EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR 

PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER 

(7/1/2007) 

EPA Registration Division contact: Julie Chao, Insecticide-Rodenticide Branch 

Team 1; (703) 308-8735 

Syngenta Crop Protection, Inc., PO Box 18300, Greensboro, NC 27419

Petition Number 0F7707

 EPA has received a pesticide petition (petition number 0F7707) from Syngenta 

Crop Protection, Inc., PO Box 18300, Greensboro, NC 27419 proposing, pursuant to 

section 408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 

346a(d), to amend 40 CFR part 180.565 by establishing tolerances for residues of

thiamethoxam {3-[(2-chloro-5-thiazolyl)methyl]tetrahydro-5-methyl-N-nitro-4H1,3,5-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 alfalfa, forage

(0.05 ppm) and alfalfa, hay (0.12 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 alfalfa, forage and alfalfa, hay).
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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-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 NOAEL 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 

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 bone marrow micronucleus study (OPPTS 870.5395) was negative 

when tested up to 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 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 
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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 hypertrophy. 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 relative kidney 

weights in males; and ovarian 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. 
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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. 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 
5

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 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 the pending seed treatment use on peanuts and 

the proposed seed treatment use on alfalfa. Percent of crop treated values were 

conservatively estimated to be 100% for all registered 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 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 food 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 
6

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 2,466 (4.0% of the aRfD of 0.35 mg/kgbw/day). The most exposed sub-population was children (1-2 years old) with a 

MOE of 1,256 (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 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 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 9,538 (1.0% 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 4,016 

(2.5% 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 Estimated Drinking Water Concentrations (EDWCs) 

of thiamethoxam were determined using Tier l screening models, SCI-GROW which 

estimates pesticide concentration in ground water, FIRST which estimates pesticide 

concentration in surface water (for proposed alfalfa seed treatment use and pending 

peanut seed treatment use), and for aquatic uses, a modified Tier I Rice Model and 

Provisional Cranberry Model which estimates pesticide concentration in tail water 

from rice paddies and cranberry bogs, respectively. EDWCs of thiamethoxam from 

the currently registered uses plus the proposed seed treatment use on alfalfa and the 

pending seed treatment use on peanuts were determined. The highest ground water 

EDWC resulting from SCI-GROW modeling was 4.12 ppb (acute and chronic) 

based on the currently registered use on grapes. The highest surface water EDWCs 

resulted from the currently registered rice use. The modified Tier I Rice model 

provided a surface water acute EDWC of 147.72 ppb and a chronic EDWC of 12.62 

ppb (adjusted for a 0.87 Percent Cropped Area (PCA) factor). Since the surface 
7

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 (alone) 

exposures 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 1,596 (6.2% of the aRfD of 0.35 mg/kg/day). Since the benchmark MOE 

for this assessment was 100 and since EPA generally has no concern for exposures 

below 100% of the acute RfD, Syngenta believes that there is a reasonable certainty 

that no harm will result from acute drinking water exposure to residues arising 

from the current and proposed uses for 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 

(7.3% of the chronic RfD of 0.012 mg/kg-bw/day). Since the Benchmark MOE for 

this assessment was 100 and since EPA generally has no concern for exposures 

below 100% of the chronic RfD, Syngenta believes that there is a reasonable 

certainty that no harm will result from chronic drinking water exposure to residues 

arising from the current and proposed use for thiamethoxam.

 2. Non-dietary exposure. A residential exposure and risk assessment was 

performed for thiamethoxam using the endpoints and uncertainty factors 

established by the EPA. Residential exposure and risk assessments were performed 

for thiamethoxam uses on turf and ornamentals (Meridian® 25WG) and for 

thiamethoxam indoor crack and crevice uses (Optigard® ZT). These product labels 

indicate that thiamethoxam is to be applied by commercial applicators only; 

therefore residential assessments were limited to post-application exposure risks for 

adults and children. The following endpoints were used for these residential risk 

assessments: NOAEL = 1.2 mg/kg/day (for adults, from a 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). Post application dermal 

exposure risks from thiamethoxam are acceptable (MOE = 4,070) for adults reentering lawn turf grass following treatment with Meridian® 25WG. Post 

application dermal plus non-dietary oral exposure risks from thiamethoxam are 

also acceptable (aggregate MOE = 1,339) for children re-entering lawn turf grass 
8

following treatment with Meridian® 25WG. Post application dermal exposure risks 

from thiamethoxam are acceptable (MOE = 900) for adults re-entering indoor 

carpeted or hard floor areas following crack and crevice treatment with Optigard® 

ZT. Post application dermal plus non-dietary oral exposure risks from 

thiamethoxam are also acceptable (short-term aggregate MOE = 1,260, 

intermediate-term aggregate MOE = 1,404) for children re-entering indoor carpeted 

or hard floor areas following crack and crevice treatment with Optigard® ZT. 

Since the children (1-6 years) and adult (20-49 years) MOEs are above the 

Benchmark MOE of 100 the residential exposure risks do not exceed the EPA’s level 

of concern.

D. Cumulative 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, pending and proposed thiamethoxam 

tolerances would result in a MOE of 1,827 (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. The 

chronic dietary exposure analysis (food plus water) showed that exposure from all 

registered and proposed thiamethoxam tolerances resulted in a MOE of 3,063 (3.3% 

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 867 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 943 (10.4% of the aRfD of 0.35 mg/kg-bw/day) for the 
9

most sensitive population subgroup, infants <1 year old, which exceeds the 

Benchmark MOE of 100. The chronic aggregate dietary (food plus water) exposure 

analysis showed that exposure from all established and proposed thiamethoxam 

uses would result in a MOE of 1,157 (8.6% of the chronic RfD of 0.012 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 1,214 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 and proposed thiamethoxam tolerances, 

including anticipated dietary exposure from food, water, and all other types of nonoccupational 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, 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.