Source: https://www.federalregister.gov/documents/2017/02/15/2017-03075/thiamethoxam-pesticide-tolerance
Timestamp: 2018-02-20 22:27:41
Document Index: 92154496

Matched Legal Cases: ['art 178', 'art 178', 'art 178', 'art 2', 'art 180', '§\u2009180']

A Rule by the Environmental Protection Agency on 02/15/2017
This regulation is effective February 15, 2017. Objections and requests for hearings must be received on or before April 17, 2017, and must be filed in accordance with the instructions provided in 40 CFR part 178 (see also Unit I.C. of the SUPPLEMENTARY INFORMATION).
82 FR 10712
10712-10718 (7 pages)
FRL-9957-00
https://www.federalregister.gov/d/2017-03075 https://www.federalregister.gov/d/2017-03075
The docket for this action, identified by docket identification (ID) number EPA-HQ-OPP-2015-0705, is available at http://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 http://www.epa.gov/​dockets.
Start Further Info Start Printed Page 10713
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-2015-0705 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 April 17, 2017. 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-2015-0705, by one of the following methods:
In the Federal Register of November 23, 2015 (80 FR 72941) (FRL-9936-73), 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 5E8401) by Syngenta Crop Protection, LLC, P.O. Box 18300, Greensboro, NC 27409-8300. The petition requested that 40 CFR part 180 be amended by establishing a tolerance for residues of the insecticide, thiamethoxam, in or on banana at 0.04 parts per million (ppm). That document referenced a summary of the petition prepared by Syngenta, the registrant, which is available in the docket, http://www.regulations.gov. Comments were received on the notice of filing. EPA's response to these comments is discussed in Unit IV.C.
Tolerances for residues of thiamethoxam are listed in 40 CFR 180.565 and are expressed in terms of the combined residues of the insecticide thiamethoxam and its metabolite CGA-322704. Metabolite CGA-322704 is also the registered active ingredient clothianidin (tolerance listings in 40 CFR 180.586). Clothianidin (hereinafter referred to as CGA-322704) has a complete toxicological database and appears to have effects in mammals that are different from those of thiamethoxam. A separate risk assessment that addresses risks from CGA-322704 residues resulting from the direct application of CGA-322704 (clothianidin), as well as risks from residues of CGA-322704 coming from thiamethoxam uses has been conducted, and there are no risk estimates of concern as a result of the proposed tolerance for thiamethoxam residues in imported bananas. This risk assessment can be found at http:www.regulations.gov in docket ID number EPA-HQ-OPP-2015-0705.
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 thiamethoxam including exposure resulting from the tolerances established by this action. EPA's assessment of exposures and risks associated with thiamethoxam follows.
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.Start Printed Page 10714
In mammals, toxicological effects are seen primarily in the liver, kidney, testes, and blood cellular system. In addition, developmental neurological effects were observed in rats. These developmental effects are being used to assess risks associated with acute exposures to thiamethoxam, and the liver and testicular effects are the basis for assessing longer-term exposures.
There is no indication of quantitative or qualitative susceptibility in the developmental toxicity studies. There is evidence of quantitative susceptibility in the developmental neurotoxicity study and both two-generation reproductive studies. However, clear no observed adverse effects levels (NOAELs) were identified for the susceptibility in the 2-generation reproduction and developmental neurotoxicity (DNT) studies and the endpoints and doses chosen for risk assessment are protective of the susceptibility observed in these studies.
Thiamethoxam is classified as “not likely to be carcinogenic to humans” at levels below which certain amounts of metabolites are produced. The liver tumors that were observed in the mouse have been demonstrated to be a result of a non-genotoxic mode of action dependent on sufficient amounts of a hepatotoxic metabolite being produced. Although humans are qualitatively capable of producing the active metabolite, thiamethoxam is unlikely to pose a cancer risk to humans unless sufficient amounts of metabolites are persistently formed to drive a carcinogenic response. The chronic endpoint selected for regulating exposure to thiamethoxam is sufficiently protective of the key events (perturbation of liver metabolism, hepatotoxicity/regenerative proliferation) in the animal mode of action. At those levels, the Agency does not expect sufficient generation of the necessary metabolites to elicit a carcinogenic response; therefore, separate quantification of carcinogenic potential is not required.
Specific information on the studies received and the nature of the adverse effects caused by thiamethoxam as well as the NOAEL and the lowest-observed-adverse-effect-level (LOAEL) from the toxicity studies can be found at http:www.regulations.gov in the document titled “Thiamethoxam. Human Health Risk Assessment for Tolerances on Imported Bananas” on page 33 in docket ID number EPA-HQ-OPP-2015-0705.
A summary of the toxicological endpoints for thiamethoxam used for human risk assessment is shown in Table 1 of this unit.
Table 1—Summary of Toxicological Doses and Endpoints for Thiamethoxam for Use in Human Health Risk Assessment
Acute dietary (All populations including infants and children) NOAEL = 34.5 mg/kg/day UFA = 10x UFH = 10x FQPA SF = 1x Acute RfD = 0.35 mg/kg/day aPAD = 0.35 mg/kg/day Rat Developmental Neurotoxicity study. LOAEL = 298.7 mg/kg/day based on decreased body weight and reduced brain morphometric measurements.
Chronic dietary (All populations) NOAEL= 1.2 mg/kg/day UFA = 10x UFH = 10x FQPA SF = 1x Chronic RfD = 0.012 mg/kg/day cPAD = 0.012 mg/kg/day 2-Generation reproduction study. LOAEL = 1.8 mg/kg/day based on increased incidence and severity of tubular atrophy in testes of F1 generation males. 2-Generation reproduction study, LOAEL = 156 mg/kg/day (males), not determined (females) based on sperm abnormalities and germ cell loss in F1 males.
Incidental oral short-term infants/children <6 years old (1 to 30 days) NOAEL= 31.6 mg/kg/day UFA = 10x UFH = 10x FQPA SF = 1x LOC for MOE = 100 28-day Dog study. LOAEL = 47.7/43.0 (M/F) mg/kg/day based on body weight loss; leukopenia and increased hematocrit, hemoglobin and erythrocyte count; increased plasma urea and creatinine; reduced thymus weight in males and females, increased thyroid weight in males and reduced brain weight in females; and, histopathological changes in liver, thymus and spleen.
Dermal short-term adults (1 to 30 days) Oral study NOAEL = 1.2 mg/kg/day (dermal absorption rate = 5% UFA = 10x UFH = 10x FQPA SF = 1x LOC for MOE = 100 2-Generation reproduction study; 1998. LOAEL = 1.8 mg/kg/day based on increased incidence and severity of tubular atrophy in testes of F1 generation males. 2-Generation reproduction study; 2004. LOAEL = 156 mg/kg/day (males), not determined (females) based on sperm abnormalities and germ cell loss in F1 males.
Dermal short-term infants/children <6 years old (1 to 30 days) Dermal study NOAEL= 60 mg/kg/day UFA = 10x UFH = 10x FQPA SF = 1x LOC for MOE = 100 Rat 28-Day Dermal Toxicity Study. LOAEL = 250 (females) mg/kg/day based on increased plasma glucose, triglyceride levels, and alkaline phosphatase activity and inflammatory cell infiltration in the liver and necrosis of single hepatocytes in females.
Inhalation short-term adults (1 to 30 days) Oral study NOAEL= 1.2 mg/kg/day UFA = 10x UFH = 10x FQPA SF = 1x LOC for MOE = 100 2-Generation reproduction study. LOAEL = 1.8 mg/kg/day based on increased incidence and severity of tubular atrophy in testes of F1 generation males. 2-Generation reproduction study. LOAEL = 156 mg/kg/day (males), not determined (females) based on sperm abnormalities and germ cell loss in F1 males.
Inhalation short-term infants/children <6 years old (1 to 30 days) Inhalation (or oral study NOAEL = 31.6 mg/kg/day (inhalation toxicity = oral toxicity) UFA = 10x UFH = 10x FQPA SF = 1x LOC for MOE = 100 28-day Dog study. LOAEL = 47.7/43.0 (M/F) mg/kg/day based on body weight loss; leukopenia and increased hematocrit, hemoglobin and erythrocyte count; increased plasma urea and creatinine; reduced thymus weight in males and females, increased thyroid weight in males and reduced brain weight in females; and, histopathological changes in liver, thymus and spleen.
Cancer (Oral, dermal, inhalation) “Not Likely to be Carcinogenic to Humans” based on convincing evidence that a non-genotoxic mode of action for liver tumors was established in the mouse. Quantification of cancer risk is not required.
Such effects were identified for thiamethoxam. In estimating acute dietary exposure, EPA used food consumption information from the United States Department of Agriculture's (USDA) National Health and Nutrition Examination Survey, What We Eat in America (NHANES/WWEIA). As to residue levels in food, EPA assumed tolerance level residues and 100 percent crop treated (PCT).
ii. Chronic exposure. In conducting the chronic dietary exposure assessment EPA used the food consumption data from USDA's NHANES/WWEIA. As to residue levels in food, the chronic analysis is based on tolerance levels and anticipated residues calculated from field trial data for selected commodities and 100 PCT.
iii. Cancer. Based on the data summarized in Unit III.A., EPA has concluded that thiamethoxam does not pose a cancer risk to humans. Therefore, a dietary exposure assessment for the purpose of assessing cancer risk is unnecessary.
2. Dietary exposure from drinking water. The Agency used screening level water exposure models in the dietary exposure analysis and risk assessment for thiamethoxam in drinking water. These simulation models take into account data on the physical, chemical, and fate/transport characteristics of thiamethoxam. Further information regarding EPA drinking water models used in pesticide exposure assessment can be found at http://www2.epa.gov/​pesticide-science-and-assessing-pesticide-risks/​about-water-exposure-models-used-pesticide. Start Printed Page 10716
Based on the Tier 1 Rice Model and Screening Concentration in Ground Water (SCI-GROW) models, the estimated drinking water concentrations (EDWCs) of thiamethoxam for acute exposures are estimated to be 131.77 parts per billion (ppb) for surface water and 4.66 ppb for ground water and for chronic exposures are estimated to be 11.31 ppb for surface water and 4.66 ppb for ground water.
Modeled estimates of drinking water concentrations were directly entered into the dietary exposure model. For the acute dietary risk assessment, the water concentration value of 131.77 ppb was used to assess the contribution to drinking water. For the chronic dietary risk assessment, the water concentration of value 11.31 ppb was used to assess the contribution to drinking water.
Thiamethoxam is currently registered for the following uses that could result in residential exposures: Turf and indoor environments (crack-and-crevice uses). EPA assessed residential exposure using the following assumptions: For residential handlers, short-term dermal and inhalation exposure is anticipated from both the lawn/turf and indoor crack-and-crevice uses. In terms of post application exposure, short-term dermal and incidental oral exposures are anticipated from both the lawn/turf and the crack-and-crevice uses. These exposures are expected from activities on turf such as playing, mowing, golfing, hand-to-mouth, object-to-mouth, incidental soil ingestion, and from contacting treated carpets. Post application inhalation exposure is also anticipated from indoor crack-and-crevice applications. The Agency selected only the most conservative, or worst case, residential adult and child scenarios to be included in the aggregate estimates, based on the lowest overall MOE (i.e., highest risk estimates). The worst case residential exposures for adults and children 1 to 2 years old were associated with post-application exposure to treated turf. Further information regarding EPA standard assumptions and generic inputs for residential exposures may be found at http://www2.epa.gov/​pesticide-science-and-assessing-pesticide-risks/​standard-operating-procedures-residential-pesticide.
Thiamethoxam is a member of the neonicotinoid class of pesticides and produces, as a metabolite, another neonicotinoid, CGA-322704. Structural similarities or common effects do not constitute a common mechanism of toxicity. Evidence is needed to establish that the chemicals operate by the same, or essentially the same, sequence of major biochemical events (EPA, 2002). Although CGA-322704 and thiamethoxam bind selectively to insect nicotinic acetylcholine receptors (nAChR), the specific binding site(s)/receptor(s) for CGA-322704, thiamethoxam and the other neonicotinoids are unknown at this time. Additionally, the commonality of the binding activity itself is uncertain, as preliminary evidence suggests that CGA-322704 operates by direct competitive inhibition, while thiamethoxam is a non-competitive inhibitor. Furthermore, even if future research shows that neonicotinoids share a common binding activity to a specific site on insect nAChRs, there is not necessarily a relationship between this pesticidal action and a mechanism of toxicity in mammals. Structural variations between the insect and mammalian nAChRs produce quantitative differences in the binding affinity of the neonicotinoids towards these receptors which, in turn, confers the notably greater selective toxicity of this class towards insects, including aphids and leafhoppers, compared to mammals. While the insecticidal action of the neonicotinoids is neurotoxic, the most sensitive regulatory endpoint for CGA-322704 is based on unrelated effects in mammals, including changes in body and thymus weights, delays in sexual maturation, and still births. Additionally, the most sensitive toxicological effect in mammals differs across the neonicotinoids (such as testicular tubular atrophy with thiamethoxam, and mineralized particles in thyroid colloid with imidacloprid). Therefore, 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 thiamethoxam and any other substances and thiamethoxam 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 thiamethoxam 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 concerning common mechanism determinations, and procedures for cumulating effects from substances found to have a common mechanism, released by OPP on EPA's Web site at http://www2.epa.gov/​pesticide-science-and-assessing-pesticide-risks/​cumulative-assessment-risk-pesticides.
2. Prenatal and postnatal sensitivity. In the developmental studies, there was no evidence of increased quantitative or qualitative susceptibility of rat or rabbit fetuses to in utero exposure to thiamethoxam. Effects in the young were seen in the presence of maternal toxicity. There was evidence of quantitative susceptibility in the developmental neurotoxicity study and both two-generation reproductive studies. Although there was evidence of increased quantitative susceptibility, there are no residual uncertainties with regard to pre- and/or postnatal toxicity following in utero exposure to rats or rabbits and pre and/or post-natal exposures to rats. Considering the overall toxicity profile and the doses and endpoints selected for risk assessment, the degree of concern for the effects observed in the studies is low because the developmental/offspring effects observed in the studies are well characterized and clear NOAELs/LOAELs have been identified in the studies for the effects of concern. Additionally, the Agency is confident that the endpoints and PODs selected Start Printed Page 10717for risk assessment are protective of potential developmental/reproductive effects.
i. The toxicity database for thiamethoxam is complete.
ii. Evidence of neurotoxicity was seen in the acute and developmental neurotoxicity studies. However, there is a low degree of concern for the potential neurotoxic effects of thiamethoxam since clear NOAELs were identified for the neurotoxic effects, the neurotoxic effects were not the most sensitive endpoint in the toxicity database and the endpoints chosen for risk assessment are protective of any potential neurotoxicity.
iii. There is no evidence that thiamethoxam results in increased susceptibility in in utero rats or rabbits in the prenatal developmental studies. There was evidence of quantitative susceptibility in the developmental neurotoxicity study and both two-generation reproductive studies, however, for the reasons cited above in section III.D.2., the Agency is confident that the endpoints and PODs selected for risk assessment are protective of potential developmental/reproductive effects.
iv. There are no residual uncertainties identified in the exposure databases. The dietary exposure assessments are based on high-end residue levels and processing factors, both of which account for parent and metabolites of concern, and the assumption of 100 PCT for all registered crops. EPA made conservative (protective) assumptions in the ground and surface water modeling used to assess exposure to thiamethoxam in drinking water. EPA used similarly conservative assumptions to assess post-application exposure of children as well as incidental oral exposure of toddlers. These assessments will not underestimate the exposure and risks posed by thiamethoxam.
1. Acute risk. Using the exposure assumptions discussed in this unit for acute exposure, the acute dietary exposure from food and water to thiamethoxam will occupy 9.5% 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 thiamethoxam from food and water will utilize 45% 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 thiamethoxam is not expected.
Thiamethoxam 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 thiamethoxam.
Using the exposure assumptions described in this unit for short-term exposures, EPA has concluded the combined short-term food, water, and residential exposures result in aggregate MOEs of 500 for adults and 580 for children 1<2 years old. Because EPA's level of concern for thiamethoxam is a MOE of 100 or below, these MOEs are not of concern.
An intermediate-term adverse effect was identified; however, thiamethoxam is not registered for any use patterns that would result in intermediate-term residential exposure. Intermediate-term risk is assessed based on intermediate-term residential exposure plus chronic dietary exposure. Because there is no intermediate-term residential exposure and chronic dietary exposure has already been assessed under the appropriately protective cPAD (which is at least as protective as the POD used to assess intermediate-term risk), no further assessment of intermediate-term risk is necessary, and EPA relies on the chronic dietary risk assessment for evaluating intermediate-term risk for thiamethoxam.
5. Aggregate cancer risk for U.S. population. As discussed in Unit III.A. and based on the lack of chronic risk discussed in Unit III.E.2., thiamethoxam is not expected to pose a cancer risk to humans.
Codex has established an MRL for thiamethoxam in bananas at 0.02 mg/kg which is different than the U.S. tolerance of 0.3 ppm. At this time, the Codex and EPA residue definitions are different (Codex's MRL is for the parent compound, thiamethoxam only, while EPA's is thiamethoxam plus metabolite CGA-322704); therefore, it is not possible to harmonize with the Codex MRL.
Three comments were received in response to the Notice of Filing. One Start Printed Page 10718simply said “Good.” The other two comments noted general concerns about approving “more herbicides and pesticides from Dow, Bayer, and Monsanto” and the toxicity of this chemical, stating, in part, that “food should not be contaminated with these chemicals.” The Agency recognizes that some individuals believe that pesticides should be banned on agricultural crops; however, the existing legal framework provided by section 408 of the Federal Food, Drug and Cosmetic Act (FFDCA) states that tolerances may be set when persons seeking such tolerances or exemptions have demonstrated that the pesticide meets the safety standard imposed by that statute. EPA has assessed the effects of this chemical on human health and determined that aggregate exposure to it will be safe. These comments provide no information to support a different conclusion.
The submitted banana field trial data support a tolerance of 0.03 ppm, instead of the petitioned-for tolerance of 0.04 ppm, in whole bananas. The petitioner used a combined limit of quantitation (LOQ) different from that used by the Agency for the input dataset of the Organization for Economic Cooperation and Development (OECD) tolerance calculation procedure. The combined LOQ used by EPA resulted in a recommended tolerance of 0.03 ppm.
Therefore, a tolerance is established for residues of thiamethoxam, including its metabolites and degradates, in or on banana at 0.03 ppm.
2. In § 180.565, add alphabetically the commodity “Banana” to the table in paragraph (a) and revise footnote 1 to read as follows:
Banana 1 0.03
1 There are no U.S. registrations for these commodities as of February 15, 2017.
[FR Doc. 2017-03075 Filed 2-14-17; 8:45 am]