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triazamate Pesticide Petition Filing 3/98



[Federal Register: March 6, 1998 (Volume 63, Number 44)]
[Notices]               
[Page 11240-11252]
>From the Federal Register Online via GPO Access [wais.access.gpo.gov]
[DOCID:fr06mr98-78]

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ENVIRONMENTAL PROTECTION AGENCY

[PF-798; FRL-5777-5]

 
Notice of Filing of Pesticide Petitions

AGENCY: Environmental Protection Agency (EPA).

ACTION: Notice.

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SUMMARY: This notice announces the initial filing of pesticide 
petitions proposing the establishment of regulations for residues of 
certain pesticide chemicals in or on various agricultural commodities.

DATES: Comments, identified by the docket control number PF-798, must 
be received on or before April 6, 1998.

ADDRESSES: By mail submit written comments to: Public Information and 
Records Integrity Branch, Information Resources and Services Divison 
(7502C), Office of Pesticides Programs, Environmental Protection 
Agency, 401 M St., SW., Washington, DC 20460. In person bring comments 
to: Rm. 119, CM #2, 1921 Jefferson Davis Highway, Arlington, VA.
    Comments and data may also be submitted electronically to: opp-
docket@epamail.epa.gov. Following the instructions under 
``SUPPLEMENTARY INFORMATION.'' No confidential business information 
should be submitted through e-mail.
    Information submitted as a comment concerning this document may be 
claimed confidential by marking any part or all of that information as 
``Confidential Business Information'' (CBI). CBI should not be 
submitted through e-mail. Information marked as CBI will not be 
disclosed except in accordance with procedures set forth in 40 CFR part 
2. A copy of the comment that does not contain CBI must be submitted 
for inclusion in the public record. Information not marked confidential 
may be disclosed publicly by EPA without prior notice. All written 
comments will be available for public inspection in Rm. 119 at the 
address given above, from 8:30 a.m. to 4 p.m., Monday through Friday, 
excluding legal holidays.

FOR FURTHER INFORMATION CONTACT: By mail: Joseph Tavano, Product 
Manager (PM) 10, Registration Division, (7505C), Office of Pesticide 
Programs, Environmental Protection Agency, 401 M St., SW., Washington, 
DC 20460. Office location, telephone number, and e-mail address: Rm. 
214, CM#2, 1921 Jefferson Davis Hwy., Arlington, VA. 22202, (703) 305-
6411; e-mail: tavano.joe@epamail.epa.gov.

SUPPLEMENTARY INFORMATION: EPA has received pesticide petitions as 
follows proposing the establishment and/or amendment of regulations for 
residues of certain pesticide chemicals in or on various raw 
agricultural commodities under section 408 of the Federal Food, Drug, 
and Comestic Act (FFDCA), 21 U.S.C. 346a. EPA has determined that these 
petitions contain data or information regarding the elements set forth 
in section 408(d)(2); however, EPA has not fully evaluated the 
sufficiency of the submitted data at this time or whether the data 
supports grantinig of the petition. Additional data may be needed 
before EPA rules on the petition.
    The official record for this notice, as well as the public version, 
has been established for this notice of filing under docket control 
number PF-798 (including comments and data submitted electronically as 
described below). 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,

[[Page 11241]]

excluding legal holidays. The official record is located at the address 
in ``ADDRESSES'' at the beginning of this document.
    Electronic comments can be sent directly to EPA at:
    opp-docket@epamail.epa.gov


    Electronic comments must be submitted as an ASCII file avoiding the 
use of special characters and any form of encryption. Comment and data 
will also be accepted on disks in Wordperfect 5.1/6.1 file format or 
ASCII file format. All comments and data in electronic form must be 
identified by the docket control number PF-798 and appropriate petition 
number. Electronic comments on this notice may be filed online at many 
Federal Depository Libraries.
    Authority: 21 U.S.C. 346a.

List of Subjects

    Environmental protection, Agricultural commodities, Food additives, 
Feed additives, Pesticides and pests, Reporting and recordkeeping 
requirements.

    Dated: March 2, 1998.

Peter Caulkins,

Acting Director, Registration Division, Office of Pesticide Programs.

Summaries of Petitions

    Below summaries of the pesticide petitions are printed. The 
summaries of the petitions were prepared by the petitioners. The 
petition summary announces the availability of a description of the 
analytical methods available to EPA for the detection and measurement 
of the pesticide chemical residues or an explanation of why no such 
method is needed.

1. Rohm and Haas Company

PP 3G4274

    EPA has received a pesticide petition (PP 3G4274)from Rohm and Haas 
Company, 100 Independence Mall West, Philadelphia, PA 19106-2399. 
proposing pursuant to section 408(d) of the Federal Food, Drug and 
Cosmetic Act, 21 U.S.C. 346a(d), to amend 40 CFR part 180 by 
establishing a tolerance for residues of triazamate [Acetic acid, [{1-
{(dimethylamino) carbonyl}-3-(1,1-dimethylethyl)-1H-1,2,4-triazol-5-y1} 
thio]-,ethyl ester] and its metabolite Acetic acid,[{1-{(dimethylamino) 
carbonyl}-3-(1,1-dimethylethyl)-1H-1,2,4-triazol-5-y1}thio]-(code 
number RH-0422 in or on the raw agricultural commodity fresh apples at 
0.1 parts per million (ppm). EPA has determined that the petition 
contains data or information regarding the elements set forth in 
section 408(d)(2) of the FFDCA; however, EPA has not fully evaluated 
the sufficiency of the submitted data at this time or whether the data 
supports granting of the petition. Additional data may be needed before 
EPA rules on the petition.

A. Residue Chemistry

    1. Plant metabolism. The metabolism of triazamate in plants 
(apples) is adequately understood for the purposes of this tolerance. 
The metabolism of triazamate involves oxidative demethylation of the 
carbamoyl group. Parent compound is rapidly metabolized and is either 
not found or found at trace levels in apples. The majority of the total 
dosage is present as other non-cholinesterase inhibiting metabolites 
whose structures do not contain the dimethylcarbamoyl moiety. Because 
the proposed experimental use program is for fresh apples, livestock 
metabolism studies are not required. Tolerances for residues of 
triazamate should be expressed as the total residue from triazamate and 
its only cholinesterase-inhibiting metabolite RH-0422.
    2. Analytical method. The metabolism of triazamate in plants 
(apples) is adequately understood for the purposes of this tolerance. 
The metabolism of triazamate involves oxidative demethylation of the 
carbamoyl group. Parent compound is rapidly metabolized and is either 
not found or found at trace levels in apples. The majority of the total 
dosage is present as other non-cholinesterase inhibiting metabolites 
whose structures do not contain the dimethylcarbamoyl moiety. Because 
the proposed experimental use program is for fresh apples, livestock 
metabolism studies are not required. Tolerances for residues of 
triazamate should be expressed as the total residue from triazamate and 
its only cholinesterase-inhibiting metabolite RH-0422.
    3. Magnitude of residues. A total of 14 field residue trials in 
apples was conducted with a 25WP formulation in geographically 
representative regions of the U.S. Three applications were made at 
either 0.25 or 0.38 lb. a.i./acre. Fruit were harvested at 40 days 
after the last application. Only trace residues of triazamate were 
detected and residues of RH-0422 did not exceed 0.06 ppm.

B. Toxicological Profile

    1. Acute toxicity. Triazamate is a moderately toxic cholinesterase 
inhibitor belonging to the carbamate class. Triazamate Technical was 
moderately toxic to rats following a single oral dose (LD50 
= 50-200 milligram/kilograms (mg/kg)), and after a 4-hr inhalation 
exposure (LC50 value of >0.47 mg/L); and was minimally to 
slightly toxic to rats following a single dermal dose (LD50 
>5,000 mg/kg). In a guideline acute neurotoxicity study with triazamate 
in the rat, the NOEL for clinical signs was 5 mg/kg based on the 
observation of cholinergic signs in 1 of 10 male rats at 25 mg/kg. 
Triazamate was practically non-irritating to the skin, moderately 
irritating to eyes in rabbits and did not produce delayed contact 
hypersensitivity in the guinea pig.
    2. Genotoxicity. Triazamate is not mutagenic or genotoxic. 
Triazamate Technical was negative (non-mutagenic) in an Ames assay with 
and without hepatic enzyme activation. Triazamate Technical was 
negative in a hypoxanthine guanine phophoribosyl transferase (HGPRT) 
gene mutation assay using Chinese hamster ovary (CHO) cells in culture 
when tested with and without hepatic enzyme activation. In isolated rat 
hepatocytes, triazamate did not induce unscheduled DNA synthesis (UDS) 
or repair when tested up to the maximum soluble concentration in 
culture medium. Triazamate did not produce chromosome aberrations in an 
in vitro assay using Chinese hamster ovary cells (CHO) or an in vivo 
mouse micronucleus assay.
    3. Reproductive and developmental toxicity. In a developmental 
toxicity study in rats with Triazamate Technical, the no-observed-
effect-level (NOEL) for developmental toxicity was 64 mg/kg (highest 
dose tested) (HDT). The NOEL for maternal toxicity was 16 mg/kg based 
on clinical signs of cholinergic toxicity at 64 mg/kg.
    In a developmental toxicity study in rabbits with Triazamate 
Technical, the NOEL for developmental toxicity was 10 mg/kg (HDT). The 
NOEL for maternal toxicity was 0.5 mg/kg based on clinical signs and 
decreased body weight at 10 mg/kg.
    In a 2-generation reproduction study in rats with Triazamate 
Technical, the NOEL for reproductive effects was 1,500 ppm (101 and 132 
milligram/kilograms/day (mg/kg/day) for males and females, 
respectively; HDT). The NOEL for parental toxicity was 10 ppm (0.7 and 
0.9 mg/kg/day for males and females, respectively) based on decreased 
plasma and RBC cholinesterase activities at 250 ppm (17 and 21 mg/kg/
day for males and females, respectively).
    The acceptable developmental studies (prenatal developmental 
toxicity studies in rats and rabbits and 2-generation reproduction 
study in rats) provided no

[[Page 11242]]

indication of increased sensitivity of rats or rabbits to in utero and 
or post-natal exposure to triazamate. Triazamate Technical is not a 
developmental or reproductive toxicant.
    4. Subchronic toxicity. In subacute and subchronic dietary toxicity 
studies, Triazamate Technical produced no evidence of adverse effects 
other than those associated with cholinesterase inhibition:
    i. In a 90-day dietary toxicity study with Triazamate Technical in 
the rat, the NOEL for blood cholinesterase inhibition was 50 ppm (3.2 
and 3.9 mg/kg/day for males and females, respectively), based on 
decreases in plasma and RBC cholinesterase activities at 500 ppm (32 
and 39 mg/kg/day for males and females, respectively). The NOEL for 
brain cholinesterase inhibition and/or clinical signs was 500 ppm (32 
and 39 mg/kg/day for males and females respectively) based on decreased 
brain cholinesterase activity and decreased body weight gain and feed 
consumption at 1,500 ppm (93 and 117 mg/kg/day for males and females, 
respectively).
    ii. In a guideline subchronic neurotoxicity study (90-day dietary 
feeding) with Triazamate Technical in the rat, the NOEL for blood 
cholinesterase inhibition was 10 ppm (0.6 and 0.7 mg/kg/day for males 
and females, respectively), based on reductions in plasma and RBC 
cholinesterase activities at 250 ppm (14.3 and 17.1 mg/kg/day for males 
and females, respectively). The NOEL for brain cholinesterase 
inhibition and/or clinical signs was 250 ppm (14.3 and 17.1 mg/kg/day 
for males and females respectively) based on decreases in brain 
cholinesterase activity and cholinergic signs at 1,500 ppm (87 and 104 
mg/kg/day for males and females, respectively).
    iii. In a 90-day dietary toxicity study with Triazamate Technical 
in the mouse, the NOEL for blood cholinesterase inhibition was 2 ppm 
(0.4 and 0.5 mg/kg/day for males and females, respectively) based on 
decreases in plasma cholinesterase activity at 25 ppm (4 and 6 mg/kg/
day for males and females, respectively). The NOEL for brain 
cholinesterase and/or clinical signs was 250 ppm (46 and 67 mg/kg/day 
for males and females, respectively) based on decreases brain 
cholinesterase and decreases body weight and feed consumption at 1,000 
ppm (164 and 222 mg/kg/day for males and females, respectively).
    iv. In a 90-day dietary toxicity study with Triazamate Technical in 
the dog, the NOEL for blood cholinesterase inhibition was 1 ppm for 
males only (0.03 mg/kg/day) based on decreases in plasma cholinesterase 
at 10 ppm (0.3 mg/kg/day). The dose of 1 ppm was a lowest-observed-
effect-level (LOEL) for females based on the presence of decreased 
plasma cholinesterase activity (24%). The NOEL for clinical signs was 
10 ppm (0.3 mg/kg/day for males and females) based a few clinical signs 
at 100 ppm (3.1 mg/kg/day for males and females).
    v. In a 21-day dermal toxicity study with Triazamate Technical, the 
NOEL blood and brain cholinesterase inhibition was 10 mg/kg based on 
decreases plasma, RBC and brain cholinesterase activities at 100 mg/kg.
    5. Chronic toxicity-- i. Rat, mouse, and dog studies. In chronic 
dietary toxicity studies, Triazamate Technical produced no evidence of 
adverse effects other than those associated with cholinesterase 
inhibition and was not oncogenic in the rat and mouse.
    In a combined chronic dietary toxicity/oncogenicity study (24 
months) in rats with Triazamate Technical, no evidence of oncogenicity 
was observed at doses up to 1,250 ppm (62.5 mg/kg/day for males and 
females; HDT). The NOEL for blood cholinesterase inhibition was 10 ppm 
(0.5 and 0.6 mg/kg/day for males and females, respectively) based on 
decreases in plasma and RBC cholinesterase activity at 250 ppm (11.5 
and 14.5 mg/kg/day in males and females, respectively). The NOEL for 
brain cholinesterase inhibition and/or clinical signs was 250 ppm (11.5 
and 14.5 mg/kg/day in males and females, respectively) based on 
clinical signs and decreases in brain cholinesterase inhibition at 
1,250 ppm (62.5 mg/kg/day for males and females).
    In a combined chronic dietary toxicity study (18 months) in mice 
with Triazamate Technical, no evidence of oncogenicity was observed at 
doses up to 1,000-1,500 ppm (130-195 mg/kg/day for males and females; 
HDT). The NOEL for blood cholinesterase inhibition was 1 ppm (0.1 and 
0.2 mg/kg/day for males and females, respectively) based on decreased 
plasma cholinesterase activity at 50 ppm (6.7 and 8.4 mg/kg/day for 
males and females, respectively). The NOEL for brain cholinesterase 
inhibition and/or clinical signs was 50 ppm (6.7 and 8.4 mg/kg/day for 
males and females, respectively) based on decreased brain 
cholinesterase activity and other evidence of systemic toxicity at 
1,000-1,500 ppm (130-195 mg/kg/day for males and females).
    In a chronic dietary toxicity study (12 months) in dogs with 
Triazamate Technical, the NOEL for blood cholinesterase inhibition was 
0.9 ppm (0.023 and 0.025 mg/kg/day for males and females, respectively) 
based on decreased plasma cholinesterase activity at 15.0 ppm (0.42 mg/
kg/day for both males and females). The NOEL for brain cholinesterase 
inhibition was 15.0 ppm (0.42 mg/kg/day for both males and females) 
based on decreased brain cholinesterase activity at 150 ppm (4.4 and 
4.7 mg/kg/day for males and females, respectively).
    ii. Human studies. A randomized double blind ascending dose study 
was conducted in human male volunteers to determine the safety and 
tolerability of Triazamate Technical and to establish a NOEL for 
adverse clinical toxicity. Single doses of Triazamate Technical, when 
administered orally by capsule to healthy male subjects, were tolerated 
up to and including a dose of 1.0 mg/kg. The 3.0 mg/kg dose of 
triazamate was not clinically tolerated well. Clinically, the NOEL was 
0.3 mg/kg of triazamate based on minimal clinical signs at 1.0 mg/kg 
that were considered possibly related to treatment. Transient decreases 
in plasma and RBC cholinesterase occurred at doses lower than the dose 
that elicited adverse clinical signs.
    Using its Guidelines for Carcinogen Risk Assessment published 
September 24, 1986 (51 FR 33992), Rohm and Haas Company considers 
triazamate to be classified as a Group ``E,'' not a likely human 
carcinogen.
    A Reference dose (RfD) of 0.01 mg/kg/day is proposed for humans, 
based on the clinical NOEL in the human study (0.3 mg/kg) and dividing 
by a safety factor of 30. The dose of 0.3 mg/kg was the highest dose in 
humans that did not produce toxicologically significant adverse effects 
(i.e., signs of cholinergic toxicity) and is 10 times lower than a dose 
that produced unequivocal signs of cholinergic toxicity in man. In 
addition, the clinical NOEL in humans is comparable to the no-
observable-adverse-effect level (NOAEL) of 0.42 mg/kg/day following 
chronic dosing in the dog, the most sensitive laboratory animal 
species. A safety factor of 10 is applied to the clinical NOEL in 
humans to account for potential variability within humans with respect 
to sensitivity towards triazamate. An additional, safety factor of 3 is 
included, since at 0.03 mg/kg (i.e., 1/10th the dose that 
was a clinical NOEL) there was a transient but measurable depression in 
plasma cholinesterase in humans. Although a change in the plasma 
pseudo-cholinesterase (i.e., butyl-cholinesterase) is not 
toxicologically significant since this enzyme is not molecularly 
similar to acetyl-cholinesterase, the additional uncertainty factor of 
3 establishes a RfD at a level where one would predict no

[[Page 11243]]

measurable response of any kind, irrespective of the toxicological 
significance of the finding.
    6. Animal metabolism. The adsorption, distribution, excretion and 
metabolism of triazamate in rats, dogs and goats was investigated. 
Triazamate is rapidly absorbed when given orally (capsule or gavage) 
but slower following dietary intake. Peak blood levels following 
dietary administration were 10-fold lower than after gavage 
administration of an equivalent mg/kg/dose. Elimination is 
predominately by urinary excretion and triazamate does not accumulate 
in tissues. The metabolism of triazamate proceeds via ester hydrolysis 
and then a rapid stepwise cleavage of the carbamoyl group. The free 
acid, (RH-0422) is the only toxicologically significant metabolite, 
given that it contains the carbamoyl group. Other metabolites of 
triazamate, which are seen in other animal and plant metabolism 
studies, do not contain the carbamoyl group and do not produce 
cholinesterase inhibition.
    7. Metabolite toxicology. Common metabolic pathways for triazamate 
have been identified in both plants (apple) and animals (rat, goat, 
hen). The metabolic pathway common to both plants and animals involves 
oxidative demethylation of the carbamoyl group. Extensive degradation 
and elimination of polar metabolites occurs in animals such that 
residue are unlikely to accumulate in humans or animals exposed to 
these residues through the diet.
    8. Endocrine disruption. The toxicology profile of triazamate shows 
no evidence of physiological effects characteristic of the disruption 
of mammalian hormones. In developmental and reproductive studies there 
was no evidence of developmental or reproductive toxicity. In addition, 
the molecular structure of triazamate does not suggest that this 
compound would disrupt the mammalian hormone system. Overall, the 
weight of evidence provides no indication that triazamate has endocrine 
activity in vertebrates.

C. Aggregate Exposure

    1. Dietary exposure. A RfD of 0.01 mg/kg/day is proposed for 
humans, based on the clinical NOEL in the human study (0.3 mg/kg) and 
dividing by a safety factor of 30.
    2. Food-- i. Acute risk. An acute dietary risk assessment (Dietary 
Exposure Evaluation Model, Novigen Sciences Inc., 1997) was conducted 
for triazamate using two approaches: (a) a Tier 1 approach using a 
tolerance level residue of 0.1 ppm and (b) Monte Carlo simulations 
using an entire distribution of field trial residues for pome fruit and 
adjusted for percent crop treated (Tier 3). Using the Tier 1 approach 
margins of exposure (MOEs) at the 95th and 99th 
percentiles of exposure for the overall U.S. population were 572 and 
199, respectively. Using the Tier 3 procedure in which residues were 
adjusted for percent crop treated, the MOEs for the 95th and 
99th percentiles were 8,769 and 1,511, respectively. Acute 
exposure was also estimated for non-nursing infants, the most sensitive 
sub-population. For this population, MOEs at the 95th and 
99th percentiles of exposure were 113 and 83, respectively. 
Using the Tier 3 method, MOEs were 909 and 396, respectively. Acute 
dietary risk is considered acceptable if the MOE is greater than 30, an 
appropriate safety factor when based on a human clinical study. Even 
under the conservative assumptions presented here, the more realistic 
estimates of dietary exposure (Tier 3 analyses) clearly demonstrate 
adequate MOEs up to the 99th percentile of exposure for all 
population subgroups.
    ii. Chronic risk. Chronic dietary risk assessments (Dietary 
Exposure Evaluation Model, Novigen Sciences Inc., 1997) were conducted 
for triazamate using two approaches: (a) using a tolerance level 
residue of 0.1 ppm assuming 100% of crop is treated and (b) using a 
tolerance level residue of 0.1 ppm adjusted for projected percent crop 
treated. The Theoretical Maximum Residue Contribution (TMRC) from the 
proposed pome fruit tolerance represents 0.91% of the RfD for the U.S. 
population as a whole. The subgroup with the greatest chronic exposure 
is non-nursing infants (less than 1 year old), for which the TMRC 
estimate represents 6.3% of the RfD. The chronic dietary risks from 
this use do not exceed EPA's level of concern.
    3. Drinking water. Both triazamate and its cholinesterase-
inhibiting metabolite RH-0422 are degraded rapidly in soil. This rapid 
degradation has been observed in both laboratory and field studies and 
makes it highly unlikely that measurable residues of either compound 
would be found in ground or surface water when triazamate is applied 
according to the proposed EUP label directions.
    4. Non-dietary exposure. Triazamate is not registered for either 
indoor or outdoor residential use. Non-occupational exposure to the 
general population is therefore not expected and not considered in 
aggregate exposure estimates.

D. Cumulative Effects

    The potential for cumulative effects of triazamate with other 
substances that have a common mechanism of toxicity was considered. It 
is recognized the triazamate, although structurally a pseudo-carbamate, 
exhibits toxicity similar to the carbamate class of insecticides, and 
that these compounds produce a reversible inhibition of the enzyme 
cholinesterase. However, Rohm and Haas Company concludes that 
consideration of a common mechanism of toxicity is not appropriate at 
this time since EPA does not have the methodology to resolve this 
complex scientific issue concerning common mechanisms of toxicity. 
Based on these points, Rohm and Haas Company has considered only the 
potential risks of triazamate and RH-0422 in its cumulative exposure 
assessment.

E. Safety Determination

    1. U.S. population. The acute and chronic dietary exposure to 
triazamate and its metabolite from the proposed use on pome fruit were 
evaluated. Exposure to triazamate and its toxicologically significant 
metabolite on pome fruit does not pose an unreasonable health risk to 
consumers including the sensitive subgroup non-nursing infants. In Tier 
1 and Tier 3 acute analyses for the 95th percentile 
exposures, MOEs were greater than 100 for the general U.S. population. 
Using the TMRC and assuming 100% of crop treated, the most conservative 
chronic approach, chronic dietary exposures represents 0.6% of the RfD 
for the U.S. population. 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.
    Using the two conservative exposure assessments described above and 
taking into account the completeness and reliability of the toxicity 
data, Rohm and Haas Company concludes that there is a reasonable 
certainty that no harm will result from aggregate exposure to residues 
of triazamate and its toxicologically significant metabolite to the 
U.S. population.
    2. Infants and children. In assessing the potential for additional 
sensitivity of infants and children to residues of triazamate, data 
from developmental toxicity studies in the rat and rabbit and 2-
generation reproduction studies in the rat are considered. The 
developmental toxicity studies are designed to evaluate adverse effects 
on the developing organism resulting from pesticide exposure during 
prenatal development

[[Page 11244]]

to one or both parents. 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 may apply an additional safety 
factor for infants and children in the case of threshold effects to 
account for pre-and post- natal effects and the completeness of the 
toxicity database. Based on current toxicological data requirements, 
the toxicology database for triazamate relative to pre- and post- natal 
effects is complete. For triazamate, developmental toxicity was not 
observed in developmental studies using rats and rabbits. The NOEL for 
developmental effects in rats was 64 mg/kg/day and rabbits was 10 mg/
kg/day. In the 2-generation reproductive toxicity study in the rat, the 
reproductive/ developmental toxicity NOEL was 101-132 mg/kg/day. These 
NOELs are 10-fold or higher than those observed for systemic toxicity, 
i.e., cholinesterase inhibition.
    In Tier 1 and Tier 3 acute dietary analyses for the 95th 
percentile exposures, MOEs were greater than 100 for non-nursing 
infants. Using the TMRC and assuming 100% of crop treated, the most 
conservative chronic approach, chronic dietary exposures represents 
6.3% of the RfD for non-nursing infants under 1 year old. Therefore 
Rohm and Haas Company concludes that there is a reasonable certainty 
that no harm will result from aggregate exposure to residues of 
triazamate and its toxicologically significant metabolite to infants 
and children.

F. International Tolerances

    There are no approved CODEX maximum residue levels (MRLs) 
established for residues of triazamate. MRLs have been established for 
apples at 0.1 ppm in the Czech Republic, at 0.02 ppm in Hungary, and at 
0.2 ppm in Korea.



[FR Doc. 98-5985 Filed 3-5-98; 8:45 am]
BILLING CODE 6560-50-F