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cymoxanil Pesticide Tolerance 4/98

 

[Federal Register: May 6, 1998 (Volume 63, Number 87)]
[Rules and Regulations]               
[Page 24941-24949]
>From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr06my98-12]

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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-300653; FRL-5788-5]
RIN 2070-AB78

 
Cymoxanil; Pesticide Tolerance

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes a tolerance for residues of the 
fungicide, cymoxanil, 2-cyano-N-[(ethylamino)carbonyl]-2-(methoxyimino) 
acetamide, in or on potatoes. E.I. DuPont de Nemours & Company 
submitted a petition under the Federal Food, Drug and Cosmetic Act 
(FFDCA), as amended by the Food Quality Protection Act of 1996 (Pub. L. 
104-170) requesting this tolerance.

DATES: This regulation is effective May 6, 1998. Objections and 
requests for hearings must be received by EPA on or before July 6, 
1998.

ADDRESSES: Written objections and hearing requests, identified by the 
docket control number, [OPP-300653], 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-300653], 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 
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-300653]. 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, Acting 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: 
Crystal Mall #2, 1921 Jefferson Davis Hwy., Arlington, VA, (703) 308-
9354, e-mail: waller.mary@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: In the Federal Register of (July 25, 1997, 
62 FR 40075)(FRL-5726-4), 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 pesticide petition (PP 7F4805) for a tolerance 
by E.I. DuPont de Nemours and Company, E. I. DuPont Agricultural 
Products, Walker's Mill,

[[Page 24942]]

Barley Mill Plaza, P.O. Box 80038, Wilmington, Deleware, 19880-0038. 
This notice included a summary of the petition prepared by E.I. DuPont 
de Nemours & Company, the registrant. No comments were received in 
response to the notice of filing.
    The petition requested that 40 CFR 180.503 be amended by 
establishing a tolerance for residues of the fungicide cymoxanil, 2-
cyano-N-[(ethylamino)carbonyl]-2-(methoxyimino) acetamide, in or on 
potatoes at 0.05 parts per million (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 percent 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 hundredfold MOE is based on the same rationale as 
the hundredfold 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 24943]]

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 percent 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 (children 1 to 6 
years old) 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 cymoxanil 
to make a determination on aggregate exposure, consistent with section 
408(b)(2), for a tolerance for residues of cymoxanil 2-cyano-N-
[(ethylamino)carbonyl]-2-(methoxyimino) acetamide in or on potatoes. 
EPA's assessment of the dietary exposures and risks associated with 
establishing this 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 is 
discussed below.
    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 for both sexes; no ocular irritation; slight 
dermal irritation and a finding that the cymoxanil is not a dermal 
sensitizer.
     2. Subchronic toxicity. a. 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 LOEL 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-effect level (NOEL) for subchronic systemic 
toxicity is 750 ppm.
     b. A subchronic oral study in mice fed doses of 50, 500, 1,750, 
3,500, or 7,000 ppm (average 8.25, 82.4, 294, 566, or 1,306 mg/kg/day, 
for males; 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 NOEL 
was established at 50 ppm for males and 500 ppm for females; the LOEL 
was 500 ppm for males and 1,750 ppm for females.
     c. A subchronic oral toxicity study was conducted in dogs fed 
doses of 100 or 200 ppm (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. The 250/500 ppm males had lower epididymal and testicular 
weights, and aspermatogenesis was observed. The LOEL is 3 mg/kg body 
weight/day (100 ppm) for dogs based on decreased body weights and food 
consumption in females. The NOEL was not established.
     d. In a 28-day dermal toxicity study, cymoxanil was applied to the 
shaved backs of rats for 6 hrs/day at doses of 50, 500, and 1,000 mg/
kg/day. There were no demonstrated effects and no compound-related 
histopathology. The NOEL for systemic toxicity and dermal irritation 
was 1,000 mg/kg/day, the highest dose tested (HDT).
    3.  Chronic toxicity. a. 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 percent and 21-40 percent 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 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

[[Page 24944]]

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 
LOEL was 30.3 mg/kg/day for males and 38.4 mg/kg/day 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 NOEL 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.
    b. A chronic toxicity study was conducted in dogs fed cymoxanil at 
doses of 25, 50, or 100 ppm for females (0.7, 1.6, or 3.1 mg/kg/day) 
and 50, 100, or 200 ppm for males (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 LOEL was 200 ppm for males, based on depressed 
weight gains through week 12 and changes in hematology and blood 
chemistry. No LOEL was established for females. The NOEL was 100 ppm.
    4.  Carcinogenicity. a. A combined chronic/carcinogenicity study, 
conducted in rats (described in the Chronic Toxicity Section, above, 
Unit II.A.3.) showed no evidence of carcinogenic potential.
    b. A carcinogenicity study was conducted in mice fed cymoxanil at 
doses of 30, 300, 1,500, and 3,000 ppm (4.19, 42.0, 216, and 446 mg/kg/
day for males; 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 percent compared to 69 percent 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. The 3,000 ppm females exhibited increased 
frequency of pallor, weakness, and hunching over. Male mice fed 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 LOEL was 300 ppm, based on toxicity to the testes and 
epididymides in males and toxicity to the gastrointestinal mucosa in 
females. The NOEL was 30 ppm. Under the conditions of this study, there 
was no evidence of a carcinogenic effect.
    5. Developmental toxicity. a. 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 LOEL was 25 mg/kg/day, based upon reduced body weight, body 
weight change, and food consumption. The maternal NOEL was 10 mg/kg/
day. The developmental LOEL 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, 150 and 150 mg/kg/day. Increased early resorptions 
resulted in reduced litter sizes. The developmental NOEL was 10 mg/kg/
day.
     b. 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 LOEL 
was not determined; the maternal and developmental NOEL 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 NOEL 
and LOEL for cymoxanil in a nonrodent species.
     c. A prenatal developmental toxicity study was conducted in 
rabbits gavaged with cymoxanil on days 6-18 of gestation at dose levels 
of 8, 16, or 32 mg/kg/day. Uncertainties regarding the source of the 
parental rabbits substantially reduced the confidence that any observed 
skeletal effects were solely related to treatment.
    d. 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 posttreatment 
increases in body weight gain at 8 and 32 mg/kg/day. The maternal LOEL 
was 8 mg/kg/day, based upon a significant dose-related rebound in 
maternal body weight. The maternal NOEL was 4 mg/kg/day. The 
developmental LOEL 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 NOEL was 4 
mg/kg/day.
    6. Reproductive toxicity. A two-generation reproduction study was 
conducted in rats fed cymoxanil at doses of 100, 500, or 1,500 ppm 
(equivalent to 6.5, 32.1, or 97.9 mg/kg/day in males and 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 LOEL was 
500 ppm based upon reduced pre-mating body weight, body weight gain, 
and food consumption for F<INF>1</INF> males; and decreased gestation 
and lactation body weight for F<INF>1</INF> females. The parental 
systemic NOEL was 100 ppm. The offspring LOEL was 500 ppm based upon 
decreased F<INF>1</INF> pup viability on postnatal days 0-4 and on a 
significant reduction in F<INF>2b</INF> pup weight. The offspring NOEL 
was 100 ppm.
    7.  Neurotoxicity. a. 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 of 
dietary doses of cymoxanil at 0, 100,

[[Page 24945]]

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 LOEL for neurobehavioral and neuropathic effects was not 
established. The NOEL for neurotoxicity was 3,000 ppm.
     b. In the combined chronic toxicity/carcinogenicity study in rats, 
increased incidence of sciatic nerve axon/myelin degeneration was 
observed in females fed cymoxanil at doses of 38.4 and 126 mg/kg/day 
for 104 weeks. Also, increased incidence and severity of retinal 
atrophy was observed in males at 30.3 and 90.1 mg/kg/day as well as in 
females at 38.4 and 126 mg/kg/day. These two findings demonstrated a 
dose-related effect. In addition, clinical observations of 
hyperactivity and aggressiveness were reported in males at 700 and 
2,000 ppm (30.3 and 90.1 mg/kg/day).
     c. In the carcinogenicity study in mice, absolute brain weight was 
decreased in both sexes at 1,500 and 3,000 ppm (216/298 mg/kg/day and 
446/582 mg/kg/day for males/females, respectively).
     d. 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 two-
generation reproduction study in rats.
     e. 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 also 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 percent), during the first 24 
hours (58-66 percent). Fecal excretion accounted for 15.7-23.6 percent 
of the dose, and radioactivity in the tissues and carcasses accounted 
for <1 percent of the dose at sacrifice for all three dosing regimens. 
A pilot study indicated that approximately 3 percent 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 
fortyfold 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 percent of the dose) was free and/or conjugated 
[<SUP>14</SUP>C]glycine, and 2-cyano-2-methoxyiminoacetic acid (IN-
W3595) (6.5-33 percent of the dose) was also found. Intact 
[<SUP>14</SUP>C]cymoxanil was not detected. In the feces, trace levels 
(<1 percent of the 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 percent 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 submitted mutagenicity 
test battery satisfied the new mutagenicity initial testing battery 
guidelines and 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-females 13+. To assess acute dietary exposure, 
the Agency used a NOEL 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 to account for enhanced 
sensitivity of infants and children (required by FQPA) should be 
reduced to 3x. An MOE of 300 is required for the acute dietary 
assessment to protect the sub-population of concern, ``Females 13+,'' 
due to neuropathological lesions seen in the chronic toxicity study in 
rats and the need for an additional developmental neurotoxicity study.
      Acute toxicity-general population. An acute dose and endpoint was 
not selected for the general population and

[[Page 24946]]

the sub-population including ``infants and children'' because there 
were no observable effects in oral toxicology studies, and no maternal 
toxicity in the developmental toxicity studies in rats or rabbits 
attributable to a single dose.
     2.  Short- and intermediate-term residential 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, at the limit dose.
     3.  Chronic residential toxicity.  Based on the use pattern, 
chronic dermal exposure is not anticipated and long-term dermal risk 
assessment is not required.
     4.  Chronic dietary toxicity.  An RfD of 0.013 mg/kg/day was 
established based on a chronic feeding study in rats with a NOEL of 
4.08 mg/kg/day and an uncertainty factor of 300.
     5. 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 (April 10, 1996).

C. Exposures and Risks

    1.  From food and feed uses. Time-limited tolerances of 0.05 ppm 
have been established in the 40 CFR 180.503(b) for residues of 
cymoxanil in or on potatoes and tomatoes under section 18 of FIFRA. In 
today's action, a tolerance will be established for residues of 
cymoxanil in or on potatoes at 0.05 ppm under section 3 of FIFRA in 40 
CFR 180.503(a) and the section 18 tolerance for potatoes will be 
removed. Risk assessments were conducted by EPA to assess dietary 
exposures and risks from cymoxanil as follows:
    a.  Acute exposure and risk. Acute dietary risk assessments are 
performed for a food-use pesticide if a toxicological study indicates 
an effect of concern may occur as a result of a 1-day or single 
exposure. For the subpopulation of concern, females 13+, the estimated 
acute MOE of 5,000 demonstrates no acute dietary concern.
    b.  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 and tomatoes and assumed 
100 percent of the crops were treated. The risk assessment resulted in 
use of <1 percent of the RfD for the general population, including 
infants (< 1 year old), and < 2 percent of the RfD for children (1-6 or 
7-12 years old).
    2.  From drinking water. No monitoring data are currently available 
to perform a quantitative drinking water risk assessment. Cymoxanil 
appears to be mobile in soils, although its rapid environmental 
dissipation precludes extensive leaching. Cymoxanil was not detected 
below 0-15 cm of soil. Degradates of cymoxanil are mobile, but short-
lived, and are not expected to 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. Surface water estimates 
derived from GENEEC assumed 7 applications of 0.12 lbs. active 
ingredient/acre would be applied. The model indicated that cymoxanil in 
surface water could reach 4.13 parts per billion (ppb) (peak 
concentration) and 0.19 ppb (average 56 day concentration ).
    a.  Acute exposure and risk.  EPA calculated drinking water levels 
of concern (DWLOC) for acute exposure by using the acute toxicity 
endpoint. The acute dietary food exposure (from the DRES analysis) was 
subtracted from the ratio of the acute NOEL (used for acute dietary 
assessments) to the ``acceptable'' MOE for aggregate exposure to obtain 
the acceptable acute exposure to cymoxail in drinking water.
     EPA has calculated DWLOCs for acute exposure to cymoxanil in 
drinking water for females (13+ years old) to be 380 ppb. The maximum 
estimated concentrations of cymoxanil in surface and ground water are 
below EPA's levels of concern for cymoxanil in drinking water as a 
contribution to acute aggregate exposure. Therefore, EPA concludes with 
reasonable certainty that residues of cymoxanil in drinking water do 
not contribute significantly to the aggregate acute human health risk.
     b.  Chronic exposure and risk. Chronic (non-cancer), drinking 
water levels of concern are 450 ppb for the U.S. population and 130 ppb 
for children (1-6 years old). The estimated average concentrations of 
cymoxanil in surface and ground water are less than EPA's levels of 
concern for cymoxanil in drinking water as a contribution to chronic 
aggregate exposure. 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.'' 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

[[Page 24947]]

case common mechanism of activity will be assumed).
     At this time, EPA does not have 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. Cymoxanil is structurally related to metazachlor, 
dimethenamid and amiphos. Of these pesticides, only dimethenamid is 
currently registered for use in the United States. 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 and that 
structurally-related chemicals will not have common toxic metabolites 
to cymoxanil.

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

     1.  Acute risk. The MOE for the acute dietary (food only) risk 
assessment for the population subgroup of concern, females 13+ years, 
was estimated at 5,000. This risk estimate does not exceed the Agency's 
level of concern. EPA has calculated drinking water levels of concern 
(DWLOCs) for acute exposure to cymoxanil in drinking water for females 
(13+ years old) to be 380 ppb. Chronic (non-cancer), drinking water 
levels of concern are 450 ppb for the U.S. population and 130 ppb for 
children (1-6 years old). 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.
     2. Chronic risk. Using the TMRC exposure assumptions described 
above, EPA has concluded that aggregate exposure to cymoxanil from food 
will utilize <1 percent of the RfD. The estimated average 
concentrations of cymoxanil in surface and ground water are less than 
EPA's levels of concern for cymoxanil in drinking water as a 
contribution to chronic aggregate exposure. Therefore, EPA concludes 
with reasonable certainty that residues of cymoxanil in drinking water 
do not contribute significantly to the potential aggregate chronic 
human health risk at the present time, considering the present uses and 
those proposed in this action.

E. 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.

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

     Safety factor for infants and children - 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 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 during 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.
     The Agency determined that for cymoxanil, the 10x factor for the 
protection of infants and children (as required by FQPA) should be 
reduced to 3x, based on the following weight of the evidence 
considerations: (1) No increased sensitivity in fetuses as compared to 
maternal animals was observed following in utero exposures in 
developmental studies in rats and rabbits; (2) no increased sensitivity 
in pups when compared to adults was seen in the two-generation 
reproduction study in rats; (3) the toxicology data base is complete 
except for the requirement to submit a developmental neurotoxicity 
study; and (4) no frank neurotoxicity was seen in the 90-day 
neurotoxicity study. The Agency has determined that a MOE of 300 is 
required because of the observance of neuropathological lesions in the 
chronic toxicity study in rats and the need for a developmental 
neurotoxicity study.

III. Other Considerations

A. Endocrine Disrupter Effects

     EPA is required to develop a screening program to determine 
whether certain substances (including all pesticides and inerts) ``may 
have an effect in humans that is similar to an effect produced by a 
naturally occurring estrogen, or such other endocrine effect....'' The 
Agency is currently working with interested stakeholders, including 
other government agencies, public interest groups, industry and 
research scientists in developing a screening and testing program and a 
priority setting scheme to implement this program. Congress has allowed 
3 years from the passage of FQPA (August 3, 1999) to implement this 
program. At that time, EPA may require further testing of this active 
ingredient and end use products for endocrine disrupter effects.

B. Metabolism in Plants and Animals

     Plants. Based on a metabolism study on potatoes, the nature of the 
residue is adequately understood. Only the parent cymoxanil compound is 
of regulatory concern.
    Animals. Based on a metabolism study in lactating goats, the nature 
of the residue in animals is adequately understood. Only the parent 
cymoxanil compound is of regulatory concern.

C. Analytical Enforcement Methodology

    An adequate enforcement method, AMR 3705-95, is available to 
enforce the tolerance on potatoes. 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, Information Resources and Services Division 
(7502C), Office of Pesticide Programs, Environmental Protection Agency, 
401 M St., SW., Washington, DC 20460. Office location and telephone 
number: Crystal Mall #2, Rm 101FF, 1921 Jefferson Davis Hwy., 
Arlington, VA (703) 305-5229.

D. Magnitude of Residues

    Residues of cymoxanil resulting from the proposed use will not 
exceed 0.05 ppm in potatoes. The tolerance on potatoes is for the raw 
agricultural commodity as defined in 40 CFR 180.1(j)(1). For risk 
assessment purposes, it was concluded that

[[Page 24948]]

residues resulting from the proposed use will not exceed 0.05 ppm in 
potatoes.

E. International Residue Limits

    There are no Codex or Canadian residue limits established for 
cymoxanil on potatoes but a Mexican maximum residue limit (MRL) of 0.05 
ppm is established for potatoes. Therefore, no compatibility problems 
exist for the proposed tolerance on potatoes.

F. Rotational Crop Restrictions

    The confined rotational crop studies provided adequate results to 
conclude that a 30-day plant back interval is sufficient for all crops.

IV. Conclusion

    Therefore, the tolerance is established for residues of cymoxanil, 
2-cyano-N-[(ethylamino)carbonyl]-2-(methoxyimino) acetamide, in or on 
the raw agricultural commodity, potatoes, at 0.05 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 July 6, 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 EPA docket for this rule making. 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 
Confidential Business Information (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 and Electronic Submissions

    EPA has established a record for this rulemaking under docket 
control number [OPP-300653] (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 a tolerance under FFDCA section 408(d) 
in response to a petition submitted to the Agency. The Office of 
Management and Budget (OMB) has exempted these types of actions from 
review under Executive Order 12866, entitled Regulatory Planning and 
Review (58 FR 51735, October 4, 1993). This final rule does not contain 
any information collections subject to OMB approval under the Paperwork 
Reduction Act (PRA), 44 U.S.C. 3501 et seq., or impose any enforceable 
duty or contain any unfunded mandate as described under Title II of the 
Unfunded Mandates Reform Act of 1995 (UMRA) (Pub. L. 104-4). Nor does 
it require any prior consultation as specified by Executive Order 
12875, entitled Enhancing the Intergovernmental Partnership (58 FR 
58093, October 28, 1993), or special considerations as required by 
Executive Order 12898, entitled Federal Actions to Address 
Environmental Justice in Minority Populations and Low-Income 
Populations (59 FR 7629, February 16, 1994), or require OMB review in 
accordance with Executive Order 13045, entitled Protection of Children 
from Environmental Health Risks and Safety Risks (62 FR 19885, April 
23, 1997).
    In addition, since these tolerances and exemptions that are 
established on the basis of a petition under FFDCA section 408(d), such 
as the tolerance in this final rule, do not require the issuance of a 
proposed rule, the requirements of the Regulatory Flexibility Act (RFA) 
(5 U.S.C. 601 et seq.) do not apply. 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 was 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 General Accounting Office

    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

[[Page 24949]]

copy of the rule, to each House of the Congress and to the Comptroller 
General of the United States. EPA will submit a report containing this 
rule and other required information to the U.S. Senate, the U.S. House 
of Representatives, and the Comptroller General of the United States 
prior to publication of the rule in the Federal Register. This rule is 
not a ``major rule'' as defined by 5 U.S.C. 804(2).

List of Subjects in 40 CFR Part 180

    Environmental protection, Administrative practice and procedure, 
Agricultural commodities, Pesticides and pests, Reporting and 
recordkeeping requirements.


    Dated: April 22, 1998.

Stephen L. Johnson,

Acting Director, 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. Section 180.503 is amended by adding text to paragraph (a) to 
read as follows and by removing the entry for ``potatoes'' in paragraph 
(b) .


Sec. 180.503  Cymoxanil; tolerances for residues.

    (a) General  . A tolerance is established for residues of the 
fungicide, cymoxanil, 2-cyano-N-[(ethylamino)carbonyl]-2-(methoxyimino) 
acetamide, in or on the following food commodity.

                                                                        
------------------------------------------------------------------------
                 Commodity                        Parts per million     
------------------------------------------------------------------------
Potatoes..................................  0.05                        
------------------------------------------------------------------------

*    *    *    *    *

[FR Doc. 98-11764 Filed 5-5-98; 8:45 am]
BILLING CODE 6560-50-F