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FERRIC PHOSPHATE
CASRN: 10045-86-0
For other data, click on the Table of Contents
Human Health Effects:
Human Toxicity Excerpts:
...SYMPTOMS OF IRON INTOXICATION INCL VOMITING, HEMATEMESIS,
DIARRHEA, LETHARGY, COMA, IRRITABILITY, SEIZURES, & ABDOMINAL
PAIN. ...INCR CARDIAC & RESP RATE...MARKED INCR IN TOTAL
PERIPHERAL VASCULAR RESISTANCE MAY MAINTAIN ARTERIAL BLOOD
PRESSURE FOR VARIABLE PERIODS BEFORE MANIFESTATIONS OF LOW
OUTPUT SHOCK... /IRON/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology:
Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982.
1665]**PEER REVIEWED**
...CONSEQUENCES OF ACUTE IRON INTOXICATION INCL METABOLIC
ACIDOSIS, DUE IN PART TO ACCUM OF LACTIC & CITRIC ACIDS, &
HYPOGLYCEMIA. /IRON/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology:
Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982.
1666]**PEER REVIEWED**
ORALLY, IRON SALTS OF BOTH VALENCE FORMS ARE NOT STRIKINGLY
TOXIC; ON THE OTHER HAND, WHEN INTRODUCED DIRECTLY INTO THE
BLOODSTREAM IRON SALTS ARE INSTANTANEOUSLY TOXIC,
PARTICULARLY FERRIC SALTS. /IRON SALTS/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology:
Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982.
1665]**PEER REVIEWED**
Emergency Medical Treatment:
EMT Copyright Disclaimer:
Portions of the POISINDEX(R) and MEDITEXT(R) database have been provided here
for general reference. THE COMPLETE POISINDEX(R) DATABASE OR
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The following Overview, *** IRON ***, is relevant for this HSDB record chemical.
Life Support:
o This overview assumes that basic life support measures
have been instituted.
Clinical Effects:
0.2.1 SUMMARY OF EXPOSURE
0.2.1.1 ACUTE EXPOSURE
A) MAJOR CLINICAL FINDINGS - Stupor, shock, acidosis,
hematemesis, bloody diarrhea or coma.
B) MINOR CLINICAL FINDINGS - Vomiting, diarrhea, mild
lethargy. Leukocytosis (WBC greater than 15,000)and
hyperglycemia are sometimes observed but are not
pathognomonic of acute iron poisoning.
C) CLINICAL COURSE (May Not Occur In All Cases) includes
the following:
1) PHASE I (0.5 to 2 h) includes vomiting, hematemesis,
abdominal pain, diarrhea, hematochezia, lethargy,
shock, acidosis, and coagulopathy. Necrosis to the GI
tract occurs from the direct effect of iron on GI
mucosa.
a) Severe gastrointestinal hemorrhagic necrosis with
large losses of fluid and blood contribute to shock.
Free iron and ferritin produce vasodilatation that
may also contribute to shock.
2) PHASE II (after phase I) includes apparent recovery
and may contribute to a false sense of security.
Observe closely.
3) PHASE III (2 to 12 hours after phase I) includes
profound shock, severe acidosis, cyanosis and fever.
a) Increased total peripheral resistance, decreased
plasma volume, hemoconcentration, decrease in total
blood volume, hypotension, CNS depression, and
metabolic acidosis have been demonstrated.
4) PHASE IV (2 to 4 days) includes possible
hepatotoxicity. Thought to be a direct action of iron
on mitochondria. Monitor liver function tests and
bilirubin. Acute lung injury may also occur.
5) Phase V (days to weeks) includes GI scarring and
strictures.
a) GI obstruction secondary to gastric or pyloric
scarring may occur due to corrosive effects of iron.
Evaluate with barium contrast studies.
b) Sustained-release preparations have resulted in small
intestinal necrosis with resultant scarring and
obstruction.
6) The phases of iron poisoning may not occur in all
patients. After massive overdose, patients may present
in shock. With less serious overdoses, the initial
gastrointestinal symptoms may be the only findings to
develop even without treatment.
7) Although serious iron poisoning in adults is rare,
deaths have been reported.
D) Carbonyl iron (also referred to as "iron carbonyl")
appears to be less toxic than other iron formulations
because of limited absorption. Please refer to the
CARBONYL IRON management for further information.
E) Case reports suggest that iron-dextran complex
overdoses may be associated with high serum iron
concentrations without evidence of a corresponding
degree of clinical symptoms and signs of toxicity.
Please refer to the IRON DEXTRAN management for further
information.
0.2.1.2 CHRONIC EXPOSURE
A) Signs and symptoms may include irritability, nausea or
vomiting, and normocytic anemia. Chronic exposure to
excess levels (greater than 50 to 100 milligram per
day) can result in pathological deposition of iron in
the body tissues causing fibrosis of the pancreas,
diabetes mellitus, and liver cirrhosis.
B) Long term excessive intake of iron containing compounds
may result in increased accumulation of iron in body,
particularly liver, spleen, and the lymphatic system.
0.2.3 VITAL SIGNS
0.2.3.1 ACUTE EXPOSURE
A) Blood pressure may be decreased following an iron
overdose.
0.2.5 CARDIOVASCULAR
0.2.5.1 ACUTE EXPOSURE
A) Blood pressure may be decreased following an iron
overdose secondary to vomiting, diarrhea, blood loss or
vasodilation. Cardiac failure has been rarely reported.
0.2.6 RESPIRATORY
0.2.6.1 ACUTE EXPOSURE
A) Noncardiogenic pulmonary edema may develop with severe
intoxication.
0.2.6.2 CHRONIC EXPOSURE
A) Inhaling dust containing iron oxide can lead to
pneumoconiosis.
0.2.7 NEUROLOGIC
0.2.7.1 ACUTE EXPOSURE
A) Lethargy, restlessness or confusion may be seen early
in the poisoning. Convulsions and coma may occur in
later phases.
0.2.7.2 CHRONIC EXPOSURE
A) Effects on the CNS can be observed in iron poisoning.
No association of occupational exposure to iron and
Parkinson's disease has been reported.
0.2.8 GASTROINTESTINAL
0.2.8.1 ACUTE EXPOSURE
A) Nausea, vomiting, diarrhea and gastrointestinal
hemorrhage may develop.
0.2.8.2 CHRONIC EXPOSURE
A) Vomiting, ulceration of the gastrointestinal mucosa,
intestinal bleeding, or even liver and kidney damages
can occur after chronic iron ingestion.
0.2.9 HEPATIC
0.2.9.1 ACUTE EXPOSURE
A) Hepatic necrosis may develop after severe poisoning,
not related to hypotension.
0.2.9.2 CHRONIC EXPOSURE
A) Chronic iron intoxication can lead to hemosiderosis in
the liver, hemochromatosis in the Kupffer cells of the
liver.
0.2.10 GENITOURINARY
0.2.10.1 ACUTE EXPOSURE
A) Acute renal failure may develop.
0.2.11 ACID-BASE
0.2.11.1 ACUTE EXPOSURE
A) Anion gap metabolic acidosis is a common early finding.
0.2.13 HEMATOLOGIC
0.2.13.2 CHRONIC EXPOSURE
A) Chronic oral iron intoxication can lead to
hemochromatosis in the reticuloendothelial cells of the
bone marrow.
0.2.14 DERMATOLOGIC
0.2.14.1 ACUTE EXPOSURE
A) Severe thermal burn with ferrous sulfate slurry has
caused classical symptoms of ingested iron poisoning.
0.2.16 ENDOCRINE
0.2.16.1 ACUTE EXPOSURE
A) Hyperglycemia is seen in the early phases of iron
poisoning. Hypoglycemia may be seen in late phases.
0.2.20 REPRODUCTIVE HAZARDS
A) Case reports of pregnant women who have received early
aggressive treatment (decontamination and/or
deferoxamine) have described good fetal outcomes.
0.2.21 CARCINOGENICITY
0.2.21.1 IARC CATEGORY
A) IARC Carcinogenicity Ratings for CAS7439-89-6 (IARC,
2004):
1) Not Listed
0.2.23 OTHER
0.2.23.2 CHRONIC EXPOSURE
A) Iron is potentially toxic in all forms and by all
routes of exposure.
Laboratory:
A) Obtain CBC, electrolytes, blood sugar, serum iron and
abdominal radiograph. Baseline PT, PTT, and LFT's should
be obtained in severe overdoses.
Treatment Overview:
0.4.2 ORAL EXPOSURE
A) GASTRIC LAVAGE: Consider after ingestion of a
potentially life-threatening amount of poison if it can
be performed soon after ingestion (generally within 1
hour). Protect airway by placement in Trendelenburg and
left lateral decubitus position or by endotracheal
intubation. Control any seizures first.
1) CONTRAINDICATIONS: Loss of airway protective reflexes
or decreased level of consciousness in unintubated
patients; following ingestion of corrosives;
hydrocarbons (high aspiration potential); patients at
risk of hemorrhage or gastrointestinal perforation; and
trivial or non-toxic ingestion.
B) Lavage with bicarbonate solutions or deferoxamine is NOT
recommended.
C) Whole bowel irrigation with polyethylene glycol is of
theoretical value in the management of patients who have
ingested substantial amounts of iron that is confirmed
radiographically because of the high morbidity and
mortality of this poisoning and a lack of other options
for gastrointestinal decontamination.
1) DOSE (PEG): ADULTS: 1.5 to 2 L/hr. CHILD: 25 mL/Kg/hr.
ENDPOINT: clear rectal effluent and/or disappearance of
radiopacities when present.
D) Because the size of orogastric tube that can be passed
in a small child may not be of sufficient diameter to
remove pills or large pill fragments and because iron is
not well adsorbed by activated charcoal,
gastrointestinal decontamination may be difficult.
1) Whole bowel irrigation may be most effective if the
ingestion occurred more than one to two hours
previously and in patients with radiographic evidence
of multiple pills beyond the pylorus.
2) In more recent ingestions or patients with retained
pills in the stomach on radiograph some clinicians
perform gastric lavage or endoscopic removal of tablets
followed by whole bowel irrigation.
3) Syrup of ipecac may be considered in young children
with large, recent ingestions; however persistent
vomiting after syrup of ipecac may interfere with the
ability to perform whole bowel irrigation, so many
clinicians prefer to use gastric lavage followed by
whole bowel irrigation even in young children.
E) EMESIS: Use is controversial. May be indicated in the
prehospital setting if administered soon (within 30
minutes) after substantial ingestion. CONTRAINDICATIONS:
loss of airway protective reflexes; CNS depression;
seizures; ingestion of a substance that might impair
airway protective reflexes or require advanced life
support within 60 minutes; ingestion of a corrosive
substance or hydrocarbon with high aspiration potential;
debilitated patient. (Dose of Ipecac Syrup: ADULT: 15 30 mL; CHILD 1 to 12 years: 15 mL; CHILD 6 to 12 months
of age: 5 - 10 mL; CHILD under 6 months of age: Not
recommended for prehospital use.).
F) MAJOR CLINICAL FINDINGS PRESENT 1) Monitor electrolytes carefully, treat shock. Blood
products may be necessary.
2) HYPOTENSION: Infuse 10 to 20 mL/kg isotonic fluid. If
hypotension persists, administer dopamine (5 to 20
mcg/kg/min) or norepinephrine (ADULT: begin infusion at
0.5 to 1 mcg/min; CHILD: begin infusion at 0.1
mcg/kg/min); titrate to desired response.
3) INSTITUTE DEFEROXAMINE THERAPY as outlined below.
4) CONSIDER EXCHANGE TRANSFUSION in severely symptomatic
patients with a serum iron exceeding 1,000 mcg/dL.
G) MINOR OR NO CLINICAL FINDINGS PRESENT 1) ASYMPTOMATIC PATIENT a) Decontamination is recommended if greater than 20
mg/Kg or unknown amount of ingestion. Patients with
ingesting more than 60 milligrams/kilogram should be
referred to a health care facility. Decontamination
efficacy should be monitored by following serial KUBS
until no pills are seen.
b) Whole bowel irrigation with polyethylene glycol may be
considered when there is radiographic evidence of iron
tablets past the pylorus or if tablets persist in the
gastrointestinal tract after other attempts at
decontamination.
1) Dose: (PEG): ADULTS: 1.5 to 2 L/hr. CHILD: 25
mL/Kg/hr. ENDPOINT: clear rectal effluent and/or
disappearance of radiopacities when present.
c) Obtain CBC, blood sugar, and serum iron (SI).
Institute deferoxamine therapy if SI is more than 350
to 500 mcg/dL, or patient is symptomatic.
2) SYMPTOMATIC PATIENT a) Evacuate stomach; obtain abdominal and chest x-ray. If
iron tablets are present in the gastrointestinal tract
begin whole bowel irrigation.
b) Determine serum iron (SI), CBC, electrolytes and blood
sugar. SI may be most useful 3 to 4 hours
postingestion for liquids/tablets. An additional level
3 to 4 hours later may be helpful with
sustained-release/enteric-coated products.
c) Begin deferoxamine therapy if the SI is more than 350
mcg/dL or SI cannot be obtained in a reasonable time
in a symptomatic patient.
H) DEFEROXAMINE - Administer by continuous intravenous
infusion at a rate of up to 15 milligram/kilogram/hour.
Faster rates or IV boluses may cause hypotension in some
individuals, but infusion rates up to 35
milligram/kilogram/hour have been used in children with
severe overdoses.
1) Duration of infusion is guided by the patient's
clinical condition. Patients with moderate toxicity are
generally treated for 8 to 12 hours, those with severe
toxicity may require deferoxamine for 24 hours or
longer. Patients should be reevaluated for evidence of
recurrent toxicity (hypotension, metabolic acidosis)
several hours after the infusion is discontinued.
Infusion duration of greater than 24 hours has been
associated with the development of ARDS.
2) Experimentally, deferoxamine and activated charcoal
given as a slurry have reduced the GI absorption of
ferrous sulfate in a small number of healthy
volunteers. Animal data did not support this finding,
but oral DFO was found to increase the rate of iron
excretion from the body, which could be enhanced by the
coadministration of sodium bicarbonate. Oral
deferoxiamine has not been studied for the treatment of
acute iron poisoning, and its routine clinical use is
not recommended at this time.
0.4.4 EYE EXPOSURE
A) Diagnosis of iron intraocular foreign body can be done
by x-ray, by computerized tomography, by establishing
that the foreign body can be moved with a magnet, and by
electroretinogram. Magnetic resonance imaging is not
recommended as movement of the foreign body may result.
Range of Toxicity:
A) Toxicity is likely following 60 mg/kg elemental iron.
Twenty to 60 mg/kg is possibly toxic.
[Rumack BH POISINDEX(R) Information System Micromedex, Inc., Englewood, CO,
2004; CCIS Volume 122, edition expires Nov, 2004. Hall AH & Rumack BH (Eds):
TOMES(R) Information System Micromedex, Inc., Englewood, CO, 2004; CCIS Volume
122, edition expires Nov, 2004.]**PEER REVIEWED**
Animal Toxicity Studies:
Non-Human Toxicity Excerpts:
IMMEDIATE CAUSE OF DEATH FROM /PARENTERAL ADMIN OF/...INORG
COMPD OF IRON IN ANIMALS IS RESP FAILURE. CLINICAL SIGNS
PRECEDING DEATH ARE ANOREXIA, OLIGODIPSIA, OLIGURIA, ALKALOSIS,
DIARRHEA, LOSS OF BODY WT, HYPOTHERMIA, & ALTERNATING
IRRITABILITY & DEPRESSION. /INORG IRON COMPD/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology:
Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982.
1665]**PEER REVIEWED**
/IN ANIMALS AFTER PARENTERAL ADMIN/...THERE IS LOSS OF WT IN MOST
ORGANS, ACCOMPANIED BY DEHYDRATION WHEN DEATH OCCURRED
EARLY, & EDEMA WHEN DEATH WAS DELAYED. VASCULAR CONGESTION
OF GI TRACT, LIVER, KIDNEYS, HEART, LUNGS, BRAIN, SPLEEN, ADRENALS,
& THYMUS GLAND IS DOMINANT HISTOPATHOLOGICAL SIGN. /INORG IRON
COMPD/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology:
Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982.
1665]**PEER REVIEWED**
...UPTAKE BY EXOGENOUS, EXCESS IRON OF ELECTRONS DONATED BY
FERRIC REDUCTASE IN MITOCHONDRIAL MEMBRANE THAT NORMALLY
CATALYZES ENDOGENOUS FERRIC IRON TO FERROUS IRON, RESULTING IN
IMMEDIATE CESSATION OF AEROBIC SYNTHESIS OF ADENOSINE
TRIPHOSPHATE, INITIATING CELLULAR ENERGY CRISIS & CELL DEATH.
/IRON/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology:
Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982.
1670]**PEER REVIEWED**
Metabolism/Pharmacokinetics:
Absorption, Distribution & Excretion:
FERROUS IRON IS GENERALLY ABSORBED FROM GI TRACT MORE READILY
THAN FERRIC IRON, PRESUMABLY BECAUSE OF GREATER SOLUBILITY OF
FERROUS COMPD. AMT OF IRON ABSORBED IS INVERSELY PROPORTIONAL
TO THE INTAKE. /IRON COMPD/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology:
Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982.
1667]**PEER REVIEWED**
NORMAL HUMAN BODY CONTAINS 4.5 G IRON; OF THIS, HEMOGLOBIN,
WHICH IS ALMOST ENTIRELY IN BLOOD, COMPRISES 72.9% OF TOTAL IRON;
MYOGLOBIN, 3.3%; PARENCHYMAL IRON (OXIDATIVE ENZYMES) 0.2%; &
STORAGE IRON (FERRITIN, HEMOSIDERIN, & UNACCOUNTED IRON) 23.5%.
MOST OF STORAGE IRON IS FOUND IN LIVER, BONE MARROW, & SPLEEN.
/IRON/
[Clayton, G. D. and F. E. Clayton (eds.). Patty's Industrial Hygiene and Toxicology:
Volume 2A, 2B, 2C: Toxicology. 3rd ed. New York: John Wiley Sons, 1981-1982.
1669]**PEER REVIEWED**
Pharmacology:
Environmental Fate & Exposure:
Natural Pollution Sources:
OCCURS IN NATURE AS MINERALS: BERAUNITE, CACOXENITE, DUFRENITE,
KONINCKITE, PHOSPHOSIDERITE, STRENGITE.
[The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 525]**PEER
REVIEWED**
...IN SMALL QUANTITIES IN PRACTICALLY ALL PHOSPHATE ROCK & IN
RATHER LARGE QUANTITIES IN SOME OF LOWER GRADES OF ROCK.
[Farm Chemicals Handbook 1981. Willoughby, Ohio: Meister, 1981.,p. B-40]**PEER
REVIEWED**
Environmental Standards & Regulations:
Federal Drinking Water Guidelines:
EPA 300 ug/l /Iron/
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee
(FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines
(11/93)]**QC REVIEWED**
State Drinking Water Standards:
(IL) ILLINOIS 1000 ug/l /Iron/
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee
(FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines
(11/93)]**QC REVIEWED**
(NC) NORTH CAROLINA 300 ug/l /Iron/
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee
(FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines
(11/93)]**QC REVIEWED**
State Drinking Water Guidelines:
(ME) MAINE 340 ug/l /Iron/
[USEPA/Office of Water; Federal-State Toxicology and Risk Analysis Committee
(FSTRAC). Summary of State and Federal Drinking Water Standards and Guidelines
(11/93)]**QC REVIEWED**
FDA Requirements:
121.101; LIMITATIONS: GRAS, NUTRIENT &/OR DIETARY SUPPLEMENT.
[Furia, T.E. (ed.). CRC Handbook of Food Additives. 2nd ed. Cleveland: The Chemical
Rubber Co., 1972. 852]**PEER REVIEWED**
Chemical/Physical Properties:
Molecular Formula:
FE.H3-O4-P
**PEER REVIEWED**
Molecular Weight:
150.83
**PEER REVIEWED**
Other Chemical/Physical Properties:
LOSES WATER ABOVE 140 DEG C; DENSITY: 2.87 /DIHYDRATE/
[The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 525]**PEER
REVIEWED**
WHITE, GRAYISH-WHITE, OR LIGHT PINK, ORTHORHOMBIC OR
MONOCLINIC CRYSTALS OR AMORPHOUS POWDER /DIHYDRATE/
[The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 525]**PEER
REVIEWED**
PRACTICALLY INSOL IN WATER; READILY SOL IN HYDROCHLORIC ACID;
SLOWLY SOL IN NITRIC ACID /DIHYDRATE/
[The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 525]**PEER
REVIEWED**
SOL IN SULFURIC ACID /DIHYDRATE/
[Weast, R.C. (ed.). Handbook of Chemistry and Physics. 60th ed. Boca Raton, Florida:
CRC Press Inc., 1979.,p. B-87]**PEER REVIEWED**
Chemical Safety & Handling:
Occupational Exposure Standards:
Threshold Limit Values:
8 hr Time Weighted Avg (TWA): 1 mg/cu m. /Iron salts, soluble, as Fe/
[American Conference of Governmental Industrial Hygienists. TLVs & BEIs: Threshold
limit Values for Chemical Substances and Physical Agents and Biological Exposure
Indices for 2002. Cincinnati, OH. 2002.37]**QC REVIEWED**
Excursion Limit Recommendation: Excursions in worker exposure levels may exceed
three times the TLV-TWA for no more than a total of 30 min during a work day, and
under no circumstances should they exceed five times the TLV-TWA, provided that the
TLV-TWA is not exceeded. /Iron salts, soluble, as Fe/
[American Conference of Governmental Industrial Hygienists. TLVs & BEIs: Threshold
limit Values for Chemical Substances and Physical Agents and Biological Exposure
Indices for 2002. Cincinnati, OH. 2002.6]**QC REVIEWED**
Manufacturing/Use Information:
Major Uses:
FOOD AND FEED SUPPLEMENT, PARTICULARLY IN BREAD ENRICHMENT;
AS FERTILIZER /DIHYDRATE/
[The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 525]**PEER
REVIEWED**
Methods of Manufacturing:
...FROM FE(H2PO4)3: REMY, BOULLE, COMPT REND 253, 2699 (1961); FROM
FE(CO)5 & H3PO4: CATE ET AL, SOIL SCI 88(3), 130 (1959); FROM PHOSPHATE
ROCK: VICKERY, US PATENT 2,914,380 (1959 TO HORIZONS INC); FROM MILL
SCALE & H3PO4: ALEXANDER, MATHES, US PATENT 3,070,423 (1962 TO
CHEMETRON CORP).
[The Merck Index. 9th ed. Rahway, New Jersey: Merck & Co., Inc., 1976. 525]**PEER
REVIEWED**
General Manufacturing Information:
CONTAINS 37% IRON.
[Rossoff, I.S. Handbook of Veterinary Drugs. New York: Springer Publishing Company,
1974. 218]**PEER REVIEWED**
A NUTRIENT AND/OR DIETARY SUPPLEMENT FOOD ADDITIVE. ALSO USED
AS TRACE MINERAL ADDED TO ANIMAL FEEDS.
[Sax, N.I. Dangerous Properties of Industrial Materials. 5th ed. New York: Van Nostrand
Rheinhold, 1979. 685]**PEER REVIEWED**
AS FEED SOURCE OF IRON (EVEN IN BREAD FOR MAN), PARTICULARLY IN
MINERAL MIXES.
[Rossoff, I.S. Handbook of Veterinary Drugs. New York: Springer Publishing Company,
1974. 218]**PEER REVIEWED**
SMALL QUANTITIES...USED AS IRON-ENRICHMENT COMPD IN FOOD
APPLICATIONS. ... ALTHOUGH IT IS INSOL IN WATER, IT IS SOL TO VARYING
DEGREES IN DIL HYDROCHLORIC-ACID SOLN, SUCH AS THOSE IN THE
STOMACH. THE DEGREE OF SOLUBILITY CAN BE CONTROLLED BY THE
METHOD OF MFR.
[Furia, T.E. (ed.). CRC Handbook of Food Additives. 2nd ed. Cleveland: The Chemical
Rubber Co., 1972. 624]**PEER REVIEWED**
ADDN OF FERRIC ORTHOPHOSPHATE TO SUPPLY NUTRITIONAL LEVELS OF
IRON DOES NOT AFFECT ASCORBIC ACID STABILITY IN FROZEN ORANGE
DRINK CONCENTRATE.
[Furia, T.E. (ed.). CRC Handbook of Food Additives. 2nd ed. Cleveland: The Chemical
Rubber Co., 1972. 107]**PEER REVIEWED**
Laboratory Methods:
Analytic Laboratory Methods:
ANALYTE: IRON; MATRIX: AIR; PROCEDURE: FILTER COLLECTION, ACID
DIGESTION, AAS. /IRON/
[U.S. Department of Health, Education Welfare, Public Health Service. Center for
Disease Control, National Institute for Occupational Safety Health. NIOSH Manual of
Analytical Methods. 2nd ed. Volumes 1-7. Washington, DC: U.S. Government Printing
Office, 1977-present.p. V5 173-1]**PEER REVIEWED**
Special References:
Synonyms and Identifiers:
Synonyms:
FERRIC ORTHOPHOSPHATE
**PEER REVIEWED**
IRON PHOSPHATE [FEPO4]
**PEER REVIEWED**
PHOSPHORIC ACID, IRON(3+) SALT (1:1)
**PEER REVIEWED**
Administrative Information:
Hazardous Substances Databank Number: 453
Last Revision Date: 20021108
Update History:
Complete Update on 11/08/2002, 1 field added/edited/deleted.
Complete Update on 07/22/2002, 1 field added/edited/deleted.
Complete Update on 05/13/2002, 1 field added/edited/deleted.
Complete Update on 08/09/2001, 1 field added/edited/deleted.
Complete Update on 05/16/2001, 1 field added/edited/deleted.
Complete Update on 05/15/2001, 1 field added/edited/deleted.
Complete Update on 09/12/2000, 1 field added/edited/deleted.
Complete Update on 06/12/2000, 1 field added/edited/deleted.
Complete Update on 02/09/2000, 1 field added/edited/deleted.
Complete Update on 02/08/2000, 1 field added/edited/deleted.
Complete Update on 02/02/2000, 1 field added/edited/deleted.
Complete Update on 12/27/1999, 1 field added/edited/deleted.
Complete Update on 11/18/1999, 1 field added/edited/deleted.
Complete Update on 09/21/1999, 1 field added/edited/deleted.
Complete Update on 08/26/1999, 1 field added/edited/deleted.
Complete Update on 11/19/1998, 1 field added/edited/deleted.
Complete Update on 11/12/1998, 1 field added/edited/deleted.
Complete Update on 06/02/1998, 1 field added/edited/deleted.
Complete Update on 03/25/1998, 4 fields added/edited/deleted.
Field Update on 02/25/1998, 1 field added/edited/deleted.
Field Update on 01/19/1996, 1 field added/edited/deleted.
Field Update on 08/23/1995, 1 field added/edited/deleted.
Field Update on 05/26/1995, 1 field added/edited/deleted.
Field Update on 04/20/1995, 1 field added/edited/deleted.
Field Update on 04/20/1995, 1 field added/edited/deleted.
Field Update on 01/26/1995, 1 field added/edited/deleted.
Field Update on 12/21/1994, 1 field added/edited/deleted.
Field Update on 08/17/1994, 1 field added/edited/deleted.
Complete Update on 03/25/1994, 1 field added/edited/deleted.
Complete Update on 08/07/1993, 1 field added/edited/deleted.
Complete Update on 02/05/1993, 1 field added/edited/deleted.
Field update on 12/12/1992, 1 field added/edited/deleted.
Complete Update on 01/23/1992, 1 field added/edited/deleted.
Field update on 12/29/1989, 1 field added/edited/deleted.
Complete Update on 12/19/1989, 1 field added/edited/deleted.
Complete Update on 12/14/1984