[Federal Register: July 16, 2004 (Volume 69, Number 136)]
[Rules and Regulations]
[Page 42560-42571]
From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr16jy04-5]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 180
[OPP-2004-0120; FRL-7367-1]
Spiroxamine; Pesticide Tolerance
AGENCY: Environmental Protection Agency (EPA).
ACTION: Final rule.
-----------------------------------------------------------------------
SUMMARY: This regulation establishes tolerances for combined residues
of spiroxamine in or on grape, banana, and hop, dried cones. Bayer
CropScience and the Interregional Research Project Number 4 (IR-4),
respectively, requested these tolerances under the Federal Food, Drug,
and Cosmetic Act (FFDCA), as amended by the Food Quality Protection Act
of 1996 (FQPA).
DATES: This regulation is effective July 16, 2004. Objections and
requests for hearings must be received on or before September 14, 2004.
ADDRESSES: To submit a written objection or hearing request follow the
detailed instructions as provided in Unit VIII. of the SUPPLEMENTARY
INFORMATION. EPA has established a docket for this action under Docket
ID number OPP-2004-0120. All documents in the docket are listed in the
EDOCKET index athttp://www.epa.gov/edocket. Although listed in the
index, some information is not publicly available, i.e., CBI or other
information whose disclosure is restricted by statute. Certain other
material, such as copyrighted material, is not placed on the Internet
and will be publicly available only in hard copy form. Publicly
available docket materials are available either electronically in
EDOCKET or in hard copy at the Public Information and Records Integrity
Branch (PIRIB), Rm. 119, Crystal Mall 2, 1801 S. St.,
Arlington, VA. This docket facility is open from 8:30 a.m. to 4 p.m.,
Monday through Friday, excluding legal holidays. The docket telephone
number is (703) 305-5805.
FOR FURTHER INFORMATION CONTACT: Sidney Jackson, Registration Division
(7505C), Office of Pesticide Programs, Environmental Protection Agency,
1200 Pennsylvania Ave., NW., Washington, DC 20460-0001; telephone
number:
[[Page 42561]]
(703) 305-7610; e-mail address:jackson.sidney@epa.gov.
SUPPLEMENTARY INFORMATION:
I. General Information
A. Does this Action Apply to Me?
You may be potentially affected by this action if you are an
agricultural producer, food manufacturer, or pesticide manufacturer.
The North American Industrial Classification System (NAICS) codes have
been provided to assist you and others in determining whether this
action might apply to certain entities. Potentially affected entities
may include, but are not limited to:
Crop production (NAICS 111), e.g., agricultural workers;
greenhouse, nursery, and floriculture workers; farmers.
Animal production (NAICS 112), e.g., cattle ranchers and
farmers, dairy cattle farmers, livestock farmers.
Food manufacturing (NAICS 311), e.g., agricultural
workers; farmers; greenhouse, nursery, and floriculture workers;
ranchers; pesticide applicators.
Pesticide manufacturing (NAICS 32532), e.g., agricultural
workers; commercial applicators; farmers; greenhouse, nursery, and
floriculture workers; residential users.
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 this unit could also be
affected. If you have any questions regarding the applicability of this
action to a particular entity, consult the person listed under FOR
FURTHER INFORMATION CONTACT.
B. How Can I Access Electronic Copies of this Document and Other
Related Information?
In addition to using EDOCKET (http://www.epa.gov/edocket/), you may
access this Federal Register document electronically through the EPA
Internet under the ``Federal Register'' listings at http://www.epa.gov/fedrgstr/.
A frequently updated electronic version of 40 CFR part 180
is available at E-CFR Beta Site Two at http://www.gpoaccess.gov/ecfr/.
II. Background and Statutory Findings
In the Federal Register of March 7, 2003 (68 FR 11088) (FRL-7290-
5), and December 10, 2003 (68 FR 68904) (FRL-7337-6), EPA issued
notices pursuant to section 408(d)(3) of FFDCA, 21 U.S.C. 346a(d)(3),
announcing the filing of pesticide petitions (PP 0F6122, 3E6538, and
3E6783) by Bayer CropScience, 2 T.W. Alexander Drive, P.O. Box 12014,
Research Triangle Park, NC 27709, and (PP 3E6518) by IR-4, 681 U.S.
Highway 1 South, North Brunswick, NJ 08902-3390, respectively.
These notices included a summary of the petitions prepared by Bayer
CropScience, the registrant. There were no comments received in
response to the notice of filing.
The petitions requested that 40 CFR part 180 be amended by
establishing tolerances for combined residues of the fungicide
spiroxamine, 8-(1,1-dimethylethyl)-N-ethyl-N-propyl-1,4-
dioxaspiro[4,5]decane-2-methanamine, and its metabolites containing the
N-ethyl-N-propyl-1,2-dihydroxy-3-aminopropane moiety (formerly known as
the aminodiol moiety), in or on grape at 1.0 parts per million (ppm),
and grape, raisin at 1.3 ppm (PP 0F6122); banana at 3.0 ppm (3E6538);
hop, dried cones (import) at 50 ppm (3E6783); and hop (United States)
at 11 ppm (3E6518). Subsequently, PP 0F6122 has been amended to delete
grape, raisin at 1.3 ppm, and PP 3E6518 has been amended to increase
the tolerance level for ``hop at 11 ppm'' to ``hop, dried cones at 50
ppm.''
Section 408(b)(2)(A)(i) of 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) of FFDCA 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) of FFDCA requires EPA to give special
consideration to exposure of infants and children to the pesticide
chemical residue in establishing a tolerance and to ``ensure that there
is a reasonable certainty that no harm will result to infants and
children from aggregate exposure to the pesticide chemical residue. . .
.''
EPA performs a number of analyses to determine the risks from
aggregate exposure to pesticide residues. For further discussion of the
regulatory requirements of section 408 of FFDCA 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) of FFDCA, EPA has reviewed the
available scientific data and other relevant information in support of
these actions. EPA has sufficient data to assess the hazards of and to
make a determination on aggregate exposure, consistent with section
408(b)(2) of FFDCA, for import tolerances for combined residues of
spiroxamine on grape at 1.0 ppm, banana at 3.0 ppm, and hop, dried
cones at 50 ppm (import and U.S. grown). EPA's assessment of exposures
and risks associated with establishing these tolerances follow.
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 spiroxamine is
discussed in Table 1 of this unit as well as the no observed adverse
effect level (NOAEL) and the lowest observed adverse effect level
(LOAEL) from the toxicity studies reviewed.
Subchronic studies show the target organ of spiroxamine toxicity is
the liver. Subchronic studies were characterized by slight to mild
hepatotoxicity, with associated elevation in liver enzymes. Mucous
membranes of the esophagus and forestomach were keratinized and
hyperplastic due to the strong irritant properties of spiroxamine.
Long-term administration of spiroxamine in the dog resulted in
hepatocytomegaly, cataracts, and liver discoloration. In the rat, it
resulted in an increased mortality in females, decreased body weights
and body weight gains in both sexes, and increased esophageal
hyperkeratosis in both sexes, while in the mouse, chronic
administration resulted in uterine nodules, hyperplasia in the adrenal
gland of males, hyperkeratosis in the esophagus, forestomach, and
tongue of females, and acanthosis in the pinnae and tails of females.
In rats, developmental effects entailed delayed ossification.
Developmental effects were not seen in rabbits. There was no evidence
of increased susceptibility of the young animals following exposure to
spiroxamine in any developmental toxicity studies in the data base.
There was evidence of mild spiroxamine-induced neurotoxicity
characterized by
[[Page 42562]]
piloerection and slight to moderate gait incoordination, and functional
observational battery (FOB) effects of decreased forelimb grip strength
and foot splay in males in the acute neurotoxicity study. No
neuropathology was seen in either the acute or subchronic toxicity
studies in rats and no neurotoxicity was detected in the subchronic
study. Spiroxamine has no carcinogenic potential, as indicated in both
the rat and the mouse carcinogenicity studies. In addition, spiroxamine
has no mutagenicity potential, based on several in vivo and in vitro
studies.
Table 1.--Subchronic, Chronic, and Other Toxicity
------------------------------------------------------------------------
Guideline No. Study Type Results
------------------------------------------------------------------------
870.3100 90-Day oral NOAEL = M: 9.3, F:
toxicity--rodents 13.2 mg/kg/day
(rats) active LOAEL = M: 54.9,
ingredient (a.i.) F: 75.1 mg/kg/day
based on
decreased body
weights and body
weight gains in
both sexes,
hyperkeratosis
and hyperplasia/
hypertrophy in
the esophagus of
both sexes and
hyperkeratosis in
the forestomach
of males. Minimal
to marked
hyperkeratosis in
the tongue of
both sexes.
Slight multifocal
hyperplasia in
the urinary
bladder of both
sexes. Minimal to
slight hyaline
droplet
degeneration in
the liver in
males.
------------------------------------------------------------------------
870.3100 90-Day oral NOAEL = M: 8.8, F:
toxicity rodents 9.7 mg/kg/day
(rats) LOAEL = M: 45.0,
Metabolite KWG F: 53.6 mg/kg/day
4168 N-oxide. based on
hyperkeratosis in
the esophagus and
forestomach
------------------------------------------------------------------------
870.3150 90-Day oral NOAEL = M: 16.19,
toxicity-- F: 15.05 mg/kg/
nonrodents (dogs) day
LOAEL = M: 20.02,
F: 21.29 mg/kg/
day based on
decreased albumin
in females,
increased
absolute and
relative liver
weights in males,
and increased
diffuse
hepatocytomegaly
in males
------------------------------------------------------------------------
870.3200 21/28-Day dermal NOAEL = 0.2 mg/kg/
toxicity (rabbit) day
LOAEL = 0.5 mg/kg/
day based on
erythema at the
application site
------------------------------------------------------------------------
870.3465 28-Day inhalation NOAEL = 23.6 mg/kg/
toxicity (rats) day (0.087 mg/L)
LOAEL = 140.5 mg/
kg/day (0.518 mg/
L) based on
decreased body
weights and body
weight gains,
increased
incidences of
clinical signs of
toxicity and
dermal
irritation,
thymic atrophy,
and toxicity to
the skin,
respiratory
system, and liver
------------------------------------------------------------------------
870.3700 Prenatal (oral) Maternal
developmental- NOAEL = 30 mg/kg/
rodents (rats) day
LOAEL = 100 mg/kg/
day based on
decreased body
weights, body
weight gains, and
food consumption
Developmental
NOAEL = 30 mg/kg/
day
LOAEL = 100 mg/kg/
day based on
increased
incidence of
delayed skeletal
development
(incomplete
ossification) of
the os
interparietal
(fetal and litter
incidences) and
os parietale
(fetal
incidences)
------------------------------------------------------------------------
[[Page 42563]]
870.3700 Prenatal (dermal) Maternal
developmental-- (Systemic)
rodents (rats) NOAEL = 5 mg/kg/
day
LOAEL = 10 mg/kg/
day based on
decreased body
weight gains
Maternal (Dermal)
NOAEL = less than
5 mg/kg/day
LOAEL (Dermal) = 5
mg/kg/day based
on very slight
erythema and/or
slight scaling of
skin
Developmental
NOAEL = 20 mg/kg/
day
LOAEL = 80 mg/kg/
day based on the
increased fetal
and litter
incidence of
incomplete/non-
ossification of
the os occipital
and the increased
non-ossification
of the left
distal phalanx of
digit number 4 of
the forelimb
------------------------------------------------------------------------
870.3700 Prenatal Maternal
developmental in NOAEL = 20 mg/kg/
nonrodents day
(rabbits) LOAEL = 80 mg/kg/
day based on
mortality,
clinical signs of
toxicity
(encrusted mouth,
anal prolapse,
and little/soft
feces), decreased
body weight
gains, and
decreased food
consumption
Developmental
NOAEL = 80 mg/kg/
day
LOAEL: Not
Achieved
------------------------------------------------------------------------
870.3800 Reproduction and Parental/Systemic
fertility effects NOAEL = M: 2.5, F:
(rats) 2.7 mg/kg/day
LOAEL = M: 10.8,
F: 11.9 mg/kg/day
based on
decreased food
consumption
during lactation
and on increased
incidences of
esophageal
hyperkeratosis in
females
Reproductive
NOAEL = M: 44.8,
F: 48.8 mg/kg/day
LOAEL = Not
achieved
Offspring
NOAEL = M: 10.8,
F: 11.9 mg/kg/day
LOAEL = M: 44.8,
F: 48.8 mg/kg/day
based on
decreased litter
size and pup
weight and
increased
clinical signs of
toxicity in the
F1 generation
------------------------------------------------------------------------
870.4100 Chronic toxicity-- NOAEL = M: 2.47,
dogs F: 2.48 mg/kg/day
LOAEL = M: 28.03,
F: 25.84 mg/kg/
day based on
hepato/
cytomegaly,
cataracts, and
decreased albumin
in males and
females; liver
discoloration and
decreased
triglycerides in
females; and
increased alanine
aminotransferase
in males
------------------------------------------------------------------------
870.4200 Carcinogenicity-- NOAEL = M: 4.22,
rats F: 5.67 mg/kg/day
LOAEL = M: 32.81,
F: 43.04 mg/kg/
day based on
increased
mortality in
females,
decreased body
weights and body
weight gains in
both sexes, and
increased
esophageal
lesions in both
sexes
No evidence of
carcinogenicity
------------------------------------------------------------------------
870.4300 Carcinogenicity-- NOAEL = M: 41.0,
mice F: 64.6 mg/kg/day
LOAEL = M: 149.8,
F: 248.1 mg/kg/
day based on
uterine nodules,
hyperplasia in
the adrenal gland
of males,
hyperkeratosis in
the esophagus,
forestomach, and
tongue of
females, and
acanthosis in the
pinnae and tails
of females
No evidence of
carcinogenicity
------------------------------------------------------------------------
870.5100 Gene mutation Negative, < plus-
(Ames Test) minus>S9 up to
cytotoxic 1,000
[mu]g/plate
------------------------------------------------------------------------
[[Page 42564]]
870.5395 Cytogenetics Negative, at
clinically toxic
i.p. dose
------------------------------------------------------------------------
870.5300 Mammalian cells in Negative, < plus-
culture minus>S9 up to
cytotoxic/
precipitation 200
[mu]g/mL
------------------------------------------------------------------------
870.5375 Chromosome Negative, < plus-
aberrations minus>S9 up to
cytotoxic doses
------------------------------------------------------------------------
870.5550 Unscheduled DNA Negative, < plus-
synthesis minus>S9 up to
severe
cytotoxicity
------------------------------------------------------------------------
870.6200 Acute NOAEL = 10 mg/kg
neurotoxicity LOAEL = 30 mg/kg
screening battery based on clinical
signs
(piloerection and
slight to
moderate gait
incoordination)
and FOB effects
(decreased
forelimb grip
strength and foot
splay) in males
------------------------------------------------------------------------
870.6200 Subchronic NOAEL = M: 2.4, F:
neurotoxicity 2.5 mg/kg/day
screening battery LOAEL = M: 10.6,
F: 11.1 mg/kg/day
based on
decreased
bodyweight gain,
food consumption
(males), and
hyperkeratosis in
the stomach,
esophagus, and
tongue
------------------------------------------------------------------------
870.7485 Metabolism and Absorption was at
pharmacokinetics least 60-70% and
(rats) began immediately
after
administration
with peak plasma
concentrations at
1.5-2 hours post-
dose at 1 mg/kg,
and delayed to 8
hours at 100 mg/
kg. More than 97%
of the recovered
radioactivity was
excreted via
urine and feces
within 48 hours
in all dose
groups and more
than 80% within
24 hours. Renal
excretion
accounted for the
majority of the
radioactivity
(1.8:1
urine:feces on
average).
------------------------------------------------------------------------
870.7600 Dermal penetration Dermal absorption
(rats) factor: 52.5% at
8 hours
------------------------------------------------------------------------
B. Toxicological Endpoints
The dose at which no adverse effects are observed (the NOAEL) from
the toxicology study identified as appropriate for use in risk
assessment is used to estimate the toxicological level of concern
(LOC). However, the lowest dose at which adverse effects of concern are
identified (the LOAEL) is sometimes used for risk assessment if no
NOAEL was achieved in the toxicology study selected. An uncertainty
factor (UF) is applied to reflect uncertainties inherent in the
extrapolation from laboratory animal data to humans and in the
variations in sensitivity among members of the human population as well
as other unknowns. An UF of 100 is routinely used, 10X to account for
interspecies differences and 10X for intraspecies differences.
Three other types of safety or uncertainty factors may be used:
``Traditional uncertainty factors''; the ``special FQPA safety
factor;'' and the ``default FQPA safety factor.'' By the term
``traditional uncertainty factor,'' EPA is referring to those
additional uncertainty factors used prior to FQPA passage to account
for data base deficiencies. These traditional uncertainty factors have
been incorporated by the FQPA into the additional safety factor for the
protection of infants and children. The term ``special FQPA safety
factor'' refers to those safety factors that are deemed necessary for
the protection of infants and children primarily as a result of the
FQPA. The ``default FQPA safety factor'' is the additional 10X safety
factor that is mandated by the statute unless it is decided that there
are reliable data to choose a different additional factor (potentially
a traditional uncertainty factor or a special FQPA safety factor).
For dietary risk assessment (other than cancer) the Agency uses the
UF to calculate an acute or chronic reference dose (acute RfD or
chronic RfD) where the RfD is equal to the NOAEL divided by an UF of
100 to account for interspecies and intraspecies differences and any
traditional uncertainty factors deemed appropriate (RfD = NOAEL/UF).
Where a special FQPA safety factor or the default FQPA safety factor is
used, this additional factor is applied to the RfD by dividing the RfD
by such additional factor. The acute or chronic Population Adjusted
Dose (aPAD or cPAD) is a modification of the RfD to accommodate this
type of safety factor.
For non-dietary risk assessments (other than cancer) the UF is used
to determine the LOC. For example, when 100 is the appropriate UF (10X
to account for interspecies differences and 10X for intraspecies
differences) the LOC is 100. To estimate risk, a ratio of the NOAEL to
exposures (margin of exposure (MOE) = NOAEL/exposure) is calculated and
compared to the LOC.
The linear default risk methodology (Q*) is the primary method
currently used by the Agency to quantify carcinogenic risk. The Q*
approach assumes that any amount of exposure will lead to some degree
of cancer risk. A Q* is calculated and used to estimate risk which
represents a probability of occurrence of additional cancer cases
(e.g., risk). An example of how such a probability risk is expressed
would be to describe the risk as one in one hundred thousand (1 x
10-\5\), one in a million(1 x 10-\6\), or one in
ten million(1 x 10-\7\). Under certain specific
circumstances, MOE calculations will be used for the carcinogenic risk
assessment. In this non-linear approach, a ``point of departure'' is
identified below which
[[Page 42565]]
carcinogenic effects are not expected. The point of departure is
typically a NOAEL based on an endpoint related to cancer effects though
it may be a different value derived from the dose response curve. To
estimate risk, a ratio of the point of departure to exposure
(MOEcancer = point of departure/exposures) is calculated.
Table 2.--Summary of Toxicological Dose and Endpoints for Spiroxamine for Use in Human Risk Assessment
----------------------------------------------------------------------------------------------------------------
Dose Used in Risk
Assessment, Special FQPA SF and
Exposure/Scenario Interspecies and Level of Concern for Study and Toxicological
Intraspecies and any Risk Assessment Effects
Traditional UF
----------------------------------------------------------------------------------------------------------------
Acute dietary (general population NOAEL = 10 mg/kg/day Special FQPA SF = 1X Acute neurotoxicity in
including infants and children) UF = 100............... aPAD = acute RfD/ rats
Acute RfD = 0.1 mg/kg/ Special FQPA SF = 0.1 LOAEL = 30 mg/kg/day
day. mg/kg/day. based on clinical
signs (piloerection
and slight to moderate
gait incoordination)
and FOB effects
(decreased forelimb
grip strength and foot
splay) in males on day
0-1
-----------------------------------------------------------------------------------------
Chronic dietary (all populations) NOAEL = 2.5 mg/kg/day Special FQPA SF = 1X Chronic oral toxicity
UF = 300............... cPAD = chronic RfD/ study in dogs
Chronic RfD = 0.0083 mg/ Special FQPA SF = LOAEL = 28.03/25.84 mg/
kg/day. 0.0083 mg/kg/day. kg/day M/F based on
hepatocytomegaly,
cataracts, and
decreased albumin in
males and females;
liver discoloration
and decreased
triglycerides in
females; and increased
alanine
aminotransferase in
males
-----------------------------------------------------------------------------------------
Dermal exposure: Short- and Dermal (or oral) study Residential LOC for MOE Prenatal toxicity study
intermediate-term (Residential) NOAEL= 5 mg/kg/day = N/A in rats (Dermal) the
maternal LOAEL
(systemic) = 20 mg/kg/
day based on decreased
body weight gains
-----------------------------------------------------------------------------------------
Dermal exposure: Long-term Oral study NOAEL = 2.5 Residential LOC for MOE Chronic oral toxicity
(Residential) mg/kg/day (dermal = N/A in dogs
absorption rate = 53%) LOAEL = 28.03/25.84 mg/
kg/day (M/F) based on
hepatocytomegaly,
cataracts, and
decreased albumin in
males and females;
liver discoloration
and decreased
triglycerides in
females; and increased
alanine
aminotransferase in
males
-----------------------------------------------------------------------------------------
Short-term inhalation (1 to 30 days) Inhalation study NOAEL Residential LOC for MOE 28-Day inhalation
(Residential) = 0.087 mg/L = 23.6 mg/ = N/A toxicity study in rats
kg/day LOAEL = 0.518 mg/L =
140.5 mg/kg/day based
on decreased body
weights and body
weight gains,
increased incidences
of clinical signs of
toxicity and dermal
irritation, thymic
atrophy, and toxicity
to the skin,
respiratory system,
and liver
-----------------------------------------------------------------------------------------
Intermediate-term inhalation (1-6 Inhalation NOAEL = Residential LOC for MOE Subchronic inhalation
months) (Residential) 0.087 mg/L = 23.6 mg/ = N/A toxicity study in rats
kg/day LOAEL = 0.518 mg/L =
140.5 mg/kg/day based
on decreased body
weights and body
weight gains,
increased incidences
of clinical signs of
toxicity and dermal
irritation, thymic
atrophy, and toxicity
to the skin,
respiratory system,
and liver
-----------------------------------------------------------------------------------------
[[Page 42566]]
Long-term inhalation (greater than 6 Oral study NOAEL = 2.5 Residential LOC for MOE Chronic oral toxicity
months) (Residential) mg/kg/day (inhalation = N/A study in dogs
absorption rate = LOAEL = 28.03/25.84 mg/
100%) kg/day M/F based on
hepatocytomegaly,
cataracts, and
decreased albumin in
males and females;
liver discoloration
and decreased
triglycerides in
females; and increased
alanine
aminotransferase in
males
----------------------------------------------------------------------------------------------------------------
C. Exposure Assessment
1. Dietary exposure from food and feed uses. Spiroxamine is a new
chemical and therefore, these are the first tolerances to be
established for the residues of spiroxamine. Tolerance level residues,
average residues from field trial data, the concentration/reduction
factors from processing studies, and 100% crop treated information were
used. Partially refined acute and chronic dietary risk assessments for
spiroxamine were conducted using the Dietary Exposure Evaluation Model
(DEEM-FCID, Version 1.33), which uses food consumption data from the
U.S. Department of Agriculture (USDA) Continuing Surveys of Food
Intakes by Individuals (CSFII) from 1994-1996 and 1998. Risk
assessments were conducted by EPA to assess dietary exposures from
spiroxamine in food as follows:
i. Acute exposure. The acute assessment was a partially refined
deterministic assessment. Tolerances were used for the nonblended and
partially blended raw agricultural commodities (3.0 ppm for bananas and
1.0 ppm for grapes). For the processed commodities of grapes, the
highest average field trial (HAFT) value of 0.613 ppm was used as the
residue value, which was computer-multiplied by the processing factors
(adjustment factors 1) of 0.67x for grape juice and 1.3x for
raisins. For the blended commodity hops, the average residue value from
the field trials for imported hops (16 ppm) was used. Data on projected
market share or percent crop treated were not used.
ii. Chronic exposure. The chronic assessment was a partially
refined deterministic assessment. Average residue values from the field
trials were used for bananas, grapes, and hops (1.13 ppm for unbagged
bananas, 0.17 ppm for grapes, and 16 ppm for imported hops.) The
tolerance level for grapes (1.0 ppm) was used for grape leaves and
wine. For the processed commodities of grapes other than wine, the
average value of 0.17 ppm was used as the residue value, which was
computer-multiplied by the processing factors (adjustment factors
1) of 0.67x for grape juice and 1.3x for raisins. Data on
projected market share or percent crop treated were not used.
iii. Cancer. Spiroxamine has been classified as not likely to be
carcinogenic to humans. Therefore, a quantitative risk assessment was
not conducted to assess cancer risk.
2. Dietary exposure from drinking water. The Agency lacks
sufficient monitoring exposure data to complete a comprehensive dietary
exposure analysis and risk assessment for spiroxamine in drinking
water. Because the Agency does not have comprehensive monitoring data,
drinking water concentration estimates are made by reliance on
simulation or modeling taking into account data on the physical
characteristics of spiroxamine.
The Agency uses the FQPA Index Reservoir Screening Tool (FIRST) or
the Pesticide Root Zone Model/Exposure Analysis Modeling System (PRZM/
EXAMS), to produce estimates of pesticide concentrations in an index
reservoir. The Screening Concentration in Groundwater (SCI-GROW) model
is used to predict pesticide concentrations in shallow ground water.
For a screening-level assessment for surface water EPA will use FIRST
(a Tier 1 model) before using PRZM/EXAMS (a Tier 2 model). The FIRST
model is a subset of the PRZM/EXAMS model that uses a specific high-end
runoff scenario for pesticides. Both FIRST and PRZM/EXAMS incorporate
an index reservoir environment, and both models include a percent crop
area factor as an adjustment to account for the maximum percent crop
coverage within a watershed or drainage basin.
None of these models include consideration of the impact processing
(mixing, dilution, or treatment) of raw water for distribution as
drinking water would likely have on the removal of pesticides from the
source water. The primary use of these models by the Agency at this
stage is to provide a screen for sorting out pesticides for which it is
unlikely that drinking water concentrations would exceed human health
levels of concern.
Since the models used are considered to be screening tools in the
risk assessment process, the Agency does not use estimated
environmental concentrations (EECs), which are the model estimates of a
pesticide's concentration in water. EECs derived from these models are
used to quantify drinking water exposure and risk as a %RfD or %PAD.
Instead drinking water levels of comparison (DWLOC) are calculated and
used as a point of comparison against the model estimates of a
pesticide's concentration in water. DWLOCs are theoretical upper limits
on a pesticide's concentration in drinking water in light of total
aggregate exposure to a pesticide in food, and from residential uses.
Since DWLOCs address total aggregate exposure to spiroxamine they are
further discussed in the aggregate risk section.
Based on the PRZM/EXAMS and SCI-GROW models, the EECs of
spiroxamine for acute and chronic exposures are estimated to be 17.8
parts per billion (ppb), and 14 ppb, respectively for surface water.
The EEC of spiroxamine for acute and chronic exposures is 0.27 ppb for
ground water.
3. From non-dietary exposure. The term ``residential exposure'' is
used in this document to refer to non-occupational, non-dietary
exposure (e.g., for lawn and garden pest control,
[[Page 42567]]
indoor pest control, termiticides, and flea and tick control on pets).
Spiroxamine is not registered for use on any sites that would
result in residential exposure.
4. Cumulative effects from substances with a common mechanism of
toxicity. Section 408(b)(2)(D)(v) of FFDCA 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.''
Unlike other pesticides for which EPA has followed a cumulative
risk approach based on a common mechanism of toxicity, EPA has not made
a common mechanism of toxicity finding as to spiroxamine and any other
substances and spiroxamine 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 spiroxamine 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 policy statements released by EPA's Office of
Pesticide Programs (OPP) concerning common mechanism determinations and
procedures for cumulating effects from substances found to have a
common mechanism on EPA's web site at http://www.epa.gov/pesticides/cumulative/
.
D. Safety Factor for Infants and Children
1. In general. Section 408 of FFDCA 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 on toxicity and exposure
unless EPA determines based on reliable data that a different margin of
safety will be safe for infants and children. Margins of safety are
incorporated into EPA risk assessments either directly through use of a
MOE analysis or through using uncertainty (safety) factors in
calculating a dose level that poses no appreciable risk to humans. In
applying this provision, EPA either retains the default value of 10X
when reliable data do not support the choice of a different factor, or,
if reliable data are available, EPA uses a different additional safety
factor value based on the use of traditional uncertainty factors and/or
special FQPA safety factors, as appropriate.
2. Prenatal and postnatal sensitivity. There was no evidence for
quantitative or qualitative susceptibility following oral or dermal
exposures to rats in utero or oral exposure to rabbits in utero.
There is no concern for neurotoxicity resulting from exposure to
spiroxamine.
3. Conclusion. The toxicology and exposure data bases for
spiroxamine are complete with the exception of certain confirmatory or
clarifying studies. The toxicity data base contains acceptable/
guideline acute and subchronic neurotoxicity studies; two acceptable/
guideline developmental toxicity studies in rats (oral and dermal), and
rabbits (oral); and an acceptable/nonguideline 2-generation rat
reproduction study. The 2-generation rat reproduction study is
classified as acceptable/nonguideline because of questions concerning
the increased lactation indices and clinical signs of toxicity in the
second generation. There are enough data to satisfy the requirements
for a 1-generation reproduction study and the study is acceptable and
potentially upgradable to an Acceptable/Guideline study (2-generation
reproduction) upon submission of clarifying data regarding the
lactation indices and clinical signs of toxicity in the second
generation.
In the acute neurotoxicity study in the rat, there was evidence of
mild spiroxamine-induced neurotoxicity characterized by piloerection
and slight to moderate gait in coordination, and FOB effects of
decreased forelimb grip strength and foot splay in males at a dose
level of 30 mg/kg/day. In subchronic neurotoxicity studies in the rat,
clinical signs, FOB, motor activity, brain weight, ophthalmology, gross
necropsy, and neuropathology were unaffected by treatment. Treatment-
related effects at 155 ppm (10.6 mg/kg/day) were limited to
hyperkeratosis of the esophagus in one male and one female. No
treatment-related effects were observed at 35 ppm (2.4 mg/kg/day).
In rat prenatal toxicity studies - oral, developmental toxicity
showed no effects of treatment on maternal survival or clinical signs.
There were no abortions, premature deliveries, or complete litter
resorptions. Similarly, there were no effects of treatment on the
number of resorptions (early or late), number of fetuses (live or
dead), post-implantation loss, or fetal sex ratio. There were no
treatment-related external, visceral, or skeletal variations.
Rat prenatal toxicity studies - dermal, showed there were no
effects of treatment on maternal survival, clinical signs, food
consumption, or gross pathologly.
In rabbit prenatal toxicity study, there were no effects of
treatment on maternal gross pathology or the number of resorptions
(early, late, or complete litter), number of fetuses (live or dead),
number of litters, post-implantation loss, fetal weights, or sex ratio.
There were no treatment-related external or skeletal variations.
4. Degree of concern analysis and residual uncertainties. There are
no concerns for residual uncertainty for prenatal toxicity in the
available developmental studies. However, until clarifying data are
provided on the 2-generation rat reproduction study, there is some
uncertainty with regard to postnatal toxicity.
A 3X (as opposed to 10X) FQPA data base uncertainty factor was
determined to be sufficient to address questions regarding the 2-
generation rat reproduction study because the available data from the
1-generation show offspring effects occurring at doses higher than the
dose that caused parental effects and the dose (2.5 mg/kg/day) used for
driving the chronic RfD is approximately 3-fold lower than the
offspring NOAEL (10.8 mg/kg/day). The 3X data base UF should be applied
only to the chronic dietary risk assessment because the required study
(2-generation reproduction toxicity study) could provide an endpoint
applicable to chronic exposure scenario, but not for an acute exposure
scenario. There are no residential uses at the present time.
Based on the above data, no special FQPA safety factor (i.e., 1X)
is required since there are no residual uncertainties for prenatal
toxicity and the lack of a fully acceptable 2-generation toxicity study
is addressed by the data base uncertainty factor of 3X.
E. Aggregate Risks and Determination of Safety
To estimate total aggregate exposure to a pesticide from food,
drinking water, and residential uses, the Agency calculates DWLOCs
which are used as a point of comparison against EECs. DWLOC values are
not regulatory standards for drinking water. DWLOCs are theoretical
upper limits on a pesticide's concentration in drinking water in light
of total aggregate exposure to a pesticide in food and residential
uses. In calculating a DWLOC, the Agency determines how much of the
acceptable exposure (i.e., the PAD) is available for exposure through
drinking water (e.g., allowable chronic water exposure (mg/kg/day) =
cPAD - (average food + residential exposure). This
[[Page 42568]]
allowable exposure through drinking water is used to calculate a DWLOC.
A DWLOC will vary depending on the toxic endpoint, drinking water
consumption, and body weights. Default body weights and consumption
values as used by the EPA's Office of Water are used to calculate
DWLOCs: 2 liter (L)/70 kg (adult male), 2L/60 kg (adult female), and
1L/10 kg (child). Default body weights and drinking water consumption
values vary on an individual basis. This variation will be taken into
account in more refined screening-level and quantitative drinking water
exposure assessments. Different populations will have different DWLOCs.
Generally, a DWLOC is calculated for each type of risk assessment used:
Acute, short-term, intermediate-term, chronic, and cancer.
When EECs for surface water and ground water are less than the
calculated DWLOCs, EPA concludes with reasonable certainty that
exposures to the pesticide in drinking water (when considered along
with other sources of exposure for which EPA has reliable data) would
not result in unacceptable levels of aggregate human health risk at
this time. Because EPA considers the aggregate risk resulting from
multiple exposure pathways associated with a pesticide's uses, levels
of comparison in drinking water may vary as those uses change. If new
uses are added in the future, EPA will reassess the potential impacts
of residues of the pesticide in drinking water as a part of the
aggregate risk assessment process.
1. Acute risk. Using the exposure assumptions discussed in this
unit for acute exposure, the acute dietary exposure from food to
spiroxamine will occupy 7.4% of the aPAD for the U.S. population, 6.2%
of the aPAD for females 13 years and older, 27% of the aPAD for infants
less than 1 year old, and 31% of the aPAD for children 1-2 years old.
In addition, there is potential for acute dietary exposure to
spiroxamine in drinking water. After calculating DWLOCs and comparing
them to the EECs for surface water and ground water, EPA does not
expect the aggregate exposure to exceed 100% of the aPAD, as shown in
Table 3 of this unit:
Table 3.--Aggregate Risk Assessment for Acute Exposure to Spiroxamine
----------------------------------------------------------------------------------------------------------------
Surface Ground
Population Subgroup aPAD (mg/ %aPAD/ Water EEC/ Water EEC/ Acute DWLOC/
kg) (Food) (ppb) (ppb) (ppb)
----------------------------------------------------------------------------------------------------------------
U.S. population 0.1 7.4 18 0.27 3,200
---------------------------------------------------------------------------
Females (13-50 years old) 0.1 6.2 18 0.27 2,800
---------------------------------------------------------------------------
Infants (less than 1 year old) 0.1 27 18 0.27 730
---------------------------------------------------------------------------
Children (1-2 years old) 0.1 31 18 0.27 690
----------------------------------------------------------------------------------------------------------------
2. Chronic risk. Using the exposure assumptions described in this
unit for chronic exposure, EPA has concluded that exposure to
spiroxamine from food will utilize 8.3% of the cPAD for the U.S.
population, 6.0% of the aPAD for females 13 years and older, 18% of the
cPAD for infants less than 1 year old, and 29% of the cPAD for children
1-2 years old. There are no residential uses for spiroxamine that
result in chronic residential exposure to spiroxamine. In addition,
there is potential for chronic dietary exposure to spiroxamine in
drinking water. After calculating DWLOCs and comparing them to the EECs
for surface water and ground water, EPA does not expect the aggregate
exposure to exceed 100% of the cPAD, as shown in Table 4 of this unit:
Table 4.- Aggregate Risk Assessment for Chronic (Non-Cancer) Exposure to Spiroxamine
----------------------------------------------------------------------------------------------------------------
Surface Ground/
Population/Subgroup cPAD/mg/kg/ %/cPAD/ Water EEC/ Water EEC/ Chronic/
day (Food) (ppb) (ppb) DWLOC(ppb)
----------------------------------------------------------------------------------------------------------------
U.S. population 0.0083 8.3 14 0.27 270
---------------------------------------------------------------------------
Females (13-50 years old) 0.0083 6.0 14 0.27 230
---------------------------------------------------------------------------
Infants (less than 1 year old) 0.0083 18 14 0.27 70
---------------------------------------------------------------------------
Children (1-2 years old) 0.0083 29 14 0.27 60
----------------------------------------------------------------------------------------------------------------
3. Aggregate cancer risk for U.S. population. Spiroxamine has been
classified as not likely to be carcinogenic to humans. Therefore,
spiroxamine is not expected to pose a cancer risk.
4. Determination of safety. Based on these risk assessments, EPA
concludes that there is a reasonable certainty that no harm will result
to the general population, and to infants and children from aggregate
exposure to spiroxamine residues.
IV. Other Considerations
A. Analytical Enforcement Methodology
A proposed enforcement method (Bayer AG Method No. 00407) for
analysis of spiroxamine and its metabolites containing the aminodiol
moiety in plants has been submitted. The method was written for grapes
and processed commodities. An independent laboratory validation (ILV)
was conducted on grapes. Minor modifications were made for analysis of
bananas and hops. The method will be adequate for establishment of
tolerances and conditional registrations when the confirmatory method
is modified to use more than single-ion monitoring or an interference
study is conducted, and when the analytical reference standard for N-
ethyl-N-propyl-1,2-dihydroxy-3-
[[Page 42569]]
aminopropane is sent to the National Pesticide Standards Repository. As
a condition of registration (for continued registration) and for
continuation of importation of bananas and hops, a method validation
for Bayer AG Method No. 00407 must be conducted by EPA's laboratory,
however, EPA has conducted a paper review of this method and found the
method acceptable.
Using the common moiety method (Bayer AG Method No. 00407),
spiroxamine residues are converted to a single analyte, N-ethyl-N-
propyl-1,2-dihydroxy-3-aminopropane (also known as aminodiol), which is
derivatized to and measured as the di-trimethylsilyl derivative. All
spiroxamine residues containing the aminodiol moiety are quantitated by
gas chromatography/mass selective detector (GC/MSD) operated in a
single-ion mode. The data collection method used for the quantitation
of residues in grape commodities from the field trial, processing, and
storage stability studies is identical to the proposed enforcement
method. Minor modifications were made for analysis of bananas and hops.
Adequate enforcement methodology (gas chromotography/mass selective
detection), Bayer AG Method No. 00407, is available to enforce the
tolerance expression. The method may be requested from: Chief,
Analytical Chemistry Branch, Environmental Science Center, 701 Mapes
Rd., Ft. Meade, MD 20755-5350; telephone number: (410) 305-2905; e-mail
address:residuemethods@epa.gov.
B. International Residue Limits
There are currently no Codex, Canadian, or Mexican maximum residue
levels or tolerances for spiroxamine. A proposal for registration of
spiroxamine on hops in the European Community (Germany) with a maximum
residue level of 50.0 ppm is consistent with the proposal for U.S.
registration of spiroxamine on hops with a tolerance of 50.0 ppm. The
U.S. tolerance of 50.0 ppm was proposed to harmonize with the European
Community's proposed maximum residue level. International harmonization
is not an issue at this time.
C. Conditions
Additional data are needed in the following areas:
Banana--Storage stability data are needed on bananas
stored frozen for 6 months. Information regarding soil types and
temperature recordings for the banana field trials should be submitted
if available.
Hops, dried cones--Additional storage stability
information is needed to support the hop field trials which were
conducted in Germany.
Clarifying data on the 2-generation reproduction study for
rat pertaining to the increased lactation indices and clinical toxicity
in the second generation.
V. Conclusion
Therefore, import tolerances are established for combined residues
of spiroxamine, 8-(1,1-dimethylethyl)-N-ethyl-N-propyl-1,4-
dioxaspiro[4,5]decane-2-methanamine and its metabolites containing the
N-ethyl-N-propyl-1,2-dihydroxy-3-aminopropane moiety, in or on grape at
1.0 ppm, banana at 3.0 ppm, and hop, dried cones at 50 ppm (import and
U.S. grown).
VI. Objections and Hearing Requests
Under section 408(g) of FFDCA, as amended by 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 FFDCA by FQPA, EPA
will continue to use those procedures, with appropriate adjustments,
until the necessary modifications can be made. The new section 408(g)
of FFDCA 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) of FFDCA, as was
provided in the old sections 408 and 409 of FFDCA. 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 ID number OPP-2004-0120 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 September
14, 2004.
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 (1900C),
Environmental Protection Agency, 1200 Pennsylvania Ave., NW.,
Washington, DC 20460-0001. You may also deliver your request to the
Office of the Hearing Clerk in Rm. 104, Crystal Mall 2, 1801
S. Bell St., Arlington, VA. 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 (703) 603-
0061.
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, 1200 Pennsylvania Ave., NW., Washington, DC 20460-
0001.
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, 1200 Pennsylvania
Ave., NW., Washington, DC 20460-0001.
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
[[Page 42570]]
inclusion in the official record that is described in Unit I.B.1. Mail
your copies, identified by docket ID number OPP-2004-0120, to: Public
Information and Records Integrity Branch, Information Resources and
Services Division (7502C), Office of Pesticide Programs, Environmental
Protection Agency, 1200 Pennsylvania Ave., NW., Washington, DC 20460-
0001. In person or by courier, bring a copy to the location of the
PIRIB described in Unit I.B.1. 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 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. Statutory and Executive Order Reviews
This final rule establishes a tolerance under section 408(d) of
FFDCA in response to a petition submitted to the Agency. The Office of
Management and Budget (OMB) has exempted these types of actions from
review under Executive Order 12866, entitled Regulatory Planning and
Review (58 FR 51735, October 4, 1993). Because this rule has been
exempted from review under Executive Order 12866 due to its lack of
significance, this rule is not subject to Executive Order 13211,
Actions Concerning Regulations That Significantly Affect Energy Supply,
Distribution, or Use (66 FR 28355, May 22, 2001). This final rule does
not contain any information collections subject to OMB approval under
the Paperwork Reduction Act (PRA), 44 U.S.C. 3501 et seq., or impose
any enforceable duty or contain any unfunded mandate as described under
Title II of the Unfunded Mandates Reform Act of 1995 (UMRA) (Public Law
104-4). Nor does it require any special considerations under Executive
Order 12898, entitled Federal Actions to Address Environmental Justice
in Minority Populations and Low-Income Populations (59 FR 7629,
February 16, 1994); or 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 section 408(d) of FFDCA, 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 section 408(n)(4) of FFDCA. For these same reasons, the Agency has
determined that this rule does not have any ``tribal implications '' as
described in Executive Order 13175, entitled Consultation and
Coordination with Indian Tribal Governments (65 FR 67249, November 6,
2000). Executive Order 13175, requires EPA to develop an accountable
process to ensure ``meaningful and timely input by tribal officials in
the development of regulatory policies that have tribal implications.''
``Policies that have tribal implications'' is defined in the Executive
Order to include regulations that have ``substantial direct effects on
one or more Indian tribes, on the relationship between the Federal
Government and the Indian tribes, or on the distribution of power and
responsibilities between the Federal Government and Indian tribes.''
This rule will not have substantial direct effects on tribal
governments, on the relationship between the Federal Government and
Indian tribes, or on the distribution of power and responsibilities
between the Federal Government and Indian tribes, as specified in
Executive Order 13175. Thus, Executive Order 13175 does not apply to
this rule.
VIII. Congressional Review Act
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: July 1, 2004.
James Jones,
Director, Office of Pesticide Programs.
0
Therefore, 40 CFR chapter I is amended as follows:
PART 180--[AMENDED]
0
1. The authority citation for part 180 continues to read as follows:
Authority: 21 U.S.C. 321(q), 346a and 371.
0
2. Section 180.602 is added to subpart C to read as follows:
Sec. 180.602 Spiroxamine; tolerances for residues.
(a) General. Tolerances are established for the combined residues
of
[[Page 42571]]
the fungicide spiroxamine (8-(1,1-dimethylethyl)-N-ethyl-N-propyl-1,4-
dioxaspiro[4,5]decane-2-methanamine) and its metabolites containing the
N-ethyl-N-propyl-1,2-dihydroxy-3-aminopropane moiety, calculated as
parent equivalent, in or on the following raw agricultural commodities:
------------------------------------------------------------------------
Commodity Parts per million
------------------------------------------------------------------------
Banana (import) 3.0
Grape (import) 1.0
Hop, dried cones 50
------------------------------------------------------------------------
(b) Section 18 emergency exemptions. [Reserved]
(c) Tolerances with regional registrations. [Reserved]
(d) Indirect or inadvertent residues. [Reserved]
[FR Doc. 04-16216 Filed 7-15-04; 8:45 am]
BILLING CODE 6560-50-S