CAS RN:118-96-7

Health Effects

    • A) TOXICOLOGY: Oxidization of iron in the hemoglobin ring to the ferric form leads to the inability of hemoglobin to bind or transport oxygen. Heme in the ferric (Fe3+) state also induces a hemoglobin conformational change increasing oxygen affinity of the remaining binding sites and decreasing the oxygen dissociation. Cyanosis occurs when more than 1.5 g/dL of hemoglobin is in the methemoglobin form, compared to 5 g/dL of deoxyhemoglobin to yield similar cyanosis. Methemoglobinemia may result from acquired or congenital causes (hemoglobin M or cytochrome b5 reductase deficiency). Acquired methemoglobinemia is caused by strong oxidizing agents, most commonly local anesthetics and dapsone, though many drugs have been implicated. In addition, recreational drugs, industrial chemicals, as well as medical conditions such as pediatric gastrointestinal infections, sepsis, surgery, or sickle cell crisis are rarely capable of inducing acquired methemoglobinemia.
    • B) EPIDEMIOLOGY: Methemoglobinemia is common, but clinically significant symptoms are uncommon, and severe toxicity is rare.
      • 1) The severity of the clinical effects observed is dependent on the quantity of methemoglobin present and are referable to the decreased oxygen-carrying capacity of the blood.
      • 2) MILD TO MODERATE TOXICITY: Cyanosis occurs at methemoglobin levels more than 1.5 g/dL. However, most patients do not have the severe ischemic symptoms that might be expected from other disease processes with the same degree of cyanosis. Cyanosis that is unresponsive to supplemental oxygen, or significant cyanosis in a patient with minimal symptoms should raise the suspicion of methemoglobinemia.
      • 3) SEVERE TOXICITY: Clinical severity increases with increased methemoglobin levels. Patients that have methemoglobin levels greater than 30% are more likely to develop severe symptoms.
      • 4) ACID/BASE: Metabolic acidosis may develop secondary to tissue hypoxia or seizures.
      • 5) CARDIOVASCULAR: Tachycardia is common. Dysrhythmias and hypotension may occur in severe cases. Myocardial infarction and abrupt cardiac arrest are rare manifestations of severe methemoglobinemia.
      • 6) GASTROINTESTINAL: Nausea and vomiting may occur.
      • 7) HEMATOLOGIC: Chocolate brown blood is classic. Hemolytic anemia may develop with some agents that cause methemoglobinemia. Hemolysis may occur in individuals with glucose-6-phosphate dehydrogenase (G6PD) deficiency.
      • 8) NEUROLOGIC: CNS effects include headache, dizziness, altered consciousness, confusion, lethargy progressing to coma, seizures and syncope which usually occurs secondary to hypoxia at levels typically of 20% or greater.
      • 9) RESPIRATORY: Dyspnea and tachypnea may occur. 1
      • 0) RISK FACTORS: Patients with underlying medical conditions such as chronic obstructive pulmonary disease (COPD), anemia or coronary artery disease, recent surgery, or increased metabolic demand (ie, shock, infection) are more susceptible to developing symptoms. The very young (less than 3 months old) and the elderly are at greater risk of developing symptomatic methemoglobinemia. In addition, individuals with a genetic deficiency of G-6-PD or nicotinamide adenine dinucleotide methemoglobin reductase are at greater risk of developing methemoglobinemia.
  • A) In the United States, commercially prepared formulas and foods for infants do not put the infant at risk for methemoglobinemia; however, infants fed formula prepared with well water remain at risk for methemoglobinemia secondary to nitrate poisoning.
    • A) A SPECIFIC REVIEW on the clinical effects and treatment of individuals exposed to this agent HAS NOT YET BEEN PREPARED. The following pertains to the GENERAL EVALUATION and TREATMENT of individuals exposed to potentially toxic chemicals.
      • 1) Exposed individuals should have a careful, thorough medical history and physical examination performed, looking for any abnormalities. Exposure to chemicals with a strong odor often results in such nonspecific symptoms as headache, dizziness, weakness, and nausea.
      • 1) Many chemicals cause irritation of the eyes, skin, and respiratory tract. In severe cases respiratory tract irritation can progress to ARDS/acute lung injury, which may be delayed in onset for up to 24 to 72 hours in some cases.
      • 2) Irritation or burns of the esophagus or gastrointestinal tract are also possible if caustic or irritant chemicals are ingested.
      • 1) A number of chemical agents produce an allergic hypersensitivity dermatitis or asthma with bronchospasm and wheezing with chronic exposure.
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