01-30915. Notice of Filing a Pesticide Petition to Establish a Tolerance for a Certain Pesticide Chemical in or on Food

AGENCY:

Environmental Protection Agency (EPA).

ACTION:

Notice.

SUMMARY:

This notice announces the initial filing of a pesticide petition proposing the establishment of regulations for residues of a certain pesticide chemical in or on various food commodities.

DATES:

Comments, identified by docket control number PF-1057, must be received on or before January 14, 2002.

ADDRESSES:

Comments may be submitted by mail, electronically, or in person. Please follow the detailed instructions for each method as provided in Unit I.C. of the SUPPLEMENTARY INFORMATION. To ensure proper receipt by EPA, it is imperative that you identify docket control number PF-1057 in the subject line on the first page of your response.

FOR FURTHER INFORMATION CONTACT:

By mail: Dani Daniel, Registration Division (7505C), Office of Pesticide Programs, Environmental Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460; telephone number: [phone]; e-mail address: [e-mail].

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

You may be affected by this action if you are an agricultural producer, food manufacturer or pesticide manufacturer. Potentially affected categories and entities may include, but are not limited to:

Categories	NAICS codes	Examples of potentially affected entities
Industry	111	Crop production
	112	Animal production
	311	Food manufacturing
	32532	Pesticide manufacturing

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

B. How Can I Get Additional Information, Including Copies of this Document and Other Related Documents?

1. Electronically. You may obtain electronic copies of this document, and certain other related documents that might be available electronically, from the EPA Internet Home Page at http://www.epa.gov/​. To access this document, on the Home Page select “Laws and Regulations” and then look up the entry for this document under the “Federal Register—Environmental Documents.” You can also go directly to the Federal Register listings at http://www.epa.gov/​fedrgstr/​.

2. In person. The Agency has established an official record for this action under docket control number PF-1057. The official record consists of the documents specifically referenced in this action, any public comments received during an applicable comment period, and other information related to this action, including any information claimed as confidential business information (CBI). This official record includes the documents that are physically located in the docket, as well as the documents that are referenced in those documents. The public version of the official record does not include any information claimed as CBI. The public version of the official record, which includes printed, paper versions of any electronic comments submitted during an applicable comment period, is available for inspection in the Public Information and Records Integrity Branch (PIRIB), Rm. 119, Crystal Mall #2, 1921 Jefferson Davis Highway, Arlington, VA, from 8:30 a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The PIRIB telephone number is [phone].

C. How and to Whom Do I Submit Comments?

You may submit comments through the mail, in person, or electronically. To ensure proper receipt by EPA, it is imperative that you identify docket control number PF-1057 in the subject line on the first page of your response.

1. By mail. Submit your comments to: Public Information and Records Integrity Branch (PIRIB), Information Resources and Services Division (7502C), Office of Pesticide Programs (OPP), Environmental Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460.

2. In person or by courier. Deliver your comments to: Public Information and Records Integrity Branch (PIRIB), Information Resources and Services Division (7502C), Office of Pesticide Programs (OPP), Environmental Protection Agency, Rm. 119, Crystal Mall #2, 1921 Jefferson Davis Highway, Arlington, VA. The PIRIB is open from 8:30 a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The PIRIB telephone number is [phone].

3. Electronically. You may submit your comments electronically by e-mail to: [e-mail], or you can submit a computer disk as described above. Do not submit any information electronically that you consider to be CBI. Avoid the use of special characters and any form of encryption. Electronic submissions will be accepted in Wordperfect 6.1/8.0 or ASCII file format. All comments in electronic form must be identified by docket control number PF-1057. Electronic comments may also be filed online at many Federal Depository Libraries.

D. How Should I Handle CBI That I Want to Submit to the Agency?

Do not submit any information electronically that you consider to be CBI. You may claim information that you submit to EPA in response to this document as CBI by marking any part or all of that information as CBI. Information so marked will not be disclosed except in accordance with procedures set forth in 40 CFR part 2. In addition to one complete version of the comment that includes any information claimed as CBI, a copy of the comment that does not contain the information claimed as CBI must be submitted for inclusion in the public version of the official record. Information not marked confidential will be included in the public version of the official record without prior notice. If you have any questions about CBI or the procedures for claiming CBI, please consult the person identified under FOR FURTHER INFORMATION CONTACT.

E. What Should I Consider as I Prepare My Comments for EPA?

You may find the following suggestions helpful for preparing your comments:

1. Explain your views as clearly as possible.

2. Describe any assumptions that you used.

3. Provide copies of any technical information and/or data you used that support your views.

4. If you estimate potential burden or costs, explain how you arrived at the estimate that you provide.

5. Provide specific examples to illustrate your concerns.

6. Make sure to submit your comments by the deadline in this notice.

7. To ensure proper receipt by EPA, be sure to identify the docket control number assigned to this action in the subject line on the first page of your response. You may also provide the name, date, and Federal Register citation.

II. What Action is the Agency Taking?

EPA has received a pesticide petition as follows proposing the establishment and/or amendment of regulations for residues of a certain pesticide chemical in or on various food commodities under section 408 of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a. EPA has determined that this petition contains data or information regarding the elements set forth in section 408(d)(2); however, EPA has not fully evaluated the sufficiency of the submitted data at this time or whether the data support granting of the petition. Additional data may be needed before EPA rules on the petition.

List of Subjects

• Environmental protection
• Agricultural commodities
• Feed additives
• Food additives
• Pesticides and pests
• Reporting and recordkeeping requirements

Dated: November 29, 2001.

Peter Caulkins,

Acting Director, Registration Division, Office of Pesticide Programs.

Summary of Petition

The petitioner summary of the pesticide petition is printed below as required by section 408(d)(3) of the Federal Food, Drug, and Cosmetic Act (FFDCA). The summary of the petition was prepared by the petitioner and represents the view of the petitioners. EPA is publishing the petition summary verbatim without editing it in any way. The petition summary announces the availability of a description of the analytical methods available to EPA for the detection and measurement of the pesticide chemical residues or an explanation of why no such method is needed.

Sygenta Crop Protection Inc.

PP 1E6349

EPA has received a pesticide petition (1E6349) from Sygenta Crop Protection Inc., P.O. Box 18300, Greensboro, NC 27419-8300 proposing, pursuant to section 408(d) of the FFDCA, 21 U.S.C. 346a(d), to amend 40 CFR part 180 by establishing a tolerance for residues of thiamethoxam and its metabolite, (N-(2-chloro-thiazol-5-ylmethyl)-N'methyl-N-nitro-guanidine, in or on the raw agricultural commodity imported green and roasted coffee beans and instant coffee at 0.05 parts per million (ppm). EPA has determined that the petition contains data or information regarding the elements set forth in section 408(d)(2) of the FFDCA; however, EPA has not fully evaluated the sufficiency of the submitted data at this time or whether the data support granting of the petition. Additional data may be needed before EPA rules on the petition.

A. Residue Chemistry

1. Plant metabolism. The primary metabolic pathways of thiamethoxam in plants (corn, rice, pears, and cucumbers) were similar to those described for animals, with certain extensions of the pathway in plants. Parent compound, thiamethoxam, and its metabolite, (N-(2-chloro-thiazol-5-ylmethyl)-N'methyl-N-nitro-guanidine, were the major residues in all crops. The metabolism of thiamethoxam in plants and animals is understood for the purposes of the proposed tolerances. Parent thiamethoxam and the metabolite, are the residues of concern for tolerance setting purposes.

2. Analytical method. Syngenta Crop Protection Inc. has submitted practical analytical methodology for detecting and measuring levels of thiamethoxam in or on raw agricultural commodities. The method is based on crop specific cleanup procedures and determination by liquid chromatography with either ultraviolet (UV) or mass spectrometry (MS) detection. The limit of detection (LOD) for each analyte of this method is 1.25 nanogram (ng) injected for samples analyzed by UV and 0.25 ng injected for samples analyzed by MS, and the limit of quantitation (LOQ) is 0.005 ppm for milk and juices and 0.01 ppm for all other substrates.

3. Magnitude of residues. A residue program was performed for thiamethoxam on coffee as prescribed in draft EPA Guidance on Import Tolerances. A total of nine trials were conducted in the major coffee producing countries of Brazil (four), Columbia (three) and Mexico (two). The applications in these trials consisted of soil applications (trench, furrow or broadcast) at the proposed maximum rate of 300 grams active ingredient per hectare. The first applications were made just after petal fall and a second application at the beginning of fruit development. There were no detectable residues <0.02 ppm of thiamethoxam or the metabolite CGA-322701 in coffee berries or dried green coffee beans.

In addition, there was a single 5X exaggerated rate processing trial conducted. There were detectable residues of thiamethoxam and its metabolite (<0.022 ppm and 0.012 ppm, respectively) in the dry beans for processing. There were no detectable residues (<0.005 ppm) of thiamethoxam or it metabolite, in roasted beans, ground roasted beans, brewed extracts, spent grounds or instant coffee.

B. Toxicological Profile

1. Acute toxicity. The acute oral LD₅₀ for thiamethoxam in the rat is 1,563 mg/kg body weight. The acute dermal LD₅₀ of thiamethoxam is >2,000 milligrams/kilogram (mg/kg) body weight. Thiamethoxam is non-toxic at atmospheric concentrations of 3.72 mg/L. Thiamethoxam is minimally irritating to the eye, non-irritating to skin, and is not a dermal sensitizer.

In an acute neurotoxicity screening study in rats (OPPTS 870.6200a), the no observed adverse effect level (NOAEL) was 100 mg/kg/day with a NOAEL of 500 mg/kg/day based on drooped palpebral closure, decrease in rectal temperature and locomotor activity and increase in forelimb grip strength (males only). At higher dose levels, mortality, abnormal body tone, ptosis, impaired respiration, tremors, longer latency to first step in the open field, crouched over posture, gait impairment, hypo-arousal, decreased number of rears, uncoordinated landing during the righting reflex test, slight lacrimation (females only), and higher mean average input stimulus value in the auditory startle response test (males only).

2. Genotoxicity. In gene mutation studies with S. typhimurium and E. coli (OPPTS 870.5100 and 870.5265), there was no evidence of gene mutation when tested up to 5,000 μg/plate and there was no evidence of cytotoxicity. In a gene mutation study with chinese hamster V79 cells at HGPRT focus (OPPTS 870.5300) there was no evidence of gene mutation when tested up to the solubility limit.

In a CHO cell cytogenetics study (OPPTS 870.5375) there was no evidence of chromosomal aberrations when tested up to cytotoxic or solubility limit concentrations.

An in vivo mouse bone marrow micronucleus study (OPPTS 870.5395) was negative when tested up to levels of toxicity in whole animals; however, there was no evidence of target cell cytotoxicity.

An UDS assay (OPPTS 870.5550) was negative when tested up to precipitating concentrations.

3. Reproductive and developmental toxicity. A prenatal developmental study in the rat (OPPTS 870.3700) resulted in maternal and developmental NOAELs of 30 mg/kg/day and 200 mg/kg/day, respectively. The maternal lowest observed adverse effect level (LOAEL) is 200 mg/kg/day based on decreased body weight, body weight gain and food consumption. The developmental LOAEL was 750 mg/kg/day based on decreased fetal body weight and an increased incidence of skeletal anomalies.

A prenatal developmental study in the rabbit (OPPTS 870.3700) resulted in maternal and developmental NOAELs of 50 mg/kg/day. The maternal and developmental LOAEL is 150 mg/kg/day. The maternal LOAEL is based on maternal deaths, hemorrhagic discharge, decreased body weight, and food intake during the dosing period. The developmental LOAEL is based on decreased fetal body weights, increased incidence of post-implantation loss and a slight increase in the incidence of a few skeletal anomolies/variations.

In a reproduction and fertility effects study in rats (OPPTS 870.3800) the parental/systemic NOAEL is 1.84 (males), 202.06 (females) mg/kg/day; the reproductive NOAEL is 0.61 (males), 202.06 (females) mg/kg/day, and the offspring NOAEL is 61.25 (males), 79.20 (females) mg/kg/day. The parental/systemic LOAEL is 61.25 (males), not determined (females) mg/kg/day based on increased incidence of hyaline change in renal tubules in F0 and F1 males. The reproductive LOAEL is 1.84 (males), not determined females mg/kg/day based on increased incidence and severity of tubular atrophy observed in testes of the F1 generation males. The offspring LOAEL is 158.32 (males), 202.06 (females) mg/kg/day based on reduced body weight gain during the lactation period in all litters.

4. Subchronic toxicity. A 90-day oral toxicity study in rats (OPPTS 870.3100) resulted in a NOAEL of 1.74 (males) and 92.5 (females) mg/kg/day. The LOAEL is 17.64 (male), 182.1 (female) mg/kg/day based on increased incidence of hyaline change of renal tubules epithelium (males), fatty change in adrenal gland of females, liver changes in females, all at the LOAEL.

A 90-day oral toxicity study in mice (OPPTS 870.3100) resulted in an NOAEL of 1.41 (males) and 19.2 (females) mg/kg/day. The LOAEL was 14.3 (male) and 231 (female) mg/kg/day based on an increased incidence of hepatocellular hypertrophy. At higher dose levels: decrease in body weight and body weight gain, necrosis of individual hepatocytes, pigmentation of Kupffer cells, and a lymphocytic infiltration of the liver in both sexes; slight hematologic effects and decreased absolute and relative kidney weights in males; and ovarian atrophy, decreased ovary and spleen weights and increased liver weights in females.

In a 90-day oral toxicity study in dogs (OPPTS 870.3150), the NOAEL is 8.23 (males) and 9.27 (females) mg/kg/day. The LOAEL is 32.0 (male), 33.9 (female) mg/kg/day based on slightly prolonged prothrombin times and decreased plasma albumin and A/G ration (both sexes); decreased calcium levels and ovary weights and delayed maturation in the ovaries (female); decreased cholesterol and phospholipid levels, testes weights, spermatogenesis, and spermatic giant cells in testes (male).

In a 28-day dermal study in rats (OPPTS 870.3200) the NOAEL was 250 (male) and 60 (female) mg/kg/day. The LOAEL was 1,000 (male),and 250 (female) mg/kg/day based on an increased plasma glucose, triglyceride levels, and alkaline phosphatase activity and an inflammatory cell infiltration in the liver and necrosis if single hepatocytes in females and a hyaline change in renal tubules and a very slight reduction in body weight in males. At higher dose levels in females, chronic tubular lesions in the kidneys and an inflammatory cell infiltration in the adrenal cortex were observed.

In a subchronic neurotoxicity screening study in rats (OPPTS 870.6200) the NOAEL was 95.4 (male) and 216.4 (female) mg/kg/day, both at the highest dose tested. The LOAEL was not determined. No treatment-related observations at any dose level. LOAEL was not achieved. May not have been tested at sufficiently high dose levels; however, a new study is not required because the weight of the evidence from other toxicity studies indicates no evidence of concern.

5. Chronic toxicity. In a chronic toxicity study in dogs (OPPTS 870.4100) the NOAEL was 4.05 (male), and 4.49 (female) mg/kg/day. The LOAEL was 21.0 (male) and 24.6 (female) mg/kg/day based on an increase of creatinine in both sexes, transient decrease in food consumption in females, and an occasional increase in urea levels, decrease in ALT, and atrophy of seminiferous tubules in males.

In a mouse carcinogenicity study (OPPTS 870.4200) the NOAEL was 2.63 (male) and 3.68 (female) mg/kg/day. The LOAEL was 63.8 (male) and 87.6 (female) mg/kg/day based on hepatocyte hypertrophy, single cell necrosis, inflammatory cell infiltration, pigment deposition, foci of cellular alteration, hyperplasia of Kupffer cells and increased mitotic activity, also an increase in the incidence of hepatocellular adenoma (both sexes). At higher doses, there was an increase in the incidence of hepatocelluar adenocarcinoma (both sexes) and the number of animals with multiple tumors, evidence of carcinogenicity. In a combined chronic caricinogenicity study in rats (OPPTS 870.4300), the NOAEL was 21.0 (male) and 50.3 (female) mg/kg/day. The LOAEL was 63.0 (male) and 255 (female) mg/kg/day based on an increased incidence of lymphocytic infiltration of the renal pelvis and chronic nephropathy in males and decreased body weight gain, slight increase in the severity of hemosiderosis of the spleen, foci of cellular alteration in liver and chronic tubular lesions in kidney in females. No evidence of carcinogenicity.

In a hepatic cell proliferation study in mice, the NOAEL was 16 (male) and 20 (female) mg/kg/day. The LOAEL was 72 (male) and 87 (female) mg/kg/day based on proliferative activity of hepatocytes. At higher dose levels, increases in absolute and relative liver weights, speckled liver, heptocellular glycogenesis/fatty change, heptocellular necrosis, apoptosis and pigmentation were observed.

In a 28-day feeding study to assess replicative DNA syntehsis in the male rat, the NOAEL was 711 mg/kg/day. The LOAEL was not established. Immunohistochemical staining of liver sections from control, and high dose animals for proliferating cell nuclear antigen gave no indication for a treatment-related increase in the fraction of DNA syntesizing hepatocytes in S-phase. Thiamethoxam did not stimulate hepatocyte cell proliferation in male rats.

In a special study to assess liver biochemistry in the mouse, the NOAEL was 17 (male) and 92 (female) mg/kg/day. The LOAEL was 74 (male) and 92 (female) mg/kg/day based on marginal to slight increases in absolute and relative liver weights, a slight increase in the microsomal protein content of the livers, moderate increases in the cytochrome P450 content, slight to moderate increases in the activity of several microsomal enzymes, slight to moderate induction of cytosolic glutathionw S-transfersase activity. Treatment did not affect peroxisomal fatty acid B-oxidation.

6. Animal metabolism. The metabolism of thiamethoxam in rats and livestock animals is adequately understood. The residues of concern have been determined to be parent thiamethoxam and its metabolite (N-(2-chloro-thiazol-5-ylmethyl)-N'methyl-N-nitro-guanidine).

7. Metabolite toxicology. For risk assessment purposes, residues of the metabolite corrected for molecular weight are considered to be toxicologically equivalent to parent thiamethoxam.

C. Aggregate Exposure

1. Dietary exposure. Permanent tolerances have been established (40 CFR 180.565) for the combined residues of the insecticide thiamethoxam, 3-[(2-chloro-5-thiazolyl)methyl]tetrahydro-5-methyl-N-nitro-4H-1,3,5-oxadiazin-4-imine and it metabolite (N-(2-chloro-thiazol-5-ylmethyl)-N'-methyl-N-nitro-guanidine), in or on a variety of raw agricultutal commodities at levels ranging from 0.02 ppm to 1.5 ppm including barley, canola, cotton, sorghum, wheat, cucurbit vegetables, fruiting vegetables, pome fruits and livestock commodities. Pending tolerances include coffee, grapes, raisins, grape juice, pecans, peanut nutmeats, peanut hay, corn grain, sweet corn (kernal with husk removed), pop corn, corn forage and stover, head and stem brassica, leafy brassica greens and leafy vegetables.

i. Food—a. Acute risk. The acute dietary risk from food use tolerances previously set as published in the Federal Register of December 21, 2000 (65 FR 80343) (FRL-6758-1) and May 23, 2001 (66 FR 28386) (FRL-6784-7) indicate that acute dietary exposure from food will occupy 3% of the acute population adjusted dose (aPAD) for the U.S. population, 2% of the aPAD for females 13-50 years old, 8% of the aPAD for infants less than 1 year old and 7% of the aPAD for children 6-11 years old. Therefore, it is expected that the proposed tolerances for coffee will have minimal impact on acute dietary risk, and that the aggregate exposure will not exceed 100% of the aPAD.

b. Chronic risk. The chronic dietary risk from food use tolerances previously set as published in the Federal Register of December 21, 2000 (65 FR 80343), and May 23, 2001 (66 FR 28386) indicate that chronic dietary exposure from food will utilize 5% of the chronic population adjusted dose (cPAD) for the U.S. population, 13% of the cPAD for children 1-6 years old. Therefore, it is expected that the proposed tolerances for coffee will have minimal impact on chronic dietary risk and the aggregate exposure will not exceed 100% of the cPAD.

c. Cancer risk. Since there were no detectable residues of thiamethoxam or its metabolite in samples from the residue trials conducted in Brazil, Columbia and Mexico, it can be concluded that there is no increased cancer risk from the proposed use on imported coffee. Syngenta DEEM analysis indicates that the proposed tolerance on coffee contributes only 3.00 x 10^E-9 lifetime dietary cancer risk.

ii. Drinking water. Since the proposed tolerance is for imported coffee, there is no potential exposure from drinking water.

2. Non-dietary exposure. Thiamethoxam is not currently registered for use on any sites that would result in residential exposure.

D. Cumulative Effects

The potential for cumulative effects of thiamethoxam, and other substances that have a common mechanism of toxicity has also been considered. Thiamethoxam belongs to a new pesticide chemical class known as the neonicotinoids. There is no reliable information to indicate that toxic effects produced by thiamethoxam would be cumulative with those of any other chemical including another pesticide. Therefore, Syngenta believes it is appropriate to consider only the potential risks of thiamethoxam in an aggregate risk assessment.

E. Safety Determination

1. U.S. population. Syngenta concludes, as described above, that there is reasonable certainty that no harm to the U.S. population will result from aggregate acute or chronic dietary exposure to thiamethoxam residues including the proposed tolerances for imported coffee.

2. Infants and children. Syngenta concludes, as described above, that there is reasonable certainty that no harm to infants and children will result from aggregate acute or chronic exposure to thiamethoxam residues, including the proposed tolerances for imported coffee.

F. International Tolerances

There are no Codex maximum residue levels established for residues of thiamethoxam on coffee.