[Federal Register Volume 65, Number 72 (Thursday, April 13, 2000)]
[Rules and Regulations]
[Pages 19842-19849]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 00-9144]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-300991; FRL-6553-7]
RIN 2070-AB78


Fenhexamid; Pesticide Tolerances

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes tolerances for fenhexamid (N-2,3-
dichloro-4-hydroxyphenyl)-1-methyl cyclohexanecarboxamide) in or on 
almond, nutmeat at 0.02 parts per million (ppm), almond, hull at 2.0 
ppm, stone fruit, except plum (fresh prune) at 6.0 ppm, plum (fresh 
prune) at 0.5 ppm, and prune, dried at 1.0 ppm. The TM-402 Fungicide 
Task Force which is comprised of Tomen Agro, Inc. and Bayer Corporation 
requested these tolerances under the Federal Food, Drug, and Cosmetic 
Act, as amended by the Food Quality Protection Act of 1996.

DATES: This regulation is effective April 13, 2000. Objections and 
requests for hearings, identified by docket control number OPP-300991, 
must be received by EPA on or before June 12, 2000.

ADDRESSES: Written objections and hearing requests may be submitted by 
mail, in person, or by courier. Please follow the detailed instructions 
for each method as provided in Unit VI. of the ``SUPPLEMENTARY 
INFORMATION.'' To ensure proper receipt by EPA, your objections and 
hearing requests must identify docket control number OPP-300991 in the 
subject line on the first page of your response.

FOR FURTHER INFORMATION CONTACT: By mail: Mary L. Waller, Product 
Manager 21, Registration Division (7505C), Office of Pesticide 
Programs, Environmental Protection Agency, Ariel Rios Bldg., 1200 
Pennsylvania Ave., NW.,Washington, DC 20460; telephone number: (703) 
308-9354; and e-mail address: [email protected].

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

    You may be affected by this action if you are an agricultural 
producer, food manufacturer, or pesticide manufacturer. Potentially 
affected categories and entities may include, but are not limited to:

------------------------------------------------------------------------
                                                          Examples of
           Categories                 NAICS codes         potentially
                                                       affected entities
------------------------------------------------------------------------
Industry                          111                 Crop production
                                  112                 Animal production
                                  311                 Food manufacturing
                                  32532               Pesticide
                                                       manufacturing
------------------------------------------------------------------------

    This listing is not intended to be exhaustive, but rather provides 
a guide for readers regarding entities likely to be affected by this 
action. Other types of entities not listed in the table could also be 
affected. The North American Industrial Classification System (NAICS) 
codes have been provided to assist you and others in determining 
whether or not this action might apply to certain entities. If you have 
questions regarding the applicability of this action to a particular 
entity, consult the person listed under ``FOR FURTHER INFORMATION 
CONTACT.''

B. How Can I Get Additional Information, Including Copies of this 
Document and Other Related Documents?

    1. Electronically. You may obtain electronic copies of this 
document, and certain other related documents that might be available 
electronically, from the EPA Internet Home Page at http://www.epa.gov/. 
To access this document, on the Home Page select ``Laws and 
Regulations'' and then look up the entry for this document under the 
``Federal Register--Environmental Documents.'' You can also go directly 
to theFederal Register listings at http://www.epa.gov/fedrgstr/.
    2. In person. The Agency has established an official record for 
this action under docket control number OPP-300991. The official record 
consists of the documents specifically referenced in this action, and 
other information related to this action, including any information 
claimed as Confidential Business Information (CBI). This official 
record includes the documents that are physically located in the 
docket, as well as the documents that are referenced in those 
documents. The public version of the official record does not include 
any information claimed as CBI. The public version of the official 
record, which includes printed, paper versions of any electronic 
comments submitted during an applicable comment period is available for 
inspection in the Public Information and Records Integrity Branch 
(PIRIB), Rm. 119, Crystal Mall #2, 1921 Jefferson Davis Hwy., 
Arlington, VA, from 8:30 a.m. to 4 p.m., Monday through Friday, 
excluding legal holidays. The PIRIB telephone number is (703) 305-5805.

II. Background and Statutory Findings

    In the Federal Register of February 25, 2000 (65 FR 10078) (FRL-
6494-2), 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 an amendment to pesticide petition (PP 7F4890) 
for tolerances, by the TM-402 Fungicide Task Force (Tomen Agro, Inc, 
100 First Street, Suite 1610, San Francisco, CA 94105 and Bayer 
Corporation, 8400 Hawthorn Road, P.O. Box 4913, Kansas City, MO 64120-
0013). This notice included a summary of the petition prepared by the 
TM-402 Fungicide Task Force. The registrant is Tomen Agro, Inc. There 
were no comments received in response to the notice of filing.
    The amended petition requested that 40 CFR 180.553 be amended by 
establishing tolerances for the fungicide, fenhexamid in or on almond, 
nutmeat at 0.02 ppm, almond, hull at 2.0 ppm, stone fruit, except plum 
(fresh prune) at 6.0 ppm, plum (fresh prune) at 0.5 ppm, and prune, 
dried at 1.0 ppm.
    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

[[Page 19843]]

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).

III. 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 
fenhexamid and to make a determination on aggregate exposure, 
consistent with section 408(b)(2), for tolerances in or almond, nutmeat 
at 0.02 ppm, almond, hull at 2.0 ppm, stone fruit, except plum (fresh 
prune) at 6.0 ppm, plum (fresh prune) at 0.5 ppm, and prune, dried at 
1.0 ppm. 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 fenhexamid are 
discussed in this unit.
    1. Acute toxicity-- i. The acute oral LD50 and acute 
dermal LD50 for rats was > 5,000 milligrams/kilogram (mg/kg) 
for both sexes. The acute inhalation LC50 for rats was > 
5.06 milligrams/liter (mg/L) for both sexes. Fenhexamid was not an eye 
or skin irritant and was not a dermal sensitizer.
    ii. In an acute neurotoxicity study, rats were gavaged with a 
single oral dose of fenhexamid at dose levels of 0, 200, 630, or 2,000 
mg/kg. The rats were observed for 14 days. Functional observational 
battery and motor activity testing were performed 7 days prior to 
dosing, approximately 20 minutes to 3 hours post-dosing, and on days 7 
and 14. The no observed adverse effect level (NOAEL) in males was 630 
mg/kg. The NOAEL in females was 2,000 mg/kg. The lowest observed 
adverse effect level (LOAEL) in males was 2,000 mg/kg based on a 
marginally decreased mean body temperature (the only treatment-related 
effect noted in the study). The LOAEL in females was not established.
    2. Subchronic toxicity-- i. In an inhalation toxicity range-finding 
study, 10 rats/sex/dose were exposed (head/nose only) to fenhexamid at 
concentrations of 0, 11.8, 97.7, or 1,092.6 mg/m3 in air for 
6 hours per day for 5 days. One-half of the rats were sacrificed 7 days 
after the first exposure and the other one-half were sacrificed 21 days 
after the first exposure. The NOAEL was 0.098 mg/L and the LOAEL was 
1,092 mg/L based on the observations of macroscopic grey coloration of 
the lungs and marginally increased lung weights.
    ii. In a 21-day dermal toxicity study, fenhexamid was applied to 
the shaved skin of 5 male and female rabbits at a dose level of 1,000 
mg/kg/day for 17 days over a 3-week period. There were no compound 
related effects. The NOAEL was 1,000 mg/kg/day and the LOAEL was > 
1,000 mg/kg/day for both systemic and local effects on the skin.
    iii. In a 28-day oral toxicity range finding study, 10 rats/sex/
dose were gavaged at dose levels of 0, 100, 300, or 1,000 mg/kg/day for 
28 days. There were no compound-related effects in mortality, clinical 
signs, body weight, food consumption, hematology, clinical chemistry, 
organ weights, or gross and histologic pathology. The NOAEL was 1,000 
mg/kg/day.
    iv. In a 90-day oral toxicity study, 10 rats/sex/dose were fed 
fenhexamid at dose levels of 0, 2,500, 5,000, 10,000, or 20,000 ppm (0, 
202, 415, 904, and 1,904 mg/kg/day for males and 0, 270, 549, 1,132, 
and 2,824 mg/kg/day for females). No treatment-related changes were 
seen in clinical signs, mortality, opthalmoscopic examinations, 
hematology, urinalyses, or gross pathology. The NOAEL was 5,000 ppm in 
males and 10,000 ppm in females. The LOAEL in males was 10,000 ppm 
based on decreased terminal body weights and body weight gains, 
increased food consumption, decreased food efficiency and increased 
Alanine amino-transferase (ALAT) levels. The LOAEL in females was 
20,000 ppm based on increased food consumption, decreased food 
efficiency, decreased liver weights and liver histopathology (Kupffer 
cell proliferation and altered hepatocyte morphology).
    v. In a 90-day oral toxicity study, 4 dogs/sex were fed fenhexamid 
at dose levels of 0, 1,000, 7,000, or 50,000 ppm (0, 33.9, 239.1, or 
1,747.7 mg/kg/day for males and 0, 37, 261, or 1,866.2 mg/kg/day for 
females). The NOAEL in males and females was 1,000 ppm. The LOAEL in 
males and females was 7,000 ppm based on significant increases in Heinz 
bodies in males and females and increased absolute and relative liver 
weights in females.
    vi. In a 90-day oral toxicity study, 10 mice/sex/dose were fed 
fenhexamid at dose levels of 0, 100, 1,000, or 10,000 ppm (0, 26.5, 
266.5, or 3,283.5 mg/kg/day in males and 0, 51.6, 453.9, or 5,151.1 mg/
kg/day in females) for 14 weeks. The NOAEL in males and females was 
1,000 ppm. The LOAEL in males and females was 10,000 ppm based on the 
observation in both sexes of: Increased serum cholesterol, bilirubin 
and creatinine, decreased kidney weights, increased water consumption, 
increased food consumption (males), decreased food efficiency (males), 
renal cortical tubular basophilia (both sexes), renal protein casts and 
cellular detritus (males), and marginal alterations of liver function 
(increased serum cholesterol, bilirubin, decreased Aspartate amino-
transferase (ASAT), ALAT, marginal increase in liver weights and 
reduced glycogen content of hepatocytes (males).
    vii. In a 56-day oral toxicity study, 10 rats/sex/dose were fed 
fenhexamid at dose levels of 0, 1,000, 5,000, 10,000, 15,000, or 20,000 
ppm (0, 57.5, 284.7, 575.7, 943.8, or 1,217.1 mg/kg/day for males and 
0, 78, 407.1, 896.5, 1,492.5, or 1,896.7 mg/kg/day for females). At 
20,000 ppm, rats had fenhexamid plasma levels below the level of 
detection. Urine samples showed measurable excretion of conjugated 
fenhexamid indicating intestinal absorption in the dose range examined. 
Males had a maximum excretion rate at 15,000 ppm indicating a 
saturation of intestinal absorption between 15,000 and 20,000 ppm. 
Urine excretion in females was somewhat lower than in males, at 
concentrations of 10,000 ppm and above. The highest value was 
determined at 20,000 ppm suggesting that saturation in intestinal 
absorption was not achieved with this dose level in females.
    3. Developmental toxicity-- i. In a developmental toxicity study, 
30 rats/dose were gavaged at dose levels of 0 and 1,000 (1,044 
determined analytically) mg/kg/day from days 6 through 15 of gestation. 
At 1,000 mg/kg/day, there were no treatment-related effects on maternal 
mortality, clinical signs, cesarean parameters or gross pathology. No 
treatment-related effects were noted in any embryo/fetal parameters. 
Under the conditions of the study, fenhexamid was not embryotoxic, 
fetotoxic or teratogenic at a dose of 1,044 mg/kg/day. The NOAEL for 
developmental and maternal toxicity was < 1,044 mg/kg/day. The LOAEL 
for maternal toxicity was 1,044 mg/kg/day based on the decreased body 
weight gain (-12% of controls) during gestation days 6-16 and a 
decrease in food consumption (10% of controls) during gestation days 6-
11.

[[Page 19844]]

    ii. In a developmental toxicity study, 16 rabbits were gavaged with 
fenhexamid at dose levels of 0, 100, 300, or 1,000 mg/kg/day from days 
6 through 18 of gestation. No treatment-related effects were seen on 
mortality, general appearance or behavior. The NOAEL for maternal 
toxicity was 100 mg/kg/day. The LOAEL for maternal toxicity was 300 mg/
kg/day based on observations at this dose and above of alterations of 
excretory products (discolored urine, small scybala), decreased body 
weight gain and feed consumption (mainly during the first week of the 
treatment period) and decreased placental weights. One abortion at 300 
mg/kg/day and one abortion and two total litter resorptions at 1,000 
mg/kg/day were not considered to be treatment-related because the 
incidences fell within the ranges of historical control data submitted 
with the study. Reduced and/or light feces were also noted at 1,000 mg/
kg/day. Pale livers were noted in the 2 dams that aborted. The NOAEL 
for developmental toxicity was 300 mg/kg/day. The LOAEL for 
developmental toxicity was 1,000 mg/kg/day based on marginally 
decreased male fetal body weights and evidence of delayed ossification. 
Fenhexamid did not induce any treatment-related fetal malformations or 
deviations at any of the doses tested under the conditions of this 
study. All effects on intrauterine development were correlated with 
maternal toxicity and, therefore, no primary developmental effect was 
evident. Fenhexamid was not teratogenic up to and including 1,000 mg/
kg/day.
    4. Reproductive toxicity. In 2-generation reproduction study, 30 
rats/sex/dose were fed fenhexamid at dose levels of 0, 100, 500, 5,000, 
or 20,000 ppm (0, 7.6, 38.2, 406, or 1,814 mg/kg/day for males and 0, 
9.0, 44.8, 477, or 2,043 mg/kg/day for females determined for the 10-
week premating period). There were no compound-related effects on 
mortality, clinical signs, behavior or reproductive parameters for 
adult animals. The NOAEL for reproductive toxicity was 20,000 ppm.
    The neonatal NOAEL was 500 ppm and the neonatal LOAEL was 5,000 ppm 
based on significantly decreased pup body weights on lactation days 14 
and 21 for the F1 (6-11% < controls) and on lactation days 
7, 14, and 21 for F2 pups (9-11% < controls). At 20,000 ppm, 
significantly decreased pup body weights were observed on lactation 
days 7, 14, and 21 for F1 pups (15-30% < controls) and for 
F2 pups (11-19% < controls). Treatment-related decreased pup 
body weights were not observed at birth or on lactation day 4. An 
additional effect observed at 20,000 ppm was an increase in the number 
of pups among the post-weaning F1 pups selected to be 
F1 parents which died, that is, 0/66, 2/68, 0/68, 0/68, and 
10/78 for the control, 100, 500, 5,000, and 20,000 ppm dose groups, 
respectively. This effect was attributed to the small size of the pups 
at weaning (30% < controls).
    The parental NOAEL was 500 ppm and the parental LOAEL in males was 
5,000 ppm based on increased creatinine levels in P-generation (but not 
F1 generation) males at premating (20%, p<0.05) and at 
termination (20%, not significant); slightly increased alkaline 
phosphatase levels in P-generation and F1-generation males 
at premating and at termination (20-34%, not significant); decreased 
absolute liver weight in P-generation and F1-generation 
males (11-12%, p0.05) and decreased liver/body weight ratios in P-
generation and F1-generation males (8-9%, p<0.05 for P-
generation and not significant for F1-generation); decreased 
absolute kidney weights in F1-generation (but not P-
generation) males (12%, p<0.05); and decreased kidney/body weight 
ratios in F1-generation (but not P-generation) males (8%, 
p>0.05). The parental LOAEL in females was based on increased alkaline 
phosphatase levels in F1-generation) (but not P-generation) 
females at premating (43%, p<0.05) and at termination (63%, p<0.05); 
and on very small increases in gamma glutamyl transferase (GGT) (not 
considered to be biologically relevant). Overall, treatment-related 
effects observed at 5,000 ppm in males and females were also observed 
at 20,000 ppm, but were slightly increased in severity. Toxicologically 
relevant additional toxicological effects observed at 20,000 ppm were 
decreased body weights and increased food consumption in males and 
increased urea nitrogen and creatinine levels, decreased kidney 
weights, decreased body weights and increased food consumption in 
females.
    5. Mutagenicity. No mutagenicity was noted in the following assays: 
Reverse gene mutation, S. typhimurium, E. coli; forward gene mutation -
Hypoxanthine guanine phophoribosyl transferase (HGPRT) locus; 
Chromosome aberration, Chinese hampster ovary (CHO) cells; unscheduled 
DNA synthesis, rat hepatocytes; and micronucleus assay in mice.
    6. Chronic toxicity-- i. In a 1-year chronic oral toxicity study, 
dogs were fed dose levels of 0, 500, 3,500, or 25,000 ppm (0, 17.4, 
124.3, or 917.8 mg/kg/day for males and 0, 19.2, 132.7, or 947.1 mg/kg/
day for females). The NOAEL in males and females was 500 ppm. The LOAEL 
was 3,500 ppm in males and females based on decreases in red blood 
cells (RBC), hemoglobin (Hb), and hematocrit (Hct) and on significant 
increases in Heinz bodies in both sexes, increased adrenal weight 
parameters in females, and the presence of intracytoplasmic vacuoles in 
the adrenal cortex of 3/4 females.
    ii. In a combined chronic toxicity/carcinogenicity study, 50 rats/
sex/dose were fed fenhexamid at dose levels of 0, 500, 5,000, or 20,000 
ppm (0, 28, 292, or 1,280 mg/kg/day for males and 0, 40, 415, 2,067 mg/
kg/day for females) for 24 months. The NOAEL in males and females was 
500 ppm. The LOAEL for chronic toxicity in males and females was 5,000 
ppm based on observations of decreased body weight gain (-6.8%) and 
food efficiency (-11.8%) in females, increased incidence of cecal 
mucosal hyperplasia in males, increased cellularity (hyperplasia) of 
the bone marrow in females and the presence of splenic extramedullary 
hematopoiesis in males. At 20,000 ppm, observations were increased food 
consumption, increased numbers of circulating reticulocytes, enlarged 
spleens observed macroscopically, increased splenic weights and thyroid 
colloid alterations (both sexes). Fenhexamid was non-oncogenic at doses 
up to and including 20,000 ppm in the diet. At doses tested, there were 
no treatment related increases in tumor incidence, tumor spectrum or 
latency when compared to controls.
    7. Carcinogenicity. In a carcinogenicity study, 50 mice/sex/dose 
were fed fenhexamid at dose levels of 0, 800, 2,400, or 7,000 ppm (0, 
247.4, 807.4, or 2,354.8 mg/kg/day for males and 0, 364.8, 1,054.5, or 
3,178.2 mg/kg/day for females) for 2 years. The NOAEL for males was 800 
ppm and the NOAEL for females was 2,400 ppm. The LOAEL for males was 
2,400 ppm based on the observation of decreased kidney weights and 
decreases in sex-specific vacuolation of the proximal tubules in the 
kidneys in males. A marginal decrease in body weights (up to 8%) and 
body weight gain (17%) was observed in males at 7,000 ppm. The LOAEL 
for females was 7,000 ppm based on significantly increased water 
consumption, decreased kidney weights, and renal histopathology 
(increased incidence of basophilic cortical tubules). Fenhexamid was 
not oncogenic in mice at doses up to and including 7,000 ppm. There 
were no treatment related increases in tumor incidence, tumor spectrum 
or latency when compared to controls.

[[Page 19845]]

    8. Dermal absorption. In a dermal absorption study, radiolabeled 
fenhexamid (50% formulation) was applied to the shaved skin of male 
rats at dose levels of 0.00138, 0.0147, or 0.148 mg/cm2. A 
volume of 100 L was applied to a skin area of approximately 
12.5 cm2 on each rat. Four rats/dose level were sacrificed 
at 0.5, 1, 2, 4, 10, 24, and 120 hours postdose. Mean total recovery of 
radioactivity ranged from 90.3% to 97.6% of the applied dose. The 
majority of radioactivity was recovered from the skin wash (69.9% to 
96.1%). Radioactivity in the skin test site ranged from 0.44% to 10.2%; 
in the urine from ``not detectable'' to 3.34%; and in the feces from 
``not detectable'' to 11.6% of the applied dose. Radioactivity in blood 
did not exceed 0.03% and in the carcass did not exceed 9.37%. Estimates 
of dermal absorption were based on the sum of radioactivity (as test 
material) in the skin test site, urine, feces, blood and carcass. The 
percentage dermal absorption decreased with increasing dose levels. The 
percentage dermal absorption at 10 hours postdose was 19.58%, 7.62%, 
and 2.63% and at 120 hours postdose was 21.0%, 6.91%, and 2.13% for the 
low, mid and high dose levels respectively.
    9. Metabolism. In a metabolism study, rats were administered 
radiolabeled fenhexamid (a single oral low dose of 1 mg/kg, a single 
oral high dose of 100 mg/kg, or 15 repeated low doses of 1 mg/kg/day). 
Radiolabeled fenhexamid was rapidly absorbed from the gastrointestinal 
(GI) tract in all dose groups. After single and repeated administration 
of the low dose, the plasma concentration peaked within 5 to 10 
minutes. After administration of the high dose, the maximum was 
detected 40 to 90 minutes postdosing. The absorption of the test 
compound was shown to be almost complete in a bile-cannulation 
experiment, as more than 97% of the administered dose was absorbed from 
the GI tract 48 hours after intra-duodenal administration. These 
results are indicative of a pronounced first pass effect and 
enterohepatic circulation. Tissue residues declined rapidly and after 
48 hours the total radioactivity residue in the body excluding the GI 
tract, was < 0.3% of the administered dose in all dose groups. Liver 
and kidney were the organs with the highest concentrations of 
radioactivcity in all dose groups. Excretion was rapid and almost 
complete with feces as the major route of excretion. Approximately 62-
81% of the recovered radioactivity was found in feces, and 15-36% in 
urine within 48 hours post-dosing. More than 90% of the recovered 
radioactivity was eliminated with bile in the bile cannulation 
experiment. Only 0.02% of the administered radioactivity was recovered 
in exhaled air. Radioactive residues in rat bodies (excluding GI tract) 
were significantly lower in females after a single high dose. There was 
significantly higher renal excretion for females in comparison with 
males after 15 repeated low doses. In both sexes renal excretion was 
significantly higher after a single low dose when compared with a 
single high dose. Metabolite characterization studies showed that the 
main component detected in excreta was the unchanged parent compound 
which accounted for 62-75% of the dose independent of the dosing regime 
and sex. Metabolite 1, the glucuronic acid conjugate of the parent 
compound, ranged from 4 to 23% of the dose. Metabolite fractions 2 and 
3 accounted for up to 3 and 7% of the dose, respectively. The proposed 
major pathway for biotransformation is via conjugation of the aromatic 
hydroxyl group with glucuronic acid. Prior to fecal excretion, 
hydrolysis in the intestine converts the conjugate back to the parent 
compound giving rise to enterohepatic circulation. Identification of 
radioactive residues ranged from 88% to 99% and was independent of dose 
and sex.

B. Toxicological Endpoints

    1. Acute toxicity. An acute toxicological endpoint was not 
identified resulting from a single oral exposure, and therefore, an 
acute Reference Dose (RfD) was not selected.
    2. Short- and intermediate-term toxicity. A short- and 
intermediate-term dermal endpoint of 1,000 mg/kg/day from the 21-day 
dermal toxicity study in rabbits was selected for occupational 
exposure. No short- and intermediate-term endpoint was selected for 
non-occupational exposure as there are no residential uses of 
fenhexamid.
    3.Chronic toxicity. EPA has established the RfD for fenhexamid at 
0.17 mg/kg/day. This RfD is based on a 1-year feeding study in dogs 
with a NOAEL = 17 mg/kg/day. An additional 3x FQPA safety factor was 
added and applies to all population subgroups resulting in a chronic 
population adjusted dose (cPAD) of 0.057 mg/kg/day.
    4. Carcinogenicity. Fenhexamid was classified as a ``not likely'' 
human carcinogen based on the lack of evidence of carcinogenicity in 
mice and rats and the lack of genotoxicity in a battery of mutagenicity 
studies.

C. Exposures and Risks

    1. Dietary-- i. From food and feed uses. Tolerances are currently 
established for fenhexamid at 40 CFR 180.553 for grapes at 4.0 ppm, 
strawberries at 3.0 ppm, and raisins at 6.0 ppm. Additional tolerances 
are being proposed as follows: almond, nutmeat at 0.02 ppm, almond, 
hull at 2.0 ppm, stone fruit, except plum (fresh prune) at 6.0 ppm, 
plum (fresh prune) at 0.5 ppm, and prune, dried at 1.0 ppm. Risk 
assessments were conducted by EPA to assess dietary exposures from 
fenhexamid as follows:
    a. 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. No toxicological endpoint attributable 
to a single (acute) dietary exposure was identified.
    b. Chronic exposure and risk. The chronic risk analysis used the 
cPAD of 0.057 mg/kg/day which applies to all population subgroups. The 
Dietary Exposure Evaluation Model (DEEMTM) which is a 
exposure analysis system that estimates exposure to a pesticide 
chemical in food comprising the diets of the U.S. population, including 
population subgroups was used to conduct the chronic (food) risk 
analysis. DEEMTM contains food consumption data as reported 
by respondents in the USDA Continuing Surveys of Food Intake by 
Individuals conducted in 1989-1992. The chronic food exposure was 
calculated assuming theoretical maximum residue contribution (TMRC) 
values, and 100% crop treated estimates. The percent of the cPAD 
utilized is as follows: 15.7 for non-nursing infants; 14.2 for all 
infants (<1 year); 10.7 for nursing infants; 9.9 for children (1-6 
years); 5.7 for non-Hispanic/non-white/non-black; 5.0 for children (7 
to 12 years); 4.6 for U.S. population (summer season); 3.7 for U.S. 
population (total) and 2.6 for females (13-50 years).
    ii. From drinking water. In soil, fenhexamid is relatively immobile 
(Koc = 446) and non-persistent (t1/2 = 
 1 day). Fenhexamid is not expected to be a ground water 
contaminant, but has some potential to reach surface water on eroded 
soil particles. In surface water, fenhexamid would be expected to 
photodegrade rapidly (t1/2 =  0.2 days).
    No monitoring data are available to perform a quantitative drinking 
water assessment. The Agency estimated surface water exposure using the 
Generic Expected Environmental Concentration (GENEEC) model, a

[[Page 19846]]

screening level model for determining concentrations of pesticides in 
surface water. GENEEC uses the soil/water partition coefficient, 
hydrolysis half life, and the maximum label rate to estimate surface 
water concentration. GENEEC contains a number of conservative 
underlying assumptions. Therefore, the drinking water concentrations 
derived from GENEEC for surface water are likely to be overestimated. 
The modeling was conducted based on the environmental profile and the 
maximum seasonal application rate proposed for fenhexamid: 0.75 lb. 
active ingredient/acre x 4 applications/acre/year. The estimated 
environmental concentrations (EECs) derived from GENEEC are 17 
g/L (peak value) and 4.8 g/L (56-day average).
    The Agency used the Screening Concentration in Ground Water (SCI-
GROW) model to estimate pesticide levels in ground water. The SCI-GROW 
model is based on actual monitoring data collected for a number of 
pesticides that serve as benchmarks to predict EECs in ground water. 
Using SCI-GROW, the EEC calculated for fenhexamid is 0.0007 g/
L (acute and chronic).
    a. Acute exposure and risk. Drinking water levels of comparison 
(DWLOCs) for acute exposure were not calculated as there was no 
appropriate toxicological endpoint attributable to a single (acute) 
dietary exposure.
    b. Chronic exposure and risk. Chronic (non-cancer) DWLOCs were 
calculated for the U.S. population and the population subgroups with 
the highest (chronic) food exposure. The DWLOCs are as follows: 480 
g/L for infants/children; 1,700 g/L for females 13-50 
yrs.); and 1,900 g/L for the U.S. population and all other 
subgroups. The EEC (0.0007 g/L from SCI-GROW, and 4.8 
g/L from GENEEC) for fenhexamid are well below the DWLOCs and 
therefore, are below the Agency's level of concern. Therefore, the 
Agency concludes with reasonable certainty that residues of fenhexamid 
in drinking water do not contribute significantly to the aggregate 
chronic human health risk.
    2. From non-dietary exposure. Fenhexamid is not registered for use 
on residential non-food sites. Therefore, no non-occupational, non-
dietary exposure and risk are expected.
    3. 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 fenhexamid 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, 
fenhexamid 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 fenhexamid 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. Acute aggregate risk is the sum of exposures 
resulting from acute dietary food + acute drinking water. The Agency 
did not identify an appropriate toxicological endpoint attributable to 
a single (acute) dietary exposure.
    2. Chronic risk. Using the TMRC, exposure assumptions described in 
this unit, EPA has concluded that aggregate exposure to fenhexamid from 
food will utilize 3.7% of the cPAD for the U.S. population. The major 
identifiable subgroup with the highest aggregate exposure is non-
nursing infants (< 1 year) discussed below. 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 fenhexamid in drinking water, EPA 
does not expect the aggregate exposure to exceed 100% of the cPAD. EPA 
concludes that there is a reasonable certainty that no harm will result 
from aggregate exposure to fenhexamid residues.
    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. Although short- and intermediate-term endpoints 
were identified, there are no residential uses for fenhexamid.
    4. Aggregate cancer risk for U.S. population. Fenhexamid was 
classified as ``not likely'' to be a human carcinogen.
    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 fenhexamid 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 fenhexamid, 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 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. Prenatal and postnatal sensitivity. Qualitatively, there is 
evidence of increased susceptibility in rat pups compared to adults, 
based on the relative severity of effects in the two-generation 
reproduction study in rats. The effects on pups were of concern 
because: significant pup body weight decreases were observed in both 
the F1 and the F2 generations; the pup body 
weight decreases in the F2 generation were observed during 
early lactation (lactation day 7 through day 21) when the pups are 
exposed to the test material primarily through the mother's milk; the

[[Page 19847]]

pup body weight decreases in the F1 generation were observed 
during late lactation (lactation days 14 through 21) when the pups are 
exposed to the test material through the mother's milk and through the 
feed; and, in the metabolism study on fenhexamid, glucuronidation of 
fenhexamid was clearly demonstrated to be the single major route of 
metabolism, detoxification and excretion of fenhexamid in adult male 
and female rats. The demonstrated poor glucuronidation capacity of rat 
pups between days 7 and 21 indicates a possibly increased sensitivity 
of pups and serves to support a concern for neonatal toxicity.
    iii. Conclusion. There is a complete toxicity data base for 
fenhexamid and exposure data are complete or are estimated based on 
data that reasonably accounts for potential exposures. Although there 
is qualitative evidence of increased susceptibility, the Agency decided 
that an additional safety factor of 3x would be appropriate based on 
the following reasons: The increased susceptibility demonstrated in the 
2-generation reproduction study was only qualitative (not quantitative) 
evidence and was observed only in the presence of parental toxicity; 
the qualitative offspring effect was limited to decreased body weight 
and no other adverse effects (e.g., decreased pup survival, behavioral 
alterations, etc.) were observed; and there is no indication of 
increased susceptibility of rat or rabbit fetuses to in utero exposure 
in the prenatal developmental toxicity studies with fenhexamid.
    2. Acute risk. An acute endpoint was not identified.
    3. Chronic risk. Using the exposure assumptions described in this 
unit, EPA has concluded that the highest aggregate exposure to 
fenhexamid from food will utilize 15.7% of the cPAD for non nursing 
infants. 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 fenhexamid 
in drinking water and from non-dietary, non-occupational exposure, EPA 
does not expect the aggregate exposure to exceed 100% of the cPAD.
    4. Short- or intermediate-term risk. There are no residential uses 
and thus these risks are not presented.
    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 fenhexamid residues.

IV. Other Considerations

A. Metabolism in Plants

    The parent compound, fenhexamid, is the only compound of concern. 
Radiolabeled fenhexamid plant metabolism studies were conducted on 
grapes, tomatoes, and apples. The qualitative nature of fenhexamid 
residues in plants is adequately understood. The data indicate very 
little translocation of residues, i.e., residues of fenhexamid are non-
systemic and are thus primarily surface residues.

B. Metabolism in Animals

    Almond hulls which are a livestock feed item contain 90% dry matter 
and its contribution to the livestock diet is a maximum of 10% each for 
beef and dairy cattle. Data from a study investigating the metabolism 
of 14C fenhexamid in a lactating goat indicated that the 
metabolism of fenhexamid in the goat is similar to that in the rat, and 
based on the experimentally determined feeding level of 133 ppm in the 
feed, the Agency calculates that the dosage was equivalent to 605x the 
maximum theoretical dietary burden of 0.22 ppm for beef and dairy 
cattle. The total radioactive residues (TRR) were 0.045-0.212 ppm in 
milk, 4.682 ppm in liver, 3.267 ppm in kidney, 0.035 ppm in muscle, and 
0.085 ppm in fat.
    The qualitative nature of the residue in ruminants is adequately 
understood. Based on the goat metabolism study, the Agency concludes 
that there is no reasonable expectation of finite residues in milk or 
ruminant tissues as a result of the currently proposed uses on almonds 
and stone fruits, and ruminant commodity tolerances are not required.

C. Analytical Enforcement Methodology

    Adequate enforcement methodology (a high performance liquid 
chromotography method with electrochemical detection) is available to 
enforce the tolerance expression. The method may be requested from: 
Calvin Furlow, PIRIB, IRSD (7502C), Office of Pesticide Programs, 
Environmental Protection Agency, Ariel Rios Bldg., 1200 Pennsylvania 
Ave., NW., Washington, DC 20460. Office location and telephone number: 
Rm 101FF, Crystal Mall #2, 1921 Jefferson Davis Hwy., Arlington, VA, 
(703) 305-5229.

D. Magnitude of Residues

    A total of five almond field trials were conducted in California. 
The almond field trial data are adequate in number and geographical 
representation. The data indicate that residues of fenhexamid will not 
exceed the proposed tolerances of 0.02 ppm in/on almond nutmeats and 
2.0 ppm in/on almond hulls following applications of the proposed 50% 
WDG formulation according to the maximum proposed use patterns. Samples 
of almond RACs were harvested 142-173 days following the last of four 
sequential applications of the 50% WDG formulation at 0.73-0.76 lb ai/
acre/application (3.0 lbs active ingredient acre/season (ai/acre/
season); 1x the proposed maximum seasonal application rate). Residues 
of fenhexamid were non-detectable (<0.02 ppm) in/on all treated almond 
nutmeat samples.
    Field trial data were submitted for cherries (sweet and tart), 
peaches, and plums, which are the three representative commodities of 
the stone fruits crop group (40 CFR 180.41, Crop Group 12). Samples 
(U.S. field trials) were harvested 0-days following the last of four 
sequential foliar applications of the 50% WDG formulation at 0.73-0.78 
lb ai/acre/application (3.0 lbs ai/acre/season; 1x the proposed maximum 
seasonal application rate). Residues of fenhexamid (uncorrected for 
method recovery and storage stability data) in/on treated samples 
ranged from 0.844-1.826 ppm for sweet cherries, 1.049-4.950 ppm for 
tart cherries, 0.327-2.131 ppm for peaches, and <0.05-0.366 ppm for 
plums. The residue data for stone fruits indicates that the maximum 
residues for tart cherries (4.950 ppm) and plums (0.366 ppm) differ by 
a factor of 13.5. On this basis, the Agency concludes that plums should 
be excluded from the proposed stone fruits crop group tolerance, and an 
individual tolerance is being established for residues of fenhexamid 
in/on plums (fresh prunes) at 0.5 ppm.
    No processing study data have been submitted for dried prunes. 
Based on the concentration factor which has previously been shown to 
occur in the processing of fenhexamid-treated grapes to raisins, it is 
probable that concentration of fenhexamid residues will occur in the 
processing of plums (fresh prunes) to dried prunes. The Agency 
concludes that the appropriate tolerance level for residues of 
fenhexamid per se in/on dried prunes is 1.0 ppm. This is based upon the 
highest average field trial (HAFT) residue value (0.264 ppm) for plums 
(fresh prunes) multiplied by the TMCF (3.4x) for dried prunes =0.90 
ppm, which is rounded up to 1.0 ppm.

E. International Residue Limits

    The Codex Alimentarius Commission has not established maximum 
residue limits (MRLs) for residues of fenhexamid or any of its 
metabolites in/on plant or animal commodities.

[[Page 19848]]

Harmonization is thus not an issue for this action.

F. Rotational Crop Restrictions

    The Agency concluded that a 30-day plantback interval is required 
for all crops without a fenhexamid tolerance.

V. Conclusion

    Therefore, tolerances are established for residues of fenhexamid in 
or on almond, nutmeat at 0.02 ppm, almond, hull at 2.0 ppm, stone 
fruit, except plum (fresh prune) at 6.0 ppm, plum (fresh prune) at 0.5 
ppm and prune, dried at 1.0 ppm.

VI. Objections and Hearing Requests

    Under section 408(g) of the FFDCA, as amended by the FQPA, any 
person may file an objection to any aspect of this regulation and may 
also request a hearing on those objections. The EPA procedural 
regulations which govern the submission of objections and requests for 
hearings appear in 40 CFR part 178. Although the procedures in those 
regulations require some modification to reflect the amendments made to 
the FFDCA by the FQPA of 1996, EPA will continue to use those 
procedures, with appropriate adjustments, until the necessary 
modifications can be made. The new section 408(g) provides essentially 
the same process for persons to ``object'' to a regulation for an 
exemption from the requirement of a tolerance issued by EPA under new 
section 408(d), as was provided in the old FFDCA sections 408 and 409. 
However, the period for filing objections is now 60 days, rather than 
30 days.

A. What Do I Need to Do to File an Objection or Request a Hearing?

    You must file your objection or request a hearing on this 
regulation in accordance with the instructions provided in this unit 
and in 40 CFR part 178. To ensure proper receipt by EPA, you must 
identify docket control number OPP-300991 in the subject line on the 
first page of your submission. All requests must be in writing, and 
must be mailed or delivered to the Hearing Clerk on or before June 12, 
2000.
    1. Filing the request. Your objection must specify the specific 
provisions in the regulation that you object to, and the grounds for 
the objections (40 CFR 178.25). If a hearing is requested, the 
objections must include a statement of the factual issues(s) on which a 
hearing is requested, the requestor's contentions on such issues, and a 
summary of any evidence relied upon by the objector (40 CFR 178.27). 
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.
    Mail your written request to: Office of the Hearing Clerk (1900), 
Environmental Protection Agency, Ariel Rios Bldg., 1200 Pennsylvania 
Ave., NW., Washington, DC 20460. You may also deliver your request to 
the Office of the Hearing Clerk in Rm. C400, Waterside Mall, 401 M St., 
SW., Washington, DC 20460. The Office of the Hearing Clerk is open from 
8 a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The 
telephone number for the Office of the Hearing Clerk is (202) 260-4865.
    2. Tolerance fee payment. If you file an objection or request a 
hearing, you must also pay the fee prescribed by 40 CFR 180.33(i) or 
request a waiver of that fee pursuant to 40 CFR 180.33(m). You must 
mail the fee to: EPA Headquarters Accounting Operations Branch, Office 
of Pesticide Programs, P.O. Box 360277M, Pittsburgh, PA 15251. Please 
identify the fee submission by labeling it ``Tolerance Petition Fees.''
    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 the waiver of these fees, you may contact James 
Tompkins by phone at (703) 305-5697, by e-mail at [email protected], 
or by mailing a request for information to Mr. Tompkins at Registration 
Division (7505C), Office of Pesticide Programs, Environmental 
Protection Agency, Ariel Rios Bldg., 1200 Pennsylvania Ave., NW., 
Washington, DC 20460.
    If you would like to request a waiver of the tolerance objection 
fees, you must mail your request for such a waiver to: James Hollins, 
Information Resources and Services Division (7502C), Office of 
Pesticide Programs, Environmental Protection Agency, Ariel Rios Bldg., 
1200 Pennsylvania Ave., NW., Washington, DC 20460.
    3. Copies for the Docket. In addition to filing an objection or 
hearing request with the Hearing Clerk as described in Unit VI.A., you 
should also send a copy of your request to the PIRIB for its inclusion 
in the official record that is described in Unit I.B.2. Mail your 
copies, identified by docket control number OPP-300991, to: Public 
Information and Records Integrity Branch, Information Resources and 
Services Division (7502C), Office of Pesticide Programs, Environmental 
Protection Agency, Ariel Rios Bldg., 1200 Pennsylvania Ave., NW., 
Washington, DC 20460. In person or by courier, bring a copy to the 
location of the PIRIB described in Unit I.B.2. You may also send an 
electronic copy of your request via e-mail to: [email protected]. 
Please use an ASCII file format and avoid the use of special characters 
and any form of encryption. Copies of electronic objections and hearing 
requests will also be accepted on disks in WordPerfect 6.1/8.0 file 
format or ASCII file format. Do not include any CBI in your electronic 
copy. You may also submit an electronic copy of your request at many 
Federal Depository Libraries.

B. When Will the Agency Grant a Request for a Hearing?

    A request for a hearing will be granted if the Administrator 
determines that the material submitted shows the following: There is a 
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(s) in the manner sought 
by the requestor would be adequate to justify the action requested (40 
CFR 178.32).

VII. Regulatory Assessment Requirements

    This final rule establishes a tolerance under FFDCA section 408(d) 
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 prior consultation as specified by Executive Order 
13084, entitled Consultation and Coordination with Indian Tribal 
Governments (63 FR 27655, May 19, 1998); special considerations as 
required by Executive Order 12898, entitled Federal Actions to Address 
Environmental Justice in Minority Populations and Low-Income

[[Page 19849]]

Populations (59 FR 7629, February 16, 1994); or require OMB review or 
any Agency action under Executive Order 13045, entitled Protection of 
Children from Environmental Health Risks and Safety Risks (62 FR 19885, 
April 23, 1997). This action does not involve any technical standards 
that would require Agency consideration of voluntary consensus 
standards pursuant to section 12(d) of the National Technology Transfer 
and Advancement Act of 1995 (NTTAA), Public Law 104-113, section 12(d) 
(15 U.S.C. 272 note). 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. In addition, the Agency has 
determined that this action will not have a substantial direct effect 
on States, on the relationship between the national government and the 
States, or on the distribution of power and responsibilities among the 
various levels of government, as specified in Executive Order 13132, 
entitled Federalism (64 FR 43255, August 10, 1999). Executive Order 
13132 requires EPA to develop an accountable process to ensure 
``meaningful and timely input by State and local officials in the 
development of regulatory policies that have federalism implications.'' 
``Policies that have federalism implications'' is defined in the 
Executive Order to include regulations that have ``substantial direct 
effects on the States, on the relationship between the national 
government and the States, or on the distribution of power and 
responsibilities among the various levels of government.'' This final 
rule directly regulates growers, food processors, food handlers and 
food retailers, not States. This action does not alter the 
relationships or distribution of power and responsibilities established 
by Congress in the preemption provisions of FFDCA section 408(n)(4).

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 this final rule in the Federal Register. This final 
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: March 30, 2000.
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. Section 180.553 is amended by alphabetically adding the 
following commodities to the table in paragraph (a) to read as follows:


Sec. 180.553  Fenhexamid; tolerances for residues.

    (a) *    *    *

 
------------------------------------------------------------------------
                                                              Parts per
                         Commodity                             million
------------------------------------------------------------------------
Almond, hull...............................................          2.0
Almond, nutmeat............................................         0.02
 
                  *        *        *        *        *
Plum (fresh prune).........................................          0.5
Prune, dried...............................................          1.0
 
                  *        *        *        *        *
Stone fruit, except plum (fresh prune).....................          6.0
 
                  *        *        *        *        *
------------------------------------------------------------------------

    *    *    *    *    *
[FR Doc. 00-9144 Filed 4-12-00; 8:45 am]
BILLING CODE 6560-50-F