<EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR PESTICIDE
PETITIONS PUBLISHED IN THE FEDERAL REGISTER (7/1/2007)>

<EPA Registration Division contact: Shaja R. Brothers<PHONE_NUMBER>)>

<FMC Corporation, 1735 Market Street, Philadelphia, PA 19103 and
Interregional Research No. 4, Rutgers, The State University of New
Jersey, 500 College Road East, Suite 201-W, Princeton, NJ 08540.>

<7E7308>

<	EPA has received a pesticide petition 7E7308 from FMC Corporation
(1735 Market Street, Philadelphia, PA 19103), and Interregional Research
No. 4 ( IR-4, Rutgers, The State University of New Jersey, 500 College
Road East, Suite 201-W, Princeton, NJ 08540) 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.>

<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]methanesulfonamide) and 3-desmethyl
sulfentrazone
(N-[2,4-dichloro-5-[4-(difluoromethyl)-4,5-dihydro-5-oxo-1H-1,2,4-triazo
l-1-yl]phenyl]methanesulfonamide)] in or on the following raw
agricultural commodities: brassica, head and stem, subgroup 5A at 0.20
parts per million (ppm); brassica, leafy greens, subgroup 5B at 0.35
ppm; melon, subgroup 9A at 0.10 ppm; vegetable, fruiting, group 8 at
0.05 ppm; okra at 0.05 ppm; pea, succulent at 0.05 ppm; flax at 0.05
ppm; strawberry at 0.05 ppm, and vegetable, tuberous and corm, subgroup
1C at 0.15 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 support granting of the
petition. Additional data may be needed before EPA rules on the
petition.>

<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 use were the major metabolites
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 detection that allows monitoring of food with
residues at or above the levels set in these tolerances. The proposed
analytical method for determining residues is hydrolysis followed by gas
chromatographic separation.>

<	3. Magnitude of residues. Sulfentrazone was applied at the maximum
label rates for broccoli, cantaloupe, flax, mustard green, pepper (bell
and non-bell), strawberry and tomatoes 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. Genotoxicty. 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 cereal grains (except sweet corn), soybeans, sunflower, sugarcane,
peanut, cabbage, horseradish, mint, corn forage, corn stover, peas,
beans, brassica, fruiting vegetables, okra, tuberous and corm
vegetables, melon, flax and strawberry.  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>

<	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.>

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[Federal Register Volume 86, Number 193 (Friday, October 8, 2021)]
[Notices]
[Page 56262]
[FR Doc No: 2021-22022]

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

DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

Combined Notice of Filings

    Take notice that the Commission has received the following Natural
Gas Pipeline Rate and Refund Report filings:

Filings Instituting Proceedings

    Docket Numbers: RP22-21-000.
    Applicants: Rover Pipeline LLC.
    Description: Sec.  4(d) Rate Filing: Summary of Negotiated Rate
Capacity Release Agreements on 10-4-21 to be effective 10/1/2021.
    Filed Date: 10/4/21.
    Accession Number: 20211004-5007.
    Comment Date: 5 p.m. ET 10/18/21.
    The filings are accessible in the Commission's eLibrary system
(https://elibrary.ferc.gov/idmws/search/fercgensearch.asp) by querying
the docket number.
    Any person desiring to intervene or protest in any of the above
proceedings must file in accordance with Rules 211 and 214 of the
Commission's Regulations (18 CFR 385.211 and 385.214) on or before 5:00
p.m. Eastern time on the specified comment date. Protests may be
considered, but intervention is necessary to become a party to the
proceeding.
    eFiling is encouraged. More detailed information relating to filing
requirements, interventions, protests, service, and qualifying
facilities filings can be found at: http://www.ferc.gov/docs-filing/efiling/filing-req.pdf. For other information, call<PHONE_NUMBER>
(toll free). For TTY, call<PHONE_NUMBER>.

    Dated: October 04, 2021.
Debbie-Anne A. Reese,
Deputy Secretary.
[FR Doc. 2021-22022 Filed 10-7-21; 8:45 am]
BILLING CODE 6717-01-P