c/EPA

EPA/690/R-21/007 F | September 2021 | FINAL

United States
Environmental Protection
Agency

Provisional Peer-Reviewed Toxicity Values for

Ammonium Salts of Inorganic Phosphates:

Monoammonium Phosphate (MAP)
(CASRN 7722-76-1)

Diammonium Phosphate (DAP)

(CASRN 7783-28-0)


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A mA United States

Environmental Protection
* ^ ^1 M % Agency

EPA 690 R-21 00 7F
September 2021
https://www.epa.gov/pprtv

Provisional Peer-Reviewed Toxicity Values for
Ammonium Salts of Inorganic Phosphates:

Monoammonium Phosphate (MAP)
(CASRN 7722-76-1)

Diammonium Phosphate (DAP)

(CASRN 7783-28-0)

Center for Public Health and Environmental Assessment
Office of Research and Development
U.S. Environmental Protection Agency
Cincinnati, OH 45268


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AUTHORS, CONTRIBUTORS, AND REVIEWERS

CHEMICAL MANAGER

Robert Mitkus, PhD, DABT, ERT

Center for Public Health and Environmental Assessment, Cincinnati, OH

DRAFT DOCUMENT PREPARED BY

SRC, Inc.

7502 Round Pond Road
North Syracuse, NY 13212

CONTRIBUTORS

Jay Zhao, MPH, PhD, DABT

Center for Public Health and Environmental Assessment, Cincinnati, OH
John Stanek, PhD

Center for Public Health and Environmental Assessment, Research Triangle Park, NC

PRIMARY INTERNAL REVIEWERS

Daniel D. Petersen, PhD, DABT

Center for Public Health and Environmental Assessment, Cincinnati, OH
Laura Carlson, PhD

Center for Public Health and Environmental Assessment, Research Triangle Park, NC

PRIMARY EXTERNAL REVIEW

Eastern Research Group, Inc.

110 Hartwell Avenue
Lexington, MA 02421-3136

PPRTV PROGRAM MANAGEMENT

Teresa L. Shannon

Center for Public Health and Environmental Assessment, Cincinnati, OH
J. Phillip Kaiser, PhD, DABT

Center for Public Health and Environmental Assessment, Cincinnati, OH

Questions regarding the content of this PPRTV assessment should be directed to the U.S. EPA
Office of Research and Development (ORD) Center for Public Health and Environmental
Assessment (CPHEA) website at https://ecomments.epa.gov/pprtv.

ii Ammonium salts of inorganic phosphates


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TABLE OF CONTENTS

COMMONLY USED ABBREVIATIONS AND ACRONYMS	iv

BACKGROUND	1

QUALITY ASSURANCE	1

DISCLAIMERS	2

QUESTIONS REGARDING PPRTVs	2

1.	INTRODUCTION	3

2.	REVIEW OF POTENTIALLY RELEVANT DATA (NONCANCER AND CANCER)	9

2.1.	HUMAN STUDIES	14

2.1.1.	Occupational Studies	14

2.1.2.	Other Human Studies	14

2.2.	ANIMAL STUDIES	15

2.2.1.	Oral Exposures	15

2.2.2.	Inhalation Exposures	18

2.3.	OTHER DATA (SHORT-TERM TESTS, OTHER EXAMINATIONS)	18

2.3.1.	Genotoxi city	18

2.3.2.	Other Animal Studies	20

2.3.3.	Metabolism/Toxicokinetic Studies	21

2.3.4.	Mode-of-Action/Mechanistic Studies	21

3.	DERIVATION 01 PROVISIONAL VALUES	22

3.1.	DERIVATION OF PROVISIONAL REFERENCE DOSES	22

3.2.	DERIVATION OF PROVISIONAL REFERENCE CONCENTRATIONS	22

3.3.	SUMMARY OF NONCANCER PROVISIONAL REFERENCE VALUES	22

3.4.	CANCER WEIGHT-OF-EVIDENCE DESCRIPTOR	23

3.5.	DERIVATION OF PROVISIONAL CANCER RISK ESTIMATES	24

APPENDIX A. SCREENING PROVISIONAL VALUES	25

APPENDIX B. DATA TABLES	28

APPENDIX C. BENCHMARK DOSE MODELING RESULTS	29

APPENDIX D. REFERENCES	34

iii Ammonium salts of inorganic phosphates


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COMMONLY USED ABBREVIATIONS AND ACRONYMS

a2u-g

alpha 2u-globulin

IVF

in vitro fertilization

ACGIH

American Conference of Governmental

LC50

median lethal concentration



Industrial Hygienists

LD50

median lethal dose

AIC

Akaike's information criterion

LOAEL

lowest-observed-adverse-effect level

ALD

approximate lethal dosage

MN

micronuclei

ALT

alanine aminotransferase

MNPCE

micronucleated polychromatic

AR

androgen receptor



erythrocyte

AST

aspartate aminotransferase

MOA

mode of action

atm

atmosphere

MTD

maximum tolerated dose

ATSDR

Agency for Toxic Substances and

NAG

\-acctyl-(}-D-gliicosaiiiiiiidasc



Disease Registry

NCI

National Cancer Institute

BMC

benchmark concentration

NOAEL

no-observed-adverse-effect level

BMCL

benchmark concentration lower

NTP

National Toxicology Program



confidence limit

NZW

New Zealand White (rabbit breed)

BMD

benchmark dose

OCT

ornithine carbamoyl transferase

BMDL

benchmark dose lower confidence limit

ORD

Office of Research and Development

BMDS

Benchmark Dose Software

PBPK

physiologically based pharmacokinetic

BMR

benchmark response

PCNA

proliferating cell nuclear antigen

BUN

blood urea nitrogen

PND

postnatal day

BW

body weight

POD

point of departure

CA

chromosomal aberration

PODadj

duration-adjusted POD

CAS

Chemical Abstracts Service

QSAR

quantitative structure-activity

CASRN

Chemical Abstracts Service registry



relationship



number

RBC

red blood cell

CBI

covalent binding index

RDS

replicative DNA synthesis

CHO

Chinese hamster ovary (cell line cells)

RfC

inhalation reference concentration

CL

confidence limit

RfD

oral reference dose

CNS

central nervous system

RGDR

regional gas dose ratio

CPHEA

Center for Public Health and

RNA

ribonucleic acid



Environmental Assessment

SAR

structure-activity relationship

CPN

chronic progressive nephropathy

SCE

sister chromatid exchange

CYP450

cytochrome P450

SD

standard deviation

DAF

dosimetric adjustment factor

SDH

sorbitol dehydrogenase

DEN

diethylnitrosamine

SE

standard error

DMSO

dimethylsulfoxide

SGOT

serum glutamic oxaloacetic

DNA

deoxyribonucleic acid



transaminase, also known as AST

EPA

Environmental Protection Agency

SGPT

serum glutamic pyruvic transaminase,

ER

estrogen receptor



also known as ALT

FDA

Food and Drug Administration

SSD

systemic scleroderma

FEVi

forced expiratory volume of 1 second

TCA

trichloroacetic acid

GD

gestation day

TCE

trichloroethylene

GDH

glutamate dehydrogenase

TWA

time-weighted average

GGT

y-glutamyl transferase

UF

uncertainty factor

GSH

glutathione

UFa

interspecies uncertainty factor

GST

g 1 u ta t h i o nc -.V-1 ra n s fc ra sc

UFC

composite uncertainty factor

Hb/g-A

animal blood-gas partition coefficient

UFd

database uncertainty factor

Hb/g-H

human blood-gas partition coefficient

UFh

intraspecies uncertainty factor

HEC

human equivalent concentration

UFl

LOAEL-to-NOAEL uncertainty factor

HED

human equivalent dose

UFS

subchronic-to-chronic uncertainty factor

i.p.

intraperitoneal

U.S.

United States of America

IRIS

Integrated Risk Information System

WBC

white blood cell

Abbreviations and acronyms not listed on this page are defined upon first use in the
PPRTV document.

iv Ammonium salts of inorganic phosphates


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EPA 690 R-21 00 7F

PROVISIONAL PEER-REVIEWED TOXICITY VALUES FOR
AMMONIUM SALTS OF INORGANIC PHOSPHATES (MONOAMMONIUM
PHOSPHATE, CASRN 7722-76-1, AND DIAMMONIUM PHOSPHATE,

CASRN 7783-28-0)

BACKGROUND

A Provisional Peer-Reviewed Toxicity Value (PPRTV) is defined as a toxicity value
derived for use in the Superfund program. PPRTVs are derived after a review of the relevant
scientific literature using established U.S. Environmental Protection Agency (U.S. EPA)
guidance on human health toxicity value derivations.

The purpose of this document is to provide support for the hazard and dose-response
assessment pertaining to chronic and subchronic exposures to substances of concern, to present
the major conclusions reached in the hazard identification and derivation of the PPRTVs, and to
characterize the overall confidence in these conclusions and toxicity values. It is not intended to
be a comprehensive treatise on the chemical or toxicological nature of this substance.

Currently available PPRTV assessments can be accessed on the U.S. EPA's PPRTV
website at https://www.epa.gov/pprtv. PPRTV assessments are eligible to be updated on a 5-year
cycle and revised as appropriate to incorporate new data or methodologies that might impact the
toxicity values or affect the characterization of the chemical's potential for causing adverse
human-health effects. Questions regarding nomination of chemicals for update can be sent to the
appropriate U.S. EPA Superfund and Technology Liaison (https://www.epa.gov/research/fact-
sheets-regional-science).

QUALITY ASSURANCE

This work was conducted under the U.S. EPA Quality Assurance (QA) program to ensure
data are of known and acceptable quality to support their intended use. Surveillance of the work
by the assessment managers and programmatic scientific leads ensured adherence to QA
processes and criteria, as well as quick and effective resolution of any problems. The QA
manager, assessment managers, and programmatic scientific leads have determined under the
QA program that this work meets all U.S. EPA quality requirements. This PPRTV was written
with guidance from the CPHEA Program Quality Assurance Project Plan (PQAPP), the QAPP
titled Program Quality Assurance Project Plan (POAPP) for the Provisional Peer-Reviewed
Toxicity Values (PPRTVs) and Related Assessments Documents (L-CPAD-0032718-OP), and the
PPRTV development contractor QAPP titled Quality Assurance Project Plan—Preparation of
Provisional Toxicity Value (I'l l ) Documents (L-CPAD-0031971-OP). As part of the QA
system, a quality product review is done prior to management clearance. A Technical Systems
Audit may be performed at the discretion of the QA staff.

All PPRTV assessments receive internal peer review by at least two CPHEA scientists
and an independent external peer review by at least three scientific experts. The reviews focus on
whether all studies have been correctly selected, interpreted, and adequately described for the
purposes of deriving a provisional reference value. The reviews also cover quantitative and
qualitative aspects of the provisional value development and address whether uncertainties
associated with the assessment have been adequately characterized.

1 Ammonium salts of inorganic phosphates


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EPA 690 R-21 00 7F

DISCLAIMERS

The PPRTV document provides toxicity values and information about the adverse effects
of the chemical and the evidence on which the value is based, including the strengths and
limitations of the data. All users are advised to review the information provided in this document
to ensure that the PPRTV used is appropriate for the types of exposures and circumstances at the
site in question and the risk management decision that would be supported by the risk
assessment.

Other U.S. EPA programs or external parties who may choose to use PPRTVs are
advised that Superfund resources will not generally be used to respond to challenges, if any, of
PPRTVs used in a context outside of the Superfund program.

This document has been reviewed in accordance with U.S. EPA policy and approved for
publication. Mention of trade names or commercial products does not constitute endorsement or
recommendation for use.

QUESTIONS REGARDING PPRTVs

Questions regarding the content of this PPRTV assessment should be directed to the
U.S. EPA ORD CPHEA website at https://ecomments.epa.gov/pprtv.

2 Ammonium salts of inorganic phosphates


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EPA 690 R-21 00 7F

1. INTRODUCTION

Phosphorus (P) is most commonly found in nature in its pentavalent form in combination
with oxygen, as phosphate (PO43 ). Phosphorus is an essential constituent of all living organisms,
and its content is quite uniform across most plant and animal tissues. Orthophosphate (anionic
salts of H3PO4) is the basic unit for all phosphates. Condensed (pyro-, meta-, and other
polyphosphates) are formed when two or more orthophosphate molecules condense into a single
molecule. Pyrophosphates refer to compounds with two condensed orthophosphates, and higher
number polymers are termed polyphosphates, sometimes preceded by a prefix indicating the
number (e.g., tri- and tetrapolyphosphates have three and four condensed phosphates,
respectively). The term "metaphosphates" is used when phosphoric acid moieties form a cyclic
(ring) structure. Inorganic phosphates (both ortho- and condensed phosphate anions) can be
grouped into four classes based on their cations: monovalent cations (sodium, potassium, and
hydrogen), divalent (calcium and magnesium), ammonium, and aluminum. The phosphoric acids
have been grouped with the other monovalent cations based on valence state.

This document addresses the available data on the toxicity of ammonium phosphate salts
(monoammonium phosphate [MAP], diammonium phosphate [DAP], and ammonium
polyphosphate [APP]). Monovalent, divalent, and aluminum phosphates are not included in this
assessment because they are expected to have differing toxicity, chemistry, and/or toxicokinetics
than the ammonium phosphates. Specifically, ammonium phosphate salts are relatively unstable,
because ammonium hydroxide is a weaker base than metal hydroxides, and ammonia can escape
as a gas (Gard. 2005). The reader is referred to the PPRTV assessments for monovalent, divalent,
and aluminum phosphates for assessments of these inorganic phosphate salts.

Ammonium phosphate salts are inorganic salts composed of a phosphate anion and an
ammonium cation. These water-soluble salts will dissociate in aqueous environments. Phosphate
is the conjugate base of phosphoric acid. Phosphoric acid is a polyprotic acid composed of three
dissociable protons with different pKa constants (pKi = 2.16, pK2 = 7.21, pK3 = 12.32) resulting
in successive deprotonation as pH increases. At very low pH values (<2) fully protonated,
neutral, phosphoric acid will predominate. In aqueous environments, at pH values between 6.5
and 8.5, phosphoric acid, and mono-, di-, and triphosphates (deprotonated anions) will all exist in
equilibrium depending on the specific pH of the system. An aqueous solution of phosphoric acid
will therefore contain some proportion of each species. Monovalent and divalent phosphate are
found in the body as inorganic anions and as functional groups on many important biomolecules.
Ammonium is the conjugate acid of ammonia. Based on its pKa of 9.25, the cation will
predominate at pH values below 9, with higher concentrations of the cation as the pH decreases
(up to 99% at physiological pH).

Commercial inorganic phosphate salts are used in many applications. The ammonium
salts of phosphoric acid addressed in this document are MAP, DAP, and APP. MAP
(monovalent: H2PO4 ) and DAP (divalent: HPO42 ) are both discrete chemicals, while APP is a
polymeric substance classified by Toxic Substances Control Act (TSCA) guidelines as "chemical
substances of unknown or variable composition, complex reaction products and biological
materials (UVCB)." Because of the variable molecular weight of APP polymers and variable
water solubility, these polymeric salts will likely behave slightly differently than the discrete
salts under both biological and environmental conditions. In general, as molecular weight
increases and water solubility decreases, bioavailability tends to decrease. However, APP

3 Ammonium salts of inorganic phosphates


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EPA 690 R-21 00 7F

polymers are susceptible to hydrolysis and will break down into smaller molecular weight
components over time.

MAP and DAP are used as fertilizers and plant nutrients, flame retardants, in
fire-extinguishers and fire-proofing agents, oral care agents, in cosmetics as buffering agents and
corrosion inhibitors, and in fermentations for yeast cultures (NLM. 2019a. b, c; CIR Expert
Panel 2016; OECD. 2007a. b, e). MAP and DAP are direct food additives classified by the
U.S. Food and Drug Administration (FDA) as generally recognized as safe (GRAS) (CIR Expert
Panel. 2016). APP salts are generally used in flame retardants for commercial furniture,
automotive fabrics, and draperies; in addition, lower molecular weight, water-soluble APP
polymers are used in foods (NRC. 2000).

In general, these salts are soluble in water; however, higher molecular weight APP
polymers tend to have lower water solubility. Ammonium phosphate salts will persist in natural
waters. In aqueous environments, both the anion (phosphates) and cation (ammonium) are
nutrients for algae, other plants, and microbes (ECHA. 2019a. b, c; CIR Expert Panel. 2016;
OECD. 2007a). In air, MAP is stable; however, DAP gradually loses up to 8% NFb upon
exposure to air (CIR Expert Panel. 2016). In aqueous systems and in soils under both aerobic and
anaerobic conditions, polyphosphate salts are susceptible to hydrolysis, with reported half-lives
ranging between 1 and 18 days (OECD. 2007b. d). In soil, ammonia is rapidly converted to
nitrate and nitrite by Nitrosomoncis and Nitrobacter bacteria, respectively (OECD. 2007a).
Human exposure to ammonium phosphate salts may occur via dermal contact through their use
in cosmetics, flame retardants, and fertilizers, or via ingestion through their use as food additives
and plant nutrients.

The empirical formulas for and physicochemical properties of the ammonium phosphate
salts are shown in Table 1.

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EPA 690 R-21 00 7F

Table 1. Identity, Molecular Weight, and Physicochemical Properties of
Ammonium Phosphate Salts3'b

Property

MAP

DAP

APP

CASRN

7722-76-1

7783-28-0

68333-79-9

Empirical formula0

NH4H2PO4

(NH4)2HP04

(NH1PO3),,

Molecular weight
(g/mol)

115.03

132.06

|97|„:d molecular weights
vary, may be as high as
30,000e

Physical state

White, tetrahedral crystals or
powder

White crystals or crystalline
powder

Wliite powder;f liquidd

Melting point (°C)

190, 193.3®

155 (decomposes)

Varies
(150-300 decomposes;d
141-225f)

Density (g/cm3 at
20°C)'

1.80

1.619

Varies
(1.74f)

pH (unitless)

4.2 (0.2 M aqueous solution)

~8

Varies
(6.5-7;d 5.0-7.0e)

Acid dissociation
constant (pKa)
(unitless)d

pKi = 2.16; pK2 = 7.21;
pK;, = 12.32 (phosphoric
acid); pK4 = 9.25 (ammonium)

pKi = 2.16; pK2 = 7.21;
pK;, = 12.32 (phosphoric
acid); pK4 = 9.25
(ammonium)

Varies

Solubility in water (at
25°C)

40.4 g/100 g water

69.5 g/100 g water

Varies

(miscible;d 4.0 g/100 g water,
max solubility 10%;e 50%
w/w, very solublef)

aOctanol-water partition coefficient, Henry's law constant, soil adsorption coefficient, atmospheric OH rate

constant, and atmospheric half-life are not applicable to inorganic phosphates.

bNLM (2019a). NLM (2019b). and NLM (2019c). unless otherwise specified.

°Weiner et al. (2001).

dOECD (2007d).

eNRC (2000). chain length = 200.
fECHA (2019c). cliain length unspecified.
gCIR Expert Panel (2016).

APP = ammonium polyphosphate; DAP = diammonium phosphate; MAP = monoammonium phosphate.

A summary of available toxicity values for ammonium phosphate salts (multiple
CASRNs) from U.S. EPA and other agencies/organizations is provided in Table 2.

5 Ammonium salts of inorganic phosphates


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EPA 690 R-21 00 7F

Table 2. Summary of Available Toxicity Values for Ammonium Phosphate
Salts (MAP, CASRN 7722-76-1; DAP, CASRN 7783-28-0; and APP,





CASRN 68333-79-9)



Source
(parameter)3'b

Value
(applicability)

Notes

Reference0

Noncancer

IRIS

NV

NA

U.S. EPA (2020)

HEAST

NV

NA

U.S. EPA (2011a)

DWSHA

NV

NA

U.S. EPA (2018)

ATSDR

NV

NA

ATSDR (2020)

IPCS/WHO (MTDI)

70 mg/kg body weight
(phosphates)

Group MTDI for P from all
sources

IPCS (2020);
WHO (1982)

CalEPA

NV

NA

CalEPA (2019);
CalEPA (2020)

OSHA

NV

NA

OSHA (2018a): OSHA
(2020); OSHA (2018b)

NIOSH

NV

NA

NIOSH (2018)

ACGIH

NV

NA

ACGIH (2018)

DOE (PAC)

MAP

PAC-1: 17 mg/m3
PAC-2: 190 mg/m3
PAC-3: 1,100 mg/m3

PAC-1 and PAC-2 based on
TEELs; PAC-3 based on rat oral
LD50

DOE (2018)

DOE (PAC)

DAP

PAC-1: 20 mg/m3
PAC-2: 210 mg/m3
PAC-3: 1,300 mg/m3

PAC-1 and PAC-2 based on
TEELs; PAC-3 based on rat oral
LD50

DOE (2018)

USAPHC
(air-MEG)

MAP

1-h critical: 500 mg/m3
1-h marginal: 350 mg/m3
1-h negligible: 50 mg/m3

Based on TEELs

U.S. APHC (2013)

USAPHC
(air-MEG)

DAP

1-h critical: 250 mg/m3
1-h marginal: 50 mg/m3
1-h negligible: 30 mg/m3

Based on TEELs

U.S. APHC (2013)

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EPA 690 R-21 00 7F

Table 2. Summary of Available Toxicity Values for Ammonium Phosphate
Salts (MAP, CASRN 7722-76-1; DAP, CASRN 7783-28-0; and APP,

CASRN 68333-79-9)

Source
(parameter)3'b

Value
(applicability)

Notes

Reference0

Cancer

IRIS

NV

NA

U.S. EPA (2020)

HEAST

NV

NA

U.S. EPA (2011a)

DWSHA

NV

NA

U.S. EPA (2018)

NTP

NV

NA

NTP (2016)

IARC

NV

NA

IARC (2019)

CalEPA

NV

NA

CalEPA (2019);
CalEPA (2020)

ACGIH

NV

NA

ACGIH (2018)

aSources: ACGIH = American Conference of Governmental Industrial Hygienists; ATSDR = Agency for Toxic
Substances and Disease Registry; CalEPA = California Enviromnental Protection Agency; DOE = U.S. Department
of Energy; DWSHA = Drinking Water Standards and Health Advisories; HEAST = Health Effects Assessment
Summary Tables; IARC = International Agency for Research on Cancer; IPCS = International Programme on
Chemical Safety; IRIS = Integrated Risk Information System; NIOSH = National Institute for Occupational Safety
and Health; NTP = National Toxicology Program; OSHA = Occupational Safety and Health Administration;
USAPHC = U.S. Army Public Health Command; WHO = World Health Organization.

Parameters: MEG = military exposure guideline; MTDI = maximum tolerable daily intake; PAC = protective
action criteria, TEEL = temporary emergency exposure limit.

°Reference date is the publication date for the database and not the date the source was accessed.

APP = ammonium polyphosphate; DAP = diammonium phosphate; LD50 = median lethal dose;
MAP = monoammonium phosphate; NA = not applicable; NY = not available; P = phosphorus.

Literature searches were conducted in April 2019 and updated in October 2020 and
July 2021 for studies relevant to the derivation of provisional toxicity values for ammonium
phosphate salts (CASRNs 7722-76-1, 7783-28-0, and 68333-79-9). Searches were conducted
using U.S. EPA's Health and Environmental Research Online (HERO) database of scientific
literature. HERO searches the following databases: PubMed, TOXLINE1 (including TSCATS1),
and Web of Science. The following resources were searched outside of HERO for health-related
values: American Conference of Governmental Industrial Hygienists (ACGIH), Agency for
Toxic Substances and Disease Registry (ATSDR), California Environmental Protection Agency
(CalEPA), Defense Technical Information Center (DTIC), European Centre for Ecotoxicology
and Toxicology of Chemicals (ECETOC), European Chemicals Agency (ECHA), U.S. EPA
Chemical Data Access Tool (CDAT), U.S. EPA ChemView, U.S. EPA Health Effects
Assessment Summary Tables (HEAST), U.S. EPA Integrated Risk Information System (IRIS),
U.S. EPA Office of Water (OW), International Agency for Research on Cancer (IARC), Japan
Existing Chemical Data Base (JECDB), National Institute for Occupational Safety and Health
(NIOSH), National Toxicology Program (NTP), Organisation for Economic Co-operation and

'Note that this version of TOXLINE is no longer updated

(https://www.nlm.nih.gov/databases/download/toxlinesubset.html): therefore, it was not included in the literature
search updates from October 2020 and July 2021.

7 Ammonium salts of inorganic phosphates


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EPA/690/R-21/007F

Development (OECD) Existing Chemicals Database, OECD Screening Information Data Set
(SIDS) High Production Volume (HPV) Chemicals via IPCS INCHEM, Occupational Safety and
Health Administration (OSHA), and World Health Organization (WHO).

A screening subchronic p-RfD for DAP has been derived in this assessment based on
compound- (DAP-) specific data, and it is expected to be protective for MAP as well, given the
physicochemical similarities between DAP and MAP (e.g., MAP possesses one less ammonium
ion). However, it should not be applied to the risk assessment of APP, which is expected to have
a much wider range of potential and variable structures, physicochemical properties, and
ammonium content (see Table 1), and for which relevant toxicity data are not available to derive
a p-RfD.

8 Ammonium salts of inorganic phosphates


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EPA/690/R-21/007F

2. REVIEW OF POTENTIALLY RELEVANT DATA
(NONCANCER AND CANCER)

Tables 3A and 3B provide overviews of the relevant noncancer and cancer evidence
bases, respectively, for ammonium phosphate salts, and include all potentially relevant acute,
repeated short-term, subchronic, and chronic studies as well as reproductive and developmental
toxicity studies identified from the literature screening results. Principal studies used in the
PPRTV assessment for derivation of provisional toxicity values are identified in bold. The phrase
"statistical significance," and term "significant," used throughout the document, indicates a
p-value of < 0.05 unless otherwise specified.

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EPA 690 R-21 00 7F

Table 3A. Summary of Potentially Relevant Noncancer Data for Ammonium Phosphate Salts
(MAP, CASRN 7722-76-1; DAP, CASRN 7783-28-0; APP, CASRN 68333-79-9)

Category"

Number of Male/Female,

Strain, Species, Study
Type, Reported Doses (if
different), Study Duration

Dosimetryb

Critical Effects

NOAELb

LOAELb

Reference
(comments)

Notes0

Human

Subchronic/
Chronic

91 fertilizer plant workers
(30 from DAP plant, 30
from urea plant, and 31 from
ammonia plant) compared
with 68 controls; of the
91 total workers, 51 were
presumed exposed <10 yr
and 40 were presumed
exposed >10 yr. Air samples
were not taken nor were
exposure levels measured.

ND

Among DAP plant workers, FVC,
FEVi, and PEFR/min were
significantly reduced compared
with controls. Among all fertilizer
workers combined, spirometry
parameters were reduced compared
with controls, with greater
reductions in the group with longer
exposure duration (>10 yr).

NDr

NDr

Bhat and

Ramaswamv (1993)

PR; due to a
lack of
exposure
information,
effect levels
could not be
established

Animal

1. Oral (mg/kg-d)

Subchronic

Toxicity subgroup: 5/sex,
Sprague Dawley rat; DAP
administered by gavage,
daily for 35 d

0, 250, 750,
1,500 (as
DAP)

Submucosal inflammation of the
stomach, stomach thickening,
horizontal banding of teeth.

NDr

250

Huntingdon (2002)
as cited in OECD
(2007b) and ECHA

PS, PR by SS;
considered
"reliable
without
restriction" by
ECHA (2002)"

(2002)

(GLP-compliant
study conducted
according to OECD
Guideline 422)



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Ammonium salts of inorganic phosphates


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Table 3A. Summary of Potentially Relevant Noncancer Data for Ammonium Phosphate Salts
(MAP, CASRN 7722-76-1; DAP, CASRN 7783-28-0; APP, CASRN 68333-79-9)

Category"

Number of Male/Female,

Strain, Species, Study
Type, Reported Doses (if
different), Study Duration

Dosimetryb

Critical Effects

NOAELb

LOAELb

Reference
(comments)

Notes0

Chronic

10 F rabbits (strain not
specified); DAP
administered in drinking
water (concentrations not
reported) for 5-16 months

300-700
(as DAP)

Parathyroid weight increased
235%. No other toxicological
parameters were assessed.

NDr

NDr

Fazekas(1954) as
cited in Weiner et al.
(2001)

PR, SS; effect
levels could not
be determined
due to the
limited
toxicological
evaluations and
limited study
details

provided in the

secondary

source

Reproductive/
Developmental

Reproductive subgroup: 10
F, 5 M, Sprague Dawley rat;
DAP administered by
gavage, daily for 28 d in
males and 53 d in females
(2 wk prior to mating,
through mating and
gestation, until LD 4)

0, 250, 750,
1,500 (as
DAP)

No reproductive or developmental
effects reported at highest dose.

1,500
(reproductive/
developmental)

NDr

Huntingdon (2002)
as cited in OECD
(2007b) and ECHA
(2002)

(GLP-compliant
study conducted
according to OECD
Guideline 422)

PR by SS;
considered
"reliable
without
restriction" by
ECHA (2002)

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Table 3A. Summary of Potentially Relevant Noncancer Data for Ammonium Phosphate Salts





(MAP, CASRN 7722-76-1; DAP, CASRN 7783-28-0; APP, CASRN 68333-79-9)





Number of Male/Female,















Strain, Species, Study















Type, Reported Doses (if









Reference



Category"

different), Study Duration

Dosimetryb

Critical Effects

NOAELb

LOAELb

(comments)

Notes0

2. Inhalation (mg/m3)

ND

"¦Duration categories are defined as follows: Acute = exposure for <24 hours; short term = repeated exposure for 24 hours to <30 days
exposure for >30 days <10% life span for humans (>30 days up to approximately 90 days in typically used laboratory animal species)
for >10% life span for humans (>~90 days to 2 years in typically used laboratory animal species) (U.S. EPA. 2002).
bDosimetry: Doses are presented as ADDs (mg/kg-day) for oral noncancer effects.

°Notes: PR = peer reviewed; PS = principal study; SS = available only as reported in secondary source.

ADD = adjusted daily dose; APP = ammonium polyphosphate; DAP = diammonium phosphate; F = female(s); FEVi = forced expiratory volume of 1 second;
FVC = forced vital capacity; GLP = Good Laboratory Practice; LD = lactation day; LOAEL = lowest-observed-adverse-effect level; M = male(s);
MAP = monoammonium phosphate; ND = no data; NDr = not determined; NOAEL = no-observed-adverse-effect level; OECD = Organisation for Economic
Co-operation and Development; PEFR = peak expiratory flow rate.

; long term (subchronic) = repeated
; and chronic = repeated exposure

12

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Table 3B. Summary of Potentially Relevant Cancer Data for Ammonium Phosphate Salts
(MAP, CASRN 7722-76-1; DAP, CASRN 7783-28-0; APP, CASRN 68333-79-9)

Category

Number of Male/Female, Strain, Species,
Study Type, Reported Doses, Study Duration

Dosimetry

Critical Effects

Reference
(comments)

Human

1. Oral (mg/kg-d)

ND

2. Inhalation (mg/m3)

ND

Animal

1. Oral (mg/kg-d)

ND

2. Inhalation (mg/m3)

ND

APP = ammonium polyphosphate; DAP = diammonium phosphate; MAP = monoammonium phosphate; ND = no data.

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2.1. HUMAN STUDIES

2.1.1.	Occupational Studies

Bhat and Ramaswamy (1993)

In a published occupational health study, 91 workers in fertilizer plants in India were
evaluated for respiratory function and compared with 68 controls matched for age, sex, body
surface area, and socioeconomic status (Bhat and Ramaswamy. 1993). Of the 91 workers,
30 worked at a DAP plant, 30 worked at a urea plant, and 31 worked at an ammonia plant.
Smokers were excluded from the study due to potential for confounding. No air samples were
taken, and DAP exposure concentrations were not reported. Spirometry parameters (forced vital
capacity [FVC], forced expiratory volume of 1 second [FEVi], and peak expiratory flow rate
[PEFR]/minute) were evaluated using a portable spirometer. The study authors did not report the
timing of spirometry measurements (e.g., before or after shift; before, during, or after a work
week) or any further information on the selected controls.

Presumed exposure to DAP had a greater association with respiratory parameters than
presumed exposure to urea or ammonia (Bhat and Ramaswamy. 1993). As reported in Table B-l,
significant reductions in FVC, FEVi, and PEFR/minute were observed in workers at the DAP
plant. Workers in all plants combined (not stratified by fertilizer type) were categorized by
duration of employment: workers exposed (presumed) 0-10 years (51), workers exposed
(presumed) for >10 years (40), and nonworker controls (68). Significant decreases in FEVi and
PEFR/minute were observed in workers exposed (presumed) 0-10 years compared to controls.
All parameters were significantly decreased in workers exposed (presumed) >10 years. Due to a
lack of any exposure information, these data are inadequate to establish effect levels.

Rahe and Ehrenbers (1985)

NIOSH conducted an occupational health survey of 43 workers at an electric power
facility construction site. At the site, insulation containing fiberglass, long-chain hydrocarbons,
and ammonium phosphate was being cut (with a saw), resulting in airborne particles. Personal
monitoring samples were collected and analyzed for formaldehyde and particulate but not for
ammonium phosphate. Workers were asked to report irritation and "constitutional" symptoms
occurring during the 24 hours and the 7 days prior to the site visit. Common symptoms reported
by the workers were chest congestion, nasal irritation, and throat irritation. No relationship was
found between exposure to the insulation particulate and prevalence of any symptom.

2.1.2.	Other Human Studies

Fire extinguishers contain large, varying amounts of MAP in powder form (34-40% in
some reports). Intentional inhalation and/or ingestion of fire extinguishing powder (during
suicide attempts) has reportedly caused electrolyte imbalance and metabolic acidosis in
numerous case studies [Becker et al. (2018) (published in German with English abstract), Dovon
and McGrath (2003) (abstract only), Lee et al. (2016). Lin et al. (2009). Senthilkumaran et al.
(2012)]. MAP doses were not estimated for these cases; however, serum phosphate levels in the
patients were reported, ranging between 9.8 and 30.6 mg/dL (normal range is 2.3-4.5 mg/dL)
[Dovon and McGrath (2003) (abstract only), Lee et al. (2016). Lin et al. (2009). Senthilkumaran
et al. (2012)]. Effects reported in the patients included respiratory tract irritation,
hyperphosphatemia, hypocalcemia, metabolic acidosis, delayed aspiration pneumonia, acute
kidney failure, and cardiac arrest. A case study (Blumenthal and Hanert-Van der Zee. 2018)
detailing autopsy results after a suicide reported a number of findings consistent with injury due
to fire extinguisher pressure (e.g., ethmoid fracture, esophageal rupture, alveolar distension and
rupture) as well as histology changes that may or may not be related to these injuries (pulmonary

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edema, vascular congestion, crystalline lattice in some alveoli). Effects attributable to
ammonium phosphate exposure could not be discerned in this case.

Two studies conducted in the 1930s evaluated the use of ammonium phosphate salts (not
further described) as urinary acidifiers, apparently to enhance the action of "urinary antiseptics"
such as hexamine. Scott (1931) administered 20 g ammonium phosphate in solution to five
volunteers 4 times/day, alternating 2 days of administration and 2 days off for 20 days (10 days
of treatment). Urine samples collected over the course of the study showed that urine tended to
be at lower pH when administered DAP when compared with samples collected on days that
DAP was not administered; no other endpoints were evaluated. A1 stead (1936) administered
"acid ammonium phosphate" in doses of 2.1-6 g to 34 hospital patient volunteers 3 or
4 times/day for an unspecified duration and compared the patients' urinary pH levels with those
seen in patients receiving sodium phosphate. The results showed decreased urinary pH with
administration of ammonium phosphate, compared with sodium phosphate.

2.2. ANIMAL STUDIES
2.2.1. Oral Exposures

Subchronic Studies

Huntingdon (2002) as cited in OECD (2007b) and EC HA (2002)

In an unpublished, Good Laboratory Practice (GLP)-compliant, OECD 422 guideline
study cited in OECD (2007b). OECD (2007f). and ECHA (2002). Sprague Dawley rats (5/sex
per toxicity subgroup; 10 females and 5 males per reproductive subgroup) were administered 0,
250, 750, or 1,500 mg DAP/kg-day [purity >87% as reported in OECD (2007b) and OECD
(2007c)1 via gavage in water for 35 days (toxicity subgroup) or through Lactation Day (LD) 4 in
females (28 and 53 days of exposure for parental males and females, respectively) of the
reproductive subgroup [Huntingdon (2002) as cited in OECD (2007b)1. Doses were analytically
verified by spectrophotometry. The source, nature, and composition of the animals' diet,
including the calcium and baseline phosphate contents, were not reported. Mortality, clinical
signs, body weight, and food consumption were monitored. In the toxicity subgroup, blood was
collected during Week 5 for determination of hematology (comprehensive endpoints including
clotting parameters) and clinical chemistry (alkaline phosphatase [ALP], alanine
aminotransferase [ALT], aspartate aminotransferase [AST], y-glutamyl transferase [GGT], total
bilirubin, albumin, total protein, urea, creatinine, glucose, total cholesterol, and electrolytes) for
the toxicity, but not the reproductive, subgroup. Functional operational battery (FOB) endpoints
(approach response, touch response, auditory startle reflex, tail pinch response, forelimb and
hindlimb grip strength, and motor activity) were evaluated after 4 weeks. The following tissues
from the toxicity subgroup were weighed: adrenals, brain, epididymides, heart, kidneys, liver,
ovaries, pituitary, prostate, seminal vesicles, spleen, testes, thymus, thyroids with parathyroid,
uterus with cervix, and vagina. Although organ weights measured in the reproductive subgroup
were not specified, the test guideline followed in the study (OECD 422) (OECD. 1996) indicates
that organs weighed for reproductive effects include gonads (testes and ovaries), accessory sex
organs (uterus and cervix, epididymides, prostate, seminal vesicles plus coagulating glands), and
vagina. In the toxicology subgroup, organs fixed for histological analysis included any with
observed abnormalities, as well as the adrenals, aorta, brain, caecum, colon, duodenum,
epididymides, eyes, heart, ileum, jejunum, kidneys, liver, lungs, lymph nodes, mammary area,
esophagus, ovaries, pancreas, pituitary, prostate, rectum, salivary glands, sciatic nerves, seminal
vesicles, skin, spinal cord, spleen, sternum (bone marrow), stomach, testes, thymus, thyroid,
trachea, urinary bladder, uterus, and vagina. In the reproductive subgroup, organs fixed for
histological analysis included those with abnormalities, as well as reproductive organs (not

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specified, but likely included gonads and accessory sex organs based on OECD 422).
Reproductive parameters (mating, gestation, and parturition parameters, including: precoital
interval, mating performance, and fertility; gestation length and gestation index; litter size; and
offspring survival indices) were assessed, and offspring were evaluated (litter size, offspring
survival indices, sex ratio, offspring body weight, and gross pathology) through Postnatal Day
(PND) 4.

Statistical tests were conducted using Fisher's exact test for categorical data and
Bartlett's test for continuous data comparisons to control, incorporating multiple comparisons
where needed. In the instance of a positive Bartlett's test, a Behrens's Fisher test was used for
pairwise comparisons; otherwise, a Dunnett's test was used.

One female in the 1,500 mg DAP/kg-day toxicity subgroup died during the study (time
point not reported); ECHA (2002) noted that findings in this animal were consistent with dosing
error.2 Dose-dependent increased incidences of the clinical signs of postdosing salivation and
reddening of the extremities were noted starting at 250 mg DAP/kg-day. Decreased body-weight
gain (78% of control value) was reported in males, but not females, of the 1,500-mg DAP/kg-day
toxicity subgroup. Food consumption was marginally suppressed in males of the
1,500-mg DAP/kg-day group only. In the reproductive subgroup, an initial decrease in
body-weight gain was noted in females during the 1st week of gestation, but body weights
recovered to control levels after the week and remained normal through PND 4. No neurological
effects were observed during the FOB. The only hematological finding was reduced activated
partial thromboplastin time in males, but not females, administered 750 or 1,500 mg DAP/kg-day
[26 and 24% less than controls, respectively; statistically significant changes reported here and
below based on ECHA (2002) and OECD (2007b) unless otherwise noted]. Clinical chemistry
alterations in males were increased ALP (32 and 31% higher than controls at 750 and
1,500 mg DAP/kg-day, respectively), decreased glucose (21% less than control) and phosphorus
(18% less than control) at 1,500 mg/kg-day, decreased total protein (7 and 9% less than control
at 750 and 1,500 mg DAP/kg-day, respectively), and a 17% increase in albumin:globulin (A/G)
ratio at 1,500 mg DAP/kg-day. Clinical chemistry alterations in females were decreased
phosphorus levels (19% less than controls) and a nonsignificant increase in ALP (22%) at
1,500 mg DAP/kg-day. Relative liver and kidney weights were increased (quantitative data not
reported) in females at 1,500 mg DAP/kg-day; no organ-weight changes were noted in males.
Both sexes exhibited horizontal banding on the incisors of teeth in the 750 and
1,500-mg DAP/kg-day dose groups; histological examination showed that this was limited to the
enamel and likely reflected direct effects on tooth mineralization. Thickening of the stomach was
also noted upon gross examination in both sexes at doses >750 mg DAP/kg-day. In the toxicity
subgroup, histological evidence of submucosal inflammation in the stomach was noted in 0/5,
3/5, 4/5, and 2/5 males and 0/5, 2/5, 4/5, and 4/5 females at doses of 0, 250, 750, and
1,500 mg DAP/kg-day, respectively (see also Table B-2). The severity of these lesions was
reported to be only minimal or slight in all cases. Incidences were statistically significant in
females at doses >750 mg DAP/kg-day and males at 750 mg DAP/kg-day. Because the available
data did not suggest sex differences in the inflammation, the incidences in males and females
were combined for this review to increase statistical power. When incidences for males and
females in the toxicity subgroup were combined (0/10, 5/10, 8/10, 6/10), the incidences at all
doses were significantly increased relative to controls (p < 0.05 by Fisher's exact test performed

2Despite the death, histopathology incidence data provided in OECD (2007b). OECD (2007f). and ECHA (2002) are
reported for five females in this group, suggesting that the animal that died prematurely was included in the results.

16 Ammonium salts of inorganic phosphates


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EPA 690 R-21 00 7F

for this review) (see Table B-2). Stomachs were not examined microscopically in the
reproductive subgroup. No other histological findings were reported. No effects were reported on
mating or fertility, and no effects on offspring were observed through PND 4 in the reproductive
subgroup.

A reproductive/developmental no-observed-adverse-effect level (NOAEL) of
1,500 mg DAP/kg-day (the highest dose tested) was identified by ECHA (2002) and OECD
(2007b); a lowest-observed-adverse-effect level (LOAEL) could not be determined. OECD
(2007f) identified a systemic NOAEL of 250 mg DAP/kg-day and a LOAEL of
750 mg DAP/kg-day for this study based on degenerative changes in the stomach,3 noting that
the incidences of histologic changes in the stomach were not statistically significant in males or
females at the low dose. ECHA (2002) identified the same effect levels, but based the LOAEL
on dental banding, which was of questionable biological relevance; ECHA (2002) attributed the
stomach effects to local irritation rather than systemic toxicity and did not consider this local
effect as a potential basis for the LOAEL. Based on the significant increase in the incidence of
stomach lesions in male and female rats (combined) at all doses in the study, the LOAEL
determined for this review is 250 mg DAP/kg-day; a NOAEL could not be determined. As noted
above, the calcium and baseline phosphate contents of the feed administered in this study were
not reported. Although the ratio of calcium to phosphate can be an important determinant of
phosphate toxicity in mammals, there were no indications of excess phosphate intake
(e.g., laxative or renal effects) in the animals, and inadequate calcium intake is not considered a
plausible cause of stomach inflammation in the current study with ammonium phosphate. The
critical effects observed in the principal study (contact irritant effects in the stomach) might be
attributable to the ammonium anion, since damage to the gastrointestinal mucosa has been
observed in rats after oral exposure to other ammonium compounds (ammonium hydroxide,
ammonium chloride, and ammonia) [reviewed by ATSDR (2004)1. Gavage bolus dosing also
would have delivered a high, instantaneous local exposure to the stomach, which may have
contributed to the observed local effects. Local stomach irritation (although more extensive,
including submucosal inflammation, epithelial hyperplasia, acantholysis, increased numbers of
mucous secreting cells) was also observed at all (identical) doses in another GLP-compliant,
OECD 422 guideline study conducted also by gavage with granular triple superphosphate
(GTSP; composed of calcium and phosphate) in rats. The effects were attributed to irritation
along with the low pH (2-3) of that test substance (OECD. 2007c). Finally, it is possible that
dental bands and/or increased serum ALP observed in Huntingdon (2002) [as cited in OECD
(2007b). OECD (2007f). and ECHA (2002)] could be related to higher phosphate intake, but
these effects occurred at higher doses (>750 mg/kg-day) than the stomach inflammation.

Chronic Studies

Fazekcis (1954) as cited in Weiner et al. (2001)

In a study published in German and summarized in a review by Weiner et al. (2001).
10 female rabbits (strain not specified) were exposed to DAP in drinking water for 5-16 months.
The review by Weiner et al. (2001) reported the doses as 300-700 mg/kg-day and indicated that
parathyroid gland weight was the only toxicological endpoint assessed in the study. According to
Weiner et al. (2001). the mean parathyroid weight was increased by 235% compared to controls.
No further information was provided in the secondary source. Effect levels could not be

3The OECD (2007f) study for phosphates also reported degenerative changes in the kidneys as a basis for the
LOAEL; however, no evidence of kidney effects was reported in the OECD (2007b) robust summary or in the
ECHA (2002) summary of the study.

17 Ammonium salts of inorganic phosphates


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EPA 690 R-21 00 7F

determined because of the limited toxicological evaluations and limited study details provided in
the secondary source.

Reproductive/Developmental Studies

The study by Huntingdon (2002) as cited in OECD (2007b) and ECHA (2002) included a
screening analysis for reproductive and developmental effects (reproductive subgroup). Details
and results are described above in the "Subchronic Studies" section. As reported there, a
reproductive/developmental NOAEL of 1,500 mg DAP/kg-day (the highest dose tested) is
identified for this study.

2.2.2. Inhalation Exposures

No repeated-dose studies of animals exposed to MAP, DAP, or APP by inhalation have
been identified in the literature searches or secondary sources reviewed.

2.3. OTHER DATA (SHORT-TERM TESTS, OTHER EXAMINATIONS)

Table 4 provides an overview of genotoxicity studies of DAP and MAP.

2.3.1. Genotoxicity

Data pertaining to the genotoxic activity of ammonium phosphate salts are very limited,
and the only studies available are unpublished studies reported in secondary sources, although
OECD and ECHA peer reviewed these primary studies. DAP was not mutagenic to Salmonella
typhimurium or Escherichia coli with or without metabolic activation [Wagner and Klug (2001)
as cited in OECD (2007b) and ECHA (2001 a) 1 and did not increase chromosomal aberrations
(CAs) in Chinese hamster ovary (CHO) cells in vitro, with or without metabolic activation [Gudi
and Brown (2001) as cited in OECD (2007b) and ECHA (2001b)1. MAP was not mutagenic to
mouse L5178Y/TK+/- lymphoma cells with or without metabolic activation (ECHA. 2010a).

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Table 4. Summary of Ammonium Phosphate Salts
(MAP, CASRN 7722-76-1; DAP, CASRN 7783-28-0; and APP, CASRN 68333-79-9) Genotoxicity

Endpoint
(substance)

Test System

Doses/
Concentrations Tested

Results
without
Activation"

Results with
Activation"

Comments

References

Genotoxicity studies in prokaryotic organisms

Mutagenicity
(DAP)

Salmonella
tvphimurium strains
TA98, TA100,
TA1535, TA1537,

Escherichia coli WP2
urvA

Experiment 1: 2.5, 7.5, 25, 75, 200, 600,
1,800, 5,000 |ig DAP/plate;

Experiment 2: 50, 150, 500, 1,500,
5,000 |ig DAP/plate





Plate incorporation assay.
Precipitation noted at
>1,800 |ig DAP/plate in
Experiment 1 and at
5,000 |ig DAP/plate in
Experiment 2, with or without
metabolic activation. No
cytotoxicity was observed. Positive
controls for each strain produced
expected results.

Wagner and Klug
(2001) as cited in
OECD (2007b)
and ECHA
(2001a)

Genotoxicity studies in mammalian cells—in vitro

Mutagenicity
(MAP)

L5178Y/TK+/-mouse
lymphoma cells

Experiment 1 (3-h exposure): 0.003, 0.03,

0.1,	0.25, 0.5, 1, 1.4, 2 (igMAP/mL
(without activation) or 0.01, 0.03, 0.1, 0.3,

1,	3, 10, 12 (igMAP/mL (with activation);
Experiment 2: 0.01, 0.03, 0.1, 0.25, 0.5, 1,
1.4, 1.8 (igMAP/mL (without activation,
24-h exposure) or 0.01, 0.1, 1, 10, 12, 14,
16, 17 (igMAP/mL (with activation, 3-h
exposure)





No cytotoxicity or precipitation
were observed. Positive controls
produced expected results.

Anonymous
(2010) as cited in
ECHA (2010a)

Clastogenicity

[CA]

(DAP)

CHO cells

165, 330, 660 |ig DAP/mL (without
activation, exposure for 4 or 20 h);
330, 660, 1,320 (ig DAP/mL (with
activation, exposure for 4 h)





Precipitate was observed at
1,320 (ig DAP/mL. Cytotoxicity
was seen at 660 |ig DAP/mL in
tests performed without activation
(4 or 20 h). Positive controls
provided expected results.

Gudi and Brown
(2001) as cited in
OECD (2007b)
and ECHA
(2001b)

a+ = positive, (+) = weak positive, - = negative, ± = equivocal.

APP = ammonium polyphosphate; CA = chromosomal aberration; CHO = Chinese hamster ovary; DAP = diammonium phosphate; MAP = monoammonium phosphate.

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2.3.2. Other Animal Studies

Ammonium phosphate salts exhibit low acute lethal potential based on unpublished data
in peer-reviewed secondary sources. Unpublished acute lethality limit tests performed according
to OECD Guideline 405 (OECD. 2021) were reported in OECD (2007a). OECD (2007b). and
OECD (2007d). The oral median lethal dose (LD50) values determined in rats were >2,000 mg/kg
for MAP, DAP, and APP, and no clinical signs or body-weight changes were reported [Merkel
(2000) as cited in OECD (2007a). OECD (2007b). and OECD (2007d)l. In a review, Weiner et
al. (2001) reported the following oral LD50 values for rats: >1,000 and 5,750 mg/kg for MAP;
>1,000, 6,500, and >25,100 mg/kg for DAP; and >2,000 mg/kg for APP, as well as the following
dermal LD50 values for rabbits: >7,940 mg/kg (MAP), >10,000 mg/kg (DAP), and >2,000 mg/kg
(APP), citing unpublished studies by Stauffer, Solutia, and Albright and Wilson. A 4-hour
inhalation median lethal concentration (LC50) value of >5.09 mg/L for APP was noted in the
same review (Weiner et al.. 2001). No details of study design or results, and no information on
clinical signs, body-weight changes, or necropsy findings were reported by Weiner et al. (2001).

In an acute lethality study of the ammonium phosphate fire retardant PHOS-CHEK 259-F
(>90% DAP and <5% guar gum according to material safety data sheet; other ingredients not
reported) (ICL. 2015) in male and female rats, gavage doses of 2,000, 2,520, 3,175, and
4,000 mg/kg resulted in the following mortality incidences: 9/10, 1/10, 8/10, and 7/10. However,
no LD50 values could be estimated from these data (Monsanto. 1992). Clinical signs of sedation,
ataxia, and ptosis, as well as gastrointestinal distress, were observed, and necropsy showed
gastrointestinal distension and darkened stomachs. Monsanto (1992) estimated an LD50 of
>5,000 mg/kg in a rabbit dermal lethality study of PHOS-CHEK 259-F. In the dermal study,
body-weight loss was noted in 7/10 rabbits, erythema and edema were observed, and at
necropsy, there was a loss of body fat (10/10 rabbits), as well as hepatic, renal, and splenic
abnormalities; in addition, enlarged gall bladder was observed in 2/5 males. Other LD50 values
for ammonium phosphate fire retardants were reported; however, these products (PHOS-CHEK
XAF and PHOS-CHEK 75-D) are of low or unknown ammonium phosphate composition. No
composition information was located for PHOS-CHEK XAF, while PHOS-CHEK 75-D is
reportedly composed of >65% diammonium sulfate, >5% DAP, and >15% MAP (ICL. 2006):
thus, these LD50 values, all higher than those reported above, are not reported here.

Following studies showing that other phosphates exhibited a cariostatic effect, DAP was
tested for prevention of dental caries (cavities) in white rats (sex and strain not reported)
(McClure. 1964). DAP administered in the diet at concentrations between 0.55 and 3.33% for
60-90 days reduced the incidence of rats with caries, the numbers of carious teeth per rat, and
the caries severity score per rat. No other toxicological endpoints were evaluated. In a study
reported only in abstract form, Ivy et al. (1974) observed lower body weight and percent femur
ash in rats administered DAP in the diet (at levels equivalent to 0.5, 0.7, or 0.9% phosphorus) for
70 days when compared with rats exposed to sodium phosphate, which provided equivalent
concentrations of phosphorus. Finally, turkeys given DAP in the diet for 8 weeks exhibited
similar tibia breaking strength when compared with those administered other dietary phosphate
sources with varying fluorine content (Struwe and Sullivan. 1975).

Clawson and Armstrong (1981) administered APP (replacing 0, 50, or 100% phosphorus
in diet, in place of defluorinated rock phosphate) to groups of seven rats (three males and four
females) for 4 weeks and observed increased food intake and weight gain, although the changes
were not monotonic with exposure. The study authors did not evaluate other toxicological
endpoints. Other studies with APP are limited to evaluations of growth in agricultural species, in

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which APP was tested as a source of nutritional nitrogen and phosphorus. Administration of APP
did not affect growth or feed consumption in pigs when compared with other supplements, such
as dicalcium phosphate (Tunmire et al.. 1983; Clawson and Armstrong. 1981; Kornegav. 1972).
In cows, Colenbrander et al. (1971) found that addition of APP in the diet for 8 weeks increased
growth and plasma phosphorus while decreasing urinary pH. In sheep and lambs, addition of
APP to the diet or in drinking water for 1-13 weeks likewise resulted in higher body-weight
gains, blood phosphorus concentrations, and retention of phosphorus (Koolivand et al.. 2019;
Hemingway and Fishwick. 1975; Fishwick and Hemingway. 1974). In 3-week experiments in
chickens, supplementation with APP in the drinking water resulted in increased food
consumption, growth, phosphorus intake, and phosphorus concentration in tibia ash compared
with controls (Damron and Flunker. 1990; Jensen and Edwards. 1980).

The ammonium phosphates (APP, MAP, and DAP), as well as PHOS-CHEK 259-F, were
considered either nonirritating or slightly to mildly irritating when applied to the skin or eyes in
tests conducted in rabbits (Weiner et al.. 2001; Monsanto. 1992; Aovama. 1975). DAP was also
determined to be nonsensitizing by the dermal route (ECHA. 2010b).

2.3.3.	Metabolism/Toxicokinetic Studies

Gastrointestinal absorption of phosphate from DAP has been studied in dogs. Summerill
and Lee (1985) administered DAP (15 mmol in two doses 2 hours apart) by stomach tube to
eight mongrel dogs and measured plasma and urinary phosphate levels for up to 4 hours. Plasma
phosphate levels were increased in exposed dogs (1.63 and 1.91 mmol/L at 1.5-2 and
3.5-4 hours, respectively, compared with 0.88 and 0.94 mmol/L in four control animals), while
creatinine clearance was unchanged. The study authors estimated phosphate absorption to be
about 50%, based on plasma phosphate levels obtained in the 4 hours after the first dose and the
assumption that phosphate was distributed evenly throughout the extracellular fluid.

2.3.4.	Mode-of-Action/Mechanistic Studies

An in vitro study used neuro-derived cell lines (PC 12 pheochromocytoma and
B35 neuroblastoma) to evaluate the neurotoxic potential of several fire retardants, including APP
(Hendriks et al.. 2014). Exposure to concentrations up to 1,300 |iM APP was not cytotoxic to
PC12 cells, but cytotoxicity was observed in B35 cells at concentrations of at least 13 [xM.
Hendriks et al. (2014) reported that APP concentrations of 7 or 700 |iM increased reactive
oxygen species production in B35 and PC12 cells but noted that the results may have been
confounded by interaction of the compound with the fluorescent dye used in the assay. APP did
not affect basal levels of intracellular calcium in either cell type but did inhibit the
depolarization-evoked rise in intracellular calcium concentration. Finally, APP reportedly
exhibited antagonistic effects on human nicotinic acetylcholine receptor at >1,300 |iM (Hendriks
et al.. 2014). The study authors concluded that APP exhibited low neurotoxic potential based on
the in vitro results.

A number of other in vitro studies were identified in which ammonium phosphate was
used as a phosphate source to evaluate mechanisms of changing membrane porosity during
mitochondrial swelling (Sitaramam and Rao. 1992; Stonerand Sirak. 1978; Hommes et al..
1975; Lundberg. 1975; Chateaubodeau et al.. 1974; Stonerand Sirak. 1971). The relevance of
these studies to mechanisms of toxicity for ammonium phosphate compounds is uncertain.

21 Ammonium salts of inorganic phosphates


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3. DERIVATION OF PROVISIONAL VALUES

3.1.	DERIVATION OF PROVISIONAL REFERENCE DOSES

No adequate repeated-dose oral toxicity studies were identified for MAP or APP. The
database of oral toxicity studies in animals exposed to DAP is limited to a German-language
chronic study in rabbits evaluating only parathyroid weight [Fazekas (1954) as cited in Weiner et
al. (2001)1 and a combined 35-day repeated-dose toxicity and 28/53 days (males/females)
reproductive/developmental screening study in rats [Huntingdon (2002) as cited in OECD
(2007b) and ECHA (2002)1. The study by Fazekas (1954) as cited in Weiner et al. (2001) is not
adequate for deriving a provisional reference dose (p-RfD). The study was published in German
with only a brief summary reported in the review by Weiner et al. (2001); furthermore, the only
endpoint evaluated was parathyroid gland weight, so effect levels could not be determined. The
study by Huntingdon (2002) as cited in OECD (2007b) and ECHA (2002) was GLP-compliant,
conducted according to OECD Test Guideline 422 (OECD. 1996). and evaluated numerous
systemic (including neurological), reproductive, and developmental endpoints. This study was
not published and is available as reported in secondary sources; therefore, this study was not
considered suitable for deriving a p-RfD. However, the study was reviewed by both OECD HPV
and ECHA, both of which are peer-review processes. The study appears to have been well
conducted, was considered "reliable without restriction" by ECHA, and provides sufficient data
to develop a screening-level subchronic p-RfD value for DAP (see Appendix A). Human and
animal data are insufficient to derive a chronic p-RfD for ammonium phosphate salts, as
discussed below.

3.2.	DERIVATION OF PROVISIONAL REFERENCE CONCENTRATIONS

Human and animal data are insufficient to derive subchronic or chronic provisional
reference concentrations (p-RfCs) for ammonium phosphate salts. The only available
repeated-exposure information consists of a published occupational health study by Bhat and
Ramaswamv (1993) and a NIOSH Human Hazard Evaluation (Ruhe and Ehrenberg. 1985);
neither study evaluated ammonium phosphate exposure levels, precluding identification of effect
levels.

3.3.	SUMMARY OF NONCANCER PROVISIONAL REFERENCE VALUES

Table 5 presents a summary of noncancer provisional references values.

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Table 5. Summary of Noncancer Reference Values for DAP
(CASRN 7783-28-0) and MAP (CASRN 7722-76-1)

Toxicity Type
(units)

Species/
Sex

Critical Effect

p-Reference
Value

POD

Method

POD

(HED)

UFc

Principal Study

Screening
subchronic p-RfD
(mg DAP/kg-d)
(see Appendix A)

Rat/both

Submucosal
inflammation in
stomach

9 x 1(T2

BMDLiq

27.7

300

Huntingdon (2002)
as cited in OECD
(2007b) and
ECHA (2002)

Chronic p-RfD
(mg/kg-d)

NDr

Subchronic p-RfC
(mg/m3)

NDr

Chronic p-RfC
(mg/m3)

NDr

BMD = benchmark dose; BMDL = 95% benchmark dose lower confidence limit on the BMD (subscripts denote
BMR: i.e., 10 = dose associated with 10% extra risk); BMR = benchmark response; DAP = diammonium
phosphate; HED = human equivalent dose; MAP = monoammonium phosphate; NDr = not determined;
POD = point of departure; p-RfC = provisional reference concentration; p-RfD = provisional reference dose;
UFC = composite uncertainty factor.

3.4. CANCER WEIGHT-OF-EVIDENCE DESCRIPTOR

Table 6 identifies the cancer weight-of-evidence (WOE) descriptor for MAP, DAP, and
APP. No human or animal studies evaluating cancer endpoints are available for any of the
chemicals. Limited in vitro genotoxicity assays of DAP and MAP available in peer-reviewed
secondary sources (see Table 4) have reported negative results. Under the U.S. EPA (2005)
cancer guidelines, the available data are inadequate for an assessment of human carcinogenic
potential, and the cancer WOE descriptor for MAP, DAP, and APP is "Inadequate Information
to Assess Carcinogenic Potential" (for both oral and inhalation routes of exposure).

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Table 6. Cancer WOE Descriptor for Ammonium Phosphate Salts (MAP,
CASRN 7722-76-1; DAP, CASRN 7783-28-0; and APP, CASRN 68333-79-9)

Possible WOE Descriptor

Designation

Route of Entry
(oral, inhalation,
or both)

Comments

"Carcinogenic to Humans"

NS

NA

There are no human carcinogenicity data
identified to support this descriptor.

"Likely to Be Carcinogenic to
Humans "

NS

NA

There are no animal carcinogenicity studies
identified to support this descriptor.

"Suggestive Evidence of
Carcinogenic Potential"

NS

NA

There are no animal carcinogenicity studies
identified to support this descriptor.

"Inadequate Information to
Assess Carcinogenic
Potential"

Selected

Both

This descriptor is selected due to the lack of
any information on carcinogenicity of MAP,
DAP, and APP.

"Not Likely to Be
Carcinogenic to Humans"

NS

NA

No evidence of noncarcinogenicity is available.

APP = ammonium polyphosphate; DAP = diammonium phosphate; MAP = monoammonium phosphate; NA = not
applicable; NS = not selected; WOE = weight of evidence.

3.5. DERIVATION OF PROVISIONAL CANCER RISK ESTIMATES

Due to a lack of carcinogenicity data, derivation of cancer risk estimates is not supported
(see Table 7).

Table 7. Summary of Cancer Risk Estimates for Ammonium Phosphate
Salts (MAP, CASRN 7722-76-1; DAP, CASRN 7783-28-0; and
APP, CASRN 68333-79-9)

Toxicity Type (units)

Species/Sex

Tumor Type

Cancer Risk Estimate

Principal Study

p-OSF (mg/kg-d) 1

NDr

p-IUR (lng/in3) 1

NDr

APP = ammonium polyphosphate; DAP = diammonium phosphate; MAP = monoammonium phosphate; NDr = not
determined; p-IUR = provisional inhalation unit risk; p-OSF = provisional oral slope factor.

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APPENDIX A. SCREENING PROVISIONAL VALUES

For reasons noted in the main Provisional Peer-Reviewed Toxicity Value (PPRTV)
document, it is inappropriate to derive provisional reference doses (p-RfDs) for any of the
ammonium phosphate salts. However, some information is available for diammonium phosphate
(DAP), which although insufficient to support derivation of a provisional toxicity value under
current guidelines, may be of limited use to risk assessors. In such cases, the Center for Public
Health and Environmental Assessment (CPHEA) summarizes available information in an
appendix and develops a "screening value." Appendices receive the same level of internal and
external scientific peer review as the provisional reference values to ensure their appropriateness
within the limitations detailed in the document. Users of screening toxicity values in an appendix
to a PPRTV assessment should understand that there may be more uncertainty associated with
the derivation of an appendix screening toxicity value than for a value presented in the body of
the assessment. Questions or concerns about the appropriate use of screening values should be
directed to CPHEA.

DERIVATION OF SCREENING PROVISIONAL REFERENCE DOSES

As discussed in the main body of the report, the only available oral study with adequate
information to derive effect levels [Huntingdon (2002) as cited in OECD (2007b) and ECHA
(2002)1 was unpublished and available as reported in a secondary source. However, this Good
Laboratory Practice (GLP)- and Organisation for Economic Co-operation and Development
(OECD) guideline-compliant study appears to have been well conducted, was peer reviewed by
the European Chemicals Agency (ECHA) and OECD and provides dose-response information
suitable for deriving a screening-level provisional toxicity value for DAP.

A lowest-observed-adverse-effect level (LOAEL) of 250 mg DAP/kg-day (the lowest
dose tested) was identified for the study by Huntingdon (2002) as cited in OECD (2007b) and
ECHA (2002) based on increased incidence of stomach submucosal inflammation in both sexes
at all doses. Benchmark dose (BMD) modeling on the stomach inflammation data (see
Table B-2) was completed using the U.S. Environmental Protection Agency (U.S. EPA)
Benchmark Dose Software (BMDS, Version 3.1.1). Combined incidences in male and female
rats (higher n vs. sex-specific) were modeled to reduce uncertainty around benchmark dose lower
confidence limit (BMDL) estimates, as consistent with Agency guidance.4 Results of BMD
modeling are summarized in Appendix C. Despite a flat dose-response, model results yielded
satisfactory fit of the data for several models after the high dose was dropped, with BMDio and
BMDLio estimates of 44.3 and 27.7 mg DAP/kg-day, respectively. ABMDLio of
27.7 mg/kg-day was therefore selected as the point of departure (POD). Confidence in this value
is increased by the recognition that it is virtually identical to that derived from an alternative
approach using the animal LOAEL of 250 mg/kg-day from the critical study as POD and
applying a LOAEL-to-no-observed-adverse-effect level (NOAEL) uncertainty factor (UFl) of
10.

Derivation of Screening Subchronic Provisional Reference Dose

U.S. EPA endorses a hierarchy of approaches to derive human equivalent doses (HEDs)
from data from laboratory animal species, with the preferred approach being physiologically
based toxicokinetic modeling. Another approach may include using chemical-specific

4Section 2.1.6 (Combining Data for a BMD Calculation) of Benchmark Dose Technical Guidance (U.S. EPA. 2012).

25 Ammonium salts of inorganic phosphates


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EPA 690 R-21 00 7F

information, including what is known about the toxicokinetics and toxicodynamics of the
chemical, to derive chemical-specific adjustments. In the absence of chemical-specific
information to derive human equivalent oral exposures, U.S. EPA endorses body-weight scaling
to the 3/4 power (i.e., BW34) as a default to extrapolate toxicologically equivalent doses of orally
administered agents from all laboratory animals to humans for the purpose of deriving an oral
reference dose (RfD) under certain exposure conditions (U.S. EPA. 2011b). More specifically,
the use of BW3 4 scaling for deriving an RfD is recommended when the observed effects are
associated with the parent compound or a stable metabolite but not typically for portal-of-entry
effects. Because the selected critical effect is stomach submucosal inflammation (portal-of-entry
effect) in rats, the use of BW3 4 scaling is not appropriate in this case.

A screening subchronic p-RfD of 9 x 10 2 mg DAP/kg-day is derived by applying a
composite uncertainty factor (UFc) of 300 (reflecting an interspecies uncertainty factor [UFa] of
10, an intraspecies uncertainty factor [UFh] of 10, and a database uncertainty factor [UFd] of 3 to
the selected POD of 27.7 mg DAP/kg-day (BMDLio) for submucosal inflammation in stomach
of rats exposed to DAP, as follows:

Screening Subchronic p-RfD = BMDLio UFc

= 27.7 mg DAP/kg-day 300
= 9 x 10"2 mg DAP/kg-day

Table A-l summarizes the uncertainty factors for the screening subchronic p-RfD for
DAP. The screening subchronic p-RfD for DAP is expected to be protective for monoammonium
phosphate (MAP) also, given the physicochemical similarities between DAP and MAP
(e.g., MAP possesses one less ammonium ion). However, it should not be applied to the risk
assessment of ammonium polyphosphate, which is anticipated to have a much wider range of
potential and variable structures, physicochemical properties, and ammonium content (see
Table 1), and for which relevant toxicity data are not available to derive a p-RfD.

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Table A-l. Uncertainty Factors for the Screening Subchronic p-RfD for
DAP (CASRN 7783-28-0) and MAP (CASRN 7722-76-1)

UF

Value

Justification

UFa

10

A UFa of 10 is applied to account for uncertainty in extrapolating from animals to humans for oral
portal-of-entry effects of DAP.

UFd

3

A UFd of 3 is applied to account for deficiencies and uncertainties in the database. The oral database
for ammonium phosphate salts includes secondary, peer-reviewed accounts of acute lethality studies
in rats, a well-conducted, GLP- and OECD guideline-compliant 35-d combined repeated-dose and
28/53 (M/F)-d reproductive/developmental screening toxicity study in rats (critical study), a chronic
study in rabbits evaluating only parathyroid gland weight, and negative genotoxicity studies. In the
critical study, no reproductive, developmental, or neurobehavioral effects were observed up to the
highest dose tested (1,500 mg/kg-d), which exceeded the limit dose, in either the toxicity or
reproductive arm of the critical study. Local toxicity at the site of administration is considered the
critical effect with DAP. Therefore, the UFd can be reduced from 10 to 3.

UFh

10

A UFh of 10 is applied to account for human variability in susceptibility to portal-of-entry effects
from oral exposure to DAP.

UFl

1

A UFl of 1 is applied for LOAEL-to-NOAEL extrapolation because the POD is a BMDLio.

UFS

1

A UFS of 1 is applied because the study length (>35 d) is of an appropriate subchronic duration.

UFC

300

Composite UF = UFA x UFD x UFH x UFL x UFS.

BMD = benchmark dose; BMDL = 95% lower confidence limit on the BMD (subscripts denote BMR:

i.e., 10 = dose associated with 10% extra risk); BMR = benchmark response; DAP = diammonium phosphate;

F = female(s); GLP = Good Laboratory Practice; LOAEL = lowest-observed-adverse-effect level; M = male(s);

MAP = monoammonium phosphate; NOAEL = no-observed-adverse-effect level; OECD = Organisation for

Economic Co-operation and Development; POD = point of departure; p-RfD = provisional reference dose;

UF = uncertainty factor; UFA = interspecies uncertainty factor; UFC = composite uncertainty factor; UFD = database

uncertainty factor; UFH = intraspecies uncertainty factor; UFL = LOAEL-to-NOAEL uncertainty factor;

UFS = subchronic-to-chronic uncertainty factor.

Because the determinant of the local toxicity (irritation) of DAP and MAP is expected to
be the ammonium ion, the toxicity of these compounds is directly related to the relative
molecular weight contribution from ammonium. Therefore, the screening subchronic p-RfD
derived above for DAP is applicable to MAP following application of a molecular-weight
adjustment and appropriate stoichiometric calculations.

Derivation of Screening Chronic Provisional Reference Dose

There are no adequate chronic-duration oral studies available for ammonium phosphate
salts. The longest available study that could serve as the basis for toxicity assessment is the
OECD 422 guideline study (combined repeated-dose toxicity study with
reproductive/developmental screening test [Huntingdon (2002) as cited in OECD (2007b) and
ECHA (2002)]). The systemic toxicity subgroup in that study was only treated for 35 days,
which is not of adequate study duration for deriving a screening chronic p-RfD. In the
reproductive component of the study, parental females were treated up to 53 days, which is of
sufficient duration to derive a chronic value. In this case, however, stomach histopathology was
only assessed in the systemic toxicity subgroup, which was treated for only 35 days. Because the
critical effect was not assessed in the reproductive toxicity subgroup, it is unclear if the
reproductive NOAEL of 1,500 mg/kg-day would be protective of stomach lesions caused by
exposure to ammonium phosphate salts in a chronic setting. Therefore, derivation of a screening
chronic p-RfD is not supported.

27 Ammonium salts of inorganic phosphates


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EPA 690 R-21 00 7F

APPENDIX B. DATA TABLES

Table B-l. Comparison between Spirometry Findings in Workers at DAP
(CASRN 7783-28-0) Fertilizer Plant and Controls3

Spirometry Parameter

Control (n = 68)

DAP Plant Workers (n = 30)

FVC (L)

3.43 ±0.21b

2.51 ±0.06* (-27%)°

FEVi (L)

2.84 ±0.10

2.08 ± 0.08* (-27%)

PEFR /mi n (L/min)

383 ±7.6

227.6 ± 18.2* (-41%)

aBhat and Ramaswamv (1993).

bMean ± SE (specified for controls in Table II of the publication).

°Value in parentheses is % change relative to control = [(treatment mean - control mean) control mean] x 100.
* Significantly different from control by paired /-test (p < 0.01), as reported by the study authors.

DAP = diammonium phosphate; FEVi = forced expiratory volume of 1 second; FVC = forced vital capacity;
PEFR = peak expiratory flow rate; SE = standard error.

Table B-2. Incidence of Minimal or Slight Submucosal Inflammation of the

Stomach in Rats Exposed to DAP (CASRN 7783-28-0) by Gavage for



35 Days3



Dose (mg DAP/kg-d)

Male (%)

Female (%)

Combined (%)

0

0/5 (0)b

0/5 (0)

0/10 (0)

250

3/5 (60)

2/5 (40)

5/10* (50)

750

4/5* (80)

4/5* (80)

8/10* (80)

1,500

2/5 (40)

4/5* (80)

6/10* (60)

"Toxicity subgroup of Huntingdon (2002) as cited in OECD (2007b) andECHA (2002).

bValues denote number of animals showing changes/total number of animals examined (% incidence).

* Significantly different from control by Fisher's exact test (one-sided p < 0.05) conducted for this review.

DAP = diammonium phosphate.

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APPENDIX C. BENCHMARK DOSE MODELING RESULTS

MODELING PROCEDURE FOR DICHOTOMOUS DATA

The benchmark dose (BMD) modeling of dichotomous data is conducted with the
U.S. Environmental Protection Agency (U.S. EPA) Benchmark Dose Software (BMDS;

Version 3.1.1 was used for this document). For these data, the Gamma, Logistic, Log-Logistic,
Probit, Log-Probit, Hill, Multistage, and Weibull dichotomous models available within the
software are fit using a benchmark response (BMR) of 10% extra risk. Alternative BMRs may
also be used where appropriate, as outlined in the U.S. EPA's Benchmark Dose Technical
Guidance fU.S. EPA. 2012/ In general, the BMR should be near the low end of the observable
range of increased risk in the study. BMRs that are too low can result in widely disparate
benchmark dose lower confidence limit (BMDL) estimates from different models (high model
dependence). Adequacy of model fit is judged based on the x2 goodness-of-fit /rvalue (p > 0.1),
magnitude of scaled residuals (absolute value <2.0), and visual inspection of the model fit.
Among all models providing adequate fit, the BMDL from the model with the lowest Akaike's
information criterion (AIC) is selected as a potential point of departure (POD), if the BMDLs are
sufficiently close (less than approximately threefold); if the BMDLs are not sufficiently close
(greater than approximately threefold), model dependence is indicated, and the model with the
lowest reliable BMDL is selected.

Dropping the High Dose

In the absence of a mechanistic understanding of the biological response to a toxic agent,
data from exposures much higher than the study's lowest-observed-adverse-effect level
(LOAEL) do not provide reliable information regarding the shape of the response at low doses.
Such exposures, however, can have a strong effect on the shape of the fitted model in the
low-dose region of the dose-response curve. Thus, if lack of fit is due to characteristics of the
dose-response data for high doses, then the Benchmark Dose Technical Guidance document
allows for data to be adjusted by eliminating the high-dose group (U.S. EPA. 2012). Because the
focus of BMD analysis is on the low-dose regions of the response curve, elimination of the
high-dose group may be reasonable for certain datasets.

Submucosal Inflammation of the Stomach in Rats Exposed to DAP by Gavage for 35 Days
[Huntingdon (2002) as cited in OECD (2007b) and ECHA (2002)1

The procedure outlined above for dichotomous data was applied to the data for
submucosal inflammation of the stomach in Sprague Dawley rats (both sexes combined) exposed
to DAP via gavage for 35 days (see Table B-2). Table C-l summarizes the BMD modeling
results. With all dose groups included, the Log-Logistic, Log-Probit, and Hill models provided
adequate fit (p > 0.1); however, the BMDs for these models varied widely (3 orders of
magnitude); and the BMDLs for both the Log-Probit and Hill models were calculated as 0, while
the Log-Logistic model yielded a BMDL estimate that was more than 12-fold lower than the
lowest experimental dose. Because of these limitations when modeling the full dataset, and since
the incidence at the high dose was lower than at the mid dose (750 mg DAP/kg-day), BMD
modeling was then performed with the high-dose group removed from analysis, as consistent
with Benchmark Dose Technical Guidance (U.S. EPA. 2012). Without the highest dose group,
additional model fit was obtained, with the Gamma, Log-Logistic, Multistage (2-degree and
1-degree), and Weibull models providing adequate fits to the data. Three separate, adequately
fitting models (Gamma, Multistage [2-degree and 1-degree], and Weibull) also estimated the
same BMDio and BMDLio values of 44.3 and 27.7 mg/kg-day, respectively, with the Multistage

29 Ammonium salts of inorganic phosphates


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and Weibull models having the lowest AICs. Based on these more acceptable fits to the data
after removing the high dose, a BMDLio of 27.7 mg/kg-day was identified for increased
incidence of stomach submucosal inflammation (minimal/slight) in rats.

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Table C-l. BMD Modeling Results for Submucosal Inflammation of the Stomach in Sprague Dawley Rats (Males and
Females Combined) Administered DAP (CASRN 7783-28-0) via Gavage for 35 Days3

Model

df

x2

X2 Goodness-of-Fit
/>-Valucb

Scaled Residual at
Dose Nearest (below)
BMD

Scaled Residual at
Dose Nearest
(above) BMDC

AIC

BMD io
(mg DAP/kg-d)

BMDLio
(mg DAP/kg-d)

Full dataset

Gammad

2

9.03

0.01

-0.0004

1.63

48.97

83.35

56.95

Log-Logistice

3

3.80

0.28

-0.0004

0.56

42.69

39.48

19.94

Multistage (3-degree/

2

9.03

0.01

-0.0004

1.63

48.97

83.35

56.95

Multistage (2-degree/

3

9.03

0.03

-0.0004

1.63

46.97

83.35

56.95

Multistage (1-degree/

2

9.03

0.01

-0.0004

1.63

48.97

83.35

56.95

Weibulld

2

9.03

0.01

-0.007

1.63

48.97

83.36

56.95

Dichotomous Hill

1

0.95

0.33

-0.0004

-4.08 x 10-5

44.30

188.19

0.00

Logistic

2

9.33

0.01

-1.91

1.03

53.27

238.16

154.31

Log-Probite

2

1.62

0.44

-0.0004

-0.39

43.04

0.17

0.00

Probit

2

9.36

0.01

-1.89

1.06

53.27

238.33

161.44

Highest dose dropped

Gammad

1

0.18

0.67

-0.0004

0.33

28.05

44.30

27.70

Log-Logistice

1

1.52 x 10-7

0.9997

-0.0004

1.72 x 10-7

27.87

43.82

10.90

Multistage (1-degree)1

2

0.18

0.91

-0.0004

0.33

26.05

44.30

27.70

Multistage (2-dcgrcc)1

2

0.18

0.91

-0.0004

0.33

26.05

44.30

27.70

Weibulld *

2

0.18

0.91

-0.0004

0.33

26.05

44.30

27.70

Dichotomous Hill

-1

1.53 x 10-'

65,535

-0.0004

-3.70 x 10-6

31.87

47.58

0

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Table C-l. BMD Modeling Results for Submucosal Inflammation of the Stomach in Sprague Dawley Rats (Males and
Females Combined) Administered DAP (CASRN 7783-28-0) via Gavage for 35 Days3

Model

df

x2

X2 Goodness-of-Fit
/>-Valueb

Scaled Residual at
Dose Nearest (below)
BMD

Scaled Residual at
Dose Nearest
(above) BMDC

AIC

BMD io
(mg DAP/kg-d)

BMDLio
(mg DAP/kg-d)

Logistic

1

3.05

0.08

-1.20

1.20

31.98

130.38

79.11

LogProbit6

0

1.78 x 10~7

NA

-0.0004

-2.97 x 10~5

29.87

46.92

0

Probit

1

3.01

0.08

-1.08

1.26

31.79

127.12

81.44

"Huntingdon (2002) as cited in OECD (2007b) and ECHA (2002).
bValues <0.10 fail to meet conventional goodness-of-fit criteria.

°Scaled residuals nearest BMDs were closest to the controls; therefore, scaled residual at nearest dose above (250 mg DAP/kg-day) were presented.

dPower restricted to >1.

eSlope restricted to >1.

fBetas restricted to >0.

*Best fitting model(s) identified in bold.

AIC = Akaike's information criterion; BMD = benchmark dose; BMDL = 95% lower confidence limit on the BMD (subscripts denote BMR: i.e., 10 = dose associated
with 10% extra risk); BMR = benchmark response; DAP = diammonium phosphate; df= degrees of freedom; NA = not applicable (computation failed).

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Frequentist Multistage Degree 1 Model with BMR of 10% Extra Risk for the BMD and

0.95 Lower Confidence Limit for the BMDL

Estimated Probability
Response at BMD
— — Linear Extrapolation
O Data
BMD
BMDL

Dose

Figure C-l. Fit of Multistage (1-degree) Model to Data for Submucosal Inflammation of the Stomach in Sprague Dawley Rats (Males
and Females Combined) Administered DAP (CASRN 7783-28-0) via Gavage for 35 Days [Huntingdon (2002) as cited in OECD

(2007b) and ECHA (2002)1

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