 

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

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

 

<INSTRUCTIONS:  Please utilize this outline in preparing the pesticide
petition.  In cases where the outline element does not apply, please
insert “NA-Remove” and maintain the outline. Please do not change
the margins, font, or format in your pesticide petition. Simply replace
the instructions that appear in green, i.e., “[insert company
name],” with the information specific to your action.>

<TEMPLATE:>

<[ Bayer CropScience LP]>

<[Insert petition number]

EPA has received a pesticide petition ([insert petition number]) from
Bayer CropScience, 2 T.W. Alexander Drive, P.O. Box 12014, Research
Triangle Park, NC  27709 proposing, pursuant to section 408(d) of the
Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to
amend 40 CFR part 180.600 

<(Options (pick one)>

<	1. by establishing a tolerance for residues of>

<	2. to establish an exemption from the requirement of a tolerance for>

<	propoxycarbazone, methyl
2-[[[(4,5-dihydro-4-methyl-5-oxo-3-propoxy-1H-1,2,4-triazol-1-yl)carbony
l]amino] sulfonyl]benzoate and its metabolite, methyl
2-[[[(4,5-dihydro-3-(2-hydroxypropoxy)
-4-methyl-5-oxo-1H-1,2,4-triazol-1-yl) carbonyl] amino]sulfonyl]benzoate
[MKH-6561] in or on the raw agricultural commodities grass forage at 20
parts per million (ppm), and grass hay at 25 ppm, and increase the
established tolerances for the residues of of propoxycarbazone, methyl
2-[[[(4,5-dihydro-4-methyl-5-oxo-3-propoxy-1H-1,2,4-triazol-1-yl)carbony
l]amino] sulfonyl]benzoate [Pr-2-OH MKH-6561], in or on the raw
agricultural commodities cattle, goat, horse, sheep meat from 0.05 ppm
to 0.1 ppm, meat byproducts from 0.3 ppm to 1.0 ppm, and milk from 0.03
ppm to 0.05 ppm..  EPA has determined that the petition contains data or
information regarding the elements set forth in section 408 (d)(2) of
the FDDCA; however, EPA has not fully evaluated the sufficiency of the
submitted data at this time or whether the data supports granting of the
petition. Additional data may be needed before EPA rules on the
petition.>

<A. Residue Chemistry>

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

<	2. Analytical method. i. Plant. The proposed tolerance expression is
MKH–6561 and Pr-2-OH MKH–6561. An analytical method was developed to
measure these two analytes in plant matrices. The method was validated
in grass tissues. Extraction of propoxycarbazone and 2-hydroxy
propoxycarbazone residue from grass forage and hay involved accelerated
solvent extraction (ASE) of a 2.0-g aliquot of the homogenized sample
using 0.050 M NH4OH as the extraction solvent. The extract was filtered
to remove the suspended solids and eluted through a small C-18 solid
phase extraction (spe) cartridge with acetonitrile (ACN)/0.1% acetic
acid (3:1). The eluate was diluted for analysis by high performance
liquid chromatography-electrospray ionization/tandem mass spectrometry
(LC/MS/MS).

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

<	3. Magnitude of residues. A total of 12 field trials were conducted to
measure the magnitude of propoxycarbazone residues in/on grasses
(pasture and rangeland) following a single foliar ground spray
application of OLYMPUS 70 WDG (water dispersible granule formulation
containing 70% propoxycarbazone-sodium) to grass at a target rate of
0.054 lb ai/A with a non-ionic surfactant (NIS) as an adjuvant (0.25%
to 0.5%, v/v).  In eleven of the field trials, duplicate composite
samples of grass forage were collected at commercial maturity at a
pre-harvest interval (PHI) of 0 day after the application and at
commercial maturity.  In one trial, duplicate composite samples of grass
forage were collected at PHIs of 0, 6, 12, 21, and 27 days following the
application to monitor residue decline. Grass hay was also collected at
Earliest Commercial Harvest (ECH), at 10 and 16 days before ECH, and at
5 and 9 days after ECH.  The residues of propoxycarbazone and its
metabolite 2-hydroxy propoxycarbazone were quantitated by high pressure
liquid chromatography/triple stage quadrupole mass spectrometry
(LC-MS/MS).  The individual analyte residues were summed to give a total
propoxycarbazone residue in parent equivalents (LOQ for each analyte was
0.05 ppm).  The HAFT (highest average field trial residue) total
propoxycarbazone residue was 11.97 ppm in/on grass forage at commercial
maturity at a PHI of 0 days. The maximum total propoxycarbazone residue
was 12.24 ppm in/on grass forage at commercial maturity at a PHI of 0
days. The HAFT total propoxycarbazone residue was 11.36 ppm in/on grass
hay at commercial maturity. The maximum total propoxycarbazone residue
was 11.38 ppm in/on grass hay at commercial maturity. The total
propoxycarbazone residue decreased with time in the decline trial hay
samples.  >

<B. Toxicological Profile>

<	1. Acute toxicity.  i. Propoxycarbazone sodium is of very low acute
toxicity to fasted rats following a single oral administration. The
acute oral LD50 is >5,000 milligrams/kilogram/body weight (mg/kg/bwt)
for males and females.

ii. Propoxycarbazone sodium is not toxic to rats following a single
dermal application. The acute dermal LD50 is >5,000 mg/kg/ bwt for males
and females.

iii. An acute inhalation study with rats showed low toxicity with a
4–hour dust aerosol LC50 5,030 mg/m3 air for males and females.

iv. An eye irritation study in rabbits showed minimal irritation
completely reversible within 48 hours.

v. A dermal irritation study in rabbits showed slight irritation
completely reversible within 48 hours.

vi. Propoxycarbazone sodium has no skin sensitizing potential under the
conditions of the maximization test in guinea pigs. >

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

<	3. Reproductive and developmental toxicity. i. In a 2–generation
reproduction study, Wistar rats were administered propoxycarbazone
sodium at levels of 0, 1,000, 4,000, or 16,000 ppm in the diet.  The no
observe adverse effect level (NOAEL) for reproductive parameters was
established at 16,000 ppm (1,231 mg/kg bwt/day in males and 1,605 mg/ kg
bwt/day in females), the highest dose tested (HDT). The parental NOAEL
was 1,000 ppm (80 mg/kg bwt/day in F1 males and 93 mg/kg bwt/day in F0
females).

ii. A developmental toxicity study was conducted with Wistar rats via
oral gavage of propoxycarbazone sodium at levels of 0, 100, 300, and
1,000 mg/kg bwt/day on days 6 through 19 of gestation. There were no
signs of maternal toxicity, embryotoxicity, fetotoxicity, or
teratogenicity at the level of 1,000 mg/ kg bwt/day. Therefore, the
maternal and developmental NOAELs for rats were established at
1,000 mg/kg bwt/day, the limit dose for this study type. No
teratogenic potential of propoxycarbazone sodium was evident in rats.

iii. Himalayan rabbits were administered propoxycarbazone sodium at
levels of 0, 20, 100, 500, or 1,000 mg/kg bwt/day by oral gavage on days
6 through 28 post coitum in a test for developmental toxicity. A
maternal NOAEL of 100 mg/kg bwt/day was established based on cold ears,
alopecia, swelling of vulva, decreased feed, and water intake, body
weight loss, gastrointestinal tract (GI) effects, liver effects, and
thyroid hormone level effects. The gestation rate NOAEL of
100 mg/kg bwt/day was based on one abortion (assessed as secondary due
to maternal toxicity) at 500 mg/kg bwt/day. The NOAEL for fetal
parameters of 500 mg/kg bwt/day was based on placental effects,
increased post-implantation loss, decreased number of fetuses, decreased
fetal weight, retarded fetal skeletal ossification, and possible
increase in lobulation of liver in fetuses at 1,000 mg/kg bwt/day. No
teratogenic potential of propoxycarbazone sodium was evident in
rabbits.>

<	4. Subchronic toxicity. i. A 28–day dermal toxicity study in Wistar
rats established a local and systemic NOAEL of 1,000 mg/kg bwt/day (the
dermal limit dose) for males and females.  

ii. A 14–week feeding study was conducted with Wistar rats at dietary
dose levels of 0, 250, 1,000, 4,000, or 20,000 ppm. The NOAEL was
determined to be 4,000 ppm (286.4 mg/kg bwt/day in males and 350.6 mg/kg
bwt/day in females) based upon increased water consumption (reversible
during the 4–week recovery period) and an irritative effect of the
forestomach epithelium (reversible during the 4–week recovery period)
in males and females dosed at 20,000 ppm as well as reduced glucose and
triglyceride levels in females only dosed at 20,000 ppm.

iii. A 91–day feeding study was conducted with B6C3F1 mice at dietary
dose levels of 0, 625, 2,500, or 10,000 ppm. The NOAELs determined for
males and females were 625 ppm (205 mg/kg bwt/day) and 2,500 ppm (1,159
mg/kg bwt/day), respectively, based on decreased body weights in 2,500
ppm males and 10,000 ppm females.

iv. A 2–month range-finding feeding study in Beagle dogs, at levels of
0, 1,000, 5,000, 10,000, and 40,000 ppm in the diet established a NOAEL
of 10,000 ppm (322.2 mg/kg bwt/day in males and 285.6 mg/kg bwt/day in
females) based on elevated hepatic biotransformation enzymes at 40,000
ppm.>

<	5. Chronic toxicity. i. A 2–year chronic/oncogenicity study was
conducted with male and female Fischer 344 rats at dietary levels of 0,
50, 500, or 1,000 mg/kg bwt/day for approximately the first seven
months of the study (dose adjustment). From approximately seven months
to study termination, the doses were 0, 1,000, 10,000, and 20,000 ppm in
the diet. A chronic toxicity NOAEL of 1,000 ppm (43 mg/kg bwt/day in
males and 49 mg/kg bwt/day in females) was determined based on increased
urine pH and decreased body weight gain at 1–year (but not 2 years) at
10,000 ppm and 20,000 ppm. No carcinogenic potential was indicated. 

ii. B6C3F1 mice were administered propoxycarbazone sodium via the diet
at levels of 0, 280, 1,400, and 7,000 ppm in a 2–year chronic
feeding/carcinogenicity study.  The chronic toxicity NOAEL was
established at 1,400 ppm (369.0 mg/kg/ day in males and 626.9 mg/kg
bwt/day in females) based on retarded body weight development. No
carcinogenic potential was indicated.

iii. A 1–year feeding study in Beagle dogs was conducted at 0, 2,000,
10,000, and 25,000 ppm in the diet. The NOAEL in males was determined to
be 10,000 ppm (258.0 mg/kg bwt/day) based upon increased absolute
adrenal gland weight without an increase in relative adrenal gland
weight and slight enlargement of zona fasciculata microscopically,
without a correlation to adrenal gland weight in males dosed at 25,000
ppm.  The NOAEL in females was determined to be 2,000 ppm (55.7 mg/kg
bwt/day) based upon decreased food consumption and decreased relative
heart weight in females dosed at 10,000 and 25,000 ppm. >

<	6. Animal metabolism. i. A single oral dose of 2 mg/kg/bwt
[triazolinone-3-14C] MKH–6561 was administered to rats. Between 22%
and 24% of the administered dose was absorbed. Maximum plasma radiation
levels were observed 0.33 hours after dosing. Within 48 hours of dosing,
between CA 88% and 97% of the radioactivity was excreted via urine and
feces.  Approximately 80–88% of the excreted radioactivity was
unchanged parent compound. The highest single metabolite concentration
was CA 3% of the administered dose. The terminal elimination half-live
for total radioactivity was CA 12–13 hours, so no bioaccumulation of
MKH–6561 or its metabolites will occur.

ii. Single oral doses of 2 mg/kg/bwt and 200 mg/kg/bwt
[phenyl-UL-14C]MKH–6561 were administered to rats. Between CA 21–31%
of the administered dose was absorbed. Maximum plasma radiation levels
were observed after 0.33 hours (low dose) and 1–hour (high dose).
Within 48 hours of dosing, CA 97–104% of the administered dose was
eliminated via urine and feces. Approximately 75–86% of the
administered dose was eliminated as unchanged parent compound. The
maximum single metabolite concentration was 8.8% of the administered
dose. At the end of the study, less than 0.25% of the administered dose
was found in organs and tissues. In a separate bile fistulation
experiment, the predominantly fecal elimination was confirmed to be due
to incomplete absorption of radioactivity from the GI tract. The
terminal elimination half-live for total radioactivity was CA 9–11
hours, so no bioaccumulation of MKH–6561 or its metabolites will
occur.

iii. Laying hens were given a daily dose of protonated MKH–6561
[phenyl-UL-14C] at 3.12 mg/kg/bwt for three consecutive days. The
residue levels were 1.343 ppm in liver, 0.017 ppm in muscle, 0.014 ppm
in fat, 0.006 ppm in the day–1 eggs, 0.009 ppm in the day–2 eggs,
and 0.012 ppm in the day–3 eggs. The residue levels based on a
theoretical 1x application rate, as determined from residue levels
observed in the propoxycarbazone sodium (MKH–6561) wheat field trials
would all be considerably less than 0.001 ppm. The major residue
identified in tissues and eggs were MKH–6561, Pr-2-OH MKH–6561,
MKH–6561 sulfonamide methyl ester, and saccharin. The major metabolic
pathway of MKH–6561 [phenyl-UL-14C] in poultry was hydrolysis of the
parent compound producing N-methyl propyl triazolinone and sulfonamide
methyl ester. The sulfonamide methyl ester was then converted to
saccharin. A minor pathway involved hydroxylation at the 2–position of
the triazolinone propoxy group. In the liver, the major metabolic
pathway led to the formation of protein bound MKH–6561 residue through
conjugation with the amino acid serine.

iv. Laying hens were given a daily dose of protonated MKH–6561
[triazolinone-3-14C] at 2.91 mg/kg/bwt for three consecutive days. The
residue levels were 0.184 ppm in liver, 0.044 ppm in muscle, 0.015 ppm
in the fat, 0.011 ppm in the day–1 egg, 0.016 ppm in the day–2 egg,
and 0.022 ppm in the day–3 egg. The residue levels in tissues and eggs
based on a theoretical 1x application, as determined from the residue
levels observed in the MKH–6561 wheat field trials, would all be
considerably less that 0.001 ppm. The metabolism of MKH–6561
[triazolinone-3-14C] appeared to involve both hydroxylation at the
2–position of the propoxy group and hydrolysis of the phenyl
sulfonamide linkage.

v. Goats were dosed with 1.0 mg/kg/bwt of MKH–6561 [phenyl-UL-14C] for
three consecutive days. Residue levels were 3.643 ppm in liver, 0.486
ppm in kidney, 0.009 ppm in muscle, 0.004 ppm in fat, 0.015 ppm in
day–1 milk and, 0.022 ppm in day–2 milk. The metabolic pathway was
based on hydrolysis of the sulfonamide to yield MKH–6561 sulfonamide
methyl ester and saccharin. The saccharin was then conjugated to
proteins which were found mainly in the liver and kidney.

vi. Goats were dosed with MKH–6561 [triazolinone-3-14C] at a dose of
0.98 mg/kg/bwt for 3 consecutive days. Residue levels were 0.171 ppm in
liver, 0.425 ppm in kidney, 0.040 ppm in muscle, 0.007 ppm in fat,
0.046 ppm in day–1 milk, and 0.057 ppm in day–2 milk. The metabolism
of propoxycarbazone sodium involved the cleavage of the phenyl
sulfonylurea side chain and the hydroxylation of the propyl side chain
on the triazolinone ring system after the cleavage of the phenyl
sulfonylurea side chain.>

<	7. Metabolite toxicology. i. 4-OH-saccharin is of low acute toxicity
to fasted rats following a single oral administration. The acute oral
LD50 is >5,000 mg/kg/bwt for males and females. 4-OH-saccharin is
considered non-mutagenic with and without S9 mix in the plate
incorporation as well as in the preincubation modification of the
Salmonella microsome test.

ii. MKH–8394 is of very low acute toxicity to fasted rats following a
single oral administration. The acute oral LD50 is>5,000 mg/kg/bwt for
males and females. MKH–8394 is considered non mutagenic with and
without S9 mix in the plate incorporation as well as in the
preincubation modification of the Salmonella microsome test.

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

iv. KTS–9304 has low to moderate acute toxicity to fasted rats
following a single oral administration. The acute oral LD50 was 263
mg/kg/bwt in males and 1,756 mg/kg/bwt in females. KTS–9304 is
considered non-mutagenic with and without S9 mix in the plate
incorporation as well as in the preincubation modification of the
Salmonella/microsome test. >

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

<C. Aggregate Exposure>

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

<	i. Food. Estimates of chronic dietary exposure to residues of
propoxycarbazone sodium utilized the current and new proposed tolerances
in grass forage and hay of 20 and 25 ppm, respectively, in cattle,
sheep, goats, horses, and hogs meat 0.1 ppm, and in cattle, sheep,
goats, horses, and hogs meat byproducts 1.0 ppm, and in milk 0.05 ppm. 
Other assumptions were that 100% of the target crop would be treated
with propoxycarbazone sodium and that no loss of residue would occur due
to processing or cooking. For chronic exposures, a reference dose (RfD)
of 0.748 mg/kg/day was assumed based on and NOAEL of 74.8 mg/kg bwt/day
from the 2-generation reproduction study in rats.  A safety factor of
100 was used based on interspecies extrapolation (10x) and intraspecies
variability (10x). The FQPA safety factor was reduced to 1x resulting in
a chronic population adjusted dose (cPAD) of 0.748 mg/kg/day. Using
these conservative assumptions, dietary residues of propoxycarbazone
sodium contribute 0.00219 mg/kg/day (0.3% of the cPAD) for children 1 to
2 years old, the most sensitive sub-population. For the U.S. population,
the exposure was 0.000504 mg/kg/day (<1% of the cPAD).  

EPA concluded in the Federal Register / Vol. 69, No. 129 / Wednesday,
July 7, 2004: “An effect of concern attributable to a single exposure
(dose) was not identified from the oral toxicity studies including the
developmental toxicity studies in rat and rabbits. Abortions seen in the
developmental toxicity study in rabbits at 1,000 mg/kg/day during GD
19–28, were not considered to be a single dose effect. Since they
occur late in gestation after repeated exposures. [sic]” >

<	ii. Drinking Water. For calculating drinking water exposure, the
Estimated Environmental Concentrations (EEC) were used as published by
EPA in the FR Vol. 69, No. 129, p. 40778, 07-Jul-04.  EPA used the FQPA
Index Reservoir Screening Tool (FIRST) or the Pesticide Root Zone
Model/Exposure Analysis Modeling System (PRZM/EXAMS), to produce
estimates of pesticide concentrations in surface water. The screening
concentration in ground water (SCI-GROW) model is used to predict
pesticide concentrations in shallow ground water.  Based on the FIRST
and SCI-GROW models, the EECs of propoxycarbazone sodium for acute
exposures are estimated to be 2.3 parts per billion (ppb) for surface
water and 0.4 ppb for ground water. The EECs for chronic exposures are
estimated to be 0.9 ppb for surface water and 0.4 ppb for ground water.
 

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

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

<D. Cumulative Effects>

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

<E. Safety Determination>

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

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

<F. International Tolerances>

<	There are currently no Codex, Canadian, or Mexican tolerances
established for propoxycarbazone sodium.  >

>

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