EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER EPA Registration Division C ontact: R e uben Baris, 703 - 305 - 7356 Nissan Chemical Industries, Ltd. 5F8367 EPA has received a pesticide petition ( 5F8367 ) from Nissan Chemical Industries, Ltd. , 3 - Chome, Kanda - Nishiki - Cho Chiyoda - Ku, Tokyo 101 - 0054 Japan request ing, pursuant to section 408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 CFR part 180 .441 by establishing tolerance s for residues of quizalofop - P - ethyl ester , [ethyl(R) - (2 - [4 - ((6 - chloroquinoxalin - 2 - yl)oxy)phenoxy)propanoate], and its acid metabolite quizalofop - P , [R - (2 - (4 - ((6 - quinoxalin - 2 - yl)oxy)phenoxy)propanoic acid and the S enantiomers of both the ester and the acid, all expressed as quizalofop - P - ethyl ester in or on the raw agricultural commodit ies Rice at 0.05 parts per million (ppm) and Crayfish at 0. 0 4 ppm . EPA has determined that the petition contains data or information regarding the elements set forth in section 408 (d)(2) of FFDCA ; however, EPA has not fully evaluated the sufficiency of the submitted data at this time or whether the data supports granting of the petition. Additional data may be needed before EPA rules on the petition. A. Residue Chemistry 1. Plant metabolism. Plant metabolism studies have been conducted for soybeans, cotton, tomatoes, potatoes, and sugar beets . These studies have been previously reviewed and accepted by EPA (see PP 3F4268 and PP0F6076 ). In addition, a rice metabolism study was initiated to investigate the metabolism of quizalofop - P - ethyl in herbicide - tolerant rice. Two labels were tested ([hydroquinone - U - 14 C] - quizalofop and [quinoxaline - phenyl - U 14 C] - quizalofop at a nominal application of 100 g ai/ha at BBCH 13 - 14 followed by 140 g ai/ha at Panicle Initiation (~BBCH 30). Quizalofop - P - ethyl was extensively metabolized and only two metabol ites were observed higher than 5% TRR, CQO and Quizalofop - P. As 14 C - residues in the grain were low, the radioactivity in grain samples was only determined by TRR. The rice metabolism study supports the known plant metabolism of Quizalofop - P - ethyl and does not indicate a difference in metabolism due to the herbicide tolerant nature of the rice. In summary, quizalofop - P - ethyl ester is metabolized by cleavage at three sites as follows. 1. Hydrolysis of the ethyl ester to form the quizalofop - P acid (primary pat hway). 2. Cleavage of the enol ether linkage in the acid, between the phenyl and quinoxalinyl rings, to form phenols. 3. Cleavage of the ether linkage between the propanic group and the phenyl ring to form a phenol.2 The plant metabolism data show that the quiz alofop - P - ethyl ester itself does not translocate, but is rapidly hydrolyzed to the corresponding acid. The phenols conjugate with the plant sugars. Metabolism studies in soybeans using the racemic mixture quizalofop ethyl ester and the resolved D+ isomer show nearly identical pathways. The nature of the quizalofop - P - ethyl ester residue in cottonseed, potatoes, tomatoes, soybeans, sugar beets, sunflower seeds, wheat, barley, and rice is adequately understood. The resi dues of concern are quizalofop - P - ethy l ester and its acid metabolite, quizalofop - P , and the S enantiomers of both the ester and the acid, all expressed as quizalofop - P - ethyl ester. 2. Analytical method. The Analytical Method Number Meth - 147 was originally developed and validated for the determina tion of residues of quizalofop - P - ethyl (QPE) as 2 - methoxy - 6 - chloroquinoxaline (MeCHQ) in wheat, barley and alfalfa raw agricultural commodities and wheat grain processed commodities at Morse Laboratories, Inc, (Morse Laboratories, Inc. Analytical Method No. Meth - 147. January 10, 2002; MRID 44967703). This method included the methanolysis to convert the residues of all possible metabolites to a common moiety analyte, 2 - methoxy - 6 - chloroquinoxaline (MeCHQ) followed by several sample clean - up steps. T he final determination of residues was performed using reverse - phase HPLC with fluorescence detection. This method was further modified using) as 2 - methoxy - 6 - chloroquinoxaline (MeCHQ) for the analysis of rice commodities at the limit of quantitation (LOQ) of 0.05 mg/kg. The modifications were used only in the sample clean - up and final determination steps for data collection purpose. A brief description of the modified method is provided below. The method involves refluxing samples with methanolic potassi um hydroxide to convert quizalofop - P - ethyl and quizalofop - P residues to a common analyte, 2 - methoxy - 6 - chloroquinoxaline (MeCHQ). The resulting extract are then centrifuged, diluted with methanol, and analyzed by LC - MS/MS with the positive ionization mode monitoring ion transition m/z 195→167 for MeCHQ. Quantitation is o btained using an external calibration curve of standard for MeCHQ. The residues are expressed in terms of the parent compound, QPE, using a molecular weight conversion factor. The limit o f quantitation (LOQ) is 0.05 mg/kg based on the lowest level of method validation. The independent lab validation (ILV) of the modified method for rice analysis is not conducted as this is used only for the data collection of rice commodities and is not to be used for enforcement purposes. 4. Magnitude of residues. Magnitude of the Residue

– Rice Crop Field Trials A total of 17 trials on rice conducted during the 2013 and 2014 growing seasons in NAFTA Regions 4 (AR, five trials; LA, six trials; MO, one trial), 5 (MO, one trial), 6 (TX, two trials), and 10 (CA, two trials) reflecting two broadcast, early - season applications of quizalofop - P - ethyl (105 g/L EC) , the first targeting 100 g ai/ha (BBCH 13 - 14, 3 - 4 leaves unfolded), and a second targeting 140 g ai/ha, with a 28 - day3 retreatment interval (240 g ai/ha/season). Total quizalofop - P - ethyl residues, determined as MeCHQ and expressed as parent equivalents, were <0.05 ppm in treated grain samples (and <0.05 - 0.194 ppm in treated straw samples, each harvest ed at normal maturity, 69 - 95 days after the last (second) application. Total quizalofop - P - ethyl residues, determined as MeCHQ and expressed as parent equivalents, were <0.05 ppm in treated grain samples (and <0.05 - 0.194 ppm in treated straw samples, each h arvested at normal maturity, 69 - 95 days after the last (second) application. At eight of the trials described above (for the 2013 growing season only), an additional treated plot (Treatment 3, side - by - side plots) was included reflecting two broadcast, early - season applications of quizalofop - P - ethyl (105 g/L EC) , the first targeting 100 g ai/ha (BBCH 11 - 12, 1 - 2 leaves unfolded), and a second targeting 140 g ai/ha, with a 14 - day retreatment interval (240 g ai/ha/season). Total quizalofop residues, determined as MeCHQ and expressed as parent equivalents, were <0.05 ppm in 12 treated grain samples and <0.05 - 0.067 ppm in 12 treated stra w samples, each harvested at normal maturity, 97 - 109 days after the last (second) application. Total quizalofop residues, determined as MeCHQ and expressed as parent equivalents, were <0.05 ppm in 12 treated grain samples and <0.05 - 0.067 ppm in 12 treate d straw samples, each harvested at normal maturity, 97 - 109 days after the last (second) application. Samples of seeds (including hulls) were analyzed for residues of quizalofop - P ethyl and quizalofop - P, express ed as quizalofop - P - ethyl, using method met h - 147. The overall recoveries in grain and straw were at 0.05 and 5.0 ppm were 73 - 117% (84±13%, n=16) and 71 - 108% (84±16%, n=14). The rice RAC samples were stored frozen for a maximum of 154 days (5.1 months) for grain and 161 days (5.3 months) for straw , from collection to analysis for residues of quizalofop - P - ethyl. The available storage stability data demonstrate that residues of quizalofop - P - ethyl and quizalofop - P are stable stored frozen in wheat grain for at least 12 months. These data support the storage intervals and conditions incurred by the residue samples in this study. Magnitude of the Residue

– Rice Processing Studies A processing study was conducted using rice grown in NAFTA Regions 4 (MO, one trial) and 6 (TX, one trial). The rice RA C samples (grain) were harvested at normal maturity, 90 days after the last (second) application, and were then processed, The treated plot received two broadcast foliar applications of a 105 g/L emulsifiable concentrate (EC) formulation of quizalofop - P - ethyl (formulation code, BAS 9152 9 H) targeting 300 + 420 g ai/ha/application (0.27 + 0.37 lb ai/A), with a retreatment interval targeting 28 days, for a total rate of 720 g ai/ha (0.64 lb ai/A/season). The first spray made at the 4 leaf growth stage (B BCH 14) for rice. The actual rates were 294 - 305 g ai/ha (1st application) and 414 - 417 g ai/ha (2nd application), at a 28 - day RTI, resulting in a total exaggerated rate of 708 - 722 g ai/ha (0.631 - 0.644 lb ai/A/season).4 The rice RAC and processed commodit y samples were analyzed using a validated method Meth - 147 (MRID 44967703). The limit of quantitation of the analytical method is 0.05 ppm. The overall recoveries in grain and straw were at 0.05 and 5.0 ppm were 73 - 117% (84±13%, n=16) and 71 - 108% (84±16%, n=14). A comparison of the residues in the RAC with those in each processed fraction indicated that total quizalofop residues do not concentrate in the processed fractions of rice: Total quizalofop residues, determined as MeCHQ and expressed as parent e quivalents, were non - quantifiable (<0.05 ppm) in all rice processed commodity samples collected during the study. Magnitude of the Residue in Animals. A ruminant feeding study has been submitted and reviewed by EPA. In summary, three groups of three lac tating dairy cows (plus a control group) were fed 0.1, 0.5, and 5.0 ppm quizalofop - ethyl (encapsulated) for 28 consecutive days. Milk was collected daily and a sub - sample was divided into skim milk and cream. Two cows were sacrificed after 28 days with sam ples of fat, skeletal muscle, liver, and kidney being collected and analyzed. The remaining cow in each test group was fed a regular diet without encapsulated quizalofop - ethyl for 7 additional days before sacrifice. Whole milk, skim milk, and cream from th e control, and the 0.1 and 0.5 ppm dose groups showed no quizalofop to < 0.02 ppm (0.05 ppm in cream). From the 5 ppm dose, quizalofop residues ranged from 0.01 to 0.02 ppm in whole, and when these samples were separated into cream and skim milk, the quiza lofop partitioned into the cream with residues plateauing at 0.26 to 0.31 ppm. No quizalofop to < 0.02 ppm was detected in skeletal muscle, and to < 0.05 ppm was detected in any liver or fat sample from any of the three doses. Quizalofop was detected in on e kidney sample as 0.05 ppm from the 5 ppm dose. From the feed items in this petition, all of the feed items in cattle diets can be treated with quizalofop - ethyl. A theoretical beef cattle diet consisting of canola meal, bean and pea forage, pea hay, and sugar beet tops which none - the - less maximizes the potential quizalofop exposure of 2.1 ppm. A theoretical dairy cattle diet consisting of pea and bean forage would none - the - less maximize the potential quizalofop exposure at 2.4 ppm. Substitutions of other feed items and varying their percentages in the diets would give a lower dietary quizalofop burden. The results of the quizalofop - ethyl bovine feeding study show that finite residues will actually occur in milk and tissues from the feeding of quizalofop - e thyl treated RACS or their processed feed items when Assure ® II is used as directed. The established quizalofop and quizalofop - ethyl tolerance in milk, and in fat, meat, and meat by - products of cattle, goats, hogs, horse, and sheep are adequate and need no t be increased from these additional uses. A poultry feeding study has been submitted and reviewed. In summary, 3 groups of 20 hens (plus 1 control group) were dosed with encapsulated quizalofop ethyl ester at 0.1, 0.5, and 5 ppm daily for 28 consecutive days. Eggs were collected daily, and after 285 days 3/4 of the hens in each test group were sacrificed, and samples of fat, liver, kidney, breast and thigh muscles were collected and analyzed. Tissues from each test group were pooled prior to analysis. The remaining five hens were fed a regular poultry diet without quizalofop - ethyl for an additional 7 days before sacrifice. No quizalofop residues were detected in the liver to < 0.05 ppm, and in breast and thigh muscles to < 0.02 ppm for any dose administered . From the 5 ppm dose, one kidney sample showed 0.09 ppm quizalofop, two fat samples were 0.05 and 0.06 ppm quizalofop, and one egg sample was 0.02 ppm quizalofop. The results of the quizalofop - ethyl poultry feeding study show that while it is not possibl e to establish with certainty whether finite residues will actually occur in eggs and tissues from the feeding of quizalofop - ethyl treated RACS or their processed feed items when Assure® II is used as directed, there is a reasonable expectation for such r esidues to occur. The established tolerance of quizalofop and quizalofop - ethyl in eggs, and in fat, meat, and meat by - products of poultry are adequ ate and need not be changed for these additional uses. Magnitude of the Residue in Animals - Crayfish A field accumulation study in crayfish was performed to test for possible accumulation of q uizalofop - P - ethyl in crayfish tissues. The r esidues (Quizalofop - P) in water reached as high as 0.0487 mg/L on Day 0 and had decreased to 0.0252 mg/L by Day 28. Pare nt residues were not detectable in water . In edible crayfish tissue, residues of q uizalofop - P were measured at 0.024 mg/kg on Day 1 - 0.017 mg/kg on Day 14 , and were below LOQ ( 0.01 mg/kg) on Days 21 and 28. Parent was not detectable any edible tissues. As a conservative estimate, an MRL of 0.04 mg/kg is proposed crayfish. The value of 0.04 mg/kg was used as part of the dietary risk calculations below. B. Toxicological Profile 1. Acute toxicity. Several acute toxicology studies were conducted, and the overall results placed technica l grade quizalofop - ethyl in toxicity Category III. These include the following studies in Category III: acute oral toxicity (LD 50 s 1480 and 1670 for female and male rats, respectively) and eye irritation (mild effects; r eversible within 4 days). Dermal toxicity (LD 50 > 5,000 mg/kg; rabbit), inhalation toxicity (LC 50 > 5.8 mg/L; rat) and dermal irritation were classified within Category IV. Technical quizalofop ethyl was not a dermal sensitizer. 2. Genotoxicty. Technic al quizalofop - ethyl was negative in the following genotoxicity tests: bacterial gene mutation assays with E. coli and S. typhimurium ; gene mutation assays in Chinese hamster ovary(CHO) cells ; in vitro DNA damage assays with B. subtillis and in rat hepatocytes; and an in vitro chromosomal aberration test in CHO cells. 3. Reproductive and developmental toxicity. A developmental toxicity study in rats administered dosage levels of 0, 30, 100, and 300 mg/kg/day. The maternal toxicity6 no - o bserved effect level (NOEL) was 30 mg/kg/day and a developmental toxicity NOEL was greater than the highest dose tested (HDT) of 300 mg/kg/day. The maternal NOEL was based on reduced food consumption and increased liver weights. A developmental toxicity s tudy in rats administered dosage levels of 0, 30, 100, and 300 mg/kg/day. The maternal toxicity no - observed effect level (NOEL) was 30 mg/kg/day and a developmental toxicity NOEL was greater than the highest dose tested (HDT) of 300 mg/kg/day. The matern al NOEL was based on reduced food consumption and increased liver weights. A developmental toxicity study in rabbits administered dosage levels of 0, 7, 20, and 60 mg/kg/day with no developmental effects noted at 60 mg/kg/day (HDT). The maternal toxicity NOEL was 20 mg/kg/day based on decreases in food consumption and body weigh t gain at 60/mg/kg/day (HDT). A two - generation reproduction study in rats fed diets containing 0, 25, 100 or 400 ppm (or approximately 0, 1.25, 5, and 20 mg/kg/day, respectively) with a developmental (systemic effects) NOEL of 1.25 mg/kg/day for F 2B wean lings based on increased liver weights and increased incidence of eosinophilic changes in the livers at 5.0 mg/kg/day. These liver changes were considered to be physiological or adaptive changes to compound exposure among weanlings. When access to the mo ther’s feed is available, it is a common observation that young rats will begin consuming chow prior to complete weaning at 21 days of age. Consumption could not be quantified; therefore, the maternal consumption was assumed as the NOEL. If normalized on a body weight basis, exposures to the weanling rats were likely higher. The parental NOEL of 5.0 mg/kg/day was based on decreased body weight and premating weight gain in males at 20 mg/kg/day (HDT) 4. Subchronic toxicity. A 90 - day study was conducted in rats fed diets containing 0, 40, 128, and 1,280 ppm (or approximately 0, 2, 6.4, and 64 mg/kg/day, respectively). The NOEL was 2 mg/kg/day, based on increased liver weights at 6.4 mg/kg. A 90 - day feeding study in mice was conducted with diets that con tained 0, 100, 316 or 1,000 ppm (or approximately 0, 15, 47.4, and 150 mg/kg/day, respectively). The NOEL was <15 mg/kg/day, the lowest dose tested (LDT), based on increased liver weights and reversible histopathological effects in the liver at the LDT. A 6 - month feeding study in dogs was conducted with diets that contained 0, 25, 100, or 400 ppm (or approximately 0, 0.625, 2.5, and 10 mg/kg/day, respectively). The NOEL was 2.5 mg/kg/day based on increased blood urea nitrogen at 10 mg/kg/day. A 21 - day dermal study was conducted in rabbits at doses of 0, 125, 500, or 2,000 mg/kg/day. The NOEL was 2,000 mg/kg/day (HDT). 5. Chronic toxicity. An 18 - month carcinogenicity study was conducted in CD - 1 mice fed diets containing 0, 2, 10, 80, or 320 ppm (or approximately 0, 0.3, 1.5, 12, or 48 mg/kg/day, respectively). No carcinogenic effects were observed under the conditions of the study at levels up to and including 12 mg/kg/day. A marginal increase in the7 incidence of hepatocellular tumors was observed at 48 mg/kg/day, the HDT, which exceeded the maximum tolerated dose (MTD). (See the discussion by the EPA Carcinogenicity Peer Review Committee. Toxicology Branch Peer Review Committee: Draft Document on Assure based on November 5, 1986 CPRC Meeting Dated December 9, 1986). A two - year chronic toxicity/carcinogenicity study was conducted in rats fed diets containing 0, 25, 100, or 400 ppm (0, 0. 9, 3.7, or 15.5 mg/kg/day for males and 0, 1.1, 4.6, or 18.6 mg/kg/day for females, respectively). No carcinogenic effects were observed under the conditions of the study at levels up to and including 18.6 g/kg/day (HDT). The systemic NOEL was 0.9 mg/kg/ day based on altered red cell parameters and slight/minimal centrilobuler enlargement of the liver at 3.7 mg/kg/day. A one - year feeding study was conducted in dogs fed diets containing 0, 25, 100, or 400 ppm (or approximately 0, 0.625, 2.5, or 10 mg/kg/d ay, respectively). The NOEL was 10 mg/kg/day (HDT). The Carcinogenicity Peer Review Committee (CPRC) of HED has evaluated the rat and mouse cancer studies on quizalofop along with other relevant short - term toxicity studies, mutagenicity studies, and str ucture activity relationships. The CPRC concluded, after three meetings and an evaluation by the EPA Science Advisory Panel (SAP), that the classification should be a Category D (not classifiable as to human cancer potential). No new cancer studies were required. (CPRC Report: Peer Review of Assure, February 6, 1987; JA Quest to RJ Taylor. SAP Findings (Assure) Document signed by Steve Johnson, December 23, 1987). The first CPRC review tentatively concluded that quizalofop should be classified as a C ategory B2 (probable human carcinogen). That classification was based on liver tumors in female rats, ovarian tumors in female mice, and liver tumors in male mice. This classification was downgraded to a Category C (possible human carcinogen) at a second CPRC review. The change in classification resulted from a reexamination of the liver tumors in female rats and ovarian tumors in female mice. The first peer review had found a statistically significant positive trend for liver carcinomas in female rats. Subsequent to this conclusion, a tumor data reevaluation showed a reduced number of carcinomas. Although there remained a statistically significant positive trend for carcinomas in the study, the CPRC concluded that the carcinomas were not biologically significant given the few carcinomas identified (one at the mid - dose and two at the high dose). Noting that this level of carcinomas was within historical levels, the CPRC concluded that administration of quizalofop did not appear to be associated with the liver carcinomas. The CPRC had first attached importance to the fact that the ovarian tumors in female mice, were statistically significant at the high dose compared to historical control values, and statistically significant when compared to concurrent controls. However, review of further historical control data showed that the level of ovarian tumors in the quizalofop study was similar to the background rate in several other studies. Given this8 information and the fact that the quizalofop study showe d no hyperplasia of the ovary, no signs of endocrine activity related to ovarian function, and no dose response relationship, the CPRC concluded that the ovarian tumors were probably not compound - related. The findings of the second CPRC review were prese nted to the SAP. The SAP concurred with the CPRC conclusion that the liver tumors in female rats and the ovary tumors in female mice showed no evidence of carcinogenicity. However, the SAP disagreed with CPRC’s classification of quizalofop as a Category C based on the liver tumors in male mice. The SAP concluded that the mouse liver tumors did not support such a classification because the tumors occurred at a dose above the MTD and because they were not statistically significant if they had a “p” value of less than 0.05. The SAP believed that such greater statistical rigor was appropriate for variable tumor endpoints such as male mouse liver tumors. Following the SAP review, the CPRC changed the classification for quizalofop to Category D. The Category D classification is based on an approximate doubling in the incidence of male mice liver tumors between controls and the high dose. This finding was not considered strong enough to warrant the finding of a Category C (possible human carcinogen), since the increase was of marginal statistical significance, occurred at a high dose that exceeded the predicted MTD, and occurred in a study in which the concurrent control for liver tumors was somewhat low compared to the historical controls; while the high dose group was at the upper end of previous historical control groups. EPA has found the evidence on the carcinogenicity of quizalofop - P - ethyl in animals to be equivocal and, therefore, concludes that quizalofop - P - ethyl does not induce cancer in animals. I mportant to this conclusion was the following evidence: (1) The only statistically significant tumor response that appears compound - related was seen at a single dose in a single sex in a single species; (2) the response was only marginally statistically signifi cant; (3) the response was only significant when benign and malignant tumors were combined; (4) the tumors were in the male mouse liver; (5) the tumors were within historical controls; and (6) the mutagenicity studies were negative. In some circumstances, a finding of animal carcinogenicity would be made despite any one, or even several, of the six factors noted. However, the combination of all of these factors casts sufficient doubt on the reproducibility of the response in the high dose male mouse and therefore, EPA concluded that the evidence on carcinogenicity is equivocal. 6. Animal metabolism. Animal metabolism studies have been conducted with laying hens and lactating goats using 14 C - phenyl and 14 C - quinoxaline quizalofop - ethyl.9 These studies were reviewed a nd accepted by EPA. EPA concluded that the metabolism of quizalofop - P - ethyl is adequately understood. The primary metabolic pathway in ruminants is via hydrolysis of the ethyl ester to form the quizalofop - - methyl. In poultry, the primary metabolic p athway is also the hydrolysis of the ethyl ester to form the quizalofop acid, followed by the methyl esterification to form the quizalofop - methyl as a minor pathway of metabolism. The residues of concern are quizalofop - ethyl, quizalofop - methyl, and quizalofop, all expressed as quizalofop - ethyl. There is no evidence that the metabolites of quizalofop ethyl, as identified in animal metabolism studies, have any toxicological significance . 7. Metabolite toxicology . There is no evidence that the metabo lites of quizalofop ethyl as identified as either the plant or animal metabolism studies are of any toxicological significance. 8. Endocrine disruption . No special studies investigating potential estrogenic or other endocrine effects of quizalofop - P - ethy l have been conducted. However, the standard battery of required toxicology studies has been completed. These include an evaluation of the potential effects on reproduction and development, and an evaluation of the pathology of the endocrine organs follo wing repeated or long - term exposure to doses that far exceed likely human exposures. Based on these studies there is no evidence to suggest that quizalofop - P - ethyl has an adverse effect on the endocrine system . C. Aggregate Exposure 1. Dietary exposure. A chronic dietary exposure and risk assessment was conducted for quizalofop - P - ethyl using the Dietary Exposure Evaluation Model (DEEM) and the USDA Continuing Survey of Food Intake by Individuals (CSFII, for 2005 - 2010, a s contained in DEEM Ver 4.02). An acute dietary exposure and risk assessment is not required because the US EPA has determined that there are no effects observed in oral toxicity studies that could be attributed to a single - dose exposure from q uizalofop - P ethyl. The chronic dietary exposure assessment was conducted using 100% crop treatment factors, tolerance level residues for all currently approved tolerances for q uizalofop - ethyl (40 CFR 180.441) and the proposed new tolerances for rice at 0.05 ppm and crayfish at 0. 04 ppm. The chronic dietary exposure included drinking water at 1 1.5 ppb. A. Acute Dietary Exposure. An acute risk assessment is not required because the US EPA has determined that there are no effects observed in oral toxicity studies that could be attributed to a single - dose exposure from q uizalofop - P - ethyl . B. Chronic Dietary Exposure. The calculated chronic dietary exposures (food + drinking water) for all populations are shown in Table 1 . The highest exposure population sub - group was infants (< 1 year old) and utilized 34.6 % cPAD. The results of the risk assessment show that for all populations the exposures are below a level of concern (< 100% cPAD). Additional refinements in the die tary risk assessment (i.e. utilizing anticipated residue values, percent crop treated values) would further reduce the10 estimated exposure values and utilized % cPAD. Table 1. Results for Quizalofop - P - ethyl Chronic Dietary Exposure (Food and Water) Considering All Commodities using DEEM - FCID

Population Exposure Estimate % cPAD Subgroups (mg/kg b.w./day) U.S. Population 0.001179 13.1 All Infants (< 1 year old) 0.003118 34.6 Children (1 - 2 years old) 0.003052 33.9 Children (3 - 5 years old) 0.002514 27.9 Children (6 - 12 years old) 0.001675 18.6 Youth (13 - 19 years old) 0.001073 11.9 Adults (20 - 49 years old) 0.000983 10.9 Adults (50+ years old) 0.000885 9.8 Females (13 - 49 years old) 0.000967 10.0 Chronic Aggregate Exposure and Risk: The chronic aggregate exposure includes food and drinking water. Therefore, the chronic dietary exposure for food and drinking water represents the chronic aggregate exposure. A short - term and intermediate term aggregate exposure assessment includes food, drinking water, and residential exposure. Quizalofop - P - ethyl does not have any uses that would result in residential exposure. Therefore, the short - term and intermediate - term aggregate exposure assessment is not required. i. Food. Not applicable as food and drinking water are included in the assessment above. ii. Drinking water . The rice use for q uizalofop - P - ethyl resulted in the highest modeled drinking water concentrations. The Tier II Rice model resulted in chronic estimated drinking water concentrations of 11.5 ug/L. The drinking water exposures were included in the c hronic dietary exposure assessment. 2. Non - dietary exposure . Quizalofop - P - ethyl is not registered for use in residential settings. D. Cumulative Effects There is no evidence to indicate or suggest that quizalofop - P - ethyl has any toxic effects on mammals that would be cumulative with those of any other chemicals . E. Safety Determination 1 . U.S. population. For the U.S. population, the calculated aggregate exposure11 from all current uses and the proposed new uses is equivalent to 13.1% of the cPAD. Because the calculated aggregate exposures, expressed as percentages of the cPAD, are well below 100%, there is reasonable certainty that the current uses and the proposed new uses of qu i zalofop - P - ethyl will not result in an unacceptable risk. 2. Infants and children . The population subgroup with the highest predicted level of chronic exposure was infants (<1 year) subgroup with an exposure of 0.003118 mg/kg bw/day . The chronic exposure for all infants (<1 year) is equivalent to 34.6% of the cPAD. Because the predicted exposures, expressed as percentages of the cPAD, for all existing and new uses are well below 100%, there is reasonable certainty that the current uses and proposed new uses for quizalofop - P - ethyl wil l not result in an unacceptable risk. F. International Tolerances There are no Mexican, Canadian or Codex MRL’s/tolerances for rice ; therefore, compatibility is not an issue .