[Federal Register Volume 78, Number 229 (Wednesday, November 27, 2013)]
[Rules and Regulations]
[Pages 70870-70877]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2013-28517]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[EPA-HQ-OPP-2011-0905; FRL-9902-39]


Etofenprox; Pesticide Tolerances

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes tolerances for residues of 
etofenprox in or on multiple commodities which are identified and 
discussed later in this document. Interregional Research Project Number 
4 (IR-4) requested these tolerances under the Federal Food, Drug, and 
Cosmetic Act (FFDCA).

DATES: This regulation is effective November 27, 2013. Objections and 
requests for hearings must be received on or before January 27, 2014, 
and must be filed in accordance with the instructions provided in 40 
CFR part 178 (see also Unit I.C. of the SUPPLEMENTARY INFORMATION).

ADDRESSES: The docket for this action, identified by docket 
identification (ID) number EPA-HQ-OPP-2011-0905, is available at http://www.regulations.gov or at the Office of Pesticide Programs Regulatory 
Public Docket (OPP Docket) in the Environmental Protection Agency 
Docket Center (EPA/DC), EPA West Bldg., Rm. 3334, 1301 Constitution 
Ave. NW., Washington, DC 20460-0001. The Public Reading Room is open 
from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal 
holidays. The telephone number for the Public Reading Room is (202) 
566-1744, and the telephone number for the OPP Docket is (703) 305-
5805. Please review the visitor instructions and additional information 
about the docket available at http://www.epa.gov/dockets.

FOR FURTHER INFORMATION CONTACT: Lois Rossi, Registration Division 
(7505P), Office of Pesticide Programs, Environmental Protection Agency, 
1200 Pennsylvania Ave. NW., Washington, DC 20460-0001; telephone 
number: (703) 305-7090; email address: [email protected].

SUPPLEMENTARY INFORMATION: 

I. General Information

A. Does this action apply to me?

    You may be potentially affected by this action if you are an 
agricultural producer, food manufacturer, or pesticide manufacturer. 
The following list of North American Industrial Classification System 
(NAICS) codes is not intended to be exhaustive, but rather provides a 
guide to help readers determine whether this document applies to them. 
Potentially affected entities may include:
     Crop production (NAICS code 111).
     Animal production (NAICS code 112).
     Food manufacturing (NAICS code 311).
     Pesticide manufacturing (NAICS code 32532).

B. How can I get electronic access to other related information?

    You may access a frequently updated electronic version of EPA's 
tolerance regulations at 40 CFR part 180 through the Government 
Printing Office's e-CFR site at http://www.ecfr.gov/cgi-bin/text-idx?&c=ecfr&tpl=/ecfrbrowse/Title40/40tab_02.tpl.

C. How can I file an objection or hearing request?

    Under FFDCA section 408(g), 21 U.S.C. 346a, any person may file an 
objection to any aspect of this regulation and may also request a 
hearing on those objections. You must file your objection or request a 
hearing on this regulation in accordance with the instructions provided 
in 40 CFR part 178. To ensure proper receipt by EPA, you must identify 
docket ID number EPA-HQ-OPP-2011-0905 in the subject line on the first 
page of your submission. All objections and requests for a hearing must 
be in writing, and must be received by the Hearing Clerk on or before 
January 27, 2014. Addresses for mail and hand delivery of objections 
and hearing requests are provided in 40 CFR 178.25(b).
    In addition to filing an objection or hearing request with the 
Hearing Clerk as described in 40 CFR part 178, please submit a copy of 
the filing (excluding any Confidential Business Information (CBI)) for 
inclusion in the public docket. Information not marked confidential 
pursuant to 40 CFR part 2 may be disclosed publicly by EPA without 
prior notice. Submit the non-CBI copy of your objection or hearing 
request, identified by docket ID number EPA-HQ-OPP-2011-0905, by one of 
the following methods:
     Federal eRulemaking Portal: http://www.regulations.gov. 
Follow the online instructions for submitting comments. Do not submit 
electronically any information you consider to be CBI or other 
information whose disclosure is restricted by statute.
     Mail: OPP Docket, Environmental Protection Agency Docket 
Center (EPA/DC), (28221T), 1200 Pennsylvania Ave. NW., Washington, DC 
20460-0001.
     Hand Delivery: To make special arrangements for hand 
delivery or delivery of boxed information, please follow the 
instructions at http://www.epa.gov/dockets/contacts.html. Additional 
instructions on commenting or visiting the docket, along with more 
information about dockets generally, is available at http://www.epa.gov/dockets.

[[Page 70871]]

II. Summary of Petitioned-For Tolerance

    In the Federal Register of December 8, 2011 (76 FR 76674) (FRL-
9328-8), EPA issued a document pursuant to FFDCA section 408(d)(3), 21 
U.S.C. 346a(d)(3), announcing the filing of a pesticide petition (PP 
1E7925) by Interregional Research Project No. 4 (IR-4), 500 College 
Road East, Suite 201 W, Princeton, NJ 08540. The petition requested 
that 40 CFR 180.620 be amended by establishing tolerances for residues 
of the insecticide etofenprox, [2-(4-ethoxyphenyl)-2-methylpropyl 3-
phenoxybenzyl ether], in or on food and feed commodities at 0.5 parts 
per million (ppm). That document referenced a summary of the petition 
prepared by Mitsui, the registrant, which is available in the docket, 
http://www.regulations.gov. There were no comments received in response 
to the notice of filing.
    Currently there are two products that contain etofenprox registered 
for mosquito control. However, the existing registrations do not allow 
treatments on or over agricultural areas. IR-4 submitted this petition 
to establish tolerances for residues of etofenprox in or on food and 
feed commodities so that the registration can be modified to allow 
repeated applications (aerial and ground) over agricultural crops, 
pasture and rangeland.
    Based upon review of the data supporting the petition, EPA has 
modified the level at which tolerances are being established. The 
reason for this change is explained in Unit IV.C.

III. Aggregate Risk Assessment and Determination of Safety

    Section 408(b)(2)(A)(i) of FFDCA allows EPA to establish a 
tolerance (the legal limit for a pesticide chemical residue in or on a 
food) only if EPA determines that the tolerance is ``safe.'' Section 
408(b)(2)(A)(ii) of FFDCA defines ``safe'' to mean that ``there is a 
reasonable certainty that no harm will result from aggregate exposure 
to the pesticide chemical residue, including all anticipated dietary 
exposures and all other exposures for which there is reliable 
information.'' This includes exposure through drinking water and in 
residential settings, but does not include occupational exposure. 
Section 408(b)(2)(C) of FFDCA requires EPA to give special 
consideration to exposure of infants and children to the pesticide 
chemical residue in establishing a tolerance and to ``ensure that there 
is a reasonable certainty that no harm will result to infants and 
children from aggregate exposure to the pesticide chemical residue. . . 
.''
    Consistent with FFDCA section 408(b)(2)(D), and the factors 
specified in FFDCA section 408(b)(2)(D), EPA has reviewed the available 
scientific data and other relevant information in support of this 
action. EPA has sufficient data to assess the hazards of and to make a 
determination on aggregate exposure for etofenprox including exposure 
resulting from the tolerances established by this action. EPA's 
assessment of exposures and risks associated with etofenprox follows.

A. Toxicological Profile

    EPA has evaluated the available toxicity data and considered its 
validity, completeness, and reliability as well as the relationship of 
the results of the studies to human risk. EPA has also considered 
available information concerning the variability of the sensitivities 
of major identifiable subgroups of consumers, including infants and 
children.
    In mammals, the major targets of etofenprox are the liver, thyroid, 
kidney, and hematopoietic system. Results from subchronic and chronic 
feeding studies in rats indicate that males may be more sensitive to 
treatment-related effects of etofenprox than females. All subchronic 
and chronic toxicity including carcinogenicity studies showed adverse 
effects (organ weights, histopathology, biochemistry, hematology, and 
clinical chemistry) in two or more of the target organs/systems. 
Additionally, decreases in body weights and food consumption were 
observed in most of the studies.
    In a mouse carcinogenicity study, the kidney was the most sensitive 
target organ, especially in males, and many deaths were attributed to 
renal lesions. Males showed a positive trend in renal cortical adenomas 
alone and in combined carcinomas and adenomas; however, tumor incidence 
was within the historical control range. Other effects included 
decreased body and thymus gland weights, and increased liver, spleen, 
and pituitary gland weights. Microscopic changes included centrilobular 
hepatocyte enlargement.
    Relevant toxicity studies showed no quantitative or qualitative 
evidence of increased susceptibility in offspring. A prenatal 
developmental toxicity study in rabbits showed no quantitative or 
qualitative evidence of increased susceptibility in offspring, in that 
the developmental effects were seen at doses that resulted in maternal 
toxicity, including death. There was no indication of increased 
susceptibility of offspring in the 1-generation/developmental study in 
rats. In the developmental portion of the study, effects were seen in 
maternal animals, while no effects were observed in the offspring. In 
the 2-generation reproductive toxicity study in rats, there was also no 
evidence of increased susceptibility of offspring.
    Although etofenprox exposure does result in some neurotoxic 
effects, these effects only occur at high doses. An acute neurotoxicity 
study in the adult rat revealed no treatment-related effects. The 
subchronic neurotoxicity study in the rat showed decreased body weight 
gains, increased liver weights in all dose groups, and increased 
incidence of rearing behavior in males and abnormal gait in females. 
The developmental neurotoxicity study in rats showed increased rearing 
behavior in mothers at the highest dose tested (HDT). In offspring, eye 
abnormalities were observed at the high-dose level and effects on 
motor/locomotor activity and auditory startle response observed at the 
high-dose level.
    The immunotoxicity studies in the rat and mouse were both negative 
for immunotoxicity.
    The cancer classification for etofenprox is ``Not likely to be 
carcinogenic to humans at doses that do not alter rat thyroid hormone 
homeostasis.'' This decision was based on the following considerations:
    i. Treatment-related thyroid follicular cell tumors were seen in 
both male and female rats at a dose level considered to be adequate, 
and not excessive, to assess carcinogenicity;
    ii. No treatment-related tumors were seen in male or female mice 
when tested at a dose that was considered adequate to assess 
carcinogenicity;
    iii. There is no mutagenicity concern for etofenprox based in vivo 
or in vitro assays;
    iv. The non-neoplastic toxicological evidence (i.e., thyroid growth 
and thyroid hormonal changes) indicates that etofenprox disrupts the 
thyroid-pituitary hormonal status; and
    v. Rats are substantially more sensitive than humans to the 
development of thyroid follicular cell tumors in response to thyroid 
hormone imbalance. The overall weight-of-the-evidence was considered 
sufficient to indicate that etofenprox induced thyroid follicular 
tumors through an antithyroid mode of action.
    Specific information on the studies received and the nature of the 
adverse effects caused by etofenprox as well as the no-observed-
adverse-effect-level (NOAEL) and the lowest-observed-adverse-effect-
level (LOAEL) from the toxicity studies can be found at http://www.regulations.gov in the document

[[Page 70872]]

titled ``Etofenprox: Section 3 Aggregate Human Health Risk Assessment 
for a Label Amendment to Remove Application Restriction Over Crop, 
Range, and Pasture land,'' pp. 36-41 docket ID number EPA-HQ-OPP-2011-
0905.

B. Toxicological Points of Departure/Levels of Concern

    Once a pesticide's toxicological profile is determined, EPA 
identifies toxicological points of departure (POD) and levels of 
concern to use in evaluating the risk posed by human exposure to the 
pesticide. For hazards that have a threshold below which there is no 
appreciable risk, the toxicological POD is used as the basis for 
derivation of reference values for risk assessment. PODs are developed 
based on a careful analysis of the doses in each toxicological study to 
determine the dose at which no adverse effects are observed (the NOAEL) 
and the lowest dose at which adverse effects of concern are identified 
(the LOAEL). Uncertainty/safety factors are used in conjunction with 
the POD to calculate a safe exposure level--generally referred to as a 
population-adjusted dose (PAD) or a reference dose (RfD)--and a safe 
margin of exposure (MOE). For non-threshold risks, the Agency assumes 
that any amount of exposure will lead to some degree of risk. Thus, the 
Agency estimates risk in terms of the probability of an occurrence of 
the adverse effect expected in a lifetime. For more information on the 
general principles EPA uses in risk characterization and a complete 
description of the risk assessment process, see http://www.epa.gov/pesticides/factsheets/riskassess.htm.
    A summary of the toxicological endpoints for etofenprox used for 
human risk assessment is shown in the Table of this unit.

   Table--Summary of Toxicological Doses and Endpoints for Etofenprox for Use in Human Health Risk Assessment
----------------------------------------------------------------------------------------------------------------
                                    Point of departure
        Exposure/scenario            and uncertainty/     RfD, PAD, LOC for     Study and toxicological effects
                                      safety factors       risk assessment
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Acute dietary (All populations)..  No adverse effects attributable to a single dose were observed in oral
                                    toxicity studies, including developmental toxicity studies in rats and
                                    rabbits. Therefore, an acute reference dose was not established.
                                  ------------------------------------------------------------------------------
Chronic dietary (All populations)  NOAEL = 3.7 mg/kg/    cRfD = 0.037 mg/kg/  Combined Chronic Toxicity/
                                    day.                  day.                 Carcinogenicity Study in Rat.
                                   UFA = 10x...........  cPAD = 0.037 mg/kg/  LOAEL = 25.5 mg/kg/day based on
                                   UFH = 10x...........   day.                 increased thyroid weights.
                                   FQPA SF = 1x........                        Related to increased liver
                                                                               weights and histopathology
                                                                               changes in liver and thyroid that
                                                                               occurred at the higher dose.
Incidental oral short- and         NOAEL = 20 mg/kg/day  LOC for MOE = 100..  Subchronic Oral Toxicity in Rat.
 intermediate-term (1 to 30 days   UFA = 10x...........                       LOAEL = 120 mg/kg/day based on
 and 1 to 6 months).               UFH = 10x...........                        decreased body weight gain,
                                   FQPA SF = 1x........                        increased liver and thyroid
                                                                               weights with corresponding
                                                                               histopathology, changes in
                                                                               hematology and clinical
                                                                               chemistry.
Incidental oral long-term (> 6     NOAEL = 3.7 mg/kg/    LOC for MOE = 100..  Combined Chronic Toxicity/
 months).                           day.                                       Carcinogenicity Study in Rat.
                                   UFA = 10x...........                       LOAEL = 25.5 mg/kg/day based on
                                   UFH = 10x...........                        increased thyroid weights.
                                   FQPA SF = 1x........                        Related to increased liver
                                                                               weights and histopathology
                                                                               changes in liver and thyroid that
                                                                               occurred at the higher dose.
Inhalation short- and              Inhalation study....  LOC for MOE = 100..  13-Week Inhalation Toxicity in
 intermediate-term (1 to 30 days   NOAEL = 10.6 mg/kg/                         Rat.
 and 1 to 6 months).                day..                                     LOAEL = 52.3 mg/kg/day based on
                                   UFA = 10x...........                        organ weight changes and
                                   UFH = 10x...........                        histopathological changes in
                                   FQPA SF = 1x........                        liver, adrenals and thyroid.
                                  ------------------------------------------------------------------------------
Cancer (Oral, dermal, inhalation)  Classification: ``Not likely to be carcinogenic to humans at doses that do
                                    not alter rat thyroid hormone homeostasis.''
----------------------------------------------------------------------------------------------------------------
FQPA SF = Food Quality Protection Act Safety Factor. LOAEL = lowest-observed-adverse-effect-level. LOC = level
  of concern. mg/kg/day = milligram/kilogram/day. MOE = margin of exposure. NOAEL = no-observed-adverse-effect-
  level. PAD = population adjusted dose (a = acute, c = chronic). RfD = reference dose. UF = uncertainty factor.
  UFA = extrapolation from animal to human (interspecies). UFH = potential variation in sensitivity among
  members of the human population (intraspecies).

C. Exposure Assessment

    1. Dietary exposure from food and feed uses. In evaluating dietary 
exposure to etofenprox, EPA considered exposure under the petitioned-
for tolerances as well as all existing etofenprox tolerances in 40 CFR 
180.620. EPA assessed dietary exposures from etofenprox in food as 
follows:
    i. Acute exposure. Quantitative acute dietary exposure and risk 
assessments are performed for a food-use pesticide, if a toxicological 
study has indicated the possibility of an effect of concern occurring 
as a result of a 1-day or single exposure. No such effects were 
identified in the toxicological studies for etofenprox; therefore, a 
quantitative acute dietary exposure assessment is unnecessary.
    ii. Chronic exposure. In conducting the chronic dietary exposure 
assessment EPA used the food consumption data from the U.S. Department 
of Agriculture's (USDA's) National Health and Nutrition Examination 
Survey, What We Eat in America (NHANES/WWEIA). The assessment assumed 
tolerance level residues for all commodities, incorporated estimated 
percent crop treated (PCT) values, and used the Dietary Exposure 
Evaluation Model Food Commodity Intake Database (DEEM-FCID) default 
processing factors. The submitted crop field trial data were conducted 
at a rate (0.07 lb ai/A) 10X greater than the proposed application rate 
of at 0.007 lb ai/A per site for mosquito control. The number and 
locations of field trials were in accordance with the initial

[[Page 70873]]

recommendations put forth by the EPA. EPA recommended field trials be 
conducted at the 1x and 10x rates and indicated that if there were 
residues detected in the samples collected above the limit of 
quantification (LOQ) at both 1x and 10x rates, then a tolerance would 
be required at the level observed at the 1x rate. However, the 
available crop field trial data do not reflect the number of 
applications proposed or the use of ground application equipment. 
Therefore, the Agency considered an analysis submitted by IR-4 of 
different modeled runs to estimate the residues resulting from multiple 
aerial applications using the Terrestrial Residue Exposure (TREX) model 
following repeated ultra low volume (ULV) applications to estimate an 
upper bound tolerance value. The EPA also evaluated the proposed 
multiple application scenarios using AGricultural DISPersal (AGDISP) 
8.25 and assumed the same application parameters (e.g., drop size 
distribution, application material, and application height) as 
considered in the TREX analysis. A deposition rate of 33% was assumed 
for aerial and ground ULV applications, which corresponds to a residue 
value of 4.8 ppm (to represent the worst case) with a wind speed of 1 
mph. These analysis result in estimated an upper bound value of 4.77 
ppm for ground and aerial applications. Therefore, the EPA determined 
that a tolerance of 5 ppm, which is based on conservative assumptions, 
is adequate to cover the expected residues. The proposed tolerance of 5 
ppm on food and feed commodities significantly increases the dietary 
burdens of etofenprox in livestock and necessitates establishing 
tolerances on livestock commodities.
    Specific information on the TREX and AGDISP analyses can be found 
at http://www.regulations.gov in the document titled ``Spray Drift 
Analysis for the Etofenprox Label Amendment (Petition No. 1E7925)'' 
docket ID number EPA-HQ-OPP-2011-0905.
    iii. Cancer. Based on the data summarized in Unit III.A., EPA has 
concluded that etofenprox does not pose a cancer risk to humans at 
doses that do not alter rat thyroid hormone homeostasis. Because the 
cPAD is protective of etofenprox's effect on thyroid hormones and 
dietary exposure to etofenprox for the purpose of assessing cancer risk 
would be the same or lower than dietary exposure relevant to other 
chronic endpoints, a dietary exposure assessment for the purpose of 
assessing cancer risk is unnecessary.
    iv. Anticipated residue and PCT information. Section 408(b)(2)(F) 
of FFDCA states that the Agency may use data on the actual percent of 
food treated for assessing chronic dietary risk only if:
     Condition a: The data used are reliable and provide a 
valid basis to show what percentage of the food derived from such crop 
is likely to contain the pesticide residue.
     Condition b: The exposure estimate does not underestimate 
exposure for any significant subpopulation group.
     Condition c: Data are available on pesticide use and food 
consumption in a particular area, the exposure estimate does not 
understate exposure for the population in such area.

In addition, the Agency must provide for periodic evaluation of any 
estimates used. To provide for the periodic evaluation of the estimate 
of PCT as required by FFDCA section 408(b)(2)(F), EPA may require 
registrants to submit data on PCT.
    In most cases, EPA uses available data from United States 
Department of Agriculture/National Agricultural Statistics Service 
(USDA/NASS), proprietary market surveys, and the National Pesticide Use 
Database for the chemical/crop combination for the most recent 6-7 
years. EPA uses an average PCT for chronic dietary risk analysis. The 
average PCT figure for each existing use is derived by combining 
available public and private market survey data for that use, averaging 
across all observations, and rounding to the nearest 5%, except for 
those situations in which the average PCT is less than one. In those 
cases, 1% is used as the average PCT and 2.5% is used as the maximum 
PCT. EPA uses a maximum PCT for acute dietary risk analysis. The 
maximum PCT figure is the highest observed maximum value reported 
within the recent 6 years of available public and private market survey 
data for the existing use and rounded up to the nearest multiple of 5%.
    The Agency estimated the PCT for proposed uses of etofenprox as a 
mosquito adulticide which may result in residues on food and feed 
commodities. The PCT estimates are for 35 agricultural crops which may 
be exposed to mosquito adulticide applications of etofenprox. The 
agricultural crops included in the analysis are apples, pears, oranges, 
rice, field com, wheat, and 29 crops grown predominantly in California. 
The EPA relied on national and state level usage data for the most 
widely used mosquito insecticides to develop percent crop treated 
estimates for new uses. The general approach to estimating PCT was to 
assume that all etofenprox mosquito adulticide applications will be 
made randomly across the landscape without regard to land use patterns. 
Except for area wide vector control programs, this approach is highly 
conservative in that mosquito adulticide applications are generally 
made to populated urban and suburban areas. However, because of the 
inherent drift of mosquito adulticides into non-target areas, it is 
realistic to assume that some residues of etofenprox may be found on 
agricultural crops in the urban-agricultural interface. Using this 
approach, PCT estimates including residues on rice, which is a 
registered use, are as follows:
    Apples: 1%; almonds: 5%; apricots: 5%; artichokes: 5%; avocados: 
5%; broccoli: 5%; Brussels sprouts: 5%; carrots: 5%; cauliflower: 5%; 
celery: 5%; chicory: 5%; dates: 5%; field corn: 1%; figs: 5%; garlic: 
5%; grapes: 5%; honeydew melon: 5%; kiwifruit: 5%; lemons: 5%; 
nectarines: 5%; olives: 5%; oranges: 15%; pears: 1%; persimmons: 5%; 
pistachios: 5%; plums: 5%; pluots: 5%; pomegranates: 5%; prunes: 5%; 
raisins: 5%; rice: 3%; tomatoes: 5%; walnuts: 5%; wheat: 1%; all other 
crops: (including livestock commodities, milk, and eggs) 3%.
    The Agency used the market leader approach to develop upper bound 
percent crop treated estimates for this new use. Under the market 
leader approach, this upper bound is estimated as the percent of the 
crop treated by the most widely used pesticide for the new use. The 
EPA's usual application of the market leader approach for deriving PCT 
traditionally focuses on broad categories of pesticides (e.g., 
insecticides, fungicides, or herbicides) applied directly to crops for 
control of agricultural pests. In this case, however, EPA determined 
that this would not be appropriate because mosquito adulticides fill a 
unique niche in the pesticide marketplace. The amount of general 
insecticide use on crops has no rational relationship to the amount of 
mosquito adulticide use. Instead of using the insecticides applied 
directly on these crops, EPA chose the most widely used mosquito 
adulticide in the states/regions that the crop is grown in. For 
occasional area wide vector control programs for West Nile Virus (WNV) 
or Vector-borne encephalitis (Western Equine Encephalitis, Eastern 
Equine Encephalitis, or St. Louis Encephalitis) this approach provides 
an accurate estimate of the PCT for agricultural crops.
    These estimates represent the upper bound of use expected during 
the pesticide's initial five years of registration; that is, PCT for 
etofenprox is a threshold of use that EPA is reasonably certain will 
not be exceeded

[[Page 70874]]

for each registered use site. The PCT recommended for use in the 
chronic dietary assessment is calculated as the average PCT of the 
market leader or leaders, (i.e., the one(s) with the greatest PCT) on 
that site over the three most recent years of available data. The 
comparisons are only made among pesticides of the same pesticide type 
(e.g., the market leader for insecticides on the use site is selected 
for comparison with a new insecticide). The market leader included in 
the estimation may not be the same for each year since different 
pesticides may dominate at different times. Typically, EPA uses USDA 
National Agricultural Statistics Service (NASS) as the source of data 
because it is publicly available and directly reports values for PCT. 
When a specific use site is not reported by USDA/NASS, EPA uses 
proprietary data and calculates the PCT given reported data on acres 
treated and acres grown. If no data are available, EPA may extrapolate 
PCT from other crops (proxies), if the crop management and pest 
spectrum are substantially similar. A retrospective analysis to 
validate this approach shows few cases where the PCT for the market 
leaders were exceeded. Further review of these cases identified factors 
contributing to the exceptionally high use of a new pesticide. Given 
the results of this review, to evaluate whether the PCT for etofenprox 
could be exceeded, EPA considered whether there may be unusually high 
mosquito pressure or disease transmission potential; whether the market 
leaders are well established for that use; and whether pest resistance 
issues with past market leaders provide etofenprox with significant 
market potential. Given currently available information, EPA concludes 
it is unlikely that actual PCT for etofenprox will exceed the estimated 
PCT for new uses during the next five years.
    Specific information on the methodology to estimate PCT can be 
found at http://www.regulations.gov in the document titled ``BEAD 
Estimate of the Percent Crop Treated for New Use (PCTn) of Etofenprox 
when used as a Mosquito Adulticide in Agricultural Areas'' docket ID 
number EPA-HQ-OPP-2011-0905.
    The Agency believes that the three conditions discussed in Unit 
III.C.1.iv. have been met. With respect to Condition a, PCT estimates 
are derived from Federal and private market survey data, which are 
reliable and have a valid basis. The Agency is reasonably certain that 
the percentage of the food treated is not likely to be an 
underestimation. As to Conditions b and c, regional consumption 
information and consumption information for significant subpopulations 
is taken into account through EPA's computer-based model for evaluating 
the exposure of significant subpopulations including several regional 
groups. Use of this consumption information in EPA's risk assessment 
process ensures that EPA's exposure estimate does not understate 
exposure for any significant subpopulation group and allows the Agency 
to be reasonably certain that no regional population is exposed to 
residue levels higher than those estimated by the Agency. Other than 
the data available through national food consumption surveys, EPA does 
not have available reliable information on the regional consumption of 
food to which etofenprox may be applied in a particular area.
    2. Dietary exposure from drinking water. The Agency used screening 
level water exposure models in the dietary exposure analysis and risk 
assessment for etofenprox in drinking water. These simulation models 
take into account data on the physical, chemical, and fate/transport 
characteristics of etofenprox. Further information regarding EPA 
drinking water models used in pesticide exposure assessment can be 
found at http://www.epa.gov/oppefed1/models/water/index.htm.
    Based on the Tier 1 Rice Model and Screening Concentration in 
Ground Water (SCI-GROW) models, the estimated drinking water 
concentrations (EDWCs) of etofenprox for chronic exposures are 
estimated to be 1.2 ppb for surface water and 3.0 x 10-3 ppb 
for ground water.
    Modeled estimates of drinking water concentrations were directly 
entered into the dietary exposure model. For chronic dietary risk 
assessment, the water concentration of value 1.2 ppb was used to assess 
the contribution to drinking water.
    3. From non-dietary exposure. The term ``residential exposure'' is 
used in this document to refer to non-occupational, non-dietary 
exposure (e.g., for lawn and garden pest control, indoor pest control, 
termiticides, and flea and tick control on pets). Etofenprox is 
currently registered for the following uses that could result in 
residential exposures: Cat and dog spot-on treatments, as a bed bug 
treatment, as indoor space and crack and crevice sprays, and as indoor 
and outdoor foggers. EPA assessed residential exposure using the 
following assumptions: Adults can potentially be exposed to etofenprox 
residues during residential application of etofenprox, including indoor 
surface-directed and aerosol space spray and outdoor fogger use. 
Handler exposure is expected to be short-term in duration and because 
there was no adverse dermal effect identified for etofenprox, risk was 
assessed only for exposure via the inhalation route. There is also 
potential for post-application exposure for individuals as a result of 
being in an environment that has been previously treated with 
etofenprox. Because of the registered indoor uses, intermediate-term 
post application exposures are possible. However, since the short- and 
intermediate-term endpoints and PODs for inhalation and oral routes are 
the same, the short-term exposure and risk estimates are considered to 
be protective of potential intermediate-term exposure and risk. Because 
adverse dermal toxicity effects were not identified for etofenprox, 
only short- and intermediate-term post-application inhalation exposures 
were assessed for adults and short- and intermediate-term post-
application inhalation and incidental oral exposures were assessed for 
children. Additionally, long-term post-application incidental oral 
exposure to children from petting treated cats or dogs was also 
assessed.
    The worst-case residential short-term exposure for adults is from 
post-application inhalation exposure from treatment of flying insects. 
The worst-case residential short-term exposure for children 1 to 2 
years old is from combined inhalation and oral hand-to-mouth post-
application exposures from treatment of flying insects. EPA typically 
combines exposures for treatments to control the same pests (e.g. flea 
treatment on surfaces and on pets) because such treatments could 
reasonably be expected to occur on the same day. But a similar 
presumption is not generally followed for exposures for treatments to 
control different pests. For etofenprox, EPA has not combined short-
term exposures from use of etofenprox to control flying insects and its 
use to control fleas, ticks, and bed bugs. Several factors support this 
approach for etofenprox. First, EPA's manner of estimating short-term 
residential exposures is very conservative. When assessing individual 
short-term residential post-application exposure scenarios, EPA assumes 
exposure occurs at the level of zero-day residues (i.e., day of 
application residues) on each day of the short-term exposure period (1-
30 days), instead of incorporating information on residue decline 
values. EPA also assumes that an individual performs the same post-
application activities, intended to represent high-end exposures as 
described in the Residential SOPs, for

[[Page 70875]]

the same amount of time every day over the short-term exposure period, 
rather than averaging post-application activity levels and exposures 
over that period. Second, these exposure estimates are then compared to 
points of departure that are typically based on weeks of dosing in test 
animals. Longer exposure periods generally produce lower points of 
departure. For etofenprox, the short-term risk assessment is 
particularly conservative because the point of departure for the short-
term (1 to 30-days) risk assessment is based on a toxicity study 
involving continuous exposure over 90 days. Third, usage survey data 
indicate that concurrent use of separate pesticide products that 
contain the same active ingredient to treat the same or different pests 
does not typically occur. Combining conservative exposure estimates 
with a conservative point of departure for an event that is itself 
improbable (co-occurrence of use of the same pesticide to control 
different pests) would unrealistically overstate exposure.
    Further information regarding EPA standard assumptions and generic 
inputs for residential exposures may be found at http://www.epa.gov/pesticides/trac/science/trac6a05.pdf.
    4. Cumulative effects from substances with a common mechanism of 
toxicity. Section 408(b)(2)(D)(v) of FFDCA requires that, when 
considering whether to establish, modify, or revoke a tolerance, the 
Agency consider ``available information'' concerning the cumulative 
effects of a particular pesticide's residues and ``other substances 
that have a common mechanism of toxicity.''
    Unlike other pesticides for which EPA has followed a cumulative 
risk approach based on a common mechanism of toxicity, EPA has not made 
a common mechanism of toxicity finding as to etofenprox. Although 
etofenprox shares some structural characteristics with synthetic 
pyrethroids, it is not included in the pyrethroid cumulative 
assessment. Naturally occurring pyrethrins and the synthetic 
pyrethroids (collectively called `pyrethroids') are grouped for 
purposes of cumulative risk assessed based on the following shared 
characteristics:
    i. Common structure. Pyrethrins and pyrethroids share a common 
structure; acid and alcohol moieties joined through an ether linkage;
    ii. Sodium channel disruption. In vitro studies demonstrate the 
ability of pyrethroids to modify mammalian sodium channel kinetics, 
leading to alterations in membrane excitability and firing potentials;
    iii. Neurotoxic effects. Pyrethroid toxicity is manifested through 
neurological syndromes described as either T (fine tremors), CS 
(choreoathetosis and salivation), or some combination thereof, 
depending on the structure. Open literature supports a correlation 
between the modification in sodium channel kinetics and the resulting 
syndrome.
    Etofenprox is not included in the pyrethroid common mechanism 
grouping or included in the cumulative risk assessment because 
etofenprox does not exhibit these key characteristics. Etofenprox is an 
ether compound; pyrethroids are esters. Etofenprox exposure does not 
result in the neurotoxic syndromes typical of pyrethroids and no 
available data suggest the molecular target for etofenprox is the 
sodium channel.
    For the purposes of this tolerance action, therefore, EPA has not 
assumed that etofenprox has a common mechanism of toxicity with other 
pyrethroids. For information regarding EPA's efforts to determine which 
chemicals have a common mechanism of toxicity and to evaluate the 
cumulative effects of such chemicals, see the policy statements 
released by EPA's Office of Pesticide Programs concerning common 
mechanism determinations and procedures for cumulating effects from 
substances found to have a common mechanism on EPA's Web site at http://www.epa.gov/pesticides/cumulative/.

D. Safety Factor for Infants and Children

    1. In general. Section 408(b)(2)(C) of FFDCA provides that EPA 
shall apply an additional tenfold (10X) margin of safety for infants 
and children in the case of threshold effects to account for prenatal 
and postnatal toxicity and the completeness of the database on toxicity 
and exposure unless EPA determines based on reliable data that a 
different margin of safety will be safe for infants and children. This 
additional margin of safety is commonly referred to as the FQPA Safety 
Factor (SF). In applying this provision, EPA either retains the default 
value of 10X, or uses a different additional safety factor when 
reliable data available to EPA support the choice of a different 
factor.
    2. Prenatal and postnatal sensitivity. There is no indication of 
increased quantitative or qualitative susceptibility of the developing 
offspring in toxicology database for etofenprox. Developmental effects 
were seen at doses that caused maternal toxicity. No developmental 
effects were seen in the rat 1-generation/developmental study. In the 
2-generation reproduction toxicity study, toxicity in the offspring 
occurred at the level of parental toxicity (increased organs weights 
and associated pathological changes occurred in both the pups and 
parents). In the developmental neurotoxicity study in rats, the 
observed eye abnormalities associated with body injuries could not be 
disassociated from possible altered, treatment-related maternal 
behavior.
    3. Conclusion. EPA has determined that reliable data show the 
safety of infants and children would be adequately protected if the 
FQPA SF were reduced to 1x. That decision is based on the following 
findings:
    i. The toxicity database for etofenprox is complete.
    ii. An acute neurotoxicity study in the adult rat revealed no 
treatment-related effects. The subchronic neurotoxicity study in the 
rat showed decreased body weight gains, increased liver weights in all 
dose groups, and increased incidence of rearing behavior and abnormal 
gait, all in the absence of histopathological changes. The 
developmental neurotoxicity study in rats showed increased rearing 
behavior in mothers. In offspring, eye lesions (including sclera and 
lens hemorrhage), which are sometimes associated with aggressive 
maternal behavior, were observed prior to weaning at the highest dose 
tested. Effects on motor/locomotor activity and auditory startle 
response were also observed in the high-dose treatment groups on PND 
58. These latter isolated, post-ontogenic effects of treatment are not 
presumed to occur following a single dose.
    Evidence of neurotoxicity was also observed in other studies. In a 
subchronic mouse study piloerection, hunched posture, lethargy, body 
tremors, and an unsteady gait were noted in both sexes above the limit 
dose. The rat developmental study showed increased salivation in all 
treatment groups of the F0 generation and decreased (non-
statistically significant) mobility (both sexes) and rearing behavior 
(males) in the F1 generation. In the 2-generation 
reproduction study F1 pups exhibited clinical signs of body 
tremors, lethargy, unsteady gait, and abnormal movements during most of 
the lactation period at the high dose.
    However, residual concern for neurotoxicity is low based on the 
following:
    a. Signs of neurotoxicity in the database occur only at the high 
dose level in each study;
    b. The studies show clear and well-defined NOAELs;

[[Page 70876]]

    c. The signs of neurotoxicity are well-characterized in terms of 
their effects in offspring; and
    d. The PODs used for risk assessment are protective of 
neurotoxicity seen in the database.
    No systemic toxicity was observed in the 28-day dermal study in 
rabbits up to 1,000 mg/kg/day. In this study, clinical signs were 
evaluated and signs such as piloerection, hunched posture, lethargy, 
body tremors, an unsteady gait and salivation, seen in the oral 
repeated dose studies discussed in this unit, were not observed. With 
neurotoxic signs occurring only at high doses in the oral studies and a 
dermal absorption factor (DAF) of 7% for etofenprox, neurotoxic 
manifestations via the dermal route are not expected below the limit 
dose. Therefore, concern for neurotoxicity following dermal exposure is 
low.
    iii. As discussed in this unit, there is no indication of increased 
quantitative or qualitative susceptibility of the developing offspring 
in the toxicology database for etofenprox.
    iv. There are no residual uncertainties identified in the exposure 
databases. The chronic dietary exposure assessment utilizes tolerance 
residue levels for all commodities based on conservative modeled 
estimates. The residue level of 5 ppm is considered an upper bound 
estimate for both ground and aerial applications that assume the 
conservative deposition onto surrounding crops following a ULV mosquito 
adulticide application. The dietary assessment also assumes 
conservative, upper-bound PCT estimates for the proposed uses. By using 
these screening level assessments, actual exposures/risks are not 
expected to be underestimated. EPA made conservative (protective) 
assumptions in the ground and surface water modeling used to assess 
exposure to etofenprox in drinking water. EPA used similarly 
conservative assumptions to assess post-application exposure of 
children as well as incidental oral exposure of toddlers. These 
assessments will not underestimate the exposure and risks posed by 
etofenprox.

E. Aggregate Risks and Determination of Safety

    EPA determines whether acute and chronic dietary pesticide 
exposures are safe by comparing aggregate exposure estimates to the 
acute PAD (aPAD) and chronic PAD (cPAD). For linear cancer risks, EPA 
calculates the lifetime probability of acquiring cancer given the 
estimated aggregate exposure. Short-, intermediate-, and chronic-term 
risks are evaluated by comparing the estimated aggregate food, water, 
and residential exposure to the appropriate PODs to ensure that an 
adequate MOE exists.
    1. Acute risk. An acute aggregate risk assessment takes into 
account acute exposure estimates from dietary consumption of food and 
drinking water. No adverse effect resulting from a single oral exposure 
was identified and no acute dietary endpoint was selected. Therefore, 
etofenprox is not expected to pose an acute risk.
    2. Chronic risk. Using the exposure assumptions described in this 
unit for chronic exposure, EPA has concluded that chronic exposure to 
etofenprox from food and water will utilize 32% of the cPAD for 
children 1-2 years old, the population group receiving the greatest 
exposure.
    There is potential chronic/long-term exposure to etofenprox via 
dietary (which is considered background exposure) and residential 
(which is considered primary) exposure pathways for children 1 to < 2 
years old. Chronic/long-term exposure to etofenprox for adults is 
expected via the dietary (background exposure) and residential 
(primary) exposure pathways; however, there is no dermal hazard 
identified for etofenprox, incidental oral exposure is not expected for 
adults, and inhalation exposure is not expected for adults from 
treating pets; therefore, chronic/long-term risk is best represented by 
the risk from dietary exposure described in this unit.
    The aggregate long-term MOE for children 1 to < 2 years old, 
including dietary exposure (food and water) and incidental oral 
exposures from contact with treated pets is 180. Because EPA's level of 
concern for etofenprox is a MOE of 100 or below, this MOE is not of 
concern.
    3. Short- and intermediate-term risk. Short- and intermediate-term 
aggregate exposure takes into account short- and intermediate-term 
residential exposure plus chronic exposure to food and water 
(considered to be a background exposure level). Etofenprox is currently 
registered for uses that could result in short- and intermediate-term 
residential exposure, and the Agency has determined that it is 
appropriate to aggregate chronic exposure through food and water with 
short- and intermediate-term residential exposures to etofenprox.
    As noted in Unit III.C.3., because the short- and intermediate-term 
endpoints and PODs for inhalation and oral routes are the same, the 
short-term exposure and risk estimates are considered to be protective 
of potential intermediate-term exposure and risk.
    Using the exposure assumptions described in this unit for short-
term exposures, EPA has concluded the combined short-term food, water, 
and residential exposures result in aggregate MOEs of 420 for children 
1- < 2 years old, and 1,700 for adults. Because EPA's level of concern 
for etofenprox is a MOE of 100 or below, these MOEs are not of concern.
    4. Aggregate cancer risk for U.S. population. Based on the data 
summarized in Units III.A. and III.C.1.iii., EPA has concluded that 
etofenprox does not pose a cancer risk to humans.
    5. Determination of safety. Based on these risk assessments, EPA 
concludes that there is a reasonable certainty that no harm will result 
to the general population or to infants and children from aggregate 
exposure to etofenprox residues.

IV. Other Considerations

A. Analytical Enforcement Methodology

    For crop commodities, adequate enforcement methodology (liquid 
chromatography/mass spectrometry/mass spectrometry (LC/MS/MS)) is 
available to enforce the tolerance expression. For livestock 
commodities, adequate enforcement methodology (gas chromatography/mass 
spectrometry (GC/MS)) is available to enforce the tolerance expression.
    The methods may be requested from: Chief, Analytical Chemistry 
Branch, Environmental Science Center, 701 Mapes Rd., Ft. Meade, MD 
20755-5350; telephone number: (410) 305-2905; email address: 
[email protected].

B. International Residue Limits

    In making its tolerance decisions, EPA seeks to harmonize U.S. 
tolerances with international standards whenever possible, consistent 
with U.S. food safety standards and agricultural practices. EPA 
considers the international maximum residue limits (MRLs) established 
by the Codex Alimentarius Commission (Codex), as required by FFDCA 
section 408(b)(4). The Codex Alimentarius is a joint United Nations 
Food and Agriculture Organization/World Health Organization food 
standards program, and it is recognized as an international food safety 
standards-setting organization in trade agreements to which the United 
States is a party. EPA may establish a tolerance that is different from 
a Codex MRL; however, FFDCA section 408(b)(4) requires that EPA explain 
the reasons for departing from the Codex level.

[[Page 70877]]

    Codex has established etofenprox MRLs on several crop and livestock 
commodities at levels that range from 0.01-8.0 ppm. These MRLs are 
different than the tolerances established for etofenprox in the United 
States. Codex and U.S. MRLs/tolerances could not be harmonized due to 
differences in the use pattern used to derive the tolerances. Codex 
MRLs were based on field trial data from foliar and granular use of 
etofenprox to kill crop pests in agricultural fields whereas the U.S. 
tolerances were based on aerial application over crops to kill 
mosquitoes. Different application amounts, frequencies, and techniques 
are used for these different use patterns and thus harmonization with 
Codex cannot be achieved.

C. Revisions to Petitioned-For Tolerances

    The proposed tolerance at 0.5 ppm was estimated using limited field 
trial data. These data were determined to be insufficient to support 
the proposed use pattern. Subsequently, the applicant submitted 
modeling results using the Terrestrial Residue Exposure Model (TREX) 
which estimated residues following repeated ULV applications and 
concluded residues were likely to peak at 1.5 ppm following repeated 
aerial applications to agricultural crops. EPA estimated an upper-bound 
crop residue estimate of 5.0 ppm following repeated ULV aerial and 
ground applications. In addition, based on the Agency review, it was 
determined that tolerances were required on livestock commodities as 
well.

 V. Conclusion

    Therefore, tolerances are established for residues of etofenprox, 
[2-(4-ethoxyphenyl)-2-methylpropyl 3-phenoxybenzyl ether], in or on 
food commodities at 5.0 ppm; feed commodities at 5.0 ppm; eggs at 0.40 
ppm; hog fat at 4.0 ppm; hog meat at 0.20 ppm; hog, meat byproducts at 
4.0 ppm; fat of cattle, goat, horse, and sheep at 10.0 ppm; meat of 
cattle, goat, horse, and sheep at 0.40 ppm; meat byproducts of cattle, 
goat, horse, and sheep at 10.0 ppm; milk at 0.60 ppm; poultry, fat at 
1.0 ppm; poultry, meat at 0.01 ppm; and poultry, meat byproducts at 1.0 
ppm.

VI. Statutory and Executive Order Reviews

    This final rule establishes tolerances under FFDCA section 408(d) 
in response to a petition submitted to the Agency. The Office of 
Management and Budget (OMB) has exempted these types of actions from 
review under Executive Order 12866, entitled ``Regulatory Planning and 
Review'' (58 FR 51735, October 4, 1993). Because this final rule has 
been exempted from review under Executive Order 12866, this final rule 
is not subject to Executive Order 13211, entitled ``Actions Concerning 
Regulations That Significantly Affect Energy Supply, Distribution, or 
Use'' (66 FR 28355, May 22, 2001) or Executive Order 13045, entitled 
``Protection of Children from Environmental Health Risks and Safety 
Risks'' (62 FR 19885, April 23, 1997). This final rule does not contain 
any information collections subject to OMB approval under the Paperwork 
Reduction Act (PRA) (44 U.S.C. 3501 et seq.), nor does it require any 
special considerations under Executive Order 12898, entitled ``Federal 
Actions to Address Environmental Justice in Minority Populations and 
Low-Income Populations'' (59 FR 7629, February 16, 1994).
    Since tolerances and exemptions that are established on the basis 
of a petition under FFDCA section 408(d), such as the tolerance in this 
final rule, do not require the issuance of a proposed rule, the 
requirements of the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et 
seq.), do not apply.
    This final rule directly regulates growers, food processors, food 
handlers, and food retailers, not States or tribes, nor does this 
action alter the relationships or distribution of power and 
responsibilities established by Congress in the preemption provisions 
of FFDCA section 408(n)(4). As such, the Agency has determined that 
this action will not have a substantial direct effect on States or 
tribal governments, on the relationship between the national government 
and the States or tribal governments, or on the distribution of power 
and responsibilities among the various levels of government or between 
the Federal Government and Indian tribes. Thus, the Agency has 
determined that Executive Order 13132, entitled ``Federalism'' (64 FR 
43255, August 10, 1999) and Executive Order 13175, entitled 
``Consultation and Coordination with Indian Tribal Governments'' (65 FR 
67249, November 9, 2000) do not apply to this final rule. In addition, 
this final rule does not impose any enforceable duty or contain any 
unfunded mandate as described under Title II of the Unfunded Mandates 
Reform Act of 1995 (UMRA) (2 U.S.C. 1501 et seq.).
    This action does not involve any technical standards that would 
require Agency consideration of voluntary consensus standards pursuant 
to section 12(d) of the National Technology Transfer and Advancement 
Act of 1995 (NTTAA) (15 U.S.C. 272 note).

VII. Congressional Review Act

    Pursuant to the Congressional Review Act (5 U.S.C. 801 et seq.), 
EPA will submit a report containing this rule 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. This action is not a ``major rule'' 
as defined by 5 U.S.C. 804(2).

List of Subjects in 40 CFR Part 180

    Environmental protection, Administrative practice and procedure, 
Agricultural commodities, Pesticides and pests, Reporting and 
recordkeeping requirements.

    Dated: November 13, 2013.
G. Jeffrey Herndon,
Acting Director, Registration Division, Office of Pesticide Programs.
    Therefore, 40 CFR chapter I is amended as follows:

PART 180--[AMENDED]

0
1. The authority citation for part 180 continues to read as follows:

    Authority:  21 U.S.C. 321(q), 346a and 371.

0
2. In Sec.  180.620, revise the table in paragraph (a) to read as 
follows:


Sec.  180.620  Etofenprox; tolerances for residues.

    (a) * * *

------------------------------------------------------------------------
                                                              Parts per
                         Commodity                             million
------------------------------------------------------------------------
Cattle, fat...............................................         10.0
Cattle, meat..............................................          0.40
Cattle, meat byproducts...................................         10.0
Egg.......................................................          0.40
All food commodities (including feed commodities) not               5.0
 otherwise listed in this subsection......................
Goat, fat.................................................         10.0
Goat, meat................................................          0.40
Goat, meat byproducts.....................................         10.0
Hog, fat..................................................          4.0
Hog, meat.................................................          0.20
Hog, meat byproducts......................................          4.0
Horse, fat................................................         10.0
Horse, meat...............................................          0.40
Horse, meat byproducts....................................         10.0
Milk......................................................          0.60
Poultry, fat..............................................          1.0
Poultry, meat.............................................          0.01
Poultry, meat byproducts..................................          1.0
Rice, grain...............................................          0.01
Sheep, fat................................................         10.0
Sheep, meat...............................................          0.40
Sheep, meat byproducts....................................         10.0
------------------------------------------------------------------------

* * * * *
[FR Doc. 2013-28517 Filed 11-26-13; 8:45 am]
BILLING CODE 6560-50-P