Document ID: EPA-HQ-OPPT-2016-0763-0001
Agency: epa
Document Type: Proposed Rule
Title: Fluoride Chemicals in Drinking Water: TSCA Section21 Petition; Reasons for Agency Response
Posted Date: 2017-02-27T05:00Z

[Federal Register Volume 82, Number 37 (Monday, February 27, 2017)]
[Proposed Rules]
[Pages 11878-11890]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2017-03829]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Chapter I

[EPA-HQ-OPPT-2016-0763; FRL-9959-74]

Fluoride Chemicals in Drinking Water; TSCA Section 21 Petition; 
Reasons for Agency Response

AGENCY: Environmental Protection Agency (EPA).

ACTION: Petition; reasons for Agency response.

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SUMMARY: This document announces the availability of EPA's response to 
a petition it received on November 23, 2016, under section 21 of the 
Toxic Substances Control Act (TSCA). The TSCA section 21 petition was 
received from the Fluoride Action Network, Food & Water Watch, Organic 
Consumers Association, the American Academy of Environmental Medicine, 
the International Academy of Oral Medicine and Toxicology, and other 
individual petitioners. The TSCA section 21 petition requested that EPA 
exercise its authority under TSCA section 6 to ``prohibit the 
purposeful addition of fluoridation chemicals to U.S. water supplies.'' 
After careful consideration,

[[Page 11879]]

EPA has denied the TSCA section 21 petition for the reasons discussed 
in this document.

DATES: EPA's response to this TSCA section 21 petition was signed 
February 17, 2017.

FOR FURTHER INFORMATION CONTACT: 
    For technical information contact: Darlene Leonard, National 
Program Chemicals Division (7404T), Office of Pollution Prevention and 
Toxics, Environmental Protection Agency, 1200 Pennsylvania Ave. NW., 
Washington, DC 20460-0001; telephone number: (202) 566-0516; fax 
number: (202) 566-0470; email address: leonard.darlene@epa.gov.
    For general information contact: The TSCA-Hotline, ABVI-Goodwill, 
422 South Clinton Ave., Rochester, NY 14620; telephone number: (202) 
554-1404; email address: TSCA-Hotline@epa.gov.

SUPPLEMENTARY INFORMATION: 

I. General Information

A. Does this action apply to me?

    This action is directed to the public in general. This action may, 
however, be of interest to individuals or organizations interested in 
drinking water and drinking water additives, including fluoride. Since 
other entities may also be interested, the Agency has not attempted to 
describe all the specific entities that may be affected by this action.

B. How can I access information about this petition?

    The docket for this TSCA section 21 petition, identified by docket 
identification (ID) number EPA-HQ-OPPT-2016-0763, is available online 
at http://www.regulations.gov or in person at the Office of Pollution 
Prevention and Toxics Docket (OPPT Docket), Environmental Protection 
Agency Docket Center (EPA/DC), EPA West Bldg., Rm. 3334, 1301 
Constitution Ave. NW., Washington, DC. Six binders containing copies of 
references were submitted along with the petition (Ref. 1). Those 
binders are not available electronically in the docket but may be 
reviewed in the Public Reading Room. The Public Reading Room is open 
from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal 
holidays. The telephone number for the Public Reading Room is (202) 
566-1744, and the telephone number for the OPPT Docket is (202) 566-
0280. Please review the visitor instructions and additional information 
about the docket available at http://www.epa.gov/dockets.

II. TSCA Section 21

A. What is a TSCA section 21 petition?

    Under TSCA section 21 (15 U.S.C. 2620), any person can petition EPA 
to initiate a rulemaking proceeding for the issuance, amendment, or 
repeal of a rule under TSCA sections 4, 6, or 8 or an order under TSCA 
sections 4, 5(e), or 5(f). A TSCA section 21 petition must set forth 
the facts that are claimed to establish the necessity for the action 
requested. EPA is required to grant or deny the petition within 90 days 
of its filing. If EPA grants the petition, the Agency must promptly 
commence an appropriate proceeding that is ``in accordance'' with the 
underlying TSCA authority. If EPA denies the petition, the Agency must 
publish its reasons for the denial in the Federal Register. 15 U.S.C. 
2620(b)(3). A petitioner may commence a civil action in a U.S. district 
court to compel initiation of the requested rulemaking proceeding 
within 60 days of either a denial or the expiration of the 90-day 
period. 15 U.S.C. 2620(b)(4).

B. What criteria apply to a decision on a TSCA section 21 petition?

    TSCA section 21(b)(1) requires that the petition ``set forth the 
facts which it is claimed establish that it is necessary'' to issue the 
rule or order requested. 15 U.S.C. 2620(b)(1). Thus, TSCA section 21 
implicitly incorporates the statutory standards that apply to the 
requested action. In addition, TSCA section 21 establishes standards a 
court must use to decide whether to order EPA to initiate rulemaking in 
the event of a lawsuit filed by the petitioner after denial of a TSCA 
section 21 petition. 15 U.S.C. 2620(b)(4)(B). Accordingly, EPA has 
relied on the standards in TSCA section 21 (and those in the provisions 
under which action has been requested) to evaluate this TSCA section 21 
petition.

III. TSCA Section 6

    Of particular relevance to this TSCA section 21 petition are the 
legal standards regarding TSCA section 6(a) rules. These standards were 
significantly altered in 2016 by the ``Frank R. Lautenberg Chemical 
Safety for the 21st Century Act,'' Public Law 114-182 (2016), which 
amended TSCA. One of the key features of the new law is the requirement 
that EPA now systematically prioritize and assess existing chemicals, 
and manage identified risks. Through a combination of new authorities, 
a risk-based safety standard, mandatory deadlines for action, and 
minimum throughput requirements, TSCA effectively creates a 
``pipeline'' by which EPA will conduct review and management of 
existing chemicals. This new pipeline--from prioritization to risk 
evaluation to risk management (when warranted)--is intended to drive 
forward steady progress on the backlog of existing chemical substances 
left largely unaddressed by the original law. (Ref. 2).
    In the initial phase of the review pipeline, EPA is to screen a 
chemical substance for its priority status, propose a designation as 
either high or low priority, and then issue a final priority 
designation within one year of starting the screening process. 15 
U.S.C. 2605(b)(1)(C). If the substance is high priority, EPA must 
initiate a risk evaluation for that substance. 15 U.S.C. 2605(b)(4)(C). 
EPA must define the scope of the risk evaluation within six months of 
starting, 15 U.S.C. 2605(b)(4)(D), and complete the risk evaluation 
within 3 to 3.5 years. 15 U.S.C. 2605(b)(4)(G). If EPA concludes that a 
chemical substance presents an unreasonable risk, EPA must propose a 
risk management rule under TSCA section 6(a) within one year and 
finalize that rule after another year, with limited provision for 
extension. 15 U.S.C. 2605(c). As EPA completes risk evaluations, EPA is 
to designate replacement high-priority substances, on a continuing 
basis. 15 U.S.C. 2605(b)(2)(C) and (b)(3)(C).
    In general, to promulgate a rule under TSCA section 6(a), EPA must 
first determine ``in accordance with section 6(b)(4)(A) that the 
manufacture, processing, distribution in commerce, use, or disposal of 
a chemical substance or mixture . . . presents an unreasonable risk.'' 
15 U.S.C. 2605(a). TSCA section (b)(4)(A) is part of the risk 
evaluation process whereby EPA must determine ``whether a chemical 
substance presents an unreasonable risk of injury to health or the 
environment,'' and thus, whether a rule under TSCA section 6(a) is 
necessary. 15 U.S.C. 2605(b)(4)(A). In particular, EPA must conduct 
this evaluation ``without consideration of costs or other non-risk 
factors, including an unreasonable risk to a potentially exposed or 
susceptible subpopulation identified as relevant to the risk evaluation 
by the Administrator, under the conditions of use.'' Id. Unless EPA 
establishes an exemption under TSCA section 6(g) (whereby certain 
unreasonable risks may be allowed to persist for a limited period) or 
EPA is addressing a persistent, bioaccumulative, and toxic substance as 
set forth in TSCA section 6(h), the standard for an adequate rule under 
TSCA section 6(a) is that it regulates ``so that the chemical

[[Page 11880]]

substance or mixture no longer presents'' unreasonable risks under the 
conditions of use. 15 U.S.C. 2605(a).
    Prior to the 2016 amendment of TSCA, EPA completed risk assessments 
that were limited to selected uses of chemical substances. The amended 
TSCA authorizes EPA to issue TSCA section 6 rules that are not 
comprehensive of the conditions of use, so long as they are consistent 
with the scope of such pre-amendment risk assessments. 15 U.S.C. 
2625(l)(4). But EPA has interpreted the amended TSCA as requiring that 
forthcoming risk evaluations encompass all manufacture, processing, 
distribution in commerce, use, and disposal activities that the 
Administrator determines are intended, known or reasonably foreseen. 
(Ref. 2, p. 7565). EPA interprets the scope of post-risk-evaluation 
rulemaking under TSCA section 6(a) in a parallel fashion: While risk 
management rules for a certain subset of the conditions of use may be 
promulgated ahead of rulemaking for the remaining conditions of use, 
rules covering the complete set of conditions of use must be 
promulgated by the deadlines specified in TSCA section 6(c). 15 U.S.C. 
2605(c). While EPA has authority under TSCA section 6(a) to establish 
requirements that apply only to ``a particular use,'' the restriction 
of just one particular use would not constitute an adequate risk 
management rule unless that particular use were the only reason that 
the chemical substance presented an unreasonable risk.
    TSCA section 21(b)(4)(B) provides the standard for judicial review 
should EPA deny a request for rulemaking under TSCA section 6(a): ``If 
the petitioner demonstrates to the satisfaction of the court by a 
preponderance of the evidence that . . . the chemical substance or 
mixture to be subject to such rule . . . presents an unreasonable risk 
of injury to health or the environment, without consideration of costs 
or other non-risk factors, including an unreasonable risk to a 
potentially exposed or susceptible subpopulation, under the conditions 
of use,'' the court shall order the EPA Administrator to initiate the 
requested action. 15 U.S.C. 2620(b)(4)(B). EPA notes that bills 
preceding the final amendment to TSCA retained language in section 21 
that resembled the pre-amendment criteria for rulemaking under section 
6. Compare 15 U.S.C. 2620(b)(4)(B)(ii) (2015) (amended 2016), 15 U.S.C. 
2605(a) (2015) (amended 2016), S. Rep. 114-67 at 135 (Ref. 3), and H.R. 
Rep. No. 114-176 at 81 (Ref. 4). But the effect of the revision in the 
final bill is to align the standard for judicial review of a TSCA 
section 21 petition with the standard for EPA's preparation of risk 
evaluation under TSCA section 6(b)(4)(A). Consistent with these 
revisions, EPA concludes that Congress intended for a petition to set 
forth facts that would enable EPA to complete a risk evaluation under 
TSCA section 6(b).
    In light of this, EPA interprets TSCA section 21 as requiring the 
petition to present a scientific basis for action that is reasonably 
comparable, in its quality and scope, to a risk evaluation under TSCA 
section 6(b). This requirement includes addressing the full set of 
conditions of use for a chemical substance and thereby describing an 
adequate rule under TSCA section 6(a)--one that would reduce the risks 
of the chemical substance ``so that the chemical substance or mixture 
no longer presents'' unreasonable risks under all conditions of use. 15 
U.S.C. 2605(a). Specifically, EPA interprets section 21(a)--which 
authorizes petitions ``to initiate a proceeding for the issuance . . . 
of a rule under . . . section 6''--as authorizing petitions for rules 
that would comply with the requirements of sections 6(a) and 6(c).
    EPA recognizes that information on a single condition of use could, 
in certain instances, suffice to demonstrate that a chemical substance, 
as a whole, presents an unreasonable risk. Nonetheless, EPA concludes 
that such information does not fulfill a petitioner's burden to justify 
``a rule under [TSCA section 6],'' under TSCA section 21, since the 
information would merely justify a subset of an adequate rule. To issue 
an adequate rule under section 6, EPA would need to conduct a catch-up 
risk evaluation addressing all the conditions of use not addressed by 
the petition, and either determine that those conditions do not 
contribute to the unreasonable risk or enlarge the scope of the rule to 
address those further conditions of use. See 15 U.S.C. 2605(a). To 
issue this rule within the time required by section 6(c), EPA would 
have to proceed without the benefit of the combined 4 to 4.5-year 
period that TSCA section 6(b) would ordinarily afford EPA (i.e., time 
to prioritize a chemical substance, conduct a careful review of all of 
its conditions of use, and receive the benefit of concurrent public 
comment). Additionally, before even initiating the prioritization 
process for a chemical substance, EPA would generally screen the 
chemical substance to determine whether the available hazard and 
exposure-related information are sufficient to allow EPA to complete 
both the prioritization and the risk evaluation processes. (Ref. 5).
    EPA's interpretation is most consonant with the review pipeline 
established in TSCA section 6. In particular, the prioritization 
process established in section 6(b) recognizes that a number of 
chemical substances may present an unreasonable risk of injury to 
health or the environment and charges EPA with prioritizing those that 
should be addressed first. EPA is required to have 10 chemical 
substances undergoing risk evaluation as of December 19, 2016, and must 
have a steady state of at least 20 high-priority substances undergoing 
risk evaluation by December 2019 (and as many as 10 substances 
nominated for risk evaluation by manufacturers). 15 U.S.C. 
2605(b)(2)(A), (B), 2605(b)(4)(E)(i). EPA is obligated to complete 
rulemakings to address any unreasonable risks identified in these risk 
evaluations within prescribed timeframes. 15 U.S.C. 2605(c)(1). These 
required activities will place considerable demands on EPA resources. 
Indeed, Congress carefully tailored the mandatory throughput 
requirements of TSCA section 6, based on its recognition of the 
limitations of EPA's capacity and resources, notwithstanding the 
sizeable number of chemical substances that will ultimately require 
review. Under this scheme, EPA does not believe that Congress intended 
to empower petitioners to promote chemicals of particular concern to 
them above other chemicals that may well present greater overall risk, 
and force completion of expedited risk evaluations and rulemakings on 
those chemicals, based on risks arising from individual uses.
    EPA recognizes that some members of the public may have safety 
concerns that are limited to a single condition of use for a chemical 
substance. But EPA's interpretation of TSCA section 21 does not deprive 
such persons of a meaningful opportunity to request that the 
Administrator proceed on their concerns. For example, such persons may 
submit a petition under the Administrative Procedure Act, requesting 
EPA to commence a ``risk-based screening'' of the chemical substance 
under TSCA section 6(b)(1)(A), motivated by their concern about a 
single condition of use.

IV. Summary of the TSCA Section 21 Petition

A. What action was requested?

    On November 23, 2016, a TSCA section 21 petition was submitted by 
the Fluoride Action Network, Food & Water Watch, Organic Consumers 
Association, the American Academy of Environmental Medicine, the

[[Page 11881]]

International Academy of Oral Medicine and Toxicology, Moms Against 
Fluoridation, and the following individuals signing on behalf of 
themselves and their children: Audrey Adams of Renton, Washington, 
Jacqueline Denton of Asheville, North Carolina, Valerie Green of Silver 
Spring, Maryland, Kristin Lavelle of Berkeley, California, and Brenda 
Staudenmaier of Green Bay, Wisconsin (Ref. 1). The general object of 
the petition is to urge EPA ``to protect the public and susceptible 
subpopulations from the neurotoxic risks of fluoride by banning the 
addition of fluoridation chemicals to water'' (Ref. 1). The specific 
action sought is a rule, under TSCA section 6(a)(2), to ``prohibit the 
purposeful addition of fluoridation chemicals to U.S. water supplies.'' 
However, such a restriction on the allowable use of fluoridation 
chemicals would actually be based on a rule under TSCA section 6(a)(5), 
not a rule under TSCA section 6(a)(2). In light of the discrepancy 
between the description of the rule sought and the cited authority, EPA 
interprets the petition as requesting both a TSCA section 6(a)(5) rule 
whereby the purposeful addition of any fluoridation chemical to a 
drinking water supply would be prohibited and a TSCA section 6(a)(2) 
rule whereby the manufacture, processing, or distribution in commerce 
of any fluoridation chemical for such use would be prohibited.

B. What support does the petition offer?

    The petition is focused on the potential for fluoride to have 
neurotoxic effects on humans; it cites numerous studies bearing on this 
issue. The petition contends that the purposeful fluoridation of 
drinking water presents an unreasonable risk to human health from 
neurotoxicity, and that a ban on this use of fluoridation chemicals is 
necessary to curtail this unreasonable risk. The following is a summary 
of the primary support given in the petition for this view:
    1. Fluoride neurotoxicity at levels relevant to U.S. population. 
The petition claims that fluoride poses neurotoxic risks to the U.S. 
population. The petition claims that the cited studies of fluoride-
exposed human populations have consistently found neurotoxic effects 
(lower-than-average IQs) at water fluoride levels below the current 
Maximum Contaminant Level Goal of 4 mg/L set by EPA's Office of Water. 
The petition argues that the difference between the fluoride levels in 
the United States and the greater levels in rural China (where most of 
the cited IQ studies were conducted) is ``lessen[ed]'' by the abundance 
of fluoridated toothpaste in the U.S.
    2. Recent epidemiological studies corroborate neurotoxic risk in 
Western populations. The petition cites two studies from Western 
populations to attempt to corroborate the assertion that exposure to 
fluoride in drinking water presents unreasonable risks for 
neurotoxicity (Refs. 6 and 7).
    3. Neurotoxic risks supported by animal and cell studies. The 
petition argues that studies on both experimental animals and cell 
cultures are consistent with cited human research linking fluoride 
exposure with neurotoxic effects in humans.
    4. Susceptible subpopulations are at heightened risk. The petition 
argues that certain subpopulations (e.g., infants, the elderly, and 
persons with nutritional deficiencies, kidney disease or certain 
genetic predispositions) are more susceptible to fluoride 
neurotoxicity.
    5. RfD/RfC derivation and uncertainty factor application. The 
petition argues that EPA's 1998 Guidelines for Neurotoxicity Risk 
Assessment support the need to apply a 10-fold uncertainty factor in 
deriving an oral Reference Dose (RfD) or inhalation Reference 
Concentration (RfC).
    6. Benefits to public health. The petition bases, in part, its 
claim of unreasonable risk on the assertion that the fluoridation of 
drinking water confers little benefit to public health, relative to the 
alleged neurotoxic risks. The petition argues that since fluoride's 
primary benefit comes from topical contact with the teeth, there is 
little benefit from swallowing fluoride, in water or any other product. 
The petition argues that there is therefore ``little justification'' in 
exposing the public to ``any risk'' of fluoride neurotoxicity.
    7. Extent and magnitude of risk from fluoridation chemicals. The 
petition bases, in part, its claim of unreasonable risk on estimates of 
the extent and magnitude of risk posed to portions of the U.S. 
population living in areas where artificial fluoridation occurs.
    8. Consequences of eliminating use of fluoridation chemicals. The 
petition argues that the risks of fluoride exposure from fluoridated 
drinking water are unreasonable, in part, because they could be easily 
and cheaply eliminated, and because alternative products containing 
topical fluoride are widely available.
    9. Link to elevated blood lead levels. The petition argues that 
artificial fluoridation chemicals are linked with pipe corrosion and 
elevated blood lead levels. The petition interprets data in several 
studies as demonstrating an association between fluoridation chemicals 
and elevated blood lead levels.
    In addition to supplying the petition, on January 30, 2017, the 
petitioners also delivered an in-person oral presentation of their 
views (Ref. 8). At their oral presentation, petitioners reiterated the 
information already supplied in writing, and requested that EPA also 
consider an additional study that was not part of the petition (Ref. 
9). EPA has discretion (but not an obligation) to consider extra-
petition materials when evaluating a petition submitted under TSCA 
section 21. In cases where the petitioners themselves attempt to 
enlarge the scope of materials under review while EPA's petition review 
is pending, EPA exercises its discretion to consider or not consider 
the additional material based on whether the material was submitted 
early enough in EPA's petition review process to allow adequate 
evaluation of the study prior to the petition deadline, the relation of 
the late materials to materials already submitted. Given the 
particularly late submittal of the additional study, EPA conducted an 
abbreviated review of the study and found that the health concerns 
covered were substantially the same as those covered in other studies 
submitted with the petition. Based on this abbreviated review, EPA does 
not believe that the new study provided any new scientific grounds for 
granting the petition.

V. Disposition of TSCA Section 21 Petition

A. What was EPA's response?

    After careful consideration, EPA denied the TSCA section 21 
petition, primarily because EPA concluded that the petition has not set 
forth a scientifically defensible basis to conclude that any persons 
have suffered neurotoxic harm as a result of exposure to fluoride in 
the U.S. through the purposeful addition of fluoridation chemicals to 
drinking water or otherwise from fluoride exposure in the U.S. In 
judging the sufficiency of the petition, EPA considered whether the 
petition set forth facts that would enable EPA to complete a risk 
evaluation under TSCA section 6(b).
    EPA also denied the petition on the independent grounds that the 
petition neither justified the regulation of fluoridation chemicals as 
a category, nor identified an adequate section 6 rule as the action 
sought. Rather than comprehensively addressing the conditions of use 
that apply to a particular chemical substance, the petition requests 
EPA to take action on a single condition of use (water

[[Page 11882]]

fluoridation) that cuts across a category of chemical substances 
(fluoridation chemicals). A copy of the Agency's response, which 
consists of a letter to the petitioners, is available in the docket for 
this TSCA section 21 petition.

B. What were EPA's reasons for this response?

    To take the actions under TSCA section 6 requested by the 
petitioners, EPA would need to make a determination of whether a 
chemical substance or substances present an unreasonable risk to human 
health or the environment. This section describes why the petitioners 
have not provided adequate and sufficient scientific information to 
make such a determination.
    1. Fluoride neurotoxicity at levels relevant to U.S. population. 
The petition ignores a number of basic data quality issues associated 
with the human studies it relies upon. Many of the human studies cited 
in the petition are cross-sectional in design, and are affected by 
antecedent-consequent bias. The antecedent-consequent bias means it 
cannot be determined whether the exposure came before or after the 
health effects, since both are evaluated at the same time. Cross-
sectional studies are most useful for developing hypotheses about 
possible causal relationships between an exposure and a health effect, 
but are rarely suitable for the development of a dose-response 
relationship for risk assessment. These studies are most useful in 
supporting more robust epidemiological studies in which defined 
exposures can be linked quantitatively to an adverse outcome.
    The petition also does not properly account for the relatively poor 
quality of the exposure and effects data in the cited human studies 
(e.g., it appears to give all studies equivalent weight, regardless of 
their quality). When an association is suggested between an exposure 
and a disease outcome, the studies need to be assessed to determine 
whether the effect is truly because of exposure or if alternate 
explanations are possible. The way to do that is to adjust for 
potential confounders, such as diet, behavior, and socioeconomic 
status, in order to appropriately assess the real relationship between 
the exposures to a specific substance and health effects. In other 
words, when these confounding factors are potentially present, but not 
recognized or controlled for, it is not possible to attribute effects 
to the contaminant of concern (fluoride) as opposed to other factors or 
exposures. The evidence presented did not enable EPA to determine 
whether various confounding factors (e.g., nutritional deficiencies) 
were indeed placing particular subpopulations at a ``heightened risk of 
fluoride neurotoxicity,'' as alleged, because the evidence did not 
adequately account for the possibility that the confounding factors 
themselves, rather than concurrent fluoride exposure, were partly or 
wholly responsible for the health effects observed. Specific 
confounding factors or variables were noted by the National Research 
Council (NRC) (Ref. 10). They may include climate, drinking water 
intake, excessive dietary fluoride, low calcium intake, drinking water 
sources with fluctuating fluoride levels, and industrial pollution such 
as use of coal for domestic heating. These factors have the potential 
to confound efforts to identify a causal relationship between drinking 
water fluoride exposure and particular health effects, either by 
introducing additional, unaccounted for sources of fluoride exposure, 
by being associated with the pertinent health endpoint through some 
mechanism other than fluoride toxicity, or by directly affecting the 
health endpoint.
    The petition relies heavily on two meta-analyses which include 
human cross-sectional (Ref. 11) and case control (Ref. 19) studies. All 
of the studies listed in Table 1 of the petition were examined in 
detail by the 2012 Choi et al. study (Ref. 11) as part of their 
systematic review and meta-analysis to investigate the possibility that 
fluoride exposure delays neurodevelopment in children. The Choi et al. 
analysis analyzes studies in which IQ was measured using various IQ 
tests, compares children of various fluoride exposure ranges without 
accounting for differences in susceptibility to fluoride by age, and 
used different exposure measures which only delineated between high and 
low exposure groups. A variety of measures of fluoride exposure were 
present across studies included in the Choi et al. study, including 
levels of fluoride in drinking water, observed dental fluorosis, coal 
burning in houses (i.e., air fluoride levels), and urine fluoride. 
Despite this disparate collection of types of measurements, all 
exposure measures were treated equally in the analysis (Ref. 11, Table 
1). The authors of the analysis identified a variety of data quality 
issues associated with this collection of studies. For example, they 
recognized that several of the populations studied had fluoride 
exposures from sources other than drinking water (e.g., coal burning; 
Refs. 13-15); they therefore controlled for this confounding factor by 
excluding such studies from their analysis. Co-exposures to other 
potentially neurotoxic chemicals (e.g., iodine) (Refs. 16-18) and 
arsenic (Refs. 19-22) were also recognized and accounted for in the 
Choi et al. analysis to understand confounding by these factors. Yet 
the petitioners include such studies in making their assertion that 
fluoride is neurotoxic, but have not indicated any attempts to control 
for the confounding factors. Choi et al. also noted that basic 
information such as the study subjects' sex and parental education was 
missing in 80 percent of the studies and household income was missing 
in 93 percent of studies; they stated that they could not therefore 
control for these co-variables in their analysis. Consideration of 
these confounding factors and their impact on the applicability of 
these studies in a risk assessment context is evident in the authors' 
discussion. The authors caution readers that ``our review cannot be 
used to derive an exposure limit, because the actual exposures of the 
individual children are not known'' and they are measured in their 
conclusions (i.e., ``our results support the possibility of adverse 
effects of fluoride exposures on children's neurodevelopment'') (Ref. 
11). The authors indicate that ``further research should formally 
evaluate dose-response relationships based on individual-level measures 
of exposure over time, including more precise prenatal exposure 
assessment and more extensive standardized measures of neurobehavioral 
performance, in addition to improving assessment and control of 
potential confounders'' (Ref. 11). EPA agrees with the conclusions by 
Choi et al. (Ref. 11) that the studies included in Table 1 of the 
petition are unsuitable for evaluating levels of fluoride associated 
with neurotoxic effects and for deriving dose-response relationships 
necessary for risk assessment.
    The petition also cites an article by Grandjean and Landrigan (Ref. 
23), for the proposition that fluoride is ``known'' to cause 
developmental neurotoxicity in humans. Grandjean and Landrigan refer 
only to the study of Choi et al. (2012), of which Grandjean is a co-
author, in discussing fluoride. EPA's observations about the 
limitations of Choi et al. (2012) thus apply with equal force to the 
cited statement from Grandjean and Landrigan. Grandjean and Landrigan 
summarize that Choi et al. (2012) ``suggests an average IQ decrement of 
about seven points in children exposed to raised fluoride 
concentrations.'' (Ref. 23). But Grandjean and Landrigan do not opine 
on whether fluoride exposures, arising from the purposeful addition of 
fluoridation chemicals to

[[Page 11883]]

U.S. water supplies, are in fact causing developmental neurotoxic 
effects to persons in the U.S. The petition itself concedes that the 
actual existence of such effects is unestablished, in urging EPA to 
conduct ``a diligent risk assessment, per EPA's Guidelines, to ensure 
that the general public, and sensitive subpopulations, are not 
ingesting neurotoxic levels'' (Ref 1, p. 3).
    The other meta-analysis cited in the petition (Ref. 12) showed 
that, based on 16 case-control studies in China, children living in an 
area with endemic fluorosis are more likely to have low IQ compared to 
children living in an area with slight fluorosis or no fluorosis. While 
this analysis may suggest an association between fluorosis and lowered 
IQ (both of which are possible effects of fluoride exposure at certain 
levels) any fluoride concentration-to-IQ effect relationship (i.e., 
dose-response relationship) is only inferred because actual fluoride 
exposures were not measured. Further, the two effects (fluorosis and 
lower IQ) both occur at fluoride exposures well above those found in 
fluoridated U.S. drinking water, such that any inference would only 
apply at fluoride concentrations not relevant to exposures in the U.S. 
The studies in the Tang et al. review (Ref. 12) correlate one effect 
(fluorosis) to another effect (neurotoxicity), but do not establish a 
dose-response relationship between fluoride exposure and neurotoxicity. 
This lack of a dose-dependent increase in effect with increasing 
exposure is a critical limitation of these data. Establishing a dose-
response relationship between exposure to a toxicant and an effect ``is 
the most fundamental and pervasive concept in toxicology. Indeed, an 
understanding of this relationship is essential for the study of toxic 
materials'' (Ref. 12). Likewise, the IQ changes noted in Table 1 (Ref. 
1) do not increase with increasing water fluoride concentration (e.g., 
dose) (Ref. 1).
    The petition suggested that a dose-response relationship between 
urinary fluoride and IQ is seen in several studies (Refs. 24-26) shown 
in Figures 1-5 of the petition (Ref. 1). Assuming, as the petitioners 
claim, that all children were malnourished in the Das and Mondal (Ref. 
26) study, it is not possible to determine whether effects on IQ were 
due to fluoride or to malnutrition (i.e., nutritional status may be an 
uncontrolled confounding factor). The study authors caution that ``it 
is difficult to determine with any degree of accuracy whether the 
difference of children's IQ scores solely depends on the exposure dose 
because many social and natural factors like economic condition, 
culture and geological environments are also responsible'' (Ref. 26). 
Hence, extrapolating relationships from this study population to other 
populations is not scientifically defensible.
    Choi et al. (2015) (Ref. 27) report that moderate and severe dental 
fluorosis was significantly associated with lower cognitive functions. 
However, associations between drinking water and urine fluoride and the 
same cognitive functions were not found to be significantly associated. 
They reached this conclusion from a study of 51 children in China and a 
comparison group of eight with dental fluorosis (Table 4 in Choi et 
al., 2015). The authors discuss potential problems associated with 
using these biomarkers of exposure to fluoride. For example, water 
samples may be imprecise because internal dose of fluoride depends on 
total water intake, and urine samples may be affected by the amount of 
water the subject drank prior to sampling. With regard to fluorosis, 
the degree of dental fluorosis is dependent not only on the total 
fluoride dose but also on the timing and duration of fluoride exposure. 
A person's individual response to fluoride exposure depends on factors 
such as body weight, activity level, nutritional factors, and the rate 
of skeletal growth and remodeling. These variables, along with inter-
individual variability in response to similar doses of fluoride, 
indicate that enamel fluorosis cannot be used as a biological marker of 
the level of fluoride exposure for an individual (Ref. 28). Hence, the 
petitioner's use of fluorosis levels as a surrogate for evidence of 
neurotoxic harm to the U.S. population is inappropriate evidence to 
support an assertion of unreasonable risk to humans from fluoridation 
of drinking water.
    The petition also cites four studies (Refs. 24, 29-31) that rely on 
human urine or serum fluoride concentrations as biomarkers of exposure 
but does not discuss the limitations associated with the biomarkers 
used in the studies. In their report, Human Biomonitoring for 
Environmental Chemicals, NRC defines properties of biomarkers and 
created a framework for grouping biomarkers of exposure (Ref. 32). 
Figure 3-1 in the NRC report illustrates the relationship between 
external dose (e.g., water), internal dose (e.g., fluoride 
concentration) and biological effects, and indicates that internal dose 
is measured through biomonitoring (e.g., fluoride concentrations 
measured in urine or serum). NRC grouped the quality of biomarkers 
based on the robustness of these relationships. NRC designated 
biomarkers for substances that have been observed in bodily fluids, but 
that lack established relationships between external dose (e.g., 
water), internal dose (e.g., urine or serum) and biological effects 
(e.g., neurotoxicity) as ``Group I'' biomarkers. Although many human 
studies have been collated and reviewed in the petition, for the 
reasons outlined previously--particularly study design and confounding 
factors--relationships between urine and serum fluoride (internal 
doses), water fluoride concentration (external dose), and neurotoxic 
effects in humans have not been established. Further, serum and urine 
biomarkers for fluoride reflect only recent exposures, not long-term 
exposures, and may be different from the exposures during the specific 
time when developmental effects can occur. A lack of established 
sampling protocols and analytical methods are also hallmarks of ``Group 
I'' biomarkers. The main studies cited in the petition which attempt to 
relate urine or serum levels to possible neurotoxic effects suffer from 
either lack of good sampling protocols or absence of documenting the 
sampling protocols. Important issues such as the timing and methods of 
sample collection were also often not reported in the studies. Using 
the NRC Framework, urine and serum fluoride levels would be at best 
``Group I'' biomarkers for fluoride-related neurotoxicity. The NRC 
Framework states ``[b]iomarkers in this category may be considered 
useless'' for risk assessment purposes (Ref. 32, p. 78).
    2. Recent epidemiological studies corroborate neurotoxic risk in 
Western populations. The petition cites two studies from Western 
populations to attempt to corroborate the assertion that exposure to 
fluoridated water presents unreasonable risks for neurotoxicity. Two 
population-level studies were cited which link fluoridated water to 
attention-deficit/hyperactivity disorder (ADHD) prevalence in the U.S. 
(Ref. 6) and drinking water exposures and hypothyroidism prevalence in 
England (Ref. 7). These studies use cross-sectional population-level 
data to examine the association between ADHD and hypothyroidism and 
fluoridated water levels. The studies make reasonable use the 
population-level data available, but causal inference cannot be made 
from these studies (Ref. 3).
    As stated in the conclusion of Malin and Till, an association has 
been reported, but ``[p]opulation studies designed to examine possible 
mechanisms, patterns and levels of exposure, covariates and moderators 
of

[[Page 11884]]

this relationship are warranted'' (Ref. 6, p. 8). In epidemiology, 
studies using cross-sectional data are most often used to generate 
hypotheses that need to be further studied to determine whether a 
``true'' association is present. Ideally, the study designs and methods 
are improved by each study that is undertaken, such as, among other 
things, identifying additional potential confounders, considering 
timing issues or resolving ambiguity in collection of samples and 
disease outcome, improving upon the exposure analysis, and evaluating 
the magnitude and consistency of the results, so that the evaluation 
can adequately assess the association (Ref. 34). For example, the 
authors assert that there are design issues with their study, 
especially related to the exposure categories, and they suggest how to 
address these issues in future studies. Although it is possible that 
there may be biological plausibility for the hypothesis that water 
fluoridation may be associated with ADHD, this single epidemiological 
study is not sufficient to ``corroborate'' neurotoxic health effects, 
as stated in the petition. More study would be needed to develop a body 
of information adequate to make a scientifically defensible 
unreasonable risk determination under TSCA.
    The Peckham et al. study (Ref. 7) suffers from similar issues noted 
in Malin and Till (Ref. 6). Adjustment for some confounders was 
considered, including sex and age, but other potential confounders 
(such as iodine intake) were not assessed. Fluoride from other sources 
and other factors associated with hypothyroidism were not assessed in 
this study. Exposure misclassification, in which populations are placed 
in the wrong exposure categories based on the water fluoridation 
status, is very possible in either of the studies presented and is a 
limitation of the study designs.
    3. Neurotoxic risks supported by animal and cell studies. The 
National Toxicology Program (NTP) conducted a systematic review of 
animal and cell studies on the effects of fluoride on learning and 
memory available up to January 2016 (Ref. 35). Almost all (159 out of 
171) of the animal and cell culture studies cited in the petition in 
Appendix D-E were included in the NTP systematic review. From among 
4,656 studies identified in the NTP database search, 4,552 were 
excluded during title and abstract screening, 104 were reviewed at the 
full-text level and 68 studies were considered relevant and were 
included in the analysis. NTP assessed each study for bias, meaning a 
systematic error in the study that can over or underestimate the true 
effect and further excluded any studies with a high risk of bias. Of 
the 68 studies, including studies provided by the Fluoride Action 
Network, 19 were considered to pose a very serious overall risk of 
bias, primarily based on concern for at least three of the following 
factors: Lack of randomization, lack of blinding at outcome assessment 
in conjunction with not using automated tools to collect information, 
lack of reporting on what was administered to animals (source, purity, 
chemical form of fluoride), lack of control for litter effects, lack of 
expected response in control animals, and lack of reporting of key 
study information such as the number or sex of animals treated. Of the 
studies cited in Table 4 in the petition, two were excluded from the 
NTP analysis because of serious concerns for study bias (Refs. 36 and 
37). Based on its review of animal and cell studies, NTP concluded that 
``[t]he evidence is strongest (moderate level-of-evidence) in animals 
exposed as adults tested in the Morris water maze and weaker (low 
level-of-evidence) in animals exposed during development'' and ``[v]ery 
few studies assessed learning and memory effects at exposure levels 
near 0.7 parts per million, the recommended level for community water 
fluoridation in the United States.'' The animal studies cited in the 
petition (Ref. 1, p. 14, Table 4) reflect these high drinking water 
exposures ranging from 2.3 mg/L to 13.6 mg/L, equivalent to 3-20 times 
the levels to which drinking water is fluoridated in the U.S. Overall, 
NTP concluded that, ``[r]esults show low-to-moderate level-of-evidence 
in developmental and adult exposure studies for a pattern of findings 
suggestive of an effect on learning and memory'' (Ref. 35, p. 52). 
Based on this review of available evidence, and the identified 
limitations in the database, NTP is currently pursuing experimental 
studies in rats to address key data gaps, starting with pilot studies 
that address limitations of the current literature with respect to 
study design (e.g., randomization, blinding, control for litter 
effects), and assessment of motor and sensory function to assess the 
degree to which impairment of movement may impact performance in 
learning and memory tests. If justified, follow-up studies would 
address potential developmental effects using lower dose levels more 
applicable to human intakes.
    Two studies included in Table 4 (Ref. 1) were not included in the 
NTP review, but do not show neurotoxicity effects at doses relevant to 
U.S. populations. One study aimed to establish vitamin A as a marker 
for fluoride neurotoxicity (Ref. 38), but changes in vitamin A were 
measured only at an excessive fluoride dose of 20 mg/L. The other study 
dosed rats with fluoride in drinking water (Ref. 39) and showed effects 
on behavior and brain neurotransmitters at a dose of 5 mg/L, a level 
well above the 0.7 parts per million level recommended for community 
water fluoridation in the United States. Other studies in Table 4, 
which, according to the title of the table, are indicative of ``Water 
Fluoride Levels Associated with Neurotoxic Effects in Rodents,'' 
erroneously report effect levels not supported by the studies 
themselves. In Wu et al. (Ref. 36), which NTP excluded based on high 
bias, no adverse effects were seen at a dose of 1 mg/kg-day as claimed 
in the petition. In fact, the behavioral effects occurred only at doses 
of 5 and 25 mg/L. In Chouhan et al. (Ref. 40), which NTP excluded in 
the initial screen for relevancy, no significant neurotoxicity was seen 
at 1 mg/L fluoride, in contrast to what the petition claims. In 
addition, the petition's statement that ``rats require 5 times more 
fluoride in their water to achieve the same level of fluoride in their 
blood as humans'' (Ref. 1) as a rationale for why higher exposure 
levels in animals are relevant to lower levels in humans is not 
supported by the NTP review in the petition. The NTP review indicates 
that ``assuming approximate equivalence [of drinking water 
concentrations in rodents and humans] is not unreasonable'' (Ref. 35, 
p. 58). These several erroneously reported studies do not change EPA's 
agreement with the conclusions of the NTP report that their ``[r]esults 
show low-to-moderate level-of-evidence in developmental and adult 
exposure studies for a pattern of findings suggestive of an effect on 
learning and memory'' (Ref. 35, p. 52).
    In cell studies cited in the petition, two studies demonstrated 
effects following exposure of artificial brain cells to fluoride at 
concentrations in the range purported to be in the bloodstream of 
humans. However, relevance of cell assays to humans is limited because 
the concentrations of fluoride experienced by cells by themselves in 
culture are not directly comparable to an animal or human exposure due 
to lack of metabolism, interactions between cells, and the ability to 
measure chronic (long-term) effects (Ref. 41). Extrapolation from 
concentrations in cell cultures to human exposures is not 
straightforward. Pharmacokinetic modeling is necessary to convert the 
concentrations to a

[[Page 11885]]

human equivalent dose relevant to risk assessment (Ref. 42), but the 
petition did not address whether data are available or lacking to 
complete such an analysis.
    4. Susceptible subpopulations are at heightened risk. The data and 
information provided in the petition do not support the claims that 
``nutritional status, age, genetics and disease are known to influence 
an individual's susceptibility to chronic fluoride toxicity.'' The only 
reference the petition presents that specifically addresses the claim 
that nutrient deficiencies (i.e., deficiencies in iodine and calcium) 
can ``amplify fluoride's neurotoxicity'' is the study by Das and Mondal 
(Ref. 26). However, the study did not measure any nutrients in their 
test subjects. Rather, they measured Body Mass Index (BMI), 
acknowledging that ``BMI is the most commonly used measure for 
monitoring the prevalence of overweight and obesity at population 
level'' and ``it is only a proxy measure of the underlying problem of 
excess body fat or underweight cases.'' Not only is the BMI an indirect 
proxy for the iodine and calcium deficiencies supposed in the petition, 
the BMI results presented in this study are themselves equivocal, as 
they show that BMIs ranged from underweight to overweight to obesity 
depending on the sex and age of the study subjects. Furthermore, the 
petition concedes that the Das and Mondal study data are only 
``suggestive'' of an area with chronic malnutrition. A few human 
studies cited provide only suggestive evidence that low levels of 
iodine may increase the effects of high levels of fluoride in children, 
but these studies suffer from study design and confounding issues 
already described previously. Other cited studies describe the effects 
of iodine or calcium on rats or rat brain cells in addition to 
irrelevantly high fluoride levels. The petition also claims that a 
certain ``COMT gene polymorphism greatly influences the extent of IQ 
loss resulting from fluoride exposure,'' citing a study by Zhang et al. 
(Ref. 29) as support. The COMT gene encodes for the enzyme, catechol-O-
methyltransferase, which is responsible for control of dopamine levels 
in the brain. Zhang et al. concludes that, ``[t]he present study has 
several limitations. First, the cross-sectional observational design 
does not allow us to determine temporal or causal associations between 
fluoride and cognition. Second, the study has a relatively small sample 
size, which limits the power to assess effects of gene-environmental 
interactions on children's IQ'' (Ref. 29). Zhang et al. continues 
``[d]espite the study limitations, this is the first gene-environment 
study investigating the potential impact of COMT single-nucleotide 
polymorphism (SNP) on the relationship between children's cognitive 
performance and exposure to elemental fluoride'' (Ref. 29). Several 
studies are cited in the petition to support the assertion that 
infants, the elderly and individuals with deficient nutritional intake 
and kidney disease are more susceptible to fluoride neurotoxicity. 
However, the level of supporting evidence from these studies (i.e., to 
specify the potentially greater susceptibility of any particular 
subpopulation) is insufficient to overcome the petition's broader 
failure to set forth sufficient facts to establish that fluoridation 
chemicals present an unreasonable risk to the general population, to 
allow EPA to reach a risk evaluation.
    5. RfD/RfC derivation and uncertainty factor application. An oral 
Reference Dose or inhalation Reference Concentration is a daily 
exposure to the human population, including sensitive subgroups, that 
is likely to be without an appreciable risk of deleterious effects 
during a lifetime (Ref. 43). The petition cites EPA's 1998 guidance 
document, Guidelines for Neurotoxicity Risk Assessment (Ref. 44), 
purporting that it demonstrates the necessity of applying an 
uncertainty factor of at least 10. It appears that the petition has 
selected the eight studies presented in Table 5 (Ref. 1, p. 19) as 
candidates for deriving a Reference Dose (RfD) or Reference 
Concentration (RfC). The petition asserts that these dose or 
concentration values are relevant oral reference values for neurotoxic 
effects. However, the petition fails to recognize that the question of 
applying an uncertainty factor does not even arise until one has first 
appropriately performed a hazard characterization for all health 
endpoints of concern (Ref. 30, Section 3.1). As outlined in EPA's 
document, A Review of the Reference Dose and Reference Concentration 
Processes (Ref. 43), the first step in deriving an RfD or RfC is to 
evaluate the available database. The petition does not set forth the 
strengths and limitations of each of the studies in the overall 
database of available studies nor any criteria or rationale for 
selecting the eight particular studies from which to derive an RfD or 
RfC. Without setting forth the strengths and limitations associated 
with each study and the weight of evidence provided by the available 
database, a necessary step in any assessment, it is not possible to 
determine whether uncertainty factors are necessary.
    Following hazard characterization and identification of suitable 
studies for an RfD or RfC, uncertainty factors are generally applied to 
a lower limit dose or concentration on the continuum of observed 
effects (dose-response curve) in an individual study (e.g., NOAEL, 
LOAEL, Benchmark Dose, etc.). The selection of uncertainty factors and 
their magnitude should be based on the quality of the data, extent of 
the database and sound scientific judgment and consider the impact of 
having adverse effects from an inadequate exposure as well as an excess 
exposure. Uncertainty factor values may be considered appropriate to 
account for uncertainties associated with extrapolating from (1) a dose 
producing effects in animals to a dose producing no effects, (2) 
subchronic to chronic exposure in animals, (3) animal toxicological 
data to humans (interspecies), (4) sensitivities among the members of 
the human population (intraspecies), and (5) deficiencies in the 
database for duration or key effects (Ref. 43). Conflicting statements 
in the petition indicate that there is both a robust and certain dose-
response relationship between fluoride exposure and IQ including for 
sensitive subpopulations. However, the petition does not clearly 
identify which sources/types of uncertainty in the data exist, nor 
which of the aforementioned uncertainty factors should be applied based 
on the review of the selected studies.
    6. Benefits to public health. The petition asserts that the 
fluoridation of drinking water confers little benefit to public health, 
claiming that the primary benefit of fluoride comes from topical 
fluoride contact with the teeth and that there is thus little benefit 
from ingesting fluoride in water or any other product. The petition 
claims there are no randomized controlled trials on the effectiveness 
of fluoridation, and that few studies adequately account for potential 
confounding factors. In addition, the petition states that modern 
studies of fluoridation and tooth decay have found small, inconsistent 
and often non-existent differences in cavity rates between fluoridated 
and non-fluoridated areas. Further, the petition questions the cost-
effectiveness of fluoridation relative to costs associated with what 
have been asserted to be fluoridation-related drops in IQ. The petition 
argues, then, that there is ``little justification'' in exposing the 
public to ``any risk'' of fluoride neurotoxicity (Ref. 1).

[[Page 11886]]

    EPA does not believe that the petition has presented a well-founded 
basis to doubt the health benefits of fluoridating drinking water. The 
petition's argument about fluoridation benefits (i.e., that the risks 
of neurotoxic health effects from fluoridation are unreasonable in part 
because they outweigh the expected health benefits arising from 
exposure to fluoride) depends on first setting forth sufficient facts 
to establish the purported neurotoxic risks, to which the 
countervailing health benefits from fluoridation could be compared. But 
as noted earlier, EPA and other authoritative bodies have previously 
reviewed many of the studies cited as evidence of neurotoxic effects of 
fluoride in humans and found significant limitations in using them to 
draw conclusions on whether neurotoxicity is associated with 
fluoridation of drinking water. Irrespective of the conclusions one 
draws about the health benefits of drinking water fluoridation, the 
petition did not set forth sufficient facts to justify its primary 
claims about purported neurotoxic effect from drinking fluoridated 
water.
    The petition cites several studies as evidence that water 
fluoridation does not have any demonstrable benefit to the prevention 
of tooth decay (Refs. 45-49). However, EPA has found substantial 
concerns with the designs of each of these studies including small 
sample size and uncontrolled confounders, such as recall bias and 
socioeconomic status. Additionally, in Bratthall et al. (Ref. 45), for 
example, the appropriate interpretation of the responses of the 55 
dental care professionals surveyed, based on the data provided in the 
paper, is that in places where water is fluoridated, the fluoridation 
is the primary reason for the reduction in dental caries. Diesendorf 
(Ref. 49) cites only anecdotal evidence and Cheng et al. (Ref. 46) is 
commentary only, with no supporting data.
    EPA is mindful of the public health significance of reducing the 
incidence of dental caries in the U.S. population. Dental caries is one 
of the most common childhood diseases and continues to be problematic 
in all age groups. Historically, the addition of fluoride to drinking 
water has been credited with significant reductions of dental caries in 
the U.S. population. In 2000, the then-Surgeon General noted that 
``community water fluoridation remains one of the great achievements of 
public health in the twentieth century--an inexpensive means of 
improving oral health that benefits all residents of a community, young 
and old, rich and poor alike.'' The U.S. Surgeon General went on to 
note, ``it [is] abundantly clear that there are profound and 
consequential disparities in the oral health of our citizens. Indeed, 
what amounts to a silent epidemic of dental and oral diseases is 
affecting some population groups.'' (Ref. 50).
    At that time, among 5- to 17-year-olds, dental caries was more than 
five times as common as a reported history of asthma and seven times as 
common as hay fever. Prevalence increases with age. The majority (51.6 
percent) of children aged 5 to 9 years had at least one carious lesion 
or filling in the coronal portion of either a primary or a permanent 
tooth. This proportion increased to 77.9 percent for 17-year-olds and 
84.7 percent for adults 18 or older. Additionally, 49.7 percent of 
people 75 years or older had root caries affecting at least one tooth 
(Ref. 50).
    More recently, from the National Health and Nutrition Examination 
Survey (NHANES) for 2011-2012, approximately 23% of children aged 2-5 
years had dental caries in primary teeth. Untreated tooth decay in 
primary teeth among children aged 2-8 was twice as high for Hispanic 
and non-Hispanic black children compared with non-Hispanic white 
children. Among those aged 6-11, 27% of Hispanic children had any 
dental caries in permanent teeth compared with nearly 18% of non-
Hispanic white and Asian children. About three in five adolescents aged 
12-19 years had experienced dental caries in permanent teeth, and 15% 
had untreated tooth decay (Refs. 51).
    Further, in 2011-2012, 17.5 percent of Americans ages 5-19 years 
were reported to have untreated dental caries, while 27.4 percent of 
those aged 20-44 years had untreated caries (Ref. 52). For those living 
below the poverty line, 24.6 percent of those aged 5-19 years and 40.2 
percent of those aged 20-44 years had untreated dental caries (Ref. 
52). Untreated tooth decay can lead to abscess (a severe infection) 
under the gums which can spread to other parts of the body and have 
serious, and in rare cases fatal, results (Ref. 53). Untreated decay 
can cause pain, school absences, difficulty concentrating, and poor 
appearance, all contributing to decreased quality of life and ability 
to succeed (Ref. 54).
    These data continue to suggest dental caries remains a public 
health problem affecting many people. Fluoride has been proven to 
protect teeth from decay by helping to rebuild and strengthen the 
tooth's surface or enamel. According to the Centers for Disease Control 
and Prevention and the American Dental Association, water fluoridation 
prevents tooth decay by providing frequent and consistent contact with 
low levels of fluoride (Refs. 55 and 56). Thus, the health benefits of 
fluoride include having fewer cavities, less severe cavities, less need 
for fillings and removing teeth, and less pain and suffering due to 
tooth decay (Ref. 55).
    Fluoride protects teeth in two ways--systemically and topically 
(Ref. 57). Topical fluorides include toothpastes, some mouth rinse 
products and professionally applied products to treat tooth surfaces. 
Topical fluorides strengthen teeth already in the mouth by becoming 
incorporated into the enamel tooth surfaces, making them more resistant 
to decay. Systemic fluorides are those ingested into the body. 
Fluoridated water and fluoride present in the diet are sources of 
systemic fluoride. As teeth are developing (pre-eruptive), regular 
ingestion of fluoride protects the tooth surface by depositing 
fluorides throughout the entire tooth surface (Ref. 56). Systemic 
fluorides also provide topical protection as ingested fluoride is 
present in saliva which continually bathes the teeth (Ref. 56). Water 
fluoridation provides both systemic and topical exposure which together 
provide for maximum reduction in dental decay (Ref. 56).
    The Surgeon General, the Public Health Service and the Centers for 
Disease Control and Prevention reaffirmed in 2015 the importance of 
community water fluoridation for the prevention of dental caries and 
its demonstrated effectiveness (Refs. 54 and 58). In the Public Health 
Service's 2015 Recommendation for Fluoride Concentration in Drinking 
Water, they note ``there are no randomized, double-blind, controlled 
trials of water fluoridation because its community-wide nature does not 
permit randomization of individuals to study and control groups or 
blinding of participants. However, community trials have been 
conducted, and these studies were included in systematic reviews of the 
effectiveness of community water fluoridation. As noted, these reviews 
of the scientific evidence related to fluoride have concluded that 
community water fluoridation is effective in decreasing dental caries 
prevalence and severity'' (Ref. 59).
    7. Extent and magnitude of risk from fluoridation chemicals. The 
petition argues that the purported risks of drinking water fluoridation 
are unreasonable in part because they are borne by a large population. 
The petition (in its discussion of the extent and magnitude of risk 
posed) cites the total U.S. population and estimates the

[[Page 11887]]

number of U.S. children under the age of 18 years who live in areas 
where artificial fluoridation occurs. That estimate is then multiplied 
by an estimate of the average decrease in lifetime earnings associated 
with IQ point loss to calculate the overall potential IQ point loss and 
associated decrease in lifetime earnings for the segment of the U.S. 
population under the age of 18 years potentially exposed to 
artificially fluoridated water. The petition concludes, based on the 
potential extent and magnitude of exposure to fluoridation chemicals, 
that fluoridation would have caused ``a loss of between 62.5 to 125 
million IQ points'' (Ref. 1, p. 24).
    The petition has not set forth a scientifically defensible basis to 
conclude that any persons have suffered neurotoxic harm as a result of 
exposure to fluoride in the U.S. through the purposeful addition of 
fluoridation chemicals to drinking water or otherwise from fluoride 
exposure in the U.S. Still less has the petition set forth a 
scientifically defensible basis to estimate an aggregate loss of IQ 
points in the U.S., attributable to this use of fluoridation chemicals. 
As noted previously, EPA has determined the petition did not establish 
that fluoridation chemicals present an unreasonable risk of injury to 
health or the environment, arising from these chemical substances' use 
to fluoridate drinking water. The fact that a purported risk relates to 
a large population is not a basis to relax otherwise applicable 
scientific standards in evaluating the evidence of that purported risk. 
EPA and other authoritative bodies have previously reviewed many of the 
studies cited as evidence of neurotoxic effects of fluoride in humans 
and found significant limitations in using them to draw conclusions on 
whether neurotoxicity is associated with fluoridation of drinking 
water. In contrast, the benefits of community water fluoridation have 
been demonstrated to reduce dental caries, which is one of the most 
common childhood diseases and continues to be problematic in all age 
groups. Left untreated, decay can cause pain, school absences, 
difficulty concentrating, and poor appearance, all contributing to 
decreased quality of life and ability to succeed (Ref. 54).
    8. Consequences of eliminating use of fluoridation chemicals. 
Apparently citing to a repealed provision of TSCA (15 U.S.C. 
2605(c)[1](A) (2015)) and guidance issued with respect to that 
statutory provision, the petition argues that the following factors are 
germane to determining whether the alleged neurotoxic risks presented 
by fluoridation chemicals are unreasonable: ``the societal consequences 
of removing or restricting use of products; availability and potential 
hazards of substitutes, and impacts on industry, employment, and 
international trade.'' Along these lines, the petition includes claims 
such as the following: That any risks of fluoridation chemicals could 
be easily reduced by discontinuing purposeful fluoridation practices; 
that alternative topical fluoride products have widespread 
availability; and that the impacts on the requested rule on industry, 
employment, and international trade would be little, if any. In short, 
the petition urges EPA to conclude that the risks of fluoridation 
chemicals are unreasonable, in part because if EPA found that the risks 
were unreasonable, the cost and non-risk factors that EPA would need to 
address in ensuing risk management rulemaking could be readily 
addressed. But this sort of ends-driven reasoning is forbidden by the 
texts of section 6(b)(4)(A) and 21(b)(4)(B)(ii) of the amended TSCA, 
which exclude ``costs or other non-risk factors'' from the unreasonable 
risk determination. It is also plainly inconsistent with Congress' 
intent, in amending TSCA, to ``de-couple'' the unreasonable risk 
decision from the broader set of issues (e.g., chemical alternatives 
and regulatory cost-effectiveness) that may factor into how best to 
manage unreasonable risks, once particular risks have been determined 
to be unreasonable. See S. Rep. 114-67 at 17 (Ref. 3); H.R. Rep. 114-
176 at 23 (Ref. 4); and 162 Cong. Rec. S3516 (Ref. 60).
    9. Link to elevated blood lead levels. To support the contention 
that TSCA (and not the Safe Drinking Water Act [SDWA]) is the 
appropriate regulatory authority, the petition asserts an association 
between fluoridation chemicals and elevated blood lead levels and 
claims that there is laboratory and epidemiological research linking 
artificial fluoridation chemicals with pipe corrosion. The petition 
then argues that issuing a rule under TSCA section 6 rather than SDWA 
would allow EPA to specifically target and prohibit the addition of 
fluoridation chemicals to drinking water. The petition argues that SDWA 
would not allow EPA to distinguish between intentionally-added, 
artificial and naturally-occurring fluoride. It is in the public 
interest, says the petition, to opt for the regulatory option that is 
less expensive and can be more narrowly tailored.
    Regarding the claims about the relative extent of legal authorities 
under TSCA and SDWA, EPA notes that the petition has not set forth any 
specific legal basis for its views on the purported limitations of 
SDWA. For this reason, and because the petition has not set forth facts 
sufficient to show that the fluoridation of drinking water presents an 
unreasonable risk under TSCA, the Agency need not resolve such legal 
questions in order to adjudicate this petition.
    EPA has further observations about the petition's claims that 
drinking water fluoridation is linked to lead hazards. The Centers for 
Disease Control and Prevention (CDC) studied the relationship between 
fluoridation additives and blood lead levels in children in the United 
States (Ref. 61). More than 9,000 children between the ages of 1-16 
years were included in the study's nationally representative sample. 
The petition argues that the study, and Table 4 in particular, shows 
that fluorosilicic acid was associated with increased risk of high 
blood lead levels. In fact, Macek et al. concluded that their detailed 
analyses did not support concerns that silicofluorides in community 
water systems cause high lead concentrations in children. The petition 
also points to another study (Ref. 62) which re-analyzed CDC's data and 
concluded that children exposed to ``silicofluoridated'' water had an 
elevated risk of having high blood lead levels. Coplan et al. (Ref. 62) 
criticized the Macek et al. approach as flawed and reevaluated the 
NHANES data comparing systems that used silicofluorides to all systems 
(e.g., a combination of fluoridated, nonfluoridated and naturally 
fluoridated) and found a small difference between the number of 
children in each group with blood lead levels >5 [micro]g/dL; the 
results were not evaluated to see if the difference was statistically 
significant. A number of other chemical characteristics are known to 
increase lead release into water sources such as pH, natural organic 
matter, water hardness, oxidant levels, and type of piping, age of 
housing; the Coplan et al. study did not evaluate these factors.
    In any event, the Agency is not persuaded that the examination of 
the relationship between fluoridation chemicals, pipe corrosion, and 
elevated blood lead levels nor their bearing on the comparative 
efficacy of TSCA or SDWA is germane to the disposition of the petition. 
Under TSCA, where the EPA Administrator determines ``that the 
manufacture, processing, distribution in commerce, use, or disposal of 
a chemical substance or mixture . . . presents an unreasonable risk of 
injury

[[Page 11888]]

to health or the environment, the Administrator shall by rule [regulate 
a] . . . substance or mixture to the extent necessary so that the 
chemical substance or mixture no longer presents such risk'' 15 U.S.C. 
2605(a). As previously discussed, the petition does not demonstrate 
that purposeful addition of fluoridation chemicals to U.S. water 
supplies presents such unreasonable risk.
    10. Regulation of fluoridation chemicals as a category. EPA has 
broad discretion to determine whether to regulate by category under 
TSCA section 26(c) rather than by individual chemical substances. In a 
prior evaluation of a section 21 petition seeking the regulation of a 
category of chemical substances, EPA explained that it does so in light 
of Congress' purpose in establishing the category authority: To 
``facilitate the efficient and effective administration'' of TSCA. See 
72 FR 72886 (Ref. 63) (citing Senate Report No. 94-698 at 31). It is of 
course self-evident that various chemical substances constituting 
``fluoridation chemicals'' would have in common their use to fluoridate 
drinking water. But as discussed in Unit III., the inquiry does not end 
there. If EPA were to grant the petitioner's request, the Agency would 
become obligated to address all conditions of use of the category. If 
certain chemical substances comprising the category present conditions 
of use that other members do not, and any of those conditions of use 
would be significant to whether the category as a whole presents an 
unreasonable risk to human health or the environment, then the overall 
approach of regulating by category is less suited to the efficient and 
effective administration of TSCA. But the petition does not set forth 
facts that would enable the Agency to reasonably evaluate whether a 
category approach on fluoridation chemicals would be consistent with 
the efficient and effective administration of TSCA. Nor does the 
petition set forth the specific chemical substances that should 
comprise the category of fluoridation chemicals.
    11. Specification of an adequate rule under TSCA section 6(a). As 
discussed earlier, the petition does not set forth facts that 
satisfactorily demonstrate to the Agency that fluoridation chemicals 
present an unreasonable risk to human health, specifically arising from 
these chemical substances' use to fluoridate drinking water. But even 
if the petition had done so, it would still be inadequate as a basis to 
compel the commencement of section 6(a) rulemaking proceeding under 
TSCA section 21. This is because the petition does not address whether 
fluoridation chemicals would still present an unreasonable risk, even 
after implementing the requested relief, arising from other conditions 
of use. As discussed earlier in Unit III., EPA interprets TSCA section 
21 as requiring a petition to address the full set of conditions of use 
for a chemical substance and thereby describe an adequate rule under 
TSCA section 6(a), as opposed to a rule that would merely address a 
particular subset of uses of special interest. The petition at issue 
pays little or no attention to the other conditions of use of the 
various fluoridation chemicals (i.e., uses other than the eponymous use 
to treat drinking water) and makes no claim for any of these chemical 
substances that the risks to be addressed by curtailing drinking water 
fluoridation would be the only unreasonable risks or even the most 
significant unreasonable risks. This problem is compounded by the 
petition's lack of specificity as to which chemical substances are 
being construed as ``fluoridation chemicals.''
    EPA acknowledges that its interpretation of the requirements of 
TSCA section 21, for petitions seeking action under TSCA section 6, was 
not available to petitioners at the time they prepared this petition. 
EPA has issued general guidance for preparing citizen's petitions, 50 
FR 56825 (1985), but that guidance does not account for the 2016 
amendments to TSCA. Particularly relevant under these circumstances, 
the Agency wishes to emphasize that its denial does not preclude 
petitioners from obtaining further substantive administrative 
consideration, under TSCA section 21, of a substantively revised 
petition under TSCA section 21 that clearly identifies the chemical 
substances at issue, discusses the full conditions of use for those 
substances, and sets forth facts that would enable EPA to complete a 
risk evaluation under TSCA section 6(b) for those substances.

VI. References

    As indicated under ADDRESSES, a docket has been established for 
this document under docket ID number EPA-HQ-OPPT-2016-0763. The 
following is a listing of documents that are specifically referenced in 
this notice. The docket itself includes both these referenced documents 
and further documents considered by EPA. The docket also includes 
supporting documents provided by the petitioner and cited in the 
petition, which are not available in the electronic version of the 
docket. For assistance in locating these printed documents, please 
consult the technical person listed under FOR FURTHER INFORMATION 
CONTACT.

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child mental work capacity: Preliminary investigation into

[[Page 11889]]

the mechanisms involved. Fluoride. Vol. 41, pp. 331-335. 2008.
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39. Sandeep, B.; Kavitha, N.; Praveena, M.; Sekhar, P.R. and Rao, 
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behavioral studies and ACh and AChE levels. International Journal of 
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63-73. 2010.
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the caries decline: What do the experts believe? European Journal of 
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water fluoridation and caries prevention: A critical review. 
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54. U.S. Department of Health and Human Services. Statement on the 
Evidence

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Supporting the Safety and Effectiveness of Community Water 
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62. Coplan, M.J.; Patch, S.C.; Masters, R.D. and Bachman, M.S. 
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Register (72 FR 72886, December 21, 2007).

List of Subjects

    Environmental protection, Fluoridation chemicals, Drinking water, 
Toxic Substances Control Act (TSCA).

    Dated: February 17, 2017.
Wendy Cleland-Hamnett,
Acting Assistant Administrator, Office of Chemical Safety and Pollution 
Prevention.
[FR Doc. 2017-03829 Filed 2-24-17; 8:45 am]
 BILLING CODE 6560-50-P