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-(tetrahydro-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 OHGP (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 
2

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 
3

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 
4

a MTD based on distinctly reduced body weights or body weight changes and 

histopathological alterations in the liver. The test substance induced changes in clinicochemical 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 
5

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)pentane1,5-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.
6

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. 
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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 subpopulations 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.
8

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
9

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
10

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 
11

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.