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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.

TEMPLATE:

[Clariant Corporation, 4000 Monroe Road, Charlotte, NC 28205]

EPA has received a pesticide petition (IN 10630] from Clariant Corporation (EPA 

Company Number 8340, 4000 Monroe Road Charlotte, NC 28205] requesting, 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 

[the use of Secondary Alkane (C13-C17) Sulfonates (C13-C17 SAS) as pesticide inert 

ingredients (as surfactants) for use in food crops in accordance with 40 CFR §180.920 (preharvest) for seed treatment and foliar applications pursuant to Section 408(d)(1) of the 

Federal Food, Drug, and Cosmetic Act (FFDCA). There are currently no approved nonfood uses or food use tolerance exemptions for C13-C17 SAS as a pesticide inert ingredient.] 

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.

[The SAS surfactant compounds are mixtures of sulfonated C13-C17 linear alkanes in 

which the sulfonate sodium salt is distributed and mainly located on the secondary carbon 

atoms in the linear alkyl chain. The following CAS RNs are supported by way of this 

petition]. 

Secondary Alkane (C13-C17) Sulfonates

CAS Registry Number (CAS RN) Name

85711-69-9 Sulfonic Acids, C13-C17 sec-alkane

97489-15-1 Sulfonic Acids, C14-C17 sec-alkane,
2

A. Residue Chemistry

1. Plant metabolism. [Not applicable/Not required for the establishment of a 

tolerance exemption for inert ingredients.]

2. Analytical method. [Not applicable/Not required for the establishment of a 

tolerance exemption for inert ingredients.]

3. Magnitude of residues. [Not applicable/Not required for the establishment of a 

tolerance exemption for inert ingredients.]

B. Toxicological Profile

The C13-C17 SAS surfactants have been generally tested as aqueous solutions (60%-30%), 

because this represents how the commercial products are generally available for 

formulation and manufacturing purposes both in the EU and US. Overall, the testing 

results may reflect the different commercial grades of C13-C17 SAS in a dose dependent 

manner that is consistent with the test concentration of C13-C17 of the SAS surfactant. The 

specific concentration of C13-C17 SAS in the test material was identified whenever 

possible. On the basis of the chemical identity analysis that toxicology data reported for 

CAS RN 85711-69-9 Sulfonic Acids, C13-C17 sec-alkane can be bridged to CAS RN

97489-15-1 Sulfonic Acids, C14-C17 sec-alkane.

1. Acute toxicity. [The C13-C17 SAS surfactants demonstrate the following acute 

toxicity data: OECD 401 (rat acute oral) data that range LD50 = 2,000 to 500 mg/kg/day 

(EPA IV - III); OECD 402 (acute dermal) not acutely toxic in mice; OECD 404 (skin 

irritant irritation), non-irritating; OECD 405 (rabbit acute eye irritation) eye irritant; and 

OECD 406 (guinea pig Buehler Assay) non-sensitizing.]

2. Genotoxicty. [The C13-C17 SAS surfactants do not display mutagenic activity in 

the following assays: AMES bacterial (OECD 471) assay with and without metabolic 

activation; In Vitro Evaluation: Mammalian Cell Gene Mutation (Similar OECD 476)

was negative with and without metabolic activation. Mouse Micronucleus Chromosome 

Aberration study (similar to OECD 474) was negative for genotoxic effects in male and 

female rats.]

3. Reproductive and developmental toxicity. [C13-C17 SAS surfactants (as a 60% 

aqueous solution) was assessed over two generations in CD rats (25/sex/dose). The test 

compound was administered in the diet in both the F0 and F1 generations at dose levels
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of 0 (vehicle control), 1000, 3000, or 10000 ppm. Treatment was given continuously to 

both sexes for 60 days prior to mating and throughout three successive pregnancies (F1A, 

F1B, F1C, F2A, F2B and F2C). Food intake, hematological parameters, absolute and 

relative organ weights as well as histopathological evaluation of tissues showed no 

adverse treatment-related effects. In the F0 generation, a slight but not statistical 

significant depression of body weight gain was observed. During the three subsequent 

pregnancies, some fluctuation in body weight gain was recorded in treated females, but

no significant inter-group variation was observed. In both generations, estrous cycles, 

mating performance and conception rates were unaffected by treatment.

Macroscopic examination, absolute and relative organ weights, and histopathological 

evaluation of F0 and F1 parent animals showed no adverse treatment-related effects. It 

was concluded from these investigations that continuous treatment with sec-alkane

The NOAEL for maternal toxicity, as well as for fertility, was 10,000 ppm in the diet 

corresponding to about 500 mg/kg bw/day. Sulfonate-sodium salts SAS (as a 60% 

aqueous solution) at a concentration level of 10,000 ppm was indicative of only slight, 

unspecific maternal toxicity.

Developmental Toxicity

The 2-generation rat reproduction study also included a Segment II phase for 

developmental toxicity. C13- C17 SAS surfactant (as a 60% aqueous solution) was tested

for reproductive function and intra-uterine development in CD rats (25/sex/dose) by 

treatment to females only during the organogenesis stage (days 6-15 of gestation). The 

female test animals received the test material at dose levels of 0 (vehicle control), 1000,

3000 or 10,000 ppm in the diet. No treatment-related adverse effects were observed in 

any of the groups treated during organogenesis. There were no indications for an 

embryotoxic or teratogenic effect related to treatment in any dose groups. There was no 

treatment related effects and no indication of fetotoxicity were observed in any of the 

dose groups throughout the study. Teratogenic effects were also not observed. The 

NOAEL with regard to developmental effects was considered to be 10,000 ppm in the 

diet corresponding to about 500 mg/kg bw/day.

DEREK Structure Activity Relationship (SAR) modeling was conducted to identify 

structural alerts for mammalian toxicology. There were no structural alerts for 

developmental (teratogenicity) or reproductive toxicity.]

4. Subchronic toxicity. [C13-C17 SAS surfactants (as a 60% aqueous solution) were 

tested for systemic subchronic toxicity using both, the oral (in rats) and dermal (in mice) 

routes of exposure. Both studies provide sufficient documentation to afford a credible 

evaluation of subchronic oral and dermal exposures. Subchronic inhalation testing is not 

available, but this is not a relevant route of exposure.
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Rat Subchronic Dietary Testing

In a feeding study, CD Sprague-Dawley rats (30/sex/dose) received C13-C17 SAS (tested as

60% aqueous solution) for a period of 52 weeks at concentrations of 0% (vehicle control),

0.08%, 0.40% and 2.0% via the diet. All rats were observed daily for clinical

signs and mortality. Food consumption was calculated weekly. Bodyweight was recorded 

weekly for the first 13 weeks, then monthly thereafter. Ophthalmoscoopic examination 

was performed prior to the start of the study, and at 26 and 52 weeks of treatment. 

Hematology (10 rats/sex/dose), clinical chemistry (5 rats/sex/dose) and urinalysis (5 

rats/sex/dose) were evaluated at 26 and 52 weeks. Organ weight histopathological 

examination was performed. At 2%, impaired grooming activity was reported in both 

males and females, when compared with the vehicle control group. Food intake was 

reduced (approximately 10%) in males at 2% over the first 19 weeks, when compared to

the vehicle control group. No effect was reported in females at 2% or any other dose level. 

Decreased body weight gain was reported in males and females at 2% when compared

with the vehicle control group. At the end of 52 weeks, males were 80% of the control 

group mean weight and female were 77% of the control group mean weight (statistical 

significance not reported). In males, absolute body weight at 52 weeks was decreased by

13% and females at 52 weeks body weight was decreased by 18% when compared with the 

vehicle control group body weight mean (statistical significance not reported). No other 

treatment-related effects were reported in the study.

Based on the study results, the no observable adverse effect level (NOAEL) in this study 

was conservatively placed at 0.40% (approximately 200 mg/kg bw/day) and the lowest 

observable adverse effect levels was 2.0% (20,000 ppm, approximately 1000 mg/kg 

bw/day) based on the decrease in body weight. At the highest level of 2% approximately

1000 mg/kg bw/day) in the diet only body weight changes were noted and the NOAEL

could be assigned as 4000 ppm, or approximately 200 mg/kg bw/day.

Mouse Dermal Subchronic Testing

A 60% aqueous formulation of C13-C17 SAS was administered to the intact skin of groups

of 25 female mice at concentrations of 0, 0.1, 0.5 (increasing to 8.0 and finally to 16.0)

and 1.0% w/v (increasing to 2.0 and finally 32.0) over periods of four or five weeks. A

constant dose of 0.1 mL / mouse was used on five days per week of treatment. 

Encrustation, skin thickening, erythema and slight sloughing were observed at the treated 

site in all mice administered 32 % w/v. Mice given 16% showed slight skin thickening 

after one week of treatment. Weight loss, without concomitant reduction of food intake, 

was seen in all mice receiving 32%. There was a return to normal growth during the 

second week at this dose level. Necropsy findings were confined to the application site 

and consisted of skin thickening, erythema, edema, sloughing and pus at 32%, and skin

thickening at 16%. Mice treated with solutions containing 8% w/v and below were 

unaffected by treatment.]
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5. Chronic toxicity. [C13-C17 SAS (as 60% aqueous solution) was tested for 

potential chronic and carcinogenic effects by the oral and dermal routes of exposure in 

rats and mice respectively. Although these studies do not adhere to current guidelines or 

GLP standards, these studies were performed according to scientific standards at the time 

of performance and of acceptable validity based on current standards. Reliability 

declarations regarding procedures and performance are available. Both studies provide 

sufficient documentation to afford a credible evaluation of carcinogenicity and systemic 

chronic toxicity through both the oral and dermal routes of exposure.

Rat Oral Carcinogenicity Testing

C13-C17 SAS as 60% aqueous solution) was tested for potential carcinogenicity in CD 

Sprague-Dawley rats (50/sex/dose) at concentrations of 0% (vehicle control), 0.08%,

0.4%, or 2.0% via the diet over a period of 2 years. Animals were observed for clinical 

signs of toxicity or mortality at least once a day; physical examinations were made at 

least weekly. Food intake wake calculated weekly. Bodyweight was recorded weekly 

for the first 13 weeks, every four weeks from weeks 14-85, and then every two weeks 

thereafter. Hematology parameters and urinalysis were measured at 26, 52 and 72 

weeks (10/sex/dose) and 104 weeks in all surviving animals. Gross pathology and 

histopathological examination was performed on all animals. The results of the study 

indicate that administration of the test compound up to 2% (w/w) in the diet resulted in 

both the non-neoplastic as well as neoplastic pathology within normal limits. Initially

a temporary impaired grooming in rats receiving the highest dietary concentration of

2.0% (w/w) was noted. No other finding was recorded in respect to appearance, 

general health condition, behavior and locomotor function. Survival was not affected. 

The cellular and chemical characteristics of blood and urine were also undisturbed by 

treatment. Macroscopic and histopathological investigations revealed no indications of 

nonneoplastic and/or neoplastic changes.

The NOAEL was set at 2% (w/w) in the diet corresponding to approximately 1000 

mg/kg bw/day. Based on these study results, there was no evidence that C13-C17 SAS 

demonstrated carcinogenic effects by the oral route of exposure.

Dermal Mouse Carcinogenicity Testing

CD-1 Mice (100/sex/dose) were treated dermally at concentrations of 0% (vehicle 

control), 0 % (untreated), 0.1%, 0.5% or 1% (w/w) C13-C17 SAS (as 60% aqueous

solution) three times each week over a scheduled period of 80 weeks that was followed 

by an observation period lasting 24 weeks. All animals were observed for clinical signs 

and mortality daily. Body weights were measured every 4 weeks, food and water 

consumption was not recorded. Gross pathology and histopathology was performed on 

all animals that died on study and those that survived until the end of the treatment 

period. Mortality was extremely high in this study with 982/1000 mice (496 males and

486 females) found dead or killed in extremis. During the first six weeks of the study, 

animals that died were replaced. The mortality was distributed among all the test groups 

and not considered to be treatment related.
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No signs of treatment related effects were recorded at any time during the total 104 week 

period. Histopathological examination of skin samples revealed that there were no 

treatment-related dermal abnormalities. Based on these study results, there was no 

evidence that C13-C17 SAS demonstrated carcinogenic effects by the dermal route of 

exposure at up to 1% (w/w).

Summary Repeat Dose Risk Analysis

A NOAEL of 200 mg/kg bw/day is proposed for oral repeat dose risk assessment for 

both for CAS RN 85711-69-9 Sulfonic Acids, C13-C17 sec-alkane that can be bridged to 

CAS RN 97489-15-1 Sulfonic Acids, C14-C17 sec-alkane.

.

Additionally body weight changes were reported at dietary levels of up to 2% (w/w)

corresponding to about 1000 mg/kg body weight per day after 90-days of exposure, the 

NOAEL is 0.4% (calculated as 200 mg/kg bw/day). The subacute dermal toxicity study 

in mice, performed with a 60% aqueous solution of C13-C17 SAS revealed no indications

of toxicity after dermal treatment at 8% (w/v) for 4 or 5 consecutive weeks. Based on the

results of this test, the NOAEL for local effects was calculated with approximately 500 mg

/ kg body per day. At higher test concentrations signs of irritation / inflammation at the 

treated skin sites were revealed. Adverse systemic toxicity effects were not observed.

Oral:

 NOAEL (chronic): 200 mg/kg bw/day (60% aqueous)

 NOAEL (subchronic): 0.4% (wt/wt) (200 mg/kg bw/day)

Dermal:

 NOAEL (subchronic): estimated to be 500 mg/kg bw/day

DEREK Modeling did not indicate structural alerts for carcinogenicity, genotoxicity, 

liver, thyroid and kidney toxicity, irritation, sensitization, or reproductive toxicity. The 

modeling report supports the findings of the subchronic and chronic toxicology database 

previously summarized.]

6. Animal metabolism. Pseudomonas sp. can metabolize primary n-alkanesulfonates to 

bisulfite and the corresponding aldehyde metabolite. By analogy it can thus be postulated 

that the C13-C17 SAS should be initially oxidized to generate bisulfite and the 

corresponding alkyl ketone metabolite. The alkyl ketone metabolite may then be further 

metabolized through oxidative degradation to presumably to alkyl acetate ester 

metabolites. Follow-on ester cleavage would yield acetate and alkyl alcohol metabolites 

which should be further metabolized by ß-oxidation fatty acid processes to ultimately 

generate carbon dioxide and water.

Toxicokinetic Studies

SAS Surfactants, rat toxicokinetic data substantiated the likelihood of a ß-oxidation 

pathway since excretion of radiolabeled CO2 was observed and that there is rapid 

excretion with the absence of bioaccumulation.
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 14C radiolabeled C13-C17 SAS administered by gavage to male rats at 

concentrations of 0.5, 5.3 or 51 mg/kg was excreted according to a biphasic 

elimination with a biological half-life of 11 hours to 65 hours. Up to 17% of the 

administered radioactivity was exhaled as CO2, approximately 30% was excreted 

via urine and about 45% with feces. In total more than 90% of the applied 

radioactivity was excreted within the first 24 hours after application. There was 

no indication of bioaccumulation as demonstrated by very low residual 

radioactivity (< 1 ppm) in organs after 7 days. Metabolites were not identified.

 Dermal application to male rats demonstrated low penetration potential of 14Cradiolabled C13-C17 SAS. Elimination half-life averaged about 41 hours (15% 

elimination in air 18% in urine and about 31% in feces. About 2.2% of the

radioactivity was found in the treated skin and 35% in the bandage used to cover 

the treated area all of which indicate a low potential for dermal absorption

(calculated 1%).]

7. Metabolite toxicology. [No Reported Data]

8. Endocrine disruption. [C13-C17 (SAS) surfactants do not belong to a class of 

chemicals known or suspected of having adverse effects on the estrogen receptor or 

endocrine system.]

C. Aggregate Exposure

1. Dietary exposure. [Clariant is proposing that the C13-C17 SAS surfactants be 

exempt from the requirement of a tolerance when used in seed treatment and foliar 

applications under 40 CFR §180.920. While no specific food use residue information is 

available for C13-C17 SAS surfactant on the basis of the physical chemical and 

environmental properties analysis crop residues are not likely. As a minor component in 

seed treatment formulations, the amount of C13-C17 SAS applied to seeds would be small 

and by the time seeds germinate, any residual C13-C17 SAS surfactant would be 

absorbed/bound to the soil (as indicated by Fugacity estimates and Koc) and should 

undergo rapid degradation. Thus, it is unlikely that the SAS surfactants could be available 

for uptake by plants.

Dietary Risk Assessment

EPA assesses potential dietary exposures to inert ingredients used in agricultural pesticide 

formulations using a screening-level model referred to as “I-DEEM,” in which the “I” 

stands for inerts and “DEEM” is the dietary exposure evaluation model that is used by EPA 

to assess dietary exposures to active ingredients in pesticide products. EPA’s Inert 

Ingredients Assessment Branch and residue chemists in the Health Effects Division of the 

Office of Pesticide Programs jointly developed I-DEEM. The model, as developed by 

EPA, uses crop-specific residue data (i.e., maximum tolerances) for 57 active ingredients as 

surrogates for potential inert ingredient residue levels. I-DEEM assumes that inert 

ingredients are used on all crops, and that 100 percent of all crops are assumed to be 

“treated” with the inert ingredient(s). I-DEEM also assumes that the inert is present at a
8

concentration of 50% in all the pesticide formulations. In addition, EPA includes potential 

residues of 100 ppb in water for potential drinking water exposures. Using these 

assumptions the chronic dietary exposure is estimated to be 0.189 mg/kg/d for the general 

U.S. population and 0.706 mg/kg/d for children 1-2 years of age (i.e., the most highly 

exposed subpopulation).

The dietary (food plus drinking water) exposures are expressed as a percentage of the 

proposed cPAD, The % cPAD for the general U.S. population and children 1-2 years old, 

the subpopulation with the highest potential exposures.

Reproductive/Developmental Toxicity, a no-observable-adverse-effect-level (NOAEL) for

C13-C17 SAS should be assigned as 200 mg/kg bw/day based on chronic testing.

The chronic reference dose (cRfD) proposed for CAS RN 97489-15-1 Sulfonic Acids, 

C14-C17 sec-alkane.is therefore 2.0 mg/kg/day.

 cRfD = 200 mg/kg bw/day /100

 cRfD/cPAD = 2 mg/kg bw/day

The data provided herein and use pattern of soil application support that the FQPA safety 

factor for C13-C17 SAS should be reduced from 10X to 1X. Therefore, only the 10X factors 

for intra- and inter- species variability should be included in calculating the chronic 

reference dose (cRfD) and the chronic population adjusted dose (cPAD).

Thus, based on I-DEEM screening level calculations, the chronic dietary exposures are 

estimated to be 9.5% of the cPAD for the general U.S. population and 35.3% of the cPAD 

for children 1-2 years old. These data demonstrate that the I-DEEM screening-level 

chronic dietary (food and drinking water) exposures are below the cPAD and are therefore 

below EPA’s established level of concern for all U.S. subpopulations.]

i. Food. [The chronic dietary exposures estimated using the conservative IDEEM screening level model (food and drinking water) are well below 100% of the 

cPAD, and are therefore below the level of concern for all U.S. subpopulations.]

ii. Drinking water. [Drinking water is included in the I-DEEM 

exposure assessment and based on anticipated concentrations expected to be 

negligible.]

2. Non-dietary exposure: None (no residential uses are proposed)

D. Cumulative Effects

[It has not been determined that the C13-C17 surfactants will have a 

common mechanism of toxicity with other substances.]
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E. Safety Determination

1. U.S. population. [Based on the conservative exposure estimates, there is a 

reasonable certainty that no harm will result to the U.S. population from the 

aggregate exposure to C13-C17 surfactants formulations in 40 CFR § 180.920 preharvest seed treatment and foliar applications with chronic dietary exposure 

estimated to be 9.5 mg/kg/day (0.095%. PAD) for the general US population.]

2. Infants and children. [The FFDCA Section 408 requires an additional 

tenfold margin of safety for the protection of infants and children in case of threshold 

effects to account for prenatal and postnatal toxicity, and an inadequate toxicity 

database. Where

an adequate and reliable database is available and there is a lack of evidence for 

increased susceptibility, the FQPA safety factor may be reduced or removed.

Based on available information discussed herein, Clariant, Inc. believes the FQPA 

safety factor should be reduced to 1X.The cRfD is therefore equivalent to the chronic 

population adjusted dose (cPAD).]

 An evaluation of susceptibility and uncertainty issues associated with the use of C13- 

C17 SAS surfactants in I-DEEM estimated chronic dietary exposures to children 1-2 

years of age (the potentially most exposed population) provided an estimated

chronic exposure of 35.3 % PAD.

 The availability of a scientifically sound mammalian toxicology database that 

includes acute, subchronic, and genotoxicity data. These test data, did not result 

in adverse developmental, reproductive and neurological endpoints or genotoxic 

effects.

 The DEREK modeling results did not indicate any structural alerts for 

carcinogenicity, genotoxicity, liver, thyroid and kidney toxicity, irritation, 

sensitization, or reproductive toxicity.

 Physicochemical/environmental properties data indicate that crop residues and 

resultant dietary exposures to sensitive populations are unlikely.

 C13-C17 SAS surfactants do not belong to a class of chemicals known or suspected 

of having adverse effects on the estrogen receptor or endocrine system.]

F. International Tolerances

[There are no known international tolerances for C13-C17 SAS Surfactants.]