EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR

PESTICIDE PETITION 

EPA Registration Division contact: Sidney Jackson (703) 305-7610

Interregional Research Project Number 4 

PP# 1E7863

EPA has received a pesticide petition (PP) 1E7863 from Interregional Research 

Project Number 4 (IR-4), IR-4 Project Headquarters, Rutgers, The State

University of New Jersey, 500 College Road East, Suite 201 W, Princeton, NJ 08540

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 180.603 by establishing a tolerance 

for residues of dinotefuran, (RS)-1-methyl-2-nitro-3-(tetrahydro-3-furylmethyl)guanidine 

and its major metabolites DN, 1-methyl-3-(tetrahydro-3-furylmethyl)guanidine, and UF, 

1-methyl-3-(tetrahydro-3-furylmethyl)urea in or on the raw agricultural commodities

berry, low growing, except strawberry, subgroup 13-07H at 0.2 parts per million (ppm); 

watercress at 5.0 ppm; onion, green, subgroup 3-07B at 6.0 ppm; onion, bulb, subgroup 

3-07A at 0.07 ppm; peach at 0.9 ppm; vegetable, tuberous and corn, subgroup 1C at 0.05 

ppm; fruit, small, vine climbing, except fuzzy kiwifruit, subgroup 13-07F at 0.9 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 support 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 dinotefuran in plants (rice, apple, potato, oilseed rape 

and lettuce) were similar to those described for animals, with certain extensions of the 

pathway in plants. Parent compound, dinotefuran, and two metabolites; 1-methyl-3-

(tetrahydro-3-furymethyl) guanidine (DN) and 1-methyl-3-(tetrahydro-3-furymethyl)-

urea (UF) were major metabolites in all crops. The metabolism of dinotefuran in plants 

and animals is understood for the purposes of the proposed tolerances. Parent 

dinotefuran and the metabolites, 1-methyl-3-(tetrahydro-3-furymethyl)guanidine (DN) 

and 1-methyl-3-(tetrahydro-3-furymethyl)-urea (UF) are the residues of concern for 

tolerance setting purposes.

2. Analytical method.

Mitsui Chemicals Agro, Inc., has submitted practical analytical methodology for 

detecting and measuring levels of dinotefuran and its metabolites, UF and DN, in or on 

raw agricultural commodities. The high-performance liquid chromatography (HPLC)

method was validated for determination of dinotefuran, DN and UF in or on tomatoes and 

peppers, cucurbits, brassica, grapes, potatoes, and lettuce for raw agricultural commodity
2

matrices and in or on tomato paste and puree, grape juice and raisins and potato chips, 

granules, and wet peel for processed commodity matrices. After extraction with a 

water/acetonitrile mixture and clean up with hexane and extraction columns, 

concentrations of dinotefuran and its metabolites were quantified after HPLC separation 

by tandem mass spectrometry (MS/MS) detection. The limit of quantitation was 0.01 

ppm for all matrices.

3. Magnitude of residues.

Crops in residue trials were treated at maximum label rates and harvested at the specified 

minimum treatment to harvest intervals. The residue method for dinotefuran, DN and UF 

in all components utilized HPLC separation with MS/MS detection. Tolerances have 

been previously proposed for combined residues of Dinotefuran, DN and UF in or on 

Leafy Vegetables (Crop Group 4), Cotton Seed Undelinted and Cotton Gin Byproducts, 

Cucurbit Vegetables (Crop Group 9), Grapes, Potatoes, Fruiting Vegetables (Crop Group 

8), Vegetables, brassica head and stem crop subgroup (Crop Subgroup 5-A), and Meat, 

Milk and Byproducts and Leafy Brassica Greens.

For Berry, low growing, subgroup 13-07H, except strawberry, residue trials were 

conducted for the representative crop, cranberry. The proposed tolerance in or on Berry, 

low growing, subgroup 13-07H, except strawberry for combined residues of Dinotefuran, 

DN, and UF is 0.2 ppm. The maximum combined residue found for the representative 

crop, cranberry, ranged from 0.02-0.09 ppm. For Watercress, residues trials were 

conducted. The proposed tolerance in or on Watercress for combined residues of 

Dinotefuran, DN, and UF is 5.0 ppm. The maximum residues found for Watercress with 

adjuvant were as follows: Dinotefuran: 2.13 ppm, DN: 0.534 ppm, UF: 0.133 ppm. The 

maximum residues found for Watercress without adjuvants were as follows: Dinotefuran: 

3.47 ppm, DN: 0.309 ppm, UF: 0.0931 ppm. For Onion, green, subgroup 3-07B, residue 

trials were conducted for the representative crop, onion (green). The proposed tolerance 

in or on Onion, green, subgroup 3-07B for combined residues of Dinotefuran, DN, and 

UF is 6.0 ppm. The maximum combined residue found for the representative crop, onion 

(green), ranged from 0.111-2.54 ppm. For Onion, bulb, subgroup 3-07A, residue trials 

were conducted for the representative crop, onion (dry bulb). The proposed tolerance in

or on Onion, bulb, subgroup 3-07A for combined residues of Dinotefuran, DN and UF is 

0.07 ppm. The maximum combined residue found for the representative crop, onion (dry 

bulb) at an application rate of 0.263lb ai/A in either a single soil drench or a single furrow 

application was <0.03 ppm. The maximum residue found for representative crop, onion 

(dry bulb) of two foliar (broadcast or directed) applications was <0.08 ppm. For Peach, 

residue trials were conducted. The proposed tolerance in or on Peach for combined 

residues of Dinotefuran, DN, and UF is 0.9 ppm. The maximum residues found for Peach 

after a total application of approximately 0.358lb ai/A and a pre-harvest interval of 2-3 

days was as follows: Dinotefuran: 0.54 ppm, DN: 0.04 ppm, UF: 0.06 ppm. For Peach 

after one soil drench application of approximately 0.268lb ai/A and a pre-harvest interval 

of 21 days, the maximum residues were as follows: Dinotefuran: 0.01 ppm. No DN or UF 

residues were observed above the lowest level of method validation of 0.01 ppm. 

B. Toxicological Profile
3

1. Acute toxicity. 

Dinotefuran has low acute oral, dermal and inhalation toxicity. The oral lethal dose 

(LD)50 in rats is 2450 mg/kg, the dermal LD50 is >2000 mg/kg and the inhalation 4-hour 

lethal concentration (LC)50 is >4.09 mg/L air. Dinotefuran is not a skin sensitizer in 

guinea pigs but is slightly irritating to the skin and eyes of rabbits. End-use formulations 

of dinotefuran have similar low acute toxicity profiles.

2. Genotoxicty.

Dinotefuran and its metabolites do not induce gene mutations in bacterial and mammalian 

cells, chromosome aberrations in mammalian cells or DNA damage in bacterial cells in in 

vitro test systems. Similarly, it does not exhibit a clastogenic effect in vivo in the mouse 

micronucleus test. Therefore, there is no evidence to suggest a genotoxic hazard at any

of the 3 main levels of genetic organization.

3. Reproductive and developmental toxicity.

In rat and rabbit developmental toxicity studies with dinotefuran, there was no evidence 

of teratogenicity or other embryotoxic effects at the highest dose levels, although 

maternal toxicity was evident. There were no treatment-related effects on litter 

parameters at any dose level in either species. In rats, 1000 mg/kg produced decreased 

food consumption and body weight gain, and increased water intake. In rabbits, 300 

mg/kg produced hypoactivity, prone position, panting, flushing of the nose and ears, 

tremors, and reduced weight gain, food consumption and water intake. Necropsy

revealed pale brown discoloration of liver and gray/white plaques in the stomach at 125 

and 300 mg/kg. The no-observable effect level (NOAEL) values in maternal rats and 

rabbits were 300 and 52 mg/kg/day, respectively. The NOAEL values in rats and rabbits 

for embryonic development and teratogenicity were the highest dose levels administered, 

1000 and 300 mg/kg/day, respectively. In a 2-generation study, parental animals of both 

sexes and both generations showed reduced body weight gain and food consumption at 

the highest dose level evaluated (10000 ppm), but there was no effect of treatment at any 

dose level in either generation on reproductive performance indicators. There were no 

treatment-related effects at any dose level on the histopathological appearance of the 

reproductive organs of either sex. Similarly, there were no effects at any dose level in 

either generation on quantitative ovarian histopathology or on sperm counts, motility and 

morphology. Reduced spleen weight in P generation animals and reduced thyroid weight 

in F1 generation parental females were apparent at 10000 ppm. F1 pup behavioral and 

sexual development was unaffected by treatment at all dose levels but pup weight gain 

during lactation was reduced at 10000 ppm in both generations. Furthermore, the spleen 

weight of F1 generation progeny was reduced at 10000 ppm. Based on reduced weight 

gain and food consumption in parental animals at 10000 ppm and reduced pre-weaning 

weight gain in the offspring, the NOAEL value for parental animals and offspring is 

241mg/kg.

4. Subchronic toxicity.
4

Dinotefuran was evaluated in 13-week oral (diet) toxicity studies in rats, mice, and dogs. 

No specific target organs were identified in any species. In the rat study, a NOAEL of 

500 ppm (34/38 mg/kg/day) for males and females) was established, based on minimal 

growth retardation in females and adrenal cortical vacuolation in males. A NOAEL was 

established at 5,000 ppm (336 / 384 mg/kg/day for males/females) based on marked 

growth retardation at 25,000 ppm (adrenal cortical vacuolation not adverse). In the 

mouse study, a NOAEL of 25,000 ppm (4,442/5414 mg/kg/day for males/females) was 

established based on growth retardation at 50,000 ppm. In the dog study, a NOAEL of 

8,000 ppm (307/323 mg/kg/day in males/females) was established based on growth 

retardation. Dinotefuran was also evaluated for dermal and inhalation toxicity for 4 

weeks in rats. Daily inhalation exposure of rats for 6 hours/day for 4 weeks did not elicit 

toxicologically significant effects at any exposure concentration up to and including the 

highest technically achievable concentration (2.08 mg/L) with a low MMAD±GSM of 

2.03 μ m ± 3.60. Dinotefuran was well tolerated and there were no treatment related 

effects on clinical condition, hematology, and clinical chemistry profiles, organ weights, 

macroscopic and microscopic pathology. Dermal application for 4 weeks at dose levels 

up to 1000 mg/kg/day did not elicit any local or systemic effects on any of the parameters 

examined. Therefore, no target organs were identified in the rat either by dermal or 

inhalation exposure. 

5. Neurotoxicity

Dinotefuran did not produce any functional or histomorphological evidence of 

neurotoxicity in acute (gavage) and 13-week (dietary) neurotoxicity studies in rats. The 

NOAEL for neurotoxicity in the acute study was 1,500 mg/kg, the highest dose level 

administered. The NOAEL for neurotoxicity in the 13-week dietary study was 50,000 

ppm (3413/3806 mg/kg/day for males and females). The NOAEL for all effects in this 

study was 5,000 ppm (327/400 mg/kg/day for males and females) based on reduced body 

weight gain and food consumption.

6. Chronic toxicity.

Chronic toxicity studies with dinotefuran have been conducted in rats, mice, and dogs. In 

common with the subchronic studies in these species, no specific target organs could be 

identified. In the 52-week dog study a NOAEL of 559/512 mg/kg/day for males/females 

was established based on decreased weight gain in both sexes and decreased food 

consumption in females. In the 78-week mouse study a NOAEL of 345/441 mg/kg/day

for males/females was established, based on decreased weight gain and a decrease in 

circulating platelet counts. In the 104-week rat study a NOAEL of 991/127 mg/kg/day

for males/females was established. This was based on a decrease in weight gain in 

females.

7. Animal metabolism.

In the rat, dinotefuran is rapidly and almost completely absorbed from the gastrointestinal 

tract into the general circulation, and is widely distributed throughout the tissues and 
5

fluids of the body. Elimination is rapid, predominantly by urinary excretion and almost 

complete within 7 days of administration. There is no evidence for tissue accumulation. 

Dinotefuran is rapidly transferred to maternal milk and widely distributed into fetal 

tissues but rapidly eliminated from them. More than 90% of orally and intravenously 

administered dinotefuran is eliminated as unchanged parent molecule, which is also the 

major radioactive component in plasma, milk, bile and most tissues. The major route of 

metabolism is an initial enzymatic hydroxylation of the tetrahydrofuran ring to form 

isomers of 6-hydroxy-5-(2-hydroxyethyl)-1-methyl-1,3-diazinane-2-ylidine-N-nitroamine 

(PHP), followed by further oxidation, reduction and acetylation of PHP to produce 

possible isomers of dinotefuran-CO, dinotefuran-DO, PHP-Ac and dinotefuranOH+COOH. Several minor pathways of metabolism of dinotefuran were identified in 

animals. The absorption, distribution, metabolism and elimination of dinotefuran is 

unaffected by sex and treatment regimen. In hens and goats, the metabolite profile was 

similar as in plant metabolism.

8. Carcinogenicity

The carcinogenic potential of dinotefuran has been evaluated in rats and mice. Survival 

incidences in the oncogenicity studies were unaffected by treatment at all dose levels. 

There were no treatment-related effects on the nature and incidence of neoplastic and 

adverse non-neoplastic histomorphological findings in either species at any dose level. 

Therefore, the NOAEL values for all effects, 991/127 mg/kg/day (male/female rats) and 

345/441 mg/kg/day (male/ female mice) are based on reduced weight gain, and also on 

reduced numbers of platelets in mice.

9. Metabolite toxicology. 

The metabolism profile for dinotefuran supports the use of an analytical enforcement 

method that accounts for parent dinotefuran and 1-methyl-3-(tetrahydro-3-

furymethyl)guanidine (DN) and 1-methyl-3-(tetrahydro-3-furymethyl)-urea (UF). Other 

metabolites are considered of equal or lesser toxicity than parent compound.

10. Endocrine disruption. 

Dinotefuran does not belong to a class of chemicals known or suspected of having 

adverse effects on the endocrine system. There is no evidence that dinotefuran has any

effect on endocrine function in developmental or reproduction studies. Furthermore, 

histological investigation of endocrine organs in chronic dog, rat and mouse studies did 

not indicate that the endocrine system is targeted by dinotefuran.

C. Aggregate Exposure

1. Dietary exposure.

i. Food.

Chronic dietary exposure assessments were conducted using a Tier I approach. This Tier I 

assessment incorporated tolerance level residues and 100% crop-treated in the DEEMTM
6

(Dietary Exposure Evaluation Model; Exponent, Inc., 2003) software system (Version 

2.16). DEEMTM utilized the food consumption data derived from the 1994-1998 USDA 

Continuing Surveys of Food Intake by Individuals (CSFII). The resulting exposures were 

compared to a RfD of 1.27 mg/kg/day, which was based on the female NOAEL of 127 

mg/kg/day from the 104-week rat study and a 100-fold uncertainty factor. Chronic dietary

exposure estimates for the overall US population and 25 population subgroups are well 

below the chronic RfD. Results of these analyses are summarized below.

Table C-1. Chronic Dietary Risk (DEEMTM) Analysis of Dinotefuran

Population Subgroup mg/kg BW/day %RfD Margin of Exposure

US population 0.005123 0.40% 24,791

All infants ( < 1 year old) 0.006062 0.50% 20,951

Non-Nursing infants 0.007155 0.60% 39,920

Children (1-6) 0.009884 0.80% 12,849

Children (7-12) 0.005746 0.50% 22,104

Females (13-50) 0.004554 0.40% 27,887

Males 20+ years 0.004468 0.40% 28,049

There are no acute toxicity concerns with dinotefuran as there is no toxicological endpoint 

attributable to a single exposure in the dinotefuran toxicology database, including the rat 

and rabbit developmental studies. Therefore, only chronic dietary exposures have been 

assessed. 

ii. Drinking water.

EPA uses the Drinking Water Level of Comparison (DWLOC) as a theoretical upper 

limit on a pesticide’s concentration in drinking water when considering total aggregate 

exposure to a pesticide in food, drinking water, and residential uses. DWLOCs are not 

regulatory standards for drinking water; however, EPA uses DWLOCs in the risk 

assessment process as a surrogate measure of potential exposure from drinking water. In 

the absence of monitoring data for pesticides, it is used as a point of comparison against 

conservative model estimates of a pesticides concentration in water.

An estimate of the drinking water environmental concentration (DWEC) in ground and 

surface water for dinotefuran has been made for this Notice of Filing. The DWEC of 

dinotefuran in groundwater was estimated to be 0.94 ppb using SCI-GROW (the 

screening model for ground water), and the DWEC for surface water was estimated to be 

6.24 ppb (for chronic and intermediate-term aggregate assessments) using FIRST (FQPA 

Index Reservoir Screening Tool).

To calculate the DWLOC for chronic aggregate exposure relative to a chronic toxicity

endpoint, the chronic dietary food exposure from DEEMTM, as addressed above, was 

subtracted from the RfD to obtain the acceptable chronic exposure to dinotefuran in 

drinking water. DWLOC’s, as presented below, were then calculated using default body

weights and drinking water consumption figures.
7

Table C-2. Chronic Aggregate Drinking Water Assessment 

Population Subgroup

Dietary

mg/kg

BW/day

Maximum water 

exposure mg/kg 

BW/day Kg BW

SCI-GROW 

(ppb)

FIRST 

(ppb)

DWLOC 

(ppb)

US Population 0.005123 1.264877 70 0.94 6.24 44,271

All Infants

(< 1 year old) 0.006062 1.263938 10 0.94 6.24 12,639

Non-nursing Infants 0.007155 1.262845 10 0.94 6.24 12,628

Children (1-6) 0.009884 1.260116 20 0.94 6.24 25,202

Children (7-12) 0.005746 1.264254 40 0.94 6.24 50,570

Females (13-50) 0.004554 1.265446 60 0.94 6.24 37,963

Males (20+ years) 0.004468 1.265532 70 0.94 6.24 44,294

Chronic RfD used in assessments - 1.27 mg/kg BW/day 

DWLOC = (Maximum water exposure*BW)/water consumption

Water consumption for adults = 2L, water consumption for children = 1L

The estimated average concentration of dinotefuran in surface water is 6.24 ppb. This 

value is less than the lowest DWLOC for dinotefuran as a contribution to chronic 

aggregate exposure (12,628 ppb for non-nursing infants, the most highly exposed 

population group for the chronic scenario). Therefore, taking into account the proposed 

uses, it can be concluded with reasonable certainty that residues of dinotefuran in food 

and drinking water will not result in unacceptable levels of human health risk.

To calculate the DWLOC for the intermediate-term aggregate exposure relative to a subchronic toxicity endpoint, the chronic dietary food exposure from DEEMTM plus the 

intermediate-term non-dietary exposures (see below) were subtracted from the NOAEL, 

divided by the target MOE (100), to obtain the acceptable intermediate-term exposure to 

dinotefuran in drinking water. DWLOC’s, as presented below, were then calculated 

using default body weights and drinking water consumption figures.

Table C-3. Intermediate-term Aggregate Drinking Water Assessment 

Population Subgroup NOAEL/MOE 

mg/kg/day

Aggregate 

Exposure 

mg/kg/day

Max. 

Water 

Exposure 

mg/kg/day

SCIGROW 

(ppb)

FIRST 

(ppb)

DWLOC 

(ppb)

Toddlers (1-6)10.307 0.143 3.068 0.94 6.24 61,360

1 Assume 20kg bodyweight

The estimated average concentration of dinotefuran in surface water is 6.24 ppb. This 

value is less than the DWLOC for dinotefuran as a contribution to intermediate-term 

aggregate exposure (61,360 ppb). Therefore, taking into account the proposed uses, it 

can be concluded with reasonable certainty that residues of dinotefuran in residential 

environments and in food and drinking water will not result in unacceptable levels of 
8

human health risk.

2. Non-dietary exposure. 

Mitsui Chemicals Agro, Inc. has considered potential non-dietary and aggregate (nondietary + dietary) exposures to adults, adult females, and children (1-6 years of age) for 

these uses. 

Applicator and post-application exposures can result from dermal and inhalation routes for 

both adults and children. Additionally, children can be exposed through the postapplication incidental ingestion route via hand-to-mouth behavior. Based on the label 

instructions and typical use patterns of these product types, only short- and intermediateterm exposure scenarios should be considered for dinotefuran products. However, since 

there are no toxicological endpoints attributable to a single or possible multiple exposures 

in a very short duration, as in a short-term scenario, only the intermediate-term exposure 

scenario has been evaluated for this document.

Dermal exposures for applicator and post-application activities were not assessed because 

the very high dermal NOAEL (>1,000 mg/kg/day) for dinotefuran indicates that dermal 

exposures are not of concern. Short-term oral (e.g., incidental ingestion) exposures for 

children, as mentioned above, were not assessed because there are no toxicological 

endpoints attributable to a single exposure or multiple exposures during a very short-term 

time frame in the dinotefuran toxicology database. Since the oral endpoint is used to 

calculate inhalation risks, short-term inhalation exposures for children and adults were 

also not evaluated since there is no toxicological endpoint attributable to a short-term 

endpoint. Intermediate-term inhalation exposures for applicator and post-application 

activities also were not assessed because the very high inhalation NOAEL (>7,000 

mg/kg/day) for dinotefuran indicates that inhalation exposures are not of concern. 

Therefore, only intermediate-term oral (incidental ingestion) exposures for children were 

assessed. These exposures were assessed for each individual dinotefuran product, as well 

as for the aggregation of all products. In the aggregate assessment, it was assumed that 

the children would be exposed to residues resulting from the agricultural uses (chronic 

dietary), all within one day. These non-dietary assessments were conducted using 

equations and default parameters from EPA’s Residential Standard Operation Procedures 

(SOPs) (US EPA, 1997 and 2001) and maximum application rates. Although these 

exposures are based on the intermediate-term time frame, the residue on the day of 

application was used in the SOP equations in order to maintain an extra level of 

conservatism. This assumption implies that children are exposed to residue levels, which 

are equivalent to levels resulting on the day of application, every day over an 

intermediate-term time frame. The resulting oral and aggregate exposures were 

compared to the NOAEL of 307 mg/kg/day observed in the 13-week dog study. These 

risk estimates (Margin of Exposures) for children (1-6 years of age) are summarized 

below. From the results below, Mitsui Chemicals Agro, Inc. concludes there is reasonable 

certainty of no harm associated with the aggregate (dietary + non-dietary) exposure to 

dinotefuran.
9

Table C-4. Intermediate-Term Aggregate MOEs

Exposure Routes

Children (1-6 years old) Margin of Exposure mg/kg BW/day

Dietary 25,202 0.009884

Aggregate 931 0.143716

D. Cumulative Effects

The potential for cumulative effects of dinotefuran and other substances that have a 

common mechanism of toxicity has also been considered. Dinotefuran belongs to a 

pesticide chemical class known as the neonicotinoids and subclass nitroguanadines. 

There is no reliable information to indicate that toxic effects produced by dinotefuran 

would be cumulative with those of any other chemical including another pesticide. 

Therefore, Mitsui Chemicals Agro, Inc. believes it is appropriate to consider only the 

potential risks of dinotefuran in an aggregate risk assessment.

E. Safety Determination

1. U.S. population.

Using the chronic exposure assumptions and the proposed RfD described above, the 

dietary exposure to dinotefuran for the U.S. population (48 states, all seasons) was 

calculated to be 0.40% of the reference dose of 1.27 mg/kg/day. The resulting DWLOC, 

44,271 ppb, is much greater than the estimated average concentration of dinotefuran in 

surface water, 6.24 ppb. Therefore, taking into account the proposed uses on berry, low 

growing, subgroup 13-07H, except strawberry; watercress; onion, green, subgroup 3-

07B; onion, bulb, subgroup 3-07A; peach; vegetable, tuberous and corm, subgroup IC; 

and fruit, small, vine climbing, subgroup 13-07F, except fuzzy kiwifruit, it can be 

concluded with reasonable certainty that residues of dinotefuran in residential 

environments and in food and drinking water will not result in unacceptable levels of 

human health risk.

2. Infants and children. 

FFDCA Section 407 provides that EPA shall apply an additional safety factor for infants 

and children to account for prenatal and postnatal toxicity and the completeness of the 

database. Only when there is no indication of increased sensitivity of infants and 

children and when the database is complete, may the extra safety factor be removed. In 

the case of dinotefuran, the toxicology database is complete. There is no indication of 

increased sensitivity in the database overall, and specifically, there is no indication of 

increased sensitivity in the developmental and multi-generation reproductive toxicity

studies. Therefore, Mitsui Chemicals Agro, Inc. concludes that there is no need for an 

additional safety factor; the RfD of 1.27 mg/kg/day and sub-chronic NOAEL of 307 
10

mg/kg/day are protective of infants and children.

Using the chronic exposure assumptions and the proposed RfD described above, the 

dietary exposure to dinotefuran for infants and children (1-6) was calculated to be 0.50 % 

of the reference dose of 1.27 mg/kg body-wt/day. The resulting DWLOC for nonnursing infants, 12,628 ppb, is much greater than the estimated average concentration of 

dinotefuran in surface water, 6.24 ppb. 

Using the intermediate-term exposure assumptions and the proposed NOAEL described 

above, the intermediate-term aggregate exposure to dinotefuran for the children (1-6) 

resulted in an MOE of 931. The resulting DWLOC, 61,360 ppb, is much greater than the 

estimated average concentration of dinotefuran in surface water, 6.24 ppb. Therefore, 

taking into account the proposed uses on berry, low growing, subgroup 13-07H, except 

strawberry; watercress; onion, green, subgroup 3-07B; onion, bulb, subgroup 3-07A; 

peach; vegetable, tuberous and corm, subgroup IC; and fruit, small, vine climbing, 

subgroup 13-07F, except fuzzy kiwifruit it can be concluded with reasonable certainty

that residues of dinotefuran in residential environments and in food and drinking water 

will not result in unacceptable levels.

F. International Tolerances

No Codex Maximum Residue Levels (MRL=s) have been established for residues of 

dinotefuran on any crops at this time.