[Federal Register Volume 65, Number 138 (Tuesday, July 18, 2000)]
[Rules and Regulations]
[Pages 44453-44468]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 00-18099]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-301015; FRL-6594-8]

RIN 2070-AB78

Vinclozolin; Pesticide Tolerances

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes tolerances for combined residues 
of vinclozolin, 3-(3,5-dichlorophenyl)-5-ethenyl-5-methyl-2,4-
oxazolidinedione and its metabolites containing the 3,5-dichloroaniline 
moiety in or on the raw agricultural commodities: succulent beans at 
2.0 parts per million (ppm); canola at 1.0 ppm; eggs, milk, and the 
meat, fat, and meat byproducts of cattle, goats, hogs, horses, and 
sheep at 0.05 ppm; and in the meat, fat, and meat byproducts of poultry 
at 0.1 ppm. These tolerances will expire and are revoked on September 
30, 2003. BASF Corporation requested these tolerances under the Federal 
Food, Drug, and Cosmetic Act, as amended by the Food Quality Protection 
Act of 1996.

DATES: This regulation is effective July 18, 2000. Objections and 
requests for hearings, identified by docket control number OPP-301015, 
must be received by EPA on or before September 18, 2000.

ADDRESSES: Written objections and hearing requests may be submitted by 
mail, in person, or by courier. Please follow the detailed instructions 
for each method as provided in Unit VII. of the SUPPLEMENTARY 
INFORMATION. To ensure proper receipt by EPA, your objections and 
hearing requests must identify docket control number OPP-301015 in the 
subject line on the first page of your response.

FOR FURTHER INFORMATION CONTACT: By mail: Mary L. Waller, Registration 
Division (7505C), Office of Pesticide Programs, Environmental 
Protection

[[Page 44454]]

Agency, Ariel Rios Bldg., 1200 Pennsylvania Ave., NW., Washington, DC 
20460; telephone number: (703) 308-9354; and e-mail address: 
[email protected].

SUPPLEMENTARY INFORMATION:

I. General Information

A. Does this Action Apply to Me?

    You may be affected by this action if you are an agricultural 
producer, food manufacturer, or pesticide manufacturer. Potentially 
affected categories and entities may include, but are not limited to:

------------------------------------------------------------------------
                                                          Examples of
           Categories                    NAICS            potentially
                                                       affected entities
------------------------------------------------------------------------
Industry                          111                 Crop production
                                  112                 Animal production
                                  311                 Food manufacturing
                                  32532               Pesticide
                                                       manufacturing
------------------------------------------------------------------------

    This listing is not intended to be exhaustive, but rather provides 
a guide for readers regarding entities likely to be affected by this 
action. Other types of entities not listed in the table could also be 
affected. The North American Industrial Classification System (NAICS) 
codes have been provided to assist you and others in determining 
whether or not this action might apply to certain entities. If you have 
questions regarding the applicability of this action to a particular 
entity, consult the person listed under FOR FURTHER INFORMATION 
CONTACT.

B. How Can I Get Additional Information, Including Copies of this 
Document and Other Related Documents?

    1. Electronically. You may obtain electronic copies of this 
document, and certain other related documents that might be available 
electronically, from the EPA Internet Home Page at http://www.epa.gov/. 
To access this document, on the Home Page select ``Laws and 
Regulations'' and then look up the entry for this document under the 
``Federal Register--Environmental Documents.'' You can also go directly 
to the Federal Register listings at http://www.epa.gov/fedrgstr/.
    2. In person. The Agency has established an official record for 
this action under docket control number OPP-301015. The official record 
consists of the documents specifically referenced in this action, and 
other information related to this action, including any information 
claimed as Confidential Business Information (CBI). This official 
record includes the documents that are physically located in the 
docket, as well as the documents that are referenced in those 
documents. The public version of the official record does not include 
any information claimed as CBI. The public version of the official 
record, which includes printed, paper versions of any electronic 
comments submitted during an applicable comment period is available for 
inspection in the Public Information and Records Integrity Branch 
(PIRIB), Rm. 119, Crystal Mall #2, 1921 Jefferson Davis Hwy., 
Arlington, VA, from 8:30 a.m. to 4 p.m., Monday through Friday, 
excluding legal holidays. The PIRIB telephone number is (703) 305-5805.

II. Background and Statutory Findings

    In the Federal Register of April 21, 2000 (65 FR 78) (FRL-6555-6), 
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) (Public Law 104-170) announcing the 
filing of a pesticide petition (PP 0F6079) for tolerances by BASF 
Corporation, Agricultural Products, P.O. Box 13528, Research Triangle 
Park, NC 27709. This notice included a summary of the petition prepared 
by BASF Corporation, the registrant. In addition, on June 2, 2000, the 
Agency added a supplemental notice of filing to the docket which 
summarized the toxicity and risk associated with the proposed 
tolerances. The Agency received comments from the Natural Resources 
Defense Council (NRDC), Earthjustice Legal Defense Fund (EJLDF), and 
BASF Corporation. The comments from outside parties are summarized in 
Unit IV below, followed by the Agency's response.
    The petition requested that 40 CFR 180.380 be amended by 
establishing tolerances for combined residues of the fungicide 
vinclozolin, 3-(3,5-dichlorophenyl)-5-ethenyl-5-methyl-2,4-
oxazolidinedione and its metabolites containing the 3,5-dichloroaniline 
moiety, in or on succulent beans at 2.0 ppm and canola at 1.0 ppm. The 
petition was later amended to request tolerances on eggs, milk, and the 
meat, fat, and meat byproducts of cattle, goats, hogs, horses, and 
sheep at 0.05 ppm and in the meat, fat, and meat byproducts of poultry 
at 0.1 ppm.
    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).

III. 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 and to 
make a determination on aggregate exposure, consistent with section 
408(b)(2), for tolerances for combined residues of vinclozolin in or on 
succulent beans at 2.0 ppm; canola at 1.0 ppm; eggs, milk, and the 
meat, fat, and meat byproducts of cattle, goats, hogs, horses, and 
sheep at 0.05 ppm; and the meat, fat, and meat byproducts of poultry at 
0.1 ppm. EPA's assessment of the 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 vinclozolin are 
discussed in this unit.
    1. Acute toxicity. A battery of acute toxicity studies placed 
technical vinclozolin in toxicity category IV for acute oral toxicity 
(LD50 of > 10,000 mg/kg), and acute inhalation toxicity 
(LC50 of 29.1 mg/l); and toxicity category III for acute 
dermal toxicity (LD50 of > 5,000 mg/kg). Technical 
vinclozolin caused minimal eye and dermal

[[Page 44455]]

irritation and the technical material is positive for skin 
sensitization.
    2. Chronic toxicity. i. A 1-year chronic feeding study in dogs fed 
dosages of 0, 1.1, 2.4, 4.9, and 48.7 mg/kg/day with a No-Observed-
Adverse-Effect Level (NOAEL) of 2.4 mg/kg/day based on the following 
effects: (1) Slight decrease in hematological and increase in clinical 
chemistry values in the 48.7 mg/kg/day dose group (highest dose 
tested--HDT); (2) increased absolute and/or relative weights for the 
testes (male only), adrenal, liver, spleen, and thyroids in the 4.9 or 
48.7 mg/kg/day dose groups; (3) a dose-related atrophy of the prostate 
in the 4.9 or 48.7 mg/kg/day dose groups; and (4) microscopic findings 
in the adrenal and testes (males) in the 48.7 mg/kg/day dose group and 
liver findings for both male and female dogs in the 48.7 mg/kg/day dose 
groups and in the females in the 4.9 mg/kg/day dose group, only.
    ii. A combination of two chronic feeding studies and one 
carcinogenicity study resulted in rats being fed combined dosages of 0, 
1.2, 2.4, 7.0, 23, 71, 143, and 221 mg/kg/day (males) and 0, 1.6, 3.1, 
7.0, 23, 71, 180, and 221 mg/kg/day (females) with a NOAEL of 1.2 mg/
kg/day (males) and 1.6 mg/kg/day (females) based on the following 
effects: (1) Decreased body weights in both male and female rats at 
dose levels  23 mg/kg/day with a progression of severity to 
the upper levels; (2) decreased food consumption in both male and 
female rats at dose levels  71 mg/kg/day with a progression 
of severity to the upper dose levels; (3) cataracts with associated 
histopathology at dose levels  23 mg/kg/day and lenticular 
changes at dose levels  7.0 mg/kg/day for male and female 
rats; (4) hematological and clinical chemistry value changes at dose 
levels  71 mg/kg/day with increase of severity at the higher 
doses tested; (5) increased absolute and/or relative weights for 
adrenal at dose levels  143 mg/kg/day, for the liver at dose 
levels  71 mg/kg/day, for the testes at dose levels 
 23 mg/kg/day, and for the ovaries at dose levels 
 143 mg/kg/day; (6) microscopic findings were observed in 
the liver, adrenal, pancreas, testes (males), ovaries and uterus 
(females) at dose levels of  7.0 mg/kg/day with a 
progression of severity of histological effects in the upper dose 
levels; and (7) an increased incidence of neoplasms occurred at dose 
levels greater than the maximum tolerated dose (MTD) of  23 
mg/kg/day in the liver, adrenal, pituitary, prostate (males), uterus 
(females), and ovaries (females) at dose levels  143 mg/kg/
day. In the testes (males), Leydig cell adenomas were seen at the MTD 
for dose levels  23.0 mg/kg/day due to the anti-androgenic 
nature of vinclozolin.
    3. Carcinogenicity. A carcinogenicity study in mice fed dosages of 
0, 2.1, 20.6, 432, and 1,225 HDT mg/kg/day (males) and 0, 2.8, 28.5, 
557, and 1,411 (HDT) mg/kg/day (females) with a NOAEL of 20.6 mg/kg/day 
(males) and 28.5 mg/kg/day (females) based on the following effects:
    i. Increased mortality in the HDT as compared to controls;
    ii. Decreased body weights and significant signs of clinical 
toxicity were observed in both male and female mice at the upper two 
dose levels with a progression of severity;
    iii. Hematological and clinical chemistry value changes were 
observed at the highest dose tested;
    iv. Increased absolute and/or relative weights for adrenal and 
liver were observed at the upper two dose levels, atrophic seminal 
vesicles and coagulation glands with reduction of the prostate (males) 
and atrophic uteri were observed at the upper two dose levels;
    v. Microscopic findings were observed in the liver, adrenal, testes 
(males), ovaries and uterus (females), and related sexual organs in the 
upper two dose levels;
    vi An increased incidence of neoplasms occurred at dose levels 
greater than the maximum tolerated dose (> 28.5 mg/kg/day) in the liver 
of female mice.
    4. Developmental toxicity. i. In four developmental toxicity 
studies, vinclozolin was given orally from gestational day (gd) 6 
through 19 as follows: Study 4--dose levels of 0, 15, 50, or 150 mg/kg/
day; study 5--dose levels of 0, 50, 100, 200 mg/kg/day, study 6--dose 
levels of 0, 200, 400 mg/kg/day and study 8--dose levels of 0, 600, and 
1,000 mg/kg/day. At the gd 20, the fetuses were evaluated.
    Maternal toxicity was demonstrated at 600 and 1,000 mg/kg/day by 
the statistically significant increase in absolute and relative adrenal 
and liver weight in study 8. This was the only study where organ 
weights were determined. A maternal NOAEL could not be established and 
therefore, the study was not considered to demonstrate any extra 
sensitivity. No histology was conducted on the organs, but other 
studies have demonstrated lipid accumulation in the adrenals, and 
centrilobular cloudiness of the liver. In addition, a dermal 
developmental study has indicated adrenal and liver weight increases 
occurred at 180 mg/kg/day and higher. Statistically significant 
increases and decreases occurred in the body weight gain and in food 
consumption with no apparent dose relatedness in any of the studies. 
The relative efficiency of food utilization was too variable to be 
definitive.
    Statistically significant male and female fetal body weight 
decrement occurred at 1,000 mg/kg/day. These weight decrements were 
considered test material related. A statistically significant decrease 
occurred in anogenital distance among male fetuses. The term 
pseudohermaphroditism was used to describe the effect because these 
males exhibited decreased anogenital distances, but exhibited 
superficially normal internal testes. The anogenital distance in male 
fetuses was statistically decreased at 50 mg/kg/day and higher in 
studies 4, 6, and 8. (The anogenital index was statistically 
significantly depressed at 150 mg/kg/day and higher). The anogenital 
distance and index were not determined in study 5. The response was 
dose related. Although the anogenital index was not statistically 
significantly depressed at 50 mg/kg/day, it was nominally depressed. 
Considering the significantly depressed anogenital distance at 50 mg/
kg/day and higher and the nominally depressed anogenital index at 50 
mg/kg/day, the NOAEL for this study was considered to be 15 mg/kg/day, 
the lowest dose tested (LDT). These results are consistent with 
hormonal or anti-hormonal effects from the test material.
    Soft tissue examination of fetuses indicated that increased 
incidence occurred in dilated renal pelvis and hydro-ureter at 400 mg/
kg/day in study 6. At higher dose levels in study 8, the incidence of 
dilated renal pelvis and hydro-ureter was nominally increased. The 
failure of the dilated renal pelvis, and hydro-ureter to be 
significantly increased in study 8 was attributed to the fewer litters 
used (7, 5, and 8 in controls, 600, and 1,000 mg/kg/day). The NOAEL for 
these renal effects is considered to be 200 mg/kg/day.
    Skeletal examination of fetuses indicated increased incidence of 
accessory 14th rib at 400 mg/kg/day and in fetuses and litters at 600, 
and 1,000 mg/kg/day. These effects on the 14th rib may be related to 
dose administration. Evaluation of the Preliminary Study suggested a 
dose related increase in 14th ribs at these high dose levels. No other 
dose related effects were reported.
    The developmental toxicity NOAEL was set at 15 mg/kg/day and the 
developmental LOAEL was 50 mg/kg/day based on decreased anogenital 
distance in males. Increased incidence of dilated renal pelvis, hydro-
ureter, and accessary 14th rib may have occurred at 400 mg/kg/day and 
higher. The maternal toxicity LOAEL was < 600 mg/kg/day based on 
increases in absolute

[[Page 44456]]

and relative adrenal and liver weight. Organ weights were not 
determined at lower dose levels.
    ii. A developmental study in rats via dermal exposure for 6 hours/
day on intact skin with dosages of 0, 60, 180, and 360 mg/kg/day HDT 
had a developmental NOAEL of 60 mg/kg/day and a maternal NOAEL of 60 
mg/kg/day based on the following: (1) Increased absolute liver weights 
at dose levels > 180 mg/kg/day; and (2) decreased anogenital distance 
and index at dose levels  180 mg/kg/day.
    iii. A developmental study in rabbits via oral gavage resulted in 
dosages of 0, 20, 80, and 300 mg/kg/day HDT with a developmental NOAEL 
of 300 mg/kg/day and a maternal NOAEL of 300 mg/kg/day based on no 
signs of maternal or meaningful fetal toxicity observed at any of the 
dose levels mentioned.
    iv. A second developmental study in rabbits via oral gavage 
resulted in dosages of 0, 50, 200, and 800 mg/kg/day HDT with a 
development toxicity NOAEL of 200 mg/kg/day and a maternal toxicity 
NOAEL of 50 mg/kg/day based on the following: (1) Severe maternal 
toxicity with simultaneous change in hematological values and high 
number of abortions at the HDT; and (2) increased absolute and/or 
relative weights for adrenal in the mid and high dose groups.
    v. A two-generation rat reproduction study (consisting of two 
studies: Study A--dose levels of 0, 2.0 and 4.1 mg/kg/day; study B--
dose levels of 0, 4.9, 29, 100, and 307 mg/kg/day) with a reproductive 
NOAEL of 4.9 mg/kg/day based on decreased epididymal weight and male's 
inability to mate at dose levels > 100 mg/kg/day and pup effects at 29 
mg/kg/day; and with a parental NOAEL of 4.9 mg/kg/day based on general 
toxicity consistent with previous rat studies at levels > 29 mg/kg/day. 
Study A was performed to clarify an equivocal finding of decreased 
absolute and relative weight of the epididymides without any 
morphological correlation in the male FY and FZ generations in Study B. 
However, the Agency concluded that the effects at the 4.9 mg/kg/day 
dose level were minimal and considered sufficiently close to the NOAEL. 
The study is acceptable and the 4.9 mg/kg/day dose level was considered 
to be the NOAEL.
    5. Mutagenicity. The following test/assays showed no evidence of 
mutagenic activity: Modified Ames Test (3 studies, point mutation); 
Host-Mediated Assay (point mutation); Mouse Lymphoma Test (point 
mutation); In Vitro CHO Cells (point mutation); In Vitro Cytogenetics--
CHO Cells (Chromosome Aberrations); In Vivo Dominant Lethal Test--Male 
NMRI Mouse (Chromosome Aberrations); Rec Assay (2 test, DNA damage and 
repair); In Vitro UDS Test Using Hepatocyte (DNA damage and repair); 
and In Vivo SCE Using Chinese Hamster (DNA damage and repair).
    6. Mechanistic studies-anti-androgenicity activity. A series of 
mechanistic studies (In Vivo and In Vitro) were conducted to define the 
anti-androgenic properties of vinclozolin. The results of these studies 
showed that vinclozolin elicits the anti-androgenic effects by binding 
to androgen sensitive organs.

B. Toxicological Endpoints

    1. Acute toxicity. EPA selected the NOAEL of 6 mg/kg/day (adjusted 
for a single dose) from a developmental toxicity study in rats based on 
decreased ventral prostate weight in male offspring observed at the 
adjusted LOAEL of 11.5 mg/kg/day. The endpoint is the most sensitive 
indicator of acute anti-androgenic developmental toxicity. The 
population subgroup of concern is females (13+) because the endpoint is 
an in utero effect applicable only to females of childbearing age. An 
uncertainty factor of 100 was used to account for interspecies 
extrapolation and intraspecies variation. On this basis, the acute 
reference dose (aRfD) is 0.06 mg/kg/day. EPA determined that a 10X FQPA 
safety factor is applicable, and the margin of exposure (MOE) for the 
population subgroup of concern, females (13+) is 1,000X. The acute 
population adjusted dose (aPAD) is 0.006 mg/kg/day. An acute dose and 
endpoint were not identified for other population subgroups.
    2. Chronic toxicity. EPA has established the Reference Dose (RfD) 
for vinclozolin at 0.012 mg/kg/day. This RfD is based on a NOAEL of 1.2 
mg/kg/day from the combined chronic toxicity/carcinogenicity study in 
rats in which histopathological lesions occurred in the lungs and 
livers of male rats, in ovaries of females, and in the eyes of both 
sexes at the LOAEL of 2.3 mg/kg/day. An uncertainty factor of 100 was 
used to account for interspecies extrapolation and intraspecies 
variation. A 10X FQPA safety factor was added resulting in a cPAD of 
0.0012 mg/kg/day.
    3. Short- and intermediate-term toxicity. For short- and 
intermediate-term dermal and inhalation toxicity, the NOAEL of 3 mg/kg/
day from a rat developmental toxicity study was selected for the 
population subgroup of concern, females (13+). The LOAEL of 6 mg/kg/day 
was based on decreased ventral prostate weights. For short- and 
intermediate-term dermal and inhalation toxicity, the NOAEL of 5 mg/kg/
day from a rat developmental toxicity study was selected for the 
population subgroup of concern, infants and children. The LOAEL of 15 
mg/kg/day was based on delayed puberty. A dermal absorption factor of 
25% was used to correct for route-to-route extrapolation (oral to 
dermal exposure) and a default inhalation absorption factor of 100% was 
assumed for oral to inhalation exposure. The MOE for females (13+), 
infants and children is 1,000X.
    4. Long-term dermal and inhalation toxicity (cancer and non- 
cancer). For chronic non-cancer and cancer dermal and inhalation 
toxicity, EPA selected the chronic NOAEL of 1.2 mg/kg/day from the 
combined rat chronic toxicity/carcinogenicity study in which 
histopathological lesions occurred in the lungs and livers of male 
rats, in ovaries of females, and in the eyes of both sexes at the LOAEL 
of 2.3 mg/kg/day. The Q1 * calculated in a low-
dose linear extrapolation is 2.9  x  10-1 (mg/kg/
day)-1. A dermal absorption factor of 25% was used to 
correct for route-to-route extrapolation (oral to dermal exposure) and 
a default inhalation absorption factor of 100% was assumed for oral to 
inhalation exposure. The cancer assessment includes not only the adult 
U.S. population but also infants and children as well.
    5. Carcinogenicity. Vinclozolin is classified as a Group C 
carcinogen based on Leydig (interstitial testicular) cell tumors in a 
perinatal rat developmental toxicity study. A non-linear (MOE) approach 
was determined to be appropriate based on a weight-of-the-evidence 
conclusion that tumor induction is via an anti-androgenic mechanism. 
Prostate weight decreases occurred at the LOAEL of 6 mg/kg/day; the 
point of departure for use in the non-linear risk assessment is 3 mg/
kg/day (NOAEL). EPA believes that use of the population adjusted dose 
(PAD) for overall anti-androgenic effects (0.0012 mg/kg/day) is also 
protective of cancer effects because it is protective of the anti-
androgenic effects that are, in effect, precursors to tumor formation.
    6. Overall anti-androgenic effects. The Agency has determined that 
use of the most sensitive regulatory toxicity endpoint and the highest 
uncertainty factor (UF) would be protective of the anti-androgenic 
effects on all population subgroups caused by vinclozolin including 
developmental/reproductive effects as well as carcinogenic effects. In 
the case of vinclozolin, the most sensitive toxicity endpoint/dose and 
UF

[[Page 44457]]

are derived from the rat oral chronic/carcinogenicity study, i.e., the 
NOAEL of 1.2 mg/kg/day and an UF of 1,000. The PAD of 0.0012 mg/kg/day 
was used in assessment of risks resulting from the anti-androgenic 
activity of vinclozolin.

C. Exposures and Risks

    1. From food and feed uses. Tolerances have been established (40 
CFR 180.380) for the combined residues of vinclozolin and its 
metabolites containing the 3,5-dichloroaniline moiety, in or on the 
following raw agricultural commodities: Belgian endive tops, cucumbers, 
wine grapes, kiwi fruit, head and leaf lettuce, dry bulb onions, bell 
peppers, raspberries, stone fruit (except plums/fresh prunes), and 
strawberries. There are no U.S. registered vinclozolin products for use 
on wine grapes, cucumbers, and peppers, and the current tolerances for 
these commodities are for imported commodities only. In addition, as a 
risk mitigation measure, BASF requested deletion of the strawberry and 
stone fruit uses from their vinclozolin label on June 30, 1998. The 
Agency published a Federal Register notice announcing the use deletion 
on July 30, 1998, (63 FR 40710) (FRL-6020-9) and under the existing 
stock plan, vinclozolin could be used on strawberries and stone fruit 
until January 30, 2000. Revocation of the stone fruit and strawberry 
tolerances are expected in the near future.
    To further mitigate risk associated with the use of vinclozolin, 
the Agency is considering a proposal submitted by the registrant which 
includes the following items to occur over the next 5 years: A phase 
out of all domestic food uses of vinclozolin except for the use on 
canola, and the reinstatement of the snap bean tolerance for a period 
of 5 years; revocation of all import tolerances except for wine grapes 
to cover residues in wine; future phase out of use on sod farms 
resulting in the remaining turf use limited to golf courses; and 
voluntary cancellation of use on ornamental plants. In addition as a 
short-term risk reduction measure, label amendments were approved on 
June 14, 2000 to add a 24-day pre-harvest interval for sod harvested 
for residential uses.
    The Agency has been petitioned by BASF Corporation to establish 
tolerances on the following commodities: Succulent beans; canola; eggs, 
milk, meat, fat, and meat byproducts of cattle, goats, hogs, horses, 
and sheep; and fat, meat, and meat byproducts of poultry. Risk 
assessments were conducted by EPA to assess dietary exposure from 
vinclozolin as a result of all current tolerances (excluding stone 
fruit and strawberries) and all proposed tolerances. Strawberries and 
stone fruit were excluded because the use of vinclozolin on these crops 
was deleted and significant residues are not expected to occur in these 
crops as the latest possible use of vinclozolin under the existing 
stocks plan was January 30, 2000.
    Section 408(b)(2)(E) authorizes EPA to use available data and 
information on the anticipated residue levels of pesticide residues in 
food and the actual levels of pesticide chemicals that have been 
measured in food. If EPA relies on such information, EPA must require 
that data be provided 5 years after the tolerance is established, 
modified, or left in effect, demonstrating that the levels in food are 
not above the levels anticipated. Following the initial data 
submission, EPA is authorized to require similar data on a time frame 
it deems appropriate. As required by section 408(b)(2)(E), EPA will 
issue a data call-in for information relating to anticipated residues 
to be submitted no later than 5 years from the date of issuance of this 
tolerance.
    Section 408(b)(2)(F) states that the Agency may use data on the 
actual percent of food treated for assessing chronic dietary risk only 
if the Agency can make the following findings: Condition 1, that the 
data used are reliable and provide a valid basis to show what 
percentage of the food derived from such crop is likely to contain such 
pesticide residue; Condition 2, that the exposure estimate does not 
underestimate exposure for any significant subpopulation group; and 
Condition 3, if data are available on pesticide use and food 
consumption in a particular area, the exposure estimate does not 
understate exposure for the population in such area. In addition, the 
Agency must provide for periodic evaluation of any estimates used. To 
provide for the periodic evaluation of the estimate of percent of crop 
treated (PCT) as required by section 408(b)(2)(F), EPA may require 
registrants to submit data on PCT.
    The Agency used PCT data for domestic crops and percent of imported 
crop treated (PICT) data for all imported crops. Data on stone fruits 
and strawberries were not included as the uses have been deleted from 
labels. For the acute analysis, the estimated maximum PCT was used and 
for the chronic analyses, the weighted average PCT was incorporated.
    The Agency believes that the three conditions listed above have 
been met. With respect to Condition 1, PCT estimates are derived from 
Federal and private market survey data, which are reliable and have a 
valid basis. EPA uses a weighted average PCT for chronic dietary 
exposure estimates. This weighted average PCT figure is derived by 
averaging State-level data for a period of up to 10 years, and 
weighting for the more robust and recent data. A weighted average of 
the PCT reasonably represents a person's dietary exposure over a 
lifetime, and is unlikely to underestimate exposure to an individual 
because of the fact that pesticide use patterns (both regionally and 
nationally) tend to change continuously over time, such that an 
individual is unlikely to be exposed to more than the average PCT over 
a lifetime. For acute dietary exposure estimates, EPA uses an estimated 
maximum PCT. The exposure estimates resulting from this approach 
reasonably represent the highest levels to which an individual could be 
exposed, and are unlikely to underestimate an individual's acute 
dietary exposure. The Agency is reasonably certain that the percentage 
of the food treated is not likely to be an underestimate. As to 
Conditions 2 and 3, regional consumption information and consumption 
information for significant subpopulations is taken into account 
through EPA's computer-based model for evaluating the exposure of 
significant subpopulations including several regional groups. Use of 
this consumption information in EPA's risk assessment process ensures 
that EPA's exposure estimate does not understate exposure for any 
significant subpopulation group and allows the Agency to be reasonably 
certain that no regional population is exposed to residue levels higher 
than those estimated by the Agency. Other than the data available 
through national food consumption surveys, EPA does not have available 
information on the regional consumption of food to which the pesticide 
may be applied in a particular area.
    The dietary (food only) risk assessments used anticipated residues 
from field trial data which EPA believes are very conservative for the 
following qualitative reasons: (1) Field trial data assumes that all 
crops are treated at the maximum application rate and harvested at the 
minimum pre-harvest interval (PHI). In practice, crops are sometimes 
treated at lower application rates and harvested at longer PHI's 
leading to lower residues in the crops; (2) Field trial data assumes no 
decline between harvest and consumption of the crop. However, residues 
of vinclozolin will decline between harvest and consumption. Data are 
not available to

[[Page 44458]]

quantify the extent of this decline; (3) Home ``processing'' was not 
accounted for in the risk assessment. Practices such as washing, 
peeling, and cooking could lead to significantly lower residues than 
those from field trial data; and (4) For the acute dietary risk 
assessment, the vinclozolin metabolites of greatest concern are those 
closely related to the parent compound. Use of field trial data in the 
acute dietary assessment assumes that all residues have structures 
closely related to the parent compound and that they all elicit the 
developmental effects of concern. In reality, many metabolites 
convertible to 3,5-DCA may have structures different from the parent 
such that they are not of acute concern.
    Although EPA cannot quantify for vinclozolin the combined residue 
reduction from the factors identified above, for many pesticides the 
difference in residues between field trial and monitoring data can be 
an order of magnitude 10X or more. The registrant is submitting 
processing (washing/cooking) studies which could allow for further 
future refinement of the dietary risk assessment.
    The Dietary Exposure Evaluation Model (DEEM), which 
incorporates consumption data generated in USDA's Continuing Surveys of 
Food Intakes by Individuals (CSFII), 1989-1992 was used to conduct the 
dietary risk assessments. For refined acute dietary risk assessments, 
the entire distribution of consumption events for individuals is 
multiplied by the distribution of residues to obtain a distribution of 
exposures in mg/kg/day. This is a probabilistic analysis, referred to 
as a ``Monte Carlo'' analysis and the risk is reported at various 
percentiles of exposure. For chronic dietary risk assessments, the 3-
day average of consumption for each population subgroup is combined 
with residues in commodities to determine average exposure in mg/kg/
day.
    i. Acute exposure and risk. Acute dietary risk assessments are 
performed for a food-use pesticide if a toxicological study has 
indicated the possibility of an effect of concern occurring as a result 
of a 1-day or single exposure. The acute dietary exposure estimates for 
the only population subgroup of concern (taking into account the 
toxicological studies on vinclozolin), females (13+), utilized the 
following percentage of the aPAD (0.006 mg/kg/day) at the various 
percentiles of exposure as indicated: 120% of the aPAD at the 
99.9th percentile; 98% of the aPAD at 99.85th 
percentile; 83% of the aPAD at the 99.8th percentile; 73% of 
the aPAD at the 99.75th percentile; 60% of the aPAD at the 
99.6th percentile; and 49% of the aPAD at the 
99.5th percentile. Because the anticipated residues are 
based on field trial data and are conservative estimates (i.e. they 
overestimate residue levels), the Agency believes that basing its 
exposure estimate on the very upper ranges of potential exposure (the 
99.5th and above) will unreasonably overestimate exposure. 
Considering this factor in choosing a population percentile of exposure 
that is adequately protective was explicitly discussed in EPA's policy 
on the use of population percentiles of exposure in acute risk 
assessments. U.S. EPA (Office of Pesticide Programs), ``Choosing A 
Percentile of Acute Dietary Exposure as a Threshold of Regulatory 
Concern'' (March 2000). In addition, as part of the reregistration 
process for vinclozolin, the registrant is proposing to further reduce 
the dietary exposure to vinclozolin, and the Agency may request future 
tolerance revocations for certain commodities as well. The very 
conservatively estimated acute dietary risk (food only) does not exceed 
the Agency's level of concern.
    ii. Chronic exposure and risk. The chronic dietary exposure 
estimates expressed as a percentage of the cPAD (0.0012 mg/kg/day) were 
4% for the U.S. population and 7% for the most highly exposed 
population subgroup, children (1-6 years old). EPA generally has no 
concern for exposures below 100% of the cPAD because the cPAD 
represents the level at or below which daily aggregate dietary exposure 
over a lifetime will not pose appreciable risk to human health. 
Therefore, the chronic dietary risk (food only) does not exceed the 
Agency's level of concern.
    iii. For cancer and anti-androgenic risk assessment. EPA believes 
that vinclozolin should be classified as a Group C carcinogen. The 
cancer risk assessment included both the U.S. population and infants 
and children. EPA believes the key concern for infants and children 
exposed to vinclozolin is the potential for developmental/reproductive 
effects related to the anti-androgenic properties of vinclozolin. In 
addition, the possibility of increased incidence of testicular Leydig 
cell tumors in adults as a result of exposure to vinclozolin as infants 
or children cannot be ruled out. However, due to the relationship 
between vinclozolin's anti-androgenic properties and its carcinogenic 
effects, the Agency believes protecting against the anti-androgenic 
effects would also be protective against potential carcinogenic effects 
to all population subgroups (including infants and children).
    Accordingly, the cPAD will be protective against potential 
carcinogenic effects as well as the developmental/reproductive effects. 
The cPAD already incorporates the full, additional 10x safety factor 
for the protection of infants and children (i.e., it is derived from 
the NOAEL of 1.2 mg/kg/day with an MOE of 1,000 - 10x for intraspecies 
extrapolation; 10x for interspecies variation; and 10x for FQPA). Since 
this approach (using the cPAD) would be more protective than the 
proposed POD for cancer risk assessment of 3 mg/kg/day, and includes an 
additional 10x factor for the protection of infants and children, a 
separate non-linear risk assessment for cancer is not necessary.
    Exposure estimates expressed as a percentage of the anti-androgenic 
PAD (0.0012 mg/kg/day) were 4% for the general U.S. population and 7% 
for the most highly exposed population subgroup, children (1-6 years 
old). In addition, as a point of comparison, the MOE was calculated to 
be 75,000 for the general U.S. population and 38,000 for children (1-6 
years old).
    2. From drinking water. In general, available monitoring data are 
of limited use because metabolite concentration measurements were not 
performed. For both surface water and groundwater, the sum of 
vinclozolin and its principal metabolites, assumed to degrade 
completely to 3,5-dichloroaniline (hereafter referred to as 3,5-DCA), 
have been used to assess the cancer risk associated with 3,5-DCA 
whereas vinclozolin per se has been used for the vinclozolin risk 
assessments.
    In the absence of reliable, available monitoring data, EPA uses 
models to calculate the estimated environmental concentrations (EECs) 
of pesticides in ground and surface water. However, EPA does not use 
these model estimates to quantify risk. Currently, EPA uses DWLOCs as a 
surrogate to capture risk associated with exposure to pesticides in 
drinking water. A DWLOC represents 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 (if any). A DWLOC will vary depending on the residue 
level in foods, the toxicity endpoint and the drinking water 
consumption patterns and body weights for specific population 
subgroups. The calculated DWLOC is compared to the model estimate 
(EEC), and if the model estimates are below the DWLOC, the risks are 
not considered to be of concern.
    For estimating groundwater concentrations of vinclozolin and 3,5-
DCA, EPA used the Screening

[[Page 44459]]

Concentration in Ground Water (SCI-GROW) model. The SCI-GROW model is 
based on scaled groundwater concentration from groundwater monitoring 
studies, and environmental fate properties (aerobic soil half-lives and 
organic carbon partitioning coefficients-Koc's). SCI-GROW provides a 
screening concentration which is an estimate of likely groundwater 
concentrations if the pesticide were used at the maximum allowed label 
rate in areas with groundwater vulnerable to contamination. In most 
cases, a majority of the pesticide use area will have groundwater that 
is less vulnerable to contamination than the areas used to derive the 
SCI-GROW estimate. Using SCI-GROW, the acute and chronic ground water 
EEC of vinclozolin per se is 0.53 parts per billion (ppb), and the 
acute and chronic ground water EEC of 3,5-DCA is 2.65 ppb.
    For estimating surface water concentrations of vinclozolin and 3,5-
DCA, EPA used tier II models, Pesticide Root Zone Model (PRZM) 3.12 and 
Exposuer Analysis Modeling System (EXAMS) 2.975, which assumed decline 
of parent vinclozolin and formation and decline of metabolites in a 
sequential degradation pattern in both field and pond such that 
degradation proceeds completely to 3,5-DCA. Vinclozolin per se is a 
major residue near application, but eventually the metabolites are the 
principal residues in both surface and drinking water. The metabolites 
are the only residues that are likely to be found in the environment 
except fairly soon after application. The scenario used in the model 
(application to onions in California) is the worst-case scenario for 
water modeling. A tier II EEC for a particular crop or use is based on 
a single site that represents a high exposure scenario for the crop or 
use. Weather and agricultural practices are simulated at the site for 
36 years to estimate the probability of exceeding a given concentration 
(maximum concentration or average concentration) in a single year. 
Maximum EECs are calculated so that there is a 10% probability that the 
maximum concentration in a given year will exceed the EEC at the site; 
peak and chronic EECs were calculated so that there is a 10% 
probability the maximum average concentration for a given duration (4-
day, 21-day, etc.) will equal or exceed the EEC at the site. This can 
also be expressed as an expectation that water concentrations will 
exceed EECs once every 10 years. The acute (peak) surface water EEC for 
vinclozolin is 5.68 ppb and for 3,5-DCA is 26 ppb. The chronic (annual 
mean) surface water EEC for vinclozolin is 0.165 ppb and for 3,5-DCA is 
3.12 ppb.
    i. Acute exposure and risk. For the population subgroup of concern, 
females (13+), the DWLOCs for vinclozolin per se at the various 
percentiles of exposure are as follows: 0 ppb at the 99.9th 
percentile; 4 ppb at the 99.85th percentile; 30 ppb at the 
99.8th percentile; 47 ppb at the 99.75th 
percentile; 80 ppb at the 99.6th percentile; and 92 at the 
99.5th percentile. At all but the very highest percentiles 
of exposure (99.85th and above), the DWLOC for vinclozolin 
per se is higher than the EEC of 5.68 ppb in surface water and 0.53 ppb 
in ground water. As explained above, given the level of refinement in 
the vinclozolin exposure estimate, EPA believes using the highest 
percentiles of exposure in estimating risk would unreasonably overstate 
risk. Therefore, EPA is reasonably certain that exposure to vinclozolin 
per se in drinking water will result in no harm.
    ii. Chronic exposure and risk. The following chronic DWLOCs were 
calculated for vinclozolin per se: general U.S. population, 41 ppb; 
females (13+) 35 ppb; and children (1-6 years old), 11 ppb. The lowest 
DWLOC of 11 ppb for children 1-6 years old is higher than the EEC of 
0.165 ppb in surface water and 0.53 ppb in ground water. Therefore, EPA 
is reasonably certain that exposure to vinclozolin in drinking water 
will result in no harm.
    3. From non-dietary exposure. There are no vinclozolin pesticide 
products registered for use by homeowners. Therefore, there is no 
potential for homeowner handler exposure to vinclozolin pesticide 
products. Vinclozolin can, however, be occupationally used in a manner 
that may lead to post-application exposures to the general population, 
in particular, golfers playing on treated golf courses and homeowners 
and their families coming into contact with or playing on sod which was 
previously treated on a sod farm. A chemical-specific turf exposure 
study was used to measure human exposure as well as residue dissipation 
over time.
    All residential exposures are considered to be short-/intermediate-
term duration (i.e., 1 day to 1 week and 1 week to several months, 
respectively), and the same endpoint applies to both durations of 
exposure. As the endpoints selected are from oral toxicity studies 
(NOAEL of 3 mg/kg/day for females (13+)) and NOAEL of 5 mg/kg/day for 
infants and children, route-to-route exposure was corrected by applying 
a 25% dermal absorption factor and a 100% default inhalation absorption 
factor was assumed. A 100% safety factor was used and a 10X FQPA safety 
factor was added raising the Agency's level of concern to 1,000.
    Post-application risks to the general population were considered 
for golfers following treatment of greens, tees, and fairways. Adult 
golfer exposures, women (13+), were less than the Agency's level of 
concern even on the day of application (MOE = 1,700). Given the 
magnitude of the MOE for adult women golfers, the Agency does not 
believe that the risks to child golfers would exceed the Agency level 
of concern either because the skin surface area/body weight ratio of 
the typical child golfer is similar to that of adults (within 15%). 
Therefore, the MOE for a child golfer is only slightly less than the 
MOE for adult golfers.
    The exposure scenario used for toddlers playing on treated sod was 
the worst case scenario. The exposure scenario assumed that toddlers 
were playing on sod which had been treated with vinclozolin on a sod 
farm that same day, cut and laid in a residential setting. The MOE for 
toddlers is 33. This MOE represents an upper-bound exposure which 
includes dermal and non-dietary ingestion pathways (dermal exposure and 
hand-to-mouth oral exposure to grass and dirt). EPA has calculated that 
foliar dislodgeable residues on the sod decline such that risks fall 
beneath the Agency's level of concern 26 days after application (MOE = 
1,100). To mitigate the unacceptable risk resulting from exposure 
before the 26-day period has elapsed; the registrant has proposed 
deletion of use on sod farms; amended the label to add a 24-day pre-
harvest interval; and initiated the immediate restickering of all 
product in the channels of trade to require a 24-day period before sod 
can be harvested. It is assumed that, at a minimum, sod harvesting and 
replanting in a residential setting would take an additional 2 days; 
thereby, providing a total of 26 days for residues of vinclozolin to 
decline to an acceptable level. Although the Agency's level of concern 
is exceeded, EPA believes that these risk reduction measures when taken 
into consideration with the extremely conservative exposure scenario 
and exposure assumptions will immediately reduce the exposure such that 
it is below the Agency's level of concern.
    4. Cumulative exposure to substances with a 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

[[Page 44460]]

effects of a particular pesticide's residues and ``other substances 
that have a common mechanism of toxicity.''
    Vinclozolin, procymidone, and iprodione are members of the imide 
group of the dicarboximide class of fungicides. Each of these three 
pesticides can metabolize to 3,5-DCA. FQPA requires EPA to estimate 
cumulative risk from consumption of food and water containing 3,5-DCA 
derived from vinclozolin, iprodione, and procymidone.
    i. Acute exposure and risk. EPA has certain evidence that these 
compounds induce similar toxic effects but has not yet determined 
whether or not these compounds modulate androgens by a common mechanism 
of toxicity. In fact, there is evidence that iprodione does not share a 
common mechanism of toxicity as it disrupts the endocrine system by 
inhibiting androgen synthesis rather than competing for the androgen 
receptor as vinclozolin does. In addition, these three chemicals do not 
have any known metabolites/degradates in common with the possible 
exception of 3,5-DCA which is structurally and toxicologically 
different from the parent compounds and unlikely to be an androgen 
receptor antagonist.
    EPA has, at this time, some data which suggests that vinclozolin 
and procymidone have a common mechanism of toxicity. An article 
published in Toxicology & Industrial Health (Vol. 15, ISS 1-2, 1999, 
page 80-93) which reports the findings by Dr. Earl Gray, National 
Health and Environmental Effects Research Laboratory, U.S. EPA, 
Research Triangle Park, NC, suggests that procymidone alters sexual 
differentiation in the male rat by acting as an androgen-receptor 
antagonist in vivo and in vitro. The Agency has yet to make a 
conclusion as to whether these data are sufficient to evaluate whether 
vinclozolin and procymidone have a common mechanism of toxicity. Within 
the next year, the Agency expects to reach a conclusion as to whether 
these data are sufficient to determine that vinclozolin and procymidone 
have a common mechanism of toxicity.
    Even if it is assumed that vinclozolin and procymidone share a 
common mechanism of toxicity, EPA believes that it can still make the 
finding of reasonable certainty of no harm for vinclozolin because any 
cumulative risk resulting from adding procymidone residues in wine to 
vinclozolin exposure is unlikely to differ significantly from the risk 
of vinclozolin alone. This conclusion is based on a number of factors. 
The exposure assessment for vinclozolin estimates that vinclozolin 
exposure through wine grapes contributes < 2% of the total vinclozolin 
exposure. The percent of imported wine grapes that are treated with 
procymidone is similar to that of vinclozolin (estimated 10% of wine 
grapes treated with vinclozolin and 9.4% of wine grapes treated with 
procymidone), and therefore, the exposure pattern for these chemicals 
is similar. In addition, the exposure estimates conservatively assume 
that all wine bearing vinclozolin residues also contain procymidone 
residues. In all likelihood, wine grapes would be treated with either 
vinclozolin or procymidone but not both chemicals. Therefore, EPA 
believes that vinclozolin exposure and procymidone exposure through 
wine grapes would each add < 2% to the ``cumulative exposure''. As 
noted above, the acute food-only risk of vinclozolin is 83% of the aPAD 
at the 99.8th percentile of exposure, and the acute ground 
water EEC of 0.53 ppb and the acute surface water EEC of 5.68 ppb are 
lower than the drinking water DWLOC which is 30 ppb at the 
99.8th percentile of exposure. EPA believes there is 
ultimately enough room in the risk cup to accommodate vinclozolin and 
procymidone risk, even, if in the future, EPA does determine that 
procymidone and vinclozolin share a common mechanism of toxicity.
    ii. Carcinogenic exposure and risk. Since 3,5-DCA is not a 
registered pesticide, there is no FIFRA toxicology data base for this 
compound. EPA has used the Q1* for p-chloroaniline (PCA) to 
assess the carcinogenicity (only toxicological endpoint identified for 
3,5-DCA) for other structurally related chloroanilines. EPA's approach 
on chloroanilines is to consider chloroaniline metabolites to be 
toxicologically equivalent to PCA unless there is sufficient evidence 
that the metabolite is not carcinogenic. A Q1* of 6.38  x  
10-2 (mg/kg/day)-1 has been calculated for p-
chloroaniline based on the spleen sarcoma rate in male rats from a 
National Toxicology Program bioassay.
    Exposure to 3,5-DCA was evaluated from the following sources: 
residues of vinclozolin- and iprodione-derived 3,5-DCA in food and 
wine, residues of procymidone-derived 3,5-DCA in imported wine, and 
3,5-DCA residues in water from domestic agricultural uses of iprodione 
and vinclozolin. There are no U.S. registrations for procymidone. 
Therefore, an evaluation of exposure to procymidone-derived 3,5-DCA in 
water is not appropriate.
    a. Food risk-- (1) From vinclozolin-derived 3,5-DCA residues. 
Cancer risks were 5.1  x  10-7 for all crops, including 
strawberries and stone fruits. Cancer risks were 2.6  x  
10-7 for all crops, excluding strawberries and stone fruits. 
Neither of these risks exceed the Agency's level of concern.
    (2) From iprodione-derived 3,5-DCA residues. As stated in the July 
1998 Iprodione RED, the cancer risk associated with 3,5-DCA derived 
from iprodione was 6  x  10-9. This risk does not exceed the 
Agency's level of concern.
    (3) From procymidone-derived 3,5-DCA residues. The cancer risk 
associated with 3,5-DCA in imported wine produced from grapes treated 
with procymidone was estimated to be 3.7  x  10-7. This risk 
does not exceed the Agency's level of concern
    b. Drinking water risk--(1) From vinclozolin derived 3,5- DCA. As 
stated previously, Tier II surface water EECs were generated using 
PRZM/EXAMS for 3,5-DCA. Onions grown in California were considered to 
be the worst-case scenario for water modeling. The highest chronic EEC 
is 3.12 ppb in surface water while the carcinogenic DWLOC for 3,5-DCA 
has been calculated to range from 0.47 ppb to 1.6 ppb. Therefore, the 
EEC exceeds the DWLOC indicating a potential for concern. The onion 
scenario was selected because this use site represents the highest 
maximum seasonal rate currently allowed on vinclozolin labels. However, 
the registrant has requested deletion of onions after this growing 
season (July 15, 2000). If the Agency accepts this request, this 
scenario is not appropriate for use in a carcinogenic risk assessment 
which represents life-time exposure.
    Assuming acceptance of BASF's use deletion request, the 
carcinogenic DWLOC for 3,5-DCA (based on the commodities available for 
consumption after this use season) has been calculated to range from 
0.46 ppb to 1.6 ppb. Using Tier II PRZM/EXAMS, the modeled EECs are 
0.64 ppb for lettuce and 0.34 ppb for canola. The use site which 
represents the highest modeled exposure in drinking water is golf 
courses. Application to golf course turf is currently permitted on 
grass mowed at 1 inch or less. Using the Tier I generic expected 
environmental concentration (GENEEC) model, the Agency has calculated a 
chronic EEC of 0.29 ppb based on application to tees and greens and a 
chronic EEC of 2.33 ppb assuming application to tees, greens, and 
fairways. These EECs were the result of refinements to the GENEEC 
model. These refinements included the incorporation of an 87 percent 
crop area (PCA) factor as well as the percentage of the golf course 
that actually receives

[[Page 44461]]

pesticide treatment, bringing the resulting PCA factor down to 17%. It 
was assumed that tees and greens comprise 2.8% of the acreage of a golf 
course. When fairways are included, an additional 16.7% of the golf 
course is treated. The EEC of 2.33 ppb exceeds the DWLOC. In evaluating 
whether this EEC indicated a risk of concern EPA considered the 
following factors:
    (i) The drinking water assessment on turf is based on GENEEC, a 
screening-level Tier I model. At present, PRZM-EXAMS, the Tier II 
model, does not have the appropriate parameters to accurately model 
turf runoff. Although GENEEC is not an ideal tool for use in drinking 
water risk assessments, it can provide high-end estimates of the 
concentrations that might be found in a confined pond of one hectare. 
Drinking water from surface water sources does not typically come from 
this type of scenario, but rather from bodies of water that are 
substantially larger than such ponds and from diverse watersheds. 
Unlike a confined pond, there is always some flow (in a river) or turn 
over (in a lake or reservoir) resulting in an over-estimation of the 
persistence of the chemicals near the drinking water utility intakes. 
Although a PCA of 17% was used to refine the model, the Agency 
recognizes that there are still uncertainties in the accuracy of the 
model to represent drinking water concentrations.
    (ii) The GENEEC model uses the 56-day average of pesticide 
concentrations immediately after an event (application of pesticide). 
This short time-period may not adequately characterize a person's 
average daily exposure over a year, even more so, over a life time of 
70 years.
    (iii) The GENEEC model assumes that once in every 10 years the EEC 
will be exceeded. For the other 9 out of 10 years the level of residue 
in drinking water is likely to be below the EEC with at least one half 
of the years falling significantly below by a factor of 5 to 10. 
Therefore, a person may be exposed to the EEC once in every 10 years or 
a total of seven times during a lifetime of 70 years. The Agency 
believes the potential for such a lifetime exposure is minimal.
    The first of these factors raises some concern because there is a 
possibility that GENEEC may underpredict residue levels although such 
underprediction would not be expected to be great. The second and third 
factors, on the other hand, could lead to a significant overstatement 
of drinking water exposure values. In light of all of these factors, 
EPA believes that it is likely there is no risk of concern from 
exposure to vinclozolin-derived 3,5-DCA.
    Nonetheless, the exceedance of the DWLOC, based on a screening 
level model, does indicate a need to take steps to insure that 
exposures do not raise a risk of concern. Therefore, the Agency is 
considering requiring the registrants of vinclozolin and iprodione to 
submit targeted surface water monitoring studies. The studies would be 
used to compare the existing modeled results to the more accurate data. 
The Agency will also consider requiring BASF to develop a survey of 
golf course superintendents to obtain current information on actual 
vinclozolin use patterns. Estimates for turf use will be examined 
further pending receipt of better usage characterization data. Lastly, 
the Agency is considering requiring additional toxicological 
information on 3,5-DCA from the registrants of vinclozolin, iprodione 
and procymidone, including data for use in evaluating the carcinogenic 
potential of this metabolite.
    (2) Iprodione 3,5-DCA. As stated in the RED, the DWLOC for 3,5-DCA 
derived from domestic uses of iprodione was estimated to be 0.55 ppb. 
The 3,5-DCA EEC in surface water associated with the use of iprodione 
alone was estimated to be 0.45 ppb. Thus, the iprodione derived 3,5-DCA 
carcinogenic DWLOC is not exceeded.
    (3) From procymidone 3,5-DCA. There is no drinking water exposure 
because procymidone is not registered for use in the United States.
    c. Cumulative risk. The cumulative, food-only cancer risk 
associated with 3,5-DCA derived from all three of these imide 
fungicides is 9.2  x  10-7 (includes stone fruit and 
strawberries) and the cumulative food-only cancer risk is 6.3  x  
10-7 when stone fruit and strawberries are excluded. There 
is uncertainty in the above risk estimates in that a surrogate 
Q1* is being used for 3,5-DCA. However, due to the 
structural similarities of 3,5-DCA and p-chloroaniline (PCA), EPA 
believes that for 3,5-DCA, the use of the PCA Q1* represents 
an upper-bound estimate. The Agency is considering requiring 
registrants of vinclozolin, iprodione, and procymidone to provide 
additional toxicological information on 3,5-DCA including data for use 
in evaluating the carcinogenic potential. The cumulative, food-only 
cancer risk estimates are conservative and are considered to be a 
negligible cancer risk.
    The 3,5-DCA DWLOC from all three imide fungicides (including 
canola, snap beans and those currently registered vinclozolin uses 
which are not being supported after this use season) ranges from 0.26 
ppb to 1.4 ppb. The estimated concentration of 3,5-DCA in water from 
applications of iprodione (1998 iprodione RED) is 0.45 ppb and falls 
within the range of the aggregated DWLOC cited above. The estimated 
concentration of 3,5-DCA in water from applications of vinclozolin 
after this use season is estimated to range from 0.29 ppb to 2.33 ppb. 
As already stated, this range could potentially present a risk of 
concern based on the model, however, based on how the model estimates 
residue concentrations for cancer assessment, EPA believes that it is 
unlikely that a cancer risk of concern is present.

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

    1. Acute risk. The acute dietary (food only) risk does not exceed 
the Agency's level of concern at the percentiles of exposure up to the 
99.8th percentile. Using anticipated residues, PCT data, and 
PICT data, the population subgroup of concern, females (13+) utilized 
83% of the dietary (food only) aPAD at the 99.8th percentile 
of exposure. For drinking water, the EEC of 5.68 ppb in surface water 
and the EEC of 0.53 in groundwater did not exceed the DWLOC of 30 ppb 
at the 99.8th percentile of exposure.
    2. Chronic risk. Using the exposure assumptions described above, 
EPA believes that aggregate dietary exposure to the U.S. population 
will use 4% of the cPAD and exposure to the most highly exposed 
population subgroup, children (1-6 year old) will use 7% of the cPAD. 
The chronic DWLOCs for vinclozolin were 41 ppb for the general U.S. 
population and 35 ppb for the most highly exposed population subgroup, 
women (13+). The chronic DWLOCs were higher than the chronic EEC of 
0.53 ppb in ground water and 0.165 ppb in surface water. EPA generally 
has no concern for exposures below 100% of the cPAD because the cPAD 
represents the level at or below which daily aggregate dietary exposure 
over a lifetime will not pose appreciable risks to human health.
    3. Short- and intermediate-term risk. Short- and intermediate-term 
aggregate exposure takes into account chronic dietary food and water 
(considered to be a background exposure level) plus indoor and outdoor 
residential exposure. All residential exposures are considered to be 
short- and intermediate-term duration and since the same endpoint 
applies to both durations of exposures, the dermal and inhalation 
exposures must be aggregated together with the food and water exposures 
for each population subgroup

[[Page 44462]]

of concern, females (13+) and infants and children. The risks currently 
exceed the Agency's level of concern. However, when considering the 
conservative method of exposure estimations previously discussed, and 
the following risk mitigation measures (stone fruit and strawberry use 
deletion, and the immediate restickering of all vinclozolin products 
for sod farm use to include a 24-day period before harvesting), the MOE 
is 1,010 for aggregate risks to the population subgroups of 
concern, females (13+) and infants and children as well as the general 
U.S. population resulting from vinclozolin uses are not of concern. 
Therefore, the risks do not exceed the Agency's level of concern.
    4. Aggregate cancer risk for U.S. population. Because the overall 
anti-androgenic effects are a prerequisite for hyperplasia and tumor 
formation, and are considered to be protective of the potential 
carcinogenic outcome of exposure to the anti-androgenic vinclozolin and 
its metabolites, the overall anti-androgenic aggregate risk which are 
identical to the chronic aggregate risk. The chronic aggregate risks 
are presented. The chronic (non-cancer) aggregate risk was below the 
Agency's level of concern for food and drinking water sources of 
exposure. Chronic food-source risks were 7% of the cPAD when 
stone fruit and strawberries are excluded (uses have been canceled). 
Estimated environmental concentrations were compared to the chronic 
DWLOCs. The chronic EEC for residues of vinclozolin per se in ground 
water (0.53 ppb) was below the chronic DWLOCs for water consumption by 
adults (41 ppb for the general U.S. population and 35 ppb for females 
(13+)) and by children (11 ppb).
    Cancer risks from vinclozolin derived 3,5-DCA were 2.6  x  
10-7 for all crops, excluding strawberries and stone fruits. 
This risk does not exceed the Agency's level of concern. The 3,5-DCA 
DWLOC from all three Imide fungicides (including canola, snap beans and 
those currently registered vinclozolin uses which are not being 
supported after this use season) ranges from 0.26 ppb to 1.4 ppb. The 
3,5-DCA EEC resulting from iprodione use is 0.45 ppb and falls with the 
range of the aggregated DWLOC cited above. The 3,5-DCA EEC resulting 
from vinclozolin use after this use season is estimated to range from 
0.29 ppb to 2.33 ppb. As already stated, this range could potentially 
present a risk of concern based on the model, however, based on how the 
model estimates residue concentrations for cancer assessment, EPA 
believes that it is unlikely that a cancer risk of concern is present.
    5. 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 vinclozolin 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 vinclozolin, 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 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 prenatal and postnatal toxicity and 
the completeness of the data base unless EPA determines that a 
different margin of safety will be safe for infants and children.
    ii. Prenatal and postnatal sensitivity. The rationale for retaining 
the 10X FQPA safety factor is explained below:
    a. There is evidence of increased susceptibility of offspring 
following in utero exposure to vinclozolin in the prenatal 
developmental toxicity study in rats.
    b. A developmental neurotoxicity study in rats with an expanded 
protocol is required for vinclozolin as a result of concern for the 
anti-androgenic properties of vinclozolin and its metabolites.
    iii. Conclusion. Based on the developmental and reproductive data 
for vinclozolin, EPA determined that an additional 10X safety factor 
for the protection of infants and children (as required by FQPA) should 
be retained.
    2. Acute risk. No study with vinclozolin indicated that acute 
exposure to vinclozolin is likely to cause an adverse effect of concern 
on infants or children or the general public with the exception of the 
in utero effects on the developing fetus. Risks to the fetus are 
estimated by examining exposure to women of child-bearing age.
    3. Chronic risk. Using the exposure assumptions described in this 
unit, EPA has concluded that aggregate exposure to vinclozolin from 
food will utilize 7% of the cPAD for infants and children. EPA 
generally has no concern for exposures below 100% of the cPAD because 
the cPAD represents the level at or below which daily aggregate dietary 
exposure over a lifetime will not pose appreciable risks to human 
health. Since the EEC's for residues of vinclozolin per se are lower 
than the chronic DWLOC's, EPA does not expect the aggregate exposure to 
exceed 100% of the cPAD.
    4. Short- or intermediate-term risk. The short- and intermediate-
term risks currently exceed the Agency's level of concern (MOE = 
1,000). However, the Agency believes the exposure estimates are 
conservative, as previously discussed, and therefore, overestimate 
risk. When the following risk mitigation measures (stone fruit and 
strawberry use deletion, and the immediate restickering of all 
vinclozolin products for sod farm use to include a 24-day period before 
harvesting) are taken into consideration, the MOE is  1,010 
for aggregate risks to infants and children resulting from use of 
vinclozolin. Therefore, the risks do not exceed the Agency's level of 
concern.
    5. 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 vinclozolin 
residues.

IV. Response to Public Comments

A. Natural Resources Defense Council Comments

    1. Comment number 1. NRDC argues that EPA is not authorized to use 
percent crop treated information in acute risk assessments. NRDC bases 
this argument on the fact that the provision explicitly addressing 
percent crop treated information, section 408(b)(2)(F), only mentions 
use of such information in chronic assessments.
    Agency response. EPA disagrees with this interpretation of the 
FFDCA. FFDCA Section 408(b)(2)(D)(vi) directs EPA, in making tolerance 
decisions, to consider ``available information concerning the aggregate 
exposure levels of consumers to the pesticide chemical residue.''
21 U.S.C. 346a(b)(2)(D)(vi). This is a broad mandate that includes all 
manner of information bearing on exposure, not the least of which would 
be percent crop treated information. Thus, EPA believes that subsection 
(b)(2)(D)(vi) authorizes use of percent crop treated information in 
both acute and chronic risk assessments.
    Congress explicitly addressed use of percent crop treated 
information in section 408(b)(2)(F) where it imposed certain conditions 
on EPA's use of

[[Page 44463]]

percent crop treated information in chronic risk assessments. Section 
408(b)(2)(F) states:

    In establishing, modifying, leaving in effect, or revoking a 
tolerance for a pesticide chemical residue, the Administrator may, 
when assessing chronic dietary risk, consider available data and 
information on the percent of food actually treated with the 
pesticide chemical (including aggregate pesticide use data collected 
by the Department of Agriculture) only if the Administrator--
    (i) finds that the data are reliable and provide a valid basis 
to show what percentage of the food derived from such crop is likely 
to contain such pesticide chemical residue;
    (ii) finds that the exposure estimate does not understate 
exposure for any significant subpopulation group;
    (iii) finds that, if data are available on pesticide use and 
consumption of food in a particular area, the population in such 
area is not dietarily exposed to residues above those estimated by 
the Administrator; and
    (iv) provides for the periodic reevaluation of the estimate of 
anticipated dietary exposure.

21 U.S.C. 346a(b)(2)(F) (emphasis added). Although this paragraph 
affirms the ability of EPA to use percent crop treated information for 
chronic dietary risk assessments, the clear thrust of this paragraph is 
to impose four limitations on the use of such information in chronic 
risk assessments (i.e. the limitations set forth in clauses (i)--(iv) 
following the ``only if''). Because the limitations expressly apply 
only ``when assessing chronic dietary risk'', Congress did not impose 
any limitation on the authority in subsection (b)(2)(D)(vi) to consider 
percent crop treated for risk assessments that consider risks other 
than chronic ones (i.e. acute risks).
    NRDC contends that subparagraph (F) impliedly bars EPA from relying 
on percent crop treated information for acute risk assessments under 
subparagraph (D)(vi) because subparagraph (F) only mentions chronic 
risk assessments. EPA, however, does not believe that the statutory 
silence on acute risk assessments in subparagraph (F) compels such an 
interpretation. In fact, the statutory structure suggests the converse 
conclusion. Subparagraph (F) clearly sets forth that percent crop 
treated information may be used in chronic risk assessments ``only if'' 
four conditions can be met. If Congress had intended that this 
provision limit EPA's general authority to consider percent crop 
treated information other than as applied to chronic risk assessments, 
the reference to chronic risk assessments should not have been included 
as part of the introductory clause but as one of the ``only if'' 
conditions. Failure to include it as one of the ``only if'' conditions 
suggests that Congress was merely setting out rules for chronic risk 
assessments and not making a broader statement about use of percent 
crop treated information generally.
    Moreover, it is not surprising that Congress chose only to address 
use of percent crop treated information in the context of chronic risk 
assessment given EPA's historical practice regarding use of percent 
crop treated data. Although EPA has considered percent crop treated 
information in chronic risk assessment for decades, use of such 
information in acute risk assessments is a relatively recent 
phenomenon, and Congress, in 1996, may have either not been aware of 
the rapidly evolving risk assessment techniques for acute hazards or 
believed that it was premature to enact statutory requirements as to 
such assessments.
    There were two key events in 1995 that triggered the use of percent 
crop treated information in acute risk assessments: (1) A new focus on 
acute hazards; and (2) a new risk methodology for assessing acute 
risks. In 1995, EPA began for the first time consistently identifying 
acute endpoints and performing acute risk assessments for each 
pesticide. EPA was initially reluctant to use percent crop treated 
information in such assessments due to the difference between acute and 
chronic risks. With chronic risk, EPA is concerned with hazards that 
occur from exposure over an extended time period. Thus, in assessing 
chronic risk, EPA generally combines percent crop treated information 
with data on residue levels to produce an estimate of the residue level 
a person is exposed to over an extended time-frame assuming the person 
gets a mixture of treated and untreated commodities. With acute 
hazards, EPA is concerned with the risk from a single exposure and thus 
is interested in the exposure that can come from a single commodity. 
Accordingly, for acute risk assessments it is inappropriate to produce 
a single estimate of the residue level in commodities if such estimate 
does not reflect high end values that are likely to occur. Use of 
percent crop treated data in the manner used in chronic assessment, 
however, reduces high-end values in proportion to percent of crop 
treated. To overcome this problem, a new risk assessment methodology 
was developed that used a complex, probabilistic model that 
incorporated all residue values, including the high end values, and 
percent crop treated information. EPA first accepted these 
probabilistic acute risk assessments late in 1995, and use of this new 
risk assessment technique in regulatory actions was still relatively 
infrequent prior to the drafting and passage of the FQPA in the summer 
of 1996.
    In sum, NRDC can demonstrate, at best, that the statute is silent 
regarding use of percent crop treated information in acute risk 
assessments. Given the general language in section 408 directing EPA to 
consider ``available information'' on aggregate exposure levels, EPA's 
interpretation of section 408 as permitting use of percent crop treated 
data in acute risk assessments is certainly reasonable. NRDC's 
interpretation, on the other hand, would erect an absolute bar to the 
use of the most advanced scientific techniques for reliably and 
accurately estimating anticipated exposure to pesticide residues.
    2.Comment number 2. EPA fails to identify the correct NOAEL for 
vinclozolin's endocrine disrupting effects. Dr. Gray has reported an 
apparent lack of a NOAEL for vinclozolin's developmental effects. 
Therefore, use of a NOAEL of 6 mg/kg/day for the acute analysis and use 
of 3 mg/kg/day as the NOAEL for short-term, intermediate-term, and 
carcinogenic risk assessments is not scientifically supportable. NRDC 
feels that a LOAEL of 3 mg/kg/day, adjusted for the lack of a true 
NOAEL, should be used as the hazard component in risk assessments.
    Agency response. First, the Agency stresses that it conducted a 
statistical analysis of anogenital distance in response to dose in the 
Gray developmental rat study, and it was determined that the NOAEL for 
acute effects was 6 mg/kg/day and the LOAEL was 12 mg/kg/day. In a 12/
8/99 memorandum, the Agency determined that decreased ventral prostate 
weight, observed at 6 mg/kg/day, was an even more sensitive indicator 
of the anti-androgenic activity of vinclozolin; the next lower dose (3 
mg/kg/day) was thus selected as the study NOAEL.
    Second, the Agency must stress that the NOAEL of 6 mg/kg/day for 
the acute dietary analysis represents the 3 mg/kg/day treatment level 
(study NOAEL) in the [multidose] perinatal oral developmental rat study 
noted above that has been adjusted by a plasma equilibrium factor to 
derive an adjusted NOAEL that reflects a single dose; the adjusted 
LOAEL causing decreased ventral prostate weight has been calculated to 
be 11.5 mg/kg/day.
    The perinatal oral developmental rat study mentioned above was also 
used as the source of the NOAEL for short-term and intermediate-term 
dermal and inhalation risk assessments for women (13-50); note that the 
study NOAEL of 3 mg/kg/day was not adjusted for the

[[Page 44464]]

plasma equilibrium factor because the applicable short-term and 
intermediate-term routes of exposure are not oral and because they 
typically reflect multiple exposure events more closely approximated by 
the multidose oral developmental rat study.
    The Agency disagrees with NRDC's suggestion that the 3 mg/kg dose 
from the Gray, et al. oral developmental rat study is a LOAEL. As noted 
above, EPA's statistical analysis shows that the anogenital distance 
effect has a NOAEL of 6 mg/kg/day in the Gray study. NRDC has not 
offered any explanation of why it does not agree with that statistical 
analysis. Second, as to the decreased ventral prostate weight effect, 
EPA's review of the data shows that this adverse affect was not present 
at 3 mg/kg; however, this adverse effect was a dose-related effect in 
male offspring at 6 mg/kg and above. No adverse effects were observed 
at the 3 mg/kg/day dose level. Thus, EPA cannot agree with NRDC that 
the 3 mg/kg/day dose should be treated as a LOAEL in conducting the 
risk assessment for vinclozolin.
    The perinatal rat developmental toxicity study was also used to 
derive the point of departure (POD = NOAEL of 3 mg/kg/day) to be used 
in the non-linear carcinogenicity risk assessments; the effect seen at 
the LOAEL of 6 mg/kg/day was prostate weight decrease, seen as an early 
manifestation of the anti-androgenic action of vinclozolin ultimately 
resulting in Leydig (testicular interstitial) cell tumors in the 
chronic/cancer studies. However, note that the NOAEL of 1.2 mg/kg/day 
from the rat chronic/cancer studies is considered to be protective of 
cancer effects because it is protective of the anti-androgenic effects 
that are the likely precursors to tumor formation. The chronic 
Population Adjusted Dose (cPAD), used to calculate risk, is derived by 
dividing the NOAEL of 1.2 mg/kg/day by the safety factor of 1,000 (10X 
for intraspecies extrapolation, 10X for interspecies variation, and 10X 
for FQPA). Because this approach (using the cPAD) would be more 
protective than the proposed POD for cancer risk assessment of 3 mg/kg/
day, and includes an additional 10X factor for the protection of 
infants and children, a separate non-linear risk assessment for cancer 
is not necessary.
    3. Comment number 3. Vinclozolin and iprodione do share a common 
mechanism of toxicity. NRDC disagrees with EPA's judgement that 
vinclozolin and iprodione do not share a common mechanism because they 
are both known anti-androgens, both have the metabolite 3,5-
dichloroaniline in common, and both cause the same effect even if the 
exact manner of androgen interference is different. In fact, they may 
act additively or synergistically as a result of affecting the androgen 
pathway at different sites as opposed to the potential competition for 
the same binding site if both act at the exact same point in the 
process.
    Agency response. FQPA requires EPA to consider available 
information concerning the cumulative effects of compounds that have a 
common mechanism of toxicity. It should be stressed, however, that EPA 
is moving in a stepwise fashion to evaluating the cumulative assessment 
of anti-androgenic pesticides.
    Vinclozolin, procymidone, and iprodione are members of the imide 
group of the dicarboximide class of fungicides. There is some evidence 
that these compounds induce similar toxic effects. Further, all of 
these fungicides appear to be anti-androgenic. The mechanistic basis 
for their anti-androgenic properties have been studied to different 
degrees. There are studies underway at EPA's National Health and 
Environmental Effects Laboratory to better elucidate the mechanism of 
toxicity for these anti-androgenic fungicides as well as mixture 
studies on how they interact. Although all three of these fungicides 
effectively reduce the level of testosterone, they do so by different 
pathways. Vinclozolin and procymidone bind and compete for the androgen 
receptor. Iprodione disrupts the endocrine system by inhibiting 
androgen synthesis rather than competing for the androgen receptor. It 
should be noted that these three chemicals do not have any known 
metabolites/degradates in common with the possible exception of 3,5-
dichloroaniline which is structurally and toxicologically different 
from the parent compounds and unlikely to be anti-androgenic.
    The androgen system may be modulated in different ways including 
competitive binding to androgen receptors, interference with gene 
control over the synthesis of several enzymes or other factors 
associated with synthesis of androgen and testosterone. All of these 
variables relate to the potency, specificity, and site of action of the 
anti-androgen and determine the expression of the anti-androgenicity 
induced by various compounds. Because of the complexity of the androgen 
system, a careful evaluation of all the available data is needed as 
well as peer review by the FIFRA Science Advisory Panel before a formal 
decision is made regarding whether or not these compounds modulate 
androgens by a common mechanism of toxicity. The evaluation of a common 
mechanism would follow the 1999 EPA Guidance for Identifying Pesticide 
Chemicals and Other Substances That Have A Common Mechanism of Toxicity 
(64 FR 5796, February 5, 1999) (FRL-6060-7). Furthermore, procymidone 
has yet to be subjected to the Reregistration Eligibility Decision 
(RED) process and, as part of this process, its toxicology database 
must meet current standards of acceptability. Although there are data 
suggesting that these dicarboximide fungicides induce some of the same 
anti-androgenic effects, the mechanism by which they cause these toxic 
effects have not been adequately evaluated.
    Even after an evaluation of all the data and a decision is made 
regarding a common mechanism of toxicity, other analyses are important 
to conduct regarding the integration of exposure and hazard data to 
determine the likelihood that such groupings might result in a 
cumulative risk as described in the Agency's Proposed Guidance on 
Cumulative Risk Assessment of Pesticide Chemicals That Have a Common 
Mechanism of Toxicity (http://www.epa.gov/scipoly/sap/1999/september/cumdoc.pdf). Only then can it be determined whether there is a need to 
conduct a cumulative risk assessment on these dicarboximide fungicides.
    Nonetheless, because of the apparent similarity of mechanism of 
toxicity between vinclozolin and procymidone EPA has considered, as 
discussed above, whether the cumulative effects from vinclozolin and 
procymidone (assuming these pesticides' effects are cumulative) would 
raise a risk of concern. EPA is unwilling, at this time, to make the 
same assumption concerning iprodione and vinclozolin. NRDC hypothesizes 
that, because iprodione and vinclozolin operate in a different manner 
on the androgen system, they are likely to have an additive anti-
androgenic effect. A conclusion that chemicals that operate at 
different stages in the androgen pathway are acting through a common 
mechanism of toxicity or otherwise merit a cumulative assessment is 
beyond any cumulative effects determination EPA has made either pre- or 
post-FQPA. That does not mean that further evaluation of the science of 
cumulative effects concerning anti-androgenic effects will not lead to 
a conclusion that iprodione and vinclozolin have a common mechanism of 
toxicity. At this time, however, given the scientific understanding of 
the mechanisms of these two pesticides, EPA is unwilling to presume 
that such common mechanism exists or that there is some other 
justification for treating

[[Page 44465]]

these pesticides as having cumulative effects.
    4. Comment number 4. EPA should not approve tolerances that exceed 
safe levels. The elevated risk numbers in the case of short-term and 
intermediate-term risk and the exceedance of the drinking water level 
of concern (DWLOC) are especially of concern and there is doubt that 
the proposed mitigation measures will alleviate the estimated risks. 
There is concern that EPA's assessments are not sufficiently 
conservative to protect public health and the Agency should not ignore 
or explain-away its own elevated risk estimates.
    Agency response. EPA has high confidence in the short-term and 
intermediate-term risk assessments (these involve treated sod) because 
a chemical-specific turf exposure study was used and because foliar 
residue dissipation over time was determined. We, therefore, have 
confidence that the mitigation measure to require a 24-day interval 
between final treatment and harvest of sod before it is shipped for 
placement in a residential setting will be protective. Only in the case 
of acute aggregate risk from vinclozolin and carcinogenic risk from 
3,5-DCA was there an indication of a potential drinking water concern. 
The exposure estimates (EECs) were based on conservative modeling. 
Also, the food exposures (subtracted from the aPAD to determine the 
DWLOC) are very conservative because they are based on field trial 
residue data. DWLOCs cannot be used in a quantitative risk assessment 
as representative monitoring data may. Rather, they are used to 
determine the magnitude of potential concern by comparison to the 
EEC's. As the 99.9th percentile of food exposure to 
vinclozolin is considered to be overly conservative given the use in 
this exposure assessment and the overly conservative drinking water 
assessment, EPA has little concern for an apparent elevated risk 
particularly in light of the registrant's mitigation proposals. 
Finally, discussion of the strengths and weaknesses of our assessments, 
the assumptions made, and our level of confidence are all part of the 
risk characterization component of risk assessment. We must provide 
qualitative descriptors to facilitate the risk management process.

B. Earthjustice Legal Defense Fund comment

    Comment. EPA is asked to consider Earthjustice's prior comments and 
objections to the previous vinclozolin tolerance.
    Agency response. EPA has addressed Earthjustice's prior comments 
and objections in the Agency letter of May 11, 2000 to the Earthjustice 
Legal Defense Fund, and therefore, the Agency believes that further 
detailed discussion is not necessary. In brief, Earthjustice's prior 
comments focused on two issues: the use of the additional safety factor 
for the protection of infants and children; and the cumulative effects 
of vinclozolin, iprodione, and procymidone. In considering 
Earthjustice's comments in the course of assessing vinclozolin, EPA has 
acceded to Earthjustice's request to retain the additional safety 
factor for the protection of infants and children and has assumed, for 
this tolerance rulemaking, that vinclozolin and procymidone have a 
common mechanism of action that will lead to cumulative effects. EPA 
decided against reaching that conclusion as to vinclozolin and 
iprodione for the reasons explained above. EPA's full response to 
Earthjustice has been included in the docket for this action.

C. BASF Corporation Comments

    1. Comment number 1. BASF has supplied information which would 
allow the Agency to further refine the acute dietary risk by using 
monitoring data provided in response to the Agency's preliminary risk 
assessment. Use of this information would significantly reduce the 
calculated acute dietary risk.
    Agency response. BASF did submit grape and lettuce metabolism 
studies and a proposal that monitoring data be used as a source of 
refined dietary exposure estimates, i.e., anticipated residues. FDA and 
USDA/Pesticide Data Program monitoring data are available for most 
foods expected to bear vinclozolin residues. However, these monitoring 
data are not useful for risk assessment purposes because these programs 
do not analyze all 3,5-DCA containing metabolites, which are the 
residues of concern. Agency review of the plant metabolism studies 
reveals that a significant portion of the vinclozolin residue may exist 
as 3,5-DCA per se or conjugates, all of which tend to increase with 
time as they are the terminal, more stable residues. Conjugates and 
3,5-DCA per se are not analyzed by either FDA or PDP. These residues 
are, however, analyzed by the data collection method used to generate 
the field trial data because the method converts all of these residues 
to a common moiety (derivatized 3,5-DCA). Also, there was significant 
variability in the ratios of vinclozolin per se to total residues with 
time, between crops, and between studies on the same crop. Therefore, 
at this time the Agency does not believe that the plant metabolism 
studies provide sufficient additional information supporting use of 
monitoring data to generate anticipated residues (ARs) and that field 
trial data should be used to calculate AR values for dietary exposure 
in food.
    2. Comment number 2. BASF has submitted or cited information it 
feels supports their contention that 3,5-DCA should not be assumed to 
be toxicologically equivalent to p-chloroaniline, i.e., that 3,5-DCA 
should not be considered to be a carcinogen like p-chloroaniline for 
risk assessment purposes. Based on physicochemical and stereochemical 
differences from p-chloroaniline, BASF thinks that 3,5-DCA would not be 
mutagenic. Calculations indicate that the amino group of p-
chloroaniline is 1,300 times more reactive than the amino group of 3,5-
DCA in a peroxidation reaction, a step necessary to generate the 
corresponding hydroxylamine which is a prerequisite for mutagenicity. 
Side-by-side Ames Bioassays demonstrated that p-chloroaniline is 
clearly mutagenic whereas 3,5-DCA is nonmutagenic in the presence of 
metabolic activation and a cocarcinogen. This indicates that the two 
chloroanilines behave different biologically.
    Agency response. While the submitted information provides some 
support for the claim that 3,5-DCA may be less potent than p-
chloroaniline, there is insufficient evidence to show that 3,5-DCA is 
not mutagenic or carcinogenic. The available mutagenicity data are 
insufficient because 3,5-DCA was tested using only one of the four or 
five Salmonella typhimurium strains usually tested in the Ames 
bioassay; also, 3,5-DCA was not the subject of any other in vitro 
mutagenicity study required for pesticide registration.
    Only long-term studies in which two mammalian species are exposed 
to a potential carcinogen can provide concrete evidence of 
carcinogenicity. Therefore, until sufficient data are submitted, DCA 
will continue to be regulated based on a Q1* calculation for 
p-chloroaniline.
    3. Comment number 3. BASF claims that recently submitted details of 
calculations of turf foliar dislodgeable residues provides evidence 
that a 9-day preharvest interval (PHI), rather than the Agency-
calculated 24-day PHI, is sufficient to bring the children's MOE to a 
level below the Agency's level of concern. Regardless of the outcome of 
the Agency review, BASF is willing to impose the 24-day PHI suggested 
in the supplemental notice.

[[Page 44466]]

    Agency response. These data are currently under review, and no 
comment can be provided at this time.

V. Other Considerations

A. Metabolism in Plants and Animals

    1. Plant metabolism. The qualitative nature of the residue in 
plants is adequately understood based on metabolism studies on 
strawberries, lettuce, peaches, and grapes. The plant metabolism 
studies indicate that metabolism in plants results from the hydrolytic 
cleavage of the oxazolidinedione ring and/or loss of the ethenyl 
moiety. Formation of conjugates and hydrolysis to 3,5-DCA occur and 
these may increase with time. The residues of concern are vinclozolin 
per se and its metabolites containing the 3,5-DCA moiety.
    2. Animal metabolism. The qualitative nature of the residue in 
livestock is adequately understood based on adequate ruminant and 
poultry metabolism studies submitted in conjunction with pesticide 
petitions PP#7H5531 and PP#9F3750. The residues of concern are 
vinclozolin, a mixture of the diastereomers of N-(3,5-dichlorophenyl)-
2-methyl-2,3,4-trihydroxybutyramide (BF 352-25), and a mixture of 
diastereomers derived by dihydroxylation of the vinclozolin vinyl group 
(BF 352-37). These metabolites are covered by the present tolerance 
expression, i.e., they contain the 3,5-DCA moiety.

B. Analytical Enforcement Methodology

    1. Plants. Adequate analytical methodology is available for data 
collection and enforcing tolerances of vinclozolin per se and its 
metabolites containing the 3,5-DCA moiety in/on plant commodities. 
Method I in PAM, Vol. II, which underwent a successful EPA method 
validation on strawberries, involves base hydrolysis of residues to 
convert vinclozolin and its metabolites to 3,5-DCA. After steam 
distillation and organic solvent extraction, the isolated DCA is 
derivatized to N-(3,5- dichlorophenyl)chloroacetamide using 
chloroacetyl chloride prior to quantitation by gas chromatography/
electron capture detection (GC/ECD). The limit of quantitation is 0.05 
ppm.
    2. Livestock. EPA has concluded that the following methods are 
available for the enforcement of tolerances for livestock tissues: 
method A9004A, a GC/ECD method, and method A9207, a High Performance 
Liquid Chromatography method. Method A9004A is based on conversion of 
vinclozolin and its metabolites to 3,5-DCA. However, it does not 
distinguish between residues of vinclozolin and other compounds 
convertible to 3,5-DCA. The LOQ is generally 0.05 ppm (0.1 ppm for 
poultry commodities). To confirm that the 3,5-DCA detected by method 
A9004A is derived from vinclozolin, method A9207 is used to measure 
2,3,4-trihydroxy-w-methylbutanoic acid-(3,5-dichloroanilide) (BF 352-
25), the major metabolite of vinclozolin in livestock commodities. The 
LOQ and the limit of detection are estimated to be 0.05 and 0.025 ppm, 
respectively. Both methods have been successfully validated.
    3. The FDA PESTDATA database dated 1/94 (PAM, Vol. I, Appendix II) 
indicates that vinclozolin is completely recovered (> 80%) using FDA 
Multiresidue Protocols D and E (oily and non-oily matrices). 
Vinclozolin metabolite B is completely recovered using Protocols D and 
E (for oily matrices), and only partially recovered (50-80%) using 
Protocol E for non-oily matrices. Metabolite E is completely recovered 
using Protocol D. Metabolite F is recovered using Protocol D but no 
quantitative information is available. Metabolite S is partially 
recovered using Protocol E (non-oily matrices). The FDA multiresidue 
methodology differentiates between vinclozolin and iprodione, a 
pesticide that also contains the DCA moiety.

C. Magnitude of Residues

    1. Snap beans. Sixteen (16) residue trials were conducted in a 
total of 7 states. Each trial consisted of a single residue sample. The 
residue trials were conducted using the Ronilin WP formulation. Eight 
of the trials involved application to lima beans and eight to snap 
beans. Ground applications were made in approximately 50 gallons of 
finish spray per acre and air applications in 5 to 15 gallons per acre. 
Samples of beans, cannery waste, green forage, and dry forage were 
analyzed. Residues in snap beans were as follows: 0.38, 0.53, 0.62, 
0.64, 0.73, 0.76, 0.95, and 2.40 ppm.
    2. Canola. Four field trials were conducted in Canada (two in 
Alberta and one each in Manitoba and Saskatchewan). These sites 
represent Regions 5, 7, and 14. A single treatment was applied at 0.22, 
0.33, or 0.45 lb active ingredient per acre (ai/A) (0.44X, 0.66X, and 
0.89X the maximum rate of 0.5 lb ai/A proposed on the U.S. label) in 40 
gallons of water per acre using ground equipment. Two major canola 
varieties were treated at 20-35% bloom; the treatment-to-harvest 
intervals were 37-57 days. The canola seed were stored frozen for 330 
days. The preponderance of data support the storage stability of the 
3,5-DCA moiety for this length of time in canola seed. At the 0.44X 
application rate, canola seed contained 3,5-DCA-containing residues of 
0.038-0.20 ppm. At the 0.33X rate, residues were detected at 0.065-0.28 
ppm. At the 0.88X rate, residues were found at 0.068-0.42 ppm. An 
additional six field trials were conducted in Canada between 1982 and 
1996 to support Section 18 requests. A single application was made at 
0.22-0.67 lb ai/A (0.44X - 1.34X) during the early bloom to the mid-
bloom stage using aerial and ground equipment. The treatment-to-harvest 
intervals were 36-69 days. Residues containing the 3,5-DCA moiety in 
canola seed were  0.93 ppm. The highest residue value 
resulted from an application of 0.44 lb ai/A (0.88X). Although some of 
the available trials do not reflect the maximum rate, others represent 
exaggerated rates. The earlier-submitted data, combined with the four 
Canadian field trials submitted with this petition, provide sufficient 
magnitude of the residue data upon which to base a canola seed 
tolerance.
    A canola seed processing study was conducted on seed harvested from 
a Saskatchewan field trial. A single treatment at 0.45 lb ai/A (0.89X) 
occurred at 40% bloom. At maturity, 49 days later, seeds were subjected 
to typical processing into oil and meal. The seed, crude oil, refined 
oil, and meal byproduct were analyzed in Germany by BASF using method 
P-14.003.02. Residues containing the 3,5-DCA moiety were detected at 
0.62 - 0.89 ppm in four replicates of seed (mean = 0.76 ppm). Residues 
in crude oil were 0.85 = 0.94 ppm (mean = 0.88 ppm) indicating very 
slight concentration in this intermediate component of the process that 
is not used for food or feed. Upon purifying, refined oil (the product 
for commerce) did not contain detectable residues (< 0.05 ppm) 
indicating residue reduction. In addition, the byproduct canola meal 
contained residue levels identical to those in the seed (0.68 - 0.89 
ppm) demonstrating a lack of concentration of vinclozolin residues in 
this livestock feed.
    3. Meat, milk, poultry, and eggs. There are no feed items 
associated with the currently registered use sites or succulent beans. 
However, canola meal may be fed to beef and dairy cows, swine, and 
poultry at up to 15% of the diet. The canola seed tolerance level of 1 
ppm was used for canola meal to calculate livestock diets because the 
processing study indicated that vinclozolin concentrations in seed 
remains the same in the meal. The meal dry matter content of 88% 
(corrected for

[[Page 44467]]

cattle only) was also used to calculate livestock diets for tolerance-
setting purposes. The dietary burdens are thus: 0.17 ppm for beef and 
dairy cattle and 0.15 ppm for swine and poultry.
    Based on livestock feeding studies, the theoretical residues in 
tissues were calculated using tissue residues at the lowest feeding 
level (100 ppm) extrapolated to the dietary burdens provided above. 
Livestock commodity residues resulting from the three feeding levels 
(100, 300, and 1,000 ppm) were fairly linear lending some support to 
the assumed linearity down to the dietary burden levels. Theoretical 
residues ranged from 0.004 ppm to 0.015 ppm in cattle tissues and milk, 
0.001 ppm to 0.004 ppm in poultry tissues and eggs, and 0.003 ppm to 
0.014 ppm in swine tissues. In accordance with 40 CFR 180.6(a)(2), EPA 
believes that the available data indicate that there is a reasonable 
expectation of finite residues of vinclozolin transferring from treated 
canola to livestock commodities via canola meal in the diet. 
Accordingly, EPA recommends that tolerances at the LOQ of the method be 
proposed as follows: 0.05 ppm in eggs, milk, and the meat, fat, and 
meat byproducts of cattle, goats, hogs, horses, and sheep; and 0.1 ppm 
in the meat, fat, and meat byproducts of poultry.

D. International Residue Limits

    CODEX maximum residue limits (MRLs) for residues of vinclozolin and 
its metabolites containing the 3,5-DCA moiety have been established in 
common bean at 2 ppm, rape seed at 1 ppm (no limit for canola), cattle 
meat and milk at 0.5 ppm, and chicken meat and eggs at 0.05 ppm. No 
Canadian or Mexican tolerances have been established for vinclozolin 
residues in succulent beans, rape, canola, meat, milk, poultry, or 
eggs.
    The CODEX MRLs for canola (rape seed), cattle meat, cattle milk, 
and poultry eggs are in harmony with the proposed tolerances associated 
with this petition. The chicken meat MRL (0.05 ppm) is not in harmony 
with the proposed tolerance in poultry meat (0.1 ppm) due to recovery 
discrepancies with the analytical method.

E. Rotational Crop Restrictions

    Based on a limited field rotational crop study which was adequate 
to satisfy the data requirement, vinclozolin residues were all < 0.05 
ppm (LOQ of method) in all plant commodities (wheat, cabbage, and 
potatoes) at the minimum plant-back interval of 30 days. Therefore, EPA 
has concluded that it is permissible to rotate to small grains, leafy 
vegetables and root crops after a 30-day interval.

VI. Conclusion

    Therefore, tolerances are established for combined residues of 
vinclozolin, 3-(3,5-dichlorophenyl)-5-ethynyl-5-methyl-2,4-
oxazolidinedione and its metabolites containing the 3,5-dichloroaniline 
moiety, in or on succulent beans at 2.0 ppm; canola at 1.0 ppm; eggs, 
milk, and the meat, fat, and meat byproducts of cattle, goats, hogs, 
horses, and sheep at 0.05 ppm; and the meat, fat, and meat byproducts 
of poultry at 0.1 ppm.

VII. Objections and Hearing Requests

    Under section 408(g) of the FFDCA, as amended by the FQPA, any 
person may file an objection to any aspect of this regulation and may 
also request a hearing on those objections. The EPA procedural 
regulations which govern the submission of objections and requests for 
hearings appear in 40 CFR part 178. Although the procedures in those 
regulations require some modification to reflect the amendments made to 
the FFDCA by the FQPA of 1996, EPA will continue to use those 
procedures, with appropriate adjustments, until the necessary 
modifications can be made. The new section 408(g) provides essentially 
the same process for persons to ``object'' to a regulation for an 
exemption from the requirement of a tolerance issued by EPA under new 
section 408(d), as was provided in the old FFDCA sections 408 and 409. 
However, the period for filing objections is now 60 days, rather than 
30 days.

A. What Do I Need to Do to File an Objection or Request a Hearing?

    You must file your objection or request a hearing on this 
regulation in accordance with the instructions provided in this unit 
and in 40 CFR part 178. To ensure proper receipt by EPA, you must 
identify docket control number OPP-301015 in the subject line on the 
first page of your submission. All requests must be in writing, and 
must be mailed or delivered to the Hearing Clerk on or before September 
18, 2000.
    1. Filing the request. Your objection must specify the specific 
provisions in the regulation that you object to, and the grounds for 
the objections (40 CFR 178.25). If a hearing is requested, the 
objections must include a statement of the factual issues(s) on which a 
hearing is requested, the requestor's contentions on such issues, and a 
summary of any evidence relied upon by the objector (40 CFR 178.27). 
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.
    Mail your written request to: Office of the Hearing Clerk (1900), 
Environmental Protection Agency, Ariel Rios Bldg., 1200 Pennsylvania 
Ave., NW., Washington, DC 20460. You may also deliver your request to 
the Office of the Hearing Clerk in Rm. C400, Waterside Mall, 401 M St., 
SW., Washington, DC 20460. The Office of the Hearing Clerk is open from 
8 a.m. to 4 p.m., Monday through Friday, excluding legal holidays. The 
telephone number for the Office of the Hearing Clerk is (202) 260-4865.
    2. Tolerance fee payment. If you file an objection or request a 
hearing, you must also pay the fee prescribed by 40 CFR 180.33(i) or 
request a waiver of that fee pursuant to 40 CFR 180.33(m). You must 
mail the fee to: EPA Headquarters Accounting Operations Branch, Office 
of Pesticide Programs, P.O. Box 360277M, Pittsburgh, PA 15251. Please 
identify the fee submission by labeling it ``Tolerance Petition Fees.''
    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 the waiver of these fees, you may contact James 
Tompkins by phone at (703) 305-5697, by e-mail at [email protected], 
or by mailing a request for information to Mr. Tompkins at Registration 
Division (7505C), Office of Pesticide Programs, Environmental 
Protection Agency, Ariel Rios Bldg., 1200 Pennsylvania Ave., NW., 
Washington, DC 20460.
    If you would like to request a waiver of the tolerance objection 
fees, you must mail your request for such a waiver to: James Hollins, 
Information Resources and Services Division (7502C), Office of 
Pesticide Programs, Environmental Protection Agency, Ariel Rios Bldg., 
1200 Pennsylvania Ave., NW., Washington, DC 20460.
    3. Copies for the Docket. In addition to filing an objection or 
hearing request with the Hearing Clerk as described in Unit VI.A., you 
should also send a copy of your request to the PIRIB for its inclusion 
in the official record that is described in Unit I.B.2. Mail your 
copies, identified by docket control number OPP-301015, to: Public

[[Page 44468]]

Information and Records Integrity Branch, Information Resources and 
Services Division (7502C), Office of Pesticide Programs, Environmental 
Protection Agency, Ariel Rios Bldg., 1200 Pennsylvania Ave., NW., 
Washington, DC 20460. In person or by courier, bring a copy to the 
location of the PIRIB described in Unit I.B.2. You may also send an 
electronic copy of your request via e-mail to: [email protected]. 
Please use an ASCII file format and avoid the use of special characters 
and any form of encryption. Copies of electronic objections and hearing 
requests will also be accepted on disks in WordPerfect 6.1/8.0 file 
format or ASCII file format. Do not include any CBI in your electronic 
copy. You may also submit an electronic copy of your request at many 
Federal Depository Libraries.

B. When Will the Agency Grant a Request for a Hearing?

    A request for a hearing will be granted if the Administrator 
determines that the material submitted shows the following: There is a 
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(s) in the manner sought 
by the requestor would be adequate to justify the action requested (40 
CFR 178.32).

VIII. 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) (Public Law 104-4). Nor 
does it require any prior consultation as specified by Executive Order 
13084, entitled Consultation and Coordination with Indian Tribal 
Governments (63 FR 27655, May 19, 1998); 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 or 
any Agency action under Executive Order 13045, entitled Protection of 
Children from Environmental Health Risks and Safety Risks (62 FR 19885, 
April 23, 1997). This action does not involve any technical standards 
that would require Agency consideration of voluntary consensus 
standards pursuant to section 12(d) of the National Technology Transfer 
and Advancement Act of 1995 (NTTAA), Public Law 104-113, section 12(d) 
(15 U.S.C. 272 note). Since 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. In addition, the Agency has 
determined that this action will not have a substantial direct effect 
on States, on the relationship between the national government and the 
States, or on the distribution of power and responsibilities among the 
various levels of government, as specified in Executive Order 13132, 
entitled Federalism (64 FR 43255, August 10, 1999). Executive Order 
13132 requires EPA to develop an accountable process to ensure 
``meaningful and timely input by State and local officials in the 
development of regulatory policies that have federalism implications.'' 
``Policies that have federalism implications'' is defined in the 
Executive Order to include regulations that have ``substantial direct 
effects on the States, on the relationship between the national 
government and the States, or on the distribution of power and 
responsibilities among the various levels of government.'' This final 
rule directly regulates growers, food processors, food handlers and 
food retailers, not States. This action does not alter the 
relationships or distribution of power and responsibilities established 
by Congress in the preemption provisions of FFDCA section 408(n)(4).

IX. Submission to Congress and the Comptroller General

    The Congressional Review Act, 5 U.S.C. 801 et seq., as added by the 
Small Business Regulatory Enforcement Fairness Act of 1996, generally 
provides that before a rule may take effect, the agency promulgating 
the rule must submit a rule report, which includes a copy of the rule, 
to each House of the Congress and to the Comptroller General of the 
United States. EPA will submit a report containing this rule and other 
required information to the U.S. Senate, the U.S. House of 
Representatives, and the Comptroller General of the United States prior 
to publication of this final rule in the Federal Register. This final 
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: June 21, 2000.
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. 321(q), (346a) and 371.

    2. In Sec. 180.380, the table to paragraph (a) is amended by 
revising the entry for ``beans, succulent'', and by adding new entries 
to read as follows:


Sec. 180.380  Vinclozolin; tolerances for residues.

    (a) *  *  *

------------------------------------------------------------------------
                                                             Expiration/
                    Commodity                     Parts per   Revocation
                                                   million       Date
------------------------------------------------------------------------
Beans, succulent................................        2.0      9/30/03
                      *      *      *      *      *
Canola..........................................        1.0      9/30/03
Cattle, fat.....................................       0.05      9/30/03
Cattle, mbyp....................................       0.05      9/30/03
Cattle, meat....................................       0.05      9/30/03
                      *      *      *      *      *
Eggs............................................       0.05      9/30/03
Goats, fat......................................       0.05      9/30/03
Goats, mbyp.....................................       0.05      9/30/03
Goats, meat.....................................       0.05      9/30/03
Hogs, fat.......................................       0.05      9/30/03
Hogs, mbyp......................................       0.05      9/30/03
Hogs, meat......................................       0.05      9/30/03
Horses, fat.....................................       0.05      9/30/03
Horses, mbyp....................................       0.05      9/30/03
Horses, meat....................................       0.05      9/30/03
                      *      *      *      *      *
Milk............................................       0.05      9/30/03
                      *      *      *      *      *
Poultry, fat,...................................        0.1      9/30/03
Poultry, meat...................................        0.1      9/30/03
Poultry mbyp....................................        0.1      9/30/03
                      *      *      *      *      *
Sheep, fat......................................       0.05      9/30/03
Sheep, mbyp.....................................       0.05      9/30/03
Sheep, meat.....................................       0.05      9/30/03
                      *      *      *      *      *
------------------------------------------------------------------------

    *      *      *      *      *
[FR Doc. 00-18099 Filed 7-17-00; 8:45 am]
BILLING CODE 6560-50-F