EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR 

PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER 

EPA Registration Division contact: [Mr. Tony Kish, (703) 308-9443]

INSTRUCTIONS: Please utilize this outline in preparing the pesticide petition. In 

cases where the outline element does not apply, please insert “NA-Remove” and 

maintain the outline. Please do not change the margins, font, or format in your 

pesticide petition. Simply replace the instructions that appear in green, i.e., 

“[Company Name],” with the information specific to your action.

TEMPLATE:

[BASF Corporation]

[PP#]

EPA has received a pesticide petition (PP# 3F8187) from BASF Corporation, 26 

Davis Drive, Research Triangle Park, NC 27709 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. by establishing a tolerance for residues of metrafenone, (3-bromo-6-

methoxy-2-methylphenyl)(2,3,4-trimethoxy-6-methylphenyl)methanone in or on the 

raw agricultural commodity Vegetables, fruiting, group 8-10 at 1.0 part per million 

(ppm). EPA has determined that the petition contains data or information regarding the 

elements set forth in section 408 (d)(2) of FDDCA; however, EPA has not fully 

evaluated the sufficiency of the submitted data at this time or whether the data supports 

granting of the petition. Additional data may be needed before EPA rules on the petition.

A. Residue Chemistry

1. Plant metabolism. [In plant metabolism studies conducted in grapevines,

cucumber, and wheat with metrafenone, the parent compound was the principal 

residue in almost all matrices. Metrafenone is metabolized through methyl and ring 

oxidative bio-transformations, followed by enzymatic glucoside conjugation reactions to 

yield the conjugates from their corresponding aglycons. All major metabolites, which 

were present at very low levels, are considered non-relevant as all were detected in the 

rat metabolism study as aglycons or conjugates, and can therefore be considered as not 

toxicologically significant. Thus, only parent metrafenone is considered relevant to 

define the residue in plants.

2. Analytical method. [The residues of parent metrafenone in/on tomato and 

pepper RAC samples were quantitated using an LC/MS/MS multi-residue 
2

QuEChERS method (BASF Study No. 398340). The method was successfully 

validated on tomatoes and peppers in conjunction with these studies prior to 

analysis of the field samples. Acceptable concurrent method recovery data for 

tomato and pepper RAC samples were also obtained for metrafenone. The 

validated limit of quantitation (LOQ) for residues of metrafenone in/on tomato and 

pepper RAC samples was 0.01 ppm. The method limit of detection (LOD) was 

0.001 ppm, or approximately 10% of the LOQ. An independent laboratory 

validation demonstrated good performance of the QuEChERS method.]

3. Magnitude of residues. [BASF has submitted field trial data for 

metrafenone (BAS 560 F) on representative crops (tomato and pepper) of the 

fruiting vegetable crop group (EPA Crop Group 8-10). A total of 28 trials were

conducted on fruiting vegetables during the 2010 growing season. Nineteen trials 

were conducted on tomato in EPA Regions 1 (NY, one trial), 2 (GA, NC, one trial

each), 3 (FL, two trials), 5 (OH, MI, one trial each), and 10 (NM, AZ, one trial each; 

CA, ten trials). The trials were performed using large-fruited, fresh market (nine 

trials), processing (eight trials), and small-fruited variety tomatoes (2 trials). Six 

trials were conducted on bell pepper in EPA Regions 2 (GA, one trial), 3 (FL, one 

trial), 5 (WI, one trial), 6 (OK, one trial), and 10 (CA, two trials). Three trials were 

conducted on nonbell pepper varieties in EPA Regions 2 (GA, one trial), 8 (KS, one 

trial), and 10 (CA, one trial). The number and locations of field trials are in 

accordance with OPPTS Guideline 860.1500. Field trials were carried out using the 

maximum label rates, the maximum number of applications, and the minimum preharvest interval (PHI) for all the crops.

A tomato processing study was conducted to determine the potential for 

concentration of residues of metrafenone (BAS 560 F) in the processed fractions of 

tomato. Four trials were conducted in Germany during the 2010 growing season.

The tomato RAC samples were separately processed using simulated commercial 

processing procedures into the currently EPA-regulated commodities of tomato 

paste and puree. Blanched tomatoes, blanching water, canned tomatoes, peeled 

tomatoes, wash water, tomato peel, wet pomace, washed tomatoes, raw juice, 

ketchup after pasteurization and vegetable stock were also generated and collected 

for analysis. A comparison of the residues in the RAC samples with those in each 

processed fraction indicated that metrafenone residues do not concentrate 

appreciably (processing factors <1 to 1.1) in any tomato processed commodities, 

except tomato peel and wet pomace (average processing factors of 6.3 and 5.1, 

respectively).

B. Toxicological Profile

1. Acute toxicity. [In an acute toxicity study with rats, metrafenone was 

practically non-toxic (EPA Tox. Category IV). In an acute neurotoxicity study with 

rats, no signs of neurotoxicity were detected up to 2,000 mg/kg b.w., the highest dose 

tested.]

2. Genotoxicty. [metrafenone was evaluated for its potential genotoxicity in 
3

vitro using bacterial and mammalian cell mutagenicity tests and a chromosome 

damage (clastogenicity) test. The results of these studies demonstrated the absence 

of a genotoxic effect. In vivo, the test substance was assessed for the induction of 

micronuclei in mice. The result of this study showed that metrafenone has no 

chromosome-damaging potential.

It is therefore concluded, that metrafenone has no mutagenic or genotoxic properties 

both in vitro and in vivo.]

3. Reproductive and developmental toxicity. [The reproductive and 

developmental toxicity of metrafenone was investigated in a 2-generation 

reproduction study in rats as well as in prenatal toxicity studies in rats and rabbits.

In the definitive 2-generation reproduction study in rats, the NOAEL for fertility 

and reproduction was 10,000 ppm (the highest concentration tested), equivalent to 

approximately 811 mg/kg b.w./day based on food consumption data during the 

premating periods. The parental NOAEL of metrafenone is 500 ppm (approximately 

39 mg/kg b.w./day based on food consumption data). The 1,000 ppm treatment 

showed statistically significant decreases in body weight and weight gain in F1 

parental males and increased absolute and relative liver weights in females. The 

NOAEL for pup (offspring) toxicity was 1,000 ppm (approximately 79 mg/kg 

b.w./day based on food consumption data); the 10,000 ppm treatment showed a 

statistically significant decrease in pup body weight (31%) during lactation, an 

increase in relative liver weights at weaning, and a delay in vaginal opening (F1 

only).

In the prenatal toxicity study in rats, there was no treatment-related maternal or 

developmental toxicity observed, even at the highest dose tested (1,000 mg/kg 

b.w./day). On the basis of these data, the maternal NOAEL of metrafenone is 1,000 

mg/kg b.w./day (highest dose tested). The 1,000 mg/kg b.w./day dose showed a 

statistically significantly increased ratio of liver weight to terminal body weights. 

However, no correlating microscopic changes were diagnosed, indicating that the 

increased relative liver weight was not considered toxicologically significant. The 

developmental NOAEL for metrafenone is 1,000 mg/kg b.w./day (no effects were 

observed at the highest dose tested). Based on the above results, metrafenone is not 

selectively toxic to the fetus. In addition, metrafenone was not teratogenic in rats.

In the rabbit prenatal toxicity study, developmental toxicity was observed in the 

presence of maternal toxicity. Specifically, the maternal NOAEL is 50 mg/kg 

b.w./day based on the following: reduced body weight gains and reduced feed 

consumption (absolute and relative) at both 350 and 700 mg/kg b.w./day. In 

addition, at these two dose levels, a dose-related, statistically significant increase in 

absolute and relative (to body weight) liver weights occurred, as compared to 

controls. Also, increased incidences and/or severities of periportal hepatocellular 

hypertrophy and diffuse and/or periportal hepatocellular vacuolation were observed 

at 350 and 700 mg/kg b.w./day. In this prenatal toxicity study in rabbits, the 

developmental NOAEL of metrafenone is 350 mg/kg b.w./day, as based on the slight 
4

but statistically significant reduction in fetal body weights at 700 mg/kg b.w./day. 

Therefore, because developmental toxicity was only observed at dose levels that 

were maternally toxic, metrafenone is not selectively toxic to the fetus. In addition, 

metrafenone was not teratogenic in rabbits.

Overall, for the reproductive and developmental toxicity studies, the lowest NOAEL 

for maternal/parental toxicity was 39 mg/kg b.w./day (two-generation reproduction 

study) and for pup toxicity was 79 mg/kg b.w./day (two-generation reproduction 

study).]

4. Subchronic toxicity. [The subchronic toxicity of metrafenone was 

investigated in a dietary 28-day study in rats, a 28-day oral toxicity study in dogs, 

and 3-month toxicity studies in rats, mice, and dogs. In addition, a 28-day 

neurotoxicity study as well as a 28-day immunotoxicity study, were conducted with 

rats. 

The signs of toxicity observed in the three species tested were overall similar and 

consisted of reduced body weight gain at the highest tested dose levels. The 

observed effects on clinical chemistry in rats and mice can be linked to the 

microscopic effects observed in the liver. The effects observed typically included 

increased cholesterol, total protein, and total bilirubin (mice only). Organ weights 

and/or pathology indicated the liver to be the only consistent target organ in all 

three species tested. The changes included, periportal cytoplasmic vacuolation in 

rats, centrilobular hepatocellular hypertrophy in mice, and increased liver weights 

in rats, mice, and dogs.

In the 28-day neurotoxicity study with rats, there was no evidence of neurotoxicity 

in all treatment groups, with a No-Observed-Adverse-Effect Level (NOAEL) for 

neurotoxicity of 15,000 in the diet (equivalent to 1,371 mg/kg b.w./day for both 

sexes, as based on food consumption data, which exceeds a limit dose of 1,000 mg/kg 

b.w./day). These results, coupled with the lack of neurotoxic effects observed in 

acute, sub-chronic and chronic studies with other species, indicate that metrafenone

is not potentially neurotoxic. 

In the 28-day immunotoxicity study with female rats, there was no evidence of 

immunotoxicity in all treatment groups, with a No-Observed-Adverse-Effect Level

(NOAEL) for immunotoxicity of 12,000 in the diet (equivalent to 1,086 mg/kg 

b.w./day, as based on food consumption data, which exceeds a limit dose of 1,000 

mg/kg b.w./day). These results, coupled with the lack of immunotoxic effects 

observed in acute, sub-chronic and chronic studies with other species, indicate that 

metrafenone is not potentially immunotoxic.]

5. Chronic toxicity. [The chronic toxicity of metrafenone was evaluated in a 1-

year oral administration study in dogs, a 24-month feeding study with rats and an 

18-month feeding study with mice.
5

Administration of metrafenone to dogs for one year resulted in mild increases in 

mean alkaline phosphatase in males after 9 and 12 months of dosing at 500 mg/kg 

b.w./day (highest dose tested). Mean absolute and relative liver weights were both 

statistically significantly increased in females at 500 mg/kg b.w./day and relative 

liver weights were statistically significantly increased in males at 500 mg/kg 

b.w./day. However, there were no associated macroscopic or microscopic findings 

in the livers of these animals. Therefore, the slight but statistically significant 

differences in liver weights and alkaline phosphatase (in males) were not considered 

to be of toxicological significance. All other parameters evaluated including 

mortality, clinical observations, body weights and food consumption data, 

ophthalmology, hematology, coagulation and urinalysis data, and macroscopic and 

microscopic examinations revealed no adverse effects due to administration of 

metrafenone. Therefore, the NOAEL for oral administration of metrafenone to 

pure-bred Beagle Dogs was 500 mg/kg b.w./day, the highest dose tested.

Treatment of Sprague-Dawley rats with metrafenone for 24 months resulted in 

markedly reduced body weight gains in females at 5,000 (26%) and 20,000/10,000 

ppm (42%) and a lesser reduction in body weight gain for males at 20,000 ppm 

(14%). Microscopic effects in the liver and kidney were associated with clinical 

chemistry changes in males and females at doses of 5,000 ppm and greater. Slight 

anemia was observed in females at 5,000 ppm and higher, which was reversed at 24 

months. An increase in the incidence of hepatocellular necrosis after 12 months and 

benign hepatocellular adenomas was observed in females at 5,000 ppm and greater 

which are dietary concentrations that exceeded the MTD. Therefore, the NOAEL 

for systemic toxicity and for oncogenic effects following dietary administration of 

metrafenone to Sprague-Dawley rats for 24 months, was 500 ppm (25 mg/kg 

b.w./day as based on food consumption data).

Treatment of albino mice with metrafenone for 18 months resulted in statistically 

significant increases in the following: liver weights (absolute and relative, in 

females), hepatocellular hypertrophy in males, renal chronic nephropathy in males 

and extramedullary hematopoiesis in the spleen of females at 1,000 ppm, the next 

highest concentration tested. Therefore, the NOAEL for systemic toxicity following 

dietary administration of metrafenone to albino mice for 18 months, was 250 ppm 

(46 mg/kg b.w./day as based on food consumption data). 

A statistically significant (P<0.01) increase in the incidence of hepatocellular 

neoplasms (adenomas and carcinomas) was observed in the livers of male mice 

receiving 7,000 ppm (19/66, 28.8%), as compared to controls (6/65, 9.2%). There 

was also a marginal increase in the incidence of hepatocellular neoplasms in females 

receiving 7,000 ppm (4/65), as compared to the control mice (2/65). The incidence of 

14/66 (21.2%) hepatocellular adenoma for males at 7,000 ppm is slightly above the 

maximum range of historical control data at the testing laboratory (14.8%) and at 

Charles River Laboratories (19.2%). The incidence of 5/66 (7.6%) hepatocellular 

carcinoma in males at 7,000 ppm is within the maximum range of historical control 

data at both the testing facility (9.2%) and Charles River Laboratories (11.5%). 
6

Although the number of hepatocellular neoplasms in males receiving 1,000 ppm was 

also slightly increased (9/65, 13.8%) compared to the untreated controls (6/65, 

9.2%), this slight increase was not statistically significant (p<0.05) and was within 

the range of the historical controls (9.2-18.5%) at the testing laboratory. The slight 

increase in hepatocellular neoplasms in male mice at 1,000 ppm may have resulted 

from increased survival observed at termination in male mice at 1,000 ppm as 

compared to controls (55 versus 45 in the surviving male controls). The incidences 

of hepatocellular neoplasms in terminally sacrificed male mice were 5/45 or 11%, 

3/53 or 6%, 8/55 or 15% and 18/54 or 33%, at respective treatment levels of 0, 250, 

1,000 and 7,000 ppm.

For females, whereas the incidence of hepatocellular adenoma was the same (2/65 or 

3.1%) at 7,000 ppm and for controls, the incidence of hepatocellular carcinoma was 

slightly increased at 7,000 ppm (2/65 or 3.1%) versus control (0/65 or 0%). Since 

this incidence of hepatocellular carcinoma (3.1%) for females at 7,000 ppm is 

slightly above the maximum range of historical control data at both the testing 

facility (1.5%) and Charles River Laboratories (2.0%), the incidence represents an 

equivocal finding. However, because this increase was very small, was not 

statistically significant, and did not demonstrate decreased latency compared to the 

controls, this finding was considered to represent only equivocal toxicologic 

significance.

Therefore, based on the weight-of-the-evidence analysis, the NOAEL for 

oncogenicity is 1,000 ppm (approximately 190 mg/kg of b.w./day, calculated from 

food consumption data and nominal concentrations) based on the increased 

incidence of hepatocellular neoplasms observed in male mice at 7,000 ppm, as 

compared to controls.

In summary, long-term exposure studies with metrafenone in dogs, rats and mice 

resulted in increased liver weights with corresponding changes in clinico-chemical 

parameters. Microscopic pathological changes were identified in the liver, kidney, 

and spleen for rats and/or mice. The main target organ was identified as the liver in 

all species. Additionally, increased incidences of primary hepatocellular neoplasms 

were observed at the highest doses in rats and mice.]

6. Animal metabolism. [Metrafenone was rapidly absorbed and efficiently 

excreted following oral administration in the rat. The amount of absorption ranged 

from approximately 89 to 92% of the administered dose of 10 mg/kg b.w. Most of 

the administered dose was eliminated via bile within 72 hours (85.2 to 90.1%) and 

feces within 7 days (84.1 to 98.8%), with a small amount (0.69 to 6.6%) in urine. 

metrafenone-related residues showed no potential for accumulation as <1.2% of the 

applied dose was retained over seven days, with highest levels of residues found in 

the liver, GI tract, plasma, blood, kidney, and fat. The tissue retention of the orally 

administered dose was less than 2% at 48-72 hours and less than 1.2% at 168 hours. 

metrafenone was extensively metabolized in the rat to multiple metabolites formed 

via demethylation of the aromatic methoxy-group(s) followed by mono-O-
7

glycosidation, hydroxylation of the bromophenyl ring, and hydroxylation of the 

methyl substituent to hydroxymethyl followed by O-glycosidation or further 

oxidation to aldehyde or lactone.]

7. Metabolite toxicology. [In plant metabolism studies conducted in grapevines 

with metrafenone, the parent compound was the principal residue in grapes. 

metrafenone is metabolized through methyl and ring oxidative biotransformations, 

followed by enzymatic glucoside conjugation reactions to yield the conjugates from 

their corresponding aglycons. All major metabolites, which were present at very 

low levels, are considered non-relevant as all were detected in the rat metabolism 

study as aglycons or conjugates, and can therefore be considered as not 

toxicologically significant. Thus, only parent metrafenone is considered relevant to 

define the residue in plants.

The results from a hydrolysis study designed to simulate different industrial and 

household processes (pasteurization, brewing, boiling and sterilization) showed that 

metrafenone is stable. Therefore, metrafenone as unchanged parent is proposed as 

the relevant residue in grapes and industrial or household preparations of grapes.

Since metrafenone is not registered for use in the United States, the toxicity of 

metabolites formed in matrices other than the raw or processed treated commodity 

(e.g., water, soil) is not relevant.]

8. Endocrine disruption. [Data from the reproduction / developmental toxicity 

and short- and long-term repeated dose toxicity studies with metrafenone in the rat, 

rabbit, mouse, or dog, do not suggest any endocrine disruption activity. This 

information is based on the absence of any treatment-related effects from the 

histopathological examination of endocrine organs as well as the low level of concern 

for possible effects on fertility, reproductive performance, or any other aspect of 

reproductive function, or on growth and development of the offspring.]

C. Aggregate Exposure

1. Dietary exposure. [Assessments were conducted to evaluate the potential 

risk due to chronic dietary exposure of the U.S. population to residues of 

metrafenone. The U.S. EPA has not established an acute reference dose for either 

the general population or females ages 13 – 49 years because no study demonstrated 

evidence of toxicity from a single dose exposure for these populations. Therefore, an 

acute exposure risk evaluation is not required. The chronic assessment was 

conducted using all currently established tolerances for metrafenone listed in 

40CFR180.624, the pending tolerance for the Pome Fruit Crop Group 11-10 of 1.5 

ppm, and the proposed new tolerances for crop group 8 – fruiting vegetables at 1.0 

ppm, crop group 9 – cucurbit vegetables at 0.5 ppm, crop subgroup 12-12A – cherry 

subgroup at 2.0 ppm, crop subgroup 12-12B – peach subgroup at 0.7 ppm, hops at 

70 ppm, and apricots at 0.7 ppm, and crop subgroup 13-07F – small fruit vine 

climbing except fuzzy kiwifruit at 4.5 ppm.]
8

i. Food. [The dietary assessment analysis followed an initial tier approach 

using 100% crop treated and current or proposed tolerance values for all 

commodities. Dietary exposure assessments were conducted using Dietary Exposure 

Evaluation Module (DEEM-FCID Ver 3.18). 

Acute Dietary Exposure Assessment

An acute assessment was not conducted because there are no relevant toxicological 

endpoints for acute dietary exposure and a risk assessment is not required. 

Chronic Dietary Exposure Assessment

Results of the chronic exposure estimates were compared against the chronic 

Population Adjusted Dose (cPAD) of 0.25 mg/kg b.w./day that was based on the 

NOAEL from the rat chronic toxicity study, a safety factor of 100, and no additional 

FQPA safety factor is required. 

Results of the chronic dietary exposure assessments are listed in Table 1. The 

highest chronic dietary exposure of 11.8% of the cPAD was for children 1-2 years 

old. 

Table 1. Chronic Dietary Food Exposure Assessment for Metrafenone.

Population

Exposure 

Estimate %cPAD

Subgroups

(mg/kg 

b.w./day)

US Population 0.005349 2.1

All infants (< 1 year) 0.021824 8.7

Children 1-2 0.029566 11.8

Children 3-5 0.017028 6.8

Children 6-12 0.007348 2.9

Youth 13-19 0.002893 1.2

Adults 20-49 0.003558 1.4

Adults 50+ yrs 0.003375 1.4

Females 13 - 49 yrs 0.003025 1.2

The results in Table 1 demonstrate there are no unreasonable risk concerns for any 

subpopulation based on established and new uses, and that the results clearly meet 

the FQPA standard of no unreasonable adverse effect.]

ii. Drinking water. [The drinking water exposure values used in this 

assessment are from the most recent U.S. EPA risk assessment for Grapes (U.S. 

EPA, March 1, 2010 “Metrafenone: Human Health Risk Assessment for Foliar Use 

on Grape”). The water values calculated by EPA are the higher values than the 

pending and proposed new uses. The chronic surface water concentration used in 

the human exposure assessment was 22.82 ug/L. 
9

Drinking water chronic exposure was assessed based on a metrafenone water 

concentration of 22.82 ug/L using drinking water consumption, and body weights 

reported in CSFII, using DEEM-FCID Ver 3.18 software. The chronic estimated 

water exposure values are summarized in Table 2. 

Table 2. Summary of chronic dietary exposure assessment for drinking water 

considering direct and indirect sources. 

Population

Subgroups

Exposure Estimate

(mg/kg b.w./day) %cPAD

US Population 0.000478 0.2

All infants (< 1 year) 0.001232 0.5

Children 1-2 0.000689 0.3

Children 3-5 0.000581 0.2

Children 6-12 0.000419 0.2

Youth 13-19 0.000348 0.1

Adults 20-49 0.000477 0.2

Adults 50+ yrs 0.000471 0.2

Females 13 - 49 yrs 0.000475 0.2

%cPAD = percent of chronic population adjusted dose 

Exposure based on the maximum estimated water concentration of 22.82 ug/L

Acute Aggregate Exposure (Food + Water)

An acute assessment was not needed because there are no relevant toxicological 

endpoints for acute dietary exposure and an aggregate risk assessment is not 

required. 

Short- and Intermediate Aggregate Exposure (Food + Water + Residential)

Metrafenone is not registered for any use which will result in residential exposure. 

Therefore, a short- or intermediate-term exposure and aggregate risk evaluation is 

not required. 

Chronic Aggregate Exposure (Food + Water)

The aggregate chronic risk includes residues of metrafenone from food and water 

(Table 3). The results demonstrate there are no unreasonable risk concerns for any 

subpopulation based on established and new uses, and that the results clearly meet 

the FQPA standard of no unreasonable adverse effect.

Table 3. Estimated chronic aggregate exposure and risk of Metrafenone

Population Subgroup cPAD 

(mg/kg/day)

Total 

Exposure, 

Food and 

Water 

(mg/kg/day)

% 

cPAD

US Population 0.25 0.005827 2.3
10

All infants (< 1 year) 0.25 0.023056 9.2

Children 1-2 0.25 0.030255 12.1

Children 3-5 0.25 0.017609 7.0

Children 6-12 0.25 0.007767 3.1

Youth 13-19 0.25 0.003241 1.3

Adults 20-49 0.25 0.004035 1.6

Adults 50+ yrs 0.25 0.003846 1.5

Females 13 - 49 yrs 0.25 0.003500 1.4

]

2. Non-dietary exposure. [Metrafenone is not registered for any use which will 

result in non-dietary residential exposure.]

D. Cumulative Effects

[At this time, there is no available information to indicate that metrafenone 

or its metabolites have a common mechanism of toxicity with other substances. 

Therefore, there is no reason to include this pesticide or its metabolites in a 

cumulative risk assessment. For the purposes of this tolerance action EPA has not 

assumed that metrafenone and its metabolites have a common mechanism of 

toxicity with other substances.]

E. Safety Determination

1. U.S. population. [Results of the analysis demonstrate no unreasonable risk 

concerns for the U.S. population based on established and new proposed uses, and 

that the results clearly meet the FQPA standard of no unreasonable adverse effect.]

2. Infants and children. [Results of the analysis demonstrate no unreasonable 

risk concerns for any U.S. population including infants and children based on 

established and new proposed uses, and that the results clearly meet the FQPA 

standard of no unreasonable adverse effect.]

F. International Tolerances

[No maximum residue levels (MRLs) have been established for metrafenone 

by the Codex Alimentarius Commission (CODEX) or in Mexico.]