Only eight countries in the world have more than 50% of their populations drinking artificially fluoridated water (Australia, Brunei, Chile, Hong Kong, Ireland, Israel, Guyana, Malaysia, New Zealand, Singapore, and the United States). In Europe, only Ireland (73%), Poland (1%), Serbia (3%), Spain (11%), and the U.K. (11%) fluoridate any of their water. Most developed countries, including Japan and 97% of the western European population, do not consume fluoridated water. 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 program first began (NRC 2006) And tooth decay is not caused by a “fluoride deficiency” (NRC 1993; Institute of Medicine 1997, NRC 2006)
Mother’s milk is remarkably low in fluoride(0.004 ppm, NRC, 2006) which 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. 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). The American Dental Association, 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.” Four 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.
According to the National Research Council (2006), “it is apparent that fluorides have the ability to interfere with the functions of the brain.” Animal experiments show that fluoride accumulates in the brain and alters mental behavior in a manner consistent with a neurotoxic agent (Mullenix 1995). 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 programs) they had morphological changes to their kidneys and brains, an increased uptake of aluminum in the brain, and the formation of beta-amyloid deposits which are associated with Alzheimer’s disease.
There have now been 33 studies from China, Iran, India and Mexico that have reported an association between fluoride exposure and reduced IQ. One of these studies (Lin 1991) indicates that even just moderate levels of fluoride exposure (e.g., 0.9 ppm in the water) can exacerbate the neurological defects of iodine deficiency. Other studies have found IQ reductions at 1.9 ppm (Xiang 2003a,b); 0.3-3.0 ppm (Ding 2011); 1.8-3.9 ppm (Xu 1994); 2.0 ppm (Yao 1996, 1997); 2.1-3.2 ppm (An 1992); 2.38 ppm (Poureslami 2011); 2.45 ppm (Eswar 2011); 2.5 ppm (Seraj 2006); 2.85 ppm (Hong 2001); 2.97 ppm (Wang 2001, Yang 1994); 3.15 ppm (Lu 2000); 4.12 ppm (Zhao 1996). In the Ding study, each 1 ppm increase of fluoride in urine was associated with a loss of 0.59 IQ points. A team of Harvard scientists whose fluoride/IQ meta-review concludes that fluoride’s impact on the developing brain should be a “high research priority.” (Choi et al., 2012). Except for two small IQ studies from New Zealand (Shannon et al., 1986; Spittle 1998) no fluoridating country has yet investigated the matter.
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). 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).
Though fluoride has been added to community water supplies for over 60 years, “there have been no randomized trials of water fluoridation” (Cheng 2007). 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 2000) NO HEALTH AGENCY IN FLUORIDATED COUNTRIES IS MONITORING FLUORIDE EXPOSURE or its side effects of those communities ingesting fluoridated water THE CENTERS FOR DISEASE CONTROL AND PREVENTION (CDC, 1999, 2001) HAS NOW ACKNOWLEDGED THAT THE MECHANISM OF FLUORIDE’S BENEFITS ARE MAINLY TOPICAL, NOT SYSTEMIC
The largest survey ever conducted in the US (over 39,000 children from 84 communities) by the National Institute of Dental Research showed little difference in tooth decay among children in fluoridated and non-fluoridated communities (Hileman 1989) 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) 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).
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 (Barnes 1992; Shiboski 2003) When fluoridation was discontinued in communities in Canada, the former East Germany, Cuba and Finland, dental decay did not increase but has generally continued to decrease (Maupomé 2001; Kunzel & Fischer, 1997, 2000; Kunzel 2000; Seppa 2000) 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).
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) (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 in perspective, the 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.
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). 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). 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).
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) and 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)
In a 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 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).
Masters and Coplan (1999, 2000, 2007), and to a lesser extent Macek (2006), show an association between the use of fluorosilicic acid (and its sodium salt) to fluoridate water and an increased uptake of lead into children’s blood. Maas et al (2007) have shown that fluoridating agents in combination with chlorinating agents such as chloroamine increase the leaching of lead from brass fittings used in plumbing.
As of January 2012, over 4,000 professionals 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 caliber 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.
All cited references in this article can be found at the Fluoride Action Network’s Online Bibliography, available at www.fluoridealert.org This document is a testament to their tireless work to rid the world of fluoridated water
Comparison of hydrofluorosilicic acid and pharmaceutical sodium fluoride as fluoridating agents—A cost–benefit analysis
Water fluoridation programs in the United States and other countries which have them use either sodium fluoride (NaF), hydrofluorosilicic acid (HFSA) or the sodium salt of that acid (NaSF), all technical grade chemicals to adjust the fluoride level in drinking water to about 0.7–1 mg/L. In this paper we estimate the comparative overall cost for U.S. society between using cheaper industrial grade HFSA as the principal fluoridating agent versus using more costly pharmaceutical grade (U.S. Pharmacopeia – USP) NaF. USP NaF is used in toothpaste. HFSA, a liquid, contains significant amounts of arsenic (As). HFSA and NaSF have been shown to leach lead (Pb) from water delivery plumbing, while NaF has been shown not to do so. The U.S. Environmental Protection Agency's (EPA) health-based drinking water standards for As and Pb are zero. Our focus was on comparing the social costs associated with the difference in numbers of cancer cases arising from As during use of HFSA as fluoridating agent versus substitution of USP grade NaF. We calculated the amount of As delivered to fluoridated water systems using each agent, and used EPA Unit Risk values for As to estimate the number of lung and bladder cancer cases associated with each. We used cost of cancer cases published by EPA to estimate cost of treating lung and bladder cancer cases. Commercial prices of HFSA and USP NaF were used to compare costs of using each to fluoridate. We then compared the total cost to our society for the use of HFSA versus USP NaF as fluoridating agent. The U.S. could save $1 billion to more than $5 billion/year by using USP NaF in place of HFSA while simultaneously mitigating the pain and suffering of citizens that result from use of the technical grade fluoridating agents. Other countries, such as Ireland, New Zealand, Canada and Australia that use technical grade fluoridating agents may realize similar benefits by making this change. Policy makers would have to confront the uneven distribution of costs and benefits across societies if this change were made.
► Arsenic in current H2O fluoridating agents causes significant cancer treatment costs. ► Arsenic in USP NaF would result in 100–500-fold fewer cancers. ► USP NaF costs about 12 times as much as current fluoridating agents. ► U.S. savings as a society using USP NaF would be $1–5 billion annually. ► Costs and savings are not distributed evenly throughout society.
Environ Health Perspect. 2012 October; 120(10): 1362–1368.
Background: Although fluoride may cause neurotoxicity in animal models and acute fluoride poisoning causes neurotoxicity in adults, very little is known of its effects on children’s neurodevelopment.
Objective: We performed a systematic review and meta-analysis of published studies to investigate the effects of increased fluoride exposure and delayed neurobehavioral development.
Methods: We searched the MEDLINE, EMBASE, Water Resources Abstracts, and TOXNET databases through 2011 for eligible studies. We also searched the China National Knowledge Infrastructure (CNKI) database, because many studies on fluoride neurotoxicity have been published in Chinese journals only. In total, we identified 27 eligible epidemiological studies with high and reference exposures, end points of IQ scores, or related cognitive function measures with means and variances for the two exposure groups. Using random-effects models, we estimated the standardized mean difference between exposed and reference groups across all studies. We conducted sensitivity analyses restricted to studies using the same outcome assessment and having drinking-water fluoride as the only exposure. We performed the Cochran test for heterogeneity between studies, Begg’s funnel plot, and Egger test to assess publication bias, and conducted meta-regressions to explore sources of variation in mean differences among the studies.
Results: The standardized weighted mean difference in IQ score between exposed and reference populations was –0.45 (95% confidence interval: –0.56, –0.35) using a random-effects model. Thus, children in high-fluoride areas had significantly lower IQ scores than those who lived in low-fluoride areas. Subgroup and sensitivity analyses also indicated inverse associations, although the substantial heterogeneity did not appear to decrease.
Conclusions: The results support the possibility of an adverse effect of high fluoride exposure on children’s neurodevelopment. Future research should include detailed individual-level information on prenatal exposure, neurobehavioral performance, and covariates for adjustment.
Intellequity Technology Services Natick, Massachusetts, United States. MYRONCOPLAN@aol.com
Silicofluorides (SiFs), fluosilicic acid (FSA) and sodium fluosilicate (NaFSA), are used to fluoridate over 90% of US fluoridated municipal water supplies. Living in communities with silicofluoride treated water (SiFW) is associated with two neurotoxic effects: (1) Prevalence of children with elevated blood lead (PbB>10microg/dL) is about double that in non-fluoridated communities (Risk Ratio 2, chi2p<0.01). SiFW is associated with serious corrosion of lead-bearing brass plumbing, producing elevated water lead (PbW) at the faucet. New data refute the long-prevailing belief that PbW contributes little to children's blood lead (PbB), it is likely to contribute 50% or more. (2) SiFW has been shown to interfere with cholinergic function. Unlike the fully ionized state of fluoride (F-) in water treated with sodium fluoride (NaFW), the SiF anion, [SiF6]2- in SiFW releases F- in a complicated dissociation process. Small amounts of incompletely dissociated [SiF6]2- or low molecular weight (LMW) silicic acid (SA) oligomers may remain in SiFW. A German PhD study found that SiFW is a more powerful inhibitor of acetylcholinesterase (AChE) than NaFW. It is proposed here that SiFW induces protein mis-folding via a mechanism that would affect polypeptides in general, and explain dental fluorosis, a tooth enamel defect that is not merely "cosmetic" but a "canary in the mine" foretelling other adverse, albeit subtle, health and behavioral effects. Efforts to refute evidence of such effects are analyzed and rebutted. In 1999 and 2000, senior EPA personnel admitted they knew of no health effects studies of SiFs. In 2002 SiFs were nominated for NTP animal testing. In 2006 an NRC Fluoride Study Committee recommended such studies. It is not known at this writing whether any had begun.
Abstracts and articles published in FLUORIDE, the peer-reviewed Journal of the International Society for Fluoride Research See http://www.fluoride-journal.com for more information on the Society.
Teotia SPS, Teotia M, Dental caries: a disorder of high fluoride and low dietary calcium interactions...
Waldbott GL, The Preskeletal Phase of Chronic Fluoride Intoxication, Fluoride, 1998, 31:1, 13-20
Chlebna-Sokól D(1), Czerwinski E(2), Bone structure assessment on radiographs of distal radial metaphysis in children with dental fluorosis, Fluoride, 1993 26:l, 37-44
SUMMARY: The effect of fluoride on bone structure was assessed in children with endemic dental fluorosis by use of radiographs of the distal radial metaphysis of test children and those of unfluoridated age-matched controls. Bone structure assessment was based on the computerized image analysis of the radiographs. In addition, the quantitative description of bone structure was analyzed in terms of correlation with age, sex, and serum calcium, magnesium, and alkaline phosphatase levels. Our findings indicate greater trabecular height and area in children with dental fluorosis than in controls. Detailed analysis of the results, in relation to age and gender, showed that the significant differences were between younger age groups and between boys. This finding indicates a stronger influence of fluoride on children of younger developmental age.
Assessment of fluoride influence on bone in children is both interesting and difficult. Fluoride exerts an effect on bones during the period of fast growth and the continuous remodelling of bone structure (1-3). In this study we analyzed bone structure of children with endemic fluorosis and of non-fluoridated age-matched children, using computerized image analysis which allowed quantitative evaluation of hone structure differences.
Materials and Methods
The investigation involved 43 children aged 11 to 15 years who had lived since birth in the village of Blaszki near Sieradz, an area in which drinking water contained naturally occurring. fluoride at 2.7 mg/liter. mottled enamel was evident in all children of this group. An age-matched control group of children without evident dental fluorosis was chosen from an area with water fluoride < 0.1 mg/liter. Clinical evaluation of the children of both groups was otherwise unremarkable. The children were divided into two sub-groups: AG-I, aged 11-12 years (average 11.8) and AG-II, aged 13.5-15.0 years (average 14.6). In both sub-groups, children were also identified by gender.
A radiograph of the left distal radial metaphysis of each child was used for bone structure assessment. High-quality film (Roentgen XS) with a TUR 1000 apparatus was used. Processing was standardized in terms of constant composition of reagents and development time (5 minutes at 20 C). All radiographs were taken and processed by the same technician.
Bone structure evaluation was based on computerized radiograph image analysis with a VFG-512-8BC (Visionetics) analyzer with resolution power of 512 x 512 pixals and 256 grey levels. Optical density was measured at 128 points in the middle of the metaphysis. The distance between these points was 0.096 mm. Microdensitometric curves obtained this way were the subject of computer analyses carried out according to the program worked out by Czerwinski (4). This program defined "radiologic trabeculae" and provided the following quantitative description of bone structure: the number of trabeculae, their width, height, area, and trabeculation density. Trabecular width is given in millimetres and density in the percentage of the cross-section enclosed by the trabeculae. Trabecular height is expressed as a percentage of the minimum and maximum of the optical density on the given radiograph. Trabecular area is expressed as a percentage of the area enclosed by the whole microdensitometric curve. The compatibility of the results of the analysis was checked together with the diagram of the curve and the diagram, in turn, with the radiologic image of the evaluated area.
In all children with dental fluorosis (DF) and in 34 children of the control group (CG), the following blood tests were performed:
- serum calcium concentration (Ca) by the method of Kovacs and Tarnoky (5);
-serum magnesium concentration (Mg) by the Lachen firm's photocolorimetric method (6);
- serum alkaline phosphatase activity (AP) by the method of King and Armstrong.
Statistical differences between the groups were assessed by variance analysis and test F according to Fisher-Snedecor. Differences of p < 0.05 were regarded as significant. In addition, linear correlation coefficients (r) by Pearson (significant at p < 0.05) were determined among some variables (7,8). Statistical calculations were performed by the Institute of Sociology of the University of Lodz.
The results of analyzed bone structure parameters are included in Table 1. Children with DF were found to demonstrate a statistically significant greater trabecular height and area (averaged and complete) than the control group (CG) children. No significant differences were found for trabecular number, width, or density.
When the age and gender sub-groups were compared, it was found that the significantly greater trabecular height and area occurred only in DF boys in AG-I. No significant trabecular differences were found in subgroup AG-II or among girls (Tables 2 and 3). Figures 1 and 2 show microdensitometric curves of digitalized radiographs (including the relative diagram of radiologic trabeculae) in a child with DF and from the control group. As Table 4 shows, the average serum calcium was higher and the alkaline phosphatase activity and serum magnesium were lower among DF children than CG children, though both sets of Ca and AP values were in the normal range and only the Mg value of DF children was slightly less than the lower limit of normal range. Table 5 contains linear correlation coefficients and their levels of significance calculated between bone structure parameters and concentration of Ca, Mg and AP blood levels. Statistically significant correlation coefficients were noted only in the DF group where the increases of trabecular height and area correlated with lower serum calcium and higher alkaline phosphatase activity levels. The detailed analysis of differentiation between groups which could suggest a direct influence of fluoride on specific ions and enzymes is not, however, the subject of this report.
Previous histomorphometric examinations have shown that fluoride causes an increase of mineralized bone mass by the increase of trabecular volume and width. This is shown by the increased absorption of radiologic radiation which increases the density shadow on radiographs (9). Because of the relatively small fluoride dosage of the children in this study, we expected to find only the initial changes of bone structure. For this evaluation, we used a computer image analysis of distal radial metaphysis to quantify bone structure parameters.
Comparing children with dental fluorosis to an age-matched control group, we found statistically significant increases in trabecular height and area in children with dental fluorosis. In addition, mean serum calcium was increased but alkaline phosphatase and serum magnesium were decreased in the DF group compared to controls. However, within the DF group, individual case analysis found a negative correlation between serum calcium and trabecular height, area and width. The decrease in alkaline phosphatase activity correlated with a decline in trabecular height and area.
Czerwinski has shown that an increase in trabecular height and area is proof of an increase in bone mineral content (10). The same process is likely to occur in children with dental fluorosis. An increase of bone mineralization could be the consequence of retarded bone resorption due to formation of less soluble fluorapatite and osteoclastic activity inhibition by fluoride ions (11-13). The decreased AP activity in children with DF indicates lower metabolic turn-over in the bone and its growth retardation (14). The statistically significant positive correlation between calcium concentration and the number of trabeculae, and the negative correlations in reference to the remaining bone structure parameters, found in children with dental fluorosis, show the slight bone structure disturbances found in this group - probably the result of the relatively small fluoride doses. It has previously been estimated that initial skeletal changes begin when the concentration of fluoride in drinking water is 8 mg/liter (15,16).
The finding of greater trabecular height and area of trabeculation occurred only in younger boys with DF (average age 11.8 years) and not among the older children (average age 14.6 years) nor among girls of both groups. This would suggest the greater influence of fluoride on the mineralization process in the earlier period of development (AG-I and boys). Boys at this time of their life are always in a younger development stage than girls (17). Similar results, from experimental examinations on rats by Bialas (18), show that the earlier the development period, the stronger is the influence of fluoride. The above suggestions agree with the results of earlier examinations which showed that an excess of fluoride in a child may inhibit growth, especially in younger boys (19).
With this technique of evaluating the bone structure of the distal radial metaphysis, significantly greater height and area of trabeculae were found in children with dental fluorosis than in the control group. These differences were not observed for number and width of trabeculae. The results indicate the effects of chronic supraoptimal doses of fluoride in increasing bone tissue mineralization. This fluoride effect is stronger in younger children.
(1) Institute of Paediatrics. Academy of Medicine, ul. Spoma 36/50, 91-738 Lodz, Poland. (2) Department of Orthopaedics. Cracow Academy of Medicine, Cracow, Poland.
editor's note: graphs, tables, pictures and references have not been reproduced here. Please contact the ISFR for subscription rates and membership
Diesendorf M., Diesendorf A., Suppression By Medical Journals Of A Warning About Overdosing Formula-Fed Infants With Fluoride, Fluoride, 1987 May, 30:2, 125, from Accountability in Research 1997, 5, 225-237
Diesendorf M, How Science Can Illuminate Ethical Debates A Case Study On Water Fluoridation, Fluoride, 1995 May, 28:2
Foulkes R, Review of Report: Investigation of Inorganic Fluoride and its Effect on the Occurrence of Dental Caries and Dental Fluorosis in Canada -- Final Report
Foulkes RG, Inorganic Fluorides, Canadian Environmental Protection Act (Priority Substances List Assessment Report, Government of Canada 1993, Fluoride, 1995 Feb, 28:1 29-3295, Review.
Summary of Report
The publication, Inorganic Fluorides (Priority Substances List Assessment Report) 1993 was prepared by the Government of Canada pursuant to the Canadian Environment Protection Act (CEPA).(1) This Act requires the Federal Ministers of the Environment and of Health to prepare and publish a Priority Substances List that identifies substances that may be harmful to the environment or constitute a danger to human health.
"Toxic" is defined in Section 11 of the Act: "...a substance is toxic if it is entering or may enter the environment in a quantity or concentration or under conditions (a) having or that may have an immediate or long-term harmful effect on the environment; (b) constituting or that may constitute a danger to the environment on which human life depends; or (c) constituting or that may constitute a danger in Canada to human life or health."
The Report states that "the assessment of whether 'inorganic fluorides' are 'toxic', was based on the determination of whether they enter or are likely to enter the Canadian environment in a concentration or quantities or under conditions that could lead to exposure of humans or other biota at levels that could cause adverse effects" (emphasis in the original).
The Report states that the data used in the study were derived from studies of humans and laboratory animals exposed to different forms of inorganic fluoride compounds. Data regarding human health published after July 1993, and on the environment after April 1993, were not considered for inclusion. With respect to the effects of fluoride on human health, it is stated: "neither dental fluorosis nor the beneficial effects of fluoride in the prevention of dental caries have been assessed in this report". The principal inorganic fluorides assessed were: hydrogen fluoride (HF); calcium fluoride (CaF2); sodium fluoride (NaF); and sulphur hexafluoride (SF6).
The conclusions were. a) that inorganic fluorides are entering the environment in quantities or under conditions that may be harmful to the environment. b) there is insufficient information to conclude whether sulphur hexafluoride is entering the environment in quantities or under conditions that may constitute a danger to the environment on which human life depends (ie, global climate change); and c) that inorganic fluorides (ie, the fluoride ion derived from such inorganic substances) are not entering the environment in quantities or under conditions that may constitute a danger to human life or health.
The strong suit in this study is the concise review of the properties, production and uses of inorganic fluorides, and uses of inorganic fluorides, and the known effects of anthropogenic sources of fluoride on plants and other biota such as ungulates and aquatic species.
In a section entitled "Exotoxicity", the Report discusses a number of key studies, selected on the basis of "proper controls, measured toxicant concentrations, acceptable protocols and identification of the most sensitive biota".
From these, those responsible for the study deduced that inorganic fluorides are entering the Canadian environment at concentrations that may cause long-term harmful effects to biota in aquatic and terrestrial ecosystems. For example, with regard to the effects on aquatic organisms, the authors extrapolate laboratory findings to the field, to yield estimated adverse effect thresholds (lethal, growth impairment, and decreased egg production) of 0.28 mg/L fluoride for fresh water species and 0.5 mg/L fluoride for marine species. These are exceeded by many anthropogenic sources.
With regard to the adverse effects of inorganic fluoride, especially air emissions, the authors review inorganic fluoride toxicity to plants and animals, especially herbivores. The white-tailed deer consuming contaminated browse, was used as a "model". The authors concluded that inorganic fluorides from anthropogenic sources result in concentrations in some Canadian plants and air that may cause long-term adverse effects to biota in terrestrial ecosystems.
The weakness of this Report that could rob it of total credibility is the obvious protection of the Government-sanctioned process of adding inorganic fluoride to drinking water. In the preceding example of the effects thresholds for aquatic organisms, no mention is made that one of the anthropogenic sources discharging inorganic fluoride into Canadian water that exceed these, is effluent from fluoridated cities that may persist, in fresh water, for some distance.
In fact, the absence of an estimate of inorganic fluoride from this source, in the text and in the accompanying table (Table 1), is conspicuous. Total inorganic fluoride emitted to the environment annually in Canada from anthropogenic sources is estimated to be 23,500 tomes. The amount released to the water is estimated to be 13,500 tonnes, 80% of which is attributed to phosphate fertilizer production (11,000 tonnes). The authors give indirect evidence to enable the reader to calculate that approximately- 10 million people in Canada are "fluoridated" and that the annual release of inorganic fluoride from this source is approximately 2000 tonnes. This puts this source in second place, behind phosphate fertilizer production, but ahead of chemical production (1362 tonnes ), coalfired power (555 tonnes), primary aluminum production (307 tonnes), and others that are identified.
In the Recommendations of the Report a request is made for information on the extent of releases from municipal drinking water fluoridation. With the authority of the Government of Canada and two Ministries, it is surprising that this information was not obtained during data collection.
The conclusion that "inorganic fluorides (ie. fluoride ions) are not entering the environment in quantities or under conditions that may constitute a danger to human life or health" is derived from a somewhat tautological argument.
The Report presents a digest of previous published reviews and secondary sources that deal with the possible adverse effects of inorganic fluoride on human health. Like previous assessments of inorganic fluoride and human health to be found in recent literature, dental fluorosis is not considered an "adverse effect". In fact, this Report ignores this effect except with regard to its occurrence in herbivores and that it does occur at a lower intake in humans than that required for skeletal changes.
The Report presents (Table 3) an estimated intake of inorganic fluoride by the general population of Canada. This table shows intake by various age groups in micrograms per kilogram body weight per day (ugm/kg bw/day). It includes breast-fed and formula-fed infants and all groups exposed to "fluoridated" and "non-fluoridated" water. The table appears to have been prepared largely from studies reported by the Environmental Health Directorate in 1992. The Table is comprehensive in as much as it shows intake form ambient air, food, soil, water (both "fluoridated" and "non-fluoridated") and household products.
Those responsible for the Report state that "available information is considered inadequate ... to assess the carcinogenicity of inorganic fluoride in humans" and recognize that the dose-response trend in the occurrence of osteosarcoma in rat experiments cannot be dismissed. The authors also recognize that there is evidence that fluoride is genotoxic, based on the outcome of in vitro and in vivo studies, and that this may be an effect of fluoride that results from its inhibition of enzymes involved in DNA synthesis and/or repair.
The authors, also, show that they have reservations regarding the potential of adverse effects upon human reproduction, development, or the central nervous and immune systems at levels required to produce skeletal effects.
Nevertheless, the authors opt to consider that effects on the skeleton are more relevant than others in assessing the toxicological effects of long-term exexposureo inorganic fluorides.
The authors present data from a number of studies and conclude that potentially adverse effects associated with skeletal fluorosis are likely to be observed at intakes of greater than approximately 200 ugm/kg bw/day fluoride. Based on the information that estimated daily intakes of inorganic fluoride range from approximately 0.5 to 160 ugm/kg bw/day by various age groups in the population, the authors conclude that these are less than the level at which adverse effects on the skeleton are anticipated.
This assessment document is an interesting addition to the literature on inorganic fluoride. The sections devoted to the ecological effects of emissions in Canada from anthropogenic sources point to serious adverse effects on aquatic and terrestrial biota. These suggest, also, that there is a need for further study of sulphur hexafluoride and its possible role in global climate change.
Overall, the Report suffers from the obvious attempt to defend the current support of fluoridation of drinking water. The deliberate omissions in the study are evidence of this, in addition to the acceptance, in the section on human health, that the development of crippling skeletal fluorosis is the adverse effect for which a threshold should be determined.
If these omissions had been included in the Report, the quantity and concentration of emissions into the aquatic ecosystem from fluoridated communities would have been shown to exceed the effect thresholds for aquatic life.
In addition, consideration would have been given to the growing view, even of spokesman from the Canadian Dental Association, that systemic fluoride does not prevent caries, but topical fluoride may have a "remineralization" effect on incipient caries. Finally, if dental fluorosis, as a clinical entity, had been fully discussed, the Report would have to present the view that it represents a continuum developing in severity along with skeletal changes. If dental fluorosis, in humans, were to be accepted as an "adverse effect", as it is in herbivores, it could easily be shown that the intake of inorganic fluoride by children living in fluoridated areas of Canada easily exceeds the effects threshold.
This Report, in spite of some excellent sections on such aspects as ecotoxicity, lacks credibility as, once again, the politics of fluoridation have pre-empted objectivity and science.
(1) Canadian Environmental Protection Act., Inorganic Fluorides, (Priority substances list assessment report), ISBN 0-662-21070-9, Cat. No. En40-215/32E, Minister of Supply and Services Canada, Canada Communication Group Publishing, Ottawa 1993.
Lee JR, Slow-Release Sodium Fluoride In The Management Of Postmenopausal Osteoporosis, Fluoride 1994 October, 27:4 227-228 (critical review -- CYC Pak et al, Annals of Internal Medicine 120 625-632 1994).
Lee JR, Fluoridation and Hip Fracture, Fluoride 1993 October, 26:4 274-277, review -- National Research Council Report: "Health Effects of Ingested Fluoride" review -- National Research Council Report: "Health Effects of Ingested Fluoride"
Lee JR, Fluoridation and Osteoporosis '92, Fluoride,1992, 25:3,162-164 (Letter to the Editor)
Li XS, et al., Effect of Fluoride Exposure on Intelligence in Children, Fluoride, 1995 Nov, 28:4, pp 189-192
Spittle B, Allergy and Hypersensitivity to Fluoride, Fluoride, 1993, 26:4, 267-273
Sutton PRN, The Failure of Fluoridation (editorial), Fluoride, 1990 January, 23:1, 1-4.
The ultimate failure of fluoridation was inevitable because it was founded on two fallacies, namely that fluorine is an essential element for man and that water containing less than approximately 1 ppm fluoride is "fluoride deficient."
The major factor which has sustained the push for fluoridation is the widely held belief that, where it operates, it has attained its objective -- that it has been shown to reduce substantially the prevalence of dental caries. This belief is based on faith in the honesty and accuracy of statements made by so-called "authorities," not because the published evidence from fluoridation trials had been investigated with the assistance of an academic statistician.
In 1978 Justice John P. Flaherty, of the Supreme Court of Pennsylvania, presided over a long (2,800 pages of testimony) court case involving fluoridation. He stated:
I seriously believe that few responsible people have objectively reviewed the evidence (1).
An early review which pointed out many of the errors in the four main trials in Grand Rapids, Newburgh and Evanston, U.S.S. and Brantford, Canada, was published by the present author as a monograph (Fluoridation: Errors and Omissions in Experimental Trials, Melbourne U.P., 1959) (2).
So great was the intolerance of some officials to any criticism of fluoridation, that Cambridge University Press (the distributor of the book in America) was approached by the Nutrition Foundation Inc., and others, in an attempt to suppress the monograph in the U.S.A. Also, the printer's type at Melbourne University Press was destroyed without authority, thus almost succeeding in preventing publication of the second edition the following year.
Having failed to suppress the monograph, it was omitted from the list of recent books and pamphlets in the Index to Dental Literature (published by the American Dental Association) and the errors it pointed out were simply ignored. Not until fairly recently have errors in those trials been tacitly acknowledged by some fluoridation promoters. In 1987 Jackson (3) stated:
On the question of efficacy, we do not have to rely on the inadequate studies of the past.
Emphasis was then placed on what were claimed to be approximately 100 more recent fluoridation trials which were stated to have "proved" the efficacy of fluoridation. For instance, in 1984 the most recent WHO book on this subject (4), Environmental Health Criteria for Fluorine and Fluorides, was written by a ten-member task group. These scientists gave as their reference, and apparently accepted without investigation, the data displayed in a poster by Murray and Rugg-Gunn in 1979 (5). They stated that "... 120 fluoridation studies from all continents showed a reduction in caries in the range of 50 to 75% for permanent teeth." These data obviously came from the same source as those in a table in a well-known book by the authors of that poster which listed 128 studies (6).
Mention of such a large number of studies Impresses the scientifically naive, who do not realize that it is not the volume but the quality of research which counts. As the statistician Sir Ronald Fisher stated many years ago (7):
If the design of an experiment is faulty, any method of interpretation which makes it out to be decisive must be faulty too.
In 1988, the scientific status of these studies was investigated. The preliminary results were published in January, 1989, in a letter to Chemical and Engineering News (8) (the official organ of the American Chemical Society) which was publishing a series of letters on fluoridation, including one from the U.S. Surgeon General. My letter stated that in 23 of those 128 fluoridation studies named by Murray and Rugg-Gunn (6) the data from the deciduous and the permanent teeth were listed separately -- as 46 studies.
Two studies which included data from more than one town were listed as six studies, and in seven cases reports in different years from the same study were listed as 14 studies. Therefore, more than a quarter of the studies were recorded more than once by Murray and Rugg-Gunn (6) to give the fictitious total of 128 studies.
The most important claim made for fluoridation is that it decreases dental caries in the permanent teeth. Contrary to the statement in that WHO book, 20 studies listed did not present any data for those teeth.
This leaves 74 studies for permanent teeth, but most of these were of very poor scientific quality. One did not refer to fluoridated water, two were anonymous, three were personal communications, and eight were essentially progress reports. Fourteen were not published in a journal but were short communications in newsletters and bulletins issued by state health departments. These obvious deficiencies, not mentioned by this WHO task group (4), were revealed by merely reading the references and a table in the book by Murray and Rugg-Gunn (6).
Four of the remaining 46 studies were the original trials, all of which were mentioned prominently in this WHO book (4), although for 25 years they had been known to be faulty (2). Sixteen of the remaining studies were short reports in state dental newsletters and journals.
A further disturbing fact in the table of Murray and Rugg-Gunn (6) which lists the studies, is that one column, with 128 entries, is headed: "Nonfluoridated Community Caries Experience," implying that each of the 128 studies listed had a control. This was not the case. Even in the remaining 26 studies -- now less than a quarter of the 120 mentioned by this WHO task group (4) -- almost every study failed to attempt to use a control or used one which was obviously unsatisfactory. These studies were not designed to estimate examiner error or to eliminate examiner bias.
An attempt was then made to examine each of the remaining 26 studies to see whether they established the claim that fluoridation decreases the prevalence of dental caries substantially. Unfortunately four of the papers listed by Murray and Rugg-Gunn (6) could not be obtained (two could not be found in the Index to Dental Literature or in the Index Medicus.) None of these studies was mentioned by this WHO task group.
Further examination revealed that three more of those 26 studies were obviously incapable of demonstrating that fluoridation is efficacious. A detailed examination was then made of the remaining 19 studies which could possibly have demonstrated the efficacy of fluoridation. Five were held in the U.S.A., five in Australia and New Zealand, three in the United Kingdom and six in other countries. However, on examination of these reports none of them showed in a scientifically-acceptable manner that fluoridation is efficacious.
Therefore, Murray and Rugg-Gunn (6), in what appears to have been comprehensive world-wide search, were unable to locate even one study which demonstrated that fluoridation reduced dental caries.
In contrast, the evidence that it has failed to reduce the number of decayed teeth Is mounting. In their 1972 paper (9) entitled "The Failure of Fluoridation in the United Kingdom," Schatz and Martin "graphed" the official results from the U.K. Department of Health's eleven-year study and showed that the slopes indicating increase in caries with age in the treated and control areas were almost identical. Their conclusion:
The official report is valuable because it so clearly reveals the failure of fluoridation in Great Britain.
The alleged benefits are thus nothing more than a statistical illusion.
More recently, Colquhoun and Mann in New Zealand (10) and Diesendorf in Australia (11) have demonstrated that fluoridation has failed in their countries. Data from a recent survey by the National Institute of Dental Research of 39,207 children aged five to seventeen years from 84 areas in the U.S.A. has shown that fluoridation has failed in America also. The number of decayed, missing and filled teeth in children who had been fluoridated all their lives was no fewer than those who had been brought up in non-fluoridated areas (12).
The original claim, made in innumerable promotional statements, was that fluoridation would reduce the prevalence of decayed teeth by about sixty percent. One of these was a WHO Press Release (WHO/45, September 4, 1957). In 1956, the authors of the Grand Rapids study (13) stated:
In children born since fluoridation was put into effect, the caries rate for the permanent teeth was reduced on the average by about 60 per cent.
It has taken forty-five years to overcome the propaganda claim that fluoridation is very efficacious. However, in 1990 it is now clear that fluoridation has failed.
1. Flaherty, J.P.: Letter to the Mayor of Auckland, New Zealand, July 31, 1979.
2. Sutton, P.R.N.: Fluoridation Errors and Omissions m Experimental Trials. Melbourne University Press, Melbourne, Australia, 1959.
3. Jackson, D.: Fluoridation: The Official Case. The Ecologist, no. 17, p. 126, 1987.
4. W.H.O.: Environmental Health Criteria 36: Fluorine and Fluorides. W.H.O., Geneva, 1984.
5. Murray, J.J. and Rugg-Gunn, A.J.: Additional Data on Water Fluoridation, Poster at XXVI ORCA Congress, 1979. (Cited from W.H.O., reference 4 above.)
6. Murray, J.J. and Rugg-Gunn, A.J.: Fluorides in Caries Prevention. 2nd ed. Wright, Briscol, 1982.
7. Fisher, R.A.: The Design of Experiments. 6th ed. Oliver and Boyd, Edinburgh, 1951.
8. Sutton, P.R.N.: Fluoridation of Water. Chemical & Engineering News, 67(4):3, January 23, 1989.
9. Schatz, A. and Martin, J.J.: The Failure of Fluoridation in the United Kingdom. Pakistan Dental Review, 22:3-7, 1972.
10. Colquhoun, J. and Mann, R.: The Hastings Fluoridation Experiment: Science or Swindle? The Ecologist, 16:243-248, 1986.
11. Diesendorf, M. Have the Benefits of Water Fluoridation Been Exaggerated? (in press), 1990.
12. Yiamouyiannis, J.: NIDR Study Shows No Relationship Between Fluoridation and Tooth Decay Rate. American Laboratory, May, 1989, p. 9-10.
13. Arnold, F.A., Jr., Dean, H.T., Jay, P. and Knutson, J.W.: Effect of Fluoridated Public Water Supplies on Dental Caries Prevalence. Publ. Hlth. Rep., 71:652-658, 1956.
Philip R.N. Sutton, D.D.Sc., F.R.A.C.D.S., Melbourne, Australia
Teotia SPS, Teotia M, Dental caries: a disorder of high fluoride and low dietary calcium interactions (30 years of personal research), Fluoride, 1994 April, 27:2, 59-66
SUMMARY: This comprehensive epidemiological study - performed during the period 1963-1993 on 0.4003 million children residing in nonendemic (F- >1.0 ppm) and endemic (F- less than or equal to 1.0 ppm) fluorosis villages of India - was designed to investigate the essentiality or otherwise of fluoride and calcium nutrition in the prevention and control of dental caries. In non-endemic areas, of the children with adequate calcium nutrition, 7 percent showed dental fluorosis and 2 percent had dental caries, while of children with inadequate calcium nutrition 14.2 percent showed dental fluorosis and 31.4 percent had dental caries. In endemic areas, of the children with adequate calcium intakes, 59 percent had dental fluorosis and 10 percent had dental caries, while in the calcium-inadequate group, 100 percent exhibited dental fluorosis and 74 percent had dental caries.
Our findings indicate that dental caries was caused by high fluoride and low dietary calcium intakes, separately and through their interactions. Dental caries was most severe and complex in calcium-deficient children exposed to high intakes of endemic fluoride in drinking water.
The only practical and effective public health measure for the prevention and control of dental caries is the limitation of the fluoride content of drinking water to <0.5 ppm, and adequate calcium nutrition (dietary calcium > 1 g/day). The World Health Organisation policy and recommendations on fluorides are not universally acceptable, especially for the environment of developing countries, with nutritional deficiencies, endemic fluorosis, and different caries prevalence trends. In the light of our scientific data, WHO recommendations require modifications to achieve dental health for all by the year AD 2000.
For the past three decades we have been continuously engaged in studies on fluorides and endemic fluorosis in India. During epidemiological studies on the prevalence of endemic fluorosis, our attention was drawn to a high level of dental caries in children living in villages endemic for fluorosis. The present study was therefore designed to discover the prevalence of dental fluorosis and dental caries in growing children residing in non-endemic and endemic fluorosis villages.
Materials and Methods
Epidemiological surveys for endemic dental fluorosis and dental caries were performed in villages throughout the 14 states of India during the period 1963-1991.
After geographical location of the villages and fluoride analysis of drinking water samples from all sources in each village, the two groups of rural child population, (i) nonendemic (F- less than or equal to 1.0 ppm) and (ii) endemic (F- >1.0 ppm) were identified. Children in both groups were further classified as calcium nutrition adequate (dietary Ca > 800 mg/day) and inadequate (dietary Ca <300 mg/day). The field team made complete house listings of the entire population, and details were recorded in a specially designed format. The total population of children surveyed was 0.80075 million, while the children who volunteered for complete examination, and inclusion in the study during the period 1963-1993, numbered 0.4003 million (Table 1). [emphasis added]
All children studied had lived in their villages since birth, and had matched socioeconomic and education backgrounds, similar dietary and food patterns, similar habits in respect to oral health and hygiene, and identical facilities for health and dental clinics.
Each child was subjected to a thorough history-taking to a clinical examination, and to nutritional assessment and dietary evaluation, in particular for calcium intake (1). The dental examinations were performed by one of the authors (SPST) assisted by trained dental, medical and public health field staff. Radiological and laboratory investigations of plasma and urine were done where found necessary. Established laboratory procedures reported previously (2-5) were employed. The alveolar bone density was determined on dental radiographs.
A group of 23,273 children, all from similar social groups with matched habits, and living in non-endemic (F- < 0.6 ppm) and endemic (F- > 2.5 ppm) areas, participated in a study designed to evaluate the effectiveness of calcium intervention in the prevention of dental caries. Their baseline dietary intakes of calcium were identical and less than 0.5 g/day. They were randomly divided into two groups. The treatment group received one gram of elemental calcium supplements per day for 5 years, and the group of children serving as controls was followed for 5 years on a placebo but received no calcium supplements. This five-year controlled calcium intervention programme was started in 10-year-olds and the results of follow-up examinations at the end of 5 years (in 15-year-olds) were compared in all the groups (Table 2).
Results and Discussion
During the period 1963-1993 extensive epidemiological, environmental, nutritional, clinical, radiological, and relevant laboratory studies were performed for aetiological prevalence (related to fluoride and calcium intakes) and pathophysiology of dental caries in rural children residing in non-endemic and endemic fluorosis villages. The possible essentiality of fluoride and calcium nutrition as caries-preventive agents was also investigated. Children of group I (non-endemic) had been drinking water with fluoride concentration of 0.50 ± 0.24 ppm and of group II (endemic) with fluoride content of 4. 19 ± 2.03 ppm. The clinical and relevant epidemiological data of the children studied are summarised in Table I.
In non-endemic villages, in children with adequate calcium nutrition, 7% showed dental fluorosis and 2% dental caries, while in children with inadequate calcium nutrition 14.2% showed dental fluorosis and 31.4% showed dental caries. In endemic areas children with adequate calcium intakes 59% had dental fluorosis and 9.8% had dental caries, while in the calcium-inadequate group practically 100% revealed dental fluorosis and 74% had dental caries. The incidence of dental fluorosis and caries increased with fluoride intakes and dietary calcium deficiency (Figure 1). Statistical analysis of the data by Student's 't' test revealed highly significant differences between non-endemic and endemic groups and between children with adequate and inadequate calcium intakes (p < 0.0001).
Our studies on the epidemiology of decayed teeth as a function of drinking water fluoride exposure and calcium nutrition revealed a very interesting situation (Figure 2). Decayed teeth per hundred children were maximum in the 5-10 year olds and minimum in the 0-5 year olds. Teeth with caries were much less frequent in children of both the groups with adequate calcium nutrition. The worst situation, with the largest, number of decayed teeth, occurred in, 5-10 year olds who had inadequate calcium nutrition and were exposed to high fluoride intakes.
The fasting plasma fluoride concentration measured in 425 children of the endemic group, with adequate calcium nutrition was 2.5 ± 0.2 uM/L and in 385 children with inadequate calcium nutrition was 6.2 ± 0.5 uM/L. This finding suggests that calcium is a strong antagonist of fluoride and inhibits its intestinal absorption, as we have previously reported (6-10). [emphasis added]
The follow-up examinations at the end of 5 years (of the children already affected with caries at the age of 10 years) revealed that the incidence of new carious lesions was greater in the children of the control group, 17% (non-endemic), 43% (endemic) compared to the incidence of 2.2% (non-endemic) and 6.8% (endemic) in the treatment group. Also at the end of 5 years the incidence of caries in new children (not affected with caries at age 10 years) was compared in all the groups (Table 2). We also observed the increased alveolar bone density in the calcium-treated children -- caused, we believe, by increased retention of calcium during the pubertal growth spurt. Increased frequency of carious teeth in children with vitamin D deficiency rickets further indicates the intimate metabolic interaction between calcium nutrition and dental caries.
Our observations in the present study are consistent with our studies on dental caries and endemic fluorosis previously reported (11-13). The effects of chronic ingestion of endemic fluoride on dental metabolism, and the possible pathophysiological mechanisms involved in the causation of dental caries, are summarized in Figure 3. Though the precise mechanism of fluoride action is not fully known (14, 15), it is our view that in children exposed to endemic fluoride the enamel and the protein matrix laid down during the period of mineralisation (12-14 years) remain diffusely hypomineralised with abnormal crystal growth (16-18).
The effects of fluoride on enamel formation also lead to insufficient closure of intercrystalline spaces, the processes responsible for the drainage of water and inorganic materials (19-21). These structural changes - immature and hypomineralised matrix, increased porosity and possible effects on dental calcium homeostasis - markedly increase the vulnerability of the teeth to bacterial invasion, and to formation of plaque which contains microorganisms. All these factors possibly operate and cannot be ignored in the etiopathogenesis of dental caries in children residing in endemic fluorosis villages.
Dental caries was more severe and complex in calcium-deficient children exposed to endemic fluoride. The interaction of fluoride and parathyroid hormone in calcium-deficient children may increase the porosity of the enamel and resorption of the teeth, and thus may aggravate the risk of dental caries. Dental caries does not occur in all children to the same degree. The various factors which could have influenced the course and severity of dental caries in our children include: 1) fluoride concentration in the drinking water; 2) daily intake of fluoride; 3) duration of fluoride exposure; 4) continuity of residence in the endemic area; 5) fluctuations in the fluoride intake; 6) age at the time of fluoride ingestion; 7) nutritional status, particularly the dietary intakes of calcium and vitamin D; 8) physical hard work in a hot environment; 9) individual oral and dental hygiene; and 10) individual consumption of refined carbohydrates.
We have not found during our 30 years of study, any appreciable change in caries prevalence trends in children of comparable socio-economic strata. Therefore time is unlikely to be an additional variable in the analysis of our results.
More than a hundred studies have reported that community water fluoridation prevents and reduces dental caries (22). However, our extensive review indicates that, in most of the reports, several parameters of vital importance in the pathogenesis of dental caries were not investigated. Some of the aspects which require in depth attention in such published reports are: 1) changing dietary and food patterns, particularly the consumption of refined carbohydrates; 2) recognition and monitoring of trends in oral health, embracing all its components, such as (a) oral and dental health education in schools and at home, (b) facilities for oral and dental health clinics, (c) public and government concern for prevention of dental caries; 3) individual and community nutritional status, particularly the dietary intakes of calcium and vitamin D; and 4) inclusion in the studies of matched communities, not exposed to fluoridated water and with similar socioeconomic backgrounds (e.g. 23, 24).
All these factors should have been recognised and assessed simultaneously with fluoridation of public water supplies and monitored during the entire length of the fluoridation studies reported. Because of these lacunae, we have reservations about the scientific documentation for the fluoridation of drinking water being the main agent responsible for the reduction in dental caries in the studies published.
From our present study two sets of important observations have emerged:
1) In India, exposure to high intakes of natural fluoride in drinking water is associated with high prevalences of dental fluorosis and dental caries, both having a very strong direct correlation with the increasing fluoride content of drinking water. Taken together, the correlation and the dose-response relationship suggest a causal relationship. Specifically, high intakes of fluoride increase the prevalence of dental fluorosis as well as dental caries. Similar observations were made by one of us (SPST in 1990) during short term surveys and examinations of schoolchildren in endemic fluorosis villages of Zilin Province of China
2) Adequate dietary calcium intakes (> 800 mg/day) provide an effective control and prevention of dental fluorosis and dental caries. Dietary calcium deficiency (Ca intakes < 300 mg/day) aggravates the toxic dental effects of fluoride making them more severe and complex. Even the marginally high intakes of fluoride (> 2.5 mg/d) continuously for more than six months in calcium deficient children may cause severe dental fluorosis and caries (25). [emphasis added]
On the basis of our comprehensive epidemiological data, supported by the benefits of intervention with calcium supplements, we recommend the limitation of fluoride in the drinking water to < 0.5 ppm, and adequate calcium nutrition (Ca intake> 1 g/day); as the most effective strategies for the prevention and control of dental caries. Oral and dental health care and avoiding consumption of refined carbohydrates are additional factors requiring attention. The World Health Organisation policy and recommendations on fluoride are not universally applicable. In the light of our studies, WHO needs to recognise that fluoridation of public water supplies cannot be documented as a scientifically proven and community-acceptable method for the prevention of dental caries. [emphasis added]
The conclusions reached in this report - we believe the most comprehensive and single largest epidemiological study on dental caries in the world literature - are based on our experience over thirty years (1963-1993) studying the effects of endemic fluoride in the drinking water and community calcium nutrition status.
The authors are indebted to and gratefully acknowledge the financial support of the Department of Environment, Department of Science and Technology and the Indian Council of Medical Research, Government of India, New Delhi, and the International Development Research Centre, Canada.
Postgraduate Department of Human Metabolism and Endocrinology, LLRM Medical College, Meerut, 250-004, India. Presented at the XXth Conference of the International Society for Fluoride Research, Kyoto, Japan, September 1992.
editor's note: graphs, tables, and references have not been reproduced here. Please contact the ISFR for subscription rates and membership.