99-14362. Notice of Filing Pesticide Petition  

  • [Federal Register Volume 64, Number 110 (Wednesday, June 9, 1999)]
    [Notices]
    [Pages 30997-31000]
    From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
    [FR Doc No: 99-14362]
    
    
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    ENVIRONMENTAL PROTECTION AGENCY
    
    [PF-876; FRL-6082-6]
    
    
    Notice of Filing Pesticide Petition
    
    AGENCY: Environmental Protection Agency (EPA).
    
    ACTION: Notice.
    
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    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-876, must 
    be received on or before July 9, 1999.
    ADDRESSES: By mail submit written comments to: Information and Records 
    Integrity Branch, Public Information and Services Division (7502C), 
    Office of Pesticides Programs, Environmental Protection Agency, 401 M 
    St., SW., Washington, DC 20460. In person bring comments to: Rm. 1132, 
    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 (CBI) should be submitted through e-mail.
        Information submitted as a comment concerning this document may be 
    claimed confidential by marking any part or all of that information as 
    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: Vera Soltero, 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. 713G, 
    Crystal Mall #2, 1921 Jefferson Davis Highway, Arlington, VA 22202, 
    (703) 308-9359; e-mail: soltero.vera@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-876] (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@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 control number (PF-876) and appropriate 
    petition number. Electronic comments on this notice may be filed online 
    at many Federal Depository Libraries.
    
    List of Subjects
    
        Environmental protection, Agricultural commodities, Feed additives, 
    Food additives, Pesticides and pests, Reporting and recordkeeping 
    requirements.
    
        Dated: May 27, 1999.
    
    James Jones,
    
    Director, Registration Division, Office of Pesticide Programs.
    
    Summaries of Petition
    
        Petitioner summary of the pesticide petition is printed below as 
    required by section 408(d)(3) of the FFDCA. The summary of the petition 
    was prepared by the petitioner and represents the views of the 
    petitioner. EPA is publishing the petition summary 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.
    
     AgrEvo USA Company
    
    PP 9E5060
    
        EPA has received a pesticide petition (9E5060) from AgrEvo USA 
    Company, Little Falls Centre One, 2711 Centerville Road, Wilmington, 
    Delaware 19808 proposing, pursuant to section 408(d) of the Federal 
    Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a(d), to amend 40 
    CFR part 180 by establishing a tolerance for residues of ethyl 5,5-
    diphenyl-2-isoxazoline-3-carboxylate (CAS 163520-33-0) herbicide 
    safener AE F122006 in or on the raw agricultural commodities (RAC) rice 
    grain at 0.05 parts per million (ppm) and rice straw
    
    [[Page 30998]]
    
    at 0.2 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 metabolism of AE F122006 (ethyl 5,5-
    diphenyl-2-isoxazoline-3-carboxylate) in rice has been investigated and 
    is understood. Total residue levels in animal and rice commodities 
    (particularly grain) were very low. The initial metabolic 
    transformation of AE F122006 in plants is hydrolysis of the prominent 
    ester function, yielding the carboxylic acid, AE F129431 (4,5-dihydro-
    5,5-diphenyl-3-isoxazolecarboxylic acid). In rice grain, the primary 
    metabolite identified was AE C637375 (-hydroxy--
    benzenepropanenitrile), which was found only in trace amounts. AE 
    F129431 and its hydroxylated analog AE F162241 (4,5-dihydro-5-(4-
    hydroxyphenyl)-5-phenyl-3-isoxazolecarboxylic acid) comprised the major 
    metabolic residues in rice straw.
        2. Analytical method. Based on the results of the metabolism 
    studies, the analytical targets selected were parent compound (AE 
    F122006), and the metabolites AE F129431, AE F162241, and AE C637375. A 
    practical analytical method utilizing capillary gas chromatography and 
    a mass spectrometer detector is available for detecting and measuring 
    levels of these residue targets. The limit of quantification (LOQ) is 
    0.02 ppm in rice grain and 0.05 ppm in rice straw.
        3. Magnitude of residues. Eighteen residue trials were conducted in 
    the major United States rice growing areas over 2-years (1996 to 1997). 
    When applied twice at a single application rate of 0.071 pound of the 
    safener per acre (80 g/ha) with the second application made at 65-days 
    before harvest, combined residues in rice grain did not exceed the LOQ 
    (0.02 ppm) with the exception of the results from one trial where the 
    residues were 0.03 and 0.04 ppm for AE F122006 and AE C637375, 
    respectively. In rice straw, the combined maximum residues did not 
    exceed 0.2 ppm. Thus, the tolerances are proposed at 0.05 ppm in rice 
    grain and 0.2 ppm in rice straw. Based on the results of the animal 
    metabolism studies, no residues are anticipated in milk, meat, and eggs 
    due to feeding rice grain or straw. Therefore, tolerances for these 
    commodities are not required.
    
    B. Toxicological Profile
    
        1. Acute toxicity. AE F122006 is slightly toxic following acute 
    oral exposure, no more than slightly toxic following acute dermal 
    exposure and practically non-toxic following acute inhalation exposure. 
    The acute rat oral LD50 of AE F122006 was 1,740 milligrams/
    kilograms (mg/kg). The acute rat dermal LD50 was greater 
    than 2,000 mg/kg and the 4-hour rat inhalation LC50 was > 5 
    milligrams per liter (mg/l). AE F122006 was slightly irritating to 
    rabbit eyes and non-irritating to rabbit skin. Based on these results, 
    AE F122006 would be classified as EPA Category III for oral and dermal 
    toxicity and eye irritation, and EPA Category IV for inhalation 
    toxicity and dermal irritation. Technical AE F122006 was shown to be a 
    dermal sensitizer in a guinea pig maximization assay, but no evidence 
    of sensitization has been observed in a Buehler assay when formulated 
    into a commercial product.
        2. Genotoxicity. No evidence of genotoxicity was noted in 
    Salmonella and E. coli reverse bacterial mutation assays, an in vitro 
    mammalian gene mutation assay in Chinese hamster lung (V79) cells, an 
    in vivo unscheduled DNA synthesis assay in rat hepatocytes, or a mouse 
    micronucleus assay. An increase in chromosomal aberrations was observed 
    in an in vitro assay in Chinese hamster lung (V79) cells, but only at 
    toxic concentrations. Thus, the overall weight of evidence indicates 
    that AE F122006 does not possess significant genotoxic activity.
        3. Reproductive and developmental toxicity. A rat developmental 
    toxicity study was conducted at dose levels of 0, 15, 120, and 1,000 
    mg/kg/day. Maternal toxicity (including one death) was noted at 1,000 
    mg/kg/day. Slight developmental toxicity (an increase in resorptions) 
    but no evidence of teratogenicity was also noted at this level. No 
    effects were noted at 120 mg/kg/day, which was considered to be the no-
    observed adverse effect level (NOAEL) for both maternal and 
    developmental toxicity.
        A rabbit developmental toxicity study was conducted at dose levels 
    of 0, 5, 50, and 500 mg/kg/day. Maternal effects at 500 mg/kg/day 
    consisted of decreased food consumption, slight weight loss during 
    gestation days 6-8, and one death. In addition, one animal at 500 mg/
    kg/day had only two empty implantation sites. No evidence of 
    teratogenicity or developmental toxicity was noted. Thus, 50 mg/kg/day 
    was considered to be the NOAEL for maternal toxicity while 500 mg/kg/
    day was the NOAEL for developmental effects.
        Although generally not a prerequisite for the establishment of 
    tolerances for an inert safener, a 2-generation rat reproduction study 
    with AE F122006 is in progress. In this study, AE F122006 was 
    administered at dietary concentrations of 0, 20, 200, and 4,000 ppm. 
    Although histopathology is still in progress, the preliminary results 
    from the in-life data indicate that the NOAEL will likely be 200 ppm, 
    based on decreased body weight (bwt) gain in both adults and weanlings 
    (beginning at day 21) at 4,000 ppm. No reproductive effects have been 
    observed at any dose level.
        4. Subchronic toxicity. In a 90-day rat feeding study, AE F122006 
    was administered at dietary concentrations of 0, 20, 200, 2,000, and 
    4,000 ppm. The NOAEL for this study was considered to be 200 ppm 
    (approximately 15.3 mg/kg/day) based on decreased weight gain at 2,000 
    ppm, and decreased weight gain, increased liver weights, and 
    centrilobular hepatocyte enlargement at 4,000 ppm.
        In a 90-day feeding study in mice, AE F122006 was administered at 
    dietary concentrations of 13, 125, 1,250, and 2,500 ppm. Decreased 
    kidney weights, increased liver weights, and histopathological changes 
    in the liver (centrilobular hepatocyte enlargement and vacuolation) 
    were noted at 1,250, and 2,500 ppm. The NOAEL for this study was 125 
    ppm (approximately 23 mg/kg/day).
        In a 90-day dog feeding study, AE F122006 was administered to 
    beagle dogs at dietary concentrations of 0, 25, 125, and 1,000 ppm. The 
    NOAEL for this study was considered to be 25 ppm (approximately 1.3 mg/
    kg/day) based on slight histopathological effects in the kidneys at 125 
    ppm, and effects on the kidneys, spleen, liver, heart, and intestines 
    at 1,000 ppm.
        5. Chronic toxicity. Long-term studies in rats, mice, and dogs have 
    not yet been completed. However, these studies are generally not a 
    prerequisite to the establishment of tolerances for inert safeners, and 
    no preneoplastic lesions were observed in any of the 90-day studies. 
    Furthermore, AE F122006 is not closely related to any known human or 
    animal oncogen, and a structure activity assessment revealed no 
    structural alerts for oncogenicity.
        6. Animal metabolism. AE F122006 was well absorbed and rapidly 
    metabolized and excreted when administered to rats as a single oral 
    dose in sesame oil. AE F122006 was poorly absorbed in dogs when 
    administered as a single oral dose in 1% gum tragacanth.
    
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     A 2-fold increase in absorption was noted in dogs when administered 
    via the diet. The primary metabolite in both rats and dogs was the 
    carboxylic acid, AE F129431, which is the same as observed in plants.
        The metabolism of AE F122006 in ruminants is adequately understood. 
    A dairy cow was dosed with the compound at a level equivalent to 10 ppm 
    in the diet for 7 days. Total residue levels were very low. Parent 
    compound was seen in fats and milk only. The carboxylic acid, AE 
    F129431, was the major metabolite identified in all of the tissues, 
    with traces also being found in the milk.
        The metabolism of AE F122006 in poultry is also adequately 
    understood. Laying hens were fed the compound at a level equivalent to 
    10 ppm in the diet for 14 days. Residue levels were low in all 
    commodities. The vast majority of the dose was excreted as AE F129431, 
    with smaller amounts of AE F162241 and AE F122006. AE F129431 was the 
    major metabolite identified in all of the tissues and yolks. Trace 
    amounts of AE F122006 and AE F162241 were detected in liver and eggs 
    with AE F122006 also being detected in the muscle.
        7. Endocrine disruption. No special studies have been conducted to 
    investigate the potential of AE F122006 to induce estrogenic or other 
    endocrine effects. However, no evidence of estrogenic or other 
    endocrine effects have been noted in any of the standard toxicology 
    studies that have been conducted with this product, and there is no 
    reason to suspect that any such effects would be likely.
    
    C. Aggregate Exposure
    
        1. Dietary exposure. AE F122006 will be used only as a herbicide 
    safener and, at this time, only for use on rice. No non-agricultural 
    uses are anticipated. Thus, the only potential sources of non-
    occupational exposure to AE F122006 would consist of any potential 
    residues in food and drinking water. As previously indicated, in the 
    absence of any acute toxicity concerns, only chronic exposures have 
    been evaluated.
        i. Food. AE F122006 is being proposed for use only in rice. In the 
    animal metabolism studies with ruminants and poultry, the concentration 
    of AE F122006 and its metabolites in the edible tissues, milk and eggs 
    were very low. Based on these results, no secondary residues of AE 
    F122006 are expected in meat, milk and eggs as a result of using AE 
    F122006 treated rice and/or rice commodities as animal feed. Thus, only 
    potential exposures from direct human consumption of rice containing 
    residues of AE F122006 were evaluated.
        The potential dietary exposures from consumption of treated rice 
    have been assessed using the Exposure 1 software system (TAS, Inc.) and 
    the 1977-78 USDA food consumption data. Two different dietary exposure 
    scenarios were evaluated. In the first, worst-case scenario, it was 
    assumed that 100% of the rice consumed contained residues of AE F122006 
    at the proposed tolerance level of 0.05 ppm. However, it is anticipated 
    that AE F122006 would be used on no more than 10% of the rice grown in 
    the United States. Furthermore, rice is a nationally distributed crop. 
    Rice treated with AE F122006 would be mixed in grain elevators and 
    processing plants with other rice which was not treated with this 
    product. Thus, a second, more realistic scenario assumed that only 10% 
    of the commodities consumed contained residues of AE F122006, but that 
    these residues remained at the proposed tolerance level of 0.05 ppm.
        ii. Drinking water. The potential for AE F122006 and its main acid 
    metabolite AE F129431 to leach into ground water and reach surface 
    water has been assessed in various laboratory studies. These studies 
    clearly demonstrate that both compounds are rapidly degraded in the 
    environment. AE F122006 is rapidly hydrolyzed in soil (half-life = 0.1-
    day) to AE F129431 which is further metabolized to carbon dioxide and 
    soil bound residue (half-life = 6.5 days).
        A screening evaluation of worst-case shallow ground water 
    concentration was conducted using the EPA model SCIGROW and a simple 
    calculation of worst-case long-term surface water concentrations 
    following use in rice paddies. The results indicate that both compounds 
    (parent and its primary degradate) will not contaminate shallow ground 
    water or surface water. Concentrations of AE F122006 and its primary 
    degradate, AE F129431 in ground or surface water were calculated to be 
    < 0.01="" ppb.="" potential="" residues="" in="" drinking="" water="" would="" be="" even="" lower.="" since="" the="" contribution="" of="" any="" potential="" residues="" of="" ae="" f122006="" in="" water="" to="" the="" total="" dietary="" intake="" of="" ae="" f122006="" would="" be="" negligible,="" these="" values="" were="" not="" included="" in="" the="" dietary="" exposure="" assessment.="" d.="" cumulative="" effects="" there="" is="" no="" information="" to="" indicate="" that="" ae="" f122006="" may="" share="" a="" common="" mechanism="" of="" toxicity="" with="" any="" other="" chemical.="" thus,="" this="" assessment="" was="" limited="" strictly="" to="" ae="" f122006.="" e.="" safety="" determination="" 1.="" u.s.="" population.="" no="" acute="" toxicity="" concerns="" were="" noted="" in="" either="" the="" acute="" toxicity="" studies="" or="" the="" developmental="" toxicity="" studies="" in="" rats="" or="" rabbits.="" since="" an="" acute="" toxicology="" endpoint="" has="" not="" been="" identified,="" an="" acute="" risk="" assessment="" with="" ae="" f122006="" is="" not="" necessary="" and="" has="" not="" been="" conducted.="" long-term="" studies="" in="" rats,="" mice="" and="" dogs,="" although="" generally="" not="" a="" prerequisite="" for="" issuance="" of="" tolerances="" for="" inert="" safeners,="" have="" not="" yet="" been="" completed.="" based="" on="" the="" subchronic="" toxicity="" data,="" it="" appears="" that="" the="" dog="" is="" the="" species="" most="" sensitive="" to="" ae="" f122006.="" therefore,="" a="" provisional="" rfd="" (adi)="" of="" 0.0013="" mg/kg/day="" has="" been="" proposed="" by="" using="" the="" noael="" of="" 1.3="" mg/kg/day="" from="" the="" 90-day="" dog="" study="" and="" a="" 1,000-fold="" (rather="" than="" 100-fold)="" margin="" of="" safety.="" the="" extra="" ten-fold="" safety="" factor="" is="" used="" to="" account="" for="" the="" fact="" that="" the="" rfd="" is="" calculated="" from="" the="" noael="" of="" a="" subchronic="" rather="" than="" chronic="" toxicity="" study.="" although="" there="" is="" no="" indication="" or="" expectation="" of="" any="" oncogenic="" effect="" from="" ae="" f122006,="" a="" worst-case="" q1*="" can="" be="" estimated="" based="" on="" the="" potential="" worst-case="" results="" from="" the="" ongoing="" rodent="" oncogenicity="" studies.="" using="" the="" linearized="" multistage="" model="" with="" hypothetical="" worst-="" case="" tumor="" responses="" from="" the="" ongoing="" studies,="" a="" hypothetical="" worst-="" case="" q1*="" was="" calculated="" to="" be="" 1.2="" x="">2 (mg/kg/day)-
    1. This hypothetical Q1* can be used to generate an upper 
    bound on any potential oncogenic risk that might result from exposure 
    to AE F122006.
        Under the most conservative, worst-case scenario, in which it is 
    assumed that all rice commodities contain residues of AE F122006 at the 
    proposed tolerance level, the potential exposures to the ``General U.S. 
    Population'' and the most highly exposed adult subgroup, ``Non-Hispanic 
    other Than Black or White,'' would utilize about 0.7% and 3.2%, 
    respectively, of the proposed provisional RfD. In a more realistic 
    scenario, in which the treated rice is assumed to represent only 10% of 
    the rice consumed in the United States and is assumed to be blended 
    with non-treated rice prior to consumption, the potential exposures to 
    the ``General U.S. Population'' and ``Non-Hispanic Other Than Black or 
    White'' subgroup would utilize about 0.1% and 0.3% of the proposed 
    provisional RfD, respectively. For chronic exposures, there is 
    generally no concern for exposures below 100% of the RfD because the 
    RfD represents the level at or below which daily exposure over a 
    lifetime would not pose
    
    [[Page 31000]]
    
    appreciable risks to human health. Therefore, these dietary exposures 
    clearly would not pose a significant risk to the health of the overall 
    U.S. population.
        As previously indicated, there is no indication that AE F122006 is 
    likely to be oncogenic. Nevertheless, an upper bound on the potential 
    oncogenic risks was estimated using the hypothetical Q1* of 1.2 x 10-
    2 (mg/kg/day)-1. Under the worst-case scenario in 
    which all rice contained tolerance level residues of AE F122006, the 
    theoretical 95% upper bound estimates of potential oncogenic risk for 
    the overall ``U.S. Population'' and ``Non-Hispanic Other Than Black or 
    White'' subgroup would be 1 x 10-7 and 5 x 10-7, 
    respectively. Taking into account the expected market share of AE 
    F122006, the upper bounds on the potential oncogenic risks for these 2 
    groups would be 1 x 10-8 and 5 x 10-8, 
    respectively. Thus, regardless of the outcome of the ongoing 
    oncogenicity studies, the potential oncogenic risks to the overall U.S. 
    population from dietary exposure to AE F122006 following its use in 
    rice are clearly negligible.
        2. Infants and children. Data from rat and rabbit developmental 
    toxicity studies and rat multigeneration reproduction studies are 
    generally used to assess the potential for increased sensitivity of 
    infants and children. The developmental toxicity studies are designed 
    to evaluate adverse effects on the developing organism resulting from 
    potential exposure during prenatal development. Reproduction studies 
    provide information relating to reproductive and other effects on 
    adults and offspring from potential prenatal and postnatal exposure to 
    the pesticide.
        FFDCA section 408 provides that EPA may apply an additional safety 
    factor for infants and children to take into account possible increased 
    sensitivity or based upon the completeness of the data base. No 
    evidence of increased sensitivity to fetuses was noted in developmental 
    toxicity studies in rats or rabbits. Although histopathology 
    examinations from the 2-generation rat reproduction study have not yet 
    been completed, there has been no indication of any reproductive 
    effects or indication of increased sensitivity to the offspring. 
    Furthermore, the proposed provisional RfD of 0.0013 mg/kg/day (which is 
    derived from the NOAEL from the 90-day dog study and a 1,000-fold 
    safety factor) is about 1,000-fold lower than the tentative (pending 
    histopathology) NOAEL of 200 ppm (about 15 mg/kg/day) in the 
    reproduction study. Thus, no additional safety factor to protect 
    infants and children is deemed necessary.
        According to the results of the dietary assessment, the population 
    subgroup with the highest potential exposures to AE F122006 under 
    scenarios previously described would be non-nursing infants (<1-year old).="" in="" the="" first,="" worst-case="" scenario,="" in="" which="" all="" rice="" and="" rice="" commodities="" contained="" residues="" of="" ae="" f122006="" at="" the="" proposed="" tolerance="" levels,="" the="" potential="" dietary="" exposure="" to="" ae="" f122006="" would="" utilize="" 4.5%="" of="" the="" proposed="" provisional="" rfd.="" taking="" into="" account="" the="" fact="" that="" less="" than="" 10%="" of="" the="" rice="" consumed="" will="" be="" treated="" with="" ae="" f122006,="" the="" potential="" exposure="" to="" infants="" and="" children="" would="" utilize="" no="" more="" than="" 0.5%="" of="" the="" proposed="" provisional="" rfd.="" these="" values="" are="" substantially="" below="" the="" rfd="" and="" therefore="" would="" not="" pose="" an="" appreciable="" risk="" to="" human="" health.="" regardless="" of="" the="" outcome="" of="" the="" ongoing="" oncogenicity="" studies,="" the="" hypothetical="" upper="" bound="" estimate="" of="" potential="" oncogenic="" risk="" to="" infants="" and="" children="" under="" the="" worst-case="" exposure="" scenario="" was="" estimated="" to="" be="" approximately="" 7="" x="">7. Under the more 
    realistic scenario incorporating percent crop treated, the potential 
    upper bound estimate of oncogenic risk would be no more than 7 x 10-
    8. Thus, even under a worst-case scenario, the use of AE 
    F122006 on rice would pose no more than a negligible risk of 
    oncogenicity to infants and children.
    
    F. International Tolerances
    
        There are no Codex Alimentarius Commission (CODEX) maximum residue 
    levels (MRLs) established for residues of AE F122006.
    [FR Doc. 99-14362 Filed 6-8-99; 8:45 am]
    BILLING CODE 6560-50-F
    
    
    

Document Information

Published:
06/09/1999
Department:
Environmental Protection Agency
Entry Type:
Notice
Action:
Notice.
Document Number:
99-14362
Dates:
Comments, identified by the docket control number PF-876, must be received on or before July 9, 1999.
Pages:
30997-31000 (4 pages)
Docket Numbers:
PF-876, FRL-6082-6
PDF File:
99-14362.pdf