What is the hydrogen sulfide content in catalytically stabilized gasoline? What are the effects of long-term exposure on the body?

The hydrogen sulfide content in gasoline varies from a few ppm to several thousand ppm. 1. Physical and chemical properties of hydrogen sulfide: Hydrogen sulfide (H2S) primarily comes from waste gases generated during production processes or in daily life. Hydrogen sulfide is a colorless gas with a rotten egg odor. Its molecular formula is H2-S, with a molecular weight of 34.08 and a relative density of 1.19. Its melting point is -82.9°C and its boiling point is -61.8°C. It is soluble in water, forming hydrosulfuric acid, which is a weak acid. It is also soluble in alcohols, petroleum solvents, and crude oil; its upper flammability limit is 45.5%, the lower limit is 4.3%, and its ignition point is 292°C. It has unstable chemical properties and is prone to burning and exploding in air. 　　2. Enterprises that may pose a hydrogen sulfide hazard Petroleum contains a certain amount of sulfur, and hydrogen sulfide is generated during the heating and decomposition process. In oil with a high sulfur content, large amounts of hydrogen sulfide gas can be released during extraction ； 　　Hydrogen sulfide is absorbed rapidly through the mucous membranes, with very little absorption through the skin. If sulfur-containing salts are ingested by mistake, hydrogen sulfide is produced upon reaction with stomach acid, which can be absorbed through the intestines and cause poisoning. 　　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. 　　Acute hydrogen sulfide poisoning generally develops rapidly, presenting with clinical manifestations primarily characterized by damage to the brain and/or respiratory system, and 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. Central nervous system damage 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 usually appear first. 　　② After exposure to high concentrations of hydrogen sulfide, encephalopathy is the prominent manifestation, 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 cessation of breathing may also lead to the stoppage of the heartbeat. 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 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 failure 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 precursor 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 leave 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, tend to recover more 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 revival; 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 appeared ； Or it may draw 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 anatomical 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. 　　(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 pain ； 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. 　　3. Symptoms of poisoning: Hydrogen sulfide has irritant and cytotoxic effects; however, due to its strong systemic toxicity, the onset of symptoms is rapid. At lower concentrations of hydrogen sulfide inhaled, noticeable irritation occurs, while at higher concentrations, the olfactory nerve endings become paralyzed, which results in the disappearance of the characteristic odor of hydrogen sulfide. Subsequently, coma may set in, and death can even occur. 　　Mild poisoning: Exposure to lower concentrations of hydrogen sulfide (70–150 mg/m3) results in obvious irritation symptoms of the eyes and upper respiratory tract, such as eye pain, tearing, photophobia, eyelid spasms, blurred vision or halos around lights, nasal discharge, coughing, chest pain, tightness in the chest, nausea, etc ； There are also gradually worsening systemic symptoms, such as dizziness, headache, fatigue, palpitations, difficulty breathing, profuse cold sweats, and even fainting. 　　At this point, moving the patient to a place with fresh air can help relieve the symptoms on their own, but systemic symptoms such as headache and fatigue take several days to subside. 　　Moderate poisoning: When exposed to higher concentrations of hydrogen sulfide (300–600 mg/m3), chemical pneumonia and chemical pulmonary edema can occur. The patient experiences increased symptoms such as difficulty breathing, chest tightness, shortness of breath, palpitations, headache, dizziness, and nausea, and quickly falls from a state of confusion into coma. On physical examination, the patient appears pale or cyanotic, with cold and wet skin; they are unconscious, have shallow and rapid breathing, a weak and rapid pulse, dull heart sounds, and dry or wet rales can be heard in the lungs ； Blood pressure may be normal or elevated at first, and then decline ； The pupils are often dilated, and various physiological reflexes are weakened or absent ； Body temperature rises. 　　Severe poisoning: It is caused by inhaling high concentrations of hydrogen sulfide (above 700 mg/m3). In severe cases, victims may fall unconscious within seconds of inhalation, in a manner similar to an electric shock; this can even lead to paralysis of the respiratory center and death. Patients often present with deep coma, generalized spasms or rigidity, incontinence of urine and feces, and cold, cyanotic skin. 　　The pupils are dilated or constricted; all physiological reflexes are absent. Breathing is shallow, rapid, and irregular, with scattered moist rales audible in the lungs. The heart sounds are weak, and the heart rate is fast and irregular ； Muscle tone is often increased. Patients in this stage often have multiple comorbidities, such as pneumonia, pulmonary edema, cerebral edema, acidosis, shock, myocardial injury, and liver and kidney damage. Treatment is difficult, and recovery may be accompanied by sequelae such as neurasthenia, autonomic nervous system disorders, and sexual dysfunction. 　 The hydrogen sulfide concentration in the air of workplaces where hydrogen sulfide is handled must be measured regularly. The health standard is 10 mg/m3.

The hydrogen sulfide content in catalytically stabilized gasoline is not clear, but someone died at the sampling point for stabilized gasoline here; it happened a few years ago, and after that all sampling cabinets were removed

Here, we take samples of regular gasoline from open openings, and there have never been any problems with that

What is the proportion of hydrogen sulfide and organic sulfur in gasoline?

Open sampling port; no problems have occurred. Be careful to stay upwind during sampling.

I have never heard of or read any reports of accidents caused by poisoning resulting from stable levels of sulfur in gasoline. Now some experts are recommending the use of sealed sampling devices; perhaps this is for that reason. In my opinion, the greatest hazard associated with exposure to gasoline is benzene contained within it

H2S needs to be guarded against, but there is no need for excessive concern. Most oil processing processes involve H2S to some extent, the difference being just the quantity. A large amount of H2S is present in dry gas; LPG contains a small amount of H2S as well as substances such as thiols and sulfur compounds. In gasoline and diesel, there is very little H2S, with most of it being substances like thiols and sulfur compounds. In fact, H2S is present in crude oil~~~

With daily sampling, I have never heard of any accidents caused by hydrogen sulfide in gasoline; a sealed sampler is currently being developed.

Based on the changes in sulfur content in the properties of the raw materials, the sulfur content of the stabilized gasoline also changes accordingly. Hydrogen sulfide is a highly toxic substance, and such accidents have occurred in many refineries.