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EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR PESTICIDE 

PETITIONS PUBLISHED IN THE FEDERAL REGISTER

EPA Registration Division contact: Cynthia Giles-Parker (703) 305-7740

Syngenta Crop Protection, LLC. Pesticide Petition # 

EPA has received a pesticide petition Pesticide Petition # 2F8113 fromSyngenta Crop Protection, 

LLC, Regulatory Affairs, P.O. Box 18300, Greensboro, NC 27419-8300 proposing, pursuant to section 

180.665 of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 CFR part 

180 by establishing a tolerance for residues of Sedaxane as a seed treatment for potato at 0.02 ppm, and 

potato, wet peel at 0.06 ppm.

EPA has determined that the petition contains data or information regarding the elements set forth 

in section 180.546 of FDDCA; however, EPA has not fully evaluated the sufficiency of the submitted 

data at this time or whether the data supports granting ofthe petition. Additional data may be needed before 

EPA rules on the petition.

A. Residue Chemistry

1. Plant metabolism. Plant metabolism data were studied for corn, wheat, soybean, Swiss 

chard, and canola to support the seed treatment uses of sedaxane. Studies for all commodities reflected 

labeling in both the phenyl and pyrazole rings. Application rates were equal to, or exaggerations of the 

currently proposed use rates, and application techniques reflect the requested use patterns.

The metabolic pathway in wheat, soybeans, and Swiss chard is substantially similar. Radioactivity 

levels were too low from corn and canola samples to elucidate the metabolic pathways in these crops. 

Following seed treatment use of sedaxane in wheat, soybean, and Swiss chard, sedaxane metabolism may 

be summarized as follows: 1) oxidative metabolism of the phenyl and cyclopropane rings, 2) Ndemethylation of the pyrazole ring and 3) cleavage between pyrazole and phenyl rings. Among the three 

crops studied, there is variation in the extent of the three reaction processes and the nature of the observed 

conjugates found.

The seed treatment data on the metabolism of sedaxane in wheat, soybean, and Swiss chard 

demonstrate that residues are generally low, but do translocate throughout the plants. The highest residues 

are generally found in the foliage or forage portions of plants, and not in the seeds or grains of these 

commodities. Crop field trial residue data were consistent with the results of the plant metabolism 

studies. Specifically, the magnitude of the residue studies showed no quantifiable residues of 

sedaxane in any human food plant parts, but low level residues were found in some livestock feedstuffs 

associated with these plants.

2. Analytical method. Various crops were analyzed for sedaxane (parent only) using a procedure for 

analysis of sedaxane (SYN524464) that can distinguish between its trans and cis isomers (SYN508210 and 

SYN508211). Plant matrices using method GRM023.01A or modified method GRM023.01B are taken through 

an extraction procedure with final determination by high performance liquid chromatography with triple 

quadrupole mass spectrometric detection (LC-MS/MS).

Method GRM023.01A (and therefore GRM023.01B, which uses the same procedure) was

validated on a range of plant commodities fortified with the trans and cis isomers SYN508210 and 

SYN508211 at the proposed limit of quantification (LOQ) of the method (0.005 mg/kg for SYN508210 

and SYN508211) and either at 10 times the LOQ or at the potential MRL. 

The plant matrices included plants from each of the crop commodities identified in OECD 

Guidance ENV/JM/MONO(2007)17, including wheat grain, wheat straw, wheat whole plant, lentils, and 

oilseed rape seed as a few of those crops tested. The mean SYN508210 and SYN508211 recoveries for 

both primary quantification and confirmatory transitions at each fortification level and overall for each 
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crop commodity tested during method validation were 76% – 102%. The limit of quantification for 

SYN508210 and SYN508211 residues in crop commodities using method GRM023.01A was established 

at 0.005 mg/kg. 

3. Magnitude of residues. 

Potato

Tolerances are proposed for sedaxane in or on potato, tuber at 0.02 ppm, and potato, wet peel at 0.06 

ppm. 

B. Toxicological Profile

1. Acute toxicity.

Sedaxane has low acute toxicity by the oral, dermal and inhalation routes. It is not a dermal sensitizer, 

causes no skin irritation and only slight eye irritation.

2. Genotoxicity 

Sedaxane was negative (non-mutagenic) in an in vitro bacterial reverse mutation assay, an in vitro gene 

mutation assay in mammalian cells, an in vitro cytogeneticsstudy, an in vivo unscheduled DNA synthesis study, 

and an in vivo rat bone marrow micronucleus assay. 

3. Reproductive and developmental toxicity

Sedaxane (SYN524464) was evaluated for potential to cause effects on reproductive and 

developmental toxicity in a multi-generation reproductive toxicity study in the rat and in pre-natal 

developmental toxicity studies in the rat and rabbit. There were no adverse effects on reproduction or fertility up 

to the top dose level of 1500 ppm. Therefore this high dose represented the NOAEL for reproductive toxicity.

There were no indications of any differences in sensitivity to sedaxane between the different 

generations or between parental animals and offspring. There were no adverse effects at a dose level of 500 

ppm in adults or pups, indicating that this was the NOAEL for parental and offspring toxicity. 

Data from both the rat and rabbit developmental toxicity studies with sedaxane showed no potential for 

teratogenic effects, and the fetal NOAEL values were equal to or higher than the maternal NOAEL values, 

indicating a lack of sensitivity of developing offspring to the effects of sedaxane.

4. Subchronic toxicity

The short-term toxicity of sedaxane has been evaluated by the oral route of administration in rats, 

dogs and mice. In addition, dermal toxicity was evaluated in rats in a 28-day study. 

Sedaxane is generally of a low order of toxicity in all species tested in short term studies. Rats were 

slightly more sensitive to the general systemic effects of sedaxane treatment than were dogs. Mice were 

relatively non-responsive except at dose levels at a limit dose for studies of this type (7000 ppm). A NOAEL 

of 28 mg/kg/day (300 ppm) was achieved in the second 90-day rat study for female rats.

 In rats, treatment-related effects were seen consistently in the liver, indicating that this is a target organ 

for sedaxane. At dose levels of 2000 ppm and 1000 ppm in the 90-day rat studies, slight increases in liver 

weight were seen in males and females, with no micropathological findings. The increases are therefore 

consistent with adaptive changes and were considered non-adverse. No effects on liver weights or 

micropathology were seen at 250 or 300 ppm in these studies. 

In male and female rats, increased incidence of thyroid follicular cell hypertrophy was observed only 

at the 4000 ppm dose level in the second 90-day rat study. There were no effects in this organ in the first 90 

day rat study. A chronic/carcinogenicity study in rats also showed similar low level changes of follicular cell 
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hypertrophy in male and female rats after 52 weeks of treatment at 1200 and 3600 ppm dose levels. Overall, 

the response in the thyroid of rats was relative mild and was variable between studies and laboratories. 

In dogs, liver weights were higher than control values in male and female dogs after one year at 200 

mg/kg/day, but in the absence of micropathology findings this was considered non-adverse. In the 90-day dog 

study, there were no effects on liver weights and no differences from control animals in liver micropathology. 

There were no adverse effects on the thyroid in any study in the dog including the 1 year study. A NOAEL of 

50 mg/kg/day was achieved in both the 90-day and 1-year dog studies, based on initially lower food 

consumption and consistently lower cumulative bodyweight gains at 150 mg/kg/day and higher. 

In mice, no adverse effects of treatment were observed in the 28-day study at dose levels up to 7000 

ppm. Decreased bodyweight gain and food utilization were observed in male mice at 7000 ppm in the 90-day 

study, but not in females. No micropathology changes were observed in either study and the few differences in 

certain hematology, clinical chemistry or organ weight values were inconsistent between the two studies and 

not considered adverse. In the 90-day study, an NOAEL of 567 mg/kg/day (3500 ppm) was achieved in male 

mice.

In a 28-day dermal toxicity study in rats, no treatment-related effects were observed at any dose level up 

to the limit dose of 1000 mg/kg/day.

In an acute neurotoxicity study in rats, no neuropathology was observed at any dose level, and the 

NOAEL for neurotoxicity was 2000 mg/kg. The NOAEL for general toxicity in this study was 30 mg/kg, 

based on effects on body weight, food consumption, and clinical signs at 250 mg/kg. For use in acute risk 

assessments, EPA derived an acute reference dose (aRfD) of 0.30 mg/kg/day based on the NOAEL of 30 

mg/kg from this acute neurotoxicity study.

In a subchronic neurotoxicity study, sedaxane did not produce any evidence of neurotoxicity in rats at 

dose levels of 0, 300, 1000 and 4000 ppm for 90 days. A NOAEL for general toxicity was observed at 1000 

ppm, equivalent to 66.0/79.7 mg/kg/day in male and female rats, respectively.

5. Chronic toxicity

Sedaxane has been evaluated for chronic toxicity in the rat and for carcinogenic potential in the rat and the 

mouse. 

In a 2 year combined rat chronic toxicity/carcinogenicity study conducted at dietary inclusion levels of 

0, 200, 1200 and 3600 ppm, there were no treatment related effects on survival. There was a marked deficit in 

body weight gain at 3600 ppm which was evidence throughout the entire study. The extent of the body 

weight effect increased substantially during the course of the study and by the end of the study represented a 

24% and 50% decrease in body weight gain in males and females, respectively. The magnitude of the effect 

at 3600 ppm was considered to be greater than that required for an adequate evaluation of carcinogenic 

potential. At 1200 ppm, body weight gain was a maximum of 11% lower than control in females, which was 

considered to be of sufficient magnitude to provide a robust assessment of carcinogenic potential. The NOEL 

was 200 ppm for both males and females, equating to 11 mg/kg/day in males and 14 mg/kg/day in females. 

The LOAEL was 1200 ppm. 

In a carcinogenicity study in the mouse, groups of 50 male and 50 female CD-1 mice were fed diets 

containing 0, 200, 1250 and 7000 ppm of Sedaxane for a period of at least 80 weeks. There were no treatment 

related effects on survival and no treatment-related clinical signs. Effects at the LOAEL and above included 

decreased body weight and body weight gain and food utilization in males and females. The NOAEL for this 

study was 1250 ppm for both sexes, equating to achieved dose levels of 157 mg Sedaxane/kg/day in males 

and 185 mg Sedaxane/kg/day in females. 

The EPA considered that sedaxane produced an increased incidence of liver tumors and thyroid tumors 

in male rats, and uterine tumors in female rats at the high dose of 3600 ppm. In the 18-month mouse study, 

EPA considered that an increase in liver tumors in male mice was treatment-related at the limit dose of 7000 

ppm. Based on these results, a Q1* value of 0.00464 (mg/kg/day)-1 was assigned for use in cancer risk 
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assessments with sedaxane. For non-cancer risk assessments of chronic exposures, a chronic reference 

dose (cRfD) of 0.11 mg/kg/day was assigned, based on the NOAEL of 11 mg/kg/day in the 2-year rat 

study.

6. Animal metabolism

In both poultry and goat, the majority of the dosed radioactivity was excreted (mainly in the faeces of 

the goat) and residues in tissues, milk and eggs were low. In the goat study, milk residues reached plateau 

very rapidly, after just 2 days (reaching a maximum of 0.045 mg/kg). Residues in eggs from the hen study 

reached a plateau after approximately 9 days (reaching a maximum of 0.015 mg/kg in egg white and 0.089 

mg/kg in egg yolk).

In both species, the highest tissue residues were observed in liver (0.26 mg/kg in hen and 0.61 mg/kg in 

goat). Residues in muscle were <0.006 mg/kg and in fat were <0.016 mg/kg). In the goat kidney residues 

represented <0.19 mg/kg).

Metabolic profiles observed in livestock commodities and excreta arise from just a few types of 

biotransformation. The principal routes of metabolism are oxidation resulting in hydroxylation of the phenyl 

ring or at the cyclopropane moiety. Additionally the same oxidations are observed following demethylation 

of sedaxane. Overall results showed that the biotransformation pathway of sedaxane in ruminants and poultry 

is very similar to that observed in the rat.

7. Metabolite toxicology.

CSCD465008 (formed via cleavage of the carboxamide link in the pyrazole labeled aerobic soil study) has 

been assessed for acute oral toxicity, in vitro genotoxicity (Bacterial reverse mutation, in vitro cytogenics and 

mammalian gene cell mutation) and repeat oral toxicity for up to 28 days. CSCD465008 was not acutely toxic by 

the oral route, not genotoxic in vitro and did not result in any toxicologically significant effects at dose levels 

exceeding 1000mg/kg bw/day, the limit dose for a 28 day toxicity study in rats. 

These data indicate that CSCD465008 is of lower toxicity than parent SYN524464 and is not therefore 

considered to be of toxicological relevance.

8. Endocrine disruption.

Sedaxane does not belong to a class of chemicals known or suspected of having adverse effects on the 

endocrine system. Furthermore, supporting developmental toxicity studies in rats and rabbits, and a 

reproduction study in rats gave no indication of any effects on endocrine function related to development 

and reproduction. Subchronic and chronic treatment did not induce any morphological changes in endocrine 

organs and tissues.

9. Immunotoxicity.

A study was conducted, as specified in US EPA OPPTS Guideline 870.7800, to provide information on 

suppression of the immune system which might occur as a result of repeated exposure to a test chemical. 

Treatment of male CD-1 mice with sedaxane on a continuous basis in the diet for a minimum of 28 days 

resulted in no suppression of the humoral immune component of the immune system, based on an evaluation 

of the spleen and thymus weights, spleen cell numbers, and the T-cell dependent antibody response of 

splenocytes (antibody forming cell assay). The no observed-effect level (NOEL) for suppression of the 

immune response in male CD-1 mice offered sedaxane on a continuous basis in the diet for a minimum of 28 

days at 0, 500, 2000, and 5500 ppm was 5500 ppm (equivalent to 1084 mg/kg/day). The only effect attributed 

to sedaxane-treatment was a slightly higher mean adjusted liver weight for the 5500 ppm group that was not 

considered adverse.

C. Aggregate Exposure

1. Dietary Exposure. Tier I acute, chronic, and lifetime cancer aggregate exposure assessments were 

performed for sedaxane (SYN524464), a mixture of SYN508210 (2’-[(1RS, 2SR)-1,1’-bicycloprop-2-yl]-3-

(difluoromethyl)-1-methylpyrazole-4-carboxanilide) and SYN508211 (2′-[(1RS, 2RS)-1,1′-bicycloprop-2-

yl]-3-(difluoromethyl)-1-methylpyrazole-4-carboxanilide) using the Dietary Exposure Evaluation Model 

software with the Food Commodity Intake Database (DEEM-FCIDTM , version 3.14). DEEM-FCID 
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software incorporates food consumption data from the National Health and Nutrition Examination 

Survey)/“What We Eat in America” (NHANES/WWEIA) dietary survey conducted in 2003-2008. 

Assessments were conducted for all current uses (canola, soybeans, and small grains), pending seed 

treatment uses on corn, sorghum, pulses (dry beans and peas, Crop Subgroup 6C), oilseed rape Crop 

Subgroup 20A, and a proposed seed piece treatment use on potatoes. The definition of the residue for 

tolerance enforcement and risk assessment purposes for crops is parent sedaxane (SYN508210 plus 

SYN508211). Percent of crop treated (%CT) was conservatively assumed to be 100% for all uses. 

Anticipated residues in meat, milk, and eggs were calculated by constructing a theoretical “maximum 

reasonably balanced diet” (MRBD) using the OPPTS 860.1000 Table 1 feedstuffs (June 2008 revision). 

Drinking water estimates were selected using the higher of the estimated drinking water concentrations 

(EDWCs) for surface and ground water.

i. Food Acute Exposure. Acute food only risk assessments for parent sedaxane (SYN508210 plus 

SYN508211) were performed for all population sub-groups using an acute reference dose of 

0.30 mg/kg-bw/day, based upon a neurotoxicity study in rats with a no observed adverse effect level 

(NOAEL) of 30 mg/kg-bw/day and an uncertainty factor of 100X. The 100X safety factor includes intraand inter-species variations; no additional FQPA safety factor was applied. For the purpose of aggregate 

risk assessment, the exposure values were expressed in terms of margin of exposure (MOE), which was 

calculated by dividing the NOAEL by the exposure for each population subgroup. In addition, exposure 

was expressed as a percent of the acute reference dose (%aRfD). Acute food exposure to the U.S. 

population resulted in a MOE of 231,799 (<0.1% of the aRfD of 0.30 mg/kg-bw/day). The most exposed 

sub-population was children (1-2 years old) with a MOE of 103,975 (0.1% of the aRfD of 0.30 mg/kgbw/day). Since the Benchmark MOE for this assessment was 100 and since the EPA generally has no 

concern for exposures above the benchmark or below 100% of the reference dose, Syngenta believes that 

there is a reasonable certainty that no harm will result from acute food exposures arising from all current, 

pending, and proposed uses of sedaxane. 

Chronic Exposure. Chronic food only risk assessments for parent sedaxane (SYN508210 plus SYN508211) 

were performed for all population sub-groups using a chronic reference dose of 0.11 mg/kg-bw/day, based 

upon a chronic rat study with a no observed adverse effect level (NOAEL) of 11 mg/kg-bw/day and an 

uncertainty factor of 100X. The 100X safety factor includes intra- and inter-species variations; no 

additional FQPA safety factor was applied. For the purpose of aggregate risk assessment, the exposure 

values were expressed in terms of margin of exposure (MOE), which was calculated by dividing the 

NOAEL by the exposure for each population subgroup. In addition, exposure was expressed as a percent of 

the chronic reference dose (%cRfD). Chronic food exposure to the U.S. population resulted in a MOE of 

220,786 (<0.1% of the cRfD of 0.11 mg/kg-bw/day). The most exposed sub-population was children (1-2 

years old) with a MOE of 84,840 (0.1% of the cRfD of 0.11 mg/kg-bw/day). Since the Benchmark MOE 

for this assessment was 100 and since the EPA generally has no concern for exposures above the benchmark 

or below 100% of the reference dose, Syngenta believes that there is a reasonable certainty that no harm will 

result from chronic food exposures arising from all current, pending, and proposed uses of sedaxane.

Cancer Risk from Food: Lifetime cancer food risk from sedaxane was evaluated by comparing exposures to 

a Q1* value of 0.0046 (mg/kg-bw/day)-1based on two rodent carcinogenicity studies. Lifetime cancer food 

risk for the U.S. population was 2.29E-07. Since the Benchmark for this lifetime cancer assessment is 

1.00E-06 and since the EPA generally has no concern for exposures below the benchmark, Syngenta 

believes that there is a reasonable certainty that no harm will result from lifetime cancer food exposures 

arising from all current, pending, and proposed uses of sedaxane.

ii. Drinking Water: To determine the Estimated Drinking Water Concentrations (EDWCs) for sedaxane, 

the Tier 1 FQPA Index Reservoir Screening Tool (FIRST v1.1.1) and the Screening Concentration in 

Ground Water (SCI-GROW v2.3) models were used for estimation of surface and ground water EDWCs, 

respectively. Sedaxane is proposed as a seed treatment at maximum field application rates of 0.050 lb/acre 

for potatoes. Seeding was modeled as granular applications with 0% spray drift and 100% efficiency and 

assumed to be seeded to a depth of 3 inches. The agricultural default Percent Cropped Area (PCA) 

adjustment for surface water of 0.91 was used.

Acute Exposure from Drinking Water: To determine the acute Estimated Drinking Water Concentrations 

(EDWCs) for sedaxane, the FIRST and SCI-GROW models were used for estimation of surface and ground 
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water EDWCs, respectively. The FIRST model provided an acute surface water EDWC of 0.851 ppb. The 

SCI-GROW model provided a ground water EDWC for sedaxane of 0.00282 ppb. Since the surface water 

EDWC exceeds the ground water EDWC, the surface water value is considered protective for any drinking 

water concentration concerns. The predicted acute surface water EDWC of 0.851 ppb (0.000851 ppm) was 

input directly into the DEEM-FCIDTM software as “water, direct and indirect, all sources” to model the 

acute drinking water exposure. Acute drinking water exposure to the U.S. population resulted in a MOE of 

>1,000,000 (<0.1% of the aRfD of 0.30 mg/kg-bw/day). The most exposed sub-population was infants <1 

year old with a MOE of 361,446 (<0.1% of the aRfD of 0.30 mg/kg-bw/day). Since the Benchmark MOE 

for this assessment was 100 and since the EPA generally has no concern for exposures above the benchmark 

or below 100% of the reference dose, Syngenta believes that there is a reasonable certainty that no harm will 

result from acute drinking water exposures arising from all current, pending, and proposed uses of sedaxane.

Chronic Exposures from Drinking Water: To determine chronic Estimated Drinking Water Concentrations 

(EDWCs) for sedaxane, the FIRST and SCI-GROW models were used for estimation of surface and ground 

water EDWCs, respectively. The FIRST model provided a chronic surface water EDWC of 0.251 ppb. The 

SCI-GROW model provided a ground water EDWC for sedaxane of 0.00282 ppb. Since the surface water 

EDWC exceeds the ground water EDWC, the surface water value is considered protective for any drinking 

water concentration concerns. The predicted chronic surface water EDWC of 0.251 ppb (0.000251 ppm) 

was input directly into the DEEM-FCIDTM software as “water, direct and indirect, all sources” to model the 

chronic drinking water exposure. Chronic drinking water exposure to the U.S. population resulted in a 

MOE of >1,000,000 (<0.1% of the cRfD of 0.11 mg/kg-bw/day). The most exposed sub-population was 

infants <1 year old with a MOE of 811,702 (<0.1% of the cRfD of 0.11 mg/kg-bw/day). Since the 

Benchmark MOE for this assessment was 100 and since the EPA generally has no concern for exposures 

above the benchmark or below 100% of the reference dose, Syngenta believes that there is a reasonable 

certainty that no harm will result from chronic drinking water exposures arising from all current, pending, 

and proposed uses of sedaxane.

Cancer Risk from Drinking Water: Lifetime cancer drinking water risk from sedaxane was evaluated by 

comparing lifetime chronic exposures to a Q1* value of 0.0046 (mg/kg-bw/day)-1based on two rodent 

carcinogenicity studies. Lifetime cancer drinking water risk for the U.S. population was 2.42E-08. Since 

the Benchmark for this lifetime cancer assessment is 1.00E-06 and since the EPA generally has no concern 

for exposures below the benchmark, Syngenta believes that there is a reasonable certainty that no harm will 

result from lifetime cancer drinking water exposures arising from all current, pending, and proposed uses of 

sedaxane.

2. Non-Dietary Exposure: There are no currently registered residential uses for sedaxane, so a non-dietary 

residential exposure assessment was not conducted.

D. Cumulative Effects

Cumulative Exposure to Substances with a Common Mechanism of Toxicity. 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”. Syngenta did not perform a cumulative risk 

assessment as part of this tolerance action for sedaxane because HED has not yet determined that there are 

any other chemical substances that have a mechanism of toxicity common with that of sedaxane.

E. Safety Determination

1. U.S. Population. Using the conservative assumptions described above, and based on the completeness 

and reliability of the toxicity data, the acute aggregate exposure analysis for all current, pending, and 

proposed uses of sedaxane resulted in a MOE of 193,597 for the U.S. population (0.1% of the aRfD of 0.30 

mg/kg-bw/day). The chronic aggregate exposure analysis for all current, pending, and proposed uses of 

sedaxane resulted in a MOE of 180,856 for the U.S. population (<0.1% of the cRfD of 0.11 mg/kg-bw/day). 

Because the worst case aggregate MOE of 180,856 for chronic aggregate exposures exceeds the Benchmark 

MOE of 100, Syngenta believes that there is a reasonable certainty that no harm will occur to the U.S. 

population from acute and chronic aggregate exposures arising from all current, pending, and proposed uses 

of sedaxane. The lifetime cancer risk analysis for all current, pending, and proposed uses of sedaxane 
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resulted in a lifetime cancer risk estimate of 2.53E-07 for the U.S. population. Because the lifetime cancer 

risk estimate was approximately 25.3% of the negligible cancer risk benchmark of 1.00E-06, Syngenta 

believes that there is a reasonable certainty that no harm will occur to the U.S. population as a result of 

aggregate cancer risk from all current, pending, and proposed uses of sedaxane.

2. Infants and children. Using the conservative assumptions described above, and based on the 

completeness and reliability of the toxicity data, the acute aggregate exposure analysis for all current, 

pending, and proposed uses of sedaxane resulted in a MOE of 91,176 for children 1-2 years old (0.1% of the 

aRfD of 0.30 mg/kg-bw/day). The chronic aggregate exposure analysis for all current, pending, and 

proposed uses of sedaxane resulted in a MOE of 78,205 for children 1-2 years old (0.1% of the cRfD of 0.11 

mg/kg-bw/day). Because the worst case aggregate MOE for chronic exposures of 78,205 for children 1-2 

years old exceeds the Benchmark MOE of 100, Syngenta believes that there is a reasonable certainty that no 

harm will occur to infants and children from acute and chronic aggregate exposures arising from all current, 

pending, and proposed uses of sedaxane. 

F. International Tolerances 

There are no Codex maximum residue levels (MRLs) established for residues of sedaxane in any 

commodity. Countries including Austria, Canada, the European Union (EU), Iceland, Japan, Malaysia, New 

Zealand, Norway, South Africa, and the United States may have country-specific MRLs established for 

residues of sedaxane in a variety of commodities.