[Federal Register Volume 63, Number 121 (Wednesday, June 24, 1998)]
[Rules and Regulations]
[Pages 34310-34318]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-16822]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-300675; FRL 5796-9]
RIN 2070-AB78


Tebufenozide; Benzoic Acid, 3,5-dimethyl-1-(1,1-dimethylethyl)-2-
(4-ethylbenzoyl) hydrazide

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes tolerances for residues of 
tebufenozide in or on pecans and grapes, wine and a time-limited 
tolerance for residues of tebufenozide in or on pears. The time-limited 
tolerance for pears is being established to allow the use of 
tebufenozide on pears under an Experimental Use Permit. Rohm and Haas 
Company requested these tolerances under the Federal Food, Drug, and 
Cosmetic Act (FFDCA), as amended by the Food Quality Protection Act of 
1996 (Pub. L. 104-170).

DATES: This regulation is effective June 24, 1998. Objections and 
requests for hearings must be received by EPA on or before August 24, 
1998.

ADDRESSES: Written objections and hearing requests, identified by the 
docket control number, [OPP-300675], must be submitted to: Hearing 
Clerk (1900), Environmental Protection Agency, Rm. M3708, 401 M St., 
SW., Washington, DC 20460. Fees accompanying objections and hearing 
requests shall be labeled ``Tolerance Petition Fees'' and forwarded to: 
EPA Headquarters Accounting Operations Branch, OPP (Tolerance Fees), 
P.O. Box 360277M, Pittsburgh, PA 15251. A copy of any objections and 
hearing requests filed with the Hearing Clerk identified by the docket 
control number, [OPP-300675], must also be submitted to: Public 
Information and Records Integrity Branch, Information Resources and 
Services Division (7502C), Office of Pesticide Programs, Environmental 
Protection Agency, 401 M St., SW., Washington, DC 20460. In person, 
bring a copy of objections and hearing requests to Rm. 119, CM #2, 1921 
Jefferson Davis Hwy., Arlington, VA.
    A copy of objections and hearing requests filed with the Hearing 
Clerk may also be submitted electronically by sending electronic mail 
(e-mail) to: <a href="/cdn-cgi/l/email-protection#452a353568212a262e20310520352428242c296b2035246b222a33"><span class="__cf_email__" data-cfemail="036c73732e676c60686677436673626e626a6f2d6673622d646c75">[email protected]</span></a>. Copies of objections and 
hearing requests must be submitted as an ASCII file avoiding the use of 
special characters and any form of encryption. Copies of objections and 
hearing requests will also be accepted on disks in WordPerfect 5.1/6.1 
file format or ASCII file format. All copies of objections and hearing 
requests in electronic form must be identified by the docket control 
number [OPP-300675]. No Confidential Business Information (CBI) should 
be submitted through e-mail. Electronic copies of objections and 
hearing requests on this

[[Page 34311]]

rule may be filed online at many Federal Depository Libraries.

FOR FURTHER INFORMATION CONTACT: By mail: Joseph M. Tavano, 
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: Crystal Mall #2, 
1921 Jefferson Davis Hwy., Arlington, VA, (703) 305-6411, e-mail: 
<a href="/cdn-cgi/l/email-protection#582c392e3936377632372b3d2830183d283935393134763d2839763f372e"><span class="__cf_email__" data-cfemail="fc889d8a9d9293d296938f998c94bc998c9d919d9590d2998c9dd29b938a">[email protected]</span></a>.

SUPPLEMENTARY INFORMATION: In the Federal Register of January 28, 1998 
(63 FR 4252) [FRL 5763-6]; March 6, 1998 (63 FR 11240) [FRL 5777-5] and 
March 27, 1998 (63 FR 14926) [5577-6]. EPA, issued notices pursuant to 
section 408 of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 
U.S.C. 346a(e) announcing the filing of pesticide petitions (PP) for 
tolerance by Rohm and Haas Company, 100 Independence mall west, 
Philadelphia, PA 19106-2399. These notices included a summary of the 
petitions prepared by Rohm and Haas Company, the registrant. There were 
no comments received in response to these notices of filing.
    The petition requested that 40 CFR 180.482 be amended by 
establishing a tolerance for residues of the insecticide, tebufenozide, 
in or on pecans, grapes, wine and pears at 0.01, 0.5, and 1.0 part per 
million (ppm) respectively.

I. Risk Assessment and Statutory Findings

    New section 408(b)(2)(A)(i) of the FFDCA allows EPA to establish a 
tolerance (the legal limit for a pesticide chemical residue in or on a 
food) only if EPA determines that the tolerance is ``safe.'' Section 
408(b)(2)(A)(ii) defines ``safe'' to mean that ``there is a reasonable 
certainty that no harm will result from aggregate exposure to the 
pesticide chemical residue, including all anticipated dietary exposures 
and all other exposures for which there is reliable information.'' This 
includes exposure through drinking water and in residential settings, 
but does not include occupational exposure. Section 408(b)(2)(C) 
requires EPA to give special consideration to exposure of infants and 
children to the pesticide chemical residue in establishing a tolerance 
and to ``ensure that there is a reasonable certainty that no harm will 
result to infants and children from aggregate exposure to the pesticide 
chemical residue. . . .''
    EPA performs a number of analyses to determine the risks from 
aggregate exposure to pesticide residues. First, EPA determines the 
toxicity of pesticides based primarily on toxicological studies using 
laboratory animals. These studies address many adverse health effects, 
including (but not limited to) reproductive effects, developmental 
toxicity, toxicity to the nervous system, and carcinogenicity. Second, 
EPA examines exposure to the pesticide through the diet (e.g., food and 
drinking water) and through exposures that occur as a result of 
pesticide use in residential settings.

A. Toxicity

    1. Threshold and non-threshold effects. For many animal studies, a 
dose response relationship can be determined, which provides a dose 
that causes adverse effects (threshold effects) and doses causing no 
observed effects (the ``no-observed effect level'' or ``NOEL'').
    Once a study has been evaluated and the observed effects have been 
determined to be threshold effects, EPA generally divides the NOEL from 
the study with the lowest NOEL by an uncertainty factor (usually 100 or 
more) to determine the Reference Dose (RfD). The RfD is a level at or 
below which daily aggregate exposure over a lifetime will not pose 
appreciable risks to human health. An uncertainty factor (sometimes 
called a ``safety factor'') of 100 is commonly used since it is assumed 
that people may be up to 10 times more sensitive to pesticides than the 
test animals, and that one person or subgroup of the population (such 
as infants and children) could be up to 10 times more sensitive to a 
pesticide than another. In addition, EPA assesses the potential risks 
to infants and children based on the weight of the evidence of the 
toxicology studies and determines whether an additional uncertainty 
factor is warranted. Thus, an aggregate daily exposure to a pesticide 
residue at or below the RfD (expressed as 100% or less of the RfD) is 
generally considered acceptable by EPA. EPA generally uses the RfD to 
evaluate the chronic risks posed by pesticide exposure. For shorter 
term risks, EPA calculates a margin of exposure (MOE) by dividing the 
estimated human exposure into the NOEL from the appropriate animal 
study. Commonly, EPA finds MOEs lower than 100 to be unacceptable. This 
100-fold MOE is based on the same rationale as the 100-fold uncertainty 
factor.
    Lifetime feeding studies in two species of laboratory animals are 
conducted to screen pesticides for cancer effects. When evidence of 
increased cancer is noted in these studies, the Agency conducts a 
weight of the evidence review of all relevant toxicological data 
including short-term and mutagenicity studies and structure activity 
relationship. Once a pesticide has been classified as a potential human 
carcinogen, different types of risk assessments (e.g., linear low dose 
extrapolations or MOE calculation based on the appropriate NOEL) will 
be carried out based on the nature of the carcinogenic response and the 
Agency's knowledge of its mode of action.
    2. Differences in toxic effect due to exposure duration. The 
toxicological effects of a pesticide can vary with different exposure 
durations. EPA considers the entire toxicity data base, and based on 
the effects seen for different durations and routes of exposure, 
determines which risk assessments should be done to assure that the 
public is adequately protected from any pesticide exposure scenario. 
Both short and long durations of exposure are always considered. 
Typically, risk assessments include ``acute,'' ``short-term,'' 
``intermediate term,'' and ``chronic'' risks. These assessments are 
defined by the Agency as follows.
    Acute risk, by the Agency's definition, results from 1-day 
consumption of food and water, and reflects toxicity which could be 
expressed following a single oral exposure to the pesticide residues. 
High end exposure to food and water residues are typically assumed.
    Short-term risk results from exposure to the pesticide for a period 
of 1-7 days, and therefore overlaps with the acute risk assessment. 
Historically, this risk assessment was intended to address primarily 
dermal and inhalation exposure which could result, for example, from 
residential pesticide applications. However, since enaction of FQPA, 
this assessment has been expanded to include both dietary and non-
dietary sources of exposure, and will typically consider exposure from 
food, water, and residential uses when reliable data are available. In 
this assessment, risks from average food and water exposure, and high-
end residential exposure, are aggregated. High-end exposures from all 
three sources are not typically added because of the very low 
probability of this occurring in most cases, and because the other 
conservative assumptions built into the assessment assure adequate 
protection of public health. However, for cases in which high-end 
exposure can reasonably be expected from multiple sources (e.g. 
frequent and widespread homeowner use in a specific geographical area), 
multiple high-end risks will be aggregated and presented as part of the 
comprehensive risk assessment/characterization. Since the toxicological 
endpoint considered in

[[Page 34312]]

this assessment reflects exposure over a period of at least 7 days, an 
additional degree of conservatism is built into the assessment; i.e., 
the risk assessment nominally covers 1-7 days exposure, and the 
toxicological endpoint/NOEL is selected to be adequate for at least 7 
days of exposure. (Toxicity results at lower levels when the dosing 
duration is increased.)
    Intermediate-term risk results from exposure for 7 days to several 
months. This assessment is handled in a manner similar to the short-
term risk assessment.
    Chronic risk assessment describes risk which could result from 
several months to a lifetime of exposure. For this assessment, risks 
are aggregated considering average exposure from all sources for 
representative population subgroups including infants and children.

B. Aggregate Exposure

    In examining aggregate exposure, FFDCA section 408 requires that 
EPA take into account available and reliable information concerning 
exposure from the pesticide residue in the food in question, residues 
in other foods for which there are tolerances, residues in groundwater 
or surface water that is consumed as drinking water, and other non-
occupational exposures through pesticide use in gardens, lawns, or 
buildings (residential and other indoor uses). Dietary exposure to 
residues of a pesticide in a food commodity are estimated by 
multiplying the average daily consumption of the food forms of that 
commodity by the tolerance level or the anticipated pesticide residue 
level. The Theoretical Maximum Residue Contribution (TMRC) is an 
estimate of the level of residues consumed daily if each food item 
contained pesticide residues equal to the tolerance. In evaluating food 
exposures, EPA takes into account varying consumption patterns of major 
identifiable subgroups of consumers, including infants and children. 
The TMRC is a ``worst case'' estimate since it is based on the 
assumptions that food contains pesticide residues at the tolerance 
level and that 100% of the crop is treated by pesticides that have 
established tolerances. If the TMRC exceeds the RfD or poses a lifetime 
cancer risk that is greater than approximately one in a million, EPA 
attempts to derive a more accurate exposure estimate for the pesticide 
by evaluating additional types of information (anticipated residue data 
and/or percent of crop treated data) which show, generally, that 
pesticide residues in most foods when they are eaten are well below 
established tolerances.
    Percent of crop treated estimates are derived from federal and 
private market survey data. Typically, a range of estimates are 
supplied and the upper end of this range is assumed for the exposure 
assessment. By using this upper end estimate of percent of crop 
treated, the Agency is reasonably certain that exposure is not 
understated for any significant subpopulation group. Further, regional 
consumption information is taken into account through EPA's computer-
based model for evaluating the exposure of significant subpopulations 
including several regional groups, to pesticide residues. For this 
pesticide, the most highly exposed population subgroup was not 
regionally based.

II. Aggregate Risk Assessment and Determination of Safety

    Consistent with section 408(b)(2)(D), EPA has reviewed the 
available scientific data and other relevant information in support of 
this action, EPA has sufficient data to assess the hazards of 
tebufenozide, benzoic acid, 3,5-dimethyl-1-(1,1-dimethylethyl)-2-(4-
ethylbenzoyl) hydrazide and to make a determination on aggregate 
exposure, consistent with section 408(b)(2), for tolerances for 
residues of tebufenozide on pecans, grapes, wine and pears at 0.01, 
0.5, and 1.0 ppm respectively. EPA's assessment of the dietary 
exposures and risks associated with establishing the tolerance follows.

A. Toxicological Profile

    EPA has evaluated the available toxicity data and considered its 
validity, completeness, and reliability as well as the relationship of 
the results of the studies to human risk. EPA has also considered 
available information concerning the variability of the sensitivities 
of major identifiable subgroups of consumers, including infants and 
children. The nature of the toxic effects caused by tebufenozide, 
benzoic acid, 3,5-dimethyl-1-(1,1-dimethylethyl)-2-(4-ethylbenzoyl) 
hydrazide are discussed below.
    1. Acute toxicity studies with technical grade: Oral 
LD<INF>50</INF> in the rat is > 5 grams for males and females - 
Toxicity Category IV; dermal LD<INF>50</INF> in the rat is = 5,000 
milligram/kilogram (mg/kg) for males and females - Toxicity Category 
III; inhalation LC<INF>50</INF> in the 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 > 5mg - Toxicity 
Category IV. Tebufenozide is not a sentizer.
    2. In a 21-day dermal toxicity study, Crl: CD rats (6/sex/dose) 
received repeated dermal administration of either the technical 96.1% 
product RH-75,992 at 1,000 mg/kg/day Limit-Dose or the formulation 
23.1% a.i. product RH-755,992 2F at 0, 62.5, 250, or 1,000 mg/kg/day, 6 
hours/day, 5 days/week for 21 days. Under conditions of this study, RH-
75,992 Technical or RH-75,992 2F demonstrated no systemic toxicity or 
dermal irritation at the highest dose tested 1,000 mg/kg/ during the 
21-day study. Based on these results, the NOEL for systemic toxicity 
and dermal irritation in both sexes is 1,000 mg/kg/day highest dose 
tested (HDT). A lowest-observable-effect level (LOEL) for systemic 
toxicity and dermal irritation was not established.
    3. A 1-year dog feeding study with a (LOEL) 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 liver showed an increased pigment 
in the Kupffer cells. The no-observed effect level (NOEL) for systemic 
toxicity in both sexes is 50 ppm (1.9 mg/kg/day).
    4. An 18-month mouse carcinogenicity study with no carcinogenicity 
observed at dosage levels up to and including 1,000 ppm.
    5. 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. 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 NOEL was 1,000 mg/kg/day.
    7. 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 NOEL was 
1,000 mg/kg/day.

[[Page 34313]]

    8. In a 1993 two-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 NOEL 
was 10 ppm (0.8/0.9 mg/kg/day for males and females, respectively) and 
the LOEL 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 
NOEL was 150 ppm. (11.5/12.8 mg/kg/day for males and females, 
respectively) and the LOEL 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 NOEL of 150 ppm (11.5/12.8 
mg/kg/day for males and females, respectively).
    9. In a 1995 two-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 NOEL was 25 
ppm (1.6/1.8 mg/kg/day in males and females, respectively), and the 
LOEL 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 NOEL was 200 ppm. (12.6/14.6 mg/kg/day in males and females), 
and the LOEL 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.
    10. 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.
    11. The pharmacokinetics and metabolism of tebufenozide were 
studied in female Sprague-Dawley rats (3-6/sex/group) receiving a 
single oral dose of 3 or 250 mg/kg of RH-5992,<SUP>14</SUP>C labeled in 
one of three positions (A-ring, B-ring or N-butylcarbon). The extent of 
absorption was not established. The majority of the radiolabeled 
material was eliminated or excreted in the feces within 48 hours within 
48 hours; small amounts (1 to 7% of the administered dose) were 
excreted in the urine and only traces were excreted in expired air or 
remained in the tissues. There was no tendency for bioacculmulation. 
Absorption and excretion were rapid.
    A total of 11 metabolites, in addition to the parent compound, were 
identified in the feces; the parent compound accounted for 96 to 99% of 
the administered radioactivity in the high dose group and 35 to 43% in 
the low dose group. No parent compound was found in the urine; urinary 
metabolites were not characterized. The identity of several fecal 
metabolites was confirmed by mass spectral analysis and other fecal 
metabolites were tentatively identified by cochromatography with 
synthetic standards. A pathway of metabolism was proposed based on 
these data. Metabolism proceeded primarily by oxidation of the three 
benzyl carbons, two methyl groups on the B-ring and an ethyl group on 
the A-ring to alcohols, aldehydes or acids. The type of metabolite 
produced varies depending on the position oxidized and extent of 
oxidation. The butyl group on the quaternary nitrogen also can be 
leaved (minor), but there was no fragmentation of the molecule between 
the benzyl rings.
    No qualitative differences in metabolism were observed between 
sexes, when high or low dose groups were compared or when different 
labeled versions of the molecule were compared.
    12. The absorption and metabolism of tebufenozide were studied in a 
group of male and female bile-duct cannulated rats. Over a 72 hour 
period, biliary excretion accounted for 30%[M] to 34%[F] of the 
administered dose while urinary excretion accounted for <nearly-eq> 5% 
of the administered dose and the carcass accounted for < 0.5% of the 
administered dose for both males and females. Thus systemic absorption 
(percent of dose recovered in the bile, urine and carcass] was 35%[M] 
to 39%[F]. The majority of the radioactivity in the bile (20% [M] to 
24% [F]) of the administered dose] was excreted within the first 6 
hours postdosing indicating rapid absorption. Furthermore, urinary 
excretion of the metabolites was essentially complete within 24 hours 
postdosing. A large amount [67%(F) to 70% (M)] of the administered dose 
was unabsorbed and excreted in the feces by 72 hours. Total recovery of 
radioactivity was 105% of the administered dose.
    A total of 13 metabolites were identified in the bile; the parent 
compound was not identified i.e. unabsorbed compound nor were the 
primary oxidation products seen in the feces in the pharmacokinetics 
study. The proposed metabolic pathway proceeded primary by oxidation of 
the benzylic carbons to alcohols, aldehydes or acids. Bile contained 
most of the other highly oxidized products found in the feces. The most 
significant individual bile metabolites accounted for 5% to 18% of the 
total radioactivity (F and/or M). Bile also contained the previously 
undetected (in the pharmacokinetics study] ``A'' Ring ketone and the 
``B'' Ring diol. The other major components were characterized as high 
molecular weight conjugates. No individual bile metabolite accounted 
for > 5% of the total administered dose. Total bile radioactivity 
accounted for <nearly-eq> 17% of the total administered dose.
    No major qualitative differences in biliary metabolites were 
observed between sexes. The metabolic profile in the bile was similar 
to the metabolic profile in the feces and urine.

B. Toxicological Endpoints

    1. Acute toxicity. 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. Thus the risk from acute exposure is 
considered negligible.
    2. Short - and intermediate - term toxicity. No dermal or systemic 
toxicity was seen in rats receiving 15 repeated dermal applications of 
the technical (97.2%) product at 1,000 mg/kg/day (Limit- Dose) as well 
as a formulated (23% a.i) product at 0, 62.5, 250, or 1,000 mg/kg/day 
over a 21-day period (MRID 42991507). The HIARC noted that in spite of 
the hematological effects seen in the dog study, similar effects were 
not seen in the rats receiving the

[[Page 34314]]

compound via the dermal route indicating poor dermal absorption. Also, 
no developmental endpoints of concern were evident due to the lack of 
developmental toxicity in either rat or rabbit studies. This risk is 
considered to be negligable.
    3. Chronic toxicity. EPA has established the RfD for tebufenozide, 
benzoic acid, 3,5-dimethyl-1-(1,1-dimethylethyl)-2-(4-ethylbenzoyl) 
hydrazide at 0.018 mg/kg/day. This RfD is based on a NOEL of 1.8 mg/kg/
day and an uncertainty factor (UF) of 100. The NOEL was established 
from the chronic toxicity study in dogs where the NOEL was 1.8 mg/kg/
day based on growth retardation, alterations in hematology parameters, 
changes in organ weights, and histopathological lesions in the bone, 
spleen and liver at 8.7 mg/kg/day. EPA determined that the 10 x factor 
to protect children and infants as required by FQPA should be removed. 
Therefore, the RfD remains the same at: 0.018 mg/kg/day. An UF of 100 
is supported by the following factors.
    (i) Developmental toxicity studies showed no increased sensitivity 
in fetuses when compared to maternal animals following in utero 
exposures in rats and rabbits.
    (ii) Multi-generation reproduction toxicity studies in rats showed 
no increased sensitivity in pups as compared to adults and offspring.
    (iii) There are no data gaps.
    4. Carcinogenicity. Tebufenozide has been classified as a Group E, 
``no evidence of carcinogenicity for humans,'' chemical by EPA.

C. Exposures and Risks

    1. From food and feed uses. Tolerances have been established (40 
CFR 180.482) for the residues of tebufenozide, in or on walnuts at 0.1 
ppm and apples at 1.0 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. Risk assessments were conducted by EPA to assess 
dietary exposures and risks from tebufenozide, benzoic acid, 3,5-
dimethyl-1-(1,1-dimethylethyl)-2-(4-ethylbenzoyl) hydrazide as follows:
    i. 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 one 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 
negligable.
    ii. Chronic exposure and risk. The RfD used for the chronic dietary 
analysis is 0.018 mg/kg/day. In conducting this exposure assessment, 
EPA has made very conservative assumptions 100% of pecans and wine and 
sherry and and pears and all other commodities having tebufenozide 
tolerances will contain tebufenozide residues and those residues would 
be at the level of the tolerance which result in an overestimate of 
human dietary exposure. Thus, in making a safety determination for this 
tolerance, HED is taking into account this conservative exposure 
assessment. 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 (31% of RfD); 
Nursing Infants (<1 year old) (41% of RfD); Non-Nursing Infants (<1 
year old) (80% of Rfd); Children (1-6 years old) (60% of RfD); Children 
(7-12 years old) (43% of Rfd); Females (13 + years old, nursing) (31% 
of RfD); Males (13-19 years old) (28% of RfD); Non-Hispanic Blacks (34% 
of RfD); Non Hispanic Others (42% of RfD) Western Region (35% of RfD). 
The subgroups listed above are: (1) the U.S. population (48 States); 
(2) those for infants and children; and, (3) the other subgroups for 
which the percentage of the RfD occupied is greater than that occupied 
by the subgroup U.S. population (48 States).
    2. From drinking water-- i. Acute exposure and risk. Because no 
acute dietary endpoint was determined, the Agency concludes that there 
is a reasonable certainty of no harm from acute exposure from drinking 
water.
    ii. 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.
    3. From 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.
    4. Cumulative exposure to substances with common mechanism of 
toxicity. 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 
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

[[Page 34315]]

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, EPA 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.

D. Aggregate Risks and Determination of Safety for U.S. Population

    1. Acute risk. Since no acute toxicological endpoints were 
established, no acute aggregate risk exists.
    2. Chronic risk. Using the conservative exposure assumptions 
described above, and taking into account the completeness and 
reliability of the toxicity data, EPA has concluded that dietary (food 
only) exposure to tebufenozide will utilize 31% 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, EPA does 
not expect the aggregate exposure to exceed 100% of the RfD.
    3. 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.

E. Aggregate Cancer Risk for U.S. Population

    Since, tebufenozide has been classified as a Group E, ``no evidence 
of carcinogenicity for humans,'' this risk does not exist.

F. Aggregate Risks and Determination of Safety for Infants and Children

    1. Safety factor for infants and children-- i. In general. In 
assessing the potential for additional sensitivity of infants and 
children to residues of tebufenozide, benzoic acid, 3,5-dimethyl-1-
(1,1-dimethylethyl)-2-(4-ethylbenzoyl) hydrazide, EPA considered data 
from developmental toxicity studies in the rat and rabbit and a two-
generation reproduction study in the rat. The developmental toxicity 
studies are designed to evaluate adverse effects on the developing 
organism resulting from maternal pesticide exposure gestation. 
Reproduction studies provide information relating to effects from 
exposure to the pesticide on the reproductive capability of mating 
animals and data on systemic toxicity.
    FFDCA section 408 provides that EPA shall apply an additional 
tenfold margin of safety for infants and children in the case of 
threshold effects to account for pre-and post-natal toxicity and the 
completeness of the database unless EPA determines that a different 
margin of safety will be safe for infants and children. Margins of 
safety are incorporated into EPA risk assessments either directly 
through use of a MOE analysis or through using uncertainty (safety) 
factors in calculating a dose level that poses no appreciable risk to 
humans. EPA believes that reliable data support using the standard 
uncertainty factor (usually 100 for combined inter- and intra-species 
variability)) and not the additional tenfold MOE/uncertainty factor 
when EPA has a complete data base under existing guidelines and when 
the severity of the effect in infants or children or the potency or 
unusual toxic properties of a compound do not raise concerns regarding 
the adequacy of the standard MOE/safety factor.
    ii. Developmental toxicity studies--a. Rats. In a developmental 
toxicity study in rats, the maternal (systemic) NOEL was 250 mg/kg/day. 
The LOEL was 1,000 mg/kg/day, based on decreased body weight and food 
consumption. The developmental (pup) NOEL was <ls-thn-eq> 1,000 mg/kg/
day (HGT)
    b. Rabbits. In a developmental toxicity study in rabbits, the 
maternal and developmental NOELs were <ls-thn-eq> 1,000 mg/kg/day 
(HDT).
    iii. Reproductive toxicity study. In a 1993 two-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 NOEL was 10 ppm (0.8/0.9 mg/
kg/day for males and females, respectively) and the LOEL 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 NOEL was 
150 ppm. (11.5/12.8 mg/kg/day for males and females, respectively) and 
the LOEL 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 NOEL of 150 ppm (11.5/12.8 mg/kg/day for 
males and females, respectively)
    In a 1995 two-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 NOEL was 25 
ppm (1.6/1.8 mg/kg/day in males and females, respectively), and the 
LOEL 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

[[Page 34316]]

epithelium and reduced uterine and ovarian weights were also observed 
at 2,000 ppm, but the toxicological significance was unknown. For 
offspring, the systemic NOEL was 200 ppm. (12.6/14.6 mg/kg/day in males 
and females), and the LOEL 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.
    iv. Pre- and post-natal sensitivity. The toxicology data base for 
tebufenozide is complete and includes acceptable developmental toxicity 
studies in both rats and rabbits as well as a two two-generation 
reproductive toxicity studies in rats.
    The EPA determined that the data provided no indication of 
increased sensitivity of rats or rabbits to in utero and/or postnatal 
exposure to tebufenozide. No maternal or developmental findings were 
observed in the prenatal developmental toxicity studies at doses up to 
1,000 mg/kg/day in rats and rabbits. In the two two-generation 
reproduction studies in rats, effects occurred at the same or lower 
treatment levels in the adults as in the offspring.
    2. Acute risk. Since no acute toxicological endpoints were 
established, no acute aggregate risk exists.
    3. Chronic risk. Using the conservative exposure assumptions 
described above, EPA has concluded that aggregate exposure to 
tebufenozide, benzoic acid, 3,5-dimethyl-1-(1,1-dimethylethyl)-2-(4-
ethylbenzoyl) hydrazide from food will utilize from 31% of the RfD for 
the U.S. population to 80% of the RfD for non-nursing infants less than 
1 year old. The potential for exposure to tebufenozide in drinking 
water does not exceed EPA's level of concern. There are currently no 
tebufenozide residential or non-dietary exposure scenarios. 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. EPA does not expect the aggregate exposure to exceed 100% of 
the RfD. EPA concludes that there is a reasonable certainty that no 
harm will result to infants and children from aggregate exposure to 
tebufenozide, benzoic acid, 3,5-dimethyl-1-(1,1-dimethylethyl)-2-(4-
ethylbenzoyl) hydrazide residues.
    4. Short- or intermediate-term risk. Since no short- and 
intermediate-term toxicological endpoints were established by EPA, no 
acute aggregate risk exists.

III. Other Considerations

A. Metabolism In Plants and Animals

    The nature of the residues of tebufenozide in/on plants is 
adequately understood. The residue of concern for both regulatory 
(tolerance expression) and risk assessment purposes is the parent 
compound, tebufenozide per se.
    There are no animal feed items associated with pecans. According to 
information supplied by the petitioner, wine grapes and wine grape 
processing commodities are not items of animal feed in Europe. 
Therefore, a discussion of potential transfer of secondary residues to 
animal commodities is not germane to these actions.

B. Analytical Enforcement Methodology

    A HPLC/UV analytical method, Enforcement Residue Analytical Method 
for RH-5992 in Pecans with HPLC-MS Confirmation is adequate for 
enforcement purposes in pecans. A successful Agency validation for an 
analytical method to detect residues of tebufenozide per se has been 
conducted by ACL/BEAD.
    The method used in the analysis of the total residue of concern in 
the European field residue trials in wine, Method AL 013/92-0, was 
developed by Rohm and Haas and independently validated. In the 
validation of this method, at levels from 0.01 to 0.5 ppm in wine 
recoveries ranged from 84 to 109%; in grapes at levels of 0.02 to 1.0 
ppm recoveries ranged from 77 to 128%. The limit of quantitation was 
given as 0.02 ppm for grapes and 0.01 ppm for wine. The method is 
different from those validated for domestic commodities but was 
determined to be adequate for data collection.

C. Magnitude of Residues

    Adequate residue data were provided to support tolerances of 0.01 
ppm for pecans and 0.5 ppm for grapes, wine and a time-limited 
tolerance for pears.
    There are no pecan or pear processed comodities of regulatory 
concern. In those instances when treated grapes were vinified, residues 
of tebufenozide in the aged wine were a third to a half of those in the 
treated grapes. The maximum residue found in the wine treated at label 
rates was 0.3 ppm; therefore, a tolerance for wine grapes would suffice 
for the wine made from them.
    Since there are no pecan or pear animal feed items and according to 
information supplied by the petitioner, wine grapes and wine grape 
processing commodities are not items of animal feed in Europe, no 
secondary residues in animals are expected.

D. International Residue Limits

    There are currently no CODEX, Canadian, or Mexican listings for 
tebufenozide residues in or on pecans or pears, therefore there are no 
harmonization issues for these crops.
    Maximum residue levels (MRL) of 0.5 ppm have been established for 
wine grapes in France, Italy, and Germany. The tolerance of 0.5 ppm in 
or on wine grapes is in harmony with these MRLs.

E. Rotational Crop Restrictions

    Since pecans, grapes, and pears are not rotated to other crops, a 
discussion of tebufenozide accumulation in rotational crops is not 
germane to this action.

IV. Conclusion

    Therefore, the tolerance is established for residues of 
tebufenozide in pecans, grapes, wine, and pears at 0.01, 0.5, and 1.0 
ppm respectively.

V. Objections and Hearing Requests

    The new FFDCA section 408(g) provides essentially the same process 
for persons to ``object'' to a tolerance regulation issued by EPA under 
new section 408(e) and (l)(6) as was provided in the old section 408 
and in section 409. However, the period for filing objections is 60 
days, rather than 30 days. EPA currently has procedural regulations 
which govern the submission of objections and hearing requests. These 
regulations will require some modification to reflect the new law. 
However, until those modifications can be made, EPA will continue to 
use those procedural regulations with appropriate adjustments to 
reflect the new law.
    Any person may, by August 24, 1998, file written objections to any 
aspect of this regulation and may also request a hearing on those 
objections. Objections and hearing requests must be filed with the 
Hearing Clerk, at the address given above (40 CFR 178.20). A copy of 
the objections and/or hearing requests filed with the Hearing Clerk 
should be submitted to the OPP docket for this rulemaking. The 
objections submitted must specify the provisions of the regulation 
deemed objectionable and the grounds for the objections (40 CFR 
178.25). Each objection must be accompanied by the fee prescribed by 40 
CFR 180.33(i). If a hearing is requested, the objections must include a 
statement of the factual issues on which a hearing is requested, the 
requestor's contentions on such issues, and a summary of any evidence 
relied upon by the requestor (40 CFR 178.27). A request for a hearing 
will be granted if

[[Page 34317]]

the Administrator determines that the material submitted shows the 
following:
    There is genuine and substantial issue of fact; there is a 
reasonable possibility that available evidence identified by the 
requestor would, if established, resolve one or more of such issues in 
favor of the requestor, taking into account uncontested claims or facts 
to the contrary; and resolution of the factual issues in the manner 
sought by the requestor would be adequate to justify the action 
requested (40 CFR 178.32). Information submitted in connection with an 
objection or hearing request may be claimed confidential by marking any 
part or all of that information as Confidential Business Information 
(CBI). Information so marked will not be disclosed except in accordance 
with procedures set forth in 40 CFR part 2. A copy of the information 
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.

VI. Public Record and Electronic Submissions

    EPA has established a record for this rulemaking under docket 
control number [OPP-300675] (including any comments and data submitted 
electronically). 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 public 
record is located in Room 119 of the Public Information and Records 
Integrity Branch, Information Resources and Services Division (7502C), 
Office of Pesticide Programs, Environmental Protection Agency, Crystal 
Mall #2, 1921 Jefferson Davis Highway, Arlington, VA.
    Electronic comments may be sent directly to EPA at: <a href="/cdn-cgi/l/email-protection#dbb4ababf6d1bfb4b8b0beaf9bbeabbab6bab2b7f5beabbaf5bcb4ad">opp-
<span class="__cf_email__" data-cfemail="d8bcb7bbb3bdac98bda8b9b5b9b1b4f6bda8b9f6bfb7ae">[email protected]</span></a>.
    Electronic comments must be submitted as an ASCII file avoiding the 
use of special characters and any form of encryption.
    The official record for this rulemaking, as well as the public 
version, as described above will be kept in paper form. Accordingly, 
EPA will transfer any copies of objections and hearing requests 
received electronically into printed, paper form as they are received 
and will place the paper copies in the official rulemaking record which 
will also include all comments submitted directly in writing. The 
official rulemaking record is the paper record maintained at the 
Virginia address in ``ADDRESSES'' at the beginning of this document.

VII. Regulatory Assessment Requirements

    This final rule establishes tolerances under FFDCA section 408(d) 
in response to a petitions submitted to the Agency. The Office of 
Management and Budget (OMB) has exempted these types of actions from 
review under Executive Order 12866, entitled Regulatory Planning and 
Review (58 FR 51735, October 4, 1993). This final rule does not contain 
any information collections subject to OMB approval under the Paperwork 
Reduction Act (PRA), 44 U.S.C. 3501 et seq., or impose any enforceable 
duty or contain any unfunded mandate as described under Title II of the 
Unfunded Mandates Reform Act of 1995 (UMRA) (Pub. L. 104-4). Nor does 
it require any prior consultation as specified by Executive Order 
12875, entitled Enhancing the Intergovernmental Partnership (58 FR 
58093, October 28, 1993), or special considerations as required by 
Executive Order 12898, entitled Federal Actions to Address 
Environmental Justice in Minority Populations and Low-Income 
Populations (59 FR 7629, February 16, 1994), or require OMB review in 
accordance with Executive Order 13045, entitled Protection of Children 
from Environmental Health Risks and Safety Risks (62 FR 19885, April 
23, 1997).
    In addition, since these tolerances and exemptions that are 
established on the basis of petitions under FFDCA section 408(d), such 
as the tolerances in this final rule, do not require the issuance of a 
proposed rule, the requirements of the Regulatory Flexibility Act (RFA) 
(5 U.S.C. 601 et seq.) do not apply. Nevertheless, the Agency has 
previously assessed whether establishing tolerances, exemptions from 
tolerances, raising tolerance levels or expanding exemptions might 
adversely impact small entities and concluded, as a generic matter, 
that there is no adverse economic impact. The factual basis for the 
Agency's generic certification for tolerance actions published on May 
4, 1981 (46 FR 24950) and was provided to the Chief Counsel for 
Advocacy of the Small Business Administration.

VIII. Submission to Congress and the Comptroller General

    The Congressional Review Act, 5 U.S.C. 801 et seq., as added by the 
Small Business Regulatory Enforcement Fairness Act of 1996, generally 
provides that before a rule may take effect, the agency promulgating 
the rule must submit a rule report, which includes a copy of the rule, 
to each House of the Congress and to the Comptroller General of the 
United States. EPA will submit a report containing this rule and other 
required information to the U.S. Senate, the U.S. House of 
Representatives, and the Comptroller General of the United States prior 
to publication of the rule in the Federal Register. This rule is not a 
``major rule'' as defined by 5 U.S.C. 804(2).

List of Subjects in 40 CFR Part 180

    Environmental protection, Administrative practice and procedure, 
Agricultural commodities, Pesticides and pests, Reporting and 
recordkeeping requirements.

    Dated:June 12, 1998.

James Jones,

Director, Registration Division, Office of Pesticide Programs.
    Therefore, 40 CFR chapter I is amended as follows:

PART 180 -- [AMENDED]

    1. The authority citation for part 180 continues to read as 
follows:

    Authority: 21 U.S.C. 346a and 371.


    2. In Sec. 180.482, by alphabetically adding the following 
commodities to the table in paragraph (b) to read as follows:


Sec. 180.482  Tebufenozide; tolerances for residues.

*      *      *      *      *
    (b)*  *  *

                                                                        
------------------------------------------------------------------------
                                                          Expiration/   
            Commodity              Parts per million    Revocation Date 
------------------------------------------------------------------------
         *        *        *        *        *        *        *        
Grapes, wine \1\................  0.5                 NA                
                                                                        
Pears...........................  1.0                 2001              
                                                                        
Pecans..........................  0.01                NA                

[[Page 34318]]

                                                                        
         *        *        *        *        *        *        *        
------------------------------------------------------------------------
\1\ There are no U.S. registrations on grapes as of June 24, 1998.      


[FR Doc. 98-16822 Filed 6-23-98; 8:45 am]
BILLING CODE 6560-50-F


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