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

EPA Registration Division contact : Jennifer Urbanski ; (703) 3 47

- 0156

Syngenta Crop Protection, LLC

[ Petition numbe r 2E8011 ]

EPA has received a pesticide petition ( [ petition number 2E8011 ] ) from Syngenta Crop Protection, LLC

, 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

by establishing a 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 agricultural commodity tea at 20 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 n ot 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 thia methoxam 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, LLC

, 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 M S 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. A total of four studies (total of eight field trials) were carried out in Japan in 1998 and 2002. Thiamethoxam was applied once as a water

-2

dispersible granule formulation containing 10% thiamethoxam al one (year 1998 studies) or in combination with lufenuron (year 2002 studies). The application rate of thiamethoxam was 100 g a.i./ha, with a dilution rate of 2000 (1 L product/ha). These studies correspond to the Japanese Good Agricultural Practices (GAP ) and common agricultural practice, since the minimum dilution rate (2000 times) is the factor relevant for regulation and not the maximum rate of a.i./ha.

Samples of tea leaves were taken at a PHI of 7 days and additionally 14 and 21 days after the appli cation. Samples of crude processed tea leaves and tea infusion were analyzed for residues of thiamethoxam and metabolite CGA322704 using the Japanese analytical method for tea. Thiamethoxam and CGA322704 residues on crude processed tea leaves sampled fro m the supervised trials at a PHI of 7 days following a single foliar application of 100 g a.i./ha ranged from 2.29

– 8.64 mg/kg and 0.08

– 0.29 mg/kg, respectively. Residues in tea infusion were similar to those in leaves, ranging from 1.54

– 8.40 mg/kg

a nd 0.07

– 0.27 mg/kg, for thiamethoxam and CGA322704, respectively.

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 870.6200a), the NOAEL was 100
mg /kg/day with a LOAEL 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 resp iration, 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

aver age 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 μg/plate an d there was no evidence of cyto to xicity.

In a gene mutation study with Chinese hamster V79 cells at HGPRT l ocus (OPPTS 870.5300) there was no evidence of gene mutation when tested up to the solubility limit.

In a CHO cell cytogenetics study (OPPTS 870.53 75) 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 cyto to xicity was observed. A UDS assay (OPPTS 870.5550) was negative when tested up to precipitating concentrations.3

3. Reproductive and developmental toxicity. A prenatal developmental study in the rat (OPPTS 870.3700a) resu lted 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 decreas ed 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 uterine contents and 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 po st

- implantation loss and a slight increase in the incidence of a few skeletal anomalies/variations.

In a reproduction and fertility effects study in rats (OPPTS 870.3800) the Parental/ systemic NOAEL is 1.84 (males), 202.06 (females) mg/kg/day; the reprodu ctive 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 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 i s 17. 6 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 870.31 00) 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 h y pertrophy. At higher dose levels: decrease in body weight and body weight gain, necrosis o f individual hepatocytes, pigmentation of Kupffer cells, and lymphocytic infiltration of the liver in both sexes; slight hematologic effects and decreased absolute and relative kidney weights in males; and ovarian atrophy, decreased ovary and spleen weight s 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 decrease d 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 spermatic giant cells in testes (mal e s ).4

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 inflam matory cell infiltration in the liver and necrosis of single hepatocytes in females and hyaline 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 inflam matory 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 deter mined. No t reatment

- related observations were observed at any dose level.. Thiamethoxam m ay 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 c oncern.

5. Chronic toxicity. In a chronic toxicity study in dogs (OPPTS 870.4100)

, the NOAEL was 4.05 (male s ), 4.49 (female s ) mg/kg/day. The LOAEL was 21.0 (male s ), 24.6 (female s ) 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 s ), 3.68 (female s ) mg/kg/day. The LOAEL was 63.8 (male s ), 87.6 (female s ) 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 carcino genicity 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 i n 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, hepatocellular g lycogenesis /fatty change, hepatocellular necrosis, apoptosis and pigmentation were observed.

In a 28 day feeding study to assess replicative DNA synthesis in the male rat, the NOAEL was 711 mg/kg/day. The LOAEL was not established. Immunohistochemical
sta ining 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 DNA5

synthesizing hepatocytes in S

- phase. CGA

- 293343 did not stimulate hepatocyte ce ll 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 live r 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 cy to solic glutathio n e S

- transfer ase 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 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 ha s 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

w ell 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 Expo sure

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 3.15) from Exponent; consumption data was from the USDA NHANES “What We Eat in America” survey, 2003

- 2008. These assessments included all current and pending uses as well as a proposed new use on imported dried tea. The Tier I acute assessments incorporated established or proposed tolerances (40CFR180.565) for the combined residues of thiamethoxam (CGA293343) and its metabolite (CGA322704) in or on a variety of raw agricultural commodities including meat and milk; percent of crop treated values were conservatively estimated to be 100% for all uses in the acute assessments. The Tier III chronic assessments incorporated field trial residue values 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. Estimate d 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 exposure assessments u sing the highest estimated drinking water concentrations (EDWCs) for surface and ground water.6

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/k g

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
ap plied. 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 95th percentile, acute (food only) exposure to the U.S. population resulted in a MOE of 2,692 (3.7% 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 1,300 (7.6% 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 reas onable 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 al l 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 exposure (MOE), which was calculated by dividing the NOAEL by the exposure for each population subgroup. In addition, exposure was expressed as a percent of the chronic reference dose (%cRfD). Chronic (food only) exposure to the U.S. population resulted in a MOE of 6,798 (1.5% of the cRfD of 0.012 mg/kg

- bw/day). The most exposed s ub

- population was children (1

- 2 years old) with a MOE of 2,622 (3.8% of the cRfD 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 dietary (food only) exposure to residues arising from all current, pending, and proposed uses of thiamethoxam.

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

ii. Drinking water

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

- GROW which estimates pesticide concentration in ground water, Tier I FIRST or Tier II PRZM/E XAMS 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 currently registered uses determined. For the proposed tea import tolerance, imported tea will be for human consumption only. Therefore, there will be no environmental exposure to ground water and/or surface water. The high est ground water7

EDWC resulting from SCI

- GROW modeling was 4.14 ppb (acute and chronic) based on the currently registered use on turf. The highest surface water EDWCs resulted from the currently registered seed treatment on dry

- seeded rice. The modified Tier I Rice model provided an acute EDWC of 161.3 ppb and a chronic EDWC of 13.78 ppb (adjusted for a 0.95 Percent Cropped Area (PCA) factor). Since the surface water EDWCs exceed the ground water EDWC, the surface water values were used for risk assessme nt purposes and will be considered protective for any ground water concentration concerns.

Acute Exposure from Drinking Water : The acute surface water EDWC of 161.3 ppb was input directly into the DEEM

- FCIDTM software as “water, direct and indirect, al l 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 + drinking water) exposures and the food exposures alone for each population su bgroup. Acute drinking water exposure U.S. population resulted in a MOE of 5,586 (1.8% 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 1,840 (5.4% 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

wa ter exposure to residues arising from all current, pending, and proposed uses of thiamethoxam.

Chronic Exposure from Drinking Water : The chronic surface water EDWC of 13.78 ppb was input directly into the DEEM

- FCIDTM software as “water, direct and indirec t, all sources” to model the chronic drinking water exposures. Chronic drinking water exposure to the U.S. population resulted in a MOE of 4,159 (2.4% of the chronic RfD of 0.012 mg/kg

- bw/day). Chronic drinking water exposure to the most exposed sub

popu lation (infants, <1 year old) resulted in a MOE of 1,613 (6.2% 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 residues arising from all current, pending, and proposed uses of thiamethoxam.

2. Non

- dietary exposure

. Residential exposur e risk assessments were performed for use of thiamethoxam formulated as Meridian 0.33G, Thiamethoxam 0.22G, Meridian 25WG, Thiamethoxam 0.40/Lambda

- cyhalothrin 0.16 ME Concentrate, Thiamethoxam 0.01/Lambda

- cyhalothrin 0.004 ME RTU, Optigard ZT, Optigard Fl ex, Tandem, or Derby. Optigard ZT, Optigard Flex, Tandem, and Derby are labeled for professional use only; therefore no residential handler exposure assessments are required for these products. Homeowner application of Meridian 0.33G, Thiamethoxam 0.22G, Meridian 25WG, Thiamethoxam 0.40/Lambda

- cyhalothrin 0.16 ME Concentrate, or Thiamethoxam 0.01/Lambda

- cyhalothrin 0.004 ME RTU is allowed; therefore residential handler exposure assessments are required. The following endpoints 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 years8

(dermal, short

- term) from a 28

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

- 6 year s (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 = 732) for adults (19+ years) treating gardens and trees with a belly grinder. Post

- ap plication exposure risk for adult gardeners (19+ years) re

- entering thiamethoxam

treated gardens and trees was acceptable (MOE = 194). Post

- application exposure risk for youth gardeners (13

- 19 years) re

- entering thiamethoxam

- treated gardens and trees

was acceptable (MOE = 284). Post

- application exposure risk for youth golfers (6

- 12 years) re

- entering thiamethoxam

- treated golf courses was acceptable (MOE = 5,427). Post

- application dermal plus non

- dietary oral hand

- to

- mouth exposure risk was acceptable for children (1

- 6 years) re

- entering thiamethoxam

- treated residential turf grass (short

- term MOE = 640). Post

- application dermal plus non

- dietary oral hand

- to

- mouth exposure risk was acceptable for children (1

- 6 years) re

- entering thiamethoxam

- treated indoor hard or carpeted surfaces areas (short

- term MOE = 693). Since the MOEs for children (1

- 6 years), youths (6

- 12 years), youths (13

- 19 years), and adults (19+ years) were above the Benchmark MOE of 100, residential exposure risks for thiamethoxam do
not exc eed 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 Agen cy 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 t olerance 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 1,816 (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 fo od, water and residential MOEs were aggregated using the inverse MOE approach. The short

- term aggregate (food, drinking water, and residential) MOE was 192 for adults (50+ years old), which exceeds the Benchmark MOE of 100. The chronic dietary exposure a nalysis (food plus water) showed that exposure from all current, pending, and proposed uses of thiamethoxam resulted in a MOE of 2,580 (3.9% of the cRfD of 0.012 mg/kg

- bw/day) for the general U.S. population, which also exceeds the Benchmark MOE of 100. B ased 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 residues9

arising from all current, pending, and proposed us es 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 970 (10.2% 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 aggregate exposure analysi s 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 605 for children (1

- 6 years), which exceeds the Benchmark MOE of 100. The chroni c 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 1,248 (8.0% of the cRfD of 0.012 mg/kg

- bw/day) for the most sensitive population subgroup, in fants <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 a rea sonable 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, including anticipated dietary exposure from food, water, and all other types of non

- occupational
exposures.

F. International Tolerances

In 2011 the Codex Alimentarius Commission established Maximum Residue Limits (MRLs) for thiamethoxam in various agricultural commodities including artichokes, bananas, barley, berries, Brassica vegetab les (head), cacao beans, celery, citrus, coffee, fruiting vegetables, cucurbits, leafy vegetables, legumes, maize, oilseeds, papayas, pecans, peppers (chili, dried), pineapples, pome fruits, popcorn, pulses, root and tuber vegetables, stone fruits, sweet c orn, tea (green, black; fermented and dried), wheat, and various meat, milk, and egg commodities.