[Federal Register Volume 64, Number 134 (Wednesday, July 14, 1999)]
[Rules and Regulations]
[Pages 37863-37870]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 99-17776]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-300886; FRL-6088-8]
RIN 2070-AB78


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

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes a tolerance for residues of 
tebufenozide in or on kiwifruit. Rohm and Haas Company requested the 
tolerance under the Federal Food, Drug, and Cosmetic Act, as amended by 
the Food Quality Protection Act of 1996.

DATES: This regulation is effective July 14, 1999. Objections and 
requests for hearings must be received by EPA on or before September 
13, 1999.

ADDRESSES: Written objections and hearing requests, identified by the 
docket control number, [OPP-300886], 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-300886], 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, Crystal 
Mall 2 (CM #2), 1921 Jefferson Davis Hwy., Arlington, VA.
    A copy of objections and hearing requests filed with the Hearing 
Clerk may be submitted electronically by sending electronic mail (e-
mail) to: [email protected]. 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

[[Page 37864]]

the docket control number [OPP-300886]. No Confidential Business 
Information (CBI) should be submitted through e-mail. Electronic copies 
of objections and hearing requests on this 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: Rm. 222, CM #2, 
1921 Jefferson Davis Hwy., Arlington, VA, (703) 305-6411, 
[email protected].

SUPPLEMENTARY INFORMATION: In the Federal Register of August 19, 1998 
(63 FR 44439) (FRL-6019-6), EPA issued a notice pursuant to section 408 
of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a as 
amended by the Food Quality Protection Act of 1996 (FQPA) (Public Law 
104-170) announcing the filing of a pesticide petition (PP) for 
tolerance by Rohm and Haas Company, 100 Independence Mall West, 
Philadelphia, PA 19106-2399. This notice included a summary of the 
petition prepared by Rohm and Haas Company, the registrant. There were 
no comments received in response to the notice 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 kiwifruit at 0.5 part per million (ppm). Tebufenozide controls 
light brown apple moth, green-headed leafroller, and brown-headed 
leafroller on kiwifruit.

I. Background and Statutory Findings

    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. For further discussion of the 
regulatory requirements of section 408 and a complete description of 
the risk assessment process, see the final rule on Bifenthrin Pesticide 
Tolerances (62 FR 62961, November 26, 1997) (FRL-5754-7).

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 a tolerance for 
residues of tebufenozide on imported kiwifruit at 0.5 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 are 
discussed in this unit.
    1. 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 
milligrams/kilograms (mg/kg) for males and females - Toxicity Category 
III; inhalation LC50 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% active ingredient (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 (HDT) 1,000 mg/kg during the 21-day study. Based on these 
results, the No Observable Adverse Effect Level (NOAEL) for systemic 
toxicity and dermal irritation in both sexes is 1,000 mg/kg/day HDT. A 
Lowest Observable Adverse Effect Level (LOAEL) for systemic toxicity 
and dermal irritation was not established.
    3. 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 Red Blood Cells (RBC), 
Hematocrit (HCT), and Hemoglobin (HGB), increases in Heinz bodies, 
methemoglobin, Mean Corpuscular Volume (MCV), Mean Corpuscular 
Hematocrit (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 NOAEL 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 study 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 milliliter (ml)/kg. There was no 
evidence of maternal or developmental toxicity; the maternal and 
developmental toxicity NOAEL 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 NOAEL 
was 1,000 mg/kg/day.
    8. 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,

[[Page 37865]]

respectively) and the 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).
    9. 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.
    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 Chinese Hampster Ovary (CHO) cells, a CHO/
Hypoxanthine guanine phophoribosyl transferase (HGPRT) assay, a reverse 
mutation assay with E. Coli, and an unscheduled DNA synthesis assay 
Unscheduled DNA Synthesis (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, 14C labeled 
in 1 of 3 positions (A-Ring, B-Ring or N-butylcarbon). The extent of 
absorption was not established. The majority of the radio labeled 
material was eliminated or excreted in the feces 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 3 benzyl 
carbons, 2 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% (Female (F)) to 34% (Male 
(M)) of the administered dose while urinary excretion accounted for 
equivalent to 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% (F) to 39% (M). The majority of the radioactivity in 
the bile 20% (F) to 24% (M) 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% (M) to 70% (F) 
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 (M and/or F). 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 equivalent to 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 termtoxicity.  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. The Agency noted that in spite of the hematological 
effects seen in the dog study, similar effects were not seen in the 
rats receiving the 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

[[Page 37866]]

either rat or rabbit studies. This risk is considered to be negligable.
    3. Chronic toxicity. EPA has established the chronic population 
adjusted dose (cPAD) for tebufenozide at 0.018 mg/kg/day. This 
Reference Dose (RfD) is based on a NOAEL of 1.8 mg/kg/day and an 
uncertainty factor (UF) of 100. The NOAEL was established from the 
chronic toxicity study in dogs where the NOAEL 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 10x factor to protect 
children and infants (as required by FQPA) should be reduced to 1x. 
Therefore, the cPAD is the same as the RfD: 0.018 mg/kg/day. Reducing 
the 10x factor to 1x 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 a variety of raw 
agricultural commodities. In today's action a tolerance will be 
established for the residues of tebufenozide in or on the raw 
agricultural commodity, kiwifruit at 0.50 ppm. Risk assessments were 
conducted by EPA to assess dietary exposures from tebufenozide as 
follows:
    Section 408(b)(2)(F) states that the Agency may use data on the 
actual percent of food treated (PCT) for assessing chronic dietary risk 
only if the Agency can make the following findings: That the data used 
are reliable and provide a valid basis to show what percentage of the 
food derived from such crop is likely to contain such pesticide 
residue; that the exposure estimate does not underestimate exposure for 
any significant subpopulation group; and if data are available on 
pesticide use and food consumption in a particular area, the exposure 
estimate does not understate exposure for the population in such area. 
In addition, the Agency must provide for periodic evaluation of any 
estimates used. To provide for the periodic evaluation of the estimate 
of PCT as required by the section 408(b)(2)(F), EPA may require 
registrants to submit data on PCT.
    The Agency used PCT information as follows:
    Estimates of PCT were used for the following crops. In all cases 
the maximum estimate was used.
    Almonds: Average <1% Maximum <1%
    Apples: Average 1% Maximum 2%
    Beans/Peas, Dry: Average 0% Maximum 1%
    Cotton: Average 1% Maximum 4%
    Sugarcane: Average 3% Maximum 5%
    Walnuts: Average 10% Maximum 16%
    The Agency believes that the three conditions, discussed in section 
408 (b)(2)(F) in this unit concerning the Agency's responsibilities in 
assessing chronic dietary risk findings, have been met. The PCT 
estimates are derived from Federal and private market survey data, 
which are reliable and have a valid basis. 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 the PCT, 
the Agency is reasonably certain that the percentage of the food 
treated is not likely to be underestimated. The regional consumption 
information and consumption information for significant subpopulations 
is taken into account through EPA's computer-based model for evaluating 
the exposure of significant subpopulations including several regional 
groups. Use of this consumption information in EPA's risk assessment 
process ensures that EPA's exposure estimate does not understate 
exposure for any significant subpopulation group and allows the Agency 
to be reasonably certain that no regional population is exposed to 
residue levels higher than those estimated by the Agency. Other than 
the data available through national food consumption surveys, EPA does 
not have available information on the regional consumption of food to 
which tebufenozide may be applied in a particular area.
    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 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 
negligable.
    ii. Chronic exposure and risk.  The residue of concern for 
tebufenozide in plant and animal commodities is the parent compound per 
se. In performing this analysis, EPA used the Dietary Exposure 
Evaluation Model (DEEM), which incorporates data from the Continuing 
Survey of Food Intakes by Individuals (CSFII), 1989 to 1992. Some 
refinement to the food exposure estimates was made through the use of 
PCT data. The resulting estimated food exposures for the United States 
(U.S.) population and various DEEM population subgroups are shown in 
the following table. Of these subgroups, the highest exposure is 
projected for children ages 1-6, whose chronic intake is estimated at 
73% of the RfD. Generally, in the absence of additional safety factors, 
EPA is not concerned with exposures less than 100% of the RfD. Thus, 
for all populations, the chronic human health risk from exposure to 
tebufenozide in foods is below EPA's level of concern. This estimate 
should be considered moderately refined. Further refinement to the 
exposure estimate, through the use of anticipated residues, more PCT 
data, or market-basket surveys, would likely result in lower exposure 
estimates.


      Chronic Dietary Exposure to Tebufenozide and Associated Risk
------------------------------------------------------------------------
                                    Eposure, mg/kg
     Population Subgroup\1\           body wt/day          % of cPAD
------------------------------------------------------------------------
U.S. Pop. (48 contiguious         0.006549..........  36
 states).
U.S. Pop. (autumn)..............  0.006634..........  37
U.S. Pop. (winter)..............  0.006742..........  38
U.S. Pop. (Western region)......  0.007230..........  40
U.S. Pop. (Pacific region)......  0.007419..........  41
Non-hispanic Blacks.............  0.006618..........  37
Not Hispanic, Black, or White...  0.007867..........  44
All Infants (< 1 yr)............  0.009369..........  52
Non-nursing Infants (< 1 yr)....  0.011223..........  62
Children (1-6 yr)...............  0.013202..........  73
Children (7-12 yr)..............  0.008301..........  46
Females (13+ yr, nursing).......  0.007604..........  42
Males (20+ yr)..................  0.005161..........  29
------------------------------------------------------------------------
\1\Subpopulations include the general U.S. population, infants and
  children, females, males, and any other groups whose exposure is
  greater than that of the general U.S. population.



[[Page 37867]]

    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 ranges from moderately persistent to 
persistent and is mobile; thus, tebufenozide could potentially leach to 
ground water and runoff to surface water under certain environmental 
conditions. There is no established Maximum Contaminant Level (MCL) for 
residues of tebufenozide in drinking water. No drinking water Health 
Advisories have been issued for tebufenozide. There is no entry for 
tebufenozide in the ``Pesticides in Groundwater Database.''
    Monitoring data are not available to assess the human exposure to 
tebufenozide via drinking water. In lieu of these, EPA has calculated 
the Tier I estimated concentrations in drinking water (DWECs) for 
tebufenozide using GENEEC (surface water) and SCIGROW (ground water) 
for use in the human health risk assessment. The maximum application 
rate for tebufenozide is 0.25 pound (lb) a.i. with 5 applications per 
year on pecans. This application scenario was used to calculate the 
DWECs for the human health risk assessment. Due to the wide range of 
aerobic soil half-life values, GENEEC and SCIGROW were run based on 
aerobic half-lives of 66 (California Loam) and 729 (worst-case soil 
with low microbial activity) days. For surface water, the chronic (56-
day) values are 13.3 parts per billion (ppb) and 16.5 ppb for the half-
lives of 66 and 729 days, respectively. The ground water screening 
concentrations are 0.16 ppb and 1.04 ppb for the half-lives of 66 and 
729 days, respectively. These values represent upper-bound estimates of 
the concentrations that might be found in surface and ground water due 
to the use of tebufenozide on pecans.
    In performing this risk assessment, EPA has calculated drinking 
water levels of comparison (DWLOCs) for each of the DEEM population 
subgroups. Within each subgroup, the population with the highest 
estimated exposure was used to determine the maximum concentration of 
tebufenozide that can occur in drinking water without causing an 
unacceptable human health risk. As a comparison value, EPA has used the 
16.5 ppb value in this risk assessment, as this represents a worst-case 
scenario. The DWLOCs for tebufenozide are above the DWEC of 16.5 ppb 
for all population subgroups. Therefore, the human health risk from 
exposure to tebufenozide through drinking water in not likely to exceed 
EPA's level of concern.
    3. From non-dietary exposure. Tebufenozide is not currently 
registered for use on any residential non-food sites. Therefore there 
is no non-dietary chronic, short- or intermediate-term exposure 
scenario.
    4. Cumulative exposure to substances with a 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.''
    EPA does not have, at this time, available data to determine 
whether tebufenozide 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 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 has a common mechanism of 
toxicity with other substances. For information regarding EPA's efforts 
to determine which chemicals have a common mechanism of toxicity and to 
evaluate the cumulative effects of such chemicals, see the final rule 
for Bifenthrin Pesticide Tolerances (62 FR 62961, November 26, 1997).

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 Anticipated Residue Contribution (ARC) 
exposure assumptions described in this unit, EPA has concluded that 
aggregate exposure to tebufenozide from food will utilize 36% of the 
cPAD for the U.S. population. The major identifiable subgroup with the 
highest aggregate exposure is children (1-6 years old) at 73% of the 
cPAD and is discussed below. 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 EPA's DWLOC. 
EPA generally has no concern for exposures below 100% of the PAD 
because the PAD 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 PAD.
    3. Short- and intermediate-term risk. Short- and intermediat-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 risks do not exist.
    4. 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.
    5. Determination of safety. Based on these risk assessments, EPA 
concludes that there is a reasonable certainty that no harm will result 
from aggregate exposure to tebufenozide residues.

E. 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, EPA considered data from 
developmental toxicity studies in the rat and rabbit and a 2-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 prenatal and postnatal toxicity and 
the completeness of the data base 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 margin of exposure (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

[[Page 37868]]

the standard uncertainty factor (usually 100 for combined inter- and 
intraspecies 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.
    Prenatal and postnatal sensitivity. The toxicology data base for 
tebufenozide included acceptable developmental toxicity studies in both 
rats and rabbits as well as a 2-generation reproductive toxicity study 
in rats. 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 2-generation reproduction studies in rats, effects 
occurred at the same or lower treatment levels in the adults as in the 
offspring.
    Conclusion. There is a complete toxicity data base for tebufenozide 
and exposure data are complete and reasonably accounts for potential 
exposures. For the reasons summarized above, EPA concluded that an 
additional safety factor is not needed to protect the safety of infants 
and children.
    2. Acute risk. Since no acute toxicological endpoints were 
established, no acute aggregate risk exists.
    3. Chronic risk. Using the exposure assumptions described in this 
unit, EPA has concluded that aggregate exposure to tebufenozide from 
food will utilize 73% of the cPAD for infants and children. EPA 
generally has no concern for exposures below 100% of the cPAD because 
the cPAD represents the level at or below which daily aggregate dietary 
exposure over a lifetime will not pose appreciable risks to human 
health. Despite the potential for exposure to tebufenozide in drinking 
water, EPA does not expect the aggregate exposure to exceed 100% of the 
PAD.
    4. Short- or intermediate-term risk. Short- and intermediate-term 
risks are judged to be negligible due to the lack of significant 
toxicological effects observed.
    5. Determination of safety. Based on these risk assessments, EPA 
concludes that there is a reasonable certainty that no harm will result 
to infants and children from aggregate exposure to tebufenozide 
residues.

III. Other Considerations

A. Metabolism in Plants and Animals

    The qualitative nature of the residue in plants is adequately 
understood based upon acceptable apple, sugar beet, and rice metabolism 
studies. EPA has concluded that the residue of regulatory concern is 
tebufenozide per se. There are no animal feed items associated with 
kiwifruit; consequently, a discussion of potential transfer of 
secondary residues to animal commodities is not relevant.

B. Analytical Enforcement Methodology

    The High Pressure Liquid Chromatography using ultra-violet 
detection (HPLC/UV) method (TR 34-95-66) used for determining residues 
of tebufenozide in/on kiwifruit is adequate for data collection. 
Adequate method validation and concurrent method recovery data have 
been submitted for this method. The limit of quantitation (LOQ) is 0.02 
ppm for residues of tebufenozide in/on kiwifruit.
    The Agency has requested that the petitioner revise the proposed 
enforcement method to correct the deficiencies noted during Agency 
method validation. Upon completion of the method revisions, the 
petitioner will be required to submit a copy suitable for publication 
in the Pesticide Analytical Manual, Volume II (PAM II).
    The method may be requested from: Calvin Furlow, PRRIB, IRSD 
(7502C), Office of Pesticide Programs, Environmental Protection Agency, 
401 M St., SW., Washington, DC 20460. Office location and telephone 
number: Rm 101FF, CM #2, 1921 Jefferson Davis Hwy., Arlington, VA, 
(703) 305-5229.

C. Magnitude of Residues

    Adequate residue data were provided to support the tolerance for 
kiwifruit at 0.5 ppm. There are no animal feed items associated with 
kiwifruit; consequently, a discussion of potential transfer of 
secondary residues to animal commodities is not relevant. There are no 
currently regulated processed food or feed items derived from 
kiwifruit; therefore, a discussion of tolerances for processed 
commodities is not relevant.

D. International Residue Limits

    A proposed Codex MRL of 0.5 ppm in/on kiwifruit is currently at 
Step 3. This is in harmonization with the proposed tolerance sought in 
this petition.

E. Rotational Crop Restrictions

    As kiwifruit is a perennial crop, confined and field rotational 
crop studies are not required for establishing a tolerance on 
kiwifruit.

IV. Conclusion

    Therefore, the tolerance is established for residues of 
tebufenozide in/on kiwifruit at 0.5ppm.

V. Objections and Hearing Requests

    The new FFDCA section 408(g) provides essentially the same process 
for persons to ``object'' to a tolerance regulation 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 September 13, 1999, 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 under the ``ADDRESSES'' section (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 
regulation. 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). EPA is authorized to waive any fee requirement 
``when in the judgement of the Administrator such a waiver or refund is 
equitable and not contrary to the purpose of this subsection.'' For 
additional information regarding tolerance objection fee waivers, 
contact James Tompkins, 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. 239, CM #2, 1921 Jefferson Davis Hwy., Arlington, VA, 
(703) 305-5697, [email protected]. Requests for waiver of tolerance 
objection fees should be sent to James Hollins, Information Resources 
and Services Division (7502C), Office of Pesticide Programs, 
Environmental Protection Agency, 401 M St., SW., Washington, DC 20460.
    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

[[Page 37869]]

(40 CFR 178.27). A request for a hearing will be granted if 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 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 regulation under docket 
control number [OPP-300886] (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 Rm. 119 of the Public Information and Records 
Integrity Branch, Information Resources and Services Division (7502C), 
Office of Pesticide Programs, Environmental Protection Agency, CM #2, 
1921 Jefferson Davis Hwy., Arlington, VA.
    Objections and hearing requests may be sent by e-mail directly to 
EPA at:

    [email protected]

    E-mailed objections and hearing requests must be submitted as an 
ASCII file avoiding the use of special characters and any form of 
encryption.
    The official record for this regulation, as well as the public 
version, as described in this unit 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 record which 
will also include all comments submitted directly in writing. The 
official record is the paper record maintained at the Virginia address 
in ``ADDRESSES'' at the beginning of this document.

VII. Regulatory Assessment Requirements

A. Certain Acts and Executive Orders

    This final rule establishes a tolerance under section 408(d) of the 
FFDCA in response to a petition 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) (Public Law 104-4). Nor 
does it require any 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 tolerances and exemptions that are established 
on the basis of a petition under FFDCA section 408(d), such as the 
tolerance 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 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.

B. Executive Order 12875

    Under Executive Order 12875, entitled Enhancing the 
Intergovernmental Partnership (58 FR 58093, October 28, 1993), EPA may 
not issue a regulation that is not required by statute and that creates 
a mandate upon a State, local or tribal government, unless the Federal 
government provides the funds necessary to pay the direct compliance 
costs incurred by those governments. If the mandate is unfunded, EPA 
must provide to OMB a description of the extent of EPA's prior 
consultation with representatives of affected State, local, and tribal 
governments, the nature of their concerns, copies of any written 
communications from the governments, and a statement supporting the 
need to issue the regulation. In addition, Executive Order 12875 
requires EPA to develop an effective process permitting elected 
officials and other representatives of State, local, and tribal 
governments ``to provide meaningful and timely input in the development 
of regulatory proposals containing significant unfunded mandates.''
    Today's rule does not create an unfunded Federal mandate on State, 
local, or tribal governments. The rule does not impose any enforceable 
duties on these entities. Accordingly, the requirements of section 1(a) 
of Executive Order 12875 do not apply to this rule.

C. Executive Order 13084

    Under Executive Order 13084, entitled Consultation and Coordination 
with Indian Tribal Governments (63 FR 27655, May 19, 1998), EPA may not 
issue a regulation that is not required by statute, that significantly 
or uniquely affects the communities of Indian tribal governments, and 
that imposes substantial direct compliance costs on those communities, 
unless the Federal government provides the funds necessary to pay the 
direct compliance costs incurred by the tribal governments. If the 
mandate is unfunded, EPA must provide OMB, in a separately identified 
section of the preamble to the rule, a description of the extent of 
EPA's prior consultation with representatives of affected tribal 
governments, a summary of the nature of their concerns, and a statement 
supporting the need to issue the regulation. In addition, Executive 
Order 13084 requires EPA to develop an effective process permitting 
elected officials and other representatives of Indian tribal 
governments ``to provide meaningful and timely input in the development 
of regulatory policies on matters that significantly or uniquely affect 
their communities.''
    Today's rule does not significantly or uniquely affect the 
communities of Indian tribal governments. This action does not involve 
or impose any requirements that affect Indian tribes. Accordingly, the 
requirements of section 3(b) of Executive Order 13084 do not apply to 
this rule.

[[Page 37870]]

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 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 25, 1999.

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. 321(q), 346a and 371.

    2. In Sec. 180.482, in paragraph (a), by adding alphabetically the 
following commodity to the table and adding footnote 1 to the table to 
read as follows:


Sec. 180.482  Tebufenozide; tolerances for residues.

    (a)     *    *    *

 
------------------------------------------------------------------------
                   Commodity                        Parts per million
------------------------------------------------------------------------
 
                          *    *    *    *    *
Kiwifruit\1\...................................                      0.5
 
                          *    *    *    *    *
------------------------------------------------------------------------
\1\ There are no U.S. registrations on kiwifruit as of June 15, 1999.

*    *    *    *    *

[FR Doc. 99-17776 Filed 7-13-99; 8:45 am]
BILLING CODE 6560-50-F