[Federal Register Volume 64, Number 18 (Thursday, January 28, 1999)]
[Rules and Regulations]
[Pages 4301-4308]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 99-1901]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-300778; FRL 6053-8]
RIN 2070-AB78


Diflufenzopyr; Pesticide Tolerance

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes a tolerance for combined residues 
of diflufenzopyr, 2-(1-[([3,5-difluorophenylamino]carbonyl)-
hydrazono]ethyl)-3-pyridinecarboxylic acid, and its metabolites 
convertible to M1 (8-methylpyrido[2,3-d]pyridazin-5(6H)-one) in or on 
field corn stover, forage and grain. BASF Corporation requested this 
tolerance under the Federal Food, Drug, and Cosmetic Act (FFDCA), as 
amended by the Food Quality Protection Act of 1996 (Pub. L. 104-170).

DATES: This regulation is effective January 28, 1999. Objections and 
requests for hearings must be received by EPA on or before March 29, 
1999.

ADDRESSES: Written objections and hearing requests, identified by the 
docket control number, [OPP-300778], must be submitted to: Hearing 
Clerk (1900), Environmental Protection Agency, Rm. M3708, 401 M St., 
SW., Washington, DC 20460. Fees accompanying objections and hearing 
requests shall be labeled ``Tolerance Petition Fees'' and forwarded to: 
EPA Headquarters Accounting Operations Branch, OPP (Tolerance Fees), 
P.O. Box 360277M, Pittsburgh, PA 15251. A copy of any objections and 
hearing requests filed with the Hearing Clerk identified by the docket 
control number, [OPP-300778], must also be submitted to: Public 
Information and Records Integrity Branch, Information Resources and 
Services Division (7502C), Office of Pesticide Programs, Environmental 
Protection Agency, 401 M St., SW., Washington, DC 20460. In person, 
bring a copy of objections and hearing requests to Rm. 119, Crystal 
Mall #2, 1921 Jefferson Davis Hwy., Arlington, VA.
    A copy of objections and hearing requests filed with the Hearing 
Clerk may also be submitted electronically by sending electronic mail 
(e-mail) to: [email protected]. 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 
or ASCII file format. All copies of objections and hearing requests in 
electronic form must be identified by the docket control number [OPP-
300778]. 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: Joanne I. Miller, 
Registration Division (7505C), Office of Pesticide Programs, 
Environmental Protection Agency, 401 M St., SW., Washington, DC 20460. 
Office location, telephone number, and e-mail address: Crystal Mall #2, 
1921 Jefferson Davis Hwy., Arlington, VA, (703) 305-6224; e-mail: 
[email protected].

SUPPLEMENTARY INFORMATION: In the Federal Register of November 21, 
1997, (62 FR 62304) (FRL 5755-4), EPA, issued a notice pursuant to 
section 408 of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21 
U.S.C. 346a(e) announcing the filing of a pesticide petition (PP) for 
tolerance by BASF Corporation, P.O. Box 13528, Research Triangle Park, 
North Carolina 27709. This notice included a summary of the petition 
prepared by BASF Corporation, the registrant. 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 combined residues of the herbicide 
diflufenzopyr, 2-(1-[([3,5-difluorophenylamino]carbonyl)-
hydrazono]ethyl)-3-pyridinecarboxylic acid, and its metabolites 
convertible to M1, (8-methylpyrido[2,3-d]pyridazin-5(6H)-one), in or on 
field corn fodder (stover), forage and grain at 0.05 part per million 
(ppm). Note that the scientific assessments relevant to establishing 
these tolerances for diflufenzopyr were conducted jointly between EPA 
and the Pest Management Regulatory Agency (PMRA) of Canada as a project 
under the North American Free Trade Agreement (NAFTA) and the Canadian 
United States Trade Agreement (CUSTA). Diflufenzopyr qualified as a 
candidate for such a program due to its classification as a reduced 
risk pesticide.

[[Page 4302]]

I. Risk Assessment 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, November 26, 1997, (62 FR 62961) (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 
diflufenzopyr and to make a determination on aggregate exposure, 
consistent with section 408(b)(2), for tolerances for combined residues 
of diflufenzopyr, 2-(1-[([3,5-difluorophenylamino] 
carbonyl)hydrazono]ethyl)-3-pyridinecarboxylic acid, and its 
metabolites convertible to M1, (8-methylpyrido[2,3-d]pyridazin-5(6H)-
one) on field corn stover, forage and grain at 0.05 ppm. EPA's 
assessment of the dietary exposures and risks associated with 
establishing the tolerance follows.

A. Toxicological Profile

    EPA has evaluated the available toxicity data and considered its 
validity, completeness, and reliability as well as the relationship of 
the results of the studies to human risk. EPA has also considered 
available information concerning the variability of the sensitivities 
of major identifiable subgroups of consumers, including infants and 
children. The nature of the toxic effects caused by diflufenzopyr are 
discussed below.
     1. Acute toxicology studies place technical-grade diflufenzopyr in 
Toxicity Category III or IV for all routes of exposure. It is not a 
dermal sensitizer.
     2. In a subchronic feeding study in rats, male and female Wistar 
rats were fed test diets containing technical diflufenzopyr, purity 
96%, at dose levels of 0, 1,000, 5,000, 10,000 and 20,000 ppm (equal to 
0, 60.8, 352, 725 and 1,513 milligram/kilogram body weight/day (mg/kg 
bw/day) for males, and 0, 72.8, 431, 890 and 1,750 mg/kg bw/day for 
females) for a period of 13 weeks, 10 rats per sex per group. An 
additional 10 rats per sex were assigned to the 0 and 20,000 ppm groups 
for a 4-week recovery period following treatment. The no observed 
adverse effect level (NOAEL) was set at 5,000 ppm (equal to 352 mg/kg 
bw/day for males, and 431 mg/kg bw/day for females) based on lower mean 
body weight gain and decreased food efficiency in the 10,000 and 20,000 
ppm groups, both sexes. Additional findings were decreased food intake 
(20,000 ppm, males only); slight increases in cholesterol (20,000 ppm, 
both sexes, and 10,000 ppm, males only) and ALAT (10,000 and 20,000 
ppm, both sexes); and slightly lower chloride (20,000 ppm, both sexes). 
Histopathological findings were an increased incidence of foamy 
macrophages in the lungs in the 10,000 and 20,000 ppm groups, both 
sexes, and testicular atrophy in the 20,000 ppm group. Following the 4-
week recovery period, the only treatment-related effects which showed 
partial or no evidence of recovery were foamy macrophages in the lungs 
and testicular atrophy.
     3. In a 13-week feeding study, male and female CD-1 mice were fed 
test diets containing technical diflufenzopyr, purity 97.1%, at dietary 
concentrations of 0, 350, 1,750, 3,500 and 7,000 ppm (equal to 0, 58, 
287, 613 and 1,225 mg/kg bw/day for males, and 0, 84, 369, 787 and 
1,605 mg/kg bw/day for females) for a period of 13 weeks, 10 mice per 
sex per group. The NOAEL was determined to be 7,000 ppm (equal to 1,225 
mg/kg bw/day for males and 1,605 mg/kg bw/day for females) since there 
were no treatment-related effects observed in male or female mice at 
any dose level tested.
     4. In a subchronic toxicity study in dogs, diflufenzopyr (98% 
a.i.) was administered to beagle dogs (4/sex/dose) by feeding at dose 
levels of 0, 1,500, 10,000, or 30,000 ppm (0, 58, 403, or 1,131 mg/kg/
day for males; 0, 59, 424, or 1,172 mg/kg/day for females) for 13 
weeks. The lowest adverse effect level (LOAEL) for this study is 10,000 
ppm (403 mg/kg/day in males and 424 mg/kg/day in females), based on the 
occurrence of erythroid hyperplasia in the bone marrow, extramedullary 
hemopoiesis in the liver, and hemosiderin deposits in Kupffer cells. 
The NOAEL is 1,500 ppm (58 mg/kg/day in males and 59 mg/kg/day in 
females).
     5. In the subchronic dermal toxicity study, technical 
diflufenzopyr, purity 96.4%, was moistened with distilled water and 
administered by dermal application to male and female New Zealand White 
rabbits, 5/sex/dose, at dose levels of 0, 100, 300 and 1,000 mg/kg bw 
per application. Duration of application was 6 hours a day, daily for 
21 to 24 consecutive days. The NOAEL for systemic toxicity was 
determined to be 1,000 mg/kg bw/day, since there were no apparent signs 
of treatment-related systemic effects observed in male or female 
rabbits at any dose level tested. A NOAEL for dermal effects could not 
be determined since local dermal irritation was observed at all dose 
levels tested (there were no corresponding findings upon 
histopathological examination).
     6. In a chronic toxicity study in dogs, diflufenzopyr (98.1% a.i.) 
was administered to beagle dogs (4/sex/dose) by feeding at dose levels 
of 0, 750, 7,500, or 15,000 ppm (0, 26, 299, or 529 mg/kg/day for 
males; 0, 28, 301, or 538 mg/kg/day for females) for 52 weeks. The 
LOAEL for this study is 7,500 ppm (299 mg/kg/day for males and 301 mg/
kg/day for females), based on erythroid hyperplasia in the bone marrow 
in bone sections, reticulocytosis, and increased hemosiderin deposits 
in the liver, kidneys, and spleen. The NOAEL is 750 ppm (26 mg/kg/day 
for males and 28 mg/kg/day for females).
     7. In a mouse carcinogenicity study, male and female CD-1 mice 
were fed test diets containing technical diflufenzopyr, purity 98.1%, 
at dietary concentrations of 0, 700, 3,500 and 7,000 ppm (equal to 0, 
100, 517 and 1,037 mg/kg bw/day for males, and 0, 98, 500 and 1,004 mg/
kg bw/day for females), 60 mice per sex per group, for a period of 78 
weeks. The NOAEL for systemic toxicity was determined to be 7,000 ppm 
(equal to 1,037 mg/kg bw/day for males and 1,004 mg/kg bw/day for 
females). There were no treatment-related effects observed at any dose 
level tested in male rats. There was a slight, but statistically 
significantly lower mean overall body weight gain for

[[Page 4303]]

females in the 7,000 ppm group, due primarily to decreased gain/
increased weight loss during the second year of the study. In the 
absence of any other treatment-related findings, this was not 
considered to be an adverse, toxicologically significant finding. There 
was no evidence of oncogenic potential of diflufenzopyr for male or 
female mice at any dose level tested.
     8. In a combined chronic toxicity/carcinogenicity study, male and 
female Wistar rats were fed test diets containing technical 
diflufenzopyr, purity 97.1% to 99.6%, at dietary concentrations of 0, 
500, 1,500, 5,000 and 10,000 ppm (equal to 0, 22, 69, 236 and 518 mg/kg 
bw/day for males, and 0, 29, 93, 323 and 697 mg/kg bw/day for females), 
72 rats per sex per group, for a period of 104 weeks. The NOAEL for 
systemic toxicity was set at 5,000 ppm (equal to 236 mg/kg bw/day for 
males and 323 mg/kg bw/day for females). Treatment-related effects in 
the 10,000 ppm group were significantly lower body weight and body 
weight gains throughout the study period and decreased food efficiency. 
There was no evidence of oncogenic potential of diflufenzopyr at any 
dose level tested. The incidences of benign and malignant tumors were 
comparable between control and treated groups.
     9. In a developmental toxicity study, technical diflufenzopyr 
(98.1% a.i.) in 0.5% aqueous methyl cellulose was administered by 
gavage to 25 female Crl: CD BR VAF/Plus (Sprague Dawley) rats/dose at 
dose levels of 0, 100, 300, or 1,000 mg/kg/day from days 6 through 15 
of gestation. The maternal NOAEL is 300 mg/kg/day and the maternal 
LOAEL is 1,000 mg/kg/day based on decreases in food consumption and 
weight gain. Developmental effects, characterized as significantly 
lower fetal body weights in males ( 5%) and skeletal variations, 
exhibited as incompletely ossified and unossified sternal centra and 
reduced fetal ossification sites for caudal vertebrae, were observed at 
1,000 mg/kg/day. The developmental LOAEL is 1,000 mg/kg/day, based on 
decreased fetal body weights and skeletal variations. The developmental 
NOAEL is 300 mg/kg/day.
     10. In a developmental toxicity study, technical diflufenzopyr 
(98.1% a.i.) in 0.5% aqueous methyl cellulose was administered by 
gavage to 20 female New Zealand White Hra: (NZW)SPF rabbits/dose at 
dose levels of 0, 30, 100, or 300 mg/kg/day from days 6 through 19 of 
gestation. The maternal LOAEL is 100 mg/kg/day, based on minimal 
reductions in body weight gain with no reduction in food consumption 
and clinical signs of toxicity (abnormal feces). The maternal NOAEL is 
30 mg/kg/day. Developmental effects, characterized as significant 
increases (p0.01) in the incidence of supernumerary thoracic 
rib pair ossification sites (12.74 vs. 12.54 for controls) occurred at 
the 300 mg/kg/day dose. No treatment-related developmental effects were 
noted at the low- or mid-doses. The developmental LOAEL is 300 mg/kg/
day based on increased skeletal variations (supernumerary rib 
ossification sites). The developmental NOAEL is 100 mg/kg/day.
     11. In a 2-generation reproduction study, technical diflufenzopyr 
(98.1% a.i.) was administered continuously in the diet to 26 Wistar 
rats/sex/dose at dose levels of 0, 500, 2,000 or 8,000 ppm in the diet 
(0, 27.3-42.2, 113.1-175.9, or 466.2-742.0 mg/kg/day). The systemic 
LOAEL is 2,000 ppm (113.1-175.9 mg/kg/day) based on reduced body weight 
gain, increased food consumption, and increased seminal vesicle 
weights. The systemic NOAEL is 500 ppm (27.3-42.2 mg/kg/day). The 
reproductive LOAEL is 8,000 ppm (466.2-742.0 mg/kg/day) based on lower 
live birth and viability indices, total pre-perinatal loss, reduced 
body weights and body weight gain during lactation, a higher proportion 
of runts, and a higher percentage of offspring with no milk in the 
stomach. The reproductive NOAEL is 2,000 ppm (113.1-175.9 mg/kg/day).
     12. In an acute neurotoxicity study, diflufenzopyr (96.4% a.i.) 
was administered by gavage to Crl:CD BR rats (10/sex/group) at dose 
levels of 0, 125, 500 or 2,000 mg/kg. The rats were evaluated for 
reactions in functional observations and motor activity measurements at 
3 hours, 7 days, and 14 days postdosing. Histopathological evaluation 
on the brain and peripheral nerves was assessed after day 14. 
Diflufenzopyr had no definite impact on neurotoxic responses, although 
a few abnormalities were observed in the functional battery on the day 
of dosing. A decrease in immediate righting responses that was observed 
in several males in all treatment groups was not concentration-
dependent. Nasal staining was observed in more rats in the 2,000 mg/kg 
treatment groups (6 males; 3 females), but was not considered a 
definite or significant response to treatment. Lower mean brain weights 
in all female treatment groups lacked associated macroscopic and 
microscopic histopathological changes, and were only 4-5% lower than 
the control brain weight. Mean locomotor activities for the 2,000 mg/kg 
female treatment groups were decreased on Days 7 ( 27%, p < 
0.05) and 14 (15%, not significant) after dosing, but the 
pattern of activity for the individual animals was similar to the 
individual controls over time. There were no definite treatment-related 
differences in body weights or food consumption in any of the treatment 
groups. There was no evidence of treatment-related neuropathology in 
the 2,000 mg/kg treatment group. A LOAEL was not established. The NOAEL 
for acute neurotoxicity is 2,000 mg/kg (the limit dose).
     13. In a subchronic neurotoxicity study, diflufenzopyr (96.4% 
a.i.) was administered in the diet to Crl: CD BR rats (10/sex/group) at 
dose levels of 0, 25, 75 or 1,000 mg/kg/day for 13 weeks. The rats were 
evaluated for reactions in functional observations and motor activity 
testing at 4 hours and during weeks 4, 8 and 13 of treatment. No 
treatment-related neurotoxicological effects were observed at any 
treatment level. A LOAEL for neurotoxicological effects was not 
established; the NOAEL was 1,000 mg/kg/day for both sexes. Treatment-
related toxic effects were observed at the 1,000 mg/kg/day treatment 
level. The toxicological LOAEL for this study is 1,000 mg/kg/day, based 
on decreased body weight gains for both sexes. The toxicological NOAEL 
is 75 mg/kg/day.
     14. In a microbial mutagenicity assay, Salmonella typhimurium 
strains TA98, TA100, TA1535, TA1537, and TA1538 were exposed to 
diflufenzopyr (97.1%) in DMSO at concentrations of 333, 667, 1,000, 
3,330, 6,670 and 10,000 g/plate in the presence and absence of 
mammalian metabolic activation. Diflufenzopyr (97.1%) was tested to 
twice the limit concentration of 5,000 g/plate and 
cytotoxicity was observed at 6,670 and 10,000 g/plate in the 
absence of activation (-S9) but not in its presence (+S9). The positive 
controls induced the appropriate responses in the corresponding 
strains. There was no evidence that the test article induced mutant 
colonies over background.
     15. In a mammalian cell gene mutation assay at the thymidine 
kinase locus, heterozygous L5178Y (TK +/-) mouse lymphoma cells 
cultured in vitro were exposed in independent repeat assays to 
diflufenzopyr technical (97.1% a.i.) in dimethyl sulfoxide at dose 
levels ranging from 0.05 to 3.0 mg/mL (50 to 3,000 g/mL) in 
the presence and absence of S9 mammalian metabolic activation in the 
first trial, and 0.05 to 2.0 mg/mL (50 to 2,000 g/mL) in the 
second. Diflufenzopyr was tested up to cytotoxic dose levels and 
mutation frequencies were determined for dose levels selected on the 
basis of relative

[[Page 4304]]

growth. Although initially declared positive by the then study 
director, application of more recent criteria for mutagenic responses 
has rendered the test article negative for forward gene mutation at the 
TK locus in mouse L5178Y cells in the presence and absence of S9 
activation. The positive controls induced the appropriate responses.
     16. In an in vivo mouse bone marrow micronucleus assay, groups of 
15 male and female ICR mice were dosed by oral gavage with 
diflufenzopyr (technical, 97.1%) in corn oil at 500, 1,667, and 5,000 
mg/kg. Bone marrow cells were harvested at 24, 48, or 72 hours and 
scored for micronucleated polychromatic erythrocytes (MPCEs). No 
mortalities or adverse clinical signs were observed at any dose 
including the limit dose of 5,000 mg/kg, and there were no changes in 
the PCE/NCE ratios (an indirect measure of cytotoxicity). The positive 
control induced significant increases in MPCEs, also in the absence of 
any target cell cytotoxicity. No significant increase in the frequency 
of MPCEs in bone marrow cells after any treatment time were recorded; 
therefore, the test article is considered negative in this micronucleus 
assay.
     17. In an unscheduled DNA synthesis assay, primary rat hepatocyte 
cultures were exposed to diflufenzopyr (97.1% a.i.) in 
dimethylsulfoxide (DMSO) at 15 concentrations ranging from 0.0250 to 
1,000 g/mL in the presence of 10Ci/ml3 
HtdR (42 Ci/mmole) for approximately 19 hours. Mutagenicity, as 
measured by unscheduled DNA synthesis (UDS), was determined for 6 
concentrations selected on the basis of cytotoxicity. The 
concentrations selected were 5.00, 10.0, 25.0, 50.0, 100, and 250 
g/mL. The highest concentration selected for UDS evaluation, 
250 g/mL, was moderately toxic (50.8% survival). There was no 
evidence that unscheduled DNA synthesis, as determined by radioactive 
tracer procedures (nuclear silver grain counts) was induced. The 
positive control induced the appropriate response.
     18. In a rat metabolism study, (phenyl-U-14C) or 
(pyridinyl-4,6-14C) diflufenzopyr was administered to five 
Wistar rats/sex/dose group as a single intravenous dose at 1 mg/kg/day, 
a single oral dose (gavage) at 10 or 1,000 mg/kg or a single dose at 10 
mg/kg following a 14-day pretreatment with unlabeled diflufenzopyr at 
10 mg/kg. Bile-duct cannulated rats from each dose group were 
sacrificed at 48 hours post-dose (Subgroup 2). Non-cannulated rats from 
each dose group were sacrificed at 72 hours (Subgroup 1) or 24 hours 
(Subgroup 3) post-dose. (14C) Diflufenzopyr was only 
partially absorbed from the GI tracts of orally dosed rats as indicated 
by the levels of excretion in urine and bile. In all orally dosed 
groups, 20-44% of the dose was excreted in the urine and 3-11% was 
excreted in the bile. In contrast, intravenously dosed rats excreted 
61-89% of the dose in urine and 4-19% of the dose in bile. For all 
orally dosed groups, the level of absorption was similar between sexes. 
Dose level and pretreatment had little effect on the proportion of the 
dose excreted in urine following oral administration. Enterohepatic 
circulation plays a role in the elimination of 14C 
diflufenzopyr in rats. 3-19% of the dose was recovered in the bile of 
all dose groups. Within 72 hours of dosing, intravenously-dosed rats 
excreted the majority of radioactivity in urine (61-89%), whereas 
orally-dosed rats excreted most of the radioactivity in feces (49-79%), 
regardless of radiolabel or sex. Pretreatment did not appear to affect 
the pattern of excretion. Bile-cannulated rats excreted lesser amounts 
in feces compared to non-cannulated rats; 3-19% of the dose was 
excreted in bile. The estimated half-lives of radiocarbon eliminated in 
urine and feces was 5.3-6.9 hours for all single intravenous and oral 
dose groups, and 7.7-10.8 hours for all repeat oral dose groups. Total 
radioactive residues in tissues from rats in all dose groups were <3% 
of the administered dose. Total tissue residue levels were highest in 
rats sacrificed at 24 hours post-dose; residue levels were highest in 
blood, blood cell, and serum for the phenyl label groups, and were 
highest in liver and kidney for the pyridinyl label groups. Blood 
residue levels for all dose groups were <1% of the administered dose at 
all sampling intervals through 72 hours post-dose. TLC and HPLC 
analyses were conducted on 0-72 and 0-48 urine and feces samples, and 
on 0-48 hour bile samples from each treatment regimen. The structures 
of the metabolites were confirmed using 2-D TLC, HPLC, LC/MS, DIP/MS, 
FAB/MS, and proton NMR. For each dose group, the metabolic profile was 
similar between sexes, except for differences in metabolite levels. 
Unchanged diflufenzopyr was identified as the major component in urine, 
feces, and bile from all dose groups using either radiolabel. Urinary 
metabolites identified in the 14C-phenyl labeled dose groups 
included: 3,5-difluoroaniline (M2; aniline) and 6-((3,5-difluorophenyl) 
carbomyl)-8-methyl-pyrido (2,3-d)-5-pyridazinone (M5; carbamoyl 
phthalazinone). Urinary metabolites identified in the 14C-
pyridinyl labeled dose groups included: 8-methyl-5-hydroxy-pyrido(2,3-
d)-pyridazine (M1; phthalazinone); carbamoyl phthalazinone (M5); 2-
acetyl nicotinic acid (M6; 2-acetyl nicotinic acid); 8-
methylpyrido[2,3-d]pyridazine-2,5(1H, 6H)-dione (M9; 2-keto-M1); 8-
hydroxymethyl-5(6H)-pyrido[2,3-d]pyridazinone (M10; 8-hydroxymethyl-
M1); and, 8-hydroxymethylpyrido[2,3-d]pyridazine-2,5(1H,6H)-dione (M19; 
2-keto-8-hydroxymethyl-M1 or Metabolite E). Fecal metabolites 
identified in the phenyl label groups included: methyl N-(3,5-
difluorophenyl)carbamate (M8) and M5. Fecal metabolites identified in 
the pyridinyl label groups included: M1, M5, M6, M9, and M10. Besides 
parent, bile samples also contained minor amounts of M5 (both labels) 
and M1 (pyridinyl label only). The data indicate that diflufenzopyr is 
excreted primarily as unchanged parent in urine, feces, and bile. Minor 
amounts of hydrolysis products (M1, M5, and M6) and hydroxylation 
products (M9, M10, and M19) were identified in excreta.

B. Toxicological Endpoints

    1. Acute toxicity. For acute dietary risk assessment, an acute 
Reference Dose (RfD) of 1.0 mg/kg/day has been selected, based on the 
developmental NOAEL of 100 mg/kg/day from the Rabbit Developmental 
Study and an uncertainty factor of 100 (10x for interspecies 
differences and 10x for intraspecies variations). The endpoint is based 
on developmental findings (increased skeletal variations) in rabbits 
which can be attributed to a single gavage dose during gestation and 
which occurred at a maternally toxic dose. The population subgroup at 
risk for this developmental effect is females of child-bearing age (13+ 
years). No appropriate toxicological endpoint is available in the data 
base for other subgroups of the population including infants and 
children.
     2. Short - and intermediate - term toxicity. Since there was no 
observed dermal or systemic toxicity in a rabbit 21-day dermal study 
with diflufenzopyr, short- and intermediate-term toxicity endpoints are 
not being established.
     3. Chronic toxicity. EPA has established the RfD for diflufenzopyr 
at 0.26 milligrams/kilogram/day (mg/kg/day). This RfD is based on bone 
marrow compensated hemolytic anemia observed in the 1-year dog feeding 
study with a NOAEL of 26 mg/kg/day.
    4. Carcinogenicity. Based on the lack of evidence of 
carcinogenicity in mice and rats at doses that were judged to be 
adequate to assess the carcinogenic

[[Page 4305]]

potential, diflufenzopyr has been characterized as ``not likely'' to be 
a human carcinogen.

C. Exposures and Risks

    1. From food and feed uses. No previous tolerances have been 
established for the combined residues of diflufenzopyr, 2-(1-[([3,5-
difluorophenylamino]carbonyl)-hydrazono]ethyl)-3-pyridinecarboxylic 
acid, and its metabolites convertible to M1, (8-methylpyrido[2,3-
d]pyridazin-5(6H)-one). Risk assessments were conducted by EPA to 
assess dietary exposures from diflufenzopyr as follows:
    i.  Acute exposure and risk. Acute dietary risk assessments are 
performed for a food-use pesticide if a toxicological study has 
indicated the possibility of an effect of concern occurring as a result 
of a one day or single exposure. An acute dietary risk assessment was 
performed for diflufenzopyr, its metabolites characterized as M1, and 
M10. The analysis was conducted using the acute RfD of 1.0 mg/kg/day, 
based on developmental findings (increased skeletal variations) 
observed in the Rabbit Developmental Study. For the population subgroup 
of concern, females 13 years and older, the estimated 95th percentile 
of exposure is equal to 0.01% of the acute RfD. The analysis is 
conservative since it assumes that 100% of corn-derived foods contain 
residues at the tolerance level (0.05 ppm).
    ii. Chronic exposure and risk. A chronic dietary risk assessment 
was performed for diflufenzopyr, its metabolites characterized as M1, 
and M10. The analysis used the RfD of 0.26 mg/kg bwt/day and assumed 
that 100% of corn-derived foods contain residues at the tolerance level 
(0.05 ppm). These assumptions result in a Theoretical Maximum Residue 
Contribution (TMRC) that is less than or equal to 0.1% of the RfD for 
the overall U.S. population (48 states) and all population subgroups.
    2. From drinking water. There are no established Maximum 
Contaminant Levels or health advisory levels for residues of 
diflufenzopyr or its metabolites in drinking water. EPA used the SCI-
GROW (Screening Concentration in Ground Water) model to estimate 
residues of diflufenzopyr in ground water and the GENEEC (Generic 
Expected Environmental Concentration) model to estimate diflufenzopyr 
residue levels in surface water. Estimated environmental concentrations 
(EECs) in ground water reflecting an application rate of 0.12 pounds of 
active ingredient per acre were 0.006 parts per billion (ppb) for acute 
and chronic exposure scenarios. EECs in surface water were 3.8 ppb for 
acute exposure scenarios and 1.95 ppb for chronic exposure scenarios. 
The computer generated EECs represent conservative estimates and should 
be used only for screening.
    i. Acute exposure and risk. EPA has calculated a drinking water 
level of comparison (DWLOC) for acute exposure to diflufenzopyr in 
drinking water for the relevant population subgroup, females 13 + years 
of age. THE DWLOC is 29,970 ug/L.
     To calculate the DWLOCs for acute exposure relative to an acute 
toxicity endpoint, the acute dietary food exposure from the DEEM 
(Dietary Exposure Evaluation Model) analysis was subtracted from the 
ratio of the acute NOAEL (used for acute dietary assessments) to the 
acceptable margin of exposure (MOE) for aggregate exposure to obtain 
the acceptable acute exposure to diflufenzopyr in drinking water. 
DWLOCs were then calculated using default body weights and drinking 
water consumption figures.
     Estimated maximum concentrations of diflufenzopyr in surface and 
ground water are 3.80 ppb and 0.006 ppb, respectively. The estimated 
maximum concentrations in water are less than EPA's level of comparison 
(29,970 ppb) for diflufenzopyr residues in drinking water as a 
contribution to acute aggregate exposure. Therefore, taking into 
account the use proposed in this action, EPA concludes with reasonable 
certainty that residues of diflufenzopyr in drinking water (when 
considered along with other sources of exposure for which EPA has 
reliable data) would not result in unacceptable levels of aggregate 
human health risk at this time.
    ii. Chronic exposure and risk. EPA has calculated drinking water 
levels of comparison (DWLOCs) for chronic exposure to diflufenzopyr in 
drinking water. For chronic (non-cancer) exposure to diflufenzopyr in 
surface and ground water, the drinking water levels of comparison are 
9,100 ug/L and 2,600 ug/L for the U.S. population and the subgroup 
children (1-6 years old), respectively.
     To calculate the DWLOCs for chronic (non-cancer) exposure relative 
to a chronic toxicity endpoint, the chronic dietary food exposure (from 
the DEEM analysis) and residential exposure were subtracted from the 
RfD to obtain the acceptable chronic (non-cancer) exposure to 
diflufenzopyr in drinking water. DWLOCs were then calculated using 
default body weights and drinking water consumption figures.
     Estimated average concentrations of diflufenzopyr in surface and 
ground water are 1.95 ppb and 0.006 ppb, respectively. The DWLOCs are 
9,100 ppb for the U.S. population and 2,600 ppb for the subgroup, 
children (1-6 years old). The estimated average concentrations of 
diflufenzopyr in surface and ground water are less than EPA's levels of 
comparison for diflufenzopyr in drinking water as a contribution to 
chronic aggregate exposure.
    3. From non-dietary exposure. There are no registered or proposed 
residential uses for diflufenzopyr.
    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 diflufenzopyr 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, 
diflufenzopyr 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 diflufenzopyr has a common mechanism of 
toxicity with other substances. For information regarding EPA's efforts 
to determine which chemicals have a common mechanism of toxicity and to 
evaluate the cumulative effects of such chemicals, see the Final Rule 
for Bifenthrin Pesticide Tolerances (62 FR 62961, November 26, 1997).

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

    1. Acute risk. For the population subgroup of concern, females 13+ 
years old, the acute dietary (food) exposure does not exceed 0.02% of 
the acute RfD. The drinking water level of comparison (DWLOC) for acute 
exposure to diflufenzopyr residues is 29,970 ug/L for females (13+ 
years). The maximum concentration of diflufenzopyr in drinking water 
(3.80 ug/L) is less than EPA's level of comparison for diflufenzopyr in 
drinking water as a contribution to acute aggregate exposure. EPA 
concludes with reasonable certainty that residues of diflufenzopyr in 
drinking water will not contribute significantly to the aggregate acute 
human health risk and that the

[[Page 4306]]

acute aggregate exposure from diflufenzopyr in food and water will not 
exceed the Agency's level of concern for acute dietary exposure.
    2. Chronic risk. Using the TMRC exposure assumptions described 
above, EPA has concluded that aggregate exposure to diflufenzopyr from 
food will utilize less than 0.1% of the RfD for the U.S. population. 
The major identifiable subgroup with the highest aggregate exposure, 
children 1-6 years old, is ``discussed below.'' EPA generally has no 
concern for exposures below 100% of the RfD because the RfD represents 
the level at or below which daily aggregate dietary exposure over a 
lifetime will not pose appreciable risks to human health. Despite the 
potential for exposure to diflufenzopyr in drinking water and from non-
dietary, non-occupational exposure, EPA does not expect the aggregate 
exposure to exceed 100% of the RfD. EPA concludes that there is a 
reasonable certainty that no harm will result from aggregate exposure 
to diflufenzopyr 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. There are no established or proposed residential 
uses for diflufenzopyr. Therefore, the short and intermediate aggregate 
risks are adequately addressed by the chronic aggregate dietary risk 
assessment.
    4. Aggregate cancer risk for U.S. population. Diflufenzopyr has 
been classifiedd 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 diflufenzopyr 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 diflufenzopyr, EPA considered data from 
developmental toxicity studies in the rat and rabbit and a two-
generation reproduction study in the rat. The developmental toxicity 
studies are designed to evaluate adverse effects on the developing 
organism resulting from maternal pesticide exposure gestation. 
Reproduction studies provide information relating to effects from 
exposure to the pesticide on the reproductive capability of mating 
animals and data on systemic toxicity.
    FFDCA section 408 provides that EPA shall apply an additional 
tenfold margin of safety for infants and children in the case of 
threshold effects to account for pre-and post-natal toxicity and the 
completeness of the database unless EPA determines that a different 
margin of safety will be safe for infants and children. Margins of 
safety are incorporated into EPA risk assessments either directly 
through use of a margin of exposure (MOE) analysis or through using 
uncertainty (safety) factors in calculating a dose level that poses no 
appreciable risk to humans. EPA believes that reliable data support 
using the standard uncertainty factor (usually 100 for combined inter- 
and intra-species variability) and not the additional tenfold MOE/
uncertainty factor when EPA has a complete data base under existing 
guidelines and when the severity of the effect in infants or children 
or the potency or unusual toxic properties of a compound do not raise 
concerns regarding the adequacy of the standard MOE/safety factor.
    ii. Pre- and post-natal sensitivity.  There is no indication of 
increased sensitivity of rats or rabbits to in utero and/or early 
postnatal exposure to diflufenzopyr in the developmental and 
reproductive toxicity studies.
    iii. Conclusion. There is a complete toxicity database for 
diflufenzopyr and exposure data is complete or is estimated based on 
data that reasonably accounts for potential exposures. Taking into 
account the completeness of the database and the toxicity data 
regarding pre- and post-natal sensitivity, EPA concludes, based on 
reliable data, that use of the standard margin of safety will be safe 
for infants and children without addition of another tenfold factor.
    2. Acute risk. No appropriate acute toxicological endpoint has been 
identified for infants and children.
    3. Chronic risk. Using the exposure assumptions described above, 
EPA has concluded that aggregate exposure to diflufenzopyr from food 
will utilize 0.1% of the RfD for infants and children. EPA generally 
has no concern for exposures below 100% of the RfD because the RfD 
represents the level at or below which daily aggregate dietary exposure 
over a lifetime will not pose appreciable risks to human health. 
Despite the potential for exposure to diflufenzopyr in drinking water, 
EPA does not expect the aggregate exposure to exceed 100% of the RfD.
    4. Determination of safety. Based on these risk assessments, EPA 
concludes that there is a reasonable certainty that no harm will result 
to infants and children from aggregate exposure to diflufenzopyr 
residues.

III. Other Considerations

A. Metabolism In Plants and Animals

    The nature of the residue in plants (field corn) and animals is 
understood. In field corn, the urea bond is cleaved to yield 
metabolites containing a new bicyclic ring system. No diflufenzopyr was 
detected in any of the corn matrices; metabolites comprising >10% total 
radioactive residue (TRR) include M1 (8-methylpyrido[2,3-d]pyridazin-
5(6H)-one), M10 (8-hydroxymethyl-5(6H)-pyrido[2,3-d]pyridazone) and its 
glucose conjugate, and M9 (8-methylpyrido[2,3-d]pyridazine-2,5(1H,6H)-
dione in forage and fodder, and 6-14% TRR lignin was found in fodder. 
Corn grain contained 3-4 discrete unknowns, all at <10% TRR or <0.05 
ppm each. The residues of concern in plants are diflufenzopyr, 2-(1-
[([3,5-difluorophenylamino]carbonyl)-hydrazono]ethyl)-3-
pyridinecarboxylic acid, and its metabolites convertible to M1 (8-
methylpyrido[2,3-d]pyridazin-5(6H)-one).
     In livestock, the majority (90%) of diflufenzopyr was 
excreted. In the ruminant, major metabolites include M1, M5 (6-((3,5-
difluorophenylcarbamoyl-8-methyl-pyrido[2,3-d]-5-pyridazinone) and M19 
(8-hydroxymethylpyrido[2,3-d]pyridazine-2,5(1H,6H)-dione. A substantial 
amount (8-50%) of diflufenzopyr was also found in milk, kidney, and 
liver. In poultry, diflufenzopyr was not detected, and M1 was the only 
significant metabolite identified, and in egg white only. Transfer of 
secondary residues to livestock is not expected .

B. Analytical Enforcement Methodology

     Adequate enforcement methodology (gas chromatography) 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, Crystal Mall #2, 1921 
Jefferson Davis Hwy., Arlington, VA 22202, (703-305-5229).

C. Magnitude of Residues

    Residues of diflufenzopyr, 2-(1-[([3,5-
difluorophenylamino]carbonyl)-hydrazono]ethyl)-3-pyridinecarboxylic 
acid, and its metabolites convertible to M1 (8-methylpyrido[2,3-
d]pyridazin-5(6H)-one) are not expected to exceed 0.05 ppm in field 
corn grain, forage and stover.

[[Page 4307]]

D. International Residue Limits

    There are no CODEX or Mexican residue limits established for 
diflufenzopyr or its metabolites. As part of the joint review, Canada 
will be setting an equivalent Maximum Residue Level (MRL) for corn 
grain. Therefore, no compatibility problems exist for the proposed 
tolerances.

E. Rotational Crop Restrictions

    The end-use product, which contains the active ingredients 
diflufenzopyr and dicamba (sodium salts), will contain a statement 
limiting the planting of rotational crops for a least 120 days after 
application. This restriction is based on rotational crop data for 
dicamba. The rotational crop study submitted for diflufenzopyr was not 
conducted in accordance with EPA guidelines. However, based on the 
results of this study, the low residues in the treated corn crop and 
diflufenzopyr's lack of persistence in soil, EPA does not expect 
residues of diflufenzopyr and its metabolites to occur in rotational 
crops at the 120-day plant-back interval, when corn is treated at the 
label rate of up to 0.125 pounds active ingredient per acre per season.

IV. Conclusion

    Therefore, tolerances are established for combined residues of 
diflufenzopyr, 2-(1-[([3,5-difluorophenylamino]carbonyl)-
hydrazono]ethyl)-3-pyridinecarboxylic acid, and its metabolites 
convertible to M1, (8-methylpyrido[2,3-d]pyridazin-5(6H)-one) in field 
corn stover, forage and grain at 0.05 ppm 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 March 29, 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 above (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 rulemaking. 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. 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 rulemaking under docket 
control number [OPP-300778] (including any comments and data submitted 
electronically). A public version of this record, including printed, 
paper versions of electronic comments, which does not include any 
information claimed as CBI, is available for inspection from 8:30 a.m. 
to 4 p.m., Monday through Friday, excluding legal holidays. The public 
record is located in Room 119 of the Public Information and Records 
Integrity Branch, Information Resources and Services Division (7502C), 
Office of Pesticide Programs, Environmental Protection Agency, Crystal 
Mall #2, 1921 Jefferson Davis Hwy., Arlington, VA.
    The official record for this rulemaking, as well as the public 
version, as described above will be kept in paper form. Accordingly, 
EPA will transfer any copies of objections and hearing requests 
received electronically into printed, paper form as they are received 
and will place the paper copies in the official rulemaking record which 
will also include all comments submitted directly in writing. The 
official rulemaking record is the paper record maintained at the 
Virginia address in ``ADDRESSES'' at the beginning of this document.

VII. Regulatory Assessment Requirements

A. Certain Acts and Executive Orders

    This final rule establishes tolerances under FFDCA section 408(d) 
in response to a petition submitted to the Agency. The Office of 
Management and Budget (OMB) has exempted these types of actions from 
review under Executive Order 12866, entitled Regulatory Planning and 
Review (58 FR 51735, October 4, 1993). This final rule does not contain 
any information collections subject to OMB approval under the Paperwork 
Reduction Act (PRA), 44 U.S.C. 3501 et seq., or impose any enforceable 
duty or contain any unfunded mandate as described under Title II of the 
Unfunded Mandates Reform Act of 1995 (UMRA) (Pub. L. 104-4). Nor does 
it require any prior consultation as specified by Executive Order 
12875, entitled Enhancing the Intergovernmental Partnership (58 FR 
58093, October 28, 1993), or special considerations as required by 
Executive Order 12898, entitled Federal Actions to Address 
Environmental Justice in Minority Populations and Low-Income 
Populations (59 FR 7629, February 16, 1994), or require OMB review in 
accordance with Executive Order 13045, entitled Protection of Children 
from Environmental Health Risks and Safety Risks (62 FR 19885, April 
23, 1997).
    In addition, since 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 has 
previously assessed whether establishing tolerances, exemptions from 
tolerances, raising tolerance levels or expanding exemptions might 
adversely impact small entities and concluded, as a generic matter, 
that there is no adverse economic impact. The factual basis for the 
Agency's generic certification for tolerance actions published on May 
4, 1981 (46 FR 24950) and was provided to the Chief Counsel for 
Advocacy of the Small Business Administration.

[[Page 4308]]

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

List of Subjects in 40 CFR Part 180

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

    Dated: January 14, 1999.

Marcia E. Mulkey,
Director, Office of Pesticide Programs.
    Therefore, 40 CFR chapter I is amended as follows:

PART 180 -- [AMENDED]

    1. The authority citation for part 180 continues to read as 
follows:

    Authority: 21 U.S.C. 346a and 371.


    2. By adding Sec. 180.549 to read as follows:


Sec. 180.549  Diflufenzopyr; tolerances for residues.

    (a) General. Tolerances are established for combined residues of 
diflufenzopyr, 2-(1-[([3,5-difluorophenylamino]carbonyl)-
hydrazono]ethyl)-3-pyridinecarboxylic acid, and its metabolites 
convertible to M1 (8-methylpyrido[2,3-d]pyridazin-5(6H)-one) in or on 
the following raw agricultural commodities.

------------------------------------------------------------------------
                                                                  Parts
                           Commodity                               per
                                                                 million
------------------------------------------------------------------------
Field corn, forage.............................................   0.05
 
Field corn, grain..............................................   0.05
 
Field corn, stover.............................................   0.05
------------------------------------------------------------------------

    (b) Section 18 emergency exemptions. [Reserved]
    (c)  Tolerances with regional registrations. [Reserved]
    (d)  Indirect or inadvertent residues. [Reserved]

[FR Doc. 99-1901 Filed 1-27-99; 8:45 am]
BILLING CODE 6560-50-F