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The physicochemical properties of appearanceProperties: colorless: gas smell pungent odor: have a rotten egg odor vapor pressure: 2026.5kPa/25.5 C flash: <-50 C: -85.5 C -60.4: boiling point C solubility: soluble in water, ethanol. Water soluble called hydrogen sulfate (hydrogen sulfide and water solubility without reaction): 1:2.6 (water soluble) density: relative density (air =1) 1.19: H2S H2+S unstable stability, heating, reversible reaction conditions: risk markers: 4 (flammable gases) application: used for chemical analysis such as identification of metal ions
Health hazards
Pathways: inhalation
Health hazards: This product is a nerve poison strong, have a strong stimulating effect on the mucosa.
Toxicology information and environmental behavior
Acute toxicity: LC50618 mg / m3 (inhalation in rats)
Subacute and chronic toxicity in rabbit: inhalation of 0.01mg/L, 2 hours / day, 3 months, the central nervous system caused by the change of function, trachea, bronchial mucosa irritation symptoms, pathological changes of the cerebral cortex. Mice exposed to Low Concentration Fluorine vulcanization, a small airway damage.
Source: hydrogen sulfide rarely used in industrial production, generally as a result of certain chemical reactions and protein decomposition and some natural ingredients and impurities, and often exist in a variety of production process and nature. Such as mining and smelting of nonferrous metals. Low temperature coking coal, sulfur oil, refining, rubber, leather, dyes, sugar and other industries have produced hydrogen sulfide. The excavation and renovation of marshes, ditches, printing and dyeing, sewers, tunnels and garbage removal, feces and other operations, as well as natural gas, volcano, jet spa is often accompanied by hydrogen sulfide is present.
Hazardous characteristics: flammable, mixed with air can form explosive mixtures, in case of fire, high heat combustion caused the explosion. With concentrated nitric acid, fuming sulfuric acid or other strong oxidants react violently, explosion. The gas is heavier than air, to a far place in the lower spread, met the fire will cause backdraft.
Combustion product: sulfur dioxide (decomposition).
Chemical formula: 2H2S+3O2==2H2O+2SO2 (O2 2H2S+O2==2H2O+2S (O2) excess)
Emergency monitoring methods
The portable gas detection instrument: hydrogen sulfide detector, Coulomb hydrogen sulfide gas sensitive electrode detector;
The rapid chemical analysis method commonly used: lead acetate test tube method, lead acetate paper indicator method "emergency treatment and monitoring of environmental pollution accidents and disposal technology of the" million too ed.
The gas measuring tube (Beijing Institute of labour protection products, Draeger Company products)
Environmental standard
Chinese (TJ36-79) the maximum allowable concentration of harmful substances in the air of workplace: 10 mg / m3
China (TJ36-79) the maximum allowable concentration of harmful substances in air of residential areas: 0.01 mg / m3 (a value)
Chinese (GB14554-93) standards for odor pollutants plant (mg / m3): level 0.03 level two; 0.06 to 0.10; three from 0.32 to 0.60
China (GB14554-93) emission standards for odor pollutants: 0.33 ~ 21kg/h
Emergency treatment and disposal methods
A leak, emergency treatment
Leakage of contaminated areas to evacuate personnel to windward, and immediately isolated, small leakage isolation 150m, large leakage isolation 300m, restricted access. Cut off the fire. Recommended emergency personnel wear self positive pressure respirator, wear protective clothing. From the windward entered the scene. As far as possible to cut off the source of leakage. Reasonable ventilation, accelerated diffusion. A spray of water dilution, dissolved. To build a large number of wastewater barrierpit to contain the. If possible, the hood will be residual gas or leak gas exhaust fan to the washing tower or connected to the tower inside. Or make it by ferric chloride aqueous solution, the pipeline loading check device to prevent the solution suck back. Leaking vessels shall be properly handled, repair, inspection and.
Two, protection measures
Respiratory protection: exceed the standard concentration in air, a transition type mask (half mask). Emergency rescue or evacuation, recommend wearing oxygen respirator or air respirator.
Eye protection: wear chemical safety goggles.
Body protection: wear anti-static overalls.
Hand protection: wear chemical protective gloves.
Other: work site smoking, eating and drinking. After work, take a shower. Timely change of clothing. Workers should learn to self-help and mutual aid. Enter the tank, confined space or other area of high concentration of work, must have a person.
Three, first aid measures
Skin contact: remove contaminated clothing, wash with water. Medical treatment.
Eye contact: immediately filed eyelid, with plenty of liquid water or saline rinse thoroughly for at least 15 minutes. Medical treatment.
Inhalation: remove to fresh air. To maintain airway patency. If breathing is difficult, give oxygen. If breathing stops, namely artificial respiration. Medical treatment.
Fire extinguishing method: all personnel must wear fire protective clothing. Cut off the gas supply. If you can not immediately cut off the gas supply, are not allowed to go out of gas burning. Water cooling containers, if possible containers from fire to open. Extinguishing agent: water spray, foam, carbon dioxide, dry powder.
Chemical property
Unstable:
H2S=H2+S (heating, reversible)
Acid:
H2S water solution is called hydrogen sulfate, a dicarboxylic acid.
2NaOH+H2S=Na2S+2H2O
Reduction:
H2S S is the -2 price, has the strong reducibility, it is easy to be SO2, Cl2, O2 oxidation.
Combustible:
Light generates sulfur dioxide and water in the air: 2H2S + 3O2 = 2SO2 + 2H2O (blue flame) (lit. If the condition is not enough air) or low temperature will generate elemental sulfur and water.
The clinical manifestations of poisoning
The general incidence of acute hydrogen sulfide poisoning quickly, appear in the brain and (or) the clinical symptoms of the respiratory system damage, can also be accompanied by heart and other organ dysfunction. The clinical presentation may be due to the concentration of hydrogen sulfide and contact factors was different.
The 1 most common central nervous system damage
(1) exposure to high concentrations of hydrogen sulfide can occur after the headache, dizziness, weakness, ataxia, mild disturbance of consciousness can occur. Often appear first eye and upper respiratory tract irritation.
(2) after exposure to high concentrations of hydrogen sulfide in encephalopathy showed noticeable, headache, dizziness, irritability, irritability, gait, confusion, delirium, epileptic seizures showed generalized tonic clonic seizure; sudden coma; can also have difficulty breathing or stop after cardiac arrest. Fundus examination showed individual cases with papilledema. Some patients may be accompanied by pulmonary edema.
Encephalopathy symptoms often appear more respiratory symptoms as early. May be due to the occurrence of mucosal stimulation requires a certain time.
(3) contact high concentrations of hydrogen sulfide after death occurred in shock like, i.e. contact within seconds or minutes after respiratory arrest, a few minutes can occur after cardiac arrest; also can immediately or within minutes of coma, and died of respiratory poly stop. Death can occur in the case when no alert, aware of hydrogen sulfide odor immediately when the smell is lost, a few cases in a coma can smell sweet moments before the turn one's stomach. Before the death of general non premonitory symptoms, can appear breathing deep and fast, then stop breathing together.
At the scene of the accident occurred coma acute poisoning, the degree of contact due to the hydrogen sulfide concentration and time vary, even with or without respiratory failure. In some cases, from the scene of the accident or transferred to hospital on the way to recovery. Still maintain vital signs when they get to the hospital patients, such as hypoxic encephalopathy, more rapid recovery. For a long time in coma after resuscitation can have have a headache, dizziness, vision or hearing loss, disorientation, ataxia or epileptic seizures, most cases can be fully restored. There have been reports of 2 cases of delayed encephalopathy, were in deep coma after 2 days of recovery, respectively at 1.5 days and 3 days respectively in the recovery of coma again, and 2 weeks after January.
Very serious symptoms of central nervous system, and mucosal irritation symptoms is not obvious, may be due to the short contact time has not yet occurred, irritation symptoms; or because of severe systemic symptoms and easy to cause the attention of the.
Acute poisoning or only early brain dysfunction but no morphological changes in anatomical imaging such as computed tomography brain scan on EEG and brain (CT) and magnetic resonance imaging (MRI) of the poor sensitivity, and single photon emission computerized brain scan (SPECT) / positron emission scanning (PET) anomaly correlation with clinical manifestations and the good neural electrophysiological examination. Such as 1 cases of poisoning after a deep coma to the cortex, CT in the bilateral globus pallidus site had lower density range. The other 1 cases of poisoning coma patients with brain CT and abnormal MRI; in the accident 3 years after the examination of PET showed bilateral temporal lobe, parietal lobe, left thalamus, striatum metabolic abnormalities; six months after SPECT showed bilateral lentiform nucleus reduced flow, no abnormal cerebral cortex. Patients with olfactory dysfunction, extrapyramidal signs, memory defects etc..
Foreign reports 15 cases of recurrent acute hydrogen sulfide poisoning history after fatigue, drowsiness, headache, agitation, anxiety, memory loss and other symptoms.
2 respiratory system injury
There may be chemical bronchitis, pneumonia, pulmonary edema, acute respiratory distress syndrome. A few cases can be poisoning clinical manifestations of pulmonary edema, and neurological symptoms lighter. May be associated with conjunctivitis. Keratitis.
3 myocardial damage
In the course of poisoning, in some cases can occur palpitations, shortness of breath, chest tightness or anginal symptoms; in a few cases, symptoms of poisoning coma recovery improved myocardial infarction like 1 weeks after the performance. The ECG showed acute myocardial infarction like graphics, but may soon disappear. The illness is lighter, shorter duration, good prognosis, and treatment of coronary atherosclerotic heart disease caused by myocardial infarction, so it is considered as diffuse toxic myocardial damage. Myocardial enzyme examination can have different degrees of abnormal.
The diagnosis is based on acute hydrogen sulfide poisoning
1, dress and breath of patients with a history of exposure to hydrogen sulfide has definitely stinky smell can be used as indicators of contact. The scene of the accident can be produced or measured hydrogen sulfide. Patients before the onset of the smell of rotten eggs smell can be used as a reference.
2, clinical features: the brain and (or) the clinical manifestations of respiratory system damage.
3, laboratory examination: at present there is no specific laboratory examination indexes.
(1) hydrogen sulfide or sulfide content in the blood increased as the absorption index, but is not consistent with the severity of poisoning, and its half-life is short, so it needs blood in a short time after cessation of exposure.
(2) urinary thiosulphate content can be increased, but by the time and determination of sulfur content in diet and other factors.
(3) the sulfur in the blood hemoglobin (Sulfhemoglobin, SHb) cannot be used as a diagnostic index, because no hydrogen sulfide combined with normal hemoglobin to form sulfur hemoglobin, which has nothing to do with the poisoning mechanism; many studies showed that there was no significant hydrogen sulfide sulfur concentration of hemoglobin in human and animal blood to death.
(4) the body containing blood and tissues can be affected by factors such as body weight decay interference, affecting its reference value.
Differential diagnosis: 4, the scene of the accident occurred shock like death should be with other chemicals such as carbon monoxide, cyanide and other acute poisoning or acute cerebrovascular disease, myocardial infarction and phase identification, also need to enter the environment and with a high concentration of methane or nitrogen and other chemicals caused by hypoxia and asphyxia caused by air phase identification. Other symptoms should be similar with other diseases or coma causes falls after trauma identification.
Rescue workers in the event of hydrogen sulfide poisoning
Handle
The 1 scene is very important, because it contains high concentrations of hydrogen sulfide in air in the field often cause much shock like death, such as the timely rescue can reduce mortality, reduce hospital number reduce illness. Even if the patient should be from the scene to fresh air. When the condition is immediately given oxygen. The rescue workers should first aid knowledge, to prevent the rescue after entering the scene autotoxicosis.
2 maintain vital signs. The respiratory or cardiac stop immediately underwent poly cardiopulmonary resuscitation. On the occurrence of respiratory arrest at the scene of the accident such as timely implementation of artificial respiration, it can avoid the occurrence of cardiac arrest. In the implementation of the implementation of the mouth to mouth breathing when should prevent H2S inhalation exhaled gas or clothes escape, so as to avoid the two poisoning.
In 3, symptomatic and supportive therapy. Hyperbaric oxygen therapy to accelerate the recovery and prevention of cerebral coma water plays an important role, where the coma patients, whether or not the recovery, should be given hyperbaric oxygen therapy as soon as possible, but must comply with the comprehensive treatment. The symptoms of poisoning should be early enough, Ming, for short term glucocorticoid, is conducive to the prevention and treatment of cerebral edema, pulmonary edema and myocardial damage. The control and prevention of pulmonary edema and convulsions, cerebral edema, and see. The heavier patients in need of electrocardiogram and myocardial enzymes, so as to discover the changes of disease, timely treatment. For eye irritation, immediately rinse with water, symptomatic treatment.
4 on the application of High-speed Rail hemoglobin forming agent indications and methods: there is no consensus. Speak High-speed Rail hemoglobin from the theory of forming agent for treatment of hydrogen sulfide in cells caused by suffocation, and invalid on the nervous system reflex inhibition of respiration. The amount of application of amyl nitrite, sodium nitrite or 4- two methyl amino phenol (4-DMAP), the High-speed Rail hemoglobin oxidation in the blood, which can be combined with the formation of sulfur free sulfhydryl High-speed Rail hemoglobin (Sulfmethemoglobin, SMHb) and detoxification; and can capture sulfur hydrogen combined with cytochrome oxidase, the enzyme complex, in order to improve hypoxia. But the indicators currently no simple and feasible in judging cell asphyxia, and sulfide in vivo quickly oxidation and inactivation, the use of these drugs aggravate tissue hypoxia. Methylene blue (Mei Lan) should not be used, because of its large doses can make the formation of High-speed Rail hemoglobin, high doses have serious side effects. The use of these drugs only by physicians to determine the clinical experience.
[edit this paragraph] cell protective effect of hydrogen sulfide
Hydrogen sulfide (hydrogen sulfide, H2S) as a toxic gas at the same time, in recent years, more and more studies have found it widely exists in mammals, but also has an important role in protecting cells. It has been called the nitric oxide (nitrogen monoxidum, NO) and carbon monoxide (carbon monoxide, CO), the third gaseous signal molecule was found, it has many physiological functions of regulating blood pressure, diastolic blood vessels. The metabolic abnormalities associated with heart disease and hypertension and other cardiovascular diseases. Myocardial injury induced by H2S in hypoxia ischemia, the effect of increasing attention. Bliksoen et al reported, endogenous H2S can protect the heart against ischemia / reperfusion induced injury in rats. Bian et al also pointed out, H2S plays an important role in the adaptability of myocardial protection of ischemic preconditioning, the effect of H2S and the activation of protein kinase C and sarcolemmal ATP sensitive potassium channel (sarcolemmal ATP-sensitive K+ channel, KATP) on. On the other hand, the donor sodium hydrosulfide H2S (sodium hydrosulfide, NaHS) can promote the proliferation of rat myocardial cells. The results of the study show that, H2S plays an important role in physiological and pathophysiological processes in the regulation of myocardial. |
