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

EPA Registration Division contact: Julie Chao ; (703) 308

- 8 73 5

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 re place the instructions that appear in green , i.e., “ [ insert
company name ] ,” with the information specific to your action.

TEMPLATE:

Syngenta Crop Protection, Inc.

[ Petition Number (2E8036) ]

EPA has received a pesticide petition ( [insert petition number ] ) from Syngenta Crop Protection, Inc.

, PO Box 18300, Greensboro, NC, 27419 request ing, 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 amending the tolerance for residues of

Thiamethoxam {3

- [(2

- chloro

- 5

- thiazolyl)methyl]tetrahydro

- 5

- methyl

- N

nitro

- 4 H

- 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 the raw

a gricultural commodity coffee from 0.05 ppm to 0.2 parts per million (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 i n 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

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 ch romatography 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 f or milk and juices, and 0.01 ppm for all other substrates

.

3. Magnitude of residues. A tolerance for coffee already exists, but new formulations for use on coffee indicate that these result in a higher level of residues. Therefore, twelve additional trials were conducted to supplement those previously submitted to EPA

-- ten in Brazil, one in Columbia, and one in Costa Rica. Coffee plants were treated at the maximum permissible labeled rate , and samples were harvested at the minimum pre

- harvest interva l permitted by the label. Residues were measured as the combined residues of thiamethoxam and its metabolite, CGA

322704, expressed as thiamethoxam . In addition to trials measuring the residues on dry green beans, processing studies were conducted to gene rate instant coffee and roasted coffee beans. The maximum combined residue for green beans was found to be 0.1 ppm. Processing studies indicated that there was no concentration of residues in either instant coffee or dry roasted coffee. The limit of quan tification (LOQ) was 0.01 mg/kg for each molecule

.

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. Thiamethoxam is minimally irritating to the eye, non

- irritating to skin and is not a dermal sensitizer.

In an acute neurotoxicity study in rats (OPPTS 870.6200 a), the NOAEL was 100 mg/kg/day with a L OAEL of 500 mg/kg/day based on drooped palpebral closure, decrease in rectal temperature and locomotor activity and increase in forelimb grip strength (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 land ing 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 870.51 00 and 870.5265 ) , there was no evidence of gene mutation when tested up to 5000 μ 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 mutatio n when tested up to the solubility3

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 up to levels of toxicity in whole animals; however, no evidence of target cell cytoxicity was observed . 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

consum ption. The developmental LOAEL was 750 mg/kg/day based on decreased fetal body weight and an increased incidence of 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 developmental 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 bod y 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 (fe males) 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 / systemic LOAEL is 61.25 (males), not determined (females) mg/kg/day based on increased 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 of fspring 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 weig ht 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 kidney4

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 prol onged prothrombin times and decreased plasma albumin and A/G ratio (both sexes; decreased calcium levels and ovary weights and delayed maturation in the ovaries (female); decreased cholesterol and phospholipid levels, testis weights, spermatogenesis, and s permatic 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 o f 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 s tudy 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 were observed at any dose level. LOAEL was not achieved. May not have b een 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 NOA EL 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 a trophy 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, infla mmatory 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 th e 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 LO AEL 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, fo ci of cellular alteration in liver and chronic tubular lesions in kidney in females. No evidence of carcinogenicity.5

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 ma le 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 sli ght 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 t o moderate induction of cystolic glutathion S

- transfer activity. Treatment did not affect peroxisomal fatty acid β

- oxidation

.

6. Animal metabolism. The metabolism of thiamethoxam in rats and livestock animals is adequately understood. The residues of c oncern 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 s tudies 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)

se lected 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

- FCIDTM, version 2.16) from Exponent. All consumption data for these assessments was taken from the USDA’s Contin uing Survey of Food Intake by individuals (CSFII) with the 1994

- 96 consumption database and the Supplemental CSFII children’s survey (1998) consumption6

database. The Tier I acute assessments incorporated established or proposed tolerances (40CFR180.565) f or the combined residues of thiamethoxam (CGA293343) and its metabolite (CGA322704) in or on a variety of raw agricultural commodities including meat and milk; percent of crop treated values were conservatively estimated to be 100% for all uses in the acut e assessments. In the Tier III chronic assessments, field trial residue values were used 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 re sidues. Estimated percent crop treated (%CT) values were incorporated into the Tier III chronic assessments based upon economic, pest, and competitive pressures. Drinking water estimates were incorporated directly into the acute and chronic dietary expos ure 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 d ose 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 safe ty 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 w as expressed as a percent of the acute reference dose (%aRfD). At the 95th percentile, acute (food only) exposure to the U.S. population resulted in a MOE of 2,464 (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 1,259 (7.8% 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 certainty 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 factor 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 e xposure (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 only) exposure to the U.S. population resulted i n a MOE of 4,807 (2.1% 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 1,598 (6.3% of the cRfD of 0.012 mg/kg

bw/day). Since the Benchmark MOE for this assessment was 100 and since the EPA
ge nerally has no concern for exposures above the Benchmark MOE or below 100%7

of the cRfD, Syngenta 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 pro posed uses of thiamethoxam.

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

ii. Drinking water

. The Estimated Drinking Water Concentrations (EDWCs) of thiamethoxam were determined using Tier l screening models, SCI

- GRO W which estimates pesticide concentration in ground water and FIRST which estimates pesticide concentration in surface water for terrestrial uses; and the modified Tier I Rice Model and Provisional Cranberry Model which estimates pesticide concentration in tail water from rice paddies and cranberry bogs, respectively. EDWCs of thiamethoxam from the currently registered uses plus pending uses on cereal grains seed treatment were determined. For the proposed revised coffee import tolerance, imported coffee will be for human consumption only. Therefore, there will be no environmental exposure to ground water and/or surface water. The highest ground water EDWC resulting from SCI

- GROW modeling was 4.14 ppb (acute and chronic) based on the currently registere d use on turf. The highest surface water EDWCs resulted from the currently registered rice use. The modified Tier I Rice model provided an 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 the ground water EDWC, the surface water values were used for risk assessment purposes and will be considered protective for any ground water concentration concerns.

Acute Exposure from Drinking Water : The acute surface water EDWC of 147.72 ppb was input directly 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 dif ference between the aggregate (food + drinking water) exposures and the food exposures alone for each population subgroup. Acute drinking water exposure U.S. population resulted in a MOE of 7,058 (1.4% of the acute RfD of 0.35 mg/kg

bw/day). The most exp osed sub

- population was all infants (<1 year old) with a MOE of 1,559 (6.3% 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, Syngenta 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 ch ronic 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 MOE 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 1,3768

(7.3% of the chronic RfD of 0.012 mg/kg

- bw/day). Since the Benchmark MOE for this a ssessment 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 residues a rising from all current, pending, and proposed uses of thiamethoxam.

2. Non

- dietary exposure

. Residential exposure risk assessments were performed for thiamethoxam formulated as Meridian 0.33G, Thiamethoxam 0.22G, Thiamethoxam 0.40/Lambda

- cyhalothrin 0.1 6 ME Concentrate, Thiamethoxam 0.01/Lambda

- cyhalothrin 0.004 ME RTU, Optigard ZT, and Optigard Flex for turf, ornamental, and indoor crack and crevice uses. Meridian 25WG, Optigard ZT and Optigard Flex are labeled for professional use only and, therefore, no residential handler exposure assessments are required. There is no prohibition against residential handler application on the labels for the other products and therefore residential handler exposure risk assessments are required. The following endpoi nts were used: a 1.2 mg/kg/day NOAEL for adults (dermal and inhalation, all durations) from a two generation oral reproduction study in rats; a 60 mg/kg/day NOAEL for children 1

- 6 years (dermal, short

- term) from a 28

- day dermal study in rats; a 8.23 mg/kg/ day NOAEL for children 1

- 6 years (dermal, short

- term) (incidental oral, all durations) from a 90

- day oral tox study in dogs. Residential handler exposure risk from thiamethoxam was acceptable (MOE = 1,327) for adults treating residential turf with a hose end sprayer. Post

- application exposure risk for adults re

- entering thiamethoxam

- treated lawn turf grass was acceptable (MOE = 4,070). Post

- application exposure risks were acceptable for adults (MOE = 8,431) and youths (MOE = 5,480) re

- entering professi onally treated golf course turf. Post

application dermal plus non

- dietary oral exposure risk was acceptable for children

re - entering thiamethoxam

- treated lawn turf grass following (short

- term MOE = 1,341; intermediate

- term MOE = 2,031). Post

- application dermal exposure risk was acceptable for adults re

- entering indoor carpeted or hard floor areas following crack and crevice treatment with Optigard® ZT or Optigard® Flex (MOE = 862). Post

- application dermal plus non

- dietary oral exposure risk was acceptabl e for children re

- entering indoor carpeted or hard floor areas following crack and crevice treatment with Optigard® ZT or Optigard® Flex (short

- term MOE = 617, intermediate

- term MOE = 688). Since the MOEs for children (1

- 6 years), youths (13

- 19 years), an d adults (20+ years) were above the Benchmark MOE of 100, residential exposure risks for thiamethoxam 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 other9

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 sub stances 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 gener al 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 822 for adults (50+ years old), which exceeds the Benchmark MOE of 100. The intermediate

- term aggregate (food, drinking water, and residential) MOE was 822 for adults (50+ years old), which exceeds the Benchmark MOE of 100. The c hronic dietary exposure analysis (food plus water) showed that exposure from all current, pending, and proposed uses of thiamethoxam resulted in a MOE of 2,326 (4.3% 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 that 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 f rom all current, pending, and proposed uses of thiamethoxam would result in a MOE of 920 (10.7% of the aRfD of 0.35 mg/kg

bw/day) for the most sensitive population subgroup, infants <1 year old, which exceeds the Benchmark MOE of 100. For the short

- term a ggregate 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 575 for children (1

- 6 years), which exceeds the Benchmar k MOE of 100. The intermediate

- term aggregate (food, drinking water, and residential) MOE was 636 for children (1

- 6 years), which exceeds the Benchmark MOE of 100. The chronic aggregate dietary (food plus water) exposure analysis showed that exposure fro m all current, pending, and proposed uses of thiamethoxam would result in a MOE of 894 (11.2% 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 complete ness 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 aggregate10

exposure to residues arising from all current, pending, and propose d uses of thiamethoxam, including anticipated dietary exposure from food, water, and all other types of non

- occupational exposures

.
F. International Tolerances Codex MRLS have been established for t hiamethoxam on various crops

.