Page 2 of 24 sulfonated, sodium salt (CAS No. 68443-05-0)) (also referred to as peroxy sulfonated oleic acids (PSOA)) (CAS No. 131 5321-93-7, 1315321-94-8, 1315321-95-9)

9-Octadecenoic acid (9Z)-, sulfonated, oxidi zed (CASRN 1315321-93-7) and the potassium and sodium salts; 9-Octadecenoic acid (9Z)-, sulfonated, oxidi zed (CASRN 1315321-94-8) potassium salts; and 9-Octadecenoic acid (9Z)-, sulfonated, oxidized (CASRN 1315321- 94-9) sodium salts.

The acute oral LD 50 in the rat is 300 mg/kg bw/day. Due to the corrosive nature of PSOA, an in

vitro skin corrosion study was conducte d 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 st udy was conducted (OECD Guidelin e 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 Ef fect 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, w ith and without metabolic activation. In the in vitro chromosome aberration study us ing human lymphocytes, PSOA wa s positive with and without metabolic activation. However, the in vivo micronucleus assay in ra ts was negative.

A developmental toxicity study with PSOA (purity 100%) was conduc ted with pregnant SpragueDawley rats. Neither maternal nor developmen tal toxicity was observe d at 50 mg/kg/day, the highest dose tested . In this st udy, the dosing was not considered adequate since it did not produce any systemic toxicity.

There are no mammalian meta bolism studies with PSOA.

There are no known chronic toxici ty studies with PSOA, however, the concerns for long term toxicity are limited due to corro sive nature of the chemical.

A neurotoxicity study was not conducted with PSOA. However, detailed functional observations were made among the parameters measured in th e 28-day subchronic oral feeding study. There were no PSOA related changes in any of th e 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 th e 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 we re seen at all doses. At 100 mg/kg/day, diarrhea, piloerection, chromodacryorrh ea, wetness of the nose /mouth area, wetness ofPage 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 tolera ted in the 28 day toxicity study and the developmental toxicity st udy. Therefore, these studies are acceptable for risk assessment. For risk assessment purposes, the conservative t oxicological endpoint of concern is 50 mg/kg bw/day which is based on the developmental study and the repeat dose subc hronic toxicity study, no toxicological effects of statistical significan ce were observed up to 50 mg/kg bw/day, which was the highest dose test ed 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 cont act surfaces in public eating places, as well as dairy processing equipment and food processing e quipment and utensils” at a maximum end-use concentration of 250 ppm. The primary use of PSOA will be in dairy pr ocessing facilities using Clean In Place (CIP) techniques which are essentiall y 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-app lication residue from treated surfaces (food contact surfaces in public eating places). The re quest is not to use PSOA on agricultural crops or otherwise in residential settings.

The Agency used the U.S. Food and Drug Admini stration (FDA) Food Contact Surface Sanitizing Solution Dietary Exposure Assessment Model to estim ate 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 exceed ed for U.S. population.

The Margins of Exposure for occupationally expose d persons are greater th an 100 and therefore do not exceed the Agency’s levels of concern for work ers handling small volumes of diluted solution. It is the Agency’s understanding th at uses involving larger volumes of material are essentially “closed system” processes. The processes ar e known industrially as “clean in place” (CIP) systems. As such there is essentially no worker contact. Minibulk contai ners with the sanitizing solution are connected via plumbing piping/tubing to the processing systems that receive the sanitizing treatment. Valves are ope ned to introduce the sanitizer a nd valves are closed to end the treatment time. The Agency cons iders “closed systems” to result in negligible exposure thus a quantitative assessment of this aspect is not necessary.

PSOA is highly toxic to freshwater fi sh. It is moderately toxic to i nvertebrates and plants. In view

of the results of EPI Suite TM 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 envi ronmental effects. The proposed use of PSOA is for indoor use only and much of that in enclosed systems. The final use

concentration is a maximu m of 250 ppm (0.025 %).

In view of the weight of the evid ence toxicologically, in view of the proposed use pattern (CIP), in view of the low maximum use concentration requ ested (250ppm), the Agency approves of the requested use of Peroxy Sulfonate d Oleic Acids as an inert i ngredient at a maximum finalPage 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 toleran ce for Peroxy Sulfonated Oleic Acids (PSOA). Specifically, the request is for a food-use unde r 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 followe d 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 (9 Z) – sulfonated (CAS No. 68988-76-1)); 9- octadecenoic acid (9Z) -, sulfonated, oxidize d, potassium salts (CAS No. 1315321-94-8) (when formed using the pre-reaction material 9-octade cenoic acid (9Z-) sulfona ted, 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. 131 5321-93-7, 1315321-94-8, 1315321-95-9)

9-Octadecenoic acid (9Z)-, sulfonated, oxidi zed (CASRN 1315321-93-7) and the potassium and sodium salts; 9-Octadecenoic acid (9Z)-, sulfonated, oxidi zed (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 agen t and a coupler. The proposed use is for Clean In Place (CIP) saniti zing 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 dilu tion 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-Octadec enoic acid (9Z)-, sulfonated, ox idized (CASRN 1315321-93-7) and the potassium and sodium salts; 9-Octadecenoic acid (9Z)-, sulfonated, oxidi zed (CASRN 1315321-94-8) potassium salts; and 9-Octadecenoic acid (9Z)-, sulfonated, oxidi zed (CASRN 1315321-94-9) sodium salts) are essentially the same with slight variance in the oxygen bonding at the en d of the 18 carbon chain.

Table 1. Physical and Chemical Properties of Peroxy Sulfonated Oleic Acids

Parameter Value Source

Molecular Formula C 18 H 36 O 7 S (compound 1, 67%)

C 18 H 36 O 6 S (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/cm 3 at 20o C Vapor Pressure 1013 hPa at 20o C

Partition Coefficient (usually the Log P or Kow) Determined Log P OW ≤ 5.04 Log K OW 1.96

IV. HAZARD ASSESSMENT O O

O 

### M2 S O O

O M 1



### OHPage 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 LD 50 > 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 na ture of PSOA via the dermal route.

According to the Applicant, due to the corrosive nature and characteristic s 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 irritati on study would waive the a dditional acute toxicity studies based on the potential corrosivity of the product.”

Repeat Dose Subchronic and Chroni c Systemic Toxicity in the Rat

A subchronic oral toxicity st udy was conducted (OECD Guideline 407) with PSOA using Sprague Dawley rats. The rats were administered 100% pure PSOA (5 animals/sex/dose) at 0 (vehiclePage 7 of 24 control), 5, 15 or 50 mg/kg bw/day by oral gava ge for 28 days. The study included additional animals in order to determine the 14-day r ecovery after cessation of treatment.

In the 14 day recovery portion of the study, the a dditional 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 additiona l 14 days without test su bstance administration.

The following were evaluated: clinical si gns, body weight, body weight changes, food consumption, ophthalmology, detailed functional observations, clinical pathology (hematology, coagulation, clinical chemis try 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 conc omitant kidney weight or histopa thology findings in the kidney. At the end of the study period, gross and microsc opic 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 anim als. Differences in incidence of dark foci in the lungs seen in male rats sacrificed on Day 29 were shown to co rrelate with alveolar he morrhage, which showed no biologically significant difference in incidenc e 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 incide ntal, as this is a co mmon background lesion.

Daily administration of PSOA by oral gavage for 28 da ys 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 pr oduce any systemic toxicity.

Genotoxicity

In vitro genotoxicity studies have been conducted with PSOA. PSOA is negative for inducing mutations in bacterial and mammalian cells, w ith and without metabolic activation. In the in vitro chromosome aberration study us ing human lymphocytes, PSOA wa s positive with and without metabolic activation. However, the in vivo micronucleus assay in rats was negative.

Table 3. Summary of Ge notoxicity 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 BohnenbergerPage 8 of 24 (Human Lymphocyte) Meta bolic 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 conduc ted 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 dosag es 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 s light 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 m ean food consumption was slightly decreased at 50 mg/kg bw/day when compared to the vehi cle control group mean for the duration of the study, particularly between Days 13 ato 20 of gest ation, 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 we re attributable to treatment with PSOA and all findings were considered to be incidental and toxicologically significan t. The parental No Observable Adverse Effect Level (NOAEL) for systemic effects was 50 mg/kg bw/day. The NOAEL for embryotoxic, fetotoxic and developmen tal 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 corrosi ve nature of the chemical. EPA

evaluated these studies and noted that there wa s no evidence of irritation in the oesophagus. Therefore requested a co nfirmatory study to demonstrate that higher doses would not have been tolerated by the animal. In response this concer n 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/d ose) were given daily doses of peroxy sulfonated oleic acids for 14 days by oral gavage using a sy ringe 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, excessivePage 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 te st 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-f ree. The modified technique was used for the remainder of the study.

On day 15 surviving animals were sacrificed and bl ood collected for analysis. The liver, adrenals, ovaries, thyroid/parathyroid, brai n, 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 fr om 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) surv ived; one female died on day 9. In the highdose group (1,000 mg/kg/day) four males and three fe males 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 includ ing diarrhea, piloer ection, chromodacryorrhea, wetness of the nose/mouth area, wetness of th e anogenital area, dyspnea, chro morhinorrhea, bloating of the abdomen, red staining of the nose/mouth area and appa rent 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 nos e/mouth area, yellow staining of the anogenital and abdominal areas, wetness of the nose/mouth and nec k, 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) abno rmal signs began on Day 2 and continued throughout until termination. Signs included red st aining 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, lacrima tion, lethargy, diarrhea, ataxia, piloerection, prostration, dyspnea, chromorhinorrhea, few feces, em aciation, apparent licking of the inside of the mouth, localized hair loss, wetne ss and yellow staining of the n eck 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 tw o females lost body weight on eith er Days 4 or 7 but regained all weight by termination.

There were no observable abnormali ties 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. Be ginning 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 th e mid-dose and high-dose groups. This increase in reticulocyte count is indicative of an erythropoietic response and is most likely co rrelated to the histopathologic findings of hemorrhaging in th e stomach. Lymphocytes were increased and eosinophils were decrease when compared to c ontrols for males in the high-dose group. These changes are within the published reference range and are consider ed 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 we re 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 increase d 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 findi ngs related to the liver although liver weights were increa se in both males and females in the high-dose group. There

were no other differences noted at terminati on 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 le sions at the necropsies of 9/10 vehicle control groups animals. Pale areas of the lungs were obs erved in one male. At necropsy of the low-dose group there were red and dark ar eas 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 area s of the lungs, wetness of the nose/mouth area, larger than normal duodenum, and yellow areas and distention (yellow liq uid 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 re d 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 disten tion of the stomach and intestines were observed in the single animal that died on Day 9. Among the high-dos e (1000 mg/kg/day) surv ivors, there were no observable abnormalities or gross lesions in the necr opsies of two out of seven animals (one male and one female). Pale areas of the stomach, red ar eas of the lungs and inte stines, 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, re d 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, abdominalPage 11 of 24 distention and red areas of the in testines were observed among one male and two females that died on Days 6 and 9.

There were no observable abnormalitie s or irregularities in measured organ weights in the control group. For males and females there were no mean ingful differences between the low- and middose groups with the control group in mean absolu te and relative spleen, liver, adrenal, kidney, heart, lung, brain, pituitary, thyr oid/parathyroid and epididymis/ ovary weight. In the high-dose group (1,000 mg/kg/day) males, m ean 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 re lative to body weight in the high-dose males were elevated over those of the control group. Becau se the mean absolute kidney and brain weights were similar between the groups, the apparent increas e were considered to be artifacts of the lower final body weight in the high-dose males. The mean absolute spleen weight s were similar between the groups. High-dose males and elevated mean and absolute and relative adrenal weights compared to the controls. There were no mean ingful differences between the high-dose and

control animals in mean absolute and relative heart, lung, pituitary, t hyroid/parathyroid and epididymides weights. The mean absolute a nd relative liver weights of high-dose males and females were greater than contro ls (15.6% and 31.4% respectively). These changes, in the absence of histopathological findings were considered a result of poor nutri tional 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 fema les in mean heart, lu ng, spleen, adrenal, pituitary, thyroid/parathyroi d and ovary weights.

The gross necropsy findings in two high-dose male s (pale areas of the stomach) were correlated with gastric epithe lial hyperplasia and hyperker atosis which are generally in response to direct gastric irritation or oral gavage procedure and is a protective re sponse mounted to preserve the integrity of the mucosal barrier.

There were no microscopic correlates for the gr oss findings observed in the mid- and high-dose groups pertaining to the intestin es 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 cons idered incidental and unrelate d to administration of PSOA.

Histopathologic lesions considered related to th e administration of PSOA were confined to the stomach (glandular and non-glandular areas ) and included epithe lial hyperplasia and hyperkeratosis of the non-glandu lar portion, as well as chronic ac tive inflammation and edema of both the glandular and non-glandular regions. In four instances, fo cal 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 consider ed incidental and unrelated to

administration of PSOA.

All other microscopic findings observed were co nsidered incidental, of the nature commonly observe in this strain and age of rats and/or were of similar inci dence and severity in the control

animals as well as the treated animals. Theref ore, 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 e ffects were diarrhea associated with staining and matting, decreased food consumption and body weight loss. At necropsy/histopathology, focal erosion, edema, inflammation, hyperkeratosis an d hyperplasia were observed in the stomach.

At the mid-dose (300 mg/kg/day) nine of 10 anim als survived and clinic al observations were associated primarily with gastro-intestinal irri tation and distress. Sustained body weight gains were observed among all the surviving animals. Increased reticulocyte counts, and changes in Alanine Aminotransferase, Aspart ate Aminotransferase and Alkalin e Phosphatase values in the absence of any gross or histopathol ogic liver findings were consid ered 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 mo rtality. The clinical pathology, body weight and organ weight results are similar to those of the vehicl e control group. The gr oss necropsy findings

were incidental and unrelated to administration of PSOA.Page 13 of 24 Table 4. Summary of Toxico logical 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 to xicity studies with PSOA.

Neurotoxicity

A neurotoxicity study was not conducted with PSOA. However, detailed functional observations were made among the parameters measured in th e 28-day subchronic oral feeding study. There were no PSOA related changes in any of th e 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 c onsidered 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 deve lopmental/reproduction toxicity st udy. There were no adverse effects noted at 50 mg/kg bw/day – it was the hi ghest 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 test ed due to highly irritati ng 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 co mpleteness of the data base 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 applyi ng 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 ir ritating 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 qualita tive assessment, the Agency did not use safety factors for assessing risk, and no additional safe ty factor is needed for assessing risk to

infants and children.

Taking into consideration the av ailable information, EPA conclude s that the additional 1X FQPA safety factor will be retained.

VI. EXPOSURE

A. Dietary Exposure

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

contacted a surface treated with an antimicrobial solution that contained PSOA as an inert ingredient. In order to estim ate possible exposure from food that has contacted a treated surface, the Agency uses the Food and Drug Administ ration (FDA) Food Contact Surface Sanitizing Solution Dietary Exposure Assessment Mode l (FDA/CFSAN OPA: Chemistry Guidance – Sanitizing Solution version 1.1; January 1993; O ffice 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 pp m) and adjusted for body weight according to current OPP policy. The results are summarized as follows:

EDI = (1 mg/cm 2 )(250 ug PSOA/1000 mg)(4000 cm 2 /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 a ssessment 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 th is document to refer to non-occupational, non-dietary exposure. Howeve r, in the particular request to use PSOA, residential exposure is not expected. The reque sted use is for “clean in place” methods of application. The requested sites of application ar e: “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 us e patterns and occupationa l exposure. Based upon the requested use, the Agency believes worker ex posure may well be chronic in nature i.e., daily exposure in the normal course of food and dairy pr ocessing. The requested end-use dilution is 250 ppm however it is presumed that occupationally exposed individua ls would be exposed to higher concentrations during the preparat ion of final dilutions. For app lications that might be employed while “flushing systems”, workers may be expose d to larger volumes of more concentrated material. Lacking more specific information, th e Agency cannot assess possible corrosive skin irritation that might result from higher volume a pplications/uses These factors were not described and the Agency does not possess these kinds of data and is therefore not ab le to estimate exposure and risk to possible hi gher volume uses.

For smaller volume applications th ere 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 Di methyl 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 dish es, 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 fo r a mixer/loader/applic ator 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 additionPage 16 of 24 to a single layer of work clot hing (long-sleeved shirt, long pant s, 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 ar e 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 * quan tity 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 sma ll quantities of material estimat ed to have been applied.

Table 5.0 Worker Exposure/Risk (single laye r 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 take s into account exposure estimates from chronic dietary consumption of food and drinking wa ter. EPA has concluded that the aggregated food and water exposures result in aggregate MO Es > 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 pl us chronic exposure to food and water (considered to be a background exposure level). Since the proposed use of PSOA is not ex pected to result inPage 17 of 24 “residential” exposures, there ar e 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 e xposure 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 th at, when considering whether to establish, modify, or revoke a tolerance, the Agency consider “available info rmation” concerning the cumulative effects of a particular pesticide's residues and “other substanc es 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 w ith other substances. For information regarding

EPA's efforts to determine which chemicals have a common mechanism of toxi city 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 (LC 50 ) 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 LC 50 = 0.75 mg/L (highly toxic) Daphnia magna 48 hr EC 50 = 3.05 mg/L (moderately toxic); NOEC = 1.28 mg/L

Pseudokirchneriella subcapitata 72 hr EC 50 = Based on growth rate: 5.44 mg/L Based on yield: 2.56 mg/L NOEC = 1.66 mg/LPage 18 of 24 Based upon the study results, PSOA is classified as hi ghly toxic to fresh water fish and moderately

toxic to invertebrates.

The Applicant used the environmental model EPA Suite TM 4.1 to estimate some environmental properties of PSOA. The use and data interpretation for EPI Suite TM are discussed in “ The Use of Structure-Activity Relationships (SAR) in the High Production Volume Chemicals Challenge Program (EPA, 1999). The EPA Suite TM model estimations were ba sed on a hydrated peroxy acid carbon chain length of C18 (i.e., PSOA primary co mponents). 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 ar e not likely to be lipophilic.

log K OW 1.96 not lipophilic vapor pressure 3.43 x 10 -14 mm Hg at 25oC non-volatile photolysis (atm- T 1/2 hr) 3.554 hr degrades in the atmosphere log BCF = 1.85 not expect ed to bioaccumulate log K OC 1.37 (based on log K OW ) indicates lo w soil binding Level III Fugacity Mode ling 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 fi sh. It is moderately toxic to i nvertebrates and plants. In view

of the results of EPI Suite TM modeling results and upon the propos ed use pattern(as a wetting agent or coupler), the use of PSOA is not expected to result in adve rse environmental effects. The proposed use of PSOA is for indoor us e 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 temperat ures experienced in the proposed use pattern, PSOA is expected to rapidly degrade to SOA and hydrogen peroxi de which further degrade rather rapidly.Page 19 of 24 X. ENVIRONMENTAL JUSTICE

Potential areas of environmental ju stice concerns, to the extent possi ble, were considered in this human health risk assessment, in accordance w ith U.S. Executive Order 12898, "Federal Actions

to Address Environmental Just ice in Minority Populations an d Low-Income Populations," http://www.eh.doe.gov/oepa/ guidance/justice/eo12898.pdf ).

As a part of every pesticide risk assessment, OP P 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 ar ound the home that involve pesticide use in a residential setting. Extensive data on food c onsumption patterns are compiled by the USDA under the Continuing Survey of Food Intake by Indivi duals (CSFII) and are used in pesticide risk assessments for all registered food uses of a pestic ide. These data are analyzed and categorized by subgroups based on age, season of the year, ethni c group, and region of the country. Additionally, OPP is able to assess dietary exposure to sma ller, 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 en tering or playing on tr eated areas post-applic ation are evaluated. Further considerations are currently in developm ent as OPP has committed resources and expertise to the development of specialized software and m odels that consider exposure to bystanders and farm workers as well as lifestyle and traditio nal dietary patterns among specific subgroups.

XI. HUMAN STUDIES

This assessment does not rely on an y studies in which human subjec ts 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 disc ussed 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 LD 50 in the rat is 300 mg/kg bw/day. A ccording 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 stud y. The results of the in vitro study show that PSOA is

corrosive to the skin.

A subchronic oral toxicity st udy was conducted (OECD Guidelin e 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 Ef fect 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, w ith and without metabolic activation. In the in vitro chromosome aberration study us ing human lymphocytes, PSOA wa s positive with and without metabolic activation. However, the in vivo micronucleus assay in ra ts was negative.

A developmental toxicity study with PSOA (purity 100%) was conduc ted with pregnant SpragueDawley rats (24 animals/dose group) (Laidlaw 2013). Neither matern al nor developmental toxicity was observed at 50 mg/kg/day, th e 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 irrita tion effects at the mid and high doses . The study confirmed findings from

earlier studies with maximum dos es of 50 mg/kg/day thus elimin ating data gaps originally identified by the Agency.

There are no known chronic to xicity studies with PSOA.

A neurotoxicity study was not conducted with PSOA. However, detailed functional observations were made among the parameters measured in th e 28-day subchronic oral feeding study. There were no PSOA related changes in any of th e parameters measured, including functional

observations. No evidence of neurotoxicity was observed.

For risk assessment purposes, the to xicological endpoint of concern is 50 mg/kg bw/day which is based on the reproduction/developmental study a nd the repeat dose subchronic toxicity study, no toxicological effects of statis tical significance were observed up to 50 mg/kg bw/day, which was the highest dose tested in those studies. As a re sult of the recently received confirmatory data in the 14-day repeated dose oral toxicity study, no additional safe ty factor is needed. EPA has determined that the available data is adequa te to assess the safety of infants and children.

The request for use is limited to “use on food cont act surfaces in public eating places, as well as dairy processing equipment and food processing e quipment 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 possibi lity of dietary exposur e as a result of postapplication residue on treated food handling su rfaces. The request is not to use PSOA on agricultural crops or otherwis e in residential settings.

The Agency used the U.S. Food and Drug Admini stration (FDA) Food Contact Surface Sanitizing Solution Dietary Exposure Assessment Model to estim ate 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 re sidues 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 Sulf onated 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 ex ceed 250 ppm when applied in antimicrobial sanitizing agents to “use on f ood contact surfaces in public eat ing places, as well as dairy processing equipment and food processing equipm ent and utensils” as described under 40 CFR 180.940(a).Page 22 of 24 ATTACHMENT



### FDA Food Contact Surface Sanitizi ng Solution Dietary Exposure

Assessment Model

(FDA/CFSAN OPA: Chemistry Guidance – San itizing Solutions “Sanitizing Solutions: Chemistry Guidelines for Food Additive Petitio ns” version 1.1; January 1993; Office of Premarket Approval now Office of Food Additive Safety).

EDI (mg/day) = (1 mg/cm 2 )(250 ug PSOA/1000 mg)(4000 cm 2 /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/cm 2 )

SA = Surface area of the treated surface wh ich comes into contact with food (cm 2 ) 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 Surfa ce Sanitizing Solution Dietary Exposure

Assessment

Parameter Value

Rationale

Residual Solution on

Surface 1 mg/cm 2 FDA assumption

Area of Treated Surface 4,000 cm 2 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 31Page 23 of 24 REFERENCES

Head, T. 2013. MRID 49295001. Technical Memorandum Toxico logy Assessment for Peroxy Sulfonated Oleic Acid: SAR, End-point Dose Selection, and De rmal 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 No rth 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 a nd 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 fo r 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. Pa ul, MN 55102. 25 SEP 14 u npublished report.Page 24 of 24