FLUORIDE ACTION NETWORK PESTICIDE PROJECT
Return to FAN's Pesticide Homepage
Return to Carfentrazone-ethyl Index Page
Carfentrazone-ethyl (FMC). June 10, 1998. Request to extend temporary pesticide tolerance. Federal Register.
http://www.epa.gov/fedrgstr/EPA-PEST/1998/June/Day-10/p15177.htm
[Federal Register: June 10, 1998 (Volume 63, Number 111)] [Notices] [Page 31768-31771] From the Federal Register Online via GPO Access [wais.access.gpo.gov] [DOCID:fr10jn98-88] ----------------------------------------------------------------------- ENVIRONMENTAL PROTECTION AGENCY [PF-810; FRL-5793-1] FMC Corporation; Pesticide Tolerance Petition Filing 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 the docket control number PF-810, must be received on or before July 10, 1998. ADDRESSES: By mail submit written comments to: Information and Records Integrity Branch, Public Information and Services Divison (7502C), Office of Pesticides Programs, Environmental Protection Agency, 401 M St., SW., Washington, DC 20460. In person bring comments to: Rm. 119, CM #2, 1921 Jefferson Davis Highway, Arlington, VA. Comments and data may also be submitted electronically by following the instructions under ``SUPPLEMENTARY INFORMATION.'' No confidential business information should be submitted through e-mail. Information submitted as a comment concerning this document may be claimed confidential by marking any [[Page 31769]] part or all of that information as ``Confidential Business Information'' (CBI). CBI should not be submitted through e-mail. Information marked as CBI will not be disclosed except in accordance with procedures set forth in 40 CFR part 2. A copy of the comment that does not contain CBI must be submitted for inclusion in the public record. Information not marked confidential may be disclosed publicly by EPA without prior notice. All written comments will be available for public inspection in Rm. 1132 at the address given above, from 8:30 a.m. to 4 p.m., Monday through Friday, excluding legal holidays. FOR FURTHER INFORMATION CONTACT: Joanne Miller, Registration Support Branch, Registration Division (7505C), Office of Pesticide Programs, Environmental Protection Agency, 401 M St., SW, Washington, DC 20460. Office location, telephone number, and e-mail address: Rm. 237, Crystal Mall CM #2, 1900 Jefferson Davis Highway, Arlington, VA 22202, (703) 305-6224; e-mail: miller.joanne@epamail.epa.gov. SUPPLEMENTARY INFORMATION: EPA has received a pesticide petition as follows proposing the establishment and/or amendment of regulations for residues of certain pesticide chemical in or on various food commodities under section 408 of the Federal Food, Drug, and Comestic 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 supports granting of the petition. Additional data may be needed before EPA rules on the petition. The official record for this notice of filing, as well as the public version, has been established for this notice of filing under docket control number [PF-810] (including comments and data submitted electronically as described below). A public version of this record, including printed, paper versions of electronic comments, which does not include any information claimed as CBI, is available for inspection from 8:30 a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The official record is located at the address in ``ADDRESSES'' at the beginning of this document. Electronic comments can be sent directly to EPA at: opp-docket@epamail.epa.gov Electronic comments must be submitted as an ASCII file avoiding the use of special characters and any form of encryption. Comment and data will also be accepted on disks in Wordperfect 5.1 file format or ASCII file format. All comments and data in electronic form must be identified by the docket number FRL-5793-1 and appropriate petition number. Electronic comments on this proposed rule may be filed online at many Federal Depository Libraries. List of Subjects Environmental protection, Agricultural commodities, Food additives, Feed additives, Pesticides and pests, Reporting and recordkeeping requirements. Dated: May 26, 1998. James Jones, Director, Registration Division, Office of Pesticide Programs. Summaries of Petitions Petitioner summaries of the pesticide petitions are printed below as required by section 408(d)(3) of the FFDCA. The summaries of the petitions were prepared by the petitioners and represent the views of the petitioners. EPA is publishing the petition summaries verbatim without editing them 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. 1. FMC Corporation PP 6G4615 EPA has received a pesticide petition (PP 6G4615) from FMC Corporation, 1735 Market Street, Philadelphia, PA 19103, proposing pursuant to section 408(d) of the Federal Food, Drug, and Cosmetic Act, 21 U.S.C. 346a(d), to amend 40 CFR part 180 by extending a temporary tolerance for the combined residue of the herbicide carfentrazone-ethyl (ethyl-alpha-2-dichloro-5-[4-(difluoromethyl)-4,5-dihydro-3-methyl-5- oxo-1H-1,2,4-triazol-1-yl]-4-fluorobenzene-propanoate) and its major wheat metabolites: carfentrazone-ethyl chloropropionic acid (alpha, 2- dichloro-5-[4-difluoromethyl)-4,5-dihydro-3-methyl-5-oxo-1H-1,2,4- triazol-1-yl]-4-fluorobenzenepropanoic acid), 3-hydroxymethyl-F8426- chloropropionic acid (alpha,2-dichloro-5-[4-difluoromethyl)-4,5- dihydro-3-hydroxymethyl-5-oxo-1H-1,2,4-triazol-l-yl]-4- fluorobenzenepropanoic acid), and 3-desmethyl-F8426 chloropropionic acid (alpha, 2-dichloro-5-[4-difluoromethyl)-4,5-dihydro-5-oxo-1H- 1,2,4-triazol-l-yl]-4-fluorobenzenepropanoic acid) in or on wheat raw agricultural commodities: 0.2 ppm in or on wheat hay, 0.2 ppm in or on wheat straw, 0.2 ppm in or on wheat grain; and extending tolerance for combined residue of the herbicide carfentrazone-ethyl (ethyl-alpha-2- dichloro-5-[4-(difluoromethyl)-4,5-dihydro-3-methyl-5-oxo-1H-1,2,4- triazol-1-yl]-4-fluorobenzene-propanoate) and its major corn metabolites: carfentrazone-ethyl chloropropionic acid (alpha, 2- dichloro-5-[4-difluoromethyl)-4,5-dihydro-3-methyl-5-oxo-1H-1,2,4- triazol-l-yl]-4-fluorobenzenepropanoic acid),and 3-desmethyl-F8426 chloropropionic acid (alpha, 2-dichloro-5-[4-difluoromethyl)-4,5- dihydro-5-oxo-1H-1,2,4-triazol-1-yl]-4-fluorobenzenepropanoic acid) in or on corn raw agricultural commodities: 0.15 ppm in or on corn forage, 0.15 ppm in or on corn fodder, 0.15 ppm in or on corn grain. 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 supports granting of the petition. Additional data may be needed before EPA rules on the petition. A. Residue Chemistry 1. Plant metabolism. The metabolism of carfentrazone-ethyl in plants is adequately understood. Corn and wheat metabolism studies with carfentrazone-ethyl have shown uptake of material into plant tissue with no significant movement into grain or seeds. All three plants extensively metabolized carfentrazone-ethyl and exhibited a similar metabolic pathway. The residues of concern are the combined residues of carfentrazone-ethyl and carfentrazone-ethyl- chloropropionic acid. 2. Analytical method There is a practical analytical method for detecting and measuring levels of carfentrazone and its metabolites in or on food with a limit of quantitation that allows monitoring of food with residues at or above the levels set in the tolerances. The analytical method for carfentrazone-ethyl involves separate analyses for parent and its metabolites. The parent is analyzed by GC/ECD. The metabolites are derivatized with boron trifluoride and acetic anhydride for analysis by GC/MSD using selective ion monitoring. 3. Magnitude of residues. Carfentrazone-ethyl 50DF was applied postemergent to 28 wheat trials, and 24 corn trials in the appropriate EPA regions. The RAC's were harvested at [[Page 31770]] the appropriate growth stages and subsequent analyses determined that the residues of carfentrazone-ethyl and its metabolites will not exceed the proposed tolerances of 1.0, 0.3, 0.2 and 0.1 ppm for wheat forage, hay, straw and grain, respectively; 0.1 ppm each for corn forage, fodder, and grain. Residue data from a cow feeding study demonstrated that no accumulation of carfentrazone-ethyl or its metabolites occurred in milk or tissues. B. Toxicological Profile 1. Acute toxicity. Carfentrazone-ethyl demonstrates low oral, dermal and inhalation toxicity. The acute oral LD<INF>50</INF> value in the rat was greater than 5,000 milligram/Kilograms (mg/kg), the acute dermal LD<INF>50</INF> value in the rat was greater than 4,000 mg/kg and the acute inhalation LC<INF>50</INF> value in the rat was greater than 5.09 mg/L/4h. Carfentrazone-ethyl is non-irritating to rabbit skin and minimally irritating to rabbit eyes. It did not cause skin sensitization in guinea pigs. An acute neurotoxicity study in the rat had a systemic no-observed-adverse-effect level (NOAEL) of 500 mg/kg based on clinical signs and decreased motor activity levels; the NOAEL for neurotoxicity was greater than 2,000 mg/kg highest dose tested (HDT) based on the lack of neurotoxic clinical signs or effects on neuropathology. 2. Genotoxicty. Carfentrazone-ethyl did not cause mutations in the Ames assay with or without metabolic activation. There was a positive response in the Chromosome Aberration assay without activation but a negative response with activation. The Mouse Micronucleus assay (an in vivo test which also measures chromosome damage), the CHO/HGPRT forward mutation assay and the Unscheduled DNA Synthesis assay were negative. The overwhelming weight of the evidence supports the conclusion that Carfentrazone-ethyl is not genotoxic. 3. Reproductive and developmental toxicity. Carfentrazone-ethyl is not considered to be a reproductive or a developmental toxin. In the 2- generation reproduction study, the NOEL for reproductive toxicity was greater than 4,000 ppm (greater than 323 to greater than 409 mg/kg/ day). In the developmental toxicity studies, the rat and rabbit maternal NOELs were 100 mg/kg/day and 150 mg/kg/day, respectively. The developmental NOEL for the rabbit was greater than 300 mg/kg/day which was the HDT and for the rat the NOEL was 600 mg/kg/day based on increased litter incidences of thickened and wavy ribs at 1,250 mg/kg/ day. These two findings (thickened and wavy ribs) are not considered adverse effects of treatment but related delays in rib development which are generally believed to be reversible. 4. Subchronic toxicity 90-day feeding studies were conducted in mice, rats and dogs with carfentrazone-ethyl. The NOEL for the mouse study was 4,000 ppm (571 mg/kg/day), for the rat study was 1,000 ppm (57.9 mg/kg/day for males; 72.4 mg/kg/day for females) and for dogs was 150 mg/kg/day. A 90-day subchronic neurotoxicity study in the rat had a systemic NOEL of 1,000 ppm (59.0 mg/kg/day for males; 70.7 mg/kg/day for females) based on decreases in body weights, body weight gains and food consumption at 10,000 ppm; the neurotoxicity NOEL was greater than 20,000 ppm (1178.3 mg/kg/day for males; 1433.5 mg/kg/day for females) which was the HDT. 5. Chronic toxicity. Carfentrazone-ethyl is not carcinogenic to rats or mice. A 2-year combined chronic toxicity/oncogenicity study in the rat was negative for carcinogenicity and had a chronic toxicity NOEL of 200 ppm (9 mg/kg/day) for males and 50 ppm (3 mg/kg/day) for females based on red fluorescent granules consistent with porphyrin deposits in the liver at the 500 and 200 ppm levels, respectively. An 18-month oncogenicity study in the mouse had a carcinogenic NOEL that was greater than 7,000 ppm (>1090 mg/kg/day for males; >1296 mg/kg/day for females) based on no evidence of carcinogenicity at the HDT. A 1- year oral toxicity study in the dog had a NOEL of 50 mg/kg/day based on isolated increases in urine porphyrins in the 150 mg/kg/day group (this finding was not considered adverse). Using the Guidelines for Carcinogen Risk Assessment, carfentrazone- ethyl should be classified as Group ``E'' for carcinogenicity -- no evidence of carcinogenicity -- based on the results of carcinogenicity studies in two species. There was no evidence of carcinogenicity in an 18-month feeding study in mice and a 2-year feeding study in rats at the dosage levels tested (DLT). The doses tested are adequate for identifying a cancer risk. Thus, a cancer risk assessment is not necessary. 6. Animal metabolism. The metabolism of carfentrazone-ethyl in animals is adequately understood. Carfentrazone-ethyl was extensively metabolized and readily eliminated following oral administration to rats, goats, and poultry via excreta. All three animals exhibited a similar metabolic pathway. As in plants, the parent chemical was metabolized by hydrolytic mechanisms to predominantly form carfentrazone-ethyl-chloropropionic acid which was readily excreted. 7. Endocrine disruption. An evaluation of the potential effects on the endocrine systems of mammals has not been determined; however, no evidence of such effects were reported in the chronic or reproductive toxicology studies described above. There was no observed pathology of the endocrine organs in these studies. There is no evidence at this time that carfentrazone-ethyl causes endocrine effects. C. Aggregate Exposure Dietary exposure--i. Acute dietary. The Agency has determine that there is no concern for an acute dietary risk assessment since the available data do not indicate any evidence of significant toxicity from a 1-day or single event exposure by the oral route Federal Register of September 30, 1997 (62, FR 189). Thus an acute dietary risk assessment is not necessary. ii. Food. Dietary exposure from the proposed uses would account for 1.3% or less of the RfD in subpopulations (including infants and children). iii. Drinking water. Studies have indicated that carfentrazone- ethyl will not move into groundwater, therefore water has not been included in the dietary risk assessment. iv. Non-dietary exposure. No specific worker exposure tests have been conducted with carfentrazone-ethyl. The potential for non- occupational exposure to the general population has not been fully assessed. No specific worker exposure tests have been conducted with carfentrazone-ethyl. D. Cumulative Effects EPA is also required to consider the potential for cumulative effects of carfentrazone-ethyl and other substances that have a common mechanism of toxicity. EPA consideration of a common mechanism of toxicity is not appropriate at this time since EPA does not have information to indicate that toxic effects produced by carfentrazone- ethyl would be cumulative with those of any other chemical compounds; thus only the potential risks of carfentrazone-ethyl are considered in this exposure assessment. E. Safety Determination 1. U.S. population. Using the conservative exposure assumptions described and based on the completeness and reliability of the toxicity data, the aggregate exposure to carfentrazone-ethyl will utilize 0.61% of the RfD for the US population. EPA generally has no concern for exposures below 100% of the RfD. Therefore, [[Page 31771]] based on the completeness and reliability of the toxicity data and the conservative exposure assessment, there is a reasonable certainty that no harm will result from aggregate exposure to residues of carfentrazone-ethyl, including all anticipated dietary exposure and all other non-occupational exposures. 2. Infants and children. In assessing the potential for additional sensitivity of infants and children to residues of carfentrazone-ethyl, EPA considers data from developmental toxicity studies in the rat and rabbit and the 2-generation reproduction study in the rat. The developmental toxicity studies are designed to evaluate adverse effects on the developing organism resulting from pesticide exposure during prenatal development. Reproduction studies provide information relating to effects on the reproductive capacity of males and females exposed to the pesticide. Developmental toxicity was not observed in developmental toxicity studies using rats and rabbits. In these studies, the rat and rabbit maternal NOELs were 100 mg/kg/day and 150 mg/kg/day, respectively. The developmental NOEL for the rabbit was greater than 300 mg/kg/day which was the HDT and for the rat was 600 mg/kg/day based on increased litter incidences of thickened and wavy ribs. These two findings are not considered adverse effects of treatment but related delays in rib development which are generally believed to be reversible. In a 2-generation reproduction study in rats, no reproductive toxicity was observed under the conditions of the study at 4,000 ppm which was the HDT. Section 408 of the FFDCA provides that EPA may apply an additional safety factor for infants and children in the case of threshold effects to account for pre- and post-natal toxicity and the completeness of the database. Based on the current toxicological data requirements, the database relative to pre- and post-natal effects for children is complete and an additional uncertainty factor is not warranted. Therefore at this time, the provisional RfD of 0.06 mg/kg/day is appropriate for assessing aggregate risk to infants and children. F. Reference Dose Using the conservative exposure assumptions described above, the percent of the RfD that will be utilized by aggregate exposure to residues of carfentrazone-ethyl for non-nursing infants (<1-year old) would be 0.28% and for children 1-6 years of age would be 1.37% (the most highly exposed group). Based on the completeness and reliability of the toxicity data and the conservative exposure assessment, there is a reasonable certainty that no harm will result to infants and children from aggregate exposure to the residues of carfentrazone-ethyl including all anticipated dietary exposure. G. International Tolerances There are no Codex Alimentarius Commission (Codex) Maximum Residue Levels (MRLs) for carfentrazone-ethyl on any crops at this time. However, MRLs for small grains in Europe have been proposed which consist of carfentrazone-ethyl and carfentrazone-ethyl-chloropropionic acid. [FR Doc. 98-15177 Filed 6-9-98; 8:45 am] BILLING CODE 6560-50-F