by establishing a tolerance for residues of Sulfentrazone
(N-[2,4-dichloro-5-[4-(difluoromethyl)-4,5-dihydro-3-methyl-5-oxo-1H-1,2
,4-triazol-1-yl]phenyl]-methanesulfonamide) and its metabolites
3-hydroxymethyl-sulfentrazone(N-[2,4-dichloro-5-[4-(difluoromethyl)-4,5-
dihydro-3-hydroxymethyl-5-oxo-1H-1,2,4-triazol-1-yl]phenyl]methanesulfon
amide) and 3-desmethyl

sulfentrazone(N-[2,4-dichloro-5-[4-(difluoromethyl)-4,5-dihydro-5-oxo-1H
-1,2,4-triazol-1-yl]phenyl]methanesulfonamide)] in or on the raw
agricultural commodity [Citrus Fruit Crop Group 10-10; Berry and Small
Fruit Crop Group 13-07; Tree Nut Crop Group 14 and Pistachio at 0.15
parts per million (ppm); Crop Group 18 Non-grass animal feed (forage,
fodder, straw and hay) : alfalfa, forage at 5 ppm; alfalfa, hay at 20
ppm; alfalfa, seed at 3 ppm; clover, forage at 5 ppm; clover, hay at 20
ppm; clover, seed at 3 ppm.  EPA has determined that the petition
contains data or information regarding the elements set forth in section
408 (d) (2) of FDDCA; however, EPA has not fully evaluated the
sufficiency of the submitted data at this time or whether the data
supports granting of the petition. Additional data may be needed before
EPA rules on the petition.

EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR PESTICIDE
PETITIONS PUBLISHED IN THE FEDERAL REGISTER

EPA Registration Division contact: Bethany Benbow<PHONE_NUMBER>

FMC Corporation, 1735 Market Street, Philadelphia, PA 19103

[1F7838]

 EPA has received a pesticide petition (1F7838) from FMC Corporation,
1735 Market Street, Philadelphia, PA 19103 proposing, pursuant to
section 408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21
U.S.C. 346a (d), to amend 40 CFR part 180.498

 A. Residue Chemistry

1. Plant metabolism. The metabolism of sulfentrazone in plants is
adequately understood for the existing and proposed tolerances. Crop
residues found after the pre-emergence and the proposed post-emergence
uses were similar in that the major metabolites were 3-hydroxymethyl
sulfentrazone and 3-desmethyl sulfentrazone. In rotational crops,
sulfentrazone is metabolized via four different pathways: (i) Oxidation
of the 3-methyl group to form 3-hydroxymethyl sulfentrazone, followed by
further oxidation to form sulfentrazone carboxylic acid which is
decarboxylated to 3-desmethyl sulfentrazone; (ii) hydrolysis of the
trifluoromethyl group to form desdifluoromethyl sulfentrazone which is
oxidized and decarboxylated to form desdifluoromethyl desmethyl
sulfentrazone; (iii) hydrolysis of the sulfonamide group to form
desmethylsulfonyl sulfentrazone; and (iv) scission of the phenyl and
triazole rings to produce methyl triazole. The corresponding phenyl
metabolites are believed to remain bound. EPA determined that tolerances
based on the parent and 3-hydroxymethyl sulfentrazone are therefore
appropriate.

2. Analytical method. There is a practical analytical method for
detecting and measuring levels of sulfentrazone and its metabolites in
or on food with a limit of quantitation that allows monitoring of food
with residues at or above the levels set or proposed in the tolerances.
The analytical enforcement method for sulfentrazone was used with minor
modification that eliminated several clean-up and derivatization steps
that was required for GC/MSD but not for LC/MS/MS.  The analytical
method for sulfentrazone involves separate analyses for parent and its
metabolites.  The parent is analyzed by evaporation and reconstitution
of the sample prior to analysis by LC/MS/MS GC/ECD.  The metabolites
samples were refluxed in the presence of acid and cleaned up with solid
phase extraction prior to analysis by LC/MS/MS.

 3. Magnitude of residues. Sulfentrazone was applied at the maximum
label rates for alfalfa, clover, citrus, tree nuts, berries and small
fruit to trials in the appropriate EPA regions.  The RACs were harvested
at the appropriate growth stages. The subsequent analyses of the RACs
and processed parts determined that the residues of sulfentrazone and
its metabolites would not exceed the established and proposed
tolerances.

B. Toxicological Profile

 1. Acute toxicity. A battery of acute toxicity studies placed technical
sulfentrazone in Toxicity Categories III and IV. No evidence of
sensitization was observed following dermal application in guinea pigs.
In an acute neurotoxicity study in rats at gavage doses of 0, 750, or
2,000 mg/kg, a NOEL of 250 mg/kg and a LOEL of 750 mg/kg were based upon
increased incidences of clinical signs, Functional Observation Battery
(FOB) findings, and decreased motor activity which were reversed by day
14 post-dose. There was no evidence of neuropathology.

2. Genotoxicity. A reverse gene mutation assay (salmonella typhimurium)
yielded negative results, both with and without metabolic activation.  A
mouse lymphoma forward gene mutation assay yielded negative results with
equivocal results without activation.  A mouse micronucleus assay test
was negative following intraperitoneal injection of 340 mg/kg.

3. Reproductive and developmental toxicity. [A prenatal oral
developmental toxicity study in the rat with dose levels at 25.0 or 50.0
mg/kg/day established a maternal NOEL of 25 mg/kg/day based on decreased
body weight gain, increased spleen weight, and microscopic changes in
the spleen, and a fetal NOEL of 10 mg/kg/day was based on fetal death,
reduced body weights, and alterations in skeletal development at higher
doses.  A supplemental oral developmental toxicity study conducted in
rats at oral dose levels of 25.0 and 50.0 mg/kg/day to test for cardiac
effects at the request of the EPA, did not reveal any significant
effects on fetal cardiac development. The results of this study
confirmed the maternal and fetal findings of the previously conducted
developmental study on sulfentrazone in rats and did not alter the study
conclusions.

In a dermal developmental study in the rat at doses of 0, 5, 25, 50, 100
and 250 mg/kg/day, a maternal (systemic) No Observed Adverse Effect
Level (NOAEL) was established at 250 mg/kg/day. Significant
treatment-related increases in the fetal and litter incidences of
incompletely ossified lumbar vertebral arches, hypoplastic or wavy ribs,
and incompletely ossified or nonossified ischia or pubes occurred at the
high-dose (250 mg/kg/day). An additional significant increase in the
high-dose fetal incidence of variations in the sternebrae (incompletely
ossified or unossified) was not judged to be treatment-related. At 250
mg/kg/day, the mean numbers of thoracic vertebral and rib ossification
sites were significantly decreased, a high-dose effect of treatment with
sulfentrazone consistent with the significant treatment-related
hypoplasia observed in the skeletal evaluation of the ribs. Therefore,
the developmental (fetal) Lowest Observed Effect Level (LOEL) is 250
mg/kg/day based on decreased fetal body weight; increased incidences of
fetal variations: hypoplastic or wavy ribs, incompletely ossified lumbar
vertebral arches, and incompletely ossified ischia or pubes; and reduced
number of thoracic vertebral and rib ossification sites. The
developmental (fetal) NOEL is 100 mg/kg/day.

A developmental toxicity study in rabbits was conducted at gavage dose
levels of 0, 100, 250, or 375 mg/kg/day. Treatment-related incidences of
decreased feces and hematuria were noted at 250 mg/kg/day or greater. In
addition, at the 375 mg/kg/day dose level, five rabbits aborted.
Significant reductions in mean body weight change were observed for the
dosing period (GD 7- 19) and for the study duration (GD 0-29, both
before and after adjustment for gravid uterine weight) at the 250 and
375 mg/kg/day dose levels. Therefore, the maternal (systemic) LOEL is
250 mg/kg/day, based upon increased abortions, clinical signs (hematuria
and decreased feces), and reduced body weight gain. The maternal
(systemic) NOEL is 100 mg/kg/day. Skeletal evaluation in fetuses
revealed dose- and treatment-related findings at the 375 mg/kg/day dose
level. These included significant increases in both the fetal and litter
incidences of fused caudal vertebrae (a malformation) and of partially
fused nasal bones (a variation). In addition, at 375 mg/kg/day,
significant treatment-related reductions in ossification site averages
were observed for metacarpals and both fore- and hindpaw phalanges.
Therefore, the developmental (fetal) LOEL is 250 mg/kg/day, based upon
increased resorptions, decreased live fetuses per litter, and decreased
fetal weight. The developmental (fetal) NOEL is 100 mg/kg/day.

A two-generation reproduction study in the rat at dietary levels of 14,
33, or 46 mg/kg/day in males and 16, 40, or 56 mg/kg/day in females
established a NOEL for systemic and reproductive/developmental
parameters of 14 mg/kg/day for males and 16 mg/kg/day for females. The
LOEL for systemic and reproductive/development parameters was 33
mg/kg/day for males and 40 mg/kg/day for females. Systemic effects were
comprised of decreased body weight gains, while
reproductive/developmental effect at the LOEL included degeneration
and/or atrophy in the testes, with epididymal sperm deficits, in the
second (F1) generation males. Male fertility in the F1 generation was
reduced at higher doses; litter size, pup survival, and pup body weight
for both generations were also effected at higher doses.

A supplemental two-generation rat reproduction study was conducted at
dietary intake levels of 50, 100, 200, or 500 ppm with a NOEL for
reproductive parameters of 200 ppm. This study confirmed the
reproductive/developmental effects observed in the first two-generation
reproductive toxicity study. It was the conclusion of the RfD/Peer
Review Committee that, under the conditions of the studies reviewed,
sulfentrazone caused developmental and reproductive toxicity. The
results of these studies elicited a high level of concern by the
Committee, since the developmental toxicity studies demonstrated
embryo/fetal toxicity at treatment levels that were not maternally
toxic, and significant toxic effects were observed primarily in the
second generation animals of the reproduction study. Because these
animals had been exposed to sulfentrazone in utero, the possibility that
the observed reproductive toxicity resulted from a developmental and/or
genotoxic mechanism was suggested.

 4. Subchronic toxicity. A 90-day subchronic toxicity study was
conducted in rats, with dietary intake levels of 0, 3.3, 6.7, 19.9,
65.8, 199.3, or 534.9 mg/kg/day for males and 0, 4, 7.7, 23.1, 78.1,
230.5, or 404.3 milligrams/kilograms/day (mg/kg/day) for females
respectively. No Observed Effect Levels (NOELs) of 19.9 mg/kg/day in
males and 23.1 mg/kg/day in females were based on clinical anemia.

A 90-day subchronic feeding study was conducted in mice by dietary admix
at doses of 0, 10.3, 17.8, 60.0, 108.4, or 194.4 mg/kg/day for males and
0, 13.9, 29.0, 79.8, 143.6, or 257.0 mg/kg/day for females,
respectively. NOELs of 60 mg/kg/day (males) and 79.8 mg/kg/day (females)
were based on decreases in body weights and/or gains; decreased
erythrocytes, hemoglobin and hematocrit values; and splenic microscopic
pathology.

In a 90-day subchronic feeding study in dogs administered by dietary
admix at doses of 0, 10, 28, or 57 mg/kg/day for males and 0, 10, 28, or
73 mg/kg/day for females, a NOEL of 28 mg/kg/day was determined for both
males and females based on decreases in hemoglobin and hematocrit,
elevated alkaline phosphatase levels, increased liver weights and
microscopic liver as well as splenic changes.

A 90-day subchronic neurotoxicity study in the rat was conducted at
dietary levels of 30, 150, or 265 mg/kg/day in males, and 37, 180, or
292 mg/kg/day in females, with a NOEL of 30 mg/kg/day in males and 37
mg/kg/day in females. The LOEL was 150 mg/kg/day for males and 180
mg/kg/day for females based on increased incidences of clinical signs,
decreased body weights, body weight gains, and food consumption in
females and increased motor activity in females at week 13. There were
no neurohistopathological effects on the peripheral or central nervous
system.

 5. Chronic toxicity. A 12-month feeding study in dogs was dosed at
levels of 0.0, 24.9, or 61.2 mg/kg/day for male dogs and 0.0, 10.4,
29.6, or 61.9 mg/kg/day for female dogs in the control through high-dose
groups, respectively, with a NOEL of 24.9 mg/kg/day for males and 29.6
mg/kg/day for females based on hematology effects and microscopic liver
changes.

An 18-month feeding/carcinogenicity study in mice was conducted with
dietary intake of 0, 46.6, 93.9, 160.5, or 337.6 mg/kg/day for males and
0, 58.0, 116.9, 198.0, or 407.1 mg/kg/day for females. A NOEL of 93.9
mg/kg/day in males and 116.9 mg/kg/day in females was based on decreases
in hemoglobin and hematocrit. There were no treatment-related increases
in tumors of any kind observed at any dose level.

In a 24-month chronic feeding/oncogenicity study in rats at dietary
doses of 0, 24.3, 40.0, 82.8, or 123.5 mg/kg/day for males and 20.0,
36.4, 67.0, or 124.7 mg/kg/day for females, an overall NOEL of mg/kg/day
in males and 36.4 mg/kg/day in females was based on hematology effects
and reduced body weights. There was no evidence of an oncogenic
response.

 6. Animal metabolism. A metabolism study in rats indicated that
approximately 84 to 104% of the orally administered dose of
sulfentrazone was excreted in the urine, and that the pooled urinary
radioactivity consisted almost entirely of 3-hydroxymethyl
sulfentrazone. Pooled fecal radioactivity showed that the major
metabolite consisted of 3-hydroxymethyl-sulfentrazone (1.26 to 2.55% of
the administered dose). The proposed metabolic pathway appeared to be
conversion of the parent compound mainly to
3-hydroxymethyl-sulfentrazone (excreted in urine and feces).

 7. Metabolite toxicology. [NA]

 8.

Endocrine disruption

.

An evaluation of the potential effects on the endocrine systems of
mammals has not been determined; however, no evidence of such effects
was reported in the chronic or reproductive toxicology studies described
above. There was no observed pathology of the endocrine organs in these
studies. There is no evidence at this time that sulfentrazone causes
endocrine effects.

C. Aggregate Exposure

 1. Dietary exposure. A short-term aggregate exposure assessment was
conducted to determine the total exposure for someone who would be
exposed to sulfentrazone residues from both dietary and non-dietary
routes over a short-term period (i.e. 1-7 days).  Aggregate exposure to
sulfentrazone was evaluated for two separate products (crop herbicide
and residential lawn/turf herbicide).  Exposure from these two uses
occurred by multiple routes (dietary, dermal and incidental ingestion).
Aggregation is conducted for dietary and non-dietary residential
exposures and it is to represent reasonable conditions of exposure. The
aggregate exposure estimates for all adults, adult females and toddlers
were less than 100% of the PAD.

 i. Food. The primary source for human exposure to sulfentrazone will be
from ingestion of both raw and processed agricultural commodities from
alfalfa, clover, citrus, tree nuts, berries and small fruit.  A DRES
chronic exposure assessment was previously conducted for asparagus,
succulent lima bean, cabbage, field corn forage, field corn stover,
field corn grain, horseradish roots, dried shelled pea and bean (except
soybean) subgroup 6C, peanut, peanut meal, peppermint tops, potato,
spearmint tops, sugarcane, sugarcane molasses and sunflower seed, raw
and processed commodities and presented in the Sulfentrazone;
Establishment of Tolerances, Final Rule (FR / Vol. 68, No. 185:
55269-55280, September 24, 2003).  A Tier 3 short-term exposure analysis
has been performed to estimate the exposure for all adults, adult
females, and toddlers (3 to 4 years of age) in the U.S. population for
these raw and processed commodities.  This analysis utilized Dietary
Exposure Evaluation Model (DEEM) software; field trial data for
registered and pending crop uses; percent crop treated information; and
consumption data from the USDA Continuing Surveys of Food Intake by
Individuals (CSFIIs). Short-term dietary exposure estimates at the
99.9th percentile for all adults, adult females and toddlers were < 2%
of the PAD.  The short-term dietary exposure to sulfentrazone has been
demonstrated to be minimal.

 ii. Drinking water. Based on the FIRST and SCI-GROW models the EECs of
sulfentrazone plus its major metabolite 3-carboxylic acid for acute
exposures are estimated to be 35.8 ppb for surface water and 26 ppb for
groundwater.  The EECs for chronic exposures are estimated to be 7.8 ppb
for surface water and 26.0 ppb for ground water.

 2.

Non-dietary exposure

.

The primary source for human non-dietary exposure to sulfentrazone will
be from post-application exposure to treated residential turfgrass.
The routes of sulfentrazone exposure were dermal post-application
exposure for adults and toddlers, and post-application incidental
ingestion of sulfentrazone due to the hand-to-mouth behavior of
toddlers.  A worst case short-term non-dietary exposure analysis was
conducted using algorithms and

default factors published in US EPA’s Standard Operating Procedures
(SOPs) for Residential Exposure Assessments.  The dermal exposure
estimates for all adults, adult females and toddlers were 0.013, 0.016
and 0.023 mg/kg/day, respectively.  The exposure estimate for incidental
ingestion due to hand-to-mouth behavior for toddlers was 0.0026
mg/kg/day. The resulting total (combined oral and dermal since the
relevant endpoints both have the same effect) non-dietary exposure
estimates were 0.013, 0.016 and 0.025 mg/kg/day for all adults, adult
females and toddlers, respectively.

D. Cumulative Effects

 Cumulative exposure to substances with common mechanism of toxicity.
Section 408(b)(2)(D)(v) 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.'' While the Agency has some information in
its files that may turn out to be helpful in eventually determining
whether a pesticide shares a common mechanism of toxicity with any other
substances, EPA does not at this time have the capability to resolve the
scientific issues concerning common mechanism of toxicity in a
meaningful way. EPA is commencing a pilot process to study this issue
further through the examination of particular classes of pesticides. The
Agency hopes that the results of this pilot process will enable the
Agency to apply common mechanism issues to its pesticide risk
assessments. At present, however, the Agency does not know how to apply
the information in its files concerning common mechanism issues to risk
assessments, and therefore believes that in most cases there is no
“available information'' concerning common mechanism that can be
scientifically applied to tolerance decisions. Where it is clear that a
particular pesticide may share a significant common mechanism with other
chemicals, or where it is clear that a pesticide does not share a common
mechanism with other chemicals, a Common mechanism issues may affect
tolerance decision. The Agency expects that most tolerance decisions
will fall into the area in between, where EPA cannot reasonably
determine whether a pesticide does or does not share a common mechanism
of toxicity with other chemicals (and, if so, how that common mechanism
should be factored into a risk assessment). In such circumstances, the
Agency will reach a tolerance decision based on the best,
currently-available and usable information, without regard to common
mechanism issues. However, the Agency will also revisit such decisions
when the Agency determines how to apply common mechanism information to
pesticide risk assessments. In the case of sulfentrazone, EPA has
determined that it does not now have the capability to apply the
information in its files to a resolution of common mechanism issues in a
manner that would be useful in a risk assessment. This tolerance
determination therefore does not take into account common mechanism
issues. The Agency will reexamine the tolerances for sulfentrazone, if
reexamination is appropriate, after the Agency has determined how to
apply common mechanism issues to its pesticide risk assessments.

E. Safety Determination

 1. U.S. population. An oral NOEL of 25 mg/kg/day was used to determine
dietary Margin of Exposures (MOEs) for all adults and adult females.
This NOEL was derived from a prenatal oral developmental toxicity study
in rats and was based on fetal death, reduced body weight and
alterations in skeletal development. A dermal NOEL of 100 mg/kg/day was
used to determine non-dietary (dermal) MOEs. This NOEL was derived from
a dermal teratology rat study and was also based upon decreased fetal
body weight and increased skeletal development variations.
Additionally, the dermal absorption of 10% was used to estimate the
absorbed (systemic) exposures for the aggregation of the oral and dermal
route exposures (note:  this is only appropriate in cases such as this
where the relevant endpoints have the same effect).  The acute dietary,
non-dietary and aggregate MOEs for all US population is 5,646, for
adults 20-49 years is 10,095, for females 13-49 years is 10,641, for
youth 13-19 years is 7,621 and for children 3-5 years old is 3,904.
Further, the calculated short-term drinking water levels of concern
(DWLOC) for all US population is 4,900 µg/L for adults 20-49 years is
4,900 µg/L, for females 13-49 years is 4,200 µg/L, for youth 13-19
years is 4,200 µg/L and for children 3-5 years old is 1,400 µg/L.
These MOEs and DWLOC are considered to be acceptable and to clearly
illustrate low risk potential.

 2.

Infants and children

.

Risk to infants and children were determined by use of developmental
toxicity studies in rats and a two-generation reproduction study in
rats. The oral developmental toxicity studies resulted in a maternal
NOEL of 25 mg/kg/day based on decreased body weight gain, increased
spleen weight, and microscopic changes in the spleen, and a fetal NOEL
of 10 mg/kg/day based on fetal death, reduced body weights, and
alterations in skeletal development at higher doses. A dermal
developmental toxicity study in rats resulted in a developmental (fetal)
NOEL of 100 mg/kg/day based on decreased fetal body weight and increased
incidences of fetal alterations, comprised primarily of skeletal
variations and reductions in mean numbers of ossification sites. A
two-generation reproduction study in rats resulted in a NOEL for
systemic and reproductive/developmental parameters of 14 mg/kg/day for
males and 16 mg/kg/day for females. The LOEL for systemic and
reproductive/development parameters was 33 mg/kg/day for males and 40
mg/kg/day for females. Systemic effects were comprised of decreased body
weight gains, and reproductive/developmental effects at the LOEL
included degeneration and/or atrophy of the testes, with epididymal
sperm deficits in the second (F1) generation males. Male fertility in
the F1 generation was reduced at higher doses; litter size, pup survival
and pup body weight for both generations were also affected at higher
doses.   FFDCA section 408 provides that EPA shall apply an additional
safety factor for infants and children in the case of threshold effects
to account for pre- and post-natal toxicity and the completeness of the
data base, unless EPA determines that such an additional factor is not
necessary to protect the safety of infants and children. Based on
current data requirements, the data base relative to pre- and post-natal
toxicity is complete. EPA has determined that there is evidence of
increased quantitative susceptibility following in-utero

exposure in the developmental toxicity studies in rats via the oral and
dermal routes, and there is evidence for increased qualitative
susceptibility following prenatal and/or postnatal exposure in the
2-generation reproduction study in rats.  The EPA performed A Degree of
Concern Analysis and concluded that concerns are low for the
quantitative susceptibility of rats fetuses observed following oral and
dermal exposures, the qualitative susceptibility of rabbit fetuses seen
via the oral route, and the qualitative susceptibility seen in the 1-
and 2-generation reproduction studies.  The EPA concluded that there is
a complete toxicity data base for sulfentrazone and exposure data are
complete or are estimated based on data that reasonably accounts for
potential exposures.  The EPA determined that the 10X safety factor to
protect infants and children should be reduced to 1X.  The percent of
the RfD that will be utilized by the aggregate exposure to sulfentrazone
for the most exposed subgroup would be < 2% of the PAD for children (1
to 6 years old) Therefore, EPA concludes that there is a reasonable
certainty that no harm will result to infants and children from
aggregate exposure to sulfentrazone.

F. International Tolerances

 There are no Codex Alimentarius Commission (Codex) Maximum Residue
Levels (MRLs) for sulfentrazone.


[Federal Register Volume 80, Number 77 (Wednesday, April 22, 2015)]
[Notices]
[Pages 22509-22510]
[FR Doc No: 2015-09222]

-----------------------------------------------------------------------

DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Project No. 2179-043--California; Project No. 2467-020--California]

Merced Irrigation District, Pacific Gas and Electric Company;
Notice of Availability of the Draft Environmental Impact Statement for
the Merced River and Merced Falls Hydroelectric Projects and Intention
To Hold Public Meetings

    In accordance with the National Environmental Policy Act of 1969
and the Federal Energy Regulatory Commission (Commission or FERC)
regulations contained in the Code of Federal Regulations (CFR) (18 CFR
Part 380 [FERC Order No. 486, 52 FR 47897]), the Office of Energy
Projects has reviewed the applications for license for the Merced River
Hydroelectric Project (FERC No. 2179), and the Merced Falls
Hydroelectric Project (FERC No. 2467) and prepared a draft multi-
project environmental impact statement (EIS) for the projects.
    Both projects are located on the Merced River. The Merced River
Project consists of the New Exchequer and McSwain developments, which
are located at river miles (RM) 62.5 and 56.3, respectively, about 23
miles northeast of the city of Merced in Mariposa County, California.
The Merced River Project occupies 3,154.9 acres of federal land
administered by the U.S. Department of the Interior, Bureau of Land
Management (BLM). The Merced Falls Project is located at RM 55 on the
border of Merced and Mariposa Counties, California. The Merced Falls
Project occupies 1.0 acre of federal land administered by BLM.
    The draft EIS contains staff's analysis of the applicants'
proposals and the alternatives for relicensing the Merced River and
Merced Falls Projects. The draft EIS documents the views of
governmental agencies, non-governmental organizations, affected Indian
tribes, the public, the license applicants, and Commission staff.
    A copy of the draft EIS is available for review at the Commission
or may be viewed on the Commission's Web site at http://www.ferc.gov,
using the ``e-Library'' link. Enter the docket number, excluding the
last three digits, to access the document. For assistance, contact FERC
Online Support at<EMAIL_ADDRESS>or toll-free at (866) 208-
3676, or for TTY, contact<PHONE_NUMBER>.
    You may also register online at http://www.ferc.gov/docs-filing/esubscription.asp to be notified via email of new filings and issuances
related to this or other pending projects. For assistance, contact FERC
Online Support.
    All comments must be filed by Friday, May 29, 2015, and should
reference Project Nos. 2179-043 and 2467-020. The Commission strongly
encourages electronic filing. Please file comments using the
Commission's efiling system at http://www.ferc.gov/docs-filing/efiling.asp. Commenters can submit brief comments up to 6,000
characters, without prior registration, using the eComment system at
http://www.ferc.gov/docs-filing/ecomment.asp. You must include your
name and contact information at the end of your comments. For
assistance, please contact FERC Online Support. In lieu of electronic
filing, please send a paper copy to: Kimberly D. Bose, Secretary,
Federal Energy Regulatory Commission, 888 First Street NE., Washington,
DC 20426.
    Anyone may intervene in this proceeding based on this draft EIS (18
CFR 380.10). You must file your request to intervene as specified
above. You do not need intervenor status to have your comments
considered.
    In addition to or in lieu of sending written comments, you are
invited to attend public meetings that will be held to receive comments
on the draft EIS. The agency scoping meeting will focus on resource
agency and non-governmental organization input, while the public
scoping meeting is primarily for public input. All interested
individuals, organizations, and agencies are invited to attend one or
both of the meetings. The time and locations of the meetings are as
follows:

Agency Meeting

    Date: Thursday, April 30, 2015.
    Time: 10:00 a.m.
    Place: El Capitan Lodge at the Merced County Fairgrounds.
    Address: 900 Martin Luther King Jr. Way, Merced, CA 95341.

Public Meeting

    Date: Thursday, April 30, 2015.
    Time: 6:00 p.m.
    Place: San Joaquin Hall at the Merced County Fairgrounds.
    Address: 900 Martin Luther King Jr. Way, Merced, CA 95341.
    At these meetings, resource agency personnel and other interested
persons will have the opportunity to provide oral and written comments
and recommendations regarding the draft EIS. The meetings will be
recorded by a court reporter, and all statements (verbal and written)
will become part of

the Commission's public record for the project. These meetings are
posted on the Commission's calendar located at http://www.ferc.gov/EventCalendar/EventsList.aspx along with other related information.
    For further information, please contact Matt Buhyoff at (202) 502-
6824 or at<EMAIL_ADDRESS>
    Dated: April 15, 2015.
Kimberly D. Bose,
 Secretary.
[FR Doc. 2015-09222 Filed 4-21-15; 8:45 am]
 BILLING CODE 6717-01-P