[Federal Register Volume 63, Number 246 (Wednesday, December 23, 1998)]
[Rules and Regulations]
[Pages 71018-71026]
From the Federal Register Online via the Government Publishing Office [www.gpo.gov]
[FR Doc No: 98-33633]


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ENVIRONMENTAL PROTECTION AGENCY

40 CFR Part 180

[OPP-300702; FRL-6024-5]
RIN 2070-AB78


Triazamate; Time-Limited Pesticide Tolerance

AGENCY: Environmental Protection Agency (EPA).

ACTION: Final rule.

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SUMMARY: This regulation establishes a time-limited tolerance relative 
to an Experimental Use Permit for combined residues of triazamate (RH-
7988) and its metabolite (RH-0422) in or on apples. Rohm and Haas 
Company requested this tolerance under the Federal Food, Drug, and 
Cosmetic Act (FFDCA), as amended by the Food Quality Protection Act 
(FQPA) of 1996 (Pub. L. 104-170). The tolerance will expire on December 
31, 2001.

DATES: This regulation is effective December 23, 1999. Objections and 
requests for hearings must be received by EPA on or before February 22, 
1999.

ADDRESSES: Written objections and hearing requests, identified by the 
docket control number, [OPP-300702], 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-300702], 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 (CM) #2, 1921 Jefferson Davis Hwy., Arlington, VA.
    A copy of objections and hearing requests filed with the Hearing 
Clerk may also be submitted electronically by sending electronic mail 
(e-mail) to: [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 
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-300702]. 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: Mark Dow, 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: CM #2, 1921 Jefferson Davis Hwy., 
Arlington, VA, 703 305-5533, e-mail: [email protected].

SUPPLEMENTARY INFORMATION: In the Federal Register of March 6, 1998 (63 
FR 11240)(FRL-5777-5), 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 
Rohm and Haas Company, 100 Independence Mall West, Philadelphia, PA 
19108-2399. This notice included a summary of the petition prepared by 
Rohm and Haas Company, 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 a time-limited tolerance for combined residues of the 
insecticide triazamate (RH-7988) and its metabolite (RH-0422), in or on 
apples at 0.1 part per million (ppm). This tolerance will expire on 
December 31, 2001.

I. Risk Assessment and Statutory Findings

    New section 408(b)(2)(A)(i) of the FFDCA allows EPA to establish a 
tolerance (the legal limit for a pesticide chemical residue in or on a 
food) only if EPA determines that the tolerance is ``safe.'' Section 
408(b)(2)(A)(ii) defines ``safe'' to mean that ``there is a reasonable 
certainty that no harm will result from aggregate exposure to the 
pesticide chemical residue, including all anticipated dietary exposures 
and all other exposures for which there is reliable information.'' This 
includes exposure through drinking water and in residential settings, 
but does not include occupational exposure. Section 408(b)(2)(C) 
requires EPA to give special consideration to exposure of infants and 
children to the pesticide chemical residue in establishing a tolerance 
and to ``ensure that there is a reasonable certainty that no harm will 
result to infants and children from aggregate exposure to the pesticide 
chemical residue. . . .''
    EPA performs a number of analyses to determine the risks from 
aggregate exposure to pesticide residues. First, EPA determines the 
toxicity of pesticides based primarily on toxicological studies using 
laboratory animals. These studies address many adverse health effects, 
including (but not limited to) reproductive effects, developmental 
toxicity, toxicity to the nervous system, and carcinogenicity. Second, 
EPA examines exposure to the pesticide through the diet (e.g., food and 
drinking water) and through exposures that occur as a result of 
pesticide use in residential settings.

A. Toxicity

    1. Threshold and non-threshold effects. For many animal studies, a 
dose response relationship can be determined, which provides a dose 
that causes adverse effects (threshold effects) and doses causing no 
observed effects (the ``no-observed effect level'' or ``NOEL'').
    Once a study has been evaluated and the observed effects have been 
determined to be threshold effects, EPA generally divides the NOEL from 
the study with the lowest NOEL by an uncertainty factor (usually 100 or 
more) to determine the Reference Dose (RfD). The RfD is a level at or 
below which daily aggregate exposure over a lifetime will not pose 
appreciable risks to human health. An uncertainty factor (sometimes 
called a ``safety factor'') of 100 is commonly used since it is assumed 
that people may be up to 10 times more sensitive to pesticides than the 
test animals, and that one person or subgroup of the population (such 
as infants and children) could be up to 10 times more sensitive to a 
pesticide than another. In addition, EPA assesses the potential risks 
to infants and children based on the weight of the evidence of the 
toxicology studies and determines whether an additional uncertainty 
factor is warranted. Thus, an aggregate daily exposure to a pesticide 
residue at or below the RfD (expressed as 100% or less of the RfD) is 
generally considered acceptable by EPA. EPA generally uses

[[Page 71019]]

the RfD to evaluate the chronic risks posed by pesticide exposure. For 
shorter term risks, EPA calculates a margin of exposure (MOE) by 
dividing the estimated human exposure into the NOEL from the 
appropriate animal study. Commonly, EPA finds MOEs lower than 100 to be 
unacceptable. This 100-fold MOE is based on the same rationale as the 
100-fold uncertainty factor.
    Lifetime feeding studies in two species of laboratory animals are 
conducted to screen pesticides for cancer effects. When evidence of 
increased cancer is noted in these studies, the Agency conducts a 
weight of the evidence review of all relevant toxicological data 
including short-term and mutagenicity studies and structure activity 
relationship. Once a pesticide has been classified as a potential human 
carcinogen, different types of risk assessments (e.g., linear low dose 
extrapolations or MOE calculation based on the appropriate NOEL) will 
be carried out based on the nature of the carcinogenic response and the 
Agency's knowledge of its mode of action.
    2. Differences in toxic effect due to exposure duration. The 
toxicological effects of a pesticide can vary with different exposure 
durations. EPA considers the entire toxicity data base, and based on 
the effects seen for different durations and routes of exposure, 
determines which risk assessments should be done to assure that the 
public is adequately protected from any pesticide exposure scenario. 
Both short and long durations of exposure are always considered. 
Typically, risk assessments include ``acute,'' ``short-term,'' 
``intermediate term,'' and ``chronic'' risks. These assessments are 
defined by the Agency as follows.
    Acute risk, by the Agency's definition, results from 1-day 
consumption of food and water, and reflects toxicity which could be 
expressed following a single oral exposure to the pesticide residues. 
High end exposure to food and water residues are typically assumed.
    Short-term risk results from exposure to the pesticide for a period 
of 1-7 days, and therefore overlaps with the acute risk assessment. 
Historically, this risk assessment was intended to address primarily 
dermal and inhalation exposure which could result, for example, from 
residential pesticide applications. However, since enaction of FQPA, 
this assessment has been expanded to include both dietary and non-
dietary sources of exposure, and will typically consider exposure from 
food, water, and residential uses when reliable data are available. In 
this assessment, risks from average food and water exposure, and high-
end residential exposure, are aggregated. High-end exposures from all 3 
sources are not typically added because of the very low probability of 
this occurring in most cases, and because the other conservative 
assumptions built into the assessment assure adequate protection of 
public health. However, for cases in which high-end exposure can 
reasonably be expected from multiple sources (e.g. frequent and 
widespread homeowner use in a specific geographical area), multiple 
high-end risks will be aggregated and presented as part of the 
comprehensive risk assessment/characterization. Since the toxicological 
endpoint considered in this assessment reflects exposure over a period 
of at least 7 days, an additional degree of conservatism is built into 
the assessment; i.e., the risk assessment nominally covers 1-7 days 
exposure, and the toxicological endpoint/NOEL is selected to be 
adequate for at least 7 days of exposure. (Toxicity results at lower 
levels when the dosing duration is increased.)
    Intermediate-term risk results from exposure for 7 days to several 
months. This assessment is handled in a manner similar to the short-
term risk assessment.
    Chronic risk assessment describes risk which could result from 
several months to a lifetime of exposure. For this assessment, risks 
are aggregated considering average exposure from all sources for 
representative population subgroups including infants and children.

B. Aggregate Exposure

    In examining aggregate exposure, FFDCA section 408 requires that 
EPA take into account available and reliable information concerning 
exposure from the pesticide residue in the food in question, residues 
in other foods for which there are tolerances, residues in groundwater 
or surface water that is consumed as drinking water, and other non-
occupational exposures through pesticide use in gardens, lawns, or 
buildings (residential and other indoor uses). Dietary exposure to 
residues of a pesticide in a food commodity are estimated by 
multiplying the average daily consumption of the food forms of that 
commodity by the tolerance level or the anticipated pesticide residue 
level. The Theoretical Maximum Residue Contribution (TMRC) is an 
estimate of the level of residues consumed daily if each food item 
contained pesticide residues equal to the tolerance. In evaluating food 
exposures, EPA takes into account varying consumption patterns of major 
identifiable subgroups of consumers, including infants and children. 
The TMRC is a ``worst case'' estimate since it is based on the 
assumptions that food contains pesticide residues at the tolerance 
level and that 100% of the crop is treated by pesticides that have 
established tolerances. If the TMRC exceeds the RfD or poses a lifetime 
cancer risk that is greater than approximately one in a million, EPA 
attempts to derive a more accurate exposure estimate for the pesticide 
by evaluating additional types of information (anticipated residue data 
and/or percent of crop treated data) which show, generally, that 
pesticide residues in most foods when they are eaten are well below 
established tolerances.
    Percent of crop treated estimates are derived from federal and 
private market survey data. Typically, a range of estimates are 
supplied and the upper end of this range is assumed for the exposure 
assessment. By using this upper end estimate of percent of crop 
treated, the Agency is reasonably certain that exposure is not 
understated for any significant subpopulation group. Further, regional 
consumption information is taken into account through EPA's computer-
based model for evaluating the exposure of significant subpopulations 
including several regional groups, to pesticide residues. For this 
pesticide, ``The chronic dietary risk (food only) for triazamate...does 
not exceed the Agency's level of concern.''

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 
triazamate and to make a determination on aggregate exposure, 
consistent with section 408(b)(2), for a time-limited tolerance for 
combined residues of triazamate (RH-7988) and its metabolite (RH-0422) 
on apples at 0.1 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

[[Page 71020]]

toxic effects caused by triazamate are discussed below.

B. Toxicological Endpoints

    1. Acute toxicity. The data base for acute toxicity is considered 
complete. No additional studies are required at this time. Acute 
toxicity categories for triazamate are: Acute oral and acute inhalation 
are toxicity category II; Acute dermal, Occular irritation and Dermal 
irritation are toxicity category IV; and Dermal sensitization is Not 
Applicable.
    Triazamate produces significant toxicity via the oral and 
inhalation routes. In the acute oral studies in the rat and the mouse, 
the LD50 values were less than 500 miligrams/kilograms (mg/
kg). In the acute inhalation study in the rat, the LC50 
value was less than 0.5 miligram/liter (mg/L).
     2. Short - and intermediate - term toxicity. The data base for 
subchronic toxicity is considered complete.
    i. Thirteen week dietary in rats.  In a subchronic toxicity study, 
RH-7988 was administered to 10 rats/sex/dose at dietary concentrations 
of 0, 50, 500, 1,500 or 3,000 ppm (mean measured concentrations of 0, 
3, 31, 93 or 192 mg/kg/day for males and 0, 4, 39, 117 or 250 mg/kg/day 
for females) for 13 weeks. In conjunction with the primary study, 10 
additional rats/sex were fed RH-7988 at 0, 50, 500, 1,500 or 3,000 ppm 
(mean measured concentrations of 0, 3, 31, 95 or 188 mg/kg/day for 
males and 0, 4, 39, 119 or 250 mg/kg/day for females) for 13 weeks to 
determine the effects of RH-7988 on cholinesterase activities.
    In the primary study, body weights for the 1,500 and 3,000 ppm 
treatment groups were significantly (p < 0.05) depressed for most or 
all weekly intervals. Body weight gains for the 1,500 and 3,000 ppm 
treatment groups were 16-23% and 27-37% lower, respectively, than the 
controls at the end of the study. Decreased food consumption by the 
1,500 ppm treatment groups was significant (p < 0.05) during the 
initial 3-4 weeks and at one or several later weekly intervals compared 
to the controls. The Lowest Observed Adverse Effect Level (LOAEL) for 
this study is 93.37 mg/kg/day (1,500 ppm) based on decreased body 
weights and decreased food consumption in both sexes. The NOEL is 31.45 
mg/kg/day (500 ppm).
    In the cholinesterase study, both sexes in the 500, 1,500, and 
3,000 ppm treatment groups exhibited concentration-dependent decreases 
in red blood cell (12-41%) and plasma (58-95%) cholinesterase 
activities compared to the controls. Both sexes in the 1,500 and 3,000 
ppm treatment groups had concentration-dependent decreases in brain 
cholinesterase activities (28-56%) compared to the controls. The LOAEL 
for this study is 30.96 mg/kg/day (500 ppm) based on decreased plasma 
cholinesterase activities in both sexes and decreased red blood cell 
cholinesterase activity in females. The NOEL is 3.09 mg/kg/day (50 
ppm).
    ii. Subchronic oral toxicity in mice. In a 3 month dietary toxicity 
study, Crl: CD-1 (ICR) BR mice (10 per group per sex) were exposed to 
triazamate at dose levels of 0, 0.5, 2, 25, 250 or 1,000 ppm (in males 
0, 0.09, 0.34, 4.55, 49.75 and 159.43 mg/kg/day; in females 0, 0.13, 
0.53, 6.56, 71.82, and 223.19 mg/kg/day). Compound related toxicity was 
observed at > 25 ppm as evidenced by cholinesterase inhibition in both 
sexes. Plasma cholinesterase levels were significantly decreased in a 
dose-dependent manner at 25 ppm in males (11-67% of control) and 
females (13-73% of control). At these same dose levels, red blood cell 
cholinesterase levels were significantly decreased in males (72-84% of 
controls) and in females (84-93% of controls). Brain cholinesterase 
levels were significantly decreased in males at 1,000 ppm (81% of 
controls). No other treatment related effects were observed.
    Based on plasma cholinesterase inhibition at 25 ppm, the NOEL and 
LOAEL were 0.34 - 0.53 mg/kg and 4.55 - 6.56 mg/kg, respectively, for 
both males and females.
    iii. Subchronic dog (non-guideline) 14-day dietary. In a non-
guideline range-finding study, triazamate (99%) was administered to 
male beagles (4/dose) at dietary levels of 0, 140, 300 or 700 ppm (0, 
5.16, 9.64 or 11.25 mg/kg/day) for a period of 2 weeks. Dose levels of 
3,500 and 7,000 ppm were initiated but the 3,500 ppm was continued for 
only one week, with recovery on basal diet (2-week average dose: 8.75 
mg/kg/day); animals receiving 7,000 ppm for one day only were fed basal 
diet for 6 days prior to use as test animals at the 300 ppm level.
    There were no unscheduled deaths in this study. The most obvious 
toxic effect of triazamate is its inhibition of cholinesterase activity 
in plasma at very low doses (140 ppm, 48% of control; 300 ppm, 54% of 
control; 700 ppm 54% of control). Other significant effects observed at 
140 ppm included only irregular feces. At 300 ppm and above, emesis was 
reported and decreases were observed in white blood cell count (86% 
control), alkaline phosphatase activity (67% control) and serum 
glutamic pyruvic transaminase (SGPT) activity (58% control). Numerous 
incidences of no fecal output were observed at 70 ppm and above.
    From the data presented in this 2-week study, the NOEL for 
triazamate is < 140 ppm (5.16 mg/kg/day) based on inhibition of plasma 
cholinesterase and irregular feces (diarrhea, soft stool, mucoid feces, 
no fecal output). The LOAEL is start  140 ppm.
    iv. Subchronic oral toxicity-13-week dog. In a subchronic toxicity 
study, triazamate (95.3%) was administered to beagle dogs (4/sex/dose) 
in the diet at dose levels of 0, 1, 10, 100 or 400 ppm (0, 0.03, 0.31, 
3.11 or 10.98 mg/kg/day for a period of 13 weeks.
    No treatment related clinical signs were observed in the 1 ppm that 
were related to treatment. In the 10 ppm group, food-like vomitus was 
observed in 2/4 males. In the 100 ppm, the same observation was made in 
2/4 males and 2/4 females. Other observations included fluid vomitus in 
1/4 females, bloated abdomen in 1/4 males, 1/4 females was considered 
thin and 1/4 females had decreased total blood protein (88% control).
    Triazamate greatly inhibited the cholinesterase activity in blood 
plasma at all dose levels but did not appear to do so in red blood 
cells or brain. No NOEL was established for cholinesterase inhibition.
    The LOAEL for inhibition of plasma cholinesterase inhibition was 
less than 1 ppm (0.03 mg/kg/day) based on inhibition of plasma 
cholinesterase activity (74% of control) in females receiving this dose 
level.
    The NOEL for systemic effects is 10 ppm (0.31 mg/kg/day) based on 
vomiting in both sexes, thin appearance in (1/4 females) and bloated 
abdomen in 1/4 males.
    The study satisfied the requirements for a subchronic nonrodent 
study and is acceptable.
    v. 21-day dermal - rat. In a 21-day dermal study groups of Crl:CD 
BR rats (6/sex/dose) received 15 repeated dermal applications of 
triazamate (97%, technical) at doses of 0, 10, 100 and 1,000 mg/kg, 6 
hours/day, 5 days /week over a three week period. An other group of 6 
male and 6 female rats received repeated dermal applications of a 
formulation product (50WP, 52% active ingredient (a.i.)) at a dose 
equivalent to 10 mg a.i./kg/day. Under the conditions of this study, 
there were no treatment-related clinical signs of toxicity for either 
product. At 10 mg/kg, there was a biologically significant decrease in 
plasma cholinesterase for both the technical (females only) and 50WP 
formulations (both sexes). At 100 mg/kg and at 1,000 mg/kg, there was a 
statistically significant decrease in

[[Page 71021]]

plasma, red cell and brain cholinesterase when compared to controls. At 
100 mg/kg, the plasma cholinesterase activity was 50% and 58% of 
control values for females and males, respectively. The red cell 
cholinesterase activity was 67% in females and 72% in males and the 
brain cholinesterase activity was 87% of control activity in both 
sexes. At 1,000 mg/kg, Plasma cholinesterase activity was 25% in 
females, and 19% of controls in males; red cell activity was 67% of 
controls in females and 72% of controls in males and brain 
cholinesterase activity was 47% in females and 42% in males. Based on 
the results of this study, for systemic toxicity, the LOAEL was 10 mg/
kg based on the biologically significant decreases in plasma 
cholinesterase activity; a NOEL was not established.
    The study satisfied the requirements for a 21-day dermal rat study 
and is acceptable.
    3. Chronic toxicity-- i. Oncogenicity. EPA has established the RfD 
for triazamate at 0.000164 (0.0002 rounded off) milligrams/kilogram/day 
(mg/kg/day). This Reference Dose (RfD) is based on a NOEL of 0.0164 mg/
kg/day and an uncertainty factor of 100; NOEL established from a 
combined chronic feeding study in the dog; LOAEL = 0.0236 mg/kg/day.
    The data base for chronic toxicity and oncogenicity is considered 
complete.
    a.  Chronic nonrodent - 1 year dog. In a chronic toxicity study 
triazamate (94.9%) was administered to purebred beagle dogs (4/sex/
dose)in the diet at dose levels of 0, 0.1, 0.3, 0.6, 0.9, 15.0 or 150 
ppm (corresponding to 0, 0.0025, 0.0078, 0.0164, 0.0236, 0.3904, or 
4.42 mg/kg/day) for 52 weeks.
    The most significant effect observed was inhibition of plasma, red 
blood cell and brain cholinesterase activity. Decreases in activity 
were reported at several dose levels. Plasma cholinesterase activity 
was decreased (9 to 87% of control value) in both sexes at the two 
highest dose levels. At 150 ppm red blood cell cholinesterase activity 
was decreased (64 to 82%) of control values. This finding was not 
reported at doses equal to and lower than 15 ppm. Brain cholinesterase 
activity was significantly decreased (53 to 80% of controls) at both 
the 15 and 150 ppm levels, but statistical significance was only 
reported for females in the 150 ppm group. Brain cholinesterase 
activity was decreased (88% of control) for males in the 0.9 ppm group. 
This decrease in activity is considered biologically significant since 
the reported decrease is greater than 10% of the control value. Brain 
cholinesterase inhibition was not observed in animals receiving 
triazamate at dose levels lower than 0.9 ppm.
    The NOEL for cholinesterase inhibition was 0.6 ppm (0.0164 mg/kg/
day) based on the inhibition of brain cholinesterase activity (88% of 
control value) in males at the LOAEL of 0.9 ppm triazamate in the diet 
(0.0236 mg/kg/day).
    No biologically significant treatment related effects were noted 
with respect to mortality, clinical signs, body weight, food 
consumption, food efficiency, hematology, clinical chemistry, 
urinalysis, organ weights, organ/body weight ratios, organ/brain weight 
ratios, or gross or microscopic pathology. The NOEL for systemic 
effects is  150 ppm (4.42 mg/kg/day); the LOAEL is > 150 
ppm.
    The study is acceptable and satisfies the requirement for a chronic 
oral non-rodent study.
    b.  Chronic oral toxicity/oncogenicity in mice. In a 78 week oral 
toxicity/oncogenicity study in mice, groups of 60 CD-1 mice/sex were 
fed dietary levels of 0, 1, 50, or 1,500 ppm triazamate (equivalent to 
0, .13, 6.7, or 210 mg/kg/day for females and 0, 0.17, 8.4 or 262 mg/
kg/day for males. At week 55, the highest dose levels were reduced to 
1,000 ppm(127 mg/kg and 146 mg/kg for males and females, respectively) 
due to high mortality. Groups of 10/sex/dose level were included for 
sacrifice at 12 months.
    At 50 ppm, plasma cholinesterase activity was decreased in males 
(64 to 75%) and in females (69 to 80%) at 6, 12, or 18 months. At the 
high dose of 1,000/1,500 ppm, a significantly decreased survival rate 
and a debilitated state of health were observed during the first 12 
months in both sexes. Body weight gains overall were depressed compared 
to controls in males and females (16%), food consumption was slightly 
decreased in males and marginal decreases in erythrocyte parameters 
(RBC, HGB and HCT) were observed at 12 and 18 months in males. An 
increase in the incidence of inhalation pneumonia was observed in both 
sexes. Inhibition of erythrocyte and brain cholinesterase activity was 
also observed at 1,000 ppm.
    The Lowest Effect Level (LEL) for cholinesterase inhibition is 50 
ppm (6.7 and 8.4 mg/kg/day in males and females, respectively) based on 
plasma cholinesterase activity. The NOEL is for cholinesterase 
inhibition is 1 ppm (0.13 and 0.17 mg/kg/day, in males and females 
respectively).
    The systemic LEL is 1,000 ppm (127 and 146 mg/kg/day , males and 
females, respectively) based on decreased body weight gains and 
inhalation pneumonia. The systemic NOEL was 50 ppm.
    There is no evidence of carcinogenic potential. Dosing was 
excessive at the highest dose (1,000/1,500 ppm) but sufficient numbers 
of mice were considered available at termination to assess the 
carcinogenicity at the highest dose. The study is Core Guideline for 
carcinogenicity and satisfies the requirement for an oncogenicity study 
in mice as per 83-2(b). For chronic toxicity, the study is core 
supplementary. No ophthalmoscopic examinations or clinical chemistry 
determinations were performed, other than for inhibition of 
cholinesterase activity.
    c. Chronic/carcinogenicity study - rats. In a combined chronic/
oncogenicity study, RH-7988 was administered to 70 Sprague-Dawley rats/
sex/dose in the diet at dose levels of 0, 10, 250, or 1,250 ppm (0, 
0.45, 11.50, and 59.18 mg/kg/day for males, and 0.58, 14.54, and 73.70 
mg/kg/day for females) for 24 months. A total of 10 rats/sex/group were 
terminated at 12 months and all remaining animals were sacrificed at 24 
months of the study.
    Chronic toxicity in rats receiving the 1,250 ppm diet was 
characterized in males by significant decreases in mean body weights 
(decrease 5-7%; p  0.05) and body weight gains ( 8-18%; p 
 0.05) and by reduced plasma (decrease 71-87%; p  
0.05), erythrocyte (decrease 37-62%; p  0.05), and brain 
cholinesterase activities (decrease 26-38%; p  0.05) in both 
males and females. In the 250 ppm group animals, reduced plasma 
(decrease 31-65%; p  0.05) and erythrocyte (decrease 16-29%; 
p  0.05) cholinesterase activities were also observed.
    The chronic LOAEL is 250 ppm (11.50 and 14.54 mg/kg/day in males 
and females, respectively) based on inhibition of plasma and 
erythrocyte cholinesterase activities in the 250 ppm animals. The 
chronic NOEL is 10 ppm (0.45 and 0.58 mg/kg/day for males and females, 
respectively).
    Under the conditions of this study, there was no evidence of 
carcinogenic potential.
    Dosing was considered adequate based on decreased body weight and 
body weight gain in the high-dose males and decreased activity of 
plasma and Red Blood Cell (RBC) cholinesterase at the mid and high 
doses and brain cholinesterase at the high dose.
    This study is classified as acceptable and satisfies the guideline 
requirements for a chronic toxicity study (Series 83-1) and a 
carcinogenicity study (Series 83-2) on the rat.

[[Page 71022]]

    ii. Developmental toxicity.  The data base for developmental 
toxicity is considered complete.
    a. Oral (gavage) developmental toxicity study - rats. In a 
developmental toxicity study, RH-7988 (95.7% a.i.) was administered to 
25 Crl:CD Br rats/dose by gavage in a corn oil suspension at dose 
levels of 0, 4, 16, or 64 mg/kg/day from days 6 through 15 of 
gestation.
    Maternal toxicity was demonstrated at 64 mg/kg/day by treatment-
related clinical signs of toxicity and decreased body weights (days 8, 
10, 13, 16, and 20, decrease 5-6%, p > 0.05), body weight gains 
(overall treatment period, decrease 25%, p > 0.05), and feed 
consumption (decrease 25 and 12%, p > 0.05, days 6-10 and 10-16, 
respectively). Clinical signs of toxicity noted during the treatment 
period in the high-dose group included fasciculations, salivation, 
rapid breathing, diarrhea, mucoid feces, tan stained perineum, and red 
stained nose. Body weights, body weight gains, feed consumption, and 
clinical signs of toxicity were unaffected by treatment at dose levels 
of 4 and 16 mg/kg/day. Cesarean section parameters were similar between 
the controls and all treated groups. No treatment-related changes were 
noted in mortality or gross pathology at any dose level. The maternal 
LOAEL is 64 mg/kg/day, based on treatment-related clinical signs of 
toxicity and decreased body weights, body weight gains, and feed 
consumption. The maternal NOEL is 16 mg/kg/day.
    There were no treatment-related effects in developmental parameters 
at any administered dose level. The developmental LOAEL was not 
observed. The developmental NOEL is 64 mg/kg/day.
    b. Developmental toxicity - rabbits. In a developmental toxicity 
study, 21 New Zealand White rabbits per group received RH-7988 
(triazamate, 94.9%) by gavage on gestational days 7-19 at dose levels 
of 0, 0.05, 0.5 or 10 mg/kg/day. Corn oil served as the control 
substance and vehicle for the test article. The study authors did not 
indicate if doses were adjusted for concentration of active ingredient. 
Analytical chemistry results demonstrated that the lowest dose was 136% 
of target, i.e. 0.068 mg/kg/day.
    Maternal toxicity was observed at 10 and 0.5 mg/kg/day as evidenced 
by increased incidences of clinical signs (soiled perineum, diarrhea 
and scant/no feces), significantly decreased body weight gain and food 
consumption during the entire gestational period. Based on these 
results, the maternal toxicity NOEL is 0.068 mg/kg/day and the maternal 
toxicity LOAEL is 0.5 mg/kg/day.
    Developmental toxicity was not observed in this study, therefore, 
the developmental NOEL was 10 mg/kg, the developmental LOAEL was not 
determined.
    iii. Reproductive toxicity  The data base for reproductive toxicity 
is considered complete.
     Two generation reproduction study in rats. In a two-generation 
reproduction study, Crl: CDBR rats (25/group) received RH-7988 
(triazamate, 94.9%) at dietary levels of 0, 10, 250, or 1,500 ppm 
(equal to 0, 0.8, 19.9 or 116.8 mg/kg/day for females and 0, 0.7, 17.0, 
or 101.4 mg/kg/day for males) during premating.
    The NOEL for systemic toxicity was 10 ppm. The LOAEL was 250 ppm 
based on decreased red blood cell and plasma cholinesterase activity in 
males and females in both generations.
    At 250 ppm, plasma cholinesterase activity was 25 to 38% of control 
value and at 1,500 ppm the plasma cholinesterase activity was 6 to 13% 
of control level. Red blood cell activity was 65 to 80% of control at 
250 ppm and 53-57% of control at 1,500 ppm. Additional findings at 
1,500 ppm included decreased body weight (F0 males, 
F1 males and F1 females), decreased food 
consumption (F0 males, F1 males and F1 
females) and an increased incidence of clinical signs (soft feces, 
small irregular shaped feces) in males in the F0 and both 
sexes in the F1.
    The NOEL for reproductive toxicity was 250 ppm (17 - 19.9 mg/kg). 
The LOAEL was 1,500 ppm (101.4 - 116.8 mg/kg) based on decreased pup 
body weight on lactation days 14 and 21 in both generations.
    iv. Neurotoxicity. Adequacy of data base for neurotoxicity (Series 
81-8, 82-5): This chemical is not an OP and hen studies were not 
performed or required. Because of the cholinesterase inhibiting 
properties of the compound, acute and subchronic neurotoxicity studies 
were conducted. The data base for neurotoxicity is considered to be 
complete. No additional studies are required at this time.
    In an Acute neurotoxicity study, RH-7988 was administered to Crl 
CD:BR rats of both sexes (10/sex/dose) by gavage at single doses of 0, 
5, 25 or 75 mg/kg. There was no neuropathology reported on brain, 
spinal cord (and ganglia) and peripheral nerves. There were no 
treatment related mortalities. Cholinesterase activity was not 
assessed.
    Based on study results the NOEL is 5 mg/kg. A threshold NOEL could 
be considered at 25 mg/kg due to the marginal effects observed in 
males, only at that dose level. This guideline [Series 81-8] acute 
neurotoxicity study is not yet classified because a formal review has 
not yet been done. The NOEL and LOAEL are tentative at this time.
    In a Subchronic neurotoxicity study RH7988 was administered to Crl 
CD:BR (Sprague-Dawley) rats of both sexes at dietary levels of 0, 10, 
250 or 1,500 ppm (0, 0.6, 14.3 or 86.8 mg/kg/day, respectively for 
males and 0, 0.7, 17.1 or 103.5 mg/kg/day for females). There was no 
effect on motor activity when dosed groups were compared to controls 
and no treatment related deaths were reported. Necropsy and 
histopathology did not reveal any lesions that could be correlated to 
treatment with the test material. Brain weights were comparable between 
groups.
    Based on the results reported, the NOEL is 10 ppm (0.6/ 0.7 mg/kg/
day[M/F]). The LOAEL is 250 ppm (14.3/17.1 mg/kg/day[M/F]) based on 
statistically and biologically significant decreases in plasma and red 
blood cell cholinesterase activity. This guideline [Series 82-5] 
subchronic neurotoxicity study is not yet classified because a formal 
review has not yet been done. The NOEL and LOAEL are tentative at this 
time.
    v. Mutagenicity.  The data base for Mutagenicity is considered 
adequate.
    vi.  Metabolism.  The data base for metabolism is considered to be 
complete.
    Groups of male and female Wistar rats were dosed with 
14C-labeled RH-7988 at oral doses of 0.3 or 30 mg/kg and at 
14-day repeated oral doses of RH-7988 at 3 ppm followed by a single 
oral dose of 14C-RH-7988 at 0.3 mg/kg. In addition, groups 
of rats were subjected to dietary administration of 14C-RH-
7988 at 300 ppm (males only) and 3,000 ppm (females only). The 
excretion of radioactivity into urine and feces was rapid and complete 
in all groups tested and most of the test compound administered was 
excreted in the urine (67-109%) and feces (10-33%) from the animals. 
Total recovery of radioactivity ranged between 101% and 128% of the 
administered dose for all tested groups within 3 to 4 days after 
dosing. No marked sex-related difference was observed in the excretion 
patterns.
    Peak plasma/whole blood 14C-concentration was attained 
5-15 minutes after oral dosing (0.3 or 30 mg/kg/day) and 12-24 hours 
after dietary administration (300 ppm or 3,000 ppm).
    At 3 days after oral administration of a low-dose (0.3 mg/kg, 
single or 14-day repeated dosing) or single high-dose (30 mg/kg), 0.6-
4% of the administered

[[Page 71023]]

radioactivity remained in the tissues (0.1-0.2%) and carcass (0.4-4%). 
There were no sex-dependent differences in retention or distribution of 
the test article. The greatest amount of radioactivity (expressed as 
percent of the administered dose) was associated with the fat, liver, 
and muscle. At 3 days after oral administration of a single low- or 
high-dose of RH-7988, thyroid contained the highest tissue 
14C-concentration (expressed as ppm equivalent/tissue).
    High Pressure Liquid Chromatography (HPLC) analysis of urine and 
feces from rats after oral administration of 30 mg/kg of 
14C-RH-7988 showed four 14C containing 
metabolites. Parent was not detected in any sample analyzed. The urine 
contained Metabolite 1 (35.5-49.4% of the dose), Metabolite 2 (9.5-
13.7%), Metabolite 3 (0.9-2.7%) and a trace of Metabolite 4. The feces 
contained only Metabolite 1 (16.7-19.8%) and a trace of Metabolite 4. 
Most of the metabolites are cleavage products of RH-7988 either at the 
carbamoyl functionality or at the ester. The authors provided a 
proposed metabolic pathway that is consistent with the available data.
    vii. Dermal absorption . In a dermal absorption study 
14-C triazamate was administered to male Crl:CDBR rats at a 
single dermal application at 0.5, 0.05 or 0.005 mg/centimeter (cm). The 
fur was removed from the intrascapular region of the back 24 hours 
prior to the administration of the test material. Dermal absorption at 
the highest concentration was less than 2% at 1, 10 and 24 hours. At 
the mid concentration, the dermal absorption ranged from less than 1% 
at 1 hour to approximately 13% after 24 hours. At the lowest 
concentration of 0.005 mg/cm, the highest percentage of absorption 
(19%) was reported at 24 hours; at 1 hour, the absorption was less than 
1%.
    Dermal Absorption Factor: A dermal absorption factor of 10% should 
be used for correcting oral dosing to dermal dosing.

C. Exposures and Risks

    1. From food and feed uses. Risk assessments were conducted by EPA 
to assess dietary exposures and risks from RH-7988 and RH-0422 as 
follows:
    i.  Acute dietary 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.
    For assessment of acute dietary risk, a maternal NOEL of 0.068 mg/
kg/day is used from a developmental toxicity study on rabbits. The 
selected endpoint is based on clinical signs and decreases in body 
weight gain and food consumption at a dose level of 0.5 mg/kg/day.
    The Margin of Exposure (MOE) is a measure of how closely the 
anticipated exposure comes to the NOEL and is calculated as a ratio of 
the NOEL to the exposure (NOEL/exposure = MOE). The Agency is not 
generally concerned unless the MOE is below 100 when the NOEL is based 
upon data generated in animal studies. The 100 factor is to take into 
account interspecies extrapolation and intraspecies variability. For 
triazamate, the Agency's level of concern is for MOEs that are below 
100.
    A dietary risk evaluation system (DRES) analysis assuming 100% crop 
treated and using the proposed tolerance level of 0.05 ppm for apples 
and average residue concentrations from field trial data for apple 
juice was conducted. Average residues for apple juice were derived The 
resulting MOEs for triazamate are summarized below.

 
------------------------------------------------------------------------
            Subgroup                NOEL mg/kg/day            MOE
------------------------------------------------------------------------
General U.S. Population.........  0.068.............  68
Infants (< 1 yr)................  0.068.............  34
Children (1-6 yrs)..............  0.068.............  45
Females (13+ yrs)...............  0.068.............  226
Males (13+ yrs).................  0.068.............  226
------------------------------------------------------------------------


    As shown above, the MOEs for adult males and females are greater 
than 100 and MOEs for the subgroups General U.S. Population, Infants (< 
1 year), and Children (1-6 years old) are below 100. However, the 
Agency determined that in reality, the MOEs will be above a level of 
concern (>100) because of the following factors: 1) While the DRES 
analysis assumes 100% crop treated, less than 5% of the crop is 
``actually'' treated with triazamate; 2) the acreage treated is 
approximately 3,000 acres, in 20 states over a 2-year period; 3) the 
field trial data show non-detectable residue levels ( < 0.01 ppm) after 
a post-treatment interval of 21 days; and 4) the unlikely leaching of 
this chemical due to its physical and chemical properties.
    ii. Chronic exposure and risk. (Anticipated Residue Contribution or 
ARC) The chronic dietary exposure analysis was conducted using a RfD of 
0.0002 mg/kg/day. The RfD is based on the NOEL for cholinesterase 
inhibition of 0.0164 mg/kg/day in male dogs from the chronic toxicity 
study in beagle dogs and an uncertainty factor of 100, applicable to 
all population subgroups.
    In conducting this chronic dietary risk assessment, EPA is assuming 
that triazamate will be applied under the experimental use permit 
directions for use: 2,107.5 lbs ai to be applied on 2,810 acres over a 
2-year period. Under these assumptions, the crop may contain triazamate 
residues when approximately 1% of the crop are treated. Anticipated 
residue values of 0.05 ppm derived from field trial data were used. 
There are no other published, pending, or section 18 tolerances for 
triazamate.
    The resulting ARCs are equivalent to the following percents of the 
RfD for the subgroups listed below.

 
------------------------------------------------------------------------
                 Subgroup                               %Rfd
------------------------------------------------------------------------
U.S. Population (48 states)...............  0.045%
Northeast Region..........................  0.056%
Western Region............................  0.054%
Hispanics.................................  0.048%
Non-Hispanic Whites.......................  0.047%
Non-Hispanic Others.......................  0.047%
Nursing Infants (< 1 yr)..................  0.329%
Non-Nursing Infants (< 1yr)...............  0.0442%
Children (1-6 yrs)........................  0.034%
Children (7-12 yrs).......................  0.060%
------------------------------------------------------------------------


    The subgroups listed above are: (1) the U.S. population (48 
states); (2) those for infants and children; and (3) the other 
subgroups for which the percentage of the RfD occupied is greater than 
that occupied by the subgroup U.S. population (48) states.
    The chronic dietary risk (food only) for triazamate therefore, does 
not exceed the Agency's level of concern.

[[Page 71024]]

    2. Drinking water risk (acute and chronic). Drinking water levels 
of concern (DWLOC) are the concentrations of triazamate in drinking 
water which would result in unacceptable aggregate risk, after 
factoring in all food exposures and other non-occupational for which 
the Agency has reliable data. To calculate the DWLOC for acute exposure 
relative to an acute dietary toxicity endpoint, the acute dietary food 
exposure is subtracted from the ratio of the acute NOEL (used for acute 
dietary assessments) to the MOE.
    However, for triazamate, the acute DWLOC could not be calculated 
because this ratio is less than the food exposure.
    To calculate the DWLOC for chronic (non-cancer) exposure relative 
to a chronic toxicity endpoint, the chronic dietary food exposure (from 
DRES) is subtracted from the RfD to obtain the acceptable chronic (non-
cancer) exposure to triazamate in drinking water. DWLOCs were then 
calculated using default body weights and drinking water consumption 
figures.
    The DWLOCs for triazamate are 6.97 /L for adults and 1.99 
/L for children (1-6 years old) which are higher than the 
estimated average concentrations for triazamate in surface (0.25 
/L) and ground water (0.000063 /L). Therefore, for 
the use proposed in this action, the Agency concludes with reasonable 
certainty that residues of triazamate in drinking water would not 
result in unacceptable levels of aggregate health risk at this time.

D. Statement of the Adequacy of the Residential Exposure Data- base to 
Assess Infants' and Children's Exposures

    There are no residential uses associated with this product, 
therefore exposures and risks for children from such uses are not a 
concern.

E. Cumulative Exposure to Substances with Common Mechanism of Toxicity

    Section 408(b)(2)(D)(v) requires that, when considering whether to 
establish, modify, or revoke a tolerance, the Agency consider 
``available information'' concerning the cumulative effects of a 
particular pesticide's residues and ``other substances that have a 
common mechanism of toxicity.'' The Agency believes that ``available 
information'' in this context might include not only toxicity, 
chemistry, and exposure data, but also scientific policies and 
methodologies for understanding common mechanisms of toxicity and 
conducting cumulative risk assessments. For most pesticides, although 
the Agency has some information in its files that may turn out to be 
helpful in eventually determining whether a pesticide shares a common 
mechanism of toxicity with any other substances, EPA does not at this 
time have the methodologies to resolve the complex scientific issues 
concerning common mechanism of toxicity in a meaningful way. EPA has 
begun a pilot process to study this issue further through the 
examination of particular classes of pesticides. The Agency hopes that 
the results of this pilot process will increase the Agency's scientific 
understanding of this question such that EPA will be able to develop 
and apply scientific principles for better determining which chemicals 
have a common mechanism of toxicity and evaluating the cumulative 
effects of such chemicals. The Agency anticipates, however, that even 
as its understanding of the science of common mechanisms increases, 
decisions on specific classes of chemicals will be heavily dependent on 
chemical specific data, much of which may not be presently available.
    Although at present the Agency does not know how to apply the 
information in its files concerning common mechanism issues to most 
risk assessments, there are pesticides as to which the common mechanism 
issues can be resolved. These pesticides include pesticides that are 
toxicologically dissimilar to existing chemical substances (in which 
case the Agency can conclude that it is unlikely that a pesticide 
shares a common mechanism of activity with other substances) and 
pesticides that produce a common toxic metabolite (in which case common 
mechanism of activity will be assumed).
    EPA does not have, at this time, available data to determine 
whether triazamate 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, 
triazamate 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 triazamate has a common mechanism of toxicity 
with other substances.

F. Aggregate Exposure and Risk Assessment/Characterization

    1. Acute aggregate exposure and risk. As indicated from the acute 
dietary (food only) risk assessment, a high-end exposure estimate was 
calculated for these subgroups: general U.S. population, infants (< 1 
year old), children (1-6 years old), females 13+ years, and males 13+.
    Three of the population subgroups, general U.S. population, infants 
(<1 year old) and children (1-6 years old), yielded MOEs below 100%. 
However, given the limited acreage proposed for use in this action, the 
low percent crop actually treated, and the physical and chemical 
properties of this chemical (e.g.,it does not leach, is not persistent, 
degrades rapidly, etc.), and based on best scientific judgement, the 
Agency concludes with reasonable confidence that residues of triazamate 
in drinking water will not contribute significantly to the aggregate 
acute human health risk when considering the use proposed by this 
action.
    2. Short- and intermediate- term aggregate exposure and risk. 
Triazamate is not currently registered for any residential uses. 
Therefore, a risk assessment for short- and intermediate- term 
aggregate risk is not required.
    3. Chronic aggregate exposure and risk. For the U.S. population, 
0.045% of the RfD is occupied by dietary (food) exposure. Triazamate is 
not currently registered for residential uses, thus, no chronic 
residential exposure is anticipated. The estimated average 
concentrations (EECs) of triazamate for the U.S. population and for 
children (1-6 years old) in surface and ground water are less than 
OPP's levels of concern for triazamate in drinking water as a 
contribution to chronic aggregate exposure when considering the use 
proposed by this action.
    4. Determination of safety (U.S. population, infants, and 
children). Triazamate has been classified as a ``not likely'' human 
carcinogen, based on a lack of evidence of carcinogenicity in mice and 
rats at dose levels judged to be adequate to assess the carcinogenic 
potential. Thus, a cancer risk assessment is not required. Triazamate 
does not have residential uses; therefore, no residential risk 
assessment is required.
    Acute dietary (food + water) risk estimates do exceed the Agency's 
level of concern for the U.S. population and for infants and children. 
Chronic dietary (food + water) risk for the U.S. population and for 
infants and children do not exceed the Agency's level of concern. 
However, given the limited acreage proposed for use in this action, the 
low percent crop actually treated, and the physical and chemical 
properties of this chemical (e.g., it does not leach, is not 
persistent, degrades rapidly, etc.), and based on best scientific 
judgement, the Agency concludes with reasonable confidence that 
residues of triazamate in drinking

[[Page 71025]]

water will not contribute significantly to the aggregate acute and 
chronic human health risk when considering the use proposed by this 
action.

III. Other Considerations

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

IV. International Tolerances

    There are no approved CODEX maximum residue levels (MRLs) 
established for residues of triazamate. No previous Experimental Use 
Permits have been requested for triazamate and no permanent or 
temporary tolerances have been established for residues of triazamate 
or its metabolites in/on raw agricultural or animal commodities.

V. Analytical Method

    Nitrogen phosphorus detector/gas liquid chromatography (NPD/GLC) 
(Method TR-34-89-37) has been submitted and validated.

VI. Conclusion

    Therefore, the tolerance is established for combined residues of 
triazamate (RH-7988) and its metabolite (RH-0422) in or on apples at 
0.1 ppm.

VII. Objections and Hearing Requests

    The new FFDCA section 408(g) provides essentially the same process 
for persons to ``object'' to a tolerance regulation issued by EPA under 
new section 408(e) and (l)(6) as was provided in the old section 408 
and in section 409. However, the period for filing objections is 60 
days, rather than 30 days. EPA currently has procedural regulations 
which govern the submission of objections and hearing requests. These 
regulations will require some modification to reflect the new law. 
However, until those modifications can be made, EPA will continue to 
use those procedural regulations with appropriate adjustments to 
reflect the new law.
    Any person may, by February 22, 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(i). If a hearing is requested, the objections must include a 
statement of the factual issues on which a hearing is requested, the 
requestor's contentions on such issues, and a summary of any evidence 
relied upon by the requestor (40 CFR 178.27). A request for a hearing 
will be granted if the Administrator determines that the material 
submitted shows the following: There is genuine and substantial issue 
of fact; there is a reasonable possibility that available evidence 
identified by the requestor would, if established, resolve one or more 
of such issues in favor of the requestor, taking into account 
uncontested claims or facts to the contrary; and resolution of the 
factual issues in the manner sought by the requestor would be adequate 
to justify the action requested (40 CFR 178.32). Information submitted 
in connection with an objection or hearing request may be claimed 
confidential by marking any part or all of that information as 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.

VIII. Public Record and Electronic Submissions

    EPA has established a record for this rulemaking under docket 
control number [OPP-300702] (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 Highway, Arlington, VA.
    Electronic comments may be sent directly to EPA at:
    [email protected].


    Electronic comments must be submitted as an ASCII file avoiding the 
use of special characters and any form of encryption.
    The official record for this rulemaking, as well as the public 
version, as described above will be kept in paper form. Accordingly, 
EPA will transfer any copies of objections and hearing requests 
received electronically into printed, paper form as they are received 
and will place the paper copies in the official rulemaking record which 
will also include all comments submitted directly in writing. The 
official rulemaking record is the paper record maintained at the 
Virginia address in ``ADDRESSES'' at the beginning of this document.

IX. Regulatory Assessment Requirements

A. Other Acts and Executive Orders

    This final rule establishes a tolerance under FFDCA section 408(d) 
in response to a petition submitted to the Agency. The Office of 
Management and Budget (OMB) has exempted these types of actions from 
review under Executive Order 12866, entitled Regulatory Planning and 
Review (58 FR 51735, October 4, 1993). This final rule does not contain 
any information collections subject to OMB approval under the Paperwork 
Reduction Act (PRA), 44 U.S.C. 3501 et seq., or impose any enforceable 
duty or contain any unfunded mandate as described under Title II of the 
Unfunded Mandates Reform Act of 1995 (UMRA) (Pub. L. 104-4). Nor does 
it require any prior consultation as specified by Executive Order 
12875, entitled Enhancing the Intergovernmental Partnership (58 FR 
58093, October 28, 1993), or special considerations as required by 
Executive Order 12898, entitled Federal Actions to Address 
Environmental Justice in Minority Populations and Low-Income 
Populations (59 FR 7629, February 16, 1994), or require OMB review in 
accordance with Executive Order 13045, entitled Protection of Children 
from Environmental Health Risks and Safety Risks (62 FR 19885, April 
23, 1997).

B. Executive Order 12875

     Under Executive Order 12875, entitled Enhancing Intergovernmental

[[Page 71026]]

Partnerships (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 the Office of Management and Budget (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.

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 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.
    In addition, since these tolerances and exemptions that are 
established on the basis of a petition under FFDCA section 408(d), such 
as the tolerance in this final rule, do not require the issuance of a 
proposed rule, the requirements of the Regulatory Flexibility Act (RFA) 
(5 U.S.C. 601 et seq.) do not apply. Nevertheless, the Agency has 
previously assessed whether establishing tolerances, exemptions from 
tolerances, raising tolerance levels or expanding exemptions might 
adversely impact small entities and concluded, as a generic matter, 
that there is no adverse economic impact. The factual basis for the 
Agency's generic certification for tolerance actions published on May 
4, 1981 (46 FR 24950) and was provided to the Chief Counsel for 
Advocacy of the Small Business Administration.

X. 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: November 18, 1998.

Joseph J. Merenda,

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

PART 180 ---- [AMENDED]

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

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

    2. Section 180.536 is added to read as follows:


Sec. 180.536  Triazamate; tolerances for residues.

    (a) General. Time-limited tolerances are established for the 
combined residues of triazamate (RH-7988) ethyl(3-tert-butyl-1-
dimethylcarbamoyl-1H-1,2,4-triazol-5-ylthio)acetate and its metabolite 
(RH0422) in or on the following commoditie(s):

 
------------------------------------------------------------------------
                                                          Expiration/
            Commodity              Parts per million    Revocation Date
------------------------------------------------------------------------
Apples..........................  0.1                 12/31/01
------------------------------------------------------------------------

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

[FR Doc. 98-33633 Filed 12-22-98; 8:45 am]
BILLING CODE 6560-50-F