EPA Registration Division contact: Venus Eagle ; (703) 30 8 - 8045

TEMPLATE: Syngenta Crop Protection, Inc. [ petition number 0F 7805 ] EPA has received a pesticide petition from Sy ngenta Crop Protection, Inc., [Sy ngenta Crop Protection, Inc., PO Box 18300, Greensboro, NC, 27419] 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.

1. by establishing a tolerance for residues of Thia methoxam {3 - [(2 - chloro - 5 - thiazolyl)methyl]tetrahydro - 5 - methyl- Nnitro - 4H - 1,3,5 - oxadiazin - 4 - imine}(CAS Reg. No. 153719 - 23 - 4) and its metabolite [ N - (2 - chloro - thiazol- 5 -ylmethyl) - N ’ - methyl- N ’ - nitro - guanidine ] in or o n buckwheat, grain at 0.02 per million (ppm) ; buckwheat, forage at 0.50 ppm; buckwheat, hay at 0.02 ppm; buckwheat, straw at 0.02 ppm; oat, grain at 0.02 ppm; oat, forage at 0.50 ppm, oat, hay at 0.02 ppm; oat, straw at 0.02 ppm; pearl millet, grain at 0.02 ppm; preal millet, forage at 0.02 ppm ; pearl millet, stover at 0.02 ppm; proso millet, grain at 0.02 ppm ; proso millet, forage at 0.02 ppm; proso millet, stover at 0.02 ppm; proso millet, straw at 0.02 ppm; rye, grain at 0.02 ppm; rye, forage at 0.50 ppm; rye, straw at 0.02 ppm; teosinte, gra in at 0.02 ppm; teosinte, forage at 0.10 ppm; teosinte, stover at 0.05 ppm; triticale, grain at 0.02 ppm; triticale, forage at 0.05 ppm; triticale, hay at 0.02 ppm; triticale, straw at 0.02 ppm; wild rice, grain at 0.02 ppm. This revised Notice of Filing is an amendment to reflect specific proposed grain tolerance and their respective animal feed commodities listed in the revised Section F of the tolerance petition [0F7805] . 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 befo re EPA rules on the petition. A. Residue Chemistry2

1. Plant metabolism. [ The primary metabolic pathways of thiam e thoxam in plants (corn, rice, pears, and cucumbers) were similar to those described for animals, with certain extensions of the pathway in plants. Parent compound and CGA -322704 were the major residues in all crops. The metabolism of thiamethoxam in plants and animals is understood for the purposes of the proposed tolerance. Parent thiamethoxam and the metabolite, CGA-322704, are the r esidues of concern for tolerance setting purposes.] 2. Analytical method. [Syngenta Crop Protection, Inc. has submitted practical analytical methodology for detecting and measuring levels of thia methoxam in or on raw agricultural commodities . This met hod is based on crop specific cleanup procedures and determination by liquid chromatography with either UV or MS detections. The limit of detection (LOD) for each analyte of this method is 1.25 ng injected for sample s analyzed by UV an d 0.25 ng injected f or samples analyzed by MS, and the limit of quantification (LOQ) is 0.005 ppm for milk and juices, and 0.01 ppm for all other substrates ] 3. Magnitude of residues.

. There is no residue data submitted with this petition as thiamethoxam is already approved for use on the representative commodities for the cereal grains (crop group 15): corn (sweet and field), rice, sorghum, and wheat. This petition is requesting that E PA establish tolerances for the rest of the commodities listed above to complete this crop group. Note that although additional residue data for the small cereal grain commodities is not provided, Syngenta Crop Protection, Inc. received feedback from an EPA ChemSAC meeting November 25, 2009 concluding that if the use patterns were similar to existing uses on barley or wheat, then wheat and barley residue data can be used to apply towards additional small cereal grain tolerances. B. Toxicological Profile 1. Acute toxicity. [The acute oral LD50 for thiamethoxam in t h e rat is 1563 mg/kg body weight. The acute dermal LD50 of thiamethoxam is >2000 mg/kg body weight. Thiamethoxam is non - toxic at atmospheric concentrations of 3.72 mg/l. Thiamthox amis minimally irritating to the eye, non - irritaing to skin and is n ot a dermal sensitizer. In an acute neurotoxicity study in rats (OPPTS 870.6200a), the NOAEL was 100 mg/kg/day with a NOAEL of 500 mg/kg/day based on drooped palpebral closure, decrease in rectal temperature and locomotor activity and increase in forelimb grip strenght (males only). At higher dose levels, mortality, abnormal body tone, ptosis, impaired respiration, tremors, longer latency to first step in the open field, crouched over po sture, gait impairment, hypo - arousal, decreased number of rears, uncoordinated landing during the righting reflex test, slight lacrimation (females only) and higher mean average input stimulus value in the auditory startle response test (males only).]3 2. Genotoxicty. [I n gene mutation studies with S. typhimurium and E. coli (OPPTS 870.5100 and 870.5265, there was no evidence of gene mutation when tested up to 5000  g/plate and there was no evidence of cytoxicity. In a gene mutation study with chinese h amster V79 cells at HGPRT focus (OPPTS 870.5300) there was no evidence of gene mutation when tested up to the solubility limit. In a CHO cell cytogenetics study (OPPTS 870.5375) there was no evidence of chromosomal aberrations when tested up to cytotoxic or solubility limit concentrations. An in vivo mouse bonemarrow micronucleus study (OPPTS 870.5395) was negative when tes t ed upto levels of toxicity in whole animals; however, no evidence of target cell cytoxicity. A UDS assay (OPPTS 870.5550) was negative when tested up to precipitating concentrations. ] 3. Reproductive and developmental toxicity. [A prenatal developmental study in the rat (OPPTS 870.3700a) resulted in Maternal and Developmental NOAELs of 30 mg/kg/day and 200 mg/kg/day, respectively . The maternal LOAEL is 200 mg/kg/day based on decreased body weight, body weight gain and food consumption. The developmental LOAEL was 750 mg/kg/day based on decreased fetal body weight and an increased incidenceof skeletal anomalies. A prenat al devel opmental study in the rabbit (OPPTS 870.3700b) resulted in ma ternal and developmental NOAELs of 50 mg/kg/day. The maternal and develomental LOAEL is 150 mg/kg/day. The maternal LOAEL is based on ma ternal deaths, hemorrhagic discharge, decreased body weig ht and food intake during the dosing period. The developmental LOAEL is based on decreased fetal body weights, increased incidence of post- implantation loss and a slight increase in the incidence of skeletal anomalies/variations. In a reproduction and fe rtility effects study in rats (OPPTS 870.3800) the Parental/sytemic NOAEL is 1.84 (males), 202.06 (females) mg/kg/day; the reproductive NOAEL is 0.61 (males), 202.06 (females) mg/kg/day and the offspring NOAEL is 61.25 (males), 79.20 (females) mg/kg/day. The parental /sytemic LOAEL is 61.25 (males), not determined (females) mg/kg/day based on inscreased incidence of hyaline change in renal tubules in F0 and F1 males. The reproductive LOAEL is 1.84 (males), not determined (females) mg/kg/day based on incre ased incidence and severity of tubular atrophy observed in testes of the F1 generation males. The offspring LOAEL is 158.32 (males), 202.06 (females) mg/kg/day based on reduced body weight gain during lactation period in all litters. ] 4. Subchronic toxicity. [A 90 day oral toxicity study in rats (OPPTS 870.3100) resulted in a NOAEL of 1.74 (males, 92.5 (females) mg/kg/day. The LOAEL is 17.4 (male), 182.1 (female) mg/kg/day based on increased incidence of hyaline change or renal tubules epithelium ( males), fatty change in adrenal gland of females, liver4

changes in females, all at the LOAEL. A 90 day oral toxicity in mice (OPPTS 870.3100) resulted in a NOAEL of 1.41 (males, 19.2 (females) mg/kg/day. The LOAEL was 14.3 (male) 231 (female) mg/kg/day based on increased incidence of hepatocellular hpertrophy. At higher dose levels: decrease in body weight and body weight gain, necrosis of individual hepatocytes, pigmentation of Kupffer cells, and lymphocytic infiltration of the liver in both sexes; slight hematologic effects and decreased absolute and erlative kidney weights in males; and ovarion atrophy, decreased ovary and spleen weights and increased liver weights in females. In a 90 day oral to xicity in dogs (OPPT S 870.3150), the NOAEL is 8.23 (males), 9.27 (females) mg/kg/day. The LOAEL is 32.0 (male), 33.9 (female) mg/kg/day based on slightly prolonged prothrombin times and decreased plasma albumin and A/G ration (both sexes; decreased calcium levels and ovary w eights and delayed ma turation in the ovaries (female); decreased cholesterol and phospholipid levels, testis weights, spermatogenesis, and spermatic giant cells in testes (male). In a 28 day dermal study in rats (OPPTS 870.3200) the NOAEL was 250 (male), 60 (female) mg/kg/day. The LOAEL was 1000 (male), 250 (female) mg/kg/day based on increased plasma glucose, triglyceride levels, and alkaline phosphatase activity and inflammatory cell infiltration in the liver and necrosis if single hepatocyts in females and hhaline change in renal tubules and a very slight reduction in body weight in males. At higher dose levels in females, chronic tubular lesions in the kidneys and inflammatory cell infiltration in the adrenal cortex were observed. In a subchronic neu rotoxicity screening study in rats (OPPTS 870.6200b) the NOAEL was 95.4 (male), 216.4 (female) mg/kg/day, both at the highest dose tested. The LOAEL was not determined. No treatment related observations at any dose level. LOAEL was not achieved. May n ot have been tested at sufficient high dose levels; however, a new study is not required because the weight o f evidence from other toxicity studies indicates no evidence of concern. ] 5. Chronic toxicity. [ In a chronic toxicity study in dogs (OPPTS 870.4100) the NOAEL was 4.05 (male), 4.49 (female) mg/kg/day. The LOAEL was 21.0 (male), 24.6 (female) mg/kg/day based on increase in creatinine in both sexes, transient decease in food consumption in females, and occasional increase in urea levels, decrease in ALT, and atrophy of seminiferous tubules in males. In a mouse carcinogenicity study (OPPTS 870.4200) the NOAEL was 2.63 (male), 3.68 (female) mg/kg/day. The LOAEL was 63.8 (male), 87.6 (female) mg/kg/day ba sed on hepatocyte hypertrophy, single cell necrosis, inflammatory cell infiltration, pigment deposition, foci of cellular alteration, hyperplasia of Kupffer cells and increased mitotic activity, also an increase in the incidence of hepatocellular adenoma (both sexes). At higher doses, there was an increase in the incidence of hepatocellular adenocarcinoma (both sexes) and the number of animals with multiple tumors, evidence of carcinogenicity.5

I n a combined carcinogenicity study in rats (OPPTS 870.4300) t he NOAEL was 21.0 (male), 50.3 (female) mg/kg/day. The LOAEL was 63.0 (male), 255 (female) mg/kg/day based on the increased incidence of lymphocytic infiltration of the renal pelvis and chronic nephropathy in males and decreased body weight gain, slight i ncrease in the severity of hemosiderosis of the spleen, foci of cellular alteration in liver and chronic tubular lesions in kidney in females. No evidence of carcinogenicity. In a hepatic cell proliferation study in mice, the NOAEL was 16 (male), 20 (female) mg/kg/day. The LOAEL was 72 (male), 87 (female) mg/kg/day based on proliferative activity of hepatocytes. At higher dose levels, increases in absolute and relative liver weights, speckled liver, haptocellular glycogenisis/fatty change, heptocellular necrosis, apoptosis and pigmentation were observed. In a 28 day feeding study to assess replicative DNA synthesis in the amle rat, the NOAEL was 711 mg/kg/day. The LOAEL was not established. Immunohistochemical staining of the liver sections from control and high dose animals for proliferating cell nuclear antigen gave no indication for a treatment related increase in the fraction of DNA synthesizing hepatocytes in S - phase. CGA293343 did not stimulate hepatocyte cell proliferation in male rats. In a special study to assess liver biochemistry in the mo use, the NOAEL was 17 (male), 20 (female) mg/kg/day. The LOAEL was 74 (male), 92 (female) mg/kg/day based on marginal to slight increases in absolute and relative liver weights, a slight increase in the microsomal protein content of the livers, moderate increases in the cytochrome P450 content, slight to moderate increases in the activity of several microsomal enzymes, slight to moderate induction of cystolic glutathion S - transfer activity. Treatment did not affect peroxisomal fatty acid  - oxidation ] 6. Animal metabolism. [The metabolism of thiamethoxam in rats and livestock animals is adequately understood. The residues of concern have been determined to be parent thiamethoxam and its metabolite [ N - (2 - chloro - thiazol- 5 -ylmethyl) - N ’ - methyl- N ’ - nitro - guanidine] expressed as thiamethoxam. ] 7. Metabolite toxicology

. [For most risk assessment purposes, residues of the metabo lite corrected for molecular weight are considered to be toxicologically equivalent to parent thiamethoxam. However, EPA has determined that the metabolite should not be included in the cancer risk assessment. ] 8. Endocrine disruption

. [There are no s pecific studies requested by the Endocrine Disruptor Screening Program (EDSP) at this time because endocrine effects have been well characterized in an acceptable 2 - generation reproduction study with a clear NOAEL and LOAEL, and the chronic reference dose (cRfD) selected for thiamethoxam risk assessments is considered protective of the observed endocrine effects. ] C. Aggregate Exposure6

1. Dietary exposure. Tier I acute, and Tier III chronic aggregate risk assessments were performed for thiamethoxam using the Dietary Exposure Evaluation Model (DEEM - FCID TM , version 2.16) from Exponent. All consumption data for these assessments was taken from the USDA’s Continuing Survey of Food Intake by individuals (CSFII) with the 1994 - 96 consumption database and t he Supplemental CSFII children’s survey (1998) consumption database. The Tier I acute assessments incorporated established tolerances (40 CFR 180.565) for the combined residues of thiamethoxam (CGA293343) and its metabolite (CGA322704) in or on a variety of raw agricultural commodities including meat and milk; the acute assessments also included anticipated residues for all pending uses and the proposed seed treatment use on buckwheat, pearl millet, proso millet, oats, rye, teosinte, triticale, and wild ri ce. Percent of crop treated values were conservatively estimated to be 100% for all uses in the acute assessments. In the Tier III chronic assessments, field trial residue values were used where thiamethoxam was applied at the maximum intended use rate a nd samples were harvested at the minimum pre harvest interval (PHI) to obtain the maximum expected residues; the chronic assessments also included anticipated residues for all pending uses the proposed seed treatment use on oats. Estimated percent crop tr eated (%CT) values were incorporated into the chronic Tier III assessments based upon economic, pest, and competitive pressures. Drinking water estimates were incorporated directly into the acute and chronic dietary exposure assessments using the highest estimated drinking water concentrations (EDWCs) for surface and ground water.

i. Food. Acute Exposure. The thiamethoxam acute food risk assessments were performed for all population subgroups using an acute reference dose of 0.35 mg/kg - bw/day based upon a developmental neurotoxicity study in rats with a no observed adverse effect level (NOAEL) of 34.5 mg/kg/day and an uncertainty factor of 100X to account for intra - and inter- species variations. No additional FQPA safety factor was applied. For th e 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 t he acute reference dose (%aRfD). At the 95 th percentile, acute (food only) exposure to the U.S. population resulted in a MOE of 2,463 (4.0% of the aRfD of 0.35 mg/kg - bw/day). The most exposed sub - population was children (1 - 2 years old) with a MOE of 1,25 5 (7.9% of the aRfD of 0.35 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 MOE or below 100% of the aRfD, Syngenta believes that there is a reasonable certain ty that no harm will result from dietary (food only) exposure to residues arising from all current, pending, and proposed uses of thiamethoxam. Chronic Exposure. The thiamethoxam chronic dietary food risk assessments were performed for all population subgroups using a chronic reference dose of 0.012 mg/kg - bw/day based upon a two generation reproduction study in rats with a no observed adverse effect level (NOAEL) of 1.2 mg/kg/day and an uncertainty factor7

of 100X to account for 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 populati on subgroup. In addition, exposure was expressed as a percent of the chronic reference dose (%cRfD). Chronic (food only) exposure to the U.S. population resulted in a MOE of 6,627 (1.5% of the cRfD of 0.012 mg/kg - bw/day). The most exposed sub - population was children (1 - 2 years old) with a MOE of 2,002 (5.0% of the cRfD of 0.012 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 MOE or below 100% of the cRfD, Syn genta believes that there is a reasonable certainty that no harm will result from dietary (food only) exposure to residues arising from all current, pending, and proposed uses of thiamethoxam.

Cancer . A quantitative risk assessment using a cancer endpoi nt was not performed. ii. Drinking water

. The Estimated Drinking Water Concentrations (EDWCs) of thiamethoxam were determined using Tier l screening models, SCI - GROW which estimates pesticide concentration in ground water, FIRST which estimates pesticide concentration in surface water (for propose d cereal grains seed treatment use), and for aquatic uses, a modified Tier I Rice Model and Provisional Cranberry Model which estimates pesticide concentration in tail water from rice paddies and cranberry bogs, respectively . The currently registered and pending uses plus the proposed seed treatment use on oats were assessed. The highest ground water EDWC resulting from SCI - GROW modeling was 4.12 ppb (acute and chronic) based on the currently registered use on grapes. The highest surface water EDWCs resu lted from the currently registered rice use. The modified Tier I Rice model provided a surface water acute EDWC of 147.72 ppb and a chronic EDWC of 12.62 ppb (adjusted for a 0.87 Percent Cropped Area (PCA) factor). Since the surface water EDWCs exceed th e ground water EDWC, the surface water values were used for risk assessment purposes and will be considered protective for any ground water exposure concerns. Acute Exposure from Drinking Water: The acute surface water EDWC of 147.72 ppb was input di rectly into the DEEM- FCIDTM software as “water, direct and indirect, all sources” to model the acute drinking water exposures. Exposure contributions at the 95% - ile of exposures were determined by taking the difference between the aggregate (food + drinkin g water) exposures and the food exposures alone for each population subgroup. Acute drinking water exposure U.S. population resulted in a MOE of 7,062 (1.4% of the acute RfD of 0.35 mg/kg bw/day). The most exposed sub - population was all infants (<1 year old) with a MOE of 1,599 (6.2% of the aRfD of 0.35 mg/kg/day). Since the Benchmark MOE for this assessment was 100 and since the EPA generally has no concern for exposures above the Benchmark MOE or below 100% of the aRfD, Syngenta8

believes that there is a reasonable certainty that no harm will result from acute drinking water exposure to residues arising from all current, pending, and proposed uses of thiamethoxam. Chronic Exposure from Drinking Water: The chronic surface water EDWC of 12.62 ppb was input directly into the DEEM- FCIDTM software as “water, direct and indirect, all sources” to model the chronic drinking water exposures. Chronic drinking water exposure to the U.S. population resulted in a MO E of 4,511 (2.2% of the chronic RfD of 0.012 mg/kg - bw/day). Chronic drinking water exposure to the most exposed sub - population (infants, <1 year old) resulted in a MOE of 1,376 (7.3% of the chronic RfD of 0.012 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 MOE or below 100% of the cRfD, Syngenta believes that there is a reasonable certainty that no harm will result from chronic drinking water exposure to resi dues arising from all current, pending, and proposed uses of thiamethoxam.

2. Non

- dietary exposure

. A residential exposure and risk assessment was performed for thiamethoxam using the endpoints and uncertainty factors established by the EPA. Residential exposure and risk assessments were performed for thiamethoxam uses on turf and ornamentals (Meridian® 25WG) and for thiamethoxam indoor crack and crevice uses (Optigard® ZT). These product labels indicate that thiamethoxam is to be applied by commercial applicators only; therefore residential assessments were limited to post- application exposure risks for adults and children. The following endpoints were used for these residential risk assessments: NOAEL = 1.2 mg/kg/day (for adults, from a tw o generation oral reproduction study in rats) and NOAEL = 60 mg/kg/day (for children 1 - 6, from a short- term dermal from a 28 - day dermal study in rats). Post application dermal exposure risks from thiamethoxam are acceptable (MOE = 4,070) for adults re ent ering lawn turf grass following treatment with Meridian® 25WG. Post application dermal plus non - dietary oral exposure risks from thiamethoxam are also acceptable (aggregate MOE = 1,339) for children re - entering lawn turf grass following treatment with Meridian® 25WG. Post application dermal exposure risks from thiamethoxam are acceptable (MOE = 900) for adults re - entering indoor carpeted or hard floor areas following crack and crevice treatment with Optigard® ZT. Post application dermal plus non - dietary oral exposure risks from thiamethoxam are also acceptable (short - term aggregate MOE = 1,260, intermediate - term aggregate MOE = 1,404) for children re - entering indoor carpeted or hard floor areas following crack and crevice treatment with Optigard® ZT. Sin ce the children (1 - 6 years) and adult (20 - 49 years) MOEs are above the Benchmark MOE of 100 the residential exposure risks do not exceed the EPA’s level of concern. D. Cumulative Effects9 [ Cumulative Exposure to Substances with a Common Mechanism of Toxicity. Section 408(b)(2)(D)(v) of FFDCA 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”. Unlike other pesticides for which EPA has followed a cumulative risk approach based on a common mechanism of toxicity, EPA has not made a common mechanism of toxicity finding as to thiamethoxam and any other substances and thiamethoxam does not appear to produce a toxic metabolite produced by other substances. For the purposes of this tolerance action, the EPA has not assumed that thiamethoxam has a common mechanism of toxicity with other substances.] E. Safety Determination 1. U.S. Population . The acute dietary exposure analysis (food plus water) showed that exposure from all current, pending, and proposed uses of thiamethoxam would result in a MOE of 1,826 (5.4% of the aRfD of 0.35 mg/kg - bw/day) for the general U.S. population, which exceeds the Benchmark MOE of 100. For the short- term aggregate exposure analysis the corresponding food, water and residential MOEs were aggregated using the inverse MOE approach. The short- term aggregate (food, drinking water, and residential) MOE was 863 for adults (20 - 49 years old), which exceeds the Benchmark MOE of 100. The chronic dietary exposure analysis (food plus water) showed that exposure from all current, pending, and proposed uses of thiamethoxam re sulted in a MOE of 2,684 (3.7% of the cRfD of 0.012 mg/kg bw/day) for the general U.S. population, which also exceeds the Benchmark MOE of 100. Based on the completeness and reliability of the toxicity data supporting these petitions, Syngenta believes th at there is a reasonable certainty that no harm will result from aggregate exposure to residues arising from all current, pending, and proposed uses of thiamethoxam, including anticipated dietary exposure from food, water, and all other types of non - occupational exposures. 2. Infants and children. The acute dietary exposure analysis (food plus water) showed that exposure from all current, pending, and proposed uses of thiamethoxam would result in a MOE of 944 (10.4% of the aRfD of 0.35 mg/kg bw/day) for t he most sensitive population subgroup, infants <1 year old, which exceeds the Benchmark MOE of 100. For the short- term aggregate exposure analysis the corresponding food, water and residential MOEs were aggregated using the inverse MOE approach. The short- term aggregate (food, drinking water, and residential) MOE was 1,225 for children (1 - 6 years), which exceeds the Benchmark MOE of 100. The chronic aggregate dietary (food plus water) exposure analysis showed that exposure from all current, pending, and proposed uses of thiamethoxam would result in a MOE of 1,048 (9.6% of the cRfD of 0.012 mg/kg bw/day) for the most sensitive population subgroup, infants <1 year old, which exceeds the Benchmark MOE of 100. Based on the completeness and reliability of the toxicity data supporting these petitions, Syngenta believes that there is a10

reasonable certainty that no harm will result to infants and children from aggregate exposure to residues arising from all current, pending, and proposed uses of thiamethoxam, inc luding anticipated dietary exposure from food, water, and all other types of non - occupational exposures

. F. International Tolerances There are currently no Maximum Residue Limits (MRLs) set for thiamethoxam for crops by the Codex Alimentarius Commission. International MRLs for the insecticide thiamethoxam have been established for various agricultural commodities in a number of countries including Argentina, Australia, Austria, Belgium, Brazil, Canada, Croatia, Czech Republic, Denmark, Europe an Union, Finland, France, Germany, Greece, Hungary, India, Ireland, Israel, Italy, Jamaica, Japan, Korea, Lithuania, Malaysia, Mexico, Netherlands, New Zealand, Norway, Poland, Portugal, Romania, Russia, South Africa, Spain, Sweden, Switzerland, Taiwan, T urkey, United Kingdom, and the United States.