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American Journal of Forensic Medicine & Pathology:
doi: 10.1097/PAF.0b013e31827ab5ad
Case Reports

Suicide by Hydrogen Sulfide Inhalation

Bott, Eleanor MBBS, BSc (Hons); Dodd, Malcolm MBBS (Hons), FRCPA, DMJ(Path), FFFLM (RCP-UK), Assoc Dip MLT, MACLM, AAIMLT, FACBS, Grad Cert Health Prof Ed

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From The Victorian Institute of Forensic Medicine, Victoria, Australia.

Manuscript received February 2, 2012; accepted June 6, 2012.

The authors report no conflict of interest.

Reprints: Eleanor Bott, MBBS, BSc (Hons), The Victorian Institute of Forensic Medicine, 57-83 Kavanagh St, Southbank, Victoria, 3006, Australia. E-mail:

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Abstract: The authors report a case of suicide by hydrogen sulfide in Australia. A young woman was located in a car wearing protective eyewear. A tub of foamy yellow substance and a quantity of hydrochloric acid and lime sulfur were also located in the rear of the vehicle. Morphological findings at autopsy were nonspecific. Toxicologic analysis of a specimen of leg blood detected elevated levels of methemoglobin.

If Australia follows a similar trend to Japan and the United States, it is possible that incidences of such cases will rise, probably because of Internet dissemination. From a public health perspective, emergency service providers and forensic case workers should be aware of the potential hazards to themselves and others when dealing with such cases.

Hydrogen sulfide (H2S) is a highly toxic and flammable gas. Hydrogen sulfide toxicity is a well-recognized occupational and industrial hazard, and cases of fatal H2S poisonings mostly occur in occupational settings.1 Fatalities of workers in occupational scenarios have involved exposure to high H2S concentrations released from petrochemical plants, sewers, volcanoes, or manure pits.

Suicides by means of H2S inhalation were first reported in Japan in 2007. Over 2000 such cases in Japan have been reported since. A number of suicides using H2S have also been described in the United States,2–6 where most of the victims have been white males. Incidences of H2S suicides are thought to be increasing because of Internet dissemination. The method of suicide involves mixing the common household chemicals hydrochloric acid (found in commercial pool cleaners) and lime sulfur (calcium polysulfide), found in common pesticides, to create H2S gas, which is then inhaled in an enclosed environment. Information about the fad spread rapidly by Internet dissemination where it has been reported that victims lose consciousness with a single intake of breath and die immediately. This has been referred to as “knock down” and is described as a painless way to kill oneself.

To the best of our knowledge, fatal intentional exposures in Australia have not been described in the literature.

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A routine patrol of a beachside car park located the body of a young white female in a car. The deceased person was kneeling on the rear seat facing the windscreen with her head slumped forward. She was fully clothed without footwear and was wearing clear plastic protective eyewear. A large plastic tub was located in the rear of the vehicle containing a foaming yellow substance. Emergency service providers reported a strong chemical smell. Containers in the rear of the vehicle contained hydrochloric acid and lime sulfur.

Medical records indicated a history of major depression, bipolar disorder, and previous self-harm.

External examination revealed early signs of decomposition including green discoloration over the lower abdomen, consistent with the estimated time between death and autopsy. It was noted that there was brown fluid over the ankles and feet. Clear plastic protective eye goggles were secured around the head with an elastic strap, and markings over the face were consistent with wearing them at the time of death. There was blood within the nostrils and dried blood smeared over the face.

Examination of the eyes revealed severe scleral and conjunctival hemorrhage, linear hemorrhage across the upper eyelids, and severe swelling of the upper eyelids. There was extensive hemorrhage involving the mucosa of the oral cavity.

There were small, punctuate burns suggestive of corrosive spatter over the face and the dorsum of the hands and fingers (Fig. 1). The skin over the palms of the hands and dorsum of the feet was rough and dry. These areas were also covered with small, irregular burns. Because the combination of chemical identified in the car results in an acid-base reaction, a mildly exothermic and violent reaction might be expected. Local irritant effects might explain the presence of multiple small burns over exposed areas in this case (Fig. 2).

Figure 1
Figure 1
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Figure 2
Figure 2
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Internal examination revealed red/brown mucoid fluid within the upper and lower airways. The underlying mucosa was hyperemic. The lung parenchyma was moderately heavy, congested, and edematous. There was nonspecific desquamation of the esophageal mucosa. Reflection of the scalp revealed 2 areas of irregular subgaleal hemorrhage over the right and left temporoparietal areas. Lack of overlying bruising suggests that these may be acute injuries perhaps sustained secondary to seizure activity, a recognized effect of H2S toxicity. Organ weights were within normal limits, and there was no evidence of any significant natural disease that may have caused or contributed to death.

Microscopically, there was evidence of pulmonary edema and congestion of the lungs and liver.

Morphological findings at autopsy in this case were similar to those described in the literature1 in that they were nonspecific for a poisoning diagnosis.

Postmortem toxicologic analysis of a specimen of leg blood sampled at the time of autopsy detected methemoglobin at approximately 5% saturation. Carboxyhemoglobin was not detected. 7-aminonitrazepam (a metabolite of nitrazepam) was detected at a level consistent with therapeutic use (approximately 0.02 mg/L). A measure of thiosulfate levels in blood was beyond the limits of the toxicology laboratory at our institution but may have been useful. Delta-9-tetrahydrocannabinol (the active form of cannabis) was also detected at a level consistent with recent use (approximately 53 ng/mL).

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Hydrogen sulfide can enter the body through the airways and a small amount through the intact skin. The toxic effect of H2S is similar to cyanide in that it binds to cytochrome-c oxidase and is classified as a cellular asphyxiant.6 H2S inhibits enzymes in mitochondria by binding with Fe3+ of cytochrome oxidase.5 This reaction blocks cellular respiration and interferes with oxygen use at the cellular level.

There are 2 major adverse effects of H2S: local irritant effects and direct neurotoxic effects. Local irritant effects often follow prolonged inhalation of low concentrations of H2S.7 These may include effects on the mucous membranes such as conjunctivitis, bronchitis, pulmonary edema. Direct neurotoxic effects are rapidly fatal and usually follow inhalation of higher concentrations of H2S. These effects are associated with sudden loss of consciousness, apnea, and rapid death. Immediate collapse has also been referred to as knock down. According to Internet communication, approximately half a cup of each product will produce approximately 1000 ppm H2S inside a confined space (Table 1).

Table 1
Table 1
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Autopsy findings on 2 individuals who died after accidental inhalation of H2S in an industrial setting described similar changes2 as were noted in this case. These included conjunctival and mucous membrane hyperemia and petechiae, esophageal erosion and submucous hemorrhages, localized erosions of the stomach and small intestinal mucosa, and slight cerebral edema. No remarkable changes except for congestion were found in other organs.

In the lungs, H2S is well absorbed into blood, where it can readily oxidize to thiosulfates and sulfides. There is sulfate in the blood and urine of healthy people, but thiosulfate content is very low.

For this reason, thiosulfate has been reported to be a useful indicator for H2S exposure.8 Levels reported in fatal human cases have ranged from 0.025 to 0.143 mmol/L2. Thiosulfate levels are believed to be strongly influenced by the atmospheric concentration of H2S the victims were exposed to and the time interval between exposure and death.4

Methemoglobin is a form of hemoglobin in which the iron in the heme group is in the Fe3+ (ferric) state, not the Fe2+ (ferrous) state and therefore cannot release bound oxygen. Normally, 1% to 2% of hemoglobin is methemoglobin. A higher percentage than this, as in this case, can be genetic, caused by exposure to various chemicals9 or a putrefaction artifact. Carboxyhemoglobin was not detected in this case. Carboxyhemoglobinemia and methemoglobinemia may occur in the setting of chemical exposure; however, these findings are nonspecific and, in cases of H2S exposure, may indicate coexposure.

From a public health perspective, H2S suicides constitute a threat to first responders, rescue personnel, and bystanders. Hydrogen sulfide is a colorless, hydrosoluble toxic gas with a distinctive “rotten egg” smell; however, above a concentration of 100 ppm, the odor is lost because of olfactory nerve paralysis.

Recognition of the hazards associated with such a scene should be discussed to prevent morbidity and mortality. Emergency service providers and forensic case workers should be aware of the hazards of H2S to adequately assess and educate bystanders and first responders to the potential hazards.

It is likely that we can expect the frequency of H2S suicides to increase as the method is popularized via Internet dissemination. Household chemicals needed to create toxic concentrations of H2S gas are readily available in stores and on the Internet.

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This case presents a suicidal death caused by H2S toxicity in a young Australian woman. This has been unusual in Australia to date, but there is evidence to suggest such cases may become more common. Findings at autopsy agree with previous reports that document nonspecific morphological changes. In addition to carboxyhemoglobin and methemoglobin levels, toxicologic analysis could include levels of blood thiosulfate as a useful indicator of H2S exposure. Emergency service providers and forensic case workers should be aware of the potential hazards of H2S exposure.

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The authors thank Dr Richard Bassed and the Victorian Institute of Forensic Medicine staff.

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1. Sidlo J, Bauer M, Bauerova J, et al.. Diagnostics of fatal hydrogen sulfide poisonings. Soud Lek. 2009; 54 (3): 37–40.

2. Ago M, Ago K, Ogata M. Two fatalities by hydrogen sulfide poisoning: variation of pathological and toxicological findings. Legal Medicine. 2008; 10: 148–152.

3. Kobayashi K, Fukushima H. Suicidal poisoning due to hydrogen sulfide produced by mixing a liquid bath essence containing sulfur and a toilet bowl cleaner containing hydrochloric acid. Chudoku Kenkyu. 2008; 21: 183–188.

4. Maebashi K, Iwadate K, Sakai K, et al.. Toxicological analysis of 17 autopsy cases of hydrogen sulfide poisoning resulting from the inhalation of intentionally generate hydrogen sulfide gas. Forensic Sci Int. 2011; 207 (1-3): 91–95.

5. Morii D, Miyagatani Y, Nakamae N, et al.. Japanese experience of hydrogen sulfide: the suicide craze in 2008. J Occup Med Toxicol. 2010; 5: 28.

6. Reedy SJD, Schwartz MD, Morgan BW. Suicide fads: frequency and characteristics of hydrogen sulfide suicides in the United States. West J Emerg Med. 2001; 7 (3): 300–304.

7. Snyder JW, Safir EF, Summerville GP, et al.. Occupational fatality and persistent neurological sequelae after mass exposure to hydrogen sulfide. Am J Emerg Med. 1995; 13: 199–203.

8. Kage S, Takekawa K, Kuroskai K, et al.. The usefulness of thiosulfate as an indicator of hydrogen sulfide poisoning: three cases. Int J Leg Med. 1997; 110: 220–222.

9. Hoffman R, Benz E, Shattil S, et al.. Hematology Basic Principles and Practice. 4th ed. New York, NY: Churchill Livingstone; 2005: 650–657.


hydrogen sulfide; suicide; post mortem

© 2013 Lippincott Williams & Wilkins, Inc.


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