2

EXECUTIVE SUMMARY

EPA received a petition (IN-10604) from Exponent Inc., (1150 Connecticut Ave., Suite 1100 

Washington, DC 20036) on behalf of the Gowan Company LLC (370 South Main Street, Yuma, 

AZ 85367) requesting a tolerance exemption for use of ammonium acetate (CAS Reg No. 631-

61-8) as an inert ingredient (buffering agent) limited to 15% in pesticide formulations under 40 

CFR Part 180.920. EPA published the notice of filing for this petition in the Federal Register on 

December 30, 2013 (78 FR 79359). No substantial comments were received in response to this 

notice. Ammonium acetate is currently approved as an inert ingredient for non-food use. 

The following information in this decision document is reproduced from the petition

submitted by the registrant (MRID 49160501), EPA document, Acetic acid and Salts summary 

document, American Chemical Council (ACC) Acetic Acid and Acetate Panels High Production 

Volume (HPV) Challenge Program.

Ammonium acetate is an ammonium salt of acetic acid. In aqueous solutions acetic acid and 

its salt ammonium acetate dissociate into the acetate anion (CH3COO-) and the respective 

cations (H+ and NH4+). The cations and ammonia (also a human metabolite) are physiological 

components of the human body. The chemical structures, physical-chemical properties, 

environmental fate behavior, and aquatic and mammalian toxicity of ammonium acetate and 

acetic acid are similar. Since limited data are available on ammonium acetate, toxicity data on 

acetic acid were used to represent toxicity due to exposure to ammonium acetate.

Acetic acid is of low acute dermal and inhalation toxicity in rats. The acute dermal LD50 was

> 1,060 mg/kg and the acute inhalation LC50 was >11.4 mg/L (equivalent to 2956 mg/kg). 

Dermal irritation was observed at > 100 mg/kg in mice and was corrosive at > 60% in rabbits. It 

was also irritating in the eyes of rabbits.

A 90-day oral toxicity study was available in rats administered acetic acid in drinking water. 

Although reduced body weight was observed at 390 mg/kg/day, the reduction in weight gain was

likely attributed to reduced appetite and food consumption observed in the study. Therefore, this 

was not considered adverse effect. Rats treated for 8 months with 60 mg/kg bw/treatment (the 

only dose tested) of acetic acid (3 times/week) via gavage, exhibited hyperplasia in the 

esophagus and forestomach but did not have tumors.

Several developmental toxicity studies were available with acetic acid. Fetal susceptibility 

was not observed in any of the studies. In rats, mice and rabbits maternal and developmental 

toxicity was not observed up to 1600 mg/kg/day. Reproduction toxicity studies were not 

available with acetic acid.

Tumors were not observed in rats treated for 8 months with 60 mg/kg bw/treatment of acetic 

acid in drinking water. 

Acetic acid was not mutagenic in an Ames test nor was it clastogenic in a cytogenetic assay 

with Chinese hamster ovary K1 cells.
3

In a toxicity study via the inhalation route of exposure, toxicity was manifested as decreased 

activity, behavioral changes and reduced work capacity following 22 days of treatment with 15 

ppm (equivalent to 10 mg/kg/day) of acetic acid in rats and mice. The NOAEL was 11 ppm 

(equivalent to 7 mg/kg/day).

Neurotoxicity studies for ammonium acetate were not available for review. However, signs 

of neurotoxicity were observed in a study conducted by Satpute et.al. that is in the literature. 

Following 4 weeks of treatment with 100 mg/kg/day of ammonium acetate via gavage to Wistar rats,

mild chromatolysis of nuclear material, moderate gliosis, and occasional neuronal vacuolation and 

edema were observed in the cortex of the brain. In the hippocampal region, moderate neuronal 

degeneration and pyknosis in the nuclei of pyramidal neurons were observed. In the cerebellum, 

there was moderate pyknosis and necrosis in Purkinje neurons. A second study (conducted by the 

registrant) in rats was conducted following the Organization for Economic Co-operation and 

Development (OECD) and good laboratory practice (GLP) guidelines. In this study, Sprague 

Dawley rats were treated for 28 days with 100 mg/kg/day of ammonium acetate via gavage. There 

was no indication of systemic toxicity, neurotoxicity, neuropathological or histological lesions. 

Immunotoxicity studies for acetic acid were not available for review. However, increased 

spleen weight was observed at 23-31 ppm (equivalent to 15-19 mg/kg/day) of acetic acid in a 

toxicity study in rats via the inhalation route of exposure. However, these effects are not due to 

an immunotoxic response but due to red blood cell destruction rather than an immunotoxic 

response. Therefore, there is no concern for potential immunotoxicity. In addition, according to 

the American Conference of Governmental Industrial Hygenists, Inc. (ACGIH), the threshold 

limit value (TLV) for occupational exposure to acetic acid is 10 ppm via inhalation. Based on 

the requested use pattern, occupational inhalation exposure is not expected. With regard to 

residential uses, exposure will be much lower because exposure is expected to occur for shorter 

periods to diluted acetic acid as compared to workers who are exposed for 8 hours continuously, 

to more concentrated acetic acid. Therefore, a qualitative assessment was conducted with regard 

to inhalation exposure.

Ammonium acetate is an ammonium salt of acetic acid. Acetic acid undergoes dissociation 

to the acetate anion and the H+ cations in aqueous media at pHs commonly found in the 

environment. Also, it is a naturally-occurring substance in plants and animals. In aerobic 

metabolism, acetic acid (as acetate) is a metabolite that combines with Co-enzyme A to form 

acetyl Co-A which subsequently enters into the Citric Acid Cycle, a common metabolic pathway 

in which food molecules are broken down to form energy. A major function of the Citric Acid 

Cycle is the oxidation of acetate. In animals, acetate is obtained from the breakdown of glucose 

molecules.

Since acetic acid dissociates to its salt, ammonium acetate, in an aqueous environment, 

toxicity due to its exposure is expected to be similar to that of acetic acid exposure. Therefore, 

based on the absence of a toxicological endpoint of concern, the regulatory history of acetic acid 

and no new toxicological data to indicate concern regarding previous decisions, a qualitative 

assessment of ammonium acetate is appropriate for all pathways of human exposure (food, 

drinking water, and residential). 
4

Occupational exposure was qualitatively assessed based on the lack of toxicity of ammonium 

acetate. 

Ammonium acetate is not expected to be toxic to aquatic organisms, terrestrial mammals and 

birds. It does not persist in the environment.

Taking into consideration all available information on ammonium acetate, EPA concludes 

that there is a reasonable certainty that no harm will result to the general population or to infants 

and children from aggregate exposure to ammonium acetate. Therefore, the establishment of an 

exemption from tolerance under 40 CFR 180.920 for residues of ammonium acetate as an inert 

ingredient (buffering agent) limited to 15 % in pesticide formulations for pre-harvest use on 

crops can be considered safe under section 408 of the FFDCA.

1. BACKGROUND

The EPA received a petition (IN-10604) from Exponent, Inc., (1150 Connecticut Street, Suite 

1100 Washington, DC 20036) on behalf of Gowan Company LLC (370 South Main Street, 

Yuma, AZ 85367) requesting a tolerance exemption for use of ammonium acetate (CAS Reg No. 

631-61-8) as an inert ingredient (buffering agent) limited to 15% in pesticide formulations under 

40 CFR Part 180.920. EPA published the notice of filing for this petition in the Federal Register 

on December 30, 2013 (78 FR 79359). No substantial comments were received in response to 

this notice. Ammonium acetate is currently approved as an inert ingredient for non-food use. 

Since ammonium acetate is an ammonium salt of acetic acid, toxicity data on acetic acid 

were used to characterize toxicity due to exposure to ammonium acetate. This document 

provides an assessment of the risk to human health and the environment for ammonium acetate 

when used as an inert ingredient in pesticide formulations. Information utilized from the petition 

submitted by the registrant (MRID 49160501), EPA documents (2008, Attachment I, 2010, 

Attachment II), American Chemical Council (ACC) Acetic Acid and Acetate Panels High 

Production Volume (HPV) Challenge Program (200la, b, Attachments III and IV) is reproduced 

and referenced in this assessment.

2. Inert Ingredient Profile

Some of the physical and chemical characteristics of ammonium acetate along with its 

structure and nomenclature, are found in Table 1.

Table 1. Physical and Chemical Properties of Ammonium Acetate

Parameter Value Source

Structure MRID 49160501
5

CAS # 631-61-8

Molecular Weight (g/mol) 77.08

Common Names Ammonium acetate, Acetic acid, 

ammonium salt; Ammonium ethanoate

Physical State Clumpy white wet powder

Melting Point (°C) 114

Boiling Point (°C) Decomposes above 160°C

pH@20°C 2.5 for 50 g/L solution

Vapor Pressure (mm Hg @ 

20°C) 0.00014

Partition Coefficient (Log Kow) -2.79

Water Solubility (g/L at 23°C) 827.29

3. Hazard Assessment

Limited data are available on ammonium acetate. Since, it is an ammonium salt of acetic 

acid, toxicity data from acetic acid were used to bridge data gaps for ammonium acetate. The 

following studies were reproduced and referenced from the petition submitted by the registrant 

(MRID 49160501), EPA document, Acetic acid and Salts summary document, American 

Chemical Council (ACC) Acetic Acid and Acetate Panels High Production Volume (HPV) 

Challenge Program.

Acute Toxicity Studies

Table 2 Acute Toxicity Profile of Ammonium Acetate

Guideline No. Study Type Results

Acute -ratsintraperitoneal 

injection

LD50= 632 mg/kg

Acute - mouseintravenous injection

LD50= 98 mg/kg

Acute Toxicity Profile of Acetic Acid

870.1000 Acute-Oral-rats LD50> 3,310 mg/kg

870.1000 Acute-Oral-mice LD50> 4,960 mg/kg

870.1100 Acute-Dermal-rats LD50> 1,060 mg/kg

870.1100 Acute-Dermal-mice > 100 mg/kg in mice produced 

irritation
6

870.1200 Acute-Inhalation-rats LC50> 11.4 mg/L(equivalent to 2956 

mg/kg)

870.2400 Acute-Eye Irritationrabbits

Irritating

870.2500 Acute-Dermal 

Irritation-rabbits

Corrosive at >60%

Toxicity studies with Ammonium Acetate

28 Day Oral-Gavage-Toxicity Study-Rat

In the study conducted by Satpute et.al. (2014), male Wistar rats (10/group) were treated with 

0 or 100 mg/kg/day of ammonium acetate for 4 weeks via gavage. Hematology, blood gas analysis 

and plasma ammonium were measured from blood samples collected at 1, 2 and 4 weeks of 

treatment. Catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione 

reductase (GR), reduced glutathione(GSH) and glutathione disulfide (GSSG) levels were measured. 

Plasma alkaline phosphatase (ALP), alanine aminotransferase (ALAT), aspartate aminotransferase 

(ASAT) and total bilirubin and were determined for liver function and plasma urea, uric acid and 

creatinine were measured for kidney function. The NH3 concentration in plasma was also measured. 

The organ–body weight index (OBI) was calculated for the brain, liver and kidney of 6 animals from 

each group. Histological examination was conducted on the brain, liver and kidney of the remaining 

4 animals from each group. 

The OBI of the brain and liver were significantly increased by 48 and 23%, respectively, in rats 

treated with ammonium acetate. CAT, SOD, GPX, GR, GSH, GSH: GSSG levels were significantly 

reduced accompanied by a significant increase in malondialdehyde levels in the brain and liver when 

compared to controls. The levels of the aforementioned enzymes in the kidney of treated animals 

were comparable to the controls. Ammonium acetate caused a significant increase in the levels of 

plasma ALP, ALAT, ASAT (263%) and bilirubin (236%). Ammonia levels were also increased after 

4 weeks of treatment with ammonium acetate. Urea, uric acid and creatinine levels and hematology 

parameters were comparable to controls. 

Microscopic evaluation showed mild chromatolysis of nuclear material, moderate gliosis, and 

occasional neuronal vacuolation and edema in the cortex of the brain and animals treated with 

ammonium acetate. In the hippocampal region, moderate neuronal degeneration and pyknosis in the 

nuclei of pyramidal neurons were observed. In the cerebellum, there was moderate pyknosis and 

necrosis in Purkinje neurons. In the liver there was moderate hepatocellular degeneration, hepatic 

vacuolation, clumping of cytoplasm, necrosis and karyolysis in hepatocytes along with the 

infiltration of polymorphonuclear cells and desquamation of endothelium of central canal. In the 

kidney there was moderate tubular degeneration, karyolysis, tubular dilation and renal parenchyma 

necrosis leading to vacuolative degeneration of convoluted tubules.

A second study was conducted by the registrant in response to the Agency’s concern regarding 

the Sapute et.al. (2014) study, a summary of this study is below.
7

Sprague Dawley rats (10/group) were treated with 0 or 100 mg/kg/day of ammonium acetate 

for 28 days via gavage. The following parameters were evaluated: viability, clinical signs, body 

weights, body weight gain, clinical chemistry parameters (alanine aminotransferase, aspartate 

aminotransferase, alkaline phosphatase, and total bilirubin), gross necropsy findings, organ weights 

and histopathology of the brain, liver and kidneys.

There were no test substance-related clinical signs or effects on body weight, body weight gain,

clinical chemistry, absolute or relative organ weights, and there were no findings at gross necropsy or 

in the histopathology of the brain, liver or kidneys (MRID 49703201). 

Repeated Dose Toxicity studies with Acetic Acid

90-Day oral-Drinking Water-Rat

A 90-day feeding study in rats was conducted with acetic acid. Rats administered up to 390 

mg acetic acid/kg/day in drinking water for 2 to 4 months had a LOAEL of 390 mg/kg/day 

(based on weight loss) and a NOAEL of 195 mg/kg/day. (Hummel, S., 2/28/07, D344771). The 

reduction in weight gain was likely attributed to reduced appetite and food consumption 

observed in the study. Therefore, this effect was not considered adverse and the NOAEL is 390 

mg/kg/day.

Developmental Toxicity Studies

Rat:

In a developmental toxicity study in albino Wistar rats, mated female rats were administered 

acetic acid (5%) via gavage at 0, 16, 74, 345 and 1600 mg/kg/day on gestation days 6-16. On 

day 20, Caesarean sections were performed. The number of implantation sites, resorption sites 

and live and dead fetuses were similar to the controls. Neither maternal nor fetal treatment 

related effects were observed up to 1600 mg/kg/day, the highest dose tested (HPV, 2001). 

Mouse:

In a developmental toxicity study in CD-1 mice, mated female mice were administered acetic 

acid (5%) via gavage at 0, 16, 74, 345 and 1600 mg/kg/day on gestation days 6-16. On day 17, 

Caesarean sections were performed. The number of implantation sites, resorption sites and live 

and dead fetuses were similar to the controls. Neither maternal nor fetal treatment related effects 

were observed up to 1600 mg/kg/day, the highest dose tested (HPV, 2001). 

Rabbit:

In a developmental toxicity study in Dutch-belted rabbits, artificially inseminated female 

rabbits were administered acetic acid (5%) via gavage at 0, 16, 74, 345 and 1600 mg/kg/day on 
8

gestation days 6-19. On day 29, Caesarean sections were performed. The number of corpora 

lutea, implantation sites, resorption sites and live and dead fetuses were similar to the controls. 

Neither maternal nor fetal treatment related effects were observed up to 1600 mg/kg/day, the 

highest dose tested (HPV, 2001).

8-Month-Oral Toxicity/Carcinogenicity Study-Rat 

In an 8-month oral toxicity study in rats, the carcinogenic potential of acetic acid was 

evaluated. In this study, nine outbred white male rats were administered 0.5ml of 3% water 

solution of acetic acid (equivalent to 60 mg/kg/treatment) via gavage three times per week for 

eight months. Rats were given N-nitrososarcosine ethyl ester (NSEE; a known carcinogen) alone 

and NSEE with an acetic acid solution, or the acetic acid solution alone. Rats treated with the 

carcinogen and NSEE had high incidences of pre-neoplastic lesions in the esophagus and 

forestomach as well as benign tumors, carcinomas and squamous cell cancer. Rats treated with 

acetic acid and NSEE had an increase in the number of benign and malignant tumors and 

carcinomas in the esophagus. Rats treated with acetic acid alone had hyperplasia in the 

esophagus and forestomach but did not have tumors (HPV, 2001).

Genotoxicity Studies

In a bacterial reverse mutation assay Salmonella typhimurium strains TA 98, TA 100, TA 

1535, TA 97 and TA 1537 were treated with acetic acid at concentrations of 100, 333, 1000 

3333, 6666 and 10,000 μg/plate with and without metabolic activation. No revertant colonies 

were observed (HPV, 2001).

In a cytogenetic assay, Chinese hamster ovary K1 cells were treated with acetic acid at 

concentrations up to 16mM. Acetic acid was not clastogenic (HPV, 2001).

Inhalation Toxicity Study

Rats and mice were treated with 11-15 ppm (equivalent to7- 10 mg/kg/day) of acetic acid via 

the inhalation route of exposure for 3-35 days. Groups of 10 rats and mice (sex unknown) were 

exposed to 15 ppm (equivalent to10 mg/kg/day) of acetic acid for 22 days or more exhibited 

decreased activity, behavioral changes and reduced work capacity. At 23-31 ppm (equivalent to

15-19 mg/kg/day), animals exhibited decreased growth, increased spleen weight, an increase of 

the level of iron stored in the spleen, signs of kidney damage and increased kidney weights. The 

LOAEL was 15 ppm (equivalent to10 mg/kg/day) based on decreased activity, behavioral 

changes and reduced work capacity. The NOAEL was 11 ppm (equivalent to7 mg/kg/day) 

(HPV, 2001).

Neurotoxicity Study
9

Neurotoxicity studies for ammonium acetate were not available for review. However, signs 

of neurotoxicity were observed in a study conducted by Satpute et.al. that is in the literature. 

Following 4 weeks of treatment with 100 mg/kg/day of ammonium acetate via gavage, mild 

chromatolysis of nuclear material, moderate gliosis, and occasional neuronal vacuolation and edema 

were observed in the cortex of the brain in Wistar rats. In the hippocampal region, moderate 

neuronal degeneration and pyknosis in the nuclei of pyramidal neurons were observed. In the 

cerebellum, there was moderate pyknosis and necrosis in Purkinje neurons. A second study in rats 

was conducted following OECD and GLP guidelines. In this study, Sprague Dawley rats were 

treated for 28 days with 100 mg/kg/day of ammonium acetate via gavage. There was no indication 

of systemic toxicity, neurotoxicity, neuropathological or histological lesions. 

Immunotoxicity Study

Immunotoxicity studies for ammonium acetate were not available for review. However, 

increased spleen weight was observed at 23-31 ppm (equivalent to 15-19 mg/kg/day) of acetic 

acid in a toxicity study in rats via the inhalation route of exposure. However, these effects are 

not due to an immunotoxic response but due to red blood cell destruction rather than an 

immunotoxic response. In addition, according to the American Conference of Governmental 

Industrial Hygenists, Inc. (ACGIH), the threshold limit value (TLV) for occupational exposure to 

acetic acid is 10 ppm via inhalation. Based on the requested use pattern, occupational inhalation 

exposure is not expected. With regard to residential uses, exposure will be much lower because 

exposure is expected to occur for shorter periods to diluted acetic acid as compared to workers 

who are exposed for 8 hours continuously, to more concentrated acetic acid. Therefore, there is 

no concern for potential immunotoxicity. 

Metabolism

Ammonium acetate is an ammonium salt of acetic acid. In aqueous solution, ammonium 

acetate dissociates into the ammonium cation (NH4+) and acetate anion (CH3COO-). The 

cations and ammonia (also a human metabolite) are physiological components of the human 

body. The toxicity assessment of the exposure and risk of acetic acid and acetate salts is driven 

by the acetate anion (which is also a human metabolite). 

Acetic acid undergoes dissociation to the acetate anion and the H+ cations in aqueous media 

at pHs commonly found in the environment. Also, it is a naturally-occurring substance in plants 

and animals. In aerobic metabolism, acetic acid (as acetate) is a metabolite that combines with 

Co-enzyme A to form acetyl Co-A which subsequently enters into the Citric Acid Cycle, a 

common metabolic pathway in which food molecules are broken down to form energy. A major 

function of the Citric Acid Cycle is the oxidation of acetate. In animals, acetate is obtained from 

the breakdown of glucose molecules. 

Table 3. Toxicology Profile for Ammonium Acetate

Guideline No./ Study 

Type

MRID No. (year)/ 

Classification /Doses

Results
10

Table 3. Toxicology Profile for Ammonium Acetate

Guideline No./ Study 

Type

MRID No. (year)/ 

Classification /Doses

Results

4 Week Oral-GavageToxicity –Wistar-Rat0 and 100 mg/kg/day NOAEL was not established.

LOAEL = 100 mg/kg/day based histopathological lesions in 

the brain, liver and kidneys.

4 Week Oral-GavageToxicity –Sprague DawleyRat0 and 100 mg/kg/day NOAEL = 100 mg/kg/day.

LOAEL was not established.

Table 4. Toxicology Profile for Acetic Acid

Study Type Doses Results

3-35 Day - inhalation -rat 11-35 ppm (equivalent to7-

23 mg/kg/day)

The NOAEL = 11 ppm (7 mg/kg/day)

The LOAEL = 15 ppm (equivalent to 10 mg/kg/day) based 

on decreased activity, behavioral changes and reduced work 

capacity.

90 day oral - F344 ratsdrinking water 195 and 390 mg/kg/day NOAEL = 390 mg/kg/day

LOAEL was not established.

8-MonthOral/Carcinogenicity 

Toxicity Study-Rat-gavage

(equivalent to96 days)

60 mg/kg/treatment The NOAEL was not established. 

LOAEL = 60 mg/kg/treatment based on hyperplasia in the 

esophagus and forestomach.

No tumors were observed.

Developmental toxicity-rat 0, 16, 74, 345 and 1600 

mg/kg bw/day

The NOAEL = 1600 mg/kg/day. 

The LOAEL was not established.

Developmental toxicitymouse0, 16, 74, 345 and 1600 

mg/kg/day

The NOAEL = 1600 mg/kg/day.

The LOAEL was not established.

Developmental toxicityrabbit0, 16, 74, 345 and 1600 

mg/kg/day

The NOAEL = 1600 mg/kg/day.

The LOAEL was not established.

Ames assay 100, 333, 1000 3333, 6666 

and 10,000 μg/plate

Negative

Cytogenetic assay <16 mM Negative
11

5. Toxicity Endpoint Selection

In an aqueous environment, acetic acid dissociates to its ammonium salt, ammonium 

acetate. Therefore, it is appropriate to expect toxicity due to exposure to ammonium acetate to 

be similar to that of acetic acid. Since there is no toxicological endpoint of concern for acetic 

acid, a qualitative assessment was appropriate for ammonium acetate for all pathways of human 

exposure (food, drinking water, and residential). A potential endpoint of concern for the 

inhalation route of exposure was identified in a toxicity study. Increased spleen weight due to 

red blood cell destruction was observed at 23-31 ppm (equivalent to 15-19 mg/kg/day) of acetic 

acid in rats. However, according to the American Conference of Governmental Industrial 

Hygenists, Inc. (ACGIH), the threshold limit value (TLV) for occupational exposure to acetic 

acid is 10 ppm via inhalation. Residential exposure to the proposed use of ammonium acetate 

via inhalation is not expected to exceed the TLV limit of 10 ppm because the residential use 

pattern would result in drastically lower opportunities for inhalation exposure than allowed 

occupational use patterns, which are limited to 10 ppm. In addition, residential exposure will be 

much lower because exposure is expected to occur for shorter periods to diluted acetic acid as 

compared to workers who are exposed for 8 hours continuously, to more concentrated acetic 

acid. Therefore, a qualitative assessment was conducted with regard to inhalation exposure.

6. Special Considerations for Infants and Children

As part of its qualitative assessment, the Agency did not use safety factors for assessing risk, 

and no additional safety factor is needed for assessing risk to infants and children. Based on the 

lack of toxicity of ammonium acetate in the available studies and its chemical properties, EPA 

has concluded that there are no toxicological endpoints of concern for the U.S. population, 

including infants and children.

7. Exposure Assessment

Dietary Exposure

In evaluating dietary exposure to ammonium acetate, EPA considered exposure under the 

petitioned for exemptions from the requirement of a tolerance. Since no endpoint of concern was 

identified for the acute and chronic dietary exposure assessment and short and intermediate 

dermal and inhalation exposure, a quantitative risk assessment for ammonium acetate is not 

necessary.

Cancer. Ammonium acetate is not expected to be carcinogenic since there was no evidence of 

carcinogenicity in an oral toxicity study in rats and there was a negative response for 

mutagenicity. Since the Agency has not identified any concerns for carcinogenicity relating to 

ammonium acetate a cancer dietary exposure assessment was not performed.
12

8. Residential (Non-Occupational) Exposure/Risk Characterization

Ammonium acetate may be used in pesticide and nonpesticide products that may be used 

around the home. However, based on the absence of a toxicological endpoint of concern, a 

qualitative assessment was conducted for residential exposure. 

9. Occupational Exposure/Risk Pathway

The Agency believes that establishing a tolerance exemption to include 40 CFR Part 180.920

will not significantly/measurably increase occupational exposure. In view of the regulatory 

history of acetic acid, its lack of toxicity and no new toxicological information to indicate 

otherwise, it is not necessary to quantitatively assess occupational exposure. Therefore, 

occupational exposure to ammonium acetate was qualitatively assessed. 

10. Cumulative Exposure:

Section 408(b)(2)(D)(v) of FFDCA requires that, when considering whether to establish, 

modify, or revoke a tolerance, 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." Unlike other pesticides for which EPA has followed a cumulative risk 

approach based on a common mechanism of toxicity, EPA has not made a common mechanism 

of toxicity finding as to ammonium acetate and any other substances and, this material does not 

appear to produce a toxic metabolite produced by other substances. For the purposes of this 

tolerance action, therefore, EPA has not assumed that ammonium acetate has 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 the policy statements released by EPA's Office of 

Pesticide Programs concerning common mechanism determinations and procedures for 

cumulating effects from substances found to have a common mechanism on EPA's website at 

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

11. Ecotoxicity and Environmental Fate

Based on the “Acetic Acid and Sodium Diacetate Proposed Interim Registration Review 

Decision (Docket Number EPA-HQ-OPP-2008-0016), ammonium acetate is not expected to be 

toxic to aquatic organisms, terrestrial mammals and birds. It does not persist in the environment. 

Therefore, the same is expected for ammonium acetate.

12. 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 
13

Actions to Address Environmental Justice in Minority Populations and Low-Income 

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

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

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

risks to population subgroups from pesticide exposures that are based on patterns of that 

subgroup’s food and water consumption, and activities in and around the home that involve 

pesticide use in a residential setting. Extensive data on food consumption patterns are compiled 

by the USDA under the Continuing Survey of Food Intake by Individuals (CSFII) and are used 

in pesticide risk assessments for all registered food uses of a pesticide. These data are analyzed 

and categorized by subgroups based on age, season of the year, ethnic group, and region of the 

country. Additionally, OPP is able to assess dietary exposure to smaller, specialized subgroups 

and exposure assessments are performed when conditions or circumstances warrant. Whenever 

appropriate, non-dietary exposures based on home use of pesticide products and associated risks 

for adult applicators and for toddlers, youths, and adults entering or playing on treated areas 

postapplication are evaluated. Further considerations are currently in development as OPP has 

committed resources and expertise to the development of specialized software and models that 

consider exposure to bystanders and farm workers as well as lifestyle and traditional dietary 

patterns among specific subgroups.

13. Risk Characterization

EPA received a petition (IN-10604) from Exponent Inc., (1150 Connecticut Ave., Suite 1100 

Washington, DC 20036) on behalf of the Gowan Company LLC (370 South Main Street, Yuma, 

AZ 85367) requesting a tolerance exemption for use of ammonium acetate (CAS Reg No. 631-

61-8) as an inert ingredient (buffering agent) limited to 15% in pesticide formulations under 40 

CFR Part 180.920. EPA published the notice of filing for this petition in the Federal Register on 

December 30, 2013 (78 FR 79359). No substantial comments were received in response to this 

notice. Ammonium acetate is currently approved as an inert ingredient for non-food use. 

Since, in an aqueous environment, acetic acid dissociates to its ammonium salt, ammonium 

acetate, toxicity due to its exposure is expected to be similar to that of acetic acid exposure. 

Therefore, based on the absence of a toxicological endpoint of concern, the regulatory history of 

acetic acid and no new toxicological data to indicate concern regarding previous decisions, a 

qualitative assessment was appropriate ammonium acetate for all pathways of human exposure 

(food, drinking water, and residential). 

Neither aggregate (i.e. residential) nor occupational exposures is of concern. 

Ammonium acetate is not expected to be toxic to aquatic organisms, terrestrial mammals and 

birds. It does not persist in the environment.

Taking into consideration all available information on ammonium acetate, EPA concludes 

that there is a reasonable certainty that no harm will result to the general population or to infants 

and children from aggregate exposure to ammonium acetate. Therefore, the establishment of an 

exemption from tolerance under 40 CFR 180.920 for residues of ammonium acetate as an inert 
14

ingredient (buffering agent) limited to 15 % in pesticide formulations for pre-harvest use on 

crops can be considered safe under section 408 of the FFDCA.
15

REFERENCES

American Chemistry Council Acetic Acid and Salts Panel, 2001, U.S.

High Production Volume (HPV) Chemical Challenge Program: Robust summaries for

Acetic acid and salts category.

Barnett, Jr., John F. (2015). A 28-Day Oral (Gavage) Repeated Dose Study of Ammonium

Acetate in Adult Rats. Laboratory Project ID 20073669. Unpublished study prepared by Charles

River Laboratories. MRID 49703201.

EPA. Hummel, S. (2007) Memorandum: Acetic Acid Registration Review Case No. 4001.DP 

Barcode D344771. November 28, 2007.

Petition for Exemption From the Requirement of a Tolerance For Residues of Ammonium Acetate 

(CAS# 631-61-8) as a Pesticide Inert Ingredient in Accordance with 40 CFR §180.920. June 13, 

2013.

Satpute, R.M., Lomash, V., Hariharakrishnan, J., Roa, P., Singh, P., Gujar, N., and Bhattacharya, 

R. (2014). Oxidative Stress And Tissue Pathology Caused By Subacute Exposure To 

Ammonium Acetate In Rats And Their Response To Treatments With Alpha-Ketoglutarate And 

N-Acetyl Cysteine. Toxicology and Industrial Health: 30(1) 12-14. MRID. 49507001.

U.S. Environmental Protection Agency (EPA), 2008. Acetic acid and salts summary document. 

Registration Review: Initial Docket, EPA-HQ-EPA- OPP-2008-0016. Case #4001,

www.regulations.gov.

U.S. Environmental Protection Agency (EPA), 2014. Acetic Acid and Sodium Diacetate Proposed 

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www.regulations.gov.