[Federal Register Volume 63, Number 176 (Friday, September 11, 1998)]
[Rules and Regulations]
[Pages 48607-48615]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-24770]


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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: [email protected]. Copies of objections and 
hearing requests must be submitted as an ASCII file avoiding the use of 
special characters and any form of encryption. Copies of objections and 
hearing requests will also be accepted on disks in WordPerfect 5.1/6.1 
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: 
[email protected].

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 LD50 at 87.2 milligrams/kilogram (mg/kg), Category III 
for acute dermal LD50 > 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 
(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 g/ml in the 
presence of mammalian metabolic activation (S9-mix) and at 
concentrations of 4.2, 12.6, 42, 126 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 g/ml in the absence of metabolic activation -S9; 420 
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 g/ml, 8.4 g/ml, 21 g/
ml, 42 g/ml respectively without exogenous metabolic 
activation (S9-mix) and at concentrations of 21 g/ml, 42 
g/ml, 84 g/ml, 210 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 F1 
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 F1 pup weights on day 21 of lactation; 
decreases in litter size and F2 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 10-9 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. However since 1992, an S,S-
isomer enriched formulation, Asana (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 is four times lower than that 
for Pydrin. 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. Bridging residue studies have shown 
Asana 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:
    [email protected].


    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