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EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR 

PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER 

EPA Registration Division contact: Cynthia Giles-Parker; Acting Product Manager, 

Team 20; (703) 305-7740 

TEMPLATE:

KIM-C1, LLC

2F8055

EPA has received a pesticide petition (2F8055) from KIM-C-1, LLC, 2547 West 

Shaw Avenue, Suite 116, Fresno, CA 93711 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

1. by establishing a temporary tolerance for residues of

N-(2-chloro-4-pyridinyl-N’-phenylurea (forchlorfenuron) in or on the raw 

agricultural commodity almond, cherry (sweet), fig, pear, pistachio, plum/prune at 0.01

parts 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. One plant metabolism study on each of three crops, 

including grapes, kiwi fruit and apple fruit, were conducted. Based on all three 

studies the residue of concern was defined as forchlorfenuron parent compound.

2. Analytical method. Two analytical methods, both based on high 

performance liquid chromatography (HPLC) procedures have been developed. 

The first method used a visible ultraviolet (UV) detector, while the second 

method used a mass spectrophotometer (MS) detector. Since the MS detector is 

capable of both qualitative as well as quantitative measurement, it is the preferred 

method. The level of quantification (LOQ) in all of the crops (i.e., almond, 

cherry, fig, pear, pistachio and plum/prune) is 0.01 ppm.
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3. Magnitude of residues. Ten field magnitude of residue trials with 

florchlorfenuron were conducted in five counties in California during the 2006 growing 

season. This included residue trials on sweet cherry, fig, pear, pistachio and plum/prune. 

In addition, three almond trials were conducted in three counties in California during the 

2005 and 2006 growing seasons. Applications on almonds were made at 11.4 grams 

a.i./A while applications on the other five crops were made at 10 grams a.i./A. 

Treatments were made with the shortest possible interval between application and harvest 

to maximize the residue level. All commodities were analyzed for parent compound. 

The validated limit of quantification (LOQ) for forchlorfenuron was set at 0.01 ppm. The 

limit of detection (LOD) was defined as 1/3 of the LOQ or 0.003 ppm for each matrix. 

Residues of forchlorfenuron were < LOQ (0.01 ppm) on all cherry, fig, pear, pistachio 

and plum/prune matrices. No residues of forchlorfenuron were found in the almond nut 

in shell samples (<0.01). Non-detectable to low levels of forchlorfenuron were found in 

almond hulls, with the highest level being 0.0841 ppm (0.0935 ppm corrected for 

concurrent mean procedural recovery). 

B. Toxicological Profile

1. Acute toxicity.

Acute toxicity endpoints for forchlorfenuron technical are as follows:

Guideline No./Study Type Results Toxicity Category

870.1100

Acute Oral – Rat

LD50 (mg/kg bw):

M = 4904; F = 4899; 

Combined = 4918

III

870.1200

Acute Dermal – Rabbit

LD50 (mg/kg bw):

M = >2000; F = 

>2000

III

870.1300

Acute Inhalation – Rat

LC50 (mg/L):

M = >3.0; F = >3.0

IV

870.2400

Primary Eye Irritation - Rabbit

Mild eye irritant III

870.2500

Primary Skin Irritation – Rabbit

Non-irritant IV

870.2600

Dermal Sensitization – Guinea 

Pig

Non-sensitizer N/A

2. Genotoxicty.

The genotoxic potential of forchlorfenuron was studied in vitro in bacteria and 

mammalian cells and in vivo in the unscheduled DNA synthesis test. The test 

systems assayed did not show any evidence of genotoxicity except in the 

bacterial mutagenicity assay, strain TA1535, without metabolic activation. 

The weight of evidence indicates that forchlorfenuron does not possess 
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significant genotoxicity concerns.

3. Reproductive	and	developmental	toxicity.

A developmental toxicity study was conducted with forchlorfenuron using rats 

gavaged with levels of 0, 100, 200 and 400 mg/kg/day. The maternal and 

developmental NOAELs were 200 mg/kg/day based on reduced body weights, 

body weight gain, food consumption, and an increased incidence of alopecia 

in dams. There were no developmental effects.

A developmental toxicity study was conducted with forchlorfenuron using 

rabbits gavaged with doses of 0, 25, 50 and 100 mg/kg/day. Maternal toxicity

(decreased body weight and body weight gains) were observed at 50 

mg/kg/day and above. The maternal NOAEL was 25 mg/kg/day and the 

developmental NOAEL was 100 mg/kg/day. There were no developmental 

effects.

A two generation reproduction study was conducted in rats in which 

forchlorfenuron was administered in the diet at levels of 0, 150, 2,000 and 

7,500 ppm. There were no adverse effects of forchlorfenuron on reproductive 

success. Parental toxicity consisted of clinical signs, inhibition of body

weight gain, reduced food consumption, and macroscopic and microscopic 

effects in the kidney. Reproductive toxicity in the highest dose consisted of 

slightly reduced live litter sizes in the F2 litters. In the pups, body weights and 

survival (late lactation period) were reduced and at the high dose, pup 

mortality and emaciation were increased. The parental, pup and reproductive 

NOAELs were 150 ppm, 150 ppm and 2,000 ppm, respectively.

4. Subchronic toxicity.

Forchlorfenuron was tested in rats in a 3-month study at 

dietary levels of 0, 200, 1,000 and 5,000 ppm Observations were decreased 

body weight, body weight gain and food efficiency. The NOAEL for males 

was 5,000 ppm (400 mg/kg/day) and in females was 1,000 ppm (84 

mg/kg/day).

Forchlorfenuron was tested in a 13-week dietary toxicity study in mice 

conducted at dose levels of 0, 900, 1,800, 3,500 and 7,000 ppm. Effects 

included decreased body weight and food consumption, increased relative 

liver weight and lymphocytic cell infiltration in the kidneys. The NOAEL 

was 3,500 ppm (609 mg/kg/day in males and 788 mg/kg/day in females).

A 13-week dietary toxicity study was conducted with forchlorfenuron in 

beagle dogs at dose levels of 0, 50, 500 and 5,000 ppm. Effects included 

decreased body weight gain, food consumption, and food efficiency. The 
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NOAEL for both sexes was 500 ppm (16.8 mg/kg/day in males and 19.1 

mg/kg/day in females).

5. Chronic toxicity.

In a 104-week combined chronic/oncogenicity study in rats, forchlorfenuron 

was administered in the diet at dose levels of 0, 150, 2,000 and 7,500 ppm. 

Findings were decreased body weight and body histopathological effects in 

the kidney. No oncogenicity was found. The NOAEL for this study was 150 

ppm (7 mg/kg/day in males and 9 mg/kg/day in females).

Forchlorfenuron was administered in the diet to mice for 78-weeks at dose 

levels of 0, 10, and 1,000 mg/kg/day. Observations were decreased body 

weight, body weight gain, food consumption, increased kidney weights and 

incidence of chronic kidney histopathological lesions. The NOAEL for both 

sexes was 10 mg/kg/day. No oncogenicity was found.

In a 12-month study, forchlorfenuron was administered in the diet given to 

dogs at dose levels of 0, 150, 3,000 and 7,500 ppm. Observations included 

reduced body weight, body weight gain, food consumption, and various 

hematology changes. The NOAEL for both sexes was 3,000 ppm (87 

mg/kg/day in males and 91 mg/kg/day in females).

6. Animal metabolism.

A rat metabolism study indicated that forchlorfenuron is almost completely

absorbed and most of the 14C-forchlorfenuron-derived radioactivity is rapidly

eliminated primarily via the urine. The majority of the metabolism of 

forchlorfenuron was via hydroxylation of the phenyl ring. The sulfate 

conjugate of the hydroxyl forchlrofenuron was the major metabolite excreted 

in the urine, accounting for as much as approximately 96% of the urinary

radioactivity. Tissue residues accounted for less than 1% of the administered 

dose at 168 hours post-dosing.

7. Metabolite toxicology. 

Metabolites occur at levels below 0.1 ppm and, therefore, are below levels 

required to be assayed in animal testing. Nevertheless, the toxicity of sulfate 

conjugate (and any other animal metabolites) was assessed during the conduct 

of the CPPU required mammalian toxicity studies.

8. Endocrine disruption. 

No special studies to investigate the potential for endocrine effects of 

forchlorfenuron have been performed. However, a large, detailed toxicology
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data base exists for the compound with studies in all required categories. 

Included are acute, sub-chronic, chronic, developmental and reproductive 

toxicology studies, with detailed histology and histopathology of numerous 

tissues, including endocrine organs, following repeated or long-term 

exposures. These studies are considered capable of revealing endocrine 

effects. The results of all of these studies show no evidence of any endocrinemediated effects and no pathology of the endocrine organs. Consequently, it 

is concluded that forchlorfenuron does not possess estrogenic or endocrine 

disrupting properties.

C. Aggregate Exposure

1. Dietary exposure.

A dietary exposure assessment was conducted looking at a number of crops 

including almond, fig, pear and prune (as well as apples, blueberries, grapes 

and kiwifruit). This assessment was conducted in connection with a previous 

EUP that was obtained for development of efficacy data on the above listed 

crops. The following information was published by EPA in FR, Vol. 69, No. 

67, pp. 18375-18380, 4/7/04. 

i. Food.

A reference dose (RfD) was calculated using the most sensitive species 

data available from the toxicological testing. The calculated RfD of 0.08 

mg/kg/day was used to calculate the impact of the estimated residue with 

results from treatment of the total acreage of all crops included in the prior 

EUP. Making the same risk exposure calculations, it was shown that there 

was no significant impact on reducing the RfD by using almonds, apples, 

blueberries, figs, grapes, kiwifruit, pears and plums in aggregate.

ii. Drinking water.

EPA stated the following in FR Vol. 73, No. 159, pp. 47841-47847, under 

“Forchlorfenuron; Permanent and Time-Limited Pesticide Tolerances” 

wherein EPA established permanent tolerances for residues of 

forchlorfenuron in or on bushberry subgroup 13-07B and time-limited 

tolerances under Petition No. 7F7246 for use on almond, cherry (sweet), 

fig, pear, pistachio and plum/prune (see FR pp. 47844); 

“The Agency used screening level water exposure models in the dietary

exposure analysis and risk assessment for forchlorfenuron in drinking 

water. Forchlorfenuron is persistent and moderately mobile in soils. 

Forchlorfenuron is also a substituted urea plant growth regulator that is

essentially stable to all routes of dissipation except sensitized

photodegradation in water. Based on the Pesticide Root Zone Model /
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Exposure Analysis Modeling System (PRZM/EXAMS) and Screening 

Concentration in Ground Water (SCI-GROW) models, the Estimated 

Environmental Concentrations (EECs) of forchlorfenuron from the newly

proposed use on bushberries and the uses on almonds, sweet cherries, figs,

pears, plums and pistachios under the EUP will not exceed the EECs from 

the grape and kiwi uses previously assessed by the Agency in document 

titled Drinking Water Assessment for Forchlorfenuron for Grape and Kiwi

Uses. Therefore, the Agency has incorporated the drinking water EEC

from the grape and kiwi analysis directly into this dietary assessment. For 

chronic dietary risk assessment, the water concentration of value 0.003 

ppb was used to assess the contribution to drinking water.”

2. Non-dietary exposure. 

EPA noted the following in FR Vol. 73, No. 159, 8/15/08 in the notice 

establishing the prior temporary tolerances under PP 7F7246 in almonds, 

sweet cherries, figs, pears, plums and pistachios in regard to non-dietary

exposure:

“The term ‘‘residential exposure’’ is used in this document to refer to nonoccupational, non-dietary exposure (e.g., for lawn and garden pest control,

indoor pest control, termiticides, and flea and tick control on pets). 

Forchlorfenuron is not registered for any specific use patterns that would

result in residential exposure.”

D. Cumulative Effects

EPA noted the following in FR Vol. 73, No. 159, 8/15/08 in the FR Notice 

establishing prior temporary tolerances under PP 7F7246 in almonds, sweet 

cherries, figs, pears, plums and pistachios in regard to cumulative effects:

“Section 408(b)(2)(D)(v) of FFDCA requires that, when considering 

whether to establish, modify, or revoke a tolerance, the Agency consider

‘‘available information’’ concerning the cumulative effects of a particular

pesticide’s residues and ‘‘other substances that have a common

mechanism of toxicity.’’ EPA has not made a common mechanism of 

toxicity finding as to forchlorfenuron and any other substances and 

forchlorfenuron does not appear to produce a toxic metabolite produced by 

other substances. For the purposes of this tolerance action, therefore, EPA 

has not assumed that forchlorfenuron has a common mechanism of 

toxicity with other substances.”

E. Safety Determination
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EPA noted the following in FR Vol. 73, No. 159, 8/15/08 in the notice 

establishing prior temporary tolerances under PP 7F7246 in almond, sweet cherry, 

fig, pear, pistachio and plum/prune relative to the Agency’s conclusions regarding 

the safety of the proposed uses under the proposed temporary tolerances for 

forchlorfenuron (which are the same tolerance levels proposed in this Petition):

“EPA has determined that reliable data show the safety of infants and children 

would be adequately protected if the FQPA SF were reduced to 1X. That decision 

is based on the following findings:

i. The toxicity database for forchlorfenuron is complete.

ii. There is no indication that forchlorfenuron is a neurotoxic chemical and 

there is no need for a developmental neurotoxicity study or additional UFs 

to account for neurotoxicity.

iii. There is no evidence that forchlorfenuron results in increased

susceptibility in in 

utero rats or rabbits in the prenatal developmental studies or in young rats 

in the 2–generation reproduction study. 

iv. There are no residual uncertainties identified in the exposure databases. 

EPA made conservative (protective) assumptions in the ground and 

surface water modeling used to assess exposure to forchlorfenuron in 

drinking water. EPA used similarly conservative assumptions to assess 

exposure to forchlorfenuron residues in food. These assessments will not 

underestimate the exposure and risks posed by forchlorfenuron.

EPA determines whether acute and chronic pesticide exposures are safe by

comparing aggregate exposure estimates to the aPAD and cPAD. The 

aPAD and cPAD represent the highest safe exposures, taking into account 

all appropriate SFs. EPA calculates the aPAD and cPAD by dividing the 

POD by all applicable UFs. For linear cancer risks, EPA calculates the 

probability of additional cancer cases given the estimated aggregate 

exposure. Short-term, intermediate-term, and chronic-term risks are 

evaluated by comparing the estimated aggregate food, water, and

residential exposure to the POD to ensure that the margin of exposure

(MOE) called for by the product of all applicable UFs is not exceeded.

1. Acute risk. An acute aggregate risk assessment takes into account 

exposure estimates from acute dietary consumption of food and drinking

water. No adverse effect resulting from a single-oral exposure was 

identified and no acute dietary endpoint was selected. Therefore, 

forchlorfenuron is not expected to pose an acute risk.

2. Chronic risk. Using the exposure assumptions described in this unit for

chronic exposure, EPA has concluded that chronic exposure to

forchlorfenuron from food and water will utilize <1% of the cPAD for the

general U.S. population and all subpopulations. There are no residential

uses for forchlorfenuron.
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3. Short-term and intermediate-term risk. Short-term and Intermediateterm aggregate exposure takes into account short-term and intermediateterm residential exposure plus chronic exposure to food and water 

(considered to be a background exposure level). Forchlorfenuron is not 

registered for any use patterns that would result in short-term and 

intermediate-term residential exposure. Therefore, the short-term and 

intermediate-term aggregate risk, individually is the sum of the risk from 

exposure to forchlorfenuron through food and water, which has already

been addressed, and will not be greater than the chronic aggregate risk.

4. Aggregate cancer risk for U.S. population. Since forchlorfenuron has

been classified as not likely to be carcinogenic, aggregate cancer risk is

not a concern.

5. Determination of safety-U.S. population and Infants & Children. Based 

on these risk assessments, EPA concludes that there is a reasonable 

certainty that no harm will result to the general population or to infants 

and children from aggregate exposure to

forchlorfenuron residues.

F. International Tolerances

The following international tolerances exist for forchlorfenuron:

Australia: An MRL of 0.01 ppm has been established for grapes and as a 

temporary MRL level for blueberries, mango and plum/prune.

European Union: Forchlorfenuron MRLs are set for table grapes and kiwifruit at 

0.05 ppm. However, a new EU MRL of 0.01 ppm is proposed because sufficient 

trials are available showing residues below 0.01 ppm

Israel: An MRL of 0.01 ppm has been established for table grapes, wine grapes 

and kiwifruit.

Japan: An MRL of 0.01 has been set for almonds.

Mexico: Has deferred to the U.S. Tolerances. Therefore, all forchlorfenuron 

tolerances established in the U.S. apply to Mexico.