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Tebufenozide - Pesticide Petition Filing for Brassica Crops 2/99


[Federal Register: February 18, 1999 (Volume 64, Number 32)]
[Notices]
[Page 8090-8102]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr18fe99-67]

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ENVIRONMENTAL PROTECTION AGENCY
[PF-859; FRL-6059-9]
Notice of Filing of Pesticide Petitions
AGENCY: Environmental Protection Agency (EPA).
ACTION: Notice.

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SUMMARY: This notice announces the initial filing of pesticide
petitions proposing the establishment of regulations for residues of
certain pesticide chemicals in or on various food commodities.

DATES: Comments, identified by the docket control number PF-859, must
be received on or before March 22, 1999.

ADDRESSES: By mail submit written comments to: Public Information and
Records Integrity Branch, Information Resources 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 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
"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: The product manager listed in the
table below:

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                                   Office location/
        Product Manager            telephone number          Address
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Melody A. Banks (PM 03).......  Rm. 205, CM #2, 703-    1921 Jefferson
                                 305-5413, e-            Davis Hwy,
                                 mail:banks.melody@epa   Arlington, VA
                                 mail.epa.gov.
Joseph M. Tavano..............  Rm. 214, CM #2, 703-    Do.
                                 305-6411, e-mail:
                                 tavano.joseph@epamail
                                 .epa.gov.
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[[Page 8091]]

SUPPLEMENTARY INFORMATION: EPA has received pesticide petitions as
follows proposing the establishment and/or amendment of regulations for
residues of certain pesticide chemicals 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 these petitions
contain 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-859] (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 (insert docket number) 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, Food additives,
Feed additives, Pesticides and pests, Reporting and recordkeeping
requirements.

    Dated: February 10, 1999.

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.

2. Rohm and Haas Company

PP 7F4824

    EPA has received a revised pesticide petition (7F4824) from Rohm
and Haas Company, 100 Independence Mall West, Philadelphia, PA
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

[[Page 8097]]

180 by establishing a tolerance for residues of tebufenozide benzoic
acid, 3,5-dimethyl-,1-(1,1-dimethylethyl)-2-(4-ethylbenzoyl) hydrazide
in or on the raw agricultural commodity crop subgroup leafy greens,
crop subgroup leaf petioles, crop subgroup head and stem Brassica and
crop subgroup leafy Brassica greens at 10.0, 2.0, 5.0, and 10.0 parts
per million (ppm) respectively. 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 tebufenozide in plants
(grapes, apples, rice, and sugar beets) is adequately understood for
the purpose of this tolerance. The metabolism of tebufenozide in all
crops was similar and involves oxidation of the alkyl substituents of
the aromatic rings primarily at the benzylic positions. The extent of
metabolism and degree of oxidation are a function of time from
application to harvest. In all crops, parent compound comprised the
majority of the total dosage. None of the metabolites were in excess of
10% of the total dosage.
    2. Analytical method. A high performance liquid chromatographic
(HPLC) analytical method using ultraviolet (UV) or mass spectrometry
(MS) detection has been validated for leafy and cole crop vegetables.
For all matrices, the methods involve extraction by blending with
solvents, purification of the extracts by liquid-liquid partitions and
final purification of the residues using solid phase extraction column
chromatography. The limit of quantitation (LOQ) of the method is 0.01
part per million (ppm) for all representative crops of these crop
subgroups except for celery which is 0.05 ppm.
    3. Magnitude of residues. Magnitude of the residue studies were
conducted in celery, and mustard greens using the maximum proposed
label rate. Samples were collected 7 days after the last application
and were analyzed for residues of tebufenozide. The residue data
support a tolerance of 5.0 ppm for the crop subgroup leaf petioles
(4A), and 10.0 ppm for the crop subgroup Leafy Brassica Green
Vegetables (5B).

B. Toxicological Profile

    1. Acute toxicity. Acute toxicity studies with technical grade:
Oral LD50 in the rat is > 5 grams for males and females -
Toxicity Category IV; dermal LD50 in the rat is = 5,000
milligram/kilogram (mg/kg) for males and females - Toxicity Category
III; inhalation LC50 rat is > 4.5 mg/l - Toxicity Category
III; primary eye irritation study in the rabbit is a non-irritant;
primary skin irritation in the rabbit > 5 mg - Toxicity Category IV.
Tebufenozide is not a sensitizer.
    2. Genotoxicty. Several mutagenicity tests which were all negative.
These include an Ames assay with and without metabolic activation, an
in vivo cytogenetic assay in rat bone marrow cells, and in vitro
chromosome aberration assay in CHO cells, a CHO/HGPRT assay, a reverse
mutation assay with E. Coli, and an unscheduled DNA synthesis assay
(UDS) in rat hepatocytes.
    3. Reproductive and developmental toxicity. In a prenatal
developmental toxicity study in Sprague-Dawley rats 25/group,
tebufenozide was administered on gestation days 6-15 by gavage in
aqueous methyl cellulose at dose levels of 50, 250, or 1,000 mg/kg/day,
and a dose volume of 10 ml/kg. There was no evidence of maternal or
developmental toxicity; the maternal and developmental toxicity no-
observed adverse effect level (NOAEL) was 1,000 mg/kg/day.
    In a prenatal developmental toxicity study conducted in New Zealand
white rabbits 20/group, tebufenozide was administered in 5 ml/kg of
aqueous methyl cellulose at gavage doses of 50, 250, or 1,000 mg/kg/day
on gestation days 7-19. No evidence of maternal or developmental
toxicity was observed; the maternal and developmental toxicity NOAEL
was 1,000 mg/kg/day.
    In a 1993 2-generation reproduction study in Sprague-Dawley rats
tebufenozide was administered at dietary concentrations of 0, 10, 150,
or 1,000 ppm (0, 0.8, 11.5, or 154.8 mg/kg/day for males, and 0, 0.9,
12.8, or 171.1 mg/kg/day for females). The parental systemic NOAEL was
10 ppm (0.8/0.9 mg/kg/day for males and females, respectively), and the
lowest-observed adverse effect level (LOAEL) was 150 ppm (11.5/12.8 mg/
kg/day for males and females, respectively) based on decreased body
weight, body weight gain, and food consumption in males, and increased
incidence and/or severity of splenic pigmentation. In addition, there
was an increased incidence and severity of extramedullary hematopoiesis
at 2,000 ppm. The reproductive NOAEL was 150 ppm. (11.5/12.8 mg/kg/day
for males and females, respectively), and the LOAEL was 2,000 ppm
(154.8/171.1 mg/kg/day for males and females, respectively) based on an
increase in the number of pregnant females with increased gestation
duration and dystocia. Effects in the offspring consisted of decreased
number of pups per litter on postnatal days 0 and/or 4 at 2,000 ppm
(154.8/171.1 mg/kg/day for males and females, respectively) with a
NOAEL of 150 ppm (11.5/12.8 mg/kg/day for males and females,
respectively).
    In a 1995 2-generation reproduction study in rats, tebufenozide was
administered at dietary concentrations of 0, 25, 200, or 2,000 ppm (0,
1.6, 12.6, or 126.0 mg/kg/day for males, and 0, 1.8, 14.6, or 143.2 mg/
kg/day for females). For parental systemic toxicity, the NOAEL was 25
ppm (1.6/1.8 mg/kg/day in males and females, respectively), and the
LOAEL was 200 ppm (12.6/14.6 mg/kg/day in males, and females), based on
histopathological findings (congestion and extramedullary
hematopoiesis) in the spleen. Additionally, at 2,000 ppm (126.0/143.2
mg/kg/day in M/F), treatment-related findings included reduced parental
body weight gain and increased incidence of hemosiderin-laden cells in
the spleen. Columnar changes in the vaginal squamous epithelium and
reduced uterine and ovarian weights were also observed at 2,000 ppm,
but the toxicological significance was unknown. For offspring, the
systemic NOAEL was 200 ppm. (12.6/14.6 mg/kg/day in males, and
females), and the LOAEL was 2,000 ppm (126.0/143.2 mg/kg/day in M/F)
based on decreased body weight on postnatal days 14 and 21.
    4. Subchronic toxicity. In a prenatal developmental toxicity study
in Sprague-Dawley rats 25/group, tebufenozide was administered on
gestation days 6-15 by gavage in aqueous methyl cellulose at dose
levels of 50, 250, or 1,000 mg/kg/day and a dose volume of 10 ml/kg.
There was no evidence of maternal or developmental toxicity; the
maternal and developmental toxicity NOAEL was 1,000 mg/kg/day.
    5. Chronic toxicity. A 1 year dog feeding study with a LOAEL of 250
ppm, 9 mg/kg/day for male and female dogs based on decreases in RBC,
HCT, and HGB, increases in Heinz bodies, methemoglobin, MCV, MCH,
reticulocytes, platelets, plasma total bilirubin, spleen weight, and
spleen/body weight ratio, and liver/body weight ratio. Hematopoiesis
and sinusoidal engorgement occurred in the spleen, and hyperplasia
occurred in the marrow of the femur and sternum. The

[[Page 8098]]

liver showed an increased pigment in the Kupffer cells. The NOAEL for
systemic toxicity in both sexes is 50 ppm (1.9 mg/kg/day).
    An 18 month mouse carcinogenicity study with no carcinogenicity
observed at dosage levels up to and including 1,000 ppm.
     A 2 year rat carcinogenicity with no carcinogenicity observed at
dosage levels up to and including 2,000 ppm (97 mg/kg/day and 125 mg/
kg/day for males and females, respectively).
    6. Animal metabolism. The adsorption, distribution, excretion and
metabolism of tebufenozide in rats was investigated. Tebufenozide is
partially absorbed, is rapidly excreted and does not accumulate in
tissues. Although tebufenozide is mainly excreted unchanged, a number
of polar metabolites were identified. These metabolites are products of
oxidation of the benzylic ethyl or methyl side chains of the molecule.
These metabolites were detected in plant and other animal (rat, goat,
hen) metabolism studies.
    7. Metabolite toxicology. Common metabolic pathways for
tebufenozide have been identified in both plants (grape, apple, rice,
and sugar beet), and animals (rat, goat, hen). The metabolic pathway
common to both plants and animals involves oxidation of the alkyl
substituents (ethyl and methyl groups) of the aromatic rings primarily
at the benzylic positions. Extensive degradation and elimination of
polar metabolites occurs in animals such that residue are unlikely to
accumulate in humans or animals exposed to these residues through the
diet.
    8. Endocrine disruption. The toxicology profile of tebufenozide
shows no evidence of physiological effects characteristic of the
disruption of the hormone estrogen. Based on structure-activity
information, tebufenozide is unlikely to exhibit estrogenic activity.
Tebufenozide was not active in a direct in vitro estrogen binding
assay. No indicators of estrogenic or other endocrine effects were
observed in mammalian chronic studies or in mammalian and avian
reproduction studies. Ecdysone has no known effects in vertebrates.
Overall, the weight of evidence provides no indication that
tebufenozide has endocrine activity in vertebrates.

C. Aggregate Exposure

    1. Dietary exposure--i. Food. Tolerances have been established (40
CFR 180.482) for the residues of tebufenozide, in or on walnuts at 0.1
ppm, apples at 1.0 ppm, pecans at 0.01 ppm and wine grapes at 0.5 ppm.
Numerous section 18 tolerances have been established at levels ranging
from 0.3 ppm in sugar beet roots to 5.0 ppm in turnip tops. Other
tolerance petitions are pending at EPA with proposed tolerances ranging
from 0.3 ppm in or on sugarcane to 10 ppm in cole crop vegetables. Risk
assessments were conducted by Rohm and Haas to assess dietary exposures
and risks from tebufenozide, benzoic acid, 3,5-dimethyl-1-(1,1-
dimethylethyl)-2-(4-ethylbenzoyl) hydrazide as follows:
    ii. Acute exposure and risk. Acute dietary risk assessments are
performed for a food-use pesticide if a toxicological study has
indicated the possibility of an effect of concern occurring as a result
of a 1 day or single exposure. Toxicity observed in oral toxicity
studies were not attributable to a single dose (exposure). No neuro or
systemic toxicity was observed in rats given a single oral
administration of tebufenozide at 0, 500, 1,000 or 2,000 mg/kg. No
maternal or developmental toxicity was observed following oral
administration of tebufenozide at 1,000 mg/kg/day (Limit-Dose) during
gestation to pregnant rats or rabbits. This risk is considered to be
negligible.
    iii. Chronic exposure and risk. The RfD used for the chronic
dietary analysis is 0.018 mg/kg/day. In conducting this exposure
assessment, Rohm and Haas has made very conservative assumptions 100%
of pecans, walnuts, wine and sherry, pome fruit, and all other
commodities having tebufenozide tolerances or pending tolerances will
contain tebufenozide residues, and those residues would be at the level
of the tolerance which result in an over estimate of human dietary
exposure. Thus, in making a safety determination for this tolerance,
Rohm and Haas is taking into account this conservative exposure
assessment. Using the Dietary Exposure Evaluation Model (Version 5.03b,
licensed by Novigen Sciences Inc.) which uses USDA food consumption
data from the 1989-1992 survey and the appropriate concentration or
reduction factors, the existing tebufenozide tolerances published,
pending, and including the necessary section 18 tolerance(s) resulted
in a Theoretical Maximum Residue Contribution (TMRC) that is equivalent
to the following percentages of the RfD:
    U.S. Population (35.8% of RfD);
    Northeast Region (37.5% of RfD);
    Western Region (39.8%);
    Pacific Region (40.9%)All Infants (<1 year) (36.3%);
    Nursing Infants (<1 year old) (16.8% of RfD);
    Non-Nursing Infants (<1 year old) (44.5% of RfD);
    Children (1-6 years old) (61.9% of RfD);
    Children (7-12 years old) (45.6% of RfD);
    Females (13 + years old, nursing) (30.6% of RfD);
    Non-Hispanic Whites (36.0%);
    Non-Hispanic Other than Black or White (43.1% of RfD).
    The subgroups listed above are subgroups for which the percentage
of the RfD occupied is greater than that occupied by the subgroup U.S.
population (48 States).
    iv. Drinking water-- Acute exposure and risk. Because no acute
dietary endpoint was determined, Rohm and Haas concludes that there is
a reasonable certainty of no harm from acute exposure from drinking
water.
    v. Chronic exposure and risk. Submitted environmental fate studies
suggest that tebufenozide is moderately persistent to persistent and
mobile. Under certain conditions tebufenozide appears to have the
potential to contaminate ground and surface water through runoff and
leaching; subsequently potentially contaminating drinking water. There
are no established Maximum Contaminant Levels (MCL) for residues of
tebufenozide in drinking water and no Health Advisories (HA) have been
issued for tebufenozide therefore, these could not be used as
comparative values for risk assessment. Therefore, potential residue
levels for drinking water exposure were calculated using GENEEC
(surface water) and SCIGROW (ground water) for human health risk
assessment. Because of the wide range of half-life values (66-729 days)
reported for the aerobic soil metabolism input parameter a range of
potential exposure values were calculated. In each case the worst case
upper bound exposure limits were then compared to appropriate chronic
drinking water level of concern (DWLOC). In each case the calculated
exposures based on model data were below the DWLOC.
    2. Non-dietary exposure. Tebufenozide is not currently registered
for use on any residential non-food sites. Therefore, there is no
chronic, short- or intermediate-term exposure scenario.

D. Cumulative Effects

    Section 408(b)(2)(D)(v) requires that, when considering whether to
establish, modify, or revoke a tolerance, the Agency consider
"available information" concerning the cumulative effects of a
particular pesticide's residues and "other substances that have a
common mechanism of toxicity." The Agency believes that "available

[[Page 8099]]

information" in this context might include not only toxicity,
chemistry, and exposure data, but also scientific policies and
methodologies for understanding common mechanisms of toxicity and
conducting cumulative risk assessments. For most pesticides, although
the Agency has some information in its files that may turn out to be
helpful in eventually determining whether a pesticide shares a common
mechanism of toxicity with any other substances, EPA does not at this
time have the methodologies to resolve the complex scientific issues
concerning common mechanism of toxicity in a meaningful way. EPA has
begun a pilot process to study this issue further through the
examination of particular classes of pesticides. The Agency hopes that
the results of this pilot process will increase the Agency's scientific
understanding of this question such that EPA will be able to develop
and apply scientific principles for better determining which chemicals
have a common mechanism of toxicity and evaluating the cumulative
effects of such chemicals. The Agency anticipates, however, that even
as its understanding of the science of common mechanisms increases,
decisions on specific classes of chemicals will be heavily dependent on
chemical specific data, much of which may not be presently available.
    Although at present the Agency does not know how to apply the
information in its files concerning common mechanism issues to most
risk assessments, there are pesticides as to which the common mechanism
issues can be resolved. These pesticides include pesticides that are
toxicologically dissimilar to existing chemical substances (in which
case the Agency can conclude that it is unlikely that a pesticide
shares a common mechanism of activity with other substances) and
pesticides that produce a common toxic metabolite (in which case common
mechanism of activity will be assumed).
    EPA does not have, at this time, available data to determine
whether tebufenozide, benzoic acid, 3,5-dimethyl-1-(1,1-dimethylethyl)-
2-(4-ethylbenzoyl) hydrazide has a common mechanism of toxicity with
other substances or how to include this pesticide in a cumulative risk
assessment. Unlike other pesticides for which EPA has followed a
cumulative risk approach based on a common mechanism of toxicity,
tebufenozide, benzoic acid, 3,5-dimethyl-1-(1,1-dimethylethyl)-2-(4-
ethylbenzoyl) hydrazide does not appear to produce a toxic metabolite
produced by other substances. For the purposes of this tolerance
action, therefore, Rohm and Haas has not assumed that tebufenozide,
benzoic acid, 3,5-dimethyl-1-(1,1-dimethylethyl)-2-(4-ethylbenzoyl)
hydrazide has a common mechanism of toxicity with other substances.

E. Safety Determination

    1. U.S. population. Using the conservative exposure assumptions
described above, and taking into account the completeness and
reliability of the toxicity data, Rohm and Haas has concluded that
dietary (food only) exposure to tebufenozide will utilize 35.8% of the
RfD for the U.S. population. Submitted environmental fate studies
suggest that tebufenozide is moderately persistent to persistent and
mobile; thus, tebufenozide could potentially leach to ground water and
runoff to surface water under certain environmental conditions. The
modeling data for tebufenozide indicate levels less than OPP's DWLOC.
EPA generally has no concern for exposures below 100% of the RfD
because the RfD represents the level at or below which daily aggregate
dietary exposure over a lifetime will not pose appreciable risks to
human health. There are no registered residential uses of tebufenozide.
Since there is no potential for exposure to tebufenozide from
residential uses, Rohm and Haas does not expect the aggregate exposure
to exceed 100% of the RfD.
     Short- and intermediate-term risk. Short- and intermediate-term
aggregate exposure takes into account chronic dietary food and water
(considered to be a background exposure level) plus indoor and outdoor
residential exposure. Since there are currently no registered indoor or
outdoor residential non-dietary uses of tebufenozide and no short- or
intermediate-term toxic endpoints, short- or intermediate-term
aggregate risk does not exist.
    Since, tebufenozide has been classified as a Group E, "no evidence
of carcinogenicity for humans," this risk does not exist.
    2. Infants and children. In assessing the potential for additional
sensitivity of infants and children to residues of tebufenozide, data
from developmental toxicity studies in the rat and rabbit, and two 2-
generation reproduction studies in the rat are considered. The
developmental toxicity studies are designed to evaluate adverse effects
on the developing organism resulting from pesticide exposure during
prenatal development to one or both parents. Reproduction studies
provide information relating to effects from exposure to the pesticide
on the reproductive capability of mating animals and data on systemic
toxicity. Developmental toxicity was not observed in developmental
studies using rats and rabbits. The NOAEL for developmental effects in
both rats and rabbits was 1,000 mg/kg/day, which is the limit dose for
testing in developmental studies.
    In the 2-generation reproductive toxicity study in the rat, the
reproductive/developmental toxicity NOAEL of 12.1 mg/kg/day was 14-fold
higher than the parental (systemic) toxicity NOAEL (0.85 mg/kg/day).
The reproductive (pup) LOAEL of 171.1 mg/kg/day was based on a slight
increase in both generations in the number of pregnant females that
either did not deliver or had difficulty and had to be sacrificed. In
addition, the length of gestation increased and implantation sites
decreased significantly in F1 dams. These effects were not replicated
at the same dose in a second 2-generation rat reproduction study. In
this second study, reproductive effects were not observed at 2,000 ppm
(the NOAEL equal to 149-195 mg/kg/day), and the NOAEL for systemic
toxicity was determined to be 25 ppm (1.9-2.3 mg/kg/day).
    Because these reproductive effects occurred in the presence of
parental (systemic) toxicity and were not replicated at the same doses
in a second study, these data do not indicate an increased pre-natal or
post-natal sensitivity to children and infants (that infants and
children might be more sensitive than adults) to tebufenozide exposure.
FFDCA section 408 provides that EPA shall 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
data base unless EPA concludes that a different margin of safety is
appropriate. Based on current toxicological data discussed above, an
additional uncertainty factor is not warranted and the RfD at 0.018 mg/
kg/day is appropriate for assessing aggregate risk to infants and
children. Rohm and Haas concludes that there is a reasonable certainty
that no harm will occur to infants and children from aggregate exposure
to residues of tebufenozide.

F. International Tolerances

    There are no approved CODEX maximum residue levels (MRLs)
established for residues of tebufenozide. (Melody Banks)

[[Page 8100]]

[FR Doc. 99-4023 Filed 2-17-99; 8:45 am]
BILLING CODE 6560-50-F