**EPA REGISTRATION**  **DIVISION -**  **COMPANY NOTICE**  **OF**

**FILING FOR PESTICIDE**  **PETITION Docket ID Number: EPA** **- HQ**  **- OPP**  **- 2014**  **- 0**  **788 EPA**  **Registration Division**  **C ontact:**  **Sidney Jackson (703)**  **305 -**  **7610 Interregional Research Project Number 4**  **Pesticide Petition Number: 4E8 3**  **2 1**  **EPA has received a pesticide petition ,**  **PP# 4**  **E8321 ,**  **from Interregional Research**  **Project Number 4 (IR -**  **4)** , **500 College Road East, Suite 201W, Princeton, NJ 08540**  **proposing, pursuant to section 408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA),**  **21 U.S.C. 346a(d), to amend 40 CFR part 180 .434**  **by establishing tolerance**  **s for residue**  **s of**  **p ropiconazole, 1**  **- [[2**  **- (2,4**  **- dichlorophenyl)**  **- 4**  **- propyl** **- 1,3**  **- dioxolan**  **- 2**  **- yl] methyl]**  **- 1H**  **- 1,2,4**  **- triazole and its metabolites determined as 2,4,**  **- dichlorobenzoic acid and expressed as**  **the stoichiometric equivalent of**  **propiconazole, in or on the raw agricultural commod**  **it ies:**  **Dill, fresh at**  **30 parts per**  **million (ppm) ; Dill, dried at 80**  **ppm ; Dill, seed at 15 ppm; Leafy brassica greens,**  **subgroup 5B at 20 ppm; Radish, tops at 0.2 ppm; Radish, roots at 0.04 ppm; Ti palm, leaves at 10 ppm; Ti palm, roots at 0.3 ppm**  **, Watercress at 6 ppm**  **, Fruit,**  **stone, group 12 -**  **12 ,**  **except plum at 4.0 ppm ;**  **Nut, tree, group 14**  **- 12 at 0.1**  **ppm and**  **Quinoa , grain**  **at 0.3 ppm. Upon approval of proposed tolerances,**  **the petitioner request**  **s remov**  **al of the established tolerances**  **under 40 CFR 180.434 in or on**  **Fruit, stone, group 12 except plum at 4.0**  **ppm ,**  **and Nut, tree, group 14 at 0.1 ppm**  **that are superseded by this action**  **. EPA has determined that the petition contains data**  **or information regarding the elements set forth in section 408 (d)(2)**  **of the FDDCA; however, EPA has not fully evaluated the sufficiency of the submitted data at this**  **time or whether the data support granting of the petition. Additional data may be needed before EPA rules on the petition.**  1. **Plant metabolism. The metabolism**  **of propiconazole as well as the nature of the residues is adequately understood for purposes of the tolerances. Plant**  **metabolism has been evaluated in five diverse crops, wheat, grapes, celery, peanuts and carrots which should serve to define the similar**  **metabolism of propiconazole in a wide range of crops. The plant metabolism pathway for propiconazole is well**  **understood. Parent metabolite CGA -**  **64250 is the major compound found in crops. Comparison of the metabolism of propiconazole in different plant**  **species shows that the differences between the respective metabolic pathways to be quantitative in**  **nature .** **2. Analytical method.**  **The metabolism data in plants and animals suggest that**

**analytical methods to detect either the phenyl or the triazole ring would be appropriate for the measurement of residues. However, because of the natural**  **occurrence of compounds that interfere with th e measurement of triazoles, methods**  **designed to detect this moiety have been proven unreliable and unacceptable. Conversely, conversion of phenyl moiety to 2,4**  **- dichlorobenzoic acid (DCBA) has**  **proven to be satisfactory for all agricultural products analyze d to date.**  **Analyti cal**  **methods AG -**  **626 and AG -**  **454A were developed for the determination of residues of**  **propiconazole and its metabolites containing the DCBA moi**  **ety. Analytical method AG** **- 626**  **has been accepted and published by EPA as the tolerance enforceme nt**  **method for crops. The limit of quantitation (LOQ) for the method is 0.05 ppm .**  **3. Magnitude of residues**  **. IR** **- 4 conducted magnitude of residue trials on**  **several crops under OPPTS 860.1500 to support the requested use**  **of propiconaozle**  **in/on on dill, leafy brassica greens, radish and watercress. These residue trials**  **satisfy the requested tolerance on these crops. EPA's Chemistry Science Advisory Council (ChemSAC)**  **agreed that for Ti palm**  **roots, a**  **tolerance of 0.3 ppm covers the rep resen**  **ta tive**  **crops in crop sub -**  **group 1B and a garden beet root tolerance and therefore, should adequately cover Ti palm**  **root residue when Ti palm is treated with the same use pattern as other** 1B crops. **ChemSAC also agreed that for Ti palm leaves ,**  **a tolerance of**  **10 ppm can be translated from the sugar beet tops established tolerance of 10 ppm, and should**  **adequately cover Ti palm leaves when it is treated with the same use pattern as leaves of root and tuber vegetables.**  **B. Toxicological Profile**  **1. Acute toxicity.**  **Propiconazole exhibits low toxicity. Available d**  **ata indicated the following: a rat acute oral**  **lethal dose (** **LD )**  **50 of 1,517**  **milligrams/kilograms (mg/kg); a rabbit acute dermal LD 50**  **>6,000 mg/kg; a rat inhalation**  **lethal concentration ( LC**  **) 50**  **> 5.8 mg/liter air; minimal skin and slight eye**  **irritation; and nonsensitization .**  **2. Genotoxicty.**  **Propiconazole exhibits low toxicity. Data indicated the following: a rat acute oral LD**  **50 of 1,517**  **mg/kg ; a rabbit acute dermal LD**  **50 >6,000**  **mg/kg; a rat inhala tion LC**  **50 >5.8 mg/liter air; minimal skin and slight eye**  **irritation; and nonsensitization. 3.**  **Reproductive and developmental toxicity. In an oral teratology study in the**  **rabbit, a maternal no observed adverse effect level (NOAEL) of 30 mg/kg was based on r**  **educed food intake but without any fetotoxicity even at the top dose of 180 mg/kg. In an oral teratology study in the rabbit, a maternal NOAEL of 100 mg/kg** 

**was based on reductions in body weight gain and food consumption and a fetal NOAEL of 250 mg/kg was**  **based on increased skeletal variations at 400 mg/kg. In an oral teratology study in the rat, a maternal and fetal NOAEL of 100 mg/kg was**  **based on decreased survival, body weight gain, and food consumption in the dams and delayed ossification in the fetus**  **es at 300 mg/kg. In a second teratology study in the rat, a maternal and fetal NOAEL of 30 mg/kg was based on reductions in body**  **weight gain and food consumption in the dams and delayed development in the fetuses at 90 and 360/300 mg/kg. A supplemental t**  **eratology study in the rat involving eight times as many animals per group as usually required showed no**  **teratogenic potential for the compound. A 2 -**  **generation reproduction study in the rat showed excessive toxicity at 5,000 ppm without any teratogenic ef**  **fects. A 2 -**  **generation reproduction study in the rat showed no effects on reproductive or fetal parameters at any dose level. Postnatal growth and survival were affected at the top**  **dose of 2,500 ppm, and parental toxicity was also evident. The NOAEL for development toxicity is 500 ppm.**  **4. Subchronic toxicity.**  **In a 21 -**  **day dermal study in the rabbit, a NOAEL of 200 mg/kg was based on clinical signs of systemic toxicity. In a 28**  **- day oral toxicity**  **study in the rat, a NOAEL of 50 mg/kg was based on increased liver weight. In a**  **subchronic feeding study in the mouse, a NOAEL of 20 ppm (3 mg/kg) was based on liver pathologic changes. In a 13 week feeding study in the male mouse, a NOAEL of**  **20 ppm (3 mg/kg) was based on liver pathologic changes. In a 90 day feedi ng study**  **in rats, the NOAEL was 240 ppm (24 mg/kg) based on a reduction in body weight gain. In a 90 day feeding study in dogs, the NOAEL was 250 ppm (6.25 mg/kg)**  **based on reduced food intake and stomach histologic changes. ]**  **5. Chronic toxicity.**  **In a 12 -**  **mo nth feeding study in the dog, a NOAEL of 50**  **ppm (1.25 mg/kg) was based on stomach histologic changes. In a 24 month oncogenicity feeding study in the mouse, the NOAEL was 100 ppm (15 mg/kg). The**  **maximum tolerated dose (MTD) was exceeded at 2,500 ppm in m**  **ales based on decreased survival and body weight. Increased incidence of liver tumor was seen in**  **these males but no evidence of carcinogenicity was seen at the next lower dose of 500 ppm in either sex. In a 24 month chronic feeding/oncogenicity study in t**  **he rat, a NOAEL of 100 ppm (5 mg/kg) was based on body weight and blood chemistry. The**  **MTD was 2,500 ppm based on reduction in body weight gain and no evidence of oncogenicity was seen. Based on the available chronic toxicity data, Syngenta**  **believes the Reference dose (RfD) for propiconazole is 0.0125 mg/kg/day. This RfD**  **is based on a 1 year feeding study in dogs with a NOAEL of 1.25 mg/kg/day (50 ppm) and an uncertainly factor of 100. No additional modifying factor for the** **nature of effects was judged to be necessary as stomach mucous hyperemia was the** 

**most sensitive indicator of toxicity in that study. Using the Guidelines for Carcinogenic Risk Assessment published on September 24,**  **1986 (51 FR 33992), the USEPA has classified propiconazole in group C f or**  **carcinogenicity (evidence of possible carcinogenicity for humans). The compound was tested in 24 month studies with both rats and mice. The only evidence of**  **carcinogenicity was an increase in liver tumor incidence in male mice at a dose level that exc**  **eeded the MTD. Dosage levels in the rat study were appropriate for identifying a cancer risk. The**  **EPA Cancer Peer Review Committee recommended**  **the RfD approach for quantitation of human risk. Therefore, the RfD is deemed protective of all chronic human**  **health effects, including cancer. 6.**  **Animal metabolism. Metabolism in animals is similar to plant metabolism.**  **In animals both the rat and the goat rapidly metabolize and excrete propiconazole. Neither animal retains significant amounts of propiconazole**  **or its metabolites in tissues. Significant quantities of parent or metabolites do not appear in goat’s milk.**  **Similar metabolites are produced by both species, and unconjugated (phase I) metabolites are similar in plants and animals.**  **The metabolism profi le supports the use of an analytical enforcement method that**  **accounts for combined residues of propiconazole and its metabolites that contain the 2,4**  **- dichlorobenzoic acid (DCBA) moiety.**  **7. Metabolite toxicology**  **. There are no metabolites of concerned based**  **on a differential metabolism between plants and animals.**  **8. Endocrine disruption**  **. Developmental toxicity studies in rats and rabbits**  **and reproduction studies in rats gave no indication that propiconazole might have any effects on endocrine function related**  **to development and reproduction. The subchronic and chronic studies also showed no evidence of a long** 

**– term effect**  **related to the endocrine system. Further, due to the moderate rate of degradation of the product, there is no risk that propiconazole may a**  **ccumulate in the environment. In animals, propiconazole is quickly excreted and has no tendency for accumulation**  **in the body. Based on these results, it is very likely that propiconazole has no potential to interfere specifically with the endocrine syste**  **m. C.**  **Aggregate Exposure 1.**  **Dietary exposure. Tier I acute, short**  **- term, and chronic aggregate exposure**  **assessments were performed for propiconazole using the Dietary Exposure Evaluation Model (DEEM**  **- FCIDTM Version 3.16) from Exponent and consumption**  **data from the USDA NHANES “What We Eat in America” survey, 2003**  **- 2008.** **Propiconazole is currently registered for uses on alfalfa; avocados; banana; beans**

**(dry and succulent); beets (garden); beets (sugar); berries (Crop Groups 13 -**  **07A, 13 -**  **07B, 13 -**  **07G); bulb vege tables (Crop Group 3); carrots; cilantro (leaves); citrus**  **fruits (Crop Group 10); corn (field, pop, sweet); cranberries; grasses; leaf petioles (Crop Group 4B); mushrooms; nectarines; ornamentals; parsley (fresh, dried);**  **peaches; peanuts; peppermint; pinea pple; pistachio; rice; small cereal grains**  **(barley, oats, rye, wheat); sorghum; soybean; spearmint; stone fruit (Crop Group 12); strawberries; sugarcane; tomatoes; tree nuts (Crop Group 14); turf grass, and**  **wild rice. A use on canola is pending. IR4 mino r uses on dill, Ti palm, radish,**  **watercress, and leafy Brassica (Crop Group 5B) are proposed. Existing 40 CFR**  **180.434 or proposed tolerances were used for all commodities. Experimental**  **p rocessing factors were used for**  **canola meal (1.48X), canola oil (0.0 3X), orange**  **juice (0.011X), pineapple juice (0.11X), pineapple process residue (1.49X), soybean oil (0.08x), sugarcane sugar (0.02X), sugarcane molasses (0.49X),**  **wheat bran (2.4x), wheat flour (0.2x)**  **. DEEM**  **TM V**  **ersion 7.87 default p rocessing factors were us**  **ed for all other commodities**  **. No adjustments were made for “percent crop treated,” i.e., 100%CT was assumed. For livestock commodities, established tolerances were**  **used. Drinking water estimates were selected using the higher of the estimated**  **drinking w ater concentrations (EDWCs)**  **for surface and ground water.** i **. Food .**  **Acute Food Risk: The acute dietary (food only) risk assessment was**  **performed for all population subgroups with an acute reference dose (aRfD) of 0.3 mg/kg**  **- body weight (** **bw )** **/day based on an acute no observed adverse effect level**  **(NOAEL) of 30 mg/kg -**  **bw/day from an acute neurotoxicity study in rats and an uncertainly factor of 100X. The 100X safety factor included intra**  **- and inter** **- species**  **variations. No additional FQPA safety factor was ap plied. For the purpose of the**  **aggregate risk assessment, the exposure value was expressed in terms of margin of exposure (MOE), which was calculated by dividing the NOAEL by the exposure for**  **each sub -**  **population. In addition, exposure was expressed as a p ercent of the acute**  **reference dose (% aRfD). At the 95th percentile, acute exposure to the U.S.**  **population resulted in a MOE of 749 or 13.4%**  **of the aRfD (Benchmark = 100; aRfD = 0.3**  **mg/kg -**  **bw/day) . Acute exposure to the most sensitive subpopulation**  **(child ren 1**  **- 2 years old) resulted in a MOE of 281 or 35.6% of the**  **aRfD (Benchmark = 100; aRfD = 0.3**  **mg/kg -**  **bw/day) . Since the Benchmark MOE for this assessment is**  **100 and since EPA generally has no concern for exposures above the benchmark or below 100% of the r**  **eference dose, Syngenta believes that there is a reasonable certainty that no harm will result from acute dietary (food) exposure to residues**  **arising from all current, pending, and proposed uses for propiconazole. Chronic Food Risk:**  **The chronic dietary (f ood only) risk assessment was performed**  **for all population subgroups with a chronic reference dose (cRfD) of 0.1 mg/kg -** **bw/day based on a 24 -**  **month oncogenicity study in mice with a NOAEL of 10**

**mg/kg -**  **bw/day and an uncertainly factor of 100X. The 100X safety factor included**  **intra -**  **and interspecies variations. No additional FQPA safety factor was applied. For the purpose of the aggregate risk assessment, the exposure values were**  **expressed in terms of MOE, which was calculated by dividing the NOAEL by the exp**  **osure for each sub -**  **population. In addition, exposure was expressed as a percent of the chronic reference dose (%cRfD). Chronic exposure to the U.S. population**  **resulted in a MOE of 819 or 12.2%**  **of the cRfD (Benchmark = 100; cRfD = 0.1**  **mg/kg -**  **bw/day) . Chro**  **nic exposure to the most exposed sub -**  **population (children 1**  **- 2 years old) resulted in a MOE of 284**  **or 35.2% of the cRfD (Benchmark = 100;**  **cRfD = 0.1 mg/kg**  **- bw/day)**  **. Since the Benchmark MOE for this assessment is 100 and since EPA generally has no concern fo**  **r exposures above the benchmark or below 100% of the reference dose, Syngenta believes that there is a reasonable**  **certainty that no harm will result from chronic dietary (food) exposure to residues arising from all current, pending, and proposed uses for p**  **ropiconazole.**

**Cancer Risk: A quantitative risk assessment using a cancer endpoint was not**  **performed. The chronic risk assessment is adequately protective for cancer risk as well as other chronic effects.** 

**- GW) and**  **ii. Drinking Water**  : **The Estimated**  **Drinking Water Concentrations ( EDWCs**  **) of**  **propiconazole were determined using Tier l Screening Concentration in Ground**  **Water (SCI -**  **GROW) (version 2.3) which estimates pesticide concentration in ground**  **water and Tier II Pesticide Root Zone Model** **/ Exposure**  **Analysis Modeling System s**  **(PRZM /EXAMS**  **) (PE version 5.0)**  **for g**  **roundwater and the Modified Tier 1 Rice**  **Model which estimate pesticide concentration in surface water for terrestrial and aquatic uses, respectively. This drinking water assessment was conducte**  **d to assess all currently registered uses, pending uses on canola as well as the proposed uses on**  **dill, watercress and leafy brassica greens, crop subgroup 5B. For groundwater, the currently registered use on turf provided the highest EDWC of 0.725 ppb (a**  **cute and chronic). For surface water, the proposed use on watercress provided an acute**  **EDWC of 272 ppb and a chronic EDWC of 174 ppb. No Percent Cropped Area (PCA) adjustments were made for surface water EDWCs.**  **Since the surface water EDWCs exceed the g**  **round water EDWC, the surface water values were used for risk assessment purposes and will be considered protective for any ground water**  **exposure concerns. Acute Exposure from Drinking Water**  **. The acute surface water EDWC of 272 ppb**  **was input directly into the DEEM -**  **FCIDTM software as “water, direct and indirect, all sources” to model the acute drinking water exposures. Exposure contributions** 

**at the 95% -**  **ile of exposures were determined by taking the difference between the**  **aggregate (food + drinking water) exposures and the food (alone) exposures for each sub**  **- population. Acute drinking water exposure U.S. population resulted in a MOE**  **of 3,627 (2.8% of the aRfD of 0.30 mg/ kg**  **- bw** **/day). The most expo sed sub**  **** **population was infants <1 year old, with a MOE of 1,216 (8.2% of the aRfD of 0.30 mg/kg/day). Since the Benchmark MOE for this assessment was 100 and since EPA**  **generally has no concern for exposures above the benchmark or below 100% of the aRfD, S**  **yngenta believes that there is a reasonable certainty that no harm will result from acute drinking water exposure to residues arising from all current, pending,**  **and proposed uses for propiconazole. Chronic Exposure from Drinking Water**  **. The chronic surface**  **water EDWC of 174 ppb was input directly into the DEEM** **- FCIDTM software as “water, direct and**  **indirect, all sources” to model the chronic drinking water exposures. Chronic drinking water exposure to the U.S. population resulted in a MOE of 2,745 (3.6% of**  **t he cRfD of 0.10 mg/kg**  **- bw/day). The most exposed sub**  **- population was infants <1**  **year old, with a MOE of 1,064 (9.4% of the cRfD of 0.10 mg/kg -**  **bw/day). Since the Benchmark MOE for this assessment was 100 and since EPA generally has no**  **concern for exposures above the benchmark or below 100% of the cRfD, Syngenta**  **believes that there is a reasonable certainty that no harm will result from chronic drinking water exposure to residues arising from the current, pending, and**  **proposed uses for propiconazole 2.**  **Non -** **di etary exposure**  **. Short** **- term exposure assessments were conducted to assess**  **exposures resulting from non -**  **dietary residential uses of propiconazole arising from uses on golf course and residential turf. Activity scenarios for adults (19+ years old)**  **included mixer/loader/applicator, high contact dermal events, mower, and golfer.**  **Activity scenarios for 11 -**  **16 year old youths included mower and golfer. Activity scenarios for 6**  **- 11 year old youths included golfer. Activity scenarios for children 1**  **- 6 years includ**  **ed re -**  **entry and various activities on treated turf. A dermal absorption value of 40% was used. For all turf and ornamental scenarios, the**  **scenario producing the highest short -**  **term exposure for each population subgroup selected. For adults 19+, the worst** **- case short**  **- term MOE was 1,639 (adult high**  **contact turf). For youths 11 -**  **16, the worst -**  **case short -**  **term MOE was 19,910 (youth golfer). For youths 6**  **- 11, the worst** **- case short**  **- term MOE was 1,639 (youth golfer).**  **For children 1 -**  **6, the worst -**  **case short -**  **term MOE was**  **764 (combined dermal +**  **hand -**  **to -**  **mouth). Exposure risks were also assessed for children’s accidental ingestion of lawn granules (MOE = 147) and were found to be acceptable**  **(Benchmark MOE = 100); the ingestion of lawn granules by children is considered to be episodic in nature and is not aggregated with dietary or other residential** **exposures. Since the Benchmark MOE for this assessment was 100 and since the** 

**EPA generally has no concern for exposures above the benchmark, Syngenta believes that there is a**  **reasonable certainty that no harm will result from short -**  **term non**  **- dietary exposures arising from all**  **current, pending, and proposed uses for**  **propiconazole. D. Cumulative Effects**  **Cumulative Exposure to Substances with a Common Mechanism of Toxicity. Secti**  **on 408(b)(2)(D)(v) requires that, when considering whether to establish, modify, or revoke a tolerance, the Agency consider “available information”**  **concerning the cumulative effects of a particular pesticide’s residues and “other substances that have a com**  **mon mechanism of toxicity”. Propiconazole is a member of the triazole**  **- containing class of pesticides. Although conazoles act similarly in**  **plants (fungi) by inhibiting ergosterol biosynthesis, there is not necessarily a relationship between this pesticida**  **l activity and their mechanism of toxicity in ma**  **mmals. Structural similarities do not constitute a common mechanism of toxicity. There is currently no evidence to indicate that conazoles share common**  **mechanisms of toxicity and the EPA is not following a cumulative risk approach**  **based on a common mechanism of toxicity for the conazoles. E. Safety Determination**  **1. U.S. population.**  **Using the conservative assumptions described above, and based on the completeness and reliability of the toxicity data, the acute aggregate**  **(food plus water) exposure calculation for all current, pending, and proposed uses of propiconazole provided a MOE o**  **f 621**  **for the U.S. population. For short -**  **term exposures, chronic dietary (food and water) exposures were aggregated with**  **residential exposures, resulting in a worst -**  **case short -**  **term aggregate MOE of 878 for the U.S. population. The chronic aggregate expos**  **ure analysis (food and water) showed that exposures from all current, pending, and proposed propiconazole uses**  **resulted in a MOE of 631 for the U.S. population. Since the worst case aggregate MOE of 621**  **(short -**  **term risk) exceeds the Benchmark MOE of 100,**  **Syngenta believes that there is a reasonable certainty that no harm will occur to the U.S.**  **population from aggregate exposures arising from all current, pending, and proposed uses for propiconazole** 

. **2. Infants and children**  **. Using the conservative assump**  **tions described above, and based on the completeness and reliability of the toxicity data, the acute**  **aggregate (food plus water) exposure calculation for all current, pending, and proposed uses of propiconazole provided a MOE of 256**  **for children 1 -**  **2 years old.**  **For short -**  **term exposures, chronic dietary (food and water) exposures were aggregated with residential exposures resulting in a short** **- term aggregate MOE of** 

**377 for children 1 -**  **2 years old. The chronic aggregate exposure analysis (food and water) showe**  **d that exposures from all current, pending, and proposed propiconazole uses resulted in a MOE of 247 for children 1**  **- 2 years old. Since the**  **worst case aggregate MOE of 247 (chronic risk)**  **exceeds the Benchmark MOE of 100, Syngenta believes that there is a r**  **easonable certainty that no harm will occur to infants and children from aggregate exposures arising from all current, pending,**  **and proposed uses for propiconazole. F. International Tolerances**  **The Codex Alimentarius Commission has established several maximum residue**  **limits (MRLs) for propiconazole in or on various raw agricultural commodities (banana; barley; coffee beans; cranberry; maize; pecan; pineapple; popcorn; rape**  **seed; rye; soya; sugar beet; sugar cane; sweet corn; triticale; wheat; and meat, milk,**  **and eggs). The Codex MRLs are expressed in terms of propiconazole per se. In addition, both Canada and Mexico have established MRLs/tolerances on several**  **commodities which also have U.S. tolerances. The U.S. tolerance expression includes all metab**  **olites determined as 2,4 -**  **dichloro -**  **benzoic acid. In conjunction with the reregistration process EPA intends to revise the tolerance expression to**  **propiconazole per se. To the extent possible, for the present petitions, U.S. tolerances have been numericall** **y harmonized with Codex, Canadian and Mexican MRLs; however, differences in use patterns and the supporting residue data have**  **precluded reducing many tolerances.**