[Federal Register Volume 60, Number 11 (Wednesday, January 18, 1995)]
[Proposed Rules]
[Pages 3607-3611]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 95-1062]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 185
[OPP-300360; FRL-4910-8]
RIN 2070-AC18
Acephate, Triadimefon, Iprodione, and Imazalil; Revocation of
Food Additive Regulations
AGENCY: Environmental Protection Agency (EPA).
ACTION: Proposed rule.
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SUMMARY: EPA is proposing to revoke food additive regulations for the
pesticides acephate, triadimefon (1-(4-chlorophenoxy)-3,3-dimethyl-1-
(1H-1,2,4-triazol-1-yl)-2-butanone), iprodione, and imazalil, which EPA
has determined ``induce cancer'' within the meaning of the Delaney
clause of section 409 of the Federal Food, Drug and Cosmetic Act
(FFDCA). As a result of a 1992 court decision regarding the Delaney
clause, EPA has initiated the process of revoking those section 409
tolerances for pesticides found to ``induce cancer.'' This proposed
rule is the second in a series of proposals to revoke affected
regulations under section 409 of the FFDCA.
DATES: Written comments, identified by the document control number
[OPP-300360], must be received on or before April 18, 1995.
ADDRESSES: By mail, submit comments to: Public Response Section, Field
Operations Division (7506C), Office of Pesticide Programs,
Environmental Protection Agency, 401 M St., SW., Washington, DC 20460.
In person, bring comments to: OPP Docket, Public Information Branch,
Field Operations Division, Rm. 1132, Crystal Mall #2, 1921 Jefferson
Davis Hwy., Arlington, VA. The telephone number for the OPP docket is
(703)-305-5805.
Information submitted as a comment concerning this document may be
claimed confidential by marking any part or all of that information as
``Confidential Business Information'' (or CBI). Information so marked
will not be disclosed except in accordance with procedures set forth in
40 CFR part 2 and in section 10 of the Federal Insecticide, Fungicide
and Rodenticide Act (FIFRA). For questions related to disclosure of
materials, contact the OPP Docket at the telephone number given above.
A copy of the comment 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. All written comments
will be available for public inspection in the OPP Docket, Rm. 1132 at
the Virginia address given above, from 8 a.m. to 4 p.m., Monday through
Friday, excluding legal holidays.
FOR FURTHER INFORMATION CONTACT: By mail: Niloufar Nazmi or Lisa
Nisenson, Special Review and Reregistration Division (7508W),
Environmental Protection Agency, 401 M St. SW., Washington, DC, 20460.
Office location and telephone number: Crystal Station #1, 2800 Crystal
Drive, Arlington, VA. Telephone 703-308-8010.
SUPPLEMENTARY INFORMATION:
I. Introduction
A. Statutory Background
The Federal Food, Drug and Cosmetic Act (FFDCA) (21 U.S.C. 301 et
seq.) authorizes the establishment of maximum permissible levels of
pesticides in foods, which are referred to as ``tolerances'' (21 U.S.C.
346a, 348). Without such a tolerance or an exemption from a tolerance,
a food containing a pesticide residue is ``adulterated'' under section
402 of the FFDCA and may not be legally moved in interstate commerce
(21 U.S.C. 342). Monitoring and enforcement of pesticide residues are
carried out by the U.S. Food and Drug Administration (FDA) and the
United States Department of Agriculture (USDA).
The FFDCA governs tolerances for raw agricultural commodities
(RACs) and processed foods separately. For pesticide residues in or on
RACs, EPA establishes tolerances, or exemptions from tolerances when
appropriate, under section 408. In processed foods, food additive
regulations setting maximum permissible levels of pesticide residues
are established under section 409. Section 409 tolerances are needed,
however, only for certain pesticide residues in processed food. Under
section 402(a)(2) of the FFDCA, no section 409 tolerance is required if
any pesticide residue in a processed food is equal to or below the
tolerance for that pesticide in or on the RAC from which it was derived
and all other conditions of section 402(a)(2) are met. This exemption
in section 402(a)(2) is commonly referred to as the ``flow-through''
provision because it allows the section 408 raw food tolerance to flow
through to the processed food form. Thus, a section 409 tolerance is
necessary to prevent foods from being deemed adulterated when the
concentration of the pesticide residue in a processed food is greater
than the tolerance prescribed for the RAC, or if [[Page 3608]] the
processed food itself is treated or comes in contact with a pesticide.
If a food additive regulation must be established, section 409 of
the FFDCA requires that the use of the pesticide will be ``safe'' (21
U.S.C. 348(c)(3)). Relevant factors in this safety determination
include: (1) the probable consumption of the pesticide or its
metabolites; (2) the cumulative effect of the pesticide in the diet of
man or animals, taking into account any related substances in the diet;
and (3) appropriate safety factors to relate the animal data to the
human risk evaluation. Section 409 also contains the Delaney clause,
which specifically provides that, with little exception, ``no additive
shall be deemed safe if it has been found to induce cancer when
ingested by man or animal'' (21 U.S.C. 348(c)(3)).
Before a pesticide may be sold or distributed, it must be
registered under the Federal Insecticide, Fungicide and Rodenticide Act
(FIFRA). To qualify for registration, a pesticide must, among other
things, perform its intended function without causing ``unreasonable
adverse effects on the environment'' (7 U.S.C. 136a(c)(5)). The term
``unreasonable adverse effects on the environment'' is defined as ``any
unreasonable risk to man or the environment taking into account the
economic, social and environmental costs and benefits of the use of any
pesticide'' (7 U.S.C. 136(bb)).
B. Regulatory Background
On May 25, 1989, the State of California, the Natural Resources
Defense Council, Public Citizen, the AFL-CIO, and several individuals
filed a petition requesting that EPA revoke several food additive
regulations and challenging EPA's de minimis interpretation of the
Delaney clause. The petition, which sought a ``zero-risk''
interpretation of the Delaney clause, requested that EPA revoke certain
food additive regulations. The petitioners argued that these food
additive regulations should be revoked because they violate the Delaney
clause.
EPA responded to the petition by revoking certain food additive
regulations, but retained several others on the grounds that the
Delaney clause provides an exception for pesticide residues posing de
minimis risk; EPA denied the petition for the food additive regulations
determined to fall under this exception.
EPA's response was challenged by the petitioners in the U.S. Court
of Appeals, Ninth Circuit. On July 8, 1992, the court ruled in Les v.
Reilly, 968 F.2d 985 (9th Cir.), cert. denied, 113 S.Ct. 1361 (1993),
that the Delaney clause barred the establishment of a food additive
regulation for pesticides which ``induce cancer'' no matter how
infinitesimal the risk.
On July 14, 1993, EPA issued a revised response to the petition
taking into account the court's ruling. That revised response granted
the original petition and revoked the food additive regulations named
in the petition. The food additive regulations for two of the four
affected pesticides, benomyl and trifluralin, have been reinstated
pending judicial review by the Court of Appeals, District of Columbia
Circuit, of several registrants' challenge to the revocation.
In implementing the court's decision in Les v. Reilly, EPA has
taken steps to identify and revoke all section 409 tolerances for
pesticides which have been found to ``induce cancer.'' EPA has issued
two lists of pesticide uses which would likely be affected by the
court's decision. The first list contains affected food and feed
additive regulations, and the second identifies uses for pesticides
that have either been found to induce cancer or are likely to be so
classified where data show a food or feed additive regulation needs to
be established. Both lists have been updated to reflect changes in data
reviews and other regulatory actions (see 59 FR 14980, March 30, 1994).
The first proposed revocation, which included 26 food additive
regulations for seven pesticides classified as ``B'', probable human
carcinogens or ``C'', possible human carcinogens subject to
quantification by a linear low-dose extrapolation model, was published
in the Federal Register of July 1, 1994 (59 FR 33941).
II. Proposed Revocation of Section 409 Tolerances Which are
Inconsistent with the Delaney Clause
EPA intends to revoke all food and feed additive regulations which
are inconsistent with the Delaney clause. This notice proposes
revocation of all food additive regulations published in the March 30,
1994 Federal Register notice which have not previously been proposed
for revocation. EPA expects to publish additional proposed revocations
for feed additive regulations in the near future.
A. Basis for Proposing Revocation
As a result of the court's 1992 decision, the only issue to be
considered for these proposed revocations is whether acephate,
triadimefon, imazalil, and iprodione qualify under the Delaney clause
as having been ``found to induce cancer when ingested by man or
animals, or it is found, after tests which are appropriate for the
evaluation of the safety of food additives, to induce cancer in man or
animal.'' 21 U.S.C. 348(c)(3)(A). If EPA finds they are human or animal
carcinogens within the meaning of the Delaney clause, the food additive
regulations must be revoked.
In construing the ``induce cancer'' standard as to animals, EPA
follows a weight-of-the-evidence approach which is guided, where
appropriate, by the principles in EPA's Cancer Assessment Guidelines.
In regard to animal carcinogenicity, EPA, in general, interprets
``induces cancer'' to mean:
The carcinogenicity of a substance in animals is established
when administration in adequately designed and conducted study or
studies results in an increase in the incidence of one or more types
of malignant (or, where appropriate, benign or a combination of
benign and malignant) neoplasms in treated animals compared to
untreated animals maintained under identical conditions except for
exposure to the test compound. Determination that the incidence of
neoplasms increases as the result of exposure to the test compound
requires a full biological, pathological, and statistical
evaluation. Statistics assist in evaluating the biological
significance of the observed responses, but a conclusion on
carcinogenicity is not determined on the basis of statistics alone.
Under this approach, a substance may be found to ``induce cancer''
in animals despite the fact that increased tumor incidence occurs
only at high doses, or that only benign tumors occur, and despite
negative results in other animal feeding studies. (See 58 FR 37863,
July 14, 1993; 53 FR 41108, October 19, 1988; and 52 FR 49577,
December 31, 1987).
Acephate, triadimefon, imazalil, and iprodione all qualify as
animal carcinogens under this test.
Summarized below is the information supporting EPA's determination
that these pesticides ``induce cancer.'' Full copies of each of these
reviews and other references in this notice are available in the OPP
Docket, the location of which is given under ADDRESSES above.
Acephate
After a full evaluation of all the data and supporting information
regarding animal carcinogenicity, EPA has concluded that exposure to
acephate results in the induction of malignant hepatocellular
carcinomas in female CD-1 mice.
Male and female CD-1 mice were fed 0, 50, 250, or 1,000 parts per
million (ppm) of acephate for 105 weeks. Although fewer low-dose and
mid-dose female mice survived to the end of the study compared with
controls, the survival of the highest dose tested (HDT) female mice and
all male mice was higher than that with the controls. Decreases in body
weight gain ranged [[Page 3609]] from 8 to 11 percent for males and 6
to 14 percent for females at the mid-dose, and about 24 percent for
males and 29percent for females at the HDT. Dose-related increasing
levels of liver toxicity, including regenerative changes, were
observed. In the female mice at the HDT, the incidence of malignant
hepatocellular carcinomas and hyperplastic nodules was significantly
increased in comparison with controls. The increased incidence of
carcinomas exceeds the testing laboratory's historical control range.
There were no increases in tumors in the two lower dosed female groups
or any of the male groups.
Male and female Charles River (CD) Sprague-Dawley rats were fed 0,
5, 50, and 700 ppm of acephate for 28 months. There was no dose-related
effect on mortality, although there was significant cholinesterase
inhibition in the mid- and high-dose male and female rats. There was a
4 to 8 percent weight loss in the HDT males.
Acephate has been tested in a wide array of genotoxicity assays.
The evidence indicates that acephate produced positive responses in
gene mutation in vitro assays with Salmonella, E. coli, and S.
cerevisiae. Acephate has been reported to produce mutations in mouse
lymphoma cells, sister chromatid exchanges (SCEs) in Chinese hamster
ovary (CHO) cells, and mitotic recombination in Saccharomyces. Several
in vivo assays for SCEs and cytogenetic endpoints have been negative.
Based on this information regarding animal carcinogenicity, the
Agency concludes that exposure to acephate results in the induction of
malignant hepatocellular carcinomas in female CD-1 mice. The incidence
exceeded the historical control range of the testing laboratory. There
is evidence that acephate is genotoxic based on in vitro studies, but
this activity may be difficult to detect in vivo. The relevance of
these data to an evaluation of acephate's potential for human
carcinogenicity is discussed in the Peer Review document of Acephate
(May 8, 1985).
Triadimefon
After a full evaluation of all the data and supporting information
regarding animal carcinogenicity, EPA has concluded that exposure to
triadimefon results in the induction of hepatocellular adenomas in both
male and female NMRI mice. Male and female NMRI mice were fed 0, 50,
300, or 1,800 ppm of triadimefon for 21 months. At the HDT, the
incidence of hepatocellular adenomas was increased in both male and
female mice by pair-wise comparison between the HDT and controls. A
positive dose-related significant trend for adenomas was found in both
sexes. The incidence of hepatocellular adenomas for each sex exceeded
the testing laboratory's historical control range for adenomas in NMRI
mice.
In another study, male and female CF1-W74 mice were fed 0, 50, 300,
or 1,800 ppm of triadimefon for 24 months. The HDT was considered
appropriate for assessing carcinogenicity based on increased
hematological changes; statistically significant increases in liver
weights accompanied by histopathological changes and weight gains at
the HDT were significantly lower than in controls.
Initially, the tumor profile was thought to provide no indication
that triadimefon had an influence on total tumor incidence, on the
number of mice with tumors or on incidence of single tumor types;
however, the pathology report indicated that more mice had hyperplastic
liver nodules at the HDT than mice in the other treated groups or the
controls. The Peer Review Committee recommended that in light of the
NMRI study results outlined above, and that the original analysis of
the study results was performed before the current criteria were put
into place, the liver nodules should be re-read with updated criteria.
The new histopathological information for the CF1-W74 mouse study
was submitted subsequent to the completion of the latest Triadimefon
Peer Review document. Only a small number of slides were available for
reexamination, and the results were deemed inconclusive. However, they
are suggestive of an effect on tumor incidence in the liver and are
consistent with the findings in the NMRI study that the liver is a
principal site for tumor induction. Lesions which were originally
classified as hyperplastic or regenerative nodules were reclassified as
either hepatocellular adenomas or carcinomas. In males, 3, 3, 2, and 3
adenomas and 1, 4, 4, and 4 carcinomas were found out of 6, 8, 7, and
13 liver samples examined at doses of 0, 50, 300, and 1,800 ppm,
respectively. This suggests that triadimefon may contribute to the
induction of liver tumors and there may be a carcinoma component.
In a 104-week study, male and female Wistar rats were fed 0, 50,
300, or 1,800 ppm of triadimefon. Triadimefon induced a positive dose-
related trend in the incidence of thyroid follicular cell adenomas/
adenomas multiple in male Wistar rats. Positive dose-related trends
were achieved in both sexes for combined incidences of thyroid
follicular cell cystic hyperplasia and adenomas/adenomas multiple.
Hepatocellular adenomas are considered to be evidence of cancer
because hepatocellular adenomas can progress to hepatocellular
carcinomas. Malignancy (carcinoma) implies a more extensive disease
process. Thus, hepatocellular adenomas represent an earlier stage than
carcinomas in the progression of cancer induction. This is one of the
major reasons that the National Toxicology Program (NTP) has used to
justify combining these two tumor types for an overall analysis of
carcinogenicity (in addition to analyzing them separately). For
triadimefon, the possible progression to carcinoma was suggested in the
CF1-W74 mouse study and is strongly supported by carcinoma induction in
close structural analogues, e.g., etaconazole, uniconazole,
cyproconazole, tebuconazole, and fenbuconazole.
Based on the above data and supporting information regarding animal
carcinogenicity, it is concluded that exposure to triadimefon results
in the induction of hepatocellular adenomas in both male and female
NMRI mice. A positive dose-related significant trend for adenomas was
also found in both sexes. This conclusion is bolstered by the extensive
structural activity support from closely structurally related triazole
compounds tested in many mouse studies that showed increased incidences
of not only adenomas but carcinomas as well. It is also noted that
although the analysis was inconclusive, there was a carcinoma response
by triadimefon in the CF1-W74 mouse study. In addition, triadimefon
induced a positive dose-related trend in the incidence of thyroid
follicular cell adenomas/adenomas multiple in male Wistar rats.
Positive dose-related trends were achieved in both sexes for combined
incidences of thyroid follicular cell cystic hyperplasia and adenomas/
adenomas multiple.
The relevance of these data to an evaluation of triadimefon's
potential for human carcinogenicity is discussed in the Peer Review
document of Triadimefon (September 26, 1990).
Iprodione
After a full evaluation of the data and supporting information
regarding animal carcinogenicity, EPA concludes that exposure to
iprodione resulted in an increased incidence of hepatocellular
malignant carcinomas in male mice and combined hepatocellular adenomas/
carcinomas in both sexes of mice, ovarian lutenomas in female mice, and
[[Page 3610]] testicular interstitial cell tumors in male rats.
Iprodione was administered to CD-1 mice (50/sex/group) at levels of
0, 160, 800, or 1,400 ppm for at least 99 weeks (or until the 52-week
interim sacrifice of 15 additional mice/sex/group). At the terminal
sacrifice, there was a significantly increased incidence of benign and
malignant liver cell tumors in both sexes compared to the control.
Analysis indicates that male mice had significant difference in the
pair-wise comparisons of the 1,400-ppm dose group with the controls for
liver adenomas, carcinomas and combined adenomas and/or carcinomas.
Female mice had significant increasing trends in liver adenomas,
carcinomas, and combined adenomas and/or carcinomas. All males in all
dose groups (including concurrent controls) displayed a higher
incidence of carcinomas than observed in historical controls. Although
there was no increase in the incidence of testicular tumors in the male
mice, there was a dose-related increase in the incidence of
interstitial cell hyperplasia at the 800- and 1,400-ppm dose levels.
In female mice, iprodione was associated with significant dose-
related increasing trends in liver adenomas, carcinomas and combined
adenomas and/or carcinomas; there were significant differences in pair-
wise comparisons with the high-dose level with controls for liver
adenomas and combined adenomas and/or carcinomas. The increased
incidences of hepatocellular tumors at the 1,400-ppm level generally
exceeded the available historical control data for these tumor types in
mice of this strain. Additionally, iprodione was associated with a
significant increasing trend in ovarian lutenomas, and there was a
significant difference in the pair-wise comparison of the 1,400-ppm
dose group with the control group and historical controls. EPA
considers the dose levels used in this study to be adequate for testing
the carcinogenicity of iprodione in mice.
Iprodione was administered in the diet to 60 Sprague-Dawley rats/
sex/group for 2 years at dose levels of 0, 150, 300, or 1,600 ppm.
There was a 52-week interim sacrifice of 10 additional rats/sex/group.
At the interim sacrifice, males at the high-dose level displayed an
increase in the incidence of lesions in the adrenals, and there was an
increase in the incidence of centrilobular hepatocyte enlargement in
males at the 300 and 600 dose levels; females displayed an increased
incidence of centrilobular hepatocyte enlargement at the highest dose
tested.
In male rats fed iprodione for 2 years, there was a significant
dose-related increasing trend and a significant difference in the pair-
wise comparison of the 1,600-ppm dose group with the controls for
testicular interstitial cell benign tumors. The incidence of both
unilateral and bilateral benign interstitial cell tumors was increased
at this dose level compared to historical control data. In addition to
the neoplastic lesions, interstitial cell hyperplasia in the testes,
reduced spermatozoa in the epididymis, and absent/empty secretory
colloid cells or reduced secretion in the seminal vesicles were
observed at the 300- and 1,600-ppm dose levels. Atrophy of the
seminiferous tubules in the testes, with atrophy of the prostate and
absence of spermatozoa in the epididymis, were observed at 1,600 ppm.
Centrilobular hepatocyte enlargement was increased in males at the
high-dose level. Adrenal lesions were observed in both sexes at the
300- and 1,600- ppm dose levels, although males displayed more lesions
than females.
In females rats fed iprodione at the high-dose level for 2 years,
there were no significant compound-related tumors observed, although
there was an increased incidence of tubular hyperplasia in the ovaries
and increased sciatic nerve fiber degeneration compared to the
controls. The dose levels chosen for this study were considered
appropriate for assessing the carcinogenicity of iprodione in rats.
Iprodione is structurally related to vinclozolin and procymidone.
Procymidone has been associated with the appearance of tumors in both
sexes in the reproductive organs and the liver, but did not have
mutagenic activity in several tests. Vinclozolin, which is currently
being tested for its carcinogenic potential, has been associated with
adverse effects on the reproductive organs and liver. With the
exception of the mouse lymphoma (forward mutation) assay, vinclozalin
was negative for mutagenicity. In mutagenicity studies, iprodione was
not mutagenic in the Ames assay, the CHO/HGPRT mammalian cell forwarded
mutation assay, the in vitro chromosome aberration assay in CHO cells,
the in vitro sister chromatid exchange assay in CHO cells and the
dominant-lethal test in mice. However, iprodione was positive in the
Bacillus subtilis assay for DNA damage without metabolic activation.
Imazalil
After a full evaluation of the data and supporting information
regarding animal carcinogenicity, EPA concludes that exposure to
imazalil is associated with an increased incidence of adenomas and
combined adenomas/adenocarcinomas of the livers of male Swiss mice and
with a significant dose-related increasing trend in hepatocellular
adenomas and combined adenomas and/or carcinomas.
Imazalil base was administered in the diet to groups of 50 male and
50 female Swiss mice and treated for 100 to 101 weeks at levels of 0,
50, 200, or 600 ppm. Male mice had a significant dose-related
increasing trends in hepatocellular adenomas and/or carcinomas. There
was a significant difference in the pair-wise comparison of the 200-ppm
dose group with the controls for hepatocellular adenomas. There were
also significant differences in the pair-wise comparisons of the 600-
ppm dose group with the controls for hepatocellular adenomas and
combined adenomas and/or carcinomas. EPA has concluded that the
malignant carcinoma response at the 600-ppm dose level was biologically
relevant and related to imazalil exposure despite the lack of pair-wise
statistical significance compared to controls. There was over a
doubling of the concurrent control incidence and a positive trend for
carcinomas. The male carcinoma incidence was also outside the
historical control data provided by the submitting company. It was
noted that about 50% of the significantly positive combined incidence
was contributed by carcinomas. Also, there appears to be a progression
towards malignancy across the dose groups.
Female mice had significant dose-related increasing trends in
hepatocellular adenomas and combined adenomas and/or carcinomas. There
were no significant differences in the pair-wise comparisons of the
dosed groups with the controls.
Nonneoplastic changes in the liver were also observed in male mice
at all dose levels. At the 200-ppm level, males had a significant
increase in the incidence of focal cellular changes, large vacuoles,
and swollen sinusoidal cells in the liver. At the highest dose tested,
males also had a significantly increased incidence of pigmentation in
the sinusoidal cells of the liver and focal cellular changes in the
pancreas, increased absolute and relative liver weight, and decreased
body weight and body weight gain. Female mice did not exhibit any
cellular changes in the liver, although there was some effect on body
weight at the 600-ppm dose and slight increases in liver weights at the
highest dose tested as well.
There is extensive structure-activity relationship (SAR) support
for the [[Page 3611]] tumor response associated with imazalil. Closely
related compounds with the chlorinated benzene moiety, e.g.,
etaconazole, cyproconazole, tebuconazole, induced hepatocellular
adenomas, and malignant carcinomas in both sexes of several strains of
mice. The mutagenicity data for imazalil did not indicate genotoxic
activity; however, a data gap was identified and additional testing is
required.
B. Proposed Food Additive Revocations
Acephate. EPA is proposing to revoke the food additive regulation
of 0.02 ppm for the combined residues of acephate (O,S-dimethyl
acetylphosphoramidothioate) and its cholinesterase-inhibiting
metabolite, methamidophos, set to cover use of the pesticide in food-
handling establishments. This food additive regulation is codified at
40 CFR185.100. EPA is proposing to revoke this food additive regulation
because the Agency has determined that acephate induces cancer in
animals. Thus, the regulation violates the Delaney clause in section
409 of the FFDCA.
Triadimefon. EPA is proposing to revoke the food additive
regulations for triadimefon (1-(4-chlorophenoxy)-3,3-dimethyl-1-(1H-
1,2,4-triazol-1-yl)-2-butanone) and its metabolite beta-(4-
chlorophenoxy)-alpha-(1,1-dimethylethyl)-1H-1,2,4triazole-1-ethanol set
to cover residues in or on milled fractions of barley (except flour)
and milled fractions of wheat (except flour). The food additive
regulations, which are codified at 40 CFR 185.800, are set at 4 ppm.
EPA is proposing to revoke these food additive regulations because the
Agency has determined that triadimefon induces cancer in animals. Thus,
the regulations violate the Delaney clause in section 409 of the FFDCA.
Iprodione. EPA is proposing to revoke the food additive regulations
for iprodione [3-(3,5-dichlorophenyl)-N-(1-methylethyl)-2,4-dioxo-1-
imidazolidinecarboxamide], its isomer [3-(1-methyl-ethyl)-N-(3,5-
dichlorophenyl)-2,4-dioxo-1-imidazolidinecarboxamide], and its
metabolite [3-(3,5-dichlorophenyl)-2,4-dioxo-1-
imidazolidinecarboxamide] set to cover residues in dried ginseng at 4
ppm and raisins at 300 ppm. The food additive regulations for iprodione
are codified at 40 CFR 185.3750. EPA is proposing to revoke these food
additive regulations because the Agency has determined that iprodione
induces cancer in animals. Thus, the regulation violates the Delaney
clause in section 409 of the FFDCA.
Imazalil. EPA is proposing to revoke the food additive regulation
for imazalil set to cover residues of the fungicide imazalil 1-[2-(2,4-
dichlorophenyl)-2-(2-propenyloxy)ethyl]-1H-imidazole and its metabolite
1-(2,4-dichlorophenyl)-2-(1H-imidazole-1-yl)-1-ethanol in citrus oil at
a level of 25 ppm. This food additive regulation is codified at 40 CFR
185.3650. EPA is proposing to revoke this food additive regulation
because the Agency has determined that imazalil induces cancer in
animals, and thus violates the Delaney clause in section 409 of the
FFDCA.
III. Consideration of Comments
Any interested person may submit comments on this proposed action
on or before April 18, 1995 at the address given in the section above
entitled ``ADDRESSES.'' Before issuing final actions, EPA will consider
all relevant comments. Comments should be limited only to the
pesticides and food additive regulations subject to this proposed
notice. After consideration of comments, EPA will issue a final order
determining whether revocation of the regulations is appropriate and
making a final finding on whether these pesticides induce cancer within
the meaning of the Delaney clause. Such order will be subject to
objections pursuant to section 409(f) (21 U.S.C. 348(f)). Failure to
file an objection within the appointed period will constitute waiver of
the right to raise issues resolved in the order in future proceedings.
IV. Executive Order 12866
Since this proposed action is being taken under the Delaney clause,
which requires the Agency to act without considering the costs or
benefits of the action, the Agency has not completed an evaluation of
the economic impacts of this particular action. Nevertheless, pursuant
to an agreement between EPA and OMB, this action was submitted to OMB
for an informal 10-day review. As required by the Executive Order, any
comments or changes made in response to OMB suggestions or
recommendations have been documented in the public record. In addition,
the Agency welcomes any comments and information regarding the impacts
of this proposed action. These could contribute to an analysis of the
impacts of similar future actions.
V. Regulatory Flexibility Act
The Regulatory Flexibility Act of 1980 (Pub. L. 96-354; 94 Stat.
1164, 5 U.S.C. 601 et seq.) requires EPA to analyze regulatory options
to assess the economic impact on small businesses, small governments,
and small organizations. As explained above, the Agency is compelled to
take this action without regard to the economic impacts. Again, EPA
welcomes any information on impacts to small businesses, governments,
and organizations.
VI. Paperwork Reduction Act
This order does not contain any information collection requirements
subject to review by Office of Management and Budget under the
Paperwork Reduction Act of 1980, 44 U.S.C. 3501 et seq.
List of Subjects in 40 CFR Part 185
Environmental protection, Administrative practice and procedure,
Agricultural commodities, Food additives, Pesticides and pests,
Recording and recordkeeping requirements.
Dated: January 10, 1995.
Lynn R. Goldman,
Assistant Administrator for Prevention, Pesticides and Toxic
Substances.
Therefore, it is proposed that 40 CFR part 185 be amended as
follows:
PART 185--[AMENDED]
1. The authority citation for part 185 continues to read as
follows:
Authority: 2l U.S.C. 346a and 348.
Sec. 185.100 [Removed]
2. By removing Sec. 185.100.
Sec. 185.800 [Removed]
3. By removing Sec. 185.800.
Sec. 185.3650 [Removed]
4. By removing Sec. 185.3650.
Sec. 185.3750 [Removed]
5. By removing Sec. 185.3750
[FR Doc. 95-1062 Filed 1-17-95; 8:45 am]
BILLING CODE 6560-50-F