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

EPA Registration Division contact: [Emily Schmid; (703) 347-0189]

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:

[Bayer CropScience]

[Insert petition number]

EPA has received a pesticide petition ([insert petition number]) from [Bayer CropScience], [800 N. Lindbergh Blvd. St. Louis, MO 63167] proposing, pursuant to section 408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 CFR part 180 by 

 Establish indaziflam tolerances for plant matrices are based on the combined residues of indaziflam ({1,3,5-triazine-2,4-diamine,N-[(1R,2S)-2,3-dihydro-2,6-dimethyl-1H-inden-1-yl]-6-[1-fluoroethyl]} and its metabolite {6-[1-fluoroethyl]-1,3,5-triazine-2,4-diaminotriazine} calculated as indaziflam equivalents. in or on the raw agricultural commodities: Crop group 17 (Grass Forage, Fodder, and Hay Group) grass forage at 30 parts per million (ppm) and grass hay at 10 ppm; in sugarcane, cane at 0.01 ppm. 
 Establish indaziflam tolerances for residues of indaziflam ({1,3,5-triazine-2,4-diamine,N-[(1R,2S)-2,3-dihydro-2,6-dimethyl-1H-inden-1-yl]-6-[1-fluoroethyl]}for animal fat, meat, meat by-products, milk, and milk fat at: 0.07, 0.01, 0.2, 0.01 and 0.25 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 and livestock metabolism. [The nature of the indaziflam residues in plants and livestock is adequately understood. 

The plant residues of concern for tolerance enforcement are the combined residues of indaziflam (N-[(1R,2S)-2,6-Dimethyl-2,3-dihydro-1H-inden-1-yl]-6-[(1R)-1-fluoroethyl]-1,3,5-triazine-2,4-diamine] and its fluoroethyl-indaziflam metabolite [6-[(1R)-1-Fluoroethyl]-1,3,5-triazine-2,4-diamine-]

In livestock the residue of concern for risk assessment is: indaziflam parent compound (N-[(1R,2S)-2,6-Dimethyl-2,3-dihydro-1H-inden-1-yl]-6-[(1R)-1-fluoroethyl]-1,3,5-triazine-2,4-diamine), indaziflam-acid ((2S,3R)-3-[[4-Amino-6-[(1R)-1-fluoroethyl]-1,3,5-triazin-2-yl]amino]-2,3-dihydro-2-methyl-1H-indene-
5-carboxylic acid), indaziflam-3 hydroxyindane ((2R,3R)-3-[[4-amino-6-[(1R)-1-fluoroethyl]-1,3,5-triazin-2-yl]amino]-2,5-dimethyl-indan-1-ol), indaziflam-3-ketohydroxymethyl ((2R,3R)-3-[[4-amino-6-[(1R)-1-fluoroethyl]-1,3,5- triazin-2-yl]amino]-5-(hydroxymethyl)-2-methyl-indan-1-one) and indaziflam-triazinediamine (6-[(1R)-1-Fluoroethyl]-1,3,5-triazine-2,4-diamine).]  Bayer proposes that the residue definition for enforcement be indaziflam parent only.

      2. Analytical method. [Indaziflam residues are quantified in raw agricultural commodities by high pressure liquid chromatography/triple stage quadrupole mass spectrometry (LC/MS/MS) using the stable isotopically labeled analytes as internal standards. The limit of quantification (LOQ) for each analyte is 0.005 ppm for all commodities.

Indaziflam residues are quantified in commodities of animal origin by high pressure liquid chromatography/triple stage quadrupole mass spectrometry (LC/MS/MS) using the stable isotopically labeled analytes as internal standards. The LOQ of each analyte is 0.01 ppm for fat, meat, meat by-produucts and feces.  The LOQ of each analyte is 0.005 ppm for milk.]

      3. Magnitude of residues. [A total of twelve field trials were conducted to measure the magnitude of indaziflam {1,3,5-triazine-2,4-diamine, N-[(1R,2S)-2,3-dihydro-2,6-dimethyl-1H-inden-1-yl]-6-[1-fluoroethyl]} residues grass (forage and hay) following broadcast applications of indaziflam. Indaziflam was applied as either a single application of 0.065 ib ai/A (0.073 Kg ai/ha) or as two applications at a rate of 0.039 lb ai/ha (0.44 Kg ai/ha) per application with a 60 day interval. 
      
Following one foliar application of Alion at a rate of 0.064 to 0.068 lb indaziflam/A (0.072 to 0.076 kg indaziflam/ha) to grass, the total indaziflam residues in grass hay collected at earliest commercial harvest (ECH) ranged from <0.010 to 21 ppm, and the total indaziflam residues in grass forage collected at a 0-day PHI ranged from 2.2 to 18 ppm.  Following two foliar applications of Alion at a total seasonal rate of 0.076 to 0.080 lb indaziflam/A (0.086 to 0.089 kg indaziflam/ha) to grass (TRTD2), the total indaziflam residues in grass hay collected at ECH ranged from 0.020 to 8.0 ppm, and the total indaziflam residues in grass forage collected at a 0-day PHI ranged from 1.4 to 5.4 ppm. 

 A total of eight field trials were conducted to measure the magnitude of indaziflam {1,3,5-triazine-2,4-diamine, N-[(1R,2S)-2,3-dihydro-2,6-dimethyl-1H-inden-1-yl]-6-[1-fluoroethyl]} residues in sugar cane (stalk) following broadcast applications of indaziflam.  Indaziflam was applied as either a single application of 0.065 ib ai/A (0.073 Kg ai/ha) or as two applications at a rate of 0.039 lb ai/ha (0.044 Kg ai/ha) per application with a 58 to 60 day interval.  Following both treatment regimens all total residue of indaziflam, in sugar cane stalk collected at ECH was below the limit of quantitation (0.01 ppm).
      
Two processing trials were conducted to measure the magnitude of indaziflam {1,3,5-triazine-2,4-diamine, N-[(1R,2S)-2,3-dihydro-2,6-dimethyl-1H-inden-1-yl]-6-[1-fluoroethyl]} residues in sugar cane and sugarcane processed commodities following  a single broadcast applications of indaziflam at a rate of 0.326 lb ai/A (0.065 Kg ai/ha), five times the maximum proposed single application use rate.
      
Following a five-fold exaggerated application of Alion to two separate processing trials of sugarcane, the total indaziflam residues in the sugarcane stalk samples were all less than the LOQ (0.01 ppm.  Since no indaziflam residues above the LOQ were observed in the sugarcane RAC study, the sugarcane processed commodities were not analyzed and no processing factors were derived.

Three trials each were conducted with wheat, turnip and soybean planted as rotational crops 22 months after a single application of indaziflam to bare soil at a rate of 0.078 lb ai/A (0.088 Kg ai/ha).   Total indaziflam residues in wheat (forage hay, grain and straw), turnip (roots and tops) and soybean seed were all less than the limit of quantitation (0.01 ppm).  The highest average field trial (HAFT) residues in soybean forage and hay were 0.021 ppm and 0.029 ppm, respectively.

 A feeding study was conducted to measure total indaziflam residue in milk, cream (milk fat), skim milk (whey), mesenteric (omental) fat, perirenal fat, subcutaneous fat, liver, kidney, muscle and excrement (feces or faeces) from lactating Holstein dairy cows (Bos taurus) following 29 consecutive days of dosing with indaziflam.  The base daily dose of indaziflam was calculated to be 31 mg/kg dry matter feed.  Three groups of cows were fed at 31 (1x), 934 (3X) and 311 (10x) mg/kg dry matter feed.  Average total indaziflam residues in milk, at the 28th day were 0.028 ppm, 0.038 ppm and 0.15 ppm, respectively at the 1x, 3x and 10x rates.  Average total indaziflam residues in fat ranged from 0.068 to 0.082 ppm, from 0.11 ppm to 0.12 ppm and from 0.27 ppm to 0.36 ppm, respectively, at the 1x, 3X and 10x rates.  Average total indaziflam residues in kidney were 0.10 ppm, 0.22 ppm and 0.74 ppm, respectively, at the 1x, 3X and 10x rates.  Average total indaziflam residues in liver were 0.20 ppm, 0.31 ppm and 1.3 ppm, respectively, at the 1x, 3X and 10x rates.  Average total indaziflam residues in muscle were < 0.05 ppm, 0.05 ppm and 0.08 ppm, respectively, at the 1x, 3X and 10x rates.  In the depuration phase, residues in all tissues and milk declined rapidly after the end of dosing.]






B. Toxicological Profile

      1. Acute toxicity. Indaziflam has low acute oral (LD50 > 2,000 mg/kg-bw; Category III), dermal (LD50 > 2,000 mg/kg-bw; Category III), and inhalation toxicity (LC50 > 2.30 mg/L air; Category IV) in male and female rats.  Indaziflam is not an eye or skin irritant (both Category IV) and is not a skin sensitizer. 

      2. Genotoxicity. Indaziflam is not genotoxic; it was negative for mutagenicity in reverse and forward gene mutation assays and negative for clastogenicity in vitro and in vivo. 

      3. Immunotoxicity. Immunotoxicity potential was evaluated with a subacute oral (diet) exposure to rats.  Immunotoxicity was not observed with indaziflam exposure, and as such the no observable adverse effect level for immunotoxicity was defined as the highest dose tested (10,000/6,000 ppm in diet, equivalent to 528 and 738 mg/kg-bw/day in males and females, respectively).

      4. Reproductive and developmental toxicity. No effects on reproduction and development were observed in the reproductive and developmental studies conducted with indaziflam, demonstrating that indaziflam is not a reproductive toxicant.  Offspring effects in the rat developmental toxicity study (i.e. decreased fetal weight) were observed only in the presence of maternal toxicity, including decreased body weight gain and food consumption.  No developmental effects were observed in rabbits up to maternally toxic doses.  Decreased pup weights and delays in preputial separation and vaginal opening were observed in the rat 2-generation reproductive toxicity study, but only in the presence of parental toxicity characterized by coarse tremors, renal toxicity, and decreased weight gain. Further, there was no indication of a teratogenic effect of indaziflam in either the rat or the rabbit. 
      
      5. Neurotoxicity. Based on evaluations in the rat (acute, chronic, and developmental neurotoxicity studies) and in the dog (subchronic and chronic studies), the nervous system is considered the major target for indaziflam toxicity, with the dog being the more sensitive species. A single oral dose of indaziflam decreased motor and locomotor activity in male (at 500 mg/kg and 2000 mg/kg) and in female ( >= 100 mg/kg) rats, with recovery within seven days. Other effects included urine, oral and perianal stains (generally resolved one to five days after treatment); tremors; increased reactivity and decreased activity (generally resolved the following day after treatment); increased salivation; cool to touch; clonic convulsions; ventrum wet/staining; and death in three females (at 2000 mg/kg only).  In male rats, acute indaziflam treatment (2000 mg/kg only) also corresponded to microscopic lesions described as focal to multi-focal individual nerve fiber degeneration, observed in the Gasserian ganglion and peripheral nerves (sciatic and tibial).  Based on these results, indaziflam exposures of 50 and 100 mg /kg-bw are the acute NOAELs for neurotoxicity in female and male rats, respectively. In the subchronic rat study, there were no mortalities.  However, similar effects in motor and locomotor activity, as well as clinical signs of neurotoxicity (tremors, repetitive chewing motion, and perianal and lacrimal staining), were noted at the highest doses tested, 10,000 ppm (585.7 mg/kg-bw/day) for male rats and 8,000 ppm (580.9 mg/kg-bw/day) for female rats.  These results establish a NOAEL for subchronic neurotoxicity in rats at 4000 ppm (243.6 mg/kg-bw/day in males and 306.9 mg/kg-bw/day in females).  In the developmental rat neurotoxicity study, the dam and offspring NOAEL was 1000 ppm (83.8 mg/kg-bw/day), based on clinical signs of toxicity in dams (tremor, dilated pupils, nasal stains, and repetitive chewing movements), marked decrease in body weight and body weight gain, and decreased food consumption in dams and offspring. There were no effects on neuropathology in this developmental neurotoxicity study. The neurotoxic effects of indaziflam in dogs, which were more sensitive than rats, are described further in subsequent sections describing subchronic and chronic toxicity. 

      6. Subchronic toxicity. Short- and intermediate-term exposures to indaziflam were assessed in the mouse, rat, and dog.  Indaziflam is not toxic by the dermal route, as there was no toxicity noted at the highest dose tested (1000 mg/kg-bw/day) in a 28-day dermal toxicity study in rats.  The only adverse treatment related effects noted in the mouse following a 90-day oral exposure were reduced body weights, body weight gain, and food consumption at the highest dose tested.  Minimal to moderate follicular cell hypertrophy of the thyroid gland was seen in male rats with a 90-day exposure (5000 and 10,000 ppm), and decreased body weights were seen with 10,000 ppm exposures in male and female rats. Adaptive, reversible findings were seen in the liver of rats, and were restricted to increased liver weight, hepatocellular hypertrophy, increased cholesterol, and lower total bilirubin.  Kidneys were enlarged in the rat, but without any corresponding weight change or pathology.  Neurotoxicity was evident in both rats and dogs receiving subchronic oral exposures to indaziflam.  Effects observed in rats included tremors; repetitive chewing movements; perianal, lacrimal, and nasal staining; and decreased motor and locomotor activity in female rats.  In dogs, effects observed included tremors, ataxia, labored breathing, and seizures in high-dose group male and female dogs.  Neuropathological lesions including axonal swelling and degeneration, as well as individual nerve fiber degeneration, were also observed in male and female dogs.  These findings were located in the brain, spinal cord, and peripheral (sciatic and tibial) nerve tracts.  The dog was the most sensitive species overall after subchronic administration of indaziflam, with the lowest NOAEL of 7.5 mg/kg-bw/day based on neurotoxicity findings in males and female dogs in the 90-day oral gavage study.

      7. Chronic toxicity. Chronic toxicity of indaziflam was evaluated in the mouse, rat, and dog, and there was no evidence of carcinogenicity in any of these species.  There were no treatment-related neoplasms in rat or mouse. Therefore, following chronic exposure, there is no indication of oncogenic potential relevant for the human health risk assessment of indaziflam.  Target organs in mice and rats included liver and kidney, and effects on the thyroid and nervous system were also targets in rats.  Following chronic exposure, mice demonstrated decreased body weight, body weight gain, and food consumption in both sexes; increased incidence of renal and hepatotoxicity in males; and, increased incidence of non-neoplastic changes in the stomach and ovaries of females, at the highest dose tested (1000 ppm).  High dose female rats (10,000 ppm) demonstrated similar signs to those observed in the acute and subchronic neurotoxicity studies (e.g. dilated pupil, reduced motor activity, limited use of limbs, uncoordinated movements, tremors, hindlimbs splayed, low alertness) following chronic administration. The incidence of treatment-related clinical signs in females decreased significantly after the dietary administration for the top dose group was decreased from 10,000 to 6000 ppm due to manifestation of clinical signs.  Clinical signs were not evident in the chronic dog at any dose level.  Organ effects noted in these studies included increased liver, kidney and thyroid weights, with centrilobular hepatocellular hypertrophy in the liver, tubular hyperplasia (male mouse only) and brown pigment in the kidney, and follicular cell hypertrophy in the thyroid (male rat only), histopathological changes to the central and peripheral nerve tracts were noted only in the dog. The dog was the most sensitive species overall after chronic administration of indaziflam, with the lowest NOAEL at 2.0 mg/kg-bw/day in males and females in the 1-year oral feeding study. 

      8. Animal metabolism. A metabolism study for indaziflam, in which male rats were given single oral doses of [indane-3-14C]- or [triazine-2,4-14C]-labeled indaziflam, demonstrated that the uptake and excretion of indaziflam was rapid.  Following oral administration, greater than 87% of the administered dose was excreted within 24 hours.  In general, the majority of the radioactivity was excreted in the feces with fecal:renal excretion ratios ranging from approximately 1:1 for the low dose experiments to approximately 10:1 for the high dose experiments.  No volatile residues were detected, and no mineralization was observed.  Residue levels in tissues were highest in gastrointestinal tract and liver.  Higher residue levels were found in the residual carcass of animals in the bile cannulation experiments.
      
Both uptake and clearance of indaziflam from the blood was rapid.  Females appeared to absorb slightly more material compared to for males.  Blood residues smoothly declined in all dose groups over time, indicating an absence of reuptake.
      
Once absorbed, the metabolism of indaziflam was rapid, occurring mainly through oxidative pathways.  The portion of the administered dose recovered as parent in the feces, particularly in the high dose experiments, was likely not absorbed.

      9. Metabolite toxicology. The two major metabolites of indaziflam are AE 2158969 (BCS-AA10717-carboxylic acid) and BCS-AA10365 (BCS-AA10717-fluoroethyldiaminotriazine, FDAT).  As AE 2158969 was a major metabolite in the rat, toxicity studies conducted with indaziflam are adequate to assess any potential toxicity of this metabolite.  An additional study of BCS-AA10365 demonstrated its lack of relevance for the neurotoxic effects of indaziflam that drive the risk assessment.  Primary mutagenicity screening tests were negative for both of these indaziflam metabolites, and therefore these metabolites are not genotoxic. 

      10. Endocrine disruption. The toxicology database for indaziflam (BCS-AA10717) is current and complete.  Studies in this database include evaluation of the potential effects on reproduction and development and an evaluation of the pathology of the endocrine organs following short- or long-term exposure.  No effects on reproduction and development were observed in the reproductive and developmental studies conducted with indaziflam.


C. Aggregate Exposure

1. Dietary exposure. [The proposed new uses of indaziflam on grass and sugarcane will have minor effects on the previous dietary aggregate risk assessment conducted for all registered uses (EPA, D408152, 2013).  Residues for the additional crop group were based on recommended tolerances.  Assessments, using the DEEM FCID Version 4.02 software, were conducted to evaluate potential risks due to chronic and acute dietary exposure of the U.S. population and selected population subgroups to residues of indaziflam.  Consumption data used in this program were taken from NHANES WWEIA 2005-2010.

The toxicological and exposure database for indaziflam is considered complete.  There was no indication of an increased sensitivity of the young in any studies including the reproductive and developmental studies in rats and rabbits.  Therefore, the special FQPA safety factor can be reduced to 1X and an uncertainty factor of 100 is adequate to account for inter- and intra- species variability.  Acute and chronic Population Adjusted Doses (aPAD and cPAD) are, therefore, the same as the reference doses for the populations and subpopulations of interest.  Acute dietary exposure was expressed as a percentage of the aPAD of 0.075 mg/kg bw/day from a NOAEL of 7.5 mg/kg bw/day, based on axonal degenerative findings in the dog subchronic gavage toxicity study, with an uncertainty factor of 100.  Chronic dietary exposure was expressed as a percentage of the chronic Population Adjusted Dose (cPAD) of 0.02 mg/kg bw/day based on a NOAEL of 2 mg/kg bw/day in the dog chronic dietary toxicity study with an uncertainty factor of 100.]

      i. Food. [Assessments were conducted to evaluate potential risks due to acute and chronic dietary exposure of the U.S. population and selected population subgroups to residues of indaziflam including all registered crops and proposed crops.  This conservative, unrefined assessment assumed recommended tolerance levels for all commodities, 100% Percent Crop Treated (PCT) and default processing factors to adjustment crop residue values.  Acute exposure (95th percentile) for food only utilizes 1.3% of the aPAD for the US Population and 4.4% for Children 1-2 yrs., the most highly exposed subpopulation.  Chronic exposure utilizes 1.3% of the cPAD for the US Population and 8% of the cPAD for Children 1-2 yrs., the most highly exposed subpopulation.]
      
      ii. Drinking water. [Estimated Drinking Water Concentrations (EDWCs) associated with indaziflam use on all crops were calculated by EFED (EPA, D356141, 2010) using SCI-GROW v2.3 and PRZM-EXAMS to calculate ground water and surface water EDWCs, respectively.  EDWCs were calculated for total indaziflam based on parent and degradates FDAT and ROI1 (a degradate of FDAT).  The maximum acute and chronic surface water concentrations estimated by SCI-GROW were 84 ppb and 26 ppb, respectively, and were higher than the ground water estimates.  The value from the highest surface water exposure scenarios were incorporated into the dietary risk assessment.  The addition of the acute estimated drinking water concentration (EDWC) of 84 ppb resulted in 7% of the aPAD utilized for the US Population and 21% utilized for Infants (< 1 yr.), the most highly exposed subpopulation.  The addition of the chronic EDWC of 26 ppb utilized 4% of the cPAD for the US Population and 12% of the cPAD for Infants (< 1 yr.), the most highly exposed subpopulation.  In conclusion, the results of the acute and chronic Tier 1 dietary exposure analyses (including drinking water) are acceptable for all population subgroups examined.  Addition of tolerance residues for the proposed crops shows a slight increase in %aPAD and %cPAD but these additions are well below the EPA level of concern of 100% of the PAD.]

2. Non-dietary exposure. Short- and intermediate-term occupational exposures were assessed. The occupational exposure and risk scenarios adequately cover the use on rangeland and pastureland grasses and sugarcane, and the risk estimates are not of concern.

The restricted entry interval (REI) listed on proposed labels is based on the acute toxicity of the technical material. Indaziflam has low acute dermal toxicity (Toxicity Category III) and is not an ocular or dermal irritant or a dermal sensitizer (Category IV). Acute toxicity Category III and IV chemicals require a 12- hour REI. Furthermore, all short-term, post-application dermal exposures resulted in MOEs greater than the level of concern (MOE>100) and therefore were not of concern. Therefore, the 12-hour REI that appears on the proposed labels is adequate and not of concern to HED.  
       

D. Cumulative Effects

The toxicological properties of indaziflam indicate that it does not have a common mechanism of toxicity with any other compounds.  Although it contains a triazine ring it does not exhibit the toxicological properties of the chlorotriazine common mechanism group.  Therefore it is not necessary to cumulate its exposure with any other compounds. 

E. Safety Determination

      1. U.S. population. [Using the conservative exposure assumptions described above and based on a completeness of toxicity data, it can be concluded that aggregate exposure to residues of indaziflam present a reasonable certainty of no harm.  Chronic aggregate dietary exposure (food and water) will utilize less than 4% of the cPAD for the US Population.  Acute aggregate dietary exposure (food and water) for the U.S. population, utilizes 7% of the aPAD.  Non-dietary and aggregate MOEs (food, drinking water, and non-dietary) are above the Level of Concern.  Therefore, the aggregate assessment for all proposed uses for indaziflam demonstrates that there is a reasonable certainty that no harm will result to the US Population and subpopulations from the use of indaziflam noted here.]

      2. Infants and children. [The developmental and reproductive toxicity of indaziflam were evaluated in developmental toxicity studies in the rat and rabbit, a 2 generation reproduction study in the rat and a developmental neurotoxicity study in the rat.  These studies are discussed under Section B (Toxicology Profile) above.  The developmental toxicity data demonstrated no increased sensitivity of rats or rabbits to in utero exposure to indaziflam.  In addition, the multi generation reproductive toxicity study did not identify any increased sensitivity of rats to in utero or post natal exposure.  The developmental toxicity studies are designed to evaluate adverse effects on the developing organism resulting from maternal pesticide exposure during gestation.  Reproduction studies provide information relating to effects from exposure to the pesticide on the reproductive capability of mating animals and data on systemic toxicity.
      
FFDCA section 408 provides that EPA shall apply an additional tenfold margin of safety for infants and children in the case of threshold effects to account for pre and post natal toxicity and the completeness of the data base unless EPA determines that a different margin of safety will be safe for infants and children.  The indaziflam database is complete for FQPA purposes and there are no residual uncertainties for pre-/post-natal toxicity for indaziflam.  Therefore, the Special FQPA Safety Factor can be reduced to 1X.
      
Based on the exposure assessments described above and on the completeness and reliability of the toxicity data, it can be concluded that the dietary exposure from all proposed uses of indaziflam consumes 21% of the aPAD at the 95th percentile and 12% of the cPAD for the most sensitive population subgroup of infants.  Short-term aggregate risk assessment of indaziflam which includes food, drinking water and residential pathways calculated a MOE of 1,400 for adults and a MOE of 530 for Children.  This is well above the Level of Concern of 100 for indaziflam.  Thus, it can be concluded that there is a reasonable certainty that no harm will result from aggregate exposure to indaziflam residues.]

F. International Tolerances

[Currently, there currently are no international (CODEX) tolerances/MRLs for indaziflam.  Several jurisdictions Canada, European Union and Japan maintain MRLs at 0.01 ppm for tree, nut and vine crops.   Korea maintains MRLs at 0.05 ppm for orchard fruits and 0.01 ppm for tree nuts.]
