Notice of Filing of Pesticide Petition 8E7411 by Interregional Research Project #4 (IR-4), 500 College Road East, Suite 201, Princeton, NJ  08540 

EPA Registration Division contact: Susan Stanton ; (703) 305-5218

	EPA has received a pesticide petition (petition number  8E7411) from Interregional Research Project #4 (IR-4), 500 College Road East, Suite 201, Princeton, NJ  08540 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. 565 by establishing a tolerance for residues of thiamethoxam {3-[(2-chloro-5-thiazolyl)methyl]tetrahydro-5-methyl-N-nitro-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 on vegetable, root, subgroup 1A (0.04 ppm), avocado (0.2 ppm), black sapote (0.2 ppm), canistel (0.2 ppm), mamey sapote (0.2 ppm), mango (0.2 ppm), papaya (0.2 ppm), sapodilla (0.2 ppm), star apple (0.2 ppm). In addition, IR-4 is requesting the tolerance expression for the Berry Crop Group 13 be revised to become the Berry and Small Fruit Crop Group 13 as per the Pesticide Tolerance Crop Grouping Program published in the Federal Register vol. 72, No. 235, Dec. 7, 2007. The proposed new tolerance expressions for the Berry and Small Fruit Crop group 13 are as follows: Caneberry subgroup 13-07A (0.35 ppm), Bushberry subgroup 13-07B, (0.2 ppm), Fruit, small, vine climbing subgroup 13-07F, except fuzzy kiwifruit (0.2 ppm), Low growing berry subgroup 13-07G except cranberry (0.3 ppm).  The existing tolerance on cranberry at 0.02 ppm will not be changed.   Also, IR-4 is requesting the following tolerance be deleted: Vegetable, root, except sugar beet, subgroup 1B (0.02 ppm), Caneberry subgroup 13A (0.35 ppm), Bushberry subgroup 13B (0.20 ppm), Grape (0.20 ppm), Strawberry (0.30 ppm), Lingonberry (0.20 ppm), Juneberry (0.20 ppm), Salal (0.20 ppm). 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.  [The primary metabolic pathways of thiamethoxam 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 residues of concern for tolerance setting purposes.]

	2. Analytical method. [Syngenta Crop Protection, Inc. has submitted practical analytical methodology for detecting and measuring levels of thiamethoxam in or on raw agricultural commodities.  This method 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 samples analyzed by UV and 0.25 ng injected for 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. [Syngenta Crop Protection, Inc. has submitted complete residue data for thiamethoxam on avocado (representing the tropical fruit subgroup containing avocado, black sapote, canistel, mamey sapote, mango, papaya, sapodilla, and star apple) and thiamethoxam on sugar beets (representing sugar beet roots, refined sugar, molasses and dried pulp)]

B. Toxicological Profile

	1. Acute toxicity.  [The acute oral LD50 for thiamethoxam in the 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.  Thiamthoxam is minimally irritating to the eye, non-irritaing to skin and is not 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 posture, 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).]

	2. Genotoxicty. [In 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 hamster 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 tested 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 prenatal developmental study in the rabbit (OPPTS 870.3700b) resulted in maternal and developmental NOAELs of 50 mg/kg/day.  The maternal and develomental LOAEL is 150 mg/kg/day.  The maternal LOAEL is based on maternal deaths, hemorrhagic discharge, decreased body weight 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 fertility 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 increased 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, liver 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 toxicity in dogs (OPPTS 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 weights and delayed maturation 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 neurotoxicity 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 not have been tested at sufficient high dose levels; however, a new study is not required because the weight of 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 based 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.

In a combined carcinogenicity study in rats (OPPTS 870.4300) the 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 increase 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.  CGA-293343 did not stimulate hepatocyte cell proliferation in male rats.

In a special study to assess liver biochemistry in the mouse, 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 metabolite 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 specific 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 Exposure

	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 the Supplemental CSFII children's survey (1998) consumption database.  In the Tier I acute assessment, in addition to 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, these exposure assessments also included pending and proposed crop tolerances.  Pending crop tolerances for foliar use of thiamethoxam (CGA293343) and its metabolite (CGA322704) include tropical fruit (avocado, black sapote, canistel, mamey sapote, mango, papaya, sapodilla and star apple - 0.2 ppm), and for the seed treatment use on beet, sugar (0.04 ppm),  beet, sugar, roots (0.04 ppm), beet, sugar, refined sugar (0.04 ppm), beet, sugar, molasses, (0.04 ppm), beet, sugar, dried pulp (0.04 ppm).  Percent of crop treated values were conservatively estimated to be 100% for all registered, pending and proposed uses.  Field trials residue values were used in the Tier III chronic assessments where thiamethoxam was applied at the maximum intended use rate and samples were harvested at the minimum pre-harvest interval (PHI) to obtain the maximum expected residues.  Calculated and projected percent crop treated (%CT) values were incorporated in these chronic Tier III assessments.  Drinking water estimates were incorporated directly into the dietary exposure assessments using the highest estimated drinking water concentrations (EDWCs) for surface and ground water.]

	i. Food. [Acute Exposure: The thiamethoxam acute dietary (food only) risk assessment was 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.  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 acute reference dose (%aRfD).  At the 95[th] percentile, acute (food only) exposure to the U.S. population resulted in a MOE of 2,569 (3.84% 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 1,352 (7.29% 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 below 100% of the aRfD, Syngenta believes that there is a reasonable certainty that no harm will result from dietary (food only) exposure to residues arising from all current and proposed uses of thiamethoxam.	

Chronic Exposure.  The thiamethoxam chronic dietary (food only) risk assessment was 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 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 (%RfD).  Chronic (food only) exposure to the U.S. population resulted in a MOE of 15,639 (0.6% of the RfD of 0.012 mg/kg-bw/day).  The most exposed sub-population was children (1-2 years old) with a MOE of 4,670 (2.1% of the 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 below 100% of the RfD, Syngenta believes that there is a reasonable certainty that no harm will result from dietary (food only) exposure to residues arising from the current and proposed uses of thiamethoxam.


Cancer.  A quantitative risk assessment using a cancer endpoint was not performed.]

	ii. Drinking water. [The EPA uses the Tier 2 model PRZM/EXAMS to estimate potential surface water concentrations and the screening model SCI-GROW to estimate potential ground water concentrations.  None of these models includes consideration of the impact that processing (mixing, dilution, or treatment) would have on the removal of pesticides from the water source prior to distribution as drinking water.  The primary use of these models is to provide a conservative approximation of the Estimated Drinking Water Concentrations (EDWCs) of specific pesticides in drinking water.  These models were used by Syngenta to provide EDWCs of thiamethoxam for proposed use on sugarbeets as a seed treatment and the proposed uses on the tropical fruits avocado, black sapote, canistel, mamey sapote, mango, papaya, sapodilla and star apple at varying maximum application rates, none greater that 0.266 lb./acre per year.  Based on these assumptions, the highest acute surface water EDWC (generated using the standard PRZM crop scenario for Florida peppers) is 12.15 parts per billion (ppb).  The highest chronic surface water EDWC, generated using the PRZM crop scenario for California lettuce, is 0.764 ppb.  The highest acute and chronic EDWC for ground water (based on an application rate of 1 x 0.266 lb./acre) is 4.12 ppb.  The highest of these values was used for the acute and chronic aggregate assessments and will be considered to be protective for all drinking water concerns.

 
Acute Exposure from Drinking Water:  The acute surface water EDWC of 12.15 ppb was input directly into the DEEM-FCID(TM) software as "water, direct and indirect, all sources".  Acute exposure (water only) to the U.S. population resulted in a MOE of 131,179 (0.08% 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 43,179 (0.23% 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 below 100% of the RfD, Syngenta believes that there is a reasonable certainty that no harm will result from acute dietary (food and drinking water) exposure to residues arising from all current, pending and proposed uses of thiamethoxam.

Chronic Exposure from Drinking Water:  The chronic EDWC of 4.12 ppb (ground water) was used to calculate the chronic drinking water exposure values for the U.S. Population and population subgroups.  Chronic drinking water estimates were incorporated directly into the DEEM-FCID(TM) software as "water, direct and indirect, all sources".  Chronic exposure (water only) to the U.S. population resulted in a MOE of 13,793 (0.7% of the chronic RfD of 0.012 mg/kg-bw/day).  The most exposed sub-population was infants (<1 year old) with a MOE of 4,211 (2.4% 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 below 100% of the RfD, Syngenta believes that there is a reasonable certainty that no harm will result from chronic drinking water exposure to residues arising from all current and proposed uses of thiamethoxam.]

	2. Non-dietary exposure. [A residential exposure and risk assessment was performed for thiamethoxam using the recently revised endpoints and uncertainty factors established by the EPA.  The residential exposure and risk assessment was performed for thiamethoxam uses on turf and ornamentals using the Meridian 0.33G and 25WG labels.  Based on these Meridian labels, there is a potential for residential handler exposure from consumers making applications to home lawns and ornamentals.  There is also a potential for post-application residential exposure to adults and children re-entering treated lawns and to adults playing golf on treated turf.  The following endpoints were used for these residential risk assessments:  NOAEL = 1.2 mg/kg/day (for adults, from a two 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).  The post-application residential MOE for children (1-6 years) from turfgrass use of Meridian 25 WG is 1,347, which exceeds the residential risk arising from the turfgrass use Meridian 0.33G (MOE = 1,650).  The resultant combined short-term MOEs were 1,347 (total post-application risk) and 2,111 (combined post-application and handler risk) for children (1-6 years) and adults (20-49 years), respectively.  Both children (1-6 years) and adults (20-49 years) MOEs are above the Benchmark MOE of 100 and thus do not exceed the EPA's level of concern.]

D. Cumulative Effects

	[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 established and proposed thiamethoxam tolerances would result in a MOE of 2,520 (3.91% of the aRfD of 0.35 mg/kg-bw/day) for the general U.S. population, which exceeds the Benchmark MOE of 100.  The chronic dietary exposure analysis (food plus water) showed that exposure from all registered and proposed thiamethoxam tolerances resulted in a MOE of 7,336 (1.4% of the chronic RfD of 0.012 mg/kg-bw/day) for the general U.S. population, which also 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 2,039 for adults (20-49 years 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 a reasonable certainty that no harm will result from aggregate exposure to residues arising from all current and proposed thiamethoxam uses, 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 established and proposed thiamethoxam uses would result in a MOE of 1,311 (7.52% of the aRfD of 0.35 mg/kg-bw/day) for the most sensitive population subgroup, children 1-2 years old, which exceeds the Benchmark MOE of 100.  The chronic aggregate dietary (food plus water) exposure analysis showed that exposure from all established, pending and proposed thiamethoxam uses would result in a MOE of 2,995 (3.3% of the chronic RfD of 0.012 mg/kg-bw/day) for the most sensitive population subgroup, children 1-2 years 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 1,279 for the children (1-6 years), 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 a reasonable certainty that no harm will result to infants and children from aggregate exposure to residues arising from all current, pending and proposed thiamethoxam tolerances, including 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, Belarus, Brazil, Canada, Czech Republic, Denmark, Estonia, Georgia, Great Britain (UK), Greece, Hungary, India, Israel, Italy, Korea (South), Latvia, Moldova, Netherlands, New Zealand, Russia, Serbia and Montenegro, Slovak Republic, Slovenia, South Africa, Spain, Switzerland, Taiwan, Ukraine, and United States.]



