Document ID: EPA-HQ-OPP-2008-0386-0002
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2008-06-13T04:00Z

<EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR PESTICIDE
PETITIONS PUBLISHED IN THE FEDERAL REGISTER  >

<EPA Registration Division contact: Jim Tompkins, telephone 703-305-5697
>

 

<INSTRUCTIONS:  Please utilize this outline in preparing the pesticide
petition.  In cases where the outline element does not apply, please
insert “NA-Remove” and maintain the outline. Please do not change
the margins, font, or format in your pesticide petition. Simply replace
the instructions that appear in green, i.e., “[insert company
name],” with the information specific to your action.>

<TEMPLATE:>

<Gowan Company>

<PP 8F7334>

<	EPA has received a pesticide petition (<PP 8F7334)> from Gowan
Company, 370 South Main Street, Yuma, AZ  85364 proposing, pursuant to
section 408(d) of the Federal Food, Drug, and Cosmetic Act (FFDCA), 21
U.S.C. 346a(d), to amend 40 CFR part 180.>

<(Options (pick one)>

<	1. by establishing a tolerance for residues of>

<	2. to establish an exemption from the requirement of a tolerance for>

<	triallate in or on the raw agricultural commodity Bermuda grass hay at
0.2 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  FDDCA; 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.>

<	2. Analytical method. Residues of triallate and its metabolite TCPSA
in Bermuda grass forage, hay, straw and seed screenings were quantitated
using a GC/MS analytical method.  The LOQ was 0.02 ppm for triallate and
0.05 ppm for TCPSA.>

<	3. Magnitude of residues. Four Bermuda grass residue trials and a
forage residue decline study were conducted in California.  Combined
residues of triallate and TCPSA were below 0.2 ppm in forage, hay, straw
and seed screenings.  Residues were highest in Bermuda grass hay.>

<B. Toxicological Profile>

<	1. Acute toxicity.  Triallate has a low order of acute oral toxicity
and is classified as a Toxicity Category III, based >on test results
that indicate the LD50 (males) = 3612 mg/kg; LD50 (females) = 3455
mg/kg; and LD50 (combined) = 3382 mg/kg.  For the general population, a
No Observed Adverse Effect Level (NOAEL) of 60 mg/kg/day has been
established based on decreased mean body weight, altered motor activity,
and changes in functional observation battery (FOB) in the rat acute
neurotoxicity study at the Lowest Observed Adverse Effect Level (LOAEL)
of 300 mg/kg/day. Because of the neurotoxic characteristics of triallate
(altered motor activity observed in both sexes 7 hours after treatment
at the mid- and high-doses that persisted up to 14 days in high-dose
females), this endpoint is considered appropriate for assessing risk in
the general population.

 

<	2. Genotoxicty. Positive genotoxicity results were observed in
Salmonella typhimurium, mouse lymphoma cells and Chinese hamster cells.>

<	3. Reproductive and developmental toxicity.  For females 13-50 years
population subgroup, a NOAEL of 5 mg/kg/day has been established based
>on increased skeletal malformations/variations in the rabbit
developmental toxicity study at the LOAEL of 15 mg/kg/day. The skeletal
malformations are presumed to occur after a single exposure (dose), and
thus, are appropriate for this (acute) risk assessment. In addition,
skeletal malformations (malaligned sternebrae) were also seen in rat
fetuses following in utero exposure to triallate.

 

<	4. Subchronic toxicity. A subchronic exposure endpoint has not been
established.>

<	5. Chronic toxicity. A chronic (non-cancer) NOAEL of 2.5 mg/kg/day was
established based on decreased survival in males and females, decreased
mean body weights in males, and increased adrenal weights in males in
the 2-year chronic toxicity/carcinogenicity study in rats at the LOAEL
of 12.5 mg/kg/day.  Triallate is classified as a Group C chemical 
(possible human carcinogen). This classification is based on the
following factors: (i) hepatocellular carcinomas found in male mice,
with a positive trend and a borderline significant increase in females;
(ii) the increased incidence in male rats of renal tubular cell adenoma
above historical control levels, although no absolute pair-wise
statistical significance was found; and (iii) triallate is considered a
mutagen because of the positive genotoxicity results discussed above.  A
linear low-dose (Q1*) approach is used to characterize human health
risk. The unit risk, Q1* based on hepatocellular carcinomas in male
mice, is  7.17 x 10-2 (mg/kg/day)-1 in human equivalents.

>

<	6. Animal metabolism. Studies on the absorption, distribution,
metabolism and excretion of triallate have been conducted with rats and
Rhesus monkeys.  Triallate is extensively metabolized via three
pathways:  (i) oxidation of the sulfur of the thiocarbamate, (ii)
hydrolysis to form the 2,3,3-trichloro-2-propene-1-thiol and (iii)
carbon oxidation.  Oxidation of the sulfur group leads to metabolite M1,
which is further oxidized to 2,3,3-trichloro-2-propenesulfonic acid
(TCPSA).  TCPSA is the only metabolite in the tolerance expression for
triallate.

>

<	7. Metabolite toxicology. TCPSA is the major metabolite of triallate
in both animals and plants.  TCPSA is less toxic than triallate.  In a
14-day feeding study with TCPSA at 1413 – 1546 mg/kg/day, no
treatment-related effects were seen, whereas triallate in a 28-day
feeding study showed a NOAEL of 75 mg/kg/day.  TCPSA showed no evidence
of genotoxicity in a Salmonella typhimurium reverse mutation assay, an
in vitro chromosome aberration test in Chinese hamster V79 cells or in a
cell mutation assay at the thymidine kinase locus in mouse lymphoma
L5178Y cells.   >

<	8. Endocrine disruption. No evidence of endocrine effects has been
observed in reproduction, developmental, neurotoxicity or chronic
toxicology studies.>

<C. Aggregate Exposure>

<	1. Dietary exposure. Bermuda grass commodities are not human foods,
and residues of triallate in plants do not translocate into meat, milk,
poultry or eggs.  The Agency has previously concluded that there is no
reasonable expectation of finite residues of triallate in animal
commodities.  Therefore no incremental human dietary exposure will be
associated with the proposed use on Bermuda grass.>

<	i. Food. [NA - Remove]>

<	ii. Drinking water. The proposed use of triallate on Bermuda grass
grown for seed is geographically limited to agricultural land in the
desert Southwest.  Runoff does not occur in these areas, and there is no
possibility of contamination of drinking water.  >

<	2. Non-dietary exposure. The proposed use of triallate is for Bermuda
grass grown for seed.  Residential use is not proposed, so non-dietary
exposure will not occur.>

<D. Cumulative Effects 	[NA - Remove]>

<E. Safety Determination>

<	1. U.S. population. The proposed use will not result in any
incremental aggregate exposure to the U.S. population.

>

<	2. Infants and children. The proposed use will not result in any
incremental aggregate exposure to infants and children.>

<F. International Tolerances	No national or transnational MRL for
triallate on Bermuda grass has been established.>

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