Ferrous sulfate

153.92300

153.90200

240-616-9

2IDP3X9OUD

3077

DTXSID0029688

White orthorhombic crystals, hygroscopic

B - Blood and blood forming organs

2833291000

82.98000

0.4255

2.99-3.08 g/cm³

64ºC

330ºC at 760 mmHg

INDEX OF REFRACTION: 1.471, 1.478, 1.486; MP 64 °C LOSING 6H2O; BP 300 °C LOSING 7H2O. /FERROUS SULFATE HEPTAHYDRATE/

soluble in water.

Low temperature, ventilation, drying ,Separate storage with food raw materials

LD50 oral in rat: 319mg/kg

-3

Standard molar enthalpy (heat) of formation at 298.15 deg K is -928.4 kJ/mol (crystal); Standard molar Gibbs energy of formation at 298.15 deg K is -820.8 kJ/mol (crystal); Standard molar entropy at 298.15 deg K is 107.5 J/mol K (crystal); Molar heat capacity at constant pressure at 298.15 deg K is 100.6 J/mol K (crystal)|Pale, bluish-green monoclinic odorless crystals or granules. Efflorescent in dry air; forms tetrahydrate @ 56.6 °C and monohydrate @ 65 °C; density 1.897. Sol in water; practically insol in alc. /Ferrous sulfate heptahydrate/|Odorless; has saline, astringent taste. /Ferrous sulfate heptahydrate/|White, triclinic crystals; index of refraction 1.526, 1.536, 1.542; density 2.2; MP 300 °C losing 5H2O; sol in cold & hot water, insol in alc. /Ferrous sulfate pentahydrate/|Green monoclinic prisms; index of refraction 1.533, 1.535; density 2.23-2.29. /Ferrous sulfate tetrahydrate/|pH 3.7 (10%) solution; hygroscopic /Ferrous sulfate heptahydrate/|Each part of ferrous sulfate heptahydrate requires 0.03 parts of oxygen or 0.126 parts of chlorine for oxidation to the ferric state. /Ferrous sulfate heptahydrate/|In moist air, oxidizes to yellow-brown basic iron(III) sulfate. Aqueous solutions tend to oxidize with the rate increasing with increasing pH, temperature, and light /Ferrous sulfate heptahydrate/|Sugar, glycerin, & many organic hydroxy acids hinder precipitation. In neutral solution, soluble carbonates, phosphates, & oxalates produce precipitation. /Ferrous salts/

Water soluble

Reducing Agents, Strong

Weak inorganic reducing agents, such as FERROUS SULFATE, react with oxidizing agents to generate heat and products that may be flammable, combustible, or otherwise reactive.

Not flammable (USCG, 1999)

3077

R25

S45

In moist air, ferrous sulfate rapidly oxidizes and becomes coated with brownish-yellow ferric sulfate . The rate of oxidation is increased by the addition of alkali or by exposure to light.

P264, P270, P280, P301+P312, P302+P352, P305+P351+P338, P321, P330, P332+P313, P337+P313, P362, P501

H302

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/

May ignite on contact with arsenic trioxide and sodium nitrate.|Potentially explosive reacition with methyl isocyanoacetate at 25 °C|Incompatible /with/ alkalies, sol carbonates, gold & silver salts, lead acetate, lime water, potassium iodide, potassium & sodium tartrate, sodium borate, tannin, vegetable astringent infusions & decoctions. /Ferrous sulfate heptahydrate/

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.

|Warning|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P280, P301+P312, P302+P352, P305+P351+P338, P321, P330, P332+P313, P337+P313, P362, and P501|H302 (100%): Harmful if swallowed [Warning Acute toxicity, oral]|Aggregated GHS information provided by 2160 companies from 14 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Mask if dust is present. (USCG, 1999)|Wear a mask if dust is present.

If material involved in fire: Extinguish fire using agent suitable for type of surrounding fire. (Material itself does not burn or burns with difficulty.)

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.

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.

If inhaled, iron is a local irritant to the lung and gastrointestinal tract. /Iron compounds/

Vacated 1989 OSHA PEL TWA 1 mg/cu m is still enforced in some states. /Iron salts (soluble, as Fe)/

Recommended Exposure Limit: 10 Hr Time-Weighted Avg: 1 mg/cu m. /Iron salts (soluble, as Fe)/

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).

The toxicity of ferrous sulfate in humans depends on the amount of iron ingested. Up to 20 mg/kg of elemental iron is not toxic, 20-60 mg/kg has mild toxicity, and more than 60 mg/kg can lead to severe symptoms and morbidity. **Overdose information** Iron containing products are the primary cause of drug overdose in children under 6 years of age. Iron is toxic to the gastrointestinal system, cardiovascular system, in addition to central nervous system. The most early reported effects following the excess ingestion of iron include nausea, flatulence, abdominal pain, diarrhea, constipation, and black/tarry stools. Symptoms of overdose in the later stages include bluish lips, fingernails, and palms, drowsiness, tachycardia, seizures, metabolic acidosis, hepatic injury, and cardiovascular dysfunction. Sequelae of iron sulfate overdose include intestinal obstruction, pyloric stenosis, and gastric scarring. If the patient is comatose or seizing, gastric lavage with sodium bicarbonate should be performed. Deferoxamine is the antidote for iron poisoning. Other supportive treatments to support fluid and electrolyte balance and correct metabolic acidosis are also advised. Hospitalization should continue for 24 h after the patient becomes asymptomatic to monitor for delayed onset of shock/gastrointestinal bleeding.

Typical replacement doses of oral iron have not been linked convincingly to serum enzyme elevations during therapy or to idiosyncratic, acute clinically apparent liver injury. In contrast, overdoses of oral iron, whether intentional or accidental, can cause liver injury, largely as a component of iron poisoning. Iron poisoning occurs most common in toddlers (1 to 3 years old) who ingest iron tablets prescribed for adults. Toxicity occurs after ingestion of 3 grams or more of ferrous sulfate (approximately 10 tablets, or ~650 mg of elemental iron), with toxic levels being more than 60 mg/kg of elemental iron and fatal levels more than 180 mg/kg. The typical sequence of events is appearance of nausea, vomiting and abdominal pain within 1 to 3 hours of the ingestion, followed by diarrhea, weakness, irritability, lethargy and stupor. Vomitus may be blood streaked or frank hematemesis. The diarrhea is generally fluid and dark (as a result of iron rather than blood). With higher doses, this initial phase is rapidly followed by pallor, hypotension and shock. Both upper and lower gastrointestinal bleeding can occur and early changes include metabolic acidosis and coagulopathy. In some instances, there is an improvement after a few hours of symptoms which can then be followed by sudden hemodynamic collapse, cardiogenic shock and severe acidosis that may be fatal. Early intervention (with gastric lavage, fluid replacement and iron chelation) appears to ameliorate the course of injury. Liver toxicity generally arises after 24 hours and may be more common in adults than children. Severe liver toxicity, with jaundice and marked aminotransferase elevations (ALT and AST greater than 25 times ULN), generally occurs only with larger overdoses and high initial serum iron levels (>1000 μg/dL). Jaundice is initially mild, while prolongation of the prothrombin time (or INR) and acidosis arise early (Case 1). The usual cause of death from iron poisoning is cardiac arrest, but deaths from hepatic failure as well as emergency liver transplantation for iron poisoning have been reported. Interestingly, the hepatic histological findings of acute iron hepatotoxicity are those of hemorrhagic, submassive necrosis which is predominantly peri-portal (zone 1), a finding typical of direct hepatotoxins that do not require hepatic metabolism for their toxicity. With more severe toxicity, the injury is massive and pan-lobular.

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.

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.

/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.

...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/

The protein binding for ferrous sulfate is equal to or greater than 90%. It is bound to transferrin and ferritin, ferroportin, myoglobin, and other enzymes. Approximately 60% of iron is located in the erythrocytes as part of hemoglobin.

HYDRATES OCCUR IN NATURE AS MINERALS: MELANTERITE, SIDEROTIL, SZOMOLNIKITE, TAUISCITE.

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. ...

Ferrous sulfate is used for the prevention and treatment of iron deficiency anemia in adults and children.

Iron is an essential heavy metal that is included in many over-the-counter multivitamin and mineral supplements and is used therapeutically in higher doses to treat or prevent iron deficiency anemia. When taken at the usual recommended daily allowance or in replacement doses, iron has little or no adverse effect on the liver. In high doses and in intentional or accidental overdoses, iron causes serious toxicities, one component of which is acute liver damage.

Trace Elements and Metals

Initial response to iron therapy ...will confirm or negate diagnosis of iron-deficiency anemia. Ferrous sulfate, 150-300 mg thrice daily, is given for 3 wk. Beginning about a wk after starting therapy, circulating hemoglobin should rise about 0.1-0.3 g % daily; less severe anemia, less daily rise.|Supplementation with 30-60 mg of iron daily (ie, 150-300 mg of ferrous sulfate) has been advocated for pregnant women ...and 0.3-0.6 mL of ferrous sulfate pediatric "drops" daily for low-birth-weight infants from 1 month until 1 yr of age. Physician must use his judgement in this regard... .|Hematinic.|MEDICATION (VET): In iron deficiency. Astringent.|For more Therapeutic Uses (Complete) data for FERROUS SULFATE (11 total), please visit the HSDB record page.

... A double-lumen perfusion tube was positioned orogastrically into a 40-cm segment of the proximal small intestine in six healthy volunteers (25 +/- 5 yr). The segment was perfused with saline and subsequently with saline containing 80 mg iron as ferrous sulfate at a rate of 10 mL/min. Intestinal fluid samples were collected at 15-min intervals. Thiobarbituric acid reactive substances concentrations as an indicator of lipid peroxidation increased significantly from 0.07 uM (range, 0-0.33 uM) during saline perfusion to 3.35 uM (range, 1.19-7.27 uM) during iron perfusion (P<0.05). Nonprotein antioxidant capacity increased significantly from 474 uM (range, 162-748 uM) to 1,314 uM (range, 674-1,542 uM) (P<0.05). These data show that a single dosage of ferrous sulfate induces oxidative damage and the subsequent release of an antioxidant in the small intestine in vivo in healthy volunteers.|Adverse effects of ferrous sulfate are those of iron compounds in general, but they are rarely severe when drug is taken in therapeutic doses; however, relatively small overdoses can cause serious intoxication in infants and children.|VET: Administer with or after feeding to help avoid gastritis.|Adverse effects are generally dose dependent; in 10% of patients they are severe enough to be intolerable. Gastrointestinal disturbances ... are most common. Ferrous sulfate is absorbed best when taken between meals, but gastrointestinal symptoms may be minimized by reducing the dose and/or giving it in divided amounts with meals or shortly thereafter. In some patients, admin of one-half the total daily dose at bedtime improves tolerance. ... Large doses of ferrous sulfate may aggravate existing gastrointestinal diseases ... . Acute severe iron poisoning is uncommon in adults but does occur in children who ingest formulations intended for adults. In young children, as little as 400 mg of elemental iron is potentially fatal.|For more Drug Warnings (Complete) data for FERROUS SULFATE (9 total), please visit the HSDB record page.

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.

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.|Gastrointestinal absorption of iron is adequate and essentially equal from...ferrous...sulfate, fumarate, gluconate, succinate, glutamate, and lactate.

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.

The half-life of orally administered iron is not readily available in the literature, with total effects lasting 2-4 months (congruent with the red blood cell life span) with an onset of action of 4 days and peak activity at 7-10 days.

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.

INGESTION: abdominal pain, retching, diarrhea, dehydration, shock, pallor, cyanosis, rapid or weak pulse, shallow respiration, low blood pressure. (USCG, 1999)

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)

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.

/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.

Aktiferrin

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).

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/

Agriculture, forestry, fishing and hunting|Sulfuric acid, iron(2+) salt (1:1): ACTIVE|Sulfuric acid, iron(2+) salt (1:?): ACTIVE

Method 426D: Automated Methylthymol Blue Method. Barium sulfate is formed by the reaction of the sulfate ion with barium chloride at a low pH. At high pH excess barium reacts with methylthymol blue to produce a blue chelate. The uncomplexed methylthymol blue is gray. The amount of gray uncomplexed methylthymol blue indicates the concentration of sulfate ion. In a single laboratory a sample with an average concentration of about 28 mg sulfate/l had a standard deviation of 0.68 mg/l and a coefficient of variation of 2.4%. In two samples with added sulfate, recoveries were 91% and 100%. /Sulfate/|Method 426A: Gravimetric Method with Ignition of Residue and Method 426B: Gravimetric Method with Drying of Residue. Sulfate is precipitated in a hydrochloric acid solution as barium sulfate by the addition of barium chloride. The precipitation is carried out near the boiling temperature, and after a period of digestion the precipitate is filtered, washed with water until free of chloride ion, ignited or dried and weighed as barium sulfate. These methods are suitable for sulfate ion concentrations above 10 mg/l. /Sulfate/|EPA Method 9038: Turbidimetric. Method 9038 is applicable to ground water, drinking and surface waters, and domestic and industrial wastes. This method is suitable for all concentration ranges of sulfate; however, in order to obtain reliable readings, use a sample aliquot containing not more than 40 mg/l of sulfate. Sulfate ion is converted to a barium sulfate suspension under controlled condition. The resulting turbidity is determined by a nephelometer, filter photometer, or spectrophotometer and compared with a curve prepared from standard sulfate solution. The minimum detectable limit is approximately 1 mg/l of sulfate. /Sulfate/

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