esfenvalerate (Asana) Pesticide Tolerance 8/98
[Federal Register: September 11, 1998 (Volume 63, Number 176)]
[Rules and Regulations]
[Page 48607-48615]
>From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr11se98-16]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 180
[OPP-300708; FRL 6026-5]
RIN 2070-AB78
Esfenvalerate; Pesticide Tolerance
AGENCY: Environmental Protection Agency (EPA).
ACTION: Final rule.
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SUMMARY: This regulation establishes tolerances for residues of
esfenvalerate, ((S)-cyano-(3-phenoxyphenyl)methyl (S)-4-chloro-alpha-
(1-methylethyl) benzeneacetate in or on the raw agricultural
commodities mustard greens at 5.0 parts per million (ppm), kiwifruit at
0.5 ppm, globe artichoke at 1.0 ppm, and kohlrabi at 2.0 ppm.
Esfenvalerate is the S,S-isomer of fenvalerate which consists of a
racemic mixture of four isomers (S,S;R,S;S,R; and RR). Technical grade
esfenvalerate, Asana, the only fenvalerate formulation sold in the
United States for agricultural use at this time, is enriched in the
insecticidally active S,S-isomer (84%). Tolerance expressions for
esfenvalerate are based on the sum of all isomers. The Interregional
Research Project Number 4 (IR-4) requested this tolerance under the
Federal Food, Drug, and Cosmetic Act (FFDCA), as amended by the Food
Quality Protection Act of 1996 (Pub. L. 104-170).
[[Page 48608]]
DATES: This regulation is effective September 11, 1998. Objections and
requests for hearings must be received by EPA on or before November 10,
1998.
ADDRESSES: Written objections and hearing requests, identified by the
docket control number, OPP-300708, must be submitted to: Hearing Clerk
(1900), Environmental Protection Agency, Rm. M3708, 401 M St., SW.,
Washington, DC 20460. Fees accompanying objections and hearing requests
shall be labeled ``Tolerance Petition Fees'' and forwarded to: EPA
Headquarters Accounting Operations Branch, OPP (Tolerance Fees), P.O.
Box 360277M, Pittsburgh, PA 15251. A copy of any objections and hearing
requests filed with the Hearing Clerk identified by the docket control
number OPP-300708, must also be submitted to: Public Information and
Records Integrity Branch, Information Resources and Services Division
(7502C), Office of Pesticide Programs, Environmental Protection Agency,
401 M St., SW., Washington, DC 20460. In person, bring a copy of
objections and hearing requests to Rm. 119, CM #2, 1921 Jefferson Davis
Hwy., Arlington, VA.
A copy of objections and hearing requests filed with the Hearing
Clerk may also be submitted electronically by sending electronic mail
(e-mail) to: opp-docket@epamail.epa.gov. Copies of objections and
hearing requests must be submitted as an ASCII file avoiding the use of
special characters and any form of encryption. Copies of objections and
hearing requests will also be accepted on disks in WordPerfect 5.1/6.1
or ASCII file format. All copies of objections and hearing requests in
electronic form must be identified by the docket control number [OPP-
300708]. No Confidential Business Information (CBI) should be submitted
through e-mail. Electronic copies of objections and hearing requests on
this rule may be filed online at many Federal Depository Libraries.
FOR FURTHER INFORMATION CONTACT: By mail: Sidney Jackson, Registration
Division (7505C), Office of Pesticide Programs, Environmental
Protection Agency, 401 M St., SW., Washington, DC 20460. Office
location, telephone number, and e-mail address: CM #2, 1921 Jefferson
Davis Hwy., Arlington, VA, 703-305-7610; e-mail:
jackson.sidney@epamail.epa.gov.
SUPPLEMENTARY INFORMATION: In the Federal Register of April 15, 1998
(63 FR 18411), (FRL 5781-9) EPA, issued a notice pursuant to section
408 of the FFDCA, 21 U.S.C. 346a(e) announcing the filing of a
pesticide petition for tolerances by DuPont Agricultural Products,
Wilmington, Delaware. This notice included a summary of the petition
prepared by DuPont Agricultural Products, Wilmington, Delaware, the
registrant. There were no comments received in response to the notice
of filing.
The petition requested that 40 CFR 180.533 be amended by
establishing tolerances for residues of the insecticide esfenvalerate,
((S)-cyano-(3-phenoxyphenyl)methyl (S)-4-chloro-alpha-(1-methylethyl)
benzeneacetate, in or on the raw agricultural commodities mustard
greens at 5.0 parts per million (ppm), kiwifruit at 0.5 ppm, globe
artichoke at 1.0 ppm, and kohlrabi at 2.0 ppm.
I. Risk Assessment and Statutory Findings
New section 408(b)(2)(A)(i) of the FFDCA allows EPA to establish a
tolerance (the legal limit for a pesticide chemical residue in or on a
food) only if EPA determines that the tolerance is ``safe.'' Section
408(b)(2)(A)(ii) defines ``safe'' to mean that ``there is a reasonable
certainty that no harm will result from aggregate exposure to the
pesticide chemical residue, including all anticipated dietary exposures
and all other exposures for which there is reliable information.'' This
includes exposure through drinking water and in residential settings,
but does not include occupational exposure. Section 408(b)(2)(C)
requires EPA to give special consideration to exposure of infants and
children to the pesticide chemical residue in establishing a tolerance
and to ``ensure that there is a reasonable certainty that no harm will
result to infants and children from aggregate exposure to the pesticide
chemical residue. . . .''
EPA performs a number of analyses to determine the risks from
aggregate exposure to pesticide residues. First, EPA determines the
toxicity of pesticides based primarily on toxicological studies using
laboratory animals. These studies address many adverse health effects,
including (but not limited to) reproductive effects, developmental
toxicity, toxicity to the nervous system, and carcinogenicity. Second,
EPA examines exposure to the pesticide through the diet (e.g., food and
drinking water) and through exposures that occur as a result of
pesticide use in residential settings.
A. Toxicity
1. Threshold and non-threshold effects. For many animal studies, a
dose response relationship can be determined, which provides a dose
that causes adverse effects (threshold effects) and doses causing no
observed effects (the ``no-observed effect level'' or ``NOEL'').
Once a study has been evaluated and the observed effects have been
determined to be threshold effects, EPA generally divides the NOEL from
the study with the lowest NOEL by an uncertainty factor (usually 100 or
more) to determine the Reference Dose (RfD). The RfD is a level at or
below which daily aggregate exposure over a lifetime will not pose
appreciable risks to human health. An uncertainty factor (sometimes
called a ``safety factor'') of 100 is commonly used since it is assumed
that people may be up to 10 times more sensitive to pesticides than the
test animals, and that one person or subgroup of the population (such
as infants and children) could be up to 10 times more sensitive to a
pesticide than another. In addition, EPA assesses the potential risks
to infants and children based on the weight of the evidence of the
toxicology studies and determines whether an additional uncertainty
factor is warranted. Thus, an aggregate daily exposure to a pesticide
residue at or below the RfD (expressed as 100% or less of the RfD) is
generally considered acceptable by EPA. EPA generally uses the RfD to
evaluate the chronic risks posed by pesticide exposure. For shorter
term risks, EPA calculates a margin of exposure (MOE) by dividing the
estimated human exposure into the NOEL from the appropriate animal
study. Commonly, EPA finds MOEs lower than 100 to be unacceptable. This
100-fold MOE is based on the same rationale as the 100-fold uncertainty
factor.
Lifetime feeding studies in two species of laboratory animals are
conducted to screen pesticides for cancer effects. When evidence of
increased cancer is noted in these studies, the Agency conducts a
weight of the evidence review of all relevant toxicological data
including short-term and mutagenicity studies and structure activity
relationship. Once a pesticide has been classified as a potential human
carcinogen, different types of risk assessments (e.g., linear low dose
extrapolations or MOE calculation based on the appropriate NOEL) will
be carried out based on the nature of the carcinogenic response and the
Agency's knowledge of its mode of action.
2. Differences in toxic effect due to exposure duration. The
toxicological effects of a pesticide can vary with different exposure
durations. EPA considers the entire toxicity data base, and based on
the effects seen for different durations and routes of exposure,
determines which risk
[[Page 48609]]
assessments should be done to assure that the public is adequately
protected from any pesticide exposure scenario. Both short and long
durations of exposure are always considered. Typically, risk
assessments include ``acute,'' ``short-term,'' ``intermediate term,''
and ``chronic'' risks. These assessments are defined by the Agency as
follows.
Acute risk, by the Agency's definition, results from 1-day
consumption of food and water, and reflects toxicity which could be
expressed following a single oral exposure to the pesticide residues.
High end exposure to food and water residues are typically assumed.
Short-term risk results from exposure to the pesticide for a period
of 1-7 days, and therefore overlaps with the acute risk assessment.
Historically, this risk assessment was intended to address primarily
dermal and inhalation exposure which could result, for example, from
residential pesticide applications. However, since enaction of FQPA,
this assessment has been expanded to include both dietary and non-
dietary sources of exposure, and will typically consider exposure from
food, water, and residential uses when reliable data are available. In
this assessment, risks from average food and water exposure, and high-
end residential exposure, are aggregated. High-end exposures from all
three sources are not typically added because of the very low
probability of this occurring in most cases, and because the other
conservative assumptions built into the assessment assure adequate
protection of public health. However, for cases in which high-end
exposure can reasonably be expected from multiple sources (e.g.
frequent and widespread homeowner use in a specific geographical area),
multiple high-end risks will be aggregated and presented as part of the
comprehensive risk assessment/characterization. Since the toxicological
endpoint considered in this assessment reflects exposure over a period
of at least 7 days, an additional degree of conservatism is built into
the assessment; i.e., the risk assessment nominally covers 1-7 days
exposure, and the toxicological endpoint/NOEL is selected to be
adequate for at least 7 days of exposure. (Toxicity results at lower
levels when the dosing duration is increased.)
Intermediate-term risk results from exposure for 7 days to several
months. This assessment is handled in a manner similar to the short-
term risk assessment.
Chronic risk assessment describes risk which could result from
several months to a lifetime of exposure. For this assessment, risks
are aggregated considering average exposure from all sources for
representative population subgroups including infants and children.
B. Aggregate Exposure
In examining aggregate exposure, FFDCA section 408 requires that
EPA take into account available and reliable information concerning
exposure from the pesticide residue in the food in question, residues
in other foods for which there are tolerances, residues in groundwater
or surface water that is consumed as drinking water, and other non-
occupational exposures through pesticide use in gardens, lawns, or
buildings (residential and other indoor uses). Dietary exposure to
residues of a pesticide in a food commodity are estimated by
multiplying the average daily consumption of the food forms of that
commodity by the tolerance level or the anticipated pesticide residue
level. The Theoretical Maximum Residue Contribution (TMRC) is an
estimate of the level of residues consumed daily if each food item
contained pesticide residues equal to the tolerance. In evaluating food
exposures, EPA takes into account varying consumption patterns of major
identifiable subgroups of consumers, including infants and children.
The TMRC is a ``worst case'' estimate since it is based on the
assumptions that food contains pesticide residues at the tolerance
level and that 100% of the crop is treated by pesticides that have
established tolerances. If the TMRC exceeds the RfD or poses a lifetime
cancer risk that is greater than approximately one in a million, EPA
attempts to derive a more accurate exposure estimate for the pesticide
by evaluating additional types of information (anticipated residue data
and/or percent of crop treated data) which show, generally, that
pesticide residues in most foods when they are eaten are well below
established tolerances.
Percent of crop treated estimates are derived from federal and
private market survey data. Typically, a range of estimates are
supplied and the upper end of this range is assumed for the exposure
assessment. By using this upper end estimate of percent of crop
treated, the Agency is reasonably certain that exposure is not
understated for any significant subpopulation group. Further, regional
consumption information is taken into account through EPA's computer-
based model for evaluating the exposure of significant subpopulations
including several regional groups, to pesticide residues. For this
pesticide, the most highly exposed population subgroup was not
regionally based.
II. Aggregate Risk Assessment and Determination of Safety
Consistent with section 408(b)(2)(D), EPA has reviewed the
available scientific data and other relevant information in support of
this action, EPA has sufficient data to assess the hazards of
esfenvalerate and to make a determination on aggregate exposure,
consistent with section 408(b)(2), for tolerances for residues of
esfenvalerate (S,S; R,S; S,R; and R,R isomers) in or on the raw
agricultural commodities mustard greens at 5 ppm, kiwifruit at 0.5 ppm,
globe artichoke at 1.0 ppm, and kohlrabi at 2.0 ppm. EPA's assessment
of the dietary exposures and risks associated with establishing the
tolerances 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 esfenvalerate are
discussed below.
1. Acute toxicity. A battery of acute toxicity studies places
technical esfenvalerate in Toxicity category II for acute oral lethal
dose LD<INF>50</INF> at 87.2 milligrams/kilogram (mg/kg), Category III
for acute dermal LD<INF>50</INF> > 2000 mg/kg and primary eye
irritation, and Category IV for primary skin irritation. Esfenvalerate
is a non-sensitizer. Acute inhalation on technical grade active
ingredient is waived due to negligible vapor pressure. The Acute
Delayed Neurotoxicity (Guideline 81-8) remains a data gap.
2. Genotoxicity--i. In a reverse gene mutation assay in bacteria,
S. typhimurium and Escherichia coli were exposed to fenvalerate in DMSO
at concentrations of 15, 50, 150, 500, 1,500, or 5,000 micrograms
(<greek-m>g)/plate in the presence and absence of mammalian metabolic
activation (S9-mix). There was no evidence of induced mutant colonies
over background.
ii. In a mammalian cell gene mutation assay at the HGPRT locus,
Chinese hamster V79 cells cultured in vitro were exposed to fenvalerate
in DMSO at concentrations of 12.6, 42, 126, 420 <greek-m>g/ml in the
presence of mammalian metabolic activation (S9-mix) and at
concentrations of 4.2, 12.6, 42, 126 <greek-m>g/milliliter (ml) in the
absence of S9-mix.
[[Page 48610]]
There was no evidence of induced mutant colonies over background. In
Chinese hamster lung fibroblasts (V79 cells) forward gene mutation
assay the test was negative up to cytotoxic and/or precipitating levels
126 <greek-m>g/ml in the absence of metabolic activation -S9; 420
<greek-m>g/ml in the presence of metabolic activation +S9).
iii. In a mammalian cell cytogenetics chromosomal aberration assay
CHO-K1 cell cultures were exposed to fenvalerate in DMSO at
concentrations of 4.2 <greek-m>g/ml, 8.4 <greek-m>g/ml, 21 <greek-m>g/
ml, 42 <greek-m>g/ml respectively without exogenous metabolic
activation (S9-mix) and at concentrations of 21 <greek-m>g/ml, 42
<greek-m>g/ml, 84 <greek-m>g/ml, 210 <greek-m>g/ml respectively with
S9-mix. There was no evidence of a significant induction of chromosomal
aberrations or polyploid cells over background.
iv. A mouse micronucleus assay was negative in male ICR mice up to
the highest dose tested (HDT) (150 mg/kg) administered by
intraperitoneal injection. Since there appears to be no sex specific
difference in the toxicity of esfenvalerate, the use of males only is
justifiable. No overt toxicity was observed, but suggestive evidence of
bone marrow cytotoxicity was seen 48 hours post-administration at the
highest dose level tested.
v. Other genetic toxicology studies submitted on racemic
fenvalerate indicate that the mixture containing equal parts of the
four stereoisomers is not mutagenic in bacteria. The racemic mixture
was also negative in a mouse host mediated assay and in a mouse
dominant lethal assay.
3. Reproductive and developmental toxicity--i. Esfenvalerate was
administered to female rats at doses of 0,2.5, 5.0, 10.0 or 20.0 mg/kg/
day from gestation days 6 through 15 (pilot study doses were 1.0, 2.0,
3.0, 4.0, 5.0 and 20 mg/kg/day). The Lowest Observed Effect Level
(LOEL) is 2.5 mg/kg/day based on behavioral/Central Nervous System
(CNS) clinical signs. The NOEL for maternal toxicity is 2.0 mg/kg/day
(from the pilot study). There was no evidence of developmental toxicity
at any dose. The NOEL is 20 mg/kg/day, the highest dose tested.
ii. Esfenvalerate was administered to rabbits at doses of 0, 3.0,
10.0 or 20.0 mg/kg/day from gestation days 7 through 19 (pilot study
doses were 0, 2.0, 3.0, 4.0, 4.5, 5.0 or 20.0 mg/kg/day). The LOEL is
3.0 mg/kg/day based on behavioral/CNS clinical signs. The NOEL is 2.0
mg/kg/day (from the pilot study). There was no evidence of
developmental toxicity at any dose. The LOEL is greater than 20.0 mg/
kg/day. The NOEL is equal to or greater than 20.0 mg/kg/day, the HDT.
iii. In a 2-generation reproduction toxicity study in rats
esfenvalerate was administered to rats at dose levels of 0, 3.75,
5.0,17.5 and 35.0/17.5 mg/kg/day. The LOEL for parental toxicity is
3.75 mg/kg/day based on decreases in mean body weights of F<INF>1</INF>
females and an increased incidence of skin lesions. The NOEL could not
be determined. The LOEL for reproductive toxicity is 5.0 mg/kg/day
based on decreases in F<INF>1</INF> pup weights on day 21 of lactation;
decreases in litter size and F<INF>2</INF> pup weights and an increased
incidence of subcutaneous hemorrhage. The NOEL is 3.75 mg/kg/day.
4. Subchronic toxicity. i. In a 90-day feeding study, rats were
administered 0, 4.7, 6.2, 7.8 or 18.7 mg/kg/day of esfenvalerate. The
LOEL is 18.7 mg/kg/day based on neurological dysfunction. The NOEL is
7.8 mg/kg/day.
ii. In another 90-day feeding study, rats were administered 0, 5,
15, 30 or 50 mg/kg/day of esfenvalerate. The LOEL is 15 mg/kg/day based
on neurological dysfunction. The NOEL is 5 mg/kg/day.
iii. Esfenvalerate was administered to mice at dose levels of 0,
10.5, 30.5 or 106 mg/kg/day (male) and 0, 12.6, 36.8 or 113 mg/kg/day
(female). The LOEL for esfenvalerate is 106 mg/kg/day. The NOEL is 30.5
mg/kg/day.
5. Chronic toxicity--i. In a 21-day probe for a 1 year feeding
study 2 male and 2 female beagles were administered 0, 2.80, 6.40 or
9.38 mg/kg/day in males and 0, 2.25, 7.37 or 8.50 mg/kg/day of
esfenvalerate. The LOEL was determined to be 6.40 mg/kg/day based on
nervous system involvement and decreases in body weight and food
consumption. The NOEL is 2.25 mg/kg/day.
ii. In a 1-year feeding study, 6 male and 6 female beagles/group
were administered 0, 0.68, 1.36 or 5.29 mg/kg/day esfenvalerate. The
LOEL was determined to be 6.40 mg/kg/day based on nervous system
involvement and decreases in body weight and food consumption. The NOEL
was determined to be 5.29 mg/kg/day. These studies are acceptable and
satisfies the requirement for a guideline series 83-1b chronic feeding
study in dogs.
6. Chronic/carcinogenicity toxicity--i. In a chronic/
carcinogenicity feeding study, rats were administered 0.050, 0.25, 1.25
or 12.5 mg/kg/day of fenvalerate in the diet for 2 years. The LOEL was
greater than or equal to 12.5 mg/kg/day. There was no increase in
tumors at 12.5 mg/kg/day. The NOEL was determined to be 12.5 mg/kg/day
the highest dose tested (HDT) in the 2 year study. The study is
supplementary and does not satisfy the requirement for a guideline
series 83-5 combined chronic/carcinogenicity study in rats.
ii. In a lifetime feeding study, rats were administered 0 or 50.0
mg/kg/day of fenvalerate in the diet. Spindle cell sarcomas were
produced in male rats only. The LOEL was 50.0 mg/kg/day based on loss
of weight and neurological effects. The NOEL was 12.5 mg/kg/day as
determined in the 2-year rat chronic/carcinogenicity feeding study
above.
The conclusion that fenvalerate is associated with the production
of spindle cell sarcomas was later retracted by EPA. The study is
supplementary and does not satisfy the requirement for a guideline
series 83-5 combined chronic/ carcinogenicity study in rats. When taken
together with chronic/carcinogenicity feeding study, the guideline
requirement for a 83-2a, cancer study in the rat is satisfied.
iii. In a 2-year feeding study mice were administered 0, 1.5, 7.5,
38.0 or 187.5 mg/kg/day fenvalerate in the diet. The LOEL was 7.5 mg/
kg/day based on granulomatous changes (related to fenvalerate only, not
esfenvalerate). The NOEL was 1.5 mg/kg/day. This study satisfies the
requirement for combined chronic feeding carcinogenicity study in mice.
iv. In an 18-month feeding study, mice were fed 0, 15.0, 45.0,
150.0 or 450.0 mg/kg/day of fenvalerate in the diet. The LOEL is 45.0
mg/kg/day based on granulomatous changes in the liver and spleen. The
NOEL is 15.0 mg/kg/day. No carcinogenicity was observed.
v. In a life span feeding study, mice were administered 0, 1.5,
4.5, 15.0 or 45.0 mg/kg/day of fenvalerate in the diet. The LOEL was
determined to be 15 mg/kg/day based on the granulomatous lesions
observed and on the change in hematological parameters. Fenvalerate was
determined not to be carcinogenic in the specific test strain of the
mouse. The NOEL was determined to be 3.48 mg/kg/day.
The following studies are considered data gaps in the toxicology
data base: general metabolism, 21 day dermal, dermal penetration, and
acute and subchronic 90-day neurotoxicity. Developmental neurotoxicity
data requirements are reserved as an upper tier study which would only
be required if effects in the acute and subchronic studies indicate
concerns for increased sensitivity of the infant or neonate. Although
these data are lacking EPA has sufficient toxicity data to support
these tolerances and these additional studies are not expected to
significantly change its risk assessment. These studies will be
required under a special Data Call-In
[[Page 48611]]
letter pursuant to section 3 (c)(2)(B) of FIFRA.
B. Toxicological Endpoints
1. Acute toxicity. EPA has established an NOEL of 2.0 mg/kg/day
through the dietary route in rat and rabbit developmental studies. This
NOEL is based on behavioral and central nervous system clinical signs.
A MOE of 100 is required.
2. Short - and intermediate - term toxicity. To assess risk from
(nonfood) short and intermediate term dermal exposure, EPA has
established a NOEL of 2.0 mg/kg/day from the rat and rabbit
developmental studies. No dermal penetration/absorption study is
available and the NOEL incorporates a 25% dermal absorption based on
the weight-of-evidence available for structurally related pyrethroids.
This NOEL is based on behavioral and central nervous system
clinical signs. For exposure via inhalation the Agency used an oral
NOEL of 2.0 mg/kg/day and assumed 100% absorption (based on the 2 mg/
kg/day used for the dermal risk assessment since no appropriate
inhalation toxicity studies are available).
3. Chronic toxicity. EPA has established the RfD for esfenvalerate
ester at 0.02 mg/kg/day. This RfD is based on a NOEL of 2.0 mg/kg/day
through the dietary exposure route in developmental study in rat. The
NOEL is based on behavioral changes and clinical signs of
neurotoxicity. This RFD is based on an uncertainty factor of 100.
4. Carcinogenicity. Esfenvalerate is classified as a Group E. There
is no evidence of carcinogenicity in either rats or mice.
C. Exposures and Risks
1. From food and feed uses. Tolerances have been established (40
CFR 180.533) for the residues of fenvalerate in or on a variety of raw
agricultural commodities. EPA notes that the acute dietary risk
assessments used Monte Carlo modeling (in accordance with Tier 3 of EPA
June 1996 ``Acute Dietary Exposure Assessment'' guidance document)
incorporating anticipated residues and percent of crop treated
refinements. Field trial data and FDA monitoring data were used to
generate anticipated residues or residue distribution for Monte Carlo
analyses. Chronic dietary risk assessments used anticipated residues
and percent crop treated refinements.
Risk assessments were conducted by EPA to assess dietary exposures
and risks from esfenvalerate as follows:
i. Acute exposure and risk. Acute dietary risk assessments are
performed for a food-use pesticide if a toxicological study has
indicated the possibility of an effect of concern occurring as a result
of a one day or single exposure. The NOEL used for the acute dietary
exposure was 2.0 mg/kg/day. Potential acute exposures from food
commodities were estimated using a Tier 3 acute dietary risk assessment
(Monte Carlo Analysis). The MOEs (99.9th percentile) for the U.S.
population based on an acute dietary exposure of 0.011717 mg/kg/day are
171. For children 1-6 years old (most highly exposed population) the
MOEs based on an acute dietary exposure of 0.019445 mg/kg/day are 103.
The Agency has no cause for concern if total acute exposure calculated
for the 99.9th percentile yields an MOE of 100 or larger.
ii. Chronic exposure and risk. Potential chronic exposures were
estimated using NOVIGEN's DEEM (Dietary Exposure Evaluation Model). The
RfD used for the chronic dietary analysis is 0.02 mg/kg/day. Using
tolerance values and anticipated residues discussed above the risk
assessment resulted in use of 1.9% of the RfD for the general U.S.
population and 4.6% of the RfD for children 1-6 years.
Section 408(b)(2)(E) authorizes EPA to consider available data and
information on the anticipated residue levels of pesticide residues in
food and the actual levels of pesticide chemicals that have been
measured in food. If EPA relies on such information, EPA must require
that data be provided 5 years after the tolerance is established,
modified, or left in effect, demonstrating that the levels in food are
not above the levels anticipated. Following the initial data
submission, EPA is authorized to require similar data on a time frame
it deems appropriate. Section 408(b)(2)(F) allows the Agency to use
data on the actual percent of crop treated when establishing a
tolerance only where the Agency can make the following findings: (1)
that the data used are reliable and provide a valid basis for showing
the percentage of food derived from a crop that is likely to contain
residues;(2) that the exposure estimate does not underestimate the
exposure for any significant subpopulation and; (3) where data on
regional pesticide use and food consumption are available, that the
exposure estimate does not understate exposure for any regional
population. In addition, the Agency must provide for periodic
evaluation of any estimates used.
The percent of crop treated estimates for esfenvalerate were
derived from federal and market survey data. EPA considers these data
reliable. A range of estimates are supplied by these data and the upper
end of this range was used for the exposure assessment. By using this
upper end of estimate of percent crop treated, the agency is reasonably
certain that exposure is not underestimated for any significant
subpopulation. Further, regional consumption information is taken into
account through EPA's computer-based model for evaluating the exposure
of significant subpopulations including several regional groups. Review
of these regional data allows the Agency to be reasonably certain that
no regional population is exposed to residue levels higher than those
estimated by the Agency. To meet the requirement for data on
anticipated residues, EPA will issue a Data Call-In (DCI) notice
pursuant to FFDCA section 408(f) requiring submission of data on
anticipated residues in conjunction with approval of the registration
under the FIFRA.
2. From drinking water. Esfenvalerate is immobile in soil and will
not leach into groundwater. Additionally, due to their insolubility and
lipophilic nature, any residues in surface water will rapidly and
tightly bind to soil particles and remain with sediment. A screening
evaluation of leaching potential of a typical potential of a typical
pyrethroid was conducted using EPA's Pesticide Root Zone Model (PRZM1).
Based on this screening assessment, the potential concentrations of a
pyrethroid in ground water at depths of 1 and 2 meters are essentially
zero (much less than 0.001 parts per billion). Therefore, EPA concludes
that residues are not expected to occur in drinking water.
i. Acute exposure and risk. Acute drinking water exposure is
estimated for the U.S. population to be 0.000039 mg/kg/day with an MOE
of 51,743. For non-nursing infants less than 1 year old the exposure is
0.000074 with a MOE of 27,042.
ii. Chronic exposure and risk. Chronic drinking water exposure is
estimated for the U.S. population to be 0.000001 mg/kg/day and for the
non-nursing infants 0.000005 mg/kg/day. Less than 0.1% of the RfD is
occupied by both population groups.
3. From non-dietary exposure. Esfenvalerate is currently registered
for use on the following residential non-food sites: spray treatments
in and around commercial and residential areas, treatments for control
of ectoparasites on pets, home care products including foggers,
pressurized sprays, crack and crevice treatments, lawn and garden
sprays, and pet and pet
[[Page 48612]]
bedding sprays. For the non-agricultural products, the very low amounts
of active ingredient they contain, combined with the low vapor pressure
(1.5 x 10<SUP>-9</SUP> mm Mercury at 25 deg.C) and low dermal
penetration, would result in minimal inhalation and dermal exposure.
Individual non-dietary risk exposure analyses were conducted using a
flea infestation scenario that included pet spray, carpet and room
treatment, and lawn care, respectively.
4. Short- and intermediate-term exposure and risk. Short- and
intermediate-term exposure and risk. The total aggregate non-dietary
exposure including lawn, carpet, and pet uses (mg/kg/day) are: 0.000023
for adults; 0.00129 for children aged 1-6 years; and 0.00138 for
infants less than 1 year old. It should be noted that carpet uses are
considered short and intermediate term exposures because available data
indicate that esfenvalerate dissipates over time and is thus
unavailable to contribute as chronic exposure and risk.
For the adults, children aged 1-6 years, and infants less than 1
year old subgroups discussed above, the MOE is > 87,000, 1,500, and
1,400, respectively. Based on potential non-dietary exposure for
esfenvalerate from existing product uses as discussed above, it can be
concluded that non-dietary risk is well below levels of concern to the
Agency.
5. Cumulative exposure to substances with common mechanism of
toxicity. Section 408(b)(2)(D)(v) requires that, when considering
whether to establish, modify, or revoke a tolerance, the Agency
consider ``available information'' concerning the cumulative effects of
a particular pesticide's residues and ``other substances that have a
common mechanism of toxicity.'' The Agency believes that ``available
information'' in this context might include not only toxicity,
chemistry, and exposure data, but also scientific policies and
methodologies for understanding common mechanisms of toxicity and
conducting cumulative risk assessments. For most pesticides, although
the Agency has some information in its files that may turn out to be
helpful in eventually determining whether a pesticide shares a common
mechanism of toxicity with any other substances, EPA does not at this
time have the methodologies to resolve the complex scientific issues
concerning common mechanism of toxicity in a meaningful way. EPA has
begun a pilot process to study this issue further through the
examination of particular classes of pesticides. The Agency hopes that
the results of this pilot process will increase the Agency's scientific
understanding of this question such that EPA will be able to develop
and apply scientific principles for better determining which chemicals
have a common mechanism of toxicity and evaluating the cumulative
effects of such chemicals. The Agency anticipates, however, that even
as its understanding of the science of common mechanisms increases,
decisions on specific classes of chemicals will be heavily dependent on
chemical specific data, much of which may not be presently available.
Although at present the Agency does not know how to apply the
information in its files concerning common mechanism issues to most
risk assessments, there are pesticides as to which the common mechanism
issues can be resolved. These pesticides include pesticides that are
toxicologically dissimilar to existing chemical substances (in which
case the Agency can conclude that it is unlikely that a pesticide
shares a common mechanism of activity with other substances) and
pesticides that produce a common toxic metabolite (in which case common
mechanism of activity will be assumed).
EPA does not have, at this time, available data to determine
whether esfenvalerate 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,
esfenvalerate 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 esfenvalerate has a common mechanism of
toxicity with other substances.
D. Aggregate Risks and Determination of Safety for U.S. Population
1. Acute risk. The acute aggregate risk assessment takes into
account exposure from food and drinking water. The potential acute
exposure from food and drinking water to the overall U.S. population
provides an acute dietary exposure of 0.011756 mg/kg/day with an MOE of
170. This acute dietary exposure estimate is considered conservative,
using anticipated residue values and percent crop-treated data in
conjunction with Monte Carlo analysis.
2. Chronic risk. Using the ARC exposure assumptions described
above, EPA has concluded that aggregate exposure to esfenvalerate will
utilize 1.9% of the RfD for the U.S. population. The major identifiable
subgroup with the highest aggregate exposure is children 1 - 6 years.
EPA generally has no concern for exposures below 100% of the RfD
because the RfD represents the level at or below which daily aggregate
dietary exposure over a lifetime will not pose appreciable risks to
human health.
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. The potential short- and intermediate-term
aggregate risk for the U.S. population is an exposure of 0.0082 mg/kg/
day with an MOE of 244.
4. Conclusion. EPA concludes that there is reasonable certainty
that no harm will result from acute, chronic or short- and
intermediate-term aggregate exposure to esfenvalerate residues.
5. Aggregate cancer risk for U.S. population. Esfenvalerate is
classified as a Group E carcinogen - no evidence of carcinogenicity in
rats or mice. Therefore, a carcinogenicity risk analysis is not
required. Based on available adequate data, EPA believes that approved
use of this pesticide does not pose a significant cancer risk.
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 esfenvalerate, 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 pre-and post-natal toxicity and the
completeness of the database unless EPA determines that a different
margin of safety will be safe for infants and children. Margins of
safety are incorporated into EPA risk assessments either directly
through use of a MOE analysis or through using uncertainty (safety)
factors in calculating a dose level that poses no appreciable risk to
humans. EPA believes that reliable data support using the standard
uncertainty factor (usually 100 for combined inter- and intra-species
variability) and not the additional tenfold MOE/uncertainty factor when
EPA has a complete data
[[Page 48613]]
base under existing guidelines and when the severity of the effect in
infants or children or the potency or unusual toxic properties of a
compound do not raise concerns regarding the adequacy of the standard
MOE/safety factor.
ii. Developmental toxicity studies. In both prenatal developmental
toxicity studies in rats and rabbits, there is no evidence of
developmental toxicity at a dose up to 20 mg/kg/day. Maternal clinical
neurotoxicity (based on behavioral and central nervous system clinical
signs) was observed at a dose as low as 2.5 or 3.0 mg/kg/day for rats
and rabbits, respectively. The maternal NOEL was 2.0 mg/kg/day.
iii. Reproductive toxicity study. In the 2-generation reproduction
study in rats, offspring toxicity was observed only at dietary levels
which were also found to be toxic to parental animals. The LOEL was 5.1
mg/kg/day based on decrease in mean body weights of females and
increased incidence of dermal lesions. The NOEL for parental systemic
toxicity was not determined. Effects on the offspring, including
decreased pup weights in both generations during early and/or late
lactation, decreased litter size, and increased incidence of
subcutaneous hemorrhage, were observed at dietary levels of 6.70 mg/kg/
day and above, with a NOEL of 5.1 mg/kg/day.
iv. Pre- and post-natal sensitivity. There is no evidence of
additional sensitivity to young rats or rabbits following pre- or
postnatal exposure to esfenvalerate.
v. Conclusion. From available adequate data, there is no
indication that the developing fetus or neonate is more sensitive than
adult animals. No developmental neurotoxicity studies are being
required at this time. A developmental neurotoxicity data requirement
is an upper tier study and required only if effects observed in the
acute and 90-day neurotoxicity studies indicate concerns for frank
neuropathy or alterations seen in the fetal nervous system in the
developmental and reproductive toxicology studies. The FQPA conditional
requirement of an additional tenfold margin of safety for pesticide
residues be applied for infants and children to take into account
potential pre-and post-natal toxicity was not imposed in this case. The
Agency believes that reliable data support use of the standard 100-fold
uncertainty factor, and that an additional ten-fold (10x) uncertainty
factor is not needed to protect the safety of infants and children.
2. Acute risk. The potential acute exposure from food and drinking
water to the most sensitive population subgroup, children 1-6 years old
is 0.019477 mg/kg/day with an MOE of 103. The Agency has no cause for
concern if total acute exposure calculated for the 99.9th percentile
yields a MOE of 100 or larger.
3. Chronic risk. Using the conservative exposure assumptions
described above, EPA has concluded that aggregate exposure to
esfenvalerate from food and drinking water will utilize 4.6% of the RfD
for children 1-6 years old, the most sensitive population subgroup
based on a dietary exposure of 0.000912 mg/kg/day. EPA generally has no
concern for exposures below 100% of the RfD because the RfD represents
the level at or below which daily aggregate dietary exposure over a
lifetime will not pose appreciable risks to human health. Despite the
potential for exposure to esfenvalerate in drinking water and from non-
dietary, non-occupational exposure, EPA does not expect the aggregate
exposure to exceed 100% of the RfD.
4. Short- or intermediate-term risk. EPA has concluded that
potential short- or intermediate -term aggregate exposure of
esfenvalerate from chronic dietary food and water (considered to be a
background exposure level) plus indoor and outdoor residential exposure
to children (1-6 years old) is 0.0113 mg/kg/day with an MOE of 177. For
infants (less than 1 year old) the exposure is 0.0098 mg/kg/day with an
MOE of 204. The Agency is not generally concerned for exposures where
the MOE value is greater than 100.
EPA concludes that there is a reasonable certainty that no harm
will result to infants and children from aggregate exposure to
esfenvalerate residues.
5. Special docket. The complete acute and chronic exposure analyses
(including dietary, non-dietary, drinking water, and residential
exposure, and analysis of exposure to infants and children) used for
risk assessment purposes can be found in the Special Docket for the
FQPA under the title ``Risk Assessment for Extension of Tolerances for
Synthetic Pyrethroids.'' Further explanation regarding EPA's decision
regarding the additional safety factor can also be found in the Special
Docket.
6. Endocrine disrupter effects. EPA is required to develop a
screening program to determine whether certain substances (including
all pesticides and inerts) ``may have an effect in humans that is
similar to an effect produced by a naturally occurring estrogen, or
such other endocrine effect...'' The Agency is currently working with
interested stakeholders, including other government agencies, public
interest groups, industry and research scientists in developing a
screening and testing program and a priority setting scheme to
implement this program. Congress has allowed 3 years from the passage
of FQPA (August 3, 1999) to implement this program. At that time, EPA
may require further testing of this active ingredient and end use
products for endocrine disrupter effects.
III. Other Considerations
A. Metabolism In Plants and Animals
The nature of the residue in plants and animals is adequately
defined. EPA has concluded that the qualitative nature of the residue
is the same for both fenvalerate and esfenvalerate. The residue to be
regulated is fenvalerate: the S,S; R,S; S,R; and R,R isomers.
B. Analytical Enforcement Methodology
There is a practical analytical method utilizing electron-capture
gas chromatography with nitrogen phosphorous detection available for
enforcement with a limit of detection that allows monitoring food with
residues at or above tolerance levels. The limit of detection for the
updated method is the same as that of the current PAM II method, which
is 0.01 ppm .
C. Magnitude of Residues
Tolerances are based on the sum of all isomers of fenvalerate.
Fenvalerate is a racemic mixture of four isomers about 25% each. This
product was registered as Pydrin<Register>. However since 1992, an S,S-
isomer enriched formulation, Asana<Register> (esfenvalerate), has been
the only fenvalerate formulation sold in the United States for
agricultural use. Since the S,S-isomer is the insecticidally active
isomer, the use rate for Asana<Register> is four times lower than that
for Pydrin<Register>. A petition is pending (PP 4F4329), to convert
tolerances (still to be expressed as the sum of all isomers) based on
the use rates for Asana<Register>. Bridging residue studies have shown
Asana<Register> residues to be 3-4 times lower than Pydrin residues.
Available residue data support the tolerance levels being established
by this Notice.
D. International Residue Limits
There are no Codex maximum residue levels (MRL's) for
esfenvalerate on crops that are the subject of this notice. MRLs have
been established for the related compound, fenvalerate, on a number of
crops that also have U. S. tolerances. Use rate and isomer pesticidal
activity are among factors that effect residue levels. The Agency will
fully evaluate MRL values for all permanent tolerances when pesticides
are reregistered.
[[Page 48614]]
IV. Conclusion
Therefore, the tolerances are established for residues of
esfenvalerate, ((S)-cyano-(3-phenoxyphenyl)methyl (S)-4-chloro-alpha-
(1-methylethyl) benzeneacetate and the S,S; R,S; S,R; and R,R isomers
in or on the raw agricultural commodities mustard greens at 5.0 parts
per million (ppm), kiwifruit at 0.5 ppm, globe artichoke at 1.0 ppm,
and kohlrabi at 2.0 ppm.
V. Objections and Hearing Requests
The new FFDCA section 408(g) provides essentially the same process
for persons to ``object'' to a tolerance regulation issued by EPA under
new section 408(e) and (l)(6) as was provided in the old section 408
and in section 409. However, the period for filing objections is 60
days, rather than 30 days. EPA currently has procedural regulations
which govern the submission of objections and hearing requests. These
regulations will require some modification to reflect the new law.
However, until those modifications can be made, EPA will continue to
use those procedural regulations with appropriate adjustments to
reflect the new law.
Any person may, by November 10, 1998, file written objections to
any aspect of this regulation and may also request a hearing on those
objections. Objections and hearing requests must be filed with the
Hearing Clerk, at the address given above (40 CFR 178.20). A copy of
the objections and/or hearing requests filed with the Hearing Clerk
should be submitted to the OPP docket for this rulemaking. The
objections submitted must specify the provisions of the regulation
deemed objectionable and the grounds for the objections (40 CFR
178.25). Each objection must be accompanied by the fee prescribed by 40
CFR 180.33(i). If a hearing is requested, the objections must include a
statement of the factual issues on which a hearing is requested, the
requestor's contentions on such issues, and a summary of any evidence
relied upon by the requestor (40 CFR 178.27). A request for a hearing
will be granted if the Administrator determines that the material
submitted shows the following: There is genuine and substantial issue
of fact; there is a reasonable possibility that available evidence
identified by the requestor would, if established, resolve one or more
of such issues in favor of the requestor, taking into account
uncontested claims or facts to the contrary; and resolution of the
factual issues in the manner sought by the requestor would be adequate
to justify the action requested (40 CFR 178.32). Information submitted
in connection with an objection or hearing request may be claimed
confidential by marking any part or all of that information as CBI.
Information so marked will not be disclosed except in accordance with
procedures set forth in 40 CFR part 2. A copy of the information that
does not contain CBI must be submitted for inclusion in the public
record. Information not marked confidential may be disclosed publicly
by EPA without prior notice.
VI. Public Record and Electronic Submissions
EPA has established a record for this rulemaking under docket
control number OPP-300708 (including any comments and data submitted
electronically). A public version of this record, including printed,
paper versions of electronic comments, which does not include any
information claimed as CBI, is available for inspection from 8:30 a.m.
to 4 p.m., Monday through Friday, excluding legal holidays. The public
record is located in Room 119 of the Public Information and Records
Integrity Branch, Information Resources and Services Division (7502C),
Office of Pesticide Programs, Environmental Protection Agency, Crystal
Mall #2, 1921 Jefferson Davis Highway, Arlington, VA.
Electronic comments may be sent directly to EPA at:
opp-docket@epamail.epa.gov.
Electronic comments must be submitted as an ASCII file avoiding the
use of special characters and any form of encryption.
The official record for this rulemaking, as well as the public
version, as described above will be kept in paper form. Accordingly,
EPA will transfer any copies of objections and hearing requests
received electronically into printed, paper form as they are received
and will place the paper copies in the official rulemaking record which
will also include all comments submitted directly in writing. The
official rulemaking record is the paper record maintained at the
Virginia address in ``ADDRESSES'' at the beginning of this document.
VII. Regulatory Assessment Requirements
A. Certain Acts and Executive Orders
This final rule establishes tolerances 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) (Pub. L. 104-4). Nor does
it require any prior consultation as specified by Executive Order
12875, entitled Enhancing the Intergovernmental Partnership (58 FR
58093, October 28, 1993), or special considerations as required by
Executive Order 12898, entitled Federal Actions to Address
Environmental Justice in Minority Populations and Low-Income
Populations (59 FR 7629, February 16, 1994), or require OMB review in
accordance with Executive Order 13045, entitled Protection of Children
from Environmental Health Risks and Safety Risks (62 FR 19885, April
23, 1997).
B. Executive Order 12875
Under Executive Order 12875, entitled Enhancing Intergovernmental
Partnerships (58 FR 58093, October 28, 1993), EPA may not issue a
regulation that is not required by statute and that creates a mandate
upon a State, local or tribal government, unless the Federal government
provides the funds necessary to pay the direct compliance costs
incurred by those governments. If the mandate is unfunded, EPA must
provide to the Office of Management and Budget (OMB) a description of
the extent of EPA's prior consultation with representatives of affected
State, local and tribal governments, the nature of their concerns,
copies of any written communications from the governments, and a
statement supporting the need to issue the regulation. In addition,
Executive Order 12875 requires EPA to develop an effective process
permitting elected officials and other representatives of State, local
and tribal governments ``to provide meaningful and timely input in the
development of regulatory proposals containing significant unfunded
mandates.''
Today's rule does not create an unfunded federal mandate on State,
local or tribal governments. The rule does not impose any enforceable
duties on these entities. Accordingly, the requirements of section 1(a)
of Executive Order 12875 do not apply to this rule.
C. Executive Order 13084
Under Executive Order 13084, entitled Consultation and Coordination
with Indian Tribal Governments (63 FR
[[Page 48615]]
27655, May 19,1998), EPA may not issue a regulation that is not
required by statute, that significantly or uniquely affects the
communities of Indian tribal governments, and that imposes substantial
direct compliance costs on those communities, unless the Federal
government provides the funds necessary to pay the direct compliance
costs incurred by the tribal governments. If the mandate is unfunded,
EPA must provide OMB, in a separately identified section of the
preamble to the rule, a description of the extent of EPA's prior
consultation with representatives of affected tribal governments, a
summary of the nature of their concerns, and a statement supporting the
need to issue the regulation. In addition, Executive Order 13084
requires EPA to develop an effective process permitting elected and
other representatives of Indian tribal governments ``to provide
meaningful and timely input in the development of regulatory policies
on matters that significantly or uniquely affect their communities.''
Today's rule does not significantly or uniquely affect the
communities of Indian tribal governments. This action does not involve
or impose any requirements that affect Indian Tribes. Accordingly, the
requirements of section 3(b) of Executive Order 13084 do not apply to
this rule.
In addition, since tolerances and exemptions that are established
on the basis of a petition under FFDCA section 408(d), such as the
tolerances in this final rule, do not require the issuance of a
proposed rule, the requirements of the Regulatory Flexibility Act (RFA)
(5 U.S.C. 601 et seq.) do not apply. Nevertheless, the Agency has
previously assessed whether establishing tolerances, exemptions from
tolerances, raising tolerance levels or expanding exemptions might
adversely impact small entities and concluded, as a generic matter,
that there is no adverse economic impact. The factual basis for the
Agency's generic certification for tolerance actions published on May
4, 1981 (46 FR 24950) and was provided to the Chief Counsel for
Advocacy of the Small Business Administration.
VIII. Submission to Congress and the Comptroller General
The Congressional Review Act, 5 U.S.C. 801 et seq., as added by the
Small Business Regulatory Enforcement Fairness Act of 1996, generally
provides that before a rule may take effect, the agency promulgating
the rule must submit a rule report, which includes a copy of the rule,
to each House of the Congress and to the Comptroller General of the
United States. EPA will submit a report containing this rule and other
required information to the U.S. Senate, the U.S. House of
Representatives, and the Comptroller General of the United States prior
to publication of the rule in the Federal Register. This rule is not a
``major rule'' as defined by 5 U.S.C. 804(2).
List of Subjects in 40 CFR Part 180
Environmental protection, Administrative practice and procedure,
Agricultural commodities, Pesticides and pests, Reporting and
recordkeeping requirements.
Dated: August 31, 1998.
James Jones,
Director, Registration Division, Office of Pesticide Programs.
Therefore, 40 CFR chapter I is amended as follows:
PART 180--[AMENDED]
1. The authority citation for part 180 continues to read as
follows:
Authority: 21 U.S.C. 346a and 371.
2. In Sec. 180.533, by alphabetically adding the following
commodities to the table in paragraph (a) to read as follows:
Sec. 180.533 Esfenvalerate; tolerances for residues
(a)* * *
------------------------------------------------------------------------
Commodity Parts per million
------------------------------------------------------------------------
Artichoke, globe.......................... 1.0
* * * * *
Kiwifruit................................. 0.5
Kohlrabi.................................. 2.0
* * * * *
Mustard greens............................ 5.0
* * * * *
------------------------------------------------------------------------
* * * * *
[FR Doc. 98-24770 Filed 9-10-98; 8:45 am]
BILLING CODE 6560-50-F
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criticism of unnamed products implied. Most of this information is historical
in nature and may no longer be applicable.
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