where the intakes are likely to approach, or be greater than, 6 mg/day, it would be appropriate to consider setting a standard or local guideline at a concentration lower than 1.5 mg/litre.” (Ref. WHO/SDE/WSH/03.04/96)

Sources of Fluoride in England

• Artificial (intentional) fluoridated water. In the UK, up to 1 mg F/litre.

• Natural fluoride. In the UK 0.1 – 1.3 mg F/litre. (There are no areas in the UK which have natural fluoride as high as 5mg F/litre.). Hartlepool has 1.9 mg F/litre diluted with non-fluoride water = 1.3mg F/litre.

• Some Natural Mineral and Spring bottled water: S. Pellegrino 0.5ppm, Badoit 1ppm

• Table Water (bottled). This is often tap water and probably contains fluoride.

• Swallowed and absorbed fluoride toothpaste. 

• Pharmaceuticals –several contain fluoride inc. Prozac, Rohypnol, Diflucan, Ventolin

• Anaesthetics – the most common one contains fluoride.

• TEA – the cheaper the tea (economy labels) the more fluoride.

• Beverages using fluoridated tap water – e.g. Pepsi Max made up with fluoridated water in Rugby by Britvic under licence to PepsiCo: Sainsbury’s traditional cider concentrate made up with 0.5ppm fluoridated water.

• Food manufactured in fluoridated areas which have water as an ingredient.

• Dental preparations: floss, mouthwash, varnishes, sealants, glass ionomer fillings, dental cement.

• Bath water. 200 litres contain 200 mg fluoride. Up to 18 mg HF as hydrofluoric acid which is absorbable through the skin. HF acid is a reportable poison.

• Bath water vapour contains hydrogen fluoride gas which is deadly at higher concentrations.

• Pesticides, chlorofluorocarbons, coal burning and industrial exposures.         

No disease, not even tooth decay, is caused by a “fluoride deficiency” (NRC 1993; Institute of Medicine 1997, NRC 2006). Not a single biological process has been shown to require fluoride. On the contrary there is extensive evidence that fluoride can interfere with many important biological processes. Fluoride interferes with numerous enzymes (Waldbott 1978). In combination with aluminium, fluoride interferes with G-proteins (Bigay 1985, 1987). Such interactions give aluminium-fluoride complexes the potential to interfere with signals from growth factors, hormones and neurotransmitters (Strunecka & Patocka 1999; Li 2003). More and more studies indicate that fluoride can interfere with biochemistry in fundamental ways (Barbier 2010).

Not being an essential nutrient, it is perhaps not surprising that the level of fluoride in mother’s milk is remarkably low (0.004 ppm, NRC, 2006). This means that a bottle-fed baby consuming fluoridated water (0.6 – 1.2 ppm) can get up to 300 times more fluoride than a breast-fed baby. There are no benefits (see reasons 11-19, only risks; see also reasons 21-36), for infants ingesting this heightened level of fluoride at such an early age, an age where susceptibility to environmental toxins is particularly high.

Healthy adult kidneys excrete 50% to 60% of the fluoride they ingest each day (Marier & Rose 1971). The remainder accumulates in the body, largely in calcifying tissues such as the bones and pineal gland (Luke 1997, 2001). Infants and children excrete less fluoride from their kidneys and take up to 80% of ingested fluoride into their bones (Ekstrand 1994). The fluoride concentration in bone steadily increases over a lifetime (NRC 2006).

No regular measurements are being made of the levels of fluoride in urine, blood, bones, hair, or nails of either the general population or sensitive sub-parts of the population (e.g., individuals with kidney disease).  The World Health Organisation recommends that surveys are carried out in order to determine the level of fluoride in a person’s body before raising the level of fluoride in drinking water.  The WHO is concerned about over-exposure.

Despite the fact that fluoride has been added to drinking water for over 60 years, “there have been no randomized trials of water fluoridation” (Cheng 2007). Randomised studies are the standard method for determining the safety and effectiveness of any purportedly beneficial medical treatment. In 2000, the British Government’s “York Review” could not give a single fluoridation trial a Grade A classification – despite 50 years of research (McDonagh et al 2000). The U.S. Food and Drug Administration (FDA) continues to classify fluoride as an “unapproved new drug.”

There is no need whatsoever, therefore, to swallow fluoride to protect teeth. Since the purported benefit of fluoride is topical, and the risks are systemic, it makes more sense to deliver the fluoride directly to the tooth in the form of toothpaste. Since swallowing fluoride is unnecessary, and potentially dangerous, there is no justification for forcing people (against their will) to ingest fluoride through their water supply.

Most western, industrialized countries have rejected water fluoridation, but have nevertheless experienced the same decline in childhood dental decay as fluoridated countries. (See data from World Health Organization presented graphically in Figure). **

The largest survey ever conducted in the US (over 39,000 children from 84 communities) by the National Institute of Dental Research (NIDR) showed little difference in tooth decay among children in fluoridated and non-fluoridated communities (Hileman 1989). According to NIDR researchers, the study found an average difference of only 0.6 DMFS (Decayed, Missing, and Filled Surfaces) in the permanent teeth of children aged 5-17 residing their entire lives in either fluoridated or unfluoridated areas (Brunelle & Carlos, 1990). This difference is less than one tooth surface, and less than 1% of the 100+ tooth surfaces available in a child’s mouth. Large surveys from three Australian states have found even less of a benefit, with decay reductions ranging from 0 to 0.3 of one permanent tooth surface (Spencer 1996; Armfield & Spencer 2004). None of these studies have allowed for the possible delayed eruption of the teeth that may be caused by exposure to fluoride, for which there is some evidence (Komarek 2005). A one-year delay in eruption of the permanent teeth would eliminate the very small benefit recorded in these modern studies.

A multi-million dollar, U.S. National Institutes of Health (NIH)-funded study found no significant relationship between tooth decay and fluoride intake among children (Warren 2009). This is the first time tooth decay has been investigated as a function of individual exposure (as opposed to mere residence in a fluoridated community).

Despite some claims to the contrary, water fluoridation cannot prevent the oral health crises that result from rampant poverty, inadequate nutrition and lack of access to dental care. There have been numerous reports of severe dental crises in low-income neighbourhoods of US cities that have been fluoridated for over 20 years (e.g., Boston, Cincinnati, New York City, and Pittsburgh). In addition, research has repeatedly found fluoridation to be ineffective at preventing the most serious oral health problem facing poor children, namely “baby bottle tooth decay,” otherwise known as early childhood caries or incisor decay (Barnes 1992; Shiboski 2003).

Where fluoridation has been discontinued in communities from Canada, the former East Germany, Cuba and Finland, dental decay has not increased but has generally continued to decrease (Maupomé 2001; Kunzel & Fischer, 1997, 2000; Kunzel 2000; Seppa 2000; PHE Bedford 2015).

Modern research shows that decay rates were coming down before fluoridation was introduced in Australia and New Zealand and have continued to decline even after its benefits would have been maximized. (Colquhoun 1997; Diesendorf 1986). As the following figure indicates, many other factors are responsible for the decline of tooth decay that has been universally reported throughout the western world.

The early trials conducted between 1945 and 1955 in North America that helped to launch fluoridation, have been heavily criticised for their poor methodology and poor choice of control communities (De Stefano 1954; Sutton 1959, 1960, 1996; Ziegelbecker 1970). According to Dr. Hubert Arnold, a statistician from the University of California at Davis, the early fluoridation trials “are especially rich in fallacies, improper design, invalid use of statistical methods, omissions of contrary data, and just plain muddleheadedness and hebetude [mental dullness].” Serious questions have also been raised about Trendley Dean’s (the father of fluoridation) famous 21-city study from 1942 (Ziegelbecker 1981).

The fluoridation program has massively failed to achieve one of its key objectives, i.e., to lower dental decay rates while limiting the occurrence of dental fluorosis (a discolouring of tooth enamel caused by too much fluoride. The goal of the early promoters of fluoridation was to limit dental fluorosis (in its very mild form) to 10% of children (NRC 1993, pp. 6-7). In 2010, however, the Centers for Disease Control and Prevention (CDC) reported that 41% of American adolescents had dental fluorosis, with 8.6% having mild fluorosis and 3.6% having either moderate or severe dental fluorosis (Beltran-Aguilar2010). As the 41% prevalence figure is a national average and includes children living in fluoridated and unfluoridated areas, the fluorosis rate in fluoridated communities will obviously be higher. The British Government’s York Review estimated that up to 48% of children in fluoridated areas worldwide have dental fluorosis in all forms, with 12.5% having fluorosis of aesthetic concern (McDonagh et al, 2000).

Because of their sole reliance on liquids for their food intake, infants consuming formula made with fluoridated water have the highest exposure to fluoride, by bodyweight, in the population. Because infant exposure to fluoridated water has been repeatedly found to be a major risk factor for developing dental fluorosis later in life (Marshall 2004; Hong 2006; Levy 2010), a number of dental researchers have recommended that parents of newborns not use fluoridated water when reconstituting formula (Ekstrand 1996; Pendrys 1998; Fomon 2000; Brothwell 2003; Marshall 2004). Even the American Dental Association (ADA), the most ardent institutional proponent of fluoridation, distributed a November 6, 2006 email alert to its members recommending that parents be advised that formula should be made with “low or no-fluoride water.” Unfortunately, the ADA has done little to get this information into the hands of parents. As a result, many parents remain unaware of the fluorosis risk from infant exposure to fluoridated water. In the fluoridated areas of England where water is dosed at 1 ppm, a 6-month-old would be overexposed by 0.6mg per day if it drank 1 litre water per day. The UK Government Committee on Toxicity recommends a maximum of 0.05mg fluoride/kg bodyweight/day for 6-month-old babies.  (CoT, para. 46 https://cot.food.gov.uk/sites/default/files/cot/fluoride.pdf  .  Thus a formula-fed fluoridated baby weighing 8 kg should drink no more than 0.4 mg fluoride/day. 1 litre formula/day made up with fluoridated tap water contains 1mg fluoride meaning that over-exposure is 0.6 mg fluoride/day.  This over-exposure is enough to cause Dental Fluorosis in the permanent teeth developing under the gum and is a causal factor leading to a reduction in intelligence (National Toxicology Programme, 2019). See 23 below.

EVIDENCE OF HARM TO OTHER TISSUES

There have been many suggestions as to the possible biochemical mechanisms underlying the development of dental fluorosis (Matsuo 1998; Den Besten 1999; Sharma 2008; Duan 2011; Tye 2011) and they are complicated for a lay reader. While promoters of fluoridation are content to dismiss dental fluorosis (in its milder forms) as merely a cosmetic effect, it is rash to assume that fluoride is not impacting other developing tissues when it is visibly damaging the teeth by some biochemical mechanism (Groth 1973; Colquhoun 1997). Moreover, whilst ingested fluoride can only cause dental fluorosis during the period before the permanent teeth have erupted (6-8 years), other tissues are potentially susceptible to damage throughout life. For example, in areas of naturally high levels of fluoride where the first indicator of harm is dental fluorosis in children, many older people develop skeletal fluorosis in the same communities.

According to the National Research Council (NRC 2006), “it is apparent that fluorides have the ability to interfere with the functions of the brain.” In a review of the literature commissioned by the US Environmental Protection Agency (EPA), fluoride has been listed among about 100 chemicals for which there is substantial evidence of developmental neurotoxicity.” Animal experiments show that fluoride accumulates in the brain and alters mental behaviour in a manner consistent with a neurotoxic agent (Mullenix 1995). In total, there have now been over 100 animal experiments showing that fluoride can damage the brain and impact learning and behaviour. According to fluoridation proponents, these animal studies can be ignored because high doses were used. However, it is important to note that rats generally require five times more fluoride to reach the same plasma levels in humans (Sawan 2010). Further, one animal experiment found effects at remarkably low doses (Varner 1998). In this study, rats fed for one year with 1 ppm fluoride in their water (the same level used in fluoridation programmes), using either sodium fluoride or aluminium fluoride, had morphological changes to their kidneys and brains, an increased uptake of aluminium in the brain, and the formation of beta-amyloid deposits which are associated with Alzheimer’s disease. Other animal studies have found effects on the brain at water fluoride levels as low as 5 ppm (Liu 2010).

This is a very important topic worthy of a page of its own.  Please go to the page entitled “Fluoride as a Toxin.”

Reduced IQ is not the only neurotoxic effect that may result from fluoride exposure. At least three human studies have reported an association between fluoride exposure and impaired visual-spatial organization (Calderon 2000; Li 2004; Rocha-Amador 2009); while four other studies have found an association between prenatal fluoride exposure and fetal brain damage (Han 1989; Du 1992; Dong 1993; Yu 1996).

Studies by Jennifer Luke (2001) show that fluoride accumulates in the human pineal gland to very high levels. In her Ph.D. thesis, Luke has also shown in animal studies that fluoride reduces melatonin production and leads to an earlier onset of puberty (Luke 1997). Consistent with Luke’s findings, one of the earliest fluoridation trials in the U.S. (Schlesinger 1956) reported that on average young girls in the fluoridated community reached menstruation 5 months earlier than girls in the non-fluoridated community. Inexplicably, no fluoridating country has attempted to reproduce either Luke’s or Schlesinger’s findings or examine the issue any further.

According to the U.S. National Research Council (2006), “several lines of information indicate an effect of fluoride exposure on thyroid function.” In the Ukraine, Bachinskii (1985) found a lowering of thyroid function, among otherwise healthy people, at 2.3 ppm fluoride in water. In the middle of the 20th century, fluoride was prescribed by a number of European doctors to reduce the activity of the thyroid gland for those suffering from hyperthyroidism (overactive thyroid) (Gorlitzer, 1932; Stecher 1960; Waldbott 1978). According to a clinical study by Galletti and Joyet (1958), the thyroid function of hyperthyroid patients was effectively reduced at just 2.3 to 4.5 mg/day of fluoride ion. To put this finding into perspective, the US Department of Health and Human Services (DHHS, 1991) has estimated that total fluoride exposure in fluoridated communities ranges from 1.6 to 6.6 mg/day. This is a remarkable fact, particularly considering the rampant and increasing problem of hypothyroidism (underactive thyroid) in the United States and other fluoridated countries. Symptoms of hypothyroidism include depression, fatigue, weight gain, muscle and joint pains, increased cholesterol levels, and heart disease. In 2010, the second most prescribed drug of the year was Synthroid (sodium levothyroxine) which is a hormone replacement drug used to treat an underactive thyroid.

Some of the early symptoms of skeletal fluorosis (a fluoride-induced bone and joint disease that impacts millions of people in India, China, and Africa), mimic the symptoms of arthritis (Singh 1963; Franke 1975; Teotia 1976; Carnow 1981; Czerwinski 1988; DHHS 1991). According to a review on fluoridation published in Chemical & Engineering News, “Because some of the clinical symptoms mimic arthritis, the first two clinical phases of skeletal fluorosis could be easily misdiagnosed” (Hileman 1988). Few, if any, studies have been done to determine the extent of this misdiagnosis, and whether the high prevalence of arthritis in America (1 in 3 Americans have some form of arthritis – CDC, 2002) and other fluoridated countries is related to growing fluoride exposure, which is highly plausible. Even when individuals in the U.S. suffer advanced forms of skeletal fluorosis (from drinking large amounts of tea), it has taken years of misdiagnoses before doctors finally correctly diagnosed the condition as fluorosis.

An early fluoridation trial (Newburgh-Kingston 1945-55) found a significant two-fold increase in cortical bone defects among children in the fluoridated community (Schlesinger 1956). The cortical bone is the outside layer of the bone and is important to protect against fracture. While this result was not considered important at the time with respect to bone fractures, it did prompt questions about a possible link to osteosarcoma (Caffey, 1955; NAS, 1977). In 2001, Alarcon-Herrera and co-workers reported a linear correlation between the severity of dental fluorosis and the frequency of bone fractures in both children and adults in a high fluoride area in Mexico.

When high doses of fluoride (average 26 mg per day) were used in trials to treat patients with osteoporosis in an effort to harden their bones and reduce fracture rates, it actually led to a higher number of fractures, particularly hip fractures (Inkovaara 1975; Gerster 1983; Dambacher 1986; O’Duffy 1986; Hedlund 1989; Bayley 1990; Gutteridge 1990. 2002; Orcel 1990; Riggs 1990 and Schnitzler 1990). Hip fracture is a very serious issue for the elderly, often leading to a loss of independence or a shortened life. There have been over a dozen studies published since 1990 that have investigated a possible relationship between hip fractures and long term consumption of artificially fluoridated water or water with high natural levels. The results have been mixed – some have found an association and others have not. Some have even claimed a protective effect. One very important study in China, which examined hip fractures in six Chinese villages, found what appears to be a dose-related increase in hip fracture as the concentration of fluoride rose from 1 ppm to 8 ppm (Li 2001) offering little comfort to those who drink a lot of fluoridated water. Moreover, in the only human epidemiological study to assess bone strength as a function of bone fluoride concentration, researchers from the University of Toronto found that (as with animal studies) the strength of bone declined with increasing fluoride content (Chachra 2010). Finally, a recent study from Iowa (Levy 2009), published data suggesting that low-level fluoride exposure may have a detrimental effect on cortical bone density in girls (an effect that has been repeatedly documented in clinical trials and which has been posited as an important mechanism by which fluoride may increase bone fracture rates).

Because of their inability to effectively excrete fluoride, people with kidney disease are prone to accumulating high levels of fluoride in their bone and blood. As a result of this high fluoride body burden, kidney patients have an elevated risk for developing skeletal fluorosis. In one of the few U.S. studies investigating the matter, crippling skeletal fluorosis was documented among patients with severe kidney disease drinking water with just 1.7 ppm fluoride (Johnson 1979). Since severe skeletal fluorosis in kidney patients has been detected in small case studies, it is likely that larger, systematic studies would detect skeletal fluorosis at even lower fluoride levels.

A U.S. government-funded animal study found a dose-dependent increase in bone cancer (osteosarcoma) in fluoride-treated, male rats (NTP 1990). Following the results of this study, the National Cancer Institute (NCI) reviewed national cancer data in the U.S. and found a significantly higher rate of osteosarcoma (a bone cancer) in young men in fluoridated versus unfluoridated areas (Hoover et al 1991a). While the NCI concluded (based on an analysis lacking statistical power) that fluoridation was not the cause (Hoover et al 1991b), no explanation was provided to explain the higher rates in the fluoridated areas. A smaller study from New Jersey (Cohn 1992) found osteosarcoma rates to be up to 6 times higher in young men living in fluoridated versus unfluoridated areas. Other epidemiological studies of varying size and quality have failed to find this relationship (a summary of these can be found in Bassin, 2001 and Connett & Neurath, 2005). There are three reasons why a fluoride-osteosarcoma connection is plausible: First, fluoride accumulates to a high level in bone. Second, fluoride stimulates bone growth. And, third, fluoride can interfere with the genetic apparatus of bone cells in several ways; it has been shown to be mutagenic, cause chromosome damage, and interfere with the enzymes involved with DNA repair in both cell and tissue studies (Tsutsui 1984; Caspary 1987; Kishi 1993; Mihashi 1996; Zhang 2009). In addition to cell and tissue studies, a correlation between fluoride exposure and chromosome damage in humans has also been reported (Sheth 1994; Wu 1995; Meng 1997; Joseph 2000).

In 2001, Elise Bassin, a dentist, successfully defended her doctoral thesis at Harvard in which she found that young boys had a five-to-seven fold increased risk of getting osteosarcoma by the age of 20 if they drank fluoridated water during their mid-childhood growth spurt (age 6 to 8). The study was published in 2006 (Bassin 2006) but has been largely discounted by fluoridating countries because her thesis adviser Professor Chester Douglass (a promoter of fluoridation and a consultant for Colgate) promised a larger study that he claimed would discount her thesis (Douglass and Joshipura, 2006). Now, after 5 years of waiting the Douglass study has finally been published (Kim 2011) but in no way does this study discount Bassin’s findings. The study, which used far fewer controls than Bassin’s analysis, did not even attempt to assess the age-specific window of risk that Bassin identified. Indeed, by the authors’ own admission, the study had no capacity to assess the risk of osteosarcoma among children and adolescents (the precise population of concern).

Fluoride administered to animals at high doses wreaks havoc on the male reproductive system – it damages sperm and increases the rate of infertility in a number of different species (Kour 1980; Chinoy 1989; Chinoy 1991; Susheela 1991; Chinoy 1994; Kumar 1994; Narayana 1994a,b; Zhao 1995; Elbetieha 2000; Ghosh 2002; Zakrzewska 2002). In addition, an epidemiological study from the US found increased rates of infertility among couples living in areas with 3 ppm or more fluoride in the water (Freni 1994), two studies have found increased fertility among men living in high-fluoride areas of China and India (Liu 1988; Neelam 1987); four studies have found reduced level of circulating testosterone in males living in high fluoride areas (Hao 2010; Chen P 1997; Susheela 1996; Barot 1998), and a study of fluoride-exposed workers reported a “subclinical reproductive effect” (Ortiz-Perez 2003). While animal studies by FDA researchers have failed to find evidence of reproductive toxicity in fluoride-exposed rats (Sprando 1996, 1997, 1998), the National Research Council (2006) has recommended that, “the relationship between fluoride and fertility requires additional study.”

In one study, which lasted 13 years, Feltman and Kosel (1961) showed that about 1% of patients given 1 mg of fluoride each day developed negative reactions. Many individuals have reported suffering from symptoms such as fatigue, headaches, rashes and stomach and gastro-intestinal tract problems, which disappear when they avoid fluoride in their water and diet (Shea 1967; Waldbott 1978; Moolenburgh 1987). Frequently the symptoms reappear when they are unwittingly exposed to fluoride again (Spittle, 2008). No fluoridating government has conducted scientific studies to take this issue beyond these anecdotal reports. Without the willingness of governments to investigate these reports scientifically, should we as a society be forcing these people to ingest fluoride?

In addition to people suffering from impaired kidney function discussed in Reason  No. 30, other subsets of the population are more vulnerable to fluoride’s toxic effects.  According to the Agency for Toxic Substances and Disease Registry (ATSDR 1993) these include: infants, the elderly, and those with diabetes mellitus. Also vulnerable are those who suffer from malnutrition (e.g., calcium, magnesium, vitamin C, vitamin D and iodine deficiencies and protein-poor diets) and those who have diabetes insipidus.  (Greenberg 1974; Klein 1975; Massler & Schour 1952; Marier & Rose 1977; Lin 1991; Chen 1997; Seow 1994; Teotia 1998. )

NO MARGIN OF SAFETY

No-one can deny that high natural levels of fluoride damage health. Millions of people in India and China have had their health compromised by fluoride. The real question is whether there is an adequate margin of safety between the doses shown to cause harm in published studies and the total dose people receive when consuming uncontrolled amounts of fluoridated water and non-water sources of fluoride. This margin of safety has to take into account the wide range of individual sensitivity expected in a large population (a safety factor of 10 is usually applied to the lowest level causing harm). Another safety factor is also needed to take into account the wide range of doses to which people are exposed. There is clearly no margin of safety for dental fluorosis (CDC, 2010) and based on the following studies nowhere near an adequate margin of safety for lowered IQ (Xiang 2003a,b; Ding 2011; Choi 2012; NTP, 2019; Bashash et al, 2017 and 2018; Green et al, 2019; Valdez-Jiminez, 2017; Malin et al 2018; Riddell, J. et al 2019; Malin and Till, 2015; Till, 2020; Malin et al 2019; NRC, 2006); lowered thyroid function (Galletti & Joyet 1958; Bachinskii 1985; Lin 1991); bone fractures in children (Alarcon Herrera 2001) or hip fractures in the elderly (Kurttio 1999; Li 2001). All of these harmful effects are discussed in the NRC (2006) review.

ENVIRONMENTAL JUSTICE

Those most likely to suffer from poor nutrition, and thus more likely to be more vulnerable to fluoride’s toxic effects, are the poor, who unfortunately, are the very people being targeted by new fluoridation programs. While at heightened risk, poor families are least able to afford avoiding fluoride once it is added to the water supply. No financial support is being offered to these families to help them get alternative water supplies or to help pay the costs of treating unsightly cases of dental fluorosis.

According to the USA’s CDC’s national survey of dental fluorosis, black and Mexican-American children have significantly higher rates of dental fluorosis than white children (Beltran-Aguilar 2005, Table 23). The recognition that minority children appear to be more vulnerable to toxic effects of fluoride, combined with the fact that low-income families are less able to avoid drinking fluoridated water, has prompted prominent leaders in the environmental-justice movement to oppose mandatory fluoridation in Georgia. In a statement issued in May 2011, Andrew Young, a colleague of Martin Luther King, Jr., a former Mayor of Atlanta and former US Ambassador to the United Nations, stated: “I am most deeply concerned for poor families who have babies: if they cannot afford unfluoridated water for their babies’ milk formula, do their babies not count? Of course they do. This is an issue of fairness, civil rights, and compassion. We must find better ways to prevent cavities, such as helping those most at risk for cavities obtain access to the services of a dentist…My father was a dentist. I formerly was a strong believer in the benefits of water fluoridation for preventing cavities. But many things that we began to do 50 or more years ago we now no longer do, because we have learned further information that changes our practices and policies. So it is with fluoridation.”

No fluoridating Government is warning African, Caribbean and Hispanic children that they have higher rates of dental fluorosis than Caucasian children (Reason No. 38). This extra vulnerability may extend to other toxic effects of fluoride. Africans have higher rates of lactose intolerance, kidney problems and diabetes, all of which may exacerbate fluoride’s toxicity.

Since dental decay is most concentrated in poor communities, we should be spending our efforts trying to increase the access to dental care for low-income families. The highest rates of tooth decay today can be found in low-income areas that have been fluoridated for many years. The real “Oral Health Crisis” that exists today in certain parts of England is not a lack of fluoride but poverty and lack of visits to the dentist.

THE LARGELY UNTESTED CHEMICALS USED IN FLUORIDATION PROGRAMS

Instead, they largely come from the wet scrubbing systems of the phosphate fertiliser industry. These chemicals which are disodium fluorosilicate and hydrofluorosilicic acid, are classified hazardous wastes contaminated with various impurities, carcinogens and heavy metals. In the USA, testing by the National Sanitation Foundation suggest that the levels of arsenic in these silicon fluorides are relatively high (up to 1.6 ppb after dilution into public water) and of potential concern (NSF 2000 and Wang 2000). Arsenic is a known human carcinogen for which there is no safe level. This one contaminant alone could be increasing cancer rates – and unnecessarily so.

The chemical usually tested in animal studies is pharmaceutical grade sodium fluoride, not industrial grade hydrofluorosilicic acid. Proponents claim that once the silicon fluorides have been diluted at the water treatment works they are completely dissociated to free fluoride ions and hydrated silica and thus there is no need to examine the toxicology of these compounds. However, while a study from the University of Michigan (Finney et al., 2006) showed complete dissociation at neutral pH, in acidic conditions (pH 3) there was a stable complex containing five fluoride ions. Thus the possibility arises that such a complex may be regenerated in the stomach where the pH lies between 1 and 2.

Studies by Masters and Coplan (1999, 2000, 2007), and to a lesser extent Macek (2006), show an association between the use of hydrofluorosilicic acid (and its sodium salt) and an increased uptake of lead into children’s blood. Because of lead’s acknowledged ability to damage the developing brain (it’s a known developmenta; neurotoxin) , this is a very serious finding. Nevertheless, it is being largely ignored by fluoridating countries. This association received some strong biochemical support from an animal study by Sawan et al. (2010) who found that exposure of rats to a combination of fluorosilicic acid and lead in their drinking water increased the uptake of lead into blood some three-fold over exposure to lead alone.

In tightly controlled laboratory experiments, Maas et al (2007) showed that fluoridating agents in combination with chlorinating agents such as chloroamine, increase the leaching of lead from brass fittings used in plumbing. While proponents may argue about the neurotoxic effects of low levels of fluoride there is no argument that lead at very low levels lowers IQ in children.

CONTINUED PROMOTION OF FLUORIDATION IS UNSCIENTIFIC

In the January 2008 issue of Scientific American, Professor John Doull, the chairman of the important 2006 National Research Council review, Fluoride in Drinking Water: A Review of EPA’s Standards, is quoted as saying: “What the committee found is that we’ve gone with the status quo regarding fluoride for many years—for too long really—and now we need to take a fresh look . . . In the scientific community people tend to think this is settled. I mean, when the U.S. Surgeon General comes out and says this is one of the top 10 greatest achievements of the 20th century, that’s a hard hurdle to get over. But when we looked at the studies that have been done, we found that many of these questions are unsettled and we have much less information than we should, considering how long this [fluoridation] has been going on.” The absence of studies is being used by promoters as meaning the absence of harm. This is an irresponsible position.

Many of those promoting fluoridation rely heavily on a list of endorsements. However, the U.S. PHS first endorsed fluoridation in 1950, before one single trial had been completed and before any significant health studies had been published. (Ch. 8 and 9 in The Case Against Fluoride for the significance of this PHS endorsement for the future promotion of fluoridation). Many other endorsements swiftly followed with little evidence of any scientific rationale for doing so. The continued use of these endorsements has more to do with political science than medical science.

Every so often, particularly when their fluoridation programme is under threat, governments of fluoridating countries hand-pick panels to deliver reports that provide the necessary re-endorsement of the practice. In their recent book Fluoride Wars (2009), which is otherwise slanted toward fluoridation, Alan Freeze and Jay Lehr concede this point when they write: “There is one anti-fluoridationist charge that does have some truth to it. Anti-fluoride forces have always claimed that the many government-sponsored review panels set up over the years to assess the costs and benefits of fluoridation were stacked in favour of fluoridation.”  A review of the membership of the various panels confirms this charge. The expert committees that put together reports by the American Association for the Advancement of Science in 1941, 1944 and 1954; the National Academy of Sciences in 1951, 1971, 1977 and 1993; the World Health Organization in 1958 and 1970; and the U.S. Public Health Service in 1991 are rife with the names of well-known medical and dental researchers who actively campaigned on behalf of fluoridation or whose research was held in high regard in the pro-fluoridation movement. Membership was interlocking and incestuous.

The most recent examples of these self-fulfilling prophecies have come from the Irish Fluoridation Forum (2002); the National Health and Medical Research Council (NHMRC, 2007) and Health Canada (2008, 2010). The latter used a panel of six experts to review the health literature. Four of the six were pro-fluoridation dentists and the other two had no demonstrated expertise on fluoride. A notable exception to this trend was the appointment by the U.S. National Research Council of the first balanced panel of experts ever selected to look at fluoride’s toxicity in the U.S. This panel of twelve reviewed the US EPA’s safe drinking water standards for fluoride. After three and half years the panel concluded in a 507- page report that the safe drinking water standard was not protective of health and a new maximum contaminant level goal (MCLG) should be determined (NRC, 2006). If normal toxicological procedures and appropriate margins of safety were applied to their findings this report should spell an end to water fluoridation. Unfortunately in January of 2011 the US EPA Office of Water made it clear that they would not determine a value for the MCLG that would jeopardize the water fluoridation program (EPA press release, Jan 7, 2011). Once again politics was allowed to trump science.

MORE AND MORE INDEPENDENT SCIENTISTS OPPOSE FLUORIDATION

Proponents of fluoridation have maintained for many years – despite the fact that the earliest opponents of fluoridation were biochemists – that the only people opposed to fluoridation are not bona fide scientists. Today, as more and more scientists, doctors, dentists and other professionals, read the primary literature for themselves, rather than relying on self-serving statements from the British Dental Association and Public Health England, they are realising that they and the general public have not been diligently informed by their professional bodies on this subject. As of January 2012, over 4,000 professionals throughout the World have signed a statement calling for an end to water fluoridation worldwide. This statement and a list of signatories can be found on the website of the Fluoride Action Network. A glimpse of the calibre of those opposing fluoridation can be gleaned by watching the 28-minute video “Professional Perspectives on Water fluoridation” which can be viewed online at the same FAN site. 

PROPONENTS’ DUBIOUS TACTICS

While pro-fluoridation officials continue to promote fluoridation with undiminished fervour, they usually refuse to defend the practice in open public debate – even when challenged to do so by organisations such as the Association for Science in the Public Interest, the American College of Toxicology, or the U.S. EPA (Bryson 2004). According to Dr. Michael Easley, a prominent lobbyist for fluoridation in the US, “Debates give the illusion that a scientific controversy exists when no credible people support the fluorophobics’ view” (Easley, 1999). In light of proponents’ refusal to debate this issue, Dr. Edward Groth, a Senior Scientist at Consumers Union, observed that, “the political pro-fluoridation stance has evolved into a dogmatic, authoritarian, essentially antiscientific posture, one that discourages open debate of scientific issues” (Martin 1991).

Many scientists, doctors and dentists who have spoken out publicly on this issue have been subjected to censorship and intimidation (Martin 1991). Dr. Phyllis Mullenix was fired from her position as Chair of Toxicology at Forsythe Dental Center for publishing her findings on fluoride and the brain (Mullenix 1995); and Dr. William Marcus was fired from the EPA for questioning the government’s handling of the NTP’s fluoride-cancer study (Bryson 2004). Many dentists and even doctors tell opponents in private that they are opposed to this practice but dare not speak out in public because of peer pressure and the fear of recriminations. Tactics like this would not be necessary if those promoting fluoridation were on secure scientific and ethical grounds.