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

EPA Registration Division contact: Tony Kish, Product Manager 22, (703)-308-9443

Pyraclostrobin alfalfa.

TEMPLATE:

BASF Corporation

9F7528

EPA has received a pesticide petition (PP#9F7528) from BASF Corporation, PO Box 13528, Research Triangle Park, North Carolina, 27709 proposing, pursuant to section 408(d) of the Federal Food, Dr ug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 CFR part 180 to establish new tolerances for pyraclostrobin, carbamic acid, [2-[[[1-(4-chl orophenyl)-1H-pyrazol-3-yl ]oxy]methyl]phenyl]methoxy-, methyl ester and its metabolite methyl-N- [[[1-(4-chlorophenyl) pyrazo l-3-yl]oxy]o-tolyl] carbamate (BF 500-3), expr essed as parent compound in or on the raw agricultural commodity alfalfa, forage at 10.0 ppm, and alfalfa, hay at 30.0 parts per million (ppm), respectively; and new tolerances for pyraclostrobin carbamic acid, [2-[[[1-(4- chlorophenyl)-1H-pyrazol-3-yl]oxy]methyl ]phenyl]methoxy-, methyl ester) and its metabolites convertible to 1-(4-chlorophe nyl)-1H-pyrazol-3-ol and 1-(3-chloro-4- hydroxyphenyl)-1H-pyrazol-3-ol (BF 500-16), expressed as parent compound in the animal commodities poultry, fat at 0.1 ppm; poultr y, meat byproducts at 0.1 ppm; poultry, meat at 0.1 ppm; and eggs at 0.1 ppm . EPA has determined that the petition contains data or information regarding the el ements set forth in se ction 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 gran ting 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 (pyraclostro bin) and BAS 500-3), methyl-N[[[1-(4- chlorophenyl) pyrazol-3yl]oxy]o-tolyl] carbam ate. In hens the residues of concern were determined to be parent compound and a hydroxlated metabolite, BAS 500-16.2

In goats the residues of concern were determined to be parent and a hydroxylated metabolite BAS 500-10

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2. Analytical method. In plants the method of analysis is aqueous organic solvent extraction, column clean up and qua ntitation by LC/MS/MS. In animals the method of analysis involves base hydrol ysis, organic extraction, column clean up and quantitation by LC/MS/MS or deri vatization (methylation) followed by quantitation by GC/MS

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3. Magnitude of residues. Field trials were carried out in order to determine the magnitude of the residues in alfalfa, forage, and alfalfa, hay, to satisfy the requirements for a tolerance of pyraclostrob in in these commodities. Field trials were carried out using the maximum proposed labeled rate, maximum proposed number of applications, and the mini mum proposed pre-harvest interval.]

B. Toxicological Profile

1. Acute toxicity. Pyraclostrobin and its formulated products have favorable acute toxicity. The acute toxicity studies pl ace technical pyraclostrobin in toxicity category IV for acute oral and acute inha lation and category III for acute dermal. Pyraclostrobin is category III for both eye a nd skin irritation, and it is not a dermal sensitizer. Two formulated end use pr oducts 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 d ermal 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

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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 investigatin g 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

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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 toxi city 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).3

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 weig ht gain. Developmental changes noted at the high dose were increased incidences of dilated renal pelvis and cervical ribs with no cartilage. The maternal NOA EL was 10 mg/kg bw and the developmental NOAEL was 25 mg/kg bw.

In the rabbit teratology study, maternal toxi city observed at the mid and high doses consisted of decreased food consumption a nd 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 resorption s. 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 indicati ve of frank developmental toxicity. The NOAEL for both maternal and developmental toxicity was 5 mg/kg bw

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4. Subchronic toxicity. The subchronic toxicity of pyraclostrobin was investigated in 90-day feeding studies wi th 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 ob served. At high dose levels in feeding studies, general findings in all three sp ecies 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 accompan ying 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 th e 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 di rect neurotoxic effect was not observed

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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. Hematologica l 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 decrea se in serum total protein, albumin, globulins and cholesterol in high dose an imals 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 same4

dose levels as in the oncogenicity study. A body weight gain depression of 10-11% in males and 14-22% in females with an a ccompanying decrease in food efficiency was observed at the high dose. There was no evidence that pyraclostrobin produced a carcinogenic effect in rats. The NOA EL for the chronic rat and the cancer rat study is 75 ppm (ca. 3.4 mg/kg bw/d ay 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 do ses 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 determin ed 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 th an the highest dose tested of 32.8 mg/kg bw/day. There was no evidence that pyracl ostrobin produced a carcinogenic effect in mice

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6. Animal metabolism. In a rat metabolism study with pyraclostrobin, 10-13% of the administered dose was excreted in th e 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 li ttle 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 hydroxylat ions, cleavage of the ether bond and further oxidation of the two resulting mole cule 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

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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 fr action (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 me tabolite in the rat is the first step in the major biotransformation process leadin g to the majority of the metabolites determined in the ma jor excretion pathway

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8. Endocrine disruption

. Endocrine effects. No specific tests have been conducted with pyraclostrobin to determ ine 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. Howe ver, there were no significant findings in other relevant toxicity studi es (i.e., subchronic and ch ronic toxicity, teratology and multi-generation reproductive studies) which would suggest that pyraclostrobin produces endocrine related effects

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C. Aggregate Exposure

1. Dietary exposure. Exposure assessments were conducted to evaluate the potential risk due to acute and chro nic dietary exposure to residues of pyraclostrobin. This analysis includes all current established tolerances for pyraclostrobin in crop and animal commoditi es and the proposed new tolerances in alfalfa, forage, alfalfa, hay, poultry, fat, poultry, meat byproducts, poultry meat, and eggs. The proposed new tolerances for alfalfa, forage, and alfalfa, hay, are 10.0 and 30.0 ppm, respectively; proposed new to lerances for poultry commodities are: poultry fat, 0.1 ppm, poultry meat bypr oducts 0.1 ppm, poultry meat, 0.1 ppm and eggs 0.1 ppm. The acute dietary assessments were conducted using 100% crop treatment factors, tolerance level or hi ghest residue levels, and experimentally derived processing factors for fruit jui ces, 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, lettu ce, citrus, pepper, mustard greens, and

tomatoes . As alfalfa is a commodity utiliz ed for animal consumption and not human consumption, no impact is anticipated on the ac ute 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 fema les 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 a ll 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 alfalfa is a commodity utilized for animal consumption and not human consumption, no impact is anticipated on the chronic dietary risk asse ssment as the proposed tolerances do not exceed those currently established for animal feed purposes.

i. Food. C onsidering 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 fe males 13-49 years of age that occupies 78.66 % of the aPAD. The results of the ac ute dietary assessment are presented in Table 1.6

Table 1. Results for Pyraclostrobin Acute Dietary Exposure Analysis Considering all Current and Proposed Tolerances Including Using DEEM-FCID at the 95 th 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 furth er reduce the estimated exposure values

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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 gro up was children 1-2 years of age at 41.5% cPAD. The results of the chronic diet ary assessment are presented in Table 2.7

Table 2. Results for Pyraclostrobin Chronic Dietary Exposure AnalysisConsidering all Current and Proposed Tolerances Using DEEMFCID

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 Aggre gate Dietary (Food and Drinking water) Exposure and Risk Assessment to Support ne w Uses on Oat Grain, Barley, Oilseed (Crop group 20), Fresh Herbs (Herbs Subgroup 10=9A), Avocado, Black Sapote, Canistel, Mamey Spoted, Mango, Papaya, Sapo dilla, 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 asse ssed based on the maximum estimated pyraclostrobin water concentrations (acu te – 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 ex posure values are summarized in Tables 3 and 4, respectively. Minimal exposure of py raclostrobin occurs through drinking water with < 0.5% the aPAD and cPAD for al l subpopulations with the exception of females 13-49 years of age with a 3.5% aPAD.8

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 dose9

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 incl udes residues of pyraclostrob in 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 1.410

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

Short-term aggregate risk from pyraclostrob in takes into account exposures from dietary consumption (food and water) and res idential 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, respectiv ely. 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 Te rm Aggregate Exposure and Risk of Pyraclostrobin

Population NOAEL (mg/kg/day ) Target MOE 1 Food Exposure (mg/kg/day ) Water Exposure (mg/kg/day ) Residential Exposure (mg/kg/day ) Total Exposure (mg/kg/day ) MOE 2

US 5.8 100 0.00581 0.000048 0.0190 0.0249 233
Child 1-2 y r 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 res ults 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 14.311

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, residen tial handler exposure was not evaluated. The exposure assessment cited in this notice of filing was transcribed from the most recent Federal Register Notice on pyraclostr obin (U.S. EPA final rule published in the Federal Register Octo ber 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) toddl ers’ incidental inge stion of pesticide residues on lawns form hand-to-mouth tr ansfer, 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 Residentia l Standard Operating Procedures and recommended approaches by an EPA scie nce advisory council. A dermal absorption value of 14% was used in the a ssessment of pyraclostrobin. The exposure and risk estimates for the residential expo sure scenarios are assessed for the day of application because adults and toddlers co uld contact treated tu rf immediately after application. All short-/intermediate term MOE were greater than 100 which indicates that exposure from all resident ial scenarios result in exposures below a level of concern

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D. Cumulative Effects

Section 408(b)(2)(D)(v) requires that, when considering whether to establish, modify, or revoke a tolerance, the Ag ency consider ``available information'' concerning the cumulative effects of a pa rticular 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 o ccurring antifungal metabolite of the mushroom Strobillurus tenacel lus (Anke et. al., 1977). The active ingredient acts in the fungal cell through inhibition of el ectron transport in the mitochondrial respiratory chain at the position of th e cytochrome-bc1 complex. The protective effect is due to the resultant death of the f ungal cells by disorganization of the fungal membrane system. Pyraclostrobin also ac ts curatively to prevent the increase and spread of fungal infections by inhibiting mycelial growth and sporulation on the leaf surface. Pyraclostrobin inhibits spo re germination, germ tube growth and penetration into the host tissues12

The EPA is currently developing methodology to perform cumulative risk assessments. At this time , there is no available da ta 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

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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

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2. Infants and children

. Based on this risk assessment, BASF concludes that there is a reasonable certainty that no ha rm will result to infa nts or children from the aggregate exposure to pyraclostrobin residues

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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 th is chemical. Since the application for registration of pyraclostrobin was revie wed jointly with the Pest Management Regulatory Agency (PMRA) of Canada, se veral Canadian MRLs for pyraclostrobin are proposed and are expected to be publis hed 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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