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fenoxaprop-ethyl (Acclaim, Horizon) Pesticide Tolerance 4/98


[Federal Register: April 22, 1998 (Volume 63, Number 77)]
[Rules and Regulations]               
[Page 19829-19837]
>From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr22ap98-8]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-300635; FRL-5782-1]
RIN 2070-AB78

 
Fenoxaprop-ethyl; Pesticide Tolerance

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes tolerances for combined residues 
of fenoxaprop-ethyl [ethyl 2-[4-[(6-chloro-2-benzoxazolyl) oxy]phenoxy] 
propanoate] and its metabolites [2-[4-] (6-chloro-2-
benzoxazolyl)oxy]phenoxy] propanoic acid and 6-chloro-2,3- 
dihydrobenzoxazol-2-one in or on the following raw agricultural 
commodities (RACs): barley, grain at 0.05 parts per million (ppm), and 
barley straw at 0.1 ppm. AgrEvo USA Company requested these tolerances 
under the Federal Food, Drug and Cosmetic Act (FFDCA), as amended by 
the Food Quality Protection Act of 1996 (Pub. L. 104-170).

DATES: This regulation is effective April 22, 1998. Objections and 
requests for hearings must be received by EPA on or before June 22, 
1998.

ADDRESSES: Written objections and hearing requests, identified by the 
docket control number, [OPP-300635], 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-300635], 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-
300635]. 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: Joanne I. Miller, Product 
Manager (PM) 23, 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: 
Crystal Mall #2, 1921 Jefferson Davis Hwy., Arlington, VA, (703) 305-
6224, e-mail: miller.joanne@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: In the Federal Register of September 17, 
1997 (62 FR 48837) (FRL-5741-1), EPA, issued a notice pursuant to 
section 408 of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 
U.S.C. 346a(e) announcing the filing of a pesticide petition (PP) for 
tolerance by AgrEvo USA Company, Little Falls One, 2711 Centerville 
Road, Wilmington, DE 19808. This notice included a summary of the 
petition prepared by AgrEvo USA Company, the registrant. There were no

[[Page 19830]]

comments received in response to the notice of filing.
    The petition requested that 40 CFR 180.430 (b) be amended by 
establishing tolerances for combined residues of the herbicide 
fenoxaprop-ethyl [ethyl 2-[4-[(6-chloro-2-
benzoxazolyl)oxy]phenoxy]propanoate] and its metabolites [2-[4-](6-
chloro-2-benzoxazolyl)oxy]phenoxy]propanoic acid and 6-chloro-2,3-
dihydrobenzoxazol-2-one, in or on the following raw agricultural 
commodities: barley, grain at 0.05 ppm; and barley straw at 0.1 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 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

[[Page 19831]]

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 
fenoxaprop-ethyl and to make a determination on aggregate exposure, 
consistent with section 408(b)(2), for tolerances for combined residues 
of fenoxaprop-ethyl [ethyl 2-[4-[(6-chloro-2-
benzoxazolyl)oxy]phenoxy]propanoate] and its metabolites [2-[4-](6-
chloro-2-benzoxazolyl)oxy]phenoxy]propanoic acid and 6-chloro-2,3-
dihydrobenzoxazol-2-one in or on the following raw agricultural 
commodities: barley, grain at 0.05 ppm; and barley straw at 0.1 ppm. 
EPA's assessment of the dietary exposures and risks associated with 
establishing these 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 fenoxaprop-ethyl 
are discussed below.
    1. Acute toxicity. A battery of acute toxicity studies is 
available, places technical fenoxaprop-ethyl in Toxicity Category III 
for acute oral (rat) ( LD<INF>50 </INF>= 2,357 milligram/kilograms (mg/
kg) (M) and 2,500 mg/kg (F) ), and acute inhalation (rat) 
LC<INF>50</INF> = >0.511 mg/L; in Toxicity Category IV for acute dermal 
(rat) = >2,000 mg/kg and rabbit =>1,000 mg/kg and skin irritation 
(slight irritant) ; and in Toxicity Category I for eye irritation 
(rabbit) with non-reversible corneal opacity at day 21. Fenoxaprop-
ethyl was determined to be a non-sensitizer in a dermal sensitization 
study (guinea pig).
    2. Genotoxicity . A battery of genotoxicity studies, none of which 
indicated any genotoxic potential. The studies submitted included: in 
vitro human lymphocyte chromosomal aberration, mouse micronucleus, in 
vitro unscheduled DNA synthesis, Ames Salmonella bacterial point 
mutation and yeast DNA repair assays.
    3. In a subchronic feeding study with rats (30/sex/dose), 
fenoxaprop-ethyl was administered at doses of 0, 1, 4 or 16 mg/kg/day 
for 90 days. The NOEL was 1 mg/kg/day and the lowest observed effect 
level (LOEL) was 4 mg/kg/day) based on relative organ weight changes. 
After the 4-week recovery period, significantly decreased liver weights 
were observed in males at the 1 mg/kg/day dose and in females at 4 mg/
kg/day.
    4. In a subchronic feeding study in dogs (6 dogs/sex/dose), 
fenoxaprop-ethyl was administered at doses of 0, 0.4, 2, or 10 mg/kg /
day were fed for 90 days. The NOEL was 0.4 mg/kg/day) and the LOEL was 
2 mg/kg/day based on histological changes of the kidneys. Inflammatory 
changes of the kidneys (interstitial pyelonephritis) were detected in 
the 2 mg/kg/day and in the 10 mg/kg/day dosed dogs.
    5. In a 21-day dermal toxicity study, Wistar rats (10/sex/dose) 
received repeated dermal applications of fenoxaprop-ethyl (96.5%, 
moistened with sesame oil) at doses of 0, 5, 10, or 20 mg/kg, 6 hours/
day, 5 days/week, for 21 total exposures. The LOEL was >5 mg/kg based 
on decreased liver weights. A NOEL was not established.
    6. In a second 21-day dermal toxicity study, Wistar rats (10/sex/
dose) received repeated dermal applications of fenoxaprop-ethyl (96.5%, 
vehicle not specified) at doses of 0, 5, or 20 mg/kg, 6 hours/day, 5 
days/week, for 21 total exposures. The study author concluded that the 
NOEL was >20 mg/kg; a LOEL was not established.
    7. In a subchronic inhalation toxicity study, Wistar rats (10-15/
sex/concentration) were exposed by nose-only inhalation to fenoxaprop-
ethyl (96.5%) at target concentrations of 0, 0.075, 0.250, or 0.750 mg/
L (analytically -determined concentrations of 0, 0.073, 0.248, or 0.727 
mg/L, respectively) for 6 hours/day, 5 days/week, for 6 weeks (28-29 
total exposures). An unequivocal NOEL was not established in this 
study. A second study using the same protocol with target 
concentrations of 0 or 0.015 mg/L (analytically determined to be 0 or 
0.0143 mg/L, respectively) was conducted. The exposure period was 
followed by a 4-week recovery period for animals in all but the 0.750 
mg/L group. A NOEL for the repeated dose inhalation was 0.015 mg/L.
    8. In a chronic toxicity study in beagle dogs (6/sex/dose) dogs 
were fed fenoxaprop-ethyl (94%) at doses of 0, 0.075, 0.375 or 1.875 
mg/kg/day for two years. The NOEL was 0.375 mg/kg/day and the LOEL was 
1.875 mg/kg/day based on decreases in body weight gain.
    9. In a carcinogenicity study with groups of 50 male and 50 female 
NMRKF (SPF71) mice, fenoxaprop-ethyl (94%) was administered at dose 
levels of 0, 0.375, 1.5, or 6 mg/kg/day for 24 months. The NOEL was >6 
mg/kg/day (HDT). A LOEL was not established.

[[Page 19832]]

    10. In a second carcinogenicity study, fenoxaprop-ethyl (96.8%) was 
administered to groups of 50 male and 50 female NMRI mice at doses of 
0, 5.7, 16.6 or 44.6 mg/kg/day in males and 0, 6.8, 19.4 or 53.7 mg/kg/
day in females for 24 months. For chronic toxicity the NOEL was 5.7 mg/
kg/day and the LOEL was 16.6 mg/kg/day based on histopathological 
findings in the liver. There was evidence of carcinogenicity at the 
highest dose tested (HDT). Statistically (p=0.05) significant increases 
were seen in liver and adrenal gland tumors. In males at the high dose, 
the incidence of hepatocellular adenomas (30%) and carcinomas (8%) were 
increased when compared to controls (2%, adenomas and 0%, carcinomas). 
Also at this dose in males, the incidence of subcapsular adenomas of 
the adrenal glands was 43% compared to 22% in controls. In addition, 
microscopic pathology indicated the hepatocellular hypertrophy was 
observed in the majority of all treated animals (both sexes). Dosing 
was considered adequate to assess the carcinogenic potential of 
fenoxaprop-ethyl based on clinical signs, increased liver weight, and 
histopathology.
    11. In a combined chronic/oncogenicity study, Wistar rats (116/sex/
dose) were dosed with fenoxaprop-ethyl (95.8%) at 0. 0.25, 1.5 or 9 mg/
kg/day for 28 months. For chronic toxicity, the NOEL was 1.5 mg/kg/day) 
and the LOEL was 9 mg/kg//day based on decreased serum lipids and 
cholesterol in the males. Under the conditions of this study, there was 
no evidence of carcinogenic potential.
    12. In an oral developmental toxicity study, pregnant Wistar rats 
(20/dose) received fenoxaprop-ethyl (93% a.i.) in sesame oil at doses 
of 0, 10, 32, or 100 mg/kg/day from days 7 through 16 of gestation. For 
maternal toxicity, the NOEL was 32 mg/kg/day and the LOEL was 100 mg/
kg/day, based on slight initial reduction in body weight and food 
consumption. There were no treatment-related effects or clinical signs, 
body weight gain, food consumption, or development of the conceptuses 
in the uterus at dose levels of less than 32 mg/kg/day. Developmental 
toxicity was demonstrated at 100 mg/kg/day as slightly impaired growth 
of the fetuses (reduced body weights and placental weights and reduced 
skeletal ossification). For developmental toxicity, the NOEL was 32 mg/
kg/day and the LOEL was 100 mg/kg/day, based on reduced fetal body 
weights, reduced placental weights, retarded skeletal ossification of 
the cranium, sternebrae and 5th metacarpals.
    13. In a second oral developmental toxicity study, pregnant 
Cr1:COBS CD (SD) BR rats were dosed with fenoxaprop-ethyl (96.2%) in 
corn oil at doses of 0, 10, 32, or 100 mg/kg/day from days 6 through 15 
of gestation. For maternal toxicity, the NOEL was 32 mg/kg/day and the 
LOEL was 100 mg/kg/day, based on decreased body weight gain and 
increased liver weights. For developmental toxicity, the NOEL was 32 
mg/kg/day and the LOEL was 100 mg/kg/day base on increase 
malformations, significant fetal weight reduction and increase total 
visceral and skeletal anomalies.
    14. In an oral developmental toxicity study with groups of 
Himalayan [(Hoe:HIMK(SPFWiga)] rabbits were dosed at doses of 
fenoxaprop-ethyl (93%) in sesame oil at 0, 0.5, 12.5, 50.0 or 200 mg/
kg/day from days 7 through 19 of gestation. For maternal toxicity, the 
NOEL was 12.5 mg/kg/day and the LOEL was 50.0 mg/kg/day, based on 
decreased food consumption and body weight gain. For developmental 
toxicity, the NOEL was 50 mg/kg/day and the LOEL was 200 mg/kg/day 
based on reduced fetal weights, placental weights, crown-rump lengths, 
and fetal survival, and increased litter and fetal incidence of rib 
anomalies and diaphragmatic hernias. No developmental toxicity was 
observed at doses of less than 50.0 mg/kg/day.
    15. In a dermal developmental toxicity study, pregnant KFM-Han 
Wistar rats (25/dose) received repeated dermal applications of 
fenoxaprop-ethyl (96.5%) in sesame oil at doses of 0, 100, 300, or 
1,000 mg/kg/day for 6 hours/day on days 6-15 of gestation. For maternal 
toxicity, the NOEL was >1,000 mg/kg/day (HDT); a LOEL was not observed. 
For developmental toxicity, the NOEL was 1,000 mg/kg/day; a LOEL was 
not observed. There were no treatment-related malformations or 
variations noted upon external, visceral, and skeletal examination of 
the fetuses.
    16. In a dermal developmental toxicity study, fenoxaprop-ethyl 
(96.5%) in sesame oil was administered dermally to 16 Chinchilla 
rabbits (SPF quality) at dose levels of 0,100, 300, or 1,000 mg/kg/day 
for 6 hours/day on days 6-18 of gestation. For maternal toxicity, the 
NOEL was 1,000 mg/kg/day (HDT); a LOEL was not observed. There was no 
developmental toxicity demonstrated at any dose level. For 
developmental toxicity, the NOEL was 1,000 mg/kg/day; a LOEL was not 
observed.
    17. In a 2-generation reproductive toxicity study, fenoxaprop-ethyl 
(97.2%) was administered to 30 WISTAR/HAN rats/sex/dose in their diet 
at doses of 0, 0.25, 1.5, or 9.0 mg/kg/day. Exposure to animals began 
at 7 weeks of age and lasted for 80 days prior to mating to produce F1a 
and F1b pups. At 21 days of age, F1b pups were selected to become the 
parents of the F2a and F2b litters. There were no treatment-related 
effects on mortality, clinical signs of toxicity, body weight, food 
consumption or reproductive parameters at any does level. For parental/
systemic toxicity, the NOEL was 0.25 mg/kg/day) and the LOEL was 1.5 
mg/kg/day based on decreased blood lipids. The NOEL for systemic 
toxicity was 0.25 mg/kg/day. For reproductive toxicity, the NOEL was 
0.25 mg/kg/day and the LOEL was 1.5 mg/kg/day based on reduced pup body 
weights (F1a).
    18. No developmental neurotoxicity data are required for 
fenoxaprop-ethyl. No effects on histopathology of the brain were 
observed in any of the studies in which these parameters were measured. 
There no evidence of developmental anomalies of the fetal nervous 
system in the prenatal developmental toxicity studies with rats or 
rabbits or in the 2-generation reproduction study in rats.
    19. Studies on metabolism: In a rat metabolism study fenoxaprop-
ethyl(U-14C-chlorophenyl; 98% radiochemical purity) was administered to 
male and female Wistar HOE: Wiskf (SPF 71) strain of rats (10-15 
animals/dose/sex) by gavage as a single dose at levels of 2 or 10 mg/
kg, or at a single dose at 2 mg/kg following a 4-day pretreatment with 
unlabeled fenoxaprop-ethyl at 2 mg/kg/day. Within 6 hours of dosing 83-
109% of the administered radioactivity was recovered in the urine and 
feces, with a majority of the dose (51-65%) being recovered within 24 
hours of dosing. Within 24 hours of dosing, urinary excretion accounted 
for 39-48% of the dose for females and 22-311% of the dose for males. 
The primary metabolite in urine of both sexes in each dose group was 6-
chlorobenzoxazole-2-mercapturic acid, accounting for 22-50% of the 
total radioactivity in the urine (15-26% of the dose) The urine of 
female rats dosed either once at 10 mg/kg or repeatedly at 2 mg/kg also 
contained high levels (23-28% of dose) of 2-(4-(6-chloro-2-
benzoxazolyloxy)-phenoxy)-propionic acid (the free acid of fenoxaprop-
ethyl). At the 10 mg/kg dose, unchanged parent accounted for 24% of the 
fecal radioactivity (15% of dose) for male rats and 6% for female rats 
(1.7% of dose).
    In a second rat metabolism study, fenoxaprop-ethyl (1-14C-
dioxyphenyl; 96% radiochemical purity) was administered by gavage as a 
single dose

[[Page 19833]]

to male and female SPF Wistar strain rats (10 animals /sex) at 10 mg/kg 
body weight and to 15 females at 2 mg/kg body weight. Within 96 hours 
of dosing, 101.3% and 87.4% of the 10 gm/kg dose was recovered from 
male and female rats, respectively, and 108.8% of the 2 mg/kg dose was 
recovered from female rats. There were sex- and dose-related 
differences in excretion. In the 0- to 24-hour urine of male rats dosed 
at 10 mg/kg, 99% of the radioactivity was identified as 2-(4-
hydroxyphenoxy)-propionic acid (HPP-acid), accounting for 47.5% of the 
administered dose. In female rats dosed at 10 mg/kg, the primary 
urinary metabolites were identified as HPP acid (27.5% of dose) and 2-
(4-6-chloro-2-benzoxazolyloxy)-phenoxy)-propionic acid (the free acid 
of fenoxaprop-ethyl; 27% of dose). In feces of the 10 mg/kg dose 
groups, fenoxaprop-ethyl and its free acid accounted for 20.1 and 16.6% 
of the dose for males and 9.0 and 11.3% of the dose for females.

B. Toxicological Endpoints

    1. Acute toxicity. EPA has selected for acute dietary risk 
assessment the NOEL of 32 mg/kg/day from the rat developmental toxicity 
study. The effects were increased incidence of fetuses with 
malformations (including skeletal defects, eye defects, absent 
innominate artery, diaphragmatic hernia and umbilical hernia at 100 mg/
kg/day (LOEL). Population subgroup of concern is females 13+ years old.
    An acute dietary risk assessment for the general population, 
including infants and children, (excluding the subgroup, females 13+ 
years old) is not required because no treatment-related effects 
attributable to a single exposure (dose) were seen in oral studies 
conducted with fenoxaprop-ethyl. A MOE of 100 is adequate to ensure 
protection for females 13+ years old.
     2. Short - and intermediate - term toxicity. No dermal or systemic 
toxicity was seen in a dermal developmental toxicity study in rats and 
rabbits following repeated dermal applications of fenoxaprop-ethyl at 
1,000 mg/kg/day (Limit-Dose). Also, no dermal or systemic toxicity was 
seen at the HDT (20 mg/kg/day) in a 21-day dermal toxicity study in 
rats.
    3. Intermediate-term inhalation toxicity. A 6-week rat inhalation 
toxicity study demonstrated a NOEL = 0.015 mg/L based on decreases in 
total lipids, increased triglycerides, increased alkaline phosphatase, 
increased liver and kidney weights, and liver hypertrophy at 0.075 mg/L 
(LOEL).

C. Cancer Dietary/Inhalation

    1. Chronic toxicity. EPA has established the RfD for fenoxaprop-
ethyl at 0.0025 milligrams/kilogram/day (mg/kg/day). This RfD is based 
on reduced pup weights observed in a 2-generation rat reproductive 
toxicity study with a NOEL of 0.25 mg/kg/day. An uncertainity factor of 
100 was used in calculating the RfD to account for both inter- and 
intra-species variations.
    2. Carcinogenicity. Characterization of the carcinogenicity of 
fenoxaprop-ethyl has been referred to EPA Health Effects Division's 
Cancer Peer Review Committee. For the interim, a worst case and 
protective risk assessment was carried out by use of a linear low dose 
extrapolation method (Q1*) based on the increases in adrenal tumors in 
male mice. The Q1* for the adrenal tumors is 9.1 x 10<SUP>-2</SUP>.

D. Exposures and Risks

    1. From food and feed uses. Tolerances have been established (40 
CFR 180.430 (a)) for the combined residues of fenoxaprop-ethyl [ethyl 
2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoate] and its 
metabolites [2-[4-](6-chloro-2-benzoxazolyl)oxy]phenoxy]propanoic acid, 
and 6-chloro-2,3-dihydrobenzoxazol-2-one in or on a variety of raw 
agricultural commodities. Risk assessments were conducted by EPA to 
assess dietary exposures and risks from fenoxaprop-ethyl 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 1 day or single exposure. The NOEL for the acute dietary exposure 
was 32 mg/kg/day from a rat study. The Agency has determined that the 
uncertainty factor of 10 to account for enhanced sensitivity of infants 
and children should be removed for fenoxaprop-ethyl, and that the MOE 
of 100 to account for inter (10) and intra (10) species variation is 
adequate to insure protection for this population from exposure to 
fenoxaprop-ethyl, because in the rat developmental toxicity study, the 
fetal effects (malformations) were seen at maternally toxic doses 
(i.e., the LOEL was the same for both adults and fetuses).
    From the acute dietary (food only) risk assessment a high-end 
exposure estimate of 0.001 mg/kg/day was calculated. This exposure 
yields a dietary (food only) MOE of 32,000 for females 13+ years, the 
population subgroup of concern. This risk estimate was highly 
conservative because it assume that 100% of barley and all other 
commodities having tolerances for residues of fenoxaprop-ethyl will 
contain residues at tolerance levels. Therefore, this is an 
overestimation of human dietary exposure. Use of anticipated residue 
values and percent crop-treated data will result in a lower acute 
dietary exposure estimate if estimated by probabilistic techniques.
    ii. Chronic exposure and risk. The anticipated residues for 
existing fenoxaprop-ethyl uses (including the use on barley) result in 
Anticipated Residue Contribution that varies between 0.000009 and 
0.000023 mg/kg/day for the population subgroups ( the U.S. Population, 
Nursing Infants (<1 year old), Non-Nursing Infants (> year old), 
Children (1-6 years old) , Children (7-12 years old) and Non-Hispanic 
Others); and occupied between 0.4% and 0.9% of the RfD.
    Section 408(b)(2)(E) authorizes EPA to use 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 five 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) states that the Agency may 
use data on the actual percent of crop treated for assessing chronic 
dietary risk only if the Agency can make the following findings: (1) 
that the data used are reliable and provide a valid a 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 fenoxaprop-ethyl were 
derived from federal and market survey data. EPA considers these data 
reliable. A range of estimates are supplied by this data and the upper 
end of this range was used for the exposure assessment. By using this 
upper end 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

[[Page 19834]]

computer-based model for evaluating the exposure of significant 
subpopulations including several regional groups. Review of this 
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 provide for the periodic evaluation of 
these estimates of percent crop treated as required by the section 
408(b)(2)(F), EPA may require fenoxaprop-ethyl registrants to submit 
data on percent crop treated. As required by section 408(b)(2)(E), EPA 
will issue a data call-in for information relating to anticipated 
residues to be submitted no later than five years from the date of 
issuance of this tolerance.
    In the absence of an Agency Cancer Assessment Review, the Health 
Effects Division of the Office of Pesticide Programs recommended a 
worst case and protective risk assessment using a linear low dose 
extrapolation method (Q1*) based on the increases in adrenal tumors in 
mice. The Q1* for the adrenal tumors was determined to be 9.1 x 
10<SUP>-2</SUP>. Based on the US population chronic dietary exposure of 
0.00001 mg/kg/day, this results in a cancer risk estimate of 9.1 x 
10<SUP>-7</SUP>.
    2. From drinking water. Based on the acute and chronic dietary 
(food) exposure and using default body weights and water consumption 
figures, acute and chronic drinking water levels of concern (DWLOC) for 
drinking water were calculated. To calculate the DWLOC, the acute or 
chronic dietary food exposure (from the DRES analysis) was subtracted 
from the acute toxicity NOEL or RfD, as appropriate. DWLOCs were then 
calculated using the default bodyweights and drinking water consumption 
figures.
    For acute drinking water exposure for both adults and children, the 
level of concern was 960 ppm. For chronic and cancer exposure in 
drinking water the levels of concern were 80 ppb and 110 ppt, 
respectively. For adults, the estimate was based on a body weight of 70 
kg and consumption of 2 liters of water per day; for children, a body 
weight of 10 kg and a consumption of 1 liter of water per day. Agency 
estimates for contamination of drinking water from the registered uses 
of fenoxaprop-ethyl is less than 1 ppb for acute exposure and less than 
100 ppt for chronic exposure. These levels are not greater than levels 
of EPA concern.
    3. From non-dietary exposure. Fenoxaprop-ethyl is currently 
registered for use on turfgrass including sod farms, commercial and 
residential turf and ornamentals. Applications to residential turf are 
done by professional applicators. There are no homeowner uses. There is 
a potential dermal exposure to infants to fenoxaprop-ethyl from the 
registered uses for lawn and turfgrass weed control but no dermal 
toxicity has been shown in animal studies. Potentially, infants and 
children may have some inhalation exposure due to residual residues of 
the pesticide on lawns but such exposure would be very low. Currently 
there are no inhalation exposure data required for post-application of 
pesticides to lawns and turf uses. As inhalation exposure for mixer/
loaders is acceptable, the risk to children and infants from inhalation 
exposure under a much lower exposure scenario is characterized 
qualitatively as being extremely low. Exposure data are required for 
hand to mouth movements of infants and children; however, no acute 
dietary toxicity endpoints have been identified for fenoxaprop-ethyl 
for infants and children. There is an acute dietary toxicity endpoint; 
however, the only population subgroup of concern is females 13+ for 
developmental effects. The risk to this subgroup will be addressed 
later in this document under ``Aggregate Risk and Determination of 
Safety for Infants and Children.'' No acute dietary toxicity endpoints 
have been identified for the general populations.
    4. 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 fenoxaprop-ethyl 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, 
fenoxaprop-ethyl 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 fenoxaprop-ethyl has a common 
mechanism of toxicity with other substances.

E. Aggregate Risks and Determination of Safety for U.S. Population

    1. Acute risk. From the acute dietary (food use) risk assessment a 
high-end exposure estimate of 0.001 mg/kg/day was determined for 
females 13+ years, the population subgroup of concern for acute 
toxicity. This exposure yields a dietary MOE of 32,000. The potential 
contribution to acute exposure from residues in drinking water is 
minimal (1,000-fold less than EPA's level of concern) and would not 
result in an aggregate acute exposure that exceeds EPA's level of 
concern. EPA concludes there is a reasonable certainty that no acute 
harm will result from aggregate exposure to fenoxapro-ethyl residues.
    2. Chronic risk. Using the ARC exposure assumptions described 
above, EPA has concluded that aggregate exposure to fenoxaprop-ethyl 
from food

[[Page 19835]]

will utilize less than 0.4% of the RfD for the U.S. population. The 
major identifiable subgroup with the highest aggregate exposure is non-
nursing infants less than one year old. 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 fenoxaprop-ethyl in drinking water and from 
non-dietary, non-occupational exposure, EPA does not expect the 
aggregate exposure to exceed 100% of the RfD. EPA concludes that there 
is a reasonable certainty that no harm will result from aggregate 
exposure to fenoxaprop-ethyl residues.
    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.
    Fenoxaprop-ethyl is currently registered for use on turfgrass 
including sod production, commercial and residential turf and landscape 
ornamentals. No short- or intermediate-term dermal toxicity endpoints 
have been identified for fenoxaprop-ethyl. An inhalation endpoint has 
been identified, however, as the uses are outdoors, exposure from 
inhalation route should be considerable less than that determined for 
worker mixer/loaders, who have an MOE of 2,800. Additionally, based on 
the low level of chronic dietary exposure, the Agency concludes that 
aggregate short- and intermediate-term exposure is at a level below 
EPA's level of concern.

F. Aggregate Cancer Risk for U.S. Population

    Based on a upper bound potency factor (Q1*) of 9.1 x 
10<SUP>-2</SUP> (mg/kg/day)<SUP>-1</SUP>, the lifetime cancer risk from 
residues of fenoxaprop-ethyl in food commodities is 9.1 x 
10<SUP>-7</SUP>. Taking into accoutn the exposure from residues in 
food, EPA has caluculated a drinking water level of concern which would 
not result in a greater negligible total cancer risk from chronic 
exposure to fenoxaprop-ethyl residues in food and water. The Agency's 
GENEEC screening model was then used to estimate maximum residues in 
surface water. This model estimates potential residues in surface water 
for use in ecological risk assessment. As such, it provides high-end 
values on the concentrations of pesticides that might be found in 
ecologically sensitive environments. The residue levels obtained for 
fenoxaprop-ethyl plus its acid metabolite in water using GENEEC do not 
exceed the drinking water level of concern. Therefore, EPA doen not 
expect there to be a greater than negligible cancer risk from chronic 
exposures to fenoxaprop-ethyl in drinking water and food.

G. Aggregate Risks and Determination of Safety for Infants and Children

    1. Safety factor for infants and children-- a. In general. In 
assessing the potential for additional sensitivity of infants and 
children to residues of fenoxaprop-ethyl, EPA considered data from 
developmental toxicity studies in the rat and rabbit and a two-
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 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.
    b. Developmental toxicity studies. In a oral developmental toxicity 
study with Wistar rats, the maternal NOEL was 32 mg/kg/day, based on 
reduction in body weight and food consumption. The developmental NOEL 
was 32 mg/kg/day, based on reduced fetal body weights, reduced 
placental weights and retarded skeletal ossification of the cranium, 
sternebrae and 5th metacarpals.
    In a second oral developmental toxicity study with Crl:COBS CD (SD) 
BR rats, the maternal NOEL was 32 mg/kg/day, based on decreased body 
weight gain and increased liver weights. The developmental NOEL was 32 
mg/kg/day, based on increase malformations, significant fetal weight 
reduction and increase total visceral and skeletal anomalies.
    In a oral developmental toxicity study with Himalayan rabbits, the 
maternal NOEL was 12.5 mg/kg/day, based on decreased food consumption 
and body weight gain. The developmental NOEL was 50mg/kg/day, based on 
reduced fetal weights, placental weights, crown-rump lengths, fetal 
survival and increased litter and fetal incidence of rib anomalies and 
diaphragmatic hernias.
    c. Reproductive toxicity study. In a rat reproduction study, the 
parental (systemic) NOEL was 0.25 mg/kg/day, based on decreased blood 
lipids. The reproductive (pup) NOEL was 0.25 mg/kg/day, based on 
reduced pup body weights.
    d. Pre- and post-natal sensitivity. The toxicological data base is 
complete and adequate to determine pre- and post-natal toxicity. The 
prenatal developmental toxicity data demonstrated no indication of 
increased sensitivity of rats or rabbits to in utero exposure or 
repeated dermal applications of fenoxaprop-ethyl. The rat reproduction 
study did not identify any increased sensitivity of rats to in utero or 
postnatal exposure. Maternal and parental NOELs were equivalent to 
developmental or offspring NOELs.
    e. Conclusion. Based on the above data, EPA determined that the 
standard safety factor would be adequate to protect the safety of 
infants and children thus the additional children's safety factor was 
removed.
    2. Acute risk. The acute dietary (food only) MOE for females 13+ 
years old (accounts for both maternal and fetal exposure) was 
determined to be 32,000. This MOE was based on the developmental NOEL 
in rats of 32 mg/kg/day. This risk assessment assumed 100% crop-treated 
and tolerance level residues on all treated crops consumed, resulting 
in a significant over-estimate of dietary exposure. Despite the 
potential for exposure to fenoxaprop-ethyl in drinking water, EPA does 
not expect the acute aggregate exposure to exceed level of concern. The 
large acute dietary MOE determined for females 13+ years old provides 
assurance that there is a reasonable certainty of no harm from both 
females 13+ years and the pre-natal development of infants.
    3. Chronic risk. Using the exposure assumptions described in this 
rule, the percentage of the RfD that will be utilized by chronic 
dietary (food only) exposure to residues of fenoxaprop-ethyl ranges 
from 0.4% for nursing infants less than one year old, up to 0.9% for 
non-nursing infants less than

[[Page 19836]]

one year old. Despite the potential for exposure to fenoxaprop-ethyl in 
drinking water, EPA does not expect the chronic aggregate exposure to 
exceed 100% of the RfD. Based on the nature of the residential uses, no 
chronic residential exposure is anticipate. EPA concludes that there is 
a reasonable certainty that no harm will result to infants and children 
from chronic aggregate exposure to fenoxaprop-ethyl regulable residues.

III. Other Considerations

A. Metabolism In Plants and Animals

    The metabolism of fenoxaprop-ethyl in plants and animals is 
adequately understood for purposes of these tolerances.

B. Analytical Enforcement Methodology

    An adequate analytical method for determining the magnitude of 
residues in the raw agricultural commodities listed in this Final Rule 
has been evaluated by EPA and is published in the Pesticide Analytical 
Manual (PAM II). The method may be requested from: Calvin Furlow, 
Public Information Branch, Field Operations Division (7502C), Office of 
Pesticide Programs, Environmental Protection Agency, 401 M St., SW., 
Washington, DC 20460. Office location and telephone number: Rm. 1130A, 
CM #2, 1921 Jefferson Davis Hwy., Arlington, VA, (703-305-5937).

C. Magnitude of Residues

    The nature of the residue in plants is adequately understood for 
the purposes of these tolerances.

D. International Residue Limits

    No CODEX Maximum Residue Levels (MRLs) have been established for 
fenoxaprop-ethyl. Canadian MRLs for combined residues of fenoxaprop-
ethyl, its free acid metabolite [2-[4-[(6-chloro-2-
benzoxazolyl)oxy]propanoic acid] and 6-chloro-2,3-dihydrobenzoxazol-2-
one have been established at 0.02 ppm for milk. This tolerance 
expression and level for milk is in harmony with subject tolerances of 
the final rule.

IV. Conclusion

    Therefore, the tolerances are established for combined residues of 
fenoxaprop-ethyl [ethyl 2-[4-[(6-chloro-2-benzoxazolyl) oxy]phenoxy] 
propanoate] and its metabolites [2-[4-] (6-chloro-2-
benzoxazolyl)oxy]phenoxy] propanoic acid and 6-chloro-2,3-
dihydrobenzoxazol-2-one, in or on the following raw agricultural 
commodities: barley, grain at 0.05 ppm; and barley straw at 0.1 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 June 22, 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 Docket

    EPA has established a record for this rulemaking under docket 
control number [OPP-300635] (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

    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

[[Page 19837]]

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 1985, April 23, 1997).
    In addition, since these 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 this 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: April 8, 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. 180.430, in paragraph (a) by alphabetically adding the 
following commodities to the table to read as follows:


Sec. 180.430  Fenoxaprop-ethyl; tolerances for residues.

    (a) * * *

                                                                        
------------------------------------------------------------------------
                                                              Parts per 
                         Commodity                             million  
------------------------------------------------------------------------
Barley, grain..............................................         0.05
Barley, straw..............................................          0.1
                                                                        
          *         *         *             *         *                 
------------------------------------------------------------------------

* * * * *

[FR Doc. 98-10395 Filed 4-21-98; 8:45 am]
BILLING CODE 6560-50-F