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Oil, also known as crude oil, is a mixture of various liquid hydrocarbons. The main components are carbon, hydrogen, nitrogen, sulfur, and oxygen, along with trace amounts of elements such as phosphorus, iron, and magnesium. Oil extraction is a complex process that involves a series of steps such as exploration, development, drilling, and oil production. During the oil production process, additional services such as well logging, testing, fracturing, and well maintenance are also required. The work cycle is long, difficult, and highly dangerous. At the same time, during oil extraction, when oil vapor mixes with air, in addition to posing a high fire risk, it also generates various gases that are toxic to humans, such as carbon monoxide, hydrogen sulfide, sulfur dioxide, nitrogen dioxide, and other such gases. Next, we will briefly explain these aspects to you, including the physical and chemical properties of these gases, routes of exposure, first aid measures, and preventive actions. Physical and chemical properties of carbon monoxide: Pure carbon monoxide (CO) is a colorless, odorless, and non-irritating gas. Molecular weight is 28.01, density is 0.967 g/L, freezing point is -207°C, and boiling point is -190°C. Its solubility in water is very low, but it is soluble in ammonia. The air-mixing explosion limit is 12.5%–74%. Occupational exposure CO gas can be produced whenever carbon-containing materials burn incompletely. There are over 70 types of tasks in industrial production that involve exposure to CO, such as coking, iron smelting, forging, casting, and heat treatment in the metallurgical industry ； Production of ammonia, propylene, phosgene, and methanol in the chemical industry ； Mine blasting and coal mine gas explosion accidents ； During the oil extraction and production process ； Manufacturing of carbon graphite electrodes ； Internal combustion engine testing ； All may be exposed to CO. **Or **the gases after the explosion contain about 30% to 60% CO. The exhaust gases from internal combustion engines that use diesel or gasoline also contain about 1% to 8% CO. Clinical manifestations after poisoning 1. Acute poisoning Acute carbon monoxide poisoning is the most common acute occupational poisoning in China in terms of incidence and mortality. CO is also one of the most lethal poisons in many **accidental cases of occupational poisoning. The occurrence of acute CO poisoning is related to the concentration and duration of CO exposure. The maximum allowable concentration of CO in workshop air in our country is 30 mg/m3. Evidence shows that when the CO concentration reaches 292.5 mg/m3, it can cause severe symptoms such as headaches and dizziness ； When the CO concentration reaches 1170 mg/m3, inhaling more than 60 mg can cause unconsciousness ； When the CO concentration reaches 11,700 mg/m3, it can be fatal within minutes. Symptoms such as headache, dizziness, palpitations, and nausea that occur after exposure to CO and disappear rapidly upon inhaling fresh air are considered to be normal exposure reactions. Those with mild poisoning experience severe headaches, dizziness, rapid heartbeat, blurred vision, weakness in the limbs, nausea, vomiting, irritability, unsteady gait, and mild to moderate disturbances in consciousness (such as confusion or a foggy state), but no coma. Several hours after leaving the poisoned area and breathing fresh air or oxygen, the symptoms gradually resolve completely. In patients with moderate poisoning, in addition to the aforementioned symptoms, there is flushing of the face, excessive sweating, a rapid pulse, and cognitive impairment manifesting as mild to moderate coma. Removing oneself from the poisoned area in a timely manner and receiving treatment allows for gradual recovery; generally, there are no significant complications or sequelae. In cases of severe poisoning, consciousness is severely impaired, resulting in a deep coma or a vegetative state. Pupillary constriction is common, with a normal or delayed light reflex; muscle tone in the limbs is increased, there is trismus, and incontinence of urine and feces may occur. As cerebral edema worsens, it manifests as persistent deep coma, a body temperature rising to 39–40°C, a rapid and weak pulse, low blood pressure, pale or cyanotic complexion, cold limbs, and tidal breathing. During the recovery from coma following treatment for severe poisoning, patients often exhibit restlessness, confusion, loss of orientation, or a loss of short-term and long-term memory. With aggressive rescue and treatment, most patients with severe poisoning can still recover completely. A few cases in a vegetative state presented with loss of consciousness, with eyes open but no speech. In patients with severe poisoning, hypoxic changes or complications in other organs may also occur. Severe myocardial damage or shock occurs ； In patients with concurrent pulmonary edema, wet rales are heard in the lungs along with difficulty breathing. 2. Effects of low concentrations of CO on the human body: Prolonged exposure to low concentrations of CO can have two types of effects on human health: (1) Nervous system: Symptoms such as dizziness, headache, tinnitus, fatigue, sleep disorders, and memory loss—characteristic of brain fatigue syndromes—are common; abnormalities can be detected through neuropsychological tests, and these symptoms usually resolve once exposure to CO is ceased. (2) Cardiovascular system: Based on survey data and combined with animal experiment studies, it is suggested that the cardiovascular system may be adversely affected by long-term exposure to low concentrations of CO. First aid measures: For patients with acute CO poisoning, they should be immediately moved to a place with fresh air, their collars loosened to keep the airways unobstructed, and they need to be kept warm. Their level of consciousness should be closely monitored. In cases of mild poisoning, oxygen inhalation can be used to alleviate symptoms while waiting for hospital treatment. Patients with moderate to severe poisoning should be promptly and actively transported to the hospital for treatment. Preventive measures: 1. In areas where CO may be generated, natural ventilation should be enhanced to prevent the accumulation of CO gas. 2. At each construction site, operational procedures must be strictly followed, and the concentration of toxic and harmful gases should be monitored regularly. When possible, a CO automatic alarm can be used. 3. When entering an environment with high CO concentrations, an oxygen-supplied gas mask must be worn for operations. 4. Prevention knowledge should be promoted to prevent incidents of CO poisoning in daily life. Physical and chemical properties of hydrogen sulfide: Hydrogen sulfide is a colorless gas. It has the smell of rotten eggs. Molecular formula: H2S. 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. Occupational exposure: Hydrogen sulfide is generated 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 tasked with removing garbage, waste, and feces, also have exposure to hydrogen sulfide. In addition, analytical chemistry laboratory workers can be exposed to this gas. Natural gas, mineral water, volcanic emissions, and water accumulated underground in mines often contain hydrogen sulfide as well. 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. 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. Clinical manifestations after 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. The target organs of acute toxicity and the mechanism of poisoning caused by hydrogen sulfide can vary depending on its concentration and duration of exposure. The higher the concentration, the more pronounced the central nervous system depressant effect; at relatively lower concentrations, the mucosal irritant effect 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 at 760 mg/m3 for 15–60 minutes leads to 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 quickly; respiratory paralysis occurs as a result of accelerated breathing, resulting in death. Acute hydrogen sulfide poisoning generally develops rapidly, presenting with clinical symptoms of poisoning characterized mainly by damage to the brain and/or respiratory system, and may also be accompanied by dysfunction in organs such as the heart. The clinical manifestations after poisoning can vary significantly depending on factors such as the concentration of hydrogen sulfide exposed to. 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 usually appear first. (2) After exposure to high concentrations of hydrogen sulfide, encephalopathy manifests itself through symptoms such as headache, dizziness, irritability, unsteady gait, restlessness, confusion, delirium, and epileptic seizures that may take the form of generalized tonic-clonic seizures ； Coma can occur suddenly ； Difficulty breathing or cessation of breathing may also lead to a stop in heartbeats. 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 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 sudden respiratory arrest. 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, 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. 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 attract attention due to severe systemic 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 those of pulmonary edema following poisoning, with milder neurological symptoms. It may be accompanied by conjunctivitis and 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. Myocardial enzyme profile tests may show abnormalities to varying degrees. 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 patients who need to be transferred to other hospitals, and alleviate the severity of the condition. The patient should be immediately removed from the scene to an area with fresh air. Provide oxygen therapy immediately if possible. First responders on site should possess knowledge of self-rescue and mutual rescue to prevent them from being poisoned after entering the scene. 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 scene of an accident, 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. For those with eye irritation symptoms, rinse immediately with clean water and provide symptomatic treatment. Preventive measures: 1. Ensure that the monitoring equipment is in good condition; those conducting monitoring in the downwind area must wear gas protection gear. Monitor the hydrogen sulfide concentration at all times during construction, and if the concentration exceeds the safe level, trigger an alarm immediately so that the workers can evacuate to a safe area promptly. 2. When measuring the liquid output from wells where hydrogen sulfide is present, the personnel performing the measurement must wear gas protection equipment. 3. The wellsite is reasonably arranged, with the duty room located on the upwind side. 4. When working on oil and gas wells containing hydrogen sulfide, sulfur-resistant wellheads and piping must be used. Physical and chemical properties of sulfur dioxide: Sulfur dioxide, also known as sulfurous anhydride, is a colorless, non-flammable gas with a strong, pungent odor. Molecular weight 64.07, density 2.3 g/L, melting point -72.7°C, boiling point -10°C. Soluble in water, methanol, ethanol, sulfuric acid, acetic acid, chloroform, and ether. It mixes easily with water to form sulfurous acid (H2SO3), which is then converted into sulfuric acid. At room temperature and pressures of 392.266–490.3325 kPa (4–5 kg/cm2), it is a colorless flowing liquid. Occupational exposure: Workers involved in tasks such as burning sulfur-containing fuels, smelting sulfide ores, burning sulfur, producing sulfuric acid and sulfurous acid, vulcanizing rubber, refrigeration, bleaching, disinfection, fumigation for pest control, magnesium smelting, petroleum refining, and certain organic syntheses, as well as those working in related fields, may be exposed to it. Additionally, it is a component of common industrial waste gases and air pollutants. Sulfur dioxide is moderately toxic and has a strong irritant effect on the eyes and respiratory tract. Inhaling high concentrations of sulfur dioxide can cause laryngeal edema, pulmonary edema, and edema and/or spasm of the vocal cords, leading to asphyxiation. Clinical manifestations after poisoning: l. Acute poisoning. After inhaling sulfur dioxide, irritation symptoms of the conjunctiva and upper respiratory tract such as tearing, photophobia, blurred vision, a burning sensation and pain in the nose, pharynx, and throat, as well as coughing, occur promptly. In more severe cases, symptoms may include hoarseness, chest tightness, pain behind the sternum, severe coughing, palpitations, shortness of breath, headache, dizziness, fatigue, nausea, vomiting, and upper abdominal pain. On examination, there is congestion and edema of the conjunctiva of the eyes; small areas of whitened, burned-looking mucosa can be seen in the cartilaginous part of the nasal septum. Dry and wet rales are audible in both lungs. In severe cases, bronchitis, pneumonia, pulmonary edema may occur, and even paralysis of the respiratory center can happen; when the inhaled concentration reaches 5240 mg/m3, it immediately causes laryngospasm and laryngeal edema, leading to rapid death. Liquid sulfur dioxide that contaminates the skin or gets into the eyes can cause skin burns and necrosis of corneal epithelial cells, leading to white patches and scars. 2. Chronic effects. Prolonged exposure to low concentrations of sulfur dioxide can lead to a decline or even loss of the sense of smell and taste, headaches and fatigue, tooth erosion, chronic rhinitis, pharyngitis, tracheitis, bronchitis, emphysema, increased lung markings, diffuse pulmonary interstitial fibrosis, and a weakened immune function. First aid measures: 1. Immediately move the patient away from the toxic environment and expose them to fresh air or oxygen; administer nebulized inhalation of 2%–5% sodium bicarbonate + aminophylline + dexamethasone + antibiotics. Thoroughly rinse the conjunctival sac and the skin contaminated by liquid sulfur dioxide with saline or clean water. 2. For those who exhibit obvious irritation symptoms due to inhalation of high concentrations of sulfur dioxide but show no physical signs, close observation for at least 48 hours is required, along with symptomatic treatment. 3. Actively prevent and treat pulmonary edema by using glucocorticoids in adequate amounts for a short period of time at an early stage. Dimethicone antifoam can be used if necessary. 4. Symptomatic and supportive treatment. Preventive measures: 1. Operations must be carried out in strict accordance with the requirements for working with hazardous toxic gases, and appropriate personal protection must be used. The sulfur dioxide concentration should be monitored at all times during construction; the maximum allowable concentration of sulfur dioxide in the air is 15 mg/m3. If the sulfur dioxide concentration exceeds this limit, an alarm should be triggered immediately, and the construction workers must evacuate to a safe area promptly. 2. When working in wells containing sulfur dioxide, workers must wear gas protection equipment. 3. The wellsite is reasonably arranged, with the control room located on the upwind side; the wellhead and piping must be of sulfur-resistant types. 4. Persons with significant respiratory and cardiovascular diseases are prohibited from engaging in work related to sulfur dioxide. Physical and chemical properties of nitrogen oxides. Nitrogen oxides include a variety of compounds such as nitrous oxide (N2O), nitric oxide (NO), nitrogen dioxide (NO2), dinitrogen trioxide (N2O3), dinitrogen tetroxide (N2O4), and dinitrogen pentoxide (N2O5), among others. Except for nitrogen dioxide, all other nitrogen oxides are highly unstable; they turn into nitrogen dioxide and nitric oxide when exposed to light, moisture, or heat, with nitric oxide subsequently converting back into nitrogen dioxide. Therefore, in the occupational environment, what is encountered is a mixture of several gases commonly referred to as gun smoke (gas), primarily nitric oxide and nitrogen dioxide, with nitrogen dioxide being the dominant component. Nitric oxide (N0) is a colorless gas with a molecular weight of 30.01, a melting point of -163.6°C, a boiling point of -151.5°C, and a vapor pressure of 101.3 lkPa at -151.7°C. Soluble in ethanol and carbon disulfide; slightly soluble in water and sulfuric acid. Solubility in water: 4.7% (20°C). It is unstable and easily oxidized to nitrogen dioxide in air (2N0 + 02 → 2N02). Nitrogen dioxide (NO2) is a reddish-brown, pungent gas at 21.1°C; it appears as a dark brown liquid below 21.1°C. At temperatures below -110°C, it is a colorless solid; under pressure, it is dinitrogen tetroxide. Molecular weight 46.01, melting point -11.2°C, boiling point 21.2°C, vapor pressure 101.3 lkPa (21°C), soluble in alkalis, carbon disulfide, and chloroform, slightly soluble in water. It has relatively stable properties. Occupational exposure: Nitrogen oxides are encountered in various occupational activities, such as the production of nitric acid or the use of nitric acid for pickling metals; the manufacture of nitrocompounds like nitro**s, nitrocellulose, and picric acid, as well as the diazotization process of aniline dyes; and when organic materials such as wood chips and paper scraps come into contact with concentrated nitric acid. Explosions of nitro**s, as well as the combustion of nitrogen-containing substances and nitric acid, also generate large amounts of nitrogen oxide gases. Gases produced during satellite launches and rocket propulsion contain significant amounts of nitrogen oxide gases as well. During welding, sub-arc welding, gas cutting, and arc lighting, the high temperatures generated can cause oxygen and nitrogen in the air to combine to form nitrogen oxides; nitrogen oxides are also present in the exhaust gases emitted by automobile internal combustion engines. Clinical manifestations after poisoning: Acute nitrogen oxide poisoning primarily damages the respiratory system as its target organ. Based on the clinical manifestations after poisoning, it is classified as: 1. Acute mild poisoning. Generally, after a latency period of several hours to 72 hours following inhalation of nitrogen oxides, symptoms such as chest tightness, coughing, and phlegm production occur, along with mild headaches, dizziness, fatigue, palpitations, nausea, and fever. There is also mild congestion of the conjunctiva and nasopharynx, as well as scattered dry rales in the lungs. Chest X-rays may show enhanced lung markings or blurred edges of the lung markings. Blood gas analysis: When breathing air, the arterial oxygen partial pressure can be 1.33–2.66 kPa (10–20 mmHg) lower than the expected value. 2. Acute moderate poisoning. There is difficulty breathing, a feeling of tightness in the chest, an increase in coughing, expectoration or coughing up blood-tinged sputum. It is often accompanied by symptoms such as dizziness, headache, fatigue, palpitations, and nausea, as well as mild cyanosis. There are dry rales or scattered wet rales in both lungs. The total number of white blood cells in the blood is increased. Chest X-rays show decreased transparency in the lung fields, increased and disordered lung markings that appear as reticular shadows; there may also be localized or scattered punctate or patchy shadows, which can merge into patchy areas with blurred edges. Blood gas analysis: An arterial oxygen partial pressure greater than 8 kPa can only be maintained when low-concentration oxygen (less than 50%) is administered. 3. Acute severe poisoning. Severe poisoning is defined by the presence of any one of the clinical manifestations following the following poisoning. (1) Pulmonary edema: respiratory distress, increased coughing, production of large amounts of white or pink frothy sputum, and significant cyanosis. Dry and wet rales can be heard in both lungs. Chest X-rays show scattered patchy shadows with low density and blurred edges in both lungs, or flocculent shadows of varying sizes; some of these shadows merge together to form larger areas of opacity. It may be accompanied by complications such as pneumothorax and mediastinal emphysema. Blood gas analysis: With inhalation of high-concentration oxygen (greater than 50%), the arterial oxygen partial pressure is less than 8 kPa (60 mmHg). (2) Coma or asphyxia. (3) Acute respiratory distress syndrome. 4. Delayed obstructive bronchiolitis: About 2 weeks after inhaling nitrogen oxide gases, without obvious acute poisoning symptoms or during the recovery phase from pulmonary edema, sudden coughing, chest tightness, progressive dyspnea, and significant cyanosis occur. Dry and wet rales or fine moist rales can be heard in both lungs. A chest X-ray shows miliary shadows throughout both lungs. Prolonged exposure to low concentrations of nitrogen oxides (above the maximum allowable concentration) can cause bronchitis and emphysema. First aid measures: 1. The patient should be quickly removed from the site of poisoning, kept warm, and allowed to rest in a quiet place. Those with breathing difficulties are given oxygen and receive necessary emergency treatment. 2. Those in close contact with nitrogen oxides should be monitored for 24–72 hours, with attention paid to any changes in their condition, and appropriate symptomatic treatment should be provided. 3. Actively prevent and treat pulmonary edema; pay attention to keeping the airways unobstructed and cooperate with the hospital’s treatment. Preventive measures: 1. Reform the manufacturing process and improve ventilation and exhaust systems to keep the concentration of nitrogen oxides in the air below the **specified maximum allowable level. 2. Regularly maintain the equipment to reduce occurrences of leaks and other issues, and strictly adhere to safety operating procedures. 3. Enhance awareness of personal protection, such as wearing air-supplied respirators as needed. 4. Individuals with severe respiratory diseases such as chronic bronchitis, emphysema, bronchitis, asthma, bronchiectasis, pulmonary heart disease, as well as serious cardiovascular diseases, should not engage in work involving nitrogen oxides. Physical and chemical properties of ozone: Ozone (O3) is a colorless gas with a distinctive odor. Molecular weight 48. Density is 1.65 g/cm3, melting point is -193°C, and boiling point is -112°C. 0.494 ml dissolves in 100 ml of water (at 25°C). Short-wave light radiation can convert oxygen in the air into ozone. Occupational exposure: Trace amounts of ozone are present in normal air. In production processes, such as the discharge process in high-voltage electrical equipment, powerful ultraviolet lamps, carbon rod arcs, electric sparks, and light emission from spectral analysis, trace amounts of ozone are generated. Ozone is also produced during welding and cutting processes. In the aforementioned production process, if ventilation in the workplace is poor, an excessive accumulation of ozone can be harmful to human health. Additionally, ozone is also encountered in processes such as disinfecting drinking water with ozone, treating industrial wastewater, bleaching paper, and \"purifying indoor air in residential areas\". Clinical manifestations after poisoning: Short-term exposure to low concentrations of ozone primarily causes dryness in the mouth and throat, a feeling of tightness under the sternum, chest discomfort, coughing, and production of sticky phlegm. Chest pain can last for 2 days, along with drowsiness or insomnia, headaches, difficulty concentrating, reduced analytical abilities, abnormal taste sensations, loss of appetite, fatigue, and weakness. There are also changes in lung function. Inhaling high concentrations of ozone for a short period of time can immediately cause mucosal irritation symptoms; after a few hours of incubation period, signs of pulmonary edema may gradually appear, with the progression of the condition being similar to that of nitrogen oxide poisoning. Long-term inhalation of low concentrations of ozone can cause bronchitis, bronchiolitis, emphysema, and pulmonary sclerosis. First aid treatment: It should be carried out in accordance with the treatment principles for toxic exposure to irritant gases, with a focus on preventing and treating pulmonary edema as early as possible. Preventive measures: Reform the manufacturing process, such as by using automatic welding; ensure comprehensive ventilation and local exhaust systems in the production areas. Strengthen individual protection, such as wearing gas masks. This post was last edited by lhm217561 on 2009-3-3 09:17.]