**EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR**

**PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER EPA Registration Division Contact:**  **Kathryn Montague (**  **703) 305 -**  **1243 INSTRUCTIONS:**  **Please utilize this outline in preparing the pesticide petition. In**  **cases where the outline element does not apply, please insert “NA -**  **Remove” and maintain the outline. Please do not change the margins, font, or format in your**  **pesticide petition. Simply replace the instructions that appear in green**  **, i.e., “ [**  **i nsert**  **company name ]**  **,” with the information specific to your action. TEMPLATE:**  **[ K** **- I CHEMICAL U.S.A., INC.**  **] [Insert petition number]**  EPA has received a pesticide petition **( [insert**  **petition number] )**  from **K -**  **I CHEMICAL U.S.A., INC. c/o Landis International**  **, Inc., P. O. Box 5126 Valdosta, GA 31603**  **- 5126**  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 b y establishing tolerances for residues of the sum of **pyroxasulfone** [3 - [ [[5 - (difluoromethox y) - 1 - methyl 3 - (trifluorometh yl ) - 1H - py razol - 4 - yl ]methyl]sulfonyl] - 4,5 - dihydro - 5,5 - dimethyl isoxazole] and its metabolite 5 - (difluoromethoxy ) - 1 - methyl - 3 - (trifluoromethyl) - 1H - py razol - 4 - carbox yl ic acid ( **M -**  **3** ) calculated as the stoichiometric equivalent of py roxasulfone, i n or on the raw agricultural commodities **corn, field, grain at**  **0.0 2**  ppm (parts per million) and **pyroxasulfone** [3 - [[[5 - (difluoromethox y) - 1 - methyl - 3 - (trifluorometh yl ) - 1H - py

razol - 4 - yl ]methyl]sulfonyl] - 4,5 - dihydro - 5,5 - dimethylisox azole] and its metabolites [5 - (difluoromethox y) - 1 - methyl - 3 - (trifluorometh yl ) - 1H - py razol - 4 - yl ]methanesulfonic acid ( **M -**  **1** ), 5 - (difluoromethoxy) - 1 - methyl - 3 - (trifluoromethyl) - 1H py razol - 4 - carbox yl ic acid ( **M -**  **3** ), and [5 - (difluoromethoxy ) - 3 - (trifluoromethyl) - 1H p yr azol - 4 - yl ]methanesulfonic acid ( **M -**  **25** ), calculated as the stoichiometric equivalent of py roxasulfone, i n or on the raw agricultural commodities **corn, field, forage at**  **0.0 9**  ppm (parts per million) . EPA has determined that the petition contains data or inf ormation regarding the elements set forth in section 408 (d)(2) of FDDCA; however, EPA has not fully evaluated the sufficiency of the submitted data at this time or whether the data supports granting of the petition. Additional data may be needed before E PA rules on the petition.2

A. Residue Chemistr

y 1. Plant Metabolism. Plant metabolism studies were conducted and accepted by the Agency

for soy bean and field corn. The plant and animal metabolism of py roxasulfone is well understood. Primary metabolic proces ses are cleavage between the two ring structures, side chain oxidation to carboxylic acid and demethylation. Py roxasulfone and its major metabolites M - 1 , M - 3 , and M - 25 were metabolites in corn and soy bean. The metabolism of py roxasulfone in plants and an imals is understood for the purposes of the propo sed tolerances. Py roxasulfone and its metabolites M - 1 , M - 3, M 25and M - 28 are the residues of concern for tolerance setting purposes for soy bean . 2. Analytical method. EPA has approved an anal yt ical enforc ement methodology including liquid chromatograph y, mass spectrometry, and mass spectrometry (L C/MS/MS) to enforce the tolerance expression for py roxasulfone. 3. Magnitude of residues. 

### Corn Residue Data Initiall y, a total of 37 corn residue raw agricul tural commodity (RAC) field trials were conducted in regions 1, 2, 3, 5, 6, 10, 11 and 12 of the United States (MRID 47701656). A total of 11 of these trials were sweet corn trials and the remaining were field corn trials. Three of these trials were residu e decline trials to determine residue decline in the respective corn RAC matrices after application. Three comparison trials, on three different soil ty

pes; fine, medium and course, were conducted to compare five different application ty

pes in different pl ots at the same site including pre - plant to surface, pre - plant incorporated, post - planting but pre - emergence of weeds or crop, earl y postemergence and split application with pre - emergence and post - emergence. Application rates for these comparison trials we re 166 g a.i./ha, 209 g a.i./ha and 300 g a.i.lha for the course, medium and fine soil ty pe, respectivel y. For the remaining 34 studies, application rates were 166 g a.i./ha on course soil ty pes and 300 g a.i./ha on medium and fine soil ty

pes. Applications for these 34 trials were post - emergence applications (approximately V4 growth stage). One trial included a plot with a 5X application rate (post - emergence) in which the grain was collected for processing. Samples were collected from each plot at the appro priate time (normal maturity except samples from the residue decline trials which were collected earlier). Matrices were extracted with acetonitrile or aqueous methanol followed by various cleanup steps depending on the matrix and ana1 yt e. Anal ys is was per formed using LC - MS/MS for py roxasu1fone and its metabolites in all matrices. The LOQ was 0.005 ppm for all matrices except two metabolites one in meal and one in oil for the LOQs which were 0.01 ppm. The residue in all field com grain samples was below LOQ . All field com processed commodity

matrix samples showed residues less than the respective LOQ for that particular matrix. A second study (MRID 48767101) was conducted to obtain RAC residue data for py roxasulfone (KIH - 485) and its metabolites M - 1, M - 3, an d M - 25 on corn following a single post - emergence application of py roxasulfone 85 WG herbicide at the V3 - V5 growth stage with and without adjuvant and fertilizer to determine if adding fertilizer3

and/or adjuvant to the spray solution affected the residues i n the harvested crop. The matrices analyzed were forage, stover, and grain, and residues of KIH - 485, M - 1, M - 3, and M - 25 were anal yz ed. The study was conducted at three trial locations in the United States including: Georgia (GA), Missouri (MO), and Nebrask a (NE), representing United States EPA Regions 2, 4 and 5, respectivel y. The protocol was designed according to a request from the EPA regarding the number of treated plots and treatments and the number of treated samples (4 treated samples collected per p lot instead of 2 as required by the guideline). In each trial, there was one non - treated plot and three treated plots. Applications were made related to the soil ty pe at a target rate of 0.148 lb ai/A (166 grams ai/ha) for the coarse textured soil site (GA ) and 0.268 lb ai/A (300 grams ai/ha) for the other two locations MO and NE (medium and fine textured soil sites, respectivel y). At the appropriate preharvest harvest intervals (PHI s), corn samples were collected for each matrix (forage, stover, and grain) , frozen and shipped frozen to the analy tical laboratory

for anal ys is. A limit of quantitation (LOQ) of 0.005 ppm was determined for the parent molecule (KIH - 485), M - 1, M - 3 and M - 25. Concurrent recoveries were conducted with fortification levels of 0.005 p pm and 0.05 ppm. Most recoveries for all anal ys es of each anal yt e in each matrix were within the accepted range (70 - 120%). No residue of the parent p yr oxasulfone molecule was seen in an y corn matrix above the LOQ of 0.005 ppm. Residues of the metabolites o f p yro xasulfone (M - 1, M - 3, and M - 25) were found in selected samples. These residues were added to the OECD MRLcalculator along with the original corn field trial residues without adjuvant to determine the appropriate tolerances. As indicted by EPA memo dated January 10, 2013 DP Barcode: D402247 (Py

roxasulfone. Summary

of Residue Data for P yroxasulfone Use on Corn with and without Adjuvant and Field Rotational Crop Residue Data) and EPA email dated March 20, 2013 the purpose of this tolerance petition is t o increase the corn forage tolerance from 0.06 ppm to 0.09 ppm due the conservative tolerance determined by the OECD MRLcalculator. C onfined Rotational Crop Study Py razole or isoxazoline ring labeled 14 C KIH - 485 was sprayed on confined plots of bare soil prior to planting soy bean, radish and wheat at 30, 120 and 365 day intervals. There were two treated plots for each plantback interval, one of which was wheat onl y and the other was planted half with soy bean and half with radish. All plots were treated at a target application rate of 300 g a.i./ha but the actual rate was 313 g a.i./ha. Samples were anal yz ed b y combustion analysis and liquid scintillation counting. All treated crops contained radioactive residue >0.01 ppm and were subjected to further analy sis. The highest total radioactive residue (TRR), 5.2 ppm was found at the 30 day rotational in wheat straw; the residue level declined to 0.02 ppm at 485 day s. The primary metabolites were M - 1 and M - 3. Field Rotational Crop Study A field rotationa l crop study was conducted in Georgia (GA) and Texas (TX) on a fine and coarse textured soil, respectivel y . The purpose of the study was to obtain raw agricultural commodity

(RAC) residue data for pyroxasulfone and its metabolites M - 1, M - 3, M - 25, M - 28, and M - 37 on rotational crops that are planted in plots that have been treated with Py

roxasulfone 85 WG at the proposed label rate and aged for various time4

intervals prior to planting the rotational plot. Each plot was treated at an appropriate time for growi ng the target crop and then allowed to age for the specified aging interval (120, 270, 300 and 365 day s, nominal intervals). There was no residue seen in any crop matrix at an y sampling interval above the LOQ except for one replicate 120 day potato top sample which showed residue of M - 1 at the LOQ (0.01 ppm). As a result, neither py roxasulfone nor any

of its metabolites are expected to accumulate in rotational crops when Py roxasulfone 85 WG is applied to target crops at the labeled rates. Cow Feeding Study Holstein dairy

cows were treated orally with gelatin capsules fortified with py roxasulfone. These were administered once daily for 28 consecutive day s at dose levels of 0, 1.8, 5.4, and 18 ppm per cow/day on a dry weight basis amounting to concentrations of control, 1X, 3X and 10X dose groups, respectively . These dose levels were equivalent to 0, 35.8 mg/cow/day , 109.9 mg/cow/day and 367.4 mg/cow/day , respectivel y. Milk samples from the high dose animals (10X) were found to contain no resi dues of the parent compound or metabolites with the exception of 3 milk samples from day 7 which contained an average of 0.003 ppm parent py roxasulfone. No other milk samples from the other dose levels were found to contain residues of pyroxasulfone or me tabolites. No other matrix (muscle, liver, kidney or fat) was found to contain residues of p yroxasulfone or metabolites above LOQ. The LOQs were 0.001 ppm in milk and 0.01 ppm in all other matrices. Therefore, no tolerances for residues of py roxasulfone and its metabolites are being proposed for meat, milk, eggs or other edible tissues of livestock or poultry . B. Toxicological Profile 1. Acute Toxicity. Py

roxasulfone was found to be of low acute toxicity via oral, dermal and inhalation routes of admin istration. It was not irritating to skin or eyes and was not a sensitizing agent. The formulated product (85WG) was also of low acute toxicity and was found to be mildly irritating to skin, moderatel y irritating to eyes and was a dermal sensitizer. In an acute neurotoxicity study in rats , there were no test substance - related effects on body weights, food consumption, clinical observations, functional observational battery assessments, motor activity measurements, or gross and microscopic neuropathology . The NOEL was demonstrated to be > 2000 mg/kg/day in adult male and female rats. 2. Genotoxicity. Py

roxasulfone and its metabolites and impurities do not induce gene mutations in bacterial cells. Py roxasulfone does not induce gene mutations or chromosomal aberrations in in vitro mammalian cells or in vivo in the mouse micronucleus test. Py

roxasulfone is non - genotoxic. 3. Reproductive and developmental toxicity. In a developmental toxicity study in rats, the NOEL for maternal and developmental toxicity w as >1000 mg/kg/day , the highest dose tested. Ina d evelopmental toxicity

s tudy i n rabbits, there were slight test substance -5

related effects on fetal weight and number of implant resorptions at 1000 mg/kg/day , the highest dose tested. T he NOEL for matern al toxicity w as 1000 mg/kg/day . The NOEL for developmental toxicity was 500 mg/kg/day . In a rat one - generation reproductive study n o reproductive toxicity

was observed up to and including the high dose of 5000 ppm. The NOEL for reproductive toxicity was > 5000 ppm, the highest dose tested. The NOEL for P 1 adult rats was 25 ppm. The NOEL for F 1 offspring was 250 ppm and the NOEL for F 1 adults was 250 ppm. In a rat two - generation reproduction study there were no test substance - related effects for reprod

uctive toxicity

at 2000 ppm, the highest concentration tested. The NOEL for reproductive toxicity was > 2000 ppm, the highest concentration tested. Test substance - related effects were observed at 2000 ppm in both adults and offspring. Therefore, the NOAEL for sy stemic toxicity was demonstrated to be 100 ppm (6.94

– 11.76 mg/kg/day) in both parents and offspring. In a developmental neurotoxicity study conducted on py

roxasulfone in mated female rats no reproductive effects were observed in the maternal ani mals at 2000 ppm, the highest concentration tested. No effects were observed on FOBs, auditory startle response habituation, pre - pulse inhibition, learning and memory of offspring. A slight (5%) decrease in absolute brain weight at 900 mg/kg/day was prese nt on PD 66, although no effect was present when evaluated on a % body weight basis. Based on the effects observed in this study , the maternal and offspring sy stemic NOAEL is 900 mg/kg/day . The NOEL for functional development was judged to be 900 mg/kg/day. A NOEL for histomorphological development of the brain of the offspring was judged to be 300 mg/kg/day . Two studies were performed to assess the availability of the test substance to the pup. These studies indicated that py roxasulfone was available i n the milk to nursing pups. 4. Subchronic toxicity. Py roxasulfone was evaluated in a 28 - day inhalation toxicity study in rats. There were no test substance - related effects. The NOELwas > 200 mg/m 3, the highest dose tested. In a 28 - day

dermal toxicity study there was a test substance - related increase in the incidence of minimal to mild cardiac m yofiber degeneration with inflammation observed in males and females dosed with 1000 mg/kg/day and cutaneous m yofiber degeneration with inflammation observed i n the treated skin of males dosed with 1000 mg/kg/day . The NOEL was 100 mg/kg/day . Immunotoxicity

was evaluated in rats and mice following dietary exposure for 28 day s. There were no test substance related effects for any of the immunotoxicity paramete rs examined. In the rat, s ys temic toxicity was limited to reductions in body weight and food consumption. The NOEL for immunotoxicity was 7500 ppm (529 and 570 mg/kg in males and females) and the NOEL for systemic effects was 250 ppm (186

and 19 mg/kg in males and females). In the mouse, the NOEL for immunotoxicity was 4000 ppm (633 mg/kg/day males: 791 mg/kg/day

females) and the NOEL for sy stemic effects was 400 ppm (61 mg/kg males: 77 mg/kg females). Py roxasulfone was evaluated in 13 - week oral toxicity studies in rats, mice and dogs. In the 13 week mouse study , no test substance - related effects on in - life and clinical pathology parameters were observed at an y level tested. Test substance - related effects at 2500 ppm were limited to an increased incidenc e of minimal to mild chronic progressive nephropath y in female mice and increased liver weight in males and females fed 2500 ppm. The NOEL was 250 ppm for female mice (51.2 mg/kg/day). The NOELfor male mice was 2500 ppm (394.0 mg/kg/day). Inthe 13 w eek rat study , a NOEL of 250 ppm for male and female rats corresponded to mean daily intake values of 16.4 and 20.6 mg/kg/day in males and females, respectivel y. Test substance related effects were increased cardiac myofiber degeneration with inflammation and diffuse mucosal hy perplasia of the urinary

bladder. In creased liver weights and centrilobular h ypertrophy were also observed in 2500 ppm males and females. In a second study evaluating recovery, full or partial recovery was evident in all the above e ffects apart from kidney weights in females with all m icroscopic findings in the liver, heart, muscle and pancreas of 5000 ppm animals comparable to control rats indicating a complete reversal of the treatment - related findings noted at the terminal sacrifi ce. In an oral 90 day

toxicity study in beagle dogs administered py roxasulfone in a capsule, the NOEL was 2.0 mg/kg. The onl y effects noted were degeneration of muscle fiber of the musculature portion of the diaphragm, hy perplasia of the satellite cell o f the muscle and nerve fiber degeneration of the sciatic nerve in one 10mg/kg/day group male only . In a second study dosed with 0 or 15 mg/kg of p yr oxasulfone, male dogs showed a decrease in body weight and histopathology similar to the full study. Py r oxasulfone was evaluated in a subchronic 90 day neurotoxicity

dietary study in rats. There were no effects on body weights, food consumption, clinical observations, FOB assessments, motor activity measurements, or gross and microscopic neuropathology . The NOELwas > 2500 ppm, the highest dose tested, for male and female rats corresponding to mean daily intake values of 161.48 and 199.59 mg/kg/day in males and females, respectivel y. 5. Chronic toxicity. Chronic toxicity studies were conducted in the rat an d dog. In the rat one ye ar chronic toxicity study t est substance - related effects occurred at 1000 ppm and above that included reduced body weight parameters and microscopic findings in the liver (centrilobular hepatocellular h ypertroph y in males), heart (i ncreased cardiom yopath y in females) and urinary bladder (mucosal hyperplasia in males and females) and urinary

bladder hy

perplasia considered to be secondary to inflammation or irritation. At 2000 ppm, these effects were accompanied b y increased clinical observations of red discharge from the penis and associated red - stained cageboards as well as increased liver and kidney weights. A slight increase in liver and kidney weights7

was observed in the 2000 ppm male and female dietary exposure groups. The NOEL i s 50 ppm (2.22 and 3.12 mg/kg/day for males and females, respectively). In a one - ye ar dog study beagle dogs/sex/dose were administered capsules containing 0.0, 0.2, 2.0 and 10.0 mg/kg/day . Adverse test article - related findings were limited to the 10.0 m g/kg/day group, the highest dose tested and not all animals at the 10 mg/kg/day

dosage had clear test - article related abnormal observation s. Adverse changes in the clinical pathology

parameters were increases in creatine kinase, aspartate aminotransferase and change in the pathology limited to the sciatic nerve and spinal cord. The NOAEL is 2.0 mg/kg/day . The carcinogenic potential of py roxasulfone was evaluated in rats and mice. The Agency has classified pyroxasulfone as “Not likely to be carcinogenic to humans” at doses that do not cause cry stals with subsequent calculi formation resulting in cellular damage of the urinary

tract. 6. Animal metabolism. In the rat, p yroxasulfone is rapidly and completel y eliminated. Between 80 to 90% of py roxasulfone was eliminated in the urine during the first 24 hours and elimination was essentiall y complete after 48 to 72 hours. Absorption was calculated (bile and urine) at 76%. Maximum plasma concentrations were achieved at 2 hours in the low and 11 hours in the high dose animals. At 96 hours only 7% of the low dose and <0.5% of the high dose was present in the carcass demonstrating the near complete elimination of py roxasulfone. Of the radioactivity present in the animals, the highest levels were seen in the l iver and kidney . The major metabolites were a carbox yl ated (py

razole ring meth ylgroup) and cleavage products between the isoxazoline and py razole ring structure with subsequent carboxylation. The absorption, distribution, metabolism and elimination of p yr oxasulfone is unaffected b y sex or treatment regimen. In a preliminary

study in the dog, py

roxasulfone is rapidly

eliminated with 76.9% of radioactivity

excreted within 24 hours. Excretion is approximately equal in urine and feces. The terminal hal f life was 89.58 hr and 40.80 hr in blood and plasma, respectivel y. The feces were found to contain only unchanged py

roxasulfone while no parent molecule was found in the urine. At 120 hr after dosing, the levels of radioactivity in the tissues were high est in the liver and blood. In a preliminary

mouse metabolism study , 73% of the applied dose of py roxasulfone was excreted in urine within 24 hours of dosing. P yroxasulfone was rapidly absorbed and distributed through the tissues of the mouse but by 24 hours after dosing, radioactivity

concentrations in the majority of tissues were indistinguishable from background levels. Metabolism studies in livestock and poultry (Nature of Residue Studies with Goat and Hen) with repeated dose established that p yro xasulfone was rapidl y metabolized and excreted and that there was minimal transmittal of residues of p yroxasulfone and its metabolites to meat or milk. For goats fed 10 ppm of radiolabeled py roxasulfone, the highest residues (TRR) were seen in liver and kidney . In the hen, fed 10 ppm, the highest re sidue was seen in liver and muscle .8 7. Metabolite toxicology. Three plant metabolites and three impurities were evaluated in acute oral toxicity studies. All six test substances evaluated showed LD50’s >20 00 mg/kg similar to the parent, p yr oxasulfone. Two metabolites were further assessed in a 14 day

toxicity study in rats. The NOELfor each of the metabolites was > 1000 mg/kg. The same three metabolites and impurities were evaluated in a bacterial gene mutation test with and without activation. All test substances were non - genotoxic. 8. Endocrine disruption. Py roxasulfone does not belong to a class of chemicals known or suspected of having adverse effects on the endocrine s ys tem. There is no eviden ce that py

roxasulfone has any

effect on endocrine function in developmental, reproduction or developmental neurotoxicity studies. Furthermore, histological investigation of endocrine organs in chronic dog, rat and mouse studies did not indicate that the e ndocrine s ys tem is targeted by py roxasulfone. C. Aggregate Exposure 1. Dietary exposure. It can be concluded with reasonable certainty that residues of py roxasulfone in food will not result in unacceptable levels of human health risk. Using proposed tol erances for corn, soy bean and wheat, both the acute and chronic dietary exposure MOEs for the overall US population and 25 population subgroups are above the EPA level of concern. i. Food. Acute and chronic dietary exposure assessments were conducted usi ng a Tier I approach. This Tier I assessment incorporated tolerance level residues and 100% crop - treated in the DEEM TM (Dietary Exposure Evaluation Model; Exponent, Inc., 2003) software s ys tem. The acute toxicological endpoint selected for assessment of risk following acute dietary

exposure was 300 mg/kg/day based on the Developmental Neurotoxicity

Study with a NOEL 300 mg/kg/day for motor activity

and brain morphology . The acute reference dose (aRfd) was determined to be 3 mg/kg/day assuming the aRdf is 1 percent of the NOEL. The chronic toxicological endpoint selected for assessment of risk following chronic dietary exposure was 2 mg/kg/day based on the one - year chronic feeding dog study with a NOE L of 2 mg/kg/day . The chronic reference dose (cRfd) was d etermined to be 0.02 mg/kg/day assuming the cRfd is 1 percent of the NOEL. Using proposed tolerances for corn, so ybean , wheat, and cotton the acute and chronic dietary

exposure Margin of Exposure (MOEs) for the overall US population and 25 population subgroups are above the EPA level of concern. It can be concluded with reasonable certainty

that residues of py

roxasulfone in food will not result in unacceptable levels of human health risk. ii. Drinking water. Based on the Pesticide Root Zone Model/Exposur e Analysis Modeling S ys tem (PRZM/EXAMS) and Pesticide Root Zone Model Ground Water (PRZM GW), the estimated drinking water concentrations (EDWCs) of py roxasulfone for acute exposure are estimated to be 17 ppb for surface water and 210 ppb for ground water. EDWCs of py

roxasulfone for chronic exposures for non - cancer assessments are estimated to be 3.2 ppb for surface water and 174 ppb for ground water. It can be9

concluded with reasonable certainty that residues of py

roxasulfone in drinking water will not res ult in unacceptable levels of human health risk. 2. Non - dietary exposure . Py roxasulfone is not intended for an y specific use patterns that would result in residential exposures. D. Cumulative Effects Py roxasulfone represents a new class of p yrazole herbicides. No other products are known to have the same mode of action as p yr oxasulfone. Therefore, a cumulative assessment is not appropriate at this time. E. Safety Determination 1. U.S. population. The toxicity database for py

roxasulfone is complet e. Based on the NOEL of 2 mg/kg/day from a 1 - ye ar toxicity

study in the dog, proposed uses represent 1 percent of the cRfD of 0.02 mg/kg/day. Based on the NOEL of 300 mg/kg/day

from a developmental neurotoxicity study , the proposed uses represent 1 percent of the RfD of 3 mg/kg/day . There is reasonable certainty that no harm to the U.S. population will result from the proposed uses of pyroxasulfone. 2. Infants and children . The toxicity database for py

roxasulfone is complete. The database includes acut e, subchronic, chronic, mutagenicity, genotoxicity , developmental, reproduction, neurotoxicity and immunotoxicity

studies on py

roxasulfone and acute mutagenicity

and genotoxicity

studies on several metabolites. The weight of evidence indicates that infant s and children are not expected to be more sensitive to py roxasulfone than are adults. Consequently , EPA reduced the FQPA Safet y Factor from 1 0 x to 1 x. F. International Tolerances Tolerances are approved on wheat, barl e y and triticale in Australia. To lerances are simultaneousl y being sought in Canada at the same levels and for the same crops as for the U.S.