Although the risk for occupational exposure to hydrogen sulfide (H2S) is widely known, it remains an unsolved issue in worker safety, particularly in the sour gas industry.1–6 In some industrial settings, H2S poisoning continues to be a significant cause of work-related morbidity and mortality.7–15 The source of H2S is both natural and artificial.16 It is present in volcanic gases, sulfur springs, undersea vents, swamps, crude petroleum, and natural gas,17–19 and it is 1 of the principal components in the natural sulfur cycle. Hydrogen sulfide is frequently found in industrial settings where it is either used as a reactant or produced as a by-product of manufacturing or industrial processes in settings such as tanneries, waste water treatment facilities, manure and sewage facilities, rayon manufacturing plants, sulfur producers, coke oven plants, Kraft paper mills,20 iron smelters,21 food processing plants,22 tar and asphalt manufacturing plants, petrochemical plants, and oil refineries.23–27 Exposure to H2S can occur by inhaling the substance, by eating or drinking it, or by skin contact. Asphyxiation is the most frequent cause of death related to occupational exposure to H2S, where it interferes with cytochrome oxidase and aerobic metabolism.6 Hydrogen sulfide operates on cytochrome oxidase, selectively on cytochrome-C oxidase, by blocking oxygen transport within the mitochondria. This enzymatic complex is situated on the internal mitochondrial membrane, and it is involved in the electron transport chain.
The activity of cytochrome-C oxidase is essential to maintain a pH gradient between both sides of the membrane. Phosphorylation of adenosine diphosphate in adenosine triphosphate depends on this gradient. Thus, the consequence of H2S action is cellular asphyxia, with early damages mainly in the central nervous system and the eyes and the lungs as well.
Despite the increased awareness of the potentially lethal consequences of occupational exposure to H2S, deaths continue to be reported. In many cases, safety measures have not been adequate; in others, workers have not complied with the correct procedures. In this article, the authors describe a fatal industrial accident in which the production of H2S caused the death of a young worker.28
In an industrial town near Perugia, a young healthy man was transferring hydrochloric acid (33%) from a bulk tank to plastic containers. Four of the 6 plastic containers (which had been used by another department for waste disposal) had previously been used to store INSOL (sodium sulfide 33%). The transfer was carried out using a plastic tube that connected the bulk tank to the containers. Maintenance duties performed monthly included the use of hydrochloric acid for descaling the pipes.
The changeover of containers was carried out manually, and throughout this operation, the worker was probably not wearing any individual protective equipment or clothing.
After approximately 10 minutes, the young man, who had filled the first container and was filling the second, was found unconscious on the ground.
The man was taken to the local hospital emergency rescue, where he appeared cyanotic and mydriatic, and heart activity and circulation were absent. The doctors declared him dead.
A chemist expert appointed by the prosecutor performed the workplace investigation. The factory had a cooperative attitude, immediately providing all the necessary information on the process and the substances used. On the basis of the advice of the chemist and the results of investigations, the prosecutor ordered to perform the autopsy and toxicological analysis to discover the cause of death.
MATERIALS AND METHODS
The medical examiner appointed by the prosecutor carried out the autopsy; the histological examination; and the toxicological analysis that was performed on the peripheral blood (femoral), the lungs, the liver, and the brain, and initially, it was directed to ascertain the presence of drugs and/or psychotropic substances. On the basis of the circumstances of the case, testing for H2S poisoning was initiated using gas chromatography–mass spectrometry by Selective Ion Monitoring mode29–31 according to the method of Poli et al.25
In the workplace investigation, it was highly likely that in the course of duties performed by the worker, there had been the production of H2S: the gas would be formed from the decomposition of 1 of its salts, sodium sulfide, by the action of hydrochloric acid inside the tank.
The workplace investigation also showed that it was the employee’s first working day in the “emulsion system” department. He probably did not comply with safety procedures and committed fatal errors: he should have been wearing standard protective equipment including a gas mask, scuba, neoprene gloves, glasses, and acid-resistant overalls, and he should have checked the plastic containers to verify the absence of any substances.
The autopsy was carried out 48 hours after the accident on the well-preserved body; the young man weighed 85 kg and was 185 cm tall.
External examination of the body revealed grayish discoloration on the vestibular side of the labial mucosa, cyanosis of the fingernails, and some mild contusions and abrasions on the left side of the body that resulted from falling.
Internal examination showed grayish coloration of the brain with massive edema and congestion; the base of the tongue and the mucous membrane of the larynx and the trachea were reddish and showed marked hyperemia; the lungs were reddish-black, heavy (right: 1610 g, left: 1560 g), and oversized with marked swelling and congestion; hemorrhagic pulmonary edema was also present; the mucous membrane of the bronchia was covered with dark-red fluid blood; and congestion was present in the liver and slightly in the spleen and the kidneys.
Histological examination confirmed massive hemorrhagic edema in both lungs, and marked congestion and edema were observed in the brain; congestion was also present in the tongue, the larynx, the trachea, and the liver and lightly in the other organs.
Toxicological evaluation did not reveal the presence of drugs and/or psychotropic substances on biological fluids and fragments of organs taken during autopsy.
Further toxicological analysis of the blood sample revealed the presence of 1.020 mM/L of thiosulfate, which was a useful indicator of H2S poisoning; it was also detected in the liver (0.266 mM/L), in the lungs (1.013 mM/L), and in the brain (1.111 mM/L).
Thiosulfate is a useful indicator of H2S poisoning because it is the major metabolite of H2S and is less volatile than H2S; thus, it remains stable for a long time in biological samples.19–30
Hydrogen sulfide enters into the body primarily through the air you breathe; much smaller amounts can enter through the skin and the gastrointestinal tract.
In the body, H2S is metabolized through 3 pathways: oxidation, methylation, and reactions with metalloproteins or disulfide-containing proteins and is rapidly excreted in the urine.
It is unstable and is primarily and rapidly oxidized to thiosulfate and sulfate in the human body; therefore, it is difficult to detect sulfide in biological samples, particularly in the blood.20–22
In addition, although sulfide can spread from the airway and from gastric fluid, thiosulfate can only diffuse from the airway because the acid conditions of gastric fluids easily decompose it.28
Therefore, the detection of thiosulfate is a reliable sulfide-poisoning indicator; its concentration can show a death-causing relationship.
Analyses performed on biological samples from the worker revealed high thiosulfate concentrations in the blood, the liver, the lungs, and the brain. The values of thiosulfate concentrations were compared with data in the literature. In particular, the results of this study are in agreement with those obtained by Maebashi et al,7 Kage et al,20 and Ago et al22 (see Table 1). These concentrations are compatible with acute H2S poisoning, although the data do not exclude the possibility that some of the thiosulfate was formed after death of the subject.28
In this case, forasmuch as the body was well preserved, the production of postmortem gases was exiguous. Therefore, the gas produced by the decomposition of the body had not impacted significantly on toxicology results.
On the basis of the results of the workplace investigations, it was concluded that the worker was exposed to a high concentration of H2S, which resulted in his death.
The autopsy findings were consistent with this hypothesis. Pulmonary edema is a common consequence of H2S poisoning22 and occurs by asphyxial phenomenon due to massive exposure.28
A careful analysis of the case highlights that worker inexperience is a prominent risk factor in causing work-related accidents.
Scientific literature notes that fatal occupation-related H2S toxicity is more common among new workers.28–31
The case highlights the fact that worker inexperience, lack of training, and failure to use personal protective equipment exposed the worker to risks that ultimately resulted in his death. Additional efforts by occupational medicine physicians and employers to train workers could prevent future deaths.32,33
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