Dinotefuran; Pesticide Tolerances, 49475-49479 [2019-18015]

Download as PDF Federal Register / Vol. 84, No. 183 / Friday, September 20, 2019 / Rules and Regulations * * * * * [FR Doc. 2019–19986 Filed 9–19–19; 8:45 am] BILLING CODE 6560–50–P ENVIRONMENTAL PROTECTION AGENCY 40 CFR Part 180 [EPA–HQ–OPP–2018–0424; FRL–9994–82] Dinotefuran; Pesticide Tolerances Environmental Protection Agency (EPA). ACTION: Final rule. AGENCY: This regulation establishes tolerances for residues of dinotefuran in or on persimmon. Mitsui Chemicals Agro, Inc., c/o Landis International, Inc. requested these tolerances under the Federal Food, Drug, and Cosmetic Act (FFDCA). DATES: This regulation is effective September 20, 2019. Objections and requests for hearings must be received on or before November 19, 2019 and must be filed in accordance with the instructions provided in 40 CFR part 178 (see also Unit I.C. of the SUPPLEMENTARY INFORMATION). ADDRESSES: The docket for this action, identified by docket identification (ID) number EPA–HQ–OPP–2018–0424, is available at https://www.regulations.gov or at the Office of Pesticide Programs Regulatory Public Docket (OPP Docket) in the Environmental Protection Agency Docket Center (EPA/DC), West William Jefferson Clinton Bldg., Rm. 3334, 1301 Constitution Ave. NW, Washington, DC 20460–0001. The Public Reading Room is open from 8:30 a.m. to 4:30 p.m., Monday through Friday, excluding legal holidays. The telephone number for the Public Reading Room is (202) 566–1744, and the telephone number for the OPP Docket is (703) 305–5805. Please review the visitor instructions and additional information about the docket available at https://www.epa.gov/dockets. FOR FURTHER INFORMATION CONTACT: Michael Goodis, Registration Division (7505P), Office of Pesticide Programs, Environmental Protection Agency, 1200 Pennsylvania Ave. NW, Washington, DC 20460–0001; main telephone number: (703) 305–7090; email address: RDFRNotices@epa.gov. SUPPLEMENTARY INFORMATION: khammond on DSKJM1Z7X2PROD with RULES SUMMARY: I. General Information A. Does this action apply to me? You may be potentially affected by this action if you are an agricultural producer, food manufacturer, or pesticide manufacturer. The following VerDate Sep<11>2014 15:59 Sep 19, 2019 Jkt 247001 list of North American Industrial Classification System (NAICS) codes is not intended to be exhaustive, but rather provides a guide to help readers determine whether this document applies to them. Potentially affected entities may include: • Crop production (NAICS code 111). • Animal production (NAICS code 112). • Food manufacturing (NAICS code 311). • Pesticide manufacturing (NAICS code 32532). B. How can I get electronic access to other related information? You may access a frequently updated electronic version of EPA’s tolerance regulations at 40 CFR part 180 through the Government Printing Office’s e-CFR site at https://www.ecfr.gov/cgi-bin/textidx?&c=ecfr&tpl=/ecfrbrowse/Title40/ 40tab_02.tpl. C. How can I file an objection or hearing request? Under FFDCA section 408(g), 21 U.S.C. 346a, any person may file an objection to any aspect of this regulation and may also request a hearing on those objections. You must file your objection or request a hearing on this regulation in accordance with the instructions provided in 40 CFR part 178. To ensure proper receipt by EPA, you must identify docket ID number EPA–HQ– OPP–2018–0424 in the subject line on the first page of your submission. All objections and requests for a hearing must be in writing and must be received by the Hearing Clerk on or before November 19, 2019. Addresses for mail and hand delivery of objections and hearing requests are provided in 40 CFR 178.25(b). In addition to filing an objection or hearing request with the Hearing Clerk as described in 40 CFR part 178, please submit a copy of the filing (excluding any Confidential Business Information (CBI)) for inclusion in the public docket. Information not marked confidential pursuant to 40 CFR part 2 may be disclosed publicly by EPA without prior notice. Submit the non-CBI copy of your objection or hearing request, identified by docket ID number EPA–HQ–OPP– 2018–0424, by one of the following methods: • Federal eRulemaking Portal: https:// www.regulations.gov. Follow the online instructions for submitting comments. Do not submit electronically any information you consider to be CBI or other information whose disclosure is restricted by statute. • Mail: OPP Docket, Environmental Protection Agency Docket Center (EPA/ PO 00000 Frm 00041 Fmt 4700 Sfmt 4700 49475 DC), (28221T), 1200 Pennsylvania Ave. NW, Washington, DC 20460–0001. • Hand Delivery: To make special arrangements for hand delivery or delivery of boxed information, please follow the instructions at https:// www.epa.gov/dockets/contacts.html. Additional instructions on commenting or visiting the docket, along with more information about dockets generally, is available at https:// www.epa.gov/dockets. II. Summary of Petitioned-For Tolerance In the Federal Register of August 14, 2018 (83 FR 40272) (FRL–9981–10), EPA issued a document pursuant to FFDCA section 408(d)(3), 21 U.S.C. 346a(d)(3), announcing the filing of a pesticide petition (PP 8E8687) by Mitsui Chemicals Agro, Inc., c/o Landis International, Inc., P.O. Box 5126, Valdosta, GA 31603–5126. The petition requested that 40 CFR part 180.603 be amended by establishing tolerances for residues of the insecticide dinotefuran (N-methyl-N′-nitro-N″;-[(tetrahydro-3furanyl)methyl)] guanidine) and metabolites DN (1-methyl-3-(tetrahydro3-furylmethyl)guanidine) and UF (1methyl-3-(tetrahydro-3-furylmethyl)urea), in or on persimmon at 2 parts per million (ppm). That document referenced a summary of the petition prepared by Mitsui Chemicals Agro, Inc., c/o Landis International, Inc., the registrant, which is available in the docket, https://www.regulations.gov. Two comments were received on the notice of filing; however, neither comment is relevant to this action. III. Aggregate Risk Assessment and Determination of Safety Section 408(b)(2)(A)(i) of 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 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 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 E:\FR\FM\20SER1.SGM 20SER1 49476 Federal Register / Vol. 84, No. 183 / Friday, September 20, 2019 / Rules and Regulations khammond on DSKJM1Z7X2PROD with RULES aggregate exposure to the pesticide chemical residue . . . .’’ Consistent with FFDCA section 408(b)(2)(D), and the factors specified in FFDCA section 408(b)(2)(D), 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 for dinotefuran including exposure resulting from the tolerances established by this action. EPA’s assessment of exposures and risks associated with dinotefuran 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. Dinotefuran is a neonicotinoid pesticide and acts as an agonist on insect nicotinic acetylcholine receptors. Typically, low to moderate levels of neonicotinoids, such as dinotefuran, activate the nicotinic acetylcholine receptors causing stimulation of the peripheral nervous system (PNS). High levels of neonicotinoids (agonists) can overstimulate the PNS, maintaining cation channels in the open state which blocks the action potential and leads to paralysis. The main target organ of toxicity for dinotefuran is the nervous system, but effects on the nervous system were only observed at high doses. Nervous system toxicity was manifested as clinical signs and decreased motor activity seen after acute dosing (in both rats and rabbits); changes in motor activity are consistent with effects on the nicotinic cholinergic nervous system seen after repeated dosing. The other significant effects were decreases in body weight and/or body weight gain, but even these effects occurred at or near the limit dose. Changes in spleen and thymus weights were seen in mice, rats, and dogs following subchronic and chronic dietary exposures. However, these weight changes were not corroborated with alterations in hematology parameters, histopathological lesions in these organs, or toxicity to the hematopoietic system. Furthermore, in the immunotoxicity studies in rats and mice, no effects on T-cell dependent antibody response (TDAR) were seen when tested up to the limit dose. There were also no changes in spleen and thymus weight, and there were no VerDate Sep<11>2014 15:59 Sep 19, 2019 Jkt 247001 histopathological lesions in these organs. In addition, the developmental immunotoxicity study showed no effects on functionality of the immune system in rats following exposure to dinotefuran at the limit dose during the prenatal, postnatal, and post-weaning periods. Because of the lack of immunotoxicity seen in the immunotoxicity studies in mice, rats, and developing rats, the thymus weight changes seen in dogs and the spleen weight changes seen in mice and rats in the subchronic and chronic oral studies were not considered to be toxicologically relevant. No systemic or neurotoxic effects were seen following repeated dermal applications at the limit dose to rats in the 28-day dermal toxicity study. Also, no systemic or portal of entry effects were seen following repeated inhalation exposure at the maximum obtainable concentrations to rats in the 28-day inhalation study. In the developmental toxicity study in rats, no maternal or developmental toxicity was seen at the limit dose. In rabbits, maternal toxicity manifested as clinical signs of neurotoxicity, but no developmental toxicity was seen. In the reproduction study in rats, parental, offspring, and reproductive toxicity was seen at the limit dose. Parental toxicity included decreased body weight weights/gains, transient decrease in food consumption, and decreased thyroid weights. Offspring toxicity was characterized as decreased forelimb grip strength or hindlimb grip strength in the F1 pups. There was no adverse effect on reproductive performance at any dose. In the developmental neurotoxicity study, no maternal or offspring toxicity was seen at any dose including the limit dose. Dinotefuran is classified as ‘‘Not Likely to be Carcinogenic to Humans’’ based on lack of evidence of carcinogenicity in rats and mice in two adequate rodent carcinogenicity studies. There was no evidence of mutagenicity in both the in vivo and in vitro assays. Dinotefuran has low acute toxicity by oral, dermal, and inhalation exposure routes. It does not irritate the eye but causes a low level of skin irritation; it is not a dermal sensitizer. Specific information on the studies received and the nature of the adverse effects caused by dinotefuran as well as the no-observed-adverse-effect-level (NOAEL) and the lowest-observedadverse-effect-level (LOAEL) from the toxicity studies can be found at https:// www.regulations.gov in document Human Health Risk Assessment to Support New Use on Imported PO 00000 Frm 00042 Fmt 4700 Sfmt 4700 Persimmon on page 18 in docket ID number EPA–HQ–OPP–2018–0424. B. Toxicological Points of Departure/ Levels of Concern Once a pesticide’s toxicological profile is determined, EPA identifies toxicological points of departure (POD) and levels of concern to use in evaluating the risk posed by human exposure to the pesticide. For hazards that have a threshold below which there is no appreciable risk, the toxicological POD is used as the basis for derivation of reference values for risk assessment. PODs are developed based on a careful analysis of the doses in each toxicological study to determine the dose at which no adverse effects are observed (the NOAEL) and the lowest dose at which adverse effects of concern are identified (the LOAEL). Uncertainty/ safety factors are used in conjunction with the POD to calculate a safe exposure level—generally referred to as a population-adjusted dose (PAD) or a reference dose (RfD)—and a safe margin of exposure (MOE). For non-threshold risks, the Agency assumes that any amount of exposure will lead to some degree of risk. Thus, the Agency estimates risk in terms of the probability of an occurrence of the adverse effect expected in a lifetime. For more information on the general principles EPA uses in risk characterization and a complete description of the risk assessment process, see https:// www2.epa.gov/pesticide-science-andassessing-pesticide-risks/assessinghuman-health-risk-pesticides. A summary of the toxicological endpoints for dinotefuran used for human risk assessment is discussed in Unit III.B of the final rule published in the Federal Register of April 10, 2013 (78 FR 21267) (FRL–9381–5). C. Exposure Assessment 1. Dietary exposure from food and feed uses. In evaluating dietary exposure to dinotefuran, EPA considered exposure under the petitioned-for tolerances as well as all existing dinotefuran tolerances in 40 CFR 180.603. EPA assessed dietary exposures from dinotefuran in food as follows: i. Acute exposure. Quantitative acute dietary exposure and risk assessments are performed for a food-use pesticide, if a toxicological study has indicated the possibility of an effect of concern occurring as a result of a 1-day or single exposure. Such effects were identified for dinotefuran. In estimating acute dietary exposure, EPA used food consumption information from the United States E:\FR\FM\20SER1.SGM 20SER1 khammond on DSKJM1Z7X2PROD with RULES Federal Register / Vol. 84, No. 183 / Friday, September 20, 2019 / Rules and Regulations Department of Agriculture (USDA) 2003–2008 National Health and Nutrition Examination Survey, What We Eat in America, (NHANES/WWEIA). As to residue levels in food, EPA assumed 100 percent crop treated (PCT) and tolerance-level residues for all current crops. ii. Chronic exposure. In conducting the chronic dietary exposure assessment EPA used the food consumption data from the USDA 2003–2008 NHANES/ WWEIA. As to residue levels in food, EPA assumed 100 PCT and tolerancelevel residues for all current crops. iii. Cancer. Based on the data summarized in Unit III.A., EPA has concluded that dinotefuran does not pose a cancer risk to humans. Therefore, a dietary exposure assessment for the purpose of assessing cancer risk is unnecessary. iv. Anticipated residue and percent crop treated (PCT) information. EPA did not use anticipated residue and/or PCT information in the dietary assessment for dinotefuran. Tolerance level residues and/or 100 PCT were assumed for all food commodities. 2. Dietary exposure from drinking water. The Agency used screening level water exposure models in the dietary exposure analysis and risk assessment for dinotefuran in drinking water. These simulation models take into account data on the physical, chemical, and fate/ transport characteristics of dinotefuran. Further information regarding EPA drinking water models used in pesticide exposure assessment can be found at https://www.epa.gov/oppefed1/models/ water/index.htm. Based on the Pesticide Root Zone Model/Variable Volume Water Model (PRZM/VVWM), Pesticide Flooded Application Model (PFAM), and Pesticide Root Zone Model Ground Water (PRZM GW), the estimated drinking water concentrations (EDWCs) of dinotefuran for acute exposures are estimated to be 84 parts per billion (ppb) for surface water and 154 ppb for ground water, and for chronic exposures for non-cancer assessments are estimated to be 19.5 ppb for surface water and 132 ppb for ground water. Modeled estimates of drinking water concentrations were directly entered into the dietary exposure model. For acute dietary risk assessment, the water concentration value of 154 ppb was used to assess the contribution to drinking water. For chronic dietary risk assessment, the water concentration of value 132 ppb was used to assess the contribution to drinking water. 3. From non-dietary exposure. The term ‘‘residential exposure’’ is used in this document to refer to non- VerDate Sep<11>2014 15:59 Sep 19, 2019 Jkt 247001 occupational, non-dietary exposure (e.g., for lawn and garden pest control, indoor pest control, termiticides, and flea and tick control on pets). Dinotefuran is currently registered for the following uses that could result in residential exposures: Turf, ornamentals, vegetable gardens, roach and ant bait, pet spot-ons, indoor aerosol sprays, crack and crevice sprays, etc. EPA assessed residential exposure using the following assumptions: Because no dermal or inhalation endpoints were chosen for dinotefuran, residential handler and post-application residential dermal and inhalation exposure scenarios were not assessed. As a result, risk assessments were only completed for post-application scenarios in which incidental oral exposures are expected. Children (ages 1 to < 2 years old) may receive shortterm hand-to-mouth exposures from post-application exposure to fogger application in indoor rooms or areas. Children (ages 1 to < 2 years old) may receive intermediate- and chronic/longterm hand-to-mouth exposures from post-application exposure to spot-on application to dogs (small). The postapplication exposure and risk estimates for all existing residential uses resulted in risk estimates that are not of concern (MOEs ranged from 1,200 to 4,600). Further information regarding EPA standard assumptions and generic inputs for residential exposures may be found at https://www.epa.gov/pesticides/ trac/science/trac6a05.pdf. 4. Cumulative effects from substances with a common mechanism of toxicity. Section 408(b)(2)(D)(v) of 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 has not found dinotefuran to share a common mechanism of toxicity with any other substances, and dinotefuran does not appear to produce a toxic metabolite produced by other substances. For the purposes of this tolerance action, therefore, EPA has assumed that dinotefuran does not have 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 EPA’s website at https:// www.epa.gov/pesticides/cumulative. PO 00000 Frm 00043 Fmt 4700 Sfmt 4700 49477 D. Safety Factor for Infants and Children 1. In general. Section 408(b)(2)(C) of FFDCA provides that EPA shall apply an additional tenfold (10X) 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 database on toxicity and exposure unless EPA determines based on reliable data that a different margin of safety will be safe for infants and children. This additional margin of safety is commonly referred to as the FQPA Safety Factor (SF). In applying this provision, EPA either retains the default value of 10X, or uses a different additional safety factor when reliable data available to EPA support the choice of a different factor. 2. Prenatal and postnatal sensitivity. In the prenatal studies, no maternal or developmental toxicity was seen at the limit dose in rats. In rabbits, maternal toxicity manifested as clinical signs of neurotoxicity, but no developmental toxicity was seen. In the rat reproduction study, parental, offspring, and reproductive toxicity was seen at the limit dose. Parental toxicity included decreased body weight gain, transient decrease in food consumption, and decreased thyroid weights. Offspring toxicity was characterized as a decreased forelimb grip strength or hindlimb grip strength in the F1 pups. There was no adverse effect on reproductive performance at any dose. In the developmental neurotoxicity study, no maternal or offspring toxicity was seen at any dose including the limit dose. 3. Conclusion. EPA has determined that reliable data show the safety of infants and children would be adequately protected if the FQPA SF were reduced to 1X. That decision is based on the following findings: i. The toxicity database for dinotefuran is complete. ii. The neurotoxic potential of dinotefuran has been adequately considered. Dinotefuran is a neonicotinoid and has a neurotoxic mode of pesticidal action. Consistent with the mode of action, changes in motor activity were seen in repeat-dose studies, including the subchronic neurotoxicity study. Additionally, decreased grip strength and brain weight were observed in the offspring of a multi-generation reproduction study albeit at doses close to the limit dose. For these reasons, a developmental neurotoxicity (DNT) study was required. The DNT study did not show evidence of a unique sensitivity of the developing nervous system; no effects on E:\FR\FM\20SER1.SGM 20SER1 49478 Federal Register / Vol. 84, No. 183 / Friday, September 20, 2019 / Rules and Regulations khammond on DSKJM1Z7X2PROD with RULES neurobehavioral parameters were seen in the offspring at any dose, including the limit dose. iii. As discussed in Unit III.D.2., there is no evidence that dinotefuran results in increased susceptibility in in utero rats or rabbits in the prenatal developmental studies or in young rats in the 2-generation reproduction study. iv. There are no residual uncertainties identified in the exposure databases. The dietary food exposure assessments were performed based on 100 PCT and tolerance-level residues, corrected for additional residues which are of concern for the risk assessment only. EPA made conservative (protective) assumptions in the ground and surface water modeling used to assess exposure to dinotefuran in drinking water. EPA used similarly conservative assumptions to assess post-application exposure of children. These assessments will not underestimate the exposure and risks posed by dinotefuran. E. Aggregate Risks and Determination of Safety EPA determines whether acute and chronic dietary pesticide exposures are safe by comparing aggregate exposure estimates to the acute PAD (aPAD) and chronic PAD (cPAD). For linear cancer risks, EPA calculates the lifetime probability of acquiring cancer given the estimated aggregate exposure. Short-, intermediate-, and chronic-term risks are evaluated by comparing the estimated aggregate food, water, and residential exposure to the appropriate PODs to ensure that an adequate MOE exists. 1. Acute risk. Using the exposure assumptions discussed in this unit for acute exposure, the acute dietary exposure from food and water to dinotefuran will occupy 10% of the aPAD for children 1–2 years old, the population group receiving the greatest exposure. 2. Chronic risk. Using the exposure assumptions described in this unit for chronic exposure, EPA has concluded that chronic exposure to dinotefuran from food and water will utilize 4.8% of the cPAD for children 1–2 years old, the population group receiving the greatest exposure. Based on the explanation in Unit III.C.3., regarding residential use patterns, chronic residential exposure to residues of dinotefuran is expected. 3. Short-term risk. Short-term aggregate exposure takes into account short-term residential exposure plus chronic exposure to food and water (considered to be a background exposure level). Dinotefuran is currently registered for uses that could result in short-term VerDate Sep<11>2014 15:59 Sep 19, 2019 Jkt 247001 residential exposure, and the Agency has determined that it is appropriate to aggregate chronic exposure through food and water with short-term residential exposures to dinotefuran. Using the exposure assumptions described in this unit for short-term exposures, EPA has concluded the combined food, water, and short-term residential exposures result in aggregate MOEs of 740. Because EPA’s level of concern for dinotefuran is a MOE of 100 or below, these MOEs are not of concern. 4. Intermediate- and long-term risk. Intermediate- and long-term aggregate exposure takes into account intermediate- and long-term residential exposure plus chronic exposure to food and water (considered to be a background exposure level). Dinotefuran is currently registered for uses that could result in intermediateterm residential exposure, and the Agency has determined that it is appropriate to aggregate chronic exposure through food and water with intermediate- and long-term residential exposures to dinotefuran. Using the exposure assumptions described in this unit for intermediateand long-term exposures, EPA has concluded that the combined food, water, and intermediate- and long-term residential exposures result in an aggregate MOE of 1,400 for children 1 to < 2 years old from background dietary exposures and post-application hand-tomouth exposures from pet spot-on applications to small dogs. Although adults are expected to also have longterm post-application exposures to dinotefuran due to the pet spot-on treatments, quantitative dermal and inhalation assessments are not required since there was no dermal and inhalation hazard identified in the toxicity database and oral exposure is not anticipated for adults. Therefore, the intermediate- and chronic/long-term aggregate assessment for adults is equivalent to the chronic dietary exposure and risk assessment for the most highly exposed adult population subgroup, adults 20–49 years old, and is not of concern. Because EPA’s level of concern for dinotefuran is a MOE of 100 or below, these MOEs are not of concern. 5. Aggregate cancer risk for U.S. population. Based on the lack of evidence of carcinogenicity in two adequate rodent carcinogenicity studies, dinotefuran is not expected to pose a cancer risk to humans. 6. Determination of safety. Based on these risk assessments, EPA concludes that there is a reasonable certainty that no harm will result to the general PO 00000 Frm 00044 Fmt 4700 Sfmt 4700 population, or to infants and children from aggregate exposure to dinotefuran residues. IV. Other Considerations A. Analytical Enforcement Methodology Adequate enforcement methodology, a high-performance liquid chromatography/tandem mass spectrometry (HPLC/MS/MS) method for the determination of residues of dinotefuran, and the metabolites DN and UF; an HPLC/ultraviolet (UV) detection method for the determination of residues of dinotefuran; and HPLC/ MS and HPLC/MS/MS methods for the determination of DN and UF) is available to enforce the tolerance expression. The method may be requested from: Chief, Analytical Chemistry Branch, Environmental Science Center, 701 Mapes Rd., Ft. Meade, MD 20755–5350; telephone number: (410) 305–2905; email address: residuemethods@ epa.gov. B. International Residue Limits In making its tolerance decisions, EPA seeks to harmonize U.S. tolerances with international standards whenever possible, consistent with U.S. food safety standards and agricultural practices. EPA considers the international maximum residue limits (MRLs) established by the Codex Alimentarius Commission (Codex), as required by FFDCA section 408(b)(4). The Codex Alimentarius is a joint United Nations Food and Agriculture Organization/World Health Organization food standards program, and it is recognized as an international food safety standards-setting organization in trade agreements to which the United States is a party. EPA may establish a tolerance that is different from a Codex MRL; however, FFDCA section 408(b)(4) requires that EPA explain the reasons for departing from the Codex level. The Codex has not established an MRL for residues of dinotefuran on persimmons. V. Conclusion Therefore, tolerances are established for residues of dinotefuran, N-methylN ′-nitro-N ″-[(tetrahydro-3furanyl)methyl)] guanidine and metabolites DN (1-methyl-3-(tetrahydro3-furmethyl)guanidine) and UF (1methyl-3-(tetrahydro-3-furmethyl)-urea), in or on persimmon at 2 ppm. VI. Statutory and Executive Order Reviews This action establishes tolerances under FFDCA section 408(d) in E:\FR\FM\20SER1.SGM 20SER1 khammond on DSKJM1Z7X2PROD with RULES Federal Register / Vol. 84, No. 183 / Friday, September 20, 2019 / Rules and Regulations response to a petition submitted to the Agency. The Office of Management and Budget (OMB) has exempted these types of actions from review under Executive Order 12866, entitled ‘‘Regulatory Planning and Review’’ (58 FR 51735, October 4, 1993). Because this action has been exempted from review under Executive Order 12866, this action is not subject to Executive Order 13211, entitled ‘‘Actions Concerning Regulations That Significantly Affect Energy Supply, Distribution, or Use’’ (66 FR 28355, May 22, 2001); Executive Order 13045, entitled ‘‘Protection of Children from Environmental Health Risks and Safety Risks’’ (62 FR 19885, April 23, 1997); or Executive Order 13771, entitled ‘‘Reducing Regulations and Controlling Regulatory Costs’’ (82 FR 9339, February 3, 2017). This action does not contain any information collections subject to OMB approval under the Paperwork Reduction Act (PRA) (44 U.S.C. 3501 et seq.), nor does it require any special considerations under Executive Order 12898, entitled ‘‘Federal Actions to Address Environmental Justice in Minority Populations and Low-Income Populations’’ (59 FR 7629, February 16, 1994). Since tolerances and exemptions that are established on the basis of a petition under FFDCA section 408(d), such as the tolerance in this final rule, do not require the issuance of a proposed rule, the requirements of the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et seq.), do not apply. This action directly regulates growers, food processors, food handlers, and food retailers, not States or tribes, nor does this action alter the relationships or distribution of power and responsibilities established by Congress in the preemption provisions of FFDCA section 408(n)(4). As such, the Agency has determined that this action will not have a substantial direct effect on States or tribal governments, on the relationship between the national government and the States or tribal governments, or on the distribution of power and responsibilities among the various levels of government or between the Federal Government and Indian tribes. Thus, the Agency has determined that Executive Order 13132, entitled ‘‘Federalism’’ (64 FR 43255, August 10, 1999) and Executive Order 13175, entitled ‘‘Consultation and Coordination with Indian Tribal Governments’’ (65 FR 67249, November 9, 2000) do not apply to this action. In addition, this action does not impose any enforceable duty or contain any unfunded mandate as described under Title II of the Unfunded VerDate Sep<11>2014 15:59 Sep 19, 2019 Jkt 247001 Mandates Reform Act (UMRA) (2 U.S.C. 1501 et seq.). This action does not involve any technical standards that would require Agency consideration of voluntary consensus standards pursuant to section 12(d) of the National Technology Transfer and Advancement Act (NTTAA) (15 U.S.C. 272 note). VII. Congressional Review Act Pursuant to the Congressional Review Act (5 U.S.C. 801 et seq.), EPA will submit a report containing this rule and other required information to the U.S. Senate, the U.S. House of Representatives, and the Comptroller General of the United States prior to publication of the rule in the Federal Register. This action is not a ‘‘major rule’’ as defined by 5 U.S.C. 804(2). 49479 ENVIRONMENTAL PROTECTION AGENCY 40 CFR Part 300 [EPA–HQ–SFUND–1999–0010; FRL–9999– 76–Region 8] National Oil and Hazardous Substances Pollution Contingency Plan; National Priorities List: Partial Deletion of the Vasquez Boulevard and I–70 Superfund Site Environmental Protection Agency (EPA). ACTION: Final rule. AGENCY: The Environmental Protection Agency (EPA) Region 8 announces the deletion of the operable unit 1 (OU1) of the Vasquez Boulevard and I–70 Superfund Site (Site) located in the City and County of Denver, CO, from the National Priorities List (NPL). The NPL, List of Subjects in 40 CFR Part 180 promulgated pursuant to section 105 of the Comprehensive Environmental Environmental protection, Response, Compensation, and Liability Administrative practice and procedure, Act (CERCLA) of 1980, as amended, is Agricultural commodities, Pesticides an appendix of the National Oil and and pests, Reporting and recordkeeping Hazardous Substances Pollution requirements. Contingency Plan (NCP). This partial deletion pertains only to OU1, the Dated: August 8, 2019. residential portion of the Site. The Michael Goodis, operable unit 2 (OU2) and operable unit Director, Registration Division, Office of 3 (OU3) will remain on the NPL and are Pesticide Programs. not being considered for deletion as part Therefore, 40 CFR chapter I is of this action. The EPA and the State of amended as follows: Colorado, through the Colorado Department of Public Health and PART 180—[AMENDED] Environment (CDPHE), have determined that all appropriate response actions ■ 1. The authority citation for part 180 under CERCLA, other than operation continues to read as follows: and maintenance, monitoring and fiveyear reviews, have been completed. Authority: 21 U.S.C. 321(q), 346a and 371. However, the deletion of these parcels does not preclude future actions under ■ 2. In § 180.603, add alphabetically the Superfund. entry ‘‘Persimmon’’ to the table in DATES: This action is effective paragraph (a)(1) to read as follows: September 20, 2019. § 180.603 Dinotefuran; tolerances for ADDRESSES: EPA has established a residues. docket for this action under Docket Identification No. EPA–HQ–SFUND– (a) * * * 1999–0010. All documents in the docket Parts per are listed on the https:// Commodity million www.regulations.gov website. Although listed in the index, some information is not publicly available, I.e., Confidential * * * * * Business Information or other Persimmon 1 .......................... 2 information whose disclosure is restricted by statute. Certain other * * * * * material, such as copyrighted material, 1 There are no U.S. registrations for use of is not placed on the internet and will be dinotefuran on this commodity. publicly available only in hard copy form. Publicly available docket * * * * * materials are available electronically [FR Doc. 2019–18015 Filed 9–19–19; 8:45 am] through https://www.regulations.gov or BILLING CODE 6560–50–P in hard copy at the site information repositories. Locations, contacts, phone numbers and viewing hours are: U.S. PO 00000 Frm 00045 Fmt 4700 Sfmt 4700 SUMMARY: E:\FR\FM\20SER1.SGM 20SER1

Agencies

[Federal Register Volume 84, Number 183 (Friday, September 20, 2019)]
[Rules and Regulations]
[Pages 49475-49479]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 2019-18015]


-----------------------------------------------------------------------

ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[EPA-HQ-OPP-2018-0424; FRL-9994-82]


Dinotefuran; Pesticide Tolerances

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

-----------------------------------------------------------------------

SUMMARY: This regulation establishes tolerances for residues of 
dinotefuran in or on persimmon. Mitsui Chemicals Agro, Inc., c/o Landis 
International, Inc. requested these tolerances under the Federal Food, 
Drug, and Cosmetic Act (FFDCA).

DATES: This regulation is effective September 20, 2019. Objections and 
requests for hearings must be received on or before November 19, 2019 
and must be filed in accordance with the instructions provided in 40 
CFR part 178 (see also Unit I.C. of the SUPPLEMENTARY INFORMATION).

ADDRESSES: The docket for this action, identified by docket 
identification (ID) number EPA-HQ-OPP-2018-0424, is available at https://www.regulations.gov or at the Office of Pesticide Programs Regulatory 
Public Docket (OPP Docket) in the Environmental Protection Agency 
Docket Center (EPA/DC), West William Jefferson Clinton Bldg., Rm. 3334, 
1301 Constitution Ave. NW, Washington, DC 20460-0001. The Public 
Reading Room is open from 8:30 a.m. to 4:30 p.m., Monday through 
Friday, excluding legal holidays. The telephone number for the Public 
Reading Room is (202) 566-1744, and the telephone number for the OPP 
Docket is (703) 305-5805. Please review the visitor instructions and 
additional information about the docket available at https://www.epa.gov/dockets.

FOR FURTHER INFORMATION CONTACT: Michael Goodis, Registration Division 
(7505P), Office of Pesticide Programs, Environmental Protection Agency, 
1200 Pennsylvania Ave. NW, Washington, DC 20460-0001; main telephone 
number: (703) 305-7090; email address: [email protected].

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this action apply to me?

    You may be potentially affected by this action if you are an 
agricultural producer, food manufacturer, or pesticide manufacturer. 
The following list of North American Industrial Classification System 
(NAICS) codes is not intended to be exhaustive, but rather provides a 
guide to help readers determine whether this document applies to them. 
Potentially affected entities may include:
     Crop production (NAICS code 111).
     Animal production (NAICS code 112).
     Food manufacturing (NAICS code 311).
     Pesticide manufacturing (NAICS code 32532).

B. How can I get electronic access to other related information?

    You may access a frequently updated electronic version of EPA's 
tolerance regulations at 40 CFR part 180 through the Government 
Printing Office's e-CFR site at https://www.ecfr.gov/cgi-bin/text-idx?&c=ecfr&tpl=/ecfrbrowse/Title40/40tab_02.tpl.

C. How can I file an objection or hearing request?

    Under FFDCA section 408(g), 21 U.S.C. 346a, any person may file an 
objection to any aspect of this regulation and may also request a 
hearing on those objections. You must file your objection or request a 
hearing on this regulation in accordance with the instructions provided 
in 40 CFR part 178. To ensure proper receipt by EPA, you must identify 
docket ID number EPA-HQ-OPP-2018-0424 in the subject line on the first 
page of your submission. All objections and requests for a hearing must 
be in writing and must be received by the Hearing Clerk on or before 
November 19, 2019. Addresses for mail and hand delivery of objections 
and hearing requests are provided in 40 CFR 178.25(b).
    In addition to filing an objection or hearing request with the 
Hearing Clerk as described in 40 CFR part 178, please submit a copy of 
the filing (excluding any Confidential Business Information (CBI)) for 
inclusion in the public docket. Information not marked confidential 
pursuant to 40 CFR part 2 may be disclosed publicly by EPA without 
prior notice. Submit the non-CBI copy of your objection or hearing 
request, identified by docket ID number EPA-HQ-OPP-2018-0424, by one of 
the following methods:
     Federal eRulemaking Portal: https://www.regulations.gov. 
Follow the online instructions for submitting comments. Do not submit 
electronically any information you consider to be CBI or other 
information whose disclosure is restricted by statute.
     Mail: OPP Docket, Environmental Protection Agency Docket 
Center (EPA/DC), (28221T), 1200 Pennsylvania Ave. NW, Washington, DC 
20460-0001.
     Hand Delivery: To make special arrangements for hand 
delivery or delivery of boxed information, please follow the 
instructions at https://www.epa.gov/dockets/contacts.html.
    Additional instructions on commenting or visiting the docket, along 
with more information about dockets generally, is available at https://www.epa.gov/dockets.

II. Summary of Petitioned-For Tolerance

    In the Federal Register of August 14, 2018 (83 FR 40272) (FRL-9981-
10), EPA issued a document pursuant to FFDCA section 408(d)(3), 21 
U.S.C. 346a(d)(3), announcing the filing of a pesticide petition (PP 
8E8687) by Mitsui Chemicals Agro, Inc., c/o Landis International, Inc., 
P.O. Box 5126, Valdosta, GA 31603-5126. The petition requested that 40 
CFR part 180.603 be amended by establishing tolerances for residues of 
the insecticide dinotefuran (N-methyl-N'-nitro-N'';-[(tetrahydro-3-
furanyl)methyl)] guanidine) and metabolites DN (1-methyl-3-(tetrahydro-
3-furylmethyl)guanidine) and UF (1-methyl-3-(tetrahydro-3-furylmethyl)-
urea), in or on persimmon at 2 parts per million (ppm). That document 
referenced a summary of the petition prepared by Mitsui Chemicals Agro, 
Inc., c/o Landis International, Inc., the registrant, which is 
available in the docket, https://www.regulations.gov. Two comments were 
received on the notice of filing; however, neither comment is relevant 
to this action.

III. Aggregate Risk Assessment and Determination of Safety

    Section 408(b)(2)(A)(i) of 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 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 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

[[Page 49476]]

aggregate exposure to the pesticide chemical residue . . . .''
    Consistent with FFDCA section 408(b)(2)(D), and the factors 
specified in FFDCA section 408(b)(2)(D), 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 for dinotefuran including exposure 
resulting from the tolerances established by this action. EPA's 
assessment of exposures and risks associated with dinotefuran 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.
    Dinotefuran is a neonicotinoid pesticide and acts as an agonist on 
insect nicotinic acetylcholine receptors. Typically, low to moderate 
levels of neonicotinoids, such as dinotefuran, activate the nicotinic 
acetylcholine receptors causing stimulation of the peripheral nervous 
system (PNS). High levels of neonicotinoids (agonists) can 
overstimulate the PNS, maintaining cation channels in the open state 
which blocks the action potential and leads to paralysis.
    The main target organ of toxicity for dinotefuran is the nervous 
system, but effects on the nervous system were only observed at high 
doses. Nervous system toxicity was manifested as clinical signs and 
decreased motor activity seen after acute dosing (in both rats and 
rabbits); changes in motor activity are consistent with effects on the 
nicotinic cholinergic nervous system seen after repeated dosing. The 
other significant effects were decreases in body weight and/or body 
weight gain, but even these effects occurred at or near the limit dose. 
Changes in spleen and thymus weights were seen in mice, rats, and dogs 
following subchronic and chronic dietary exposures. However, these 
weight changes were not corroborated with alterations in hematology 
parameters, histopathological lesions in these organs, or toxicity to 
the hematopoietic system. Furthermore, in the immunotoxicity studies in 
rats and mice, no effects on T-cell dependent antibody response (TDAR) 
were seen when tested up to the limit dose. There were also no changes 
in spleen and thymus weight, and there were no histopathological 
lesions in these organs. In addition, the developmental immunotoxicity 
study showed no effects on functionality of the immune system in rats 
following exposure to dinotefuran at the limit dose during the 
prenatal, postnatal, and post-weaning periods. Because of the lack of 
immunotoxicity seen in the immunotoxicity studies in mice, rats, and 
developing rats, the thymus weight changes seen in dogs and the spleen 
weight changes seen in mice and rats in the subchronic and chronic oral 
studies were not considered to be toxicologically relevant.
    No systemic or neurotoxic effects were seen following repeated 
dermal applications at the limit dose to rats in the 28-day dermal 
toxicity study. Also, no systemic or portal of entry effects were seen 
following repeated inhalation exposure at the maximum obtainable 
concentrations to rats in the 28-day inhalation study. In the 
developmental toxicity study in rats, no maternal or developmental 
toxicity was seen at the limit dose. In rabbits, maternal toxicity 
manifested as clinical signs of neurotoxicity, but no developmental 
toxicity was seen. In the reproduction study in rats, parental, 
offspring, and reproductive toxicity was seen at the limit dose. 
Parental toxicity included decreased body weight weights/gains, 
transient decrease in food consumption, and decreased thyroid weights. 
Offspring toxicity was characterized as decreased forelimb grip 
strength or hindlimb grip strength in the F1 pups. There was no adverse 
effect on reproductive performance at any dose. In the developmental 
neurotoxicity study, no maternal or offspring toxicity was seen at any 
dose including the limit dose.
    Dinotefuran is classified as ``Not Likely to be Carcinogenic to 
Humans'' based on lack of evidence of carcinogenicity in rats and mice 
in two adequate rodent carcinogenicity studies. There was no evidence 
of mutagenicity in both the in vivo and in vitro assays.
    Dinotefuran has low acute toxicity by oral, dermal, and inhalation 
exposure routes. It does not irritate the eye but causes a low level of 
skin irritation; it is not a dermal sensitizer.
    Specific information on the studies received and the nature of the 
adverse effects caused by dinotefuran as well as the no-observed-
adverse-effect-level (NOAEL) and the lowest-observed-adverse-effect-
level (LOAEL) from the toxicity studies can be found at https://www.regulations.gov in document Human Health Risk Assessment to Support 
New Use on Imported Persimmon on page 18 in docket ID number EPA-HQ-
OPP-2018-0424.

B. Toxicological Points of Departure/Levels of Concern

    Once a pesticide's toxicological profile is determined, EPA 
identifies toxicological points of departure (POD) and levels of 
concern to use in evaluating the risk posed by human exposure to the 
pesticide. For hazards that have a threshold below which there is no 
appreciable risk, the toxicological POD is used as the basis for 
derivation of reference values for risk assessment. PODs are developed 
based on a careful analysis of the doses in each toxicological study to 
determine the dose at which no adverse effects are observed (the NOAEL) 
and the lowest dose at which adverse effects of concern are identified 
(the LOAEL). Uncertainty/safety factors are used in conjunction with 
the POD to calculate a safe exposure level--generally referred to as a 
population-adjusted dose (PAD) or a reference dose (RfD)--and a safe 
margin of exposure (MOE). For non-threshold risks, the Agency assumes 
that any amount of exposure will lead to some degree of risk. Thus, the 
Agency estimates risk in terms of the probability of an occurrence of 
the adverse effect expected in a lifetime. For more information on the 
general principles EPA uses in risk characterization and a complete 
description of the risk assessment process, see https://www2.epa.gov/pesticide-science-and-assessing-pesticide-risks/assessing-human-health-risk-pesticides.
    A summary of the toxicological endpoints for dinotefuran used for 
human risk assessment is discussed in Unit III.B of the final rule 
published in the Federal Register of April 10, 2013 (78 FR 21267) (FRL-
9381-5).

C. Exposure Assessment

    1. Dietary exposure from food and feed uses. In evaluating dietary 
exposure to dinotefuran, EPA considered exposure under the petitioned-
for tolerances as well as all existing dinotefuran tolerances in 40 CFR 
180.603. EPA assessed dietary exposures from dinotefuran in food as 
follows:
    i. Acute exposure. Quantitative acute dietary exposure and risk 
assessments are performed for a food-use pesticide, if a toxicological 
study has indicated the possibility of an effect of concern occurring 
as a result of a 1-day or single exposure.
    Such effects were identified for dinotefuran. In estimating acute 
dietary exposure, EPA used food consumption information from the United 
States

[[Page 49477]]

Department of Agriculture (USDA) 2003-2008 National Health and 
Nutrition Examination Survey, What We Eat in America, (NHANES/WWEIA). 
As to residue levels in food, EPA assumed 100 percent crop treated 
(PCT) and tolerance-level residues for all current crops.
    ii. Chronic exposure. In conducting the chronic dietary exposure 
assessment EPA used the food consumption data from the USDA 2003-2008 
NHANES/WWEIA. As to residue levels in food, EPA assumed 100 PCT and 
tolerance-level residues for all current crops.
    iii. Cancer. Based on the data summarized in Unit III.A., EPA has 
concluded that dinotefuran does not pose a cancer risk to humans. 
Therefore, a dietary exposure assessment for the purpose of assessing 
cancer risk is unnecessary.
    iv. Anticipated residue and percent crop treated (PCT) information. 
EPA did not use anticipated residue and/or PCT information in the 
dietary assessment for dinotefuran. Tolerance level residues and/or 100 
PCT were assumed for all food commodities.
    2. Dietary exposure from drinking water. The Agency used screening 
level water exposure models in the dietary exposure analysis and risk 
assessment for dinotefuran in drinking water. These simulation models 
take into account data on the physical, chemical, and fate/transport 
characteristics of dinotefuran. Further information regarding EPA 
drinking water models used in pesticide exposure assessment can be 
found at https://www.epa.gov/oppefed1/models/water/index.htm.
    Based on the Pesticide Root Zone Model/Variable Volume Water Model 
(PRZM/VVWM), Pesticide Flooded Application Model (PFAM), and Pesticide 
Root Zone Model Ground Water (PRZM GW), the estimated drinking water 
concentrations (EDWCs) of dinotefuran for acute exposures are estimated 
to be 84 parts per billion (ppb) for surface water and 154 ppb for 
ground water, and for chronic exposures for non-cancer assessments are 
estimated to be 19.5 ppb for surface water and 132 ppb for ground 
water.
    Modeled estimates of drinking water concentrations were directly 
entered into the dietary exposure model. For acute dietary risk 
assessment, the water concentration value of 154 ppb was used to assess 
the contribution to drinking water. For chronic dietary risk 
assessment, the water concentration of value 132 ppb was used to assess 
the contribution to drinking water.
    3. From non-dietary exposure. The term ``residential exposure'' is 
used in this document to refer to non-occupational, non-dietary 
exposure (e.g., for lawn and garden pest control, indoor pest control, 
termiticides, and flea and tick control on pets). Dinotefuran is 
currently registered for the following uses that could result in 
residential exposures: Turf, ornamentals, vegetable gardens, roach and 
ant bait, pet spot-ons, indoor aerosol sprays, crack and crevice 
sprays, etc. EPA assessed residential exposure using the following 
assumptions: Because no dermal or inhalation endpoints were chosen for 
dinotefuran, residential handler and post-application residential 
dermal and inhalation exposure scenarios were not assessed. As a 
result, risk assessments were only completed for post-application 
scenarios in which incidental oral exposures are expected. Children 
(ages 1 to < 2 years old) may receive short-term hand-to-mouth 
exposures from post-application exposure to fogger application in 
indoor rooms or areas. Children (ages 1 to < 2 years old) may receive 
intermediate- and chronic/long-term hand-to-mouth exposures from post-
application exposure to spot-on application to dogs (small). The post-
application exposure and risk estimates for all existing residential 
uses resulted in risk estimates that are not of concern (MOEs ranged 
from 1,200 to 4,600). Further information regarding EPA standard 
assumptions and generic inputs for residential exposures may be found 
at https://www.epa.gov/pesticides/trac/science/trac6a05.pdf.
    4. Cumulative effects from substances with a common mechanism of 
toxicity. Section 408(b)(2)(D)(v) of 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 has not found dinotefuran to share a common mechanism of 
toxicity with any other substances, and dinotefuran does not appear to 
produce a toxic metabolite produced by other substances. For the 
purposes of this tolerance action, therefore, EPA has assumed that 
dinotefuran does not have 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 EPA's website at https://www.epa.gov/pesticides/cumulative.

D. Safety Factor for Infants and Children

    1. In general. Section 408(b)(2)(C) of FFDCA provides that EPA 
shall apply an additional tenfold (10X) 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 database on toxicity 
and exposure unless EPA determines based on reliable data that a 
different margin of safety will be safe for infants and children. This 
additional margin of safety is commonly referred to as the FQPA Safety 
Factor (SF). In applying this provision, EPA either retains the default 
value of 10X, or uses a different additional safety factor when 
reliable data available to EPA support the choice of a different 
factor.
    2. Prenatal and postnatal sensitivity. In the prenatal studies, no 
maternal or developmental toxicity was seen at the limit dose in rats. 
In rabbits, maternal toxicity manifested as clinical signs of 
neurotoxicity, but no developmental toxicity was seen. In the rat 
reproduction study, parental, offspring, and reproductive toxicity was 
seen at the limit dose. Parental toxicity included decreased body 
weight gain, transient decrease in food consumption, and decreased 
thyroid weights. Offspring toxicity was characterized as a decreased 
forelimb grip strength or hindlimb grip strength in the F1 
pups. There was no adverse effect on reproductive performance at any 
dose. In the developmental neurotoxicity study, no maternal or 
offspring toxicity was seen at any dose including the limit dose.
    3. Conclusion. EPA has determined that reliable data show the 
safety of infants and children would be adequately protected if the 
FQPA SF were reduced to 1X. That decision is based on the following 
findings:
    i. The toxicity database for dinotefuran is complete.
    ii. The neurotoxic potential of dinotefuran has been adequately 
considered. Dinotefuran is a neonicotinoid and has a neurotoxic mode of 
pesticidal action. Consistent with the mode of action, changes in motor 
activity were seen in repeat-dose studies, including the subchronic 
neurotoxicity study. Additionally, decreased grip strength and brain 
weight were observed in the offspring of a multi-generation 
reproduction study albeit at doses close to the limit dose. For these 
reasons, a developmental neurotoxicity (DNT) study was required. The 
DNT study did not show evidence of a unique sensitivity of the 
developing nervous system; no effects on

[[Page 49478]]

neurobehavioral parameters were seen in the offspring at any dose, 
including the limit dose.
    iii. As discussed in Unit III.D.2., there is no evidence that 
dinotefuran results in increased susceptibility in in utero rats or 
rabbits in the prenatal developmental studies or in young rats in the 
2-generation reproduction study.
    iv. There are no residual uncertainties identified in the exposure 
databases. The dietary food exposure assessments were performed based 
on 100 PCT and tolerance-level residues, corrected for additional 
residues which are of concern for the risk assessment only. EPA made 
conservative (protective) assumptions in the ground and surface water 
modeling used to assess exposure to dinotefuran in drinking water. EPA 
used similarly conservative assumptions to assess post-application 
exposure of children. These assessments will not underestimate the 
exposure and risks posed by dinotefuran.

E. Aggregate Risks and Determination of Safety

    EPA determines whether acute and chronic dietary pesticide 
exposures are safe by comparing aggregate exposure estimates to the 
acute PAD (aPAD) and chronic PAD (cPAD). For linear cancer risks, EPA 
calculates the lifetime probability of acquiring cancer given the 
estimated aggregate exposure. Short-, intermediate-, and chronic-term 
risks are evaluated by comparing the estimated aggregate food, water, 
and residential exposure to the appropriate PODs to ensure that an 
adequate MOE exists.
    1. Acute risk. Using the exposure assumptions discussed in this 
unit for acute exposure, the acute dietary exposure from food and water 
to dinotefuran will occupy 10% of the aPAD for children 1-2 years old, 
the population group receiving the greatest exposure.
    2. Chronic risk. Using the exposure assumptions described in this 
unit for chronic exposure, EPA has concluded that chronic exposure to 
dinotefuran from food and water will utilize 4.8% of the cPAD for 
children 1-2 years old, the population group receiving the greatest 
exposure. Based on the explanation in Unit III.C.3., regarding 
residential use patterns, chronic residential exposure to residues of 
dinotefuran is expected.
    3. Short-term risk. Short-term aggregate exposure takes into 
account short-term residential exposure plus chronic exposure to food 
and water (considered to be a background exposure level).
    Dinotefuran is currently registered for uses that could result in 
short-term residential exposure, and the Agency has determined that it 
is appropriate to aggregate chronic exposure through food and water 
with short-term residential exposures to dinotefuran.
    Using the exposure assumptions described in this unit for short-
term exposures, EPA has concluded the combined food, water, and short-
term residential exposures result in aggregate MOEs of 740. Because 
EPA's level of concern for dinotefuran is a MOE of 100 or below, these 
MOEs are not of concern.
    4. Intermediate- and long-term risk. Intermediate- and long-term 
aggregate exposure takes into account intermediate- and long-term 
residential exposure plus chronic exposure to food and water 
(considered to be a background exposure level).
    Dinotefuran is currently registered for uses that could result in 
intermediate-term residential exposure, and the Agency has determined 
that it is appropriate to aggregate chronic exposure through food and 
water with intermediate- and long-term residential exposures to 
dinotefuran.
    Using the exposure assumptions described in this unit for 
intermediate- and long-term exposures, EPA has concluded that the 
combined food, water, and intermediate- and long-term residential 
exposures result in an aggregate MOE of 1,400 for children 1 to < 2 
years old from background dietary exposures and post-application hand-
to-mouth exposures from pet spot-on applications to small dogs. 
Although adults are expected to also have long-term post-application 
exposures to dinotefuran due to the pet spot-on treatments, 
quantitative dermal and inhalation assessments are not required since 
there was no dermal and inhalation hazard identified in the toxicity 
database and oral exposure is not anticipated for adults. Therefore, 
the intermediate- and chronic/long-term aggregate assessment for adults 
is equivalent to the chronic dietary exposure and risk assessment for 
the most highly exposed adult population subgroup, adults 20-49 years 
old, and is not of concern. Because EPA's level of concern for 
dinotefuran is a MOE of 100 or below, these MOEs are not of concern.
    5. Aggregate cancer risk for U.S. population. Based on the lack of 
evidence of carcinogenicity in two adequate rodent carcinogenicity 
studies, dinotefuran is not expected to pose a cancer risk to humans.
    6. Determination of safety. Based on these risk assessments, EPA 
concludes that there is a reasonable certainty that no harm will result 
to the general population, or to infants and children from aggregate 
exposure to dinotefuran residues.

IV. Other Considerations

A. Analytical Enforcement Methodology

    Adequate enforcement methodology, a high-performance liquid 
chromatography/tandem mass spectrometry (HPLC/MS/MS) method for the 
determination of residues of dinotefuran, and the metabolites DN and 
UF; an HPLC/ultraviolet (UV) detection method for the determination of 
residues of dinotefuran; and HPLC/MS and HPLC/MS/MS methods for the 
determination of DN and UF) is available to enforce the tolerance 
expression.
    The method may be requested from: Chief, Analytical Chemistry 
Branch, Environmental Science Center, 701 Mapes Rd., Ft. Meade, MD 
20755-5350; telephone number: (410) 305-2905; email address: 
[email protected].

B. International Residue Limits

    In making its tolerance decisions, EPA seeks to harmonize U.S. 
tolerances with international standards whenever possible, consistent 
with U.S. food safety standards and agricultural practices. EPA 
considers the international maximum residue limits (MRLs) established 
by the Codex Alimentarius Commission (Codex), as required by FFDCA 
section 408(b)(4). The Codex Alimentarius is a joint United Nations 
Food and Agriculture Organization/World Health Organization food 
standards program, and it is recognized as an international food safety 
standards-setting organization in trade agreements to which the United 
States is a party. EPA may establish a tolerance that is different from 
a Codex MRL; however, FFDCA section 408(b)(4) requires that EPA explain 
the reasons for departing from the Codex level.
    The Codex has not established an MRL for residues of dinotefuran on 
persimmons.

V. Conclusion

    Therefore, tolerances are established for residues of dinotefuran, 
N-methyl-N '-nitro-N ''-[(tetrahydro-3-furanyl)methyl)] guanidine and 
metabolites DN (1-methyl-3-(tetrahydro-3-furmethyl)guanidine) and UF 
(1-methyl-3-(tetrahydro-3-furmethyl)-urea), in or on persimmon at 2 
ppm.

VI. Statutory and Executive Order Reviews

    This action establishes tolerances under FFDCA section 408(d) in

[[Page 49479]]

response to a petition submitted to the Agency. The Office of 
Management and Budget (OMB) has exempted these types of actions from 
review under Executive Order 12866, entitled ``Regulatory Planning and 
Review'' (58 FR 51735, October 4, 1993). Because this action has been 
exempted from review under Executive Order 12866, this action is not 
subject to Executive Order 13211, entitled ``Actions Concerning 
Regulations That Significantly Affect Energy Supply, Distribution, or 
Use'' (66 FR 28355, May 22, 2001); Executive Order 13045, entitled 
``Protection of Children from Environmental Health Risks and Safety 
Risks'' (62 FR 19885, April 23, 1997); or Executive Order 13771, 
entitled ``Reducing Regulations and Controlling Regulatory Costs'' (82 
FR 9339, February 3, 2017). This action does not contain any 
information collections subject to OMB approval under the Paperwork 
Reduction Act (PRA) (44 U.S.C. 3501 et seq.), nor does it require any 
special considerations under Executive Order 12898, entitled ``Federal 
Actions to Address Environmental Justice in Minority Populations and 
Low-Income Populations'' (59 FR 7629, February 16, 1994).
    Since tolerances and exemptions that are established on the basis 
of a petition under FFDCA section 408(d), such as the tolerance in this 
final rule, do not require the issuance of a proposed rule, the 
requirements of the Regulatory Flexibility Act (RFA) (5 U.S.C. 601 et 
seq.), do not apply.
    This action directly regulates growers, food processors, food 
handlers, and food retailers, not States or tribes, nor does this 
action alter the relationships or distribution of power and 
responsibilities established by Congress in the preemption provisions 
of FFDCA section 408(n)(4). As such, the Agency has determined that 
this action will not have a substantial direct effect on States or 
tribal governments, on the relationship between the national government 
and the States or tribal governments, or on the distribution of power 
and responsibilities among the various levels of government or between 
the Federal Government and Indian tribes. Thus, the Agency has 
determined that Executive Order 13132, entitled ``Federalism'' (64 FR 
43255, August 10, 1999) and Executive Order 13175, entitled 
``Consultation and Coordination with Indian Tribal Governments'' (65 FR 
67249, November 9, 2000) do not apply to this action. In addition, this 
action does not impose any enforceable duty or contain any unfunded 
mandate as described under Title II of the Unfunded Mandates Reform Act 
(UMRA) (2 U.S.C. 1501 et seq.).
    This action does not involve any technical standards that would 
require Agency consideration of voluntary consensus standards pursuant 
to section 12(d) of the National Technology Transfer and Advancement 
Act (NTTAA) (15 U.S.C. 272 note).

VII. Congressional Review Act

    Pursuant to the Congressional Review Act (5 U.S.C. 801 et seq.), 
EPA will submit a report containing this rule and other required 
information to the U.S. Senate, the U.S. House of Representatives, and 
the Comptroller General of the United States prior to publication of 
the rule in the Federal Register. This action is not a ``major rule'' 
as defined by 5 U.S.C. 804(2).

List of Subjects in 40 CFR Part 180

    Environmental protection, Administrative practice and procedure, 
Agricultural commodities, Pesticides and pests, Reporting and 
recordkeeping requirements.

    Dated: August 8, 2019.
Michael Goodis,
Director, Registration Division, Office of Pesticide Programs.
    Therefore, 40 CFR chapter I is amended as follows:

PART 180--[AMENDED]

0
 1. The authority citation for part 180 continues to read as follows:

     Authority: 21 U.S.C. 321(q), 346a and 371.


0
2. In Sec.  180.603, add alphabetically the entry ``Persimmon'' to the 
table in paragraph (a)(1) to read as follows:


Sec.  180.603  Dinotefuran; tolerances for residues.

    (a) * * *

------------------------------------------------------------------------
                                                             Parts per
                        Commodity                             million
------------------------------------------------------------------------
 
                                * * * * *
Persimmon \1\...........................................               2
 
                                * * * * *
------------------------------------------------------------------------
\1\ There are no U.S. registrations for use of dinotefuran on this
  commodity.

* * * * *
[FR Doc. 2019-18015 Filed 9-19-19; 8:45 am]
BILLING CODE 6560-50-P
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.