 

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

<EPA Registration Division contact: Shaunta Hill, 703-347-8961>

Pyraclostrobin soybean.

 

<>

<TEMPLATE:>

<BASF Corporation>

<9F7590>

<	EPA has received a pesticide petition (9F7590) from BASF Corporation],
PO Box 13528, Research Triangle Park, North Carolina, 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 to establish
tolerances for pyraclostrobin, carbamic acid,
[2-[[[1-(4-chlorophenyl)-1H-pyrazol-3-yl]oxy]methyl]phenyl]methoxy-,
methyl ester and its metabolite methyl-N-[[[1-(4-chlorophenyl)
pyrazol-3-yl]oxy]o-tolyl] carbamate (BF 500-3); expressed as parent
compound in or on the raw agricultural commodity soybean, forage, and
soybean, hay at 11.0 and 14.0 parts per million (ppm), respectively. 
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.>

<A. Residue Chemistry>

<	1. Plant metabolism. Plant and animal metabolism. Nature of the
residue studies (OPPTS 860.1300) were conducted in grape, potato and
wheat as representative crops in order to characterize the fate of
pyraclostrobin in all crop matrices.  Pyraclostrobin demonstrated a
similar pathway and fate in all three crops. In all three crops the
pyraclostrobin Residues of Concern (ROC) of were characterized as parent
(pyraclostrobin) and BAS 500-3), methyl-N[[[1-(4-chlorophenyl)
pyrazol-3yl]oxy]o-tolyl carbamate.  In hens the residues of concern were
determined to be parent compound and a hydroxlated metabolite, BAS
500-16.  In goats the residues of concern were determined to be parent
and a hydroxylated metabolite BAS 500-10. 

>

<	2. Analytical method. In plants the method of analysis is aqueous
organic solvent extraction, column clean up and quantitation by
LC/MS/MS.  In animals the method of analysis involves base hydrolysis,
organic extraction, column clean up and quantitation by LC/MS/MS or
derivatization (methylation) followed by quantitation by GC/MS.>

<	3. Magnitude of residues. Field trials were carried out in order to
determine the magnitude of the residues in soybean, forage, and soybean,
hay, to satisfy the requirements for a tolerance of pyraclostrobin in
these commodities.  Field trials were carried out using the maximum
proposed labeled rate, maximum proposed number of applications, and the
minimum proposed pre-harvest interval. >

  

<B. Toxicological Profile>

<	1. Acute toxicity.  Pyraclostrobin and its formulated products have
favorable acute toxicity. The acute toxicity studies place technical
pyraclostrobin in toxicity category IV for acute oral and acute
inhalation and category III for acute dermal.  Pyraclostrobin is
category III for both eye and skin irritation, and it is not a dermal
sensitizer.  Two formulated end use products are proposed, an
Emulsifiable Concentrate (EC) and an Extruded Granule (EG).  The EC has
an acute oral toxicity category of II, acute dermal of III, acute
inhalation of IV, eye and skin irritation categories of III, and is not
a dermal sensitizer.  The EG has acute oral and dermal toxicity
categories of III, acute inhalation of IV, eye irritation of III, skin
irritation of IV and is not a dermal sensitizer.>

<	2. Genotoxicty. Pyraclostrobin was negative for inducing mutations in
both an in vitro Ames test and an in vitro CHO/HGPRT Locus Mammalian
Cell Mutation Assay.  Pyraclostrobin also demonstrated no chromosomal
effects in an in vitro V79 Cells CHO Cytogenetic Assay and an in vivo
Mouse Micronucleus test.  An additional in vitro study investigating DNA
damage and repair also showed no effects. Pyraclostrobin has been tested
in a total of 5 genetic toxicology assays consisting of in vitro and in
vivo studies.  It can be stated that pyraclostrobin did not show any
mutagenic, clastogenic or other genotoxic activity when tested under the
conditions of the studies mentioned above.  Therefore, pyraclostrobin
does not pose a genotoxic hazard to humans.>

<	3. Reproductive and developmental toxicity. The reproductive and
developmental toxicity of pyraclostrobin was investigated in a
2-generation rat reproduction study as well as in rat and rabbit
teratology studies.  There were no adverse effects on reproduction,
systemic toxicity to adults or developmental toxicity in the
two-generation study so the NOAEL is the highest dose tested of 300 ppm
(approximately 32.6 mg/kg bw/day).>  

No teratogenic effects were noted in either the rat or rabbit
developmental studies.  In the rat study, maternal toxicity observed at
the mid and high dose consisted of decreased food consumption and body
weight gain.  Developmental changes noted at the high dose were
increased incidences of dilated renal pelvis and cervical ribs with no
cartilage.  The maternal NOAEL was 10 mg/kg bw and the developmental
NOAEL was 25 mg/kg bw.

In the rabbit teratology study, maternal toxicity observed at the mid
and high doses consisted of decreased food consumption and body weight
gain (severe at the high dose).  An increased postimplantation loss was
also observed at the mid and high doses due to an increase in early
resorptions.  In rabbits, these types of effects are often observed with
significant stress on the mothers (as seen by the body weight gain
decrease in this study) and not indicative of frank developmental
toxicity.  The NOAEL for both maternal and developmental toxicity was 5
mg/kg bw.

<	4. Subchronic toxicity. The subchronic toxicity of pyraclostrobin was
investigated in 90-day feeding studies with rats, mice and dogs, and in
a 28-day dermal administration study in rats.  A 90-day neurotoxicity
study in rats was also performed.  Generally, mild toxicity was
observed.  At high dose levels in feeding studies, general findings in
all three species were decreased food consumption and body weight gain
and a thickening of the duodenum.  Anemia occurred at high dose levels
in both rats and mice with accompanying extramedullary hematopoiesis of
the spleen in rats.  In rats only, a finding of liver cell hypertrophy
was indicative of a physiological response to the handling of the
chemical.   The lowest NOAEL in the 90-day feeding studies was from the
dog study and determined to be 5.8 mg/kg bw/day.

In the 28-day repeat dose dermal study, no systemic effects were noted
up to the highest dose tested of 250 mg/kg bw/day.   

In a 90-day rat neurotoxicity study, a direct neurotoxic effect was not
observed.>

<	5. Chronic toxicity. Pyraclostrobin was administered to groups of 5
male and 5 female purebred Beagle dogs in the diet at concentrations of
0, 100, 200 and 400 ppm over a period of 12 months.   Signs of toxicity
were observed at the high dose.  Diarrhea was observed throughout the
study period for both sexes. High dose males and females initially lost
weight and body weight gain was decreased for the entire study period
for females.  Hematological changes observed were an increase in white
blood cells in males, and an increase in platelets in both sexes at the
high dose.  Clinical chemistry demonstrated a decrease in serum total
protein, albumin, globulins and cholesterol in high dose animals of both
sexes possibly due to the diarrhea and reduced nutritional status of the
animals.  The NOAEL was 200 ppm (ca. 5.5 mg/kg bw/day males; 5.4 mg/kg
bw/day females).

	

In an oncogenicity study, pyraclostrobin was administered to groups of
50 male and 50 female Wistar rats at dietary concentrations of 0; 25;
75, and 200 ppm for 24 months.  In a companion chronic toxicity study,
20 rats/sex were used at the same dose levels as in the oncogenicity
study.  A body weight gain depression of 10-11% in males and 14-22% in
females with an accompanying decrease in food efficiency was observed at
the high dose.  There was no evidence that pyraclostrobin produced a
carcinogenic effect in rats.  The NOAEL for the chronic rat and the
cancer rat study is 75 ppm (ca. 3.4 mg/kg bw/day males; 4.7 mg/kg bw/day
females).

Pyraclostrobin was administered to groups of 50 male and 50 female
B6C3F1 mice at dietary concentrations of 0, 10, 30, 120 and 180 ppm
(females only) for 18 months.  Body weights were reduced at the highest
doses tested in both males and females.  At the high dose, body weight
gain decreases of 27% in females and 29% in males with an accompanying
decrease in food efficiency were observed.  No other signs of toxicity
were noted at any dose level.  The NOAEL was found to be 30 ppm (ca. 4.1
mg/kg bw/day) for males. The Agency determined that the body weight
effect at the high dose in females was not sufficient to determine an
MTD.  Therefore the NOAEL for females is considered greater than the
highest dose tested of 32.8 mg/kg bw/day.   There was no evidence that
pyraclostrobin produced a carcinogenic effect in mice.]>

<	6. Animal metabolism. In a rat metabolism study with pyraclostrobin,
10-13% of the administered dose was excreted in the urine and 74-91% in
the feces within 48 hours.  Excretion via bile was significant
accounting for 35-38% of the administered dose. By 120 hours after
dosing, very little radioactivity remained in tissues. Pyraclostrobin
was rapidly and almost completely metabolized.  Very little unchanged
parent was detected.  The phase one biotransformation is characterized
by N-demethoxylation, various hydroxylations, cleavage of the ether bond
and further oxidation of the two resulting molecule parts.  Conjugation
of the formed hydroxyl groups by glucuronic acid or sulfate also
occurred. In summary, pyraclostrobin is extensively metabolized and
rapidly eliminated primarily via the bile, with no evidence of
accumulation in tissues.>

<	7. Metabolite toxicology. A comparison of the rat metabolism results
with the plant metabolism/residue results indicates that toxicology
studies performed with the parent pyraclostrobin are sufficient to cover
dietary exposure.  Plant residues are primarily the parent compound with
a fraction (up to 10-20% at most) being the demethoxylated parent.  This
metabolite is referred to as BF 500-3 in the plant studies and as 500M07
in the rat study.  This metabolite in the rat is the first step in the
major biotransformation process leading to the majority of the
metabolites determined in the major excretion pathway.>

<	8. Endocrine disruption. Endocrine effects. No specific tests have
been conducted with pyraclostrobin to determine whether the chemical may
have an effect in humans that is similar to an effect produced by a
naturally occurring estrogen or other endocrine effects.  However, there
were no significant findings in other relevant toxicity studies (i.e.,
subchronic and chronic toxicity, teratology and multi-generation
reproductive studies) which would suggest that pyraclostrobin produces
endocrine related effects.>

<C. Aggregate Exposure>

<	1. Dietary exposure. Exposure assessments were conducted to evaluate
the potential risk due to acute and chronic dietary exposure to residues
of pyraclostrobin.  This analysis includes all current established
tolerances for pyraclostrobin in crop and animal commodities and the
proposed new tolerances in soybean, forage, and soybean, hay.  The
proposed new tolerances for soybean, forage, and soybean, hay, are 11.0
and 14.0 ppm, respectively.  The acute dietary assessments were
conducted using 100% crop treatment factors, tolerance level or highest
residue levels, and experimentally derived processing factors for fruit
juices, tomato, and wheat commodities.  The chronic assessment was
conducted using tolerance or average residues levels, 100% crop
treatment factors, and experimentally derived processing factors for
fruit juices, tomato, and wheat commodities.  Average residues were used
for apple, broccoli, celery, collards, grape, lettuce, citrus, pepper,
mustard greens, and tomatoes.  As soybean forage and hay are commodities
utilized for animal consumption and not human consumption, no impact is
anticipated on the acute dietary risk assessment as the proposed
tolerances do not exceed those currently established for animal feed
purposes.

The pyraclostrobin chronic reference dose (cRfD) is 0.034 mg/kg bw/day
based on the NOAEL of 3.4 mg/kg bw/day in the rat chronic toxicity study
and a 100X safety factor.  The acute reference dose (aRfD) is 3 mg/kg
b.w./day for the general population based on a NOAEL from the acute
neurotoxicity study of 300 mg/kg bw/day and a 100X safety factor.  For
females of child bearing years (13-49 years), the aRfD is 0.05 mg/kg
b.w./day based on the NOAEL of 5 mg/kg bw/day from the rabbit teratology
study and a 100X safety factor.  The EPA determined that the FQPA safety
factor should be 1X for all exposure scenarios.  Therefore, the acute
Population Adjusted Dose (aPAD) and the chronic Population Adjusted Dose
(cPAD) are the same as the aRfD and cRfD, respectively.  As soybean
forage and soybean hay are commodities utilized for animal consumption
and not human consumption, no impact is anticipated on the chronic
dietary risk assessment as the proposed tolerances do not exceed those
currently established for animal feed purposes.

>

<	i. Food. Considering the exposure assumptions discussed above,
pyraclostobin acute dietary exposure from food is less than 2.5 % aPAD
for the U.S. population and all sub-populations except females 13-49
years of age that occupies 78.66 % of the aPAD.  The results of the
acute dietary assessment are presented in Table 1.

Table 1.	Results for Pyraclostrobin Acute Dietary Exposure Analysis
Considering all Current and Proposed Tolerances Including Using
DEEM-FCID at the 95th Percentile 

Population	Exposure Estimate	%aPAD

Subgroups	(mg/kg b.w./day)*	 

U.S. Population	0.041503	1.38

All Infants (< 1 year old)	0.055564	1.85

Children (1-2 years old)	0.066579	2.22

Children (3-5 years old)	0.060633	2.02

Children (6-12 years old)	0.043994	1.47

Youth (13-19 years old)	0.033506	1.12

Adults (20-49 years old)	0.037625	1.25

Adults (50+ years old)	0.040381	1.35

Females (13-49 yr old) 	0.039331	78.66

aPAD = acute population adjusted dose 

The results of the analysis show that for all sub-populations, the
exposures are below the Agency's level of concern (< 100% aPAD). 
Additional refinements in the dietary risk assessment would further
reduce the estimated exposure values.

Considering the exposure assumptions discussed above, pyraclostobin
chronic dietary exposure from food for the U.S. population was 17.1 % of
the cPAD.  The most highly exposure population sub group was children
1-2 years of age at 41.5% cPAD.   The results of the chronic dietary
assessment are presented in Table 2. 

Table 2. 	Results for Pyraclostrobin Chronic Dietary Exposure Analysis
Considering all Current and Proposed Tolerances Using DEEM-FCID 

Population	Exposure Estimate	%cPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population	0.005814	17.1

All Infants (< 1 year old)	0.01138	33.5

Children (1-2 years old)	0.014104	41.5

Children (3-5 years old)	0.011	32.4

Children (6-12 years old)	0.006626	19.5

Youth (13-19 years old)	0.004016	11.8

Adults (20-49 years old)	0.004825	14.2

Adults (50+ years old)	0.005629	16.6

Females (13-49 years old)	0.004553	13.4

cPAD = chronic  population adjusted dose 

The results of the analysis show that for all sub-populations, the
exposures are below a level of concern (< 100% cPAD).  Additional
refinements in the chronic dietary risk assessment (i.e. utilizing %
crop treatment factors) would further reduce the estimated exposure
values.  ]>

<	ii. Drinking water. [The water exposure values used for this analysis
are from the most recent EPA assessment for pyraclostrobin (February 11,
2008, “Pyraclostrobin. Acute and Chronic Aggregate Dietary (Food and
Drinking water) Exposure and Risk Assessment to Support new Uses on Oat
Grain, Barley, Oilseed (Crop group 20), Fresh Herbs (Herbs Subgroup
10=9A), Avocado, Black Sapote, Canistel, Mamey Spoted, Mango, Papaya,
Sapodilla, and Star Apple.”  The highest water exposure values were
from aerial application on ornamentals which resulted in an acute
exposure of 35.6 ug/L and chronic exposure of 2.3 ug/L. 

Drinking water contributions were assessed based on the maximum
estimated pyraclostrobin water concentrations (acute – 35.6 ug/L,
chronic 2.3 ug/L), and water consumption and body weights reported in
CSFII, using DEEM-FCID software.  The acute and chronic estimated water
exposure values are summarized in Tables 3 and 4, respectively.  Minimal
exposure of pyraclostrobin occurs through drinking water with < 0.5% the
aPAD and cPAD for all subpopulations with the exception of females 13-49
years of age with a 3.5% aPAD.

Table 3. 	Results for Pyraclostrobin Acute Water Exposure Analysis
Considering the Maximum Estimated Acute Drinking Water Concentration
using 

DEEM-FCID 

Population	Water Exposure Estimate	%aPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population	0.00186	0.06

All Infants (< 1 year old)	0.007012	0.23

Children (1-2 years old)	0.002918	0.10

Children (3-5 years old)	0.002666	0.09

Children (6-12 years old)	0.001856	0.06

Youth (13-19 years old)	0.001509	0.05

Females (13-49 years old)	0.001723	0.06

Adults (20-49 years old)	0.001556	0.05

Adults (50+ years old)	0.001733	3.47

aPAD = acute  population adjusted dose



Table 4. 	Results for Pyraclostrobin Chronic Water Exposure Analysis
Considering the Maximum Estimated Chronic Drinking Water Concentration
using DEEM-FCID 

Population	Water Exposure Estimate	%cPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population	0.000048	0.1

All Infants (< 1 year old)	0.000159	0.5

Children (1-2 years old)	0.000072	0.2

Children (3-5 years old)	0.000067	0.2

Children (6-12 years old)	0.000046	0.1

Youth (13-19 years old)	0.000035	0.1

Females (13-49 years old)	0.000045	0.1

Adults (20-49 years old)	0.000048	0.1

Adults (50+ years old)	0.000045	0.1

cPAD = chronic  population adjusted dose

Acute Aggregate Exposure and Risk (Food and water)

The aggregate acute risk includes residues of pyraclostrobin from food
and water (Table 5). Exposures from residential uses are not included in
the acute aggregate assessment.  The results demonstrate that there are
no safety concerns for any subpopulation based on established and new
uses, and that the results clearly meet the FQPA standard of reasonable
certainty of no harm.

Table 5. 	Estimated Acute Aggregate Exposure and Risk of Pyraclostrobin 


Population Subgroup	aPAD (mg/kg/day)	Food Exposure (mg/kg/day)	Water
Exposure (mg/kg/day)	Total Exposure (mg/kg/day)	% aPAD

U.S. Population	3	0.041503	0.001860	0.043363	1.4

All Infants (< 1 yr old)	3	0.055564	0.007012	0.073591	2.5

Children 1-2 years	3	0.066579	0.002918	0.063551	2.1

Children 3-5 years	3	0.060633	0.002666	0.046660	1.6

Children 6 – 12 years	3	0.043994	0.001856	0.035362	1.2

Youth 13-19 years	3	0.037625	0.001509	0.039134	1.3

Females 13-49 years	0.05	0.039331	0.001733	0.041064	82.1

Adults 20-49 years	3	0.037625	0.001723	0.042104	1.4

Adults + 50	3	0.040381	0.001556	0.040887	1.4



Short- and Intermediate Term Aggregate Exposure and Risk (food, water,
and residential)

Short-term aggregate risk from pyraclostrobin takes into account
exposures from dietary consumption (food and water) and residential
exposure from turf use.  Post application exposure from the turf use is
considered short-term.  The aggregate MOEs from food, water, and
residential exposure are 119 and 233 for children 1-2 years old and the
US population, respectively.  These MOEs are greater than the target MOE
of 100 which indicates there is no safety concern.  The results of the
analysis are shown in Table 6. 

Table 6. 	Estimated Short/Intermediate Term Aggregate Exposure and Risk
of Pyraclostrobin  

Population	NOAEL (mg/kg/day)	Target MOE1	Food Exposure (mg/kg/day)	Water
Exposure (mg/kg/day)	Residential Exposure (mg/kg/day)	Total Exposure
(mg/kg/day)	MOE2

US	5.8	100	0.00581	0.000048	0.0190	0.0249	233

Child 1-2 yr old	5.8	100	0.01410	0.000072	0.0345	0.0487	119

1 Target MOE is 100.

2 Aggregate MOE = (NOAEL / (Food + Water + Residential Exposure)

 Chronic Aggregate Exposure and Risk (food and water)

The aggregate chronic risk includes residues of pyraclostrobin from food
and water (Table 7). Exposures from residential uses are not included in
the chronic aggregate assessment.  The results demonstrate there are no
safety concerns for any subpopulation based on established and new uses,
and that the results clearly meet the FQPA standard of reasonable
certainty of no harm. 

  Table 7. 	Estimated Chronic Aggregate Exposure and Risk of
Pyraclostrobin  

Population Subgroup	cPAD (mg/kg/day)	Food Exposure (mg/kg/day)	Water
Exposure (mg/kg/day)	Total Exposure (mg/kg/day)	% cPAD

U.S. Population	0.034	0.005814	0.000048	0.005862	17.2

All Infants (< 1 yr old)	0.034	0.011380	0.000159	0.011539	33.9

Children 1-2 years	0.034	0.014104	0.000072	0.014176	41.7

Children 3-5 years	0.034	0.011000	0.000067	0.011067	32.6

Children 6 – 12 years	0.034	0.006626	0.000046	0.006672	19.6

Youth 13-19 years	0.034	0.004016	0.000035	0.004051	11.9

Females 13-49 years	0.034	0.004553	0.000045	0.004598	13.5

Adults 20-49 years	0.034	0.004825	0.000045	0.004870	14.3

Adults + 50	0.034	0.005629	0.000048	0.005677	16.7

>

<	2. Non-dietary exposure. Pyraclostrobin is registered for use on
residential and recreational turf.  The applications to turf will be
made only by professional pest control operators.  Therefore,
residential handler exposure was not evaluated.  The exposure assessment
cited in this notice of filing was transcribed from the most recent
Federal Register Notice on pyraclostrobin (U.S. EPA final rule published
in the Federal Register October 29, 2004 [Vol 69, No. 209, p 63083 –
63100).  The EPA evaluated the following post-application exposure
scenarios 1) adults and toddler post-application dermal exposure 2)
toddlers’ incidental ingestion of pesticide residues on lawns form
hand-to-mouth transfer, 3) toddlers’ object-to-mouth transfer from
mouthing pesticide-treated turfgrass, and 4) toddlers’ incidental
ingestion of soil from pesticide-treated residential areas.  The
post-application exposure assessment was based on generic assumptions
specified in the Recommended Revisions to the Residential Standard
Operating Procedures and recommended approaches by an EPA science
advisory council.  A dermal absorption value of 14% was used in the
assessment of pyraclostrobin. The exposure and risk estimates for the
residential exposure scenarios are assessed for the day of application
because adults and toddlers could contact treated turf immediately after
application.  All short-/intermediate term MOE were greater than 100
which indicates that exposure from all residential scenarios result in
exposures below a level of concern.>

<D. Cumulative Effects>

<	Section 408(b)(2)(D)(v) requires that, when considering whether to
establish, modify, or revoke a tolerance, the Agency consider
``available information'' concerning the cumulative effects of a
particular pesticide's residues and ``other substances that have a
common mechanism of toxicity.'  Pyraclostrobin is a foliar fungicide
which belongs to the new class of strobilurin chemistry.  It is a
synthetic analog of strobilurin A, a naturally occurring antifungal
metabolite of the mushroom Strobillurus tenacellus (Anke et. al., 1977).
The active ingredient acts in the fungal cell through inhibition of
electron transport in the mitochondrial respiratory chain at the
position of the cytochrome-bc1 complex.  The protective effect is due to
the resultant death of the fungal cells by disorganization of the fungal
membrane system.  Pyraclostrobin also acts curatively to prevent the
increase and spread of fungal infections by inhibiting mycelial growth
and sporulation on the leaf surface. Pyraclostrobin inhibits spore
germination, germ tube growth and penetration into the host tissues

The EPA is currently developing methodology to perform cumulative risk
assessments.  At this time, there is no available data to determine
whether pyraclostrobin 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,
pyraclostrobin does not appear to produce a toxic metabolite common to
other substances.>

<E. Safety Determination>

<	1. U.S. population. Based on this risk assessment, BASF concludes that
there is a reasonable certainty that no harm will result to the general
population from the aggregate exposure to pyraclostrobin residues.>

<	2. Infants and children. Based on this risk assessment, BASF concludes
that there is a reasonable certainty that no harm will result to infants
or children from the aggregate exposure to pyraclostrobin residues.>

<F. International Tolerances. No Codex or Mexican maximum residue levels
(MRLs) have been proposed or are established for residues of
pyraclostrobin.  Therefore, no tolerance discrepancies exist between
countries for this chemical.  Since the application for registration of
pyraclostrobin was reviewed jointly with the Pest Management Regulatory
Agency (PMRA) of Canada, several Canadian MRLs for pyraclostrobin are
proposed and are expected to be published soon.  However, the joint
review is expected to have eliminated the potential for discrepancies
between U.S. tolerances and Canadian MRLs.>

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