[Federal Register Volume 82, Number 37 (Monday, February 27, 2017)]
[Proposed Rules]
[Pages 11878-11890]
[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,

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:<PHONE_NUMBER>; fax
number:<PHONE_NUMBER>; email address<EMAIL_ADDRESS>    For general information contact: The TSCA-Hotline, ABVI-Goodwill,
422 South Clinton Ave., Rochester, NY 14620; telephone number: (202)
554-1404; email address<EMAIL_ADDRESS>
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

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

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

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

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

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

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).

    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

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

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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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