Hydrogen Sulfide Toxicity


Practice Essentials

Hydrogen sulfide (H2S) is a colorless, flammable gas that has strong odor of rotten eggs. H2S poisoning is a rarity, mainly observed in industrial settings. However, the deliberate mixture of household chemicals to create hydrogen sulfide is increasingly used as means of committing suicide, and these cases pose a potential risk for first responders. Emergency physicians must be aware of the presentation and management of hydrogen sulfide poisoning because rapid identification and treatment is essential for recovery.


Significant hydrogen sulfide poisoning usually occurs by inhalation. Local irritant effects, along with arrest of cellular respiration, may follow. Hydrogen sulfide forms a complex bond to the ferric moiety causing inhibition of mitochondrial cytochrome oxidase (iron-containing protein), thereby arresting aerobic metabolism in an effect similar to cyanide toxicity. Very high lipid solubility allows it to penetrate easily through biologic membranes.

As a cellular poison, hydrogen sulfide affects all organs, particularly the CNS and pulmonary system. The spectrum of illness depends on the concentration and duration of exposure, with concentration being more important than duration.[1] High concentrations (>700 ppm or >975 mg/m3) have the potential to cause sudden death, theoretically due to hydrogen sulfide’s effect on the brainstem respiratory center.


Hydrogen sulfide most often is encountered as a byproduct of the petroleum, viscose rayon, rubber, and mining industries.[1] The petroleum industry is responsible for most cases of hydrogen sulfide toxicity in North America. Organic decomposition of sulfur compounds in sewers, barns, liquid manure pits, ships' holds, and sulfur springs also produces hydrogen sulfide. In nature, hydrogen sulfide can be found in caves, sulfur springs, underground deposits of natural gas, or as result of volcanic eruptions.

The use of hydrogen sulfide as a means of committing suicide became a trend in Japan in 2007.[2] In these cases, bath sulfur was mixed with toilet bowl cleaner to produce the gas. Subsequently, the practice spread to the United States—facilitated by Web sites providing instructions on the technique—and its use appears to be increasing.[2, 3]

In these cases, hydrogen sulfide is created by mixing household chemicals (eg, an acidic detergent such as a toilet bowl cleaner, which acts as a proton donor, and a sulfur source such as a pesticide or bath salts), leading to the terms detergent suicide and chemical suicide. These are mixed in an enclosed space, such as a closet or an automobile, and despite the fact that suicide victims often place warning signs on closet doors or car windows, rescue workers and others entering the space have been affected.[3]


In the United States from 1999 to 2007, 45 deaths from hydrogen sulfide exposure occurred, all of them unintentional.[2] In occupationally-related hydrogen sulfide deaths, 25% of fatalities usually involve rescuers, professionals, or bystanders.[4]

Since 2008, approximately 2000 people in Japan have committed suicide by inhaling hydrogen sulfide.[5] In the United States, use of hydrogen sulfide for suicide reportedly resulted in 2 deaths in 2008, 10 in 2009, and 18 in 2010; however, the incidence is probably underreported.[2] In addition to deaths, at least 80% of hydrogen sulfide suicides “have resulted in injuries to police officers, firefighters, emergency workers or civilians exposed to the gas.”[5]

In 2017, 646 single exposures to hydrogen sulfide exposure were reported to Poison Control Centers in the United States. Major outcomes occurred in seven cases, along with one death.[6]


Low-level exposures to hydrogen sulfide usually produce local eye and mucous membrane irritation, while high-level exposures rapidly produce fatal systemic toxicity.[7] Exposures of 700-800 ppm or greater can cause loss of consciousness and cardiopulmonary arrest. Complications include the following:

Occurrence of long-term neurologic sequelae from hydrogen sulfide exposure is unknown but appears to be linked to longer sublethal exposures. Paradoxically, high-concentration exposures of hydrogen sulfide may have no long-term effects.


The presence of hydrogen sulfide usually is apparent because of the characteristic rotten egg smell. However, concentrations above 150 ppm may overwhelm the olfactory nerve so that the victim may have no warning of exposure. Similarly, continuous exposure to low concentrations of hydrogen sulfide result in olfactory fatigue/paralysis and loss of the ability to smell or detect the gas even if it is still present in the environment.

Exposures can be subdivided into low-, high-, and very high-level categories. Low-level exposure often is more chronic in nature and usually is seen in industrial settings. Chronic low-level exposure of hydrogen sulfide results primarily in irritation to mucous membranes and the respiratory system. Other toxic effects are headaches, asthenia, bronchitis, pronounced deficits in balance and reaction time, dizziness, insomnia, and overpowering fatigue.[8]

High-level exposures of hydrogen sulfide result in more neurologic and pulmonary symptoms, as follows:

Very high concentrations lead to the following manifestations:

Physical Examination

Low-level exposure of hydrogen sulfide most often affects the mucous membranes and may show the following few physical signs:

High-level exposure of hydrogen sulfide may manifest as follows:

Perform a secondary survey to rule out traumatic injuries. Historically, these have been found in about 10% of victims.

Approach Considerations

Arterial blood gas (ABG) testing usually reveals a marked uncompensated metabolic acidosis. Acidosis is associated with an elevation in serum lactate level. Oxygen tension (pO2) and calculated oxygen saturation are within the reference range unless the patient has concomitant pulmonary edema. As with other hemoglobinopathies, however, measured oxygen saturation often is low and indicates a saturation gap.

Venous blood gas may indicate abnormally high oxygen tension (because of decreased oxygen utilization) resulting in a decrease in the PO2 gradient between arterial and venous blood. Hydrogen sulfide toxicity may be associated with carboxyhemoglobin or methemoglobinemia, depending on the source of the hydrogen sulfide and co-exposure to other toxic gases.

An electrocardiogram may reveal ischemia or infarction patterns.

Chest radiographic findings initially may be normal, but up to 20% of patients present with clinical evidence of acute lung injury. Acute respiratory distress syndrome (ARDS) is viewed as a complication of hydrogen sulfide poisoning. Computed tomography or magnetic resonance imaging scans of the head may also be initially normal, with abnormal findings (eg, basal ganglia lesions) delayed.

Blood levels of sulfide (which is an unstable metabolite) and thiosulfate may be elevated in cases of significant exposure, but these assays are rarely available, especially on short notice.

With significant acute exposure, respiratory paralysis may terminate ongoing exposure and decrease the amount of hydrogen sulfide absorbed and blood levels may be surprisingly low.

Measurement of sulfide and thiosulfate levels is more appropriate for the evaluation of low-level chronic exposures.

Approach Considerations

Initial treatment of hydrogen sulfide exposure requires immediate removal of the victim from the contaminated area into a ventilated/fresh-air environment. Emergency responders must take hazardous materials precautions to avoid exposure to the gas; recommendations on recognizing and responding to chemical suicides are available from Chemical Hazards Emergency Medical Management.[9] Precautions include using respirator devices (self-contained breathing apparatus [SCBA]).

In severe cases, intubation may be necessary for ventilatory support and airway protection. Establish intravenous (IV) access or initiate other initial supportive care as necessary. Search the patient's pockets for discolored copper coins, which can be an early diagnostic clue.

In the emergency department, high-flow (100%) oxygen is the mainstay of therapy for hydrogen sulfide poisoning. Supportive therapy includes aggressive ventilation and possible use of positive pressure ventilation for the patients with evidence of acute lung injury.

IV fluids and vasopressors should be administered to hypotensive patients. Correction of acidosis based on arterial blood gas and serum lactate values is indicated.

Based on the similarities in cyanide and hydrogen sulfide toxicity, induced methemoglobinemia may be used in hydrogen sulfide toxicity. Methemoglobin acts as a scavenger, and it has a stronger affinity to hydrogen sulfide than to cytochrome oxidase. Administer 10 mL of 3% sodium nitrite IV over 2-4 minutes (adult dose). Obtain a methemoglobin level 30 minutes after administration of antidote. However, there is a lack of research evidence supporting efficacy.[10]   Hydroxocobalamibin and its precurser Cobinamide have both been studied in animal models but are not currently recomended.[11]

Patients who have suffered significant exposure (ie, anything other than chronic low-level exposure with mucous membrane irritation) should be admitted to the intensive care unit. Patients who are unresponsive to intravenous nitrites or who have persistent or delayed neurologic sequelae should be considered for hyperbaric oxygen therapy (HBO). Anecdotal reports indicate a salutary effect. All patients should be discussed with the local poison center and/or a medical toxicologist.

Medication Summary

Antidotal treatment of hydrogen sulfide (H2 S) poisoning is based on the creation of methemoglobinemia. Symptomatic treatment includes the use of bronchodilators for patients with bronchospasm.

Sodium thiosulfate & sodium nitrite (Nithiodote)

Clinical Context:  Although approved for use in cyanide poisoning, sodium nitrite is the initial drug of choice for hydrogen sulfide poisoning. Because high methemoglobin concentrations can cause fatal reduction of oxygenation and perfusion, methemoglobin concentrations should be closely monitored and kept below 30%.

Sodium thiosulfate should not be used in the treatment of hydrogen sulfide poisoning. In the classic cyanide antidote kit, sodium nitrite and sodium thiosulfate are provided. The nitrites cause the formation of methemoglobinemia, scavenging both cyanide and hydrogen sulfide. In cyanide poisoning, sodium thiosulfate enhances the activity of the enzyme rhodanese, a mammalian enzyme that likely evolved in response to the ubiquitous presence of cyanide in nature. Rhodanese catalyzes the transfer of sulfate from sodium thiosulfate to cyanide to form thiocyanate, a less toxic form that is excreted by the kidneys. This does not share the crossover treatment that sodium nitrites do with hydrogen sulfide (ie, it is useless in hydrogen sulfide poisoning).

Class Summary

Nitrite administration leads to formation of methemoglobinemia. H2 S has a much greater affinity for methemoglobin than for cellular cytochromes, leading to lower metabolic toxicity.


Chip Gresham, MD, FACEM, Emergency Medicine Physician, Medical Toxicologist, and Intensive Care Consultant, Department of Emergency Medicine, Clinical Director of Medication Safety, Middlemore Hospital; Consultant Toxicologist, National Poisons Centre; Director, Auckland Regional Toxicology Service; Senior Lecturer, Auckland University Medical School, New Zealand

Disclosure: Nothing to disclose.


Emma A Lawrey, MBChB, Dip Paeds, PG Cert ClinEd, FACEM, Emergency Medicine Consultant and Clinical Toxicology Fellow, Department of Emergency Medicine, Middlemore Hospital, New Zealand

Disclosure: Nothing to disclose.

Chief Editor

Michael A Miller, MD, Clinical Professor of Emergency Medicine, Medical Toxicologist, Department of Emergency Medicine, Texas A&M Health Sciences Center; CHRISTUS Spohn Emergency Medicine Residency Program

Disclosure: Nothing to disclose.


John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Occupational and Environmental Medicine, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

David C Lee, MD Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School

David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Sujal Mandavia, MD, FRCP(C), FACEP Clinical Assistant Professor of Emergency Medicine, USC, Department of Emergency Medicine, Cedars-Sinai Medical Center, Los Angeles County-University of Southern California Medical Center

Sujal Mandavia, MD, FRCP(C), FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, and American College of Emergency Physicians

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.


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