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Federal Food, Drug, and Cosmetic Act (FFDCA) Considerations for Tetraacetylethylenediamine 

(TAED) and its metabolite Diacetylethylenediamine (DAED)

Docket ID Number: EPA-HQ-OPP-2013-0277

Date: August 29, 2014

Section 408(c)(2)(A)(i) of FFDCA allows the EPA to establish an exemption from the requirement for a 

tolerance (the legal limit for a pesticide chemical residue in or on a food) only if the EPA determines that 

the exemption is “safe.” Section 408(c)(2)(A)(ii) of FFDCA defines “safe” to mean that “there is a 

reasonable certainty that no harm will result from aggregate exposure to the pesticide chemical residue, 

including all anticipated dietary exposures and all other exposures for which there is reliable information.” 

This includes exposure through drinking water and in residential settings but does not include occupational 

exposure. Pursuant to FFDCA section 408(c)(2)(B), in establishing or maintaining in effect an exemption 

from the requirement of a tolerance, the EPA must take into account the factors set forth in FFDCA section

408(b)(2)(C), which require the EPA to give special consideration to exposure of infants and children to the 

pesticide chemical residue in establishing a tolerance exemption, and to “ensure that there is a reasonable 

certainty that no harm will result to infants and children from aggregate exposure to the pesticide chemical 

residue....” Additionally, FFDCA section 408(b)(2)(D) requires that the EPA consider “available 

information concerning the cumulative effects of [a particular pesticide's] . . . residues and other substances 

that have a common mechanism of toxicity.”

The EPA performs a number of analyses to determine the risks from aggregate exposure to pesticide 

residues. First, the EPA determines the toxicity of pesticides. Second, the EPA examines exposure to the 

pesticide through food, drinking water, and through other exposures that occur as a result of pesticide use in 

residential settings.

I. Summary of Petitioned-for Tolerance Exemption

In the Federal Register of October 25, 2013, (78 FR 63941), the EPA issued a notice pursuant to FFDCA 

section 408(d)(3), 21 U.S.C. 346a(d)(3), announcing the filing of a pesticide tolerance petition (PP 3F8148)

by Technology Sciences Group, Inc., on behalf of Agri-Neo, Inc., 3485 Ashby Saint-Laurent (Quebec), 

H4R 2K3, Canada. The petition requested that 40 CFR part 180 be amended by establishing an exemption 

from the requirement of a tolerance for residues of Tetraacetylethylenediamine (TAED) and its metabolite

Diacetylethylenediamine (DAED). The notice referenced a summary of the petition prepared by the 

petitioner, Technology Sciences Group, Inc., (on behalf of Agri-Neo, Inc.), which is available in Docket ID 

Number EPA-HQ-OPP-2013-0277 via http://www.regulations.gov.

II. Toxicological Profile

Consistent with section 408(b)(2)(D) of FFDCA, the EPA reviewed the available scientific data and other 

relevant information on Tetraacetylethylenediamine (TAED) and its metabolite Diacetylethylenediamine 

(DAED), and considered its validity, completeness, and reliability, as well as the relationship of this 

information to human risk. The EPA also considered available information concerning the variability of the 

sensitivities of major identifiable subgroups of consumers, including infants and children.

A. Overview of Tetraacetylethylenediamine (TAED) and its metabolite

 Diacetylethylenediamine (DAED).

Tetraacetylethylenediamine, commonly abbreviated TAED (CAS No. 10543-57-4), is a federally registered 

antimicrobial active ingredient used most often as a bleaching activator. As a pesticide, TAED is present 
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in combination with two other biochemical active ingredients (potassium silicate, and sodium percarbonate) 

in an end use product intended for the early season control of bacterial and fungal pathogens on turf grass, 

golf courses, greenhouses and in nursery or in field-grown rice and strawberries. As an antimicrobial 

active ingredient, TAED is often present with sodium percarbonate for the sole purpose of generating 

peroxyacetic acid (PAA) and hydrogen peroxide. For pesticidal uses, the end use product is in granular 

form. The product must be tank mixed with water. As a result of the tank mixing, part of the TAED 

molecule generates PAA and the remaining part of the TAED molecule metabolizes into 

diacetylethylenediamine (DAED). The potassium silicate, also a part of the tank mixing, remains 

unchanged in the mixture and enhances systemic acquired resistance (SAR) to bacterial and fungal 

pathogens in the treated plants. 

Based on the above chemical reactions, it can be concluded that TAED has no direct pesticidal activity. 

Additionally, upon completion of the chemical reaction, the substances which are exhibiting the pesticidal 

activity are PAA, hydrogen peroxide and potassium silicate. DAED, although present on the commodities 

at the time of application, exhibits no pesticidal activity and is considered to be a metabolite of TAED. 

All of the biochemical active ingredients in this product that are present either at the start or formed upon 

tank-mixing, are exempt from the requirement of tolerance as follows:

 Potassium silicate: All food commodities when applied at rates not exceeding 1% by weight in 

aqueous solutions (40 CFR 180.1268)

 Sodium percarbonate: exempted under as hydrogen peroxide, since it is converted to hydrogen 

peroxide immediately when in contact with water and it is the hydrogen peroxide that is the residue 

of concern. 

 Hydrogen peroxide is exempt from the requirement of a tolerance in or on all food commodities 

when applied at < 1% per application (40 CFR 180.1197)

 Peroxyacetic Acid: In or on all food commodities (40 CFR 180.1196(c))

Currently, there are registered antimicrobial uses for TAED/DAED as a commercial laundry sanitizer and 

hard surface disinfectant used in medical settings only. Therefore, the uses of TAED/DAED as a pesticide, 

as described above, are considered as a new use/first food use.

TAED is not classified as a biochemical active ingredient because it is not a naturally occurring substance, 

does not have a nontoxic mode of action, nor a history of exposure to humans and the environment 

demonstrating minimal toxicity. However, since TAED generates PAA, a biochemical active ingredient, 

data and other information submitted in support of the registration of a new use/first food use for TAED as 

a fungicide/bactericide under Section 3(c)(5) of the Federal Insecticide, Fungicide and Rodenticide Act 

(FIFRA) has been reviewed by the Biopesticides and Pollution Prevention Division (BPPD), and it has 

been determined that the current data requirements (40 CFR part 158.2010 through 158.2070) for 

registration of a new use/first food use for a pesticide have been satisfied.

B. Biochemical Pesticide Toxicology Data Requirements

All applicable mammalian toxicology data requirements supporting the request for an exemption from the 

requirement of a tolerance for residues of Tetraacetylethylenediamine (TAED) and its metabolite 

Diacetylethylenediamine (DAED) in or on rice and strawberries have been fulfilled with data or 

information submitted by the petitioner or data waiver requests that have been granted by the EPA.
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As described in the overview section of this document, certain chemical reactions between the a.i.s, sodium 

percarbonate and TAED occur, when in the presence of water in the tank mix. As a result of the chemical

reaction, TAED generates PAA and DAED, a metabolite of TAED. Due to the potential that residues of 

TAED’s metabolite, DAED, could be present on food commodities, all TGAI Tier I human health data 

requirements were required including information on the toxicity on the metabolite. Information from a

recent kinetic study has shown that TAED is converted >99% to DAED (HERA, 2002). In support of this 

application and petition for the requirement of a tolerance exemption, the majority of the available toxicity

studies submitted were conducted on TAED with a few studies tested on DAED. However, given that 

almost all of TAED is converted to DAED, and the recognized structural-similarity of TAED and DAED, 

EPA has assumed that both chemicals have similar toxicity; and therefore, TAED toxicity data will be used 

for DAED.

The following is a summary of EPA’s review of the toxicity profile of this biochemical:

 

1. Acute Toxicity (OCSPP Guideline Nos. 870.1100, 870.1200, 870.1300, 870.2400, 870.2500, and 

870.2600; Master Record Identification (MRID) Nos. 48653202, 48653203, 48653204, 48653205, 

48653206, 48653207, 45299702, 49043703, 45712902, 46204801, 45712903, & HERA 2002,):

The petitioner submitted data on the proposed End Use Product (EP), Ato Cide Granular (EPA File Symbol 

No. 88306-G), in order to fulfill the biochemical pesticide date requirements for Acute Toxicity. 

The acute oral median lethal dose (LD50) in rats was equal to 1,750 milligrams per kilogram (mg/kg) 

bodyweight in rats. There were no observed toxicological effects on the EP in the acute oral study 

submitted by the petitioner. The EP is further classified as Toxicity Category III for acute oral toxicity. 

The acute dermal LD50 in rats was greater than 5,050 mg/kg bodyweight in rabbits. The EP

is further classified as Toxicity Category IV for acute dermal toxicity. 

The acute inhalation median lethal concentration (LC50) was greater than 

2.26 milligrams per liter (mg/L) in rats and showed no significant inhalation 

toxicity. The EP is classified as Toxicity Category IV for acute inhalation toxicity. 

A primary eye irritation study on rabbits indicates that EP caused eye iritis, corneal opacity, a conjunctivae 

(redness and chemosis) in rabbit eyes. Redness and chemosis was observed in all three animals after 1 hour 

and lasted until day 10 (redness) and day 17 (chemosis). Iritis was observed in one animal after 24 hours 

and lasted until day 10. Corneal opacity was observed in three animals after 24 hours and lasted in one 

animal through 21 days when experiment was terminated. The EP is classified as severely irritating to the 

eye; therefore is classified as Toxicity Category I for primary eye irritation.

A skin irritation study on rabbits indicates that the EP is caused slight to severe erythema through day 14 

and very slight to slight edema at 24 hours through day 10 in rabbits. The substance was scored moderately 

irritating; however, based on the presence of necrosis in one animal, the EP is classified as corrosive. The 

EP is classified as Toxicity Category I. for primary dermal irritation.

Data indicates very faint to faint erythema in 17 of 20 test animals after challenge treatment. The EP is 

considered a dermal sensitizer.

Due to this likely potential of residues of TAED/DAED being present on food commodities, the petitioner 

also submitted data on the TAED, and its metabolite DAED.
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The acute oral median lethal dose (LD50) in rats was equal to 7,940 milligrams per kilogram (mg/kg) 

bodyweight in rats. There were no observed toxicological effects on TAED in the acute oral study

submitted by the petitioner. TAED is further classified as Toxicity Category IV for acute oral toxicity. 

The HERA (2002) document indicates that a submitted acute oral toxicity study on DAED is defined as 

non-toxic by the study authors. LD50 > 2,000 mg/kg body weight in rats (highest dose tested).

The acute dermal LD50 in rats was greater than 2,000 mg/kg bodyweight in rabbits (highest dose tested). 

TAED and its metabolite DAED is further classified as Toxicity Category III for acute dermal toxicity. 

The acute inhalation median lethal concentration (LC50) was greater than 

2.08 milligrams per liter (mg/L) in rats and showed no significant inhalation 

toxicity. TAED and its metabolite is classified as Toxicity Category IV for acute inhalation toxicity. 

A primary eye irritation study on rabbits indicates that caused produced minimal ocular irritation in 2 of 6 

animals. Effects at 24 hours consisted of minimal palpebral redness. All irritation had ameliorated at 72 

hours. TAED is classified as minimally irritating to the eye.

Two skin irritation studies were performed for TAED on rabbits. The first study, the test substance 

produced minimal cutaneous irritation in 3 of 6 animals. Effects at the 24 hours consisted of barely 

perceptible erythema, with one site showing minimal edema. All irritation had disappeared at 72 hours. The 

second study, no dermal irritation was noted at any time during the study. Based on the results of the two 

studies, TAED is classified as minimally irritating to non-irritating to the skin. TAED and its metabolite 

DAED is classified as Toxicity Category IV. for primary dermal irritation.

Data indicates that TAED and its metabolite are not dermal sensitizers.

2. Subchronic Toxicity, Developmental Toxicity, and Mutagenicity Testing (Tier I) (OCSPP Guideline 

Nos. 870.3100, 870.3250, 870.3465; 870.3700, 870.5100, 870.5300, 870.5375; MRID Nos. 45299704, 

45274306, 49043703, 45547201, 45547202 & HERA, 2002):

A 90-day oral toxicity study was conducted on TAED. TAED was administered to Sprague Dawley rats 

orally at dosages of 25, 500, and 1,000 mg/kg/day. A group of 10 animals/sex received the test vehicle, 1% 

carboxymethylcellulose. No mortality was observed in any dose group and no treatment-related clinical 

signs were noted. Dose-related decreases in body weights were noted with 10, 15, and 25% in the low, mid, 

and high-dose groups in males and 10 and 15% in the mid- and high-dose groups in females. Food 

consumption was decreased in these groups with statistical significances in the high-dose males. In the 

clinical pathology there were significant increases in red blood cells, total protein, albumin, and cholesterol, 

and decreases in hemoglobin, hematocrit, MCV, MCH, glucose, creatinine, AST, chloride, and 

triglycerides mostly in the mid-dose or high-dose males and/or females; however, the study authors felt that 

these increases/decreases were not clinically significant. The liver was considered to be the target organ 

based on changes in organ weight, gross necropsy, and microscopic pathology. The livers were enlarged in 

the high-dose males and females and accompanied by an increase in absolute and relative organ weights in 

the high-dose males and the mid- and high-dose females. There was centrilobular cytomegaly in the mid 

and high-dose males and females and a mild degeneration of the seminiferous tubules in the high-dose 

males. Based on body weight changes there would not be a NOEL in males, but a NOEL of 25 mg/kg/day 

in females. Based on microscopic changes in the liver, the NOAEL would be 25 mg/kg/day in males and 

females. 
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Another 90-day oral toxicity study was performed on Sprague-Dawley rats at daily dose levels of 0, 90, 

250, and 800 mg/kg/day and summarized in the HERA document on TAED (Ref 1 and 3). No mortality

occurred in any dose group and salivation observed in the high-dose group was the only clinical finding. 

Total body weight gain was decreased in male and female rats in high-dose groups. Slightly decreased

hematocrit values in all male dose groups and increased leukocytes in female high-dose group were 

observed were observed. Increased protein values in males and females of the high-dose group and 

increased cholesterol values in female high-dose group were also observed. Relative liver and testes 

weights were significantly increased in male rats of the 250 mg/kg/day dose group. Absolute and relative 

liver weights of males and females and relative adrenal and testes weights in males were statistically 

significantly increased in the 800 mg/kg/day dose group. Histopathological examination revealed 

centrilobular hypertrophy of hepatocytes in all high-dose group animals. This effect reversed completely

with the 28 day recovery period. Centrilobular hypertrophy was also noted in some of the male and female 

rats in the 90 and 250 mg/kg/day groups; however, the effect was borderline not considered a clear 

substance related effect since it was also noted in some of the control animals. Adverse effects were clearly 

noted in the 800 mg/kg/day dose group and changes in organ weights were present in the 250 mg/kg/day

dose group; therefore, the NOAEL is 90 mg/kg/day and the LOAEL is 250 mg/kg/day. 

The HERA document also makes mention of a 13-week rat feeding study on DAED with a NOEL of 5,700 

mg/kg/day reported in a handbook of environmental chemistry; however, no reference was given in the 

handbook so the study could not be validated (Ref. 1).

A 90-day dermal toxicity study was performed on Sprague-Dawley rats at daily dose levels of 0, 20, 200, 

and 2,000 mg/kg/day and submitted (Ref. 3). The daily doses were delivered by dermal application once a 

day for six hours. One control male, two 200 mg/kg/day females, and one 2,000 mg/kg/day female did not 

survive to termination of the study; however, these deaths were attributed to the wrapping procedure and 

not result of the TAED since no clinical signs were noted prior to death that would have suggested an effect 

from the test substance. No treatment related effects were noted at the 0, 20, or 200 mg/kg/day in clinical 

observations, body weight and food consumption data, ophthalmologic findings, clinical pathology 

findings, gross necropsy findings, and organ weight data. The only effect found was minimal centrilobular 

hypertrophy (cytomegaly) in 8/10 males and 4/10 females at the 2,000 mg/kg/day dose. This effect was not 

found in the lower dosed rats that died in the study or had gross lesions associated with the liver. The 

NOEL is determined to be of equal to or greater than 200 mg/kg/day. Based on the minimal effects seen at 

the high dose group, the NOEL is likely to be much closer to 2,000 mg/kg/day than 200 mg/kg/day.

A 13-week inhalation toxicity study was performed on three groups of 12 male Wistar rats at daily dose 

levels of 12.2, 60.3, and 99.7 mg/m3and summarized in the HERA document on TAED (Ref 1 and 3). 

Male rats were exposed in whole body inhalation chambers to TAED for six hours a day, five days a week, 

for 13 weeks. Male rats were used as they were more sensitive than females in the acute inhalation study. 

Following exposure, six rats were killed and examined by whole body necropsy. The remaining six rats of 

each dose group were maintained without further treatment for 13 weeks to investigate the reversibility of 

treatment-related effects. There was no mortality in any dose group. There were statistically significant 

increases in absolute and relative liver and kidney weights; however, all organ weights returned to normal 

values following the recovery period except for a small increase in liver weight for the high-dose group. 

There was a statistically significant reduction in hemoglobin and an increase in platelet numbers in the 

high-dose group and an increase in the number of monocytes in the high and mid-dose groups; however, 

these values returned to normal following the recovery period. Glucose levels and aspirate transaminase 

activity were reduced in all dose groups. Increased CA+2, serum total protein, and albumin and reduced 

alanine transaminase activity were found in the high and mid-dose groups and increases in total cholesterol 
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and pseudocholinesterase activity and reduced alkaline phosphatase activity in the high-dose group; 

however, these values returned to normal following the recovery period. Following necropsy, one rat in the 

high-dose group had a slight enlargement of the liver, but no other abnormal features were noted in any of 

the other rats. Microscopic examination showed no treatment-related effects in the lungs. There was a 

systemic response as reported by significant increases in kidney weights in the high and mid-dose groups 

and in liver weights in all dose groups. Hypertrophy of centrilobular hepatocytes was considered to be due 

to induction of hepatic microsomal drug metabolizing enzymes based on further ultrastructural studies that 

demonstrated proliferation of smooth endoplasmatic reticulum in these hepatocytes. Eosinophilic droplets 

in the tubular epithelial cells in kidneys were also noted, usually referred to as hyaline droplets composed 

principally of the normal male rat urinary protein α2μ-globulin. Due to the fact that in another study where 

female and male rats were fed TAED and male rats developed this same kidney issue and female rats did 

not, the kidney findings in this study are specific to the male rat and not relevant to humans. Examination 

of recovery rats showed that these effects were reversible and returned to normal. The NOAEL for systemic 

effects cannot be determined from this study as the whole body of the animal was exposed to TAED dust 

and the oral ingestion of unquantifiable amounts of TAED would have occurred due to normal grooming 

practices. Under the condition of the study, the NOAEL in rat lungs, respiratory tract or nasal mucosa is 

99.7 mg/m3.

A developmental toxicity study was performed on pregnant Sprague-Dawley rats during days 6 through 15 

of pregnancy at daily dose levels of 0, 40, 200, and 1,000 mg/kg/day and submitted (Ref. 3). On day 20, the 

pregnant females were caesarean-sectioned and subjected to post-mortem examination. No clinical signs, 

behavioral changes, death or abortion were noted in any dose group. A dose-related lower mean body

weight gain and mean daily food consumption was observed in the 200 and 1,000 mg/kg/day dose groups. 

No embryotoxic effects were found. In the 40 and 200 mg/kg/day dose groups, there were statistically

lower mean fetal weight and higher percentage of skeletal variants, these values were well within the range 

of historical control values; therefore, these effects were considered not toxicologically significant. 

However, mean fetal weight and placental weight were lower and skeletal variants were higher in the 1,000 

mg/kg/day dose group. The maternal toxicity NOEL was determined to be 40 mg/kg/day. The 

developmental toxicity NOEL was determined to be 200 mg/kg/day.

A bacterial reverse mutation assay (Ames test) with five strains of Salmonella typhimurium with and 

without metabolic activation at dose concentrations of 10, 100, 1,000, and 10,000 μg/plate was performed 

and submitted (Ref 3). The results of the test indicated that TAED exerted no bactericidal/static properties 

and all strains were non-mutagenic. In another bacterial reverse mutation assay as summarized in the 

HERA document on TAED, DAED was evaluated in the presence of four strains of S. typhimurium and one 

strain of E. coli with and without S9 metabolic activation (Ref. 1 and 3). Prior to the main study, a range 

finding assay was performed with one strain of S. typhimurium without metabolic activation to determine 

cytotoxicity. DAED assayed at concentrations from 0.1 to 10,000 μg/plate in triplicates and found not to be 

cytotoxic and not mutagenic. In the main assay study, DAED was tested at 5,000 μg/plate. A statistically

significant increase in the number of colonies was not observed with DAED; therefore, DAED was 

determined to be non-mutagenic.

Two in vitro mammalian chromosome aberration tests conducted in human lymphocytes were performed 

and submitted (Ref. 3). Four treatment conditions were used, 4 hours of exposure to TAED in the presence 

of S9 metabolic activation with cell harvest at 16 and 40 hours later, and 20 and 44 hour continuous 

exposures in the absence of metabolic activation. In experiment one, 20-hour harvest cultures were exposed 

to eight concentrations of TAED, 17.81, 35.63, 71.25, 142.5, 285, 570, 1,140, and 2,280 μg/ml. The three 

highest dose concentrations, 570, 1,140, and 2,280 μg/ml were selected for chromosomal analysis. The test 

substance did not induce any significant increases in the frequency of cells with aberrations either with or 
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without S9 metabolic activation. The test substance also did not induce any significant increase in the 

numbers of polyploid cells at any of the dose levels. In experiment two, three dose concentrations, 570, 

1,140, and 2,280 μg/ml were harvested at 20-hours and observed for chromosomal analysis similar to 

experiment one; however, the highest dose concentration, 2,280 μg/ml, was also harvested at 44 hours and 

observed for chromosomal analysis. The 44 hour mitotic index data indicated a toxic effect at the maximum 

dose level tested of 2,280 μg/ml (~35% reduction in mean mitotic index) with and without S9 metabolic 

activation, although there was some inter-culture variation. Statistical analysis indicated that only a single 

significant increase in aberrant cell frequency in TAED treated cultures (at 570 μg/ml with S9 mix, 20 hour 

harvest, experiment two, p = 0.03); however, there was no such statistical increase in experiment one and 

the results were not reproducible. The test material did not induce a significant increase in the numbers of 

polyploid cells at any dose level in experiment two. Based on the results of the two experiments, the test 

substance, TAED, did not induce biologically or reproducible statistically significant increases in the 

frequency of cells with chromosome aberrations with or without S9 metabolic activation and is considered 

to be non-clastogenic to human lymphocytes in vitro. In another in vitro mammalian chromosome 

aberration test as summarized in the HERA document on TAED, TAED was evaluated in V79 cells of the 

Chinese hamster (Ref. 1 and 3). The V79 cells were exposed to TAED for four hours with and without S9 

metabolic activation and harvested at 7, 18, and 28 hours and evaluated for chromosome aberrations. The 

TAED concentrations tested were 500 μg/ml in cultures harvested at 7 and 28-hours and 20, 200, and 500 

μg/ml in cultures harvested after 18-hours. The mitotic index was only slightly reduced in the 500 μg/ml 

concentration at the 7 hour harvest with and without S9 activation. There was no relevant increase in cells 

with structural aberrations. Based on these results, TAED was determined to be non-clastogenic in V79 

cells of the Chinese hamster in vitro. 

One in vivo mammalian micronucleus test was conducted in mice and submitted (Ref. 3-5). The test 

substance, TAED, was given to ten mice (five males and five females) at the dose concentrations of 312.5, 

625, and 1,250 mg/kg bw. The control and 1,250 mg/kg dose group were sacrificed at 24, 48, and 72 hours 

after dosing. The 312.5 mg/kg, 625 mg/kg, and positive control dose groups were sacrificed at 24 hours 

after dosing. Bone marrow was extracted from the femurs and smear preparations were made and stained. 

There were no statistically significant increases in the frequency of micronucleated polychromatic 

erythrocytes in the treatment groups compared to the control groups. No significant change in the 

polychromatic/normochromatic erythrocytes (PCE/NCE) ratio was observed (compared to the positive test 

control) after dosing with the test material, but the presence of clinical observations and premature deaths 

(three animals dosed at 1,250 mg/kg) indicated that systemic absorption had occurred. Based on the test 

results, TAED was considered to be non-genotoxic. In another in vivo mammalian micronucleus test in 

mice as summarized in the HERA document (Ref.1) on TAED, TAED was tested at dose levels of 250, 

1,250, and 2,500 mg/kg bw administered twice, separated by an interval of 24 hours (Ref. 1 and 3). The 

animals were sacrificed at 30 hours after the first test substance application and bone marrow smears were 

prepared. No premature deaths occurred and the mean micronucleated cell count of TAED was comparable 

to the negative control at all dose levels. No significant change to the PCE/NCE ration was observed, but 

the presence of clinical observations indicates that the systemic absorption had occurred. Based on the test 

results, TAED was considered to be non-genotoxic.

Toxicity endpoints and points of departure (PODs) for residential and occupational exposure scenarios to 

TAED are summarized below. Description of studies used as the basis for the selected endpoints are as 

follow:

Acute Dietary Endpoint: An acute endpoint was not selected based on the absence of an appropriate 

endpoint attributable to a single dose. 
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Chronic Dietary Endpoint: The chronic dietary endpoint was derived from the rat 90 day oral study, where 

the NOAEL was 90 mg/kg/day. The LOAEL is 250 mg/kg/day based on significant increase in relative 

liver and testes weights in male rats. This study is also protective of the maternal and developmental 

effects observed in the developmental toxicity study (MRID 45299704).

Short (1-30 days) Term incidental Oral Endpoint: The short-term incidental oral endpoint was derived 

from the 90 day study in rats, where the NOAEL was 90 mg/kg/day. The LOAEL is 250 mg/kg/day based 

on significant increase in relative liver and testes weights in male rats. This study is appropriate for the 

duration of exposure as well as it is protective for the population of concern (young children). This study is 

also protective of the maternal and developmental effects observed in the developmental toxicity study

(MRID 45299704).

Short (1-30 days) Term Dermal Endpoint: A dermal endpoint was not selected based on the absence of an 

appropriate endpoint from the available dermal study. An affect was not observed at the limit dose of 2000 

mg/kg/day. 

Short (1-30 days) Term Inhalation Endpoint: An inhalation endpoint was not selected based on the absence 

of an appropriate endpoint from the available inhalation study. An effect was not observed the highest dose 

tested (99.7 mg/m3). 

Residue study on rice or strawberries were not submitted; therefore, the Agency calculated residues using 

the known environmental fate information for TAED and DAED and the revised application rates from 

label, intervals, and timing for rice and strawberries as inputs in the Agency’s Terrestrial Residue Exposure 

(T-REX) model. The Agency used a default foliar dissipation half-life value of 35 days in calculating 

estimated residues in its T-REX model Version 1.5.2. Tank mixture data (the proposed EP, Ato Cide 

Granular, mixed with water) submitted by the applicant under MRID 49043702 showed that at the time of 

application, TAED from the proposed EP had reacted with hydrogen peroxide (hydrogen peroxide was 

formed from the reaction of sodium percarbonate from the proposed EP with the water in the mixing tank) 

to form peroxyacetic acid (PAA) and its metabolite DAED. The amount of DAED formed from the 

reaction of TAED and hydrogen peroxide in the tank mixture was approximately 50% of the initial amount 

of TAED in the proposed EP. Based on the application use rates and intervals, the amount of potential 

DAED is 2.23 ppm on rice and 8.79 ppm on strawberries. The Agency also calculated residues in drinking 

water sources from use of the pesticide using the screening model, FQPA Index Reservoir Screening Tool 

(FIRST). 

The FIRST model calculated surface water estimated drinking water concentrations (EDWCs) of 74 ppb.

Based on the residues estimated in the T-REX model from the application rates and intervals on the 

proposed EP label, the percent of the chronic Population Adjusted Dose (%cPAD) calculated in the Dietary

Exposure Evaluation Model-Food Commodity Intake Database (DEEM-FCIDTM) Version 3.16 analysis for 

dietary exposure is the highest in the population subgroups, Non-nursing infants and Children (age 1-2), at 

9.2%. The Agency’s Level of Concern (LOC) for %cPAD is 100; therefore, the calculated %cPAD for 

DAED is well below the Agency’s LOC for the quantitative chronic dietary risk assessment. In addition, 

any possible quantifiable dietary exposure is expected to be mitigated even further due to the use of the 

pesticide product containing TAED/DAED as an effective control of early season fungus and bacterial 

diseases that will be applied well before any food commodity is harvested.
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III. Aggregate Exposure

In examining aggregate exposure, FFDCA section 408 directs the EPA to consider available information

concerning exposures from the pesticide residue in food and all other non-occupational exposures, 

including drinking water from ground water or surface water and exposure through pesticide use in 

gardens, lawns, or buildings (residential and other indoor uses).

The Agency aggregated exposure of potential short (1-30 days) term residential post-application incidental 

oral exposure and chronic dietary exposure for the population subgroup, children (age 1 to < 2). The 

quantitative exposures via the diet and residential uses (post-application incidental oral) for this pesticidal 

use. 

The aggregate MOE for the population subgroup, children (age 1 to < 2), is 7400 MOEs greater than 1000 

do not exceed the Agency’s LOC; therefore, aggregate risks for this new pesticidal use of TAED/DAED 

are not considered to be of concern. Based on the results of the aggregate risk assessment, unreasonable 

adverse effects are not anticipated when the pesticide product is used according to label instructions.

EPA recognizes that there are additional uses for TAED/DAED Antimicrobial Division. The two current

federally registered end-use products are for use in institutional and commercial laundry sanitization (EPA 

Reg. No. 16930-5) and part of a two-part system to create an end use hard surface disinfectant solution in 

medical/dental/veterinary facilities (EPA Reg. No. 1043-125). These two products have a similar 

perhydrolysis reaction that yields PAA and hydrogen peroxide, along with the metabolite, DAED. The 

current dietary and residential risk assessment for this new pesticidal use is highly conservative and 

protective of any potential exposure to these additional antimicrobial uses because the aggregate MOE of 

7400 is well above the Agency’s LOC of 1000. For additional information on these antimicrobial uses, 

refer to the preliminary work plan for TAED (docket ID number EPA-HQ-OPP-2013-0608; 

www.regulations.gov), which is currently undergoing registration review.

In consideration of the above information, the Agency has determined the risk from aggregate exposure 

(via oral, dermal, and inhalation exposures) is negligible; there is reasonable certainty that no harm will 

result to the general population or to infants and children from aggregate exposure to TAED and its

metabolite, DAED.

Food Exposure: In the absence of residue data on rice or strawberries; the Agency calculated residues 

using the known environmental fate information for TAED and DAED and the revised application rates, 

intervals, and timing for rice and strawberries as inputs in the Agency’s T-REX model Version 1.5.2. In the 

absence of chemical-specific half-life data, the Agency used the Environmental Fate and Effects Division’s 

(EFED’s) default foliar dissipation half-life of 35 days in calculating estimated residues in its T-REX 

model. The Agency used EFED’s default foliar dissipation half-life value of 35 days, which represents the 

upper bound of the half-lives reported in Willis and McDowell (1987). For more information on the use of 

this default foliar dissipation half-life value of 35 days in T-REX modeling, refer to the T-REX User’s 

Guide located at the following website: 

http://www.epa.gov/oppefed1/models/terrestrial/trex/t_rex_user_guide.htm. Tank mixture data (the 

proposed EP, Ato Cide Granular, mixed with water) submitted by the applicant under MRID 49043702 

showed that at the time of application, TAED (from the proposed EP) had reacted with hydrogen peroxide 

(hydrogen peroxide was formed from the reaction of sodium percarbonate from the proposed EP with the 

water in the mixing tank) to form PAA and the metabolite of TAED, DAED. The amount of DAED formed 

from the reaction of TAED and hydrogen peroxide in the tank mixture was approximately 50% of the 

initial amount of TAED in the proposed EP. Based on the application use rates and intervals, the amount of 
10

potential DAED is 2.23 ppm on rice and 8.79 ppm on strawberries. The T-REX Version 1.5.2 inputs to 

determine the potential residues were as follows: 1) EFED’s default foliar dissipation half-life of 35 days, 

2) application rate (from label) of 0.3 lbs a.i./acre (DAED), 3) application interval (from label) of 7 days, 

and 4) max number of applications (from label) of 2 for rice and 3 for strawberries. The application rate of 

0.3 lbs a.i./acre of DAED was calculated by multiplying the application rate of 3 lbs product/acre by 10% 

DAED. The T-REX upper bound Kenaga worksheet values for rice and strawberries (represented by the 

dietary-based estimated environmental concentrations [EECs] “fruits/pods/seeds”) were 8.42 ppm and 

11.83 ppm, respectively; however, these residue values do not take into consideration any pre-harvest 

intervals (PHIs). The T-REX Version 1.5.2 model worksheets do provide residue values for each day up to 

370 days after first application based on first-order decay rates (see T-REX User’s Guide for details on 

residue calculations 

http://www.epa.gov/oppefed1/models/terrestrial/trex/t_rex_user_guide.htm#Section3_1); therefore, based 

on the proposed product PHIs of 60 days for rice and 15 days for strawberries, the amount of potential 

DAED is 2.23 ppm for rice and 8.79 ppm for strawberries.

Timing of Application in Rice and Strawberries

For rice, the product would be applied at least 60 days prior to harvest; therefore, very little DAED residue 

would be expected at the time of harvest due to the following facts: 1) the rice kernel is not fully formed at 

application 60 days before harvest and 2) DAED is readily biodegradable (HERA, 2002). To further 

expand on the timing of application in rice and the potential for residues, additional information was 

submitted in MRID 49266701, pages 4-6. The information explained outlined rice production. Specifically, 

that there are four major milestones in a growing season of U.S. rice: 1) planting, 2) panicle initiation, 3) 

heading, and 4) harvest. From planting to harvest, the typical U.S. rice growing season is 130 days. At the 

panicle initiation, which is approximately at the half-way point of the growing season (60-70 days), most 

fungicides and bactericides, including this proposed EP, are sprayed by aerial application onto the rice crop 

since it is at this time that many rice pathogens attack the plant and induce disease. The rice diseases in the 

U.S. that the EP is intended to control are the bacterial panicle blight and the fungal pathogens sheath 

blight, blast, smut, stem rot, and narrow brown leaf spot. The EP is intended to control all of these diseases 

preventively so the diseases cannot establish on the rice crop as this is when the EP is most effective. The 

EP is not intended to be applied on the crop once the disease is already present and established as it is not 

intended to be a cure-all. In addition, the EP contains the a.i., potassium silicate, a known Systemic 

Acquired Resistance (SAR) inducer, which stimulates crop plant immunity to disease. Applying this EP 

early in the growing season induces SAR and further protects the plant against any surviving bacteria or 

fungi that may remain on the plant or in the field. The EP will be applied no later than 60-70 days after 

planting during the panicle initiation stage, which is at least 60 days prior to harvest. The edible portion of 

the plant, the rice kernels, have not yet been formed. At the heading stage, which is 100 days after planting 

and 30-40 days after application of the EP, the fertilized flowers have turned into the rice grains or kernels. 

These rice grains or kernels ripen over the next 30 days and are harvested around day 130. Based on the 

provided information that the EP is applied around days 60-70 (panicle initiation stage), the edible rice 

grain or kernel forming around day 100 (heading stage), and the rice grain or kernel harvested at day 130, 

the applicant expects that it is highly unlikely that any DAED residue would be present on the edible 

portion of the rice crop. The Agency agrees that it is highly unlikely that DAED residue would remain on 

the edible portion of the rice crop at the time of harvest, which is approximately 60-70 days after 

application of the EP based on the preceding information; however, a quantitative risk assessment was 

conducted for this use on rice to assess potential risks (if any) from dietary exposure.

For strawberries, data was submitted on the timing of the application in strawberries and the potential for 

residues under the cover letter dated 10/15/2013 (value proposition information section) and in MRID 
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49266701, pages 7-8. The data indicated that the growing season for strawberries after transplant is 

typically 90-120 days in Florida and California and the EP would be applied within the first 30-45 days of 

the growing season. The EP is applied in the early part of the growing season to control three major plant 

diseases, angular leaf spot, botrytis, and powdery mildew. For angular leaf spot, caused by the bacterium, 

Xanthomonas fragariae, and powdery mildew, caused by the fungus, Podosphaera aphanis, the plant 

diseases are generally transmitted to the field by contaminated transplants; therefore, it is recommended to 

apply pesticides early in the growing season to control the diseases before they are established in the 

strawberry plant or contaminate other strawberry plants in the field. For grey mould, caused by the fungus, 

Botrytis cinerea, the plant disease is from spores that lie dormant on dead strawberry leaves in the field and 

cover young flowers until fertilization and fruit set occur. At that stage the spores germinate and the fungus 

makes the fruit rot (MRID 49266701, page 7). Like with the other two main strawberry plant diseases, it is 

recommended to apply fungicides early in the growing season to kill the grey mould spores before the 

disease can get a foothold on the strawberry crop later in the season. As previously stated, the EP contains 

the a.i., potassium silicate, a known SAR inducer, which stimulates crop plant immunity to disease. 

Applying the EP early in the growing season allows the strawberry plant to trigger SAR and further 

protects the plant from fungal spores that remain on the plant or in the field. The first harvest of 

strawberries is at least 60 days into the growing season and subsequent harvests occur weekly after the first 

harvest. Based on the proposed labeling, the final application of the product would occur approximately 15 

days prior to the first harvest; therefore, potential residues of DAED would be expected to be less than the 

calculated residue of 8.79 ppm from the T-REX modeling and less in subsequent harvests since T-REX 

modeling does not take into consideration biodegradation of DAED and any loss of residues based on 

processing of the strawberry crop. (Ref 3)

Drinking Water Exposure: To estimate drinking water exposure to DAED, EDWCs were generated by

BPPD using the OPP’s standard suite of models. The generated EDWCs were used in DEEM-FCIDTM 

Version 3.16 to calculate the potential dietary exposure of DAED in drinking water sources. The screening 

model FQPA Index Reservoir Screening Tool (FIRST) was used to calculate surface water EDWCs. The 

FIRST model and its description are available at the following EPA website: 

http://www.epa.gov/oppefed1/models/water/.The following inputs were used to estimate surface water 

EDWCs in the FIRST screening model: 1) 0.26 lbs a.i. (DAED)/acre based on highest support use rate for 

turf and landscape applications on the proposed EP label, 2) maximum number of applications of 121 per 

year and application interval of 3 days for turf and landscape applications on the proposed EP label, 3) 

OPP’s EFED default percent cropped area (PCA) factor of 0.87 for turf uses, 4) Koc of 25 ml/g, 5) 35 days 

for soil aerobic metabolic half-life (EFED default foliar dissipation half-life value used in T-REX 

modeling), 6) EFED default of 2 days for non wetted-in pesticide, 7) EFED default for ground spray

application of 6.4% for %drift and 99% for application efficiency, 8) no soil incorporation depth (0.0 

inches), 9) water solubility of 2 g/l (converted to 2002 ppm), 10) 70 days for aerobic aquatic metabolic 

half-life (EFED default of 2x the soil aerobic metabolic half-life if unknown), and 11) 365 days for 

photolysis half-life. The inputs for Koc and water solubility were taken from the HERA document (2002) 

and the Agency’s Registration Review Preliminary Work Plan (PWP) on TAED (EPA, 2014). For the 

photolysis half-life input, the Agency used 365 days as data/information listed in the HERA document 

(2002) and the Agency’s PWP on TAED (2014) indicate that DAED appears to be stable in this setting. 

Chronic exposure of DAED in surface drinking water sources is represented by annual average 

concentrations estimated by the FIRST model. Upper-bound Tier I modeling predicts that the 

concentrations of DAED in surface drinking water sources are not likely to exceed 74 ppb (or 0.074 ppm) 

for the chronic annual average concentrations. DEEM-FCIDTM Version 3.16 Results using Residues from TREX and FIRST Modeling Dietary risk assessment incorporates both exposure and toxicity of a given 

pesticide. For chronic assessments, the risk is expressed as a percentage of a maximum acceptable dose 

(i.e., the dose that EPA has concluded will result in no unreasonable adverse health effects). This dose is 
12

referred to as the population adjusted dose (PAD). The PAD is equivalent to the point of departure (POD, 

NOAEL, LOAEL, e.g.) divided by the required uncertainty or safety factors. For non-cancer chronic 

exposures, EPA is concerned when estimated dietary risk exceeds 100% of the PAD. References that 

discuss chronic risk assessments in more detail are available on the EPA/pesticides web site: “Available 

Information on Assessing Exposure from Pesticides, A User’s Guide,” 21-JUN-2000, web link: 

http://www.epa.gov/fedrgstr/EPA-PEST/2000/July/Day-12/6061.pdf; or see SOP 99.6 (20-AUG-1999).

To evaluate chronic dietary exposure to residues of DAED when used as a pesticide on food (rice and 

strawberry crops) and drinking water sources, the Agency conducted a chronic dietary exposure assessment 

using the Dietary Exposure Evaluation Model software with the Food Commodity Intake Database DEEMFCIDTM, Version 3.16, which incorporates consumption data from USDA’s National Health and Nutrition 

Examination Survey, What We Eat in America, (NHANES/WWEIA). This dietary survey was conducted 

from 2003 to 2008. The data are based on the reported consumption of more than 20,000 individuals over 

two non-consecutive survey days. Foods “as consumed” (e.g., apple pie) are linked to EPA-defined food 

commodities (e.g. apples, peeled fruit - cooked; fresh or N/S; baked; or wheat flour - cooked; fresh or N/S, 

baked) using publicly available recipe translation files developed jointly by USDA/ARS and EPA. For 

chronic exposure assessment, consumption data are averaged for the entire U.S. population and within 

population subgroups. Based on analysis of the 2003-2008 WWEIA consumption data, which took into 

account dietary patterns and survey respondents, EPA concluded that it is most appropriate to report risk 

for the following population subgroups: the general U.S. population, all infants (<1 year old), children 1-2, 

children 3-5, children 6-12, youth 13-19, adults 20-49, females 13-49, and adults 50+ years old.

For a chronic dietary exposure assessment, an estimate of the residue level in each food or food-form (e.g., 

orange or orange juice) on the food commodity residue list is multiplied by the average daily consumption 

estimate for that food/food form to produce a residue intake estimate. The resulting residue intake estimate 

for each food/food form is summed with the residue intake estimates for all other food/food forms on the 

commodity residue list to arrive at the total average estimated exposure. Exposure is expressed in mg/kg 

body weight/day and as a percent of the chronic Population Adjusted Dose (cPAD). This procedure is 

performed for each population subgroup. The Agency used the following inputs for the DEEM-FCIDTM 

analysis: 1) calculated residue of 2.23 ppm for rice and 8.79 ppm for strawberries from the T-REX 

modeling, 2) 0.074 ppm for “water, direct, all sources” and “water, indirect, all sources” food categories for 

drinking water from the FIRST modeling, and 3) the chronic Reference Dose (cRfD) or chronic Population 

Adjusted Dose (cPAD) of 0.09 mg/kg bw/day. A PAD is an estimate (with consistent applications of 

generally order-of-magnitude uncertainty factors) of a daily dietary exposure to the human population 

(including sensitive subgroups) that is likely to be without an appreciable risk of deleterious effects during 

a lifetime. The uncertainty factor (UF) that is generally used is 1000, which represents 10X uncertainty

factor for interspecies (extrapolation from animal data to humans), 10X uncertainty factor for intraspecies 

(variability of humans), and the 10X FQPA safety factor. The PAD is represented by the equation below:

Point of Departure (e.g., NOAEL)

PAD = ------------------------------------------

Uncertainty Factors (e.g., 1000)

The chronic PAD (cPAD) was calculated by dividing the NOAEL of 90 mg/kg/day from the 90-day oral 

toxicity study on TAED by the uncertainty factor of 1000, which results in a cPAD of 0.09 mg/kg bw/day.

DEEM-FCIDTM analysis calculates a percent of the cPAD (%cPAD) for each population subgroup by

dividing the dietary exposure (estimated in DEEM-FCIDTM) by the cPAD and multiplying the result by

100%. EPA is concerned when dietary risk exceeds 100% of the cPAD. The %cPAD is represented by the 

equation below:
13

Exposure

%cPAD = ------------- * 100%

cPAD

Based on the residues estimated in the T-REX and FIRST models from the application rates and intervals 

on the proposed EP label, the %cPAD is the highest in the population subgroups, Non-nursing infants and 

Children (age 1-2), at 9.2%. As stated above, for chronic dietary assessments, the Agency is concerned 

when dietary risks exceeds 100% of the cPAD; therefore, the calculated %cPAD for DAED is well below 

the Agency’s LOC.

Based on the preceding information, if dietary exposure to humans occurs, the Agency has determined that 

there is reasonable certainty of no harm to humans when exposed to residues of DAED, the metabolite of 

TAED, from pesticidal use from this particular pesticide product when label instructions are followed. (Ref. 

3)

Other Non-occupational Exposure: The residential post-application exposure risk assessment was 

conducted using a POD of 90 mg/kg bw/day (the NOAEL from the 90-day oral toxicity study) for the 

incidental oral route of exposure. The short (1-30 days) term incidental oral endpoint selected for DAED is 

appropriate for the duration of exposure as well as it is protective for the population of concern (young 

children). This endpoint is also protective of the maternal and developmental effects observed in the 

developmental toxicity study (MRID 45299704). BPPD used the POD inputs in the residential postapplication exposure calculation spreadsheet developed in the OPP’s HED (spreadsheets available at the 

following EPA website: http://www.epa.gov/pesticides/science/residential-exposure-sop.html). The body

weight of 11 kg (age 1 to < 2 years) was used for incidental oral exposure scenario since the endpoint 

selected was not developmental and/or fetal effects. The body weights of: 80 kg (adults), 57 kg (age 11 to < 

16 years), and 32 kg (age 6 to < 11 years) were not used in this residential post-application exposure 

scenario since the only endpoint selected was for short (1-30 days) term incidental oral exposure. The 

application rate used for the residential exposure was the maximum application rate on the turf and 

landscape sub label of 0.26 lbs a.i./acre. The application rate input was calculated by multiplying the 

maximum application rate for the turf and landscape use by 10%. The 10% represents the concentration of 

DAED that is applied to the turf and landscape based on the known chemical reaction of the EP with water 

in the tank mix and the results of the tank mix study which showed that at the time of application, DAED is 

approximately 50% of the initial amount of TAED in the product.

The Agency’s LOC is 1000 for residential post-application incidental oral exposure. MOEs were greater 

than the Agency’s LOC of 1000 for all residential post-application incidental oral exposure scenarios. The 

exposure scenario with the lowest MOE was hand to mouth for the population subgroup, children (age 1 to 

< 2), of 23000. Based on the results of the residential post-application incidental oral exposure risk 

assessment, unreasonable adverse effects for children (age 1 to < 2) to DAED are not anticipated when the 

pesticide product is used according to label instructions. (Ref 3)

IV. 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.”
14

EPA has not found TAED nor its metabolite, DAED to share a common mechanism of toxicity with any

other substances, and TAED nor its metabolite, DAED does not appear to produce a toxic metabolite 

produced by other substances. For the purposes of this tolerance action, therefore, EPA has assumed that 

TAED nor its metabolite, DAED does not have a common mechanism of toxicity with other substances. 

For information regarding EPA’s efforts to determine which chemicals have a common mechanism of 

toxicity and to evaluate the cumulative effects of such chemicals, see EPA’s website at 

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

V. Determination of Safety for the United States Population, Infants and Children

FFDCA section 408(b)(2)(C) provides that, in considering the establishment of a tolerance or tolerance 

exemption for a pesticide chemical residue, EPA shall assess the available information about consumption 

patterns among infants and children, special susceptibility of infants and children to pesticide chemical 

residues, and the cumulative effects on infants and children of the residues and other substances with a 

common mechanism of toxicity. In addition, FFDCA section 408(b)(2)(C) provides that EPA shall apply an 

additional tenfold (10X) margin of safety for infants and children in the case of threshold effects to account 

for prenatal and postnatal toxicity and the completeness of the database on toxicity and exposure, unless 

EPA determines that a different margin of safety will be safe for infants and children. This additional 

margin of safety is commonly referred to as the Food Quality Protection Act Safety Factor. In applying this 

provision, EPA either retains the default value of 10X, or uses a different additional or no safety.

Based on the currently available toxicity data, EPA has retained the FQPA Safety Factor (10X). The 

available toxicology database for TAED indicate a potential increase susceptibility under FQPA. In the 

available developmental study, the maternal effects of dead fetuses and decrease food consumption were 

observed along with developmental effects of ↓ fetal weight and placental weights. In addition, since a 2 

generation reproductive study is not available, the severity and extend of these toxicity effects cannot fully

be examined. Therefore, to be protective of sensitive subpopulations, including infants and children, the 

10X FQPA safety factor was retained. Should additional toxicity information on TAED become available 

to the Agency, retaining the FQPA safety factor will be determined. 

VI. Conclusions

EPA concludes that there is a reasonable certainty that no harm will result to the U.S. population, including 

infants and children, from aggregate exposure to residues of Tetraacetylethylenediamine (TAED) and its 

metabolite Diacetylethylenediamine (DAED). Therefore, an exemption is established for residues of the 

pesticide Tetraacetylethylenediamine (TAED) and its metabolite Diacetylethylenediamine (DAED) in or on

rice and strawberries when used in accordance with label directions and good agricultural practices as a 

bactericide and a fungicide.

VII. References

1. HERA. 2002. Human and Environmental Risk Assessment on ingredients of European household 

cleaning products. Targeted Risk Assessment of Tetraacetylethylenediamine (TAED). December 2002

http://www.heraproject.com/files/2-F-04-HERA%20TAED%20full%20web%20wd.pdf

2. Hill, E.F. 1993. Acute and subacute toxicology in evaluation of pesticide hazard to avian wildlife. In: 

Up and Down Procedure Peer Panel Report, July 25, 2000 Meeting, Appendix P-3, National 

Toxicology Program. P45-P67. 

http://ntp.niehs.nih.gov/iccvam/docs/acutetox_docs/udpProc/udpfin01/append/AppP3.pdf
15

3. U.S. EPA 2014. Memorandum from Colin G. Walsh to Menyon Adams. Science Review in Support of 

the Registration of Ato Cide (EPA File Symbol No. 88306-G), an End-Use Product (EP), Containing 

42.50%, 19.99%, and 9.94% of Sodium Percarbonate, Tetraacetylethylenediamine (TAED), and 

Potassium Silicate as its Active Ingredients (A.I.s) and Tolerance Exemption Petition Review in 

Support of TAED, and its Degradate, Diacetylethylenediamine (DAED) (First Food Use). U.S. 

Environmental Protection Agency Office of Pesticide Programs. August 26, 2014.

4. U.S. EPA 2014. Memorandum from Colin G. Walsh to Menyon Adams. Science Review in Support of 

the Registration of Ato Cide (EPA File Symbol No. 88306-G), an End-Use Product (EP), Containing 

42.50%, 19.99%, and 9.94% of Sodium Percarbonate, Tetraacetylethylenediamine (TAED), and 

Potassium Silicate as its Active Ingredients (A.I.s) and Tolerance Exemption Petition Review in 

Support of TAED, and its Degradate, Diacetylethylenediamine (DAED) (First Food Use). U.S. 

Environmental Protection Agency Office of Pesticide Programs. February 27, 2014.

5. U.S. EPA. 2012a. Memorandum from Colin G. Walsh to Menyon Adams. Science Review in Support 

of the Registration of Ato Cide (EPA File Symbol No. 88306-G), an End-Use Product (EP), Containing 

42.50%, 19.99%, and 9.94% of Sodium Percarbonate, Tetraacetylethylenediamine (TAED), and 

Potassium Silicate as its Active Ingredients (A.I.s). U.S. Environmental Protection Agency Office of 

Pesticide Programs. August 8, 2012.

6. U.S. EPA. 2012b. Memorandum from Colin G. Walsh to Menyon Adams. Science Review in Support 

of the Registration of Ato Cide (EPA File Symbol No. 88306-G), an End-Use Product (EP), Containing 

42.50%, 19.99%, and 9.94% of Sodium Percarbonate, Tetraacetylethylenediamine (TAED), and 

Potassium Silicate as its Active Ingredients (A.I.s). U.S. Environmental Protection Agency Office of 

Pesticide Programs. November 28, 2012.

7. U.S. EPA. Dietary Exposure Evaluation Model - Food Commodity Intake Database (DEEMFCID)/Calendex http://www.epa.gov/pesticides/science/deem/

8. U.S. EPA. FIRST (FQPA Index Reservoir Screening Tool)

http://www.epa.gov/oppefed1/models/water/

9. U.S. EPA. SCI-GROW (Screening Concentration In Ground Water)

http://www.epa.gov/oppefed1/models/water/

10. U.S. EPA. Occupational Pesticide Post-application Exposure Data

http://www.epa.gov/pesticides/science/post-app-exposure-data.html

11. U.S. EPA. Standard Operating Procedures (SOP) for Residential Pesticide Exposure Assessment

http://www.epa.gov/pesticides/science/residential-exposure-sop.html