## Interregional Research Project Number 4 (IR**- 4)** 

**PP# 4E8311 EPA has received a pesticide petition**  **( 4E8311**  **) from**  **Interregional Research Project Number 4 (IR** **- 4), 500 College Road East, Suite 201W, Princeton, NJ 08540**  **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 180.507 as follows: B** **y establishing tolerance s**  **for residues of flubendiamide, (**  **N 2** 



## - **1,1 -**  **dim ethyl** **- 2**  **- (methylsulfonyl)ethyl** **- 3**  **- iodo**  **- N**  **1**



## -**2 -**  **methyl -** **4 -**  **1,2,2,2 -** **tetrafluoro -**  **1 -**  **(trifluoromethyl)ethylphenyl -**  **1,2 -** **benzenedicarboxamide)** in or on the following: **Bushberry subgroup 13 -**  **07B at**  **8 .0**  **parts per million (** **ppm );**  **Vegetable , fruiting**  **group 8 -**  **10 at**  **0.6 0**  **ppm ;**  **Fruit, pome, group 11**  **- 10**  **at 1.5**  **ppm ;**  **Fruit , stone,**  **group 12**  **- 12**  **at 1.6**  **ppm ;**  **Nut , tree,**  **group 14 -**  **12 at**  **0.06 ppm**  **; and**  **Sunflower ,**  **subgroup 20 B**  **at 5**  **.0 ppm**  **. Upon the approval of the aforementioned tolerances, to remove**  **the established tolerances for**  **flubendiamide, ( N**  **2**



## - **1,1 -**  **dimethyl -** **2 -**  **(methylsulfonyl)ethyl****** **3 -** **iodo -**  **N 1** 



## -**2 -**  **methyl -** **4 -**  **1,2,2,2 -** **tetrafluoro -**  **1 -**  **(trifluoromethyl)ethylphenyl -**  **1,2 -**  **benzenedicarboxamide)** in or on the following : Fruit, pome, group 11 at 1.5 ppm; Fruit, stone, group 12 at 1.6 ppm; Nut, tree, group 14 at 0.06 ppm; Safflower, seed at 5.0 ppm; and Sunflower, seed at 5.0 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 in plants was limited, with parent flubendiamide being the major residue observed in all of the studies (tomato,**  **cabbage, apple, and corn). NNI -**  **0001 -**  **des -** **iodo, a minor metabolite found in the plant metabolism studies, was formed by reductive deiodination of flubendiamide.**  2. Analytical me thod. **Independently validated, analytical methods for crop ma** **trices have been submitted for measuring flubendiamide. Typically, plant ma** **trices samples are extracted, concentrated, and quantified by LC/MS/MS using deuterated internal standards.**  3. Magnitude of residues. **Magnitude of the residue data were conducted on lowbush blueberry**  **and highbush blueberry ( Bushberry subgroup 13**  **- 07B**  **) according to OPPTS Guideline 860.1500.**  **The data supports revising the requested**  **tolerances.**

### 2



## B. Toxicological Profile 1. Acute toxicity. **Technical flubendiamide and the formulated products show low acute toxicity (Toxicity Category III or IV) via the oral, dermal and inhalation**  **routes of exposure. Flubendiamide technical exhibits very low acute oral (LD 50**  

## : **>2, 000 mg/kg bw), dermal (LD**  **50** 

## : >2,000 mg/kg bw) and inhalative toxicity (LC **50** 

## : **>68.5 mg/m 3**  

## air; the mean maximum attainable concentration) in male and female **rats. Though a slight irritant to the eye, flubendiamide is non -** **irritating to skin and**  **it shows no skin sensitization potential under the conditions of the guinea pig**  **maximization test. There were no neurotoxicity concerns based on the acute neurotoxicity study.**  2. Genotoxicty. **Flubendiamide was tested for its genotoxic potential in a battery of**  **in v itro**  **or in vivo**  **studies covering all required end -** **points (gene mutations, chromosomal aberrations, and DNA damage and repair). There was no**  **evidence of genotoxicity.** 3. Reproductive and developmental toxicity. **Flubendiamide shows no evidence**  **of primary developmental or reproductive effects. In the prenatal developmental toxicity studies in rats and rabbits and in the two**  **- generation reproduction study in**  **rats, toxicity to the offspring occurred at equivalent or higher doses than maternal**  **toxicity. No effect on embryo/fetal development was observed in rabbits and no evidence to suggest that flubendiamide possesses a teratogenic potential was noted**  **in either species. There were no neurotoxicity concerns based on the developme ntal**  **neurotoxicity (DNT) study. An enlargement of the eyeball (** **buphthalmia ) was noted in rat offspring in the**  **reproductive and DNT studies. Supplemental studies designed to investigate the cause of the eye effect were able to establish a link to the unique inability of the**  **female rat, unlike other mammalian species including hu mans, to oxidize the parent**  **compound, resulting in a higher body burden and subsequent exposure to flubendiamide.**  **As a conservative estimate buphthalmia was selected as the endpoint to establish the acute reference dose (aRfD) using the DNT, two**  **** **generatio n, and one** **- generation reproduction studies in the rat as co**  **- critical studies**  **with a NOAEL of 99.5 mg/kg (the highest NOAEL) and a LOAEL of 127 mg/kg (the lowest LOAEL). Using the NOAEL for buphthalmia from the DNT study, which**  **had the shortest duration of exposure (**  **36 days), in conjunction with the lowest LOAEL observed in the database for this effect result in a more refined acute**  **dietary risk assessment.** 4. Subchronic toxicity. **The subchronic toxicity of flubendiamide was investigated via the oral rou**  **te in 90 -**  **day feeding studies in mouse, rat and dog, and via the dermal route in a 30**  **- day dermal toxicity study in rat. Animals generally**  **responded to exposure to flubendiamide with signs of nonspecific toxicity. Rats, dogs, and mice tolerated the chemica** **l in excess of the limit dose without mortalities or clinical signs. Effects were similar in the chronic studies. In rats, there is a** 

### 3



## pronounced difference between the sexes in their susceptibility to flubendiamide **exposure. Female rats were much more s ensitive to the toxic actions of**  **flubendiamide than male rats, which was principally attributed to a diminished capacity of the female rat to oxidatively metabolize relative to the male rat. The**  **primary target organ in rats and mice was the liver. In the rat, liver changes**  **typically observed first in the female rat with respect to dose and time included increased liver weight, periportal (microvesicular) fatty change of hepatocytes,**  **decreased alkaline phosphatase activity, and increased -**  **glutamyl transpe ptidase**  **activity. In the mouse liver, hepatocellular centrilobular hypertrophy, fatty change of hepatocytes, and dark** **- colored tissue were observed in both sexes. Alterations in**  **red blood cell parameters were also noted and included declines in mean corpu**  **scular volume, hematocrit and hemoglobin concentration, increased platelet count, and decreased total bilirubin. A further target in the rat was the thyroid,**  **characterized by the occurrence of follicular cell hypertrophy in both sexes but emerging later i** **n the male with respect to dose and time; the thyroid pathology was not accompanied by alterations in circulating thyroid hormones despite evidence of**  **slightly increased serum TSH levels. Targets were similar in the 30 -**  **day rat dermal toxicity study. In t** **he dog, moderate liver effects (increased: alkaline phosphatase, triglycerides, liver weight) were also observed; however, generating a pronounced**  **systemic toxicity proved challenging, even using high doses that exceeded the limit dose of 1,000 mg/kg body**  **weight. The 90 -**  **day oral NOAEL was 13.1 mg/kg/based on a indications of a slight hepatotoxicity in the female rat. In the mouse and dog, the**  **NOAEL was 11.9 and 2.58 mg/kg bw/day, respectively. The NOAEL was 100 mg/kg/day in the rat dermal toxicity study.**  5. Chronic toxicity. **Over the chronic duration via the oral route, the primary target organs across dogs, rats and mice are liver, kidney and thyroid; with an**  **increase in organ weight, fatty change, and hypertrophy. Changes in hematocrit, hemoglobin, me**  **an corpuscular volume and eosinophil counts were noted in the 1 -**  **year rat and 2 -** **year rat studies. For the chronic Reference Dose (cRfD), the 1 -** **year chronic toxicity study in the rat, 1**  **- year chronic toxicity in the dog, and the 2**  **- year**  **rat cancer study were s elected as three co**  **- critical studies with a NOAEL/LOAEL of**  **2.4/33.9 mg/kg/day (highest NOAEL of 2.4 mg/kg/day from 1 -** **year chronic rat study and lowest LOAEL of 33.9 mg/kg/day from 2**  **- year chronic rat study; although the**  **1 -** **year dog had NOAELs of 2.21/2.51 mg /kg/day**  **- the lowest NOAELs from each**  **study was considered when comparing NOAELs among the three studies), respectively, based on the consistent liver toxicity reported across multiple studies,**  **different durations, and multiple species. The NOAEL in the o**  **ncogenic mouse study**  **was 4.44 mg/kg bw/day, based on liver and thyroid effects. Flubendiamide is not likely to be carcinogenic, based on rat and**  **mouse bioassays as well as negative in vivo**  **and in vitro**  **mutagenic effects.** 6. Animal metabolism. **Following oral administration of flubendiamide to rats, blood and plasma levels peaked approximately 6 to 12 hours after dosing followed**  **by continuous decline. The flubendiamide was fairly well distributed among blood**

### 4



## and most of the organs and tissues wi**th some preference for liver, adrenal glands, and fat. Male rats showed a more rapid clearance of residues than in the female**  **animals. In general, excretion of flubendiamide residues was rapid, with feces being the predominant excretion route. Renal exc**  **retion accounted for only 2% and <1% of the dose in male and female rats, respectively. Absorption was demonstrated by**  **bile fistula studies. Metabolism of flubendiamide in the male rat was primarily by oxidation and that in female rats was by oxidation a**  **nd glutathione conjugation. Parent flubendiamide, NNI** **- 0001**  **- benzylalcohol and NNI**  **- 0001**  **- benzoic acid were**  **the major residues identified in the feces. In the ruminant and poultry metabolism studies, NNI**  **- 0001**  **- iodophthalimide was the only significant metabol** **ite, and is included in the risk assessment.**  7. Metabolite toxicology

. **As the metabolism of flubendiamide was very limited, no significant testing of metabolites has been conducted. Acute oral and**  **mutagenic testing (bacterial reverse mutation) was condu cted on NNI** **- 0001**  **- des**  **** **iodo, NNI -**  **0001 -** **3 -**  **OH and NNI -**  **0001 -** **iodophthalimide metabolites. Overall, relative to the parent compound, neither an acute nor a mutagenic concern emerged**  **following toxicological screening of these metabolites derived from exposure to f**  **lubendiamide technical. NNI -**  **0001 -**  **des -** **iodo was the major plant metabolite but it was present at levels of less than 4% of the total residue in field trials. It was not**  **found in animals but was present as an impurity in flubendiamide technical, the test ma** **terial for toxicity studies.** 8. Endocrine disruption

. **The toxicology database for flubendiamide is current and complete. Studies in this database include evaluation of the potential effects on**  **reproduction and development and an evaluation of the pathol ogy of the endocrine**  **organs following short -**  **or long -** **term exposure. At the higher doses, possible endocrine effects following exposure to flubendiamide were noted in the adrenal**  **(increased weight in rats; cortical hypertrophy in dogs), ovary (interstitial cell**  **vacuolation in rats), and thyroid (increased weight and follicular cell hypertrophy in rats). The reversibility of histological thyroidal effects was demonstrated in**  **subchronically -** **treated female rats during a four -** **week recovery period. Thyroid fol** **licular cell hypertrophy emerged as one major endpoint in all rat studies. In the case of F344 rats, the activation of the thyroid is consistent with an indirect**  **hypothesis, involving increased TSH secretion from the pituitary in order to restore depresse**  **d levels of circulating thyroid hormone brought about by a chemically****** **induced increase in thyroxine metabolism. Consistent with this hypothesis, an increase in hepatic UDP** **- GT activity was measured in female F344 rats in a special**  **28 -**  **day thyroid hormone st udy. In general, chemically** **- induced interference with**  **thyroid regulation, through enhanced metabolism of circulating thyroxine, is considered a greater toxicological concern to rodents than humans.**  C. Aggregate Exposure 1. Dietary exposure. **The toxicology database for flubendiamide is complete for the purposes of this risk assessment and the characterization of potential pre** **-**

### 5



## and postnatal risks to infants and children. **Although susceptibility was identified in the toxicological database (ey** **e effects), the selected regulatory points of departure (PODs) are protective of these effects, and therefore, the human health risk**  **assessments are protective. There are no treatment** **- related neurotoxic findings in**  **the acute neurotoxicity and developmenta l neurotoxicity studies in rats. Based on**  **the data, EPA has reduced the FQPA Safety Factor to 1**  **X and, therefore, an**  **uncertainty factor of 100 is adequate to account for inter -**  **and intra -**  **species variability. Acute and chronic Population Adjusted Doses (a**  **PAD and cPAD) are, therefore, the same as the reference doses for the populations and subpopulations of**  **interest. Acute dietary exposure was expressed as a percentage of the aPAD of**  **0.995 mg/kg bw/day**  **from a highest NOAEL of 99.5**  **mg/kg bw/day established from the**  **co -**  **critical DNT, one generation and two generation reproductive studies in the rat with an uncertainty factor of 100. Chronic dietary exposure was expressed as a**  **percentage of the chronic Population Adjusted Dose (cPAD) of 0.024**  **mg/kg bw/day base**  **d on the highest NOAEL of 2.4**  **mg/kg bw/day established from the co**  **- critical 1**  **- year chronic toxicity study in the rat, 1**  **- year chronic toxicity in the dog, and the 2**  **- year rat cancer study.**  i. Food. **Food exposure estimates were calculated using DEEM -** **FCID Ver.**  **3.16 software , with**  **NHANES WWEIA 2003 to 2008 consumption**  **data. Acute assessments assumed that 100% of crops with registered**  **and pending uses of flubendiamide are treated, and that all treated crops contain residues at tolerance level.**  **In addition, toler ance level**  **residues for livestock commodities were also included in the analyses to account for the potential transfer of plant residues to livestock**  **tissues. The**  **refined c**  **hronic assessments assumed average percent of**  **crops with registered and pending use s of flubendiamide are treated,**  **and that all treated crops contain residues at the average residue levels found in crop field trials.**  **Experimentally determined processing factors were incorporated, where available.**  **In addition, Maximum Reasonable Balance**  **d Diet estimation of residues for livestock commodities were also included in the chronic analyses to**  **account for the potential transfer of plant residues to livestock tissues. Acute exposure (95**  **th** 

## percentile) for food only utilizes **4 % of the aPAD**  **for the US Population and**  **8.8 % for Children 1**  **- 2, the most highly**  **exposed subpopulation. Chronic exposure for food only utilizes 3.6**  **% of the cPAD for the US Population and**  **5.8 % of the cPAD for**  **Children 1 -** **2, the most highly exposed subpopulation.** ii. Drinking water

. **Estimated Drinking Water Concentration (EDWCs) associated with flubendiamide use on all crops were calculated using**  **PRZM -**  **GW (ver. 1.0). The highest potential drinking water exposure**  **from registered and pending uses of flubendiamide was from ground**  **water us ing the**  **Wisconsin corn scenario. For acute exposure, the EDWC of 116**  **g/L used in the assessment. For chronic exposure the EDWC of 112**  **g/L used in the assessment. EDWCs were** 

### 6 

## incorporated **into exposure assessments using DEEM** **- FCID 3.16.**  **Incorporation of the acute EDWC of 116**  **g/L resulted in**  **acute aggregate dietary exposure (food and water) of 4.4% aPAD for the**  **overall U.S. population. For the most highly exposed population subgroup, children 1**  **- 2 yrs., acute aggregate exposure (food and**  **water) was 9.3% of the aPAD.**  **Incorporation of the chronic EDWC of 112**  **g/L into the**  **exposure assessment resulted in chronic aggregate**  **dietary exposure (food and water) of 13% cPAD for the overall U.S. population. For the most highly exposed population subgroup,**  **childre n 1**  **- 2 yrs., chronic aggregate exposure (food and water) was**  **31% of the cPAD.** 2. Non

- dietary exposure

. **The maximum seasonal and single use rate has not changed and no new methods of application or field post application activities are**  **introduced by the additional crops. There have been updates to the unit exposures**  **as EPA transitions from PHED to AHETF unit exposures and has refined the default post application initial DFR and TC values. However, based on the MOEs**  **originally calculated by the Agency, th ese refinements do not alter the**  **determination that the MOEs all exceed 100. Hence, a risk to bystanders, field workers, and applicators is not expected to change from the current acceptable**  **levels.** D. Cumulative Effects **At this time, there is no available information to indicate that flubendiamide or its metabolites have a common mechanism of human toxicity with other**  **substances. Flubendiamide is a ryanodine receptor agonist belonging to the chemical class of phthalic ac** **id diamides. The biological mode of action of flubendiamide is not reflected by the results of the multiple** **- dose feeding studies in**  **rodents and dogs. For this class of chemistry, EPA has not yet conducted a detailed review of common mechanisms to determi** **ne whether it is appropriate, or how to include these chemicals in a cumulative risk assessment. Flubendiamide does not**  **appear to produce a toxic metabolite produced by other substances. For the purposes of these tolerance actions, therefore, EPA has not**  **assumed that flubendiamide has a common mechanism of toxicity with other substances.**  E. Safety Determination 1. U.S. population. **Using the conservative exposure data from GLP conducted trials to determine dietary exposure and**  **conservative models to cal**  **culate drinking water exposure and based on the completeness of the toxicity data, it can be**  **estimated that aggregate exposure (dietary plus water) to residues of flubendiamide from all proposed uses will utilize 4.4% of the aPAD for the U.S. population an**  **d 13.3% of the cPAD for the U.S. population. These estimates are well below HED's**  **level of concern (100% of the aPAD or cPAD). Therefore, there is reasonable certainty that no harm will result to the general U.S. population from aggregate** 

### 7



## exposure to flu **bendiamide residues from proposed uses .**  2. Infants and children

. **Based on the completeness of the database and the conservative nature of the assumptions used in the exposure assessment, the FQPA**  **safety factor for infants and children has been reduced to 1X. Using the conservative exposure data from GLP conducted trial** **s to determine dietary exposure and conservative models to calculate drinking water exposure, the**  **aggregate (food and water), acute dietary exposure occupies 9.3% of the aPAD for the most highly exposed subpopulation, children 1**  **- 2 yrs. and the aggregate (f**  **ood and water), chronic dietary exposure occupies 31% of the cPAD for the most highly**  **exposed subpopulation, children 1 -** **2 yrs.. These estimates are well below HED's level of concern (100% of the aPAD or cPAD). Therefore, there is reasonable**  **certainty th at no harm will result to infants or children from aggregate exposure to**  **flubendiamide residues from proposed uses .** 

F. International Tolerances **International tolerances established for Flubendiamide can be found in the table below.**  **Crop a**  **US EU**  **b CODEX**  **Japan c**  **Taiwan Korea**  APPLE 1.5 0.8 0.8 1 1 1 APRICOT 1.6 0.8 2 2 1 ARTICHOKE, GLOBE 1.6 0.01 0.01 BALSAM PEAR 0.2 0.15 0.2 2 BEAN, ADZUKI, DRY 0.6 1 1 1 BEAN, BROAD(FAVA BEAN), DRY 0.6 1 1 1 0.05 BEAN, FIELD, DRY 0.6 1 1 1 BEAN, KIDNEY, DRY 0.6 1 1 1 0.05 BEAN, LABLAB, DRY 0.6 1 1 1 BEAN, LIMA, DRY 0.6 1 1 1 0.05 BEAN, MOTH, DRY 0.6 1 1 1 BEAN, MUNG, DRY 0.6 1 1 1 0.05 BEAN, NAVY, DRY 0.6 1 1 1 BEAN, PINTO, DRY 0.6 1 BEAN, RICE, DRY 0.6 1 1 1 0.05 BEAN, TEPARY, DRY 0.6 1 1 1 BEAN, URD, DRY 0.6 1 1 1 BLUEBERRY, LOW BUSH 1.5 0.01 0.01 1 BROCCOLI 3 0.01 4 5 1 3 BROCCOLI RAAB 25 0.01 25 BRUSSELS SPROUTS 3 0.01 4 4 1 CABBAGE 3 4 4 4 1 1 CABBAGE, CHINESE, BOK CHOY 25 0.01 5 1 3

### 8

**Crop a**  **US EU**  **b CODEX**  **Japan c**  **Taiwan Korea**  CABBAGE, CHINESE, MUSTARD, GAI CHOY 3 0.01 1 CABBAGE, CHINESE, NAPA 3 0.01 5 1 1 CANTALOUPE 0.2 0.06 0.2 0.05 1 CATTLE, BY PRODUCTS 0.6 1 1 1 CATTLE, FAT 0.7 2 2 CATTLE, KIDNEY 0.6 1 1 1 CATTLE, LIVER 0.6 1 1 1 CATTLE, MEAT 0.08 2 2 1 CAVALO BROCCOLO 3 CELERY 11 5 5 5 5 CHAYOTE, FRUIT 0.2 0.15 0.2 2 CHERRY, SW EET 1.6 2 2 2 1 1 CHERRY, TART 1.6 2 2 2 1 1 CHICKEN, FAT 3 0.01 0.01 CHICKEN, LIVER 0.6 0.01 0.01 CHICKEN, MEAT 0.1 0.01 0.01 COLLARDS 25 0.01 25 CORN SALAD 11 0.01 25 CORN, GRAIN 0.03 0.02 0.02 0.05 0.05 CORN, POP 0.02 0.01 0.05 CORN, SW EET, KERNELS PLUS COB WI TH HUSKS REMOVED 0.01 0.02 0.02 0.05 0.02 COTTONSEED 0.9 1.5 1.5 2 1.5 CRESS, GARDEN 11 0.01 CRESS, UPLAND 11 0.01 0.01 CUCUMBER 0.2 0.15 0.2 0.7 1 CUCUMBER, CHINESE 0.2 EGGPLANT 0.6 0.2 1 0.7 EGGS, CHICKEN 0.4 0.01 0.01 ENDIVE (ESCAROLE) 11 0.01 0.01 3 FENNEL, BULB 11 0.01 25 GHERKIN, W EST INDIAN 0.2 0.15 0.2 GRAPE, TABLE 1.4 2 2 2 2 GRAPE, W INE 1.4 2 2 2 2 HOG, BY PRODUCTS 0.15 1 1 1 HOG, FAT 0.15 2 2 HOG, KIDNEY 0.15 1 1 1 HOG, LIVER 0.15 1 1 1 HOG, MEAT 0.03 2 2 1 1 KALE 25 0.01 25 3 KIW IFRUIT, HARDY 1.4 0.01 0.1 0.5 LETTUCE, HEAD 11 7 5 15 5 LETTUCE, LEAF 11 7 7 15 10 LETTUCE, ROMAINE (COS) 11 7 15 10 MELON, CASABA 0.2 0.06 0.2 0.05 1 MELON, CITRON 0.2 0.2 0.05 MELON, CRENSHAW 0.2 0.06 0.2 0.05 1 MELON, GOLDEN PERSHAW 0.2 0.06 0.05 1 MELON, HONEY BALL 0.2 0.06 0.2 0.05 1 MELON, HONEYDEW 0.2 0.06 0.2 0.05 1 MELON, MANGO 0.2 0.06 0.2 1

### 9

**Crop a**  **US EU**  **b CODEX**  **Japan c**  **Taiwan Korea**  MELON, PERSIAN 0.2 0.06 0.2 0.05 1 MELON, PINEAPPLE 0.2 0.06 0.05 1 MELON, SANTA CLAUS 0.2 0.06 0.05 1 MELON, SNAKE 0.2 0.06 0.2 1 MILK FAT, CATTLE 1 0.1 5 MILK, CATTLE 0.15 0.1 0.1 0.1 MUSKMELON 0.2 0.06 0.2 0.05 1 1 MUSTARD GREENS 25 0.01 25 3 MUSTARD SPINACH 25 0.01 25 1 NECTARINE 1.6 0.8 2 2 1 NUT, BEECH 0.06 0.1 0.1 0.1 NUT, BRAZIL 0.06 0.1 0.1 0.1 NUT, BUTTER 0.06 0.1 0.1 NUT, CASHEW 0.06 0.1 0.1 0.1 0.05 NUT, CHESTNUT 0.06 0.1 0.1 0.1 0.05 NUT, HICKORY 0.06 0.1 0.1 0.1 NUT, MACADAMIA 0.06 0.1 0.1 0.1 0.06 0.05 NUT, PECAN 0.06 0.1 0.1 0.1 0.05 NUT, PISTACHIO 0.06 0.1 0.1 0.1 0.05 OKRA 0.3 0.01 2 0.7 ORACH 11 PEA, FIELD, DRY 0.6 1 1 1 0.05 PEACH 1.6 0.8 2 0.05 0.7 PEANUT OIL, EDIBLE 0.03 0.01 PEAR 1.5 0.8 0.8 1 1 PEAR, ASIAN 1.5 0.8 0.8 1 PEPINO 0.6 0.2 0.1 2 PEPPER, BELL 0.6 0.2 0.7 3 1 PEPPER, NON

- BELL 0.6 0.2 0.7 10 1 PLUM, CHERRY 1.6 0.01 2 2 PLUM, CHICKASAW 1.6 0.01 2 2 PLUM, DAMSON 1.6 0.01 2 2 PLUM, GREENGAGE 1.6 0.01 2 PLUM, JAPANESE 1.6 0.01 2 2 PLUM, PRUNE, FRESH 1.6 0.01 2 2 1 PLUMCOT 1.6 2 PUMPKIN 0.2 0.06 0.2 0.2 1 QUINCE 1.5 0.8 0.8 0.8 0.5 RADICCHIO (RED CHICORY) 11 0.01 1 3 RAPE GREENS 25 0.01 25 RICE, GRAIN 0.5 0.2 0.5 SAFFLOWE R, SEED 5 0.01 0.01 0.05 SHEEP, BY PRODUCTS 0.6 1 1 0.01 SHEEP, FAT 0.7 2 0.01 SHEEP, KIDNEY 0.6 1 1 0.01 SHEEP, LIVER 0.6 1 1 0.01 SHEEP, MEAT 0.08 2 2 0.01 SORGHUM, GRAIN 5 0.01 0.01 0.05 SOYBEAN 0.25 0.01 1 1 0.05 SOYBEAN (IMMATURE SEED) 0.5 0.5 2 5 0.05 SPINACH 11 10 0.01 10 SPINACH, NEW ZEALAND 11 10 5

### 10

**Crop a**  **US EU**  **b CODEX**  **Japan c**  **Taiwan Korea**  SPINACH, VINE 11 0.01 5 SQUASH, ACORN 0.2 0.06 0.2 0.2 1 SQUASH, BUTTERNUT 0.2 0.06 0.2 0.2 1 SQUASH, CROOKNECK 0.2 0.15 0.2 0.2 1 SQUASH, HUBBARD 0.2 0.06 0.2 0.2 1 SQUASH, SCALLOP 0.2 0.15 0.2 0.2 1 SQUASH, SPAGHETTI 0.2 0.06 0.2 0.2 1 SQUASH, STRAIGHTNECK 0.2 0.15 0.2 0.2 1 STRAW BERRY 1.5 2 1 SUGAR CANE 0.3 0.01 0.01 SUNFLOWE R, SEED 5 0.01 0.01 0.05 SW ISS CHARD 11 0.01 25 3 TOMATILLO 0.6 0.2 5 TOMATO 0.6 0.2 2 2 0.7 TURKEY, FAT 3 0.01 0.01 TURKEY, LIVER 0.6 0.01 0.01 TURKEY, MEAT 0.1 0.01 0.01 TURNIP, TOPS 25 0.01 25 WA LNUT, BLACK 0.06 0.1 0.1 0.1 0.05 WA LNUT, ENGLISH (PERSIAN) 0.06 0.1 0.1 0.1 0.05 WATERMELON 0.2 0.06 0.2 0.05 1 ZUCCHINI 0.2 0.15 0.2 0.2 1 **a** MRL data extracted from Federal Registry and / or FAS MRL Database (www.mrldatabase.com) **b** Default MRL in Europe = 0.01 ppm **c** Default MRL in Japan = 0.01 ppm