Page 2 of 24

sulfonated, sodium salt (CAS No. 68443-05-0)) (also referred to as peroxy sulfonated oleic acids 

(PSOA)) (CAS No. 1315321-93-7, 1315321-94-8, 1315321-95-9) 

9-Octadecenoic acid (9Z)-, sulfonated, oxidized (CASRN 1315321-93-7) and the potassium and 

sodium salts; 

9-Octadecenoic acid (9Z)-, sulfonated, oxidized (CASRN 1315321-94-8) potassium salts; and 

9-Octadecenoic acid (9Z)-, sulfonated, oxidized (CASRN 1315321-94-9) sodium salts. 

The acute oral LD50 in the rat is 300 mg/kg bw/day. Due to the corrosive nature of PSOA, an in 

vitro skin corrosion study was conducted with PSOA rather than the in vivo rat dermal corrosion 

study. The results of the in vitro study show that PSOA is corrosive to the skin. 

A subchronic oral toxicity study was conducted (OECD Guideline 407) with PSOA. PSOA was 

administered for 28 days by oral gavage to Sprague Dawley rats. There were no treatment related 

changes in any of the parameters tested. The No Observable Adverse Effect Level (NOAEL) was 

50 mg/kg bw/day. In this study, the dosing was not considered adequate since it did not produce 

any systemic toxicity. 

In vitro genotoxicity studies have been conducted with PSOA. PSOA is negative for inducing 

mutations in bacterial and mammalian cells, with and without metabolic activation. In the in vitro

chromosome aberration study using human lymphocytes, PSOA was positive with and without 

metabolic activation. However, the in vivo micronucleus assay in rats was negative. 

A developmental toxicity study with PSOA (purity 100%) was conducted with pregnant SpragueDawley rats. Neither maternal nor developmental toxicity was observed at 50 mg/kg/day, the 

highest dose tested . In this study, the dosing was not considered adequate since it did not produce 

any systemic toxicity. 

There are no mammalian metabolism studies with PSOA. 

There are no known chronic toxicity studies with PSOA, however, the concerns for long term 

toxicity are limited due to corrosive nature of the chemical. 

A neurotoxicity study was not conducted with PSOA. However, detailed functional observations 

were made among the parameters measured in the 28-day subchronic oral feeding study. There 

were no PSOA related changes in any of the parameters measured, including functional 

observations. No evidence of neurotoxicity was observed. 

An immunotoxicity study was not conducted with PSOA. There was no indication of any systemic 

toxicity in the database. 

The Agency requested additional confirmatory data that the higher doses of PSOA cannot be used 

in toxicity studies due to highly irritating property of the test article. A 14-day toxicity study was 

conducted with 0, 100, 300 and 1,000 mg/kg/day of PSOA administered to rats via gavage. 

Clinical signs of toxicity due to the irritant property of PSOA were seen at all doses. At 100 

mg/kg/day, diarrhea, piloerection, chromodacryorrhea, wetness of the nose/mouth area, wetness of 
Page 3 of 24

the anogenital area, dyspnea, chromorhinorrhea, bloating of the abdomen, red staining of the 

nose/mouth area and apparent licking of the inside of the mouth was reported. The results of this 

14-day study confirms that higher doses would not have been tolerated in the 28 day toxicity study 

and the developmental toxicity study. Therefore, these studies are acceptable for risk assessment. 

For risk assessment purposes, the conservative toxicological endpoint of concern is 50 mg/kg 

bw/day which is based on the developmental study and the repeat dose subchronic toxicity study, 

no toxicological effects of statistical significance were observed up to 50 mg/kg bw/day, which 

was the highest dose tested in those studies. 

EPA has determined that the available data are adequate to assess the safety of infants and 

children. Therefore it is not necessary to apply an additional safety factor as described in the Food 

Quality Protection Act (FQPA). 

The request for use is limited to “use on food contact surfaces in public eating places, as well as 

dairy processing equipment and food processing equipment and utensils” at a maximum end-use 

concentration of 250 ppm. The primary use of PSOA will be in dairy processing facilities using 

Clean In Place (CIP) techniques which are essentially closed systems. As such, the general public 

is not expected to be exposed to PSOA as a result of “residential use”. However there is the 

possibility of dietary exposure as a result of post-application residue from treated surfaces (food 

contact surfaces in public eating places). The request is not to use PSOA on agricultural crops or 

otherwise in residential settings. 

The Agency used the U.S. Food and Drug Administration (FDA) Food Contact Surface Sanitizing 

Solution Dietary Exposure Assessment Model to estimate dietary exposure. The model was run at 

the maximum requested concentration level of 250 ppm. The model indicates the Agency’s level 

of concern is not exceeded for U.S. population. 

The Margins of Exposure for occupationally exposed persons are greater than 100 and therefore do 

not exceed the Agency’s levels of concern for workers handling small volumes of diluted solution. 

It is the Agency’s understanding that uses involving larger volumes of material are essentially 

“closed system” processes. The processes are known industrially as “clean in place” (CIP) 

systems. As such there is essentially no worker contact. Minibulk containers with the sanitizing 

solution are connected via plumbing piping/tubing to the processing systems that receive the 

sanitizing treatment. Valves are opened to introduce the sanitizer and valves are closed to end the 

treatment time. The Agency considers “closed systems” to result in negligible exposure thus a 

quantitative assessment of this aspect is not necessary. 

PSOA is highly toxic to freshwater fish. It is moderately toxic to invertebrates and plants. In view 

of the results of EPI SuiteTM modeling results and upon the proposed use pattern (as a wetting 

agent or coupler), the use of PSOA is not expected to result in adverse environmental effects. The 

proposed use of PSOA is for indoor use only and much of that in enclosed systems. The final use 

concentration is a maximum of 250 ppm (0.025 %). 

In view of the weight of the evidence toxicologically, in view of the proposed use pattern (CIP), in 

view of the low maximum use concentration requested (250ppm), the Agency approves of the 

requested use of Peroxy Sulfonated Oleic Acids as an inert ingredient at a maximum final 
Page 4 of 24

concentration not to exceed 250 ppm when applied in antimicrobial sanitizing agents to “use on 

food contact surfaces in public eating places, as well as dairy processing equipment and food 

processing equipment and utensils” as described under 40 CFR 180.940(a). 

II. BACKGROUND 

The firm Exponent (1150 Connecticut Ave., N.W. Suite 1100, Washington, D.C. 20036) on behalf 

of the firm Ecolab (370 N. Wabasha St., St. Paul, MN 55102) has submitted a request for an 

exemption from the requirement of a tolerance for Peroxy Sulfonated Oleic Acids (PSOA). 

Specifically, the request is for a food-use under 40 CFR 180.940(a) which is for “use on food 

contact surfaces in public eating places, as well as dairy processing equipment and food processing 

equipment and utensils.” The request is to use a maximum of 250 ppm PSOA in a final use 

dilution of an antimicrobial product. Typically uses are expected to be “clean in place” (CIP) 

applications which are not followed by a potable water rinse. 

Peroxy sulfonated oleic acids are defined as: 

9-octadecenoic acid (9Z) -, sulfonated, oxidized (CAS No. 1315321-93-7) (when formed using the 

pre-reaction material 9-octadecenoic acid (9Z) – sulfonated (CAS No. 68988-76-1)); 9-

octadecenoic acid (9Z) -, sulfonated, oxidized, potassium salts (CAS No. 1315321-94-8) (when 

formed using the pre-reaction material 9-octadecenoic acid (9Z-) sulfonated, potassium salt (CAS 

No. 68609-93-8)); and 9-octadecenoic acid (9Z) -, sulfonated, oxidized, sodium salts, (CAS No. 

1315321-95-9) (when formed using the pre-reaction material 9-octadecenoic acid (9Z) -, 

sulfonated, sodium salt (CAS No. 68443-05-0)) (also referred to as peroxy sulfonated oleic acids 

(PSOA)) (CAS No. 1315321-93-7, 1315321-94-8, 1315321-95-9) 

9-Octadecenoic acid (9Z)-, sulfonated, oxidized (CASRN 1315321-93-7) and the potassium and 

sodium salts; 

9-Octadecenoic acid (9Z)-, sulfonated, oxidized (CASRN 1315321-94-8) potassium salts; and 

9-Octadecenoic acid (9Z)-, sulfonated, oxidized (CASRN 1315321-94-9) sodium salts. 

III. INERT INGREDIENT PROFILE 

 A. The purpose of PSOAs is to serve as a surfactant/wetting agent and a coupler. The 

proposed use is for Clean In Place (CIP) sanitizing of food preparation surfaces, food processing 

equipment, dairy processing equipment and utensils. An antimicrobial sanitizer will be placed on 

the surface, or if appropriate, equipment submerged in, or the sanitizer flushed through the 

plumbing (i.e., piping) of processing equipment. No potable water rinse will follow. The 

maximum final end-use dilution is 250 ppm (0.025%). 

 B. Physical/Chemical Properties 

The primary chemical structure of 9-Octadecenoic acid (9Z) sulfonated is: 
Page 5 of 24

All three structures (9-Octadecenoic acid (9Z)-, sulfonated, oxidized (CASRN 1315321-93-7) and 

the potassium and sodium salts; 

9-Octadecenoic acid (9Z)-, sulfonated, oxidized (CASRN 1315321-94-8) potassium salts; and 

9-Octadecenoic acid (9Z)-, sulfonated, oxidized (CASRN 1315321-94-9) sodium salts) are 

essentially the same with slight variance in the oxygen bonding at the end of the 18 carbon chain. 

Table 1. Physical and Chemical Properties of 

Peroxy Sulfonated Oleic Acids 

Parameter Value Source 

Molecular Formula 

C18H36O7S (compound 1, 67%) 

C18H36O6S (compound 2, 10%) 

Ecolab Submission 

Pages 8-12/111 

Molecular Weight 396 compound 1 

380 compound 2 

Common Names 

Persulfonated oleic acid 

Peroxy sulfonated oleic acids 

Prehydrolyzed sulfonated oleic acid 

Physical State White Liquid at 20o C 

Boiling Point (°C) 100.2o C 

Density 1.0484 g/cm3 at 20o C 

Vapor Pressure 1013 hPa at 20o C 

Partition Coefficient 

(usually the Log P or Kow)

Determined Log POW 

≤ 5.04 

Log KOW 1.96 

IV. HAZARD ASSESSMENT 

O

O

O

M2

S O

O

O

M1

OH
Page 6 of 24

 TOXICOLOGY PROFILE 

Acute Toxicity 

Table 2. Summary of Acute Toxicity of PSOA* 

Species Study Results Reference 

Toxicity 

Category

Rat Acute Oral - rat LD50 > 

300 mg/kg 

bw/day 

Single dose toxicity study of 

PSOA by Oral Gavage in rats 

with a 14 day recovery period 

cited in Petition for Exemption from 

the Requirement of a Tolerance for 

PSOAs. Petition IN-10549; 15 FEB 

2013. 

II 

Rat Acute Dermal 

toxicity 

NA** NA I 

Rat Acute Inhalation - 

toxicity 

N/A** NA I 

In Vitro human 

skin 

Dermal Irritation Corrosive In Vitro Skin Corrosion: 

Human Skin Model Test with 

PSOA 

I 

Rabbit Primary Eye 

Irritation 

NA** NA I 

Guinea Pig Dermal 

Sensitization 

NA** NA NA 

* Table taken from ECOLAB submission p 18/111. 

** No study conducted based on corrosive nature of PSOA via the dermal route. 

According to the Applicant, due to the corrosive nature and characteristics of the compound(s) as 

an organic acid, PSOA is corrosive. “In the interest of animal welfare, an in vitro skin corrosion 

study was conducted with PSOA rather than the in vivo rat dermal corrosion study. The results of 

the in vitro study show that PSOA is corrosive to the skin. The Applicant cites 

(http://www.epa.gov/opp00001/science/acute-data-waiver-guidance.pdf) in the “classification of 

Toxicity Category I from the acute skin irritation study would waive the additional acute toxicity 

studies based on the potential corrosivity of the product.” 

 Repeat Dose Subchronic and Chronic Systemic Toxicity in the Rat 

A subchronic oral toxicity study was conducted (OECD Guideline 407) with PSOA using Sprague 

Dawley rats. The rats were administered 100% pure PSOA (5 animals/sex/dose) at 0 (vehicle 
Page 7 of 24

control), 5, 15 or 50 mg/kg bw/day by oral gavage for 28 days. The study included additional 

animals in order to determine the 14-day recovery after cessation of treatment. 

In the 14 day recovery portion of the study, the additional animals (5/sex/dose) were administered 

PSOA by oral gavage at dose levels of 0 (vehicle control) and 50 mg/kg bw/day for a period of 28 

days then maintained on the study for an additional 14 days without test substance administration. 

The following were evaluated: clinical signs, body weight, body weight changes, food 

consumption, ophthalmology, detailed functional observations, clinical pathology (hematology, 

coagulation, clinical chemistry and urinalysis) gross necropsy findings, organ weights and 

histopathologic examinations. 

There were no treatment related changes in any of the parameters tested. Lower urine volumes 

noted in animals dosed at 15 and 50 mg/kg bw/day were considered to not be toxicologically 

significant in the absence of concomitant kidney weight or histopathology findings in the kidney. 

At the end of the study period, gross and microscopic findings observed were of the nature and 

incidence commonly seen in rats of the age and strain on studies of the type and, or were of similar 

incidence in control and treated animals. Differences in incidence of dark foci in the lungs seen in 

male rats sacrificed on Day 29 were shown to correlate with alveolar hemorrhage, which showed 

no biologically significant difference in incidence between treated and controls. The increase 

incidence of minimal hemorrhage in the thymus of treated animals which were sacrificed after the 

recovery period on Day 43 is considered incidental, as this is a common background lesion. 

Daily administration of PSOA by oral gavage for 28 days was well tolerated in rats at levels of 5, 

15 and 50 mg/kg bw/day. Based on these results, the No Observable Adverse Effect Level 

(NOAEL) is considered to be 50 mg/kg bw/day. In this study, the dosing was not considered 

adequate since it did not produce any systemic toxicity. 

Genotoxicity 

In vitro genotoxicity studies have been conducted with PSOA. PSOA is negative for inducing 

mutations in bacterial and mammalian cells, with and without metabolic activation. In the in vitro

chromosome aberration study using human lymphocytes, PSOA was positive with and without 

metabolic activation. However, the in vivo micronucleus assay in rats was negative. 

Table 3. Summary of Genotoxicity Testing for PSOA 

Study Result In 

Vitro/InVivo 

Reference 

Bacterial Reverse Mutation 

Assay 

(Ames test) 

Negative with and 

without 

metabolic activation 

In vitro Sokolowski 

(2011) 

Gene Mutation Assay in Chinese 

Hamster V79 Cells (V79/HPRT) 

Negative with and 

without 

metabolic activation 

In vitro Wollny 

(2011) 

Chromosome Aberration Study Positive with and without In vitro Bohnenberger 
Page 8 of 24

(Human Lymphocyte) Metabolic activation (2012) 

Micronucleus Assay I Bone 

Marrow Cells of the Rat with 

PSOA 

Negative In vivo Roth (2012) 

 

Reproductive and Developmental Toxicity (OECD 414) 

A developmental toxicity study with PSOA (purity 100%) was conducted with pregnant SpragueDawley rats (24 animals/dose group) (Laidlaw 2013). Animals were dosed by oral gavage every 

day from Day 6 to Day 19 of gestation at dosages of 0, (vehicle control) 5, 15, and 50 mg/kg 

bw/day PSOA. The study was conducted according to OECD Guideline 414. 

No test substance related mortality was reported. Clinical observations were reported in two 

animals at the high dose level (50 mg/kg bw/day) and included piloerection in both animals and 

hunched posture in one animal. There was a slight reduction in group mean body weight gain 

(9%) over the course of the study at 50 mg/kg bw/day when compared to the vehicle control group 

means. It was not statistically significant. Group mean food consumption was slightly decreased 

at 50 mg/kg bw/day when compared to the vehicle control group mean for the duration of the 

study, particularly between Days 13 ato 20 of gestation, but this change was not statistically 

significant. 

Pregnancy performance and fetal weights were comparable throughout the groups and slight 

intergroup differences in pregnancy performance and fetal weights were considered not to be 

treatment related. No abnormalities or variations were attributable to treatment with PSOA and all 

findings were considered to be incidental and toxicologically significant. The parental No 

Observable Adverse Effect Level (NOAEL) for systemic effects was 50 mg/kg bw/day. The 

NOAEL for embryotoxic, fetotoxic and developmental effects was also 50 mg/kg bw/day, the 

highest dose tested. In this study, the dosing was not considered adequate since it did not produce 

any systemic toxicity. 

 14-Day Repeated-Dose Oral Toxicity Study 

The dosing was not considered as adequate for the 28-day oral toxicity study and developmental 

toxicity study since there was no evidence of any systemic toxicity. The registrant claim that the 

higher dose levels were not used in these two studies due to corrosive nature of the chemical. EPA 

evaluated these studies and noted that there was no evidence of irritation in the oesophagus. 

Therefore requested a confirmatory study to demonstrate that higher doses would not have been 

tolerated by the animal. In response this concern by the EPA, the registrant submitted a study on 

30 September 2014, new study to the Agency (Yasso, B. 2014. MRID 4948070. PSOA: 14-Day 

Repeated-Dose Oral Toxicity Study in Rats unpublished report by MB Research Laboratories, 

1765 Wentz road, P.O. Box 178, Spinnerstown, PA 18968, 25 SEPTEMBER 2014). Twenty male 

and twenty female Sprague Dawley rats (5/sex/dose) were given daily doses of peroxy sulfonated 

oleic acids for 14 days by oral gavage using a syringe and dosing needle. The vehicle was water. 

Doses were 0 (vehicle/control), 100 mg/kg/day (low dose), 300 mg/kg/day (mid-dose) and 1,000 

mg/kg/day (high dose) which is the limit dose. On Day 1 immediately following dosing, excessive 
Page 9 of 24

salivation and wetness of the nose/mouth area were observed in several animals in the high dose. 

The response was attributed to test article residue on the gavage needle. The dosing technique was 

modified so the gavage needle was attached to the syringe after it was filled with the test article so 

that the needle would be residue-free. The modified technique was used for the remainder of the 

study. 

On day 15 surviving animals were sacrificed and blood collected for analysis. The liver, adrenals, 

ovaries, thyroid/parathyroid, brain, testes, pituitary, stomach, kidneys, epididymides, heart, gross 

lesions, spleen, urinary bladder and lungs were weighed and/or preserved. Microscopic 

examination was performed on the tissues noted above from the high-dose group (1,000 

mg/kg/day) and control group (0 mg/kg/day) and gross lesions from animals in all treatment 

groups. All animals in the control group survived the 14 day test period. Five male and four 

females in the mid-dose group (300 mg/kg/day) survived; one female died on day 9. In the highdose group (1,000 mg/kg/day) four males and three females survived. The deaths in the high-dose 

group occurred on Day 6 (1 male and 1 female) and on Day 9 (1 female). 

In the low-dose group, signs including diarrhea, piloerection, chromodacryorrhea, wetness of the 

nose/mouth area, wetness of the anogenital area, dyspnea, chromorhinorrhea, bloating of the 

abdomen, red staining of the nose/mouth area and apparent licking of the inside of the mouth were 

observed. Abnormal signs were observed beginning on Day 3 then sporadically among the 

animals through till Day 15. 

Among surviving animals in the mid-dose group (300 mg/kg/day), the onset of abnormal signs 

began on Day 1 with more significant findings on Day 10 and continuing until termination. Signs 

included red staining of the nose/mouth area, yellow staining of the anogenital and abdominal 

areas, wetness of the nose/mouth and neck, anogenital areas, piloerection, dyspnea, 

chromorhinorrha, yellow and red staining of the neck area, lethargy, ataxia and bloating of the 

abdomen. 

In the high-dose group (1,000 mg/kg/day) abnormal signs began on Day 2 and continued 

throughout until termination. Signs included red staining and wetness of the nose/mouth area, red 

and yellow staining, wetness and bloating of the abdomen, red substance in pan liner, 

chromodacryorrhea, hunched posture, lacrimation, lethargy, diarrhea, ataxia, piloerection, 

prostration, dyspnea, chromorhinorrhea, few feces, emaciation, apparent licking of the inside of the 

mouth, localized hair loss, wetness and yellow staining of the neck area and soiling, wetness and 

yellow staining of the anogenital area. 

All animals in the control, low- and mid-dose groups gained body weight throughout the test. In 

the high-dose group one male and two females lost body weight on either Days 4 or 7 but regained 

all weight by termination. 

There were no observable abnormalities in water or feed consumption in the control and low-dose 

groups. In the mid-dose group there were no observable abnormalities in water and feed 

consumption however diminished feed and water consumption was observed on Days 7 and 8 prior 

to the unscheduled death of one female. Beginning on Day 3 and throughout the study period, 
Page 10 of 24

diminished food and/or water consumption was observed periodically among animals in the highdose group. 

White blood cell counts were increased in males and females in the high-dose group. Reticulocyte 

counts were increased for males and females in the mid-dose and high-dose groups. This increase 

in reticulocyte count is indicative of an erythropoietic response and is most likely correlated to the 

histopathologic findings of hemorrhaging in the stomach. Lymphocytes were increased and 

eosinophils were decrease when compared to controls for males in the high-dose group. These 

changes are within the published reference range and are considered incidental. There were no 

other differences noted at termination between the treated groups or when compared to the control 

group in any other hematological value. 

Clinical chemistry parameters affected by the administration of PSOA were indicative of liver 

damage, most likely due to the poor nutritional status of the animals at the end of the study. 

Alanine Aminotransferase (ALT) was increased in males in the high-dose group. Aspartate 

Aminotransferase (AST) and Alkaline Phosphatase (ALP) were decreased for males in the middose and high-dose groups however these changes were within the published reference range and 

were below that of the control values. There were no histopathological findings related to the liver 

although liver weights were increase in both males and females in the high-dose group. There 

were no other differences noted at termination between the PSOA-treated groups or when the 

PSOA-treated groups were compared to the control group in any other clinical chemistry values. 

There were no observable abnormalities or gross lesions at the necropsies of 9/10 vehicle control 

groups animals. Pale areas of the lungs were observed in one male. At necropsy of the low-dose 

group there were red and dark areas as well as darker than normal lungs and red stained 

nose/mouth areas among one male and one female. The necropsies of the remaining low-dose 

group animals revealed no observable abnormalities or gross lesions. Among the nine survivors in 

the mid-dose group (300 mg/kg/day), there were no observable abnormalities in three males and 

one female. Necropsy revealed red and dark areas of the lungs, wetness of the nose/mouth area, 

larger than normal duodenum, and yellow areas and distention (yellow liquid and gas) of the 

intestines in two males. Among three of four females, red and brown staining of the nose/mouth 

area, red and dark areas of the lungs, dark red areas on the thymus were observed. Emaciated 

appearance, red staining of the nose/mouth area, yellow staining of the anogenital and abdominal 

areas as well as pronounced distention of the stomach and intestines were observed in the single 

animal that died on Day 9. Among the high-dose (1000 mg/kg/day) survivors, there were no 

observable abnormalities or gross lesions in the necropsies of two out of seven animals (one male 

and one female). Pale areas of the stomach, red areas of the lungs and intestines, wetness, red and 

yellow staining of the nose/mouth area, yellow staining of the anogenital area, dark lungs, 

emaciated appearance and larger than normal duodenum were observed among the three surviving 

males and two females. 

A larger than normal adrenal gland, soiling and yellow staining of the anogenital area, yellow 

staining of the abdominal area, red staining of the nose/mouth area, dark red areas of the stomach 

and a thick white fluid in the stomach, distention of the stomach, darkened and dark red areas of 

the lungs, emaciated appearance, wetness of the nose/mouth and anogenital areas, abdominal 
Page 11 of 24

distention and red areas of the intestines were observed among one male and two females that died 

on Days 6 and 9. 

There were no observable abnormalities or irregularities in measured organ weights in the control 

group. For males and females there were no meaningful differences between the low- and middose groups with the control group in mean absolute and relative spleen, liver, adrenal, kidney, 

heart, lung, brain, pituitary, thyroid/parathyroid and epididymis/ovary weight. In the high-dose 

group (1,000 mg/kg/day) males, mean relative liver weight was 20.4% greater than that of the 

control males. The mean absolute liver weight in the high-dose males was similar to that of the 

controls. The mean kidney and brain weights relative to body weight in the high-dose males were 

elevated over those of the control group. Because the mean absolute kidney and brain weights 

were similar between the groups, the apparent increase were considered to be artifacts of the lower 

final body weight in the high-dose males. The mean absolute spleen weights were similar between 

the groups. High-dose males and elevated mean and absolute and relative adrenal weights 

compared to the controls. There were no meaningful differences between the high-dose and 

control animals in mean absolute and relative heart, lung, pituitary, thyroid/parathyroid and 

epididymides weights. The mean absolute and relative liver weights of high-dose males and 

females were greater than controls (15.6% and 31.4% respectively). These changes, in the absence 

of histopathological findings were considered a result of poor nutritional status from the gastric 

irritation caused by the administration of PSOA. The mean relative kidney and brain weights in 

the high-dose group were elevated over those of the controls. There were no meaningful 

differences between the high-dose and control females in mean heart, lung, spleen, adrenal, 

pituitary, thyroid/parathyroid and ovary weights. 

The gross necropsy findings in two high-dose males (pale areas of the stomach) were correlated 

with gastric epithelial hyperplasia and hyperkeratosis which are generally in response to direct 

gastric irritation or oral gavage procedure and is a protective response mounted to preserve the 

integrity of the mucosal barrier. 

There were no microscopic correlates for the gross findings observed in the mid- and high-dose 

groups pertaining to the intestines or duodenum. The gross findings of lung discoloration, reported 

among low- mid- and high-dose animals were generally correlated to areas of atelectasis. All of 

the non-gastric findings were considered incidental and unrelated to administration of PSOA. 

Histopathologic lesions considered related to the administration of PSOA were confined to the 

stomach (glandular and non-glandular areas) and included epithelial hyperplasia and 

hyperkeratosis of the non-glandular portion, as well as chronic active inflammation and edema of 

both the glandular and non-glandular regions. In four instances, focal erosion and ulceration of the 

gastric mucosa occurred. These changes occurred in all high-dose males and females as well as 

three of four mid-dose females. All other lesions were considered incidental and unrelated to 

administration of PSOA. 

All other microscopic findings observed were considered incidental, of the nature commonly 

observe in this strain and age of rats and/or were of similar incidence and severity in the control 

animals as well as the treated animals. Therefore, the effects were considered unrelated to 

administration of PSOA. 
Page 12 of 24

At the high-dose (1,000 mg/kg/day) the primary effects of PSOA were on the gastrointestinal 

system. The clinical manifestations of these effects were diarrhea associated with staining and 

matting, decreased food consumption and body weight loss. At necropsy/histopathology, focal 

erosion, edema, inflammation, hyperkeratosis and hyperplasia were observed in the stomach. 

At the mid-dose (300 mg/kg/day) nine of 10 animals survived and clinical observations were 

associated primarily with gastro-intestinal irritation and distress. Sustained body weight gains 

were observed among all the surviving animals. Increased reticulocyte counts, and changes in 

Alanine Aminotransferase, Aspartate Aminotransferase and Alkaline Phosphatase values in the 

absence of any gross or histopathologic liver findings were considered to be secondary responses 

to decreased nutritional status of the rats caused by local gastric irritation from PSOA. 

At the low-dose (100 mg/kg/day) there was no mortality. The clinical pathology, body weight and 

organ weight results are similar to those of the vehicle control group. The gross necropsy findings 

were incidental and unrelated to administration of PSOA. 

 
Page 13 of 24

Table 4. Summary of Toxicological Endpoints for PSOA. 

Study Dose Levels 

mg/kg bw/day 

NOAEL 

mg/kg bw/day 

Effects 

28 Day Oral Toxicity 

in Rats 

0,5,15,50 50 No observed effects 

up to the highest dose 

Developmental 

Toxicity in Rats 

0,5,15,50 50 Fetal & Maternal: No 

observed effects up to 

the highest dose 

tested 

14-day Repeat-dose 

Oral Toxicity in Rats 

0, 100, 300, 1,000 100 g.i. irritational and 

related effects at the 

mid and high dose, no 

effects at the low dose

Chronic Toxicity/Carcinogenicity 

There are no known chronic toxicity studies with PSOA. 

 Neurotoxicity 

A neurotoxicity study was not conducted with PSOA. However, detailed functional observations 

were made among the parameters measured in the 28-day subchronic oral feeding study. There 

were no PSOA related changes in any of the parameters measured, including functional 

observations (FOB). No evidence of neurotoxicity was observed. 

 Immunotoxicity 

An Immunotoxicity study was not conducted with PSOA. However, minimal hemorrhage in the 

thymus was observed after the recovery period in the 14 day study with rats. Since, this effect is a 

common background lesion it is not considered indicative of potential immunotoxicity. Therefore, 

an immunotoxicity study is not required at this time. 

 Metabolism 

There are no available PSOA mammalian metabolism studies. 

 TOXICITY ENDPOINT SELECTION 

The toxicological endpoint selected for risk assessment purposes is 50 mg/kg bw/day from the 28-

day feeding study and from the developmental/reproduction toxicity study. There were no adverse 

effects noted at 50 mg/kg bw/day – it was the highest dose tested in those studies. The Agency 

selected this conservative NOAEL as the end point of concern for risk assessment purposes since 

higher doses cannot be tested due to highly irritating property of the PSOA. 
Page 14 of 24

V. Special Consideration for Infants and Children (FQPA Safety Factor)

 Section 408(b)(2)(c) of FFDCA provides that EPA shall apply an additional tenfold (10X) 

margin of safety for infants and children in the case of threshold effects to account for 

prenatal and postnatal toxicity and the completeness of the database on toxicity and 

exposure unless EPA determines based on reliable data that a different margin of safety 

will be safe for infants and children. This additional margin of safety is commonly referred 

to as the FQPA safety factor (SF). In applying this provision, EPA either retains the default 

value of 10X, or uses a different additional safety factor when reliable data available to 

EPA support the choice of a different factor. 

Based on lack of any systemic toxicity and the irritating property of the chemical which precluded 

testing at a higher doses, EPA has concluded that there are no toxicological endpoints of 

concern for the U.S. population, including infants and children, and has conducted a 

qualitative assessment. As part of its qualitative assessment, the Agency did not use safety 

factors for assessing risk, and no additional safety factor is needed for assessing risk to 

infants and children. 

Taking into consideration the available information, EPA concludes that the additional 1X FQPA 

safety factor will be retained.

VI. EXPOSURE

A. Dietary Exposure 

Dietary exposure to PSOA by the general population could occur from ingesting food that 

contacted a surface treated with an antimicrobial solution that contained PSOA as an inert 

ingredient. In order to estimate possible exposure from food that has contacted a treated surface, 

the Agency uses the Food and Drug Administration (FDA) Food Contact Surface Sanitizing 

Solution Dietary Exposure Assessment Model (FDA/CFSAN OPA: Chemistry Guidance – 

Sanitizing Solution version 1.1; January 1993; Office of Premarket Approval now Office of Food 

Additive Safety). The model is presented in the attachment. The model was run using the 

maximum concentration expected for PSOA (250 ppm) and adjusted for body weight according to 

current OPP policy. The results are summarized as follows: 

EDI = (1 mg/cm2)(250 ug PSOA/1000 mg)(4000 cm2/person/day = 1000 ug/person/day = 1 mg/person/day 

Mg/kg bw/day 

Adult 1 mg/day ÷ 80 kg bw = 0.0125 mg/kg bw/day 

Child 1 mg/day ÷ 11 kg bw = 0.091 mg/kg bw/day 

Margin of Exposure (MOE) = NOAEL (50 mg/kg bw/day)/Exposure 

Adult 50 mg/kg bw/day/0.0125 mg/kg bw/day = 4000 

Child 50 mg/kg bw/day/0.091 mg/kg bw/day = 550 

Since all MOEs exceed 100, using conservative assessment techniques, the proposed use does not 

exceed the Agency’s level of concern. 
Page 15 of 24

 

 

B. Residential (Non-Occupational) Exposure 

From non-dietary exposure. The term “residential exposure” is used in this document to refer to 

non-occupational, non-dietary exposure. However, in the particular request to use PSOA, 

residential exposure is not expected. The requested use is for “clean in place” methods of 

application. The requested sites of application are: “use on food contact surfaces in public eating 

places, as well as dairy processing equipment and food processing equipment and utensils.” Thus, 

while inadvertent dietary exposure might occur from residues remaining on treated food contact 

surfaces, the proposed use pattern is expected to be from commercial use, not residential i.e. 

homeowner use. 

 C. Occupational Exposure 

Limited information was presented regarding use patterns and occupational exposure. Based upon 

the requested use, the Agency believes worker exposure may well be chronic in nature i.e., daily 

exposure in the normal course of food and dairy processing. The requested end-use dilution is 250 

ppm however it is presumed that occupationally exposed individuals would be exposed to higher 

concentrations during the preparation of final dilutions. For applications that might be employed 

while “flushing systems”, workers may be exposed to larger volumes of more concentrated 

material. Lacking more specific information, the Agency cannot assess possible corrosive skin 

irritation that might result from higher volume applications/uses These factors were not described 

and the Agency does not possess these kinds of data and is therefore not able to estimate exposure 

and risk to possible higher volume uses. 

For smaller volume applications there is the possibility of dermal and inhalation exposure from 

applying the sanitizing solution to fixed “surfaces” or “utensils”. As such, the Agency has 

estimated occupationally related exposures to PSOA based upon information contained in the 

“Reregistration Eligibility Decision for Alkyl Dimethyl Benzyl Ammonium Chloride (ADBAC)” 

(U.S. EPA Publication EPA739-R-06-009; August 2006) 

(www.epa.gov/oppsrrd1/REDs/adbac_red.pdf). 

The RED document discusses occupational exposures as a result of using antimicrobial agents in 

“food handling/storage establishments premises and equipment”. As such, five methods of 

application to indoor hard surfaces (including dishes, utensils and equipment) are described. It 

should be noted that the ADBAC document only assessed inhalation exposure. To assess the 

dermal component, the dermal unit exposure was taken from: “Occupational Pesticide Handler 

Unit Exposure Surrogate Reference Table” (Office of Pesticide Programs, U.S. EPA, March 

2013). The dermal unit exposure selected is for a mixer/loader/applicator using a manually 

pressurized hand-wand applying material to “food handling establishments, warehouses, 

residential living spaces, childcare centers/schools. A worker using protective gloves in addition 
Page 16 of 24

to a single layer of work clothing (long-sleeved shirt, long pants, shoes plus socks) has a unit 

exposure of 8600 μg/lb handled (8.6 mg/lb handled). The dermal unit exposure is used as a “best 

fit” surrogate since dermal unit exposures are not expressed in the RED document. 

The Agency assumes the density of a typical end-use product is 8.0 lb/gallon. The requested 

maximum use rate concentration is 250 ppm PSOA. 250 ppm = 0.025 % therefore 0.025 * 8.0 lb 

gallon = 0.2 lb PSOA/gal. 

The algorithm used to estimate exposure is 

Unit exposure * application rate * quantity handled per day ÷ body weight. 

Lacking information to the contrary, the Agency assumes 100 % absorption via the dermal and 

inhalation routes of exposure. A toxicological endpoint of 50 mg/kg bw/day is used to calculate 

Margin of Exposure. The level of concern is for MOE < 100. As is summarized in Table 5.0 the 

estimated dermal and inhalation MOEs are > 100 and therefore do not exceed the Agency’s level 

of concern Also note the small quantities of material estimated to have been applied. 

Table 5.0 Worker Exposure/Risk (single layer work clothing plus protective gloves) 

Application 

method 

Dermal 

Unit 

Exposure 

mg/lb 

handled 

Inhalation 

Unit 

Exposure 

mg/lb 

handled 

Application 

Rate 

Quantity 

Handled 

(treated) 

Per Day 

Dermal 

Dose 

mg/kg/day 

Inhalation 

Dose 

mg.kg/day 

Dermal 

MOE 

Inhalation 

MOE 

Lowpressure 

hand-wand 

8.6 

0.681 

0.2 lb/gal 

2 gal 0.043 0.0034 1160 14700 

Mop 2.38 2 gal 0.043 0.0119 1160 4200 

Wipe 67.3 0.26 gal 0.0059 0.044 8470 1140 

Trigger 

pump 

sprayer 

1.3 0.26 gal 0.0059 0.00085 8470 59000 

Immersion 

Flooding 

Circulation 

1.89 2 gal 0.043 0.0095 1160 5300 

VII. AGGREGATE RISK 

Acute Aggregate Risk. There was no hazard attributable to a single exposure seen in the toxicity 

database for PSOA. Therefore, PSOA is not expected to pose an acute risk. 

Chronic risk. A chronic aggregate risk assessment takes into account exposure estimates from 

chronic dietary consumption of food and drinking water. EPA has concluded that the aggregated 

food and water exposures result in aggregate MOEs > 1000 for adults in the general population. 

The MOE for children age 1-2 years is 550 which does not exceed the Agency’s level of concern 

i.e., MOE <100. 

Short- and intermediate-term Aggregate risks. Short-term aggregate exposure takes into account 

short-term residential exposure plus chronic exposure to food and water (considered to be a 

background exposure level). Since the proposed use of PSOA is not expected to result in 
Page 17 of 24

“residential” exposures, there are no “residential” exposures that must be added to estimated 

dietary exposures. 

Aggregate cancer risk for U.S. population. Due to insufficient information it was not possible for 

the Agency to estimate the potential for carcinogenicity from exposures to PSOA. 

Residential Post-application Exposure

Assessments of Residential Post-application exposure are not necessary since the proposed use 

pattern is not expected to result in residential exposures. 

VIII. CUMULATIVE EXPOSURE 

Cumulative effects from substances with a common mechanism of toxicity. Section 

408(b)(2)(D)(v) of 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 found PSOA to share a common mechanism of toxicity with any other 

substances, and PSOA does do not appear to produce a toxic metabolite produced by other 

substances. For the purposes of this tolerance action, therefore, EPA has assumed that the PSOA 

does not have a common mechanism of toxicity with other substances. For information regarding 

EPA's efforts to determine which chemicals have a common mechanism of toxicity and to evaluate 

the cumulative effects of such chemicals, see EPA's website at 

http://www.epa.gov/pesticides/cumulative. 

IX. ENVIRONMENTAL FATE & EFFECTS 

Acute toxicity studies have been conducted with PSOA on Rainbow Trout, Daphnia magna and 

the alga Pseudokirchneriella subcapitata. Summary test results are presented below. 

Table 6.0 Summary of Environmental Fate and Effects 

OCSPP Guideline 

OECD Guideline

Study Title 

OECD 203 Determination of Acute Toxicity (LC50) of PSOA to Rainbow Trout (96 h Continuous Flow 

850.1010 

OECD 202 

Acute Toxicity of PSOA to Daphnia magna in a 48-hour Immobilization Test 

850.5400 

OECD 201 

Growth Inhibition Test of PSOA on the Alga Pseudokirchneriella subcapitata 

Species Duration Result 

Rainbow Trout 96 hr LC50 = 0.75 mg/L (highly toxic) 

Daphnia magna 48 hr EC50 = 3.05 mg/L (moderately toxic); NOEC = 1.28 mg/L 

Pseudokirchneriella 

subcapitata 

72 hr EC50 = 

Based on growth rate: 5.44 mg/L 

Based on yield: 2.56 mg/L 

NOEC = 1.66 mg/L 

 
Page 18 of 24

Based upon the study results, PSOA is classified as highly toxic to fresh water fish and moderately 

toxic to invertebrates. 

The Applicant used the environmental model EPA SuiteTM 4.1 to estimate some environmental 

properties of PSOA. The use and data interpretation for EPI SuiteTM are discussed in “The Use of 

Structure-Activity Relationships (SAR) in the High Production Volume Chemicals Challenge 

Program (EPA, 1999). The EPA SuiteTM model estimations were based on a hydrated peroxy acid 

carbon chain length of C18 (i.e., PSOA primary components). Overall it was concluded that 

PSOA is unlikely to persist in aquatic or terrestrial organisms or in the environment since the 

compounds which comprise PSOA are not likely to be lipophilic. 

log KOW 1.96 not lipophilic 

vapor pressure 3.43 x 10-14 mm Hg at 25oC non-volatile 

photolysis (atm- T1/2 hr) 3.554 hr degrades in the atmosphere 

log BCF = 1.85 not expected to bioaccumulate 

log KOC 1.37 (based on log KOW) indicates low soil binding 

Level III Fugacity Modeling Not persistent 

Table 7.0 Primary Level III Fugacity 

Environmental 

Compartment 

Mass Amount

(percent 

Half-Life

(hr) 

Emissions

(kg/hr) 

Air 0.022 7.11 1000 

Water 21.7 55.9 1000 

Soil 78.2 112 1000 

Sediment 0.064 50 0 

Table 8.0 Ultimate Level III Fugacity 

Environmental 

Compartment 

Mass Amount

(percent 

Half-Life

(hr) 

Emissions

(kg/hr) 

Air 0.0037 7.11 1000 

Water 18.8 360 1000 

Soil 81.1 720 1000 

Sediment 0.129 3.24e003 0 

PSOA is highly toxic to freshwater fish. It is moderately toxic to invertebrates and plants. In view 

of the results of EPI SuiteTM modeling results and upon the proposed use pattern(as a wetting agent 

or coupler), the use of PSOA is not expected to result in adverse environmental effects. The 

proposed use of PSOA is for indoor use only and the great majority of that is in enclosed systems. 

The final use concentration is a maximum of 250 ppm (approximately 0.025 %). Further, upon 

exposure to light and high temperatures experienced in the proposed use pattern, PSOA is expected 

to rapidly degrade to SOA and hydrogen peroxide which further degrade rather rapidly. 
Page 19 of 24

X. ENVIRONMENTAL JUSTICE 

Potential areas of environmental justice concerns, to the extent possible, were considered in this 

human health risk assessment, in accordance with U.S. Executive Order 12898, "Federal Actions 

to Address Environmental Justice in Minority Populations and Low-Income Populations," 

http://www.eh.doe.gov/oepa/guidance/justice/eo12898.pdf). 

As a part of every pesticide risk assessment, OPP considers a large variety of consumer subgroups 

according to well-established procedures. In line with OPP policy, HED estimates risks to 

population subgroups from pesticide exposures that are based on patterns of that subgroup’s food 

and water consumption, and activities in and around the home that involve pesticide use in a 

residential setting. Extensive data on food consumption patterns are compiled by the USDA under 

the Continuing Survey of Food Intake by Individuals (CSFII) and are used in pesticide risk 

assessments for all registered food uses of a pesticide. These data are analyzed and categorized by 

subgroups based on age, season of the year, ethnic group, and region of the country. Additionally, 

OPP is able to assess dietary exposure to smaller, specialized subgroups and exposure assessments 

are performed when conditions or circumstances warrant. Whenever appropriate, non-dietary 

exposures based on home use of pesticide products and associated risks for adult applicators and 

for toddlers, youths, and adults entering or playing on treated areas post-application are evaluated. 

Further considerations are currently in development as OPP has committed resources and expertise 

to the development of specialized software and models that consider exposure to bystanders and 

farm workers as well as lifestyle and traditional dietary patterns among specific subgroups.

XI. HUMAN STUDIES

This assessment does not rely on any studies in which human subjects were intentionally exposed 

to a pesticide. 

XII. RISK CHARACTERIZATION

Based upon the proposed use pattern, upon the maximum limit on use rate and upon the 

physical/chemical characteristics of PSOA as discussed above, the EPA concludes that there is a 

reasonable certainty that no harm will result to any subpopulation since the MOEs are > 100 

The acute oral LD50 in the rat is 300 mg/kg bw/day. According to the Applicant, due to the 

corrosive nature of PSOA, an in vitro skin corrosion study was conducted with PSOA rather than 

the in vivo rat dermal corrosion study. The results of the in vitro study show that PSOA is 

corrosive to the skin. 

A subchronic oral toxicity study was conducted (OECD Guideline 407) with PSOA. PSOA was 

administered for 28 days by oral gavage to Sprague Dawley rats. There were no treatment related 

changes in any of the parameters tested. The No Observable Adverse Effect Level (NOAEL) was 

50 mg/kg bw/day. 
Page 20 of 24

There are no available PSOA mammalian metabolism studies. 

In vitro genotoxicity studies have been conducted with PSOA. PSOA is negative for inducing 

mutations in bacterial and mammalian cells, with and without metabolic activation. In the in vitro

chromosome aberration study using human lymphocytes, PSOA was positive with and without 

metabolic activation. However, the in vivo micronucleus assay in rats was negative. 

A developmental toxicity study with PSOA (purity 100%) was conducted with pregnant SpragueDawley rats (24 animals/dose group) (Laidlaw 2013). Neither maternal nor developmental toxicity 

was observed at 50 mg/kg/day, the highest dose tested . 

The Agency recently received new toxicological data from a 14-day repeated dose oral toxicity 

study at doses of 100 mg/kg/day, 300 mg/kg/day and 1000 mg/kg/day. The effects were primarily 

gastro-intestinal irritation effects at the mid and high doses. The study confirmed findings from 

earlier studies with maximum doses of 50 mg/kg/day thus eliminating data gaps originally 

identified by the Agency. 

There are no known chronic toxicity studies with PSOA. 

A neurotoxicity study was not conducted with PSOA. However, detailed functional observations 

were made among the parameters measured in the 28-day subchronic oral feeding study. There 

were no PSOA related changes in any of the parameters measured, including functional 

observations. No evidence of neurotoxicity was observed. 

For risk assessment purposes, the toxicological endpoint of concern is 50 mg/kg bw/day which is 

based on the reproduction/developmental study and the repeat dose subchronic toxicity study, no 

toxicological effects of statistical significance were observed up to 50 mg/kg bw/day, which was 

the highest dose tested in those studies. As a result of the recently received confirmatory data in 

the 14-day repeated dose oral toxicity study, no additional safety factor is needed. 

EPA has determined that the available data is adequate to assess the safety of infants and children. 

The request for use is limited to “use on food contact surfaces in public eating places, as well as 

dairy processing equipment and food processing equipment and utensils” at a maximum end-use 

concentration of 250 ppm. As such, the general public is not expected to be exposed to PSOA as 

a result of any “residential use”. There is the possibility of dietary exposure as a result of postapplication residue on treated food handling surfaces. The request is not to use PSOA on 

agricultural crops or otherwise in residential settings. 

The Agency used the U.S. Food and Drug Administration (FDA) Food Contact Surface Sanitizing 

Solution Dietary Exposure Assessment Model to estimate dietary exposure. The model was run at 

the maximum requested concentration level of 250 ppm. The model indicates the Agency’s level 

of concern is not exceeded for toddlers exposed as a result of ingesting residues transferred to food 

from treated surfaces.

In view of the data and reasons summarized above and the results of the FDA dietary model, the 

Agency approves of the use of Peroxy Sulfonated Oleic Acids (CAS Reg. No. 1315321-93-7, 
Page 21 of 24

CAS Reg. No. 1315321-94-8, and CAS Reg. No. 1315321-95-9) for use as an inert ingredient at a 

maximum final end-use concentration not to exceed 250 ppm when applied in antimicrobial 

sanitizing agents to “use on food contact surfaces in public eating places, as well as dairy 

processing equipment and food processing equipment and utensils” as described under 40 CFR 

180.940(a). 

 
Page 22 of 24

ATTACHMENT 

FDA Food Contact Surface Sanitizing Solution Dietary Exposure 

Assessment Model 

 (FDA/CFSAN OPA: Chemistry Guidance – Sanitizing Solutions “Sanitizing Solutions: 

Chemistry Guidelines for Food Additive Petitions” version 1.1; January 1993; Office of 

Premarket Approval now Office of Food Additive Safety).

EDI (mg/day) = (1 mg/cm2

)(250 ug PSOA/1000 mg)(4000 cm2/person/day = 1000 ug/person/day = 1 mg/person/day 

 

DDD (mg/kg/day) = 

Adult 1 mg/day ÷ 80 kg bw = 0.0125 mg/kg bw/day 

Child 1 mg/day ÷ 11 kg bw = 0.091 mg/kg bw/day 

Margin of Exposure (MOE) = NOAEL (50 mg/kg bw/day)/Exposure 

Adult 50 mg/kg bw/day/0.0125 mg/kg bw/day = 4000 

Child 50 mg/kg bw/day/0.091 mg/kg bw/day = 550 

It is assumed that 100% of the residue is transferred to the exposed individual 

 

Where: 

AR = Application rate (ppm) 

RS = Residual solution (mg/cm2

) 

SA = Surface area of the treated surface which comes into contact with food (cm2

) 

BW = Body weight (kg) 

The input parameters listed in Table below and equations 1 and 2 above are used to calculate EDI, DDD and %PAD 

for the two population subgroups (average adult and infants/children) 

Input Parameters for Food Contact Surface Sanitizing Solution Dietary Exposure 

Assessment 

Parameter

Value

Rationale

Residual Solution on 

Surface 1 mg/cm2 FDA assumption 

Area of Treated Surface 4,000 cm2 FDA assumption for food 

utensils/surfaces 

concentration in diluted 

solution 250 ppm 

Diluted Solution concentration, based 

on maximum concentration (expressed 

in ppm). 

Fraction Transferred 100% US EPA Antimicrobials Div. SOP for 

Residential Exposure 3.1.1 

Body Weight (kg) 

Average adult = 

Child = 

80 

11 EPA (2011) Hot sheet 31 
Page 23 of 24

REFERENCES 

Head, T. 2013. MRID 49295001. Technical Memorandum Toxicology Assessment for Peroxy 

Sulfonated Oleic Acid: SAR, End-point Dose Selection, and Dermal Exposure Considerations. 

30 DEC 2013. Unpublished report. 

Laidlaw, K. 2013. An Embryo-foetal Developmental Study of PSOA by Oral Gavage in Rats. 

unpublished. Study sponsor: Ecolab Inc. 370 North Wabasha Street. St. Paul, MN 55102. Study 

Director: Karen Laidlaw. 11 January 2013. 130 pp. 

NIH 2012. http://toxnet.nlm.nih.gov

U.S. EPA. 2005. Oleic Acid Sulfonates and Related Compounds: Antimicrobials Division Risk 

Assessment for the Reregistration Eligibility Decision (RED) Document and for Tolerance 

Reassessment. Office of Prevention, Pesticides and Toxic Substances. Barcode 323799. 

September 30, 2005. 

U.S. EPA. 2005. Reregistration Eligibility Decision (RED) for Oleic Acid Sulfonates. September 

30 2004/September 2005. 

U.S. EPA. 2006. DDAC Dietary Risk Assessment. Memornandum J. Patel to T. Brody and R. 

Lee (Versar Inc.) to N. Shamin, USEPA. Jaunary 23, 2006. 

U.S. EPA. 2006. “Reregistration Eligibility Decision for Alkyl Dimethyl Benzyl Ammonium 

Chloride (ADBAC)” (U.S. EPA Publication EPA739-R-06-009; August 2006) 

(www.epa.gov/oppsrrd1/REDs/adbac_red.pdf). 

U.S. EPA. 2013. “Occupational Pesticide Handler Unit Exposure Surrogate Reference Table”

(Office of Pesticide Programs, U.S. EPA, March 2013). 

Yasso, B. 2014. MRID 49480701. PSOA: 14-Day Repeated-Dose Oral Toxicity Study in Rats 

MB Research Laboratories 1765 Wentz Road, P.O. Box 178 Spinnerstown, PA 18968 sponsored 

by Ecolab Inc. 370 North Wabasha St., St. Paul, MN 55102. 25 SEP 14 unpublished report. 
Page 24 of 24