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EPA REGISTRATION DIVISION COMPANY NOTICE OF FILING FOR 

PESTICIDE PETITIONS PUBLISHED IN THE FEDERAL REGISTER 

EPA Registration Division contact: PV Shah, (703) 308-1846

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.

Stepan Company

[IN-10805]

EPA has received a pesticide petition (IN-10805) from Stepan Company, 22 West 

Frontage Road, Northfield, Illinois 60093 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.

to establish an exemption from the requirement of a tolerance for

N,N-dimethyltetradecanamide (CAS Reg. No. 3015-65-4) when used as an inert 

solvent applied to growing crops or harvested crops under 40 CFR 180.910 in pesticide 

formulations. 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 NA remove

1. Plant metabolism.

2. Analytical method. NA remove

3. Magnitude of residues. NA remove

B. Toxicological Profile Toxicity data were evaluated for the petitioned substance when 

they were available. When data were not available, toxicity of a commercial mixture of 

surrogate compounds with structural and metabolic similarity to N,Ndimethyltetradecanamide was assessed. The mixture contains 50–65% N,N-
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dimethyloctanamide, 37–50% of N,N-dimethyldecanamide, 0–5% N,Ndimethylhexanamide, and 0–2% N,N-dimethyldodecanamide.

1. Acute toxicity. The acute oral LD50 of the mixture of N,N-dimethyloctanamide, 

N,N-dimethyldecanamide, N,N-dimethylhexanamide, and N,N-dimethyldodecanamide 

was determined to be 1770 mg/kg body weight. It was classified as EPA Toxicity 

Category III for acute oral toxicity. The dermal LD50 of the dimethylalkylamide mixture 

was determined for male rats to be approximately 2,000 mg/kg and for females, between 

400 and 2,000 mg/kg. It was classified as EPA Toxicity Category II for acute dermal 

toxicity. The acute inhalation LC50 was determined to be >3.55 mg/L in rats exposed in 

nose/head only chambers. Clinical signs of toxicity were reported for the groups exposed 

to 0.586 mg/L and higher. The surrogate dimethylalkylamide mixture is classified as EPA 

Toxicity Category IV for acute inhalation toxicity. The dimethylalkylamide mixture is 

classified as EPA Toxicity Category I for dermal irritation and ocular irritation and was 

not sensitizing in guinea pigs according to the Buehler method.

2. Genotoxicty. The mixture of N,N-dimethyloctanamide, N,Ndimethyldecanamide, N,N-dimethylhexanamide, and N,N-dimethyldodecanamide 

produced negative results in a HGPRT assay in Chinese hamster lung cells, in an in vitro 

chromosome aberration assay in Chinese hamster ovary cells, and in an Ames assay in 

Salmonella typhimurium tester strains TA1537, TA98, TA100, and TA1535 in the 

presence and absence of metabolic activation. There is no evidence for genotoxicity of 

the surrogate mixture or the petitioned substance, N,N-dimethyltetradecanamide.

3. Reproductive and developmental toxicity. Two developmental toxicity studies 

were carried out on the mixture of N,N-dimethyloctanamide, N,N-dimethyldecanamide, 

N,N-dimethylhexanamide, and N,N-dimethyldodecanamide: one in the rat and one in the 

rabbit. Pregnant female rats received gavage doses of 0, 50, 150, or 450 mg/kg bw/day on 

gestation days 6-15. On gestation day 21, dams were sacrificed and fetuses were 

removed by Caesarean section and examined. Dams in the high dose group exhibited 

clinical signs of toxicity, a significant decrease in food consumption, and significantly

lower body weight gain on days 18 and 19 of gestation. The corrected weight gain in 

controls throughout gestation was 7.8%, and in the high dose group the corrected weight 

gain was 4.9%. There was also a significant decrease in fetal body weight in the 450 

mg/kg group and an increased incidence of fetuses with common skeletal abnormalities 

and delayed developmental growth. There were no developmental abnormalities 

observed in the absence of maternal toxicity. The maternal NOAEL and LOAEL from 

this study were 150 and 450 mg/kg/day, respectively. The developmental NOAEL and 

LOAEL were the same as the maternal values. 

In an OECD TG 414 study, rabbits received doses of the dimethylalkylamide mixture on 

post-coitum days 6-18. Sacrifice took place on day 28 post-coitum. The food

consumption of high dose animals was reduced during the dosing period (post coitum 

days 6-19); this difference was statistically significant during post-coitum days 11-15. 

There was no significant difference from controls on any reproductive or fetal endpoint 

for treated fetuses. Study authors concluded that the NOAEL for maternal systemic 
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effects was 300 mg/kg bw based on the decrease in food consumption during dosing. The 

NOAEL for reproductive and embryotoxicity/teratogenicity was the highest dose of 1000 

mg/kg bw.

4. Subchronic toxicity. In a 90-day oral study (OECD TG 406), the surrogate 

substance (the mixture of N,N-dimethyloctanamide, N,N-dimethyldecanamide, N,Ndimethylhexanamide, and N,N-dimethyldodecanamide) was administered in the diet of 

Wistar rats at 0, 400, 2000, or 10,000 ppm for 13 weeks, and at 0 or 10,000 ppm for 13 

weeks followed by a 28-day recovery period. Body weight gain was impaired in females 

and males at the highest dose, but this did not last into the recovery period. Increases in 

liver weights of high dose females were not accompanied by changes in clinical 

chemistry, gross pathological or histopathology that indicated effects on the function of 

the liver. The relative spleen weights among females were significantly higher even after 

the recovery period. There were no accompanying changes in spleen morphology. High 

dose males showed an increased incidence of basophilic regenerative tubules in the renal 

cortex as well as a slight increase in the amount of protein excreted in the urine. These 

effects were not significant after the recovery period. The NOAEL in this study was 

2000 ppm in males based on reversible kidney effects, and 10,000 ppm in females, 

equivalent to approximately 136.8 mg/kg bw/day in males and 894.6 mg/kg bw/day in 

females.

5. Chronic toxicity. The data available suggest that N,N-dimethyltetradecanamide

is not carcinogenic. These include a lack of positive results in all genotoxicity testing in 

the surrogate chemical mixture of N,N-dimethyloctanamide, N,N-dimethyldecanamide, 

N,N-dimethylhexanamide, and N,N-dimethyldodecanamide.

6. Animal metabolism. N,N-dimethyltetradecanamide is expected to be 

metabolized via carboxyamide hydrolysis by amidase enzymes, producing tetradecanoic

acid, a fatty acid. Fatty acids are metabolized by beta oxidation in the mitochondria to 

produce acetyl-CoA, which can enter the citric acid cycle and produce energy.

7. Metabolite toxicology. N/A Remove

8. Endocrine disruption. Toxicity related to endocrine disruption was not 

observed in the currently available N,N-dimethyltetradecanamide database, or that of the

surrogate chemical mixture of N,N-dimethyloctanamide, N,N-dimethyldecanamide, N,Ndimethylhexanamide, and N,N-dimethyldodecanamide. As the science develops and 

resources allow, screening of additional compounds may be added to the Endocrine 

Disruptor Screening Program (EDSP), at which point N,N-dimethyltetradecanamide may

be subjected to additional screening and/or testing to better characterize effects related to 

endocrine disruption.

C. Aggregate Exposure
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1. Dietary exposure. The estimated dietary exposure to N,Ndimethyltetradecanamide was determined using methods to estimate chronic dietary

exposure for a generic inert ingredient. This assessment considers drinking water and 

crop-specific residues from pre-harvest applications of agricultural insecticides, 

herbicides and fungicides, assuming the highest established tolerance level residue for 

each commodity. The assessment assumes that the inert ingredient is used on all crops, 

and that 100% of all crops are treated with the inert. The inert ingredient is assumed to 

be present in all commodities treated with 57 of the most significant active ingredients at 

the maximum tolerance level as identified by the U.S. EPA for the default assessment. 

Chronic dietary exposure estimates were derived for the general US population and subgroups of the population using the Dietary Exposure Evaluation Model, DEEMTM. The 

estimated chronic exposure for the total US population is 0.189 mg/kg/day, 12.6% of the 

chronic Population Adjusted Dose (cPAD). Children age 1 to 2 years old have the 

highest estimated exposure at 0.706 mg/kg/day, or 47.1% of the cPAD.

i. Food. Dietary exposures of concern are not anticipated for N,Ndimethyltetradecanamide due to its ready biodegradation in the environment and low 

general toxicity.

ii. Drinking water. N,N-dimethyltetradecanamide exposure via drinking water 

from use as an inert ingredient is not expected to be significant. Based on the physical 

chemical characteristics, the compound is expected to partition primarily to the soil, and 

the comparatively small amounts that enter the water will readily biodegrade. Exposure 

via the drinking water was estimated in the DEEM dietary exposure assessment assuming 

a concentration of 100 ppb

2. Non-dietary exposure. Residential exposures of concern are not anticipated for 

N,N-dimethyltetradecanamide due to its ready biodegradation in the environment and 

low general toxicity.

D. Cumulative Effects Section 408(b)(2)(D) (9v) of the FFDCA 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.” EPA has not 

made a common mechanism of toxicity finding as to N,N-dimethyltetradecanamide and 

other compounds. N,N-dimethyltetradecanamide does not appear to produce toxic 

metabolites in common with other substances. 

E. Safety Determination

1. U.S. population. There is a reasonable certainty that no harm to humans will 

result from the use of N,N-dimethyltetradecanamide as an inert ingredient in pesticide 

products. A NOAEL of 150 mg/kg/day in a developmental toxicity study of rats exposed 
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to the mixture of surrogate dimethylalkylamides was used to derive the chronic 

population adjusted dose (cPAD). Intraspecies and interspecies uncertainty factors were 

combined for a total uncertainty factor of 100. The resulting cPAD is 1.5 mg/kg/day. 

For the total US population, the estimated chronic dietary exposure from food and 

drinking water for N,N-dimethyltetradecanamide, calculated as 50% of all agricultural 

formulations, is 12.6 % of cPAD, well below any level of potential concern. 

2. Infants and children. There is a reasonable certainty that no harm to infants and 

children will result from the use of N,N-dimethyltetradecanamide as an inert ingredient in 

pesticide products. Mammalian teratology tests in rats and rabbits demonstrate that the 

chemical mixture of N,N-dimethyloctanamide, N,N-dimethyldecanamide, N,Ndimethylhexanamide, and N,N-dimethyldodecanamide does not cause adverse effects on 

fetal development in the absence of maternal toxicity. Thus at this time there is no 

concern for potential sensitivity to infants and children, and therefore the default 10X 

FQPA safety factor may be reduced to 1X. 

F. International Tolerances

N/A Remove