and complete          conduct an opacity
                               corrective actions..  test
                                                     If opacity
                                                     greater than 10%
                                                     are observed,
                                                     initiate and
                                                     complete corrective
                                                     actions
Clay ceramics kilns with no   To demonstrate        To demonstrate
 add-on control, or            compliance with       compliance with
 intending to comply with      dioxins/furans        dioxins/furans
 dioxin/furan standard         standard:             standard:
 without an ACI system.        Monitor       Monitor
                               kiln operating        kiln stack
                               temperature..         temperature
                               Maintain at   Maintain at
                               or above average      or below highest
                               operating             stack temperature
                               temperature during    during dioxin/furan
                               dioxin/furan test..   test
------------------------------------------------------------------------

V. Summary of Significant Comments and Responses

    The EPA received a total of 52 public comment letters on the
proposed BSCP Manufacturing NESHAP. (See Docket ID No. EPA-HQ-OAR-2013-
0291 for the complete public comments.) The EPA received a total of
seven public comment letters on the proposed Clay Ceramics
Manufacturing NESHAP. (See Docket ID No. EPA-HQ-OAR-2013-0290 for the
complete public comments.) The following sections summarize the major
public comments received on the proposal and present the EPA's
responses to those comments.

A. Health-Based Standards

    Comment: Two commenters disagreed with setting standards under CAA
section 112(d)(4) for emissions of HCl, HF, and Cl2 from new
and existing BSCP and clay ceramics sources. One commenter questioned
whether the EPA has the authority to set CAA section 112(d)(4)
standards for these acid gases. The commenter asserted that it would be
arbitrary and capricious for the EPA to set risk-based standards for
these pollutants when the EPA previously decided not to set CAA section
112(d)(4) standards for HCl, HF, and Cl2 in air toxics
rulemakings for industrial boilers and power plants. For power plants,
the EPA stated that the agency ``does not have sufficient information
to establish CAA section 112(d)(4) health-based emission standards and
we did not receive such data during the comment period.''\1\ The
commenter noted that the EPA reached a similar conclusion with respect
to industrial boilers, declining to set risk-based standards because of
a lack of information on emissions.\2\ The commenter asserted that the
health and scientific data regarding emissions of acid gases from BSCP
and clay ceramics plants similarly fail to provide justification for
setting HBEL for these pollutants. The commenter asserted the EPA must
instead set MACT standards.
---------------------------------------------------------------------------

    \1\ ``Responses to Public Comments on National Emission
Standards for Hazardous Air Pollutants from Coal- and Oil-Fired
Electric Utility Steam Generating Units.'' Docket Item No. EPA-HQ-
OAR-2009-0234-20126.
    \2\ National Emission Standards for Hazardous Air Pollutants for
Major Sources: Industrial, Commercial, and Institutional Boilers and
Process Heaters, 75 FR 32006, 32031 (June 4, 2010).
---------------------------------------------------------------------------

    Similarly, the second commenter expressed concern over using CAA
section 112(d)(4) and health-based risk assessment for setting the HCl,
HF and Cl2 standards for BSCP Manufacturing and Clay
Ceramics Manufacturing. The commenter noted that this would be the
first time the EPA used the health-based risk assessment approach under
CAA section 112(d)(4) to set emission standards for HF and
Cl2; although the EPA has used this approach in the past to
establish health-based standards for other source categories, it was
restricted to ``HCl emissions for discrete units within the facility''
(79 FR 75639).
    The commenter supported focusing on pollutants that pose the
greatest risks but expressed concern that the EPA has not adequately
established that the approaches used are appropriate. The commenter
asserted that the EPA's approach represented a far-reaching and
significant change in the manner in which MACT standards are
established under CAA section 112(d) and that it was inappropriate for
the EPA to propose such changes in a rulemaking for individual source
categories instead of discussing the approach with all affected
parties. The commenter noted that Congress established section 112 of
the CAA to rely on a technology-based approach to avoid the gridlock of
the unsuccessful risk-based methods used before the adoption of the
1990 CAA Amendments. Accordingly, while the CAA includes language under
section 112(d)(4) allowing the use of risk in the establishment of
MACT, it should be used only under limited and very specific
circumstances, and the commenter stated that the EPA's proposal did not
adequately make the case for the use of CAA section 112(d)(4).
    Conversely, two other commenters stated that the EPA has clear
legal authority to set HBEL and ample justification to do so for the
BSCP source category. The commenters stated that under the terms of
this provision, the EPA may set an emission standard at a level higher
than would be required by CAA section 112(d)(4), provided that: (1) The
pollutant(s) being regulated is a threshold pollutant and (2) the
standard provides an ample margin of safety. The

commenters stated that both of these criteria are met in this case.
    The commenters asserted that the proposed standard is consistent
with Congress's expectations regarding the implementation of CAA
section 112(d)(4). According to the Senate report accompanying the
legislation, ``For some pollutants a MACT emission limitation may be
far more stringent than is necessary to protect public health and the
environment'' and in such situations, ``[t]o avoid expenditures by
regulated entities which secure no public health or environmental
benefit, the Administrator is given discretionary authority to consider
the evidence for a health threshold higher than MACT at the time the
standard is under review.'' \3\ The commenters stated that for this
rulemaking, MACT would result in emission standards that are far more
stringent than are needed to protect health and the environment and
asserted that Congress enacted CAA section 112(d)(4) to allow emission
standards to be tailored to protect public health without imposing
unreasonable and unnecessary standards on affected sources.
---------------------------------------------------------------------------

    \3\ S. Rep. No. 101-228, 101st Cong. 1st sess. at 171.
---------------------------------------------------------------------------

    Response: The EPA disagrees with the commenters that we do not have
the authority to establish CAA section 112(d)(4) standards in this
rulemaking. The EPA also disagrees that the decision to establish CAA
section 112(d)(4) standards is inconsistent with our decisions on other
rulemakings. The commenters' more detailed arguments and the EPA's
responses are provided in the remainder of this section.
1. Health Thresholds
    Comment: One commenter stated that a pollutant is not a threshold
pollutant under CAA section 112(d)(4) unless the EPA establishes that
it cannot cause cancer at any level of exposure. The commenter asserted
that HCl, HF, and Cl2 do not have already-established safe
health thresholds and the EPA's proposed standards would not provide
``an ample margin of safety.''
    Conversely, two commenters agreed with the EPA that the available
health data indicate that HCl, HF, and Cl2 are all threshold
pollutants. The commenters stated that the data show that each of these
pollutants has a discernible exposure threshold below which adverse
human health effects are not expected to occur; in addition, none of
the available data suggest that these pollutants reasonably should be
expected to act as a carcinogen or mutagen, or exhibit a mode of action
that would result in non-threshold effects.
    Response: The EPA disagrees with the first commenter regarding HCl,
HF and Cl2 not having thresholds accepted by the scientific
community, and we acknowledge the support of the other two commenters.
The EPA's conclusion that HCl, HF and Cl2 are threshold
pollutants is based on the best available toxicity database considered
in hazard identification and dose response assessments. There is
agreement on using a similar threshold approach for these chemicals
across agencies, i.e., the EPA's Integrated Risk Information System
(IRIS) Program, Agency for Toxic Substances and Disease Registry
(ATSDR) and the California Environmental Protection Agency (CalEPA).
The toxicity assessments, which include noncancer and/or cancer
toxicity assessments, provided by these authoritative bodies are widely
vetted through the scientific community and undergo rigorous peer
review processes before they are published. In addition, the Science
Advisory Board (SAB) has endorsed the use of the reference values
derived by these sources to support the EPA's risk assessments in the
residual risk and technology review (RTR) program.
    Specifically, none of the compounds discussed here has been
classified as a carcinogen or as ``suggestive of the potential to be
carcinogenic,'' individually or in combination, by existing
authoritative bodies, including EPA, CalEPA, International Agency for
Research on Cancer (IARC), Organisation for Economic Co-operation and
Development (OECD), and the European Community. In light of the absence
of evidence of carcinogenic risk for any of these pollutants, and the
evidence of an existing threshold below which HCl, HF and
Cl2 are not expected to cause adverse effects, the EPA
considers it appropriate to set health threshold standards under CAA
section 112(d)(4) for these pollutants. The existing health effects
evidence on HCl, HF and Cl2 that provide support for this
determination is described below.
    Potential health effects of HCl:
     There are limited studies on the carcinogenic potential of
HCl in humans. The occupational data are limited to a couple of studies
(Steenland et al., 1988, Beaumont et al., 1986)\4,5\ where the subjects
were exposed to a mixture of acid gases (mainly sulfuric acid)and other
chemicals (including metals) that may have contained HCl. These studies
failed to separate potential exposure of HCl from exposure to other
substances shown to have carcinogenic activity and are therefore not
appropriate to evaluate the carcinogenic potential of HCl. Another
occupational study failed to show evidence of association between
exposure to HCl and lung cancer among chemical manufacturing plant
employees showing that there is no evidence that HCl is a human
carcinogen.\6\
---------------------------------------------------------------------------

    \4\ Steenland, K., T. Schnorr, J. Beaumont, W. Halperin, T.
Bloom. 1988. Incidence of laryngeal cancer and exposure to acid
mists. Br. J. of Ind. Med. 45: 766-776.
    \5\ Beaumont, J.J., J. Leveton, K. Knox, T. Bloom, T. McQuiston,
M Young, R. Goldsmith, N.K. Steenland, D. Brown, W.E. Halperin.
1987. Lung cancer mortality in workers exposed to sulfuric acid mist
and other acid mists. JNCI. 79: 911-921.
    \6\ Bond G.G., Flores G.H., Stafford B.A., Olsen G.W. Lung
cancer and hydrogen chloride exposure: results from a nested case-
control study of chemical workers. 1991. J Occup Med; 33(9), 958-61.
---------------------------------------------------------------------------

     Consistent with the human data, chronic inhalation studies
in animals have reported no carcinogenic responses after chronic
exposure to HCl (Albert et al., 1982; Sellakumar et al., 1985).\7,8\
---------------------------------------------------------------------------

    \7\ Albert, R.E., A.R. Sellakumar, S. Laskin, M. Kuschner, N.
Nelson and C.A. Snyder. 1982. Gaseous formaldehyde and hydrogen
chloride induction of nasal cancer in rats. J. Natl. Cancer Inst.
68(4): 597-603.
    \8\ Sellakumar, A.R., C.A. Snyder, J.J. Solomon and R.E. Albert.
1985. Carcinogenicity for formaldehyde and hydrogen chloride in
rats. Toxicol. Appl. Pharmacol. 81: 401-406.
---------------------------------------------------------------------------

     Hydrogen chloride has not been demonstrated to be
genotoxic. The genotoxicity database consists of two studies showing
false positive results potentially associated with low pH in the test
system (Morita et al., 1992; Cifone et al., 1987).\9,10\
---------------------------------------------------------------------------

    \9\ Morita, T., T. Nagaki., I. Fukuda, K. Okumura. 1992.
Clastogenicity of low pH to various cultured mammalian cells. Mutat.
Res. 268: 297-305.
    \10\ Cifone, M.A., B. Myhr, A. Eiche, G. Bolcsfoldi. 1987.
Effect of pH shifts on the mutant frequency at the thymidine kinase
locus in mouse lymphoma L5178Y TK=/- cells. Mutat. Res. 189: 39-46.
---------------------------------------------------------------------------

     Chronic exposure to HCl at concentrations below the
current IRIS reference concentration (RfC) are not expected to cause
adverse effects.
    Potential health effects of HF:
     There are a limited number of studies investigating the
carcinogenic potential of HF. These studies are unreliable on the issue
of possible carcinogenicity of HF and/or fluorides, in general, because
of many confounding factors (e.g., exposure to multiple unknown
chemicals and smoking habits not accounted for) and because no
breakdown was done by type of fluoride exposure.\11\
---------------------------------------------------------------------------

    \11\ U.S. Department of Health and Human Services, Agency for
Toxic Substances and Disease Registry. Toxicological Profile for
Fluorides, Hydrogen Fluoride and Fluorine. 2003. Available at http://www.atsdr.cdc.gov/toxprofiles/tp11.pdf.

---------------------------------------------------------------------------

     Chronic exposure at or below the current CalEPA reference
exposure level (REL) is not expected to cause adverse effects.
    Potential health effects of Cl2:
     The existing studies of workers in the chemical industry
have not found any evidence that Cl2 is carcinogenic.
     Chronic bioassays in rodents and long-term studies in non-
human primates have shown no evidence for carcinogenicity in
respiratory tract as target tissue or other tissues.
     Chronic exposure to Cl2 at concentrations below
the current ATSDR minimal risk level (MRL) are not expected to cause
adverse effects.
    We disagree with the comment that the EPA's proposed HBEL does not
provide an ample margin of safety, for the following reasons.
    First, the limit is based on the facility in the source category
with the highest potential exposure to nearby residents. The HBEL at
this single facility reflects a ratio of exposure concentration over
the reference value of up to 1 (at an exposure concentration below the
RfC is considered to be health protective). As such, exposures will not
exceed the established health threshold at this facility. In addition,
the exposure estimate used to set the limit is very health protective
in that it assumes constant exposure for 70 years. Actual exposures
from emissions from this facility are expected to be lower (i.e.,
because persons will spend time away from home). This conservative
exposure scenario is consistent with the ``ample margin of safety''
requirement in CAA section 112(d)(4).
    Second, the ratios at the other facilities (not the highest
facility noted above) from this source category are lower and in most
cases significantly lower, with approximately 90 percent of these
facilities having a ratio of 0.5 or less, which provides a further
increased margin of safety beyond the ample margin of safety
established at the facility with the highest potential exposure.
    Comment: One commenter stated that, according to the EPA, an RfC is
merely ``an estimate (with uncertainty spanning perhaps an order of
magnitude)'' of an exposure that is ``likely to be'' without health
risks.\12\ By definition, this ``estimate'' is not by itself a ``safe
threshold'' of exposure that ``presents no risk'' of adverse health
effects. The commenter stated the EPA cannot lawfully use a pollutant's
RfC as a default ``safe threshold'' under CAA section 112(d)(4) because
an RfC does not pose ``no'' health risks, as the commenter asserted the
CAA requires.
---------------------------------------------------------------------------

    \12\ U.S. EPA, Glossary, http://www.epa.gov/risk_assessment/glossary.htm (last updated Apr. 28, 2014).
---------------------------------------------------------------------------

    The commenter stated that the EPA is authorized to set risk-based
standards only where it has direct evidence of the level at which there
are no adverse effects observed and that proceeding with HBEL without a
no observed adverse effect level (NOAEL) is unlawful. Another commenter
stated the use of health-based standards should only be considered for
HAP that have been thoroughly evaluated by the EPA and are contained in
the IRIS database with a high level of confidence in the RfC. With
respect to HCl, the IRIS confidence levels are ``Low'' for the
inhalation RfC. In ``Carcinogenicity Assessment for Lifetime
Exposure,'' IRIS states, ``This substance/agent has not undergone a
complete evaluation and determination under the EPA's IRIS program for
evidence of human carcinogenic potential.'' \13\ In the proposal, the
EPA acknowledged that ``[t]he EPA has not classified HCl for
carcinogenicity'' and ``[l]ittle research has been conducted on its
carcinogenicity'' (79 FR 75639).
---------------------------------------------------------------------------

    \13\ U.S. EPA, Integrated Risk Information System--Hydrogen
chloride. http://www.epa.gov/iris/subst/0396.htm#coninhal.
---------------------------------------------------------------------------

    The commenter also stated that IARC concluded that ``[t]here is
inadequate evidence for the carcinogenicity in humans of hydrochloric
acid,'' that ``[t]here is inadequate evidence for the carcinogenicity
in experimental animals of hydrochloric acid,'' and that HCl ``is not
classifiable as to its carcinogenicity to humans.'' \14\ The commenter
stated that the EPA did not identify any evidence that HCl is not
carcinogenic and noted that the only study the EPA referenced is ``one
occupational study'' that ``found no evidence of carcinogenicity'' (79
FR 75639). Because the EPA did not provide a citation for the study or
otherwise identify it or discuss it, the public are unable to
adequately comment on it.
---------------------------------------------------------------------------

    \14\ IARC, Hydrochloric Acid (Monograph), available at http://monographs.iarc.fr/ENG/Monographs/vol54/mono54-8.pdf.
---------------------------------------------------------------------------

    Response: The EPA's risk assessments are supported by the best
available toxicity assessments from authoritative bodies including the
EPA's IRIS Program, ATSDR and CalEPA. The SAB has endorsed the use of
the reference values derived by these sources to support EPA's risk
assessments in the RTR program. These authoritative bodies derive
health protective reference values at or below which no adverse effects
are expected to occur. As mentioned previously in this section, the
toxicity assessments, which include noncancer and/or cancer toxicity
assessments, provided by these authoritative bodies are widely vetted
through the scientific community and undergo rigorous peer review
processes before they are published.
    The commenter stated that there is not a NOAEL and that based on
that, the EPA cannot set a HBEL for HCl. The EPA toxicity assessments
consider the entire toxicity database for specific chemicals and are
conducted following well-established EPA guidance on how to assess
potential hazard of a chemical and conduct dose response assessments.
These assessments include the derivation of an RfC, which is likely to
be without appreciable risk of adverse health effects to the human
population (including susceptible subgroups and all life stages) over a
lifetime. According to EPA guidelines, RfCs can be derived from a
NOAEL, lowest observed adverse effect level (LOAEL) or benchmark dose,
with uncertainty factors applied to reflect the limitations of the data
used. In particular for HCl, the point of departure for the RfC (15
milligrams per cubic meter (mg/m \3\)) was selected from chronic
inhalation studies in rodents and was adjusted to reflect a lifetime of
exposure (2.7 mg/m \3\) and extrapolated to a human equivalent
concentration (6.1 mg/m \3\) based on differences in the effects of a
gas in the respiratory system between rats and humans. Uncertainty
factors (total of 300, yielding an RfC of 0.02 mg/m \3\) were applied
to account for interspecies differences, intraspecies extrapolation and
extrapolation from a LOAEL to NOAEL. It is important to note that in
the IRIS assessment for HCl it is stated that a reasonable estimate of
the NOAEL in humans is in the range of 0.3-3 mg/m \3\. This estimate
resulted from an expert review workshop and is based on examination of
the HCl literature, a comparison with sulfuric acid toxicity, and the
judgment of those in attendance at the review workshop. In addition,
this value is generally consistent with identified NOAELs in subchronic
animal studies (OECD, 2002). Based on this information, we are
confident that the IRIS HCl RfC represents a conservative health
protective benchmark below which adverse health effects are not
expected to occur.
    As part of the risk analysis conducted to support this rule, the
EPA thoroughly evaluated all the available and relevant scientific
evidence on HCl (discussed previously in this section) and concluded
that there is no evidence that HCl is a carcinogen and that this
information is sufficient for this regulatory determination. The 2002

OECD assessment of HCl drew similar conclusions:

    For genetic toxicity, a negative result has been shown in the
Ames test. A positive result in a chromosome aberration test using
Hamster ovary cells is considered to be an artifact due to the low
pH. For carcinogenicity, no pre-neoplastic or neoplastic nasal
lesions were observed in a 128-week inhalation study with SD male
rats at 10 ppm hydrogen chloride gas. No evidence of treatment
related carcinogenicity was observed in other animal studies
performed by inhalation, oral or dermal administration. In humans,
no association between hydrogen chloride exposure and tumor
incidence was observed.\15\
---------------------------------------------------------------------------

    \15\ United Nations Environment Programme 2002, Organisation for
Economic Co-operation and Development (OECD), Screening Information
Dataset (SIDS) Initial Assessment Report for SIAM 15, Hydrogen
Chloride: CAS N[deg]:7647-01-0. October 25, 2002. http://www.inchem.org/documents/sids/sids/7647010.pdf.

Additionally, the EPA conducted a screening level literature review in
2003 and did not identify any critical studies that would change the
conclusions in the 1995 HCl IRIS assessment. Based on the information
available, the EPA concludes that this information is sufficient to
support setting an HBEL under CAA section 112(d)(4) for HCl.
    Comment: One commenter stated that the EPA proposed to base the HCl
emission standards on the HCl RfC and argued it is unlawful to do so
where the EPA has ``low confidence'' in the RfC. The commenter stated
that it is arbitrary to claim there is an established, safe health
threshold based on a reference value in which the EPA has low
confidence. According to the commenter, having low confidence in the
RfC is the same as admitting that the EPA has ``low confidence'' in the
proposed emission standards. The fact that the EPA was unable to
determine a no-effect level in a robust and reliable scientific study
demonstrates concern that chronic exposure to even very low levels of
HCl can compromise health, especially in sensitive subpopulations.
Therefore, the EPA cannot state that HCl presents no risk of adverse
health effects.
    The commenter stated that the EPA used a non-cancer health
threshold for HCl based on a chronic inhalation study on rats.\16\ The
EPA has determined the RfC to be 0.02 mg/m\3\ (0.0134 part per million
(ppm)), based on rat studies by Albert, et al., demonstrating
hyperplasia of the nasal mucosa (the protective cell lining of the
nasal tract and cavities), larynx, and trachea.\17\ The commenter
asserted that because these rat studies failed to identify a NOAEL, the
EPA based the RfC on a LOAEL (i.e., the lowest dose in the study that
induced a measurable adverse health effect in treated animals). The
commenter asserted that CAA section 112(d)(4) does not permit risk-
based standards where a NOAEL has not been determined; at a minimum,
Congress required that a threshold be based on the `` `no observable
[adverse] effects level' (NOAEL) below which human exposure is
presumably `safe.' '' \18\ The EPA has similarly recognized that ``the
legislative history of CAA section 112(d)(4) indicates that a health-
based emission limit under CAA section 112(d)(4) should be set at the
level at which no observable effects occur'' (79 FR 75642). The
commenter stated that, if there is no established non-zero threshold
level at which it has been shown that the pollutant has no deleterious
health effects, then the EPA cannot be certain that exposure to the
pollutant at a given level presents no harm. The commenter stated that
without a NOAEL, no established threshold can exist, and the EPA does
not have the authority under CAA section 112(d)(4) to set an HBEL for
HCl.
---------------------------------------------------------------------------

    \16\ EPA, Integrated Risk Information System: Hydrogen Chloride.
    \17\ Albert, R.E., et al., Gaseous formaldehyde and hydrogen
chloride induction of nasal cancer in rats, 68(4) J. Natl. Cancer
Inst. 597 (1982).
    \18\ S. Rep. No. 101-228, at 171, 176.
---------------------------------------------------------------------------

    Response: The EPA's chemical-specific toxicity assessments are
derived using the EPA's risk assessment guidelines and approaches that
are well established and vetted through the scientific community, and
follow rigorous peer review processes.\19\ The RTR program gives
preference to EPA values (i.e., RfCs for noncancer assessments) for use
in risk assessments and uses other values, as appropriate, when those
values are derived with methods and peer review processes consistent
with those followed by the EPA. The approach for selecting appropriate
toxicity values for use in the RTR Program has been endorsed by the
SAB.\20\
---------------------------------------------------------------------------

    \19\ Integrated Risk Information System (IRIS). IRIS Guidance
documents available at http://www.epa.gov/iris/backgrd.html.
    \20\ Science Advisory Board. Memorandum to Lisa Jackson,
Administrator, U.S. EPA. Review of EPA's draft entitled, ``Risk and
Technology Review (RTR) Risk Assessment Methodologies: For Review by
the EPA's Science Advisory Board with Case Studies--MACT I Petroleum
Refining Sources and Portland Cement Manufacturing.'' May 7, 2010.
Available at: http://yosemite.epa.gov/sab/sabproduct.nsf/
4AB3966E263D943A8525771F00668381/$File/EPA-SAB-10-007-unsigned.pdf.
---------------------------------------------------------------------------

    The EPA's RfCs are assigned confidence levels of high, medium and
low based on the completeness of the supporting database. High
confidence RfCs are considered less likely to change substantially with
the collection of additional information, while low confidence RfCs are
recognized as being based on less complete data and so may be subject
to change if additional data is developed.\21\ It is important to note
that a ``low confidence'' label does not indicate that the EPA believes
that the RfC is unreliable. For a given chemical, if there are not
adequate or appropriate data with which to derive an RfC, one is not
calculated. All RfCs, even those with low confidence, are appropriate
for regulatory use.
---------------------------------------------------------------------------

    \21\ U.S. EPA Air: Fate, Exposure, and Risk Analysis Web site.
Air Toxics Assessment Reference Library, Volume 1. 2004. Available
at http://www2.epa.gov/sites/production/files/2013-08/documents/volume_1_reflibrary.pdf.
---------------------------------------------------------------------------

    We disagree with the comment that without a NOAEL, no established
threshold can exist. The EPA toxicity assessments for specific
chemicals are conducted using well-established EPA guidance on how to
assess potential hazard of chemicals and how to conduct dose response
assessments to arrive at a chemical concentration below which we do not
expect adverse effects to occur (i.e., threshold). These assessments
include the derivation of a RfC which is likely to be without
appreciable risk of adverse health effects to the human population
(including susceptible subgroups and all life stages [e.g., children])
over a lifetime. According to EPA guidelines, RfCs can be derived from
a NOAEL, LOAEL or benchmark dose, with uncertainty factors applied to
account for relevant extrapolations, including extrapolation from LOAEL
to NOAEL, and to reflect additional limitations of the data used.\22
23\
---------------------------------------------------------------------------

    \22\ U.S. EPA. 1994. Methods for Derivation of Inhalation
Reference Concentrations and Application of Inhalation Dosimetry.
EPA/600/8-90/066F, Oct 1994. Docket Item No. EPA-HQ-OAR-2013-0291-
0160.
    \23\ U.S. EPA. 2002. A Review of the Reference Dose and
Reference Concentration Processes. EPA/630/P-02/002F, Dec 2002.
---------------------------------------------------------------------------

    Comment: One commenter stated that the studies the EPA relied upon
only investigated respiratory effects and did not consider other ways
HCl could cause harm. The commenter noted the EPA has acknowledged that
the RfC is an ``inhalation RfC'' and represents the health risk and
toxicity associated with the inhalation pathway of exposure only (75 FR
32031). The commenter stated that the EPA identified no studies that
indicate whether exposure to HCl--at 0.02 mg/m\3\ or any other
concentration--harms other bodily systems.
    Response: The EPA disagrees with the comment that the agency
investigated only respiratory effects and that it did not consider
other ways in which HCl can cause harm. In the principal studies

upon which the RfC is based, a complete necropsy was performed on all
animals. Histologic sections were prepared from the nasal cavity, lung,
trachea, larynx, liver, kidneys, testes, and other organs where gross
pathological signs were present. Due to the reactive nature of HCl,
however, portal of entry effects are anticipated to occur first and at
lower exposure concentrations. The IRIS assessment \24\ for HCl
included a comprehensive review of all the available toxicity data for
HCl. No effects are expected to occur at exposures of HCl at or below
the level of the RfC.
---------------------------------------------------------------------------

    \24\ IRIS Summary for Hydrogen Chloride. http://www.epa.gov/iris/subst/0396.htm (Accessed on July 24, 2015)
---------------------------------------------------------------------------

    Comment: One commenter stated that the RfC is an inadequate basis
for establishing a threshold because it ``did not reflect any potential
cumulative or synergistic effects of an individual's exposure to
multiple HAP or to a combination of HAP and criteria pollutants'' and
noted that the EPA recognized the potential for cumulative and
synergistic effects was important in its consideration of risk-based
standards in two recent rulemakings (see 75 FR 32031 and 76 FR 25050).
    The commenter stated that there is no ``established'' threshold at
the RfC for HCl, because the CalEPA has determined a lower and more
health-protective value than the RfC. The EPA's chronic inhalation RfC
is 0.02 mg/m\3\, while California's chronic inhalation REL is 0.009 mg/
m\3\.\25\ The commenter stated that CalEPA's REL is based on the same
science as the IRIS RfC but was developed more recently than the EPA's
RfC, which was last revised in 1995.\26\ The REL is ``the concentration
level at or below which no health effects are anticipated in the
general human population,'' and the EPA's process for developing RELs
``is similar to that used by EPA to develop IRIS values and
incorporates significant external scientific peer review.'' \27\ The
commenter asserted that the EPA and CalEPA disagree about the
concentration of HCl exposure at which no health effects are expected
and that the disagreement stems from how to account for uncertainty and
variability in interpreting the study results.
---------------------------------------------------------------------------

    \25\ California Office of Environmental Health Hazard Assessment
(OEHHA), OEHHA Acute, 8-Hour and Chronic Reference Exposure Levels
(REL)s, http://www.oehha.ca.gov/air/Allrels.html (last accessed Mar.
12, 2015).
    \26\ California OEHHA, Chronic RELs and Toxicity Summaries Using
the Previous Version of the Hot Spots Risk Assessment Guidelines at
311 (1999), available at http://oehha.ca.gov/air/hot_spots/2008/AppendixD3_final.pdf.
    \27\ EPA, Risk Assessment to Determine a Health-Based Emission
Limitation for Acid Gases for the Brick and Structural Clay Products
Manufacturing Source Category, May 19, 2014, Docket Item No. EPA-HQ-
OAR-2013-0291-0132.
---------------------------------------------------------------------------

    The fact that two agencies have determined significantly different
``safe'' levels, the commenter contended, demonstrates as a matter of
law that there is no ``established'' health threshold for HCl and
precludes the EPA from lawfully setting CAA section 112(d)(4) standards
for HCl. The commenter stated that the statute requires that a health
threshold ``has been established'' and argued the legislative history
indicates Congress intended for CAA section 112(d)(4) limits to be used
only where there was a ``well-established'' level that presents ``no
risk'' of adverse effects and about which there was no ``dispute.''
\28\ The commenter asserted that Congress did not grant the
Administrator the authority to establish the threshold itself and that
the EPA does not have authority to set CAA section 112(d)(4) standards
in situations where there is disagreement among expert agencies as to
what the correct health threshold should be.
---------------------------------------------------------------------------

    \28\ S. Rep. No. 101-228, at 171.
---------------------------------------------------------------------------

    The commenter asserted that by failing to address the CalEPA REL,
the EPA contravened its obligation under administrative law to address
significant evidence that detracts from the agency's conclusion. The
commenter stated that for the EPA to rely solely on the IRIS RfC, the
EPA would need to explain why the CalEPA REL is incorrect and why the
IRIS RfC reflects the best available science and risk assessment
practices, particularly when the IRIS RfC and CalEPA REL thresholds are
based on the same science and when the EPA relied upon CalEPA RELs at
several other points in its proposal (e.g., the EPA used the CalEPA REL
for acute inhalation exposure to HCl as the basis for its CAA section
112(d)(4) standards). If the EPA considers CalEPA's acute REL for HCl
to reflect a reliable value, then the commenter stated it is arbitrary
to disregard CalEPA's chronic REL for HCl. The commenter further noted
the EPA relied upon the CalEPA chronic REL for HF in order to determine
a threshold for HF and argued that using the CalEPA REL for HF but not
for HCl is arbitrary.
    Response: At an initial point, with respect to the comment that
different agencies have identified different thresholds and so ``as a
matter of law'' there is no ``established'' health threshold for HCl,
the EPA disagrees that the phrase ``has been established'' in CAA
section 112(d)(4) means that there is universal agreement on the health
threshold level and that differences between CalEPA and the EPA
demonstrate that no health threshold ``has been established.'' The
statute does not clearly identify who must establish the health
threshold or how such threshold should be established. In the absence
of such specificity in the statute, the EPA reads CAA section 112(d)(4)
to authorize the EPA to set health-based limits where, in the EPA's
expert judgment, there is a health threshold for the pollutant below
which no adverse health effects are expected to occur.
    Further, we disagree with the comment that there is no established
threshold at the RfC because CalEPA developed a reference value at a
lower concentration than the RfC. The approaches used by both agencies
are similar and assume a threshold below which adverse health effects
would not be expected; however, there are some differences between
agencies in methods for deriving the estimate for a threshold that may
affect the final resulting values. Both agencies use the best available
science to support their risk assessments. The EPA has an approach for
selecting appropriate health benchmark values and, in general, this
approach places greater weight on the EPA derived health benchmarks
than those from other agencies. The approach favoring EPA benchmarks
(when they exist) has been endorsed by the SAB and ensures use of
values most consistent with well-established and scientifically-based
EPA science policy.\29\
---------------------------------------------------------------------------

    \29\ Science Advisory Board. Memorandum to Lisa Jackson,
Administrator, U.S. EPA. Review of EPA's draft entitled, ``Risk and
Technology Review (RTR) Risk Assessment Methodologies: For Review by
the EPA's Science Advisory Board with Case Studies--MACT I Petroleum
Refining Sources and Portland Cement Manufacturing.'' May 7, 2010.
Available at: http://yosemite.epa.gov/sab/sabproduct.nsf/
4AB3966E263D943A8525771F00668381/$File/EPA-SAB-10-007-unsigned.pdf.
---------------------------------------------------------------------------

    Specifically for HCl, we selected the IRIS RfC for HCl as the most
appropriate chronic noncancer health threshold to use for this rule. In
the case of HF, there is not an EPA RfC available and the only chronic
reference value from an authoritative source and appropriate for use in
this rule is the California REL.
    Comment: Several commenters disagreed with the EPA's decision to
set a HBEL for HF. These commenters contended the EPA does not have the
authority to set HF standards under CAA section 112(d)(4) because the
scientific data supporting the EPA's findings regarding the
carcinogenic potential of HF are insufficient and unreliable. Three
commenters asserted that the EPA should not adopt HBEL for

HF due to uncertainty about the vulnerabilities of children, infants,
and fetuses to HF exposures at the REL concentration used by the EPA to
set the HF emissions standards. Two commenters noted that the proposal
states, ``There is limited/equivocal evidence of the carcinogenic
potential of HF'' (79 FR 75641) and ``[t]he EPA has not classified HF
for carcinogenicity'' (79 FR 75640) and questioned how the agency could
be confident that HF is eligible to be a threshold pollutant if its
status as a non-carcinogen is uncertain.
    One commenter noted that the EPA failed to identify an established,
well-defined health-based threshold, below which HF does not cause
cancer, that is based on reliable science and has a high level of
certainty. The EPA has stated that ``carcinogenicity via inhalation of
fluoride is not considered to be likely by most investigators reporting
in the existing literature'' (79 FR 75641) and that the EPA ``has not
classified HF for carcinogenicity'' (79 FR 75640). The commenter stated
that it is possible that HF causes cancer because increased rates of
cancer have been observed in workers exposed to a mixture of chemicals
that included fluoride \30\ and noted that the EPA acknowledged data
suggesting that those with occupational exposure to HF have greater
than normal occurrences of cancer.\31\ The commenter stated that,
because of the data showing possible carcinogenic effect, as well as
the data showing mutagenic effect in animals, the EPA does not have
enough evidence to classify HF as a threshold pollutant with any level
of confidence. The commenter stated that the EPA failed to explain how
it weighed the conflicting evidence of HF's carcinogenicity and
considered EPA's conclusion to be arbitrary and capricious. Three
commenters noted that the EPA does not consider HF in its IRIS database
but noted that HF breaks down into fluorine, which is included in
IRIS.\32\ One commenter stated that IRIS indicates no data are
available to determine an RfC for chronic inhalation exposure to
fluorine.\33\ This commenter further noted that IARC ``has determined
that the carcinogenicity of fluoride to humans is not classifiable.''
\34\ Another commenter stated that health-based standards should be
considered only for HAP that are contained in IRIS with a high level of
confidence in the RfC.
---------------------------------------------------------------------------

    \30\ Gallerani, M., et al., Systemic and topical effects of
intradermal hydrofluoric acid, 16 Am. J. Emer. Med. 521, 522 (1998).
    \31\ EPA, Technology Transfer Network Air Toxics Web site:
Hydrogen Fluoride, http://www.epa.gov/ttn/atw/hlthef/hydrogen.html
(last updated Oct. 18, 2013).
    \32\ EPA, Integrated Risk Information System: Fluorine (Soluble
Fluoride) (CASRN 7782-41-4), http://www.epa.gov/iris/subst/0053.htm
(last updated Oct. 31, 2014).
    \33\ Id.
    \34\ ATSDR, Toxicological Profile for Fluorides, Hydrogen
Fluoride, and Fluorine at 8.
---------------------------------------------------------------------------

    One commenter noted that although the National Air Toxics
Assessment (NATA) database does not contain HF,\35\ the database does
provide evidence that HF has a mutagenic effect in animals. This
conclusion was supported by other scientific reviews \36\ and by the
National Academy of Sciences (NAS), which states that ``the overall
evidence from human animal studies is mixed'' on the question of
whether fluoride is carcinogenic when inhaled.\37\
---------------------------------------------------------------------------

    \35\ EPA, National Scale Air Toxics Assessment Overview: The 33
Pollutants, http://www.epa.gov/ttn/atw/nata/34poll.html (last
updated Jan. 6, 2015).
    \36\ See, e.g., National Research Council of the National
Academies, Emergency and Continuous Exposure Guidance Levels for
Selected Submarine Contaminants vol.3 at 91-92, available at http://www.ncbi.nlm.nih.gov/books/n/nap12741/pdf.
    \37\ National Research Council of the National Academies,
Emergency and Continuous Exposure Guidance Levels for Selected
Submarine Contaminants vol.3 at 91-92, available at http://www.ncbi.nlm.nih.gov/books/n/nap12741/pdf.
---------------------------------------------------------------------------

    Four commenters questioned the EPA's reliance on a CalEPA risk
assessment, noting that the CalEPA REL is based on a study of adults
exposed to HF in the workplace \38\ and therefore, did not include any
children. Two commenters stated that a 10X ``intraspecies'' factor was
applied to account for variability among humans, but noted that CalEPA
expressed concern about ``the potentially greater susceptibility of
children to the effects of inhaled fluorides, considering the rapid
bone growth in early years.'' \39\ One commenter recommended the EPA
use an additional default factor of at least 10X to account for
uncertainty regarding health risks to children, infants, and fetuses.
The commenter stated that a 10X factor would be consistent with the NAS
recommendation\40\ and with the 10X factor enacted by Congress in the
Food Quality Protection Act (FQPA).\41\ Another commenter stated that
recent science not considered at the time CalEPA adopted the REL
provides further support for prior research showing that HF has
neurodevelopmental effects on children and that children living in
high-fluoride areas have been observed to have lower IQ scores than
those living in low-fluoride areas.\42\ The commenter asserted that the
adverse effects of fluoride on children are likely to be more severe,
and long-lasting, compared with effects on adults.
---------------------------------------------------------------------------

    \38\ Derryberry O.M., et al., Fluoride exposure and worker
health-The health status of workers in a fertilizer manufacturing
plant in relation to fluoride exposure, 6 Arch. Environ. Health. 503
(1963).
    \39\ OEHHA Chronic RELs and Toxicity Summaries, at 280.
    \40\ National Research Council of the National Academies,
Science and Decisions: Advancing Risk Assessment, at 190-93 (2009).
    \41\ 21 U.S.C. 346a(b)(2)(C) (requiring that, in establishing,
modifying, leaving in effect, or revoking a tolerance or exemption
for a pesticide chemical residue, ``for purposes of clause (ii)(I)
an additional tenfold margin of safety for the pesticide chemical
residue and other sources of exposure shall be applied'' to protect
infants and children).
    \42\ See Choi, A.L., et al., Developmental Fluoride
Neurotoxicity: A Systematic Review and Meta-Analysis, 120 Envtl.
Health Perspect. 1362 (Oct. 2012), http://ehp.niehs.nih.gov/1104912/
(reviewing and discussing findings from over 20 studies); Choi,
A.L., et al., Association of Lifetime Exposure to Fluoride and
Cognitive Functions in Chinese Children: A Pilot Study, 47 Neurotox.
& Teratology 96 (Jan.-Feb. 2015).
---------------------------------------------------------------------------

    One commenter stated that the CalEPA REL is based on a study that
only examined the increased bone density (skeletal fluorosis) endpoint
and noted that CalEPA stated that ``[t]he primary uncertainty in the
study was the lack of a comprehensive health effects examination.''
\43\ The commenter stated that the EPA does not know whether
neurodevelopmental harm, or other health effects, are more sensitive
than skeletal harm; therefore, the EPA cannot lawfully set a ``safe''
threshold at a concentration that poses ``no risk'' of health effects
with ``an ample margin of safety'' based on a study that lacks ``a
comprehensive health effects examination.''
---------------------------------------------------------------------------

    \43\ OEHHA, Chronic RELs and Toxicity Summaries, at 280.
---------------------------------------------------------------------------

    Another commenter asserted that the EPA has insufficient data
showing exposure to HF at the REL value ``presents no risk'' of harm to
other bodily systems. The commenter noted that HF is a possible
reproductive toxin,\44\ that occupational studies of women exposed to
fluoride identified increased rates of menstrual irregularities,\45\
and that animal studies have found that fluoride impairs reproduction
and increases the rates of fetal bone and teeth malformation.\46\ In
addition, chronic inhalation of hydrofluoric acid can cause irritation
and congestion of the nose and throat

and bronchitis,\47\ and animal studies found increased rates of kidney
and liver damage from hydrofluoric acid inhalation.\48\ Further, HF
readily penetrates the skin, causing deep tissue layer destruction,\49\
and ingestion of HF may result in vomiting and abdominal pain, with
painful necrotic lesions, hemorrhagic gastritis, and pancreatitis
reported after significant exposure.\50\
---------------------------------------------------------------------------

    \44\ Massachusetts Toxics Use Reduction Institute, Massachusetts
Chemical Fact Sheet: Hydrofluoric Acid, at 1, available at http://www.turi.org/content/download/3663/44840/file/Fact_Sheet_Hydrofluoric_Acid.pdf.
    \45\ EPA, Health Issue Assessment: Summary Review of Health
Effects Associated with Hydrogen Fluoride and Related Compounds,
EPA/600/8-89/002F (1988).
    \46\ ATSDR, Toxicological Profile for Fluorides, Hydrogen
Fluoride and Fluorine; EPA, Health Issue Assessment: Summary Review
of Health Effects Associated with Hydrogen Fluoride and Related
Compounds.
    \47\ CalEPA, Technical Support Document for the Determination of
Noncancer Chronic Reference Exposure Levels.
    \48\ EPA, Health Issue Assessment: Summary Review of Health
Effects Associated with Hydrogen Fluoride and Related Compounds.
    \49\ Burgher, Francois, et al., Experimental 70% hydrofluoric
acid burns: histological observations in an established human skin
explants ex vivo model, 30.2 Cutaneous & Ocular Toxicology 100
(2011).
    \50\ CDC, National Institute for Occupational Safety and Health
(NIOSH): Hydrogen Fluoride/Hydrofluoric Acid, http://www.cdc.gov/niosh/ershdb/emergencyresponsecard_29750030.html.
---------------------------------------------------------------------------

    The commenter stated the CalEPA REL was developed by CalEPA using
an outdated version of CalEPA's Hot Spots Risk Assessment Guidelines
(1999) that has been ``superseded'' by the more recent guidelines
released in February 2015.\51\ The commenter noted the 1999 version
required updating in part because it did not include sufficient
consideration of ``infants and children in assessing risks from air
toxics.''
---------------------------------------------------------------------------

    \51\ OEHHA Chronic RELs and Toxicity Summaries at 1; CalEPA,
OEHHA, Air Toxics Hot Spots Program: Guidance Manual for Preparation
of Health Risk Assessments (Feb. 2015), available at http://oehha.ca.gov/air/hot_spots/2015/2015GuidanceManual.pdf.
---------------------------------------------------------------------------

    Response: The EPA has not reviewed HF in the IRIS program. However,
we concur with the two recent authoritative assessments by ATSDR (2003)
\52\ and the European Union (2002) \53\ that the available evidence
does not support classifying HF as ``Carcinogenic to Humans,'' ``Likely
to Be Carcinogenic to Humans'' or as having ``Suggestive Evidence of
Carcinogenic Potential'' (U.S. EPA Guidelines for Carcinogen Risk
Assessment (2005)).
---------------------------------------------------------------------------

    \52\ Agency for Toxic Substances and Disease Registry (2003)--
``Although elevated cancer rates have been reported in some
occupational groups exposed to hydrogen fluoride and fluoride dusts,
these studies were not controlled for the multiple substance
exposures to which industrial workers are generally exposed. Because
of these multiple exposures and the problem inherent in all
occupational studies in identifying appropriate reference
populations, only limited evidence from such studies is specifically
relevant to the investigation of possible carcinogenic effects of
long-term dermal exposure to hydrofluoric acid and inhalation
exposure to hydrogen fluoride and/or fluoride dusts in human beings.
As noted previously, IARC has determined that the carcinogenicity of
fluoride to humans is not classifiable.''
    \53\ European Union Risk Assessment Report (2001)--
``Carcinogenicity studies, in which HF has been tested, are not
available. Studies with NaF may provide insight in the
carcinogenicity of HF, especially for systemic tumours. With the
latter substance 4 animal studies have been performed, 2 in which
NaF was supplied in the drinking water to rats and mice, and two in
which NaF was administered via the diet, again to rats and mice . .
. .In the rat drinking water study, equivocal indications for
osteosarcomas in males were obtained, but the rat diet study was
negative, despite clear indications of fluoride intoxication. The
mouse drinking water study was also negative. The mouse diet study
was confounded by the presence of a retrovirus which may have (co)-
induced the growth of benign osteomas thus thwarting the
interpretation of the study. In the diet studies (Maurer et al.
1990; Maurer et al. 1993) bone fluoride levels were higher than in
the drinking water studies (NTP 1990), while in the diet studies no
indications for osteosarcomas were obtained. Furthermore, the
osteomas were considered to be reminiscent of hyperplasias rather
than true bone neoplasms. It was concluded that the available data
is sufficient to suggest that fluoride is not a carcinogenic
substance in animals (Janssen and Knaap 1994) . . . Based on
epidemiological data IARC (1982) concluded that the evidence for
carcinogenicity of orally taken fluoride in humans is inadequate.
Recent studies (cited in CEPA 1993; Janssen and Knaap 1994) did not
supply evidence of a relationship between fluoride in drinking water
and cancer mortality, either. US-EPA, reviewing the epidemiological
data for fluoride, stated that no conclusion can be drawn as to the
carcinogenicity of fluoride after inhalatory exposure, because in
all studies available, humans were exposed to other substances as
well (Thiessen 1988).''
---------------------------------------------------------------------------

    All of the studies cited by the commenter are from exposure to
fluoride and not from inhalation exposures to HF. Neurodevelopmental
effects may be relevant to high fluoride exposures, but the existing
evidence shows these effects may occur at fluoride exposure levels
beyond those that would cause respiratory effects if HF were the sole
source of exposure. In the study of Lund (1997),\54\ plasma fluoride
concentrations were shown to increase in the nanogram per milliliter
(ng/ml) range from exposures to HF in the mg/m\3\ level (e.g.,
elevations of approximately 20 nanograms fluoride per milliliter in
plasma resulted from 1-hour exposure to 2 mg/m\3\ HF, with notable
respiratory and eye irritation effects). Reproductive and developmental
effects in rats have been noted from experiments \55\ with plasma F
levels in the 150 ng/ml range maintained for over 4 months. The primary
issue in causing neurodevelopmental effects (which have yet to be
quantified) is likely associated with aggregate and cumulative exposure
from multiple sources of fluorides (e.g., water, food, toothpaste)
which are greater contributors to total fluoride body burden and
uncontrollable variables in establishing this rule, which deals with
exposures to HF only.
---------------------------------------------------------------------------

    \54\ Lund K, Ekstrand J, Boe J, S[oslash]strand P, and Kongerud
J. (1997) Exposure to hydrogen fluoride: an experimental study in
humans of concentrations of fluoride in plasma, symptoms, and lung
function. Occup Environ Med. 54(1):32-37.
    \55\ Oencue, M, Kocak, A, Karaoz, E; Darici, H; Savilk, E; and
Gultekin, F (2007) Effect of long-term fluoride exposure on lipid
peroxidation and histology of testes in first- and second-generation
rats. Biological Trace Element Research 118:260-268.
---------------------------------------------------------------------------

    The EPA also disagrees with the comment that a children's default
safety factor of 10 should be added to the CalEPA REL for HF. In
response to the 10X factor enacted by Congress in the FQPA (1996)\56\
to the EPA non-cancer reference value derivation, the agency evaluated
its methods for considering children's risk in the development of
reference values. As part of its response, the EPA (i.e., the Science
Policy Council and Risk Assessment Forum) established the RfD/RfC
Technical Panel to develop a strategy for implementing the FQPA and
examine the issues relative to protecting children's health and
application of the 10X safety factor. One of the outcomes of the
Technical Panel's efforts was an in depth review of a number of issues
related to the RfD/RfC process (U.S. EPA 2002). The most critical
aspect in the derivation of a reference value pertaining to the FQPA
has to do with variation between individual humans and is accounted for
by a default uncertainty factor when no chemical-specific data are
available. The EPA reviewed the default UF for inter-human variability
and found the EPA's default value of 10 adequate for all susceptible
populations and lifestages, including children and infants. The EPA
also recommends the use of chemical-specific data in preference to
default uncertainty factors when available (U.S. EPA, 1994, 2011) and
is developing Agency guidance to facilitate consistency in the
development and use of data-derived extrapolation factors for RfCs and
reference doses (RfDs) (U.S. EPA, 2011).57 58 In agreement
with the recommendations of the RfC review, CalEPA chronic REL for HF
was derived using an inter-individual uncertainty factor of 10, which
is considered adequate by the EPA for accounting for all susceptible
populations and lifestages, including children and infants.
---------------------------------------------------------------------------

    \56\ U.S. Environmental Protection Agency, Pesticide: Regulating
Pesticides. The Food Quality Protection Act (FQPA). 1996. Available
at http://www.epa.gov/pesticides/regulating/laws/fqpa/backgrnd.htm.
    \57\ U.S. EPA (1994). Methods for derivation of inhalation
reference concentrations and application of inhalation dosimetry.
(EPA/600/8-90/066F). Research Triangle Park, NC. Docket Item No.
EPA-HQ-OAR-2013-0291-0160.
    \58\ U.S. EPA (2011). Office of the Science Advisor, Risk
Assessment Forum. Recommended Use of Body Weight\3/4\ as the Default
Method in Derivation of the Oral Reference Dose. February 2011. EPA/
100/R11/0001.
---------------------------------------------------------------------------

    Regarding the comment that CalEPA's Hot Spots Risk Assessment
Guidelines

(1999) have been ``superseded'' by the more recent guidelines released
in February 2015, the EPA reviewed the February 2015 Guidelines
information provided by the commenter and concluded that this
information does not include methods for conducting hazard
identification and dose response assessments, which are the analyses
that preclude the derivation of a reference value. Therefore, the
information provided by the commenter does not apply to the CalEPA REL
derivation methods.
    The commenter's assertion that the NATA database does not contain
HF is incorrect; NATA 2005 (cited above by the commenter) does include
noncancer risk estimates for HF. The HF cancer risks are not included
in NATA because a quantitative cancer analysis for HF does not exist.
    Comment: Several commenters disagreed with the EPA's decision to
set a HBEL for Cl2 and stated the EPA does not have the
authority to set Cl2 standards under CAA section 112(d)(4)
because the EPA does not have reliable scientific data demonstrating a
``safe'' threshold for Cl2 and has not demonstrated
Cl2 presents no cancer risk. Two commenters noted that in
the proposal, the EPA stated that, ``the agency presumptively considers
Cl2 to be a threshold pollutant.'' The commenters asserted
that a presumption is not adequate for EPA to justify setting a health-
based standard for Cl2 under CAA section 112(d)(4).
    One commenter stated that it is possible that Cl2 is
carcinogenic and noted that Cl2 has not undergone a complete
evaluation and determination of human carcinogenic potential under the
IRIS program.\59\ The IARC and the Department of Health and Human
Services (DHHS) have not classified Cl2 gas for human
carcinogenicity. The commenter stated that the absence of data showing
carcinogenicity is not the same as data demonstrating that a substance
is not carcinogenic.
---------------------------------------------------------------------------

    \59\ EPA, Integrated Risk Information System: Chlorine, http://www.epa.gov/iris/subst/0405.htm (last updated Oct. 31, 2014).
---------------------------------------------------------------------------

    According to the commenter, Congress authorized CAA section
112(d)(4) standards only where a threshold ``has been established.'' In
other words, there must be an already-established threshold for which
there is direct evidence that the pollutant presents ``no'' harm at the
threshold level of exposure, and the law requires ``well-established''
factual evidence.\60\ The commenter asserted that the EPA is not
authorized to set risk-based standards based on a ``presumption'' of
the existence of a safe level of exposure and that by doing so, the EPA
would violate the law and fail to ensure adequate protection from the
health risks of hazardous pollution.
---------------------------------------------------------------------------

    \60\ S. Rep. No. 101-228, at 171.
---------------------------------------------------------------------------

    The commenter stated that the EPA cannot set a health threshold for
Cl2 based on a chronic inhalation study on monkeys because
that study did not determine a NOAEL. The commenter asserted that CAA
section 112(d)(4) does not permit risk-based standards where a NOAEL
has not been determined. The commenter stated that, at a minimum,
Congress required that a threshold be based on the `` `no observable
[adverse] effects level' (NOAEL) below which human exposure is
presumably `safe.' '' \61\ If there is no established non-zero
``threshold'' level at which it has been shown that the pollutant has
no deleterious health effects, then the commenter asserted that the EPA
cannot be certain that exposure to the pollutant at a given level
presents ``no'' harm.
---------------------------------------------------------------------------

    \61\ S. Rep. No. 101-228, at 171, 176.
---------------------------------------------------------------------------

    Two commenters stated that IRIS contains ``no data'' on an RfC for
chronic inhalation exposure.\62\ The ATSDR MRL on which the proposed
Cl2 threshold is based is a ``screening value[] only'' and
``[is] not [an] indicator[] of health effects.'' \63\ According to the
ATSDR, ``Exposures to substances at doses above MRLs will not
necessarily cause adverse health effects and should be further
evaluated,'' ``MRLs are intended to serve only as a screening tool to
help you decide if you should more closely evaluate exposures to a
substance found at a site,'' and ``uncertainties are associated with
[the] techniques'' used to derive MRLs.\64\
---------------------------------------------------------------------------

    \62\ EPA, Integrated Risk Information System: Chlorine.
    \63\ ATSDR, Public Health Assessment Guidance Manual (2005
Update): Appendix F, http://www.atsdr.cdc.gov/hac/PHAManual/appf.html (last updated Nov. 30, 2005).
    \64\ ATSDR, Toxicological Profile for Chlorine, at 14.
---------------------------------------------------------------------------

    One commenter stated that the MRL does not account for the
potentially greater susceptibility of children, infants, and fetuses to
Cl2 exposures \65\ and noted that CalEPA has recognized that
Cl2 is a toxic air contaminant ``that may disproportionately
impact infants and children'' because it can exacerbate asthma.\66\
Therefore, the commenter asserted the MRL does not reflect an
``established'' safe health threshold at which exposure presents ``no''
adverse effects and that it is unlawful for the EPA to set CAA section
112(d)(4) standards for Cl2.
---------------------------------------------------------------------------

    \65\ ATSDR, Toxicological Profile for Chlorine at 20-21
(observing that a value similar to the MRL could be calculated using
the lowest observed adverse effect level (LOAEL) approach if an
uncertainty factor of only 3 for human variability is used and no
child-safety uncertainty factor is used).
    \66\ CalEPA, Prioritization of Toxic Air Contaminants Under the
Children's Environmental Health Protection Act, at 27-28.
---------------------------------------------------------------------------

    Response: The EPA disagrees with the comment. As part of the risk
analysis conducted to support this rule, the EPA thoroughly evaluated
all the available and relevant scientific evidence on Cl2
(as discussed in detail previously in this section) and concluded that
there is no evidence that Cl2 is a carcinogen and that this
information is sufficient to support this regulatory decision. The MRL
for Cl2 was developed using the benchmark dose analysis
method, which has been widely adopted across the risk assessment
community and by the EPA's Risk Assessment Forum \67\ as a more
reliable estimate of a threshold for an effect than a NOAEL or LOAEL.
As a result, the REL for Cl2 does define a threshold.
---------------------------------------------------------------------------

    \67\ U.S. EPA (2012) Benchmark Dose Technical Guidance. Risk
Assessment Forum, Washington, DC 20460. EPA/100/R-12/001, June 2012.
Available online at http://www2.epa.gov/sites/production/files/2015-01/documents/benchmark_dose_guidance.pdf.
---------------------------------------------------------------------------

    Regarding the assertion that the MRL does not take into
consideration the potential for greater potential effects in children,
in the development of the Toxicological Profile for Chlorine,\68\ ATSDR
performed an exhaustive review of all of the relevant health effects
data available at the time. Until new information becomes available,
the Cl2 MRL is the most credible, scientifically grounded
toxicity assessment for Cl2 and the most appropriate
reference value to use in this regulatory action.
---------------------------------------------------------------------------

    \68\ Agency for Toxic Substances and Disease Registry (ATSDR).
2010. Toxicological profile for Chlorine. Atlanta, GA: U.S.
Department of Health and Human Services, Public Health Service.
---------------------------------------------------------------------------

    In the light of the absence of evidence of carcinogenic risk from
Cl2 exposure and the evidence of an existing threshold below
which Cl2 is not expected to cause adverse effects, the EPA
considers it appropriate to set health threshold standards under CAA
section 112(d)(4) for Cl2.
    Comment: One commenter referenced an NAS review of chemical health
evaluations in the United States that concluded improvements in both
chemical testing and risk assessment are needed to assure current risk
evaluations protect people from toxic chemicals.\69\ The NAS
recommended the EPA use ``A consistent, unified

approach for dose-response modeling that includes formal, systematic
assessment of background disease processes and exposures, possible
vulnerable populations, and modes of action that may affect a
chemical's dose-response relationship in humans; that approach
redefines the RfD or RfC as a risk-specific dose that provides
information on the percentage of the population that can be expected to
be above or below a defined acceptable risk with a specific degree of
confidence.'' The NAS also observed that ``[n]oncancer effects do not
necessarily have a threshold, or low-dose nonlinearity'' and found that
``[b]ecause the RfD and RfC do not quantify risk for different
magnitudes of exposure but rather provide a bright line between
possible harm and safety, their use in risk-risk and risk-benefit
comparisons and in risk-management decision-making is limited.'' \70\
---------------------------------------------------------------------------

    \69\ See National Research Council of the National Academies,
Toxicity Testing in the Twenty-First Century: A Vision and a
Strategy (2007); National Research Council of the National
Academies, Phthalates and Cumulative Risk Assessment: The Tasks
Ahead (2008); NAS, Science and Decisions.
    \70\ Janssen, S., et al., Strengthening Toxic Chemical Risk
Assessments to Protect Human Health (2012), available at http://www.nrdc.org/health/files/strengthening-toxic-chemical-riskassessments-report.pdf (citing NAS, Science and Decisions).
---------------------------------------------------------------------------

    The commenter stated that there may be no safe threshold in the
human population for many chemicals and that newer studies show many
chemicals increase the risk of various noncancer health effects--such
as reproductive harm and neurological effects--at low doses, without
any scientifically identifiable threshold.\71\ The commenter noted that
even if a threshold is established for an individual, when risk is
assessed across a diverse population, it is unlikely the same threshold
applies to all individuals because some people are more vulnerable than
others.
---------------------------------------------------------------------------

    \71\ Janssen et al., Strengthening Toxic Chemical Risk
Assessments to Protect Human Health.
---------------------------------------------------------------------------

    The commenter stated that, to address the fact that very low levels
of non-carcinogen exposures can pose health risks, NAS recommended that
cancer and chronic non-cancer risk assessment use the same
approach.\72\ The commenter noted that the use of RfCs for dose-
response risk assessment of chronic non-cancer health effects may
significantly underestimate risk: ``For these health effects, risk
assessments focus on defining the reference dose (RfD) or reference
concentration (RfC), which is defined as a dose `likely to be without
an appreciable risk of deleterious effects' over a lifetime of
exposure. In actual fact, these levels may pose appreciable risks.''
\73\
---------------------------------------------------------------------------

    \72\ NAS, Science and Decisions, at 8-9, 265-66.
    \73\ Janssen, S., et al., Strengthening Toxic Chemical Risk
Assessments to Protect Human Health at 10.
---------------------------------------------------------------------------

    The commenter asserted that the EPA ignored the best available,
current science showing that pollutants have health effects at low
doses in its evaluation of health thresholds for HCl, HF, and
Cl2 and ignored NAS's recommendation that the EPA use
similar approaches for chronic non-cancer as for cancer risk
assessment, which presumes deleterious health effects for any amount of
exposure. According to the commenter, the EPA lacked sufficient data to
demonstrate that these pollutants do not cause harm at low levels of
exposure over time and cannot be certain that there exists an
established, safe health threshold at the proposed thresholds. The
commenter also stated that, because it must be assumed that these
pollutants cause harm at low doses, it is impossible for the EPA to
meet the CAA's requirement for an ``ample margin of safety.'' The
commenter concluded the EPA's use of CAA section 112(d)(4) standards
for HCl, HF, and Cl2 is indefensible because the EPA
determined the thresholds based on studies that did not identify a
level at which no health effects were observed (i.e., a NOAEL) and the
EPA itself has low confidence in the proposed thresholds.
    Response: The NAS has recognized that many of the recommended
changes for the IRIS Program will need to be incorporated over a number
of years and further recommended that assessments continue to be
developed as the recommendations are implemented (i.e., the regulatory
process should not be halted until all recommendations can be enacted).
Improvements will thus be made over time and the best science available
will be used in the interim. Further, the EPA has a legal obligation to
proceed with regulatory action based on the best, currently available
tools.
    The EPA's conclusion that HCl, HF and Cl2 are threshold
pollutants is based on the best available toxicity database considered
in hazard identification and dose response assessments. There is
agreement on using a similar threshold approach for these chemicals
across agencies, e.g., the EPA's IRIS Program, ATSDR and CalEPA. The
toxicity assessments (which may include noncancer and/or cancer
toxicity assessments) provided by these authoritative bodies are widely
vetted through the scientific community and undergo rigorous peer
review processes before they are published. In addition, the SAB has
endorsed the use of the reference values derived by these sources to
support EPA's risk assessments in the RTR program.
    Specifically, none of the compounds discussed here has been
classified as carcinogenic or suggestive of the potential to be
carcinogenic, individually or in combination by existing authoritative
bodies including the EPA, CalEPA, IARC, OECD, and the European
Community. In light of the absence of evidence of carcinogenic risk for
any of these pollutants, and the evidence of an existing threshold
below which HCl, HF and Cl2 are not expected to cause
adverse effects, the EPA considers it appropriate to set health
threshold standards under CAA 112(d)(4) for these pollutants.
2. Co-Benefits
    Comment: One commenter stated that the EPA's proposal not to set
MACT standards for acid gases did not fully consider the co-benefits of
controlling criteria pollutants. The commenter noted that the
legislative history makes clear that employing a CAA section 112(d)(4)
standard rather than a conventional MACT standard ``shall not result in
adverse environmental effect which would otherwise be reduced or
eliminated.'' \74\ The EPA asserted that where there is an established
health threshold, the agency may weigh additional factors in making a
judgment as to whether to set CAA section 112(d)(4) standards or MACT
standards, including ``[c]o-benefits that would be achieved via the
MACT standard, such as reductions in emissions of other HAP and/or
criteria pollutants'' (79 FR 75622). The commenter asserted that it is
impossible to make this assessment without evaluating the full
collateral benefits of a MACT standard.
---------------------------------------------------------------------------

    \74\ S. Rep. No. 101-228, at 171.
---------------------------------------------------------------------------

    The commenter noted that the EPA has recognized that MACT standards
for HCl in other source categories resulted in reductions in emissions
of PM, hydrogen cyanide, and other criteria and HAP pollutants and has
relied upon the co-benefits of these reductions as a basis for not
setting risk-based standards for those other source categories.\75\

However, for BSCP and clay ceramics plants, the EPA only considered the
co-benefits of reductions in sulfur dioxide (SO2). The
commenter argued the EPA should have considered the significant
reductions in PM, hydrogen cyanide, and other pollutants that would
likely result from MACT standards for HCl, HF, and Cl2, as
these are the same reductions that the EPA considered in its past
rulemakings. The commenter stated that these reductions will provide
enormous health and environmental benefits that would not occur if CAA
section 112(d)(4) standards are finalized instead.
---------------------------------------------------------------------------

    \75\ See, e.g., National Emission Standards for Hazardous Air
Pollutants from the Portland Cement Manufacturing Industry and
Standards of Performance for Portland Cement Plants, 75 FR 54970,
54984 (Sept. 9, 2010) (``Setting technology-based MACT standards for
HCl . . . would likely also result in additional reductions in
emissions of mercury, along with condensable PM, ammonia, and semi-
volatile compounds.''); id. at 54,985 (``Setting an HCl standard
under 112(d)(2) and (3) allows the Agency to also address'' HCN,
ammonia, and other pollutants.); National Emission Standards for
Hazardous Air Pollutants from the Portland Cement Manufacturing
Industry, 74 FR 21136, 21160 (May 6, 2009) (``[S]etting a MACT
standard for HCl is anticipated to result in a significant amount of
control for other pollutants emitted by cement kilns, most notably
SO2 and other acid gases, along with condensable PM,
ammonia, and semi-volatile compounds.''); 75 FR 32030 (``[S]etting
conventional MACT standards for HCl as well as PM . . . would result
in significant reductions in emissions of other pollutants, most
notably SO2, non-condensable PM, and other non-HAP acid
gases (e.g., hydrogen bromide) and would likely also result in
additional reductions in emissions of mercury and other HAP metals
(e.g., selenium).''); 76 FR 25051 (``[S]etting conventional MACT
standards for HCl as well as PM . . . would result in significant
reductions in emissions of other pollutants, most notably
SO2, PM, and other non-HAP acid gases (e.g., hydrogen
bromide) and would likely also result in additional reductions in
emissions of Hg and other HAP metals (e.g., Se).'').
---------------------------------------------------------------------------

    Response: Although not explicitly stated in the preamble to the
proposed rule, the EPA agrees with the commenter that MACT standards
for acid gases for BSCP manufacturing facilities are associated with
additional reductions of PM emissions (approximately 460 tpy in the
third year following promulgation of the standards) and non-Hg HAP
metals emissions. No additional PM or non-Hg HAP metals emission
reductions would be expected from sanitaryware tunnel kilns because it
is anticipated that all sanitaryware tunnel kilns could meet the MACT
floor emission limits for HF and HCl without additional APCD. The EPA
has no information suggesting that HCN is emitted from BSCP or clay
ceramics manufacturing facilities, so no reduction in HCN would be
expected from MACT standards for HF, HCl, and Cl2.
    For the past rulemakings in which the EPA considered co-benefits as
part of a CAA section 114(d)(4) evaluation, the EPA did not quantify
the PM emissions reductions associated with MACT standards (see 79 FR
75641, footnote 27), so a direct comparison of the co-benefits of the
BSCP Manufacturing NESHAP and the Clay Ceramics Manufacturing NESHAP
with the co-benefits of these other rules for PM is not possible. The
only pollutant with quantified emissions reductions in the co-benefits
analyses for these other rulemakings was SO2, so that was
the pollutant highlighted in the co-benefits analysis for BSCP and clay
ceramics at proposal. The additional nationwide reductions of
SO2 that would be attributable to MACT standards for acid
gases in the BSCP Manufacturing NESHAP are estimated to be only 4,700
tpy in the third year following promulgation of the standards. No
additional nationwide reductions of SO2 would be
attributable to MACT standards for acid gases in the Clay Ceramics
Manufacturing NESHAP because it is anticipated that all sanitaryware
tunnel kilns could meet the MACT floor emission limits without
additional APCD. As noted at proposal, these reductions are
substantially lower than the co-benefits from MACT standards for other
industries for which the EPA has decided not to set a HBEL, and it
would not be expected to provide a significant public health benefit.
3. Ecosystem Impacts
    Comment: One commenter expressed concern about the ecological
impacts of the proposed HBEL for acid gases. The commenter stated that
federal, state and local agencies have struggled for years to reduce
emissions of SO2 and other acid gases to prevent the
devastating effects of acid rain on large ecosystems and noted the
proposed standards would likely result in the acidification of the
ecosystems in close proximity to BSCP and clay ceramics manufacturing
sources. The commenter asserted the ecological impact analysis of the
emissions standards for this proposal is inadequate.
    Response: The EPA disagrees with the commenter that the ecological
analysis is inadequate. The environmental screening analysis evaluated
potential damage and reduced productivity of plants due to chronic
direct exposure to HCl and HF emitted by clay ceramics manufacturing
facilities and BSCP manufacturing facilities into the air. The chronic
90-day benchmarks used in the environmental risk screen for the acid
gases are shown in Table 7 of this preamble and discussed in the
following section.

 Table 7--Acid Gas Benchmarks Included in the Environmental Risk Screen
------------------------------------------------------------------------
                                                          Chronic 90-day
                        Acid gas                           benchmark in
                                                          [mu]g/m\3\ \a\
------------------------------------------------------------------------
Hydrochloric acid--LOEL.................................           \b\50
Hydrofluoric acid--Plant Community LOEL.................             0.5
Hydrofluoric acid--Plant Community LOEL.................             0.4
------------------------------------------------------------------------
\a\ Micrograms per cubic meter.
\b\ Note that the human health RfC is 20 [micro]g/m\3\, which is lower
  than the ecological benchmark.

    For HCl, the EPA identified chronic benchmark concentrations as
described in a 2009 EPA document on RTR risk assessment
methodologies.\76\ The chronic benchmark for HCl was based on a lowest
observed effects level (LOEL) from a short-term exposure (20 minutes)
that related HCl concentration to ``changes'' in the leaves of 7 out of
8 plant species as reported by Lerman et al.\77\ It was the lowest
exposure concentration at which effects of any type were seen (visible
injury to some proportion of leaves). Haber's law was used to
extrapolate the 1.5 mg/m\3\ LOEL concentration (20-minute exposure) to
a 0.5 mg/m\3\ concentration expected to produce the same effect after 1
hour. The 1-hour estimated LOEL was extrapolated to a chronic benchmark
by dividing by a factor of ten to yield 0.050 mg/m\3\, or 50 [micro]g/
m\3\.
---------------------------------------------------------------------------

    \76\ U.S. EPA, 2009. Risk and Technology Review (RTR) Risk
Assessment Methodologies: For Review by the EPA's Science Advisory
Board with Case Studies--MACT I Petroleum Refining Sources and
Portland Cement Manufacturing. EPA-452/R-09-006. Docket Item No.
EPA-HQ-OAR-2013-0291-0044.
    \77\ Lerman, S., O.C. Taylor, and E.F. Darley, 1976.
Phytotoxicity of Hydrogen Chloride Gas with a Short-Term Exposure.
Atmospheric Environment, Vol. 10, pp. 873-878.
---------------------------------------------------------------------------

    For HF, the EPA used two chronic benchmark concentrations for
plants in the environmental screening analysis. The value of 0.5 [mu]g
HF/m\3\ is based on the Washington State criterion for gaseous HF and
represents a LOEL. The value of 0.4 [mu]g HF/m\3\ is based on the
Environment Canada criteria and also represents a LOEL.
    To protect vegetation from adverse effects resulting from HF
exposure, the Canadian Council of Ministers of the Environment \78\
recommends that HF concentrations not exceed 0.4 [mu]g/m\3\ over a 30-
to 90-day period; HF concentrations can be higher for shorter
exposures). Environment Canada \79\ defined the effect represented by
the level of 0.4 [mu]g HF/m\3\ as:
---------------------------------------------------------------------------

    \78\ CCME. 1999b. Canadian National Ambient Air Quality
Objectives: Process and Status. In: Canadian Environmental Quality
Guidelines, 1999, Canadian Council of Ministers of the Environment,
Winnipeg. Publication No. 1299, ISBN 1-896997-34-1. Available at
http://ceqg-rcqe.ccme.ca/download/en/133/.
    \79\ EC. (Environment Canada). 1996. National Ambient Air
Quality Objectives for Hydrogen Fluoride (HF). Science Assessment
Document. A Report by the CEPA/FPAC Working Group on Air Quality
Objectives and Guidelines. July. ISBN 0-662-25641-7, Catalogue En42-
17/6-1997. Available online at: http://www.bape.gouv.qc.ca/sections/mandats/ap50_rio_tinto_alcan/documents/DQ3.1.1.pdf.

    The level above which there are demonstrated effects on human
health and/

or the environment. It is scientifically based and defines the
boundary between the lowest observed adverse effect level (LOAEL)
and the no observed adverse effect level (NOAEL). It is considered
to be the level of exposure just below that most likely to result in
a defined and identifiable but minimal effect. The reference levels
have no safety factors applied to them, as they are related directly
to the LOAEL, and are the most conservative estimates of the effect
---------------------------------------------------------------------------
level.

    High concentrations of HF in the air have also been linked to
fluorosis in livestock. However, the HF concentrations at which
fluorosis in livestock occur are higher than those at which plant
damage begins. Therefore, the benchmarks for plants are protective of
both plants and livestock.
    For Clay Ceramics Manufacturing facilities, the environmental risk
screen indicated that the area-weighted average modeled concentration
of HCl around each facility (i.e., the area-weighted average
concentration of all offsite data points in the modeling domain) did
not exceed the ecological benchmark. In addition, the ecological
benchmark was not exceeded at any offsite receptor location for any
facility. For HF, the environmental risk screen indicated that the
area-weighted average modeled concentration of HF around each Clay
Ceramics Manufacturing facility did not exceed the ecological
benchmark. There were multiple facilities with modeled concentrations
of HF at offsite receptor locations that exceeded the ecological
benchmark, but the area over which the value was exceeded was no
greater than 1 percent of the offsite modeling domain for each
facility, indicating that there would not be any significant or
widespread environmental effects.
    For BSCP Manufacturing facilities, the environmental risk screen
indicated that the area-weighted average modeled concentrations of HCl
and HF around each facility (i.e., the area-weighted average
concentration of all offsite data points in the modeling domain) did
not exceed the ecological benchmarks. In addition, the area over which
the HCl or HF benchmarks were exceeded was less than 1 percent of the
offsite modeling domain for each facility in the category, indicating
that there would not be any significant or widespread environmental
effects.
    The EPA did not conduct an assessment of the potential for
emissions of HCl to cause acidification in close proximity to the
sources in this category. Acid deposition, more commonly known as acid
rain, primarily occurs when emissions of SO2 and nitrogen
oxides (NOX) react in the atmosphere (with water, oxygen,
and oxidants) to form various acidic compounds.\80\ Although some
studies indicate that HCl emissions could contribute to acidification
around emission sources in certain environments,\81\ its overall effect
relative to NOX and SO2 emissions would be small.
In addition, the commenter did not provide any data to support their
assertion that the proposed standards would result in the acidification
of the ecosystems in close proximity to BSCP and structural clay
products manufacturing facilities.
---------------------------------------------------------------------------

    \80\ National Acid Precipitation Assessment Program Report to
Congress, 2005. Also see--http://www.epa.gov/acidrain/reducing/index.html.
    \81\ Hydrochloric Acid: An Overlooked Driver of Environmental
Change. Environmental Science and Technology 2011, 45, 1187-1894.
---------------------------------------------------------------------------

4. Cumulative Effects
    Comment: One commenter expressed concern that the EPA did not fully
consider the cumulative effects of exposure to HAP when proposing the
health-based standard under CAA section 112(d)(4). The commenter
asserted that the agency assumed there are no cumulative health and
environmental impacts of concern and argued the EPA cannot ensure that
its proposed standards include an ample margin of safety without
properly accounting for the additive and/or synergistic effects of
multiple pollutants and the cumulative effects of nearby emissions.
    Another commenter stated that the EPA made no adjustments to the
HBEL it selected to account for the potential for harm from exposures
other than to the amounts of HCl, HF, and Cl2 it proposed to
allow. Specifically, the EPA must consider emissions of HCl, HF, and
Cl2 and other pollutants with biologically similar endpoints
(i.e., that cause respiratory harm) from sources in the source category
as well as from any co-located sources and other stationary or mobile
sources located such that their emissions affect people who are also
exposed to the emissions subject to the NESHAP. The commenter asserted
that the EPA cannot lawfully set limits ``with an ample margin of
safety'' when it ignores other sources of exposure and cumulative
health effects. The commenter asserted that, to protect exposed
populations, the regulated sources must reduce their emissions to a
level that ensures the total concentration of pollutants will remain
below the pollutants' respective health thresholds. The commenter
asserted that the EPA's decision to ignore the impact of other
emissions and background concentrations in the implementation of the
HBEL is therefore arbitrary, capricious, an abuse of discretion, and
otherwise not in accordance with law.
    If the ambient concentration of a particular pollutant is already
at or near the health threshold, the commenter asserted that an
additional source of that pollutant or another pollutant with a
biologically similar endpoint can push the exposure over the threshold,
even if the additional source emits the pollutant at low
concentrations. The total risk that is unacceptable for the most-
exposed person in each source category must be reduced to consider the
cumulative effect of these additional exposures and to create a total
risk from all regulated source categories. The commenter stated that
EPA's assessment of cumulative risks posed by HCl, HF, and
Cl2 emissions ignored emissions from co-located sources (for
BSCP kilns), nearby sources and all other potential sources that could
contribute to background levels. The commenter noted that the EPA has
emissions information about co-located and nearby sources in its own
databases but failed to evaluate whether cumulative exposures would
exceed the health thresholds and to consider combined exposures. The
commenter reviewed reports from the EPA's Enforcement and Compliance
History Online (ECHO) Web site for a number of BSCP and clay ceramics
facilities and provided notes on other major source facilities in close
proximity. The commenter stated that the EPA's justifications regarding
cumulative nearby emissions are legally inadequate and factually
inaccurate. The commenter stated that general assertions that other
operations are not ``commonly'' co-located with BSCP and clay ceramics
facilities, that such facilities are ``typically'' located on large
tracts of land, and that facilities are set back from property lines in
rural areas are insufficient to set the emissions standard at a level
that protects all people living near such facilities.
    The commenter stated that information in the EPA's own databases
demonstrates that BSCP and clay ceramics facilities are not
predominantly located in rural, sparsely populated areas, as the EPA
assumes. Many of the BSCP facilities are located in urban areas,
including Boral Bricks in Terre Haute, Indiana; Hanson Brick in
Columbia, South Carolina; General Shale Brick in Denver, Colorado; and
Cherokee Brick & Tile in Macon, Georgia.\82\ Similarly, in the clay

ceramics source category, only two of the sources are located in areas
considered ``rural'' by the United States Census Bureau: American
Marazzi Tile in Sunnyvale, Texas, and the Kohler Wisconsin Plant
outside of Sheboygan, Wisconsin.\83\
---------------------------------------------------------------------------

    \82\ U.S. Census Bureau, 2010 Census Urban and Rural
Classification and Urban Area Criteria: Lists of 2010 Census Urban
Areas, http://www2.census.gov/geo/docs/reference/ua/ua_list_all.xls.
    \83\ U.S. Census Bureau, 2010 Census Urban and Rural
Classification and Urban Area Criteria,  https://www.census.gov/geo/reference/ua/urban-rural-2010.html (revised Feb. 9, 2015) (searching
plant location by city listed in address).
---------------------------------------------------------------------------

    The commenter stated that the EPA's assessment of cumulative risks
does not meet generally accepted good practices in risk assessment. The
SAB recommended in May 2010 that the EPA incorporate ``aggregate and
cumulative risks, including background concentrations and contributions
from other sources in the area'' into its risk analysis.\84\ The
commenter stated that the EPA must assess the total and cumulative risk
burden, rather than only looking at each type of risk in a discrete,
separate way, and the EPA should be integrating its assessments and
performing a ``comprehensive risk assessment'' as the NAS has
emphasized. After first assessing the total cancer, chronic non-cancer,
and acute risks, for both inhalation and multipathway exposure, the EPA
also must assess the total risks.\85\ The EPA must aggregate health
risk for each pollutant, and each type of health risk, to create a
cumulative risk determination for an individual with maximum exposure.
Without a combined health risk metric, the EPA cannot make an ample
margin of safety determination that is based on the full picture of
health risk for these source categories.
---------------------------------------------------------------------------

    \84\ Memorandum from Science Advisory Board, U.S. EPA, to Lisa
Jackson, Adm'r, U.S. EPA re: Review of EPA's Draft, EPA-SAB-10-007
at 6 (May 7, 2010).
    \85\ CalEPA, OEHHA, Cumulative Impacts at 19-21, 25 (describing
total ``pollution burden'' as sum of exposures, public health
effects, and environmental effects); EPA, Concepts, Methods and Data
Sources for Cumulative Health Risk Assessment of Multiple Chemicals,
Exposures and Effects, at 4-42 to 4-46 (Aug. 2007).
---------------------------------------------------------------------------

    Finally, the commenter stated that this proposal is contrary to the
EPA's recent conclusion in its regulation of power plant electric
generating units that ``the potential cumulative public health and
environmental effects of acid gas emissions'' did not allow for CAA
section 112(d)(4) standards.\86\ In that rulemaking, the EPA did not
receive facility-specific emissions information for all the acid gases
from units in the source category, co-located sources, and all nearby
sources. The EPA concluded that ``cumulative impacts of acid gases on
public health were not assuaged by the comments received.'' The
commenter stated that the EPA did not consider that information in this
rulemaking either, and just as in the power plant rulemaking, HBEL are
not lawful.
---------------------------------------------------------------------------

    \86\ Responses to Public Comments on EPA's National Emission
Standards for Hazardous Air Pollutants from Coal- and Oil-Fired
Electric Utility Steam Generating Units, vol. 1. Docket Item No.
EPA-HQ-OAR-2009-0234-20126.
---------------------------------------------------------------------------

    Response: The EPA disagrees with the commenter that the EPA did not
consider the potential impacts of nearby BSCP and clay ceramics
facilities or other nearby facilities in the determination of the HBEL
for each source category. The limit reflects the impacts of all
facilities in the source category. While the risk assessment did not
perform a detailed modeling analysis of other nearby facilities, based
on a proximity analysis of sources emitting acid gases, the EPA
concludes that the emissions from these facilities would not have
significantly impacted the analysis for several reasons. First, the
limit reflects a hazard index (HI) less than or equal to one at the
highest impacted receptor at each facility. For source categories like
BSCP and clay ceramics where emission release heights are low, the
highest impacted receptor is always very near (e.g., shares a common
fenceline) the facility, and ambient concentrations fall quickly with
distance from the source. Because of this, other facilities would have
to be very near a BSCP or clay ceramics facility and have relatively
high emissions to have any significant impact on the receptor with the
highest estimated concentration from the BSCP or clay ceramics
emissions. As in risk assessments performed under the Risk and
Technology Review program, the EPA did not model the nearby sources in
the National Emissions Inventory (NEI) because that inventory has not
received the same level of review and quality assurance that the BSCP
emissions have for the purposes of this rulemaking.
    Although the EPA did not model the other nearby facilities, the EPA
did compare the location of all sources emitting acid gases with the
locations of the BSCP and clay ceramics facilities. The EPA found that
only four facilities emitted acid gases within 1 kilometer of any BSCP
facility. Beyond 1 kilometer, we would expect very little coincidental
impacts from multiple low level sources emitting the same pollutants.
The largest of these facilities emitted less than 12 tpy of HCl-
equivalent emissions, or less than 5 percent of the emissions limit.
The estimated HI for this BSCP facility was 0.6, so an increase of 5
percent in emissions would result in an increase in HI of at most 5
percent and, thus, not increase the HI above a value of 1. There are no
other sources emitting acid gases within 1 kilometer of any clay
ceramics facility.
    Also, for the BSCP plant with the highest estimated HI, there are
no other acid gas emissions indicated in the NEI within 5 kilometers of
the facility. For the clay ceramics plant with the highest estimated
HI, there are no other acid gas emissions indicated in the NEI within
10 kilometers of the facility. Thus, we would not expect emissions of
acid gases from other sources to contribute significantly at the
receptors where the maximum HI occurs due to BSCP or clay ceramic
emissions, and the HI at these receptors would not exceed 1.
5. Risk Assessment
    Comment: One commenter stated that the Human Exposure Model (HEM-3)
meteorological data used for dispersion calculations was insufficient
because it included data for only 1 year (2011) from only 824
meteorological stations. The commenter asserted that this provides a
very limited snapshot of air quality data and, therefore, is
insufficient to determine with confidence that exposures at the
proposed emissions standards pose ``no risk'' of adverse health
effects. The commenter stated that it is unlawful and arbitrary to set
CAA section 112(d)(4) standards without more extensive air quality
information.
    Response: The EPA disagrees with the commenter that the
meteorological data were insufficient to perform the risk assessment.
Although 5 years of meteorological data are preferred for assessing
chronic exposures and risks, we use a single year (2011) of
meteorological data in our risk assessments because of model run times
for the Human Exposure Model (HEM-3) air dispersion model (AERMOD).
Because we frequently run AERMOD for an entire source category with
many individual emissions points and for many receptors, using 5 years
of meteorological data would increase already significant model run
times by a factor of five compared to a single year. In a sensitivity
analysis of the impact of using a single year of meteorological data
compared to 5 years,\87\ we found that modeled concentrations differed
by less than 10 percent on average and, thus, the use of

1 year of meteorological data is not likely to appreciably affect the
results of the risk assessment.
---------------------------------------------------------------------------

    \87\ U.S. EPA, 2009. Risk and Technology Review (RTR) Risk
Assessment Methodologies: For Review by the EPA's Science Advisory
Board with Case Studies--MACT I Petroleum Refining Sources and
Portland Cement Manufacturing. EPA-452/R-09-006. Docket Item No.
EPA-HQ-OAR-2013-0291-0044.
---------------------------------------------------------------------------

    The meteorological data we used were obtained from the Automated
Surface Observing Systems (ASOS) program, which is a joint effort of
the National Weather Service (NWS), the Federal Aviation Administration
(FAA), and the Department of Defense (DOD). The ASOS serves as the
nation's primary surface weather observing network and is designed to
support weather forecast activities and aviation operations and, at the
same time, support the needs of the meteorological, hydrological, and
climatological research communities. With the largest and most modern
complement of weather sensors, ASOS has significantly expanded the
amount of available meteorological information. The ASOS works non-
stop, updating observations every minute, 24 hours a day, every day of
the year. The ASOS is installed at more than 900 airports across the
country, and our meteorological library for the year 2011 includes all
of these that are without a significant number of missing hours (824
stations).
    Comment: Two commenters stated that the EPA's modeling understates
chronic health risk by assuming that chronic exposure to HAP from BSCP
and clay ceramic manufacturing sources occurs at the census block
centroid and not at the facility fence or property line. The commenters
stated that exposures are likely to be higher for people living closest
to the plants, especially because census blocks can cover a large area
and the center of a census block is almost always farther away from the
facility than the facility's property line. One commenter noted that
even if the area near the property line is not developed, over time
homes and businesses could locate closer to the facility. While it is
possible that population distribution is homogenous over a census
block, the commenter stated this assumption is not necessarily accurate
in considering the predicted impacts from the location of a source.
    One commenter stated that no effort was made to move receptor
points closer to the facility to assess chronic or cancer risk, even in
those instances where local residents live nearer to a facility than
the geographic centroid of the census block. This conflicts with the
recommendation of the SAB, which has urged the EPA to consider
``specific locations of residences.'' \88\ The commenter stated that
the EPA failed to adjust receptor points for residents living on the
fence-line even though the HEM-AERMOD system allows for such an
adjustment, and that such an adjustment was appropriately made for the
estimation of acute health risks (see, e.g., 79 FR 75644). The
commenter stated that the EPA cannot justify failing to analyze chronic
health effects in a similar manner.
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    \88\ Memorandum from Science Advisory Board, U.S. EPA, to Lisa
Jackson, Administrator, U.S. EPA re: Review of EPA's Draft entitled,
``Risk and Technology Review (RTR) Risk Assessment Methodologies:
For Review by the EPA's Science Advisory Board with Case Studies--
MACT I Petroleum Refining Sources and Portland Cement
Manufacturing'' at 4. May 7, 2010.
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    Another commenter agreed and stated that the EPA can use HEM-3 to
identify the maximum individual risk at any point in a census block
that is within a 50-kilometer radius from the center of the modeled
facility. The commenter recommended the EPA not use the predicted
chronic exposures at the census block centroid as a surrogate for the
exposure concentrations for all people living in that block; instead,
the EPA should use the maximum individual risk in its risk assessments,
irrespective of its location in the census block.
    Response: The EPA disagrees with the commenters' assertion that we
relied solely on the census block centroids as receptors for human
exposure. As we have noted in the development of RTR regulations, in a
national-scale assessment of lifetime inhalation exposures and health
risks from facilities in a source category, it is appropriate to
identify exposure locations where it may be reasonably expected that an
individual will spend a majority of his or her lifetime. Further, in
determining chronic risks, it is appropriate to use census block
information on where people actually reside, rather than points on a
fenceline, to locate the estimation of exposures and risks to
individuals living near such facilities.
    Census blocks are the finest resolution available as part of the
nationwide population data (as developed by the U.S. Census Bureau);
each is typically comprised of approximately 50 people, or about 20
households. In the EPA risk assessments, the geographic centroid of
each census block containing at least one person is used to represent
the location where all the people in that census block live. The census
block centroid with the highest estimated exposure then becomes the
location of maximum exposure, and the entire population of that census
block is assumed to experience the maximum individual risk. In some
cases, because actual residence locations may be closer to or farther
from facility emission points, this may result in an overestimate or
underestimate of the actual annual concentrations (although there is no
systematic bias for average levels). Given the relatively small
dimensions of census blocks in densely populated areas, there is little
uncertainty introduced by using the census block centroids in lieu of
actual residence locations. There is the potential for more uncertainty
when census blocks are larger, although there is still no systematic
bias. The EPA concludes that the most appropriate locations at which to
estimate chronic exposures and risks are the census block centroids
because: (1) Census blocks are the finest resolution available in the
national census data, (2) facility fencelines do not usually represent
locations where chronic exposures are likely and (3) there is no bias
introduced into the estimate of the MIR by using census block centroid
locations. In addition, in its peer review of the methodologies used to
estimate risks as part of the RTR rulemaking efforts, the EPA's SAB
endorsed this approach.
    In addition to the approach described above, the EPA recognizes
that where a census block centroid is located on industrial property or
is large and the centroid is less likely to be representative of the
block's residential locations, the block centroid may not be the
appropriate surrogate. For BSCP facilities, in cases where a census
block centroid was within 300 meters of any emission source (and
therefore possibly on facility property), we viewed aerial images of
the facility to determine whether the block centroid was likely located
on facility property. Likewise, we examined aerial images of all large
census blocks within 1 kilometer of any emission source. If the block
centroid did not represent the residential locations within that block,
we relocated it to better represent them and/or we added additional
receptors for residences nearer to the facility than the centroid. For
this source category, we relocated 14 census blocks that appeared to be
on facility property or were otherwise not representative of the
population within the block, and we modeled an additional 15 receptors
in cases where the single block centroid was inadequate to characterize
the population within the census blocks.
    Comment: One commenter stated that the EPA's risk assessment did
not account for the synergistic health effects from the potential
exposure to multiple acid gas pollutants. Specifically, the EPA did not
demonstrate that no health effects would occur if a person is
chronically exposed to a combination of

HCl, HF, and Cl2, even if the sum of the exposures
(converted into ``equivalent'' units) does not exceed the ``HCl-
equivalent'' limit. The commenter also argued the EPA failed to provide
evidence showing that the acid gases would not have synergistic effects
that could cause harm at a chronic exposure concentration that is lower
than the RfC, REL, or MRL of each pollutant. The commenter asserted the
EPA did not seek outside peer review by the SAB or other body or
request public comment on its use of dose-response values to exchange
exposures of one acid gas pollutant for another prior to proposing use
of ``HCl-equivalents'' standards.
    The commenter stated that since the EPA based the ratio for
comparing HF and Cl2 emissions to HCl emissions on the RfC,
REL or MRL values, and those values are uncertain and flawed (see
previous comments in this section V.A, explaining that values were not
based on a NOAEL, and the EPA has ``low'' confidence in the HCl RfC),
the HCl-equivalent method cannot assure ``an ample margin of safety.''
The commenter asserted that CAA section 112(d)(4) requires the EPA to
set separate standards for HCl and HF, and the EPA's decision to set a
HCl-equivalent emissions standard is unlawful and arbitrary.
    Response: The EPA believes that groups of chemicals can behave
antagonistically or synergistically, such that combined exposure can
either cause less or more harm, depending on the chemicals. To address
pollutant mixtures in the determination of the HBEL, the EPA generally
used the same methodology used in RTR assessments, which is to follow
the EPA's mixture guidelines.89 90 This methodology has been
formally peer reviewed by the SAB.\91\ Following the mixture
guidelines, the EPA aggregated noncancer hazard quotients (HQs) of HAP
that act by similar toxic modes of action or that affect the same
target organ. This process creates, for each target organ, a target-
organ-specific hazard index (TOSHI), defined as the sum of HQs for
individual HAP that affect the same organ or organ system. All TOSHI
calculations were based exclusively on effects occurring at the
``critical dose'' (i.e., the lowest dose that produces adverse health
effects). The EPA actually calculated the HBEL conservatively by
including HF in the calculation of equivalent emissions even though it
affects a different target organ than HCl and Cl2, thereby
allowing the development of a single emissions limit for all acid
gases. The conservatism in the limit due to the inclusion of pollutants
with different target organ systems would have the effect of
ameliorating potential synergism of the acid gases.
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    \89\ U.S. EPA, 1986. Guidelines for the Health Risk Assessment
of Chemical Mixtures. EPA-630-R-98-002. September 1986.
    \90\ U.S. EPA, 2000. Supplementary Guidance for Conducting
Health Risk Assessment of Chemical Mixtures. August 2000.
    \91\ U.S. EPA Science Advisory Board, 2010. Review of EPA's
draft entitled, ``Risk and Technology Review (RTR) Risk Assessment
Methodologies: For Review by the EPA's Science Advisory Board with
Case Studies--MACT I Petroleum Refining Sources and Portland Cement
Manufacturing.'' May 7, 2010. Available at: http://yosemite.epa.gov/
sab/sabproduct.nsf/4AB3966E263D943A8525771F00668381/$File/EPA-SAB-
10-007-unsigned.pdf.
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6. Ample Margin of Safety
    Comment: One commenter disagreed with the EPA's decision to set an
HCl-equivalent HBEL, rather than set separate HBEL for HCl, HF, and
Cl2. The commenter stated that, by setting one ``HCl-
equivalent emissions'' limit at 250 tpy (57 lb/hr) for BSCP tunnel
kilns and 600 tpy (140 lb/hr) for clay ceramics sources, each source is
free to emit whatever combination of HCl, HF, and Cl2 it
would like, provided the aggregate of the ``HCl-equivalent emissions''
does not exceed the limit. The commenter also noted that the HCl-
equivalent HBEL for clay ceramics does not include Cl2 and
requested that the EPA explain how it converted Cl2 into
HCl-equivalent emissions.
    The commenter stated that CAA section 112(d)(2) mandates that the
EPA ``shall require the maximum degree of reduction in emissions of the
hazardous air pollutants subject to this section.'' The commenter
asserted that it is unlawful for the EPA not to set an emissions limit
for a CAA section 112-listed pollutant (Nat'l Lime Ass'n, 233 F.3d at
634) and concluded that even if the EPA believes the health risks posed
by HF and Cl2 emissions can be translated into HCl-
equivalent units, the proposed ``HCl-equivalent'' limit contravenes the
EPA's obligation to set CAA section 112(d) standards for each
pollutant.
    The commenter also stated that the EPA's approach raises questions
about whether the use of ``HCl-equivalents'' results in limits that
protect people against all of a pollutant's health risks with ``an
ample margin of safety,'' as required by CAA section 112(d)(4). The
commenter argued that because pollutants cause different adverse health
effects, they are not ``equivalent'' pollutants that cause
``equivalent'' health effects at ``equivalent'' concentrations of
exposure. The commenter further argued the RfC for HCl is based on a
study of respiratory toxicity and is meant to protect individuals
against respiratory harms from chronic exposures, while the REL used
for HF is based on a study of skeletal fluorosis (increased bone
density) and is meant to protect individuals against skeletal harm from
chronic exposures.\92\ The commenter noted that the EPA focused only on
the respiratory harm caused by the pollutants, when skeletal harm is
the most sensitive effect for HF, and the EPA failed to explain why
skeletal harm caused by a certain quantity of HF can be converted into
respiratory harm caused by HCl.
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    \92\ OEHHA, Chronic RELs and Toxicity Summaries, at 278. CalEPA
made it clear that its REL is for ``[i]ncreased bone density
(skeletal fluorosis),'' that the NOAEL was for ``chronic skeletal
fluorosis,'' and that ``[c]hanges in bone density . . . appear[s] to
be the most sensitive health effect for chronic exposure.'' OEHHA,
Chronic RELs and Toxicity Summaries at 272, 278-79. The principal
study on which the REL is based did observe an increase in the
incidence of acute respiratory disease, too, id. at 271, but the REL
was not primarily based on that health effect.
---------------------------------------------------------------------------

    The commenter also noted that the EPA does not claim to be using
HCl as a surrogate for HF or Cl2. The commenter stated that
the EPA previously stated that HCl cannot act as a surrogate for the
other acid gases because pollutants that act on humans in different
manners, at different doses, cannot stand in for one another (see 76 FR
25049 and 75 FR 32031).
    Another commenter expressed concern the HCl-equivalent emissions
limit could mask exposures or emissions of concern for the most toxic
gas because the comparison would be dominated by a higher concentration
pertinent to the less toxic gases. The commenter asserted that there is
no analysis that justifies this combined metric and noted it would be
more justifiable if the substances were in the same order of magnitude
for potential potency. The commenter recommended that the EPA consider
whether these gases could contribute to the acid component of ambient
air that is thought to potentially contribute to cancer and other
effects because these impacts appear not to have been considered by the
EPA.
    Response: The EPA disagrees with the commenters' assertion that the
HBEL cannot be based on equivalent emissions of a single pollutant. For
the BSCP Manufacturing rulemaking, the EPA used an approach specific
for this NESHAP to set health-protective emissions limits that would
account for the multiple acid gas pollutants emitted by the BSCP
facilities. By converting the emissions of each acid gas or combination
of acid gases (HCl, Cl2 and

HF) to an HCl-equivalent emission, the EPA can estimate a single
exposure concentrations for comparison with the HCl reference value
(RfC). If the ratio of HCl exposure concentration to the HCl RfC value
remains at or below 1, the HBEL (HCl-equivalent emissions) would ensure
that the threshold values for any individual or combination of acid
gases would not be exceeded (i.e., remain at or below 1). The EPA used
the same approach to convert emissions of HF to an HCl-equivalent and
determine the HBEL for the Clay Ceramics Manufacturing NESHAP; the only
difference is that there are no valid Cl2 emissions data for
clay ceramics facilities, so Cl2 is not included in the
HBEL.
    Comment: Two commenters generally supported the proposed HBEL and
stated that the EPA has conclusively demonstrated that the proposed
HBEL would provide an ample margin of safety for HCl, HF, and
Cl2 emissions from affected facilities. As the EPA explained
in the proposal, the analysis was based on site specific data from each
tunnel kiln, and the proposed HBEL was developed at a level that would
result in an HQ of 1 at the worst-case facility. Because the potential
risks at facilities other than the worst-case facility are predicted to
be well below 1, the commenters stated that this analysis assures that
an ample margin of safety will be provided for the ``worst case''
facility in the industry and more than an ample margin will be provided
for all other affected facilities.
    Conversely, another commenter contended that the EPA's proposed
HBEL under CAA section 112(d)(4) does not include ``an ample margin of
safety.'' The commenter disagreed with the approach the EPA used to
determine the CAA section 112(d)(4) limits. Specifically, the commenter
stated that by setting the limits at precisely the same level as the
threshold value, the EPA proposed to allow plants to emit acid gas
pollution that would expose people to amounts of pollution that reach
threshold levels.
    The commenter stated that these limits do not include any ``margin
of safety,'' let alone an ``ample'' one, as the EPA is required to
include for CAA section 112(d)(4) standards. The commenter expressed
concern that under the EPA's approach, even the slightest uncertainty
in the EPA's estimates or low background levels of pollution can place
health at risk because plants can emit at the health threshold. The
commenter stated that the EPA did not explain how these limits would
protect public health with ``an ample margin of safety.'' \93\ The
commenter asserted that a margin of safety is supposed to provide
additional safety and account for uncertainty and variability that
might result in harm to individuals below the threshold. The commenter
further stated that an ``ample'' margin of safety must assure not only
extra room for safety, but a ``generous'' margin for safety.\94\
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    \93\ Mountain Commc'ns v. FCC, 355 F.3d 644, 648-49 (D.C. Cir.
2004) (agency must ``explain how its position can be reconciled''
with statutory requirements).
    \94\ Webster's Seventh New Collegiate Dictionary (1971) defines
``margin'' as ``a spare amount or measure or degree allowed or given
for contingencies or special situations'' and ``ample'' as
``generous or more than adequate in size, scope, or capacity.''
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    The commenter noted that a TOSHI (which is the sum of the HQs) of
``one'' does not necessarily represent a safe level of exposure. The
commenter asserted the EPA characterizes a TOSHI or HQ of ``one'' or
less as exposures that ``are not likely to cause adverse health
effects'' (79 FR 75643), but did not provide any explanation why this
level would meet the statutory standard. According to the commenter,
Congress intended the standard to be set at a level at which there is
``no risk'' of ``adverse health effects,'' plus ``an ample margin of
safety (and not considering cost).'' \95\ For these reasons, the
commenter concluded that the proposed limits do not comply with the CAA
and could put public health at risk.
---------------------------------------------------------------------------

    \95\ S. Rep. No. 101-228, at 171.
---------------------------------------------------------------------------

    The commenter also expressed concern that the EPA did not take
steps to adjust the limits to reflect the uncertainties regarding
health exposures and effects. The EPA has factored in uncertainties and
vulnerability factors in other rulemakings, such as when determining a
Target Margin of Exposure under the FQPA, where the EPA considered
whether risks below the Target Margin of Exposure warranted increased
scrutiny and changes to allowable exposures.\96\ The commenter also
stated that the EPA's proposed limits would allow human exposures to
exceed the level that CalEPA has identified is the safety minimum.
Allowing human exposure to HCl concentrations above a threshold a state
agency determined may cause respiratory harm, the commenter contended,
would not provide the ample margin of safety required by law.
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    \96\ See, e.g., EPA, Sulfuryl Fluoride; Proposed Order Granting
Objections to Tolerances and Denying Request for a Stay, Proposed
Rule, 76 FR 3422, 3427 (Jan. 19, 2011) (explaining use of MOE).
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    The commenter further stated that the ``ample margin of safety''
language in CAA section 112(d)(4) requires that any standard that is
set under this authority must be sufficient to protect against
significant unforeseen consequences.\97\ The commenter stated that
because the ``ample margin of safety'' requirement is meant to protect
against risks that have not yet been identified in research, a CAA
section 112(d)(4) standard cannot be justified on grounds that the EPA
does not have sufficient evidence about the health risks posed by a HAP
or does not have the time or inclination to review the evidence that is
available.
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    \97\ See, e.g., Envtl. Def. Fund v. EPA, 598 F.2d 62, 81 (D.C.
Cir. 1978) (holding that the phrase `ample margin of safety' in the
Clean Water Act's toxic provisions required the EPA to protect
against as yet unidentified risks to human health, including those
``which research has not yet identified'').
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    Response: For several reasons, the EPA disagrees with the commenter
who stated that the HBEL does not include an ample margin of safety.
First, the limit is based on the single facility in the source category
with the worst-case combination of meteorology and distance to nearest
residential receptor that leads to the highest ambient concentrations.
While the EPA estimates that the limit reflects an HI of one at this
facility, the HI at most other facilities would be significantly lower,
with approximately 90 percent of the facilities having an estimated HI
less than or equal to 0.5. Further as the standard is based on a 1-hour
emission limit, in determining chronic impacts, the analysis
conservatively assumes that each plant emits at the 1-hour HBEL for an
entire year (8,760 hours). Also, the limit is based on estimated
ambient concentrations and not exposure concentrations. Exposure
concentrations are typically lower than ambient concentrations because
they reflect that people's activities (e.g., work, school) remove them
from their residential exposure locations for significant amounts of
time. For these reasons, the EPA concludes that the emission limit is
health protective (i.e., exposures will remain below the threshold
values) and this conservative exposure scenario is consistent with the
``ample margin of safety'' requirement in CAA section 112(d)(4).
    Comment: One commenter expressed concern that the EPA
underestimated acute health risks in the evaluation of the risk of
acute harm from short-term exposures by ignoring variability in short-
term emissions. The commenter noted that the EPA calculated the 1-hour
emissions estimates for its modeling of acute harm by dividing the
annual emissions level by 8,760 hours per year instead of using a
default factor or emissions multiplier to account for higher-than-
average short-term

emissions. The commenter noted actual emissions over a 1-hour period
will at times exceed the average hourly emissions level used in the
modeling. The commenter asserted the EPA did not explain how this
approach captures peak short-term emissions levels or adequately
protects people from short-term exposures at levels above the average.
    The commenter stated that the EPA has used emissions multipliers to
scale up average hourly emissions in air dispersion modeling for other
risk assessments.\98\ The commenter asserted that although emission
multipliers in risk assessments still underestimate risk, these