Page 2 of 38

8E7362 and 8E7363; 2 - (2’ - hydroxy - 3’, 5’ - di - tert - amylphenyl) benzotriazole (CAS Reg. No. 25973 - 55 - 1) and Phenol, 2 - (2H - benzotriazole - 2 - yl) - 6 - dodecyl - 4 - methyl (CAS Reg. No. 23328 - 53 - 2) ). Much of the current document discussion is taken from the Agency’s 14 July 2010 assessment. CAS Reg. No. 25973 - 55 - 1 and CAS Reg. No. 23328 - 53 - 2 are currently used as packaging stabilizers (preventing UV light from y ellowing or hardening product packages). They are also used in paints and coatings. In addition, the Food and Drug Administration (FDA), under 21 CFR 175.105, has approved the use of CAS Reg. No. 25973 - 55 - 1 as an indirect food additive for use in food pack aging. Phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2) is classified among the phenolic benzotriazole (PBTZ) class of chemicals. The PBTZ class of chemicals consists of mono and di - substituted phenolic derivatives of 1,2, 3 - benzotriazole. Data have been published regarding a number of PBTZ chemicals regarding chemical properties, mammalian toxicity and environmental fate and effects. There are five compounds which are structurally and toxicologically similar to phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - . They are: 1) drometrizole (Tinuvin ® P; CAS Reg. No. 2440 - 22 - 4); 2 - (2’ - hydroxy - 5’ - methylphenyl benzotriazole 2) octrizole (UV 329; CAS Reg. No. 3147 - 75 - 9); 2 - (2’ - hydroxy - 5’ - octylphenyl benzotriazole 3) HDBB (CAS Reg. No. 3846 - 71 - 1); phenol, 2 - (2H - benzotriazol - 2 - yl) - 4,6 - bis(1,1 - dimethyl) - 4) 4) Tinuvin ® 234 (CAS Reg. No. 70321 - 86 - 7); 2 - (2H - benzotriazole - 2 - yl - 4,6 - bis(1 - methyl - 1 - phenylethyl) phenol and 5) Tinuvin ® 328 (CAS reg. No. 25973 - 55 - 1); 2 - (2’ - hydrox y - 3’,5’ - di - t - amylphenyl)benzotriazole. Acute studies revealed low acute toxicity with an oral LD 50 >2325 mg/kg based on the highest dose tested. Acute inhalation, acute dermal toxicity, skin and eye irritation and skin sensitization studies have not been conducted on either of the chemicals contained in this petition; however, evidence does exist for structurally similar chemicals contained within the High Production Volume ( HPV ) document. Acute inhalation and dermal studies resulted in LC 50 >1420 mg/m 3 an d LD 50 >2000 mg/kg, respectively. Skin irritation studies on rats and mice showed n o local irritation and no systemic toxicity. The Agency concluded in the HPV document that CAS Reg. No. 2440 - 22 - 4 was slightly irritating to rabbit eyes. The document states that CAS Reg. No. 2440 - 22 - 4, in skin sensitization studies on guinea pigs, showed skin sensitization; however, studies conducted on humans showed no sensitization. In a 90 - day study Wistar rats were given the test substance via their diet at 100, 200, 4 00, 800, or 1600 ppm ( approximately 5, 10, 20, 40, or 80 mg/kg/day ). Decreased hemoglobin and packed cell volume were seen in males administered ≥~20mg/kg/day and increases in glucose - 6 - phosphatase activity was noted at all dietary concentrations; however , these values were within the normal range of variability and therefore, are not considered to be of toxicological significance. Liver, kidney, spleen, and testes weights were increased in higher exposure groups with an indication of increased thyroid wei ghts. Increases in testes weights were seen at ~20, ~40, and ~80 mg/kg/day; however, the testes weights were reported as testes weight per 100g body weight. The increase in testes weight may be caused by the decreased body weight and not a toxicologically significantPage 3 of 38

finding. Reproductive organs were not evaluated microscopically. The primary target organ was the liver which showed a greenish - drab discoloration in males and females at higher exposure levels. “Microscopic examination revealed foci of necrosi s and slight proliferation of bile duct epithelia.”(HPV, 2009) Enlargement of the parenchymal cells was also observed. Tubular necrosis was reported in the kidney of some males in the higher does groups. A treatment related yellowish brown pigmentation was seen in the cytoplasm of the proximal tub u lar cells of females. No mortality was observed. The NOAEL of 20 mg/kg/day is based on blood, liver, and kidney effects seen at the LOAEL of 40 mg/kg/day. In a 90 - day dog study male and female Beagles were admi nistered 0, 15, 30, 60, 120, or 240 mg/kg/day through their diet. Animals in the high - dose group showed decreases in body weight and food consumption. Males were more sensitive than females with mortality of one male dog in the highest dose group. Anemia a nd slight changes in blood chemistry parameters including increased serum bilirubin levels and gamma glutamyl transpeptidase (GTP), glutamyl oxalacetic transaminasae (GOT) and alkaline phosphatase activity were noted in the animals from the two highest dos e groups. Males from these groups showed decreases in testes, prostrate, and epididymal weights and females showed deceases in body weight and uterus weight in the three highest dose groups. In higher dose groups, some animals showed atrophy of uterus , abn ormal spermiogenesis, and atrophy of the prostate. The liver was reported to be the primary target organ for toxicity. Although the full study was not available, the submission summary for the HPV program states that at treatment levels of 60, 120, and 240 mg/kg/day, reduced food consumption and body weights were seen. In addition, histopathologic effects were noted in the liver, kidney, and testes of the 3 highest dose groups (details not provided). Increased liver weights associated with liver damage incl uding icterus (jaundice) were observed upon gross and histopathological examination in a few dogs in the 120 and 240 mg/kg/day dose groups. Microscopically, fatty degeneration of hepatocytes, presence of protein globules in the cytoplasm, Kupffer cell hyp erplasia and centrilobular choleostatis were seen. (HPV) The NOAEL for this study is 30 mg/kg/day based on body weight, liver, and kidney effects seen at the LOAEL of 60 mg/kg/day. Developmental studies have been conducted on two structurally similar che micals. In one study rats and mice received the test substance containing CAS Reg. No. 2440 - 22 - 4 on days 6 - 15 of gestation. No maternal toxicity was evident and the rates of implantation and embryotoxicity were not affected by treatment. No teratogenic eff ects were observed however, the study did not specify what developmental endpoints were examined. The NOAEL for maternal and developmental toxicity was 1000 mg/kg/day (highest dose tested). A second developmental rat study showed no maternal toxicity at a ny dose tested for CAS Reg. No. 70321 - 86 - 7 on gestation days 6 - 15. A significant reduction in fetal body weight and an increased delay of skeletal maturation was observed in the 1000 mg/kg dose group. However, there were no similar effects in the high dose group indicating that these effects may be “incidental”. An omphalocele was seen in one fetus in the high dose group. The maternal toxicity NOAEL was 3000 mg/kg/day (highest dose tested). A developmental toxicity NOAEL of 1000 mg/kg/day was chosen based on the omphalocele seen at the LOAEL of 3000 mg/kg/day. All genetic toxicity tests ( in vitro and in vivo ) conducted on the chemicals assessed in the HPV document indicated that this group of chemicals are not mutagenic and will not undergoPage 4 of 38

chromosomal abe rrations. A 104 week feeding study administered up to 142 mg/kg/day to rats did not find evidence of carcinogenicity. The Agency does not believe that CAS Reg. No. 25973 - 55 - 1 and CAS Reg. No. 23328 - 53 - 2 will be carcinogenic in humans. No clinical signs of neurotoxicity were seen in any of the repeat dose studies. After evaluating the available data and the expected exposure from the intended use pattern of this inert ingredient, the Agency does not feel that CAS Reg. No. 25973 - 55 - 1 and CAS Reg. No. 23328 - 53 - 2 will cause neurotoxicity. A combined repeated dose toxicity study with the reproduction/developmental toxicity screening test (OECD 422) was conducted using drometrizole (CAS Reg. No. 2440 - 22 - 4). Male and female Crl:CD(SD) rats (12/sex/group) were adm inistered drometrizole by gavage at dose levels of 0, 30, 100 or 300 mg/kg/day in olive oil. An additional group of 5 rats/sex were placed on test for the control and high dose group as recovery animals (15 days). Males were administered the test material for 42 days and females from 14 days prior to mating to d 4 of lactation. Offspring were terminated on PND 4. Mortality was unaffected by treatment and no clinical signs of toxicity were observed. No treatment - related effects were observed on body wei ghts, food consumption, reflex/reaction, grip strength, locomoter activity, hematology parameters or reproductive parameters. The reproductive/developmental toxicity NOAEL was the highest dose tested at 300 mg/kg/day . The NOEL in males was considered to be < 30 mg/kg/day based on increased relative liver weights observed in all dose groups and 30 mg/kg/day based on effects on liver and kidney weights and kidney histopathology. The NOAEL was concluded to be 300 mg/kg/day for males and 30 mg/kg/day for fe males based on kidney lesions. In an extended one - generation oral reproduction study (OECD Test Guideline 443) with the rat (MRID 49358004), the no - observed - effect - level (NOAEL) for phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - for parental and r eproductive toxicity was 10000 ppm (equal to 618 mg/kg/day, the highest dose tested). The NOAEL for offspring toxicity was 5000 ppm (equal to 311 mg/kg/day) based on decreased body weight, and body weight gain, increased absolute spleen weights in males an d increased incidence of splenic extramedullary hematopoiesis in males observed in pups at the LOAEL of 10000 ppm (equal to 618 mg/kg/day). The data from the combined repeated dose toxicity study allow the Agency to remove the additional 10X uncertainty f actor originally applied due to data gaps. Based on the discussion summarized above, Margins of Exposure > 100 based upon conservative (protective) assumptions, the Agency approves the use of phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl (CAS Reg. N o. 23328 - 53 - 2) as an inert ingredient used in pesticide formulations under 40 CFR § 180.920 on agricultural crops at a maximum end - use concentration not to exceed 10 % by weight II. BACKGROUND The U.S. Environmental Protection Agency (EPA or “the Agenc y”) received a request (Pesticide Petition IN - 10704 ; 9 April 2014) from Pyxis Regulatory Consulting, Inc. (4110 136 th St., N.W., Gig Harbor, WA 98332) on behalf of Loveland Products, Inc. (3005 Rocky Mountain Ave., Loveland, CO 80538) to amend the exempti on from the requirement of a tolerance of phenol, 2 -Page 5 of 38

(2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2) to allow for its use under 40 CFR § 180.920 at a maximum of 10% (0.10) in final pesticide formulations applied to growing crops. . Phe nol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - is used as an ultraviolet (UV) stabilizer in pesticide formulations. The current tolerance exemption for 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - is for use at a maximum of 0.6% on adzuki beans, canola , chickpeas, cotton, fava beans, field peas, lentils, linola, linseed, lucerne, lupins, mung beans, navy beans, pigeon peas, safflower, sunflower and vetch. On 14 July 2010, the Agency previously assessed the use of phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dod ecyl - 4 - methyl - (Memorandum, D. Sunderland, Decision Document for Petition Numbers 8E7362 and 8E7363; 2 - (2’ - hydroxy - 3’, 5’ - di - tert - amylphenyl) benzotriazole (CAS Reg. No. 25973 - 55 - 1) and Phenol, 2 - (2H - benzotriazole - 2 - yl) - 6 - dodecyl - 4 - methyl (CAS Reg. No. 2 3328 - 53 - 2) ). Portions of the current document are taken from the Agency’s 14 July 2010 assessment. Phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - was originally approved for use under 40 CFR § 180. 9 20 at a maximum of 0.6% on adzuki beans, canola, c hickpeas, cotton, fava beans, field peas, lentils, linola, linseed, lucerne, lupins, mung beans, navy beans, pigeon peas, safflower, sunflower and vetch. The Agency’s existing regulatory decision regarding phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl 4 - me thyl - includes use of a 10X uncertainty factor ( U F) as required by the Food Quality Protection Act (FQPA) due to what was viewed as an incomplete data base d on the lack of a ny reproduction toxicity data . In its request to remove the FQPA 10X SF and to i ncrease the maximum permitted concentration in formulated pesticide products, the petitioner has submitted an extended one generation reproduction study using the rat in addition to other data not previously considered by the Agency. Phenol, 2 - (2H - benzotr iazol - 2 - yl) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2) is classified among the phenolic benzotriazole (PBTZ) class of chemicals. The PBTZ class of chemicals consists of mono and di - substituted phenolic derivatives of 1,2,3 - benzotriazole. Data have bee n published regarding a number of PBTZ chemicals regarding chemical properties, mammalian toxicity and environmental fate and effects. There are five compounds which are structurally and toxicologically similar to p henol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecy l - 4 - methyl - . They are: 1) drometrizole ( Tinuvin ® P; CAS Reg. No. 2440 - 22 - 4) ; 2 - (2’ - hydroxy - 5’ - methylphenyl benzotriazole 2) octrizole ( UV 329; CAS Reg. No. 3147 - 75 - 9) ; 2 - (2’ - hydroxy - 5’ - octylphenyl benzotriazole 3) HDBB (CAS Reg. No. 3846 - 71 - 1); phe nol, 2 - (2H - benzotriazol - 2 - yl) - 4,6 - bis(1,1 - dimethyl) - 4) 4) Tinuvin ® 234 (CAS Reg. No. 70321 - 86 - 7) ; 2 - (2H - benzotriazole - 2 - yl - 4,6 - bis(1 - methyl - 1 - phenylethyl) phenol and 5) Tinuvin ® 328 (CAS reg. No. 25973 - 55 - 1) ; 2 - (2’ - hydroxy - 3’,5’ - di - t - amylphenyl)benzotr iazole . III. PHYSICAL/CHEMICAL PROPERTIES (Taken from MRID 49358001) Molecular Weight........................................393.57 Molecular Formula.......................................C 24 H 35 N 3 O Color........................................................YellowPage 6 of 38

Physical State..............................................Liquid Odor.........................................................Faint Odor pH... .........................................................5.4 Melting Point............................................... - 54°C Boiling Point...............................................174°C Density at 25°C............................................1.003 gm/cm 3 Octanol/water partition coefficient (K OW )............ .. log P = 8.9 @ 20 - 25°C Water solubility............................................<0.0003 mg/L @ 20°C Vapor Pressure.............................................0.1 hPa @ 20°C

Molecular Structure (Taken from www.chemblink.com ) Also known a s: Tinuvin 571 UV 571 2 - (2H - benzotrialzol - 2 - yl) - 6 - dodecyl - 4 - methyl phenol benzotriazolyl docecyl

– cresol (linear) 2 - (3’ - dodecyl - 2’ - hydroxy - 5’ - methylphenyl)benzotriazole 2 - (3’ - dodecyl - 5’ - methyl - 2’ - hydroxyphenyl)benzotriaole IV. HAZARD CHARACTERIZATION Muc h of the discussion of the toxicological profile is taken from MRID 49358002 as well as the Agency’s 2010 assessment cited earlier . The EPA has previously considered phenol, 2 - (2H benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - ( CAS Reg. No. 23328 - 53 - 2 ) in Petitio n Numbers 8E7362 and 8E7363. In addition to the available, previously reviewed data, the petitioner has submitted additional , new data/information not reviewed by the Agency as well as an extended, one generation reproduction study. Acute Oral Toxicity ( Rat) An acute oral toxicity study on phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - is not available. Acute oral toxicity studies are available on drometrizole, octrizole, Tinuvin 328 and Tinuvin 234. The acute oral toxicities of these compounds r anges from an LD 50 of < 1000 mg/kg for octrizole to >10000 mg/kg for d ro metrizole. Acute Dermal Toxicity (Rabbit)Page 7 of 38

An acute dermal toxicity study is not available for phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - . However, the acute dermal toxicit y of Tinuvin 234 has been studied and the LD 50 is >2000 mg/kg. Acute Inhalation Toxicity ( Rat ) An acute inhalation toxicity study is not available for phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl 4 - methyl - . However the acute inhalation LC 50 for drometrizo le is >1420 mg/cm 3 or 1.42 mg/L. Acute Eye Irritation (Rabbit ) Drometrizole was considered minimally irritating to the eyes of 2/6 rabbits at a dose of 100 mg/eye. Acute Dermal Irritation (Rats and Mice) Drometrizole did not cause any dermal irritatio n when applied to rats and mice at doses of 5% to 0.4 cm 2 (rat) and 0.1 cm 2 (mouse). Dermal Sensitization (Guinea pigs) Thirty per cent drometrizole in Vas e line was used in the induction phase and 20 % in Vas e line was used in the challenge phase of the t est. At the 48 hr time point, 90% of the animals had positive reactions to the challenge. Drometrizole was considered to be a strong dermal sensitizer. Tinuvin P was tested using the mouse local lymph node assay. Tinuvin P did not cause an increase in the stimulation index in any test group and was considered to be negative in the assay. REPEAT DOSE TOXICITY In a 28 - day oral toxicity study MR Wistar rats (5/sex/group) were administered octrizole (CAS Reg. No. 3147 - 75 - 9) in the diet at 0, 1.2, 2.5 or 5 % (corresponding to 0, 1.286, 2.594 or 5.658 mg/kg/day respectively) according to OPPTS Guideline 870.3050; MRID 49358002). Body weights and food consumption were recorded. Gross necropsy was performed and apparently some histopathology performed on som e organs. There were no deaths nor clinical signs of toxicity. Body weights and food consumption were not affected by the treatment. Hydronephrosis was noted in 3 control and 4 high dose rats

– a finding common with this strain. There were no treatment related lesions. The no observed adverse effect level ( NOAEL ) was determined to be 5658 mg/kg/day. In a 90 - day oral toxicity study (OPPTS 870.3050; MRID 49359002) with Wistar - derived rats, animals were administered drometrizole (CAS Reg. No. 2440 - 22 - 4) in the diet at levels of 0, 0.2, 1.0 and 5.0% (equivalent to 0, 100, 500 or 2500 mg/kg/day, respectively) for 14 weeks. Body weight was recorded weekly and food consumption was determined weekly during the first 4 weeks of the study and then in the 11 th and 12 th week of the study. Blood was collected at week 13 for hematological evaluation. Rats were sacrificed at 14 weeks and gross necropsy conducted.Page 8 of 38

Organ weights were recorded for the liver, kidney, spleen, heart, brain, testes, ovary, adrenal, thyr oid, pituitary and thymus. There were no significant effects on food consumption. Erythrocyte counts were statistically decreased and leucocyte counts statistically increased in males at the high dose. Statistical differences in relative organ weights w ere noted as follows: liver weights were increased in both sexes at the mid and high dose; kidney weight was increased in both sexes at the high dose; testes weights were decrease at the mid and high dose; spleen weights were increase at the high dose in females; and adrenal weights were increase at the mid and high dose in females. An increased incidence and severity of nephropathy was observed in male rats at the mid and high dose. Two males in the high dose group had liver changes consisting of bile d uct proliferation, an increase in the number of Kupffer cells, extended sinusoid and often enlarged parenchymal cells with irregular nuclei. A slight increase in l y mphatic tissue in the sp l een was observed. No other treatment - related microscopic lesions were observed. The no observed adverse effect level (NOAEL) was determined to be at the 0.2% level of the diet or approximately 100 mg/kg/day based on the effects on body weights, hematology parameters, liver weights and kidney histopathology observed at the mid and high doses. In a 90 - day oral toxicity study using Tinuvin 328 (CAS Reg. No. 25973 - 55 - 1) , Wistar - derived rats (10/sex/group) were administered dietary dose levels of 0, 100, 200, 400, 800 or 1600 ppm (approximately 0, 5, 10, 20, 40 or 80 mg/k g/day respectively) for 90 days. Body weights were recorded weekly and food consumption was determined per gr o up in the first four weeks and in the 11 th and 12 th weeks. Blood was drawn to evaluate hematological parameters at week 12. The following organ s were weighed: heart, liver, kidney, spleen, brain, testes/ovary, thymus, pituitary, thyroid an adrenal. Glucose - 6 - phosphatase activity was determined in the liver. Histopathology was performed on the liver and kidney. Body weights were statistically de creased in males at 1600 ppm throughout the study and in females at the 2 - week time period. Food consumption and food efficiency were decreased in males at 1600 ppm. Percentage packed cell volume was statistically decreased at ≥ 200 ppm in males and in f emales at 800 and 1600 ppm. Hemoglobin levels were decreased or statistically decreased at ≥ 400 ppm in males and at 800 and 1600 ppm in females. Liver glucose - 6 - phosphatase activity was increased in males at the lower dose, but not at the high dose leve ls. Statistical significance was not indicated. Liver weights were statistically increased in males and females at 100 and 400 ppm and kidney weights were statistically increased in females at 1600 ppm in the subgroup of rats treated for 4 weeks. In the rats sacrificed after 90 days of treatment, liver weights were statistically increased in both sexes at al l dose levels tested and kidney weight were statistically decreased in both sexes at ≥ 400 ppm. In the 4 - week subgroup rats, microscopic examination of the liver revealed very enlarged parenchymal cells in the 400 ppm group and slightly enlarged parenchym al cells at 100 ppm. No microscopic findings were observed in the kidneys. In the rats in the 90 - day group, foci of necrosis and extremely enlarged parenchymal cells in males and in a smaller number of females in the 800 and 1600 ppm groups. There was a slight proliferation of the bile duct. These findings occurred to a lesser extent in the lower dose groups . Foci of necrosis w e re absent in males at doses below 800 ppm and occurred incidentally in females. Parenchymal cells were enlarged at the lower dose levels. The no observed effect level (NOEL) was considered to be < 100 ppm and the NOAEL was considered to be 100 ppm (about 20 mg/kg/day) based on increased liver weights and microscopic findings in the liver.Page 9 of 38

A 90 - day oral toxicity study was condu cted using Tif:RAif(SPF) rats (20/sex/group). Test animals were administered Tinuvin 234 (CAS Reg. No. 70321 - 86 - 7) (according to OPPTS Guideline 870.3100) in the diet at dose levels of 0, 50, 300, 2000 and 10000 ppm for 92 to 94 days. The dose levels cor respond to 0, 2.5, 15, 100 and 500 mg/kg/day respectively. Body weights and hematology, clinical chemistry and urinalysis parameters were unaffected by treatment. No treatment - related ophthalmic or gross macroscopic findings were observed. Mean absolute and relative (to body and brain weights) liver weights were statistically increased i n both sexes at ≥ 300 ppm. Slight to moderate hypertrophy and or cytoplasmic vacuolization of hepatocytes were observed in both sexes ≥ 300 ppm. Based upon findings in the liver at 300 ppm (about 15 mg/kg/day), the NOAEL was considered to be 50 ppm or ab out 2.5 mg/kg/day. A 17 - day oral toxicity study was conducted using HDBB (UV 320) (CAS Reg. No. 3846 - 71 - 1) administered by gavage in corn oil to preweanling Crl:CD(SD) rats at dose levels of 0, 0.1, 0.5, 2.5 or 12.5 mg/kg/day from post - natal days ( PND ) 4 to 21 . Dams were observed daily for clinical signs of toxicity and body weights were recorded on days 0, 10 and 20 of pregnancy and on days 0, 10, 20 and 22 after delivery. All pups were observed daily before and three to four hours after dosing for clini cal signs of toxicity. Body weights were recorded on PBD 0, 4, 6, 8, 10, 12, 16, 18, 21 and 22. On PND 22 blood was collected from two male and two female pups per litter. Plasma was evaluated for clinical chemistry parameters. At necropsy, th4e heart , lung, liver, spleen, kidney and adrenals were weighed. The liver and heart were examined microscopically. No treatment - related mortality, clinical signs of toxicity or effects on body weight were observed. In male and female pups, albumin , aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels were statistically increased at the high dose. Statistically increased blood urea nitrogen (BUN) levels in males and lactate dehydrogenase (LDH) in females were observed at the high dose. In m ale and female pups, liver weights (absolute and relative) were statistically increased and spleen weights were statistically decreased. The effects on spleen and adrenal weights were not correlated to any histopathologic findings. In the liver, an incre ased incidence of nucleolar enlargement in hepatocytes, hepatocellular anisokaryosis, hepatocellular hypertrophy, hepatocellular eosinophilic granular change and decrease hepatocellar glycogen were seen. The NOEL was 0.5 mg/kg/day based on increase relati ve liver weigh t s in male and female pups observed at 2.5 mg/kg/day. The NOAEL was 2.5mg/kg/day in male and female pups based on liver pathology observed at 12.5 mg/kg/day. In a 28 - day oral toxicity study (OPPTS 870.3100) HDBB (CAS Reg. No. 3846 - 71 - 1) w as administered in corn oil by gavage to Crj:CD (SD)IGS rats (10/sex/group for controls and high dose and 5/sex in the other groups). Daily dose levels were 0 (corn oil), 0.5, 2.5, 12.5, and 62.6 mg/kg/day for 28 days. Five rats/sex/group were sacrificed after the last dose for assessment of hematology and blood biochemi s try parameters, organ weights and macroscopic and microscopic pathology. The remaining 5 rats/sex/group were maintained on the control diet for a 14 - day recovery period. Animals were ob served for clinical signs of toxicity at 1 and 4 hours after dosing. Body weights and food consumption were recorded weekly. Urine was collected for analysis o day 25 of the dosing period and on day 11 of the recovery period. Blood was collected for eva luation of hematology and clinical chemistry parameters prior to necropsy. Selected organs were weighed and microscopic examination of a full set of tissues/ organs were examined in thePage 10 of 38

control and high dose groups. The liver, heart, kidneys, spleen and t hyroid of the mid and low dose groups were also examined microscopically. No mortality or clinical signs were observed. Body weights, food consumption and urinalysis parameters were unaffected by treatment. A significant decrease in red blood cells (RBC s) hematocrit and hemoglobin was observed at doses of ≥ 2.5 mg/kg/day in males, but not females. Fibrinogen levels were statistically decreased at doses of ≥ 2.5 mg/kg/day in males and at the high dose in females. A statistically significant increase in the A/G ratio at ≥ 0.5 mg/kg/day, glucose at ≥ 2.5 mg/kg/day , albumin, ALT and ALP at ≥ 12.5 mg/kg/day and BUN and AST at the high dose in males. In females, a statistically significant increase in glucose, A/G ratio, total cholesterol, triglycerides and ALT was observed at the high dose only. Relative liver weights were statistically increase in males at all dose levels, while absolute liver weights were statistically increased at ≥ 12.5 mg/kg/day. Absolute kidney weights were increased in male and fem ales in the high dose and relative weight at the high dose in males only. Microscopically, an increased incidence of hypertrophy of hepatocytes at ≥ 2.5 mg/kg/day, bile duct proliferation at 12.5 and 62. 6 mg/kg/day, vacuolar degeneration of hepatocytes at ≥ 2.5 mg/kg/day and of focal necrosis and increased mitosis of hepatocytes were seen in males at the high dose. Further, males had an increased incidence of cell infiltration in the heart (≥ 2.5 mg/kg/day ), degeneration of the myocardium (12.5 and 62.6 m g/kg/day), hypertrophy of the myocardium (62.6 mg/kg/day) and hypertrophy of tubular epithelium (62.6 mg/kg/day). In females, an increased incidence of hypertrophy of hepatocytes was observed at 12.5 mg/kg/day and 62.6 mg/kg/day and of degeneration of the myocardium at the high dose only. The NOAEL was determined to by <0.5 mg/kg/day in males and 2.5 mg/kg/day in females based on the increased A/G ratio observed in males at all dose levels and effects on liver weights and liver histopathology in females a t 12.5 mg/kg/day. In a 90 - day oral toxicity study, HDBB (CAS Reg. No. 3846 - 71 - 1) was administered once daily in corn oil by oral gavage to Crj:CD(SD)IGS rats (10/sex/group) at doses of 0 (corn oil), 0.1, 0.5 or 2.5 mg/kg/day (males) and of 0 (corn oil), 0 .5, 2.5 or 12.5 mg/kg/day (females). Body weights and food consumption were recorded weekly. Prior to necropsy, blood was drawn for the evaluation of hematology and clinical chemistry parameters and urine collected for determination of urinalysis paramet ers. Selected organs were weighed and microscopic examination of a full set of tissues/organs were examined in the control and high dose groups. The liver, heart, kidneys, spleen and thyroid of the mid and low dose groups were also examined microscopical ly. No clinical signs of toxicity were observed. Body weight gain was s tatistically decreased in males in the 2.5 mg/kg/day group from study day 36 until the end of the study. In males, the following statistically significant findings were noted on he matology parameters: RBCs were decreased at the high dose; hemoglobin levels were decreased at the mid and h i gh dose; and platelet count was increased at the high dose. In females, hematocrit and mean corpuscular volume (MCV) were statistically decreased and mean cell hemoglobin concentration (MCHC) was statistically increased. A/G ratio was statistically increased in males at 0.5 and 2.4 mg/kg/day and in females at 12.5 mg/kg/day . In males, additional statistical si gnificance was noted in: decreased α 1 and α 2 - globulin and β - globulin levels at the mid and high doe; and increased albumin, ALP, glucose and BUN at the mid and high dose. In females, total protein and albumin levels were statistically increased at the hi gh dose and α 2 - globulin and β - globulin levels were decreased at the high dose. Absolute heart, testes, kidney and brain weights were statistically increased at the high dose malesPage 11 of 38

and absolute liver weights were increased in the mid and high dose. Absolu te liver weights were statistically increased at the high dose females. An increased incidence of centrilobular hypertrophy of hepatocytes w a s observed in mid and high dose males and at the high dose in females. The NOAEL was determined to be 0.1 mg/kg/da y in males and 2.5 mg/kg/day if females based on hematology and clinical chemistry findings, increased liver weights and liver pathology observed in males at 0.5 mg/kg/day and in females at 12.5 mg/kg/day . In a 90 - day oral toxicity study with the dog, d rometrizole (CAS Reg. No. 2440 - 22 - 4) was administered in the feed to beagle dogs (6/sex/group) at dose levels of 0, 1000, 3000 and 10000 ppm ( ~32.9, 98.7 or 329 mg/kg/day respectively) for 13 weeks. One dose/sex/group was fed the control diet for a month to test for recovery. No mortality or clinical signs of toxicity were observed. Body weight gain and food consumption were decreased at 10000 ppm. There were no effects on ophthalmology or auditory perception. Mean levels of alanine aminotransferase at 3000 and 10000 ppm and γ - glutamyl transpeptidase at 10000 ppm were increased. No treatment - related gross or microscopic changes were observed. The NOAEL was determined to be 1000 ppm or 31.75 mg/kg/day in males and 34.6 mg/kg/day in females based on inc reased levels of alanine aminotransferase at 3000 ppm. In a 90 - day oral toxicity study with the dog, Tinuvin 328 (CAS Reg. No. 25973 - 55 - 1) was administered daily in the feed to beagle dogs at dose rates of 15, 30, 60, 120 and 240 mg/kg/day for three month s. Controls consisted of 5 dogs/sex/group and were fed untreated diet. Dogs were examined daily for mortality and clinical signs of toxicity. Food consumption was monitored daily and recorded per week, and body weights were recorded every three days. O phthalmology examinations were conducted on all dogs. Hematology, clinical chemistry and urinalysis parameters were evaluated pretest and monthly after the start of test material administration. Gross necropsy was performed on all dogs and the following organs weights were recorded: brain heart, lung, liver, kidneys, spleen, hyp o physis, thyroid, adrenals, testes, epididymis, prostate and thymus . Selected organs/tissues from all dogs were examined microscopically. One male dog in the high dose group die d during week 8. Mean body weight was decreased in dogs receiving ≥ 60 mg/kg/day . Food consumption was decreased in males at 120 and 240 mg/kg/day and in females at 240 mg/kg/day . No treatment - related ophthalmic findings were observed. A decrease in th e number of erythrocytes, a decrease in packed cell volume and decreased hemoglobin levels were observed in the 120 and 240 mg/kg/day groups. Slight effects were observed in bilirubin levels, and guanosine 5’ - triphosphate (GTP) and glutamic - oxaloacetic tr ansaminase (GOT) and alkaline phosphatase activities. No effects were observed on urinalysis parameters. Enlarged livers were observed with severe liver damage in the 120 and 240 mg/kg/day groups. Microscopic changes in the liver consisted of fatty dege neration of hepatocytes, protein globules in the cytoplasm, Kupffer cell hyperplasia and centrolobular choleostatisis. Kidney effects were observed but there was no clear dose response. In some dogs in the higher dose groups, atrophy of the uterus (≥ 60 mg/kg/day ), abnormal spermiogenesis (240 mg/kg/day ) and atrophy of the prostate (≥ 60 mg/kg/day ) were observed. The NOAEL was considered to be 30 mg/kg/day based on body weight effects and histopathology observed at 60 mg/kg/day .Page 12 of 38

CHRONIC TOXICITY A chro nic toxicity study (OECD Guideline 452) was conducted using Crj: CD (SD) IGS rats. HDBB (CAS Reg. No. 3846 - 71 - 1) was administered in corn oil once daily for 52 weeks by oral gavage at doses of 0 (corn oil), 0.1, 0.5 or 2.5 mg (males) and of 0 (corn oil), 0.5, 2.5 or 12.5 mg/kg/day (females). Animals were observed daily prior to and after dosing for clinical signs of toxicity. Body weight and food consumption were recorded weekly for the first 13 weeks and then every four weeks after that. Prior to necrop sy, blood was drawn for hematology evaluation and clinical chemistry parameters. Urine was collected for urinalysis. Selected organs were weighed and microscopic examination of a full set of tissues/organs in the control and high dose groups. The liver, heart, kidneys, spleen and thyroid of the mid and low dose groups were also examined microscopically. Two males in the 0.1 mg/kg/day group were found dead on days 231 or 357 of the dosing period and one female was moribund on day 354. No clinical sign s of toxicity were observed in males or females. Body weight was decreased in males at the high dose from day 36 to the end of the 52 week study. RBCs were statistically decreased in males at the mid and high dose and hematocrit at the high dose. Platel et count was increased at the high dose. In females, platelet count was increased at the high dose. A/G ratio, albumin levels and ALP activity were statistically increased in males at 0.5 and 2.5 mg/kg/day . The following additional statistically signifi cant findings were noted in males: decreased α 1 and α 2 - globulin levels at the mid and high dose; decreased β - globulin levels at the high dose; and increased BUN at the mid and high dose. In females, albumin levels were statistically increased at the high dose. Absolute pituitary, heart, brain, thyroid, lung, testes, kidney and epididymides w eights were statistically increased in high dose males and absolute liver weighs were increased in the mid and high dose. Absolute liver weights were statistically i ncreased in the high dose females. An increased incidence of centrilobular hypertrophy of hepatocytes was observed in mid and high dose males and at the high dose in females. An increase incidence of lipofuscin deposition in hepatocytes was observed at t he high dose; also altered hepatocellular foci at the mid and high dose and of cystic degeneration of hepatocytes at the high dose in males only. The NOAEL was 0.1 mg/kg/day in males and 2.5 mg/kg/day in females based on hematology and clinical chemistry findings, increased liver weights and liver pathology observed in males at 0.5 mg/kg/day and of hematology findings, increased liver weights and liver pathology in females at 12.5 mg/kg/day . COMBINED CHRONIC TOXICITY/CARCINOGENICITY (Rat) A combined chr onic toxicity/carginogenicity study was conducted using CFY rats ( 50/sex/group). Drometrizole (CAS Reg. No. 2440 - 22 - 4) was administered in the diet for 104 weeks at dose levels of 0, 100, 300, 1000 and 3000 ppm which corresponds to 0, 4 to 6, 14 to 17, 47 to 58 and 142 to 169 mg/kg/day , respectively. Mortality, clinical signs of toxicity, body weight and food consumption were monitored. Hematology and clinical chemistry were evaluated. Body weight gain was statistically decreased in males during the sec ond year of the study and food consumption was statistically decreased in females from study week 53 to week 80 at 3000 ppm. Mortality was slightly increased in male rats at the high dose; however the increase was not statistically significant. A reducti on in blood urea nitrogen was observed at study termination in males of the high dose group. Relative thyroid/parathyroid weights were statistically increasePage 13 of 38

compared to the control group in males at 1000 ppm and females at the 1000 and 3000 ppm groups. No correlating histopathology was observed in the thyroid/parathyroid. No microscopic non neoplastic or neoplastic lesions attributable to treatment were seen. The NOAEL was established at 1000 ppm (47 to 58 mg/kg/day ) based on effects on body weights an d BUN in males at 3000 ppm. Drometrizole was not carcinogenic under the conditions of the study. CARCINOGENICITY (Mouse) A carcinogenicity study (OPPTS 870.4200) was conducted using Tif: MAGf(SPF) mice (50/sex/group). Mice were administered drometrizo le (CAS Reg. No. 2440 - 22 - 4) for 24 months in the diet at dose rates of 0, 5, 50 or 500 ppm which corresponds respectively to 0, 0.8, 6.5 and 64 mg/kg/day in males and 0, 0.8, 6.7 and 62 mg/kg/day in females. Mice were housed 5/cage. Mortality, clinical s igns of toxicity, body weight and food consumption were monitored. No treatment related effects were observed on mortality, clinical signs of toxicity, body weights or food consumption. Liver weight was decreased in males at the 50 ppm group and adrenal weights were slightly increased in treated females. Nor correlating histopathology was observed in those organs. No treatment - related microscopic non neoplastic or neoplastic lesions were seen. The NOAEL was determined to be > 64 mg/kg/day in males and 6 2 mg/kg/day in females. Drometrizole was not carcinogenic to mice under the conditions of the study. GENOTOXICITY A dominant lethal assay study was conducted on NMRI - derived mice (20/group) (OPPTS 870.5450). Male mice were administered a single dose of drometrizole (CAS Reg. No. 2440 - 22 - 4) in aqueous carboxymethyl cellulose by gavage at dose levels of 0, 1000 or 3000 mg/kg. Immediately after treatment each male mouse was placed in a cage with 2 untreated female mice. After one week, the female mice were removed and replaces by two additional females. This was done for 6 weeks. Females were examined daily for the presence of a vaginal plug. The day a plug was observed was designated as gestation day 0. On day 14 of pregnancy, the females were necro psied. The number of live embryos and embryonic deaths were recorded. The uteri were examined for embryonic resorptions. Drometrizole was tested for it s ability to produce dominant lethals in NMRI - derived mice. Mating ratio, the number of implantations and embryonic deaths were unaffected by treatment. Drometrizole was determined to be negative for producing dominant lethals in mice. A somatic mutation assay (non - guideline) was conducted on Chinese hamsters (3/sex/group). Drometrizole (CAS Reg. No. 2440 - 22 - 4) was administered by oral gavage for 2 consecutive days at dose levels of 0, 500, 1000 or 2000 mg/kg. Hamsters were sacrificed 24 hours after the last dose and one marrow was harvested from the shaft of both femura. Bone marrow cells (1000/ani mal) were scored for chromosomal anomalies. The positive control was cyclophosphamide (128 mg/kg). The positive control produced the expected response. Drometrizole was negative for producing chromosomal anomalies in this test. A mammalian bone marrow chromosomal aberration test (OPPTS 870.5385) was conducted using Chinese hamsters . Drometrizole (CAS Reg. No. 2440 - 22 - 4) was administered by gavage for 2 consecutive days at dose levels of 0, 500, 1000 or 2000 mg/kg. A control group consisted ofPage 14 of 38

8 female s and 9 males and was administered the vehicle (2.0% sodium carboxymethyl cellulose). Groups receiving the test material consisted of 8 females and 4 males/group. A group of hamsters (10 females and 9 males) received the positive control, cyclophosphamid e (64 mg/kg). Animals were injected intraperitoneally (i.p.) with colcemide (10 mg/kg) two hours after administration of the second dose. They were sacrificed 4 hours later and bone marrow from 2 females and 2 males/group was harvested. The bone marrow was analyzed for chromosomal aberrations. No chromosomal aberrations were observed in the test groups. The positive control produced the expected positive results. Drometrizole was negative for inducing chromosomal aberrations in this test. A bacterial reverse mutation (Ames) test was conducted (OPPTS 870.5100) on Salmonella sp. The Salmonella strains were TA98, TA100, TA 1535 and TA1537 with and without metabolic activation. Test concentrations were 0, 10, 30, 90, 270 and 810 μg.0.1 ml. No increase in mutation frequency was observed. Drometrizole was considered negative for inducing genetic mutations. A reverse mutation (Ames) test was conducted on Salmonella tester strain TA98 with metabolic activation. Five dose levels (not stated) of drometrizo le (CAS Reg. No. 2440 - 22 - 4) were tested with duplicate plates in two independent assays. The S9 was prepared from the livers of male Sprague - Dawley rats treated with phenobarbital and 5,6 - benzoflavone. The solvent was dimethylsulfoxice (DMSO). No increa se in mutation frequency was observed and under the conditions of this study drometizole was considered negative to induce mutations. Drometrizole (CAS Reg. No. 2440 - 22 - 4) was used in an unscheduled DNA synthesis in mammalian cells in culture test (OP PTS 870.5550). The test material was dissolved in DMSO at concentrations of 0, 11.9, 17.8, 26.7, 40 and 60 μg/ml. The concentrations were selected based on results from a preliminary toxicity range finding study where the threshold for toxicity was deter mined to be between 6.5 and 65 μg/ml. The positive control was 7,12 - dimethylbenzanthracene. Primary cultures of rat hepatocytes were prepared from a male Sprague Dawley rat. Cells were exposed to the test material and incubated with 3 H - thymidine. The c ultures were prepared on coverslip and processed for autoradiography. At least 50 cells from each treatment group (25 cells from each coverslip) were scored and mean grain counts determined. The test concentrations were 0, 2.3, 3.5, 5.3, 7.9, 11.9, 17.8, 26.7, 40 and 60 μg/ml. The 40 and 60 μg/ml concentrations were toxic yielding no cells for evaluation at the highest dose tested. The mean net grain count per nuclei as ≤ 5 for dose levels of ≥ 11.9 μg/ml. The response was dose related. The positive c ontrol produced the expected positive results. Drometrizole was considered to be positive for inducing UDS in primary rat hepatocytes. Octrizole (CAS Reg. No. 3147 - 75 - 9) was used in a bacterial reverse mutation test (OPPTS 870.5100) (OECD Guideline 471). Octrizole was tested in Salmonella typhimurium strains TA 98, TA100, TA1535, and TA1537 and in E. coli WP2uvrA at concentrations of 20.5, 61.7, 185.2, 555.5, 1666.6 and 5000 μg/plate with and without metabolic activation. The solvent was DMSO and approp riate positive controls were used. No increase in the mean number of revertant colonies was observed with any tester strain in the presence or absence of metabolic activation. Positive controls produced the expected results. Octrizole was considered neg ative in the Ames Salmonella test.Page 15 of 38

Tinuvin 328 (CAS Reg. No. 25973 - 55 - 1) was used in a Salmonella microsome mutagenicity test using Salmonella tester strains TA98, TA100, TA1535, and TA 1537 in the presence or absence of metabolic activation at concentrat ions of 25, 75, 225 and 2025 μg/0.1ml. No increase in mutant frequency was observed in the presence or absence of metabolic activation. Tinuvin 328 is considered negative in this study. Tinuvin 328 (CAS Reg. No. 25973 - 55 - 1) was used in a bacterial rever se mutation assay (OPPTS 870.5100) with Salmonella tester strain TA98 with and without metabolic activation. S9 was prepared fro m the livers of male Sprague - Dawley treated with phenobarbital and 5,6 - benzoflavone. Five dose levels (not specified) were use d and the solvent was DMSO. No increase in the frequency of mutations was observed and Tinuvin 328 is considered negative in this study. Tinuvin 234 (CAS Reg. No. 70321 - 86 - 74 ) was used in a nucleus anomaly test on somatic interphase nuclei of Chinese ham ster bone marrow cells. Chinese hamsters (6/sex/group) were administered the test material for two consecutive days by oral gavage at dose levels of 0, 1250, 2500 or 5000 mg/kg. The vehicle was 0.5% carboxymethyl cellulose. Animals were sacrificed 24 ho urs after the last dose and bone marrow was harvested from the shafts of both fem ora. Bone marrow cells (1000/animal) were examined for nuclear anomalies. The positive control was cyclophosphamide (128 mg/kg). The number of single Jolly bodies, fragment s of nuclei in erythrocytes, micronuclei in erythroblasts, micronuclei in leucopoietic cells, bizarre forms of nuclei and polyploidy cells were counted. The results were that the percentage of cells displaying nuclear anomalies did not statistically diffe r from the negative control group. The positive control group produced the expected response. Tinuvin 234 was negative in this test. An in vivo sister chromatid exchange test was conducted using Tinuvin 234 (CAS Reg. No. 70321 - 86 - 74 ). Chinese hamster s (4/sex/group) were administered the test substance once by oral gavage in 0.5% carboxymethyl cellulose at dose levels of 0, 1250, 2500, or 5000 mg/kg. They were injected i.p. with colcemide 22 hours after administration of the test material and were sac rificed 2 hours later. The positive control was 7,12 - dimethylbenzanthracene (100 mg/kg in 0.5 % carboxymethyl cellulose). Bone marrow slides were prepared and examined for sister chromatid exchange. The results were that there was no increase in the incid ence of sister chromatid exchanges occurred in the dosed groups compared to the control. Tinuvin 234 was negative for inducing sister chromatid exchanges in Chinese hamsters. A bacterial reverse mutation test (OPPTS 870.5100) was conducted using Tinuvi n 234 (CAS Reg. No. 70321 - 86 - 74 ). Salmonella typhimurium strains TA98, TA100, TA1535 and TA 1537 were tested at concentrations of 25, 75, 225, 675 and 2025 μ g/plate with and without metabolic activation. The solvent was acetone and positive controls were used. The results were no increase in mutant frequency was observed in the presence or absence of metabolic activation. Tinuvin 234 was negative in this test. An autoradiographic DNA repair test was conducted on rat hepatocytes using Tinuvin 234 (CAS Reg. No. 70321 - 86 - 74 ). The test material was dissolved in acetone at concentrations of 0, 0.4, 2, 10 and 50 μg/ml for the definitive study. The positive control was DMN (100mM). Primary cultures of rat hepatocytes were prepared from a male Tif:Ralf (SP F) rat. Cells werePage 16 of 38

exposed to the test material and incubated with 3 H - thymidine. The cultures were prepared on cover slips and processed for autoradiography. At least 150 cells from each treatment group (50 cells from each coverslip; total of 3 coversli ps) were scored and mean grain counts were determined. Mean nuclear counts ≥ were considered a positive response. There was no increase in the mean number of silver grans per nucleus seen in the cultures of the treated groups. Tinuvin 234 was negative f

or inducing unscheduled DNA synthesis in the primary rat hepatocyte assay. PRENATAL DEVELOPMENTAL TOXICITY Drometrizole (CAS Reg. No. 2440 - 22 - 4) was the test substance in a prenatal developmental toxicity study in the rat. Study methods closely followed OECD Guideline 414 (“Teratogenicity”). Pregnant Sprague - Dawley rats were administered drometrizole by gavage at dose levels of 0 (vehicle; 2% aqueous carboxymethyl cellulose), 150, 500 or 1000 mg/kg/day from gestation days 6 to 15. During the treatment period, clinical signs, weight gain, and food consumption were monitored and recorded daily. Caesarean sections were conducted on gestation day 21. Fetuses were examined for external, visceral and skeletal abnormalities. No maternal toxicity was observe d and there were no effects of treatment o the number of implantations. No embryotoxicity was seen and no teratogenic were observed. The NOAEL for maternal and developmental toxicity was determined to be 1000 mg/kg/day which was the limit dose in this st udy. Drometrizole (CAS Reg. No. 2440 - 22 - 4) was used in a prenatal developmental toxicity study in the mouse. Study methods follow OECD Guideline 414 “Teratogenicity”. Pregnant NMRI derived mice were administered drometrizole by gavage at dose levels of 0 (vehicle control; 2% aqueous carboxymethyl cellulose), 150, 500 and 1000 mg/kg/day from gestation days 6 through 15. During the treatment time, clinical signs, weight gain and food consumption were monitored. Caesarean sections were conducted on gestat ion day 18. Fetuses were examined for external, visceral and skeletal anomalies. No maternal toxicity was observed and there were no treatment related effects on number of implantations. No embryotoxicity was observed and no teratogenic effects were not ed. The NOAEL for maternal and developmental toxicity was determined to be 1000 mg/kg/day , the limit dose of this study. Tinuvin 234 (CAS Reg. No. 70321 - 86 - 74 ) was the test substance in a prenatal developmental toxicity study in the rat (OPPTS 870.370 0). Pregnant Tif: RAIF (SPF) rats were administered the test substance from gestation day 6 to 15 by oral gavage at dose levels of 0, 300, 1000 and 3000 mg/kg/day . The number of pregnant rats/group and vehicle was not specified. During treatment, gener al condition, weight gain, food consumption and clinical signs of toxicity were checked daily. Just prior to parturition, the females were sacrificed and the uteri examined. Live fetuses were weighed, sexed and evaluated for external, visceral and/or ske letal abnormalities. Maternal body and food consumption were comparable to the controls. No embryo or fetal mortality was observed at necropsy. Neither were observed at the high dose. The maternal NOAEL was set at 3000 mg/kg/day and the developmental N OAEL at 10 00 mg/kg/day based on the findings at 3 000 mg/kg/day .Page 17 of 38

REPRODUCTIVE TOXICITY A recently submitted extended one - generation reproduction study with the rat (OECD 443) was conducted using Tinuvin 571 (CAS Reg. No. 23328 - 53 - 2). Wistar rats (25/se x/group) were administered Tinuvin 571 in the diet at dose levels of 0, 2500, 5000 or 10000 ppm. Parental male rats were administered the diets four weeks prior to mating, during mating and during the post mating period until F 1 animals were weaned. Pare ntal females were administered the diets for four weeks prior to mating, during mating and throughout the gestation and lactation periods up to the day of termination after weaning of offspring. After weaning, F 1 rats were maintained on the diets until te rmination on post - natal day (PND) 56. Rats were examined once daily for clinical signs and twice daily for mortality and morbidity. Body weights of males were determined weekly during the treatment period. Females were weighed weekly prior to mating, on gestation day 0, 7, 14 and 20 and during lactation on day 0, 4, 7, 14 and 21. Food consumption was monitored with the body weight determinations. Estrus cyclicity was evaluated over a two week period. Parental animals were observed for neurobehavioral parameters once weekly. Blood was collected for evaluation of hematology and clinical chemistry parameters and for analysis of thyroxine ( T4 ) and thyroid stimulating hormone ( TSH ) . A vaginal smear was taken at termination for estrus staging. The number of corpora lutea and implantation sites was recorded. At termination, sperm was collected for evaluation of motility and morphology and homogenization - resistant testicular spermatids and cauda epididymal sperm were counted. Selected organ weights were r ecorded and selected tissues/organs were examine microscopically. On PND 4 litters were culled to five males and five females per litter. On PND 0 and 4 body temperature was recorded and reaction to handling was evaluated. Ano - genital distance was measu red on PND0 for all pups. Pup body weights were recorded on PND 0, 4, 7, 14 and 21. Blood was collected on PND 4 for determination of T4 and on PND 22 and 56 for determination of T4 and TSH and evaluation of clinical chemistry and hematology parameters. Urinalysis was conducted. Body weights of selected F 1 animals were recorded weekly until termination on PND 56. Sexual developmental landmarks were evaluated. F 1 rats were examined for neurobehavioral effects weekly after weaning. Selected organ weigh s were recorded at termination on PND 56. A vaginal smear was taken from all F 1 females after attaining vaginal patency until day of sacrifice. The results were no effects on body weight, food consumption, neurobehavioral parameters, hematology or clini cal chemistry parameters, organ weighs, reproductive parameters, T4 or TSH levels, sperm evaluations, estrus cyclicity or upon microscopic examination of tissues/organs. In pups at 10000 ppm, statistically significant lower body weight and body weight gai n were observed in both sexes when compared to the controls. However, on PND 4, body temperature of male and female pups was statistically significantly decreased at 5000 and 10000 ppm compared to the concurrent control groups. However, the changes in bod y temperature was slight without significant systemic toxicity and therefore, not considered adverse. On PND 4 serum levels of T4 were comparable with concurrent control group. T4 levels were unaffected by treatment on PND 22 and PND56 pups. However, TSH levels were statistically increased in PND 22 females at 5000 and 10000 ppm without a clear dose response and in males at 10000 ppm. The changes in T4 and TSH were not consistent, changes were small in magnitude, and not collaborated with histopatholo gy, therefore, they were not considered as adverse. There were no treatment - related effects on body weight, body weight change, feed consumption, clinical pathology, or sexual development in F1 animals. Absolute liver weight in males was significantly inc reased at the midPage 18 of 38

and high doses in F1 animals. In females, absolute liver weight was significantly increased at the mid - dose only, while relative liver weights at the mid and high dose were also significantly increased. In the absence of correlating fin dings in clinical chemistry parameters and histopathology, the liver effects were considered treatment - related but non - adverse. Absolute spleen weight was significantly increased in males of the high dose and associated with an increased incidence of sple nic extramedullary hematopoiesis (17/20). The incidence was significantly increased (p < 0.05; calculated by the reviewer) compared to the incidence in the males of the control group (9/20). Therefore, under the conditions of this study, the offspring to xicity LOAEL for Tinuvin 571 in rats is 10,000 ppm (equal to 618 mg/kg bw/day in males, and 870 mg/kg bw/day in females), based on increased spleen weight associated with increased incidence of splenic extramedullary hematopoiesis, body weights and body we ight gain from PNDs 4 - 21 were significantly decreased in males and females. The offspring systemic NOAEL is 5000 ppm (equal to 311 mg/kg bw/day in males and 432 mg/kg bw/day in females) (MRID 49358004) . A combined repeated dose toxicity study with the reproduction/developmental toxicity screening test (OECD 422) was conducted using drometrizole (CAS Reg. No. 2440 - 22 - 4). Male and female Crl:CD(SD) rats (12/sex/group) were administered drometrizole by gavage at dose levels of 0, 30, 100 or 300 mg/kg/day in olive oil. An additional group of 5 rats/sex were placed on test for the control and high dose group as recovery animals (15 days). Males were administer e d the test material for 42 days and females from 14 days prior to mating to d 4 of lactation. Offspring were terminated on PND 4. Animals were examined for mortality and cl inical signs of toxicity. Body weights and food consumption were recorded. A functional observation battery (FOB) was conducte d and motor activity was evaluated. The length of estrous cycles were re c orded as were the number of mated pairs, pregnant fema les and pairing days until copulation. The copulation index and fertility indices were calculated and parturition and lactation were monitored for abnormalities. Hematology, clinical chemistry parameters were evaluated at termination for parental males a nd females. The thymus, adrenals, heart, kidneys, spleen, liver, brain, testes and epid id ymides were weighed. Selected organs/tissues were examined microscopically. Mortality was unaffected by treatment and no clinical signs of toxicity were observed. No treatment - related effects were observed on body weights, food consumption, reflex/reaction, grip strength, locomoter activity, hematology parameters or reproductive parameters . Increased protein was observed in the urine of males at ≥ 100 mg/kg/day which returned to normal during the recovery period in the high dose group. Plasma levels of phospholipid were statistically increased in males and females at the high dose as were cholesterol levels in females. The values of both of these parameters returned to control levels during the recovery period. Relative liver weight was statistically increased in males at ≥ 30 mg/kg/day and absolute liver weight at the high dose. In fem ales, absolute and relative liver and kidney weights were statistically increase at 100 and 300 mg/kg/day . The incidence of hepatocellular hypertrophy was statistically increased in male and female rats at 300 mg/kg/day . The presence of eosinophilic bodi es in the kidney was statistically increased in males at 300 mg/kg/day . One female in the 100 mg/kg/day group and 2 in the 300 mg/kg/day group had hydropic changes in the proximal tubule compared to none in the control group. The reproductive/development al toxicity NOAEL was the highest dose tested at 300 mg/kg/day . The NOEL in m ales was considered to be < 30 mg/kg/day based on incre ased relativePage 19 of 38

liver weights observed in all do s e groups and 30 mg/kg/day based on effects on liver and kidney weights and k idney histopath o logy. The NOAEL was concluded to be 300 mg/kg/day for males and 30 mg/kg/day for females based on kidney lesions. NEUROTOXICITY There are no neurotoxicity studies available on CAS Reg. NO. 23328 - 53 - 2 or its surrogates. However, there were no indications of toxicity observed in any of the repeated dose studies discussed above. Further, FOB parameters and motor activity was evaluated in an extended one generation rat reproduction study and no effects were observed up to a dose of 10000 ppm (~500 mg/kg/day ). METABOLISM In an OPPTS 870.7485 metabolism study (MRID 49358002), four male albino rats (strain not specified) were administered 14 C - drometrizole (5.07 μgCi/mg) as a single oral dose of 10 mg/kg dissolved in polyethylene glycol 40 0. Urine and feces were collected in 24 hour periods until 168 hours post - treatment. The test material was labelled in the benzene ring and in the 5’ - methyl group. The radioactive purity was determined to be >99%. By 168 hours post - treatment, 73% of th e radioactivity was excreted in the urine and 27% in the feces. Residual radioactivity in tissues was below the blood level of 0.017 μg/g except in the kidney, aorta and liver (0.10

– 0.22 μg/g). The highest level of radioactivity was in the liver at 0.1 % of the initial dose. V. TOXICITY ENDPOINT SELECTION In this 2014 review, the Agency relies upon its original selection of toxicological endpoint as was discussed in the Agency’s 2010 assessment. The point of departure for the risk assessment for all d urations and routes of exposure was from the 90 - day toxicity study in rats. The NOAEL was 20 mg/kg/day and the LOAEL was 40 mg/kg/day based on increases in liver, kidney, spleen, and testes weights. Although the chronic point of departure was selected fr om a subchronic study, longer - term studies are available that shows the lack of toxicity even at higher doses (NOAEL higher than 60 mg/kg/day in carcinogenicity studies). No additional uncertainty factor is needed for extrapolating from subchronic to chron ic exposure. In this assessment a 100 fold uncertainty factor is used for the chronic exposure (10X interspecies extrapolation, 10X for intraspecies variability). The need for a 10X FQPA factor used in previous risk assessment is no longer necessary in light of the findings in the recently submitted “Extended One - Generation Reproduction Toxicity Study of Tinuvin 571 in Wistar Rats” (MRID 493 58004) . The NOAEL of 20 mg/kg/day was used for all exposure duration via dermal and inhalation routes of exposure. The residential, occupational, and aggregate level of concern (LOC) is for MOEs that are less than 100 and is based on 10X interspecies extrapolation and 10X for intraspecies variability . Dermal absorption is estimated to be 10% based on SAR analysis . A 100% inhalation is assumed. Special Consideration for Infants and Children (FQPA Safety Factor)Page 20 of 38 Section 408 (b)(2)(c) of the FFDCA provides that EPA shall apply an additional margin of safety for infants and children in the case of threshold effe cts to account for prenatal and post natal toxicity and the completeness of the database on toxicity and exposure unless EPA determines that a different margin of safety will be safe for infants and children. EPA concludes that the 10X FQPA safety factor c an be reduced to 1X is not necessary due to the recently submitted reproductive toxicity study data that fills the original “data gap”. VI. EXPOSURE Dietary Exposure/Risk Characterization The proposed use of this chemical as an inert ingredient in pes ticide products under the current petition is restricted to a maximum concentration of 10.0 % in the final formulation when applied to all agricultural crops . Using the I - DEEM dietary exposure model to estimate the exposure to all subpopulations ( see the at tachment ), it was determined that the exposure from the use of this inert ingredient at the proposed concentration (including exposure through drinking water) and crop use pattern would result in nominal exposure to all subpopulations. All subpopulations showed a % RfD of 7 0 % or less. The subpopulation with the greatest % RfD is for children 1 - 2 years old 70.6 % of cPAD . It is important to note that the I - DEEM Model assumes a default value of 100 ppb for the concentration of the inert in all sources of drinking water. Based on the physical and chemical properties of th is chemical and the intended use pattern, exposure through drinking water is unlikely; therefore, these results are highly conservative in regards to the exposure through drinking water.
Table 1 : Summary of Dietary (Food and Drinking Water) Exposure and Risk for CAS 25973 - 55 - 1 and 23328 - 53 - 2 Results Taken from I - DEEM Model Population Subgroup Acute Dietary (95 th Percentile) Chronic Dietary Dietary Exposure (mg/kg/day) % aPAD Dieta ry Exposure (mg/kg/day) % cPAD General U.S. Population
No acute endpoint selected 0.0 37869 18.9 All Infants (< 1 year old) 0.0 78886 39.4 Children 1 - 2 years old 0. 141248 70.6 Children 3 - 5 years old 0.0 97327 48.6 Children 6 - 12 years old 0.0 5011 1 25.1 Youth 13 - 19 years old 0.0 26960 13.5 Adults 20 - 49 years old 0.0 28948 14.5 Adults 50+ years old 0.0 30358 15 .2Page 21 of 38 Table 1 : Summary of Dietary (Food and Drinking Water) Exposure and Risk for CAS 25973 - 55 - 1 and 23328 - 53 - 2 Results Taken from I - DEEM Model Population Subgroup Acute Dietary (95 th Percentile) Chronic Dietary Dietary Exposure (mg/kg/day) % aPAD Dieta ry Exposure (mg/kg/day) % cPAD Females 13 - 49 years old 0.0 29267 14.6 The most highly exposed subgroup is bolded. Residential (Non - Occupational) Exposure/Risk Cha racterization The Agency’s 2010 assessment contained estimates of non - occupational (“residential”) exposures from “handling” (i.e., applying) pesticides and from post - application exposures. For purposes of comparison and characterization, non - occupationa l “handler” exposures are revised and presented. The revisions reflect current Agency policy regarding “Unit Exposures” and “body weight” and are explained along with the exposure estimates. The methodology used to estimate exposure and risk are the same as w ere presented in the 2010 assessment. The backpack sprayer method of application was substituted for the trigger pump ready to use sprayer as th at is not a practical method of application to lawns and turf. In addition, the backpack method is consid ered a high exposure situation thus provides a conservative, screening measure of safety or risk. The assessment methodology was developed by the Health Effects Division Science Advisory Council on Exposure (EXPOSAC) and is standard Agency operating proc edure. The basic algorithm is: ADD = UE x Amount/Day x AF ÷ BW where: ADD = Average Daily Dose UE = Unit Exposure expressed as mg of inert per pound of product handled. UE is activity specific. UE are taken from: “Standard Operating Procedures for Re sidential Pesticide Exposure Assessment”. Health Effects Division/Office of Pesticide Programs/OCSPP/EPA, January 2012. Amount/day = from 2010 EPA assessment (see below) . AF = absorption factor; 10% dermal absorption and 100 % inhalation absorption fro m 2010 EPA assessment BW = body weight; 80 kg; HED Hot Sheet # 31 Use of New Human Body Weight Data as Presented in the EPA’s Exposure Factors Handbook: 2011 edit. The 2010 assessment used the assumption that five (5) gallons of formulated pesticide pro duct are used per day. A product density of 9.0 lb/gallon was assumed to be a typical product density. The product was assumed to be diluted at a 1 to 10 ratio with water. Thus: 5 gal. formulated product * 9 lb/gal * (1part product/10 parts water) = 4. 5 lb product per day. The amount of product per day is adjusted according to the per cent inert ingredient, in the case of this request, 10 % (0.10). Therefore 4.5 lb product/day * 10% inert = 0.45 lb inert handled/applied per day.Page 22 of 38

Table 2. Resi dential Pesticide Handler/Applicator Estimated Exposure and Risk Exposure Scenario (Formulation/ Application) Quantity

Handled/ per day Dermal

Unit Exposure (mg/lb inert 3 Inhalation

Unit Exposure (mg/ lb inert) Dermal Dose

(mg/kg /day) Inhalation

Dose (mg/ kg/ day) Baseline

Dermal MOE Baseline

Inhalation MOE Liquids/ Low Pressure Handwand 0.45 lb 63 0.0 18 0.035 0.000101 571 198000 Liquids/ Hose End Sprayer, Lawn 0.45 lb 13.4 0.0 22 0.0075 0.000124 2666 161290 Backpack Sprayer 0.45 lb 130 0.014 0.073 0. 000078 273 25 6 410 Risks were calculated using the Margin of Exposure (MOE) approach, which is a ratio of the body burden to the toxicological Po int of Departure (PoD). For this material a MOE greater than 100 indicates that the exposure scenario does no t exceed the Agency’s level of concern. For all residential handler scenarios, risk estimates are not of concern for both the dermal and inhalation assessments. These exposure models are highly conservative and therefore the true risk of the anticipated exposure to these chemicals is believed to be less than what is shown . Margins of Exposure (MOE) express the Agency’s Level of Concern (LOC). For this review, MOE < 100 exceed the Agency’s level of concern. MOEs are the ratio of toxicological endpoint (NOAEL) to estimated Dose, both are expressed as mg inert/kg bw/day. MOE = NOAEL ( mg/kg/day )/Dose ( mg/kg/day ). Since the estimated MOEs exceed 100, the proposed use patterns do not exceed the Agency’s level of concern.

Table 3. Residential Po sta pplication Short - term Exposures and Risks for 23328 - 53 - 2 Exposure Scenario Application Rate Exposed Population & Exposure Duration Daily Dose (mg/kg/day) MOE Outdoor Lawn Products Dermal Exposure to Treated Lawns 0.45 lb/day Adult 0.00091 21,980 Ch ild 0.0017 11,770 Hand - to - Mouth from Treated Lawn Child 0.00066 30,300 Object - to - Mouth from Treated Lawn Child 0.000042 476,000 Soil Ingestion Child 0.000 0 98 20,400 Total Lawn Combined Exposures* Child 0.00 25 8,000 The Agency’s 2010 assessm ent included some assessments of intermediate - term exposures i.e., exposures from one to six months. In the current re - evaluation, the Agency does not expect intermediate - term exposures for the use patterns listed. This is consistent with the guidance se t forth in the “Standard Operating Procedures for Residential Pesticide Exposure Assessment” (Health Effects Division/Office of Pesticide Programs/U.S. EPA; January 2012). Intermediate term exposures are exposures expected for a period of 1

– 6 months tha t are continuous or a series of intermittent exposures. Intermediate - term residential are generally not required becausePage 23 of 38

individuals are not expected to re - treat the same sites repeatedly day after day for this duration, nor are a large number of pesticid e applications resulting in intermediate - term exposures expected over this duration (Section 1 page 8). Further, due to dissipation over time for intermediate - term post application exposures, short - term exposures are generally considered to be protective of intermediate - term exposures . However, for the sake of continuity, adjusted Margins of Exposure are presented. The 2010 assessment was based upon 0.6 % concentration. The current request is for the use of 10 % concentration, an increase of approximate ly 17 times the original amount. The Health Effects Division assumes a linear response relationship to increases or decreases in dose and subsequent Margin of Exposure. Therefore, the 2010 intermediate - term Margins of Exposure (which were quite large) ar e divided by 17 and presented here. Table 4. Intermediate - term Residential Post - application Margins of Exposure Exposure Scenario Exposed

Population & Exposure Duration MOE 2010 Assessment MOE 2015 Assessment Dermal Exposure to Treated Lawns Adult IT 63000 3705 Child IT 38000 2235 Hand - to - Mouth from Treated Lawn Child IT 100000 5882 Object - to - Mouth from Treated Lawn Child IT 200000 11764 Soil Ingestion Child IT 15000000 882352 Total Lawn Combined Exposures* Child IT 28000 1647 Residen tial Postapplication Outdoor Exposure and Risk Calculations Potential dermal postapplication exposure was calculated using the following formulas: Adult and Child Dermal Exposure to Treated Lawns (from SOP 2.2) :
Where: ADD= Average Daily Dose (mg/kg /day) TTR= Turf Transferable Residue (μg/cm 2 ) TC = Transfer Coefficient (cm 2 /hr) (14,500 cm 2 /hr for adults, 5,200 cm 2 /hr for children for short term exposure durations) ET = Exposure Time (2 hr) CF1 = Conversion Factor (1 mg / 1000 μg) DA = Dermal Absorpti on Factor (%) (10%) BW = Body Weight (70 kg for adult, 15 kg for toddler) ADD = TTR * TC * ET * CF 1 * DA

BWPage 24 of 38

Where: AR = Application Rate ( 0.45 lb inert/ day as derived from 2010 assessment ) F = fraction of inert retained on foliage or 5% (unitless) D = fraction of residue that dissipate s daily or 10% (unitless) t = number of days after application day (Day 0; day of application) CF1 = 4.54 x 10 8 μg/lb CF2 = 24.7 x 10 - 9 acre/cm 2 0.45 lb inert/day * 0.05 (%) * 4.54 8 μg/lb * 2.47 - 9 A/cm 2 = 0.025μg/cm 2 0.025μg/cm 2 * 14,500 cm 2 /hr * 2h r * 1 mg/1000 μ g * 10 % (DA) ÷ 80 kg = 0.00091 mg/kg/day (adult) 0.025μg/cm 2 * 5,200 cm 2 /hr * 2hr * 1 mg/1000 μ g * 10 % (DA) ÷ 15 kg = 0.0017 mg/kg/day (toddler) Assumptions for Dermal Dose from Pesticide Residues on Turf:  On the day of application, it was assumed that 5% of the application rate is available from the turfgrass as dislodgeable residue.  Postapplication exposure is assessed on the same day the pesticide is applied because it is assumed that the homeowner could be exposed to turfgrass im mediately after application. Therefore, postapplication exposures and risk are based on residues expected to be present on day 0 (i.e., the day of application).  The upper percentile dermal transfer coefficient is assumed to be 14,500 cm 2 /hr for adults a nd 5,200 cm 2 /hr for children for short - term durations. The transfer coefficient cm 2 /hr is a calculated mean, based on the Jazzercise method, which is believed to result in an upper percentile estimate of the transfer coefficient for this scenario.  The dur ation of exposure for children and adults is assumed to be 2 hours per day. The 95 th percentile value for playing on grass is 121 minutes per day for both age groups 1 - 4 years and 18 - 64 years (U.S. EPA 1996). Hand to Mouth (HTM) Exposure to Child on Tre ated Turf (from SOP 2.3.2): The following equation is used to calculate the nondietary ingestion exposures that are attributable to hand - to - mouth behavior on treated turf.

Where: ADD = Average daily dose (mg/kg/day) TTR= turf transferable residue (μg /cm 2 ) SA= Surface area of child hand - 3 fingers (20 cm 2 /event) SE = Saliva Extraction Factor (0.5) TTR = AR * (1 - D) t * F * CF1 * CF2

ADD = TTR * SA * SE * Freq * CF1 * ET BWPage 25 of 38

Freq = Frequency of hand - to - mouth events (20 events/hr for short - term exposures, 9.5 events/hr for long - term exposures) CF1 = 1 mg/ 1000 μg ET = Exposure Tim e (2 hours) BW = Body weight (15 kg for toddler) 0.025μg/cm 2 * 20 cm 2 /event * 0.5 (saliva extraction) * 20 events/hr * 1mg/1000 μ g * 2 hr = 0.00066 mg/kg/day 15 kg bw Assumptions for Potential Dose among children from Incidental Nondietary Ingest ion of Pesticide Residues on Residential Lawns from Hand - to - Mouth Transfer:  On the day of application, it was assumed that 5% of the application rate is available on the turfgrass as dislodgeable residue.  Postapplication activities are assessed on the sa me day that the pesticide is applied because it is assumed that children could play on the lawn immediately after application.  The surface portion of three fingers of a toddler’s hand put in mouth is 20 cm 2 .  The Hand - to - Mouth (HTM) exposure frequency is 20 times per hour for short term exposures.  The duration of exposure for toddlers is assumed to be 2 hours per day. The 95 th percentile value for playing on grass is 121 minutes per day for both age groups 1 - 4 years and 18 - 64 years (U.S. EPA 1996).  Toddl ers (age 3 years), used to represent the 1 to 6 year old age group, are assumed to weigh 15 kg. (U.S. EPA 1996).  The saliva extraction factor is 50%. Object to Mouth (OTM) Exposure to Child (from SOP 2.3.3) : The following equation is used to calculate t he nondietary ingestion exposures that are attributable to object - to - mouth behavior on treated turf:

Where: TTR = object transferable residue (μg/cm 2 ) IgR = Ingestion Rate for mouthing per day (25 cm 2 /day) CF1 = 1 mg / 1000 μg BW = Body weight (15 kg for child) 0.025 μg/cm 2 * 25 cm 2 /day * 1 mg/1000 μ g/ 15 kg bw = 0.000042 mg/kg/day Assumptions for Potential Dose among Toddlers from the Ingestion of Pesticide - Treated Turfgrass: ADD = TTR * I g R * CF1

BWPage 26 of 38

 On the day of application, it may be assumed that 20% of the applica tion rate is available on the turfgrass as dislodgeable residue.  Postapplication activities are assessed on the same day that the pesticide is applied because it is assumed that children could play on the lawn immediately after application.  The assumed i ngestion rate for grass for toddlers (age 3 years) is 25 cm 2 /day. This value is intended to represent the approximate area from which a child may grasp a handful of grass. Soil Ingestion Exposure to Child (from SOP 2.3.4): The following equation is us ed to calculate the nondietary ingestion exposures that are attributable to soil ingestion on treated turf:

Where: ADD = Average daily dose (mg/kg/day) SR = Soil Residue, 1 cm depth of surface soil, (μg/g) IgR = Ingestion Rate for daily soil ingestio n (100 mg/day) CF1 = Conversion Factor (1 g / 1,000,000 μg) BW = Body weight (15 kg for child)

Where: AR= application rate (lb inert/ A) CF1 = Conversion factor (4.54 x 10 8 μg/lb) CF2 = Conversion factor (2 . 47 x 10 - 9 acre/cm 2 ) CF3 = Conversion factor (0.67 cm 3 / g soil) F = fraction of inert retained on soil or 100% (unitless) D = fraction of residue that dissipates daily (unitless) t = postapplication day on which exposure is being assessed (t = 0, day of application) 19.6 lb inert/A * 4.54 8 * 2 . 47 - 9 A/cm 2 * 0.67 cm 3 /g soil * 1 on day zero. = 14 . 7 μ g /g thus: 14 . 7 μ g/g * 100 mg / day * 1 g/1,000,000 μ g ÷ 15 kg bw = 0.000 0 98 mg/kg/day NOTE: As has been noted above and in keeping with the Agency’s 2010 assessment, the amount handled/applied per day is five gallons of product which in this case equals 0.45 lb inert per day. According to HED policy, five gallons applied per day is for 1000 square feet or a “a spot treatment” . Therefore to derive the amount of inert per acre: 43,580 ft 2 /A ÷ 1000 ft 2 /0. 45 lb inert = 19.6 lb inert per acre. Soil Residue (SR) = AR * CF1 * CF2 * CF3 * F * (1 - D) t ADD = SR * I g R * CF1

BWPage 27 of 38

Assumptions for Potential Dose among Toddlers from Incidental Ingestion of Soil from Pesticide Treated Residential Areas:  On the day of application “Day 0”, it was assumed that 100% of the application rate is located within the soil’s uppermost 1 cm.  Postapplication exposure was assessed on the same day the pesticide is applied because it is assumed that toddlers could play on the lawn or other outdoor treated areas immediately after application.  The assumed soil ing estion rate for children (age 1 - 6 years) is 100 mg/day (U.S. EPA 1996). Where HED has identified a common endpoint for this inert ingredient for the dermal and oral routes of exposure; it is HED’s policy to conduct an aggregate residential assessment whi ch combines a child’s dermal exposure from contact with treated turf with the incidental oral exposure from the hand - to - mouth exposure from exposures that occur on treated turf. Once daily dermal and incidental oral (non - dietary) exposures are combined, t hey are then compared to the appropriate PoD.Page 28 of 38

Occupational Exposure Estimates of occupational exposure and risk are derived in the same manner as the Agency’s 2010 assessment. However, the current estimates are adapted to reflect current policy re garding Unit Exposure (UE) and body weight. As with the 2010 assessment, the rates of application are taken from: ‘‘JITF Inert Ingredients. Residential and Occupational Exposure Assessment Algorithms and Assumptions Appendix for the Human Health Risk As sessments to Support Proposed Exemption from the Requirement of a Tolerance When Used as Inert Ingredients in Pesticide Formulations’’ (D364751, 5/7/09, Lloyd/LaMay in docket ID number EPA

– HQ

– OPP

– 2008

– 0710) found at http://www.regulations.gov . The rates of application are typical insecticide formulations and are adjusted for the requested 10% maximum versus the 0.6% assessed in 2010. Only short - term exposures are presented as they are the highest (most conservati ve) as compared to intermediate - term exposures also reported in 2010. Occupational Unit Exposures are taken from “Occupational Pesticide Handler Unit Exposure Surrogate Reference Table” , Health Effects Division , Office of Pesticide Programs, U.S. Environ mental Protection Agency, March 2013 and are for a single layer of work clothing (long sleeved shirt, long pants, shoes plus socks) a nd the use of protective gloves. Pilots in enclosed cockpits are considered to have the engineering control of the enclose d cockpits. Flaggers are assumed not to wear protective gloves. For occupational assessment the algorithm is: AR x Units x UE x AF ÷ BW where AR = Application rate in lb inert/A (adjusted for 10% maximum requested) Units = Acres treated/day UE = Unit Exp osure in mg per pound handled AF = Absorption Factor (10% dermal; 100% inhalation) BW = body weight (80 kg average adult).Page 29 of 38

Table 5. Estimated Exposure and Risk for Occupation Pesticide Handlers Exposure Scenario (Formulation/ Application/ Crop) Applicati on

Rate (lb inert/ A) Area

Treated Daily (acres) Dermal

Unit Exposure (mg/lb inert) Inhalation

Unit Exposure ( m g/ lb inert) Baseline

Dermal Dose (mg/kg /day) Baseline

Inhalation Dose (mg/kg/ day) Baseline

Dermal MOE Baseline

Inhalation MOE Liquids/ Aeri al Application/ High Acreage Crops (ST) 0.2 1200 0.0376 0.000219 0.011 0.000 657 1 , 8 20 30 , 440 Liquids/ Groundboom/ High Acreage Crops (ST) 0.2 200 0.00 188 0.000 11 10 , 640 181 , 800 Liquid/ Aerial Application/ High Acreage Crops (ST ) 0 . 2 1200 Eng control on ly: 0.00 2 Eng control

only: 0.0 000049 0.000 6 0.00001 5 33 , 000 1.3M Groundboom/ High Acreage Crops (ST) 0.2 200 0.0161 0. 00034 0.000 81 0.000 17 24 , 700 118 , 650 Liquid/ Low Pressure Handwand/ Ornamentals (ST) 0. 72 5 0.39 0.0039 0.0 018 0.000 18 11,100 111 , 100 Liquid/ Flagger/ High Acreage Crops (ST) 0.2 1200 0.011 0. 00035 0.0 033 0.00 11 6 , 100 18,200 Margins of Exposure (MOE) express the Agency’s Level of Concern (LOC). For this review, MOE < 100 exceed the Agency’s level of concern. MOEs are the ratio of tox icological endpoint (NOAEL) to estimated Dose, both are expressed as mg inert/kg bw/day. MOE = NOAEL ( mg/kg/day )/Dose ( mg/kg/day ). Since the estimated MOEs exceed 100, the proposed use patterns do not exceed the Agency’s level of concern. VII. AGGRE GATE RISK In addition to consideration of single, acute exposures, the Agency also considers to possibility of aggregate exposures. Aggregate exposure refers to the sum(s) of individual exposures that might occur within a limited time frame. Aggregate e xposure assessments are conducted for non occupationally exposed individuals i.e., for adults and toddlers (residents). In this case aggregate exposures consider oral (dietary) exposure, handler (residential applicator) exposure and post application expos ure from treated lawns or turf. For adults the Agency uses the highest residential applicator exposure (use of back - pack sprayer), dietary exposure as estimated by the I - DEEM model (results attached) and from estimated post application exposure. For to ddlers, the Agency combines post - application dermal exposure from treated lawns with hand - to - mouth exposure from treated lawns and dietary exposure as estimated with the I - DEEM model. Residential Handler/Backpack sprayer 0.073 mg/kg/day Adult Post - a pplication dermal exposure/treated lawn 0.0091 mg/kg/day Adult Dietary exposure/I - DEEM model 0.0378 mg/kg/day Total Adult Aggregate Exposure 0.1199 mg/kg/day Toddler/Total Exposure from lawn and turf (Dermal + Hand - to - Mouth) 0.0034 mg/kg/day Toddler Dietary from I - DEEM 0.141248 mg/kg/day Total Toddler Aggregate Exposure 0.145 mg/kg/dayPage 30 of 38

Margins of Exposure for aggregate exposures. Margin of exposure is: NOAEL ÷ Total Aggregate Exposure thus For adult 20 mg/kg/da y ÷ 0 .1199 mg/kg/day = 1 70 . For toddler 20 mg/kg/day ÷ 0.145 mg/kg/day = 1 40 . Table 6. Intermediate - term Aggregate Exposure: 2010 Estimates Adjusted for Rate Increase

Population 2010 Estimated

Aggregate MOE (food and residential) 2015 Adjusted

Aggregate M OE Adult Male 55000 3235 Adult Female 54000 3176 Child 16000 941 The estimated exposures are based upon highly conservative (protective) assumptions. The margins of exposure exceed 100 therefore, the estimated risks do not exceed the Agency’s level of concern. 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 Phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - to share a common mechan ism of toxicity with any other substances, and Phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - 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 Ph enol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - do es 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 e ffects of such chemicals, see EPA's website at http://www.epa.gov/pesticides/cumulative . IX. ENVIRONMENTAL FATE & EFFECTS It was noted earlier in this document, there is not a complete data set for p henol, 2 - (2H benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2) with regards to toxicological effects on mammals and the same is true with regards to environmental fate and effects. Also as discussed earlier p henol, 2 - (2H - benzotriazol - 2 - yl ) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2) is classified among the phenolic benzotriazole (PBTZ) class of chemicals. The PBTZ class of chemicals consists of mono and di - substituted phenolic derivatives of 1,2,3 - benzotriazole. DataPage 31 of 38

have been publishe d regarding a number of PBTZ chemicals regarding chemical properties, mammalian toxicity and environmental fate and effects. Much of the discussion of environmental fate and effects is taken from MRID 49358003. There are four compounds which are structu rally and toxicologically similar to phenol, 2 - (2H benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - and which the Agency has previously reviewed relative to environmental fate and effects . The Agency’s High Production Volume (HPV) Challenge Program contains the res ults of that review and may be found in http://www.epa.gov/chemrtk/index.htm and in http://www.epa.gov/chemrtk/pubs/general/guidocs.htm . The four compounds similar to p henol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2) are: 1) drometrizole (Tinuvin ® P; CAS Reg. No. 2440 - 22 - 4) 2) octrizole (UV 329; CAS Reg. No. 3147 - 75 - 9) 3 ) Tinuvin ® 234 (CAS Reg. No. 703 21 - 86 - 7) and 4 ) Tinuvin ® 328 (CAS R eg. No. 25973 - 55 - 1). Phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2) is currently approved for use under 40 CFR § 180.020 at a maximum of 0.6% on adzuki beans, canola, chickpeas, cotton, f

a v a beans, field peas, lentils, linola, linseed, lucerne, lupins, mung beans, navy beans, pigeon peas, safflower, sunflower and vetch. Drometrizole is approved for use in cattle ear tags at a maximum of 0.5%. Regarding environmental fate and effects, t he Agency found that the phenolic benzotriazoles are solids with low water solubilities and low to negligible vapor pressures. They are expected to have low mobility in soil. Volatilization of phenolic benzotriazoles is considered low based on the respec tive Henry’s Law constant. The rate of hydrolysis of phenolic benzotriazoles cannot be measured due to a lack of water solubility. However, the chemical structures of these compounds suggests that hydrolysis is likely to be negligible under environmental conditions. The rate of atmospheric photooxidation is considered rapid for CAS Reg. No. 2440 - 22 - 4 and CAS Reg. No. 70321 - 86 - 7 and moderate for CAS Reg. No. 3147 - 75 - 9 and CAS Reg. No. 25973 - 55 - 1. CAS Reg. No. 2440 - 22 - 4 is expected to have low potential f or bioaccumulation but CAS Reg. No. 3147 - 75 - 9 and CAS Reg. No. 25973 - 55 - 1 are expected to have high potentials for bioaccumulation and CAS Reg. No. 70321 - 86 - 7 is expected to have moderate potential for bioaccumulation. However, the relatively low solubili ty of these compounds may mitigate the potential to bioaccumulate. All four phenolic benzotriazole derivatives are expected to have high persistence though the phenolic portion resembles many antioxidant phenols which might suggest that that portion of th e molecule could oxidize. An acute toxicity study with the rainbow trout (Oncorhynchus mykiss ) was conducted using (CAS Reg. No. 2440 - 22 - 4); 2 - (2’ - hydroxy - 5’ - methylphenyl benzotriazole at concentrations of 0.022, 0.037, 0.061, 0.10 and 0.17 mg/L for 96 hr under static conditions. The highest dose tested approximated the limit of water solubility for the compound. No mortality or adverse effects were noted in the test. The 96 hr LC 50 (mg/L) is determined to be > 0.17 mg/L. The Agency indicatedPage 32 of 38

that since no effects were seen in fish at the limit of solubility, no further aquatic toxicity testing was necessary (MRID 49358003). An acute toxicity study was conducted using zebra fish. 2 - (2’ - hydroxy - 5’ - methylphenyl benzotriazole (CAS Reg. No. 2440 - 22 - 4; Tinuvin P) was used in a limit test at a concentration of 100 mg/L according to OECD Guideline 203. Ten fish were exposed in duplicate 20 L glass aquaria to the test substance. The control group consisted of 10 fish. The test was a “static” test. Te st vessels were dosed at a concentration of 0.09 g/L for 96 hr. No mortality or adverse effects were noted in any of the test or control fish. The 96 hr LC 0 and 96 hr LC 50 values were > 100 mg/L. In another static acute toxicity test , 2 - (2’ - Hydroxy - 5’ - o ctylphenyl)benzotriazole (CAS Reg. No. 3147 - 75 - 9) and 4 mg alky p lhenolpolyglycol ether per liter were used according to OECD Guideline 203. Ten zebra fish per concentration were dosed at 10, 18, 32, 58 and 100 mg/L for 96 hr in 20L aquaria. The control t anks contained water with 4 mg alky lp henolpolyglycol ether/L of water. Fish were not fed during the test period. At the end of the test (96 hr), there were no mortality or adverse effe c ts observed in any of the test fish or control fish. The 96 hr LC 50 was determined to be 100 mg/L. An acute static toxicity test was conducted using zebra fish and 2 - (2’ - Hydroxy - 3,5 - di,5 - tert amylphenyl)benzotriazole (CAS Reg. No. 25973 - 55 - 1). A limit test was conducted under static conditions according to OECD Guideline 203. Ten zebra fish were exposed in duplicate to the test material. The control group consisted of ten fish. Test vessels were dosed at 0.08 g/L for 96 hr. No mortality occurred in treated or control tests. However, in the treated tests, a precipitat e formed indicating that the limit of solubility of the test material had been exceeded. The 96 hr LC 50 value was > 100 mg/L. An acute static toxicity test was conducted using Daphnia pulex . Nine benzo phenolic triazoles were tested including: (CAS Reg . No. 23328 - 53 - 2) p henol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - ; (CAS Reg. No. 3147 - 75 - 9); 2 - (2’ - hydroxy - 5’ - octylphenyl benzotriazole; (CAS reg. No. 25973 - 55 - 1); 2 - (2’ - hydroxy - 3’,5’ - di - t - amylphenyl)benzotriazole; (CAS Reg. No. 70321 - 86 - 7); 2 - (2H - ben zotriazole 2 - yl - 4,6 - bis(1 - methyl - 1 - phenylethyl) phenol; HDBB (CAS Reg. No. 3846 - 71 - 1); phenol, 2 - (2H benzotriazol - 2 - yl) - 4,6 - bis(1,1 - dimethyl) - 4). Stock solutions were prepared in tetrahydrofuran (THF). No more than 0.01% (v/v) of THF was used in the fi nal exposure so l utions . Solvent controls showed no adverse effects at this level of solvent concentration. Daphnia pulex (20 neonates/dose level) were placed in 30 mL glass beakers exposed to 25 mL of test solutions. Test concentrations ranged from 0.1 to 10 mg/L for all compounds tested. The 24 - and 48 - hr LC 50 values for p henol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl were 6.35 and 2.59 mg/L respectively. No acute toxic effects were observed for the other phenolic benzotriazoles tested. An acute static toxicity test was conducted on Daphnia magna using (CAS reg. No. 25973 - 55 - 1); 2 - (2’ - hydroxy - 3’,5’ - di - t - amylphenyl)benzotriazole. The test was a component of the High Production Volume (HPV) testing program. Daphnia magna were exposed to concentrat ions of 5.8, 10, 18, 32, 58 and 100 mg/L. A slight precipitate was noted at all levels indicating the limit of solubility in water had been exceeded. Ten Daphnia were exposed to each test solution and aPage 33 of 38

control solution for 24 hr. The EC 0 concentration was determined to be 58 mg/L. Two daphnids were immobilized at 100 mg/L. The EC 50 was determined to be > 100 mg/L. Numerous other studies yielded similar results indicating the low levels of toxicity of benzotriazoles to aquatic invertebrates. In an acute toxicity test to aquatic plants (CAS Reg. No. 3147 - 75 - 9); 2 - (2’ - hydroxy - 5’ - octylphenyl benzotriazole was used in an algal growth inhibition test (EEC Guideline 87/302). The toxicity of CAS Reg. No. 3147 - 75 - 9 was tested on the green alga Scenedesmus subspicatus. The test substance was mixed with acyl phenol polyglycol ether solution and nominal test concentrations were 1.23, 3.7, 11, 33 and 100 mg/L. Initial cell density was 10 4 cells/mL. The control group was exposed to water and water plus 3.6 mg alkylphenolpolyglycol ether. The 72 hr EC 50 was determined to be > 100 mg/L. A number of additional studies yield confirmative results indicating low toxicity of phenolic triazoles to aquatic plants. X. DETERMINATION OF SAFETY For phenol, 2 - (2H - benzot riazol - 2 - yl) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2), aggregate risk include dietary exposure from food and water, exposure to adults from handling (applying the material) and from post - application dermal exposure. Exposures to toddlers (the most hi ghly exposed population subgroup from dietary sources) include food and water, post - application dermal exposure and post - application “hand - to - mouth” exposures. “Residential exposures (adult and toddler) are discussed in Sections VI and VII earlier in this memorandum. D ietary exposure estimates for food and drinking water are below the Agency’s level of concern (<100% cPAD) for the U.S. population and all population subgroups. The total dietary exposure for food and drinking water is 18.9 % of the cPAD for the U.S. population and 70.6 % of the cPAD for children 1 - 2 yrs old, the most highly exposed population subgroup . XI. 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 u se of pesticide products and associated risks for adult applicators andPage 34 of 38

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 resource s 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. XII. HUMAN STUDIES This assessment does not rely on any studies in which human subjects were intentionally exposed to a pesticide. XIII INTERNATIONAL LIMITS: There are no international limits on CAS Reg. No. 23328 - 53 - 2. XIV. RISK CHARACTERIZATION CAS Reg. No. 25973 - 55 - 1 and CAS Reg. No. 23328 - 53 - 2 are currently used as packaging stabilizers (preventing UV light from yellowing or hardening product packages). They are also used in paints and coatings. In addition, the Food and Drug Administration (FDA), under 21 CFR 175.105, has approved the use of CA S Reg. No. 25973 - 55 - 1 as an indirect food additive for use in food packaging. Acute studies revealed low acute toxicity with an oral LD 50 >2325 mg/kg based on the highest dose tested. Acute inhalation, acute dermal toxicity, skin and eye irritation and skin sensitization studies have not been conducted on either of the chemicals contained in this petition; however, evidence does exist for structurally similar chemicals contained within the HPV document. Acute inhalation and dermal studies resulted in LC 5 0 >1420 mg/m 3 and LD 50 >2000 mg/kg, respectively. Skin irritation studies on rats and mice showed n o local irritation and no systemic toxicity. The Agency concluded in the HPV document that CAS Reg. No. 2440 - 22 - 4 was slightly irritating to rabbit eyes. The document states that CAS Reg. No. 2440 - 22 - 4, in skin sensitization studies on guinea pigs, showed skin sensitization; however, studies conducted on humans showed no sensitization. In a 90 - day study Wistar rats were given the test substance via their die t at 100, 200, 400, 800, or 1600 ppm ( approximately 5, 10, 20, 40, or 80 mg/kg/day ). Decreased hemoglobin and packed cell volume were seen in males administered ≥~20mg/kg/day and increases in glucose - 6 - phosphatase activity was noted at all dietary concent rations; however, these values were within the normal range of variability and therefore, are not considered to be of toxicological significance. Liver, kidney, spleen, and testes weights were increased in higher exposure groups with an indication of incre ased thyroid weights. Increases in testes weights were seen at ~20, ~40, and ~80 mg/kg/day; however, the testes weights were reported as testes weight per 100g body weight. The increase in testes weight may be caused by the decreased body weight and not a toxicologically significant finding. Reproductive organs were not evaluated microscopically. The primary target organ was the liver which showed a greenish - drab discoloration in males and females at higher exposure levels. “Microscopic examination revealed foci of necrosis and slight proliferation of bile ductPage 35 of 38

epithelia.”(HPV, 2009) Enlargement of the parenchymal cells was also observed. Tubular necrosis was reported in the kidney of some males in the higher does groups. A treatment related yellowish brown pigmentation was seen in the cytoplasm of the proximal tub u lar cells of females. No mortality was observed. The NOAEL of 20 mg/kg/day is based on blood, liver, and kidney effects seen at the LOAEL of 40 mg/kg/day. In a 90 - day dog study male and female B eagles were administered 0, 15, 30, 60, 120, or 240 mg/kg/day through their diet. Animals in the high - dose group showed decreases in body weight and food consumption. Males were more sensitive than females with mortality of one male dog in the highest dose group. Anemia and slight changes in blood chemistry parameters including increased serum bilirubin levels and gamma glutamyl transpeptidase (GTP), glutamyl oxalacetic transaminasae (GOT) and alkaline phosphatase activity were noted in the animals from the two highest dose groups. Males from these groups showed decreases in testes, prostrate, and epididymal weights and females showed deceases in body weight and uterus weight in the three highest dose groups. In higher dose groups, some animals showed atroph y of uterus , abnormal spermiogenesis, and atrophy of the prostate. The liver was reported to be the primary target organ for toxicity. Although the full study was not available, the submission summary for the HPV program states that at treatment levels of 60, 120, and 240 mg/kg/day, reduced food consumption and body weights were seen. In addition, histopathologic effects were noted in the liver, kidney, and testes of the 3 highest dose groups (details not provided). Increased liver weights associated with l iver damage including icterus (jaundice) were observed upon gross and histopathological examination in a few dogs in the 120 and 240 mg/kg/day dose groups. Microscopically, fatty degeneration of hepatocytes, presence of protein globules in the cytoplasm, Kupffer cell hyperplasia and centrilobular choleostatis were seen. (HPV) The NOAEL for this study is 30 mg/kg/day based on body weight, liver, and kidney effects seen at the LOAEL of 60 mg/kg/day. Developmental studies have been conducted on two structur ally similar chemicals. In one study rats and mice received the test substance containing CAS Reg. No. 2440 - 22 - 4 on days 6 - 15 of gestation. No maternal toxicity was evident and the rates of implantation and embryotoxicity were not affected by treatment. No teratogenic effects were observed however, the study did not specify what developmental endpoints were examined. The NOAEL for maternal and developmental toxicity was 1000 mg/kg/day (highest dose tested). A second developmental rat study showed no matern al toxicity at any dose tested for CAS Reg. No. 70321 - 86 - 7 on gestation days 6 - 15. A significant reduction in fetal body weight and an increased delay of skeletal maturation was observed in the 1000 mg/kg dose group. However, there were no similar effects in the high dose group indicating that these effects may be “incidental”. An omphalocele was seen in one fetus in the high dose group. The maternal toxicity NOAEL was 3000 mg/kg/day (highest dose tested). A developmental toxicity NOAEL of 1000 mg/kg/day w as chosen based on the omphalocele seen at the LOAEL of 3000 mg/kg/day. All genetic toxicity tests ( in vitro and in vivo ) conducted on the chemicals assessed in the HPV document indicated that this group of chemicals are not mutagenic and will not undergo chromosomal aberrations. A 104 week feeding study administered up to 142 mg/kg/day to rats did not find evidence of carcinogenicity. The Agency does not believe that CAS Reg. No. 25973 - 55 - 1 and CAS Reg. No. 23328 - 53 - 2 will be carcinogenic in humans. No cl inical signs of neurotoxicityPage 36 of 38

were seen in any of the repeat dose studies. After evaluating the available data and the expected exposure from the intended use pattern of this inert ingredient, the Agency does not feel that CAS Reg. No. 25973 - 55 - 1 and CAS R eg. No. 23328 - 53 - 2 will cause neurotoxicity. A combined repeated dose toxicity study with the reproduction/developmental toxicity screening test (OECD 422) was conducted using drometrizole (CAS Reg. No. 2440 - 22 - 4). Male and female Crl:CD(SD) rats (12/sex /group) were administered drometrizole by gavage at dose levels of 0, 30, 100 or 300 mg/kg/day in olive oil. An additional group of 5 rats/sex were placed on test for the control and high dose group as recovery animals (15 days). Males were administered the test material for 42 days and females from 14 days prior to mating to d 4 of lactation. Offspring were ter minated on PND 4. Mortality was unaffected by treatment and no clinical signs of toxicity were observed. No treatment - related effects were observed on body weights, food consumption, reflex/reaction, grip strength, locomoter activity, hematology parame ters or reproductive parameters. The reproductive/developmental toxicity NOAEL was the highest dose tested at 300 mg/kg/day . The NOEL in males was considered to be < 30 mg/kg/day based on increased relative liver weights observed in all dose groups and 30 mg/kg/day based on effects on liver and kidney weights and kidney histopathology. The NOAEL was concluded to be 300 mg/kg/day for males and 30 mg/kg/day for females based on kidney lesions. In an extended one - generation oral reproduction study (OECD Test Guideline 443) with the rat (MRID 49358004), the no - observed - effect - level (NOAEL) for phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - for parental and reproductive toxicity was 10000 ppm (equal to 618 mg/kg/day, the highest dose tested). The NOA EL for offspring toxicity was 5000 ppm (equal to 311 mg/kg/day) based on decreased body weight, and body weight gain, increased absolute spleen weights in males and increased incidence of splenic extramedullary hematopoiesis in males observed in pups at th e LOAEL of 10000 ppm (equal to 618 mg/kg/day). The data from the combined repeated dose toxicity study allow the Agency to re duce to the FQPA safety factor from 10X ( originally applied due to data gaps ) to 1X. Based on the discussion summarized above, M argins of Exposure > 100 based upon conservative (protective) assumptions, the Agency approves the use of phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl (CAS Reg. No. 23328 - 53 - 2) as an inert ingredient used in pesticide formulations under 40 CFR § 180 .920 on all agricultural crops at a maximum end - use concentration not to exceed 10 % by weight .Page 37 of 38 REFERENCES E.P.A. 2010. Memorandum, D. Sunderland, Decision Document for Petition Numbers 8E7362 and 8E7363; 2 - (2’ - hydroxy - 3’, 5’ - di - tert - amylpheny l) benzotriazole (CAS Reg. No. 25973 - 55 - 1) and Phenol, 2 - (2H - benzotriazole - 2 - yl) - 6 - dodecyl - 4 - methyl (CAS Reg. No. 23328 - 53 - 2) ). Federal Register. 2010. EPA - HQ - OPP - 2008 - 0601 and EPA - HQ - OPP - 2008 - 0602; FRL - 8836 - 3. Volume 75, No. 159/Wednesday 18 August 2010. Pp 50884

– 50890. 2 - (2’ - hydroxy - 3’, 5’ - di - tert - amylphenyl) benzotriazole and Phenol, 2 - (2H - benzotriazole - 2 - yl) - 6 - dodecyl - 4 - methyl; Exemption fro the Requirement of a Tolerance. MRID 49358001. Physical and Chemical Properties of Phenol, 2 - (2H - b enzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2); Tinuvin ® 571) and related Phenolic Benzotriazides. Sponsored by Loveland Products, Inc., P.O. Box 1286, Greeley, CO 80632; 6 November 2013 . 67 pp. MRID 49358002 . Mammalian Toxicity of Phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2); Tinuvin ® 571) and related Phenolic Benzotriazides. Sponsored by Loveland Products, Inc., P.O. Box 1286, Greeley, CO 80632; 25 March 2014. 303pp. MRID 49358003. Ecologica l Effects and Environmental Fate of Phenol, 2 - (2H - benzotriazol - 2 - yl) - 6 - dodecyl - 4 - methyl - (CAS Reg. No. 23328 - 53 - 2); Tinuvin ® 571) and related Phenolic Benzotriazides. Sponsored by Loveland Products, Inc., P.O. Box 1286, Greeley, CO 80632; 2 7 January 20 14. 169 pp. MRID 49358004. Extended One - Generation Reproductive Toxicity Study of Tinuvin 571 in Wistar Rats. Sponsored by Loveland Products, Inc., P.O. Box 1286, Greeley, CO 80632; 27 January 2014. 1322pp.Page 38 of 38 ATTACHMENT DEEM - FCID – Phenol, 2 - (2H - benzotriazol - 2 - yl - 6 - dodecyl - 4 - methyl January 2015 US EPA Ver. 3.16, 03 - 08 - d DEEM - FCID Chronic analysis for PHENOL NHANES 2003 - 2008 2 - day Residue file name: J: \ P henol \ INERTS_57ACTIVE_100PPBH2OREV.R08 Adjustment factor #2 used. Analysis Date 01 - 21 - 2015/13:37:36 Residue file dated: 01 - 21 - 2015/13:36:42 Reference dose (RfD, Chronic) = .2 mg/kg bw/day NOEL (Chron ic) = 20 mg/kg bw/day COMMENT 1: Inert 57 active ingredients + drinking water (100ppb) =============================================================================== Total exposure by population subgroup

------------------------------- ------------------------------------------------ Total Exposure

----------------------------------- Population mg/kg Margi n of Percent Subgroup body wt/day Exposure of RfD

-------------------------------------- ------------- ---------- ---------- Total US Population 0.037869 528 18.9% Hispan ic 0.041352 484 20.7% Non - Hisp - White 0.037160 538 18.6% Non - Hisp - Black 0.035190 568 17.6% Non - Hisp - Other 0.044671 448 22.3% Nursing Infants 0.049641 403 24.8% Non - Nursing Infants 0.091947 218 46.0% Female 13+ PREG 0.0330 48 605 16.5% Children 1 - 6 0.109335 183 54.7% Children 7 - 12 0.045482 440 22.7% Male 13 - 19 0.026752 748 13.4% Female 13 - 19/NP 0.027186 736 13.6% Male 20+ 0.028199 709 14.1% Female 20+/NP 0.030632 653 15.3% Seniors 55+ 0.030537 655 15.3% All Infants 0.078886 254 39.4% Female 13 - 50 0.029281 683 14.6% Children 1 - 2 0.141248 142 70.6% Children 3 - 5 0.097127 206 48.6% Children 6 - 12 0.050111 399 25.1% Youth 13 - 19 0.026960 742 13.5% Adults 20 - 49 0.028948 691 14.5% Adults 50 - 99 0.030358 659 15.2% Female 13 - 49 0.029267 683 14.6%

--- ----------------------------------------------------------------------------

RDI: PV Shah, K. Leifer M.I.Dow:S7 958 :PY1:(703)305 - 5533: IIA B:7505P