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

EPA Registration Division Contact: Kathryn Montague (703) 305-1243 

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:

[K-I CHEMICAL U.S.A., INC.]

[Insert petition number]

	EPA has received a pesticide petition ([insert petition number]) from
K-I CHEMICAL U.S.A., INC. c/o Landis International, Inc., P. O. Box 5126
Valdosta, GA  31603-5126 proposing, pursuant to section 408(d) of the
Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to
amend 40 CFR part 180 by establishing  tolerances for residues of the
sum of pyroxasulfone
[3-[[[5-(difluoromethoxy)-1-methyl-3-(trifluoromethyl)-1H-pyrazol-4-yl]m
ethyl]sulfonyl]-4,5-dihydro-5,5-dimethylisoxazole] and its metabolite
5-(difluoromethoxy)-1-methyl-3-(trifluoromethyl)-1H-pyrazol-4-carboxylic
 acid (M-3) calculated as the stoichiometric equivalent of
pyroxasulfone, in or on the raw agricultural commodities corn, field,
grain at 0.02 ppm (parts per million) and pyroxasulfone
[3-[[[5-(difluoromethoxy)-1-methyl-3-(trifluoromethyl)-1H-pyrazol-4-yl]m
ethyl]sulfonyl]-4,5-dihydro-5,5-dimethylisoxazole] and its metabolites
[5-(difluoromethoxy)-1-methyl-3-(trifluoromethyl)-1H-pyrazol-4-yl]methan
esulfonic acid (M-1),
5-(difluoromethoxy)-1-methyl-3-(trifluoromethyl)-1H-pyrazol-4-carboxylic
 acid (M-3), and
[5-(difluoromethoxy)-3-(trifluoromethyl)-1H-pyrazol-4-yl]methanesulfonic
acid (M-25), calculated as the stoichiometric equivalent of
pyroxasulfone, in or on the raw agricultural commodities corn, field,
forage at 0.09 ppm (parts per million).  EPA has determined that the
petition contains data or information regarding the elements set forth
in section 408 (d)(2) of  FDDCA; however, EPA has not fully evaluated
the sufficiency of the submitted data at this time or whether the data
supports granting of the petition. Additional data may be needed before
EPA rules on the petition.

Residue Chemistry

1. Plant Metabolism. Plant metabolism studies were conducted and
accepted by the Agency for soybean and field corn.  The plant and animal
metabolism of pyroxasulfone is well understood. Primary metabolic
processes are cleavage between the two ring structures, side chain
oxidation to carboxylic acid and demethylation.  Pyroxasulfone and its
major metabolites M-1, M-3, and M-25 were metabolites in corn and
soybean.  The metabolism of pyroxasulfone in plants and animals is
understood for the purposes of the proposed tolerances.  Pyroxasulfone
and its metabolites M-1, M-3, M-25and M-28 are the residues of concern
for tolerance setting purposes for soybean.

	2. Analytical method. EPA has approved an analytical enforcement
methodology including liquid chromatography, mass spectrometry, and mass
spectrometry (LC/MS/MS) to enforce the tolerance expression for
pyroxasulfone. 

	3. Magnitude of residues. 

Corn Residue Data

Initially, a total of 37 corn residue raw agricultural commodity (RAC)
field trials were conducted in regions 1, 2, 3, 5, 6, 10, 11 and 12 of
the United States (MRID 47701656). A total of 11 of these trials were
sweet corn trials and the remaining were field corn trials. Three of
these trials were residue decline trials to determine residue decline in
the respective corn RAC matrices after application. Three comparison
trials, on three different soil types; fine, medium and course, were
conducted to compare five different application types in different plots
at the same site including pre-plant to surface, pre-plant incorporated,
post-planting but pre-emergence of weeds or crop, early postemergence
and split application with pre-emergence and post-emergence. Application
rates for these comparison trials were 166 g a.i./ha, 209 g a.i./ha and
300 g a.i.lha for the course, medium and fine soil type, respectively.
For the remaining 34 studies, application rates were 166 g a.i./ha on
course soil types and 300 g a.i./ha on medium and fine soil types.
Applications for these 34 trials were post-emergence applications
(approximately V4 growth stage). One trial included a plot with a 5X
application rate (post-emergence) in which the grain was collected for
processing. Samples were collected from each plot at the appropriate
time (normal maturity except samples from the residue decline trials
which were collected earlier). Matrices were extracted with acetonitrile
or aqueous methanol followed by various cleanup steps depending on the
matrix and ana1yte. Analysis was performed using LC-MS/MS for
pyroxasu1fone and its metabolites in all matrices. The LOQ was 0.005 ppm
for all matrices except two metabolites one in meal and one in oil for
the LOQs which were 0.01 ppm. The residue in all field com grain samples
was below LOQ. All field com processed commodity matrix samples showed
residues less than the respective LOQ for that particular matrix.

A second study (MRID 48767101) was conducted to obtain RAC residue data
for pyroxasulfone (KIH-485) and its metabolites M-1, M-3, and M-25 on
corn following a single post-emergence application of pyroxasulfone 85
WG herbicide at the V3-V5 growth stage with and without adjuvant and
fertilizer to determine if adding fertilizer and/or adjuvant to the
spray solution affected the residues in the harvested crop. The matrices
analyzed were forage, stover, and grain, and residues of KIH-485, M-1,
M-3, and M-25 were analyzed. The study was conducted at three trial
locations in the United States including: Georgia (GA), Missouri (MO),
and Nebraska (NE), representing United States EPA Regions 2, 4 and 5,
respectively. The protocol was designed according to a request from the
EPA regarding the number of treated plots and treatments and the number
of treated samples (4 treated samples collected per plot instead of 2 as
required by the guideline). In each trial, there was one non-treated
plot and three treated plots. Applications were made related to the soil
type at a target rate of 0.148 lb ai/A (166 grams ai/ha) for the coarse
textured soil site (GA) and 0.268 lb ai/A (300 grams ai/ha) for the
other two locations MO and NE (medium and fine textured soil sites,
respectively). At the appropriate preharvest harvest intervals (PHIs),
corn samples were collected for each matrix (forage, stover, and grain),
frozen and shipped frozen to the analytical laboratory for analysis. A
limit of quantitation (LOQ) of 0.005 ppm was determined for the parent
molecule (KIH-485), M-1, M-3 and M-25. Concurrent recoveries were
conducted with fortification levels of 0.005 ppm and 0.05 ppm. Most
recoveries for all analyses of each analyte in each matrix were within
the accepted range (70-120%). No residue of the parent pyroxasulfone
molecule was seen in any corn matrix above the LOQ of 0.005 ppm.
Residues of the metabolites of pyroxasulfone (M-1, M-3, and M-25) were
found in selected samples. These residues were added to the OECD MRL
calculator along with the original corn field trial residues without
adjuvant to determine the appropriate tolerances. As indicted by EPA
memo dated January 10, 2013 DP Barcode:  D402247 (Pyroxasulfone. Summary
of Residue Data for Pyroxasulfone Use on Corn with and without Adjuvant
and Field Rotational Crop Residue Data) and EPA email dated March 20,
2013 the purpose of this tolerance petition is to increase the corn
forage tolerance from 0.06 ppm to 0.09 ppm due the conservative
tolerance determined by the OECD MRL calculator. 

Confined Rotational Crop Study

Pyrazole or isoxazoline ring labeled 14C KIH-485 was sprayed on confined
plots of bare soil prior to planting soybean, radish and wheat at 30,
120 and 365 day intervals.  There were two treated plots for each
plantback interval, one of which was wheat only and the other was
planted half with soybean and half with radish.  All plots were treated
at a target application rate of 300 g a.i./ha but the actual rate was
313 g a.i./ha.  Samples were analyzed by combustion analysis and liquid
scintillation counting.  All treated crops contained radioactive residue
>0.01 ppm and were subjected to further analysis.  The highest total
radioactive residue (TRR), 5.2 ppm was found at the 30 day rotational in
wheat straw; the residue level declined to 0.02 ppm at 485 days.  The
primary metabolites were M-1 and M-3.  

Field Rotational Crop Study

A field rotational crop study was conducted in Georgia (GA) and Texas
(TX) on a fine and coarse textured soil, respectively. The purpose of
the study was to obtain raw agricultural commodity (RAC) residue data
for pyroxasulfone and its metabolites M-1, M-3, M-25, M-28, and M-37 on
rotational crops that are planted in plots that have been treated with
Pyroxasulfone 85 WG at the proposed label rate and aged for various time
intervals prior to planting the rotational plot. Each plot was treated
at an appropriate time for growing the target crop and then allowed to
age for the specified aging interval (120, 270, 300 and 365 days,
nominal intervals).  There was no residue seen in any crop matrix at any
sampling interval above the LOQ except for one replicate 120 day potato
top sample which showed residue of M-1 at the LOQ (0.01 ppm).    As a
result, neither pyroxasulfone nor any of its metabolites are expected to
accumulate in rotational crops when Pyroxasulfone 85 WG is applied to
target crops at the labeled rates.      

   

Cow Feeding Study

	Holstein dairy cows were treated orally with gelatin capsules fortified
with pyroxasulfone.  These were administered once daily for 28
consecutive days at dose levels of 0, 1.8, 5.4, and 18 ppm per cow/day
on a dry weight basis amounting to concentrations of control, 1X, 3X and
10X dose groups, respectively.  These dose levels were equivalent to 0,
35.8 mg/cow/day, 109.9 mg/cow/day and 367.4 mg/cow/day, respectively. 
Milk samples from the high dose animals (10X) were found to contain no
residues of the parent compound or metabolites with the exception of 3
milk samples from day 7 which contained an average of 0.003 ppm parent
pyroxasulfone.  No other milk samples from the other dose levels were
found to contain residues of pyroxasulfone or metabolites.  No other
matrix (muscle, liver, kidney or fat) was found to contain residues of
pyroxasulfone or metabolites above LOQ.  The LOQs were 0.001 ppm in milk
and 0.01 ppm in all other matrices.  Therefore, no tolerances for
residues of pyroxasulfone and its metabolites are being proposed for
meat, milk, eggs or other edible tissues of livestock or poultry.

B. Toxicological Profile

1.  Acute Toxicity. Pyroxasulfone was found to be of low acute toxicity
via oral, dermal and inhalation routes of administration.  It was not
irritating to skin or eyes and was not a sensitizing agent.  The
formulated product (85WG) was also of low acute toxicity and was found
to be mildly irritating to skin, moderately irritating to eyes and was a
dermal sensitizer.  In an acute neurotoxicity study in rats, there were
no test substance-related effects on body weights, food consumption,
clinical observations, functional observational battery assessments,
motor activity measurements, or gross and microscopic neuropathology.
The NOEL was demonstrated to be >2000 mg/kg/day in adult male and female
rats.

2.  Genotoxicity. Pyroxasulfone and its metabolites and impurities do
not induce gene mutations in bacterial cells.  Pyroxasulfone does not
induce gene mutations or chromosomal aberrations in in vitro mammalian
cells or in vivo in the mouse micronucleus test.  Pyroxasulfone is
non-genotoxic.

3.  Reproductive and developmental toxicity. In a developmental toxicity
study in rats, the NOEL for maternal and developmental toxicity was
>1000 mg/kg/day, the highest dose tested.

	In a developmental toxicity study in rabbits, there were slight test
substance-related effects on fetal weight and number of implant
resorptions at 1000 mg/kg/day, the highest dose tested.  The NOEL for
maternal toxicity was 1000 mg/kg/day. The NOEL for developmental
toxicity was 500 mg/kg/day.

	In a rat one-generation reproductive study no reproductive toxicity was
observed up to and including the high dose of 5000 ppm.  The NOEL for
reproductive toxicity was >5000 ppm, the highest dose tested.  The NOEL
for P1 adult rats was 25 ppm.  The NOEL for F1 offspring was 250 ppm and
the NOEL for F1 adults was 250 ppm.

	In a rat two-generation reproduction study there were no test
substance-related effects for reproductive toxicity at 2000 ppm, the
highest concentration tested.   The NOEL for reproductive toxicity was
>2000 ppm, the highest concentration tested. Test substance-related
effects were observed at 2000 ppm in both adults and offspring.
Therefore, the NOAEL for systemic toxicity was demonstrated to be 100
ppm (6.94 – 11.76 mg/kg/day) in both parents and offspring.

	In a developmental neurotoxicity study conducted on pyroxasulfone in
mated female rats no reproductive effects were observed in the maternal
animals at 2000 ppm, the highest concentration tested. No effects were
observed on FOBs, auditory startle response habituation, pre-pulse
inhibition, learning and memory of offspring.  A slight (5%) decrease in
absolute brain weight at 900 mg/kg/day was present on PD 66, although no
effect was present when evaluated on a % body weight basis.  Based on
the effects observed in this study, the maternal and offspring systemic
NOAEL is 900 mg/kg/day. The NOEL for functional development was judged
to be 900 mg/kg/day. A NOEL for histomorphological development of the
brain of the offspring was judged to be 300 mg/kg/day.

	Two studies were performed to assess the availability of the test
substance to the pup.  These studies indicated that pyroxasulfone was
available in the milk to nursing pups.

	4.  Subchronic toxicity. Pyroxasulfone was evaluated in a 28-day
inhalation toxicity study in rats.  There were no test substance-related
effects.  The NOEL was >200 mg/m3, the highest dose tested.

	In a 28-day dermal toxicity study there was a test substance-related
increase in the incidence of minimal to mild cardiac myofiber
degeneration with inflammation observed in males and females dosed with
1000 mg/kg/day and cutaneous myofiber degeneration with inflammation
observed in the treated skin of males dosed with 1000 mg/kg/day.  The
NOEL was 100 mg/kg/day.

	Immunotoxicity was evaluated in rats and mice following dietary
exposure for 28 days.  There were no test substance related effects for
any of the immunotoxicity parameters examined.  In the rat, systemic
toxicity was limited to reductions in body weight and food consumption. 
The NOEL for immunotoxicity was 7500 ppm (529 and 570 mg/kg in males and
females) and the NOEL for systemic effects was 250 ppm (18 and 19 mg/kg
in males and females).  In the mouse, the NOEL for immunotoxicity was
4000 ppm (633 mg/kg/day males: 791 mg/kg/day females) and the NOEL for
systemic effects was 400 ppm (61 mg/kg males: 77 mg/kg females).

	Pyroxasulfone was evaluated in 13-week oral toxicity studies in rats,
mice and dogs. In the 13 week mouse study, no test substance-related
effects on in-life and clinical pathology parameters were observed at
any level tested. Test substance-related effects at 2500 ppm were
limited to an increased incidence of minimal to mild chronic progressive
nephropathy in female mice and increased liver weight in males and
females fed 2500 ppm.  The NOEL was 250 ppm for female mice (51.2
mg/kg/day).  The NOEL for male mice was 2500 ppm (394.0 mg/kg/day).

	 In the 13 week rat study, a NOEL of 250 ppm for male and female rats
corresponded to mean daily intake values of 16.4 and 20.6 mg/kg/day in
males and females, respectively.  Test substance related effects were
increased cardiac myofiber degeneration with inflammation and diffuse
mucosal hyperplasia of the urinary bladder.  Increased liver weights and
centrilobular hypertrophy were also observed in 2500 ppm males and
females. In a second study evaluating recovery, full or partial recovery
was evident in all the above effects apart from kidney weights in
females with all microscopic findings in the liver, heart, muscle and
pancreas of 5000 ppm animals comparable to control rats indicating a
complete reversal of the treatment-related findings noted at the
terminal sacrifice.

	In an oral 90 day toxicity study in beagle dogs administered
pyroxasulfone in a capsule, the NOEL was 2.0 mg/kg. The only effects
noted were degeneration of muscle fiber of the musculature portion of
the diaphragm, hyperplasia of the satellite cell of the muscle and nerve
fiber degeneration of the sciatic nerve in one 10mg/kg/day group male
only.  In a second study dosed with 0 or 15 mg/kg of pyroxasulfone, 
male dogs showed a decrease in body weight and histopathology similar to
the full study.

	Pyroxasulfone was evaluated in a subchronic 90 day neurotoxicity
dietary study in rats.  There were no effects on body weights, food
consumption, clinical observations, FOB assessments, motor activity
measurements, or gross and microscopic neuropathology. The NOEL was
>2500 ppm, the highest dose tested, for male and female rats
corresponding to mean daily intake values of 161.48 and 199.59 mg/kg/day
in males and females, respectively.

5.  Chronic toxicity. Chronic toxicity studies were conducted in the rat
and dog. In the rat one year chronic toxicity study test
substance-related effects occurred at 1000 ppm and above that included
reduced body weight parameters and microscopic findings in the liver
(centrilobular hepatocellular hypertrophy in males), heart (increased
cardiomyopathy in females) and urinary bladder (mucosal hyperplasia in
males and females) and urinary bladder hyperplasia considered to be
secondary to inflammation or irritation.  At 2000 ppm, these effects
were accompanied by increased clinical observations of red discharge
from the penis and associated red-stained cageboards as well as
increased liver and kidney weights. A slight increase in liver and
kidney weights was observed in the 2000 ppm male and female dietary
exposure groups. The NOEL is 50 ppm (2.22 and 3.12 mg/kg/day for males
and females, respectively).

	In a one-year dog study beagle dogs/sex/dose were administered capsules
containing 0.0, 0.2, 2.0 and 10.0 mg/kg/day.  Adverse test
article-related findings were limited to the 10.0 mg/kg/day group, the
highest dose tested and not all animals at the 10 mg/kg/day dosage had
clear test-article related abnormal observations.  Adverse changes in
the clinical pathology parameters were increases in creatine kinase,
aspartate aminotransferase and change in the pathology limited to the
sciatic nerve and spinal cord.  The NOAEL is 2.0 mg/kg/day.

	The carcinogenic potential of pyroxasulfone was evaluated in rats and
mice. The Agency has classified pyroxasulfone as “Not likely to be
carcinogenic to humans” at doses that do not cause crystals with
subsequent calculi formation resulting in cellular damage of the urinary
tract.

6.  Animal metabolism.  In the rat, pyroxasulfone is rapidly and
completely eliminated.  Between 80 to 90% of pyroxasulfone was
eliminated in the urine during the first 24 hours and elimination was
essentially complete after 48 to 72 hours.  Absorption was calculated
(bile and urine) at 76%.  Maximum plasma concentrations were achieved at
2 hours in the low and 11 hours in the high dose animals.  At 96 hours
only 7% of the low dose and <0.5% of the high dose was present in the
carcass demonstrating the near complete elimination of pyroxasulfone. 
Of the radioactivity present in the animals, the highest levels were
seen in the liver and kidney.  The major metabolites were a carboxylated
(pyrazole ring methyl group) and cleavage products between the
isoxazoline and pyrazole ring structure with subsequent carboxylation. 
The absorption, distribution, metabolism and elimination of
pyroxasulfone is unaffected by sex or treatment regimen.   

	In a preliminary study in the dog, pyroxasulfone is rapidly eliminated
with 76.9% of radioactivity excreted within 24 hours.  Excretion is
approximately equal in urine and feces. The terminal half life was 89.58
hr and 40.80 hr in blood and plasma, respectively.  The feces were found
to contain only unchanged pyroxasulfone while no parent molecule was
found in the urine.  At 120 hr after dosing, the levels of radioactivity
in the tissues were highest in the liver and blood. 

	In a preliminary mouse metabolism study, 73% of the applied dose of
pyroxasulfone was excreted in urine within 24 hours of dosing. 
Pyroxasulfone was rapidly absorbed and distributed through the tissues
of the mouse but by 24 hours after dosing, radioactivity concentrations
in the majority of tissues were indistinguishable from background
levels.

	Metabolism studies in livestock and poultry (Nature of Residue Studies
with Goat and Hen) with repeated dose established that pyroxasulfone was
rapidly metabolized and excreted and that there was minimal transmittal
of residues of pyroxasulfone and its metabolites to meat or milk.  For
goats fed 10 ppm of radiolabeled pyroxasulfone, the highest residues
(TRR) were seen in liver and kidney.  In the hen, fed 10 ppm, the
highest residue was seen in liver and muscle.  

7.  Metabolite toxicology. Three plant metabolites and three impurities
were evaluated in acute oral toxicity studies.  All six test substances
evaluated showed LD50’s >2000 mg/kg similar to the parent,
pyroxasulfone.  Two metabolites were further assessed in a 14 day
toxicity study in rats.  The NOEL for each of the metabolites was > 1000
mg/kg.  The same three metabolites and impurities were evaluated in a
bacterial gene mutation test with and without activation.  All test
substances were non-genotoxic.  

8.  Endocrine disruption. Pyroxasulfone does not belong to a class of
chemicals known or suspected of having adverse effects on the endocrine
system.  There is no evidence that pyroxasulfone has any effect on
endocrine function in developmental, reproduction or developmental
neurotoxicity studies.  Furthermore, histological investigation of
endocrine organs in chronic dog, rat and mouse studies did not indicate
that the endocrine system is targeted by pyroxasulfone.

C. Aggregate Exposure

	1. Dietary exposure. It can be concluded with reasonable certainty that
residues of pyroxasulfone in food will not result in unacceptable levels
of human health risk. Using proposed tolerances for corn, soybean and
wheat, both the acute and chronic dietary exposure MOEs for the overall
US population and 25 population subgroups are above the EPA level of
concern.

	i. Food. Acute and chronic dietary exposure assessments were conducted
using a Tier I approach.  This Tier I assessment incorporated tolerance
level residues and 100% crop-treated in the DEEMTM (Dietary Exposure
Evaluation Model; Exponent, Inc., 2003) software system.  The acute
toxicological endpoint selected for assessment of risk following acute
dietary exposure was 300 mg/kg/day based on the Developmental
Neurotoxicity Study with a NOEL 300 mg/kg/day for motor activity and
brain morphology. The acute reference dose (aRfd) was determined to be 3
mg/kg/day assuming the aRdf is 1 percent of the NOEL. The chronic
toxicological endpoint selected for assessment of risk following chronic
dietary exposure was 2 mg/kg/day based on the one-year chronic feeding
dog study with a NOEL of 2 mg/kg/day. The chronic reference dose (cRfd)
was determined to be 0.02 mg/kg/day assuming the cRfd is 1 percent of
the NOEL. Using proposed tolerances for corn, soybean, wheat, and cotton
the acute and chronic dietary exposure Margin of Exposure (MOEs) for the
overall US population and 25 population subgroups are above the EPA
level of concern. It can be concluded with reasonable certainty that
residues of pyroxasulfone in food will not result in unacceptable levels
of human health risk. 

	ii. Drinking water. Based on the Pesticide Root Zone Model/Exposure
Analysis Modeling System (PRZM/EXAMS) and Pesticide Root Zone Model
Ground Water (PRZM GW), the estimated drinking water concentrations
(EDWCs) of pyroxasulfone for acute exposure are estimated to be 17 ppb
for surface water and 210 ppb for ground water. EDWCs of pyroxasulfone
for chronic exposures for non-cancer assessments are estimated to be 3.2
ppb for surface water and 174 ppb for ground water. It can be concluded
with reasonable certainty that residues of pyroxasulfone in drinking
water will not result in unacceptable levels of human health risk. 

	2. Non-dietary exposure. Pyroxasulfone is not intended for any specific
use patterns that would result in residential exposures. 

D. Cumulative Effects

	Pyroxasulfone represents a new class of pyrazole herbicides.  No other
products are known to have the same mode of action as pyroxasulfone.
Therefore, a cumulative assessment is not appropriate at this time.

E. Safety Determination

	1. U.S. population. The toxicity database for pyroxasulfone is
complete. Based on the NOEL of 2 mg/kg/day from a 1-year toxicity study
in the dog, proposed uses represent 1 percent of the cRfD of 0.02
mg/kg/day.  Based on the NOEL of 300 mg/kg/day from a developmental
neurotoxicity study, the proposed uses represent 1 percent of the RfD of
3 mg/kg/day.  There is reasonable certainty that no harm to the U.S.
population will result from the proposed uses of pyroxasulfone.

	2. Infants and children. The toxicity database for pyroxasulfone is
complete.  The database includes acute, subchronic, chronic,
mutagenicity, genotoxicity, developmental, reproduction, neurotoxicity
and immunotoxicity studies on pyroxasulfone and acute mutagenicity and
genotoxicity studies on several metabolites.  The weight of evidence
indicates that infants and children are not expected to be more
sensitive to pyroxasulfone than are adults.  Consequently, EPA reduced
the FQPA Safety Factor from 10x to 1x.

F. International Tolerances.

	Tolerances are approved on wheat, barley and triticale in Australia.
Tolerances are simultaneously being sought in Canada at the same levels
and for the same crops as for the U.S.  

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