EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR

PESTICIDE PETITION EPA Registration Division contac t: 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 di notefuran, ( RS ) - 1 - methyl - 2 - nitro - 3 - (tetrah ydro - 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 o n the raw agricultural commodities be rry , low growing, except strawberry , subgroup 13 - 07H at 0.2 parts per million (ppm) ; w atercress at 5.0 ppm ; o nion, green, subgroup 3 - 07B at 6.0 ppm; o nion, bulb , sub group 3 - 07A at 0.07 ppm; p each at 0.9 ppm; v egetable, tuberous and corn, subgroup 1C at 0.05 ppm; f ruit, 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 full y 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 peti tion. A. Residue Chemistry 1 . Plant metabolism. The primary

metabolic pathway s 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. Pare nt compound, dinotefuran, and two metabolites; 1 - methyl - 3 - (tetrah ydro - 3 - fury

methyl) guanidine (DN) and 1 - methyl - 3 - (tetrah ydro - 3 - fury methyl) - urea (UF) were major metabolites in all crops. The metabolism of dinotefuran in plants and animals is understood fo r the purposes of the proposed tolerances. Parent dinotefuran and the metabolites, 1 - methyl - 3 - (tetrahydro - 3 - fury methyl)guanidine (DN) and 1 - methyl - 3 - (tetrahydro - 3 - fury methyl) - urea (UF) are the residues of concern for tolerance setting purposes. 2. Analy tical method. Mitsui Chemicals Agro, Inc., has submitted practical anal yt ical methodology for detecting and measuring levels of dinotefuran and its metabolites, UF and DN, in or on raw agricultural commodities. The h igh - performance liquid chromatography ( HPL C ) 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 commodity2

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 HPL C separation with MS/MS detection. Tolerances have been previousl y proposed for combined residues of Dinotefuran, DN and UF in or on Leafy Vegetables (Crop Gro up 4), Cotton Seed Undelinted and Cotton Gin By products, 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 By

products and L eafy 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 residue s 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 0.263 lb ai/A in either a single soil drench or a sing le 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 c ombined residues of Dinotefuran, DN, and UF is 0.9 ppm. The maximum residues found for Peach after a total app lication of approximately 0.358 lb ai/A and a pre - harvest interval of 2 - 3 day s was as follows: Dinotefuran: 0.54 ppm, DN: 0.04 ppm, UF: 0.06 ppm. F or Peach after one soil drench app lication of approximately 0.268 lb ai/A and a pre - harvest interval of 21 day s, 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 Profile3 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 met abolites 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 sy stems. Similarly , it does not exhibit a clastogenic effect in vivo in the mouse micronucl eus 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 ev idence 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 an y dose level in either species. In rats, 1000 mg/kg produced decrea sed food consumption and body weight gain, and increased water intake. In rabbits, 300 mg/kg produced h ypoactivity , prone position, panting, flushing of the nose and ears, tremors, and reduced weight gain, food consumption and water intake. Necropsy revea led pale brown discoloration of liver and gray /white plaques in the stomach at 125 and 300 mg/kg. The no - observable effect level (NO A EL ) values in maternal rats and rabbits were 300 and 52 mg/kg/day , respectivel y. The NO A EL values in rats and rabbits for embryonic development and teratogenicity were the highest dose levels administered, 1000 and 300 mg/kg/day , respectivel y. 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 an y 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 thy roid weight in F1 generation parental females were apparent at 10000 ppm. F1 pup behavioral and sexual development was unaffected b y treatment at all dose levels but pup weight gain during lactation was reduced at 10000 ppm in both generations. Further more, the spleen weight of F1 generation progen y 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 NO A EL value for parental animals and off spring 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 NO A EL 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 (a drenal 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 NO A EL of 8,000 ppm (307/323 mg/kg/day in males/fem ales) 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 an y exposure concentration up to and including the highest technicall y 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, hematolog y, 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 sy stemic effects on any of the parameters examined. Therefore, no target organs were identified in the rat either b y dermal or inhalation exposure. 5. N eu rotoxicity Dinotefuran did not produce an y functional or histomorphological evidence of neurotoxicity

in acute (gavage) and 13 - week (dietary) neurotoxicity studies in rats. The NO A EL for neurotoxicity in the acute study

was 1,500 mg/kg, the highest dose level administered. The NO A ELfor neurotoxicity in the 13 - week dietary

study was 50,000 ppm (3413/3806 mg/kg/day for males and females). The NO A EL 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. Inthe 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 establish ed. 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 and5

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 widel y d istributed into fetal tissues but rapidly

eliminated from them. More than 90% of orally and intravenousl y administered dinotefuran is eliminated as unchanged parent molecule, which is also the major radioactive component in plasma, milk, bile and most tis sues. The major route of metabolism is an initial enzy matic hydrox yl ation of the tetrah ydrofuran ring to form isomers of 6 - hydrox y - 5 - (2 - hydroxyeth yl ) - 1 - methyl - 1,3 - diazinane - 2 - yl idine -N - nitroamine (PHP), followed b y further oxidation, reduction and acetyl at ion of PHP to produce possible isomers of dinotefuran - CO, dinotefuran - DO, PHP - Ac and dinotefuran OH+COOH. Several minor pathway s of metabolism of dinotefuran were identified in animals. The absorption, distribution, metabolism and elimination of dinotefuran is unaffected b y 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 onc ogenicity 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 dinotefura n supports the use of an anal yt ical enforcement method that accounts for parent dinotefuran and 1 - methyl - 3 - (tetrah ydro - 3 - fury methyl)guanidine (DN) and 1 - methyl - 3 - (tetrahydro - 3 - fury methyl) - urea (UF). Other metabolites are considered of equal or lesser toxi city 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 s ys tem. There is no evidence that dinotefuran has any effect on endocrine function in dev elopmental or reproduction studies. Furthermore, histological investigation of endocrine organs in chronic dog, rat and mouse studies did not indicate that the endocrine s ys tem 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 DEEM TM6

(Dietary Exposure Evaluation Model; Exponent, Inc., 2003) software s ys te m (Version 2.16). DEEM TM utilized the food consumption data derived from the 1994 - 1998 USDA Continuing Survey s 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 NOAELo f 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 anal ys es are summarized below. T able C - 1. Chronic Dietary Risk (DEEM TM ) 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 inf

ants 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% 28,0 49 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, onl y chronic dietary exposures have been assessed. ii. Drinking water. EPA uses the Drinking Water Level of Comparison (DWL OC) 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 DWL OCs 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. T he 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 ass essments) 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 DEEM TM , 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 Popu lation Subgroup Dietary mg/kg BW/day Maxim um w ater

exposure mg/kg BW/day Kg BW SCI - GROW (ppb) FIRST

(ppb) DWLOC

(ppb) US Population 0.005123 1.26 4877 70 0.94 6.24 44, 271 All Infants (< 1 year old) 0.006062 1.26 3938 10 0.94 6.24 12,6 39 Non - n ursing Infants 0.007155 1.26 2845 10 0.94 6.24 12,6 28 Children (1 - 6) 0.009884 1.26 0116 20 0.94 6.24 25,2 02 Children (7 - 12) 0.005746 1.26 4254 40 0.94 6.24 50, 570 Females (13 - 50) 0.004554 1.26 5446 60 0.94 6.24 37,9 63 Males (20+ years) 0.004468 1.26 5532 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 c oncentration of dinotefuran in surface water is 6.24 ppb. This value is less than the lowest DWL OC for dinotefuran as a contribution to chronic aggregate exposure (12,628 ppb for non - nursing infants, the most highl y exposed population group for the chroni c 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 sub chronic toxicity

endpoint, the chronic dietary food exposure from DEEM TM 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 Drinkin g Water Assessment Population Subgroup NOAEL/MOE mg/kg/day Aggregate

Exposure mg/kg/day Max.

Water Exposure mg/kg/day SCI GROW (ppb) FIRST

(ppb) DWLOC

(ppb) Toddlers (1 - 6) 1 0.307 0.143 3.068 0.94 6.24 61,360 1 Assume 20kg bodyweight The estimated avera ge 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 certaint y that residues of dinotefuran in residential environments and in food and drinking water will not result in unacceptable levels of8

human health risk. 2. Non - dietary exposure . Mitsui Chemicals Agro, Inc. has considered potential non - dietary and aggregate (non dietary + 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. A dditionally , children can be exposed through the post application incidental ingestion route via hand - to - mouth behavior. Based on the label instructions and ty

pical use patterns of these product ty pes, onl y short - and intermediate term 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 or al (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 toxico logy 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, onl y 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, 199 7 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 imp lies 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 o bserved 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 ag gregate (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 an y other chemical including another pesticide. Therefore, Mitsui Chemicals Agro, Inc. believes it is appropriate to consider only the pote ntial 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 stat es, all seasons) was calculated to be 0. 4 0% 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 pro posed 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 ki wifruit , 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 safet y factor for infants and children to account for prenatal and postnatal toxicity and the completeness of the database. Onl y when there is no indication of increased sensitivity of infants and children and when the d atabase is complete, may the extra safet y 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 specificall y, there is no indication of increased s ensitivity

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 30710

mg/kg/day

ar e 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/d ay . The resulting DWL OC for non nursing infants, 12,6 28 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, th e intermediate - term aggregate exposure to dinotefuran for the children (1 - 6) resulted in an MOE of 931 . The resulting DWL OC, 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 Resid ue Levels (MRL = s) have been established for residues of dinotefuran on an y crops at this time.