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:

By establishing tolerances for residues of 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:

Bushberry subgroup 13-07B at 8.0 parts per million (ppm); Vegetable, fruiting

group 8-10 at 0.60 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 20B

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)ethyl3-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 method. Independently validated, analytical methods for crop 

matrices have been submitted for measuring flubendiamide. Typically, plant 

matrices 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 (LD50: 

>2,000 mg/kg bw), dermal (LD50: >2,000 mg/kg bw) and inhalative toxicity (LC50: 

>68.5 mg/m3air; 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 vitro 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 developmental 

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 humans, 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, twogeneration, 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 route 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 chemical 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 sensitive 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 transpeptidase 

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 

corpuscular 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 in 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 the 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, mean 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 selected 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 oncogenic 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 with 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 excretion 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 and 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 metabolite, 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 conducted on NNI-0001-desiodo, 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 

flubendiamide 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 

material 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 pathology 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 

follicular 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 

depressed levels of circulating thyroid hormone brought about by a chemicallyinduced 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 study. 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 (eye 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 developmental neurotoxicity studies in rats. Based on 

the data, EPA has reduced the FQPA Safety Factor to 1X and, therefore, an 

uncertainty factor of 100 is adequate to account for inter- and intra- species 

variability. Acute and chronic Population Adjusted Doses (aPAD 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 

based 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, tolerance 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 chronic assessments assumed average percent of 

crops with registered and pending uses 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 Balanced 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 (95th 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 using 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, 

children 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, these 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 acid 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 determine 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 calculate 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 and 

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 flubendiamide 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 trials 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 (food 

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 that 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.

Cropa US EUb CODEX Japanc

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, LOWBUSH 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

Cropa US EUb CODEX Japanc

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, SWEET 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, SWEET, KERNELS PLUS COB 

WITH 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, WEST INDIAN 0.2 0.15 0.2

GRAPE, TABLE 1.4 2 2 2 2

GRAPE, WINE 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

KIWIFRUIT, 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

Cropa US EUb CODEX Japanc

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

SAFFLOWER, 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

Cropa US EUb CODEX Japanc

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

STRAWBERRY 1.5 2 1

SUGAR CANE 0.3 0.01 0.01

SUNFLOWER, SEED 5 0.01 0.01 0.05

SWISS 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

WALNUT, BLACK 0.06 0.1 0.1 0.1 0.05

WALNUT, 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