The hydrogen sulfide accident kept me awake all night! ! !

Yes, hydrogen sulfide is a very dangerous substance~But in practice, we tend to rely on luck~And many emergencies occur suddenly, with no way of predicting them. In my opinion, employees are responsible for ensuring that nothing goes wrong during their working hours, while managers are responsible for ensuring that the equipment functions properly. I hope that employees will not rely on luck, but even more so, I hope that managers will avoid relying on luck as well and will pay more attention to the safety of their employees by providing more protective equipment and putting more effort into safety management.

Indeed, almost every production facility contains it; it is highly toxic, and its presence in the air is required to be controlled

Hydrogen sulfide; CAS: 7783-06-4. Its physical and chemical properties are those of a colorless gas. It has the smell of rotten eggs. Molecular formula H2-S. Molecular weight 34.08. Relative density 1.19. Melting point -82.9°C. Boiling point -61.8°C. It is soluble in water, as well as in alcohols, petroleum solvents, and crude oil. The upper flammability limit is 45.5%, and the lower limit is 4.3%. The ignition point is 292°C. Opportunities for exposure to hydrogen sulfide arise in industries such as mining and the extraction of copper, nickel, cobalt, etc., from ores; low-temperature coking of coal; the extraction and processing of sulfur-containing petroleum; as well as in industries related to rubber, rayon, tanning, sulfonic dyes, papermaking, pigments, vegetable pickling, sugar production from beets, and animal glue. Workers involved in the excavation and remediation of swamps, ditches, wells, sewers, tunnels, as well as those responsible for removing garbage, waste, and feces, also have opportunities to be exposed to hydrogen sulfide. Hydrogen sulfide is often present in natural gas, mineral water, volcanic emissions, and water accumulated underground in mines. Since hydrogen sulfide is soluble in water and oil, it can sometimes flow away from the source along with water or oil, leading to accidental poisoning incidents. Route of entry: Hydrogen sulfide is rapidly absorbed through the mucous membranes, with very little absorption through the skin. Accidental ingestion of sulfide salts, which produce hydrogen sulfide when reacting with stomach acid, can be absorbed through the intestines and cause poisoning. Introduction to Toxicology: Hydrogen sulfide is a neurotoxin. It is also a asphyxiating and irritating gas. The main targets of its toxic effects are the central nervous system and respiratory system; damage to multiple organs such as the heart may also occur. The tissues most sensitive to this toxicity are the brain and the areas in contact with mucous membranes. Human inhalation of LCL0: 600 ppm/30M, 800 ppm/5M. Human (male) inhalation LCL0: 5700 ug/kg. Rat inhalation LC50: 444 ppm. Mouse inhalation LC50: 634 ppm/1H. In the body, hydrogen sulfide is mostly detoxified through oxidative metabolism to form thiosulfate and sulfate, with glutathione possibly playing a catalytic role in this metabolic process ； A small portion can be metabolized through methylation to form less toxic methylmercaptan and dimethyl sulfide, but high concentrations of methylmercaptan have an effect on the central nervous system. Metabolic products in the body are excreted in the urine within 24 hours, some are excreted in feces, and a small portion is exhaled through the lungs in their original form. It does not accumulate in the body. The target organs and mechanisms of acute toxicity of hydrogen sulfide can vary depending on its concentration and duration of exposure. The higher the concentration, the more pronounced the central nervous system depression; at relatively lower concentrations, mucosal irritation is significant. When humans inhale 70–150 mg/m3 for 1–2 hours, symptoms of irritation to the respiratory tract and eyes occur; after 2–5 minutes of inhalation, olfactory fatigue sets in and they can no longer detect the foul smell. Inhalation of 300 mg/m3 for 1 hour causes acute eye irritation symptoms within 6–8 minutes, while prolonged exposure leads to pulmonary edema. Inhalation of 760 mg/m3 for 15–60 minutes caused pulmonary edema, bronchitis, and pneumonia, as well as headache, dizziness, unsteady gait, nausea, and vomiting. Inhaling 1000 mg/m3 for a few seconds leads to acute poisoning rapidly; an accelerated breathing rate followed by respiratory paralysis results in death. Pathogenesis 1. High concentrations of hydrogen sulfide in the blood can directly stimulate the chemoreceptors in the carotid sinus and aortic area, leading to reflexive respiratory depression. 2. Hydrogen sulfide can act directly on the brain, with low concentrations having an excitatory effect ； High concentrations have an inhibitory effect, causing coma and paralysis of the respiratory and vasomotor centers. Since hydrogen sulfide is a potent inhibitor of cytochrome oxidase, it can bind to the trivalent iron ions in the oxidized form of cytochrome oxidase within the respiratory chain of the mitochondrial inner membrane, thereby inhibiting electron transfer and oxygen utilization, leading to a lack of oxygen inside the cells and causing cellular asphyxiation. Since brain tissue is most sensitive to hypoxia, it is the most vulnerable to damage. Both of these effects occur rapidly and can lead to respiratory arrest, resulting in a shock-like death. If exposure is stopped in a timely manner at the onset of the illness, many cases can recover rapidly and completely, likely due to hydrogen sulfide being quickly oxidized and inactivated in the body. 3. Secondary hypoxia is caused by a decrease in blood oxygen levels due to factors such as apnea or pulmonary edema induced by hydrogen sulfide; it can exacerbate the condition, prolong neurological symptoms, and lead to multiple organ failure. 4. Hydrogen sulfide decomposes upon contact with the moisture on the surfaces of the eyes and respiratory tract mucosa, and reacts with alkaline substances in the tissues to produce hydrosulfyl groups, sulfur and hydrogen ions, hydrogen sulfide, and sodium sulfide. These substances have a strong irritant and corrosive effect on the mucosa, causing chemical inflammatory reactions of varying degrees. Coupled with intracellular anoxia, this causes the most severe damage to deeper tissues and can easily lead to pulmonary edema. 5. The mechanism of myocardial damage, especially delayed damage, remains unclear. Acute poisoning presents with myocardial infarction-like symptoms, which may be caused by the direct effect of hydrogen sulfide leading to coronary vasospasm, myocardial ischemia, edema, inflammatory infiltration, and oxidative dysfunction within myocardial cells. The autopsy findings in cases of death due to acute hydrogen sulfide poisoning are often related to the duration of the illness; cerebral edema and pulmonary edema are common, followed by myocardial lesions. Generally, the corpse shows obvious cyanosis; a hydrogen sulfide odor is detected during dissection, the blood is fluid in consistency, and the internal organs appear slightly green. Cerebral edema is the most common; there are punctate hemorrhages, necrosis, and areas of softening in the brain tissue ； Degeneration of spinal nerve tissue is visible. Autopsy of electrocution-like deaths revealed non-specific asphyxia. Clinical manifestations: Acute hydrogen sulfide poisoning usually develops rapidly, presenting with clinical symptoms primarily related to damage to the brain and/or respiratory system; it may also be accompanied by dysfunction in organs such as the heart. Clinical manifestations can vary significantly depending on factors such as the concentration of hydrogen sulfide exposure. 1. Damage to the central nervous system is the most common: (1) Exposure to high concentrations of hydrogen sulfide can cause headache, dizziness, fatigue, ataxia, and mild disturbances in consciousness. Symptoms of irritation in the eyes and upper respiratory tract often appear first. (2) After exposure to high concentrations of hydrogen sulfide, encephalopathy becomes evident, with symptoms such as headache, dizziness, irritability, unsteady gait, restlessness, confusion, delirium, and epileptic seizures that may present as generalized tonic-clonic seizures ； Coma can occur suddenly ； Difficulty breathing or cardiac arrest may also occur following respiratory arrest. Fundus examination revealed papilledema in individual cases. Some cases may be accompanied by pulmonary edema as well. Symptoms of encephalopathy often appear earlier than those of respiratory symptoms. It may take some time due to mucosal irritation. (3) Exposure to extremely high concentrations of hydrogen sulfide can lead to electrocution-like death, that is, respiratory arrest occurs within a few seconds or minutes after exposure, and cardiac arrest can follow a few minutes later ； Coma can also occur immediately or within a few minutes, followed by respiratory arrest and death. Death can occur without any warning; loss of the sense of smell happens immediately when the smell of hydrogen sulfide is detected. In a few cases, an unpleasant sweet smell can be perceived in the moments before losing consciousness. There are usually no preceding symptoms before death; deep and rapid breathing may occur first, followed by the cessation of breathing. In cases of acute poisoning, unconsciousness usually occurs at the scene of the accident, with its severity varying depending on the concentration and duration of exposure to hydrogen sulfide; respiratory failure may or may not be present. Some patients recover as soon as they are removed from the accident scene or on their way to the hospital. Patients who still have vital signs when they arrive at the hospital, and who do not suffer from hypoxic encephalopathy, usually recover quickly. Those who have been in a coma for an extended period may experience headaches, dizziness, reduced vision or hearing, disorientation, ataxia, or epileptic seizures after recovery; the vast majority of cases recover completely. There have been reports of 2 cases of delayed encephalopathy; both patients regained consciousness 2 days after falling into a deep coma, became comatose again after 1.5 days and 3 days respectively, and regained consciousness again after 2 weeks and 1 month respectively. The central nervous system symptoms are extremely severe, while the mucosal irritation symptoms are not obvious; this may be because the exposure time was short and irritation symptoms have not yet developed ； Or it may attract attention due to severe systemic symptoms. In the early stages of acute poisoning, or in cases where there is only cerebral dysfunction without any morphological changes, patients show poor sensitivity to electroencephalography and brain imaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI). In contrast, abnormalities detected by single-photon emission computed tomography (SPECT)/positron emission tomography (PET) are well correlated with clinical manifestations and neuroelectrophysiological findings. For example, in one case, deep coma due to poisoning was followed by a decorticate state, and CT showed areas of reduced density in the bilateral globus pallidus. Head CT and MRI showed no abnormalities in another patient with toxic coma ； A PET scan performed 3 years after the accident showed abnormal metabolism in both temporal lobes, the areas beneath the parietal lobes, the left thalamus, and the striatum ； Half a year later, SPECT showed reduced blood flow in both globus pallidus regions, with no abnormalities in the cerebral cortex. The patient presents with decreased sense of smell, extrapyramidal signs, memory deficits, and other symptoms. Foreign reports describe 15 cases of individuals with a history of recurrent acute hydrogen sulfide poisoning presenting with symptoms such as fatigue, drowsiness, headache, irritability, anxiety, and memory loss. 2. Respiratory system damage: Chemical bronchitis, pneumonia, pulmonary edema, acute respiratory distress syndrome, etc., may occur. In a few cases of poisoning, the clinical manifestations are primarily pulmonary edema, with milder neurological symptoms. It may be accompanied by conjunctivitis. Keratitis. 3. Myocardial damage: During the course of poisoning, some cases may experience symptoms such as palpitations, shortness of breath, chest tightness, or angina-like symptoms ； In a few cases, myocardial infarction-like symptoms occurred 1 week after recovery from coma and improvement of toxic symptoms. The ECG shows a pattern consistent with acute myocardial death, but it can disappear quickly. Its condition is mild, the course of the disease is short, and the prognosis is good. The treatment methods differ from those used for myocardial infarction caused by coronary atherosclerotic heart disease; therefore, it is considered to be diffuse toxic myocardial damage. Myocardial enzyme profile tests may show abnormalities to varying degrees. The main criteria for diagnosing acute hydrogen sulfide poisoning are: 1. A clear history of exposure to hydrogen sulfide; the foul egg-like odor on the patient’s clothing and in their breath can serve as an indicator of such exposure. Hydrogen sulfide can be generated or detected at the accident site. It can be useful as a clue if the patient smelled an odor similar to rotten eggs before the onset of the illness. 2. Clinical features: Clinical manifestations primarily characterized by the aforementioned damage to the brain and/or respiratory system occur. 3. Laboratory tests: There are currently no specific laboratory test markers available. (1) An increased level of hydrogen sulfide or sulfides in the blood can serve as an indicator of absorption, but it does not correspond to the severity of poisoning; moreover, its half-life is short, so blood sampling must be conducted shortly after exposure ceases. (2) Urine thiosulfate levels may increase, but they can be affected by factors such as the timing of testing and the sulfur content in the diet. (3) Sulfhemoglobin (SHb) in the blood cannot be used as a diagnostic indicator, as hydrogen sulfide does not bind to normal hemoglobin to form sulfhemoglobin, and the latter is not related to the mechanism of poisoning ； Many studies have shown that there is no significant concentration of methemoglobin in the blood of humans and animals killed by hydrogen sulfide. (4) The sulfur content in the blood and tissues of corpses can be affected by factors such as corpse decay, which impacts its reference value. 4. Differential diagnosis: In cases of death resembling electrocution at the accident scene, it is necessary to differentiate from acute poisoning caused by other chemicals such as carbon monoxide or cyanide, acute cerebrovascular diseases, myocardial infarction, etc. It is also important to distinguish from asphyxiation resulting from exposure to an environment with high concentrations of chemicals such as methane or nitrogen that lead to oxygen deficiency in the air. Other symptoms must also be differentiated from similar diseases caused by other etiologies or injuries resulting from falls following coma. First aid measures: 1. On-site rescue is extremely important, as very high concentrations of hydrogen sulfide in the air can cause multiple deaths similar to electric shock at the scene. Timely rescue can reduce the mortality rate, decrease the number of people who need to be transferred to other hospitals, and alleviate the severity of the condition. The patient should be immediately removed from the area to a place with fresh air. Provide oxygen therapy immediately if possible. First responders at the scene should possess knowledge of self-rescue and mutual rescue to prevent them from being poisoned after entering the site. 2. Maintain vital signs. CPR should be performed immediately on those with respiratory or cardiac arrest. If artificial respiration is administered promptly to those who experience respiratory arrest at the accident scene, cardiac arrest that may follow can be prevented. When performing mouth-to-mouth resuscitation, the performer should avoid inhaling the patient’s exhaled air or hydrogen sulfide escaping from the patient’s clothing to prevent secondary poisoning. 3. Treatment is mainly symptomatic and supportive. Hyperbaric oxygen therapy plays an important role in accelerating the recovery from coma and preventing cerebral edema. All comatose patients, whether they have recovered or not, should receive hyperbaric oxygen therapy as soon as possible, but it must be combined with comprehensive treatment. For those with obvious symptoms of poisoning, adrenal glucocorticoids should be administered early, in sufficient doses, and for a short period of time; this helps to prevent and treat cerebral edema, pulmonary edema, and myocardial damage. For controlling seizures and preventing and treating cerebral edema and pulmonary edema, see and. Patients with more severe conditions require electrocardiographic monitoring and myocardial enzyme testing in order to detect any changes in their condition promptly and take appropriate action. For those with eye irritation symptoms, rinse immediately with clean water and provide symptomatic treatment. 4. There is no consensus yet on the indications and methods for using methemoglobin-forming agents. Theoretically, methemoglobin-forming agents are suitable for treating intracellular asphyxia caused by hydrogen sulfide, but they are ineffective against the reflexive respiratory depression in the nervous system. Appropriate use of isopentyl nitrite, sodium nitrite, or 4-dimethylaminophenol (4-DMAP) etc., oxidizes hemoglobin in the blood to methemoglobin; this latter can bind with free hydrothiol groups to form sulfmethemoglobin (SMHb), thereby enabling detoxification ； It can also seize the hydrosyl group bound to cytochrome oxidase, reactivating the enzyme to alleviate hypoxia. However, at present there are no simple and feasible indicators for determining intracellular asphyxia, and sulfides are rapidly oxidized and inactivated in the body; the use of the aforementioned drugs actually exacerbates tissue hypoxia. Methylene blue should not be used, as it is only at high doses that it can cause methemoglobin formation, and excessive doses lead to severe side effects. At present, the use of such drugs can only be determined based on a physician’s clinical experience. Standard workshop air hygiene standards: China’s MAC is 10 mg/m3; the U.S. ACGIH TLV-TWA is 14 mg/m3 (10 ppm), with a STEL of 21 mg/m3 (15 ppm)

Hydrogen sulfide is everywhere in refineries. Every operator must know which process in the workshop generates the most hydrogen sulfide, as well as which areas are prone to hydrogen sulfide leaks. This requires starting with basic technical knowledge, including an understanding of the properties of raw materials, the processing techniques, and the characteristics of hydrogen sulfide. Generally speaking. Hydrogenation units, catalytic cracking units, double desulfurization units (acid water and liquefied gas desulfurization), sulfur recovery units, delayed coking units, etc., are relatively dangerous. This post was last edited by redsun1 on 2009-4-16 14:47.]

Yes, hydrogen sulfide is extremely dangerous; just inhaling a small amount of it can be fatal. One of my colleagues almost lost his life during a maintenance task. That’s why we need to be extra careful in our daily work. When dealing with dehydration issues, we should stand in the upwind direction. In the event of a hydrogen sulfide leak, we must immediately put on gas masks or air respirators before entering the area – we shouldn’t try to handle the situation blindly, as that would only lead to worse consequences!

What was said upstairs is absolutely correct! Just a small inhalation of hydrogen sulfide can be fatal to us! Therefore, our equipment has a specific requirement: the dehydration process must be carried out by at least two people, who should stand in the upwind direction; it is essential to wear gas masks or air respirators when entering the area!

We had a hydrogen sulfide poisoning incident here, resulting in 3 deaths. We have an ethylene tank (which contains naphtha after hydrogenation); the internal floating roof of the tank was damaged, causing hydrogen sulfide gas to escape, which poisoned 5 people, 3 of whom died. It’s really scary!

As long as safety measures are properly implemented, hydrogen sulfide accidents can be prevented. It is advisable to install clear warning signs in areas with high levels of hydrogen sulfide; regular testing of the alarm devices on site should be carried out; field workers should be equipped with hydrogen sulfide alarms during their inspections; regular drills related to hydrogen sulfide accidents should be conducted to help employees learn safety precautions and enhance their awareness of safety

As long as everyone pays close attention and follows the operating procedures, there is generally no danger:loveliness:

I’ve worked in acidic water; to be honest, over time neither the managers nor I paid much attention to it. Once, I almost left it there. It is still necessary to improve the safety mechanisms from top to bottom; otherwise, there will be endless problems. This post was last edited by Refiner on 2009-4-17 17:31]

Our company has experienced several hydrogen sulfide poisoning incidents, but no deaths have occurred. We now attach great importance to hydrogen sulfide poisoning; for the discharge of catalyzed acidic gases and acidic water, an application must be submitted, a risk analysis must be prepared, and work must be carried out using positive-pressure air respirators, with at least two people present. So we haven’t had any accidents since then

A truly terrifying killer! Our company has also experienced several cases of hydrogen sulfide poisoning, but fortunately everyone was saved! It’s terrifying, but it’s preventable! Our company is placing increasing emphasis on management in this area. 1. Install hydrogen sulfide detection and alarm devices on-site. (Ensure regular maintenance and inspection) 2. Operators must carry portable hydrogen sulfide detectors when conducting on-site inspections. 3. To strengthen employee training, it is necessary to popularize knowledge related to hydrogen sulfide and raise awareness. 4. Conduct regular accident drills related to hydrogen sulfide leaks to improve emergency response capabilities and awareness. For reference only, sorry about that; P! !

It’s good that the original poster brought up this topic. One of my colleagues resolved an issue with the instruments at midnight, and then went on to deal with the level measurement in the reflux tank of the hydrogenation unit; unfortunately, he lost his life to hydrogen sulfide. It’s terrifying every time I think about it. This requires us to pay attention to it in our daily thinking, to practice more, and to truly learn how to use air respirators so that we can utilize them in dangerous situations to protect ourselves and our colleagues around us.

Our company recently experienced a hydrogen sulfide poisoning incident involving 6 people; fortunately, none of them are in life-threatening condition, but they will definitely suffer from some aftereffects. It’s quite terrifying to think about. It’s not about discovering and providing help quickly; in the blink of an eye, all 6 people can be gone.

If you walk by the river often, your shoes will get wet eventually. It’s useless to be afraid; one can still get injured while walking on the road. The key is to start with ourselves, improve our professional knowledge, eliminate potential hazards, and follow procedures strictly in order to minimize the likelihood of accidents.

It is essential to have a portable hydrogen sulfide detector – you cannot afford to skimp on this! Because the hydrogen sulfide concentration is high, no odor can be detected.

It is hoped that every operator will work in pairs, and every refinery worker should be fully aware of the severity of hydrogen sulfide

Hydrogen sulfide poisoning is extremely dangerous. One of our plant’s instrument technicians suffered an accident while repairing a level gauge, as a result of inhaling residual hydrogen sulfide; another technician also felt dizzy. Fortunately, prompt action was taken and no further incidents occurred. Everyone needs to be vigilant, after all, life is only once – if one person gets hurt, it can affect many others!

Our dry gas liquid separation tank needs to have its liquid removed on a daily basis; usually, the pressure from the dry gas is used to push the liquid back into the gasoline tank. Some colleagues, in order to save trouble, simply discharge the liquid into the sewer system. When liquid is removed, hydrogen sulfide levels rise sharply, triggering alarms, and I’m very worried that an accident might occur. The leaders never know, because they rarely spend time with the workers. Very bureaucratic. This post was last edited by Refiner on 2009-4-25 10:53]

To strengthen safety management, it is necessary to have a sense of safety, safety knowledge, safety warning devices, and an emergency plan in case of safety incidents. Life is the most important thing. I have been to some oil refineries in Shandong, and the entire plants were filled with a foul smell reminiscent of rotten eggs; I wonder what the plant managers were thinking. Respecting life, maintaining family harmony, and ensuring social peace – I support the original poster for raising this topic.