Lab result explainedBlood count (CBC)Last updated November 11, 2026

Methemoglobin (MetHb): normal range, what a high level means and the causes of methemoglobinemia

Methemoglobin (MetHb) · CO-oximetry (arterial or venous blood gas with co-oximetry) · reported in percent of total hemoglobin (% MetHb); some labs also report g/dL

Methemoglobin (MetHb) is hemoglobin whose iron has been oxidized from the ferrous (Fe2+) to the ferric (Fe3+) state, which leaves it unable to bind oxygen. A small amount forms all the time and is constantly converted back by an enzyme in red cells, so a normal methemoglobin level is under 1 to 2 percent of total hemoglobin. When the level climbs above that, from a drug, a chemical or a rare inherited enzyme deficiency, the condition is called methemoglobinemia: the blood turns chocolate brown, the skin and lips take on a blue-gray tinge at around 10 to 15 percent, and levels above 20 to 30 percent cause headache, breathlessness, confusion and a racing heart. Above 50 percent there is a risk of seizures, coma and death, and above 70 percent it is usually fatal without treatment.

In practice almost every case is acquired, and most are caused by medicines. Benzocaine sprays and gels used to numb the throat before endoscopy or sold over the counter for teething, mouth ulcers and sore throats are the single best-known trigger and can push methemoglobin above 30 percent within an hour of a few sprays; dapsone, used for skin conditions and infection prophylaxis, is the commonest cause of a chronic, lower-grade rise; and nitrates and nitrites, from contaminated well water in infants, inhaled poppers, some fertilizers and industrial chemicals, account for most of the rest. Infants under 6 months are especially vulnerable because their reducing enzyme is immature.

The clue that often leads to the test is a pulse oximeter stuck around 85 percent that does not improve with oxygen, in someone who looks blue but is less breathless than that reading would suggest. A blood gas then shows a normal calculated oxygen level, a mismatch called the saturation gap, and the co-oximeter reports the methemoglobin percentage directly. Treatment, for people who are symptomatic or above about 20 to 30 percent, is intravenous methylene blue, which restores normal hemoglobin within an hour.

MetHb at a glance

What it is: the fraction of hemoglobin with oxidized (ferric) iron that cannot carry oxygen, measured by co-oximetry on an arterial or venous sample.
Normal: under 1–2% of total hemoglobin (most people 0.5–1%); a pulse oximeter cannot measure it and misreads it.
Symptoms by level: 10–20% blue-gray skin and lips and chocolate-colored blood; 20–30% headache, anxiety, fatigue, fast heart rate, breathlessness; 30–50% confusion, dizziness, chest pain; above 50% seizures, coma, arrhythmia; above 70% usually fatal.
Common causes: benzocaine sprays and gels, dapsone, prilocaine and lidocaine, nitrates and nitrites (well water in infants, poppers), aniline dyes, naphthalene mothballs, primaquine, phenazopyridine, rasburicase.
Pulse-ox clue: saturation stuck around 82–88% despite oxygen, with a normal oxygen level on the blood gas (saturation gap).
Treatment: stop the cause; methylene blue for symptoms or levels above about 20–30% (lower if anemic or with heart or lung disease); it does not work and can cause hemolysis in G6PD deficiency.

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What MetHb measures

Hemoglobin carries oxygen only when the iron at the center of each heme group is in the reduced ferrous state. Everyday oxidative stress converts about 3 percent of hemoglobin to the ferric form each day, and the enzyme cytochrome b5 reductase (NADH-methemoglobin reductase) in red cells converts it back, keeping the steady-state level under about 1 percent. A second, normally minor pathway uses NADPH, and it is this pathway that methylene blue switches on to treat poisoning. Methemoglobin cannot bind oxygen and, worse, it makes the remaining normal hemoglobin hold on to its oxygen more tightly, so the oxygen deficit in tissues is greater than the percentage alone suggests.

The test is a co-oximetry measurement, usually part of an arterial or venous blood gas. The analyzer shines light at multiple wavelengths through the lysed sample and separates oxyhemoglobin, deoxyhemoglobin, carboxyhemoglobin and methemoglobin by their absorption spectra, reporting each as a percentage of total hemoglobin. Venous blood is adequate. Samples should be run promptly and kept cool, because methemoglobin continues to form in a tube left standing. Methylene blue and sulfhemoglobin absorb at similar wavelengths and can produce falsely high readings on some analyzers, so a repeat level is normally taken an hour or more after treatment rather than minutes after it.

The reason a pulse oximeter fails is that methemoglobin absorbs the red and infrared light used by two-wavelength oximeters almost equally, which the device interprets as a saturation of about 85 percent regardless of the true value. At low methemoglobin levels the oximeter under-reads and at very high levels it over-reads, converging on 85 percent. A blood gas analyzer, by contrast, calculates saturation from the dissolved oxygen pressure and will report a normal value, producing a saturation gap of more than 5 percentage points between the two; a gap that size with a cyanosed patient who does not improve on oxygen is methemoglobinemia until proved otherwise. Newer multi-wavelength pulse co-oximeters can estimate methemoglobin non-invasively but are less accurate than a blood sample.

Normal range for MetHb

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (percent of total hemoglobin (% MetHb); some labs also report g/dL)	Notes
Normal	Below 1–2%	Most healthy people are 0.5–1%. Some labs print an upper limit of 1.5% and others 3%; use the range on your report.
Mild elevation, usually without symptoms	3–10%	Seen with dapsone, chronic nitrate exposure and mild congenital enzyme deficiency; pulse oximetry starts to read low.
Visible cyanosis	10–20%	Blue-gray lips, fingertips and skin appear once about 1.5 g/dL of hemoglobin is methemoglobin (about 10% at a normal hemoglobin); blood drawn looks chocolate brown and does not redden in air. Often few other symptoms.
Symptomatic	20–30%	Headache, anxiety, light-headedness, fatigue, fast heart rate, shortness of breath; most guidelines recommend methylene blue at this level.
Moderate to severe	30–50%	Confusion, weakness, chest pain, dizziness, worsening breathlessness; metabolic acidosis begins.
Severe	50–70%	Seizures, coma, arrhythmias, severe acidosis; risk of death.
Usually fatal untreated	Above 70%	Tissue oxygen delivery is insufficient to sustain life.
Congenital cytochrome b5 reductase deficiency (type I)	Typically 10–35% lifelong	People are blue but generally well; treated with oral methylene blue or vitamin C for cosmetic reasons if at all.
Threshold for treatment in anemia, heart or lung disease, or infants	Symptoms at lower percentages; treat at 10–20% or with any symptoms	A smaller oxygen reserve means less methemoglobin is tolerated.

High methemoglobin (methemoglobinemia)

A methemoglobin above 1 to 2 percent means hemoglobin is being oxidized faster than your red cells can reduce it back. The significance scales with the number, with your hemoglobin level and with how healthy your heart and lungs are. A level of 3 to 8 percent in someone taking dapsone is common and usually causes nothing more than a slightly low pulse oximeter reading, although it can worsen fatigue and breathlessness in people who are also anemic. Levels of 10 to 20 percent produce the characteristic blue-gray color of the lips and fingertips and a brown tinge to drawn blood, often with surprisingly few other complaints. Above 20 to 30 percent the oxygen deficit becomes symptomatic, and above 50 percent it becomes life-threatening.

The level is interpreted together with the oxygen reserve. Someone with a hemoglobin of 8 g/dL and a methemoglobin of 20 percent has far less functional hemoglobin than someone with a hemoglobin of 15 and the same percentage, and people with coronary disease, heart failure, COPD or sepsis, and infants, tolerate much less. For that reason treatment with methylene blue is given for any symptoms, or for a level above about 20 to 30 percent in a healthy adult, rather than waiting for a particular number; most people respond within 30 to 60 minutes, and a second dose is given if the level is still above 20 percent an hour later. Methylene blue is ineffective in G6PD deficiency and can trigger hemolysis, so exchange transfusion or hyperbaric oxygen are used instead.

Finding the cause matters as much as treating the level. An acute rise within an hour or two of a procedure almost always means a topical anesthetic (benzocaine spray for endoscopy or bronchoscopy, prilocaine or lidocaine for a block or EMLA cream over a large area in a baby). A chronic, fluctuating rise points to dapsone or another regular medication, or to a nitrate source in well water, and a rise in an infant with diarrhea and acidosis may have no external cause at all. Dapsone and its metabolites persist for days, so methemoglobin can rebound 6 to 12 hours after methylene blue and people on dapsone are usually observed for 24 to 48 hours. A lifelong mild cyanosis in an otherwise healthy person suggests one of the inherited forms.

Common causes

Benzocaine sprays, gels and lozenges
The commonest cause of severe acute methemoglobinemia in US hospital data; one or two sprays of a 20 percent benzocaine throat spray before endoscopy can raise methemoglobin above 30 to 40 percent within 20 to 60 minutes. The FDA has warned against over-the-counter benzocaine teething gels for children under 2 and advises against routine use in adults.
Dapsone
Used for dermatitis herpetiformis, leprosy, some blistering skin diseases and Pneumocystis prophylaxis; its hydroxylamine metabolite oxidizes hemoglobin continuously, giving methemoglobin of 5 to 15 percent in many users and higher in overdose. The most frequent cause of chronic elevation.
Other local anesthetics (prilocaine, lidocaine, articaine)
Prilocaine, including the prilocaine-lidocaine cream EMLA applied over large areas or under occlusion in infants, and high-dose lidocaine for nerve blocks or airway topicalization, are well-documented causes; infants and people with G6PD or reductase deficiency are at highest risk.
Nitrates and nitrites
Well water with nitrate above the EPA limit of 10 mg/L nitrate-nitrogen is converted to nitrite by gut bacteria in babies under 6 months, causing blue baby syndrome; inhaled alkyl nitrite poppers, swallowed poppers, sodium nitrite (sometimes mistaken for table salt or taken deliberately), nitroglycerin and nitroprusside infusions, and nitrate-rich vegetable purees in infants are other sources.
Aniline dyes, naphthalene and industrial chemicals
Aniline in dyes, shoe polish and marking inks, naphthalene in mothballs (especially if ingested by children), nitrobenzene, chlorates and some herbicides are absorbed through the skin or gut and are potent oxidants.
Antimalarials and antibiotics
Primaquine, chloroquine, sulfonamide antibiotics (including trimethoprim-sulfamethoxazole) and nitrofurantoin can oxidize hemoglobin, particularly in people with G6PD deficiency.
Phenazopyridine, metoclopramide, rasburicase and inhaled nitric oxide
Phenazopyridine (the urinary analgesic Pyridium) in high doses or kidney disease, metoclopramide in neonates, rasburicase in G6PD-deficient patients, and inhaled nitric oxide in intensive care all cause methemoglobinemia often enough that levels are monitored.
Infant diarrhea, acidosis and sepsis
Babies under 6 months have only about half the adult level of cytochrome b5 reductase and more easily oxidized fetal hemoglobin; dehydration, metabolic acidosis and gut infection alone can raise methemoglobin to 10 to 20 percent with no drug exposure.
Congenital cytochrome b5 reductase deficiency
An autosomal recessive condition; type I (red cell only) causes lifelong methemoglobin of 10 to 35 percent with cyanosis but good health, type II (all tissues) causes severe neurological disability. Heterozygous carriers are normal day to day but develop methemoglobinemia readily when exposed to oxidant drugs.
Hemoglobin M disease
A group of dominantly inherited hemoglobin variants with an amino-acid change near the heme iron that stabilizes the ferric state; causes cyanosis from birth (or from about 6 months for beta-chain variants), does not respond to methylene blue and needs no treatment.

Symptoms that can go with it

Blue-gray or slate-colored lips, nail beds, ears and skin that does not improve with oxygen (from about 10–15%)
Blood that looks dark brown or chocolate-colored when drawn and stays brown on a white gauze
Headache, light-headedness, anxiety and fatigue (20–30%)
Shortness of breath, fast heart rate and palpitations
Confusion, weakness, nausea and chest pain (30–50%)
Seizures, collapse, irregular heartbeat or coma at higher levels
In infants: unusual fussiness or lethargy, poor feeding and a gray-blue color, sometimes after a procedure, a numbing gel or well water formula

Read it alongside

Arterial or venous blood gas — shows a normal partial pressure of oxygen and calculated saturation despite low pulse oximetry (the saturation gap); a metabolic acidosis marks severe cases.
Carboxyhemoglobin — measured on the same co-oximetry run; also invisible to pulse oximetry and relevant in smoke inhalation and chemical exposures.
Hemoglobin and hematocrit — anemia lowers the tolerable methemoglobin percentage and shifts the treatment threshold down; a falling hemoglobin after treatment suggests hemolysis.
G6PD test — needed before or soon after methylene blue, which is ineffective and can cause hemolysis in G6PD deficiency; the result is unreliable during an acute hemolytic episode.
LDH, bilirubin, haptoglobin and reticulocyte count — detect the hemolysis that oxidant drugs and methylene blue can cause alongside methemoglobinemia.
Lactate — rises as tissue oxygen delivery falls; a level above 4 mmol/L supports treating promptly.
Pulse oximetry versus co-oximetry — a pulse-ox reading stuck at 82–88 percent with a normal or near-normal blood gas is the classic pattern.
Peripheral blood smear — Heinz bodies and bite cells point to oxidant hemolysis, often in G6PD deficiency.

What usually happens next

Stop and record every recent drug, spray, cream, anesthetic, supplement, chemical and water source; the cause is identified from the history far more often than from further tests.
If symptomatic or above about 20 to 30 percent, expect intravenous methylene blue (1 to 2 mg/kg over 5 minutes) with a repeat co-oximetry about an hour later; levels usually fall below 10 percent within an hour, and a second dose is given if not.
Ask whether a G6PD level has been checked, especially if you are of African, Mediterranean, Middle Eastern or South Asian ancestry; it changes the treatment to ascorbic acid, exchange transfusion or hyperbaric oxygen.
After dapsone or other long-acting causes, expect observation for 24 to 48 hours because methemoglobin can rebound as the drug continues to be metabolized.
Lifelong, mild, unexplained cyanosis warrants enzyme activity testing for cytochrome b5 reductase deficiency and hemoglobin electrophoresis for hemoglobin M; relatives can be tested.
Record the offending agent in your medical record and allergy list; people who have had methemoglobinemia should avoid benzocaine, prilocaine, dapsone and other oxidant drugs in future, and tell endoscopy and dental staff beforehand.

Diet, lifestyle and natural levers with evidence

What can move MetHb once the cause is known. Nothing here replaces finding the cause.

Avoid over-the-counter benzocaine products

Strong evidence

No food, herb or supplement lowers methemoglobin in a healthy person; the levers are about avoiding the triggers. Benzocaine gels, liquids, sprays and lozenges for teething, canker sores, sore throats and dental pain are the leading cause of severe acquired methemoglobinemia; the FDA asked manufacturers to stop marketing them for children under 2 in 2018 and warns adults to use them sparingly, never more than four times a day and never on broken tissue. Anyone who has had methemoglobinemia, has G6PD deficiency, heart or lung disease or anemia should avoid them entirely.

Test well water for nitrate before using it for infant formula

Strong evidence

Private wells are not regulated, and nitrate above the EPA limit of 10 mg/L (as nitrate-nitrogen) is common in agricultural areas. Infants under 6 months fed formula made with such water can develop methemoglobin of 10 to 40 percent within days, and cases still occur in the US every year. Boiling concentrates nitrate rather than removing it; use bottled or tested water for infant formula and test wells annually, and after flooding.

Vitamin C (ascorbic acid) in congenital methemoglobinemia

Preliminary evidence

Oral ascorbic acid 300 to 1,000 mg a day in divided doses reduces methemoglobin by roughly a third to a half in case series of people with hereditary cytochrome b5 reductase deficiency, by slowly reducing ferric iron directly, and high-dose intravenous vitamin C has been used in acquired cases when methylene blue is contraindicated or unavailable. It works too slowly to treat acute poisoning and is not needed by people with normal levels.

Long-term doses above 1 g a day increase kidney stone risk, particularly in men; discuss with the hematologist managing the condition.

Riboflavin in congenital enzyme deficiency

Preliminary evidence

Riboflavin 20 to 30 mg a day has lowered methemoglobin in small case series of cytochrome b5 reductase deficiency by supporting the alternative NADPH-flavin reductase pathway; it is sometimes used with or instead of daily methylene blue for cosmetic cyanosis. There is no evidence it helps acquired methemoglobinemia or that it prevents drug-induced episodes.

Know your G6PD status if you take or may be given oxidant drugs

Moderate evidence

About 1 in 10 African American men and many people of Mediterranean, Middle Eastern and South Asian ancestry carry G6PD deficiency, which both increases the chance of methemoglobinemia and hemolysis from dapsone, primaquine, sulfonamides, rasburicase and nitrofurantoin and makes methylene blue dangerous. A one-time G6PD test before starting these drugs, which several guidelines now recommend, avoids both problems. Poppers (alkyl nitrites) are a common recreational cause and should be avoided by anyone with G6PD deficiency or anemia.

When to see a clinician promptly

Blue or gray lips, skin or nail beds that do not improve with rest or oxygen, especially within hours of a numbing spray or gel, a dental or endoscopy procedure, a new medication, poppers or a chemical exposure: this is an emergency; call emergency services.
Breathlessness, racing heart, confusion, chest pain, fainting or a seizure with any of the above, or a pulse oximeter reading stuck in the 80s that oxygen does not correct.
A baby under 6 months with blue-gray coloring, unusual sleepiness, poor feeding or fast breathing, particularly if fed formula made with well water or given a teething gel: go to an emergency department.
A methemoglobin above 10 percent on any blood test, even without symptoms, to identify and stop the cause; above 20 percent or any symptoms need treatment the same day.
Anyone on dapsone, primaquine or phenazopyridine who develops fatigue, breathlessness or dusky skin, so the level can be checked and the drug reviewed.
Lifelong mild blueness of the lips or fingers in an otherwise well person, or a family history of it, to be tested for inherited methemoglobinemia before any surgery or anesthesia.

Frequently asked questions

What is a normal methemoglobin level?

Under 1 to 2 percent of total hemoglobin; most healthy people are between 0.5 and 1 percent, because the small amount that forms each day is continuously converted back by the enzyme cytochrome b5 reductase. Some laboratories print an upper limit of 1.5 percent and others up to 3 percent. Levels of 3 to 10 percent are abnormal but usually without symptoms; symptoms begin above about 10 to 20 percent.

What level of methemoglobin is dangerous?

Cyanosis appears at about 10 to 15 percent, symptoms such as headache, breathlessness and a fast heart rate at 20 to 30 percent, confusion and chest pain at 30 to 50 percent, and seizures, coma and death above 50 to 70 percent. Treatment with methylene blue is usually given for any symptoms or for a level above 20 to 30 percent in a healthy adult, and at lower levels in people who are anemic, have heart or lung disease, or are infants, because they have less oxygen reserve.

What causes methemoglobinemia?

Almost always a drug or chemical. The commonest are benzocaine sprays and gels, dapsone, prilocaine or lidocaine, and nitrates and nitrites (contaminated well water in infants, poppers, sodium nitrite); others include aniline dyes, mothballs, primaquine, sulfonamide antibiotics, phenazopyridine, rasburicase and inhaled nitric oxide. Infants with diarrhea and acidosis can develop it without any exposure. Rare inherited forms are cytochrome b5 reductase deficiency and hemoglobin M disease, which cause lifelong mild cyanosis.

How does benzocaine cause methemoglobinemia?

Benzocaine is metabolized to compounds that oxidize the iron in hemoglobin faster than red cells can reduce it back. Throat sprays deliver a large, poorly controlled dose to a mucous membrane that absorbs it quickly, so one or two sprays before an endoscopy can push methemoglobin above 30 percent within an hour; teething gels and mouth-ulcer gels do the same in small children. The FDA has warned against benzocaine products for children under 2 and advises adults to use them sparingly. People who have had an episode should avoid benzocaine for life and tell procedural staff.

Why does my pulse oximeter read 85 percent with methemoglobinemia?

Standard pulse oximeters compare absorption of red and infrared light, and methemoglobin absorbs both almost equally, which the device interprets as a saturation of about 85 percent whatever the real value. At the same time a blood gas calculates a normal oxygen level from the dissolved oxygen, producing the saturation gap that points to the diagnosis. Giving oxygen does not change the pulse-ox reading. Only a co-oximeter (on a blood sample or a multi-wavelength finger probe) measures methemoglobin itself.

How is methemoglobinemia treated?

By stopping the cause and, for symptomatic people or levels above about 20 to 30 percent, giving intravenous methylene blue, which activates a backup enzyme pathway and typically brings the level under 10 percent within an hour. Oxygen is given but does not fix the problem on its own. In G6PD deficiency methylene blue does not work and can cause hemolysis, so high-dose vitamin C, exchange transfusion or hyperbaric oxygen are used instead. Mild cases from dapsone may just need the drug stopped and observation for a day or two because levels can rebound.

Can nitrates in food or water cause methemoglobinemia?

In infants under 6 months, yes: nitrate in well water above 10 mg/L (nitrate-nitrogen) or in home-made purees of nitrate-rich vegetables such as spinach, beets and carrots can be converted to nitrite in the gut and cause blue baby syndrome. Older children and adults convert nitrate far less and have mature reducing enzymes, so dietary nitrate from vegetables or processed meats does not cause methemoglobinemia at normal intakes; adult cases involve concentrated sources such as sodium nitrite powder, poppers or contaminated food.

Is methemoglobinemia hereditary?

Rarely. Most cases are acquired. The inherited forms are cytochrome b5 reductase deficiency (recessive; type I causes lifelong methemoglobin of 10 to 35 percent with blue coloring but good health, type II adds severe neurological problems) and hemoglobin M disease (dominant; cyanosis from infancy, no treatment needed). People who carry one copy of a reductase deficiency gene are normal day to day but develop methemoglobinemia easily after oxidant drugs, so a family history of unexplained blueness or a bad reaction to a local anesthetic is worth mentioning before procedures.

References

Methemoglobinemia. MedlinePlus Medical Encyclopedia, US National Library of Medicine (2023)
Methemoglobinemia. Merck Manual Professional Version (2024)
Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology, and clinical management. Annals of Emergency Medicine (1999)
Iolascon A, Bianchi P, Andolfo I, et al.. Recommendations for diagnosis and treatment of methemoglobinemia. American Journal of Hematology (2021)
Ash-Bernal R, Wise R, Wright SM. Acquired methemoglobinemia: a retrospective series of 138 cases at 2 teaching hospitals. Medicine (Baltimore) (2004)
Cortazzo JA, Lichtman AD. Methemoglobinemia: a review and recommendations for management. Journal of Cardiothoracic and Vascular Anesthesia (2014)
Guay J. Methemoglobinemia related to local anesthetics: a summary of 242 episodes. Anesthesia and Analgesia (2009)
Risk of serious and potentially fatal blood disorder prompts FDA action on oral over-the-counter benzocaine products used for teething and mouth pain and prescription local anesthetics. US Food and Drug Administration, Drug Safety Communication (2018)
Barker SJ, Curry J, Redford D, Morgan S. Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry: a human volunteer study. Anesthesiology (2006)
Percy MJ, Lappin TR. Recessive congenital methaemoglobinaemia: cytochrome b5 reductase deficiency. British Journal of Haematology (2008)
Knobeloch L, Salna B, Hogan A, Postle J, Anderson H. Blue babies and nitrate-contaminated well water. Environmental Health Perspectives (2000)
Skold A, Cosco DL, Klein R. Methemoglobinemia: pathogenesis, diagnosis, and management. Southern Medical Journal (2011)

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