Document ID: EPA-HQ-OPP-2009-0797-0003
Agency: epa
Document Type: Supporting & Related Material
Title: 
Posted Date: 2010-01-06T05:00Z

Docket #:  EPA-HQ-OPP-2009-0797 

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

<EPA Registration Division contact: Sidney Jackson[James Tompkins, 703
703-305-5761097]>

 

<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:>

<[Interregional Research Project Number 4Canyon Group LLC, c/o Gowan
Company, 370 South Main Street, Yuma, Arizona 85364]>

<[PP9E7577xxxxxx]>

<	EPA has received a pesticide petition ([PP9E7577xxxxxx]) from the
Interregional Research Project Number 4(IR-4)[C in cooperation with
Canyon Group LLC], [c/o Gowan Company, 370 South Main Street, Yuma,
Arizona 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 180.479 >

<(Options (pick one)>

<	1. by establishing a tolerance for residues of 

>

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

<	[halosulfuron-methyl] in or on the raw agricultural commodities [pea
and bean, succulent shelled (subgroup 6B); pea and bean, dried shelled,
except soybean (subgroup 6C);, vegetables, tuberous and corm (subgroup
1C); bushberry (subgroup 13-07B);, apple; ,  and rhubarb; and okra at
[0.05 ] parts per million (ppm).  It has also been requested that the
existing tolerance for vegetables, fruiting (except cucurbits) group
(group 8) be redefined as “vegetables, fruiting (except cucurbits)
group plus okra (group 8).  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 . [The metabolism of halosulfuron-methyl as well
as the nature of the residues in plants is adequately understood for the
purposes of these tolerances.  Metabolism studies were conducted with
three crops, vis.; field corn, sugarcane and soybeans.  Metabolism
depends on the mode of application.  Preemergent applications result in
rapid soil degradation of halosulfuron-methyl followed by crop uptake of
the resulting pyrazole moiety.  The pyrimidine ring binds tightly to
soil and is eventually converted to carbon dioxide by microbial
degradation.  In postemergent applications, little metabolism and
translocation take place, resulting in unmetabolized parent compound as
the major residue on the directly treated foliar surfaces.  Very low
residue levels of the metabolite
3-chloro-1-methyl-5-sulfamoylpyrazole-4-carboxylic acid (3-CSA) are
found in grain.]>

<	2. Analytical method. [A practical analytical method, gas
chromatography with a nitrogen-specific detector, is available for
enforcement purposes.  The limit of detection is 0.003 ppm.]>

<	3. Magnitude of residues. [Samples from 13 apple trials, 6 blueberry
trials, 4 rhubarb trials, 9 potato trials, 12 dry bean trials and 12
succulent pea trials were analyzed for halosulfuron and its metabolites.
 Samples from an additional apple trial treated a 5X the proposed rate
were also analyzed.  Combined residues were below 0.05 ppm in every
sample.]>

<B. Toxicological Profile>

<	1. Acute toxicity.  [Acute toxicological studies placed
technical-grade halosulfuron-methyl in Toxicity Category III.  The
Agency has derived an acute PAD of 0.17 mg/kg based upon a rabbit
developmental toxicity study.  The NOAEL was 50 mg/kg, and the Agency
applied an Uncertainty Factor of 300 (10X for interspecies
extrapolation, 10X for intraspecies variability and 3X due to the lack
of a developmental neurotoxicity study.]>

<	2. Genotoxicty. [Bacterial and mammalian microsomal mutagenicity
assays showed halosulfuron-methyl not to be mutagenic.  Gene mutation
and chromosomal aberration studies were negative.  An unscheduled DNA
test in primary rat hepatocytes was negative.  An in vivo mouse
micronucleus assay did not cause a significant increase in the frequency
of micronucleated polychromatic erythrocytes in bone marrow cells.]>

<	3. Reproductive and developmental toxicity. [A developmental toxicity
study in rats resulted in a developmental LOAEL of 750 mg/kg/day, based
on decreases in mean litter size and fetal body weight and increases in
resorptions, resorptions per dam, post-implantation loss and in fetal
and litter incidences of soft tissue and skeletal variations.  The
developmental NOAEL in this study was 250 mg/kg/day.  The maternal LOAEL
was 750 mg/kg/day, based on increased incidence of clinical
observations, reduced body weight gains, and reduced food consumption
and food efficiency.  The maternal NOAEL was 250 mg/kg/day.

A developmental toxicity study in rabbits resulted in a developmental
LOAEL of 150 mg/kg/day, based on decreased mean litter size and
increases in resorptions, resorptions per dam and post-implantation
loss.  The developmental NOAEL was 50 mg/kg/day.  The maternal LOAEL was
150 mg/kg/day, based on reduced body weight gain and reduced food
consumption and food efficiency, and the maternal NOAEL was 50
mg/kg/day.

A dietary 2-generation reproduction study in rats resulted in parental
toxicity at 223 mg/kg/day in males and 261 mg/kg/day in females, based
on decreased body weights, decreased body weight gains, and reduced food
consumption during the premating period.  Very light effects were noted
in body weight of the offspring at this dose.  This effect was
considered to be developmental toxicity (developmental delay) rather
than a reproductive effect.  No effects were noted on reproductive or
other developmental toxicity parameters.  The systemic/developmental
toxicity LOAEL was 223 mg/kg/day in males and 261 mg/kg/day in females; 
the systemic/developmental toxicity NOAEL was 50 mg/kg/day in males and
59 mg/kg/day in females.  The reproductive NOAEL was greater than or
equal to 223 mg/kg/day for males and 261 mg/kg/day for females.]>

<	4. Subchronic toxicity. [A 90-day feeding study in rats resulted in a
NOAEL of 116 mg/kg/day in males and 147 mg/kg/day in females.  The LOAEL
was 497 mg/kg/day for males and 640 mg/kg/day in females.]>

<	5. Chronic toxicity. [A 1-year chronic oral toxicity study in dogs
resulted in a LOAEL of 40 mg/kg/day based on decreased weight gain and a
NOAEL of 10 mg/kg/day.  In a 78-week carcinogenicity study in mice, a
LOAEL of 972 mg/kg/day was based upon decreased body weight gains and an
increased incidence of microconcretion/mineralization in the testis and
epididymis in males.  No treatment-related effects were observed in
females.  The systemic NOAEL was 410 mg/kg/day, and the study showed no
evidence of carcinogenicity.  A combined chronic and carcinogenicity
study in rats resulted in a LOAEL of 108 mg/kg/day on males and 56
mg/kg/day in females.  The study showed no evidence of carcinogenicity. 
The Agency has derived a chronic PAD of 0.03 mg/kg/day based upon a
NOAEL of 10 mg/kg/day in the dog study and an Uncertainty Factor of
300.]>

<	6. Animal metabolism. [The Agency has determined that the nature of
the residue in ruminants is adequately understood.  In the tissues and
milk of goats, the major extractable residue was the unmetabolized
parent compound.  The Agency has not required tolerances for residues in
poultry.  In the rat metabolism study, parent compound was absorbed
rapidly but incompletely.  Excretion was relatively rapid at all doses
tested, and the majority of the radioactivity was eliminated in the
urine and feces within 72 hours.  Fecal elimination was the result of
unabsorbed parent compound.]>

<	7. Metabolite toxicology. [Various toxicity studies have shown that
the metabolite 3-CSA is of lower toxicity than the parent compound, and
the Agency has concluded that it should not be included in the tolerance
expression.  However, in the residue analytical method for animal
products, halosulfuron-methyl and all of its metabolites are hydrolyzed
to 3-CSA, which is analyzed and the results expressed as parent
equivalents.  The tolerance expression for plant commodities consists of
only parent compound.]>

<	8. Endocrine disruption. [No specific tests have been conducted with
halosulfuron-methyl to determine whether the chemical may have an effect
in humans that is similar to an effect produced by a naturally occurring
estrogen, or other endocrine effects.  However, there were no
significant findings in relevant toxicology studies,;  e.g., teratology
and reproduction studies, which suggest that halosulfuron-methyl
produces effects characteristic of the estrogen disruption.]>

<C. Aggregate Exposure>

<	1. Dietary exposure. [Tolerances have previously been established for
residues in a variety of raw agricultural commodities (40 CFR 180.479). 
Additionally, tolerances have been established for halosulfuron-methyl
and its metabolites in the meat byproducts of cattle, goats, hogs,
horses and sheep.   The Agency’s exposure and risk assessments for
these commodities were discussed in FR 70 (168) 51615 – 51623 (August
31, 2005).]>

<	i. Food. [No detectable residues were observed in soybeans treated
even at an exaggerated use rate.  Therefore, the proposed use of
halosulfuron-methyl on soybeans does not alter the Agency’s previous
conclusions regarding risk resulting from dietary exposure.]>

<	ii. Drinking water. [The Agency has not conducted a comprehensive
dietary exposure analysis of halosulfuron-methyl in drinking water.  The
Agency, however, has estimated concentrations in surface water using the
First Index Reservoir Screening Tool (FIRST) or the Pesticide Root Zone
Model / Exposure Analysis Modeling System (PRZM/EXAMS).  Concentrations
in ground water were estimated using the Screening Concentration in
Ground Water Modeling System (SCI-GROW).  None of these models includes
consideration of the impact of processing (dilution and treatment) of
raw water.  The Agency conservatively estimated maximum residues of
0.105 ppm in surface water and 0.000065 ppm in ground water.  The use of
halosulfuron-methyl on soybeans proposed here does not alter the
Agency’s previous calculations.]>

<	2. Non-dietary exposure.  [Halosulfuron-methyl is registered for use
on residential turfgrass and landscaped areas.  The short-term aggregate
risk assessment estimates risks that are likely to result from exposures
up to 30 days.  The same toxicological effect upon which endpoints were
defined (decreased bodyweight gain) was observed across all routes of
exposure.   The Agency’s level of concern is a short-term aggregate
(food + water + residential) MOE of less than 300.  However, the Agency
has previously calculated aggregate MOEs of 3,100 or greater.  The
proposed use of halosulfuron-methyl on soybeans does not alter the
Agency’s previous calculations.

Similarly, an intermediate-term aggregate risk assessment evaluates
risks that are likely to result from exposures of 1 to 6 months.  Again
the same effect upon which endpoints were defined (decreased bodyweight
gain) was observed across all routes of exposure, and the Agency’s
level of concern for intermediate-term aggregate exposure is an MOE of
less than 300.  The Agency has previously calculated an
intermediate-term aggregate risk of 819 for the most highly exposed
subgroup.  Therefore, short-term and intermediate-term aggregate
exposure is not of concern.]>

<D. Cumulative Effects>

<	[EPA has not made a common mechanism of toxicity finding regarding
halosulfuron-methyl and any other substance.  Halosulfuron-methyl does
not appear to produce a toxic metabolite that is produced by any other
substance.  Therefore, for the purposes of this tolerance action, EPA
has not assumed that halosulfuron-methyl has a common mechanism of
toxicity with other substances.]>

<E. Safety Determination>

<	1. U.S. population. [The Agency has evaluated acute aggregate risk
assessment only for females 13 – 50 years old.  The Agency has
calculated that exposure to this subpopulation occupies 1% of the aPAD. 
There is no indication that halosulfuron-methyl could cause adverse
effects to the general population from a single dose.  EPA previously
concluded that chronic exposure occupies 3% of the cPAD for the general
U.S. population, 8% for infants <1 year old and 4% for children 1-5. 
EPA previously concluded that intermediate-term aggregate exposure
results in MOEs greater than 480 for all population subgroups, whereas
the Agency’s Level of Concern is MOEs below 300.  Halosulfuron-methyl
is not carcinogenic.

]>

<	2. Infants and children. [The Agency has not set a special FQPA safety
factor for infants and children.  The Agency has concluded that an acute
risk assessment for infants and children is not required.  Short-term,
intermediate-term and chronic exposure assessments for infants and
children indicate that risk is below the Agency’s level of concern. 
Therefore, based on these risk assessments, the Agency has concluded
that there is a reasonable certainty that no harm will result to the
general population and to infants and children from aggregate exposure
to halosulfuron-methyl residues.]>

<F. International Tolerances>

<	Mexico and Japan each has a Maximum Residue Level (MRL) of 0.05 ppm
for halosulfuron-methyl on dry beans.]  Japan has also set provisional
MRLs for halosulfuron-methyl of 0.02 ppm on apples, blueberries, peas
and potatoes.  There  are no Canadian, Codex or EU MRLs for these
commodities.  >

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