i

EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR 

PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER 

EPA Registration Division contact: Thomas C. Harris 703-308-9423 

Syngenta Crop Protection, LLC

PP # 3F8184

 EPA has received a pesticide petition PP # 3F8184 from Syngenta Crop 

Protection, LLC, 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

1. by establishing a tolerance for residues of 

 abamectin in or on the raw agricultural commodity corn, field, sweet and 

pop at 0.01 ppm; soybean at 0.01 ppm; corn, field and pop, forage at 0.2 ppm; 

corn, field and pop, grain at 0.01 ppm; corn, field and pop, stover at 0.6 ppm; 

corn, sweet, forage at 0.2 ppm; corn, sweet, kernel plus cob with husk removed 

at 0.01 ppm; corn, sweet, stover at 0.5 ppm; soybean forage at 0.3 ppm; 

soybean, hay at 1 ppm; and soybean, seed at 0.01 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 metabolism of abamectin in plants is adequately 

understood and the residues of concern include the parent insecticide abamectin 

(also referred to as avermectin B1 which is a mixture of a minimum of 80% 

avermectin B1a and a maximum of 20% avermectin B1b) and the delta 8,9-isomer 

of the B1a and of the B1b components of the parent insecticide. 

 2. Analytical method. The analytical methods involve homogenization,

filtration, partition, and cleanup with analysis by high performance liquid 

chromatography (HPLC)-fluorescence detection. The methods are sufficiently 

sensitive to detect residues at or above the tolerances proposed. All methods 

have undergone independent laboratory validation. 

A. 3. Magnitude of residues.
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Results of MOR Studies with the Abamectin on Soybean 

Twenty crop-field trials were successfully conducted in the United States to 

support the registration of abamectin on soybeans resulting from a combination 

of a seed treatment application with Abamectin 500 FS (A14006B), a flowable 

concentrate for seed treatment (FS) formulation, and two foliar applications of 

Abamectin SC (A15368D), a suspension concentrate (SC) formulation. The 

seed treatment application was made at a nominal rate of 0.15 mg ai/seed, and 

the two foliar applications were made at the maximum proposed label use rate of 

0.019 lb ai/A/application. At each site, one treated plot was established for 

forage and hay sample collection with foliar applications made nominally 14 ± 1 

and 7 ± 1 days before forage harvest and cutting of hay. At each site, another 

treated plot was established for seed sample collection with foliar applications 

made nominally 35 ± 1 and 28 ± 1 days before seed harvest. The foliar 

applications included an adjuvant [non-ionic surfactant (NIS) or crop oil 

concentrate (COC)] in the spray solutions as specified for each site following the 

manufacturer’s recommended label rate. At two sites, another treated plot was 

established that was treated in the same manner and timing as described above 

for seed harvest, but at a 5× rate (0.095 lb ai/A/application) to produce seed for 

processing into aspirated grain fractions (AGF), meal, hulls, and refinedbleached-deodorized (RBD) oil. 

Forage samples were collected and hay samples cut 7 ± 1 days after the last 

application (DALA) during the blooming period. The hay samples were allowed 

to dry to ~80-90% dry matter prior to collection. Seed samples were collected 28 

± 1 DALA at normal crop maturity. At two trial sites, additional RAC samples 

were collected (1, 3, 10, and 14 DALA for forage and hay; 20-21, 23-24, 31-32, 

and 34-35 DALA for seed) to generate residue decline data. 

Residues of abamectin, a mixture containing avermectin B1a (parent B1a + 8,9-Z 

B1a) and avermectin B1b, were determined in or on all of the collected soybean 

forage, hay, seed, AGF, meal, hulls, and RBD oil samples. The fortification 

levels were 0.002 (LOQ), 0.0336, and 3.36 ppm for B1a, and 0.002 (LOQ) and 

0.20 ppm for B1b and 8,9-Z isomer. 

 

Residues above the LOQ were not found in any of the non-treated control 

samples of any soybean matrix except for two hay samples with residues just 

above the LOQ (0.00246 ppm from Trial -15 and 0.00202 ppm from Trial -20) 

and one AGF sample (0.00320 ppm from Trial -20). 

Results of MOR Studies with the Abamectin in Field Corn and Popcorn

Twenty crop-field trials on field corn and three crop-field trials on popcorn were 

successfully conducted in the United States to support the registration of 

abamectin on field corn and popcorn resulting from a combination of a seed 
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treatment application with Abamectin 500 FS (A14006B), a flowable concentrate 

for seed treatment (FS) formulation, and two foliar applications of Abamectin SC 

(A15368D), a suspension concentrate (SC) formulation. The seed treatment 

application was made at a nominal rate of 0.25 mg ai/seed, and the two foliar 

applications were made at the maximum proposed label use rate of 0.019 lb 

ai/A/application. At each field corn site, one treated plot was established for 

forage sample collection with foliar applications made nominally 14 ± 1 and 7 ± 1 

days before field corn forage harvest. At each field corn and each popcorn site, 

another treated plot was established for grain and stover sample collection with 

foliar applications made nominally 28 ± 1 and 21 ± 1 days before grain/stover 

harvest. The foliar applications included an adjuvant [non-ionic surfactant (NIS) 

or crop oil concentrate (COC)] in the spray solutions as specified for each site 

following the manufacturer’s recommended label rate. At two field corn sites, 

another treated plot was established that was treated in the same manner and 

timing as described above for grain harvest, but at a 5× rate (0.095 lb 

ai/A/application) to produce grain for generation of aspirated grain fractions 

(AGF) and for processing into grits, meal, flour, and refined-bleached-deodorized 

(RBD) oil from dry milling, and starch and RBD oil from wet milling. 

Field corn forage (with ears) samples were collected nominally 7 ± 1 days after 

the last application (DALA) at the late dough to early dent stage. Field corn and 

popcorn grain and stover samples were collected nominally 21 ± 1 DALA at 

normal crop maturity. At two field corn trial sites, additional RAC samples were 

collected (1, 3, 10, and 14 DALA for forage; 14, 17-18, 24-25, and 27-28 DALA 

for grain and stover) to generate residue decline data. 

Residues of abamectin, a mixture containing avermectin B1a (parent B1a + 8,9-Z 

B1a) and avermectin B1b, were determined in or on all of the collected field corn 

forage, grain, stover, AGF, grits, meal, flour, RBD oil (dry milling and wet milling) 

and starch samples and all of the collected popcorn grain and stover samples. 

The abamectin method of analysis was verified on field corn forage, grain, stover, 

meal, flour, grits, starch, and refined oil (dry milling) prior to field sample analysis. 

The fortification levels were 0.002 (LOQ), 0.0336, and 3.36 ppm for B1a, and 

0.002 (LOQ) and 0.20 ppm for B1b and 8,9-Z isomer. The overall mean 

recoveries for all analytes in all matrices ranged 71-111% and the relative 

standard deviations (RSD) ranged 5.8-22% (all ≤20% except for B1b in grain). 

Concurrent procedural recovery samples were analyzed in conjunction with each 

analytical set for quality control purposes. The overall mean recoveries for all 

analytes in all matrices ranged 61-112% (within 60-120%) and the relative 

standard deviations (RSD) ranged 5.3-28% (all ≤20% except for B1a in popcorn 

stover). 

 
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Residues above the LOQ were not found in any of the non-treated control 

samples of any field corn or popcorn matrix except for one forage sample with 

avermectin B1a residues of 0.00409 ppm. When this sample was reanalyzed, 

residues were ND; therefore, the initial residues in the control sample appear to 

be laboratory contamination. 

 

Results of MOR Studies with the Abamectin in Sweet Corn

Twelve crop-field trials were successfully conducted in the United States to 

support the registration of abamectin on sweet corn resulting from a combination 

of a seed treatment application with Abamectin 500 FS (A14006B), a flowable 

concentrate for seed treatment (FS) formulation, and two foliar applications of 

Abamectin SC (A15368D), a suspension concentrate (SC) formulation. The 

seed treatment application was made at a nominal rate of 0.25 mg ai/seed, and 

the two foliar applications were made at the maximum proposed label use rate of 

0.019 lb ai/A/application. The two foliar applications were made 14 ± 1 and 7 ± 1 

days before fresh market harvest of forage and kernel + cob with husk removed 

(K+CWHR) and cutting of the stover samples. The foliar applications included an 

adjuvant [non-ionic surfactant (NIS) or crop oil concentrate (COC)] in the spray 

solutions as specified for each site following the manufacturer’s recommended 

label rate. 

Forage and K+CWHR samples were harvested 7 ± 1 days after the last 

application (DALA). The stover samples were cut 7 DALA and allowed to dry to 

~80-85% dry matter. At two trial sites, additional RAC samples were collected (1, 

3, 10, and 14 DALA) to generate residue decline data. 

Residues of abamectin, a mixture containing avermectin B1a (parent B1a + 8,9-Z 

B1a) and avermectin B1b, were determined in or on all of the collected sweet 

corn forage, K+CWHR, and stover samples. The abamectin method of analysis 

was verified on sweet corn forage, K+CWHR, and stover prior to field sample 

analysis. The fortification levels were 0.002 (LOQ), 0.0336, and 3.36 ppm for 

B1a, and 0.002 (LOQ) and 0.20 ppm for B1b and 8,9-Z isomer. The mean 

recoveries for all analytes in all matrices ranged 78-100% and the relative 

standard deviations (RSD) ranged 10-23% (all <20% except for 8,9-Z in 

K+CWHR and stover). 

Concurrent procedural recovery samples were analyzed in conjunction with each 

analytical set for quality control purposes. The mean recoveries for all analytes 

in all matrices ranged 72-100% (within 70-120%), and the relative standard 

deviations (RSD) ranged 10-18% (all <20%). 

 

Residues above the LOQ were not found in any of the non-treated control 

samples of any sweet corn matrix. 
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B. Toxicological Profile

 1. Acute toxicity. The database includes the following studies with 

Syngenta’s technical abamectin products: 

Abamectin Technical: 

i. A rat acute oral study with an LD50 of 13.6 mg/kg. 

ii. A rat acute oral study with an LD50 of 214-232 mg/kg. 

iii. A rabbit acute dermal study with an LD50 of 2000 mg/kg. 

iv. A rat acute inhalation study with an LC50 of 0.21 mg/L (nose only). 

v. A primary eye irritation study in rabbits which showed no irritation. 

vi. A primary skin irritation study in rabbits which showed slight irritation. 

vii. A dermal sensitization study (Buehler) in guinea pigs which was negative. 

Abamectin Technical II 

i. A rat acute oral study with an LD50 of 372.5 mg/kg 

ii. A rat acute dermal study with an LD50 of >200 mg/kg but <2000 mg/kg 

ii. A rat acute inhalation study with an LC50 of >0.0518 mg/L (nose only) 

v. A primary eye irritation study in rabbits which showed no irritation. 

vi. A primary skin irritation study in rabbits which showed slight irritation. 

vii. A dermal sensitization study (Buehler) in guinea pigs with Abamectin 

Technical supports the registration of this technical. 

 2. Genotoxicty. The Ames assays conducted with and without metabolic 

activation were both negative. The V–79 mammalian cell mutagenesis assays 

conducted with and without metabolic activation did not produce mutations. In an 

alkaline elution/rat hepatocyte assay, abamectin was found to induce single 

strand DNA breaks without significant toxicity in rat hepatocytes treated in vitro at 

doses greater than 0.2 millimole per liter (mM). This in vitro dose of 0.2 mM is 

biologically unobtainable in vivo, due to the toxicity of the compound. However, at 

these potentially lethal doses, in vivo treatment did not induce DNA single strand 

breaks in hepatocytes. In the mouse bone marrow assay, abamectin was not 

found to induce chromosomal damage. There are also, many studies and a great 

deal of clinical and follow-up experience with regard to ivermectin, a closely 

similar human and animal drug.

 3. Reproductive and developmental toxicity. In a 2-generation study in rats 

the NOAEL was established at 0.12 mg/kg/day in pups based upon retinal folds, 

decreased body weight (bwt), and mortality. The NOAELs for systemic and 

reproductive toxicity were 0.4 mg/kg/day. In the 1-generation reproduction study 

in rats with the delta 8,9-isomer, the NOAEL was 0.4 mg/kg/day and the lowest 

observed adverse effect level (LOAEL) was greater than 0.4 mg/kg/day highest 

dose tested (HDT). In an oral developmental toxicity study in rabbits the maternal 
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NOAEL was 1.0 mg/kg/day based upon decreased body weights and tremors. 

The fetal NOAEL was 1.0 mg/kg/day based upon clubbed feet. In an oral 

developmental toxicity study in rats the maternal and fetal NOAEL was 1.6 

mg/kg/day, the HDT. In an oral developmental toxicity study the maternal NOAEL 

in CF-1 mice that expressed P-glycoprotein was greater than 1.5 mg/kg/day, the 

highest and only dose tested. No cleft palates were observed in fetuses that 

expressed normal levels of P-glycoprotein, but fetuses with low or no levels of Pglycoprotein had increased incidence of cleft palates. In a developmental 

neurotoxicity study in rats the maternal NOAEL was 0.4 mg/kg/day, the HDT, and 

the offspring NOAEL was 0.12 mg/kg/day with an offspring LOAEL of 0.2 

mg/kg/day based on slight pup body weight loss. In a second developmental 

neurotoxicity study in rats the maternal NOAEL was 0.4 mg/kg/day, the HDT, and 

the offspring NOAEL was 0.2 mg/kg/day with an offspring LOAEL of 0.4 

mg/kg/day based on decreased body weight in both sexes. There was no 

evidence of neurotoxicity in the offspring.

 4. Subchronic toxicity. Subchronic toxicity studies included the following: 

i. A rat 14–week oral toxicity study with a NOAEL of 0.4 mg/kg/day, the HDT. 

ii. A dog 12–week feeding study with a NOAEL of 0.5 mg/kg/day based upon 

mydriasis. 

iii. A dog 18–week oral study with a NOAEL of 0.25 mg/kg/day based upon 

mortality. 

 5. Chronic toxicity. A rat 53–week carcinogenicity feeding study was 

negative for carcinogenicity, with a NOAEL of 1.5 mg/kg/day based upon 

tremors. A CD–1 mouse 94–week carcinogenicity feeding study was negative for 

carcinogenicity, with a NOAEL of 4 mg/kg/day based upon decreased body 

weights. A dog 53–week chronic feeding study resulted in a NOAEL of 0.25 

mg/kg/day based upon mydriasis.

 6. Animal metabolism. Rats were given oral doses of 0.14 or 1.4 mg/kg 

bwt/day of abamectin or 1.4 mg/kg bwt/day of the delta 8,9 isomer. Over 7–days, 

the percentages excreted in urine were 0.3–1% of the administered dose of 

abamectin and 0.4% of the dose of the isomer. The animals eliminated 69–82% 

of the dose of abamectin and 94% of the dose of isomer in feces. In rats, goats, 

and cattle, unchanged parent compound accounted for up to 50% of the total 

radioactive residues in tissues. The 24-hydroxymethyl derivative of abamectin 

was found in rats, goats, and cattle treated with the compound and in rats treated 

with the delta 8,9 isomer, and the 3’’-O-demethyl derivative was found in rats and 

cattle administered abamectin and in rats administered the isomer.

 7. Metabolite toxicology. There are no metabolites of concern based on a 

differential metabolism between plants and animals. The potential hazard of the 

24-hydroxymethyl or the 3’’-O-demethyl animal metabolites was evaluated in 

toxicology studies with abamectin photolytic break-down product, the delta 8,9-

isomer. 
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 8. Endocrine disruption. There is no evidence that abamectin is an 

endocrine disrupter. Evaluation of the rat multigenerational study demonstrated 

no effect on the time to mating or on the mating and fertility indices, suggesting 

no effects on the estrous cycle, on mating behavior, or on male or female fertility 

at doses up to 0.4 mg/kg/day, the HDT. Furthermore, the range finding study 

demonstrated no adverse effect on female fertility at doses up to 1.5 mg/kg/day, 

the HDT. Similarly, chronic and subchronic toxicity studies in mice, rats, and 

dogs did not demonstrate any evidence of toxicity to the male or female 

reproductive tract, or to the thyroid or pituitary (based upon organ weights and 

gross and histopathologic examination). In the developmental studies, the pattern 

of toxicity observed does not seem suggestive of any endocrine effect. Finally, 

experience with ivermectin in breeding animals, including sperm evaluations in 

multiple species, shows no adverse effects suggestive of endocrine disruption. 

The EPA notified registrants of the EPA’s first group of specified active 

ingredients and manufacturers of the EPA’s first group of specified inert 

ingredients that the Agency was initiating the Endocrine Disruptor Screening 

Program for these compounds. In 2010 the EPA issued Data-Call In’s the 

endocrine assays required for specified active ingredients including abamectin. 

The Abamectin EDSP Consortium is generating the required assays 

C. Aggregate Exposure

 1. Dietary exposure. Tier III/IV acute, short-term, and chronic aggregate 

exposure evaluations were made for abamectin using the Dietary Exposure 

Evaluation Model software with the Food Commodity Intake Database (DEEMFCIDTM , version 3.14), which incorporates food consumption data from the 

National Health and Nutrition Examination Survey/“What We Eat in America” 

(NHANES/WWEIA) dietary survey conducted in 2003-2008. These assessments 

included all current foliar, food handling establishment (FHE), and residential 

uses for abamectin, pending uses on cotton and strawberries, and a proposed 

new IR-4 use on caneberries (Crop Group 13-07A). For these exposure 

assessments, residue data were taken from field trial residue studies in which 

abamectin was applied at the maximum intended use rate and samples were 

harvested at the minimum pre-harvest interval (PHI) to obtain maximum residue 

values. Drinking water estimates were incorporated directly into the dietary 

exposure assessment using the higher of the estimated drinking water 

concentrations (EDWCs) for surface and ground water. Percent crop treated 

values were estimated based upon economic, pest, and competitive pressures. 

Residue values for milk and livestock commodities were obtained from the EPA’s 

July 18, 2011 abamectin dietary risk assessment (D380796). 

 i. Food. Acute Exposure. The abamectin acute dietary (food only) risk 

assessment was performed for all population subgroups with an acute reference 

dose of 0.005 mg/kg-bw/day based on a 12-week dose-range finding study in 
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dogs with a No Observed Adverse Effect Level (NOAEL) of 0.5 mg/kg-bw/day 

and an uncertainty factor of 100X. The 100-fold safety factor includes intra- and 

interspecies variations and no additional FQPA safety factors were included in 

these acute assessments. For the purpose of the aggregate risk assessment, 

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 also expressed as a percent of the acute 

reference dose (%aRfD). Acute (food only) exposure to the U.S. population 

resulted in a MOE of 719 (13.9% of the acute RfD of 0.005 mg/kg-bw/day). The 

most sensitive sub-population was children (1-2 years old) with a MOE of 376 

(26.6% of the aRfD). Since the Benchmark MOE for this assessment was 100 

and since the EPA generally has no concern for exposures above the benchmark 

or below 100% of the reference dose, Syngenta believes that there is a 

reasonable certainty that no harm will result from acute food exposure to 

residues arising from all current, pending, and proposed uses for abamectin. 

Chronic Exposure. The abamectin chronic dietary (food only) risk assessment 

was performed for all population subgroups with a chronic reference dose of 

0.0004 mg/kg-bw/day based on combined data from three reproduction studies 

and two developmental neurotoxicity studies with a No Observed Adverse Effect 

Level (NOAEL) of 0.12 mg/kg-bw/day and an uncertainty factor of 300X. The 

300-fold safety factor includes intra- and interspecies variations (100X) and the 

additional FQPA safety factors of 3X for the steepness of the dose-response 

curve and the severity of effects. For the purpose of the aggregate risk 

assessment, 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 also expressed as a percent of 

the chronic reference dose (%RfD). Chronic (food only) exposure to the U.S. 

population resulted in a MOE of 2,936 (10.2% of the chronic RfD of 0.0004 

mg/kg-bw/day). The most sensitive sub-population was children (1-2 years old) 

with a MOE of 669 (44.8% of the chronic RfD). Since the Benchmark MOE for 

this assessment was 300 and since the EPA generally has no concern for 

exposures above the benchmark or below 100% of the reference dose, Syngenta 

believes that there is a reasonable certainty that no harm will result from chronic 

food exposure to residues arising from all current, pending, and proposed uses 

for abamectin. 

 ii. Drinking water. The Estimated Drinking Water Concentrations (EDWCs) 

of abamectin were determined using Tier 1SCI-GROW which estimates pesticide 

concentration in ground water and Tier 2 PRZM/EXAMS which estimates 

pesticide concentration in surface water. EDWCs of abamectin from the 

currently registered and pending uses as well as a proposed use on caneberries 

were determined using EPA’s model inputs. Based on the SCI-GROW modeling, 

the highest groundwater EDWC for abamectin is 0.00188 ppb (acute and 

chronic) based on the currently registered/pending use on strawberries. Based 

on the PRZM/EXAMS modeling, the currently registered use on dry beans 
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provided the highest surface water EDWCs of 2.35 ppb for acute and 1.39 ppb 

for chronic. 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 exposure concerns. 

Acute Exposure from Drinking Water. The acute surface water EDWC of 2.35 

ppb was incorporated directly into the DEEM software as “water, direct and 

indirect, all sources” to model the acute drinking water exposures by taking the 

difference between the aggregate (food + drinking water) exposures and the food 

(alone) exposures for each population subgroup at the 99.9%-ile of exposures. 

Acute drinking water exposure to the U.S. population resulted in a MOE of 4,808 

(2.1% of the acute RfD of 0.005 mg/kg-bw/day). The most exposed subpopulation was all infants (<1 year old) with a MOE of 3,106 (3.2% of the aRfD of 

0.005 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 or 

below 100% of the reference dose, 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 for abamectin. 

Chronic Exposure from Drinking Water. The chronic surface water EDWC of 

1.271 ppb was input directly into the DEEM 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 4,123 (7.3% 

of the chronic RfD of 0.0004 mg/kg-bw/day). Chronic drinking water exposure to 

the most exposed sub-population (infants, <1 year old) resulted in a MOE of 

1,599 (18.8% of the chronic RfD of 0.0004 mg/kg-bw/day). Since the Benchmark 

MOE for this assessment was 300 and since the EPA generally has no concern 

for exposures above the benchmark or below 100% of the reference dose, 

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 for abamectin. 

 2. Non-dietary exposure. Residential exposure risk assessments were 

performed for use of abamectin formulated as Varsity® Fire Ant Bait and 

Optigard® Fire Ant Bait for residential turf. Residential adult handler/applicator 

assessments were performed for activities including push spreader, belly grinder, 

spoon, cup, hand dispersal, and shaker can. Residential post-application 

exposure scenarios assessed included adult and child high contact dermal, adult 

and youth mower, adult and youth golfer, and child hand-to-mouth, object-tomouth, soil ingestion, and ingestion of granules. The most-exposed adult (19+ 

years) handler/applicator scenario was for belly-grinder applications, with a shortterm MOE of 899,348 (Benchmark = 300). The most-exposed youth (11-16 

years) post-application scenario was for the youth golfer, with a short-term MOE 

of 15,753,170 (Benchmark = 300). The most-exposed youth (6-11 years) postapplication scenario was for the youth golfer, with a short-term MOE of 

13,418,308 (Benchmark = 300). The most-exposed children’s (1-6 years) post-
10

application scenario was via hand-to-mouth and dermal exposures resulting from 

play activities on treated turf, with a combined short-term MOE of 343,564 

(Benchmark = 300). Incidental oral ingestion of granules by children had a shortterm MOE of 48,017 (Benchmark = 300; granule ingestion is not aggregated with 

other exposure scenarios). 

D. Cumulative Effects

Cumulative Exposure to Substances with a Common Mechanism of 

Toxicity. Section 408(b)(2)(D)(v) 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”. If, in the 

future, EPA obtains new data suggesting that abamectin shares a common 

mechanism of toxicity with other chemical substances, the Agency will revisit the 

need for a cumulative risk assessment. For the purposes of this filing, Syngenta 

has not assumed that abamectin has a common mechanism of toxicity with other 

substances

E. Safety Determination

 1. U.S. population. The acute dietary exposure analysis (food plus drinking 

water) showed that exposure from all current, pending, and proposed abamectin 

crop uses result in a MOE of 625 (16.0% of the aRfD, Benchmark MOE = 100) 

for the general U.S. population. The short-term exposure analysis (food plus 

drinking water plus residential) showed that exposure from all current, pending, 

and proposed abamectin uses result in a MOE of 1,711 (Benchmark MOE = 300) 

for the general U.S. population. The chronic dietary exposure analysis (food plus 

drinking water) showed that exposure from all current, pending, and proposed 

abamectin crop uses result in a MOE of 1,715 (17.5% of the chronic RfD, 

Benchmark MOE = 300) for the general U.S. population. Based on the 

completeness and reliability of the toxicity data supporting these uses, Syngenta 

believes that there is a reasonable certainty that no harm will result to the general 

U.S. population from aggregate exposure to residues arising from all current, 

pending, and proposed abamectin uses, including anticipated dietary exposure 

from food, water, and all other types of non-occupational residential exposures. 

 2. Infants and children. The acute dietary exposure analysis (food plus 

drinking water) showed that exposure from all current, pending, and proposed 

abamectin uses results in a MOE of 342 (29.2% of the aRfD) for children 1-2 

years old (the most sensitive population subgroup). For the short-term aggregate 

assessments, children 1-2 years old had an aggregate MOE of 542 (Benchmark 

MOE = 300) for all current, pending, and proposed abamectin uses. The chronic 

dietary exposure analysis (food plus drinking water) showed that exposure from 

all current, pending, and proposed abamectin uses result in a MOE of 542 

(55.3% of the cRfD) for children 1-2 years old (the most sensitive population 
11

subgroup). Based on the completeness and reliability of the toxicity data 

supporting these uses, Syngenta believes that there is a reasonable certainty 

that no harm will result to infants and children from aggregate exposure to 

residues arising from all current, pending, and proposed abamectin uses, 

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

non-occupational residential exposures. 

F. International Tolerances

Codex has established Maximum Residue Levels (MRLs) for abamectin on a 

number of commodities including almonds, apples, citrus, cotton, cucumbers, 

hops, lettuce, meat, milk, and related commodities (beef and goat), melons, 

pears, peppers, potatoes, squash, strawberries, tomatoes, and walnuts. In 

addition, country or region-specific international MRLs for abamectin have been 

established or proposed in a number of countries including: Argentina, Australia, 

Brazil, Canada, Chile, China, France, Germany, Greece, Hungary, Italy, Japan, 

Korea, Mexico, Russia, South Africa, Spain, Switzerland, Taiwan, Turkey, United 

Kingdom, and the United States.