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Toxicity, Hydrogen Sulfide

Author: 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
Contributor Information and Disclosures

Updated: Mar 24, 2009

Introduction

Background

Hydrogen sulfide (H2 S) is a colorless gas that has strong odor of rotten eggs. H2 S poisoning is a rarity, mainly observed in industrial settings. Emergency physicians must be aware of the presentation and management of H2 S poisoning because rapid identification and treatment is essential for recovery.

Pathophysiology

Significant H2 S poisoning usually occurs by inhalation. Local irritant effects, along with arrest of cellular respiration, may follow. H2 S 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, H2 S affects all organs, particularly the CNS and pulmonary system. The spectrum of illness depends on the concentration and duration of exposure, with high concentrations (>700 ppm or >975 mg/m3) causing sudden death possibly due to hydrogen sulfide effect on the brainstem respiratory center.

Frequency

United States

According to the 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System, 1134 single exposures and 13 fatal outcomes were reported.1

It is very important to realize that 25% of fatalities usually involve rescuers, professionals, or bystanders.2

Mortality/Morbidity

  • Low-level exposures of hydrogen sulfide usually produce local eye and mucous membrane irritation, while high-level exposures rapidly produce fatal systemic toxicity.
  • Exposures of 700-800 ppm or greater can cause loss of consciousness and cardiopulmonary arrest.

Sex

Because hydrogen sulfide exposures predominantly occur in industrial exposures, it is conceivable that the majority of patients will be middle-aged men.

Age

If exposed to hydrogen sulfide, children are more vulnerable than adults.

Clinical

History

The presence of H2 S 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. 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. Patients exposed to continuous low-level concentrations or after acute exposure to the very high concentrations of hydrogen sulfide can lose their ability to smell/detect the gas even though it is still present in the environment (olfactory fatigue/paralysis).
    • Headaches
    • Asthenia
    • Bronchitis
  • High-level exposures of hydrogen sulfide result in more neurologic and pulmonary symptoms.
    • Cough
    • Dyspnea
    • Vertigo
    • Confusion
    • Nausea and vomiting
    • Possible loss of consciousness
    • Hemoptysis
  • Very high concentrations lead to cardiorespiratory arrest because of brainstem toxicity.
    • Myocardial infarction
    • Sudden loss of consciousness ("knockdown") 
    • Seizure
    • Cardiopulmonary arrest

Physical

  • Low-level exposure of hydrogen sulfide most often affects the mucous membranes and may show the following few physical signs:
    • Conjunctivitis (even at levels of only 4 ppm)
    • Pharyngitis
    • Green-gray line on gingiva
    • Wheezing
  • High-level exposure of hydrogen sulfide may elicit the following signs:

Causes

  • H2 S most often is encountered as a byproduct of the petroleum, viscose rayon, rubber, and mining industries.
  • Organic decomposition of sulfur compounds in sewers, barns, liquid manure pits, ships' holds, and sulfur springs also produces H2 S.
  • The petroleum industry is responsible for most cases of H2 S toxicity in North America.
  • In nature, hydrogen sulfide can be found in caves, sulfur springs, underground deposits of natural gas, or as result of volcanic eruptions.
  • Hydrogen sulfide has recently been implicated in suicides in Japan.3

More on Toxicity, Hydrogen Sulfide

Overview: Toxicity, Hydrogen Sulfide
Differential Diagnoses & Workup: Toxicity, Hydrogen Sulfide
Treatment & Medication: Toxicity, Hydrogen Sulfide
Follow-up: Toxicity, Hydrogen Sulfide
References
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References

  1. Bronstein AC, Spyker DA, Cantilena LR Jr, Green JL, Rumack BH, Heard SE. 2007 Annual Report of the American Association of Poison Control Centers' National Poison Data System (NPDS): 25th Annual Report. Clin Toxicol (Phila). Dec 2008;46(10):927-1057. [Medline].

  2. Fuller DC, Suruda AJ. Occupationally related hydrogen sulfide deaths in the United States from 1984 to 1994. J Occup Environ Med. Sep 2000;42(9):939-42. [Medline].

  3. Truscott A. Suicide fad threatens neighbours, rescuers. CMAJ. Aug 12 2008;179(4):312-3. [Medline].

  4. Gregorakos L, Dimopoulos G, Liberi S, Antipas G. Hydrogen sulfide poisoning: management and complications. Angiology. Dec 1995;46(12):1123-31. [Medline].

  5. Hall AH, Rumack BH. Hydrogen sulfide poisoning: an antidotal role for sodium nitrite?. Vet Hum Toxicol. Jun 1997;39(3):152-4. [Medline].

  6. Hessel PA, Herbert FA, Melenka LS, et al. Lung health in relation to hydrogen sulfide exposure in oil and gas workers in Alberta, Canada. Am J Ind Med. May 1997;31(5):554-7. [Medline].

  7. Kilburn KH, Warshaw RH. Hydrogen sulfide and reduced-sulfur gases adversely affect neurophysiological functions. Toxicol Ind Health. Mar-Apr 1995;11(2):185-97. [Medline].

  8. Milby TH, Baselt RC. Hydrogen sulfide poisoning: clarification of some controversial issues. Am J Ind Med. Feb 1999;35(2):192-5. [Medline].

  9. Richardson DB. Respiratory effects of chronic hydrogen sulfide exposure. Am J Ind Med. Jul 1995;28(1):99-108. [Medline].

  10. Smilkstein MJ, Bronstein AC, Pickett HM, Rumack BH. Hyperbaric oxygen therapy for severe hydrogen sulfide poisoning. J Emerg Med. 1985;3(1):27-30. [Medline].

  11. Snyder JW, Safir EF, Summerville GP, Middleberg RA. Occupational fatality and persistent neurological sequelae after mass exposure to hydrogen sulfide. Am J Emerg Med. Mar 1995;13(2):199-203. [Medline].

  12. Watt MM, Watt SJ, Seaton A. Episode of toxic gas exposure in sewer workers. Occup Environ Med. Apr 1997;54(4):277-80. [Medline].

  13. Whitcraft DD, Bailey TD, Hart GB. Hydrogen sulfide poisoning treated with hyperbaric oxygen. J Emerg Med. 1985;3(1):23-5. [Medline].

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Further Reading

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Keywords

hydrogen sulfide toxicity, hydrogen sulfide exposure, hydrogen sulfide poisoning, rotten egg odor, H2 S toxicity, H2 S poisoning, H2 S, inhalation of hydrogen sulfide

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Contributor Information and Disclosures

Author

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.

Medical Editor

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.

Pharmacy Editor

John T VanDeVoort, PharmD, Regional Director of Pharmacy, Sacred Heart & 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.

Managing Editor

John G Benitez, MD, MPH, FACMT, FACPM, FAAEM, Associate Professor, Department of Medicine, Clinical Pharmacology Division, Vanderbilt University; Managing Director, Tennessee Poison Center
John G Benitez, MD, MPH, FACMT, FACPM, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD, Assistant Professor, Department of Surgery, Section of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital
Disclosure: Nothing to disclose.

 
 
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