EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR 

PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER 

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

9443]

Pyraclostrobin sugarcane.

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:

[BASF Corporation]

[2F8038]

EPA has received a pesticide petition 2F8038 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 new 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 sugarcane, 

cane at 0.2 parts per million (ppm). No tolerances are proposed for the processed 

commodities, refined sugar and molasses, as no concentration of pyraclostrobin residues 

are expected in these commodities. 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-
2

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 sugarcane and the processed commodities, refined 

sugar and molasses, to satisfy the requirements for a tolerance of pyraclostrobin in 

this commodity. Field trials were carried out using the maximum proposed labeled 

rate, maximum proposed number of applications, and the minimum proposed preharvest interval. 

Based on the results of a processing study, residues of pyraclostrobin do not 

concentrate in refined sugar or molasses. The use in sugarcane does not result in a 

maximum reasonable feed burden for cattle, poultry or swine in excess of that 

already determined for registered uses. No additional data were needed in support 

of residues in meat, milk, poultry and eggs. 

 

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 
3

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 
4

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.]
5

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 currently registered uses and the 

proposed new tolerances in sugarcane. The proposed new tolerance for sugarcane, 

cane is 0.2 ppm. 

The pyraclostrobin chronic population adjusted dose (cPAD) is 0.034 mg/kg bw/day 

based on the NOAEL of 3.4 mg/kg bw/day in the rat chronic toxicity study, a 

standard safety factor of 100X and a FQPA safety factor of 1X . The acute 

population adjusted dose (aPAD) is 3 mg/kg b.w./day for all subpopulation except 

females 13-49 years of age based on a NOAEL from the acute neurotoxicity study of 

300 mg/kg bw/day, a standard safety factor of 100X and a FQPA safety factor of 1X. 

For females ages 13-49 years, the aPAD is 0.05 mg/kg b.w./day based on the NOAEL 

of 5 mg/kg bw/day from the rabbit teratology study, a standard safety factor of 

100X, and a FQPA safety factor of 1X. 

i. Food. [Acute Dietary Exposure Assessment

The estimated acute dietary exposure is based on the proposed tolerance of 0.2 

mg/kg for sugarcane and tolerance values for all registered commodities except as 

follows: use of highest average field trial residues of for crop groups 4A (23.38 

mg/kg) except that specific highest field trial residues were used for head lettuce 

(14.8 mg/kg), leaf lettuce (21.2 mg/kg) and crop groups 4b celery (10.7 mg/kg) and 

crop group 6C dry bean (0.21 mg/kg) and dry pea (0.1 mg/kg). Experimental 

processing factors of 0.1 and 0.3 were used for sugarcane, refined sugar and 

molasses, respectively. Experimental processing factors were also used for sugar 

beet, sugar, apple juice, grape juice , citrus juice, cottonseed oil, tomato paste, 

tomato puree, tomato juice, soybean oil, wheat flour, wheat germ and mint oil with 

default process factors used for all other commodities. The evaluation used 100% 

crop treated. The consumption data was from the USDA Continuing Survey of Food 

Intake by Individuals (CSFII 1994 - 1996, 1998) and the EPA Food Commodity 

Ingredient Database (FCID) using Exponent's Dietary Exposure Evaluation Module 

(DEEM-FCID) software. The results of the assessment for the population of females 

age 13 to 49 years was a utilization of 80.54% aPAD at the 95th percentile based on 

all users, while the highest utilization for all other populations was that of children 

age 1-2 year at 2.45% aRfD.
6

Table 1. Results for Pyraclostrobin (BAS 500 F) Acute Dietary Exposure 

Analysis Considering All Tolerances and 100 % Crop Treated using DEEM-FCID 

at the 95th Percentile (Food only)

Population Exposure Estimate %aPAD

Subgroups (mg/kg b.w./day)

U.S. Population 0.043299 1.44

All Infants (< 1 year old) 0.059113 1.97

Children (1-2 years old) 0.073358 2.45

Children (3-5 years old) 0.06372 2.12

Children (6-12 years old) 0.046582 1.55

Youth (13-19 years old) 0.034726 1.16

Adults (20-49 years old) 0.038416 1.28

Adults (50+ years old) 0.040873 1.36

Females (13 – 49 years old) 0.04027 80.5

Chronic Dietary Exposure Assessment

BASF has estimated chronic dietary exposure estimates based on the proposed 

tolerance of 0.2 mg/kg for sugarcane and tolerance values for all registered 

commodities except as follows: use of average field trial residues for crop group 4A 

(11.77 mg/kg) except for specific values for head lettuce (0.59 mg/kg) and leaf 

lettuce(7.68 mg/kg), for crop group 4b (5.02 mg/kg), for crop group 5a (1.10 mg/kg), 

for crop group 5b (5.74 mg/kg), highest residue for crop group 6C (0.21 mg/kg), 

orange (0.3 mg/kg), apple (0.31 mg/kg) and grape (0.768 mg/kg). ). Experimental 

processing factors of 0.1 and 0.3 were used for sugarcane, refined sugar and 

molasses, respectively. Experimental processing factors were also used for sugar 

beet, sugar, apple juice, grape juice , citrus juice, cottonseed oil, tomato paste, 

tomato puree, tomato juice, soybean oil, wheat flour, wheat germ and mint oil with 

default process factors used for all other commodities. The evaluation used 100% 

crop treated. The consumption data was from the USDA Continuing Survey of Food 

Intake by Individuals (CSFII 1994 - 1996, 1998) and the EPA Food Commodity 

Ingredient Database (FCID) using Exponent's Dietary Exposure Evaluation Module 

(DEEM-FCID) software. The exposure of the general population utilized 19.5% 

cRfD while the most highly exposed population sub-group children 1-2 years of age 

utilized 53.4% cPAD.
7

Table 2. Results for Pyraclostrobin (BAS 500 F) Chronic Dietary Exposure Analysis 

Considering all Tolerances and 100 % Crop Treated using DEEM-FCID (Food 

only)

Population Exposure Estimate %cPAD

Subgroups (mg/kg b.w./day)

U.S. Population 0.006635 19.5

All Infants (< 1 year old) 0.012892 37.9

Children (1-2 years old) 0.018145 53.4

Children (3-5 years old) 0.013672 40.2

Children (6-12 years old) 0.008301 24.4

Youth (13-19 years old) 0.004877 14.3

Adults (20-49 years old) 0.005276 15.5

Adults (50+ years old) 0.005961 17.5

Females (13-49 years old) 0.005133 15.1

 ]

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.
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 3.5

aPAD = acute population adjusted dose
9

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

(Food and Drinking Water) 

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 0.043299 0.001860 0.045159 1.5

All Infants (< 1 yr 

old) 3

0.059113 0.007012 0.080370 2.7

Children 1-2 years 3 0.073358 0.002918 0.066638 2.2

Children 3-5 years 3 0.063720 0.002666 0.049248 1.6

Children 6 – 12 years 3 0.046582 0.001856 0.036582 1.2

Youth 13-19 years 3 0.038416 0.001509 0.039925 1.3

Females 13-49 years 0.05 0.040270 0.001733 0.042003 84.0

Adults 20-49 years 3 0.038416 0.001723 0.042596 1.4

Adults + 50 3 0.040873 0.001556 0.041826 1.4
10

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 110 and 226 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 (Food, Drinking Water, and Residential exposure)

Population

Target 

MOE1

Food 

Exposure 

(mg/kg/day)

Water 

Exposure 

(mg/kg/day)

Residential 

Exposure 

(mg/kg/day)

Total 

Exposure 

(mg/kg/day) MOE2

US 100 0.00664 0.000048 0.0190 0.0257 226

Child 1-2 yr 

old 100 0.01815 0.000072 0.0345 0.0527 110

1 Target MOE is 100.

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

5.8 mg/kg b.w./day. 

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

(Food and Drinkiing water) 

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 0.006635 0.000048 0.006683 19.7

All Infants (< 1 yr old) 0.034 0.012892 0.000159 0.013051 38.4

Children 1-2 years 0.034 0.018145 0.000072 0.018217 53.6

Children 3-5 years 0.034 0.013672 0.000067 0.013739 40.4

Children 6 – 12 years 0.034 0.013672 0.000046 0.008347 24.6

Youth 13-19 years 0.034 0.008301 0.000035 0.004912 14.4

Females 13-49 years 0.034 0.005133 0.000045 0.005178 15.2

Adults 20-49 years 0.034 0.005276 0.000045 0.005321 15.7
11

Adults + 50 0.034 0.005961 0.000048 0.006009 17.7

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
12

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 maximum residue levels (MRLs) have been established for 

residues of pyraclostrobin. Therefore, no tolerance discrepancies exist between 

countries for this chemical.]