Food Labeling: Health Claims; Sugar Alcohols and Dental Caries

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DEPARTMENT OF HEALTH AND HUMAN SERVICES

Food and Drug Administration

21 CFR PART 101

[Docket No. 95P-0003]

Food Labeling: Health Claims; Sugar Alcohols and Dental Caries

AGENCY: Food and Drug Administration, HHS.

ACTION: Proposed rule.

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SUMMARY: The Food and Drug Administration (FDA) is proposing to

authorize the use, on food labels and in food labeling, of health

claims on the association between sugar alcohols and the nonpromotion

of dental caries. In addition, FDA is proposing to exempt sugar

alcohol-containing foods from certain provisions of the health claims

general requirements regulation. FDA is proposing these actions in

response to a petition filed by the National Association of Chewing Gum

Manufacturers, Inc., and an ad hoc working group of sugar alcohol

manufacturers (hereinafter referred to as the petitioners).

DATES: Written comments by October 3, 1995. The agency is proposing

that any final rule that may issue based upon this proposal become

effective 30 days following its publication.

ADDRESSES: Written comments to the Dockets Management Branch (HFA-305),

Food and Drug Administration, rm. 1-23, 12420 Parklawn Dr., Rockville,

MD 20857.

FOR FURTHER INFORMATION CONTACT: Joyce J. Saltsman, Center for Food

Safety and Applied Nutrition (HFS-165), Food and Drug Administration,

200 C St. SW., Washington, DC 20204, 202-205-5916.

SUPPLEMENTARY INFORMATION:

I. Background

A. The Nutrition Labeling and Education Act of 1990

On November 8, 1990, the President signed into law the Nutrition

Labeling and Education Act of 1990 (the 1990 amendments) (Pub. L. 101-

535). This new law amended the Federal Food, Drug, and Cosmetic Act

(the act) in a number of important ways. One of the most notable

aspects of the 1990 amendments was that they confirmed FDA's authority

to regulate health claims on food labels and in food labeling. As

amended by the 1990 amendments, section 403(r)(1)(B) of the act (21

U.S.C. 343(r)(1)(B)) provides that a product is misbranded if it bears

a claim that characterizes the relationship of a nutrient to a disease

or health-related condition, unless the claim is made in accordance

with the procedures and standards contained in regulations adopted by

FDA.

Under section 403(r)(3)(B)(i) of the act, the Secretary of Health

and Human Services (and, by delegation, FDA) shall promulgate

regulations authorizing such claims only if he or she determines, based

on the totality of publicly available scientific evidence (including

evidence from well-designed studies conducted in a manner which is

consistent with generally recognized scientific procedures and

principles), that there is significant scientific agreement, among

experts qualified by scientific training and experience to evaluate

such claims, that the claim is supported by such evidence.

Section 403(r)(3)(B)(ii) and (r)(3)(B)(iii) of the act describes

the information that must be included in any claim authorized under the

act. The act provides that the claim shall be an accurate

representation of the significance of the substance in affecting the

disease or health-related condition, and that it shall enable the

public to comprehend the information and understand its significance in

the context of the total daily diet. Finally, section 403(r)(4)(A)(i)

of the act provides that any person may petition FDA to issue a

regulation authorizing a health claim.

The 1990 amendments, in addition to amending the act, directed FDA

to consider 10 substance-disease relationships as possible subjects of

health claims.

B. FDA's Response

In the Federal Register of January 6, 1993 (58 FR 2478), FDA

adopted a final rule that implemented the health claim provisions of

the act. In that final rule, FDA adopted Sec. 101.14 (21 CFR 101.14).

The regulation sets out the circumstances in which a substance is

eligible to be the subject of a health claim (Sec. 101.14(b)), adopts

the standard in section 403(r)(3)(B)(i) of the act as the standard that

the agency will apply in deciding whether to authorize a claim about a

substance-disease relationship (Sec. 101.14(c)), sets forth general

rules on how authorized claims are to be made in food labeling

(Sec. 101.14(d)), and establishes limitations on the circumstances in

which claims can be made (Sec. 101.14(e)). The agency also adopted

Sec. 101.70 (21 CFR 101.70), which establishes a process for

petitioning the agency to authorize health claims about a substance-

disease relationship (Sec. 101.70(a)) and sets out the types of

information that any such petition must include (Sec. 101.70(d)). These

regulations became effective on May 8, 1993.

In addition, FDA conducted an extensive review of the evidence on

the 10 substance-disease relationships listed in the 1990 amendments.

FDA has authorized claims that relate to 8 of these 10 relationships.

The present rulemaking on sugar alcohols and dental caries

represents the first rulemaking that FDA has conducted in response to a

health claim petition.

C. History of Sugar Alcohol Labeling

In a set of findings of fact and a tentative order on label

statements for special dietary foods that the agency issued on July 19,

1977 (42 FR 37166), FDA addressed the issue of the use of the terms

``sugar free,'' ``sugarless,'' and ``no sugar.'' The agency stated that

consumers may associate the absence of sugar in a product with weight

control and with foods that are low calorie or that have been altered

to reduce calories significantly. At that time, FDA viewed foods

intended to be useful in maintaining or reducing calorie intake or body

weight as foods for special dietary use, that is, as foods intended for

supplying particular dietary needs that exist by reason of a physical,

physiological, pathological, or other condition.

Evidence had been introduced at a public hearing in the 1977

rulemaking to show that the ``sugarless'' claim is useful to identify

foods like chewing gum, which is in sustained contact with the teeth,

in which the use of a sweetener other than a fermentable or cariogenic

carbohydrate may not promote tooth decay. The secretary of the American

Dental Association's Council on Dental Therapeutics supported the

importance of advertising and labeling sugarless chewing gum and mints

as noncariogenic, in the sense that they did not contribute to the

development of dental caries (Ref. 80).

In the final rule on label statements for special dietary foods

published in the Federal Register of September 22, 1978 (43 FR 43248),

FDA required a statement that a food is not low calorie or calorie

reduced (unless it is in fact, a low or reduced calorie food) when a

``sugar free,'' ``sugarless,'' or ``no sugar'' claim is made for the

food. The agency decided to allow ``useful only in not promoting tooth

decay'' as an alternative statement to accompany such claims. The

agency stated that the statements that the food is not low calorie or

not useful for weight control, as well as ``useful only in not

promoting tooth decay,'' were needed because the

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term ``sugar free'' meant only that the food was sucrose free. A

``sugar free'' food could contain other fermentable carbohydrates.

Thus, the information about the effect of sugar alcohol-containing

foods on the risk of developing dental caries was originally placed on

the food label primarily to clarify that the product was not

necessarily useful in weight control, not to highlight the effect of

sugar alcohol on dental caries production.

In the Federal Register of November 27, 1991 (56 FR 60421), in

response to the 1990 amendments, FDA published a proposed rule entitled

``Food Labeling: Nutrient Content Claims, General Principles,

Petitions, Definition of Terms'' (the nutrition labeling general

principles proposal). In that document, FDA recognized that

developments in nutrition science had established that the focus of

nutrient content claims for providing dietary guidance had shifted from

special populations with particular conditions to the general

population (see 56 FR 60421). Therefore, in the nutrition labeling

general principles proposal, FDA proposed to treat several claims that

had been subject to regulation in Sec. 105.66 (21 CFR 105.66) as

special dietary use claims as nutrient content claims for the general

population. To eliminate redundancy in the regulations and to conform

Sec. 105.66 to the 1990 amendments, FDA proposed to define these claims

in part 101 (21 CFR part 101) and to remove them from part 105 (21 CFR

part 105). Specifically, FDA proposed to adopt definitions for terms

such as ``low calorie'' and ``reduced calorie,'' for other comparative

calorie claims, and for sugar claims under section 403(r)(2) of the act

and to codify them in Sec. 101.60. It also proposed to delete these

claims from Sec. 105.66.

In the Federal Register of January 6, 1993 (58 FR 2302), FDA

published its final rules on nutrient content claims. FDA adopted

definitions for claims for the calorie content of foods in Sec. 101.60

(58 FR 2302 at 2415). FDA defined claims regarding the sugars content

of a food, e.g., ``sugar free,'' ``free of sugar,'' ``no sugar,'' in

Sec. 101.60(c). In addition, FDA published a final rule that deleted

these claims from Sec. 105.66 (58 FR 2427).

However, based on its consideration of comments on the use of the

statement ``useful only in not promoting tooth decay'' to qualify the

``sugarless'' claim, FDA concluded that the statement was actually an

unauthorized health claim (58 FR 2302 at 2326). The claim is a health

claim because it characterizes the relationship of a substance (sugar

alcohols) to a disease (dental caries).

In the nutrient content claim general principles proposal (56 FR

60421 at 60437), the agency stated that it intended to reevaluate the

usefulness of chewing gums sweetened with sugar alcohols in not

promoting tooth decay. The agency stated that the data supporting the

claim were over 20 years old and requested that new data be submitted

in accordance with the final rule on health messages. In the nutrient

content claim final rule, FDA stated that it had received data on the

validity of a claim about this nutrient-disease relationship, and that

it would make a determination on whether to authorize a claim in

accordance with the final rule on health claims (58 FR 2302 at 2326).

On February 5, 1993, under the procedure established in section

701(e) of the act (21 U.S.C. 371(e)), a group of sugar alcohol

manufacturers submitted an objection to the revocation of

Sec. 105.66(f) (Ref. 2) and asked for a hearing on their objection. At

the same time, the group petitioned for reconsideration of the agency's

decision and for a stay of any administrative action by FDA pursuant to

the determination announced in the preamble of the nutrient content

claims rules that ``useful only in not promoting tooth decay'' is an

unauthorized health claim.

Filing objections to the revocation of Sec. 105.66(f) stayed the

effect of the final rule as a matter of law. FDA's response to these

objections and to the petitions is set forth elsewhere in this issue of

the Federal Register.

In the Federal Register of August 18, 1993 (58 FR 44036), FDA

published technical amendments to the health claim regulations in

response to comments that the agency received on the implementation

final rule that was published with the other final rules that responded

to the 1990 amendments in January of 1993 (see 58 FR 2066, August 18,

1993). One of the comments stated that if a petition were submitted for

the claim ``Useful Only in Not Promoting Tooth Decay,'' virtually none

of the sugar-free products on the market would be eligible to bear the

claim based on the requirements of a subsection of health claims

general principles regulation, Sec. 101.14(e)(6). FDA acknowledged that

certain food products of limited nutritional value that have been

specially formulated relative to a specific disease condition, such as

dental caries, may be determined to be appropriate foods to bear a

health claim (58 FR at 44036). The agency commented that it was its

intention to deal with such situations within the regulations

authorizing specific health claims. Therefore, FDA amended

Sec. 101.14(e)(6) to state that:

Except for dietary supplements or where provided for in other

regulations in part 101, subpart E, the food contains 10 percent or

more of the Reference Daily Intake or the Daily Reference Value for

vitamin A, vitamin C, iron, calcium, protein, or fiber per reference

amount customarily consumed prior to any nutrient addition.

II. Petition for the Noncariogenicity of Sugarless Food Products

Sweetened With Sugar Alcohol

A. Background

On August 31, 1994, the petitioners submitted a health claim

petition to FDA requesting that the agency authorize a health claim on

the relationship of sugar alcohols (i.e., xylitol, sorbitol, mannitol,

maltitol, lactitol, isomalt, hydrogenated starch hydrolysates, and

hydrogenated glucose syrups) in sugarless foods to dental caries (Ref.

1). On September 15, 1994, FDA sent the petitioners a letter stating

that study reports that are needed to support the petition, and that

are required for a health claim petition under Sec. 101.70, were not

included in the petitioners' submission. The agency stated that no

further action would be taken until that information was received (Ref.

3).

On September 27, 1994, the petitioners filed an amendment to their

petition submitting the required information. On October 7, 1994, the

agency sent the petitioners a letter acknowledging receipt of the

additional information and stating that the agency had begun its

scientific review of the petition (Ref. 4).

In this document, the agency will consider whether a health claim

on the relationship between sugar alcohols and dental caries is

justified under the standard in section 403(r)(3)(B)(i) of the act and

Sec. 101.14(c) of FDA's regulations. In addition, the agency will

consider the petitioners' request that the agency provide in any

regulation authorizing a claim that foods sweetened with sugar alcohols

be exempt from the requirement in Sec. 101.14(e)(6). The following is a

review of the health claim petition.

B. Preliminary Requirements

1. The Substances That Are the Subjects of the Petition

Sugar alcohols are a class of organic compounds that contain chains

of carbon atoms that bear two or more hydroxyl groups and have only

hydroxyl functional groups (Ref. 1). The hydroxyl groups replace ketone

or aldehyde groups that are found in sugars (Sec. 101.9(c)(6)(iii)).

The specific sugar alcohols that are the subject of this petition are

xylitol, sorbitol, mannitol,

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maltitol, maltitol syrup, maltitol solution, isomalt, lactitol, and

mixtures of sugar alcohol substances, i.e., hydrogenated glucose syrup

(HGS) and hydrogenated starch hydrolysate (HSH) products.

Xylitol is a monosaccharide polyhydric alcohol with a 5-carbon

backbone. It occurs naturally in fruits (e.g., plums, strawberries, and

raspberries) and vegetables (e.g., cauliflower and endive) (Refs. 82

and 83). Xylitol is made commercially by the hydrogenation of D-xylose.

Sorbitol is a monosaccharide polyhydric alcohol with a 6-carbon

backbone. It is found naturally in many types of berries and fruits and

in seaweeds and algae (Ref. 82). Sorbitol is made by hydrogenation of

glucose.

Mannitol is also a 6-carbon, monosaccharide polyhydric alcohol. It

occurs widely in nature in plants (e.g., pumpkins, mushrooms, onions,

beets, celery, and olives), algae, and fungi. Like sorbitol, mannitol

is made commercially by the hydrogenation of glucose.

Maltitol is a disaccharide alcohol (4-D-glucopyranosyl-D-sorbitol)

with a 12-carbon backbone. It is produced commercially by hydrogenation

of maltose.

Lactitol is also a disaccharide alcohol (-D-

galactopyranosyl D-sorbitol) with a 12-carbon backbone. It is produced

by hydrogenation of lactose (Ref. 84).

HSH and HGS are mixtures of sugar alcohols manufactured by

hydrogenation of corn starch or glucose syrups. The composition of the

sugar alcohols in the final product will depend on the manufacturing

process. Therefore, HSH and HGS products from different manufacturers

may contain different proportions of the same sugar alcohols. One HSH

product, under the trade name ``Lycasin,'' was first produced in Sweden

by hydrogenation of potato starch. The Swedish product contained a

mixture of sorbitol, maltitol, maltotrititol, and hydrogenated

dextrines of various molecular weights. When the manufacturing process

was moved to France in the 1970's, the production process was also

changed (Ref. 85). The French product, ``Lycasin 80/55,'' was made from

the hydrogenation of corn starch and contained 6 to 8 percent sorbitol,

50 to 55 percent hydrogenated disaccharides, 20 to 25 percent

trisaccharides, and 10 to 20 percent hydrogenated polysaccharides (Ref.

75). Lycasin 80/55, or HSH 80/55, is less fermentable and produces less

acid than the Swedish product (Ref. 85).

Isomalt, also known by the commercial name ``Palatinit,'' is an

equimolar mixture of the disaccharide alcohols of -D-

glucopyranosyl-D-sorbitol and -D-glucopyranosyl-D-mannitol.

It is produced by treating sucrose with enzymes, followed by

hydrogenation of the resulting mixture.

2. The Substances are Associated With a Disease for Which the U.S.

Population is at Risk

Dental caries is recognized in The Surgeon General's Report on

Nutrition and Health (Surgeon General's report) as a disease or health-

related condition for which the United States population is at risk

(Ref. 7). The overall prevalence of dental caries imposes a substantial

burden on Americans. Of the 13 leading health problems in the United

States, dental diseases rank second in direct costs (Ref. 7).

Based on this fact, FDA tentatively concludes that sugar alcohols

meet the requirement in Sec. 101.14(b)(1).

3. The Substances Are Food

Sugar alcohols are used as replacements for simple and complex

sugars as sweeteners and bulking agents in foods (Ref. 1). Thus sugar

alcohols are consumed for their taste and for their effect as a

stabilizer and thickener (21 CFR 170.3(o)(28)). Therefore, FDA

tentatively concludes that these substances satisfy the preliminary

requirements of Sec. 101.14(b)(3)(i).

4. The Substances Are Safe and Lawful

Several of the sugar alcohols that are the subject of this

proceeding are currently listed in FDA's food additive and generally

recognized as safe (GRAS) regulations, i.e., xylitol (21 CFR 172.395),

mannitol (Sec. 180.25 (21 CFR 180.25)), and sorbitol (Sec. 184.1835 (21

CFR 184.1835)). Moreover, GRAS affirmation petitions have been

submitted for each of the remaining substances, i.e., maltitol (GRASP

6G0319), maltitol syrups (HGS syrups) (GRASP 3G0286), isomalt (GRASP

6G0321), lactitol (GRASP 2G0391), HSH (GRASP 5G0304) and HSH syrups

(GRASP 1G0375).

The agency notes that these GRAS affirmation petitions are under

consideration and that any positive action resulting from this proposed

rule should not be interpreted as an indication that the agency has

affirmed those uses of the sugar alcohols as GRAS. Such determinations

can only be made after the agency has completed its review of the GRAS

petitions. A preliminary review of the GRAS affirmation petitions

reveals that they contain significant evidence supporting the safety of

these substances.

The agency also points out, however, that some concerns about the

safety of sugar alcohols do exist. For example, in a filing notice for

the affirmation of the GRAS status of lactitol (58 FR 47746, September

10, 1993), FDA stated that ``the agency's notice of filing of GRASP

2G0391 should not be interpreted either as a determination, preliminary

or otherwise, that the issue of Leydig cell tumors has been resolved or

that lactitol qualifies for GRAS affirmation.'' Also, by notice in the

Federal Register of December 13, 1994 (59 FR 64207), the agency

announced the filing of a food additive petition (FAP 4A4412) to amend

the interim food additive status of mannitol to permit an alternate

method of manufacture. In this notice, the agency pointed out concerns

about data from studies on mannitol that demonstrate a significant

incidence of benign thymomas, and an abnormal growth of thymus gland

tissue, in female rats fed mannitol. In addition, the safety of sugar

alcohols has been examined by the Federation of American Societies for

Experimental Biology (FASEB) (Ref. 90), as well as internationally by

the Joint Expert Committee on Food Additives (Ref. 91). The agency also

notes that two of the sugar alcohols that are listed in FDA's food

additive and GRAS regulations, i.e., mannitol (Sec. 180.25) and

sorbitol (Sec. 184.1835), require a warning label regarding laxation if

daily consumption of these sugar alcohols is expected to exceed 20

grams (g) per day for mannitol and 50 g per day for sorbitol. Nothing

in this proposal alters these requirements.

Based on the totality of the evidence, the agency is not

challenging, at this time, the petitioner's position that the use of

sugar alcohols is safe and lawful. Although FDA tentatively concludes

that the petitioner has satisfied the requirements of

Sec. 101.14(b)(3)(ii), the agency requests comments on its tentative

conclusion.

III. Review of Scientific Evidence

A. Introduction

The development of dental caries is the result of an interaction

between sugars (and other fermentable carbohydrates, such as refined

flour) and oral bacteria in a suitable environment (Ref. 71).

Microorganisms, and Streptococcus mutans (S. mutans) in particular, in

dental plaque metabolize available dietary sugars, producing acid and

sticky polysaccharides that adhere to the tooth as plaque. Acid

produced from rapid and complete fermentation of sugars creates an acid

environment within the

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plaque, characterized by a pH of usually less than 5.0, that is capable

of demineralizing tooth enamel and causing a carious lesion.

Studies designed to measure the cariogenicity of a food assess the

potential to cause caries if it is consumed in a standard way by a

highly susceptible subject (Ref. 8). The methods used to measure

cariogenic potential include long-term controlled human caries trials,

in vivo and in vitro plaque pH measurement, demineralization and

remineralization techniques, and rat caries models (Refs. 8 through

11). Because long-term clinical caries trials are difficult to conduct,

an integration of the plaque pH, animal caries, and demineralization

methodologies has been recommended as the best measure for establishing

the cariogenic potential of a food (Ref. 12). Experts recommend,

however, that these methods be used with appropriate controls, such as

sucrose, to assess experimental results (Ref. 13).

Plaque acidity studies are useful in providing evidence on the

effects of many microbial and physiological factors on the cariogenic

potential of foods (Ref. 78). An acidic plaque environment at the tooth

surface, specifically a pH of less than 5.5, suggests microbial

fermentation of a substrate resulting in microbial growth, plaque and

acid production, and promotion of carious lesions from enamel

decalcification. Factors that can modify these effects include the

presence of promoters or inhibitors in food products that affect

bacteria growth, the nature of the acids produced as a result of

bacterial metabolism of food carbohydrates (Ref. 78), intraplaque

buffering, and the pH of mixed saliva (Ref. 74).

B. Review of Scientific Evidence

1. Evidence Considered in Reaching the Decision

The petitioners submitted scientific evidence on the various sugar

alcohols and their effects on plaque, plaque pH, and dental caries.

This evidence included human (in vivo and epidemiological), animal, and

in vitro studies regarding the association between consumption of sugar

alcohols from chewing gum and other foods and plaque pH, acid

production, plaque quantity and quality, bacteria levels, and the

incidence of caries. The petition included four tables that summarized

the information for: (1) Human plaque and demineralization, (2)

bacteriological studies, (3) animal experiments, and (4) human

longitudinal and field studies. A fifth table provided a summary of

review articles.

In addition to the information submitted by the petitioner, the

agency considered other studies and reviews, such as the reports on

health aspects of sugar alcohols by the Life Sciences Research Office

(LSRO) and the FASEB (Refs. 14 through 16). The agency also considered

the results of additional human epidemiological studies on caries

incidence and demineralization; studies of animal caries; and in vitro

plaque pH studies.

2. Criteria for Selection of Human Studies

The criteria that the agency used to select pertinent studies were

that the studies: (1) Present data and adequate descriptions of study

design and methods; (2) be available in English; (3) provide daily

intakes of the sugar alcohol or enough information to estimate their

daily intakes; (4) include in vivo or in vitro assessment of the

changes in plaque pH or plaque acid production; (5) for intervention

studies on caries development, be of no less than 2 years (yr) in

duration; and (6) be conducted in persons who generally represent the

healthy United States' population (adults or children).

In selecting human studies for review, the agency decided that only

those studies investigating the use of sugar alcohols in chewing gums

and other foods, including mouth rinses that would be representative of

beverages, were appropriate for review. The agency excluded studies

that were published in abstract form because they lacked sufficient

detail on study design and methodologies, and because they lacked

necessary primary data. In selecting animal and in vitro studies for

review, the agency chose those studies that measured caries

development, plaque pH, or acid production from plaque bacteria.

3. Criteria for Evaluating the Relationship Between Sugar Alcohols and

Human Dental Caries

The subject of the petitioned health claim is the nonpromotion of

dental caries by sugar alcohol-containing foods, especially chewing gum

and confectioneries. To support this claim, there needs to be

significant scientific evidence to show that the sugar alcohol or sugar

alcohol mixture, e.g., HSH, makes no contribution to the progression of

dental carious lesions in humans. It would be difficult, if not

impossible, to design and execute a study that would directly address

this issue because such a study would require a control group that

consumed foods containing no sugars, fermentable carbohydrates, or

sugar alcohols.

In the absence of studies that directly evaluate the nonpromotion

of dental caries by sugar alcohol-containing foods, the agency gave the

greatest weight to those studies that evaluated in vivo the acidogenic

potential of plaque and plaque pH of sugar alcohols and sucrose in

representative food systems (e.g., confectioneries and solutions).

These in vivo measures can provide specific information about the

effect of sugar alcohols in the oral environment and, more

specifically, about the effect of sugar alcohols on pH at the interface

between dental plaque and tooth surfaces. The more acidic the

environment on the tooth surface, the greater the chance for enamel

demineralization and caries formation.

The agency also considered in vitro studies that measured plaque pH

and acid production of sugar alcohols in solution, and long-term caries

trials that evaluated caries development in a population using foods

containing sugar alcohols and sucrose. Studies investigating in situ

the demineralization or remineralization of enamel as a result of the

action of sugar alcohols on human dental plaque were considered as

supporting evidence by the agency.

C. Human Studies

1. Evaluation of Human Studies

FDA evaluated the results of studies against general criteria for

good experimental design, execution, and analysis. The criteria that

the agency used in evaluating these studies included appropriateness of

subject selection criteria; adequacy of the description of the

subject's oral health before intervention; extent of evaluation of

subject's type of dental plaque (i.e., sticky or nonsticky, thick or

thin); methods of plaque collection; adequacy of methods used to assess

study endpoints (e.g., in vivo versus in vitro assessment of plaque

pH); and other study design characteristics, including randomization of

subjects, appropriateness of controls, report of attrition rates

(including reasons for attrition), frequency of snack or substance

consumption, recognition and control of confounding factors (for

example, the subject's use of fluoride during the test period), and

appropriateness of statistical tests and comparisons. The agency also

considered it desirable if information on treatment and control diets,

the sugar alcohol content of the test substance, and daily sugar

alcohol and nutrient intakes was available.

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A review of the studies evaluating the effect of sugar alcohols on

plaque pH and acid production and of the in vitro microbiological

studies is provided in Table 1. Table 2 provides a review of

epidemiological studies evaluating the incidence of dental caries and

studies on demineralization and remineralization.

2. Summary of Evidence Relating Sugar Alcohol and Plaque pH or Acid

Production

Bibby and Fu (Ref. 38) measured human plaque pH in vitro using 0.1-

, 1.0-, or 10-percent solutions of the following sweeteners: Sucrose,

HSH, mannitol, isomalt, xylitol, isomaltulose, sorbose, saccharin, and

aspartame. Results showed the lowest plaque pH was attained with

sucrose (1- and 10- percent solution: pH less than 5.0). Plaque pH

decreased with increasing concentrations of isomalt, sorbitol,

mannitol, and HSH. The lowest pH attained for isomalt was about 5.6,

for sorbitol 5.82, for mannitol 5.22, and for HSH about 5.0. Negligible

acid production was measured from aspartame, saccharin, and xylitol.

Solution mixtures of xylitol (5 to 20 percent) and sucrose (10 percent)

were fermented to the same low pH as sucrose alone. Thus, the presence

of xylitol in a sucrose and xylitol mixture did not affect acid

production in plaque from sucrose.

The results of this study support the contention that xylitol does

not promote dental caries by lowering plaque pH below 5.5. However, the

results for sorbitol, mannitol, isomalt, and HSH do not support a

``nonpromotion'' claim. The results suggest that when higher

concentrations of these sweeteners are present in food, the plaque pH

may reach a level that will promote decalcification of dental enamel.

Birkhed and Edwardsson (Ref. 39) measured plaque pH and acid

production of human plaque samples in solutions of mannitol, xylitol,

maltitol, sorbitol, French HSH, Swedish HSH, fructose, and glucose

syrups. Results showed that plaque pH in the presence of xylitol,

maltitol, mannitol, and French HSH increased or slightly decreased from

baseline (pH remaining at 6.8 or above). Sorbitol showed a slight

decrease in plaque pH, but the final pH attained was about 6.0. The

other sweeteners, including Swedish HSH, depressed plaque pH below pH 6

over the 30-min (min) test period. The results of this study showed

that mannitol and xylitol produced no plaque acid compared to sucrose.

Maltitol and sorbitol produced plaque acid at rates that were 10 to 30

percent of that of sucrose. French HSH produced 20 to 40 percent and

Swedish HSH 50 to 70 percent of the acid produced by sucrose.

Birkhed et al. (Ref. 40) measured acid production in vitro and

plaque pH changes in vivo over a 30-min period following a 30-second(s)

mouth rinse with 10-percent glucose or sorbitol solutions. To determine

whether plaque microorganisms can adapt to the presence of sorbitol,

i.e., use it as a source of energy like sucrose, with repeated exposure

to the sugar alcohol, investigators measured plaque pH and acid

production at the end of a 6-week (wk) period. During the 6-wk period,

each subject rinsed their mouth six times per day for approximately 2

min at a time with a 10-percent sorbitol solution. At the end of 6 wk,

plaque pH was again measured for a 30-min period following a mouth

rinse with glucose and sorbitol. The study results showed acid

production in the presence of sorbitol, before adaptation, to be 11.3

percent of that from glucose. After the adaptation period, plaque acid

production from sorbitol increased to 30 percent of the glucose rate.

After the adaptation period to sorbitol, the glucose rinse produced

mean plaque pH values that were higher than before the adaptation

period. The differences in plaque pH, however, were only significant at

2 and 5 min following the rinse.

Overall results of this study suggest that sorbitol produces very

little plaque acid. Mean plaque pH values after sorbitol adaptation in

the presence of the 10-percent sorbitol rinse showed only a slight

decrease from the baseline value. The differences in mean plaque pH,

compared to baseline, at 5, 10, 20, and 30 min following the rinse were

significant. The authors noted that the fermentability of sorbitol was

more pronounced after the adaptation period than before.

Birkhed et al. (Ref. 41) studied the effects on in vivo plaque pH

and in vitro acid production from HSH (Swedish HSH), maltitol,

sorbitol, and xylitol. Subjects in each group sucked on two lozenges a

day, containing 0.5 g of one of the four sweeteners and 0.5 g of gum

arabic, four times daily between meals (total of eight lozenges per

day) for 3 months (mo). Changes in plaque pH over a 30-min period were

measured in each of the sugar alcohol groups after a 30-s mouth rinse

with a 50-percent solution containing the same sweetener as the

lozenge. The rinse was used 1 wk before and 1 wk after the lozenge

period. A control group consumed no lozenges but rinsed with each of

the four sweeteners. At least 1 wk separated each mouth rinse

experiment. Acid production activity (APA) from dental plaque suspended

in glucose and each of the four sugar alcohols was determined 1 wk

before and 1 wk after the 3-mo consumption period.

The results with HSH showed that although plaque pH values differed

before and after the lozenge period, differences were not statistically

significant, and that the lowest plaque pH attained was above 6.0. In

the maltitol group, plaque pH before the lozenge period was higher than

the pH following the lozenge period. Differences at 2, 10, and 30 min

were statistically significant. However, there were no significant

differences in plaque pH at any time compared to baseline. The lowest

plaque pH recorded was about 6.9. Plaque pH in the xylitol group

changed very slightly, remaining around pH 7. Plaque pH in the sorbitol

group was higher before than after the lozenge period. Differences in

pH at times 0 to 20 min and 0 to 30 min before compared with after the

test period were statistically significant (p6), then gradually decreased to a final pH

of 4.6 to 5.1 after 24 h.

The results of the demineralization test showed highly significant

differences (p) sorbitol > isomalt > xylitol > control. An in vitro

microbiological experiment was performed to test acid production

capacity of plaque microorganisms in 10 percent solutions of isomalt,

glucopyranosido mannitol (GPM), glucopyranosido sorbitol (GPS),

sorbitol, mannitol, sucrose, and fructose. GPS and GPM are the two

components that make up isomalt. Sucrose produced acid rapidly and had

the greatest acid formation. Sorbitol and mannitol produced acid

slowly, and isomalt and its two components had practically no acid

production in vitro.

Karle and Gehring (Ref. 63) evaluated the cariogenicity of isomalt

in rats. Six groups of rats received the basic diet without low

molecular weight carbohydrates in addition to xylitol, sorbose,

isomalt, lactose, and sucrose. The control group received only the

basic diet. Sweetener concentrations were increased slowly up to 30

percent by weight of the basic feed. The highest number of fissure

caries were caused by sucrose (about 33) followed by lactose (25),

isomalt (about 13), sorbose (about 12), xylitol (about 7) and the

control (5). Differences in caries incidence between the sucrose and

the other groups were significant.

Larje and Larson (Ref. 64) fed rats a caries diet, diet 2000, to

which various sweeteners were added. The caries diet, containing 56

percent sucrose, was used as a control ration. Sucrose substitutes used

in at least one of the experiments included glucose, fructose,

mannitol, sorbitol, potato starch, starch/sucrose mixtures, or HPS

(contains sorbitol and hydrogenated dextrins). In the first experiment

each group was fed diet 2000 for a few days, then they were changed to

one of the diets containing a sucrose substitute. Each test diet was

fed for 7 out of every 14 days followed by rotation back to the control

diet. The diets were changed every 2 or 3 days according to a

predetermined schedule. A second experiment was designed to determine

the effect of feeding the sucrose diet after the period of bacterial

implantation on diets containing sucrose substitutes. The animals

consumed one of the test diets the first week while being inoculated

with S. mutans, followed in the final 7 wk by the control diet

containing sucrose. A third experiment was designed to determine the

effect of feeding sucrose and sucrose-substitute diets intermittently

after the period of bacterial implantation on the sucrose diet. The

animals consumed diet 2000 the first wk, followed in the final 7 wk by

diets containing the sugar substitutes.

The results of the first experiment showed significantly (p in candy.

`The Roslagen study','' Acta Odontologica Scandinavica, 32:235-253,

1974.

32. Glass, R. L., ``A two year clinical trial of sorbitol gum,''

Caries Research, 17:365-368, 1983.

33. Ikeda, T., K. Ochiai, Y. Doi, T. Mukasa, and S. Yagi,

``Maltitol and SE58 in rats and decalcification as human intraoral

substrate, Nihon University Journal of Oral Science, 25:1-5, 1975.

34. Yagi, S., ``Effects of maltitol on insoluble glucan synthesis

by S. mutans and change of enamel hardness,'' Nihon University Journal

of Oral Science, 4:136-144, 1978.

35. Leach, S. A., G. T. R. Lee, and W. M. Edgar, ``Remineralization

of artificial caries-like lesions in human enamel in situ by chewing

sorbitol gum,'' Journal of Dental Research, 68:1064-1068, 1989.

36. Rundegren, J., T. Koulourides, and T. Ericson, ``Contribution

of maltitol and Lycasin to experimental enamel demineralized

in the human mouth,'' Caries Research, 14:67-74, 1980.

37. Creanor, S. L., R. Strang, W. H. Gilmour, R. H. Foye, J. Brown,

D. A. M. Geddes, and A. F. Hall, ``The effect of chewing gum use on in

situ enamel lesion remineralization,'' Journal of Dental Research,

71:1895-1900, 1992.

38. Bibby, B. G., and J. Fu, ``Changes in plaque pH in vitro by

sweeteners,'' Journal of Dental Research, 64:1130-1133, 1985.

39. Birkhed, D., and S. Edwardsson, ``Acid production from sucrose

substitutes in human dental plaque,'' Proceedings of ERGOB Conference,

pp. 211-217, 1978.

40. Birkhed, D., S. Edwardsson, B. Svensson, F. Moskovitz, and G.

Frostell, ``Acid production from sorbitol in human dental plaque,''

Archives of Oral Biology, 23:971-975, 1978.

41. Birkhed, D., S. Edwardsson, M. L. Ahlden, and G. Frostell,

``Effects of 3 mo frequent consumption of hydrogenated starch

hydrolysate (Lycasin), maltitol, sorbitol and xylitol on human dental

plaque,'' Acta Odontologica Scandinavica, 37:103-115, 1979.

42. Frostell, G., ``Dental plaque pH in relation to intake of

carbohydrate products,'' Acta Odontologica Scandanavia, 27:3-29, 1969.

43. Toors, F. A., and J. I. B. Herczog, ``Acid production from a

nonsugar licorice and different sugar substitutes in Streptococcus

mutans monoculture and pooled plaque-saliva mixtures,'' Caries

Research, 12:60-68, 1978.

44. Gallagher, I. H., and S. J. Fussell, ``Acidogenic fermentation

of pentose alcohols by human dental plaque microorganisms,'' Archives

of Oral Biology, 24:673-679, 1979.

45. Gehring, F., and H. D. Hufnagel, ``Intra- and extraoral pH

measurements on human dental plaque after rinsing with some sugar and

sucrose substitute solutions,'' Oralprophylaxe, 5:13-19, 1983.

46. Havenaar, R., J. H. J. Huis In't Veld, O. Backer Dirks, and J.

D. de Stoppelaar, ``Some bacteriological aspects of sugar

substitutes,'' Proceedings from ERGOB Conference, pp. 192-196, 1978.

47. Jensen, M. E., ``Human plaque acidogenicity studies with

hydrogenated starch hydrolysates,'' unpublished.

48. Maki, Y., K. Ohta, I. Takazoe, Y. Matsukubo, Y. Takaesu, V.

Topitsoglou, and G. Frostell, ``Acid production from isomaltulose,

sucrose, sorbitol, xylitol in suspensions of human dental plaque,''

Caries Research, 17:335-339, 1983.

49. Park, K. K., B. R. Schemehorn, J. W. Bolton, and G. K. Stookey,

``Comparative effect of sorbitol and xylitol mints on plaque

acidogenicity,'' presented at the International Association for Dental

Research, April 17-21, 1991.

50. Soderling, E., K. K. Makinen, C.-Y. Chen, H. R. Pape, and P.-L.

Makinen, ``Effect of sorbitol, xylitol and xylitol/sorbitol gums on

dental plaque,'' Caries Research, 23:378-384, 1989.

51. Birkhed, D., and G. Skude, ``Relation of amylase to starch and

Lycasin metabolism in human dental plaque in vitro,''

Scandinavian Journal of Dental Research, 86:248-258, 1978.

52. Havenaar, R., J. S. Drost, J. D. de Stoppelaar, J. H. J. Huis

in't Veld, and O. Backer Dirks, ``Potential cariogenicity of Lycasin

80/55 in comparison to starch, sucrose, xylitol, sorbitol and L-sorbose

in rats,'' Caries Research, 18:375-384, 1984.

53. Havenaar, R., J. S. Drost, J. H. J. Huis in't Veld, O. Backer

Dirks, and J. D. de Stoppelaar,, ``Potential cariogenicity of Lycasin

80/55 before and after repeated transmissions of the dental plaque

flora in rats,'' Archives of Oral Biology, 29:993-999, 1984.

54. Havenaar, R., J. H. J. Huis In't Veld, J. D. de Stoppelaar, and

O. Backer Dirks, ``A purified cariogenic diet for rats to test sugar

substitutes with special emphasis on general health,'' Caries Research,

17:340-352, 1983.

55. Havenaar, R., J. D. Huis in't Veld, J. D. J. de Stoppelaar, and

O. B. Dirks, ``Anti-cariogenic and remineralizing properties of xylitol

in combination with sucrose in rats inoculated with Streptococcus

mutans,'' Caries Research, 18:269-277, 1984.

56. Grenby, T. H., and J. Colley, ``Dental effects of xylitol

compared with other carbohydrates and polyols in the diet of laboratory

rats,'' Archives of Oral Biology, 28:745-758, 1983.

57. Karle, E. J., and F. Gehring, ``Kariogenitatsuntersuchungen von

zuckeraustauschstoffen an xerostomierlen ratten. (Studies on the

cariogenesis of sugar substitutes in xerostomized rats),'' Deutsche

Zahnarztliche Zeitschrift, 34:551-554, 1979.

58. Muhlemann, H. R., R. Schmid, T. Noguchi, T. Imfeld, and R. S.

Hirsch, ``Some dental effects of xylitol under laboratory and in vivo

conditions,'' Caries Research, 11:263-276, 1977.

59. Shyu, K.-W., and M.-Y Hsu, ``The cariogenicity of xylitol,

mannitol, sorbitol and sucrose,'' Proceedings of the National Science

Council ROC, 4:21-26, 1980.

60. Bramstedt, F., F. Gehring, and E. J. Karle, ``Comparative study

of the cariogenic effects of Palatinit, xylitol and

saccharose in animals,'' unpublished, 1976.

61. Izumiya, A., T. Ohshima, and S. Sofue, ``Caries inducibility of

various sweeteners,'' Academy of Pedodontia, p. 65, May 1984.

62. Gehring, F., and E. J. Karle, ``The sugar substitute

Palatinit with special emphasis on microbiological and

caries-preventing aspects,'' Zeitschrift Ernahrungswiss, 20:96-106,

1981.

[[Page 37529]]

63. Karle, E. J., and F. Gehring, ``Palatinit-A New Sugar

Substitute and its Carioprophylactic Assessment,'' Deutsche

Zalnarztliche Zeitschrift 33:189-191, 1978.

64. Larje, O., and R. H. Larson, ``Reduction of dental caries in

rats by intermittent feeding with sucrose substitutes, Archives of Oral

Biology, 15:805-816, 1970.

65. Muhlemann, H. R., ``Effect of topical application of sugar

substitutes on bacterial agglomerate formation, caries incidence and

solution rates of molars in the rat,'' unpublished, 1978.

66. Ooshima, T., A. Izumitani, T. Minami, T. Yoshida, S. Sobue, T.

Fujiwari, and S. Hamada, ``Non-cariogenicity of maltitol in SPF rats

infected with mutans streptococci,'' submitted for publication.

67. Tate, N., S. Wada, H. Tani, and K. Oikawa, ``Experimental

studies on correlations between progressive caries and sugar intake,''

unpublished.

68. Leach, S. A., and R. M. Green, ``Effect of xylitol-supplemented

diets on the progression and regression of fissure caries in the albino

rat,'' Caries Research, 14:16-23, 1980.

69. Mukasa, T., ``The possibility of maltitol and SE 58 as non-

cariogenic sweeteners: their utilization by Streptococcus mutans for

insoluble glucan synthesis and experimental dental caries in rats,''

Nihon University Journal of Oral Science, 3:266-275, 1977.

70. Hoeven, J. S. van der, ``Cariogenicity of disaccharide alcohols

in rats,'' Caries Research, 14:61-66, 1980.

71. Burt, B. A., and A. I. Ismail, ``Diet, nutrition, and food

cariogenicity,'' Journal of Dental Research, 65 (Special Issue): 1475-

1484, 1986.

72. National Research Council, National Academy of Sciences, ``Diet

and Health,'' National Academy Press, Washington, DC, 1989.

73. Hoeven, J.S. van der, ``Carigenicity of lactitol in program-fed

rats,'' Caries Research, 20:441-443, 1986.

74. Imfeld, T., and H. R. Muhlemann, ``Cariogenicity and

acidogenicity of food, confectionery and beverages,'' Pharmacology and

Therapeutic Dentistry, 3:53-68, 1978.

75. Imfeld, T., ``Identification of Low Caries Risk Dietary

Components,'' Monographs in Oral Science, vol. 11, Karger, Basel,

Switzerland, pp. 1-8 and 117-144, 1983.

76. Grenby, T. H., A. Phillips, and M. Mistry, ``Studies of the

dental properties of lactitol compared with five other bulk sweeteners

in vitro,'' Caries Research, 23:315-319, 1989.

77. Grenby, T. H., and A. Phillips, ``Dental and metabolic effects

of lactitol in the diet of laboratory rats,'' British Journal of

Nutrition, 61:17-24, 1989.

78. Edgar, W. M., and D. A. M. Geddes, ``Plaque acidity models for

cariogenicity testing--some theoretical and practical observations,''

Journal of Dental Research, 65 (Special Issue): 1498-1502, 1986.

79. Birkhed, D., S. Kalfas, G. Svensater, and S. Edwardsson,

``Microbiological aspects of some caloric sugar substitutes,''

International Dental Journal, 35:9-17, 1985.

80. Schrotenboer, G. H., ``In the Matter of Revising the Regulation

for Foods for Special Dietary Uses,'' Docket No. FDC-78, March 4, 1970

at 6-7.

81. Saltsman, Joyce J., CFSAN, FDA, Memorandum to file--

Environmental Assessment of Health Claim Petition, December 23, 1994.

82. Ayers, C. S., and R. A. Abrams, ``Noncariogenic sweeteners,

sugar substitutes for caries control,'' Dental Hygiene, April, 162-

167:1987.

83. Rugg-Gunn, A. J., and W. M. Edgar, ``Sweeteners and dental

health,'' Community Dental Health, 2:213-223, 1985.

84. Grenby, T. H., ``Nutritive sucrose substitutes and dental

health,'' In: Developments in Sweeteners, editors: T. H. Grenby, K. J.

Parker, and M. G. Lindley, Elsevier Science, Inc., 2:51-88, 1983.

85. Rugg-Gunn, A. J., ``Lycasin and the prevention of

dental caries,'' In: Progress in Sweeteners, editor: T. H. Grenby,

Elsevier Science, Inc., pp. 311-328, 1989.

86. Loesche, W. J., ``The rationale for caries prevention through

use of sugar substitutes,'' International Dental Journal, 35:1-8, 1985.

87. Mandel, I. D., ``Dental caries,'' American Scientist, 67:680-

688, 1979.

88. Koulourides, T., R. Bodden, S. Keller, L. Manson-Hing, J.

Lastra, and T. Housch, ``Cariogenicity of nine sugars tested with an

intraoral device in man,'' Caries Research 10:427-441, 1976.

89. Baer, A., ``Significance and promotion of sugar substitution

for the prevention of dental caries,'' Lben.-Wiss U. Technology,

Academic Press, 22:46-53, 1989.

90. LSRO, FASEB ``Health Aspect of Sugar Alcohols and Lactose,''

Bethesda, MD, December 1986.

91. Joint FAO/WHO Expert Committee on Food Additives, ``Evaluation

of Certain Food Additives and Contaminants,'' Geneva, Switzerland, pp.

16-17, 1993.

List of Subjects in 21 CFR Part 101

Food labeling, Nutrition, Reporting and recordkeeping requirements.

Therefore, under the Federal Food, Drug, and Cosmetic Act and under

authority delegated to the Commissioner of Food and Drugs, it is

proposed that 21 CFR part 101 be amended as follows:

PART 101--FOOD LABELING

1. The authority citation for 21 CFR part 101 is revised to read as

follows:

Authority: Secs. 4, 5, 6 of the Fair Packaging and Labeling Act

(15 U.S.C. 1453, 1454, 1455); secs. 201, 301, 402, 403, 409, 701 of

the Federal Food, Drug, and Cosmetic Act (21 U.S.C. 321, 331, 342,

343, 348, 371).

2. New Sec. 101.80 is added to subpart E to read as follows:

Sec. 101.80 Health claims: dietary sugar alcohols and dental caries.

(a) Relationship between dietary sugar alcohols and dental caries.

(1) Dental caries, or tooth decay, is a disease caused by many factors.

Both environmental and genetic factors can affect the development of

dental caries. Risk factors include tooth enamel crystal structure and

mineral content, plaque quantity and quality, saliva quantity and

quality, individual immune response, types and physical characteristics

of foods consumed, eating behaviors, presence of acid producing oral

bacteria, and cultural influences.

(2) The relationship between dietary sugars consumption and tooth

decay is well established. Sucrose is one of the most, but not the

only, cariogenic sugar in the diet. Bacteria found in the mouth are

able to metabolize sugars producing acid and forming dental plaque.

Prolonged exposure of the tooth enamel to acids from dental plaque

causes tooth enamel to demineralize, or decay. Frequent between-meal

consumption of sugary foods, particularly foods that easily stick to

the teeth, can cause tooth decay.

(3) U.S. diets tend to be high in sugars consumption. Although

there has been a decline in the prevalence of dental caries in the

United States, per capita consumption of sugars has not declined, and

the disease remains widespread throughout the population. Federal

government agencies and nationally recognized health professional

organizations recommend decreased consumption of sugars.

(4) Dietary sugar alcohols can be used to replace dietary sugars in

food. Sugar alcohols are significantly less cariogenic than dietary

sugars. Thus, replacing dietary sugars with sugar alcohols helps to

maintain dental health.

(b) Significance of the relationship between sugar alcohols and

dental caries. Sugar alcohols do not promote

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dental caries because they are slowly metabolized by bacteria to form

some acid. The rate and amount of acid production is significantly less

than that from sucrose and does not cause the loss of important

minerals from tooth enamel.

(c) Requirements. (1) All requirements set forth in Sec. 101.14

shall be met, except that sugar alcohol-containing foods are exempt

from section Sec. 101.14(e)(6).

(2) Specific requirements. (i) Nature of the claim. A health claim

relating sugar alcohols and the nonpromotion of dental caries may be

made on the label or labeling of a food described in (c)(2)(ii) of this

section, provided that:

(A) The claim shall state ``does not promote,'' ``useful in not

promoting,'' or ``expressly for not promoting'' dental caries.

(B) In specifying the disease, the claim uses the following terms:

``dental caries'' or ``tooth decay.''

(C) For packages with a total surface area available for labeling

of 15 or more square inches, the claim shall indicate that dental

caries depends on many factors.

(D) Packages with a total surface area available for labeling of

less than 15 square inches are exempt from paragraph (C) of this

section.

(E) The claim shall not attribute any degree of nonpromotion of

dental caries to the use of the sugar alcohol-containing food.

(ii) Nature of the food. (A) The food shall meet the requirement in

Sec. 101.60(c)(1)(i) with respect to sugars content.

(B) The sugar alcohol in the food shall be xylitol, sorbitol,

mannitol, maltitol, isomalt, lactitol, hydrogenated starch

hydrolysates, hydrogenated glucose syrups, or a combination of these.

(C) The sugar alcohol-containing food shall not lower plaque pH

below 5.7 by bacterial fermentation either during consumption or up to

30 minutes after consumption, as measured by in vivo tests.

(d) Optional information. (1) The claim may include information

from paragraphs (a) and (b) of this section, which describe the

relationship between diets containing sugar alcohols and dental caries.

(2) In referring to sucrose, the claim may use the term ``sucrose''

or ``sugar.''

(3) The claim may identify one or more of the following risk

factors for dental caries: Frequent consumption of sucrose or other

fermentable carbohydrates; presence of oral bacteria capable of

fermenting sugars; length of time sugars are in contact with the teeth;

lack of exposure to fluoride; individual susceptibility; socioeconomic

and cultural factors; and characteristics of tooth enamel, saliva, and

plaque.

(e) Model health claim. The following model health claims may be

used in food labeling to describe the relationship between sugar

alcohol and dental caries.

(1) For packages with total surface area available for labeling of

less than 15 square inches:

(i) Useful only in not promoting tooth decay;

(ii) Does not promote tooth decay; and

(iii) [This product] does not promote tooth decay.

(2) For packages with total surface area available for labeling of

15 or more square inches:

(i) Tooth decay is a disease caused by many factors including

frequent between meal consumption of sugary foods. [Name of sugar

alcohol] does not promote tooth decay.

(ii) [Reserved].

Dated: July 7, 1995.

William B. Schultz,

Deputy Commissioner for Policy.

Note: The following tables will not appear in the annual Code of

Federal Regulations.

BILLING CODE 4160-01-P

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[FR Doc. 95-17505 Filed 7-19-95; 8:45 am]

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