 

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

<EPA Registration Division contact: James Tompkins, Registration Support
Branch, Registration Division (7505C), Office of Pesticide Programs,
Environmental Protection Agency, 401 M Street, SW, Washington, DC 20460;
telephone number: (703) 305-5697; e-mail address: tompkins.jim@epa.gov

>

<BASF Corporation>

<PP 0E7788>

<<	EPA has received a pesticide petition (PP 0E7788) from BASF
Corporation, P.O. Box 13528, Research Triangle Park, NC  27709
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 by
establishing a tolerance for residues of  tepraloxydim,
(2-[1-[[[(2E)-3-chloro-2-propenyl]oxy]imino]propyl]-3-hydroxy-5-(tetrahy
dro-2H-pyran-4-yl)-cyclohexene-1-one) and its metabolites convertible to
GP (3- (tetrahydropyran-4-yl)pentane-1,5-dioic acid) and OH-GP
(3-hydroxy-3-(tetrahydropyran-4-yl)pentane-1,5-dioic acid), calculated
as tepraloxydim, in or on the raw agricultural commodities pea and bean,
dried shelled, except soybean, subgroup 6C, at 0.10 parts per million
(ppm), and Sunflower Subgroup 20B, at 0.25 ppm for imported commodities.
 EPA has determined that the petition contains data or information
regarding the elements set forth in section 408 (d)(2) of 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 qualitative nature of the residues of
tepraloxydim in plants is adequately understood for the purposes of
establishing these tolerances.  Nature of the residue studies were
conducted in soybean, canola, and sugar beet in order to characterize
the fate of tepraloxydim amongst different crop types.  Tepraloxydim and
its metabolites convertible to GP
(3-(tetrahydropyran-4-yl)pentane-1,5-dioic acid) and OH-GP
(3-hydroxy-3-(tetrahydropyran-4-yl)pentane-1,5,-dioic acid),  expressed
as the parent compound, comprise the relevant residues.  >

<	2. Analytical method. The analytical method involves extraction,
concentration, precipitation, centrifugation/filtration, oxidation,
partition, and clean-up. Samples are then analyzed by GC-MS (selected
ion monitoring). The limit of quantitation (LOQ) is 0.05 ppm for each
analyte, parent and metabolite.

>

<	3. Magnitude of residues.  Residue crop field trials were conducted in
North Dakota, South Dakota, Manitoba, and Quebec to represent the dry
bean production regions of Canada.  Residue crop field trials were
conducted in North Dakota, Wisconsin, Manitoba, and Saskatchewan, to
represent the sunflower production regions of Canada.  In addition, a
processing study was conducted to determine the potential for residues
of tepraloxydim to concentrate in sunflower processed fractions.   All
field trials were carried out using the maximum or higher labeled rates,
maximum number of applications, and the proposed pre-harvest interval. 
In the dry bean trials, there were no residues detected above the limit
of quantitation (0.05 ppm) for either tepraloxydim or its metabolites
convertible to the analytes GP and OH-GP.  The combined residues of
tepraloxydim in the treated sunflower seed samples ranged from <0.10 ppm
(less than the combined LOQ) to 0.18 ppm.  Only two of the ten treated
samples contained quantifiable residues (combined residues of 0.10 and
0.18 ppm).  A comparison of the residues in the RAC with those in the
processed fractions indicated that residues of tepraloxydim do not
concentrate in sunflower processed fractions (meal and refined oil).

>

<B. Toxicological Profile>

<	1. Acute toxicity.>  Tepraloxydim is characterized by low acute
toxicity by the oral, dermal and inhalation route of administration. 
The acute toxicity studies place technical tepraloxydim in toxicity
category IV for acute inhalation and skin irritation.  Tepraloxydim is
in toxicity category III for acute oral, acute dermal toxicity and eye
irritation.  The technical material is not a dermal sensitizer.  An
acute neurotoxicity study conducted with tepraloxydim showed a LOAEL of
500 mg/kg, but a NOAEL was not identified.

<	2. Genotoxicty.  In the five mutagenicity studies consisting of both
in vitro and in vivo studies, tepraloxydim showed no mutagenic,
clastogenic or other genotoxic activity.  Tepraloxydim did not induce
mutations in either an in vitro Ames test or an in vitro CHO/HPRT locus
mammalian cell assay.  Tepraloxydim had no chromosomal effects in an in
vitro cytogenetics chromosome aberration test in CHO cells or in an in
vivo mouse micronucleus test.  Tepraloxydim also did not induce
DNA-damage and -repair in the unscheduled DNA synthesis (UDS) test. 
Therefore, tepraloxydim does not pose a genotoxic hazard to humans.>

<	3. Reproductive and developmental toxicity.>  The reproduction
toxicity of tepraloxydim was investigated in a 2-generation study as
well as in prenatal toxicity studies in rats and rabbits.  In the
2-generation study the NOAEL for reproductive function was the highest
dose tested, 2500 ppm (approximately 260 mg/kg bw male).  The NOAEL for
systemic toxicity for the parental animals in the 2-generation study was
500 ppm (50.6 mg/kg bw male, 55 mg/kg bw female).  The NOAEL for
developmental toxicity was 500 ppm (50.6 mg/kg bw male, 55 mg/kg bw
mg/kg bw female) in the 2-generation study.

	A prenatal toxicity study in rats observed a slight increased rate of
malformations in the highest dose group (360 mg/kg bw), in which
distinct maternal toxicity was also observed.    A slight increase in
skeletal variations was observed at the mid dose (120 mg/kg bw). 
Although there was no maternal toxicity at this dose, the skeletal
variations were most likely related to reduced pup weights at this dose.
 No treatment-related developmental effects were observed at the low
dose level (40 mg/ kg bw).

	No embryotoxic or teratogenic findings were detected in a prenatal
toxicity study in rabbits at any dose level, including one dose level
where there was clear maternal toxicity.

	The lowest NOAEL for maternal/parental toxicity was 50.6 mg/kg bw
(2-generation study, male rat), and the lowest NOAEL for developmental
toxicity was 40 mg/kg bw (prenatal toxicity study, rat).

<	4. Subchronic toxicity.  The short-term toxicity of tepraloxydim was
investigated in 28-day range-finding studies as well as in 3-month
studies in rats, mice, and dogs.  The signs of toxicity observed in the
three species were quite similar. The target organs were the liver and
the kidneys, with the observed clinicochemical findings linked to either
liver or kidney toxicity. In dogs the NOAEL was 12.9 mg/kg bw male and
14.3 mg/kg bw female based upon increased weights of the liver and
thyroid and histopathology of the spleen at the mid dose (63.3 mg/kg bw
male, 68 mg/kg bw female).

In a 4-week dermal toxicity study in rats no substance-related findings
were detected up to the highest dose level tested of 1,000 mg/kg bw.

	The overall lowest subchronic NOAELs from oral administration studies
were 22 mg/kg bw for rats (male), 95 mg/kg bw for mice and 12.9 for dogs
(male).

A subchronic oral neurotoxicity study in rats found the NOAEL was 1500
pm (103 mg/kg bw males, and 124 mg/kg bw females) based on increased
motor activity, decreased body weight and decreased food consumption at
the high dose (6000 ppm, 428 mg/kg bw male, 513 mg/kg bw female).>

<	5. Chronic toxicity. A 12-month dog study with doses of 0, 100, 400
and 2000 ppm found a slight anemia, detected only at the highest dose
level, with subsequent alterations in the bone marrow and the spleen.
This phenomenon was only observed in dog studies, so the dog was
determined to be the most sensitive species with regard to the anemic
process. Furthermore, an impairment of liver function was detected with
associated hepatocellular hypertrophy at the highest dose tested.  The
high toxic dose levels caused weight reductions of epididymides and
testes, combined with signs of reduced function of epididymides and
degeneration and atrophy of the germinal epithelium in the testes. In
the urinary bladder, hyperplasia of the transitional epithelium was
found in animals from high dose levels.  From the toxico-pathological
point of view, liver, urinary bladder and the haematopoietic system were
identified as primary target organs in dogs. Effects on the male gonadal
tissues may be regarded as secondary due to reduced nutritional status
and anemia.

The results of a 24-month chronic toxicity study and a carcinogenicity
study with dose levels at 0, 100, 600, 3000 (male) and 4,000 ppm
(female) in rats showed that the highest dose level (3,000 ppm in males
and 4,000 ppm in females) clearly fulfilled the criteria for a MTD based
on distinctly reduced body weights or body weight changes and
histopathological alterations in the liver. The test substance induced
changes in clinico-chemical parameters that are associated with liver
toxicity. Histopathological effects were found in the liver, therefore
this organ was identified as the target. In the carcinogenicity study,
females at the top dose showed a slight trend towards an increased
incidence of hepatocellular adenomas and carcinomas, which was virtually
within the historical control range. In top dose males of the chronic
toxicity study, a trend towards a slightly elevated increase of
carcinomas was detected.  Additional mechanistic investigations (Foci
initiation study in rats) demonstrated that tepraloxydim does not
possess an initiating potential for a liver carcinogenic process.  
Rather, Tepraloxydim can reversibly enhance cell proliferation at high
dose levels as indicated by an S-phase response study in rat.  This
mechanism that results in an increased incidence of liver tumors is
relevant only at dose levels at the MTD.  Combined with the absence of
gene or chromosome damaging effect, it can be concluded that the
increased incidence of rat liver neoplasia was not related to a
genotoxic mode of action and Tepraloxydim does not have an oncogenic
potential of biological relevance.

The result of the carcinogenicity study in mice with dose levels of 0,
200, 1800 and 5000 ppm demonstrates that the high dose level of 5,000
ppm exceeded the criteria of an MTD as evidenced by drastically reduced
body weights or body weight changes. A trend towards an increased
incidence of liver neoplasia occurred only in females at the high dose
level and therefore cannot be extrapolated to dose levels below the MTD.
Relative liver weights were distinctly increased at the highest dose
level, associated with foci of cellular alteration and hypertrophy of
hepatocytes. In female animals of the high dose levels, hyalinization of
the uterus was found as well as a reduced ovarian activity, which may be
a consequence of the reduced terminal body weights.

The overall lowest NOAELs obtained in long-term oral administration
studies were 5 mg/kg bw for male rats, 37 mg/kg bw for male mice, and
11.5 mg/kg bw for male dogs.  These chronic NOAELs demonstrate that the
rat is the most sensitive species.  Tepraloxydim has been reviewed by
the Agency for carcinogenicity classification. In accordance with the
EPA Draft Guidelines for Carcinogenic Risk Assessment (July, 1999), the
Agency has classified tepraloxydim as data are inadequate for an
assessment of human carcinogenic potential because some evidence is
suggestive of carcinogenic effects, but other equally pertinent evidence
does not confirm a concern. The Agency concluded that quantification of
human cancer risk is not required because although there was some
evidence of carcinogenicity in female rats based on an increased
incidence of liver tumors at the high dose, this finding was not
supported by the results 

of the chronic study. The Agency also concluded that female mice
developed liver tumors at an excessively toxic dose, and although male
mice had non-neoplastic liver changes similar to or exceeding those seen
in female mice at the same dose, there was no increase in liver tumor
incidence in males. Further more tepraloxydim was not mutagenic in a
battery of assays. Therefore a cancer risk assessment was not
performed.>

<	6. Animal metabolism. Tepraloxydim is extensively metabolized and
rapidly eliminated, with no evidence of accumulation in tissues. 
Pharmacokinetic studies demonstrate that tepraloxydim is readily
absorbed orally in rats, but is rapidly excreted mainly via the urine
(65 - 80%) and to a minor degree via the feces (15 - 25%). 
Approximately 35 - 55% of the dose was excreted via the bile, which when
compared to the excretion via the feces suggests an enterohepatic
recirculation.  Based on the amount of radioactivity excreted via the
bile and urine, the bioavailability of tepraloxydim is virtually 100%.

The biotransformation of tepraloxydim in rats resulted in a large number
of metabolites in urine, feces and bile. The main metabolic pathways
were the oxidation at the pyran ring to the lactone via the
hydroxy-metabolite, and the cleavage of the oxime ether group with the
imine and oxazol as products. Plasma, liver and kidney almost
exclusively contained parent.>

<	7. Metabolite toxicology. Tepraloxydim, hydroxylated in the 5-position
of the cyclohexenone ring (5-OH-DP), was tested in toxicological studies
(acute oral rat, 90-day feeding rat, Ames Test, in vitro UDS, ex vivo
USD, Micronucleus Test, prenatal toxicity rat).  This metabolite has
been shown to be the main metabolite of the active ingredient in oilseed
rape and soybeans, but not in mammals.  The results of these studies
showed that this metabolite is not more toxic than the parent compound
and does not have mutagenic or teratogenic properties.>

<	8. Endocrine disruption.  No specific tests have been conducted with
tepraloxydim 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 other relevant toxicity studies (i.e., subchronic and
chronic toxicity, teratology and multi-generation reproductive studies)
that would suggest that tepraloxydim produces endocrine related
effects.>

<C. Aggregate Exposure>

<	1. Dietary exposure. Exposure assessments were conducted to evaluate
the potential risk due to acute and chronic dietary exposure of the U.S.
population to residues of tepraloxydim.  

This herbicide and its metabolites convertible to GP
(3-(tetrahydropyran-4-yl)pentane-1,5-dioic acid) and OH-GP
(3-hydroxy-3-(tetrahydropyran-4-yl)pentane-1,5,-dioic acid) in or on raw
agricultural commodities, animal fat, liver, kidney, meat, and meat
byproducts, milk, and eggs were expressed as the parent compound.  The
tolerance values previously established for cotton, soybeans, canola,
and animal products are listed in the U.S. EPA final rule published in
the Federal Register August 2, 2001 (Vol 66, No. 149, p 40141 –
40150).  Additional tolerances established for the imported commodities
flax, seed; lentil, seed; and pea, dry, seed, are listed in the U.S. EPA
final rule published in the Federal Register September 26, 2007 (Vol 72,
No. 186, p 54584 – 54588) and in U.S. 40 CFR § 180.573.  The analysis
presented below included all current and proposed import tolerance
values for pea and bean, dried shelled, except soybean, subgroup 6C, at
0.1 parts per million (ppm), and Sunflower Subgroup 20B, at 0.25 ppm.>

<	i. Food. >

Acute Dietary Exposure Assessment

The acute dietary exposure estimates were highly conservative using
proposed and established tolerance values, default processing factors,
and 100% crop treated values for all commodities.  The tolerance values
included current and proposed import tolerances for pea and bean, dried
shelled, except soybean, subgroup 6C, at 0.1 parts per million (ppm),
and Sunflower Subgroup 20B, at 0.25 ppm.  The consumption data was from
the USDA Continuing Survey of Food Intake by Individuals (CSFII 1994 -
1996, 1998) and the EPA Food Commodity Ingredient Database (FCID) using
Exponent's Dietary Exposure Evaluation Module (DEEM-FCID) software.  

The EPA has determined that different acute population adjusted doses
(aPAD) should be used for assessing the acute dietary risk of
tepraloxydim.  The justification for this has been described in the
final rule published in the Federal Register September 26, 2007 (Vol 72,
No. 186, p 54584 – 54588), and in the Human Health Risk Assessment
available in docket ID EPA-HQ-OPP-2007-0145.   In brief, the 10X FQPA
Safety Factor was applied to the endpoint used in assessing the acute
dietary risk to the general US population (including infants and
children), but it was reduced to 1X when applied to the endpoint for
assessing the acute dietary risk to females (13-49 years of age).   The
aPAD used for the general population is 0.5 mg/kg bw/day, and for
females (13-49 years of age) the aPAD is 0.4 mg/kg bw/day.   

The results of the acute dietary assessment are presented in Table 1. 
The results of the analysis show that for the relevant sub-populations,
the exposures are below the Agency's level of concern (< 100% aPAD). 
Considering the exposure assumptions discussed above, the acute dietary
exposure to 95th percentile residues in food is 5.5 % aPAD for the
population group (infants <1 year old) receiving the greatest exposure. 
Additional refinements in the dietary risk assessment (i.e. utilizing
anticipated residue values, processing factors, percent crop treated
values and percent imported commodities for all crops) would further
reduce the estimated exposure values.  

Table 1.	Summary of Tepraloxydim Acute Dietary Exposure Analysis
Considering all Current and Proposed Tolerances, Default Processing
Factors, and 100% Crop Treated Using DEEM-FCID at the 95th Percentile 

Population	Exposure Estimate	%aPAD

Subgroup	(mg/kg b.w./day)	 

	95th Percentile

	U.S. Population	0.010813	2.16

All Infants (< 1 year old)	0.027537	5.51

Children (1-2 years old)	0.021466	4.29

Children (3-5 years old)	0.018472	3.69

Children (6-12 years old)	0.013214	2.64

Youth (13-19 years old)	0.008824	1.76

Adults (20-49 years old)	0.006999	1.40

Adults (50+ years old)	0.005446	1.09

Females (13-49 years old)*	0.006582	1.65

aPAD = acute population adjusted dose 

* The endpoint applied for females age 13 to 49 is different from the
other population subgroups.

Chronic Dietary Exposure Assessment

The chronic dietary exposure estimates were highly conservative using
proposed and established tolerance values, default processing factors,
and 100% crop treated values.  The consumption data was from the USDA
Continuing Survey of Food Intake by Individuals (CSFII 1994 - 1996,
1998) and the EPA Food Commodity Ingredient Database (FCID) using
Exponent's Dietary Exposure Evaluation Module (DEEM-FCID) software.  The
tolerance values included current and proposed import tolerances for pea
and bean, dried shelled, except soybean, subgroup 6C, at 0.1 parts per
million (ppm), and Sunflower Subgroup 20B, at 0.25 ppm.

The chronic population adjusted dose (cPAD) used for U.S. population and
all sub-populations is 0.05 mg/kg bw/day. Considering the exposure
assumptions discussed above, tepraloxydim chronic dietary exposure from
food for the U.S. population was 8.0%of the cPAD.  The most highly
exposed population sub-group was children 1-2 years of age at 22.3%
cPAD.   The results of the chronic dietary assessment are presented in
Table 2.

The results of the analysis show that for all sub-populations, the
exposures are below a level of concern (< 100% cPAD).  Additional
refinements in the chronic dietary risk assessment (i.e. utilizing
anticipated residue values, processing factors, percent crop treated
values) would further reduce the estimated exposure values.

Table 2. 	Summary of Tepraloxydim Chronic Dietary Exposure Analysis
Considering all Current and Proposed Tolerances, Default Processing
Factors, and 100% Crop Treated Using using DEEM-FCID

Population	Exposure Estimate	%cPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population (total)	0.004017	8.0%

All infants (< 1 year)	0.009576                	19.2%

Children 1-2 yrs	0.011169                	22.3%

Children 3-5 yrs	0.009572                	19.1%

Children 6-12 yrs	0.006414                	12.8%

Youth 13-19 yrs	0.003881                 	7.8%

Adults 20-49 yrs	0.003102                 	6.2%

Adults 50+ yrs	0.002485                 	5.0%

Females 13-49 yrs	0.002921                 	5.8%

cPAD = chronic population adjusted dose 

<	ii. Drinking water. The estimated maximum tepraloxydim surface water
and groundwater values were taken from the Federal Register, September
26, 2007 (Vol 72, No. 186, p 54584 – 54588).  Surface water acute and
chronic values were listed as 1.4 and 0.7 ppb, respectively.  The
groundwater value was 0.002 ppb (acute and chronic).

Drinking water contributions were assessed based on the maximum
estimated tepraloxydim water concentrations (acute – 1.4 ug/L, chronic
0.7 ug/L), and water consumption and body weights reported in CSFII,
using DEEM-FCID software.  The acute and chronic estimated water
exposure values are summarized in Tables 3 and 4, respectively.  Minimal
exposure of tepraloxydim occurs through drinking water with < 1.0% the
aPAD and < 1.0 % cPAD for the U.S. population and all subpopulations.

Table 3. 	Results for Tepraloxydim Acute Water Exposure Analysis
Considering the Maximum Estimated Acute Drinking Water Concentration
using DEEM-FCID 

Population	Water Exposure Estimate	%aPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population (total)	0.000074	0.01

All infants (< 1 year)	0.000292	0.06

Children 1-2 yrs	0.000117	0.02

Children 3-5 yrs	0.000106	0.02

Children 6-12 yrs	0.000074	0.01

Youth 13-19 yrs	0.000061	0.01

Adults 20-49 yrs	0.000068	0.01

Adults 50+ yrs	0.000061	0.01

Females 13-49 yrs	0.000069	0.02

aPAD = acute  population adjusted dose

Based on estimated acute surface water value of 1.4 ug/L from the
Federal Register September 26, 2007 (Vol 72, No. 186, p 54584 –
54588)>

Table 4. 	Results for Tepraloxydim Chronic Water Exposure Analysis
Considering the Maximum Estimated Chronic Drinking Water Concentration
using DEEM-FCID 

Population	Water Exposure Estimate	%cPAD

Subgroups	(mg/kg b.w./day)	 

U.S. Population (total)	0.000015	0.0%

All infants (< 1 year)	0.000048	0.1%

Children 1-2 yrs	0.000022	0.0%

Children 3-5 yrs	0.000021	0.0%

Children 6-12 yrs	0.000014	0.0%

Youth 13-19 yrs	0.000011	0.0%

Adults 20-49 yrs	0.000014	0.0%

Adults 50+ yrs	0.000014	0.0%

Females 13-49 yrs	0.000014	0.0%

cPAD = chronic  population adjusted dose

Based on estimated chronic surface water value of 0.7 ug/L from the
Federal Register September 26, 2007 (Vol 72, No. 186, p 54584 – 54588)

Acute Aggregate Exposure and Risk (Food and Water)

The aggregate acute risk includes residues of tepraloxydim from food and
water (Table 5). Exposures from residential uses are not included in the
acute aggregate assessment.  The results demonstrate that there are no
safety concerns for any subpopulation based on established and proposed
new uses, and that the results clearly meet the FQPA standard of
reasonable certainty of no harm.

Table 5. 	Estimated Acute Aggregate Exposure and Risk of Tepraloxydim  

Population Subgroup	aPAD (mg/kg/day)	Food Exposure (mg/kg/day)	Water
Exposure (mg/kg/day)	Total Exposure (mg/kg/day)	% aPAD

U.S. Population (total)	0.5	0.010813	0.000074	0.010887	2.18

All infants (< 1 year)	0.5	0.027537	0.000292	0.027829	5.57

Children 1-2 yrs	0.5	0.021466	0.000117	0.021583	4.32

Children 3-5 yrs	0.5	0.018472	0.000106	0.018578	3.72

Children 6-12 yrs	0.5	0.013214	0.000074	0.013288	2.66

Youth 13-19 yrs	0.5	0.008824	0.000061	0.008885	1.78

Adults 20-49 yrs	0.5	0.006999	0.000068	0.007067	1.41

Adults 50+ yrs	0.5	0.005446	0.000061	0.005507	1.10

Females 13-49 yrs	0.4	0.006582	0.000069	0.0066510	1.66



Chronic Aggregate Exposure and Risk (food and water)

The aggregate chronic risk includes residues of tepraloxydim from food
and water (Table 6). Exposures from residential uses are not included in
the chronic aggregate assessment.  The results demonstrate there are no
safety concerns for any subpopulation based on established and proposed
new uses, and that the results clearly meet the FQPA standard of
reasonable certainty of no harm. 

Table 6. 	Estimated Chronic Aggregate Exposure and Risk of Tepraloxydim

Population Subgroup	cPAD (mg/kg/day)	Food Exposure (mg/kg/day)	Water
Exposure (mg/kg/day)	Total Exposure (mg/kg/day)	% cPAD

U.S. Population (total)	0.05	0.004017	0.000015	0.0040320	8.06

All infants (< 1 year)	0.05	0.009576                	0.000048	0.0096240
19.25

Children 1-2 yrs	0.05	0.011169                	0.000022	0.0111910	22.38

Children 3-5 yrs	0.05	0.009572                	0.000021	0.0095930	19.19

Children 6-12 yrs	0.05	0.006414                	0.000014	0.0064280	12.86

Youth 13-19 yrs	0.05	0.003881                 	0.000011	0.0038920	7.78

Adults 20-49 yrs	0.05	0.003102                 	0.000014	0.0031160	6.23

Adults 50+ yrs	0.05	0.002485                 	0.000014	0.0024990	5.00

U.S. Population (total)	0.05	0.002921                 	0.000014
0.0029350	5.87



<	2. Non-dietary exposure. Tepraloxydim is not registered for
residential use, therefore, residential and occupational exposure risk
assessments for the incidental oral, dermal, and inhalation exposure
routes are not required.>

<D. Cumulative Effects>

<

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 EPA is currently developing methodology to perform cumulative risk
assessments.  At this time, there is no available data to determine
whether tepraloxydim has a common mechanism of toxicity with other
substances or how to include this pesticide in a cumulative risk
assessment.>

<E. Safety Determination>

<	1. U.S. population. Based on the risk assessments, BASF concludes that
there is a reasonable certainty that no harm will result to the general
population from the aggregate exposure to tepraloxydim residues.>

<	2. Infants and children. Based on the risk assessments, BASF concludes
that there is a reasonable certainty that no harm will result to infants
or children from the aggregate exposure to tepraloxydim residues.>

<F. International Tolerances>

<No Codex or Mexican maximum residue levels (MRLs) have been proposed or
are established for residues of tepraloxydim.  Therefore, no tolerance
discrepancies exist between countries for this chemical.  >

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