I Fenoxaprop-p-ethyl Human Health Risk Assessment DP No. 403928 and 411289 

UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON, D.C. 20460 

MEMORANDUM 

Date: March 20, 2014 

OFFICE OF 

CHEMICAL SAFETY AND 

POLLUTION PREVENTION 

SUBJECT: Fenoxaprop-p-ethyl. Registration Review Preliminary Risk Assessment and 

Proposed New Use on Grass Grown for Seed. 

PC Code: 129092 DP Barcode: D403928 and D411289 

Decision No.: 477911; 466648 Registration No.: 264-666 

Petition No.: 2E8051 Regulatory Action: Registration Review and New Use 

Assessment 

Risk Assessment Type: Risk Assessment 

TXRNo.: NA 

CaseNo.: NA 

CAS No.: 66441-23-4 

MRIDNo.: NA 40 CFR: 180.430 

FROM: Shalu Shelat, Industrial Hygienist 

Christopher Schlosser, Toxicologist 

Donald Wilbur, Chemist 

Risk Assessment Branch VI 

Health Effects Division (7509P) 

THROUGH: Donna S. Davis, Acting Branch Chief 

Risk Assessment Branch VI 

TO: 

Health Effects Division (7509P) 

Andrew Ertman/ Barbara Madden, Risk Managers 

Risk Integration Minor Use, and Emergency Response Branch 

Registration Division (7505P) 

And 

Molly Clayton, Chemical Review Manager 

Risk Management and Implementation Branch III 

Pesticide Re-evaluation Division (7508P) 

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Introduction

The Health Effects Division (HED) of the Office of Pesticide Programs (OPP) is charged with 

estimating the risk to human health from exposure to pesticides. Fenoxaprop-p-ethyl (FPE) is 

currently registered for use on barley, cotton, rice, soybeans, and wheat. FPE is also registered 

for non-agricultural use on conservation reserve lands, ornamentals, rights-of-way, and turf. The 

Interregional Research Project No. 4 (IR-4) has submitted a petition requesting a new use on 

grass grown for seed in the states of Oregon, Washington, and Utah only. The Registration 

Division (RD) of OPP has requested that HED evaluate the hazard and exposure data and 

conduct dietary, residential, occupational, and aggregate exposure assessments, as needed, to 

estimate the risk to human health that will result from the existing and newly proposed use of 

FPE. The Pesticide Re-evaluation Division has also requested that an assessment be drafted in 

support of registration review of the currently registered uses of FPE. This document has been 

developed to assess both the new use as well as in support of registration review for FPE.

HED has evaluated the toxicity and exposure databases for FPE and has conducted a human 

health risk assessment which is provided in this document. Based on this assessment, HED has 

determined that there are no potential risk estimates of concern for the proposed use and 

currently registered uses of FPE with the addition of PPE (i.e., chemical-resistant gloves).

The HED team members contributing to this risk assessment include Donald Wilbur (residue 

chemistry and dietary exposure assessment), Shalu Shelat (occupational and residential exposure 

assessments and risk assessment), and Christopher Schlosser (hazard assessment). Chuck Peck 

of the Environmental Fate and Effects Division (EFED) performed the drinking water 

assessment.
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Table of Contents

1.0 Executive Summary............................................................................................................. 5

2.0 HED Recommendations....................................................................................................... 8

2.1 Data Deficiencies ............................................................................................................. 8

2.2 Tolerance Considerations................................................................................................. 8

2.2.1 Enforcement Analytical Method............................................................................... 8

2.2.2 Established Tolerances.............................................................................................. 9

2.2.2.1 Revisions to Established Tolerances................................................................... 10

2.2.3 Petitioned-For Tolerances....................................................................................... 10

2.2.3.1 Revisions to Petitioned-For Tolerances .............................................................. 10

2.2.4 International Harmonization ................................................................................... 11

2.3 Label Recommendations................................................................................................ 11

2.3.1 Recommendations from Residue Reviews ............................................................. 11

2.3.2 Recommendations from Occupational Assessment................................................ 11

2.3.3 Recommendations from Residential Assessment ................................................... 11

3.0 Introduction........................................................................................................................ 11

3.1 Chemical Identity ........................................................................................................... 11

3.2 Physical/Chemical Characteristics................................................................................. 12

3.3 Pesticide Use Pattern...................................................................................................... 13

3.4 Anticipated Exposure Pathways..................................................................................... 15

3.5 Consideration of Environmental Justice ........................................................................ 15

3.6 Incident Reports ............................................................................................................. 15

4.0 Hazard Characterization and Dose-Response Assessment................................................ 16

4.1 Toxicology Studies Available for Analysis ................................................................... 16

4.2 Absorption, Distribution, Metabolism, & Elimination (ADME)................................... 17

4.2.1 Dermal Absorption.................................................................................................. 17

4.3 Toxicological Effects ..................................................................................................... 17

4.4 Safety Factor for Infants and Children (FQPA Safety Factor)....................................... 18

4.4.1 Completeness of the Toxicology Database............................................................. 19

4.4.2 Evidence of Neurotoxicity ...................................................................................... 19

4.4.3 Evidence of Sensitivity/Susceptibility in the Developing or Young Animal ......... 19

4.4.4 Residual Uncertainty in the Exposure Database..................................................... 19

4.5 Toxicity Endpoint and Point of Departure Selections.................................................... 20

4.5.1 Dose-Response Assessment.................................................................................... 20

4.5.2 Recommendation for Combining Routes of Exposures for Risk Assessment........ 22

4.5.3 Cancer Classification and Risk Assessment Recommendation.............................. 22

4.5.4 Summary of Points of Departure and Toxicity Endpoints Used in Human Risk 

Assessment............................................................................................................................ 23

4.6 Endocrine Disruption ..................................................................................................... 24

5.0 Dietary Exposure and Risk Assessment ............................................................................ 25

5.1 Metabolite/Degradate Residue Profile ........................................................................... 25

5.1.1 Summary of Plant and Animal Metabolism Studies............................................... 25

5.1.2 Summary of Environmental Degradation ............................................................... 26

5.1.3 Comparison of Metabolic Pathways....................................................................... 26

5.1.4 Residues of Concern Summary............................................................................... 27
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5.2 Food Residue Profile...................................................................................................... 27

5.3 Water Residue Profile .................................................................................................... 28

5.4 Dietary Risk Assessment................................................................................................ 29

5.4.1 Description of Residue Data Used in Dietary Assessment..................................... 29

5.4.2 Acute Dietary Risk Assessment.............................................................................. 29

5.4.3 Chronic Dietary Risk Assessment .......................................................................... 29

5.4.4 Summary Table....................................................................................................... 30

6.0 Residential (Non-Occupational) Exposure/Risk Characterization .................................... 30

6.1 Residential Handler Exposure........................................................................................ 30

6.2 Post-Application Exposure............................................................................................. 33

6.3 Combined Residential Risk Estimates (Multiple Exposure Scenarios) ......................... 34

6.4 Residential Risk Estimates for Use in Aggregate Assessment ...................................... 35

6.5 Residential Bystander Post-application Inhalation Exposure ........................................ 36

6.6 Spray Drift...................................................................................................................... 36

7.0 Aggregate Exposure/Risk Characterization....................................................................... 37

7.1 Acute Aggregate Risk .................................................................................................... 37

7.2 Short-Term Aggregate Risk ........................................................................................... 37

7.3 Chronic Aggregate Risk................................................................................................. 38

8.0 Cumulative Exposure/Risk Characterization..................................................................... 38

9.0 Occupational Exposure/Risk Characterization .................................................................. 38

9.1 Short- and Intermediate-term Handler Risk................................................................... 38

9.2 Short- and Intermediate-term Post-Application Risk..................................................... 47

9.2.1 Dermal Post-application Risk ................................................................................. 47

9.2.2 Inhalation Post-application Risk............................................................................. 49

10.0 References.......................................................................................................................... 49

Appendix A. Toxicology Profile and Executive Summaries....................................................... 51

Appendix B. International Residue Limits Table ..................................................................... 78

Appendix C. Spray Drift Summary Tables.................................................................................. 80
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1.0 Executive Summary

Fenoxaprop-p-ethyl [FPE; (+)-ethyl 2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoate] is 

a selective aryloxy phenoxy-propionate herbicide used to control grass weeds after emergence. 

FPE is an enriched isomer formulation (95% d, the herbicidally active enantiomer). Originally, 

the product was registered as racemic mixture known as fenoxaprop ethyl (FE, PC Code 

128701). FE is no longer a registered active ingredient. FPE is currently registered for use on 

barley, cotton, rice, soybeans, and wheat. FPE is also registered for non-agricultural use on 

conservation reserves, ornamentals, rights-of-way, and turf. The Interregional Research Project 

No. 4 (IR-4) has submitted a petition requesting a new use on grass grown for seed in the states 

of Oregon, Washington, and Utah only. This document is being drafted in support of registration 

review of FPE as well as the assessment of the new use on grass grown for seed.

The toxicology database for FPE is complete based on studies submitted for both FPE and FE. 

Based on the analysis of the submitted studies, HED found that the toxicological effects of FE 

and FPE across species, duration, and route of exposure are similar. Most of the toxicological 

data available involved testing of the FE, not FPE. However, HED has concluded that the 

similarity between the FE and FPE data is such that the database for FE could be bridged with 

FPE. Acute and subchronic neurotoxicity studies were not available; however, HED’s Hazard 

and Science Policy Council (HASPOC) determined that the studies may be waived.

The major target organs following short-term and long-term oral administration of FE and FPE 

in rats and mice are the liver and kidneys, with rats being the most sensitive species. The primary 

toxic effect is altered lipid metabolism characterized by decreased lipids and cholesterol, and 

increased liver weights in rats, and slightly increased lipids, cholesterol, proteins, and liver 

weights in mice. It is also important to note that no increases in toxicity are observed over time 

for FE when comparing the 28-day and 90-day subchronic studies, the 2-generation reproductive 

toxicity study, and the 2-year chronic toxicity/carcinogenicity study in rats, or in FPE when 

comparing the 28-day and 90-day subchronic toxicity studies in rats. 

FPE has low acute toxicity following the oral, dermal, and inhalation routes of exposure. No 

evidence of Immunotoxicity, reproductive, or neurological toxicity was identified in the 

database. No developmental effects were identified in rabbits. In mice, a treatment-related 

increase in tumor incidence of hepatocellular adenomas and carcinomas, mainly adenomas, was 

observed in males at 320 ppm (30%) compared to the control (2%). Although a treatmentrelated increase in tumor incidence of hepatocellular adenomas and carcinomas, mainly 

adenomas, was observed in male mice and microscopic pathology indicated that hepatocellular 

hypertrophy was observed in the majority of treated animals (both sexes), there was no evidence 

of a mutagenic effect in a comprehensive battery of genetic toxicology assays with both isomers. 

No evidence of tumors was identified in rats. In accordance with EPA’s Final Guidelines for 

Carcinogen Risk Assessment (2005), CARC classified FE/FPE as “Suggestive Evidence of 

Carcinogenic Potential”. 

For short-term incidental oral exposure (1-30 days), a 28-day oral toxicity study in rats with a no 

observed adverse effect level (NOAEL) of 6 mg/kg/day was selected based on altered lipid 

metabolism (decreased HDL-cholesterol, HDL-phospholipids, and total lipids, increased 
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triglycerides, and ketonuria) and increased liver and kidney weights at the study the Lowest 

Observed Adverse Effect Level (LOAEL) of 26/28 (M/F) mg/kg/day. 

For short and intermediate-term dermal exposure, a 28-day dermal toxicity study in rats with a 

NOAEL of 20 mg/kg/day was selected (FPE) based on non-regenerative anemia, decreased 

serum cholesterol, total lipids, and protein (beta 1 globulins), and increased liver and kidney 

weights seen at the study LOAEL of 100 mg/kg/day. There is no long-term exposure from 

existing or proposed uses; therefore, a risk assessment for long-term dermal exposure is not 

required. 

For short and intermediate-term inhalation exposure, a 28-day inhalation toxicity study in rats 

with a NOAEL of 0.07 mg/L was selected (FPE). In the study, the LOAEL is 0.3 mg/L (M) 

based on slight normocytic anemia, decreases in serum cholesterol and total lipids, and increases 

in liver and kidney weights and urea nitrogen. An inhalation study was used therefore the 

resulting human equivalent concentrations (HECs) are 0.14 mg/L and 0.57 mg/L, respectively.

There is no long-term exposure from existing or proposed uses; therefore, a risk assessment for 

long-term inhalation exposure is not required. 

No acute reference dose (aRfD) was established to assess acute dietary risks since there was no 

evidence of toxicity attributable to a single dose for the general U.S. population, infants and 

children, or females 13-49 years of age in any studies. For the chronic dietary risk assessment, a 

chronic reference dose (cRfD) of 0.015 mg/kg/day was established for assessments of all 

populations, with a NOAEL of 1.5 mg/kg/day and a LOAEL of 9 mg/kg/day based on decreased 

serum lipids and cholesterol, and changes in liver weights. 

For acute and chronic dietary, incidental oral and dermal risk assessments, a 100X uncertainty 

factor is applied (interspecies factor of 10X and intraspecies factor of 10X). For inhalation risk 

assessment, a 30X uncertainty factor is applied, which includes interspecies (3X) and 

intraspecies (10X) extrapolation. The interspecies factor was reduced from l0Xto 3X due to the 

HEC calculation accounting for pharmacokinetic (not pharmacodynamic) interspecies 

differences

The risk assessments conducted for FPE were based on the most sensitive endpoints in the 

toxicity database, and the NOAELs selected for risk assessment are considered protective of 

potential developmental, neurotoxic, and immunotoxic effects for infants and children. There is 

no evidence of increased qualitative or quantitative susceptibility in the rat 2-generation 

reproduction study or the rat and rabbit developmental studies. There is no evidence of 

neurotoxicity in any of the submitted studies for FPE. There is also no residual uncertainty in the 

exposure database. Therefore, reduction of the 10X FQPA safety factor to 1X is considered 

appropriate.

The residue chemistry database is considered complete for FPE for the purposes of the proposed 

use as well as for registration review. The nature and magnitude of the residue in plants has been 

adequately delineated. The residue of concern in plants and livestock consists of fenoxapropethyl, its free acid metabolite, and 6-chloro-2,3-- dihydrobenzoxazol-2-one. No FPE residues are 

expected in poultry livestock commodities based on the submitted ruminant metabolism study 

and the calculated dietary burden. The requirements for residue analytical methods are fulfilled 
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for the purposes of the proposed use as well as for registration review. Adequate methods are 

available for tolerance enforcement and data collection purposes for plant and animal 

commodities. The enforcement methods are not stereo-specific and cannot differentiate between 

FE and FPE (i.e., cannot distinguish the level of enrichment of the d enantiomer).

Since an acute reference dose was not selected for FPE, the Agency conducted only a chronic 

dietary (food and drinking water) exposure and risk assessment. This assessment was conducted 

using tolerance level residues, 100% crop treated, and DEEMTM default processing factors. 

Using assumptions considered to be highly conservative, the chronic dietary risk estimates are 

below HED’s level of concern (<100% of the chronic population adjusted dose (cPAD)), and 

range from 8.9% of the cPAD for youth 13-19 years old to 27.5% of the cPAD for the highest 

exposed population subgroup of all infants < 1 years old.

The registered uses of FPE on ornamentals and turf may result in adult residential handler and 

post-application exposure. This exposure is expected to be only short-term in duration (i.e., 1 to 

30 days) as intermediate- or long-term exposures are not likely based on the intermittent nature 

of applications by homeowners. These assessments were conducted according to HED’s 2012 

Residential Standard Operating Procedures (SOPs). All route specific (dermal and inhalation) 

exposure scenarios do not exceed HED’s level of concern (LOC) (MOEs ≥ 100 for dermal and 

MOEs ≥ 30 for inhalation) and all combined dermal and inhalation exposure scenarios for 

handlers result in aggregate risk index (ARI) values that are ≥ 1. ARI values were used to 

illustrate the combined exposures because the inhalation and dermal exposures have different 

LOCs. For residential post-application exposure, there are no risk estimates of concern 

identified for the dermal or incidental oral routes of exposure (all MOEs ≥ 100) from turf or 

ornamental use sites. Inhalation post-application exposure is not assessed for the registered use 

scenarios. 

A non-occupational spray drift assessment was conducted for FPE based on the highest 

agricultural application rate currently registered (0.173 lbs ai/acre for use on sod farms). The 

edge of field adult dermal and children (1 to < 2 years) dermal and incidental oral MOEs do not 

exceed HED’s level of concern (MOEs ≥ 100). 

Since there are no acute points of departure identified, an acute aggregate risk assessment was 

not conducted. HED has conducted short-term and long-term (chronic) aggregate risk 

assessments for FPE. The short-term aggregate assessment includes residential post-application 

and dietary (food and water) exposures. Short-term aggregate MOEs do not exceed HED’s level 

of concern (MOEs ≥ 100). The long-term (chronic) aggregate assessment includes only dietary 

(food and water) exposure as long-term residential exposure is not expected. Chronic dietary 

risk is not of concern. 

Occupational handler risks were assessed for the inhalation and dermal route of exposure. All 

estimated short- and intermediate-term handler combined (dermal and inhalation) risk estimates 

do not exceed HED’s level of concern (ARIs ≥ 1) with the use of chemical resistant gloves. 

Similarly, the short- and intermediate-term post-application dermal risk estimates ranging from 

220 to 12,000 do not exceed HED’s of concern (MOEs ≥100) on the day of treatment (i.e., Day 

0) for all of the post-application exposure activities. Based on the Agency's current practices, a 
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quantitative occupational post-application inhalation exposure assessment was not performed for 

FPE at this time. 

This risk assessment relies, in part, on data from studies in which adult human subjects were 

intentionally exposed to a pesticide or other chemical. These data, which include the Pesticide 

Handlers Exposure Database Version 1.1 (PHED 1.1); the Agricultural Handler Exposure Task 

Force (AHETF) database; the Outdoor Residential Exposure Task Force (ORETF) database; the 

Agricultural Re-entry Task Force (ARTF) database; and the Residential SOPs (Handler, Turf, 

and Gardens SOP) are subject to ethics review pursuant to 40 CFR 26, have received that review, 

and are compliant with applicable ethics requirements. For certain studies that review may have 

included review by the Human Studies Review Board.

2.0 HED Recommendations

There are no recommendations based on the toxicological database.

HED has examined the residue chemistry database for FPE. Pending submission of a revised 

Section F (see requirements under Revisions to Petitioned-For Tolerances below) there are no 

residue chemistry issues that would preclude the establishment of a tolerance with regional 

restriction on grass, hay. Additionally, all regulatory requirements related to residue chemistry 

for FPE are considered adequate for registration review.

HED recommends that all registered and proposed occupational use labels contain chemicalresistant gloves for handler exposure activities.

2.1 Data Deficiencies

There are no data deficiencies relating to toxicology, residue chemistry, or occupational exposure

associated with this action. 

2.2 Tolerance Considerations

2.2.1 Enforcement Analytical Method

An adequate analytical method is available to enforce tolerances for FE in plant and animal 

commodities. A gas chromatography with electron capture detection (GD-ECD) method, based 

on Hoechst HRAV Analytical Method HRAV-4B, was previously reviewed by the Agency and 

was incorporated into the Food and Drug Administration (FDA) Pesticide Analytical Manual, 

Volume II (PAM II). The method has a limit of quantitation (LOQ) of 0.05 ppm in all matrix 

types. HED notes that his method is not stereospecific, and therefore, does not distinguish 

between residues of FE and FPE in foods. 

The method is described as follows. Briefly, samples are refluxed with a solution of acetonitrile, 

concentrated HCl, and water for 6 hours and filtered through filer paper. An aliquot is 

transferred onto an Extrelut column and equilibrated with the column matrix. The hydrolysis 

product 6-chlorobenzoxazolone is eluted with hexane: diethyl ether and evaporated to dryness. 
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The residue is dissolved with ethyl acetate and the ethyl acetate evaporated to dryness. The 

residue is then derivatized in a mixture of toluene, acetic anhydride, and pyridine for 2 hours at 

130° C. The residue with reaction product acyl 6-chlorobenzoxazolone (AE F083312) is dried, 

and cleaned up on a silica gel SPE cartridge. FE and its metabolites are then determined as 

6-chlorobenzoxazolone (AE F083312) by GC-ECD. Total residue is then expressed as FE 

equivalents.

FE has also been subjected to analysis by the Food and Drug Administration (FDA) multiresidue method (MRM) protocols. Multi-residue methods are available for residues of FE and 

the metabolites of concern under Protocols 1 through 4.

2.2.2 Established Tolerances

FPE is an enriched isomer formulation (95% d, the herbicidally active enantiomer). Originally, 

the product was registered as racemic mixture known as FE. Tolerances were at that time 

established under 40CFR 180.30 for FE, and the tolerance expression included both enantiomers 

(d and l) with no ratio specified. Therefore, since both enantiomers are included in the tolerance

expression and the data-collection and tolerance enforcement methods are not stereo-specific and 

cannot differentiate between FE and FPE (i.e., cannot distinguish the level of enrichment of the d

enantiomer), the previously established tolerances for FE are adequate to cover residues from the 

application of FPE. For this reason, any discussion of tolerances with respect to FPE is 

described in terms of FE in this document.

Currently there are tolerances established for residues of FE as listed in Table 2.2.2 below. The 

tolerance expression for FE is as follows:

Compliance with the tolerance levels specified is to be determined by measuring only the sum of 

fenoxaprop-ethyl, (±)-ethyl 2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoate, and its 

metabolites, 2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoic acid and 6-chloro-2,3-

dihydrobenzoxazol-2-one, calculated as the stoichiometric equivalent of fenoxaprop-ethyl.

Table 2.2.2. Tolerance Summary for Fenoxaprop-ethyl

Commodity Tolerance (ppm) Comments

Correct Commodity Definition

180.430 (a) General

Barley, grain 0.05

Barley, straw 0.1

Cattle, fat 0.05

Cattle, meat byproducts 0.05

Cattle, meat 0.05

Cotton, undelinted seed 0.05

Goat, fat 0.05

Goat, meat byproducts 0.05

Goat, meat 0.05

Hog, fat 0.05

Hog, meat byproducts 0.05

Hog, meat 0.05

Horse, fat 0.05
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Table 2.2.2. Tolerance Summary for Fenoxaprop-ethyl

Commodity Tolerance (ppm) Comments

Correct Commodity Definition

Horse, meat byproducts 0.05

Horse, meat 0.05

Milk 0.02

Peanut 0.05

Peanut, hulls 0.05 Revoke, no longer a regulated 

commodity

Rice, grain 0.05

Sheep, fat 0.05

Sheep, meat byproducts 0.05

Sheep, meat 0.05

Soybean 0.05 Soybean, seed

Wheat, grain 0.05

Wheat, straw 0.05

180.430 (b) Section 18 emergency exemptions

Grass, forage 0.05 Expires 12/31/2013

Grass, hay 0.05 Expires 12/31/2013

2.2.2.1 Revisions to Established Tolerances

HED is recommending that certain existing tolerances be amended to reflect current polices. 

The commodity definition for soybean should be changed from soybean to soybean, seed. 

Additionally, the tolerance on peanut, hulls may be revoked since that commodity is no longer a 

regulated raw agricultural commodity (RAC).

2.2.3 Petitioned-For Tolerances

For the purposes of this petition, tolerances for residues of FE in/on grass, hay were not derived 

using the Organization for Economic Cooperation and Development Maximum Residue Level 

(OECD MRL) Calculation Procedures since all of the residue values were less than the limit of 

quantification (<LOQ) of the analytical method. 

Table 2.2.3 Proposed Tolerance Summary for FE

Commodity Proposed 

Tolerance 

(ppm)

HED-Recommended 

Tolerance (ppm)

Comments 

180.430 (c) Tolerances with regional restrictions

Grass, hay 0.15 0.09 For the states of WA, OR, and 

UT only

2.2.3.1 Revisions to Petitioned-For Tolerances

HED is recommending that a tolerance with regional restriction be set for grass, hay as requested 

by the petitioner with the change noted below. The method used for data-collection (as well as 

tolerance enforcement) converts the residues of concern for FE to acyl 6-chlorobenzoxazolone 

for detection. It is necessary to then convert this residue value to parent equivalents. Since the 

residues found on grass, hay were less than the LOQ of 0.05 ppm for acyl 
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6-chlorobenzoxazolone, HED multiplied this 0.05 ppm value by the ratio of the molecular 

weights (1.71) to arrive at a recommended tolerance of 0.09 ppm.

The requested change to the proposed tolerance level is shown in Table 2.2.3 above.

2.2.4 International Harmonization

There are no international harmonization issues related to the existing or proposed uses of FPE.

Please see Appendix B for a summary of international maximum residue limits (MRLs).

2.3 Label Recommendations

2.3.1 Recommendations from Residue Reviews

There are no label recommendations based on residue chemistry identified for this petition. 

2.3.2 Recommendations from Occupational Assessment

HED recommends that all registered and proposed occupational use labels contain chemicalresistant gloves for handler exposure activities. 

2.3.3 Recommendations from Residential Assessment

There are no label recommendations for the currently registered residential uses of fenoxaprop-pethyl.

3.0 Introduction

FPE is a selective aryloxy phenoxy-propionate herbicide used to control grass weeds after 

emergence. FPE is currently registered for use on barley, cotton, rice, soybeans, and wheat. FPE 

is also registered for non-agricultural use on conservation reserve lands, ornamentals, rights-ofway, and turf. Since both enantiomers are included in the tolerance expression, and the datacollection and tolerance enforcement methods are not stereo-specific and cannot differentiate 

between FE and FPE, the previously established tolerances for FE are adequate to cover residues 

from the application of FPE.

The chemical structure and nomenclature of FPE are presented in Table 3.1, and the 

physicochemical properties of the technical grade of FPE are provided in Table 3.2.

3.1 Chemical Identity

Table 3.1 Fenoxaprop-p-ethyl Nomenclature
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Table 3.1 Fenoxaprop-p-ethyl Nomenclature

Chemical Structure

Empirical Formula

Common Name Fenoxaprop-p-ethyl

Company experimental name AE F046360

IUPAC name

ethyl (R)-2-[4-(6-chloro-1,3-benzoxazol-2-yloxy)phenoxy] propionate

or

ethyl (R)-2-[4-(6-chlorobenzoxazol-2-yloxy)phenoxy]propionate

CAS Name ethyl (2R)-2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoate

CAS Registry Number 71283-80-2

3.2 Physical/Chemical Characteristics

FPE has low water solubility. Its octanol/water partition coefficient suggests that it is a 

hydrophobic compound that is more fat soluble than water soluble, exhibiting a tendency to 

dissolve in fats, oils, lipids, and non-polar solvents more readily than in water. Further, FPE has 

a low vapor pressure. The full complement of physiochemical properties for this active 

ingredient is shown in Table 3.2. 

Table 3.2. Physicochemical Properties of the Technical Grade FPE

Parameter Value Reference

Melting Point/Range (C) 86.5 Health Canada 

Fenoxaprop-p-ethyl 

Proposed ReEvaluation Decision

(PRVD2011-04)

Density (g/cm3) 1.32

Water Solubility ( 20 C, pH 5.8) (mg/L) 0.7

Solvent Solubility (g/L at 20C) n-hexane 7.0

acetone >400

toluene >480

dichloromethane >400

methanol 43.1

isopropanol 14.2

ethyl acetate >380

Vapor Pressure (Pa) 5.3 x 10-

7

at 20°C

1.4 x 10-

6

at 25°C

1.1 x 10-4at 50°C

Dissociation Constant (pKa) Not possible to measure 

in water in the pH range 

1-13 (no acidic or basic 

groups on the molecule)

Octanol/Water Partition Coefficient Log (Kow) 4.58

UV/Visible Absorption Spectrum Not expected to absorb at 
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Table 3.2. Physicochemical Properties of the Technical Grade FPE

Parameter Value Reference

λ > 300nm

3.3 Pesticide Use Pattern

The only FPE end-use formulation currently registered is as a liquid formulation which may be 

applied post-emergent for the use on various agricultural crops (barley, cotton, rice, soybeans, 

and wheat), ornamentals, turf (residential lawns and sod farms), conservation reserve lands, and 

right-of-ways. There is also a proposed new use for grasses grown for seed in Oregon, 

Washington, and Utah.

A summary of the existing and proposed use patterns for FPE are shown in Tables 3.3a and 3.3b

below. 

Table 3.3a. Summary of Directions for Use of Currently Registered Fenoxaprop-p-ethyl Uses

Applic. 

Timing, Type, 

and Equip.

EPA Reg. 

No.

Max 

Applic. 

Rate (lb 

ai/A)

Max. No. 

Applic. per 

Season

Max. 

Seasonal 

Applic. Rate 

(lb ai/A)

PHI 

(days)

Use Directions and 

Limitations

Barley

Groundboom 

and Aerial 

applications

264-666

264-1073

264-1075

0.083 1 0.083 57 No chemigation

24 hour REI

Conservation Reserve Lands

Groundboom 

and Aerial 

applications

264-647 0.1 NS 0.142 N/A No chemigation

24 hour REI

Cotton

Groundboom 

and Aerial 

applications

100-1059 0.105 1 0.105 90 No chemigation

24 hour REI

Ornamentals 

Groundboom 

and handheld 

applications

432-950 0.173

0.002 lbs 

ai/gal

3 0.531 N/A No chemigation

24 hour REI

Ornamentals (Residential)

Handheld 

applications 72155-74

0.076

0.0009 

lbs ai/gal

0.008 lbs 

ai/bottle

NS 0.531 N/A N/A
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Table 3.3a. Summary of Directions for Use of Currently Registered Fenoxaprop-p-ethyl Uses

Applic. 

Timing, Type, 

and Equip.

EPA Reg. 

No.

Max 

Applic. 

Rate (lb 

ai/A)

Max. No. 

Applic. per 

Season

Max. 

Seasonal 

Applic. Rate 

(lb ai/A)

PHI 

(days)

Use Directions and 

Limitations

Rice

Groundboom 

and Aerial 

applications

264-647

264-682

0.108

(SLN) 1 0.142 65 No chemigation24 hour REI

Right of Way

Groundboom 

and Aerial 

applications

100-1059

432-950

0.173 

0.017 

(lbs 

ai/gal)

3 0.531 N/A No chemigation

24 hour REI

Soybean

Groundboom 

and Aerial 

applications

100-1059

264-647 0.1 2 0.128 90 No chemigation24 hour REI

Turf (sod/commercial)

Groundboom 

and Aerial 

applications

432-950 0.173 NS 0.531 NS No chemigation

24 hour REI

Turf (residential lawns)

Ready to use 

Hose-end 

sprayer and 

concentrate 

solutions 

through 

handheld 

equipment

228-7161

72155-74

72155-77

72155-78

0.076

0.0009 

lbs ai/gal

0.008 lbs 

ai/bottle

NS NS N/A

No aerial, groundboom, or 

chemigation

Wheat

Groundboom 

and Aerial 

applications

100-1429

264-666

264-1073

264-1075

0.083 1 0.083 70 No chemigation

24 hour REI

SLN= Special Local Needs 

1. The currently registered label 228-716 has a maximum application rate of 0.1 lbs ai/acre for residential lawn 

applications; however, Bayer Crop Science has submitted a commitment letter to revise the application rate to 

0.076 lbs ai/acre for all residential lawn applications. The letter is discussed and appended to D416000, 

D416003 (S. Shelat, 1/23/2014).

Table 3.3b. Summary of Directions for Use of Proposed Fenoxaprop-p-ethyl Uses

Applic. 

Timing, Type, 

and Equip.

Formulation 

[EPA Reg. 

No.]

Max 

Applic. 

Rate (lb 

ai/A)

Max. No. 

Applic. per 

Season

Max. 

Seasonal 

Applic. 

Rate (lb 

ai/A)

PHI 

(days)

Use Directions and 

Limitations

Proposed Grass grown for seed (Oregon, Washington, Utah)

Groundboom 

application 264-266 0.082 NS NS 60 No chemigation no aerial applications

NS= not specified
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3.4 Anticipated Exposure Pathways

In addition to the preliminary risk assessment for Registration Review, this document addresses 

the Registration Division’s request of a human health risk to support the proposed new use of 

fenoxaprop-p-ethyl on grass grown for seed. Humans may be exposed to fenoxaprop-p-ethyl in 

food and drinking water, since fenoxaprop-p-ethyl may be applied directly to growing crops and 

application may result in fenoxaprop-p-ethyl reaching surface and ground water sources of 

drinking water. There are residential uses of fenoxaprop-p-ethyl, so there is likely to be 

exposure in residential or non-occupational settings. In an occupational setting, applicators may 

be exposed while handling the pesticide prior to application, as well as during application. There 

is also a potential for post-application exposure for workers re-entering treated fields. 

Risk assessments have been previously prepared for the existing uses of fenoxaprop-p-ethyl. 

This risk assessment considers all of the aforementioned exposure pathways based on the 

proposed new use of fenoxaprop-p-ethyl, but also considers the existing uses as well. 

3.5 Consideration of Environmental Justice

Potential areas of environmental justice concerns, to the extent possible, were considered in this 

human health risk assessment, in accordance with U.S. Executive Order 12898, "Federal Actions 

to Address Environmental Justice in Minority Populations and Low-Income Populations," 

(http://www.eh.doe.gov/oepa/guidance/justice/eo12898.pdf. As a part of every pesticide risk 

assessment, OPP considers a large variety of consumer subgroups according to well-established 

procedures. In line with OPP policy, HED estimates risks to population subgroups from 

pesticide exposures that are based on patterns of that subgroup’s food and water consumption, 

and activities in and around the home that involve pesticide use in a residential setting. 

Extensive data on food consumption patterns are compiled by the USDA under the Continuing 

Survey of Food Intake by Individuals (CSFII) and are used in pesticide risk assessments for all 

registered food uses of a pesticide. These data are analyzed and categorized by subgroups based 

on age, season of the year, ethnic group, and region of the country. Additionally, OPP is able to 

assess dietary exposure to smaller, specialized subgroups and exposure assessments are 

performed when conditions or circumstances warrant. Whenever appropriate, non-dietary 

exposures based on home use of pesticide products and associated risks for adult applicators and 

for toddlers, youths, and adults entering or playing on treated areas post-application are 

evaluated. Further considerations are currently in development as OPP has committed resources 

and expertise to the development of specialized software and models that consider exposure to 

bystanders and farm workers as well as lifestyle and traditional dietary patterns among specific 

subgroups.

3.6 Incident Reports

HED completed a review of FPE incidents in the OPP Incident Data System (IDS) and the 

Centers for Disease Control and Prevention/National Institute for Occupational Safety and 

Health (CDC/NIOSH) Sentinel Event Notification System for Occupational Risk-Pesticides 

(SENSOR) databases. Based on the low frequency and severity of incident cases reported for 
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FPE in both IDS and NIOSH SENSOR-Pesticides, there does not appear to be a concern at this 

time that would warrant further investigation. The Agency will continue to monitor the incident 

information and if a concern is triggered, additional analysis will be conducted.

The Agricultural Health Study (AHS) is also a potential source of information associated with 

human health effects associated with certain pesticides. FPE is included in the AHS, but it is 

only in phase III and there are no studies available yet to consider. Further detail is provided in 

the Tier I Updated Review of Human Incidents for Preliminary Risk Assessment (D416023, 

November 13, 2013).

4.0 Hazard Characterization and Dose-Response Assessment

4.1 Toxicology Studies Available for Analysis

FE was first registered as a 50:50 racemic mixture of d and l enantiomers. Since registration, the 

more herbicidally active isomer d, FPE has been registered. HED held a joint Toxicology 

Science Advisory Committee/Hazard and Science Council (ToxSAC/HASPOC) meeting on 

April 17, 2008 to determine if bridging of fenoxaprop-ethyl (FE) toxicity data was appropriate 

for FPE (Kidwell, 2008). Based on the analysis of the acute and subchronic toxicity studies, 

HED found that the toxicological effects of FE and FPE across species, duration, and route of 

exposure are similar. It was, therefore, concluded that the similarity between the FE and FPE 

data was such that the database for FE could be bridged with FPE. HED further concluded that 

the enriched isomer is approximately an order of magnitude less toxic than the racemic mixture.

Based on bridging, the toxicology database on FPE is sufficient for assessing the toxicity and 

characterizing the hazard of FPE. The toxicology studies for FPE are summarized in Table A.1 

in Appendix A. The database includes the following studies. 

 Subchronic: 90-day oral toxicity (rat, mouse, dog)

 Dermal: 30-day dermal toxicity (rat)

 Inhalation: 28-day inhalation toxicity (rat)

 Developmental toxicity: developmental toxicity (rat and rabbit)

 Immunotoxicity: 28-day dietary (rat)

 Other: Mutagenicity battery, metabolism, dermal absorption, in vitro dermal penetration 

comparison of humans vs. rats

The database for the racemic fenoxaprop ethyl (FE) includes the following studies. 

 Chronic/Carcinogenicity: 2-year oral toxicity (rat and mouse)

 Chronic: 1-year oral toxicity (dog)

 Subchronic: 90-day oral toxicity (rat, mouse, and dog)

 Dermal: 21-day and 30-day dermal toxicity (rat)

 Inhalation: 28-day inhalation toxicity (rat)

 Developmental toxicity: oral (rat, mouse, and rabbit); dermal (rat and rabbit)

 Reproductive toxicity: 2-generation (rat)

 Other: Mutagenicity, metabolism, dermal absorption
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The studies available for consideration of FPE toxicity provide a comprehensive database, with 

routes of administration that are consistent with potential exposure scenarios. 

4.2 Absorption, Distribution, Metabolism, & Elimination (ADME)

In studies with the racemic FE, 83-109% of the administered radioactivity was recovered in the 

urine and feces, with the majority of the dose (51-65%) being recovered within 24 hours of 

dosing. Sex-related differences in the pattern of excretion were apparent. Female rats 

metabolized the chemical more rapidly and excreted more of the total radioactivity in the urine 

(54-70% of dose) than the males (37-58% of dose). Within 24 hours of dosing, urinary excretion 

accounted for 39-48% of the dose for females and 22-31% of the dose for males. Over the course

of the study, radioactivity in feces accounted for 39-62% of the dose for males and 30-43% of 

the dose for females. Dose-related differences in excretion were not evident in females, but high 

dose males had a higher level (62% of dose) of excretion in the feces than low-dose males (39-

40% of dose). A very small amount of unchanged parent compound is excreted in the feces. No 

bioaccumulation occurred. 

A comparison and evaluation of the metabolism and pharmacokinetics of FPE was conducted in 

rats using single and repeat (15 doses, once daily) oral doses of 2 and 10 mg/kg. Excretion via 

the urine and feces is in the same order of magnitude as FE. At 168 hours after exposure with 

FPE, ~95% of the administered dose was recovered, with slightly higher urinary excretion in 

females (56.9 to 65.0%) than males (42.8 to 54.1%). The highest residue concentrations were 

identified in the kidneys at 168 hours following exposure. Comparison of metabolic pathways 

demonstrated that they are identical for FE and FPE, and that the optical activity is preserved in 

the animal body.

4.2.1 Dermal Absorption

In an in vivo study, a single dermal application of 2.72 ± 0.03 or 617.5 ± 125.6 μg/cm2 was 

applied to male rats. Each dose was washed after eight hours of exposure and 4/group were 

sacrificed at 8, 24, 72 and 120 hrs. Recovery of the applied dose (mass balance) was acceptable 

at both dose levels (96.3 and 90.8%, respectively). Estimates of dermal absorption were based on 

the sum of residues retained in the urine (including cage wash and rinse), gastrointestinal tract 

and contents, feces, carcass, and blood and increased in a contact time-dependent manner from 

6.212% of the applied dose at eight hours and 9.6% of the applied dose at 24 hours after 

initiation of treatment to 16.31% of the applied dose at 120 hours after initiation of treatment for 

the low dose. For the high dose, total absorption was 0.6% of the applied dose eight hours after 

initiation of treatment, 1.3% after 24 hours, and increased to 2.012% of the applied dose by 120 

hours. 

4.3 Toxicological Effects

FPE is a post-emergent herbicide of the oxyphenoxy acid ester group (aryloxy phenoxypropionate class). Its pesticidal mechanism of action is to interfere with fatty acid biosynthesis, 

specifically to inhibit acetyl CoA carboxylase. The major target organs following short-term and 
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Page 18 of 84

long-term oral administration of FE and FPE in rats and mice are the liver and kidneys, with rats 

being the most sensitive species. The primary toxic effect is altered lipid metabolism 

characterized by decreased lipids and cholesterol, and increased liver weights in rats, and slightly 

increased lipids, cholesterol, proteins, and liver weights in mice. Additionally, increased enzyme 

activity (ASAT, ALAT, and ALP), hypertrophy, and single cell necrosis were observed in mice. 

In the kidneys, increases in ketones and kidney weights were observed in rats and evidence of 

proximal renal tubular injury were observed in mice following 90 day administration of FPE. 

However, no effects on the kidneys were observed following chronic administration of FE to 

rats, mice, or dogs. In both species, males were slightly more sensitive to the liver effects of FE 

and FPE. It is also important to note that no increases in toxicity are observed over time for FE 

when comparing the 28-day and 90-day subchronic studies, the 2-generation reproductive 

toxicity study, and the 2-year chronic toxicity/carcinogenicity study in rats, or in FPE when 

comparing the 28-day and 90-day subchronic toxicity studies in rats. 

FPE has low acute toxicity following the oral, dermal, and inhalation routes of exposure. No 

evidence of immunotoxicity, reproductive or neurological toxicity was identified in the database. 

Developmental toxicity occurred in rats as evidenced by skeletal anomalies (longitudinally 

displaced, fragmented, fused, dysplastic sternebrae or dislocated sternebrae) and skeletal 

retardations (weak or non-ossification of one or several cranial bones). Developmental effects 

only occurred in the rat in the presence of maternal toxicity (decreased body weight, body weight 

gain, and heart weight). No developmental effects were identified in rabbits. In mice, a 

treatment-related increase in tumor incidence of hepatocellular adenomas and carcinomas, 

mainly adenomas, was observed in males at 320 ppm (30%) compared to the control (2%). In 

addition, microscopic pathology indicated that hepatocellular hypertrophy was observed in the 

majority of treated animals (both sexes). There was, however, no evidence of a mutagenic effect 

in a comprehensive battery of genetic toxicology assays with both isomers. No evidence of 

tumors was identified in rats. In accordance with EPA’s Final Guidelines for Carcinogen Risk 

Assessment (2005), CARC classified FE/FPE as “Suggestive Evidence of Carcinogenic 

Potential”. 

4.4 Safety Factor for Infants and Children (FQPA Safety Factor)

The HED recommends that the FQPA Safety Factor be reduced to 1X based on adequate toxicity 

database and exposure data. There is no evidence of susceptibility/sensitivity and there are no 

residual uncertainties concerning pre- or post-natal toxicity. No evidence of neurotoxicity was 

identified throughout the database for FE or FPE. All endpoints used in this risk assessment are 

protective of developmental effects in FE and FPE. The dietary and residential assessments are 

based on reliable data and will not underestimate exposure.
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4.4.1 Completeness of the Toxicology Database

The toxicology database for FPE is complete based on bridging to FE. Acceptable rat and rabbit 

developmental toxicity studies, a rat 2-generation reproduction study, a non-guideline 

developmental toxicity study, and an immuno toxicity study are available. The Hazard and 

Science Policy Council (HASPOC) (Report dated November 27, 2012, TXR 0056489, 

determined that the acute neurotoxicity study and subchronic neurotoxicity studies may be 

waived. 

4.4.2 Evidence of Neurotoxicity

No evidence of neurotoxicity was observed in any of the submitted studies for FPE or FE. The 

HASPOC determined that the acute neurotoxicity study and subchronic neurotoxicity studies are 

not required at this time based on the following rationale: 1) the lack of neurotoxicity in the 

available toxicology database for FE and FPE; 2) the target organs of FPE and FE are the kidney 

and liver, and the mechanism of action for FPE and the chemical class do not target the nervous 

system; 3) developmental effects and decreased total blood lipids/cholesterol are the most 

sensitive effects seen in the FE database and provide the most sensitive POD for risk assessment; 

4) there is low concern for neurotoxicity in other members of this class of chemicals (i.e., the 

arloxy phenoxy-propionate class); and 5) using an oral POD, the acute and chronic dietary risk 

estimates (food only) for FE utilize <1% of the aPAD and cPAD, respectively. 

4.4.3 Evidence of Sensitivity/Susceptibility in the Developing or Young Animal

The available data do not provide evidence of any increased susceptibility in the offspring in 

either of the two developmental toxicity studies for FPE or in the two-generation reproduction 

study for FE. Delayed ossification was the primary effect in the developmental toxicity study 

and only occurred in the presence of maternal toxicity and a clearly defined NOAEL and 

LOAEL were achieved. 

In the rat developmental toxicity study with FPE, longitudinally displaced, fragmented, fused, 

dysplastic sternebrae or dislocated sternebrae and weak or non-ossification of one or several 

cranial bones were noted at 100 mg/kg (highest dose tested). These incidences occurred only in 

the presence of maternal toxicity (decreased gestational body weights, body weight gains, and 

food consumption.). No developmental effects occurred in rabbits. In the 2-generation rat 

reproductive toxicity study on FE, no reproductive or developmental effects were observed. An 

increase in alkaline phosphatase (ALP) activity and liver weights were identified in the offspring

at 9.0 mg/kg. These effects occurred in the presence of parental toxicity (increased liver weight 

and decreased lipids) and are consistent with hepatotoxicity, the primary toxic effect of FPE, 

observed across the database.

4.4.4 Residual Uncertainty in the Exposure Database

There are no residual uncertainties in the exposure database. Since the dietary and residential 

exposure estimates were based on conservative assumptions, HED is confident that this 

assessment does not underestimate dietary (food and water) or residential exposure. 
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The unrefined chronic analysis is based on tolerance-level residues, 100% crop treated (%CT) 

assumptions, and DEEM default processing factors. The drinking water assessment used water 

concentration values generated by models and associated modeling parameters which are 

designed to produce conservative, health protective, high-end estimates of water concentrations 

which are not likely to be exceeded. For these reasons it can be concluded that the chronic 

dietary exposure analysis does not underestimate risk from chronic exposure to FPE.

Similarly, HED does not believe that the residential exposure estimates are underestimated 

because they are also based on conservative assumptions including maximum application rates 

and standard values for inputs such as unit exposures, transfer coefficients, and amount handled. 

4.5 Toxicity Endpoint and Point of Departure Selections

4.5.1 Dose-Response Assessment

A detailed description of the toxicity studies used for selecting toxicity endpoints and points of 

departure for various exposure scenarios is presented in Appendix A.

For acute dietary assessment, no appropriate toxicological endpoints attributable to a single 

exposure were identified for general populations or females age 13 to 49. Consequently, there 

was no basis for selecting a dose and endpoint for an acute RfD for general populations including 

infants and children, and females ages 13-49.

For chronic dietary exposure and risk assessment, the chronic/carcinogenicity and 2-generation 

reproductive toxicity studies in rats, conducted on FE, were selected with a NOAEL of 1.5 

mg/kg/day identified in both studies. The LOAEL is 9 mg/kg/day based on decreased serum 

lipids and cholesterol, and changes in liver weights in both studies, as well as increased ALP and 

liver weights in pups from the 2-generation reproductive toxicity study. These studies are 

considered to be the most appropriate for chronic dietary dose and endpoint selection. A lower 

NOAEL of 0.375 mg/kg/day was identified in the chronic dog study for FE. However, this was 

not considered a critical NOAEL as only minimal effects occurred (10-12% reduction in body 

weights), and subchronic toxicity studies in the dog for FPE showed no effects up to 77.7 

mg/kg/day.

For short-term incidental oral exposure (1-30 days), a 28-day oral toxicity study in rats with a 

NOAEL of 6 mg/kg/day was selected (FPE). In the study, the LOAEL is 26 mg/kg/day (M/F) 

based on altered lipid metabolism (decreased HDL-cholesterol, HDL-phospholipids, and total 

lipids, increased triglycerides, and ketonuria) and increased liver and kidney weights. 

Intermediate exposure is not expected based on current use patterns; therefore, risk assessment 

for intermediate incidental oral exposure is not required.

For short and intermediate-term dermal exposure, a 28-day dermal toxicity study in rats with a 

NOAEL of 20 mg/kg/day was selected (FPE). In this study, the LOAEL is 100 mg/kg/day (M/F) 

based on non-regenerative anemia, decreased serum cholesterol, total lipids, and protein (beta 1 

globulins), and increased liver and kidney weights. There is no long-term exposure from existing 

or proposed uses; therefore, a risk assessment for long-term dermal exposure is not required. 
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For short and intermediate-term inhalation exposure, a 28-day inhalation toxicity study in rats 

with a NOAEL of 0.07 mg/L was selected (FPE). In the study, the LOAEL is 0.3 mg/L (M) 

based on slight normocytic anemia, decreases in serum cholesterol and total lipids, and increases 

in liver and kidney weights and urea nitrogen. There is no long-term exposure from existing or 

proposed uses; therefore, a risk assessment for long-term inhalation exposure is not required.

The methods and dosimetry equations described in EPA's reference concentration (RfC) 

guidance (1994) are suited for calculating HECs based on the inhalation toxicity NOAEL for use

in MOE calculations. The regional-deposited-dose ratio (RDDR), which accounts for the 

particulate diameter (mass median aerodynamic diameter [MMAD] and geometric standard 

deviation [<σg] of aerosols), can be used to estimate the different dose fractions deposited along 

the respiratory tract. The RDDR is also based on interspecies differences in ventilation and 

respiratory-tract surface areas. Thus, the RDDR can be used to adjust an observed inhalation 

particulate exposure of an animal to the predicted inhalation exposure for a human. For the 4-

week inhalation study with FPE, a MMAD and geometric standard deviation were not reported 

due to the type of particle collection system. An MMAD of 1.2 μm and standard deviation (<σg) 

of 2.80 were estimated based on the cumulative 50th percentile (50% of particles being ≤) 

ranging from 1.2-1.5 μm and between 74-97% of particles ≤ 4 μm. Therefore, an RDDR of 2.7 

was estimated using the above values and the respiratory-tract surface area of the rat relative to 

the human (see Appendix A.5 for detailed calculations). Since the rat inhalation study was 

carried out for 6 hrs/day for 5 days/week, the only exposure adjustment made was in the 

assumption of 8 hrs/day for human occupational exposures, and 2 hrs/day for human residential 

exposures. The resulting HECs are 0.14 mg/L and 0.57 mg/L, respectively. 

4.5.1. Inhalation Endpoints and Points of Departures for Fenoxaprop-p-ethyl

Inhalation 

Short-Term

(1-30 days) and 

Intermediate-Term

(1 – 6 months)

NOAEL = 0.07 

mg/L (males)

0.3 mg/L 

(females)

UFA = 3x

UFH = 10x

FQPA SF= 1X

LOC for MOE 

= 30

21-Day Inhalation toxicity (rat)

MRID 47113307 (1989)

LOAEL = 0.3 mg/L (males only)

Based on slight normocytic anemia, 

decreases in serum cholesterol and total 

lipids, and increases in liver weight and 

urea nitrogen.

Occupational 

HEC = 0.14 

mg/L

Residential 

HEC = 0.57 

mg/L

HED = 6.8 

mg/kg/day

NOAEL =no-observed adverse-effect level, LOAEL- lowest-observed adverse-effect level

MOE= margin of exposure, HEC =human-equivalent concentration; HED =human-equivalent dose.

Occupational HEC =rat NOAEL*(daily duration adjustment)*weekly daily duration adjustment *RDDR*

= 0.07 mg/L * (6hr/8hr)*(l)*2.7 = 0.1417 or 0.14 mg/L.

Residential HEC =rat NOAEL*(daily duration adjustment)*weekly daily duration adjustment *RDDR*

= 0.07 mg/L * (6hr/2hr)*(l)*2.7 = 0.567 or 0.57 mg/L.

HED = HEC*human-specific conversion factor*daily duration

= 0.1417 mg/L • 6.0 l/hr/kg*8hr = 6.81 or 6.8 mg/kg/day.
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For acute and chronic dietary, incidental oral, and dermal risk assessments, a 100X uncertainty 

factor is applied (interspecies factor of 10X and intraspecies factor of 10X). For inhalation risk 

assessment, a 30X uncertainty factor is applied, which includes interspecies (3X) and 

intraspecies (10X) extrapolation. The interspecies factor was reduced from l0Xto 3X due to the 

HEC calculation accounting for pharmacokinetic (not pharmacodynamic) interspecies 

differences.

4.5.2 Recommendation for Combining Routes of Exposures for Risk Assessment

When there are potential occupational and residential exposures to a pesticide, the risk 

assessment must address exposures from three major sources: incidental oral, dermal, and 

inhalation. For FPE, inhalation, dermal, and oral routes can be combined since toxicological 

effects are the same.

4.5.3 Cancer Classification and Risk Assessment Recommendation

In accordance with EPA’s Final Guidelines for Carcinogen Risk Assessment (2005), the Cancer 

Assessment Review Committee (CARC) classified FPE as “Suggestive Evidence of 

Carcinogenicity” based on increased liver adenomas and carcinomas observed male mice in the 

chronic toxicity/carcinogenicity study (7/29/2013, TXR 0056683). The liver tumor response 

induced by FE/FPE occurred only in the male mice; no liver tumors were seen in the female 

mice or in the guideline chronic/carcinogenicity study in rats. The tumors were benign with no 

progression to malignancy. Mutagenicity has been ruled out as an MOA for this response. 

Additionally, the adrenal cortex subcapsular Type B adenomas were determined to be not 

treatment-related. The CARC concluded that data were not sufficient to support the proposed 

MOA for liver tumors. When there is suggestive evidence of carcinogenicity, the Agency does 

not attempt a dose-response assessment as the nature of the data generally would not support 

one. Therefore, quantification of risk using a non-linear approach (i.e. the chronic reference dose 

(cRfD)) will adequately protect for all chronic toxicity, including carcinogenicity that could 

result from exposure to FE/FPE.
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4.5.4 Summary of Points of Departure and Toxicity Endpoints Used in Human Risk 

Assessment.

Table 4.5.4. Summary of Toxicological Doses and Endpoints for Fenoxaprop-p-ethyl for Use 

in Human Health Risk Assessments

Exposure/

Scenario

Point of 

Departure

Uncertainty/

FQPA Safety 

Factors

RfD/PAD, 

Level of 

Concern for 

Risk 

Assessment

Study and Toxicological Effects

Acute Dietary 

(General 

Population) No appropriate endpoint attributable to a single dose was identified. An acute RfD was not 

Acute Dietary established.

(Females 13-49 

years of age)

Chronic Dietary 

(All Populations)

NOAEL = 1.5 

mg/kg/day

UFA 10X

UFH 10X

FQPA SF = 1X

Chronic RfD = 

0.015 

mg/kg/day

cPAD = 0.015 

mg/kg/day

Chronic Toxicity/Carcinogenicity (rat)

MRIDs: 00149664, 0149665, 00151564, 

00151565

2-Generation Reproductive Toxicity (rat)

MRID: 00159920

LOAEL = 9 mg/kg/day, based on 

decreased serum lipids and cholesterol, and 

altered liver weights

Incidental Oral

Short-Term

(1-30 days)

NOAEL = 6 

mg/kg/day

UFA = 10X

UFH = 10X

FQPA SF = 1X

LOC for MOE 

= 100

28-Day Oral Toxicity (rat)

MRID 47113304 (1986)

LOAEL = 26 mg/kg/day, based on altered 

lipid metabolism (decreased HDLcholesterol, HDL-phospholipids, and total 

lipids, increased triglycerides, and 

ketonuria) and increased liver and kidney 

weights.

Dermal

Short-Term

(1 – 30 days) and 

Intermediate-Term

(1 – 6 months)

NOAEL = 20 

mg/kg/day

UFA = 10X

UFH = 10X

FQPA SF= 1X

LOC for MOE 

= 100

28-Day Dermal Toxicity (rat)

MRID 47113306 (1987)

LOAEL = 100 mg/kg/day, based on nonregenerative anemia, decreased serum 

cholesterol, total lipids, and protein (beta 1 

globulins), and increased liver and kidney 

weights were observed. Additionally, 

cholesterol remained decreased following a 

15-day recovery period.

Inhalation

Short-Term

(1-30 days) and 

Intermediate-Term

(1 – 6 months)

NOAEL = 0.07 

mg/L (males)

0.3 mg/L 

(females)

UFA = 3X

UFH = 10X

FQPA SF= 1X

LOC for MOE 

= 30

21-Day Inhalation toxicity (rat)

MRID 47113307 (1989)

LOAEL = 0.3 mg/L (males only)

Based on slight normocytic anemia, 

decreases in serum cholesterol and total 
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Table 4.5.4. Summary of Toxicological Doses and Endpoints for Fenoxaprop-p-ethyl for Use 

in Human Health Risk Assessments

Exposure/

Scenario

Point of 

Departure

Uncertainty/

FQPA Safety 

Factors

RfD/PAD, 

Level of 

Concern for 

Risk 

Assessment

Study and Toxicological Effects

Occupational 

HEC = 0.14 

mg/L

Residential 

HEC = 0.57 

mg/L

HED = 6.8 

mg/kg/day

lipids, and increases in liver weight and 

urea nitrogen.

Cancer (oral)

Classification: "Suggestive evidence of carcinogenic potential"; quantification of risk using a 

non-linear approach; i.e., RfD, for FPE will adequately account for all chronic toxicity, including 

carcinogenicity, that could result from exposure to FPE.

Point of Departure (POD) = A data point or an estimated point derived from observed dose-response data and used to mark 

the beginning of extrapolation to determine risk associated with lower environmentally relevant human exposures. NOAEL 

= no observed adverse effect level. LOAEL = lowest observed adverse effect level. UF = uncertainty factor. UFA = 

extrapolation from animals to humans (interspecies). UFH = potential variation in sensitivity among members of the human 

population (intraspecies). FQPA SF = FQPA Safety Factor. cPAD = chronic population adjusted dose. RfD = reference 

dose. N/A = not applicable. HEC = human equivalent concentration. HED = human equivalent dose.

4.6 Endocrine Disruption 

As required by FIFRA and FFDCA, EPA reviews numerous studies to assess potential adverse 

outcomes from exposure to chemicals. Collectively, these studies include acute, subchronic and 

chronic toxicity, including assessments of carcinogenicity, neurotoxicity, developmental, 

reproductive, and general or systemic toxicity. These studies include endpoints which may be 

susceptible to endocrine influence, including effects on endocrine target organ histopathology, 

organ weights, estrus cyclicity, sexual maturation, fertility, pregnancy rates, reproductive loss,

and sex ratios in offspring. For ecological hazard assessments, EPA evaluates acute tests and 

chronic studies that assess growth, developmental and reproductive effects in different 

taxonomic groups. As part of its most recent registration decision for FPE, EPA reviewed these 

data and selected the most sensitive endpoints for relevant risk assessment scenarios from the 

existing hazard database. However, as required by FFDCA section 408(p), FPE is subject to the 

endocrine screening part of the Endocrine Disruptor Screening Program (EDSP). 

EPA has developed the EDSP to determine whether certain substances (including pesticide 

active and other ingredients) may have an effect in humans or wildlife similar to an effect 

produced by a “naturally occurring estrogen, or other such endocrine effects as the Administrator 

may designate.” The EDSP employs a two-tiered approach to making the statutorily required 

determinations. Tier 1 consists of a battery of 11 screening assays to identify the potential of a 

chemical substance to interact with the estrogen, androgen, or thyroid (E, A, or T) hormonal 

systems. Chemicals that go through Tier 1 screening and are found to have the potential to 

interact with E, A, or T hormonal systems will proceed to the next stage of the EDSP where EPA 
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will determine which, if any, of the Tier 2 tests are necessary based on the available data. Tier 2 

testing is designed to identify any adverse endocrine-related effects caused by the substance, and 

establish a dose-response relationship between the dose and the E, A, or T effect. 

Under FFDCA section 408(p), the Agency must screen all pesticide chemicals. Between October 

2009 and February 2010, EPA issued test orders/data call-ins for the first group of 67 chemicals, 

which contains 58 pesticide active ingredients and 9 inert ingredients. A second list of chemicals 

identified for EDSP screening was published on June 14, 20131 and includes some pesticides 

scheduled for registration review and chemicals found in water. Neither of these lists should be 

construed as a list of known or likely endocrine disruptors.

FPE is on List 2. List 2 represents the next set of chemicals for which EPA intends to issue test

orders/data call-ins in the near future.

5.0 Dietary Exposure and Risk Assessment 

See memos D415999, D416002 (D. Wilbur; 11/14/2013) and D415998, D416001 (D. Wilbur; 

12/5/13) for additional details.

5.1 Metabolite/Degradate Residue Profile

5.1.1 Summary of Plant and Animal Metabolism Studies

Plant

HED has previously concluded that the metabolism of fenoxaprop-ethyl is adequately 

understood. A comparison of the metabolism of FE and FPE was submitted for soybeans, rice, 

and wheat (MRID 47113302). The results showed that there is no significant difference in the 

metabolism for FE and FPE. Plant metabolism studies have been submitted for barley, soybeans, 

rice, cotton, peanuts, and wheat. It has been concluded that the metabolic pathway for 

fenoxaprop-ethyl is similar in these plants. The parent compound fenoxaprop-ethyl is cleaved to 

yield 2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoic acid which subsequently loses 

phenoxypropionic acid to yield 6-chloro-2,3--dihydrobenzoxazol-2-one. The residue of concern 

in plants consists of fenoxaprop-ethyl, its free acid metabolite {2-[4-[(6-chloro-2-

benzoxazolyl)oxy]phenoxy]propanoic acid,} and 6-chloro-2,3-- dihydrobenzoxazol-2-one.

Livestock

The nature of the residue in livestock for FPE based on the currently registered and proposed 

uses is considered to be adequately understood. Both ruminant and poultry metabolism studies 

were submitted/reviewed and found to be scientifically acceptable. The metabolic pathway in 

ruminants and poultry is similar; therefore a swine metabolism study was not required.

The metabolism of fenoxaprop-ethyl in animals has been previously considered in lactating 

ruminants (PP#6F3316, N. Dodd, 02/04/1986). It was reported that 6-chloro-2,3-

dihydrobenzoxazol-2-one constituted 75% of the residue in milk and 50% of the residue in the 

tissues of liver and kidney. No information was available concerning the relative amounts of 

parent and the two metabolites in ruminant tissues, since the analytical method used in the 

ruminant study was the enforcement method resulting in a common analyte, 6-chloro-2,3-
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dihydrobenzoxazol-2-one. In HED reviews of 02/02/90 and 12/14/90, (PP#9F3714), it was 

concluded that the residue of concern in ruminants and swine are parent compound, its free acid, 

fenoxaprop, and 6-chloro-2,3-dihydrobenzoxazol-2-one.

A poultry metabolism study (MRID #43426201, 01/22/1998) was submitted. The nature of the 

residue in poultry has been adequately delineated. The principal route of metabolism is deesterification to the free acid, followed by cleavage of the ether linkage to yield 6-chloro-2,3-

dihydrobenzoxazol-2-one and phenoxypropionic acid. Further, based on the low levels of TRR 

found in edible tissues of poultry following dosing at highly exaggerated rates, there is no 

reasonable expectation of finite residues (180.6(a)(3)). Therefore, a poultry feeding study is not 

required, nor are tolerances for poultry/eggs required.

Rotational Crops

Confined rotational crop data were submitted, reviewed and found to be scientifically acceptable. 

Based on the results of this study and the results of the studies from EFSA, no field accumulation 

studies are required.

A confined rotational crop study was submitted and reviewed in support of an experimental use 

permit (EUP) on soybeans (8340-EUP-T, 01/04/1984). Rotational crops were planted at 120 and 

364 days after the first application of radiolabeled FE. Wheat, lettuce, carrots, radishes, 

soybeans, and corn were then allowed to grow to maturity. Samples of these representative 

rotational crops did not show significant uptake of radiolabeled FE after 120 and 364 days. The 

parts of the plants that had measurable levels of radioactivity are not used for human 

consumption. Only total radioactive residue (TRR) was measured in the study.

5.1.2 Summary of Environmental Degradation

FPE has limited solubility in water and is moderately mobile. FPE is also quite lipophilic. Once 

deposited, either at the site of application or farther afield through spray drift (or through erosion 

of FPE bearing soil particles), the parent molecule is expected to degrade quickly through 

multiple fate processes (half-lives of hours to several days) under environmental conditions.

FPE is hydrolyzed moderately rapidly in acidic conditions and neutral conditions, and quickly in 

alkaline conditions. The two major hydrolytic degradates identified were fenoxaprop-p acid and 

chlorobenzoxazolone. Both FPE and fenoxaprop-p acid may hydrolyze to chlorobenzoxazolone, 

which was observed in the hydrolysis study. When considering the combined residues, however, 

they were stable to hydrolysis at all pHs. While FPE degrades quickly via aqueous photolysis 

and is quickly biodegraded in aerobic soils and aerobic and anaerobic aquatic systems, the total 

residues of concern (FPE, fenoxaprop-p acid (AE F088406), chlorobenzoxazolone (AE 

F054014), and 4-(6-chloro-2-benzoxazolyloxy) phenol (AE F040356), are relatively stable in the 

environment (half-lives > 200 days).

5.1.3 Comparison of Metabolic Pathways

The metabolism of FPE in plants is similar. The parent compound is rapidly metabolized to 

yield 2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoic acid which subsequently loses 

phenoxypropionic acid to yield 6-chloro-2,3--dihydrobenzoxazol-2-one. Residues in plants tend 
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to be surface residues with no translocation to newly formed leaves or plants parts. There is no 

difference between the metabolic profiles of FE and the enriched FPE.

Metabolism studies performed in rat, goat, and laying hen showed a common metabolic pathway 

in animals. FPE is metabolized in animals primarily by de-esterification to the free acid, 

followed by cleavage of the ether linkage to yield 6-chloro-2,3-dihydrobenzoxazol-2-one and 

phenoxypropionic acid. 

5.1.4 Residues of Concern Summary 

Table 5.1.4 Summary of Metabolites and Degradates to be included in the Risk 

Assessment and Tolerance Expression

Matrix Residues included in Risk Assessment Residues included in 

Tolerance Expression

Plants

Primary Crop

fenoxaprop-ethyl,

2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoic 

acid, 

6-chloro-2,3 dihydrobenzoxazol-2-one

Same as those

included in RA

Rotational 

Crop Not Applicable Not Applicable

Livestock Ruminant and 

Poultry

fenoxaprop-ethyl

2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoic 

acid 

6-chloro-2,3 dihydrobenzoxazol-2-one

Same as those 

included in RA

Drinking Water fenoxaprop-ethyl and all degradates containing the 6-

chloro-2-benzoxazol moiety Not Applicable

5.2 Food Residue Profile

The results from plant metabolism for FPE indicate that the residues of concern are fenoxapropethyl, its free acid metabolite {2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoic acid,} 

and 6-chloro-2,3-- dihydrobenzoxazol-2-one. These data also show that FPE undergoes limited 

translocation with plants. Supplemental metabolism studies on FE and FPE demonstrated that 

there is no significant difference in metabolism and no racemisation occurs. The metabolism of 

FE and FPE follows the same path leading to the metabolic pathway being identical for the two 

compounds.

Adequate residue chemistry data are available for FPE. Field trials showed levels of FPE 

residues to be less than the LOQ (<0.05 ppm) for all crops with the exception of some animal 

feedstuffs (barley and wheat straw) where very few detects were seen slightly above the LOQ. 

The data were generated using a validated data collection method and are adequately supported 

by frozen storage stability data. Sufficient processing studies are available to elucidate the fate 

of FPE in processed commodities, with no concentration seen in any crop matrix. Tolerances 

have been set on ruminant livestock commodities based on the previously calculated high-end 

dietary burden. HED believes that these tolerances are protective for all uses of FPE since the 

method used was much more conservative that the current method of using a maximum 

reasonably balanced diet (MRBD). HED has determined that the uses of FPE are classified as 
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180.6 (a) (3), no reasonable expectation of finite residues with respect to residues in poultry 

commodities. Metabolism in rotational crops was seen to be limited; with radioactive residues 

less than the LOQ found at 30-days, 120-days, or 365-days in leafy vegetables, root vegetables, 

and small grains.

5.3 Water Residue Profile

FPE is partially soluble in water, dissolving at 0.7 mg/L at 20°C and pH 5.8. FPE residues are

considered moderately mobile. The compound is not expected to volatilize significantly due to 

its low vapor pressure of 1.4 x 10-8torr (20°C). The octanol-water partition coefficient of FPE is 

38,000, with a relatively high bioconcentration factor (BCF) observed in fish viscera (1021x) 

compared to the edible fish portions (129x). The BCF for whole fish portions was 510x, which 

does not exceed reporting thresholds for concern for bioconcentration.

FPE is hydrolyzed moderately rapidly in acidic conditions (t1⁄2 = 19.6 d at pH 5) and neutral 

conditions (t1⁄2 = 24.6 d at pH 7), and quickly in alkaline conditions (t1⁄2 = 0.7 d at pH 9). Two 

major hydrolytic degradates were identified: fenoxaprop-p acid (AE F088406) and 

chlorobenzoxazolone (AE F054014). Both FPE and fenoxaprop-p acid may hydrolyze to 

chlorobenzoxazolone, which was observed in the hydrolysis study at up to 64% of the applied at 

pH 5(30 DAT), 23% of the applied at pH 7 (30 DAT), and 20% of the applied at pH 9 (30 DAT). 

When considering the combined residues however, they were stable to hydrolysis at all pHs. 

FPE also degrades quickly via aqueous photolysis, with an estimated half-life of 0.95 days. FPE 

was quickly biodegraded in aerobic soils (t1⁄2 ≤ 1.63 d), in aerobic aquatic systems (t1⁄2 < 1 d) and 

in anaerobic aquatic systems (t1⁄2 ≤ 2.4 d). 

The computer models PRZM and EXAMS and the Tier I Rice model were used to generate 

surface water EDWCs for use in the human health dietary risk assessment, while the PRZM-GW 

and SCI-GROW models were used to generate groundwater EDWCs. In 2007, HED identified 

FPE and its two degradates, fenoxaprop-p acid ((D+)-2-[4-(6-chloro-2-benzoxazolyloxy) 

phenoxy] propanoate, AE F088406) and chlorobenzoxazolone (4-(6-chloro-2-benzoxazolyloxy) 

phenol, AE F054014), as residues of concern in drinking water because these residues retained 

the 6-chloro-2-benzoxazol moiety. Newly submitted environmental fate studies indicated that a 

fourth degradate, 4-(6-chloro-2-benzoxazolyloxy) phenol (AE F040356), also contained the 6-

chloro-2-benzoxazol moiety. This degradate was included as a residue of concern, so the parent 

plus the three degradates were assessed using a total toxic residue (TTR) approach. 

Additionally, as high levels (e.g., >20%) of non-extracted residues (NER) were found in all 

environmental fate studies and these NER were found to contain levels of two degradates of 

concern (fenoxaprop-p acid and chlorobenzoxazolone) when subjected to harsh mineral acid 

extraction, NER were also included in the TTR approach. However, it is uncertain as to how 

available these residues are to reaching surface water and groundwater drinking water sources. 

As such, EFED modeled FPE TTR with and without NER to bracket the EDWCs. Descriptions 

of the models are available at the EPA internet site: http://www.epa.gov/oppefed1/models/water/.

The maximum acute and chronic surface EDWCs (110 and 69 μg/L, respectively) were 

associated with application to rice. Surface water EDWCs for the proposed new use of grass 

grown for seed were much lower than the maximum values (acute EDWC of 1.65 μg/L and a 
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chronic EDWC of 0.62 μg/L). For groundwater sources of drinking water, the maximum acute 

and chronic estimated concentrations of FPE TTR in shallow groundwater from PRZM-GW for 

applications to turf were 0.17 and 0.032 μg/L, respectively. The maximum groundwater EDWC 

reported from SCI-GROW was 0.096 μg/L for the chemical’s use on turf. Maximum EDWCs 

for FPE residues in surface water and groundwater recommended for dietary assessment are 

presented in Table 2. Water residues were incorporated in the DEEM-FCID into the food 

categories “water, direct, all sources” and “water, indirect, all sources.” 

Table 5.3 Summary of Estimated Surface Water and Groundwater Concentrations 

for Fenoxaprop-p-ethyl

Scenario Surface Water Conc., ppb a Groundwater Conc., ppb b

Acute 110 0.17

Chronic (non-cancer) 68.6 0.032

Chronic (cancer) N/A N/A

a From the Tier I Rice Model. Input parameters are based on foliar rice with first app at 0.108 lbs a.i./A, 14 

day RTI, second app at 0.034 lbs a.i./A, and third app at 0.046 lbs a.i./A.

b From the PRZM-GW model. Input parameters are based on aerial foliar turf with 0.173 lbs a.i./A applied 3 times 

and fourth app at 0.012 lbs a.i./A. (RTI = 14 days)

Reference: C. Peck, D411291, D404234, 09/25/2013

5.4 Dietary Risk Assessment

5.4.1 Description of Residue Data Used in Dietary Assessment

This chronic dietary exposure and risk analysis is based on tolerance-level residues, 100% crop 

treated assumptions, and default processing factors.

5.4.2 Acute Dietary Risk Assessment

An acute reference dose has not been established for either the general population or for females 

13-49 years of age since there were no appropriate studies that demonstrated evidence of toxicity 

attributable to a single dose for these populations.

5.4.3 Chronic Dietary Risk Assessment

The DEEM-FCID analyses estimate the dietary exposure and risk of the U.S. population and 

various population subgroups. The results reported in Table 5.4.5 below are for the general U.S. 

Population, all infants (<1 year old), children 1-2, children 3-5, children 6-12, youth 13-19, 

females 13-49, adults 20-49, and adults 50-99 years. Combined chronic dietary exposure 

estimates for food and drinking water are below HED’s level of concern for all population 

subgroups, including those of infants and children. The most highly exposed population 

subgroup is all infants at 27.5% of the cPAD, while the general U.S. population utilized 11.7% 

of the cPAD. 
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5.4.4 Summary Table

Table 5.4.5. Summary of Dietary (Food and Drinking Water Exposure and Risk for 

Fenoxaprop-p-ethyl

Population Subgroup

Acute Dietary Chronic Dietary Cancer

Dietary 

Exposure 

(mg/kg/day)

% aPAD

Dietary 

Exposure

(mg/kg/day)

% cPAD

Dietary 

Exposure

(mg/kg/day)

Risk

General U.S. Population

N/A N/A

0.001757 12

N/A N/A

All Infants (< 1 year old) 0.004121 28

Children 1-2 years old 0.003361 22

Children 3-5 years old 0.002634 18

Children 6-12 years old 0.001810 12

Youth 13-19 years old 0.001340 9.0

Adults 20-49 years old 0.001671 11

Adults 50+ years old 0.001617 11

Females 13-49 years old 0.001646 11

6.0 Residential (Non-Occupational) Exposure/Risk Characterization

There are currently several registered labels with residential turf and ornamental use sites for 

FPE. The residential uses have not previously been assessed by HED and therefore, have been 

assessed in this risk assessment document and the accompanying occupational and residential 

exposure risk assessment (S. Shelat, D416003, 1/23/2014) to reflect updates to HED’s 2012 

Residential SOPs1along with policy changes for body weight assumptions. The residential 

exposures assessed will impact the human health aggregate risk assessment for FPE.

6.1 Residential Handler Exposure

HED uses the term “handlers” to describe those individuals who are involved in the pesticide 

application process. HED believes that there are distinct tasks related to applications and that 

exposures can vary depending on the specifics of each task. Residential handlers are addressed 

somewhat differently by HED as homeowners are assumed to complete all elements of an 

application without use of any protective equipment.

The quantitative exposure/risk assessment developed for residential handlers is based on the 

following scenarios: 

 Manually-pressurized handwand

 

1 Available: http://www.epa.gov/pesticides/science/residential-exposure-sop.html
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 Hose-end Sprayer

 Backpack

 Trigger-sprayer

The residential handler non-cancer risk estimates from the registered non-occupational uses of 

FPE do not result in risk estimates of concern for dermal (MOEs ≥ 100) nor inhalation routes of 

exposure (MOEs ≥ 30). Dermal MOEs range from 1,200 to 120,000 and inhalation MOEs 

range from 420,000 to 190,000,000. An ARI approach was used to calculate the combined 

dermal and inhalation exposure risk estimates because the levels of concern are different for the 

two routes as determined by the uncertainty factors discussed in Section 4.5.1. The ARIs for the 

combined dermal and inhalation exposures are ≥ 1 and therefore do not exceed HED’s level of 

concern. The ARIs range from 12 to 1200 and are provided below in Table 6.1.
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Table 6.1. Short-term Residential Handler Non-cancer Exposure and Risk Estimates for Fenoxaprop-p-ethyl.

Exposure Scenario Use Site

Dermal Unit 

Exposure 

(mg/lb ai)

Inhalation 

Unit Exposure 

(mg/lb ai)

Maximum 

Application 

Rate1

Area Treated or 

Amount Handled 

Daily2

Dermal Inhalation Combined

Dose 

(mg/kg/day)3 MOE4 Dose (mg/kg/day)5 MOE6 ARI7

Mixer/Loader/Applicator

Manually pressurized 

handwand

(Liquid Concentrate)

Gardens/Trees

63 0.018

0.0009

lbs ai/gallon 5 gallons 0.0035 5,600 0.000001 6,700,000 56

0.00000174 

lbs ai/ft2 1200 ft2 0.0016 12,000 0.00000047 14,000,000 120

Lawns/Turf 0.0009 

lbs ai/gallon 5 gallons 0.0035 5,600 0.000001 6,700,000 56

Hose-end sprayer 

(Liquid Concentrate)

Gardens/Trees 58 0.0014

0.00000174 

lbs ai/ft2 1200 ft2 0.0015 13,000 0.000000037 190,000,000 130

0.0009

lbs ai/gallon 11 gallons 0.0072 2,800 0.00000017 39,000,000 28

Lawns/Turf 13.4 0.022 0.076 

lbs ai/acre 0.5 acres 0.0064 3,100 0.00001 650,000 31

Hose-end sprayer

(Ready to Use)

Gardens/Trees

6.26 0.034

0.00000174 

lbs ai/ft2 1200 ft2 0.00016 120,000 0.00000089 7,700,000 1200

0.0009

lbs ai/gallon 11 gallons 0.00077 26,000 0.0000042 1,600,000 260

Lawns/Turf 0.076 

lbs ai/acre 0.5 acres 0.003 6,700 0.000016 420,000 67

Backpack

(Liquid Concentrate)

Gardens/Trees

130 0.14

0.00000174 

lbs ai/ft2 1200 ft2 0.0034 5,900 0.0000037 1,900,000 59

0.0009 

lbs ai/gallon 5 gallons 0.0073 2,700 0.0000079 860,000 27

Lawns/Turf 0.0009 

lbs ai/gallon 5 gallons 0.0073 2,700 0.0000079 860,000 27

Trigger-spray bottle

(Ready to Use)

Gardens/Trees 85.1 0.061 0.008 

lbs ai/bottle

2 bottles 0.017 1200 0.000012 560,000 12

Lawns/Turf 1 bottle 0.0085 2400 0.0000061 1,100,000 23

1 Based on registered labels (see Table 3.3 or D411289).

2 Based on HED’s 2012 Residential SOPs (http://www.epa.gov/pesticides/science/residential-exposure-sop.html).

3 Dermal Dose = Dermal Unit Exposure (mg/lb ai) × Application Rate (lb ai/ft2 or gal) × Area Treated or Amount Handled (ft2/day or gallons/day)÷ Body Weight (kg).

4 Dermal MOE = Dermal NOAEL (mg/kg/day) ÷ Dermal Dose (mg/kg/day).

5 Inhalation Dose = Inhalation Unit Exposure (mg/lb ai) × Application Rate (lb ai/ ft2 or gal) × Area Treated or Amount Handled (ft2/day or gallons/day) ÷ Body Weight (kg).

6 Inhalation MOE = Inhalation NOAEL (mg/kg/day) ÷ Inhalation Dose (mg/kg/day).

7 ARI = Aggregate Risk Index = 1÷ [(Dermal LOC ÷ Dermal MOE) + (Inhalation LOC ÷ Inhalation MOE)].
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6.2 Post-Application Exposure

There is the potential for post-application exposure for individuals exposed as a result of being in 

an environment that has been previously treated with FPE. The quantitative exposure/risk 

assessment for residential post-application exposures is based on the following scenarios: 

 Adults High Contact Lawn Activities

 Children 1 to <2 years old High Contact Lawn Activities

 Adults Mowing Turf

 Children 11 to < 16 years old Mowing Turf

 Adults Ornamental Garden Activities

 Children 6 to < 11 years old Ornamental Garden Activities

The lifestages selected for each post-application scenario are based on an analysis provided as an 

Appendix in the 2012 Residential SOPs2. While not the only lifestage potentially exposed for 

these post-application scenarios, the lifestage that is included in the quantitative assessment is 

health protective for the exposures and risk estimates for any other potentially exposed lifestage.

Dislodgeable Foliar Residues: 

This assessment uses HED’s default assumption that 25% of the application is available for 

transfer on day 0 following the application to ornamental use sites and the residues dissipate at a 

rate of 10% each following day. EPA is not requiring additional 40CFR DFR data.

Turf Transferable Residue Study:

A Turf Transferable Residue (TTR) study for FPE was submitted to the Agency and reviewed 

for use in this assessment. For the purposes of this risk assessment, the highest measured TTR 

value (0.0091 μg/cm2) adjusted for application rate was used in the post-application exposure 

assessment for turf uses of FPE. (S.Shelat, D416436, 1/23/2014)

Table 6.2.1 Summary of Fenoxaprop-p-ethyl Turf Transferable Residue Study (MRID 45251301)

Location Average Application 

Rates (lbs ai/acre)

Highest Mean 

Measured Residue 

(μg/cm2)

Timing of Highest 

Measured Residue

Adjusted TTR 

value for 

Residential Use1

North Rose, New 

York 0.0885 0.0091 0DAT2

0.0078 μg/cm2

Columbia, Missouri 0.0867 0.0047 0DAT5

Ivor, Virginia 0.089 0.0067 0DAT2

1. Maximum application rate for residential lawn/turf use is 0.076 lbs ai/acre, therefore the TTR value for the residential 

lawn/turf assessment was calculated as follows: (0.076 lbs ai/acre * 0.0091 μg/cm2)/0.089 lbs ai/acre = 0.0078 μg/cm2). 

0.089 lbs ai/acre represents the application rate during application treatment 2, after which the highest measured residue 

was collected.

 

2 Available: http://www.epa.gov/pesticides/science/residential-exposure-sop.html
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Since dermal and incidental oral exposure routes share a common toxicological endpoint, risk 

estimates have been combined for those routes. The incidental oral scenarios (i.e., hand-tomouth and object-to-mouth) should be considered inter-related. Combining these scenarios with 

the dermal exposure scenario would be overly-conservative because of the conservative nature of 

each individual assessment. Therefore, the post-application exposure scenarios that were 

combined for children 1 to < 2 years old are the dermal and hand-to-mouth scenarios. This 

combination should be considered a protective estimate of children’s exposure to pesticides used 

outdoors.

Summary of Residential Post-application Non-Cancer Exposure and Risk Estimates

Table 6.2.2 Short-term Residential Post-application Non-cancer Exposure and Risk Estimates for 

Fenoxaprop-p-ethyl.

Lifestage

Post-application Exposure 

Scenario Application 

Rate1

Dose 

(mg/kg/day)2 MOEs3

Combined Routes

(X indicates 

included in 

Combined MOE)

Combined 

MOEs4

Use Site Route of 

Exposure

Adult

Turf- High 

contact lawn 

activity

Dermal 0.076 0.026 760

Child

(1 to <2 years)

Dermal 0.076 0.052 390 X

370 Hand to Mouth 0.076 0.001 5,600 X

Object to Mouth 0.076 0.00003 190,000

Soil Ingestion 0.076 0.0000034 1,800,000

Adult

Turf- Mowing 

turf

Dermal 0.076 0.0005 37,000

Child 

(11 to < 16 

years)

Dermal 0.076 0.0006 33,000

Adult

Ornamentals

Dermal 0.076 0.049 410

Child 

(6 to < 11 

years)

Dermal 0.076 0.033 600

1 Based on registered labels (see Table 3.3).

2 Dose (mg/kg/day) equations provided in D411289 and D403926.

3 MOE = POD (mg/kg/day) ÷ Dose (mg/kg/day).

4 Combined MOE = 1 ÷ (1/dermal MOE) + (1/incidental oral MOE), where applicable.

6.3 Combined Residential Risk Estimates (Multiple Exposure Scenarios)

For FPE, there is the potential for multiple exposure scenarios to be combined. Of the registered 

non-occupational uses of FPE, the use on turf and ornamentals in the residential setting is 

registered on the same label (72155-74), increasing the likelihood that the exposures from these 

application sites may occur on the same day(s) for both the adult handler and post-application 

scenarios. The multiple exposure scenario risk estimate for the handler, which includes both 

dermal and inhalation exposures, do not exceed HED’s level of concern (ARI ≥ 1) and the 

multiple exposure estimate for post-application, which includes only dermal exposure, results in 

an MOE of 267 and is similarly not of concern. The results are provided in Table 6.3. 
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Table 6.3. Short-term Adult Residential Combined (Multiple Exposure Scenarios) Non-Cancer Exposure and Risk 

Estimates for Fenoxaprop-p-ethyl (EPA Reg No 72155-74).

Combined 

Exposure 

Scenario

Exposure Scenario Route of 

Exposure

Dose 

(mg/kg/day)1

Combined 

Total Dose 

(mg/kg/day)2

Total MOEs3 Total ARI4

Outdoor 

Scenario 

(Turf/Garden)

Handler

Turf – Sprays with Trigger 

Pump Sprayer

Dermal 0.0085 Dermal:

0.0255 780

8

Inhalation 0.0000061

Garden – Sprays with 

Trigger Pump Sprayer

Dermal 0.017 Inhalation:

0.000018 376,000 Inhalation 0.000012

Post-application

Turf - Sprays Dermal 0.026 Dermal:

0.075 267 N/A

Garden - Sprays Dermal 0.049

1 Dose (mg/kg/day) taken from Tables 6.1 and 6.2.2.

2 Combined Total Dose (mg/kg/day) = combined dermal + inhalation doses for handlers or combined dermal + inhalation + incidental oral postapplication doses. Handler exposures should not routinely be combined with post-application exposures. 

3 Total MOEs = POD (mg/kg/day) ÷ Total Dose (mg/kg/day).

4 ARI = Aggregate Risk Index = 1÷ [(Dermal LOC ÷ Dermal MOE) + (Inhalation LOC ÷ Inhalation MOE)].

6.4 Residential Risk Estimates for Use in Aggregate Assessment

Table 6.4 reflects the residential risk estimates that are recommended for use in the aggregate 

assessment for FPE.

 The recommended residential exposure for use in the adult aggregate assessment reflects 

post-application dermal exposure from applications to turf and gardens via sprays.

 The recommended residential exposure for use in the children 1 to <2 years old aggregate 

assessment reflects dermal and hand-to-mouth exposures from post-application high 

contact lawn activity exposure from turf applications.

Table 6.4 Recommendations for the Residential Exposures for the Fenoxaprop-p-ethyl Short-term 

Aggregate Assessment.1

Lifestage

Dose (mg/kg/day)2,4 MOE3,5

Dermal Inhalation Oral Total Dermal Inhalation Oral Total ARI 

or MOE

Residential Handler

Adult 0.0255 0.000018 N/A 0.0255 780 376,000 N/A 8 (ARI)

Residential Post-application

Adult 0.075 N/A N/A 0.075 267 N/A N/A 267 (MOE)

Child 0.052 N/A 0.001 0.053 390 N/A 5,640 370 (MOE)

1 Bolded risk estimates should contribute to the residential exposure portion of the aggregate assessment. 

2 Residential Handler Dose = the highest handler dose for each applicable lifestage of all residential handler scenarios assessed. Total = 

dermal + inhalation.

3 Residential Handler MOE = the MOEs associated with the highest residential handler doses. ARI = Aggregate Risk Index = 1÷ [(Dermal 

LOC ÷ Dermal MOE) + (Inhalation LOC ÷ Inhalation MOE)].

4 Residential Post-application Dose = the highest post-application dose for each applicable lifestage of all post-application scenarios assessed. 

Total = dermal + inhalation + incidental oral (where applicable).

5 Residential Post-application MOE = the MOEs associated with the highest post-application doses. Total = Dermal MOE + Inhalation MOE 

+ Incidental Oral MOE (where applicable). 
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6.5 Residential Bystander Post-application Inhalation Exposure

Based on the Agency's current practices, a quantitative post-application inhalation exposure 

assessment was not performed for FPE at this time. However, volatilization of pesticides may be 

a source of post-application inhalation exposure to individuals nearby pesticide applications. 

The Agency sought expert advice and input on issues related to volatilization of pesticides from 

its Federal Insecticide, Fungicide, and Rodenticide Act Scientific Advisory Panel (SAP) in 

December 2009, and received the SAP’s final report on March 2, 20103. The Agency is in the 

process of evaluating the SAP report and may, as appropriate, develop policies and procedures to 

identify the need for and, subsequently, the way to incorporate post-application inhalation 

exposure into the Agency's risk assessments. If new policies or procedures are developed, the 

Agency may revisit the need for a quantitative post-application inhalation exposure assessment 

for FPE.

6.6 Spray Drift

Off-target movement of pesticides can occur via many types of pathways and it is governed by a 

variety of factors. Sprays that are released and do not deposit in the application area end up offtarget and can lead to exposures to those it may directly contact. They can also deposit on 

surfaces where contact with residues can eventually lead to exposures (e.g., children playing on 

lawns where residues have deposited next to treated fields). The potential risk estimates from 

these residues can be calculated using drift modeling coupled with methods employed for 

residential risk assessments for turf products. The approach to be used for quantitatively 

incorporating spray drift into risk assessment includes assessing exposures for children (1 to < 2 

years old) and adults who have contact with turf where residues are assumed to have deposited 

via spray drift thus resulting in an exposure scenario. Aside from the predicted residues 

available for transfer, the routes of exposure and assessment methodology is analogous to how 

exposures to turf products are considered in risk assessment. 

The spray drift risk estimates are based on an estimated deposited residue concentration as a 

result of the screening level agricultural application scenarios. FPE is used on a variety crops 

and turf sites and can be applied via groundboom and aerial equipment at a maximum 

application rates ranging from 0.083 to 0.173 lbs ai/acre. Dermal risk estimates were calculated 

for adults. Dermal and incidental oral risk estimates for children 1 to <2 years old were 

combined because the toxicity endpoint for each route of exposure is the same. The total 

applicable Level of Concern is 100 so MOEs < 100 represent risk estimates that exceed HED’s 

level of concern. Adult and children dermal and children’s incidental oral risk estimates from 

indirect exposure to FPE related to spray drift result in buffers of 0 feet for groundboom and 

aerial applications, (i.e., all MOEs ≥ 100 at the edge of the field). Results for the drift scenarios 

of the highest application rate and chemical-specific TTR values are provided in Appendix C. 

 

3 Available: http://www.epa.gov/scipoly/SAP/meetings/2009/120109meeting.html
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7.0 Aggregate Exposure/Risk Characterization

In accordance with the FQPA, HED must consider and aggregate (add) pesticide exposures and 

risks from three major sources: food, drinking water, and residential exposures. In an aggregate 

assessment, exposures from relevant sources are added together and compared to quantitative 

estimates of hazard (e.g., a NOAEL or PAD), or the risks themselves can be aggregated. When 

aggregating exposures and risks from various sources, HED considers both the route and 

duration of exposure.

7.1 Acute Aggregate Risk

Acute aggregate risk estimates include exposure to residues in food and water alone; therefore, 

the acute aggregate risk estimates are equivalent to the acute dietary risk assessment. However, 

for FPE, no toxic effects attributable to a single dose were observed in the toxicology database. 

As a result, an acute aggregate risk assessment is not required for this chemical. 

7.2 Short-Term Aggregate Risk

There is a potential for short-term exposure to FPE via dietary and residential exposure 

pathways. To estimate short-term aggregate risk, HED combined chronic dietary (average food 

and water) exposures (as a measure of average background dietary exposure) with short-term 

residential exposures. These pathways lead to exposure via oral (background), dermal, and 

incidental oral (hand to mouth) (primary) routes.

The most conservative residential exposure scenario was chosen for the adult population which 

reflects dermal exposure from post-application exposure to turf and gardens (refer to Table 6.3 

and 6.4). The residential exposure for use in the children 1 to <2 years old aggregate assessment 

reflects dermal and hand-to-mouth exposures from post-application high contact lawn activity 

exposure from turf applications.

For adult male background dietary exposure, the adult sub-population with the highest exposure 

(adults 20-49) was chosen since this is protective for all other adult sub-populations. For 

children 1 to < 2 years old, the children 1 to 2 years old background dietary exposure was chosen 

for the short-term aggregate risk assessment. The 1/MOE approach was used for the aggregate 

assessment because route specific toxicological data was available for the different routes of 

exposure.

Short-term aggregate margins of exposure for adults (all adult sub-populations) and children (1 

to < 2 years old) are above the LOC of 100 and do not exceed HED’s level of concern (MOEs ≥ 

100). Short-term aggregate risk estimates are shown below in Table 7.2. 

Table 7.2 Short-Term Aggregate Risk Calculations

Population Short-Term Scenario
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LOC for 

Aggregate 

Risk1

Dietary

MOE2

MOE Oral 

Residential 

Exposure3

MOE 

Dermal 

Residential 

Exposure4

MOE 

Inhalation 

Residential 

Exposure5

Aggregate 

MOE (food, 

water, and 

residential)6

Adult 100 3590 N/A 267 N/A 249

Child 100 1790 5640 390 N/A 302

1 10X interspecies uncertainty factor and 10X intraspecies uncertainty factor totaling 100

2 MOE dietary = [(6 mg/kg/day)/(chronic dietary exposure)] (Table 5.4.5).

3 MOE oral = [(6 mg/kg/day)/(hand-to-mouth residential exposure)] (Table 6.4).

4 MOE dermal = [(20 mg/kg/day)/(high end dermal residential exposure)] (Table 6.4).

5 Not applicable

6 MOE Aggregate = 1/[(1/MOE dietary) + (1/MOE oral) + (1/MOE dermal)]

7.3 Chronic Aggregate Risk

As there are no uses that are expected to result in long-term residential exposure, long-term 

(chronic) aggregate risk includes only chronic dietary (food and water) exposure. As noted in 

Section 5.4.4, there are no chronic dietary risks of concern for FPE.

8.0 Cumulative Exposure/Risk Characterization

Unlike other pesticides for which EPA has followed a cumulative risk approach based on a 

common mechanism of toxicity, EPA has not made a common mechanism of toxicity finding as 

to FPE and any other substances and FPE 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 FPE has a common mechanism of toxicity with other substances. For information 

regarding EPA’s efforts to determine which chemicals have a common mechanism of toxicity 

and to evaluate the cumulative effects of such chemicals, see the policy statements released by 

EPA’s Office of Pesticide Programs concerning common mechanism determinations and 

procedures for cumulating effects from substances found to have a common mechanism on 

EPA’s website at http://www.epa.gov/pesticides/cumulative/.

9.0 Occupational Exposure/Risk Characterization

9.1 Short- and Intermediate-term Handler Risk

HED uses the term handlers to describe those individuals who are involved in the pesticide 

application process. HED believes that there are distinct job functions or tasks related to 

applications and exposures can vary depending on the specifics of each task. Job requirements 

(amount of chemical used in each application), the kinds of equipment used, the target being 

treated, and the level of protection used by a handler can cause exposure levels to differ in a 

manner specific to each application event. 

Based on the anticipated use patterns and current labeling, types of equipment and techniques 

that can potentially be used, occupational handler exposure is expected from the registered and 

proposed uses of FPE. The quantitative exposure/risk assessment developed for occupational 

handlers is based on the following scenarios: 
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 Mixer/Loader for aerial and groundboom equipment

 Applicators for aerial and groundboom equipment

 Flagger for aerial spray applications

 Mixer/Loader/Applicator for backpack equipment

 Mixer/Loader/Applicator for manually-pressurized handwand equipment

 Mixer/Loader/Applicator for mechanically-pressurized handgun equipment

The above exposure scenarios best represent the registered and proposed use patterns for FPE. 

Chemigation applications are prohibited on the product labels.

For FPE, based on the registered and proposed uses, short- and intermediate-term exposures are 

expected because a number of the registered uses allow for multiple applications over the 

growing season. The toxicological endpoints for FPE are the same for both the short-and 

intermediate-term durations, therefore the short-term assessment is protective for the longer 

duration. 

Estimates of dermal and inhalation exposure presented for “baseline,” defined as a single layer of 

clothing consisting of a long sleeved shirt, long pants, shoes plus socks, no protective gloves, and 

no respirator. Most of the currently registered and proposed labels of FPE require PPE in 

addition to baseline attire. PPE on the registered labels ranges from the addition of chemicalresistant gloves to also requiring coveralls, goggles and face shields. Respirators are not required 

PPE on the currently registered or proposed FPE labels.

A total aggregate risk index (ARI) was used since the LOC values for dermal exposure (100) and 

inhalation exposure (30) are different. The target ARI is 1; therefore, ARIs of less than 1 are risk 

estimates of concern. 

For mixer/loaders with baseline attire, ARIs range from 0.56 to 43. With the addition of gloves, 

the mixer/loader ARIs range from 3.1 to 3,900,000. For applicators with baseline attire (except 

for aerial applicators which are always assessed with engineering controls), the ARIs range from 

9 to 31 and with chemical-resistant gloves for groundboom applicators the ARIs range from 45 

to 150. Flagger ARIs range from 21 to 130 and 23 to 140 for baseline attire and chemicalresistant gloves, respectively. For mixers/loaders/applicators the handheld equipment ARIs 

range from 2 to 28 with baseline attire and 3.1 to 440 with the addition of chemical-resistant 

gloves. Risk estimate summary tables are provided below. 
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Table 9.1.1. Short- and Intermediate-term Occupational Handler Non-Cancer Exposure and Risk Estimates for Fenoxapropp-ethyl. All estimates are at Baseline Attire*.

Exposure Scenario Crop or Target

Dermal Unit 

Exposure (ug/lb ai)1

Inhalation Unit 

Exposure (ug/lb ai)1 Maximum 

Application 

Rate2

Area 

Treated or 

Amount 

Handled 

Daily3

Dermal Inhalation Total

Baseline Attire No Respirator Dose 

(mg/kg/day)4 MOE5 Dose (mg/kg/day)6 MOE7 ARI8

Mixer/Loader

Aerial

Nursery

220 0.219

0.173 60 0.0285 700 0.0000284 240000 7

Sod 0.173 350 0.166 120 0.000166 41000 1.2

Rice 0.108

1200

0.356 56 0.000355 19000 0.56

Barley and 

Wheat 0.083 0.274 73 0.000273 25000 0.73

Cotton 0.105 0.346 58 0.000345 20000 0.58

Soybeans 0.1 0.33 61 0.000329 21000 0.61

Conservation 

Reserve Land 0.1 0.33 61 0.000329 21000 0.61

Groundboom

Field-grown 

Ornamentals

220 0.219

0.173 40 0.019 1100 0.000019 360000 11

Nursery 

Ornamentals 0.173 60 0.0285 700 0.0000284 240000 7

Greenhouse 

Ornamentals 0.173 60 0.0285 700 0.0000284 240000 7

Sod 0.173 80 0.038 530 0.0000379 180000 5.3

Rice 0.108

200

0.0594 340 0.0000591 120000 3.4

Barley and 

Wheat 0.083 0.0456 440 0.0000455 150000 4.4

Cotton 0.105 0.0578 350 0.0000575 120000 3.5

Soybean 0.1 0.0699 290 0.0000695 98000 2.9

Conservation 

Reserve Land 0.1 0.0699 290 0.0000695 98000 2.9

Grass Grown 

for Seed 220 0.219 0.082 80 0.018 1100 0.000018 380000 11

Mechanically PressurizedHandgun Right of Ways 220 0.219 0.0017 1000 

gallons 0.00468 4300 0.00000465 1500000 43

Applicator
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Table 9.1.1. Short- and Intermediate-term Occupational Handler Non-Cancer Exposure and Risk Estimates for Fenoxapropp-ethyl. All estimates are at Baseline Attire*.

Exposure Scenario Crop or Target

Dermal Unit 

Exposure (ug/lb ai)1

Inhalation Unit 

Exposure (ug/lb ai)1 Maximum 

Application 

Rate2

Area 

Treated or 

Amount 

Handled 

Daily3

Dermal Inhalation Total

Baseline Attire No Respirator Dose 

(mg/kg/day)4 MOE5 Dose (mg/kg/day)6 MOE7 ARI8

Aerial

*Engineering Controls

Nursery

2.08 0.0049

0.173 60 0.00027 74000 0.000000636 11000000 740

Sod 0.173 350 0.00158 13000 0.00000371 1800000 130

Rice 0.108

1200

0.00338 5900 0.00000794 860000 59

Barley and 

Wheat 0.082 0.00256 7800 0.00000603 1100000 78

Cotton 0.105 0.00328 6100 0.00000771 880000 61

Soybeans 0.1 0.00313 6400 0.00000735 930000 64

Conservation 

Reserve Land 0.1 0.00313 6400 0.00000735 930000 64

Groundboom

Field-grown 

Ornamentals

78.6 0.34

0.173 40 0.0068 2900 0.0000294 230000 29

Nursery 

Ornamentals 0.173 60 0.0102 2000 0.0000441 150000 20

Greenhouse 

Ornamentals 0.173 60 0.0102 2000 0.0000441 150000 20

Sod 0.173 80 0.0136 1500 0.0000589 120000 15

Rice 0.108

200

0.0213 940 0.0000918 74000 9.4

Barley and 

Wheat 0.083 0.0163 1200 0.0000705 96000 12

Cotton 0.105 0.0206 970 0.0000893 76000 9.7

Soybean 0.1 0.0196 1000 0.000085 80000 10

Conservation 

Reserve Land 0.1 0.0196 1000 0.000085 80000 10

Grass Grown 

for Seed 78.6 0.34 0.082 80 0.0065 3100 0.0000279 240000 31

Mechanically PressurizedHandgun Right of Ways 1300 3.9 0.0017

lbs ai/gallon

1000

gallons 0.0276 720 0.0000829 82000 7.2

Flagger
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Table 9.1.1. Short- and Intermediate-term Occupational Handler Non-Cancer Exposure and Risk Estimates for Fenoxapropp-ethyl. All estimates are at Baseline Attire*.

Exposure Scenario Crop or Target

Dermal Unit 

Exposure (ug/lb ai)1

Inhalation Unit 

Exposure (ug/lb ai)1 Maximum 

Application 

Rate2

Area 

Treated or 

Amount 

Handled 

Daily3

Dermal Inhalation Total

Baseline Attire No Respirator Dose 

(mg/kg/day)4 MOE5 Dose (mg/kg/day)6 MOE7 ARI8

All aerial applications 

(Flagger)

Nursery

11 0.35

0.173 60 0.00143 14000 0.0000454 150000 140

Sod 0.173 350 0.00833 2400 0.000265 26000 23

Rice 0.108 350 0.0052 3800 0.000165 41000 37

Barley and 

Wheat 0.083 350 0.004 5000 0.000128 53000 49

Cotton 0.105 350 0.00505 4000 0.000161 42000 39

Soybeans 0.1 350 0.00481 4200 0.000154 44000 41

Mixer/Loader/Applicator

Backpack Sprayer

Greenhouse 

Ornamentals 13200 140

0.002 

lbs ai/gallon 40 

gallons

0.0133 1500 0.00014 49000 15

Nursery 13200 11200 0.0133 1500 0.00014 49000 15

Landscape 

Turf 8260 2.58 0.00826 2400 0.00000258 2600000 24

Right of Ways 8260 2.58

0.0017 

lbs ai/gallon 0.00703 2800 0.00000219 3100000 28

Manually-pressurized 

Handwand

Greenhouse 

Ornamentals

100000 30

0.002 

lbs ai/gallon

40 

gallons Nursery 0.1 200 0.00003 230000 2

Landscape 

Turf

Mechanically-pressurized 

Handgun

Greenhouse 

Ornamentals 3500 120

0.002 

lbs ai/gallon

1000 

gallons 0.0875 230 0.003 2300 2.2

Nursery 1300 3.9

0.002 

lbs ai/gallon

1000

gallons

0.0325 620 0.0000975 70000 6.2

Landscape 

Turf

1300 3.9

0.002 

lbs ai/gallon

1000

gallons

0.0325 620 0.0000975 70000 6.2

1140 1.9 0.173 lbs 

ai/acre 5 acres 0.0123 1600 0.0000205 330000 16

1 Based on the “Occupational Pesticide Handler Unit Exposure Surrogate Reference Table” ([May 2013]); Level of mitigation: Baseline, PPE, Eng. Controls.
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2 Based on registered and proposed labels (Table 4.1 & 4.2).

3 Exposure Science Advisory Council Policy #9.1.

4 Dermal Dose = Dermal Unit Exposure (μg/lb ai) × Conversion Factor (0.001 mg/μg) × Application Rate (lb ai/acre or gal) × Area Treated or Amount Handled Daily (A or gal/day) ÷ BW (kg).

5 Dermal MOE = Dermal NOAEL (mg/kg/day) ÷ Dermal Dose (mg/kg/day).

6 Inhalation Dose = Dermal Unit Exposure (μg/lb ai) × Conversion Factor (0.001 mg/μg) × Application Rate (lb ai/acre or gal) × Area Treated or Amount Handled Daily (A or gal/day) ÷ BW (kg).

7 Inhalation MOE = Inhalation NOAEL (mg/kg/day) ÷ Inhalation Dose (mg/kg/day).

8 Aggregate Risk Index (ARI) = 1÷ (1 ÷ RIdermal) + (1 ÷ RIinhalation) Where: Risk Index (RI) = MOE ÷ LOC 

Table 9.1.2. Short- and Intermediate-term Occupational Handler Non-Cancer Exposure and Risk Estimates for Fenoxapropp-ethyl. All estimates are at Baseline Attire plus Chemical-Resistant Gloves*.

Exposure Scenario Crop or Target

Dermal Unit 

Exposure (ug/lb ai)1

Inhalation Unit 

Exposure (ug/lb ai)1 Maximum 

Application 

Rate2

Area 

Treated or 

Amount 

Handled 

Daily3

Dermal Inhalation Total

Baseline plus 

gloves No Respirator Dose (mg/kg/day)4 MOE5 Dose (mg/kg/day)6 MOE7 ARI8

Mixer/Loader

Aerial

Nursery

37.6 0.219

0.173 60 0.00488 4100 0.0000284 240000 41

Sod 0.173 350 0.0285 700 0.000166 41000 7

Rice 0.108

1200

0.0609 330 0.000355 19000 3.3

Barley and 

Wheat 0.083 0.0434 460 0.000273 25000 4.3

Cotton 0.105 0.0468 430 0.000345 20000 3.4

Soybeans 0.1 0.0593 340 0.000329 21000 3.5

Conservation 

Reserve Land 0.1 0.0593 340 0.000329 21000 3.5

Groundboom

Field-grown 

Ornamentals

37.6 0.219

0.173 40 0.00325 6200 0.000019 360000 62

Nursery 

Ornamentals 0.173 60 0.00488 4100 0.0000284 240000 41

Greenhouse 

Ornamentals 0.173 60 0.00488 4100 0.0000284 240000 41

Sod 0.173 80 0.0065 3100 0.0000379 180000 31

Rice 0.108

200

0.0102 2000 0.0000591 120000 20

Barley and 

Wheat 0.083 0.0078 2600 0.0000455 150000 26

Cotton 0.105 0.00988 2000 0.0000575 120000 20

Soybean 0.1 0.0119 1700 0.0000695 98000 17
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Table 9.1.2. Short- and Intermediate-term Occupational Handler Non-Cancer Exposure and Risk Estimates for Fenoxapropp-ethyl. All estimates are at Baseline Attire plus Chemical-Resistant Gloves*.

Exposure Scenario Crop or Target

Dermal Unit 

Exposure (ug/lb ai)1

Inhalation Unit 

Exposure (ug/lb ai)1 Maximum 

Application 

Rate2

Area 

Treated or 

Amount 

Handled 

Daily3

Dermal Inhalation Total

Baseline plus 

gloves No Respirator Dose (mg/kg/day)4 MOE5 Dose (mg/kg/day)6 MOE7 ARI8

Conservation 

Reserve Land 0.1 0.0119 1700 0.0000695 98000 17

Grass Grown 

for Seed 37.6 0.219 0.082 80 0.00309 6500 0.000018 380000 65

Mechanically PressurizedHandgun Right of Ways 37.6 0.219 0.0017 1000 

gallons 0.0008 25000 0.00000465 1500000 3900000

Applicator

Aerial

*Engineering Controls

Nursery

2.08 0.0049

0.173 60 0.00027 74000 0.000000636 11000000 740

Sod 0.173 350 0.00158 13000 0.00000371 1800000 130

Rice 0.108

1200

0.00338 5900 0.00000794 860000 59

Barley and 

Wheat 0.082 0.00256 7800 0.00000603 1100000 78

Cotton 0.105 0.00328 6100 0.00000771 880000 61

Soybeans 0.1 0.00313 6400 0.00000735 930000 64

Conservation 

Reserve Land 0.1 0.00313 6400 0.00000735 930000 64

Groundboom

Field-grown 

Ornamentals

16.1 0.34

0.173 40 0.00139 14000 0.0000294 230000 140

Nursery 

Ornamentals 0.173 60 0.00209 9600 0.0000441 150000 94

Greenhouse 

Ornamentals 0.173 60 0.00209 9600 0.0000441 150000 94

Sod 0.173 80 0.00279 7200 0.0000589 120000 71

Rice 0.108

200

0.00435 4600 0.0000918 74000 45

Barley and 

Wheat 0.083 0.00334 6000 0.0000705 96000 59

Cotton 0.105 0.00423 4700 0.0000893 76000 46

Soybean 0.1 0.00403 5000 0.000085 80000 49

Conservation 0.1 0.00403 5000 0.000085 80000 49
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Table 9.1.2. Short- and Intermediate-term Occupational Handler Non-Cancer Exposure and Risk Estimates for Fenoxapropp-ethyl. All estimates are at Baseline Attire plus Chemical-Resistant Gloves*.

Exposure Scenario Crop or Target

Dermal Unit 

Exposure (ug/lb ai)1

Inhalation Unit 

Exposure (ug/lb ai)1 Maximum 

Application 

Rate2

Area 

Treated or 

Amount 

Handled 

Daily3

Dermal Inhalation Total

Baseline plus 

gloves No Respirator Dose (mg/kg/day)4 MOE5 Dose (mg/kg/day)6 MOE7 ARI8

Reserve Land

Grass Grown 

for Seed 16.1 0.34 0.082 80 0.00133 15000 0.0000279 240000 150

Mechanically PressurizedHandgun Right of Ways 390 3.9 0.0017

lbs ai/gallon

1000

gallons 0.00829 2400 0.0000829 82000 24

Flagger

All aerial applications 

(Flagger)

Nursery

12 0.35

0.173 60 0.00156 13000 0.0000454 150000 130

Sod 0.173 350 0.00909 2200 0.000265 26000 21

Rice 0.108 350 0.00568 3500 0.000165 41000 34

Barley and 

Wheat 0.083 350 0.00436 4600 0.000128 53000 45

Cotton 0.105 350 0.00551 3600 0.000161 42000 35

Soybeans 0.1 350 0.00525 3800 0.000154 44000 37

Mixer/Loader/Applicator

Backpack Sprayer

Greenhouse 

Ornamentals 11200 140

0.002 

lbs ai/gallon

40 

gallons

0.0112 1800 0.00014 49000 18

Nursery 11200 140 0.0112 1800 0.00014 49000 18

Landscape 

Turf 8260 2.58 0.00826 2400 0.00000258 2600000 24

Right of Ways 8260 2.58

0.0017 

lbs ai/gallon

40 

gallons

0.00703 2800 0.00000219 3100000 28

Manually-pressurized 

Handwand

Greenhouse 

Ornamentals

430 30

0.002 

lbs ai/gallon

40 

gallons Nursery 0.00043 47000 0.00003 230000 440

Landscape 

Turf

Mechanically-pressurized 

Handgun

Greenhouse 

Ornamentals 2500 120

0.002 

lbs ai/gallon

1000 

gallons 0.0625 320 0.003 2300 3.1
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Table 9.1.2. Short- and Intermediate-term Occupational Handler Non-Cancer Exposure and Risk Estimates for Fenoxapropp-ethyl. All estimates are at Baseline Attire plus Chemical-Resistant Gloves*.

Exposure Scenario Crop or Target

Dermal Unit 

Exposure (ug/lb ai)1

Inhalation Unit 

Exposure (ug/lb ai)1 Maximum 

Application 

Rate2

Area 

Treated or 

Amount 

Handled 

Daily3

Dermal Inhalation Total

Baseline plus 

gloves No Respirator Dose (mg/kg/day)4 MOE5 Dose (mg/kg/day)6 MOE7 ARI8

Nursery 390 3.9

0.002 

lbs ai/gallon

1000

gallons

0.00975 2100 0.0000975 70000 21

Landscape 

Turf 390 3.9

0.002 

lbs ai/gallon

1000

gallons

0.00975 2100 0.0000975 70000 21

Turf/Sod 880 1.9 0.173 lbs 

ai/acre 5 acres 0.00951 2100 0.0000205 330000 21

1 Based on the “Occupational Pesticide Handler Unit Exposure Surrogate Reference Table” ([May 2013]); Level of mitigation: Baseline, PPE, Eng. Controls.

2 Based on registered and proposed labels (Table 4.1 & 4.2).

3 Exposure Science Advisory Council Policy #9.1.

4 Dermal Dose = Dermal Unit Exposure (μg/lb ai) × Conversion Factor (0.001 mg/μg) × Application Rate (lb ai/acre or gal) × Area Treated or Amount Handled Daily (A or gal/day) ÷ BW (kg).

5 Dermal MOE = Dermal NOAEL (mg/kg/day) ÷ Dermal Dose (mg/kg/day).

6 Inhalation Dose = Dermal Unit Exposure (μg/lb ai) × Conversion Factor (0.001 mg/μg) × Application Rate (lb ai/acre or gal) × Area Treated or Amount Handled Daily (A or gal/day) ÷ BW (kg).

7 Inhalation MOE = Inhalation NOAEL (mg/kg/day) ÷ Inhalation Dose (mg/kg/day).

8 Aggregate Risk Index (ARI) = 1÷ (1 ÷ RIdermal) + (1 ÷ RIinhalation) Where: Risk Index (RI) = MOE ÷ LOC 
Fenoxaprop-p-ethyl Human Health Risk Assessment DP No. 403928 and 411289

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9.2 Short- and Intermediate-term Post-Application Risk

9.2.1 Dermal Post-application Risk

HED uses the term post-application to describe exposures that occur when individuals are 

present in an environment that has been previously treated with a pesticide (also referred to as reentry exposure). Such exposures may occur when workers enter previously treated areas to 

perform job functions, including activities related to crop production, such as scouting for pests 

or harvesting. Post-application exposure levels vary over time and depend on such things as the 

type of activity, the nature of the crop or target that was treated, the type of pesticide application, 

and the chemical’s degradation properties. In addition, the timing of pesticide applications, 

relative to harvest activities, can greatly reduce the potential for post-application exposure.

Transfer Coefficients:

It is the policy of HED to use the best available data to assess post-application exposure. 

Sources of generic post-application data, used as surrogate data in the absence of chemicalspecific data, are derived from ARTF exposure monitoring studies, and, as proprietary data, are 

subject to the data protection provisions of FIFRA. The standard values recommended for use in 

predicting post-application exposure that are used in this assessment, known as “transfer 

coefficients”, are presented in the ExpoSAC Policy 34” which, along with additional information 

about the ARTF data, can be found at the Agency website5.

Dislodgeable Foliar Residues: 

This assessment uses HED’s default assumption that 25% of the application is available for 

transfer on day 0 following the application and the residues dissipate at a rate of 10% each 

following day.

Turf Transferable Residues:

Chemical-specific turf transferable residue (TTR) data have been submitted for FPE. Therefore, 

this assessment uses the highest measured residue adjusted for the maximum commercial sod 

application rate. A description of the TTR study is provided in Section 6.2. 

Table 9.2: Summary of Occupational/Commercial Post-application Risk Estimates for Fenoxaprop-p-ethyl.

Crop/Site Activities DFR/TTR1 DAT MOE

2

Barley

Scouting

0.233

0 780

Mechanical Harvesting/Swathing/non-Handset 

Irrigation/ Baling Straw - -

Cotton

Scouting

0.294

0 3200

Hand weeding 0 9700

Mechanical wedding/non-Handset Irrigation - -

Ornamentals –

Nursery Crop

Handset Irrigation

0.485

0 220

6 410

Hand harvesting, pruning, weeding, transplanting, 

grafting, propagating, pinching, tying/training, 0 1800

 

4 Available: http://www.epa.gov/pesticides/science/exposac_policy3.pdf

5 Available: http://www.epa.gov/pesticides/science/post-app-exposure-data.html
Fenoxaprop-p-ethyl Human Health Risk Assessment DP No. 403928 and 411289

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Table 9.2: Summary of Occupational/Commercial Post-application Risk Estimates for Fenoxaprop-p-ethyl.

Crop/Site Activities DFR/TTR1 DAT MOE

2

Mechanical wedding, harvesting, non-handset 

irrigation, fertilizing, spreading bins - -

Ornamentals –

Greenhouse Crop

Hand harvesting, pruning, weeding, transplanting, 

grafting, propagating, pinching, tying/training, 0.485

0 1800

Mechanical wedding, harvesting, non-handset 

irrigation, fertilizing, spreading bins - -

Rice

Scouting

0.303

0 600

Hand weeding 0 9400

Mechanical weeding, non-hand set irrigation - -

Sod Maintenance, Slab harvesting, Transplanting/planting 0.0177 0 1700

Roll harvesting - -

Soybean

Scouting

0.28

0 650

Hand weeding 0 10000

Mechanical weeding, non-hand set irrigation - -

Wheat, spring/winter

Scouting

0.233

0 780

Hand weeding 0 12000

Mechanical Harvesting/Swathing/non-Handset 

Irrigation/ Baling Straw - -

Proposed Use

Grass Grown for 

Seed

(Surrogate: Forage 

Crop)

Handset Irrigation

0.23

0 460

Scouting, 0 790

Non-handset Irrigation, , Mechanical harvesting, 

fertilizing - -

1. Default DFR calculation for liquid formulations was utilized. Chemical specific TTR data was utilized for the commercial sod application.

2. MOE = POD (mg/kg/day) / Daily Dermal Dose. Daily Dermal Dose = [DFR/TTR (μg/cm2) x TC x 0.001 mg/μg x 8 hrs/day ]  BW (kg)

In accordance with 40CFR158, DFR data are required for all occupational (e.g., crop, nursery, 

greenhouse use sites) or residential (e.g., ornamental and vegetable gardens, pick your own 

farms, retail tree farms) uses that could result in post-application exposure to foliage. In the 

absence of chemical-specific DFR data, EPA uses default values. The 2012 Standard Operating 

Procedures for Residential Pesticide Exposure Assessment includes an analysis of a number of 

DFR studies, which resulted in the selection of a revised default values for the fraction of the 

application rate available for transfer after a foliar application (FAR). These values are based on 

an analysis of 19 DFR studies. The results indicate a range of FAR values from 2% to 89%. In 

the data, a large range of transferability is observed and this variability can potentially be 

attributable to many factors such as active ingredient; formulation; field conditions in the studies; 

weather conditions (e.g., humidity); or many other difficult to quantify factors. Although 

witnessed across multiple chemicals, this range in FAR values is not expected when considering 

DFR data for a single chemical. EPA selected 25% as the reasonable, high-end default value. 

Because DFR data are not available for FPE, EPA is using the default value of 25%. Although 

there may be a small degree of uncertainty in the use of the default DFR value for FPE (i.e., there 

is a small chance that the FAR value may exceed the applicable default value), it is likely that the 

health-protective aspects of EPA’s residential and occupational post-application assessment 

methodology will more than compensate for this potential uncertainty. For example, when 

assessing residential and occupational post-application exposure, EPA assumes the following: 

exposures occur to zero-day (i.e., day of application ) residues every day of the assessed 

exposure duration (i.e., EPA assumes that no dissipation or degradation occurs, it doesn’t rain, 

etc); individuals perform the same post-application activities performed in the transfer 
Fenoxaprop-p-ethyl Human Health Risk Assessment DP No. 403928 and 411289

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coefficient study day after day (e.g., weeding, harvesting, pruning, etc.); and individuals engage 

in these post-application activities for a high-end amount of time every day (represented by data 

reflecting time spent gardening based on survey data). In actuality, residues will dissipate to 

some degree depending on the chemical; in the residential setting, individuals do not garden 

every day; children do not spend all of their outdoor time in vegetable or ornamental gardens or 

“pick your own” farms; and high-end levels of activity will not occur every day even if 

individuals are in treated areas. In the occupational post-application setting, it is possible that 

individuals may not enter a treated field day 0 after treatment, may not engage in the same type 

of post-application activity, and may not conduct those activities throughout the duration 

assessed. 

Given the conservatisms discussed above and the potential compounding nature of these 

conservatisms, EPA is able to rely upon the calculated exposure estimates with confidence that 

exposure is not being underestimated. 

The highest estimated occupational post-application exposure risk estimate (i.e., nursery crop 

hand set irrigation scenario) using default DFR values for FPE is minimal in comparison to the 

level of concern. EPA is not requiring additional 40CFR DFR data.

9.2.2 Inhalation Post-application Risk

Based on the Agency's current practices, a quantitative post-application inhalation exposure 

assessment was not performed for FPE at this time. However, there are multiple potential 

sources of post-application inhalation exposure to individuals performing post-application 

activities in previously treated fields. These potential sources include volatilization of pesticides 

and resuspension of dusts and/or particulates that contain pesticides. The Agency sought expert 

advice and input on issues related to volatilization of pesticides from its Federal Insecticide, 

Fungicide, and Rodenticide Act Scientific Advisory Panel (SAP) in December 2009, and 

received the SAP’s final report on March 2, 20106. The Agency is in the process of evaluating 

the SAP report as well as available post-application inhalation exposure data generated by the 

ARTF and may, as appropriate, develop policies and procedures, to identify the need for and, 

subsequently, the way to incorporate occupational post-application inhalation exposure into the 

Agency's risk assessments. If new policies or procedures are put into place, the Agency may 

revisit the need for a quantitative occupational post-application inhalation exposure assessment 

for FPE.

Although a quantitative occupational post-application inhalation exposure assessment was not 

performed, an inhalation exposure assessment was performed for occupational/commercial 

handlers. Handler exposure resulting from application of pesticides outdoors is likely to result in 

higher exposure than post-application exposure. Therefore, it is expected that these handler 

inhalation exposure estimates would be protective of most occupational post-application 

inhalation exposure scenarios.

10.0 References

 

6 Available: http://www.epa.gov/scipoly/SAP/meetings/2009/120109meeting.html
Fenoxaprop-p-ethyl Human Health Risk Assessment DP No. 403928 and 411289

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D. Wilbur, December 5, 2013, D415998 and D416001, Fenoxaprop-p-ethyl. Petition for the 

Establishment of a Permanent Tolerance and Registration for Use on Grass Grown for 

Seed (Grass Hay). Summary of Analytical Chemistry and Residue Data for Registration 

Review.

D. Wilbur. November 14, 2013, D415999 and 416002, Fenoxaprop-p-ethyl. Chronic 

Aggregate Dietary (Food and Drinking Water) Exposure and Risk Assessment for 

Registration Review and a New Use on Grass Hay.

J. Kidwell. May 13, 2008, FPE/FE: Joint ToxSAC/HASPOC Meeting to Discuss Briding of 

Mixed and Enriched Isomers.

S. Shelat, January 23, 2014, D411289 and D403928, Fenoxaprop-p-ethyl. Occupational and 

Residential Exposure Assessment for the Registration Review Preliminary Risk 

Assessment and Proposed New Use on Grass Grown for Seed.

S. Shelat, January 23, 2014, D416436, Fenoxaprop-p-ethyl..Determination of Transferable Turf 

Residues on Turf Treated with Fenoxaprop-p-ethyl.

C. Peck, September 25, 2013, D411291 and D404234, Fenoxaprop-p-ethyl Drinking Water 

Assessment for Registration Review and Section 3 New Use Registration

S. Recore, November 13, 2013, D416023, Fenoxaprop-p-ethyl: Tier I Updated Review of 

Human Incidents for Preliminary Risk Assessment
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Appendix A. Toxicology Profile and Executive Summaries

A.1 Toxicology Data Requirements

The requirements (40 CFR 158.340) for the food use for FE/FPE are in Table 1. Use of the new guideline numbers 

does not imply that the new (1998) guideline protocols were used.

Test Technical

Required Satisfied

870.1100 Acute Oral Toxicity

870.1200 Acute Dermal Toxicity

870.1300 Acute Inhalation Toxicity

870.2400 Primary Eye Irritation

870.2500 Primary Dermal Irritation

870.2600 Dermal Sensitization

yes

yes

yes

yes

yes

yes

yes 

yes

yes

yes

yes

yes

870.3100 Oral Subchronic (rodent)

870.3150 Oral Subchronic (nonrodent)

870.3200 21-Day Dermal

870.3250 90-Day Dermal

870.3465 90-Day Inhalation

yes

yes

yes

no

no

yes

yes

yes

no

yesa

870.3700a Developmental Toxicity (rodent)

870.3700b Developmental Toxicity (nonrodent)

870.3800 Reproduction

yes

yes

yes

yes

yes

yes

870.4100a Chronic Toxicity (rodent)

870.4100b Chronic Toxicity (nonrodent)

870.4200a Oncogenicity (rat)

870.4200b Oncogenicity (mouse)

yes

no

yes

yes

yes

yes

yes

yes

870.5100 Mutagenicity—Gene Mutation - bacterial

870.5300 Mutagenicity—Gene Mutation - mammalian

870.5395 Mutagenicity—Other Genotoxic Effects

yes

yes

yes

yes

yes

yes

870.6100a Acute Delayed Neurotox. (hen)

870.6100b 90-Day Neurotoxicity (hen)

870.6200a Acute Neurotox. Screening Battery (rat)

870.6200b 90-Day Neuro. Screening Battery (rat)

870.6300 Developmental Neurotoxicity

no

no

yes

yes

CR

no

no

waivedb

waivedb

no

870.7485 General Metabolism

870.7600 Dermal Penetration

870.7800 Immunotoxicity

yes

no

yes

yes

yes

yes

Special Studies for Ocular Effects no no

a) A 28 day inhalation study is suitable for risk assessment based on the current proposed use pattern, and a 90 day inhalation study is not 

required at this time.

b) Acute and subchronic neurotoxicity studies are not required for FPE (HASPOC TXR#0056489, November 27, 2012)
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A.2 Toxicity Profiles

Acute Toxicity Profile – Fenoxaprop-p-ethyl

Guideline No. Study Type MRID(s) Results Toxicity Category

870.1100 Acute oral [Rats] 42009612

42009613

LD50 = 3.04♂/♀2.09 g/kg

LD50 = 4.0♂ g/kg III

870.1200 Acute dermal [Rat] 42009614 LD50 > 2.0 g/kg III

870.1300 Acute inhalation 42009615 LD50 > 0.604 mg/L III

870.2400 Acute eye irritation 

42009616

No corneal opacity, no iris 

effects, irritation reversible 

within 72 hrs

III

870.2500 Acute dermal irritation

42009617

Very slight irritation, 

resolved by 48 hours

Irritancy index 0.33

IV

870.2600 Skin sensitization

42009618

Buehler method-negative

Magnusson & Kligmanallergic potentialN/A

Fenoxaprop-p-ethyl Toxicity Profile

Guideline 

No. 

Study Type MRID No. (year)/ 

Classification /Doses

Results

870.3100 28-Day oral 

toxicity (Wistar 

rat) (FPE)

47113304 (1986)

Acceptable/non-guideline

20, 80, 320 ,1280, 5120 

ppm

M: 2, 6, 26, 95, and 126 

mg/kg/day

F: 2, 6, 28, 94, and 144 

mg/kg/day

NOAEL = 80 ppm (6 mg/kg/day)

LOAEL = 320 ppm (26/28 mg/kg/day)

Based on altered lipid metabolism (decreased HDLcholesterol, HDL-phospholipids, and total lipids, 

increased triglycerides, and ketonuria) and increased 

liver and kidney weights.

870.3100 90-Day oral 

toxicity (Wistar rat, 

feeding) (FPE)

47113310 (1987)

Acceptable/Guideline

10, 80, 640 ppm

M: 0.7, 5.8, 49 mg/kg/day

F: 0.8, 6.3, 51.8 

mg/kg/day

NOAEL = 5.8/6.3 mg/kg/day

LOAEL = 49/51.8 mg/kg/day

Based on decreased body weights (-11 to 19%), 

increased liver and kidney weights, and altered lipid 

metabolism (decreased HDL-cholesterol, HDLphospholipids, and total lipids, increased triglycerides, 

and ketonuria).
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Fenoxaprop-p-ethyl Toxicity Profile

Guideline 

No. 

Study Type MRID No. (year)/ 

Classification /Doses

Results

870.3100 90-Day oral 

toxicity 

(NMRI/KFM mice,

feeding) (FPE)

47113305 (1987)

47113309 (1987)

Acceptable/Guideline

90-day study: 10, 80, or 

640 ppm (M: 1.4, 11.9, 

and 100.8 mg/kg/day; F: 

2.0, 16.5, and 122.4 

mg/kg/day)

28-day study: 20, 80, 320 

and 1280 ppm (M: 3, 14, 

56, and 260 mg/kg/day; F: 

4, 16, 61, and 280 

mg/kg/day) 

NOAEL = 80 ppm (11.9/14 mg/kg/day)

LOAEL = 320 ppm (56/61 mg/kg/day)

Based on increased liver weight, hepatocellular 

hypertrophy, single or group cell necrosis in the liver, 

and proximal renal tubular injury.

870.3150 90-Day oral 

toxicity (Beagle 

dog, capsule) 

(FPE)

47113308 (1986)

47113303 (1986)

Acceptable/Non-guideline

80, 400, or 2000 ppm

M: 3.0, 15.6, and 77.7 

mg/kg/day

F: 3.2, 16.2, and 83.4 

mg/kg/day

NOAEL = 77.7 mg/kg/day in males

 = 83.4 mg/kg/day in females

No LOAEL was achieved. However, this study is 

acceptable based on bridging to FE. 

870.3200 30-Day dermal 

toxicity (Wistar 

rat) (FPE)

47113306 (1987)

Acceptable/Guideline

10, 20, 100, 500 

mg/kg/day

Systemic NOAEL = 20 mg/kg/day

Systemic LOAEL = 100 mg/kg/day

Based on non-regenerative anemia, decreased serum 

cholesterol, total lipids, and protein (beta 1 globulins), 

and increased liver and kidney weights. Cholesterol 

remained decreased following a 15-day recovery 

period. 

Dermal Toxicity NOAEL is equal to or greater than 

500 mg/kg/day as no toxicologically relevant effects 

were identified.

870.3465 28-Day inhalation 

toxicity 

(Wistar rat) 

(FPE)

47113307 (1989)

Acceptable/Guideline

0.015, 0.07, 0.3 mg/L

NOAEL = 0.07 mg/L in males

 = 0.3 mg/L in females

LOAEL = 0.3 mg/L in males

Based on slight normocytic anemia, decreases in serum 

cholesterol and total lipids, and increases in liver and 

kidney weights and urea nitrogen.
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Fenoxaprop-p-ethyl Toxicity Profile

Guideline 

No. 

Study Type MRID No. (year)/ 

Classification /Doses

Results

870.3700a Prenatal 

developmental 

(Wistar rats) (FPE)

47113318 (1985)

Acceptable/Guideline

10, 32, 100 mg/kg/day

GD 7-16

Maternal NOAEL = 32 mg/kg/day

 LOAEL = 100 mg/kg/day

Based on decreased gestational body weights, body 

weight gains, and food consumption. 

Developmental NOAEL = 32 mg/kg/day

 LOAEL = 100 mg/kg/day based 

Based on decreased fetal body weight (-18%) and 

crown rump length (-10%), and longitudinally 

displaced, fragmented, fused, dysplastic sternebrae or 

dislocated sternebrae, and weak ossification or nonossification of one or several cranial bones. 

870.3700b Prenatal 

developmental 

(rabbit) (FPE)

47113319 (1986)

Acceptable/Guideline

10, 32, 100 mg/kg/day

GD 7-19

Maternal NOAEL = 32 mg/kg/day

 LOAEL = 100 mg/kg/day

Based on decreased body weights gain and food 

consumption.

Developmental NOAEL = 100 mg/kg/day

There were no treatment-related external, visceral, or 

skeletal malformations or variations. There were no 

effects of treatment on fetal body weights, fetal crown 

to rump lengths, or placental weights. Incidences of 

skeletal retardations in the treated groups were similar 

to the concurrent controls and were within historical 

control ranges.

NonGuidelineDevelopmental

Toxicity (Wistar 

rats) (FPE)

47113320 (1986)

Acceptable/non-guideline

10, 32, 100 mg/kg

GD 7-16

Maternal NOAEL = 32 mg/kg

 LOAEL = 100 mg/kg

Based on decreased gestational body weights, body 

weight gains, and food consumption. 

Developmental NOAEL = 32 mg/kg/day

 LOAEL = 100 mg/kg/day

Based on decreased pup body weights.

870.3800 2-Generation 

Reproduction and 

fertility effects

(Wistar rat) (FE)

00159920 (1986)

Acceptable/Guideline

5, 30, 180 ppm (0.25, 1.5, 

9.0 mg/kg)

Parental NOAEL = 1.5 mg/kg

 LOAEL = 9 mg/kg

Based on decreased total lipids and increased liver 

weights. 

Reproductive NOAEL = 9.0 mg/kg 

Offspring NOAEL = 1.5 mg/kg

 LOAEL = 9.0 mg/kg

Based on increased ALP and liver weights. 
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Fenoxaprop-p-ethyl Toxicity Profile

Guideline 

No. 

Study Type MRID No. (year)/ 

Classification /Doses

Results

870.4100b Chronic toxicity 

(Beagle dog, 

capsule) (FE)

00151566 (1985)

Acceptable/Guideline

3, 15, 75 ppm

0.075, 0.375, 1.875 mg/kg

NOAEL = 0.375 mg/kg/day

LOAEL = 1.875 mg/kg/day

Based on reduced body weights (10-12%) and body 

weight gains.

870.4300 Combined chronic 

toxicity/carcinogen

icity (SpragueDawley rat) (FE)

00149664

00149665

00151564

00151565

Acceptable/Guideline

5, 30, 180 ppm 

~0.25, 1.5, 9 mg/kg

NOAEL = 1.5 mg/kg/day

LOAEL = 9 mg/kg/day 

Based on decreased serum lipids, cholesterol and 

relative liver weights in male rats. 

No evidence of carcinogenicity. 

Note: Dosing was considered adequate by CARC based 

on the findings of the 90-day feeding study in rats 

(MRID 00130028) with data showing liver toxicity at 

320 ppm.

870.4200 Carcinogenicity

(NMRI-mice) (FE)

44157402 (1996)

Acceptable/Guideline

40, 115, 320 ppm 

M: 5.7, 16.6, 44.6 mg/kg

F: 6.8, 19.4, 53.7 mg/kg

NOAEL = 5.7/6.8 mg/kg

LOAEL = 16.6/19.4 mg/kg

Based on liver histopathology including hypertrophy, 

single cell necrosis, pigmentation in microphages and 

lipofuscin deposit and increased liver weights. 

Note: No appreciable differences in survival were 

reported for the vehicle control and test groups at any 

dose. All test animals survived to study termination. 

The only clinical sign of note was an increased 

incidence of swollen abdomens in the mid- and highdose males and females. In addition, microscopic 

pathology indicated that hepatocellular hypertrophy 

was observed in the majority of male animals treated 

with 115 or 320 ppm fenoxaprop-ethyl and the majority 

of females at 320 ppm. Dosing was, therefore, 

considered adequate by the CARC based on clinical 

signs (swollen abdomen), increased liver weights, and 

histopathology data at the high dose. 

Gene 

Mutation

870.5100 

Bacterial reverse 

mutation test 

(FPE)

47113314

Acceptable/Guideline

0, 4, 20, 100, 500, 2500, 

5000 μg/plate +/-S9; two 

independent trials.

Negative in S. typhimurium TA1535, TA100, TA1537, 

and TA98 & E. coli WP2 uvrA up to a cytotoxic limit 

dose. 

Cytogenetics 

870.5300

In vitro 

mammalian cell 

gene mutation test 

(FPE)

47113316

Acceptable/Guideline

0, 6.25, 12.5, 25.0, 50.0, 

100 μg/mL +/-S9; two 

independent trials. 

Negative up to an insoluble concentration (40 μg/mL 

+/-S9). No cytotoxicity at any level.
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Fenoxaprop-p-ethyl Toxicity Profile

Guideline 

No. 

Study Type MRID No. (year)/ 

Classification /Doses

Results

Other Effects 

870.5375

In vitro 

chromosome 

aberrations in 

human 

lymphocytes assay 

(FPE)

47113313

Acceptable/Guideline

5.0-125 μg/mL +/-S9. . 

Cells, treated either 

continuously for 24 hrs & 

harvested (-S9) or for 2 

hrs. & harvested at 12 or 

24 hrs (+S9).

Negative up to an insoluble concentration (100 μg/mL 

+/-S9). No cytotoxicity at any level. No clear effects 

(≥50% ↓) on the mitotic index.

Other Effects 

870.5395

Mammalian 

Micronucleus assay

(NMRI Mouse) 

(FPE)

47113317

Acceptable/Guideline

0, 1000, 2000, 4000 

mg/kg oral gavage. 

Negative up to a level that exceeds the limit dose (2000 

mg/kg). Toxic signs at 4000 mg/kg included: narrowed 

palpebral fissures & reduced spontaneous activity. No 

cytotoxic effect on the bone marrow.

Other Effects 

870.5550

Unscheduled DNA 

synthesis in A 549 

human HeLa cells 

(FPE)

47113315

Acceptable/Guideline

0, 0.1, 0.3, 1, 3, 10, 30, 

100 μg/mL +/-S9; two 

independent trials. 

Negative up to the highest soluble concentration (100 

μg/mL +/-S9). No cytotoxicity at any level.

Other Effects 

870.5575

Mitotic gene 

conversion in 

Saccharomyces 

cerevisiae D4 

(FPE)

47113312

Acceptable/Guideline

0, 1.25, 2.50, 5, 10, 20 

μg/mL +/-S9; two 

independent trials

Negative at the ade-2 and try-5 loci up to an insoluble 

concentration (20 μg/mL +/-S9). No cytotoxicity at 

any level.

Other Effects 

NonGuideline

Forward mutations 

in 

Schizosaccharomy

ces pombe P1 

assay (FPE)

47113311

Acceptable/NonGuideline

0, 2.5, 5.0, 10.0, 20.0, 

40.0 μg/mL +/-S9; two 

independent trials.

Negative up to an insoluble concentration (40 μg/mL 

+/-S9). No cytotoxicity at any level.

870.6200a Acute 

neurotoxicity 

screening battery

Waived by HASPOC

870.6200b Subchronic 

neurotoxicity 

screening battery

Waived by HASPOC

870.7485 Metabolism and 

pharmacokinetics

(Sprague-Dawley 

rat) (FPE)

MRID 47113323 (1988)

Acceptable/NonGuideline

HOE 033171 and HOE 046360 were both excreted 

rapidly. ~75% of admin. Dose was recovered in excreta 

0-48 hrs sampling interval. Females tend to excrete 

slightly higher % of admin. Dose via urine than males, 

but is not influenced by dose or number of admins. 

Residue concentrations of several tissues at 168 hrs 

showed no sex differences in either HOE 033171 or 

HOE 046360, highest concern always in kidney. For 

HOE 046360, no racemization occurs after 

administration of dose to rats. The unchanged parent 

and its free acid HOE 088406 stay in their D+-

configuration. The metabolism pathway for both HOE 

033171 and 046360 is identical.
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Fenoxaprop-p-ethyl Toxicity Profile

Guideline 

No. 

Study Type MRID No. (year)/ 

Classification /Doses

Results

870.7600 Dermal penetration

(Sprague-Dawley 

rat) (FPE)

47113321 (2002)

Acceptable/NonGuideline

2.72 ± 0.03 and 617.5 ± 

125.6 μg ai/cm2 skin. 

0.0276 and 6.9 mg/animal 

Estimates of dermal absorption based on the sum of 

residues retained in the urine (including cage wash and 

rinse), GIT and contents, feces, carcass, and blood 

ranged from 6.212% of the applied dose at eight hours 

after initiation of treatment to 16.31% of the applied 

dose at 120 hours after initiation of treatment for the 

low dose and 0.6% of the applied dose eight hours after 

initiation of treatment that increased to 2.012% of the 

applied dose by 120 hours in the high-dose group. 

In Vitro Dermal 

penetration – Rat 

vs. Human (FPE)

47113322 (2000)

Acceptable/NonGuideline

Absorption was ~0.34 μg/cm2/hr for human skin and 

2.32 μg/cm2/hr for rat skin (or ~6.8 times greater for 

rat skin than human skin) when applied at a nominal 

concentration of 550 μg/cm2. When the test material 

was applied diluted 75-fold as for end use, rat skin was 

only slightly more permeable (~1.6 times) than human 

skin. Absorption through human skin was ~0.02 

μg/cm2/hr and 0.034 μg/cm2/hr for rat skin when 

fenoxaprop-p-ethyl was applied at a nominal 

concentration of 7.3 μg/cm2. 

870.7800 Immunotoxicity

(Female Wistar 

Rat) (FPE)

48445201 (2011)

Acceptable/Guideline

70, 210, 630 ppm 

5.5, 16, or 47 mg/kg/day

Systemic NOAEL = 210 ppm (16 mg/kg/day)

 LOAEL = 630 ppm (47 mg/kg/day) 

Based on decreased body weight gains and food 

consumption.

Under conditions of this study, the immunotoxicity 

NOAEL is 630 ppm (47 mg/kg/day) (HDT)

HDT= highest dose tested

A.3 Hazard Identification and Endpoint Selection

A.3.1 Chronic Reference Dose (cRfD)

Study Selected: Combined Chronic Toxicity/Carcinogenicity Study and 2-Generation 

Reproductive Toxicity Study in rats. 

MRIDs: 00149664, 0149665, 00151564, and 00151565 (Chronic), and 00159920 (2-Gen)

Dose and Endpoint for Risk Assessment: NOAEL=1.5 mg/kg/day based on decreased serum 

lipids and cholesterol, and altered liver weights, as well as increased ALP and liver weights in 

pups from the 2-generation reproductive toxicity study at LOAEL of 9 mg/kg/day (M/F).

Uncertainty Factor: 100x (10x interspecies extrapolation, 10x intraspecies variability, 1x FQPA 

Safety Factor)

Comments on Study/Endpoint/Uncertainty Factors: The studies are of appropriate duration. 

The Chronic Toxicity/Carcinogenicity and 2-Generation Reproductive Toxicity studies are 

considered to be co-critical as systemic effects from both studies and developmental effects from 

the two-generation study were observed at the same NOAEL and LOAEL. It is also protective of 

developmental effects seen at LOAEL of 32 mg/kg/day in the rat developmental study, and 

systemic effects in the rat and mouse subchronic and chronic studies throughout the FE/FPE 
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database. A lower NOAEL of 0.375 mg/kg/day was identified in the chronic dog study with FE. 

However, this was not considered a critical NOAEL, taking into consideration the minimal 

effects that occurred in the study (10-12% reduction in body weights) and no toxicity was 

observed in the 90-day dog study with FPE. 

Chronic RfD = 

100( )

1.5mg/kg/day

UF

= 0.015 mg/kg/day

A.3.2 Incidental Oral Exposure (Short-term, 1-30 days)

Study Selected: 28-Day Feeding Study in Rats (FPE)

MRID No.: 47113304

Dose and Endpoint for Risk Assessment: NOAEL=6 mg/kg/day based on altered lipid 

metabolism (decreased HDL-cholesterol, HDL-phospholipids, and total lipids, increased 

triglycerides, and ketonuria) and increased liver and kidney weights.

Uncertainty Factor: 100x (10x interspecies extrapolation, 10x intraspecies variability, 1x FQPA 

Safety Factor)

Comments on Study/Endpoint/Uncertainty Factors: The endpoint of concern in this study is 

appropriate for the population (infant and children) and the duration of concern.

A.3.3. Dermal Exposure (Short- and Intermediate-Term)

Study Selected: 28-Day Dermal Toxicity Study in Rats (FPE)

MRID No.: 47113306

Dose and Endpoint for Risk Assessment: NOAEL=20 mg/kg/day based on non-regenerative 

anemia, decreased serum cholesterol, total lipids, and protein (beta 1 globulins), and increased 

liver and kidney weights were observed at a LOAEL of 100 mg/kg/day. 

Uncertainty Factor: 100x (10x interspecies extrapolation, 10x intraspecies variability, 1x FQPA 

Safety Factor)

Comments: This study is appropriate for the short and intermediate duration as no increase in 

toxicity occurred over time throughout the FPE or FE database. There is no proposed long-term 

use; therefore, risk assessment for long-term dermal exposure is not required.

A.3.4 Inhalation Exposure (Short-, and Intermediate-Term)

Study Selected: 28-Day Inhalation Study 

MRID No.: 47113307

Dose and Endpoint for Risk Assessment: NOAEL=0.07 mg/L based on slight normocytic 

anemia, decreases in serum cholesterol and total lipids, and increases in liver and kidney weights 

and urea nitrogen at LOAEL of 0.03 mg/L (M/F). 

Uncertainty Factor: 30x (3x interspecies extrapolation, 10x intraspecies variability, 1x FQPA 

Safety Factor)
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Comments on Study/Endpoint/Uncertainty Factors: This study is appropriate for the short 

and intermediate duration as no increase in toxicity occurred over time throughout the FPE or FE 

database. There is no proposed long-term use; therefore, risk assessment for long-term inhalation 

exposure is not required.

A.4 Executive Summaries

A.4.1 Subchronic Toxicity

870.3100 28-Day Oral Toxicity – Rat (FPE)

In a 28-day oral toxicity study (MRID 47113304) HOE 046360 (Batch no. OH ZC960002; 

95.6%) was administered to 5 Wistar, KFM-han., SPF rats/sex/dose in the diet at levels of 0, 20, 

80, 320, 1280 and 5120 ppm (equivalent to 0, 2, 6, 26, 95 and 126 mg/kg/day, in males and 0, 2, 

6, 28, 94 and 144 mg/kg/day, in females). The males and females dosed at 5120 ppm were killed 

due to severe systemic toxicity on exposure day 9; the remaining exposure groups received the 

test diets for at least 28 days.

Based on study results, there were no compound-related effects on hematology or gross and 

histological pathology. Animals dosed at 5120 ppm lost body weight and became emaciated; as 

noted, these animals were killed on day 9 of exposure. Clinical signs in these animals included 

curved posture and ruffled fur in addition to emaciation. Clinical examinations were not 

conducted on the remaining animals. Body weights, body weight gain, and food consumption 

were significantly decreased in the 1280 ppm group in both sexes. Compound-related changes in 

clinical chemistry parameters indicated altered lipid metabolism and included decreased levels 

of total cholesterol and HDL-cholesterol at 320 (-31.2 and -50%, respectively) and 1280 ppm ( -

51.8 and -74.5%, respectively) in males, decreased HDL-phospholipids at 80 ppm and above in 

males (-17.9, -27.8 and -42.6%, respectively), increased triglyceride at 320 ppm in females 

(+47%) and 1280 ppm in both sexes (M: +129%, F: +153%). Additionally, compound-related 

changes in urinalysis parameters included detection of ketones at 80 ppm in males and at 320 and 

1280 ppm in both sexes. Alkaline phosphatase (M: +61.8%, F: +101%) and leucine 

aminotransferase activities (M: +14.5%, F: +27%) were increased at 1280 ppm in both sexes 

without correlative histopathological changes in the liver. Bilirubin and urobilinogen were seen 

in males at 320/1280 ppm and 80 ppm and above, respectively. Decreased creatinine and 

creatinine clearance were also seen at 1280 ppm in males, which may be an indication of 

decreased glomerular function. An increased level of lactate dehydrogenase (LDH) was 

observed in females at 1280 ppm. Absolute and liver relative weights were increased at 320 ppm 

and above in both sexes. Compound-related increases in relative kidney weights were seen at 

320 and 1280 ppm in both sexes. Clinical chemistry changes at 80 ppm were not considered 

adverse in the absence of corresponding liver weight changes. 

The Systemic Toxicity LOAEL is 320 ppm (26 mg/kg/day), based on altered lipid metabolism 

(decreased HDL-cholesterol, HDL-phospholipids, and total lipids, increased triglycerides, and 

ketonuria) and increased liver and kidney weights.

The Systemic Toxicity NOAEL is 80 ppm (6 mg/kg/day).
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This 28-day oral toxicity study in the rat is Acceptable/Non-guideline. There is no guideline for 

a range-finding study. Many parameters that should have been assessed were omitted; 

deficiencies are listed in the Study/Report Deficiencies section of this DER. This study can be 

used to support a guideline study in the rat.

870.3100 90-Day Oral Toxicity- Rat (FPE)

In a 90-day oral toxicity study (MRID 47113310), HOE 046360 (Batch no. OH ZC960002; 

95.6% a.i.) was administered to 10 Wistar, KFM-han., SPF rats/sex/dose in the diet at dietary 

levels of 0, 10, 80 and 640 ppm (equivalent to 0, 0.7, 5.8 and 49 mg/kg/day, in males and 0, 0.8, 

6.3 and 51.8 mg/kg/day, in females) for 13 weeks. Ten additional rats/sex/dose received dietary 

levels of 0, 80 and 640 ppm for 13 weeks and a recovery evaluation was performed on these 

animals for 4 weeks after the termination of exposure.

There were no significant compound-related effects on mortality, clinical signs, eyes or gross 

pathology. The following significant compound-related effects were seen at 640 ppm: decreased 

body weight (19% in males, 11% in females) and body weight gain (31% in males, 11% 

females); increased serum alkaline phosphatase activity in both sexes (163% males, 23% 

females), altered lipid metabolism: decreased concentrations of total cholesterol (-37%) and 

HDL-phospholipids in males (-32%), decreased HDL-cholesterol in both sexes (-61% males, -

13% females), increased triglyceride in females (24%), and ketonuria in males; and increased 

absolute and relative liver weights in males (23 and 46%, respectively) and females (20 and 

32%, respectively). These results suggest a treatment-related perturbation in lipid metabolism as 

well as impaired liver function. Absolute and relative kidney weights were also increased in 

high-dose female rats (13 and 25%, respectively). 

The LOAEL is 640 ppm (49 and 51.8 mg/kg/day in males and females, respectively) based on 

decreased body weights (-11 to 19%), increased liver and kidney weights, and altered lipid 

metabolism (decreased HDL-cholesterol, HDL-phospholipids, and total lipids, increased 

triglycerides, and ketonuria). The Systemic Toxicity NOAEL in this study is 80 ppm (5.8 and 6.3 

mg/kg/day in males and females, respectively). 

This 90-day oral toxicity study in the rat is Acceptable/Guideline and satisfies the guideline 

requirement for a 90-day oral toxicity study (OPPTS 870.3100; OECD 408) in rat when taken 

together with MRID 00130028. Although this second subchronic rat study was conducted with 

the racemic Fenoxaprop-ethyl (FE) rather than the enriched compound, Fenoxprop-p-Ethyl 

(FPE), the ToxSAC and HASPOC determined that FE studies can be bridged with FPE.

870.3100 90-Day Oral Toxicity – Mouse (FPE)

In a subchronic oral toxicity study, HOE 046360 technical was tested in NMRI/KFM-han 

outbred mice by dietary treatment for 28 or 90 days. Results of both studies are presented in this 

report. In the dose range-finding study (MRID 47113305), HOE 046360 Technical (95.6% a.i., 

Batch No. OH ZC06 002) was administered to mice (5/sex/dose) in the diet at dose 

concentrations of 0, 20, 80, 320 and 1280 ppm (equivalent to 0, 3, 14, 56, and 260 mg/kg bw/day 
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for males and 0, 4, 16, 61, and 280 mg/kg bw/day for females) for 28 days. In the 90-day oral 

toxicity study (MRID 47113309), HOE 046360 Technical (95.6% a.i., Batch No. OH ZC06 002)

was administered to mice (10/sex/dose) in the diet at dose concentrations of 0, 10, 80, or 640 

ppm (equivalent to 0, 1.4, 11.9, and 100.8 mg/kg/day for males and 0, 2.0, 16.5, and 122.4 mg/kg 

bw/day for females. 

In the 28-day feeding study, dietary treatment at doses up to 1280 ppm did not cause adverse 

effects on clinical signs, survival, body weight, body weight gain, or food consumption. 

Treatment-related findings at 1280 ppm included significant increases in aspartate aminotransferase (356%), and alkaline phosphatase (452%) activities in males as well as alanine 

aminotransferase activity in males (997%) and females (396%), increases in protein concentration (25%) and sodium concentration (10%) in males and albumin (17%-33%) concentration in 

both sexes. Effects on organs included increased liver weights (172%-265%) associated with 

hepatocellular hypertrophy (100%) and single cell necrosis (40%-100%), as well as increased 

incidences of renal tubular injury in both sexes (33%-100%). At 320 ppm, there were significant 

increases in sodium concentration (9%) in males, increase in relative liver weights (33%-74%) 

and liver hypertrophy (100%) in both sexes, and single cell necrosis (40%) in males as well as 

renal tubular injury (20%-80%) in both sexes. The statistically significant increase in absolute 

kidney weights in females at 80 ppm was not considered to be toxicologically relevant. No 

adverse effects were seen following treatment with 20 ppm.

Following oral administration HOE 046360 Technical for 90 days, there were no adverse effects 

on survival, body weight and body weight gain, food consumption, and hematology. At 640 

ppm, the treatment-related effects seen in one or both sexes consisted of significant increases in 

alanine aminotransferase (102%) and alkaline phosphatase (171%) activities and albumin concentration (13%) in males, as well as increased absolute (100-137%) and relative (93%-140%) 

liver weights, hepatocellular hypertrophy (100%), and group cell necrosis (10%-20%). These 

changes were toxicologically significant and indicative of liver toxicity. The liver effects were 

more pronounced in males than in females. Proximal renal tubular injury noted at 640 ppm 

(50% in males, 100% in females) and renal cortical calcification (100% in females) was 

accompanied by increase in urea (91% in females) and sodium concentration (13% in males). 

Based on the combined results of both studies, the Systemic Toxicity LOAEL is 320 ppm 

(61 and 56 mg/kg/day, for females and males, respectively) increased liver weight, 

hepatocellular hypertrophy, single or group cell necrosis in the liver, and proximal renal 

tubular injury.

The Systemic Toxicity NOAEL is 80 ppm (16.5 and 14 mg/kg/day, for females and males, 

respectively)

The 28-day oral toxicity study in mice is a dose range-finding study and therefore, is not 

intended to meet the guideline requirements. The 13-week oral toxicity study in mice is

Acceptable/ Guideline and as such satisfies the guideline requirements for the 90-day oral 

toxicity study (OPPTS 870.3100; OECD 408) in mice.

870.3150 90-Day Oral Toxicity – Dog (FPE)
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In a 90-day oral toxicity study (MRID 47113308), HOE 046360 Technical (95.6% a.i., Sample 

No. 13646) was administered to four beagle dogs/sex/dose in diet at dose levels of 0, 80, 400, or 

2000 ppm (equivalent to 0, 3.0, 15.6, and 77.7 mg/kg bw/day, in males and 0, 3.2, 16.2, and 83.4 

mg/kg bw/day, in females). Doses were based on results of a 28-day range-finding dietary study 

in beagles (MRID 47113303).

No deaths occurred, no clinical signs related to treatment were observed, and no treatmentrelated changes were noted in ophthalmoscopic findings, hematologic, clinical chemistry and 

urinalysis findings, organ weights and their ratios, or macroscopic and microscopic findings. 

Body weight gain in high-dose males was consistently reduced compared to controls, with the 

body weight gain over the dosing interval of Days 0-90 reduced by 41%. However, as the 

reduced body weight gain did not follow a clear dose-response and were not accompanied by 

changes in absolute body weight, they are not considered to be treatment related. Compared to 

controls, high-dose females had a biologically significant reduction in body weight gain over 

Days 20-42 (-50% of controls; not statistically significant) that was accompanied by a reduction 

in food consumption (reduced by 11% and 7% over weeks 22-28 and 36-42; respectively). 

However, as the reduced body weight gain and food consumption were transient, and no effects 

on absolute body weight were reported, these changes were not considered to be adverse. 

The study authors considered the decreased alanine aminotransferase activity in the high-dose 

male and female groups and increased total protein in the high-dose male group to be an effect of 

treatment. However, these values were not biologically significant and were within the historical 

control range that was supplied in the study report (Attachment 6 of MRID 47113308). 

Additionally, the changes were not accompanied by any other indications of toxicity such as 

gross or microscopic changes. Therefore, the reviewer does not agree that these changes are an 

adverse effect of treatment.

The Systemic Toxicity NOAEL is 77.7 mg/kg/day (2000 ppm) and 83.4 mg/kg bw/day (2000 

ppm) in females.

This 90-day oral toxicity study in the dog is Acceptable/Guideline and as such satisfies the 

guideline requirement for a 90-day oral toxicity study (OPPTS 870.3150; OECD 409) in dogs. 

No LOAEL was achieved in this study. Based on the range-finding study (no effects up to and 

including 1280 ppm), the animals could have tolerated a higher dose. However, based on 

bridging with FE, the study is acceptable. 

870.3200 21/28-Day Dermal Toxicity – Rat (FPE)

In a 30-day dermal toxicity study (MRID 47113306), Hoe 046360 (Fenoxaprop-p-ethyl; 95.6% 

a.i., batch/lot# not reported) in sesame oil was applied to the clipped skin of groups of Wistar 

[Hoe: WISKf(SPF71)] rats, under occlusive conditions, 6 hours/day, 5 days/week, for a total of 

21 treatments during a 30-day period. Animals were treated at dose levels of 0, 10, 20, 100, or 

500 mg/kg bw/day (6/sex/dose were treated at dose levels of 10 or 20 mg/kg bw/day and 

12/sex/dose at 100 or 500 mg/kg). Six animals/sex/dose (all dose levels) were killed on Day 30, 
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and satellite groups of 6 male and 6 female animals from the control, and the 100 and 500 mg/kg 

groups were killed on Day 44, after a 14-day recovery period. 

There were no deaths during the study, and clinical signs were limited to local effects (dry, 

chapped skin, with or without fine or coarse scales) at the application sites. No treatment related 

toxicologically relevant effects were identified on body weights, food consumption, water 

consumption, ophthalmoscopic examination, or sacrifice and pathology. 

On day 30, the males in the 100 and 500 mg/kg groups had mild normocytic, normochromic, 

non-regenerative anemia (hematocrit: 48%, 44%, and 43% for control, 100 and 500 mg/kg, 

respectively; p<0.05). 100 mg/kg males showed partial recovery by Day 44, but the high-dose 

males did not (hematocrit: 47%, 45%, and 43% for control, 100 and 500 mg/kg, respectively). In 

addition, reticulocytes remained decreased in high-dose males between day 30 (n.s.) and day 44 

(2.6% vs. 6.7% for controls; p<0.05). In males, decreased serum cholesterol and a concomitant 

decrease in total lipids were seen in the 100 and 500 mg/kg groups on day 30 (cholesterol: 1.60, 

1.19, and 1.10 mmol/L in ascending dose order), and both parameters remained decreased at the 

high-dose on Day 44 (cholesterol: 1.58 vs. 1.92 mmol/L in controls). Decreases in serum protein 

concentration and the β1-globulin fraction were seen in males at 100 and 500 mg/kg on day 30, 

only. In females, treatment-related effects on clinical pathology parameters occurred only at the 

high-dose and on Day 30; these included decreased reticulocytes (2.6% vs. 4.5% for controls; 

p<0.05) and decreased serum cholesterol (1.05 vs. 1.48 mmol/L for controls; p<0.05).

High-dose males had increased absolute and relative liver and kidney weights and decreased 

heart and spleen weights (liver: +37%/+40%; kidney: +13%/+15%; heart: -17%/-16%; spleen: 

-25/-23), but by day 44, only the heart weight remained affected (-17%/-16% absolute/relative). 

In 100 mg/kg males, liver and kidney weights were increased on day 30 only (liver: 

+16%/+15%; kidney: +10%/+9% absolute/relative). High-dose females had increased liver and 

kidney weights on day 30 only (liver: +15%/+20%; kidney: +11%/+16% absolute/relative). 

There were no treatment-related effects on gross or microscopic pathology, other than local 

microscopic changes at the application sites.

Decreases in serum cholesterol and total lipids, and increases in liver weight are consistent with 

altered lipid metabolism and were also observed in the 28- and 90-day oral toxicity studies. In 

addition, increases in urine ketone bodies may be indicative of increased breakdown of lipids. 

The treatment-related hematological effects are considered to be toxicologically relevant as 

decreases were greater than 5% of the concurrent controls. The fact that the high-dose males 

showed little if any increase in erythrocyte mass during recovery, and decreased reticulocytes 

were observed in high-dose animals of both sexes is also significant. Decreases in reticulocytes 

may consistent with a bone marrow alteration and/or kidney dysfunction, and the decrease in 

high-dose males is of particular concern, as it is an inappropriate response in the face of anemia. 

The decreased spleen weight in high-dose males is consistent with impaired erythropoiesis, as 

well. Additionally, transferrin is the chief component of the β1 globulin fraction, and a decrease 

in transferrin has the potential to alter iron metabolism and thus erythrocyte production. 
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The Systemic Toxicity LOAEL is 100 mg/kg/day, based on non-regenerative anemia, 

decreased serum cholesterol, total lipids, and protein (beta 1 globulins), and increased liver 

and kidney weights. The Systemic Toxicity NOAEL is 20 mg/kg/day.

The Dermal Toxicity NOAEL is equal to or greater than 500 mg/kg/day as no 

toxicologically relevant effects were identified.

This study is Acceptable/Guideline and as such satisfies the guideline recommendations for a 

28-day dermal toxicity study (OPPTS 870.3200; OECD 410) in rats. 

870.3465 28-Day Inhalation – Rat (FPE)

In a 28-day inhalation toxicity study, (MRID 47113307) [Hoe 046360 (Code Hoe 046360 OH 

ZC96 0002, 95.6 % purity)] four groups of rats consisting of 15 males and 15 females per group 

were administered the test material by nose-only exposure at concentrations of 0, 0.015, 0.07, or 

0.3 mg/L. The exposures were for six hours per day, 5 days per week for a total of 28 exposures. 

Ten males and ten females were killed and necropsied one day after the last exposure, and the 

remainder were killed and necropsied after a recovery period of 29 days.

In males rats, hemoglobin concentration (-9.8%), hematocrit (-10.9%), and thromboplastin time 

(-17.8%) were decreased (p<0.05) in the 0.3 mg/L group. Thromboplastin time was also 

decreased in males in the mid-dose group (0.07 mg/L). The effects in male rats persisted 

throughout the 29-day recovery period. Activated partial thromboplastin (APTT) time was 

increased in females at the high concentration compared to controls (p<0.05). There were no 

correlating histological findings to the observed hematology changes relative to controls and no 

effects were observed in the female rats following the 29-day recovery period. 

There was a decrease in cholesterol and total lipids in both males and females at the high 

exposure level accompanied by an increase in urea nitrogen (p<0.05). Males at the high exposure 

level showed increases in triglycerides and decreases in α2-globulin that may be treatment 

related due to the possible interactions with lipoproteins and lipid metabolism. There were no 

correlating histological findings to the observed clinical chemistry changes relative to controls. 

However, at the end of the 4-week recovery period, the hemoglobin concentration, hematocrit, 

and thromboplastin time remained decreased (p<0.05) in males relative to controls.

In males, significant increases (p<0.05) in absolute liver weights were observed at all dose 

levels, and significant increases in relative liver weights were observed in the mid- and high-dose 

groups. At the high-dose, significant increases in relative liver weights were also identified 

following the 29-day recovery period. Significant increases in kidney weights observed for both 

sexes in the high-dose group but did not persist following the 29-day recovery period. 

Additionally, females showed increased absolute and relative liver weights in the top dose 

following the exposure were comparable to controls following 29-day recovery. 

Decreases in both hemoglobin (-9.8%) and hematocrit (-0.9%) values, which persisted after the 

29-day recovery period may indicate slight normocytic anemia in male rats. Evidence of slight 

normocytic anemia was also observed in male rats following the 30-day dermal toxicity study. 
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In both sexes, decreases in serum cholesterol and total lipids, and increases in liver weight and 

urea nitrogen are consistent with altered lipid metabolism. These effects were only observed in 

male rats following the 29-day recovery period, and were therefore not considered to be adverse 

in females. 

The Systemic Toxicity LOAEL for male rats is 0.3 mg/L following 28 days of inhalation 

exposure to Hoe 046360 based on slight normocytic anemia, decreases in serum cholesterol 

and total lipids, and increases in liver and kidney weights and urea nitrogen. The Systemic 

Toxicity for male rats is NOAEL is 0.07 mg/L. 

The Systemic Toxicity NOAEL for female rats is 0.3 mg/L, the highest-tested dose. 

Submission by Registrant (Dana Sargent, Feb 20, 2008): Doses selected based on subchronic 

feeding study (MRID 4713310). Due to the type of particle collection system used in this study, 

a calculated MMAD and GSD were not provided for this study. Particle sizes generated in this 

study were generally very small, as stated in the report, “98% of the particles had an 

aerodynamic diameter less the 7 microns in all treatment groups, and 22 to 49% were less than 1 

micron.” Pg 25. The reason for the small particle size was that the test substance could not be 

dispersed in its original state. Therefore, HOE 046360 was micronized and used as a fine dust. 

Based on the cumulative distribution tables and graphs for median mass diameter of the particles 

collected (starting p 230 of the report) at multiple time points for each dose level, between 74-

97% of the particles were below 4 μm, with diameter values at the cumulative 50th percentile 

(50% of the particles being ≤) ranging from 1.2-1.5 μm. Therefore, while an overall MMAD 

was not presented in the study, the distribution of particle size is within the current guideline 

requirements.

This 28-day inhalation toxicity study in the rat is Acceptable/Guideline and as such satisfies the 

guideline requirement (OPPTS 870.3465 [§82-4], OECD 413) for a subchronic inhalation study 

in the rat.

A.4.2 Prenatal Developmental Toxicity

870.3700a Prenatal Developmental Toxicity Study – Rat (FPE)

In a developmental toxicity study (MRID 47113318), HOE 046360 (fenoxaprop-p-ethyl; >99% 

a.i.; Serial No. 0321, OH ZB99 0002) was administered by oral gavage to presumed pregnant 

Wistar rats (20/sex/dose) at doses of 0, 10, 32, or 100 mg/kg bw/day from gestation days (GD) 7-

16. On GD 21, all dams were euthanized, and the uterus was removed via cesarean section and 

its contents examined. Fetuses were examined for external, visceral, and skeletal malformations 

and variations.

All dams survived until the end of the study. At 100 mg/kg, a slight increase in incidence of 

increased urinary excretion was noted (20% treated vs 0% controls). Increased urinary excretion 

was observed in 2 dams during GD 13-16 and 20-21, in 1 dam during GD 11-16, and in 1 dam 

during GD 19-21. The biological relevance for this observation is unclear. The intake of fluids 

was not monitored.
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At 100 mg/kg/day, decreased maternal body weights and maternal body weight gains were 

observed. Decreased (p≤0.05) body weight was noted on GD 17 (decreased 15% and outside the 

normal range of historical control data) and GD 21 (decreased 13%; within the normal range of 

historical control data). Body weight gains were decreased by 45-90% during GD 7-14 and GD 

14-17. Overall body weight gain (GD 0-21) was decreased by 30%. Food consumption differed 

(p≤0.05 and outside the normal range of historical control data) from controls during GD 14-17 

(decreased 1%) and 17-21 (increased 13%). Thus, during GD 17-21, a slight increase in food 

consumption was noted at the same time there was a slight decrease in body weight gain, 

suggesting decreased food efficiency (not calculated). Decreased (not statistically significant; 

NS) food consumption was also noted during GD 7-14 (decreased 32%), which corresponded to 

the decrease in body weight gain of 90% observed during this period. 

Additionally, heart weight was decreased (p≤0.05; outside of the normal historical control range) 

at 100 mg/kg (decreased 17%). This may be due to decreased body weights. No histopathology 

was available for the heart.

The Maternal Toxicity LOAEL is 100 mg/kg bw/day based on decreased body weight, body 

weight gain, and heart weight. The Maternal Toxicity NOAEL is 32 mg/kg/day.

At 100 mg/kg/day, the following findings were observed: 2 abortions (vs 0 controls), 2 dead 

fetuses (vs 0 controls), and 22 resorptions (vs 11 controls); increased post-implantation loss 

(10.0% treated vs 4.1% controls); and decreased (p≤0.05) placental weight (decreased 16%). 

One 32 mg/kg/day dam aborted; however, there was no further evidence to corroborate toxicity 

at this dose level. There were no premature deliveries and no effect on sex ratio at any dose. 

Also, there was no change in litter size between control and treated groups.

Decreased (p≤0.05) mean fetal weight (decreased 18%) and crown to rump length (decreased 

10%) were noted at 100 mg/kg/day. Increased (p≤0.05) incidences of retardations were observed 

as follows: (i) weak ossification or non-ossification of one or several cranial bones at all doses 

(30.5-65.5% fetuses in 65.0-88.9% litters) compared to controls (19.5% fetuses in 60.0% litters); 

(ii) non-ossification of one sternebra at 100 mg/kg/day (56.4% fetuses in 83.3% litters) compared 

to controls (5.3% fetuses in 25.0% litters); and (iii) non-ossification of os metacarpal 5 at all 

doses (33.6-91.8% fetuses in 68.4-94.4% litters; NS at 10 mg/kg/day) compared to controls 

(23.3% fetuses in 60.0% litters).

Increased incidences of the following developmental anomalies were observed: (i) bent, 

thickened ribs at 32 mg/kg/day (15.2% fetuses in 47.4% litter; p≤0.05) and 100 mg/kg/day (4.5% 

fetuses in 22.2% litters compared to controls (1.5% fetuses in 10% litters); (ii) longitudinally 

displaced, fragmented, fused, dysplastic sternebrae or dislocated sternebrae at 100 mg/kg/day 

(23.6% fetuses in 66.7% litters) compared to controls (1.5% fetuses in 5.0% litters); and (iii) 

anlage of the 14th thoracic vertebra and of a normal length and/or short 14th rib on this vertebra at 

100 mg/kg/day (4.5% fetuses in 16.7% litters) compared to controls (0%).

No treatment-related findings were observed on external malformation or anomalies or visceral 

anomalies. One 100 mg/kg/day fetus (among 104 fetuses) had an abdominal fissure with 
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protruding abdominal coils, and one 100 mg/kg/day fetus (among 110 fetuses) had various 

vertebral malformations. 

The Developmental Toxicity LOAEL is 100 mg/kg bw/day based on decreased fetal body 

weight (-18%) and crown rump length (-10%), and longitudinally displaced, fragmented, 

fused, dysplastic sternebrae or dislocated sternebrae, and weak ossification or nonossification of one or several cranial bones. The Developmental Toxicity NOAEL is 32 

mg/kg/day.

This study is classified Acceptable/Guideline and as such with the additional information, 

satisfies the guideline requirement for a developmental toxicity study (OPPTS 870.3700; OECD 

414) in rats. 

870.3700b Prenatal Developmental Toxicity Study - Rabbit (FPE)

In a developmental toxicity study (MRID 47113319), HOE 046360 (fenoxaprop-p-ethyl; >99% 

a.i.; Serial No. 0321) in sesame oil was administered by oral gavage (0.5 mL/kg) once daily to 

inseminated Himalyan rabbits (15/dose group) at dose levels of 0, 10, 32, or 100 mg/kg bw/day 

from gestation days (GD) 7-19. On GD 29, all dams were euthanized. The uterus was removed 

via cesarean section, and its contents examined. Fetuses were examined for external, visceral, 

and skeletal malformations and variations.

In the dams, no treatment-related effect was observed on mortality. Furthermore, no 

macroscopic abnormalities and no adverse effects on organ weights were observed.

At 100 mg/kg/day, decreased defecation was noted (4/15 dams in treated group vs 0/15 controls). 

Decreased body weight gains were observed throughout the treatment period, where body weight 

gain was approximately 0. Before and after the treatment period body weight gain was similar to 

the controls. Overall body weight gain (GD 0-29) was decreased by 24%. Relative food 

consumption (g/100 g-bw) was decreased during the treatment period by 22% (not statistically 

significant) at GD 7-14 and by 42% (p≤0.05, but within the normal range of historical controls) 

at GD 14-20.

The Maternal Toxicity LOAEL is 100 mg/kg bw/day based on decreased food consumption 

and body weight gain. The Maternal Toxicity NOAEL is 32 mg/kg/day.

Abortions were noted in one 32 mg/kg/day dam and two 100 mg/kg/day dams, and a premature 

delivery was noted in one 10 mg/kg/day dam; however, these values were within the range of 

historical controls. There were no effects of treatment on numbers of litters, live fetuses, dead 

fetuses, or sex ratio.

There were no treatment-related external, visceral, or skeletal malformations or variations. 

There were no effects of treatment on fetal body weights, fetal crown to rump lengths, or 

placental weights. Incidences of skeletal retardations in the treated groups were similar to the 

concurrent controls and were within historical control ranges.
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The Developmental Toxicity NOAEL is equal to or greater than 100 mg/kg/day.

This study is classified Acceptable/Guideline and as such with the additional information, 

satisfies the guideline requirement for a developmental toxicity study (OPPTS 870.3700; OECD 

414) in rabbits. 

Non-Guideline Developmental Toxicity Study - Rat (FPE)

In a non-guideline, developmental toxicity study (MRID 47113320), Fenoxaprop-p-ethyl (Hoe 

046360; 95.6% a.i.; Serial # 13646, OH ZC96 0002) in sesame oil was administered by daily oral 

gavage to 20 presumed pregnant Wistar (Hoe WISKf [SPF71]) rats/dose at levels of 0, 10, 32, or 

100 mg/kg/day (dose volume 5 mL/kg) on gestation days (GD) 7-16. The dams were allowed to 

litter normally and rear their offspring for 21 days. Pups were examined daily for viability and 

clinical signs of toxicity, weighed at regular intervals, and examined for physical development. 

All animals were killed on post-natal days (PND) 21-23 and necropsied. The purpose of this 

study was to determine if repeated doses of Fenoxaprop-p-ethyl administered during pregnancy 

impaired the post-natal development of offspring.

There were no treatment-related effects on mortality, clinical observations, organ weights, gross 

pathology, or reproductive performance.

In the 100 mg/kg/day females, body weights were decreased (statistics not presented) by 7-10% 

during GD 14-21, resulting in decrease of 16% in overall (GD 0-21) gestational body weight 

gains, and absolute and relative food consumption were decreased by 16-25% during treatment 

(GD 7-17).

The Maternal Toxicity LOAEL is 100 mg/kg/day, based on decreased gestational body 

weights, body weight gains, and food consumption. The Maternal Toxicity NOAEL is 32 

mg/kg/day.

At 100 mg/kg/day, mean pup body weights were decreased by 4-8% during PND 0-21, and 

overall (PND 0-21) body weight gains were decreased by 3%. As these mean body weights were 

observed to be near the minimum or slightly below the range of historical controls, these 

decreases were considered adverse.

The Offspring Systemic/Developmental Toxicity LOAEL for offspring toxicity 100 

mg/kg/day, based on decreased pup body weights. The Offspring Systemic/Developmental 

Toxicity NOAEL is 32 mg/kg/day.

This study is classified as Acceptable/Non-Guideline. 

A.4.3 Reproductive Toxicity

870.3800 Reproduction and Fertility Effects – Rat (FE)
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In a 2-generation reproduction study (MRID# 00159920) HOE 33171 (97.2% a.i.) was 

administered to 30 WISTAR/HAN rats/sex/dose in the diet at dose levels of 0, 5, 30, or 180 ppm 

(calculated by the reviewer to be the equivalent to doses of 0.25, 1.5, or 9.0 mg/kg/day). 

Exposure to F0 animals began at 7 weeks of age and lasted for 80 days prior to mating to 

produce Fla and F1b pups. At 21 days of age, F1b pups were selected to become the parents of 

the F2a and F2b litters. Fl animals were given test diets for 101 days prior to mating the first 

time. Exposure of the test material to all animals was continuous in the diet throughout the study 

and all pups were given the same concentration of the test diet as their dam.

Parental toxicity was noted at 180 ppm as treatment- related decreases in total lipids (27-56%, 

p≤0.05, Fl males and females) and total cholesterol (16-36%, p≤0.05, Fl males) Decreases (12-

25%, p≤0.05) in total lipid and cholesterol were also noted at 5 ppm in the Fl parents, however, 

these effects were considered borderline. In addition for parental males dosed at 180 ppm, 

increased absolute (8%, p<0.05, Fl), relative to body (5-7%, F0 and Fl, p≤0.01), and relative to 

brain (l0%, p≤0.0l, Fl) liver weights were noted. Treatment-related increases in the absolute (9-

12%, p≤0.01, Fl males and females), relative to body (6-l2%, p≤0.0l or ≤0.05, F0 and Fl males, 

Fl females), and relative to brain (5-13%, p≤0.0l or ≤0.05, F0 and Fl males) kidney weights were 

also observed at the high-dose. Histopathology was not reported for this study, however, 

increased incidences of nephrocalcinosis at the 180 ppm dose level was reported in the previous 

study. There were no treatment-related effects on mortality, clinical signs of toxicity, body 

weight, food consumption or reproductive parameters at any dose level.

The Parental Systemic Toxicity LOAEL is 180 ppm (9 mg/kg/day) based on decreased 

blood lipids with increases in liver and kidney weights. The Parental Systemic Toxicity 

NOAEL is 30 ppm (1.5 mg/kg/day).

There were no effects on reproductive parameters. The Reproductive Toxicity LOAEL is 

greater than 180 ppm. The Reproductive Toxicity NOAEL is greater than or equal to 180 

ppm.

Offspring toxicity was demonstrated as increased pup liver weights on day 21 postpartum in the 

all F2 groups at 180 ppm. Several organ weights and organ weight ratios were decreased at the 

high dose, including lungs and spleen weights. These effects were considered to be secondary to 

the debility of the animals. Alkaline phosphatase was increased in the pups at the mid- and highdoses. 

The Developmental/Offspring Systemic Toxicity LOAEL is 180 ppm (9 mg/kg/day) based 

on increased liver weights and increased alkaline phosphatase. The 

Developmental/Offspring Systemic Toxicity NOAEL is 30 ppm (1.5 mg/kg/day).

This study is classified Acceptable/Guideline and satisfies the guideline requirements 

(OPPTS 870.3800; OECD 416) for a multigeneration reproduction study in rats. 

A.4.4 Chronic Toxicity

870.4100b Chronic Toxicity – Dog (FE)
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In chronic toxicity study (MRID # 00151566), HOE 33171 (technical, 94% a.i.) was 

administered in the diet for two years to beagle dogs (6/sex/dose, English beagle dog, 

Hoe:BEAK strain) at dose levels of 0, 3, 15, or 75 ppm (calculated by the reviewers to be 

equivalent to 0, 0.075, 0.375, or 1.875 mg/kg/day, based on a dry diet).

Treatment with HOE 33171 for up to two years did not affect mortality, behavior, clinical 

findings, food consumption, hematology, kidney and liver function, or urinalysis. Neurologic, 

ophthalmologic, otologic, dental, and mucosal health was similar in the treated and control 

animals. In addition, dosing did not cause toxicologically significant effects on organ weights, 

organ-to-body weight ratios, or gross and histopathological findings. At termination, the highdose animals had lower (p ≤ 0.05) mean body weights (10-13%) and body weight gains (51-

53%) than the controls. The mean body weights of the mid-dose males were also significantly (p 

≤ 0.05) decreased (11%), but mean weight gain did not differ significantly from the controls. 

Additionally, body weights in the mid-dose were 8% lower than controls at study initiation. 

Therefore, the body weight difference at the mid-dose was not considered to be adverse. 

The LOAEL is 75 ppm (1.875 mg/kg/day) based on reduced body weights and body weight 

gains. The NOAEL is 15 ppm (0.375 mg/kg/day).

This study is classified as Acceptable/Guideline and as such satisfies the guideline 

recommendations for a (OPPTS 870.4100; OECD 452 (1981); EEC 87/302 B) chronic oral 

toxicity study in dogs.

A.4.5 Carcinogenicity

870.4300a Combined Chronic Toxicity/Carcinogenicity – Rat (FE)

In combined chronic/carcinogenicity studies (MRID Nos. 00145638, 00149664, 00149665, 

00151564, 00151565), HOE 33171 (technical, 94 and 95.8% a.i.) was administered to 116 

Wistar rats/sex/dose in the diet at dose levels of 0, 5, 30, or 180 ppm (calculated by the reviewers 

to be equivalent to approximately 0, 0.25, 1.5, or 9 mg/kg/day) for up to 28 months. At each of 

the 6 and 12 month interim sacrifices, 10 rats/sex/group were terminated and at the 24 month 

sacrifice, 20 rats/sex/group were terminated. In addition, at 26 months, hepatic and renal 

(BSP/PSP clearance) function tests were performed in 6 rats/sex/group, and at 28 months, 60 

rats/sex/group were terminated.

Treatment with HOE 33171 for up to 28 months did not affect mortality, behavior, clinical 

findings, body weight, food consumption, haematology, kidney function, or urinalysis. In 

addition, dosing did not cause toxicologically important effects on gross and histopathological 

findings. Significantly decreased absolute and relative liver weights were identified in male rats 

at 24 months, and significantly decreased relative liver weights only at 28 months. All clinical 

chemistry parameters were similar in dosed and control groups with the exception that in the 

high-dose males, there were significant (p<0.05) decreases in serum cholesterol levels at 26, 54, 

and 107 weeks (1.19-22%) and in total lipids at 107 weeks (-24%) . The decreases in cholesterol 
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(17-18%) and total lipids (19%) observed in the high-dose females were not statistically 

significant.

The Chronic Toxicity LOAEL is 180 ppm (equivalent to 9 mg/kg/day) based on decreased 

serum lipids, cholesterol and relative liver weights in the males and the Chronic Toxicity 

NOAEL is 30 ppm (equivalent to 1.5 mg/kg/day).

There was no evidence of carcinogenicity (no increase in tumors) in Wistar rats under these 

study conditions. 

Note: Dosing was considered adequate by CARC (TXR #0056683) based on the findings of the 

90-day feeding study in rats (MRID 00130028) with data showing liver toxicity at 320 ppm.

This study is classified Acceptable/Guideline and as such satisfies the guideline 

recommendations (OPPTS 870.4300; OECD 452) for a chronic oral toxicity/carcinogenicity 

study in rats. 

870.4200b Carcinogenicity (feeding) – Mouse (FE)

In a carcinogenicity toxicity study in mice (MRID 44157402), Fenoxaprop-ethyl (96.8% a.i.,

Lot/Batch 04663) was administered to NMRI mice (50/sex/group, Hoe:NMRI(SPF71) obtained 

from Hoechst-AG, Kastengrund) via the diet at dose levels of 0, 40, 115, or 320 ppm (0, 5.7, 

16.6, or 44.6 mg/kg/day for males and 0, 6.8, 19.4, or 53.7 mg/kg/day for females, respectively) 

for 105 weeks.

Clinical observations indicated an increased, incidence of swollen abdomen in both sexes at 115 

and 320 ppm from week 55 onward. No other significant findings were noted on mortality and 

clinical observations. Absolute liver weight was increased at 320 ppm (males only) while relative 

liver weight was increased at 115 and 320 ppm (males only). Microscopic pathology showed that 

alterations occurred in the liver including hypertrophy, single cell necrosis, pigmentation in 

macrophages and lipofuscin deposit at 115 ppm (males only) and 320 ppm (both sexes). 

The Systemic Toxicity LOAEL is 115 ppm (16.6 mg/kg/day for males and 19.4 mg/kg/day 

for females) based on histopathological findings in the liver. The Systemic Toxicity

NOAEL is 40 ppm (5.7 mg/kg/day for males or 6.8 mg/kg/day for females).

At the doses tested, there was a treatment related increase in tumor incidence of hepatocellular 

adenoma and carcinoma when compared to controls. A significant increase in liver tumors, 

mainly adenomas, was observed in males at 320 ppm (30%) compared to the ‘control (2%). In 

addition, microscopic pathology indicated that hepatocellular hypertrophy was observed in: the 

majority of all treated animals (both sexes). Dosing was considered adequate based on clinical 

signs (swollen abdomen), increased liver weight, and histopathology data at the high dose. 

Note: No appreciable differences in survival were reported for the vehicle control and test groups 

at any dose. All test animals survived to study termination. The only clinical sign of note was an 

increased incidence of swollen abdomens in the mid- and high-dose males and females. In 
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addition, microscopic pathology indicated that hepatocellular hypertrophy was observed in the 

majority of male animals treated with 115 or 320 ppm fenoxaprop-ethyl and the majority of 

females at 320 ppm. Dosing was, therefore, considered adequate by the CARC (TXR #0056683)

based on clinical signs (swollen abdomen), increased liver weights, and histopathology data at 

the high dose.

This study is classified as Acceptable-Guideline and as such satisfies the guideline 

recommendations for a carcinogenicity study in mice (OPPTS 870.3200; OPP §82-2).

A.4.6 Mutagenicity (FPE)

STUDY FPE

870.5100

Bacterial /mammalian 

microsome reverse gene 

mutation assay

MRID 47113314: 0, 4, 20, 100, 500, 2500, 

5000 μg/plate +/-S9; two independent 

trials. Negative in S. typhimurium

TA1535, TA100, TA1537, and TA98 & E. 

coli WP2 uvrA up to a cytotoxic limit 

dose. 

Non-Guideline

Forward mutations in 

Schizosaccharomyces 

pombe P1 assay

MRID 47113311: 0, 2.5, 5.0, 10.0, 20.0, 

40.0 μg/mL +/-S9; two independent trials. 

Negative up to an insoluble concentration 

(40 μg/mL +/-S9). No cytotoxicity at any 

level. 

870.5300

In vitro gene mutations in 

Chinese hamster V79 cells 

(HGPRT locus) assay

MRID 47113316: 0, 6.25, 12.5, 25.0, 

50.0, 100 μg/mL +/-S9; two independent 

trials. Negative after a 6- or 9-day 

expression time up to an insoluble 

concentration (100 μg/mL +/-S9). No 

cytotoxicity at any level.

870.5375

In vitro chromosome 

aberrations in human 

lymphocytes assay

MRID 47113313: 5.0-125 μg/mL +/-S9. 

Cells, treated either continuously for 24 hrs 

& harvested (-S9) or for 2 hrs. & harvested 

at 12 or 24 hrs (+S9). Cells exposed to 0, 

50, 79, 125 μg/mL +/-S9 were scored. 

Negative up to an insoluble concentration 

(100 μg/mL +/-S9). No cytotoxicity at any 

level. No clear effects (≥50% ↓) on the 

mitotic index.

870.5395

NMRI Mouse (M/F) 

Micronucleus assay

MRID 47113317: 0, 1000, 2000, 4000 

mg/kg oral gavage. Negative up to a level 

that exceeds the limit dose (2000 mg/kg). 

Toxic signs at 4000 mg/kg included: 

narrowed palpebral fissures & reduced 

spontaneous activity. No cytotoxic effect 

on the bone marrow.

870.5575 MRID 47113312: 0, 1.25, 2.50, 5, 10, 20 
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STUDY FPE

Mitotic gene conversion in 

Saccharomyces cerevisiae 

D4

μg/mL +/-S9; two independent trials. 

Negative at the ade-2 and try-5 loci up to 

an insoluble concentration (20 μg/mL +/-

S9). No cytotoxicity at any level.

870.5550

Unscheduled DNA 

synthesis in A 549 human 

HeLa cells

MRID 47113315: 0, 0.1, 0.3, 1, 3, 10, 30, 

100 μg/mL +/-S9; two independent trials. 

Negative up to the highest soluble 

concentration (100 μg/mL +/-S9). No 

cytotoxicity at any level. 

A.4.7 Neurotoxicity

870.6200 Acute Neurotoxicity Screening Battery- Rat

Waived by HASPOC.

870.6200 Subchronic Neurotoxicity Screening Battery -Rat

Waived by HASPOC.

A.4.8 Metabolism

870.7485 Metabolism – Rat (FE)

In a rat metabolism study (MRID 00148476), HOE 33171 (FE) (U-14C-chlorophenyl; 98% 

radiochemical purity) was administered to male and female Wistar HOE:WISKf (SPF 71) strain 

rats (10-15 animals/dose/sex) by gavage as a single dose at levels of 2 or 10 mg/kg, or as a single 

dose at 2 mg/kg following a 14-day pretreatment with unlabeled HOE 33171 at 2 mg/kg/day.

Within 96 hours of dosing, 83-109% of the administered radioactivity was recovered in the urine 

and feces, with the majority of the dose (51-65%) being recovered within 24 hours of dosing. 

Sex-related differences in the pattern of excretion were apparent. Female rats metabolized the 

chemical more rapidly and excreted more of the total radioactivity in the urine (54-70% of dose) 

than the males (37-58% of dose). Within 24 hours of dosing, urinary excretion accounted for 39-

48% of the dose for females and 22-31% of the dose for males. Over the course of the study, 

radioactivity in feces accounted for 39-62% of the dose for males and 30-43% of the dose for 

females. Dose-related differences in excretion were not evident in females, but high dose males 

had a higher level (62% of dose) of excretion in the feces than low-dose males (39-40% of dose).

The primary metabolite in urine of both sexes in each dose group was 6-chlorobenzoxazole-2-

mercapturic acid, accounting for 22-50% of the total radioactivity in urine (15-26% of dose). 

However, urine of female rats dosed either once at 10 mg/kg or repeatedly at 2 mg/kg also 

contained high levels (23-28% of dose) of 2-(4- (6-chloro-2-benzoxazolyloxy)-phenoxy)-

propionic acid (the free acid of fenoxaprop-ethyl). This metabolite in urine accounted for 4.7% 

of the dose from single low-dose females and ≤ l.3% of the dose from males of all dose groups. 
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The primary fecal metabolite, which was common to both sexes, was the free acid of 

fenoxaprop-ethyl, accounting for 21-39% of the fecal radioactivity (8.4-21.7% of dose). 

Unchanged parent accounted for approximately 17% of the fecal radioactivity (5.7-6.3% of dose) 

in rats dosed once at 2 mg/kg and approximately 4% of the fecal radioactivity (1.1-1.4% of dose) 

in rats dosed repeatedly at 2 mg/kg. At the 10 mg/kg dose, unchanged parent accounted for 24% 

of the fecal radioactivity (15% of dose) for male rats and 6% for female rats (1.7% of dose)

870.7485 Metabolism – Rat (FE)

In a rat metabolism study (MRID 00148477), HOE 33171 (FE) (1-14C-dioxyphenyl; 96% 

radiochemical purity) was administered by gavage as a single dose to male and female SPF 

Wistar strain rats (10 animals/sex) at 10 mg/kg body weight and to 15 females at 2 mg/kg body 

weight.

The administered radioactivity was quantitatively recovered from the urine and feces of rats at 

each dosing regimen. Within 96 hours of dosing, 101.3% and 87.4% of the 10 mg/kg dose was 

recovered from male and female rats, respectively, and 108.8% of the 2 mg/kg dose was 

recovered from female rats. For each sex and dose level, the majority of the dose (66-80%) was 

recovered within 24 hours of dosing. Sex- and dose-related differences in excretion were noted. 

For the 10 mg/kg dose groups, females eliminated 54.9% of the dose in urine and 32.5% of the 

dose in feces; whereas, males eliminated 47.9% and 53.4% of the dose in urine and feces, 

respectively. In addition, females dosed at 2 mg/kg had a higher rate of urinary excretion (70.9% 

of dose) than did females dosed at 10 mg/kg, although levels of fecal elimination were similar 

for females from both dose levels.

Sex- and dose-related differences were also apparent in the metabolic profiles. In the 0- to 24-

hour urine of male rats dosed at. 10 mg/kg, 99% of the radioactivity was identified as 2-(4-

hydroxyphenoxy)-propionic acid (HPP-acid), accounting for 47.5% of the administered dose. In 

female rats dosed at 10 mg/kg, the primary urinary metabolites were identified as HPP acid 

(27.5% of dose) and 2-(4-(6-chloro-2-benzoxazolyloxy) phenoxyl-propionic acid (the free acid 

of fenoxaprop-ethyl; 27% of dose). These metabolites were also identified in the urine of lowdose females at a ratio of approximately 2:1 (49.6 and 21.3% of dose, respectively).

In 0- to 24-hour feces from each dose group, 63-69% of the radioactivity was identified as either 

fenoxaprop-ethyl or its free acid metabolite. In feces of the 10 mg/kg dose groups, fenoxapropethyl and its free acid accounted for 20.1 and 16.6% of the dose for males and 9.0 and 11.3% of 

the dose for females. In feces from the low-dose females, parent and the free acid metabolite 

accounted for 6.6 and 17.5% of the dose, respectively. Minor amounts (≤ 1% of dose) of HPP 

acid metabolite were also detected in feces from each dose group.

870.7600 Dermal Absorption - Rat (FPE)

In a dermal penetration study (MRID 47113321), fenoxaprop-p-ethyl (~99%) was administered 

to four male Sprague Dawley Crl:CD BR rats /dose to a 10.3 cm2 area on the shaved dorsolumbar surface at concentrations of 2.72 ± 0.03 and 617.5 ± 125.6 μg ai/cm2

skin. The applied 
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concentrations were equivalent to 0.0276 and 6.9 mg/animal for the low- and high-exposure 

groups, respectively. The animals were exposed for eight hours. Four rats/exposure 

interval/group were sacrificed at 8, 24, 72, 120 hours after initiation of treatment. 

The average recovery of the radiolabel was 96.3% and 90.8% for the low- and high-groups, 

respectively. The maximum concentration of radiolabel recovered in the blood and plasma of 

the low-dose group was 15.4 and 25.1 ng equivalents/g at eight hours after initiation of treatment 

and 403 and 622 ng equivalent/g, respectively, at 24 hours after initiation of treatment for the 

high dose. The majority of the administered dose was recovered from the wash solutions and

dressings at both treatment concentrations. Approximately 70-80% of the applied low-dose and 

87-90% of the high-dose were retained in these media. Estimates of dermal absorption based on 

the sum of residues retained in the urine (including cage wash and rinse), GIT and contents, 

feces, carcass, and blood ranged from 6.212% of the applied dose at eight hours after initiation of 

treatment to 16.31% of the applied dose at 120 hours after initiation of treatment for the low dose 

and 0.6% of the applied dose eight hours after initiation of treatment that increased to 2.012% of 

the applied dose by 120 hours in the high-dose group. Following treatment, approximately twothirds of the absorbed radiolabel was recovered in the urine/cage wash with the remainder 

recovered in the feces. The 250-fold difference between the low-dose (meant to simulate the 

spray-strength concentration) and the high-dose resulted in a 28-fold difference in the amount 

absorbed (444 ng equivalents/cm2for the low-dose and 12,445 ng equivalents/cm2for the highdose) strongly suggested the absorption process was saturated at the high-dose.

This study in the rat is Acceptable/Nonguideline and does not satisfy the guideline requirement 

for a dermal penetration study (870.7600) in rats. The study does provide, however, useful 

information on the absorption of fenoxaprop-p-ethyl at expected use concentrations. Study 

deficiencies are listed in the Deficiency Section

Non-Guideline Dermal Absorption – Rat vs. Human (FPE)

In an in vitro dermal penetration study (MRID 47113322), fenoxaprop-p-ethyl (>99% a.i. 

unlabeled, Lot No. 28283-133 and >99% a.i. radiolabeled, Lot No. Z 28084-1 uniformly labeled 

on the phenyl ring) was applied to 0.64 cm2skin preparations from male Sprague Dawley rats 

and from a human female at nominal concentrations of 7.3 and 550 μg/cm2. The radiolabeled 

test material was in contact with the epidermal tissue for 24 hours. Absorption through the 

prepared tissue samples was determined by monitoring the amount of radioactivity in the 

receptor fluid.

Absorption was ~0.34 μg/cm2/hr for human skin and 2.32 μg/cm2/hr for rat skin (or ~6.8 times 

greater for rat skin than human skin) when applied at a nominal concentration of 550 μg/cm2. 

When the test material was applied diluted 75-fold as for end use, rat skin was only slightly more 

permeable (~1.6 times) than human skin. Absorption through human skin was ~0.02 μg/cm2/hr 

and 0.034 μg/cm2/hr for rat skin when fenoxaprop-p-ethyl was applied at a nominal 

concentration of 7.3 μg/cm2.

However, following OECD guidelines, calculations should be conducted using the receptor fluid, 

material left on the skin site, and the cell wash + receptor chamber contents. Using these values, 
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the percent absorption from rats and humans is 38.9 and 59.6%, respectively, indicating high 

penetration through human skin.

This in vitro study with rat and human skin Acceptable/Nonguideline.

A.4.9 Immunotoxicity

870.7800 Immunotoxicity- Rat (FPE)

In an immunotoxicity study (MRID 48445201), fenoxaprop-p-ethyl (94.5% a.i., batch# 

EFLC000572) was administered to female Wistar rats (10/dose) via diet at dose levels of 0, 70, 

210, or 630 ppm (0, 5.5, 16, or 47 mg/kg/day, respectively) for 4-weeks. The positive control 

consisting of 10 female Wistar rats were administered cyclophosphamide (3.5 mg/kg/day) by 

gavage for 28 days. Animals were observed daily for mortality and clinical signs. Body weight 

and food consumption were recorded once weekly. A detailed physical examination was 

performed once during the acclimatization phase and at least weekly throughout the study. 

On Day 26, all animals were immunized with 0.5 mL Sheep Red Blood Cell (2.5 x 108

SRBC/mL) antigen by intravenous injection via the tail vein. On Day 30, blood samples were 

collected from the retro-orbital venous plexus of each animal for specific anti-SRBC IgM 

analysis with an Enzyme-Linked Immunosorbent Assay (ELISA). 

There were no effects on mortality, clinical signs, organ weight or gross pathology findings. At 

630 ppm, mean body weight was reduced 4% to 6% (not statistically significant) during the 

course of the study, when compared to the controls. Between Study Days 1 to 8, mean body 

weight gain was reduced by 54% (p<0.01), compared to controls. Between Study Days 8 to 15, 

and 15 to 22, effect was less pronounced and not statistically significant. Overall mean absolute 

body weight gain between Study Days 1 and 29 was reduced by 29% (p≤0.05). Mean food 

consumption was statistically significantly lower than controls (-10% to -13%, p<0.05 to p≤0.01) 

throughout the study. At 210 and 70 ppm, there were no treatment-related effects on any of the 

parameters assessed.

The systemic toxicity NOAEL is 210 ppm (16 mg/kg/day) and the LOAEL was 630 ppm (47 

mg/kg/day) based on decreased body weight gains and food consumption.

For immunotoxicity, mean anti-SRBC IgM concentrations were similar to the untreated control 

group at all dose levels tested. A high inter-individual variability was noted in all the treatment 

groups as well as in the control group. Evaluation of individual animal data did not show any 

trend or distribution that would demonstrate significant suppression of SRBC antibody response.

For positive control group, cyclophosphamide induced no mortalities, clinical signs, body weight 

or food consumption effects and no gross pathology findings. Lower mean absolute and relative 

spleen weights were observed, compared with the control group (-16% to -17%, p≤0.05). 

Following immunization with SRBC antigen, the mean anti-SRBC IgM concentration was 

markedly lower than the corresponding control group (-92%, p<0.01). The positive control 
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animals confirmed the sensitivity of the test system to detect immunosuppressive effects and 

confirmed the validity of the study design. 

The NK cells activity was not evaluated. Evaluation of toxicity database of fenoxaprop-p-ethyl 

reveals no evidence of treatment-related effects on the immune system. Under the HED 

guidance, if the TDAR assay is negative and evaluation of observational endpoints from all 

available toxicology database provide no evidence of immunotoxicity, the test article is 

considered negative for immunotoxicity and evaluation of NK cells activity is not necessary.

Under conditions of this study, the immunotoxicity NOAEL is 630 ppm (47 mg/kg/day) and 

the LOAEL was not established.

This immunotoxicity study in rats is classified as Acceptable/Guideline and satisfies the 

guideline requirement for an immunotoxicity study (OPPTS 870.7800).
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Appendix B. International Residue Limits Table

Fenoxaprop-p-ethyl (129092), Fenoxaprop-ethyl (128701; 09/09/2013)

Summary of US and International Tolerances and Maximum Residue Limits 

Residue Definition:

US Canada Mexico1 Codex

40 CFR 180.430:

Plant and Livestock: Compliance with the 

tolerance levels specified is to be 

determined by measuring only the sum of 

fenoxaprop-ethyl, (±)-ethyl 2-[4-[(6-

chloro-2-

benzoxazolyl)oxy]phenoxy]propanoate, 

and its metabolites, 2-[4-[(6-chloro-2-

benzoxazolyl)oxy]phenoxy]propanoic acid 

and 6-chloro-2,3-dihydrobenzoxazol-2-

one, calculated as the stoichiometric 

equivalent of fenoxaprop-ethyl

(RS)-ethyl-2-[4-(6-

chloro-1,3-benzoxazol-2-

yloxy)

phenoxy]propanoate, 

including the metabolites 

2-[4-

[(6-chloro-2-

benzoxazolyl)-

oxy]phenoxy]propionic

acid and 6-chloro-2,3-

dihydrobenzoxalazol-2-

one

None

Commodity Tolerance (ppm) /Maximum Residue Limit (mg/kg)

US Canada Mexico1 Codex

Barley, grain 0.05 0.05

Barley, straw 0.1

Cattle, fat 0.05

Cattle, meat byproducts 0.05

Cattle, meat 0.05

Cotton, undelinted seed 0.05

Goat, fat 0.05

Goat, meat byproducts 0.05

Goat, meat 0.05

Hog, fat 0.05

Hog, meat byproducts 0.05

Hog, meat 0.05

Horse, fat 0.05

Horse, meat byproducts 0.05

Horse, meat 0.05

Milk 0.02 0.02

Peanut 0.05

Peanut, hulls 0.05

Rice, grain 0.05 0.05

Sheep, fat 0.05

Sheep, meat byproducts 0.05

Sheep, meet 0.05

Soybean 0.05 0.05 dry soybeans

Wheat, grain 0.05 0.05

Wheat, straw 0.50

Proposed Tolerances

Grass, hay** 0.15

Completed: M. Negussie; 9/11/13

1 Mexico adopts US tolerances and/or Codex MRLs for its export purposes.

** Grass hay is a new use. Grass, hay also has a time-limited tolerance of 0.05 ppm expiring 12/31/2013.
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*** Time limited tolerance expiring 12/31/2013.

(b) Section 18 emergency exemptions. Time-limited tolerances are established for residues of the 

herbicide fenoxaprop-ethyl, including its metabolites and degradates, in or on the commodities in the 

table in this paragraph in connection with use of fenoxaprop-ethyl under section 18 emergency 

exemptions granted by EPA. Compliance with the tolerance levels specified in this paragraph is to be 

determined by measuring only the sum of fenoxaprop-ethyl, (±)-ethyl 2-[4-[(6-chloro-2-

benzoxazolyl)oxy]phenoxy]propanoate, and its metabolites, 2-[4-[(6-chloro-2-

benzoxazolyl)oxy]phenoxy]propanoic acid and 6-chloro-2,3-dihydrobenzoxazol-2-one, calculated as the 

stoichiometric equivalent of fenoxaprop-ethyl, in or on the commodity. The tolerances expire and are 

revoked on the dates specified in the table in this paragraph.

Commodity Parts per million

Expiration/

revocation date

Grass, forage 0.05 12/31/13

Grass, hay 0.05 12/31/13
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Appendix C. Spray Drift Summary Tables

The spray drift risk estimates are based on an estimated deposited residue concentration as a 

result of the screening level agricultural application scenarios. FPE is used on a variety crops 

and turf sites and can be applied via groundboom and aerial equipment at a maximum 

application rates ranging from 0.083 to 0.173 lbs ai/acre. The recommended drift scenario 

screening level options are listed below: 

 Groundboom applications are based on the AgDrift option for high boom height and 

using very fine to fine spray type using the 90th percentile results. 

 Aerial applications are based on the use of AgDrift Tier 1 aerial option for a fine to 

medium spray type and a series of other parameters which will be described in more 

detail below (e.g., wind vector assumed to be 10 mph in a downwind direction for entire 

application/drift event).7

In addition to the screening level spray drift scenarios described above, additional results are 

provided which represent viable drift reduction technologies (DRTs) that represent potential risk 

management options. In particular, different spray qualities have been considered as well as the 

impact of other application conditions (e.g., boom height, use of a helicopter instead of fixed 

wing aircraft, crop canopy conditions).

Dermal risk estimates were calculated for adults. Dermal and incidental oral risk estimates for 

children 1 to <2 years old were combined because the toxicity endpoint for each route of 

exposure is the same. The total applicable Level of Concern is 100 so MOEs < 100 represent 

risk estimates of concern. Adult and children dermal and children’s incidental oral risk estimates 

from indirect exposure to FPE related to spray drift result in buffers of 0 feet for groundboom 

and aerial applications, (i.e., all MOEs ≥ 100 at the edge of the field). Results for the drift 

scenarios of the highest application rate and chemical-specific TTR values (as described in 

Section 5.2) are presented in Tables C.1 and C.2. 

 

7 AgDrift allows for consideration of even finer spray patterns characterized as very fine to fine. However, this 

spray pattern was not selected as the common screening basis since it is used less commonly for most agriculture. If 

assessors identify this use pattern it should be used as the screening criteria and deposition values associated with it 

are provided in Table 1 below. Justification for including this spray quality should be included in any assessment 

based on specific label directions for its use.
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Table C.1 Adult Risk Estimates (MOEs) Related to Indirect Exposure to Spray Drift for Fenoxaprop-p-ethyl for the Dermal Route of Exposure

Crop/Rate 

Group

Spray Type/ 

Nozzle 

Configuration

Appl. 

Rate (lb 

ai/A)

TTR 

(ug/c

m2)

At 

Edge

10 

Feet

25 

Feet

50 

Feet

75 

Feet

100 

Feet

125 

Feet

150 

Feet

200 

Feet

250 

Feet

300 

Feet

Right of Way/ Commercial Turf (Sod Farms)/ Ornamentals

Aerial

Fine to Medium

0.173 0.018

 1,300 1,600 2,000 2,600 3,400 4,400 5,300 6,200 8,200 9,900 12,000 

Medium to Coarse 1,600 2,100 2,900 4,100 5,800 7,600 9,600 12,000 16,000 21,000 26,000 

Coarse to Very 

Coarse 1,800 2,700 4,100 6,300 9,100 12,000 15,000 19,000 26,000 34,000 42,000 

Very Fine to Fine 900 990 1,100 1,300 1,500 1,700 1,900 2,200 2,600 3,100 3,500 

AT401, M, 10 mph, 

37% SD

 

1,400 

 

1,800 

 

2,400 

 

3,200 

 

4,300 

 

5,600 

 

6,800 

 

8,000 

 

10,000 

 

13,000 

 

16,000 

WASP, M, 10 mph, 

37% SD

 

1,500 

 

2,000 

 

2,600 

 

3,900 

 

5,300 

 

6,800 

 

8,400 

 

9,900 

 

13,000 

 

16,000 

 

19,000 

AT401, C, 10 mph, 

25% SD

 

1,700 

 

2,400 

 

3,400 

 

5,000 

 

7,100 

 

9,300 

 

12,000 

 

14,000 

 

20,000 

 

26,000 

 

30,000 

WASP, C, 10 mph, 

25% SD

 

2,000 

 

2,800 

 

4,000 

 

6,300 

 

8,800 

 

12,000 

 

15,000 

 

19,000 

 

26,000 

 

34,000 

 

37,000 

AT401, VC, 10 

mph, 20% SD

 

1,900 

 

2,900 

 

4,700 

 

7,600 

 

11,000 

 

15,000

 

19,000 

 

24,000 

 

34,000 

 

42,000 

 

56,000 

WASP, VC, 10 

mph, 20% SD

 

2,400 

 

3,800 

 

5,900 

 

9,300 

 

13,000 

 

18,000 

 

24,000 

 

28,000 

 

42,000 

 

48,000 

 

56,000 

Groundboom

High Boom Very 

fine to Fine

 

1,800 

 

3,600 

 

6,000 

 

9,600 

 

13,000 

 

17,000 

 

20,000 

 

24,000 

 

30,000 

 

42,000 

 

48,000 

Low Boom Very 

fine to Fine

 

3,900 

 

10,000 

 

17,000 

 

26,000 

 

34,000 

 

42,000 

 

48,000 

 

56,000 

 

67,000 

 

84,000 

 

110,000 

High Boom Fine to 

Medium/Coarse

 

6,800 

 

18,000 

 

26,000 

 

37,000 

 

48,000 

 

56,000 

 

67,000 

 

67,000 

 

84,000 

 

110,000 

 

110,000 

Low Boom Fine to 
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Medium/Coarse 10,000 28,000 42,000 56,000 67,000 84,000 110,000 110,000 170,000 170,000 170,000 

Table C.2 Children (1 to <2 years old) Risk Estimates (MOEs) Related to Indirect Exposure to Spray Drift for Fenoxaprop-p-ethyl for the Combined Dermal and Oral 

Routes of Exposure

Crop/Rate 

Group

Spray Type/ 

Nozzle 

Configuration

Appl. 

Rate (lb 

ai/A)

TTR 

(ug/cm2)

At 

Edge

10 

Feet

25 

Feet

50 

Feet

75 

Feet

100 

Feet

125 

Feet

150 

Feet 200 Feet 250 Feet 300 Feet

Right of Way/ Commercial Turf (Sod Farms)/ Ornamentals

Aerial

Fine to Medium

0.173 0.018

 

620 

 

760 

 

940 

 

1,200 

 

1,600 

 

2,100 

 

2,500 

 

2,900 

 

3,900 

 

4,700 

 

5,700 

Medium to 

Coarse

 

750 

 

1,000 

 

1,400 

 

1,900 

 

2,700 

 

3,600 

 

4,500 

 

5,500 

 

7,500 

 

9,900 

 

12,000 

Coarse to Very 

Coarse

 

870 

 

1,300 

 

1,900 

 

3,000 

 

4,300 

 

5,700 

 

7,200 

 

8,800 

 

12,000 

 

16,000 

 

20,000 

Very Fine to 

Fine

 

420 

 

470 

 

520 

 

600 

 

700 

 

800 

 

910 

 

1,000 

 

1,200 

 

1,500 

 

1,700 

AT401, M, 10 

mph, 37% SD

 

680 

 

870 

 

1,100 

 

1,500 

 

2,000 

 

2,600 

 

3,200 

 

3,800 

 

4,900 

 

6,100 

 

7,500 

WASP, M, 10 

mph, 37% SD

 

730 

 

930 

 

1,200 

 

1,800 

 

2,500 

 

3,200 

 

4,000 

 

4,700 

 

6,100 

 

7,500 

 

8,800 

AT401, C, 10 

mph, 25% SD

 

800 

 

1,100 

 

1,600 

 

2,400 

 

3,400 

 

4,400 

 

5,500 

 

6,600 

 

9,300 

 

12,000 

 

14,000 

WASP, C, 10 

mph, 25% SD

 

930 

 

1,300 

 

1,900 

 

3,000 

 

4,200 

 

5,700 

 

6,900 

 

8,800 

 

12,000 

 

16,000 

 

18,000 

AT401, VC, 10 

mph, 20% SD

 

910 

 

1,400 

 

2,200 

 

3,600 

 

5,100 

 

6,900 

 

8,800 

 

11,000 

 

16,000 

 

20,000 

 

26,000 

WASP, VC, 10 

mph, 20% SD

 

1,100 

 

1,800 

 

2,800 

 

4,400 

 

6,300 

 

8,300 

 

11,000 

 

13,000 

 

20,000 

 

23,000 

 

26,000 

Groundboom High Boom 

Very fine to 

 

850 

 

1,700 

 

2,800 

 

4,500 

 

6,300 

 

7,900 

 

9,300 

 

11,000 

 

14,000 

 

20,000 

 

23,000 
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Fine

Low Boom 

Very fine to 

Fine

 

1,900 

 

4,900 

 

7,900 

 

12,000 

 

16,000 

 

20,000 

 

23,000 

 

26,000 

 

32,000 

 

40,000 

 

53,000 

High Boom 

Fine to 

Medium/Coarse

 

3,200 

 

8,300 

 

12,000 

 

18,000 

 

23,000 

 

26,000 

 

32,000 

 

32,000 

 

40,000 

 

53,000 

 

53,000 

Low Boom 

Fine to 

Medium/Coarse

 

4,800 

 

13,000 

 

20,000 

 

26,000 

 

32,000 

 

40,000 

 

53,000 

 

53,000 

 

79,000 

 

79,000 

 

79,000 
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