[Federal Register Volume 64, Number 103 (Friday, May 28, 1999)]
[Rules and Regulations]
[Pages 28917-28924]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 99-13656]
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ENVIRONMENTAL PROTECTION AGENCY
40 CFR Part 180
[OPP-300866; FRL-6082-7]
RIN 2070-AB78
Fenhexamid; Pesticide Tolerance
AGENCY: Environmental Protection Agency (EPA).
ACTION: Final rule.
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SUMMARY: This regulation establishes tolerances for fenhexamid (N-2,3-
dichloro-4-hydroxyphenyl)-1-methyl cyclohexanecarboxamide) in or on
grapes at 4.0 parts per million (ppm), strawberries at 3.0 ppm, and
raisins at 6.0 ppm. The TM-402 Fungicide Task Force comprised of Tomen
Agro, Inc. and Bayer 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 May 28, 1999. Objections and
requests for hearings must be received by EPA on or before July 27,
1999.
ADDRESSES: Written objections and hearing requests, identified by the
docket control number, [OPP-300866], must be submitted to: Hearing
Clerk (1900), Environmental Protection Agency, Rm. M3708, 401 M St.,
SW., Washington, DC 20460. Fees accompanying objections and hearing
requests shall be labeled ``Tolerance Petition Fees'' and forwarded to:
EPA Headquarters Accounting Operations Branch, OPP (Tolerance Fees),
P.O. Box 360277M, Pittsburgh, PA 15251. A copy of any objections and
hearing requests filed with the Hearing Clerk identified
[[Page 28918]]
by the docket control number, [OPP-300866], must also be submitted to:
Public Information and Records Integrity Branch, Information Resources
and Services Division (7502C), Office of Pesticide Programs,
Environmental Protection Agency, 401 M St., SW., Washington, DC 20460.
In person, bring a copy of objections and hearing requests to Rm. 119,
Crystal Mall 2 (CM #2), 1921 Jefferson Davis Hwy., Arlington, VA.
A copy of objections and hearing requests filed with the Hearing
Clerk may be submitted electronically by sending electronic mail (e-
mail) to: opp-docket@epa.gov. Copies of objections and hearing requests
must be submitted as an ASCII file avoiding the use of special
characters and any form of encryption. Copies of objections and hearing
requests will also be accepted on disks in WordPerfect 5.1/6.1 file
format or ASCII file format. All copies of objections and hearing
requests in electronic form must be identified by the docket control
number [OPP-300866]. No Confidential Business Information (CBI) should
be submitted through e-mail. Electronic copies of objections and
hearing requests on this rule may be filed online at many Federal
Depository Libraries.
FOR FURTHER INFORMATION CONTACT: By mail: Mary L. Waller, Product
Manager 21, Registration Division (7505C), Office of Pesticide
Programs, Environmental Protection Agency, 401 M St., SW., Washington,
DC 20460. Office location, telephone number, and e-mail address: Rm.
249, CM #2, 1921 Jefferson Davis Hwy., Arlington, VA, (703) 308-9354,
waller.mary@epa.gov.
SUPPLEMENTARY INFORMATION: In the Federal Register of November 20, 1998
(63 FR 64498) (FRL-6042-1), EPA issued a notice pursuant to section 408
of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 U.S.C. 346a as
amended by the Food Quality Protection Act of 1996 (FQPA) (Pub. L. 104-
170) announcing the filing of a pesticide petition (PP 7F4890) for
tolerances by the TM-402 Fungicide Task Force comprised of Tomen Agro,
Inc. and Bayer Corporation. The notice included a summary of the
petition prepared by the TM-402 Fungicide Task Force. There were no
comments received in response to the notice of filing.
The petition requested that 40 CFR part 180 be amended by
establishing tolerances for the fungicide, fenhexamid in or on grapes
at 4.0 ppm, strawberries at 3.0 ppm, and raisins at 6.0 ppm.
I. Background and Statutory Findings
Section 408(b)(2)(A)(i) of the FFDCA allows EPA to establish a
tolerance (the legal limit for a pesticide chemical residue in or on a
food) only if EPA determines that the tolerance is ``safe.'' Section
408(b)(2)(A)(ii) defines ``safe'' to mean that ``there is a reasonable
certainty that no harm will result from aggregate exposure to the
pesticide chemical residue, including all anticipated dietary exposures
and all other exposures for which there is reliable information.'' This
includes exposure through drinking water and in residential settings,
but does not include occupational exposure. Section 408(b)(2)(C)
requires EPA to give special consideration to exposure of infants and
children to the pesticide chemical residue in establishing a tolerance
and to ``ensure that there is a reasonable certainty that no harm will
result to infants and children from aggregate exposure to the pesticide
chemical residue....''
EPA performs a number of analyses to determine the risks from
aggregate exposure to pesticide residues. For further discussion of the
regulatory requirements of section 408 and a complete description of
the risk assessment process, see the final rule on Bifenthrin Pesticide
Tolerances (62 FR 62961, November 26, 1997) (FRL-5754-7).
II. Aggregate Risk Assessment and Determination of Safety
Consistent with section 408(b)(2)(D), EPA has reviewed the
available scientific data and other relevant information in support of
this action. EPA has sufficient data to assess the hazards of
fenhexamid and to make a determination on aggregate exposure,
consistent with section 408(b)(2), for tolerances in or grapes at 4.0
ppm, strawberries at 3.0 ppm, and raisins at 6.0 ppm. EPA's assessment
of the dietary exposures and risks associated with establishing the
tolerances follows.
A. Toxicological Profile
EPA has evaluated the available toxicity data and considered its
validity, completeness, and reliability as well as the relationship of
the results of the studies to human risk. EPA has also considered
available information concerning the variability of the sensitivities
of major identifiable subgroups of consumers, including infants and
children. The nature of the toxic effects caused by fenhexamid are
discussed in this unit.
1. Acute toxicity--i. The acute oral LD50 and acute
dermal LD50 for rats was > 5,000 milligrams/kilograms (mg/
kg) for both sexes. The acute LC50 for rats was > 5.06 mg/
liters (L) for both sexes. Fenhexamid was not an eye or skin irritant
and was not a dermal sensitizer.
ii. In an acute neurotoxicity study, rats were gavaged with a
single oral dose of fenhexamid at dose levels of 0, 200, 630, or 2,000
mg/kg. The rats were observed for 14 days. Functional Observational
Battery and motor activity testing were performed 7 days prior to
dosing, approximately 20 minutes to 3 hours post-dosing, and on days 7
and 14. The no observed adverse effect level (NOAEL) in males was 630
mg/kg. The NOAEL in females was 2,000 mg/kg. The lowest observed
adverse effect level (LOAEL) in males was 2,000 mg/kg based on a
marginally decreased mean body temperature (the only treatment-related
effect noted in the study). The LOAEL in females was not established.
2. Subchronic toxicity--i. In an inhalation toxicity range-finding
study, 10 rats/sex/dose were exposed (head/nose only) to fenhexamid at
concentrations of 0, 11.8, 97.7 or 1,092.6 mg/m3 in air for
6 hours per day for 5 days. One-half of the rats were sacrificed 7 days
after the first exposure and the other one-half were sacrificed 21 days
after the first exposure. The NOAEL was 0.098 mg/L and the LOAEL was
1.092 mg/L based on the observations of macroscopic grey coloration of
the lungs and marginally increased lung weights.
ii. In a 21-day dermal toxicity study, fenhexamid was applied to
the shaved skin of 5 male and female rabbits at a dose level of 1,000
mg/kg/day for 17 days over a 3-week period. There were no compound
related effects. The NOAEL was 1,000 mg/kg/day and the LOAEL was >
1,000 mg/kg/day for both systemic and local effects on the skin.
iii. In a 28-day oral toxicity range finding study, 10 rats/sex/
dose were gavaged at dose levels of 0, 100, 300, or 1,000 mg/kg/day for
28 days. There were no compound-related effects in mortality, clinical
signs, body weight, food consumption, hematology, clinical chemistry,
organ weights, or gross and histologic pathology. The NOAEL was 1,000
mg/kg/day.
iv. In a 90-day oral toxicity study, 10 rats/sex/dose were fed
fenhexamid at dose levels of 0, 2,500, 5,000, 10,000 or 20,000 ppm (0,
202, 415, 904, and 1,904 mg/kg/day for males and 0, 270, 549, 1,132,
and 2,824 mg/kg/day for females). No treatment-related changes were
seen in clinical signs, mortality, opthalmoscopic examinations,
hematology, urinalyses, or gross pathology. The NOAEL was 5,000 ppm in
males and 10,000 ppm in females.
[[Page 28919]]
The LOAEL in males was 10,000 ppm based on decreased terminal body
weights and body weight gains, increased food consumption, decreased
food efficiency and increased Alanin amino-transferase (ALAT) levels.
The LOAEL in females was 20,000 ppm based on increased food
consumption, decreased food efficiency, decreased liver weights, and
liver histopathology (Kupffer cell proliferation and altered hepatocyte
morphology).
v. In a 90-day oral toxicity study, 4 dogs/sex were fed fenhexamid
at dose levels of 0, 1,000, 7,000 or 50,000 ppm (0, 33.9, 239.1, or
1,747.7 mg/kg/day for males and 0, 37, 261, or 1,866.2 mg/kg/day for
females). The NOAEL in males and females was 1,000 ppm. The LOAEL in
males and females was 7,000 ppm based on significant increases in Heinz
bodies in males and females and increased absolute and relative liver
weights in females.
vi. In a 90-day oral toxicity study, 10 mice/sex/dose were fed
fenhexamid at dose levels of 0, 100, 1,000 or 10,000 ppm (0, 26.5,
266.5 or 3,283.5 mg/kg/day in males and 0, 51.6, 453.9, or 5,151.1 mg/
kg/day in females) for 14 weeks. The NOAEL in males and females was
1,000 ppm. The LOAEL in males and females was 10,000 ppm based on the
observation in both sexes of: increased serum cholesterol, bilirubin
and creatinine, decreased kidney weights, increased water consumption,
increased food consumption (males), decreased food efficiency (males),
renal cortical tubular basophilia (both sexes), renal protein casts and
cellular detritus (males), and marginal alterations of liver function
(increased serum cholesterol, bilirubin, decreased Aspartate amino-
transferase (ASAT), ALAT), marginal increase in liver weights and
reduced glycogen content of hepatocytes (males).
vii. In a 56-day oral toxicity study, 10 rats/sex/dose were fed
fenhexamid at dose levels of 0, 1,000, 5,000, 10,000, 15,000, or 20,000
ppm (0, 57.5, 284.7, 575.7, 943.8, or 1,217.1 mg/kg/day for males and
0, 78, 407.1, 896.5, 1,492.5, or 1,896.7 mg/kg/day for females). At
20,000 ppm, rats had fenhexamid plasma levels below the level of
detection. Urine samples showed measurable excretion of conjugated
fenhexamid indicating intestinal absorption in the dose range examined.
Males had a maximum excretion rate at 15,000 ppm indicating a
saturation of intestinal absorption between 15,000 and 20,000 ppm.
Urine excretion in females was somewhat lower than in males, at
concentrations of 10,000 ppm and above. The highest value was
determined at 20,000 ppm suggesting that saturation in intestinal
absorption was not achieved with this dose level in females.
3. Developmental toxicity--i. In a developmental toxicity study, 30
rats/dose were gavaged at dose levels of 0 and 1,000 (1,044 determined
analytically) mg/kg/day from days 6 through 15 of gestation. At 1,000
mg/kg/day, there were no treatment-related effects on maternal
mortality, clinical signs, cesarean parameters, or gross pathology. No
treatment-related effects were noted in any embryo/fetal parameters.
Under the conditions of the study, fenhexamid was not embryotoxic,
fetotoxic, or teratogenic at a dose of 1,044 mg/kg/day. The NOAEL for
maternal toxicity was < 1,044="" mg/kg/day.="" the="" developmental="" noael="" was="" 1,044="" mg/kg/day.="" the="" loael="" for="" maternal="" toxicity="" was="" 1,044="" mg/kg/day="" based="" on="" the="" decreased="" body="" weight="" gain="" (-12%="" of="" controls)="" during="" gestation="" days="" 6-16="" and="" a="" decrease="" in="" food="" consumption="" (10%="" of="" controls)="" during="" gestation="" days="" 6-11.="" ii.="" in="" a="" developmental="" toxicity="" study,="" 16="" rabbits="" were="" gavaged="" with="" fenhexamid="" at="" dose="" levels="" of="" 0,="" 100,="" 300,="" or="" 1,000="" mg/kg/day="" from="" days="" 6="" through="" 18="" of="" gestation.="" no="" treatment-related="" effects="" were="" seen="" on="" mortality,="" general="" appearance="" or="" behavior.="" the="" noael="" for="" maternal="" toxicity="" was="" 100="" mg/kg/day.="" the="" loael="" for="" maternal="" toxicity="" was="" 300="" mg/="" kg/day="" based="" on="" observations="" at="" this="" dose="" and="" above="" of="" alterations="" of="" excretory="" products="" (discolored="" urine,="" small="" scybala),="" decreased="" body="" weight="" gain="" and="" feed="" consumption="" (mainly="" during="" the="" first="" week="" of="" the="" treatment="" period)="" and="" decreased="" placental="" weights.="" one="" abortion="" at="" 300="" mg/kg/day="" and="" one="" abortion="" and="" two="" total="" litter="" resorptions="" at="" 1,000="" mg/kg/day="" were="" not="" considered="" to="" be="" treatment-related="" because="" the="" incidences="" fell="" within="" the="" ranges="" of="" historical="" control="" data="" submitted="" with="" the="" study.="" reduced="" and/or="" light="" feces="" were="" also="" noted="" at="" 1,000="" mg/="" kg/day.="" pale="" livers="" were="" noted="" in="" the="" 2="" dams="" that="" aborted.="" the="" noael="" for="" developmental="" toxicity="" was="" 300="" mg/kg/day.="" the="" loael="" for="" developmental="" toxicity="" was="" 1,000="" mg/kg/day="" based="" on="" marginally="" decreased="" male="" fetal="" body="" weights="" and="" evidence="" of="" delayed="" ossification.="" fenhexamid="" did="" not="" induce="" any="" treatment-related="" fetal="" malformations="" or="" deviations="" at="" any="" of="" the="" doses="" tested="" under="" the="" conditions="" of="" this="" study.="" all="" effects="" on="" intrauterine="" development="" were="" correlated="" with="" maternal="" toxicity="" and,="" therefore,="" no="" primary="" developmental="" effect="" was="" evident.="" fenhexamid="" was="" not="" teratogenic="" up="" to="" and="" including="" 1,000="" mg/="" kg/day.="" 4.="" reproductive="" toxicity.="" in="" 2-generation="" reproduction="" study,="" 30="" rats/sex/dose="" were="" fed="" fenhexamid="" at="" dose="" levels="" of="" 0,="" 100,="" 500,="" 5,000="" or="" 20,000="" ppm="" (0,="" 7.6,="" 38.2,="" 406,="" or="" 1,814="" for="" males="" and="" 0,="" 9.0,="" 44.8,="" 477,="" or="" 2,043="" mg/kg/day="" for="" females="" determined="" for="" the="" 10-week="" premating="" period).="" there="" were="" no="" compound-related="" effects="" on="" mortality,="" clinical="" signs,="" behavior="" or="" reproductive="" parameters="" for="" adult="" animals.="" the="" noael="" for="" reproductive="" toxicity="" was="" 20,000="" ppm.="" the="" neonatal="" noael="" was="" 500="" ppm="" and="" the="" neonatal="" loael="" was="" 5,000="" ppm="" based="" on="" significantly="" decreased="" pup="" body="" weights="" on="" lactation="" days="" 14="" and="" 21="" for="" the="">1 (6-11% < controls)="" and="" on="" lactation="" days="" 7,="" 14,="" and="" 21="" for="">2 pups (9-11% < controls).="" at="" 20,000="" ppm,="" significantly="" decreased="" pup="" body="" weights="" were="" observed="" on="" lactation="" days="" 7,="" 14,="" and="" 21="" for="">1 pups (15-30% < controls)="" and="" for="">2 pups (11-19% < controls).="" treatment-related="" decreased="" pup="" body="" weights="" were="" not="" observed="" at="" birth="" or="" on="" lactation="" day="" 4.="" an="" additional="" effect="" observed="" at="" 20,000="" ppm="" was="" an="" increase="" in="" the="" number="" of="" pups="" among="" the="" post-weaning="">1 pups selected to be
F1 parents which died viz. 0/66, 2/68, 0/68, 0/68 and 10/78
for the control, 100, 500, 5,000, and 20,000 ppm dose groups,
respectively. This effect was attributed to the small size of the pups
at weaning (30% < controls).="" the="" parental="" noael="" was="" 500="" ppm="" and="" the="" parental="" loael="" in="" males="" was="" 5,000="" ppm="" based="" on="" increased="" creatinine="" levels="" in="" p-generation="" (but="" not="">1 generation) males at premating (20%, p<0.05) and="" at="" termination="" (20%,="" not="" significant);="" slightly="" increased="" alkaline="" phosphatase="" levels="" in="" p-generation="" and="">1-generation males
at premating and at termination (20-34%, not significant); decreased
absolute liver weight in P-generation and F1-generation
males (11-12%, p<0.05) and="" decreased="" liver/body="" weight="" ratios="" in="" p-="" generation="" and="">1-generation males (8-9%, p<0.05 for="" p-="" generation="" and="" not="" significant="" for="">1-generation); decreased
absolute kidney weights in F1-generation (but not P-
generation) males (12%, p<0.05); and="" decreased="" kidney/body="" weight="" ratios="" in="">1-generation (but not P-generation) males (8%,
p>0.05). The parental LOAEL in females was based on increased alkaline
phosphatase levels in F1-generation) (but not P-generation)
females at premating (43%, p<0.05) and="" at="" termination="" (63%,=""><0.05); and="" on="" very="" small="" increases="" in="" gamma="" glutamyl="" transferase="" (ggt)="" (not="" considered="" to="" be="" biologically="" relevant).="" overall,="" treatment-related="" effects="" observed="" at="" 5,000="" ppm="" in="" males="" and="" females="" were="" also="" observed="" at="" 20,000="" [[page="" 28920]]="" ppm,="" but="" were="" slightly="" increased="" in="" severity.="" toxicologically="" relevant="" additional="" toxicological="" effects="" observed="" at="" 20,000="" ppm="" were="" decreased="" body="" weights="" and="" increased="" food="" consumption="" in="" males="" and="" increased="" urea="" nitrogen="" and="" creatinine="" levels,="" decreased="" kidney="" weights,="" decreased="" body="" weights,="" and="" increased="" food="" consumption="" in="" females.="" 5.="" mutagenicity.="" no="" mutagenicity="" was="" noted="" in="" the="" following="" assays:="" reverse="" gene="" mutation,="" s.="" typhimurium,="" e.="" coli;="" forward="" gene="" mutation="" -="" hypoxanthine="" guanine="" phophoribosyl="" transferase="" (hgprt)="" locus;="" chromosome="" aberration,="" chinese="" hampster="" ovary="" (cho)="" cells;="" unscheduled="" dna="" synthesis,="" rat="" hepatocytes;="" and="" micronucleus="" assay="" in="" mice.="" 6.="" chronic="" toxicity--i.="" in="" a="" 1-year="" chronic="" oral="" toxicity="" study,="" dogs="" were="" fed="" dose="" levels="" of="" 0,="" 500,="" 3,500,="" or="" 25,000="" ppm="" (0,="" 17.4,="" 124.3,="" or="" 917.8="" mg/kg/day="" for="" males="" and="" 0,="" 19.2,="" 132.7,="" or="" 947.1="" mg/kg/="" day="" for="" females).="" the="" noael="" in="" males="" and="" females="" was="" 500="" ppm.="" the="" loael="" was="" 3,500="" ppm="" in="" males="" and="" females="" based="" on="" decreases="" in="" red="" blood="" cells="" (rbc),="" hemoglobin="" (hb),="" and="" hematocrit="" (hct)="" and="" on="" significant="" increases="" in="" heinz="" bodies="" in="" both="" sexes,="" increased="" adrenal="" weight="" parameters="" in="" females,="" and="" the="" presence="" of="" intracytoplasmic="" vacuoles="" in="" the="" adrenal="" cortex="" of="" 3/4="" females.="" ii.="" in="" a="" combined="" chronic="" toxicity/carcinogenicity="" study,="" 50="" rats/="" sex/dose="" were="" fed="" fenhexamid="" at="" dose="" levels="" of="" 0,="" 500,="" 5,000="" or="" 20,000="" ppm="" (0,="" 28,="" 292,="" or="" 1,280="" mg/kg/day="" for="" males="" and="" 0,="" 40,="" 415,="" 2,067="" mg/="" kg/day="" for="" females)="" for="" 24="" months.="" the="" noael="" in="" males="" and="" females="" was="" 500="" ppm.="" the="" loael="" for="" chronic="" toxicity="" in="" males="" and="" females="" was="" 5,000="" ppm="" based="" on="" observations="" of="" decreased="" body="" weight="" gain="" (-6.8%)="" and="" food="" efficiency="" (-11.8%)="" in="" females,="" increased="" incidence="" of="" cecal="" mucosal="" hyperplasia="" in="" males,="" increased="" cellularity="" (hyperplasia)="" of="" the="" bone="" marrow="" in="" females="" and="" the="" presence="" of="" splenic="" extramedullary="" hematopoiesis="" in="" males.="" at="" 20,000="" ppm,="" observations="" were="" increased="" food="" consumption,="" increased="" numbers="" of="" circulating="" reticulocytes,="" enlarged="" spleens="" observed="" macroscopically,="" increased="" splenic="" weights,="" and="" thyroid="" colloid="" alterations="" (both="" sexes).="" fenhexamid="" was="" non-oncogenic="" at="" doses="" up="" to="" and="" including="" 20,000="" ppm="" in="" the="" diet.="" at="" doses="" tested,="" there="" were="" no="" treatment="" related="" increases="" in="" tumor="" incidence,="" tumor="" spectrum,="" or="" latency="" when="" compared="" to="" controls.="" 7.="" carcinogenicity.="" in="" a="" carcinogenicity="" study,="" 50="" mice/sex/dose="" were="" fed="" fenhexamid="" at="" dose="" levels="" of="" 0,="" 800,="" 2,400,="" or="" 7,000="" ppm="" (0,="" 247.4,="" 807.4,="" or="" 2,354.8="" mg/kg/day="" for="" males="" and="" 0,="" 364.8,="" 1,054.5,="" or="" 3,178.2="" mg/kg/day="" for="" females)="" for="" 2="" years.="" the="" noael="" for="" males="" was="" 800="" ppm="" and="" the="" noael="" for="" females="" was="" 2,400="" ppm.="" the="" loael="" for="" males="" was="" 2,400="" ppm="" based="" on="" the="" observation="" of="" decreased="" kidney="" weights="" and="" decreases="" in="" sex-specific="" vacuolation="" of="" the="" proximal="" tubules="" in="" the="" kidneys="" in="" males.="" a="" marginal="" decrease="" in="" body="" weights="" (up="" to="" 8%)="" and="" body="" weight="" gain="" (17%)="" was="" observed="" in="" males="" at="" 7,000="" ppm.="" the="" loael="" for="" females="" was="" 7,000="" ppm="" based="" on="" significantly="" increased="" water="" consumption,="" decreased="" kidney="" weights,="" and="" renal="" histopathology="" (increased="" incidence="" of="" basophilic="" cortical="" tubules).="" fenhexamid="" was="" not="" oncogenic="" in="" mice="" at="" doses="" up="" to="" and="" including="" 7,000="" ppm.="" there="" were="" no="" treatment-related="" increases="" in="" tumor="" incidence,="" tumor="" spectrum,="" or="" latency="" when="" compared="" to="" controls.="" 8.="" dermal="" absorption.="" in="" a="" dermal="" absorption="" study,="" radiolabeled="" fenhexamid="" (50%="" formulation)="" was="" applied="" to="" the="" shaved="" skin="" of="" male="" rats="" at="" dose="" levels="" of="" 0.00138,="" 0.0147,="" or="" 0.148="">2. A
volume of 100 L was applied to a skin area of approximately
12.5 cm2 on each rat. Four rats/dose level were sacrificed
at 0.5, 1, 2, 4, 10, 24, and 120 hours postdose. Mean total recovery of
radioactivity ranged from 90.3% to 97.6% of the applied dose. The
majority of radioactivity was recovered from the skin wash (69.9% to
96.1%). Radioactivity in the skin test site ranged from 0.44% to 10.2%;
in the urine from ``not detectable'' to 3.34%; and in the feces from
``not detectable'' to 11.6% of the applied dose. Radioactivity in blood
did not exceed 0.03% and in the carcass did not exceed 9.37%. Estimates
of dermal absorption were based on the sum of radioactivity (as test
material) in the skin test site, urine, feces, blood and carcass. The
percentage dermal absorption decreased with increasing dose levels. The
percentage dermal absorption at 10 hours post-dose was 19.58%, 7.62%,
and 2.63% and at 120 hours post-dose was 21.0%, 6.91%, and 2.13% for
the low, mid and high dose levels respectively.
9. Metabolism. In a metabolism study, rats were administered
radiolabeled fenhexamid (a single oral low dose of 1 mg/kg, a single
oral high dose of 100 mg/kg, or 15 repeated low doses of 1 mg/kg/day).
Radiolabeled fenhexamid was rapidly absorbed from the gastrointestinal
(GI) tract in all dose groups. After single and repeated administration
of the low dose, the plasma concentration peaked within 5 to 10
minutes. After administration of the high dose, the maximum was
detected 40 to 90 minutes post-dosing. The absorption of the test
compound was shown to be almost complete in a bile-cannulation
experiment, as more than 97% of the administered dose was absorbed from
the GI tract 48 hours after intra-duodenal administration. These
results are indicative of a pronounced first pass effect and
enterohepatic circulation. Tissue residues declined rapidly and after
48 hours the total radioactivity residue in the body excluding the GI
tract, was < 0.3%="" of="" the="" administered="" dose="" in="" all="" dose="" groups.="" liver="" and="" kidney="" were="" the="" organs="" with="" the="" highest="" concentrations="" of="" radioactivcity="" in="" all="" dose="" groups.="" excretion="" was="" rapid="" and="" almost="" complete="" with="" feces="" as="" the="" major="" route="" of="" excretion.="" approximately="" 62-="" 81%="" of="" the="" recovered="" radioactivity="" was="" found="" in="" feces,="" and="" 15-36%="" in="" urine="" within="" 48="" hours="" post-dosing.="" more="" than="" 90%="" of="" the="" recovered="" radioactivity="" was="" eliminated="" with="" bile="" in="" the="" bile="" cannulation="" experiment.="" only="" 0.02%="" of="" the="" administered="" radioactivity="" was="" recovered="" in="" exhaled="" air.="" radioactive="" residues="" in="" rat="" bodies="" (excluding="" gi="" tract)="" were="" significantly="" lower="" in="" females="" after="" a="" single="" high="" dose.="" there="" was="" significantly="" higher="" renal="" excretion="" for="" females="" in="" comparison="" with="" males="" after="" 15="" repeated="" low="" doses.="" in="" both="" sexes="" renal="" excretion="" was="" significantly="" higher="" after="" a="" single="" low="" dose="" when="" compared="" with="" a="" single="" high="" dose.="" metabolite="" characterization="" studies="" showed="" that="" the="" main="" component="" detected="" in="" excreta="" was="" the="" unchanged="" parent="" compound="" which="" accounted="" for="" 62="" to="" 75%="" of="" the="" dose="" independent="" of="" the="" dosing="" regime="" and="" sex.="" metabolite="" 1,="" the="" glucuronic="" acid="" conjugate="" of="" the="" parent="" compound,="" ranged="" from="" 4="" to="" 23%="" of="" the="" dose.="" metabolite="" fractions="" 2="" and="" 3="" accounted="" for="" up="" to="" 3="" and="" 7%="" of="" the="" dose,="" respectively.="" the="" proposed="" major="" pathway="" for="" biotransformation="" is="" via="" conjugation="" of="" the="" aromatic="" hydroxyl="" group="" with="" glucuronic="" acid.="" prior="" to="" fecal="" excretion,="" hydrolysis="" in="" the="" intestine="" converts="" the="" conjugate="" back="" to="" the="" parent="" compound="" giving="" rise="" to="" enterohepatic="" circulation.="" identification="" of="" radioactive="" residues="" ranged="" from="" 88%="" to="" 99%="" and="" was="" independent="" of="" dose="" and="" sex.="" b.="" toxicological="" endpoints="" 1.="" acute="" toxicity.="" an="" acute="" toxicological="" endpoint="" was="" not="" identified="" resulting="" from="" a="" single="" oral="" exposure,="" and="" therefore,="" an="" acute="" reference="" dose="" (rfd)="" was="" not="" selected.="" 2.="" short-="" and="" intermediate-term="" toxicity.="" a="" short-="" and="" intermediate-term="" [[page="" 28921]]="" dermal="" endpoint="" of="" 1,000="" mg/kg/day="" from="" the="" 21-day="" dermal="" toxicity="" study="" in="" rabbits="" was="" selected="" for="" occupational="" exposure.="" no="" short-="" and="" intermediate-term="" endpoint="" was="" selected="" for="" non-occupational="" exposure="" as="" there="" are="" no="" residential="" uses="" of="" fenhexamid.="" 3.="" chronic="" toxicity.="" epa="" has="" established="" the="" rfd="" for="" fenhexamid="" at="" 0.17="" mg/kg/day.="" this="" rfd="" is="" based="" on="" 1-year="" feeding="" study="" in="" dogs="" with="" a="" noael="17" mg/kg/day.="" an="" additional="" 3x="" fqpa="" safety="" factor="" was="" added="" and="" applies="" to="" all="" population="" subgroups="" resulting="" in="" a="" chronic="" population-adjusted="" dose="" (chronic="" pad)="" of="" 0.057="" mg/kg/day.="" 4.="" carcinogenicity.="" fenhexamid="" was="" classified="" as="" a="" ``not="" likely''="" human="" carcinogen="" based="" on="" the="" lack="" of="" evidence="" of="" carcinogenicity="" in="" mice="" and="" rats="" and="" the="" lack="" of="" genotoxicity="" in="" a="" battery="" of="" mutagenicity="" studies.="" c.="" exposures="" and="" risks="" 1.="" from="" food="" and="" feed="" uses.="" fenhexamid="" is="" a="" new="" chemical="" and="" no="" tolerances="" are="" currently="" established.="" in="" today's="" action,="" tolerances="" are="" being="" established="" at="" 40="" cfr="" 180.553="" for="" grapes="" at="" 4.0="" ppm,="" strawberries="" at="" 3.0="" ppm,="" and="" raisins="" at="" 6.0="" ppm.="" risk="" assessments="" were="" conducted="" by="" epa="" to="" assess="" dietary="" exposures="" from="" fenhexamid="" as="" follows:="" i.="" acute="" exposure="" and="" risk.="" acute="" dietary="" risk="" assessments="" are="" performed="" for="" a="" food-use="" pesticide="" if="" a="" toxicological="" study="" has="" indicated="" the="" possibility="" of="" an="" effect="" of="" concern="" occurring="" as="" a="" result="" of="" a="" 1-day="" or="" single="" exposure.="" no="" toxicological="" endpoint="" attributable="" to="" a="" single="" (acute)="" dietary="" exposure="" was="" identified.="" ii.="" chronic="" exposure="" and="" risk.="" the="" chronic="" risk="" analysis="" used="" the="" chronic="" pad="" of="" 0.057="" mg/kg/day="" which="" applies="" to="" all="" populations="" subgroups.="" the="" dietary="" exposure="" evaluation="" model="" (deem)="" which="" is="" a="" exposure="" analysis="" system="" that="" estimates="" exposure="" to="" a="" pesticide="" chemical="" in="" food="" comprising="" the="" diets="" of="" the="" u.s.="" population,="" including="" population="" subgroups="" was="" used="" to="" conduct="" the="" chronic="" (food)="" risk="" analysis.="" deem="" contains="" food="" consumption="" data="" as="" reported="" by="" respondents="" in="" the="" usda="" continuing="" surveys="" of="" food="" intake="" by="" individuals="" conducted="" in="" 1989-1992.="" the="" chronic="" food="" exposure="" was="" calculated="" assuming="" theoretical="" maximum="" residue="" contribution="" (tmrc)="" values="" and="" 100%="" crop="" treated="" estimates.="" the="" percent="" of="" the="" chronic="" pad="" utilized="" is="" as="" follows:="" 6.6%="" for="" nursing="" infants="">< 1="" year);="" 4.8%="" for="" children="" (1-6="" years);="" 3.6%="" for="" females="" (13+/nursing)="" and="" for="" all="" infants="">< 1="" year);="" 2.7%="" for="" the="" pacific="" regions;="" 2.4%="" for="" non-nursing="" infants="">< 1="" year),="" western="" region,="" and="" non-hispanic="" other="" than="" black="" or="" white;="" and="" 1.8%="" for="" the="" u.s.="" population="" (48="" states-all="" seasons).="" 2.="" from="" drinking="" water.="" in="" soil,="" fenhexamid="" is="" relatively="" immobile="">oc = 446) and non-persistent (t\1/2\ = 1 day).
Fenhexamid is not expected to be a ground water contaminant, but has
some potential to reach surface water on eroded soil particles. In
surface water, fenhexamid would be expected to photodegrade rapidly
(t\1/2\ = 0.2 days).
No monitoring data are available to perform a quantitative drinking
water assessment. The Agency estimated surface water exposure using the
Generic Expected Environmental Concentration (GENEEC) model, a
screening level model for determining concentrations of pesticides in
surface water. GENEEC uses the soil/water partition coefficient,
hydrolysis half life, and the maximum label rate to estimate surface
water concentration. GENEEC contains a number of conservative
underlying assumptions. Therefore, the drinking water concentrations
derived from GENEEC for surface water are likely to be overestimated.
The modeling was conducted based on the environmental profile and the
maximum seasonal application rate proposed for fenhexamid: 0.75 lb.
active ingredient/acre x 4 applications/acre/year. The estimated
environmental concentrations (EECs) derived from GENEEC are 17
g/L (peak value) and 4.8 g/L (56-day average).
The Agency used the Screening Concentration in Ground Water (SCI-
GROW) model to estimate pesticide levels in ground water. The SCI-GROW
model is based on actual monitoring data collected for a number of
pesticides that serve as benchmarks to predict EECs in ground water.
Using SCI-GROW, the EEC calculated for fenhexamid is 0.0007 g/
L (acute and chronic).
i. Acute exposure and risk. Drinking water levels of comparison
(DWLOCs) for acute exposure were not calculated as there was no
appropriate toxicological endpoint attributable to a single (acute)
dietary exposure.
ii. Chronic exposure and risk. Chronic (non-cancer) DWLOCs were
calculated for the U.S. population and the population subgroups with
the highest (chronic) food exposure. The DWLOCs are as follows: 530
g/L for infants/children; 1,700 g/L for females 13+;
1,900 g/L for the U.S. population - pacific region; and 2,000
g/L for U.S. population (48 states, all seasons). The EECs
(0.0007 g/L from SCI-GROW, and 4.8 g/L from GENEEC)
for fenhexamid are well below the DWLOCs and therefore, are below the
Agency's level of concern. Therefore, the Agency concludes with
reasonable certainty that residues of fenhexamid in drinking water do
not contribute significantly to the aggregate chronic human health
risk.
3. From non-dietary exposure. Fenhexamid is not registered for use
on residential non-food sites. Therefore, no non-occupational, non-
dietary exposure and risk are expected.
4. Cumulative exposure to substances with common mechanism of
toxicity. Section 408(b)(2)(D)(v) requires that, when considering
whether to establish, modify, or revoke a tolerance, the Agency
consider ``available information' concerning the cumulative effects of
a particular pesticide's residues and ``other substances that have a
common mechanism of toxicity.'
EPA does not have, at this time, available data to determine
whether fenhexamid has a common mechanism of toxicity with other
substances or how to include this pesticide in a cumulative risk
assessment. Unlike other pesticides for which EPA has followed a
cumulative risk approach based on a common mechanism of toxicity,
fenhexamid does not appear to produce a toxic metabolite produced by
other substances. For the purposes of this tolerance action, therefore,
EPA has not assumed that fenhexamid has a common mechanism of toxicity
with other substances. For information regarding EPA's efforts to
determine which chemicals have a common mechanism of toxicity and to
evaluate the cumulative effects of such chemicals, see the final rule
for Bifenthrin Pesticide Tolerances (62 FR 62961, November 26, 1997).
D. Aggregate Risks and Determination of Safety for U.S. Population
1. Acute risk. Acute aggregate risk is the sum of exposures
resulting from acute dietary food + acute drinking water. The Agency
did not identify an appropriate toxicological endpoint attributable to
a single (acute) dietary exposure.
2. Chronic risk. Using the TMRC, exposure assumptions described in
this unit, EPA has concluded that aggregate exposure to fenhexamid from
food will utilize 1.8% of the chronic PAD for the U.S. population. The
major identifiable subgroup with the highest aggregate exposure is
nursing infants (< 1="" year)="" discussed="" below.="" epa="" generally="" has="" no="" concern="" for="" exposures="" below="" 100%="" of="" the="" chronic="" pad="" because="" the="" chronic="" pad="" represents="" the="" level="" at="" or="" below="" which="" daily="" aggregate="" dietary="" exposure="" over="" a="" lifetime="" will="" not="" pose="" appreciable="" risks="" to="" human="" health.="" despite="" the="" [[page="" 28922]]="" potential="" for="" exposure="" to="" fenhexamid="" in="" drinking="" water,="" epa="" does="" not="" expect="" the="" aggregate="" exposure="" to="" exceed="" 100%="" of="" the="" chronic="" pad.="" epa="" concludes="" that="" there="" is="" a="" reasonable="" certainty="" that="" no="" harm="" will="" result="" from="" aggregate="" exposure="" to="" fenhexamid="" residues.="" 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.="" although="" short-="" and="" intermediate-term="" endpoints="" were="" identified,="" there="" are="" no="" residential="" uses="" for="" fenhexamid.="" 4.="" aggregate="" cancer="" risk="" for="" u.s.="" population.="" fenhexamid="" was="" classified="" as="" ``not="" likely''="" to="" be="" a="" human="" carcinogen.="" 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="" fenhexamid="" 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="" fenhexamid,="" epa="" considered="" data="" from="" developmental="" toxicity="" studies="" in="" the="" rat="" and="" rabbit="" and="" a="" 2-generation="" reproduction="" study="" in="" the="" rat.="" the="" developmental="" toxicity="" studies="" are="" designed="" to="" evaluate="" adverse="" effects="" on="" the="" developing="" organism="" resulting="" from="" maternal="" pesticide="" exposure="" gestation.="" reproduction="" studies="" provide="" information="" relating="" to="" effects="" from="" exposure="" to="" the="" pesticide="" on="" the="" reproductive="" capability="" of="" mating="" animals="" and="" data="" on="" systemic="" toxicity.="" ffdca="" section="" 408="" provides="" that="" epa="" shall="" apply="" an="" additional="" tenfold="" margin="" of="" safety="" for="" infants="" and="" children="" in="" the="" case="" of="" threshold="" effects="" to="" account="" for="" pre-and="" 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.="" margins="" of="" safety="" are="" incorporated="" into="" epa="" risk="" assessments="" either="" directly="" through="" use="" of="" a="" margin="" of="" exposure="" (moe)="" analysis="" or="" through="" using="" uncertainty="" (safety)="" factors="" in="" calculating="" a="" dose="" level="" that="" poses="" no="" appreciable="" risk="" to="" humans.="" epa="" believes="" that="" reliable="" data="" support="" using="" the="" standard="" uncertainty="" factor="" (usually="" 100="" for="" combined="" inter-="" and="" intra-species="" variability)="" and="" not="" the="" additional="" tenfold="" moe/="" uncertainty="" factor="" when="" epa="" has="" a="" complete="" data="" base="" under="" existing="" guidelines="" and="" when="" the="" severity="" of="" the="" effect="" in="" infants="" or="" children="" or="" the="" potency="" or="" unusual="" toxic="" properties="" of="" a="" compound="" do="" not="" raise="" concerns="" regarding="" the="" adequacy="" of="" the="" standard="" moe/safety="" factor.="" ii.="" pre-="" and="" postnatal="" sensitivity.="" qualitatively,="" there="" is="" evidence="" of="" increased="" susceptibility="" in="" rat="" pups="" compared="" to="" adults,="" based="" on="" the="" relative="" severity="" of="" effects="" in="" the="" 2-generation="" reproduction="" study="" in="" rats.="" the="" effects="" on="" pups="" were="" of="" concern="" because:="" significant="" pup="" body="" weight="" decreases="" were="" observed="" in="" both="" the="">1 and the F2 generations; the pup body
weight decreases in the F2 generation were observed during
early lactation (lactation days 7 through day 21) when the pups are
exposed to the test material primarily through the mother's milk; the
pup body weight decreases in the F1 generation were observed
during late lactation (lactation days 14 through 21) when the pups are
exposed to the test material through the mother's milk and through the
feed; and, in the metabolism study on fenhexamid, glucuronidation of
fenhexamid was clearly demonstrated to be the single major route of
metabolism, detoxification and excretion of fenhexamid in adult male
and female rats. The demonstrated poor glucuronidation capacity of rat
pups between days 7 and 21 indicates a possibly increased sensitivity
of pups and serves to support a concern for neonatal toxicity.
iii. Conclusion. There is a complete toxicity data base for
fenhexamid and exposure data are complete or are estimated based on
data that reasonably accounts for potential exposures. Although there
is qualitative evidence of increased susceptibility, the Agency decided
that an additional safety factor of 3x would be appropriate based on
the following reasons: the increased susceptibility demonstrated in the
2-generation reproduction study was only qualitative (not quantitative)
evidence and was observed only in the presence of parental toxicity;
the qualitative offspring effect was limited to decreased body weight
and no other adverse effects (e.g., decreased pup survival, behavioral
alterations, etc.) were observed; and there is no indication of
increased susceptibility of rat or rabbit fetuses to in utero exposure
in the prenatal developmental toxicity studies with fenhexamid.
2. Acute risk. An acute endpoint was not identified and this risk
assessment was not required.
3. Chronic risk. Using the exposure assumptions described in this
unit, EPA has concluded that highest aggregate exposure to fenhexamid
from food will utilize 6.6% of the chronic PAD for all infants (< 1="" year).="" epa="" generally="" has="" no="" concern="" for="" exposures="" below="" 100%="" of="" the="" chronic="" pad="" because="" the="" chronic="" pad="" represents="" the="" level="" at="" or="" below="" which="" daily="" aggregate="" dietary="" exposure="" over="" a="" lifetime="" will="" not="" pose="" appreciable="" risks="" to="" human="" health.="" despite="" the="" potential="" for="" exposure="" to="" fenhexamid="" in="" drinking="" water="" and="" from="" non-dietary,="" non-occupational="" exposure,="" epa="" does="" not="" expect="" the="" aggregate="" exposure="" to="" exceed="" 100%="" of="" the="" chronic="" pad.="" 4.="" short-="" or="" intermediate-term="" risk.="" there="" are="" no="" residential="" uses="" and="" thus="" these="" risks="" are="" not="" presented.="" 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="" fenhexamid="" residues.="" iii.="" other="" considerations="" a.="" metabolism="" in="" plants="" and="" animals="" the="" parent="" compound,="" fenhexamid,="" is="" the="" only="" compound="" of="" concern.="" radiolabeled="" fenhexamid="" plant="" metabolism="" studies="" were="" conducted="" on="" grapes,="" tomatoes,="" and="" apples.="" the="" qualitative="" nature="" of="" fenhexamid="" residues="" in="" plants="" is="" adequately="" understood.="" the="" data="" indicate="" very="" little="" translocation="" of="" residues,="" i.e.,="" residues="" of="" fenhexamid="" are="" non-="" systemic="" and="" are="" thus="" primarily="" surface="" residues.="" there="" are="" no="" animal="" feedstuffs="" associated="" with="" the="" uses="" of="" fenhexamid="" on="" grapes,="" strawberries,="" and="" ornamentals.="" therefore,="" no="" animal="" metabolism="" data="" were="" submitted="" or="" required.="" b.="" analytical="" enforcement="" methodology="" adequate="" enforcement="" methodology="" (a="" high="" performance="" liquid="" chromotography="" method="" with="" electrochemical="" detection)="" is="" available="" to="" enforce="" the="" tolerance="" expression.="" the="" method="" may="" be="" requested="" from:="" calvin="" furlow,="" prrib,="" irsd="" (7502c),="" office="" of="" pesticide="" programs,="" environmental="" protection="" agency,="" 401="" m="" st.,="" sw.,="" washington,="" dc="" 20460.="" office="" location="" and="" telephone="" number:="" rm.="" 101ff,="" 1921="" jefferson="" davis="" hwy.,="" arlington,="" va,="" (703)="" 305-5229.="" c.="" magnitude="" of="" residues="" an="" adequate="" number="" of="" geographically="" representative="" field="" trials="" were="" submitted="" to="" support="" the="" proposed="" uses="" on="" grapes="" and="" strawberries.="" these="" studies="" were="" conducted="" via="" use="" patterns="" approximating="" those="" proposed="" by="" the="" petition="" requesting="" these="" tolerances.="" the="" data="" indicate="" that="" residues="" of="" fenhexamid="" will="" not="" exceed="" the="" proposed="" tolerances.="" residues="" concentrated="" an="" average="" of="" 1.9x="" in="" raisins.="" multiplying="" 1.9x="" by="" the="" highest="" [[page="" 28923]]="" average="" field="" trial="" residue="" value="" in="" grapes="" (2.3="" ppm),="" yields="" 5.3="" ppm="" as="" the="" maximum="" residue="" expected="" in="" raisins="" which="" is="" below="" the="" proposed="" tolerance="" of="" 6.0="" ppm.="" the="" concentration="" factor="" was=""> 0.25x in
juice and 0.5x in wine grapes based on data from red and
white wine grapes.
D. International Residue Limits
There are no codex, Canadian or Mexican maximum residue limits
established for this chemical. This petition was jointly reviewed with
Canada's Pest Management and Regulatory Agency and the tolerances
proposed have been harmonized with Canada.
E. Rotational Crop Restrictions
The Agency concluded that a 30-day plantback interval is required
for all crops without a fenhexamid tolerance.
IV. Conclusion
Therefore, tolerances are established for residues of fenhexamid in
or on grapes at 4.0 ppm, strawberries at 3.0 ppm, and raisins at 6.0
ppm.
V. Objections and Hearing Requests
The new FFDCA section 408(g) provides essentially the same process
for persons to ``object'' to a tolerance regulation as was provided in
the old section 408 and in section 409. However, the period for filing
objections is 60 days, rather than 30 days. EPA currently has
procedural regulations which govern the submission of objections and
hearing requests. These regulations will require some modification to
reflect the new law. However, until those modifications can be made,
EPA will continue to use those procedural regulations with appropriate
adjustments to reflect the new law.
Any person may, by July 27, 1999, file written objections to any
aspect of this regulation and may also request a hearing on those
objections. Objections and hearing requests must be filed with the
Hearing Clerk, at the address given under the ``ADDRESSES'' section (40
CFR 178.20). A copy of the objections and/or hearing requests filed
with the Hearing Clerk should be submitted to the OPP docket for this
regulation. The objections submitted must specify the provisions of the
regulation deemed objectionable and the grounds for the objections (40
CFR 178.25). Each objection must be accompanied by the fee prescribed
by 40 CFR 180.33(i). EPA is authorized to waive any fee requirement
``when in the judgement of the Administrator such a waiver or refund is
equitable and not contrary to the purpose of this subsection.'' For
additional information regarding tolerance objection fee waivers,
contact James Tompkins, Registration Division (7505C), Office of
Pesticide Programs, Environmental Protection Agency, 401 M St., SW.,
Washington, DC 20460. Office location, telephone number, and e-mail
address: Rm. 239, CM #2, 1921 Jefferson Davis Hwy., Arlington, VA,
(703) 305-5697, tompkins.jim@epa.gov. Requests for waiver of tolerance
objection fees should be sent to James Hollins, Information Resources
and Services Division (7502C), Office of Pesticide Programs,
Environmental Protection Agency, 401 M St., SW., Washington, DC 20460.
If a hearing is requested, the objections must include a statement
of the factual issues on which a hearing is requested, the requestor's
contentions on such issues, and a summary of any evidence relied upon
by the requestor (40 CFR 178.27). A request for a hearing will be
granted if the Administrator determines that the material submitted
shows the following: There is genuine and substantial issue of fact;
there is a reasonable possibility that available evidence identified by
the requestor would, if established, resolve one or more of such issues
in favor of the requestor, taking into account uncontested claims or
facts to the contrary; and resolution of the factual issues in the
manner sought by the requestor would be adequate to justify the action
requested (40 CFR 178.32). Information submitted in connection with an
objection or hearing request may be claimed confidential by marking any
part or all of that information as CBI. Information so marked will not
be disclosed except in accordance with procedures set forth in 40 CFR
part 2. A copy of the information that does not contain CBI must be
submitted for inclusion in the public record. Information not marked
confidential may be disclosed publicly by EPA without prior notice.
VI. Public Record and Electronic Submissions
EPA has established a record for this regulation under docket
control number [OPP-300866] (including any comments and data submitted
electronically). A public version of this record, including printed,
paper versions of electronic comments, which does not include any
information claimed as CBI, is available for inspection from 8:30 a.m.
to 4 p.m., Monday through Friday, excluding legal holidays. The public
record is located in Rm. 119 of the Public Information and Records
Integrity Branch, Information Resources and Services Division (7502C),
Office of Pesticide Programs, Environmental Protection Agency, CM #2,
1921 Jefferson Davis Hwy., Arlington, VA.
Objections and hearing requests may be sent by e-mail directly to
EPA at:
opp-docket@epa.gov
E-mailed objections and hearing requests must be submitted as an
ASCII file avoiding the use of special characters and any form of
encryption.
The official record for this regulation, as well as the public
version, as described in this unit will be kept in paper form.
Accordingly, EPA will transfer any copies of objections and hearing
requests received electronically into printed, paper form as they are
received and will place the paper copies in the official record which
will also include all comments submitted directly in writing. The
official record is the paper record maintained at the Virginia address
in ``ADDRESSES'' at the beginning of this document.
VII. Regulatory Assessment Requirements
A. Certain Acts and Executive Orders
This final rule establishes tolerances under section 408(d) of the
FFDCA in response to a petition submitted to the Agency. The Office of
Management and Budget (OMB) has exempted these types of actions from
review under Executive Order 12866, entitled Regulatory Planning and
Review (58 FR 51735, October 4, 1993). This final rule does not contain
any information collections subject to OMB approval under the Paperwork
Reduction Act (PRA), 44 U.S.C. 3501 et seq., or impose any enforceable
duty or contain any unfunded mandate as described under Title II of the
Unfunded Mandates Reform Act of 1995 (UMRA) (Pub. L. 104-4). Nor does
it require any special considerations as required by Executive Order
12898, entitled Federal Actions to Address Environmental Justice in
Minority Populations and Low-Income Populations (59 FR 7629, February
16, 1994), or require OMB review in accordance with Executive Order
13045, entitled Protection of Children from Environmental Health Risks
and Safety Risks (62 FR 19885, April 23, 1997).
In addition, since tolerances and exemptions that are established
on the basis of a petition under FFDCA section 408(d), such as the
tolerances in this final rule, do not require the issuance of a
proposed rule, the requirements of the Regulatory Flexibility Act (RFA)
(5 U.S.C. 601 et seq.) do not apply. Nevertheless, the Agency
previously assessed whether establishing tolerances, exemptions from
tolerances,
[[Page 28924]]
raising tolerance levels or expanding exemptions might adversely impact
small entities and concluded, as a generic matter, that there is no
adverse economic impact. The factual basis for the Agency's generic
certification for tolerance actions published on May 4, 1981 (46 FR
24950), and was provided to the Chief Counsel for Advocacy of the Small
Business Administration.
B. Executive Order 12875
Under Executive Order 12875, entitled Enhancing the
Intergovernmental Partnership (58 FR 58093, October 28, 1993), EPA may
not issue a regulation that is not required by statute and that creates
a mandate upon a State, local or tribal government, unless the Federal
government provides the funds necessary to pay the direct compliance
costs incurred by those governments. If the mandate is unfunded, EPA
must provide to OMB a description of the extent of EPA's prior
consultation with representatives of affected State, local, and tribal
governments, the nature of their concerns, copies of any written
communications from the governments, and a statement supporting the
need to issue the regulation. In addition, Executive Order 12875
requires EPA to develop an effective process permitting elected
officials and other representatives of State, local, and tribal
governments ``to provide meaningful and timely input in the development
of regulatory proposals containing significant unfunded mandates.''
Today's rule does not create an unfunded Federal mandate on State,
local, or tribal governments. The rule does not impose any enforceable
duties on these entities. Accordingly, the requirements of section 1(a)
of Executive Order 12875 do not apply to this rule.
C. Executive Order 13084
Under Executive Order 13084, entitled Consultation and Coordination
with Indian Tribal Governments (63 FR 27655, May 19, 1998), EPA may not
issue a regulation that is not required by statute, that significantly
or uniquely affects the communities of Indian tribal governments, and
that imposes substantial direct compliance costs on those communities,
unless the Federal government provides the funds necessary to pay the
direct compliance costs incurred by the tribal governments. If the
mandate is unfunded, EPA must provide OMB, in a separately identified
section of the preamble to the rule, a description of the extent of
EPA's prior consultation with representatives of affected tribal
governments, a summary of the nature of their concerns, and a statement
supporting the need to issue the regulation. In addition, Executive
Order 13084 requires EPA to develop an effective process permitting
elected officials and other representatives of Indian tribal
governments ``to provide meaningful and timely input in the development
of regulatory policies on matters that significantly or uniquely affect
their communities.''
Today's rule does not significantly or uniquely affect the
communities of Indian tribal governments. This action does not involve
or impose any requirements that affect Indian tribes. Accordingly, the
requirements of section 3(b) of Executive Order 13084 do not apply to
this rule.
VIII. Submission to Congress and the Comptroller General
The Congressional Review Act, 5 U.S.C. 801 et seq., as added by the
Small Business Regulatory Enforcement Fairness Act of 1996, generally
provides that before a rule may take effect, the Agency promulgating
the rule must submit a rule report, which includes a copy of the rule,
to each House of the Congress and the Comptroller General of the United
States. EPA will submit a report containing this rule and other
required information to the U.S. Senate, the U.S. House of
Representatives and the Comptroller General of the United States prior
to publication of the rule in the Federal Register. This rule is not a
``major rule'' as defined by 5 U.S.C. 804(2).
List of Subjects in 40 CFR Part 180
Environmental protection, Administrative practice and procedure,
Agricultural commodities, Pesticides and pests, Reporting and
recordkeeping requirements.
Dated: May 19, 1999.
Susan B. Hazen,
Acting Director, Office of Pesticide Programs.
Therefore, 40 CFR chapter I is amended as follows:
PART 180-[AMENDED]
1. The authority citation for part 180 continues to read as
follows:
Authority: 21 U.S.C. 321(q), (346a) and 371.
2. Section 180.553, is added to subpart C to read as follows:
Sec. 180.553 Fenhexamid; tolerances for residues.
(a) General. Tolerances are established for the residues of the
fungicide fenhexamid (N-2,3-dichloro-4-hydroxyphenyl)-1-methyl
cyclohexanecarboxamide) in or on the following commodities:
------------------------------------------------------------------------
Commodity Parts per million
------------------------------------------------------------------------
Grapes......................................... 4.0
Raisins........................................ 6.0
Strawberries................................... 3.0
------------------------------------------------------------------------
(b) Section 18 emergency exemptions. [Reserved]
(c) Tolerances with regional registrations. [Reserved]
(d) Indirect or inadvertent residues. [Reserved]
[FR Doc. 99-13656 Filed 5-27-99; 8:45 am]
BILLING CODE 6560-50-F
