32(1) 1999
| FLUORIDE |
International Society for Fluoride Research | Table of Contents 32(1) 1999 |
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Research Report
THE DISTRIBUTION OF URINARY FLUORIDE
CONCENTRATION IN THE UK
Peter Mansfield,* M.D.
Grimoldby, Louth, Lincolnshire, UK
SUMMARY: During 1997-1998, fluoride-specific electrode analyses were conducted on urine specimens from 268 users of a health facility and 261 respondents to a press appeal in the United Kingdom. Among residents of areas with artificial water fluoridation, the median urinary fluoride concentration was 1.2 ppm, and in nonfluoridated areas it was 0.7 ppm. Two percent of the samples from the fluoridated areas showed F levels of 4 ppm or higher. In one of the fluoridated areas, individuals with a medically confirmed bone degeneration had significantly higher urinary fluoride concentrations (median 1.75 ppm) than age- and sex-matched controls from the same neighborhood (median 1.2 ppm). These findings indicate an urgent need to base epidemiological comparisons of fluoridated and nonfluoridated populations on individual fluoride excretion.
Keywords: Artificial fluoridation, Bone, Epidemiology, Fluoridation, Osteoarthrosis, Osteoporosis, Spondylosis, Urinary fluoride concentration.
INTRODUCTION
In 1983 I was surprised to discover that a girl, then 5 years old had, on two separate occasions two years apart, ailed dramatically from using fluoridated toothpaste and recovered promptly when it was withdrawn. The National Health Service could not provide a clinical test to help me confirm the role of fluoride in her illness. After preliminary inquiries I established a laboratory facility in my own practice and began doing routine urinary fluoride analyses in 1990. All new clients since 1990 have had routine urinary fluoride determinations, regardless of their reason for attendance.
MATERIALS AND METHODS
All the data are from assays conducted personally by the author during 1997-98 using the same apparatus. Most testing sessions included samples from both the East and West Midlands.
An ELIT 221 fluoride-selective electrode was used. Ten-mL aliquots of urine were diluted to 50 mL containing commercial 50% TISAB. Comparison of the electrode potential in this solution with a straight-line plot of potential vs log[F concentration], obtained from four standard fluoride solutions, gave the F concentration with an accuracy of ± 10%.
Since 1997, 268 urine specimens have been analyzed routinely from the local East Midlands and South Yorkshire population. In May 1997 the author solicited urine specimens from residents in the West Midlands region, whose water supply had been artificially fluoridated for 35 years. A total of 261 postal samples were analyzed. Many respondents reported illnesses which could not be verified, but 39 volunteers from the Osteoporosis support group had diagnoses verified by a doctor. Each of these was matched for age and sex with a neighboring control without any known bone disease. These controls were also selected without access to any urinary fluoride result.
From 54 volunteers during 1990-1996, 24-hour urine samples were collect-ed with no exclusion because of fluoride concentration. The mean, median and mode volumes were 1.7, 1.5 and 1.5 liters respectively (standard deviation 0.7).
Statistical significance testing was performed using the Student’s t-test on the square root of fluoride data, and the x2 test on demographic data.
RESULTS
Results from the East Midlands are presented in Table 1. Fifteen residents of naturally fluoridated areas were excluded, leaving 88 from artificially fluoridated and 165 from non-fluoridated addresses. The demographic distribution of these two groups was similar, and the distribution of urinary fluoride (F) concentration in both was bimodal, but otherwise differed significantly (P <0.002). In the artificially fluoridated group, 60% were excreting ≥ 1 ppm F and 18% ≥ 2 ppm F, compared to 39% and 8%, respectively, in the non-fluoridated group.
|
Urine F (ppm) |
Fluoridated No. (percent) |
Non-fluoridated No. (percent) |
| < 0.3 | 4 (4.5) | 16 (9.7) |
| 0.3 < 0.7 | 20 (22.7) | 63 (38.2) |
| 0.7 < 1.0 | 11 (12.5) | 21 (12.7) |
| 1.0 < 1.3 | 22 (25.0) | 33 (20.0) |
| 1.3 < 1.7 | 10 (11.4) | 9 (5.5) |
| 1.7 < 2.0 | 5 (5.7) | 10 (6.1) |
| 2.0 < 2.3 | 5 (5.7) | 3 (1.8) |
| 2.3 < 2.7 | 4 (4.5) | 5 (3.0) |
| 2.7 < 3.0 | 2 (2.3) | 1 (0.6) |
| 3.0 < 3.3 | 1 (1.1) | 1 (0.6) |
| 3.3 < 3.7 | 1 (1.1) | 1 (0.6) |
| 3.7 < 4.0 | 2 (2.3) | 1 (0.6) |
| ≥ 4.0 | 1 (1.1) | 1 (0.6) |
| Total No. | 88 (99.9) | 165 (100.1) |
| Mean F | 1.28 | 0.96 |
| Median F | 1.1 | 0.7 |
| Populations are the same: x2(5) = 5.8. Difference between columns is highly significant: |t| = 3.21, v = 251. P < 0.002. | ||
The West Midlands and East Midlands samples are demographically different, presumably because of the differing mode of recruitment. The distribution of urinary fluoride concentration in the two fluoridated areas is shown in Table 2. Apart from loss of the bimodal pattern, they do not differ markedly, notwithstanding the demographic contrast. This fact makes it unlikely that the West Midlands fluoride measurements are significantly biased.
| Urine F (ppm) |
West Midlands No. (percent) |
East Midlands No. (percent) |
| < 0.3 | 4 (1.5) | 4 (4.5) |
| 0.3 < 0.7 | 30 (11.5) | 20 (22.7) |
| 0.7 < 1.0 | 60 (23.0) | 11 (12.5) |
| 1.0 < 1.3 | 49 (18.8) | 22 (25.0) |
| 1.3 < 1.7 | 31 (11.9) | 10 (11.4) |
| 1.7 < 2.0 | 28 (10.7) | 5 (5.7) |
| 2.0 < 2.3 | 25 (9.6) | 5 (5.7) |
| 2.3 < 2.7 | 8 (3.1) | 4 (4.5) |
| 2.7 < 3.0 | 9 (3.4) | 2 (2.3) |
| 3.0 < 3.3 | 4 (1.5) | 1 (1.1) |
| 3.3 < 3.7 | 4 (1.5) | 1 (1.1) |
| 3.7 < 4.0 | 4 (1.5) | 2 (2.3) |
| ≥ 4.0 | 5 (1.9) | 1 (1.1) |
| Total No. | 261 (99.9) | 88 (99.9) |
| Mean F | 1.46 | 1.28 |
| Median F | 1.2 | 1.1 |
| Populations differ - x2(5) = 17.9 - due to different sampling methods. | ||
The results from two age- and sex-matched sub-samples from the West Midlands, differing by the presence or absence of known degenerative bone disease, are depicted in Table 3. Despite the assortment of diagnoses, those individuals with bone damage show a significantly higher urinary fluoride concentration than their controls (P = 0.02). This difference was not diminish-ed when the ten subjects with osteoporosis (and their controls) were excluded.
DISCUSSION
These data explain in part why epidemiological studies of hip fracture comparing populations distinguished by the fluoridation status of their drinking water1-6 have agreed so poorly. They have very low discriminating power.
| Urine F (ppm) | Bone-Damaged No. (percent) |
ControlsNo. (percent) |
| < 0.5 | 0 (0) | 0 (0) |
| 0.5 < 1.0 | 7 (18) | 15 (38) |
| 1.0 < 1.5 | 10 (26) | 8 (21) |
| 1.5 < 2.0 | 6 (15) | 7 (18) |
| 2.0 < 2.5 | 3 (8) | 6 (15) |
| 2.5 < 3.0 | 4 (10) | 0 (0) |
| 3.0 < 4.0 | 7 (18) | 1 (3) |
| 4.0 < 6.0 | 2 (5) | 2 (5) |
| Total | 39 (100) | 39 (100) |
| Mean | 2.04 | 1.47 |
| Median | 1.75 | 1.2 |
| Student’s test on square root of value: |t| = 2.38 (v = 76) P = 0.02. Differences are significant. | ||
Total fluoride intake is distributed widely, with considerable overlap between populations distinguished in this way (Table 1). In order to be detected, differences between these groups would have to be quite large.
Urinary fluoride concentration is well established7-10 as a way to estimate total fluoride intake in individuals from the general population, and is regularly used for special purposes in various countries.11-13 This method of estimation varies by ± 50% in individual cases, but the distribution in a population is considered reliable.9
McClure7 in 1944 pointed out the close correspondence of the concentrations of fluoride in drinking water and in the urine of people drinking it. His result was an average value, because his method was to pool the urine of up to 20 national service recruits from a given area. The variance of individual samples is therefore not apparent. Something has, nevertheless, clearly changed since 1944. The wide range of individual urinary fluoride concentration reported here bears no obvious relationship to the water concentration, which does not exceed 1 ppm in the present series. Even so, individual urine concentrations range as high as in McClure’s series, in which water fluoride was as high as 5 ppm.
Two differences are noteworthy. Since 1944 fluoride has been introduced into many water supplies as sodium hexafluorosilicate, which may exhibit different biodynamic properties14,15 from naturally-occurring water-borne fluoride. This possibility has not been adequately investigated.
The second difference is the increased availability of fluoride from other sources, particularly in crowded industrialized countries. It is present at up to 1500 ppm in most toothpastes, in many foods as residues from agricultural fertilizers and biocidal sprays, in foods processed in areas with fluoridated water, and still to some extent in the air as an industrial effluent, the Clean Air Act notwithstanding.16
The findings of this study contribute to anxieties about the possible consequences of current life-long consumption of fluoride. It has been suggested17 (originally in relation to workers exposed to cryolite dust) that a urinary fluoride concentration consistently above 4 ppm may lead to significant skeletal fluorosis. That criterion applies to 1.9% of our West Midlands sample.
The case-control data presented here independently suggest that bony degeneration may be causally related to habitual fluoride consumption. Recent tea-drinking did not explain the finding. Negative fluoride balance (due to porotic lysis of fluorotic bone) has not been ruled out, but the prior fluoride accumulation required for that to occur could well have caused the osteoporotic process in the first place.
CONCLUSION
Urinary fluoride concentrations have risen markedly since 1944 in relation to increases in the fluoride content of drinking water. The frequency distribution of urine concentration is wide in all areas, but distributions differ significantly between artificially fluoridated and unfluoridated areas. In a small case-control study of bony degeneration in a fluoridated area, cases had significantly higher urinary fluoride concentrations than age-, sex- and neighborhood-matched controls.
These findings indicate the possibility of eventual bone damage from life-long consumption of fluoride at levels prevailing in Britain. Studies in individuals, linking 24-hour urinary fluoride excretion with bone fluoride concentrations, are urgently needed to probe this possibility.
Presented in part to the XXIInd Conference of the International Society for Fluoride Research, Bellingham, Washington, USA, August 24-27, 1998
REFERENCES
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