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EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR 

PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER 

EPA Registration Division contact: [Richard Gebkin, (703) 305-6701]

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., “[insert 

company name],” with the information specific to your action.

TEMPLATE:

Gowan Company

[Insert petition number]

EPA has received a pesticide petition ([insert petition number]) from Gowan

Company, LLC, P.O. Box 556 Yuma, AZ 85366 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.

(Options (pick one)

1. by establishing a tolerance for residues of

Fenazaquin, [3-[2-[4-(1,1-dimethylethyl) phenyl] ethoxy] quinazoline] 

in or on the raw agricultural commodity for Tree Nut crop group 14-12 at 0.02 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. Apple metabolism work (MRID 45029914) demonstrates

that TRR are reduced to less than 25% of their original value at 70 DAT after a late 

season treatment and are reduced to between 1 - 4% of their original value at 105 

DAT after an early season application. Virtually all of the TRR at 0 DAT is solvent 

washable fenazaquin on the surface of the apples. At 70 DAT identified parent

fenazaquin is less than 35% TRR. At 105 DAT, 12 - 21% TRR was identified as 

parent fenazaquin. At harvest, fenazaquin is the predominant residue in apples with 

smaller amounts of other metabolites. 
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2. Analytical method. The basic analytical method was previously reviewed by

the Agency in association with the establishment of the current tolerances with 

registrations of multiple commodities. Residues of fenazaquin are extracted from 

the sample matrices by blending with acetonitrile. An aliquot is transferred to a 

separatory funnel and partitioned between water and methylene chloride. A 10% 

portion of the methylene chloride layer is evaporated and the residue is 

reconstituted in acetonitrile for instrumental analysis by LC/MS/MS with positiveion electrospray ionization tandem mass spectrometry. The method had a Limit of 

Quantitation of 0.01 ppm and a Limit of Detection of 0.003 ppm. 

3. Magnitude of residues. Residues of fenazaquin ranged from not detected to 0.02

ppm in tree nuts. The Agency previously reviewed residue data and concluded the 

following: 

Trials were conducted with the representative commodities pecan (5 trials) and 

almonds (5 trials). The pecan data yielded a tolerance estimate of 0.02 ppm, and the 

almond data yielded a tolerance estimate of 0.015 ppm. The higher value, 0.02 ppm, 

was used as the tolerance for the tree nuts group.

Trial samples (5) were also analyzed for almond hulls, and the tolerance estimate is 4 

ppm. 

B. Toxicological Profile

1. Acute toxicity. EPA has reviewed the acute toxicity database and has

determined that fenazaquin belongs in Category II for oral toxicity; Category III for 

both inhalation exposure and eye irritation; and Category IV for dermal exposure 

and skin irritation.

2. Genotoxicity. A number of mutagenicity studies were conducted. The

genotoxic database is complete. All test results for genotoxicity with fenazaquin have 

been negative.

3. Reproductive and developmental toxicity. In rat and rabbit developmental

toxicity studies, no evidence of increased quantitative or qualitative susceptibility

exists following in utero exposure to fenazaquin. There are no qualitative or 

quantitative pre-natal susceptibility issues and no residual uncertainties in the rat

two-generation reproduction study.

4. Subchronic toxicity. The major findings following repeated oral

administration in rats, hamsters and dogs were decreases in body weight, body 

weight gain, food intake, and food efficiency. The lowest NOAEL observed during

these studies was 5 mg/kg/day in a 90-day feeding study in dogs.

5. Chronic toxicity. At the doses used in chronic toxicity studies (up to 35
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mg/kg/day), there were no organ specific toxicity findings. Effects on body weight 

and weight gain and food intake efficiency were identified in parental animals of the

rat developmental and reproduction studies and in the offspring of the reproduction

rat study. There were no developmental findings in the rat study (up to 40 mg/kg) 

and no parental or developmental findings of any kind up to 60 mg/kg/day in the

rabbit developmental study.

The EPA Health Effects Division Cancer Assessment Review Committee reviewed

the carcinogenicity study in hamsters, as well as the carcinogenicity study conducted

in rats, the mutagenicity studies, and discussed the possible carcinogenic mode of

action of fenazaquin. Based on the weight of evidence of these studies, and in

accordance with the 2005 Guidelines for Carcinogen Risk Assessment, the members

concluded that the negative hamster findings along with the negative tumor findings

in the 24-month rat study and negative mutagenicity findings support a cancer

classification of "Not likely to Be Carcinogenic to Humans" for fenazaquin. 

6. Animal metabolism. In rat, goat and hen metabolism studies, orally

administered fenazaquin was quickly excreted in the feces. Excretion of the dose

was rapid with no accumulation or apparent target organ. The metabolites found 

were the result of oxidation or hydrolysis. A new hen study demonstrates

metabolism similar to rats and goats. 

7. Metabolite toxicology. No toxic metabolites were detected in any

metabolism study.

8. Endocrine disruption. There is no evidence of endocrine disruptor effects in

the fenazaquin database.

C. Aggregate Exposure

1. Dietary exposure. Dietary Exposure from food. A dietary risk assessment

for all registered crops has been completed by the Agency (Federal Register, May 6, 

2015, pages 25952-25958).

i. Food. Acute Exposure. The acute dietary exposure risk estimate utilizes

2.77% (0.004156 mg/kg/day) of the acute population-adjusted dose (aPAD) for the 

U.S. population at the 95th percentile of exposure. The most highly-exposed 

population subgroup was children 1 to 2 years old which utilized 9.64% (0.014463 

mg/kg/day) of the aPAD at the 95th percentile of exposure. 

Chronic Exposure. The proposed tolerances for fenazaquin in tree nut crop group

will not add to dietary risk. Chronic dietary exposures to registered and proposed 

crops range from 0.000658 mg/kg/day (1.3% of cPAD) for adults 20 – 49 years to 

0.004253 (8.5% of cPAD) for children aged 1-2 years old, the most highly-exposed 

population subgroup. Chronic dietary exposure for the U.S. population is estimated 

to be 0.000995 mg/kg/d (2.0% of cPAD). Thus, chronic dietary exposure to 

fenazaquin for all population subgroups is not of concern.
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ii. Drinking water. The Agency has previously used screening level surface

water exposure models in dietary exposure analysis and risk assessment for 

fenazaquin in drinking water. Based on the Pesticide Root Zone Model /Exposure 

Analysis Modeling System (PRZM/EXAMS), the estimated drinking water 

concentration (EDWC) of fenazaquin for acute and chronic exposures were 

estimated to be 5.74 parts per billion (ppb). (Federal Register, May 6, 2015, pages 

25952-25958). 

2. Non-dietary exposure. EPA has previously assessed residential exposure.

Since there is no residential incidental oral exposure expected for children 1<2 years 

old on ornamental plants, a post-application exposure assessment was not 

conducted. The inhalation exposure assessment performed for residential handlers 

is representative of worst-case inhalation exposure and is considered protective for 

post-application inhalation scenarios. 

D. Cumulative Effects

EPA has not found fenazaquin to share a common mechanism of toxicity 

with any other substances, and fenazaquin does not appear to produce a toxic 

metabolite produced by other substances. 

E. Safety Determination

1. U.S. population. Acute risk. Total acute dietary exposure to the US

population from the proposed food uses is 0.020052 mg/kg/day, representing 13.37% 

of the acute reference dose. 

Short-and intermediate term risk. Short-term aggregate exposure takes into account 

short-term residential exposure plus chronic exposure to food and water (considered 

to be a background exposure level). Fenazaquin is currently registered for uses that 

could result in short-term residential exposure, and the Agency has determined that 

it is appropriate to aggregate chronic exposure through food and water with shortterm residential exposures to fenazaquin. 

Chronic risk. The total chronic exposure to the US population was 0.000995 

mg/kg/day, representing 2.0% of the chronic reference dose. 

2. Infants and children. EPA previously has determined that reliable data

show the safety of infants and children would be adequately protected if the FQPA 

SF were reduced to 1X. The highest risks calculated for any pre-teen dietary 

subgroup were 23.03% of the acute reference dose for children 1-2 years old and 

6.6% of the chronic reference dose for the same subpopulation. 

F. International Tolerances 

The Codex has not established a MRL for fenazaquin.