[Federal Register Volume 79, Number 88 (Wednesday, May 7, 2014)]
[Rules and Regulations]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2014-10214]
ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 180
Fenoxaprop-ethyl; Pesticide Tolerances
AGENCY: Environmental Protection Agency (EPA).
ACTION: Final rule.
SUMMARY: This regulation establishes a tolerance for residues of
fenoxaprop-ethyl (FE), in or on grass hay. Interregional Research
Project Number 4 (IR-4) requested this tolerance under the Federal
Food, Drug, and Cosmetic Act (FFDCA).
DATES: This regulation is effective May 7, 2014. Objections and
requests for hearings must be received on or before July 7, 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-2012-0588, 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].
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-2012-0588 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
July 7, 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-2012-0588, 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
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.
II. Summary of Petitioned-For Tolerance
In the Federal Register of September 28, 2012 (77 FR 59578) (FRL-
9364-6), 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
2E8051) by IR-4, 500 College Road East, Suite 201W., Princeton, NJ
08540. The petition requested that 40 CFR 180.430 be amended by
establishing tolerances for residues of the herbicide fenoxaprop-ethyl,
[()-ethyl 2-[4- [(6-chloro-2-
benzoxazolyl)oxy]phenoxy]propanoate] and its metabolites 2-[4-[(6:-
chloro-2-benzoxazolyl) oxy]phenoxy] propanoic acid and 6-chloro-2,3-
dihydrobenzoxazol-2-one, each expressed as the parent compound, in or
on grass, hay at 0.15 part per million (ppm). Based on the regional
residue data submitted from Washington and Oregon, and the petitioner's
intent for this to be a regional pesticide tolerance, the tolerance is
being established as a ``Tolerance with regional registration'' with
use restricted to Oregon, Washington, and Utah. That document
referenced a summary of the petition prepared by Bayer CropScience, the
registrant, which is available in the docket, http://www.regulations.gov.
Comments were received on the notice of filing. EPA response to
those comments is discussed in Unit IV.C.
Based upon review of the data supporting the petition, EPA has
modified the level at which the tolerance is being established. The
reason for this change is explained in Unit IV.D.
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 fenoxaprop-p-ethyl (FPE)
including exposure resulting from the tolerances established by this
action. EPA's assessment of exposures and risks associated with FPE
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
FPE is an enriched isomer formulation (95% d and 5% l enantiomers)
based on the previously registered product FE which is a 50:50 racemic
mixture of d and l enantiomers. FE is no longer a registered active
ingredient. The toxicology database for FPE is complete based on
studies submitted for both FPE and FE. Based on the analysis of the
submitted studies, EPA found that the toxicological effects of FE and
FPE across species, duration, and route of exposure are similar. Most
of the toxicological data available involved testing of the FE, not
FPE. However, EPA has concluded that the similarity between the FE and
FPE data is such that the database for FE could be bridged with FPE.
The major target organs following short-term and long-term oral
administration of FE and FPE in rats and mice are the liver and
kidneys, with rats being the most sensitive species. The primary toxic
effect is altered lipid metabolism characterized by decreased lipids
and cholesterol, and increased liver weights in rats, and slightly
increased lipids, cholesterol, proteins, and liver weights in mice.
Additionally, increased enzyme activity (aspartate amino transferase
(ASAT), alanine amino transferase (ALAT), and alkaline phosphatase
(ALP)), hypertrophy, and single cell necrosis were observed in mice. In
the kidneys, increases in ketones and kidney weights were observed in
rats and evidence of proximal renal tubular injury were observed in
mice following 90-day administration of FPE. However, no effects on the
kidneys were observed following chronic administration of FE to rats,
mice, or dogs. In both species, males were slightly more sensitive to
the liver effects of FE and FPE. It is also important to note that no
increases in toxicity are observed over time for FE when comparing the
28-day and 90-day subchronic studies, the 2-generation reproductive
toxicity study, and the 2-year chronic toxicity/carcinogenicity study
in rats, or in FPE when comparing the 28-day and 90-day subchronic
toxicity studies in rats.
FPE has low acute toxicity following the oral, dermal, and
inhalation routes of exposure. No evidence of immunotoxicity,
reproductive or neurological toxicity was identified in the database.
Developmental toxicity occurred in rats as evidenced by skeletal
anomalies (longitudinally displaced, fragmented, fused, dysplastic
sternebrae or dislocated sternebrae) and skeletal retardations (weak or
non-ossification of one or several cranial bones). Developmental
effects only occurred in the rat in the presence of maternal toxicity
(decreased body weight, body weight gain, and heart weight). No
developmental effects were identified in rabbits. In mice, a treatment-
related increase in tumor incidence of hepatocellular adenomas and
carcinomas, mainly adenomas, was observed in males at 320 ppm (30%)
compared to the control (2%). In addition, microscopic pathology
indicated that hepatocellular hypertrophy was observed in the majority
of treated animals (both sexes). There was, however, no evidence of a
mutagenic effect in a comprehensive battery of genetic toxicology
assays with both isomers. No evidence of tumors was identified in rats.
The only tumor response induced by FE/FPE occurred in the liver of
male mice; no liver tumors were seen in the female mice or in the
guideline chronic/carcinogenicity study in male and female rats. The
tumors were benign with no progression to malignancy. Mutagenicity has
been ruled out as a mode of action (MOA) for this response. The
presence of a single non-mutagenic tumor type in one sex and species--
here, benign liver tumors in the male mouse, a common tumor in mice--
provides no more than a weak suggestion of possible carcinogenic
effects and thus does not support a linear assessment of risk based on
the tumor incidence. Given the doses at which the benign mouse tumors
were seen, EPA concludes that the chronic reference dose (cRfD) for FPE
will adequately protect for all chronic toxicity, including
carcinogenicity, that could result from exposure to FE/FPE.
The Agency has waived the requirements for acute and subchronic
neurotoxicity studies based on the following rationale:
1. The lack of neurotoxicity in the available toxicology database
for FE and FPE.
2. The target organs of FPE and FE are the kidney and liver, and
the mechanism of action for FPE and the chemical class do not target
the nervous system.
3. Developmental effects and decreased total blood lipids/
cholesterol are the most sensitive effects seen in the FE database and
provide the most sensitive POD for risk assessment.
4. There is low concern for neurotoxicity in other members of this
class of chemicals (i.e., the arloxy phenoxy-propionate class).
Specific information on the studies received and the nature of the
adverse effects caused by FPE 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 titled ``Fenoxaprop-p-ethyl.
Registration Review Preliminary Risk Assessment and Proposed New Use on
Grass Grown for Seed'' on pages 52-57 in docket ID number EPA-HQ-OPP-
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 (LOC) 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 FPE used for human
risk assessment is shown in Table 1 of this unit.
Table 1--Summary of Toxicological Doses and Endpoints for FPE for Use in Human Health Risk Assessment
POD and uncertainty/ RfD, PAD, LOC for
Exposure/scenario safety factors risk assessment Study and toxicological effects
Acute dietary (general population No appropriate endpoint attributable to a single dose was identified. An
including infants and children acute RfD was not established.
and females 13-50 years of age).
Chronic dietary (all populations) NOAEL = 1.5 mg/kg/ Chronic RfD = 0.015 Chronic toxicity/carcinogenicity
day. mg/kg/day. (rat) 2-generation reproductive
UFA = 10x........... cPAD = 0.015 mg/kg/ toxicity (rat).
UFH = 10x........... day. LOAEL = 9 mg/kg/day, based on
FQPA SF = 1x........ decreased serum lipids and
cholesterol, and altered liver
Incidental oral short-term....... NOAEL = 6 mg/kg/day. LOC for MOE = 100.. 28-day oral toxicity (rat).
(1 to 30 days)................... UFA = 10x........... LOAEL = 26 mg/kg/day, based on
UFH = 10x........... altered lipid metabolism
FQPA SF = 1x........ (decreased HDL-cholesterol, HDL-
phospholipids, and total lipids,
increased triglycerides, and
ketonuria) and increased liver
and kidney weights.
Dermal short-term (1 to 30 days) Dermal study NOAEL = LOC for MOE = 100.. 28-day dermal toxicity (rat).
and intermediate-term (1 to 6 20 mg/kg/day. LOAEL = 100 mg/kg/day, based on
months). UFA = 10x........... non-regenerative anemia,
UFH = 10x........... decreased serum cholesterol,
FQPA SF = 1x........ total lipids, and protein (beta 1
globulins), and increased liver
and kidney weights were observed.
remained decreased following a 15-
day recovery period.
Inhalation short-term (1-30 days) Inhalation study. LOC for MOE = 30... 21-day inhalation toxicity (rat).
and intermediate-term (1-6 NOAEL = 0.07 mg/L LOAEL = 0.3 mg/L (males only)
months). (males) 0.3 mg/L Based on slight normocytic
(females). anemia, decreases in serum
UFA = 3x............ cholesterol and total lipids, and
UFH = 10x........... increases in liver weight and
FQPA SF = 1x........ urea nitrogen.
Cancer (oral, dermal, inhalation) Quantification of risk using a non-linear approach; i.e., RfD, for FPE will
adequately account for all chronic toxicity, including carcinogenicity, that
could result from exposure to FPE.
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 FPE, EPA considered exposure under the petitioned-for
tolerances as well as all existing FE tolerances in 40 CFR 180.430. EPA
assessed dietary exposures from FPE and FE 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
FPE; therefore, a quantitative acute dietary exposure assessment is
ii. Chronic exposure. In conducting the chronic dietary exposure
assessment EPA used the food consumption data from the United States
Department of Agriculture's (USDA's) National Health and Nutrition
Examination Survey, What We Eat in America, (NHANES/WWEIA). As to
residue levels in food, EPA use an unrefined analysis based on
tolerance-level residues, 100 percent crop treated (PCT) assumptions,
and Dietary Exposure Evaluation Model (DEEM) default processing
iii. Cancer. Based on the data summarized in Unit III.A., EPA has
concluded that a nonlinear RfD approach is appropriate for assessing
cancer risk to FPE. Cancer risk was assessed using the same exposure
estimates as discussed in Unit III.C.1.ii.
iv. Anticipated residue and PCT information. EPA did not use
anticipated residue or PCT information in the dietary assessment for
FPE or FE. Tolerance level residues and 100 PCT were assumed for all
2. Dietary exposure from drinking water. The Agency has identified
FPE and its three degradates, fenoxaprop-p acid ((D+)-2-[4-(6-chloro-2-
benzoxazolyloxy) phenoxy] propanoate, AE F088406), chlorobenzoxazolone
(4-(6-chloro-2-benzoxazolyloxy) phenol, AE F054014), and 4-(6-chloro-2-
benzoxazolyloxy) phenol (AE F040356), as residues of concern in
drinking water. The parent plus the three degradates were assessed
using a total toxic residue (TTR) approach.
The Agency used screening level water exposure models in the
dietary exposure analysis and risk assessment for FPE and its three
degradates in drinking water. These simulation models take into account
data on the physical, chemical, and fate/transport characteristics of
FPE and its three degradates. 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 Pesticide Root Zone Model Ground
Water (PRZM GW), the estimated drinking water concentrations (EDWCs) of
FPE and its degradates (TTR) for
chronic exposure assessments are estimated to be 68.6 parts per billion
(ppb) for surface water and 0.032 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 68.6 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). FPE is currently
registered for the following uses that could result in residential
exposures: Residential turf and home garden. EPA assessed residential
exposure using the following assumptions: For residential handlers,
both short-term dermal and short-term inhalation exposure is expected
as a result of applying FPE to ornamentals and turf.
There is the potential for short-term dermal and incidental short-
term oral post-application exposure for individuals exposed as a result
of being in an environment that has been previously treated with FPE.
The quantitative exposure/risk assessment for residential post-
application exposures is based on the following scenarios:
Adults High Contact Lawn Activities
Children 1 to <2 years old High Contact Lawn Activities
Adults Mowing Turf
Children 11 to <16 years old Mowing Turf
Adults Ornamental Garden Activities
Children 6 to <11 years old Ornamental Garden Activities
The most conservative residential exposure scenario for adults
reflects dermal exposure from post-application exposure to turf and
gardens. The most conservative residential exposure for children
reflects dermal and hand-to-mouth exposures from post-application high
contact lawn activity exposure from turf applications.
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.''
EPA has not found FPE to share a common mechanism of toxicity with
any other substances, and FPE does not appear to produce a toxic
metabolite produced by other substances. For the purposes of this
tolerance action, therefore, EPA has assumed that FPE does not have a
common mechanism of toxicity with other substances. 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 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
2. Prenatal and postnatal sensitivity. The available data do not
provide evidence of any increased susceptibility in the offspring in
either of the two developmental toxicity studies for FPE or in the 2-
generation reproduction study for FE. Delayed ossification was the
primary effect in the developmental toxicity study and only occurred in
the presence of maternal toxicity and a clearly defined NOAEL and LOAEL
In the rat developmental toxicity study with FPE, longitudinally
displaced, fragmented, fused, dysplastic sternebrae or dislocated
sternebrae and weak or non-ossification of one or several cranial bones
were noted at 100 mg/kg (highest dose tested). These incidences
occurred only in the presence of maternal toxicity (decreased
gestational body weights, body weight gains, and food consumption). No
developmental effects occurred in rabbits. In the 2-generation rat
reproductive toxicity study on FE, no reproductive or developmental
effects were observed. An increase in ALP activity and liver weights
were identified in the offspring at 9.0 mg/kg. These effects occurred
in the presence of parental toxicity (increased liver weight and
decreased lipids) and are consistent with hepatotoxicity, the primary
toxic effect of FPE, observed across the database.
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
i. The toxicity database for FPE is complete.
ii. There is no indication that FPE is a neurotoxic chemical and
there is no need for a developmental neurotoxicity study or additional
UFs to account for neurotoxicity.
iii. There is no evidence that FPE results in increased
susceptibility in in utero rats or rabbits in the prenatal
developmental studies or in young rats in the 2-generation reproduction
iv. There are no residual uncertainties identified in the exposure
databases. The dietary food exposure assessments were performed based
on 100 PCT and tolerance-level residues. EPA made conservative
(protective) assumptions in the ground and surface water modeling used
to assess exposure to FPE 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 FPE.
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,
FPE is not expected to pose an acute risk.
2. Chronic risk. Using the exposure assumptions described in this
chronic exposure, EPA has concluded that chronic exposure to FPE and FE
from food and water will utilize 28% of the cPAD for all infants less
than 1 year old, the population group receiving the greatest exposure.
Based on the explanation in Unit III.C.3., regarding residential use
patterns, chronic residential exposure to residues of FPE is not
3. Short-term risk. Short-term aggregate exposure takes into
account short-term residential exposure plus chronic exposure to food
and water (considered to be a background exposure level).
FPE is currently registered for uses that could result in short-
term residential exposure, and the Agency has determined that it is
appropriate to aggregate chronic exposure through food and water with
short-term residential exposures to FPE.
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 worst case MOEs of 249
for adults and 302 for children. Because EPA's level of concern for FPE
is a MOE of 100 or below, these MOEs are not of concern.
4. Intermediate-term risk. Intermediate-term aggregate exposure
takes into account intermediate-term residential exposure plus chronic
exposure to food and water (considered to be a background exposure
An intermediate-term adverse effect was identified; however, FPE is
not registered for any use patterns that would result in intermediate-
term residential exposure. Intermediate-term risk is assessed based on
intermediate-term residential exposure plus chronic dietary exposure.
Because there is no intermediate-term residential exposure and chronic
dietary exposure has already been assessed under the appropriately
protective cPAD (which is at least as protective as the POD used to
assess intermediate-term risk), no further assessment of intermediate-
term risk is necessary, and EPA relies on the chronic dietary risk
assessment for evaluating intermediate-term risk for FPE.
5. Aggregate cancer risk for U.S. population. EPA considers the
chronic aggregate risk assessment to be protective of any aggregate
6. 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 FPE and FE residues.
IV. Other Considerations
A. Analytical Enforcement Methodology
Adequate enforcement methodology (gas chromatography with electron
capture detection (GD-ECD) method, based on Hoechst HRAV Analytical
Method HRAV-4B) is available to enforce the tolerance expression.
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.
The Codex has not established a MRL for FPE in or on grass hay.
C. Response to Comments
Two comments that were received were not related to FPE and
therefore, do not need to be addressed here. A third comment was
received stating that FPE is an endocrine disruptor and America does
not need any more of those. In the available toxicity studies on FPE,
there was no estrogen, androgen, and/or thyroid mediated toxicity. The
Agency currently has no evidence that FPE is an endocrine disruptor.
D. Revisions to Petitioned-For Tolerances
EPA has modified the tolerance from the proposed level of 0.15 ppm
to 0.09 ppm for the following reason: The method used for data-
collection (as well as tolerance enforcement) converts the residues of
concern for FPE to acyl 6-chlorobenzoxazolone for detection. It is
necessary to then convert this residue value to parent equivalents.
Since the residues found on grass, hay were less than the limit of
quantitation (LOQ) of 0.05 ppm for acyl 6-chlorobenzoxazolone, EPA
multiplied this 0.05 ppm value by the ratio of the molecular weights
(1.71) to arrive at a recommended tolerance of 0.09 ppm.
Therefore, a tolerance with regional registration is established
for residues of fenoxaprop-ethyl, [()-ethyl 2-[4- [(6-
chloro-2-benzoxazolyl)oxy]phenoxy]propanoate] and its metabolites 2-[4-
[(6:-chloro-2-benzoxazolyl) oxy]phenoxy] propanoic acid and 6-chloro-
2,3-dihydrobenzoxazol-2-one, each expressed as the parent compound, in
or on grass, hay at 0.09 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
Dated: April 29, 2014.
Director, Registration Division, Office of Pesticide Programs.
Therefore, 40 CFR chapter I is amended as follows:
1. The authority citation for part 180 continues to read as follows:
Authority: 21 U.S.C. 321(q), 346a and 371.
2. In Sec. 180.430, revise paragraph (c) to read as follows:
Sec. 180.430 Fenoxaprop-ethyl; tolerances for residues.
* * * * *
(c) Tolerances with regional registrations. Tolerances with
regional registration, as defined in Sec. 180.1(l), are established
for residues of the herbicide fenoxaprop-ethyl, including its
metabolites and degradates, in or on the commodities in the table in
this paragraph when fenoxaprop-ethyl is used in the states of Oregon,
Washington, and Utah. Compliance with the tolerance levels specified in
this paragraph is to be determined by measuring only the sum of
fenoxaprop-ethyl, ()-ethyl 2-[4-[(6-chloro-2-
benzoxazolyl)oxy]phenoxy]propanoate, and its metabolites, 2-[4-[(6-
chloro-2-benzoxazolyl)oxy]phenoxy]propanoic acid and 6-chloro-2,3-
dihydrobenzoxazol-2-one, calculated as the stoichiometric equivalent of
fenoxaprop-ethyl, in or on the commodity
Grass, hay.............................................. 0.09
* * * * *
[FR Doc. 2014-10214 Filed 5-6-14; 8:45 am]
BILLING CODE 6560-50-P