EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR

PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER EPA Registration Division contact: James Tompkins, Registration Support Branch, Registration Division (7505C ), Office of Pesticide Programs, Environmental Protection Agency, 401 M Street, SW, Washington, DC 20460; telephone number: (703) 305 - 5697; e - mail address: tompkins.jim@epa.gov BASF Corporation PP 0E7788 EPA has received a pesticide petition ( PP 0E7788 ) from BASF Corporation, P .O. Box 13528, Research Triangle Park, NC 27709 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 by

establishing a tolerance for residue s of tepralox ydim , (2 - [1 - [[[(2E) - 3 - chloro - 2 - propenyl]oxy]imino]propyl] - 3 - hydrox y- 5 - (tetrah ydro - 2H - py ran - 4 - yl ) - cyclohexene - 1 - one) and its metabolites convertible to GP (3 - (tetrahydrop yran - 4 - yl )pentane - 1,5 - dioic acid) and OH - GP (3 - hydrox y - 3 - (tetrahydrop yr an - 4 - yl )pentane - 1,5 - dioic acid), calculated as tepralox ydim, in or on the raw agricultural commodities pea and bean, dried she lled, except soy bean, subgroup 6C , at 0.1 0 parts per million (ppm), and S unflower Subgroup 20B , at 0. 25 ppm for imported commoditie s . EPA has determined that the petition contains data or information regarding the elements set forth in section 408 (d)(2) of F F DCA; 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. The qualitative nature of the residues of tepraloxydim in plants is adequatel y understood for the purposes of establishi ng these tolerance s . Nature of the residue studies were conducted in so ybean, canola, and sugar beet in order to characterize the fate of tepralox ydim amongst different crop ty pes. Tepraloxydim and its metabolites convertible to GP (3 - (tetrah ydrop yran - 4 - yl )pentane - 1,5 - dioic acid) and OH GP (3 - hydroxy- 3 - (tetrahydropy ran - 4 - yl )pentane - 1,5, - dioic acid), expressed as the parent compound, comprise the relevant residues. 2. Analytical method. The anal yt ical method involves extraction, concentration, precipitation, centrifugation/filtration, oxidation, partition, and clean - up. Samples are then anal yz ed b y GC - MS (selected ion monitoring). The limit of quantitation (LOQ) is 0.05 ppm for each anal yt e, parent and metabolite. 3. Magnitude of residues. Resid ue crop field trials were conducted in North2

Dakota, South Dakota, Manitoba, and Quebec to represent the dry bean production regions of Canada. Residue crop field trials were conducted in North Dakota, Wisconsin, Manitoba, and Saskatchewan, to represent the sunflower production regions of Canada. In addition, a processing study was conducted to determine the potential for residues of tepralox ydim to concentrate in sunflower processed fractions. All field trials were carried out using the maximum or high er labeled rates, maximum number of applications, and the proposed pre - harvest interval. In the dry bean trials , there were no residues detected above the limit of quantitation (0.05 ppm) for either tepralox ydim or its metabolites convertible to the anal y tes GP and OH - GP. The combined residues of tepralox ydim in the treated sunflower seed samples ranged from <0.10 ppm (less than the combined LOQ) to 0.18 ppm. Only two of the ten treated samples contained quantifiable residues (combined residues of 0.10 and 0.18 ppm). A comparison of the residues in the RAC with those in the processed fractions indicated that residues of tepraloxydim do not concentrate in sunflower processed fractions (meal and refined oil). B. Toxicological Profile 1. Acute toxici ty. Tepraloxydim is characterized by low acute toxicity

by the oral, dermal and inhalation route of administration. The acute toxicity studies place technical tepralox ydim in toxicity

category IV for acute inhalation and skin irritation. Tepralox ydim i s in toxicity category III for acute oral, acute dermal toxicity and eye irritation. The technical material is not a dermal sensitizer. An acute neurotoxicity study conducted with tepralox ydim showed a LOAEL of 500 mg/kg, but a NOAEL was not identified . 2. Genotoxicty. In the five mutagenicity studies consisting of both in vitro and in vivo studies, tepralox ydim showed no mutagenic, clastogenic or other genotoxic activity . Tepralox ydim did not induce mutations in either an in vitro Ames test or an in vitro CHO/HPRT locus mammalian cell assay . Tepraloxydim had no chromosomal effects in an in vitro cy

togenetics chromosome aberration test in CHO cells or in an in vivo mouse micronucleus test. Tepraloxydim also did not induce DNA - damage and - repair in the unscheduled DNA sy

nthesis (UDS) test. Therefore, tepraloxydim does not pose a genotoxic hazard to humans. 3. Reproductive and developmental toxicity. The reproduction toxicity of tepralox ydim was investigated in a 2 - generation study as well as in prenatal toxicity studies in rats and rabbits. In the 2 - generation study the NOAEL for reproductive function was the highest dose tested, 2500 ppm (approximately 260 mg/kg bw male). The NOAEL for s ys temic toxicity for the parental animals in the 2 - gener ation study was 500 ppm (50.6 mg/kg bw male, 55 mg/kg bw female). The NOAEL for developmental toxicity was 500 ppm (50.6 mg/kg bw male, 55 mg/kg bw mg/kg bw female) in the 2 - generation study. A prenatal toxicity

study in rats observed a slight increased rate of malformations in the highest dose group (360 mg/kg bw), in which distinct maternal toxicity was also observed. A slight increase in skeletal variations was observed at the mid dose (120 mg/kg bw). Although there was no maternal toxicity at thi s dose, the skeletal variations3

were most likel y related to reduced pup weights at this dose. No treatment - related developmental effects were observed at the low dose level (40 mg/ kg bw). No embryotoxic or teratogenic findings were detected in a prenat al toxicity study in rabbits at any dose level, including one dose level where there was clear maternal toxicity . The lowest NOAEL for maternal/parental toxicity was 50.6 mg/kg bw (2 - generation study, male rat), and the lowest NOAEL for developmental tox icity was 40 mg/kg bw (prenatal toxicity study , rat). 4. Subchronic toxicity. The short - term toxicity of tepraloxydim was investigated in 28 - day range - finding studies as well as in 3 - month studies in rats, mice, and dogs. The signs of toxicity

observe d in the three species were quite similar. The target organs were the liver and the kidney s, with the observed clinicochemical findings linked to either liver or kidney toxicity . In dogs the NOAEL was 12.9 mg/kg bw male and 14.3 mg/kg bw female based upon increased weights of the liver and thy roid and histopathology

of the spleen at the mid dose (63.3 mg/kg bw male, 68 mg/kg bw female). In a 4 - week dermal toxicity study in rats no substance - related findings were detected up to the highest dose level tested of 1,000 mg/kg bw. The overall lowest subchronic NOAELs from oral administration studies were 22 mg/kg bw for rats (male), 95 mg/kg bw for mice and 12.9 for dogs (male). A subchronic oral neurotoxicity study in rats found the NOAEL was 1500 pm (103 mg/kg bw males, and 124 mg/kg bw females) based on increased motor activity , decreased body weight and decreased food consumption at the high dose (6000 ppm, 428 mg/kg bw male, 513 mg/kg bw female). 5. Chronic toxicity. A 12 - month dog study with doses of 0, 100, 400 and 2000 ppm found a slight anemia, detected only at the highest dose level, with subsequent alterations in the bone marrow and the spleen. This phenomenon was onl y observed in dog studies, so the dog was determined to be the most sensitive spe cies with regard to the anemic process. Furthermore, an impairment of liver function was detected with associated hepatocellular hy pertrophy at the highest dose tested. The high toxic dose levels caused weight reductions of epididy mides and testes, combin ed with signs of reduced function of epididy mides and degeneration and atrophy of the germinal epithelium in the testes. In the urinary bladder, hyperplasia of the transitional epithelium was found in animals from high dose levels. From the toxico - patholo gical point of view, liver, urinary

bladder and the haematopoietic s ys tem were identified as primary target organs in dogs. Effects on the male gonadal tissues may be regarded as secondary due to reduced nutritional status and anemia. The results of a 24 - month chronic toxicity study and a carcinogenicity study with dose levels at 0, 100, 600, 3000 (male) and 4,000 ppm (female) in rats showed that the highest dose level (3,000 ppm in males and 4,000 ppm in females) clearl y fulfilled the criteria for4

a MTD b ased on distinctly reduced body

weights or body

weight changes and histopathological alterations in the liver. The test substance induced changes in clinico chemical parameters that are associated with liver toxicity . Histopathological effects were found i n the liver, therefore this organ was identified as the target. In the carcinogenicity study , females at the top dose showed a slight trend towards an increased incidence of hepatocellular adenomas and carcinomas, which was virtually within the historical control range. In top dose males of the chronic toxicity study , a trend towards a slightl y elevated increase of carcinomas was detected. Additional mechanistic investigations (Foci initiation study

in rats) demonstrated that tepraloxydim does not possess an initiating potential for a liver carcinogenic process. Rather, Tepraloxydim can reversibl y enhance cell proliferation at high dose levels as indicated by an S - phase response study in rat. This mechanism that results in an increased incidence of liver tumors is relevant onl y at dose levels at the MTD. Combined with the absence of gene or chromosome damaging effect, it can be concluded that the increased incidence of rat liver neoplasia was not related to a genotoxic mode of action and Tepralox ydim doe s not have an oncogenic potential of biological relevance. The result of the carcinogenicity study in mice with dose levels of 0, 200, 1800 and 5000 ppm demonstrates that the high dose level of 5,000 ppm exceeded the criteria of an MTD as evidenced b y dra stically reduced body weights or body weight changes. A trend towards an increased incidence of liver neoplasia occurred onl y in females at the high dose level and therefore cannot be extrapolated to dose levels below the MTD. Relative liver weights were distinctly increased at the highest dose level, associated with foci of cellular alteration and h ypertroph y of hepatocytes. In female animals of the high dose levels, hyalinization of the uterus was found as well as a reduced ovarian activity , which may be a consequence of the reduced terminal body weights. The overall lowest NOAEL s obtained in long - term oral administration studies were 5 mg/kg bw for male rats, 37 mg/kg bw for male mice, and 11.5 mg/kg bw for male dogs. These chronic NOAEL s demonstrate th at the rat is the most sensitive species. Tepralox ydim has been reviewed b y the Agency for carcinogenicity classification. In accordance with the EPA Draft Guidelines for Carcinogenic Risk Assessment (July , 1999), the Agency

has classified tepralox ydim as data are inadequate for an assessment of human carcinogenic potential because some evidence is suggestive of carcinogenic effects, but other equally

pertinent evidence does not confirm a concern. The Agency concluded that quantification of human cancer ri sk is not required because although there was some evidence of carcinogenicity in female rats based on an increased incidence of liver tumors at the high dose, this finding was not supported by the results of the chronic study. The Agency also concluded that female mice developed liver tumors at an excessivel y toxic dose, and although male mice had non - neoplastic liver changes similar to or exceeding those seen in female mice at the same dose, there was no increase in liver tumor incidence in males. Furthe r more tepralox ydim was not mutagenic in a battery of assay s. Therefore a cancer risk assessment was not performed. 6. Animal metabolism. Tepralox ydim is extensively metabolized and rapidly eliminated, with no evidence of accumulation in tissues. Phar macokinetic studies5

demonstrate that tepraloxydim is readil y absorbed orally in rats, but is rapidly excreted mainly via the urine (65 - 80%) and to a minor degree via the feces (15 - 25%). Approximately

35 - 55% of the dose was excreted via the bile, whi ch when compared to the excretion via the feces suggests an enterohepatic recirculation. Based on the amount of radioactivity

excreted via the bile and urine, the bioavailability of tepraloxydim is virtually 100%. The biotransformation of tepralox ydim in rats resulted in a large number of metabolites in urine, feces and bile. The main metabolic pathway s were the oxidation at the py ran ring to the lactone via the hydrox y- metabolite, and the cleavage of the oxime ether group with the imine and oxazol as pro ducts. Plasma, liver and kidney almost exclusively contained parent. 7. Metabolite toxicology . Tepralox ydim, h ydrox yl ated in the 5 - position of the cyclohexenone ring (5 - OH - DP), was tested in toxicological studies (acute oral rat, 90 - day feeding rat, Am es Test, in vitro UDS, ex vivo USD, Micronucleus Test, prenatal toxicity rat). This metabolite has been shown to be the main metabolite of the active ingredient in oilseed rape and so ybeans, but not in mammals. The results of these studies showed that th is metabolite is not more toxic than the parent compound and does not have mutagenic or teratogenic properties. 8. Endocrine disruption . No specific tests have been conducted with tepralox ydim to determine whether the chemical may have an effect in humans that is similar to an effect produced b y a naturall y occurring estrogen or other endocrine effects. However, there were no significant findings in other relevant toxicity studies (i.e., subchronic and chronic toxicity , teratology and multi - generation reproductive studies) that would suggest that tepralox ydim produces endocrine related effects. C. Aggregate Exposure 1. Dietary exposure. Exposure assessments were conducted to evaluate the potential risk due to acute and chronic dietary exposure o f the U.S. population to residues of tepralox ydim. This herbicide and its metabolites convertible to GP (3 - (tetrah ydrop yran - 4 - yl )pentane 1,5 - dioic acid) and OH - GP (3 - hydroxy- 3 - (tetrahydropy ran - 4 - yl )pentane - 1,5, - dioic acid) in or on raw agricultural comm odities, animal fat, liver, kidney , meat, and meat by products , milk, and eggs were expressed as the parent compound. The tolerance values previously

established for cotton, soy beans, canola, and animal products are listed in the U.S. EPA final rule publis hed in the Federal Register August 2, 2001 (Vol 66, No. 149, p 40141

– 40150) . Additional tolerances established for the imported commodities flax, seed; lentil, seed; and pea, dry , seed, are listed in the U.S. EPA final rule published in the Federal Regi ster September 26, 2007 (Vol 72, No. 186, p 54584

– 54588 ) and in U.S. 40 CFR § 180.573. The analy sis presented below included all current and proposed import tolerance values for pea and bean, dried shelled, except soy bean, subgroup 6C, at 0.1 parts per million (ppm), and Sunflower Subgroup 20B, at 0.25 ppm .6 i. Food. Acute Dietary

Exposure Assessment The acute dietary

e xposure estimates were highly c onservative using proposed and established tolerance values, default process ing factors, and 100% cro p treated values for all commodities. The tolerance values included current and proposed import tolerances for pea and bean, dried shelled, except soy bean, subgroup 6C, at 0.1 parts per million (ppm), and Sunflower Subgroup 20B, at 0.25 ppm. The consumption data was from the USDA Continuing Survey o f Food Intake by

Individuals (CSFII 1994 - 1996, 1998) and the EPA Food Commodity Ingredient Database (FCID) using Exponent's Dietary Exposure Evaluation Module (DEEM - FCID) software. The EPA has determined that different acute population adjusted dose s (aPAD) should be used for assessing the acute dietary risk of tepraloxydim. The justification for this has been described in the final rule published in the Federal Register September 26, 2007 (Vo l 72, No. 186 , p 54584

– 54588) , and in the Human Health Risk Assessment available in docket ID EPA - HQ - OPP - 2007 - 0145. Inbrief, the 10X FQPA Safety F actor was applied to the endpoint used in assessing the acute dietary risk to the general US population (including inf ants and children) , but it was reduced to 1X when applied to the endpoint for assessing the acute dietary risk to females (13 - 49 years of age). The aPAD used for the general population is 0.5 mg/kg bw/day , and for females (13 - 49 years of age ) the aPAD is 0. 4 mg/kg bw/day . The results of the acute dietary a ssessment are presented in Table 1. The results of the anal ys is show that for the relevant sub - population s , the exposures are below the Agency's level of concern (< 100% aPAD). Considering the expo sure assumptions discussed above, the acute dietary

e xposure to 95 th percentile residues in food is 5. 5 % aPAD for the population group (infants <1 ye ar old) receiving the greatest exposure. Additional refinements in the dietary risk assessment (i.e. util izing anticipated residue values, process ing factors, percent crop treated values and percent imported commodities for all crops) would further reduce the estimated exposure values.7

Table 1. Summary of Tepraloxydim Acute Dietary Exposure Analysis Con sidering

all Current and Proposed Tolerances , Default Processing Fa ctors, and 100% Crop Treated U sing DEEM - FCID at the 95 th Percentile Population Exposure Estimate %aPAD Subgroup (m g/kg b.w./day) 95 th Percentile U.S. Population 0.010813 2.16 All I nfants (< 1 year old) 0.027537 5.51 Children (1 - 2 years old) 0.021466 4.29 Children (3 - 5 years old) 0.018472 3.69 Children (6 - 12 years old) 0.013214 2.64 Youth (13 - 19 years old) 0.008824 1.76 Adults (20 - 49 years old) 0.006999 1.40 Adults (50+ years o ld) 0.005446 1.09 Females (13 - 49 years old)* 0.006582 1.65 aPAD = acute population adjusted dose * The endpoint applied for females age 13 to 49 is different from the other population subgroups. Chronic Dietary

Exposure Assessment The chronic dietary exposure estimates were highl y conservative using proposed and established tolerance values, default process ing factors, and 100% crop treated values. The consumption data was from the USDA Continuing Survey o f Food Intake by Individuals (CSFII 1994 - 199 6, 1998) and the EPA Food Commodity Ingredient Database (FCID) using Exponent's Dietary E xposure Evaluation Module (DEEM - FCID) software. T he tolerance values included current and proposed import tolerances for pea and bean, dried shelled, except soy bean, subgroup 6C, at 0.1 parts per million (ppm), and Sunflower Subgroup 20B, at 0.25 ppm. The chronic population adjusted dose (cPAD) used for U.S. population and all sub populations is 0.05 mg/kg bw/day . Considering the exposure assumptions discussed above, tepraloxydim chronic dietary e xposure from food for the U.S. population was 8.0%of the cPAD. The most highl y exposed population sub - group was children 1 - 2 ye ars of age at 22.3% cPAD. The results of the chronic dietary a ssessment are presented in Table 2 . The results of the anal ys is show that for all sub - populations, the exposures are below a level of concern (< 100% cPAD). A dditional refinements in the chronic dietary risk assessment (i.e. utilizing anticipated residue values, processing factors, perce nt crop treated values) would further reduce the estimated exposure values.8

Table 2 . Summary of Tepraloxydim Chronic Dietary Exposure Analysis

Considering all Current and Proposed Tolerances , Default Processing Factors, and 100% Crop Treated Using using DEEM - FCID Population Exposure Estimate %cPAD Subgroups (m g/kg b.w./day) U.S. Population (total) 0.004017 8.0% All infants (< 1 year) 0.009576 19.2% Children 1 - 2 y

rs 0.011169 22.3% Children 3 - 5 y

rs 0.009572 19.1% Children 6 - 12 y

rs 0.006414 12.8% Youth 13 - 19 y

rs 0.003881 7.8% Adults 20 - 49 y

rs 0.003102 6.2% Adults 50+ yrs 0.002485 5.0% Females 13 - 49 y

rs 0.002921 5.8% cPAD = chronic population adjusted dose ii. Drinking water. The estimated maximum tepralox ydim surface water and groundwater values were taken from the Federal Register , September 26, 2007 (Vol 72, No. 186, p 54584

– 54588) . Surface water acute and chronic values were listed as 1.4 and 0.7 ppb, respectivel y. The groundwater value was 0.00 2 ppb (acute and chronic). Drinking water contributions were assessed based on the maximum estimated tepralox ydim water concentrations (acute

– 1.4 ug/L , chronic 0.7 ug/L), and water consumption and body

weights reported in CSFII, using DEEM - FCID software. The acute and chronic estimated water exposure values are summarized in Tables 3 and 4, respectivel y. Minimal exposure of tepralox ydim occurs through drinking wat er with < 1.0% the aPAD and < 1.0 % cPAD for the U.S. population and all subpopulations. Table 3. Results for Tepraloxydim Acute Water Exposure Analysis

Considering the Maximum Estimated Acute Drinking Water Concentration using DEEM - FCID Population Wate r Exposure Estim ate %aPAD Subgroups (m g/kg b.w./day) U.S. Population (total) 0.000074 0.01 All infants (< 1 year) 0.000292 0.06 Children 1 - 2 y

rs 0.000117 0.02 Children 3 - 5 y

rs 0.000106 0.02 Children 6 - 12 y

rs 0.000074 0.01 Youth 13 - 19 y

rs 0.000061 0.01 Adults 20 - 49 y

rs 0.000068 0.01 Adults 50+ yrs 0.000061 0.019 Females 13 - 49 y

rs 0.000069 0.02 aPAD = acute population adjusted dose Based on estimated acute surface water value of 1.4 ug/L from the Federal Register Septem ber 26, 2007 (Vol 72, No. 1 86, p 54584

– 54588) Table 4. Results for Tepraloxydim Chronic Water Exposure Analysis

Considering the Maximum Estimated Chronic Drinking Water Concentration using DEEM - FCID Population Water Exposure Estim ate %cPAD Subgroups (m g/kg b.w./day) U.S. P opulation (total) 0.000015 0.0% All infants (< 1 year) 0.000048 0.1% Children 1 - 2 y

rs 0.000022 0.0% Children 3 - 5 y

rs 0.000021 0.0% Children 6 - 12 y

rs 0.000014 0.0% Youth 13 - 19 y

rs 0.000011 0.0% Adults 20 - 49 y

rs 0.000014 0.0% Adults 50+ yrs 0.000014 0 .0% Females 13 - 49 y

rs 0.000014 0.0% cPAD = chronic population adjusted dose Based on estimated chronic surface water value of 0.7 ug/L from the Federal Register Septem ber 26, 2007 (Vol 72, No. 186, p 54584

– 54588) Acute Aggregate Exposure and Risk (Fo od and W ater) The aggregate acute risk includes residues of tepraloxydim from food and water (Table 5). Exposures from residential uses are not included in the acute aggregate assessment. The results demonstrate that there are no safety concerns for an y subpopulation based on established and proposed new uses, and that the results clearl y meet the FQPA standard of rea sonable certainty of no harm. Table 5. Estimated Acute Aggregate Exposure and Risk of Tepraloxydim Population Subgroup aPAD (m g/kg/day) Food Exposure

(m g/kg/day) Water

Exposure (m g/kg/day) Total

Exposure (m g/kg/day) % aPAD U.S. Population (total) 0.5 0.010813 0.000074 0.010887 2.18 All infants (< 1 year) 0.5 0.027537 0.000292 0.027829 5.57 Children 1 - 2 y

rs 0.5 0.021466 0.000117 0.02158 3 4.32 Children 3 - 5 y

rs 0.5 0.018472 0.000106 0.018578 3.72 Children 6 - 12 y

rs 0.5 0.013214 0.000074 0.013288 2.6610 Youth 13 - 19 y

rs 0.5 0.008824 0.000061 0.008885 1.78 Adults 20 - 49 y

rs 0.5 0.006999 0.000068 0.007067 1.41 Adults 50+ yrs 0.5 0.005446 0.00 0061 0.005507 1.10 Females 13 - 49 y

rs 0.4 0.006582 0.000069 0.0066510 1.66 Chronic Aggregate Exposure and Risk (food and water) The aggregate chronic risk includes residues of tepralox ydim from food and water (Table 6). Exposures from residential uses are not included in the chronic aggregate assessment. The results demonstrate there are no safety concerns for any subpopulation based on established and proposed new uses, and that the results clearly meet the FQPA standard of reasonable certainty of no h arm. Table 6. Estimated Chronic Aggregate Expo sure and Risk of Tepraloxydim Population Subgroup cPAD (m g/kg/day) Food Exposure

(m g/kg/day) Water

Exposure (m g/kg/day) Total

Exposure (m g/kg/day) % cPAD U.S. Population (total) 0.05 0.004017 0.000015 0.00 40320 8.06 All infants (< 1 year) 0.05 0.009576 0.000048 0.0096240 19.25 Children 1 - 2 y

rs 0.05 0.011169 0.000022 0.0111910 22.38 Children 3 - 5 y

rs 0.05 0.009572 0.000021 0.0095930 19.19 Children 6 - 12 y

rs 0 .05 0.006414 0.000014 0.0064280 12.86 Youth 13 - 19 y

rs 0.05 0.003881 0.000011 0.0038920 7.78 Adults 20 - 49 y

rs 0.05 0.003102 0.000014 0.0031160 6.23 Adults 50+ yrs 0.05 0.002485 0.000014 0 .0024990 5.00 U.S. Population (total) 0.05 0.002921 0.000014 0.0029350 5.87 2. Non - dietary exposure . Tepralox ydim is not registered for residential use, therefore, residential and occupational exposure risk assessments for the incid ental oral, dermal, and inhalation exposure rout es are not required . D. Cumulative Effects Section 408(b)(2)(D)(v) requires that, when considering whether to establish, modify , or revoke a tolerance, the Agency consider “available information” concer ning the cumulative effects of a particular pesticide's residues and “other substances that have a common mechanism of toxicity . ” The EPA is currently

developing methodology to perform cumulative risk assessments. At this time, there is no available d ata to determine whether tepraloxydim11

has a common mechanism of toxicity with other substances or how to include this pesticide in a cumulative risk assessment. E. Safety Determination 1. U.S. population. Based on the risk assessment s , BASF conclude s that there is a reasonable certainty

that no harm will result to the general population from the aggregate exposure to tepralox ydim residues. 2. Infants and children . Based on the risk assessment s, BASF concludes that there is a reasonable certainty that no harm will result to infants or children from the aggregate exposure to tepralox ydim residues . F. International Tolerances No Codex or Mexican maximum residue levels (MRL s) have been proposed or are established for residues of tepralox ydim. Therefore, no tolerance discrepancies exist between countries for this chemical.