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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) 308-8735

INSTRUCTIONS: Please utilize this outline in preparing the pesticide petition. In 

cases where the outline element does not apply, please insert “NA-Remove” and 

maintain the outline. Please do not change the margins, font, or format in your 

pesticide petition. Simply replace the instructions that appear in green, i.e., “[insert 

company name],” with the information specific to your action.

TEMPLATE:

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 requesting, 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-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 on the raw 

agricultural 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 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.
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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. 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 interval permitted by the label. Residues 

were measured as the combined residues of thiamethoxam and its metabolite, CGA322704, expressed as thiamethoxam. In addition to trials measuring the residues on 

dry green beans, processing studies were conducted to generate 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 quantification (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 870.6200a), 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 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 μg/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 
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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 

consumption. 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 

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 /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 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 
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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 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 (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 of 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 were observed 

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.
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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 male 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 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 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 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-FCIDTM, 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 
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database. 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. 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 residues. 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 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 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 2,464 (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 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 

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/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% 
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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 cancer endpoint 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 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 registered 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 difference 

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/kgbw/day). The most exposed 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 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 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 1,376 
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(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 residues arising 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 0.16 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 

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 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 professionally treated golf course turf. Postapplication 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 acceptable 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), and 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 other 
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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/kgbw/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 shortterm 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 chronic 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 from all current, pending, and proposed uses of 

thiamethoxam would result in a MOE of 920 (10.7% of the aRfD of 0.35 mg/kgbw/day) for the 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 575 for children (1-6 years), which exceeds the Benchmark 

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 from all current, pending, and proposed uses of 

thiamethoxam would result in a MOE of 894 (11.2% of the cRfD of 0.012 mg/kgbw/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 a 

reasonable certainty that no harm will result to infants and children from aggregate 
10

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

Codex MRLS have been established for thiamethoxam on various crops.