Fenhexamid; Pesticide Tolerances
[Federal Register: April 13, 2000 (Volume 65, Number 72)]
[Rules and Regulations]
[Page 19842-19849]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr13ap00-12]
-----------------------------------------------------------------------
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.
-----------------------------------------------------------------------
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: waller.mary@epa.gov.
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 tompkins.jim@epa.gov,
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: opp-docket@epa.gov.
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
![[logo] US EPA](http://www.epa.gov/epafiles/images/logo_epaseal.gif){kind=logo}