The Journal of the American Dental Association
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Am Dent Assoc, Vol 133, No 2, 157-165.
© 2002 American Dental Association
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by BELTRÁN-AGUILAR, E. D.
Right arrow Articles by LOCKWOOD, S. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by BELTRÁN-AGUILAR, E. D.
Right arrow Articles by LOCKWOOD, S. A.

TRENDS

COVER STORY
JADA Continuing Education

Prevalence and trends in enamel fluorosis in the United States from the 1930s to the 1980s



EUGENIO D. BELTRÁN-AGUILAR, D.M.D., M.P.H., M.S., Dr.P.H., SUSAN O. GRIFFIN, Ph.D. and STUART A. LOCKWOOD, D.M.D., M.P.H.


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 STUDY LIMITATIONS
 PUBLIC HEALTH IMPLICATIONS
 CONCLUSION
 REFERENCES
 
Background. The National Survey of Dental Caries in U.S. School Children: 1986–1987 conducted by the National Institute of Dental Research, or NIDR, remains the only source of national data about the prevalence of enamel fluorosis. The authors analyze these data and describe changes in the prevalence of enamel fluorosis since the 1930s, as reported by H. Trendley Dean.

Methods. A sample of children comparable to those described in the 1930s was selected from the NIDR data set among children living in households served by public water systems during the child’s first eight years of life. The type of water system (that is, natural, optimal and suboptimal) for each household had been recorded in the NIDR data set using data from the 1985 U.S. Fluoridation Census. The NIDR data set included information about the children’s history of fluoride exposure obtained from parents.

Results. In the 1986–1987 period, the prevalence of enamel fluorosis (ranging from very mild to severe) was 37.8 percent among children living in residences with natural fluoride (0.7 to 4.0 parts per million fluoride ions, or F –), 25.8 percent in the optimal fluoride group (0.7 to 1.2 ppm F –) and 15.5 percent in the suboptimal fluoride group (< 0.7 ppm F –). The largest increase in fluorosis prevalence from the 1930s to the 1980s was in the suboptimal fluoride group (6.5 to 15.5 percent).

Conclusions and Clinical Implications. Exposure to multiple sources of fluoride may explain the increase in enamel fluorosis from the 1930s to the 1980s. The exposure to fluoride from sources such as dietary supplements has decreased since the 1980s because of reductions in the recommended dosage, but these changes occurred too late to have an effect on the study cohort. Evidence of simultaneous use of systemic fluorides indicates the need to reinforce guidelines for the appropriate use of fluorides and promote research on measuring total fluoride exposure.

During the 1930s, H. Trendley Dean conducted a series of epidemiologic studies in the Midwest and Southwest that established a direct association between the natural concentration of fluoride in the drinking water and the prevalence and severity of cosmetic changes in the tooth enamel, subsequently termed "enamel fluorosis."1 More important, Dean also reported an inverse association between the concentration of fluoride in the drinking water and the prevalence of dental caries.2

Evidence of simultaneous use of systemic fluorides indicates the need to reinforce guidelines for the appropriate use of fluorides.

Since then, other U.S. researchers have reported an increase in the prevalence of enamel fluorosis among children, but usually in cohorts of limited representativeness.3–6 The U.S. Public Health Service compiled a comprehensive review of fluorosis studies conducted in North America up to 1985.7 Two follow-up studies, one from Illinois8 and the other from New York,9 reported conflicting results in regard to the increase in enamel fluorosis in optimally fluoridated communities during the 1985–1995 period. A recent review of published data compared the prevalence of enamel fluorosis in the 1930s with that in the late 1980s and concluded that there was an increase in enamel fluorosis in communities with less than 0.3 parts per million fluoride ions, or F–, in the drinking water. A less evident increase was observed in optimally fluoridated communities.10

In 1986–1987, the National Institute of Dental Research, or NIDR, conducted the only assessment to date of the prevalence of enamel fluorosis in a representative sample of U.S. schoolchildren; the results, published in an abstract,11 indicated that 22.3 percent of all U.S. schoolchildren had enamel fluorosis, measured as very mild, mild, moderate or severe.

A secondary analysis of the 1986–1987 NIDR data12 suggested the need for a re-evaluation of current recommendations for fluoride concentration in the drinking water (that is, 0.7 to 1.2 ppm F–) because of the relatively high prevalence and severity of enamel fluorosis in children who drink water with fluoride concentrations greater than 0.6 ppm, as assessed at their schools. The objectives of our study were as follows:

– to perform a comprehensive analysis of the 1986–1987 NIDR data regarding the prevalence and severity of enamel fluorosis;
– to compare these results with those reported by Dean in the 1930s;
– to discuss the public health implications associated with current levels of enamel fluorosis in the United States.
The prevalence and severity of enamel fluorosis did not differ substantially according to history of use of fluoride drops or tablets.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 STUDY LIMITATIONS
 PUBLIC HEALTH IMPLICATIONS
 CONCLUSION
 REFERENCES
 
The NIDR data on enamel fluorosis were collected as part of the National Survey of Dental Caries in U.S. School Children: 1986–1987.13 In this survey, 40,693 children attending kindergarten through 12th grade (ages 5 to 17 years) were selected by a multistage probability sample to represent 41 million children attending U.S. schools in the middle 1980s. The methods and diagnostic criteria are reported elsewhere.13,14 In our report, we provide information about aspects of the survey directly related to our analysis.

In the NIDR survey, 14 trained dental examiners collected information about the fluorosis status of fully erupted permanent teeth.13 Teeth with more than one-half of the visible surface obscured by a restoration, caries or an orthodontic appliance were excluded from assessment. Each tooth was assigned a level of the ordinal Dean’s fluorosis index,13,14 which is based on the percentage of the surface affected by fluorosislike lesions. The teeth were not dried before scoring. We used Dean’s definition of fluorosis to assign a fluorosis score to each child, using the "severest form of dental fluorosis recorded for two or more teeth."1 Unless otherwise noted, we used an estimate of the prevalence of enamel fluorosis in children with very mild, mild, moderate or severe fluorosis.

As part of the 1986–1987 national survey, each child’s parent or guardian completed a questionnaire that included demographic information and information about whether the child was exposed (yes or no) to fluoride drops, fluoride tablets or fluoride treatment in a dental office, as well as the ages at which these exposures occurred. We restricted our analysis to the dichotomous "yes" or "no" for each fluoride vehicle because only one time period was assigned to each fluoride vehicle on the questionnaire. The parent or guardian also provided the child’s residential history, including the moving dates to and from each residence and whether each residence was served by a public water system.

In addition, for residences served by a public water system, NIDR staff used the information from the questionnaire and the 1985 fluoridation census15 (collected by the Centers for Disease Control and Prevention, or CDC) to categorize each residence as having

– optimal fluoride, or OF, defined as having adjusted fluoride concentrations between 0.7 and 1.2 ppm;
– natural fluoride, or NF, defined as having naturally occurring fluoride between 0.7 and 4.0 ppm
– suboptimal fluoride, or SF, defined as water systems not reported in the census, suggesting that they had fluoride concentrations of less than 0.7 ppm F–.

In this report, we refer to this water fluoride exposure variable as the type of water system.

We used a stepwise process to select from the 1986–1987 NIDR data set a subgroup of children comparable to those in Dean’s studies. The boxGo ("Selection Criteria for Enamel Fluorosis Sample") illustrates the number of children excluded at each level. The final sample size was 3,763 children, which represented 41 percent of all 12- to 14-year-old children in the data set (a total of 9,089 children) and more than 4 million schoolchildren.


View this table:
[in this window]
[in a new window]
  		SELECTION CRITERIA FOR ENAMEL FLUOROSIS SAMPLE.*

 
We reviewed and tabulated the data from the 21 cities assessed by Dean.1 We included cities with water fluoride concentrations between 0.7 and 1.9 ppm because the subjects in these cities exhibited prevalences of enamel fluorosis comparable to those observed in the NIDR survey.

We calculated weighted percentages of children with fluorosis at each level of Dean’s index for each of the three types of water systems, and compared these prevalence values with those reported by Dean. All analyses were conducted using a statistical software package (SUDAAN, Release 7.5, Research Triangle Institute, Research Triangle Park, N.C.), with the weights and stratification variables suggested by NIDR.14


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 STUDY LIMITATIONS
 PUBLIC HEALTH IMPLICATIONS
 CONCLUSION
 REFERENCES
 
Table 1Go shows the distribution of the sample and the population represented by type of water system. About 55 percent of all children were classified in the SF group, 38 percent were classified in the OF group and 6 percent were classified in the NF group.


View this table:
[in this window]
[in a new window]
  		TABLE 1 DISTRIBUTION OF STUDY COHORT BY TYPE OF WATER SYSTEM.*{dagger}

 
Table 2Go shows the distribution of the sample according to use of fluoride tablets, fluoride drops or both. About 23 percent of children in the SF group reported receiving fluoride tablets or drops and 13 percent reported receiving both. Between about 6 and 8 percent of children in the OF and NF groups reported that they used fluoride tablets or drops, and between about 2 and 3 percent reported that they used both.


View this table:
[in this window]
[in a new window]
  		TABLE 2 HISTORY OF FLUORIDE SUPPLEMENT USE BY TYPE OF WATER SYSTEM.*{dagger}

 
Our analysis found that the prevalence and severity of enamel fluorosis by type of water system did not differ substantially according to history of use of fluoride drops or tablets. Among those children whose parents reported no use of fluoride supplements, the prevalence of enamel fluorosis ranging from very mild to severe was highest in the NF group (38 percent), followed by the OF group (26 percent) and then the SF group (15.5 percent) (Figure 1Go, page 161). The prevalence of moderate and severe fluorosis was 8.6 percent in the NF group, 1.5 percent in the OF group and 0.6 percent in the SF group (Figure 1Go). The prevalence and severity of enamel fluorosis in the 12- to 14-year-old children not meeting the selection criteria (57 percent) were similar to those in children in the OF group (data not shown).



View larger version (47K):
[in this window]
[in a new window]
  		Figure 1. Prevalence and severity of enamel fluorosis in 12- to 14-year-old children with no history of fluoride supplement use, according to the National Survey of Dental Caries in U.S. School Children: 1986–1987.13

 
In seven communities studied by Dean, the prevalence of enamel fluorosis ranged from 6.5 percent (Pueblo, Colo.) to 48 percent (Galesburg, Ill.) (Figure 2Go, page 161). These communities had fluoride concentrations in the drinking water of between 0.7 and 1.9 ppm. Dean did not include children living in communities with water fluoride concentrations of 0.8, 1.0, 1.1, 1.5, 1.6 or 1.7 ppm. He reported moderate fluorosis only in Elmhurst, Ill. (1.8 ppm F–), and Galesburg, Ill. (1.9 ppm F–). Severe fluorosis was not observed in any city, even those with water fluoride concentrations of 1.9 ppm F–.



View larger version (47K):
[in this window]
[in a new window]
  		Figure 2. Prevalence and severity of enamel fluorosis in children in seven communities in the 1930s.1,2

 
In comparing the enamel fluorosis data from the 1930s with that of 1986–1987 (Figure 3Go, page 162), we observed a similar prevalence (15 percent) in children in the SF group in the 1980s (< 0.7 ppm F–) and in children in Aurora, Ill., in the 1930s (1.2 ppm F–). We also observed a similar prevalence (about 26 percent) among children in the OF group in the 1980s (0.7 to 1.2 ppm F–) and children in Joliet, Ill., in the 1930s (1.2 to 1.3 ppm F–). Finally, children in the NF group in the 1980s (0.7 to 4.0 ppm F–) and children in Elmhurst in the 1930s (1.8 ppm F–) had a prevalence of enamel fluorosis of about 37 to 40 percent.



View larger version (51K):
[in this window]
[in a new window]
  		Figure 3. Historical comparison of enamel fluorosis prevalences (very mild to severe) in the 1930s1,2 with those in the 1980s.13

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
STUDY LIMITATIONS
 PUBLIC HEALTH IMPLICATIONS
 CONCLUSION
 REFERENCES
 
For most teeth, excluding third molars, the risk period for developing enamel fluorosis—the time during which the tooth might develop fluorosis if exposed to excessive fluoride over the long term—is the first eight years of life.16 That time is restricted to the first six years for most anterior teeth. Central incisors seem to be at greater risk of excessive exposures of as brief as four months after the 22nd month of life.17 We know from Dean’s studies1 that enamel fluorosis was present in children living in communities with very low concentrations of natural fluoride in the drinking water (ranging from negligible levels to less than 0.6 ppm F–) and, at that time, fluoride in the water was the predominant source of fluoride.

Therefore, we know there has always been a trade-off in regard to fluoride use—namely, we expect that a small proportion of the population will develop milder forms of enamel fluorosis in exchange for a vast majority (including those with such fluorosis) benefiting from its preventive effect in regard to dental caries. This trade-off is not unique to fluorides. Other public health preventive interventions, such as vaccines, carry specific side effects. The advantage of community water fluoridation over some other public health preventive interventions is that its only known side effect (enamel fluorosis) is a possible cosmetic problem, with no functional implications or associated morbidity.18

Therefore, when discussing enamel fluorosis, we cannot ignore the caries-preventive benefits achieved after more than 50 years of fluoride use in general and water fluoridation in particular. The Centers for Disease Control and Prevention19 has identified fluoridation of the drinking water as one of 10 great achievements in public health during the 20th century.

In our analysis of the NIDR data, we found that the prevalence of enamel fluorosis varied according to the type of water system. We found the highest prevalence in children living in areas with public systems served with naturally fluoridated water, followed by children living in optimally fluoridated areas and, finally, children in suboptimally fluoridated areas. The CDC fluoridation census data that were used to classify these public water systems include the actual fluoride level as reported by each public water system; however, the NIDR data set does not include such data.

For our analyses, we assumed that most of the water systems in the SF group were served with water with natural fluoride at concentrations of less than 0.7 ppm, because otherwise they would have been classified as having optimal or natural fluoride levels. However, the actual distribution within this group is impossible to determine from the data set. Unfortunately, the fluoride range in the NF group was wider than that for the other two groups. This limitation in the data set precludes a more precise analysis of the effect of higher fluoride levels and changes in fluorosis prevalence from the 1930s to the 1980s. However, only 7 percent of our cohort was in the NF group.

Fluorosis indexes. The 1986–1987 survey used Dean’s index of enamel fluorosis. Some criticism has been raised concerning this index,20 especially in regard to the nature of Dean’s "questionable" category. Other indexes, especially the Tooth Surface Index of Fluorosis21 and the Thylstrup and Fejerskov, or TF, Index,22 have been used in many epidemiologic studies. Each of these three indexes, however, has advantages and disadvantages and their results are not directly comparable.20 Dean’s fluorosis index, however, was designed strictly as an epidemiologic tool and, as such, exhibits an important characteristic: the person is the unit of measurement, which allows for the assessment of prevalence. This is not true for the other indexes, which use the tooth surface as the unit of measurement and report the percentage of surfaces affected with a certain level of fluorosis.

In computing and reporting the prevalence of enamel fluorosis, Dean did not include the "questionable" category.1 As one would expect, prevalence figures in our analysis and in Dean’s data increased substantially when children in this category were included (data not shown). Other indexes do not have this latitude and it seems, for example, that the 55 percent fluorosis prevalence reported by Burt and associates in Durham, N.C.,23 using the TF Index, included children who may have been classified as "questionable" by Dean. In fact, the prevalence of fluorosis in our comparable OF group (0.7 to 1.2 ppm F–) was 63 percent when children in the "questionable" category were included.

Lack of biological indicator. Researchers have not agreed on a way to measure total fluoride exposure because of the lack of a practical and noninvasive tool (that is, a biological indicator). A good biological indicator would allow the modification of current fluoride dosages so that the probability of deleterious effects can be reduced. Enamel fluorosis is not a good biological indicator of fluoride exposure,24 because by the time the first permanent tooth erupts, it is too late to introduce any fluoride modification that could affect the other teeth.

The only known etiologic factor for enamel fluorosis is ingested fluoride.

Two noninvasive biological indicators of fluoride exposure have been tested. The World Health Organization recommends the urinary fluoride excretion rate (milligrams of fluoride excreted in 24 hours).25 This technique has been used to monitor fluoride ingestion in salt and milk fluoridation programs.26–30 One recent study reported fluoride excretion rates in U.S. children living in areas with different natural fluoride concentrations in the drinking water.31 Similarly, studies of fluoride concentrations in fingernails and hair have shown promising results.32,33

Sources of ingested fluoride. The only known etiologic factor for enamel fluorosis is ingested fluoride. Between 1972 and 1983, when the NIDR study cohort was younger than age 8 years—and therefore at risk of developing fluorosis—children were exposed to fluoride from multiple sources: water, infant formula, foods, foods and drinks prepared with fluoridated water, and dietary fluoride supplements (tablets, drops or both), as well as from vehicles intended to be used topically (mainly fluoride toothpaste). Moreover, we believe that shifts in fluoride exposure occurred during and after the teeth of this cohort were at risk of developing fluorosis.

For example, in the case of infant formula, manufacturers began processing products with water containing negligible levels of fluoride in 1979.34 The effect of this fluoride on the risk of developing fluorosis may have been higher among children in fluoridated communities whose parents used water-diluted formula,35 and may have continued after manufacturers reduced the concentration of fluoride in the formulas—a direct effect of the fluoridated water used to dilute powdered or concentrated formula.36

The 1986–1987 NIDR data indicate that between 6 and 8 percent of the children drinking water with optimal and natural fluoride levels reportedly received dietary fluoride supplements. Even though we did not find a significant increase in enamel fluorosis at the population level when we included these children in our analysis, other studies have demonstrated a clear association between supplement use and enamel fluorosis.35–38 Since dietary fluoride supplements were introduced in the late 1960s, their prescription has been tailored to the concentration of fluoride in the drinking water. The schedule for dietary fluoride supplementation in the United States has been revised twice, first in 1979 and then in 199439–41; therefore, children in the 1986–1987 NIDR study, especially those in the SF group, were probably exposed to the 1979 schedule at the time they were at risk of developing fluorosis (1972–1983).

One important source of unintended fluoride ingestion in young children is fluoride toothpaste. Ingestion of toothpaste may occur when parental supervision is absent or inadequate. Many studies have focused on the risk of developing enamel fluorosis associated with ingestion of fluoridated toothpaste by young children.35,37,38,42,43 Researchers in the NIDR survey did not measure the use of fluoride toothpaste; however, between 1972 and 1983, when the children in our analysis were at risk of developing enamel fluorosis, fluoride toothpaste sales in the U.S. market increased from about 70 percent to more than 95 percent.44 Therefore, ingestion of fluoride toothpaste probably contributed to the prevalence of enamel fluorosis observed.


   STUDY LIMITATIONS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 STUDY LIMITATIONS
PUBLIC HEALTH IMPLICATIONS
 CONCLUSION
 REFERENCES
 
Recall bias. Some of the information obtained via questionnaries may be subject to recall bias. This is especially true in the case of fluoride dietary supplementation because of the amount of time that would have elapsed since the children received the supplements. Furthermore, it is possible that the lack of difference in fluorosis prevalence between positive and negative responders to the question about fluoride supplementation may be the consequence of the inability to identify those subjects truly exposed to supplements for long periods. Residency history is less subject to recall bias because most people can recall their addresses from the past 10 to 15 years.

Trend analysis. Our analysis of trends from the 1930s to the 1980s also is subject to shortcomings. Dean was the only examiner in his surveys, and he modified and improved his index as he collected data.1 In the NIDR survey, 14 trained and standardized examiners assessed fluorosis along with other conditions. Dean’s fluorosis index requires an estimation of the percentage of the tooth affected by fluorosislike lesions. This is clinically difficult but critical to categorize a tooth in the questionable, very mild and mild categories, and, to a lesser extent, in the moderate category. For this reason, the risk exists for some misclassification in determining prevalence as the lower end of the fluorosis spectrum moves from "questionable" to "very mild." Unfortunately, the NIDR study reported only overall examiner consistency,14 rather than individual intraexaminer and interexaminer reliability. We can assume that all examiners achieved a good level of interexaminer and intraexaminer consistency because of the following:

– examiners were carefully assigned across examination sites to avoid bias;
– each examiner was recalibrated on site twice during the six months of field activity;
– during recalibrations, no statistical differences were observed between the reference dentist and the examiners when agreement was assessed within one level of Dean’s fluorosis index.14

Other shortcomings include the small sample size at some of Dean’s sites and the lack of sites with fluoride concentrations of 0.8, 1.0 or 1.1 ppm (Figure 2Go). Finally, the wide range of fluoride levels in the NF group precludes a more meaningful comparison of trends between the 1930s and the 1980s.

Despite these limitations, the data are of great interest in regard to changes in the prevalence of enamel fluorosis between the 1930s and the 1980s (Figure 3Go). In our analysis, enamel fluorosis prevalence increased proportionately more in the SF group than it did in the OF group. However, one important difference between the 1930s and 1980s data (a difference less subject to misclassification) is the presence of moderate and severe enamel fluorosis in the SF group. This severity was not observed in the 1930s among children drinking water with less than 1.3 ppm F–.

As more fluoride vehicles become available, children are more likely to be exposed to greater amounts of fluoride. When water fluoridation is the only or main source of fluoride, however, the prevalence of fluorosis remains close to the levels reported by Dean. For example, in 1962, Arnold and colleagues45 reported questionable (7.5 percent), very mild (2.7 percent) and mild (0.5 percent) fluorosis in children aged 12 to 16 years in Grand Rapids, Mich., after 15 years of water fluoridation. In a recent study conducted in Japan, where fluoride supplements are absent and fluoride toothpaste is not popular, Tsutsui and colleagues46 reported enamel fluorosis prevalences that were comparable to those reported by Dean in the 1930s.

Despite the limitations, the NIDR data remain the only national source of information about the prevalence of enamel fluorosis in the United States. Currently, the Fourth National Health and Nutrition Examination Survey, or NHANES IV, is collecting fluorosis data in a representative sample of the U.S. population. Comparison of NHANES IV and NIDR data should enable researchers to determine if changes in the prevalence and severity of enamel fluorosis have occurred during the last 15 years, and if professional recommendations pertaining to the reduction in exposure to systemic fluorides from infant formulas, toothpaste and fluoride supplements have had some effect.

However, the issue with the greatest policy implications is whether an increase in fluorosis prevalence can be attributed to any one fluoride vehicle. If we assume that children in the late 1980s required the same amount of total daily fluids as children in the 1930s, it seems unreasonable to attribute the observed higher enamel fluorosis prevalence only to drinking optimally fluoridated water. On the contrary, because fluoride toothpaste and supplements were not available in the 1930s, it seems more plausible to attribute any additional fluorosis to the ingestion of fluoride from these sources by young children who also drink optimally fluoridated water.35,36,47


   PUBLIC HEALTH IMPLICATIONS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 STUDY LIMITATIONS
 PUBLIC HEALTH IMPLICATIONS
CONCLUSION
 REFERENCES
 
There are at least two public health implications of these results. First, there is a need to reinforce current recommendations for appropriate fluoride use. Children younger than 8 years of age should receive fluoride according to their needs rather than routinely. Use of fluoride toothpaste should follow current recommendations (that is, supervised toothbrushing and a pea-sized amount48) or dispensing toothpaste transversally to the long axis of the toothbrush.49 In addition, researchers have suggested that a low-fluoride-concentration toothpaste should be manufactured for use by young children.47,50 Such products are sold in other countries, but their introduction into the United States as a preventive agent will have to follow evidence in regard to efficacy, as determined by the U.S. Food and Drug Administration.

The CDC has made recommendations in regard to the appropriate use of fluorides in the United States,51 reinforcing the supervised and controlled use of fluoride toothpaste by young children. Since the late 1970s, infant formula manufacturers have reduced the concentration of fluoride in their products. However, it seems that infants living in fluoridated areas who ingest formula may be at higher risk of developing enamel fluorosis.36 This is an area that requires further research, followed by effective public health interventions, if needed.

The second implication is the need to determine whether current enamel fluorosis prevalence warrants a re-evaluation and possible reduction in the fluoride concentration in water, as has been suggested by some investigators.12 The argument in favor of this action centers on the premise that the fluoride concentration in water may be the most controllable of all fluoride modalities. Most overexposure to fluoride in the age groups at risk of developing fluorosis, however, comes from sources that were not intended to be used concomitantly with fluoridated water, such as dietary supplements, or from sources not designed to be ingested, such as fluoridated toothpaste.

If dental and medical practitioners prescribe supplements according to the recommended schedules, and toothpaste is used according to current recommendations, the prevalence and severity of enamel fluorosis should decrease in younger cohorts. Still, the way we measure fluoride exposure (by its effects at least six years after exposure) remains an inappropriate method for evaluating the impact of such intervention. To date, no data are available in the United States that are compelling enough to prompt a change in public policy in regard to recommended fluoride concentrations in the drinking water.


   CONCLUSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 STUDY LIMITATIONS
 PUBLIC HEALTH IMPLICATIONS
 CONCLUSION
REFERENCES
 
Within the limitations of the data, enamel fluorosis in 12- to 14-year-old schoolchildren who drank water from public water systems during the middle 1980s varied according to the level of fluoride in the drinking water. The prevalence of enamel fluorosis increased from the 1930s, as fluoride became more widely available and other vehicles were used concomitantly with water fluoridation. Evaluation of the public health impact of enamel fluorosis must be balanced against the benefits attributable to fluoride in general and to water fluoridation in particular. Future studies are needed to measure total fluoride exposure and enamel fluorosis prevalence in successive cohorts of the population before we can assess the impact of changes in fluoride use at the population level.



View larger version (93K):
[in this window]
[in a new window]
  		Dr. Beltrán-Aguilar is an epidemiologist, Surveillance, Investigations and Research Branch, Division of Oral Health, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta, Ga. 30341-3724, e-mail "edb4{at}CDC.gov". Address reprint requests to Dr. Beltrán-Aguilar.

 


View larger version (84K):
[in this window]
[in a new window]
  		Dr. Griffin is a health care economist, Surveillance, Investigations and Research Branch, Division of Oral Health, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta.

 


View larger version (76K):
[in this window]
[in a new window]
  		At the time of this study, Dr. Lockwood was a dental officer, Surveillance, Investigations and Research Branch, Division of Oral Health, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, Atlanta. He now is state dental director in Alabama.

 


   FOOTNOTES
 

Some of the results in this study were presented at the annual meeting of the International Association for Dental Research, Washington, April 2000.


More detailed data about enamel fluorosis prevalence and severity are available from Dr. Beltrán-Aguilar.


   REFERENCES
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 STUDY LIMITATIONS
 PUBLIC HEALTH IMPLICATIONS
 CONCLUSION
 REFERENCES
 

  1. Dean HT. The investigation of physiological effects by the epidemiological method. In: Moulton FR, ed. Fluorine and dental health. Washington: American Association for the Advancement of Science; 1942: 23–31.

  2. Dean HT. Endemic fluorosis and its relation to dental caries. Public Health Rep 1938;53:1443–52.

  3. Leverett D. Prevalence of dental fluorosis in fluoridated and non-fluoridated communities: a preliminary investigation. J Public Health Dent 1986;46:184–7.[Medline]

  4. Heifetz SB, Driscoll WS, Horowitz HS, Kingman A. Prevalence of dental caries and dental fluorosis in areas with optimal and above-optimal water-fluoride concentrations: a 5-year follow-up survey. JADA 1988;116:490–5.

  5. Szpunar SM, Burt BA. Dental caries, fluorosis, and fluoride exposure in Michigan schoolchildren. J Dent Res 1988;67:802–6.[Abstract/Free Full Text]

  6. Kumar JV, Green EL, Wallace W, Carnahan T. Trends in dental fluorosis and dental caries prevalences in Newburgh and Kingston, NY. Am J Public Health 1989;79:565–9.[Abstract/Free Full Text]

  7. U.S. Public Health Service. Review of fluoride benefits and risks. Report of the Ad Hoc Subcommitee on Fluoride of the Committee to Coordinate Environmental Health and Related Programs. Washington: U.S. Public Health Service; 1991:48–62.

  8. Selwitz RH, Nowjack-Raymer RE, Kingman A, Driscoll WS. Prevalence of dental caries and dental fluorosis in areas with optimal and above-optimal water fluoride concentrations: a 10-year follow-up survey. J Public Health Dent 1995;55(2):85–93.[Medline]

  9. Kumar JV, Swango PA, Lininger LL, Leske GS, Green EL, Haley VB. Changes in dental fluorosis and dental caries in Newburgh and Kingston, New York. Am J Public Health 1998;88:1866–70.[Abstract/Free Full Text]

  10. Rozier RG. The prevalence and severity of enamel fluorosis in North American children. J Public Health Dent 1999;59:239–46.[Medline]

  11. Brunelle JA. The prevalence of dental fluorosis in U.S. children, 1987 (abstract). J Dent Res 1989;68(special issue):995.

  12. Heller KE, Eklund SA, Burt BA. Dental caries and dental fluorosis at varying water fluoride concentrations. J Public Health Dent 1997;57:136–43.[Medline]

  13. U.S. Department of Health and Human Services. Oral health of United States children. The National Survey of Dental Caries in U.S. School Children: 1986–1987. Bethesda, Md.: U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health; 1989. NIH publication 89–2247.

  14. National Institute of Dental Research. Oral health of United States children. The National Survey of Oral Health in U.S. School Children: 1986–1987. Public use datafile documentation and survey methodology, 1992. Bethesda, Md.: Epidemiology and Oral Disease Prevention Program of the National Institute of Dental Research.

  15. U.S. Department of Health and Human Services. Fluoridation Census: 1985. Atlanta: Centers for Disease Control; 1988.

  16. Larsen MJ, Richards A, Fejerskov O. Development of dental fluorosis according to age at start of fluoride administration. Caries Res 1985;19:519–27.[Medline]

  17. Evans RW, Stamm JW. An epidemiologic estimate of the critical period during which human maxillary central incisors are most susceptible to fluorosis. J Public Health Dent 1991;51:251–9.[Medline]

  18. National Research Council. Health effects of ingested fluoride. Washington: National Academy Press; 1993.

  19. Centers for Disease Control and Prevention. Achievements in public health, 1900–1999: fluoridation of drinking water to prevent dental caries. MMWR Morb Mortal Wkly Rep 1999;48:933–40. Available at: "www.cdc.gov/mmwr/PDF/wk/mm4841.pdf". Accessed Jan. 4, 2002.

  20. Rozier RG. Epidemiologic indices for measuring the clinical manifestations of dental fluorosis: overview and critique. Adv Dent Res 1994;8(1):39–55.[Abstract]

  21. Horowitz HS, Driscoll WS, Meyers RJ, Heifetz SB, Kingman A. A new method for assessing the prevalence of dental fluorosis: the Tooth Surface Index of Fluorosis. JADA 1984;109:37–41.

  22. Thylstrup A, Fejerskov O. Clinical appearance of dental fluorosis in permanent teeth in relation to histologic changes. Community Dent Oral Epidemiol 1978;6:315–28.[Medline]

  23. Burt BA, Keels MA, Heller KE. The effects of a break in water fluoridation on the development of dental caries and fluorosis. J Dent Res 2000;79:761–9.[Abstract/Free Full Text]

  24. Den Besten PK. Dental fluorosis: its use as a biomarker. Adv Dent Res 1994;8(1):105–10.[Abstract]

  25. World Health Organization. Monitoring of renal fluoride excretion in community preventive programmes on oral health. Geneva: World Health Organization; 1999. Publication WHO/NCD/NCS/ORH/99.1.

  26. Collado J. Fluoruria en jóvenes de 16 a 22 años de San Ignacio de Acosta y Siquirres, Costa Rica. Fluoruración al Día 1991–1992;1(2): 18–21.

  27. Villa AE, Salazar G, Fernández O, Villa CV, Andrade M. Estudios de excreción urinaria de flúor en niños pre-escolares [Studies on urinary fluoride excretion in preschoolers]. Santiago, Chile: Departamento Odontológico, Ministerio de Salud de Chile; 1996.

  28. Villa AE, Salazar G, Anabalón M, Cabezas L. Estimation of the fraction of an ingested dose of fluoride excreted through urine in pre-school children. Commmunity Dent Oral Epidemiol 1999;27:305–12.

  29. Marthaler TM, Steiner M, Menghini G, De Crousaz P. Urinary fluoride excretion in children with low fluoride intake or consuming fluoridated salt. Caries Res 1995;29(1):26–34.[Medline]

  30. Warpeha RA, Marthaler TM. Urinary fluoride excretion in Jamaica in relation to fluoridated salt. Caries Res 1995;29(1):35–41.[Medline]

  31. Baez RJ, Baez MX, Marthaler TM. Urinary fluoride excretion by children 4–6 years old in a south Texas community. Rev Panam Salud Publica 2000;7:242–8.[Medline]

  32. Whitford GM, Sampaio FC, Arneberg P, von der Fehr FR. Fingernail fluoride: a method for monitoring fluoride exposure. Caries Res 1999;33:462–7.[Medline]

  33. Villena RS, Villena HM, Cury JA. Dental fluorosis and caries prevalence in Peruvian children residing at an altitude of 3700m: preliminary study (abstract). J Dent Res 2000;79(special issue):303.

  34. Feigal RJ. Recent modifications in the use of fluorides for children. Northwest Dent 1983;62(5):19–21.[Medline]

  35. Pendrys DG, Katz RV, Morse DE. Risk factors for enamel fluorosis in a fluoridated population. Am J Epidemiol 1994;140:461–71.[Abstract/Free Full Text]

  36. Pendrys DG, Katz RV. Risk factors for enamel fluorosis in optimally fluoridated children born after the US manufacturers’ decision to reduce the fluoride concentration of infant formula. Am J Epidemiol 1998;148:967–74.[Abstract/Free Full Text]

  37. Osuji OO, Leake JL, Chipman ML, Nikiforuk G, Locker D, Levine N. Risk factors for dental fluorosis in a fluoridated community. J Dent Res 1988;67:1488–92.[Abstract/Free Full Text]

  38. Pendrys DG, Katz RV. Risk of enamel fluorosis associated with fluoride supplementation, infant formula, and fluoride dentrifice use. Am J Epidemiol 1989;130:1199–208.[Abstract/Free Full Text]

  39. American Academy of Pediatrics, Committee on Nutrition. Fluoride supplementation: revised dosage schedule. Pediatrics 1979;63(1):150–2.[Abstract/Free Full Text]

  40. American Dental Association. Accepted dental therapeutics. 38th ed. Chicago: American Dental Association; 1979:321.

  41. Dosage schedule for dietary fluoride supplements. Proceedings of a workshop. Chicago, Illinois, USA. January 31–February 1, 1994. J Public Health Dent 1999;59:203–4.[Medline]

  42. Riordan PJ, Banks JA. Dental fluorosis and fluoride exposure in Western Australia. J Dent Res 1991;70:1022–8.[Abstract/Free Full Text]

  43. Mascarenhas AK, Burt BA. Fluorosis risk from early exposure to fluoride toothpaste. Community Dent Oral Epidemiol 1998;26:241–8.[Medline]

  44. Heifetz SB, Horowitz HS. Fluoride dentifrices. In: Newbrun E, ed. Fluorides and dental caries. 3rd ed. Springfield, Ill.: Thomas; 1986:50–70.

  45. Arnold FA, Likins RC, Russell AL, Scott DB. Fifteenth year of the Grand Rapids fluoridation study. JADA 1962;65:780–5.

  46. Tsutsui A, Yagi M, Horowitz AM. The prevalence of dental caries and fluorosis in Japanese communities with up to 1.4 ppm of naturally occurring fluoride. J Public Health Dent 2000;60(3):147–53.[Medline]

  47. Beltrán ED, Szpunar SA. Fluoride in toothpaste for children: suggestion for change. Pediatr Dent 1988;10(3):185–8.[Medline]

  48. United States Preventive Services Task Force. Guide to clinical preventive services. 2nd ed. Baltimore: Williams & Wilkins; 1996: 717–8.

  49. Villena RS. An investigation of the transverse technique of dentifrice application to reduce the amount of fluoride dentifrice for young children. Pediatr Dent 2000;22:312–7.[Medline]

  50. Horowitz HS. The need for toothpastes with lower than conventional fluoride concentrations for preschool-aged children. J Public Health Dent 1992;52:216–21.[Medline]

  51. Recommendations for using fluoride to prevent and control dental caries in the United States. Centers for Disease Control and Prevention. MMWR Morb Mortal Wkly Rep 2001;50(RR-14):1–42.[Medline]




This article has been cited by other articles:


Home page
 J Dent EducHome page
S. Narendran, J. T. Chan, S. D. Turner, and H. J. Keene
Fluoride knowledge and prescription practices among dentists.
J Dent Educ., September 1, 2006; 70(9): 956 - 964.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by BELTRÁN-AGUILAR, E. D.
Right arrow Articles by LOCKWOOD, S. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by BELTRÁN-AGUILAR, E. D.
Right arrow Articles by LOCKWOOD, S. A.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS