[Federal Register Volume 78, Number 96 (Friday, May 17, 2013)]
[Rules and Regulations]
[Pages 29032-29034]
[FR Doc No: 2013-11681]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 52

[EPA-R04-OAR-2012-0888; FRL-9814-3]

Approval and Promulgation of Implementation Plans Tennessee:
Revisions to Volatile Organic Compound Definition

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: EPA is taking final action to approve changes to the Tennessee
State Implementation Plan (SIP), submitted by the State of Tennessee,
through the Tennessee Department of Environment and Conservation (TDEC)
on September 3, 1999. Tennessee's September 3, 1999, SIP adds 17
compounds to the list of compounds excluded from the definition of
``Volatile Organic Compound'' (VOC). EPA is approving this SIP revision
because the State has demonstrated that it is consistent with the Clean
Air Act (CAA or Act).

DATES: This rule is effective June 17, 2013.

ADDRESSES: EPA has established a docket for this action under Docket
Identification No. EPA-R04-OAR-2012-0888. All documents in the docket
are listed on the www.regulations.gov Web site. Although listed in the
index, some information is not publicly available, i.e., Confidential
Business Information or other information whose disclosure is
restricted by statute. Certain other material, such as copyrighted
material, is not placed on the Internet and will be publicly available
only in hard copy form. Publicly available docket materials are
available either electronically through www.regulations.gov or in hard
copy at the Regulatory Development Section, Air Planning Branch, Air,
Pesticides and Toxics Management Division, U.S. Environmental
Protection Agency, Region 4, 61 Forsyth Street SW., Atlanta, Georgia
30303-8960. EPA requests that if at all possible, you contact the
person listed in the FOR FURTHER INFORMATION CONTACT section to
schedule your inspection. The Regional Office's official hours of
business are Monday through Friday, 8:30 to 4:30 excluding federal
holidays.

FOR FURTHER INFORMATION CONTACT: Sean Lakeman, Regulatory Development
Section, Air Planning Branch, Air, Pesticides and Toxics Management
Division, U.S. Environmental Protection Agency, Region 4, 61 Forsyth
Street SW., Atlanta, Georgia 30303-8960. The telephone number is (404)
562-9043. Mr. Lakeman can be reached via electronic mail at
<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

Table of Contents

I. Analysis of the State's Submittal
II. Response to Comments
III. Final Action
III. Statutory and Executive Order Reviews

I. Analysis of the State's Submittal

    Tennessee's September 3, 1999, SIP submission changes rule 1200-3-
9-.01 by adding a total of 17 compounds to the list of compounds
excluded from the definition of VOC to be consistent with EPA's
definition of VOC at 40 CFR 51.100(s). The SIP submittal is in response
to EPA's revision to the definition of VOC, (at 40 CFR 51.100(s))
published in the Federal Register on August 25, 1997 (62 FR 44900) and
April 9, 1998 (63 FR 17331) adding the 16 compounds listed below in
Table--1 and the compound methyl acetate, respectively. These compounds
were added to the exclusion list for VOC on the basis that they have a
negligible effect on tropospheric ozone formation. The compounds were
added by EPA through a rulemaking action which provided for public
notice and comment. Today's action approves a SIP revision to update
the Tennessee SIP to be consistent with federal law.
    Tropospheric ozone, commonly known as smog, occurs when VOC and
nitrogen oxide (NOX) react in the atmosphere. Because of the
harmful health effects of ozone, EPA limits the amount of VOC and
NOX that can be released into the atmosphere. VOC are those
compounds of carbon (excluding carbon monoxide, carbon dioxide,
carbonic acid, metallic carbides, or carbonates, and ammonium
carbonate) which form ozone through atmospheric photochemical
reactions. Compounds of carbon (or organic compounds) have different
levels of reactivity; they do not react at the same speed, or do not
form ozone to the same extent. It has been EPA's policy that compounds
of carbon with a negligible level of reactivity need not be regulated
to reduce ozone (42 FR 35314, July 8, 1977). EPA determines whether a
given carbon compound has ``negligible'' reactivity by comparing the
compound's reactivity to the reactivity of ethane. EPA lists these
compounds in its regulations at 40 CFR 51.100(s), and excludes them
from the definition of VOC. The chemicals on this list are often called
``negligibly reactive.'' EPA may periodically revise the list of
negligibly reactive compounds to add compounds to or delete them from
the list.
    TDEC's September 3, 1999, SIP revision changes rule 1200-3-9-.01 to
add a total of 17 compounds to the list of compounds excluded from the
definition of VOC in accordance with the federal list of compounds
designated as having negligible photochemical reactivity at 40 CFR
51.100(s).

                    Table 1-16--Compounds Added to the List of Negligibly Reactive Compounds
----------------------------------------------------------------------------------------------------------------
             Compound                                              Chemical name
----------------------------------------------------------------------------------------------------------------
HFC-32...........................  Difluoromethane.
HFC-161..........................  Ethylfluoride.
HFC-236fa........................  1,1,1,3,3,3-hexafluoropropane.
HFC-245ca........................  1,1,2,2,3-pentafluoropropane.
HFC-245ea........................  1,1,2,3,3-pentafluoropropane.
HFC-245eb........................  1,1,1,2,3-pentafluoropropane.
HFC-245fa........................  1,1,1,3,3-pentafluoropropane.
HFC-236ea........................  1,1,1,2,3,3-hexafluoropropane.
HFC-365mfc.......................  1,1,1,3,3-pentafluorobutane.
HCFC-31..........................  Chlorofluoromethane.
HCFC-123a........................  1,2-dichloro-1,1,2-trifluoroethane.
HCFC-151a........................  1-chloro-1-fluoroethane.
C4F9OCH3.........................  1,1,1,2,2,3,3,4,4-nonafluoro-4-methoxybutane.
(CF3)2CFCF2OCH3..................  2-(difluoromethoxymethyl)-1,1,1,2,3,3,3-heptafluoropropane.
C4F9OC2H5........................  1-ethoxy-1,1,2,2,3,3,4,4,4-nonafluorobutane.

(CF3)CFCF2OC2H5..................  2-(ethoxydifluoromethyl)-1,1,1,2,3,3,3-heptafluoropropane.
----------------------------------------------------------------------------------------------------------------

II. Response to Comments

    On February 19, 2013 (78 FR 11583), EPA published a direct final
action and parallel proposed action to approve Tennessee's September 3,
1999, SIP submission to change rule 1200-3-9-.01 to add a total of 17
compounds to the list of compounds excluded from the definition of VOC
to be consistent with EPA's definition of VOC at 40 CFR 51.100(s). EPA
published a parallel proposal action in the event that adverse comments
were received such that the direct final rule would need to be
withdrawn. Specifically, in the direct final rule, EPA stated that if
adverse comments were received by March 21, 2013, the direct final rule
would be withdrawn and not take effect. EPA further stated that the
corresponding proposed rule would remain in effect and that any adverse
comment comments received would be responded to in a final rule
provided EPA was able to address such comments.\1\ On March 21, 2013,
EPA received a comment. EPA interprets this comment as adverse although
notably, it is arguably not a significant adverse comment requiring a
response. EPA nonetheless withdrew the direct final rule. A summary of
the comment received and EPA's response is provided below.
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    \1\ EPA also noted that an additional public comment period
would not be instituted for the action.
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    Comment: The Commenter stated ``[w]e are against and want
disapproved the desired changes.''
    Response: The Commenter provided a one-sentence statement with no
rationale or basis as to why EPA should not approve Tennessee's
September 3, 1999, SIP revision, except to state that the Commenter
(and all who the Commenter purports to represent) are against it. In
response to the comment which EPA interpreted as adverse, EPA withdrew
the direct final rule. As mentioned in EPA's direct final rulemaking
and again in today's final rule, Tennessee's September 3, 1999, SIP
revision was in direct response to EPA's changes to the federal
definition of VOC, and the purpose of the revision is to ensure that
the Tennessee SIP is consistent with federal regulations. The Commenter
raises no basis on which EPA could take any action other than a full
approval of Tennessee's SIP submittal. Thus, EPA is now taking final
action to approve Tennessee's September 3, 1999, SIP revision.

III. Final Action

    EPA is approving the aforementioned changes to the State of
Tennessee SIP, because they are consistent with EPA's definition of VOC
and the CAA.

III. Statutory and Executive Order Reviews

    Under the CAA, the Administrator is required to approve a SIP
submission that complies with the provisions of the Act and applicable
federal regulations. 42 U.S.C. 7410(k); 40 CFR 52.02(a). Thus, in
reviewing SIP submissions, EPA's role is to approve state choices,
provided that they meet the criteria of the CAA. Accordingly, this
action merely approves state law as meeting federal requirements and
does not impose additional requirements beyond those imposed by state
law. For that reason, this action:
     Is not a ``significant regulatory action'' subject to
review by the Office of Management and Budget under Executive Order
12866 (58 FR 51735, October 4, 1993);
     does not impose an information collection burden under the
provisions of the Paperwork Reduction Act (44 U.S.C. 3501 et seq.);
     is certified as not having a significant economic impact
on a substantial number of small entities under the Regulatory
Flexibility Act (5 U.S.C. 601 et seq.);
     does not contain any unfunded mandate or significantly or
uniquely affect small governments, as described in the Unfunded
Mandates Reform Act of 1995 (Pub. L. 104-4);
     does not have Federalism implications as specified in
Executive Order 13132 (64 FR 43255, August 10, 1999);
     is not an economically significant regulatory action based
on health or safety risks subject to Executive Order 13045 (62 FR
19885, April 23, 1997);
     is not a significant regulatory action subject to
Executive Order 13211 (66 FR 28355, May 22, 2001);
     is not subject to requirements of Section 12(d) of the
National Technology Transfer and Advancement Act of 1995 (15 U.S.C. 272
note) because application of those requirements would be inconsistent
with the CAA; and
     does not provide EPA with the discretionary authority to
address, as appropriate, disproportionate human health or environmental
effects, using practicable and legally permissible methods, under
Executive Order 12898 (59 FR 7629, February 16, 1994).
    In addition, this rule does not have tribal implications as
specified by Executive Order 13175 (65 FR 67249, November 9, 2000),
because the SIP is not approved to apply in Indian country, and EPA
notes that it will not impose substantial direct costs on tribal
governments or preempt tribal law.
    The Congressional Review Act, 5 U.S.C. 801 et seq., as added by the
Small Business Regulatory Enforcement Fairness Act of 1996, generally
provides that before a rule may take effect, the agency promulgating
the rule must submit a rule report, which includes a copy of the rule,
to each House of the Congress and to the Comptroller General of the
United States. EPA will submit a report containing this action and
other required information to the U.S. Senate, the U.S. House of
Representatives, and the Comptroller General of the United States prior
to publication of the rule in the Federal Register. A major rule cannot
take effect until 60 days after it is published in the Federal
Register. This action is not a ``major rule'' as defined by 5 U.S.C.
804(2).
    Under section 307(b)(1) of the CAA, petitions for judicial review
of this action must be filed in the United States Court of Appeals for
the appropriate circuit by July 16, 2013. Filing a petition for
reconsideration by the Administrator of this final rule does not affect
the finality of this action for the purposes of judicial review nor
does it extend the time within which a petition for judicial review may
be filed, and shall not postpone the effectiveness of such rule or
action. Parties with objections to this direct final rule are
encouraged to file any comment in response to the parallel notice of
proposed rulemaking for this action published in the proposed rules
section of today's Federal Register, rather than file an immediate
petition for judicial review of this direct final rule, so that EPA can
withdraw this direct final rule and address the comment in the proposed
rulemaking. This action may not be challenged later in proceedings to
enforce its requirements. See section 307(b)(2).

List of Subjects in 40 CFR Part 52

    Environmental protection, Air pollution control, Incorporation by
reference, Intergovernmental relations, Reporting and recordkeeping
requirements, Volatile organic compounds.

    Dated: May 7, 2013.
A. Stanley Meiburg,
Acting Regional Administrator, Region 4.
    40 CFR part 52, is amended as follows:

PART 52--[AMENDED]

0
1. The authority citation for part 52 continues to read as follows:

    Authority: 42 U.S.C. 7401 et seq.

Subpart RR--Tennessee

0
2. In Sec.  52.2220, table 1 in paragraph (c) is amended by revising
the entry in Table 1 for ``Section 1200-3-9.01'' to read as follows:

Sec.  52.2220  Identification of plan.

* * * * *
    (c) * * *

                                   Table 1--EPA Approved Tennessee Regulations
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                                                         State
     State citation             Title/subject       effective date   EPA approval date         Explanation
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                                                  * * * * * * *
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                               CHAPTER 1200-3-9 CONSTRUCTION AND OPERATING PERMITS
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1200-3-9-.01............  Definitions.............       6/27/2011  5/17/2013 [Insert    On 5/17/2013 EPA
                                                                     first page of        revised this section
                                                                     publication].        to add 17 compounds to
                                                                                the list of compounds
                                                                                excluded from the
                                                                                definition of VOC that
                                                                                was state effective on
                                                                                9/3/1999.
                                                                                EPA is approving
                                                                                Tennessee's July 29,
                                                                                2011, SIP revisions to
                                                                                Chapter 1200-3-9-.01
                                                                                with the exception of
                                                                                the term ``particulate
                                                                                matter emissions'' at
                                                                                1200-03-09-.01(4)(b)47
                                                                                (vi) as part of the
                                                                                definition for
                                                                                ``regulated NSR
                                                                                pollutant'' regarding
                                                                                the inclusion of
                                                                                condensable emissions
                                                                                in applicability
                                                                                determinations and in
                                                                                establishing emissions
                                                                                limitations.
                                                                                EPA approved
                                                                                Tennessee's May 28,
                                                                                2009 SIP revisions to
                                                                                Chapter 1200-3-9-.01
                                                                                with the exception of
                                                                                the ``baseline actual
                                                                                emissions''
                                                                                calculation revision
                                                                                found at 1200-3-9-.01
                                                                                (4)(b)45(i)(III),
                                                                                (4)(b)45(ii)(IV),
                                                                                (5)(b)1(xlvii)(I)(III)
                                                                                and
                                                                                (5)(b)1(xlvii)(II)(IV)
                                                                                of the submittal.

                                                  * * * * * * *
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[FR Doc. 2013-11681 Filed 5-16-13; 8:45 am]
BILLING CODE 6560-50-P


[Federal Register: September 16, 2009 (Volume 74, Number 178)]
[Notices]
[Page 47571-47572]
[DOCID:fr16se09-50]

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ENVIRONMENTAL PROTECTION AGENCY

[EPA-HQ-OPPT-2003-0004; FRL-8437-5]

Access to Confidential Business Information by CGI Federal Inc.

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice.

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SUMMARY: EPA has authorized contractor, CGI Federal Inc. of Fairfax,
VA, to access information which has been submitted to EPA under all
sections of the Toxic Substances Control Act (TSCA). Some of the
information may be claimed or determined to be Confidential Business
Information (CBI).

DATES: Access to the confidential data will occur no sooner than
September 23, 2009.

FOR FURTHER INFORMATION CONTACT: For general information contact: Colby
Lintner, Regulatory Coordinator, Environmental Assistance Division
(7408M), Office of Pollution Prevention and Toxics, Environmental
Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460-
0001; telephone number:<PHONE_NUMBER>; e-mail address: TSCA-
<EMAIL_ADDRESS>    For technical information contact: Scott Sherlock, Environmental
Assistance Division (7408M), Office of Pollution Prevention and Toxics,
Environmental Protection Agency, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460-0001; telephone number:<PHONE_NUMBER>; fax
number:<PHONE_NUMBER>; e-mail address<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Notice Apply to Me?

    This action is directed to the public in general. This action may,
however, be of interest to all who manufacture, process or distribute
industrial chemicals. Since other entities may also be interested, the
Agency has not attempted to describe all the specific entities that may
be affected by this action. If you have any questions regarding the
applicability of this action to a particular entity, consult the
technical person listed under FOR FURTHER INFORMATION CONTACT.

B. How Can I Get Copies of this Document and Other Related Information?

    1. Docket. EPA has established a docket for this action under
docket identification (ID) number EPA-HQ-OPPT-2003-0004. All documents
in the docket are listed in the docket index available at http://
www.regulations.gov. Although listed in the index, some information is
not publicly available, e.g., CBI or other information whose disclosure
is restricted by statute. Certain other material, such as copyrighted
material, will be publicly available only in hard copy. Publicly
available docket materials are available electronically at http://
www.regulations.gov, or, if only available in hard copy, at the OPPT
Docket. The OPPT Docket is located in the EPA Docket Center (EPA/DC) at
Rm. 3334, EPA West Bldg., 1301 Constitution Ave., NW., Washington, DC.
The EPA/DC Public Reading Room hours of operation are 8:30 a.m. to 4:30
p.m., Monday through Friday, excluding Federal holidays. The telephone
number of the EPA/DC Public Reading Room is<PHONE_NUMBER>, and the
telephone number for the OPPT Docket is<PHONE_NUMBER>. Docket visitors
are required to show photographic identification, pass through a metal
detector, and sign the EPA visitor log. All visitor bags are processed
through an X-ray machine and subject to search. Visitors will be
provided an EPA/DC badge that must be visible at all times in the
building and returned upon departure.
    2. Electronic access. You may access this Federal Register document
electronically through the EPA Internet under the ``Federal Register''
listings at http://www.epa.gov/fedrgstr.

II. What Action is the Agency Taking?

    Under Contract Number GS-35F4797H, Task Order Number 1518,
contractor CGI of 12601 Fair Lakes Circle, Fairfax, VA., will assist
the Office of Pollution Prevention and Toxics (OPPT) in developing a
scalable, target-solutions architecture and strategic plan with the
design to handle all TSCA content starting with an appropriate data
mapping/modeling effort. The TSCA-wide aspect of this effort shall
include, but not be limited to, Section 8(a), 8(b) Inventory Update
Report, 8(e), 8(d), Section 4, and Section 12(b) notices.
    In accordance with 40 CFR 2.306(j), EPA has determined that under
Contract Number GS-35F4797H, Task Order Number 1518, CGI will require
access to CBI submitted to EPA under all sections of TSCA to perform
successfully the duties specified under the contract. CGI personnel
will be given access to information submitted to EPA under all sections
of TSCA.
    EPA is issuing this notice to inform all submitters of information
under all sections of TSCA that EPA may provide CGI access to these CBI
materials on a need-to-know basis only. All access to TSCA CBI under
this contract will take place at EPA Headquarters in accordance with
EPA's TSCA CBI Protection Manual.
    Access to TSCA data, including CBI, will continue until March 30,
2012. If the contract is extended, this access will also continue for
the duration of the extended contract without further notice.
    CGI personnel will be required to sign nondisclosure agreements and
will be briefed on appropriate security procedures before they are
permitted access to TSCA CBI.

List of Subjects

    Environmental Protection, Confidential Business Information.

    Dated: September 9, 2009.
 Matthew Leopard,
Acting Director, Information Management Division, Office of Pollution
Prevention and Toxics.

[FR Doc. E9-22291 Filed 9-15-09; 8:45 am]

BILLING CODE 6560-50-S


Phillips et al., ( 2002) F344 rat ( male and female adolescents) Drinking water 6 months, 0, 20, 72, 161 mg/ kg/ day Neuromuscular and neurobehavioral abnormalities in all dosed groups, spinal cord neuropathology in mid and highdose groups  20 Published abstract. Neurotoxicity and neuropathology only end points examined. Drinking Water Criteria Document for Brominated Acetic Acids Table VIII 3. Summary of Oral Studies of DBA Toxicity Reference Species Route Exposure Duration; Doses Endpoints NOAEL LOAEL Comments mg/ kg/ day EPA/ OW/ OST/ HECD VIII 21 Draft, do not cite or quote Reproductive Toxicity Studies ( by duration of treatment)

Linder et al., 1994a Sprague Dawley rat ( male) Oral Gavage in water Acute single dose, up to 28 day recovery; 0 or 1250 mg/ kg Reproductiveorgan weight changes, decreased serum testosterone, sperm quality changes,

reproductivetract histopathology  1250 A single dose level was used.

Vetter et al., 1998 Crl: CD ( SD) Br rat ( male) Oral Gavage in water Acute single dose; 0, 600, 1200 mg/ kg Testes histopathology  600 Sperm analysis was limited to motility and membrane permeability, with no adverse effects reported.

Cummings and Hedge, 1998 Holtzman rat ( female) Oral Gavage in water Gestation days 1 8; 0, 62.5, 125, 250, 500 mg/ kg/ day Clinical observation 250 500 ( FEL) Reproductive parameters were not affected at 250 mg/ kg/ day or less and were not measured in the high dose group due to overt toxicity.

Linder et al., 1994b Sprague Dawley rat ( male) Oral Gavage in water 14 daily doses; 0, 10, 30, 90, or 270 mg/ kg Reproductivetract histopathology  10 None Drinking Water Criteria Document for Brominated Acetic Acids Table VIII 3. Summary of Oral Studies of DBA Toxicity Reference Species Route Exposure Duration; Doses Endpoints NOAEL LOAEL Comments mg/ kg/ day EPA/ OW/ OST/ HECD VIII 22 Draft, do not cite or quote Linder et al., 1995 Sprague Dawley rat ( male) Oral Gavage in water 2, 5, 9, 16, 31, or 42 days; 0, 250 mg/ kg/ day Decreased reproductive performance on Day 8   14 mating and day 15  21 mating. Decreased fertility of male sperm day 16 and 31. Altered sperm parameters beginning on day 9.  250 None Linder et al., 1995 and Linder et al., 1997a Sprague Dawley rat ( male) Oral Gavage in water Up to 79 days; 0, 2, 10, or 50 mg/ kg/ day 42 days; 250 mg/ kg/ day Reproductivetract histopathology 2 10 ( equivocal) Histopathology analysis presented in Linder et al., 1997 Effects at LOAEL became significant at 31 days.

Veeramachaneni et al., 2000 Dutchbelted rabbits ( male) Drinking water Dams gestation days 15 through life, male offspring through 24 weeks; 0, 0.97, 5.05, 54.2 mg/ kg/ day At 24 weeks, fertility of sperm tested in artificially inseminated does nd 0.97 Published abstract does not provide adequate details for definitive review. Drinking Water Criteria Document for Brominated Acetic Acids Table VIII 3. Summary of Oral Studies of DBA Toxicity Reference Species Route Exposure Duration; Doses Endpoints NOAEL LOAEL Comments mg/ kg/ day EPA/ OW/ OST/ HECD VIII 23 Draft, do not cite or quote Christian et al., 1999 Sprague Dawley rat ( male and female) Drinking water Sires from study day ( SD) 1 70: 10, 20, 36, 66 mg/ kg/ day; Dams from SD 1 15: 15, 30, 49, 82 mg/ kg/ day; from gestation day ( GD) 0 21: 15, 39, 49, 82 mg/ kg/ day; from lactation day ( LD) 1 29: 44, 87, 151, 212 mg/ kg/ day Slight nonsignificant decrease in mating performance and number of mated pairs at highest dose tested; reduced body wt gain, body wt, water consumption, food intake attributed to taste aversion of DBAtreated water 66 ( sires)

> 60 ( dams)

> 82 ( developmental  Mean daily water intake and corresponding mean DBA daily doses significantly increased in pregnant and lactating females Drinking Water Criteria Document for Brominated Acetic Acids Table VIII 3. Summary of Oral Studies of DBA Toxicity Reference Species Route Exposure Duration; Doses Endpoints NOAEL LOAEL Comments mg/ kg/ day EPA/ OW/ OST/ HECD VIII 24 Draft, do not cite or quote Chlorine Chemistry Council, 2001; Christian et al., ( 2002) Sprague Dawley rat ( male and female) Drinking water Two generation reprod. toxicity study, 0, 50, 250, 650 ppm in water; estimated daily doses are: P males  SD 1 92: 0, 4.4, 22, 52 mg/ kg/ day; P females  SD 1 70: 0, 6, 28, 69 mg/ kg/ day; GD 0 21: 0, 6, 30, 76 mg/ kg/ day; LD 1 15: 0, 12, 56, 132; F1 males: 0, 5 6, 22 30; 55 75 mg/ kg/ day; F1 females: Premating: 0, 7, 32, 83 mg/ kg/ day; GD 0 21: 0, 6, 29, 67 mg/ kg/ day; LD 1 15: 0, 10, 50, 115 mg/ kg/ day Impaired spermatogenesis, testicular histopathology in P and F1 males; no treatmentrelated effects in females Reduced body wt gain, body wt, water consumption, food intake in P, F1, F2 animals and changes in organ weights in P and F1 attributed to taste aversion effects of DBA treated water 4 ( P males)

> 5 ( F1 males) 22 ( P males)

> 22 ( F1 males) Study report was reviewed by an independent scientific advisory panel Recently published in International Journal of Toxicology 21: 237 276, 2002.

Developmental Toxicity Studies Drinking Water Criteria Document for Brominated Acetic Acids Table VIII 3. Summary of Oral Studies of DBA Toxicity Reference Species Route Exposure Duration; Doses Endpoints NOAEL LOAEL Comments mg/ kg/ day EPA/ OW/ OST/ HECD VIII 25 Draft, do not cite or quote Narotsky et al., 1996 CD 1 mouse ( female) Oral Gavage in water Gestation days 6 15; 0, 24, 50, 100, 200, 392, 610, or 806 mg/ kg/ day Increased postnatal mortality; decreased pup weight, tail defects 392 610 Published abstract does not provide adequate details for definitive review.

Maternal toxicity was limited to decreased maternal motor activity at the high dose.

Narotsky et al., 1997 CD 1 mouse ( female) Oral Gavage in water Gestation days 6 15; 0, 50, 100, or 400 mg/ kg/ day Fetal malformations; hydronephrosis 50 100 Published abstract does not provide adequate details for definitive review.

Hydronephrosis and renal agenesis at 400 mg/ kg/ day.

B. 3.1 One Day Health Advisory for DBA The acute oral toxicity data for DBA are very limited. Linder et al. ( 1994a) reported an LD 50 of 1737 mg/ kg in Sprague Dawley rats. However, LD 50 studies are not suitable for the development of One day health advisories. In the same paper, Linder et al. ( 1994a) assessed the effects of a single oral dose of 0 or 1250 mg/ kg/ day on the male reproductive system. After dosing, the animals were followed for up to 28 days. The single dose tested was spermatotoxic,

and induced severe changes in sperm quality parameters and reproductive tract histopathology. Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 26 Draft, do not cite or quote The absence of dose response data limits the utility of this study for health advisory derivation. In a similar acute dosing study validating a new test method, Vetter et al. ( 1998) also evaluated the spermatotoxicity of DBA in male Crl: CD( SD) Br rats given single oral doses of 0, 600, or 1200 mg/ kg DBA. The high dose, but not the low dose, resulted in clinical observations of toxicity and testes histopathology, but no effects on sperm motility, morphology, or cell membrane permeability; analysis was limited to evaluation of these measures. Due to the limited doseresponse and the testing for a limited number of endpoints, this study is not suitable for deriving a One day health advisory.

B. 3.2 Ten Day Health Advisory for DBA A number of toxicity studies have been reported for DBA that are of suitable duration for derivation of a Ten day health advisory. These studies have evaluated reproductive and developmental toxicity endpoints, as well as some indices of systemic toxicity.

Two studies by Narotsky and colleagues ( Narotsky et al., 1996; Narotsky et al., 1997)

observed adverse developmental effects, including skeletal and soft tissue malformations, in the offspring of pregnant mice administered DBA by gavage on GD 6 15. Full study reports have not been published, so these studies are not appropriate for the derivation of a health advisory.

Male fertility and sperm parameters were also evaluated in groups of rats administered 0 or 250 mg/ kg/ day DBA by gavage for 2 42 days ( Linder et al., 1995), but only a single high dose was Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 27 Draft, do not cite or quote tested. Linder et al. ( 1994b) identified an equivocal LOAEL of 10 mg/ kg/ day based on histopathological changes of the seminiferous tubules in adult male Sprague Dawley rats administered 14 daily gavage doses of DBA; a NOAEL could not be determined. In a study of female reproductive function and fetal development, gavage doses of up to 125 mg/ kg/ day on GD 1 8 had no effects on reproductive parameters or clinical observations of toxicity in rats ( Cummings and Hedge, 1998). The highest dose tested in this study ( 500 mg/ kg/ day) was lethal and not evaluated for reproductive outcome. None of these reproductive studies are appropriate for the derivation of a Ten day health advisory for a 10 kg child because the findings are only relevant to sexually mature animals and not to children.

Two other studies were of an appropriate duration for derivation of a Ten day health advisory, but these studies did not include evaluation of a complete array of systemic endpoints.

Parrish et al. ( 1996) evaluated the ability of DBA to induce oxidative DNA damage in the livers of mice treated with DBA in drinking water for 21 days. Increased liver weight and levels of 8

OHdG, a measure of oxidative stress, were observed at 125 mg/ kg/ day, but the absence of histopathology or clinical chemistry data makes it unclear whether the observed increase in liver weight was adverse. Other organ systems and end points were not evaluated. In an immunotoxicity screening assay comprised of 4 short term studies ( NTP, 1999), female mice treated with DBA in the drinking water for 28 days exhibited an array of immunotoxic effects;

however, many of these effects were inconsistent and/ or did not exhibit a dose response. Based on decreased spleen IgM antibody forming response, the NOAEL was 38 mg/ kg/ day and the Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 28 Draft, do not cite or quote LOAEL was 70 mg/ kg/ day. Thymus and spleen weights were also evaluated, but other organs and end points were not assessed. Therefore, neither of these studies ( Parish et al., 1996; NTP,

1999) are considered to be suitable for derivation of a Ten day health advisory in the absence of other toxicity studies that have adequately evaluated systemic toxicity.

B. 3.3 Longer Term Health Advisory for DBA A number of studies that examined the reproductive or developmental toxicity of DBA were evaluated for the potential derivation of a Longer term HA. As described previously,

published abstracts are available for two developmental toxicity studies in mice ( Narotsky et al.,

1996, 1997), which demonstrated adverse developmental effects including increased postnatal mortality, and skeletal ( tail defects) and soft tissue ( kidney defects) malformations. A published abstract for a neurotoxicity study in rats has shown that DBA produces neurobehavioral toxicity,

including neuromuscular abnormalities, decreased sensorimotor responsiveness, and increased motor activity, as well as spinal cord neuropathology indicative of axonal degeneration ( Phillips et al., 2002). However, none of these studies have been published and, thus, these results are not suitable for the derivation of human health advisories.

Linder et al. ( 1995, 1997a) evaluated the spermatotoxicity and fertility in male Sprague

Dawley rats administered daily gavage doses of DBA of 0, 2, 10, or 50 mg/ kg/ day for up to 79 days. In a companion study, male rats were gavaged with either 0 or 250 mg/ kg/ day daily for 42 Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 29 Draft, do not cite or quote days, at which time dosing was terminated due to severe overt toxicity. Fertility in the dosed males was assessed through day 213 by mating treated males with untreated females at different time periods. Based on the results of these studies, DBA is clearly spermatotoxic and effects on sperm histopathology appear to be the most sensitive endpoint, because these effects are observed in the absence of other reproductive toxicity endpoints. Changes in retention of Step 19 spermatids was the only effect that occurred at the lowest dose. This effect was equivocally noted following repeated dosing with 10 mg/ kg/ day, but not 2 mg/ kg/ day, for 31 or 79 days. However,

the biological significance of this finding for a Longer term human health advisory is unclear because changes in sperm count, morphology, and motility were observed at higher doses ( 50 mg/ kg/ day) than those associated with these early and mild histopathological changes, and male fertility was significantly affected only at 250 mg/ kg/ day ( Linder et al., 1995). At doses of 50 mg/ kg/ day and lower, there were no significant effects on reproductive outcome as indicated by a number of different measures and indices of successful mating behavior were not significantly altered. These results are described in detail in Section V. Although it has been proposed that the fertility of rodents may be less sensitive to changes in sperm count than fertility in humans ( U. S.

EPA, 1996a; Zenick et al., 1994), human data are highly variable and generally inconsistent across studies. Further, there may be significant differences in the susceptibility of different species and rodent strains to DBA induced reproductive toxicity. In an acute spermatotoxicity study by Vetter et al. ( 1998), changes in sperm motility and morphology were not observed in male Crl: CD( SD) BR rats at acute gavage doses of up to 1200 mg/ kg, whereas Linder et al. ( 1994a) Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 30 Draft, do not cite or quote observed significant alterations in both of these parameters in male Sprague Dawley rats following an acute gavage dose of 1250 mg/ kg. A published abstract by Veeramachaneni et al.

( 2000) reported that male Dutch belted rabbits exposed in utero from GD 15 through lactation and post weaning for 24 weeks exhibited decreased fertility, as evidenced by reduced conception in females artificially inseminated with sperm from treated animals, at drinking water doses as low as 0.97 mg/ kg/ day. However, a full report of this study has not been published, and thus these results cannot be comprehensively evaluated. It is also not known whether humans would be less,

or more, sensitive to DBA induced male reproductive tract toxicity than rats or rabbits. No reproductive epidemiologic data on DBA are available, and comparative in vitro studies have not been conducted.

Although the studies by Linder et al. ( 1994a, 1994b, 1995, 1997) adequately characterize the male reproductive hazards in rats repeatedly administered DBA by oral gavage, these studies are not considered to be suitable for quantitative dose response assessment in the absence of subchronic and chronic toxicity studies that have adequately evaluated DBA systemic toxicity. In the recent two generation reproductive/ developmental toxicity study conducted by the ( Chlorine Chemistry Council, 2001; Christian et al., 2002), impaired spermatogenesis was also observed in male rats of the P and F1 generations at DBA drinking water concentrations of 250 ppm and above ( equivalent to a LOAEL of 22 mg/ kg/ day for the P generation, and not less than 22 mg/ kg/ day for the F1 generation); abnormal pathology of the testes and epididymes was noted in some males of the F1 generation at 650 ppm ( equivalent to a LOAEL of not less than 75 Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 31 Draft, do not cite or quote mg/ kg/ day). The corresponding NOAEL was 4 mg/ kg/ day in the P generation and at least 5 mg/ kg/ day in the F1 generation. However, in contrast with the shorter term study that showed adverse mating performance effects at 250 mg/ kg/ day and higher ( Linder et al., 1995), no adverse treatment related effects on mating performance, gestation length, fertility, pup mortality and viability, and other functional indices of successful reproductive behavior were observed at DBA drinking water concentrations up to 650 ppm ( 52 to 132 mg/ kg day) ( Chlorine Chemistry Council, 2001; Christian et al., 2002). Alternatively, these studies in combination may define a NOAEL/ LOAEL boundary for functional effects of DBA on reproduction. No treatment related adverse developmental effects other than impaired spermatogenesis were noted in either males or females of the F1 and F2 generations. To date, other developmental toxicity studies have only been published in abstract form and thus cannot be comprehensively evaluated until full study reports are available for review. Subchronic and chronic toxicity testing of DBA is planned or in progress ( NTP, 2000c). A number of additional studies are currently ongoing. Therefore, it is not appropriate to develop a Longer term health advisory at this time.

B. 3.4. Reference Dose and Drinking Water Equivalent Level for DBA As discussed in the previous section on the Longer term health advisory, the toxicity database for DBA is currently limited, and there are no suitable studies of appropriate design and duration to derive an oral RfD at this time. Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 32 Draft, do not cite or quote C. Carcinogenic Effects No epidemiology or animal studies were identified to develop a quantitative cancer risk assessment for MBA, BCA, or DBA. No studies were identified that directly evaluated the human carcinogenicity of MBA, BCA, or DBA. Rather, most of the human health data for brominated acetic acids are as components of complex mixtures of water disinfection byproducts. These complex mixtures of disinfection byproducts have been associated with increased potential for cancer ( Boorman et al., 1999), but brominated acetic acids have not been specifically implicated.

C. 1. Monobromoacetic acid No epidemiology or animal studies were identified that evaluated the carcinogenicity of MBA. The data are inadequate for determining whether MBA is genotoxic. The mutagenicity of MBA might be metabolism dependent, based on different results for these compound in the presence or absence of microsomal activation in S. typhimurium strain TA100. MBA was reported to be mutagenic in three independent studies in bacteria ( Giller et al., 1997; Kohan et al.,

1998; NTP 2000a), but MBA did not induce DNA repair as measured by the SOS chromotest ( Giller et al., 1997). Due to the limited database, there is insufficient evidence to determine the genotoxicity of MBA. Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 33 Draft, do not cite or quote Following the EPA's 1986 ( U. S. EPA, 1986) Guidelines for Cancer Risk Assessment,

MBA is best classified as Group D, " not classifiable as to human carcinogenicity". This classification is appropriate because no data are available on human or animal carcinogenicity.

Under the 1999 Draft Guidelines for Carcinogen Risk Assessment ( U. S. EPA, 1999b), the data are " inadequate for an assessment of human carcinogenic potential" of MBA.

C. 2. Bromochloroacetic acid No epidemiology studies have evaluated the carcinogenicity of BCA. The carcinogenicity of BCA has not been tested in a full cancer bioassay. However, BCA is currently slated for testing ( NTP, 2000b). The only carcinogenicity testing data in animals for BCA that was identified was reported in a published abstract ( Stauber et al., 1995). The abstract reported preliminary data suggesting that BCA induces hepatic tumors in B6C3F1 mice. However, no experimental details were provided in the brief study summary and the full study report has not been published. BCA was reported as positive in the single standard assay identified, a Salmonella reverse mutation assay ( NTP, 2000b). The reports of Austin et al. ( 1996) and Parrish et al. ( 1996) demonstrated that BCA treatment could induce oxidative DNA damage in the livers of treated mice. While these data are suggestive of genotoxic potential, BCA has not been sufficiently tested to make a determination as to its genotoxicity. Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 34 Draft, do not cite or quote Following the EPA's 1986 Guidelines for Carcinogen Risk Assessment, BCA is best classified as Group D, " not classifiable as to human carcinogenicity" ( U. S. EPA, 1986). This classification is appropriate because no data are available on human carcinogenicity and there are only preliminary animal carcinogenicity data. Under the 1999 Draft Guidelines for Carcinogen Risk Assessment ( U. S. EPA, 1999b), the data are " inadequate for an assessment of human carcinogenic potential" of BCA.

C. 3. Dibromoacetic acid No epidemiology studies have evaluated the carcinogenicity of DBA. The carcinogenicity of DBA has not been tested in a full cancer bioassay. However, DBA is currently undergoing testing ( NTP, 2000c). In published abstracts, So and Bull ( 1995) reported that DBA induces aberrant crypt foci in the colon of rats, and Stauber et al. ( 1995) reported that DBA induces liver tumors in mice. Experimental details are not available for either of these studies because neither has been published in peer reviewed journals, but the findings of So and Bull ( 1995) might be of particular significance since colon cancer has been implicated as a potential cancer site in humans exposed to drinking water disinfectant by products, including haloacetic acids ( Boorman et al.,

1999).

Much of the concern for the potential carcinogenicity of DBA arises from the demonstrated high dose rodent liver tumorigenicity of its chlorinated analog, dichloroacetic acid Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 35 Draft, do not cite or quote ( DCA). The ability of both compounds to induce a similar spectrum of noncarcinogenic toxic effects suggests the possibility that this might also be the case for carcinogenic effects. For example, both compounds are potent spermatotoxicants and induce a similar spectrum of effects in the male reproductive tract ( Linder et al., 1997b). Both compounds also affect the liver.

Treatment with DBA or DCA resulted in increased liver weight, although only DBA increased the formation of oxidative DNA damage in this study ( Parrish et al., 1996). DBA and DCA also appear to have similar kinetics ( Schultz et al., 1999), but insufficient data are available on DBA metabolism, renal elimination, and tissue distribution to fully compare the kinetics of DBA and DCA. These similarities between DBA and DCA suggest that, like DCA, DBA might also be tumorigenic at high drinking water doses administered for a lifetime. However, the weight

ofevidence for DCA genotoxicity indicates that DCA is nongenotoxic except possibly at high doses that also induce cytotoxicity. In contrast, although the DBA database for genotoxicity/

mutagenicity is more limited than that for DCA, the weight of evidence to date indicates that DBA is genotoxic Thus, although both DBA and DCA exhibit similar toxicokinetics and similar systemic and reproductive toxicity, they may well differ in their carcinogenic potential and mode( s) of carcinogenic action.

Thus, insufficient data are available to assess DBA carcinogenic hazard, and DBA is classified as Group D, " not classifiable as to human carcinogenicity" under the 1986 Carcinogen Risk Assessment Guidelines. Under the 1999 Draft Guidelines for Carcinogen Risk Assessment Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD VIII 36 Draft, do not cite or quote ( U. S. EPA, 1999b), the data are " inadequate for an assessment of human carcinogenic potential" of DBA.

D. Summary In the absence of a comprehensive toxicity database, no adequate studies of suitable design and/ or duration were identified to serve as the basis for any health advisories for MBA,

BCA, or DBA.

MBA, BCA, and DBA are all classified as " not classifiable as to human carcinogenicity" under the 1986 Carcinogen Risk Assessment Guidelines , and " inadequate for an assessment of human carcinogenic potential" under the 1999 Draft Guidelines for Carcinogen Risk Assessment ( U. S. EPA, 1999b). Drinking Water Criteria Document for Brominated Acetic Acids EPA/ OW/ OST/ HECD IX 1 Draft, do not cite or quote Chapter IX. References Anderson, W. B., P. G. Board, B. Gargano and M. W. Anders. 1999. Inactivation of glutathione transferase zeta by dichloroacetic acid and other fluorine lacking alpha haloalkanoic acids. Chem.

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