Ferrous Sulfate

Herbicides

Active substance -> EU Pesticides database: Approved

1.9 at 59 °F (USCG, 1999) - Denser than water; will sink

3.56 g/cu cm

Density 2.970 at 25 °C; off-white, monoclinic crystals. /Ferrous sulfate monohydrate/

3.65 @25 °C

White to yellow crystalline powder. Sol in water. Loses water @ about 300 °C; decomp @ higher temp. /Ferrous sulfate monohydrate/

Soluble in water.

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Antianaemia medicines

Ferrous sulfate appears as a greenish or yellow-brown crystalline solid. Density 15.0 lb /gal. Melts at 64 °C and loses the seven waters of hydration at 90 °C. The primary hazard is the threat to the environment. Immediate steps should be taken to limit its spread to the environment. Used for water or sewage treatment, as a fertilizer ingredient.

Large Crystals; CBI; Dry Powder; Other Solid; Liquid; Dry Powder; Large Crystals

White hygroscopic solid; [HSDB] Blue-green odorless crystals; [MSDSonline]

Warning

H302: Harmful if swallowed [Warning Acute toxicity, oral]

P264, P264+P265, P270, P280, P301+P317, P302+P352, P305+P351+P338, P321, P330, P332+P317, P337+P317, P362+P364, and P501 (click each P-code to see the statement)

This chemical does not meet GHS hazard criteria for 0.2% (4 of 2130) of reports.

Warning

H302 (99.8%): Harmful if swallowed [Warning Acute toxicity, oral]

Chemical: Sulfuric acid, iron(2+) salt (1:1)

Commission Regulation (EC) No 2229/2004

Sulfuric acid, iron(2+) salt (1:1) is listed on the EPA's Chemical Data Reporting (CDR) system. Manufacturers and importers of Sulfuric acid, iron(2+) salt (1:1) are required to report information about their production and use of this chemical to the EPA under the Toxic Substances Control Act (TSCA). (40 eCFR Part 711)

2008/127, Reg. (EU) 2017/195, Reg. (EU) 2020/1160, Reg. (EU) 2021/745, Reg. (EU) 2022/708, Reg. (EU) 2023/1446, Reg. (EU) No 540/2011, Reg. (EU) No 637/2012

Status: Active Update: 23-03-2023 https://echa.europa.eu/registration-dossier/-/registered-dossier/15513

Ferrous sulphate: Does not have an individual approval but may be used under an appropriate group standard

An irritant to the skin, eyes, and mucous membranes; Toxic by ingestion: hemorrhagic gastroenteritis, shock, and liver damage; [Merck Index] A skin and eye irritant; [eChemPortal: ERMA; ESIS] See Ferrous sulfate heptahydrate. See Iron salts, soluble.

Substance added directly to human food affirmed as generally recognized as safe (GRAS).

Trace minerals added to animal feeds. These substances added to animal feeds as nutritional dietary supplements are generally recognized as safe when added at levels consistent with good feeding practice. All substances listed may be in anhydrous or hydrated form. Iron sulfate is included on this list.

Ferrous sulfate used as a nutrient and/or dietary supplement in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice.

USEPA/ORD; Steel Industry Pickling Waste and its Impact on Environment (1981) EPA-600/9-81-017. This report reviews the impact of steel industry pickling waste, incl ferrous sulfate, on the environment.

California Environmental Protection Agency/Department of Pesticide Regulation; Toxicology Data Review Summaries. Available from: http://www.cdpr.ca.gov/docs/toxsums/toxsumlist.htm on Ferrous sulfate as of September 15, 2004.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 1000 lb or 454 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

INGESTION: give milk immediately and then induce vomiting by stroking the pharynx with a blunt object such as a spoon handle. Gastric lavage with 1 pint of 5% aqueous solution of mono- or disodium phosphate if promptly available; otherwise use water. Get medical attention. (USCG, 1999)

Environmental considerations: Water spill: Adjust pH to neutral (pH= 7). Allow to aerate. Neutralize with agricultural lime (CaO), crushed limestone (CaCO3), or sodium bicarbonate (NaHCO3). Adjust pH to neutral (pH= 7). Use mechanical dredges or lifts to remove immobilized masses of pollutants and precipitates.

Environmental considerations: Land spill: Dig a pit, pond, lagoon, holding rea to contain liquid or solid material. /SRP: If time permits, pits, ponds, lagoons, soak holes, or holding areas should be sealed with an impermeable flexible membrane liner./ Cover solids with a plastic sheet to prevent dissolving in rain or fire fighting water.

During transport: stable; storage temp: ambient; venting: open.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

Precipitation & landfill: Treat water or scrap material with soda ash or dilute sodium hydroxide to precipitate iron. Separate the precipitate and dispose of in an approved landfill. /Iron sulfate heptahydrate/

Personnel protection: Keep upwind. ... Avoid breathing vapors or dusts. Wash away any material which may have contacted the body with copious amounts of water or soap and water.

SRP: The scientific literature for the use of contact lenses in industry is conflicting. The benefit or detrimental effects of wearing contact lenses depend not only upon the substance, but also on factors including the form of the substance, characteristics and duration of the exposure, the uses of other eye protection equipment, and the hygiene of the lenses. However, there may be individual substances whose irritating or corrosive properties are such that the wearing of contact lenses would be harmful to the eye. In those specific cases, contact lenses should not be worn. In any event, the usual eye protection equipment should be worn even when contact lenses are in place.

All ... /iron/ prepn should be kept in child-proof bottles. /Iron prepn/

If material not involved in fire: keep material out of water sources and sewers. Build dikes to contain flow as necessary.

1.0 [mg/m3], as Fe (soluble iron salts)

8 hr Time Weighted Avg (TWA) 1 mg/cu m /Iron salts, soluble, as Fe/

Excursion Limit Recommendation: Excursions in worker exposure levels may exceed 3 times the TLV-TWA for no more than a total of 30 minutes during a work day, and under no circumstances should they exceed 5 times the TLV-TWA, provided that the TLV-TWA is not exceeded. /Iron salts, soluble, as Fe/

0.52 [mg/m3]

5.7 [mg/m3]

38 [mg/m3]

Mask if dust is present. (USCG, 1999)

Wear a mask if dust is present.

A 19 yr old female patient ingested an estimated 50-60 ferrous sulfate tablets, representing approx 9.8-11.7 g of elemental iron. At the time of admission, she had a serum iron level of 915 ug/dL and a total iron binding capacity of 515 ug/dL. ...

Simultaneous administration of iron as ferrous sulfate reduced absorption and caused significant decrease in serum concentration of tetracycline, oxytetracycline, methacycline, and doxycycline in man.

Oral ferrous sulfate appears to impair the GI absorption of various tetracyclines, possibly because of chelation or other type of binding in the gut.

It is suggested that the magnesium trisilicate either changes the ferrous sulfate into less easily absorbed iron salts, or increases its polymerization, thereby rendering it less easily absorbed. Sodium bicarbonate causes the formation of poorly absorbed iron complexes.

A 250 mg tablet of levodopa was taken with and without a 325 mg tablet of ferrous sulfate by 8 normal subjects in a randomized crossover trial. When levodopa was taken with ferrous sulfate, there was a 55% decrease in peak levodopa levels (3.5 plus or minus 2.6 vs 1.6 plus or minus 0.82 nmol/mL; p<0.05) and a 51% decrease in area under concentration-time curve (AUC) (257 plus or minus 133 vs 125 plus or minus 51 nmol min/mL; p<0.01). Levodopa levels were significantly higher at 40 and 50 min when the subjects received levodopa alone. Persons with the highest peak levodopa levels and AUC after levodopa alone had the greatest reduction of peak levodopa levels and AUC after levodopa ingestion with ferrous sulfate.

For more Interactions (Complete) data for FERROUS SULFATE (9 total), please visit the HSDB record page.

LC50 Artemia salina (Brine shrimp) 186 umol/L/24 hr; static

LC50 Asellus aquaticus (Aquatic sowbug) 419.2 mg/L/55 hr (95% confidence interval: 357.6-480.8 mg/L); static

LC50 Brachionus calyciflorus (Rotifer) 230 umol/L/24 hr; static

LC50 Cyprinus carpio (Common carp, juvenile) 560 ug/L/96 hr; renewal

For more Ecotoxicity Values (Complete) data for FERROUS SULFATE (9 total), please visit the HSDB record page.

/AQUATIC SPECIES/ The hatching success of Cyprinus carpio var communis eggs was impaired by addition of ferrous sulfate. The impairment was concentration-related. Also an increased proportion of deformed larva which had little survival potential was observed. The chief deformity in the hatchlings as a result of exposure was a curvature of the caudal region and poor development of the vertebral column and the body beyond the yolk sac.

/OTHER TOXICITY INFORMATION/ Small amounts of ferrous sulfate do not show radiographically 30 min post ingestion.

/SIGNS AND SYMPTOMS/ Severe gastritis or gastroenteritis with abdominal pain, retching, ...vomiting, beginning 10-60 min after ingestion. Vomitus may become bloody. Diarrhea is sometimes violent; feces are watery & later tarry. Dehydration becomes intense. Shock, pallor, cyanosis & coldness. Rapid, weak or imperceptible pulse, low blood pressure, rapid & shallow respirations. Sometimes breathing is deep & rapid, reflecting accompanying metabolic acidosis. Drowsiness, hyporeflexia, dilated pupils, coma. Liver injury, consisting of hemorrhagic necrosis which is usually reversible. Death from shock, usually in 4-5 hr. Sometimes following apparent recovery, pneumonia with fever or secondary shock may cause death 1 to 3 days later. Among survivors pyloric stenosis & mild hepatic cirrhosis may be encountered as persistent sequelae, but recovery is usually complete.

/SIGNS AND SYMPTOMS/ In children, ingestion of large quantities may cause vomiting, hematemesis, hepatic damage, tachycardia, peripheral vascular collapse... .

/CASE REPORTS/ ... A 22-month-old male was brought to the emergency department by his parents after ingesting an estimated 50 ferrous sulfate tablets (60 mg elemental iron/tablet) several hours earlier. Despite spontaneous emesis and gastric lavage his condition deteriorated and he was found to have a serum iron of 2992 mumol/L (16,706 micrograms/dL). During the first four days in the intensive care unit, he developed coma, metabolic acidosis, hypovolemic and cardiogenic shock, liver failure, coagulopathy and adult respiratory distress syndrome. He was treated with a unique deferoxamine dosage schedule (25 mg/kg/h for 12 h/d x 3 d), mechanical ventilation, Swan-Ganz catheter monitoring, dopamine/nitroprusside therapy, blood product, bicarbonate, electrolyte and volume replacement. After a prolonged hospital course complicated primarily by gastric outlet obstruction he was dismissed on full oral feedings, gaining weight, and neurologically intact. Swan-Ganz catheter monitoring guided the management of this patient's shock, iron-induced cardiac failure, and deferoxamine mesylate induced adult respiratory distress syndrome.

For more Human Toxicity Excerpts (Complete) data for FERROUS SULFATE (11 total), please visit the HSDB record page.

/LABORATORY ANIMALS: Acute Exposure/ Experiments .../have/ shown that large doses of ferrous sulfate produce severe liver damage ...At post mortem in naturally occurring cases only organ consistently affected is liver, characteristic finding being periportal necrosis. Local action on gut is shown by edema and ulceration of stomach ...brown staining of its mucous membranes.

/LABORATORY ANIMALS: Acute Exposure/ Retinal degeneration was produced in frogs and albino rats by intravitreal injections of ferrous sulfate. Treatment resulted in the loss of long-chain polyunsaturated fatty acids and the accum of lipid hydroperoxides in isolated rod outer segments.

/LABORATORY ANIMALS: Acute Exposure/ ... In this study both NaFeEDTA and carbonyl Fe were compared with FeSO(4), the most common form of iron for dietary supplements, to obtain information relevant to the acute toxicological profile in young rats. With FeSO(4) and NaFeEDTA, total liver nonheme iron increased with increasing dose, but the response was approximately 50% lower with NaFeEDTA compared with FeSO(4). Serum iron peaked at approximately 0.5 to 1 h for both FeSO(4) and carbonyl Fe, while NaFeEDTA was elevated up to 4 h. FeSO(4) had an LD(50) of 1.1 g Fe/kg and was approximately 45 times more toxic than carbonyl Fe, which had an LD(50) greater then 50 g Fe/kg. NaFeEDTA had an LD(50) of 1.3 g Fe/kg and, when compared with FeSO(4), had approximately the same level of toxicity.

/LABORATORY ANIMALS: Acute Exposure/ ...After oral administration by gavage of the LD50 of iron to Wistar rats, the pharmacokinetics of iron, baseline and peak serum iron levels, and mortality rates were compared between sexes. Prepubertal females died... more /frequently/ than males (p<0.01), pubertal females died... earlier than males (p<0.04), and the same was true among adult rats (p=0.02). Baseline serum iron levels were not significantly different between prepubertal female and male rats, but female pubertal rats had significantly higher baseline iron levels than males (p=0.006). After iron administration, females had significantly higher peak serum iron concentrations (p<0.03).

For more Non-Human Toxicity Excerpts (Complete) data for FERROUS SULFATE (16 total), please visit the HSDB record page.

...There is concern that the individual with metabolic defects that impair the ability to regulate iron absorption will be at risk from excessive exposure to iron, primarily as a result of acceleration of accumulation of iron in the body and an earlier onset of clinical symptoms of the disease. /Iron salts/

A 19 yr old female patient ingested an estimated 50-60 ferrous sulfate tablets, representing approx 9.8-11.7 g of elemental iron. ...This paper supports the safety and efficacy of a slow iv infusion of deferoxamine in an adult patient, using a regimen recommended for a pediatric patient.

Give milk ... induce vomiting by stroking pharynx with blunt object ... Alternately Induce ... with syrup of ipecac. Gastric lavage with 1 pint of 5% solution of mono- or disodium phosphate ... otherwise use water. After lavage, leave 2-3 oz of phosphate solution in stomach. X-ray of abdomen may show ... tablets ... sometimes removed with saline cathartic or fleet enema. Deferoxamine mesylate ... in water may be left in stomach instead of phosphate solution. In patients not in shock, give deferoxamine im ... In patients /experiencing/ cardiovascular collapse ... deferoxamine mesylate may be given by slow iv infusion ... . Bismuth subcarbonate 0.2 g every 4 hr in young children as a demulcent. Iv 5% glucose in saline to correct dehydration. ... Transfusion with plasma or whole blood if shock becomes severe. Oxygen therapy as indicated. Exchange transfusion may be employed. Antibiotics at first sign of infection ... . Observe patient carefully for signs of relapse (48 hr) or late stricture formation (several days to weeks).

Basic treatment: Establish a patent airway. Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if necessary. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for shock and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with normal saline during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 ml/kg up to 200 ml of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool. /Iron and related compounds/

Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious. Monitor cardiac rhythm and treat arrhythmias if necessary ... . Start an IV with lactated Ringer's /SRP: "To keep open", minimal flow rate/. Watch for signs of fluid overload. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Iron and related compounds/

For more Antidote and Emergency Treatment (Complete) data for FERROUS SULFATE (7 total), please visit the HSDB record page.

LD50 Mouse iv 65 mg/kg

LD50 Mouse oral 1,520 mg/kg

LD50 Rat oral 319 mg/kg

LD50 Rat dermal 155 mg/kg

For more Non-Human Toxicity Values (Complete) data for FERROUS SULFATE (8 total), please visit the HSDB record page.

Substance added directly to human food affirmed as generally recognized as safe (GRAS).

Trace minerals added to animal feeds. These substances added to animal feeds as nutritional dietary supplements are generally recognized as safe when added at levels consistent with good feeding practice. All substances listed may be in anhydrous or hydrated form. Iron sulfate is included on this list.

Ferrous sulfate used as a nutrient and/or dietary supplement in animal drugs, feeds, and related products is generally recognized as safe when used in accordance with good manufacturing or feeding practice.

Persons in charge of vessels or facilities are required to notify the National Response Center (NRC) immediately, when there is a release of this designated hazardous substance, in an amount equal to or greater than its reportable quantity of 1000 lb or 454 kg. The toll free number of the NRC is (800) 424-8802; In the Washington D.C. metropolitan area (202) 426-2675. The rule for determining when notification is required is stated in 40 CFR 302.4 (section IV. D.3.b).

Ferrous sulfate is designated as a hazardous substance under section 311(b)(2)(A) of the Federal Water Pollution Control Act and further regulated by the Clean Water Act Amendments of 1977 and 1978. These regulations apply to discharges of this substance. This designation includes any isomers and hydrates, as well as any solutions and mixtures containing this substance.

B - Blood and blood forming organs

QB - Blood and blood forming organs

B03AA02; B03AA07

Ferrous sulfate replenishes iron, an essential component in hemoglobin, myoglobin, and various enzymes. It replaces the iron that is usually found in hemoglobin and myoglobin. Iron participates in oxygen transport and storage, electron transport and energy metabolism, antioxidant and beneficial pro-oxidant functions, oxygen sensing, tissue proliferation and growth, as well as DNA replication and repair.

Iron is required to maintain optimal health, particularly for helping to form red blood cells (RBC) that carry oxygen around the body. A deficiency in iron indicates that the body cannot produce enough normal red blood cells. Iron deficiency anemia occurs when body stores of iron decrease to very low levels, and the stored iron is insufficient to support normal red blood cell (RBC) production. Insufficient dietary iron, impaired iron absorption, bleeding, pregnancy, or loss of iron through the urine can lead to iron deficiency. Symptoms of iron deficiency anemia include fatigue, breathlessness, palpitations, dizziness, and headache. Taking iron in supplement form, such as ferrous sulfate, allows for more rapid increases in iron levels when dietary supply and stores are not sufficient. Iron is transported by the divalent metal transporter 1 (DMT1) across the endolysosomal membrane to enter the macrophage. It can then can be incorporated into ferritin and be stored in the macrophage or carried of the macrophage by ferroportin. This exported iron is oxidized by the enzyme to ceruloplasmin to Fe3+, followed by sequestration by transferrin for transport in the serum to various sites, including the bone marrow for hemoglobin synthesis or into the liver. Iron combines with porphyrin and globin chains to form hemoglobin, which is critical for oxygen delivery from the lungs to other tissues.

Coagulopathy is a hallmark of severe ferrous sulfate poisoning in humans and lab animals. At iron concn comparable to those of previous animal investigations, the coagulopathy, in other words, the dose-related prolongation of the prothrombin, thrombin, and partial thromboplastin time, was reproduced in human plasma in vitro. Studies of the mechanism by which iron prevents a normal plasma coagulation revealed that the proenzymes of the coagulation cascade and fibrinogen were not damaged by iron. Fibrinogen coagulability and fibrin monomer aggregation were unaffected by very high iron concn. Instead, thrombin was markedly inhibited by iron in its clotting effect on fibrinogen and, specifically, in its fibrinopeptide A-generating capacity, the inhibitory effect being reversible upon iron removal by ethylenediaminetetraacetic acid chelation and gel filtration. Thrombin generation in the presence of iron was reduced as well, indicating an inhibition of one or several other enzymes of the intrinsic coagulation cascade. Because the amidolytic activity of human thrombin as well as factor Xa, kallikrein, and bovine trypsin was also reversibly suppressed by ferrous sulfate, it is considered likely that coagulopathy occurring in iron poisoning is the consequence of a general, physiologically important phenomenon: the susceptibility of serine proteases to nontransferrin-bound iron(3+)

The mechanism of acute iron cardiotoxicity was investigated in isometrically contracting left atrial strips and right ventricular papillary muscles isolated from rabbit hearts. A 90 min exposure to iron (1.8 mM; as ferrous sulfate) reduced the peak-developed tension and the maximal rate of tension development.

... Iron is stored in the liver in the oxidized or ferric state & is tightly bound to protein as ferric ferritin. Xanthine oxidase appears to be involved in the conversion of ferric ferritin to ferrous ferritin. The reduced form of iron is less tightly bound to ferritin and thus is more easily released for utilization. Therefore, a possible inverse relationship between hepatic xanthine oxidase activity & hepatic iron storage exists. Theoretically, the xanthine oxidase inhibitor allopurinol should decrease the activity of xanthine oxidase & increase hepatic iron storage.

The metabolism of iron is complex. Normally, iron exists in the ferrous (Fe2+) or ferric (Fe3+) state, but since Fe2+ is oxidized to Fe3+, which hydrolyzes to insoluble iron(III)hydroxides in neutral aqueous solutions, iron binds to plasma proteins and is either transported or stored throughout the body. There are three proteins that serve to regulate the storage and transport of ingested iron. The first protein , transferrin, transports iron in both the plasma and extracellular fluid. Ceruloplasmin in the plasma and hephaestin on the enterocyte participate in the oxidation and binding of iron to transferrin. The main role of transferrin is the chelation of iron to prevent the production of reactive oxygen species, while facilitating its transport into cells. The transferrin receptor, located on many cells that require iron, binds the transferrin complex and internalizes this complex. Ferritin is a protein that stores iron, making it readily available for body requirements.

Approximately 5 – 10% of dietary iron is absorbed, and this absorption rate increases to up to 30% in iron deficiency states. Oral iron supplements are absorbed up to 60% via active and passive transport processes. Gastrointestinal absorption of iron occurs via strict regulation by the enterocyte and duodenal cytochrome and ferric reductase enzymes. The hormone hepcidin heavily regulates iron absorption and distribution throughout the body. The median time to maximum serum concentration (Tmax) is generally 4 hours after administration. Between 2-8 hours post administration, average serum iron concentrations fluctuate by 20%, according to one study. Bioavailability of iron depends on whether it is administered in a film coated tablet or enteric coated tablet. One pharmacokinetic study in healthy volunteers revealed a 30% bioavailability for enteric coated tablets. The AUC of enteric coated tablets varied between a lower limit of -46.93 to 5.25 µmolxh/l. Cmax is higher for film coated tablets, ranging from 3.4 to 22.1 µmol/h/l. It is advisable to take ferrous sulfate with ascorbic acid, as this practice may increase absorption. Avoid antacids, tea, coffee,tea, dairy products, eggs, and whole-grain bread for at least an hour after taking ferrous sulfate. Calcium can decrease iron absorption by 33% if taken concomitantly.

Oral iron is recycled, with some loss in the urine, sweat, and desquamation. Some iron can be lost during menstrual bleeding This loss is balanced by changes in intestinal absorption. The enzyme hepcidin promotes the excretion of iron via the sloughing of enterocytes with ferritin stores into the feces.

About 60% of iron is distributed the erythrocytes. The remainder of the iron is found in muscle tissues (as a part of myoglobin), and in a variety of different enzymes, as well as in storage form. Most stored iron is in the form of ferritin, which can be found in the liver, bone marrow, spleen and, and muscle. Iron crosses the placenta and is also found in breast milk.

... The bioavailability studies were carried out using four groups of 30 female mice each. In two groups, we studied the absorption of ferrous ascorbate and ferrous sulfate, both in water as reference standards, which show absorptions of 13.1+/-4.9% and 13.2+/-4.3%, respectively. With the third group, we studied the absorption of ferrous sulfate in milk; its value, 7.9+/-3.2%, is significantly lower than that of the remaining groups, with a p < 0.01. The studies with SFE-171 in milk, were performed on the fourth group, with a result of 11.6+/-4.5%, demonstrating that its absorption does not differ significantly from that of the reference standards. The absorption mechanism was determined by means of in vivo self-displacement studies of the ferrous ion and the SFE-171, taking ferrous sulfate as the reference compound. For this study, 210 female mice were used, and no significant difference between the absorption mechanism of both products could be observed.

We investigated the iron bioavailability of microencapsulated ferrous sulfate (SFE-171) in a diet based on powdered milk by using the prophylactic method in rats.The SFE-171 was added into fluid milk and industrially processed into powdered milk, which was then mixed in our laboratory with a normalized diet (17.2 +/- 2.1 mg Fe/kg). A reference standard diet using ferrous sulfate as iron-fortifying source (19.8 p+/- 2.9 mg Fe/kg) and a control diet without added iron (4.6 +/- 0.8 mg Fe/kg) were prepared in the laboratory in a similar way. These diets were administered to different groups of weaning rats for 28 d as the only solid nourishment. The iron bioavailability of the different sources was calculated as the relation between the mass of iron incorporated into hemoglobin during the treatment and the total iron intake per animal. The iron bioavailability values of SFE-171 and ferrous sulfate in the fortified diets were 41.6 +/- 6.6% and 42.6 +/- 4.2%, respectively; these results were significantly higher (P < 0.01) than the iron bioavailability of the control diet (28.8 +/- 8.1%).

A prospective analytical study was conducted to determine the relationship between nonprotein-bound iron and serum iron concentrations following gastric instillation of ferrous sulfate. Four female pigs (2022 kg) with indwelling central venous lines and gastrostomy tubes were studied. A 5% solution of ferrous sulfate (20 mg elemental iron/kg bwt) was administered through the gastrostomy tube over 1 to 2 min. Six hourly blood samples were collected, and serum samples were subjected to ultrafiltration with the filtrate representing nonprotein-bound iron. Iron concentrations were determined by atomic absorption spectrophotometry. Baseline (mean | SD) iron concentrations were 73 | 25 mug/dL as the serum total and 21 | 4 mug/dL as nonprotein-bound iron. The serum iron and nonprotein-bound iron concentrations achieved a peak of 191 | 66 and 23 | 10, respectively, at 2 h and declined to near baseline values at 6 h. The mean ratio of filtrate to serum iron concentration was 0.

Used as a mordant in textile dyeing; [www.ci.tucson.az.us/arthazards/medium.html] Used to make iron compounds and in engraving, lithography, water treatment, aluminum etching, and qualitative analysis (brown ring test for nitrates); Also used in iron electroplating baths, fertilizers and pesticides, food and feed supplements, radiation dosimeters, wood preservative, inks, leather dyes, polymerization catalysts, and pharmaceuticals (iron deficiency anemia); [Merck Index] Used as iron oxide pigment, catalyst (especially for synthetic ammonia), and food supplement; [Hawley]

Electroplating [Category: Plate]

Textile arts [Category: Hobbies]

In manufacture of iron, iron cmpd, other sulfates; in iron electroplating baths; in fertilizer; as food and feed supplement; in radiation dosimeters; as reducing agent in chemical processes; as wood preservative; as weed killer; in prevention of chlorosis in plants; in other pesticides; in writing ink; in process engraving and lithography; as dye for leather; in etching aluminum; in water treatment; in qualitative analysis ("brown ring" test for nitrates); as polymerization catalyst.

MEDICATION: hematinic

MEDICATION (VET): In iron deficiency, astringent.

IRON OXIDE PIGMENTS AND SALTS, 75%; FERTILIZER, 7%; ANIMAL FEED ADDITIVE, 6%; WATER TREATMENT, 6%; OTHER, 6% (1985).

CHEMICAL PROFILE: Ferrous Sulfate. Lawn, garden and commercial fertilizer, 35%; animal feed additive, 32%; water treatment, 30%; other, 3%. (The dominant end-use for moist material is in iron oxide pigments and salts).

CHEMICAL PROFILE: Ferrous sulfate. Demand: 1987: 53,000 tons; 1988: 57,000 tons; 1992 /projected/: 64,500 tons (Totals are for dried material only. Total moist demand is in excess of 200,000 tons, with most of it supplied by imports. Since the majority of the moist material is used internally by a broad spectrum of buyers, precise demand figures are elusive).

Prepared commercially by the action of sulfuric acid on iron. /Ferrous sulfate heptahydrate/

By-product from pickling of steel and many chemical operations. ...Oxidation of pyrites in air followed by leaching and treatment with scrap iron. /Heptahydrate/

Available as a by-product of the manufacture of titanium dioxide. /Ferrous sulfate heptahydrate/

Official USP tablets contain 300 mg iron sulfate. 7H2O or equivalent amount of dried (anhydrous) ferrous sulfate. It is also available as syrup and as elixirs.

It is usually dispensed as pills or tablets, coated to protect them from moisture. Salt is mixed with glucose or lactose to protect it against oxidation.

Available in heptahydrate (20% iron) and monohydrate (30% Fe) grades.

Grade: Technical, anhydrous, CP, USP /Heptahydrate/

Food Additives -> NUTRIENT_SUPPLEMENT -> JECFA Functional Classes

Cosmetics -> Astringent

All Other Basic Inorganic Chemical Manufacturing

Sulfuric acid, iron(2+) salt (1:1): ACTIVE

Sulfuric acid, iron(2+) salt (1:?): ACTIVE