[Federal Register Volume 85, Number 117 (Wednesday, June 17, 2020)]
[Rules and Regulations]
[Pages 36504-36506]
[FR Doc No: 2020-10835]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 52

[EPA-R06-OAR-2020-0229; FRL 10009-40-Region 6]

Air Plan Approval; Texas; Approval of Substitution for Dallas-
Fort Worth Area Transportation Control Measures

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule; notice of administrative change.

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SUMMARY: The Environmental Protection Agency (EPA) is making an
administrative change to update the Code of Federal Regulations (CFR)
to reflect a change made to the Texas State Implementation Plan (SIP)
on February 21, 2020, as a result of EPA's concurrence on substitute
transportation control measures (TCMs) for the Dallas-Fort Worth (DFW)
8-hour ozone nonattainment area portion of the Texas SIP. EPA has
determined that the substitution of the TCMs is consistent with the
Clean Air Act and EPA's national guidance on such substitutions, and
therefore falls within the ``good cause'' exemption in the
Administrative Procedure Act (APA) which, upon finding ``good cause,''
authorizes an agency to make an action effective immediately.

DATES: This action is effective June 17, 2020.

ADDRESSES: The EPA has established a docket for this action under
Docket ID No. EPA-R06-OAR-2020-0229. All documents in the docket are
listed on the http://www.regulations.gov website. Although listed in
the index, some information is not publicly available, e.g.,
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 electronically through http://www.regulations.gov.

FOR FURTHER INFORMATION CONTACT: Jeff Riley,<PHONE_NUMBER>,
<EMAIL_ADDRESS>Out of an abundance of caution for members of
the public and our staff, the EPA Region 6 office may be closed to the
public to reduce the risk of transmitting COVID-19. Please call or
email the contact listed above if you need alternative access to
material indexed but not provided in the docket.

SUPPLEMENTARY INFORMATION: Under Clean Air Act (CAA) section 176(c)(8),
States are allowed to substitute TCMs in approved SIPs for replacement
TCMs which achieve equivalent or greater emissions reductions without
having to undertake the standard SIP revision process.\1\ The DFW area
metropolitan planning organization, the North Central Texas Council of
Governments (NCTCOG),\2\ identified for substitution three TCMs
originally approved as High-Occupancy Vehicle (HOV) lanes into the DFW
SIP as follows:
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    \1\ The Safe, Accountable, Flexible, Efficient Transportation
Equity Act: A Legacy for Users (SAFETEA-LU) transportation funding
and authorization bill, which was signed into law on August 10,
2005, revised the CAA's section 176(c) transportation conformity
provisions to allow states to substitute or add TCMs into approved
SIPs without the standard SIP revision process. These revisions
facilitate compliance with the transportation conformity rule's
requirements for timely implementation of TCMs (40 CFR 93.113) by
expediting the TCM substitution process.
    \2\ As the Metropolitan Planning Organization for the DFW area,
NCTCOG is delegated authority under 30 Texas Administrative Code
Sec.  114.270 to implement SIP-approved TCMs for the DFW ozone
nonattainment area.

               Table 1--Approval of TCMs Into the DFW SIP
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          SIP revision               EPA approval             TCM
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April 2000 DFW 1-Hour Ozone       September 27, 2005   IH 35
 Attainment Demonstration.         (70 FR 56374).      East corridor
                                                       (Stemmons
                                                       Freeway) HOV lane
                                                       between IH 635
                                                       and SH 121.
                                                       IH 635
                                                       West corridor
                                                       (LBJ Freeway) HOV
                                                       lane between Luna
                                                       Road/IH 35 E and
                                                       US 75.
May 2007 DFW 1997 8-Hour Ozone    January 14, 2009     IH 635
 Attainment Demonstration.         (74 FR 1903).       East corridor
                                                       (LBJ Freeway) HOV
                                                       lane between Coit
                                                       Road and
                                                       Greenville
                                                       Avenue.
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    The NCTGOC determined that since the opening of these HOV lanes,
increased congestion in these corridors had resulted from increased
population and vehicle miles traveled. As a result, the HOV lanes no
longer provided the needed congestion relief and associated nitrogen
oxide (NOX) and volatile organic compound (VOC) air quality
benefits approved into the DFW SIP as detailed in Table 1.
    As a part of the TCM substitution concurrence process required
under CAA section 176(c)(8), the NCTCOG published notice on November 7,
2019 in 20 DFW area newspapers and circulars announcing a November 11,
2019 public meeting to provide information on the proposed TCM
substitutions and begin a 30-day public comment period. No public
comments were received, and EPA did not provide comment or concurrence
during this comment period. On December 12, 2019, the NCTCOG Regional
Transportation Council adopted a resolution to substitute these HOV
lane TCMs for traffic signalization project TCMs to offset any
NOX and VOC emission reduction credits lost by removing
these corridors from HOV lane usage and keep equivalent emission
reduction controls in place.
    On February 21, 2020, EPA issued concurrence letters to the Texas
Commission on Environmental Quality (TCEQ) and the NCTCOG stating that
the substitution of the DFW area IH 35E/IH 635 HOV Lane TCMs with
traffic signalization project TCMs met the CAA section 176(c)(8)
requirements for substituting TCMs in an area's approved SIP, including
the requirement that the substitute measures achieve equivalent or
greater emission reductions than the control measure to be replaced. On
February 18, 2020, the TCEQ issued similar concurrence letters to EPA
Region 6 and the NCTCOG. Each of the above-noted concurrence letters
are included in the docket to this rulemaking as part of the State of
Texas' April 8, 2020 submittal to EPA. See EPA's Guidance for
Implementing the Clean Air Act Section 176(c)(8) Transportation Control
Measure Substitution and Addition Provision dated January 2009.
    Upon issuance EPA's February 21, 2020 concurrence letters, the HOV
Lane substitutions took effect as a matter of federal law.\3\ In
accordance with the requirements for TCM substitution, on April 8,
2020, the State of Texas submitted through the TCEQ a request for EPA
to update the DFW portion of the Texas SIP to reflect EPA's February
21, 2020 approval of the TCM substitution of the HOV Lanes with the
traffic signalization project TCMs in its SIP (the subject of this
administrative change). Today, EPA is taking administrative action to
update the non-regulatory provisions of the Texas SIP in 40 CFR
52.2270(e) to reflect EPA's concurrence on the substitution to convert
the IH 35E/IH 635 HOV Lane TCMs to traffic signalization project TCMs:
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    \3\ CAA section 176(c)(8)(B) stipulates that concurrence by the
MPO, State air pollution control agency and the EPA shall constitute
adoption of the substitute control measures, and that once adopted,
the substitute measures become, by operation of law, part of the SIP
and become federally enforceable.

------------------------------------------------------------------------
                                                               State
     Name of nonregulatory SIP           Applicable       submittal date/
             provision                  geographic or        effective
                                     nonattainment area        date
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DFW nine-county area IH-35E/IH-635  Dallas-Fort Worth...        4/8/2020
 HOV Lane TCMs to traffic
 signalization TCMs. Affected
 counties are Dallas, Tarrant,
 Collin, Denton, Parker, Johnson,
 Ellis, Kaufman, Rockwall.
------------------------------------------------------------------------

    Under section 553 of the APA, an agency may find good cause where
procedures are ``impractical, unnecessary, or contrary to the public
interest.'' EPA's January 2009 guidance establishes EPA's rationale for
utilizing the good cause provision under the APA to take actions
relating to TCM substitutions without additional need for public
comment because the substitution was originally made through the
process approved into the Texas SIP (79 FR 5287) in addition to the CAA
section 176(c)(8) statutory provision as applicable, and because the
public has had the opportunity to comment on the specific substitution
during NCTCOG's public comment period.\4\ Effective immediately,
today's action codifies provisions which are already in effect. The
public had an opportunity to comment on this substitution during the
public comment period prior to approval of the substitution. Immediate
notice of this action in the Federal Register benefits the public by
providing the updated Texas SIP Compilation and ``Identification of
Plan'' portion of the CFR.
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    \4\ EPA's rationale for applicability of the APA ``good cause''
exemption to TCM substitution rulemakings is provided in its January
2009 Guidance for Implementing the Clean Air Act Section 176(c)(8)
Transportation Control Measure Substitution and Addition Provision,
EPA-420-B-09-002. https://nepis.epa.gov/Exe/ZyPDF.cgi/P1002W66.PDF?Dockey=P1002W66.PDF.

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Statutory and Executive Order Reviews

A. General Requirements

    Under Executive Orders 12866 (58 FR 51735, October 4, 1993) and
13563 (76 FR 3821, January 21, 2011), this administrative action is not
a ``significant regulatory action'' and is therefore not subject to
review by the Office of Management and Budget. This action is not
subject to Executive Order 13211, ``Actions Concerning Regulations That
Significantly Affect Energy Supply, Distribution, or Use'' (66 FR
28355, May 22, 2001) because it is not a significant regulatory action
under Executive Order 12866. Because the Agency has made a ``good
cause'' finding that this action is not subject to notice-and-comment
requirements under the APA or any other statute as indicated in the
Supplementary Information section above, it is not subject to the
regulatory flexibility provisions of the Regulatory Flexibility Act (5
U.S.C. 601 et seq.), or to sections 202 and 205 of the Unfunded
Mandates Reform Act (UMRA) of 1995 (Pub. L. 104-4). In addition, this
action does not significantly or uniquely affect small governments or
impose a significant intergovernmental mandate, as described in
sections 203 and 204 of UMRA.
    This administrative action also does not have a substantial direct
effect on one or more Indian tribes, on the relationship between the
federal government and Indian tribes, or on the distribution of power
and responsibilities between the federal government and Indian tribes,
as specified by Executive Order 13175 (65 FR 67249, November 9, 2000),
nor will it have substantial direct effects on the states, on the
relationship between the national government and the states, or on the
distribution of power and responsibilities among the various levels of
government, as specified in Executive Order 13132 (64 FR 43255, August
10, 1999).
    This administrative action also is not subject to Executive Order
13045 (62 FR 19885, April 23, 1997), because it is not economically
significant. This administrative action does not involve technical
standards; thus the requirements of section 12(d) of the National
Technology Transfer and Advancement Act of 1995 (15 U.S.C. 272 note) do
not apply. The administrative action also does not involve special
consideration of environmental justice related issues as required by
Executive Order 12898 (59 FR 7629, February 16, 1994). This
administrative action does not impose an information collection burden
under the Paperwork Reduction Act of 1995 (44 U.S.C. 3501 et seq.).

B. Submission to Congress and the Comptroller General

    The Congressional Review Act (CRA) (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. Section 808 allows the issuing agency to
make a rule effective sooner than otherwise provided by the CRA if the
agency makes a good cause finding that notice and public procedure is
impracticable, unnecessary or contrary to the public interest. Today's
administrative action simply codifies a provision which is already in
effect as a matter of law in Federal and approved state programs. 5
U.S.C. 808(2). These announced actions were effective upon EPA's
concurrence. 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 this action in the Federal Register. This update to
Texas' SIP Compilation is not a ``major rule'' as defined by 5 U.S.C.
804(2).

List of Subjects in 40 CFR Part 52

    Environmental protection, Air pollution control, Incorporation by
reference, Nitrogen dioxide, Ozone, Volatile organic compounds.

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

    Dated: May 14, 2020.
Kenley McQueen,
Regional Administrator, Region 6.

    For the reasons stated in the preamble, EPA amends 40 CFR part 52
as follows:

PART 52--[AMENDED]

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

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

SUBPART SS--TEXAS

0
2. In Sec.  52.2270, in paragraph (e), amend the table titled ``EPA
Approved Nonregulatory Provisions and Quasi-Regulatory Measures in the
Texas SIP'' by adding an entry for ``DFW nine-county area IH-35E/IH-635
HOV Lane TCMs to traffic signalization TCMs'' at the end of the table
to read as follows:

Sec.  52.2270  Identification of plan.

* * * * *
    (e) * * *

              EPA Approved Nonregulatory Provisions and Quasi-Regulatory Measures in the Texas SIP
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                                       Applicable
      Name of SIP provision          geographic or     State submittal/   EPA approval date        Comments
                                   nonattainment area   effective date
----------------------------------------------------------------------------------------------------------------

                                                  * * * * * * *
DFW nine-county area IH-35E/IH-   Dallas-Fort Worth:           4/8/2020  6/17/2020 [Insert    ..................
 635 HOV Lane TCMs to traffic      Dallas, Tarrant,                       Federal Register
 signalization TCMs.               Collin, Denton,                        citation].
                                   Parker, Johnson,
                                   Ellis, Kaufman and
                                   Rockwall Counties.
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* * * * *
[FR Doc. 2020-10835 Filed 6-16-20; 8:45 am]
BILLING CODE 6560-50-P


1 This report supersedes the previous HIARC report dated March 4, 2002 ( TXR No. 0050586). It differs from the previous report in that it reflects the most recent formatting, and it delineates the selection of the FQPA factor. No decision regarding the FQPA factor was made previously.

TXR NO. 0051692 DATE: April 9, 2003 MEMORANDUM SUBJECT: PCNB  Report of the Hazard Identification Assessment Review Committee.

FROM: Elizabeth A. Doyle, Chief Toxicology Branch Health Effects Division ( 7509C)

THROUGH: Jess Rowland, Co Chair and Elizabeth Doyle, Co Chair Hazard Identification Assessment Review Committee Health Effects Division ( 7509C)

TO: Diana Locke, Risk Assessor Toxicology Branch Health Effects Division ( 7509C)

PC Code: 056502 On December 10, 2002, the Health Effects Division ( HED) Hazard Identification Assessment Review Committee ( HIARC) reviewed the recommendations of the toxicology reviewer for PCNB with regard to the potential for increased susceptibility of infants and children from exposure to PCNB was also evaluated as required by the Food Quality Protection Act ( FQPA) of 1996 in accordance with the 2002 OPP 10X Guidance Document. The conclusions drawn at this meeting are presented in this report.

Committee Members in Attendance 2 Members present were: Ayaad Assaad, William Burnam, Jonathan Chen, Elizabeth Doyle, John Liccione, Susan Makris, Elizabeth Mendez, David Nixon, Jess Rowland, and Brenda Tarplee Member( s) in absentia: Steve Knizner ( RARC Rep.) and Pamela Hurley Data evaluation prepared by: Elizabeth Doyle, Toxicology Branch Also in attendance were: Paula Deschamp and Mark Dow Data Evaluation / Report Presentation Elizabeth A. Doyle Chief, Toxicology Branch 3 INTRODUCTION On December 10, 2002, the Health Effects Division ( HED) Hazard Identification Assessment Review Committee ( HIARC) reconvened to evaluate the potential for increased susceptibility of infants and children from exposure to PCNB as required by the Food Quality Protection Act ( FQPA) of 1996 in accordance with the 2002 OPP 10X Guidance Document, and discussed the magnitude and rationale for required uncertainty factors. The conclusions drawn at both meetings are presented in this report.

I. FQPA HAZARD CONSIDERATIONS 1. Adequacy of the Toxicity Data Base Acceptable developmental toxicity studies in rats ( MRID# 40588601 and41361201) and rabbits ( MRID # 41361301 and 40717102) and reproduction studies ( MRID# 43469301, 43469302, 43469303 and 41918701) are available and adequate for FQPA considerations. Data gaps were identified in data on thyroid hormone levels, significance of ALT/ AST enzyme levels, pharmacokinetics, and in cytogenetic toxicity. The data base is not complete.

2. Evidence of Neurotoxicity Acute delayed neurotoxicity, acute and subchronic neurotoxicity studies and a developmental neurotoxicity studies are not required at this time since there is no evidence that the compound is a neurotoxicant.

3. Developmental Toxicity Study Conclusions a. Developmental Toxicity Study in the Rat ( gavage) OPPTS 870.3700 Executive Summary: In an oral developmental toxicity study ( MRID 40588601), 25 ( presumed) pregnant Sprague Dawley COBS CD rats/ dose group were administered pentachloronitrobenzene ( PCNB tech., 96.0% a. i.; 0.025% hexachlorobenzene contaminant) by gavage in 0.2% high viscosity carboxymethylcellulose ( 10 ml/ kg body wt.) at dose levels of 0, 30, 600 or 1200 mg/ kg/ day from gestation days 6 through 15, inclusive.

There were no treatment related maternal or developmental effects observed at any dose level tested. The highest dose tested ( 1200 mg/ kg/ day) exceeded the limit dose requirement. The maternal toxicity LOAEL is > 1200 mg/ kg/ day ( HDT) and the NOAEL is

1200 mg/ kg/ day. The developmental toxicity LOAEL is > 1200 mg/ kg/ day and the NOAEL is

1200 mg/ kg/ day.

This study is classified Acceptable/ Guideline ( § 83 3a; OPPTS 870.3700) and satisfies the guideline requirement for a developmental toxicity study in the rat. 4 b. Developmental Toxicity Study in the rat ( gavage) OPPTS 870.3700 Executive Summary: In an oral developmental toxicity study ( MRID 41361201), 25 ( presumed) pregnant CRL: CD ® ( SD) BR rats/ dose group were administered pentachloronitrobenzene ( PCNB tech., 98.5% a. i.; hexachlorobenzene contamination 0.09%) at doses of 0, 250, 750 or 1500 mg/ kg/ day from days 6 through 15 of gestation, inclusive. Doses were given by gavage in 1% aqueous carboxymethyl cellulose vehicle ( 10 ml/ kg body weight).

Maternal toxicity: No treatment related effects were observed. The highest dose level tested ( 1500 mg/ kg/ day) exceeded the limit dose. The maternal toxicity LOAEL is > 1500 mg/ kg/ day and the NOAEL is

1500 mg/ kg/ day.

Developmental toxicity: At 750 and 1500 mg/ kg/ day, small but statistically significant increases in the average number of thoracic vertebrae/ fetus ( 13.05, 13.16, 13.23 and 13.21, control to high dose; historical control range 13.00 to 13.13), average pairs of thoracic ribs/ fetus ( 13.03, 13.13, 13.17 and 13.15; historical control range 13.00 to 13.09), and decreases in the average number of lumbar vertebrae/ fetus ( 5.94, 5.84, 5.77 and 5.79; historical control range 5.85 to 6.00) were reported ( all historical data from 4852 fetuses in 573 litters, 26 studies). The biological significance of these findings is uncertain due to relatively small magnitude of the changes and lack of a clear dose response. No treatment related fetal malformations were observed. The HIARC concluded that these small differences observed in thoracic vertebrae were very marginal effects and not biologically significant. Decreases in number of lumbar vertebra/ fetus suggest that increases in thoracic vertebra per fetus may not be adverse and similar effects were not seen in the Uniroyal rat study ( MRID 40588601). Hence, the developmental toxicity LOAEL is > 1500 mg/ kg/ day and the NOAEL is > 1500 mg/ kg/ day ( HDT).

This study is classified Acceptable/ Guideline ( § 83 3a; OPPTS 870.3700) and satisfies the guideline requirement for a developmental toxicity study in the rat.

c. Developmental Toxicity Study in the Rabbit ( Gavage) OPPTS 87.3700 Executive Summary: In an oral developmental toxicity study ( MRID 41361301), 20 ( presumed) pregnant New Zealand White rabbits/ dose group were administered pentachloronitrobenzene ( PCNB tech., 98.5% a. i.; 0.09% hexachlorobenzene contaminant) by gavage at 0, 100, 300 or 900 mg/ kg/ day in 10 ml aqueous 1% carboxymethylcellulose vehicle/ kg body weight from gestation days 6 through 18, inclusive.

Maternal toxicity: At 900 mg/ kg/ day, abnormal feces ( soft, liquid or dried; total incidence 45 in 11 does vs. 15 in 4 does, controls), decreased weight gain during dosing ( 75% less than controls; not statistically significant), slightly decreased food consumption ( 16% less than controls; not statistically significant) were observed. Abortions ( days 24 and 25, 2/ 20 vs. 0/ 20, controls) and premature delivery ( day 25, 1/ 20 vs. 0/ 20, controls) were observed and these 3 does also had associated abnormal feces, weight loss and decreased food consumption. The doe with premature delivery also had decreased motor activity and a fluid filled cecum, one abortive female had gastric ulceration and the other had a litter with 4 late resorptions out of 6 conceptuses. No mortality was observed. The maternal toxicity LOAEL is 900 mg/ kg/ day, based on clinical signs of toxicity, decreased body weight gain and food consumption during dosing, 5 abortions and premature delivery. The maternal toxicity NOAEL is 300 mg/ kg/ day.

Developmental toxicity: There were no treatment related developmental effects reported in this study with the exception of a slightly increased incidence of abortions at the 900 mg/ kg dose level considered by HIARC as developmental toxicity due to the associated fetal mortality. The developmental toxicity LOAEL is 900 mg/ kg/ day and the developmental toxicity NOAEL is 300 mg/ kg/ day.

This study is classified Acceptable/ Guideline ( § 83 3b; OPPTS 870.3700) and satisfies the Guideline requirement for a developmental toxicity study in the rabbit.

d. Developmental Toxicity Study in the Rabbit ( gavage) OPPTS 870.3700 Executive Summary: In an oral developmental toxicity study ( MRID # 40717102) groups of 16 pregnant New Zealand White rabbits were given daily doses of 0 ( two groups) s, 6.25, 12.5, 125 ( two groups) and 250 mg/ kg/ day PCNB ( 96%) by gavage on days 7 through 19 of gestation.

Maternal Toxicity: At the highest dose tested there was mortality, abortions, weight loss during gestation and decreased food consumption. The only effects observed in the 125 mg/ kg/ day dose groups were decreased body weight and weight gain. Group mean maternal body weight was statistically significantly less than control values only during the second of the two trials that were conducted at that dose level. Based on these results, a LOAEL for maternal toxicity was established at 125 mg/ kg/ day and NOAEL was established at 12.5 mg/ kg/ day.

Developmental Toxicity: Based on statistically significant decreased fetal weights reported in the highest dose group, the LOAEL for developmental toxicity was established at 250 mg/ kg/ day and the NOAEL was determined to be 125 mg/ kg/ day in rabbits.

This study is classified Acceptable ( § 83 3b; OPPTS 870.3700) and satisfies the Guideline requirement for a developmental toxicity study in the rabbit.

4. Reproductive Toxicity Study Conclusions Two Generation Reproduction Study in Rats ( dietary) OPPTS 870.3800 Executive Summary: In a 2 generation reproductive toxicity study ( MRID 41918701), 26 Sprague Dawley COBS ® CD rats/ sex/ dose group were administered pentachloronitrobenzene ( PCNB tech., > 99% a. i.; < 0.1% hexachlorobenzene contaminant) in their diet at concentrations of 0, 20, 3000 or 6000 ppm ( equivalent to 1.2/ 1.4, 169/ 213 or 344/ 468 mg/ kg/ day, males and 1.5/ 1.7, 218/ 255 or 455/ 640 mg/ kg/ day, females, based on mean F0/ F1 premating compound consumption values), beginning in 55 day old F0 animals at 81 days prior to mating or in weanling F1 animals for at least 90 days prior to mating. Each parental generation was mated twice to produce F1/ F2 a and b litters. Dosing of the F0 and F1 parental animals was continued throughout the study period until termination of the animals after day 21 of the second lactation period ( females) or after the second mating period ( males).

Parental toxicity: At 3000 ppm, statistically significantly decreased mean premating body weights 6 were observed in F0 males prior to both matings ( 7% less than controls) and in F1 females prior to the first mating ( 5.7% to  10%; due to decreased initial weights of the F1 weanlings assigned to be parental animals). At 6000 ppm, significantly decreased mean premating body weights ( F0 males  9 to  10% less than controls and females  7%; F1 males, initial weights  35%; thereafter  16%; females initial weights  37%; thereafter  14% to  16%). The small size of almost all F1 animals at 6000 ppm and emaciation in 4 females was related to these decreases. Food consumption was decreased, primarily during the first weeks of each premating period. Increased incidence of pulmonary foci was also observed in F0 females ( 4/ 26) and in F1 males ( 5/ 26) and females ( 8/ 26) ( no controls affected in either sex). The parental systemic toxicity LOAEL is 3000 ppm ( 169 mg/ kg/ day, males and 218 mg/ kg/ day, females), based on decreased body weight/ weight gain. The NOAEL is 20 ppm ( 1.2 mg/ kg/ day, males and 1.5 mg/ kg/ day, females).

Reproductive/ developmental toxicity: At 3000 ppm, decreased mean pup weight ( 6.8% to  8.7% less than controls at lactation day 21, both sexes; statistically significant) was observed in F1a, F1b and F2b pups. At 6000 ppm, decreases in male and female pup weights in all 4 litters were pronounced ( 30% to  41% at lactation day 21). The reproductive/ developmental LOAEL is 3000 ppm ( 169 mg/ kg/ day), based on decreased mean pup weight in most generations. The NOAEL is 20 ppm ( 1.2 mg/ kg/ day).

The Offspring NOAEL: Based on decreases in mean pup weights of F1a, F1b, and F2b animals, the offspring NOAEL is 1.2 mg/ kg/ day and the LOAEL is 169 mg/ kg/ day.

This study is classified Acceptable/ Guideline ( § 83 4; OPPTS 870.3800) and satisfies the Guideline requirement for a multigeneration reproductive toxicity study in the rat.

5. Additional Information from Literature Sources 1. A number of older studies have been identified in the data base but most of these studies are associated with testing of the older manufactured technical ( high in HCB and other contaminants) and therefore these data cannot be used as part of the present assessment on the currently marketed technical.

2. A kinetic study was identified in the literature [ W. Kogel et al, ( 1979) Uptake, Body Distribution, Storage and Excretion of Pentachloronitrobenzene 14 C in Rhesus Monkeys, Chemosphere No. 2, pp 89 95l. Pergamon Press Ltd] which despite, study deficiencies, demonstrated some ability of PCNB to accumulate over time. The half life of PCNB ( in monkeys) was 1.5 1.7 days at a low dose of 2 mg/ kg , with only 81 85% of the dose recovered in excreta after 15 days. At the higher dose of 91 mg/ kg only 59.5% of the dose had been recovered in excreta after 20 days. Feeding studies at 2 ppm, indicated that a plateau was reached after 30 40 days. Because of concerns about the uncertainties of the half life and thus for the accumulation potential of the chemical, the HIARC recommended that a study to determine the biological half life on PCNB be requested ( See 7. Data Gaps).

3. PCNB studies consistently show decreases in serum enzyme activities. AST/ ALT activities decrease in a dose dependent manner by as much as 30 80%. It is known that penicillamine, cycloserine, hydralazine, and in particular the anti tuberculin drug isoniazid can decrease the 7 activities of AST and ALT at therapeutic doses. The mechanism by which this occurs is through a biochemical interaction between the drug and Vitamin B6. With isoniazid [ Balazs et al. Arch. Toxicol, Suppl. 1, 159 163 ( 1978)] this is thought to occur through combination with pyridoxal or pyridoxal phosphate to form a hydrazone.

Vitamin B6 compromises a group of closely related compounds, pyridoxine, pyridoxal and pyridoxamine, that are phosphorylated in vivo by pyridoxal kinase to form pyridoxal phosphate. Pyridoxal phosphate serves as a cofactor in many reactions, including decarboxylation and transamination of amino acids, deamination of hydroxy amino acids and cysteine, conversion of tryptophan to niacin, metabolism of fatty acids, protein metabolism, and the transport of certain amino acids across cell membranes. The inhibition of pyridoxal kinase by the isoniazid pyridoxal complex occurs at concentrations 1000 times less than those required to inhibit the enzyme containing the cofactor.

The dose dependent decreases of AST/ ALT activities found consistently in subchronic and chronic studies suggest that PCNB disrupts transferase and other enzyme activities that require pyridoxal phosphate, perhaps by affecting Vitamin B6 homeostasis. Whether the mechanism is similar to that of the isoniazid is not known and cannot be determined from the subchronic or chronic studies. However, the clinical data suggests a disturbance of protein and amino acid metabolism. This is supported not only by the decreased activities of AST/ ALT but also by the dose dependent excretion of triple phosphate crystals in the urine. The excretion of triple phosphate and calcium phosphate, which are urine buffering systems, suggests a disturbance of systemic acid base balance. It is also of interest to note at terminal sacrifice the presence of tyrosine phosphate crystals in urine. Typically these crystals suggest severe hepatic toxicity. However, the clinical pathology of the liver did not suggest toxicity sufficient to disrupt hepatic function. All that was typically found was hepatocellular hypertrophy. Although tyrosine phosphate crystals may have originated from impaired hepatic function, they could have also arisen from tyrosine overload. Excess tyrosine could have resulted from the chronic and cumulative inhibition of various transaminases, particularly tyrosine transaminase, that are essential for protein and amino acid metabolism.

Therefore, in the PCNB studies submitted, it might be reasonable ( in the absence of other relevant kinetic data) to consider the decreases of AST/ ALT as adverse effects. This would generally reduce NOAEL's and LOAEL's by at least an order of magnitude. PCNB appears to induce a chronic and progressive inhibition of transferase activity and to confirm this would require additional study.

4. Hepatocellular hypertrophy occurs following the administration of chlorinated benzenes, polyhalogenated biphenyls, TCDD, and other polyhalogenated hydrocarbons. These compounds induce hepatic microsomal enzymes that ultrastructurally result in cellular changes consistent with those reported in the chronic and subchronic PCNB studies. Likewise, the induction of thyroid follicular hyperplasia and hypertrophy in animals is a well documented effect of many polyhalogenated aromatic hydrocarbons. Current evidence suggests that the induction of certain hepatocellular microsomes increases metabolism of thyroxine, thereby inducing a hypothyroid state ( and it seems likely that PCNB induces primary hypothyroidism in both male and female rats). However, without analysis of TSH, this cannot be firmly established nor can the severity of the hypothyroidism be determined. Further, what effects might be superimposed, or whether the 8 effects would be potentiated, additive, synergistic, or antagonistic is unclear at this time. For this and other reasons, adequate kinetic data should be available for use in the risk assessment process.

6. Pre and/ or Postnatal Toxicity The HIARC concluded that there is not a concern for pre and/ or postnatal toxicity resulting from exposure to PCNB.

A. Determination of Susceptibility There was no quantitative or qualitative evidence of increased susceptibility of rat or rabbit fetuses after in utero exposure, or after pre or postnatal exposure to rats in multigeneration reproduction studies.

B. Degree of Concern Analysis and Residual Uncertainties This analysis was not conducted because there was no evidence of qualitative or quantitative susceptibility.

C. Special FQPA Safety Factor( s)

The special FQPA factor can be reduced to 1x because there are no residual uncertainties for pre and/ or postnatal toxicity.

The Special FQPA Safety Factor recommended by the HIARC assumes that the exposure databases ( dietary food, drinking water, and residential) are complete and that the risk assessment for each potential exposure scenario includes all metabolites and/ or degradates of concern and does not underestimate the potential risk for infants and children.

7. Recommendation for a Developmental Neurotoxicity Study The HIARC concluded that there is not a concern for developmental neurotoxicity resulting from exposure to PCNB.

A. Evidence that suggest requiring a Developmental Neurotoxicity study:

There is no evidence supporting the requirement for a DNT.

B. Evidence that do not support a need for a Developmental Neurotoxicity study:

There was no evidence of neurotoxicity in the toxicity data base for PCNB.

Based on the weight of evidence presented, the HIARC concluded that a developmental neurotoxicity study is not required for PCNB.

The HIARC, however, did require a comparative thyroid assay in young and adult rats which 9 included hormonal measurements for thyroid function, since thyroid weights were increased in a number of chronic and subchronic studies in rats, and TSH, T3, and T4 levels were affected in a 90 day special oral study in male rats.

The absence of the comparative thyroid study resulted in a database uncertainty factor of 10x ( UF DB of 10x) which was applied to the dietary ( acute and chronic) as well as all residential exposure ( incidental oral, dermal and inhalation) scenarios. The HIARC determined that the 10X UF DB is required since the available data provide no basis to support reduction or removal of the default 10X factor.

II. HAZARD IDENTIFICATION 1. Acute Reference Dose ( aRfD)  An endpoint attributable to a single dose ( exposure) was not available in the database.

2. Chronic Reference Dose ( cRfD)

Study Selected: Combined chronic toxicity/ carcinogenicity  rat § OPPTS 870.4300 MRID No.: 41987301 Executive Summary: In an oral chronic toxicity/ carcinogenicity study ( MRID 41987301), 50 Charles River CD ® rats/ sex/ dose group were administered pentachloronitrobenzene ( PCNB tech., 99.4% a. i.) in the diet at concentrations of 0, 20, 3000 or 6000 ppm ( equivalent to estimated average daily intakes of 0, 1, 150 or 300 mg/ kg/ day; estimated based on a standard conversion factor of 0.05) for 24 months. An additional 10 animals/ sex/ dose group were included for interim sacrifice at 12 months.

At 3000 ppm, statistically significantly increased relative liver weight in males (+ 20% above controls), absolute thyroid/ parathyroid weight in males (+ 26%), relative thyroid/ parathyroid weight (+ 35%, males and + 24%, females), and significantly increased incidence of microscopic lesions including mild hepatocellular hypertrophy ( 27%, males and 38%, females vs. 0%, controls), mild thyroid hyperplasia ( 15%, males vs. 4%, controls and 16%, females vs. 0%, controls) and thyroid hypertrophy ( 42%, males vs. 0%, controls and 36%, females vs. 2%, controls) were observed. Sporadic significantly decreased mean body weights in both sexes were not considered biologically significant. At 6000 ppm, these effects showed a dose response and in addition, statistically significantly decreased mean body weight/ weight gain throughout treatment ( at termination,  11%/ 15% less than controls in males and  12%/ 18% in females), decreased food consumption during the first 6 months, increased serum cholesterol ( females), significantly increased relative liver weight in both sexes (+ 25%, males and + 20%, females) and increased incidence of thyroid colloid cysts in males ( 16% vs. 4.1%, controls) were observed. At the 12 month interim sacrifice, both sexes showed slight ( not statistically significant) increases in liver and thyroid weights at mid and high dose and in high dose females, there was a slightly increased incidence of visible tan foci in the lungs. There were no treatment related clinical or 10 ophthalmologic observations and no effects on mortality, hematology or urinalysis parameters.

The systemic toxicity LOAEL is 3000 ppm ( 150 mg/ kg/ day), based on hepatocellular hypertrophy, hepatocellular hyperplasia ( females) and thyroid hypertrophy and hyperplasia. The systemic toxicity NOAEL is 20 ppm ( 1 mg/ kg/ day).

PCNB caused an increased incidence of thyroid follicular cell adenomas in males ( 0%, 0%, 12.5% and 10.2%, control to high dose; p< 0.05 at 3000 ppm) and a significantly increasing trend ( p< 0.01). Incidence in females was 2.0%, 0%, 4.0% and 8.7% ( control to high dose; not significant); however, a significantly increasing trend ( p< 0.05) was observed. The incidence of thyroid follicular cell carcinoma was increased at 6000 ppm only in males ( males 0%, 2.0%, 0% and 4.1%; females 2.0%, 0%, 0% and 2.2%). The combined incidence of thyroid follicular cell adenomas and carcinomas was significantly increased in males at 3000 and 6000 ppm ( control to high dose, 0%, 2.0%, 12.5%, 14.3%; p< 0.05) but not females ( 4.0%, 0%, 4.0% and 10.9%), with a significant trend in both sexes ( females p< 0.05 and males p< 0.01). The incidence of follicular cell adenoma in historical control data from this laboratory did not exceed 11.1% in males or 3.2% in females. The incidence of carcinoma did not exceed 9.4% in males or 3.2% in females.

This study is classified Acceptable/ Guideline ( § 83 5; OPPTS 870.4300) and satisfies the Guideline requirement for a chronic toxicity/ carcinogenicity study in the rodent.

Dose and Endpoint for Establishing cRfD: NOAEL = 1 mg/ kg/ day based on hepatocellular hypertrophy, hepatocellular hyperplasia ( females) and thyroid hypertrophy and hyperplasia at The LOAEL = 150 mg/ kg/ day.

Uncertainty Factor( s): 1000 ( 10x for interspecies extrapolation, 10x for interspecies differences, and UF DB for lack of comparative thyroid assay).

Comments about Study/ Endpoint/ Uncertainty Factor: This study is appropriate for the population and duration considered in a chronic risk assessment.

4. Incidental Oral Exposure: Short Term ( 1 30 days)

Study Selected: Subchronic Oral Toxicity in male rats § Nonguideline MRID No.: 42630801 Executive Summary: In a special ( nonguideline) subchronic oral toxicity study ( MRID 42630801), 75 male Charles River CD ® rats/ dose were administered pentachloronitrobenzene ( PCNB tech., 99.09% a. i.) in their diet at levels of 0, 20 or 6000 ppm ( equivalent to average daily intakes of 0, 1.0 or 333 mg/ kg/ day). Groups of 15 animals/ dose were sacrificed at 7, 14, 30 or 90 days. The remaining 15 animals/ dose group at day 90 were fed only basal diet for a recovery Chronic RfD = ( NOAEL) 1 mg/ kg/ day = 0.001 mg/ kg/ day ( UF) 1000 11 period of at least 90 days ( sacrificed on day 180 or 183). Levels of circulating thyroid hormones ( TSH, T3 and T4) and thyroid/ liver weights and pathology were evaluated at each sacrifice time.

At 20 ppm, hypertrophy of the liver ( trace) and thyroid ( mild) were observed in 14/ 15 and 15/ 15 animals, respectively ( 0/ 15, controls). At 6000 ppm, statistically significantly decreased mean body weight throughout most of treatment ( at termination,  6.1% less than controls) and decreased body weight gain ( at termination,  20%, due largely to a pronounced decrease during Week 1), decreased food consumption during Week 1 only ( 23% below controls), increased TSH (+ 31% to + 132% above controls; significant at most time points), decreased T3 ( 9 to  26% less than controls; significant at most time points), decreased T4 ( 48 to  54% less than controls, significant at all time points), decreased rT3 ( 28% at day 90; significant), increased relative liver weight (+ 12 to + 18% above controls), decreased absolute thyroid/ parathyroid weights ( 14%, day 30) and increased follicular epithelial hypertrophy of the thyroid ( trace to mild, all animals at all sacrifice times vs. 0/ 15 controls) and hepatocellular hypertrophy ( moderate, all animals at 90 days, vs. 0/ 15, controls). There were no treatment related deaths or clinical signs observed. Animals maintained on basal diet for an additional 90 days showed complete recovery. The following were not evaluated: hematology, urinalysis, organ weights and gross/ microscopic pathology, with the exception of liver, thyroid/ parathyroids. The study LOAEL is 20 ppm ( 1.0 mg/ kg/ day), based on liver and thyroid histopathology. The study NOAEL was not determined.

This study is classified Acceptable/ nonguideline ( § 82 1a). It does not satisfy the guideline requirement for a subchronic oral toxicity study in the rodent because it is not a complete Guideline subchronic study. This was a special non guideline study designed only to assess effects of PCNB on the thyroid hormone levels, rather than a complete Guideline subchronic study, and was adequately conducted to provide this information. However, only males were tested, only two doses were utilized and hematology, urinalysis, organ weights, and gross and microscopic pathology ( with the exception of thyroid/ parathyroids and liver) were not assessed.

Dose and Endpoint for Risk Assessment: 1 mg/ kg/ day. Although a NOAEL was not identified in the above non guideline male study at 90 days, no effects were observed at the 1 mg/ kg/ day dose level at interim sacrifice/ hormone assessment intervals conducted at 7, 14, and 30 days. This finding was considered an appropriate endpoint for risk assessment by HIARC for periods up to 30 days.

Comments about Study/ Endpoint: Although no effects were observed in this special study at the 1 mg/ kg/ day dose level during interim assessments up to 30 days, it must be recognized that this is not a guideline study and was intended only for a limited assessment of the thyroid and liver function. In addition, it included no assessment for potential effects on females ( since none were utilized in the study), it only utilized two dose levels, and did not include routine assessments in males for hematology, urinalysis, organ weights and gross and microscopic pathology ( with the exception of liver and thyroid/ parathyroids) and other endpoints. HIARC concluded that the effects observed in this study are appropriate for the population ( infants and children) and duration of concern ( 1 30 days).

5. Incidental Oral Exposure: Intermediate Term ( 1  6 Months) 12 Study Selected: Subchronic Oral Toxicity in male rats § Nonguideline MRID No.: 42630801 Executive Summary: See Short Term ( 1 day to 1 month) Incidental Oral Exposure section.

Dose and Endpoint for Risk Assessment: 1 mg/ kg/ day. A NOAEL was not identified in this study. As noted above under the short term incidental oral exposure, no adverse effects were seen up to 30 days. The HIARC determined that the effects seen at the 1 mg/ kg/ day at termination were minimal and therefore this dose is appropriate for this exposure risk assessment.

Comments about Study/ Endpoint: Although no effects were observed in this special study at the 1 mg/ kg/ day dose level during interim assessments up to 30 days, it must be recognized that this is not a guideline study and was intended only for a limited assessment of the thyroid and liver function. In addition, it included no assessment for potential effects on females ( since none were utilized in the study), it only utilized two dose levels, and did not include routine assessments in males for hematology, urinalysis, organ weights and gross and microscopic pathology ( with the exception of liver and thyroid/ parathyroids) and other endpoints. In consideration of these issues, HIARC considered the observed effects to be appropriate for the population ( infants and children and duration of concern ( 1 6 months).

6. Dermal Absorption Dermal Absorption Factor: 33%

A dermal penetration study ( MRID no. 250698 and 255226) was available; two formulations ( 20% dust and 75% wettable powder) were tested in rats for four hours or 5 days. After 4 hours, recovery/ dermal penetration was 1.3% for the wettable powder and 3.1% for the dust. After 5 days, the recovery was 32.3% for the wettable powder and 33.8% for the dust.

The HIARC did not use this study since this study: ( 1) did not follow current guidelines; ( 2) test materials are significantly different from the technical product currently marketed: ( 3) the lot number of the test materials was not reported; and ( 4) the report did not account for all radioactivity.

The HIARC extrapolated a dermal absorption factor of 33% based on the ratio of 333 mg/ kg/ day ( based on the presence of thyroid hormone changes observed at 7, 14, and 30 days at the 333 mg/ kg/ day dose level observed in the male 90 day rat feeding study) and the LOAEL of 1000 mg/ kg/ day in the 21 day dermal toxicity study. In rats, it was noted that thyroid toxicity was the common toxicity seen via both routes in the same species 7. Dermal Exposure: Short Term ( 1 30 days) Exposure Study Selected: 21 Day Dermal Toxicity Study § OPPTS 870.3200 13 MRID No.: 42416002 Executive Summary: In a 21 day dermal toxicity study ( MRID# 42416002), Charles River rats were exposed dermally to PCNB ( 98% a. i) by application of the moistened solid ( distilled water vehicle) to the shaved dorsal skin at doses of 0, 100, 300 and 1000 mg/ kg for 6 hours per day, five days per week.

In the high dose males, dilatation of the thyroid follicles was observed in 3/ 5 animals and hypertrophy of the thyroid follicular epithelium was observed in 4/ 5 animals. These changes were not observed in any of the other dose groups, including controls or in any females. No other treatment related effects were observed in either males or females. Based on these findings, the NOAEL is 300 mg/ kg/ day and the LOAEL is 1000 mg/ kg/ day based on thyroid effects.

Dose and Endpoint for Risk Assessment: NOAEL = 300 mg/ kg/ day based on hypertrophy of the thyroid follicular epithelium and dilation of the thyroid follicles in males only at the LOAEL = 1000 mg/ kg.

Comments about Study/ Endpoint: This study is appropriate for the route and duration of exposure concerns.

8. Dermal Exposure: Intermediate Term ( 1  6 Months)

Study Selected: 21 Day Dermal Toxicity Study § OPPTS 870.3200 MRID No.: 42416002 Executive Summary: See Short term Dermal ( 1 day to 1 month) Exposure Dose and Endpoint for Risk Assessment: NOAEL = 300 mg/ kg/ day based on hypertrophy of the thyroid follicular epithelium and dilation of the thyroid follicles in males at the LOAEL = 1000 mg/ kg/ day.

Comments about Study/ Endpoint: This study is appropriate for the route and duration of exposure concerns.

9. Dermal Exposure Long Term (> 6 Months)

Study Selected: Combined Chronic Toxicity/ Carcinogenicity Study  Rat § OPPTS 870.4300 MRID No.: 41987301 Executive Summary: See Chronic Reference Dose ( RfD)

Dose and Endpoint for Risk Assessment: 1 mg/ kg/ day based on hepatocellular hypertrophy, hepatocellular hyperplasia ( females) and thyroid hypertrophy and hyperplasia at 150 mg/ kg/ day. 14 Comments about Study/ Endpoint: This dose/ end point study was also used to establish the chronic RFD. Since an oral dose was identified, 33% dermal absorption should be used in routeto route extrapolation.

10. Inhalation Exposure: Short  Term ( 1 30 days)

Study Selected: Subchronic Oral Toxicity Study in Male Rats § Nonguideline MRID No.: 42630801 Executive Summary: See Short Term ( 1 day to 1 month) Incidental Oral Exposure Dose/ Endpoint for Risk Assessment: 1 mg/ kg/ day. Although a NOAEL was not identified in the non guideline male study at 90 days, no effects were observed at the 1 mg/ kg/ day dose level at interim sacrifice/ hormone assessment intervals conducted at 7, 14, and 30 days. This finding was considered an appropriate endpoint for risk assessment by HIARC for periods up to 30 days.

Comments about Study/ Endpoint: In the absence of an inhalation study, an oral study was selected. Absorption by the inhalation route should be considered to be equivalent to absorption by the oral route.

11. Inhalation Exposure: Intermediate Term ( 1 6 Months)

Study Selected: Subchronic Oral Toxicity Study in Male Rats § Nonguideline MRID No.: 42630801 Executive Summary: See Short Term ( 1 day to 1 month) Incidental Oral Exposure Dose/ Endpoint for Risk Assessment: 1 mg/ kg/ day. Although a NOAEL was not identified in the non guideline male study at 90 days, no effects were observed at the 1 mg/ kg/ day dose level at interim sacrifice/ hormone assessment intervals conducted at 7, 14, and 30 days. This finding was considered an appropriate endpoint for risk assessment by HIARC for periods up to 30 days.

Comments about Study/ Endpoint: In the absence of an inhalation study, an oral study was selected. Absorption by the inhalation route should be considered to be equivalent to absorption by the oral route.

12. Inhalation Exposure: Long Term (> 6 Months)

Study Selected: Combined Chronic Toxicity/ Carcinogenicity Study  Rat § OPPTS 870.4300 MRID No.: 41987301 Executive Summary: See Chronic Reference Dose ( RfD) 15 Dose/ Endpoint for Risk Assessment: 1 mg/ kg/ day based on hepatocellular hypertrophy, hepatocellular hyperplasia ( females) and thyroid hypertrophy and hyperplasia at 150 mg/ kg/ day.

Comments about Study/ Endpoint: In the absence of an inhalation study, an oral study was selected. Absorption by the inhalation route should be considered to be equivalent to absorption by the oral route.

13. Margins of Exposure Summary of target Margins of Exposure ( MOEs) for risk assessment.

Route Duration Short Term ( 1 30 Days) Intermediate Term ( 1  6 Months) Long Term (> 6 Months)

Occupational ( Worker) Exposure Dermal 100 100 100 Inhalation 100 100 100 Residential ( Non Dietary) Exposure Oral 1000 1000 N/ A Dermal 1000 1000 1000 Inhalation 1000 1000 1000 For Occupational exposure: This is based on the conventional uncertainty factor of 100X ( 10X for intraspecies extrapolation and 10X for interspecies variation)

For Residential exposure: This is based on the conventional uncertainty factor of 100X ( 10X for intraspecies extrapolation and 10X for interspecies variation) in addition to a 10X UF DB due to the lack of a comparative thyroid study.

14. Recommendation for Aggregate Exposure Risk Assessments As per FQPA, 1996, when there are potential residential exposures to the pesticide, aggregate risk assessment must consider exposures from three major sources: oral, dermal and inhalation exposures. The toxicity endpoints selected for these routes of exposure may be aggregated as follows:

A common toxicological endpoint of concern ( thyroid toxicity) was identified for the oral, dermal, and inhalation ( oral equivalent) routes of exposure. Therefore, for short, intermediate and long term exposure aggregate risk assessments, these routes/ durations can be aggregated for the appropriate populations. 16 III. CLASSIFICATION OF CARCINOGENIC POTENTIAL 1. Combined Chronic Toxicity/ Carcinogenicity Study in Rats OPPTS 870.4300 MRID No.: 41987301 Executive Summary: In an oral chronic toxicity/ carcinogenicity study ( MRID 41987301), 50 Charles River CD ® rats/ sex/ dose group were administered pentachloronitrobenzene ( PCNB tech., 99.4% a. i.) in the diet at concentrations of 0, 20, 3000 or 6000 ppm ( equivalent to estimated average daily intakes of 0, 1, 150 or 300 mg/ kg/ day; estimated based on a standard conversion factor of 0.05) for 24 months. An additional 10 animals/ sex/ dose group were included for interim sacrifice at 12 months.

At 3000 ppm, statistically significantly increased relative liver weight in males (+ 20% above controls), absolute thyroid/ parathyroid weight in males (+ 26%), relative thyroid/ parathyroid weight (+ 35%, males and + 24%, females), and significantly increased incidence of microscopic lesions including mild hepatocellular hypertrophy ( 27%, males and 38%, females vs. 0%, controls), mild thyroid hyperplasia ( 15%, males vs. 4%, controls and 16%, females vs. 0%, controls) and thyroid hypertrophy ( 42%, males vs. 0%, controls and 36%, females vs. 2%, controls) were observed. Sporadic significantly decreased mean body weights in both sexes were not considered biologically significant. At 6000 ppm, these effects showed a dose response and in addition, statistically significantly decreased mean body weight/ weight gain throughout treatment ( at termination,  11%/ 15% less than controls in males and  12%/ 18% in females), decreased food consumption during the first 6 months, increased serum cholesterol ( females), significantly increased relative liver weight in both sexes (+ 25%, males and + 20%, females) and increased incidence of thyroid colloid cysts in males ( 16% vs. 4.1%, controls) were observed. At the 12 month interim sacrifice, both sexes showed slight ( not statistically significant) increases in liver and thyroid weights at mid and high dose and in high dose females, there was a slightly increased incidence of visible tan foci in the lungs. There were no treatment related clinical or ophthalmologic observations and no effects on mortality, hematology or urinalysis parameters. The systemic toxicity LOAEL is 3000 ppm ( 150 mg/ kg/ day), based on hepatocellular hypertrophy, hepatocellular hyperplasia ( females) and thyroid hypertrophy and hyperplasia. The systemic toxicity NOAEL is 20 ppm ( 1 mg/ kg/ day).

This study is classified Acceptable/ Guideline ( § 83 5; OPPTS 870.4300) and satisfies the Guideline requirement for a chronic toxicity/ carcinogenicity study in the rodent.

Discussion of Tumor Data: PCNB caused an increased incidence of thyroid follicular cell adenomas in males ( 0%, 0%, 12.5% and 10.2%, control to high dose; p< 0.05 at 3000 ppm) and a significantly increasing trend ( p< 0.01). Incidence in females was 2.0%, 0%, 4.0% and 8.7% ( control to high dose; not significant); however, a significantly increasing trend ( p< 0.05) was observed. The incidence of thyroid follicular cell carcinoma was increased at 6000 ppm only in males ( males 0%, 2.0%, 0% and 4.1%; females 2.0%, 0%, 0% and 2.2%). The combined incidence of thyroid follicular cell adenomas and carcinomas was significantly increased in males 17 at 3000 and 6000 ppm ( control to high dose, 0%, 2.0%, 12.5%, 14.3%; p< 0.05) but not females ( 4.0%, 0%, 4.0% and 10.9%), with a significant trend in both sexes ( females p< 0.05 and males p< 0.01). The incidence of follicular cell adenoma in historical control data from this laboratory did not exceed 11.1% in males or 3.2% in females. The incidence of carcinoma did not exceed 9.4% in males or 3.2% in females.

Adequacy of the Dose Levels Tested: The dose levels are considered adequate. Systemic toxicity was seen at the mid and high dose levels tested.

B. Executive Summary: In a Chronic Toxicity/ Oncogenicity study ( MRID 43015801), groups of 60 male and 60 female Crl: CDBR Sprague Dawley rats were given 0, 5, 50, 500, or 1000 mg/ kg bodyweight pentachloronitrobenzene ( Technical 98%) by gavage five days per week for up to two years. When adjusted for continuous exposure, these dose levels were equivalent to 0, 3.6, 36, 357 or 714 mg/ kg/ day. T 3, T 4 and TSH parameters were not examined.

No apparent effects on body weight, food intake, clinical observations, or survival were found. At all dose levels and at all measured time points ( 6, 12, and 18 months and study termination), dose dependent decreases in serum AST and ALT activities and the excretion of triple phosphate crystals in the urine were found in both sexes. At 36 mg/ kg/ day and above, increases in minimal to slight hepatocellular hypertrophy were observed in males ( ranging from 9/ 60 to 26/ 60 versus 2/ 60 in controls; p < 0.05 at 36 mg/ kg/ day; p < 0.01 at 357 mg/ kg/ day and above). At 357 mg/ kg/ day and above, increases in minimal to slight hepatocellular hypertrophy were observed in females ( ranging from 10/ 60 to 22/ 60 versus 1/ 60 in controls; p < 0.01). Increases in thyroid follicular cell hypertrophy/ hyperplasia were observed in both sexes ( 6/ 60 versus 2/ 60 in males and 5/ 59 versus 1/ 59 in females) however, the increases were not statistically significant. High dose male rats had an approximate 30% increase of absolute and relative liver weight and an approximate 22% increase in absolute thyroid/ parathyroid weight at necropsy. Microscopically, increases in thyroid follicular cell hypertrophy/ hyperplasia ( mostly minimal to slight; 12/ 60 versus 2/ 60 for males and 10/ 60 versus 1/ 59 for females; p < 0.01) were found. Based on the hepatocellular hypertrophy and the thyroid follicular cell hypertrophy/ hyperplasia, the NOAEL was 3.6 mg/ kg/ day for males and 36 mg/ kg/ day for females. The corresponding LOAELS would be 36 mg/ kg/ day for males and 357 mg/ kg/ day for females. No treatment related increase in neoplasia was found.

The study is classified as core guideline and satisfies the requirements for an § 83 5 Oral Chronic/ oncogenicity Study.

Discussion of Tumor Data: No treatment related increase in neoplasia was noted.

Adequacy of Dosing: Previous concerns for PCNB carcinogenicity were linked to the high HCB concentrations in earlier studies. However, in the Uniroyal feeding study ( MRID No. 41987301), only 0.04% HCB was reported in the test material and this study demonstrated a positive carcinogenic potential. On the other hand, the Amvac study ( MRID No. 41987301) was negative for carcinogenicity. This is a gavage study with administration of the test material ( 98% PCNB) only 5 days per week. The interruption in dosing may tend to allow some time for test material body burden to decrease and for for recovery, as compared to a dietary feeding study. This 18 difference in dosing regimen might tend to explain the negative carcinogenicity results, although other similar thyroid findings were noted. HIARC concluded that the dose levels tested were judged to be adequate based on thyroid toxicity observed at the mid and high dose levels.

2. Carcinogenicity Study in Mice MRID No.: 45609101 Citation: National Toxicology Program. March, 1986. NTP Technical Report on the Toxicology and Carcinogenesis Studies of Pentachloronitrobenzene in B6C3 F1 Mice. ( Pre publication draft report no. NIH 86 2581)

Executive Summary: In an oral carcinogenicity study, ( MRID No. 45609101) 50 B6C3F1 mice per sex per dose group were administered PCNB ( purity not reported) in the diet at concentrations of 0, 2500, or 5000 ppm for 103 weeks. At the end of the feeding period, test diets were withdrawn and the animals were fed control diets during a one week observation period before termination of the study.

No increase in the incidence of neoplastic lesions was observed in the treated mice, but the test substance may have predisposed the female mice of the high dose group to a bacterial infection which significantly decreased their survival after 86 weeks. PCNB did not exhibit carcinogenic potential under the conditions of the experiment.

Due to the decreased survival rate, since the lot and concentration of the test material used in the study are not indicated, and the suggestion that study interpretation may have been confounded due to infection, this study is classified as unacceptable and does not satisfy the requirement for a mouse carcinogenicity study.

Discussion of Tumor Data: No carcinogenic effects were noted.

Adequacy of Dosing: Dosing may have been adequate, but survival was reduced associated with a bacterial infection.

3. Classification of Carcinogenic Potential The carcinogenicity of PCNB was assessed in reviews of 1977 ( special review) and in 1986 and 1992. In 1992, HED's Carcinogenicity Peer Review Committee ( CARC) classified PCNB as a Group C  possible human carcinogen and recommended that for the purpose of risk characterization, the Reference Dose approach should be used for quantification of human risk.

IV. MUTAGENICITY The HIARC concluded that there is not a concern for mutagenicity resulting from exposure to PCNB. 19 Pentachloronitrobenzene was selected for genetic toxicology screening by the National Toxicology Program ( NTP). Testing included: the Salmonella/ mammalian microsome test, induction of forward gene mutations in L5178Y mouse lymphoma cells and induction of chromosome aberrations and sister chromatid exchanges ( SCEs) in Chinese hamster ovary ( CHO) cells. Although formal DERs do not exist for these assays, they are considered acceptable by HED.

GENE MUTATIONS 1. Salmonella typhimurium/ mammalian microsome reverse gene mutation assay: Using the preincubation procedure, PCNB ( 95%) was negative in S. typhimurium strains TA1535, TA1537, TA198 and TA 100 up to high doses of 6666.7 to 10,000 ug/ plate without S( activation and with S9 activation derived from rat and hamster livers induced with Aroclor 1254. Compound precipitation was seen at > 1000ug/ plate. The study is acceptable and satisfies the guideline requirement for a bacterial gene mutation assay.

2. L5178Y mouse lymphoma cell forward gene mutation assay: Independent trial were negative up to the highest doses tested ( 15 or 30

g/ mL  S9; 15

/ mL + S9). The study is acceptable and satisfies the guideline requirement for a mammalian cell gene mutation assay.

CHROMOSOMAL ABERRATIONS 3. In vitro cytogenetics assay in Chinese hamster ovary ( CHO) cells: the test was positive in the absence of S( activation with a significant ( p< 0.05) increase in chromosome aberrations over a concentration range of 7.5 75

g/ mL. With S9 activation, results were equivocal at the highest dose tested ( 75

g/ mL). The study is acceptable and satisfies the guideline requirement for an in vitro cytogenetic assay.

OTHER MUTAGENIC MECHANISMS 4. In vitro SCE assay in CHO cells: The test was negative up to the highest concentration tested ( 7.5

g/ mL  S9; 75

g/ mL+ S9). The study is acceptable and satisfies the guideline requirement for an in vitro SCE assay.

Results from the NTP genetic toxicology testing indicate that PCNB ( lot and % a. i. not specified) is not mutagenic in bacteria or in cultured mammalian cells. There is, however, evidence showing that PCNB is clastogenic in the absence of S9 activation and equivocal in the presence of S9 activation. PCNB was also negative for the induction of SCEs in vitro. Based on these data, it is recommended that the in vitro test results of clastogenicity be examined in an in vivo cytogenetic assay.

CITATIONS Haworth, S., Lawlor, T., Mortelmans, K., Speck, W., and Zeiger, E. ( 1983). Salmonella mutagenicity test results for 250 chemicals. Environ Mutagen 5( Suppl 1): 3 142 20 Galloway, S. M., Armstrong, M. A., Reuben, C., Colman, S., Brown, B., Cannon, C. et al ( 1987). Chromosome aberration and sister chromatid exchange in Chinese ovary cells: Evaluation of 108 chemicals. Environ Molec Mutagen 10( Suppl 10): 1 176.

Helsley, D ( 2000). Personal communication between d. Helsley, cellular and Genetic toxicology Branch, NTP and N. E. McCarroll, OPP/ HED/ Tox 1   mouse lymphoma data.

V. HAZARD CHARACTERIZATION The Metabolism Assessment Review Committee ( MARC) convened on October 14, 2001 to consider the Uniroyal and Amvac PCNB data bases. They concluded that they could find no evidence that the chemical composition ( i. e. impurity levels) differences among the formulations tested in the toxicity studies affected the NOAELS/ LOAELS and endpoints found. This is interpreted as indicating that the data bases for the two technicals should be combined for purposes of risk assessment PCNB is used as a non systemic soil treatment fungicide for vegetables, field crops, turf, ornamentals and as a post harvest treatment on banana stems and rose bushes. It is also a seed dressing agent. It is primarily applied as a spray, through sprinkler irrigation systems or granular preparations to soil and is formulated as an emulsifiable concentrate, granules or wettable powder. Acute toxicities are low , with most study results in Toxicity Categories III or IV, although ( Uniroyal) PCNB has been identified as a weak sensitizer.

Data from several 1970' s monkey studies suggest that PCNB bioaccumulates, to some degree, in mammals. In these studies, only a few animals are utilized but data suggest that the half live might be as long as 4 or more days. These investigators also noted that after 20 days only 59% of a given dose was eliminated. It was also suggested that from day 30 to 40, the excretion curve paralleled the dose which means that an equilibrium between uptake and excretion was reached, resulting in a plateau of the storage curve. These data clearly raise an uncertainty as to the biological half life for PCNB and therefore as to its potential for bioaccumulation. Additional data are necessary before finalization of the risk assessment process.

Subchronic and chronic studies indicate that the thyroid and the liver are target organs for PCNB. Limited evidence suggest that the thyroid effects might be due, at least in part, to disturbance of thyroid homeosthasis. ( Also see discussion in Section 5.5, Additional Information from Literature Sources)

Aminotransferase activities ( AST/ ALT, particularly ALT) decrease in dose dependent manner by as much as 30 80% in rats and dogs. However, data are inadequate to evaluate the toxicological significance of these findings. ( Also see discussion in Section 5.5, Additional Information from Literature Sources). The Registrant has been requested to address these issues of thyroid activity and transaminase enzymatic activity.

Results from the NTP genetic toxicology testing indicate that PCNB ( lot and % a. i. not specified) is not mutagenic in bacteria or in cultured mammalian cells. There is, however, evidence showing that PCNB is clastogenic in the absence of S9 activation and equivocal in the presence of S9 activation. PCNB was 21 also negative for the induction of SCEs in vitro. The HIARC recommended that the in vitro test results of clastogenicity be examined in an in vivo cytogenetic assay.

The carcinogenicity of PCNB was assessed in reviews of 1977 ( special review) and in 1986 and 1992. In 1992, the CPRC classified PCNB as a Group C possible human carcinogen and recommended that for the purpose of risk characterization, the Reference Dose approach should be used for quantification of human risk.

No findings of significant toxicological concern have been identified in developmental toxicity or reproduction study data. No neurotoxicity studies have been identified and no neurobehavioral alterations nor evidence of neuropathological effects have been observed in available data.

VI. DATA GAPS / REQUIREMENTS 1. Although the thyroid is a target organ for PCNB, thyroid hormone and TSH determinations have been performed only in one nonguideline study ( 90 day study in male rats) using inappropriate dosing ( 0, 1, & 333 mg/ kg/ day) which precludes a meaningful assessment of doseresponse and time course features of the effect. The HIARC requests that the Registrant conduct a study to assess thyroid toxicity in adults vs. offspring development. The study should include: ( a) Assays of appropriate hormones ( b) Organ Weights ( c) Histopathology. The study should be conducted utilizing an adequate dosing regimen allowing for meaningful toxicological assessment of dose response and comparison to other submitted toxicological studies. In addition, it should be integrated with appropriate kinetic data. The registrant is requested to consult the Agency in the design of this study.

2. Aminotransferase activities ( AST/ ALT, particularly ALT) decrease in dose dependent manner by as much as 30 80% in rats and dogs. Although the literature indicates that Aminotransferase inhibition, may result in increases in GABA, hepatocellular tyrosine, and other aminoacid related compounds, there are no data to evaluate the toxicological significance of the inhibition data for PCNB. The Registrant is requested to address the toxicological significance of these alterations in AST/ ALT activities on the risk assessment of the subject chemical. ( Also see Section 5.5, Additional Information from Literature Sources)

3. Limited kinetic data have been identified in the literature which suggest that PCNB will likely accumulate within mammalian tissues potentially impacting upon the risk assessment process. Because of concerns about the uncertainties of the half life and thus for the accumulation potential of the chemical, the HIARC recommended that a study to determine the biological half life on PCNB be requested. It is therefore requested that the Registrant perform a guideline metabolism study of PCNB ( including a mass balance of radioactivity in excreta, tissues, and carcass) including a Tier II study of blood kinetics, to determine a half life of PCNB. The Registrant should consult the Agency as to the details of the protocol.

4. There is evidence showing that PCNB is clastogenic in the absence of S9 activation and equivocal in the presence of S9 activation. PCNB was also negative for the induction of SCEs in vitro. The HIARC requests that the in vitro test results of clastogenicity be examined in an in 22 vivo cytogenetic assay.

5. There are no subchronic inhalation toxicity data on PCNB. Due to the greenhouse use of PCNB the HIARC requests that a 90 day inhalation toxicity study of PCNB be conducted. It is recommended that interim thyroid hormone analyses be made at 7, 14, 30 and 90 days. 23 VII. ACUTE TOXICITY Acute Toxicity of PCNB ( Uniroyal)

Guideline No. Study Type MRIDs # Results Toxicity Category 81 1 Acute Oral 43198201 LD 50 = > 5000 mg/ kg IV 81 2 Acute Dermal 43198202 LD 50 = > 5000 mg/ kg IV 81 3 Acute Inhalation 43118201 LC 50 = > 1.7 mg/ L III 81 4 Primary Eye Irritation 43198203 Slight irritant III 81 5 Primary Skin Irritation 43198204 Non irritant IV 81 6 Dermal Sensitization 4060901 Weak sensitizer 81 8 Acute Neurotoxicity Acute Toxicity of PCNB ( Amvac)

Guideline No. Study Type MRIDs # Results Toxicity Category 81 1 Acute Oral 41443101 LD 50 = > 5050 mg/ kg IV 81 2 Acute Dermal 41443102 LD 50 = > 2020 mg/ kg III 81 3 Acute Inhalation 41443103 LC 50 = > 6.49 mg/ L III 81 4 Primary Eye Irritation 41443109 Slight irritant III 81 5 Primary Skin Irritation 41443105 PII = 0.0175 IV 81 6 Dermal Sensitization 40734001 Non sensitizer 81 8 Acute Neurotoxicity 24 VIII. SUMMARY OF TOXICOLOGY ENDPOINT SELECTION Summary of Toxicological Dose and Endpoints for PCNB Exposure Scenario Dose Used in Risk Assessment, UF Special FQPA SF* and Level of Concern for Risk Assessment Study and Toxicological Effects Acute Dietary ( All populations) N/ A N/ A None selected Chronic Dietary ( All populations) NOAEL= 1.0 mg/ kg/ day UF = 1000 Chronic RfD = 0.001 mg/ kg/ day FQPA SF = 1X cPAD = chronic RfD FQPA SF = 0.001 mg/ kg/ day Chronic/ Oncogenicity Study  rat LOAEL = 150 mg/ kg/ day based on hepatocellular hypertrophy, hepatocellular hyperplasia, and thyroid hypertrophy Short Term Incidental Oral ( 1 30 days) NOAEL= 1.0 mg/ kg/ day Residential LOC for MOE = 1000 Occupational = NA 90 Day Subchronic  Rat LOAEL = 1.0 mg/ kg/ day based on no toxicity at 30 days Intermediate Term Incidental Oral ( 1 6 months) NOAEL= 1.0 mg/ kg/ day Residential LOC for MOE = 1000 Occupational = NA 90 Day Subchronic  Rat LOAEL = 1.0 mg/ kg/ day based on threshold effects ( liver and thyroid lesions) seen at the lowest dose tested Short ( 1 to 30 days) and Intermediate Term Dermal ( 1 to 6 months) Dermal NOAEL= 300 mg/ kg/ day Residential LOC for MOE = 1000 Occupational LOC for MOE = 100 21 Day Dermal  Rat LOAEL = mg/ kg/ day based on hypertrophy of the thyroid follicular epithelium and dilation of the thyroid follicles in males at 1000 mg/ kg/ day Long Term Dermal (> 6 months) Oral NOAEL= 1.0 mg/ kg/ day ( dermal absorption rate = 33% of oral) Residential LOC for MOE = 1000 Occupational LOC for MOE = 100 Chronic/ Oncogenicity Study  rat LOAEL = 150 mg/ kg/ day based on hepatocellular hypertrophy, hepatocellular hyperplasia, and thyroid hypertrophy Exposure Scenario Dose Used in Risk Assessment, UF Special FQPA SF* and Level of Concern for Risk Assessment Study and Toxicological Effects 25 Short Term Inhalation ( 1 to 30 days) Oral NOAEL= 1.0 mg/ kg/ day ( inhalation absorption = 100% of oral) Residential LOC for MOE = 1000 Occupational LOC for MOE = 100 90 Day Subchronic  Rat LOAEL = 1.0 mg/ kg/ day based on no toxicity at 30 days Intermediate Term Inhalation ( 1 to 6 months) Oral NOAEL = 1.0 mg/ kg/ day ( inhalation absorption rate = 100% of oral) Residential LOC for MOE = 1000 Occupational LOC for MOE = 100 90 Day Subchronic  Rat LOAEL = 1.0 mg/ kg/ day based on threshold effects ( liver and thyroid lesions) seen at the lowest dose tested Long Term Inhalation (> 6 months) Oral NOAEL= 1.0 mg/ kg/ day ( inhalation absorption rate = 100% of oral) Residential LOC for MOE = 1000 Occupational LOC for MOE = 100 Chronic/ Oncogenicity Study  rat LOAEL = 150 mg/ kg/ day based on hepatocellular hypertrophy, hepatocellular hyperplasia, and thyroid hypertrophy Cancer ( oral, dermal, inhalation) HED's Carcinogenicity Peer Review Committee ( CARC) classified PCNB as a Group C  possible human carcinogen and recommended that for the purpose of risk characterization, the Reference Dose approach should be used for quantification of human risk.

UF = uncertainty factor, FQPA SF = Special FQPA safety factor, NOAEL = no observed adverse effect level, LOAEL = lowest observed adverse effect level, PAD = population adjusted dose ( a = acute, c = chronic) RfD = reference dose, MOE = margin of exposure, LOC = level of concern, NA = Not Applicable NOTE: The Special FQPA Safety Factor recommended by the HIARC assumes that the exposure databases ( dietary food, drinking water, and residential) are complete and that the risk assessment for each potential exposure scenario includes all metabolites and/ or degradates of concern and does not underestimate the potential risk for infants and children. 26 REVIEWER NOTES:

Subsequent to the HIARC meeting of November 27, 2001, the presenting reviewer, Laurence Chitlik, added the following additional comments:

1. It does not appear appropriate for the HIARC to select the use of a non guideline study conducted only in male rats for use as part of a risk assessment process to protect females. In addition even for males, this study only evaluated a very few parameters far short of what would be included in a typical 90 day study. For example, the study did not include hematology or even gross and histopathology for tissues other than the thyroid, parathyroids, pituitary, and liver.

Certainly, the risk assessment process must include low dose hazards identified in this study. However, consideration of the lack of toxicity observed at certain interim time points does not constitute an appropriate endpoint for safety assessment especially since so little was assessed in this study and only in one sex.

2. The second comment relates to the need for a new mouse oncogenicity study since previous reviews had identified a number of shortcomings ( including bacterial infection) in the study which appear to confound interpretation of study data. Although this issue was presented to the HIARC, it did not appear to the reviewer that a consensus was reached by the committee not to require a new study. Some committee members did suggest continued use of the mouse oncogenicity study, but clearly there was no actual vote by the committee and relative to such a critical issue.

Since PCNB was originally registered in the 1950' s, the contaminants present in the technical have changed dramatically. The NTP mouse oncogenicity study listed in this review was completed in 1987 and a number of significant deficiencies have been identified in this study. Previous reviews of the study indicated that nonneoplastic lesions observed in female mice were secondary to bacterial infection. The investigators attempted to explain the high levels of infection observed in this study by suggesting that the test material might have predisposed the female mice ( but curiously not the males) to the infection. The infection was identified as Klebsiella. The mouse onco study appears compromised due to infection confounding interpretation of the study results as well as affecting the longevity of the animals on test. In addition, the lot # of the test material is not identified and there is no indication in the report that the test diets were analyzed. Lack of diet analysis by itself is often considered adequate for invalidation of a carcinogenicity study. Also, a review by R. Gardner, 2/ 2/ 89, states that it is " prudent to use the mouse study in the absence of better data" but at this time I do not find this a reason to continue to use this study as was done in the 1993 Cancer review. There is also a review by the California Department of Food and Agriculture which states that the study is unacceptable because among other things, only two doses were used, many missing tissues in histopathology examination, a questionable MTD was utilized, and effects of an infectious agent compromised the study.

3. Due to the significance of current data gaps, conduct of a meaningful risk assessment especially as it might relate to FQPA is questionable at this time. The HIARC concurred that significant additional data will be required from the registrants to assist in the risk assessment process. Until these basic data are available, it is the opinion of this reviewer that a meaningful risk assessment cannot be performed for PCNB. Certainly, without adequate kinetic data demonstrating the potential for bioaccumulation and determination of steady state levels, even a meaningful MOE assessment cannot be performed.


[Federal Register: October 14, 2010 (Volume 75, Number 198)]
[Notices]
[Page 63166-63167]
[DOCID:fr14oc10-52]

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DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Docket No. DI10-19-000]

Howard Rosenfeld; Notice of Declaration of Intention and
Soliciting Comments, Protests, and/or Motions To Intervene

October 6, 2010.
    Take notice that the following application has been filed with the
Commission and is available for public inspection:
    a. Application Type: Declaration of Intention.

    b. Docket No: DI10-19-000.
    c. Date Filed: September 17, 2010.
    d. Applicant: Howard Rosenfeld.
    e. Name of Project: Warren Energy Independence Hydroelectric
Project.
    f. Location: The proposed Warren Energy Independence Hydroelectric
Project will be located on Sucker Brook, a.k.a. Lake Waramaug Brook,
tributary to Aspetuck River and the Housatonic River, near the town of
Warren, Litchfield County, Connecticut.
    g. Filed Pursuant to: Section 23(b)(1) of the Federal Power Act, 16
U.S.C. 817(b).
    h. Applicant Contact: Paul V. Nolan, 5515 North 17th Street,
Arlington, VA 22205-2722; telephone:<PHONE_NUMBER>; Fax: (703) 538-
5257; e-mail<EMAIL_ADDRESS>    i. FERC Contact: Any questions on this notice should be addressed
to Henry Ecton,<PHONE_NUMBER>, or E-mail address:
<EMAIL_ADDRESS>    j. Deadline for filing comments, protests, and/or motions: November
08, 2010.
    All documents should be filed electronically via the Internet. See
18 CFR 385.2001(a)(1)(iii) and the instructions on the Commission's Web
site at http://www.ferc.gov/docs-filing/efiling.asp. If unable to be
filed electronically, documents may be paper-filed. To paper-file, an
original and seven copies should be filed with: Secretary, Federal
Energy Regulatory Commission, 888 First Street, NE., Washington, DC
20426.
    Commenters can submit brief comments up to 6,000 characters,
without prior registration, using the eComment system at http://
www.ferc.gov/docs-filing/ecomment.asp. Please include the docket number
(DI10-19-000) on any comments, protests, and/or motions filed.
    k. Description of Project: The proposed Warren Energy Independence
Hydroelectric Project will consist of: (1) An existing natural lake;
(2) an existing 80-foot-long, 4-foot-wide, 5-foot-high masonry dam; (3)
a proposed 18-inch-diameter, 535-foot-long PVC penstock; (4) an
existing 22-foot-long, 22-foot-wide, 25-foot-high existing mill
building, containing a new 10-kW turbine/generator; (5) a bank of
batteries for use on site; and (6) appurtenant facilities.
    When a Declaration of Intention is filed with the Federal Energy
Regulatory Commission, the Federal Power Act requires the Commission to
investigate and determine if the interests of interstate or foreign
commerce would be affected by the proposed project. The Commission also
determines whether or not the project: (1) Would be located on a
navigable waterway; (2) would occupy or affect public lands or
reservations of the United States; (3) would utilize surplus water or
water power from a government dam; or (4) if applicable, has involved
or would involve any construction subsequent to 1935 that may have
increased or would increase the project's head or generating capacity,
or have otherwise significantly modified the project's pre-1935 design
or operation.
    l. Locations of the Application: Copies of this filing are on file
with the Commission and are available for public inspection. This
filing may be viewed on the web at 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. You may also
register online at http://www.ferc.gov/docs-filing/esubscription.asp to
be notified via e-mail of new filings and issuances related to this or
other pending projects. For assistance, please contact FERC Online
Support at<EMAIL_ADDRESS>or toll-free at<PHONE_NUMBER>,
or TTY, contact<PHONE_NUMBER>. A copy is also available for inspection
and reproduction at the address in item (h) above.
    m. Individuals desiring to be included on the Commission's mailing
list should so indicate by writing to the Secretary of the Commission.
    n. Comments, Protests, or Motions to Intervene--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,
.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.
    o. Filing and Service of Responsive Documents--Any filings must
bear in all capital letters the title ``COMMENTS'', ``PROTESTS'', AND/
OR ``MOTIONS TO INTERVENE'', as applicable, and the Docket Number of
the particular application to which the filing refers. A copy of any
motion to intervene must also be served upon each representative of the
Applicant specified in the particular application.
    p. Agency Comments--Federal, state, and local agencies are invited
to file comments on the described application. A copy of the
application may be obtained by agencies directly from the Applicant. If
an agency does not file comments within the time specified for filing
comments, it will be presumed to have no comments. One copy of an
agency's comments must also be sent to the Applicant's representatives.

Kimberly D. Bose,
Secretary.
[FR Doc. 2010-25793 Filed 10-13-10; 8:45 am]
BILLING CODE 6717-01-PGPO Galley End:?>