How to cite this article: Iseki K, Ozawa A, Seino K, Goto K, Tase C. The Suicide Pandemic of Hydrogen Sulfide Poisoning in Japan. Asia Pac J Med Toxicol 2013;3:13-7.

Introduction

Hydrogen sulfide (H2S) is a colorless, highly inflammable toxic gas, with a characteristic odor of rotten eggs (1-3). It is found in crude petroleum, natural gas, volcanic gas, and hot springs. It is also generated from industrial processes and natural deposits in sewers and manholes (1,4). Thus, H2S poisoning can occur following accidental exposure.

The toxicity of H2S poisoning is reversible by inhibiting cytochrome oxidase in the respiratory system (5). The clinical features of H2S poisoning depend on the concentration of inhaled gas. At a concentration of over 30 parts per million (ppm), its odor can be detected and the olfactory nerve may become paralyzed at a level of over 150 ppm (3,4). Pulmonary and eye irritations occur at a level of over 200 ppm (4). Coma and cardiopulmonary arrest occur at a level of over 700 ppm due to brain respiratory center paralysis, asphyxia, and cardiac failure (4,6). A high H2S concentration (≥ 1000 ppm) immediately leads to unconsciousness and cardiopulmonary arrest; this is referred to as “knock down” (1).

H2S suicides are frequent in Japan (1,7-9). Furthermore, individuals who try to help the victims or those who are present at the scene may be exposed to the gas and suffer from secondary poisoning. The objective of this study was to describe the epidemiologic profile of an outbreak of H2S suicides in Japan.

Method

In September 2008, questionnaires about patients involved with H2S poisoning were sent to 250 hospitals, including emergency medical centers and university hospitals, in Japan. Data collected from each patient included gender, age, clinical manifestations, date of event, location of suicide, source of H2S, treatments and neurological outcome. The Cerebral Performance Category (CPC) was used to assess neurological outcome at hospital discharge (10):

CPC1. Conscious, alert, possible mild neurological or psychological deficit, able to work; CPC2. Conscious, moderate neurological disability, conscious, sufficient cerebral function for independent activities of daily life, able to work in sheltered environment; CPC3. Conscious, severe neurological disability, dependent on others for daily support because of impaired brain function; CPC4. Coma or vegetative state; and CPC 5. Brain death: apnea, areflexia, EEG silence.

The data are shown in terms of frequency and percentage using Microsoft Office Excel® 2010 (Microsoft Corp., Redmond, WA, USA). The data on age are shown as mean (SD). Statistical analysis was performed with Statview 5.0® (SAS Institute Inc., Cary, NC, USA). Student's t test was used to compare age between two groups and compare continuous variables and the chi-square was used to analyze categorical variables.

Result

 A total of 90 subjects (60 men, 30 women) from 34 (response rate: 13.6%) hospitals responded (Table 1). There were 60 cases (42 men, 18 women) of attempted suicide by inhalation of H2S gas (suicide group) and the 30 cases (18 men, 12 women) of gas exposure after attempting to rescue the victims or from being present in the scene (secondary exposure group). The first cases of H2S poisoning were reported in September 2006 and reached a peak in April 2008 (Figure 1).

Suicide group

In the suicide group, the mean age was 28.8 (9.1) years (range: 17–51 years) (Figure 2). The cases of attempted suicide were more frequent among men and women in their twenties (34 cases; 57%). Cardiopulmonary arrest at the scene was reported in 39 cases (65%); while in two of those cases, there was return of spontaneous circulation; however, they died 4 and 22 days after the suicide attempt, respectively. Patients who suffered from cardiac arrest at the scene due to high concentration of H2S did not survive despite cardiopulmonary resuscitation and antidote administration. However, the patients who escaped early from H2S gas were successfully treated.

Twenty-three subjects (38%), in total were admitted to hospitals. Their clinical manifestations included coma in 14 cases, convulsion in 1 case, and lung edema in 1 case (Table 1). In 51 cases, H2S was generated by mixing hydrochloric acid detergent with any of the following: sulfur-based bath additive (MUTOHAP®) in 40 cases (78%), sulfur-based pesticide in 8 cases (16%), sulfur-based bath powder in 2 cases (4%), or a combination of sulfur-based bath additive (MUTOHAP®) and sulfur-based pesticide in 1 case (2%) (Table 2).

The place where the gas was generated was reported in 58 cases including bathroom in 25 cases (43%), car in 12 cases (20%), bedroom in 10 cases (17%), and toilet in 7 cases (12%) (Figure 3). Among those admitted to the hospital (suicide inpatient group: 23 cases), 9 patients were intubated (39%); antidote therapy was given using inhaled amyl nitrite, followed by intravenous sodium nitrate in 3 cases (13%) or sodium nitrate in 5 cases (22%); and hyperbaric oxygen therapy was used in 2 cases (9%) (Table 1).

The outbreak of H2S suicide was found to be associated with available information of producing this substance on the internet (1,8). A website describing how to use H2S for suicide was available and it listed the methods to generate H2S gas, including the adequate amount of hydrochloric acid detergent and sulfur-based bath additive (MUTOHAP®) and provided information on how to make this gas available to others (1). Furthermore, the website recommended using a confined place to generate a high concentration H2S gas, for example, in a car or a toilet. At the same time, newspapers, television and other mass-media reported daily H2S suicides, reaching a peak around April 2008 (8,9). Considering the increase in H2S suicide attempts, newspapers and television offered access limitation to the substance and the website was restricted to access. Moreover, unrelated to the abovementioned events, MUTOHAP® was discontinued in April 2008. Accordingly, the number of the H2S suicide attempts decreased gradually, although they are still reported. In the same manner, the same setup was observed in the United States with the dissemination of information about suicide methods via the internet (16).

The H2S poisoning mostly manifests with neurological and/or pulmonary signs and symptoms. Central nervous system effects include dizziness, headache, convulsions, coma, and respiratory center paralysis (2,17,18). Pulmonary effects include wheezing, dyspnea, bronchiolitis, pulmonary edema, and acute respiratory distress syndrome (ARDS) (2,17,18). Myocardial symptoms such as arrhythmia and dilated cardiomyopathy have also been reported in some cases (2,18,19). Furthermore, Arnold et al. reported that unconsciousness, headache, nausea/vomiting, dyspnea, disequilibrium, lung edema and convulsion can be found in subjects with occupational exposure to H2S (18).

In this study, 42 patients (46%) in total developed cardiopulmonary arrest at the scene. Correspondingly, Inoue et al. and Amino et al. reported 2 cases of sudden death due ardial effects related to H2S poisoning are noticeable when high concentrations of the gas are inhaled (2). Accordingly, patients with secondary exposure in the present study that were less exposed to the gas and not in direct contact in the very first minutes, experienced this complication in a much lesser extent.

The initial management of patients with H2S poisoning includes immediate removal from the area of gas exposure, supplemental oxygen, and eye and skin decontamination (5). Intubation and ventilation should be performed, depending on the patient’s condition. Additionally, administration of nitrites has been widely used in the treatment of H2S poisoning (2). This treatment should be initiated with inhalation of amyl nitrite until sodium nitrite can be injected intravenously (22). Recently, hydroxocobalamin was reported to be effective on reducing serum concentration of sulfide and thiosulfate, in patients with H2S poisoning (3). Hyperbaric oxygen therapy has also been shown effective in some cases of H2S poisoning (23-25). In this study, intravenous sodium nitrite combined with inhaled amyl nitrite was administered to 3 cases. However, no patient was treated with intravenous hydroxocobalamin. Moreover, it was found that patients with suicidal attempt had poorer prognosis and needed to more aggressive treatments compared to patients with secondary exposure.

Limitations

In this study, data were not directly collected by the researchers and were collected retrospectively with questionnaires, which may cause bias in data collection. Although some emergency departments in Japan cooperated with this study, all patients with H2S poisoning could not be covered and hence the actual condition may not be properly reflected.

Conclusion

Suicide with H2S poisoning has recently been a serious social problem especially in younger generation in Japan. There is extensive information on H2S suicide methods on the internet. Management of access to websites describing suicide methods is an immediate necessity together with counseling for suicide prevention.

Acknowledgments

The authors would like to thank Izumi Sato of Yamagata University for technical assistance. Also, we are very thankful to the staff of all hospitals in Japan that contributed to this study.

Conflict of Interest: None to be declared.

Funding and support: None.