Ferrous sulfate has many useful applications, all of which involve potential contact with handlers as well as the environment. As ferrous sulfate is a chemical, it is not 100% safe for people or nature and consequently requires handling with care. Here, we will discuss its toxicity to humans and the environment.
Toxicity to humans
Ferrous sulfate is fairly non-toxic, with an acute oral LD50 at 132-881 mg Fe/kg (rat) and chronic oral NOAEL 57-65 mg Fe/kg/d (rat,90 days) (1). However, it may cause skin and eye irritation. If inhaled, it may also cause headaches, nausea, and respiratory irritations. This chemical is not listed as a carcinogen by NTP, IARC, or OSHA.
The common recognized injury from ferrous sulfate is local tissue irritation. In short, the irritating action is often from hydrolysis to form sulfuric acid and may occur from ingestion, skin or eye contact, or inhalation of dust and mists. Remove victims from contaminated areas.
- Routes of Entry: Skin or eye contact, ingestion, or inhalation of dust and mists.
- SKIN / EYES: May cause corneal burns or severe irritation in eyes. Fumes or mists may cause irritation or burns to skin.
- INGESTION:Oral and gastrointestinal irritation. Local tissue damage. In addition, nausea, vomiting, diarrhea, and gastrointestinal bleeding may follow. Can be fatal if swallowed in sufficient quantities.
- INHALATION:Irritation of the respiratory system. Long term exposure may cause bronchial irritation, coughing, and bronchial pneumonia. Medical conditions generally aggravated are acute and chronic respiratory diseases.
Toxicity to the environment
Single-dose toxicity testing indicates ferrous sulfate is low in toxicity to birds. However it is moderately toxic to mammals, fish, and other aquatic organisms.
Sealife
Plantlife
Animals
In brief, the forms of iron that may result in toxicity are:
- Ferrous fumarate
- Ferrous sulfate
- Ferric phosphate
- Ferrous carbonate
Toxic levels of iron cause damage to the stomach and intestinal lining. It can also cause severe liver damage and heart damage.
Dogs are more easily affected by iron overdoses than people because they do not have a way to excrete excessive iron from their bodies. If low doses of iron are given over a period of time, toxicity can still develop since their body cannot get rid of the iron already present. (4)
A study in Clinical Toxicology Journal found that ferrous sulfate also can be toxic to wildlife in high enough doses, mostly damaging their digestive tract. (5)
Accidental release of ferrous sulfate
According to its safety data sheet, these precautions should be taken for an accidental release of ferrous sulfate:
- Wear PPE appropriate for handling the material.
- No smoking or eating in spill areas.
- Absorb small spills with sand or vermiculite.
- Place contaminated material in appropriate container for disposal.
- If spilled on the ground, the affected area should be removed to a depth of 1 to 2 inches and after that placed in an appropriate container.
- Handle large spills according to a predetermined plan.
- Do not flush material to public sewer systems, or likewise, to any waterways.
- Wear appropriate protective clothing and equipment during cleanup activities.
- Ensure adequate decontamination of tools and equipment following cleanup.
- Adequate ventilation is required when neutralizing spills / leaks.
Environmentally friendly ferrous sulfate practices at Affinity Chemical
Affinity Chemical adheres to the safest handling practices to protect the environment as well as our people and customers who work with ferrous sulfate. Moreover, we produce our ferrous in a manner which minimizes pollution. Learn more about our zero-emission (aka “green”) facilities.
Need ferrous sulfate? Give us a call today!
Resources
Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.
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From: Department of Medicine 4, Christian Medical College, Vellore, Tamil Nadu, India
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From: Department of Medicine 4, Christian Medical College, Vellore, Tamil Nadu, India
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From: Department of Medicine 4, Christian Medical College, Vellore, Tamil Nadu, India
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Acute iron toxicity is usually seen in children with accidental ingestion of iron-containing syrups. However, the literature on acute iron toxicity with suicidal intent in adults is scant. We report, the first instance of two adults with fatal ingestion of a single drug overdose with iron tablets from India. Two young adults developed severe gastro-intestinal bleeding and fulminant hepatic failure 48 h after deliberate consumption of large doses of iron tablets. Serum iron levels measured 36 h after ingestion were normal presumably due to the redistribution of iron to the intracellular compartment. Despite aggressive supportive management in medical intensive care unit of a tertiary care hospital, the patients succumbed to the toxic doses of iron.
Keywords: Adults, fatal, iron tablets, overdose
Intentional iron tablets overdose in adults is uncommon. The majority of acute iron toxicity cases occur in children less than 5 years of age who present with accidental ingestion of iron supplements.[1] Clinical outcome is variable and depends on the quantity of iron ingested, other drugs ingested and the delay to treatment. Severe iron overdose can cause acute hepatic necrosis and lead to multi-organ failure and death.[2,3] Most of the literature on iron overdose in adults is on multiple-drug overdose usually with paracetamol or other hepatotoxic drugs. This report is unique in that our patients allegedly consumed only iron tablets and both died as a result of direct toxicity of iron alone.
A 25-year-old lady allegedly consumed 200 tablets of ferrous sulphate with suicidal intent. The total dose amounted to 13.5 g of elemental iron (270 mg/kg). She had abdominal pain with vomiting and was given gastric lavage along with supportive care at a primary health center. She was referred to our hospital after 24 h of ingestion for further management. At presentation, she was hemodynamically stable with a normal pulse rate and blood pressure. Complete blood count (CBC) showed hemoglobin-14.1 g/dl, total white blood cell (WBC) count-19,300/cu mm (90% neutrophils) and platelet count-283,000/cu mm. Serum iron level as measured by spectrophotometric analysis was 73 μg/dl (normal range 40-145 μg/dl) and the total iron binding capacity was 350 g/dl (normal range 250-350 μg/dl). Liver function tests (LFT) showed marked elevation in liver enzymes (serum glutamic oxaloacetic transaminase [SGOT]-11,000 U/L and serum glutamic pyruvic transaminase [SGPT]-11,420 U/L), total bilirubin (2.6 mg%), direct bilirubin (1.1 mg%), protein (4.6 g%), albumin (2.8 g%) and alkaline phosphatase (161 U/L). Serum creatinine was 1.9 mg%, bicarbonate was 15 mmol/l and blood sugar level was 81 mg/dl. Chelation therapy with desferrioxamine was started as an intravenous infusion of 15 mg/kg/h and increased to 25 mg/kg/h. 24 h after admission, she developed severe gastro-intestinal (GI) bleeding and went into a state of circulatory shock. Hemoglobin dropped from 14.1 to 7 gm%. Activated partial thromboplastin time (aPTT) was 71.3 s and prothrombin time (PT) was 24.5 with an international normalized ratio (INR) of 1.9. Arterial blood gas analysis showed severe metabolic acidosis with a pH of 6.96. She became progressively drowsy with un-recordable blood pressure, for which she was intubated and ventilated and supported with multiple inotropes. Aggressive blood product supports were given and hemodialysis was initiated for metabolic acidosis. Despite these measures, she continued to deteriorate and died within 36 h of admission due to multi-organ failure.
A 17-year-old lady allegedly consumed 300 tablets of ferrous sulfate amounting to a total dose of 20 g of elemental iron (400 mg/kg). She was initially taken to a local hospital with abdominal pain and vomiting and gastric lavage given. Further treatment details are unknown. After 48 h, she developed multiple episodes of hematemesis and melena and progressively became oliguric and drowsy. She was intubated and referred to our hospital 48 h after ingestion. At presentation, pulse and blood pressure were not recordable and resuscitated with colloids. CBC profile showed hemoglobin-2.8 g/dl, total WBC count-4,500/cu mm, platelet count-52,000/cu mm. LFT showed marked elevation in liver enzymes (SGOT-4,250 U/L and SGPT-3,908 U/L), total bilirubin (0.7 mg%), direct bilirubin (0.5 mg%), protein (2.2 g%), albumin (0.7 g%) and alkaline phosphatase (72 U/L). Serum iron levels were not measured as the patient presented more than 48 hours after ingestion. Serum creatinine was 2.4 mg%, bicarbonate was 10 mmol/l, blood sugar level was 27 mg/dl, aPTT was >3 min and PT was >2 min with an INR of >10. Aggressive supportive management along with desferrioxamine as a 15 mg/kg/h infusion was initiated. Hemodialysis was planned, but could not be instituted as the patient had refractory hypotension and had a cardiac arrest within 2 hours of presentation. Despite ventilator and inotropic supports, she continued to deteriorate with circulatory collapse and could not be resuscitated. She died within 3 h of presentation to our hospital.
Iron is the most abundant trace element in the body and is essential in most biological systems. Acute iron poisoning causes GI, cardiovascular, metabolic, hepatic and central nervous system toxicity. This is due to a direct caustic effect of iron on the GI mucosa and the toxicity of free unbound iron in the circulation. Clinically, iron toxicity manifests in four stages. Stage I/stage of GI toxicity (0-6 h since ingestion) causes vomiting, hematemesis, abdominal pain and lethargy; Stage II/stage of apparent stabilization (6-12 h since ingestion) when symptoms subside; Stage III/stage of mitochondrial toxicity and hepatic necrosis (12-48 h since ingestion) where patients may develop acute liver failure, coagulopathy, acute tubular necrosis, metabolic acidosis and shock. Patients who survive this phase go into Stage IV/stage of gastric scarring (4-6 weeks since ingestion) characterized by gastric scarring and pyloric stricture.[2]
Acute liver failure and cardiovascular collapse are the main causes of death due to iron overdose. In 2005, a review of 70 patients with iron toxicity showed hepatotoxicity in 13 patients with severe toxicity (alanine transaminase/SGPT >1,000 U/L) in nine patients. Ten of these patients (all <18 years) died with one of them requiring liver transplantation.[3] Kozaki et al. reported a patient with massive iron ingestion successfully treated with liver transplantation.[4] A literature search for adult cases of iron poisoning associated with hepatotoxicity yielded only three cases that were older than 15 years of age.[5] The only reported adult death directly attributed to iron toxicity without ingestion of other drugs was that of a 30-year-old pregnant lady who consumed 70 mg/kg of elemental iron.[6] She died of fulminant hepatic failure 2 weeks later. Ingestion of more than 60 mg/kg is associated with high toxicity and the lethal dose of elemental iron is said to be 200-250 mg/kg.[7]
A serum iron level of more than 350 μg/dl between 2 and 6 h post-ingestion is supposed to indicate a significant intoxication and levels more than 500 μg/dl suggest serious risk of acute liver failure. However, serum iron levels as measured by spectrophotometric analysis may not be reliable in diagnosis or prognostication if the patient presents late as iron is redistributed to the intracellular compartment within 6-12 h.[2,8] There is also a possibility of idiosyncratic reaction to iron. Our patients presented more than 24 h after ingestion of the tablets, which explains normal serum iron levels with severe toxicity.
Treatment of acute iron poisoning includes early decontamination of the gut, chelation with parenteral desferrioxamine and intensive supportive therapy. Administration of desferrioxamine after acute intoxication may color the urine a pinkish red, a phenomenon termed “vin rose urine.” Whole bowel irrigation (WBI) may be useful in children if abdominal X-ray reveals radio opaque iron tablets beyond the pylorus or throughout the GI tract.[7] X-ray abdomen in both our patients did not show any radio-opaque pills and WBI was not done.
In conclusion, though iron tablets overdose with suicidal intent is uncommon, delay in diagnosis and administration of chelation therapy may rapidly allow progession of toxicity to multi-organ failure and death even in adults. Serum iron levels may not be reliable for diagnosis and prognostication if the patient presents late.
Source of Support: Nil
Conflict of Interest: None declared.
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