 COMPANY FEDERAL REGISTER DOCUMENT SUBMISSION TEMPLATE ( 1/ 1/ 2006)

EPA Registration Division contact: [ Ms. Joanne Miller, PM 23, ( 703) 305 6224]

INSTRUCTIONS: Please utilize this outline in preparing tolerance petition documents. In cases where the outline element does not apply please insert " NARemove and maintain the outline. The comment notes that appear on the left margin represent hidden typesetting codes designed to expedite the processing of the Federal Register document. Please do not remove or alter these comment notes or change the margins, font, or format in your document. Simply replace the instructions that appear in italics and brackets, i. e., "[ insert company name]," with the information specific to your action.]

TEMPLATE:

Bayer CropScience [ 5F6959]

EPA has received a pesticide petition ( 5F6959) from Bayer CropScience, 2 T. W. Alexander Drive, P. O. Box 12014, Research Triangle Park, NC 27709 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 180.600 by increasing established tolerances for the residues of propoxycarbazone, methyl 2[[[( 4,5 dihydro 4 methyl 5 oxo 3 propoxy 1H 1,2,4 triazol 1 yl) carbonyl] amino] sulfonyl] benzoate and its metabolite, methyl 2[[[( 4,5 dihydro 3( 2 hydroxypropoxy)  4 methyl 5 oxo 1H 1,2,4 triazol 1 yl) carbonyl] amino] sulfonyl] benzoate in or on the raw agricultural commodities wheat forage from 1.5 parts per million ( ppm) to 11 ppm, and of propoxycarbazone, methyl 2[[[( 4,5 dihydro 4 methyl 5 oxo 3 propoxy 1H 1,2,4 triazol 1 yl) carbonyl] amino] sulfonyl] benzoate, in or on the raw agricultural commodities cattle, goat, horse, sheep, meat byproducts from 0.05 ppm to 0.3 ppm, and milk from 0.004 ppm to 0.03 ppm. EPA has determined that the petition contains data or information regarding the elements set forth in section 408 ( d)( 2) of the 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.

A. Residue Chemistry 1. Plant metabolism. The metabolism of propoxycarbazone sodium ( MKH  6561) in wheat was rapid, as only minor amounts of propoxycarbazone sodium were found in some of the wheat matrices. The primary metabolic pathway in wheat appeared to be hydroxylation of the propoxy side chain of propoxycarbazone sodium to give Pr 2 OH MKH  6561, methyl 2[[[( 4,5 dihydro 3( 2 hydroxypropoxy) 4 methyl 5 oxo 1H 1,2,4 triazol 1 yl) carbonyl] amino] sulfonyl] benzoate. Hydrolysis of Pr 2 OH MKH  6561 then gave Pr 2 OH NMT and, probably the sulfonamide methyl ester which was not observed in any wheat matrices. Hydrolysis of the sulfonamide methyl ester gave sulfonamide acid, which was in equilibrium with saccharin. A minor metabolic pathway was demethylation of propoxycarbazone sodium to yield N desmethyl MKH  6561.

2. Analytical method. i. Plant. The proposed tolerance expression is MKH  6561 and Pr 2 OH MKH  6561. An analytical method was developed to measure these two analytes in plant matrices. The method was validated in wheat tissues. MKH  6561 and Pr 2 OH MKH  6561 were extracted from the wheat tissues with 0.05 M NH4OH using accelerated solvent extraction. Trifluoroacetic acid ( 0.5 mL) and an isotopically labeled internal standard were added to the extract. The whole extract was loaded onto a C  18 solid phase extraction ( SPE) cartridge. The C  18 SPE cartridge was washed with aqueous trifluoroacetic acid ( 0.1%) and aqueous acetic acid ( 0.1%). A three to one mixture of acetonitrile and aqueous acetic acid ( 0.1%) was used to elute the analytes from the C  18 SPE cartridge. Water and acetic acid were added to the sample which was analyzed by LC/ MS/ MS. ii. Animal. The proposed tolerance expression is MKH  6561. An analytical method was developed to measure this analyte in animal tissues and milk. The method was validated in animal tissues and milk. MKH  6561 was extracted from the tissues with 0.05 M NH4OH. using accelerated solvent extraction. Trifluoroacetic acid ( 0.5 mL) and an isotopically labeled internal standard were added to the extract which was then centrifuged at 2,000 rpm for 10 minutes. Approximately half of the sample was loaded onto a C  18 SPE cartridge. The C  18 SPE cartridge was washed with aqueous trifluoroacetic acid ( 0.1%) and aqueous acetic acid ( 0.1%). A three to one mixture of acetonitrile and aqueous acetic acid ( 0.1%) was used to elute the analytes from the C  18 SPE cartridge. Water and acetic acid were added to the sample which was analyzed by LC/ MS/ MS. Milk samples were analyzed by amending an aliquot of milk with trifluororacetic acid ( 0.5 mL) and isotopically labeled internal standard. The sample was purified by C  18 SPE as described above. The resultant sample was analyzed by LC/ MS/ MS.

3. Magnitude of residues. Twenty ( 18 ' harvest'; 2 ' decline') spring or winter wheat trials were conducted to measure the residues on wheat forage at a 0 day Preharvest Interval ( PHI). Following one foliar spray application with propoxycarbazone sodium 70% WG( 70 g ai/ 100 g product) to wheat at BBCH 12   30 growth stage and a total seasonal target rate of 0.040 lb ai/ A ( 45 g ai/ ha) and harvest immediately after the application, the highest average field trial ( HAFT) total propoxycarbazone residue as well as the maximum total propoxycarbazone single residue was 11 ppm for wheat forage. B. Toxicological Profile 1. Acute toxicity. i. Propoxycarbazone sodium is of very low acute toxicity to fasted rats following a single oral administration. The acute oral LD50 is > 5,000 milligrams/ kilogram/ body weight ( mg/ kg/ bwt) for males and females. ii. Propoxycarbazone sodium is not toxic to rats following a single dermal application. The acute dermal LD50 is > 5,000 mg/ kg/ bwt for males and females. iii. An acute inhalation study with rats showed low toxicity with a 4  hour dust aerosol LC50 5,030 mg/ m3 air for males and females. iv. An eye irritation study in rabbits showed minimal irritation completely reversible within 48 hours. v. A dermal irritation study in rabbits showed slight irritation completely reversible within 48 hours. vi. Propoxycarbazone sodium has no skin sensitizing potential under the conditions of the maximization test in guinea pigs.

2. Genotoxicty. The genotoxic action of Propoxycarbazone sodium was studied in bacteria and mammalian cells with the aid of various in vitro test systems ( Salmonella microsome test, hypoxanthine guanine phophoribosy transferase ( HGPRT) test with chinese hamster V79 cells, cytogenetic study with chinese hamster V79 cells, and unscheduled DNA synthesis ( UDS) test) and in one in vivo test ( micronucleus test). None of the tests revealed any evidence of a mutagenic or genotoxic potential of propoxycarbazone sodium. The compound did not induce point mutation, DNA damage or chromosome aberration ( CA).

3. Reproductive and developmental toxicity. i. In a 2  generation reproduction study, Wistar rats were administered propoxycarbazone sodium at levels of 0, 1,000, 4,000, or 16,000 ppm in the diet. The no observe adverse effect level ( NOAEL) for reproductive parameters was established at 16,000 ppm ( 1,231 mg/ kg bwt/ day in males and 1,605 mg/ kg bwt/ day in females), the highest dose tested ( HDT). The parental NOAEL was 1,000 ppm ( 80 mg/ kg bwt/ day in F1 males and 93 mg/ kg bwt/ day in F0 females). ii. A developmental toxicity study was conducted with Wistar rats via oral gavage of propoxycarbazone sodium at levels of 0, 100, 300, and 1,000 mg/ kg bwt/ day on days 6 through 19 of gestation. There were no signs of maternal toxicity, embryotoxicity, fetotoxicity, or teratogenicity at the level of 1,000 mg/ kg bwt/ day. Therefore, the maternal and developmental NOAELs for rats were established at 1,000 mg/ kg bwt/ day, the limit dose for this study type. No teratogenic potential of propoxycarbazone sodium was evident in rats. iii. Himalayan rabbits were administered propoxycarbazone sodium at levels of 0, 20, 100, 500, or 1,000 mg/ kg bwt/ day by oral gavage on days 6 through 28 post coitum in a test for developmental toxicity. A maternal NOAEL of 100 mg/ kg bwt/ day was established based on cold ears, alopecia, swelling of vulva, decreased feed, and water intake, body weight loss, gastrointestinal tract ( GI) effects, liver effects, and thyroid hormone level effects. The gestation rate NOAEL of 100 mg/ kg bwt/ day was based on one abortion ( assessed as secondary due to maternal toxicity) at 500 mg/ kg bwt/ day. The NOAEL for fetal parameters of 500 mg/ kg bwt/ day was based on placental effects, increased post implantation loss, decreased number of fetuses, decreased fetal weight, retarded fetal skeletal ossification, and possible increase in lobulation of liver in fetuses at 1,000 mg/ kg bwt/ day. No teratogenic potential of propoxycarbazone sodium was evident in rabbits.

4. Subchronic toxicity. i. A 28  day dermal toxicity study in Wistar rats established a local and systemic NOAEL of 1,000 mg/ kg bwt/ day ( the dermal limit dose) for males and females. ii. A 14  week feeding study was conducted with Wistar rats at dietary dose levels of 0, 250, 1,000, 4,000, or 20,000 ppm. The NOAEL was determined to be 4,000 ppm ( 286.4 mg/ kg bwt/ day in males and 350.6 mg/ kg bwt/ day in females) based upon increased water consumption ( reversible during the 4  week recovery period) and an irritative effect of the forestomach epithelium ( reversible during the 4  week recovery period) in males and females dosed at 20,000 ppm as well as reduced glucose and triglyceride levels in females only dosed at 20,000 ppm. iii. A 91  day feeding study was conducted with B6C3F1 mice at dietary dose levels of 0, 625, 2,500, or 10,000 ppm. The NOAELs determined for males and females were 625 ppm ( 205 mg/ kg bwt/ day) and 2,500 ppm ( 1,159 mg/ kg bwt/ day), respectively, based on decreased body weights in 2,500 ppm males and 10,000 ppm females. iv. A 2  month range finding feeding study in Beagle dogs, at levels of 0, 1,000, 5,000, 10,000, and 40,000 ppm in the diet established a NOAEL of 10,000 ppm ( 322.2 mg/ kg bwt/ day in males and 285.6 mg/ kg bwt/ day in females) based on elevated hepatic biotransformation enzymes at 40,000 ppm.

5. Chronic toxicity. i. A 2  year chronic/ oncogenicity study was conducted with male and female Fischer 344 rats at dietary levels of 0, 50, 500, or 1,000 mg/ kg bwt/ day for approximately the first seven months of the study ( dose adjustment). From approximately seven months to study termination, the doses were 0, 1,000, 10,000, and 20,000 ppm in the diet. A chronic toxicity NOAEL of 1,000 ppm ( 43 mg/ kg bwt/ day in males and 49 mg/ kg bwt/ day in females) was determined based on increased urine pH and decreased body weight gain at 1  year ( but not 2 years) at 10,000 ppm and 20,000 ppm. No carcinogenic potential was indicated. ii. B6C3F1 mice were administered propoxycarbazone sodium via the diet at levels of 0, 280, 1,400, and 7,000 ppm in a 2  year chronic feeding/ carcinogenicity study. The chronic toxicity NOAEL was established at 1,400 ppm ( 369.0 mg/ kg/ day in males and 626.9 mg/ kg bwt/ day in females) based on retarded body weight development. No carcinogenic potential was indicated. iii. A 1  year feeding study in Beagle dogs was conducted at 0, 2,000, 10,000, and 25,000 ppm in the diet. The NOAEL in males was determined to be 10,000 ppm ( 258.0 mg/ kg bwt/ day) based upon increased absolute adrenal gland weight without an increase in relative adrenal gland weight and slight enlargement of zona fasciculata microscopically, without a correlation to adrenal gland weight in males dosed at 25,000 ppm. The NOAEL in females was determined to be 2,000 ppm ( 55.7 mg/ kg bwt/ day) based upon decreased food consumption and decreased relative heart weight in females dosed at 10,000 and 25,000 ppm. 6. Animal metabolism. i. A single oral dose of 2 mg/ kg/ bwt [ triazolinone 3 14C] MKH  6561 was administered to rats. Between 22% and 24% of the administered dose was absorbed. Maximum plasma radiation levels were observed 0.33 hours after dosing. Within 48 hours of dosing, between CA 88% and 97% of the radioactivity was excreted via urine and feces. Approximately 80  88% of the excreted radioactivity was unchanged parent compound. The highest single metabolite concentration was CA 3% of the administered dose. The terminal elimination half live for total radioactivity was CA 12  13 hours, so no bioaccumulation of MKH  6561 or its metabolites will occur. ii. Single oral doses of 2 mg/ kg/ bwt and 200 mg/ kg/ bwt [ phenyl UL 14C] MKH  6561 were administered to rats. Between CA 21  31% of the administered dose was absorbed. Maximum plasma radiation levels were observed after 0.33 hours ( low dose) and 1  hour ( high dose). Within 48 hours of dosing, CA 97  104% of the administered dose was eliminated via urine and feces. Approximately 75  86% of the administered dose was eliminated as unchanged parent compound. The maximum single metabolite concentration was 8.8% of the administered dose. At the end of the study, less than 0.25% of the administered dose was found in organs and tissues. In a separate bile fistulation experiment, the predominantly fecal elimination was confirmed to be due to incomplete absorption of radioactivity from the GI tract. The terminal elimination half live for total radioactivity was CA 9  11 hours, so no bioaccumulation of MKH  6561 or its metabolites will occur. iii. Laying hens were given a daily dose of protonated MKH  6561 [ phenyl UL 14C] at 3.12 mg/ kg/ bwt for three consecutive days. The residue levels were 1.343 ppm in liver, 0.017 ppm in muscle, 0.014 ppm in fat, 0.006 ppm in the day  1 eggs, 0.009 ppm in the day  2 eggs, and 0.012 ppm in the day  3 eggs. The residue levels based on a theoretical 1x application rate, as determined from residue levels observed in the propoxycarbazone sodium ( MKH  6561) wheat field trials would all be considerably less than 0.001 ppm. The major residue identified in tissues and eggs were MKH  6561, Pr 2 OH MKH  6561, MKH  6561 sulfonamide methyl ester, and saccharin. The major metabolic pathway of MKH  6561 [ phenyl UL 14C] in poultry was hydrolysis of the parent compound producing N methyl propyl triazolinone and sulfonamide methyl ester. The sulfonamide methyl ester was then converted to saccharin. A minor pathway involved hydroxylation at the 2  position of the triazolinone propoxy group. In the liver, the major metabolic pathway led to the formation of protein bound MKH  6561 residue through conjugation with the amino acid serine. iv. Laying hens were given a daily dose of protonated MKH  6561 [ triazolinone 3 14C] at 2.91 mg/ kg/ bwt for three consecutive days. The residue levels were 0.184 ppm in liver, 0.044 ppm in muscle, 0.015 ppm in the fat, 0.011 ppm in the day  1 egg, 0.016 ppm in the day  2 egg, and 0.022 ppm in the day  3 egg. The residue levels in tissues and eggs based on a theoretical 1x application, as determined from the residue levels observed in the MKH  6561 wheat field trials, would all be considerably less that 0.001 ppm. The metabolism of MKH  6561 [ triazolinone 3 14C] appeared to involve both hydroxylation at the 2  position of the propoxy group and hydrolysis of the phenyl sulfonamide linkage. v. Goats were dosed with 1.0 mg/ kg/ bwt of MKH  6561 [ phenyl UL 14C] for three consecutive days. Residue levels were 3.643 ppm in liver, 0.486 ppm in kidney, 0.009 ppm in muscle, 0.004 ppm in fat, 0.015 ppm in day  1 milk and, 0.022 ppm in day  2 milk. The metabolic pathway was based on hydrolysis of the sulfonamide to yield MKH  6561 sulfonamide methyl ester and saccharin. The saccharin was then conjugated to proteins which were found mainly in the liver and kidney. vi. Goats were dosed with MKH  6561 [ triazolinone 3 14C] at a dose of 0.98 mg/ kg/ bwt for 3 consecutive days. Residue levels were 0.171 ppm in liver, 0.425 ppm in kidney, 0.040 ppm in muscle, 0.007 ppm in fat, 0.046 ppm in day  1 milk, and 0.057 ppm in day  2 milk. The metabolism of propoxycarbazone sodium involved the cleavage of the phenyl sulfonylurea side chain and the hydroxylation of the propyl side chain on the triazolinone ring system after the cleavage of the phenyl sulfonylurea side chain.

7. Metabolite toxicology. i. 4 OH saccharin is of low acute toxicity to fasted rats following a single oral administration. The acute oral LD50 is > 5,000 mg/ kg/ bwt for males and females. 4 OH saccharin is considered non mutagenic with and without S9 mix in the plate incorporation as well as in the preincubation modification of the Salmonella microsome test. ii. MKH  8394 is of very low acute toxicity to fasted rats following a single oral administration. The acute oral LD50 is> 5,000 mg/ kg/ bwt for males and females. MKH  8394 is considered non mutagenic with and without S9 mix in the plate incorporation as well as in the preincubation modification of the Salmonella microsome test. iii. KTS  9061 ( Pr 2 OH MKH  6561) is not toxic to fasted rats following a single oral administration. The acute oral LD50 is> 5,000 mg/ kg/ bwt for males and females. KTS  9061 is considered non mutagenic with and without S9 mix in the plate incorporation as well as in the preincubation modification of the Salmonella/ microsome test. KTS  9061 is considered non clastogenic with and without S9 mix CA test in vitro using chinese hamster V79 cells. Wistar rats were administered KTS  9061 via the diet at levels of 0, 800, 4,000, and 10,000 ppm for approximately four weeks. The NOAEL was determined to be 10,000 ppm ( 905.3 mg/ kg bwt/ day in males and 880.0 mg/ kg bwt/ day in females), the HDT. iv. KTS  9304 has low to moderate acute toxicity to fasted rats following a single oral administration. The acute oral LD50 was 263 mg/ kg/ bwt in males and 1,756 mg/ kg/ bwt in females. KTS  9304 is considered non mutagenic with and without S9 mix in the plate incorporation as well as in the preincubation modification of the Salmonella/ microsome test.

8. Endocrine disruption. There is no evidence to suggest that propoxycarbazone sodium has an effect on the endocrine system. Studies in this data base include evaluation of the potential effects on reproduction and development, and an evaluation of the pathology of the endocrine organs following short term and long term exposure. These studies revealed no endocrine effects due to propoxycarbazone sodium.

C. Aggregate Exposure 1. Dietary exposure. Using the Dietary Exposure Evaluation Model software with the Food Commodity Intake Database ( DEEM FCID), ver. 2.0, and the USDA 1994  1996 and 1998 Nationwide Continuing Surveys of Food Intake by Individuals ( CSFII) database, the dietary exposure and risk from food and drinking water was calculated.

i. Food. Estimates of chronic dietary exposure to residues of propoxycarbazone sodium utilized the current and new proposed tolerances in wheat forage, wheat hay, wheat straw, and wheat grain of 11, 0.15, 0.05, 0.02, respectively, in cattle, sheep, goats, horses, and hogs meat, and meat byproducts , of 0.05 and 0.3 ppm, respectively, and in milk of 0.03 ppm. Other assumptions were that 100% of the target crop would be treated with propoxycarbazone sodium and that no loss of residue would occur due to processing or cooking. For chronic exposures, a reference dose ( RfD) of 0.748 mg/ kg/ day was assumed based on and NOAEL of 74.8 mg/ kg bwt/ day from the 2 generation reproduction study in rats. A safety factor of 100 was used based on interspecies extrapolation ( 10x) and intraspecies variability ( 10x). The FQPA safety factor was reduced to 1x resulting in a chronic population adjusted dose ( cPAD) of 0.748 mg/ kg/ day. Using these conservative assumptions, dietary residues of propoxycarbazone sodium contribute 0.001316 mg/ kg/ day ( 0.2% of the cPAD) for children 1 to 2 years old, the most sensitive sub population. For the U. S. population, the exposure was 0.000305 mg/ kg/ day (< 1% of the cPAD). EPA concluded in the Federal Register / Vol. 69, No. 129 / Wednesday, July 7, 2004: " An effect of concern attributable to a single exposure ( dose) was not identified from the oral toxicity studies including the developmental toxicity studies in rat and rabbits. Abortions seen in the developmental toxicity study in rabbits at 1,000 mg/ kg/ day during GD 19  28, were not considered to be a single dose effect. Since they occur late in gestation after repeated exposures. [ sic]"

ii. Drinking Water. For calculating drinking water exposure, the Estimated Environmental Concentrations ( EEC) were used as published by EPA in the FR Vol. 69, 129, p. 40778, 04 Jul 04. EPA used the FQPA Index Reservoir Screening Tool ( FIRST) or the Pesticide Root Zone Model/ Exposure Analysis Modeling System ( PRZM/ EXAMS), to produce estimates of pesticide concentrations in surface water. The screening concentration in ground water ( SCI GROW) model is used to predict pesticide concentrations in shallow ground water. Based on the FIRST and SCI GROW models, the EECs of propoxycarbazone sodium for acute exposures are estimated to be 2.3 parts per billion ( ppb) for surface water and 0.4 ppb for ground water. The EECs for chronic exposures are estimated to be 0.9 ppb for surface water and 0.4 ppb for ground water.

EECs derived from these models are incorporated in the calculation of the dietary risk and included in the above expression of the % cPAD.

2. Non dietary exposure. There are no current non food uses for propoxycarbazone sodium registered under the Federal Insecticide, Fungicide, and Rodenticide Act, as amended. No non food uses are proposed for this active ingredient and no non dietary exposures are expected for the general population.

D. Cumulative Effects Propoxycarbazone sodium is a sulfonamide herbicide. There is no information to suggest that any chemical in this class of herbicides has a common mechanism of mammalian toxicity or that chemicals in this class produce similar effects so it is not appropriate to combine exposures of propoxycarbazone sodium with other herbicides.

E. Safety Determination 1. U. S. population. As presented previously, the exposure of the U. S. general population to propoxycarbazone sodium is low, and the risks, based on comparisons to the RFD, are minimal. The margins of safety from the use of propoxycarbazone sodium are well within EPA's acceptable limits. Bayer Corporation concludes that there is a reasonable certainty that no harm will result to the U. S. population from aggregate exposure to propoxycarbazone sodium residues.

2. Infants and children. The complete toxicological data base including the developmental toxicity and 2  generation reproduction studies were considered in assessing the potential for additional sensitivity of infants and children to residues of propoxycarbazone sodium. The developmental toxicity studies in rats and rabbits revealed no increased sensitivity of rats or rabbits to in utero exposure to propoxycarbazone sodium. The 2  generation reproduction study did not reveal any increased sensitivity of rats to in utero or postnatal exposure to propoxycarbazone sodium. Furthermore, none of the other toxicology studies revealed any data demonstrating that young animals were more sensitive to propoxycarbazone sodium than adult animals. In the FR Vol. 69, 129, p. 40778, 04 Jul 04 EPA concluded: " The toxicology database is complete for FQPA purposes and there are no residual uncertainties for pre/ post natal toxicity. Based on the quality of the exposure data, EPA determined that the 10X SF to protect infants and children should be removed."

F. International Tolerances There are currently no Codex, Canadian, or Mexican tolerances established for propoxycarbazone sodium. The European Community has established cereal ( incl. wheat) tolerances of 0.02 ppm.


[Federal Register Volume 77, Number 130 (Friday, July 6, 2012)]
[Notices]
[Pages 40037-40039]
[FR Doc No: 2012-16441]

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

ENVIRONMENTAL PROTECTION AGENCY

[FRL-9697-3]

Notice of the Peer Review Meeting for EPA's Draft Report Entitled
An Assessment of Potential Mining Impacts on Salmon Ecosystems of
Bristol Bay, AK

AGENCY: U.S. Environmental Protection Agency (EPA).

ACTION: Notice of external peer review meeting.

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

SUMMARY: The U.S. Environmental Protection Agency (EPA) is announcing
that Versar, Inc., an EPA contractor for external peer review, has
convened a panel of experts and will organize and conduct an
independent expert external peer review meeting on August 7-9, 2012, to
review the draft report entitled An Assessment of Potential Mining
Impacts on Salmon Ecosystems of Bristol Bay, Alaska. Versar, Inc.
invites the public to register to attend the first two days of this
meeting as observers. In addition, Versar, Inc. invites the public to
register to provide oral testimony

during Day 1 (August 7, 2012) of the external peer review meeting. The
panel will meet privately on Day 3 (August 9, 2012) of the meeting. The
expert panel is charged with reviewing the scientific and technical
merit of the draft assessment. The panel will not be making
recommendations to the EPA concerning any potential future actions or
policies. Therefore, the peer review meeting will focus on issues of
science relevant to the assessment, rather than its policy
implications. The panel will have access to public comments received in
the official public docket (docket ID number EPA-HQ-ORD-2012-0276)
during the assessment's public comment period, as well as oral comments
made on Day 1 of the peer review meeting. The draft assessment is
available through www.regulations.gov and at www.epa.gov/bristolbay. In
preparing the final assessment, EPA will consider Versar, Inc.'s report
of the comments and recommendations from the external peer review
meeting, as well as written public comments received through the
official public docket. The final peer review report prepared by
Versar, Inc. will be made available to the public. EPA has released
this draft assessment for the purposes of public comment and peer
review. This draft assessment is not final as described in EPA's
information quality guidelines, and it does not represent and should
not be construed to represent Agency policy or views.

DATES: The public peer review panel meeting will be held on August 7-8,
2012, beginning and ending at approximately 8:30 a.m. and 5:00 p.m.
(AKDT) on both days.

ADDRESSES: The independent expert external peer review meeting will be
held at the Dena'ina Civic & Convention Center, located at 600 West
Seventh Avenue, Anchorage, Alaska.
    Meeting Background: As part of the peer review process for the
EPA's draft assessment report, the public portion of the peer review
meeting will be held on August 7-8, 2012 at the Dena'ina Civic &
Convention Center in Anchorage, Alaska. On both days, the meeting will
begin at 8:30 a.m. (AKDT) and will end at approximately 5:00 p.m.
(AKDT). Members of the public and any other interested parties may
register to attend both days of the meeting as observers, and to offer
oral testimony on the first day of the meeting.
    The focus of this peer review meeting is the scientific content and
merit of the EPA's draft assessment. Public speakers are encouraged to
focus on issues directly relevant to science-based aspects of the
assessment, and to address specific scientific points in their oral
testimony. The peer review process is separate from the EPA public
comment meetings held in early June that enabled members of the public
to provide comments and voice opinions concerning the EPA's draft
assessment report and its potential policy implications for the public
docket.
    Day 1 of the meeting (August 7, 2012) will be dedicated to hearing
oral comments on the draft assessment. Members of the public who have
registered in advance to provide oral comments will have the
opportunity to speak during the observer comment session. Each speaker
will be allowed between 3-5 minutes, depending on number of speakers
registered. Given time constraints, a maximum of 100 speakers will be
allowed to offer testimony. If more than 100 speakers register to
provide oral comments, speakers will be selected by Versar in a manner
designed to optimize representation from all organizations,
affiliations, and present a balance of science issues relevant to the
Agency's science assessment. Additional information on selection of
speakers and speaking times will be sent out by August 3, to all
individuals who register to speak.
    To accommodate as many speakers as possible, registered speakers
will present oral comments only, without visual aids or written
material. All members of the public, including registered observers and
speakers, are encouraged to submit written comments and materials to
the official public docket for the draft assessment (docket ID number
EPA-HQ-ORD- 2012-0276) by the close of the public comment period on
July 23, 2012. Panel members will have access to any written comments
and materials submitted to the official public docket by this deadline.
Registered observers and speakers will not be allowed to distribute any
written materials directly to the peer review panel. To submit written
comments, please follow one of the methods outlined in the previous
Federal Register notice, issued on May 25, 2012, initiating the
assessment's public comment period: Federal Register Volume 77, Number
102 (http://www.gpo.gov/fdsys/pkg/FR-2012-05-25/html/2012-12808.htm).
    Day 2 of the meeting (August 8, 2012) will be devoted to
deliberations of the EPA's draft assessment by the peer review panel,
guided by the charge questions provided to the public for public
comment. Registered observers may attend and observe the peer review
panel deliberations on Day 2, but will not be allowed to address the
panel or provide oral or written comments.
    Registration: To attend the August 7-8 public portion of the peer
review meeting, you must register for the meeting by 11:59 p.m. (EDT)
on July 23, 2012. You can register for the meeting by visiting http://www.versar.com/epa/bristolbayregistration.html, completing the online
registration form, and submitting the required information. You can
also register through U.S. Postal Service or overnight/priority mail by
sending the necessary registration information (see Required
Registration Information) to the Versar Meeting Coordinator, Ms.
Brittany Ekstrom, Versar, Inc., 6850 Versar Center, Springfield, VA
22151; Telephone:<PHONE_NUMBER>. Registrations sent via U.S. Postal
Service or overnight/priority mail must be received by 11:59 p.m. (EDT)
on July 23, 2012. There will be no on-site registration, so members of
the public who do not register by July 23, 2012 via one of the methods
detailed above will not be able to attend the peer review meeting.
    Required Registration Information: To register for the meeting
online or via post, you must provide your full name, organization or
affiliation, and contact information. You must also indicate which days
you plan to attend the meeting and if you are interested in making an
oral statement during the public comment session on Day 1 of the
meeting. If you register to speak, you must also indicate if you have
any special requirements related to your oral comments (e.g.,
translation).
    If you indicate that you wish to make oral comments, you will be
asked to select one category most closely reflecting the content of
your comments. These comment categories are: (i) Mine scenario and
operational modes; (ii) potential failures and probabilities; (iii)
hydrology; (iv) toxicity; (v) potential effects on Alaska Native
culture; (vi) potential effects on fish; (vii) potential effects on
wildlife; and (viii) other issues. Should more than 100 speakers
register, these categories will be used to ensure that a balance of
substantive science issues relevant to the assessment are heard.

FOR FURTHER INFORMATION CONTACT: Questions regarding logistics or
registration for the external peer review meeting should be directed to
Ms. Brittany Ekstrom, Versar, Inc., 6850 Versar Center, Springfield,
VA, 22151; telephone:<PHONE_NUMBER>; or via email at
<EMAIL_ADDRESS>
SUPPLEMENTARY INFORMATION:

I. Information About the Project

    The EPA conducted this assessment to determine the significance of
Bristol Bay's ecological resources and evaluate the potential impacts
of large-scale mining on these resources. The EPA will use the results
of this assessment to inform the consideration of options consistent
with its role under the Clean Water Act. The assessment is intended to
provide a sound scientific and technical foundation for future decision
making. The Web site that describes the project is www.epa.gov/bristolbay.

II. Information About the Peer Review Panel

    The EPA released the draft assessment for the purposes of public
comment and peer review on May 18, 2012. Consistent with guidelines for
the peer review of highly influential scientific assessments, EPA asked
a contractor (Versar, Inc.) to assemble a panel of experts to evaluate
the draft report. Versar, Inc. evaluated the 68 candidates nominated
during a previous public comment period (February 24, 2012 to March 16,
2012) and sought other experts to complete this peer review panel. The
twelve peer review panel members were made public in EPA's previous
FRN, issued on June 5, 2012. The panelist's names are included below,
with corrections made to account for errors present in the June 5, 2012
FRN:

Mr. David Atkins, Watershed Environmental, LLC.--Expertise in mining
and hydrology.
Mr. Steve Buckley, WHPacific--Expertise in mining and seismology.
Dr. Courtney Carothers, University of Alaska Fairbanks--Expertise in
indigenous Alaskan cultures.
Dr. Dennis Dauble, Washington State University--Expertise in fisheries
biology and wildlife ecology.
Dr. Gordon Reeves, USDA Pacific NW Research Station--Expertise in
fisheries biology and aquatic biology.
Dr. Charles Slaughter, University of Idaho--Expertise in hydrology.
Dr. John Stednick, Colorado State University--Expertise in hydrology
and biogeochemistry.
Dr. Roy Stein, Ohio State University--Expertise in fisheries and
aquatic biology.
Dr. William Stubblefield, Oregon State University--Expertise in aquatic
biology and ecotoxicology.
Dr. Dirk van Zyl, University of British Columbia--Expertise in mining.
Dr. Phyllis Weber Scannell--Expertise in aquatic ecology and
ecotoxicology.
Dr. Paul Whitney--Expertise in wildlife ecology and ecotoxicology.

    Dated: June 29, 2012.
Darrell Winner,
Acting Director, National Center for Environmental Assessment.
[FR Doc. 2012-16441 Filed 7-5-12; 8:45 am]
BILLING CODE 6560-50-P


[Federal Register Volume 80, Number 251 (Thursday, December 31, 2015)]
[Notices]
[Page 81818]
[FR Doc No: 2015-32917]

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

DEPARTMENT OF ENERGY

Federal Energy Regulatory Commission

[Docket No. EL11-66-000]

Martha Coakley, Massachusetts Attorney General; Connecticut
Public Utilities Regulatory Authority; Massachusetts Department of
Public Utilities; New Hampshire Public Utilities Commission;
Connecticut Office of Consumer Counsel; Maine Office of the Public
Advocate; George Jepsen, Connecticut Attorney General; New Hampshire
Office of Consumer Advocate; Rhode Island Division of Public Utilities
and Carriers; Vermont Department of Public Service; Massachusetts
Municipal Wholesale Electric Company; Associated Industries of
Massachusetts; The Energy Consortium; Power Options, Inc.; and the
Industrial Energy Consumer Group, v. Bangor Hydro-Electric Company;
Central Maine Power Company; New England Power Company d/b/a National
Grid; New Hampshire Transmission LLC d/b/a NextEra; NSTAR Electric and
Gas Corporation; Northeast Utilities Service Company; The United
Illuminating Company; Unitil Energy Systems, Inc. and Fitchburg Gas and
Electric Light Company; Vermont Transco, LLC;

Notice of Filing

    Take notice that on December 23, 2015, the New England Transmission
Owners (NETOs) submitted tariff filing per: Refund Report to be
effective N/A, pursuant to the Commission's Opinion No. 531-A, issued
on October 16, 2014.\1\
---------------------------------------------------------------------------

    \1\ Martha Coakley, Mass. Attorney Gen., et al. v. Bangor Hydro-
Elec. Co., et al., Opinion No. 531, 147 FERC ] 61,234 (2014)
(Opinion No. 531), order on paper hearing, Opinion No. 531-A, 149
FERC ] 61,032 (2014) (Opinion No. 531-A).
---------------------------------------------------------------------------

    Any person desiring to intervene or to protest this filing must
file in accordance with Rules 211 and 214 of the Commission's Rules of
Practice and Procedure (18 CFR 385.211, 385.214). Protests will be
considered by the Commission in determining the appropriate action to
be taken, but will not serve to make protestants parties to the
proceeding. Any person wishing to become a party must file a notice of
intervention or motion to intervene, as appropriate. Such notices,
motions, or protests must be filed on or before the comment date.
Anyone filing a motion to intervene or protest must serve a copy of
that document on the Applicant and all the parties in this proceeding.
    The Commission encourages electronic submission of protests and
interventions in lieu of paper using the ``eFiling'' link at http://www.ferc.gov. Persons unable to file electronically should submit an
original and 5 copies of the protest or intervention to the Federal
Energy Regulatory Commission, 888 First Street NE., Washington, DC
20426.
    This filing is accessible on-line at http://www.ferc.gov, using the
``eLibrary'' link and is available for electronic review in the
Commission's Public Reference Room in Washington, DC. There is an
``eSubscription'' link on the Web site that enables subscribers to
receive email notification when a document is added to a subscribed
docket(s). For assistance with any FERC Online service, please email
<EMAIL_ADDRESS>or call<PHONE_NUMBER> (toll free). For
TTY, call<PHONE_NUMBER>.

Comment Date: 5:00 p.m. Eastern Time on January 13, 2016.

    Dated: December 24, 2015.
Nathaniel J. Davis, Sr.,
Deputy Secretary.
[FR Doc. 2015-32917 Filed 12-30-15; 8:45 am]
BILLING CODE 6717-01-P


                       NACAA Consultation Documentation

Memo to Docket Record of EPA consultation with NAACA Permitting Sub-Committee on the renewal of the Information Collection Request (ICR) for 40 CFR part 70 Federal Operating Permit Program (EPA tracking number 1587.15; OMB tracking number 2060-0243.)

Date of Call: June 26, 2015.

Participants:      * EPA:  Juan Santiago, Associate Division Director, Air Quality Policy Division of the Office of Air Quality Planning and Standards (OAQPS); Vera Kornylak, Operating Permits Group (OPG) Leader, OAQPS; Jeff Herring, Environmental Scientist, OPG, OAQPS; Dylan Mataway-Novak, Environmental Specialist, OPG, OAQPS.     * National Association of Clean Air Agencies (NACAA): Permitting Committee Monthly Conference Call Attendees.

Purpose of Call: The EPA participated in a conference call with members from the NACAA permitting sub-committee who joined the call, regarding a previously established agenda topic to consult with the EPA and discuss any comments on the part 70 ICR renewal set to expire on October 31, 2015. At the time of the call, the first part 70 ICR renewal Federal Register notice asking for comments had been issued, and the EPA was seeking input from NACAA before submitting the ICR renewal to OMB for review and final approval.

Comments for NACAA and EPA response

NACAA Comment: Representatives from some of the states and local permitting authorities participating on the committee expressed comments that all the costs of title V did not appear to be included in the ICR. Specific examples given included consideration of monitoring and enforcement costs for emissions standards, the costs of permit renewals and significant modifications, the labor rates assumed for states, ambient monitoring costs, and enforcement related costs. While this was not necessarily the consensus of the members present, there were several state and local representatives who raised this comment.

EPA Response: The EPA provided some background information on the nature and scope of ICRs, including that the ICR is an assessment of the paperwork burdens of the program, rather than of all burdens and costs of the permitting program. The commenters appeared to be under the impression that any activities that a state or local permitting authority would consider for permit fee purposes should also be included in the ICR consideration of program burden and costs. The EPA has issued several prior guidance memoranda on the costs and activities that state and local agencies are required to cover for state permit fee purposes. Some of the activities that commenters suggested should be included in the ICR are not actually part of the ICR consideration, but they are included in title V related considerations. In addition, some activities identified, such as ambient monitoring, source monitoring, enforcement of emissions standards derived from applicable requirements, are covered separately under ICRs for those requirements. In addition, the EPA explained the mathematical nature of the ICR assumptions as averages, variability among permitting authorities, and the data used to develop the information provided in the ICR.

After considering these comments, the EPA will revise the support statement for the part 70 ICR to explain in greater detail the nature of the ICR assessment. This will include explaining that separate ICRs exist for much of the burden that state and local permitting authorities might otherwise attribute to title V.

In light of these comments, the EPA will review the assumptions and analysis in the supporting statement to see if any changes are necessary. As a general matter, revising the burden estimates would typically need to be supported by national data and/or national consensus by the state and local permitting authorities. NACAA expressed an interest in potentially providing such data for the next part 70 ICR renewal in 2018. For the next part 70 ICR renewal in 2018, the EPA will work with NACAA to review the assumptions and analysis for the part 70 ICR.