[Federal Register: September 24, 2009 (Volume 74, Number 184)]
[Rules and Regulations]
[Page 48659-48662]
[DOCID:fr24se09-6]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 52

[EPA-R05-OAR-2009-0293; FRL-8961-6]

Approval and Promulgation of Air Quality Implementation Plans;
Indiana; Lead (Pb) Maintenance Plan Update for Marion County

AGENCY: Environmental Protection Agency (EPA).

ACTION: Direct final rule.

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SUMMARY: EPA is approving a request submitted by the Indiana Department
of Environmental Management (IDEM) on April 1, 2009, to revise the
Indiana State Implementation Plan (SIP) for lead (Pb). The State has
submitted an update to its Pb maintenance plan for Marion County for
continued attainment of the 1.5 micrograms per cubic meter ([mu]g/m\3\)
National Ambient Air Quality Standard (NAAQS) promulgated in 1978. This
update satisfies section 175A of the Clean Air Act (CAA), and is in
accordance with EPA's May 10, 2000, approval of the State's
Redesignation Request and Maintenance Plan for the Marion County Pb
nonattainment areas. Additionally, this Pb maintenance plan satisfies
the requirements for maintenance plans contained in the September 4,
1992, EPA memorandum entitled ``Procedures for Processing Requests to
Redesignate Areas to Attainment.''

DATES: This direct final will be effective November 23, 2009, unless
EPA receives adverse comments by October 26, 2009. If adverse comments
are received, EPA will publish a timely withdrawal of the direct final
rule in the Federal Register informing the public that the rule will
not take effect.

ADDRESSES: Submit your comments, identified by Docket ID No. EPA-R05-
OAR-2009-0293, by one of the following methods:
    1. http://www.regulations.gov: Follow the on-line instructions for
submitting comments.
    2. E-mail<EMAIL_ADDRESS>    3. Fax:<PHONE_NUMBER>.
    4. Mail: John M. Mooney, Chief, Criteria Pollutant Section, Air
Programs Branch (AR-18J), U.S. Environmental Protection Agency, 77 West
Jackson Boulevard, Chicago, Illinois 60604.
    5. Hand Delivery: John M. Mooney, Chief, Criteria Pollutant
Section, Air Programs Branch (AR-18J), U.S. Environmental Protection
Agency, 77 West Jackson Boulevard, Chicago, Illinois 60604. Such
deliveries are only accepted during the Regional Office normal hours of
operation, and special arrangements should be made for deliveries of
boxed information. The Regional Office official hours of business are
Monday through Friday, 8:30 a.m. to 4:30 p.m., excluding Federal
holidays.
    Instructions: Direct your comments to Docket ID No. EPA-R05-OAR-
2009-0293. EPA's policy is that all comments received will be included
in the public docket without change and may be made available online at
http://www.regulations.gov, including any personal information
provided, unless the comment includes information claimed to be
Confidential Business Information (CBI) or other information whose
disclosure is restricted by statute. Do not submit information that you
consider to be CBI or otherwise protected through http://
www.regulations.gov or e-mail. The http://www.regulations.gov Web site
is an ``anonymous access'' system, which means EPA will not know your
identity or contact information unless you provide it in the body of
your comment. If you send an e-mail comment directly to EPA without
going through http://www.regulations.gov your e-mail address will be
automatically captured and included as part of the comment that is
placed in the public docket and made available on the Internet. If you
submit an electronic comment, EPA recommends that you include your name
and other contact information in the body of your comment and with any
disk or CD-ROM you submit. If EPA cannot read your comment due to
technical difficulties and cannot contact you for clarification, EPA
may not be able to consider your comment. Electronic files should avoid
the use of special characters, any form of encryption, and be free of
any defects or viruses.
    Docket: All documents in the docket are listed in the http://
www.regulations.gov index. 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 either
electronically in http://www.regulations.gov or in hard copy at the
Environmental Protection Agency, Region 5, Air and Radiation Division,
77 West Jackson Boulevard, Chicago, Illinois 60604. This facility is
open from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding
Federal holidays. We recommend that you telephone Andy Chang,
Environmental Engineer, at<PHONE_NUMBER> before visiting the Region 5
office.

FOR FURTHER INFORMATION CONTACT: Andy Chang, Environmental Engineer,
Criteria Pollutant Section, Air Programs Branch (AR-18J), U.S.
Environmental Protection Agency, Region 5, 77 West Jackson Boulevard,
Chicago, Illinois 60604,<PHONE_NUMBER><EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION: Throughout this document whenever ``we,''
``us,'' or ``our'' is used, we mean EPA. This supplementary information
section is arranged as follows:

I. Background
    A. Why did the State make this submittal?
    B. Did the State hold public hearings for the maintenance plan
update?
II. What criteria is EPA using to evaluate this submittal?
III. What is EPA's analysis of this submittal?
    A. Requirements of Section 175A of the CAA
    B. Consistency With the September 4, 1992, Memorandum
    1. Emissions Inventory
    2. Maintenance Demonstration
    3. Monitoring Network
    4. Verification of Continued Attainment
    5. Contingency Plan
IV. What action is EPA taking?
V. Statutory and Executive Order Reviews

I. Background

A. Why did the State make this submittal?

    On November 6, 1991, EPA designated a portion of Franklin Township
in Marion County as a primary nonattainment area for Pb under section
107 of the CAA (56 FR 56694). On the same date, EPA designated a
portion of Wayne Township in Marion County as an unclassifiable area
for Pb.
    On March 2, 2000, IDEM submitted a Redesignation Request and
Maintenance Plan for the Marion County nonattainment areas. IDEM's
submittal included ambient monitoring data showing that the areas met
the 1978 Pb NAAQS for the prior three years, air quality improvements
that could be attributed to reductions in Pb emissions which are
permanent and enforceable, and a maintenance plan that assured
continued attainment of the standard. As a result, on May 10, 2000 (65
FR 114223), EPA approved the request.
    The State's updated maintenance plan satisfies the requirements of
section 175A(b) of the CAA, which mandates that the State shall submit
an additional revision to the maintenance plan eight years after
redesignation of any area as an attainment area. It is also consistent
with the requirements for maintenance plan elements outlined in a
September 4, 1992, memorandum from the Director of EPA's Air Quality
Management Division, entitled ``Procedures for Processing Requests to
Redesignate Areas to Attainment.'' The State submitted the updated
maintenance plan to EPA on April 1, 2009, and supplemented its
submittal with two technical addenda on June 5, 2009, and July 6, 2009.

B. Did the State hold public hearings for the maintenance plan update?

    Public notice was given on February 20, 2009, in the Indianapolis
Star News.

II. What criteria is EPA using to evaluate this submittal?

    In addition to the general requirements in section 175A of the CAA,
guidance for maintenance plans and maintenance plan updates are
provided in the September 4, 1992, memorandum, which states that the
following five components need to be addressed: Attainment Inventory,
Maintenance Demonstration, Monitoring Network, Verification of
Continued Attainment, and Contingency Plan.

III. What is EPA's analysis of this submittal?

A. Requirements of Section 175A of the CAA

    Section 175A contains four subsections pertaining to maintenance
plans. Section 175A(a) establishes requirements for initial SIP
redesignation request maintenance plans, as addressed in EPA's May 10,
2000 approval of the Indiana plan. Section 175A(b) requires states to
submit an update to the maintenance plan eight years following the
original redesignation to attainment, and IDEM has satisfied the
requirements of this element with its current submittal. It also
requires that within this update, the State must outline methods for
maintaining the pertinent NAAQS for ten years after the expiration of
the ten-year period referred to in subsection (a), i.e., Indiana's
maintenance plan update must outline methods for maintaining the 1.5
[mu]g/m\3\ Pb NAAQS through 2020. In a June 5, 2009, technical
addendum, Indiana provided Pb emissions projections that satisfy this
requirement. Section 175A(c) does not apply to this rulemaking, given
that EPA has previously redesignated Marion County to attainment for
Pb. The contingency provisions requirements outlined in section 175A(d)
will be addressed in detail in Section B5, below.

B. Consistency With the September 4, 1992, Memorandum

    As discussed above, EPA's interpretation of section 175A of the CAA
is contained in the September 4, 1992, memorandum. Indiana has
addressed the five major elements of that policy, as follows:
1. Emissions Inventory
    The State is required to develop an attainment emissions inventory
to identify a level of emissions in the area which is protective of the
1.5 [mu]g/m\3\ Pb NAAQS. In its submittal, IDEM provided a
comprehensive emissions inventory of major and minor permitted sources
in Marion County for the base year and attainment year (1996) compared
to the most recent emissions inventory (2007). The State demonstrated
that annual Pb emissions in Marion County from permitted sources have
decreased by over 1.78 tons (61.58%) from 1996 to 2007. This decrease
can be attributed to a number of factors, including Federally mandated
programs, the closings of permitted stationary sources, and source-
specific operating provisions. Additionally, the State demonstrated
that the actual 2007 emissions were 2.032 tons less than the projected
2010 emissions. The State has satisfied the attainment inventory
requirement for maintenance plan updates.
2. Maintenance Demonstration
    The State may generally demonstrate maintenance of the 1.5 [mu]g/
m\3\ Pb NAAQS by either showing that future Pb emissions will not
exceed the level of the attainment inventory, or by modeling to show
that the future mix of sources and emission rates will not cause a
violation of the Pb NAAQS. The demonstration should be for a period of
ten years following the redesignation, i.e., until 2020 for the
maintenance plan update.
    In its submittal, IDEM showed, using ambient monitoring data
collected between 1999 and 2008, that the County is meeting the 1.5
[mu]g/m\3\ Pb NAAQS, which is based on a quarterly average. The highest
quarterly average in this

time period was less than 0.20 [mu]g/m\3\, which equates to 13% of the
1.5 [mu]g/m\3\ Pb NAAQS. Pb emissions are expected to decrease from
2.897 tons per year in 1996 to 0.63 tons per year in 2020. As 1996 was
the base year for attainment with an emissions inventory of 2.897 tons,
any projected emissions below that level will also lead to attainment.
Therefore, the State has satisfied the maintenance demonstration
requirement for maintenance plan updates.
3. Monitoring Network
    Once an area has been redesignated, the State should continue to
operate an appropriate air quality monitoring network, in accordance
with 40 CFR Part 58, to verify the attainment status of the area. In
its submittal, IDEM specifically identifies two monitoring sites
located in Marion County, which are Air Quality Systems (AQS) I.D. 18-
097-0063 (7601 Rockville Road) and AQS I.D. 18-097-0076 (230 South
Girls School Road). The monitors have been in operation since January
1, 1984, and May 6, 1991, respectively. IDEM commits to continue
monitoring Pb in these areas to ensure that Pb concentrations remain
well below the 1.5 [mu]g/m\3\ Pb NAAQS. Furthermore, IDEM commits to
consult with EPA should changes to the existing monitoring network be
needed. The State has satisfied the monitoring network requirements for
the maintenance plan update.
4. Verification of Continued Attainment
    The State should ensure that it has the legal authority to
implement and enforce all measures necessary to attain and to maintain
the NAAQS. One such measure for maintaining the NAAQS is the
acquisition of ambient and source emission data to demonstrate
attainment and maintenance.
    IDEM has included quality-assured data in its submittal in
accordance with 40 CFR 58.10 (Supbart B--Monitoring Network) and the
Indiana Quality Assurance Manual. The data were found to be valid, and
was recorded in the AQS database, which is available to the public.
IDEM commits to continue its quality assurance and validation processes
in accordance with 40 CFR Part 58 and the Indiana Quality Assurance
Manual. Furthermore, the State commits to enter all data in the AQS
database in a timely basis in accordance with Federal guidelines. The
State has satisfied the verification of continued attainment
requirements for maintenance plan updates.
5. Contingency Plan
    Section 175A(d) of the CAA requires that a maintenance plan include
contingency provisions, as necessary, to promptly correct any violation
of the NAAQS that occurs after redesignation of an area. The September
4, 1992, memorandum further requires that the contingency provisions
identify the measures to be adopted, a schedule and procedure for
adoption and implementation, and a specific time limit for action by
the State.
    In its April 1, 2009, submittal, Indiana commits to the same
contingency measures that EPA previously approved on May 10, 2000 (65
FR 11423). In a July 6, 2009, technical memorandum, the State added one
new trigger and associated timeline for contingency measures: if the
State determines that Pb levels and emissions are increasing and action
is necessary to reverse that trend, IDEM will implement any necessary
contingency measures within 18 months of the monitoring data being
submitted to EPA's AQS database. The State has satisfied the
contingency plan requirements pursuant to section 175A(d) of the CAA as
well as those of the September 4, 1992, memorandum.

IV. What action is EPA taking?

    We are approving this update to the Pb maintenance plan for Marion
County. The State of Indiana has complied with requirements of section
175A of the CAA, as interpreted by the guidance provided in the
September 4, 1992, memorandum. Indiana has shown through its submittal
that Pb emissions in Marion County have remained well under the level
of the 1.5 [mu]g/m\3\ NAAQS, and that they are expected to remain so
until at least 2020.
    We are publishing this action without prior proposal because we
view this as a noncontroversial amendment and anticipate no adverse
comments. However, in the Proposed Rules section of this Federal
Register publication, we are publishing a separate document that will
serve as the proposal to approve the state plan if relevant adverse
written comments are filed. This rule will be effective November 23,
2009 without further notice unless we receive relevant adverse written
comments by October 23, 2009. If we receive such comments, we will
withdraw this action before the effective date by publishing a
subsequent document that will withdraw the final action. All public
comments received will then be addressed in a subsequent final rule
based on the proposed action. EPA will not institute a second comment
period; therefore, any parties interested in commenting on this action
should do so at this time. If we do not receive any comments, this
action will be effective November 23, 2009.

V. Statutory and Executive Order Reviews

    Under the CAA, the Administrator is required to approve a SIP
submission that complies with the provisions of the CAA 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 Clean Air Act; 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 located in the state, 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 Clean Air Act, petitions for
judicial review of this action must be filed in the United States Court
of Appeals for the appropriate circuit by November 23, 2009. 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 a 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, Lead, Reporting and
recordkeeping requirements.

    Dated: September 14, 2009.
Walter W. Kovalick Jr.,
Acting Regional Administrator, Region 5.

0
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 P--Indiana

0
2. Section 52.797 is amended by adding paragraph (e) to read as
follows:

Sec.  52.797  Control strategy: Lead.

* * * * *
    (e) On April 1, 2009, Indiana submitted an updated maintenance plan
under section 175A of the CAA for Marion County for the continued
attainment of the 1.5 [mu]g/m\3\ lead standard.

[FR Doc. E9-22922 Filed 9-23-09; 8:45 am]

BILLING CODE 6560-50-P


[Federal Register Volume 85, Number 171 (Wednesday, September 2, 2020)]
[Notices]
[Pages 54558-54559]
[FR Doc No: 2020-19382]

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DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Project No. 2816-050]

North Hartland, LLC; Notice of Application Accepted for Filing,
Soliciting Motions To Intervene and Protests, Ready for Environmental
Analysis, and Soliciting Comments, Recommendations, Terms and
Conditions, and Prescriptions

    Take notice that the following hydroelectric application has been
filed with the Commission and is available for public inspection.
    a. Type of Application: New Major License.
    b. Project No.: 2816-050.
    c. Date filed: November 26, 2019.
    d. Applicant: North Hartland, LLC (North Hartland).
    e. Name of Project: North Hartland Hydroelectric Project (North
Hartland Project).
    f. Location: The North Hartland Project is located on the
Ottauquechee River in Windsor County, Vermont. The North Hartland
Project occupies 20.8 acres of land managed by the U.S. Army Corps of
Engineers (Corps).
    g. Filed Pursuant To: Federal Power Act 16 U.S.C. 791(a)-825(r).
    h. Applicant Contact: Andrew J. Locke, President, Essex Hydro
Associates, LLC, 55 Union Street, Boston, MA 02108; Phone at (617) 367-
0032, or email at<EMAIL_ADDRESS>    i. FERC Contact: Bill Connelly,<PHONE_NUMBER> or
<EMAIL_ADDRESS>    j. Deadline for filing motions to intervene and protests, comments,
recommendations, terms and conditions, and prescriptions: 60 Days from
the issuance date of this notice; reply comments are due 105 days from
the issuance date of this notice.
    The Commission strongly encourages electronic filing. Please file
motions to intervene and protests, comments, recommendations, terms and
conditions, and prescriptions using the Commission's eFiling system at
https://ferconline.ferc.gov/FERCOnline.aspx. Commenters can submit
brief comments up to 6,000 characters, without prior registration,
using the eComment system at https://ferconline.ferc.gov/QuickComment.aspx. You must include your name and contact information
at the end of your comments. For assistance, please contact FERC Online
Support at<EMAIL_ADDRESS>(866) 208-3676 (toll free), or
(202) 502-8659 (TTY).
    The Commission's Rules of Practice require all intervenors filing
documents with the Commission to serve a copy of that document on each
person on the official service list for the project. Further, if an
intervenor files comments or documents with the Commission relating to
the merits of an issue that may affect the responsibilities of a
particular resource agency, they must also serve a copy of the document
on that resource agency.
    k. This application has been accepted for filing and is ready for
environmental analysis at this time.
    l. Project Description: The existing North Hartland Project
consists of: (1) A steel-lined intake structure in the Corps' North
Hartland Dam that is equipped with trashracks with 2-inch clear bar
spacing; (2) a 470-foot-long, 12-foot-diameter steel penstock that
provides flow to a 4.0-megawatt (MW) adjustable blade, vertical shaft
turbine-generator unit located inside of a 59-foot-long, 40-foot-wide
concrete powerhouse; (3) a 12-foot-diameter bypass conduit that
branches off of the 12-foot-diameter penstock about 100 feet before the
powerhouse, and that empties into a 60-foot-long concrete-lined channel
through a bypass control gate; (4) a 30-inch-diameter steel penstock
that branches off of the 12-foot-diamater bypass conduit about 50 feet
upstream of the bypass control gate, and that provides flow to a
0.1375-MW fixed geometry, horizontal pump turbine-generator unit
located on a raised platform outside of the southern wall of the
powerhouse; (5) a 400-foot-long, 50 to 150-foot-wide tailrace channel;
(6) a

transmission line that comprises an approximately 600-foot-long, 12.5
kilovolt (kV) underground segment, and a 4,000-foot-long, 12.5-kV
overhead segment that connect the generators to Green Mountain Power
Corporation's Clay Hill Road Line 66 Transmission Project No. 12766;
and (9) appurtenant facilities.
    The project is managed to meet daily peak electrical system demand,
as needed using the available head and reservoir outflow from the
Corps' North Hartland dam. The current license requires North Hartland
to release a continuous minimum flow of 23 cubic feet per second (cfs)
from July 1 through October 31, and 40 cfs during the remainder of the
year (or inflow to the reservoir, whichever is less), for the purpose
of protecting and enhancing aquatic resources in the Ottauquechee
River. The project has an average annual generation of approximately
13,991,990 kilowatt-hours from 2014 through 2018.
    North Hartland proposes to release the following minimum and
maximum flows, respectively, to the downstream reach: (1) 60 and 700
cfs from October 1 through March 31; (2) 160 and 835 cfs from April 1
through April 31; (3) 160 and 550 cfs from May 1 through May 31; (4)
140 and 450 cfs from June 1 through June 30; and (5) 60 and 300 cfs
from July 1 through September 30.
    m. In addition to publishing the full text of this notice in the
Federal Register, the Commission provides all interested persons an
opportunity to view and/or print the contents of this notice, as well
as other documents in the proceeding (e.g., license application) via
the internet through the Commission's Home Page (http://www.ferc.gov)
using the eLibrary link. Enter the docket number excluding the last
three digits in the docket number field to access the document (P-
2816). At this time, the Commission has suspended access to the
Commission's Public Reference Room due to the proclamation declaring a
National Emergency concerning the Novel Coronavirus Disease (COVID-19)
issued by the President on March 13, 2020. For assistance, contact FERC
at<EMAIL_ADDRESS>or call toll-free,<PHONE_NUMBER> or
(202) 502-8659 (TTY).
    You may also register online at https://ferconline.ferc.gov/FERCOnline.aspx to be notified via email of new filings and issuances
related to this or other pending projects. For assistance, contact FERC
Online Support.
    n. Anyone may submit comments, a protest, or a motion to intervene
in accordance with the requirements of Rules of Practice and Procedure,
18 CFR 385.210, .211, and .214. In determining the appropriate action
to take, the Commission will consider all protests or other comments
filed, but only those who file a motion to intervene in accordance with
the Commission's Rules may become a party to the proceeding. Any
comments, protests, or motions to intervene must be received on or
before the specified comment date for the particular application.
    All filings must: (1) Bear in all capital letters the title
PROTEST, MOTION TO INTERVENE, COMMENTS, REPLY COMMENTS,
RECOMMENDATIONS, TERMS AND CONDITIONS, or PRESCRIPTIONS; (2) set forth
in the heading the name of the applicant and the project number of the
application to which the filing responds; (3) furnish the name,
address, and telephone number of the person protesting or intervening;
and (4) otherwise comply with the requirements of 18 CFR 385.2001
through 385.2005. All comments, recommendations, terms and conditions
or prescriptions must set forth their evidentiary basis and otherwise
comply with the requirements of 18 CFR 4.34(b). Agencies may obtain
copies of the application directly from the applicant. A copy of any
protest or motion to intervene must be served upon each representative
of the applicant specified in the particular application. A copy of all
other filings in reference to this application must be accompanied by
proof of service on all persons listed in the service list prepared by
the Commission in this proceeding, in accordance with 18 CFR 4.34(b)
and 385.2010.
    o. A license applicant must file no later than 60 days following
the date of issuance of this notice: (1) A copy of the water quality
certification; (2) a copy of the request for certification, including
proof of the date on which the certifying agency received the request;
or (3) evidence of waiver of water quality certification.
    p. Procedural Schedule: The application will be processed according
to the following schedule. Revisions to the schedule will be made as
appropriate.

------------------------------------------------------------------------
               Milestone                           Target date
------------------------------------------------------------------------
Filing of interventions, protests,       October 2020.
 comments, recommendations, preliminary
 terms and conditions, and preliminary
 fishway prescriptions.
Commission issues Environmental          May 2021.
 Assessment.
Comments on Environmental Assessment...  June 2021.
------------------------------------------------------------------------

    Final amendments to the application must be filed with the
Commission no later than 30 days from the issuance date of this notice.

    Dated: August 27, 2020.
Nathaniel J. Davis, Sr.,
Deputy Secretary.
[FR Doc. 2020-19382 Filed 9-1-20; 8:45 am]
BILLING CODE 6717-01-P


       UNITED STATES ENVIRONMENTAL PROTECTION AGENCY

WASHINGTON, DC 20460

             OFFICE OF  PREVENTION, PESTICIDES,  AND TOXIC SUBSTANCES

DATE:	August 29, 2008

MEMORANDUM

SUBJECT:	Creosote - Endpoint Selection Report.

FROM:	Timothy F. McMahon, Ph.D.

Senior Toxicologist, Antimicrobials Division

TO:		Jacquie McFarlane

PM Team 34 / RMB II

Antimicrobials  Division (7510P)

PC Code: 025004

On April 1, 1999, the Health Effects Division's Hazard Identification
Assessment Review Committee evaluated the toxicology data base of
creosote   and selected toxicological endpoints for short-term,
intermediate-term, and long-term occupational/residential exposure risk
assessments.    An acute and chronic Reference Dose (RfD) was not
selected, as there are no food uses for creosote or expected dietary
exposure to creosote. The HIARC also addressed the potential enhanced
sensitivity of infants and children from exposure to creosote as
required by the Food Quality Protection Act (FQPA) of 1996, as there are
potential residential exposures to creosote.  On September 3, 2003, the
Antimicrobials Division Toxicity Endpoint Selection Committee (ADTC) met
to verify the selected endpoints for long-term dermal risk assessments
for creosote and  inhalation risk assessment, and also discussed whether
dermal and inhalation Margins of Exposure should be combined for
creosote risk assessment.  On December 6, 2007, members of the
Antimicrobials Division’s Toxicity Endpoint Selection Committee and
members of the Health Effects Division’s Carcinogenicity Assessment
Review Committee met to discuss the quantitative carcinogenicity
analysis  performed for creosote by the Pest Management Regulatory
Agency, Health Canada and to determine an appropriate potency factor for
creosote.

Chemical Name:  Creosote

I. DIETARY

A. ACUTE DIETARY (Acute RfD)

Type of Study Proposed:

MRID No.:

Executive Summary:

Dose and Endpoint Proposed for Consideration:

Uncertainty Factor(s) Proposed for Consideration:

Proposed ACUTE  RfD:

Comments about Study/Endpoint/Uncertainty Factor(s): An acute dietary
risk assessment  is not required for creosote, as there is no
anticipated dietary exposure to creosote.

This Risk Assessment  is not required.

B. CHRONIC DIETARY [Reference Dose (RfD)]

Type of Study:

MRID No.:

Executive Summary:

Dose Proposed for Consideration:

Uncertainty Factor(s) Proposed for Consideration:

Proposed RfD:

Comments about Study/Endpoint/Uncertainty Factor(s):  A chronic dietary
risk assessment is not required for creosote, as dietary exposure is not
anticipated for this chemical.

This risk assessment is not required.

C.  OCCUPATIONAL / RESIDENTIAL EXPOSURE

1.    DERMAL ABSORPTION

In 2003, the Toxicology disciplinary chapter for  the reregistration
eligibility decision (RED) document included toxicity endpoints of
concern, among them an estimation of the magnitude of dermal absorption
for creosote.  As there were no data at that time specifically examining
dermal absorption of creosote, a factor of 50% was estimated, based on
comparison of the  oral and dermal LOAELs from the developmental
toxicity study in rats (MRID # 43584201) and the 90-day dermal toxicity
study in rats (MRID # 43616101) using the P1/P13 blend. The oral LOAEL
of 175 mg/kg/day observed in the developmental toxicity study, when
compared to the dermal LOAEL of 400 mg/kg/day observed in the dermal
toxicity study, yields an absorption factor of 44%, which was rounded up
to 50% by the Committee.  The rounding to 50% took  into account the
significant dermal irritation which occurs from dermal exposure to
creosote.

Beginning in 2005, a series of meetings were held involving scientific
and regulatory staff of the Antimicrobials Division and the Health
Effects Division, Office of Pesticide Programs, U.S. Environmental
Protection Agency, the Pest Management Regulatory Agency, Health Canada,
and the Creosote Council III as the Creosote Couincil did not agree with
the 50% dermal absorption factor determination.  Over the next two
years, a study protocol was discussed to examine dermal absorption of
the creosote mixture. The study protocol was  approved in 2007 and the
dermal absorption study was submitted for review by the Office of
Pesticide Programs in 2007.  The studies submitted consisted of an in
vivo dermal absorption study in the rat as well as an in vitro dermal
absorption study using both rat and human skin.  The executive summaries
of these studies are reproduced below from the data evaluation records.

CITATION:	Fasano, W. (2007) AWPA P1-P13 Creosote: In vivo dermal
absorption in the rat. E.I. du Pont de Nemours and Company, HaskellSM
Laboratory for Health and Environmental Sciences, Newark, Delaware.
Laboratory Project ID:  DuPont-19622, July 2, 2007. MRID 47179501.
Unpublished.

SPONSOR:	The Creosote Council III, P.O. Box 160, Valencia, Pennsylvania
16059.

EXECUTIVE SUMMARY:  In a dermal penetration study (MRID 47179501) AWPA
P1-P13 Creosote (98.5% a.i.) spiked with eight radiolabeled target
chemicals (approx. 43% of the chemicals in creosote) was applied to the
clipped dorso-lumbar skin (10.5 cm2) of eight male Sprague-Dawley rats
at a dose of 10.7 mg/cm2 skin (10 µL/cm2, total radioactivity 16.7
µCi). The exposure duration was 8 hours.  At the end of 8 hours,
animals were removed from the metabolism cages, and the application
sites were washed with 2% Ivory soap solution followed by a water rinse
and then a dry natural sponge. Four rats were then euthanized (0 hours
post-exposure) while the other 4 rats were  returned to the metabolism
cages for further excreta collection. These 4 rats were sacrificed at
496 hours post-exposure.

The mean percent recovery of the radioactivity in the applied dose was
95.009% (±2.569%) and 96.609% (±3.628%) at 0 and 496 hours
post-exposure, respectively. The majority of the administered dose was
recovered from the skin wash sponges; the mean percent recovery was
59.283% (±12.54%) for the 0-hr post-exposure group and 56.822%
(±8.294%) for the 496-hr post-exposure group. The mean percent absorbed
dose was 6.342% (±0.808%) at 0 hours post-exposure and 33.959%
(±8.445%) at 496 hours post-exposure, with a mean percent of 1.553%
(±0.299%) and 0.005% (±0.003%), respectively, present in the skin
after removal of the stratum corneum. Most of the absorbed dose had been
excreted by 496 hours post-exposure, with a mean of 18.97% (±4.97%) of
the dose eliminated in the urine and 12.60% (±4.11%) eliminated in the
feces.

In a supplemental dermal penetration study intended to clarify the
results for the 496 post-exposure group in the initial main study, AWPA
P1-P13 Creosote (98.5% a.i.) spiked with eight radiolabeled target
chemicals was applied to the shaved dorsal skin (10.5 cm2) of four male
Sprague-Dawley rats at a dose of 10.7 mg/cm2 skin (10 µL/cm2, total
radioactivity 18.9 µCi). The exposure duration was 8 hours. Animals
were sacrificed at 496 hrs post-exposure (504 hrs post-dosing). In the
supplemental absorption study, the O-ring, which demarcated the
application area, was applied without glue following the dose
application, and was removed at the end of the 8-hr exposure. In the
main study, the O-ring had been glued to the skin one day prior to dose
application and remained in place until study termination.

In the supplemental study, the mean percent recovery of the
radioactivity in the applied dose was 92.775% (±2.70%) at 496 hours
post-exposure. The majority of the administered dose was recovered from
the body wrap (34.228±6.328%), skin wash (22.240±7.818%), and O-ring
(27.452±3.680%).   Although the mean percent absorbed dose was reported
in this supplemental experiment as 8.853±1570%, with a mean percent of
0.005% present in the skin after removal of the stratum corneum, the
presence of a significant amount of radioactivity in the body wrap after
8 hours adds uncertainty as to the actual available dose.  In addition,
in the first experiment, dermal absorption was still evident after
washing of the skin at 8 hours and monitoring of urinary and fecal
excretion of radioactivity from 8 hours onward. Therefore, the data are
not conclusive of a reduced dermal absorption based on the contention
that the O-ring or the glue had an influence on dermal absorption.

In a preliminary plasma kinetic (dermal bioavailability) study, neat
creosote was applied to the clipped dorso-lumbar skin (10.5 cm2) of four
male Sprague-Dawley rats (10 µL/cm2) for an exposure duration of 8
hours; animals were sacrificed 168 hours post-dosing (160 hours
post-exposure). None of the twelve target creosote chemicals analyzed in
the plasma were detected above their detection limit.

This study in the rat is ACCEPTABLE-NON-GUIDELINE  Although only one
exposure duration and one exposure concentration were evaluated, this
was part of an agreement in study design between the Antimicrobials
Division and the registrant.

EXECUTIVE SUMMARY:  In an in vitro dermal absorption study using rat and
human skin preparations (MRID 47179502), AWPA P1-P13 Creosote (98.5%
a.i.) spiked with eight radiolabeled target chemicals was applied to 6
rat and 6 human skin preparations mounted in individual static diffusion
cells at a nominal dose of 10,700 µg creosote/cm2 (1 µCi/skin).
Samples were collected from the receptor chambers at 0.5, 1, 2, 4, and 8
hours post-application. The skin was washed 8 hours post-application and
the study terminated. The amount of the applied dose absorbed was
considered to be the amount of radioactivity measured in the receptor
fluid.

The mean total recovery of the applied dose for the rat and human skin
was 78.3% and 83.9%, respectively. The mean absorbed dose was 15.1% for
the rat skin and 3.34% for the human skin. The mean rate of penetration
was 85.3 µg equiv/cm2/hr for the rat skin and 19.7µg equiv/cm2/hr for
the human skin. The mean rate of penetration and the mean total
penetration for the rat skin were approximately 4.3 times and 4.4 times
greater than that for the human skin, respectively.

This in vitro study using rat and human skin sample preparations is
currently not acceptable for regulatory purposes. Additional data must
be provided in order to consider the data in this study for assessment
of dermal absorption in conjunction with the submitted in vivo dermal
absorption study  (MRID 47179501).  Deficiencies are listed at the end
of this review.

Recent Developments

The in vitro study was determined to be unacceptable for regulatory
purposes from initial review, based on the lack of data demonstrating
that the concentration of the creosote solution did not exceed
solubility limits and therefore did not have an artefactual influence on
the magnitude of absorption in the in vitro test system.

The Office of Pesticide Programs further determined that from the in
vivo data, a value of  33.9 (34%) was appropriate for the magnitude of
dermal absorption in the in vivo test system. This was concluded on the
basis of data demonstrating continued absorption of the creosote mixture
after 8 hours as evidenced by urinary and fecal excretion of radiolabel.
The registrant presented an argument that the O-ring used in the initial
study may have acted as a depot for creosote-derived readioactivity and
should therefore be considered artefactual, based on a supplemental
study conducted where the O-ring was not glued to the skin of the
animal.  However, significant radioactivity was recovered from the body
wrap used in this supplemental study, compromising interpretation of the
supplemental study results.

In January of 2008, the Creosote Council met again with scientific and
regulatory staff of the Office of Pesticide Programs to discuss their
interpretation of the dermal absorption data.  The main point of their
presentation was that the Office of Pesticide Programs should consider
the ratio of absorption of creosote in rat skin vs. human skin based on
the submitted data. These data show an approximate 8-fold difference in
absorption through rat skin vs. human skin (34% in rat skin in vivo and
in vitro vs. 4.2% in human skin in vitro).

Conclusions

The scientific personnel involved in the dermal absorption discussion
have determined that, based on the available data, that the 8-fold
factor for rat skin vs. human skin with respect to absorption of
creosote is supported by the submitted data. However, uncertainties
still exist with these data:

1) The registrant submitted data on solubility limits of the 8 marker
components used in the in vivo dermal absorption protocol as
representative of creosote. The registrant did not submit solubility
limits for the actual creosote mixture itself. While the solubility data
submitted by the registrant indicated that the solubility limits were
not exceeded for any of the 8 marker compounds used as radiolabelled
tracers, there is uncertainty as to how the mixture behaves.

2) There is uncertainty regarding absorption after 8 hours exposure.
The O-ring data are not conclusive of an effect of the O-ring  acting as
a depot, as absorption is still seen after 8 hours of exposure and
washing of the skin surface contained by the O-ring.

Based on the uncertainties, 8-fold factor describing the difference in
dermal absorption between rat and human skin is acceptable, but the
dermal absorption value for creosote is concluded to be 5% (34% value
from the rat study divided by 8 and rounded upward).

Percentage (%) Dermal Absorption:  5%

2. SHORT-TERM DERMAL (1 - 7 days)

 Study Selected: Developmental Toxicity in Rats (P1/P13)

MRID No.: 43584201

Executive Summary:  In a developmental toxicity study using P1/P13
creosote (MRID # 43584201), pregnant female Sprague-Dawley rats
(30/dose) were administered P1/P13 creosote at dose levels of 0, 25, 50,
and 175 mg/kg/day on gestation days 6 through 15 inclusive.  Decreased
body weight and food consumption were observed at the 175 mg/kg/day dose
level in this study in maternal rats.   Decreased uterine weight was
observed in maternal rats at the high dose, which is reflected partly by
the decreased live fetuses per litter at the high dose (although mean
fetal weight was not affected).   Cesarean section observations showed
significantly increased resorptions and post-implantation loss as well
as decreased number of live fetuses per litter at the 175 mg/kg/day
dose.   Based on the results of this study, the Maternal NOAEL is 50
mg/kg/day, and the Maternal LOAEL is 175 mg/kg/day, based on decreased
body weight gain and food consumption during the study.

No treatment-related malformations (external, visceral or skeletal)
were observed in any of the fetuses at 25 mg/kg bw/day. At 50 mg/kg
bw/day, the overall incidence of malformations on a fetal and litter
basis were statistically elevated compared to controls. However, these
individual malformations were not seen at higher dose levels and/or fell
within the range of historical control data. At 175 mg/kg bw/day there
was (i) an overall significant increased incidence of developmental
malformations, (ii) increased incidence of cardiovascular, vertebral and
digital malformations, compared to lower dose levels, concurrent
controls or historical controls (2429 and 2898 fetuses examined
viscerally and skeletally respectively) and (iii) an increased incidence
of malformations at this dose level in spite of increased fetal loss
(resorptions) (Beck and Lloyd, 1963) thus resulting in fewer fetuses
available for teratogenic examination. Although the incidence of fetal
malformations observed at 175 mg/kg bw/day dose level in rats was low
and could be related to maternal stress (decreased body weight gain and
food consumption), the teratogenic potential of P1/P13 Creosote cannot
be ruled out. Based on these data, the developmental toxicity NOAEL is
50 mg/kg/day, and the developmental toxicity LOAEL is 175 mg/kg/day,
based on increased post-implantation loss, increased mean resorptions,
decreased live fetuses per litter, and increased developmental
malformations.

Dose and Endpoint: Maternal NOAEL of 50 mg/kg/day, based on decreased
body weight gain during the study at 175 mg/kg/day.

Comments about Study/Endpoint: Although a 90-day dermal toxicity study
was available, the developmental toxicity study was chosen  for the
following reasons:  1) dermal toxicity studies (including the 2-week
range-finding studies) did not measure developmental endpoints, which
are present in both developmental toxicity studies;  2) the results of
dermal toxicity studies would not be protective of infants and children
from residential exposure to creosote.  An uncertainty factor (MOE) of
100 is applied to this risk assessment.  The dermal absorption factor of
5% should be used when converting from an oral to dermal risk
assessment.

This risk assessment is required.

3.  INTERMEDIATE-TERM DERMAL (1-Week to Several Months)

 Study Selected: 90-Day Dermal Toxicity Study in Rats         Guideline
#:  82-3

MRID No.: 43616201

Executive Summary: In a 90-day dermal toxicity  study (MRID # 43616201),
Charles River rats ( 10/sex/dose) were given dermal applications of P2
creosote in corn oil at dosage levels of 0, 4, 40 or 400 mg/kg bw/day.
There was no mortality observed in this study at any dose level. Body
weight in high dose males was decreased 7-8% during weeks 9-12 of the
study, and bodyweight gain decreased 15% in high dose males for the
treatment period. Food consumption in high dose males was decreased
during weeks 2-4 and week 6 by 4-10% vs control. Only slight dermal
irritation was observed in high dose males. No effects were observed on
hematology or clinical chemistry. Treated skin in the 400 mg/kg/day dose
groups (male and female) was observed with increased incidence of dermal
inflamation.  Based on the results of this study, the systemic LOAEL is
400 mg/kg/day, based on decreased body weight gain in male rats. The
systemic NOAEL is 40 mg/kg/day.  For females,  the NOAEL is set at 400
mg/kg bw/day since no systemic toxic effects were noted in any of the
treated groups.

Dose and Endpoint:  NOAEL of 40 mg/kg/day, based on decreased body
weight gain at 400 mg/kg/day.

Comments about Study/Endpoint:   an uncertainty factor (MOE) of 100 is
applied to this risk assessment. As a dermal endpoint was used, the
dermal absorption factor does not need to be employed for this risk
assessment.

This risk assessment is required.

4.  LONG-TERM DERMAL (Several Months to Lifetime)

Type of Study:    2-Generation Reproduction
Guideline #:  83-4

MRID No.:  N/A (reviewed by CAL EPA )

Executive Summary:  In this study, Charles River Crl:CD rats,
26/sex/group, were dosed by gavage with P1/P13 creosote in corn oil at
doses of 0, 25, 75, and 150 mg/kg/day. Pre-mating treatment phase lasted
approximately 17 weeks, which may have contributed to the decreased
fertility observed in this study.  Systemic effects observed in this
study for parental animals included decreased body weight during the
pre-mating period at all dose levels, with a dose-response noted for
this effect. Salivation was also observed at 75 mg/kg/day and above in
the F1 generation.  Effects in offspring included a dose-related
decrease in growth of offspring of the F0 generation starting at 25
mg/kg/day (as shown by decreased pup weight). For the F0 pups, mean
number of liver pups per litter was decreased at 75 and 150 mg/kg/day,
and percent live pups at 175 mg/kg/day was also decreased. In the F1
pups, the percent live pups was decreased at 75 nad 150 mg/kg/day, but
pup growth was affected only at 150 mg/kg/day as shown by decreased mean
pup weight. Decreased fertility and pregnancy indices were observed in
the F1 female parental rats at all dose levels, but this was not
interpreted as a treatment-related effect, as it was more likely related
to the fact that the critical weight for fertility was exceeded by the
17-week pre-mating interval. Based on the results of this study, the
Parental Systemic NOAEL is < 25 mg/kg/day, and the Parental Systemic
LOAEL is 25 mg/kg/day, based on decreasedpre-mating body weight.  The
developmental NOAEL in this study is < 25 mg/kg/day, and the
developmental LOAEL is 25 mg/kg/day, based on a dose-related decrease in
pup body weight for the F0 pups from days 14-21. The reproductive NOAEL
is < 25 mg/kg/day, and the reproductive LOAEL is 25 mg/kg/day, based on
reduced pregnancy and fertility indices in F1 female parental rats.

Dose and Endpoint:  Parental LOAEL of 25 mg/kg/day, based on decreased
pre-mating body weight.

Comments about Study/Endpoint:   An extra uncertainty factor of 3x is
applied to the MOE of 100,  based on  the use of a LOAEL .  The dermal
absorption factor of 5% should be used when converting from oral to
dermal risk assessment.

This risk asessment is required.

  5a.   INHALATION-Creosote (any time period)

Type of Study: 90-day inhalation toxicity in rats         Guideline #:
82-4

MRID No.: 43600901

Executive Summary: In a 13-week inhalation toxicity study (MRID #
43600901), 20 Sprague-Dawley rats/sex/group were treated for 5
days/week, 6 hours/day with P2 Creosote CTM via whole body exposure at
doses of 0, 4.7, 48 or 102 mg/m3 (0, 0.005, 0.048 or 0.102 mg/L ) in air
measured gravimetrically.  The aerosol size MMAD was between 2.4 and 2.9
microns with a geometric standard deviation between 1.85 and 1.91.
Subsequent to the exposure period 10 rats/sex/group were allowed to
recover from treatment for 6 weeks.

During the exposure period, two animals (low dose female; mid dose male)
were sacrificed in extremis and the cause of morbidity was not related
to treatment.  Significant treatment-related findings in mid and high
dose animals included decreased terminal body weight and body weight
gain (m/f), altered hematological parameters (decreased hemoglobin
content, hematocrit, erythrocyte and platelet counts; increased
reticulocyte counts and mild poikilocytosis, m/f) and biochemical
parameters (increased serum cholesterol levels, m/f).  In both sexes
macroscopic discolouration of the lungs persisted through the recovery
period and correlated with the presence of black pigment granules within
alveolar macrophages.  Both sexes showed increased absolute and relative
liver and thyroid weights and increased lung/trachea/body weight ratios.
 Absolute and relative thyroid weights of high dose animals actually
increased after the recovery period.  An increased incidence of lesions
of the nasal cavity epithelium (chronic inflammation) was noted
following treatment (all treatment groups, m/f) but appeared to lessen
in incidence and severity during the recovery period (mainly the high
dose group, m/f).  During exposure an increased incidence of thyroid
follicular epithelial cell hypertrophy occurred in all male groups
including control and in the high dose female group.  At recovery the
male incidence remained similar to that observed at exposure while the
incidence in females of the high dose group had declined.  The incidence
of thyroid follicular cell hypertrophy was slightly increased in low and
mid dose females after the recovery period. Slightly increased incidence
of mild poikilocytosis was observed in all treatment groups (m/f)
including the low dose group and control, which persisted through the
recovery period. Low dose animals exhibited lesions of the nasal cavity
epithelium which had resolved after the recovery period.  Based on the
results of this study, the systemic LOAEL is 48 mg/m3  , based on
decreased body weight and weight gain, altered hematology ad clinical
chemistry, increased absolute and relative weight of the liver ad
thyroid, and increased incidence of lesions of the nasal cavity. The
systemic NOAEL is set at 4.7 mg/m3 (0.0047 mg/L )  for P2 Creosote CTM
in rats.

Dose and Endpoint: NOAEL of 0.0047 mg/L, based on decreased body weight
gain, altered hematology and clinical chemistry, and increased absolute
and relative weight of the liver and thyroid observed at 0.048 mg/L.

Comments about Study/Endpoint:  A Margin of Exposure of 100 is
considered adequate for this risk assessment.

This risk assessment is required.

5b. Inhalation – Naphthalene (any time period)

For worker risk, naphthalene was selected as an indicator because 100
percent of the inhalation samples monitored at the pressure treatment
facilities were detectable.  For naphthalene, the Antimicrobials
Division used the inhalation reference concentration (RfC) for
naphthalene published in the EPA’s IRIS database adjusted for the work
week (i.e., EPA recognizes that the 24 hour/day 7 day/week adjustment to
the RfC is not representative of a typical work day).  The RfC was
derived from a 2 year chronic inhalation study in the mouse in which
exposure was for 6 hours/day, 5 days/week.  The inhalation
route-specific LOAEL is 52 mg/m3 with a target MOE of 300 (10x intra
species variability, 10x inter species extrapolation, and 3x for a lack
of a NOAEL).

Although there is a 13-week inhalation study with creosote from which an
endpoint was derived (as noted above),  an endpoint is selected for
naphthalene and used for inhalation risk assessment to workers because
in the inhalation monitoring study, there were several significant
deficiencies, including (1) no attempt by the study sponsors to relate
inhalation levels found for polynuclear aromatics (PNAs) and coal tar
pitch volatiles (CTPVs) to "total creosote" -- a significant weakness
with the study; (2) analytical problems encountered with the CTPV
samples (all samples were non-detect); (3) the overall inhalation field
fortification percent recoveries for the coal tar pitch volatiles
(CTPVS) were poor (51-57%).  Therefore, EPA did not rely on the CTPV
inhalation exposure monitoring results.  Instead, risk concerns are
indicated using the results of the naphthalene inhalation samples.

D. Margins of Exposure for Occupational / Residential Risk Assessments

A Margin of Exposure of 100 is adequate for short-term and
intermediate-term dermal and inhalation risk assessments for creosote.
A Margin of Exposure of 300 is adequate for long-term dermal risk
assessments for creosote. For inhalation risk assessment, a Margin of
Exposure of 100 is adequate for creosote;  for naphthalene,  a Margin of
Exposure of 300 is adequate. The extra 3x uncertainty factor is added to
the standard factor of 100 for use of a LOAEL from the 2-year study on
naphthalene.

E. Recommendation for Aggregate Risk Assessments

There is the potential for post-application exposures to creosote.
However, the dermal and incidental oral exposures to creosote that may
occur from scenarios such as railroad ties used as landscape timbers are
expected to be episodic in nature and of short duration. Thus, an
aggregate assessment is not  necessary.

III.  Classification of Carcinogenic Potential:

 A large body of experimental evidence exists which shows a positive
relationship between exposure to creosote and development of tumors in
experimental animals.  In addition to its tumor-promoting potential, the
ability of creosote to induce lung tumors after dermal application was
examined. Dermally applied creosote  (0.25ml undiluted, twice weekly for
8 months) induced 5.8 lung adenomas per mouse in mice housed in
stainless steel cages, while untreated controls showed 0.5 lung
adenomas/mouse (Roe et al, Cancer Res. 18: 1176-1178, 1958).
Carcinogenicity of two high-temperature derived creosote oils was
studied by Poel and Kammer (JNCI 18: 41-55, 1957).  The light creosote
fraction is composed mainly of benzene, toluene, xylene, and solvent
naphtha, while the blended oil is composed of creosote oil, anthracene
oil, and oil drained from recovery of naphthalene. Oils were applied by
drops to the skin of mice at concentrations of 20%, 50%, or 80% three
times a week for life.  By weeks 21-26, both oils had induced skin
tumors.  Several mice exhibited metastases to the lungs or regional
lymph nodes.

In an oral carcinogenicity study conducted by  Culp et al. (1996), the
carcinogenicity of two coal tar mixtures and pure benzo[a]pyrene (BaP)
was studied.  Coal tar mixture 1 (CTM-1) was a composite of coal tar
samples from seven coal gasification plant waste sites and was dosed at
0.0, 0.01, 0.03, 0.1, 0.3, 0.6, and 1.0% of diet.  Coal tar mixture 2
(CTM-2) was a composite of coal tars from three waste sites with high
BaP content and was dosed at 0.0, 0.01, 0.03, 0.1, 0.3% of diet.  An
additional group was dosed with pure BaP at 0, 0.0005, 0.0025, and 0.01
% in diet.  A control group received solvent control in diet.  Each
group consisted of 48 mice.

In mice exposed to coal tar, coal tar acted as a systemic carcinogen
and induced a dose-related increase in hepatocellular adenomas and
carcinomas, alveolar/bronchiolar adenomas and carcinomas, forestomach
squamous epithelial papillomas and carcinomas, small intestine
adenocarcinomas, histiocytic sarcomas, hemangiosarcomas in multiple
organs, and sarcomas in several tissues.

The incidence of forestomach tumors increased sharply between the 0.1
and 0.3% doses.  However, there was not a proportional increase in
forestomach tumors above 0.3% because these mice died from
adenocarcinomas of the small intestine.  Tumors of the esophagus,
observed in BaP treated mice, were not observed in the CTM1 or CTM-2
treated groups.  Lung and hepatocellular tumors observed in the CTM1 and
CTM2 groups were not observed in BaP treated animals.

Multiple neoplasms were noted in liver, lung, forestomach, and the small
intestines of exposed mice.  Liver neoplasms occurred in 1, 0,  and 4
mice fed 0.03, 0.1 and 0.3% CTM-1, respectively.  Lung neoplasms
occurred in 21, 11 and 13 mice fed 0.3% , 0.6% , 1.0% CTM-1,
respectively.  Eight mice in the 0.3% CTM-2 group had multiple lung
neoplasms.  Forestomach carcinomas were found in 2 and 1 mice fed 0.6%
or 1.0% CTM-1, respectively.  Adenocarcinomas were found in the small
intestines (jejunum) of 2 and 12 mice fed 0.6% and 1.0% CTM-1,
respectively.  Groups dosed with (0.3% CTM-1 or CTM-2 had significantly
reduced survival.

 The incidence of forestomach tumors increased steeply between 5 and 25
ppm, equivalent to 20.5 and 104 μg BaP/day.  Tumors of the esophagus
were not observed in the CTM1 or CTM-2 treated groups.  Lung and
hepatocellular tumors, observed in CTM treated mice, were not observed
in mice fed BaP.

Multiple neoplasms of the forestomach occurred in 8 and 21 mice fed 25
and 100 ppm BaP, respectively.  Multiple neoplasms of the esophagus and
tongue were noted in 6 and 3 mice, respectively, fed 100 ppm BaP.  It
should be noted that all animals in 100 ppm group died before
termination of the study.

In humans, evidence for carcinogenicity of creosote varies. Several
studies have associated occupational exposure to creosote with
development of skin cancer, with a latency period of 20-25 years. These
studies are very old (1920's to 1940's), when occupational safety
practices were much more lax than today.  More recent reports (1980)
show no increase in risk of skin, bladder, or lung cancer in wood
treatment plant workers, or after treatment for 4 years with coal-tar
medicinal therapy for treatment of dermatitis.  These reports, however,
were limited in scope. Those reports associated with therapeutic use of
coal tar did not mention the fact that the composition of the coal tar
used therapeutically is different than that used for wood treatment.  In
the report on wood treatment workers, the population studied was small,
and the follow-up period was too short to allow a long enough latency
for tumor development.

The Agency in 1988 acknowledged limitations on conducting a quantitative
risk assessment from use of a single component of creosote (Guidance for
the Reregistration of Pesticide Products Containing Coal Tar/Creosote As
the Active Ingredient, USEPA, 1988), but it was also observed that
creosote mixtures are “complex mixtures with known synergistic
effects” on carcinogenicity.

Based on the availability and analysis of the Culp et al. (1998) data,
and in conjunction with the Pest Management Regulatory Agency, Health
Canada, a  quantitative risk assessment on carcinogenicity of creosote
has been performed. A dermal carcinogenicity study by Bushmann et al.
(1997) was also available, but was determined not suitable for
quantitative assessment of carcinogenicity. Ulceration of the skin was
significant finding of the dermal carcinogenicity study which
potentially affected tumor response. In addition, systemic toxicity was
not examined, and complete histopathology data were not available. Based
upon the analysis of the Culp et al. data, an oral cancer potency factor
of 6.28 x 10-6 (µg/kg/day)-1 for the coal tar mixture 1 tested in this
study was selected, on the basis of forestomach tumors observed. The
Agency has not formally updated the classification of creosote using the
2005 guidelines for Carcinogen Risk Assessment, but quantitation has
been performed for the creosote mixture.

IV. MUTAGENICITY

 In consideration of the available evidence that creosote is a positive
mutagen, the Agency waived the requirement for the standard mutagenicity
battery, and instead required dominant lethal testing of both the P1/P13
and P2 blends. The executive summaries of these studies are shown below.

In a  rat dominant lethal assay (MRID not available), male
HSD:Sprague-Dawley CD rats were treated orally once per day for five
consecutive days with Cresosote P1/P13 at target doses of 725, 362.5 or
181.25 mg/kg body weight/day in a volume of 2.5 mL/kg.  Actual doses
determined by chemical analysis were 857.5, 330.5 and 230.8 mg/kg/day.
Twenty-one rats were dosed at the two lower doses and 26 rats at the
highest dose.  The vehicle was corn oil.  Seven days after the initial
dosing, each male was mated with two untreated females per week for 10
weeks. Females were sacrificed 13 days after the midweek of the
presumptive mating day and the following data collected:  total
implantations per female, corpora lutea per female, preimplantation
losses per female, live implantations per female, dead implantations per
female, proportion of females with one or more dead implantations,
proportion of females with two or more dead implantations and dead
implantations/total implantations (expressed as a percentage).  The
fertility index, computed as the number of fertile females (with corpora
lutea present) per number of mated females, was also determined.

Creosote P1/P13 was tested to toxic doses.   In the dominant lethal
study, all rats in the top two treatment groups but none in the low dose
group showed decreased activity following dosing and all rats in the
high dose group had dyspnea.  Two animals in the low dose group and two
in the high dose group had material around the nose and mouth. Other
pharmacotoxic signs were limited to a few animals in the high dose group
and included lacrimation, deposition of the test material around the
eyes, increased salivation and anogenital staining.  One high dose rat
died following the fourth dose.  A dose-related decrease in body weight
in the low-, mid-, and high-dose animals, compared to the solvent
controls, was seen during the dosing period, and this initial weight
loss was not recovered in mid- and high-dose rats during the ten week
mating period.   Statistically significant differences from control
values were seen in a number of endpoints throughout the study;;
however, with the exception of results from mating group nine, none were
endpoints indicative of a dominant lethal effect.  In mating group nine,
statistically significant increases were seen in dead implantations per
female, the percentage of females with ( one implantation, the
percentage of females with ( two implantations and the percent dead
implantations per total implantations. These increases were seen at the
low and mid doses but not at the high dose.  Also, the vehicle control
values in mating group nine were unusually low compared to those in the
other weekly mating groups (there were fewer preimplantation losses
(0.85 per female) and fewer dead implantations (0.41 per female) than
seen for the vehicle controls in the other mating groups (1.53 ± 0.37
and 0.85 ± 0.20 per female, respectively) and values for percentage of
females with ( one and two dead implantations and the percent dead
implantations per total implantations were depressed).  The  results,
although statistically significant, are thus not considered biologically
significant.  Positive and solvent control values were appropriate
except where noted for the vehicle controls in mating group nine.  Based
on the results of this study, there was no evidence that Creosote P1/P13
induced dominant lethals in any germ cell stage in male rats as tested
in this study.

In a  rat dominant lethal assay (MRID not available), male
HSD:Sprague-Dawley CD rats were treated orally once per day for five
consecutive days with Creosote P2 at target doses of 775, 387.5 or
193.75 mg/kg body weight/day in a volume of 2.5 mL/kg.  Actual doses by
chemical analysis were 866.3, 431, or 199.3 mg/kg body weight/day.
Twenty-one rats were dosed at the two lower doses and 26 rats at the
highest dose.  The vehicle was corn oil.  Seven days after the initial
dosing, each male was mated with two untreated females per week for 10
weeks. Females were sacrificed 13 days after the midweek of the
presumptive mating day and the following data collected:  total
implantations per female, corpora lutea per female, preimplantation
losses per female, live implantations per female, dead implantations per
female, proportion of females with one or more dead implantations,
proportion of females with two or more dead implantations and dead
implantations/total implantations (expressed as a percentage). The
fertility index, computed as the number of fertile females (with corpora
lutea present) per number of mated females, was also determined.

Creosote P2 was tested to an adequate dose.  All rats in all treatment
groups showed decreased activity following dosing.  Other clinical
signs, limited to a few animals in which there was a back-up of test
material during dosing, were lacrimation, deposition of the test
material around the eyes and increased salivation in one high-dose male,
labored breathing in one low-dose male and two high-dose males, and
material around nose and mouth in two low-dose, one medium-dose and four
high-dose males.  Reduced food consumption was seen in all high-dose
rats.  No dosing- or test material-related deaths occurred during the
study.  A dose-related decrease in body weight in the low-, mid-, and
high-dose animals, compared to the solvent controls, was seen during the
dosing period, and this initial weight loss was not recovered in mid-
and high-dose rats during the ten week mating period.  Statistically
significant differences from solvent control values (p ( 0.05) were seen
for a number of endpoints during the first nine weekly mating intervals
but, with one exception, not in endpoints considered indicative of
dominant lethality.  The one exception was a significant increase in the
number of dead implants over the solvent control value in the sixth
mating group at the lowest Creosote P2 dose.  This increase was not
considered biologically relevant because no significant increases were
seen at higher doses or in other endpoints concerning dead implants.  In
the tenth mating group (exposure to the test material at the
spermatogonial stem cell stage), an apparently dose-related increase was
seen in the number of dead implantations per female, the percentage of
females with ( 1 dead implant, the percentage of females with ( 2 dead
implants and the percentage of dead implantations per total
implantations.  The increases reached statistical significance at the
highest dose for the first two endpoints.   Positive and solvent control
values were appropriate.  The data in this study, while indicating a
positive effect at week 10 of treatment, are not considered to be
treatment-related, based on the conclusion that while dead implantations
per female was significantly increased at the highest dose tested at
mating week 10, the number of live implants/female was not significantly
reduced (<5% lower than control).  In addition,  no dominant lethal
effects were seen at weeks 8 or 9, which would also sample
spermatogonial cells.   Therefore, creosote P2 is considered to be
negative for dominant lethal effects in rats.

V.  CONSIDERATIONS for Special Sensitivity

1.  Neurotoxicity Data

  There are no current Agency guideline neurotoxicity studies available
for creosote.  Of the existing studies available, there is no evidence
of neurotoxicity for either the P1/P13 or P2 blends of creosote,
although there is valid concern for some of the components of creosote,
which are known to be neurotoxic (i.e. naphthalene).  Data  from the
ATSDR Toxicological profile for Creosote  showed increased brain-to-body
weight ratios after exposure of male and female rats to beechwood
creosote (used therapeutically in the past as a disinfectant and
expectorant, and composed mainly of phenol, cresols, guaicol, xylenol,
and creosol)  to 257 mg/kg/day in the diet for 3 months in male rats, or
exposure of female rats for 52 weeks to 297 mg/kg/day in the diet, or
exposure of male and female rats for 96 weeks in the diet to 143 and 394
mg/kg/day, respectively. Acute exposure of male and female rats to 600
and 313 mg/kg beechwood creosote resulted in  convulsions. Although
signs of neurologic involvement were evident,  no treatment-related
pathological findings of the central nervous system were noted at
necropsy in these studies.

 Based on the above data, and realizing that creosote is currently
registered only for non -food use and is a restricted use pesticide, no
additional neurotoxicity testing will be required at this time.

2.  Developmental & Reproductive Toxicity

(i)  Developmental Toxicity:

    In a developmental toxicity study using P1/P13 creosote (MRID #
43584201), pregnant female Sprague-Dawley rats (30/dose) were
administered P1/P13 creosote at dose levels of 0, 25, 50, and 175
mg/kg/day on gestation days 6 through 15 inclusive.  Decreased body
weight and food consumption were observed at the 175 mg/kg/day dose
level in this study in maternal rats.   Decreased uterine weight was
observed in maternal rats at the high dose, which is reflected partly by
the decreased live fetuses per litter at the high dose (although mean
fetal weight was not affected).   Cesarean section observations showed
significantly increased resorptions and post-implantation loss as well
as decreased number of live fetuses per litter at the 175 mg/kg/day
dose.   Based on the results of this study, the Maternal NOAEL is 50
mg/kg/day, and the Maternal LOAEL is 175 mg/kg/day, based on decreased
body weight gain and food consumption during the study.

No treatment-related malformations (external, visceral or skeletal) were
observed in any of the fetuses at 25 mg/kg bw/day. At 50 mg/kg bw/day,
the overall incidence of malformations on a fetal and litter basis were
statistically elevated compared to controls. However, these individual
malformations were not seen at higher dose levels and/or fell within the
range of historical control data. At 175 mg/kg bw/day there was (i) an
overall significant increased incidence of developmental malformations,
(ii) increased incidence of cardiovascular, vertebral and digital
malformations, compared to lower dose levels, concurrent controls or
historical controls (2429 and 2898 fetuses examined viscerally and
skeletally respectively) and (iii) an increased incidence of
malformations at this dose level in spite of increased fetal loss
(resorptions) (Beck and Lloyd, 1963) thus resulting in fewer fetuses
available for teratogenic examination. Although the incidence of fetal
malformations observed at 175 mg/kg bw/day dose level in rats was low
and could be related to maternal stress (decreased body weight gain and
food consumption), the teratogenic potential of P1/P13 Creosote cannot
be ruled out. Based on these data, the developmental toxicity NOAEL is
50 mg/kg/day, and the developmental toxicity LOAEL is 175 mg/kg/day,
based on increased post-implantation loss, increased mean resorptions,
decreased live fetuses per litter, and increased developmental
malformations.

In  a developmental toxicity study (MRID # 43584202), pregnant female
Sprague-Dawley rats (30/dose) were administered P2 creosote by gavage
on gestation days 6 through 15 inclusive at dose levels of 0, 25, 75,
and 225 mg/kg/day.

 Decreased body weight gain and food consumption were observed at all
dose levels and are considered treatment-related. Cesarean section data
observed at 225 mg/kg/day  showed  decreased live fetuses per litter,
decreased fetal body weight, and increased post-implantation loss.
Based on the data in this study, the Maternal NOAEL is determined to be
< 25 mg/kg/day, and the Maternal LOAEL is determined to be 25 mg/kg/day,
based on decreased body weight gain and food consumption.   The
Developmental NOAEL is determined to be 75 mg/kg/day, and the
Developmental LOAEL is determined to be 225 mg/kg/day.

(ii)  Reproductive Toxicity:

In this study, Charles River Crl:CD rats, 26/sex/group, were dosed by
gavage with P1/P13 creosote in corn oil at doses of 0, 25, 75, and 150
mg/kg/day. Pre-mating treatment phase lasted approximately 17 weeks,
which may have contributed to the decreased fertility observed in this
study.  Systemic effects observed in this study for parental animals
included decreased body weight during the pre-mating period at all dose
levels, with a dose-response noted for this effect. Salivation was also
observed at 75 mg/kg/day and above in the F1 generation.  Effects in
offspring included a dose-related decrease in growth of offspring of the
F0 generation starting at 25 mg/kg/day (as shown by decreased pup
weight). For the F0 pups, mean number of liver pups per litter was
decreased at 75 and 150 mg/kg/day, and percent live pups at 175
mg/kg/day was also decreased. In the F1 pups, the percent live pups was
decreased at 75 nad 150 mg/kg/day, but pup growth was affected only at
150 mg/kg/day as shown by decreased mean pup weight. Decreased fertility
and pregnancy indices were observed in the F1 female parental rats at
all dose levels, but this was not interpreted as a treatment-related
effect, as it was more likely related to the fact that the critical
weight for fertility was exceeded by the 17-week pre-mating interval.
Based on the results of this study, the Parental Systemic NOAEL is < 25
mg/kg/day, and the Parental Systemic LOAEL is 25 mg/kg/day, based on
decreasedpre-mating body weight.  The developmental NOAEL in this study
is < 25 mg/kg/day, and the developmental LOAEL is 25 mg/kg/day, based on
a dose-related decrease in pup body weight for the F0 pups from days
14-21. The reproductive NOAEL is < 25 mg/kg/day, and the reproductive
LOAEL is 25 mg/kg/day, based on reduced pregnancy and fertility indices
in F1 female parental rats.

3. Determination of Susceptibility

 There are no existing food uses for creosote.  Therefore, an FQPA
assessment is

 not necessary but the available data on developmental, reproductive,
and neurotoxicity was

examined. The available evidence on developmental and reproductive
effects

 of creosote suggests potential infants and children’s susceptibility
of creosote,

based on the severity of offspring vs. maternal effects  observed with
testing of

creosote in the P1/P13 blend developmental toxicity study in rats at the
175

mg/kg/day dose level. Testing of the P2 blend of creosote also showed
evidence of

developmental effects at doses below those producing maternal toxicity.

4.  Determination of the Need for Developmental Neurotoxicity Study

  There is no requirement for a developmental neurotoxicity study for
creosote at this time.

VI.  HAZARD CHARACTERIZATION

Acute Toxicity of  P1/P13 Creosote

Guideline No.

Study Type

MRIDs #

Results

Toxicity Category

81-1

Acute Oral

43032101

LD50 =  2451 mg/kg (M); 1893 mg/kg  (F)

III

81-2

Acute Dermal

43032102

LD50 > 2000 mg/kg

III

81-3

Acute Inhalation

43032103

LC50 > 5 mg/L

IV

81-4

Primary Eye Irritation

43032104

irritation clearing in 8-21 days

II

81-5

Primary Skin Irritation

43032105

erythema to day 14

III

81-6

Dermal Sensitization

43675301

study unacceptable

81-8

Acute Neurotoxicity

no study available

Acute Toxicity of P2 Creosote

Guideline No.

Study Type

MRIDs #

     Results

   Toxicity     Category

   81-1

Acute Oral

43032301

LD50 =  2524 mg/kg (M); 1993 mg/kg  (F)

   III

    81-2

Acute Dermal

43032302

LD50 > 2000 mg/kg

    III

    81-3

Acute Inhalation

43032303

LC50 > 5.3  mg/L

    IV

   81-4

Primary Eye Irritation

43032304

irritation clearing within 7 days

   III

81-5

Primary Dermal Irritation

43032305

no irritation after 72 hours, but study must be upgraded

81-6

Dermal Sensitization

43675201

study  unacceptable

81-7

Acute Neurotoxicity

no study available

Subchronic dermal testing with both the P1/P13 and P2 blends of creosote
show a minimum of toxic effects in experimental animals (rats).  Using
the P2 blend, one mortality of questionable significance was observed at
a dose of 400 mg/kg/day, while testing of the P1/P13 blend produced
decreases in body weight gain.  Effects on the skin in both studies were
minimal to moderate.

Subchronic inhalation testing with creosote produced a wider spectrum
of effects.  At a dose of 0.049 mg/L, exposure to the P1/P13 blend
produced myocardial pathology (degeneration, hemorrhage, cardiomyopathy)
in males and females. Altered hematological parameters (decreased
hemoglobin, hematocrit, erythrocytes; increased reticulocytes,
polychromasia, poikilocytosis, anisocytosis) were also observed in males
and females.  Testing of the P2 blend by the inhalation route also
produced altered hematological parameters, and also resulted in
increased absolute and relative liver and thyroid weights. Follicular
cell hypertrophy was observed. Lesions of the nasal cavity were also
observed with the P2 blend.

Developmental and reproductive testing of creosote showed potential
sensitivity of offspring to the P1/P13 blend.  Decreased body weight
gain and decreased food consumption were observed in maternal animals at
a dose of 175 mg/kg/day, but at this same dose, increased
post-implantation loss, increased mean resorptions, and decreased live
fetuses per litter were also observed. An overall significant increase
in incidence of developmental malformations was also observed at the 175
mg/kg/day dose.  Testing of the P2 blend did not show any apparent
susceptibility of developing offspring to creosote, and reproductive
testing of P1/P13 creosote did not show any apparent susceptibility, but
the reproductive toxicity study contained several deficiencies that
compromised interpretation of the data, such as a low fertility and
pregnancy index for F1 female parental rats. Thus, there is some
uncertainty associated with concluding that creosote is devoid of any
reproductive effects.  In this light, the addtional safety factor
mandated by FQPA was employed to account for this uncertainty as well as
for the effects observed from developmental toxicity testing of P1/P13
creosote.

The mutagenicity database for creosote shows positive effects from in
vitro studies, although dominant lethal testing of both the P1/P13 and
P2 blends failed to show a positive effect.

There are no reliable metabolism data on creosote, as the chemical is a
complex mixture of several classes of polycyclic aromatic chemicals.
Assays are in development to identify marker compounds to determine
exposure to creosote.

A large body of experimental evidence exists which shows a positive
relationship between dermal exposure to creosote and development of
tumors in experimental animals.  In addition to its tumor-promoting
potential, the ability of creosote to induce lung tumors after dermal
application wqas examined. Dermally applied creosote  (0.25ml undiluted,
twice weekly for 8 months) induced 5.8 lung adenomas per mouse in mice
housed in stainless steel cages, while ntreated controls showed 0.5 lung
adenomas/mouse (Roe et al, Cancer Res. 18: 1176-1178, 1958).
Carcinogenicity of two high-temperature derive creosote oils was studied
by Poel and Kammer (JNCI 18: 41-55, 1957). The light creosote fraction
is composed mainly of benzene, toluene, xylene, and solvent naphtha,
while the blended oil is composed of creosote oil, anthracene oil, and
oil drained from recovery of naphthalene. Oils were applied by drops
tothe skin of mice at concentrations of 20%, 50%, or 80% three times a
week for life. By weks 21-26, both oils had induced skin tumors.
Several mice exhibited metastases to the lungs or regional lymph nodes.

Based on the availability and analysis of the Culp et al. (1998) data,
and in conjunction with the Pest Management Regulatory Agency, Health
Canada, a  quantitative risk assessment on carcinogenicity of creosote
has been performed. A dermal carcinogenicity study by Bushmann et al.
(1997) was also available, but was determined not suitable for
quantitative assessment of carcinogenicity. Ulceration of the skin was
significant finding of the dermal carcinogenicity study which
potentially affected tumor response. In addition, systemic toxicity was
not examined, and complete histopathology data were not available. Based
upon the analysis of the Culp et al. data, an oral cancer potency factor
of 6.28 x 10-6 (µg/kg/day)-1 for the coal tar mixture 1 tested in this
study was selected, on the basis of forestomach tumors observed. The
Agency has not formally updated the classification of creosote using the
2005 guidelines for Carcinogen Risk Assessment, but quantitation has
been performed for the creosote mixture.

VII. Summary of Toxicology Endpoint Selection for Creosote

EXPOSURE

SCENARIO

Endpoint (mg/kg/day) and Margin of Exposure (MOE)

Effect

Study selected

Acute and Chronic Dietary

 Acute and Chronic Dietary risk assessments not required

Carcinogenicity

(dermal)

Creosote has been shown to exert positive mutagenic effects in vitro,
and has been shown to be positive for carcinogenicity in an
initiation/promotion study.  Creosote  has been classified as a B1
carcinogen in IRIS. An oral cancer slope factor of 6.28 x 10-6  (µg
CTM1/kg/day)-1 was selected for creosote using the data of Culp et al
(1998) for the coal tar mixture 1 (CTM1) on the basis of forestomach
tumors.

Short-Term  (Dermal)

Oral NOAEL=50

MOE = 100

 decreased body weight gain at 175 mg/kg/day

 Developmental Toxicity - Rat

Intermediate-term

(Dermal)

Dermal NOAEL = 40

MOE = 100

Decreased body weight gain at 400 mg/kg/day

90-Day Dermal Toxicity Study in the Rat

Long-Term (Dermal)a

Oral  LOAEL = 25 mg/kg/day

MOE = 300

decreased pre-mating body weight

2-generation reproduction study - Rat

Inhalation-creosote

(any  time period)b

NOAEL = 0.0047mg/m3

MOE = 100

decreased body  weight, body weight gain, altered hematology

90-day Inhalation Study in the Rat with P2 creosote (MRID 43600901)

Inhalation-naphthalene (any time period)

HEC = 52 mg/m3

MOE = 300	nasal effects: hyperplasia and metaplasia in respiratory and
olfactory epithelium respectively

Two year inhalation toxicity study - mouse (USEPA, IRIS)

Dermal absorption c

5%, determined from the results of in vivo / in vitro testing in rats
and in vitro testing using human skin (MRIDs 47179501 and 47179502).

  aafter re-examination of the toxicology data, the ADTC concluded that
the 2-generation reproduction toxicity study was appropriate for
long-term dermal risk assessment for the following reasons: the duration
of the 2-generation reproduction study is more representative of the
time frame (i.e. long-term) than the 90-day dermal study, and is
consistent with OPP policy regarding duration of the study vs.  route of
exposure;  body weight gain decreases in the 2-generation reproduction
toxicity study were observed in the F2 generation, supporting  the time
frame for the long-term endpoint (i.e. > 6 months).  The 90-day dermal
study effects are not as representative of the time frame for the
long-term dermal risk assessment.  However, the two studies can be
considered co-critical studies for this endpoint. Correction of the
LOAEL from the 2-generation reproduction toxicity study for dermal
absorption (50%) and use of a LOAEL (3x extra UF) yields a MOE and
endpoint (300 and 50 mg/kg/day) similar to the 90-day dermal toxicity
study (40 mg/kg/day and MOE of 300 [extra 3x to extrapolate to long-term
endpoint]).

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ation toxicity study showed significant effects on body weight gain
early in the study (one week) and is therefore relevant for short-term
assessment (2)  it is also a route-specific study; and (3) the
inhalation NOAEL is more sensitive than the developmental NOAEL.
Therefore, the inhalation study will remain as the study for the
short-term inhalation endpoint.

cdermal absorption of creosote was determined from submitted in vivo and
in vitro studies on creosote (MRIDs 47179501 and 47179502).

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