IRON
HAZARDTEXT ®
Information to help in the initial response for evaluating chemical incidents
-IDENTIFICATION
SYNONYMS
ANCOR EN 80 ANCOR EN 80/150 ARMCO IRON EFV 250/400 EO 5A FERROVAC E FERRUM GS 6 IRON IRON, ELECTROLYTIC IRON, ELEMENTAL IRON, POWDERED IRON, REDUCED (FCC) LOHA NC 100 PZH-1M3 PZH-2 PZH1M1 PZH2M1 PZH2M2 PZH3 PZH3M PZH4M PZh2M PZhO REMKO SUY-B 2 3ZhP AMMONIUM IRON SULFATE FERROUS FERROUS ION FERROUS METAL BORINGS, SHAVINGS, TURNINGS, OR CUTTINGS IRON (FE 2+) IRON (II) ION IRON (III) CHLORIDE, SOLUTION IRON OXIDE DUST AND FUME IRON SESQUICHLORIDE IRON(2+) IRON, ION(FE 2+) JEWELER'S ROUGE NATURAL HEMATITE VOGEL'S IRON RED ZELAZA TLENKI (POLISH)
IDENTIFIERS
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures.
FERRIC PYROPHOSPHATE CITRATE: Fe4(C6H4O7)3(H2P2O7)2(P2O7) IRON: Fe IRON SUCROSE: [Na2Fe5O8(OH).3H2O]n.m(C12H22O11) SODIUM FERRIC GLUCONATE COMPLEX: [NaFe2O3(C6H11O7)(C12H22O11)5]n of approximately 200
SYNONYM REFERENCE
- (AAR, 1998; Clayton & Clayton, 1994; HSDB , 1999; Lewis, 1996; RTECS , 1999)
USES/FORMS/SOURCES
INDUSTRIAL/COMMERCIAL USES Iron is primarily used in powder metallurgy and serves as a catalyst in chemical reactions (AAR, 1998). Iron is a component of carbon steels, cast iron, high-speed steels, high-strength low-alloy steels, manganese alloy steels, and stainless steels (Ashford, 1994). Steel is the most important alloy of iron. It contains 0.25-2% of carbon. Tensile strength increases with increase in carbon content (Clayton & Clayton, 1994). Alloyed with carbon (C), manganese (Mn), chromium (Cr), nickel (Ni) and other elements, iron is used to form steel (Budavari, 1996; Sittig, 1991)
Wrought iron is almost pure iron (Clayton & Clayton, 1994). Ignition of a mixture of iron and potassium perchlorate generates heat sufficient for metal welding (Urben, 1995). Iron uses include magnets, dyes, pigments, abrasives, and polishing compounds such as jeweler's rouge (Harbison, 1998). Iron is used to increase the density of fluids used in oil-well drilling (ILO, 1998). HAND WARMER: Iron powder is used in hand warmers available worldwide, especially in Japan, Canada and the United States. The iron powder and other contents of the hand warmer (activated charcoal, salt and vermiculite) create an exothermic chemical reaction when exposed to air or moisture (Tam et al, 2008). One patient developed a "warm sensation" in her mouth and epigastrium after ingesting a piece of a hand warmer (Hot Hands 2) containing 5 to 8 grams of elemental iron. Laboratory results revealed a serum iron concentration of 235 mcg/dL obtained 6 hours postingestion. Some heat warmers may contain up to 60 g of iron powder (Weiland & Sherrow, 2015).
BIOLOGICAL/ENVIRONMENTAL USES Iron is essential to life. It is a constituent of biological pigments such as hemoglobin, cytochromes and ferrichromes (Lewis, 1998). Iron is believed to be essential for normal growth and nutrition of all living cells, including microorganisms (Baselt & Cravey, 1995; Dragun, 1988; Lewis, 1997). Iron, one of the ten trace elements, is required in the diet of higher animals, including humans, and is the most abundant trace metal in the human body (Schardein, 1993; Baselt & Cravey, 1995). RECOMMENDED DAILY INTAKE: Adults require 10-20 mg of elemental iron daily. This amount is supplied through average diet (Baselt & Cravey, 1995). During pregnancy, the daily requirement increases to 30 mg (TERIS , 1999).
Injections of iron dextran (complex of ferric hydroxide and dextran) are used to treat iron deficiency anemia in humans and piglets (Clayton & Clayton, 1994). Iron isotopes 55Fe and 59Fe are used in tracer studies (Budavari, 1996). 55Fe is used as a biological tracer (Budavari, 1996). Its half-life is 2.91 years (Lewis, 1997). 59Fe (half-life 46.3 days) emits beta and gamma radiation. It is used in medicine and as a tracer element in biochemical and metallurgical research (Lewis, 1997).
Iron participates in cellular oxidative processes (Lewis, 1997). Iron ions are involved in various biological processes, such as oxygen transport, electron transport, and nitrogen fixation (Budavari, 1996; Zenz, 1994). The body burden of a human, weighing 70 kg, is about 4.1 g (ranges 3-5 g) (Clayton & Clayton, 1994; Zenz, 1994). Iron is a constituent of hemoglobin (Lewis, 1997). Hemoglobin contains about 67% of the body iron (Clayton & Clayton, 1994; Zenz, 1994). About 27% (ranges 20-30%) of the body iron is stored in the liver as ferritin (physiological) or hemosiderin (pathological conditions) (Clayton & Clayton, 1994; Zenz, 1994).
Iron is essential for proper functioning of myoglobin, heme-containing enzymes, and metalloflavoprotein enzymes (Harbison, 1998). Iron tablets, used to orally treat iron deficiency, contain soluble iron salts and are potentially toxic. Ingestion of 0.5 g of iron may result in vomiting, ulceration of the gastrointestinal mucosa, intestinal bleeding, and possibly liver and kidney damage (Zenz, 1994).
INDUSTRIAL FORMS Powdered iron is a gray lustrous substance (AAR, 1998; (HSDB , 1999). Iron is a silver-white metal (Lewis, 1997; Clayton & Clayton, 1994; Lewis, 1996; HSDB , 1999). Also available as crystals, whiskers, and iron sponge (Lewis, 1997). Common valences are 2 and 3 (Budavari, 1996) Lewis, 1997), seldom 1, 4, 6 (Budavari, 1996; HSDB , 1999). Four naturally occurring isotopes (Lewis, 1997; Budavari, 1996; HSDB , 1999): - 54 (5.82%)
- 56 (91.66%)
- 57 (2.19%)
- 58 (0.33%)
Four artificial, radioactive isotopes (Lewis, 1997; Budavari, 1996): Although iron occurs in pure form, it is more commonly found as oxide or carbonate (Clayton & Clayton, 1994; Lewis, 1998), or as sulfide or silicate (Clayton & Clayton, 1994). Iron carbonyl (iron pentacarbonyl) equals 2.58% iron.
Important source ores (Budavari, 1996; Harbison, 1998; HSDB , 1999; ILO, 1998; Lewis, 1997; Zenz, 1994): Derivatives obtained during iron production include aniline, copper, ferric chloride, ferroboron, ferrocene, ferrosilicon, ferrous chloride, ferrovanadium and iron pentacarbonyl (Ashford, 1994). INDUSTRIAL SOURCES DIETARY SOURCES The required daily amount of iron of 10-20 mg for adults is supplied through average diet (Baselt & Cravey, 1995). The average daily intake for adults is 15 mg (Clayton & Clayton, 1994). In the United States, supplemental iron is contained in flour, some breakfast cereals and vitamin preparations (Baselt & Cravey, 1995). EPA set the Federal Drinking Water Guidelines for iron at 300 mcg/L (HSDB , 1999).
ENVIRONMENTAL SOURCES Iron is found in 5.1% of the earth's crust. It is the second most abundant metal (Budavari, 1996) and the fourth most abundant element (Clayton & Clayton, 1994). The content in the earth's crust is 50,000 ppm (Clayton & Clayton, 1994). It is believed that the earth's core consist mainly of iron (Budavari, 1996). Native iron, found in Greenland, exists as small grains or nodules in basalt (HSDB , 1999).
SYNONYM EXPLANATION
- For information regarding CARBONYL IRON or IRON DEXTRAN please see individual managements.
-CLINICAL EFFECTS
GENERAL CLINICAL EFFECTS
- USES: Found primarily as a nutritional supplement in vitamins. Used for the treatment and prevention of iron-deficiency anemia.
- PHARMACOLOGY: Iron is required in the function of multiple essential protein and enzyme complexes including hemoglobin, myoglobin, and cytochromes.
- TOXICOLOGY: Iron is a general cellular poison and is directly corrosive to the GI mucosa.
- EPIDEMIOLOGY: Historically, a common poisoning which was one of the leading causes of pediatric toxicologic deaths. Exposure has been reduced in recent years with improved packaging, but still has the potential for significant morbidity and mortality.
MILD TO MODERATE POISONING: Vomiting and diarrhea may occur within 6 hours of ingestion. SEVERE POISONING: Severe vomiting and diarrhea, lethargy, metabolic acidosis, shock, GI hemorrhage, coma, seizures, hepatotoxicity, and late onset GI strictures. CLINICAL COURSE (May Not Occur In All Cases) includes the following: PHASE I (0.5 to 2 hours) 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. Severe gastrointestinal hemorrhagic necrosis with large losses of fluid and blood contribute to shock. PHASE II includes apparent recovery; continue to observe patient closely. PHASE III (2 to 12 hours after phase I) includes profound shock, severe acidosis, cyanosis, and fever. Increased total peripheral resistance, decreased plasma volume, hemoconcentration, decrease in total blood volume, hypotension, CNS depression, and metabolic acidosis have been demonstrated. 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. Phase V (days to weeks) includes GI scarring and strictures. GI obstruction secondary to gastric or pyloric scarring may occur due to corrosive effects of iron. Sustained-release preparations have resulted in small intestinal necrosis with resultant scarring and obstruction.
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. 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.
- POTENTIAL HEALTH HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
Inhalation of material may be harmful. Contact may cause burns to skin and eyes. Inhalation of Asbestos dust may have a damaging effect on the lungs. Fire may produce irritating, corrosive and/or toxic gases. Some liquids produce vapors that may cause dizziness or suffocation. Runoff from fire control may cause pollution.
ACUTE CLINICAL EFFECTS
PHARMACOLOGY: Iron is required in the function of multiple essential protein and enzyme complexes including hemoglobin, myoglobin, and cytochromes. TOXICOLOGY: Iron is a general cellular poison and is directly corrosive to the GI mucosa. EPIDEMIOLOGY: Historically, a common poisoning which was one of the leading causes of pediatric toxicologic deaths. Exposure has been reduced in recent years with improved packaging, but still has the potential for significant morbidity and mortality. ADVERSE EFFECTS OVERDOSE MILD TO MODERATE POISONING: Vomiting and diarrhea may occur within 6 hours of ingestion. SEVERE POISONING: Severe vomiting and diarrhea, lethargy, metabolic acidosis, shock, GI hemorrhage, coma, seizures, hepatotoxicity, and late onset GI strictures. CLINICAL COURSE (May Not Occur In All Cases) includes the following: PHASE I (0.5 to 2 hours) 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. Severe gastrointestinal hemorrhagic necrosis with large losses of fluid and blood contribute to shock. PHASE II includes apparent recovery; continue to observe patient closely. PHASE III (2 to 12 hours after phase I) includes profound shock, severe acidosis, cyanosis, and fever. Increased total peripheral resistance, decreased plasma volume, hemoconcentration, decrease in total blood volume, hypotension, CNS depression, and metabolic acidosis have been demonstrated. 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. Phase V (days to weeks) includes GI scarring and strictures. GI obstruction secondary to gastric or pyloric scarring may occur due to corrosive effects of iron. Sustained-release preparations have resulted in small intestinal necrosis with resultant scarring and obstruction.
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. 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.
ACIDOSIS: Anion gap metabolic acidosis is a common early finding in significant ingestions (Carlsson et al, 2008; Schonfeld & Haftel, 1989; Wu et al, 1998). Severe metabolic acidosis may persist for days in severe overdoses.
HYPOTENSION: Hypotension may develop 2 to 6 hours after severe poisoning secondary to vomiting, diarrhea, blood loss or vasodilation. HEART FAILURE: Cardiac failure has been reported on the second day following severe acute iron poisoning (Tenenbein & Israels, 1988). Iron-mediated lipid peroxidation of myocyte organelle membranes (Watts, 1999) and impairment of cardiac mitochondrial respiratory enzyme activity (Link, 1998) are the proposed mechanism. Cardiac toxicity is a well-known complication of chronic iron overload.
HYPOGLYCEMIA: Hypoglycemia secondary to hepatic failure may be seen late (2 to 4 days) in severe overdoses. HYPERGLYCEMIA: Serum glucose concentration greater than 150 mg/dL has been reported (Lacouture et al, 1981; Mann et al, 1989).
Nausea, vomiting, and diarrhea may develop following an overdose (Carlsson et al, 2008; Wu et al, 2003). Hemorrhage, ulceration and necrosis of the esophagus, stomach, and bowel are common autopsy findings in fatal iron overdoses. Gastrointestinal hemorrhage may be seen in the first few hours after ingestion.
Iron particles as foreign bodies in the cornea or sclera principally have local effects; whereas, if they are in the posterior part of the globe, in the vitreous humor, or in the vicinity of the lens, the effect may be widespread and serious (Grant & Schuman, 1993).
COAGULOPATHY: Early coagulopathy (4 to 8 hours postingestion) has been reported rarely and may be due to interference with enzymes of the coagulation cascade by free iron (Tenenbein & Israels, 1988). It is related to plasma concentrations of ferric iron. Late coagulopathy (24 hours or more postingestion) is associated with severe hepatotoxicity and decreased levels of factors V, VII, IX, X, and fibrinogen (Tenenbein & Israels, 1988).
HEMOCHROMATOSIS: Hemochromatosis may rarely occur after chronic ingestion of excessive iron (Green et al, 1989). Patients receiving parenteral iron therapy may be at more risk to develop iron overload because the intestinal regulatory mechanisms are bypassed (Burns & Pomposelli, 1999). LEUKOCYTOSIS: Leukocyte counts greater than 15,000/mm(3) have been reported following iron poisoning, but is nonspecific (Lacouture et al, 1981; Mann et al, 1989).
HEPATOTOXICITY: BACKGROUND: Hepatotoxicity leading to death can occur following acute iron poisoning. Based on a review of the literature, patients developed hepatotoxicity within 24 to 48 hours and effects appear to be dose related. The primary site of hepatic injury is the periportal areas of the hepatic lobule (the principal site for hepatic regeneration), which may explain the increase in mortality and poorer prognosis. Rapid onset and periportal injury were also consistently reported in animal studies due to iron poisoning (Tenenbein, 2001). MECHANISM: Iron-induced hepatotoxicity is a presumed result of free radical generation and lipid peroxidation. Iron catalyzes hydroxyl radical formation (the most potent-free radical), which initiates lipid peroxidation. Based on limited data, antioxidants may have a hepatoprotective role in iron poisoning. Further research is suggested to establish efficacy (Tenenbein, 2001). INCIDENCE: Periportal hepatic necrosis is described in fatal cases, although it occurs rarely (McGuigan, 1996). Significant elevations of AST, ALT, LDH, and bilirubin occur 1 to 4 days postingestion in severe cases (Gleason, 1979; Comes et al, 1993). DOSE-DEPENDENT RELATIONSHIP: Robertson & Tenenbein (2005) looked at 73 cases of iron poisoning to determine if hepatotoxicity due to iron poisoning is a dose-related effect. Sixty patients had no signs of hepatotoxicity, 4 patients developed mild hepatotoxicity, and 9 patients developed severe hepatotoxicity (transaminase greater than 1000 Units/L). The serum iron levels of only 3 patients with severe hepatotoxicity were obtained early and prior to deferoxamine therapy. The values ranged from 1821 to 20,900 mcg/dL. The authors concluded that clinically significant hepatotoxicity is not likely to occur with serum iron levels less than 700 mcg/dL (Robertson & Tenenbein, 2005).
ANAPHYLACTOID REACTIONS: Reports of anaphylactoid reactions have occurred with therapeutic administration of parenteral iron. In one study, doses of 500 mg or more were associated with severe reactions (Burns & Pomposelli, 1999).
Lethargy, restlessness and/or confusion have been noted (30 minutes to 2 hours) (Carlsson et al, 2008; Chyka & Butler, 1993). Seizures and coma may be seen in Phase III or IV (2 hours to 4 days) (Chyka & Butler, 1993).
ACUTE LUNG INJURY: Acute lung injury may develop in severe iron intoxication 12 hours to several days after ingestion. Use of high doses of deferoxamine for longer than 24 hours may contribute to the development of acute lung injury (Tenenbein et al, 1988). PULMONARY ASPIRATION: CASE SERIES: Sixteen cases of ferric chloride poisoning between the years of 1990-2001 were analyzed, and aspiration pneumonia was reported in 18.8% of patients (Wu et al, 2003). PNEUMOCONIOSIS: Inhaling dust containing iron oxide can lead to pneumoconiosis, but no definitive conclusions as to its role in lung cancer. Based on animal data, iron oxide dust is suspected as a "co-carcinogenic" substance (ILO, 1998). Although it is considered by IARC to be group 3. Iron oxide particles or dust may be caught in the remaining iron oxide accumulates in lymphoid tissue along bronchi, around blood vessels, or at the bifurcation of bronchi(Harbison, 1998a).
CHRONIC CLINICAL EFFECTS
- Chronic iron inhalation (as iron oxide) leads to accumulation in the lungs and a characteristic stippled appearance on X-rays. This condition, called SIDEROSIS, is considered benign in that it does not interfere with lung function and does not predispose to other disease.
- Iron appears to be preferentially released from quartz particles in the lungs of patients with more severe fibrosis (Tourmann & Kaufmann, 1994). A similar release of iron was seen in the lungs of rats following pulmonary instillation of silica, together with increases in oxidant stress and decreased levels of antioxidants (Ghio et al, 1994). Iron may play a central role in development of fibrosis through some oxidative mechanism(s).
- Clinical signs of iron overload appear when the total body iron is 5 to 10 times higher than normal (Lynch, 1995).
- Neurobehavioral defects including decreased activity, habituation, reflex startle, and conditioned avoidance response performance, were seen in rats fed excess iron (20,000 ppm) in the diet for 12 weeks, but similar effects were also seen in iron-deficient animals. It is therefore likely that these behavioral effects are secondary to general toxicity (Sobotka et al, 1996).
- Iron DEFICIENCY, measured as lower serum iron and transferrin levels, has been linked with major depression; decreased iron may be the result of immune-inflammatory response in depression (Maes et al, 1996).
- Sodium ferrous citrate has been linked with photosensitivity (Kawada et al, 1996). Contact hypersensitivity to ferric and ferrous salts has been shown in patch testing (Hemmer et al, 1996).
- High serum iron levels were associated with an increased risk of fatal acute myocardial infarction (MI) in a group of 9920 Canadian men and women. Persons with serum iron levels greater than or equal to 175 mcg/dL had double the risk for men, and over 5 times the risk for women of having a fatal MI (Morrison et al, 1994). It has been hypothesized that iron plays a role in atherosclerosis and coronary heart disease, because its incidence in women is only 30% to 50% of that in men, and women are typically iron-deficient. While at least 7 epidemiologic studies have found an association between iron and CHD, 18 have not. Most of the epidemiologic data since the original Finnish study have failed to find an association between increasing levels of serum ferritin and risk of heart attack (Meyers, 1996; Sempos et al, 1996).
-FIRST AID
FIRST AID AND PREHOSPITAL TREATMENT
-MEDICAL TREATMENT
LIFE SUPPORT
- Support respiratory and cardiovascular function.
SUMMARY
- FIRST AID - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
Move victim to fresh air. Call 911 or emergency medical service. Give artificial respiration if victim is not breathing. Administer oxygen if breathing is difficult. Remove and isolate contaminated clothing and shoes. In case of contact with substance, immediately flush skin or eyes with running water for at least 20 minutes. Ensure that medical personnel are aware of the material(s) involved, and take precautions to protect themselves.
INHALATION EXPOSURE INHALATION: Move patient to fresh air. Monitor for respiratory distress. If cough or difficulty breathing develops, evaluate for respiratory tract irritation, bronchitis, or pneumonitis. Administer oxygen and assist ventilation as required. Treat bronchospasm with an inhaled beta2-adrenergic agonist. Consider systemic corticosteroids in patients with significant bronchospasm. If bronchospasm and wheezing occur, consider treatment with inhaled sympathomimetic agents.
EYE EXPOSURE DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
ORAL EXPOSURE
-RANGE OF TOXICITY
MINIMUM LETHAL EXPOSURE
Fatalities have occurred following pediatric ingestions of 1200 mg to 4500 mg of elemental iron. Adult fatalities have been reported when only supportive care was provided or deferoxamine treatment was delayed. Lethality may be modified by adequate supportive care and treatment. Of 17 pediatric cases reported prior to the use of deferoxamine, 8 (47%) resulted in death (Spencer, 1951; Forbes, 1947; Thomson, 1947; Thomson, 1950; Roxburgh, 1949). For ferrous iron, the estimated lethal dose is 0.3 grams/kg body weight (Baselt, 2000). Acute iron intoxication occurs more often in children than in adults, and is believed to be responsible for several hundred pediatric deaths annually (Baselt, 2000). Fatal poisoning is accompanied with the following autopsy findings: hemorrhage and necrosis of gastrointestinal mucosa, degenerative changes in liver, and hemorrhagic bronchopneumonia (Baselt, 2000). FATAL HEPATIC INJURY - The lowest serum iron level that was associated with hepatic injury was 1700 mcg/dL (304 mcmol/L) in a 17-year-old pregnant female who died of iron overdose-induced hepatic failure (Tenenbein, 2001).
PEDIATRIC In a series of 12 children who all received gastric lavage and deferoxamine, all survived (Whitten et al, 1965). In a review of cases of children who developed severe iron intoxication, defined as coma or shock, definitive therapy (chelators, exchange transfusion) resulted in survival in 12 of 14 (86%), supportive care resulted in survival in 14 of 26 (54%), and no therapy resulted in survival in 0 of 10 (Whitten et al, 1965). In another series of 28 children with shock or coma due to iron poisoning, 25 (89%) survived after deferoxamine therapy (Westlin, 1966). TABLE of fatal PEDIATRIC iron ingestions
ADULT TABLE of fatal ADULT iron ingestions
MAXIMUM TOLERATED EXPOSURE
- Ingestion of less than 40 mg/kg generally does not cause significant toxicity, although mild GI irritation may develop (Manoguerra et al, 2005).
- One case series found that hospital referral values as high as 61 mg/kg of iron do not adversely impact patient outcomes (Benson et al, 2003).
- In one study, 27.6% of 380 children with an iron ingestion of 40 mg/kg to 60 mg/kg became symptomatic (Oderda et al, 1987).
- In one series of 59 iron-poisoned children 15/20 with serum iron greater than 500 mcg/dL were symptomatic and were considered to be moderately or severely poisoned (James, 1970). In addition, another study found a significant correlation between serum iron levels above 500 mcg/dL and coma. Nine of 13 with serum iron less than 300 mcg/dL were mildly poisoned or asymptomatic (Chyka & Butler, 1993).
- Of 22 patients with initial levels between 300 and 500 mcg/dL, 14 were moderately or severely poisoned and 8 were mildly poisoned or asymptomatic (James, 1970).
HAND WARMERS: One patient developed a "warm sensation" in her mouth and epigastrium after ingesting a piece of a hand warmer (Hot Hands 2) containing 5 to 8 grams of elemental iron. Laboratory results revealed a serum iron concentration of 235 mcg/dL obtained 6 hours postingestion. Some heat warmers may contain up to 60 g of iron powder (Weiland & Sherrow, 2015). HIGH-DOSE DEFEROXAMINE: A 22-year-old woman with an extremely high serum iron concentration (4573 mcg/dL) after ingesting 180 tablets of 300 mg ferrous sulfate (216 mg/kg elemental iron), received high-dose IV deferoxamine (15 mg/kg/hr started 8 hours after ingestion, increased to 30 mg/kg/hr 2 hours later, and then decreased to 15 mg/kg/hr 4 hours later). Despite severe gastrointestinal complications and metabolic acidosis, she rapidly recovered following supportive care and did not developed any adverse effects from high-dose deferoxamine (Noble et al, 2015). An 18-year-old woman presented with persistent vomiting, abdominal pain, lethargy, altered mental status, tachycardia (124 beats/min), and severe anion gap metabolic acidosis (pH 7.16, PaO2 122 mmHg, PCO2 20 mmHg, bicarbonate 6.9 mmol/L, base excess -21.5 mmol/L) about 8 hours after ingesting 50 ferrous sulfate tablets (100 mg of elemental iron per 335 mg tablet; 100 mg/kg of elemental iron). Following supportive care, including gastric lavage, whole bowel irrigation, continuous renal replacement therapies, continuous venovenous hemodiafiltration, and deferoxamine therapy, her condition gradually improved. Her serum iron concentration decreased from 2150 to 160 mcg/dL (reference range: 40 to 150 mcg/dL) 24 hours after ingestion (Gumber et al, 2013). PEDIATRIC: An 18-month-old boy (weight 11 kg) presented with diarrhea and vomiting after ingesting about 1625 mg (147 mg/kg) of ferrous sulfate. He later became drowsy, requiring intubation and ventilation. X-ray of the abdomen revealed 13 tablet fragments. Despite standard therapy (gastric lavage, whole bowel irrigation, and intravenous deferoxamine 15 mg/kg/hr, total at least 360 mg/kg in 24 hours), his serum iron concentration increased to 700 mcmol/L (3906 mcg/dL) 6 hours after ingestion. He developed elevated ALT (359 Units/L) and coagulopathy with kaolin partial thromboplastin time at 74.5 s and prothrombin time at 16.5 s, requiring vitamin K, fresh frozen plasma, and cryoprecipitate. Approximately 14 hours postingestion, he underwent continuous veno-venous hemofiltration (CVVH) for 17 hours and his serum iron concentration quickly decreased to 24.5 mcmol/L (137 mcg/dL). Despite signs of organ damage, he gradually recovered and was discharged on day 5 (Milne & Petros, 2010). PEDIATRIC - An 18-month-old girl (12 kg) presented to the emergency department after the ingestion of 5300 mg of iron (442 mg/kg of elemental iron; serum iron concentration of 447 mcg/dL on admission). Despite standard therapy (gastric lavage, whole bowel irrigation, and intravenous deferoxamine) for 2 hours, her serum iron increased to 1362 mcg/dL (244 mcmol/L). Exchange transfusion 9 hours post-ingestion reduced serum iron to 134 mcg/dL (24 mcmol/L). Her serum iron level decreased further to 40 mcg/dL (7 mcmol/L) after plasmapheresis for 5 hours. She was extubated 18 hours after the exchange transfusion (Carlsson et al, 2008). PEDIATRIC - A 7-week-old girl was brought to the hospital 4 hours after the maternal grandmother accidently gave the infant approximately 1.5 ounces (400 mg/kg of elemental iron) of ferrous sulfate suspension from a baby bottle thought to contain juice. The infant was lethargic and shortly after arrival developed metabolic acidosis (pH 7.22; PCO2 58 mm Hg) and shock. Initial serum iron level was 671 mcg/dL, and the level decreased to 194 mcg/dL and 46 mcg/dL following 6 and 20 hours of deferoxamine chelation therapy, respectively. Treatment was complicated by the immaturity of the infant, but a full recovery without sequelae was noted at a follow-up several months after the incident (Valentine et al, 2009). ADULT - Iron ingestions of 20 mg/kg by 6 fasted adults resulted in nausea, malaise, and diarrhea in all subjects, with 4 requiring intravenous fluids (Burkhart et al, 1991).
- Carcinogenicity Ratings for CAS7439-89-6 :
ACGIH (American Conference of Governmental Industrial Hygienists, 2010): Not Listed ; Listed as: Iron salts, soluble, as Fe EPA (U.S. Environmental Protection Agency, 2011): Not Listed IARC (International Agency for Research on Cancer (IARC), 2016; International Agency for Research on Cancer, 2015; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2010a; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2008; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2007; IARC Working Group on the Evaluation of Carcinogenic Risks to Humans, 2006; IARC, 2004): Not Listed NIOSH (National Institute for Occupational Safety and Health, 2007): Not Listed ; Listed as: Iron salts (soluble, as Fe) MAK (DFG, 2002): Not Listed NTP (U.S. Department of Health and Human Services, Public Health Service, National Toxicology Project ): Not Listed
TOXICITY AND RISK ASSESSMENT VALUES
- EPA Risk Assessment Values for CAS7439-89-6 (U.S. Environmental Protection Agency, 2011):
References: Clayton & Clayton, 1994 Lewis, 1996 OHM/TADS, 1999 RTECS, 1999
-STANDARDS AND LABELS
WORKPLACE STANDARDS
- ACGIH TLV Values for CAS7439-89-6 (American Conference of Governmental Industrial Hygienists, 2010):
Editor's Note: The listed values are recommendations or guidelines developed by ACGIH(R) to assist in the control of health hazards. They should only be used, interpreted and applied by individuals trained in industrial hygiene. Before applying these values, it is imperative to read the introduction to each section in the current TLVs(R) and BEI(R) Book and become familiar with the constraints and limitations to their use. Always consult the Documentation of the TLVs(R) and BEIs(R) before applying these recommendations and guidelines.
- AIHA WEEL Values for CAS7439-89-6 (AIHA, 2006):
- NIOSH REL and IDLH Values for CAS7439-89-6 (National Institute for Occupational Safety and Health, 2007):
- OSHA PEL Values for CAS7439-89-6 (U.S. Occupational Safety, and Health Administration (OSHA), 2010):
- OSHA List of Highly Hazardous Chemicals, Toxics, and Reactives for CAS7439-89-6 (U.S. Occupational Safety and Health Administration, 2010):
ENVIRONMENTAL STANDARDS
- EPA CERCLA, Hazardous Substances and Reportable Quantities for CAS7439-89-6 (U.S. Environmental Protection Agency, 2010):
- EPA CERCLA, Hazardous Substances and Reportable Quantities, Radionuclides for CAS7439-89-6 (U.S. Environmental Protection Agency, 2010):
- EPA RCRA Hazardous Waste Number for CAS7439-89-6 (U.S. Environmental Protection Agency, 2010b):
- EPA SARA Title III, Extremely Hazardous Substance List for CAS7439-89-6 (U.S. Environmental Protection Agency, 2010):
- EPA SARA Title III, Community Right-to-Know for CAS7439-89-6 (40 CFR 372.65, 2006; 40 CFR 372.28, 2006):
- DOT List of Marine Pollutants for CAS7439-89-6 (49 CFR 172.101 - App. B, 2005):
- EPA TSCA Inventory for CAS7439-89-6 (EPA, 2005):
SHIPPING REGULATIONS
- DOT -- Table of Hazardous Materials and Special Provisions (49 CFR 172.101, 2005):
- ICAO International Shipping Name (ICAO, 2002):
LABELS
- NFPA Hazard Ratings for CAS7439-89-6 (NFPA, 2002):
-HANDLING AND STORAGE
STORAGE
Stable in dry air. Readily oxidizes in moist air, forming "rust" (HSDB , 1999). For incompatibilities with other chemicals see "REACTIVITY HAZARD" in the "PHYSICAL HAZARD MANAGEMENT" section.
-PERSONAL PROTECTION
SUMMARY
- RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
- Wear protective gloves, boots and goggles when handling this substance. If substance is on fire or involved in fire, do not breath in dusts and fumes (AAR, 1998).
- Contaminated shoes and clothing should be removed and isolated at spill site (AAR, 1998).
- Upon contact with eyes or skin, immediately flush with running water for at last 15 minutes (AAR, 1998).
- Fittings for hydrogen peroxide handling systems should not contain iron (Urben, 1995)
- Protective clothing should consist of goggles, leather gauntlets, dust or welding masks, steel-toed shoes as needed (Sittig, 1991).
EYE/FACE PROTECTION
- If material contacts eyes or skin, immediately flush with running water for at last 15 minutes (AAR, 1998).
- Dust or welding masks should be used (Sittig, 1991).
RESPIRATORY PROTECTION
- Refer to "Recommendations for respirator selection" in the NIOSH Pocket Guide to Chemical Hazards on TOMES Plus(R) for respirator information.
- Depending on the air concentration, the following respiratory equipment (above 500 mg/m3 with full facepiece) is suggested (Sittig, 1991):
fume respirator high efficiency particulate filter respirator, supplied-air respirator, self-contained breathing apparatus (positive pressure mode), powered air-purifying respirator with high efficiency particulate filter, Type C supplied-air respirator (positive pressure mode), Combination of Type C supplied-air respirator with full facepiece and auxiliary self-contained air supply (both in positive pressure mode).
PROTECTIVE CLOTHING
- CHEMICAL PROTECTIVE CLOTHING. Search results for CAS 7439-89-6.
ENGINEERING CONTROLS
- Use local exhaust and general ventilation to control dust levels (HSDB , 1999).
-PHYSICAL HAZARDS
FIRE HAZARD
Editor's Note: This material is not listed in the Emergency Response Guidebook. Based on the material's physical and chemical properties, toxicity, or chemical group, a guide has been assigned. For additional technical information, contact one of the emergency response telephone numbers listed under Public Safety Measures. POTENTIAL FIRE OR EXPLOSION HAZARDS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004) Some may burn but none ignite readily. Containers may explode when heated. Some may be transported hot.
Powdered iron may undergo reaction with water, giving off the flammable gas hydrogen. The heat produced during this chemical reaction may be sufficiently high to ignite the hydrogen gas (AAR, 1998). Stabilization of pyrophoric iron particles may be achieved through heat treatment with oxygen-containing gases in two stages, first at 25-45 degree C, then at 50-70 degree C (Urben, 1995). Heating of oily iron dust in a collecting vessel under oxidative conditions resulted in vaporization of oil, ignition, and subsequent explosion (Urben, 1995). Exceeding a critical specific surface area results in the development of pyrophoricity of finely divided metal powders. Underlying cause for this property seems to be high heat of oxide formation upon exposure to air. Relatively low concentration of oxygen and an inert gas allow for safe handling (Urben, 1995). An explosion occurred when liquid chlorine was added to carbon disulfide in an iron cylinder, but not when glassware was used. The explosion was due to the iron-catalyzed chlorination of carbon disulfide to carbon tetrachloride (Urben, 1995). Iron powder ignites on contact with polystyrene in the presence of friction or spark (Lewis, 1996). Iron ignites in dry chlorine gas at ambient temperature (Urben, 1995; Lewis, 1996). In liquid fluorine, iron powder (100-mesh, but not 20-mesh) ignites (Urben, 1995; Lewis, 1996). At ambient temperature, reduced iron ignites in dinitrogen tetraoxide gas (Urben, 1995; Lewis, 1996). Iron powder ignites on contact with hydrogen peroxide, nitryl fluoride, peroxyformic acid, potassium dichromate, potassium perchlorate, and sodium peroxide (at 240 degrees C) (Lewis, 1996). Wet iron dust may ignite during drying (Lewis, 1996). Iron dust has moderate flammability when exposed to heat or flame (OHM/TADS , 1999; HSDB , 1999). Combining iron and hydrogen peroxide results in immediate ignition if trace amounts of manganese dioxide are present (HSDB , 1999) Reaction between iron and chlorine trifluoride results in incandescence (HSDB , 1999). At ordinary temperature, nitrogen dioxide decomposes in the presence of reduced iron, resulting in incandescence (HSDB , 1999).
- FLAMMABILITY CLASSIFICATION
- NFPA Flammability Rating for CAS7439-89-6 (NFPA, 2002):
- INITIATING OR CONTRIBUTING PROPERTIES
Heating of oily iron dust in a collecting vessel under oxidative conditions resulted in vaporization (of oil), ignition, and subsequent explosion (Urben, 1995). Hot filtration of aqueous liquor from reduction of a nitro compound with reduced iron powder resulted in formation of iron oxide residues. When air was suctioned through, these residues rapidly heated (Urben, 1995). A mixture of iron flake powder and polystyrene beads, blended together in a high-speed mixer, ignited and burned rapidly upon discharge into a polyethylene bag. Ignition may have been due to rapid oxidation of the finely divided metal and / or static discharge. Surface coating the iron powder with stearic acid prevented ignition (Urben, 1995). Possibly wet ferrous scrap was stored in sealed steel tubes for several years. Pressure was noticed when holes were drilled into the tubes. In one tube, drilling holes resulted in ignition and explosion, which was attributed to the generation of hydrogen during storage (Urben, 1995). At ambient or slightly elevated temperatures, reaction between bromine pentafluoride and iron is violent and may lead to ignition (Urben, 1995). An explosion occurred when liquid chlorine was added to carbon disulfide in an iron cylinder, but not when glassware was used. The explosion was due to the iron-catalyzed chlorination of carbon disulfide to carbon tetrachloride (Urben, 1995). Iron ignites in dry chlorine gas at ambient temperature (Urben, 1995; Lewis, 1996). The reaction between iron and chlorine trifluoride occurs at ambient or slightly elevated temperatures, is violent, and often causes a fire. The severity of the reaction may depend on the state of subdivision (Urben, 1995). In liquid fluorine, iron powder (100-mesh, but not 20-mesh) ignites (Urben, 1995; Lewis, 1996). At ambient temperature, reduced iron ignites in dinitrogen tetraoxide gas (Urben, 1995; Lewis, 1996). In the presence of trace amounts of manganese dioxide, addition of hydrogen peroxide to powdered iron results in ignition upon contact (Urben, 1995). Addition of 2-3 drops of approximately 90% peroxyformic acid to iron powder results in very rapid auto-combustion if traces of manganese dioxide are present (Urben, 1995). Mixtures of finely divided iron and sodium peroxide ignite under high friction at 240 degree C (Urben, 1995). Powdered iron may undergo reaction with water, giving off the flammable gas hydrogen. The heat produced during this chemical reaction may be sufficiently high to ignite the hydrogen gas (AAR, 1998). Stabilization of pyrophoric iron particles may be achieved through heat treatment with oxygen-containing gases in two stages, first at 25-45 degree C, then at 50-70 degree C (Urben, 1995). Exceeding a critical specific surface area results in the development of pyrophoricity of finely divided metal powders. Underlying cause for this property seems to be high heat of oxide formation upon exposure to air. Relatively low concentration of oxygen and an inert gas allow for safe handling (Urben, 1995). Iron powder ignites on contact with polystyrene in the presence of friction or spark (Lewis, 1996). Iron powder ignites on contact with hydrogen peroxide, nitryl fluoride and heat, peroxyformic acid, potassium dichromate, potassium perchlorate, sodium peroxide (at 240 degrees C) (Lewis, 1996). Wet iron dust may ignite during drying (Lewis, 1996). Iron dust has moderate flammability when exposed to heat or flame (OHM/TADS , 1999; HSDB , 1999). Combining iron and hydrogen peroxide results in immediate ignition if trace amounts of manganese dioxide are present (HSDB , 1999). Reaction between iron and chlorine trifluoride results in incandescence (HSDB , 1999). At ordinary temperature, nitrogen dioxide decomposes in the presence of reduced iron, resulting in incandescence (HSDB , 1999).
- FIRE CONTROL/EXTINGUISHING AGENTS
- SMALL FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
- LARGE FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
Water spray, fog or regular foam. Move containers from fire area if you can do it without risk. Do not scatter spilled material with high pressure water streams. Dike fire-control water for later disposal.
- TANK FIRE PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
Cool containers with flooding quantities of water until well after fire is out. Withdraw immediately in case of rising sound from venting safety devices or discoloration of tank. ALWAYS stay away from tanks engulfed in fire.
- NFPA Extinguishing Methods for CAS7439-89-6 (NFPA, 2002):
- If powdered iron is on fire or involved in fire, use water only if volume is sufficient to flood area. Otherwise use graphite, soda ash, powdered calcium chloride, or suitable dry powder to extinguish fire (AAR, 1998).
- If powdered iron is not on fire or involved in fire, do not use water. Keep iron powder dry. Keep sources of ignition, such as sparks and flames, away from spilled iron. Prevent spillage of iron into water sources and sewers (AAR, 1998).
EXPLOSION HAZARD
- Heating of oily iron dust in a collecting vessel under oxidative conditions resulted in vaporization (of oil), ignition, and subsequent explosion (Urben, 1995).
- Grinding iron to sizes below 1 micrometer makes it liable to explosive oxidation (Urben, 1995).
- Mixing chloric acid and iron leads to the formation of explosive compounds (Urben, 1995; Lewis, 1996).
- Powdered iron is explosively ignited by chloroformamidinium nitrate (Urben, 1995; Lewis, 1996).
- At ambient or slightly elevated temperatures, reaction between bromine pentafluoride and iron is violent and may lead to ignition (Urben, 1995; Lewis, 1996).
- An explosion occurred when liquid chlorine was added to carbon disulfide in an iron cylinder, but not when glassware was used. The explosion was due to the iron-catalyzed chlorination of carbon disulfide to carbon tetrachloride (Urben, 1995).
- Preparation of iron(III) chloride from iron powder and chlorine gas using a chlorinated pyridine solvent resulted in an explosion (Urben, 1995).
- Ammonium nitrate decomposes violently and may explode in the presence of 0.1% of iron(III) chloride (Urben, 1995; Lewis, 1996).
- Chemical interaction between ammonium salt, galvanized iron and ammonia may lead to the formation of the explosive compound tetraamminezinc peroxodisulfate (Urben, 1995).
- In the presence of iron(II) catalysts, oxidative rearrangement of 2-amino-4-methyloxazole to 4-hydroperoxy-5-hydroxy-4-methylimidazolidin-2-one needs to be controlled carefully because the latter may become explosive at ambient temperature (Urben, 1995).
- Maximum temperatures of 1090 degrees C were observed on ignition of explosive mixtures (1:1 wt) of iron and potassium dichromate (Urben, 1995).
- The reaction between iron and chlorine trifluoride occurs at ambient or slightly elevated temperatures, is violent and often causes a fire (Urben, 1995; Lewis, 1996)
- Rubbing sodium acetylide in mortar containing finely divided iron may result in a violent reaction (Lewis, 1996; Urben, 1995).
- Violent dissolution of iron takes place in the presence of slightly acidic ammonium peroxodisulfate (Urben, 1995; Lewis, 1996).
DUST/VAPOR HAZARD
- Heating of oily iron dust in a collecting vessel under oxidative conditions resulted in vaporization (of oil), ignition, and subsequent explosion (Urben, 1995; Lewis, 1996).
- Rust-containing dust violently react with hydrogen peroxide (Urben, 1995).
- For dust, explosion potential is moderate when exposed to heat or flame (HSDB , 1999).
REACTIVITY HAZARD
- Iron becomes more reactive as it is more finely divided. Ultrafine iron powder is pyrophoric and has the potential to explode (Lewis, 1996).
- In the presence of air and water or oil:
Powdered iron may undergo reaction with water, giving off the flammable gas hydrogen. The heat produced during this chemical reaction may be sufficiently high to ignite the hydrogen gas (AAR, 1998). Iron is a strong reducing agent. It readily oxidizes in the presence of moist air. When hot, it reacts with steam, yielding iron oxide and hydrogen gas (Lewis, 1997). Wet iron dust may ignite during drying (Lewis, 1996).
Hot filtration of aqueous liquor from reduction of a nitro compound with reduced iron powder resulted in formation of iron oxide residues. When air was suctioned through, these residues rapidly heated (Urben, 1995). A mixture of iron flake powder and polystyrene beads, blended together in a high-speed mixer, ignited and burned rapidly upon discharge into a polyethylene bag. Ignition may have been due to rapid oxidation of the finely divided metal and/or static discharge. Surface coating the iron powder with stearic acid prevented ignition (Urben, 1995). Rust was found to catalyze the spontaneous, exothermic reaction between iron powder or turnings with water in the absence of chlorides (Urben, 1995).
- In the presence of acetaldehyde:
- In the presence of chloric acid:
- In the presence of chloroformamidinium nitrate:
- In the presence of bromine pentafluoride:
At ambient or slightly elevated temperatures, reaction between bromine pentafluoride and iron powder is violent and may lead to ignition (Urben, 1995; Lewis, 1996).
- In the presence of chlorine:
An explosion occurred when liquid chlorine was added to carbon disulfide in an iron cylinder, but not when glassware was used. The explosion was due to the iron-catalyzed chlorination of carbon disulfide to carbon tetrachloride (Urben, 1995). Preparation of iron(III) chloride from iron powder and chlorine gas using a chlorinated pyridine solvent resulted in an explosion. These reactions were accompanied by formation of heat and evolution of hydrogen chloride (Urben, 1995). Iron ignites in dry chlorine gas at ambient temperature (Urben, 1995).
- In the presence of chlorine trifluoride:
The reaction between iron and chlorine trifluoride occurs at ambient or slightly elevated temperatures, is violent, and often causes a fire (Urben, 1995; Lewis, 1996). The severity of the reaction may depend on the state of subdivision (Urben, 1995).
- In the presence of fluorine:
In liquid fluorine, iron powder (100-mesh, but not 20-mesh) ignites (Urben, 1995). Powdered iron reacts with fluorine below redness (incandescence) (HSDB , 1999). Mixture of iron and phosphorus may become incandescent when heated (HSDB , 1999).
- In the presence of ammonium nitrate:
- In the presence of ammonium peroxodisulfate:
- In the presence of dinitrogen tetraoxide:
- In the presence of hydrogen peroxide:
Iron, iron salts and rust-containing dust violently react with hydrogen peroxide (Urben, 1995). In the presence of iron(II) catalysts, oxidative rearrangement of 2-amino-4-methyloxazole to 4-hydroperoxy-5-hydroxy-4-methylimidazolidin-2-one needs to be controlled carefully because the latter may become explosive at ambient temperature (Urben, 1995). In the presence of trace amounts of manganese dioxide, addition of hydrogen peroxide to powdered iron results in ignition upon contact (Urben, 1995). In peroxide handling systems, iron oxide (especially rust) must be thoroughly excluded. This applies to both parent metals and their alloys (Urben, 1995).
- In the presence of nitryl fluoride:
Passing mildly warmed nitryl fluoride over iron results in glowing or white incandescence of the fluoride (Urben, 1995). Ignition occurs on contact between iron, nitryl fluoride, and heat (Lewis, 1996).
- In the presence of peroxyformic acid:
Addition of 2-3 drops of approximately 90% peroxyformic acid to iron powder results in very rapid autocombustion only if traces of manganese dioxide are present (Urben, 1995). Iron ignites on contact with peroxyformic acid (Lewis, 1996).
- In the presence of potassium dichromate:
Maximum temperatures of 1090 degrees C were observed on ignition of explosive mixtures (1:1 wt) of iron and potassium dichromate (Urben, 1995). Iron ignites on contact with potassium dichromate (Lewis, 1996).
- In the presence of potassium perchlorate:
- In the presence of sodium peroxide:
- In the presence of sodium acetylide:
- In the presence of diethyl sulfate:
Diethyl sulfate, stored in a sealed iron drum, was hydrolyzed by water in the moisture to sulfuric acid, leading to corrosion of the metal, generation of hydrogen, development of high internal pressure and rupture of the drum (Urben, 1995).
EVACUATION PROCEDURES
- Editor's Note: This material is not listed in the Table of Initial Isolation and Protective Action Distances.
- SPILL - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171(ERG, 2004)
Increase, in the downwind direction, as necessary, the isolation distance of at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids in all directions.
- FIRE - PUBLIC SAFETY EVACUATION DISTANCES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
If tank, rail car or tank truck is involved in a fire, ISOLATE for 800 meters (1/2 mile) in all directions; also, consider initial evacuation for 800 meters (1/2 mile) in all directions.
- PUBLIC SAFETY MEASURES - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
CALL Emergency Response Telephone Number on Shipping Paper first. If Shipping Paper not available or no answer, refer to appropriate telephone number: MEXICO: SETIQ: 01-800-00-214-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5559-1588; For calls originating elsewhere, call: 011-52-555-559-1588.
CENACOM: 01-800-00-413-00 in the Mexican Republic; For calls originating in Mexico City and the Metropolitan Area: 5550-1496, 5550-1552, 5550-1485, or 5550-4885; For calls originating elsewhere, call: 011-52-555-550-1496, or 011-52-555-550-1552; 011-52-555-550-1485, or 011-52-555-550-4885.
ARGENTINA: CIQUIME: 0-800-222-2933 in the Republic of Argentina; For calls originating elsewhere, call: +54-11-4613-1100.
BRAZIL: PRÓ-QUÍMICA: 0-800-118270 (Toll-free in Brazil); For calls originating elsewhere, call: +55-11-232-1144 (Collect calls are accepted).
COLUMBIA: CISPROQUIM: 01-800-091-6012 in Colombia; For calls originating in Bogotá, Colombia, call: 288-6012; For calls originating elsewhere, call: 011-57-1-288-6012.
CANADA: UNITED STATES:
For additional details see the section entitled "WHO TO CALL FOR ASSISTANCE" under the ERG Instructions. As an immediate precautionary measure, isolate spill or leak area in all directions for at least 50 meters (150 feet) for liquids and at least 25 meters (75 feet) for solids. Keep unauthorized personnel away. Stay upwind.
- AIHA ERPG Values for CAS7439-89-6 (AIHA, 2006):
- DOE TEEL Values for CAS7439-89-6 (U.S. Department of Energy, Office of Emergency Management, 2010):
Listed as Iron TEEL-0 (units = mg/m3): 2 TEEL-1 (units = mg/m3): 6 TEEL-2 (units = mg/m3): 40 TEEL-3 (units = mg/m3): 75 Definitions: TEEL-0: The threshold concentration below which most people will experience no adverse health effects. TEEL-1: The airborne concentration (expressed as ppm [parts per million] or mg/m(3) [milligrams per cubic meter]) of a substance above which it is predicted that the general population, including susceptible individuals, could experience notable discomfort, irritation, or certain asymptomatic, nonsensory effects. However, these effects are not disabling and are transient and reversible upon cessation of exposure. TEEL-2: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience irreversible or other serious, long-lasting, adverse health effects or an impaired ability to escape. TEEL-3: The airborne concentration (expressed as ppm or mg/m(3)) of a substance above which it is predicted that the general population, including susceptible individuals, could experience life-threatening adverse health effects or death.
- AEGL Values for CAS7439-89-6 (National Research Council, 2010; National Research Council, 2009; National Research Council, 2008; National Research Council, 2007; NRC, 2001; NRC, 2002; NRC, 2003; NRC, 2004; NRC, 2004; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; United States Environmental Protection Agency Office of Pollution Prevention and Toxics, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2009; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2008; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2007; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2005; National Advisory Committee for Acute Exposure Guideline Levels for Hazardous Substances, 2006; 62 FR 58840, 1997; 65 FR 14186, 2000; 65 FR 39264, 2000; 65 FR 77866, 2000; 66 FR 21940, 2001; 67 FR 7164, 2002; 68 FR 42710, 2003; 69 FR 54144, 2004):
- NIOSH IDLH Values for CAS7439-89-6 (National Institute for Occupational Safety and Health, 2007):
CONTAINMENT/WASTE TREATMENT OPTIONS
SPILL OR LEAK PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004) Do not touch or walk through spilled material. Stop leak if you can do it without risk. Prevent dust cloud. Avoid inhalation of asbestos dust.
RECOMMENDED PROTECTIVE CLOTHING - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004) LAND SPILLS Liquid or solid material should be contained in a pit, pond, lagoon or other holding area (AAR, 1998). Covering solids with plastic sheet should prevent dissolution in rain or fire fighting water (AAR, 1998). Surface flow should be diked using soil, sandbags, foamed polyurethane, or foamed concrete (AAR, 1998).
WATER SPILLS Spill travel should be limited by using natural barriers or oil spill booms (AAR, 1998). Material should be trapped at bottom of body of water by utilizing natural deep water pockets, excavated lagoons, or sand bag barriers (AAR, 1998). Use suction hoses to remove trapped material (AAR, 1998).
Suggested disposal methods are landfilling (Sittig, 1991) or salvage (OHM/TADS , 1999).
SMALL SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004) SMALL DRY SPILL PRECAUTIONS - EMERGENCY RESPONSE GUIDEBOOK, GUIDE 171 (ERG, 2004)
Suggested disposal methods are landfilling (Sittig, 1991) or salvage (OHM/TADS , 1999). Soluble iron salts can be treated either with Sodium-bicarbonate (NaHCO3, from grocery store) or with a cation exchanger (water softener supplies). The precipitated hydroxides can then be removed with an electromagnet (salvage operators) (OHM/TADS , 1999). Waste management activities associated with material disposition are unique to individual situations. Proper waste characterization and decisions regarding waste management should be coordinated with the appropriate local, state, or federal authorities to ensure compliance with all applicable rules and regulations.
-ENVIRONMENTAL HAZARD MANAGEMENT
POLLUTION HAZARD
- Groundwater naturally contains 0.01-10 ppm of iron. In brine, thermal springs and mine areas, concentrations up to 1000 ppm may be found (Dragun, 1988).
- Four naturally occurring isotopes (Lewis, 1997; Budavari, 1996; HSDB , 1999):
54 (5.82%) 56 (91.66%) 57 (2.19%) 58 (0.33%)
- Four artificial, radioactive isotopes (Lewis, 1997; Budavari, 1996):
- Although iron occurs in pure form, it is more commonly found as oxide or carbonate (Clayton & Clayton, 1994; Lewis, 1998), or as sulfide or silicate (Clayton & Clayton, 1994).
Important source ores (Budavari, 1996; Harbison, 1998; HSDB , 1999; ILO, 1998; Lewis, 1997) Zenz, 1994):
- Iron is found in 5.1% of the earth's crust. It is the second most abundant metal (Budavari, 1996) and the fourth most abundant element (Clayton & Clayton, 1994).
- The content in the earth's crust is 50,000 ppm (Clayton & Clayton, 1994).
- It is believed that the earth's core consist mainly of iron (Budavari, 1996).
- Native iron, found in Greenland, exists as small grains or nodules in basalt (HSDB , 1999).
ENVIRONMENTAL FATE AND KINETICS
TERRESTRIAL The natural color of soil is largely influenced by its redox status, which in turn strongly influences the oxidative state of Fe (Dragun, 1988). Red, yellow and reddish brown soil colors are found mainly under oxidizing conditions. Reducing soil conditions result in gray, black or subdued soil colors (Dragun, 1988).
Using oil field brine as dust control or to de-ice roads may lead to increased dissolution of iron in the soil to replenish the concentration of uncomplexed iron in water (Dragun, 1988). Iron is extensively absorbed by a fulvic acid (Dragun, 1988).
OTHER Iron concentrations of 500 mg/L of waste water sludge completely inhibited sludge digestion. Digestion inhibition was already seen at 300 mg/L. No gas production was observed at concentrations of 1500 to 2000 mg/L (OHM/TADS , 1999). In aqueous solution, reduction of ferrous iron to ferric iron may be coupled to the production of superoxide anion and peroxide, resulting in the reduction of molecular oxygen (Lewis, 1998). In the presence of iron, reaction between superoxide anion and peroxide may result in generation of the extremely toxic hydroxyl radical, with concurrent release of oxygen (Lewis, 1998). Homolytic cleavage of peroxide into hydroxyl ion and the highly reactive hydroxyl radical is catalyzed by iron(II) ions (Fenton reaction) (Klaassen, 1996).
ENVIRONMENTAL TOXICITY
- Freshwater Toxicity Values (OHM/TADS , 1999):
LDLo - CARP: 0.9 ppm -- pH 5.5 LDLo - PIKE, TENCH, TROUT: 1 ppm -- pH 5-6.7 LDLo - DOGFISH: 5 ppm for 3H LDLo - TROUT: 10 ppm for 0.1H
- Saltwater Toxicity Values (OHM/TADS , 1999):
TLm - MARINE FISH: 14 ppm for 48H LC50 - PRAWN: 39 ppm for 48H LC50 - SHRIMP: 56 ppm for 48H LC50 - COCKLE: 190 ppm for 48H LC50 - CRAB: 90-100 ppm for 48H
- Other Toxicity Values (OHM/TADS , 1999):
-PHYSICAL/CHEMICAL PROPERTIES
MOLECULAR WEIGHT
- FERRIC PYROPHOSPHATE CITRATE: 1313 daltons (Prod Info TRIFERIC(R) not applicable solution, 2015)
- IRON: 55.85 (Budavari, 1996)
- IRON SUCROSE: Approximately 34,000 to 60,000 daltons (Prod Info Venofer(R) intravenous injection, 2015)
- SODIUM FERRIC GLUCONATE COMPLEX: 289,000 to 440,000 daltons (Prod Info Ferrlecit intravenous injection, 2011)
DESCRIPTION/PHYSICAL STATE
- FERRIC PYROPHOSPHATE CITRATE is a clear solution that is slightly yellow/green in color (Prod Info TRIFERIC(R) not applicable solution, 2015).
- IRON is a silvery-white or gray, soft, ductile, malleable, somewhat magnetic metal, that takes on a bright polish. In powder form, it is black to gray (HSDB, 2005; Budavari, 1996).
Iron (chemical symbol Fe, from the Latin word ferrum) has the atomic number 26 and belongs to the Group VIII transition elements of the periodic table (Clayton & Clayton, 1994). Iron can be rolled, hammered, and bent, particularly when red hot (Budavari, 1996). Iron's magnetism is held only after hardening (as alloy steel, such as Alnico) (Budavari, 1996). Iron is supplied as ingots, powder, wire, sheets, and other forms (Budavari, 1996). Iron is stable in dry air and readily oxidizes in moist air, forming "rust" (Budavari, 1996). Commercial forms of iron usually contain carbon (C), phosphorus (P), silicon (Si), sulfur (S) and manganese (Mn) (Budavari, 1996). Iron is the only metal that can be tempered (Lewis, 1997).
- IRON SUCROSE is a brown, aqueous solution with an osmolarity of 1250 milliosmoles/L (Prod Info Venofer(R) intravenous injection, 2015).
- SODIUM FERRIC GLUCONATE COMPLEX is a deep red solution (Prod Info Ferrlecit intravenous injection, 2011).
PH
- IRON SUCROSE: 10.5 to 11.1 (Prod Info Venofer(R) intravenous injection, 2015)
- SODIUM FERRIC GLUCONATE COMPLEX: 7.7 to 9.7 (Prod Info Ferrlecit intravenous injection, 2011)
VAPOR PRESSURE
- 1 mmHg (at 1787 degrees C) (HSDB, 2005)
DENSITY
- OTHER TEMPERATURE AND/OR PRESSURE
- TEMPERATURE AND/OR PRESSURE NOT LISTED
PURE: 7.86 (HSDB, 2005; OHM/TADS, 2005; Budavari, 1996; Clayton & Clayton, 1994) CAST: 7.76 (Budavari, 1996) WROUGHT: 7.25 to 7.78 (Budavari, 1996) STEEL: 7.6 to 7.78 (Budavari, 1996)
FREEZING/MELTING POINT
PURE: 1535 degrees C (HSDB, 2005; OHM/TADS, 2005; Budavari, 1996; Clayton & Clayton, 1994; Lewis, 1996) PURE: 1536 degrees C (Lewis, 1997) CAST: 1000 to 1300 degrees C (HSDB, 2005; Budavari, 1996) WROUGHT: 1500 degrees C (HSDB, 2005; Budavari, 1996) STEEL: 1300 degrees C (HSDB, 2005; Budavari, 1996)
BOILING POINT
- 3000 degrees C (HSDB, 2005; OHM/TADS, 2005; Budavari, 1996; Lewis, 1997)
- 2750 degrees C (Clayton & Clayton, 1994)
SOLUBILITY
Readily attacked by diluted mineral acids (HSDB, 2005; Budavari, 1996) Not appreciably attacked by cold concentrated sulfuric acid (H2SO4) or nitric acid (HNO3), but attacked by hot acids (HSDB, 2005; Budavari, 1996) Attacked or dissolved by organic acids (HSDB, 2005; Budavari, 1996) Soluble in acids (Clayton & Clayton, 1994) Dissolves in sulfuric and hydrochloric acid, and in cold dilute nitric acid (Lewis, 1997) Insoluble in alkali solutions (HSDB, 2005)
OTHER/PHYSICAL
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