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cymoxanil Pesticide Tolerance 1/99

  


[Federal Register: February 10, 1999 (Volume 64, Number 27)]
[Rules and Regulations]               
[Page 6532-6539]
>From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr10fe99-16]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-300782; FRL-6056-4]
RIN 2070-AB78

 
Cymoxanil; Pesticide Tolerance

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes tolerances for residues of the 
fungicide, cymoxanil, [2-cyano-N-[(ethylamino)carbonyl]-2-
(methoxyimino) acetamide], in or on imported tomatoes and grapes. E. I. 
DuPont De Nemours and Co., Inc. requested this tolerance under the 
Federal Food, Drug, and Cosmetic Act, as amended by the Food Quality 
Protection Act of 1996.

DATES: This regulation is effective February 10, 1999. Objections and 
requests for hearings must be received by EPA on or before April 12, 
1999.

ADDRESSES: Written objections and hearing requests, identified by the 
docket control number, [OPP-300782], 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-300782], 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, Crystal 
Mall #2, 1921 Jefferson Davis Hwy., Arlington, VA.
    A copy of objections and hearing requests filed with the Hearing 
Clerk may be submitted electronically by sending electronic mail (e-
mail) to: opp-docket@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 file 
format or ASCII file format. All copies of objections and hearing 
requests in electronic form must be identified by the docket control 
number [OPP-300782]. 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: Mary Waller, Product Manager 
(PM) 21, 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: Rm. 247, Crystal 
Mall #2, 1921 Jefferson Davis Hwy., Arlington, VA, (703)-308-9354, 
waller.mary@epa.gov.

SUPPLEMENTARY INFORMATION: In the Federal Register of November 15, 1995 
(60 FR 57419-57422) (FRL-4971-5), EPA issued a notice pursuant to 
section 408 of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 
U.S.C. 346a as amended by the Food Quality Protection Act of 1996 
(FQPA) (Pub. L. 104-170) announcing the filing of a pesticide petition 
(PP) for tolerance by DuPont, DuPont Agricultural Products, P.O. Box 
80038, Wilmington, DE 19880-0038. This notice included a summary

[[Page 6533]]

of the petition prepared by DuPont, the registrant. There were no 
comments received in response to the notice of filing.
    The petition requested that 40 CFR 180.503 (e) be amended by 
establishing tolerances for residues of the fungicide, cymoxanil, [2-
cyano-N-[(ethylamino)carbonyl]-2-(methoxyimino) acetamide], in or on 
imported tomatoes and grapes at 0.1 part per million (ppm).

I. Background and Statutory Findings

    Section 408(b)(2)(A)(i) of the FFDCA allows EPA to establish a 
tolerance (the legal limit for a pesticide chemical residue in or on a 
food) only if EPA determines that the tolerance is ``safe.'' Section 
408(b)(2)(A)(ii) defines ``safe'' to mean that ``there is a reasonable 
certainty that no harm will result from aggregate exposure to the 
pesticide chemical residue, including all anticipated dietary exposures 
and all other exposures for which there is reliable information.'' This 
includes exposure through drinking water and in residential settings, 
but does not include occupational exposure. Section 408(b)(2)(C) 
requires EPA to give special consideration to exposure of infants and 
children to the pesticide chemical residue in establishing a tolerance 
and to ``ensure that there is a reasonable certainty that no harm will 
result to infants and children from aggregate exposure to the pesticide 
chemical residue....''
    EPA performs a number of analyses to determine the risks from 
aggregate exposure to pesticide residues. For further discussion of the 
regulatory requirements of section 408 and a complete description of 
the risk assessment process, see the final rule on Bifenthrin Pesticide 
Tolerances (62 FR 62961, November 26, 1997) (FRL-5754-7).

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 cymoxanil 
and to make a determination on aggregate exposure, consistent with 
section 408(b)(2), for a tolerance for residues of Cymoxanil on 
imported tomatoes and grapes at 0.1 ppm. EPA's assessment of the 
dietary exposures and risks associated with establishing the tolerance 
follows.

A. Toxicological Profile

    EPA has evaluated the available toxicity data and considered its 
validity, completeness, and reliability as well as the relationship of 
the results of the studies to human risk. EPA has also considered 
available information concerning the variability of the sensitivities 
of major identifiable subgroups of consumers, including infants and 
children. The nature of the toxic effects caused by cymoxanil are 
discussed in this unit.

    1. Acute toxicity. A battery of acute toxicity studies resulted in 
an acute oral LD<INF>50</INF> > 760 milligrams/kilograms (mg/kg) for 
males and LD<INF>50</INF> > 1,200 mg/kg for females; an acute dermal 
LD<INF>50</INF> > 2,000 mg/kg for both sexes; an acute inhalation 
LC<INF>50</INF> > 5.06 mg/L for both sexes; no ocular irritation; 
slight dermal irritation and a finding that the cymoxanil is not a 
dermal sensitizer.
    2. Subchronic toxicity. i. A subchronic oral toxicity/neurotoxicity 
study in rats fed cymoxanil at dose levels of 0, 100, 750, 1,500, or 
3,000 ppm (0, 6.54, 47.6, 102, or 224 mg/kg/day for males, and 0, 8.0, 
59.9, 137, or 333 mg/kg/day for females) for approximately 97 days. A 
group of 10 rats/sex/dose were evaluated for subchronic systemic 
toxicity and a group of 10 rats/sex/dose underwent neurobehavioral 
testing at pre-test, 5, 9, and 13 weeks. The control and high-dose 
groups were assessed for neuropathology. The lowest-observed-adverse-
effect level (LOAEL) for subchronic systemic toxicity is 1,500 ppm 
based on decreases in body weights, body weight gains, and food 
efficiency in the females, and body weight decreases and testicular and 
epididymal changes in the males. The no-observed-adverse-effect level 
(NOAEL) for subchronic systemic toxicity is 750 ppm.
    ii. A subchronic oral toxicity study in mice fed doses of 0, 50, 
500, 1,750, 3,500, or 7,000 ppm (average 0, 8.25, 82.4, 294, 566, or 
1,306 mg/kg/day, for males; 0, 11.3, 121, 433, 846, or 1,130 mg/kg/day, 
for females) for 98 days showed a decrease in body weight gains in 
males dosed at 500, 1,750, and 3,500 ppm. An increase in the absolute 
liver and spleen weights was seen in females fed doses of 1,750 and 
3,500 ppm. The NOAEL was established at 50 ppm for males and 500 ppm 
for females; the LOAEL was 500 ppm for males and 1,750 ppm for females.
    iii. A subchronic oral toxicity study was conducted in dogs fed 
doses of 0, 100 or 200 ppm (0, 3 or 5 mg/kg/day) for 13 weeks, or at 
250 ppm (5 mg/kg/day) for 2 weeks followed by 500 ppm (11 mg/kg/day) 
for 11 weeks. Reduced body weight gain and food consumption were 
observed in the 100 and 200 ppm females, and in both sexes from the 
250/500 ppm groups and final body weights were reduced 32% for males 
(250 ppm group) and 42% for females (500 ppm group), compared to the 
controls. Both sexes in the 200 and 250/500 ppm treatment groups 
exhibited reduced red blood cell parameters, and an increased incidence 
of ketonuria. Red blood cell counts, hemoglobin and hematocrit values 
were lower in both sexes. Decreased calcium, total protein, albumin, 
phosphorus, and chloride concentrations, and A/G ratio were also 
observed in the blood serum of the 250/500 ppm males and females. Males 
in the 250/500 ppm group had lower epididymal and testicular weights, 
and aspermatogenesis was observed. The 250/500 ppm females had lower 
kidney, liver, and thyroid gland weights. No associated microscopic 
lesions or corresponding decreases in relative organ weights were 
observed. One euthanized female from the 250/500 ppm group had dark red 
contents and reddened mucosa throughout the gastrointestinal tract. The 
LOAEL is 3 mg/kg/day (100 ppm) for dogs based on decreased body weights 
and food consumption in females. The NOAEL was not established.
    iv. In a 28-day dermal toxicity study, cymoxanil was applied to the 
shaved backs of rats, for 6 hrs/day at doses of 0, 50, 500, and 1,000 
mg/kg/day. There were no demonstrated effects and no compound-related 
histopathology. The NOAEL for systemic toxicity and dermal irritation 
was 1,000 mg/kg/day, the highest dose tested (HDT).
     3. Chronic toxicity. i. A combined chronic/carcinogenicity study 
was conducted in rats fed cymoxanil at doses of 0, 50, 100, 700, or 
2,000 ppm (0, 1.98, 4.08, 30.3, and 90.1 mg/kg/day for males, and 0, 
2.71, 5.36, 38.4, and 126 mg/kg/day for females) for 23 months. A 
satellite group was included and terminated at 52 weeks. Because of 
poor survival in controls and treated rats, the study was terminated 
after 23 months. Survival was 24-45% and 21-40% in the male and female 
groups, respectively.
    Chronic toxicity observed at 126 mg/kg/day in females, included 
significant decreases in mean body weight and body weight gains, a 
decrease in food efficiency, and increased incidences of non-neoplastic 
lesions in several organ systems including the lungs, intestines, and 
mesenteric lymph nodes. In females receiving 38.4 mg/kg/day, chronic 
toxicity was characterized by increased incidences of non-neoplastic 
lesions of the lungs, liver, sciatic nerve, and eyes (retinal atrophy). 
Chronic toxicity in the males dosed at 30.3 or 90.1 mg/kg/day included 
aggressiveness and/or

[[Page 6534]]

hyperactivity, decreased mean body weight and body weight gain, 
decreased food efficiency, and increased incidence of elongate 
spermatid degeneration and retinal atrophy. No important effects were 
observed in the low- and low-mid-dose groups. No increases in the 
incidences of any neoplasm was observed in dosed animals. The chronic 
LOAEL was 30.3 mg/kg/day for males and 38.4 mg/kg/day for females based 
on histologic changes detected in several organs of the females and 
decreased body weight, body weight gains, and food efficiency observed 
in the males and females. The chronic NOAEL is 4.08 mg/kg/day for males 
and 5.36 mg/kg/day for females. Under the conditions of this study, 
there was no evidence of carcinogenic potential.
    ii. A chronic toxicity study was conducted in dogs fed cymoxanil at 
doses of 0, 25, 50 or 100 ppm for females (0, 0.7, 1.6, or 3.1 mg/kg/
day) and 0, 50, 100, or 200 ppm for males (0, 1.8, 3.0, or 5.7 mg/kg/
day) for 52 weeks. The only effect seen in females in the 100 ppm 
treatment group was weight loss during the first week of the study. No 
effect was observed in females in the 25 or 50 ppm group, or in males 
in the 50 or 100 ppm group. The LOAEL was 200 ppm for males based on 
depressed weight gains through week 12 and changes in hematology and 
blood chemistry. No LOAEL was established for females. The NOAEL was 
100 ppm.
    4. Carcinogenicity. i. A combined chronic/carcinogenicity study, 
conducted in rats (described in the chronic toxicity section in Unit 
II.A.3.i in the preamble of this document) showed no evidence of 
carcinogenic potential.
    ii. A carcinogenicity study was conducted in mice fed cymoxanil at 
doses of 0, 30, 300, 1,500, and 3,000 ppm (0, 4.19, 42.0, 216, and 446 
mg/kg/day for males; 0, 5.83, 58.1, 298, and 582 mg/kg/day for females) 
for approximately 80 weeks. Two additional groups were sacrificed at 
31-32 days for cell proliferation and biochemical evaluation.
    Males and females dosed at 300 ppm and above exhibited alterations 
in organ weights and microscopic pathology. Affected organs were the 
testes and epididymis in males, the gastrointestinal tract in females, 
and the liver in both sexes. Male mice fed 300 ppm exhibited treatment-
related increased frequency of sperm cyst/cystic dilation, tubular 
dilation, and increased lymphoid aggregate. Centrilobular apoptotic 
hepatocytes, pigment-containing macrophages, and granuloma were 
detected in males dosed with 300 ppm. Elevated centrilobular 
hepatocellular hypertrophy and associated significant increases in 
liver weight in males dosed with 300 ppm was considered a pharmacologic 
response to cymoxanil. Hyperplastic gastropathy increased significantly 
in 300 ppm female mice and cystic enteropathy of the small intestine 
showed a significant positive trend. At the 1,500 ppm dose, decreases 
in body weight, body weight gain, and food efficiencies were observed 
in males and females. In addition to the testicular and epididymal 
abnormalities observed at the lower dose, the 1,500 ppm males exhibited 
increased incidence of sperm granuloma and bilateral oligospermia. 
Females at 1,500 ppm exhibited the microscopic liver abnormalities seen 
in males at the lower dose. Cystic enteropathy was observed in males at 
1,500 ppm. At 3,000 ppm, there were significant reductions in body 
weight, body weight gain, food consumption, and food efficiencies in 
males and females. Survival over 18 months was decreased in the 3,000 
ppm females, 57% compared to 69% in controls. Early deaths among high-
dose females were attributed to pancreatic acinar cell necrosis and/or 
stress, evidenced by splenal and thymic atrophy and bone marrow 
congestion. Females dosed with 3,000 ppm exhibited increased frequency 
of pallor, weakness, and hunching over. Male mice dosed with 3,000 ppm 
showed hematological signs of decreased circulating erythrocyte mass at 
the 12-month evaluation. The high dose also resulted in gross and 
microscopic pathology of the liver, gastrointestinal tract, and testes. 
Dosing was considered adequate based on decreased body weight gains and 
an increase in non-neoplastic lesions in both sexes relative to the 
controls at the highest dose level.
    The LOAEL was 300 ppm based on toxicity to the testes and 
epididymides in males and toxicity to the gastrointestinal mucosa in 
females. The NOAEL was 30 ppm. Under the conditions of this study, 
there was no evidence of a carcinogenic effect.
    5. Developmental toxicity. i. A prenatal developmental toxicity 
study was conducted in rats gavaged with cymoxanil on days 7-16 of 
gestation at dose levels of 0, 10, 25, 75, or 150 mg/kg/day. The 
maternal LOAEL was 25 mg/kg/day based upon reduced body weight, body 
weight change, and food consumption. The maternal NOAEL was 10 mg/kg/
day. The developmental LOAEL was 25 mg/kg/day based upon a significant 
increase in overall malformations and a generalized dose-related delay 
in skeletal ossification. Fetal body weights were significantly 
decreased at 75 and 150 mg/kg/day. At 150 mg/kg/day, increased early 
resorptions resulted in reduced litter sizes. The developmental NOAEL 
was 10 mg/kg/day.
    ii. A prenatal developmental toxicity study was conducted in 
rabbits gavaged with cymoxanil on days 6-18 of gestation at dose levels 
of 0, 4, 8, or 16 mg/kg/day. There was no evidence of treatment-related 
maternal or developmental toxicity. A maternal and developmental LOAEL 
was not determined. The maternal and developmental NOAEL was 
<gr-thn-eq> 16 mg/kg/day. When considered along with other prenatal 
developmental toxicity studies in rabbits, this study provides 
acceptable information that assists in determining the overall maternal 
and developmental NOAEL and LOAEL for cymoxanil in a nonrodent species.
    iii. A prenatal developmental toxicity study was conducted in 
rabbits gavaged with cymoxanil on days 6-18 of gestation at dose levels 
of 0, 8, 16, or 32 mg/kg/day. Evaluation of litter data and assessment 
of embryonic and fetal development revealed treatment-related increases 
in the incidence of malformations in all treated groups. The maternal 
LOAEL was 32 mg/kg/day based upon increased incidences of cold ears, 
anorexia, and/or few feces and body weight loss during the first four 
days of treatment; the maternal NOAEL was 16 mg/kg/day. The 
developmental LOAEL was 8 mg/kg/day based upon an increase in skeletal 
malformations of the cervical and thoracic vertebrae and ribs. The 
developmental NOAEL was <ls-thn-eq> 8 mg/kg/day but could not be 
determined. Although the results of this study suggested an additional 
susceptibility of fetal rabbits to in utero exposure with cymoxanil, 
uncertainties regarding the source of the parental rabbits 
substantially reduce the confidence that the observed skeletal 
anomalies are solely related to treatment.
    iv. A prenatal developmental toxicity study was conducted in 
rabbits gavaged with cymoxanil on days 6-18 of gestation at dose levels 
of 0, 1, 4, 8, or 32 mg/kg/day. The females showed significant post-
treatment increases in body weight gain at 8 and 32 mg/kg/day. The 
maternal LOAEL was 8 mg/kg/day based upon a significant dose-related 
rebound in maternal body weight. The maternal NOAEL was 4 mg/kg/day. 
The developmental LOAEL was 8 mg/kg/day based upon an increase in 
skeletal malformations of the cervical and thoracic vertebrae and ribs; 
and, at 32 mg/kg/day, cleft palate was observed. The developmental 
NOAEL was 4 mg/kg/day.

[[Page 6535]]

    6. Reproductive toxicity. i. A 2-generation reproduction study was 
conducted in rats fed cymoxanil at doses of 0, 100, 500, or 1,500 ppm 
(equivalent to 0, 6.5, 32.1, or 97.9 mg/kg/day in males and 0, 7.9, 
40.6, or 130 mg/kg/day in females), over two consecutive generations. 
No effects of treatment were observed at 100 ppm. The parental systemic 
NOAEL was 100 ppm. The parental systemic LOAEL was 500 ppm, based upon 
reduced pre-mating body weight, body weight gain, and food consumption 
for F1 males; and decreased gestation and lactation body weight for F1 
females. The offspring NOAEL was 100 ppm and the offspring LOAEL was 
500 ppm, based upon decreased F1 pup viability on postnatal days 0-4 
and on a significant reduction in F2b pup weight.
    7. Neurotoxicity. i. The neurotoxicity portion of the subchronic/
neurotoxicity study in rats demonstrated no effects on the Functional 
Observation Battery or on motor activity after 5, 9, and 13 weeks at 
dietary doses of cymoxanil of 0, 100, 750, 1,500, or 3,000 ppm (0, 
6.54, 47.6, 102, or 224 mg/kg/day for males, and 0, 8.0, 59.9, 137, or 
333 mg/kg/day for females), for 97 days. There were no treatment-
related gross or microscopic findings detected in the nervous system or 
skeletal muscles. Grip strength and foot splay measurements were 
decreased (non-significantly) in males at 224 mg/kg/day in the 13-week 
subchronic neurotoxicity study in rats, although these findings 
occurred in conjunction with decreased body weight. A LOAEL for 
neurobehavioral and neuropathic effects was not established. The NOAEL 
for neurotoxicity was 3,000 ppm.
    ii. No evidence of developmental anomalies of the fetal nervous 
system were observed in the prenatal developmental toxicity studies in 
either rats, or rabbits at maternally toxic oral doses up to 25 and 32 
mg/kg/day, respectively. In addition, there was no evidence of 
behavioral or neurological effects on the offspring in the 2-generation 
reproduction study in rats.
    iii. There were no major data gaps for the assessment of potential 
neurotoxicological effects due to cymoxanil. However, following a 
weight-of-the evidence review of the database, which suggested that 
neuropathological lesions, changes in brain weight, axon/myelin 
degeneration, and retinal atrophy could result from long-term exposure 
to cymoxanil, the Agency will require a confirmatory developmental 
neurotoxicity study in rats.
    8. Mutagenicity. Mutagenicity studies with cymoxanil included gene 
mutation assays in bacterial and mammalian cells, a mouse micronucleus 
assay and an in vivo/in vitro unscheduled DNA synthesis (UDS) assay in 
rats. These studies did not demonstrate mutagenicity. An in vitro 
unscheduled DNA synthesis assay-primary rat hepatocytes was positive 
from 5-500 <greek-m>g/mL and cytotoxicity was seen at concentrations of 
<gr-thn-eq>500 <greek-m>g/mL. A chromosome aberrations in human 
lymphocytes assay was positive at 100 - 1,500 <greek-m>g/mL, positive 
at 1,250 and 1,500 <greek-m>g/mL -S9 and 850-1,500 <greek-m>g/mL +S9.
    9. Metabolism. A metabolism study was conducted by gavaging rats 
with single doses of radiolabeled cymoxanil at 2.5 or 120 mg/kg, or as 
a single dose (2.5 mg/kg) following a 14-day pretreatment with 
unlabeled cymoxanil (2.5 mg/kg/day). Radiolabeled cymoxanil was readily 
absorbed through the intestinal tract. Maximum plasma concentrations 
were attained within 3-5 hours of dosing, then declined steadily. Dose 
rate and pretreatment did not appear to affect absorption.
    Elimination was not dependent on sex or dosing regimen; occurring 
predominantly in the urine (63.8-74.8%), during the first 24 hours (58-
66%). Fecal excretion accounted for 15.7-23.6% of the dose, and 
radioactivity in the tissues and carcasses accounted for <1% of the 
dose at sacrifice for all three dosing regimens. A pilot study 
indicated that approximately 3% of the dose would be expected to be 
respired as <SUP>14</SUP>CO<INF>2</INF>.
    For each dosing regimen, there was also no difference between male 
and female rats in the distribution of radioactivity in tissues. No 
accumulation of radioactivity was observed over time in any tissues. 
However, in comparison, concentrations of radioactivity were highest in 
liver and kidney and lowest in brain tissue at 96 hours post-dosing 
sacrifice.
    Peak plasma concentrations for the low and high dose groups were 
attained within 3-5 hours of dosing, and both dose groups had similar 
elimination half-lives from plasma, suggesting that the metabolic 
process was not saturated by the high dose. In addition, there was a 
40-fold difference in the area under the curve for plasma from the low 
and high dose groups, approximating the 48-fold difference in the dose 
levels.
    The metabolite profile in urine and feces was similar between sexes 
and among dose groups. In the urine, the majority of the radioactivity 
(36.7-55% of the dose) was free and/or conjugated 
[<SUP>14</SUP>C]glycine, and 2-cyano-2-methoxyiminoacetic acid (IN-
W3595) (6.5-33% of the dose) was also found. Intact [<SUP>14</SUP>C] 
cymoxanil was not detected. In feces, trace levels (<1% dose) of 
[<SUP>14</SUP>C] cymoxanil and IN-W3595 were detected, but the majority 
of radioactivity was the free and conjugated [<SUP>14</SUP>C] glycine 
(8.5-13.1% of the dose). The data indicate that the principal pathway 
for the elimination of cymoxanil from rats is via renal elimination.
    Based on the data, the proposed metabolic pathway involves 
hydrolysis of cymoxanil to IN-W3595, which is then degraded to glycine. 
Subsequently, glycine is incorporated into natural constituents or 
further metabolized.
    10. Other toxicological considerations. The available studies 
indicate that cymoxanil is not mutagenic in bacterial or cultured 
mammalian cells. There is, however, confirmed evidence of clastogenic 
activity and UDS induction in vitro. In contrast, cymoxanil was neither 
clastogenic nor aneurogenic in mouse bone marrow cells and did not 
induce a genotoxic response in rat somatic or germinal cells. 
Accordingly, the negative results from the mouse bone marrow 
micronucleus assay support the lack of carcinogenic effect in the rat 
and mouse long-term feeding study.
    Similarity of clinical signs were observed in the micronucleus and 
in vivo UDS assay, but the confidence in the negative findings of the 
in vivo UDS assay was not high because of a failure to demonstrate that 
test material reached either target tissue. It was concluded that the 
test may have been inadequate because of the short interval between 
dosing and cell harvest. Therefore, the Agency will be requiring that a 
supplemental rat dominant lethal assay be conducted to determine if any 
effects are noted which are associated with genetic damage to male 
germinal cells.

B. Toxicological Endpoints

     1. Acute toxicity. To assess acute dietary exposure in the 
subpopulation of concern (females 13+), the Agency used a NOAEL of 4 
mg/kg/day from prenatal developmental toxicity studies in rabbits based 
on an increase in skeletal malformations of the cervical and thoracic 
vertebrae and ribs at 8 mg/kg/day. EPA determined that the 10x factor 
for infants and children (required by FQPA) should be reduced to 3x and 
an MOE of 300 is required because of neuropathological lesions observed 
in the chronic toxicity study in rats and the need for a developmental 
neurotoxicity study. A dose and endpoint were not selected for the 
general population (including infants and children) because there were 
no

[[Page 6536]]

effects observed in oral toxicology studies, including maternal 
toxicity in the developmental toxicity studies in rats or rabbits, that 
could be attributable to a single exposure.
     2. Short- and intermediate- term toxicity. The Agency determined 
that this dose and endpoint was not applicable for risk assessment 
because no dermal or systemic toxicity was seen in a 28 day dermal 
toxicity study.
    3. Chronic toxicity. i. EPA has established the Reference dose 
(RfD) for cymoxanil at 0.013 mg/kg/day. This RfD is based on a chronic 
feeding study in rats with a NOAEL of 4.08 mg/kg/day and an uncertainty 
factor of 300.
    ii. Based on the use pattern, chronic dermal exposure is not 
anticipated; therefore, a long-term dermal risk assessment is not 
required.
    4. Carcinogenicity. Based on the lack of evidence of 
carcinogenicity in mice and rats, EPA has classified cymoxanil as a 
``not likely'' human carcinogen, according to EPA's Proposed Guidelines 
for Carcinogen Risk Assessment.

C. Exposures and Risks

    1. From food and feed uses. Tolerances have been established (40 
CFR 180.503 (a)) for the residues of cymoxanil, in or on potatoes and 
for the Section 18 emergency exemption use of cymoxanil in or on 
tomatoes (40 CFR 180.503 (b)). Risk assessments were conducted by EPA 
to assess dietary exposures from cymoxanil 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 acute exposure analysis for the 
females (13+) subgroup was performed using tolerance level residues and 
assuming 100% crop treated. The resulting MOE's are as follows: 2,100 
for females (13+/pregnant/not nursing), 2,200 for females (13+/
nursing), 980 for females (13-19 yrs/not pregnant or nursing), 1,500 
for females (20+ years/not pregnant or nursing), and 1,200 for females 
(13-50 years). The estimated acute MOEs of 980 or more (MOE of 300 
required) demonstrate no acute dietary concern.
    ii. Chronic exposure and risk. The chronic dietary risk analysis 
used the RfD of 0.013 mg/kg/day. Chronic dietary exposure estimates 
utilized tolerance level residues on potatoes, tomatoes, and grapes, 
and assumed 100% of the crops were treated. The risk assessment 
resulted in use of < 3% of the RfD for the general population, < 2% of 
the RfD for infants ( < 1 year), and < 5% of the RfD for children (1-6 
years). The chronic dietary risk does not exceed the Agency's level of 
concern.
    2. From drinking water. Cymoxanil appears to be mobile in soils. 
However, the rapid dissipation of cymoxanil in the environment 
precludes the possibility of extensive leaching. No detections of 
cymoxanil were observed below the 0-15 cm soil depth. The degradates of 
cymoxanil are mobile but the aerobic soil metabolism study showed they 
are short-lived. Therefore, cymoxanil and its degradates should not 
pose a threat to ground water.
    EPA estimated surface water exposure using the Generic Expected 
Environmental Concentration (GENEEC) model, a screening level model for 
determining concentrations of pesticides in surface water. GENEEC uses 
the soil/water partition coefficient , hydrolysis half life, and 
maximum label rate to estimate surface water concentration. In 
addition, the model contains a number of conservative underlying 
assumptions. Therefore, the drinking water concentrations derived from 
GENEEC for surface water are likely to be overestimated.
    EPA uses drinking water levels of comparison (DWLOCs) as a 
surrogate measure to capture risk associated with exposure to 
pesticides in drinking water. A DWLOC is the concentration of a 
pesticide in drinking water that would be acceptable as an upper limit 
in light of total aggregate exposure to that pesticide from food, 
water, and residential uses. A DWLOC will vary depending on the residue 
level in foods, the toxicity endpoint and with drinking water 
consumption patterns and body weights for specific subpopulations
    i.  Acute exposure and risk. The acute DWLOC for cymoxanil was 
calculated for the subpopulation of concern, females (13+ years) to be 
280 parts per billion (ppb). The estimated maximum concentration of 
cymoxanil in surface water (4.13 ppb) derived from GENEEC is much lower 
than EPA's DWLOC of 280 ppb. Therefore, EPA concludes with reasonable 
certainty that residues of cymoxanil in drinking water do not 
contribute significantly to the aggregate acute human health risk.
    ii. Chronic exposure and risk. The chronic DWLOCs are 440 ppb for 
the U.S. population and 120 ppb for the most sensitive subgroup, 
children (1-6 years). The DWLOCs are substantially higher than the 
GENEEC 56-day estimated environmental concentration of 0.19 ppb for 
cymoxanil in surface water. Therefore, EPA concludes with reasonable 
certainty that residues of cymoxanil in drinking water do not 
contribute significantly to the aggregate chronic human health risk.
    3. From non-dietary exposure. Cymoxanil is not registered for use 
on residential non-food sites. Therefore, no non-occupational, non-
dietary exposure and risk are expected.
    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.''
    EPA does not have, at this time, available data to determine 
whether cymoxanil 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, 
cymoxanil 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 cymoxanil has a common mechanism of toxicity 
with other substances. For information regarding EPA's efforts to 
determine which chemicals have a common mechanism of toxicity and to 
evaluate the cumulative effects of such chemicals, see the final rule 
for Bifenthrin Pesticide Tolerances (62 FR 62961, November 26, 1997).

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

    1. Acute risk. For the population subgroup of concern, females (13+ 
years old), the lowest calculated MOE for dietary (food only) exposure 
is 980. The acute DWLOC for cymoxanil in females (13+ years old) is 280 
ppb. The Agency concludes that there is a reasonable certainty that no 
harm will result from acute aggregate exposure to cymoxanil residues 
for children.
    2. Chronic risk. Using the TMRC exposure assumptions described in 
this unit, EPA has concluded that aggregate exposure to cymoxanil from 
food will utilize 2 % of the RfD for the U.S. population. The major 
identifiable subgroup with the highest aggregate exposure is children 
1-6 years 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 cymoxanil 
in drinking water and from non-dietary, non-occupational exposure, EPA 
does not expect the aggregate exposure to exceed

[[Page 6537]]

100% of the RfD. EPA concludes that there is a reasonable certainty 
that no harm will result from aggregate exposure to cymoxanil residues.
    3. Aggregate cancer risk for U.S. population. EPA has classified 
cymoxanil as a ``not likely'' human carcinogen, based on the lack of 
evidence of carcinogenicity in mice and rats, and therefore has a 
reasonable certainty that no harm will result from exposure to residues 
of cymoxanil.
    4. Determination of safety. Based on these risk assessments, EPA 
concludes that there is a reasonable certainty that no harm will result 
from aggregate exposure to cymoxanil residues.

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

    1. Safety factor for infants and children-- i. In general. In 
assessing the potential for additional sensitivity of infants and 
children to residues of cymoxanil, 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 margin of exposure (MOE) analysis or through using 
uncertainty (safety) factors in calculating a dose level that poses no 
appreciable risk to humans. EPA believes that reliable data support 
using the standard uncertainty factor (usually 100 for combined inter- 
and intra-species variability) and not the additional tenfold MOE/
uncertainty factor when EPA has a complete data base under existing 
guidelines and when the severity of the effect in infants or children 
or the potency or unusual toxic properties of a compound do not raise 
concerns regarding the adequacy of the standard MOE/safety factor.
    ii. Pre- and post-natal sensitivity. The Agency determined that a 
developmental neurotoxicity study is required for cymoxanil. Evidence 
that support requiring a developmental neurotoxicity study include (1) 
clinical neurotoxicity in the database, (2) clinical observations of 
hyperactivity and aggressiveness were reported in males at 700 and 
2,000 ppm (30.3 and 90.1 mg/kg/day) in the chronic toxicity study in 
rats, (3) diarrhea was noted in males in the subchronic dog study at 5-
11 mg/kg/day, (4) grip strength and foot splay measurements were 
decreased (non-significantly) in males at 224 mg/kg/day in the 13-week 
subchronic neurotoxicity study in rats, although it was noted that 
these findings occurred in conjunction with decreased body weight, (5) 
brain weight changes and/or neuropathology in the cymoxanil database, 
particularly following long-term exposure, (6) absolute brain weight 
was decreased in both sexes at 1,500 and 3,000 ppm (216/298 and 446/582 
mg/kg/day for M/F, respectively) in the chronic toxicity study in mice, 
(7) equivocal incidences of myelin degeneration were observed in males 
at 3,000 ppm (224 mg/kg/day) in the 13-week neurotoxicity study in 
rats, (8) axon/myelin degeneration of the sciatic nerve was observed in 
females at 700 and 2,000 ppm (38.4 and 126 mg/kg/day) in the chronic 
toxicity study in rats, and (9) retinal atrophy was reported in both 
sexes at 700 and 2,000 ppm (30.3/38.4 and 90.1/126 mg/kg/day, 
respectively) in the chronic toxicity study in rats.
    The developmental toxicity and multigeneration reproduction study 
data demonstrated no indication of increased susceptibility of rats or 
rabbits in utero and/or postnatal exposure to cymoxanil. Overall, in 
the developmental toxicity studies in rats and rabbits, and in the 2-
generation reproductive toxicity study with cymoxanil in rats, 
offspring toxicity was observed only at treatment levels which were 
toxic to parental adults. Although increased fetal susceptibility was 
suggested by the results of one prenatal developmental toxicity study, 
in which the fetal NOAEL was lower than the maternal NOAEL, 
uncertainties regarding the source of the rabbits substantially reduced 
the confidence that observed skeletal anomalies were solely related to 
treatment, and the results of this study were not duplicated in other 
rabbit developmental studies.
    iii. Conclusion. Except for the pending requirements for a 
developmental neurotoxicity study and a rat dominant lethal study (both 
in rebuttal), there is a complete toxicity database for cymoxanil and 
exposure data is complete or is estimated based on data that reasonably 
accounts for potential exposures. The Agency determined that for 
cymoxanil, the 10x factor should be reduced to 3x, taking into account 
all of the following information: no sensitivity to perinatal animals, 
no data gaps for evaluating potential effects on offspring following in 
utero and/or postnatal exposure to cymoxanil by standard required 
studies and a weight-of-evidence review indicating that 
neuropathological lesions could result from long-term exposure to 
cymoxanil. A developmental neurotoxicity study and a rat dominant 
lethal study (both in rebuttal) were required to resolve concerns for 
potential genetic damage to male germinal cells that may be associated 
with the effects noted in the reproduction, developmental subchronic 
and chronic studies.
    2. Acute risk.  The MOE for the acute dietary (food only) risk 
assessment for the population subgroup of concern, females 13+ years, 
not pregnant or nursing, was estimated at 980. This risk estimate does 
not exceed the Agency's level of concern. EPA has calculated drinking 
water levels of comparison (DWLOCs) for acute exposure to cymoxanil in 
drinking water for females (13+ years old) to be 280 ppb. Therefore, 
EPA concludes with reasonable certainty that the potential risks from 
aggregate acute exposure (food & water) would not exceed the Agency's 
level of concern.
    3. Chronic risk. Using the exposure assumptions described above, 
EPA has concluded that aggregate exposure to cymoxanil from food will 
utilize less than 5% of the RfD for infants and children. 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 cymoxanil in drinking water, EPA 
does not expect the aggregate exposure to exceed 100% of the RfD.
    4. Determination of safety. Based on these risk assessments, EPA 
concludes that there is a reasonable certainty that no harm will result 
to infants and children from aggregate exposure to cymoxanil residues.

III. Other Considerations

A. Metabolism In Plants and Animals

    The nature of the residue in plants and animals is adequately 
understood. Only the parent cymoxanil compound is of regulatory 
concern. There are no animal feed items currently associated with 
grapes and tomatoes.

[[Page 6538]]

B. Analytical Enforcement Methodology

    An adequate enforcement method, AMR 3060-94, is available to 
enforce the tolerance on grapes and tomatoes. Quantitation is by HPLC/
UV. These methods have been submitted for publication in PAM I. The 
methods are available to anyone who is interested in pesticide residue 
enforcement from: Calvin Furlow, Public Response and Program Resources 
Branch, Field Operations Division (7506C), Office of Pesticide 
Programs, Environmental Protection Agency, 401 M St., S.W., Washington, 
DC 20460. Office location and telephone number: Crystal Mall #2, Rm 
101FF, 1921 Jefferson Davis Hwy., (701) 305-5229.

C. Magnitude of Residues

    EPA has concluded that residue data submitted in support of the 
tolerances for grapes and tomatoes at 0.1 ppm, indicate that the 
tolerances requested by the petitioner are adequate.

D. International Residue Limits

    There are no Codex or Canadian residue limits established for 
cymoxanil on grapes or tomatoes. Therefore, no compatibility problems 
exist for the proposed tolerances.

E. Rotational Crop Restrictions

    Rotational crop restrictions are not an issue as there are no U.S. 
registrations associated with imported tolerances.

IV. Conclusion

    Therefore, tolerances are established for residues of cymoxanil, 
[2-cyano-N-[(ethylamino)carbonyl]-2-(methoxyimino) acetamide] in or on 
the raw agricultural commodities, imported grapes and tomatoes 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 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 April 12, 1999, 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 under the ADDRESSES section (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 
regulation. 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). EPA is authorized to waive any fee requirement 
``when in the judgement of the Administrator such a waiver or refund is 
equitable and not contrary to the purpose of this subsection.'' For 
additional information regarding tolerance objection fee waivers, 
contact James Tompkins, 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: Rm. 239, Crystal Mall #2, 1921 Jefferson Davis Hwy., 
Arlington, VA, (703) 305-5697, tompkins.jim@epa.gov. Requests for 
waiver of tolerance objection fees should be sent to James Hollins, 
Information Resources and Services Division (7502C), Office of 
Pesticide Programs, Environmental Protection Agency, 401 M St., SW., 
Washington, DC 20460.
     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 regulation under docket 
control number [OPP-300782] (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 Hwy., Arlington, VA.
     Objections and hearing requests may be sent by e-mail directly to 
EPA at:
     opp-docket@epa.gov.

    E-mailed objections and hearing requests must be submitted as an 
ASCII fileavoiding the use of special characters and any form of 
encryption.
    The official record for this regulation, as well as the public 
version, as described in this unit 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 record which 
will also include all comments submitted directly in writing. The 
official 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 a tolerance under section 408(d) of the 
FFDCA in response to a petition submitted to the Agency. The Office of 
Management and Budget (OMB) has exempted these types of actions from 
review under Executive Order 12866, entitled Regulatory Planning and 
Review (58 FR 51735, October 4, 1993). 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 specficed by Executive Order 
12875, entitled Enhancing the Intergovernmental Partnership (58 FR 
58093, October 28, 1993), or special considerations as required by 
Executive

[[Page 6539]]

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).
    In addition, since tolerances and exemptions that are established 
on the basis of a petition under FFDCA section 408(d), such as the 
tolerance/exemption 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 
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.

B. Executive Order 12875

    Under Executive Order 12875, entitled Enhancing the 
Intergovernmental Partnership (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 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 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 officials 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.

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 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: January 25, 1999.

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. 180.503 by adding paragraph (e) to read as follows:


Sec. 180.503  Cymoxanil; tolerance for residues.

* * * * *
    (e) Import. Import tolerances are established for residues of the 
fungicide [2-cyano-N-[(ethylamino)carbonyl]-2-(methoxyimino) acetamide] 
expressed as cymoxanil in or on the following food commodities:


------------------------------------------------------------------------
                 Commodity                        Parts per million
------------------------------------------------------------------------
Grapes, imported..........................  0.1
Tomatoes, imported........................  0.1
------------------------------------------------------------------------


[FR Doc. 99-3249 Filed 2-9-99; 8:45 am]
BILLING CODE 6560-50-F