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Fluoride

9. Does water fluoridation pose risks?

  • 9.1 When can teeth be affected by dental fluorosis?
  • 9.2 Is water fluoridation causing dental fluorosis?
  • 9.3 How can bones be affected by skeletal fluorosis?
  • 9.4 At what intake levels does fluoride cause skeletal fluorosis?

9.1 When can teeth be affected by dental fluorosis?

The source document for this Digest states:

Dental fluorosis

Since the publication of the WHO (1994) assessment on the quantitative relationship between dental fluorosis and fluoride intake, a large number of further studies have been published on the matter. A recent meta-analysis (McDonagh et al., 2000) of such studies is presented in Figures 2 and 3.

Fluoride level

Note: Fluoride level plotted on the log scale because there was an approximately linear association between this and the log (odds) of fluorosis.

Fig. 2. Proportion of the population with dental fluorosis by water fluoride level together with the 95% upper and lower confidence limits for the proportion

[Reproduced with permission from Br Med J (2000) 321: 855–859 ]

Dental fluorosis is a condition that results from the intake of excess levels of fluoride during the period of tooth development, usually from birth to approximately 6–8 years of age. It has been termed a hypoplasia or hypomineralization of dental enamel and dentine and is associated with the excessive incorporation of fluoride into these structures. The severity of this condition, generally characterized as ranging from very mild to severe, is related to the extent of fluoride exposure during the period of tooth development. Mild dental fluorosis is usually typified by the appearance of small white areas in the enamel; individuals with severe dental fluorosis have teeth that are stained and pitted ("mottled") in appearance. In human fluorotic teeth, the most prominent feature is a hypomineralization of the enamel. In contrast to many animal species, fluoride-induced enamel hypoplasia (indicating severe fluoride disturbance of enamel matrix production) seems to be rare in fluorosed human enamel. The staining and pitting of fluorosed dental enamel are both posteruptive phenomena (i.e., acquired after tooth eruption and occur as a consequence of the enamel hypomineralization). The incorporation of excessive amounts of fluoride into enamel is believed to interfere with its normal maturation, as a result of alterations in the rheologic structure of the enamel matrix and/or effects on cellular metabolic processes associated with normal enamel development (WHO, 1994; Aoba, 1997; Whitford, 1997). Experimental animal studies suggest that this hypomineralization results from fluoride disturbance of the process of enamel maturation (Richards et al., 1986).

Unlike skeletal fluorosis, which is considered to be a marker of long-term exposure to fluoride (due to the ongoing process of bone remodelling), dental fluorosis is considered to be indicative of the level of exposure to fluoride only during the period of enamel formation. Exposure to excessive levels of fluoride after tooth development appears to have little influence on the extent of fluorosis.

Graphic Proportion of population with fluorisis/Fluoride level

Note: Fluoride level plotted on the untransformed scale because there was an approximately linear association between this and the log (odds) of "aesthetic fluorosis."

Fig. 3. Proportion of the population with fluorosis of aesthetic concern by water fluoride level [Reproduced with permission from Br Med J (2000) 321: 855–8 59]

Re-evaluation of classical fluorosis data (Dean et al., 1941, 1942; Richards et al., 1967; Butler et al., 1985) has shown that even at low fluoride intake from water, a certain level of dental fluorosis will be found (Fejerskov et al., 1996). A dose–response relationship was also demonstrated. The data demonstrated an increase of the fluorosis community index by 0.2 for every dose increase of 0.01 mg fluoride

Source & ©: IPCS "Environmental Health Criteria for Fluorides", (EHC 227),
Chapter 8: Effects on humans, section 8.1.3.8: Dental effects
 

9.2 Is water fluoridation causing dental fluorosis?

The source document for this Digest states:

Over the past 30–40 years, there has been an increase in the prevalence of dental fluorosis among populations consuming either fluoridated or non-fluoridated drinking-water. Although greater numbers of individuals are now being served by fluoridated drinking-water, for the most part this increased prevalence in dental fluorosis has been attributed to the widespread intake of fluoride from sources other than drinking-water, especially in areas served by non-fluoridated drinking-water. Unlike the situation in the 1930s, when the primary sources of exposure to fluoride were limited to drinking-water and foodstuffs, now there is potential exposure to fluoride from a variety of additional sources, such as toothpastes, mouth rinses, fluoride supplements and topically applied dental gels, solutions and varnishes. Exposure to fluoride may also result from the ingestion of fluoridated salt or fluoridated milk.

The prevalence of dental fluorosis is also elevated in certain areas of the world where the intake of fluoride may be inordinately high, due in large part to the elevated fluoride content of the surrounding geological environment. In China, large numbers of people exhibit dental fluorosis (Liu, 1995). In addition to the actual consumption of often large amounts of drinking-water containing naturally occurring elevated levels of fluoride, the indoor burning of coal rich in fluoride, the preparation of foodstuffs in water containing increased fluoride levels and the consumption of specific foodstuffs naturally rich in fluoride, such as tea, are believed to contribute to the elevated intake of fluoride, with the resultant development of dental fluorosis (Chen et al., 1993, 1996; Grimaldo et al., 1995; Han et al., 1995; Liu, 1995; Xu et al., 1995).

Source & ©: IPCS "Environmental Health Criteria for Fluorides", (EHC 227),
Chapter 8: Effects on humans, section 8.1.3.8: Dental effects
 

9.3 How can bones be affected by skeletal fluorosis?

The source document for this Digest states:

Skeletal fluorosis is a pathological condition that may arise following long-term exposure (either by inhalation or by ingestion) to elevated levels of fluoride. Although the incorporation of fluoride into bone may increase the stability of the crystal lattice and render the bone less soluble, bone mineralization is delayed or inhibited (Grynpas, 1990), and consequently the bones may become brittle and their tensile strength may be reduced. The severity of the effects associated with skeletal fluorosis is related to the amount of fluoride incorporated into bone. In a preclinical phase, the fluorotic patient may be relatively asymptomatic, with only a slight increase in bone mass, detected radiographically. Sporadic pain and stiffness of the joints, chronic joint pain, osteosclerosis of cancellous bone and calcification of ligaments are associated with the first and second clinical stages of skeletal fluorosis. Crippling skeletal fluorosis (clinical phase III) may be associated with limited movement of the joints, skeletal deformities, intense calcification of ligaments, muscle wasting and neurological deficits (Krishnamachari, 1987; Kaminsky et al., 1990; US DHHS, 1991). A consistent finding in cases of chronically elevated fluoride uptake is an increase in mineralization lag time of bone, which can be demonstrated by dynamic histomorphometry (Boivin et al., 1989). Osteomalacia may be observed in fluorotic individuals with a reduced or suboptimal intake of calcium; secondary hyperparathyroidism may also be observed in a subset of patients (Krishnamachari, 1987; US DHHS, 1991). Apparently in combination with nutritional deficiencies, high intakes of fluoride and the subsequent osteomalacia may also lead in children to bone deformities such as genu valgum, originally described as Kenhardt bone disease (Jackson, 1962; Krishnamachari & Krishnaswamy, 1973; Krishnamachari, 1976; Chakma et al., 2000). In osteoporotic patients, fluoride can stimulate bone formation to such an extent that, despite calcium supplementation, calcium deficiency, secondary hyperparathyroidism and osteomalacia occur (Dure-Smith et al., 1996).

The concentration of fluoride in the bone of individuals in the preclinical or crippling stages of skeletal fluorosis may be between 3500 and 5500 mg/kg bone or greater than 8400 mg/kg bone, respectively, compared with the reference values of 500–1000 mg/kg bone ash weight (US DHHS, 1991).

A number of factors, such as age, nutritional status, renal function and calcium intake, in addition to the extent and duration of exposure, can influence the amount of fluoride deposited in bone and, consequently, the development of skeletal fluorosis (US DHHS, 1991). Individuals with impaired renal function, such as those with diabetes, may be more prone to developing fluoride-related toxicological effects (i.e., fluorosis) due to their diminished excretion of fluoride (Kaminsky et al., 1990; US DHHS, 1991). Skeletal fluorosis may be reversible to some degree in a manner that is dependent upon the extent of bone remodelling (Grandjean & Thomsen, 1983).

Felsenfeld & Roberts (1991) reported the case of a 54-year-old woman who, after having consumed drinking-water containing approximately 8 mg fluoride/litre over a period of 7 years, had osteosclerosis and stiffness in her knees and hips.

Source & ©: IPCS "Environmental Health Criteria for Fluorides", (EHC 227),
Chapter 8: Effects on humans, section 8.1.3.2: Skeletal fluorosis
 

9.4 At what intake levels does fluoride cause skeletal fluorosis?

The source document for this Digest states:

Five cases of crippling skeletal fluorosis in the USA have been reported over the past 40 years; the total intake of fluoride by some of these individuals over a 20-year period was estimated to be approximately 15–20 mg/day (US DHHS, 1991) (equivalent to a daily intake of 230–310 µg fluoride/kg body weight per day in an adult weighing 64 kg). There have been no systematic studies of the prevalence of this disease in the USA.

The occurrence of endemic skeletal fluorosis has been well documented in case reports and surveys of individuals residing in certain areas of the world (e.g., India, China, northern, eastern, central and southern Africa), where the intake of fluoride may be inordinately high as a result of the often significant consumption of drinking-water containing substantial amounts of naturally occurring fluoride, the indoor burning of fluoride-rich coal for heating and cooking, the preparation of foodstuffs in water containing increased fluoride and/or the consumption of specific foodstuffs naturally rich in fluoride (Haimanot et al., 1987; Krishnamachari, 1987; Pettifor et al., 1989; Kaminsky et al., 1990; Tobayiwa et al., 1991; Mithal et al., 1993; Wang et al., 1994; Abdennebi et al., 1995; Liu, 1995; Michael et al., 1996; Zhao et al., 1996; Teotia et al., 1998). Large numbers of individuals residing in India and China are afflicted with skeletal fluorosis, which in some cases may be severely crippling. In addition to an increased intake of fluoride from foodstuffs and drinking-water with high levels of fluoride, other factors, such as nutritional status as well as climate and other factors influencing fluid intake, may possibly play a significant role in the development of endemic skeletal fluorosis (Krishnamachari, 1987; Haimanot, 1990; Zang et al., 1996). These issues make it difficult to characterize the exposure–response relationship in studies of skeletal fluorosis, such as those outlined below.

In China, endemic fluorosis associated with coal burning has been identified in epidemiological investigations. Local residents absorb high doses of fluoride through inhalation and/or ingestion, as a consequence of the indoor use of high-fluoride coal in cooking, heating and drying of food (the average concentrations of fluoride in coal were 200–1500 mg/kg, with the highest up to 3000 mg/kg). In those areas, the intakes of fluoride via drinking-water were relatively low (range from 0.1 to 0.52 mg/day per person) (Table 10). The number of cases of coal-burning-type skeletal fluorosis has been estimated to be 1.5 million (Hou, 1997; Liang et al., 1997).

Table 10. Daily fluoride intake in different endemic areas in China using high-fluoride coal for cooking and drying foodstuffs indoors

Endemic area Coal type Daily intake (mg/person)
Food Drinking-water Air Total
Sichuan Soft coal 8.86 0.1 0.67 9.63
Hubei Anthracite 4.12 0.45 0.55 6.12
Jiangxi Anthracite 2.54 0.5 0.24 3.28
Hunan Anthracite 1.81 0.52 0.31 2.64
Hubei Anthracite 1.86 0.42 0.15 2.43
Jiangxi
(control)
Firewood 1.14 0.24 0.11 1.49

In a short communication with few details, the relationship between air, well-water and dietary fluoride and skeletal fluorosis (no information on diagnostic criteria provided) was studied among 6792 individuals in Inner Mongolia (Xu et al., 1997) (Table 11). The concentrations of fluoride in air and diet were low, and that in drinking-water showed a correlation of 0.87 with the prevalence of fluorosis. The skeletal fluorosis prevalence was <0.21% for fluoride concentrations of 0.65 mg/litre or lower and reached 19.9% for fluoride concentrations of 6.9 mg/litre.

Table 11. Prevalence of skeletal fluorosis in villages in Inner Mongolia, China a

Fluoride content of drinking-water Skeletal fluorosis
Cases %
a From Xu et al. (1997).
0.4 0 0
0.65 2 0.21
1.4 93 7.72
1.6 109 12.3
3.2 101 12.7
3.4 132 15.2
4.7 42 19.6
6.9 166 19.9

The relationship between fluoride concentrations in drinking-water and the prevalence of skeletal fluorosis was also reported in another Chinese study (Liang et al., 1997) (Table 12).

Table 12. Prevalence of skeletal fluorosis in China as a function of drinking-water fluoride concentration a

Fluoride concentration in drinking-water (mg/litre) Prevalence of skeletal fluorosis (%) among individuals with normal nutrition b Prevalence of skeletal fluorosis (%) among individuals with deficient nutrition c
a From Liang et al. (1997).
b Normal nutrition = protein >75 g/day, high-quality protein >20% of total protein, calcium >600 mg/day.
c Deficient nutrition = protein <20 g/day, high-quality protein <10% of total protein, calcium <400 mg/day.
<0.3 0 0
0.6–1.0 0 0
>4.0 43.8 69.2

According to an early estimate, the number of persons at risk of developing skeletal fluorosis was 5 million in Punjab and more in Andhra Pradesh and Madras, India (Siddiqui, 1970).

The frequency of skeletal fluorosis (as identified by the clinical picture) among children 3–10 years of age was 39% (18/46) in a village in India, where the fluoride concentrations in the three wells were 0.6, 4.0 and 1.34 mg/litre (Shivashankara et al., 2000). It was not possible to discern, from the information available, the contribution of each well to the drinking-water of the residents.

In a clinical survey for fluorosis in a random sample of residents in five areas in Tamil Nadu, South India, the drinking-water fluoride concentration was directly related to the prevalence of dental fluorosis in children (8–15 years of age) and adults. Among children, no skeletal fluorosis (no information on diagnostic criteria provided) was observed; among adults, the prevalence of fluorosis was 34% (157 individuals surveyed) in the area with the highest drinking-water fluoride concentration (summer month average 6.8 mg/litre, non-summer month average 5.6 mg/litre) (estimated total daily fluoride intake 20 mg), while no skeletal fluorosis was observed in the other areas, where the mean fluoride concentrations were 2.2 (summer months) and 1.8 (non-summer months) mg/litre or lower, with estimated total daily fluoride intakes less than 10 mg (Karthikeyan et al., 1996).

A correlation between average water fluoride concentration and prevalence of skeletal fluorosis (assessed by X-ray) was found among adults in 15 villages in Dungapur district in Rajasthan, India (Choubisa et al., 1997) (Table 13). The prevalence ranged from 4.4% at a water fluoride level of 1.4 mg/litre to 63.0% at the level of 6.0 mg/litre. Crippling fluorosis was consistently observed in villages with fluoride concentrations of >3 mg/litre.

Table 13. Relationship between drinking-water fluoride concentration and skeletal fluorosis in Rajasthan, India a

Village Fluoride concentration (mg/litre) Prevalence of fluorosis % Crippling fluorosis
Mean Range
a From Choubisa et al. (1997).
Amaliya Fala 1.4 0.5–1.8 4/92 4.3 No
Doja 2 1.2–2.0 10/102 9.8 No
Selaj 2 1.5–2.5 4/85 4.7 No
Anturi 2.3 0.3–3.5 16/180 8.9 No
Batikada 2.4 1.3–3.1 16/120 13.3 No
Devsomnath 2.5 0.0–3.1 14/188 7.4 No
Masania 2.6 1.0–2.6 28/176 15.9 No
Dora 3 1.2–3.9 22/96 22.9 Yes
Dolwaniya Ka Oda 3 2.5–3.5 14/78 17.9 Yes
Palvasi 3.4 2.3–4.2 38/114 33.3 Yes
Jogiwara 3.4 1.0–4.3 27/106 25.5 Yes
Kolkhanda 4.5 4.2–4.7 52/106 49.1 Yes
Banda Ghanti 5.7 3.8–6.7 61/115 53.0 Yes
Hadmatiya 6 3.9–8.3 118/205 57.6 Yes
Pantali 6 2.4–10.8 121/192 63.0 Yes

In four villages in the Faridabad district, North India, the percentage of people with skeletal fluorosis (assessed by the clinical appearance of impaired mobility) was 57, 43, 18 and 17, while the respective means (ranges) of the water fluoride contents were 3.2 (0.25–8.0), 3.7 (0.3–7.0), 2.5 (0.3–5.4) and 1.0 (0.7–1.6) mg/litre (Susheela et al., 1993).

A cross-sectional study in Punjab also reported the relationship between water fluoride and the prevalence of skeletal fluorosis (Jolly et al., 1968). Skeletal fluorosis was rare (assessed by X-ray) (2.4%) in a village where the average well-water fluoride concentration was 1.4 mg/litre, but its incidence was 71% in the village with the highest water fluoride concentration, 9.7 mg/litre. In five villages where the water fluoride concentration was 3–4 mg/litre, the prevalence of skeletal fluorosis was 10–42%. It was suggested that lower calcium concentrations in some water sources were associated with higher skeletal fluorosis prevalence.

The dependence of skeletal fluorosis on duration of exposure and age was studied in a village in Andhra Pradesh, India, where the drinking-water was derived from five wells, in which the fluoride concentrations were between 7.2 and 10.7 mg/litre (average 9.0 mg/litre); it was estimated that the daily water consumption was 4.6 litres, which would lead to a daily dose of 36–54 mg fluoride (Saralakumari & Ramakrishna Rao, 1993). Skeletal fluorosis started to appear after 10 years of residence in the village and reached 100% after 20 years.

In a cross-sectional study of 50 randomly selected adults who had been residents of one of two villages for all their lives in Senegal, kyphosis was used as an indicator of skeletal fluorosis (and was radiologically confirmed to be fluorosis in three cases) (Brouwer et al., 1988). The prevalence of severe kyphosis was 4 out of 55 (7%) in Guinguineo, where the well-water fluoride concentration was 3.9 mg/litre, and 11 out of 42 (26%) in Darou Rahmarie Fall, where the fluoride concentration was 7.4 mg/litre.

Source & ©: IPCS "Environmental Health Criteria for Fluorides", (EHC 227),
Chapter 8: Effects on humans, section 8.1.3.2: Skeletal fluorosis
 


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