[Federal Register Volume 68, Number 188 (Monday, September 29, 2003)]
[Rules and Regulations]
[Pages 55833-55849]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 03-24565]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-2003-0058; FRL-7327-9]


Glufosinate Ammonium; Pesticide Tolerance

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes a tolerance for combined residues 
of glufosinate ammonium and its metabolites in or on certain raw 
agricultural commodities. Aventis CropScience USA, now Bayer 
CropScience, and Interregional Research Project Number 4 (IR-4) 
requested these tolerances under the Federal Food, Drug, and Cosmetic 
Act (FFDCA), as amended by the Food Quality Protection Act of 1996 
(FQPA).

DATES: This regulation is effective September 29, 2003. Objections and 
requests for hearings, identified by docket ID number OPP-2003-0058, 
must be received on or before November 28, 2003.

ADDRESSES: Written objections and hearing requests may be submitted 
electronically, by mail, or through hand delivery/courier. Follow the 
detailed instructions as provided in Unit VI. of the SUPPLEMENTARY 
INFORMATION.

FOR FURTHER INFORMATION CONTACT: Joanne I. Miller, Registration 
Division (7505C), Office of Pesticide Programs, Environmental 
Protection Agency, 1200 Pennsylvania Ave., NW.,Washington, DC 20460-
0001; telephone number: 703-305-6224; e-mail address: 
[email protected].

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

    You may be potentially affected by this action if you are an 
agricultural producer, food manufacturer, or pesticide manufacturer. 
Potentially affected categories and entities may include, but are not 
limited to:
    [bull] Crop production (NAICS 111)
    [bull] Animal production (NAICS 112)
    [bull] Food manufacturing (NAICS 311)
    [bull] Pesticide manufacturing (NAICS 32532)
    This listing is not intended to be exhaustive, but rather provides 
a guide for readers regarding entities likely to be affected by this 
action. Other types of entities not listed in the table could also be 
affected. The North American Industrial Classification System (NAICS) 
codes have been provided to assist you and others in determining 
whether or not this action might apply to certain entities. If you have 
questions regarding the applicability of this action to a particular 
entity, consult the person listed under FOR FURTHER INFORMATION 
CONTACT.

B. How Can I Get Copies of this Document and Other Related Information?

    1. Docket. EPA has established an official public docket for this 
action under docket identification (ID) number OPP-2003-0058. The 
official public docket consists of the documents specifically 
referenced in this action, any public comments received, and other 
information related to this action. Although a part of the official 
docket, the public docket does not include Confidential Business 
Information (CBI) or other information whose disclosure is restricted 
by statute. The official public docket is the collection of materials 
that is available for public viewing at the Public Information and 
Records Integrity Branch (PIRIB), Rm. 119, Crystal Mall 2, 
1921 Jefferson Davis Hwy., Arlington, VA. This docket facility is open 
from 8:30 a.m. to 4 p.m., Monday through Friday, excluding legal 
holidays. The docket telephone number is (703) 305-5805.
    2. Electronic access. You may access this Federal Register document 
electronically through the EPA Internet under the ``Federal Register'' 
listings at http://www.epa.gov/fedrgstr/. A frequently updated 
electronic version of 40 CFR part 180 is available at http://www.access.gpo.gov/nara/cfr/cfrhtml_00/Title_40/40cfr180_00.html/, a 
beta site currently under development. To access the OPPTS Harmonized 
Guidelines referenced in this document, go directly to the guidelines 
at http://www.epa.gov/opptsfrs/home/guidelin.htm.
    An electronic version of the public docket is available through 
EPA's electronic public docket and comment system, EPA Dockets. You may 
use EPA Dockets at http://www.epa.gov/edocket/ to submit or view public 
comments, access the index listing of the contents of the official 
public docket, and to access those documents in the public docket that 
are available electronically. Although not all docket materials may be 
available electronically, you may still access any of the publicly 
available docket materials through the docket facility identified in 
Unit I.B.1. Once in the system, select ``search,'' then key in the 
appropriate docket ID number.

II. Background and Statutory Findings

    In the Federal Register of May 19, 2000 (65 FR 31904) (FRL-6558-2), 
EPA issued a notice pursuant to section 408 of FFDCA, 21 U.S.C. 346a, 
as amended by FQPA (Public Law 104-170), announcing the filing of a 
pesticide petition (PP 0F6140) by Aventis CropScience USA, now Bayer 
CropScience, PO Box 12014, 2 T. W. Alexander Drive, Research Triangle 
Park, NC 27709. That notice included a summary of the petition prepared 
by Bayer CropScience, the registrant. There were no comments received 
in response to the notice of filing.
    In the Federal Register of July 24, 2002 (67 FR 48465) (FRL-7184-
6), EPA issued a notice pursuant to section 408 of FFDCA, 21 U.S.C. 
346a, as amended by FQPA (Public Law 104-170), announcing the filing of 
a pesticide petition (PP OF6210) by Aventis CropScience USA, now Bayer 
CropScience, PO Box 12014, 2 T. W. Alexander Drive, Research Triangle 
Park, NC 27709. That notice included a summary of the petition prepared 
by Bayer CropScience, the registrant. Comments on the petition were 
filed by Neil J. Carman, Ph.D. of the Sierra Club

[[Page 55834]]

Genetic Engineering Committee. A response to these comments is provided 
in Unit VI.
    In the Federal Register of August 21, 2002 (67 FR 54196) (FRL-7190-
9), EPA issued a notice pursuant to section 408 of FFDCA, 21 U.S.C. 
346a, as amended by FQPA (Public Law 104-170), announcing the filing of 
a pesticide petition (PP 2E6404) by Interregional Research Project 
Number 4 (IR-4), 681 US Highway 1 South, North Brunswick, NJ 
08902-3390. That notice included a summary of the petition prepared by 
IR-4, the petitioner. There were no comments received in response to 
the notice of filing.
    In the Federal Register of August 15, 2003 (68 FR 48908) (FRL-7322-
9), EPA issued a notice pursuant to section 408 of FFDCA, 21 U.S.C. 
346a, as amended by FQPA (Public Law 104-170), announcing the filing of 
amended pesticide petitions (PP 0F6140 and PP OF6210) by Bayer 
CropScience, PO Box 12014, 2 T. W. Alexander Drive, Research Triangle 
Park, NC 27709. That notice included a summary of the petition prepared 
by Bayer CropScience. Two hundred and sixty five comments were filed. A 
response to these comments is provided in Unit VI.
    The petitions requested that 40 CFR 180.473(a)(1) be amended by 
establishing tolerances for residues of the herbicide glufosinate 
ammonium (butanoic acid, 2-amino-4-(hydroxymethylphosphinyl)-, 
monoammonium salt) and its metabolite, 3-methylphosphinico-propionic 
acid, expressed as 2-amino-4-(hydroxymethylphosphinyl)butanoic acid 
equivalents in or on the raw agricultural commodities derived from 
cotton, undelinted seed at 3.5 parts per million (ppm) and gin 
byproducts at 12.0 ppm; and blueberry, lingonberry, juneberry and salal 
at 0.10 ppm and that 40 CFR 180.473(a)(2) be amended by establishing 
tolerances for residues of the herbicide glufosinate ammonium (butanoic 
acid, 2-amino-4-(hydroxymethylphosphinyl)-, monoammonium salt) and its 
metabolites, 3-methylphosphinico-propionic acid, and 2-acetamido-4-
methylphosphinico-butanoic acid expressed as 2-amino-4-
(hydroxymethylphosphinyl)butanoic acid equivalents in or on the raw 
agricultural commodities derived from transgenic cotton tolerant to 
glufosinate ammonium: undelinted seed at 3.5 ppm and gin byproducts at 
12.0 ppm and transgenic rice tolerant to glufosinate ammonium: grain at 
1.0 ppm, straw at 1.6 ppm.
    IR-4 and Bayer CropScience subsequently amended the petitions to 
request that 40 CFR 180.473(a)(1) be amended by establishing tolerances 
for residues of the herbicide glufosinate ammonium (butanoic acid, 2-
amino-4-(hydroxymethylphosphinyl)-, monoammonium salt) and its 
metabolites, 2-acetamido-4-methylphosphinico-butanoic acid and 3-
methylphosphinico-propionic acid, expressed as 2-amino-4-
(hydroxymethylphosphinyl)butanoic acid equivalents, in or on the 
following food commodities: Bushberry subgroup, lingonberry, juneberry 
and salal at 0.15 ppm, cattle, fat at 0.40 ppm, cattle, meat at 0.15 
ppm, cattle, meat byproducts at 6.0 ppm, cotton, gin byproducts at 15 
ppm, cotton, undelinted seed at 4.0 ppm, egg at 0.15 ppm, goat, fat at 
0.40 ppm, goat, meat at 0.15 ppm, goat, meat byproducts at 6.0 ppm, 
hog, fat at 0.40 ppm, hog, meat at 0.15 ppm, hog, meat byproducts at 
6.0 ppm, horse, fat at 0.40 ppm, horse, meat at 0.15 ppm, horse, meat 
byproducts at 6.0 ppm, Milk at 0.15 ppm, poultry, fat at 0.15 ppm, 
poultry, meat at 0.15 ppm, poultry, meat byproducts 0.6 ppm, sheep, fat 
at 0.40 ppm, sheep, meat at 0.15 ppm, and sheep, meat byproducts at 6.0 
ppm.
    Bayer CropScience subsequently amended the petitions to request 
that 40 CFR 180.473(a)(2) be amended by establishing tolerances for 
residues of the herbicide glufosinate ammonium (butanoic acid, 2-amino-
4-(hydroxymethylphosphinyl)-, monoammonium salt) and its metabolites, 
2-acetamido-4-methylphosphinico-butanoic acid and 3-methylphosphinico-
propionic acid, expressed as 2-amino-4-
(hydroxymethylphosphinyl)butanoic acid equivalents, in or on the 
following raw agricultural and processed commodities derived from 
transgenic cotton and rice that are tolerant to glufosinate ammonium: 
Cotton, gin byproducts at 15 ppm, cotton, undelinted seed at 4.0 ppm, 
rice, grain at 1.0 ppm, rice, straw at 2.0 ppm, and rice, hull at 2.0 
ppm. These amendments were included in the August 15, 2003 notice of 
filing.
    Section 408(b)(2)(A)(i) of the FFDCA allows EPA to establish a 
tolerance (the legal limit for a pesticide chemical residue in or on a 
food) only if EPA determines that the tolerance is ``safe.'' Section 
408(b)(2)(A)(ii) of the FFDCA defines ``safe'' to mean that ``there is 
a reasonable certainty that no harm will result from aggregate exposure 
to the pesticide chemical residue, including all anticipated dietary 
exposures and all other exposures for which there is reliable 
information.'' This includes exposure through drinking water and in 
residential settings, but does not include occupational exposure. 
Section 408(b)(2)(C) of the FFDCA requires EPA to give special 
consideration to exposure of infants and children to the pesticide 
chemical residue in establishing a tolerance and to ``ensure that there 
is a reasonable certainty that no harm will result to infants and 
children from aggregate exposure to the pesticide chemical 
residue....''
    EPA performs a number of analyses to determine the risks from 
aggregate exposure to pesticide residues. For further discussion of the 
regulatory requirements of section 408 of the FFDCA and a complete 
description of the risk assessment process, see the final rule on 
Bifenthrin Pesticide Tolerances (62 FR 62961, November 26, 1997) (FRL-
5754-7).

III. Aggregate Risk Assessment and Determination of Safety

    Consistent with section 408(b)(2)(D) of the FFDCA, EPA has reviewed 
the available scientific data and other relevant information in support 
of this action. EPA has sufficient data to assess the hazards of and to 
make a determination on aggregate exposure, consistent with section 
408(b)(2) of the FFDCA, for a tolerance for combined residues of 
glufosinate ammonium and its metabolites on bushberry subgroup, 
lingonberry, juneberry and salal at 0.15 ppm, cattle, fat at 0.40 ppm, 
cattle, meat at 0.15 ppm, cattle, meat byproducts at 6.0 ppm, cotton, 
gin byproducts at 15 ppm, cotton, undelinted seed at 4.0 ppm, egg at 
0.15 ppm, goat, fat at 0.40 ppm, goat, meat at 0.15 ppm, goat, meat 
byproducts at 6.0 ppm, hog, fat at 0.40 ppm, hog, meat at 0.15 ppm, 
hog, meat byproducts at 6.0 ppm, horse, fat at 0.40 ppm, horse, meat at 
0.15 ppm, horse, meat byproducts at 6.0 ppm, milk at 0.15 ppm, poultry, 
fat at 0.15 ppm, poultry, meat at 0.15 ppm, poultry, meat byproducts at 
0.60 ppm, sheep, fat at 0.40 ppm, sheep, meat at 0.15 ppm, and sheep, 
meat byproducts at 6.0 ppm, cotton, gin byproducts at 15 ppm, rice, 
grain at 1.0 ppm, rice, straw at 2.0 ppm, and rice, hull at 2.0 ppm. 
EPA's assessment of exposures and risks associated with establishing 
the tolerance follows.

A. Toxicological Profile

    EPA has evaluated the available toxicity data and considered its 
validity, completeness, and reliability as well as the relationship of 
the results of the studies to human risk. EPA has also considered 
available information concerning the variability of the sensitivities 
of major identifiable subgroups of consumers, including infants and 
children. The nature of the

[[Page 55835]]

toxic effects caused by glufosinate ammonium and its metabolites are 
discussed in Tables 1, 2 and 3 of this unit as well as the no-observed-
adverse-effect-level (NOAEL) and the lowest-observed-adverse-effect-
level (LOAEL) from the toxicity studies reviewed.

  Table 1.--Glufosiante-ammonium: Acute, Subchronic, Chronic, and Other
                                Toxicity
------------------------------------------------------------------------
         Guideline No.              Study Type            Results
------------------------------------------------------------------------
81-1                            Acute oral         LD50 = 4,010 mg/kg
                                                    (milligram/kilogram)
                                                    in males
                                                   LD50 = 3,030 mg/kg in
                                                    females
------------------------------------------------------------------------
870.3100                        90-Day oral        NOAEL = 6.2-8.8 mg/kg/
                                 toxicity in rats   day in males
                                 (males only)      LOAEL = 64-90 mg/kg/
                                                    day in males, based
                                                    on glutamine
                                                    synthetase
                                                    inhibition in the
                                                    brains
------------------------------------------------------------------------
870.3100                        N-acetyl-L-        NOAEL = 65-90 mg/kg/
                                 glufosinate        day in males
                                 disodium          LOAEL = 657-935 mg/kg/
                                90-Day oral         day in males, based
                                 toxicity in rats   on glutamine
                                 (males only).      synthetase
                                                    inhibition in the
                                                    brains
------------------------------------------------------------------------
870.3100                        90-Day oral        NOAEL = 48 mg/kg/day
                                 toxicity in        in males, 192 mg/kg/
                                 mouse              day in females
                                                    Highest Dose Tested
                                                    (HDT)
                                                   LOAEL = 192 mg/kg/day
                                                    in males based on
                                                    the changes in
                                                    clinical
                                                    biochemistry and
                                                    liver weights in
                                                    males
------------------------------------------------------------------------
870.3200                        21/28-Day dermal   NOAEL = 100 mg/kg/day
                                 toxicity in rat   LOAEL = 300 mg/kg/day
                                                    based on clinical
                                                    observations
                                                    (aggressive
                                                    behavior,
                                                    piloerection, and a
                                                    high startle
                                                    response)
------------------------------------------------------------------------
870.3700                        Prenatal           Maternal: NOAEL = 10
                                 developmental in   mg/kg/day
                                 rats (three       LOAEL = 50 mg/kg/day
                                 studies            based on vaginal
                                 combined)          bleeding and
                                                    hyperactivity
                                                   Developmental: NOAEL
                                                    = 50 mg/kg/day
                                                   LOAEL =250 mg/kg/day
                                                    based on dilated
                                                    renal pelvis
------------------------------------------------------------------------
870.3700                        Prenatal           Maternal: NOAEL = 6.3
                                 developmental in   mg/kg/day
                                 rabbit            LOAEL = 20.0 mg/kg/
                                                    day based on reduced
                                                    food consumption,
                                                    body weight and
                                                    weight gains
                                                   Developmental: NOAEL
                                                    = 6.3 mg/kg/day
                                                   LOAEL = 20.0 based on
                                                    decreased body
                                                    weights and fetal
                                                    death
------------------------------------------------------------------------
870.3800                        Reproduction and   Parental/Systemic
                                 fertility          NOAEL = 18.0 mg/kg/
                                 effects in rat     day (HDT)
                                                   LOAEL = not
                                                    established
                                                   Reproductive NOAEL =
                                                    6.0 mg/kg/day
                                                   LOAEL = 18.0 mg/kg/
                                                    day based on
                                                    decreased number of
                                                    viable pups
                                                   Offspring NOAEL = 6.0
                                                    mg/kg/day
                                                   LOAEL = 18.0 mg/kg/
                                                    day based on
                                                    decreased number of
                                                    viable pups
------------------------------------------------------------------------
870.4100                        Chronic toxicity   NOAEL = 5.0 mg/kg/day
                                 in dogs           LOAEL = 8.5 mg/kg/day
                                                    based on mortality
                                                    (week 2) and
                                                    alterations in the
                                                    electrocardiogram at
                                                    6 months
------------------------------------------------------------------------
870.4200                        Carcinogenicity    NOAEL = 45.4 mg/kg/
                                 in rats            day in males, 57.1
                                                    mg/kg/day in females
                                                   LOAEL = 228.9 mg/kg/
                                                    day in males and
                                                    281.5 based on
                                                    increased incidences
                                                    of retinal atrophy.
                                                   No evidence of
                                                    carcinogenicity
------------------------------------------------------------------------
870.4300                        Chronic Feeding /  NOAEL = 24.4 mg/kg/
                                 Carcinogenicity    day in males, 8.2 mg/
                                 in rats            kg/day in females
                                                   LOAEL = not achieved
                                                    in males and 28.7
                                                    based on inhibition
                                                    of brain glutamate
                                                    synthetase in
                                                    females at 130 weeks
                                                   No evidence of
                                                    carcinogenicity
------------------------------------------------------------------------
870.4300                        Carcinogenicity    NOAEL = 10.82 mg/kg/
                                 mice               day in males, 16.19
                                                    mg/kg/day in females
                                                   LOAEL = 22.60 mg/kg/
                                                    day in males, 63.96
                                                    mg/kg/day in females
                                                    based on increased
                                                    mortality and
                                                    glucose levels and
                                                    consistent changes
                                                    in glutathione
                                                    levels in males,
                                                    increased glucose
                                                    levels and decreased
                                                    albumin and total
                                                    proteins
                                                   No evidence of
                                                    carcinogenicity
------------------------------------------------------------------------
870.5265                        Reverse Mutation   Glufosinate ammonium
                                 Assay              failed to cause
                                                    reverse mutations in
                                                    bacteria with and
                                                    without metabolic
                                                    activation.
------------------------------------------------------------------------
870.5300                        Detection of gene  Glufosinate ammonium
                                 mutations in       did not increase the
                                 somatic cells in   mutation frequency
                                 culture            at the thymidine
                                                    kinase locus
------------------------------------------------------------------------
870.5395                        In vivo mammalian  The results indicated
                                 cytogenetic        glufosinate ammonium
                                 tests              had no effect on
                                                    micronucleus
                                                    formation
------------------------------------------------------------------------

[[Page 55836]]

 
870.5500                        Bacterial DNA      glufosinate ammonium
                                 damage or repair   failed to cause
                                 test               damage to DNA that
                                                    could be detected by
                                                    this repair assay
------------------------------------------------------------------------
870.5550                        Unscheduled DNA    There was no evidence
                                 synthesis in       that unscheduled DNA
                                 mammalian cells    synthesis was
                                 in culture         induced by
                                                    glufosinate
                                                    ammonium.
------------------------------------------------------------------------
870.6200                        Acute              NOAEL = 500 mg/kg in
                                 neurotoxicity in   males and females
                                 rat (2 studies)    (HDT)
                                                   LOAEL = Not
                                                    established in both
                                                    sexes
------------------------------------------------------------------------
870.6200                        Repeat Dose        NOAEL = 1.5 mg/kg/day
                                 Neurotoxicity in   in males, 1.8 mg/kg/
                                 rat                day in females
                                                   LOAEL = 14.9 mg/kg/
                                                    day in males, 17.1
                                                    mg/kg/day in
                                                    females, based on
                                                    the inhibition of
                                                    glutamate synthetase
                                                    in the brain
------------------------------------------------------------------------
870.7485                        Metabolism and     The majority of the
                                 pharmacokinetics   radioactivity (95-
                                 in rat             98% of the dose) was
                                                    eliminated during
                                                    the first 24 hrs
                                                    after dosing. The
                                                    parent compound,
                                                    glufosinate
                                                    ammonium, accounted
                                                    for most of the
                                                    eliminated
                                                    radioactivity in the
                                                    urine and feces of
                                                    both males (80% of
                                                    the dose) and
                                                    females (73% of the
                                                    dose). The
                                                    metabolite, 3-
                                                    methylphosphinico-
                                                    propionic acid, was
                                                    consistently found
                                                    in both urine and
                                                    feces of both sexes.
------------------------------------------------------------------------
870.7485                        Metabolism and     The majority of the
                                 pharmacokinetics   radioactivity was
                                 in rat             eliminated during
                                                    the first 24 to 48
                                                    hrs after dosing.
                                                    The parent compound,
                                                    glufosinate
                                                    ammonium, accounted
                                                    for the majority of
                                                    the radioactivity
                                                    eliminated in the
                                                    excreta of both
                                                    males ([]80% of
                                                    the dose) and
                                                    females (88% of the
                                                    dose). The
                                                    metabolite, 3-
                                                    methylphosphinico-
                                                    propionic acid, was
                                                    consistently found
                                                    in both urine (0.22-
                                                    1.20% of the dose)
                                                    and feces (0.44-
                                                    1.36% of the dose)
                                                    of both sexes. 2-
                                                    acetamido-4-
                                                    methylphosphinico-
                                                    butanoic acid was
                                                    found in feces (0.28-
                                                    1.72% of the dose)
                                                    of both male and
                                                    female rats and
                                                    barely above or at
                                                    the level of the
                                                    detection in the
                                                    urine of both sexes
                                                    (0.02-0.04% of the
                                                    dose). Very little
                                                    if any of
                                                    administered
                                                    glufosinate ammonium
                                                    was sequestered in
                                                    any tissues
                                                    examined.
------------------------------------------------------------------------
870.7485                        Metabolism and     The major route of
                                 pharmacokinetics   excretion was via
                                 in rat             feces (88% and 84%
                                                    of the administered
                                                    radioactivity for
                                                    males and females,
                                                    respectively).
                                                    Within 7 days of
                                                    post dosing, greater
                                                    than 94% of the dose
                                                    was eliminated.
                                                    Kinetics analysis
                                                    indicated that the
                                                    process of excretion
                                                    was a two-phase
                                                    process. The tissue
                                                    radioactivity level
                                                    for kidneys, liver
                                                    and gonads was just
                                                    above the background
                                                    level.
------------------------------------------------------------------------
870.7485                        Metabolism and     The majority of the
                                 pharmacokinetics   radioactivity was
                                 in rat             excreted within 24
                                                    hrs after the last
                                                    dose. The major
                                                    route of elimination
                                                    was via feces. There
                                                    was also a two-
                                                    phased elimination
                                                    process. More
                                                    radioactivity was
                                                    found in the tissues
                                                    of animals dosed
                                                    repeatedly than that
                                                    of animals receiving
                                                    a single dose.
------------------------------------------------------------------------
870.7600                        Dermal             The results indicate
                                 penetration        that at the low dose
                                                    (0.1 mg) 42.5 to
                                                    50.8% of the applied
                                                    radioactivity was
                                                    absorbed whereas at
                                                    the high dose (10
                                                    mg) 26% was
                                                    absorbed. After
                                                    removal and washing
                                                    of the treated skin
                                                    a substantial amount
                                                    of the radioactivity
                                                    still remained in
                                                    the skin, and it was
                                                    gradually absorbed
                                                    and eliminated.
                                                    Radioactivity was
                                                    found in both feces
                                                    and urine samples,
                                                    but the majority of
                                                    glufosinate ammonium
                                                    was eliminated in
                                                    the urine. In all
                                                    organs/tissues
                                                    examined,
                                                    radioactivity was
                                                    found to reach a
                                                    maximum level either
                                                    at 4 or 10 hrs after
                                                    exposure.
                                                    Subsequently, the
                                                    radioactivity
                                                    dropped rapidly. The
                                                    amount of
                                                    radioactivity found
                                                    in the brain was
                                                    very minimal
                                                    relative to that of
                                                    kidneys and liver.
------------------------------------------------------------------------


    Table 2.--3-Methylphosphinico-propionic Acid: Subchronic Toxicity
------------------------------------------------------------------------
          Guideline No.               Study Type            Results
------------------------------------------------------------------------
870.3100                          90-Day dermal       NOAEL = 102 mg/kg/
                                   toxicity in rats    day in males, 113
                                                       mg/kg/day in
                                                       females
                                                      LOAEL = 420 mg/kg/
                                                       day in males, 439
                                                       mg/kg/day in
                                                       females based on
                                                       increased
                                                       reticulocytes and
                                                       increased
                                                       absolute and
                                                       relative liver
                                                       weights in males
------------------------------------------------------------------------
870.3100                          90-Day dermal       NOAEL = 1,121 mg/
                                   toxicity in mice    kg/day in males,
                                                       1,340 mg/kg/day
                                                       in females
                                                      LOAEL = Not
                                                       established
------------------------------------------------------------------------

[[Page 55837]]

 
870.3700                          Prenatal            Maternal: NOAEL =
                                   developmental in    300 mg/kg/day
                                   rodents in rats    Maternal: LOAEL =
                                                       900 mg/kg/day
                                                       based on one
                                                       death and
                                                       clinical findings
                                                       (persistent
                                                       piloerection and/
                                                       or increased
                                                       urinary output)
                                                      Developmental:
                                                       NOAEL = 300 mg/kg/
                                                       day
                                                      Developmental:
                                                       LOAEL = 900 mg/kg/
                                                       day based on
                                                       increases in the
                                                       incidences of
                                                       total litter loss
                                                       and in the fetal
                                                       and litter
                                                       incidences of
                                                       wavy and/or
                                                       thickened ribs.
------------------------------------------------------------------------
870.3700                          Prenatal            Maternal: NOAEL =
                                   developmental in    50 mg/kg/day
                                   rabbits            Maternal: LOAEL =
                                                       100 mg/kg/day
                                                       based on
                                                       increased
                                                       abortions,
                                                       mortality, and
                                                       reductions in
                                                       food and water
                                                       consumption, body
                                                       weight gain, and
                                                       fecal output
                                                      Developmental:
                                                       NOAEL = 200 mg/kg/
                                                       day
                                                      Developmental:
                                                       LOAEL = Not
                                                       observed
------------------------------------------------------------------------


     Table 3.--Metabolite, 2-acetomido-4-methylphosphinico-butanoic:
                      Subchronic and Other Toxicity
------------------------------------------------------------------------
         Guideline No.              Study Type            Results
------------------------------------------------------------------------
870.3100                        90-Day oral        NOAEL = 147 mg/kg/day
                                 toxicity rodents   in males, 162 mg/kg/
                                 in rats            day in females
                                                   LOAEL = 738 mg/kg/day
                                                    in males, 800 mg/kg/
                                                    day in females based
                                                    on glutamine
                                                    synthetase
                                                    inhibition in the
                                                    brain
------------------------------------------------------------------------
870.3100                        90-Day oral        NOAEL = Not
                                 toxicity rodents   established for
                                 in mice            males, 110 mg/kg/day
                                                    in females
                                                   LOAEL = 83 mg/kg/day
                                                    in males, 436 mg/kg/
                                                    day in females based
                                                    on glutamine
                                                    synthetase
                                                    inhibition in the
                                                    brain
------------------------------------------------------------------------
870.3150                        Subchronic         NOAEL = 19 mg/kg/day
                                 Nonrodent Oral     in males, 21 mg/kg/
                                 Toxicity in dogs   day in females
                                                   LOAEL = 72 mg/kg/day
                                                    in males, 79 mg/kg/
                                                    day in females based
                                                    on glutamine
                                                    synthetase
                                                    inhibition in the
                                                    brain
------------------------------------------------------------------------
870.3700                        Prenatal           Maternal: NOAEL =
                                 developmental in   1,000 mg/kg/day
                                 rodents-rat       Maternal: LOAEL = Not
                                                    observed
                                                   Developmental: NOAEL
                                                    = 1,000 mg/kg/day
                                                   Developmental: LOAEL
                                                    = Not observed
------------------------------------------------------------------------
870.3700                        Prenatal           Maternal: NOAEL = 64
                                 developmental in   mg/kg/day
                                 rabbits           Maternal: LOAEL = 160
                                                    mg/kg/day based on
                                                    reduced feed
                                                    consumption
                                                   Developmental: NOAEL
                                                    = 64 mg/kg/day
                                                   Developmental: LOAEL
                                                    = 160 based on uni-
                                                    or bilateral extra
                                                    at the 13th thoracic
                                                    vertebra
------------------------------------------------------------------------
870.6200                        Acute              NOAEL = 1,000 mg/kg
                                 Neurotoxicity in   in males and females
                                 rats              LOAEL = 2,000 mg/kg
                                                    in males and females
                                                    based on clinical
                                                    signs of toxicity
                                                    including sedation,
                                                    ruffled fur, and
                                                    diarrhea
------------------------------------------------------------------------
870.6200                        Acute              NOAEL = 100 mg/kg in
                                 Neurotoxicity in   males and females
                                 rats              LOAEL = 1,000 mg/kg
                                                    in males and females
                                                    based on decreased
                                                    body weight gain
------------------------------------------------------------------------
870.6200                        Repeat Dose        NOAEL = 158.9 mg/kg/
                                 Neurotoxicity in   day in males, 179.4
                                 rats               mg/kg/day in females
                                                   LOAEL = Not
                                                    established in males
                                                    and females
------------------------------------------------------------------------

B. Toxicological Endpoints

    The dose at which no adverse effects are observed (the NOAEL) from 
the toxicology study identified as appropriate for use in risk 
assessment is used to estimate the toxicological level of concern 
(LOC). However, the lowest dose at which adverse effects of concern are 
identified (the LOAEL) is sometimes used for risk assessment if no 
NOAEL was achieved in the toxicology study selected. An uncertainty 
factor (UF) is applied to reflect uncertainties inherent in the 
extrapolation from laboratory animal data to humans and in the 
variations in sensitivity among members of the human population as well 
as other unknowns. An UF of 100 is routinely used, 10X to account for 
interspecies differences and 10X for intraspecies differences. A 10x 
data base uncertainty factor, due to the lack of a developmental 
neurotoxicity study, was applied to all dietary and residential dermal, 
inhalation, and incidental oral exposure assessments. For residential 
inhalation exposure assessments an additional 10x data base uncertainty 
factor was applied due to the lack of an adequate inhalation study and 
high concern for exposure via the inhalation route (10,000). Agency 
policy limits the total uncertainty factor applied for any particular 
chemical to no more than 3,000 (see EPA report ``A Review of the 
Reference Dose and Reference Concentration Processes:'' EPA/630/P-02/
022F, December 2002; a Notice of Availability of the Final Report was 
published in the Federal Register of

[[Page 55838]]

May 21, 2003 (68 FR 27805) (FRL-7501-8).
    For dietary risk assessment (other than cancer) the Agency uses the 
UF to calculate an acute or chronic reference dose (acute RfD or 
chronic RfD) where the RfD is equal to the NOAEL divided by the 
appropriate UF (RfD = NOAEL/UF). Where an additional safety factors 
(SF) is retained due to concerns unique to the FQPA, this additional 
factor is applied to the RfD by dividing the RfD by such additional 
factor. The acute or chronic Population Adjusted Dose (aPAD or cPAD) is 
a modification of the RfD to accommodate this type of FQPA SF.
    For non-dietary risk assessments (other than cancer) the UF is used 
to determine the LOC. For example, when 100 is the appropriate UF (10X 
to account for interspecies differences and 10X for intraspecies 
differences) the LOC is 100. To estimate risk, a ratio of the NOAEL to 
exposures (margin of exposure (MOE) = NOAEL/exposure) is calculated and 
compared to the LOC.
    The linear default risk methodology (Q*) is the primary method 
currently used by the Agency to quantify carcinogenic risk. The Q* 
approach assumes that any amount of exposure will lead to some degree 
of cancer risk. A Q* is calculated and used to estimate risk which 
represents a probability of occurrence of additional cancer cases 
(e.g., risk is expressed as 1 x 10-6 or one in a million). 
Under certain specific circumstances, MOE calculations will be used for 
the carcinogenic risk assessment. In this non-linear approach, a 
``point of departure'' is identified below which carcinogenic effects 
are not expected. The point of departure is typically a NOAEL based on 
an endpoint related to cancer effects though it may be a different 
value derived from the dose response curve. To estimate risk, a ratio 
of the point of departure to exposure (MOEcancer = point of 
departure/exposures) is calculated. A summary of the toxicological 
endpoints for glufosinate ammonium and its metabolite used for human 
risk assessment is shown in Table 4 of this unit:

  Table 4.--Summary of Toxicological Dose and Endpoints for Glufosinate ammonium and its Metabolites for Use in
                                              Human Risk Assessment
----------------------------------------------------------------------------------------------------------------
                                                                 FQPA SF* and Level of
          Exposure Scenario               Dose Used in Risk         Concern for Risk     Study and Toxicological
                                            Assessment, UF             Assessment                Effects
----------------------------------------------------------------------------------------------------------------
Acute Dietary (Females 13-50 years of  NOAEL = 6.3 mg/kg/day    FQPA SF = 1              Prenatal Developmental
 age)                                  UF = 1,000.............  aPAD = acute RfD / FQPA   Toxicity Study in non-
                                       Acute RfD = 0.0063 mg/    SF = 0.0063 mg/kg/day.   rodents - rabbit
                                        kg/day.                                          LOAEL = 20.0 mg/kg/day
                                                                                          based on decreased
                                                                                          body weights and fetal
                                                                                          death
-----------------------------------------------------------------------------------------
Chronic Dietary (All populations)      NOAEL = 6.0 mg/kg/day    FQPA SF = 1 cPAD =       ``Weight-of-evidence''
                                       UF = 1,000.............   chronic RfD / FQPA SF    approach from several
                                       Chronic RfD = 0.006 mg/   = 0.006 mg/kg/day        studies; NOAEL = 6.0
                                        kg/day.                                           mg/kg/day; brain
                                                                                          glutamine synthetase
                                                                                          inhibition and
                                                                                          alterations in the
                                                                                          electrocardiogram.
-----------------------------------------------------------------------------------------
Short-Term Dermal (1 to 30 days)       Oral study NOAEL = 6.3   LOC for MOE = 1,000      Prenatal Developmental
 (Residential)                          mg/kg/day (dermal        (Residential)            Toxicity Study in non-
                                        absorption rate = 50%)                            rodents - rabbits
                                                                                         LOAEL = 20 mg/kg/day
                                                                                          based on reduced fetal
                                                                                          body weights,
                                                                                          increased fetal
                                                                                          mortality, reduced
                                                                                          food consumption, body
                                                                                          weight, and body
                                                                                          weight gain
-----------------------------------------------------------------------------------------
Short-Term Inhalation (1 to 30 days)   Oral study NOAEL = 6.3   LOC for MOE = 3,000      Prenatal Developmental
 (Residential)                          mg/kg/day (inhalation    (Residential)            Toxicity Study in non-
                                        absorption rate =                                 rodents - rabbits
                                        100%)                                            LOAEL = 20 mg/kg/day
                                                                                          based on reduced fetal
                                                                                          body weights,
                                                                                          increased fetal
                                                                                          mortality, reduced
                                                                                          food consumption, body
                                                                                          weight, and body
                                                                                          weight gain
----------------------------------------------------------------------------------------------------------------
*The reference to the FQPA SF refers to any additional SF retained due to concerns unique to the FQPA.

C. Exposure Assessment

    1. Dietary exposure from food and feed uses. Tolerances have been 
established (40 CFR 180.473) for the combined residues of glufosinate 
ammonium and its metabolites, in or on almond hulls, apples, bananas, 
meat, milk, fat, meat byproducts, eggs, grapes, potatoes, tree nuts and 
food commodities derived from transgenic canola, transgenic field corn, 
transgenic soybean and transgenic sugar beets. Risk assessments were 
conducted by EPA to assess dietary exposures from combined residues of 
glufosinate ammonium and its metabolites as follows:
    i. Acute exposure. Acute dietary risk assessments are performed for 
a food-use pesticide if a toxicological study has indicated the 
possibility of an effect of concern occurring as a result of a one day 
or single exposure. The Dietary Exposure Evaluation Model-Food 
Consumption Intake Database (DEEM-FCID[reg]) analysis 
evaluated the individual food consumption as reported by respondents in 
the USDA 1994-1996 and 1998 nationwide Continuing Surveys of Food 
Intake by Individuals (CSFII) and accumulated exposure to the chemical 
for each commodity. The following assumptions were made for the acute 
exposure assessments: 100% crop treated for all registered and proposed 
commodities (Tier 1 analysis) and, depending on the level of blending 
of a commodity, tolerance level residues, highest field trial, or 
average field trial.
    ii. Chronic exposure. In conducting this chronic dietary risk 
assessment the DEEM-FCID[reg] analysis evaluated the 
individual food consumption as reported by respondents in the USDA 
1994-1996 and 1998 nationwide CSFII and accumulated exposure to the 
chemical for each commodity. The following assumptions were made for 
the chronic exposure assessments: 100% crop treated for all registered 
and proposed commodities (Tier 1 analysis) excluding apple, canola, 
corn and grape, where 3 year weighted average percent crop treated was 
used, and, depending

[[Page 55839]]

on the level of blending of a commodity, tolerance level residues or 
average field trial.
    iii. Cancer. No evidence of carcinogenicity at doses tested were 
observed in the mouse and rat carcinogenicity studies. A quantitative 
cancer risk assessment was not performed for glufosinate ammonium.
    iv. Anticipated residue and percent crop treated (PCT) information. 
Section 408(b)(2)(F) of the FFDCA states that the Agency may use data 
on the actual percent of food treated for assessing chronic dietary 
risk only if the Agency can make the following findings: Condition 1, 
that the data used are reliable and provide a valid basis to show what 
percentage of the food derived from such crop is likely to contain such 
pesticide residue; Condition 2, that the exposure estimate does not 
underestimate exposure for any significant subpopulation group; and 
Condition 3, if data are available on pesticide use and food 
consumption in a particular area, the exposure estimate does not 
understate exposure for the population in such area. In addition, the 
Agency must provide for periodic evaluation of any estimates used. To 
provide for the periodic evaluation of the estimate of PCT as required 
by section 408(b)(2)(F) of the FFDCA, EPA may require registrants to 
submit data on PCT.
    The Agency believes that the three conditions listed in Unit IV. 
have been met. With respect to Condition 1, PCT estimates are derived 
from Federal and private market survey data, which are reliable and 
have a valid basis. EPA uses a weighted average PCT for chronic dietary 
exposure estimates. This weighted average PCT figure is derived by 
averaging State-level data for a period of up to 3 years, and weighting 
for the more robust and recent data. A weighted average of the PCT 
reasonably represents a person's dietary exposure over a lifetime, and 
is unlikely to underestimate exposure to an individual because of the 
fact that pesticide use patterns (both regionally and nationally) tend 
to change continuously over time, such that an individual is unlikely 
to be exposed to more than the average PCT over a lifetime. For acute 
dietary exposure estimates, EPA uses an estimated maximum PCT. The 
exposure estimates resulting from this approach reasonably represent 
the highest levels to which an individual could be exposed, and are 
unlikely to underestimate an individual's acute dietary exposure. The 
Agency is reasonably certain that the percentage of the food treated is 
not likely to be an underestimation. As to Conditions 2 and 3, regional 
consumption information and consumption information for significant 
subpopulations is taken into account through EPA's computer-based model 
for evaluating the exposure of significant subpopulations, including 
several regional groups. Use of this consumption information in EPA's 
risk assessment process ensures that EPA's exposure estimate does not 
understate exposure for any significant subpopulation group and allows 
the Agency to be reasonably certain that no regional population is 
exposed to residue levels higher than those estimated by the Agency. 
Other than the data available through national food consumption 
surveys, EPA does not have available information on the regional 
consumption of food to which glufosinate ammonium may be applied in a 
particular area.
    2. Dietary exposure from drinking water. The Agency lacks 
sufficient monitoring exposure data to complete a comprehensive dietary 
exposure analysis and risk assessment for glufosinate ammonium in 
drinking water. Because the Agency does not have comprehensive 
monitoring data, drinking water concentration estimates are made by 
reliance on simulation or modeling taking into account data on the 
physical characteristics of glufosinate ammonium. Based on 
environmental fate data the residues of concern in drinking water are 
glufosinate ammonium, 3-methylphosphinico-propionic acid, 2-
methylphosphinico-acetic acid and N-acetyl-glufosinate.
    The Agency uses the First Index Reservoir Screening Tool (FIRST) or 
the Pesticide Root Zone/Exposure Analysis Modeling System (PRZM/EXAMS), 
to produce estimates of pesticide concentrations in an index reservoir. 
The SCI-GROW model is used to predict pesticide concentrations in 
shallow groundwater. For a screening-level assessment for surface water 
EPA will use FIRST (a tier 1 model) before using PRZM/EXAMS (a tier 2 
model). The FIRST model is a subset of the PRZM/EXAMS model that uses a 
specific high-end runoff scenario for pesticides. While both FIRST and 
PRZM/EXAMS incorporate an index reservoir environment, the PRZM/EXAMS 
model includes a percent crop area factor as an adjustment to account 
for the maximum percent crop coverage within a watershed or drainage 
basin.
    None of these models include consideration of the impact processing 
(mixing, dilution, or treatment) of raw water for distribution as 
drinking water would likely have on the removal of pesticides from the 
source water. The primary use of these models by the Agency at this 
stage is to provide a coarse screen for sorting out pesticides for 
which it is highly unlikely that drinking water concentrations would 
ever exceed human health levels of concern.
    Since the models used are considered to be screening tools in the 
risk assessment process, the Agency does not use estimated 
environmental concentrations (EECs) from these models to quantify 
drinking water exposure and risk as a %RfD or %PAD. Instead, drinking 
water levels of comparison (DWLOCs) are calculated and used as a point 
of comparison against the model estimates of a pesticide's 
concentration in water. DWLOCs are theoretical upper limits on a 
pesticide's concentration in drinking water in light of total aggregate 
exposure to a pesticide in food, and from residential uses. Since 
DWLOCs address total aggregate exposure to glufosinate ammonium they 
are further discussed in the aggregate risk sections in Unit III.E.
    Based on the PRZM-EXAMS and SCI-GROW models the EECs of glufosinate 
ammonium and its degradates for acute exposures are estimated to be 94 
[mu]g/liter for surface water and 9 [mu]g/liter for ground water. The 
EECs for chronic exposures are estimated to be 43 [mu]g/liter for 
surface water and 9 [mu]g/liter for ground water.
    3. The term ``residential exposure'' is used in this document to 
refer to non-occupational, non-dietary exposure (e.g., for lawn and 
garden pest control, indoor pest control, termiticides, and flea and 
tick control on pets).
    Glufosinate ammonium is currently registered for use on the 
following residential non-dietary sites: Home use for spot treatment of 
weeds, grass, bushes and vines. The risk assessment was conducted using 
the following residential exposure assumptions: Application rate of 
0.0312 lb active ingredient (ai) per 1,000 ft2, dermal unit 
exposure of 11 mg/lb and inhalation exposure of 0.016 mg/lb from hose 
end application and dermal unit exposure of 56 mg/lb and inhalation 
exposure of 0.0065 mg/lb from low pressure hand wand application.
    4. Cumulative exposure to substances with a common mechanism of 
toxicity. Section 408(b)(2)(D)(v) of the FFDCA requires that, when 
considering whether to establish, modify, or revoke a tolerance, the 
Agency consider ``available information'' concerning the cumulative 
effects of a particular pesticide's residues and ``other substances 
that have a common mechanism of toxicity.''

[[Page 55840]]

    EPA does not have, at this time, available data to determine 
whether glufosinate ammonium has a common mechanism of toxicity with 
other substances. Unlike other pesticides for which EPA has followed a 
cumulative risk approach based on a common mechanism of toxicity, EPA 
has not made a common mechanism of toxicity finding for glufosinate 
ammonium and any other substances and glufosinate ammonium does not 
appear to produce a toxic metabolite produced by other substances. For 
the purposes of this tolerance action; therefore, EPA has not assumed 
that glufosinate ammonium has a common mechanism of toxicity with other 
substances. For information regarding EPA's efforts to determine which 
chemicals have a common mechanism of toxicity and to evaluate the 
cumulative effects of such chemicals, see the policy statements 
released by EPA's Office of Pesticide Programs concerning common 
mechanism determinations and procedures for cumulating effects from 
substances found to have a common mechanism on EPA's website at http://www.epa.gov/pesticides/cumulative/.

D. Safety Factor for Infants and Children

    1. In general. Section 408 of the FFDCA provides that EPA shall 
apply an additional tenfold margin of safety for infants and children 
in the case of threshold effects to account for prenatal and postnatal 
toxicity and the completeness of the data base on toxicity and exposure 
unless EPA determines that a different margin of safety will be safe 
for infants and children. Margins of safety are incorporated into EPA 
risk assessments either directly through use of a MOE analysis or 
through using uncertainty (safety) factors in calculating a dose level 
that poses no appreciable risk to humans.
    2. Prenatal and postnatal sensitivity. The studies examining 
prenatal and postnatal toxicity showed:
    a. No quantitative or qualitative evidence of increased 
susceptibility following in utero exposure in the prenatal 
developmental study in rats.
    b. Qualitative evidence of increased susceptibility in the prenatal 
developmental study in rabbits and quantitative evidence of increased 
susceptibility in the 2-generation reproduction study in rats. In this 
study, a decrease in the number of viable pups was observed in the 
absence of parental toxicity at any dose.
    Since there is qualitative evidence of increased susceptibility of 
the young following exposure to glufosinate ammonium, EPA performed a 
degree of concern analysis to: Determine the level of concern for the 
effects observed when considered in the context of all available 
toxicity data; and identify any residual uncertainties after 
establishing toxicity endpoints and traditional uncertainty factors to 
be used in the risk assessment of this chemical. In the rabbit 
developmental study the degree of concern observed as low noting that 
the fetal effects of concern occurred only at the highest dose tested 
and that a clear NOAEL for effects was established. In the 2-generation 
reproduction study the degree of concern for the effects observed as 
low noting that clear NOAELs and LOAELs were identified for the 
offspring effects of concern and the dose-response well-characterized.
    3. Conclusion. There is not an adequate toxicity data base for 
glufosinate ammonium and its metabolites although the exposure data are 
complete or are estimated based on data that reasonably account for 
potential exposures. EPA identified the following data gaps:
    a. Acute neurotoxicity study conducted in the rat which includes 
glutamine synthetase activity measurement in the liver, kidneys, and 
brain.
    b. A developmental neurotoxicity (DNT) study conducted in the rat 
which includes comparative glutamine synthetase activity measurement in 
the liver, kidneys, and brain of the pups and mothers.
    c. A 28-day inhalation toxicity study in rats with glutamine 
synthetase activity measurements in brain, kidney, liver and lung.
    EPA is also requesting additional data to confirm that liver and 
kidney changes, observed in the absence of histopathological changes, 
are an adaptive response and not an adverse effect. These studies are 
required because the glutamine synthetase measurements are not 
available in young and adult animals. Therefore, EPA has applied 
additional data base uncertainty factors in this risk assessment. The 
results of these studies are expected to eliminate any uncertainty that 
may be associated in characterizing the toxicity of glufosinate 
ammonium.
    For dietary risk assessment, an FQPA additional 10X safety factor, 
retained as a data base uncertainty factor due to the lack of a 
developmental neurotoxicity (DNT) study that measures glutamine 
synthetase activity in the young and adult animals, was applied to all 
dietary and residential dermal, inhalation, and incidental oral 
exposure assessments. For residential inhalation exposure assessments 
an additional 10x data base uncertainty factor was applied due to the 
lack of an adequate inhalation study and high concern for exposure via 
the inhalation route with a total uncertainty factor of 3,000 applied 
based on EPA policy cited in Unit III.B.

E. Aggregate Risks and Determination of Safety

    To estimate total aggregate exposure to a pesticide from food, 
drinking water, and residential uses, the Agency calculates DWLOCs 
which are used as a point of comparison against the model estimates of 
a pesticide's concentration in water (EECs). DWLOC values are not 
regulatory standards for drinking water. DWLOCs are theoretical upper 
limits on a pesticide's concentration in drinking water in light of 
total aggregate exposure to a pesticide in food and residential uses. 
In calculating a DWLOC, the Agency determines how much of the 
acceptable exposure (i.e., the PAD) is available for exposure through 
drinking water [e.g., allowable chronic water exposure (mg/kg/day) = 
cPAD - (average food + residential exposure)]. This allowable exposure 
through drinking water is used to calculate a DWLOC.
    A DWLOC will vary depending on the toxic endpoint, drinking water 
consumption, and body weights. Default body weights and consumption 
values as used by the USEPA Office of Water are used to calculate 
DWLOCs: 2 liter (L)/70 kg (adult male), 2L/60 kg (adult female), and 
1L/10 kg (child). Default body weights and drinking water consumption 
values vary on an individual basis. This variation will be taken into 
account in more refined screening-level and quantitative drinking water 
exposure assessments. Different populations will have different DWLOCs. 
Generally, a DWLOC is calculated for each type of risk assessment used: 
Acute, short-term, intermediate-term, chronic, and cancer.
    When EECs for surface water and groundwater are less than the 
calculated DWLOCs, EPA concludes with reasonable certainty that 
exposures to the pesticide in drinking water (when considered along 
with other sources of exposure for which EPA has reliable data) would 
not result in unacceptable levels of aggregate human health risk at 
this time. Because EPA considers the aggregate risk resulting from 
multiple exposure pathways associated with a pesticide's uses, levels 
of comparison in drinking water may vary as those uses change. If new 
uses are added in the future, EPA will reassess the potential impacts 
of residues of the pesticide in drinking water as a part of the 
aggregate risk assessment process.

[[Page 55841]]

    1. Acute risk. Using the exposure assumptions discussed in this 
unit for acute exposure, the acute dietary exposure from food to 
glufosinate ammonium will occupy 48% of the aPAD for females 13 years 
and older. In addition, there is potential for acute dietary exposure 
to glufosinate ammonium in drinking water. After calculating DWLOCs and 
comparing them to the EECs for surface water and groundwater, EPA does 
not expect the aggregate exposure to exceed 100% of the aPAD, as shown 
in Table 5 of this unit:

                 Table 5.--Aggregate Risk Assessment for Acute Exposure to Glufosinate ammonium
----------------------------------------------------------------------------------------------------------------
                                                                               Surface       Ground      Acute
                                                    aPAD (mg/      % aPAD     Water EEC    Water EEC     DWLOC
               Population Subgroup                     kg)         (Food)      ([mu]g/      ([mu]g/     ([mu]g/
                                                                                liter)       liter)      liter)
----------------------------------------------------------------------------------------------------------------
Females (13-50 years old)                               0.0063           48           94            9         98
----------------------------------------------------------------------------------------------------------------

    2. Chronic risk. Using the exposure assumptions described in this 
unit for chronic exposure, EPA has concluded that exposure to 
glufosinate ammonium from food will utilize 10% of the cPAD for the 
U.S. population, 20% of the cPAD for all infants and 27% of the cPAD 
for children (1-2 years old). Based on the use pattern, chronic 
residential exposure to residues of glufosinate ammonium is not 
expected. In addition, there is potential for chronic dietary exposure 
to glufosinate ammonium in drinking water. After calculating DWLOCs and 
comparing them to the EECs for surface water and groundwater, EPA does 
not expect the aggregate exposure to exceed 100% of the cPAD, as shown 
in Table 6 of this unit:

          Table 6.--Aggregate Risk Assessment for Chronic (Non-Cancer) Exposure to Glufosinate ammonium
----------------------------------------------------------------------------------------------------------------
                                                                             Surface       Ground      Chronic
                                                 cPAD mg/kg/     % cPAD     Water EEC    Water EEC      DWLOC
              Population Subgroup                    day         (Food)      ([mu]g/      ([mu]g/      ([mu]g/
                                                                              liter)       liter)       liter)
----------------------------------------------------------------------------------------------------------------
U.S. Population                                        0.006           10           43            9          189
----------------------------------------------------------------------------------------------------------------
Youth (13-19 years old)                                0.006            9           43            9          164
----------------------------------------------------------------------------------------------------------------
Females (13-50 years old)                              0.006            7           43            9          167
----------------------------------------------------------------------------------------------------------------
Adults (20-49)                                         0.006            8           43            9          194
----------------------------------------------------------------------------------------------------------------

    3. Short-term risk. Short-term aggregate exposure takes into 
account residential exposure plus chronic exposure to food and water 
(considered to be a background exposure level).
    Glufosinate ammonium is currently registered for use that could 
result in short-term residential exposure and the Agency has determined 
that it is appropriate to aggregate chronic food and water and short-
term exposures.
    Using the exposure assumptions described in this unit for short-
term exposures, EPA has concluded that food and residential exposures 
aggregated result in aggregate risk index (ARI) of 5.42 for the U.S. 
population, 6.35 for females (13-49 years old) and 5.75 for youth (13-
19 years old). The registered spot treatment of weeds is expected to 
result in residential exposure only to adults. Therefore, short-term 
aggregate assessments were not conducted for infants and children. 
These aggregate ARIs do not exceed the Agency's level of concern of 
less than 1 for aggregate exposure to food and residential uses. In 
addition, short-term DWLOCs were calculated and compared to the EECs 
for chronic exposure of glufosinate ammonium in groundwater and surface 
water. After calculating DWLOCs and comparing them to the EECs for 
surface and ground water, EPA does not expect short-term aggregate 
exposure to exceed the Agency's level of concern, as shown in Table 7 
of this unit:

               Table 7.--Aggregate Risk Assessment for Short-Term Exposure to Glufosinate ammonium
----------------------------------------------------------------------------------------------------------------
                                                               Aggregate
                                                             ARI\1\ (Food    Surface       Ground     Short-Term
                    Population Subgroup                            +        Water EEC    Water EEC   DWLOC (ppb)
                                                             Residential)     (ppb)        (ppb)
----------------------------------------------------------------------------------------------------------------
U.S. Population                                                      5.42           43            9          180
----------------------------------------------------------------------------------------------------------------
Females (13-49 years old)                                            6.35           43            9          159
----------------------------------------------------------------------------------------------------------------
Youths (13-19 years old)                                             5.75           43            9          156
----------------------------------------------------------------------------------------------------------------
\1\ ARI = MOEcalculated ( i.e., food, dermal, inhalation) / MOEacceptable

    4. Aggregate cancer risk for U.S. population. No evidence of 
carcinogenicity at doses tested were observed in the mouse and rat 
carcinogenicity studies. Therefore, no cancer risk is expected.
    5. Determination of safety. Based on these risk assessments, EPA 
concludes that there is a reasonable certainty that no harm will result 
to the general population, and to infants and children from aggregate 
exposure to glufosinate ammonium residues.

[[Page 55842]]

IV. Other Considerations

A. Analytical Enforcement Methodology

    Adequate enforcement methodology (example--gas chromatography) is 
available to enforce the tolerance expression. The method may be 
requested from: Chief, Analytical Chemistry Branch, Environmental 
Science Center, 701 Mapes Rd., Ft. Meade, MD 20755-5350; telephone 
number: (410) 305-2905; e-mail address: [email protected].

B. International Residue Limits

    Codex and Mexico do not have maximum residue limits (MRLs) for 
glufosinate ammonium and its metabolites for the proposed crops or 
livestock commodities. Canada does not have MRLs for glufosinate 
ammonium and its metabolites for the proposed crops, poultry 
commodities or milk, but does have a MRL of 1 ppm for ruminant liver 
and kidney.

V. Conclusion

    Therefore, the tolerance is established for combined residues of 
glufosinate ammonium and its metabolites in or on bushberry subgroup, 
Lingonberry, juneberry and salal at 0.15 ppm, cattle, fat at 0.40 ppm, 
cattle, meat at 0.15 ppm, cattle, meat byproducts at 6.0 ppm, cotton, 
gin byproducts at 15 ppm, cotton, undelinted seed at 4.0 ppm, egg at 
0.15 ppm, goat, fat at 0.40 ppm, goat, meat at 0.15 ppm, goat, meat 
byproducts at 6.0 ppm, hog, fat at 0.40 ppm, hog, meat at 0.15 ppm, 
hog, meat byproducts at 6.0 ppm, horse, fat at 0.40 ppm, horse, meat at 
0.15 ppm, horse, meat byproducts 6.0 ppm, Milk at 0.15 ppm, poultry, 
fat at 0.15 ppm, poultry, meat at 0.15 ppm, poultry, meat byproducts 
0.60 ppm, sheep, fat at 0.40 ppm, sheep, meat at 0.15 ppm, and sheep, 
meat byproducts 6.0 ppm, cotton, gin byproducts at 15 ppm, rice, grain 
at 1.0 ppm, rice, straw at 2.0 ppm, and rice, hull at 2.0 ppm.

VI. Response to Comments

    The overall thrust of the comments from the Sierra Club was that 
``large quantities of glufosinate ammonium herbicide will be utilized 
on transgenic rice crops in the United States and abroad . . . even 
though the herbicide may have side effects on humans, farm animals and 
beneficial insects.'' The testing of pesticides will often reveal that 
a pesticide has the potential to create adverse effects in animals and/
or insects; those risks are addressed via registration under FIFRA. The 
critical issue addressed by FFDCA is whether there is an adequate 
margin of safety between the aggregate exposure level of humans to the 
pesticide and the level that potentially may be harmful. As EPA 
described in Unit III.E. above, EPA's risk assessment showed that an 
adequate margin was available for EPA to conclude that there is a 
reasonable certainty of no harm for the general population including 
infants and children.
    EPA has reprinted each of Sierra Club's more specific comments 
below and responded to each individually.
    1. Comment--plant metabolism of glufosinate. A concern is other 
plant metabolites of glufosinate ammonium may occur in addition to the 
two primary metabolites identified in the grain and straw, since the 
two substances did not appear to account for 100% of the total 
radioactive residues in the two plant tissues tested. While more than 
80% appeared to be accounted for, Aventis needs to identify whether 
additional metabolites were produced. The two primary metabolites 
identified as being typical of plant metabolism in the grain at harvest 
were 3-methylphosphinicopropionic acid, being--70% of the total 
radioactive residues (TRR). Another residue in the grain was N-acetyl-
L-glufosinate (2-acetamido-4-methylphosphinicobutanoic acid), at about 
11% of the TRR and parent at 5-6% of the TRR. In the straw, 3-
methylphosphinicopropionic acid was the major metabolite comprising 
approximately 60% of the TRR. Lesser amounts of the parent (about 17% 
of the TRR) and N-acetylglufosinate (10-13% of TRR) were found in the 
straw fraction.
    Agency response. The transgenic rice metabolism study was conducted 
according to the regulatory guideline requirements (OPPTS 860.1500) and 
conformed to EPA Good Laboratory Practice (GLP) Standards (the % TRR 
figures given below are averages of four samples). The study indicated 
that glufosinate ammonium, N-acetyl-glufosinate, and 3-MP accounted for 
88% and 91% of the total radioactive residue (TRR) found in rice grain 
and rice straw, respectively (grain and straw are the only rice raw 
agricultural commodities (RACs)). The remainder of the radioactivity 
was identified as 2-methylphosphinico-acetic acid (grain--1% TRR; 
straw--2% TRR), several unknowns when combined accounted for 2% TRR 
(rice grain) and 3% TRR (rice straw), and fiber bound residues (grain--
8% TRR; straw--5% TRR). The petitioner identified/characterized 99% and 
101% of the TRR in rice grain and rice straw, respectively. In 
previously submitted transgenic canola and non-transgenic apple, corn, 
lettuce, soybeans, and wheat metabolism studies, the petitioner 
demonstrated the incorporation of radioactivity into nature plant 
constituents. On the basis of the transgenic rice metabolism study and 
the previously submitted metabolism studies, EPA concluded that the 
residue identification/characterization procedures performed were 
adequate and the residues of concern in transgenic rice, for purposes 
of tolerance enforcement and risk assessment, are glufosinate ammonium, 
N-acetyl-glufosinate, and 3-methylphosphinico-propionic acid (3-MP).
    2. Comment--analytical method. We ask EPA if any independent 
sampling and gas chromatography analyses were conducted besides that 
performed by Aventis and its contractors. We request that an 
independent sampling and G.C. analysis program be carried out if 
Aventis has not had a third party independent contractor, since we are 
skeptical of Aventis' sampling data and analyses. We generally agree 
that the enforcement analytical method of utilizing gas chromatography 
appears to be acceptable for detecting and measuring levels of 
glufosinate ammonium and metabolites with a general limit of 
quantification of 0.05 ppm to allow detection of glufosinate residues 
at or above the proposed tolerances. We wonder if glufosinate residues 
might have been found between 0.01 ppm and 0.05 ppm, and that due to 
its toxicity, EPA should have required a lower detectability limit be 
utilized to demonstrate if glufosinate residues were missed below 0.05 
ppm or 50 parts per billion (ppb) concentration down to 1 ppb.
    Agency response. The rice magnitude of the residue study was 
conducted according to the regulatory guideline requirements (OPPTS 
860.1500) and conformed to EPA GLP Standards. The rice grain and straw 
samples were analyzed using a method similar to that previously 
validated by an independent laboratory and by the EPA. Based on these 
validation procedures and the validation and concurrent recovery data 
submitted with the transgenic rice field trials, EPA concluded that the 
method was appropriate for data collection purposes.
    EPA understands that residues below the level of quantification (< 
LOQ) does not mean that residues are not present. The dietary analyses 
assumed average field trial residues for rice commodities. When 
calculating the average, half LOQ residues were assumed for residues < 
LOQ. Therefore, the dietary risk assessment took into account the 
possibility of residues between 0.01 and

[[Page 55843]]

0.05 ppm. For further information on EPA's rationale for assuming half 
LOQ residues see ``Values to Non-Detectable/Non-Quantifiable Residues 
in Human Health Food Exposure Assessments'' (faxed upon request; 
telephone: (202) 401-0527; item: 6047).
    3. Comment--magnitude of glufosinate residues. The reason that we 
are requesting independent sampling and gas chromatography analyses be 
conducted besides that performed by Aventis and its contractors is the 
potential for higher glufosinate residue concentrations to be confirmed 
above the 0.74 ppm level in rice grain and 1.48 ppm level in rice straw 
when sampled at 70 days or more after the last treatment. We are 
concerned that Aventis' sampling protocol may have been biased in some 
unidentified manner and that samples above the 0.74 ppm level in rice 
grain and 1.48 ppm level in rice straw were missed in the field residue 
trials. While EPA emphasizes that the treatment regime was selected to 
represent the use pattern that is the most likely to result in the 
highest residues, we are concerned that sampling bias may have 
transpired and resulted in bias in the G.C. analyses. We are also 
concerned that glufosinate treatment may have occurred closer to the 
sampling period than is the case and higher glufosinate concentrations 
were missed. After all, a higher concentration factor of approximately 
2.3 was found for rice hulls compared to the grain and straw. We also 
question that the finding that no detectable concentration of the 
residues occurred when rice whole grain was processed into polished 
grain and bran, whereas a glufosinate residue concentration may have 
been present at less than the 0.05 ppm (50 ppb) detection limit.
    Agency response. The rice magnitude of the residue (15 field trials 
conducted throughout the rice growing regions in the United States; 2 
composite samples collected at each site) and processing studies were 
conducted according to the regulatory guideline requirements (OPPTS 
860.1500 and 860.1520) and conformed to EPA GLP Standards. It is 
difficult to further address the potential for bias since the comment 
gave no specific criteria for the concern. The comment does make 
reference to the processing study and the concentration of residues in 
rice hull and the lack of concentration of residues in rice bran and 
polished rice. The following paragraph is a summary of the rice 
processing study.
    Processing studies are required to determine if residues reduce or 
concentrate during food processing (processing factor = concentration 
in processed commodity / concentration in unprocessed commodity). 
Processing factors are dependent on several factors including the 
location of the residues (surface or translocated residues), loss of 
water as in dried commodities, and/or the physical chemical properties 
of the residues. The rice processing study (conducted at 5x the 
proposed rate) resulted in quantifiable concentrations of glufosinate 
ammonium, N-acetyl-glufosinate, and 3-MP in/on all commodities 
excluding glufosinate ammonium and N-acetyl-glufosinate in/on rice hull 
(residues at the LOQ assumed for calculation of processing factor). 
Based on the combined glufosinate ammonium, N-acetyl-glufosinate, and 
3-MP residues in/on the processed and unprocessed commodities, the 
following processing factors were calculated: rice hull--2.8x, rice 
bran--0.9x, and polished rice--1.3x. The dietary analyses assumed 
average field trial residues and a processing factor of 1.3 for all 
rice commodities excluding rice bran where a processing factor of 0.9 
was assumed (rice hull is not a human food commodity).
    4. Comment--acute toxicity. EPA states that glufosinate ammonium 
has been classified as toxicity category III for acute oral, dermal, 
and inhalation toxicity; and for eye irritation. EPA finds that 
glufosinate ammonium is not a dermal irritant (toxicity category IV) 
nor is it a dermal sensitizer. The oral LD50 is 2 g/kg in 
male rats, and 1.62 g/kg in female rats. But we are concerned about 
acute toxicity because of the published finding that glufosinate causes 
convulsions in humans and experimental rodents by brain cell glutamate 
receptor activation (glufosinate and glutamate are structurally 
similar) according to Matsumura et al. Has EPA considered the 
structural similarities between glufosinate and glutamate receptor 
activation. We request that EPA review all of the relevant 
toxicological literature on human and rat brain cell glutamate receptor 
activation and speak with scientists who performed this research as to 
the significance of glufosinate tampering with glutamate receptors. 
Evidence also exists that glufosinate stimulates nitric oxide 
production in the brain through N-methyDaspartate (NMDA) receptors. We 
request that EPA investigate this published finding to determine if the 
requested herbicide tolerance concentrations are set too high which, is 
a possibility.
    Agency response. EPA has evaluated both the published and 
petitioner submitted toxicity studies. The oral, dermal, and inhalation 
toxicity categories assigned by EPA are based on studies conducted 
according to the EPA toxicity testing guidelines and were conducted in 
compliance with EPA GLP. In an acute oral toxicity study in rats, the 
oral LD50 was found to be 1,620 and 2,000 mg/kg/day in 
female and male rats, respectively. In this study, no effects were seen 
in rats at doses up to 630 mg/kg/day.
    The commenter cites two acute exposure studies. Matsumura et al. 
have shown that an acute dose of 80 mg/kg injected intraperitoneally 
into mice was convulsive and that this effect was partially antagonized 
by NMDA antagonists, suggesting that NMDA receptors may mediate this 
effect. Nakaki et al. found that injection of glufosinate ammonium 
directly into the brain stimulated nitric oxide production as a result 
of stimulation of NMDA receptors in rat brain, another neurochemical 
effect. But neither of these published studies provide sufficient 
appropriate evidence to establish an acute endpoint for risk assessment 
from oral, dermal, or inhalation exposures because the routes that they 
used, intraperitoneal injection or direct injection into the brain, are 
not directly relevant to potential routes of human exposure to 
pesticides, i.e., oral, dermal, or inhalation exposure.
    The herbicidal mechanism of action of glufosinate ammonium is 
inhibition of the enzyme glutamine synthetase. This enzyme is also 
present in mammalian systems. In mammals, glutamine synthetase 
facilitates the conversion of glutamate and ammonia to glutamine and is 
therefore involved in the metabolism of nitrogen and ammonia. In 
addition, glutamate is a major excitatory neurotransmitter in the 
nervous system; inhibition of glutamine synthetase has been shown to 
impair its ability to serve as a neuroprotectant by controlling 
glutamate concentrations in neurons. More generally in the body, 
ammonia is buffered for extracellular transport through its interaction 
with glutamate to form glutamine by glutamine synthetase.
    EPA also reviewed mechanistic studies submitted by the petitioner 
as well as the published studies, and, where applicable and 
appropriate, incorporated findings from these studies in the human 
health risk assessment. In fact, the intermediate-term and long-term 
incidental oral endpoints and the chronic dietary endpoint are based on 
brain glutamine synthetase inhibition, the most sensitive indicator of 
glufosinate ammonium toxicity in humans and experimental animals.

[[Page 55844]]

    After reviewing all of the submitted data, EPA confirms that the 
tolerances, as proposed, are safe.
    5. Comment--genotoxicity. EPA claims that ... based on results of a 
complete genotoxicity data base, there is no evidence of mutagenic 
activity in a battery of studies, including: Salmonella spp., E. coli, 
in vitro mammalian cell gene mutation assays, mammalian cell chromosome 
aberration assays, in vivo mouse bone marrow micronucleus assays, and 
unscheduled DNA synthesis assays. EPA needs to inquire with the FDA, 
USDA, ATSDR, medical doctors and scientists as to whether there are 
reports of glufosinate induced mutations and gene toxicity which appear 
to be glossed over in the Aventis petition.
    Agency response. Glufosinate ammonium was clearly negative in the 
acceptable guideline mutagenicity studies. The test battery included: a 
Salmonella typhimurium and Escherichia coli reverse gene mutation 
assay, in vitro mammalian cell gene mutation and chromosome aberration 
assays, in vivo mouse bone marrow micronucleus assay and an in vitro 
unscheduled DNA synthesis assay. All studies were performed in 
accordance with the specified Office of Prevention, Pesticides, and 
Toxic Substances (OPPTS) Harmonized Mutagenicity Test Guidelines Series 
870 and satisfied the testing requirements of the Federal Insecticide, 
Fungicide, and Rodenticide Act (FIFRA), the Toxic Substances Control 
Act (TSCA), and the Organization for Economic Cooperation and 
Development (OECD). Further, each study meets the requirement of 40 CFR 
part 160, Good Laboratory Practice (GLP) and was subjected to a Quality 
Assurance(QA) inspection. Based on the negative responses observed in 
these assays, EPA concluded that there is no concern for mutagenicity 
from exposure to glufosinate ammonium. In addition, no evidence of 
carcinogenicity was observed in mice and rats in acceptable guideline 
carcinogenicity studies. As indicated previously, EPA evaluated both 
petitioner submitted guideline studies and published scientific 
studies. In addition, the petitioner is required by law under FIFRA 
(6)(a)2) to report any adverse finding to EPA.
    No mutagenicity studies were found in the open literature and the 
Agency for Toxic Substances and Disease Registry (ATSDR) has no 
finalized, draft, or ``under development'' toxicological profile for 
glufosinate ammonium. Finally, FDA has evaluated the human safety of 
multiple crops with resistance to glufosinate ammonium and has no 
concerns for human safety but has no mutagenicity or toxicity data in 
the Biotechnology Notification Files on this herbicide.
    6. Comment--reproductive and developmental toxicity. We are 
skeptical of EPA's findings because, based on peer-reviewed studies in 
the published literature, birth defects have been caused by exposure of 
the human father to the herbicide. EPA needs to thoroughly investigate 
these findings and reconsider the glufosinate herbicide tolerance 
limits requested by Aventis as entirely unsafe and unacceptably high. 
It is rather distressing to note that there does not seem to be peer 
reviewed studies on the metabolism of the high levels of acetyl 
glufosinate in harvested GM crops to highly neurotoxic and teratogenic 
glufosinate. Certainly, gut bacteria are well known to contain enzymes 
that remove acetyl groups from glufosinate and mammalian enzymes may 
also be capable of removing the acetyl group from glufosinate. Even 
though glufosinate is being used widely with GM crops in North America 
its safety is far from proven and its impact on humans and farm animals 
is difficult to trace because the GM products are not labeled for 
consumption. We request that EPA obtain more technical data and 
information to better define the neurotoxicity and teratogenicity of 
glufosinate and its metabolites, especially in humans. Glufosinate, for 
example, was found to trigger apoptosis (programmed cell suicide) in 
the developing brain of the embryonic mouse. Numerous, well established 
studies showing brain damage and birth defects seem to have been 
ignored by those regulating use of the herbicide. We request that the 
EPA conduct a more comprehensive investigation of available literature 
on glufosinate and make requests for unpublished information from 
independent scientists such as their expert opinions on the adverse 
health effects of glufosinate and its metabolites.
    We request the same under subchronic, chronic, animal metabolism, 
and metabolite toxicology as requested for Reproductive and 
Developmental toxicity.
    Agency response. The study authors (cited study by Garcia et al) 
state in their conclusion that ``these findings warrant further 
investigation.'' In this study, only 16 individuals out of 261 
referenced glufosinate ammonium. The results of this study indicated 
that there was a marginally significant increased risk of paternally 
related developmental toxicity. However, in this study various 
contributing factors such as smoking, work habits etc. were not 
evaluated and therefore, this epidemiological evaluation does not 
establish a causal definitive link to paternally related developmental 
toxicity. The potential for glufosinate ammonium to cause developmental 
or reproductive effects due to exposure (male or female) has been 
evaluated in acceptable guideline studies in rats and rabbits. Based on 
these studies, glufosinate ammonium is not teratogenic in rats and 
rabbits.
    The petitioner has submitted acute, subchronic, chronic, 
developmental, and reproductive toxicity studies conducted with 
glufosinate ammonium. The petitioner has also submitted developmental 
toxicity studies (rat and rabbit) and subchronic studies (rat, mouse, 
and dog) with N-acetyl-glufosinate and 3-MP. All of these studies were 
conducted according to the regulatory guideline requirements (OPPTS 870 
series) and conformed to EPA GLP Standards. EPA has reviewed all of 
these studies and selected the most sensitive endpoints. Based on a 
comparison of the common studies conducted with the parent and 
metabolites, the metabolites exhibited toxic effects at doses equal to 
or greater than the parent and EPA concluded that N-acetyl-glufosinate 
and 3-MP are not likely to be more toxic than glufosinate ammonium. In 
regards to the enzyme that can remove acetyl groups from substrates, 
these enzymes are present in the toxicology test systems used to 
evaluate the parent and metabolites.
    In the cited study by Watanabe, mouse embryo cultures were exposed 
to glufosinate ammonium. This is an in vitro experiments which indicate 
apoptosis in the developing brain of cultured mouse embryos. It should 
be noted that apoptosis is a normal part of the brain development 
process. This experiments did not use whole animals and the current 
scientific knowledge is not sufficient to allow extrapolation of in 
vitro results to whole animals.
    7. Comment--endocrine disruption. We find EPA's statements on the 
potential of glufosinate to function as an endocrine-disrupting 
substance in humans and animals as not founded on logical information 
or peer-reviewed studies. In fact EPA states that no special studies 
have been conducted to investigate the potential of glufosinate 
ammonium to induce estrogenic or other endocrine effects. Given the 
enormous complexities of mammalian hormonal regulatory systems and the 
current uncertainties existing in this field of knowledge as revealed 
by EPA's Endocrine Disruptor Advisory Committee several years ago about 
how to screen for potential endocrine-disrupting substances, we feel 
it's totally premature for EPA at this time to dismiss all concerns 
about glufosinate

[[Page 55845]]

as an endocrine-disrupting substance. EPA stresses that no evidence of 
estrogenic or other endocrine effects have been noted in any of the 
toxicology studies that have been conducted with this product and there 
is no reason to suspect that any such effects would be likely. Due to 
the millions of Americans and their children exposed to glufosinate and 
its metabolites, EPA needs to conclusively determine if this herbicide 
has endocrine-disrupting potential.
    Agency response. EPA is required under the FFDCA, as amended by the 
FQPA, to develop a screening program to determine whether certain 
substances, including all pesticide active and other ingredients, ``may 
have an effect in humans that is similar to an effect produced by a 
naturally occurring estrogen, or other such endocrine effects as the 
Administrator may designate.'' Following the recommendations of its 
Endocrine Disruptor Screening and Testing Advisory Committee (EDSTAC), 
EPA determined that there was scientific bases for including, as part 
of the program, the androgen and thyroid hormone systems, in addition 
to the estrogen hormone system. EPA also adopted EDSTAC's 
recommendation that the Program include evaluations of potential 
effects in wildlife. For pesticide chemicals, EPA will use Federal 
Insecticide, Fungicide and Rodenticide Act (FIFRA) and, to the extent 
that effects in wildlife may help determine whether a substance may 
have an effect in humans, FFDCA has authority to require the wildlife 
evaluations. As the science develops and resources allow, screening of 
additional hormone systems may be added to the Endocrine Disruptor 
Screening Program (EDSP).
    When the appropriate screening and/or testing protocols being 
considered under the Agency's EDSP have been developed, glufosinate 
ammonium may be subjected to additional screening and/or testing to 
better characterize effects related to endocrine disruption. The 
studies submitted as guideline studies as well as the data reviewed in 
the open literature did not provide any obvious indications that 
glufosinate ammonium and/or its metabolites have specific endocrine 
disruptive effects.
    8. Comment--dietary exposure. EPA states that tolerances have been 
established (40 CFR 180.473) for the combined residues of glufosinate 
ammonium and metabolites in or on a variety of RACs. EPA further 
maintains that no appropriate toxicological endpoint attributable to a 
single exposure was identified in the available toxicity studies. This 
is why EPA has not established an acute RfD for the general population 
including infants and children. An acute RfD of 0.063 mg/kg/day was 
established, however, for the females 13+ subgroup. Therefore, an acute 
dietary analysis was conducted for this sub-population; whereas, 
chronic dietary analysis was conducted for the usual populations. We 
request that EPA reconsider and reevaluate the health information 
finding that no appropriate toxicological endpoint attributable to a 
single exposure was identified in the available toxicity studies as too 
being limited and erroneous.
    Agency response. EPA has evaluated the published toxicity studies 
and considered the relevant petitioner submitted studies. On the basis 
of these studies, no appropriate endpoint of concern attributable to a 
single exposure was identified. EPA has asked the petitioner to conduct 
a study to evaluate potential effects of glufosinate ammonium following 
a single exposure (acute effects) with glutamate synthetase 
measurements. Until such data are available, EPA has applied additional 
data base UF to account or allow for uncertainty about those potential 
effects of acute exposure.
    9. Comment--infants and children. We are very concerned that EPA 
finds that the toxicological data base is sufficient for evaluating 
prenatal and postnatal toxicity for glufosinate ammonium in human 
infants and children using exclusively results from rats and rabbits. 
Although EPA states that there are no prenatal or postnatal 
susceptibility concerns for infants and children, based on the results 
of the rat and rabbit developmental toxicity studies and the 2-
generation reproduction study, we are concerned that human infants and 
children may possess genetic predispositions, biochemical 
individualities and behavioral patterns very different from rats and 
rabbits. EPA needs to do a more thorough literature review and 
interview scientists and medical doctors who may have relevant 
information on the prenatal and postnatal toxicity for glufosinate 
ammonium in human infants and children.
    As EPA notes, Based on clinical signs of neurological toxicity in 
short and intermediate dermal toxicity studies with rats, the agency 
has determined that an added FQPA safety factor of 3x is appropriate 
for assessing the risk of glufosinate ammonium derived residues in crop 
commodities. Using the conservative assumptions described in the 
exposure section above, the percent of the chronic RfD that will be 
used for exposure to residues of glufosinate ammonium in food for 
children 1-6 (the most highly exposed sub-group) is 61%. Infants 
utilize 37% of the chronic RfD. As in the adult situation, drinking 
water levels of comparison are higher than the worst case DWECs and are 
expected to use well below 100% of the RfD, if they occur at all. 
Therefore, there is a reasonable certainty that no harm will occur to 
infants and children from aggregate exposure to residues of glufosinate 
ammonium.
    Agency response. The short-term (dermal, inhalation, and incidental 
oral) and acute dietary (females 13-50 years) endpoints are based on 
reduced fetal body weight and increased fetal death seen in the rabbit 
developmental toxicity study (6.3 mg/kg/day). An acute dietary endpoint 
for the general population, including infants and children, could not 
be identified due to no adverse effects seen in the relevant studies. 
The chronic dietary endpoint is based on a weight-of-evidence approach 
from several studies which demonstrated brain glutamine synthetase 
inhibition and alterations in the electrocardiogram (6.0 mg/kg/day). 
EPA concluded that the toxicological data base for glufosinate ammonium 
was not complete and requested the submission of the following studies: 
(1) Acute neurotoxicity study conducted in the rat which includes 
glutamine synthetase activity measurement in the liver, kidneys, and 
brain; (2) a developmental neurotoxicity (DNT) study conducted in the 
rat which includes comparative glutamine synthetase activity 
measurement in the liver, kidneys, and brain of the pups and mothers; 
and (3) a 28-day inhalation toxicity study in rats with glutamine 
synthetase activity measurements in brain, kidney, liver and lung. EPA 
also requested additional data to confirm that liver and kidney 
changes, observed in the absence of histopathological changes, are an 
adaptive response and not an adverse effect. Kidney and liver function 
assays should be performed in addition to glutamine synthetase activity 
measurements. Pending the submission of the requested data, a 10x data 
base uncertainty factor was applied to all oral and dermal risk 
assessments and a 100x uncertainty factor was applied to all inhalation 
risk assessments. These uncertainty factors combined with the 
traditional 100x inter/intra species uncertainty factor, resulted in a 
total uncertainty factor of 1,000x for dermal and oral exposure 
assessments and 3,000x for inhalation exposure assessments (10,000x 
uncertainty factor reduced to 3,000x based on Agency policy cited in 
Unit III.B.).

[[Page 55846]]

    EPA concluded that there is no qualitative or quantitative evidence 
of increased susceptibility in the developmental toxicity study 
conducted in rats. Qualitative evidence of increased susceptibility is 
demonstrated in the rabbit developmental toxicity study since fetal 
deaths were observed in the presence of lesser maternal toxicity at the 
same dose. There is also quantitative evidence of increased 
susceptibility in the rat 2-generation reproduction study. In this 
study, a decrease in the number of viable pups was observed in the 
absence of parental toxicity at any dose. Since there is qualitative 
evidence of increased susceptibility of the young following exposure to 
glufosinate ammonium, EPA performed a degree of concern analysis to: 
(1) Determine the level of concern for the effects observed when 
considered in the context of all available toxicity data; and (2) 
identify any residual uncertainties after establishing toxicity 
endpoints and traditional uncertainty factors to be used in the risk 
assessment of this chemical. Based on the data gaps listed above, the 
EPA did not identify any other residual uncertainties. The established 
endpoints are protective of pre-/postnatal toxicity following acute and 
chronic exposures.
    The Notice of Filing (NOF) published in the Federal Register of 
July 24, 2002 (67 FR 48465)(FRL-7184-6) represents a summary of the 
petition prepared by the petitioner and represents the views of the 
petitioner. As such, and in this case, discrepancies may arise between 
what is stated in the NOF and the procedures/conclusions employed by 
EPA when assessing human health risk. For instance, the toxicological 
data base for glufosinate ammonium has been reevaluated by EPA since 
July 2002, and some of the conclusions presented in the NOF concerning 
the toxicity of glufosinate ammonium do not reflect current EPA 
conclusions.
    10. Comment--cumulative effects section 408(b)(2)(D)(v). We are 
deeply concerned about the potential for cumulative effects of 
glufosinate and its metabolites, and therefore request that EPA not 
approve the Aventis tolerance petition unless or until peer-reviewed 
confirming scientific evidence is available that glufosinate and its 
metabolites do not cause any cumulative effects. It is not acceptable 
public health policy to dismiss cumulative effects of glufosinate and 
its metabolites because of lack of scientific evidence and lack of any 
studies. Law requires that, when considering whether to establish, 
modify, or revoke a tolerance, the EPA must consider ``available 
information'' concerning the cumulative effects of a particular 
pesticide's residues and ``other substances that have a common 
mechanism of toxicity.'' EPA has indicated that, at this time, the 
Agency does not have available data to determine whether glufosinate 
ammonium has a common mechanism of toxicity with other substances or 
how to include this pesticide in a cumulative risk assessment. Unlike 
other pesticides for which EPA has followed a cumulative risk approach 
based on a common mechanism of toxicity, EPA suggests that glufosinate 
ammonium does not appear to produce a toxic metabolite produced by 
other substances. For the purposes of this tolerance petition, 
therefore, it has not been assumed that glufosinate ammonium has a 
common mechanism of toxicity with other substances. We disagree with 
EPA's illogical and unscientific assumption that glufosinate ammonium 
has a common mechanism of toxicity with other substances. We propose 
that further study is necessary to conclusively confirm such an 
assumption.
    Agency response. Section 408(b)(2)(D)(v) of the FFDCA requires 
that, when considering whether to establish, modify, or revoke a 
tolerance, the Agency consider ``available information'' concerning the 
cumulative effects of a particular pesticide's residues and ``other 
substances that have a common mechanism of toxicity.''
    EPA does not have, at this time, sufficient data to determine 
whether glufosinate ammonium has a common mechanism of toxicity with 
other substances. Unlike other pesticides for which EPA has followed a 
cumulative risk approach based on a common mechanism of toxicity (i.e., 
organophosphates), EPA has not made a common mechanism of toxicity 
finding as to glufosinate ammonium and any other substances and 
glufosinate ammonium does not appear to produce a toxic metabolite 
produced by other substances. For the purposes of this tolerance 
action, therefore, EPA has not assumed that glufosinate ammonium has a 
common mechanism of toxicity with other substances. For information 
regarding EPA's efforts to determine which chemicals have a common 
mechanism of toxicity and to evaluate the cumulative effects of such 
chemicals, see the policy statements released by EPA's Office of 
Pesticide Programs concerning common mechanism determinations and 
procedures for cumulating effects from substances found to have a 
common mechanism on EPA's website at http://www.epa.gov/pesticides/cumulative/.
    11. Comment--safety determination U.S. population. We believe that 
EPA has not done an adequate scientific job with respect to its safety 
determination for the U.S. population. By using what EPA claims (and 
may be a flawed set of assumptions) are the conservative assumptions 
described above and based on the completeness and reliability of the 
toxicity data, it is concluded that chronic dietary exposure to the 
registered and proposed uses of glufosinate ammonium will utilize at 
most 25% of the chronic RfD for the U.S. population. We disagree with 
EPA's assumption that the actual exposure is likely to be significantly 
less than predicted by this analysis as data and models that are more 
realistic are developed. We disagree with EPA's assumption that 
exposures below 100% of the reference dose (RfD) are generally assumed 
to be of no concern because the RfD represents the level at or below 
which daily aggregate exposure over a lifetime will not pose 
appreciable risk to human health. We dispute that the acute population 
of concern, female 13+ utilizes 34% of the acute RfD. We disagree with 
EPA's assumption that this is a Tier One highly conservative assessment 
and actual exposure is likely to be far less. Drinking water levels of 
comparison based on dietary exposures are greater than highly 
conservative estimated levels, and would be expected to be well below 
the 100% level of the RfD, if they occur at all, assuming that EPA's 
set of assumptions are reasonably accurate which they may not be. We 
believe that EPA has erroneously concluded that it is not appropriate 
to aggregate non-dietary exposures with dietary exposures in a risk 
assessment because the toxicity end-points are different. We strongly 
dispute EPA's concluding assumption that there is a reasonable 
certainty that no harm will occur to the U.S. population from aggregate 
exposure (food, drinking water and nonresidential) to residues of 
glufosinate ammonium and metabolites.
    Agency response. Contrary to what was written in the Notice of 
Filing prepared by the petitioner, EPA did aggregate dietary (food + 
drinking water) and residential exposures. Glufosinate ammonium is 
currently registered for application in the residential setting for 
lawn renovation and spot treatment purposes. Since the lawn renovation 
use resulted in exposures greater than EPA's level of concern, 
revocation of this use was recommended. Therefore, aggregate exposures 
were conducted by combining dietary exposure and residential exposure 
resulting from the spot treatment use. The resulting

[[Page 55847]]

combined exposures were subtracted from the appropriate dose and 
drinking water levels of comparison (DWLOCs) were calculated and 
compared to EECs in groundwater and surface water. The EECs were 
generated using SCIGROW (groundwater) and PRZM-EXAMS (surface water). 
SCIGROW is a regression model designed to estimate a screening level of 
a pesticide concentration at an agricultural site which is highly 
vulnerable to leaching due to permeable soil overlaying shallow ground 
water. PRZM-EXAMS is used to estimate concentration that might occur in 
vulnerable surface water (assumes 87% of the basin is cropped and 
entire cropped area is treated). Both models assumed 3 applications at 
1.5 lbs ai/acre (highest registered/proposed rate). The resulting EECs 
were less than the DWLOCs indicating aggregate exposures are less than 
EPA's level of concern.
    12. Comment. Additional issues not apparently being addressed by 
EPA such as negative impacts on beneficial insects. Bystander or 
beneficial insects have been detrimentally effected by the herbicide. 
Kutlesa and Caveny found that the herbicide had a number of neurotoxic 
impacts on the skipper butterfly at levels of herbicide experienced in 
the field. Ahn et al found that glufosinate was toxic to some but not 
all predatory insects at levels of the herbicide experienced in the 
field. Studies showing that helpful predatory insects or bystander 
insects are poisoned by the herbicide seem to have been ignored by 
regulators of the herbicide.
    Agency response. This comment raises an issue concerning the 
pesticide's registrability under FIFRA and is not directly relevant to 
the safety determination under FFDCA. For registrations of a pesticide 
under FIFRA, EPA requires non-target insect data if the proposed use 
will result in exposure to honey bees (40 CFR 158.590). Two studies on 
the toxicity of glufosinate ammonium to bees indicates that the 
herbicide (technical and a formulated product) is practically non-toxic 
to bees via contact and oral routes. The cited studies suggest that 
glufosinate ammonium may cause mortality to insects, other than bees, 
and mites may also be affected. The issues of the hazard to non-target 
insects will be addressed via registration under FIFRA.
    13. Comment. Additional issues not apparently being addressed by 
EPA such as glufosinate residues in other crop varieties. Muller et al 
studied glufosinate metabolites in transgenic and unmodified sugar 
beet, carrot, purple foxglove and thorn apple, and they found that 
unmodified (i.e., non-genetically engineered) crops contained 
glufosinate mainly while GM crops contained higher levels of 
glufosinate and acetyl glufosinate. Beriault et al studied phloem 
transport of glufosinate and acetylglufosinate in canola in GM canola 
and unmodified canola and found that both chemicals were highly mobile.
    Agency response. Common toxicity studies conducted with glufosinate 
ammonium, N-acetyl-glufosinate, and 3-MP indicate that N-acetyl-
glufosinate and 3-MP exhibit toxic effects at doses equal to or greater 
than glufosinate ammonium. Based on these toxicity studies, EPA 
concluded that N-acetyl-glufosinate, and 3-MP are not likely to be more 
toxic than glufosinate ammonium (risk assessment assumes they are of 
equal toxicity to parent). The field trial data were submitted for the 
transgenic crops monitored for residues of glufosinate ammonium, N-
acetyl-glufosinate, and 3-MP in/on all food/feed commodities. 
Therefore, the higher residues in transgenic crops and/or greater 
mobility of the residues of concern has been taken into consideration.
    14. Comment. Two hundred and twenty four comments were received 
that were opposed to establishing tolerances for glufosinate ammonium 
in genetically engineered (GE) rice and cotton. They included some or 
all of the following comments from the campaign to halt the 
introduction of GE Crops:
    I am writing in reference to Bayer CropScience's August 15th 
petition to establish a tolerance for Glufosinate in or on Rice and 
cotton. I believe that by approving the residues requested by Bayer 
you will be exposing the public to unnecessary health risks, 
potentially increasing use of toxic herbicides on rice and cotton, 
and endangering the livelihoods of farmers by shutting off valuable 
export markets that are rejecting transgenic crops. I am concerned 
about the loss of overseas markets for farmers growing transgenic 
crops and for farmers whose own ability to market their crops is 
threatened by genetic pollution. Many countries throughout the world 
are refusing transgenic crops and USDA organic standards strictly 
prohibit the use of transgenic seeds. Glufosinate tolerance levels 
have not been established by the international food standards 
commission, Codex Alimentarius. Events such as StarLink and last 
year's ProdiGene incident highlight the inadequacies of our current 
system in keeping transgenic crops segregated. In Canada, farmers 
growing transgenic crops have detected triple herbicide resistance 
in weeds and volunteer canola plants as a result of gene transfer, 
rendering the herbicides useless. If Bayer's petition is approved, 
it will only be a matter of time before red rice, which is the same 
species as cultivated rice and also one of the most virulent weeds 
on rice farms, becomes resistant to Glufosinate. Similar gene 
transfer in rice will lead to the need for new, more toxic 
herbicides. Peer-reviewed scientific studies have shown Glufosinate 
to be ``highly toxic'' to aquatic animals such as clams, oysters, 
water fleas, fish and birds at doses as low as 0.5 ppm. As rice is 
grown in an aquatic environment, the adoption of Glufosinate 
tolerant rice will have tragic impacts for the ecosystems of rice 
growing areas. The EPA classifies Glufosinate as ``persistent'' and 
it has been found in the edible parts of spinach, wheat and radishes 
more than 120 days after being sprayed with the chemical. The 
approval of Glufosinate tolerant rice and cotton will send us a step 
backward in our efforts toward a more sustainable agriculture. 
Please take action to ensure that our current system of agriculture 
moves toward one that is less reliant on chemicals, and ensures our 
farmers a prosperous livelihood. I strongly urge you to deny Bayer's 
request for approval of Glufosinate tolerance and to work with other 
government agencies to enact a more rigorous approval and testing 
process for transgenic crops.
    Forty one comments were in favor of establishing the tolerances for 
glufosinate ammonium. They stated that growers need the new technology 
to control weed species.
    Agency Response. EPA has concluded that there is a reasonable 
certainty that no harm will result to the general population, and to 
infants and children from aggregate exposure to glufosinate-ammonium 
and its metabolites from established and proposed tolerances. The 
issues of the hazard to non-target organisms and crop resistance will 
be addressed via registration under FIFRA. The growing of Herbicide 
Tolerant crops and potential effects on shipment of crops overseas is 
addressed by USDA and FDA in their pre-marketing review of Plant-
Incorporated Protectant Seeds. EPA is responsile for the safety of the 
pesticide to be applied to the growing crop.

VII. Objections and Hearing Requests

    Under section 408(g) of the FFDCA, as amended by the FQPA, any 
person may file an objection to any aspect of this regulation and may 
also request a hearing on those objections. The EPA procedural 
regulations which govern the submission of objections and requests for 
hearings appear in 40 CFR part 178. Although the procedures in those 
regulations require some modification to reflect the amendments made to 
the FFDCA by the FQPA, EPA will continue to use those procedures, with 
appropriate adjustments, until the necessary modifications can be made. 
The new section 408(g) of the FFDCA provides essentially the same 
process for persons to ``object'' to a regulation for an exemption from 
the requirement

[[Page 55848]]

of a tolerance issued by EPA under new section 408(d) of FFDCA, as was 
provided in the old sections 408 and 409 of the FFDCA. However, the 
period for filing objections is now 60 days, rather than 30 days.

A. What Do I Need to Do to File an Objection or Request a Hearing?

    You must file your objection or request a hearing on this 
regulation in accordance with the instructions provided in this unit 
and in 40 CFR part 178. To ensure proper receipt by EPA, you must 
identify docket ID number OPP-2003-0058 in the subject line on the 
first page of your submission. All requests must be in writing, and 
must be mailed or delivered to the Hearing Clerk on or before November 
28, 2003.
    1. Filing the request. Your objection must specify the specific 
provisions in the regulation that you object to, and the grounds for 
the objections (40 CFR 178.25). If a hearing is requested, the 
objections must include a statement of the factual issues(s) on which a 
hearing is requested, the requestor's contentions on such issues, and a 
summary of any evidence relied upon by the objector (40 CFR 178.27). 
Information submitted in connection with an objection or hearing 
request may be claimed confidential by marking any part or all of that 
information as CBI. Information so marked will not be disclosed except 
in accordance with procedures set forth in 40 CFR part 2. A copy of the 
information that does not contain CBI must be submitted for inclusion 
in the public record. Information not marked confidential may be 
disclosed publicly by EPA without prior notice.
    Mail your written request to: Office of the Hearing Clerk (1900C), 
Environmental Protection Agency, 1200 Pennsylvania Ave., NW., 
Washington, DC 20460-0001. You may also deliver your request to the 
Office of the Hearing Clerk in Rm.104, Crystal Mall 2, 1921 
Jefferson Davis Hwy., Arlington, VA. The Office of the Hearing Clerk is 
open from 8 a.m. to 4 p.m., Monday through Friday, excluding legal 
holidays. The telephone number for the Office of the Hearing Clerk is 
(703) 603-0061.
    2. Tolerance fee payment. If you file an objection or request a 
hearing, you must also pay the fee prescribed by 40 CFR 180.33(i) or 
request a waiver of that fee pursuant to 40 CFR 180.33(m). You must 
mail the fee to: EPA Headquarters Accounting Operations Branch, Office 
of Pesticide Programs, P.O. Box 360277M, Pittsburgh, PA 15251. Please 
identify the fee submission by labeling it ``Tolerance Petition Fees.''
    EPA is authorized to waive any fee requirement ``when in the 
judgement of the Administrator such a waiver or refund is equitable and 
not contrary to the purpose of this subsection.'' For additional 
information regarding the waiver of these fees, you may contact James 
Tompkins by phone at (703) 305-5697, by e-mail at [email protected], 
or by mailing a request for information to Mr. Tompkins at Registration 
Division (7505C), Office of Pesticide Programs, Environmental 
Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460-
0001.
    If you would like to request a waiver of the tolerance objection 
fees, you must mail your request for such a waiver to: James Hollins, 
Information Resources and Services Division (7502C), Office of 
Pesticide Programs, Environmental Protection Agency, 1200 Pennsylvania 
Ave., NW., Washington, DC 20460-0001.
    3. Copies for the Docket. In addition to filing an objection or 
hearing request with the Hearing Clerk as described in Unit VII.A., you 
should also send a copy of your request to the PIRIB for its inclusion 
in the official record that is described in Unit I.B.1. Mail your 
copies, identified by docket ID number OPP-2003-0058, to: Public 
Information and Records Integrity Branch, Information Resources and 
Services Division (7502C), Office of Pesticide Programs, Environmental 
Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460-
0001. In person or by courier, bring a copy to the location of the 
PIRIB described in Unit I.B.1. You may also send an electronic copy of 
your request via e-mail to: [email protected]. Please use an ASCII 
file format and avoid the use of special characters and any form of 
encryption. Copies of electronic objections and hearing requests will 
also be accepted on disks in WordPerfect 6.1/8.0 or ASCII file format. 
Do not include any CBI in your electronic copy. You may also submit an 
electronic copy of your request at many Federal Depository Libraries.

B. When Will the Agency Grant a Request for a Hearing?

    A request for a hearing will be granted if the Administrator 
determines that the material submitted shows the following: There is a 
genuine and substantial issue of fact; there is a reasonable 
possibility that available evidence identified by the requestor would, 
if established resolve one or more of such issues in favor of the 
requestor, taking into account uncontested claims or facts to the 
contrary; and resolution of the factual issues(s) in the manner sought 
by the requestor would be adequate to justify the action requested (40 
CFR 178.32).

VIII. Statutory and Executive Order Reviews

    This final rule establishes a tolerance under section 408(d) of the 
FFDCA in response to a petition submitted to the Agency. The Office of 
Management and Budget (OMB) has exempted these types of actions from 
review under Executive Order 12866, entitled Regulatory Planning and 
Review (58 FR 51735, October 4, 1993). Because this rule has been 
exempted from review under Executive Order 12866 due to its lack of 
significance, this rule is not subject to Executive Order 13211, 
Actions Concerning Regulations That Significantly Affect Energy Supply, 
Distribution, or Use (66 FR 28355, May 22, 2001). This final rule does 
not contain any information collections subject to OMB approval under 
the Paperwork Reduction Act (PRA), 44 U.S.C. 3501 et seq., or impose 
any enforceable duty or contain any unfunded mandate as described under 
Title II of the Unfunded Mandates Reform Act of 1995 (UMRA) (Public Law 
104-4). Nor does it require any special considerations under Executive 
Order 12898, entitled Federal Actions to Address Environmental Justice 
in Minority Populations and Low-Income Populations (59 FR 7629, 
February 16, 1994); or OMB review or any Agency action under Executive 
Order 13045, entitled Protection of Children from Environmental Health 
Risks and Safety Risks (62 FR 19885, April 23, 1997). This action does 
not involve any technical standards that would require Agency 
consideration of voluntary consensus standards pursuant to section 
12(d) of the National Technology Transfer and Advancement Act of 1995 
(NTTAA), Public Law 104-113, section 12(d) (15 U.S.C. 272 note). Since 
tolerances and exemptions that are established on the basis of a 
petition under section 408(d) of the FFDCA, such as the tolerance in 
this final rule, do not require the issuance of a proposed rule, the 
requirements of the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et 
seq.) do not apply. In addition, the Agency has determined that this 
action will not have a substantial direct effect on States, on the 
relationship between the national government and the States, or on the 
distribution of power and responsibilities among the various levels of 
government, as specified in Executive Order 13132, entitled 
Federalism(64 FR 43255, August 10, 1999). Executive Order 13132 
requires EPA to develop an accountable process

[[Page 55849]]

to ensure ``meaningful and timely input by State and local officials in 
the development of regulatory policies that have federalism 
implications.'' ``Policies that have federalism implications'' is 
defined in the Executive order to include regulations that have 
``substantial direct effects on the States, on the relationship between 
the national government and the States, or on the distribution of power 
and responsibilities among the various levels of government.'' This 
final rule directly regulates growers, food processors, food handlers 
and food retailers, not States. This action does not alter the 
relationships or distribution of power and responsibilities established 
by Congress in the preemption provisions of section 408(n)(4) of the 
FFDCA. For these same reasons, the Agency has determined that this rule 
does not have any ``tribal implications'' as described in Executive 
Order 13175, entitled Consultation and Coordination with Indian Tribal 
Governments (65 FR 67249, November 6, 2000). Executive Order 13175, 
requires EPA to develop an accountable process to ensure ``meaningful 
and timely input by tribal officials in the development of regulatory 
policies that have tribal implications.'' ``Policies that have tribal 
implications'' is defined in the Executive order to include regulations 
that have ``substantial direct effects on one or more Indian tribes, on 
the relationship between the Federal Government and the Indian tribes, 
or on the distribution of power and responsibilities between the 
Federal Government and Indian tribes.'' This rule will not have 
substantial direct effects on tribal governments, on the relationship 
between the Federal Government and Indian tribes, or on the 
distribution of power and responsibilities between the Federal 
Government and Indian tribes, as specified in Executive Order 13175. 
Thus, Executive Order 13175 does not apply to this rule.

IX. Congressional Review Act

    The Congressional Review Act, 5 U.S.C. 801 et seq., as added by the 
Small Business Regulatory Enforcement Fairness Act of 1996, generally 
provides that before a rule may take effect, the agency promulgating 
the rule must submit a rule report, which includes a copy of the rule, 
to each House of the Congress and to the Comptroller General of the 
United States. EPA will submit a report containing this rule and other 
required information to the U.S. Senate, the U.S. House of 
Representatives, and the Comptroller General of the United States prior 
to publication of this final rule in the Federal Register. This final 
rule is not a ``major rule'' as defined by 5 U.S.C. 804(2).

List of Subjects in 40 CFR Part 180

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


    Dated:September 23, 2003.
Debra Edwards,
Director, Registration Division, Office of Pesticide Programs.

0
Therefore, 40 CFR chapter I is amended as follows:

PART 180--[AMENDED]

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

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

0
2. Section 180.473 is revised to read as follows:


Sec.  180.473  Glufosinate ammonium; tolerances for residues.

    (a) General. (1) Tolerances are established for residues of the 
herbicide glufosinate ammonium (butanoic acid, 2-amino-4-
(hydroxymethylphosphinyl)-, monoammonium salt) and its metabolites, 2-
acetamido-4-methylphosphinico-butanoic acid and 3-methylphosphinico-
propionic acid, expressed as 2-amino-4-
(hydroxymethylphosphinyl)butanoic acid equivalents, in or on the 
following food commodities:

------------------------------------------------------------------------
                      Commodity                        Parts per million
------------------------------------------------------------------------
Almond, hulls........................................               0.50
Apple................................................               0.05
Banana...............................................               0.30
Banana, pulp.........................................               0.20
Bushberry subgroup 13B...............................               0.15
Cattle, fat..........................................               0.40
Cattle, meat.........................................               0.15
Cattle, meat byproducts..............................                6.0
Cotton, gin byproducts...............................                 15
Cotton, undelinted seed..............................                4.0
Egg..................................................               0.15
Goat, fat............................................               0.40
Goat, meat...........................................               0.15
Goat, meat byproducts................................                6.0
Grape................................................               0.05
Hog, fat.............................................               0.40
Hog, meat............................................               0.15
Hog, meat byproducts.................................                6.0
Horse, fat...........................................               0.40
Horse, meat..........................................               0.15
Horse, meat byproducts...............................                6.0
Juneberry............................................               0.10
Lingonberry..........................................               0.10
Milk.................................................               0.15
Nut, tree, group 14..................................               0.10
Potato...............................................               0.80
Potato, chips........................................               1.60
Potato granules and flakes...........................               2.00
Poultry, fat.........................................               0.15
Poultry, meat........................................               0.15
Poultry, meat byproducts.............................               0.60
Salal................................................               0.10
Sheep, fat...........................................               0.40
Sheep, meat..........................................               0.15
Sheep, meat byproducts...............................                6.0
------------------------------------------------------------------------

    (2) Tolerances are established for residues of the herbicide 
glufosinate ammonium (butanoic acid, 2-amino-4-
(hydroxymethylphosphinyl)-, monoammonium salt) and its metabolites, 2-
acetamido-4-methylphosphinico-butanoic acid and 3-methylphosphinico-
propionic acid, expressed as 2-amino-4-
(hydroxymethylphosphinyl)butanoic acid equivalents, in or on the 
following food commodities derived from transgenic canola, transgenic 
cotton, transgenic field corn, transgenic rice, transgenic soybean and 
transgenic sugar beet that are tolerant to glufosinate ammonium:

------------------------------------------------------------------------
                                                              Parts per
                         Commodity                             million
------------------------------------------------------------------------
Aspirated grain fractions..................................         25.0
Beet, sugar, molasses......................................          5.0
Beet, sugar, roots.........................................          0.9
Beet, sugar, tops (leaves).................................          1.5
Canola, meal...............................................          1.1
Canola, seed...............................................          0.4
Corn, field, forage........................................          4.0
Corn, field, grain.........................................          0.2
Corn, field, stover........................................          6.0
Cotton, gin byproducts.....................................           15
Cotton, undelinted seed....................................          4.0
Rice, grain................................................          1.0
Rice, hull.................................................          2.0
Rice, straw................................................          2.0
Soybean....................................................          2.0
Soybean, hulls.............................................          5.0
------------------------------------------------------------------------

    (b) Section 18 emergency exemptions. [Reserved]
    (c) Tolerances with regional restrictions. [Reserved]
    (d) Indirect or inadvertent residues. [Reserved]

[FR Doc. 03-24565 Filed 9-26-03; 8:45 am]
BILLING CODE 6560-50-S