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CFR Citation: 40 CFR Part 180

OPP ID: [OPP-2003-0270; FRL-7324-5]

NOTICE: RULES

ACTION: Pesticides; tolerances in food, animal feeds, and raw agricultural commodities:

DOCUMENT ACTION: Final rule.

SUBJECT CATEGORY: Sulfentrazone; Pesticide Tolerances

DATES: This regulation is effective September 24, 2003. Objections and requests for hearings, identified by docket ID number OPP20030270, must be received on or before November 24, 2003.

DOCUMENT SUMMARY: This regulation establishes tolerances for combined residues of the herbicide sulfentrazone and its metabolites in or on asparagus; bean, lima, succulent; cabbage; corn, field, forage; corn, field, grain; corn, field, stover; horseradish, roots; pea and bean, dried shelled, except soybean, subgroup 6C; peanut; peanut, meal; peppermint, tops; potato; spearmint, tops; sugarcane, cane; sugarcane, molasses; and sunflower, seed. EPA is also deleting certain sulfentrazone tolerances that are no longer needed as result of this action. The Interregional Research Project Number 4 and FMC Corporation requested these tolerances under the Federal Food, Drug, and Cosmetic Act (FFDCA), as amended by the Food Quality Protection Act of 1996 (FQPA).

SUMMARY: Sulfentrazone,

SUPPLEMENTAL INFORMATION

A. Does this Action Apply to Me?

You may be affected by this action if you are an agricultural producer, food manufacturer, or pesticide manufacturer. Potentially affected categories and entities may include, but are not limited to: [sbull] Crop production (NAICS 111)
[sbull] Animal production (NAICS 112)
[sbull] Food manufacturing (NAICS 311)
[sbull] Pesticide manufacturing (NAICS 32532)

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This listing is not intended to be exhaustive, but rather provides a guide for readers regarding entities likely to be affected by this action. Other types of entities not listed in this unit could also be affected. The North American Industrial Classification System (NAICS) codes have been provided to assist you and others in determining whether this action might apply to certain entities. If you have any questions regarding the applicability of this action to a particular entity, consult the person listed under FOR FURTHER INFORMATION CONTACT.
B. How Can I Get Copies of this Document and Other Related Information?

1. Docket. EPA has established an official public docket for this action under docket identification (ID) number OPP20030270. The official public docket consists of the documents specifically referenced in this action, any public comments received, and other information related to this action. Although a part of the official docket, the public docket does not include Confidential Business Information (CBI) or other information whose disclosure is restricted by statute. The official public docket is the collection of materials that is available for public viewing at the Public Information and Records Integrity Branch (PIRIB), Rm. 119, Crystal Mall 2, 1921 Jefferson Davis Hwy., Arlington, VA. This docket facility is open from 8:30 a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The docket telephone number is (703) 3055805.

2. Electronic access. You may access this Federal Register document electronically through the EPA Internet under the ``Federal Register'' listings at http://www.epa.gov/fedrgstr/. A frequently updated electronic version of 40 CFR part 180 is available at http://www.access.gpo.gov/nara/cfr/cfrhtml_00/Title_40/40cfr180_00.html , a
beta site currently under development. To access the OPPTS Harmonized Guidelines referenced in this document, go directly to the guidelines at http://www.epa.gov/opptsfrs/home/guidelin.htm.

An electronic version of the public docket is available through EPA's electronic public docket and comment system, EPA Dockets. You may use EPA Dockets at http://www.epa.gov/edocket/ to submit or view public comments, access the index listing of the contents of the official public docket, and to access those documents in the public docket that are available electronically. Although not all docket materials may be available electronically, you may still access any of the publicly available docket materials through the docket facility identified in Unit I.B.1. Once in the system, select ``search,'' then key in the appropriate docket ID number.

II. Background and Statutory Findings

In the Federal Register of March 7, 2003 (68 FR 11096) (FRL7290 1), EPA issued a notice pursuant to section 408 of FFDCA, 21 U.S.C. 346a, as amended by FQPA (Public Law 104170), announcing the filing of pesticide petitions (PP 0E6149, 1E6311, 2E6405, 2E6498, and 2E6500) by the Interregional Research Project Number 4 (IR4), and 681 U.S. Highway 1 South, North Brunswick, NJ 08902, and PP 0F6116 and 2F6391 by FMC Corporation, Agricultural Products Group, 1735 Market Street, Philadelphia, PA 19103. That notice included a summary of the petitions prepared by FMC Corporation, the registrant. There were no comments received in response to the notice of filing.

The petitions requested that 40 CFR 180.498 be amended by establishing tolerances for combined residues of the herbicide sulfentrazone, [N(2,4dichloro5(4(difluoromethyl)4,5dihydro3 methyl5oxo1H1,2,4triazol1ylphenylmethansulfonoamide and its metabolites HMS (N(2,4dichloro5(4(difluoromethyl)4,5dihydro3 hydroxymethyl5oxo1H1,2,4triazol 1yl)phenyl)methanesulfonamide) and DMS (N(2,4dichloro5(4(difluoromethyl)4,5dihydro5oxo1H
1,2,4triazol1yl)phenyl)methanesulfonamide), in or on food
commodities as follows: Sunflower, seed at 0.2 parts per million (ppm) (PP 0E6149); horseradish, roots at 0.2 ppm (PP 1E6311); cabbage at 0.2 ppm (PP 1E6311); peppermint, tops and spearmint, tops at 0.3 ppm (1E6311); potato at 0.1 ppm (PP 2E6405); bean, lima, succulent at 0.15 ppm (PP 2E6498); asparagus at 0.15 ppm (2E6500); peanut nutmeat and its processed parts at 0.2 ppm and sugarcane and its processed parts at 0.1 ppm (PP 0F6116); corn, field forage at 0.25 ppm (PP 2F6391); corn, field stover at 0.35 ppm (PP 2F6391); pea and bean, dried shelled, except soybean, subgroup 6C at 0.15 ppm (PP 2F6391). Pesticide petitions 0F6116, 2F6391 and 2E6405 were subsequently amended to propose tolerances for peanut at 0.20 ppm; peanut, meal at 0.40 ppm; sugarcane, cane at 0.15 ppm; sugarcane, molasses at 0.20 ppm; corn, field, forage at 0.20 ppm; corn, field, grain at 0.15 ppm; corn, field, stover at 0.30 ppm and potato at 0.15 ppm. EPA is also deleting several timelimited tolerances established in connection with section 18 emergency exemption under 40 CFR 180.498(b) that are no longer needed, as a result of this action. The deletions to 40 CFR 180.498(b) are as follows:

1. Delete horseradish, roots at 0.1 ppm; replace with horseradish, roots at 0.20 ppm.

2. Delete pea, dry, seed at 0.10 ppm; replace with pea and bean, dried shelled, except soybean, subgroup 6C at 0.15 ppm.

3. Delete potato at 0.10 ppm; potato, granules/flakes at 0.20 ppm; and potato, wet peel at 0.15 ppm; replace with potato at 0.15 ppm.

4. Delete sugarcane at 0.05 ppm; replace with sugarcane, cane 0.15 ppm and sugarcane, molasses at 0.20 ppm.

5. Delete sunflower at 0.1 ppm; replace with sunflower, seed at 0.20 ppm.

Section 408(b)(2)(A)(i) of the FFDCA allows EPA to establish a tolerance (the legal limit for a pesticide chemical residue in or on a food) only if EPA determines that the tolerance is ``safe.'' Section 408(b)(2)(A)(ii) of the FFDCA defines ``safe'' to mean that ``there is a reasonable certainty that no harm will result from aggregate exposure to the pesticide chemical residue, including all anticipated dietary exposures and all other exposures for which there is reliable information.'' This includes exposure through drinking water and in residential settings, but does not include occupational exposure. Section 408(b)(2)(C) of the FFDCA requires EPA to give special consideration to exposure of infants and children to the pesticide chemical residue in establishing a tolerance and to ``ensure that there is a reasonable certainty that no harm will result to infants and children from aggregate exposure to the pesticide chemical residue. . . .''

EPA performs a number of analyses to determine the risks from aggregate exposure to pesticide residues. For further discussion of the regulatory requirements of section 408 of the FFDCA and a complete description of the risk assessment process, see the final rule on Bifenthrin Pesticide Tolerances (62 FR 62961, November 26, 1997) (FRL 57547).

III. Aggregate Risk Assessment and Determination of Safety

Consistent with section 408(b)(2)(D) of the FFDCA, EPA has reviewed the available scientific data and other relevant information in support of this action. EPA has sufficient data to assess the hazards of and to make a determination on aggregate exposure, consistent with section 408(b)(2) of the
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FFDCA, for tolerances for combined residues of sulfentrazone and its major metabolites on asparagus at 0.15 ppm; bean, lima, succulent at 0.15 ppm; cabbage at 0.20 ppm; corn, field, forage at 0.20 ppm; corn, field, grain at 0.15 ppm; corn, field, stover at 0.30 ppm; horseradish, roots at 0.20 ppm; pea and bean, dried shelled, except soybean, subgroup 6C at 0.15 ppm; peanut at 0.20 ppm; peanut, meal at 0.40 ppm; peppermint, tops at 0.30 ppm; potato at 0.15 ppm; spearmint, tops at 0.30 ppm; sugarcane, cane 0.15 ppm; sugarcane, molasses 0.20 ppm; and sunflower, seed at 0.20 ppm. EPA's assessment of exposures and risks associated with establishing the tolerances follows.

A. Toxicological Profile

EPA has evaluated the available toxicity data and considered its validity, completeness, and reliability as well as the relationship of the results of the studies to human risk. EPA has also considered available information concerning the variability of the sensitivities of major identifiable subgroups of consumers, including infants and children. The nature of the toxic effects caused by sulfentrazone are discussed in Table 1 of this unit as well as the no observed adverse effect level (NOAEL) and the lowest observed adverse effect level (LOAEL) from the toxicity studies reviewed.
Table 1.Subchronic, Chronic, and Other Toxicity Guideline No. Study Type Results 870.3100 90Day oral NOAEL = 19.9 toxicity rodents milligrams/ (rats) kilogram/day (mg/ kg/day) for males and 23.1 mg/kg/ day for females LOAEL = 65.8 mg/kg/ day for males and 78.1 mg/kg/day for females based on clinical signs of anemia (reduced hematocrit, hemoglobin, mean cell volume, and mean cell hemoglobin values during treatment) 870.3100 90Day oral NOAEL = 60 mg/kg/ toxicity rodents day for males and (mice) 79.8 mg/kg/day for females LOAEL = 108.4 mg/ kg/day for males and 143.6 mg/kg/ day for females based on decreased body weights, body weight gains, red blood cells, hemoglobin, hematocrit, and severity of splenic micropathology (increased incidence and severity of extramedullary hematopoiesis) 870.3150 90Day oral NOAEL = 28 mg/kg/ toxicity in day
nonrodents (dogs) LOAEL = 57 mg/kg/ day for males and 73 mg/kg/day for females based on decreased body weights (710%) and body weight gains during first 5 weeks of study; decreased hemoglobin, hematocrit, mean cell volume, mean cell hemoglobin and mean cell hemoglobin concentration, and increased absolute liver weights and alkaline phosphatase levels, and microscopic changes in the liver and spleen (pigmented sinusoidal microphages in the liver, swollen centrilobular hepatocytes and pigmented reticuloendotheli al cells in the spleen) 870.3200 21/28Day dermal Systemic and toxicity dermal NOAEL = 1,000 mg/kg/day, highest dose tested (HDT) 870.3700 Prenatal Maternal developmental in NOAEL = 25 mg/kg/ rodents (rats) day
LOAEL = 50 mg/kg/ day based on increased relative splenic extramedullary hematopoiesis Developmental NOAEL = 10 mg/kg/ day
LOAEL = 25 mg/kg/ day based on decreased mean fetal weights, and retardation in skeletal development evidenced by an increased number of litters with any variation and by decreased number of caudal vertebral and metacarpal ossification sites [[Page 55272]]
870.3700 Prenatal Maternal developmental in NOAEL = 250 mg/kg/ rodents (rats) day
LOAEL was not established. Developmental NOAEL = 100 mg/kg/ day
LOAEL = 250 mg/kg/ day based on decreased fetal body weight; increased incidence of fetal variations: hypoplastic or wavy ribs, incompletely ossified lumbar vertebral arches, and incompletely ossified ischia or pubis; and reduced number of thoracic vertebral and rib ossification sites 870.3700 Prenatal Maternal developmental in NOAEL = 100 mg/kg/ nonrodents day
(rabbits) LOAEL = 250 mg/kg/ day based on increased abortions, clinical signs (hematuria and decreased feces), and reduced body weight gain Developmental NOAEL = 100 mg/kg/ day
LOAEL = 250 mg/kg/ day based on increased resorptions, decreased live fetuses per litter, and decreased fetal weights 870.3800 2Generation Parental/Systemic reproduction and NOAEL = 14 mg/kg/ fertility effects day for males and (rats) 16 mg/kg/day for females LOAEL = 33 mg/kg/ day for males and 40 mg/kg/day for females based on decreased maternal body weight/body weight gain during gestation in both generation (P and F1) and reduced premating body weight gain in second generation (F1) males Reproductive NOAEL = 14 mg/kg/ day for males and 16 mg/kg/day for females LOAEL = 33 mg/kg/ day for males and 40 mg/kg/day for females based on increased duration of gestation in females and degeneration and/ or atrophy of the germinal epithelium of the testes and oligospermia and intratubular degenerated seminal material in the epididymis of F1 males Offspring NOAEL = 14 mg/kg/ day for males and 16 mg/kg/day for females LOAEL = 33 mg/kg/ day for males and 40 mg/kg/day for females based on reduced prenatal viability (fetal and litter), reduced litter size, increased number of stillborn pups, reduced pup and litter postnatal survival and decreased pup body weights throughout lactation 870.3800 Reproduction and Parental/Systemic fertility effects NOAEL = 20 mg/kg/ (rat) day
Nonguideline LOAEL = 51 mg/kg/ day (F1 females) based on decrease in premating body weight gain (10%) Offspring and Reproductive NOAEL = 16 mg/kg/ day
LOAEL = 40 mg/kg/ day based on reduced gestation day 20 fetal weights; decreased postnatal day 0, 4 and 7 pup weights; decreased pup survival; delayed vaginal patency; reduced epididymal, prostate, and testicular weights Additional information supports the conclusions reached in the 2 generation reproduction study in rats [[Page 55273]]
870.4100 Chronic toxicity NOAEL = 24.9 mg/kg/ dogs day for males and 29.6 mg/kg/day for females LOAEL = 61.2 mg/kg/ day for males and 61.9 mg/kg/day for females based on compensated normochromic microcytosis 870.4200 Carcinogenicity NOAEL = 93.9 mg/kg/ mice day for males and 116.9 mg/kg/day for females LOAEL = 160.5 mg/ kg/day for males and 198.0 mg/kg/ day for females based on dose related decreases in hemoglobin and hematocrit by study termination No evidence of carcinogenicity 870.4300 Combined chronic NOAEL = 40 mg/kg/ toxicity/ day for males and carcinogenicity 36.4 mg/kg/day in rats females LOAEL = 82.2 mg/kg/ day for males and 67 mg/kg/day for females based on doserelated decreased body weights (11 and 19%), body weight gains (13 and 26%), food consumption (13 and 19%), hemoglobin, hematocrit, mean cell volume, and mean cell hemoglobin. Increased nucleated red blood cells and reticulocytes in bone of females at 124.7 mg/kg/ day
No evidence of carcinogenicity 870.5100 Gene mutation No evidence of compoundinduced cytotoxicity was evident in Salmonella typhimurium strains TA1535, TA1538, TA1537, TA98 and TA100 either in presence or in absence of S9 activation. The positive controls induced the expected mutagenic responses in the appropriate tester strain. Sulfentrazone was considered not mutagenic under any test condition. 870.5300 In vitro mammalian In a forward gene cell gene mutation assay, mutation assay sulfentrazone at (mouse lymphoma) precipitating levels was equivocally positive in the absence of S9 activation. This response was not repeated at doses up to 1,800 [mu]g/ ml in the presence of S9 activation. 870.5395 Mammalian The test was erythrocyte negative in mice micronucleus test administered single intraperitoneal doses of 85 to 340 mg/kg. The 340 mg/kg dose was estimated to be approximately 80% of the LD50. No evidence of a cytotoxic effect on the target organ and no significant increase in the frequency of micronucleated polychromatic erythrocytes in bone marrow cells. 870.5450 Dominant lethal There were no assay rodent significant difference from negative controls in the proportion of early dead: total implants, and (total) dead: total implants. Based on the results, sulfentrazone is considered negative for inducing dominant lethal mutations in premeiotic, meiotic, and post meiotic germ cells of male rats under conditions of this assay up to the estimated MTD. 870.6200 Acute NOAEL = 250 mg/kg/ neurotoxicity day
screening battery LOAEL = 750 mg/kg/ day based on increased incidence of clinical signs, FOB findings, and decreased motor activity which was reversed by day 14 postdose. No evidence of neuropathology at any dose tested. [[Page 55274]]
870.6200 Subchronic NOAEL = 30 mg/kg/ neurotoxicity day for males and screening battery 37 mg/kg/day for females LOAEL = 150 mg/kg/ day for males and 180 mg/kg/day for females based on increased incidence of clinical signs; decreased body weight, body weight gains, and food consumption in females; and increased motor activity in females. At 5,000 ppm, included increased mortality; decreased body weights, and body weight gains in males; decreased hindlimb grip strength and increased tail flick latency in males at week 8; distended bladders with red fluid and enlarged spleen. No evidence of neuropathology at 2,500 and 5,000 ppm. 870.7485 Metabolism and Sulfentrazone pharmacokinetics (Phenyl 14C (rats) sulfentrazone) was readily absorbed and 84 to 104% of the administered dose was excreted in urine and feces within 72 hours. There were no major sex differences in the pattern of excretion. Almost all the radioactivity in the urine was 3 hydroxymethyl F6285 (84 104% of the administered dose). In the feces, HMS accounted for 1.26 to 2.55% of the administered dose. The proposed metabolic pathway appeared to be conversion of the parent compound mainly to 3 hydroxymethyl F6285 (excreted in the urine). A small amount of 3 hydroxymethyl F6285 was also converted to 3 carboxylic acid F6285 (excreted in the urine and feces). B. Toxicological Endpoints

The dose at which no adverse effects are observed (the NOAEL) from the toxicology study identified as appropriate for use in risk assessment is used to estimate the toxicological level of concern (LOC). However, the lowest dose at which adverse effects of concern are identified (the LOAEL) is sometimes used for risk assessment if no NOAEL was achieved in the toxicology study selected. An uncertainty factor (UF) is applied to reflect uncertainties inherent in the extrapolation from laboratory animal data to humans and in the variations in sensitivity among members of the human population as well as other unknowns. An UF of 100 is routinely used, 10X to account for interspecies differences and 10X for intraspecies differences.

For dietary risk assessment (other than cancer) the Agency uses the UF to calculate an acute or chronic reference dose (acute RfD or chronic RfD) where the RfD is equal to the NOAEL divided by the appropriate UF (RfD = NOAEL/UF). Where an additional safety factors (SF) is retained due to concerns unique to the FQPA, this additional factor is applied to the RfD by dividing the RfD by such additional factor. The acute or chronic Population Adjusted Dose (aPAD or cPAD) is a modification of the RfD to accommodate this type of FQPA SF.

For nondietary risk assessments (other than cancer) the UF is used to determine the LOC. For example, when 100 is the appropriate UF (10X to account for interspecies differences and 10X for intraspecies differences) the LOC is 100. To estimate risk, a ratio of the NOAEL to exposures (margin of exposure (MOE) = NOAEL/exposure) is calculated and compared to the LOC.

The linear default risk methodology (Q*) is the primary method currently used by the Agency to quantify carcinogenic risk. The Q* approach assumes that any amount of exposure will lead to some degree of cancer risk. A Q* is calculated and used to estimate risk which represents a probability of occurrence of additional cancer cases (e.g., risk is expressed as 1 x 10⁶ or one in a million). Under certain specific circumstances, MOE calculations will be used for the carcinogenic risk assessment. In this nonlinear approach, a ``point of departure'' is identified below which carcinogenic effects are not expected. The point of departure is typically a NOAEL based on an endpoint related to cancer effects though it may be a different value derived from the dose response curve. To estimate risk, a ratio of the point of departure to exposure (MOEcancer = point of departure/exposures) is calculated. A summary of the toxicological endpoints for sulfentrazone used for human risk assessment is shown in Table 2 of this unit:

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Table 2.Summary of Toxicological Dose and Endpoints for Sulfentrazone for Use in Human Risk Assessment FQPA SF^* and Level of Exposure Scenario Dose Used in Risk Concern for Risk Study and Toxicological Assessment, UF Assessment Effects Acute dietary (females 1350 years of NOAEL = 25 mg/kg/day FQPA SF = 1X Developmental toxicity age) UF = 100............... aPAD = acute RfD/FQPA study in rats Acute RfD = 0.25 mg/kg/ SF = 0.25 mg/kg/day. LOAEL = 50 mg/kg/day day. based on decreased live fetuses, and increased early resorptions Acute dietary (general population NOAEL = 250 mg/kg/day FQPA SF = 1X Acute neurotoxicity including infants and children) UF = 100............... aPAD = acute RfD/FQPA study in rats Acute RfD = 2.5 mg/kg/ SF = 2.5 mg/kg/day. LOAEL = 750 mg/kg/day day. based on increased incidence of clinical signs and FOB parameters and decreased motor activity. Chronic dietary (all populations) NOAEL= 14 mg/kg/day FQPA SF = 1X 2Generation UF = 100............... cPAD = chronic RfD/FQPA reproduction study Chronic RfD = 0.14 mg/ SF = 0.14 mg/kg/day. LOAEL = 33 mg/kg/day kg/day. based on decreased body weight and body weight gains Shortterm (1 to 30 days) and Offspring LOC for MOE = 100 2Generation intermediateterm (1 to 6 months) NOAEL = 14 mg/kg/day... (Residential) reproduction study incidental oral LOAEL = 33 mg/kg/day based on decreased pup body weights during lactation in both generations Shortterm dermal (1 to 30 days), Dermal study NOAEL= 100 LOC for MOE = 100 Dermal developmental intermediateterm dermal (1 to 6 mg/kg/day (Residential) study in rats months) and longterm dermal (>6 (dermal absorption rate LOAEL = 250 mg/kg/day months) = 10%). based on decreased fetal body weight; increased incidences of fetal variations: hypoplastic or wavy ribs, incompletely ossified lumbar vertebral arches, and incompletely ossified ischia or pubes; and reduced number of thoracic vertebral and rib ossification sites Shortterm inhalation (1 to 30 days), Oral study NOAEL = 14 LOC for MOE = 100 2Generation intermdiateterm inhalation (1 to 6 mg/kg/day (inhalation (Residential) reproduction study months) and longterm inhalation (> rate = 100% LOAEL = 33 mg/kg/day 6 months) based on decreased body weight and body weight gains Cancer (oral, dermal, inhalation) Not applicable Not applicable No evidence of carcinogenicity in rats and mice ^*The reference to the FQPA SF refers to any additional SF retained due to concerns unique to the FQPA. C. Exposure Assessment

1. Dietary exposure from food and feed uses. Tolerances have been established (40 CFR 180.498) for the combined residues of
sulfentrazone, in or on soybean, seed at 0.05 ppm. Timelimited tolerances (set to expire on December 31, 2004) are established in connection with section 18 emergency exemptions for bean, succulent seed without pod at 0.1; horseradish, roots at 0.1 ppm; chickpea, seed at 0.10 ppm; pea, dry, seed 0.10 ppm; potato at 0.10 ppm; potato, wet peel at 0.15; flax, seed at 0.20 ppm; potato, granules/flakes at 0.20 ppm; strawberry at 0.60 ppm. Timelimited tolerances (set to expire on December 31, 2005) are established in connection with section 18 emergency exemptions for sugarcane at 0.05 ppm and sunflower at 0.1 ppm. Tolerances are also established for indirect or inadvertent residues in or on cereal grain (excluding sweet corn). Risk assessments were conducted by EPA to assess dietary exposures from sulfentrazone in food as follows:

i. Acute exposure. Acute dietary risk assessments are performed for a fooduse pesticide if a toxicological study has indicated the possibility of an effect of concern occurring as a result of a 1day or single exposure. In conducting the acute dietary risk assessment EPA used the Dietary Exposure Evaluation Model software with the Food Commodity Intake Database (DEEM^TM) which incorporates food consumption data as reported by respondents in the United States Department of Agriculture (USDA) 19941996 and 1998 nationwide Continuing Surveys of Food Intake by Individuals (CSFII) and accumulated exposure to the chemical for each commodity. Separate Tier I, acute dietary exposure assessments were performed for females 13 to 49 years old and for the general U.S. population (including infants and children) using tolerancelevel residues and 100 percent crop treated (PCT).

ii. Chronic exposure. In conducting this chronic dietary risk assessment EPA used the DEEM^TM software with the Food Commodity Intake Database which incorporates food consumption data as reported by respondents in the USDA 19941996 and 1998 nationwide CSFII and accumulated exposure to the chemical for each commodity. An unrefined, Tier I chronic dietary exposure assessment was performed using tolerancelevel residues and 100 PCT.

2. Dietary exposure from drinking water. Sulfentrazone and the degradate 3carboxylic acid sulfentrazone are the residues of concern for the drinkingwater risk assessment. Environmental
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fate data suggest that sulfentrazone and 3carboxylic acid
sulfentrazone are persistent and mobile. Based on the structure similarity, 3carboxylic acid sulfentrazone could potentially have similar toxicity as the parent.

The Agency lacks sufficient monitoring exposure data to complete a comprehensive dietary exposure analysis and risk assessment for sulfentrazone in drinking water. Because the Agency does not have comprehensive monitoring data, drinking water concentration estimates are made by reliance on simulation or modeling taking into account data on the physical characteristics of sulfentrazone.

The Agency uses the FQPA Index Reservoir Screening Tool (FIRST) or the Pesticide Root Zone Model/Exposure Analysis Modeling System (PRZM/ EXAMS), to produce estimates of pesticide concentrations in an index reservoir. The Screening Concentrations in Ground Water (SCIGROW) model is used to predict pesticide concentrations in shallow ground water. For a screeninglevel assessment for surface water EPA will use FIRST (a Tier 1 model) before using PRZM/EXAMS (a Tier 2 model). The FIRST model is a subset of the PRZM/EXAMS model that uses a specific highend runoff scenario for pesticides. FIRST and PRZM/EXAMS incorporate an index reservoir environment, and both models include a percent crop area factor as an adjustment to account for the maximum percent crop coverage within a watershed or drainage basin.

None of these models include consideration of the impact processing (mixing, dilution, or treatment) of raw water for distribution as drinking water would likely have on the removal of pesticides from the source water. The primary use of these models by the Agency at this stage is to provide a coarse screen for sorting out pesticides for which it is unlikely that drinking water concentrations would exceed human health levels of concern.

Since the models used are considered to be screening tools in the risk assessment process, the Agency does not use estimated environmental concentrations (EECs) from these models to quantify drinking water exposure and risk as a %RfD or %PAD. Instead drinking water levels of comparison (DWLOCs) are calculated and used as a point of comparison against the model estimates of a pesticide's concentration in water. DWLOCs are theoretical upper limits on a pesticide's concentration in drinking water in light of total aggregate exposure to a pesticide in food, and from residential uses. Since DWLOCs address total aggregate exposure to sulfentrazone, they are further discussed in the aggregate risk sections in Unit E.

Based on the FIRST and SCIGROW models the EECs of sulfentrazone plus its major metabolite 3carboxylic acid for acute exposures are estimated to be 35.8 parts per billion (ppb) for surface water and 26.0 ppb for ground water. The EECs for chronic exposures are estimated to be 7.8 ppb for surface water and 26.0 ppb for ground water.

3. From nondietary exposure. The term ``residential exposure'' is used in this document to refer to nonoccupational, nondietary exposure (e.g., for lawn and garden pest control, indoor pest control, termiticides, and flea and tick control on pets). Sulfentrazone is proposed for use on use on turf by professional lawn care operators as a broadcast spray at a maximum application rate of 0.03 lbs active ingredient. Based on the proposed use pattern, potential residential/ nonoccupational postapplication exposures include the following: Shortterm oral turfgrass exposure (toddler handtomouth, objectto mouth); shortterm dermal turfgrass exposure (adult and toddler) and shortterm dermal golfer exposure (adult and adolescent). Incidental ingestion of soil is assumed to be negligible. Exposure over intermediateterm (16 months) or longterm (chronic, more than 6 months) exposure is not expected. Homeowner handler exposure is not expected since sulfentrazone will be applied by professional lawn care operators.

4. Cumulative effects from substances with a common mechanism of toxicity. Section 408(b)(2)(D)(v) of the FFDCA 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 common mechanism of toxicity.''

EPA does not have, at this time, available data to determine whether sulfentrazone has a common mechanism of toxicity with other substances. Unlike other pesticides for which EPA has followed a cumulative risk approach based on a common mechanism of toxicity, EPA has not made a common mechanism of toxicity finding as to sulfentrazone and any other substances and sulfentrazone does not appear to produce a toxic metabolite produced by other substances. For the purposes of this tolerance action, therefore, EPA has not assumed that sulfentrazone has a common mechanism of toxicity with other substances. For information regarding EPA's efforts to determine which chemicals have a common mechanism of toxicity and to evaluate the cumulative effects of such chemicals, see the policy statements released by EPA's Office of Pesticide Programs concerning common mechanism determinations and procedures for cumulating effects from substances found to have a common mechanism on EPA's website at http://www.epa.gov/pesticides/cumulative/ .

D. Safety Factor for Infants and Children

1. In general. Section 408 of the FFDCA provides that EPA shall apply an additional tenfold margin of safety for infants and children in the case of threshold effects to account for prenatal and postnatal toxicity and the completeness of the data base on toxicity and exposure unless EPA determines that a different margin of safety will be safe for infants and children. Margins of safety are incorporated into EPA risk assessments either directly through use of a MOE analysis or through using uncertainty (safety) factors in calculating a dose level that poses no appreciable risk to humans.

2. Prenatal and postnatal sensitivity. There is evidence of increased quantitative susceptibility following in utero exposure in the developmentaltoxicity studies in rats via the oral and dermal routes, and there is evidence for increased qualitative susceptibility following prenatal and/or postnatal exposure in the 2generation reproduction study in rats. A Degree of Concern Analysis was performed by EPA and it was concluded that concerns are low for the quantitative susceptibility of rat fetuses observed following oral and dermal exposures, the qualitative susceptibility of rabbit fetuses seen via the oral route, and the qualitative susceptibility seen in the 1 and 2generation reproduction studies. The conclusion was based on the following:
[sbull] The doseresponse was well characterized.
[sbull] There were clear NOAELs and LOAELs for developmental, offspring, maternal, and parental toxicities.
[sbull] The developmental effects in rabbits and the offspring effects in the rats were seen in the presence of maternal and parental toxicities, respectively.
[sbull] The parental reproductive and offspring effects were reproducible between the two reproductive studies.

3. Conclusion. There is a complete toxicity data base for sulfentrazone and
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exposure data are complete or are estimated based on data that reasonably accounts for potential exposures. EPA determined that the 10X safety factor to protect infants and children should be reduced to 1X for the following reasons:

1. There are no residual uncertainties for prenatal and/or postnatal toxicities via the oral route since the doses selected for overall risk assessments would address the concerns for the developmental and offspring toxicities seen in the above mentioned studies.

2. There are no residual uncertainties for prenatal and/or postnatal toxicities via the dermal route since the dose/endpoint/ study/species of concern was used for dermalrisk assessment.

3. The toxicology data base is complet

FOR FURTHER INFORMATION CONTACT Hoyt Jamerson, Registration Division (7505C), Office of Pesticide Programs, Environmental Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 204600001; telephone number: (703)3089368; email address: jamerson.hoyt@epa.gov.